Skip to main content

Full text of "You and Heredity"

See other formats

uspiadaas steele Sehe 
Srarepr eterna ante: 
Trelelyistetg ste bens 
+1 Banal 


Cotieserr ss 
Tee lp eins 


ibis eiclete! 
ebm ee gee gra ly 


Sree etite 

tel y as Ty heagheeoe and 

fog ririee rt 




ware more 


iv ay 



ritierttele eg 

Seni ya tates 


SF aes Oe PC TE OE 74 pe FO Fal HS oh 

aS Gris eaw ak 





ee eh 



eet ett 



Phage or ty 

sad 3 



SOS ml 

Beireeeetertrri see 


He Fat 


ig ees 

Sra ® 

so ph bal 



hes ta? 



tr eDew Es eels kgs 





plppige paws 

ierse pepe serss: 
sttesine sans 








PErteestare tetas 
papeer Sees 
. os Fi 
epi geteit® 
prcrsreseor ne 
rektrse nese 
> Tha? 
AO IED fa90 
{ates 15 es 




sa eo bee 

at Yee 



pi heS e 

S33 pha Stee 









ae Pere roe 



peri iie 

sats # Fee 

“Woe A rer 
SME Oe se 
Rita bi 



ae i 





ae ie 

went Sa AS 

rhe HES SEIS: 

Can Have ae 

Blond, aN Haired, Blue- pale, Children 

May Have Various Types of Children, 


(For Results of Other Matings, See Text) 

YOU and 


assisted in the genetic sections by 
MO RONG Deis GriW HIER) Ph.D: 



With four color-plates and seventy-five draw- 
ings, maps and diagrams 

Including an original study of The Inheritance 
of Musical Talent cite 

NENTS AY pat ge 

Garden City, New York Bp y | 



All rights reserved. No part of this 
work may be reproduced without the 
written permission of the publishers. 

H \/ JI3dO 

we, | 




GarDEN City Pus.isHiNnc Co. Reprint Edition, 1945, by special 
arrangement with J. B. LIPPINCOTT Co. 

Gh Ga \ 2 Printed in the United States of America 



Mosr books on scientific subjects addressed to the general public 
are written from the inside looking out—that is to say, from the 
viewpoint of the scientist looking out, and not infrequently down, 
to the reader. 

This book is written from the outside looking in—from the view- 
point of a layman peering into the laboratories of the scientists (in 
this case those concerned with the study of human heredity) and 
reporting back to others what he has seen, heard and learned. 

The two viewpoints differ in many respects, and especially is 
this true of the subject here dealt with. The scientist studying 
heredity is preoccupied chiefly with the processes by which the 
findings in his field were achieved and which pave the way for 
future discoveries. When, and if, he stops to consider the practical 
aspects of his science in relation to human life, he is inclined to 
think in terms of broad averages, of large masses and many gen- 
erations, and of individuals as mere fragments in a limitless mosaic. 

But the layman is interested primarily in himself and in the im- 
mediate application of the scientific findings to his own life and 
to his own little world which will come to an end when he 
passes on. 

The difference in viewpoints underlies the motivation and, I 
hope, the justification for this book. Had any scientist made easily 
available to me all the facts about human heredity which I wished 
to know, and which many years of writing for the general public 
have taught me that others wish to know, this book would never 
have been written, nor should I have had the temerity to think of 
writing it. When I began my study of the subject, it was solely with 
the practical purpose of utilizing some facts about human heredity 
in a projected work of fiction. Before very long I discovered that 
the findings in this field so completely shattered my own precon- 
ceived notions and the ideas held by all but an initiated few, as to 

obliterate my original plans. I became convinced that the most in- 


teresting and important task before me was to acquire as thorough 
a knowledge of this subject as I could and then, in some way, to 
communicate what I had learned to others. 

The subsequent steps included my enrolment (at a mature age; 
for a college course in genetics and the setting aside of all other 
activity for several years to devote myself to further study and re- 
search. The first fruits came with a series of articles on human 
heredity which I wrote for a popular magazine. These proved to 
my own satisfaction that the subject could be expounded to laymen 
without putting them through the technical mazes of meiosis and 
mitosis, the formation of spindle fibers and polar bodies, of linkage, 
cross-over, nondisjunction of chromosomes, tetraploidy, etc., all con- 
sidered essentials in almost every college course and treatise’ on 

From the articles grew the plan for a book, but even when the 
contract for it was signed with my publishers, nothing like the 
present work was contemplated. That it did grow to its present 
proportions was due to many factors, not the least of which was 
the quite unexpected aid and encouragement given it by the very 
scientists and other authorities who, I had feared, would look 
askance at such a project undertaken by one outside their fold. 

Thus, well aware that a layman writing on a scientific subject 
must, like Caesar’s wife, be~or try to be—above suspicion, I am 
heartened by the thought that in every phase of this book I have 
had expert counsel and guidance, and that, as a happy consequence, 
my acknowledgments of indebtedness are many. 

In my toddling steps I was aided by Dr. Henry J. Fry of the 
New School For Social Research. Later, as the necessity for an ac- 
tive scientific associate grew imperative, through the friendly offices 
of Prof. Donald C. Lancefield, then of Columbia University and 
now of Queens College, I was brought in touch with Dr. Morton 
D. Schweitzer of the Cornell University Medical College. 

Dr. Schweitzer’s participation in this enterprise proved one of 
the happiest events that could have befallen it. To him fell the task 
of gathering most of the material for the chapters dealing with 
hereditary diseases and defects, and of preparing the data for the 
extensive “black” gene lists; of working out genetic ratios for the 


various “forecast” tables and other parts involving genetic pre- 
dictions; and in general, of casting a trained eye over all the facts 
and statements in the book coming within the scope of his knowl- 
edge as a geneticist. I can say unreservedly that without his en- 
thusiastic cooperation, painstaking research and meticulous editing, 
this book would have fallen short of such scientific validity as it 
may now possess. 

Because human genetics is correlated with all other sciences deal: 
ing with human beings, it was necessary to seek further for in- 
formation and counsel from physicians, sociologists, psychologists, 
anthropologists and various other experts. This aid was so gra- 
ciously and generously given wherever sought that every part of 
this book can be said to have had the benefit in its preparation of 
careful reading, discussion, criticism or editing by some qualified 
expert. With both pride and gratitude I therefore acknowledge my 
great indebtedness to the following: 

Prof. Lancefield, for reading all the first twenty chapters; Dr. 
George W. Henry, Associate Professor of Psychiatry at Cornell 
University Medical College, for reading and discussing “Sick 
Minds,” “The Twilight Sexes” and “Sexual Behavior”; Dr. Walter 
Bromberg, Senior Psychiatrist, Bellevue Psychiatric Hospital, and 
Psychiatrist of the New York Criminal Courts, for editing the afore- 
mentioned three chapters and “Enter the Villain”; Dr. Alfred J. 
Lotka, of the Metropolitan Life Insurance Company, for editing 
and aiding, with members of his staff, in the preparation of 
charts for “How Long Will You Live?”, and to Prof. Ray- 
mond Pearl, of Johns Hopkins University, for reading and dis- 
cussing that chapter; Dr. Dwight F. Chapman, of the Department 
of Psychology, Columbia University, for helpful criticisms and sug- 
gestions regarding “The Battle of the IQ’s” and “Personality”; Prof. 
Carl E. Seashore, of the University of Iowa, for reading “Musical 
Talent” and giving pertinent advice regarding the original study 
presented therein; Dr. Gene Weltfish, of the Department of An- 
thropology, Columbia University, for her suggestions regarding 
“Race” and her invaluable aid in the preparation of maps for that 
chapter; and to Frederick Osborn, Associate in Anthropology, 
American Museum of Natural History, for reading and discussing 

“Ancestry,” “The Giddy Stork,” “Eugenics: Negative” and “Pro- 

gram for Tomorrow.” 

(In all of these acknowledgments no responsibility is implied on 
the part of the individuals named for any errors of fact or judgment 
that may still have survived in the text. The responsibility for any 
failings of commission or omission, or for any opinions expressed 
in this book, I accept fully as my own.) 

On behalf of Dr. Schweitzer, as well as on my behalf, thanks are 
extended to the following who discussed with him special phases 
of disease inheritance: Dr. James Ewing, Director of the Memorial 
Hospital for the Treatment of Cancer; Dr. May Wilson, Associate 
Professor of Pediatrics at Cornell University Medical College (child- 
hood rheumatism); Dr. Eugene Opie, Professor of Pathology at 
Cornell (tuberculosis); and also to Drs. William Schmidt, Harold 
Aaron, Emanuel Klein, Nathan Kaliss and Emil Smith. 

Overseas our thanks go to Prof. J. B. S. Haldane of the University 
of London who, in editing this book for British publication, made 
many important suggestions by which we have profited. For several 
other corrections we may thank Prof. S. J. Holmes of the University 
of California. 

For discussion of problems relating to intelligence I am indebted 
to Prof. Gertrude H. Hildreth of Teachers College, Columbia 
University; Dr. Beth L. Wellman of the University of Iowa; Dr. 
Donah B. Lithauer, Psychologist of the Hebrew Orphan Asylum, 
New York; and Dr. I. Newton Kugelmass. 

Special thanks, which I am sure will be echoed by all music 
lovers, are due to the scores of musicians and singers who con- 
tributed data for the study of the Inheritance of Musical Talent, to 
their concert managements and personal representatives who aided 
in enlisting their cooperation, and to Ernest Hutcheson, President 
of the Juilliard Institute; also, for the auxiliary study of Voice 
Types, to Miss Rose Held and members of the Schola Cantorum. 

To Prof. Gregory G. Pincus and to the Anatomical Record I am 
indebted for permission to reproduce the photograph of the human 
ovum; to Dr. Seymour F. Wilhelm, of Beth Israel and Montefiore 
Hospitals, New York City, for the slide from which the spermato- 
zoa photograph was made; to Prof. Lewis M. Terman of Stanford 
University and to the McGraw-Hill Company, for permission to 


use material from “Sex and Personality”; and to the Macmillan 
Company for permission to quote from “Human Heredity,” by 
Baur, Fischer and Lenz. 

My memory has undoubtedly failed me with regard to others 
who have been of great help. Also, while I do not name them, mem- 
bers of my family and many friends know how deep is my grati- 
tude for innumerable services and considerate acts which con- 
tributed toward the production of this book. 

Finally, I wish to acknowledge my debt to all the many geneti- 
cists, scientists and research workers from whose painstaking 
studies I have gleaned, and in the conveyance of whose findings 
my role has been merely that of a reporter. It is my hope that 
the indebtedness will be repaid in some measure by. such added in- 
terest as this book may stimulate in their work. 

To acknowledge my great debt to my publishers would be 
superfluous, for the make-up of this book itself will speak for their 
faith in this enterprise and the unlimited support and encourage- 

ment which they gave it. 

New York City, 
June 1, 1939. 

n é a4 \ 
esas ¥ 
Se pach of 

As . i} 
Pie tate 

















EYE COLOR . : n : * 









3 I 
















PERSONALITY) soe Iho sn ae 




RACE (2s oR epee ask @ Bane Ver: 
ANCESTRY) 5" ntect ited Reanim Pala eat in 
THE ‘GIDDY (STORK its ae ee 
YOU ‘AND: HEREDITY 12 7) eee yk tee 
APPENDIX eMedia stu sics kloan CM a een 

INDEX . . . ° ° ¢ e e 






Parents and offspring (color plate). . . .  . Frontispiece 

The human egg and human sperms (from a photograph) 

The homunculus 

Fertilization i Hee 

Human dhiearmeree as hey radi nck if Ait it in pairs 

Human chromosomes, as they look under the microscope 

Genes, or section of chromosome 

The heredity process 

How a fertilized egg-cell aan 

How sperms are produced . 

Compatibility in mating 

F ingers representing chromosomes . 

“Finger” chromosomes in combinations . 


Fertilized human egg (eee) 

Relationship between mother and ide 

How sex is determined 

Our “chain-gangs” (chromosomes and genes) 

One of Mendel’s experiments with peas . 

Diagram of the eye 

What makes your eye color Ge plate) uirict paindeeeny 
What makes your hair color (color plate) . . . facing 
esin, color (color plate) — . genie eimirey joao) Yl facing 

How the “nose-bridge” gene works . 
Nose-shapes, “dominance” and “recessiveness” 
“Eye-shape” genes . 
“Hairdresser” genes 
Head shapes 






The laws of. chance 

Homely parents: beautiful child. Eanes Parente Herel 

child . 
How twins are produced 
How triplets may be precited” 
The Dionne quintuplets (diagram) . 
How the Dionne quintuplets were ed ced 
Tuberculosis and environment . 
“Sex-linked” inheritance 
Pattern baldness 
How baldness is inherited . 
The ductless glands 
Hand abnormalities 
Negro albinos (from a photograph) 
The human life span 
As incomes drop, deaths of Rabie rise 
Death and occupations . 
Females live longer! 
Oddities in sex 
How a gynandromorph may ae poner 
Human intersexes . 
“Black” gene symbols (Key to “Black” Gene Tables) 
Your blood type ; 
IQ’s of children in relavion't to father’ s status . 
IQ differences in twins, unrelated children, etc. . 
Kirsten Flagstad’s musical pedigree . 
The Toscanini family (diagram) 
How musical talent may be inherited 
Talent results from various matings 


The late Leopold Auer (from a sketch by the nisthor) bane 
Heredity or training? Samuel Reshevsky, chess champion 

(from a photograph) es 
The Dionnes (from a photograph) . 
Homicides—United States and other countries 








Raine “Map OritierWiited later ys a gure y tes) had 
Masculine and feminine characteristics (table) . . beats 
The “ink-blot” tests for “masculinity” and “femininity” .  . 313 
“Masculinity” and “femininity” in men and women by occu- 
Patlons aye. A aH Nh REAR AGRA 9) NITE 
Sex characteristics in fesike Sa ig ACA, MOR RE i ae i a be 22 
MCD Caincetiist’ Chickenlomer otro Mimrti le) pune lama eee 2b) 
SiierCVOLOLION OL Inala OPO pine Mmm nt, hy ide ee amanaceh 2a0 
he orci of races.( map yo... 0D A) Sp Rae ae AA 
The melting pots of Europe (series of Tee) . 344 
Birth, American: Culture, Chinese (from a Bho aay 
facing 354 
Oldiconceptopancesttvagn cer ape Wanna gars Hire by ital cite OR 
The Kallikak family tree... sla lay: cada Mri Ba 
The birth-rate “differential” aran\is SEE, ae RARNY henge 200 
Wittstemication comadraccomplish yin tal vol Glo mensiwnoen Wih 870 

Dest toler traits iy AVOMeTENae HU CR Vite, PW men ee Ale ME sey 

Behe dy, 

ee ee Wr aes oe 

Pee 6 oe 

ty coe i a WENA. aay A ats eae bi e ’ SL a 
yee ; a ny rg en Wate Se ; J 
has oar 1 be ast eRe TGR ok eee ee 
A } | prt (A i ip ‘ ‘ x i ae Me ' 
SRE Rb A veanter He oy cD re - 


~ e x ° 5 

Ehediiys Ra isan me Ce 

% tes ee 4 one nt uid! per pant bod. 
' a t Pd WB ee aes we a 


Srop and think about yourself: 

In all the history of the world there was never any one else exactly 
like you, and in all the infinity of time to come there will never be 

Whether or not you attach any importance to that fact, undoubt- 
edly you have often wondered what made you what you are; what 
it was that you got from your parents and your ancestors and how 
much of you resulted from your own efforts or the effects of en- 
vironment; and finally, what of yourself you could pass on to your 

Until comparatively recently, all this was a matter of theory and 
speculation. Not until the dawn of this century was anything 
definitely established about the mechanism of heredity, and for 
some years thereafter the most important points were bandied about 
like footballs among the biologists. Then, dramatically climaxing 
a series of some of the most remarkable experiments in all scientific 
history, the whole field of genetics (the study of heredity and 
variation among living things) became brilliantly illumined, and 
what had been theory became fact. 

With American geneticists, led by the Nobel Prize winner, 
~ Thomas Hunt Morgan, in the vanguard, the work has been pro- 
ceeding on many broad fronts throughout the world. New data are 
- pouring in with increasing volume from geneticists, pathologists, 
and other scientists. Experiments are repeated countless times, state- 
ments checked and rechecked. If the reader is inclined to be 
skeptical regarding some of the conclusions, let him be advised 
that no greater skeptics can be found than the geneticists themselves. 
Their rigid determination to take nothing for granted, and to 

subject the reports of even their most brilliant colleagues to the 


severest tests, has made genetics one of the most exact of all biologi- 
cal sciences. 

Thus it can be said with assurance that the mechanism of 
heredity—among humans as among other living and growing 
things—now stands clearly revealed. While all of its intricacies are 
by no means laid bare, the basic principles are as unmistakably 
clear as the workings of a watch. Problems of heredity that con- 
founded the greatest thinkers and scientists of the past, from 
Aristotle to Darwin, have been solved. Long-standing mysteries 
about birth and development have been unraveled. Endless popular 
beliefs, theories and superstitions have been completely discredited. 
Existing social philosophies have been called into question and the 
way pointed to a reconstruction of humanity itself. 

And yet, vitally important as all this is, very little of it has so far 
seeped through to the general public. If nobody believes in the 
stork any more, it is astonishing what people still do believe about 
heredity. The fault, however, is not that of the layman. Develop- 
ments in the field of genetics have been too rapid and recent to 
reach widespread circulation, and most of the published reports 
have been of so technical a nature as to have little appeal for the 
average reader. Even where isolated phases of the subject are popu- 
larly treated in newspapers and magazines, the layman is generally 
left confused through lack of sufficient understanding of the basic 

So we come to the purpose of this book, which is: 

1. To sift out from the genetics laboratories and research fields 
the outstanding facts about heredity directly applicable to human 

2. To present these facts in clear-cut, untechnical language, dia- 
grams and illustrations. 

3. To point out what their significance may be to the individual . 
and to society, leaving the reader to draw his own conclusions. 

The steps and processes by which these findings were arrived at 
will be largely omitted. It is assumed that you, the reader, do not 
care two raps about the love life of sea urchins or about the inter- 
action of hereditary factors for coat colors in mice, or what happens 
when a yellow-bodied Drosophila melanogaster (fruit-fly) with 


double-bar eyes and vestigial wings is crossed with a gray-bodied, 
long-winged, normal red-eyed one. True, without laborious study 
of these lowlier creatures the geneticists could never have arrived 
at the facts about human beings, for not the least of their amazing 
discoveries has been that the mechanism of heredity is almost the 
same in all living things. 

Nevertheless, the facts about the laboratory creatures can wait. 
What you probably wish to know, as directly as possible, are the 
answers to the innumerable questions about your own heredity and 
that of your fellow humans. These questions we hope have been 
anticipated and answered in the following pages. 

The fact has not been overlooked that many readers may already 
know more or less about the subject of heredity; but for the sake 
of the many others to whom this is all quite new, it is our plan 
to presuppose no previous knowledge whatsoever. And so, in the 
vernacular, we are going to start from “scratch.” 



A sperm and an egg: You, like every other human being and 
most other animals, began life as just that. 

A single sperm enters a single egg and a new individual: is started 
on its way. 

Leaving aside for the present the part played by the ie we 
know that a father’s rdle in his child’s heredity is fixed the moment 
that it is conceived. Whatever it is that the father passes on to his 
child must be contained within that single sperm. 

But to find out exactly what that sperm contains has not been so 
simple a matter. 

Consider, first, its size: 

One hundred million sperms may be present in a single drop 
of seminal fluid. Two billion sperms—two thousand million, as 
many as were needed to father all the people in the world today— 
could be comfortably housed in the cap of a small-sized tube of 

The microscope had to be well perfected before a sperm could be 
even seen. Then, in the first flush of discovery, carried away by 
their desire to believe, just as children and lovers imagine that they 
see a man in the moon, some scientists (circa 1700 a.D.) reported 
excitedly that every sperm contained a tiny embryonic being. With 
professional gravity they gave it the name of “homunculus” (little 
man), and scientific papers appeared showing careful drawings of 
the little being in the sperm—although there was some dispute as 
to whether it had its arms folded or pressed against its side, and 
whether or not its head had any features. 

Presently, however, it became apparent that imagination had run 
away with scientific perspicacity. The head of the sperm—in which 
interest rightfully centered, as the tail was merely a means for 


Photographed from a 
slide prepared by Dr. 
Seymour F. Wilhelm. 

Magnification about 
Behe same as egg 
above, showing rela- 
tive size of a single 
sperm compared 
with the humanegg. 



A two-day old un- 
fertilized human 
ovum, photograph- 
ed by Dr. Gregory 
G. Pincus. 

Magnification and 
enlargement about 
600 diameters, or 
millions of times by 

The black spot at 

upper center is the 
region of the nu- 


propelling it—proved to be a solid little mass that defied all attempts 
at detailed study. Even the great Darwin, who was so right about 
many things, could never more than guess at what the sperm head. 
_comprised—and his guess was a. wrong one. Many scientists thought 
it was hopeless to try to find out. Others concluded that if the 

sperm head itself could never be 
dissected and its contents exam- 
ined, they might still find out 
what it carried if they could 
learn what happened after it 
entered the egg. And in this 
they were right. 

Crowning years of painstak- 
ing study, we know at last that 
what a human sperm carries— 
the precious load that it fights 
so desperately to deliver—are 
twenty-four minute things called 

When the sperm enters the 

egg, and penetrates its substance, 
the head begins to unfold and 
reveal itself as having been 
made up of the twenty-four 
closely packed chromosomes. As 
they represent everything that 
enters the egg, we know beyond 
any doubt that these chromo- 




THE HOMUNCULUS (or Manikin) 
which early scientists believed was 
contained in the sperm. 

After drawings by 
(a) Hartsoeker—1694 
(b) Dalempatius—1699 

somes must comprise all the hereditary material contributed by the 


What of the egg? Although many thousands of times larger 
than the sperm, the egg is yet smaller than a period on this page, 
barely visible to the naked eye. Under the microscope we see 
that it consists largely of foodstuffs with the exception of a tiny 
globule, or nucleus. What that contains we see when the sperm 
head enters the egg and releases its chromosomes. Almost at the 
Same time, the egg nucleus breaks up and releases tts twenty-four 


similar chromosomes—the contribution ofthe mother to the child’s 

eee @ 
(A) Sperm-head enters egg (B) Sperm-head and nucleus 

of egg each release 
their chromosomes. 

Thus, the new individual is started off with forty-eight chromo- 

In order to reveal the otherwise colorless chromosomes special 
dyes have to be applied. When this is done, they appear as colored 
bodies. Hence their name “chromosomes” (color-bodies). 

But almost immediately another remarkable fact becomes ap- 
parent. We find that the chromosomes are of twenty-four different 
kinds as to shape, size, etc., with one of each kind contributed 

by each parent. If we could arrange all the pairs in a line they 
would look like this: 



How human chromosomes would look 
if arranged in pairs. 

These forty-eight chromosomes comprised all the physical heritage 
with which you began your life. 

By a process of division and redivision, as we shall see in detail 
later, these initial forty-eight chromosomes are so multiplied that 


eventually every cell in the body contains an exact replica of each 
and every one of them. This is not mere theory. If you were will- 
ing to lend yourself to a bit of dissection, an expert could: take 
some of your own cells and show you the chromosomes in them 
looking just about like those pictured here. 

As we viewed them up to this point, the chromosomes are in 
their compressed form. But at certain times they may stretch out 
into filaments ever so much 
longer, and then we find that 
what they consist of appar- 
ently are many gelatinous 
beads closely strung together. 

These beads either are, in 
themselves, or contain the 
paves wandstt ts-the genes 
which, so far as science can 
now establish, are the ultt- 
mate factors of heredity. Un- 
der the most powerful mag- 
nification, differences are ap- 
parent among these chromo- 
some sections in size, depth 
of shading, and patterns of 
striping. But whether or not 
differences are revealed to the eye, we know beyond any question 
that each gene has a definite function in the creation and develop- 
ment of the individual. 

Of all the miraculous particles in the universe, one can hardly 
conceive of anything more amazing than these infinitesimally tiny 
units. We say again “infinitesimally tiny” for want of another. and 
better expression. Think of the microscopic size of a sperm. Then 
recall that the head of a sperm alone contains twenty-four chromo- 
somes. And now consider that strung in a single chromosome might 
be anywhere from scores to hundreds of genes—with a single 
gene, in some cases, able to change the whole life of an’ indi- 
vidual! | 

To grasp all this you must prepare yourself for a world’ in 


As they look under the 


which minuteness is carried to infinity. Contemplating the heavens, 
you already may have adjusted yourself to the idea of an infinity 
of bigness. You can readily believe that the sun is millions of miles 
away, that stars, mere specks of light, may be many times larger 
than the earth; that the light from a star which burned up six 
thousand years ago, is reaching us only now; that there are bil- 
lions of stars in the space beyond space which our most power- 


A. Section of a chromosome Cy 
stretched out. The beads are & 
the genes or contain the ‘SS 
genes. ‘2 
O | 
4 C. The whole string, 
or chromosome, | 
B. The same section much compressed | 
with the genes and dyed, as it | 
drawn together. looks under the | 


ful telescopes cannot yet reveal. This is the infinity of bigness out- 
side of you. 

Now turn to the world inside of you. Here there is an infinity of 
smallness. As we trace further and further inward we-come to the 
last units of life that we can distinguish—the genes. And here 
with our limited microscopes, we must stop, just as we are stopped 
in our exploration of the stars by the limitations of our telescopes. 
But we can make some pretty good guesses about what the genes 
are from what we already know about what they can do. 

You believe the astronomer when he tells you that, on October 
26, in the year 2144, at thirty-four minutes.and twelve seconds past 
twelve o’clock noon there will be a total eclipse of the sun. You 
believe this because time and again the predictions have come 


You must now likewise prepare yourself to believe the geneticist 
when he tells you that a specific gene, which cannot yet be seen, 
will nevertheless at such and such a time do such and such things 
and create such and such effects—under certain specified condi- 
tions. The geneticist must make many more reservations than the 
astronomer, for genetics as a science is but a day-old infant com- 
pared to astronomy, and the genes are living substances whose action 
is complicated by innumerable factors. But despite all this, so much 
has already been established about our gene workings that we 
must stand in greater awe than ever at this latest revelation of 
how fearfully and wonderfully we are made. 


At conception received 
24 Chromosomes from Each parent 

or 48 in all 
22 In mating 
~ “4 Each passes 
—I on half OA 
\ Poea ixelrantres eye Te 
er, her J 
j a chromosomes ‘ 
d ait aGs f ay 
Be) axe 
IW We 
—> —7 <—— Cat 
Q vay | 

The FATHER'S role 24 (24 —The MOTHER, 

is merely that of SPs Wy although she also — 

passing on half eS Ye) acts as incubator — 
otf his Chromosomes AN a, and nourisher for 4 

by way of a les vy : the egg .con- 
cola “| These 48 chromo.[) SIVuSe> Re mores 
somes comprise co the child = 

heredity than 
ackareninea tee | doce ne Father 
heredity of 
the child 



No less important than knowing what heredity is, is knowing 
what it zs not. Before we examine the chromosomes and their 
genes in detail, let us first find out how the sperms or eggs which 
carry them are produced in the parent. That in itself will clear 
away much of the deadwood of the past with innumerable false 
theories, beliefs and superstitions about the life processes. 

Not so long ago the most learned of scientists believed that 
whatever it was that the sperms or eggs contained, these were 
products of the individual, in which were incorporated in some 
way extracts of themselves. That is to say, that each organ or part 
of a person’s body contributed something to the sperm or egg. 
Darwin, a proponent of that theory, called these somethings “gem- 
mules.” | 

By the “gemmule” theory, all the characteristics of both parents 
could be transmitted to the child, to be blended in some mysteri- 
ous way within the egg and reproduced during development. A 
child would therefore be the result of what its parents were at the 
time it was conceived. As the parents changed through life, so 
would their eggs or sperms, and the chromosomes in them, also 
change. All that is what scientists believed not so long ago, and 
what the vast majority of people today still believe—erroneously. 

The theory that sperms or eggs change as the individual changes 
has now been upset. Because we have learned finally that the 
chromosomes which they contain are not new products of the in- 
dividual and are most certainly not made up of “gemmules” or 
contributions from the various parts of the body. 

As we have seen, a human being starts life as just a single 
cell containing forty-eight chromosomes. That initial cell must be 

multiplied countless times to produce a fully developed person, 

12 YY O°U ASN(D2 EE REE Diletta 


(1) Original cell. (Only four (2) Each chromosome splits in 
chromosomes shown, for sim- half, lengthwise 
plification ) 


(3) The halved chromosomes go » (4) The halved chromosomes 
to opposite sides and wall grow to full size, resulting in 
forms between them as cell two cells, each a replica of 
begins to divide the original 

and this is accomplished by a process of division and redivision, as 
shown in the accompanying illustration. 

Continuing in the same way, the two cells become four, the 
four eight, and this goes on into the billions—the material with 
which to make the cells, after that in the egg is exhausted, 
coming from the mother. 

But the cells do not all remain the same, by any means. After 
the earliest stages, when they are still very limited in number, 
they begin “specializing.” Some give rise to muscle cells, some 
to skin, blood, brain, bone and other cells, to form different 
parts’ of the body. But a certain number of cells remain aloof. 

They take no part in building the body proper, and at all odds 

ee eee ee ee ee 


preserve their chromosomes unchanged and unaffected by any- 
thing that happens outside of them—short of death itself. 

These “reserve” cells are the germ cells, dedicated to posterity. 
It ts from these cells that the sperms or eggs are derived. 

When a boy is born, he already has in his testes all the germ 
cells out of which sperms will eventually be produced. When 
he reaches puberty, a process is inaugurated that will continue 
throughout his life—or most of his life, at any rate. In the same 
way that billions of cells grew from one, millions of more germ 
cells are manufactured from time to time by division and re 
division. Up to a certain point the process is the same as that pre. 
viously explained—but just before the sperms themselves are to 
be formed, something different occurs. The chromosomes in the 
germ cell remain intact and the cell merely splits in half, each 
half getting only twenty-four chromosomes, or one of every pair. 

The process of forming the sperms is illustrated on the following 
page (several stages omitted for simplification). This should make 
clear how, from a parent germ cell with the regular quota of forty- 
eight chromosomes, two sperms are formed, each carrying only 
twenty-four chromosomes. The reason and necessity for this “reduc- 
tion division” will be explained presently. 

Before we go on, let us stop to answer a question which has 
undoubtedly caused concern to many a man: 

“Is it true that the number of sperms in a man is limited, and 
that if he ts wasteful with them in early life, the supply will run 
out later?” 

No, for as we have seen, the sperms are made out of germ cells 
thrown off without decreasing the “reserve” stock. Endless billions 
of sperms can continue to be discharged from a man’s body 
(200,000,000 to 500,000,000 in a single ejaculation) and the original 
quota of germ cells will be there to provide more—so long as 
the reproductive machinery functions and the body can supply 
the material out of which to make them. (However, dissipation to 
an extreme point which might injure or weaken the body—and 
similarly, disease, accident, or old age—can curtail the produc- 
tion of sperms, or greatly reduce the number of those that are 


(1) Germ cell, containing forty-eight (2) The paired chromosomes sep- 
chromosomes arate, going to opposite sides of 
the cell, and the cell divides 

(3) There are now two half-cells, with . (4) The chromosomes mass to- 
only twenty-four single chromo- gether, and part of the cell con- 
somes in each tents forms a sheath around 


(5) The sheath shapes the chromosomes into a tightly packed 
mass forming the head. The rest of the cell contents is 
squeezed out behind to form the tail 



In the female, although the eggs are also manufactured out 
of germ cells, the process does not provide for an endless num- 
ber, running into billions, as in the case of the sperms. The 
female, when she reaches puberty, will be required normally to 
mature only one egg a month, for a period of about thirty-five 
years. So, when a girl baby is born, the fundamental steps in 
the process have already been taken, and the germ cells have 
already been turned into eggs. In other words, her ovaries at 
birth contain tiny clusters of all the eggs (in rudimentary form) 
which will mature years later. The chromosomes which she will 
pass on to her future children are, however, already present and 
will not be changed in any way. The maturing process will merely 
increase the size of the egg by loading it with a store of food 
material with which to start a new individual on its way. 

Although we can ignore the complicated details of the egg- 
formation process, it may be pointed out that before the eggs 
are formed from the germ cells there is a “reduction” division, 
just as there is in the case of the sperms. This gives each egg, 
like each sperm, only half of the parent’s quota of the chromosomes. 
But when the sperm, with its twenty-four single chromosomes, 
unites with the egg, with its twenty-four corresponding single 
_chromosomes, the result is an individual with two each of every 
chromosome—twenty-four pairs, or forty-eight, the required quota 
for a human being. 

If that reduction process hadn’t taken place, each sperm or egg 
would carry 48 chromosomes; on uniting they would start off an 
individual with 96 chromosomes; the next generation would begin 
‘with 192, and so on to an absurd and impossible infinity. However, 
this reduction division, it will soon be seen, has much more than 
a mathematical significance. 

One fact should be constantly kept in mind: Regardless of the 
differences in their processes of formation, the sperms or eggs 
receive chromosomes which are replicas of those which the parents 
themselves received when they were conceived. Nothing that hap- 
pened to the body cells of the parents throughout their lives could 
have been communicated to their germ cells so as to alter the genes, 
or hereditary factors, which their child would receive. 


Does this mean that a gene can never change? No, for as we 
shall see in a later chapter, a change (“mutation”) might take 
place at rare intervals in any given human gene, either spontane- 
ously or through some outside influence about which we know very 
little. But nothing that we ourselves do can change the make-up 
of our germ cells. 

It is as if, when Nature creates an individual, she hands over 
to him billions of body cells to do with as he wishes, and in 
addition, wrapped up separately, a small number of special germ 
cells whose contents are to be passed on to the next generation. 
And, because Nature apparently does not trust the individual, she 
sees to it that the hereditary factors in those germ cells are so 
sealed that he cannot tamper with them or alter them in the 
slightest degree. 


Mgn since the world began have taken comfort in the thought 
that they could pass on to their children not merely the posses- 
sions they had acquired, but also the physical and mental attributes 
they had developed. 

To both types of inheritance, as previously conceived, serious 
blows have been dealt within recent years. The passing on of 
worldly goods has been greatly limited by huge inheritance taxes 
in most countries, and abolished (almost) entirely in Russia. As 
for physical heredity, all preexisting conceptions have been shaken 
by the finding we have just dealt with: 

The chromosomes in our germ cells are not affected by any 
change that takes place within our body cells. 

What this means is that no change that we make in ourselves 
or that is made in us in our lifetimes, for better or for worse, can 
be passed on to our children through the process of physical 
heredity. Such changes—made in a person by what he does, or 
what happens to him—are called acquired characteristics. Whether 
such characteristics could be passed on has provided one of the 
most bitter controversies in the study of heredity. It has been 
waged by means of thousands of experiments, and is still being 
carried on by a valiant few. But now that the smoke of battle 
has cleared away, there remains standing no verified evidence to 
prove that any acquired characteristic can be inherited. 

Reluctantly we must abandon the belief that what we in one 
generation do to improve ourselves, physically and mentally, can 
be passed on through our germ-plasm to the next generation. It 
may not be comforting to think that all such improvements will 
go to the grave with us. And yet the same conclusion holds for 
the defects developed in us, of the things we may do in our life- 



times to weaken or harm ourselves. If we cannot pass on the 
good, we cannot likewise pass on the bad. 

Why we can’t should now be obvious. Knowing that all that 
we transmit to our children, physically, are the chromosomes, it 
means that in order to pass on any change in ourselves, every 
such change as it occurred would have to be communicated to 
the germ cells and accompanied by some corresponding change in 
every specific gene in every specific chromosome concerned with 
the characteristic involved. 

Just imagine that you had a life-sized, plastic statue of your- 
self and that inside of it was a small, hermetically sealed con- 
tainer filled with millions of microscopic replicas of this statue. 
Suppose now that you pulled out of shape and enlarged the 
nose of the big statue. Could that, by any means you could con- 
ceive, automatically enlarge all the noses on all the millions of 
little statues inside? Yet that is about what would have to hap- 
pen if a change in any feature or characteristic of a parent were 
to be communicated to the germ cells, and thence to the child. 
It applies to the binding of feet by the Chinese, to circumcision 
among the Jews, to facial mutilation and distortion among savages, 
to all the artificial changes made by people on their bodies through- 
out generations, which have not produced any effect on their off- 
spring. And it applies to the mind as well. 

Nature performs many seeming miracles in the process of 
heredity. But it would be too much to ask that every time you 
took a correspondence course or deepened a furrow in your brain, 
every gene in your germ cells concerned with the mental mecha- 
nism would brighten up accordingly. Or that, with every hour 
you spent in a gymnasium, the genes concerned with the muscle- 
building processes would increase their vigor. 

Thinking back to your father, you will see that what he was, 
or what he made of himself in his lifetime, might have little re- 
lation to the hereditary factors he passed on to you. 

Remember, first, that your father gave you only half of his 
chromosomes—and which ones he gave you depended entirely on 
chance. It may he possible that you didn’t receive a single one 


of the chromosomes which gave your father his outstanding charac- 
teristics. : 

Aside from this fact, what your father was or is may not at 

all indicate what hereditary factors were in him. The genes, as 
we shall see presently, do not necessarily determine characteristics. 
What they determine are the possibilities for a person’s develop- 
ment under given circumstances. 
_ Thus, your father may have been a distinguished citizen or a 
derelict, a success or a failure, and yet this may provide no clear 
indication of what chromosomes were in him. But whether or 
not the nature of his chromosomes did reveal themselves through 
his characteristics, you can make only a guess as to which of 
them came to you by studying unusual traits that your father and 
you have in common. 

You may already be thinking, “What about my children? How 
much of myself did I, or can I, pass on to them?” 

Let us first see what you can’t pass on. 

You may have started life with genes that tended to make you 
a brilliant person, but sickness, poverty, hard luck or laziness kept 
you from getting an education. Your children would be born with 
exactly the same mental equipment as if you had acquired a string 
of degrees from Yale to Oxford. — 

Suppose you are a woman who had been beautiful in girl- 
hood, but through accident, suffering or hardship, had lost your 
looks. The children born to you at your homeliest period would 
be not one whit different than had you developed into a movie 

Suppose you are a World War veteran who was shell-shocked, 
blinded, crippled and permanently invalided. If you had a child 
today his heredity would be bastcally the same as in one you might 
have fathered in your fullest vigor when you marched off to the 

Suppose you are old. 

The sperms of a man of ninety-five, if he is still capable of 
producing virile sperms (and there are records of men who were) 
would be the same in their hereditary factors as when he was 
sixteen. And although the span of reproductive life in a woman is 


far shorter than in a man, the eggs of a woman of forty-five 
would similarly be no different in their genes than when she was 
a young girl. 

Nevertheless, there may be considerable difference in the off- 
spring born to parents under different conditions. But not because 
of heredity. 

Let us take the case of drunkenness. On this point alone end- 
less controversy raged in previous years. Certain experiments were 
reported as proving that drunkenness, and other dangerous habits, 
could be passed on by heredity. All these “findings” have since 
been discredited. But you may ask: “If drunkenness is not in- 
herited, how explain that children of drunkards are so often 
drunkards themselves?” 

The most likely and obvious explanation would be, “through 
precept and example.” 

As often as not, similarities between child and parent (mother 
as well as father), which are ascribed to heredity are really the 
effects of similar influences and conditions to which they have 
been exposed. In fact, so interrelated and so dependent on each 
other are the forces of environment and heredity in making us what 
we are that they cannot be considered apart, and at every stage in 
this book will be discussed together. 

Thus where heredity may fall down, environment may be there 
to carry on. And if you ask, “Can I pass on to my child any of 
the accomplishments or improvements I have made in myself?” 
the answer may be, “Yes! You can pass on a great deal—not by 
‘ieredity, but by training and environment!” 

The successful, educated, decent-living father can give his son 
a better start in life. The athletic father can, by example and 
training, insure his child a better physique. The healthy, intel- 
ligent, alert mother can insure her child a more favorable entry 
into the world, and after it is born, can influence it for the bet- 
ter in innumerable ways. 

There are, however, limits to what environment can accom- 

lish. Exaggerated claims made for it in previous years have been 
refuted by the findings in genetics. The theory of the extreme 
“behaviorists” that any kind of person could be produced out of 

WE le aE wie DION OWL ODN ERAT 21 

any stock by the proper training, has been deflated. On the other 
hand, the extreme “hereditarians” who in the first flush of dis- 
covering the mechanism of heredity attributed everything to its 
workings, have also been given a setback. 

All that we can do here is to present the facts about heredity and 
environment. As to their relative influence on your own life, on 
that of your children or others, you will be left to draw your own 



Or the various myths about mating and parenthood, one that 
has been most ardently cherished is that which many loving 
couples cling to about “putting themselves in the right state for 
the conception of a child.” To disillusion them may be almost as 
bad as telling children there is no Santa Claus. But what we have 
just learned should convince us of the sad, unromantic fact that 
whether a child is conceived during a glamorous sojourn on sunny 
strands, or in the depressing air of a dingy tenement, whether 
in the height of passion or when its parents are barely on speak- 
ing terms with one another, the hereditary factors transmitted to 
it will be not one whit different. 

What, then, of a “love child’? Popular belief is that a child born 
out of wedlock is in some ways different from a legitimate child 
—that it is likely to be more delicate, more sensitive, developing 
to extremes—often a criminal or a genius. It need hardly be stated 
that Nature takes no note of marriage certificates. Yet, strangely 
enough, an illegitimate child, as such, may well be different from 
a legitimate child. Not, however, because of any genetic difference, 
but again because of environment. 

The worry of the unmarried mother, the improper care she 
generally receives and the furtiveness often preceding and fol- 
lowing the birth may leave their mark on the illegitimate child. 
Subsequently the bad start may be overcome, but too often ad- 
verse conditions, both physical and psychological, attend the de- 
velopment of the illegitimate child and continue through life, 
strongly influencing its constitution and character, and sometimes 
giving it that queer twist which may lead it to great depths or great 
heights. Here we have a clear case of where environmental effects 

may be confused with those of heredity; for under the same con- 


ditions as stated, a legitimate child might be expected to turn out 
exactly like the illegitimate one. 

The age of parents is also believed to affect the nature of the 
child, but where it does, it is only through environmental influ- 
ences. A “child of old age,” born, let us say, when a mother is in 
mid-forty and the father in his sixties, frequently appears to be 
frailer and sicklier than others. The explanation will be found not 
in any weakness in the parent’s sperm or egg, but (1) in the less 
favorable intra-uterine environment provided by the older mother; 
(2) in the greater opportunity she has had to become affected by 
disease over the years; and (3) in the fact that such late births 
are generally unwanted .and occur mostly where conditions for 
childbearing are bad. Following birth other factors enter. The 
“child of old age,” surrounded as is often the case by mature 
brothers, sisters and their friends, in addition to the older parents, 
is frequently pampered and spoiled, and may quite understandably 
become high-strung and precocious. 

In children born to very young mothers (under seventeen), both 
the intra-uterine and post-natal conditions are also likely to be un- 

It should be hardly necessary now to dwell long on certain 
other erroneous beliefs associated with mating and parenthood, 
which, while prevalent largely among breeders of domestic animals, 
are also applied to human beings: 

“Telegony” is the theory that if a female is mated with two or 
more successive males, the influence of an earlier sire may carry over 
to offspring of a later father. 

Similarly, by “infection,” that a male mated first with an un- 
desirable female (a blooded bull with a scrub cow) may com- 
municate some of her characteristics to offspring of the next female 
with whom he is mated. 

Or that continued mating together may cause a male and female 
to resemble each other, and that by “saturation” the oftener a 
female is mated with the same male, the more the successive off- 
spring will resemble him. 

In the last two cases, the explanation which should readily occur 
is that individuals who live together for a long time, whether 


lower animals or humans, may show common effects of the same 
environment, diet, habits and other living conditions. Husbands 
and wives sometimes may get to look alike in the same way that 
any persons living in the same environment may develop similari- 
ties of physique and appearance. One often hears it said of a 
couple, “You’d think they were brother and sister!” The same 
environmental influence also tends to increase the resemblance be- 
tween children and parents. 

The myths and superstitions associated-with mating and parent- 
hood could fill a book by themselves. Back of all of them lie 
sometimes coincidences, sometimes mistaken assumptions of pater- 
nity, and most often the cropping out of hidden factors (recessive 
genes) which will be dealt with more fully further along. 

One common question regarding mating may deserve special 

“Can there be such a thing as ‘conflict’ between the chromosomes 
of one person.and another—a genetic incompatibility that would 
seriously affect or prevent birth of children?” 

Yes, but only as applied to certain individuals, not to “races,” 
groups or “types” of human beings. This is an important distinc- 
tion. Later we shall see how in given persons there may be specific 
“dangerous” genes or other genetic factors which may seriously 
affect their having children if mated with each other. But one 
shouid not jump to the conclusion that this would single out per- 
sons of radically different “surface types.” For the fact is that all 
human beings, regardless of “race,” “type,” “color” or any other 
classification in which they are placed, are, as members of the same 
species, sexually and genetically compatible with one another. 

No such chromosome incompatibility exists between any two 
kinds of humans as there does between animals of different species 
—a cat and a dog, a chicken and a goose, etc. The tallest, blondest 
“Nordic” could mate with the smallest, blackest pigmy and pro- 
duce children perfectly normal in the eyes of Nature. This, how- 
ever, has certain qualifications, for if a tall, big-boned European 
mated with a pigmy woman, the child might be too large for 
her to bear without danger to it or to herself. The same, how- 
ever, would apply to the mating of any extremely large man with 

99 66 


A Cat and a Dog 

Cannot mate and have offspring 
together because they are of dif- 
ferent species, 

—and their chromosomes dif- 
fering in kind and number are 
‘not compatible. 

HBS eg 
$°¢ ae 
co Beary 
? Obits 

an 78 ON 

A Horse and a Donkey 

Although of different species can mate and produce MULE offspring. 
But these are sterile because 


produces eggs or produces eggs or work together 
sperms containing sperms with an- somehow to pro- 
one kind of chro- other kind of chro- duce MULE off- 

mosomes. mosomes. spring 

—While these can — The conflicting 

chromosomes can- 
not form in the 
Mule fertile germ 

BUT All Varieties of Human Beings Are Fertile With One Another 

—All humans are of the 
same species with the 
same kind of chromo- 
somes. Thus, the smallest 

—and the tallest Nordic 
could mate and produce 
a child perfectly normal 
in the eyes of Nature. 


a very small woman, even of the same “race,” where sometimes a 
Caesarian operation is required to deliver the child. 

The theory has been advanced that in the mating of parents 
of radically different types, serious disharmonies may result in 
the bodily structure and features of their offspring. The evidence 
on that score is far from conclusive, and until proved otherwise, 
must be placed among “beliefs” rather than facts, with which we 
are dealing. 

As matters stand “incompatibility” of chromosomes or of their 
genetic take-up need hardly be a bogey to any except relatively 
few prospective parents. 



Wuat was the most thrilling, perilous, extraordinary adven- 
ture in your lifer 

Whatever you might answer, you are almost certain to be wrong. 
For the most remarkable and dramatic series of events that could 
possibly have befallen you took place before you were born. 

In fact, it was virtually a miracle that you were born at all! 

Consider what had to happen: 

First, you—that very special person who is you and no one else 
in this universe—could have been the child of only two spectfic 
parents out of all the untold billions past and present. Assuming 
that you had been ordered up in advance by some capricious 
Power, it was an amazing enough coincidence that your parents 
came together. But taking that for granted, what were the chances 
of their having had you as a child? In other words, how many 
different kinds of children could they have had, or could any 
couple have, theoretically, if the number were unlimited? 

This is not an impossible question. It can be answered by calcu- 
lating how many different combinations of chromosomes any two 
parents.can produce in their eggs or sperms. For what every parent 
gives to a child is just half of his or her chromosomes—one repre- 
sentative of every pair taken at random. In that fact you will 
find the explanation of why you are different from your brothers 
and sisters, why no two children (except “identical” twins) can 
ever be the same in their heredity. 

Putting yourself in the réle of parent, think for a moment of 
your fingers (thumbs excluded) as if they were four pairs of 
chromosomes, of which one set had come to you from your father, 
‘one set from your mother. (To distinguish between the two, we’ve 



Representing chromosomes Representing chromosomes 
received from one's received from one's 

i= ae 

made the paternal set black in the diagram, the maternal set white.) 

Now suppose that these “chromosomes” were detachable and 
that you had countless duplicates of them. If you could give a set 
of four to every child, and it didn’t make any difference whether 
any “chromosome” was a right- or left-hand one—in other words, 
whether it had come from your father or your mother—how many 
different combinations would be possible? 

Sixteen (see the diagram opposite), in which every combination 
differs from any other in from one to four “chromosomes,” 

But this is with just fowr pars involved. If now you put the 
thumb of each hand into play, representing a fifth pair of chromo- 
somes, you could produce twice the number of combinations, or 32. 
In short, as our mathematician friends can quickly see, with every 
added pair of factors the number of possible combinations is dou- 
bled. So in the case of the actual chromosomes, with twenty-four 
pars involved—where one from each pair is taken at random— 
every parent can theoretically produce 16,777,216 combinations of 
hereditary factors, each different from any other in anywhere from 
one to all twenty-four chromosomes. 

Whether we are dealing with the millions of sperms released by 
a male at one time, or the single egg matured by a woman, the 
chance of any specific combination occurring would be that once 
in 16,777,216 times. 

But to produce a given individual, both a specific sperm and a 

THEW MAR A Ci BOR aeYoU.. 29 

Illustrating combinations of chromosomes 
produced with four pair 

ally le vdeo lle 

Ade vile wade tly 
able Wy whe athe 
Ml whe the ile 

specific egg must come together. So think now what had to happen 
for you to have been born: 

At exactly the right instant, the one out of 16,777,216 sperms 
which represented the potential half of you had to meet the one 
specific egg which held the other potential half of you. That 
could happen only once in some 300,000,000,000,000 times! Adding 
to this all the other factors involved (as we shall presently see), 
the chance of there having been or ever being another person ex- 
actly like you is virtually nil. 

At this point you might say, with modesty or cynicism, “So 

Well, perhaps it wasn’t worth all the fuss, or perhaps it wouldn’t 
have made any difference whether or not you were born. But it 
was on just such a miraculous coincidence—the meeting of a specific 
sperm with a specific egg at a specific time—that the birth of a 
Lincoln, or a Shakespeare, or an Edison, or any other individual 
in history, depended. And it is by the same infinitesimal sway of 


chance that a child of yours might perhaps be a genius or a numb- 
skull, a beauty or an ugly duckling! 

However, that first great coincidence was only the beginning. 

The lucky sperm, which has won out in the spectacular race 
against millions of others, enters the chosen egg which has been 
waiting in the fallopian tube of the mother. Immediately, as we 
previously learned, the sperm and the nucleus in the egg each re- 
leases its quota of chromosomes, and thus the fertilized egg starts 
off on its career. 

Already, from this first instant, the fertilized egg is an individual 

with all its inherent capacities mapped out—so far as the hereditary 
factors can decide. Will the baby have blue eyes or brown eyes? 
Dark hair or blond hair? Will it have six fingers or a tendency 
to diabetes? Will it live to nineteen or to ninety? These and 
thousands of other characteristics are already largely predetermined 
by genes in its particular chromosomes. 
- But as yet the individual consists of only one cell, like the most 
elemental of living things (i.e, the ameba). To develop it into a 
- full-fledged human being, trillions of cells will be required. How this 
multiplication is effected we have seen in a previous chapter: The 
chromosomes split in half and separate, then the cell divides, mak- 
ing two cells, each with exact replicas of the forty-eight chromo- 
somes that there were in the original whole. Again the process is 
repeated, and the two cells become four. Again, and the four 
cells become eight. So it continues, and as you could figure out if 
you wished, the doubling process would have to be repeated only 
forty-five times to provide the twenty-six trillion cells which, it is 
estimated, constitute a fully developed baby. 

However, as the cells go on to “specialize,” some divide and 
multiply much more slowly than others. But regardless of how 
they multiply or what they turn into, to the very last cell, each 
one will still carry in its nucleus descendants of each of the original 
forty-eight chromosomes. 



We have followed the first stage in Your Greatest Adventure— 
the remarkable coincidence by which you were conceived. But con- 
ception is a long way from birth. The beginnings of life, as science 
has now disclosed them, are beset with far more hazards than any 
one has ever imagined. 

In the first days after fertilization, while all the cell-division 
and activity has been going on inside the egg, it has been slowly 
making its way down the fallopian tube toward the mother’s uterus. 
Within a few more days the egg finds itself at the entrance of 
what—to this tiny droplet of substance, smaller than a period on 
this page—must be a vast, foreboding universe. If you can think 
of YouRSELF at that stage, your life hung precariously in the balance. 
Innumerable adverse forces confronted you. At any moment you 
might be swept away to destruction. In short, the odds were most 
heavily against your survival. 

But to become impersonal once more, the immediate concern of 
the human egg at this stage is to take root somewhere. Already 
it has prepared itself for this by developing microscopic little “ten- 
drils” from its outer surface, so that it somewhat resembles a tiny 
thistle. Thus it can attach itself to the mother’s membrane, as- 
suming—which is not always the case—that that membrane is re- 
ceptive. If luck is with the egg, it is hospitably received—a hungry 
and thirsty little egg that has almost exhausted the store of food 
with which it started out. Immediately, with the maternal tissues 
cooperating, arrangements are begun for its food, oxygen and water 
supply through the development of a receiving surface—the placenta 
—which grows into the mother’s membrane but does not become 
part of it. And so, about nine days from the start of its existence— 



Once every 28 days (about the 
middle of the menstrual cycle) an 
egg ripens in the human ovary 
and is released from its follicle— 

The egg is caught up into the fun- 
nel-end of the fallopian tube and 
begins its journey— 

Meanwhile (if chance has so willed} 
many sperms, of millions released 
simultaneously, have found their 
way up the tube and to the egg—v 

And if the time is favorable ~ 
which may be for only a day or 
two in every month — a sperm 
enters the egg and fertilization 
takes place. 

The fertilized egg now continues 
its journey by slow stages for 
about a week, toward the uterus. 

But by the time it reaches the 
opening to the uterus it has grown 
little burr-like tendrils on its out- 

By means of these tendrils in a 
few more days it may attach itself 
to the wall of the uterus and begin 
to grow. 

NOTE: The “rhythm” theory for women is based on the facts presented. above. 



the most perilous days in any person’s life—the new individual 
becomes what is really a parasite on its mother. 

And now we may ask, how far can the mother, from this point 
on, affect the development and future of the child? The answer, 
as revealed by the latest findings in embryology, should do much 
to clear away many popular misconceptions. 

Skipping some of the early stages, we presently find the embryo 
encased in a fluid-filled sack, suspended from the placenta by the 
umbilical cord which acts as the con- 
duit that brings in the food from the 
mother and carries out the waste 
products. But the umbilical cord is not, 
as is commonly supposed, a tube that 
goes directly into the mother’s body. In 
fact, there is no direct connection any- 
where, and at any time, between the 
mother and child. The child is from 
the earliest stage until birth as distinct 
an individual as if it were developing 

Actual Size -> ee 

outside of the mother’s body, like a Exterior of HUMAN EGG 
chick within the eggshell. (embryo) at time of implan- 

tati bout twelfth 
There is a wall between the mother (about twelfth day] 

and child. On one side, the open ends of some of the mother’s blood 
vessels empty into the wall. But the mother’s blood, as such, never 
reaches the child, nor do any mother and child have a single drop 
of blood in common. For what happens is that the food substances 
in the mother’s blood—chiefly sugars, fats and protein elements— 
are strained out by osmosis, like moisture soaking through a blotter. 
And it is these which are drawn into the placenta pressed hungrily 
on the other side of the wall, and then conducted by the umbilical 
cord to the embryo. As Professor C. H. Waddington has phrased it, 
if it were not for that wall or filter between mother and child, “the 
embryo would actually be killed by foreign proteins, since each 
animal is a chemical individual which has to be respected.” 
Science, by the way, now overrules the decision by the late great 
Justice Oliver Wendell Holmes, from a Massachusetts bench in 
1884, that an unborn child is not an individual, but “part of its 



Hee & <— NERVES 
an, wy arse ferwne®. SO 

> of . hte . 


mother’s bowels.” The decision, used only recently in a Chicago 
court as a precedent, will, we feel sure, eventually be nullified. 

Not only is there no direct blood connection between mother 
and child, but there is, moreover, no nerve connection, and hence 
no such mental or psychological relationship as mothers have al- 
ways liked to believe exists between them and the little one they 
are carrying. In the light of all this, another batch of myths, about 
prenatal influences and maternal impressions, about “strawberry 
marks” or other marks and deformities in the child resulting from 
the mother’s having seen.or done this or that vanish into thin 
air. (We say “vanish” with reservations, for myths die hard, and 
even some of the most enlightened mothers still cherish a few of 

If the mother goes to concerts while she is carrying the child, 
that will not make it one whit more musical. Thinking pure 
thoughts, reading elevating books, doing kind deeds, can have their 
effect only in relaxing the mother and improving her physical 
condition. And, as already noted, if she is ardently in love with her 
husband—as sharply contrasted to hating him—the only difference it 
could make to her child would be to put her in a happier frame 
of mind and condition for bearing it. 


Adversely, however, the effect of the mother may be great. First, 
of course, she is its food provider and if her supply is inadequate, 
the baby, being a voracious little parasite, will suffer malnutrition. 
Then, in her role as nurse—a nurse who is inseparably linked with 
the child throughout the crucial prenatal period—she may even 
unwittingly do it great injury. If her physical condition is bad, or 
if she suffers any great shock, severe chill or strong emotional re- 
action, the life of the potential child may be snuffed out. But 
there are other hazards, for we find that the wall between the 
embryo and the mother is, unfortunately, not a barrier against every- 

First, various drugs may pass from the mother to the embryo. If 
she smokes or drinks to excess, the nicotine or alcohol in her sys- 
tem may reach the child with harmful, or even disastrous effects. 
A large amount of alcohol penetrating to the child may result in 
its death or malformation. “Monsters” are often supposedly due 
to such prenatal alcoholization. Another serious result might be 
deafness in the child, which can also be caused by the mother’s ex- 
cessive use of quinine. 

Among other substances which may pass from the mother to the 
embryo are lead and arsenic (the fumes of which may be inhaled 
in certain industrial operations) and—especially dangerous—nar- 
cotics. If the mother is addicted to the use of morphine or opium 
to the point where her tissues are saturated with the drug, the child 
may actually come into the world as a drug addict. 

Certain disease germs, notably those of diphtheria, typhoid, in- 
fluenza and syphilis, may also penetrate to the child. And whether 
through germs or through her condition, where the mother suffers 
from typhoid fever, scarlet fever, cholera, smallpox, erysipelas, pneu- 
monia, sleeping sickness or malaria, in a great many cases the child 
will be killed before birth. 

The birth of babies with syphilis has given rise to the belief 
(widely but erroneously promulgated through Ibsen’s “Ghosts”) 
that the disease can be inherited. Actually, no sperm and—so far 
as we have record—no human egg could carry a disease germ of 
any kind and function. What has happened when a child is born 
with syphilis is that the mother has been infected, and that she has 


then transmitted it to the child before or during the process of 

Here, in the prenatal period, we have our first clear-cut ex- 
amples of what is due to heredity, and what to environment. 

From the very first instant—we might say even before concep- « 
tion—both heredity and environment are at work. 

An egg might start off with one or more defective chromosomes 
—or bad heredity—which might under average conditions destine 
it to be killed off. But if the mother’s condition is unusually good, 
in other words if the environment is extremely favorable, the 
“weak” egg may develop through to birth and the individual may 

On the other hand, an egg might start off with the finest of 
chromosomes—the best of heredity. But through bad environment 
or influences (the poor condition of the mother, an accident or 
one of innumerable circumstances) the individual might be killed 
off or be permanently impaired. Under the same conditions, how- 
ever, the egg with the better heredity will have a much brighter 
future. ! 

In the nine months before birth every human being faces the 
severest test that he will ever undergo. With ruthlessness Nature 
exercises her “Law of Selection,” killing off the weak more relent- 
lessly than ever the ancient Greeks ventured to do. Undoubtedly, 
many worthy individuals are sacrificed in the effort to weed out 
the defectives. In fact, so stringent is the initial ordeal that ex- 
perts believe the children who are born represent only a portion 
of all the eggs fertilized. In other words, in innumerable instances 
—perhaps a majority of cases—women conceive and the egg is 
killed off without their even knowing it. What frequently are de- 
scribed as “false alarms” may have been actual conceptions. 

On the whole, however, parents should be grateful for this rigid 
pre-selection, for without it the world might be overrun with some 
pretty bad specimens. As it is, plenty of them do survive, but these 
are fortunately in the great minority. Where birth is achieved, it 
can generally be taken as a stamp of approval by Nature, qualify- 
ing the individual to face life. From that point on it is “up” to 
his parents, to himself and to the environment created by society. 


Next to being born, the most important single fact attending 
your coming into the world was whether you were to be a male 
or a female. Undoubtedly, that is the first question that occurs ta 
prospective parents. Before you read this chapter, you may find it 
of interest to test your present knowledge as to what determines 
sex. Which of these statements would you say is right, which 

1. The sex of an unborn child can be influenced before or during 
conception by (a) the stars, (b) the climate, (c) the mother’s diet. 
2. It can be influenced by other factors within two months after con- 
. It is the mother who determines the sex of the child. 
. More boys are born than girls because boys are stronger. 
. On an average, as many boys are conceived as girls. 
. A mother’s age or condition has no effect on her chances of giving 
birth to a boy or a girl. 
7, Whether mothers are White or Negro the chances of their baby 
being a boy are exactly the same. 

AVI & Ww 

Every one of the foregoing statements, you will presently find, 
1s wrong! 

The scene is a regally furnished bedchamber, in medieval times. 

A beautiful young woman is lying in a luxurious, canopied bed. 
She is to become a mother, but although this will not occur for 
many months, already there is much to do. 

A midwife carefully adjusts her so that she lies on her right 
side, her hands held with thumbs out. Over her now a bearded 
necromancer swings with precise up-and-down motions a tiny in- 
cense-burner. (Heaven forfend that it be allowed to describe a 



circle!) At the foot of the bed an abbot kneels in prayer. In one 
corner an astrologer mumbles incantations as he studies an almanac. 
In another corner an alchemist prepares a potion in which are 
boiled the wattles of a rooster, some heart-blood of a lion, the head 
of an eagle and certain parts of a bull—the essence of all these 
will be blended with thrice-blessed wine and given to the young 
woman to drink. And meanwhile, surrounded by high counselors, 
the young woman’s noble spouse—none other than the mighty 
Sovereign of the Realm—looks anxiously on. 

By this time you have probably guessed that all the ceremonial 
and hocus-pocus was for a single purpose: To make sure that the ex- 
pected child would be a son and heir to the throne. 

Synthetic as this particular scene might be, in effect it occurred 
many times in history. But if it were only a matter of dim history 
we would not be dealing with it here. The fact is, however, that 
to this very present day, throughout the world and in our own 
country, a fascinating variety of potions, prayers, midwives’ for- 
mulas, “thought applications,” diets, drugs or quasi-medical treat- 
ments is still being employed by expectant mothers to influence 
the sex of the future child. Most often, undoubtedly, the objec- 
tive is a, boy. But an ample list could also be compiled of the 
“what-to-do’s” to make it a girl. 

Alas then, whatever the methods employed, primitive or sup- 
posedly enlightened, all are now equally dismissed by science with 
this definite and disillusioning answer: 

The sex of every child is fixed at the instant of conception—and 
it 1s not the mother, but the father, who is the determiner. 

The moment that the father’s sperm enters the mother’s egg, the 
child is started on its way to being a boy or a girl. Subsequent events 
or influences may possibly affect the degree of “maleness” or “female- 
ness,” or thwart normal development, but nothing within our power 
from that first instant on can change what is to be a girl into a 
boy, or vice versa. 

The solution of the mystery of sex-determination came about 
through this discovery: 

That the only difference between the chromosomes of a man and 


a woman ltes in just one of the pairs—in fact, in a single chromo- 
some of this pair. | 

Of the twenty-four pairs of chromosomes, twenty-three pairs— 
which we could number from A to W, inclusive—are alike in both 
men and women. That is to say, any one of them could just as 
readily be in either sex. But when we come to the twenty-fourth 
pair, there is a difference. For, as we see in the accompanying dia- 
gram, every woman has in her cells two of what we call the “X” 
chromosome, but a man has just one “X”—its mate being the tiny 
“Y.” It is the presence of that “Mutt and Jeff” pair of chromosomes 
in the male (the “XY” combination) and the “XX” in the female 
that sets the machinery of sex development in motion and results 
later in all the differences that there are between a man and a 

We have already seen how when human beings form eggs or 
sperms, each gets just half the respective parent’s quota of chromo- 
somes. When the female, then, forms eggs and gives to each egg 
one chromosome of every pair, as she has two X’s, each egg gets an 
X. But when the male forms sperms and the different pairs of 
chromosomes split up, one chromosome to go into this sperm, 
the other into that sperm, one of every two sperms will get an X, 
the other a Y. 

We find, then, with regard to the sex factor, that the female 
produces only one kind of egg, every egg containing an X. But 
the male produces two kinds of sperm—in exactly equal numbers. 
(Which is to say, that of the 200,000,000 to 500,000,000 sperms re- 
leased by a man each time, exactly half would be X-bearers, half 

Science having established that only one sperm fertilizes an egg 
(as a wall forms about the egg the instant it enters, shutting out, 
all others), the result should be self-evident. If a sperm with an X 
gets to the egg first, it pairs up with the X already there, an XX 
individual is started on its way and eventually a girl baby is pro- 
duced. But should a Y-bearing sperm win the race, the result will 
be an XY individual, or a boy. 

Here at last is the comparatively simple answer to what was 
long considered an unfathomable mystery! 


This is what makes all the differences 
there are between a woman and a man: 

qt 0g) 



4 (dyes 
i <a 

Qgi bly 

p> 4 

Nyy gi8! 


In every cell of every 
female there are two 
chromosomes like this, 

called '"'X''s 



Ip ft ilty 


b> It 




fT] fn 



gs ti 
a7 7 










P 4 



Every cell of every male 

has only one ''X"'. Its 

mate, much smaller, is 
called a "Y" 

For geproductiony a female forms eggs, a male sperms, 

to eac 

of which they contribute only HALF their quota 

of chromosomes, or just one from every pair: 

Zince a female has TWO ''X''s, each 
agg gats one "X", so in this respect 
every egg is the same: 

But as the male has only ONE "X", 
paired with a "Y", he forms TWO 

kinds of sperms: 


AN "X's 
a EO 

A ike GR 

Thus: If an'"X"-bearing sperm enters the egg, 
the result is an individual with TWO "X"s 


ES Ga A St 

...lfa"Y"-bearing sperm enters the egg, 
the result is an "XY" individual, or 

aT (<2) A BOY 
Lites 7520 a4 
\ ! 


Seow OR OC PRL-f?2 4) 

But hardly have we solved this when we are confronted with 
a new mystery: 

The world has always taken it pretty much for granted that 
there are about as many males as females conceived, and that if 
about 5 or 6 percent more boys are born than girls this is due 
to the “fact” that boys are stronger and better able to survive the 
ordeal of being born. The actual sttuation, as now revealed by 
science, 1s radically different. 

All evidence now points to the fact that more boys are born 
because more boys are conceived. Why should this be, you may 
ask, if the “male”-producing and “female”-producing sperms are 
exactly equal in number? Because they are apparently not the 
same in character. The assumption follows that the sperm con- 
taining the small Y has some advantage over the one with the 
X, so that, on an average, it gets to the mark oftener—so much 
oftener, various scientists have stated, that the ratio at conception 
may be as high as 20 to 50 percent more males. 

(The most recent investigator, however, believes these previous 
estimates are exaggerated, but that, nevertheless, the excess of males 
over females conceived is still greater than the ratio at birth.) 

On what are these estimates based? On the fact that the mor- 
tality among male embryos averages about 50 percent higher than 
among female embryos—completely contradicting the old belief 
that boys are better able to survive the ordeal of birth. 

About one-quarter of the known pregnancies result in still-births. 
Great numbers of these aborted babies have been examined, and 
some surprising data obtained. In embryos aborted when they are 
about three months old, specialists can already distinguish sex, 
and in these early mortalities they have found that the males 
outnumber the females almost four to one. These, however, are 
but a small percentage of the total still-births. In those in the fourth 
month, aborted males are double those of females, in the fifth 
month, 145 males to 100 females, in the next few months the pro- 
portion drops further, but just before birth there is a rise to almost 
140 males aborted to every 100 females. 

All this leads to another conclusion: That before birth, certainly, 
males as a class are not only not stronger than females, but, quite 


on the contrary, are weaker. If we look beyond birth, we find, 
moreover, that at almost every stage of life, males drop out at a 
higher rate than females. It may very well be, then, that a canny 
Nature enters more males than females at the start of life’s race 
in order to counterbalance the difference in mortality. 

The theory as to why males are less able to survive will be 
brought out in a later chapter. For the present, assuming that the 
male embryo is the likeliest to be carried off under adverse condi- 
tions, we might gather that where the condition of a mother is 
more unfavorable, the possibility of a son being born will be less- 

Some evidence has been advanced to support this. Among mothers 
who have had a considerable number of previous pregnancies the 
later children show a drop in percentage of sons. Among colored 
mothers, in general, perhaps because they may receive inferior 
care during pregnancy, there is a markedly smaller percentage of 
sons born than among white women. It has also been reported, 
from other countries, that births among unmarried mothers show 
a lower than average ratio of sons, but recent figures for the United 
States do not seem to bear this out. 

A popular question is whether a tendency to bear sons may not 
run in certain families or individuals. Quite possibly, yes, although 
researches are not yet sufficiently adequate to permit a definite 
answer. One might guess that exceptionally active or virile sperms 
on the part of males, or exceptionally favorable conditions for 
motherhood on the part of women, would lead to an above-average 
ratio of male births. But a “run” of either sons or daughters in 
any given family may be as much a matter of chance as a run 
of “sevens” in a dice game. 

Other questions you might ask, “What about the influence of 
hormones and glands on sex after birth? ‘What part does heredity 
play in ‘masculine women’ and ‘feminine men’?” etc., will be dis- 
cussed in a later chapter. One question, however, might be an- 
swered here: 

_ Knowing that an X-bearing sperm produces a girl, a Y-bearing 
sperm a boy, might not a way be found of separating the two kinds 

and then, by artificial insemination, producing boys and girls at 

Yes—it seems only a matter of time before this will be possible. 
Already, in a number of laboratories, geneticists are working to- 
ward this goal. The distinct differences between the X sperm and 
Y sperm have provided a basis for their experiments. Definite 
affirmative results are already reported at this writing, and it is 
considered likely that in a not too distant future many persons— 
or those, at least, to whom the laboratory facilities will be avail- 
able—will be able to have a boy or girl baby, as they wish. 

For the time being the matter of “boy or girl?” remains one of 
chance, with this qualification, as we have seen: The better pre- 
pared a woman is for motherhood, the slightly greater will be the 
odds that as the anxious father paces the hospital corridor, the nurse 
will report, 

“It’s a boy!” 


Sex is but one of the myriad characteristics potentially determined 
by your genes at the instant of conception. 

But how, and by what processes, do the genes do their work 
during that long dark interval between conception and birth? 

Recall that a single gene is millions of times smaller than the 
smallest speck you could see with your naked eye. How can 
such minute bits of substance do such astounding things as mold- 
ing the shape of your nose, determining the color of your eyes 
or hair, actually making you sane or insane? 

What, to begin with, zs a gene? 

At the present stage of our knowledge (and it is only yester- 
day, as science computes it, that we even knew about genes) no 
one can answer definitely, because it has so far not been possible 
to isolate a gene and to analyze it. But geneticists know a great 
deal of what genes do and how they do it. They are convinced 
(most of them) that a gene acts like an enzyme, a substance which 
produces a certain chemical change in a compound without in it- 
self being affected. 

Every housewife knows that a bit of yeast will make dough 
rise and that a pellet of rennet will turn milk into “junket.” Home 
brewers of the prohibition era remember the potent effects of a 
few raisins in their jug of mash. Manufacturers are familiar with 
hundreds of substances (small pieces of platinum, for instance) 
used in various processes to bring about desired chemical changes. 

And finally, if one is still puzzled by the smallness of the gene 
and the bigness of its effect, one has only to think of how a droplet 
of deadly poison, such as cobra venom, can speedily bring about 
chemical changes which will convert a hulking, roaring giant of 
a man into a lifeless mass of flesh and bone. 



In creating an individual, the genes work first upon the raw 
material in the egg, then upon the materials which are sent in by 
the mother, converting these into various products. These, in turn, 
react again with the genes, leading to the formation of new prod- 
ucts. So the process goes on, meanwhile specific materials being 
sorted out to go into and construct the various cells of the body. 

Where the genes are unique is that they are alive and able to 
reproduce themselves. It is not impossible that genes may be made 
up of smaller particles, but so far as science can trace back today 
the gene ts the ultimate unit of life. 

We cannot therefore regard genes as mere chemical substances. 
When we consider what they do, we may well think of them as 
workers endowed with personalities. No factory, no industrial or- 
ganization, has so varied an aggregation of workers and specialists 
as the genes in a single individual, and no army of workers can do 
more amazing things. Architects, engineers, plumbers, decorators, 
chemists, artists, sculptors, doctors, dieticians, masons, carpenters, 
common laborers—all these and many others will be found among 
the genes. In their linked-together form (the chromosomes) we can 
think of them as “chain-gangs” twenty-four of these gangs of 
workers sent along by each parent to construct the individual. 

Turn back to the moment of conception. The chain-gangs con- 
tributed by your mother are packed together closely in a shell (the 
nucleus) suspended in the sea of nutrient material which constitutes 
the egg. Suddenly, into that sea, is plunged a similar shell (the 
sperm) filled with the chain-gangs sent by your father. Its entrance 
causes both shells to break, and out come the chain-gangs with 
their workers, stirred to activity. 

The first impulse of the workers, after their long confinement, 
is to eat (which seems natural enough). They gorge themselves on 
the sea of materials around them, and as we have already noted 
before, they double in size, split in half, and form two of them- 
selves. The sne-cell egg divides into two cells, the two into four, the 
four into eight, etc—a replica of each original chain-gang going 
into each cell. 

Up to this point the genes have all been doing ordinary construc- 
tion work. But now, while the process of multiplying themselves 


The CHROMOSOMES may be thought of as 
“Chain-Gangs," twenty-four of which are sent 
ang Ry ey parent to ereaty the child. Every Chonieeere 
gang’ consists of many linked-together work- ‘ 

ers, each assigned to given tasks. 

~ Colorist 


Engineer ete 
Architect Colorist 
e eae 
oe ae y 
Sa A Plumber 
FATHER Carpenter 

NOTE that in each of 
these ''mated" chains, 
the workers (“genes'| 

at corresponding points, are ase« 

signed to exactly the same type of | 



and the cells continues, the specialists get into action and begin 
constructing different kinds of cells at different locations. 

The details of how this is done—such details as are known or 
surmised—fill tens of thousands of pages in scientific treatises. 
Briefly stated, we can assume that on set cues the different genes 
step out for their special tasks, snatching at this bit of material or 
element, combining it with other stuffs, fashioning a product, set- 
ting it in place, etc., all the time working in cooperation with the 
other genes. 

Throughout one’s lifetime the genes are in a constant ferment of 
activity, carrying on and directing one’s life processes at every stage. 
Everything seems to be done according to plan, as if the most de- 
tailed blueprints were being followed. The step-by-step process has 
been explained as a sequence of reactions, the workers being moti- 
vated to each step by the effects of the preceding one. By observing 
the process in lower experimental animals we can see how first 
the broad general construction of the body is worked out; then 
how certain cells are marked off for the organs, certain ones for the 
respiratory and digestive systems, certain ones for the muscles, 
others for the skin, features, etc. 

The generalized cells now begin to develop into special ones. In 
those marked off for the circulatory system the rudiments of hearts, 
veins and arteries begin to be formed (here is where the “plumber” 
genes step in to construct the great chain of pumps and pipe-lines) ; 
from the generalized bone cells the skeleton begins to be shaped; 
from the skin cells, the rudiments of features, etc. With each stage 
the specialization is carried further along in the developing embryo. 
The amazing way in which the development of every human being 
parallels that of every other proves how infinitely exact and pre- 
determined are the genes in their workings. 

Another remarkable feature of the process is this: That despite 
the growing differences in the various specialized cells, zvto every 
cell, as it is being created and constructed, go exact replicas of all 
the chromosomes with their genes. Thus, the same gene which 
produced eye color in your eye cells will also be found in your 
big toe cells, and the same gene which directed the fashioning of 
your big toe will also be found in your eye cells—or in your ear 


and liver cells, for that matter! Probably, then, in addition to every 
special task that each gene performs, it also takes part in general 
activities which make its presence required everywhere. 

But we recall now that the individual starts life with two chromo- 
somes of every kind, which means also two genes of every kind. 
If, in terms of chain-gangs, we designate the chromosomes by letter, 
there would be two Chain A’s, two Chain B’s, two Chain C’s, 
and so on up to the last pair—where in the case of a girl, as noted 
in the preceding chapters, there would be two Chain X’s, but in 
the case of 4 boy, only one X Chain, the other being a Y Chain. 
With this latter exception, the corresponding chain-gangs (AA, BB, 
CC, etc.) would be exactly alike in the number of workers each 
contained, and in the type of worker at each point in the chain. 

If the No. 1 gene in Chain A contributed to you by your father 
was an architect, so would be the No. 1 gene in the Chain A from 
your mother. The No. 2’s in line might be carpenters, the No. 3’s 
decorators, etc. All the way from Chain A to Chain X, the genes 
at each point in all human beings are exactly the same in the type 
of work to which they are assigned. In other words, every in- 
dividual starts life with two workers for each job, one sent by the 
mother, one by the father. , 

But the corresponding genes in’any two human beings are far 
from the same. To be sure, they are sufficiently alike in their effects 
so that the difference between even our pigmy Hottentot friend 
and our tall blond “Nordic” are insignificant compared to the differ- 
ence between either one and an ape. Nevertheless, within the range 
of human beings, the corresponding genes are exceedingly variable 
in their workings, leading to many peculiar effects and the marked 
differences that might exist between individuals, even those in the 
same family. 


Auruoucu there are no statistics on the subject, we dare say that 
millions of husbands since the world began, and a not inconsider- 
able number of mothers, noting that some child in no way re- 
sembled them, have had the cold suspicion creep up that it actually 
was not theirs. 

Many times, perhaps, in the case of husbands, this suspicion has 
been justified; and in rare instances, possibly (but much more rarely 
now) the wrong infant may have been wittingly or unwittingly 
foisted upon the mother. In the majority of cases, however, the 
doubts were groundless, and today can often be quickly dissipated 
as the result of the findings of two men. 

One, an obscure Austrian monk of Civil War days, who culti- 
vated garden peas. 

The other, a living American scientist, who cultivated, and still 

How can ordinary garden peas (the same peas that you get at 
any Rotary Club luncheon with your chicken and candied sweets) 
and fruit-flies (the sort that buzz around bunches of bananas—and 
not the best bananas, either), how can these have any bearing on 
the parentage of a child? They can because, as we know now, the 
mechanism of heredity in peas and flies, and in all other living 
things, is basically the same as it is in man. This is one of the 
amazing facts that is being made increasingly more evident, and 
that is one of the hardest for the layman to accept. 

When in 1857 the plump Abbot Gregor Mendel, waddling about 
in the garden of the monastery at Brinn, Austria (now held by 
Germany), set out to clarify his mind about the heredity of peas, 
he himself did not dream that he was at the same time about to 
throw lasting light on the heredity of human beings. Mendel had 



RED 29 << WHITE 
(A) vy (8) 


2 Nd 


-But when any 4 
of these offspring 

were mated, they 


Zrd. “AW 


3 in 4 RED LiIN4 WHITE 
(Like Grandparent “A’) (Like Grandpt. B ) 



a brilliant mind, but it was simple and direct. And this is why he 
succeeded where others failed. He resolved to confine his studies 
to his own little thirty-by-seven-foot patch and not to wander afield 
(possibly because he was too fat to travel comfortably). In his 
garden were plants with many different characteristics. Mendel 
decided to concentrate on just one character at a time. So, as one 
instance, he set out to see what would happen when he mated 
plants of a pure red-flowering strain with those that habitually bore 
white flowers. Thorough in his methods, he bred together hundreds 
of such plants. And this was the result: The offspring were all red- 

Had the influence of the white parent been completely lost? No, 
because when Mendel mated any two second-generation red- 
flowered plants together, the offspring were three in four red- 
flowered, but one out of four was pure white like the white grand- 
parent. This proved that the white factor had been carried along 
hidden in the preceding generation. 

Further investigation showed that the third generation red- 
flowered plants were not all alike, even though they looked the 
same. In only one out of three cases were they “pure” red-flowered, 
like the grandparent, and when mated with each other would pro- 
duce only red flowers. In the other instances the plants had mixed 
factors, both red and white, like their immediate parents. 

Mendel checked the results in planting after planting. Mean- 
while, in different patches of his garden, he experimented with other 
matings—breeds of tall pea plants with breeds of short ones; plants 
having yellow seeds with those having green; wrinkled seeds with 
smooth, etc. For everything he kept exact figures, carefully tabu- 
lated, until finally the evidence pointed overwhelmingly to these 
conclusions, now often referred to as | 


1. The inherited characteristics are produced by genes (called 
by Mendel “factors”) which are passed along unchanged from 
one generation to another. 

2. In each individual these genes are found in pairs, and where 
the two genes in a pair. are different in their effects, one gene 


dominates the other so that it might be referred to as a “dominant,” 
the other as a “recessive.” 

3. When seeds are formed in any individual, the members of 
each pair of genes segregate out, independently of the other pairs, 
with just one of every two mated genes going from each parent to 

each offspring. 

These conclusions Mendel embodied in a paper which he read 
before his local scientific society and which was then printed. But 
almost no attention was paid to it. The scientific world of the time 
was in a turmoil over Darwin’s theory of evolution. The few who 
saw Abbot Mendel’s paper ignored it. And so Mendel, little aware 
of the scientific treasure he had unearthed, turned to other things 
and passed on at the age of sixty-two. 

But recognition did come—sixteen years too late. In 1900, three 
biologists, almost at the same time (although they were working 
independently) chanced on Mendel’s paper and quickly realized its 
importance. Their reports set the world of biology feverishly experi- 
menting to see whether the Mendelian findings applied to other 
living things—including man. Yes, in many cases Mendel’s “laws” 
did seem to operate. But in other instances the results were either 
inconclusive or flatly contradictory. Biologists were floundering 
about in confusion, and might still have been had not a very large 
man named Thomas Hunt Morgan happened to become intensely 
interested in a very little fly named Drosophila melanogaster. 

The drama which might be called “Man Meets Fly” began in 
1907. Professor Morgan, then at Columbia University, found the 
fruit-fly an ideal subject for his experiments. For one thing, the 
Drosophilz, mere and pére, do not believe in birth control. At the 
age of twelve days they are ready to breed and within another 
twelve days each female produces some 300 offspring. Starting 
from scratch, within two years one can get sixty generations of flies, 
as many as there have been generations of mankind from the time 
of Christ. Moreover, the fly has many easily distinguished variations 
and the cost of boarding it is trifling. The reward for all this is 
that the Drosophila has today become the most famous experimental 


animal in science, and is assured immortality, even though individu- 
ally it might prefer a speckled banana. 

With the Drosophila, then, Morgan was able to prove that while 
the Mendelian principles held firmly, the mechanism of heredity 
was not nearly so simple as Mendel had suggested. There were 
many complicated forms of gene operation, Morgan showed, and 
many environmental factors that influenced the genes. All this he 
and a brilliant corps of students and collaborators made indispu. 
tably clear. They identified hundreds of special genes in the Drosoph. 
ila. They showed at which points on the flies’ chromosomes these 
genes were located. And they actually bred flies of almost any kind 
specified as easily as a pharmacist would compound a prescription. 

All this time, everything learned about the gene workings in 
flies was being applied to the study of other living things, up the 
scale from the most elemental creatures to man himself. Jennings 
with the paramecium, Goldschmidt with moths, Castle with 
rabbits, Wright with guinea-pigs, Stockard with dogs, Davenport 
with studies of humans—these are but a handful of the hundreds 
of brilliant investigators who pyramided the facts on which our 
present knowledge of the genes so firmly rests. 

So it is by way of Mendel with his peas and Morgan with his 
flies that we have finally arrived at an understanding of the com- 
plexities of human heredity. If you turn back again now to the 
figurative drawings of our “chain-gangs” (chromosomes) you will 
see why we have shown that while genes at corresponding points 
in the paired chains are the same in the type of work to which they 
are assigned, they are not necessarily the same in their characters. 
The two “A-1” architect genes, one coming from your father, the 
other from your mother, may have been as different in their manner 
of working as are any two human architects. So, too, just as any 
two plumbers might differ, or any two masons might differ (even 
though they belonged to the same union) any two paired genes 
might differ greatly in what they do and how they do it. 

There are strong genes, weak genes, alert genes, and inactive 
genes; temperamental genes and freak genes; constructive genes 
and destructive genes; in fact, if we endow them with personalities 
genes individually have almost as many different characteristics as 


have the people they create. Ever present, moreover, are the factors 
of environment, which may make any given gene act one way 
under some conditions, another way under other conditions, just 
as the work of a human artisan is affected by food, weather, acci- 
dent, spats with fellow-workers, etc. 

The best way of illustrating all this is to tell what genes do with 
regard to our own features, organs and characteristics. It will then 
be clear why in some instances we needn’t be at all surprised if we 
have a child that looks nothing like either parent, whereas in other 
instances a child of an unexpected type may rightly be regarded 
with suspicion. 



Amonc the characteristics of a child which most often are un- 
expected and baffling to parents are the coloring of its eyes and hair 
—and sometimes its skin. 

Nevertheless, because color is on the surface and is quite definite 
in its nature, it offers us one of the simplest means of studying and 
analyzing the action of genes. 

Color, to begin with, is not a positive substance but an effect 
produced by the reflection of light on different materials. When we 
speak, then, of different genes “producing” different colors, what 
is meant is that given genes take part in the production of differen. 
pigment materials. The color effect of these pigments is not impor- 
tant to Nature. Where pigment is produced in the skin, eyes or 
hair, it is usually to insure protection from the sunlight. The pig- 
ment deposited in the otherwise translucent iris of the eye shades 
the retina within; the pigment in the skin protects the flesh under- 
neath. Even the pigment in the hair affords protection to the hair 
cells and the scalp. 

In the eye we have our most interesting range of color effects. 
Geneticists believe that the first human beings all had very dark 
brown or black eyes, and that by mutations throughout the ages 
the original eye-pigment genes gave rise to variations which now 
provide us with all the many known lighter shades. 

To produce the color effects, the genes do not mix pigments, 
nor, in fact, are different pigments produced to correspond with 
what we know as the eye colors. There are really only one or two 
basic eye pigments, and a few variations of these. What any given 
eyes look like is determined by the amount of these pigments and 
the way in which they are distributed in the iris. 

The iris, as you probably know, is the small disk around the pupil. 



(Or, rather, one should say that the pupil is the hole in the iris.) 
Without any pigment the iris would look something like a tiny, 
transparent doughnut. It has, however, two clearly defined parts 
as if it had been slit in half and pasted together again. Thus we 
speak of the part facing out as the “front” of the iris and the 
other half as the “rear.” 

While a number of genes participate in the pigmenting process, it 
is a single “key” gene that usually determines the result. 

Cross - section Side View 
Front View of Eye (Part in front of dotted line 
shown ‘in color - plate) 

In BLuE Eyes the gene is a weakling which produces no pigment 
whatsoever in the front of the iris, but manages to produce a 
certain amount in the rear. But this pigment is a dark substance, 
not blue. The blue eye color that results is an optical effect, just 
as is the blue of the sky, and is caused by the reflection and diffrac- 
tion of light by the pigment and other particles in the eye. 

In fact, all eyes are basically just as “blue” as blue eyes. The other 
eye colors are due to the addition of pigment in the front of the irts. 

In GREEN Eyes the rear of the iris has the same kind of pigmenta- 
tion as in blue eyes, but in addition the “key” gene or a special 
gene lays down a certain number of dilute brown or yellow pigment 
cells in the front of the iris. Superimposed on the “blue” back- 
ground, these produce the effect of green. 

In cray EyeEs the gene involved distributes lightly a number of 
black (or dark brown) pigment cells in the front, and these against 
the blue-appearing background produce the gray effect. 




If "true" blue-eyed 
you carry two 
"blue-eye" genes 

BLUE ie 
as is due to 
reflection of 
light from 
tiny dark 
pigment granules in 
An optical illusion OF IRIS 

(There is no blue pigment 

(One alone is recessive to 
all others except Albino) 

in the eye) 



(yellow ++ blue = green) 


is due to 
scattered yellow 
pigment in 
acting with the 
blue reflection 


is due to 
scattered dark 

pigment in 


screening blue 


from behind 

(Gene action of green 
and gray eyes not yet 
clearly established) 

Two brown-eye 

—BROWN Effect genes 
is due to 
dark pigment in 
FRONT or One 
OF IRIS one @+ of 
paring blue any 
re ection lighter 
(The heavier the Epes 

pigmentation, the 
darker the eye) 

= P| N K Effect An albino carries 
(Albino) is due to two albino genes 
reflection from ae - 

An Illusion 

(The eye is really 

blood vessels 

But persons of any 

other eye color including 

blue may be carrying 
a hidden albino gene 

4 : f a ' ley Ne ae ? . 
‘ ‘ . : ‘ Ld t 

rr’ " eh Wa ie . we aotee) |) Ls 
7 “/ at =Sier Doiee id _ : 

¥ at 

F ar ant how iy, uN 


In Brown EyEs the “key” gene is active enough to so fill the 
front of the iris with pigment that no blue reflection can be seen. 

And finally, in stack ryzs the gene is of the most vigorous type, 
and lays down an intense deposit of pigment in the front of the iris 
(and perhaps the rear also). 

All the other in-between eye-color effects are produced by the 
varying degrees of pigmentation, and also by the “pattern” in which 
the pigment is distributed. 

ALBINO EYES should be dealt with separately because they are not 
due to any cye-color gene but to a defective “general” gene which 
interferes with all pigmentation processes. Thus, the true albino 
eyes have no pigment whatsoever, in either the front or rear of 
the iris. The pink effect is due partly to tiny blood-vessels in the 
partition of the otherwise colorless iris, and partly to the reflection 
from other blood-vessels behind. 

Let us .see now what happens when an individual receives one 
kind of eye-color gene from one parent, a different gene from the 
other parent. 

In eye color, as in most other processes, some genes can do the 
same work singly as well as if there were two. The blackest, or 
darkest eye-color gene, if only one is transmitted, will produce the 
same effect as if two were transmitted. That is to say, if a child 
should receive just one dark-eye-color gene from one parent, no 
matter what other gene it received from the other parent—green, 
gray, blue or even albino—that child would have dark brown eyes. 

This follows the principle of dominance and recessiveness which 
Mendel discovered. Just as the gene for red-flower dominated that 
for white-flower in his garden peas, in human beings the gene for 
black (or brown) eyes dominates that for blue eyes (or any other 
of the lighter shades). But, you might ask, doesn’t the blue-eye or 
other recessive gene do anything when coupled with the dominant 
brown-eye gene? 

Possibly you may recall having gone to a party planning to sing, 
or to play the piano or exhibit some other accomplishment, and 
just as you were preparing to perform, some one else got up and 
did the same sort of thing, much more forcefully than you could 


do it. If you were an ordinarily shy person, the chances are that 
you kept your performance to yourself for the rest of the evening. 

That is what happens when a little Blue-Eye gene arrives and 
finds a big domineering Brown-Eye gene on the scene. Little Blue- 
Eye sits back with never a peep out of it through all the long 
lifetime of the individual in which it finds itself. But there is 
always “another time.” Just as you might go to the next party, and 
in the absence of a menacing competitor, perform handsomely, so 
the Blue-Eye gene need not be permanently squelched. To a gene, 
the “next time” means the next individual to which it is sent—that 
is, to some future child. Again little Blue-Eye gene goes forth hope- 
fully (and if necessary again and again, generation after generation) 
until in some child it finds itself coupled, not with a “bully” Brown- 
Eye gene, but with a kindred Blue-Eye gene. And this time, glory 
be, the two Blue-Eye genes happily fall to work, and the result is a 
blue-eyed baby! 

In all mixed matings the blue-eye gene has a hard time of it, for 
it is also dominated by the light-brown, green and gray-eye genes; 
by all the rest, in fact, except the albino gene, which all normal 
genes dominate. As for the other contests, the general rule is that 
the genes for darker colors dominate those for the lighter shades. 
But present evidence is still not clear as to what happens when a 
green-eye gene and a gray-eye, both of apparently equal potency, 
get together. 

From all the foregoing, you may make these guesses about the 
eye-color genes you are carrying: 

If you have black or brown eyes: 

(1) Where both your parents, all your brothers and sisters and 
all your near relatives also have dark eyes, in all probability you 
carry two black (or brown-eye) genes. 

(2) Where both your parents have dark eyes, but one or more 
of your brothers and sisters or other near relatives have eyes of a 
lighter shade (gray, green, ‘blue) you may be carrying, in addition 
to the dark-eye gene, a “hidden” gene for the lighter shade. The 
greater the number in your family who have light-colored eyes, the 
‘greater the chance that you carry such a gene. 

(3) Where one of your parents has black or brown eYes and the 


other light-colored eyes you definitely carry one dark-eye gene and 
one for a lighter shade. If the light-eyed parent has gray or green 
eyes, your “hidden” gene may be either a gray, green, or blue one. 
If the parent has blue eyes, then you definitely carry a hidden 
blue-eye gene. 

If you have gray or green eyes: 

Regardless of what eye colors your parents have, you carry no 
dark, but only light-colored genes, which may be gray, green or 
blue. If one parent has blue eyes, however, then you definitely 
carry at least one “hidden” blue-eye gene. 

If you have blue eyes: 3 

Regardless of the eye colors of your parents, you are almost certain 
to be carrying two blue-eye genes. 

If you have albino eyes: 

You must be carrying two albino genes. 

To all the foregoing deductions there may be, more or less rarely, 
some exceptions. As we have learned, environmental factors can 
swerve a gene from its course and alter its workings. One cannot 
always be positive that a person whose eyes are, or appear to be, 
blue, really carries two blue-eye genes. In rare instances a person 
may receive at conception one, or even both genes, of some darker 
shade, and at some stage thereafter something may happen to 
inhibit or modify the usual gene workings so that blue or blue- 
appearing eyes result. Disease and age may be among such modify- 
ing influences. Any mother knows that her brown-eyed child was 
born with slate-blue eyes, and that it may take up to two years or 
more before the “true” eye color of a child is revealed and that 
even thereafter the color may never be constant. In old age, brown 
eyes may again become bluish. Cataracts, or some other eye defect, 
may also rob brown eyes of their color and make them appear to be 
a watery-blue. One cannot therefore always tell. merely by looking 
at people’s eyes what genes they may be carrying. 

Still another modifying influence in human eye color is that of 
pattern in pigment distribution, also determined by genes. There 
are eye types with the pigment in rings, in clouds, in radial stripes, 
or spread over the whole iris. The pattern genes have not been too 
closely studied, but it appears that where parents have a radial, 


ring or cloud-eye pattern, most of the children will have the same. 
If, however, a child receives different “pattern” genes than a given 
parent, even though the color genes are the same, the eyes may 
look different. 

One peculiar phenomenon, which occurs about once in a thou- 
sand times, is that of unmatched eyes—the two eyes in the same 
person being of different colors. Among motion-picture celebrities, 
Colleen Moore and Lionel Stander have this eye-condition. How 
it occurs may be explained in several ways: A person may inherit 
one brown-eye gene and one blue-eye gene, which would normally 
make both eyes brown. But in the very earliest stages something 
may happen to the brown-eye gene in the rudimentary eye cell on 
one side of the face, leaving the field on that side to the blue-eye 
gene. Or, starting with two blue-eye genes some pathological con- 
dition may increase the pigment production in one of the eyes, 
making it brown. 

While most unmatched eyes are believed due to environmental 
factors, this condition might also be inherited as the result of a one- 
sided eye-nerve defect which can be transmitted through a certain 
gene. The condition, by the way, is prevalent among many domestic 
animals, including dogs, cats and cattle. 

Sex also seems to play a part in eye color. Women’s eyes as a 
general rule are slightly darker than those of men. There are more 
brown-eyed girls than boys, and, generally, more males with blue 
eyes than females. These conclusions have been reached through 
studies of several hundred thousand school children, with additional 
studies made in the adult population. Exceptions have been noted 
in the cases of Russians, Scots, and Bulgarians, among whom, for 
some reason, the sex-factor in eye color does not seem to be 

Although the range of human eye color is normally confined to 
variations of brown, blue, green and gray eyes, rare cases have been 
reported of persons with eyes of tortoise-shell color (mottled yellow 
and black), and also of persons with ruby-colored eyes. But we may 
eventually see eyes of many other colors. Even so serious a geneti- 
cist as Professor Jennings believes that new eye colors in man 
could conceivably be produced by means of chemicals. We may 


therefore yet see the time when some women will change the color 
of their eyes just as they now change that of their hair. When that 
day comes, and a man says to a girl, “Where did you get those 
big blue eyes?” she may reply: “At Antoine’s, corner of De Peyster 
Avenue and Thirty-second Street!” 



GENTLEMEN (and particularly a certain European dictator) we are 
told prefer blondes. , 

There must be some truth in this, for otherwise how account 
for the great number of women who go to beauty parlors to have 
their dark hair bleached? Is there any record of blondes convert-— 
ing themselves into brunettes? (Unless, perhaps, to avoid the police.) 

Even more than blond hair, red hair has a certain social sig- 
nificance. Which might lead to this question, assuming that you 
are a prospective parent: 

“What are the chances of a child of yours being a blond or a 
red-head ?” 

As you already have gathered, looking at your own hair and that 
of your mate may not in itself provide the answer. You must try 
to ascertain what genes for hair color you both carry. 

Pigmentation of the hair follows the same general principles as 
does that of the eyes. Often, in fact (but not always), the two are 
related. In hair we deal with the pigmentation of hair cells, and 
just as in eyes the basic actions of the color genes may be modified 
or changed by “meddling” genes and by many environmental 

A dark-brown pigment known as melanin is chemically the prin- 
cipal element in our hair coloring. If the “key” hair-color gene acts 
to produce a heavy -deposit of melanin in the hair cells, the result 
is black hair; a little less melanin, very dark brown hair; still less, 
light brown; and very dilute, blond hair. The shade of hair color 
is further influenced by the way the hair cells are constructed, by | 
their air content and by their amount of natural oil, or greasiness. 

Red hair is due to a supplementary gene which produces a dif- 

fuse red pigment. It is often present with the “key” melanin gene. 





hair cells 

produced by 

produced by 
red pigment 
diffused with 
the scattered 
pigment granules 

produced by 
heavy deposit of 
pigment granules 
(The heavier the 
déposit, the darker 
the brown) 

deposit of 


(If white hair is 
not due to age or 


(But all hair 
color types may be 
carrying one hidden 

White-Hair Gene) 




(The "Red-Hair” Gene 
is a special one 
which shows its 

effect if not 
masked by 
very "Dark-Hair” 

Red Gene may make 

hair reddish-brown) 

06: 0@ 

or Gene 

ee1 |. 




If the melanin gene is very active, making the hair black or dark 
brown, the effect of the red gene will be completely obscured. (The 
claim has been made, however, that a hidden red gene may betray 
its presence in black-haired persons by a glossiness of the hair.) 
Where the melanin gene is weaker, the red-hair gene can manifest 
itself, and the result will be a reddish-brown, or chestnut shade. 
If the brown-hair gene is an utter weakling, or if it is absent, dis- 
tinctive red hair will be produced. 

In relation to a “blond” gene, we are not so sure of the action 
of the red-hair gene. Theoretically, it should dominate the blond, 
but we have cases, nevertheless, where blond parents have a red- 
haired child. With rare exceptions, however, the blond gene is defi- 
nitely recessive to those for all darker-hair shades. 

This leads to these conclusions: 

If you have dark hair, you are'carrying either two dark-hair genes, 
or one dark and one for any other shade. 

If you have blond hair, you carry two blond genes. 

If you have red hair you are carrying either one or two red genes, 
supplementing blond or brown genes. 

The basic hair-color genes are found among all peoples, although 
not by any means in the same proportions. Red-heads are found 
even among Negroes and are quite frequent among the usually 
black-haired Latins. While blonds also are not uncommon among 
Latins and other black-haired peoples, we have no way of know- 
ing to what extent the blond gene may have arisen among them 
by mutation, or to what extent it was introduced through inter- 
breeding. The mutation theory seems to be the most plausible one 
in the case of blond Indians found among certain black-haired 
tribes, notably in Panama. 

White hair can be due to various factors, genetic and otherwise. 
In its most striking form it is caused by the albino gene, which, 
as we have already seen, also robs the eye of color. White hair 
might also be due to an extremely weak blond gene, or to some 
“inhibiting” gene or condition which would interfere only with 
the hair-pigmenting process. White-haired persons of this type, quite 
common among Norwegians, Swedes, etc., differ from albinos in 
that they are normal in eye and skin pigmentation. And finally, 


there is the white hair due to age, disease, etc. In fact, in all hair 
colors there is the constant possibility that other factors may alter 
the effects of the “key” genes. 

Age plays a much more important part in hair color than it does 
in eye color. The hair-color genes may be slow in expressing them- 
selves. Often mothers have wailed as they have seen the golden 
locks of their young child turn later into an indefinite murky brown. 
On the other hand, a child born with black hair may have the sec- 
ond growth of hair much lighter in shade. 

Light hair as a rule has a tendency to turn darker from child- 
hood on through maturity. This also applies to red hair. Rarely does 
hair become lighter in color as a child grows up. Constant exposure 
to the sun, or bleaching by salt water, drugs, or some other artificial 
means, can of course easily lighten or change hair color, and cli- 
mate can also be an influence. But regardless of surface changes, 
the pigment particles will still be there, so that under a microscope 
a scientific Sherlock Holmes could easily tell whether a blond was 
natural or artificial. 

The hair-color change that comes with age is one of decoloriza- 
tion. Not merely the pigment, but the air content, oil content and 
structure of the hair are affected. The time at which hair pigmenta- 
tion begins to slow down often seems to be governed by heredity. 
Where a parent has grayed prematurely, in many cases a child 
will begin to gray at about the same time. 

Nerves or gland disorders, diseases and other physiological factors 
may also affect or change the color of hair. The belief has long been 
prevalent that sudden shock can turn a person’s hair white “over- 
night.” Quite possibly some sudden nerve upset might affect the 
hair-pigmenting process, causing the new hair to grow out white; 
but a little study of the hair structure will show that no shock 
could be communicated instantly along the whole length of all the 
hairs already grown out, to destroy the pigment there. For lack of 
authenticated cases the “turning white overnight” stories will have 
to be lumped with the myths about children being born with 
white hair because their mothers were frightened during pregnancy. 

In passing, it might be noted that localized environmental condi- 
tions in different parts of the body may account for discrepancies 


in color or shade between the hair on the head and that elsewhere. 
Gland-action, perspiration, under-exposure to air, etc., may cause 
such differences. Thus, men with brown head-hair may have fair 
or reddish pubic hair. Strangely enough, where in men the tend- 
ency is for this hair to be lighter than the head-hair, in blond 
women the pubic hair is usually darker than their head-hair. 

We have dealt with environmental influences at some length be- 
cause it is important for parents to rule out these factors before 
they can ascertain what hair-color genes they may be carrying and 
can pass on to their children. Unless changes in parents’ hair are 
caused by genes, they can have no meaning with regard to the hair 
color of their child. 


Jupy O’Grapy and the Colonel’s lady, both being white, might 
very well be sisters under the skin. But whether the black man, 
yellow man and white man are brothers under the skin is a ques- 
tion that has long agitated the world and still causes strife and 

Scientifically, the matter of skin color is important because it 
has long been used as a basis for the broad classification of human 
beings into so-called “White,” “Black” and “Yellow” races. Although 
the “blending” effects in offspring of mixed matings was thought 
to contradict the Mendelian laws, we are now able to show clearly 
that the “skin-color” genes act in precisely the same way as do 
other genes. 

One’s skin is in some respects like a wrapping. The skin serves 
many purposes, among them that of protecting the flesh beneath. 
For one thing, it must shade the delicate blood-vessels from strong 
sun or light rays. Nature therefore calls on certain genes to fill 
the skin with pigment particles; and because the human being is 
a migratory animal, the amount of pigment produced is governed 
to some extent by the needs of the individual, varying with the 
seasons and other influences (including disease). 

Persons of the so-called “White races” may range all the way 
from the very light-skinned “Nordics” of the cold climates to the 
extremely dark-skinned southern Italians and almost-black Arabs. 
The difference in complexions among Whites in various countries 
is due in part to gene variations, in part to the degree of exposure 
to the hot sun. The black skin of the Negro is, however, not due 
to such exposure, although it may be modified by more or less 

sunlight. Shakespeare was laboring under a familiar misapprehen- 


sion when he had the Prince of Morocco refer to his complexion 
as “The shadow’d livery of the burnish’d sun.” 

It might be noted that the terms “White” or “Black” are often 
used arbitrarily without regard to skin color, and may have dif- 
ferent meanings in different parts of the world. In the south of 
the United States a person who has any distinguishable fraction 
of Negro blood is grouped with the “Blacks” and must ride with 
them in the “Jim Crow” cars. In South Africa, on the other hand, 
a fraction of white blood makes a person “White.” The “Jim Crow” 
laws there apply only to those who are full-blooded Negroes. 

The skin-color genes among the various peoples differ not merely 
in the amount but in the type of pigment they produce. In Whites 
the basic pigment is the brown melanin, diffusely distributed in 
the epidermis so that the blood-vessels below shine through and 
produce the “flesh color” which artists suffer agonies trying to copy. 
Among Mongols, Eskimos and American Indians, the brown-color 
gene is either supplemented with or replaced by one producing yel- 
low or yellowish-red pigment. In Negroes it is believed that several 
skin-color genes are at work, some producing yellowish and dark- 
brown pigments in greater intensity than in lighter-skinned peoples. 

Examples of how “multiple” genes operate are offered in mat- 
ings between full-blooded Negroes and Whites. Although at first 
glance the skin color of their children might seem to evidence a 
blended action of the black and white parental genes, analysis shows 
that the color genes are at work independently, and that only in 
the effect they produce is there any blending. The segregation of the 
genes is revealed if, in the next generation, the mulatto offspring 
mate with similar mulatto offspring. Had the genes blended, all 
the offspring would have the mulatto color of their parents. Instead, 
such offspring are of a variety of shades, ranging from the darkest 
black of any Negro grandparent, to the light skin of the fairest 
white grandparent. 

How this sorting out and recombination of the genes takes place 
is shown in our accompanying color-plate. We can see by this why 
a truly black-skinned child can be produced only if both parents 
carry some Negro-skin-color genes. This should dispose of the 
old superstition, common in yesterday’s fiction, of how a woman 


with some hidden Negro blood, “passing” as white and married 
to a White, might give birth to a coal-black baby. Where a black 
baby does unexpectedly turn up, it can be taken for granted that 
(a) both parents have Negro ancestry, or (b) that the parentage 
is doubtful. In reverse, it would be equally impossible for a Negress 
with hidden white blood to be mated with a full-blooded Negro and 
give birth to a white child. 

Apart from the pigment they produce, the skin-color genes may 
also influence the manner in which skins react to strong sunlight. 
Take the familiar examples of stenographers on their vacations. In 
the case of one, the more she is exposed to glaring sunlight, the 
more her genes will rally to increase pigmentation. A beautiful tan 
will result. In another girl (usually true of very fair-skinned peo- 
ple) the pigment genes may be unequal to the task. Unless she 
properly protects herself, her flesh may actually be broiled, some- 
times with serious results. 

There are white persons who through constant exposure to a 
hot sun can become almost as dark as some Negroes. However, 
their coat of tan can never offer them the same protection from 
the sun’s rays as does the natural pigmentation of the Negro. Where 
normally fair Whites do become dark-skinned, it should be clea: 
that this is only an acquired characteristic that can have no effect 
on their children. White families can live in the tropics for gen- 
erations, and yet their children will continue to be born as fair- 
skinned as if their forebears had never strayed out of Hoboken, 
New Jersey. 

Do Negroes become lighter when they are kept out of the sun? 
Yes, somewhat. While the basic skin color of the full-blooded Negro 
is always dark, it may vary in intensity under different conditions. 
Some Negroes, however, are genetically lighter-skinned than others. 
Increasing intermarriage, with the constant admixture of white- 
skin genes, has greatly diluted the “mean” (average) color of the 
Negro population. It is estimated, in fact, that the Negro popula- 
tion of the United States today does not contain more than 5 per- 
cent of “full” Negroes, who have no white blood whatsoever. 

Matings between Whites and Yellow people have also been ex- 
tensively studied, but are of less importance to us. Of interest, how- 


The white has 
two sets of 
“white-skin" genes 

The ''full'’ Negro has 
TWO sets of 
"Negro skin-color'' genes 


Each parent contributes to every child 
ONE set. (One "A" gene and one "'B") 

Every child is of a ‘blended" (mulatto) shade 

WHEN TWO MULATTOS (like child above) MAT 

The genes segregate, and each parent 
may give to a child any of these four 
combinations of "A'' and "B" genes: 

eo” 4G ASi«l¢ >| 

Mulatta Mulatto 
Skin Genes Skin Genes 
4 @° From both parents together a child may get 
any of nine combinations, including these: 
All four Three Two One All four 
“Negro” genes: "| genes: “Negro” genes: "Negro" gene: "White" genes: 

@|@ 2° e 
eo @0 O16 @10 O'1O 

Aen Oe OF VARIOUS $ Orr 

Black Dark Medium Light White 

(NOTE: Only two types of skin color genes are shown, but there probably are more) 

Tints th SO 

i eae 

i a y a st 



ever, are the instances of where a remote Mongol ancestor may 
reveal himself in a European or American infant through the “Mon- 
golian spot.” This is a patch, or concentration of pigment cells, 
toward the lower end of the spine occurring as a hereditary effect 
in many, if not almost all, infants among Eskimos, Indians, Chinese 
and kindred peoples. It disappears by the end of the first year. 
Where this spot appears not infrequently among infants of Austrian 
or Hungarian descent, or sometimes among those of some other 
nationality, it often reveals the presence of some Mongolian in- the remote branches of the family tree. 

Freckles provide a more familiar example of spotting in humans, 
which may have a definite hereditary basis. Freckling is often 
transitory, appearing in childhood and disappearing with maturity. 
Frequently it is associated with red hair and white skin, indicat- 
ing the likelihood of some multiple gene action. A rarer form of 
spotting in humans, just as in lower animals,-is the presence from 
birth of permanent white patches over the body, due to an eccentric 
dominant gene. 

In the general skin-pigmenting process, the genes do not assert 
themselves in full strength until after infancy. Characteristic pig- 
mentation begins during the embryonic stage. Negro babies at 
birth have skin of a light sepia color. “White” babies are anything 
but white at birth (as every one knows!). Their flaming redness 
is due to the fact that their as yet very thin, and very sparsely pig- 
mented, skin allows the blood-vessels beneath to shine through. 

Changes in skin color in later years may be due to various other 
influences besides those already mentioned. “Addison’s disease” gives 
the sufferer a bronzed skin. Pregnancy also tends to darken the 
skin in a woman. Jaundice produces a yellowish skin, as does ad- 
diction to certain drugs. Tuberculosis may give a person white skin 
with very red cheeks. Still other diseases produce their characteristic 
skin effects. But, as we must constantly keep in mind, all such in- 
fluences can in no way change the skin-color genes which the in- 
dividuals transmit ta their children. 



Ir we expect to find in the plastic features of our face (nose, eye- 
shape, ears, lips, etc.) and in our body form as a whole, such clear- 
cut examples of gene dominance and recessiveness as occur in our 
coloring processes, we are due for a measure of disappointment. 

This is not because the “sculptor” genes are less definite in their 
work than the “color” genes. It is because we know less about 
them. Their effects are much harder to study, our plastic features 
being not nearly so independent in their development as are our 
color effects, and being also influenced by many more external fac- 
tors. Added to all this is the difficulty of classification. 

In eye color, for instance, “blue” is blue, applied to any one the 
world over. We know exactly what is meant by “blue” when we 
say a child or a man of sixty has blue eyes, a girl or a boy has blue 
eyes. But in describing features or form we can use such terms as 
“large,” “small,” “broad,” “narrow,” etc., only relatively. A nose 
that would be large on a child would be small on an adult; a nose 
that would be broad on an Englishman would be considered narrow 
among Negroes; a nose that would look handsome on a Leslie 
Howard would be a monstrosity on a Greta Garbo. | 

Consider the members of your own family, or your friends. You 
say that this one of you has a “large” nose, that one a “small” 
nose. If you measured the noses you would be surprised to find that 
the difference between them might be no more than three-sixteenths 
or a quarter of an inch. Similarly, you would find that the differ- 
ence between what we call “enormous” eyes and average eyes might 
not be more than an eighth of an inch in width. 

For this reason, geneticists and anthropologists who have studied 
human features have confined themselves largely to crosses between 
peoples with marked differences—Whites and Negroes, Europeans 



and Chinese, etc. (This is why, also, in this book so much atten- 
tion has been and will be given to “mixed” matings.) Nevertheless, 
the “inter-racial” studies have been checked sufficiently with obser- 
vations of matings among people of all kinds to lead to certain 
fairly definite conclusions regarding our specific features. 

Tue Nossr. The “nose” genes are among those that can be most 
clearly analyzed. Some studies might indicate that there is one 
“key” gene producing the general shape of the nose, but most 
authorities agree that three, and possibly four genes are at work, 
each on a different part. That is, there would be separate genes 
for the bridge (its shape, height and length); the nostrils (breadth, 
shape and size of apertures); the root of the nose and its junc- 
ture with the upper lip; and the “bulb,” or point of the nose. 

Often, it is true, the nose as an entire unit appears to be “in- 
herited” from one parent, as might be almost the entire face. (The 
present J. Pierpont Morgan, for instance, bears a striking resem- 
blance to his late father.) Where such resemblance occurs in a set 
of features between a parent and a child, it can be assumed that 
the different genes involved were passed over in combination and 
were almost all of them dominant over those of the other parent. 

Very often, on the other hand, a child has a nose which seems 
to be a “cross” between that of both parents. This would bear out 
the theory that several unit factors are involved. At any rate, it is 
clear that distinctive genes are at work, and that they sort out inde- 
pendently. If this were not so, the nose of every child would be a 
“blend” of its parents’ noses, and eventually in a fairly homogenous 
population, the noses of all persons would look alike. But we know, 
of course, that this is not so; that even in the most inbred peoples 
roses of every shape and size appear, proving the Mendelian segre- 
gation and sorting out of the “nose” genes. 

In the bridge, the most important part of the nose, shape and size 
are dependent on how far out from the skull and at what angle, 
the “bridge” gene works until it stops. 

At the same time other “nose” genes are acting to determine 
the breadth of the nose, ranging from the thin bridge found among 

“Nordics” to the broad bridge found among Negroes; and these, 
or still other genes, are at work on the nostrils and the “bulb” or 



—lf a bit further 
down, an average- 
length nose; if much 
further down, a 


@ If the "bridge" 
gene in its 
workings stops 
short, result is a 


—If it makes just 
a small angle, re- 
sult is a 


3) If the ''bridge’' 
gene pushes out 
far, at a big angle, 
result is a ROMAN 

eet (or prominent) nose 

tip of the nose. What happens when the paired genes from the 
two parents are radically different is suggested by the illustration. 

With the various nose genes sorting out independently, we can 
see how persons may have a large nose with small nostrils, a small 
nose with a wide bridge and large nostrils, or any other combina- 
tion. The full effects of the nose genes do not assert themselves 
until maturity; in fact, the genes may keep on working throughout 
life. As many readers have learned to their regret, the pertest, 
daintiest little noses of childhood may blossom out after adolescence 
into veritable monstrosities. Moreover, during and after middle age, 
there may be a final “spurt” in nose development, so that often, 
in later years, racial or familial characteristics become most apparent. 

Being the most prominent of the features, the nose may also be 
most affected by environmental factors. Nose diseases (such as 


The gene DOMINATES The gene 

for for 

Prominent and Moderate and 
Convex Straight 

The gene The gene 

-O On| 

ae (_) 

| High and Narrow Low and Broad Bridge 
i Bridge (As in Negroes) 
| The gene DOMINATES The gene 

for for 

rp)? Oey) 

N 4 
| Broad Nostrils arrow Nostrils 

NOTE: It should be clear that it is not any type of nose itself that “dominates” another 
| nose, but the gene producing the nose effect that dominates the other gene. 



sinusitis), structural disorders (deviated septums), childhood ac- 
cidents, blows, blood disorders, alcoholism, etc., all can wreak havoc 
with nose shapes. Despite all this, however, the genes do manage 
to assert themselves and a knowledge of what “nose” genes the 
parents carry can lead to a pretty fair prediction of what the noses 
of their children will look like. 

Tue Eyes. The form and shape of the eye, as we see it, are con- 
ditioned by the shape of the individual socket, and by the way the 
lids grow. A “large” eye may be due either to the fact that the 
eyeball and the socket are large, or because the eyeball protrudes 
and pushes back the lids around it (which may happen through 
some disease, as for instance, goiter). Where normal, the gene for 
wide eye dominates that for narrow. 

The “slant” or “almond” eye is often confused with the Mongolian 
eye found among Chinese, Japanese, Eskimos, etc. In the slant eye, 
the inner corner is rounded, the outer pointed, and slightly higher. 
The Mongolian eye, however, is due to a skin fold overlapping 
the inner corner of the eye which gives it its oblique appearance. 
While the gene for “slant” eye is recessive to that for “straight,” the 
gene for Mongolian eye is usually dominant. 

Another dominant (fortunate for the ladies) is the one stilt 
produces long eyelashes. Where a mother has long lashes she can 
count on one of every two daughters “inheriting” them. 

Tue Ear. In ear-shape the Mendelian inheritance of several char- 
acteristics has been noted: 

The gene for long ear seems to dominate that for short. 

The gene for wide ear dominates that for narrow ear. 

The gene for free lobe dominates that for affixed (although not 
always completely). 

(A rare abnormality has also been uncovered recently where smali, 
turned-in cup-shaped ears are inherited as a dominant.) 

Ears, by the way, like the nose, may continue to grow and de- 
velop until late in life. 

Tue Mourtu anp Teetu. Lips are so delicately shaped and formed 
that only in crosses between widely divergent races can we find 
clear instances of how conflicting genes work. 

The “broad lip” gene of the Negro appears to dominate the “thin 


The gene The gene 
for— for— 
© DOMINATES @e ie 
(Not Chinese type) 




On } | DOMINATES Oe a 
©). via DOMINATES Oy Lo) x 

(An abnormality) 



lip” gene of the White. Among Whites themselves, characteristic 
lip forms have been noted in various families, but geneticists have 
not yet studied this feature sufficiently to enable us to say what 
happens when a “cupid’s-bow” gene meets a “thin-lip” gene, etc. 

An abnormal condition, the Hapsburg lip (named for its preva- 
lence in the Spanish royal family) reveals itself clearly as due to 
a dominant gene. The Hapsburg jaw also goes with the lip, an 
example of how the shape of the lips may be conditioned by the 
underlying teeth and jaw formations. 

In teeth, genes are at work to produce the many characteristics 
noted among individuals, but little attempt has been made as yet 
to single out the modes of inheritance. (Except in cases of serious 
teeth defects which will be dealt with later.) Prominence of teeth 
and jaws, however, has been set down as a nearly recessive condition. 

Hair Form. The hair has been subjected in times past and pres- 
ent, throughout the world, to more artificial changes than probably 
any other human feature. But of all hairdressers the greatest are 
the infinitesimal “hairdresser” genes with which a person starts 
life. They determine whether one’s hair is to be straight, wavy, 
curly, or kinky as in Negroes. Of course, we may artificially alter 
the surface effects of the genes’ work; or environmental influences, 
such as age, climate, disease, may somewhat modify hair form. But 
under the microscope we can see that the different forms of hair 
are actually different in their construction, which explains their 
eccentricities of growth. 

In cross-section, straight hair is round; wavy hair is slightly ellip- 
tical; curly hair is more elliptical; and kinky hair is almost flat. 
Kinky hair is also characterized by the “bunching” of the hair in 
spirally twisted locks. In woolly hair, the extreme form of kinky, 
these spiral twists are very small and clumped together close to the 
scalp. (In addition to the gene which produces the form of the in- 
dividual’s hair, there may be another gene that determines its col- 
lective growth.) Although common among Negroes and typical of 
the Bushmen of Australia, woolly hair appears sometimes among 
Whites in whom there can be no presumption of Negro blood. 

The basic differences in hair form are caused by the way the 




— = 2 @ea ee 
2 IAS ic 


cow ee ow won 


Me aucee by 
genes shaping 

_ OPENING! d Slight Ova! Almost 
aa El iptical, | flat, 
Siow, Straight Curved Verycurved Bent 

genes shape the follicles, or pipelets, up and out of which the hair 
grows. If you use toothpaste, you know that there are some tubes 
from which the paste comes out like a flat ribbon, from others 
perfectly round, from still others almost square. The form is de- 
pendent on the shape of the opening in the tube. In the same 
way, by the manner in which they shape the follicles, the “hair- 
dresser” genes determine the form of the hair. By additional slight 
differences in construction and through environmental factors, the 
minor variations in hair form are created. 

In the matter of dominance and recessiveness, the workings of 
the hair-form genes seem fairly distinct. They appear to be graded 
in potency by the degree of curliness they produce. The “woolly” 

Where a different kind of gene is received from each 
parent, the effect is as follows in order of dominance: 


age gene “CURLY gee “WAVY “gene “STRAIGHT « gene 
| Ominar? Q “omin ore? Q Comin ake? Q 


— a 


gene is the most potent, and seems to dominate all others. The 
“kinky” gene, in turn, dominates the “curly,” the “curly” dominates 
the “wavy” and the “wavy” dominates the “straight.” Thus, 
for straight hair there could only be “straight” genes involved. As 
proof of this two straight-haired parents almost invariably have all 
straight-haired children. In matings between parents with other 
hair-forms the results cannot be so easily predicted unless we have 
a fair idea as to which two genes each one is carrying. 

‘A special gene, which determines the “stiffness” of the hair, may 
also be at work to complicate matters. The “stiff-hair” gene found 
among Chinese and Filipinos is a dominant. Apart from this spe- 
cial gene, hair-thickness (i.e. coarse hair vs. fine hair) has not yet 
been clearly analyzed. Thus, in matings between two Americans of 
relatively the same descent, where one has thick hair and the other 
fine hair, we cannot yet predict what type of hair their ae 
may inherit. 

An interesting hair-characteristic is the whorl, the manner in 
which the hair grows wheel-like around the point at the top of 
the head. Some people appear to inherit a “clockwise” whorl; others 
a “counter-clockwise.” The “clockwise” gene is reported as domi- 
nant, studies made in Germany revealing that the clockwise whorl 
appears in about 74 percent of the population; that about 20 per- 
cent have the counter-clockwise whorl; that among the very small 
remainder there is a double whorl. 

The distribution of body hair, the forms of beard and mustache, 
the shapes of eyebrows (and their growing together, as among 
Greeks and Turks) are all determined or strongly influenced by 

Tue Sxin. Complexions, skin-thickness, folds of the skin, ridges 
on the palms and soles of the feet and fingerprints are among other 
surface characteristics in which heredity plays a part. But how the 
genes work with regard to these details is not sufficiently known, 
or even where known may be too involved to be dealt with here. 
(Fingerprints and palm patterns, however, will be discussed again 
in the chapter on twins.) 

Tue Face. Viewing the face as a whole, one of the most interest- 
ing points about the “feature” genes, and something that we have 


taken for granted, is the precision and symmetry with which they 
do their work when they produce two features of the same kind— 
two eyes, two ears, corresponding teeth, and the two sides of the 
face in general. Here we have evidence of how consistently the 
genes do their work. If the genes did not construct the features in 
specified ways, down to the most minute details, one eye would 
be radically different from the other, one ear from another ear, 
etc. (The theoretical mechanism by which the features are repro- 
duced in reverse is too involved for explanation here.) As it is, 
minor differences do exist between corresponding features and sides 
of the face, but except in some abnormal instances these result from 
the slightly different conditions encountered by the duplicate genes, 
or from external effects as the body develops. 

During the intra-uterine stage something may happen to make 
one side of the face different from the other; in early infancy there 
is always the possibility of some slight accident; throughout the 
formative period and even. well into life, sleeping habits, habits of 
speech and eating, and various eccentricities, may produce changes 
in the shape of the mouth, jaw and cheekbones which are char- 
acteristic of individuals or of entire groups or nations; and age, 
through a gradual slight increase in the size of mouth, ears, nose, 
etc., continuing throughout life, may greatly modify appearance. 
Environmental influences, however, do not produce nearly so great 
an effect on the individual features as they do on the body as a 
whole. This we shall see when we turn now to the general body 
form and stature. : 



Ir you are short or tall, fat or thin, did you “inherit” the tendency 
for your type of figure? 

The marked differences between body form in peoples of diverse _ 
races and nations—between Europeans and Hottentots, Chinese and 
Moors, American Indians and Dutch burghers, etc.—might lead 
one to suppose that all such differences were hereditary; and fur- 
ther, that among individuals of the same race these differences 
would be inherited in the same way. Which is to say, that because 
tall Scotchmen kept on breeding tall children, and pigmies kept 
on breeding pigmies, stature was fixed by heredity, and all tall 
parents would have tall children and all short parents would have 
short children. 

Anthropologists have tried for ‘years to find some structural or 
constitutional basis for classifying humans into various groups. But 
today it becomes increasingly clear that while genetic factors most 
certainly are at work in laying out the general skeletal and con- 
stitutional aspects of the body, so many different kinds of genes 
are at work—and, what is more important, so many environmental 
factors are involved—that the classification of peoples on this basis 
is a formidable, if not impossible, task. 

Where groups of human beings have been isolated in the same 
environment for generations, and where there has been considerable 
inbreeding, we do find that all individuals of one group may pos- 
sess many distinctive characteristics in contrast with all individuals 
of some other extreme group—the pigmies, for instance, compared 
with the tall Galloway Scots. But when we look for similar marked 
characteristics differentiating larger groups—Whites, Negroes, Mon- 
gols, or even Scandinavians, English, Italians, etc—we meet with 

confusion. Within a general world population we will find Blacks 


that are as tall as the tallest Whites and hulking Chinese and Japa- 
nese wrestlers that will dwarf many a “Nordic.” (The tallest of 
“peoples,” by the way, are the Negroes of the Lake Chad region of 
Africa, the males averaging 6 feet 1 inch.) With the few excep- 
tions that are the result of selective processes, there are no body 
forms exclusively typical of any “race.” 

Comparing one individual with another, however, there are dif- 
ferences in bodily proportions which often have a hereditary basis. 
But these differences are relatively slight, for we find no such 
hereditary variability among humans as we do among other ani- 
mals of the same species—the giant St. Bernard dog, for instance, 
compared with the pint-sized Mexican Chihuahua. Between the 
very tallest of humans—the Lake Chad Negroes—and the smallest 
pigmy Negrillos (who average 4 feet 6 inches in height) there is 
a difference in height of little more than 25 percent. Even with 
these, we cannot be quite sure to what extent their differences are 
due to “stature” genes, and to what extent to other factors. 

Two interesting “experiments” are on record where an attempt 
was made to deliberately breed tall people or short people. The 
Prussian king, Friedrich Wilhelm I, set out to produce a race of 
tall soldiers by marrying his giant grenadiers to tall women. His 
death stopped the experiment. (We may assume that left to their 
own devices, his grenadiers probably picked out the shortest and 
most petite Gretchens they could find.) 

Catherine de’ Medici, who had many cute ideas, took the op- 
posite tack by setting out to breed a race of dwarfs. She did pro- 
mote quite a number of dwarf matches, but these unfortunately 
(or perhaps fortunately) proved sterile, as such matches usually 
do. Misshapen dwarfs (achondroplastics), by the way, should not 
be confused with midgets (ateleotics) who are normally propor- 
tioned. Where midgets are mated with midgets, and the female 
succeeds in having a child, it is usually of normal size. 

From the moment of conception and through puberty, innumer- 
able factors bear upon the action of the “stature” genes. The mother’s 
health, gland disorders, food habits, climate, living conditions, oc- 
cupation, exercise, modes of walking and sleeping, all influence the 
body structure. This is strikingly illustrated when we transplant 


a group of people to another environment, and watch the effect on 
their offspring, who grow up under different conditions than their 
parents. In the United States, the anthropologist Franz Boas found 
that within one generation children of immigrants (notably Jews 
and Japanese) grew to an average height of two inches more than 
their parents. The better conditions for development offered chil- 
dren here in more recent years are undoubtedly responsible. 

This applies also to the children of native stock. In various studies 
it is reported that American college students today are not only 
taller but heavier than were those of twenty years ago; and even 
ten years ago evidence was advanced (by Horace Gray) that Amer- 
ican boys of native stock averaged two inches taller than those of 
fifty years before. A similar increase in stature is reported in coun- 
tries throughout the world where living conditions, hygiene and 
nurture have been improved. All this is no surprise to livestock 
breeders, who know that proper or improper feeding and care may 
produce, from the same strain, huge prize dairy cattle or stunted 
animals with a “scrub-cow” look. 

Granted that their environments were approximately the same 
(the environment is never exactly the same, even in twins), the dif- 
ferences in height between individuals can then be ascribed to the 
general influence of genes. But how these “stature” genes operate is 
still not too clear. It does appear, though, that the genes for tall- 
ness are usually recessive to those for shortness. This would imply 

Two “normally” tall parents are probably both carrying “tall- 
ness” genes, and will have all tall children. But— 

Two “normally” short parents may be carrying hidden “tallness” 
genes in addition to the dominant “shortness” genes, and can there- 
fore have children who, while for the most part short, may also 
include some of any height. In other words, it is much more_likely 
that short parents may have a tall child than that tall parents will 
have a short child. 

SKULL Form, or head-shape, has been extensively studied by an- 
thropologists in search of an “index” for classifying “races.” While 
there is unquestioned evidence that in head-shape, as in stature 
genes do play an important part, there is also unquestioned proof 



(Brachycephalic) (Dolicocephalic) 
a mr, 
TOP y ( 0 
> an ia a 
al v7 

that environmental factors can and do greatly modify head form. 

Broadly speaking, people are classified as “round-headed” or 
“long-headed”; or, as your hat-store man might say, “long oval” 
or “broad oval.” In general terms, the “long oval” is most common 
among Negroes; the “round oval” is most common among many 
“Nordic” Whites. Yet one can quite easily find a great many 
Negroes with round heads, rounder than those of many Whites, 
and many Whites with long heads, longer than those of the aver- 
age Negro. The best that can be said at the present stage is that 
the factor, or factors, for the broad-and-short head appear to domi- 
nate those for long-headedness. 

Quite possibly some of the genes for head-shape work through 
the glands, whose peculiar effects may often be hereditary. Dr. 
Charles R. Stockard, in his studies of dogs, attributes to glandular 


workings many of the differences which distinguish dogs of the 
various types—bulldog, dachshund, etc. While no such extreme vari- 
ability exists in humans, he believes that the “bulldog” type of 
human head, the “dachshund” type (long and thin), the “Pekinese” 
type (big eyes, little nose) may similarly be caused by gland dif- 
ferences. 3 

The artificial shaping of heads, as is widely known, is practised 
among some primitive peoples. Almost in the same way, habits of 
eating, sleeping, and talking may modify the head-shapes of people 
in our own civilization. In the United States there -seem to be 
“normalizing” conditions at work; we see that the children of 
“long-headed” Sicilians and Scots tend to develop shorter heads; 
that the children of Jews from Eastern or Central Europe, whose 
parents are often characterized by broad skulls, develop longer and 
narrower heads. The marked round heads in certain sections of 
Germany are also held to be in part due to environmental factors 
peculiar to the locality. 

Environment plays its largest role in head-shape before and dur- 
ing birth, and in infancy. The shape of the mother’s pelvis may 
exert an important influence in the prenatal period. During infancy, 
the manner in which the infant sleeps, and in the ensuing early 
_ years the type of cap, hat or head covering the child wears (which 
differs among various peoples) all may be instrumental in modify- 
ing the head form. 

Bopy Form. If we find difficulties in isolating the genetic factors 
for stature and head-shape, they are as nothing compared to iden- 
tifying those for weight and girth. Innumerable environmental in- 
fluences may produce in people degrees of leanness or stoutness. 
Moreover, while stature is virtually “set” after puberty, body weight 
may fluctuate throughout life. In the face of this, nevertheless, at- 
tempts have been made to classify human form according to types. 
Various indices have been used, but the most familiar classification 
is of three types, common to both sexes: 

The “asthenic’—tall and slender, somewhat flat-chested, with nar- 
row, drooping shoulders. 

The “pyknic’—short and fat, thick-neck, protruding abdomen, 
barrel-shaped thorax. 



The “athletic’—the intermediate type, with broad, square shoul- 
ders, muscular limbs, large hands and feet. 

The assumption is that while environmental factors may modify 
or alter the human form, generally in a given population persons 
are destined for one body type or another by inheritance. Also, an 
attempt has been made to show that the “asthenic” type is char- 
acteristic of the “Nordics,” the “pyknic” type of the Alpine peoples, 

~ and the “athletic” type of the Dinaric peoples (southeastern Euro- 

peans). The theory involved falls down when we see that all the 
types are represented in all races, and that while the proportions 
may vary in the races, environmental factors may explain these dif- 
ferences just as easily as might genetic factors. 

Applied only to individuals, however, there does seem to be fair 
evidence that slenderness or obesity “runs” in certain families, and 
that under average conditions there are genes which will condition 
a person’s weight. It appears, moreover, that obesity may be caused 
by dominant factors. Slender parents as a rule have slender chil- 
dren, whereas fat parents will have some children who are fat, and 
others who may be of varied figures. 

Whether through heredity or not, it is clear that certain persons 
are predisposed to plumpness, whatever they do and whatever they 
eat, and that others are not. | 

Bopy Deraizs. Almost any detail of the body structure, on ex- 
amination, indicates that characteristic genes are at work. The 
types of breasts found among women show the influence of heredity. 
In some peoples, for instance, they are apt to be placed high and 
closer to the armpits, with the nipples larger. 

An interesting peculiarity among Hottentot and Bushman women 
is the condition known as steatopygia, which may be politely de- 
scribed as a protuberance of the rear anatomy. Whether or not this 
is due to a special gene confined to these peoples, or due to the 
overactivity of a gene also found among White females (who might 
therefore have relative degrees of steatopygia) is not known. 

Oruer Deratts. The shapes of the hips and pelvis among women 
of different nationalities, the length of legs and arms (as in Negroes 
compared with Whites), the length and shapes of various muscles, 
the size and weight of bones, and many other bodily details in- 


dicate specific inheritance. Occupation and living habits may, how- 
ever, be responsible for various differences among individuals. If 
the son of a blacksmith has brawny arms, like his father, should 
we conclude that his arms were “inherited,” or may we not also 
assume that he developed such arms by working in the smithy, just 
as his father did? Very often, as we look at families of tailors, or 
families of policemen, or families of farmers, etc., we are likely to 
confuse the bodily characteristics that resulted from similar work- 
ing and living habits with those that might be due to heredity. 

In your own case, you may find that many of your bodily char- 
acteristics which seem an integral part of you are merely the re- 
sults of “conditioning.” Whether they are, or on the other hand © 
whether they have a hereditary basis, becomes important when you 
try to guess what your children will look like. And this is now 
what we're about to help you do. 


We have gone far enough in identifying genes linked with various 
characteristics so that, given certain facts about you and your mate, 
we could make some fairly accurate predictions as to what your 
children would look like. 

Were we able to breed people as the geneticist breeds flies, we 
could make many more predictions, with greater accuracy. By con- 
stant breeding and inbreeding, geneticists have established strains 
of Drosophila, ranged in rows of bottles in their laboratories, whose 
genes they know almost as well as the chemist knows the make-up 
of his various compounds. In fact, with almost the same precision 
that the chemist mixes compounds, the geneticist can “mix,” by 
mating, two flies of any strains and predict the types of offspring 
that will result. 

We cannot, of course, ever expect to do anything like that with 
human beings. Pure strains of humans cannot be produced, like 
flies, by long inbreeding of parents with children, brothers with 
sisters, etc. And where flies have 300 offspring at a time and three 
generations to a month, human couples do not average more than 
four offspring to a marriage, and only three or four generations 
to a century. 

So, genetically, in most respects we humans are unknown quan- 
tities. With regard to your own genes, you can only make guesses, 
but in this you will be helped considerably not merely by the char- 
acteristics which you yourself reveal, but by those which appear in 
your parents, grandparents, brothers, sisters and other close rela- 
tives. As was noted in the “Eye Color” chapter, if you are dark- 
eyed, the chances of your carrying a “hidden” blue-eye gene in- 
crease according to the number of your relatives who have blue 

eyes, and their closeness to you. Going further, if you marry a 


blue-eyed person and have a blue-eyed child, then you know def- 
nitely that you carry a blue-eye gene. On the other hand, if two, 
three, four children in a row are all dark-eyed, the presumption 
grows that you haven’t a blue-eye gene. 

Likewise, where both parents are dark-eyed, the appearance of 
a blue-eyed baby is proof conclusive that both carry “hidden” blue- 
eye genes. But if all the children are dark-eyed, it still might mean 
only that one of the parents has no blue-eye gene. 

These qualifications hold for every case where persons have some 
characteristic due to a dominant gene (dark hair, curly or kinky 
hair, thick lips, etc.) and wish to know what chance they have of 
carrying a “hidden” gene which might produce a different trait in 
their child. 

But before we try to make any predictions these facts should 
be clear: 

All forecasts as to the types of children people will have are 
based on averages determined by the laws of chance. 

Wherever dominant and recessive genes are involved, it is like 
tossing up coins with heads and tails. Toss up coins long enough, 
and the number of heads and tails will come out even. So if you 
are carrying one dominant and one recessive gene for any char- 
acteristic, were it possible for you to have an unlimited number 
of children, you’d find that exactly half would get the dominant, 
half the recessive gene. 

With zwo parents involved, the results will be like those obtained 
in “matching” coins. This, of course, conforms with Mendel’s laws. 

When we think in terms of the characteristic produced, the re- 
sult in “mixed” matings will be that the dominant characteristic 
(dark eyes, dark hair, etc.) will show up three out of four times, 
the recessive only one in four, as it requires a matching of the 
recessive genes. 

Of course, where one parent carries two dominant genes, all the 
children will show the dominant trait. Where one parent carries 
a dominant and a recessive, and the other parent two recessives, 
balf the children will show the dominant trait, half the recessive. 

But here is something else to bear in mind: 

Wherever it is a question of a child’s getting one gene or an- 

|—6hhindatimes 2 in 4 times ONE 
ws 7) ‘ aT | DOMINANT 

ONE HEADS child wi @ @ Nie 

_ No matter how many times No matter how many children 


The odds are exactly even When you mate, the odds 
that it will ane are exactly even that 
any child will receive 

v \ 
o © 

Lin 2 times Lin2times Lin2 times Lined times 


You: Your Mate: 
Rene © G © @ 

Every time you have a child 
he Odds are exacty 

Lin4 times 

-The odds are exactly 

1 in4times 

BOTH Child will 
HEADS receive © @ dominants 
1 in 4times 1 in sab nE S BOTH 
BOTH Child will 
TAILS receive O Orecessives 

coins are tossed, the odds you have or how many “ing row” 
will always be exactly the Gre the same type, the odds will 
_ Same for the next toss bé exactly the same for the next 



other, or having such and such a characteristic, the odds for every 
child are exactly the same. 

Some gamblers might dispute this, but if you toss up a coin 
one time, and it comes up heads, that does not mean that the next 
time there is any better chance of its coming up tails. There is the 
same fifty-fifty chance on each toss-up. Even, if through an unusual 
“run,” there would be ten heads in succession, on the eleventh 
toss there would still be an exactly even chance for either “heads” 
or “tails.” (This applies to dice, roulette or any other game of chance. 
Many a gentleman has lost a fortune trying to disprove it.) 

So, let us say, if the odds are even for your having a blue-eyed 
child, and your first one is brown-eyed, that doesn’t mean that the 
odds are any better that the next will be blue-eyed. Even if four 
or five children in a row are born with brown eyes, there is still 
that same fifty-fifty chance, no more and no less, that the next 
child will have either brown or blue eyes. 

But perhaps we need not have gone into all this. In the “boy or 
girl?” question we say that there is a 106 to 100 chance that the 
child will be a boy. And yet, authorities like Eddie Cantor will 
tell you that the fact of their having had two, three or four girls in 
a row in no way bettered the odds that the next one would not 
be a girl! 7 

In “boy or girl?”, however, it is a simple question of one or the 
other. But in the case of features or form—in fact, of any detail in 
the body—there are innumerable variations to contend with. If you 
and your mate conform to the average, you will find the forecasts 
here presented fairly dependable. Always, however, allow for ex- 
ceptions and—whatever happens, do not blame us (or the geneticists 
on whose studies these tables are. based) if the baby does not turn 
out the way the forecast indicated. 

And now to Sir Oracle! 


First: If this is to be your first child, find out as much as possible about 
what genes you and your mate may be carrying by consulting the detailed 
treatments of each feature in preceding chapters, and by studying other 
metbers of your iamilies.* Make allowances for all characteristics influenced 
by environment. 

Second: If you have already had one or more children, also study each 
child for additional clues as to your genes. 

Third: Remember that no matter how many children you have had, or 
what they look like, the odds that your next child will receive a given 
characteristic are exactly the same as if it had been the first. 

Fourth; In consulting the tables, look for your own characteristic in esther 
of the ‘‘parent’s’’ columns. (They each apply equally to father or mother.) 
If you and your mate are of different types, look first for the type most 
pronounced—the darkest coloring, the most extreme hair form, etc. 

Fifth: Remember that these ‘‘forecasts’’ are based on averages in large 
numbers of matings. With just one child, that child might be the exception. 

Sixth: Wherever age is a factor, make due allowances for its future effects 
or changes that may be expected to take place. 

*In the following pages, “family” refers not only to parents, brothers, and sisters, but to 
grandparents and other close relatives. 




Type r. 
_ family were dark-eyed 

Type 2. Where some in 
this parent’s family have 
lighter-colored eyes 
(gray, green or blue) 



ALBINO (Colorless) 

Ifallthisparent’s X 



No Matter 
What Color 

Brown, Type 2 

Gray, Green 
or Blue 

Gray, Green 

or Blue 


Normal-eyed par- 
ent of any eye- 

xX Albino 

Child’s Eyes 
Will Be: 

Almost certainly dark 

Probably brown, but pos- 
sibly some other color 

Even chance brown or 
lighter color (most likely 
like that of lighter-eye 

parent) sie 

Probably gray or green, 
but possibly blwe. (Rarely 

Almost certainly blue. 
(Rarely a darker shade, 
the possibility being less 
if parents’ eyes are light~ 

Normal, leaning to shade 
of normal parent’s eyes, 

unless this parent carries — 

hidden ‘‘albino’’ gene, 
when x in 2 chance of 
child being albino 

Definitely albino 

Width: Where just one parent has wide eyes, child will quite likely 

have them. 

Slant: If one parent has slant-eyes (but not of Chinese type) child will not | 
be likely to have them unless slant-eyes also appear in the family of the | 
other parent. If, however, the parent’s eyes are of the Chinese, or Mon- | 

golian, type there is great likelihood that child will have them. 

Lashes: Where just one parent has long lashes, child may be expected - 

to have them. 




DARK (Brown or Black) 

Type z. Where allinthis X No Matter What Almost certainly dark 
parent’s family had dark 

x Dark, Type 2 Probably dark, but pos- 
sibly some lighter shade 
Type 2. Where there ate|xX Red About equal chance (a) 
lighter shades among dark ot (b) red-brown ot, 
others in this parent’s red, with (c) some slight 
family possibility of blond 
x Blond Probably dark, but pos- 
sibly blond—tarely red 
RED xX Red Most probably red, and 
or blond 
x Blond Even chances, (a) red or 
—(b) light-brown or blond 
Type x. If medium shade X Blond Fairly certain blond, with 

tarely brown. (Red pos- 
sibly if this shade is 
present in either parent’s 


Typez. Ifflaxenorwhite X Blond—Flaxen Certainly blond, but 
: or white with shade of darker 
parent apt to prevail 





Type xz. If all in this par- 
ent’s family are curly- 

Type 2. If some wavy or 
straight in this parent's 



Type x. If no straight- 
haired persons in this 
parent’s family 

Type 2. If there are some 
with straight hair in this 
parent's family 


Type z. Where all in this 

parent’s family are kinky- 

Typez. Whereother hair- 
forms appear in this par- 
ent’s family 


Any Form, except 
kinky or woolly 

Curly, Type 2 



Wavy or Straight 



No Matter What 
Hair Form 

Curly or Wavy 


Child’s Hair 
Will Be: 

Almost certainly curly 
(rarely any other) 

Probably curly, possibly 
wavy or straight 

Even chance (a) curly or 
(b) possibly wavy or oc- 
casionally straight 

Probably curly or wavy, 
possibly straight 

Almost certainly wavy, 
rarely straight 

Even chance wavy or 
straight. Rarelyanything 

Almost certainly straight 

Almost certainly kinky 

Even chance (a) kinky or 
(b) curly or wavy; rarely 

Almost same as above, 
but with greater possi- 
bility of straight 

Woollv: While fairly frequent among Negroes, it is rare among Whites. 
Where, however, it appears in even ~ne parent half the children will have 

woolly hair. 




CNose-shape is not ‘‘inherited’’ as a unit. Different characteristics of the 
aose may be ‘‘inherited’’ separately, one detail sometimes from one parent, 
another from the other parent. Environmental factors also have great 
influence. ) 

Generally: Where both parents have about the same type of nose, a child 
on maturity will have a similar type. 

But: If just one parent has a broad nose, a long nose, or a prominent nose, and 
the other parent a moderate nose, the child’s nose will very likely be of the 
more extreme type (on maturity). 

Where any nose peculiarity has appeared in several generations of either 
parent’s family there is an even chance that the child will ‘‘inherit’’ it. 

Large. If just one parent has large ears, the child will very likely have 
similar ears. 
Affixed Lobes. Where only one parent has affixed ear-lobes, or absence of 
lobes, and the condition does not appear in the other parent’s sey there 
is little likelihood that the child will have such ears. 

Lips. If just one parent has thick lips, the child will probably have them. 
If just one parent has a heavy, or protruding underlip CHapsburg type) 
the child has an even chance of “‘inheriting”’ it. 


Both parents tall. The child on maturity will almost certainly be tall, or 
taller than average. 
. Both parents short. The child will probably be inclined to shortness, but 
may possibly be taller than the parents, and even very tall. 
One parent tall, one short. The child will probably incline toward the 
shorter parent. 
If both parents are slender, the child will be more likely to be like them 
than if both parents are fleshy. But build is a highly variable characteristic, 
dependent on so many conditions and genes that it can hardly be predicted. 

(For the inheritance of ‘tabnormal” conditions and characteristics of all 
kinds, in features, form and appearance, see later chapters.) 



Bald Black, straight 
Murky-green us 

eyes Dull-brown eyes 
Long-lashes lost Drooping eyelids 
rough disease Ba d skin 


‘(local disorder) 


Misshapen mouth 
due to bad teeth 

Bad nose due to 

BUT they may carry and pass on to 

their child hidden genes for RESULT: A 
Fees curly heir “BEAUTY CONTEST" 
ue eyes 
Long lashes WINNER 
Pretty nose 

Cupid's-bow mouth 
Lovely complexion 


Curly, black hair ey Blond 
Large, black tif 

eyes, long Blue eyes 
lashes Long lashes 
Well-shaped aay Regular teeth « 
mouth and 


Ws ; ( ee Pretty mouth 

BUT they may carry and pass on to 
their child hidden genes for 

=—Dull-brown, straight hair RESULT: AN 
Murky-green, small ith gem " " 
short Ibekes : eb ca Xs <p) UGLY DUCKLING 

Protruding jaw and teeth 
(and, alas, other irregularities) 



You have seen what produces your external appearance. But you 
are much more than a hollow doll with such and such kind of eyes, 
hair, skin, etc. While your “looks” may be extremely important, 
your real importance as an individual lies in what is within your 
shell: your organs—brain, nerves, heart, lungs, glands and other 
functional parts. These are “what make you tick” and they are 
what account for the greatest differences between individuals. 

In fashioning and constructing every one of our organs we know 
that genes are involved. We know that differences in the organs 
of different individuals are often inherited. But the task of iden- 
tifying these hereditary differences is vastly more complicated than 
it was in the case of features, for we are here dealing not with 
easily recognizable characteristics but with functions and effects. 
In that regard, mere appearances are of very little help to us, for 
in very few cases have we yet been able to establish by mere sur- 
face inspection the nature of the important organs and their heredi- 
tary aspects. 

We have reason to believe that different types of brains, hearts. 
livers, lungs, stomachs, etc., are inherited, but we have not yet 
been able to identify and classify such genetic differences, even be- 
tween the organs of our by now familiar examples, the “Nordics” 
and the Hottentots. In the construction of every organ, many genes © 
must be involved. However, only when a specific gene takes a 
strange and unusual turn, producing some easily recognizable ab- 
normality, do we have any clue to what it does. 

The glands form a group of organs which hold special interest 
because almost every peculiarity in humans is being ascribed to 
them these days. When people talk of “glands” they do not mean 
such old standbys as the liver and kidneys, or the gastric and salivary 



glands, etc. They refer to the “ductless” (endocrine) glands—the 
pituitary, thyroid, parathyroids, pancreas (one part), suprarenals, 
pineal, thymus and the testes or ovaries. These introduce into the 
blood certain all-powerful substances called “hormones,” the effects 
of which are often confused with the direct action of genes. It is 
quite true that the glands are conditioned by heredity; but glandu- 
lar differences among individuals may equally be due to environ- 
ment. All this will be clarified later. 

As general or specific effects of the glands and other organs, there 
are a vast number of characteristics which show distinct hereditary 
influences. Among these may be cited the age and onset of menstru- 
ation, of puberty and of “change of life.” All of the functional heredi- 
tary effects of the glands and other organs reveal themselves, as 
we have. said, when they deviate from the “normal.” Where these. 
differences are so extreme as to be classed as “abnormal,” we have 
our most striking illustrations of gene activity. 

“Normal” and “abnormal,” by the way, are vague words wholly 
inadequate to express what we mean. “Abnormal” means “not nor- 
mal”; but “normal” cannot be defined except in relation to some 
standard that in itself is usually highly variable. For instance, if a 
man eats three pounds of meat at a sitting, we'd say he has an 
“abnormal” appetite; but suppose that man were seven feet tall 
and weighed three hundred pounds? An abnormal appetite for 
others would be normal for him. Four feet six inches would be 
an abnormal height for a man in northern Scotland and five feet 
eight would be normal; but five feet eight inches would be an 
abnormal height among pigmies, whereas four feet six would 
be normal. 

In other words, an abnormality is a deviation from some arbi- 
trary standard which may vary according to the point of view. It 
should not be confused with a “defect,” for an abnormality may be 
favorable or unfavorable. An idiot is abnormal, but so also is a 
genius. All of this again will be dealt with in much greater detail 
presently. | 

But first let us consider the primary “abnormality” in humans: 
where one individual immediately after conception becomes two, 
three, four or even five individuals. 



In any discussion of heredity, one question is sure to pop up, 
like a heckler at a political meeting. The inevitable question is: 

“W hich ts more important, heredity or environment?” 

We have tried to bring out that both forces go hand in hand 
in shaping any one’s life, and that consideration of one without the 
other is impossible. You will therefore understand why the geneticist 
counters with, “Which is more important, the fish or the water in 
which it swims?” 

The first question can have meaning only when it is applied to 
some specific characteristic or circumstance. Millions of young men 
have been killed in battle. In their case, which factor was more 
important in bringing on early death, heredity or environment? 
Obviously, environment. On the other hand, we know of many 
conditions which are produced by heredity, and which nothing yet 
within our power can change. A person is an achondroplastic dwarf 
—with a large, misshapen head and stunted arms and legs—due to 
defective genes. Which is more important in causing this condi- 
tion, heredity or environment? This time, obviously heredity. 

But when we deal with more general circumstances and char- 
acteristics, with the sum total of any individual’s life, the question 
becomes infinitely more complicated. In your own case, you may 
often have thought, how would you with your given heredity have 
turned out under different conditions? Or, under the same condi- 
tions, to what extent might you have been different with a slightly 
different heredity? 

That is what geneticists, as well as psychologists and sociologists, 
are trying to answer. And the only way it could be answered—or 
at best, partly answered—is this: 



1. If there were two of you to start with and each were exposed 
to different conditions; or 

2. If you started life with somebody else at the same time within 
the same mother and after you were both bor developed under 
approximately the same conditions. 

Is either of these situations at all possible? 

Yes, for Nature has most thoughtfully provided us with twins, 
who, willy-nilly, are human guinea-pigs for such experiments. 

For the first experiment we have “identical” twins; for the sec- 
ond, “fraternal” twins. The two types differ in this way: 

Identical twins are the product of a single fertilized egg which, 
shortly after it begins to grow, splits in half to form two individuals. 
Each has exactly the same hereditary factors, and they are therefore 
always of the same sex. 

Fraternal twins, on the other hand, are the product of two en- 
tirely different eggs which happen to have been simultaneously 
matured by the mother and fertilized, approximately at the same 
time, by two entirely different sperms. They may therefore each 
carry quite different genes, and be as unlike as any other two chil- 
dren in the same family, as often as not, in fact, being of opposite 

In other words, identical twins are, from the standpoint of 
heredity, exactly the same individual in duplicate. 

Fraternal twins are two entirely different individuals who merely 
through chance were born together. 

The important distinction between the two types of twins was 
not known nor fully realized until recently. In earlier years, twins 
were considered “identical” if they were of the same sex or resem- 
bled each other fairly closely. Even when the “one-egg” and “two- 
egg” distinctions became known and when biological facts of their 
birth were considered, mistakes in diagnosing them were frequently 
made. It was believed that the “one-egg” (identical) twins were 
always encased in a single fetal sac, with one placenta, whereas the 
two-egg (fraternal) twins invariably had separate fetal sacs and sepa- 
rate placentas. While generally true, it has now been found that 
this is not an invariable rule. Sometimes the sacs and placentas of 
fraternal twins are fused; and sometimes in identical twins (or even 


Are products of 
A single and 

A single 


In an early stage 
the embryo divides 
on to become 

separate / : 
individuals a) a 

Usually — but not always — identical 
twins share the same placenta and 
fetal sac 

The halves go 

But regardless of how they develop, 
they carry the same genes and are 

Always of the same sex — two boys 
or two girls 



Are products of TWO different eggs 
fertilized by TWO different sperms 


They have different genes and may 
develop in different ways, usually— 
but not always — having separate 
placentas and separate fetal sacs 

Also, as they are totally different ine. 
dividuals, they may be 

of the 

Two boys 


triplets, quadruplets, etc.) where their division has taken place at 
an early stage, each may grow a separate placenta and become en- 
cased in a separate sac. : 

Today, in classifying twins as “identical” or “fraternal” geneticists 
no longer consider midwives’ or even doctors’ reports. They have 
much more certain evidence in the form of “correlation” tests. By 
comparing the twins with regard to many characteristics known 
to be definitely inherited or influenced by heredity, they can tell 
whether or not the degree of resemblance, or “correlation,” is high 
enough to stamp them as “identicals.’ Among the characteristics 
used for comparison are sex, blood groups, blood pressure, pulse 
and respiration; eye color, and vision; skin color; hair color, hair 
form and hair whorls; palm, sole and finger patterns; height, 
weight and head-shape, and facial details. The correlation in these 
characteristics is so much greater between two identical twins than 
between two fraternal twins that.there is almost no possibility of 
confusing them. 

Now why are geneticists so concerned about this acd? Be- 
cause on it depends whatever conclusions may be drawn from study- 
ing twins. 

Inasmuch as identical twins have exactly the same heredity, what- 
ever differences there are between them must be due to environ- 
ment. Or, on the other hand, when identical twins develop in dif- 
ferent environments—there being instances where they were sepa- 
rated in infancy—distinctive characteristics which have developed 
in both of them might be ascribed to heredity. Thus we may get 
some light on the question of what might have happened had 
there been two of you. 

The study of fraternal twins takes a different direction. Inasmuch 
as fraternal twins have a much more similar environment and 
developmental experience than individually born persons, the ques- 
tion is how much more alike this similarity in environment makes 

If heredity were everything, then identical twins would be exactly 
like each other in all respects, even if reared apart. But innumerable 
studies show that they are far from exactly alike. 

On the other hand if environment were everything, then fra- 


ternal twins, reared under the same conditions, would also be 
alike, regardless of how different were their genes. But here we 
find that although they show a closer resemblance to each other 
than do non-twin brothers and sisters, “fraternals’ even when of 
the same sex are less alike than are identicals reared apart. 

The various studies of twins have comprised an important source 
of evidence for geneticists, and some of the conclusions will be 
presented in succeeding chapters. You will always have to keep 
in mind, however, that these conclusions can never be absolute. 
No identical twins are really identical because they cannot possibly 
have had identical environments, even before birth. If their en- 
vironments were always identical there would never be any in- 
stances, as there frequently are, of one identical twin being born 
alive while the other is dead. They would either both be dead, or 
both born alive. | 

Differences between identical twins may also be due to the man- 
ner in which they were separated in the first stages. If the separa- 
tion takes place in the earliest embryonic stage, before any body 
differentiation has begun, twins are as identical as possible. But if 
the division takes place later, when the potential right and left 
sides of the embryo are already laid out, the twin that comes from 
the right half might develop a little in advance of the other, and 
might be born slightly heavier and with greater vigor. This slight 
lead may be carried on throughout life, and may be productive of 
other differences, both physical and psychological. 

“Mirrorimaging,” or reverse-patterning, in identical twins is an 
interesting phenomenon that often results when their division takes 
place after the embryo has begun to differentiate. (See page 104.) 

Thus, the one that developed from the half that was marked 
out for the right side might be right-handed, and the other left- 
handed. Similarly, in the hair whorls the whorl of one may be 
clockwise, of the other counter-clockwise. Dental irregularities in 
twins, birthmarks, freckle patterns and other details also often 
occur on reverse sides in the paired identical twins. 

Freak twins of various kinds occur when there is an incomplete 
separation of the halves of the original embryo. In Siamese twins 
the separation is sometimes almost complete, but only in rare in- 


stances is the link between them so slight that it can be severed 
by operation without danger. Where the division is only partial 
such freaks may result as twins with one body and two heads, or 
one body with four legs and four arms, or duplicated organs, etc. 
All but a few of such human monsters perish before birth, fortu- 
nately, and are of little interest to us here because there is no evi- 
dence that they are due to heredity. 


Hair whorl —~4 ( AY Q)axyiar whorl coun 
clockwise ter clocKwis€ 

Larger tye \ Larger eye 
on right | fc © Paes TAR cole left 

Birthmark on Birthmark on 

right cheek 4—-> ¢ at..@29ce: | left cheek 

Bad ee “x ZL Bad tooth 
on right on left 

Think of the early human embryo as a solid sphere with a design 
running straight through. Cut in half (like an apple) the halves 
would show the parts of the design in reverse. 

Normal twinning, however, does apparently have some heredi- 
tary basis, as the tendency of twinning to run in certain families is 
well known. In the case of idetiticals, should a specific g gene play 
any part in causing the initial egg or embryo to split in half, then 
such a gene could just as easily be carried in the sperm as in the 
egg, and the twinning could therefore be due to the father as well 
as the mother. In fraternal twins, it devolves upon the mother to 
mature two or more eggs simultaneously. The tendency to do this 
might be inherited, or, in the opinion of some authorities, might 
be induced by external factors. 

In either identical or fraternal twins, conception is one thing, but 
the bringing forth of the twins is another, and is greatly dependent 
upon the mother’s condition. An interesting fact is that twins occur 
in the United States (and European countries) about once in every 


go births, whereas in Japan they occur only once in about 160 births. 
Does that mean that “twinning” genes are only half as common 
among Japanese women as among American women? A more 
likely conclusion might be that the smallness of the Japanese women 
their narrower pelves, and perhaps some other constitutional or en- 
vironmental factors do not enable them to bring forth twins as 

The age of mothers seems to be an important influence in pro-. 
ducing fraternal twins, but not identicals, indicating that the ma- 
turing of two eggs at a time is more a matter of environment. Older 
mothers have a better chance of producing fraternal twins than do 
younger ones. The frequency of two-egg twin births increases with 
the age of the mother up to the years between 35 and 40, and there- 
after declines. However, even mothers between 45 and 50 average 
more twins than do young mothers between 15 and 20. 

We have confined ourselves so far, in the matter of multiple 
births, only to twins. But all the basic facts brought out in this 
chapter also apply to the higher multiples. 

Once in about 8,000 births triplets occur, and because there are 
three of them, it is possible for all three to be identicals—devel- 
oped from one egg, or for two of them to be identical twins, de- 
veloped from one egg, and the third a fraternal, developed from 
a different egg. Interesting examples of this latter kind of triplets 
are three well-known American scientists—Robert, Wallace and 
Malcolm Brode, physicist, chemist and zoologist, respectively. Rob- 
ert and Wallace in relation to.each other are identical twins, but 
each in relation to Malcolm is fraternal. 

Quadruplets occur once in about every 700,000 births, with only 
a few sets surviving. Here various combinations are possible: (1) 
All four identicals; (2) three identicals and one fraternal; (3) two 
identicals and two fraternals; (4) or, more rarely perhaps, all four 
fraternals. The well-known Keys quadruplets, Roberta, Mona, Mary 
and Leota, of Hollis, Oklahoma, are probably of the No. 3 type, 
derived from three eggs, two of the girls being identical twins and 
two fraternal twins, 

Among lower animals, it may be noted, the kittens or puppies in 
a litter are usually “fraternals’—products of different eggs. How- 



Single sperm fertilizes Two separate sperms fertilize 
single egg two separate eggs 

Fertilized egg ~£ .) 
as in twins lf < she 
eae The 
as one sa 
@ individual naa PY! 
to form 

One twins 

“set and 

oes on 
9 to Other 
develop divides 

again ] 

noe W) 

RESULT: Triplets, two of whom are 
really identical twins, the other a fran | 
ternal twin of theirs, of the same ob 
opposite sex. 


(Always of same sex) 

A. third type, of "unmatched" triplets, can result from the union of 
three separate sperms and three separate eggs. 

ever, one species of mammal, the armadillo, habitually gives birth 
to four “identical” offspring at a time, suggesting’ the possibility 
that in humans, too, a tendency to give birth to such higher mul- 
tiples may be inherited. | 

Finally we come to the rarest and, to date, the. most remarkable 
of all multiple births among humans. But that is sufficiently impor- 
tant to justify a special chapter. 



On a night in May, 1934, Nature poured into the lap of science a 
lavish gift—the Dionne quintuplets. | 
If twins are of value in the study of heredity, how infinitely 

more valuable would be five children born at one time! 

Such an event is believed to have happened not more than sixty 
times in the last five hundred years—and in all cases the babies 
perished soon after birth. Never before, in the history of medical 
science, had all five members of a set of quintuplets survived. 

What made the Dionnes even more distinctive, and thus more 
valuable for study, was the fact that all five were “denticals,’ the 
product of a single egg and therefore all carrying exactly the same 
hereditary factors—to the very last of their thousands of genes. 

This, by the way, was not established until later. From certain 
conditions attending their birth, good Dr. Allan Dafoe, who ushered 
them into the world and miraculously kept them there, came to 
the conclusion that they were identicals, developed from a single 
egg. But certain other reputable authorities considered them 
“fraternals.” However, as the quintuplets grew and an intensive 
study of them was carried on by a group of scientists of the Uni- 
versity of Toronto, it became apparent that Dr. Dafoe had been 
right—that there wasn’t a chance in the world of their being any- 
thing but identicals. 

Some of the many points of similarity in the Dionnes, including 
such an unusual characteristic as mild “webbing” between their sec- 
ond and third toes, will be listed later. But also there are some im- 
portant differences. And it is these differences which give us a clue 
as to how the Dionnes were born. 

The quintuplets could have been. produced, theoretically, in vari 
ous ways. Starting with the single egg (or embryo) they would 

first have had to divide into two. But from that point on: 
| 107 


(A) SIMILARITIES —And all five have the same 
"Webbed Toes" (2nd and| 
3rd)—on each foot. 

Blood group "O" 
Medium-brown eyes mixed with gray 

Same eye pattern, same eyelashes, 

All same light-brown eyebrows 
have Same hair-color (dark, slightly red- 
same dish-brown) 

Same hair-form: Wavy 
Same feet pattern 

Same complexion: Light and fair 

(B) DIFFERENCES (At age of three) 



pe Nese dl 
ane a Right 

+1. 25V 

(Most far- 

v4 Stills sav 

Cross -EYES 

nel b=, 

SVE Peau 

Sli rar ai 
“sight ted) 

trace oF 


1. One-half might have doubled and then redoubled, forming 
four individuals, while the second half went on to develop by it- 
self, intact. 

2. Or the two halves might have each redoubled, forming four 
individuals, and then one of these could have divided again to make 
the required five. This, it is believed, 1s the way the Dionnes were 

It also would have been theoretically possible for even more divi- 
sions to have taken place, with six, seven or eight individuals cre- 
ated, of whom only the five survived. Dr. Dafoe did believe that 
there were six and that one of these failed to develop. 

There is, however, interesting evidence to support our theory that 
the Dionnes were in the early stage four individuals, and that one 
of these re-divided again to make the added fifth child. Our clue 
is provided by the differences among the children. 

We find that three of the Dionnes—Cecile, Annette and Yvonne, 
are similar zn all characteristics noted. But both Emilie and Marie 
differ from the others in several respects. 

Both Marie and Emilie are more far-sighted (Marie the most) 
than the other three, whose vision (eye refractive error) is uniform. 

Both Marie and Emilie were mildly cross-eyed long after this 
condition (strabismus), found in all infants, disappeared in their 
sisters. In Emilie it had at last reports almost disappeared but was 
still showing in Marie. 

Both Marie and Emilie have slenderer faces and more sloping 
palates than their sisters. 

Both Marie and Emilie, as infants, displayed a peculiar mannerism 
in grasping things—holding a spoon, for instance, as indicated on 
the chart—Marie with her right hand and Emilie with her left. 
The other quintuplets did not have this mannerism. 

Both Marie and Emilie, at the age of three, had seventeen teeth, 
whereas their sisters had only sixteen, 

Ali the foregoing facts would indicate that Marie and Emilie 
were in some way paired and set apart from the others. As this 
could not possibly be due to any differences in heredity, we must 
look for some environmental factor, and the most logical one would 

be this: 



(Theoretical probability) 

1. Asingle sperm united 
with a single egg. Se) 


2. The embryo divided 
to form “identical 

rs 7a 

3. The “twins" again di- 
vided to form ‘quad- 
i ' 
4. But at this point, three ; ; 
i t 
' pane a ! 

went on, ‘'set,"' to de- 

velop as individuals— ' 

§. The fourth again di- eo sts 
vided. a, Ap 

That when the embryo reached the four-division stage, three of 
the divisions were “set” and went on to form Cecile, Annette and 
Yvonne, respectively. 

But that the fourth part divided again, one-half going to form 
Emilie and the other, Marie. 

We can go even further: Granted that Emilie and Marie came 


from the same fourth-part embryo, if differentiation had already 
begun before they divided, then the characteristics of “hair whorl” 
and “handedness” would already have been set. A division at this 
stage would then result in “mirror-imaging,” and this is just what 
we find in these two! 

Marie’s hair whorl is clockwise, whereas that of Emilie (as of 
the other three) is counter-clockwise. 

Emilie, in turn, is /eft-handed, whereas Marie (like the others). is 

This “mirror-imaging” in Emilie and Marie, which does not 
occur in the others, is further proof of their linkage. 

If we are right, then, in assuming that Emilie and Marie were 
the last to form and develop, then we might expect them to be the 
smallest at birth. This, too, accords with the facts. Even at the 
present writing they still are the smallest and lightest. The pos- 
sibility is further suggested that Marie’s development came slightly 
behind Emilie’s because she is the “baby” of them all. 

But there are still other deductions. In our preceding chapter we 
pointed out that not even twins ever have exactly the same intra- 
uterine environment. How much more so would this be true of not 
two, but five individuals growing all at once! We noted further 
that if one twin has even a slight initial advantage over the other, 
that advantage might be increased and carried along throughout 
their subsequent development, bringing in ‘its wake other differ- 
ences. And that is just what we find with regard to the Dionnes. 

The theory that Emilie and Marie were at a disadvantage before 
birth in comparison with their sisters seems to be borne out by the 
fact that they are the most far-sighted, that their cross-eye con- 
dition lingered longer, that they were the smallest at birth and still 
are, and that they continue to be the most retarded in almost all 
other phases of their development, with Marte consistently the last. 

The mentality, achievement and behavior of the Dionnes will be 
discussed in later chapters. For the present we need go no further 
than their physical make-up to prove for ourselves this significant 

1A photograph of the quintuplets, with their heights and weights as of August, 
1938, is reproduced in Chapter XXXIV. 


That with four years of life behind them, and reared under the 
most scientific and most uniform environment that has ever been 
provided for any group of children in history, the Dionne quin- 
tuplets, despite their exactly identical heredity, are nevertheless not 
all the same and are not developing in an identical way. As with 
any other individual the minor differences with which the quin- 
tuplets started life were sufficient to develop in each a special in- 
ternal and external environment of her own. The child who had 
any slight advantage to begin with over another might tend to in- 
crease that advantage. Or here and there other factors might enter 
to create new advantages or nullify old ones. One might eat a bit 
more than the next, one might learn a little faster than the next, 
one might exercise a bit more than the next, one might be slightly 
more exposed, or more susceptible, to a cold than the next. Little 
by little jigsaw patterns of circumstance are being fitted together to 
make each of the Dionnes an unmistakably distinct individual. 
Already their parents and others close to them can, although not 
too easily, distinguish any one from the others. 

If such differences can develop among five children with identical 
sets of genes, and with as uniform environments as science can 
create, we can now realize how almost futile it is te answer, in the 
case of ordinary individuals, “Which is more important, heredity 
or environment?” 

The story and the lesson of the Dionnes are far from being 
finished. While the entire world prays that they will live a long 
and happy life, geneticists are even more ardent in their prayers 
for them. No human experiment holds forth greater promise. 
Secretly many a scientist wishes that there were another set of 
identical quintuplets that could be separated at the instant of birth 
and that each of these could be reared in an entirely different en- 
vironment, as deliberately different as science could make it. One 
child might be reared in the slums; a second in the wealthiest of 
homes surrounded by every luxury; a third perhaps among half- 
starved illiterate mountaineers in Kentucky; a fourth in the home 
of a professor at Harvard; and perhaps a fifth in just an average 
middle-class home of an average couple, or on an average mid- 
western farm. 


How would such a set of quintuplets, dispersed among such 
widely different environments, compare with the Dionnes? Would 
they still resemble each other? Or would they, despite the similarity 
for which their genes had destined them, be radically different in 
their figures, features, manners, health, intellects, behavior, accom- 
plishments, in their adjustments to life, in their failures or successes, 
in the men they would marry, in the time when the final curtain 
would be lowered on their lives? 

Not until an experiment of this kind is performed to provide 
a basis of comparison can even the study of the Dionne quintuplets 
give us the conclusive proof that we seek. Nevertheless, the Dionnes 
can teach us a great deal, and we shall all continue to watch them 
anxiously, waiting to see what different paths their lives may 
take despite their identical heredity. One thing we have already 
learned is that not even in the case of these five does Nature ever 
repeat herself in creating the substance and pattern of an individual. 



Henry Forp, Mr. General Motors or Mr. Rolls-Royce could 
hardly be blamed if he disapproved of Mother Nature as a producer 
of mechanisms. 

No reputable automobile manufacturer would think of turning 
out a car unless it had been rigidly inspected and every part found 
as free from flaws as he could make it. But Nature exercises no 
such care with regard to the human machine. For reasons of her 
own, perhaps, which we little mortals are not privileged to under- 
stand, she creates individuals with every conceivable kind of flaw, 
defect or “abnormality.” 

No human being is free from hereditary imperfections. But in 
most of us, fortunately, the defects are so slight that they hamper 
not at all, or very little, our progress through life. In some persons, 
however, the defects are serious enough to interfere with important 
functions, to produce abnormal appearance which may make social 
adjustment difficult or, in rare cases, to cause premature death. 
Wherever genes produce such detrimental effects we have given 
them the name of “black” genes. And only when these “black” 
genes are involved in producing a defect, disease or abnormality 
can we consider it, in the scientific sense, as hereditary. 

The greatest error that was made in the past was to assume that 
because a condition was inborn or congenital, present in an individ- 
ual at birth, or because it appeared in successive generations, it was, 
per se, inherited. An example of where this error is still commonly 
made is in syphilis. 

Syphilis is not, never was and never can be inherited. 

One of the most dramatic episodes in our experience bears upon 
this point. Some years ago we were conducting a “baby contest” in 
a large state, the ostensible purpose of which was to select that 


THE “"BLACK’ ‘GENE's 115 

state’s most “perfect” baby. A more important objective was to 
have babies, considered “perfect” by their parents, brought in for 
examination by doctors who might uncover unsuspected diseases 
or defects. 

With a first prize of $1,000 and other attractive prizes as a lure, 
thousands of babies were entered. At the end of weeks of examina- 
tions and reexaminations the field was narrowed down to a half- 
dozen or so infants brought together in a central place. Every one 
of them was already in line for a prize. The question now was 
merely in which order the prizes would be awarded. 

Proudly the mothers took their infants into the final examining 
room where a jury of leading pediatricians waited to make the 
selections. Only the doctors and the writer were left in the room 
with the babies. Never were babies more carefully scrutinized. 
Suddenly one of the specialists who was examining a two-year-old 
baby, whispered excitedly to his colleagues, “Look at this!” 

The others crowded around. And then came the gruesome pro- 
nouncement, “Congenital syphilis!” 

No one else, of the various doctors that had examined the child, 
had detected the almost imperceptible symptoms. The child had 
already been publicly proclaimed as among the prize-winning final- 
ists. All that could be done would be to award it the last prize. 

A shudder still runs through us as we recall how the mother 
was officially presented with the handsome token for her baby as 
one of the most perfect in the state, and then taken aside and 
informed that the child had syphilis. But that was not all. As she 
returned with her baby to her home town, where proud towns- 
people and relatives were waiting to welcome them as conquering 
heroines, the mother carried with her the knowledge that the child 
had acquired the disease from her. 

For the only way that a child can be born with syphilis rs through 
the infection by its mother while she is carrying it. The mother 
herself may have had the disease to begin with; she may have been 
infected by her husband when the child was conceived or at any 
subsequent time up to its birth. But the germs had to be in her 
to be transmitted to the child. All this is also true of gonorrhea. 

A father, no matter how diseased, could not transmit syphilis or 


gonorrhea directly to his child through his sperms. No sperm cell 
can carry a venereal disease germ (or any other germ known today) 
and function. The germs can, however, be carried in the seminal 
fluid together with the sperms. Where germs enter the embryo 
after development is well under way, the child as a result of the 
disease acquired may be born blind, deaf or with any of various 
abnormalities. If, however, the germs are not transmitted until the 
moment of birth, or just before, the disease may net manifest itself 
outwardly until later. 

We have dealt at such length with syphilis because ever since 
Ibsen’s “Ghosts” startled the world, the belief has prevailed that 
the disease can be inherited, and that a “syphilitic” taint may 
persist in a family for generations. Attending this was the theory, 
called “blastophthoria,” that syphilis, as well as drunkenness, drug 
addiction, prostitution, etc., might in some way permanently affect 
the germ cells in a family strain, leading to increasing degeneracy 
and progressive weakening from generation to generation. The 
cases of the poor Jukes and Kallikaks, the classic “horrible examples” 
of the eugenists, have been cited as evidence. But as we have seen 
in previous chapters, no disease, drug or habit can alter the genes 
in the germ cells, and there can therefore be no such thing as an 
“acquired” hereditary taint. 

When a child is born into the world with syphilis, or some ter- 
rible affliction resulting from it, the question as to whether the 
condition should be termed “congenital” or “inherited” may seem 
to be mere quibbling. But this is emphatically not so. For if a 
congenital condition is cured (as syphilis can now be cured) the 
child—no matter how diseased its parents were—can grow to a 
healthy maturity and marry and have children without the slightest 
fear that they will zmherit that defect. But where a condition is 
inherited, no matter whether it 1s cured or not, and no matter 
how healthy the individual himself may be when he marries, there 
is always the ,possibility that he may pass on the “black” genes 
that may reproduce that condition in his children. Syphilis may be 
wiped from the face of the earth in a few generations merely by 
treatment and prevention. Inherited conditions may persist forever, 


for they could be eliminated only by preventing all carriers of the 
“black” genes from breeding. 

Hence the importance of distinguishing between diseases or ab- 
normalities acquired before or after birth and those truly inherited. 

Mere familial inheritance—the occurrence of a condition in the 
mother and in several of her children—may be misleading. Rickets 
was long considered as being hereditary because it clearly “ran” in 
families. And yet now we know that it is a disease due to dietary 
deficiency, the result mostly of poverty, and that it is the poverty 
running in families that causes it. 

In cases where the inheritance seems always to. stem from the 
mother—and affects children of both sexes—there may be every 
presumption that not heredity, but a faulty zntra-uterine environment 
is to blame. Cretinism and “Mongolian” idiocy are two such condi- 
tions which are directly due to the unfavorable condition of the 
mother. Innumerable other defects, diseases, and abnormalities are 
traceable either directly or indirectly to the mother’s influence, but 
for the most part these must be ruled out here as having no bearing 
on the mechanism of heredity. 

Before a condition is stamped as hereditary the geneticist subjects 
it to the most searching study and analysis. The chance of error in 
considering human pedigrees is great because methods of diagnoses 
are variable, the identity of the male parent is not always certain, 
facts about other relatives or ancestors not living may be mere 
hearsay, etc. Where, therefore, in the following pages, a condition 
is unqualifiedly cited as inherited, it may be taken for granted that it 
is so considered by leading authorities; but where the statement is 
qualified, the implication is that while many, even a majority of 
the authorities consider it hereditary, there are others who may not 
be convinced. 

So we come to specific cases. The list of “black” genes already 
definitely identified, or whose existence is clearly suspected, is a long 
and formidable one. Coming suddenly on the rather gruesome 
array, you may have a sinking feeling. Let us assure you, then, that 
the great majority of known “black” genes are of minor importance 
to society at large because the conditions they produce are rare. In 
only a few of the major diseases or defects that afflict mankind 


are “black” genes known to play an important role—and in many 
of these cases the way already has been pointed to prevention or 
cure. : 

Many “black” genes, however, produce what we call direct inherit- 
ance. Certain malformations of the features (deformed ears, teeth, 
etc.), skeletal defects (curved spine, extra fingers and toes, etc.) 
and other easily recognizable defects are passed on from parents to 
children, always in the same form, generation after generation, 
with no way yet known of preventing their appearance. But in 
diseases due to hereditary defects in the functioning of organs or 
parts. of the body, there is generally no such direct inheritance. The 
“black” genes involved usually have a tendency to produce undesir- 
able effects, but under some conditions they will, and under other 
conditions they won't. All this will be brought out when we deal 
with specific cases. 

It is our plan to present here in more or less detail all human 
defects, diseases, disorders or “abnormalities” in which heredity is 
known, believed or assumed to play any part—and which may be 
of interest to any considerable number of our readers. We do not 
intend to bore the many for the sake of the few. Even as it is, you 
may be inclined to skip lightly through the next several chapters, 
stopping only at those items that touch you personally. To make 
this easier, we have arranged the “black” genes in sections and 
under easily found headings. 

Finally, all the “black” genes” dealt with, and additional ones of 
minor interest, will be summarized in a later chapter, in which 
you will also find “inheritance” predictions. 


Tue twelve diseases which take the largest toll of deaths in the 
United States yearly are: 

_ per 100,000 
EAGare, Ciscasest ats opiates) aac so¥ gst Re stab a tales adr 266 
(mincer (inalionant tumOn enn iio saa ba III 
PTR UIOU LA! Cen as ci wee sy MA ee) tah cr Wa aaicg Oe 93 
Nephritis (kidney disease—acute and chronic) ... 83 
Cerebral hemorrhage (brain softening) ......... 81 
PRIDE ECULOSES TMT MeN aS emer e rate: : MBN olla MLR 56 
Briteterezai eens ay eR RN FUER Men, ens 26 
Diabete sparred i CUsh ee oy. eee mene ie are isialsy atin 24 
PRD DOHCIEIE IS Ue Bilton CMR Mme asian dane fi 13 
Intantile diarrhea; enteritismiaw uprima ohne aes 12 
Hernia, intestinal obstructions ja Poel cil ss « 10.5 
SVDEITS pM we chs) 1s ane enh Maes uate aa 10 
DIVE EIT DOSES is us... Ui aN A City da thle) iat 8 

Of all these, heredity has so far been clearly indicated as a domi- 
nating influence only in diabetes and in one form of heart disease, 
namely, rheumatic heart disease. 

In tuberculosis, there is no possibility of direct inheritance, but 
some believe that heredity may be a contributory cause in the form 
of constitutional defects (such as a weak respiratory system) which 
may make certain individuals an easier prey to the tuberculosis 

In cancer, some authorities believe that there may be a hereditary 
influence, but proof of direct inheritance exists so far only with 

regard to certain rare cancers. 


Appendicitis has been linked with heredity by only a few author- 
ities and is very much in the doubtful class. 

In nephritis (kidney disease), cirrhosis of the liver, and infantile 
diarrhea, no inheritance has been shown. 

Syphilis, pneumonia, influenza—all “germ” diseases—have already 
been ruled out. 

So, as we turn to the detailed consideration of the most serious 
diseases, we are immediately limited to only four: Heart disease, 
diabetes, cancer and tuberculosis. 

Hearr Disease. The “common” forms are rheumatic heart dis- 
ease, the severe form of children’s rheumatism which strikes down 
mostly children and persons under forty; high blood pressure (in- 
cluding hardening of the arteries), which generally does not occur 
until late in life; and syphilitic heart disease. 

As previously stated, only childhood rheumatism shows any clear 
evidence of hereditary influence. In some of the various high-blood- 
pressure diseases, recent evidence has indicated a presumption of 
heredity, but no adequate proof. Of the remaining important types 
of heart ailment, congenital heart disease shows little evidence of 
heredity, and sypAzlitic heart disease is obviously not inherited. 

Childhood rheumatism, which is characterized by joint pains, 
fever and inflammation of the heart, is one of the most puzzling 
of diseases. It affects 2 percent of the childhood population, and 
accounts for 80 percent or more of all deaths from heart disease 
of persons under forty (or 25 percent of all “heart” deaths). In 
addition to its fatal consequences, childhood rheumatism every 
year makes many thousands of children invalids for life in 
greater or less degree, the heart condition often becoming worse 
with each repeated attack. (St. Vitus’ dance, a nervous condition, 
is believed by most authorities to be one of its manifestations.) 

Childhood rheumatism had long been known to run in families, 
but only recently, after long research, has the réle of heredity been 
proved. Evidence points to the conclusion that a single pair of 
recessive genes is involved. Where a child receives such a gene from 
each parent, the two genes together should be expected to produce 
the disease. But that does not always happen, because what is inher- 


ited is not the disease itself, but a susceptibility to its development 
under certain conditions. 

One of the peculiarities of childhood rheumatism is that certain 
environments may partially or completely suppress its appearance. 
Most striking is the fact that the disease 1s very widespread among 
the poor and relatively rare among the rich. In New York City, 
for instance, in the squalid tenements of Third Avenue, there is an 
extremely high proportion of children with childhood rheumatism. 
Yet a stone’s-throw away, on fashionable Park Avenue, the inci- 
dence of the disease among the children of the wealthy is far below 
average expectancy! (The same contrast prevails in London.) 

Another peculiarity of childhood rheumatism is its prevalence in 
certain climates. The disease has very seldom been observed in the 
tropics, but as we go farther away in either direction within the 
temperate zones we find it more and more prevalent. In the north- 
ern cities of the United States—New York, Chicago—the disease 
is common. In southern cities, particularly New Orleans and 
Tucson, Arizona, or semi-tropical Florida and Puerto Rico it has 
rarely been reported. Yet among Puerto Ricans*who have settled 
in New York, among adults as well as children, the disease takes 
a heavy toll. Once again, why? We may know, perhaps, in the 
near future. But as yet, childhood rheumatism continues to be one 
of the most baffling afflictions of mankind. 

Also baffling in its nature, but not nearly so clear as to its inherit- 
ance, is “high blood pressure’ (which includes several ailments). 
It directly causes half the heart-disease deaths, carrying off one in 
every 1,000 persons yearly. Many others are incapacitated by it. 

One fortunate aspect is that high blood pressure does not gener- 
ally occur until late in life. However, this greatly hampers the study 
of its possible inheritance, for in families where research is being 
carried on, many individuals have already died as the result of 
other ailments, and there is as yet no way of knowing if they 
had not also carried genes for high blood pressure. Some recent 
evidence indicates that susceptibility to this condition may be in- 
herited, but there is considerable doubt. 

Cancer. While proof of the inheritance of common cancer has as 

yet not been brought forward, the question is still undecided. Why 


this should be so, with almost 150,000 persons dying annually of the 
disease in the United States alone, with millions of dollars being 
spent and thousands of experts engaged in its study, becomes clear 
only when we consider what cancer 1s. 

Cancer is not the name of a specific disease, as is diabetes or 
childhood rheumatism. Cancer is a ‘general term for malignant 
growths which attack organs or tissues of the body. There are 
hundreds of different kinds of cancers, unlike each other in many 
ways, having only this in common: They are abnormal and destruc- 
tive growths which begin by attacking some specific part or type 
of tissue. 

These cancer growths are not introduced into the body from the 
outside, like some malignant seed, germ or parasite. How then, 
do cancers originate? Through some irritation, or perhaps spon- 
taneously, a few cells at a given location undergo some malignant 
change and begin to multiply, forming a mass. Often some of these 
now cancerous cells become detached and migrate through the 
blood-stream to other locations, thus hastening their destructive 
action. Breast cancer cells may become implanted in the stomach, 
lungs, or other parts. A lung cancer therefore might be due either 
to cancerous cells that had originated in the lungs, or to breast 
cancer cells that had migrated. In fact, a cancer in one part of the 
body might have originated at one of many other points. There are 
more different kinds of cancer than there are of all other known 
human diseases. All this has vastly complicated the problem of 
diagnosing specific cancers. 

You hear it said “cancer runs in that family.” A grandmother, 
a mother and a daughter all have cancer of the breast, one of the 
most common forms of cancer in women. Should you not conclude 
that this condition is clearly hereditary? Let us see. 

We find that there are more than a score of known varieties of 
breast cancer. Some of these cancers grow to large size, others may 
be no larger than a pinhead. Some grow rapidly, causing death 
in a few weeks, others may develop slowly, over a period of thirty 

ears. Some remain localized, others fragment and are carried in 
the blood-stream to different parts of the body, to the bones, lungs, 
etc., where they take root. Some cancers are very susceptible to 


X-ray and radium and may be easily destroyed or cured by surgery. 
Others are highly resistant. 

Thus, in grandmother, mother and daughter, where all have 
breast cancers, each of their cancers may be entirely unrelated to 
the others. The grandmother’s cancer might be a slow, small 
growth that originated in old age and did not interfere with her 
normal life; the mother’s cancer might have appeared at the age 
of 40, and have been successfully eradicated by X-ray treatment. 
The daughter’s cancer, however, might have appeared when she 
was just sixteen years old, and might have been so malignant as to 
cause her death a few months later. The breast cancers in the three 
generations of women might therefore be no more related than 
three cases of stomach trouble, one resulting from overeating, an- 
other from drinking bad liquor and a third due to stomach ulcers. 
But, while this might well be so, on the other hand it does not rule 
out the possibility that the cancers might equally be influenced by 
hereditary factors. 

The suspicion that some of the common cancers might be inher- 
ited may be an important aid in combating the condition. Where 
a patient has obscure symptoms the knowledge that other relatives 
have had cancer in the same region of the body has sometimes 
permitted earlier diagnosis and treatment. This is particularly true 
of stomach cancer, which has in the past frequently escaped recog- 
nition until the sufferer was incurably ill or had already been 
claimed by death. This has been reported as running in families. 

Many cases are known in which non-hereditary factors are di- 
rectly responsible for producing certain types of cancer. As an 
example, cancer of the mouth ‘shows a definite correlation with 
poor mouth hygiene—broken and neglected teeth, badly fitted artifi- 
cial teeth or diseased gums. These may result in abrasions, irritations 
or sores, whose end result may be cancer (although certainly not 
in every case). The worse the condition of the mouth, the greater 
the danger of developing a cancer growth. 

In certain cancers of the intestines and in the skin cancer known 
as neurofibromatosis and in a few other less common types, we 
know of no external agent which may play a part, leading to the 
conclusion that in these hereditary factors are primarily responsible. 


Other types are known in which both hereditary and external 
factors seem to be necessary for the cancers to develop. And finally, 
there are a few rare types—malignant freckles and certain tumors 
of the eye and skin, to be discussed later—which have been defi- 
nitely proved to have a hereditary basis. But again the reader is - 
cautioned not to confuse these rare types with the common types, 
nor the proved cases of the inheritance of specific types of cancer 
in other animals, such as mice, with those in humans. 

The human species is generally susceptible to cancer. Given a 
prolonged exposure to cancer-producing factors it is believed that 
most persons will eventually succumb. The reader may recall the 
case of the girls who worked in the watch factory in New Jersey 
painting luminous dials with radium paint. Almost every one of 
those girls died of malignant cancer. Nevertheless, present evidence 
indicates that under ordinary conditions of exposure to cancer- 
producing factors, there seems to be a definitely greater susceptt- 
bility of persons of certain families to the disease than others. Fig- 
ures in the United States have led some authorities to conclude that 
the presence of cancer in a near relative increases tenfold the possi- 
bility that a person may die of the disease. However, the relative 
difference between susceptible and immune strains for cancer is 
much less than for many other proved hereditary diseases, such as 

The mechanism of transmission of human cancer factors, for all 
except the few rare types noted, can only be guessed at. Almost 
certainly, authorities believe, no genes working singly produce the 
common forms of cancer, and the interaction of a number of 
genes is probably required. One interesting theory as to the way 
cancer-producing agencies work is that they start all the trouble in 
just a single cell, by precipitating a malignant “mutation” or upset 
in one or more of its genes or chromosomes, which would make 
the cell lose its property of orderly growth and harmony with 
other parts. It may thus become an “outlaw,” growing and multiply- 
ing without restraint, preying on the rest of the body without 
contributing to its orderly processes. 

The theories are plentiful. But in many of its major aspects 
cancer still remains a stubborn and inscrutable foe. 


Drazetes. Diabetes (the “sugar-sickness”) which afflicts about one 
percent of the population, is produced in most cases through the 
inheritance of genes which make one vulnerable to its attack. 

The disease results from a failure of the pancreas to secrete 
sufficient znsulin—vitally necessary for the conversion of sugar in 
the body processes. This is why large amounts of sugar accumulate 
in the blood, causing degeneration in the kidneys and also produc- 
ing poisons that may cause death. Recent genetic studies indicate 
that a pair of recessive genes are responsible. 

Inheritance of two “diabetic” genes need not, however, portend 
the certain development of the disease. The disease does not usually 
manifest itself until the age of fifty, and may even then develop in 
some individuals only if they become very fat, if they overeat, worry 
excessively or overstrain themselves. There are almost twice as 
many cases of diabetes in women as in men. Consequences of 
childbirth are held responsible for this, as in unmarried women 
the diabetic rate is no higher than in men. 

During the World War the number of diabetic deaths fell in all 
countries where there was a shortage of food, and rose again 
immediately as normal food rations were restored. In accordance 
with the principle involved, diabetic sufferers were formerly sub- 
jected to mild starvation, a treatment particularly dangerous to 
afflicted children who, through malnutrition, rarely were able to 
survive. Today, however, with the momentous discovery that insulin 
derived from other animals can be artificially supplied to the body, 
diabetics may be enabled to lead almost normal lives. 

Several unrelated hereditary conditions, some of whose symptoms 
approximate those of diabetes, are often confused with it and cause 
unnecessary fear. 

Diabetes insipidus is related to true diabetes only in name, and in 
the fact that, as in diabetes, there may be abnormal thirst and fre 
quent urination. Aside from the possible inconvenience, it has no 
harmful effects. There is no abnormal production of sugar in the 
blood or urine, and there is no danger that the condition will de- 
velop into diabetes or produce its other harmful effects. This con- 
dition, which is believed to be a pituitary gland disorder, differs 


from true diabetes further in that it is inherited through a simple 
dominant gene. 

Sugar urine (renal glycosuria) is the condition in which there 
is an excessive amount of sugar in the urine, but with none of the 
harmful effects which attend a similar symptom in diabetes. It is 
inherited, probably, as a dominant. (When you are told by an 
insurance company that there is sugar in your urine it might be 
the result of this harmless condition.) 

Tusercutosis. The prevailing opinion among tuberculosis experts 
is that heredity is no ally of this Public Enemy No. 1 of our youth. 
As every one now knows, tuberculosis is caused by a germ—the 
tubercle bacillus. Intimate contact with a tubercular person is neces- 
sary to acquire the disease. Inasmuch as tuberculosis germs breed 
most easily in sunless and poorly ventilated quarters, and find their 
readiest victims among those who are poorly nourished, the disease 
is usually correlated with slum conditions and poverty. 

Tuberculosis germs are found in countless billions almost every- 
where we turn in civilized countries. At one time or another un- 
doubtedly they have invaded all individuals; it is quite likely that 
almost every one of us has had tuberculosis in a mild, usually im- 
perceptible degree. In most of us, fortunately, the condition is soon 
suppressed or never develops to the stage where it can be called a 
disease. Only when the germs get out of hand, multiply enormously 
and begin to destroy the tissues of the lung do we call a person 

Once tuberculosis gets a foothold in one member of a family, 
undisputed evidence shows that it spreads to others in the house- 
hold. But not every one will acquire the disease under the same 
exposure. The reason that some do not succumb, authorities believe, 
is that they may have been rendered immune as the result of a 
previous mild attack (explained in the preceding paragraph). 

The “acquired immunity” theory, however, has been disputed in 
some quarters, where it is maintained that some persons develop 
tuberculosis more easily than others because they have “inherited” 
weaker respiratory systems. This belief was widely held in previous 
days, but has failed to stand up under searching investigation. The 
spectacular decrease in tuberculosis mortality, during the last gener- 


(As indicated by average (Approximate 
monthly rentals) averages 

per 1,000 pop.) 


(Based on figures compiled in Cleveland, O.., 
for 1928-32, by Howard Whipple Green) 


ation, which has attended the improvement in living conditions 
gives evidence that this disease is chiefly a social. problem. 

Gorrer. The question of whether this disease is inherited is open 
to doubt. We refer here to the common form of goiter, attended by 
a swelling of the thyroid gland in the throat. It has long been con- 
sidered hereditary, and still is so considered by many authorities. 
One thing is now clear: That the disease is the direct result of 
iodine deficiency in the body processes, either because of lack 
of iodine in the diet, or because of the failure of the thyroid gland 
to convert it properly. 

While it is theoretically possible for defective thyroid glands to be 
inherited, one may now seriously question the earlier conclusions 
that the high incidence of goiter in certain localities and regions 
(such as the vicinity of the Great Lakes) was proof of such inherit- 
ance. In one experiment made among schoolgirls at Akron, Ohio, 
in the so-called “goiter belt,” it was shown that of 2,100 who were 
fed minute amounts of iodine for three years, only five developed 
goiter, as compared with 495 cases of goiter that developed among 
2,305 of their schoolmates with an iodine insufficiency. 

Another fact which might indicate that goiter is primarily an 
environmental, rather than a hereditary disease, is this: As is well 
known, it occurs much more frequently among women than 
among men, and also, where it “runs” in the family, it usually 
appears to have come through the mother. Thus, we have the 
strong likelihood that not defective genes, but a failure of the 
mother to supply her children with sufficient iodine in their intra- 
uterine stage led to their acquiring the disease. One of the most 
unfortunate consequences of thyroid deficiency in a mother may be 
the birth of a cretin—a type of defective child that formerly always 
grew up to be a deformed imbecile. Today, however, by glandular 
treatments, medicine has made it possible for such children to 
develop normally. 

On the basis of present evidence we may conclude that common 
goiter, where apparently transmitted through the mother, is acquired 
or congenital, and not hereditary. 

Dicestive Diszases. Of all the many diseases associated with the 
digestive processes, few have been definitely linked with heredity. 


Except for diabetes, there is not a single one of these conditions of 
any importance which can be conclusively blamed on “black” genes. 

In alcers of the stomach and intestines, heredity has been claimed, 
but has not been established. Polycystic disease of the kidneys, a 
rare disorder, serious in pregnant women, is generally considered 
hereditary, but the manner of transmission is uncertain. Acholuric 
family jaundice, characterized by fragile blood cells, with occasion- 
ally anemia, jaundice and enlarged spleen, has been established as 
due to a dominant gene. 

Autercic Diszases. Asthma, hay fever, eczema and allergies to 
various foods and substances, have been extensively studied. Many 
investigators claim that allergies are definitely inherited through 
dominant genes, but the evidence is somewhat clouded by the fact 
that in almost every family there is some one who is allergic to 
something—ranging from colds and cats to—actually—the ink on 
colored comics in the Sunday papers! | 

Migraine (sick headache) which some consider as also allergic in 
origin, has likewise been reported asa hereditary condition, but 
the evidence for this is inadequate. 


A sincLe “black” gene in one little boy may well have been a 
motivating factor in bringing on the Russian Revolution and in 
changing the course of the world’s history. 

The gene was that for the dread “bleeding” disease, hemophilia, 
which found its way, by one of Queen Victoria’s grand- 
daughters, to the last little Czarevitch. As the world knows, it was 
because of his affliction that his credulous parents, the Czar and 
Czarina, became victims of the designing Rasputin, who held out 
hopes of a cure through supernatural powers. From Rasputin, as 
from a spider, spread a web of intrigue, cruelty, debauchery, demor- 
alization and mass indignation which may have brought on the 
collapse of the empire. Jf the Czarevitch hadn’t had hemophilia, zf 
his parents hadn’t become the prey of Rasputin, 7f Rasputin hadn’t 
demoralized the court ... Thus a momentous structure of “ifs” 
can be built up, like an inverted pyramid, resting on that infinitesi- 
mal bit of substance constituting a single gene. 

What interests us here, however, is the long-standing mystery of 
why hemophilia, and scores of other diseases and defects, are always 
transmitted only by way of mothers to their sons. 

Poor males! In the chapter on “Boy or Girl?” we pointed out 
that the chance of survival among males is considerably less than 
among females. Now science pours further salt on their wounds by 
showing why men are an easier prey to many ills than their 
supposedly weaker opposites. 

We saw that the only initial difference (in the primary cell stage) 
between a male and a female is that the female has two X chromo- 
somes and the male just one X paired with a bit of a chromosome 
designated as a Y. Very clearly the Y contains many fewer genes 

than the X; in fact, it may be considered as only a fragment of 


some original X. Thus, while a daughter inherits the same amount 
of genes from each parent, a son inherits more genes from his 
mother than from his father. And that means that he can also 
receive more defective genes from her. 

So here’s the answer to our mystery: 

If a female gets one “black” gene in one of her X chromosomes, 
the chances are that there will be a normal gene for the job in the 
other chromosome. (Like a motorist with a spare tire when there’s 
a blow-out.) 

If, however, a male gets just one “black” gene in his single X 
chromosome, he is headed for trouble, because usually there is no 
corresponding gene in his Y chromosome to do the job. (So he’s 
like a motorist who hasn’t any spare tire when there’s a blow-out.) 
Thus, the defective “blood coagulating” gene being in the X 
chromosome, if just one of these is received by a male, he will 
have hemophilia. The disease is usually fatal in early life. While 
comparatively rare, it has achieved prominence chiefly because of 
its occurrence among some of the progeny of Queen Victoria of 
England, who was a carrier. Her son, King Edward, and his 
descendants, escaped, but two of her granddaughters, the Czarina 
and the Queen of Spain received the gene, the latter transmitting 
it to Alfonso’s son, the hemophiliac Count of Covadonga. This 
tragic young man, after battling the disease all his life, was finally 
claimed when he bled to death in September, 1938, from wounds 
sustained in an automobile accident at Miami, Fla. 

For a female to be victimized by hereditary hemophilia, she 
would have to receive a hemophilic gene in both “X” chromosomes. 
Theoretically, this could happen, but no case is known of a woman 
with true hemophilia. The explanation, it is believed, is that two 
hemophilic genes together prove /ethal, killing the individual before 
birth. A number of women have shown symptoms of mild hemo- 
philia, but this may have been another blood disease or perhaps 
their one normal gene was not sufficiently strong to counteract the 
“black” one. 

Cotor-BLINDNEss: A much more common condition than hemo 
philia (if not so dramatic) that victimizes males is hereditary 
color-blindness, the inability to distinguish between red and green. 


The'""X""chromosome (\_----------=: > The "Y' chromosome 
is many times larger ----------> lacks duplicates of al- 
thanthe'"Y." ££ \--=---=---<-- > most all the ''X'’ 
BGaS ney! LN eae > genes. 
Se 5 
Oe aU ee ee 

If a recessive 'black-X" gene is circulating in a family, 

Receiving one "'color-blindness'’ gene Receiving a "color-blindness" gene in 
usually has in her second "'X" a normal his single ''X'' has no normal gene to 
gene to block it. . block it. 

Result: Perfectly NORMAL (but a carrier) Result: COLOR-BLIND 


(1) WOMAN As in Hemophilia 

Normal, but a carrier 

‘Bleeding’ gene cov- (2) ONE-IN-TWO 
ered by normal one. SONS 


. All his sons receiving 

only his "Y" are normal. 
(3) Every one of 

daughters is car- 

rier, like grand- 

mother. Vip cece eat repeated as from No. }, 


About 4 percent of all males are color-blind. (An immediate ques- 
tion is, how can they distinguish between red and green traffic 
signals? They can, because the red light appears to them different 
in intensity than the green.) 

The gene for color-blindness is also carried in the X chromosome, 
and if the one X that a male gets has that gene, he will be color- 
blind. In a woman color-blindness results only when she receives 
two such genes—one in each X. This happens to about % of 1 
percent of women, who are color-blind. These women then pass 
on a defective X to each son, so that every one of their sons is 
almost certain to be color-blind. Their daughters, however, will be 
solor-blind only if the father also is color-blind; otherwise they 
will get a “normal” X from him which will counteract the one 
from the mother. 

A number of additional eye defects and various other conditions 
which strike particularly at males have been tracked down to “sex- 
linked” genes. As the X chromosomes must contain a great many 
genes still not identified, there is every indication that as investiga- 
tion proceeds, the list of conditions “for men only” will be increased. 

In a few cases, however, sex-linked genes may strike particularly 
at women. Here’s why: 

In hemophilia, color-blindness, etc., the defective gene involved 
is recessive to the “normal” one. It is only because a male gets only 
this gene, and no normal one to counteract it, as a woman usually 
does, that it asserts itself. But some conditions now known are 
caused by a dominant “black” gene in the X chromosome to which 
the-normal gene is recessive. In this case women, therefore, would 
be particularly vulnerable because their two X’s open them to a 
double chance of getting the gene. An example is a certain condition 
in which such a gene produces defective enamel in the teeth. 

The genes in the Y chromosome are still a mystery. Geneticists 
are investigating one queer toe condition (a peculiar kind of 
“webbed” toes), passed on only from fathers to sons, in the belief 
that this may involve a “black” Y gene. Should there be any 
defective Y genes it would make matters still worse for the males. 
As it is, with the majority of “black” genes in the X being 
recessive, the males, for reasons explained, are already special objects 


of attack. But, alas, their disadvantage as compared with females 
doesn’t stop there. In addition to the “sex-linked” genes they may 
be victimized by what the geneticist calls a “sex-limited” gene, one 
effect of which, if you are a man, you may know only too well. 
We refer to the following: ; 

Batpness: Comes a time when the hair on the head of the rugged 
male begins to loose its hold like the seeds of an autumn dandelion, 
presently to be gone with the wind. 

Dejectedly, fearfully, he watches the teeth of his comb, as if 
they were some devouring monster, gobbling up more and more 
of his precious locks. What to do? 


Starting at Starting at Over whole 
center of crown temples top of head 

(Baldness patterns tend to be alike in men of the same family) 

In some cases, it is true, falling hair is the result of some disease 
or scalp disorder. In many other cases, perhaps the majority,- the 
hair of a man, healthy in every way, falls out for no apparent 
reason. What adds to the mystery is that women, even if they 
have the same scalp condition or disease that a man has, rarely 
lose their hair to the same extent. When we speak of “baldness” 
in a woman we usually mean only partial baldness (complete bald- 
ness in women is almost never seen), and if it is, may be attributed 
to certain diseases. 

The why of all this has long been a mystery. Some “specialists,” 
and many “baldness-cure” advertisements, continue to repeat the old 
theories that men become bald, while women do not, because 


through the ages men have cut their hair short, have worn tight 
hats, have not taken such good care of their hair and scalps as 
women have, etc. All of these statements have as much evidence 
to support them as the theory that if you cut off the tails of 
puppy dogs for a number of generations, the offspring will be 
born with stub tails. 

What, then, is the explanation? 

Geneticists find it in a special type of “black” gene, called a “sex- 
limited” gene. Unlike that for hemophilia or color-blindness, it is 
not carried in the “sex” chromosome but in one of the “general” 
chromosomes which both sexes have in common, and which they 
therefore inherit equally. However, it does not act in the same way 
in both sexes. The “baldness” gene—an example of the “sex-limited” 
gene, is a dominant in men—one only being required to produce 
baldness. But in women the gene acts as a recessive, with two 
necessary to produce even partial baldness. Again, why? 

Apparently the glandular make-up of the two sexes has a lot to do 
with the way the gene manifests itself. One theory is that the 
female hormones suppress the action of a single “baldness” gene, 
but cannot fully cope with two. Another theory is that the male 
hormones stimulate the action of the gene. In this connection it is 
claimed that eunuchs do not become bald, perhaps because they do 
not produce in themselves the hormones which would make them 
as susceptible to baldness as are other men. 

Whatever the explanation, it appears that ordinary ‘ ‘pattern” 
baldness can be inherited through a single gene in men and through 
two genes in women. If a man has this inherited condition, there- 
fore, he may be carrying either one or two “baldness” genes, for 
the effect is the same in either case. Carrying one gene, however, 
he will transmit baldness to an average of half his sons; but with 
two genes, to all his sons. 

A woman, as we have noted, can carry one “baldness” gene with- 
out any effect on her. But the gene will, as likely as not, reveal 
itself in her sons; for even if she is married to a normal-haired 
man, one in two of her sons may be expected to get her hidden 
“baldness” gene and to become bald. Where a woman carries two 
baldness genes, the theory is that on maturity she will have sparse 



@ .. . "BALDNESS" GENE (Symbol). 

In Men—Dominant. One produces baldness. 

In Women—Recessive or completely suppressed. 
Two genes required to produce any degree of 
baldness in a woman. 

wo ..-. "NORMAL HAIR" GENE (Symbol). 




{All of this man’s sons will be bald, 
and if wife is Type A, daughters also) 


(Same effect as two genes, but only 
one-in-two sons of this man will be 





No baldness in this man's sons unless 
his wife is Type A or Type B 


A Q 

Produces thin hair or partial bald- 
ness in women. (All sons will be bald) 



No effect on woman herself, but 
one-in-two sons will be bald 


No baldness in this woman's sons 
unless her husband is bald 



hair and in later life partial baldness. With such a condition, she 
may be expected to transmit baldness to all her sons. 

The Samson episode in the Bible has given rise to the belief that 
a large amount of hair is correlated with virility. But many sturdy 
men from Julius Caesar down through Bob Fitzsimmons (the prize- 
fighter) and on to Postmaster-General James Farley—all with heads 
like billiard balls—belie this theory. Also, the saying goes, “Grass 
doesn’t grow on busy streets.” The implication is that intellectual 
men are inclined to baldness because of their brain activity. But 
this theory can be refuted by a glance at our Supreme Court judges 
—Judge Brandeis and the late Judge Cardozo, for instance, with 
their thick shocks of white hair (and both of them of a people with 
whom nervousness and high tension are commonly associated)— 
and also by a study of the faculty roster of any university. 

In addition to “pattern” baldness, there are a number of less- 
common types of baldness, whole or partial, which have a hereditary 
basis. These, however, are not due to “sex-limited” genes, and 
affect women as well as men. (They will be found listed in the 
“Black” Gene Tables in Chapter XXVII.) 

Also to be noted as non-hereditary causes of baldness are many 
diseases and constitutional disorders. Among these are syphilis, 
typhoid fever, pneumonia, tuberculosis, diabetes, rheumatism and 
certain glandular, nervous and local scalp disorders. Some of the 
diseases produce only temporary hair-fall; in others the resulting 
thin hair or baldness may be permanent. To what extent these 
acquired cases of baldness can be cured we are not prepared to say. 
But where “baldness institutes” claim today that they can also cure 
the common hereditary “pattern” baldness, we might venture the 
opinion that they are being, to put it mildly, optimistic. 

We come then to this question: If, for no apparent reason your 
hair begins to fall out, and from the fact that baldness preceded 
‘you in your family you have reason to believe that the condition 
is hereditary, what should you, or what can you do about it? 

We can answer feelingly, for the position is one in which we, 
who write this, also found ourselves a few years ago. We happened 
to be living in Paris at the time and when our undue fall of hair 


became disquietingly evident, a friend sent us post-haste to the 
outstanding hair specialist of all France. 

Monsieur le Professeur occupied an elaborate apartment, betoken- 
ing his eminence and inspiring great hope for our thinning locks. 
An assistant took down the case-history of the “chute des cheveux.” 
As is the French custom, he tested us for many irrelevant symptoms, 
filled out a long blank and took it away. At last we were ushered 
into the inner sanctum of Le Professeur himself. The great man 
sat at his desk, our case-history before him. He looked at the 
report, he looked at us, and then smilingly bent over. In the center 
of his head was a most decided bald spot! 

“Voila,” he said. There was an eloquent silence. Finally the writer 
sadly asked, “J/ n’y a rien a faire?” (Is there nothing one can do?) 

“Out,” answered the great specialist. “Il faut choisir vos parents!” 

Which means, as you have probably surmised, “Yes. The one 
thing you can do is to pick your parents.” 

And even at this writing, despite anything the barbers or adver- 
tisements might tell you, we still don’t know of any other way to 
prevent or cure hereditary baldness. 



Mosr apparent of the human “abnormalities,” by their very nature, 
are those which affect external appearance or sensory functions. 

At circus sideshows you can see some of the more startling 
examples of “black” gene caprice—midgets, dwarfs with misshapen 
heads and bodies, Negro albinos, “India-rubber” men, etc. But for 
each one of these there are dozens of other surface or structural 
defects found in the everyday walks of life. In fact, it may be said 
that most persons have some inherited structural abnormality—if 
we include as “abnormal,” conditions that are unusual, but not 
necessarily harmful or defective. Going further, and taking into con- 
sideration “hidden” recessive genes which singly produce no effect, 
it is pretty certain that every one of us is carrying some one or 
another of these genes. 

Any detailed recital of defects or ailments, as we already have 
said, cannot help but be a dreary one. So, having little faith in the 
readability of this chapter, we can only suggest again that you scan 
the pages for those items which interest you personally. To make 
this easier we have grouped the various conditions under general 
headings. (Further, we have omitted some of the minor conditions 
or variations, or have left out, among many conditions discussed, 
details about modes of inheritance. These all will be found included 
in the later Summary Tables.) 

Growrn. The familiar stage or circus midgets (ateleotic dwarfs) 
have normal proportions, but usually do not grow beyond 42 inches 
in height. Of a different type is the misshapen achondroplastic 
dwarf, with a large head and normal torso, but stubby arms and 
legs. Both types are hereditary, with multiple genes probably 
being involved. This explains why it is not uncommon for a pair 
of circus midgets to produce normal children, and why, in turn, 



—''Pacemaker." Reg- —Structural defects 
ulates growth and de- such as gigantism, - 
velopment; stimulates dwarfism, acromegaly 
sex-functioning. and sexual disorders. 
— "Thermostat." Reg- —Goitre, cretinism, 
ulates metabolism. myxedema. 
—Govern bone- for- —Bone softening spasms 
mation and "tone™ in children, 

nervous system. 

—''Sugar’’ gland. 
Produces insulin, reg- —Diabetes. 
ulating sugar-conver- 

—''Emotional" glands. —Addison's disease. 
Affect nervous, emo- Also, in females, sec- 
tional and sex proc- ondary male character- 
esses. istics; in boys, prema- 

ture growth. 

? a Gonads 

—Sex glands (Ova- 

ries in women, testes —Sterility. “Maleness" 

in men). Affect sex in females, 'femaleness” 
iy processes and char- in males. 


Z 140 


it is from normal parents that dwarfs usually derive. (Pigmies 
should not be confused with dwarfs, as their small stature is due 
to “small growth” genes and is not attended by any glandular 

There are a number of other growth abnormalities due to glandu- 
lar upsets, which are not hereditary. Acromegaly, characterized by 
very large head, protruding jaw, oversized hands and feet and 
thick lips, results from overactivity of the pituitary gland in adult 
life. Myxedema, characterized by obesity, puffiness, thick dry skin 
and sluggishness, also comes on in adult life as the result of a 
thyroid deficiency. Cretinism. (mentioned under goiter) is another 
thyroid-deficiency effect. 

Hanps anv Feer. The very first proved case of Mendelian inherit- 
ance in man was that of “stub fingers” (brachyphalangy) in which 
the middle joint is missing in each finger. Various other hand 
abnormalities (extra fingers, split hand, stiff fingers, webbed fingers, 
spider hand), are shown in an accompanying plate. In many in- 
stances the abnormality is duplicated in the feet. Also to be noted 
is that every one of these is due to a dominant gene, so that parents 
with any of these conditions will pass them on to half of their 

SKELETAL. “Brittle bones” (blue sclerotic, so called because one of 
its attendant effects is bluish eye-whites) is a not uncommon con- 
dition in which the bones are so brittle that they may break at the 
slightest strain. (In one classic case reported by Professor Mohr, a 
young man broke his ankle when he turned to look at a pretty girl.) 

A number of spinal deformities are inherited. One condition is 
the result of incomplete construction of the spine and spinal cord. 
Some hunchback conditions are due to this defect, but most are the 
result of tuberculosis of the spine (non-hereditary). 

Cleft palate and hare-lip (due to failure of these parts to fuse) 
may sometimes be the result of heredity, but may also be caused by 
intra-uterine conditions. Where inherited, it is believed that recessive 
or multiple genes are involved. 

Teri. While most teeth defects which send people to the dentist 
are clearly due to environment, there are a few for which we can 
blame heredity. The most serious of those is “fang-mouth,” in which 



(All inherited through dominant genes) 






(All conditions above may be repeated in 
the feet and toes of the same individual) 

none of the teeth, except the four canines, ever grow out. In an- 
other condition the two upper incisors are the only ones which 
do not appear. On the other hand, we find the hereditary quirk 
which produces teeth at birth. 

Several defective enamel conditions are hereditary. In some the 
enamel is soon lost or pitted, in others it is discolored, usually 
bluish. One condition producing brown teeth—a dominant sex- 


linked one, carried in the X—has already been noted in the preced- 
ing chapter. It should be borne in mind, however, that many cases 
of defective enamel, especially where they are prevalent in a com- 
munity, are due to such extraneous causes as fluorine or other 
harmful chemicals in the water or foods. 

Some teeth defects occur in combination with such conditions as 
“cranial soft-spot,” brittle bones and cleft-palate, where the mouth 
and jaws are affected, and with other conditions to be mentioned 

Eye Derecrs. The human eye, because of its importance and 
accessibility, has been so extensively studied that hundreds of heredi- 
tary defects or anomalies (unusual conditions) already have been 
brought to light. Some of these are of slight importance, but others 
produce defective vision ranging up to total blindness. 

Out of the blind population in the United States about ro percent 
of the cases are attributed to heredity. The blindness may be 
present from birth through the failure of “black” genes to construct 
an iris, retina or some other vital part of the eye; or the blindness 
may develop later as an aftermath of other hereditary defects, which 
may at first produce only partial blindness, such as cataracts, glau- 
coma, optic atrophy, retinitis pigmentosa, and “small eyes.” Some 
of these conditions may also be caused by environment. In most 
cases where children are born blind, or become blind during child- 
hood, not heredity, but a disease of the mother—often syphilis or 
gonorrhea—is responsible. 

Cataract, or opacity of the lens, appears in different forms in 
different families. It is considered hereditary in all cases except 
those which come on in old age (these still being doubtful) or 
which are due to environmental causes (such as infection or indus- 
trial hazards). The time of onset—birth, childhood, puberty or 
middle-age—varies in different families and also appears to be deter- 
mined by heredity. The genes which cause hereditary cataracts of 
every type are usually dominant. 

Glaucoma is a serious, and rather common condition, in which 
heredity has been definitely established only in the case of the 
infantile type, which is usually associated with small eyes. Recessive 
genes are responsible. In the adult type, however (which may lead 


to blindness), while there is a possibility that dominant or “sex- 
linked” genes may be involved, this has not yet been proved. 

(The less common hereditary conditions which lead to blindness 
are listed in the Summary Tables.) 

Errors of refraction (near-sightedness, far-sightedness, etc.) may 
be inherited through variability in the way in which the genes con- 
struct the eye. But in these as in all eye defects it should be kept 
constantly in mind that the gene effects may be greatly modified 
or influenced by the treatment accorded the eyes, by diseases, by con- 
ditions encountered, etc. In one rare congenital condition, miosis, 
or “pin-point” pupil, which formerly doomed a child to blindness, 
it has now been found that a permanent cure can be rapidly effected 
by artificially dilating the pupil in the infant. 

Cross-eyes are sometimes inherited. 

Color-blindness (dealt with in the preceding chapter) is one of 
various “sex-linked” eye conditions which include Leber’s disease, 
paralysis of the ocular muscles (the hereditary type) and several 
others. Also “sex-linked” is one type of nystagmus, which produces 
a tremor of the eye. (Sometimes, though, this condition may result 
from such work as mining.) 

“Night blindness” (inability to see in dim light), of which several 
types have been cited as hereditary, has recently been reported 
as due to Vitamin A deficiency, throwing some doubt on its 
hereditary derivation. (“Day blindness,” “Mirror-reading,” Double 
eyelashes and other eye conditions not discussed here will all be 
found in the Summary Tables, page 188.) 

Far. At least 10 percent of the cases of deafness (and perhaps 
as high as 25 percent) are considered hereditary. In some instances 
“black” genes produce deafness at birth but usually their effects 
are gradual, beginning with partial deafness in childhood and 
reaching a more serious state in maturity, especially among women 
after they have been pregnant. 

As in blindness, most of the cases of total deafness are due not to 
heredity but to other causes, chiefly syphilis, contracted from the 
mother in the intra-uterine state; and also childhood illnesses such 
as meningitis, scarlet fever, and mumps. (Then, of course, there 
are later illnesses and accidents.) In tracing deafness back through 




Absence of 

Sweat Glands 

Woolly Hair 


White Blaze 


(As in Microce- 
phalic idiots) 


Extra Fingers 



Pattern patches of white 

Necessity to pant when 

Found among Whites as 
well as Negroes 

Lack of pigment in eyes, 
skin and hair 

Patch of white hair over 

No hair on head or any 
other part of body 

Tiny, undeveloped head 

Very small size but nor- 
mal proportions 

Occurring on one or more 
hands and feet 

Shortened limbs 



Cows, dogs, etc. 

Dogs, wolves 


Almost every animal from 

mice to elephants 

Horses (“‘Star’’ forehead) 

Mexican hairless dog 

Russian wolfhounds 

‘““Toy’’ dogs 

Cats, guinea-pigs 



several generations these primary causes are often unknown or 
ignored. ‘The mere fact that a parent and grandparent were deaf 
is not sufficient ground for fear that a child will inherit deafness. 
However, if it can be ascertained that the deafness was not due to 
extraneous influences, there is a fair presumption of inheritance. 

Mutism is a natural concomitant of deafness, where a person is 
born deaf, or stricken with deafness in early infancy and therefore 
cannot learn to imitate sounds. Only when deafness has come after 
one has learned to speak is it not accompanied by mutism. 

The usual form of hereditary childhood deafness is believed due 
to a recessive gene or genes, these frequently coming together in 
a child when the parents are closely related. That more than one 
set of genes is involved seems evidenced by the fact that children 
with normal hearing can be born to two parents both of whom are 
apparently hereditary deaf-mutes. 

A common form of hearing impairment is middle-ear deafness 
(otosclerosis), coming on in maturity and believed due to multiple 
genes. The fact, however, that it more frequently affects women 
after childbirth suggests that environment may play a part in its 

“Word deafness” is perhaps more a defect of the brain than of 
the ear, as the hearing is normal but the individual is unable to un- 
derstand the meaning of sounds. It affects many more males than 
females, and appears in infancy. 

In the outer ear there are several hereditary abnormalities, in- 
cluding complete absence of the ear, usually on one side. (Other 
abnormalities are noted in the Summary Tables.) 

Skin. Because, like eyes, skin disorders or abnormalities are 
quickly recognized, they have been intensively studied, and a great 
many of them have becn established as hereditary. Most of these 
are not functionally serious, but derive their importance from their 
effect on the social and economic life of the individual. Such con- 
ditions as “scaly skin,” “shedding skin,” “elephant skin” or “blotched 
face” (large birthmarks) may greatly interfere with the victim’s 
chance of employment, social adjustment and marriage. Some skin 
conditions, however, may have serious constitutional effects, and a 
few may even prove fatal. 

(sm9st) Saoqqoag Surysury qui Sursvoddp ) 

‘sourqyy Aur jo SastIJoIDvILYD ‘s399Jop yII93 pur (sTTeqeA2 Surav[]Ioso) suuSessku savy osye AY], 
-(sosodind vosztqryxe JO} MOIS wisy1 SujII2] pur spuvsas ATTOOM 241 INO Zurquiod Aq p2onpoad 392y9 ppo 242) ey uaxey pu sodo on]q aed 
(sye014} J19q3 2300) suTys s17YM savy Ady], “SOUTqTY yeo1dAa ose sIayIOIq BS9y2 ‘PIOISIN] VstMI39YIO pur “vA ‘oyouroY UT sjuased yoxr]q JO UIOg 



“Rubber-skin” is one of the skin “oddities.” The familiar “India- 
rubber” men may have skin so elastic that it can be pulled out five 
or six inches on the chest. This is possible because the connective 
tissues which hold the skin in place are absent. The defect is pro- 
duced by a rare gene. 

Another “oddity” is thick nails, which are. sometimes so thick 
that a hammer and chisel are needed to trim them. 

Large hereditary birthmarks (naevi) are of various types, some 
due to blood-vessel swellings, some raised, some merely pigmented 
patches of the skin. The blood type (vascular) when it appears on 
the cheek is due to a dominant gene. A familiar type of hereditary 
birthmark is the “Nevus of Unna” appearing on the nape of the 

“Dog-men” are those who have a rare condition, absence of sweat 
glands, due to a “sex-linked” gene, and therefore affecting chiefly 
men. The victim cannot perspire and as in the case of dogs, who 
also have no sweat glands, must pant when the body is overheated. 
An added effect may be an incomplete set of teeth, sharp-pointed. 

Albinism, already mentioned, is primarily a skin defect. The 
gene for this (a recessive, two being required to produce the con- 
dition, as will be recalled) is found among all peoples, light or 
dark. The highest incidence of albinism is among the San Blas In- 
dians of Central Panama (7 in 1,000). Albinoidism is a mild form 
of albinism, due to a different and dominant gene. The skin 
and hair are lightly pigmented, the hair is not as fine as in true 
albinos, and the eyes are normal. Partial albinism has several mani- 
festations. One of these is the condition that produces a “blaze,” or 
patch of white hair above the center of the forehead. The common 
type is present from birth. 

Among the serious hereditary skin conditions are these: 

Coffee-colored spots (neurofibromatosis) which appear at birth 
over various parts of the body, spreading later, and possibly de- 
veloping into local cancer. Less common is another cancer-produc- 
ing condition, malignant freckles. This is a peculiar type of freckles 
appearing shortly after birth, and bringing death before puberty in 
most cases. } 

In “scaly skin” the skin is dry and scaly, easily inflames and con 


tinually sheds. In “horny skin” the skin is hard at birth, becomes 
cracked at the joints and may prove fatal. The milder cases may 
disappear in later life. One peculiarity of this condition is that it 
is frequently accompanied by small, deformed ears. 

Blistering takes two main forms: (a) (simplex), where blisters 
are readily produced on hands and feet, but heal without scarring. 
This begins in childhood. In the serious form (b) (dystrophica), 
scars are left after healing. Of several types, the most severe is ac- 
companied by nail deformities and may be fatal in infancy. 

Light sensitivity (Porphyrinuria congenita), also produces blis- 
ters, but on exposed parts in spring and summer, with skin easily 
bruising. In the worst forms the hair falls out and blindness may 
result. Another peculiar effect may be redness of the urine. 

In “shedding skin” the skin thickens and falls off, in some cases 
the complete cast of the palms and soles being shed in the autumn. 
There is a milder form, where the skin over the entire body flakes 

Fatty skin growths, due to a hereditary defect in the fat metab- 
olism of the body, are serious only when they appear in the internal 
organs, where they may form tumors and cause death. Usually, 
however, they are confined to the face and scalp, and produce no 
ill effects. 

Hair. The most common hereditary hair defect, baldness, already 
has been discussed. Some other hair conditions, all due to dominant 
genes, are: 

Complete hairlessness (hypotrichosis), absence of hair over the 
entire body, associated with loss of teeth and deformed nails. 

Juvenile hairlessness (alopecia) in which the infantile soft down 
is retained and no real hair develops. 

“Beaded” hair (monilithrix) in which the scalp hair is scanty and 

Muscres anp Nerves. Inherited muscular defects are not very com- 
mon. The most serious ones are those in which muscles “shrivel” 
(atrophy) and become incapable of functioning. Since muscle ac- 
tivity is controlled by nerves, often a nerve defect may lead to in- 
activity and shriveling of the muscle, so that it is not always easy 


to tell in a given case whether a defective “muscle” gene or a defec- 
tive “nerve” gene is responsible. 

Ataxia (hereditary), of which Friedreich’s ataxia is the most 
common, comes on in childhood and is symptomized by wobbly 
gait, defective speech and curvature of the spine. Spastic paralysis, 
which also appears in childhood, attacking the lower limbs and 
spreading upward, is dominant in some families, in others recessive. 

(Various other types of muscular and nerve defects are listed in 

the Summary Tables, page 188.) 




In the seventeenth century three brothers came to the United 
States bringing with them one of the most terrible of all known 
“black” genes. 

Through these three who settled in New England hundreds of 
persons in the United States have come to as horrible an end as 
any one could imagine—death from Huntington’s chorea. 

A single dominant gene causes this condition. 

A man (or woman) to all appearances normal, perhaps even bril- 
liant or outstanding, goes on into maturity with no sign of any 
waiting doom. Then, quite suddenly, perhaps at the age of thirty- 
five or forty, he begins literally to disintegrate. His speech becomes 
thick, his brain and nervous system go to pieces, his body collapses. 
In a few years the individual is a helpless wreck, shortly to be car- 
ried off by merciful death. And no cure for this condition is yet 

But this is not all. An individual with a gene for Huntington’s 
chorea may marry and raise a family before the disease strikes. Be- 
cause the gene is a dominant, all the children of the victim are thus 
suddenly confronted with the one-in-two possibility that they like- 
wise may be doomed—and there is no way of finding out before- 
hand. To make matters worse, those with the gene may not always 
develop the disease, so that they can never be certain that they are 
not carriers. 

The drama in this horrible situation, which confronts scores of 
persons in the United States today, was recognized by Eugene 
O’Neill when he used it in his play “Strange Interlude.” * Lest the 

1 Mr. O’Neill has written to us: “. . . No, I cannot say that I had the hereditary 
mental defect in ‘Strange Interlude’ identified as Huntington’s chorea. On the other 
hand, I knew what I wrote was valid because it was based on an actual history. 
Evidently, from what you say, this must have been a case of Huntington’s chorea, 



reader be unduly alarmed, we might say that the disease is an ex- 
tremely rare one, and that no other type of insanity is known 
to be inherited in this way. Society has little to fear from Hunting- 
ton’s chorea. Now that the mechanism of its transmission is known, 
there is every reason to believe that, either through the voluntary 
action of the individuals concerned, or through outside pressure, 
the spread of the disease will be greatly curtailed. 

Of far greater importance to society are the much more preva- 
lent types of mental defects—feeble-mindedness, epilepsy, idiocy, 
schizophrenia (dementia praecox) and manic-depressive insanity. 
Are these inherited? And if so, how? 

First, let us remember that the human mind is not an organ, but 
is the end result of a group of functions embracing instincts, emo- 
tions, intellect, operations of will, etc., stemming primarily from the 
activity of the brain. Because of this, when we speak of “hereditary” 
defects in mentality we cannot be quite so explicit as we were when 
we dealt with purely physical defects; nor can we generally track 
down a mental defect to a single gene as we can with Huntington’s 

Think of your automobile. What makes it go? The motor? No, 
the motor without the gasoline, spark-plugs, gears, transmission, 
wheels, etc., would be useless. Every functional part of the auto- 
mobile must be in working order, for a defect in just one part may 
stop the whole process or seriously disturb it. Suppose that an in- 
telligent savage who had never seen an autotnobile watched you 
fumbling under the hood. You take out a spark-plug; the car 
comes to a dead stop. You put back the spark-plug; the car runs. 
The savage might conclude that it was the spark-plug which makes 
the car go. 

This actually expresses the “unit” conception of mentality which 
prevailed not so many years ago. Because insanity, feeble-minded- 
ness or brilliance seemed to “run” in given families, it was con- 
cluded that the different types of minds were inherited as units, 
with one or two genes determining whether a person was to be 
although I never heard it described except by the general term of hereditary in- 

sanity. So I think your mention of the disease in ‘Strange Interlude’ is justified by 
the fact, even though it gives me more credit as a diagnostician than I deserve.” 


brilliant, mediocre or feeble-minded. On such a premise rested the 
detailed studies of our pet horrible examples, the Jukes and the 
Kallikaks. The factor of environment in governing mentality was 
almost completely overlooked. 

Today we are aware that everything that happens to a person, 
inside his body and out, from the moment he is conceived, affects his 
mentality. We no longer venture to say, when an individual is men- 
tally “abnormal,” to what extent we can blame heredity unless we 
are quite clear regarding the various circumstances to which that 
person, his parents and ancestors were exposed. The fact that a 
feeble-minded child had a reputedly feeble-minded grandfather, or 
that two persons in the same family are insane, is no longer prima 
facie evidence of heredity. Only when a mental defect manifests it- 
self in the same way in successive generations under different condi- 
tions, and with some clear evidence of genetic ratios, can we con- 
clude that it is inherited. 

We find, therefore, that most of our evidence regarding the in- 
heritance of any of the more general types of insanity and mental 
deficiency is still presumptive. While authorities are convinced that. 
insanity and mental deficiency can be, and more or less frequently 
are, inherited, the gene mechanism by which most mental defects 
can be transmitted is by no means conclusively established. 

ScHIZOPHRENIA (or dementia praecox) is a collective term for 
various mental derangements that manifest themselves after puberty, 
the first symptoms usually being “inversion” or a lack of interest in 
outside things. These types of insanity, geneticists have come to be- 
lieve, can be (but not always are) inherited through mulzzple reces- 
sive genes (more than one pair). 

An unusual feature of schizophrenia may be its effect on the in- 
dividual sexually. That is to say, it commonly leads to a loss of 
interest in the opposite sex so that the individuals do not fall in love, 
or, if they are already married, frequently leave their wives or hus- 
bands, as the case may be. Thus the disease has a self-sterilizing ef- 
fect, which, coupled with the fact that the individuals are usually 
short-lived, often acts as a bar to their reproduction. Granted that 
the condition is hereditary, this latter effect can be considered for- 
tunate by society as it prevents schizophrenics from reproducing. 


Manic-DepressiveE Insanity, which usually comes on about ma- 
turity (although it sometimes appears earlier or in late life) mani- 
fests itself by a depressed condition alternating with maniacal 
tendencies. Unlike the schizophrenics, the manic-depressive insane 
may be cured after a short stay in an institution, perhaps not more 
than ten to twenty-five weeks. A dangerous aspect of this condi- 
tion, however, is that an individual once cured may as a result of 
undue stress have a sudden relapse. Manic-depressive insanity can be 
inherited, not directly but as a “susceptibility” which, under shock 
or adverse circumstances will lead to a breakdown. For example, 
following the stock market crash in 1929 and in the years following, 
there was a “wave” of manic-depressive cases among some who had 
lost their fortunes. 

The incidence of mental disorders in the general population is 
much greater than is usually realized. In New York State, it is 
estimated that one out of every twenty adults at some time or an- 
other spends a period in a mental institution. Schizophrenia and 
manic-depressive insanity are responsible for about half of the ad- 
missions. Represented among the other half are such conditions as 
alcoholic insanity, paresis (syphilis) and senile dementia, which 
have not been discussed here for lack of any link with heredity. 

FEEBLE-MINDEDNESS. As high as 5 percent of the population in the 
United States (according to some authorities) is estimated to be 
feeble-minded. But what do we mean by “feeble-minded”? Like “in- 
sanity,” it is a general term. In insanity, a person is mentally nor- 
mal up to a certain age, and then, more or less suddenly, begins to 
act queerly. He may even be brilliant at one time and then be a 
blubbering maniac at another time. A feeble-minded person, how- 
ever, is not one with a normal mind gone wrong, but with an 
arrested or incomplete mental development, i.e., a subnormal mind. 
In every other way he may be perfectly normal. 

“Subnormal” intelligence, however, is not so easily defined. In 
the lowest types of human intelligence, those of the idiot or im- 
becile, we can be fairly clear as to the meaning of “subnormal,” or 
“feeble-minded,” But as we go up the scale, we are forced more 
and more to accept rather arbitrary definitions based on existing in- 


telligence tests. If you score between go and 110, you are considered 
as having a normal “IQ” (intelligence quotient). But if a person 
scores below 90, he is rated according to the accompanying scale: 

go-80: Dull 
80-70: On the borderline between dulness and subnormalcy 
Below 70: Feeble-minded (mentally defective): 

70-62: High-grade moron 

62-55: Mid-grade moron 

55-50: Low-grade moron 

50-25: Imbecile 

25- 0: Idiot 

We can see from the gradings that even if we accept the tests as 
being conclusive, any variability in the way a person responds 
under different conditions, or a slight error on the part of the ex- 
aminer, could lead to faulty classification. 

With all this in mind, we can therefore be clear only about the 
most pronounced types of mental defectives, especially those at the 
bottom of the scale. 

Iprors. These have the mentality of an infant and are almost as 
helpless. A familiar type is the Mongolian idiot (misnamed through 
some resemblance of the features to those of Mongols). Such unfor- 
tunates remain underdeveloped, mentally and sexually. Although 
this form of idiocy was once believed to be clearly hereditary, many 
authorities now dispute this conclusion and attribute the condition 
to some nutritive deficiency on the part of the mother while the 
child is being carried. As evidence is cited the fact that the mother’s 
age plays an important part in the possibility of having such a child. 

About 75 percent of Mongolian idiots are born to either young 
mothers under twenty or to those over thirty-five. The percentage 
is considerably higher among the latter, especially when it is the 
mother’s first child. Mongoloids are rarely born twice to the same 
mother. This leads to the belief that the intra-uterine defect or de- 
ficiency which might produce a Mongolian idiot can be corrected 
through the process of giving it birth. If this form of idiocy is in- 
herited—which, as was noted, seems doubtful—it would have to be 


due to a defect in the mother or to genes in the child which ex- 
press themselves only if the mother’s condition is unfavorable. 

The microcephalic idiot is an unfortunate with a “pinhead,” 
sometimes exhibited as a “what’s-it” in circus side-shows, whose 
mental age never goes beyond that of an imbecile. It is fairly clear 
that in some cases microcephaly is due to recessive genes, but it 
may sometimes be due to other causes. 

The cretin, another form of idiot, is dwarfed in body and mind 
by the failure of the thyroid gland to function properly. At the age 
of twenty-five a cretin may look and act like a very dull small boy. 
Cretinism may run in families and is believed to be the result of a 
thyroid deficiency in the mother which communicates itself to the 
embryonic child, but whether this deficiency is hereditary or not is 
in dispute. 

The idiots as a class, tragic as may be their condition to therm. 
selves and their families, are not the mental defectives who present 
the most serious problem to society. They are proportionately few 
in number; there is no clear evidence that their condition is in- 
herited; they are rarely allowed at large; and they seldom can 

It is the very large class of the higher type of feeble-minded, the 
morons; which concerns us most. 

Morons. Those classed as morons reach a mental development at 
maturity no further than that of a hypothetical “normal” child of 
twelve. Only by an intelligence test can they be distinguished from 

ersons of normal mentality. (One must be careful not to confuse 
lack of education with lack of intelligence.) While environment is 
believed to be a dominant causative factor in many cases of sub- 
normal mentality, there is also reason to believe that some cases are 
due to heredity. However, the uncertainty as to the réle of in- 
heritance in producing morons—especially those whose intelligence 
shades into the almost “normal” brackets—is still so great that no 
agreement has been reached among geneticists as to the genes in- 

Epriepsy. The brain being part of the nervous system, there is a 
popular cendency to confuse or link with defective mentality any 


derangement of a person’s nervous system that affects behavior. This 
is why epilepsy (falling sickness) has so often in the past been 
associated erroneously with insanity; why, in fact, in so many insti- 
tutions epileptics were, and still are, housed together with the in- 
sane. While the two conditions sometimes do go together the fact 
that they are far from synonymous is shown by the number of 
great men and geniuses throughout history who were epileptics. 

Epilepsy is a general term referring to various convulsive dis- 
orders. In fact, it is regarded as a symptom, and not a disease itself. 
Usually epilepsy takes the form of convulsive fits, falling, foaming 
at the mouth, etc., an unhappy spectacle which perhaps every reader 
has seen. In some cases the epileptic does not fall but becomes pale 
and stares blankly, being wholly or partly unconscious meanwhile. 
During such states a person may commit strange acts, even crimes, 
and not be aware later of what he has done. History, from its earliest 
recorded pages, contains strange stories of epileptics. 

The belief that epilepsy is inherited has long been held. Never- 
theless, in some cases diseases and brain injuries or infections have 
been proved responsible. (In fact, many authorities now believe 
that all epilepsy is so caused.) But where no such external motivat- 
ing causes are known, some authorities still hold to the belief that 
the condition is hereditary. 

The process, however, whereby epilepsy may be inherited is ap- 
parently much more complicated than earlier analysts thought when 
they ascribed it to simple recessive genes. Now it would appear that 
multiple factors, probably several pairs of genes, are involved. All 
that can be said with assurance is that where a parent has epilepsy, 
the chance is much greater than average that a child will be epi- 
leptic. (One rare form of epilepsy, myoclonus, which comes on in 
childhood and differs from the ordinary type in that there is no 
loss of consciousness, is definitely hereditary and appears due to a 
single pair of recessive genes.) 

In all the foregoing conditions we must never lose sight of the fact 
that while heredity may be responsible, similar effects might be 
produced by external causes. There are many prenatal and post- 
natal influences, comprising a host of diseases, internal disordezs, and 


accidents, which individually or in combination might turn what 
otherwise would have been a normal person into one with an un- 
balanced mind or defective nervous system. Before, then, you begin 
worrying about insanity in your family background, rule out by 
careful study and with the aid of your doctor, every possibility that 
the cases may have been caused by other and non-hereditary factors. 



One often hears, “So-and-so is of long-lived stock,” or, “So-and-so 
is of short-lived stock.” 

Genetically, there may be some basis for such assertions—but not 

Within certain limits, the life-span of human beings, as of all 
living things, seems to be set by inherited factors. 

The oldest living things are trees. Different varieties are charac- 
terized by different limits of longevity, the most venerable of all 
being the macrozamia trees of Australia which have reached the 
age of 15,000 years. Soil, climate and other conditions are, of course, 
vitally important factors, but there is also something in the nature 
of trees that determines their potential age and that makes a tree 
of one variety live longer than another growing by its side. 

Animals, whose mechanism is much more complex, and whose 
lives are far more hazardous, are rigidly limited in their life-spans, 
but these limits likewise vary with different species. Under the best 
of conditions elephants die at the age of between go and 100, horses 
at 45, dogs and cats at about 20, oxen at 30. 

How long can a man live? 

Cold-eyed scientists and insurance actuaries are now skeptical 
about ancient records of human longevity. Figures in the Bible are 
believed to be based on a different method of computing years—in 
fact, on two different methods than were later employed. For in- 
stance, the age of Adam is given as 930, of Methuselah as 969, of 
Cainan as 970, Jared, 962, etc. But all these were pre-flood person- 
ages. After the flood we find the ages cut to one-fourth—Abraham, 
175, Isaac, 180, Jacob, 147, Mosés, 120—leading to the belief that a 
“year” had a different meaning before and after the deluge. 

As we come down to comparatively recent times we find that only 


obscure persons, usually in obscure localities, have been credited 
with phenomenal ages. England’s champion oldster is listed as 
Thomas Parr (“Old Parr”) a Shropshire farmer who died in 1635 
at the age (according to tradition) of 152. From less conservative 
countries come reports of ages ranging up to 185. 

To all such figures scientists now raise skeptical eyebrows, at- 
tributing them to errors, hearsay testimony, etc. Insurance actuaries 
believe that human beings have not lived, and do not live, much 
beyond 106 years. Only three persons in 100,000 in the United States 
attain the age of 100. The “all time” record for this country, which 
has any claim to authenticity, is that of a woman who lived to be 
110 years and 321 days. 

Let us say, then, that 110 years represents the known maximum 
span of human life. The average life is a little more than half of 
this (namely, 60 years for males and 64 years for females). Never- 
theless, studies show that there are apparently short-lived and long- 
lived families. This has led to the belief that the degree of longevity 
is to a large extent inherited through genes, which by acting on 
specific parts or on the body as a whole, set potential limits to one’s 

Perhaps, as in automobiles, every Rieian being starts life with a 
qualified “guarantee” as to how many years he can be kept going. 
We might call this “conditioned longevity.” That word “condi- 
tioned” is extremely important, for nowhere does environment play 
so significant a part as it does in relation to longevity. 

Quite true, Mr. So-and-so may boast that he comes of “long-lived 
stock,” and may produce figures to show that his parents and all 
his ancestors lived to the age of ninety. But let Mr. So-and-so, driv- 
ing home from the club some winter night with one-too-many un- 
der his belt, try to round an icy horseshoe curve on high, and all the 
statistics as to his potential longevity may be of no avail. 

In the matter of longevity we can think only in terms of broad 
general averages. You read everywhere that the life-span has been 
steadily increasing, how in George Washington’s time the average 
expectation of life was about thirty-five years, how in 1901 it was 
about fifty years and that today it is more than sixty. But applied to 
yourself, that does not mean that because your parents lived to an 

apr] UPHOdoayWy “}UEUIEdaG jeD1;51404S yO ple YpM posedosg 

‘ory O2ue INSU 

STL. ‘ doko, MMED yyy 
ING 920 eee. 

. J 7 “phe a o ty x * 1? hy’ A/, : 
oe geG ash DO LAVIN. sul QIN df y 34 BS YH o. IN gpg Se LUMLEY G 

<N2NY WIP ay 

“hee Ab Yi, A “ar 


. (3U1) P3330p Aq uMOUS 
obp sa03k 2 - 13434) 
j P39NP34 uU3s3q BADY UZDOd 'SIY 
Ul S3/>07SqO 34} AlUO : p3At|-4AzBUO} 40 


ff suryo ‘saiwwas 
B'str og ‘satww 


11L9/9 Ly Ti 

fa Pee OTP A is MN pa Ee be) Meagan? sah feos ge gigi Aide) : EULA 
fica k BP DONAAY  winotipanpy TE Ris | Gav ey pale 

BES pay i SSO Dea ko PAN IOS OUI: Soyo a7! Wad 

OTA ge LO ON ope gh Sym Wy OP sa ty 


(4A 7.02.dn)  -Hiwaa 40 
Adu 4.u} sasnv> 
“Wd lONIdd 

ODvV SuVv3aX 

, (‘sak 6T 07 T) 
300 PIO Ry Pingoyy —-_ HANA, PU POOUPI!YD 
J ‘surig ‘“saqwwaa 
[S34 Op ‘saqvi 




average age of seventy, you will live to be eighty. What has been 
increased, through hygiene, improved medical knowledge and better 
living conditions, is not the potential longevity of human beings, but 
the chances of survival. 

The very young are the ones who have had their expectation of 
life most sharply increased. The death rate from measles, diphtheria, 
scarlet fever, whooping-cough—the most fatal enemies of childhood 
—has dropped more than 80 percent. Many plagues and epidemics 
that formerly carried off vast numbers of children as well as older 
persons have been stamped out. All this has projected into later 
life many individuals who formerly would never have passed into 

Thus, the disconcerting fact is that for people in middle age today 
the expectation of life 1s no greater than it formerly was. 

But granted that each individual has his potential limits of life, 
by what genetic mechanism could these limits be set? 

There are various theories as to the direct causes of the body’s 
“natural” breakdown which lead to death. Some lay the blame on 
fermentation (Metchnikoff) ; some on changes in the arteries (Osler, 
Brown-Séquard); some on breakdown of the ductless glands 
(Lorand), etc. But there is also the belief that in whichever parts of 
the body the “crack-up” might originate, specific genes are con- 
cerned in fixing the “natural” span, or time-limit, for each part. 
Death might come through a single gene which sets a time-limit 
for the heart, or through many genes which set limits for the work- 
ings of various parts in cooperation with each other. 

Have we identified any of such “killer” genes? 

Yes. Geneticists have discovered that “killer” genes are found in 
great numbers among all living things, both plants and animals. 
Most drastic are the “lethals” which may kill off an individual in 
the very earliest stages or soon after birth. While many of these 
have already been identified in experimental animals, it has not yet 
been possible to uncover more than a few lethal genes among hu- 
mans. All authorities, however, are agreed that there must be many. 
In fact, there is reason to believe that in numerous instances of 
“false” pregnancy the woman actually was pregnant, but the embryo 


was killed off by lethal genes; and that many cases of miscarriage 
can also be attributed to them. 

Obviously, no lethal gene could bring death working always 
singly. If it did, it could never be passed on, for no individual who 
carried it would live to propagate. Lethal genes, therefore, must 
work in twos, one contributed by each parent. Those genes which 
singly produce serious effects and which, with two together, have 
their effects greatly intensified are among the principal lethals. Ex- 
amples of this are believed to be the genes for brachyphalangy (stub 
fingers) and for hemophilia. There is no case on record of any in- 
dividual definitely known to carry a pair of either of these genes, 
leading to the belief that a “double dose” of them proves fatal. 

Three other human genes which have been established as lethal 
if inherited in pairs are those for “elephant skin,” multiple bone 
fractures in the embryo, and familial jaundice of the newly born. 
Familial jaundice, however, is a condition which no longer can be 
considered truly lethal, as it can be cured permanently by giving 
the infant born with it an immediate blood transfusion. This raises 
the question as to whether the term “killer” can continue to be ap- 
plied to this, or to other genes now termed “lethal,” when and if 
cures for their effects are discovered. 

In addition to these lethals there are “killer” genes (some men- 
tioned in preceding chapters) which may bring death prematurely. 
One of such genes is that for glioma retina (eye tumor) usually 
fatal in infancy. This is the condition which recently figured in the 
news with regard to a Chicago infant, when an “ethical” jury was 
called on to decide whether to try and save her life by operation 
or to let nature take its course. 

Amaurotic family idiocy, malignant freckles and progressive spinal 
muscular atrophy of infants are also fatal in early life, while hemo- 
philia in a male is generally deadly by maturity. (A few other pre- 
maturely fatal conditions will be found listed in the Summary 

It is conceivable that if there are genes which produce a fatal 
breakdown at early stages of life, there might also be genes 
“timed” to bring death at later periods. On this theory (which, let 
us emphasize, still lacks scientific corroboration) rests the belief 
that there may be sets of genes, collectively inherited in given fam- 


ilies, which in a general way make some of them potentially “long- 
lived” and others “short-lived.” 

At first glance the evidence on this score would seem to be con- 
clusive. Extensive studies have been made of hundreds of thousands 
of individual records by leading insurance companies of the United 
States, in which the ages at death of parents and sons were com- 
pared. The findings were these: 

Men with the best parental longevity show unmistakably lower 
mortality at every age. 

At the age of twenty, persons whose parents had a good longevity 
record have a minimum of two and a half years’ greater expectation 
of life than those with a poor ancestral history. 

In men aged thirty, the probability of living to the age of eighty 

was 26.6 percent for those whose parents had both lived to, be sev- 
enty-five, compared with only 20.3 percent for those whose parents 
had died under sixty. The chance of reaching the four-score mark 
was therefore almost one-third greater for those with long-lived 
parents than for the others. 
. Further, in another study by Dr. Raymond Pearl it was found 
that among those who lived to a very old age (ninety to one hun- 
dred) almost 87 percent had had one or more long-lived parents 
and a large proportion had had two or more long-lived grandparents. 
In comment Dr. Pearl said, “Taking all the evidence in this study 
as a whole it would seem to leave no doubt as to the importance of 
heredity in determination of the longevity of the individual human 
being.” * | } 

All the foregoing findings, however, demand certain qualifica- 
tions. The comparative “longevity” records may be weighted in favor 
of the long-lived families by the fact (as we shall see presently) that 
the rates vary in different social and occupational levels and are in- 
fluenced by various other factors. To quote from “Length of Life,” 
by Drs. Louis I. Dublin and Alfred J. Lotka: 

“The superior longevity of persons with a good family record may 
be the result, in part, of more favorable environment as well as a 

1Dr. Pearl has stressed the fact that, in his opinion, it is the total genetic con- 
stitution or make-up of the individual, rather than any particular genes (lethal or 
other), that is most important as a factor in determining length of life. As he points 
out, the significant réle of lethal genes is in the fairly early (prenatal) develop- 
mental stages. 



(As shown 1,000 BIRTHS 
by monthly (Deaths under 
rental paid) one year of age) 
500 [20 

RENTAL ~*~. 

*IQOM, os 



$5 ; “ZO 

(Based on a survey made in Cleveland, O. by Howard Whipple Green — 1932) 

better physical inheritance. We know that those with a good family 
history have the benefit of more favorable environment than those 
with a poor family history. To have parents survive to old age means 
in most cases to enjoy a more protected and a more fayorable in- 
fancy and childhood. 

“The premature death of either parent often results in the break- 
ing up of the home, with all its consequent evils to the children. If 

——— ~——.. - Ln 


it is the mother who dies, the children often receive poor care and 
improper nourishment; and the premature death of the father 
usually means an even severer handicap for the children than the 
early death of the mother. The family is often reduced to poverty 
and destitution. Consequently, the children are badly housed, badly 
fed and poorly clothed. Moreover, many of them are compelled to 
leave school and go to work as soon as the law permits. 

“All these factors are hazards to the life and health of this group, 
[comprising those with a poor ancestral history] and it is therefore 
not surprising that its longevity is lower than that of groups more 
favorably situated. In these circumstances the-influence of inheritance 
and environment are intertwined. Both undoubtedly operate to ac- 
count for the differences [in longevity |.” 

With so many environmental factors—both internal and external 
—involved, tracing the inheritance of longevity is an extremely com- 
plicated procedure. Taking up other instances, there is an exceed- 
ingly high death rate among insane persons, idiots and imbeciles. 
Half of these die between the ages of ten and twenty, and few pass 
far into maturity. Does this mean that the genes for low mentality 
also produce short-livedness? In some cases they do, but in general 
we can find another answer: That mental defectives, being unable 
to care for themselves and usually receiving inadequate treatment 
at the hands of others, are easier prey to ills than are normal indi- 

In fact, not merely native intelligence, but position in life has a 
great deal to do with one’s life-span. The higher up the soctal scale 
you are in earnings and position, the longer you may expect to live. 
Professional men, scientists and notables in “Who’s Who” live 
longer than do average men. In current mortality tables we find 
that deaths among men in middle age range about as follows: 

For Men Between Ages of 55-64 
Annual deaths 
per 100,000 

Class (Approx.) 
Upper and: professional classes ...2....-.......... 2,247 
Partly skilled or skilled workers and craftsmen .... 2,490 

Unskilled workers and casual laborers ............ 3,060 


COLLEGE GRADUATES have mortality rates definitely 
below the average. 

CLERGYMEN live considerably longer than the general 
average man. 

DOCTORS have a somewhat higher death rate than 
other professional men, no doubt because of their 
special occupational hazards. 

LAWYERS have among the lowest death rates in the 
professional group. 

TEACHERS have among the lowest death rates for 

women in any occupation. 

FARMERS are particularly long-lived. 

UNSKILLED LABORERS have the highest mortality rate. 

Farmers are in a special class, with a death rate almost the same 
as that of the “upper” classes, either because their conditions tend 
to develop health and strength, or because they have to be healthier 
and stronger to continue as farmers. 

The facts regarding mortality are even more striking in the case 


of babies. Deaths among infants in the so-called “lowest” classes are 
several times as high as those in the “upper” classes. In other words 
(speaking always in terms of general averages) studies in the large 
cities of the United States have shown that infant mortality goes 
higher and higher, step by step, as the incomes of the fathers drop 
lower and lower. Would this prove that the babies of the poor have 
“poorer” genes? Hardly. With lower income, of course, is corre- 
lated lower educational status, poorer hygiene and living conditions, 
shorter intervals between births and many other adverse factors. All 
these are responsible for the higher mortality not only among the 
infants but among the adults as well. Nevertheless, in the same so- 
cial and economic levels and within the same environments, there 
are other factors that produce differences in degrees of longevity 
among individuals. 3 

First we have the pronounced difference as between males and 
females. The fact that there is a far higher mortality among male 
embryos than female was brought out in the “Boy or Girl?” chapter. 
This discrepancy in death rates continues throughout “life, but to 
a lesser degree. Of babies dying during the first year, there are at 
least 20 percent more boys than girls. In childhood and youth the 
males continue to fall in greater numbers, so that before maturity 
is reached the females have overcome the 6 percent lead that males 
had at birth, and have caught up with them numerically. Then the 
females begin to draw ahead. In middle life there are about 15 per- 
cent more females than males, and finally, in the very old-age 
group, there are about twice as many females as males surviving. 

There is but one logical conclusion: That it is not the male, but 
the female who constitutes the stronger sex. Here science gives the 
laugh to the deep-rooted idea, perpetuated through the ages no 
doubt by men themselves, of masculine superiority. For even grant- 
ing that men have stronger surface development, yet if “fitness” 
and “strength” are to be judged by the power of survival, then un- 
questionably women are by considerable odds the strongest and 
most fit. 

Why males are less able to survive cannot yet be told with au- 
thority. But inasmuch as the only initial difference between the 
sexes is the lack of an extra “X” in the male (its place, remember, 




saa ek 6 vy, MORE BOYS 



YOUTH a7’. ar. ae EQUAL 

MATURITY i. Welt taceie a ee PROPORTION 



RS Eh gb tee dace will Damaged a pt 




being taken by the abbreviated “Y”) the answer may lie here, in 
the fact that females get more genes than do males. As we have seen 
in preceding chapters, the X chromosome contains many genes 
which, when defective, produce the “sex-linked” conditions that 
especially victimize males (because they have no alternative normal 
X to protect them). There may be more genes in the X, still un- 


known, which affect other vital processes. It is not unlikely, there- 
fore, that the two X’s which a female receives, compared to the 
single X of the male, may make her more resistant to early adverse 
conditions and give her a better start that carries through life. (Per- 
haps Nature has intended this, as Dr. Alfred Lotka suggests, to bet- 
ter prepare women for childbearing.) 

Hormonal or constitutional differences (in which, of course, the 
genes also play a part), and perhaps environmental differences later, 
may help to explain the differential death rate between men and 
women. But the fact remains that at every stage the expectation of 
life for a woman is higher than it is for a man. is the accompany- 
ing table.) 

(For Whites) 
A man may expect A woman may expect 

At the age of to live: to live: 
Zieh ee ana 38 more years AI more years 
TG Oa? SRG NE 29 more years 32 more years 
aye biked wing Nema Oe 22 more years 24 more years 
(SLES UG a Sen ea - 15 more years 16 more years 
TOMeME eyed va) ne. Q more years IO more years 
COME Re ee 5 more years 54 more years 

(Computed by Statistical Bureau, Metropolitan Life Insurance Co., according to 
U. S. mortality statistics for 1935.) 

Among both men and women, insurance actuaries report that 
mortality is greater for the young ones below average height and 
weight and for those over forty who are overweight. No clear de- 
ductions can be drawn, however, as to any correlation between body- 
build and longevity. A better-appearing body may be the result of 
the same favorable environmental factors that generally are con- 
ducive to longer life; an undersized, underweight, or misshapen 
body may result from the same adverse factors which are prejudicial 
to longer life. 

One hears various theories: Brunettes live longer than blondes; 
short people live longer than tall (or vice versa); premature gray 
hairs mean early death; bald-headed men die before those not bald; 
men with more hair on their chest live longer than those with little 


hair, etc. Not one of these theories has yet been found to have any 
scientific basis. | 

Another variable field of speculation has been that regarding the 
effect of alcoholic drinking on one’s age. The best existing evidence 
is that moderate drinkers live as long as do abstainers but that those 
who drink to ex¢ess have their lives shortened. 

We may pause now to ask, first, this question: 

Does anything brought out here throw any light on how long you 
may expect to live? 

Well, perhaps not too much. The fact, of course, is that at present 
we know so little about what lies ahead of any “normal” individua! 
(excluding the relatively few who are afflicted with serious heredi- 
tary defects) that it would be folly to attempt any ae estimates 
of longevity on the basis of family records alone. 

Or, in other words, as matters stand today, you must look to your 
own physical condition and to the way that you live your life for 
the best forecast of how long you can expect to live. At best, none 
of us can expect to live (even if we wished) any longer than the 
potential limit that has prevailed apparently from the dawn of civili- 

What of future life-expectations for our children and grandchil- 
dren and later descendants? Do we imply that the “conditioned 
longevity” of humans is forever “set”? 

No, for in the opinion of most authorities, the human life-span 
very likely will be increased. However, even the most optimistic of 
the scientists believe that so long as the human animal is a function- 
ing mechanism, with life being a continual process of building up 
and tearing down cells, the potential longevity limits will never be 
far from where they are today. Estimates for the “maximum” theo- 
retical life-span range from 120 years, in the opinion of Voronoff, 
to 185 according to the most optimistic Russian, Metchnikoff. 

The idea of extreme longevity has been given no little impetus 
by the feat of Dr. Alexis Carrel in showing how living tissue can be 
kept alive indefinitely. Doing this with an isolated piece of tissue 
is far from the same thing as keeping all the vital parts and organs _ 
of a complete human body growing and Aunctioning uniformly .— 


through all the varied experiences which come to one in a lifetime. 
But who knows what science may accomplish? 

There is one other interesting possibility: Russian scientists, work- 
ing in the Arctic, found that plants which had been frozen into the 
ice for a thousand years or more could be revived and made to grow 
again. Said Professor P. N. Kapterev: “As a result of our experi- 
ments, it can be stated that there is really a possibility of resuscitat- 
ing organisms long after they have been frozen.” 

Again, who knows? Perhaps, some day, one of us, fresh out of 
college, will be frozen by the method described in the frozen-food 
advertisements: “Wuam! A blast of Arctic cold strikes suddenly and 
seals in all the freshness. . . .” We could then be kept in status quo 
indefinitely under perfect De lvediod: and a hundred or two hun- 
dred years hence we could be “defrosted” and enabled to begin liv- 
ing and moving again in another world, as characters in drama 
and fiction have already done. 

The only immediate method in sight, therefore, of prolonging 
oui days seems to be by spending a stretch of years in an icebox. 




“Male and female created he them... . 
—Gen. I: 27. 

From a corridor in the office of our psychiatrist friend came 
the voices of a woman and child. The child’s voice was that of 
a little girl. It broke into a tinkle of bell-like laughter, and then, 
with a hippety-hop, into our view came, not a little girl, but a boy 
of about five. 

We say “boy.” But only the clothes would identify him as such. 
His head was covered with golden ringlets; from his pink-and- 
white face shone the bluest of blue eyes, fringed with long dark 
lashes; his every gesture was that of a little girl. Behind fol- 
lowed his mother, her expression reflecting the tragedy of the 
situation. For through some strange circumstance or quirk of 
birth, this child of hers, although healthy in every way, was of 
a type considered by the world as “abnormal.” 

“Sad case, that,” remarked our psychiatrist friend, when the 
mother and child had left. The little boy, he explained, had shown 
these feminine traits almost from infancy. His parents at first had 
been overjoyed by his unusual beauty. Now they were desperately 
worried. Both highly educated persons, they knew all about psycho- 
analysis, “fixations,” complexes, etc. But this child did not merely 
act like a little girl; he looked like a little girl. Whatever early 
environmental upsets might have been involved in “conditioning” 
the child’s behavior, how could they account for his appearance, for 
the so-called sexual characteristics which were so much more like 
those of a young female than of a male? Was the child born that 
way? Or, going further, could he have inherited such a condi- 



The answer, as given by many geneticists today, might very 
well be, “Yes.” There are frequent cases of “abnormal” sexuality in 
humans, as in all other animals, which may be caused directly by 
“abnormal” sex-genes, by derangements of the chromosome work- 
ings or by upsets in the sex glands, due either to primary genetic 
causes or to later environmental influences. 

The Bible says, “Male and female created he them. . . .” There 
is no need to dispute that. But however distinctly the first man 
and woman might have been differentiated the one from the other, 
in the billions that are assumed to have sprung from them one 
can find every gradation of sexuality. In short, sex is a highly 
variable characteristic, and there is not quite the clear-cut distinc- 
tion between “male” and “female” which we’ve always assumed 
that there was. 

Think back to the chapter on “Boy or Girl?” We learned that 
the matter of sex determination depends upon which combination of 
“sex chromosomes” an individual receives at conception. 

An X and a Y produce a male. 

Two X’s produce a female. 

This is fundamentally correct. But as in all other human charac. 
teristics, the best laid plans of the chromosomes gang aft agley, 
In the earlier chapter there was no need to bring up the exceptions 
to the rule or to go into the involved details which explain these 
exceptions. In fact, it was not until recently that geneticists them. 
selves came to understand the intricacies of sex-determination and 
to be able to explain how various sex abnormalities are produced. 

First: The X and Y chromosomes are not the sole arbiters of sex. 
If there are a great many “sex” genes, as we believe, they are not 
confined to the X and Y, but may be distributed among the other 
chromosomes, just as many other genes that have nothing to do 
with sex are found in the X and Y. Which is to say, in the mat- 
ter of sex development it is believed that various, and perhaps all, 
the chromosomes, are involved. 

The X and Y most probably carry the “directing” genes, which 
start sex development off in one direction or another. But we 
know now that all individuals carry in them the potentialities for 
either sex, and that sex determination is merely a process of modify 


ing the rudimentary sex glands so that they produce hormones of 
one kind or another. These in turn lead to the development of male 
or female reproductive organs and secondary sex characteristics. 

Thus, the combination of “sex” genes in two X’s starts the in- 
dividual off in the direction of femaleness. 

In the XY combination, either the absence of the extra set of 
X genes, or perhaps the presence of certain other genes in the Y, 
steers the individual toward maleness. But—between the initial 
steps taken by the “sex directing” genes and the final result many 
things can happen. In fact, the type of sexuality of any individual 
can be changed tn degree or varied at every stage of life. 

If we turn to the lower animals, we can see some rather amaz- 
ing instances of deviation from what we think of as sex “normalcy.” 
There are creatures that are normally double-sexed, performing both 
sex functions either simultaneously or alternately. These are known 
as “hermaphrodites.” But they are not freaks. It is normal for the 
snail, earthworm or oyster—and many other creatures—to be double- 
sexed, just as are most plants and flowers. For them to be single- 
sexed would be abnormal. 

But how do such queer manifestations apply to human beings? 
Can a human being also be “double-sexed,” or be born as a male 
and turn into a female, or vice versa? ; 

Let us see first how this can happen in the lower animals. 
Strangely enough, in even the snail or the earthworm, the sex- 
chromosome mechanism is basically the same as it is in humans. 
They, too, start out with the potentialities for either sex. But 
instead of their genes sending them off in either one sex direc- 
tion or another, they allow both potentialities to assert themselves, so 
that the organs of both sexes develop. In the oyster, the sex genes 
are so gaged that they allow first the male organs to develop, and 
later have these give way to the development of the female or- 

But there are “freak” types, occurring in animals normally single- 
sexed in which commonly half the body is of one sex, and another 
half of the other sex. These are known as “gynandromorphs.” They 
are fairly common in many species, including butterflies, moths, 
wasps, bees, flies, ants and spiders. If you were a “child natu- 



while also double-sexed, have their sex organs 
so placed that each individual must mate with 
another of its kind, but playing both male and 
female roles. 

is hermaphroditic (double-sexed), each section 
complete with both male and female organs, 
and able to fertilize itself. 

alternates from one sex to another. It starts the same egg, if fertilized, will preduce a fe- 
| life as a male, becomes a female, may turn into male; if not fertilized, will develop into a male.-: 

| ‘a male again, etc. 


® female may turn outwardly into a "male," or a male into a female," as a result of some upset in 
the sex organs or hormonal balance. 



ralist” you may have caught one of these freaks, in which the 
creature had one kind of pattern or form on one side, and a 
different appearance on the other side. Or, as frequently happens, 
the gynandromorph is male in the front half of its body and 
female in the rear half, or vice versa. 

One way in which a gynandromorph might be produced is shown 
in the accompanying diagram. At conception a certain individual 
receives two X’s, normally destining it to be a female. But at the 
very first stages of cell division something happens so that one of 
the X’s is left out of a primary cell, this cell giving rise to others 
with only one X in each. Here, then, is an individual starting 
life with part of its body containing XX cells, the other part 
single X cells. The XX part proceeds to develop femaleness. The 
part with the single X goes on to develop maleness, for as we 
have seen, the Y chromosome is not essential. 

In some cases gynandromorphs have the genitalia of both sexes, 
but whether with one set of sex organs or both, as a rule they 
cannot reproduce. In contrast to these freaks, hermaphrodites have 
the reproductive organs of both sexes, either simultaneously or 
alternately, and are normally capable of functioning as both sexes, 
either at the same time, or first as one sex, later as another. 

Now in what way do such queer conditions apply to humans? 

We find, first, that true gynandromorphs in which one half of 
the body is completely male, the other half female can occur only 
among the more elementary creatures, such as insects, which have 
no sex hormones as humans have. In human beings or in other 
mammals, even where a derangement of the sex chromosomes 
might occur, the sex hormones circulating in the body would pro- 
duce a “blending” effect throughout. Circus freaks, claiming to 
be “half man and half woman,” are sometimes seen, but these 
may be set down as spurious. (In these cases the freak is prob- 
ably a male in whom one breast is overdeveloped, giving him a 
female contour on one side, a male contour on the other.) 

True hermaphroditism in human beings, where an individual 
may have organs and characteristics of both sexes, is, however, 
not at all impossible. Every sort of sexual intergradation has been 

. Individual starts out as a potential 

. In early stage, when chromosomes and 

. As the cells multiply, those on one 

. The result is a creature male on one 

(Half-in-half creature) 


female with two "X's. 

cells double, an "X" may get left out 
of one of the halves. 

side have only one "'X,"' all those 
on the other side two "X's." 

side, female on the other. (The one 
here shown is a fruit-fly, [Drosophila,] 

(After Morgan) 



found, from males with undeveloped masculine genitalia to males 
with all degrees of female genital development, grading into females 
with undeveloped or incomplete female organs and ranging up 
to those with rudimentary male organs. 

Recently Professor Hugh Hampton Young, of Johns Hopkins 
Jniversity, published an exhaustive treatise on the condition. Dr. 
Young reports knowledge of twenty indisputable cases of true 
hermaphroditism, in which the same individuals had within them- 
selves both ovaries and testes. 

A much more common condition, estimated to occur as often 
as once in every 1,000 persons, is that of “pseudo-hermaphroditism.” 
In this, the individual has either ovaries or testes, but not both, 
yet nevertheless may have external organs of both sexes (with one 
type usually predominant). Thus, while genetically either a male or 
female, the pseudo-hermaphrodite may be mistakenly classified in 
infancy or childhood as of the wrong sex. A number of such cases 
have lately come to the fore where individuals reared as females 
have achieved prominence as champion “women” athletes. One 
of these later underwent an operation which “transformed” her 
into a male by suppressing the rudimentary female organs. 

If we seem to be stressing sex abnormalities it is with a purpose. 
We can imagine no aspect of heredity more important than the 
fundamental one of sex. By clarifying what are considered as ab- 
normalities we may come to a better understanding of what is 
considered “normal.” For what do we mean by “normal” sexuality 
in human beings? Dictionaries define “male” as a person having 
organs for “procreating young or producing sperm for the im- 
pregnation of an ovum,” and “female” as a “person with organs 
for conceiving and bringing forth young or producing ova.” And 
yet as we have just seen, there are individuals characterized by 
society as “male” or “female” who do not correspond with either 
definition, who may have both kinds of sex organs, or who may 
have one kind so defective that it cannot be used for reproduction. 
It is to these persons that we apply the term of “twilight sexes.” 

The difficulty in defining “male” and “female” is as nothing 
compared to the task confronting us when we try to define “mas- 


culine” and “feminine.” These terms geneticists now recognize 
as being capable of highly variable interpretation. Most authorities 
believe that drologically, no person is completely “masculine” or 
completely “feminine”; that we all begin life with potentialities 
for either sex; and that only because Nature has found it expedient 

MAN (Extremely rare) WOMAN 

Between normal’ male and ''normal'' female there is every type shading from 
"maleness" to "femaleness'' and ''femaleness"’ to 'maleness'’ 

for our reproduction does she usually, but not always, provide a 
mechanism to tip the balance of sexuality in either one direction 
or the other. 

Nevertheless, as we have seen, only with respect to a single 
chromosome of the 48 are males and females genetically different. 
With “sex” genes scattered through all the other chromosomes, 
so-called “female” characteristics may just as well be transmitted 
by a father to his daughter as by a mother, and “male” charac- 
teristics just as well by a mother to her son. This is no news to 
animal breeders. They have long known that the milking qualities 
of a prize cow can be carried by a bull offspring and passed on by 

him to his daughter; that the fighting qualities of a bull sire 

can be passed on through a daughter to her son. 

In human beings there is reason to believe that a gene or genes 
for fertility or twinning can be passed along by a mother through 
her son just as well as through her daughter. The gene for a father’s 
beard pattern could be passed on to his daughter, and while 
not manifesting itself in her, could be passed on by her in turn 
to her son, where it would assert itself. The list could be ex- 
tended greatly to include a host of “secondary” sex characteristics, 
the genes for which both sexes carry equally. 

As further evidence of all this, when there is some upset in 
the sex glands of either male or female, the latent secondary sex 
characteristics of the opposite sex may crop out. Startled farmers 
have sometimes reported that one of their hens became trans- 
formed into a rooster. This can actually happen. In a classic case 
(reported by Crew) the transformation was due to the destruc- 
tion of the ovary in a hen, allowing the male glands and organs, 
always present in a rudimentary form, to develop. The claim was 
made that this “hen-rooster” actually functioned as both “mother” 
and “father,” first laying eggs and then, in the rooster stage, pro- 
ducing sperm and “fathering” chicks. While the evidence regarding 
the double functioning is not considered conclusive, experiments 
have repeatedly shown that when the ovaries of hens are removed 
they do develop the secondary male characteristics of a rooster— 
comb, plumage, etc. 

In the human female, removal of the ovaries after puberty is not 
known to have any such corresponding effect. However, if re- 
moved before puberty, when the secondary sexual characteristics of 
the body are not yet developed, they might seriously alter the 
physical characteristics of a girl. Even if the ovaries are not affected, 
some upset in the sex balance or some glandular disturbance, es- 
pecially if happening in early life, may well produce in a human 
female secondary male characteristics, such as male body propor- 
tions and, later, deep voice, hairiness of body and face, ete. 

Among human males the results of castration before puberty are 
well known. But (as in females) even without an operation it 


is possible that early derangement of the sex glands or sex balance 
might cause a boy to grow up with “eunochoid” characteristics— 
secondary sexual characteristics resembling those of a female— 
large hips, narrow sloping shoulders, absence of beard and body 
hair, high-pitched feminine voice, etc. In maturity, also, especially 
in old age, changes in the glandular make-up may often cause 
men to develop high-pitched voices and perhaps some other sec- 
ondary female sex characteristics. 

To upset a popular fallacy, it might also be made clear that 
in netther sex, male nor female, does removal of the “gonads” 
(testes or ovaries) after puberty, necessarily interfere with sex func- 
tioning. Eunuchs may have sex relations as other men. The “sex 
impulse” in men—in its physical aspects—is engendered and sex 
functioning governed not by the testes alone but also by hormonal, 
nervous and psychic stimult. 

It might also be said that popular impressions as to what con- 
stitute “masculine” or “feminine” secondary physical characteristics 
are also not too well grounded. Hairiness of body and strong 
muscular development are considered characteristic of males, and 
yet there are many “normal” women with more body hair or 
with bigger muscles than the average man. Delicate features, smooth 
skin and rounded contours are considered “feminine” characteristics, 
and yet there are many “normal” men who have these charac- 
teristics in greater degree than many women. In short, there are 
biologically normal women who look more “masculine” than a 
good many males, and biologically normal males who look more 
“feminine” than do a good many women. 

It is not hard to see, therefore, how difficult it is to try to identify 
genes that produce abnormal sexual characteristics. Only in the case 
of obvious genital defects or abnormalities has it so far been pos- 
sible to do this. Among such hereditary abnormalities, some of 
which are known to “run” in families, are these: 

Supernumerary nipples—extra nipples, occurring in males and 
females. Some individuals have as many as six nipples, the pairs 
ranged one below the other. (A condition, by the way, abnormal 
for humans but normal in lower animals.) 


Hypospadias—a misplaced opening of the urethra. This occurs 
in males only, is present from birth and is believed due to a 
dominant gene. 

Sterility may also be inherited, unbelievable as that may seem 
at first thought. It can be produced quite simply by two recessive 
genes coming together, just as in the case of lethals. There are 
several such types of genes which produce incomplete develop- 
ment of the reproductive organs, and with it, sterility. Sterility 
in a male might be produced by a gene transmitted only through 
mothers. But in the majority of cases of sterility in either males 
or females it is questionable whether hereditary factors play any 
great part. 

Fertility is also believed by many authorities to be influenced 
by certain genes. The prolific child-bearing which seems to charac- 
terize certain human strains is thought to have some hereditary 
basis, just as the number of offspring in a litter or the frequency 
of reproduction among various species of other animals is ap- 
parently genetically controlled. No “excess fertility” genes, however, 
have yet been identified. 

The “timing” of sex development is also, quite clearly, influ- 
enced by genes. It is no accident that puberty, adolescence, maturity, 
the climacteric in women, etc., come to most human beings at 
about the same time, and that in various strains or families there is 
a frequent deviation from the average “timing.” Where the cycles 
appear to arrive consistently in families either earlier or later, and 
where no environmental factors seem to be involved, genes are 
apparently responsible. In rare cases (but not believed due to heredi- 
tary factors) the workings of the sex glands are so abnormally 
speeded up that they can produce fully developed sex organs in 
children of the age of two or three. 

Only a beginning has been made in the study of the genetic 
aspects of sex and of the rdle of heredity with regard to sex abnor- 
malities. As has been said previously, no characteristics could be 
considered of greater importance. If we think back to the little 
boy at the beginning of this chapter, and with him include others 
who deviate sexually from what is considered “normal,” we might 


ask ourselves to what extent such deviations may affect or alter 
their actions and behavior, and influence the attitude of others 
toward them. This will be dealt with in later chapters, when we 
take up the possible inheritance of abnormal instincts and behavior 
—characteristics as yet too vague to be identified or classified here 
with the “black” genes. 


Tuts is not a happy chapter. 

It summarizes and brings together all the “black” genes previ- 
ously discussed and some additional ones of lesser import. Also 
—which is its most ominous aspect—it forecasts the chances of 
transmitting any given defect, disease or abnormality to a child. 

At first glance the array of “black” genes may appear to be 
Tables of Doom. But really, there are some brighter sides to the 
picture. As we have pointed out, the list of known hereditary 
defects is as nothing compared to the interminable array of non- 
hereditary ills that fill volume after volume in the medical treatises. 
Moreover, few of the known hereditary conditions are sufficiently 
common to present grave problems to society, and many of them 
are serious to the individual only when he considers them as such. 

For instance, most of the eye conditions: Near-sightedness or 
far-sightedness, in their usual form, can hardly be thought of as 
spelling doom—not, certainly, when there is an optician around 
the corner. In certain professions and trades (such as soldiering) 
weak eyes may be a bar or a serious handicap. But we prefer tc 
think of one of the most near-sighted of men, Arturo Toscanini, 
and of how the very fact of his weak eyes tended to develop in 
him the miraculous memory which has contributed to his achieve- 

If a deviation from the standard for any characteristic is a de- 
fect, then we are all, each and every one of us, defectives. Look- 
ing through the list of “black” genes (and remember, not all 
the minor ones are here included), it is more than likely that 
you will find at least one condition that strikes home to you per- 

sonally, or that is present in your immediate family. Most cases 


justify no further comment than, “My, my—so that’s inherited. 
How interesting!” 

But, unfortunately, many conditions cannot be dismissed so 
lightly. For example, blindness, or conditions that lead to blind- 
ness; deafness; diseases such as diabetes, hemophilia and other 
blood disorders; certain tumors; serious and unpleasant skin con- 
ditions; deformities of the features and of the body; grave mental 
disorders; etc. If any of such conditions are present in you or in 
your immediate family (bearing in mind always that we are speak- 
ing of the hereditary types) then they may well give you pause. 
This is when you should study seriously the “forecast” tables. 

Even where a condition has already been transmitted, or may 
be transmitted, an optimistic view may be that a cure or treat- 
ment exists or will be made available. Many hereditary condi- 
tions or defects once considered extremely grave have had their 
importance much diminished by the discovery of cures, and there 
is every prospect that medicine and surgery will provide cures 
for others. But this, of course, may have no bearing on the im- 
mediate present, and will not affect the transmission of the genes 
~ Another fact which may hearten the individual is that no re- 
cessive condition, even if present in one parent, will crop out in 
a child unless a gene for that condition is also carried by the 
other parent. No one individual parent can transmit to a child 
rheumatic fever, diabetes, albinism, feeble-mindedness or any other 
condition where two recessive genes are required. But this does 
not console society, for actually, as will be more clearly explained 
in a later chapter, it is the recessive “hidden” conditions that con- 
stitute our greatest problem. 

The zme of onset of any condition is also of great importance. 
To the lay mind a condition which is present from birth, or that 
manifests itself in childhood, with perhaps fatal consequences, is 
considered more ominous than one which does not appear until 
late in life. Although late-appearing conditions may be more fa- 
vorable to the individual, from the standpoint of society quite the 
reverse is true, in many respects. Where conditions do not come 
on until after puberty they may permit the afflicted individual to 


reproduce and pass on the genes. Thus, if you are still young, 
and a condition which has its onset in maturity is known to run 
in your family, there is always the possibility that it may yet ap- 
pear in you and that you may transmit it. 

As we said, we are not here listing every single one of the 
known “black” genes, down to the rarest and the most minor ones 
which are often merely variations of others that are listed. To 
have attempted such thoroughness would have been to give this 
book the character of a medical treatise, which we heartily wished 
to avoid. However, a conscientious effort has been made to present 
every condition that could be of interest to any considerable num- 
ber of readers. Further, to permit any “skipping over” desired, the 
relative importance of the various conditions has been indicated 
by the use of different type. 

A final word of caution: In reading the brief description of each 
condition, be careful not to confuse it with something else which 
might have similar symptoms, or which is not hereditary. Also be 
sure to make allowances for the réle of environment—disease, ac- 
cident, etc—and for time of onset. Wherever in doubt—and cer- 
tainly for every serious condition—it would be well to consult 
your physician. 

We now turn to the tables, presenting first, the lists of the “black” 
genes, and following them with the “forecasts.” 



DOMINANT Gene. Only One required to pro- 
duce effect. : 

A parent with a dominant condition will pass it 
on to one in two children. 

RECESSIVE Gene (Simple). Two required ” to 
produce effect. Ke 

For a child to have a recessive condition each 
parent must contribute the same gene. 

SEX-LINKED RECESSIVE Gene. Carried by ‘X" 
Chromosome. Only one needed to produce 
effect in male, but two required in female 
(as with any other recessive). 

"D" after ''S-L" means that the Sex-Linked gene 
is Dominant (rare), producing effect singly in 
females as well as males. 

RECESSIVE PLUS. Condition is caused by two 
or more different pairs of recessive genes 
acting together. 

DOMINANT PLUS. Condition is caused by two 
or more different dominant genes acting 

QUALIFIED. Genes may not always produce 
their effects, or may not always work in sarne 
way, or environment is a factor. 

QUESTION MARK after name of condition 
indicates “heredity doubtful or uncertain.” 

After gene’ symbols it means “gene mechanism 
not established." 

BLACK CROSS after gene ohn means the 

condition is fatal in early life. 



Herewith are listed all leading or unusual defects, diseases or “‘abnormal” 
conditions, in which heredity has been proved or the possibility of inheri- 
tance presumed. (Nore to physicians: Some of the conditions listed as heredi- 
tary may be clinically similar to conditions caused by acquired diseases, for 
example, eye-muscle paralysis, where the hereditary type is present from 
birth while the non-hereditary type is a sequel to meningitis.) 

The relative importance of the conditions is broadly indicated by the 
type in which their names are set: 

Black Type—Prevalent or common. 
‘Medium Type—Fairly common. : 
Small Type—Rare. 

Condition Description 
Diabetes ‘Sugar Sickness’’. Due to pancreas defect. 

False Diabetes 


High Blood 
Pressure ? 


(Common) ? 

Rare Cancers 
and Tumors 

Middle-age; sometimes childhood. 

Some symptoms of true Diabetes, but none 
of serious effects: 

a. Sugar urine. 

b. Diabetes insipidus. Thirst, excessive 

urine. g 

Joint pains, chorea, heart effects. Child- 

Due to hardening of arteries. Late life. 
Heredity uncertain. 

a. Multiple cysts, serious in pregnant 

b. Urinary disorders. (Black, reddish, etc.) 

(Stomach, breast, etc.) Inheritance doubt- 


a. Malignant freckles. Dark, freckle-like 
inflammations from sun, leading to cancer. 
Infancy or childhood, usually fatal. 





@ D(q) 

@@ R(q) 


@@ R +} 





Rare Cancers 
and Tumors 

Bleeding Diseases 

- Anemia 


b. Sebaceous adenoma. Tumors of skin, 
brain, etc. Childhood. Frequently fatal. 
c. Retinal angioma. Blood tumor of eye. 
d. Eat-nerve tumor, causing deafness, 
blindness, frequently death. 

e. Glioma retina. Tumor of eye, fatal un- 
less eye removed. Birth or infancy. 

f. Polyposis of the colon. May lead to 
cancer. Maturity. 

g. See also under skin: Birthmarks—a; 
Coffee-colored spots CNeurofibromatosis); 
Fatty Skin Growth—d; and Scalp Cysts. 

a. Hemophilia. Defective blood-clotting. 
Birth, usually fatal before maturity. 

b. Pseudo-hemophilia. Unrelated to above, 
far less severe. In both sexes. 

c. Nose-bleed—Thrombasthenia. Child- 
hood. More common and serious in females. 
Other effects. Childhood. 

d. Nose-bleed—Telangiectasis. Similar to 
above, but purple areas on skin. Usually 
childhood. Increasing with age. 

Heredity claimed in some cases; but not 

a. Achlorhydric. Common. 

b. Mediterranean. Also bone effects. Fatal. 
a. Red corpuscles sickle-shaped. Mainly 

Negroes. Birth. Occasionally severe ane- 
mia, sometimes fatal. 

b. Oval-shaped. Not harmful. Birth, 



@ D(q) Bh 

@ D>} 



@ S-L 
(Men only) 
@ D(q) 

@ S-LD 



@ D 







Stomach Ulcers 2 




a. In new-born, with anemia. Transfusion 
required, otherwise usually fatal. 

b. Acholuric. Fragile blood cells some- 
times with anemia. Childhood or adult. 
Sometimes fatal. 

Heredity doubtful. 

a. In males: Abnormal opening in ureter. 

b. In both sexes: Extra nipples or breasts. 

a. Sensitivity to certain substances, caus- 
ing asthma, hay fever, rash, etc. Onset 
early. Some authorities doubt heredity. 

b. Angioneurotic oedema. Sudden skin or 
membrane swelling. If in larynx or vital 
organs may cause death. Puberty or later. 

Considered a form of allergy. Heredity in 


Amaurotic Idiocy 

Epilepsy ? 


a Brain degeneration with blindness, 
paralysis, idiocy. Infancy or childhood. 

b. Juvenile and adult forms. Frequently 

c. Eye effect only. Brain normal. Puberty. 
May be fatal. 

Various spontaneous convulsive disorders. 
Cause unknown. Heredity claimed but not 

(Rare. ) Consciousness not lost during seiz- 
ures. Childhood. 




@@ R(q) 

@ D(q) 


@ D 


@ D 

@@ RG 

@ D> 
or S-L 




BRAIN AND NERVE (Continued) 

Idiocy ? 



Description Required 
Congenital idiocy due to some intra-uterine 
effect on embryo. Heredity doubtful. ? 
Extreme or ‘‘Pinhead’’. @@+R-+ ? 

a. Sydenham’s, St. Vitus Dance (see Child- 

hood Rheumatism under INTERNAL). 

b. Huntington’s. Progressive mental de- 
terioration (see text). Usually middle-age. @ D 

c. Wilson’s Disease. With liver cirrhosis, 
muscular rigidity. Youth. @@ R 

a. Schizophrenia. Various forms of adoles- 
cent insanity. (See text.) @e-+R-+? 
b. Manic Depressive. Mental depression, 
sometimes maniacal tendencies. Usually in 

maturity following undue strain. @@+R+? 
Beep puace ties: a. Sub-normal mentality, with no physical 

symptoms. Not always hereditary. @@+R+ 

b. With paralysis on both sides. COne- 

sided generally due to birth injury.) @@R 

c. Phenylpyruvic amentia, with metabolic 

disorder and swellings on nerves. @@ R 

Cerebral Sclerosis 

Mirror Reading 
and Writing 



| Cataract 



Gradual failure of intelligence, vision, 
muscular power. Childhood or youthh @@®R 

Seeing in reverse and upside-down. Some- 
times with stuttering. Birth. @ D(q) 

Opaque lens; common cause of blindness. 
Onset, type, varying in different families. 
Old-age cataracts may not be hereditary. @ D(q) 

a. Adult: Pressure in eye-ball, leading to 
blindness. Usually middle-age. Several 
types. @ D(q) 



Condition Description Required 
EYES (Continued) m.@ SL 
Glaucoma b. Juvenile type (rare). Onset in nee orp 
(Continued) @@ 
c. Infantile type. @®@e@rR 
Retinitis Gradual filling of retina with pigment in( @ D 
Pigmentosa youth, leading to blindness by middle-age. @@ R 
Sometimes with deafness. (or S-L 
Optic Atrophy Withering optic nerve, leading to blindness: 
a. Birth type. Occasionally associated with 
deafness. @ D 
b. Childhood type. @@R? 
c. Adult type CLeber’s disease). Blindness m.@ S-L (q) 
only in center of eye. fi @@ 
d. Associated with ataxia. © D ? 
Small Eyes a. Entire eye undersized, frequently with @ D 
other eye defects. Birth. or S-L 
b. Same, with teeth defects also. @@R 
c. Extreme form, eye completely absent, 
thus blindness fon birth. @@+ R+ ? 
Glioma Retinae Tumor of eye. (See under Rare Cancers—e.) 
Pin-Hole Pupil Iris almost closed; may cause blindness. 
Birth. @ D 
Astigmatism Defective focusing. Birth. Heredity un- 
certain. @D? 
Far-Sightedness Inability to see clearly close-hand. Birth, 
(Extreme) decreasing with age: @ D(q) 
a. Slight. Not pathological. 
b. Extreme, with other eye effects. @@ R 
Near-Sightedness 4. Distant vision blurred. Birth, increasing @@ R 
(Extreme) with age. (or S-L) 
b. Associated with oscillating eyes and @ D 
poor vision. (Nystagmus) or S-L 



EYES (Continued) 

Color Blindness 

Day Blindness 

Night Blindness 


Oscillating Eyes 


Drooping Eyelids 

Defective Cornea 

Description Required 

Confusion of red and green. Birth. Several m.@ S-L 

types. £.@®@ 
Blurred vision in strong light; also com- 
plete color blindness. Birth. @@R 

Vision failing in dim light, otherwise nor- 
mal. Birth. (Most cases due to Vitamin A 

a. With no other eye defect. @ D 

b. With near-sightedness. 99% of cases m.@ S-L 
males. .@@ 

c. With extreme near-sightedness. @@R 
d. Japanese type, like type a. @@ R 

Eyes not focusing together. Childhood, @@ R 
may disappear later. Not always hereditary. or @ D 

Eye tremor, usually weak vision. Birth. m.@ S-L 

a. Common type, occurring by itself. £.@@ 
b. With head-twitching. 

@ D 
Inability to move eye. Birth or later, in- @ D or 
creasing in severity. (May be result of m.@ 
meningitis.) £.@@ 

(Ptosis) Inability to raise lids. Birth. @ D 

a. Cloudiness over lens, impairing vision. 

Onset variable. @ D(q) 

b. Opaque ring over iris, giving “‘specta- 

cled’” appearance. Childhood. @ D 

c. Cone-shaped cornea, causing extreme 

astigmatism. Childhood, progressing.  @@R 
m.@ S-L 

d. Enlarged cornea. Vision usually normal. f, @ @ 
or @ D 



EYES (Continued) 
Displaced Lens 

Defective Iris 

Inner Lid Fold 

Pink Eye Color 

Mirror Reading 

Unmatched Eyes 

Double (Multiple) 

Descriprion Required 
a. Due to atrophied suspensory ligament. 
Sometimes at birth, sometimes adult. @ D(q) 
b. Same, with displaced pupil. ee R ? 
@ D(q) 
a. Segment of iris missing. Birth. Also R 
or S-L 
b. Complete absence of iris. Birth. @D 

Fold across inner-eye angle. (Somewhat 
like Mongolian fold.) @ D(q) 

Only eyes unpigmented, with no other @ S-L 
albino effects. Birth. Confined to males. (Men only) 

(See under BRAIN.) 

Each eye of different color or shade. Infancy. 
Heredity uncertain. 

Double row of lashes on each lid. @D? 



Outer Ear 

About 30% of cases of deafness hereditary: 

a. Deaf-mutism: Deafness at birth, pre- 

venting speech learning. @@R? 

b. Middle-ear deafness (COtosclerosis): 
Noises in ear. More common in women. | 
Maturity. Slowly progressive. @@+ R+? 

c. Inner-ear deafness (Labyrinthine). 
Middle-age. Slowly progressive. @D 
d. Ear-nerve tumor. (See Rare Cancers, 

All of the following present at birth: 
a. Absence of ear, usually one side only. @ D 
b. Cup-shaped ear (ear turned in). @ D(q) 






Outer Ear 
' Deformities 

Ear Fistula 

Word Deafness 


Cleft Palate 
and Harelip 

Defective Enamel 

‘Teeth at Birth 
: Missing Teeth 

— Teeth 

[Auxiliary Teeth 
| Defects 


Description Required 

c. Affixed ear-lobe (in varying degrees). @@ R(q) 
d. Imperfect double ear Cone or both). @D? 

_@. Tube-like passage, occasionally soreness 
or ear discharge. Birth. @ D(q) 
b. Internal opening near tonsil. Birth. @ D(q) 
Hearing normal but inability to interpret 
sound. More common in males. ~ @ D(q) 
Failure of palate to fuse, sometimes with 
teeth defects. Birth. @@-+- R-+- ? 
a. Teeth discolored, usually brown; child- 
hood. @ D 
b. ‘‘Honeycombed”’ teeth. May have fits 
at puberty. @ D 
c. Rare forms, affecting mostly females. @ S-L D 
Incisors present at birth. @ D(q) 
a. Upper lateral incisors absent or small. @ D(q) 
b. All teeth missing except canines. @D? 
Frequently associated with cleft palate. @ D? 
Concomitants of various conditions. Gee 
Brittle Bones, p. 196, Small eyes, b, p. 192.) 
a. “‘Lilliputian’’—adults less than 4 feet, 
but proportions normal. @-+ D+(q) 
b. Achondroplastic—Abnormally stunted 
limbs, head and body average. @+ D+(q) 





SKELETAL (Continued) 

Hand and Foot 

Cranial Opening 
Brittle Bones 

Deformed Spine 

Many different types, single genes produc- 
ing variable effects within same family. 
Most common: Stub-fingers—middle finger 
joints missing; extra fingers and toes; stiff 
fingers—joints fused; webbed fingers or toes; 
split foot or hand. (See illustration, p. 142.) 

Infant ‘‘soft spot’’ in skull persisting to 
maturity, with other bone defects. 

Fragile bones with bad teeth, deafness, 
bluish eye-whites. Birth. 

(Spina bifida.) With various other effects. 


Muscular Atrophy 

Muscle Disorders 

Muscle Cramp 


Shriveling or degeneration of muscles: 

a. Peroneal. Only hands and feet. Child- 

b. Spinal. Infancy. Fatal. 
c. Progressive, associated with cataract, 
sterility, etc. Maturity. 

Various types, affecting special muscles, 
with different onsets and genes. 

Thomsen’s Disease. Muscle stiffness, delay- 
ing movements. Childhood. 

a. Spastic. Rigidity lower limbs, spreading 
upward. Childhood. 

b. Agitans. Tremor, rigidity, slowness. 

c. Soft-muscle. More common in males. 




@ D(q) 
—@ Dq) 
@ D(q) 

@ D(q) 

@ D or 
R or S-L 

@@® RH 

@ D(q) 


or @ D 


@ D(q) 







Leg Swelling 



a ores Spots 


Malignant Freckles 




Description Required 
Wobbly gait, speech defects. Childhood. @ D(q) 
a. Slight involuntary movements, begin- 
ning in childhood. @® D 
Nerve inflammation. Childhood, pro- 
gressing. @D 

(Trophoedema.) Chronic inflammation of 
vasomotor nerves. Birth or later, spreading. @ D(q) 

a. Several types: Red, brown or raised. 
May be start for cancer-growths. Heredity 
uncertain. ? 

b. Slight depression over eyebrows, ex- 
tending to temple. 

c. Numerous pigmented marks of variable 

d. Mongolian Spot—Slate-blue patch over 
base of spine, characterizing Mongoloid 
peopies. Disappears in childhood. 

@ D 


Neurofibromatosis. Dangerous, may lead to 
cancer, blindness, paralysis or internal 
effects. Birth or childhood, increasing. 

@ D(q) 

Dark, freckle-like inflammations. Infancy 
or childhood. (See Rare Cancers, p. 188.) 

Lack of pigmentation in skin and hair. 
a. Complete—Skin and hair ‘‘dead’’ white, 
with also pink eyes. 

b. Partial—White patches on skin. 

c. White forelock or ‘‘blaze’’. Unpigmented 
patch of skin on scalp, growing white 
hair. From birth, both sexes; or puberty, 
‘aales only. 

@ D(q) 



Condition Description Required 

SKIN (Continued) 

Albinism a. Piebald—Stripe on back, sometimes with 
(Continued ) patches of white elsewhere. In vitiligo, 
somewhat similar “‘patch’’ effect, heredity : 

doubtful.) @® D : 

e. Albinoidism—Nearly ‘‘albino’’ skin and 
hair, at birth, some pigment developing 
later. Eyes normal. @ D(q) 

Fatty Skin a. On eyelids (Xanthoma) often with dis- | 
Growth coloration. May also be elsewhere. Puberty. @ D 

b. Lipoidosis—Numerous small growths | 
on face, scalp. Sometimes in larynx, re- | 
quiring operation. Birth. @@R 

Blistering a. Blisters easily raised. Childhood. @ D(q) | 

b. Same, leaving scars. Birth. Sometimes | 
with defective nails, or baldness. @@ R(q) 

c. Sunlight blistering; scarring. Especially | 
males. @@ KR? | 
d. Extreme (Bullosa connata). Often causes i 
bleeding, death in infancy. @@R |, 

) | 

e. Sensitivity to light. Urine frequently 
ted. Birth. Sometimes leads to baldness, 
blindness, later. @@R 

Scaly or a. Common type, with shedding. Infancy. @ D | 
Horny Skin (or S-L R) | 

b. Cracked skin, ears often defective. Birth, 

may disappear later. Sometimes fatal. @@R 
c. ‘‘Elephantskin’’—Extreme form of above. 
Causes premature birth, death. @@RE. 

d. Psoriasis—Mottled scaly patches de- 
creasing with age. If hereditary, only as 
tendency. e 


SKIN (Continued) 



Thick, or 
Shedding Skin 

Biireat-Gland Defects 




Rubber Skin 

! Scalp Cysts 

i| ° 5 
Defective Hair 


Description Required 


a. Skin flaking off over entire body. Birth @@ R 
b. Same, but skin thicker. Several types, 

one with casts of palms and soles shedding. 

Birth or puberty. @ D 

c. Thick or discolored skin on limbs, but 

not shedding. Childhood, more among 

males. ; @ D(q) 

a. Complete inability to sweat—panting 
in hot weather, as by dogs. May also be ™.@ S-L 

hair, teeth, growth defects. Birth. £.@@ 
b. Mild type of above, more among males. @ D(q) 
c. Excessive sweating. @ D 

Absence of connective tissue, making pos- 
sible freak stretching of skin. Childhood. @ D(q) 

Sometimes on face also. Several types. 
Puberty or later. @ D(q) 


a. Pattern—almost exclusively in males. @ D 

Maturity. (See text.) (Men only) 
b. Patch baldness—small bald area on 
scalp; may spread. Birth or puberty. @ D(q) 

c. Congenital—Hair defective or never de-( @@ R 
veloping. Various types, associated with, @ D 
teeth, nail or scalp defects. (or S-L) 
d. Susceptibility to scalp infection (sebor- 

rhea) leading to baldness. In adults, mostly 


a. Infantile down remaining through life. @ D 

_b. Beaded hair. May lead to baldness. 

Infancy. @ D(q) 




HAIR AND NAILS (Continued) 

Defective Hair 
(Continued ) 

Woolly Hair 


White Forelock 

Defective Nails 

c. Excessive long, soft hair on face and 
elsewhere. Other effects. C‘‘Dog-face’’.) 

d. Defective hair with abnormal nails. 
Mostly among French Canadians. Puberty. 

e. Follicle defects, causing hair-loss, 
goose-flesh; frequent growth and mind 
defects. Several types. Birth or childhood. 

Short, tightly-curled (not to be confused 
with Negro hair); may be any color. In- 

Head-hair only. No effect on life-span. 
Begins in adolescence. 

(Or Blaze.) See ATpinieet p- 197.) 

a. Nails absent, partially or wholly. 

b. Thick nails. Skin on palms, soles also 
thick. Birth. 

c. Thick nails, protruding at angle. Birth. 
d. Small, thin, soft nails. Birth. 

e. Bluish-white spots on nails. Birth. 

f. Flat and thin nails. Birth. 




@ D(q) 
@ D 

@ D(q) 
(or S-L) 

@ D 


or @ D 

@ D | 
@ D(q) 


—You are still young, and there is some condition known in your family, 
generally appearing in later life, which you are worried may also appear 
in you. 

—You are planning to marry, and are worried that some condition in either 
you of your prospective mate, or one that appears in your families, may 
be passed on to your children. 

—You are married and already have children, and are worried that some 
condition may crop out in them later. 


—The condition you have in mind is the one listed in our tables. 

—That, where there are various ways in which it can be inherited, you know 
which gene mechanism applies in your case. 

—That, where environment is a factor in its expression, you have ruled out 
the possibility that the condition has not been covered up, or that, even 
if the genes are transmitted, it might not be prevented from developing 
in a child. 

—That, where a condition can also be caused by environment, the one you 
have in mind is of the hereditary type. 

—That you have paid full attention to the question of ‘‘onset’’ (for instance, 
where a condition appears late, you cannot be sure that the genes are, or 
are not, present until the person reaches the required age). 


In All Cases It Is Best to Consult Your Family Doctor! 

| ‘at 


(The most common form of ‘‘black’’ gene inheritance. Because of the vast 
number of persons that are carrying a ‘‘hidden’’ recessive gene for various 
conditions, complete assurance can never be given that any common recessive 
condition may not crop up in some child. But the possibility that it will crop 
up diminishes with the infrequency that it appears in the parents’ families. 
The more prevalent the condition in the general population, however, the 
more likely it is to turn up unexpectedly—especially if the parents are 

closely related.) CHANCES CHILD 

1. IF BOTH PARENTS ARE AFFECTED * Almost certainly 


a. His or her father or mother is affected, or a 
child with the defect has already appeared: Even chance 
b. A brother, sister, or grandparent is affected: Less than even 
c. Some mote remote relative is affected: Possible, but not 

d. No one, near or far, has been known to have 
the condition: Very unlikely 

a. The condition occurs on both sides in one of their 
parents, or in a brother or sister, or has already 

appeared in a child: One-in-four 
b. The condition occurs or has occurred in more 
distant relatives of the families of both: Extremely unlikely, | 

but yet possible | 
c. The condition is wholly unknown in the family 
of either: Virtually nil 

*NOTE FOR ALL ABOVE: Certain recessive conditions (childhood rheumatism, diabetes, 
etc.) may be strongly influenced in their expression by environment. The fact, then, that parents | 
or their families are affected does not positively indicate whether, or to what extent, their child | 
might develop the condition if the environment is favorable. Or the fact that the parents them- | 
selves do not show the condition, when it appears in others in their families, is not conclusive | 
oe that they are free of the genes involved. All this applies to the ‘‘qualified’’ recessives | 

io — 



@@ R@$ 

The chances of inheriting the gemes are exactly the same as shown in 
Table I, but the chances of the condition actually appearing in the child may 
be altered by the circumstances stated in the preceding footnote. In general, 
however, the odds are somewhat lower than in simple recessives for each 
type of mating. 


The situations are about the same as in Table I, but with the probability 
lessened in most cases. 

males @ 
—— S-L 
females @@ 
(Where the ‘‘black’’ gene is carried in the ‘*X’’ chromosome, and therefore 
acts as a dominant in the case of males, as a recessive in the case of females. 
Examples: Color blindness, hemophilia, nystagmus, enlarged cornea.) 

1. IF BOTH PARENTS ARE AFFECTED: Almost certainly in 
all their children 
FREE OF IT: Certainforeveryson, 
, but no daughter 

a. Her father, mother or a sister has or had the 

condition: Even chance in any 
b. One of her brothers is affected: One-in-four for any 
c. One of her more remote relatives is affected: Extremely unlikely, 
but yet possible 
ad. No known case in her family: Virtually nil 

' OCCURS IN THE MOTHER’S FAMILY (in the | daughter, but for 
Same situations as noted above): sons same odds as 

in 3-4.b.c.d. above 


@ D 

(For all conditions which can be produced in either sex by one gene acting 
singly, as in acholuric jaundice, drooping eyelids, various hand defects, etc.) 


ts ed IF BOTH PARENTS ARE AFFECTED: Very probable 


a. If the condition is always known to show itself Nil 
when the gene is present: 

b. *If the gene action is sometimes known to be Some likelihood, 
suppressed by environment: but not great 

* NOTE: In every case where the gene action is irregular, or influenced by environment, we 
have the situation following of 

® D@ 

In all ‘‘qualified’’ dominant conditions, such as mirror-reading, extreme 
far-sightedness, adult glaucoma, etc., the predictions are modified downward © 
from those shown in preceding table, the forecasts depending upon the 
degree to which the gene expresses itself or is suppressed by environment. 

@+ D+ 
(Rare, as in dwarfism and rare defective enamels.) Relative probabilities 
are about as shown in Table V, but greatly reduced in most cases. : 
@ S-LD 

(As in thrombasthenia type nose-bleed.) If mother has condition, ratios for 
all offspring, male and female, will be the same as in Table V-1, 2. Where — 
father has condition, every daughter, and only the daughters, will get it. | 

204 | 


Tuere used to be a jolly old judge in Milwaukee who specialized 
in doubtful paternity .cases, or what the state so bluntly calls 
“bastardy actions.” 

By “specialized” we mean that he showed a special aptitude 
for trying these cases, and accordingly most of them were as- 
signed to him. For one thing, he seemed fully aware of the fact 
that such actions permitted no strict adherence to legal procedure. 
The evidence offered—aside from the highly contradictory state- 
ments of the plaintiff and defendant—was hearsay and much col- 
ored by perjury. Recognizing that it was largely a matter of de- 
ciding who was lying and who wasn’t, the judge viewed the pro- 
» ceedings as a family squabble in which he had to play the rdle 
of an impartial father. 

One case in particular (of the many before him which we covered 
as a “cub” reporter) stands out in our memory. The young woman 
plaintiff had given rather convincing testimony, and the young 
man whom she named as the father of her child had taken the 
stand. Under a barrage of cross-examination he admitted having 
“sat up” with the young woman on the night in question, but 
insisted that his deportment had been blameless. No amount of 
forceful questioning could shake him. At this point the judge inter. 

“Tell me,” the judge asked, “was there by any chance a moon 
shining that night?” 

The young man thought a moment and innocently replied, 
“Why, yes, sir. I think there was.” 

The judge nodded with mock gravity, then sat back in his big 
chair and gazed at the ceiling, seemingly in deep thought. “Ah!” 
he said at last, and bent forward as if to take the entire court- 



room into his confidence. “It’s all very simple. Some man had 
to be the father of the child. Well, there was a moon shining that 
night. All we have to decide is whether it was this young fel- 
low or the man in the moon.” 

Now, any lawyer could tell you that such a remark coming 
from a judge was improper. But, as we said before, the entire 
procedure in doubtful paternity cases was (and usually still is) 
highly questionable. The “paternity” laws have little concern with 
the individual. They do not seek to compensate the mother nor 
to punish the errant father. Their primary purpose is to insure the 
state against the possibility of the child becoming a public charge. 

The justice or injustice of the law, however, is not an issue 
here. What we wish to point out is that the whole matter of 
deciding parentage in disputed cases has been befogged with un- 
certainty, and that fortunately a fairer, and more scientific, ap- 
proach is in sight. 

The first constructive step has already been taken through the 
“blood” tests which are just beginning to be used in doubtful 
paternity cases. Here the law formally recognizes, and makes prac- 
tical application, for the first time, of our knowledge of the gene 
mechanism of heredity. ! 

What are the “blood” tests? They are based on the discovery that 
the blood of all human beings can be classified into four hereditary 
groups—which provides one of the clearest examples we have of 
Mendelian gene action. Only three “key” blood genes are involved 
in producing the four groups. These genes may be designated by 
the letters 4, B and O. To describe their effects as simply and un- 
technically as possible, we may say that each of them produces dif- 
ferent substances in the blood. 

Gene A produces, principally, a substance known as “Antigen 
A.” | 

Gene B produces, principally, “Antigen B.” 

Gene O produces neither antigen, but only certain milder sub- 

Every one of us inherits two of these genes—a single one from 
each parent. We may therefore receive two genes of the same 
kind—AA, BB, or OO—or a mixed pair, AB, AO or BO. It is 


Was inherited through a pair of any of these genes—two of the same kind or a mixed 
pair—one gene coming from each parent: | 

(Symbols) @ 

Each gene pice ee different blood substances. Genes "A" and "B" are of equal strength, and 

when brou 
or '"B," does not function. Accordingly: 


t together, work independently. But Gene ''O" is recessive; and if coupled with "A" 

©+® @+® 



Containing Containing Containing 
"B eat and "Bt only nc 
substance substances substance 


—Containing both "A" and 
B "B" substances, most easily 
/ \ receives the others 




—Being "weakest,"’ is least able 
to receive any of the others 

—But, because it also has some- 
thing foreign to each, ‘clashes 
most if infused, producing 

—But can be transfused into 
the others with the least clot- 


when the genes differ that their relative effects become apparent. 
How they work to produce the blood types is illustrated on p. 207. 

As each of the bloods has its own peculiarities, they are incom- 
patible with one another in greater or less degree. All this is of 
tremendous importance in connection with blood transfusions— 
much more important than in the infrequent cases of determining 
parentage. Until the discovery of the blood groups was made the 
medical world could not understand why in some cases the blood 
of even the closest relatives—mother and child perhaps—would 
not mix, and why transfusions were sometimes fatal. Now, of 
course, the mystery has been solved. We can see that it is just 
as possible for a mother to have one kind of blood and her child 
another kind, as it is for her to have brown eyes and her child 
blue eyes. 

To return to the subject of determining parentage, the blooa- 
group tests now enable us to make certain deductions. Previously 
in this book (in the “feature” forecasts and the “black” gene tables) 
we asked, “Given parents with certain characteristics, what can 
_ we predict about their child?” 

Now our question is reversed: 

Given a specific baby whose parentage (usually paternity) is in 
doubt, what can we determine about its parents? 

Here is where the blood tests may provide definite clues. An 
actual case (in 1936) in the New York City courts will serve as the 
best illustration. 

A young woman sued a prominent society man for a huge sum, 
claiming that on his promise to marry her she had borne him a 
son. Under authorization of the “blood test” statute, passed a short 
time before, the court assigned the blood specialist, Dr. Rufus E. 
Stetson, to make tests of the mother, the child and the alleged 
father. And this is what Dr. Stetson reported: 

The mother’s blood was of the O type. The child’s was of the 4 
type. This meant that as the mother could have given the child 
only an O gene, the 4d gene must have come from the father. 
The father would therefore have had to be of either 4 or AB type 
blood. But what Dr. Stetson found was that the accused man had O 
type blood—conclusive proof that he could not have been the father 

of that child. So without further ado the judge dismissed the ac- 


But suppose these first tests show that a man’s blood is of one 
of the required types?—which would be more than likely. 
At this point an accused man has still another “out.” In addition 
to the 4, B and O genes, it has been discovered that there are two 
minor supplementary blood genes, the M and WN genes. Every one 
carries two of these genes (one received from each parent); either 
two of the same kind, MM or NN, or a mixed pair, MN, in addi- 
tion to the main ones. The M and N genes also produce substances 
in the blood which, while having no effect in transfusions (nor, 
so far as we yet know, any other important effect), nevertheless 
reveal themselves in tests. And it is by these additional tests that 
sometimes conclusive proof may be obtained. 

Another actual happening (reported in the Journal of Immunol- 
ogy) will again serve as an illustration: 

This was a most unusual case. A married woman came into 
court to prove that her child was tllegitimate—that not her hus- 
band, but a lover, was its father. And it was her husband whoa 
was contesting the claim. True enough, the first tests, on the 
basis of the A, B, AB and O groupings, did show that he could 
have been the father. But unfortunately for him, and perhaps for 
the child, when the M and NV tests were made it was found that he 
could not have been the father. 

All the various situations in which blood tests may offer proof 
of non-paternity are presented in the tables on page 210. Note, 
however, that they are of value only when negative. Dr. Stetson 
informs us that of quite a number of such tests that he has made 
since the one mentioned (these others, however, being in cases 
that were never brought to court) only about 20 to 25 percent 
provided disproof of parentage. Where the results are positive, it 
does not mean that the accused man 7s the father. It only implies 
that he could be, as could be any of tens of millions of other 
men with the same type of blood. 

Another important failing of the blood tests is that they cannot 
be made until the blood of the child in question is “set” and its 


(Assuming that you’re a man and that its paternity is in doubt) 

O No Matter Which AB 
AB No Matter Which O 
A O ot B O or B 
B OorA OorA 
M No Matter What N 
N No Matter What M 




blood type revealed, which may not be until a year or more 
after birth. 

When the blood tests fail, genetics now makes possible many 
other tests, gradually being recognized by the courts. An imme- 
diate source of evidence is provided through distinctive surface 
abnormalities which are known to be clearly inherited. This was 
first recognized by a Norwegian court in the case of an illegitimate 
child who had the hand abnormality known as brachyphalangy, 
in which the middle finger joints are missing. The mother, nor- 
mal, accused a certain paperhanger in her community of being the 
child’s father. He was brought into court. “Let’s see your hands!” 
the judge ordered. And when the unfortunate man held up his 
stub-fingers (a condition in which he was unique in the entire 
community) the court promptly adjudged him the father. 

Any other inherited surface abnormality in a child caused by 
a dominant gene—which, if not revealed in the mother must have 
come from the father—can provide similar evidence. The “Mon- 
golian” spot in a child, where the mother is without question 
“pure” White might be evidence against an Oriental or Indian 
accused of being its father. Many conditions listed in the “feature” 
-or “black” gene chapters could also provide evidence, but most 
of these conditions occur so rarely that they are of little general 
value. Nevertheless, even through the common genes in plentiful 
circulation, we have at our disposal many valuable clues. 

By considering combinations of various characteristics instead of 
merely single ones, a new field is opened for establishing parentage. 
A child is blue-eyed and blond. The mother is blue-eyed and 
blond. The reputed father is blue-eyed and blond. That proves 
nothing. But we find also that the child has curly hair—its mother 
has straight—but the reputed father also has curly hair. The child 
is freckled—its mother isn’t—dut the reputed father is freckled. The 
child has a Hapsburg lip—its mother hasn’t—but the reputed 
father has this peculiarity. By means of various points of genetic 
similarity, or dissimilarity, in combination, evidence could be built 
up for or against parentage. But you might say, “This is merely 
circumstantial evidence!” True enough, but if you think about 
it, there has never been and can never be anything but circum- 


Child *‘A’’, about six months old, has drooping eyelids (ptosis). Its mother 
is free of the condition, but Man ‘‘X”’ alleged to be the father, is found to 
have the condition. This in itself is insufficient proof of paternity, for 
drooping eyelids occur quite frequently in the population. But a comparison 
of other traits in the child, the mother and the man reveal the following: 

Black Hair Blond Hair — Dark Hair 
Blue Eyes Blue Eyes Blue Eyes 
Curly Hair Straight Hair Curly Hair 
Affixed Ear-lobes Free Ear-lobes Affixed Ear-lobes 

Because in each trait there is evidence that he could have contributed to 
the child the required gene, Man “*X”' is in all probability the father. 


Child ‘‘B’’, about a year old. Two men, “‘Y’’ and “*Z’’ are equally under 
suspicion of being the father. 

A A B O 
Blood MN M N NI 
Eyes Green, Black, Brawn, Blue, 
Slant Slant Straight Slant 

Eyelashes Very long Short - Short Very long 
Hair Blond Black Black Red 

With regard to blood type, the premise is that the child must be carrying 
a hidden O gene, otherwise both men should have been ruled out. On this 
assumption, then, the odds would be greater that Man ‘*Z’’ contributed 
this gene to the child. (in the matter of the ‘‘N’’ gene both men are equal.) 

In all the other traits, however, the odds are also higher that Man “‘Z”’ 
contributed the required genes. Accordingly, Man ‘‘Z’’ is in all probability 
the father of the child. 



stantial evidence in questions regarding the paternity of a child. 

We have confined ourselves largely to cases of doubtful paternity, 
because these are the ones usually at issue. Rarely now, with in- 
fants so scrupulously identified at birth, are “changelings” possible. 
Nevertheless, all the tests here mentioned can be used with regard 
to the mother, or even with regard to both parents, should the 
need arise. 

Genetic knowledge, at its present stage, may or may not offer 
definite proof of parentage in many cases, but it can certainly help 
to throw light on almost any case. With the knowledge increasing 
rapidly, more and more clues will be made available. In these 
days when experts can tell that a given hair came from a given 
head, that a certain rung in a ladder came from such and such 
a tree in such a forest, that a certain bullet was fired from a speci- 
fied revolver, that a brush-stroke on a painting was made by the 
hand of a certain old master dead four hundred years, it would 
be strange if we should continue unable to determine whether a 
child, with a host of characteristics differentiating it from other 
children, did or did not stem from such and such a parent. 

We have every reason to anticipate the discovery before many 
years of other hereditary factors in the blood and perhaps in 
the glandular secretions, of many more feature and structural genes, 
of the establishing of hereditary factors in fingerprints, palm and 
foot patterns, and of the identification of so many additional clues 
that doubtful paternity cases will become among the easiest to 




Wirn this chapter we enter a new phase in our book. Up to 
this point we have been considering human beings as mechanisms. 
Now we begin thinking of you, and all the rest of us, as social 

As mechanisms we have seen that every one of us is created 
differently from any other individual, that a great deal of how 
each of us looks and functions physically is determined by heredity. 
Now we ask whether the differences in social behavior among in- 
dividuals may not also be greatly influenced by heredity. 

Are some individuals predestined to success, and others to failure, 
by their znherent natures? What keeps large masses of people sub- 
merged at the same low social level, and enables others to emerge 
from the depths and reach the heights? Why, in the very same 
family, is one person stupid, one brilliant; one son a law-abiding 
citizen, the other a criminal; one member kindly and happily 
adjusted, the other mean and anti-social? Are these differences due 
mainly or in part to different combinations of genes, as are the 
different features of members in the same family? Or are they 
due entirely to environmental influences? 

Genetics can already throw much light on these questions. But 
as you will soon see, answers regarding the social traits of human 
beings can be given with no such surety as were those regarding 
our surface characteristics and organic make-up. For we may 
say at once that we are now venturing into uncertain territory. 
Previously we confined ourselves to the presentation almost exclu- 
sively of scientific facts. But from this point on, as we begin to 
analyze the rdle of heredity in such variable and intangible human 

characteristics as mentality, personality, talent, temperament, crimi- 


nality, sexual behavior, etc., we will find our facts becoming more 
and more diluted with theory. 

Our genetic evidence, like a stream of clear, fresh water flowing 
into an arm of the sea, now begins to intermingle with theories 
of psychology, anthropology, sociology, economics and even politics. 
And it will be increasingly difficult to sift out the facts from 
the theories—theories which, even in the case of leading authori- 
ties, are often tempered by unconscious prejudices or emotional re- 
actions. : ! | 

The social phases of human heredity are viewed through varied 
lenses, sometimes rose-tinted, sometimes dark or almost opaque, 
so that the outlook ranges from bright to dismal; again, the lenses 
may be concave or convex, offering to some a long view, to others 
a short view. The very directions which researches into human 
genetics may take, and the findings arrived at, may differ in the 
degree that the investigators themselves differ in personality, back- 
ground and emotional make-up. The descendants of Mayflower 
stock and the offspring of recent immigrants, the hidebound reac- 
tionary and the confirmed Marxist, the Russian, English, German 
and American biologists as groups often react differently toward the 
same evidence. 

Thus, you also will find yourself taking sides in the ensuing chap- 
ters. If you are socially and financially secure, and come of a worthy | 
family, your reactions will be different from those of the man at 
the bottom or of insignificant stock. You may say of this, “That 
sounds unreasonable,” or of that, “I don’t believe it.” And there 
may be no denying you the right to say it, for often the problems 
we are coming to are so involved, the play of heredity and en- 
vironment so tangled, that no absolute and definitive answers can 
yet be given. ; 

Further, you may find yourself chafing, as we did in our own 
researches, at the constant procession of “ifs” and “buts” which 
dot the ensuing discussions. But remember, genetics is a new 
science, and its application to human behavior is most recent of 
all. The experts are feeling their way cautiously into the new fields. 
Few wish to commit themselves definitely on controversial points, 
for nothing is so damaging to a scientist’s reputation as the espousal 


of a theory that is subsequently upset. Accordingly, many state- 
ments and findings are presented with more qualifications than 
they deserve, giving the impression of greater doubt than really 

So we frankly advise you that from now on in our book, with 
regard to conclusions, you will be more and more “on your 


Here are two orphaned infants, available for adoption at a 
placement bureau: They look the same and are “guaranteed” to 
be equally sound and fit. You are eager to adopt one, and as 
there is ae no choice, you are about to toss a coin to decide. 

Then the matron 
tells you that Baby “A” 
is the offspring of a 
charwoman and an il- 
literate day-laborer. 

Baby “B” is the off- 
spring of a young 
woman writer and a 
young physician. 

Would you still feel 

Basy “A” there was no choice? Basy “B” 
Or would you pick Baby “B” on the chance that it had inherited a 
higher degree of mentality? 

Around this question, or others closely related, centers one of — 
the greatest controversies in the study of human heredity. There 
are authorities who say that no evidence exists which would 
justify a choice in favor of Baby “B.” There are many others who 
disagree with them. 

What is the basis for the arguments pro and con? Let us start 
at the beginning. 

We have seen that various eee: and pies: of abnormal intelli- 

¢$e,0¢ 8904 

ee 820 

wrench into any complex machine would ‘tell us about its normal 



In lower animals, true enough, we know that a normal mouse 
inherits a certain type of brain, a cat another type, a dog still an- 
other, etc. Also, that within each species itself there seem to be 
degrees of brain activity. In dogs, breeds vary in alertness; in mice, 
geneticists have bred strains, one dull, one bright. 

If degrees of “normal” intelligence are inherited among other 
animals, why not among human beings? There’s the rub! For 
should we prove that gradations of human intelligence we see 
about us in the workaday and social world are conditioned to 
any great extent by heredity, then we'd be faced with the possi- 
bility that dulness, mediocrity and superiority are inherent in in- 
dividuals, and that failure and success may be to a large extent 

No wonder that beneath the placid surface of scientific research 
on this subject a struggle is going on between the “hereditarians” 
-and the “environmentalists.” The “hereditarians” are out to prove 
that certain individuals come to the top, like cream in a milk bottle, 
because of inherent superiority, thus tending to form classes at 
various intellectual levels. The “environmentalists” challenge this 
analogy. They are set on proving that if we shake the bottle and 
equalize the environment, the levels of mentality in which classes 
of people now appear to be stratified would disappear. 

How are we to settle this? 

Our great difficulty in analyzing intelligence is that it can be 
measured only by arbitrary standards, such as those set up by 
the current intelligence tests. We saw in the chapter on “Sick 
Minds” how the tests are used to determine degrees of mental 
defectiveness: the idiot scoring an IQ of under 25; the imbecile, 
25-50; the moron, 50-70. Those who score from 70 to 80 are 
placed on the borderline. Above that, now, we come to non-defective 
mentality, with the ratings as shown in the accompanying table. 

BO QO rats iiss ikraiy tiene ap hae acy rares tan toe dull 

QOrT TO te aa mins ok ag aes eta hae normal 

TE Or E 2O pC slog babe a oe) <) 4 tate Us wee cae superior 
T2O“TAO Ven Guarani ss uC an oer ara very superior 
TA0' OF OVED Wi sc eae Veet genius * 

1 Used in a technical sense, and not implying that individuals with this score are 


As between a person with an IQ of go and a person with an 
IQ of 130 there can be little doubt that the tests do indicate a 
marked difference in mental capacity. But with regard to the lesser 
gradations, those closer to the normal range, there is disagreement 
as to the significance of IQ scores. The same person may score 108 
one day when he isn’t feeling well, and 113 the next day; or he 
may be given one score by one examiner and a lower or higher 
score by a different examiner. It has also been claimed that the 
tests are not equally fair to all, that they are not consistent at 
the different ages and that they measure “classroom” intelligence 
rather than general intelligence. 

Despite the foregoing and other criticisms, the standard intelli- 
gence tests are considered sufficiently reliable so that they are in 
wide use throughout our educational system. If you live in New 
York City (as one of many places) and you have a child, that 
child will be placed in a class with backward pupils, or average 
pupils, or superior pupils, on the basis of its IQ. If you are 
seeking admission to some highly selective university, medical col- 
lege, dental college, law school, etc., your IQ might decide your 
acceptance or rejection. And in various corporations and research 
institutions your IQ may be a factor in winning a job. 

For all practical purposes, then, the intelligence tests must be 
seriously considered. But how significant they are when used to 
study the inheritance of intelligence is another matter. For only 
if the IQ scores are proved to reveal a fixed capacity—born in the 
individual and but little affected by environment—can they have 
meaning to the geneticist. In other words, inasmuch as all the studies 
made to date of the inheritance of intelligence are based on IQ 
scores, the interpretation of these studies must depend upon the 
importance attached to the intelligence tests and to their actual or 
implied weaknesses. 

Here is where the authorities fall out. You will not be surprised 
to learn, therefore, that the findings of various studies made on 
the same questions may differ markedly. All we can do is to 
summarize what we consider the most valid studies, theories and 

opinions on all sides, leaving you to form your own. conclusions. 

Let us now follow the procedure of the investigators. First they 


ask themselves questions. Then they set out to find the answers. 
We'll start with this: 

1. Do people of different “classes’ show different degrees of 

As measured by intelligence tests, yes. Extensive studies reveal 
that the higher up the social and economic scale one goes, the 
higher is the average IQ. That is to say, unskilled laborers and 
farmhands as a group have lower IQ’s than skilled laborers and 
farmers; above these rank skilled factory workers, “white-collar” 
workers and small business men; above these, semi-professional 
people, bigger business men and managers, and at the top of the 
IQ structure are the professional men. Obviously, however, there 
is much overlapping among the groups, some unskilled workers 
having higher IQ’s than those in levels above, and some profes- 
sional men having lower IQ’s than those in levels below. 

Bearing in mind that we are speaking always in general terms 
and allowing for individual exceptions, it would seem that lower 
intelligence goes with lower work. But does this mean that the 
unskilled laborer has a very low IQ because conditions have 
thwarted his mental development, or does it mean that he is an 
unskilled laborer because he has a low IQ? Which came first, the 
low condition or the low IQ? 

We ask another question: 

2. Are the intelligence levels of children related to those of thet» 

Yes. Children of a group of parents of high intelligence almost 
uniformly—on the average—are reported as having greater mental 
capacity than children of parents of low intelligence. 

Studies in Boston (Stuart M. Stokes) and in New York (Lita 
Hollingworth) indicate that rarely, if ever, where both parents are 
of inferior mentality, does a superior child result. 

Comparing offspring of parents at various social and economic 
levels, it is found that children of unskilled laborers have the lowest 
IQ’s, children of professional men the highest, with those of the 
groups in between being similarly correlated (as shown in our 
accompanying diagram). 

We must note, as with their fathers, that the differences be- 


tween adjacent groups of children are not radically great, the entire 
range in IQ’s, from lowest to highest, averaging within twenty 

A criticism regarding the above data is that the comparison 

of child 






(Based on studies by Terman and Merrill, reported in 
"Measuring Intelligence’) 

made is not of the intelligence of children and fathers, but of the 
IQ’s of children compared with the assumed intelligence of their 
fathers as reflected by occupational rank. If, as is claimed, the 
intelligence tests are weighted in favor of “book learning,” chil- 
dren from homes of poorly educated workers would be retarded 


in comparison with those from better educated circles. An addi- 
tional criticism is that the different occupational groups do not 
have the same ethnic make-up, the unskilled and “lower” groups 
having a larger proportion of foreign-born and Negroes, and that 
children from such parentage are therefore at a further disad- 
vantage because the intelligence tests are presumably designed for 
native Whites. 

So again we might draw two conclusions: (a) that the children 
of parents in the lower intellectual levels have inherited their lower 
mentality; or (b) that the lower mentality has been thrust upon 
them by inferior environment. 

Which is right? We go on: 

3. When children are taken away from their parents in infancy 
and reared elsewhere, do their IQ’s still show the influence of their 

According to some studies, yes; to behers: no. 

Tests have been made in various places of large numbers of 
illegitimate children placed in institutions or adopted soon after 
birth. The fathers of these children were of all classes. In the in- 
stitutions the environment for all children was the same. Yet it 
was reported that the IQ’s of the children bore almost the same 
relation to the levels of their fathers (whom most had never seen) 
as IQ’s of children on the outside. 

Studies of children adopted and. reared in private homes con- 
flict in their findings. Some report that the IQ’s of adopted chil- 
dren accorded very closely with the levels of their fathers, and 
were but slightly influenced by the levels of their foster parents. 

But from the University of Iowa where studies are being made 
of about 150 waifs, of generally inferior parentage, adopted into 
superior homes, comes the report that the IQ’s of these children 
follow not the low levels of their true parents but the higher in- 
telligence levels of their foster parents. 

(Discrepancies in the foregoing and other studies of adopted 
or orphaned children have been attributed to various factors, among 
them: that investigators have taken different directions and studied 
differing groups of children under not fairly comparable circum- 
stances; that “superior” couples tend to select, or to be offered for 


adoption, the brightest infants; that the paternity of illegitimate 
children may be in doubt; that orphaned and illegitimate children 
receive a worse physical start than others; and that even the 
most conscientious foster parents might not rear an adopted child 
in the same way they would their own. It is also claimed that 
where an average difference of 6 or 7 points is reported, this is 
not statistically conclusive.) 

We'll leave this question open and go on: 

4. When children are transferred from bad environments to bet- 
ter homes or institutions, do their IQ’s improve? 

The evidence on this point is also variable. In one study (Rogers, 
Durling and McBride, 1928) a group of American girls aged four 
to thirteen, taken from bad environments, were tested before and 
after being placed in improved environments. Their IQ’s were not 
found to have been changed. In another study, made in Glasgow, 
Scotland (Dawson, 1934), children taken from slums and sent 
to a better environment also showed no improvement in IQ. 

Contrariwise, a study made at the Hebrew Orphan Asylum in 
New York (Donah B. Lithauer and Otto Klineberg, 1933) showed 
that children taken from disrupted homes increased their IQ’s 
by an average of about 6 points when being placed in a more 
stable environment. (Here, however, the change was largely one 
in psychological atmosphere.) 

Several other studies on the effects of change in environment also 
report some increase in IQ, but none averaging more than about 7 

5. How far can training -nold intelligence? 

Again, studies in orphanages revealed that children reared from 
early age under almost uniform conditions showed the same degrees 
of differences in IQ as children on the outside reared under diver- 
gent conditions. This would suggest that there were inherent mental 
differences in the children to begin with. 

At the State Teachers College at Jersey City, 140 primary school 
children were studied before and after they were given the very best 
training possible. It was found that there was no significant im- 
provement in their IQ’s, regardless of the length of training. (Edna 
E. Lamson, 1938.) 


On the other hand, Dr. Wellman of the University of Iowa re- 
ports findings that IQ’s of children can be raised materially if they 
are subjected in early life to stimulating schooling. Commenting on 
the criticism that intelligence tests made of very young children 
(the point of departure for her study) are unreliable, she has written 
to us: “I believe this is an erroneous conclusion which has arisen 
from the fact that changes in IQ occur. I do not believe we should 
discredit the measuring instrument because changes are registered, 
any more than we should discard a thermometer because tempera- 
tures vary.” 

Continuing, we may ask: 

6. Does heredity unalterably fix the intelligence of an individual? 

We turn once more to our human laboratory subjects, twins. If 
heredity alone determined one’s intelligence, then identical twins, 
with exactly the same genes, should always have exactly the same 
IQ’s. But they don’t. IQ’s of identical twins do often differ, although 
on an average they are much more altke than those of fraternal 
twins, and decidedly more alike than those of ordinary brothers and 
sisters in the same family. Most interesting are the comparisons re- 
ported (by Professor H. H. Newman and others) of identical twins 
who were separated in early life and reared in different environ- 
ments. In several instances their IQ’s were found to differ by as 
much as 18 points, but on an average the IQ’s of identical twins 
even when reared apart are found to be as alike as, or slightly more 
alike than, those of fraternal twins reared together. Moreover, while 
identical twins become neither more nor less alike in intelligence 
as they grow older, fraternal twins become increasingly different in 
IQ as time passes. 

Fascinating to watch will be the mental progress of the Dionne 
quintuplets. While their IQ’s have not yet been announced, the little 
girls as a group are reported to be somewhat retarded (which was 
to be expected because of their underdevelopment at birth). But of 
greatest importance to us is the fact that there are differences among 
them in mental achievement and behavior responses which seem to 
be correlated with the physical differences we have previously dis- 
cussed. Marie, physically the weakest, ranks the lowest in mental 
achievement and responses: Emilie, her “other half,” is next lowest; 




(a) Reared together: 

(a) Reared together: 

(b) Reared apart: 

F\.} 17.72 

(Based on tables from "Heredity and Environment,” by Gladys C. Schwesinger } 


Yvonne ranks the highest and Cecile and Annette alternate for sec- 
ond place. 

How great the IQ differences among the quintuplets are we do 
not yet know, but if as time goes on they become marked, we will 
have a striking illustration of how even slight inequalities in en- 
vironment may modify hereditary intellectual capacities. The other 
twin studies, however, have already proved that heredity does not 
unalterably fix intelligence, but that it does play a great pais in de- 
termining the general degree of intelligence. 

Suggested by the differences among the Dionnes is our next 

7. Does a poor body produce a poor mind? 

Or, conversely, does a healthy body make a healthy mind? 

To the surprise of most of us, there is little proof on this point. 

In the population at large, there is a general tendency for more 
intelligent children to have fewer constitutional physical defects and 
less disease than children of lower intelligence. But it may be not 
the poor bodies that produce the poor minds, but the fact that the 
less intelligent children are usually found to come from less favor- 
able environments, which would tend to suppress both their bodily 
and mental development at the same time. 

To clarify this further, we may ask another question: 

8. Does malnutrition during early life permanently affect the in- 
telligence of children? 

One of the classic studies was made in Germany to see whether 
the extreme undernourishment of the children during the World 
War had lowered their IQ’s. It was reported that even where chil- 
dren had been literally starved for two or three years, their basic 
intelligence rarely appeared to be affected. 

Malnutrition, by the way, is not a synonym for starvation, and is 
not something confined to the poor. It refers to any defective nutri- 
tion or failure of the individual to assimilate food properly, and oc- 
curs among the very wealthiest children as well as the poorest. Deal- 
ing, then, with malnutrition rather than starvation, various investi- 
gators (Hunt, Dowe and others) have concluded that “under- 
nourished children, whatever their other handicaps, are no whit in- 
ferior mentally to well-nourished children of the same race and 

THE* BATTLE OF THE. 100s” 227 

social status.” Also, it was found that when undernourished children 
are fed properly, their physical condition may improve greatly, their 
intelligence very little. 

9. Does disease retard mental development? 

If we eliminate, obviously, mental diseases, the answer appears to 
be sometimes Yes, sometimes No. 

Consider adenoids or bad tonsils. Popular belief is that when dull- 
witted Johnny Jones, who has a bad case of adenoids, gets them re- 
moved, he will brighten up immediately. But studies show that 
after children have had adenoid or tonsil operations, there is no in- 
crease in their basic intelligence. 

In hookworm, directly correlated with poverty among children of 
the South, the more serious the condition, the lower the intelli- 
gence. But again the possibility is that the disease is severest where 
the conditions would ordinarily be most unfavorable for mental 

Syphilis, ominous as this disease is, has not yet been shown to have 
any effect of itself on intellectual capacity, unless, or until, the dis- 
ease causes some severe breakdown or mental derangement. 

No disease which does not attack the central nervous system is 
known to diminish intelligence. A few diseases such as spinal men- 
ingitis, epilepsy, hardening of the arteries (arteriosclerosis) and 
brain fever (epidemic encephalitis) may lower the sufferer’s IQ, but 
not invariably. 

Many physical defects do, however, adversely affect intelligence. 
Deafness might retard a child’s mental development by two or three 
years, and defects of the eye (which retard the capacity to learn) 
are also known to affect intelligence. Accidents may directly affect 
the brain; and as we've already seen, certain harmful intra-uterine 
influences (alcoholism or drug addiction of the mother, injuries at- 
tending birth, etc.) may even produce idiocy in a child. But, on the 
other hand, history is starred with individuals who rose to the 
greatest heights despite every sort of physical and even psychotic 
handicap, sometimes dating from birth, sometimes suffered later. 
(This will be enlarged upon in our later discussion of “genius.”) 

Among normal, healthy individuals we find it quite impossible 



to establish any correlation between basic physical characteristics 
and basic mentality. For instance: 

10. Does head size have any bearing on mentality? 

Not that we can discover. Disregarding imbeciles and “pinhead” 
idiots, exhaustive studies fail to prove that loftier foreheads mean 
higher IQ’s (as the late Arthur Brisbane, who himself had a high- 
domed forehead, so frequently maintained). Eskimos have bigger 
heads than Whites, and the skulls of some prehistoric men had a 
bigger cranial capacity than the record head of modern times, that 
of Ivan Turgenev, the Russian novelist (2,030 cubic centimeters). 
Studies of brain size among men of different occupations, ranging 
from scientists to unskilled laborers, have likewise failed to reveal 
that there is any special correlation between one’s brain dimensions 
and one’s achievements. 

In women, their smaller heads, as compared with those of men, 
have been cited as the reason for their “lower mentality.” But that 
statement is open to question, Which brings us to this: 

11. Are women mentally inferior to men? 

No!—at least, according to IQ scores. 

Undoubtedly women think in different ways than do men about 
many problems. This may or may not be due largely, if not entirely, 
to differences in the way the sexes are reared and conditioned. But 
regarding “quantitative,” or measurable differences in the mentality 
of the two sexes, Professor Lewis M. Terman, one of the highest 
authorities in the field, has this to say: 

“Intelligence tests . . . have demonstrated for all time the falsity 
of the once widely prevalent belief that women as a class are ap- 
preciably or at all inferior to men in the major aspects of intellect. 
The essential equality of the sexes has further been shown by psy- 
-chometric methods to obtain also in various special fields, such as 
musical ability, artistic ability, mathematical ability and even me- 
chanical ability. The enfranchisement of women and their invasion 
of political, commercial and other fields of action formerly reserved 
to men have accorded increasingly convincing evidence that sex 
differences in practical abilities are also either nonexistent or far less 
in magnitude than they have commonly been thought to be.” 

From the standpoint of intellectual achievement, it need hardly 


be disputed that women still rank below men. This might be ex- 
plained by their social limitations, or perhaps by physical limitations. 
It has been suggested that because women mature earlier (correlated 
with the earlier onset of puberty) they become mentally “set” sooner. 
This would seem to be borne out in literature, the theater and a 
number of professions where women achieve fame at an earlier age 
than men, but do not as a rule progress as far. As we write this, 
Dr. Richard J. Block of New York reports that he has found chemi- 
cal differences between male and female brains. But this we know: 
There cannot be any difference in the “mental” genes that men 
and women carry, with the reservation that if there are any “mental” 
genes in the X chromosomes, women receive more of them than 
do men. 

The difficulty in measuring comparative intelligence of any two 
dissimilar masses of people is brought out by our next question: 

12. Do different races and nationalities have different degrees of 

This, too, cannot be answered with scientific certainty. We may 
be able to measure comparative intelligence of individuals within 
the same country and within the same race, but the question arises 
as to how fairly we can apply IQ tests, devised by investigators of 
one country for their own kind, to those of an entirely different 
country and civilization. To remedy this, psychologists are work- 
ing on new tests of a non-verbal nature which may be univer- 
sally applicable. 

At present we can only go by what has been learned about chil- 
dren brought up and educated under relatively the same condi- 
tions. In California, then, Chinese and Japanese children were 
found to have just as high IQ’s as American and European chil- 
dren. The children of Jewish immigrants were found to score higher 
than those of other immigrant stocks. Negro children, tested in 
various parts of the United States, average much lower in their 
IQ’s than do Whites. But let us not forget that the conditions and 
Opportunities among the Negroes are greatly inferior to those of 
the others-tested. Negro children in the North, with better oppor- 
tunities, score higher IQ’s than do those in the South—in New 
York City the average among them being about 7 points higher. 


That this is not due to selective immigration has been brought out 
in a study by Professor Klineberg. 

By now you have seen that while the “intelligence” studies have 
thrown doubt on many points previously taken for granted, few, if 
any of our main questions, have been answered decisively. So you 
may ask: 

13. Why cannot science tell us something more definite about 
the inheritance of intelligence? 

First, because we haven’t determined what we mean by “intel- 
ligence.” The intelligence tests, as we have already pointed out, 
were devised by educators chiefly for their own domain, the realm 
of the classroom. But academic intelligence and practical intelli- 
gence as judged in the larger world outside are not necessarily the 
same.’ Often the tasks and problems of everyday life demand 
mental attributes that the standard intelligence tests do not re- 
veal—character, will-power, intuition, humor, understanding, abil- 
ity to get along with people, and so on. 

Before we can make accurate studies of the inheritance of intel- 
ligence, we must be clear as to what we are studying. Further, we 
must have a way of measuring inherent mental capacity, stripped 
of environmental influences and by standards which can be fairly 
and uniformly applied to people of all ages, types, races, back- 
grounds, occupations and degrees of education. In these respects 
the existing tests fall short. However, even if they were scientifically 
acceptable, the present intelligence tests have not been in existence 
long enough so that we could yet have any comparative records 
of IQ’s of parents and children at the same ages and successive 
stages through to maturity. Possibly when the present generation of 
school children grows up and produces families we may be able 
to make some fairly accurate genetic studies without waiting for 
more acceptable tests. 

Meanwhile most geneticists, while agreeing that differences in 
intellectual capacity among humans may be inherited, shy away 
from further commitments. Several have toyed with theories of 

1 Mendel, father of genetics, twice failed in an important examination in botany 

at the University of Vienna, largely because he had been self-taught and his academic 
knowledge was deficient. 

THE*BATTGE OF THE “lo $8” 231 

the genes involved in producing intelligence, and have even made 
guesses as to the types and numbers of these genes. But certainly 
no geneticist would yet venture to predict what ratios and degrees 
of intelligence to expect in the children of parents with such and 
such IQ scores. 

Which brings us back to the beginning of this chapter, and our 
final question: , 

14. What, then, is one to decide regarding a choice on the basis 
of intelligence between Baby “A,” the offspring of a charwoman 
and a day-laborer, and Baby “B,” the offspring of a young woman 
writer and a physician? 

As we cannot find the answer in scientific fact, we might look 
for guidance to the opinions of leading authorities (geneticists, an- 
thropologists, psychiatrists and psychologists) who have given de- 
tailed attention to all the evidence we have summarized. To the 
best of our knowledge, these opinions would take two main and 
divergent directions: 

1. There are those who would say that no choice is justified, 

“We have no proof of the extent to which intellectual attain- 
ments are due to heredity or to environment. Even with the use 
of the present ‘intelligence’ tests, faulty as they are, it is clear that 
what we call ‘intelligence’ is greatly influenced by education and 
conditioning. We have no right, therefore, to compare by the same 
tests people whose environments are radically different and to con- 
sider that their relative scores have any bearing on their relative 
inherited mental capacities. 

“Assuming that there are genes which produce degrees of in- 
telligence, in view of the complexity of the mental. processes there 
would obviously have to be a great many of such genes; which 
makes it difficult to conceive how, with the constant intermingling 
that has taken place among people of all levels, ‘superior’ and ‘in- 
ferior’ intelligence genes could have become noticeably segregated 
in different proportions within our different occupational groups, 
especially in so short a time. 

“Therefore we have no basis for assuming that parents in the 
unskilled laboring group carry, or will transmit to their offspring, 


genes for intelligence inferior to those of parents in the professional 

“Accordingly, we are justified in concluding with regard to 
the intelligence of the two hypothetical infants that there should 
be no choice between Baby ‘A,’ born of a charwoman and a day- 
laborer, and Baby ‘B, born of an authoress and a physician.” 

2. On the other hand, we know of authorities who would answer: 

“The view that, lacking clear scientific evidence of how in- 
telligence is inherited, we are not justified in making deductions 
regarding it, is shortsighted and unwarranted. All the general find- 
ings of genetics point to the inheritance of degrees of intellectual 
capacity in the same way that other characteristics and capacities 
are inherited. Therefore, 

“Without knowing what the ‘intelligence’ genes are, we may 
still rightfully assume that there are some which make for greater 
intellectual capacity and others for lesser capacity. 

“Allowing for all possible powers of environment to depress or 
to raise intelligence, we know that many bright individuals born 
into lower social levels rise to higher levels, and many dull in- 
dividuals born into upper levels sink to lower levels. With this 
process having gone on throughout civilization we may reason that 
in two large social groups differing radically in intellectual attain- 
ment, there would be more of the ‘superior’ genes in the superior 

“The average IQ difference of 20 points between offspring of 
the unskilled laboring classes and those of the professional classes 
cannot be dismissed as without significance unless it is ascribed 
entirely to differences in environment. There is no proof that this 
is so. Knowing that in the same environment, even in members 
of the same family, great differences in intelligence exist, the burden 
of proving that environment alone is responsible for all these dif- 
ferences rests on those who make the assertion. 

“At the very best, in the situation cited, one can only say that 
Baby ‘A’ might be expected to be as inheren‘ly intelligent as Baby 
‘B.’ No one would venture to say, and not a single study has in- 
dicated, that children of unskilled laborers as a group would be 
expected to have a better intellectual heritage than those of pro- 


fessional people. On the other hand, many studies do indicate that 
there is a possibility, if not a probability, that the average child of 
professional people will turn out to be more intelligent than the 
average child of those in the lowest occupational groups. 

“The question thus becomes one of odds. Baby ‘A’ might in- 
deed turn out to be more intelligent than Baby ‘B.’ But the odds 
are surely greater—although we cannot say how much greater— 
that Baby ‘B,’ offspring of the authoress and the physician, would 
have inherited the better mental equipment. 

“Therefore, everything else being equal, on the basis of intel- 
ligence there should be a choice in favor of Baby ‘B.’” 

So here are two clearly conflicting interpretations of the same 
set of facts. How are you, the layman, to decide? For remember, 
the two theoretical babies are before you, and you can take only 
one of them. | 

You might beg the question by saying, “We are dealing, after 
all, not with objects but with human beings, helpless infants. So 
long as there is uncertainty, the humane thing to do, and the 
democratic thing to do, would be not to condemn Baby ‘A’ as in- 
ferior purely on theoretical grounds, but to give it the benefit of 
the doubt and consider it as equal.” There is merit in this view- 
point, but our problem here is not a humanitarian one but essen- 
tially a scientific one. You are called on to decide, solely on the 
basis of the evidence, whether the offspring of the one set of parents 
would be likely to turn out more intelligent than the offspring of 
the other set of parents. 

If you conclude that the facts presented are not conclusive enough 
to warrant a choice, and that you should leave the selection entirely 
to a toss of the coin, we can assure you that there are high-ranking 
authorities who will approve your stand. 

But if you prefer to be guided by the weight of opinion, at least 
in a numerical sense, we may say this: 

It is our belief that the majority of qualified experts of all kinds 
would subscribe to the second viewpoint previously stated, and 
would unequivocably advise you to keep your coin in your pocket 
and to choose Baby “B,” child of the authoress .nd the physician. 

(An Original Genetic Study) 

A urtte boy, hugging a violin, walks out onto the stage at New 
York’s Carnegie Hall. There is a flutter of applause from the thou- 
sands of persons filling the auditorium. The little boy tucks his 
violin under his chin and begins to play. The audience, skeptical, 
watches, listens. A tiny hand sweeps the bow back and forth, tiny 
fingers fly over the strings, streams of melody, now shrill, now 
full-throated, cascade forth. Already, in those first minutes, many 
mature musicians out front know that in all their years of study 
and work they have not been able to achieve such mastery. Soon 
they, and the others, forget that this is a little boy who is playing. 
As if drawn by invisible bonds, they are carried out of the hall, 
into the night, higher and higher, so high they can scarcely breathe. 
Then suddenly there is a burst of notes like a rocket’s shower of 
golden stars ... the music stops ... a sensation of dream-falling 

. and they are all back again in Carnegie Hall, incredulously 
storming with their bravos a little boy—a very little boy who in a 
few hours may be crying because he isn’t allowed to stay up and 
play with his toy soldiers. 

The scene has been enacted a number of times in each genera- 
tion, but not too many times, for little boys like this do not appear 
often. It may have been elsewhere than Carnegie Hall—in Paris, 
London, Vienna—possibly in your own town. And sometimes it was 
not a violin that the child played, but a piano. So Chopin, Mozart, 
Mendelssohn, Liszt, Schumann, César Franck, and of living mu- 
sicians, Heifetz, Hofmann, Kreisler, Rosenthal and Menuhin, among 
many others, revealed their genius to the world as children. 

In no other field of human achievement do the young so strik- 



ingly scale the heights. Not even in the other arts—painting, sculp- 
ture, literature—is there any such early ripening of genius which 
enables a child to compete on equal terms with adults. How can 
we explain this? Is it due to a divine spark, an inexplicable gift? 
Is it the practical result of unusual environment and training? Or 
is it merely another something with a physical basis, produced by 
genes and inherited as are other unusual characteristics? 

Scientists began wondering about this long before modern genetics 
offered any clear approach to the subject. Many studies of musical 
genius were made in the past. The fact that this form of genius 
ran in certain families was apparent in the case of the Bachs, 
Mozarts and Webers, and of the families of Beethoven, Brahms, 
Schubert and Liszt. Most notable of these were the Bachs, in which 
genius was traced in an unbroken line through five generations of 
males. Johann Sebastian Bach himself sired five noted musicians. 
Johann’s father and his father’s brother were identical twins who 
were reported to be markedly similar not only in the way they 
‘played, but in their speech, temperaments and physical character- 
istics. (Even their deaths came close together.) 

But these striking examples were not in themselves evidences of 
heredity, as we know now. Where musical achievement did run in 
families one could easily argue that it was due to environment, 

recept and training—just as “banking” achievement ran in the 
Rothschild family—for in previous times, much more than today, 
sons tended to follow the calling of their fathers. But—and there 
is that ever-present “but”—even in former times, where a father was 
outstanding in some field that called for unusual ability not every 
son was chosen to follow in his footsteps. Only those sons who 
showed the required talent or aptitude were trained to carry on. 
So we come back to the question, “Where does talent come from?” 

With the question still so much in doubt, we felt that perhaps 
we could learn something if, instead of again stirring up the ashes 
of bygone personages, we inquired into the careers of great musi- 
cians of our own time. And thus was inspired a detailed study made 
especially for this book, in which, we are happy to say, we received 
the fullest cooperation of the artists themselves and of leading fig- 
ures in the musical world. 


Our study was carried on among three groups of artists, in two 
fields of music, instrumental and vocal (the reason for distinguish- 
ing between the two fields soon to be apparent): 

1. Thirty-six outstanding instrumental musicians of the world— 
that is, those universally conceded to be leading figures on our 
present-day concert platform. 

2. Thirty-six principals of the Metropolitan Opera Company 
(season 1937-38) concededly representing a large proportion of our 
best-known and most talented singers at this writing. 

3. Fifty students of the Juilliard Graduate School of Music, 
comprising a highly selected group of younger musicians and 
singers, many of whom are already active in the professional 

In all three groups direct questions were asked and answered 
by each artist personally (with two exceptions: one, of Arturo Tos- 
canini, where, in his absence, the data were supplied by some one 
very close to him ofhcially; and in the case of Yehudi Menuhin, 
where the data came from his father). The result is a rather impos- 
ing array of facts which we will present in detail because, aside 
from what they may prove, they afford you a splendid opportunity 
for seeing how genetic studies are made, evidence analyzed and 
conclusions derived. In fact, we hope that you will study the data 
carefully and try to form your own conclusions before you look for 

Tue Virtuost InstrruMENTALists: We come first to the noted fig- 
ures in the instrumental field. You will see that our list includes 
a large majority of those likely to be known to you. (Space did not 
permit us to include every one, and here and there a few outstand- 
ing individuals whom we wished to include could not be reached, 
or for some personal reasons did not.wish to be represented in these 
studies.) Whatever may be said about the relative worth of these 
artists, we feel sure that the talent of each one is beyond ques- 
tion. They have risen from the ranks of tens of thousands of mu- 
sicians, from many countries and many backgrounds. Week after 
weck and year after year they have faced the most critical of audi- 


ences, and have continued to be acclaimed. So we may well say 
that as a scientist first tests his materials before he begins his study, 
here is a group of persons as thoroughly tested for the same char- 
acteristic, basic musical talent, as any that could be assembled. 

What now can we learn from these artists about the source of 
their talents? From our first table (see ff. pages) certain facts are 
immediately apparent: 

Taare I: The Musicians Themselves. The average age at which 
talent was expressed was under five. It might be said, “Ha! You’d 
expect a musician to say that his talent was expressed early!” But 
this is quite clearly answered by the next fact. 

The professional débuts were made at the average of thir- 
teen. By “professional” début is meant, in the sense that it is used 
by most of the musicians, not the mere first public appearance, or 
even the first paid performance, but the formal launching of their 
careers. Note the four debuts after twenty-one—Brailowsky, Giese- 
king, Rodzinski and Smeterlin. Brailowsky, for instance, had already 
given minor concerts before his professional début, and the others 
had also performed publicly. Inquiry revealed that zn all four cases 
their musical careers were delayed by service in the World War 
and by these other factors: Smeterlin’s father had first “sent him 
off to be a Latin and Greek scholar”; Rodzinski (although his im- 
pulse toward music was not expressed until late) had started out 
with the study of law; and Gieseking, definitely of “prodigy” caliber, 
was retarded in making his début by the fact that his father, a 
physician, did not believe that careers should be begun in childhood. 

Except for these four the professional débuts of the others were 
made in their ’teens, with many of them achieving fame at an age 
when other children were still in grade school. 

To put it another way, our facts indicate quite definitely that 
great achievement tn this field 1s correlated with an extremely early 
start. But what is the reason for that early start—something from 
outside of the individual or something inside of him? 

Wherever such a question occurs, the first thing the geneticist 
does is to explore thoroughly the family backgrounds of the indi- 

viduals, If there is any presumption that an unusual condition has 

“snr 03 osuodsax poxseur Inq ‘yu2[¥3 Surdeyd ou sayrusis ,.ON,, plOM 943 JO ****** Jopun ©, caddy, 4 

(Avyoq Je Ay) saratjenb, AS1poad ($6, Castuetg) 
eee fe (OY SOX” CSAy Sz fay8nvaun ouvid q ONIMASAID ULLIVAN 
HR {Caddy} souvivodde (16,) (STUTTOTA ) 
x Jpurry = g Et). 2 So Ree ee or onqnd asanq § - NVWTIS VHOSIW 
pSticlousst)- a, ‘puoy JOSUIS (-puoo se) (79,) (astueid-"puo7) 
x» USN b CH) 489K SPX 61 ouvid Surdefg 9 HOSOUNVC UALIVA 
»% UPUPIL) ane ‘TYD)  s8urms urjora (61,) CsturforA ) 
x JPUPIQD = xt = 6) SPR SAK v Supe], t OdvV.Lsnd VIIND 
uyjora Aeyd (16 ,) (asturfor, ) 
x JpueIgn = (4) ~89X sax HE OrurSog == HE HoOsnd ATOGV 
CAepq eM) —sayaez wos (96,) (@asturtg) = 
Zee «tT () 8®9A ON tt ss suosspy oud og QS RMSMOTIVU UAAGNVXATV & 
qsI) outid (42,) (so1onpu07) 
ae Z CE) sox ON Ot Aejd oa Buy4I, AMZNVdOd UNALUV 
(asturpora) ISNUT 03 (£2,) Qastuetg) 
wee Poe (P= SOK SOK Or — esuodsosyensnuy) = € wanvd GIOUVH 
xUISNO) xx - oppso pue (66 |) (ast][29-"puoD) 
x2PUN WH = Z ) *89X ON TI uyora urdetg Y ITIOWNUVA NHOI 
pea) =(‘ON 
Ur MIN 4410 TPL, I0T) sqiwy  4sqiow aay mor ip 
"S4SES GP “S04 
76) UJOd Jeo 
JO fice Gea sorte yeas) cee Sons QHssdadxa ‘eonena ur 2n3tq) 


(Sh +d 209 ‘uotsyyngqvs sof 3477 004 paatas9y, ) 

e@oe0ec8e@ I 

e@eee Z 

ey 7 

ae ¢ 

Gee al 
SI9TN va | 
ar al 

spun Z 

xx4UPW x eee 
xxx d IQ 7 


sox  o9wos 

eee eee 


sox ON 
Sox ON 
ON Sox 

‘puoy Josuts 











ysasoqUT psounouolg 34 € 

O88 ISIT[IvS Iv 

SJsnuE UT parysifoq 

$1J20U09 18 SUT[OTA 
03 asuodsay 

§ durosoe ‘Sursuts 
‘yoaid aanjosqy 

 UI[OIA Surce Tq, , 

oueid ur 3sosa,Uy 

yoard sanjosqe 
JO UOTSsassog 

ouvid 3oF otsnur 



JqulIear Te pray “AV 

geo [eoIsnur o3ndy 
zy ye Sutsoduros 

pidnd s sayavy 
sv uljorA Surhe[g 



(96,) (asturig) 

(90,) G@stuTpoTA ) 

(vo,) @sturjor, ) 

(41, (asturfor,A) 

(vZ,) Qsturtg) 

(SZ,) (-duros-astutpor A) 

($6) (‘puod-istuvig) 
IgUun.Li Asol 

(2Z,) Gstuetg) 

(06) (asturtg) 

(10,) (astutfor, ) 

(7%g,) (sasoduros-1stuetg) 


(£6) (-dutoo-astutpora-"puo7) 



SUISNO’) . I (7) ON ON 
Sretumt) alse: seu 6 (9) ON ON 
¥* Caddy) 
nent S . . PON- —-ON 
eeeceo jo cveceee (£) ON AIDA, 
»% JPUrIOH 1 (S$) SOX soz 
suIsno’) SLe' 6 6 ene (0) er at tie! ele: SOX 
¥ (9) SPR Sax 
el -@)~ -sax..-0N 
peas CON 
ury 409NT 42410 “je L 10) 40G1O 7 4dG10IN 

(Ariqe Tensnun 
JO [euoTssajoid sa}0Uap JvIS) 


Sutketd oueid 

OI $,JoIsIs polepnMy 9 
€ 1e youd 
sinjosqy ‘osensury] 
9 .2U0S,, SUIS) I 

youd aanjosqe 
OI ode sIyi Iv pry b 

(‘puos -3dQ) (ae, voys ‘Apnis 
gt me Aq ist Avlaq) OT 

ouvid Surkeyd 
61 uvSog v 

24S av sosodurod 

Li ‘ouvid Surdeig v 
(ast[[99 4st) «6 av seurour9 sunod 
Cr [eco] ur surdvepg AIDA, 
s JoyIey uO 
£ SpIO092I ue mouy AI 
apy mop aay 
TVNOIS Gussdud xy 


moe CASTIET = 

(68 ,) Gasturig) 

(79) (astuvtg) 

(¥6,) (so19npuo09) 

(¢Z,) (-duros-3stuvtg) 


(16) (-duros-astuetg) 

(£0,) Gst]]29) 

(66,) (xox9pu09) 

(usjoqg Je3 
:sasoyquored ur an81J) 




€1 6 Li “stk Wer ‘sik Vey 
sury ivou =| S$ ‘piuyey, | — 
joy10 ur «=| Orr =yeioy | Fv ‘y auI0S iz "7, awos :3nqaq : passoidxy 
quo{eI "SISES St ‘pauyey, | OF ‘pauyey, | [euotssajorg|  udyey, SNVIDISAW 9£ 
Ssuis0day Lp “SOLG 549G40 J S49q 40 sy ‘SAVY | o8y ‘SAV SSTV.LOL 
urjora Zurkeyd (68,) CSTUTTOTA ) 
Bee (9) *89X ON gt mE é LSITVAWIZ Wawdd 
oer (86,) Cpuos-ast{]29) 
age Le (a. eSeA 9 SON II assy sry Sony, E NIGZLSNATIVA GaaITV 
(‘puos se 61) (x23 939) (L9 =) (to19Npuo’)) : 
#208IN ye3 ONS ON br eApats naeoT = 8 ININVOSO.L OUNLUV J 
x AUP] urjora Avyd (<6 ,) (ASTUTTOT A ) 
»% JPUrIDH I (1) SAX = Apsregq €1 03 Surdx ‘BurSuig 44 E LLADIZS HaASOL 

(Aepaq Jem) 3% 38 ‘yos0 yITM (76) (astuvig) 

ees | (z) GNe e ON ert: 2 o1souco pakeig = Z NITYa.LAWS NVf 
sojeos SurysinSun “SOW (Sz,) Csturtgq) 
eke re (Z%) 4S°9X ON vy  ——-stp fypard yo asuag 6 ISSNAZONATIS HLAY 
; Zurdeyd s oy30Iq (v0, (astuerg) 
otee S (4) “saxe aN 9 OVI 03 pas, = T NIsuas ATOGAU 
Zuosm pofeyd opoun (66, ) GSTUTTOIA ) 
coos Sa ON ON VI voymsunnuy py € 

ee ee eee ees ee 



a hereditary basis, there should be a much higher than average in- 
cidence of the condition among the parents, brothers and sisters 
and near relatives of the individual. So we turn to: 

The Instrumentalists’ Families: First, were the parents musically 

Of the mothers, half are reported as having musical talent or 
“musicality” of some kind. (At this point we may explain that 
the question of evaluating talent in relatives was left to the artists 
themselves; but both the data, and “check-ups” here and there with 
others, have convinced us that fair and honest appraisals were made 
—so far as such appraisals can be made without scientific tests. 
Above all, the reputations of the artists, and the fact that their re- 
ports are here presented for all to see, should give assurance that 
their judgments are authoritative.) 

We may note also that sometimes where a parent or other rela- 
tive was not credited with performing talent, the musicians took 
pains to report “appreciation” or “response.” This refers to an “ear” 
for music, which often may indicate latent talent that for lack of 
training or for other reasons may not have had a chance to express 

Of the fathers, three-fourths were musical, at least nine being 
professional musicians and several (including the fathers of Dam- 
rosch, Goossens and Barbirolli) being outstanding. 

Considering mothers and fathers together, in only five instances 
were both parents reported as unqualifiedly not talented—Iturbi, 
Schnabel, Seidel, Smeterlin and Toscanini. (The interesting case 
of Arturo Toscanini will be dealt with later.) 

What of the brothers and sisters? 

We find talent in Aalf of the total number of brothers and sisters. 
Several (including Leon Goossens, Amparo Iturbi and Hephzibah 
Menuhin) are concert artists of note. In only five instances where 
there is more than one brother or sister do we find no others with 

As for the other near relatives, talent was reported in one-third 
of the cases. As a whole, Barbirolli, Busch, Bustabo, Damrosch, 
Goossens, Elman, Szigeti and Rachmaninoff may be said to have 


stemmed ‘from distinctly musical lineages. To complete our aiudy 
of familial talent we have still another question: 

What of the children of musicians? 

With six exceptions at this writing, all the musicians are married, 
and of these thirty—all men—only eighteen have children, with a 
total of thirty-seven among them. 

Are these children usually talented? We have compiled the an- 
swers of the fathers themselves, in Tasie II (page 244). 

Taste II: Offspring. Here we have included “talent” data about 
the wives of the musicians also, because obviously they must be 
considered equally in regard to the children’s heredity. With only 
three stated exceptions, all of them are also musical, many being 
professional musicians. (Mrs. Lhevinne is a distinguished concert 
pianist in her own right; Mrs. Zimbalist was Alma Gluck, a for- 
mer opera star; and Mmes. Prokofieff and Schnabel are also singers.) 
In half the cases, also, there were musicians in the wife’s background. 

On the whole, we can consider that from both sides the prospects 
were exceptionally favorable for the expression of talent in the 
children, either through environment or heredity. Has the prom- 
ise been fulfilled? 

Three-fourths of the children are cited as talented, or if still very 
young, as showing musical aptitude. That the parents are not too 
prejudiced is indicated by the several instances where zo talent is 
reported, and in the several instances where one child is cited as 
talented, the others not. 

A truly musical family is that of the Schnabels, all three of the 
children having shown marked talent, one son, Karl Ulrich 
Schnabel, now rivaling his father as a pianist. Also worth watch- 
ing in the future is the Serkin child, whose grandfather is Adolf 

Looking back over three, and in some instances four, generations 
of our musicians, there is unquestionable proof that musical talent 
“runs” in these strains. But, we hasten to add, this in itself ts no 
evidence that the talents were inherited, for everything might still 
be accredited to environment. However, had we not found the 
high familial incidence, then the case for heredity would have 





Musical? Family? 
ADOLF BUSCH Yes ey ane 
| Grandf.* 
(Pianist) » 
(Singer) parents) 
ARTUR RUBINSTEIN Yes f.; cond s* 
| (Singer) (many) 
(A. Busch) 
CA. Gluck) 

TOTALS—Wives: Talented, 14; Not, 3; ?, 1. 
Children: Of 37, 27 Talented. 





P Rp A 




Both, to a degree 

All 4 
1 yes,* 3 no 



Daughter, yes; 
son, no 

Both talented but 
not trained 

(44, 334) Both 

All. Karl Ulrich, pianist; 
other son actor, singer; 
daughter, composer. 

Yes (2%) - 

Yes, but chiefly 
critical ability 

1 daughter, criti- 
cal ability only 



fallen down at once." So, still keeping our minds open, let us con- 
tinue to the second part of our study—that of the Metropolitan 
Opera singers. 

THe Metropotitan Srncers. Every one has heard, with regard to 
this or that vocally gifted person, “She inherited her voice from 
her mother” (or he from his father, etc.). To throw light on 
‘whether this is so or not, we present now the genetic backgrounds 
of exactly the same number of vocal artists as we did of instru- 
mental artists. 

The vocal study was confined to one brilliant group—the prin- 
cipals of the Metropolitan Opera Company. Originally we had 
planned to select singers from the field at large, but it quickly be- 
came evident that vocal artists cannot be evaluated with any such 
clarity as can instrumentalists, and that, had we sought to exercise 
our own judgment, we would have been beset with numerous 

The simplest procedure was to make a “unit” study of an out- 
standing group, obviously the Metropolitan ensemble, whose singers 
include a majority of the best-known vocal artists now appearing 
before the public. These, too, like the instrumentalists, have come 
from many countries, and have risen to the top through the ranks 
of tens of thousands of other singers. 

We are well aware that there are many distinguished singers 
outside of the present Metropolitan cast; and if we think in terms 
of basic ability rather than public recognition, there are probably 

1 As we were going to press we received from her native Brazil these data sent by 
Guiomar Novaes: 

Talent expressed: At age of less than four, playing by ear. 

Professional début: Age of 8. 

Mother: Pianist and her first teacher. 

Father: Not musical, but a poet. 

Brothers and sisters: Seventeen. None talented, but some appreciative. 

Other near kin: None with any exceptional talent. 

Note the remarkable fact that Mme. Novaes has, or had, seventeen brothers and 
sisters, none of whom showed musical talent. She points out, however, that some 
are “appreciative.” We regret that time did not permit us to ascertain how many 
were meant by “some,” and to what extent circumstances might have suggested that 
there was latent talent in these which had been suppressed. 

Mme. Novaes reports further that she is married to a musical man of a musical 
family, and that the happy result is two children who are both musical. 


‘une ‘apug) 4 8§86(S) | SOX 
L T (1) Sox 
‘sntuy Auvpy (£) %SOXK 
SIOSUIS Be ey Cpu05) 
‘sna Aurpy ss € (£) S29 X 
[@I9AIg (7) sox 
eeeee (0) ON 
Po) eltia ies 
* JPUETS) (0) sox 
ee eee (zt) sox 
ro) elisa I (7) ON 
eeeeve (7) ON 
ury “S1585 4oqt0.q 
APINT 42410 bp “SOAT 
(qu2]e], [eoIsnyy JO) 














1u9vy, sy 

C-adog ‘wviq) 
NOsdaf NaTaH 
C:adog ‘ureiq) 
(-adog ‘ureiq) 
_ (ouvsdos) 
C-adog ‘weiq) 
C:adog *s4'J) 
awd VOTH 
~ (oursdog) 
C-adog ‘wviq) 



ass 1 
cao 1 

Pe z 
etic 2 
wpuryy ¢ 
‘ € 
quny A 




#59 A 






















‘ow £*tA Gt ‘our p rh g 









Cadog *[o9 *s4'T) 

‘Cadog ‘weiq) 

C:adog ‘ureiq) 

C:3dog *Jo9) 

C:3adog ‘wreiq) 

Cadog "109 *14'7) 

C:adog *14"T) 

C:adog *34°T) 

(-adog *314J) 


eececoe ee (v1) O N 
eoecoe ee (7) 3 
oEeetS) Ee AA) ON 
RS xt @) SOX 
BS sdpuetsy <= -(C) ON 
: KEX 
eoecee € (9) IWIOS 
eevee (Vv) ON 
"JpurIo Z (2) SUIOS 
eoeoe 1 (£) %SIK 
Ee sox 
ury “S4548 ays] 
SPIN 42410 Lp “Soa 
(QuzTe I, [eIIsny JO) 


4G 10WW 


















tue y, ay 

_ Gousy) 
(‘jO1g osseg) 


(sous |, *I4'T) 
Vunddaia Nvi 


(soudy, “I4'T) 
(sous, *44T) 
Caousy, ‘s4'T) 

(10u2T, ‘Wwesq) 



oat et 

91 €p (fOr) sax IZ SOR EZ ‘OWL IAQT ‘OUIG'I4G 11? “of aSvaaap 
Se ee ee en se ee ae Oe ee ee eee 
OL CZs CK) Sok ZI SOX PL ‘ourZ'rAST ‘ourpssg Saj0Uua J 
ec el 
9 Stes. COS): as SIIAG Sok 6 ‘ours JALT ‘ows 'JAII sav —aSo4oay 
(ou011Ieg ) 
(auoiseg *IA'T) ¢ 
aie ne a sox SOX 61 8 SVWOHLL ‘SVHO NHOL 
(ossvg ) 
eng xt © é ON 61 é VZNId OIZd 
sunof | (4OUDT, ITOIDE) 

(sous, ‘A4"T) 
ant ss Teo) sox sox gi L INILUVW ONIN 


very many talented artists whom we have excluded. But by and 
large, we believe that our list is a representative selection of vocal 
artists whose backgrounds can be intelligently compared, for the 

urpose of this study, with the data regarding our instrumentalists. 

Taste III: The Singers Themselves. Perhaps the first fact that 
will strike you is the preponderance of women in the “vocal” table 
compared with the mere four in the instrumental tables. Unbal- 
anced as this may seem, the comparative ratios actually are about 
those which prevail in the field at large. That is to say, women 
predominate among the better-known singers, whereas in the in- 
strumental field there are exceedingly few women in the front 

Second, we see that the age at which vocal talent appeared (ac- 
cording to the artists’ own statements) averaged about eight and 
a half years in women, and eleven and a half in men. We may 
compare this with the appearance of talent at the’ average age of 
less than five among the instrumental artists. _ 

Note also that we did not ask for “age at professional début” in 
the vocal field, but “when training was begun.” The principal rea- 
son was that “professional début” in the singing field is much more 
variable in its meaning than in the instrumental field. (Another 
reason: Many vocal artists are reluctant to give any figures which 
would be a clue to their ages.) To be on the safe side, therefore, 
we confined ourselves to the age at which training began, which 
in some cases was but a short time before the professional début, 
in others quite a number of years earlier. Nevertheless, by indi- 
rect comparison a significant fact stands out: 

The average age when training began in the vocal field was 
directly correlated with the period terminating puberty. (Fifteen 
and a half for the female artists, seventeen and a half for the males.) 

Here is a striking environmental factor in the vocal field that 
does not occur in the instrumental field, namely, the purely physical 
requirement that the voice must first weather the rigors of puberty 
and be “set” before it can be trained. Thus, averaging male and 
female singers, vocal training did not begin until the age of sixteen 
and a half—more than three years after the average instrumentalist 
had already been launched on his or her career. 


The Singers’ Families: Turning to the family histories of our 
vocalists, we find, however, that they tell very much the same story 
as do those of the instrumentalists. A larger number of mothers and 
a slightly smaller number of fathers are reported as talented, but 
the average for both parents together is about the same. Also, while 
there are not quite as many brothers and sisters with talent, there 
are still almost half.* In other near kin (grandparents, uncles, aunts, 
cousins, etc.) the talent count is about the same for the singers as 
for the instrumentalists. 

Again we have clear evidence that where there is a high degree 
of musicality in individuals—this time expressing itself in singing— 
there is an unusually high incidence of talent in their families. 

Now to our third group. 

Tue Juriiarp Group. With the aid of Ernest Hutcheson, the 
noted pianist previously listed who is president of the Juilliard 
School of Music, the third part of our study was conducted among 
graduate students of this distinguished institution. 

“Students” may convey an erroneous impression of this group, for 
all of them have won their spurs as unusually talented individuals, 
and many are professional musicians. Ranging in age from the re- 
quired minimum of sixteen up to the maximum of thirty, they 
were chosen from a great many applicants. How keen is the com- 
petition for admission into the Juilliard Graduate School may be 
gathered from the fact that there is no tuition and that private in- 
struction by leading concert artists and music teachers is provided 
without cost. 

All those included in this group, therefore, may be accepted as 
among the most talented of the new generation of musicians in 
this country. We say “new generation” because, although some may 
be as old as some of the celebrities in our virtuoso groups, their 
average age puts them almost a generation behind; and profes- 

1The large quota of fourteen non-talented brothers and sisters reported by 
Martinelli may have tended to reduce the percentage somewhat, but not greatly, as 
we shall explain later: Another factor might have been that we queried the singers 
primarily regarding vocal talent, and although we suggested also that other musical 
talent be named, it is possible that some may have reported an unqualified “No” 
for relatives who could not sing but were otherwise musical. 


sionally, also, they may on the whole still be considered “juniors” 
compared with the others. We therefore have the interesting oppor- 
tunity of comparing musically gifted groups of different genera- 
tions, chronologically and professionally. 

Data from fifty Juilliard students were secured, our returns being 
taken just as they came in, with the number limited only by the 
fact that our impending publication date made it necessary to halt. 
Although these constitute somewhat less than one-third of the gradu- 
ate student body, in the opinion of the school authorities they rep- 
resent a fair and accurate sampling. | 

Both instrumentalists and vocalists are included in this group, but 
the instrumentalists are in the great majority. As it happens (quite 
by coincidence) there are thirty-six of them, exactly the same num- 
ber as in each of the other two major groups. An easy numerical 
comparison is therefore made possible between the Juilliard in- 
strumentalists and the “senior” instrumental artists, with the one 
interesting difference that half the Juilliard group are young women. 
Space limitations here preclude our listing the Juilliard students 
individually. We therefore, in Table IV, give merely the summaries, 

Age Talent Expressed: The average age at which the Juilliard 
instrumentalists revealed talent was about 574 years—somewhat less 
for the girls, somewhat more for the boys. This is about a year 
higher than among the major instrumentalists, but shows, never- 
theless, the early appearance of talent. (The “professional début” 
question was naturally not asked because most of the Juilliard 
group have still to begin their formal careers.) 

Talent in Family: Two-thirds of all the parents are reported as 
having musical talent, a somewhat higher proportion than among 

1 The following are the members of the Juilliard group represented in the study: 
Maro Ajemian, Hinda Barnett, Emma Beldan, Edna Bockstein, Sophie Bostelmann, 
Eleanor Brownell, V. Condon, Diana Dipson, Leah Effenbach, Sue Elson, Ruth Free- 
man, Gertrude Gibson, Jane Glenn, Mary Eliz. Henderson, Drusilla Huffmaster, Rivka 
Iventosch, Eugenie Limberg, Miriam Mann, Estelle Andron, Elizabeth Morgan, Esther 
Schure, Vivienne Simon, Maxine Stillman, Barbara Pentland, Berenice Robinson, 
Helen Van Loon, Richard. Browning, Dean Dixson, James de la Feunte, Edmond 
de Luca, Wendel Diebel, Michael Field, William Gephart, Norman Goldblatt, Leonid 
Hambro, John Calvin Jackson, Charles S. Kent, Richard Korn, Frederick Loadwick, 
Billy Masselos, Walter Mourant, Carl Nicholas, Peter Page, Charles S. Rugg, Robert 
Stevenson, David Stiner, Elie Siegmeister, Bernhard Tiede, Earl C. Voorhies, Harry 
Wilson, Joseph Wood, C. Wister Yearsley. 



Average Age 
Talent Expressed: 

Talent in Mothers: 
(a) Definitely Yes 
(b) Some Talent or 

(c) Totals of Both 

Talent in Fathers: 
(a) Definitely Yes 
(b) Some Talent or 

(c) Totals of Both 

Brothers and Sisters: 
Number in Families 
(a) Definitely Tal- 

(b) Some Talent or 

(c) Totals of Both 

Talent in Other Kin: 
(a) Those reporting 
talent in one 
or more grand- 

- (b) Those reporting 
talent in near 
kin of any 
kind, includ- 
ing grand- 


Females Males 
(18) (8) 

8 6 
13(72%) 10(56%) 
3 1 
16(89%) 11(61%) 
10(56%)  8(44%) 
2 z 
12(67%) 10(56%) 
31 30 
21(68%) 13(43%) 
6 3 
27(87%) 16(53%) 
739%) 950%) 
13072%) 13(72%) 





5(63 7%) 






5(63 %) 






5(83 %) 





5(83 %) 



534 yrs. 










the major artists but chiefly due to the much greater number of 
musical mothers reported. 

Among brothers and sisters, again more than two-thirds are 
listed’ as musical, likewise a higher proportion than among the 
major artists. (An interesting revelation is that the total number 
of children in the families of this newer generation is about half 
the size of those in the senior groups—a significant indication of a 
drop in birth-rate.) 1 

Further, we find more than twice as many of the Juilliard in- 
strumentalists reporting musicality in their grandparents or other 
near kin as either of the two major groups. Can it be that there 
actually is more musical talent in the backgrounds of these “junior” 
artists than among the families of the outstanding major artists? 
We will come to that presently. 

The Juilliard Vocalists: As our study here (at the time we were 
forced to halt) netted only fourteen individuals, a detailed analysis 
of their backgrounds would not be too significant. Nevertheless, 
all the important facts with regard to early appearance of talent, 
high incidence of talent in parents, brothers and sisters and near 
kin is consistent with the data of their fellow Juilliard students. 
While talent appeared earlier among them than among the Metro- 
politan singers, it is interesting to note that, comparing the two 
sexes, there is the same later manifestation of talent among the 
males as there was in the Metropolitan ete 

The eae may have occurred dpe the records of the indi- 
viduals we studied were by some chance not representative of musi- 
cal artists in general. We, therefore, dipped at random into the back- 
grounds of other contemporary virtuosi. We found the stories the 
same: Josef Hofmann (his father a conductor, his mother an 
operatic star), making his début at six; Ignace Paderewski, born 
in a small Polish town, playing piano at three, taught by a musical 
mother; Feodor Chaliapin, rising to operatic triumph from a child- 
hood of abject poverty in Russia during which his training con- 
sisted chiefly of apprenticeships at cobbling and carpentry; Georges 
Enesco, in Roumania, repeating:in early childhood the songs of 
gipsies, making his violin début at eleven; Emanuel Feuermann, 


in Austria, from a highly musical family, showing precocity at 
the cello and also making his début at eleven. 

No, the data from those we have studied are representative of 
others in the world of music. So now, as we look at our “evidence,” 
we may ask in the words of Sherlock Holmes, “What do you make 
of it?” 


(An Original Genetic Study) 

WHEN we begin to analyze the assembled data regarding the 122 
musically gifted individuals represented in our study, we are struck 
by this fact: in all of these three unrelated groups—whether the 
individuals are instrumentalists or singers, males or females, young 
or old, foreign or American, famous or still to make their mark— 
the general story is the same (see Table V, page 259). 

Nevertheless, before we jump to any conclusions about heredity, 
we must first find out what we can or can’t attribute to environ- 
ment. For instance, take the fact that the talents of almost all, 
with a few exceptions, appeared in early childhood. Could not this 
have been the result of “conditioning”? 

A similar question occurred more than twenty years ago to 
Prof. Carl E. Seashore of the University of Iowa, when he set out 
to study musical aptitude. (This, however, as will be explained 
later, is not quite the same as musical talent.) First, he had to find 
some standards of measurement, so he “broke down” musical apti- 
tude into what he considered its components—sense of pitch, sense 
of time, sense of intensity (or degrees of loudness and softness), 
sense of consonance (or harmony), sense of rhythm, and tonal 
memory. For each of these “senses” he devised tests to discover to 
what extent they might be inherent in persons, and to what extent 
they could be cultivated. 

In the years that have followed he and others (notably Prof. 
Hazel M. Stanton in this country, Prof. Jon Alfred Mjoen of 
Norway, and Prof. J. Philiptschenko of Russia) have used the 
Seashore tests or similar tests to measure the musical aptitudes of 

many thousands of individuals. Children in public schools, students 



in music schools and adults at large were tested before and after 
periods of training. And this seems to have been revealed: 

The various “senses” required for musical aptitude do have a 
constitutional basts. 

In other words (according to the Seashore studies) the sense of 
pitch is zmnate—developed quickly in the individual—and can- 
not be materially improved by training, nor can the “elemental” 
sense of time be improved; the sense of intensity cannot be 
imparted by training, apparently because it seems to depend mainly 
upon delicacy of ear structure; and the senses of harmony and of 
rhythm can be developed only to the extent made possible by the 
individual’s inherent capacities. Prof. Stanton reported that by the 
time a child is ten years old its future musical performance can be 
clearly determined, and at sixteen an individual is musically “set.” 

Prof. Seashore gathered that for each of the musical “senses” there 
is a mental process. (Recently Dr. F..A. Gibbs of Harvard an- 
nounced evidence of the location of brain cells which are concerned 
with recording sounds of different pitch.) It has also been shown 
that the different “musical” senses may be independent not only 
of one another, but of other mental factors. That is to say, an 
individual with an acute sense of pitch might have no sense of 
rhythm, or one with a sense of rhythm may have no sense of 
harmony; and—as many of you who read this may know all too 
well—a highly intelligent person may be almost devoid of musical- 
ity, while a nitwit may be highly musical. (There are many cases 
of feeble-minded persons who are good musicians, although, of 
course, never virtuosi.) 

These findings would tend to prove that there is something zn 
people, from childhood on, which determines or influences the 
degree of their musical aptitude. But this brings us to the point 
that musical aptitude does not necessarily imply true talent in the 
sense that musicians would understand it. A person may have well- 
developed senses of pitch, rhythm, time, etc., and yet be as mechani- 
cal as a nickel-in-the-slot player-piano. Aptitude is the basis for 
technique, but while technique is highly essential, by itself it cannot 
produce talent. This is true not only in music but in painting, 
writing and other arts. 


Commenting on this point recently, Josef Hofmann said, “My 
hand is a bad one for the piano—too small, my fingers not long 
enough for everything—and my technique is limited. I have pupils 
who have far bigger technique than I.” 

For talent--and especially great talent—an additional “something” 
is required. This, in the opinion of Harold G. Seashore (Prof. 
Seashore’s nephew), who has specialized in the study of great 
musical talents, is the “artistic deviation from the pure, the true, 
the exact, the perfect, the rigid, the even and the precise.” He has 
shown (with unusual graph-recordings) that each virtuoso artist 
deviates from exactness and preciseness in a characteristically differ- 
ent way. Such artistic deviation must be dictated by extreme sensi- 
tivity, great emotion, and high intelligence. These qualities, we 
may assume, are probably some of the components of great talent. 
In addition, for the talent to reach full fruition, the artist must 
have unusual powers of muscular coordination and also the ability 
to concentrate. 

When we add together, then, both ihe basic “aptitude” require- 
ments and the added “talent” requirements, our next question is 
whether these essentials can be implanted in individuals by envir- 
onment during early childhood, the stage at which they appeared 
among the artists we have studied. And this would imply some 
uniform influence in the early backgrounds of all the individuals. 

But no such environmental uniformity can be found. True 
enough, the backgrounds of many of the musicians and singers 
were highly favorable for talent development, but then we also 
find individuals like Toscanini, Rubinstein, Seidel, Smeterlin, 
Schnabel, Iturbi, Grace Moore, Gladys Swarthout, Rose Pauly, 
Martinelli, etc., emerging from homes where neither parent was 
musical. In some instances the background might have been con- 
sidered almost deadening for musical expression. Again and again 
we find evidence of talent cropping out with apparent spontaneity, 
as an orchid might suddenly appear in a field of dandelions. 

Arturo Toscanini was born in a humble home in Parma, Italy. 
His father (a Garibaldi veteran) was a tailor, his mother an un- 
pretentious homebody, neither being musical. No talent had ever 
been reported in grandparents, aunts, uncles or other kin, and 


there was none, moreover, in any of the other Toscanini children. 
There was therefore no reason to look for musicality in young 
Arturo. Yet by the time he was nine his tendency toward music 
had asserted itself sufficiently so that his parents sent him to the 
local conservatory. He soon “found” himself with the cello, and 
within a short time was winning honors. At fourteen he was 
conducting the school orchestra in pieces of his own composition 
and playing, professionally, in the town orchestra outside of school 
hours. At nineteen he made his début as a conductor at Rio de 

Can something “special” in his environment be credited with 
having produced the genius of Toscanini? 

Yehudi Menuhin’s parents were also not musicians. His mother 
“dabbled” a bit on the piano, as any young woman might. His 
father couldn’t read a note and to this day—as he lamented to us— 


Virtuosi Metropolitan Juilliard Totals 
Instrumental Opera Graduate for All 
Artists Singers Students Groups 
G6 in all) (36 in all) (yo in all) (222 in all) 
Average Age 
Talent Expressed 43/, yrs. 934 yts. 534 yrs. 634 yrs. 
Mothers Talented or | 
Musical in Some 
Degree 17 (47%) 24 (67%) 37 (74%) 78 (647%) 

Fathers Talented or 
Musical in Some 

Degree 29 (81%) 25 (69%) 29 (58%) 83 (68%) 
Brothers and Sisters, | 

Total _ II0 103 72 285 

Talentedor Musical 

in Some Degree 55 (50%) 43 (42%) 51 G1%) 148 (52%) 

Number reporting 
Talent in Addi- 

tional near kin 13 (36%) 16 (44%) 37:(74%) 66 (54%), 


“can’t even turn the pages for his son.” The two, however, 
ardently loved music. They went to symphony concerts in San 
Francisco (where Mr. Menuhin was principal of a Hebrew school) 
and, the family budget not permitting a maid, took their baby with 
them. Soon they were aware that the infant was listening raptly 
to the music, but was especially drawn to the violins. One day 
they took him up to the conductor, Louis Persinger. He became 
interested in the baby, and as soon as Yehudi was old enough 
to finger a violin began giving him lessons. To what extent can 
environment claim credit for this brilliant young artist? 

Artur Rubinstein was born in a poor home in Warsaw where 
no musical instrument was to be heard. Yet as a baby he began 
to sing little songs of his own making to express what he wanted 
or to designate various members of the family. He clung to his 
“song language” and could not be taught to talk until he was three. 
By that time musicians had taken note of this unusual child. Lessons 
began soon thereafter, and within a few years little Artur made 
his début, 

Many stories of this kind lurk behind the terse sentences in our 
Table I. Eugene Ormandy, at 114 years, being able to distinguish 
each of the fifty or sixty records on his father’s hurdy-gurdy... . 
Toscha Seidel, at the age of three having “tantrums” when his 
uncle, whom he describes as an earnest but not talented “fiddler,” 
played the wrong notes. . . . Guila Bustabo, found “tweaking” the 
strings of her father’s violin and not being made happy until she 
was given one of her own.... Alfred Wallenstein, who had 
already been playing the piano, instinctively tuning the first cello 
placed in his hands on his seventh birthday—a feat which any 
cellist would applaud. 

Wallenstein, as it happened, had (as he still has) an acute musi- 
cal ear or “absolute pitch”—the highest development of the sense 
of pitch—which might be described as a sort of “mental tuning- 
fork.” This enables the fortunate musician or singer so endowed 
to “hit” any note accurately, or to judge the accuracy of any note, 
without the aid of any instrumental cue. Among others of our 
instrumentalists who revealed this gift in childhood are Hutcheson, 
_ Heifetz, Lhevinne, Rosenthal, Rubinstein and Miss Slenczynski. 



Maternal Maternal Maternal Paternal Paternal 
Singer Violinist Cellist (not musical) 

: Pitch 
| a 
‘Pianist, Op- Violinist, 
| tratic Coach Conductor 
| aed ene 
\ 1ER 
Absclute Singer Cellist, Pianist 

| ‘The latter is reported as also having been able to distinguish, at the 
early age of nine months, between major and minor scales. 
| Of the singers, there is the unusual case of Kirsten Flagstad, 
| where absolute pitch is reported not only in herself, but in her 
| mother, her mother’s father and her mother’s uncle. (This ‘ ‘pedigree 
of pitch” came to our attention through Prof. Mjoen, and is illus- 
trated in the accompanying diagram.) Although “absolute pitch” 
is by no means a prerequisite for great musical achievement, it is, 
of course, a valuable asset. Many others in our lists report such 
| acuteness of musical ear or the spontaneous manifestation of one 
| of the other musical senses during their first few years of life. 

eee aoe 


The possibility that something unusual in the environment can 
have produced these early manifestations becomes more remote 
when we see that a home can be as musical as possible and yet 
no talent may appear, or it may appear in one child and not in 
another. Here is Efrem Zimbalist, married to the famous singer, 
Alma Gluck, and reporting that neither of their two children 
has talent. Again there are Toscanini’s three children, only one 
of whom shows “musicality,” and this only in the form of critical 
ability. There is Josef Lhevinne, whose wife is also a concert artist, 
and yet reporting that one child is talented, the other not. Our 
data provide numerous parallels, and any one in musical circles 
can add many other instances where children in the most musical 
homes “fail to respond.” 

It would seem very much, then, that one is, or is not born with 
great musical capacity. What do musicians and singers themselves 
think about this? Their opinions, of course, have no scientific 
validity, but they might prove interesting. So, with that thought in 
mind, we asked each one, “Do you believe that you inherited 
your talent?” 

It is perhaps a mere coincidence that almost the same sized 
majority in each group answered “Yes.” Some answered, “In Part,” 



(Answers to the question: ‘‘Do you believe you inherited your talent?’’) - 

Instrumental Metropolitan Juilliard 

Virtuosi Singers Students Totals 

esis. Me a aie 18 19 28 65 
In Partita icededic able 3 Io 16 | 
Nol vise ade oe 7 9 IO 26 | 
Doubtful or | 

No Opinion........ 8 5 2 15 
ToraL ANSWERS..... , 36 36 50 122 


and a number were doubtful or offered no opinion. But about 
20 to 25 percent answered quite definitely “No.” (The “vote” is 
tabulated in Table VI.) 

One type of comment, however, is of special interest. Some of 
the artists said that they didn’t believe they inherited their talent, 
but that they were “just born with it.” Now, if a person is born 
with talent, and it isn’t due to heredity, then it must be due to 
some intra-uterine influence. (In the way, for instance, that some 
forms of idiocy are produced!) This would mean that musical 
talent could be instilled by some shock, blow, nutritive agent or 
chemical conveyed by the mother to the embryonic child. Do you 
believe that? We are quite sure that no biologist does. When, in 
fact, the situation was made clear to some of the musicians whe 
answered “inborn” they said, “I suppose, then, I must mean ‘inher- 
ited.’ ” 

So it begins to look very much as if musical talent zs inherited. 
But a mere guess isn’t sufficient for the geneticist. He would like 
to see some evidence of genetic ratios. That is to say, where a 
condition exists in individuals or is presumed to exist, 7 should 
appear in their offspring in given proportions. 

So now we assemble some of our data in a new form. In all 
our groups we have 122 matings represented between the parents 
of the individuals studied. For our genetic study we will arrange 
the matings in three groups: 

(1) Where both parents are musical. 

(2) Where one parent is musical, the other not. 

(3) Where neither parent is musical. (Although, of course, hav- 
ing produced one highly talented child—the one represented in our 
study—we assume that one of the parents at least is a “carrier” for 

In our first computation we will eliminate the “doubtful” cases, 
where judgment is uncertain regarding the talent of a parent or, 
in a few instances, of a brother or sister. Thus, we set to one side 
the families of Elman, Menuhin, Milstein, Morini and Rodzinski, 

1JIn all cases where a definite “Yes” or “No” was given by the artists, we have 

accepted their estimates. The value of our data, or the importance attached to the 
ensuing conclusions, must be governed by the faith placed in these estimates. 


Pinza, List, Crooks, Queena Mario and Hackett, and about a half- 
dozen among the Juilliard group. 

Our next step is to count only the brothers and sisters of the 
individuals we have studied because, if we included the artists 
themselves, we would be “loading” the evidence—giving each 
family a “send off” with one talented individual. The omission of 
this one need not upset the ratios, for if you recall, the laws of 
chance prescribe that the odds that any condition will turn up are 
always the same for the next child. 

So now if musical talent is produced by genes, this should be 
evident: Where both parents are musical, we should expect a 
higher incidence of musical talent in their children than if only 
one parent is musical; and where one parent is talented, there 
should be more talented offspring than where neither parent is 
talented. That 1s exactly what our figures reveal. (See Table VII.) 

In each of the groups different results from the three types of 
matings are clearly apparent. There were about 12 to 15 percent 
more talented offspring resulting from the “double talent” matings 
than from the “one parent \talented” matings, and a strikingly 
small proportion produced where neither parent was talented. 

To test our evidence further, we compiled the “doubtful” cases 
according to the fairest guess possible, and found that they yielded 
about the same ratios. Again, other more technical genetic calcula- 
tions (grouping the families according to size, then including the 
artists themselves, etc.) also produced results consistent with the 
previous findings. And finally we tabulated the results of the 
marriages among our virtuosi instrumentalists—eighteen of whom, 
as you recall, had children. As almost all of these were “double 
talent” matings they offered no basis for comparison among them- 
selves. But it may be noted that these matings produced almost the 
same percentage of talented offspring as did the similar matings 
among the Juilliard parents who are of the same modern genera- 

The following deductions could therefore be made: 

Where both parents were talented, in most matings one-half to 
three-fourths of the children were talented. 



Where only one parent was talented, in most matings one-half 
of the children were talented. 

Where neither parent was talented (referring only to parents 
whose capacity to produce a talented child had been demonstrated) 
the average of talented offspring was one-fourth or less. 

With this strong indication that heredity is involved, we next ask, 
“What type or types of genes could produce these ratios?” 

Remember, we are dealing with zalent, not merely with “apti- 


(Totals of other talented offspring produced by parents of the musicians and 
singers we have studied, in addition to these artists themselves. Furthei 
“omitted are the results of those matings which were in doubt.) 

Bros. & Sisters 
of Instrumental 
(26 families) 

Bros. & Sisters 
of Metropolitan 
(26 families) 

Bros. & Sisters 

| of Juilliard 

| Graduates 

| Gz families) 
Totals for All 

_ Three Groups 

Where Both 
Had Talent 
Number Number 
of Other With 
Children* Talent 

31 22 
42 26 
21 19 
94 67 

*In addition to the artists themselves. 

** Note: It should be kept in mind that. this refers only to the parents who had already 
| produced a highly talented child. 

Where Only One 

Had Talent 
Number Number 
of Other With 
Children* Talent 
35 21 
16 8 
20 14 
71 43 

Where Neither 
Had Talent ** 
Number Number 
of Other With 
Children * Talent 
a7, & 

ys Z 

14 4 

(66 10 


tude.” It is not unlikely that there are genes for each of the 
musical aptitude “senses” (of pitch, time, rhythm, etc.). But these 
genes are believed to be in such wide circulation that almost every 
one who can carry a tune, play the ukulele or harmonize in a 
barber-shop must have them in some degree. Nevertheless, as we 
have indicated, these ordinary aptitudes might not in themselves 
constitute talent. What we are after, then, are rare and “special” 
genes which might be acting either to intensify the effects of the 
common ones or to produce some unusual supplementary gifts. 

Could a single dominant gene do this? 

Apparently not, for if it could, as in any dominant condition, 
wherever there was a musical child the talent would also show 
in the parent that carried that gene. And as we’ve seen, many of 
our virtuosi reported neither parent talented. 

Could one pair of recessive genes produce the talent? 

Again, apparently not, for if musical talent were a simple recessive 
condition (like blue eyes or blond hair) wherever both parents 
were talented, all of their children would be talented. Our table 
would rule out this theory if we accept evidence that such matings 
have produced an average of 30 percent offspring without talent. 

Evidently, then, the situation is more complex and demands that 
we look for multiple genes. Without taxing you further, we may 
say that the simplest multiple-gene mechanism which might ex- 
plain the ratios would be that of two different dominant genes. In 
such a hereditary process both genes must come together to produce 
their joint effect. But where the double-dominant genes differ from 
a pair of simple recessives (like the blue-eye-color genes) is in 
this way: The simple recessive genes are exact duplicates of each 
other and only one of them can be received from the same parent. 
For any recessive condition to crop out, therefore, both parents 
would have to contribute the same gene to the child. In a double- 
dominant condition, however, as the two genes involved are of 
different kinds, one parent alone may give a child both of them. 
(All this is made clearer in the diagrams, pages 268-269.) 

Thus, assuming for the moment that our hypothesis regarding 
the two dominant “musical talent” genes is correct, we could ex- 
plain many puzzling facts in our study. 


SYMBOLS & A) Eyer) 


The Maestros The Maestro's 
Father Mother 


(mildly musical 
but not 

ing diab VLADIMIR 

(At 4-No talent) (At 8 -no talent) ri 3/2- talented) 

How could so great a talent as Toscanini’s have emerged from 
so unmusical a background? 

Our explanation might be that on the maestro’s paternal side 
only one of the required genes had been carried, while on the 
maternal side the other one had been handed along—neither effec- 
tive by itself. It may have taken many generations for both genes 
to be brought together through the mating of Father Toscanini 

(An hypothesis) 

Granted that a person has the ordinary "aptitude" genes (see text), the additional - 
"something" required for musical talent may be produced by 


RN zy, Wes 
We J Ge - 
(symMBOL) TE 
will | é; 
Each gene is ineffective by itself, but s(A)e> MUSICAL 
when both come together in the same CADE o ae x 
individual the result is: (Be TALENT 

The ordinary ''A" or "B" genes, which ie man 
most persons carry, produce ''blanks’’: @> 

Thus, receiving a pair of genes ("talent" or ordinary) from each parent, individuals | 
may carry any of the following 

(All have the same effect.) 






(While in each case above no talent will show in the individual, the more talent” | 
genes carried—as is also true of those with talent—the greater the chance that one's | 
children will be talented.) | 



tT | 

[Pe eB, 



| {ln each case it is assumed that the ordinary “aptitude” genes are also handed on to the children.) 

t. BOTH PARENTS —Have an almost one-in-two chance of producing 
! but of this same "talent-gene" type: of these types: 
2. ONE TALENTED PARENT —Would have, three out of four times, 
—of this —mated to one NON-TALENTED CHILDREN 
type: with no "talent of these types: 


» Clearer: 


Jay ee 


| of these types —of this rata 

bee oe 
G2 as } 6 a gh 

—but of these types (rare): ra} o 

Through any of these matings (Nos. 3, 4 or 5) every child would receive the required 
two "talent" genes. 

Note: In general, the more talented relatives there are on both sides, the greater will 
be the probability of children with talent. 



and Mother Toscanini. Then the chance of the combination appear- 
ing in one of their offspring was one in four or less, and as it hap- 
pened, out of their four children, Arturo was so favored. 

Why has the maestro’s talent failed to appear in his children? 

The young woman whom Arturo Toscanini married had sung 
in a local choral ensemble, but whether or not she had unusual 
talent, or was presumably carrying the required “talent” genes, we 
do not know. Granted that she did have these genes, the odds 
would still be about even that a child of theirs might not receive 
both genes together. It would therefore not be surprising that out 
of three children, only one, the youngest daughter, Wanda, has 
shown any true musicality, and this only in the way of a keen 
critical sense. (Sufficiently acute, however, for her father to take 
stock in her comments on his performances.) But proceeding into 
another generation, this daughter is married to the pianist Vladimir 
Horowitz, and there is every indication that their little girl is 
highly talented. 

With two dominant genes involved, as you can see by the 
diagram, almost any kind of talent combination could be possible 
in a family. Both parents talented (as the Zimbalists) might pro- 
duce no talented children, or (as with the Lhevinnes) only one in 
two talented children; and neither parent talented (or at least, not 
outwardly so, as in the case of the Menuhins) might produce all 
talented children. 

You may have wondered how Martinelli could have had fourteen 
brothers and sisters with no talent among them. So did we, and 
so did Martinelli. He thought and thought when our question was 
put to him and finally said, almost plaintively, “But what can I do? 
My brothers and sisters had no talent—not one!” (It was only by 
accident that Martinelli’s own talent was discovered, and not until 
he was nineteen years old. While he was in service in the Italian 
army a keen-eared officer heard him singing in the barracks and 
arranged for his vocal instruction.) 

Consulting our ratios, we can see that with two non-musical 
parents we need not have expected talent in more than one in four 
of the Martinelli family, which is to say in no more than three of 

the other children. It is not so surprising, then, that by the laws 


of chance, talent cropped out in only one. However, an additional 
possibility is that the ordinary “aptitude” genes might have been 
sparse in the Martinelli lineage, so that even given the “talent” 
genes, where one or more of the basic “aptitude” genes were miss- 
ing, a brother or sister might still have shown no musicality. 

While our data would seem to favor the hypothesis of two dif- 
ferent dominant “talent” genes, plus certain “basic aptitude” genes, 
earlier investigators have suggested other gene mechanisms to 
explain the production of “musicality.” About ten years ago the 
able Russian geneticist, J. Philiptschenko, reported the belief that 
four pars of genes of different kinds were involved, both recessives 
and dominants, some acting to produce basic aptitude and others 
to intensify the effects. We are not sure, however, in view of the 
fact that Philiptschenko’s studies were apparently not confined to 
so highly specialized a group as ours, whether he was dealing with 
mere musical aptitude or the talent we have in mind. Neverthe- 
less, our findings need not be considered radically different from his. 

In any case, while our conclusions must await confirmation by 
further studies in the field before they can make any pretense to 
finality, this much seems to have been settled (in refutation of 
earlier theories): Where both parents are highly talented, there is 
no guarantee that their children will be talented; and where 
neither parent is talented, there is still the possibility that they may 

roduce a musical genius—if they carry the required genes. For, 
above all, to answer the main question raised by this study: 

Musical talent is in all probability inherited through a number 
of genes acting together, and without the required genes there can 
be no musical talent. : 

This does not by any means dismiss the influence of environment. 
If the best musical environment cannot create talent, an unfavor- 
able environment might well suppress talent. As the father of 
Yehudi Menuhin, Moishe Menuhin, said to us, “I am sure that 
there are many other young men now nobodies who might have 
become as great artists as my son if their talents had been immedi- 
ately recognized by their parents and they had been given equal 
opportunities for training and development.” 

The “veto” power of environment is plainly revealed in our 


data. We can see, as we trace backward into preceding generations, 
that wherever opportunity was more limited, less talent appeared. 
Most strikingly is this shown among women. We find that our 
virtuosi instrumentalists reported many fewer mothers, grand- 
mothers and aunts with talent than did the Juilliard students, 
their juniors in both age and achievement. Certainly there could 
not have been any lesser amount of “talent” genes in the families 
of the world-famous musicians. The explanation must lie in the 
fact that their women forebears, most of whom had lived in humble 
surroundings abroad, had been given little chance for their talents 
to assert themselves. Among the women of a later day, as repre- 
sented by the sisters of the artists, we find as many with talent 
reported as among their brothers. ) 

But even today, while women may have an equal opportunity 
to show musical talent, this is far from saying that their achieve- 
ments in music are equal to those of men. Very few women, as 
our Virtuosi Table bears out, are in the front ranks of the instru- 
mentalists. Why? Erica Morini has this to say: 

“In my opinion it is because only a few women have the great 
power of concentration, the strength and the energy required for 
such achievement. A complete absorption is necessary, and a readi- 
ness to give up the pleasures which most women seek.” 

Others believe that woman’s failure to keep pace with male musi- 
cians is due not to any inherent inferiority but solely to discrimina- 
tion against them. The professional world of music, it is claimed, 
is largely a world of men which does not welcome the intrusion 
of women. At the same time, audiences (including ladies’ cultural 
clubs) seem to show a preference for male artists. Thus, the “veto” 
power of environment over talent in women may be continuing 
to assert itself. 

In the vocal field, there is no such suppression of musicality in 
women, for operas and musical presentations of all kinds demand 
their equal representation. But nevertheless among singers of both 
sexes the negative effects of environment appear to be much greater 
than among instrumentalists. As we saw clearly in our tables, train- 
ing among the singers is dependent upon what happens to their 
voices during puberty. Regardless of talent or ability, the singer is 


Are voice types inherited? While not a direct part of the talent study, an 
effort was made to throw light on the inheritance of voice types by ques- 
‘tioning members of the Metropolitan Opera Company and, in addition, 
about 100 members of the celebrated Schola Cantorum of New York City. 
‘The data regarding the voices of these artists and of members of their families, 
are tabulated below. As can be seen, a general correlation between voices of 
children and parents is indicated. Where both parents had high voices, most 
of the children were in the high range. The 26 tenor fathers listed produced 
‘no bass sons and only 2 contralto daughters; but fathers with bass voices, 
.and contralto mothers, had a considerable proportion of low-voiced children. 
(A question mark indicates “‘singing voice of parent unknown.’’) 

| Matings Sopr.  Mezz. Contr. Ten.  Barit. Bass 
7m Dalit: oor OOD. 28 14 2; 19 1, 
12, :| Barit.,,.X,, Mezz. 12 3 2 3, 
Fo Bertt os Xo. Contr. 6 3 3 31 4 
Ey a Darit: jx ? 6 4 4 3 3 
zo” léenhor® 9° Soper! 16% * 5 2 
fon, Lenotae x. MezZ. 3 4 2 ihe Os ce 
py Lenor x . Contr, I 
Sis. henoroX ? 3 2 6 I 
ieee weASS) us aes ii ODL. 6 2 4 - 7 
Bw Bass’) 1<\).Mezz. 2: 
Pee Dasstanw.) nONtr: I 
Be ASS. OK ? 2 3, I 
19 - 4X OOPT. 2I 3 3 14 Rens v2: 
8 oir Mezz. es 2 4 5 8 
7 PoarersyGOntte! ? ot3 I 6 4 5 

131 (Total matings) CE OMIT TN IO eH Bey aL, 
(Total offspring—3 67) 


continually at the mercy of his or her physical equipment. One can 
buy a violin if it breaks, but one can’t buy another set of vocal 

“I don’t think you can consider a talent for singing in the same 
way you would a talent for music, as such,” Richard Bonelli (one 
of the Metropolitan stars) said to us. “Altogether aside from the 
talent for music which a singer should—and usually does—have, 
there is the question of physical fitness and the very peculiar mental 
aptitude toward vocal technique which are necessary to make real 
singers. Consequently, you find thousands of people with fine musi- 
cal talent who can’t sing a lick, and you also find plenty of people 
with at best an indifferent musical talent, yet who make wonderful 
singers, simply because they happen to combine the physical and 
mental qualities necessary.” 

Without doubt, physical appearance and personality are more 
important to the vocalists than they are to the instrumentalists. 
But while these factors may sometimes lift singers to an eminence 
unmerited by their true talents, their careers are all too often 
unjustly cut short by age, public fickleness or professional difficul- 
ties. To a much less extent is this true among the instrumental 
artists. Rarely is the career of a great pianist, violinist or conductor 
terminated by anything but voluntary retirement or death. 

However, granted that environment, in the form of early influ- 
ences, educational opportunities and chance are important in any 
human career, one more question remains: 

To what extent are the achievements of our great musicians and 
singers to be credited to heredity, and to what extent to environ- 

This is of course a rhetorical question to which no scientific 
answer can be given. But it has been asked so many times, often 
by the artists themselves and innumerable times by persons who 
have called on them for judgment and advice, that we thought it 
worth while to secure their opinions once again. For this question 
we “polled” only the two senior groups. The answers showed some 
marked differences of opinion. (See Table VIII.) The largest num- 
ber took the conservative view that inherited talent and training are © 
both equally important or that no opinion could be given. Those 


that thought talent more important were almost equally balanced 
by those who thought training more important. (Note, however, 
that a majority of the men singers believed training played the 
biggest role in their careers.) 

The general views of the artists in both groups, as expressed to 
us, are reflected in the following selections from their comments: 

Sergei Rachmaninoff: “I am inclined to believe that heredity and 
training are inseparable and indispensable in any art achievement. 
I consider that capacity for hard work is also a talent and that 
only those few artists who have inherited both musical and work- 
ing talents attain the highest peak of their profession.” 

Alexander Brailowsky: “Genuine talent is the basic requirement 
and is bound to manifest itself sooner or later; training is an indis- 
pensable accessory.” 

Eugene Goossens: “Heredity unquestionably lays the solid founda- 
tion for musical achievement. Proper training lies principally in 
early apprenticeship to the profession.” | 



(Opinions of the artists) 

Instrumental — Metropolitan 

Virtuosi Singers Totals 
Both Equally Important.......... 16 12 (10 women 28 
Talent More Important.........+¢ 6 10 ( 5 women 16 
5 men ) 
Training More Important........ ma II ( 2 women x 
| g9men_ ) 

Uncertain or No Opinion........ 8 3 Cwomen_ ) II 

M Ootalvcnswers..iiis. ae ea 36 36 yp? 


Fritz Kreisler: “Heredity and training contribute probably in 
equal measure.” 

Nathan Milstein: “Talent is, in my opinion, inborn and inde- 
pendent of training and home influence. But however great, it 
will remain futile without real training, which is the means and 
the only one of developing it and nzaking it productive.” 

Jan Smeterlin: “Heredity without training would not go far, 
but training without heredity would not go anywhere.” 

Artur Rodzinski: “Training and above all luck.” 

Grace Moore: “I had a voice even when very young, and all my 
natural emotional expression was toward music. I only felt com- 
pletely myself when I sang. That I call inheritance of a special 
spirit and emotional values. The rest was training.” 

Lily Pons: “One must first be born with a voice, and next the 
musical background during youth is important. But training makes 
the difference between the person who just sings and the one who 
becomes a truly fine singer.” 

Lotte Lehmann: “Everybody with a fine voice can be trained to 
become a good singer, but to be a real artist you must have. inborn 
or inherited talent. Nobody can ever learn that.” 

Lauritz. Melchior: “By heredity came intelligence, ear and ‘ove 
of music—the qualities that make an artist and which no teacher 
can give you.” 

Mario Chamlee: “Training plays a greater part. With extraordi- 
nary vocal equipment and no training singers seldom develop. 
With little natural voice but consistent effort and training voices 
have developed to great extents.” 

Jan Kiepura: “Heredity counts only physically. I received my 
voice as though given a violin. Training did for me what learning 
to play would do for a violinist.” 

Lawrence Tibbett: “I believe heredity may have played some 
part in my singing ability, but so far as achievement goes, I attrib- 
ute the greater part of it to training.” 

Reviewing all the data and opinions in this study of ours, we 
feel justified in leaving you with the conclusion that some unusual 
hereditary endowment is essential for great musical achievement. 


That opportunity and training are also essentials need hardly be 
debated, but the important fact is that the talent must be there 
first before it can be cultivated. 

How does this apply to you? If you happen to be an average 
person in whose life virtuoso talent hasn’t entered, the question 
of your “musicality” must have come up at one time or another. 

So our study suggests that if you have tried to play or sing and 
just haven’t been able to, or if you do play and sing but have 
“never gotten anywhere with it,” the fault may not have been in 
your background, efforts or training, but in your genes. In which 
case, it is as idle to blame yourself for your musical shortcomings 
as to blame yourself for not being as tall as you’d like to be. 

It suggests that if you have a child and that child shows little or 
no response to music, you must not try to force musical training 
upon. it. 

It suggests that with musical talent having a constitutional basis, 
often independent of intelligence, it is unfair to penalize children 
in school for backwardness in music, or to average in “music” 
marks with those for other studies. 

It suggests that when parents are both highly musical they should 
not frown on a child of theirs who shows no musicality, and that 
when parents are not at all musical, they should nevertheless keep 
an eye open for the possibility that a child of theirs may be talented, 
and give it every opportunity to develop. (The possibility that a 
talented child will be produced by average non-musical parents is, 
however, ever so much more remote than is indicated by the 
“neither-parent-talented” matings in our study. The fact that the 
latter matings had already produced an exceptional child was 
proof that the parents carried hidden “talent” genes, whereas aver- 
age non-musical parents are unknown quantities.) 

With awareness of the basis of musical talent there should be 
a wiser understanding of which children to train intensively and 
which ones to teach music to only casually, or not at all. Many 
a tragedy might have been averted if parents had not tried to turn 
a Jimmy into a Jascha. 

All of which brings to mind the pleasant remembrance of a 
visit which we had with Professor Leopold Auer, one of the great- 


est violinists of his time, and in later years one of the most famous 
of music teachers. (As every one in the musical world knows, he 
was a vital force in the careers of many of our present violin 
virtuosi, who were trained by him at the Imperial Conservatory 
at St. Petersburg, now Leningrad.) 

When we saw Professor Auer it was in 1926, a few years before 
his death. A tiny little man, past eighty, he was then established 
in a big stone house off Riverside Drive, New York, which pupils, 
friends and a grateful public had provided after the post-war up- 
heaval had driven him from abroad. 

Chatting about his celebrated: pupils, we happened to bring up 
the “coincidence” that various of them had given names ending 
in “cha”—Jascha Heifetz, Toscha Seidel, Mischa Elman, etc. These, 
Professor Auer explained, were his affectionate Russian diminu- 
tives for their real'names, Jacob, Thomas, Michael, etc., which he 
had applied to them in special recognition of their talents, and 
which they later adopted professionally. 

“Ah,” we sighed, “now we know why we could not become a 
great violinist. Our name should have been ‘Amscha.’” 

The little man’s eyes twinkled. “Perhaps,” he answered with 
laughter in his tinkling voice. “But don’t forget that these others 
had the talent before they got the name.” 


pepe cr 

(a is We C Reta, je yf YG 

: L926 

As sketched by the author on the occasion mentioned in the text. 



Ir there is a hereditary basis for musical talent, a logical inference 
would be that heredity plays a part in other specialized talents and 

There is every reason to believe that this is so, but, unfortunately, 
genetic exploring in other fields is not nearly so easy as it is in 
music. You will understand why when you recall that our music- 
talent studies were confined to performing or interpretive ability— 
the rendering of set pieces of music whereby individuals of all ages 
and nationalities can be measured by the same standards. But only 
in music is this possible, and only in interpretive music. Had we 
ventured into the field of composing we would have been beset 
with difficulties. For composing is creative art, the very essence of 
which is individuality; and individuality cannot be measured by 
any yardstick. That is why we did not include composers in our 
study, unless by coincidence ey also happened to be outstanding 

The difficulty of evaluating creative achievement impedes genetic 
study similarly in the other arts—painting, sculpture, literature, etc. 
—with the added difficulty that in these fields there is no interpre- 
tive art as there is in music. Moreover, where in interpretive music 
great achievement, with attendant recognition, may come in child- 
hood, in the creative arts talent requires many years to ripen, and 
recognition may not come until long after—if ever. In all history, 
we are not aware of a single important piece of creative work 
done by a pre-adolescent child. 

Many composers, artists and. writers did give early evidence of 
potential creative talent, but innumerable others were nothing to 
brag about as children. Of course, the talent may have been latent 
and unrevealed for the lack of aptitude tests. It is to remedy this 



that many special tests have been and are now being devised which 
seek to measure aptitude in other arts and fields (including business, 
mechanical pursuits, science, etc.) as the Seashore tests do in music. 

Although the heredity of other specific artistic talents may be 
harder to discover, if we consider them all together, a trend toward 
artistry in general does seem to run in given families. One member 
might become a musician, another a writer, another an actress or 
dancer, etc. We have many instances of this, suggesting that all the 
arts have certain “genes” in common. In music, writing, painting, 
sculpture, drama, architecture or esthetic dancing, one encounters 
the same basic principles of composition, tempo, rhythm, form, 
tonality or shading. In each field, however, there are certain special 
requirements: In writing, a knowledge of and “feeling” for lan- 
guage; in painting, a sense of color; in music, an “ear,” etc. 

If we think, then, of all the various artistic elements as being 
correlated with genes, we can easily see why, although two persons 
in a family may each carry many of the same “artistry” genes, a 
difference between them in a single “key” gene may send them off 
into different channels. An individual with many “artistry” genes 
who yet lacks the “color” gene may become an etcher or a black- 
and-white artist. A child of musical parents, failing to get the 
“musical-ear” genes, may become a painter, sculptor or writer. Or 
one lacking genes for manual facility may become an actor, or 
dancer. But of course, this is still theory. 

Whatever the genetic explanation, the relationship of the various 
arts is clearly shown by the fact that so many persons talented in 
one field are also talented in other fields. To cite only living 
examples, Deems Taylor is a composer, writer and skilled cabinet- 
maker. George M. Cohan and Noel Coward write, compose, act. 
John Held, Jr., the cartoonist and writer, is also an accomplished 
musician. Professor John Erskine, educator and author, also appears 
as a concert pianist. John Barrymore, the actor, began his career 
as an artist, and Paul Muni might have ended up as a violinist. 
The writers, Joseph Hergesheimer and Somerset Maugham, started 
out as painters, while Hendrik Willem van Loon, E. E. Cummings 
and John Dos Passos are among many who continue to “double” 
in both fields of writing and art. Sinclair Lewis, Nobel-Prize- 


winning author, is one of our most gifted mimics. Angna Enters. 
mime and dancer, also paints and writes. These are but a handful 
of instances that come to our mind. As we think further, it is 
almost a rule that a person greatly talented in one of the arts 
should also show talent for some other art. (Of course, the greatest 
of all exemplars of versatility was Leonardo da Vinci, of whom 
we shall speak later.) 

Not to be overlooked as an outstanding factor in the develop- 
ment of any creative artist is our old friend, Environment. A talent 
may be all dressed up with no place to go. If a talent for art 
crops out in an environment where no one wants art, it may die 
a-borning. Again, under modern conditions, with insistence on 
specialization, a person with various talents is forced to decide early 
which talent to cultivate. The wrong choice may lead him to 
failure where the cultivation of an alternative talent might have 
led to success. Few question that environment has stifled many 
more talents than have ever come to fruition. 

Where there is no true talent or aptitude for a given pursui’, 
but conditioning has created an “imitation” of it, the results may be 
as unfortunate as the stifling of talent. Thus, the child of a musician, 
writer, artist or actor—or of a doctor, lawyer, engineer or business 
man—may, through precept and training, acquire tendencies which 
are eagerly seized on as symptoms of his being a “chip of the old 
block.” Yet he may lack the inherent factors necessary for achieve- 
ment. This may explain in part why so many sons who attempt to 
follow in the footsteps of illustrious fathers come to grief. A clear 
understanding of the required basic aptitudes and talents would 
greatly reduce the many sad failures who fill the arts and profes- 

Here is where the aptitude tests in all fields may prove of great 
value. Six hundred American colleges which offer pre-medical 
courses now give aptitude tests to candidates for admission. Many 
deutal colleges also give tests for prospective dentists. Tests for 
almost every profession are being given by the “Human Engineer- 
ing Laboratories,” the one at the Stevens Institute of Technology, 
Hoboken, N. J., the other in Boston. Some 20,000 adults and 
children over eleven years of age have been tested in the past few 


years for their capacities, with the purpose of directing them into 
the proper channels. 

In the fields outside of the arts, such as law, medicine, business, 
trades, etc., we have reason to believe that environment or training, 
rather than inherent capacities, have heretofore been chiefly respon- 
sible for sending individuals into specific channels. On this premise 
the fact that there are families of doctors, lawyers, clergymen, 
business men, etc., might have no more genetic significance than 
that there are families of house-painters, railroad men or plumbers. 
Caution must be used in speaking of this or that family, group or 
race as inheriting specialized tendencies. One hears it said that 
Jews have “business” minds, Germans “technical” minds, French- 
men “artistic” minds, etc. This is no more valid than saying, from 
what we see in the United States, that the Chinese have “launder- 
ing” or “chop suey restaurant” minds, the Greeks “shoe-shining” 
minds, the Armenians “rug-peddling” minds, the Irish “police” 
minds, etc. 

Genetics emphasizes constantly the danger of generalizing and 
the necessity of thinking in terms of individuals and individual 
characteristics. For instance, let us say that one of the requisites 
for achievement in science, engineering or business is a “head for 
figures.” By isolating the single unit factor of “mathematical” 
talent (if there is one!) we could look for its appearance in given 
families. Thus, college records have revealed a correlation between 
the standings in mathematics of fathers and sons, and alse of 
brothers, which has led to the belief that mathematical talent has 
a hereditary basis. (Some authorities go so far as to ascribe it to 
a dominant gene.) If a few more unit factors which play a part 
in business achievement are found to run in families, we might 
then, but only then, be justified in saying that “business ability” is 

Some investigators have also reported an apparent correlation 
between mathematical and musical talent, pointing out that musi- 
cians must have a “feeling” for numerical ratios. We might then 
expect that some mathematicians (granted that they also had a 
few of the required “music” genes) would be able to play. A few 
isolated examples prove nothing, but it is interesting to point to 


Prof. Albert Einstein, and perhaps to former Vice-President Charles 
Dawes, a banker, as men with “heads for figures” who are both 
accomplished violinists. 

Also considered closely allied with mathematical ability is vir- 

tuosity in chess. That there may be a hereditary basis for chess 
virtuosity seems indicated by the several instances where chess 
talent cropped out at an early age, notably in Jose Capablanca, 
former world chess champion; Paul Morphy of New Orleans, an- 
other chess expert; and, most strikingly, in the present chess cham- 
pion of the United States, Samuel Reshevsky. 
, As many may recall, Reshevsky (now twenty-six) burst upon our 
chess horizon when, at the age of eight, he came from Poland 
with his father and made a spectacular tour of the United States, 
playing matches sometimes with as many as twenty or thirty players 
simultaneously. At one of the cities he visited, we were sent (in our 
reportorial capacity) to a private home, where he was being 
boarded, to interview the prodigy. Loud outcries greeted us from 
the rear yard. Investigation revealed a frail, undersized youngster 
shouting at some neighbor lads, in language unintelligible to them, 
that he was the great chess player. (His adversaries seemed totally 
unimpressed, and only a timely rescue prevented lése-majesté from 
being committed.) 

In other words, the prodigy appeared to be no different from any 
other small boy. Yet that night we saw this frail, undersized child 
suavely and single-handed engaging a roomful of adult and expert 
chess players, moving with bewildering swiftness from board to 
board and in short order defeating all but two, who were declared 
tied because little Sammy was getting sleepy. 

The “something uncanny” which people associate with prodigies 
might be nothing more than the premature development of certain 
“unit” characteristics of the mind. An exceptional development of 
the power of memory might of itself produce prodigy qualities in 
a child. One prodigy of our acquaintance, a young miss whose IQ 
at twelve was one of the highest on record, had not only a remark- 
able memory, but the ability to “see in chunks” (as she put it)—to 
read not by word or phrase but by whole paragraphs at a time. 
The two gifts in combination enabled her to take her studies in 


kangaroo leaps. In most other respects, however, she was no differ- 
ent than other children of twelve, and at last reports she has grown 
up to be a bright, but not outstanding, young married woman. 

The foregoing case, and that of Reshevsky, illustrate the fact that 
in many prodigies only part of a child’s mentality may be prema- 
turely developed. It may very well be that certain genes, or perhaps 
environmental factors, have acted to stimulate an early growth of 
such mental characteristics, in the same way that there are genes 
or factors which may force the premature arrival of puberty. The 
mistake, however, is to assume that the entire mental process has 
been advanced, and also to overlook the rdle of experience in 
producing maturity. By therefore confusing precocity in only limited 
respects with adult mentality, and forcing prodigies into adult levels 
to which they were not adjusted, much grief has been caused them 
in the past. 

The tendency now is to recognize unusual brilliance in a child 
as merely a “unit” manifestation, in the same way that children 
may have unusual athletic ability or musical talent and yet be 
quite average in other respects. Accordingly, advanced school sys- 
tems are now providing extra outlets for the mental energies of 
superior children, the while keeping them at average class levels 
and in association with other children of their age. 

Talent, aptitude and creative ability reach their fullest expression 
in those most remarkable of all human phenomena—the true 
geniuses, whose intellectual and creative powers carry them to such 
heights that long after they are gone humanity continues to be 
illumined by their achievements. Think a moment of Leonardo 
da Vinci, whose talents ran a bewildering gamut—art, architecture, 
poetry, music, engineering, anatomy, biology, invention, city plan- 
ning—with outstanding contributions in each field. How are we 
to account for him? Or for such other geniuses, less versatile, but 
no less great, as Shakespeare, Michelangelo, Plato, Sophocles, 
Spinoza, Newton and the few score others of similar caliber in all 

Because geniuses seem to arise spontaneously, with apparently no 
relationship to their family, background or training, they were 
formerly looked upon as divine, supernatural and inexplicable 

Kubli photo 


Samuel Reshevsky, later to be United States’ chess champion, is here shown, at the age 
of eight, on the occasion referred to in the text when he played thirty opponents 


human phenomena. Geneticists now incline toward a more prosaic 
explanation: That great geniuses were, or are, merely the result of 
rare and unusual combinations of “superior” genes, interacting 
with the necessary environmental conditions. The very fact that 
such men have arisen from every type of background, sometimes 
in the face of extreme adversity, and all sorts of handicaps, rules 
out the theory that it is environment which produces genius. 
Nothing in the background or training of a Shakespeare, Leonardo, 
Lincoln or Edison was any more unusual than that of countless 
others who never rose beyond mediocrity. 

A gene hypothesis similar to that which we advanced for the 
inheritance of musical talent might be elaborated to explain the 
derivation of genius of any kind. Naturally, for different types of 
geniuses, different gene combinations would be required, and 
the rarer the genius, the rarer and more complex the combination 
of genes would have to be. (Mind you, we are speaking theoreti- 
cally.) % 

Taking Shakespeare as an example, if we tried to “break down” 
the components of his genius, we might say that they must have 
included an extraordinary intelligence, an unusual memory, intense 
emotional feeling, an extreme sensitivity to “sound effects” in 
words, remarkable powers of imagination, a sense of harmony, 
composition and rhythm, a response to color, etc.; and coupled 
with all that, an unusual “drive” which enabled him to produce 
his masterpieces in so short a time. Each of these attributes of his 
may have been due to one or many genes, and every single one 
of these genes would have been required to make the potential 
Shakespeare. The absence of just one “key” gene might have re- 
duced the whole combination to mediocrity. 

We can thus see (again theoretically) why Shakespeare’s parents 
as individuals were nonentities in spite of the fact that they might 
have carried a large number of the precious genes; and why, with 
only half of his genes passed on to any child, Shakespeare’s genius 
never again repeated itself in his descendants. So with Lincoln, 
Wagner, or any other genius in history. It would then be little 
wonder that there is no record of two truly great geniuses following 
each other in the same family. 


Again it should be emphasized that the mere presence of the 
requisite combination of superior genes would not insure the flower- 
ing of a genius. We have no way of telling how many equally 
great or perhaps even greater potential geniuses than those on 
record were suppressed by some unfavorable circumstance. Espe- 
cially does this suggest itself with regard to the failure of women 
to keep pace with men in achieving greatness. Everything we have 
learned in genetics (as we pointed out in the preceding chapter) 
proves conclusively that any combination of “superior” genes that 
could occur in a man could also occur in a woman; in fact, that 
as women carry more genes, the combination would be even likelier 
to occur. We must therefore conclude that (a) our social environ- 
ment, in which women have always been kept subordinate to men, 
is responsible for suppressing their potentialities, or (b) that some- 
thing constitutional—possibly hormonal, or such factors as mother- 
hood—acts as an inhibitory influence. As to the latter, we have seen 
that in hardly more than a generation since women have been given 
comparative freedom in careers, but not yet equality, they have 
produced many notable persons. Until they are given full equality 
and full opportunity we cannot conclude that there is something 
inherent in women which prevents their being geniuses. 

One other question that is bound to come up in any discussion 
of genius: 

Is it true that geniuses are always a little “queer” mentally or 

The belief that such is the case has been and still is widespread. 
Back about 50 a.p. Seneca said, “There is no great genius without 
a tincture of madness.” In the seventeenth century John Dryden 

“Great wits are sure to madness near allied, 
And thin partitions do their bounds divide.” 

And capping mere adages with weighty scientific thought, Lom- 
broso, a generation ago, brought forth reams of data to prove that 
genius was akin to insanity. Others have followed with added testi- 
_mony that many great men were “queer” or physically warped. 
Reported as epileptics were Mohammed, Paul of Tarsus, Julius 


Caesar, Francis of Assisi, Alfred the Great, Peter the Great, 
Napoleon I, Dostoefisky. Listed as emotionally unstable or of a 
“hysterical” temperament were Bismarck, Poe, Goethe, Kant, Pascal, 
Rousseau, Baudelaire, Wagner, Schopenhauer, Tolstoy, etc. Insanity 
—or suicide—ended the careers of Schumann, Nietzsche, Van Gogh 
and many others. This and that man was sexually abnormal. So we 
could continue to fill pages. 

The implication from all this, taken at face value, is that genius 
carries with it an evil destiny, or that genius can only flower in 
unhealthy soil. This is far from a universal fact. While it is quite 
true that many great men were mentally or physically abnormal, 
many more great men were apparently not physically or mentally 
abnormal. The records of the great men of our own country or 
of our own time will bear this out. We have only to think of 
Washington, Franklin, Jefferson, and Lincoln, of Mark Twain, 
Emerson, Henry James and of George Bernard Shaw, Toscanini, 
Sibelius; Einstein, Darwin; Justices Oliver Wendell Holmes and 
Brandeis. Neither insanity, nor morbidity, so far as we know, 
characterized or characterizes any of these men. 

Why, then, has genius always been linked with madness. or 
some pathological condition? Perhaps the first reason, as various 
authorities suggest, is what may be bluntly termed the “sour grapes” 
attitude of more ordinary mortals—the wish to explain achievement 
far beyond them as due to something undesirable. Many early scien- 
tists were looked upon as sorcerers and many great men were 
hounded or even executed because their words or talents were 
believed to have an evil source. 

If a large number of geniuses or other celebrated figures were 
“queer,” so have been innumerable persons who weren’t great. With 
regard to insanity or nervous disorders, also, we know that the 
incidence in the general population is high enough to explain why 
a fair percentage of great men should also be so afflicted. And 
when we get right down to it, how many of us who aren’t geniuses 
could prove that we are at all times, and under all conditions, fully 

Because the records of great men were carefully kept, and their 
lives subjected to close scrutiny, it should be expected that their 


“abnormalities” would loom up out of all proportion to those in 
the general population. Nevertheless, it is also possible that the 
strain, the responsibilities and the abnormal social environment sur- 
rounding great men and geniuses might have tended to make 
them eccentric, or to undermine their health. 

“I wouldn’t want my child to be a genius!” is something that 
you yourself might have said. There may be a sound basis for 
this, not because of any evidence that geniuses are doomed to 
unhappiness by something inherent in them, but because the world 
isn’t fully prepared for geniuses. As was brought out earlier, steps 
are now being taken to make the development and adjustment of 
superior children easier. In the opinion of genetic authorities the 
genes requisite for genius abound throughout the world in all 
classes and among all peoples. Not an “unhealthy” soil, but a 
healthy social environment, they believe, will eventually result in 
the bumper crop of geniuses that may lift all humanity to new 
and far higher levels. 



Ir people in real life were like characters in the movies and the 
comic strips, we could make these definite assertions: 

All fat people are ARISE frank and easily moved to 
Jaughter or tears. 

All blond women are dumb Bat frivolous, or else are cold, cal- 
culating and morally loose. 

All black-haired men with swarthy skins and sharp noses are 

All red-heads are passionate; all men with high foreheads are 
intellectual; all men with receding chins are timid. 

The list could be extended indefinitely to include the various fea- 
tures and looks that are supposed to indicate jealousy, meanness, 
criminality, aristocracy, treachery, affectionate disposition, etc. 

But is there actually such a correlation? If there were, then know- 
ing that heredity influences one’s appearance, we might go further 
and ask whether heredity does not also make a person act the way 
he looks? 

Much attention has been given recently by scientists to these 
very points. As in other studies, we begin with the lower animals. 
Here we do find indications of what the scientists call inherited 
“behavior patterns,” which characterize not merely the different 
species, but subdivisions of the same species. It is well known that 
various types of birds build their nests in various ways, that dif- 
ferent breeds of dogs behave differently—fox-terriers being nervous 
and aggressive, St. Bernards calm, bulldogs persistent, etc. Is there 
a parallel in different strains of men? 

Approaching the subject objectively, scientists now say that our 
behavior may have a genetic basis just as well-founded as that in 
the lower animals. As Professor James Gray of Cambridge expresses 




it: “...1 do not believe we can put our finger on any of our 
mental powers and say, ‘Herein are we a race apart, elevated above 
the rest of the animal world.” To illustrate, Professor Gray re- 
ports his discovery that even the lowly fish have not merely auto- 
matic movements but powers of forming associations between 
events, of memory in carrying out highly complicated excursions, 
and also power to display emotion. 

On a physical basis, all such activity in the fish is explained as 
being the result of a series of “reflexes.” If a fireman is awakened 
in the middle of the night by a gong he automatically jumps out 
of bed, pulls on his trousers, shirt, socks, shoes, slides down the 
brass pole, etc. This sequence of acts, initiated by the gong and one 
act giving rise to the next, might also be thought of as “reflexes.” 
Further, were such a pattern of actions “inherited,” we might ex- 
pect that a fireman’s child, hearing a gong for the first time, would 
go through the same procedure (assuming that the clothing, pole, 
etc., were at hand). 

Strangely enough, scientists believe that not too dissimilar pat- 
terns of behavior can be inherited among the lower animals. In 
the fish, a certain stimulus produces a certain reflex, etc., the chain 
of events often resulting in highly complex actions. These reflexes 
may be provoked or conditioned by environment and by imitation 
of others. Nevertheless, widely separated individuals among fish 
as well as other lower animals often act in the same way, so on 
the whole the various behavior patterns which are characteristic 
of the different species with respect to sex or food-gathering, or nest- 
building among birds, dam-building among beavers, honeycomb- 
building among bees, etc., may be considered as due to something 
inherited rather than acquired. 

All this, and studies of humans themselves, have led to the be- 
lief that there may be laws of inheritance which apply to human 
behavior just as there are laws of inheritance that apply to our 
physical structure. Or, in other words, that there are genes which 
govern our temperament, disposition and behavior in the same way 
that there are genes for other characteristics. 

It is when we try to isolate and identify these “behavior” genes 
in the light of our present limited knowledge that we encounter 


difficulties. Much more than in the case of mentality, human be- 
havior is influenced and modified by training and environment, 
and any comparison between humans and lower animals falls short 
if it does not take this into account. As just one factor, our young 
remain helpless and dependent for a much longer time than do 
the young of any other animals. This long formative period of 
itself offers great opportunity in humans for shaping and perhaps 
distorting whatever inherited behavior patterns we may have. 

A girl is blond, blue-eyed, beautiful. Does a certain kind of tem- 
perament, character, behavior, go with that combination? Or does 
beauty in a girl produce a certain kind of environment about her 
which in turn molds her temperament and behavior? Here is where 
we must consider two kinds of environment—the external environ- 
ment which one encounters in any society, and the internal en- 
vironment which a person himself or herself creates. 

If a girl is beautiful as a child, she evokes quite different re- 
sponses and attitudes toward her than does the homely girl, and 
it would be strange indeed if her character were not affected. As 
she carries her beauty into maturity its effect on others—family, 
friends, masculine admirers, employers—increases and reacts again 
on herself. To the extent that these experiences and effects are simi- 
lar in all beautiful girls, it may be said that beauty is accompanied 
by a certain type of personality. The mistake would lie in assum- 
ing that the genes which tended to produce beauty also produced 
this temperament. 

Consider the case of the very tall girl. If her growth comes early, 
she must begin dressing as a grown-up before her classmates do. 
The discrepancies between her mature appearance and her im- 
maturity of experience may tend to produce in her a sense of mal- 
adjustment. Finally, the man problem comes along. The tall girl 
encounters difficulty in finding dancing partners, boy friends or 
mates. Often forced to be with herself a great deal, the tall girl 
may turn to reading and reflection, and become more sober and 

The very fat girl, always a target for pleasantries, may build up 
a defense by being the first to laugh at herself in order to disarm 
others. You may have observed that at costume parties big, fat 


girls often dress in “kiddy” costumes, to expose fully the plump- 
ness of their arms and legs, just as do the fat ladies in the circus. 
Never feeling themselves quite at ease, it would not be surpris- 
ing if fat girls as a class are emotionally not too well balanced. 

Similarly, very short girls appear in children’s costumes (those 
of little boys or little girls). In buying clothes they must patronize 
the junior-misses’ or even children’s departments. Men good- 
naturedly toss the little girls about, bigger girls baby them, people 
constantly jest about their size. These and other factors may make 
the small girl hypersensitive, high-spirited, high-strung. 

The effects of extreme homeliness on a girl should be obvious. The 
lack of welcome she receives, the indifference of men, the greater 
difficulty in finding jobs and in making a place for herself in society, 
the many unpleasant experiences she encounters, could well explain 
certain aspects of her temperament; and yet most people confuse the 
resentfulness, the anti-social attitude often displayed by homely girls 
with something basic in their make-up. 

A psychologist would extend this type of analysis to every other 
kind of person. In men, very short men, like very small girls, tend 
to be sensitive and eager to dominate; handsome men, to whom 
many things come too easy, may often be ne’er-do-wells. So too, great 
physical strength on the one hand or sickliness on the other may 
each be correlated with a type of personality. 

Now all of these cases (which may conjure up pictures of some 
of your friends, and perhaps even of yourself) are important because 
they illustrate the fact that appearance can influence personality and 
behavior. If, then, appearance in turn is due to certain genes, we 
might conclude that a child who inherited genes which make him 
Took like his father would automatically grow up to act like his 
father. In other words, that people who looked the same would act 
the same. But this is not necessarily true. 

A person with one type of “personality” in one environment might 
have developed into quite a different person in another environ- 
ment. Consider our girl types again: If our tall girl found herself 
in a society of uniformly tall people, she would no longer be mal- 
adjusted; nor would the short girl be exceptional in a society of 
very short women, nor the fat girl in a country of fat women. The 


blonde with the streamlined, hipless figure who may be so popular 
in New York society might quickly develop an inferiority complex 
in a Turkish outpost where plump women are preferred. 

So much for certain kinds of Jooks that alter actions. But there are 
also certain kinds of actions that alter Jooks. In fact, human appear- 
ance is much more plastic than is generally imagined. 

As every one knows, habits of occupation and of living may pro- 
duce marked differences not merely in behavior but in physical ap- 
pearance and facial expression, Scientists now have a term, “muscle 
tone,” which they apply to the degree of contraction of a muscle, 
pr in other words to the manner in which it works. ‘The “tone” of 
” muscle results from the way in which one habitually uses it. The 
face is a network of innumerable muscles, large and small, govern- 
ing every movement of the features. Through use and habit starting 
from infancy, every facial muscle develops its “tone,” its peculiar 
way of working, or relaxing. A person’s facial expression in repose 
or in action, therefore, would be the sum of his facial-muscle “tones.” 
Similarly, all acquired mannerisms of walking, moving the hands, 
posture, etc., would be due to the “tones” of the muscles involved. 

When we add to the muscle tones the effects of other living-habits 
—diet, sleep, work, etc——we can see why persons in the same occu- 
pation, farmers, policemen, firemen, teachers, clerks, etc—may de- 
velop certain similarities of appearance. Even more emphatically, per- 
sons in the same country or locality with similar habits and condi- 
tions may develop characteristics—of moving the hands, talking, 
walking, etc——which are erroneously assumed to be basic and 

To hark back now to the habit of associating a certain kind of 
appearance with a certain kind of personality, we find that inter- 
pretations may vary markedly with the locality or country. Why are 
villains depicted among us as dark-haired men with swarthy skins, 
sharp noses and heavy black eyebrows? Probably because in Amer- 

1 The imteresting theory has beén advanced that eating habits among various 
peoples or individuals may be influenced by inherited variations in the sense of 
taste. In support of this theory are findings (by Dr. A. F. Blakeslee and Prof. 
L. H. Snyder among others) that certain chemicals or substances taste differently 
to various individuals and that these taste reactions are apparently inherited. We 

have not stressed this point because there are as yet no data regarding the heredity 
6f taste reactions to any common foods—for instance, spinach. 


ica, and perhaps in England, the type was that of the foreigner who 
differed radically from the prevailing native stock. It is human to 
view strangers with suspicion; and we dare say that among many 
black-haired, dark-skinned people, the villains would be depicted as 
blond and light-skinned. 

There is also a tendency, in associating appearance with personal- 
ity, to resort to allegorical interpretation. “Black” connotes mystery, 
death, tragedy, and sinister influences; it is easy to see why vil- 
lains would be depicted as “dark.” And similarly why the Little 
Evas and the innocent heroines would be depicted as blond, blue- 
eyed and white-skinned. 

A radio psychologist recently made the assertion that all pop-eyed 
persons are talkative, and all people with deep-set eyes are reticent. 
This theory does not conform to fact. The “pop-eye” correlation is 
based on the idea that goiter or thyroid conditions frequently cause 
pop-eyes, and that often the “hyper-thyroid” person is given to ver- 
bosity. But this far from implies that all people who are hyper- 
thyroid types or all persons with goiter are talkative, or that all per- 
sons with pop-eyes produced by other causes are also talkative. 

The idea that protruding eyes mean “protruding” personality or 
vocal assertiveness, may have as its converse the idea that deep-set, 
receding eyes connote reticence or “receding” personality. A similar 
notion is that receding chins indicate a “receding” or weak character, 
while a protruding jaw indicates pugnaciousness and bravery. Sci- 
ence, however, offers nothing to substantiate this. Surely, there is no 
evidence that peoples with more receding chins, such as American 
Indians and Chinese, are inherently less brave than big-jawed Euro- 


Although countless detailed studies have been made and are in 
process of being made, we are not yet able to point to any particu- 
lar type of body, face, head or skeletal structure in normal indi- 
viduals as definitely correlated with any given type of behavior. The 
German psychiatrist, Ernst Kretschmer, some years ago presented 
evidence that dementia praecox cases were most frequently found 
among long and thin persons of the “asthenic” type, and that manic- 
depressives were most frequently of the short and rounded “pyknic” 
physiques. But his claims of other correlations, in non-pathological 


cases, between physical structure and behavior have not stood up. 

Glandular disturbances or nerve and mental disorders obviously 
can result in abnormal behavior. It is therefore logical to suppose 
that inasmuch as the glands, through their hormones, are known to 
influence greatly both physical development and emotional states 
among all individuals, the degree in which “gland” genes might vary 
among even normal persons would have some bearing on their dif- 
ferences in behavior. This implies not that “gland” genes directly 
determine personality, but that they are important influences in 
its production. 

According to Professor Gordon W. Allport, Harvard psychologist, 
a newborn infant can be considered as lacking personality, for per- 
sonality must be thought of as developing from birth onward. But 
the child is by no means a mass of clay in this respect, to be molded 
solely by the forces of environment, as the extreme “behaviorists” 
formerly maintained. Forces inside every child—implanted by hered- 
ity—work together from the very beginning with forces from the 
outside to develop its personality. 

Psychologists may be adding nothing to what mothers know when 
they report that one can detect distinct differences in personality 
among the youngest infants. Alertness, dulness, restlessness placid- 
ity, enterprise, laziness, fretfulness, calmness, responsiveness to peo- 
ple about them or indifference—these and many other traits in vary- 
ing degrees may be noted among infants whose environments are 
approximately the same. In fact, in these early manifestations some 
authorities see portents of the child’s future personality. 

However, whatever inner “personality” factors there are can be 
considered only as related to potentialities. That is, one must con- 
sider each individual as having from the beginning not a definite 
personality but the potentialities for a wide range of personalities— 
the form which his personality will take depending upon the circum- 
stances encountered. Nor can we consider that the personality will 
take any fixed form. A moment’s thought will make clear that one’s 
personality is never constant and may undergo continuous changes. 
But again, when we remember that there are “time” genes which 
do not come into play until given stages in a person’s life are reached 
—genes acting at puberty, maturity or old age, such as those for 


baldness, mental defects, many diseases, etc—it may readily be 
gathered that heredity as well as environment acts throughout life 
to effect such personality changes. 

(An interesting note in passing is the observation by Prof. 
Jennings that the personalities of dull persons may be influenced 
more by heredity than those of bright individuals, because the lat- 
ter are more responsive to their environments.) \ 

As for the role of environment, the most significant evidence we 
have is provided by our study of identical twins. If there are dif- 
ferences in personality between identical twins, with exactly the same 
genes, these differences must be directly attributed to environment. 
Especially illuminating, then, would be a study of five individuals 
with the same genes. So we turn again to those invaluable little 
aides of science, the Dionne quintuplets. 

After two years of careful observation, Drs. W. E. Blatz and 
D. A. Millichamp, psychologists of the University of Toronto, re- 
port that the quintuplets show variations in behavior, personality 
and temperament, even greater than they do with regard to their 
physical make-up and mentality. However, it is the physical dif- 
ferences, as we saw, that form the point of departure for their other 

The personality studies of the Dionnes were made along the 
most approved scientific lines. The quintuplets were compared in 
their social behavior both with the standards for average children 
of their own age and in relation to one another. The observers 
noted every action and incident which had a social significance— 
that is, which threw some light on the attitude of any one of the 
quintuplets toward others in the group, and their responses in turn 
toward her. If any child did something to attract the attention of 
the others, or if she showed more interest in one sister than in an- 
other, this was carefully recorded. And these were the findings: 

Yvonne is the most popular one within the group. Although the 
most advanced in general development, she is nevertheless the least 
socially aggressive, quite good-naturedly letting the others take the 
initiative in play. So distinct is her personality that she has been 
dubbed by the psychologists “The Matriarch.” 

Annette is the most aggressive. She clamors for attention and is 


watched the most by the others. This attention that she receives, 
say the psychologists, stimulates her to “further aggressive social be- 
havior in order to satisfy the developed need of an audience.” 

Emilie is a happy-go-lucky little individual, not caring much 

“who starts what or does which,” and is the most self-sufficient of 
the five. 

Cecile is set down as the “unknown quantity,” her behavior with 
regard to the others being the most variable and most unpredictable, 

And finally we have little Marie—Fortune’s Stepchild of the quin. 
tuplets. Starting off with physical handicaps, these led to handicaps 
in mentality and achievement, and these in turn now conspire against 
her socially. The baby of the group, she is the least skilled in manipu- 
lating materials, in play and in enterprise. Poor little Marie! She 
tries so hard to initiate contacts, but only motherly Yvonne pays 
much attention to her. 

Let us stop a minute. We have almost forgotten that we are 
dealing with “identical” quintuplets who look so much alike in 
the pictures that we cannot tell them apart. And yet here are these 
striking differences in personality among them—Yvonne at one 
extreme, Marie at the other—despite the fact that all five carry 
exactly the same types of whatever genes there are for behavior, 
personality and temperament. 

Is it any wonder that we have such difficulty in determining 
how much of an ordinary individual’s personality is inherited or 
“basic,” and how much is due to environment? 

What, for instance, would we call the “basic” personality of the 
Dionnes, even if we considered them all together as a group? What 
has been the effect upon them of their training, their association 
with good Dr. Dafoe and their nurses, their consciousness of being 
watched, and all the other unusual influences in their “hothouse” 
environment? The psychologists cannot help wondering what the 
personalities of the quintuplets would be now (a) had they all 
been separated at the beginning and reared in different environ- 
ments, (b) had they been kept together, but reared in free asso- 
ciation with other children, or (c) had they been left with Papa 
and Mama Dionne, to be reared any which way with the large 
brood of older brothers and sisters. 


Of this there seems to be no doubt, that the personalities of the 
quintuplets will always be distinct from one another, the differences 
probably increasing with the years, and that they would have been 
different and distinct under any circumstances. In short, that the 
environment can never be exactly the same for any two individuals, 
and that even with exactly the same genes present, the slightest 
environmental changes can produce differences in personality. 

On the other hand, emphasis must also be placed on the evi- 
dence, provided by many other twin studies, of the effects of 
heredity. After long and detailed study of large numbers of twins, 
Professor Newman has reported: 

Identical twins do show marked similarity in behavior and per- 
sonality which cannot be entirely explained on the ground of similar 

Even when reared apart, identical twins, although differing in 
many ways, are nevertheless more alike than fraternal twins reared 
together, tending to prove that there is a genetic basis for “personal- 
“At the same time, the resemblance in personality between any 
two identical twins—whether reared together or apart—is much less 
than their similarity in physical characteristics. Or, to sum up 
Prof. Newman’s conclusions, on the basis of the twin studies, it 
appears that physical characteristics are affected least by environ- 
ment; intelligence more; education and achievement still more; 
and personality and temperament the most. 

Among psychologists in general the belief prevails that of the 
various factors involved in producing personality, the likelihoods 
of their being influenced by heredity are as follows: 

Most likely to be influenced by heredity: Basic abilities, such as 
intelligence, speed of reaction, motor skills, sensory discrimination, 

Less likely to be influenced by heredity: ‘Temperamental traits, 
such as emotionality, alternation or evenness of mood, activity or 
lethargy, and other characteristics in which gland activity is con- 
ceivably involved. 

Least likely to be influenced by heredity (if at all): Attitudes, 

World Copyright, 1938, NEA Service, Inc. 


Ht., 3914 in. 39 in. 391% in. 391% in. 3914 in. 
Wt., 4014 lbs. 3614 lbs. 3934 lbs. 41 lbs. 3834 lbs. 

The early differences among the five, due to differences in pre-natal environment are here 
shown to have persisted. The photograph was taken in August, 1938, some months after 
their fourth birthday. Note the marked contrast between Yvonne, “‘matriarch’’ of the group, 
| and Marie, the ‘‘baby’’; also the fact that Marie and Emilie, the ‘‘twinned’’ pair, are still 
| closest in Measurements. 


stylistic traits, beliefs, values and other such characteristics in which 
training or conditioning are clearly major factors. 

To sum up this chapter, every trail of scientific evidence and 
reasoning points to the existence of genes which influence behavior, 
temperament and personality. Where, within the same family, 
under a similar environment, great differences in personality ap- 
pear among the children, we may ascribe these differences in some 
degree to different combinations of genes. We can also assume that 
some of the similarity in personality between parents and their 
children is produced by genes. But we are still unable to identify 
any of these genes, or to gage the extent of their effects, or to 
hazard any predictions as to what the personality of a given child 
will be on the basis of what we know about its parents. What is 
fully clear is that such genes as may be involved in molding per- 
sonality are highly susceptible to outside influences. We can there- 
fore hardly consider them as producing such distinct effects as do 
the genes for many physical traits which we have noted, or as 
chatting a definite course for an individual’s personality. 

Nor do we know of any other influences that can chart a fixed 
course for one’s personality. There are many myths and supersti- 
tions, and not a few pseudo-scientific theories, regarding the influ- 
ence of the stars, planets, atmospheric conditions and various cos- 
mic factors on the behavior, temperaments and achievements of 
individuals—all implying that a person born at certain times, under 
certain conditions, will have such and such a personality. Regard- 
ing these we can only say that science offers no corroborative evi- 
dence whatsoever. To discuss these “influences” at greater length 
would be like setting up stuffed dummies for the sole purpose of 
promptly knocking them down again. 

Neither through the genes, then, nor through other influences, 
are we prepared to say that any normal human being is “pre- 
destined” to act in any certain way. This still leaves open the 
question of “abnormal” behavior—such as criminality, which we 
consider next. 



Ticers and wolves are “killers.” Jackals and buzzards are scav- 
engers. Magpies and cuckoos are thieves. Leeches are parasites. If 
these and hosts of other animals were judged by human standards, 
we would say that they were all of them congenitally “anti-social.” 

But we do not hold the lower animals strictly to account for 
what they do because we do not credit them with the same sort 
of intelligence that we have, or with any will or conscience. We 
ascribe their acts to “instincts,” to uncontrollable impulses; we say 
“they were born that way.” On the other hand, what the himan 
animal does we like to think of as dictated by intelligence and 
reasoning powers. On this assumption, that what we do is done 
wilfully, are based all our existing codes of law and morality, of 
responsibility for our acts, with punishment for “bad” behavior 
and reward for “good” behavior. 

Are we entirely right? Disquieting theories have been advanced 
that many human criminals are no more responsible for their acts 
than are the lower animals; that they, too, are impelled by un- 
controllable impulses and inherited anti-social instincts. If this were 
so, it would be highly important for geneticists to ascertain the 
genes responsible for criminal behavior, so that these could be listed 
prominently among the “black” genes. 

Long before the mechanics of heredity was revealed, the belief 
was prevalent that the tendency to commit murder or crimes of 
every kind “ran as a taint” in certain families. Toward the end of 
the nineteenth century, the Italian criminologist, Cesare Lombroso, 
startled the world with his theory that there was a definite correla- 
tion between criminality and bodily constitution, and that various 

kinds of criminals were of specified physical types. Back of this 


lay the thought that one could be born predestined to a life of 

Lombroso’s theory did not stand up well under an onslaught 
of contradictory evidence, and was abandoned by most criminol- 
ogists and psychologists. Recently, however, some of the principles 
have been revived. One of our own prominent scientists, Professor 
Ernest Hooton, says his personal studies of criminals suggest that 
there is an unduly large proportion of very short fat men among 
sex offenders and an excess of tall, slender men among murderers. 
Others, pointing to the fact that there is every type represented 
among criminals and murderers, look skeptically at the “predestina- 
tion” theories. | 

Most closely approaching factual evidence are the studies that 
have been made of criminality in twins. Professor J. Lange, who 
studied twins in German prisons, reported that in almost every 
instance where one member of a pair of identical twins had 
taken to crime, the other had also become a criminal. What was 
more, the types of crime committed by the twins were the same, 
or closely related. Among fraternal twins (who had different heredi- 
tary factors) he did not find a corresponding similarity. All this 
would tend to indicate that heredity played an overwhelming part 
in criminality and that the criminal twins had an inborn tendency 
to a life of crime. 

Lange’s work, which was based on a limited number of cases, 
inspired further study of criminality in twins, including studies 
in the United States. These later studies with many more cases 
recorded modify somewhat Lange’s findings. They do indicate a 
much greater likelihood that identical twins will both become crimi- 
nals than that fraternal twins or any two ordinary brothers will both 
become criminals. But also, many cases are revealed where only one 
member of a pair of identical twins went astray, and where the 
other, with exactly the same heredity, did not. This rules out the 
possibility that crime is znvariably predestined, and suggests that 
slight differences in environment may make one twin a criminal 
while the other goes straight. It also suggests that in many in- 
stances where both twins become criminals, a similarity in their 

> i | 


Number of persons 

Killed in years stated, | 
1 CARON WR Mice Miele = ARON Ses | 
\ J f ! | | I 

per 100,000 population: 

United States ('35) 

Roumania ('33) 

Hungary ('34) 
Czecho-Slovakia ('35) Woes | 

Italy ('34) ) 
Switzerland ('35) } 
Belgium ('34) | Peas 
Canada ('35), Germany ('34) | 
N. Ireland ('35) Hs 7 
; _ *Homicides include not only murders : 
eae el but justifiable, excusable or unin- q 
P tentional killings. 
Holland ('34) | 
neces sae ee The year stated for each country 
path was the latest for which a report 
England, Wales P| was obtainable. . 
and Scotland ('35) ’ 

environment, and their close association with each other, may be 
responsible. | 

While the evidence as to the rdle of heredity in crime is meager, 
there is no such uncertainty regarding the influence of environ- 
ment. Consider the most serious of crimes, murder: 

The murder rate in the United States is far above that of any 
large European country. For homicides (which include manslaugh- = 
ter) the rate per 100,000 population in large American cities is | 
almost twenty times higher than in England and Wales and about | 


three to four times higher than in Germany or Italy, with the 
rates for other countries-somewhere in between. 

Knowing that the hereditary factors of the people of the United 
States can be no different than that of their European progenitors, 
we are forced to conclude that there is something in the environ- 
ment of this country which produces more murders. This becomes 
even clearer as we examine comparative murder statistics within 
the United States itself: ; 

In 1936 there were no murders in such fair-sized cities as Daven- 
port, Iowa, Lynn, Massachusetts, and Berkeley, California; only g 
murders each in Boston and Milwaukee; and 118 murders in At- 
lanta, and 70 in Birmingham, Alabama, each of these last two 
cities with about one-third the population of Boston. Certainly an 
uneven distribution! 

Almost uniformly, the homicide rate in southern cities is over- 
whelmingly greater than in our cities elsewhere—including Chicago 
and New York. (None of the ten largest cities of the country, in 
fact, are in the list of the thirty with the highest murder rate.) 
The high murder rate among Negroes in the South has a bear- 
ing on the situation, but by no means accounts for all of it, be- 
cause the murder rate among southern Whites is also far higher 
than among Whites elsewhere. 

Thus once more, as no one would claim that the Whites of 
the South have a much more “murderous” heredity than those of 
the North, or that, comparing cities elsewhere, the people of Den- 
ver, Colorado (with a murder rate of 10 per 100,000), are by heredity 
five or six times as murderous as those of Boston and Milwaukee, 
we must look for an explanation to environmental differences. And 
we can readily find it. Wherever living conditions, poverty and 
ignorance are the worst, politics most corrupt, graft most rampant, 
the police most inefficient and the courts most lax, there the mur- 
der and crime rate will be the highest. 

Perhaps you remember this story: 

In a “hell-roaring” mining town of Wild West days, there was 
a commotion one evening. An old “Forty-niner” stuck his head 
out of a barroom and saw his son being led to jail by the sheriff. 

“Hey!” he called out. “What’s my Willy done?” 

Oo} Naeay 

oe te "1084 
a. lO =u0"4S OH 


Oan‘i2) Ax!D 



; ee om. 

ae OAD 3 
oie » we we es aH ha 
Puowiyrie — 69 ALAS] (8) O quodu3ang 
3 ; — ie wr) 
wes Wizz) SHH 
piud3po\tud a ye obp>iu> 
Ax19 ~ anomity 
yao, om : 
Suoysog o1%3576 sijodpsuuiy 
elt pulrqtog 44910 

‘suoljeindod saya 0} uotysodoid 
ul (spoyzows je Aq) suapunus oyes1p 
“ul ,sun6,, jo sozis SAILEIOY “GES 
Ul sdapsnu yo Jaquunu Moys seunbi4, 


osty | 


. s23buy $07 
Bas) | 
3 &® 
a sO 
| MOTs 
IHL JO Be) wuoy 

dVW ,IGUINW, V eel) ae 


The sheriff yelled back, “He got mad and killed one of them 

Eastern dudes!” 

“Shucks,” said the old-timer, going back to his tippling. “I 
thought mebbe Willy’d stole a horse.” 

This is not so far-fetched. Horse-stealing was a hanging offense 
in the frontier days, when a murder was often looked upon as 
an indiscretion. A not too dissimilar easy atttitude toward murder 
on the part of juries today, coupled with lack of restriction against 
“totin’ a gun,” has a lot to do with high murder rates, not only 
in individual sections of the country but in the United States as 
a whole compared with European countries. No one doubts, for 
instance, that the tendency of our chivalric juries to all but pin 
a medal on fair murderesses, after they have dutifully recited “.. . 
He struck me... then everything went dark” has acted as a 
“go ahead” signal for many whose husbands or lovers prove an- 

Although it might appear obvious that environment is to blame 
for differences in murder rates between one group of Americans 
and another, or between Americans in general and Europeans, 
there is nevertheless an undercurrent of belief that differences in 
murder rates among various nationalities in our midst are due to 
heredity. This belief was one of the important reasons for check- 
ing immigration and fixing quotas, it being felt that many of the 
immigrant peoples (especially those from southern Europe) were 
by nature predisposed to criminality. 

How true is it, for instance, that Italians are more “hot-blooded,” 
and therefore more easily moved to murder or crime in general 
than other people? Statistics do show that in certain large cities 
there is a higher percentage of murders by Italians than by native 
Whites of British or German descent. But further investigation 
will show that the comparison is unfair, because the mass of Italians 
in these cities live under conditions far more unfavorable than do 
most of these others. 

We also might find that many of the murders by Italians here 
were committed by members of the old Mafia or Black Hand who 
came to our shores and who had no more in common with other 
Italians than some of our native gangsters have with other Amer- 


icans. As a final commentary, an elaborate study of Italian con- 
victs in western Pennsylvania prisons has resulted in these con- 
clusions: That crimes of violence: are not a racial trend of the 
Italians; that the crime rate among second-generation Italians is 
not notably greater than among other native Whites; that the 
Italians in the area covered by the survey were not professional, 
but rather accidental, criminals, their crimes being the result of 
factors that generally are conducive to crime—want, unemploy- 
ment, low mentality, etc. 

Negroes, too, are popularly thought of as more “hot-blooded” 
and inherently criminal than Whites, but it is now being shown 
that where their crime rate is high, one should look first to 
environment instead of blaming heredity. If bad conditions can 
explain high crime rates among Whites, the immeasurably worse 
conditions under which Negroes live can explain a far greater de- 
gree of criminality. In Birmingham, Alabama, where illiteracy 
among Negroes was decreased one-half, the murder rate was also 
decreased one-half. 

The whole question of crime in relation to our foreign-born 
was thoroughly investigated by the National Commission on Law 
Observance and Enforcement, in 1931. Studying the high delin- 
quency areas, or slums in American cities, the Commission found 
that while these areas were inhabited largely by the foreign-born, 
it was not the nationalities of the people, but the conditions sur- 
rounding them, that produced the high crime rates. Although the 
nationalities of the people in these areas changed almost completely 
over a period of twenty years, the rate of delinquency in these 
areas remained about the same. Furthermore, when the older 
national groups moved to more favorable sections, the delinquency 
among their children consistently declined. 

Coming back to murder, we are led to the conclusion that no 
group of people in the United States is by nature more murderous 
than any other, but that bad environment increases the murder 
rate in any group. This still leaves open the possibility that among 
individuals in the same bad environment, under the same condi- 
tions, there are some who will kill, while others will not, because 
of an inherited tendency teward murder. (Or, as some suggest, 


because of emotional instability or warped intelligence.) The dif- 
ficulty, however, in finding the genetic basis for any such “murder 
instinct” is the same as that we encountered with regard to cancer. 

The motivations for, and types of, murder are of every con- 
ceivable kind, just as are cancers. The fact that there was a mur- 
derer in several successive generations of the same family proves 
nothing. One might have killed in revenge, another for love, an- 
other in self-defense, and another while insane. In different cir- 
cumstances none of these murders might have been committed. 
Only when murder is linked with certain violent forms of in- 
sanity (paranoid psychosis) does it appear to have a definitely in- 
herent basis; that is to say, a demented individual may be im- 
pelled to kill for fancied slights or injuries. 

Back of the theory that there is a “killer” instinct in people, 
lurks the more ominous thought that war is a wholesale expres- 
sion of that instinct and is therefore inevitable. But yet entire gen- 
erations have grown up and passed on in many countries, such 
as Holland, Switzerland, Iceland, Norway and Sweden, without 
ever having gone to war. We can hardly imply that the present 
inhabitants of these countries have lost any possible “fighting” 
genes that their ancestors might have had. For peaceful as the 
Dutch, Swiss and Scandinavians may now appear to be, we know 
that in former times they were as warlike as any. In fact, not a 
nation, race or people anywhere in the world would be surviving 
today were it not that in previous times it had battled for its 

War, too, if considered as a form of “mass” murder, may be 
set down as depending for its expression on environment. Likewise, 
the “inevitability” of war must remain open to doubt until it can 
be proved that there is an inherited “murder” or “fighting” in- 
stinct in human beings. That there zs not is the belief of more than 
go percent of several hundred American psychologists who were 
recently polled on the question. 

Regarding other forms of crime or wrongdoing—burglary, theft, 
embezzlement, suicide, prostitution, sex-crimes, drunkenness, etc.— 
the rdle of heredity is being similarly minimized, the réle of en- 
vironment emphasized. 


Crimes in the theft category are obviously correlated with eco- 
nomic factors. While the “stealing point” in some people is lower 
than in others, if there is a “theft” instinct almost all of us can 
be said to have it in some degree. (Will all those kindly step 
forward who never stole fruit, flowers or candy when they were 
young? Who never filched a sign or gadget for their college room? 
Who never absconded with an ash-tray or hotel towel, or a Chinese 
soup-spoon from a chop-suey restaurant? Or who never, never 
beat the government out of any income tax?) There are, of course, 
thefts, swindles, and financial breaches of every kind, “harmless” 
and “serious,” “impulsive” and “deliberate,” but until we can ac- 
curately weigh all types in our moral scale we, will be hard put 
to identify “genes” for thievery. 

Prostitution, because it takes toll of so many millions of women 
throughout the world, has been thoroughly investigated everywhere. 
The most recent of the studies is that made by Dr. Tage Kemp in 
Copenhagen, where all common prostitutes must be registered. He 
found, as investigators have found almost everywhere, including 
the United States, that many of the prostitutes are mentally de- 
fective, some of them psychopathic; that most of them had been 
brought up in the very worst surroundings; and that many had 
had drunken fathers and some, mothers or sisters who were pros- 
titutes. In a number of cases, however, the women came from 
fairly good homes, so bad upbringing cannot be considered as suf- 
ficient in itself to explain their delinquency. And in many cases, 
also, prostitutes are of high intelligence. In New York City, in 
fact, Dr. Walter Bromberg, criminal court psychiatrist, reports that 
he has found prostitutes no different mentally or pei 
from the average run of women. 

As Dr. Kemp points out, his information relates principally to 
the poorer type of prostitute, as the “higher type,” who does not 
ply her trade openly, is not registered. On the whole, his studies 
bear out previous conclusions that prostitution is largely the prod- 
uct of bad environment. But again we must keep in mind that 
not all women in the same environment, even those mentally defi- 
cient or psychopathic, become prostitutes. There is still the possibil- 
ity that heredity may produce a weaker will or lower moral re- 


sistance which may increase the chance that a woman will turn 
to prostitution under given conditions. But those conditions have 
to be there first. 

Because this question is frequently asked, it may be said that 
neither Dr. Kemp’s studies, nor any others, show that there is any 
basic sexual difference between prostitutes and other women. Few 
of those studied by Dr. Kemp were oversexed or perverted. In fact, 
many authorities incline to the belief that prostitutes are more 
often undersexed and that their comparative lack of emotion and 
indifference to sex relations facilitates their taking up and carry- 
ing on their pursuit. From this, and the preceding observations, 
it may be concluded that no inherent constitutional basis for the 
“oldest of professions” has yet been established. 

Suicide, included spiritually if not legally among crimes, has also 
been said to “run” in families. That the suicide of a parent may 
induce morbidity which might influence a child to take the same 
step is not hard to see, nor need one dispute the fact that an un- 
balanced mind (which may be inherited) may lead to the suicide 
of several individuals in the same family. But that there is any 
hereditary tendency toward suicide itself is still to be proved. Every 
available fact, on the contrary, would indicate that the causes of 
suicide are predominantly environmental. The suicide waves in the 
United States following the stock-market crashes and in Austria 
following the Nazi invasions, and the general rise in suicides every- 
where in recent years, bear sad testimony to this. In “normal” times 
suicide (in the words of one writer) is “a phenomenon of social 
isolation.” The highest rate is among divorced persons, with next 
in order those who have never married. 

The attitude toward suicide, as toward murder, may also be 
considered a factor in its frequency. Where the concept of suicide 
as a serious crime is prevalent, suicides are at a minimum. The 
recent rise in suicides both here and abroad, often explained as 
being due to increased tension of modern life, may be equally 
ascribed to growing “individualism” and a modification of the at- 
titude toward self-destruction. 

This brings us to the point that “anti-social” acts of human 
beings in general may be motivated less by any inherent tendencies 


than by the atmosphere in which people are reared. The whole 
subject of “right” and “wrong-doing” rests on the shifting sands 
of prevailing social viewpoints. Murder may at one time and place 
be condemned and in another time and place be extolled as a noble 
deed—as, for instance, the assassination of Premier Dollfuss of Aus- 
tria. Prostitution has been and still is considered among some peo- 
ples a “respectable,” or even a noble calling. Suicide was looked 
upon as an honorable deed in earlier civilizations, and is still 
thought of as such among the Japanese. Theft is a virtue among 
certain Bedouins. There is probably not a crime, social breach or 
type of dereliction on our police registers that in certain locali- 
ties in the world, or among certain groups within our own coun- 
try, is not considered quite proper. 

To sum up: Genetic studies of the possible role of heredity in 
human wrong-doing bog down because of our inability to disen- 
tangle any inherent crime tendencies from the environmental factors 
in which they are enmeshed. We have no proof of a direct 
correlation between any specific crime and any given type of body 
structure, physical characteristic, mental state or racial identity. On 
the other hand, it seems to be clear that an atmosphere of degrada- 
tion, ignorance and poverty will breed crime and that lax prosecu- 
tion or public indifference to any type of crime will foster its 

So, where the hereditary factors are so vague, and the environ- 
mental factors so clear, it would seem that if we want to do any- 
thing about crime we should worry less about what is inside of 
people and more about what is outside of them. 



No phase of human behavior is more important than that of sex, 
and none presents greater difficulties when we try to find the 
hereditary basis for such of its various manifestations as are con- 
sidered “abnormal” or “anti-social.” 

From what we have already learned, there is every reason to be- 
lieve that basic patterns of sex behavior are inherited by human 
beings just as they obviously are by the lower animals. But on the 
other hand, human sex behavior is so highly variable and so strongly 
influenced by training, laws, taboos, regional customs, habits, etc., 
that it is extremely difficult to ascertain what may be due to in- 
born tendencies and what to environmental influences. Neverthe- 
less, advances have been made in clarifying many phases of the 

Like any other characteristic, sexual behavior in either men or 
women can be judged only in relation to accepted standards. Almost 
immediately, then, we are confronted with the fact that there are 
no scientifically determined standards for “normal” human sexual 
behavior. "Chere is not even a real definition available for what con- 
stitutes “masculine” and what “feminine” behavior, or what is 
“manly” and what “womanly.” Look up these words in your dic- 
tionary and you will find that “manly” and “masculine” are de- 
fined approximately as “having the characteristics of a man,” and 
“womanly” and “feminine” as “having the characteristics becoming 
to woman.” But the views as to what these characteristics might 
be have changed from age to age and continue to vary with each 
country and each locality. As Margaret Mead showed in her studies 
of primitive peoples, many of our accepted patterns for masculine 
and feminine behavior are completely reversed among certain tribes. 
And within our own United States, and in our own time, we have 



| | Whether You Are a Man or a Woman 




Exploit and adventure 

Outdoor activity and physi- 
cally strenuous occupations 

Machinery and tools 

Science, physical phenomena 
and inventions 

Business and commerce 







Blunt of manner and speech 




Domestic affairs 

Art, literature, music 

Sedentary and indoor occu- 

Ministering to the helpless 
and distressed 

“Moral" activities 







Sentimental and affectionate 

seen radical changes not only in the views regarding sex, but in 
sexual behavior itself. , 

It was clear that before any progress could be made in study- 
ing the subject there would have to be some standards to follow. 
So, as sequels to the “intelligence” tests and the “personality” and 
various other behavior tests, a series of “masculinity-femininity” 
(“M-F”) tests were recently devised by Prof. Lewis M. Terman and 
Catherine Cox Miles of California for measuring degrees of human 
sexuality. These “M-F” tests comprise a series of questions (the 
same for both men and women) to each of which an individual 
can give either a response considered “masculine,” or one considered 
“feminine.” Thus, an answer indicating physical callousness might 
be set down as “masculine,” one indicating tenderness as “feminine.” 


What do these pictures suggest? Check the word you 

think most descriptive of each: 

1. ax E 1. bow 
2. boat 2. chain 
3. chopper 3. footprints 
4. moon 4. tie 
1. brush G 1. baby 
2. centipede 2. buoy 
Stree 3. comb 3. lady 
4. teeth 4. valve 
1. flame H 1. chimney 
2. flower 2. coil 
3. snake 3. smoke 
\ / 4, worm 4. thread 
1. baby | 1. funnel 
2. bell 2. horn 
3. idol 3. jack 
4, incense 4. vase 
. boat J I. couch 
. door . 2. cow 
. hat 3. deer 
. stump 4. horse 


puza [uz] 2 [uz}usay 2a |uza] 2 [oat 2 
[3 fasfuaafaa] 2 fs] 3. fae pez] ass 

_ * From “Sex and Personality”, by Terman and Miles 


| Masculine: 



For every “masculine” response the individual is given a “-+-1” 
mark; for every “feminine” response a “—x” mark. 

Testing 4,000 individuals, Terman and Miles found that the 
“M-F” scores of male adults range from “+200” to “—100” (for 
inverts), with an average of “+52”; while female adults score 
from’ “~-100" to “+200,” with an. average, (ofM)—70. -alamatner 
words, the difference in “M-F” response between an average man 
and woman is quite great, revealing the expected distinction be- 
tween them in sexual personality. But in individual cases, some 
men (with the high “minus” scores) are revealed as being more 
“feminine” in their responses than a good many women, and some 
women (with the high “plus” scores) as being more “masculine” 
than many men. . 

Classifying men and women into various groups, we see some 
striking differences. The most “masculine” men—but remember, 
only on the basis of the Terman tests!—are college athletes and 
engineers; the least “masculine” men are artists and clergymen. 
And much to our surprise we find that policemen and firemen 
have the lowest “masculinity” scores in the occupational classes! 
The Terman-Miles study indicates that this is in line with the 
“feminizing” influence of social-welfare work, but also suggests that 
policemen and firemen are likely to be drawn from the ranks of 
men who are by nature lacking in marked mechanical interests 
and financial objectives, who are seeking job security and who are 
amenable to discipline (all considered “feminine” characteristics). 
In other words, the “M-F” tests would lead us to believe that our 
proud wearers of civic uniforms may really be sheep in wolves’ 

Among women, the most “feminine” are domestics, the least 
“feminine” are the superior female athletes. (Scores for all classes 
are given in the diagram opposite.) Thus, in both men and 
women, athletic pursuits are correlated with “masculinity.” But one 
should be careful not to confuse external appearance with _per- 
sonality, for various authorities have pointed out that the appear- 
ance of roughness or ruggedness presented by either a rawboned, 
swaggering male or by a heavy-set, homely female, may mask a 
soft, feminine nature; and that a delicate-appearing man, equally 

oo aes 


(How various classifications of men and women rank according to average scores int 
the ''M-F"' tests) 

(Degrees shown by ? (Degrées shown by 
"plus" signs) ‘minus’ sign) 
+100 Domestics —7, -JO0 
. Oe tices (Hignest Femininity) 
A ; , Stenographers, 
+90 CH ghest masculinity) Dressmakers, a 
3 Hairdressers 220 
4 Ava. 
Engineers, Architects Women in Arts, GO yroid 
+80 | Housewives, npg 
3 i High-school Boys Business Occupaths Re 
z Clicks, Secretaries] 4o-ola 
rofessions I Avg.29- 
Male College Students ale Lae e8 
(Average) | -710 
Lawyers, Salesmen, ; 
Bankers, Executives -60 
Women College 
Dentists, Teachers Students (Avirags) | -~50 
— Mechanical Occupations r ip 
OW Clerks and Merchants. Who's Who 
Building Trades -40 
( 5\ Farmers 
» S9& POP) We Who's Who" Men ~ Women Doctors x 
iE or Ph.D’s 
A +30 | 
(‘Oo Police and y -30 i 
| Men of Firemen 2 
(gen. pop) , by 
. U 
Journalists, Di Din ay Ae 
a ie y Artists Mal< Inverts 20 a 
“A Clergymen Superior 
4 Womtn 
“ Athletes 4 e 
7 Dip | 
M 1 
my 60 ( tra) 40 

Nee pope lation) ae 

(Based on reports by Terman and Miles in “Sex and Personality") 


with a pretty and petite girl, may sometimes be at heart as relent. 
less and daring as the steeliest soldier. 

Generally, however, physical factors do seem to play a part in 
molding sexual personality, and this is especially true of age. Study- 
ing their records, Terman and Miles report that both men and 
women tend to become more “feminine” as they grow older. At 
the age of 20, males average “M-F” scores of “+58,” but at 70 the 
average has gone down to “+3,” that is, 55 points in the direction 
of “femininity.” In part, this is ascribed to the “feminizing” 
effect of marriage and domestication. In females the change is not 
nearly so marked, the scores for females at 20 averaging “—75,” 
and at the age of 60, “—8g,” only 14 points of “femininity” greater. 

These tests are interesting, but it must be kept in mind that 
they record “masculinity” and “femininity” from an arbitrary point 
of view, influenced or conditioned by general standards. For in- 
stance, “courage” and “hardihood” are popularly linked with physi- 
cal activity. And yet the supposedly “feminine” artists, writers or 
musicians as a group are often required, in pursuing their careers, 
to cope with privation, insecurity and professional hazards that 
would intimidate many an average “masculine” man. A shy little 
“—yo0” dressmaker, casting herself adrift in marriage with some 
comparatively unknown man, may be proving more adventure- 
some than an Arctic explorer. The habitual “wallflower” going 
doggedly to a dance to face masculine slights, the stammerer get- 
ting up to make a public speech, the clergyman who takes issue 
with his “big-wig” deacons, these and many others may be con- 
stantly displaying on the social battlefield courage of the highest 
sort, which ordinary standards of “masculinity” may disregard. 

Like the intelligence tests, the “M-F” tests are the same for both 
males and females, also disregarding the fact that boys and girls 
are trained from infancy to act differently, and that throughout 
life males and females have radicaliy different environments. Thus, 
these tests do not gage basic sexual personality, as is clearly shown 
by the fact that the “M-F” scores, especially of men, change radi- 
cally with age. Nor do the tests attempt to measure the sex impulse 
of the individual—the functional aspect of sex which concerns so- 
ciety the most. 


The assumption has always persisted that degrees of intensity 
of the sex impulse have a hereditary basis. Some individuals (and 
some “races”) are popularly thought of as inherently more 
strongly sexed than others. Also, where there are unusual types of 
sex behavior, these too are spoken of as “running” in families. To 
the extent that sex-functioning is motivated by organs, glands and 
constitutional factors, it is not illogical to suppose that heredity 
may play a part in its various manifestations. But only where there 
is some easily recognized “abnormality’—that is, some marked 
deviation from what we consider “normal” sexual behavior—are 
we able to look for a hereditary basis. 

In devising the mechanism of sex, it has long been assumed 
that Nature had only one objective—to provide a means for propa- 
gation of the species. Among most lower animals, sex-function and 
reproduction are in fact synonymous. That this should also be so 
among humans has been the widely held belief in civilized so- 
ciety. Any manifestation of sex, or any exercise of the sex func- 
tions that adversely affects or prevents reproduction has therefore 
been considered anti-social and often, from the religious point of 
view, immoral. And most strongly has condemnation been directed 
toward that form of sexual behavior known as homosexuality, 
which swerves individuals away from relations with members of 
the opposite sex and inclines them toward relations with those of 
their own sex. 

The subject of homosexuality is not a happy one to discuss. Con- 
ditioned as most persons have been to avoid open mention of it— 
just as venereal disease was not discussed in polite society until 
recent years—they prefer to think of homosexuality as something 
far removed from their own lives. These facts—gleaned from lead- 
ing authorities—will therefore come as somewhat shocking: 

From 3 percent to 5 percent of all males everywhere are believed 
to be homosexual. (Active, or “overt,” homosexuality is implied in 
the case of men in the large cities. Elsewhere the percentage of 
“overt” homosexuals may not be so great.) 

In one of the largest American universities the medical staff re- 
ports that 4 percent of the students have homosexual tendencies. 
(By this is probably meant, also, homosexual interests.) 


{n the population at large, tt is estimated that an average of one 
man in every thirty is strongly enough inclined to homosexuality 
to find relationship with the opposite sex difficult. 

it might be added that while the number of female homosexuals 
is also considered far greater than is generally supposed, no defi- 
nite estimates can be made for them because homosexuality in 
women is much harder to trace than it is in men. 

With the revelation of this rather large proportion of individuals 
who would be considered by society as seriously “abnormal,” it 
becomes important to determine the basis for the condition. 

From a moral point of view, homosexuality has often been 
pointed out as the product of a degenerate civilization, a concomi- 
tant or a portent of the collapse of a nation. However that might 
be, we find undisputed evidence that it exists in regions where 
civilization has never penetrated, at widely scattered points through- 
out the world, and that, in fact, among many peoples it is a social 
institution as well recognized as marriage. When we link this with 
evidence that homosexuality is also found among the lower ani- 
mals we must begin to look for other than merely environmental 

As the first step in their studies, authorities point out that there 
are two kinds of homosexuals—the “active” and the “passive.” In 
either sex it is the “active” homosexual who plays the part of the 
male, the “passive” one the part of the female. Thus the “active” 
male homosexual, even though he prefers the company of males, 
may be outwardly no different from other men; he may, in fact 
(as Prof. Terman’s studies have shown), be actually more “mascu- 
line” than the average man. Similarly the “passive” female homo- 
sexual, who plays the part of the female in relations with other 
women, is often intensely feminine in her behavior. Both “active” 
male homosexuals and “passive” females may therefore outwardly 
show no sign of abnormality and are difficult to recognize. 

It is the “passive” male, who acts like a female, and the “active” 
female, who often looks and acts like a male, whom we usually 
have in mind when we think of homosexuals. As we saw in the 
chapter on “The Twilight Sexes,” where a man looks and acts 
like a female, and a female looks and acts like a male, there is 


ground for believing that some glandular disturbance, or some 
other physical factor, is responsible. What is significant, then, is 
that many authorities today look upon all cases of homosexuality, 
whether “active” or “passive,” and regardless of outward appear- 
ance—so long as persons show a sexual preference for those of 
their own sex—as likewise having a constitutional basis which 
might conceivably have been inherited. 

Searching for evidence to bear out this latter theory, some inves- 
tigators (Hirschfeld, Van Romer, Walter Wolf, et al.) reported that 
35 percent of the homosexuals they studied came from families in 
which the trait had made its appearance in other members, often 
a brother and sister both being homosexual. 

But even more significant might seem the studies made of homo- 
sexuality in twins (if we can consider the limited number studied 
as fair evidence). Where one member of a pair of identical twins 
was a homosexual, in almost every instance the other twin was 
also a homosexual. This same correlation was not found to exist 
among fraternal twins, for where one was homosexual, the other 
usually was not. Dr. J. Sanders, Director of the Dutch Institute for 
Human Genetics, who recently summarized the reports on this 
subject, believes that they prove heredity to be an important factor 
in this condition. 

“Direct” inheritance of homosexuality hardly seems possible. 
What is usually implied is the inheritance of a tendency toward 
homosexuality which depends for its expression on certain environ- 
mental or psychological factors. Among both men and women, 
for instance, the lack of available members of the opposite sex, or 
for one reason or another any acquired aversion to relations with 
members of the opposite sex, would favor the expression of such 
a tendency. 

As for the homosexual tendency itself, the most probable basis, 
in the opinion of authorities, appears to be some glandular disorder 
which upsets the hormonal balance of the individual. In the lower 
animals we can readily prove by experiment that maleness and 
femaleness of behavior are biochemically determined. We have 
already seen how secondary physical characteristics in the sexes 


can be changed. Sexual behavior, too, can be radically altered by 
sex-gland operations, especially if performed at an early age. Even 
after maturity hens can be made not only to look but to act like 
roosters; and pigeons, mice, guinea-pigs and other animals of one 
sex can have their sexual behavior radically changed or turned 
into that of the opposite sex. All this has been done in laboratories 
time and again. 

Naturally, no such deliberate experiments have been performed 
on humans, but some not too dissimilar results have been noted 
from sex-gland operations performed through necessity, or from 
some pathological condition which altered the individual’s glands 
or hormonal balance. Also, the failure of the sex organs to develop 
properly, preventing normal sexual relations, has been cited as a 
motivating cause of abnormal behavior. Thus, with a constitutional 
basis indicated, it is believed that an individual might sometimes 
or often be born with the conditions which would predispose him 
or her to homosexuality or to some other deviation from “normal” 
sexual behavior. 

Summarized (according to prevailing views) the possible causes 
of abnormal sexual behavior would be these: 

1. Tendencies inherited through “abnormal” genes.* 

2. Pre-natal factors: Possibly infiltration of mother’s hormones 
(in a male); failure of some necessary elements for developing the 
glands to reach the embryo; some intra-uterine accident affecting 
development of the sex organs, etc. 

3. Some glandular or other upset after birth (probably during 
puberty) due to either internal or external causes, and impeding 
the proper development of the sex organs. 

4. Inversion through necessity—lack of available persons of the 
opposite sex. 

5. Psychic causes: Shock; adverse early conditioning; “fixations” 
and “complexes”; an instilled impression that sex relationships are 
immoral; fear in women of pregnancy or in men of fathering a 
child; ugliness in a woman, or homeliness or “unmanly” appearance 

1 Prof, Richard Goldschmidt has suggested that, based on his findings in certain 
lower animals, it is possible that homosexuality may result from an unbalance in 
the sex-determining genes, which may swerve a femaie toward “maleness” or a male 
toward “femaleness.” 


in a male, prompting avoidance of those of the opposite sex; some 
mental derangement; etc. 

Psychoanalysts and psychiatrists are inclined to psychic explana- 
tions for most cases of abnormal sexual behavior. While undue 
stress is often placed on psychological factors, it is not at all impos- 
sible for some experience or chain of experiences to so act upon 
the nervous system, and through it in turn upon the glands, as to 
produce the same effects which might come through direct physical 
action or change. Mental or nervous influences of this kind, which 
lead to physical disturbances, are called “psychogenic” factors, and 
have been known to produce a wide variety of conditions, ranging 
from eye symptoms to (in women) symptoms of pregnancy. Far- 
fetched as it might seem, it would therefore be conceivable that 
some early psychological disturbance in a boy and its corresponding 
psychogenic effect on his glands, might lead not merely to his 
acting like a girl, but to his looking like a girl, at least with 
regard to certain secondary sexual characteristics. Similarly, a girl 
might conceivably get to act and look like a boy. 

All this is, of course, still theory. Some authorities, notably 
Dr. George W. Henry of New York, report that homosexual 
patients may show deviations from the average in certain secondary 
sexual characteristics. In homosexual males, he observes, there 
may be the “feminine carrying angle of the arm, narrow hips, 
deficient hair on face, chest and back, feminine distribution of pubic 
hair, high-pitched voice, excess of fat on shoulders, etc.” In homosex- 
ual females, conversely, there may be characteristics usually associ- 
ated with males, “firm adipose tissue, deficient fat in shoulders, 
firm muscles, excess hair on face and chest, tendency to masculine 
distribution of pubic hair, underdevelopment of breasts, low-pitched 
voice, etc.” However, not all authorities have found this to be 
generally so, and certainly, the facts do not apply to all homosexuals, 
many of whom, as we have pointed out, are more masculine looking 
than average men, and if womea, extremely feminine in appearance. 

But whether or not abnormal physical factors are present, and 
regardless of how they originated (particularly with or without 
some hereditary basis), it appears clear that the expression or 


development of any abnormal sexual tendency is largely condi- 
tioned by environment. 

The most recent views on the subject have been expressed by 
Dr. Henry, who is at this writing engaged in a study of both 
male and female homosexuals. Here are some of his conclusions: 

“Personality forces and human interrelations contributing to a 
homosexual development cannot be traced to their ultimate sources, 
but it appears that the more closely a relative or friend is associated, 
especially in childhood, the more direct and decisive is the influence 
exerted, This means that the parents are in most instances chiefly 
responsible for the homosexual developments in their children. Not 
uncommonly a nursemaid, a brother or sister, a cousin, an uncle 
or an aunt may be involved in the distortion of a child’s psychosex- 
ual development. It appears, also, that boarding and non-coeduca- 
tional schools are more likely to favor a homosexual development. 
It is generally recognized that any segregation of the sexes is likely 
to bring about overt expression of latent homosexual desires. 

“Whatever these external influences may be, the majority of 
persons do not succumb to them and the minority who do succumb 
appear to be fundamentally predisposed. Some of this predisposi- 
tion may be inherited through the germ plasm, but in the cases 
studied thus far it is rare to find overt homosexuals in more than 
one generation. The tendency may nevertheless be inherited, be- 
cause the difference between latent and overt homosexuality is 
often very slight. Undoubtedly there are many instances of overt 
homosexuality in the family of which the informants are unaware.” 

So finally we come to this question: Assuming that an individual 
does reveal “abnormal” sexual tendencies, either in childhood or 
later, what can be done about it? : 

Where the condition is considered chiefly psychological or environ- 
mental, it might perhaps be best treated by a psychiatrist. Where 
morphological, due to a defect in the sex organs making “normal” 
relations difficult, an operation might help. If the tendency is 
revealed as having a glandular or hormonal basis, there is a possi- 
bility that its expression (in the future) may be repressed by hor- 
monal treatment, just as diabetes can be curbed through insulin. 
Indeed, many scientists are now at work identifying, isolating and 


even artificially producing the various hormones concerned with 
sexuality. But while hormonal treatments at this writing are being 
given to some homosexuals, it is still too early to report any positive 

All this is predicated on the assumption that homosexuality 


Angle, corresponding Straight Slightly knock-kneed Straight 

to knock-knees 


eee ee eee we we we ie 

should be cured and eliminated, an assumption well justified by 
the fact that in our preseut society this condition seriously militates 
against an individual’s adjustment and happiness. We need hardly 
enlarge on this phase of the subject. But at the same time, if it 
should be proved that this form of sexual behavior is a natural one 
with many individuals—that they have either inherited the tendency 
or acquired it without any volition—and that nothing can be done— 
or possibly even should be done—about it, the question arises as to 
whether the attitude of society should not be changed. 


Viewed from any standpoint, the subject calls for more sympathy 
and understanding than is now being given it by the public and 
by the law. In the light of what little we already know, the hound- 
ing of homosexuals as criminals, classifying them with degenerates, 
drug-fiends and insane, exhibiting them on the stage as freaks and 
subjecting them to scorn, ridicule and ostracism, seems hardly in 

keeping with a supposedly enlightened age. 



Tuinxinc back over the manv odd and various human character- 
istics that we have been discussing, you, undoubtedly have won- 
dered, “How did they all originate? Where did all the different 
kinds of people there are in this world come from?” 

Some eighty years ago Charles Darwin, claiming to have the 
answer for those very questions, threw a bombshell into thinking 
society with his theories of evolution. The resulting explosion set 
thundering against him avalanches of wrath from many quarters, 
which still echo as stray rocks of denunciation come rumbling 

The most violent of the reactions, as every one knows, was 
occasioned by Darwin’s implied assault on the Biblical story of 
creation. Darwin dismissed the idea that man was dropped into 
the world ready-made, and, on the contrary, advanced the belief 
that man was the end result of a step-by-step development from 
the most elemental living things through fish, reptiles, lower 
mammals, up to apes and then, by some “missing link,” to primitive 

All this may seem like an old story, but the fact is that the 
Darwinian theories are very much alive and are constantly being 
tested by scientists. The mass of evidence has now established most 
of Darwin’s theories as accepted fact. But in one conclusion it 
appears that he was most See wrong. And this involves the 
hoary old enigma: 

“Which came first, the chicken or the egg?” 

Or, from the standpoint of evolution, and thinking of chickens 
as symbolical of various species: Did a new kind of chicken arise, 
which then produced a new kind of egg? 




. First there was a I. 

certain kind of 

. It laid and hatched 

. Which produced off- ° 
spring similar to it- 
self. But— 

. As they developed, 
different environ- 
ments, habits, etc. 
produced changes in 
the descendants, 

. Which ACQUIRED changes | 

were communicated and 


. Until, with many | 

such changes in 
successive gen- 
erations added 
together, even- 
tually there re- 


. Which then produced the 
characteristic | 

So by this reasoning 




First there was a cer- 

tain kind of egg, 

iy . Which produced a 


. Which produced 

characteristic kind of 


But in some of these 
birds something hap- 
pened to produce 

Which resulted in their 

laying eggs with certain Pot 9 




birds differing from 
their parents. And as 
mutations continued, 

In the course of ages 
there resulted A NEW 

Which produced 

Thus, as science 

now indicates, 







Or did a new kind of egg originate, which then produced a new 
kind of chicken? 

Darwin held with the first theory. He took it for granted, as did 
almost every scientist until the gene mechanism was revealed (long 
after his death), that heredity, and with it “upward evolution,” was 
a blending process. By such a process the improvements or changes 
that each generation made in itself would be added to and blended 
in with those of the preceding one and the combination passed 
along to the next generation. Thus: 

1. Giraffes got their long necks by stretching higher and higher 
for choice leaves on trees, each generation benefiting by the stretch- 
ing done by their parents. 

2. Apes developed their brains and muscles be the effort of 
keeping up with their respective Joneses, and passed on their 
accomplishments to their offspring. 

3. And, conversely, in various species, organs became atrophied 
or lost through disuse, the classic example being that of the fish 
who swam into dark caves and by staying there generation after 
generation eventually gave rise to a race of blind fish. 

All this summarizes the theory of the inheritance of acquired 
characteristics, which as we said at the very beginning of the book, 
has been completely discredited. Darwin, however, believed it, and 
so did most of his contemporaries. But then some of them began 
to think about it. Why hadn’t the principle worked with regard to 
the binding of feet by the Chinese, circumcision by the Jews, tattoo- 
ing by the savages, and the many other changes made by people 
in their bodies, through customs, habits, etc., for generation after 
generation—with no effect on their offspring? Skeptics among the 
scientists began to experiment. August Weismann (in 1880) 
gravely cut off the tails of mice for twenty successive generations, 
but in the last litter—just as he expected—the mice showed not 
the slightest shortening of their tails as compared with their an- 

The “cave-blindness” theory was tested by keeping flies in pitch- 
blackness for fifty successive generations; and at the end, once again, 
the last batch of offspring, when born into the light, had just as 

normal eyes as ordinary fruit-flies. 


What about accomplishments in mentality and behavior? In- 
numerable experiments have since been performed by geneticists 
in training successive generations of animals to do certain things 
or act in certain ways; and yet no effect of this training shows in 
their offspring. (Pavlov thought at first that he had produced 
hereditary “reflex” improvements in mice by training, but later 
discovered that his conclusions were erroneous. In experiments of 
this kind, very often, it is not that the animals become more 
responsive but that the investigators become more adept in training 

Could a child inherit the habit of drunkenness from a drunkard 
father? Geneticists kept generations of mice, rabbits, guinea-pigs 
and poultry virtually stupefied with alcohol. There wasn’t the 
slightest evidence that such alcoholization produced any changes 
in the genes, although, true enough, when the mother was alcohol- 
ized, some of her weaker offspring were killed off in embryo, so 
that successive generations were in some cases actually stronger. 

The experiments made along these lines run into many hundreds. 
Finally, as perhaps the best evidence, geneticists stopped to reason: 
Recessive genes, paired with dominants, may be carried hidden for 
generations in bodies of persons with entirely different character- 
istics than those which the recessives tend to produce, and yet 
these genes are never affected. The blue-eye gene isn’t changed if 
coupled with a brown-eye gene and made for a lifetime 
in brown eyes. No “normal” gene of any kind is affected by 
living in an “abnormal” body; and no “abnormal” gene is “normal- 
ized” by living in a normal body. This in itself is held prima facie 
evidence that the internal environment of an individual cannot 
change his genes. 

As Prof. Thomas Hunt Morgan has summed it up, the belief 
in the inheritance of acquired characteristics is not based on scien- 
tific evidence, but on the very human desire to pass on one’s 
acquisitions to one’s children. 

If, then, the material for evolution was not provided by acquired 
characteristics, from where did it come? It probably came—almost 
all geneticists are now agreed—through spontaneous changes in 
chromosomes which we have already referred to as mutations. 


Darwin himself was not unaware that new characteristics inex- 
plicably cropped out in living things. But he did not believe that 
these happened often, and not knowing anything about genes, he 
attached little importance to them. Today, however, the entire 
concept of evolution centers about mutations. 

As geneticists look back, they see that mutated genes must have 
been responsible for innumerable new characteristics in all kinds of 
animals and plants within the last few hundred years. In 1791 a 
Massachusetts farmer found in his flock a peculiar lamb with a 
long sagging back and very short legs. It offered to him a distinct 
advantage: It couldn’t jump the fences and get away. So from this 
single mutant (of course he didn’t think of it as such) he bred 
the strain of sheep known as Ancon, which was so popular for 
many years and is still extant. 

In 1889 a hornless Hereford calf appeared in a Kansas herd, 
and from this has been bred the present “polled” (hornless) 
Hereford cattle, valued because they suffer fewer injuries than 
horned cattle. 

The list of comparatively recent mutations recorded among all 
sorts of animals could be greatly extended. Vastly more numerous 
are those that have been observed in the plant kingdom even within 
our own time. Many of these have given rise to unusual new types 
of flowers or of highly desirable fruits, vegetables and grains. 
Geneticists believe, also, that mutations of various kinds have taken 
place in human beings in our own times and are still taking place. 
Especially interesting is the recent theory that the gene for hemo- 
philia which Queen Victoria passed on to her descendants arose in 
her through mutation. 

But what causes gene mutations? They happen so rarely under 
natural conditions that geneticists had little opportunity to find out. 
Even among the carefully watched Drosophile, tens of thousands 
of flies had to be counted for every mutation that was found— 
usually of an almost imperceptible kind. One had to sit and wait 
for a mutation to happen, and there wasn’t a clue as to when 
or how. 

Then, in 1927, came the epochal discovery by Prof. Herman J. 
Muller that zf fltes were exposed to X-rays, the mutations would 


occur about 150 times as often. Immediately, under X-ray bombard- 
ment, mutations in the Drosophila began coming thick and fast. 
Thus Prof. Muller’s discovery led to the speculation that perhaps 
some sort of natural emanations or atmospheric disturbances—for 
instance, cosmic rays—produced the mutations in nature. Flies were 
taken up into different altitudes, or into mines or regions. where 
natural radiations were known to be more intense, and, true enough, 
it was found that the rate of mutations was speeded up. In a 
recent balloon ascension into the stratosphere, flies were taken to 
a height of over thirteen miles, and it was shown that the mutation 
rate was accelerated to five times its pace at sea level. 

Seizing on the “cosmic-ray” theory, H. G. Wells, in his unusual 
book, “Star-Begotten,” projected the fanciful idea that inhabitants of 
Mars, presumably far advanced beyond us earthlings, have per- 
fected a method of bombarding us with rays which cause “superior” 
mutations, and in turn “superior” humans. Assuming that there 
is a grain of truth in all this, you might ask, “Do we have to 
wait for the inhabitants of Mars to bombard us with rays? Couldn’t 
we ourselves use X-rays on people to produce mutations in their 
germ cells?” We probably could, but the weakness of the idea 
(which also applies to the Wellsian concept) lies in the fact that 
rays are random shots in the dark, which hit genes indiscriminately. 
There is no way of predicting which gene will be hit, or what 
the mutation will be. Most mutations are so slight as to be hardly 
noticeable—a minute change in eye color, a slight change in form. 
But whatever the effect, in the vast majority of cases it is harmful. 
Only once in many times does a mutation produce any change that 
could be considered beneficial. 

Knowing now that rays of some kind, X-ray or cosmic, can 
cause a gene to mutate, we have some clue as to what happens. 
The gene, in the opinion of many geneticists, is a molecule of 
living stuff made up of many atoms held together. The number 
of atoms in each gene, and the way they are arranged, is believed 
to determine its behavior. Suppose now there is a sudden shock, 
caused by a ray. The arrangement of the atoms might be changed, 
or some of them might be knocked out. And there would be a 
“mutated” gene, with a different kind of behavior! 


Applying this principle to the theory of evolution we could start, 
back in some infinite past, with a single gene. (We make no at- 
tempt to explain whence it came.) The single gene gives rise to 
many genes like itself, and each forms a simple cell functioning 
in the same simple way. Possibly in some of the cells, a few ‘of 
the genes cling together. Then in a flash, something happens to 
make one of the genes mutate. Now we have a cell with two kinds 
of genes, able to do something the others can’t do. If what it 
does is advantageous, this cell reproduces itself more prolifically 
than the simple ones until there are many two-gene cells. Be- 
fore long there is another mutation, and another variety of gene 
is created, which chance links together with the other two genes. 
More and different genes are created, and the work they can do 
in cooperation grows in complexity as they utilize new and dif- 
ferent materials. And all the time the chains of genes grow longer, 
forming the chromosomes. 

With more and more “mutated” genes being created and linking 
together, the chromosomes become longer and longer. Now, as 
they lash about in their cell activities, in “crack-the-whip” fashion 
the chromosomes may break into two, each half forming a separate 
and distinct chromosome. With further mutations, any number 
and kind of chromosomes can result. So here the mechanism is at 
hand for producing an endless variety of genes and chromosomes, 
and through these, of animals more and more complex and dif- 

Thus, starting with a single gene, we can theoretically account 
for all the changes and processes by which the innumerable types 
and species of living things, including man, were evolved. (All 
this would have had to take millions of years, but why not? Na- 
ture had an infinity of time behind and ahead of her, and needn’t 
have been in any hurry.) Generally speaking, the higher types of 
animals seem to have more genes, but the number of chromo- 
somes in which these are arranged has little significance. Where 
one animal has more chromosomes than another, it may mean 
merely that it has fewer genes to a chromosome. 

Through the mutations of genes and their arrangement, com- 
bination and recombination in sets of chromosomes, we have there- 


fore the raw materials provided by nature for the evolution oj 
man. But these raw materials were not in themselves sufficient. 
They had to be used, and first they had to be selected and tested, 
for they weren’t ordered in response to the needs of any indi- 
vidual (most often, in fact, quite the contrary). They popped up 
from nowhere at irregular and unexpected times. Each species 
found the materials for its evolution dumped on its doorstep, so 
to speak, the good with the bad. And from this point on Dar- 
win’s theories as to how evolution proceeded have been greatly 
strengthened by the recent findings in genetics. 

We know, unquestionably, that under natural conditions nature 
spawns an infinitely greater number of individuals for each species 
than there could possibly be room for. There must therefore be 
a constant battle between the individuals and their environment, 
or between the individuals themselves, for survival. So we have 
Darwin’s theories of the struggle for existence and the survival of 
the fittest. 

These theories now call for some modifications. As we have 
noted, the vast majority of mutations are harmful, in reality caused 
by an injury to a gene. Where these produced serious functional 
defects in an individual, he usually perished. But in some cases 
the mutations produced merely adverse reactions to certain de- 
grees of temperature, or moisture, or nutrition. In other cases 
they were minor physical variations. Where these characteristics 
were disadvantageous only in. a certain environment or under cer- 
tain conditions, the individual was frequently able to move to 
another environment, or, in man’s case, to change the conditions, 
Often, in fact, what in one environment had been a serious defect 
in another became a decided advantage. (And many times, as 
in the case of the dinosaurs and other extinct species, what made 
them supreme in one environment made it impossible for them 
to survive as conditions changed.) 

However, among the many mutations produced, there were 
some that proved highly useful to the individual. Such improve- 
ments—stronger and better organs, keener eyesight, better teeth, 
more flexible muscles, keener intelligence, etc—also enabled him 
to excel, and perhaps eliminate, the weaker members of his species, 


and so (according to Darwin) would tend to promote the gradual 
upward trend of evolution. 

For back of all this lies the thought that evolution was a process 
upward, always toward some higher objective. The weak were 
weeded out, the fittest survived. But, one might ask, the fittest for 
what? Sometimes those that survived might have perished in an- 
other environment; sometimes those that perished might have 
flourished in a different environment. The survival of the fittest, 
categorically stated, would imply that certain individuals were pre- 
destined to survive even before the environment which their de- 
scendants were to encounter had been created. 

Tf we think, from our own viewpoint, of man as the ultimate 
stage in the evolution of animals, we would have to believe that 
back in the dim Proterozoic era when all was water and swamp, 
already changes were taking place in certain primordial creatures 
which were planned for the millions of years hence, when they 
would evolve into majestic man. It would mean clearly that some 
great directing Force was at work, planning and producing muta- 
tions for future needs, not as yet apparent, for an environment that 
was anticipated but not yet in existence. This might also be called 
the theory of predestination, or purposive evolution. 

But if we think of all the vast majority of haphazard, harmful 
mutations that have no rhyme nor reason, and the very few that 
could possibly be advantageous, we might have to conclude that 
man was no more foreordained among other animals than Pike’s 
Peak, Lake Winnepesaukee in New Hampshire, or some oasis in 
the Sahara was foreordained among the earth’s physical features. 
Many scientists believe that man was a biological accident, hap- 
pily able to survive in the environment in which he found him- 
self. But what if there had been a different environment, if the 
water had still covered the earth, with only marshes sticking out 
here and there? Or what if today, through some cosmic cataclysm, 
there is an upheaval of the earth’s surface, if the temperature changes 
radically, if the chemical composition of the atmosphere is al- 
tered, making it impossible for man and other higher vertebrates 
to survive, while lowly fish and insects might find themselves quite 


at home? Do we not, in contemplating such a dire possibility, 
have to revise our ideas of “fitness”? 

So we add another to the list of arbitrary terms euch as “superior,” 
“inferior,” “normal” and “abnormal,” which we must be careful 
in using with regard to humans. And most especially must we be 
careful, as geneticists point out, when we take it for granted that 
the onward march of time has been synonymous with “upward 
evolution” and that we are here, and other earlier races of man 
are not, because of our inherent superiority and greater “fitness.” 
All this may become clearer when we turn from generalities and 
try to determine by what steps and processes primitive man, once 
he arrived, gave rise to the specific types of people we now have 
in the world. 


Tue subject of “race” has an ominous significance today when 
men are again writing their theories regarding it in blood. The 
validity of these theories can now be weighed in the light of recent 
scientific findings. 3 

Our preceding chapter sketched roughly the processes by which 
the most elemental creatures evolved into the highest types of 
mammals. All this must have required many millions of years, 
but how many would be only a guess. The scientist prefers to 
talk about the vague pristine stretches in terms of eras divided into 
periods, subdivided again into epochs, and these in turn into ages. 
Thus, he will tell you that the first primate, or forerunner of 
man, appeared in an early epoch of an early period of the Cenozoic 
era. This was at least ten million and possibly fifty million years 
ago. At any rate, it was exceedingly long ago. 

The new creature that arose may have been chiefly distinguished 
from any other mammal by its slightly more specialized brain. 
But this first primate was not yet an ape, any more than it was 
a man. It had a long way to go to develop into either. For if it 
is any comfort to you, anthropologists now hold that man did not 
descend from any existing type of ape, but both apes and man 
descended from a common primate ancestor. The subtle difference 
is that instead of thinking of ourselves as descendants of the apes 
we see, we may consider them as merely our remote cousins. 

From the same primate (perhaps somewhere in India) it is now 
believed that the descendants took two main evolutionary routes, 
one leading “ape-ward” and the other “man-ward.” The routes were 
by no means direct. Any number of “trial and error” variations 
must have been evolved before anything like an ape resulted along 
one route, and anything like a man on the other route. 





(3°38 0C0’OSZ) 

(epeunxosdde ose soyeq) 


eto ac vee WIM DY 

S43y p3spoUIbiuo 




(‘3 O00'00S) 
NVWw ; 
9y30150135H (( 

Sf Ci (38 90000) 

ease ) NMOGIId 


RACE 357 

Our first glimpse of one of the creatures on the “man” route 
—a true “missing link” which Darwin had sought in vain—is in 
the form of fossilized (or petrified) bones, found in Java. To the 
creature from whom these bones came anthropologists have given 
the name of Pithecanthropus erectus, because, as his skeletal con- 
formations show, he walked not like other mammals on all fours, 
but almost erect. Popuiarly he is referred to as the “Java Man,” 
although he was far from being a man in the present sense of the 

The “Java Man” is believed to have lived about a million years 
ago. There follow long blank periods in which only here and 
there have lucky finds brought to light other glimpses of man- 
creatures—the “Pekin Man” (dated about 750,000 B.c.), the “Heidel- 
berg Man” (about 500,000 8.c.) and the “Piltdown Man” (about 
300,000 B.c.). Alf these creatures had heavy, chinless lower jaws 
and many apelike traits. 

Not until about 100,000 B.c., with the coming of the Ice Age, 
do the mists of man’s past begin really to clear away. Now 
emerges the “Neanderthal Man,” definitely of the genus Homo. 
We have more than a hundred skeletons to attest the fact that 
the Neanderthaler was about five feet three inches high, thick- 
set, beetle-browed, long-armed, with a massive jaw, little chin, 
big teeth, a large aquiline nose and other primitive features. Never- 
theless, he could think. He fashioned wooden spears and chipped 
tools of flint (the latter by some process which still eludes us), 
he used fire and respectfully laid out his dead. It is with this 
man that our cultural history begins. 

The days of the Neanderthaler, however, were numbered. For, 
beginning with about 50,000 B.c., there was being fashioned in 
the crucible of evolution a new type of man. To the best of our 
knowledge this New Man arose in the region of Mesopotamia. 
Quite likely his ancestors had also been Neanderthalers. But of 
whatever species of Homo they were, they had stumbled into 
what was then one of the most favored habitats of the world. 
It had the best of climates, an abundance of game, fruits, nuts 
and foods of every kind. Compared to other regions where the 
scattered hordes of man-creatures battled for existence against great 


odds, this was a veritable Paradise. Here there was every oppor- 
tunity for a species to thrive and develop, and by an accumula- 
tion of mutations in the course of time to give rise to a new 

Thus, if you are so inclined, you may think of this region 
as the Garden of Eden, and of the New Man that arose in its 
midst as Adam, first of the species Homo saptens. 

We must not assume that this Adam (the Hebrew for “man”) 
sprang into being overnight. Various new genes had been arising 
over a long period, and, proving their worth, had been multi- 
plying and coming together in individuals who supplanted those 
less favored. Even in this region of abundance there must have 
been a struggle for existence. But eventually Homo sapiens and his 
descendants reigned supreme—and alone. 

For here is our second important point: That every human being 
on earth today, civilized or primitive, descended from the same 
stock and belongs to the same species, Homo sapiens. 

The first point we noted was that mankind descended not from 
apes, but with them, from a common primate ancestor. Together, 
then, the two points controvert earlier evolutionary theories, still 
cherished by some anthropological die-hards, that different divisions 
of men stemmed from different types of apes (the inference being, 
of course, that “superior” humans came from “superior” apes). 
The evidence to substantiate our new theory of common origin 
is based principally on the fact that all men, from Nordics to 
Pigmies, are fertile with one another, and from the genetic find- 
ings that the differences in basic traits among them are extremely 
few. This is not true of the apes, which include a variety of 
species differing radically in their genes and chromosomes, mak- 
ing some types of monkeys or apes infertile with others. In fact, 
there are much greater differences between gorillas and some other 
types of apes than there are between gorillas and men. 

To suppose, then, that starting from different species of primates 
and within a comparatively short evolutionary period the various 
races of man could have achieved the biologic unity which they 
possess, is quite inconceivable. We can therefore safely assume that 
the history of all modern mankind begins with the same single 


group of the species Homo sapiens, clustered, as we believe, at 
the crossroads of Asia, Europe and Africa. 

Favored by environment as this group was, it must have mullti- 
plied rapidly. Within five or six hundred years it is not incon- 
ceivable that from a single pair of humans (Adam and Eve, if you 
wish) there could have developed a population of one million. 
Inevitably, dispersal followed, for in those early days very little 
was required to set people a-moving. There was no strong sense 
of fixity in habitat, no dwellings, no cultivated fields, no cattle, 
nothing to hold people down. Bands of humans roved about, 
following the hunt or good weather, a dispersed by quarrels, 
natural forces or enemies. In terms of today, floods, dust-storms 
and earthquakes, tornadoes and severe cold spells, food shortage, 
or wars and oppression of minorities, would quickly set large 
groups of people moving to new territories. 

So bands of Homo sapiens fared forth among such other species 
of men as still roved the continents. We cannot say that the New 
Man was superior to all others, for some isolated species of man 
wiped out by ill chance might have been superior to Homo sapiens 
both mentally and physically. (Often, in fact, we have reason to 
wonder how well our species deserves the name “sapiens,” which 
means “wise.”) The New Man may have killed off the men from 
whom he differed radically, or may have blended with those whom 
he found compatible. Recent evidence (in Palestine) indicates that 
he did mate with some of the lingering Neanderthalers. But 
whether Homo sapiens exterminated or absorbed other men, before 
long, as we said, he had the world to himself. 

Now came another period of integration. Large groups had 
drifted far enough apart to become isolated, and for a sufficiently 
long time (at least many thousands of years) so that various muta- 
tions could take place which would differentiate one group from 
another. Thus there developed in the region of China the “Yellow- 
Brown” or Mongolian race, in Africa the “Black” or Negro race, 
at the crossroads of Europe and Asia the “White” or Eurasiatic 
race, and in the South Pacific the Australoid race, somewhat akin 
to the Negro, but whose derivation is not certain. 

The genetic differences that developed among the races were, 


“i. , = | “D'8 00'S $F YoNg—"y “Dg 00'S t20qy—g : 
‘J'a 000'SZ #OGQY—z_ —«“D'8_000'0$ sNoqy—=ry 

> Be "sabes operipus suoquinyy | 
hh) "Tnoaw Sova JO NIDIWO JHL 
I a | 
t suv pu ai mune j 
Ud IBY > 3 
Ww Z —~ 
ey UNOS ° < BS ES ZN, : : S23! yord | 
wv ee ee ee ee ee - > : y, Z Be ee eae GEES -\ -— og 
Vat YOLVNDA *. hire Crea ; 4 " K ssousan)\ Al 
“AR. s¥DIPUI ut CNA Vp ON = | 
oe Sy) —~ Upriasiuy as je LS, / 
*S_, SOARS }04}.U35 ool . QV 3 = 
Sn S233hY NY ‘e aig —— : aye oe ee 
AEN , 7 oN aly] 
PA aN /~| jean Veh A | 
; Fm (\supipuy \ i ie 47+ | 
ee foosys & NS aeteaay 
= UOnN«\ fh | | SNDIVS | coud LZ | 
tN a . OWON 3 seid A. | 
sOUL)> Sh SS 3 ee en Pe. gL oe 
s IN aS) en ero YK Ss 
‘> 0900'S! iN ae ann ——- ya Vi ee Oy | 
inocavy — 7 a oS Sa ee ge ete wa SaIPAON | 
: ye J 

GNV1 YySWYOS : : ; 

RACE 341 

so far as we now can see, largely in surface traits which seem 
to have had little significance. The shades of skin color, contrary 
to former beliefs, have not been proved to have any correlating 
adaption to climate. Mongols do just as well with their yellow- 
brown skins in the cold regions as in the tropics, and “Northern- 
ized” Negroes, we find, can become sunburned on sudden ex- 
posure to a hot sun just as well as Whites." (The terms “Yellow,” 
“Black” and “White” races are misnomers. Within each race there 
are many shades of skin color, some overlapping with shades of 
the other races.) 

Why, in the same latitudes and climates, but in regions apart, 
did some peoples develop kinky hair, others woolly, others curly and 
wavy, and others straight? How could the specific hair forms help 
them? What advantage does a broad, flat nose confer on the 
Negro in a hot climate, a round head on an Alpine mountaineer? 
What benefit is derived by Mongolians from the epicanthic fold 
which gives them their slant-eye effect? We do not really know. 
Wanting evidence, we might gather that these various surface 
traits arose through haphazard mutations as mere idle pranks 
of nature. Possibly some localized cosmic ray or other special 
influence produced certain mutations in one region and not in 
another; and possibly the resulting traits served for a time to bring 
together individuals who had them, in the belief that they were 
more closely related than others not so distinguished. This is 
speculation. But we must not assume that the surface changes nec- 
sarily implied that important changes had also taken place in the 
characters or functional aspects of the peoples. Especially is it a 
mistake to judge degrees of “primitiveness” in humans by ex: 
ternal aspects. 

-A little unprejudiced study by scientists has shown, in fact, that 
many of the peoples formerly considered most primitive are farther 
removed in various traits from the primate than are modern Euro- 
peans. The Negro is extremely curly-headed, and has very little 
body hair, in these respects being much less apelike than the 

1“The death-rates from the effects of heat throughout the South run from two 
to more than six times as high among Negroes as among White persons, perhaps 
on account of greater occupational exposure of the Negro.’—From “Twenty-five 
Years of Health Progress,” by Drs. Louis I. Dublin and Alfred J. Lotka. (1937) 


White Europeans and aboriginal Australians, who both have straight 
or wavy hair and considerable body hair. With regard to skin color, 
the Negro is also farther away from the brown ape than is the 
European. Again, the full, fleshy lips of the Negro are a highly 
specialized and advanced human feature, for it is the thin lip 
that characterizes the ape. To point out, on the other hand, that 
Europeans may possess certain features less apelike than those of 
the Negro would have just as little meaning. 

With many thousands of genes involved in producing a human 
being, the proved segregation of a few for surface traits within 
given groups cannot be considered highly significant. This will 
become clearer when we follow the further trend of the races. 

The clearest trail is that of the Mongols. Beginning with about 
15,000 B.c. we can follow their trek up from China, through 
Siberia and then over by way of Alaska (probably connected at the 
time with Asia) and into North America. Generation by genera- 
tion the migration pushed ahead until by about 8,000 B.c. the tip 
of South America had been reached. Meanwhile, also, groups had 
strayed off in different directions, giving rise eventually to the 
Eskimos, the North American Indians, the Aztecs, Incas and other 
groups. (Here in the Americas, among the Mongol offshoots, we 
have interesting evidence of how much—or how little—genetic 
variation can take place in isolated groups of people of common 
stock within given periods.) 

Back in Asia, Mongols had been moving in all directions, but 
with no such clear paths ahead as had their brethren in America. 
For the other races had also been on the march. A blending process 
was beginning. Mongols, Whites, Blacks, and Australoids joined 
in populating India. South of the Sahara, while the Negroes were 
branching off into various groups, some of the Eurasiatics from 
the north and east were blending with them. A mixed stream com- 
pounded of Whites, Yellow-Browns and even some Blacks poured 
into Europe and gave rise, as human puddles collected at various 
points, to the Nordic, the Alpine and the Mediterranean peoples. 
These, in turn, mingled with offshoots of each other and of in- 
vading hordes from Asia to form still further subdivisions of peoples. 

Note that we have said “peoples” and not “races.” “Race” sig- 

RACE 343 

nifies a sufficiently long continuity of common ancestry and a 
uniqueness of hereditary traits to distinguish one group of peoples 
from another. The primary White, Yellow-Brown and Black races 
did experience such isolation while leisurely forming in prehis- 
toric times. But their offshoots were developing within a much 
smaller space of time, and when growing population and culture 
were bringing men closer and closer together. There were, as there 
still are, some isolated outposts of mankind, but in the civilized 
world we have ample evidence that for the last few thousand 
years the genetic fences among humans have been knocked down 
in all directions. Today, among civilized peoples, no “pure” races 
can be said to exist. 

So it is that while some still speak of a “Nordic race,” “Alpine 
race,” “Mediterranean race,” etc., and others go even farther and 
talk of an “Italian race,” “German race,” or “English race,” lead. 
ing authorities are now speaking of these as “ethnic groups,” o1 
“peoples.” They know well that if on the map of Europe one 
tried to indicate the paths of all the various peoples that went 
to make up the different nations, the effect would be very much 
like a confetti shower during the height of a New Year’s Eve 

Here we may pertinently (or perhaps impertinently!) quote 
from the well-known German treatise on human heredity by 
Baur, Fischer and Lenz, a standard text in the field of genetics. 
Wrote Professor Erwin Baur (one of Germany’s greatest geneti- 
cists) : 

“What we today term a nation or a people is, biologically con- 
sidered, a mishmash of the most extraordinarily diversified ele- 
ments. . . . It cannot be too emphatically insisted that that which 
is common to the people of one nation, such as the German, 
the British or the French, and that which unites them as a nation, 
is not, properly speaking, their ‘race, but first and foremost, 
a common speech and culture. Racial distinctions, such as the dif- 
ferences between the before-mentioned peoples, are never anything 
more than relative distinctions, insofar as the quantitative propor- 
tions out of which the mixture is made up in the various peoples 
differ to some extent, some racial elements being more strongly 


These were the primary sources of your ancestry if your descent is— 


: . 7 

O/ ! 
wa hese 1 or ie) 
rate Reema hice S/ SAPP 
Wr. Y w v bw) WwW MM 
o/E fal aki ge / 
= fa) Salary 1 
Gia festa! | o4, Tria, 2 
E/O zy Les yl ve Lee 
0/9 | pe clew fed 
WK) g! joz | gisk locli 
Lin? pee eee Ss 1 
BED LS PES USS ts vals iE Bi 
eiw [ui (kl gS \Oo!! 
Clo Ped (We O ec 2144 
hee lol iw | EF a) 
Aichi lrg keen ee 
ra Vol Oy 
a eh aes 


; \\ 
English \\ aK \\ 

1200 -!500% NAY 

SNS \ 
Norsemen en 

ay 7 
Iberians | pe an 4/0 
from N.Africa_-~ Lit 18 
GR eOOOR Co ety a(S 


Vikings ©)> 

9 and tothe, < 

(Fred'kK Barbaross« 
1154 AD. 


— ee ee ee 

800 B.C. 


we peoples 
500 AD, 


_— —, ‘ak 

lbsrians ae Ph eg” ley ee — 
from N-Africa = === 4--==:4) Romans 


Oe ate Carthaginians 
eer(S) (originally Photnicians) 
| (See also cut on p. 346.) 

_---@) Finns (from Siberia) 


Vikings BAS hom 
1300 A.D. Vu ete tamcnoaans Huns 
Bese a5 

peoples ~T50 AD. 



coe ae om aa 

tay 100 A.D 
Vy Also 9OO-1000 AD 
@) Finns 
4 / 
| / 
: } R | 
Bolly Geamanie Oo 
t£oples wa 
ote Denrnark i Wl 
10,000 B.C. (4) £3) Later Teutons ~ 1700 B.c 

HUNGARIAN: Slave (2) Vandals 300 AD. 
Germanic 6) F H 
n uns and 
Spates eaten (3) ne oH » Avars 
ey | ie 
oths Hee \ rue a pea 800 AD. 
palace phat i] om ae 
Germans (7}=== 5 [ - 


=e = v <== 
ees ===-== CELTIC fa ! 
ig TRIBES =< | 
me A SSS oo j 
x ated FSS) lartars | 
(1) Ss 240 AD. | 

2 AD 4 SS Tories Tanedhe | 
ee j SSS rides 
@) Italians SE® 1300-1400 

All maps in this chapter were prepared with the aid of Dr. Gene Weltfish, Dept. of Anthro-| 
pology, Columbia University. | 


RACE 347 

represented in one nation and others in another. Moreover, unmis- 
takably anthropological distinctions between nations by no means 
necessarily coincide with the boundary-lines between folk-speeches.” 
(The italics are ours.) 

We should explain that the quotation is from an edition pub- 
lished in 1929, prior to the time that certain political changes caused 
many German scientists to modify their yews (at least publicly). 
Scientists elsewhere, however, will heartily sponsor the conclusion 
that the chief differences to be noted among various peoples in the 
civilized world are cultural in origin. The findings of genetics, as 
we have previously reported, reveal how often the effects of en- 
vironment are mistaken for hereditary effects, and how difficult it 
is, with regard to the complex traits of human behavior, to dis- 
sociate and separately appraise the two influences. But chiefly, 
genetics has brought out that with many genes required for com- 
plex traits, important basic differences could hardly have developed 
among the various minor subdivisions of humans in their brief 
span of existence and under the circumstances noted. 

Think, as an average American, just what it is that identifies 
in our minds a Frenchman, a German, a Swede, or an Italian. 
In all probability, the pictures will be those compounded for us 
by the stage, movies, comic-strips and popular fiction—portrayals 
dependent upon accent, costume and make-up. Without such acces- 
sories, we dare say that not even our cleverest actors could pre- 
sent recognizable characterizations of the various nationalities. The 
problem, moreover, is general. Look at the pictures of “races of 
mankind” in any encyclopedia, dictionary, school geography or 
even technical treatise and you will see that resort must be made 
to costume, hair-dress and other accessories. 

If we have such difficulty in distinguishing among ethnic groups 
by simple outward traits, it is highly questionable how far we 
can ascribe to them temperamental differences so complex that 
the genes, or the mechanisms for producing them, have not yet 
been identified. We might therefore discount greatly the sweeping 
generalizations that the Irish are inherently “pugnacious,” the Japs 
“sly,” the Chinese “inscrutable,” the Swedes “stolid,” the Germans 
“militaristic,” or “craving regimentation,” etc. We have seen very 


clearly in the United States that in a little space of time children 
of every nationality take on a common American character, to such 
an extent that when they reach maturity and travel abroad Euro- 
peans think of them all as Americans. 

Underlying the attempts to prove that there are great basic dif- 
ferences among peoples is the thought that one group (usually 
that of the speaker or writer) is “superior” to another. Leaving 
aside the question of what is meant by “superiority,” scientists are 
inclining more and more to the view that such attempts are fruit- 
less and will remain so until we can set up uniform standards of 
measurement that will apply fairly to all peoples. Geneticists agree 
that mankind in general is today probably not much different in 
basic intelligence or capacity from his early ancestors in the New 
Stone Age. If this is true, and if it is also true that all existing 
peoples have the same common ancestry, the advance of one and 
the backwardness of another group might readily be attributed to 
differences in opportunity and environment. 

To retrace our steps, we have evidence that our present civiliza- 
tion had its primary source in the peoples who inhabited Mesopo- 
tamia—the “Garden of Eden” to which we referred. Not greater 
capacity, it is believed, but greater opportunity in the form of 
abundant resources gave them a “head start” over others. But 
by no means did they have a monopoly of culture. There is evi- 
dence that throughout the world similar ideas, inventions, codes 
of behavior and other cultural factors arose independently among 
peopics far apart. This suggests that there may be much the same 
cultural capacities in all peoples which they may reveal if given 
full opportunity for development. 

We are reminded of the Arctic explorer who was telling about 
the crude diet of the Eskimos, when a well-meaning but not too 
bright old lady expressed surprise that Eskimos didn’t drink milk. 

“Madam,” replied the explorer, “have you ever tried to milk 

There are many things, important to the development of culture, 
which one cannot “milk” out of an environment where they do 
not exist. People cannot learn to fashion metals where there are no 
metal deposits, nor cultivate crops in frozen ground, nor breed 

RACE 349 

cattle where there are only bears and walruses. When we think of 
their limited resources, it is not surprising that the Eskimos have 
remained backward in many respects. Far south their more favored 
cousins, the Aztecs and Incas, did achieve a high degree of civili- 
zation. But on the other hand, another set of cousins, some of the 
American Indians, with great resources at hand, lagged behind. 
Thus it is not so easy to ascribe reasons for the failure of some 
peoples to develop culturally. 

Too often an entire people is judged by a few gifted members 
who may not at all reflect the make-up of the mass. Differences be- 
tween individuals in the same ethnic group are infinitely greater 
than the average difference between any two races or peoples. When 
we say that one people is superior to another, we generally refer 
only to its few outstanding individuals. The subsequent idea of 
attributing to the mass the prowess of these few harks back to 
the eras when a champion was picked by one tribe to do battle 
with the champion of another. The qualities of each group were 
supposed to be transmuted within its representative, and a triumph 
by the champion “proved” the superiority of his followers. The 
same concept still permeates undergraduates of rival colleges during 
a football game. It also hovered in a racial sense over the prize- 
fight between the Negro, Joe Louis, and the German, Max 

No more than the last-named contest proved that Negroes as 
a race are better fighters than Germans, is there proof that a tem- 
porary flurry of champions in art, literature, science, invention, 
commerce or war indicates the inherent superiority of one people 
over another. Commenting on the claim of “Nordic” supremacy, 
Professor Lancelot Hogben (himself an Englishman) has pointed 
out that the Black Moors were highly cultured at the time when 
the Nordics were little better than barbarians. He quotes a Moorish 
savant of Toledo as writing of the northern peoples, “They are 
of cold temperament and never reach maturity; they are of great 
stature and of a white color. But they lack all sharpness of wit 
and penetration of intellect.” This, as Professor Hogben adds, was 
at a time when few priests in northern Europe could read or write 


and when washing the body was still considered a heathen and a 
dangerous custom. 

History reveals many instances where peoples who were on 
top at one stage were on the bottom at another, and vice versa. 
The rapidity with which the transitions have occurred has sug- 
gested that social and cultural influences were chiefly responsible. 

Thus, there is question now as to whether the reign of art among 
the Athenians, the era of conquest among the Romans, the exploits 
of the Vikings, the Renaissance among the Italians, and so on, 
can be considered proof of inherent superiority. Would we say 
that the present American reign in business proves that Americans 
carry superior “business” genes? Hardly, for we know very well 
that favorable conditions gave impetus to American enterprise. And 
we know also that these or other conditions, and not any hereditary 
failings, were responsible for what many Europeans long con- 
sidered the “incapacity” of Americans for response to or expres- 
sion in the higher forms of culture. Knowing this, we might 
ask whether many of our own judgments regarding the basic 
natures or capacities of other peoples are justified. 

Are Negroes as a race definitely inferior to Whites in intelli- 
gence and cultural capacity? Few authorities today would echo 
the confident “Yes!” of former times, when Negroes were con- 
sidered a sub-species of man. Though studies are available which 
might seem to prove Negro inferiority in some respects, the fair- 
ness of these have been challenged on the ground, quite logically, 
that they have been made by Whites in a White civilization and 
according to White standards. But even by these standards, and 
in an environment still prejudicial, the amazing transition of 
Negroes from a primitive state to one where they are producing 
writers, scientists, musicians, educators and leaders of high type 
must be regarded as evidence that their true capacities are far 
from having been ascertained. As Professor J. B. S. Haldane has 
observed regarding the question of Negro “inferiority,” “Not merely 
has nothing been proved, but it is going to be exceedingly dif- 
ficult to prove anything within the next few generations.” 

We come finally to the race problem that at the moment com- 

RACE 354 

mands the greatest attention—that which the present rulers of 
Germany choose to term “Aryan” versus “Non-Aryan.” 

Anthropologists tell us that there is not and never was an “Aryan” 
race, or even an “Aryan” people. The word “Aryan” was intended 
by the philologist* who coined the term—Friedrich Max Mueller, 
himself a German—to designate a large group of languages, both 
European and Asiatic. They include the Celtic, Teutonic, Italic, 
Hellenic, Albanian, Armenian, Indo-Iranian and Balto-Slavonic lan- 
guages. Used in the sense of “race,” “Aryan” would have to take 
in a wide sweep of the most diverse peoples, ranging from the 
Irish to the Vedda Negroes of Ceylon (one of the most primi- 
tive tribes in existence). 

No more than there is an “Aryan race” is there a “Semitic 
race,” for “Semitic” also refers to a large family of languages, 
among them the Hebrew. However, on the basis of language, the 
terms “Hebrew” and “Jewish” are not synonymous. The mass of 
Jews, especially in Europe, have little knowledge of Hebrew (using 
it only in their religious services, as Catholics use Latin) but 
have for centuries employed as their written and spoken language 
the Yiddish, a compound largely with an old German base. Judged 
by language, then, most Jews would be properly included among 
the “Aryans.” 

The stress laid by Nazi German leaders upon the “Aryan” 
issue is one of the attempts to provide standards by which Ger- 
mans might set themselves apart from other peoples as a “racial 
unit.” In accordance with what their own authority, Professor 
Baur, has pointed out, such attempts are in conflict with fact. Ger- 
many includes within its boundaries many ethnic groups—Nordics, 
Alpines, Slavs and Mediterraneans—blended, through countless 
wars, invasions, and migrations, with the blood of almost every 
other people in Europe and Asia. To endow Germans with “racial 
unity” and to refer to them as “blood brothers” on the basis of 

1 Prof. Friedrich Max Mueller, noted German philologist, wrote in 1883: “I have 
declared again and again if I say Aryan, I mean neither blood nor bones, nor hair, 
nor skull; I mean simply those who speak an Aryan language. ...To me an 
ethnologist who speaks of Aryan race, Aryan blood, Aryan eyes and hair, is as great 
a sinner as a linguist who speaks of a dolicocephalic [long-headed] dictionary or a 
brachycephalic [round-headed] grammar.” 


a common language and national ties would be equivalent to ea. 
dowing all citizens of the United States—from Mayflower de- 
scendants to southern Negroes—with biological unity and “blood 
brotherhood” because they all speak English. 

Bearing further on the Jewish question, it should be clear that 
the Jews, also, do not constitute a “race” in the sense which we 
have defined it. While undoubtedly more homogeneous than many 
other groups, the Jews are none the less compounded of diverse 
peoples. Originally they were a mixture of Eurasiatics, chiefly 
Arabian and Mediterranean stocks. However, their troubled history 
bears witness to the fact that in their wanderings they must have 
absorbed bloods of every type. 

It is not surprising, then, that anthropologists have not been able 
to find any physical traits which would identify Jews as a people 
and set them apart biologically from other Whites. While a few 
characteristics thought of as “Jewish” are found among some Jews, 
each of these traits is also found among non-Jews; and among 
Jews in general there is every type of eye, lip, nose, hair form, 
coloring, head-shape and facial contour common to other Whites. 
Further, Jews long rooted in different countries differ markedly in 
appearance, an old-line Spanish Jew looking much more like a 
Spaniard, and an old-line German Jew much more like a German, 
than they resemble each other. (This bears out the findings of 
Professor Boas that environment may do a great deal to alter 

As to what, then, constitutes a Jew, there is a growing tendency 
to look to cultural factors—the effects of common religion, tradi- 
tions, training, habits and to some extent diet, similarities in social 
experience, reactions to oppression and other influences. But whether 
cultural influences alone can explain the story, or as some might 
term it, the phenomenon, of the Jews, is debatable. 

Currently the Jews seem to be the victims of a general move- 
ment toward isolation and integration which has been launched 
in many countries. Illogically, however, some of the nations which 
are most ardently seeking to cement themselves into “racial units” 
are also clamoring for expansion. History, physics and genetics all 
teach that these policies of contraction and expansion are in con- 

RACE 353 

flict. Empires cannot be created without sending part of the ex- 
panding peoples out into the new territories, and inevitably a 
mingling of bloods must ensue. It has not infrequently happened 
that a small body of conquerors has been absorbed by a large body 
of conquered. In any event, unless a nation welcomes the admix- 
ture of foreign blood, history teaches that conquest and expansion 
are hardly compatible with a policy of “racial integration.” 

The Negro problem in the United States has aspects somewhat 
illustrative of the above. Taken into our midst as a conquered and 
subject people, the Negroes have been gradually intermingling 
with the Whites until today it is believed that only a fraction of 
the Negro population is without White blood. It would be folly 
to assume that all the mixing has been in one direction. Much 
Negro blood has undoubtedly found its way into the White 
stream, especially by way of intermarriages with Mexicans, In- 
dians or other peoples who do not too closely draw the “color 
line.” As the Negro population becomes “Whiter” one may won- 
der how far and for how long the two races can be kept definitely 

Everything points to the fact that the possibility of long main- 
taining any “pure” people in this world of changing humans is 
exceedingly remote. Taking Germany as an example, even if she 
drew the most rigid lines about herself, she would be starting 
out with almost every type of gene known to Homo sapiens, in- 
cluding an ample proportion of “Non-Aryan” genes. Supposing 
again that for a full thousand years she practised the most intensive 
selection in breeding, casting out the genes she considered unde- 
sirable; nevertheless, replicas of many of these genes would be aris- 
ing through mutation. The evolutionary process, it should always 
be kept in mind, is still going on. No human force can control 
it, and to the extent that there are “superior” genes or “inferior” 
genes, no people can hope to maintain a corner on the one kind 
or exclude the other. In effect, any people theoretically starting out 
as “pure” would before long be rendered “impure.” 

The question then arises, “How important is it to humanity to 
maintain ‘pure races’?” Or, stated in another way, “Is ‘race-crossing,’ 
or interbreeding between different peoples, undesirable?” 


There is much disagreement on these points. Some have argued 
that the “purest” peoples have made the greatest advances, and 
yet, in rebuttal, one need only point to the achievements of the 
highly mixed population of the United States. From the physical 
standpoint, some geneticists have claimed that crossing between 
markedly different peoples may result in misshapen offspring— 
with big teeth in small jaws, etc. Other authorities dispute these 
claims on the ground that skeletal parts in humans differ so little 
that they can freely blend together. The most serious argument 
against race-crossing is that where peoples of widely diverse type 
are mated, their differences in temperament, behavior, backgrounds 
and family connections will make for social conflict that will react 
unfavorably on their offspring. 

We can thus see that all our major “race” problems revolve 
about the same points: How great are the fundamental differences 
among various subdivisions of mankind, and to what extent are 
these differences due to hereditary or to cultural factors? While 
we have brought out some factual evidence, and a good deal of 
circumstantial evidence bearing on these points, for the present 
conclusions must rest on opinion. 

As one final commentary, we believe that most leading an- 
thropologists, geneticists and psychologists would agree to this 
somewhat far-fetched hypothesis: | 

That if a child fathered by Adolf Hitler were by some whimsy 
of fate exchanged at birth with the child of a Jewish rabbi, and 
each were reared unwittingly by the wrong father, in all likeli- 
hood Hitler’s child would grow up to be “Jewish” in temperament, 
behavior and social viewpoint, and the rabbi’s child would be 
goose-stepping, storm-trooping and “Heil-Hitlering” with the most 
rabid of the Aryans. 

And we might make similar comparisons in the case of a child 
of Stalin’s reared by Hitler, or an Eskimo child reared by a Hindu, 
or an Italian child reared by a Swede, or a Turkish child reared 
by a Boston Cabot. Or, as our photograph proves, of an American 
child reared by a Chinese. 

sup £9 0f0qq 

‘ysysuq surusvay ‘ssvyo 
UAAOYS IJDY st 2» ‘sosn3 
-va} sty Aq ATUO D9¥I 9Y2 
jo sioquiszul wow 9sIq¥ 
-YsInsuTIsIp sem oy Avy 
yooyno pur ysqvy ‘ysoeds 
‘JuUTW, UT asauTYyy) 
A] Ysno010Y2 Os sWOd 

-9q pry ay ‘soIvig pou 
243 02 YIq IYsnoIg 
‘UMO J1943 JO UO sv 
dsauTY) 942 Suowlv posvas 
stm 24 6[ Sv oy [HUQ 
‘euIyD 02 WIY Yoo? oym 
asouryy ev Aq poidope pur 
*€ JO a3v 94) Iv poasosop 
sum “XX “N ‘puis, Zuo7T 
uo §‘sjusird = urooWy 
fomraic Gout y ydosof 
ujog ‘Sunoy yomy sung 





oe Pk 
oa a 
ie) io 
ayy a he 
oe & 
Ny? p 


ta Gre 

Lon ye 


es: 4 

i, At : 

» [39 See 


Mr. Recrnatp Twomsiey Dunn-Twerep, who is not very bright 
and weighs 110 pounds—of which a good part is front teeth—likes 
to boast that he is descended from William the Conqueror, and that 
the steel-blue blood of ancient warriors flows in his veins. To prove 
it he will show you his family tree and a beautiful hand-painted 
crest, prepared by a genealogist in Boston for fifty dollars. 

Even in these United States there are still a lot of people like 
Reginald, who point with pride to some remote ancestor; and, no 
doubt, others who feel humbled because they haven’t any to point 
to. You yourself may have been among them. We say “may have 
been” because by now you must have gathered that the whole an- 

cestry business has been shaken pretty badly by our genetic findings. 
__ The importance previously attached to ancestry rested on a num- 
ber of fallacies. First was the pre-genetic concept that heredity was 
a process of passing on “blood’—the blood of the parents being 
blended together to form that of the child. No matter how far one 
traced back, therefore, there was always a little of the blood of any 
ancestor “flowing” in one’s veins. Also, as blood was thought to 
carry factors that influenced character, the greater the percentage of 
“blue” or noble blood one carried, the more superior one would be; 
and the more “common” blood in one’s veins, the more inferior one 
would be. Likewise, touches of genius, of great courage, of brilliance 
—or taints of criminality, shiftlessness and depravity were thought 
to be carried in the blood. All that, of course, has been shattered by 
our knowledge that blood is merely a product of each individual’s 
body and that not even a mother and her child have a single drop 
of blood in common. 

Knowing now that all that we inherit are 24 chromosomes from 
each parent, ancestry has been reduced to a simple mathematical 




-Paternal: -Maternal: 



blood poured h 

Parents’ blood 
poured into the 


formula: With each generation farther back the average number of 
chromosomes you may have received from any ancestor is reduced 
by half. Note the qualification “average number.” You can be quite 
certain you received 24 chromosomes from each of your parents, 
but in the combination from your father, for instance, any number 
of these 24 may have been derived from /is father, with the rest 
from his mother. On an average, however, you can assume that you 
received 12 chromosomes from each of your grandparents, that an 
average of six of these came from each great-grandparent, an average 


of three from each great-great-grandparent, and so on, the number 
from any ancestor being halved with each generation back. 

Thus, as you will see by the Ancestry Table on page 358, when 
we get to the fourth generation you might have received from 
any ancestor on an average of three chromosomes, and from any 
specified individual in the preceding generation, either one or two. 
From that point back, the more remote the ancestor, the greater the 
odds that you did not receive a single one of his chromosomes. In 
other words, if you claimed descent from Miles Standish, the odds 
may be 20 to 1 that you are no more related to him than is any one 
else in town. 

That, however, should be qualified. Wherever there was a mar- 
riage in your family between two individuals with some common 
ancestor, the chance of getting a chromosome from that ancestor 
increased. If both your parents claimed descent from Miles Standish, 
the chance of your carrying one of his chromosomes would be in- 
creased to 1 in 10. Further, if there were marriages between other 
Pilgrim descendants farther back in your ancestry, you might very 
likely be chock-full of Mayflower chromosomes. Thus, in families 
with considerable inbreeding, such as the European royalty, or in 
any peoples who have tended to hold together (the Irish, Scotch, 
Jews, etc.) the possibility of carrying one or more chromosomes of 
some vaunted ancestor increases. 

At the same time, with each marriage between related persons in 
your ancestry, the number of your ancestors is reduced. Were it not 
for this, you can readily see that the number of your potential an- 
cestors, if you continued to double them with each generation back, 
would reach impossible figures. As the number of possible ancestors 
is limited, it has therefore been estimated that all persons of English 
descent are at least thirtieth cousins; and of course, if we go far back 
enough, we all have ancestors in common. 

Even if one could be certain of carrying one or two chromosomes 
of some famous ancestor the claim to distinction on that account 
becomes rather ridiculous when we recall that a full complement of 
48 chromosomes is required to make an individual. Nor is there any 
guarantee that the one or two vaunted chromosomes which one 
might have received did not contain the very worst of genes. 


The only possible hereditary link which you can have with any ancestor is through inheri- 
tance of one or more chromosomes. This table shows the average number of chromosomes which 
you might have received from any specified ancestor in any generation back, or the odds against 
having received even a single chromosome.* However, as noted in the text, marriages between 
telatives in your line of descent intensified your link with any preceding ancestor. 



(Your parents) 






No. of 
Approx. Year and Generation Ancestors 
1890 4 
(The ‘‘Nineties’’) 
1860 8 
(Generation of Lincoln) 
1830 16 
(Generation of C. Vanderbilt) 
1800 22 
(Generation of Napoleon) 
1770 64 
(Revolutionary War heroes) 
1740 | 128 
(Benj. Franklin, etc.) 
1700 2.56 
CWilliam IID) 
1670 512 
(John Bunyan) 
1635 1,024 
(The Pilgrims) 
1600 2,048 
(Capt. John Smith) 
1570 4,096 
(Mary, Queen of Scots) 
1535 8,192 
(Martin Luther) 
1500 16,384 
(Henry VIID 
1470 32,768 

No. of Chromosomes 

Each (Av.) 




Odds Against Having 
Received Even One 
Chromosome from Any 
Given Ancestor 

4 to 3 
8 to 3 
5 to l 
10 to 1 
-21 to 1 
85 to 1 
170 to 1 
340 to 1 

680 to 1 

*It is theoretically possible for chromosomes to be passed on in fractions by the process 
known as “‘cross-over,’’ but this would not affect the odds or general averages shown. 



A second fallacy is that of completely disregarding the unimpor- 
tant ancestors, and in many families the remoter women ancestors. 
In our first paragraph we mentioned William the Conqueror. While 
his father was of royal blood, it is seldom pointed out that William’s 
mother was a humble miller’s daughter who bore him illegitimately. 

In fact, with regard to all family trees the practise has been to lop 
off the ignoble branches in each generation, so that eventually only 
the limited few “distinguished” ancestors are left dangling. When a 
geneticist therefore is confronted with a lineage dating back say, 
twenty generations, in which at best a selected few hundred out of 
a possible many thousands are listed, he may be besoned for not 
taking it seriously. 

A third fallacy in the ancestry field is that of comparing human 
families to strains of domestic animals—aristocrats to thoroughbreds 
and ordinary folks to mongrels. True enough, there are genetic aris- 
tocracies among horses, dogs, cows and cats; but bear in mind that 
they were derived only by the closest inbreeding—fathers with 
daughters, mothers with sons, brothers with sisters—and also by 
controlling every mating and by discarding those not wanted from 
every generation or litter. So far as we know, no family of human 
aristocrats lays claim to having been thus derived. (We're not saying 
it couldn’t or won’t be done. No one can predict what certain Euro- 
pean dictators may be up to next.) But as matters stand, human 
breeding has been a haphazard process, and even the bluest of our 
blue-blooded families are a hodgepodge of unidentifiable genes. To 
quote the famed biologist, W. Johannsen, “From the point of view 
of a pure-bred dog, we are all curs.” 

We cannot deny, however, that there are families which by the 
consistent achievement of an unduly large percentage of their mem- 
bers do suggest that they carry many “superior” genes. Among such 
families may be cited the Darwins and the Huxleys in England, and 
the Adamses, the Edwardses and the Roosevelts in the United States. 
But it is also clear that even in the greatest of families there are 
mediocrities who ride along, as in a trailer, pulled by their family 
influence, opportunity or wealth and who, left to their own power, 
would get nowhere. 

“Ancestry” or “family” has significance only when individuals 


themselves show clear evidence of continued superiority. But, alas, 
all our records show that combinations of “superior” genes do not 
long hold together. Rarely do we find any dynasty of superior hu- 
mans continuing for as much as four or five generations. (In the 
Bible we find a suggestion, in another way, that there are limits to 
the effects of ancestral influence. We are told that “the iniquity of 
the fathers” is visited “upon the children unto the third and fourth 
generation . . .” [Ex. 20:5.] This might also be interpreted as apply- 
ing to ancestral virtues.) 

When we turn now to “inferior” ancestry we find that the same 
fallacies underlie the compilation of “bad” pedigrees as of “superior” 
ones. The motives, however, are quite different. As we might ex- 
press it in verse— 

There was a Bostonese 

Who searched out pedigrees 

Which she stored in the middle of her forehead; 

And when they were good, they were very, very good, 
But when they were bad—they were horrid! 

Which is by way of saying that compilers of pedigrees may be 
motivated by the very human urge to prove extremes. Those who 
compile genealogies of persons of “superior” stock are out to show 
how very good these people are. In the compilation of pedigrees of 
“inferior” stock investigators may unconsciously yield to the oppo- 
site impulse. Nowhere has this been more clearly illustrated than in 
those classic horrible examples of yesterday’s sociology books—the 
two distinct clans referred to as the “Kallikaks” and the “Jukes.” 
In case you’ve forgotten, here are the main facts: 

First, the “Kallikaks.” In 1898 Dr. H. H. Goddard, then director 
of an institution for mental defectives in New Jersey, chanced on 
the strange fact that there were two family groups in the vicinity, 
distantly related to each other, and yet as different in character as 
the proverbial night and day. The one branch comprised upright, 
intelligent, prosperous citizens; the other abounded in degenerates, 
mental defectives, drunks, paupers, prostitutes and criminals. Struck 
with the contrast, Dr. Goddard coined for the family the name 
“Kallikak” (compounded of Greek words meaning “good” and 


“bad”) and after long research into the pedigrees, produced this ex- 

Both clans had stemmed from the same remote ancestor—Martin 
“Kallikak,” a Revolutionary War soldier—but through two dtffer- 
ent matings. Martin Kallikak, himself, it appeared, was of good 
stock, and after the war had married a worthy young Quakeress by 
whom he had seven children—progenitors of all the “good” Kalli- 
kaks. But— 

Before he had married, and while a-soldiering, Martin had met a 
feeble-minded girl in a tavern, and with her had had an affair. He 
went his way, and presently the girl bore an illegitimate male child 
to whom she gave the name of Martin Kallikak, Jr. This lad grew 
up to be so wicked he was known as “Old Horror,” and to make 
matters worse, sired ten worthless offspring. It was from these that 
Dr. Goddard traced all the several hundred dad Kallikaks. 

Clearly, looking first at the very, very good Kallikaks, and then at 
the very, very bad Kallikaks, their differences would seem to have 
been caused by the two radically different females from whom they 
descended—the worthy Quakeress and the feeble-minded slattern. 
For a long time this was held up as a fine illustration of “superior” 
ancestry and “inferior” ancestry. But, remember, this study was be- 
gun in 1898, before there was any science of genetics. Today we can 
view the situation quite differently. 

The comparison rests largely on the assumption that the illegiti- 
mate child whom the feeble-minded mother chose to call Martin 
Kallikak, Jr., was indeed the son of the man she designated, which 
no court would accept as evidence. But supposing that she were cor- 
rect, a nice point in genetics intrudes itself: 

Granted that “Old Horror” (Kallikak, Jr.) was a degenerate be- 
cause of bad heredity (and there is as yet no evidence that “degen- 
eracy” is inherited) by what gene mechanism did he become that 
way? No single dominant gene could produce any such complex 
condition, nor is there any known gene that can singly produce even 
feeble-mindedness. Recessive genes would have had to be involved. 
Which means that as such genes must come from both parents for 
the effect to assert itself, no matter how chock-full of “black” genes 
the feeble-minded mother was, the worthy Martin Kallikak, Sr., 

$59q 94} UtIM 'sueWunY jo 
edAy Aujsom sou ey} jo 
Spespuny owes esey}, wol4 

*Apipasoy 4SiOM 
Ou} UFIM 'sUeLUNY 4seMOo] BUF 4O 
speipuny poumeds oym usspyiya 
Ue} BWPD JONOL PjO,, Wos4 



1942) — 7 *yexiyey UILJeW, 
peje? ous WOUM uos ® 340q ous 

*usspjiya 44Bidn ‘Aupeoy 
"oul, UBAOS WIY B10 9YS 

NE Bieri re 

sseseyency) Bunok Aujsom @ 
pelssew ey Jem out J01j0— 

js16 userey papuiw-9j)qe0} @ 
YHA Peep ay S21Ases Ul SIIUAA 

Pawou JaIpjos D sDM asay] Sawi} IDM AsJDUOIINJOAaY UY 



himself had to be carrying such genes tf the condition of his pre- 
sumptive son, “Old Horror,” was due to heredity. And that would 
mean, in turn, that the “good” Kallikaks also received some of those 
“black” genes! 

Before we go on to a number of other points that any geneticist 
might raise, let’s look into the case of the “Jukes” (also a coined 

The Jukes family, another unsavory clan abounding 1n every 
known type of human riff-raff, was investigated long before the 
Kallikaks. It was in 1874 that R. L. Dugdale, a New York Prison 
Association inspector, chanced upon this worthless aggregation, 
clustered in one locality. Tracing back, he discovered that they all 
had a common ancestry in two eighteenth-century brothers who had 
married a pair of disreputable sisters. Intensifying their relationship 
was the fact that the Jukes were much inbred. 

In 1916 the Jukes study was brought up to date with an investiga- 
tion of the ensuing generations. Degeneracy, immorality and defec- 
tiveness were still rampant among the new crop of Jukes, but to a 
smaller degree. Many of the family, in fact, were honest, hard-work- 
ing citizens, some even “superior” and prosperous. This improve- 
ment was ascribed to reduced inbreeding and the infusion of “good 
outside” blood. 

If we now analyze the Jukes studies, we find them quite as ques- 
tionable from a genetic standpoint as we found the Kallikak stud- 
ies. When Dugdale investigated the Jukes, not only was nothing 
known of the mechanism of heredity, but sociology was in its in- 
fancy. Dugdale blandly assumed, as did others at the time, that 
“pauperism,” prostitution and criminality—even the tendency to 
have illegitimate children—had an hereditary basis. His conclusions 
were that starting with a bad heredity, the Jukes had created for 
themselves a bad environment and that this envirenment had pro- 
duced bad traits which in turn became hereditary. (Or, in other. 
words, that morals, habits and other acquired bad traits are inherited 
—which, of course, we now know is unfounded.) 

We can well suspect that in the original study of the Jukes there 
were many errors in the dogmatic classification of individuals as 
“prostitutes,” “criminals” or “degenerates” (especially when we con- 


sider that some of the individuals classified had been dead for any- 
where from 25 to 100 years). But even more strongly can we ques- 
tion the data regarding mental defectiveness, for at that time there 
were not even IQ scores to go by. Nor were there in the first 
studies of the Kallikaks. Moreover, in both studies, the individuals 
traced represented only @ part of all the descendants. This is im- 
portant, for it is one thing to prove that there are 300 degenerates 
out of 600, and another that there are 300 out of 6,000. 

With all these reservations, however, there is no gainsaying that 
the bad Jukes who were observed, like the bad Kallikaks, were an 
unusually undesirable lot. We needn’t argue how bad or how de- 
generate they were. What concerns us is the extent to which their 
degeneracy and their lowness can be blamed on bad heredity. 

Let us try to picture one of the Jukes girls, at the time of Dug- 
dale’s investigation, in the Seventies: 

Mamie Jukes lived in a dark, squalid nest of hovels, with a 
drunken, thieving father, a slattern of a mother and a swarm of 
untidy, ill-fed brothers and sisters. Mamie didn’t go to school, be- 
cause there was no compulsory education and the district school- 
house wouldn’t take any of the brood. Decent folks kept away 
from the Jukes and whipped their children if they were even seen 
talking to Mamie. She was pretty lonely until, when she got to be 
about fourteen or fifteen, some men who hung around a pool hall 
began to take an interest in her. Mamie was a little bewildered, and 
pathetically flattered by this sudden attention. She was too dumb to 
understand what was happening, or how it happened, but soon she 
became diseased. . . . And one day, months later in a dark corner 
where Mamie cowered like a sick animal, another illegitimate, “un- 
fit” child was added to the Jukes clan. 

Yes, this is a synthetic picture, but no one who has studied the 
records would deny that it is a typical one. Can we still say that 
the new Jukes child—or any similar child—starting out life under 
such conditions was predestined to inferiority because of “black” 
genes? Or could we not equally predict a bad end, regardless of the 
genes that child carried, on the basis of its “black” environment? 

It is because earlier investigators did not quite see this distinction 


that their studies are now greatly discounted. To quote Professor 
Thomas Hunt Morgan: 

“The numerous pedigrees that have been published showing a 
long history of social misconduct, crime, alcoholism, debauchery and 
venereal diseases, are all open to the same criticism from a genetic 
point of view, for it is obvious that these groups of individuals have 
lived under demoralizing social conditions that might swamp a 
family of average persons. It is not surprising that, once begun, 
from whatever cause, the effects may be to a large extent communi- 
cated rather than inherited.” 

And as a coup de grace, we may add this from another famed 
geneticist, Professor Lancelot Hogben: “If social biology ever be- 
comes an exact science, the dreary history of the Jukes will be re- 
garded as we now regard alchemy.” 



“We hold these truths to be self-evident, that all men are created 

Everything we have learned about human heredity challenges this 
statement in our Declaration of Independence. While genetics gives 
no support to the concept of hereditary “superior” or “inferior” 
classes (to paraphrase Professor Jennings) neither does it support 
the theory of genetic equality. We have been shown beyond the 
shadow of doubt that individuals are ushered into the world with 
every type of inequality in body and mind, and when we add to this 
the obvious inequalities in environment and opportunity, we are 
forced to conclude that the statement of the Founding Fathers was 
a flight of poetic fancy (as indeed they may have meant it to be!). 

Without inquiring further into the causes of human differences, 
there is general agreement that we would like to see more of some 
kind of people in this world than of others. (Which probably means 
more of “our” kind of people—vague as that might be.) So when we 
now take a broad view of the population, it is disconcerting to dis- 
cover—or so we are told—that the kind of people we do want are 
being created not nearly so fast as the kind of people we don’t want. 
Here is a new sort of “population fear.” 

For a long time the fear was that the world would become over- 
run with human beings. In 1800 all humanity totaled not more than 
750 million souls. A phenomenal growth began, due principally to 
lowered death-rates and improved means of subsistence. Within a 
few generations the population doubled. (Now it is almost triple.) 
The specter of a world choking itself to death with overpopulation 
arose. To meet this came a spread of the Malthusian doctrines that 

human population growth was a biologically self-regulating process, 


and that wars, plagues, famines, etc., etc., would automatically step 
in from time to time to keep the population within bounds. 

The Malthusian doctrines, like others we have mentioned, are 
now being abandoned. For it is becoming apparent that our popula- 
tion growth, in numbers, kind and quality, is controlled not by nat- 
ural biologic forces but by artificial factors. And again there is 
alarm, this time that unless we begin planning the growth of our 
population, as we do our crops, we are headed for disaster. 

The first fact cited is that not only has the growth of population 
in this and many other countries slowed down, but that a decline is 
on the point of setting in. “What of it?” you ask, as you view the 
many unemployed and the many undesirables. “We might be a lot 
‘better off with fewer people in this world.” That may well be so, 
but, like the lady in the reducing class, some authorities aoe 
that the decrease is in the wrong quarters. 

Viewing the world at large, we find that the populations of our 
Western countries are being outdistanced by those of Oriental na- 
tions. Next, in Europe, the birth-rates in Germany and Italy, under 
dictatorial stimulus, have begun to go up while the birth-rates in 
England and France continue to drop. (Which, of course, is cause 
for alarm only in the democracies.) Finally, coming home, we find 
that the birth-rate in the United States has declined 25 percent in 
the last ten years, and that we now have 1,600,000 fewer children 
under ten than we had only five years ago! 

The census figures tell you that our population is still growing, 
which is true; and it is also true that the birth-rate is still higher 
than the death-rate. But this is because the great increase in lon- 
gevity within the past generation has swelled our numbers by mil- 
lions of middle-aged and old people who would not have been here 
before. If we thought of our population in terms of an army, a 
large percentage of veterans have been kept in service far beyond 
the time when they previously would have been mustered out. Thus, 
though the number of annual recruits (babies) is rapidly declining, 
for the time being the army ranks (our total population) appear 
to be full and even growing. But within twenty years or so the 
temporary advantage gained by the veterans in the ranks will be 


overcome, and from then on (about the year 1960) official estimates 
are that our actual numbers will begin to decline. 

In post-Revolutionary War days, American women living through 
the child-bearing period were producing an average of almost eight 
children each. Today the average is about ¢wo children. Yet this far 
from tells the whole story, for it refers to the general average. Ac- 
tually the birth-rate is unevenly distributed in various levels, being 
lowest among those in the upper social and economic levels, and 
highest among those in the lower social and economic levels. 

Disregarding for the moment the question of why some people 
are on a lower level than others, as we said at the beginning of this 
chapter, there cannot be much doubt that certain persons will make 
better parents than other persons. If we think of those best quali- 
fied as “plus” and those least qualified as “minus” we might picture 
two contrasting types: 

The “Pluses” are able, willing, intelligent, hard-working, socially- 
conscious, forward-looking couples who want as many children as 
they can have. 

The “Minuses’ are the unstable, shiftless, indifferent, unintelli- 
gent, unsocially-minded couples, living from hand to mouth in sor- 
did and unhealthy surroundings and looking upom added children 
as necessary inflictions. By the “Minuses” are further meant not “de- 
pression” victims, but those who, even in average times, answer the 
description given. 

So we come to the complaint, which is that the “Pluses” of the 
United States (and of other countries, too) who want children most 
and are able to give them the best start in life, are having the small- 
est families, while the “Minuses” who least desire children and who 
offer them the worst start in life, are having the largest families. 
Remember, this is referring to broad averages. It does not imply 
that all those with small families are “Pluses,” and all those with 
large families are “Minuses.” (Our ambassador to England, Joseph 
P. Kennedy, has a family of nine splendid children and many a 
good American can boast an equal or an even greater number.) 

For the country at large, the highest birth-rates are in the most im- 
poverished rural areas, chiefly of the South and West. In the worst 
of the areas the population is reproducing rapidly enough to double 


(As Viewed by a Population Expert) * 


x 6% Professional and most-favored 
oy Soke o ee = be | groups 


Lowest are BEST- ITTED we 30% Intelligent, honest, willing, able, hard- 

ee) oe F OR PARENTHOOD . working, dependable, socially-con- 
Here pea ah Sal aigian Teil scious, good citizens of all kinds 

30% The middle group, fluctuating be- 
tween both extremes, some rising, 
some dropping 

oF % 


Nef be o 


30% Unstable, shiftless, indifferent, unin- 
telligent, unsocially-minded, most un- 

Highest productive 


3% Socially inadequate 
V2 of 1% Known defectives 

* This should be considered as an individual opinion. Other experts might make 
different estimates of the percentages of “best-fitted” and “least-fitted.” 

its numbers in one generation. On the other hand, in the more 
favorable economic areas—which are chiefly urban—fertility is much 
lower. In some of the large cities fertility is less than 75 percent of 
that required for replacement, and within the cities proper, the fer- 
tility is highest among the poor, the less educated and those in the 
least favorable circumstances, and lowest among those in the higher 
income brackets who are engaged in business or professions. 


Where the decline in births first took place in the cities, it is now 
rapidly extending to the rural districts. And here, again, the falling 
off in births is greatest among the most favorably situated farmers 
and rural inhabitants. In short, throughout the country, wherever 
education and standards of living have gone up, with only few ex- 
ceptions has the birth-rate not gone down. 

What are the causes of this disproportion? First and foremost is 
the growing practise of birth control, which is most widespread 
among those in the “upper” social and economic strata, least com- 
mon among those in the “lower” strata. Education and improved 
living standards bring with them the desire to insure better oppor- 
tunities for children. Which means that the educated and conscien- 
tious parents, with the knowledge of birth-control methods at hand, 
are now regulating the size and spacing of their families to conform 
with their incomes, health, and opportunities for child-raising. On 
the other hand, parents in the lowest social and economic levels, who 
are largely ignorant of birth-control methods or are indifferent to 
their use, are letting nature take its course. 

Comparing city and country, the pressure for limitation of fam- 
ilies is not so great in the rural areas. Added children on farms do 
not mean moving to new quarters with higher rent, as they do in 
the city. Also, schooling in farm areas is more limited, so that chil- 
dren do not remain dependent for so long; in fact, children on 
farms:are often an economic asset, especially among the most back- 
ward, where they are put to work at some task from the earliest 

Another cause of the disproportion in birth-rates is difference in 
age at marriage. Persons in the “upper” levels, where education and 
training are prolonged, marry later; and as the educational require- 
ments for entrance into the professions have steadily increased, the 
average age at marriage has been pushed forward. A natural result 
has been a decline in the number of children. Over a period of 80 
years it has been found that college graduates have been producing 
consistently fewer children than their own brothers or cousins who 
have not attended college. 

Among women, the effects of education have been even more 
acute. Not only may a college education postpone the time when a 


young woman will marry and begin bearing children, but in many 
cases it acts to forestall marriage altogether. Alumnae records of our 
leading women’s colleges show a strikingly high proportion of grad- 
uates who remain unmarried. Whether it is because college women 
become more “choosey” about men, or because careers distract them, 
the fact remains that where there are diplomas there are all too fre- 
quently no marriage licenses or birth certificates. 

There are “social sterility” factors of. many kinds. Not only for 
women but for men, certain careers, such as writing, art, music and 
the theater, where the road upward is long and uncertain and earn- 
ings precarious, keep many from marrying or from having children 
when they do marry. Even where money is not at issue psycho- 
logical or social forces which prevent settling down may inhibit 
reproduction. A glance back at the notable instrumental musicians 
represented in our study will show that all thirty-six, of whom only 
four are under thirty, have produced but thirty-seven children. An- 
other study we made with regard to birth-rate, of one hundred 
married “Who’s Who” American authors represented in the collec- 
tion of books presented by publishers to the White House, showed 
that all these authors together produced about one hundred and 
fifty children. Eleven of these authors were women, and their total 
number of children was twelve. With about three children to a 
couple being required for population replacement it will be seen 
that the birth-rate among all these gifted individuals is well un- 
der par. 

Several exceptions should be noted to the rule that the “higher 
up” one goes, the fewer the number of children. Studies at Yale 
and Harvard showed that among the most successful of the gradu- 
ates, and among the faculty, those with the highest standing had 
the largest families. More recently another study of graduates of 
Brown University of the class of ’24 showed that the “high” men 
produced substantially more offspring than the “low” men, and 
solely because they married earlier and in larger proportions. It is 
apparent, however, within the ranks of college men as among so- 
cially awakened persons in general, that lower incomes mean fewer 

Apart from the social factors cited (which by no means constitute 


all the socio-economic factors involved) it is estimated that. one 
couple in every ten is childless largely because of physical reasons. 
The sterility, as might be expected, is usually in the woman, but 
there is a considerable incidence: of complete or partial sterility in 
men. (Further facts on this subject. will be given in the chapter on 
“Program for ‘Tomorrow.”) 

Most serious among the physical factors affecting the birth-rate 
are abortions, both spontaneous and induced. Dr. Frederick Taussig, 
who has made an exhaustive study of the subject, has recently re- 
ported that there must be close to 700,000 abortions in the United 
States annually—or one abortion to every three confinements. From 
25 to 30 percent of the abortions are therapeutic—medically sanc- 
tioned as necessitated by the: mother’s condition. (In all countries 
nephritis—kidney disease—in a pregnant mother is legal ground for 
abortion.) However, 60 to 65 percent of the abortions are: illegally 
induced, only half of these being performed by physicians; and it is 
the illegal abortions that are largely responsible for the annual death 
toll of 8,000 women from such operations. 

Of significance with regard to the birth-rate is the fact that almost 
go percent of the abortions (according to Dr. Taussig) now occur 
among married women, most of them between 25 and 35 years 
of age, and especially where they have had. several children. Fur- 
ther, among married women in the cities, there are proportion- 
ately twice as many abortions as among women in the country dis- 
tricts, who have less reason to fear the advent of an extra child. 

All this again confronts us with the paradox that children are be- 
ing forced upon many people who do not want them, or should not 
have them, and are being kept from many people who do want 
them, and should have them. 

The Stork, it seems, has no sense of direction. What shall we do 
to steer it right? 



Nor so many years ago the word “eugenics” conjured up a picture 
of an athletic young man in a leopard skin being mated to a robust 
young woman in a bathing suit while over them, in an inset signify- 
ing “The Future” hovered a large brood of youngsters posed ath- 
letically (in their birthday suits) to show the effects of good hered- 
ity and a diet of cracked wheat and vegetables. 

Later on the picture changed to one of determined reformers shoo- 
ing the Stork away from slums and hovels while shouting their 
war-cry, “Sterilize! Sterilize!” 

Whatever “eugenics” may now suggest to the popular mind, we 
dare say that it is still viewed as “just another of those reform 
movements.” If so, the blame attaches to the earlier “eugenists” who 
got it off to a bad start. And this is unfortunate, for eugenics, prop- 
erly interpreted, may be one of the great forces for good on our 
social horizon. 

“Eugenics” (based on the Greek word ‘ Busts! —“well-born”) 
was the term used by Sir Francis Galton in 1883 to designate his 
movement for improving the human race by scientific breeding. 
However, as the mechanism of heredity had not yet been discovered, 
Galton and his followers were motivated by many of the fallacious 
ideas about ancestry which we previously mentioned. They believed 
quite strongly that those on top were there largely because of “su- 
perior” heredity, while those at the bottom were there because of 
“inferior” ancestry. Accordingly, they drew strong support from the 
aristocracy and the “old-line families,” in both England and the 
United States, and at the same time aroused the resentment of the 
more democratically minded. 

When the Mendelian findings did come out, and an array of 
“black” genes in humans was revealed, the eugenists seized on this 



as confirmation of their belief that most of the major ills in the 
world were due to bad heredity. The quickest way, and the only 
way, to improve the world, they argued, was by breeding better hu- 
mans. This was violently contested by the “environmentalists” and 
“behaviorists,” who insisted that heredity was of little account and 
that education, hygiene and social improvements alone could 
duce a more perfect humanity. Today, as the smoke of battle begins 
to clear, we find both sides ready to compromise. 

Recognizing that heredity and environment are inter-operating 
forces that cannot be considered apart, the “hereditarians” have 
come to realize that many defects previously attributed to bad hered- 
ity are due primarily to outside influences, and no matter how 
greatly we can improve our heredity, our efforts will be of little 
avail unless we can also improve our environment. The “environ- 
mentalists,” on the other hand, faced with proof that many ills and 
undesirable characteristics are directly due to or influenced by 
heredity, must concede that no plan for human betterment can 
ignore the importance of improving our genetic make-up. 

Thus has been formulated this two-fold “eugenics program” in 
which both environmental and genetic measures are included: 

Negative Eugenics, embodying all measures that might reduce the 
proportion of “unfit” individuals. 

Positive Eugenics, embodying all measures that might increase 
the proportion of “fit” individuals. 

Not to give the impression that a definite platform has been 
drawn up (as by a party convention), we may say at once that the 
eugenics “program” we are presenting is merely a summary of all 
the various proposals made for improvement of the human stock. 
Some of these measures are already being carried out in this or 
other countries, some are still nebulous proposals, some meet with 
general approval and others are being hotly debated. All will be 
discussed impartially. 

First, “negative” eugenics: The obvious way to reduce the pro- 
portion of “unfit” children is to reduce the birth-rate among “unfit” 
parents. The cause of their unfitness, as previously explained, is 
here set aside. No one need deny that couples who are insane, or 
morons, or deaf mutes, or who are horribly diseased or malformed, 



or who are criminal or degenerate, can hardly be “fit” parents. (At 
least under average conditions.) Nor need we deny that a husband 
and wife who are poverty-stricken, uneducated, living in squalor 
and already with several children for whom they are unable to pro- 
vide properly, cannot give a fair start to more children. Yet these 
parents produce an unduly large number of offspring, chiefly be- 
cause, through ignorance or indifference—and often against their 
will—they let nature take its course. 

To combat this situation, eugenists favor the spread of birth-con- 
trol information. As has been shown, the more educated and in 
many instances the more desirable individuals in our population are 
fully informed on the subject and are widely practising birth-control 
methods. Only by placing the same information and facilities at the 
disposal of the more backward persons in our population (the con- 
tention is) can we prevent our population growth from becoming 
adversely one-sided. 

“Planned parenthood” is a better term than “birth control” to 
characterize the eugenic objectives. In many instances what is sought 
is not a reduction in the size of families, but the proper “spacing” 
of children, so that they will come when the mother, the home and 
the family budget are best prepared for their advent into the world. 
Children, like any guest in a home, it is felt, should arrive only 
when they are welcome. : 

But what about persons who are considered unfit to have any 
children? For these, the extreme form of birth control is proposed— 
that of sterilization. 

Sterilization, as you probably know, is not an wnsexing operation. 
It in no way inhibits sex desires or interferes with normal sex- 
functioning. In men, sterilization is the simple process of cutting 
and tying up the vas deferens, the tube through which the sperms 
must issue. In women, sterilization is more serious. Here the opera- 
tion consists of making an abdominal incision and tying the fal- 
lopian tubes down which the eggs must travel. (See page 32.) 
While conception is rendered impossible, the ovaries are in no way 
affected (any more than sterilization affects the testes in men). 

Sterilization for eugenic reasons is not new. In the United States 
it dates back forty years, when a prison doctor in Indiana first began 


performing such operations on habitual criminals (with their con- 
sent). Before long sterilization began to be advocated for mental de- 
fectives and in 1907 the first sterilization laws were passed in Indiana 
and California. Twenty-six other states have since followed suit. To 
date some 27,000 persons (60 percent females) have been sterilized 
in the United States, nearly half of these in California alone. 

What has been accomplished, and what can be accomplished by 

The first thought was that it would be a quick and easy method 
of wiping out all serious hereditary conditions. Let us assume (but 
with great reservations to be noted later) that the persons sterilized 
to date did carry serious “black” genes and that thereby the birth 
of many defective children has already been prevented. But this is 
the merest beginning. Suppose from: now on that we have a free 
hand so that we can sterilize anybody and everybody, those in insti- 
tutions and outside, who may be carrying serious hereditary defects. 
Which ones are sufficiently grave to warrant sterilization? 

We can confine ourselves to the more acute mental defects, the 
severe organic disorders and various malformations or loathsome 
conditions which make impossible a normal or happy existence. But 
at the very outset, when we seek to eliminate any given “black” 
gene, we must consider the gene mechanism involved—dominant, 
recessive, sex-linked, etc—for in each case the problem is distinctly 

The simplest gene mechanism is that of the dominant gene which 
singly produces its effect. Every person with a dominant condition 
will transmit it to one in every two children. Sterilize every domi- 
nant “black” gene victim and we could almost wipe these conditions 
from the earth within a single generation. We say “almost,” because 
here and there the condition may arise through mutation, but chiefly 
because, in such maladies as that of Huntington’s chorea, or glau- 
coma, the individual may marry and have children before the condi- 
tion asserts itself. Where this factor is not involved, the serious dom- 
inant conditions that we could eliminate immediately (ear-nerve 
tumor, complete absence of iris, optic atrophy, etc.) are all so rare 
as to be of little significance. 

Our next category comprises sex-linked genes, conditions such as 


the classic hemophilia, where a single gene produces the effect in 
males only, with two such genes required to make a female defec- 
tive. Here our problem becomes complicated. In hemophilia, it is 
dangerous to try to sterilize the victims (all males) because being 
“bleeders,” any operation might prove fatal to them. This isn’t too 
important, as few hemophiliacs survive to maturity, and those that 
do today would hardly venture to have children. Few pedigrees of 
hemophilia run for more than two or three generations. Mutations, 
it is believed, are responsible for keeping up the supply of “hemo- 
philia” genes, as well as those for a number of other serious defects. 

In other sex-linked conditions such as juvenile glaucoma, absence 
of sweat glands, retinitis pigmentosa, adult Leber’s disease, eye- 
muscle paralysis, peroneal muscular atrophy, etc., where the bleeding 
factor is not involved, sterilization could of course reduce the circu- 
lation of the genes by both male victims, carrying one gene, and 
female victims, with two. 

But in all the above conditions—including hemophilia—we would 
still have with us the much larger number of women carrying the 
single hidden “black” genes. How are we to identify these women 
when they are in themselves perfectly normal? Remember in 
Queen Victoria’s case that only until hemophilia appeared among 
her descendants was it known that she was a “carrier.” (It might 
be interesting to speculate what would have happened to history 
had Queen Victoria been forced to undergo sterilization!) 

The problem of what to do about “carriers,” or suspected “car- 
riers” of serious “black” genes comes upon us with full force when 
we turn to the recessives. Almost all the serious hereditary ills— 
diabetes, rheumatic fever, certain types of mental defect, etc—are in 
the recessive or multiple gene category. And it is these conditions, © 
where at least two genes are required, that constitute our greatest 
menace and confront us with our principal eugenic predicament. 

Consider the hereditary mental defectives. The most serious types 
—absolute idiots and imbeciles—are either sterile or, being institu. 
tionalized, do not reproduce. Our problem is with the morons, or 
feeble-minded. The estimates as to their number vary from 14 of 
I percent of our population to as high as 5 percent (which latter 
tnust surely include those who are merely retarded, rather than de- 


fective) and do not differentiate between those whose condition 
might be due to heredity, or those defective through environment. 

Confining ourselves to the hereditary cases, let us assume that we 
have as many as 500,000 feeble-minded whose condition is due to 
“black” genes. But this would mean, as geneticists have figured out, 
that there are at least ten times as many normal persons, or 5,000,000 
in the population, each carrying a hidden one of those genes. Thus, 
because the “carriers” would still continue to produce their quota, 
it is pointed out that sterilization of all the mental defectives would 
cut down the number of them in the next generation by not more 
than perhaps 10 percent—some say less, some say as high as 30 

In the next generation sterilization could pick off only the defec- 
tive children of normal parents who were carriers. Perhaps, through 
law or voluntary action, these parents themselves would be sterilized 
as soon as a defective child appeared, preventing further spread of 
the genes. Nevertheless, with each successive generation the effects 
of sterilization would be reduced. To thus make any sizeable dent 
in the hereditary feeble-minded population might take a thousand 
years, but never could the genes involved be completely eliminated. 

All this applies to every other recessive condition caused by “black” 
genes, with various additional complications occurring wherever 
environmental influences are concerned. In manic-depressive insanity 
and schizophrenia, there is first the uncertainty as to what genes, 
and how many are responsible; then, as in Huntington’s chorea, 
the appearance of the condition may be long delayed until the vic- 
tim has already had children; or, again, it may be completely sup- 
pressed by favorable environment, so that persons genetically “posi- 
tive” (with the required genes) for insanity may swell the propor- 
tion of normal persons who are “carriers.” 

In all other conditions that do not assert themselves until after 
maturity, or that may be suppressed by favorable environment, such 
as diabetes, glaucoma, childhood rheumatism, certain types of deaf- 
ness, progressive muscular atrophy, etc., the possibilities in steriliza- 
tion would be similarly limited. Further, the rarer any gene, the 
harder it would be to eliminate. Even in so obvious a gene defect as 
albinism, which shows itself at birth under all conditions, it might 


both sexes 

(Single gene producing a serious detect.} 
By sterilizing all with the defect... 

L '- oe oe 
7@=y Cer 
L é Jams 

. \ 
36) Og: 

Next Generation: No more of these 
defectives (except for rare new muta- 

(Where a pair of the genes produce a 
serious defect.) By sterilizing all with the 

genes in carriers would still be | 
passed on, thus... 

Next generation: Proportion of these 
defectives only slightly reduced 


(Single gene producing serious defect 
in male, two genes required for female.) 

By sterilizing all the defectives, 

ry tsk ee < 

sey yee 

female carriers would still remain... 
Next generation: No more females with 
ema this defect, but many carriers, and many 
: defective males receiving “black'’ gene | 
from carrier mothers. 


take two thousand years to reduce the percentage of albinos by 
one-half. With no recessive defect could sterilization accomplish 
much in the long run unless all normal persons who were “car- 
riers” could also be sterilized. And that would mean—assuming that 
“carriers” could be detected, which they can’t be as yet—that almost 
every one of us would have to be sterilized. 

That the enthusiasm for sterilization might have gone too far 
was pointed out last year by a committee of the American Neuro- 
logical Association, headed by Dr. Abraham Myerson of Boston. 
Special emphasis was placed on the ethical and legal aspects of 
sterilization, wholesale and peremptory sterilizations being sharply 
denounced. Sterilization is justified, the committee stated, only in 
especially selected cases of insanity, feeble-mindedness, epilepsy and 
a limited number of other conditions we have mentioned, when 
these show every evidence of being hereditary; and even then, only 
after careful study of each individual case by experts. 

Regarding “carriers” the neurologists reported, “Our knowledge 
of human genetics has not the precision or amplitude which would 
warrant the sterilization of people who themselves are normal in 
order to prevent the appearance (of a condition) in their descend- 
ants.” A kind word was said for the feeble-minded: “In a world 
which has much low-grade work to be done, there is still room 
for the people of low-grade mentality, of good character.” Regard- 
ing criminals or prison inmates (you will recall that, these were the 
first to be sterilized by law): “There is at present no sound scien- 
tific basis for sterilization on account of immorality or character 
defect.” And finally, “Any law concerning sterilization under the 
present state of our knowledge should be voluntary and regulatory 
rather than compulsory, and should be applicable not only to public 
charges but also to those in private institutions or at large in the 

That sterilization may be invoked recklessly, and perhaps fool- 
ishly, was pointed to in the case of a Kansas institution for girls 
where wholesale sterilizations were carried out in some of the 
girls merely because—according to official reports—they were ob- 
streperous, incorrigible, fighters or “near degenerates.” This was in 


spite of the fact that the state law specifically lists idiocy and social 
disease as the only legal grounds for sterilization. 

Another cause célébre, at this writing still before the courts, is 
that of a young woman, daughter of a noted inventor, who is suing 
her mother for having had her sterilized on the grounds of feeble- 
mindedness. Here is something to think about: Assuming that the 
girl was mentally retarded (which has not been proved) might she 
not also have been carrying valuable “superior” genes of her in- 
ventor father? And in such a case, would society be justified in risk- 
ing the passing on of “feeble-minded” genes in order to conserve 
the “superior” genes? 

As we have now seen, a good deal of cold water has been thrown 
on the high hopes for the eugenic uses of sterilization. While it can 
undoubtedly eliminate many defectives, it has serious limitations 
and many inherent dangers. The situation may be altered somewhat 
if means are discovered to produce sterilization without an opera- 
tion, and especially temporary sterilization. Experiments in the lat- 
ter direction are already being made, with some positive results re- 
ported. This would relieve sterilization of much of its drastic sig- 
nificance, would increase the number of those voluntarily allowing 
themselves to be sterilized, would permit curtailment of reproduc- 
tion among venereal disease sufferers until they were cured, and 
would permit “probationary” sterilization of those whose heredi- 
tary defectiveness or social undesirability was in doubt. In any 
event, the final decision as to who should and should not be steril- 
ized, and how that should be accomplished, saaule be left to com- 
petent medical authorities. 

Where sterilization falls down with regard to “carriers,” eugenics 
offers as a partial remedy the prohibition of marriages between 
such persons, that is, if they are suspected of carrying hidden 
“black” genes for the same condition. Particularly does this apply to 
marriages between cousins and other closely related individuals. 
But first let’s be clear about this much-misunderstood phase of hu- 
man heredity. 

Cousin marriages, or inbreeding, suggests to many persons an ar- 
ray of idiots, imbeciles, monsters, weaklings, blind, deaf and other 


defective children that are supposed to ensue. To what extent does 
this accord with fact? 

Genetically, the marriage of first cousins means only this: Inas- 
much as they have two grandparents in common, at least one- 
quarter of their genes, on an average, will be exactly the same. 
Thus, if their mutual grandparents were carrying any hidden 
“black” genes, there will be a much greater than average danger 
that these will come together in their children. In marriages between 
second-cousins, the possibility of the same genes coming together is 
reduced very much, and it continues to decrease as relationship 
becomes more distant. But wherever there is inbreeding, there is 
more chance that recessive defects will crop out than there is in mar- 
riages between unrelated persons. 

Much substantiating evidence is available. Some thirty years ago 
Alexander Graham Bell made a study of vast numbers of the na- 
tion’s blind and deaf, and found a high percentage of cousin mar- 
riages among their parents. In certain inbred families of Martha’s 
Vineyard there was the abnormally high incidence of 11 percent of 
deaf-mutism. Where similar inbreeding prevailed, great numbers 
of feeble-minded were found among the so-called hill-folk of New 
England, while many dwarfs were found in one of the peninsulas 
of Chesapeake Bay. 

It is estimated that the complete prohibition of first cousin mar- 
riages would reduce the incidence of congenital deaf-mutism by 25 
percent, juvenile amaurotic idiocy by 15 percent, xeroderma pig- 
mentosum (a fatal skin disease) by nearly 50 percent, and all other 
types of recessive defects by varying percentages. But we must not 
conclude from this that a ban on all cousin marriages is justified, 
or that inbreeding in itself is harmful, sinister or immoral. 

Existing laws or scruples against cousin marriages date far back 
to times when next to nothing was known about the mechanism 
of heredity. That superstition played a part in compounding these 
scruples is indicated by this fact: In the Middle Ages the ban on 
marriages between “related” persons was extended even to those 
without any blood tie, who merely had had the same godfather or 

It is incorrect to assume that there is a deep-rooted or instinctive 


fear against inbreeding among humans. In Biblical times Jacob 
wedded his first cousins, Rachel and Leah, while Abraham mar- 
ried his half-sister, and Moses, his aunt. The Egyptian Pharaohs 
and Ptolemies mated with their sisters wherever possible—Cleo- 
patra having been the offspring of six generations of such brother- 
sister marriages, while she herself, in turn, was married to her 
younger brother. The ancient Peruvian rulers also believed that 
the only bride royal enough for a king was his own sister. The 
Spartans were highly inbred; there were many cousin marriages 
among our Puritans; and coming down to the present, the sturdy 
Pitcairn Islanders are the highly inbred descendants of the famed 
mutineers of the Bounty. In all the foregoing cases there is no 
evidence that inbreeding had any harmful effects. 

This brings up the point that where no “black” genes are in 
circulation, and the family is of unusual stock, cousin marriages 
or other inbreeding may in fact result in superior children. Charles 
Darwin, married to his first cousin, produced proof of this in his 
distinguished offspring. Turning to domestic animals, we have 
ample evidence that constant and intense inbreeding, far from 
being harmful, has made possible some of our most valuable 
strains. However, as we noted in the chapter on “Ancestry,” the 
breeder of domestic animals has the privilege of discarding the 
defectives that crop out and rigorously selecting for matings only 
the superior animals. If something like this could be done among 
humans (but we're not saying that it should be done!) cousin 
marriages would be of immense eugenic value. Thinking in terms 
of the present, however, we must conclude that unless a family 
is of unusually high quality, and known to be free of serious heredi- 
tary defects, cousin marriages should be discouraged. 

But equally, matings between any unrelated two individuals in 
whose families the same serious hereditary defects occur should 
also be discouraged. The most direct way of doing this is by en- 
couraging prospective couples to compare the genetic histories 
of their families before they seek a marriage license. A campaign 
to popularize such precautions is being carried on in England, by 
the Eugenics Society, which distributes printed “pedigree” forms, 
known as “Pre-Marital Health Schedules.” These are designed to 


bring out all facts about the family background or physical state 
of the individual, which have any eugenic significance. | 

All this implies voluntary action by parties to a proposed mar- 
riage, and can be expected only of the most enlightened and so- 
cially minded individuals. Hevering in the background, therefore, 
is the suggestion that just as venereal disease tests are now re- 
quired in many states, the filling out of such “pre-marital health 
schedules” should ultimately be made compulsory; and that when 
analysis of the facts reveals a strong possibility of defective chil- 
dren ensuing, marriage licenses should be denied. ) 

In this, as in all “negative” eugenic proposals, little account 
is taken of Cupid. We dare say that any stringent action to greatly 
hamper Cupid’s activities will bring on an uprising in his defense. 
In fact, when we look back now over all the various “negative” 
eugenic proposals, it seems pretty clear that whatever is done, 
at least under democratic rule, to limit the production of “unfit” 
children will for a long while to come depend largely upon the 
voluntary action of individuals themselves. 



Every farmer knows that improvement of crops or livestock 
depends on the two factors, “Seed” and “Feed.” These are synonyms 
for what some biologists call “Nature” and “Nurture” or others 
call “Heredity” and “Environment.” 

If the farmer is intelligent and his crops have been running down, 
he looks first to the “feed”—the soil or his agricultural methods— 
before he begins bombarding the state farm bureau for new “seed”; 
and if his cattle and sheep are below par, he looks first to their 
pasturage and care before he clamors for new animal “seed” (or 

So in humans, the program of “Positive Eugenics,” which seeks 
to increase the proportion of the “fit,” turns first to “feed,” or in 
other words, environment. We have seen that the reasons for the 
decline in births among the “fit” were primarily social or eco- 
nomic—late marriages, forced limitation of offspring by limited 
budgets, etc. To counteract these influences, most eugenic measures 
proposed for the immediate future are also social or economic. 
They invite little controversy, because they might be included in 
almost any program for human betterment. 

To illustrate these proposals, let us apply them to two hypo- 
thetical young people, John Smith and Mary Jones. Both are as 
“fit” as can be, healthy and intelligent. John is twenty-three, 
just out of college, and “breaking into” a profession on a small 
salary. Mary is two years younger, with a high-school education 
and is working as a secretary. Thev’re much in love and want to 
get married, but feel they’d better wait until John can properly 
support a wife. 

Says Eugenics: Don’t wait! If money is the problem, this might 



Marriage grants: Wherever possible, parents should be encour: 
aged to make substantial “setting up” gifts to young people; or 
provide dowries (shades of the Old Country!) Otherwise the state 
should provide marriage loans or grants. (Already being done 

Salary increases for married men: Popularize the practise of rais- 
ing the wages or salaries of men when they marry. 

Jobs for married women: Combat prejudices against women 
continuing to work after marriage, or employers’ discrimination 
against hiring them. 

Housing projects: The biggest bugaboo of young couples—high 
rent—might be shooed away if the government or ‘states would 
provide “honeymoon” apartments with special rent concessions for 
the first years of married life. 

John Smith and Mary Jones have been induced to wed. They 
both want a child, but their budget is slim, and they feel they 
ought to wait until John’s salary is large enough to provide for 
the hospital expenses. So Eugenics suggests: 

Lower maternity costs: State grants to maternity hospitals to 
make possible a cut in bills. 

Pre-maternal care: Recognize expectant mothers as the direct 
concern of the state, establish more pre-maternity clinics and in- 
sure that each pregnant woman is given all necessary food and 

These measures may relieve the Smiths of some of their wor- 
ries. But suppose Mrs. Smith can’t afford to risk losing her job? 

Maternity leaves for working mothers: Impress employers with 
the patriotic duty of keeping jobs open for women who take time 
out to have babies. 

Ease burdens of working mothers: Provide diet kitchens, milk 
services and public laundries (yes, we mean for diapers!). As the 
babies grow, provide public nurseries and, later, pre-schools to 
look after them while the mothers are at work. 

All these various measures should induce the Smiths not to de- 
lay too long about having their first child. But we don’t want 
them to stop there, To encourage larger families: 


Rental concessions: Public housing projects with a decreasing 
scale per room for larger families. 

Tax cuts: Larger tax reductions for each child, increasing as the 
child grows, to keep pace with the added expense. 

Educational grants: Relieve parents of the worry about educa- 
tion by providing special scholarships for children from large 

Let us now look back. Do all the various eugenic proposals seem 
vague and impractical? Almost every one of them is already in 
operation either in the United States or in some other country! 
As an impressive illustration of how effective a “positive” eugenics 
measure can be—even though it wasn’t deliberately planned as such 
—consider the case of the New York City public-school teachers: 

When we were children “teacher” was a synonym for “spinster,” 
and, in truth, school teachers almost invariably were spinsters— 
because they Aad to be. When women teachers married they lost 
their jobs. That was the situation in New York City some twenty- 
odd years ago. But see what has happened: 

In 1915, after the issue was fought through the courts, the Board 
of Education was forced to rescind the ban on married women 
teachers. Today, out of some 30,000 women teachers in New York 
City, between 40 and 45 percent are married. Of the rest, many 
more are still young enough to be confidently looking forward to 
marrying. But teachers couldn’t always be so confident. And that 
is another phase of our story. 

At the time the ban on marriages was still in effect, the salaries 
for New York teachers in the lower grades ranged from $600 to 
$1,200 a year. By a series of increases it has now been brought 
to the range of $1,608 to $3,339—with teachers in the upper grades 
and high schools receiving considerably more. Thus teaching has 
become one of the most lucrative steady jobs open to women. 
And presto! Teachers who were once thought of by many men 
as “queer” or “old maids” by temperament have now become 

As for their having children, the New York system provides for 
a maternity leave for teachers with no loss of seniority. The re 
sult is that large numbers begin having children in their best 


years, while many, as soon as their husbands are able to carry 
on alone, resign to increase the size of their families. 

The story of the New York teachers (which is paralleled in many 
other cities) is emphatic proof of how “social sterility” factors, that 
have been operating to prevent many eminently qualified indi- 
viduals from marrying and having children, can be easily elimi- 
nated. In New York City alone thousands of women teachers 
now happily married and mothers of children would have remained 
spinsters under the old rules. Nor is all this past history, for in 
many communities the ban on teacher marriages still persists. In 
fact, as a recent report of the John Dewey Society brought out, 
some communities still go so far as to enjoin young women teachers, 
by rule or contract, from even “keeping company” with young 

Another “social sterility” factor, is that which forces many women 
to postpone marriage, often until it is too late, in order to care 
for old or sick parents or younger members of the family. Pen- 
sions for aged or sick parents, and educational grants for younger 
brothers and sisters, would set many of these women free. In fact, 
when we think of the millions of fine women who are forced 
to remain unmarried, a great proportion for no justifiable reason 
whatsoever, we can be very sure that many other “social sterility” 
factors are. at work which should be uncovered and rooted out. 

More apparent are the cases of physical sterility. Let us retrace 
our steps to the young Smiths. Suppose that the economic path has 
been cleared for parenthood, but that after they wait and wait for 
several years, the Stork shows no inclination to arrive? This, as 
we saw, happens with about 10 percent of our couples. 

Having cited the Smiths as a “fit” couple, we rule out the pos- 
sibility of venereal disease, one of the principal causes of sterility. 
For cases like theirs, then, the widespread establishment of “sterility 
clinics” is recommended. Many of these are already in operation. 
(In New York City, at the Harlem, Mt. Sinai and Beth Israel 
hospitals, among others.) The function of such clinics is, first, to 
look for obvious causes of sterility both in the woman applicant 
and in her husband. (Not infrequently the seminal fluid of a 


sexually normal man may be devoid of sperms or may contain 
all, or a high percentage of, defective sperms.) 

Where the sterility is in the man, diseases, accidents or other 
factors may be responsible, and if the effects of these can be over- 
come, fertility may be restored. In women, too, where diseases are 
involved, a cure may restore fertility. However, in normal and 
healthy women, the cause of sterility is often a minor obstruction 
in the fallopian tubes. This may usually be remedied by quick 
and simple treatment. Hormonal and X-ray treatments and even 
psychological ministrations, have also been reported as useful in 
overcoming sterility. The clinics claim success in cing: con- 
ceptions in about 25 percent of the cases. 

We come now to this question: Suppose our fine young Smith 
couple discover that, through the incapacity of either, or both, 
they will not be able to have children? To the tens of thousands of 
couples in that position, the answer is: 

Adopt a child, for an adopted child may often be reared ta be 
quite as much like you as a child of your own. 

What, by the way, is meant by a child “of one’s own”? 

We have seen how, with regard to its hereditary factors, every 
child is a gamble. No one can predict to what extent a child 
will be genetically like or unlike its parents. True enough, we 
can make some forecasts about physical characteristics, and here 
and there about defects. But no one can predict the character, dis- 
position, mentality or behavior of any given child of normal par- 
entage. These factors are determined or influenced by such a mul: 
titude of genes, inter-operating with so many environmental fac: 
tors that as individuals we can’t possibly expect to reproduce our- 
selves. A true “chip of the old block” in humans is a genetic myth. 

All this is by way of saying that there may be infants at large, 
available for adoption, who may have the same kind of genes that 
a child of your own might be expected to get. 

But while the genetic make-up of any child of yours is to a 
great extent unpredictable, you do have considerable power to 
control the environment which you will provide for it. Thus, in 
the opinion of many authorities, if you took a child of genetically 
normal stock, and raised it carefully, it might in many respects 


turn out to be as much like you in character and in degrees of 
social resemblance as many a potential child of “your own.” 

And so, encouragement of more adoptions constitutes another 
plank in the “Positive Eugenics” platform. But the demand for 
adoptable infants already exceeds the supply. Where shall we get 
more of them? 

In our previous chapter we spoke of abortions—that one out 
of every four conceptions in the United States is thwarted by this 
means. In many cases, undoubtedly, the expectant mother would 
be happy to give birth to the child if she were properly cared 
for and were sure the child would have a happy entrance into 
the world. On this principle a number of private institutions have 
been established where unmarried mothers can have their babies 
under the most favorable conditions, and with the knowledge that 
the infant will be eagerly welcomed by some worthy couple on 
the institution’s waiting list. 

Among other proposals to combat sterility are some of a more 
radical nature, still to have their efficacy tested, and which are 
certain to evoke widespread dissent. They would involve, in fact, 
sharp revision in prevailing concepts regarding marriage and sexual 
morality. We may add that while advanced by eminent authori- 
ties, these proposals are not yet incorporated in any formal Eugenics 
program. Your own judgment must determine how worthy they 
are of consideration. 

First, artificial insemination (technically known as eutelegenesis). 
This is the process of artificially impregnating a female with the 
sperms of a male without any contact between them. In the breed- 
ing of domestic animals it has long passed the experimental stage, 
and is now being widely used in many countries. Sperms are 
drawn off, transferred to vials and kept under refrigeration for 
days, to be used as needed. Thus, in breeding cattle, for instance, 
the services of a superior bull may be vastly multiplied and car- 
ried over wide areas. (Sperms from pedigreed South American 
bulls have been recently brought to the United States by airplane.) 
Other advantages of artificial insemination are that females can 
be impregnated at the most propitious times, that the chances 


of conception are increased and the possibility of disease trans- 
mission greatly reduced. 

If we think only of its practical aspects, here is how artificial in- 
semination could be applied to human beings: 

1. Where conception in a woman is difficult for organic rea- 
sons, the husband’s sperms may be artificially inseminated, greatly 
increasing the chances of conception. 

2. Where a husband is sterile but the wife fertile, instead of a 
couple being forced to adopt a child wholly unrelated to them, 
the wife could be impregnated with the sperms of some other 
man with no infraction of the moral code. This has already been 
done in many instances. (We are reliably informed that there is 
a private clinic in New York which arranges for “sperm” donors 
—some of them selected young college men—whose identity remains 
unknown to the recipient.) 

3. Where the husband is not sterile, but where it is feared he 
may transmit some dangerous hereditary factor; or where husband 
and wife are fearful that they each carry the same recessive “black” 
genes (as in first cousins), the sperms from some other man may 
be used, and a child at least “half their own,” genetically, may be 

Some biologists hold out high hopes that once the practise of 
artificial insemination in humans is popularized, the sperms of 
some eminent or highly desirable man could be used to procreate a 
yast number of children. Prof. Muller estimates that 50,000 is a 
reasonable estimate with technical methods now at hand. Going 
further, he believes that it may be possible in the future to take 
sperm-tissues from a man and keep the culture going for many 
years, so that his sperms will be available long after his death. 
(The recent experiments by Dr. Alexis Carrel, in keeping detached 
organs alive with the aid of the Lindbergh apparatus, gives en- 
couragement to this theory.) 

Artificial insemination also opens up the possibility that we may 
eventually be able to overcome the shortage of marriageable men 
by controlling the proportionate birth-rate of the sexes. In our early 
chapters we discussed the suggestion that this might be done by 

separating male-bearing from female-bearing sperms. Significant 


experiments toward this goal have been reported recently, and con- 
fidence is expressed that in some not-far-off time, by the artificial 
insemination of the one or the other kind of sperms, parents will 
be able to have boys or girls as they desire. There would probably 
be an overproduction of boys to begin with, but through the well- 
known law of supply and demand the demand for girls, too, 
might be expected soon to equalize the ratio. 

Back of all the more radical human “breeding” proposals hovers 
the thought that we may some day be able to breed a race of 
“superior” humans. Once we have determined the specific genes re- 
sponsible for the manifold characteristics in human beings, no 
biologist doubts that, by assembling various combinations of genes 
in given individuals, we could breed people of specific types, for 
specific purposes, just as we now breed animals. But that is far 
from the thought of any democratically-minded eugenist, for it 
implies the assumption by the state of supreme dictatorial powers 
over all matings. An unwelcome idea, but not an impossible one. 
It happened in Sparta long ago, and today we have only to think 
what has already been done and what can be done in the totalitarian 

Planned human breeding, carried to the extreme, would demand 
that the state take charge of all children, virtually from infancy, 
raising and training each one for special tasks. From the same 
parents, one child might be selected as the type for a common la- 
borer, another for a scientist. Families as units would no longer 
exist, until, after many generations of breeding, true genetic fami- 
lies had been achieved, with all the individuals sufficiently alike 
in mind, temperament, aptitudes and vocation so that the state 
would see no need of separating them. 

Certainly, from our present American viewpoint, any such dis- 
regard of the wholesome influence of home environment and the 
right of individuals to free mating and parenthood would be carry- 
ing specialization a bit too far. It brings to mind the story about the 
old country doctor whose son, studying to be a doctor also, wrote 
to him, “There’s nothing in this general practise, Dad. I’ve de- 
cided to specialize on disorders of the foot.” To which his father 
wrote back, “Which toe?” 


Finally, for those who cherish the dream of a race of “superior” 
individuals to be achieved by intensively selective breeding, biolo- 
gists pose this question: “What do we mean by ‘superior’?” “Su- 
perior” in one environment may mean “inferior” in another. We 
need only point out that the dictators of three European countries, 
considered as the ultimate of human superiority—almost as demi- 
gods—within their own borders, are looked upon by millions else- 
where as the most vicious, anti-social and undesirable of human 

For an analogy closer home, consider women. If we had the 
power to breed women to order, what type would we aim at—leav- 
ing it to both men and women to decide? Beauty, delicacy of fea- 
tures, slim figure, tapering wrists and ankles, small, regular teeth, 
vivaciousness, intelligence but no profundity of intellect—this might 
perhaps be a general description of feminine desirability. And yet— 
as our chart (page 394) shows—these characteristics would be quite 
the opposite of those best suited to motherhood or making for 
superiority in a woman from a practical point of view. 

“Styles” in women and in men change with time and place, and 
standards of “desirability” or “superiority” in human beings, as in 
fashion, or art, are far too variable to permit of precise evaluation. 
Left to the judgment of their contemporaries, some of our greatest 
men would have been doomed to oblivion (as undoubtedly many 
unsung prophets must have been). The paintings of Van Gogh, 
Gaugin, Cézanne, would have been consigned to ash-heaps had the 
recognized “superior” artists of their day been left to decide. In 
every one of the other arts as in almost every other important field 
of human achievement—religion, social reform, invention, science, 
business—many men who were far in advance of their time were 
ignored, looked down upon and sometimes persecuted by their con- 

Even among average individuals it is not always so easy to deter- 
mine which qualities of mind or character are superior, which in- 
ferior. The lying child with an overdeveloped imagination may 
sometimes be the forerunner of a gifted writer; the boy who balks 
at discipline may sometimes develop into a blazer of new social 
trails. Extreme righteousness may often be coupled with intolerance, 


and bravery may sometimes mean callousness. The requirements 
for success in many fields may go with such undesirable social quali- 
ties as ruthlessness, insensitivity, unscrupulousness and selfishness. 
As human beings, many obscure little men who never get anywhere 
may be superior to some of those on top. 



Beauty unimportant 

Beauty first 
Delicate features Strong features 
No “deep” intellect High intelligence 


Slim fi 
im figure Sturdy figure 
Tiny waist 
Ample waist 
Small hips 
Broad hips 
Dainty wrists 
and hands Sturdy wrists, 

ae . strong hands 
ender, so 

tapering limbs Solid, sturdy 

“ : limbs and 
Slim ankles ankles; good- 
Tiny feet sized feet 

So, having sifted the various eugenic proposals, both “positive” 
and “negative,” we may be left with these conclusions: 

No radical change in the genetic make-up of human beings cai. 
be expected for a long, long time. Nor are we justified, with what 
little we now know about our genes and their workings, and with 
our uncertain and short-sighted viewpoint, to plan any drastic 
change. We can and should try to root out the most serious of the 
“black” genes which do not appear to have a single point in their 


favor; we can and should restrain reproduction of individuals who 
at any stage of civilization would be considered undesirable; and 
we can and should encourage propagation among those individuals, 
to be found in all classes and among all peoples, who by every broad 
rule of human existence can be considered fit and desirable. 

In short, modern eugenics places its greatest hope for improve- 
ment in the human stock on such changes in the social environment 
as will bring about the most eugenic distribution of births. Better 
education, better hygiene, better standards of living, can far more 
easily and more rapidly reduce the number of “unfit” than can any 
arbitrary process of breeding. Such genetic improvements as’ we can 
effect, short of those possible through the comparatively limited em- 
ployment of compulsory sterilization, must depend at present on 
voluntary action. Individuals who are genetically defective must be 
encouraged to refrain from reproducing, and individuals who are 
genetically desirable must be awakened to the importance of repro- 
ducing themselves. To go much further, and by ban and edict of 
the state to launch into a program of breeding human beings to 
order, might bring upon our heads a deluge of evils that might far 
outweigh the good to be derived. 

We were talking about John Smith and Mary Jones at the be- 
ginning of this chapter. They signify to us an average desirable 
American couple. If we can correctly interpret the aims of American 
eugenics we believe these aims would be to bring to all the Johns 
and Marys the kind and number of sons and daughters that their 
own minds and hearts and longings would prescribe for them. 


Tuis book began, as you may recall, with “Stop and think about 

Now that we reach its end, we hope that you are clearer as to 
the why and how of yourself and your fellow human beings. But 
you may rightfully ask, “How can this knowledge be usefully ap- 
plied to my own life? Of what practical value to me are all these 
facts about the inheritance of features, diseases, defects, social traits 
and talents, about race, ancestry, eugenics and so on?” 

What can you do with the information concerning the heredity 
of features and surface details? Yes, it may help to satisfy a natural 
curiosity about your appearance and the looks of your children. 
We frankly concede, however, that such knowledge has as yet little 
practical value to the layman except in doubtful-paternity cases. If 
you are single, your choice in marriage would hardly be affected by 
the possibility of your offspring having such or such hair or eyes. 
And we doubt that you would jilt your sweetheart because you 
knew that your alliance might result in a child with attached ear- 
lobes, or even a Hapsburg lip. 

But as you will recall, the study of the inheritance of surface 
traits, initiated by Mendel with his peas, has made possible all our 
other knowledge about heredity, and leads directly to the under- 
standing of how you may have inherited truly important and vital 
traits, how your children may inherit them, and what constructive 
steps can be taken with regard to many problems. This can be best 
illustrated by considering the hereditary defects and diseases. 

Let us assume that some serious “black” gene condition appears 
in you or runs in your family. (You are indeed fortunate if this 
is not the case.) What light have our studies thrown on your course 

ef action? 


We have previously brought out what society should, might or 
can do about the “black” genes. But the problem confronting you 
as an individual when a “black” gene strikes home cannot always 
be viewed from the broad standpoint of society. To you the problem 
is not one of tens of thousands of matings with definitely predictable 
ratios. Everything, in your case, may be staked on a single turn 
of the wheel of chance. It may give you little comfort to know that 
the odds are one in four that a defective child will result, for your 
first child might be that defective one—which would be calamity 
enough—and the possibility lurks that you might have two in 

You must be governed, therefore, by the special circumstances or 
considerations which apply to your case. Consider the following 
hypothetical situations: 

You yourself are afflicted with some serious hereditary condition. 
Should you risk having children? 

If the condition is a dominant one, where a single gene from one 
parent can cause the damage, you know that there is a straight 
fifty-fifty risk. With the odds so great you must act as if it is almost 
a certainty that you will have a defective child. Your decision then 
must be based on the seriousness of the condition, the degree to 
which it has hampered your own life or impaired your happiness, 
the willingness of yourself and mate to have a child similarly 
afflicted and your capacity to compensate it for the handicap. In the 
few unqualified dominant conditions so serious that many sufferers 
have said, “I wish I had never been born,” your answer could 
well be “No.” 

In recessive conditions produced only when two of the same 
genes come together, the problems are more numerous and more 
involved, although usually all for the good. That is to say, while 
the range of odds and circumstances to be considered are much 
more varied than in the simple dominant conditions, the probability 
of transmitting a recessive defect is in most cases much less. 

Is there insanity in your family? 

Then you know that, as all identified hereditary insanities (ex- 
cept for the rare Huntington’s chorea) are due to recessive genes, 
even if you yourself were insane or definitely carry a hidden gene 


for insanity, no child of yours could inherit insanity from you alone. 
This is true of all recessive defects—feeblemindedness, childhood 
rheumatism, diabetes, deaf-mutism and others—which constitute 
numerically the vast proportion of common “black” gene conditions. 
No one of these defects could be inherited by your child unless it 
recetved exactly the same gene from both you and your mate. 

Here is one of the most far-reaching, important and constructive 
findings of genetics. How many hapless individuals, parents of a 
defective child, have had salt poured on their wounds or been 
scourged by their mates with the words, “You know the child in- 
herited it from you! You know it runs in your family!” What you 
cannot impress on yourself and others too strongly, therefore, is 
that wherever there is a child with any recessive defect, the in- 
heritance has stemmed from both parents, and wherever a mar- 
riage or conception is being avoided for fear that such a child may 
result, the family histories on both sides should be considered with 
equal thoroughness. 

The dangerous aspects of recessives lie in the mating of two 
persons with the same gene. If both you or your mate are normal 
but “carriers” (which is certain if you each had a parent with the 
same recessive affliction) then the odds are one-in-four that you 
will have a child with the defect. If one of you is afflicted, the 
other a “carrier,” the odds are one-in-two. But, most dangerous of 
all, if you and the person you marry both have the same recessive 
condition, every one of your children will inherit it. For instance, 
if you have diabetes and you marry a diabetic, every one of Has 
children will be diabetic. 

So to this problem: 

You are in love or engaged, and have just learned that the pos- 
sibility of having a seriously defective child lurks in your contem- 
plated marriage. 

If children are not important to you, the situation can resolve 
itself easily. But if having children is a primary objective in your 
marriage, you may have to weigh the “black” gene odds against 
your affections—even to the point, where the risk is menacing, of 
considering marriage to some one else. However, as you have 
learned, in only a small proportion of cases (among them, some- 


times, those involving first cousins) need such a predicament arise. 
Generally, where the risk is not too great, you are justified 1 in being 
swayed by the redeeming possibilities in your marriage. 

We assume next that your problems of mating are far in the 

Your children have all been ushered into the world and no heredt- 
tary defect has yet appeared in any of them. What good will it do 
to worry about defects appearing later? 

The knowledge of what conditions might be expected to develop 
in a child, and what conditions might not, can do an immense 
amount of good. Wherever a defect or disease is amenable to treat- 
ment and the approximate time of its onset is known, foreknowl- 
edge by your doctor of an hereditary tendency may be an invaluable 
aid to him in preventing its development, arresting its progress or 
effecting a cure. To cite some specific cases: 

—Where diabetic inheritance is suspected, control of diet, ab- 
stinence from over-eating, keeping down of excess weight and fre- 
quent medical inspection may thwart the development of the dis- 
ease or greatly impede its progress. 

—Where childhood rheumatism lurks in family backgrounds, 
notably among the poor, its development in many children may be 
prevented by assuring them plenty of fresh air, proper living- 
conditions and periodic medical examinations of their hearts and 
nervous systems. 

—In insanity, the foreknowledge of a familial tendency may make 
possible precautionary steps or early treatment which would save 
a large proportion of the victims. 

—In polyposis of the colon, a cancer-inducing condition, the 
suspicion of inheritance may be of vital importance in insuring 
prompt treatment. With regard to common cancer, although the 
question of its inheritance is still entirely open, specialists tell us 
that a sharp lookout for and early recognition of its symptoms 
might save as many as 50 percent of those afflicted. 

This brings us to another point. You may have been thinking 
that all of this searching into ourselves is a wet blanket on romance, 
that it may take the joy out of life and arouse many fears. In some 
instances this might be true, but on the whole we believe that 


genetics analysis can do far more to allay fears than to arouse them. 

At the moment that we write this, the newspapers carry the re- 
port that a young mother on Long Island has slain her two children 
(aged two and five) and attempted suicide because she feared that 
they had inherited cancer from her. Her mother had died of cancer 
a year before, and the poor woman herself had just undergone an 
operation for the removal of a growth which she believed, errone- 
ously, was also cancerous. Before the slaying she had sought fran- 
tically among her friends for information. We quote from the re- 

. She asked the cook all sorts of questions, how long did 
people live with cancer, and was it hereditary, and did she think 
the children had inherited it. The cook was unable to answer most 
of the questions.” 

Had the distracted mother been aware of the very facts with 
which you are now acquainted, her children would still be alive. 
For she would have known that there was no evidence that she had 
inherited cancer and, in view of its complexity, no chance that she 
herself could have transmitted it directly to any child. 

In innumerable other cases ungrounded fears regarding disease 
inheritance have wrecked people’s lives. Sometimes the fear itself, 
through psychogenic (mentally-induced) effects, may produce 
symptoms of the condition feared. This is especially true of in- 
sanity. Whatever the condition, the truth as to whether it is heredi- 
tary or not should usually prove more helpful than harmful to 
the individual, and is invariably of immense value to the physician, 
for an essential factor in combating any ailment is the knowledge 
of how it originates, 

To the further credit of genetics as a Micaeen lever it can be 
said that a host of conditions formerly thought hereditary have 
been proved otherwise, and few, if any important conditions not 
formerly considered hereditary have been added to the list. Fears 
about the inheritance of syphilis or any other acquired condition 
have been dismissed. Mothers can rest easier as to what they can 
or cannot do to the child they are carrying, In fact, genetic findings 
have swept away so many groundless fears that an average couple 


can today have children with less worry regarding heredity than 
ever before. 

Turning to the social traits, of intelligence, behavior, character, 
personality, etc., limited as may yet be our genetic knowledge, it is 
sufficient to also allay a host of longstanding fears. Many of the 
undesirable social traits in human beings have been indicated as 
due primarily to environment, and there has been. much to chal- 
lenge prevalent beliefs and suspicions regarding the hereditary 
“criminality,” “immorality,” or general “undesirability’ of mem- 
bers of this or that group, class or race. These findings, too, may 
be of use in your own life. If you have had the uneasy feeling that 
one of the forementioned traits, or some crudity, unpleasant man- 
nerism, inability to “get along” or other social deficiency in you 
was due to an inherited and incurable “streak,” you may see by 
now that your suspicions were probably unfounded. Again, in mar- 
riage, employment, friendship or any other relationship, if any 
individual you have in mind is personally desirable and of good 
character, you need not be greatly worried because he is of this or 
that race or nationality, or be much concerned because a grand- 
father had a penchant for abducting horses, or a great-aunt was no 
better than she should have been. 

This does not imply that you should ignore the important réle 
that genes obviously play in the development of mind, character 
and personality. But in these complex social characteristics, only 
where an individual himself shows some markedly adverse trait, 
or where it consistently appears in his family with no evidence that 
it is due to environment, can we consider him genetically suspect. 
Among members of your own family, and your intimates, where 
there are great differences in behavior and achievement which 
cannot be traced to environmental influences, you are justified in 
ascribing them in considerable measure to different gene combina- 
tions. Practically applied to your children, such knowledge might 
lead you to deal more sympathetically with the “black sheep” and 
to endeavor to make up to them by guidance and training, for 
inherited deficiencies. 

Further, with the strong indication that special talents, capacities 
and aptitudes are inherited, you may avoid forcing specialized train- 


ing on a child not inherently fitted for it, while at the same time 
encouraging the child who does reveal such capacities. We may 
add that with our knowledge regarding the inheritance of social 
traits constantly growing, problems of child guidance and training 
and of adapting individuals to the work and life for which they 
are best fitted will be increasingly simplified. 

So far we have been dealing with the practical application to 
your life of genetic facts. But, as we have seen, in all major aspects 
of our lives we cannot dissociate the effects of heredity from those 
of environment. It is of interest to note, therefore, that the tech- 
nique developed for sifting hereditary factors can be admirably 
adapted to the analysis of environmental influences. 

In much the same way that our genetic make-up is determined 
by biologic genes passed on from one generation to another, we 
may consider that our social make-up is determined by “soctal 
genes,” also passed on from one generation to another. These 
“social genes” would include all the factors that go to make for 
education, technical knowledge, habits, customs, mannerisms, at- 
titudes, beliefs, etc., and also for the physical effects of our social 
environment. Thus, you, like every other person, are the product 
of both biologic genes and “social genes,” with this difference be- 
tween them: The biologic genes were passed on to you through 
the stream of germ-plasm which has flowed from the dawn of life, 
with the only changes made being those produced by mutation. 
No human force has ever had the power to change a single one 
of these biologic genes; and not even today can we do more than 
cast out a limited number of the most defective ones, and that only 
by controlling reproduction. 

But our “social genes” are no inherent part of our germ-plasm 
or of our make-up. They were every one of them acquired. 

Suppose for a moment that you and your mate were set down, 
like another Adam and Eve, on an uncharted island where no 
man had ever been before and which no other human could ever 
reach. And suppose at the same time, that you were struck by 
some force that blotted out completely every thought, every mem- 
ory, everything you had learned from the moment of birth, and 
‘all consciousness of the past. Would you be able to talk, think, 


act or cope with existing conditions any better than did the most 
primitive Stone Age man? Science, as we have observed, says 
“No!” For your biologic genes would be hardly different than his, 
and despoiled of all the “social genes” acquired and accumulated 
in twenty thousand years, you and your descendants would have to 
travel the same long road of social evolution that stretched ahead 
of the Stone Age man. You would have to begin all over again 
learning the simplest facts by trial and error or accident. Genera- 
tions and scores of generations would pass before your descendants 
would learn to build dwellings, plant seeds, fashion the simplest 
mechanisms and develop a written language. 

So if you, or any one of us living today, differ from men of any 
previous generation in mental development, behavior or other 
social characteristics, or in the possession of any superior inven- 
tions, appliances or objects, it is because we'have had passed on to 
us an accumulation of “social genes” from the past, with their 
many resulting products. But this does not mean that all of the 
“social genes” of each generation were passed along, or that the 
best of them were carried over. Each generation has been the heir 
of all the preceding generations, and from what we know of heirs 
we have little reason to doubt that in many instances some of the 
best “social genes” in the successive legacies were lost, destroyed 
or tossed foolishly away. When we think of all the wars, barbaric 
invasions and blotting out of whole civilizations, of the whims 
and judgments of ruling despots that often dictated the course of 
culture as it is being dictated even today, we have good reason to 
believe that numerous “social genes” of inestimable value were not 
passed on, while some of the worst were. 

Just as we have identified many biologic “black” genes, we can 
easily point to “social black genes” linked with or producing pov- 
erty, ignorance, social and contagious diseases, injuries from acci- 
dent, vice, crime, suicide, corruption, strife, conflict and finally war. 
Look back through our pages and you will find little to suggest 
that these blights on mankind are inherent in our germ-plasm. 
Those who point to them as part and parcel of “human nature” 
ignore the fact that the impulses of the vast majority of people 
are toward sociality, kindness, peacefulness, tolerance, the desire 


to be and let be. We have only to think of the sacrifices of parents 
for their children, of the spontaneity with which we respond to our 
fellow creatures in time of fire, flood, disaster or distress, of the 
millions praying each day to be made better and worthier, of 
countless individuals working throughout the world to uplift others. 
Back of these impulses we can find many of our superior “social 

Herein, then, lies the hope for whatever improvement can be 
made in mankind, or that you, as an individual, can in your re- 
stricted sphere help to make in your children: 

1. Through the selection, by regulating and controlling human 
breeding, of the biologic genes which we pass on. 

2. Through the selection, by education, laws or other measures 
of the “social genes” which we pass on. 

As for our biologic genes, we have brought out in preceding 
chapters what might be accomplished eugenically. By sterilization 
and birth control we might reduce somewhat the proportion of 
the “unfit,” and by stimulating births in other quarters we might 
increase somewhat the proportion of the “fit.” This is on the basis 
of our present knowledge of human genetics, which is little com- 
pared to what we know about the breeding of plants and domestic 

The application of genetic principles to agriculture and livestock 
breeding has been so sweeping that there is today hardly a fruit, 
grain or vegetable which you eat, and no egg, poultry or meat 
from the better farms or ranches, in whose production genetic 
principles have not been employed. If you have any lingering doubt 
about the reality of genes and chromosomes, and of the certainty 
with which they can be identified and combined, we refer you to 
the yearbooks of the United States Department of Agriculture for 
1936 and 1937, the former devoted almost in full and the latter in 
part, to practical genetics. Here you will find hundreds of pages 
filled with details regarding the genes and chromosomes of every 
important cultivated plant and food animal, and with facts which 
every alert farmer and breeder is applying today. 

If the knowledge of human genetics has lagged behind, it is not 
entirely because of our inability to experiment with human beings. 


Also responsible is the fact that the importance of human genetics 
has not yet been popularly realized and that our all too few trained 
geneticists have been forced, by practical considerations, to devote 
themselves chiefly to the problems of crops and livestock in which 
state or national governments are immediately interested. Once 
we know proportionately as much about the genetics of humans 
as we do about the heredity of plants and livestock, there is no pre- 
dicting what we may be able to do. 

However, at the moment we have no need to stake our hopes 
for an improved mankind on future genetic findings or on radical 
changes in our biological make-up. We can consider that we have 
not even begun to tap the genetic resources at our command. We 
have in our biologic genes now in circulation, scientists tell us, all 
the potentialities for a race of supermen—#f we can properly direct 
and control our environment. In other words, all our studies have 
led to renewed confidence in “human nature”—in our inherent im- 
pulses and capacities—and to the belief that not our biologic genes, 
but our acquired “social genes,” are responsible for most of our 
social ills. 

We noted in the chapter on “Race” that large groups and whole 
peoples have been praised for the virtues of the few gifted indi- 
viduals who have raised the general level of those about them. 

Similarly, the many have been damned for the excesses of the 
few. If the advancement of mankind has come through the efforts 
of a handful, civilization has again and again been hurled back 
by a few individuals, who, like cancers, have corrupted the rest. 
We have no more right, therefore, even in these questionable times, 
to condemn all civilization as hopeless because of some of its evil 
specimens than we have to consider that all persons are diseased be- 
cause a few have hemophilia or Huntington’s chorea. 

Today, evil “social genes” as embodied in the acts of malignant 
individuals present a greater menace than ever. Mankind has been 
brought so closely together that it must now be considered as one 
body. Whatever happens to a group of humans anywhere in the 
world can sooner or later affect others. “J/ faut cultiver votre jardin” 
(“Cultivate your own garden”), said Voltaire. Which was another 
way of saying, “Look to your own backyard!” But if that was ever 


good advice, it is so no longer. We cannot ignore what is happen- 
ing in the backyards of our neighbors or of our fellow men, be 
they ever so far away. We have learned that a malarial swamp on 
one man’s farm may menace others for vast stretches around, that 
a plague in China may reach us here, that a bank crash, a crop 
failure, a strike, a financial depression and most certainly a war, 
no matter where, may start a chain of effects spreading throughout 
the world and ultimately to you. There is no “social black gene” 
that might not some day strike at you and yours and no biologic 
“black” gene that might not find its way to your children or your 

So, if you are concerned with the practical application of genetic 
findings to yourself and to your children, you must think both in 
biologic and in social terms, and not only of your own family, but 
of others. Biologically, your action is limited by the children you 
have or do not have. Socially, even if you are childless, there is no 
limit to the influence you can exert. But nothing that is done to- 
ward biologic or social improvement can have permanent meaning 
if it is confined to one family, one group, or even to one nation. 
All that we have learned proves that one section of mankind can- 
not long maintain a corner on “superior” genes, biologic or “social,” 
or rid itself and keep free of the “inferior” genes in circulation. 
Only by improving others also can we improve ourselves, and only 
by promoting progress on a broad front, throughout mankind, can 
we give our own advancement significance or permanency. 

That something should and can be done to improve humanity 
is the view of many of us who do not consider that this is the 
best of all possible worlds and that it can run itself without plan- 
ning. We have seen and are seeing that the good, the superior, the 
“fittest” in genes, persons or doctrines are not automatically being 
swept on to survival, and that the bad, the inferior and the most 
“unfit” are not automatically swept into the discard. Those of us 
who are at the top of the social heap can no longer smugly ascribe 
this all to our greater intrinsic worth, diligence and perseverance. 
And where as individuals we have failed in what we have set out 
to do, if we have not reached the heights in our profession, busi- 
ness or in one of the arts, we cannot so easily blame ourselves. No 


one fully aware of the findings of genetics and related sciences can 
still cling to the old theories of predestination, or, contrariwise, to 
the belief that the individual is the “master of his fate and the 
captain of his soul.” Knowing that our lives are governed, if not 
dictated, by both biologic and “social genes,” we may look at both 
the shining successes above us, and at the criminals, the paupers, 
the drunkards, the misfits at the bottom and well say, “There but 
for the grace of my genes go I.” 

But if we today are the products largely of chance, our descendants 
do not have to be. We have had a long enough spell, all the thou- 
sands of years since Homo Sapiens made his appearance, of leav- 
ing our destinies to the fates or to the tides of circumstance, largely 
because we were ignorant of what otherwise to do. But here at 
last we have the first glimmers of true light as to why we are what 
we are, and what we can do to make the world better. Genetics and 
the related sciences have proved beyond question that we can guide, 
if not control, the destinies of those who follow us by selecting 
the units of biologic and social inheritance which we pass on to 
them. To make this selection intelligently, we must first under- 
stand ourselves, the sources of the good and the bad in us. It has 
been the lack of such understanding in individuals, and between 
one person and another, between man and woman, parent and 
child, class and class, nation and nation, race and race, that has been 
responsible for much of the strife, misery and unhappiness in this 
world. If we are called on to decide what first to include in our 
legacy to succeeding generations, our wisest choice might well be 
whatever genes there are, biologic and social, that make for better 
human understanding. 

fey be 



; ne 
ho ed | 

Append eo 


th Seiten a % 


i ay ae 
sv aan 


An a, 
‘ Bi 



Tue following compilation has been abstracted and adapted 
from the extensive “Chronology of Genetics” prepared by Robert 
Cook, Editor of The Journal of Heredity, and appearing in the 
Yearbook of the United States Department of Agriculture for 1937. 

As Dr. Cook notes, although domestic animals had been bred 
for many thousands of years, it was not until the end of the seven- 
teenth century that the dark mantle of superstition and gross ig- 
norance about the processes of heredity began to be pierced by 
the first intelligent experiments and researches. By the latter half 
of the eighteenth century the foundations of important livestock 
breeds were already being laid, chiefly in England, through care- 
ful inbreeding and selection. With the dawn of the nineteenth cen- 
tury, the march of knowledge leading to our present science of 
genetics had begun as herewith recorded. 

1809 J. B. P. de Lamarck (France) publishes “Philosophie Zoo- 

logique,” first attempt at a comprehensive theory of evo- 
lntion Waa 

1820 C. F. Nasse (Germany) suggests law of male sex-linked in- 
heritance, based on study of hemophilia. 

1822 John Goss (England) reports but does not interpret domi- 
nance and recessiveness, and segregation in peas. 

1826 A. Sageret (France) cites unit characters in human eye color, 
and uses term “dominant.” 

1841 R. A. von Kolliker (Switzerland) proves spermatozoa arise 
from parent body and are not parasites as previously 

1849 (1) Sir Richard Owen (England) enunciates principle of 
the continuity of the germ-plasm. This idea culminated in 
the:modern gene theory. 



2) G. Thuret (France), studying seaweed, is first to ob- 

serve union of sperm cell and egg cell (fertilization) and 

later shows that egg would not develop without fertiliza- 

1858 R. Virchow (Germany) enunciates principle that every cell 
arises from another cell, disposing of theory of spontaneous 
generation and establishing continuity of all life from re- 
mote beginnings. 

1859 Charles Darwin (England) publishes his “Origin of Species” 
marking turning point in scientific thought and the be- 
ginning of the modern experimental approach to biologi- 
cal problems. 

1865 F. Schweigger-Seidel and A. von la Valette St. George (Ger- 
many) independently prove that a sperm is a single cell. 

1866 (1) Gregor Mendel (Austria) publishes in the Proceedings 
of the Brinn Natural History Society his now famous 
paper, “Versuche tiber Pflanzen-Hybriden,” on inheritance 
in peas. His paper receives little critical attention and is 
destined to remain in obscurity for 34 years. 

(2) E. Haeckel (Germany) predicts that the cell nucleus 
will play a star role in heredity. 

1875 (x) E. Strasburger (Germany) describes the chromosomes. 

(2) Oscar Hertwig (Germany) proves that fertilization con- 
sists of union of two parental nuclei contained in the sperm 
and ovum, demonstrating that sexual reproduction is a 
process contributed to essentially equally by both sexes. 

1883 P. J. van Beneden (Belgium) reports reduction of chromo- 
some number in egg cells to half that in body cells, and 
draws important conclusion that chromosomes have a 
genetic continuity throughout the life cycle. 

1884-5 Identification of the cell nucleus as the basis of inheri- 
tance made independently by Hertwig, Strasburger, Kol- 
liker and A. Weismann (Germany). 

1885-7. Weismann publishes a theory of chromosome behavior 
throwing great light on what happens during cell division 
and fertilization. 

1886 (1) Francis Galton (England) devises correlation table for 









applying statistical methods to many biological problems. 

(2) Hugo de Vries (Holland) discovers mutations in prim- 
rose plants which form basis for his later mutation theory 
of evolution. 

W. Roux (Germany) suggests that longitudinal splitting of 
chromosomes when dividing means that many different 
qualities are arranged single file in the chromosome and 
can by the splitting process all be passed along when the 
cell multiplies. 

Chromosomes named by W. Waldeyer (Germany). 

Th. Boveri (Germany) and L. Guignard (France) formulate 
law of numerical equality of paternal and maternal chromo: 
somes at fertilization. 

Weismann promulgates his “germ-plasm” theory, refuting the 

_ widely held idea that acquired characteristics can be in- 

Flemming counts human chromosomes, finding 24 in eye tis- 
sue. (Later study is to reveal 24 pairs.) 

L. Cuénot (France) working with animals, and Strasburger 
(Germany) with plants, advance theory that sex is con- 
trolled within the germ cell, not by environment. 


Rediscovery and verification of Mendel’s principles indepen- 
dently by De Vries (Holland), Correns (Germany), and E. 
von Tschermak (Austria), marking the beginning of 
modern genetics. 

(1) Bateson and Saunders report identifying 26 paired hered- 
itary factors in various plants and animals. Also suggest 
that polydactylism (extra finger) in man may be inherited 
according to Mendelian principles. 

(2) De Vries publishes his “Mutation Theory of Evolution.” 

(3) E. C. McClung offers first clues to the existence of “sex” 
chromosomes on basis of his studies with insects. 

(4) Cuénot first demonstrates Mendelian inheritance in ani- 
mals (normal and albino mice). 



1902-3 W. W. Sutton (United States) shows that body chromo- 










somes are individually recognizable. 

W. L. Johannsen (Denmark) advances “pure line” concept 
and defines difference between “phenotype”’—the appear- 
ance of an individual, and “genotype”—the genetic make- 

(1) C. B. Davenport (United States) confirms Mendelian in- 
heritance of polydactylism in man. 

(2) Thomas Hunt Morgan becomes professor of zoology at 
Columbia University, founding the famed “Columbia 
group” of genetic research workers. — 

N. M. Stevens and E. B. Wilson (United States) confirm 
McClung’s theory linking sex-determination with the “sex” 

(1) The term “genetics” is coined by W. Bateson. | 

(2) C. W. Woodworth and W. E. Castle (United States) “dis- 
cover” Drosophila as an invaluable aid in genetic study. 

Correns advances theory that there are two kinds of male 
germ cells—male-determining and female-determining. 

Cuénot discovers a lethal factor in mice—that for yellow 
color—which, if inherited from both parents, kills the em- 
bryo early in development. This was the first of the many 
“killer” genes discovered in animals and man. 

The Galton Laboratory at the University of London, the 
first laboratory devoted to the study of human heredity, is 
founded with a bequest from Sir Francis Galton. 

(1) L. Epstein and R. Ottenberg (United States) point out 
that human blood groups follow Mendelian principles in 

(2) Morgan proposes explanation of sex-linked inheritance 
and publishes report of first gene mutation (white eye) 
found in Drosophila. | 

(3) Morgan announces the gene theory and the locating of 
specific genes at fixed points on Drosophila chromosomes. 

W. E. Castle and J. C. Philips (United States) by transplant- 
ing ovaries in mice, show that inherited traits transmitted 
to offspring are not changed by the intra-uterine environ- 
ment of the mother. 


1915 Morgan, A. H. Sturtevant, C. B. Bridges and H. J. Muller 
(United States) publish “The Mechanism of Mendelian 
Heredity,” an epoch-making book. 

1917 W. B. Kirkham, H. L. Ibsen and E. Steigleder (United 
States) prove the lethal action of the yellow gene in the 
mouse by embryological studies—an important step in the 
tracing of gene effects in the earliest possible stages of de- 

1918 H. D. King (United States) reports results of inbreeding 
rats for 25 consecutive generations, showing that close in- . 
breeding need not in itself be harmful if there are no bad 
hereditary factors in the stock. 

1919 Morgan and others publish “The Physical Basis of Heredity,” 
setting forth in detail the gene theory. 

1921 Morgan estimates that the gene has a diameter between 20 
and 70 microns. 

1923 F. A. Crew (Great Britain) finds the first lethal in livestock, 
that producing the “bulldog” calf, a non-living monster 
frequently appearing in crosses of Dexter and Kerry cattle. 

1927 Mutations are produced artificially through X-rays by Mul- 
ler, in Drosophila, and by L. J. Stadler, in plants, vastly 
facilitating genetic studies. 

1930-37 Analysis of inheritance in man is greatly enhanced through 
perfecting of the gene-frequency technique by F. Bernstein 
(Germany), L. Hogben, J. B. S. Haldane and L. S. Pen- 
rose (England), A. S. Wiener and L. S. Snyder (United 

1931 Wright gives first comprehensive picture of evolution in Men- 
delian terms, with stress on the balance and interplay be- 
tween selection intensity, mutation rates, inbreeding, isola- 
tion and migration. . 

1934 Painter discovers that giant salivary gland chromosorres make 
possible detailed studies of chromosome structure and lead 
to very exact location of genes. 

(Many genetic findings of recent years and those of the last few 

years are not here listed because sufficient time has not elapsed to 

definitely establish or fully evaluate them.) 



WE present here merely a selection of useful references, for our 
available space would not permit, or the nature of this work justify, 
a full listing of the several thousand books, papers and articles con- 
sulted or drawn upon. 

Preference has been given to the latest works, with few excep- 
tions anything published prior to 1y30 being omitted in view of the 
fact that all earlier publications of importance will be found sum- 
marized or referred to among the references cited. 

In the first classification (GENERAL) which follows, the books 
starred are those least technical and dealing chiefly with human 
heredity. The others are for the most part textbooks, and unless the 
titles indicate otherwise, deal with all phases of genetics. 


Bavr, E., Fiscuer, E., and Lenz, F. Human Heredity. Macmillan. °31. 
(Also revised edition in German—Menschliche Erblichkeit Lehre 
und Rassenhygiene. Lehmann, Munich. ’36.) 

CasTLE, W. E. Genetics and Eugenics. 4th ed. Harvard U. Press. *30., E. G. Heredity and Environment in the Development of Men. 
6th ed. Princeton U. Press. ’30. 

Dunn, L. C. Heredity and Variation. University Society, N. Y. 734. 

Fasten, N. Principles of Genetics and Eugenics. Ginn. 35. 

Gates, R. R. Heredity in Man. Macmillan. 731. 

Hocsen, L. Nature and Nurture. Norton. ’33. 

Genetic Principles in Medicine and Social Science. Knopf. °31. 

Jennines, H. S. *Biological Basis of Human Nature. Norton. ’30. 

*Genetics. Norton. 35. 
Morean, T. H. *Scientific Basis of Evolution. Norton. ’32. 
Theory of the Gene. Yale U. Press. ’28. 

Mutter, H. J. *Ouz of the Night: A Biologist’s View of the Future. 
Vanguard. ’35. 



Newman, H. H. Evolution, Genetics and Eugenics. 3d ed. U. of 
Chicago Press. *32. 

SHutt, A. F. Heredity. 3d ed. McGraw-Hill. ’38. 

Sinnott, E. W., and Dunn, L. C. Principles of Genetics. 2d ed. 
McGraw-Hill. ’32 

Snyper, L. H. Principles of Heredity. Heath. ’35. 

StocKarD, C. R. Physical Basis of Personality. Norton. ’31. 

Wa ter, H. E. Genetics. 4th ed. Macmillan. ’38. 

We ts, H. G., et al. *Science of Life. Doubleday. ’31. (Many parts deal- 
ing with human heredity scattered throughout.) 


For quicker identification, book listings are in larger type than those 
of papers or articles and are given first. 

Pre-Natal Development 
Davenport, C. B. How We Came by Our Bodies. Holt. ’36. 
WappincTon, C. H. How Animals Develop. Norton. ’36. 
The Human Egg (with Photographs) 
Lewis, W. H. Bulletin, Johns Hopkins Hospital. 48:368. ’31. 
Pincus, Grecory G. Anat. Rec. 69:163. Sept. ’25, ’37. 
Human Chromosomes 

Evans, H. M., and Swezey, O. Chromosomes in Man, etc. Memoirs, U. of C2!. 
Press. 9:1-65. °29. 

Demerec, M. What Is a Gene? J. of Hered. 24:369. °33. 
GoupscHMIDT, R. B. Theory of the Gene. Sci. Monthly, Mar. ’38. 
(Also see Morgan, T. H., under GENERAL.) 

Sex Determination 
Parsutey, H. M. Science of Human Reproduction. Norton. °33. 
(Also discussed in most text books listed under GENERAL.) 


KrocMan, W. M. Inheritance of Non-Pathological Physical Traits in Man. Eusg. 
News, Nov.-Dec. ’36. 

(Also detailed discussions in Baur, et al., and Gates, listed under 
Newman, H. H., et al. Twins, A Study of Heredity and Environment. 
U. of Chicago Press. ’37. 
Dionne Quintuplets 
Buatz, W. E., et al. Collected Studies of the Dionne Quintuplets. U. 
of Toronto Press. ’37. 


Disease and Defect Inheritance 
Biacker, C. P. Chances of Morbid Inheritance. Lewis, London. 34. 
Cockayne, E. A. Inherited Abnormalities of the Skin. H. Milford, 
London. ’33. 
Monr, O. Heredity and Disease. Norton. ’34. 
MuckERMANN, Herrmann. Vererbung und Entwicklung. Dimmler, 
Berlin. ’37. 
Gun, W. Y. J. Hemophilia in the Royal Caste. Eug. Rev., Jan. ’38. 
Mackin, Mapce. The Role of Heredity in Disease. Medicine. 14:1-75. 35. 
Wassinx, W. F. Heredity of Cancer. Genetica. 17:103. °35. 
Eye Defects 
WaarDENBuRG, P. J. Das menschliche Auge und seine Erbanglagen. 
The Hague. ’32. (Also in Bibliographia Genetica. Vol. VII.) 
Mental Defects 
Henry, G. W. Essentials of Psychopathology. (Chap. I. on Heredity.) 
William Wood. ’35. 

MERRIMAN, W. E. Psychoses in Identical Twins. Psychiat. Quart. 7:37-49. °33. 
Pottocx, H. M., et al. Heredity and Environment in Dementia-Praecox and 
Manic-Depressive Psychoses. Psychiat. Quart. Vol. IX, Jan. and Apr. ’35; Vol. 
X, Jan. and June, ’36. 
RosanorF, A. J., et al. Insanity in Twins. 
(a) Manic-depressive. Am. Jour. Psychiat. 91:247. °34. 
(b) Schizophrenia. Am. Jour. Psychiat. 91:724. 35. 
SutaTER, E. Inheritance of Mental Disorder. Eug. Rev., Jan. ’37. 
Other Defects and Diseases 
See Index Medicus, Quarterly Cumulative. A. M. A. 
Dust, L. I., and Lorxa, A. J. Length of Life. Ronald Press. 36. 
Peart, R. J. and R. De W. Ancestry of the Long-Lived. Johns Hop- 
kins Press. ’34. 
MauisorF, W. M. Span of Life. Lippincott. 37. 
Eaton, O. N. Summary of Lethal Characters in Animals and Man. J. of Hered., 
Sexual Abnormalities 
Gotpscumipt, R. B. Die sexuellen Zwischenstufen. (Intersexes.) J. 
Springer, Berlin. ’31. 
Younc, Hucn Hampton. Genital Abnormalities, Hermaphroditism 
and Related Adrenal Diseases. Williams & Wilkins. 737. 
Blood Tests | 
SnypvEr, L. H. Blood Groupings in Relation to Clinical and Legal 
Medicine. Williams & Wilkins. ’27. 

Present Status of Medicolegal Applications, etc. Eug. News. 21:45. May-June, 


LevINE, Puitip. Application of Blood Groups in Forensic Medicine. Am. J. Politi- 
cal Science. 3:157. 732. 


WIENER, A. S. Blood Grouping Tests in the N. Y. Courts. U. S. Law Rev., Dec. 

eee Parentage. Scientific Monthly, Apr. ’35. 

Freeman, F. S. Individual Differences: The Nature and Causes of 

Variation in Intelligence and Special Abilities. Holt. ’34. 
Kurneserc, Orto. Race Differences. Harper. ’35. 7 

Negro Intelligence. Columbia U. Press. 35. 

ScuwesincEr, G. C. Heredity and Environment. (Detailed treatment 
of intelligence studies, with large bibliography including most 
references up to 1933.) Macmillan. ’33. 

TERMAN, L. M., and Merriti, M. A. Measuring Intelligence. (Revised 
intelligence tests.) Houghton Mifflin. ’37. 

CaTTELL, R. B. Is National Intelligence Declining? (British study.) Eug. Rev., 

Papers referred to in text, reporting original studies: 
Lamson, E. E., J. of Educ. Psych., Jan. 738. 
Leany, A. M., J. Am. Statist. Assn. 30:281. 735. 
— LirHaver, Donan B., and KLINEBERG, O., J. of Genet. Psych. 733. 
—  SKEELs, Harotp M., J. of Consult. Psych., Mar.-Apr. ’38. 
—— WELLMAN, BETH L., J. of Exper. Educ., Dec. ’37; J. of Nat'l. Educ. Assn., 
Feb. ’38; and J. of Consult. Psych., July-Aug. ’38. 
Musical Talent 
Myjoen, Jon A. Die Vererbung der musikalischen Begabung. Metzner, 
Berlin. *34. 
SrasHoreE, Caru E, (Author or Editor). Studies in the Psychology of 
Music. University of Iowa: 
Vol. II. By Hazex M. Stanton. Measurement of Musical Talent. 
(With chapter on Inheritance.) ’37. 
Vol. IV. Objective Analysis of Musical Performance. ’37. 

PHILIPTSCHENKO, J. (In Russian.) Studies on Inheritance of Musical Talent. Bul- 
letin of the Bureau of Genetics and Plant Breeding, Vol. V. Leningrad. ’27. 

Exuis, Havetocx. A Study of British Genius. Houghton Mifflin. ’26. 
Henry, G. W. Essentials of Psychiatry. 350-55. (Discussion of abnor- 
malities in famous persons.) Williams & Wilkins. 38. 
Terman, L. M., et al. Studies of 1,000 Gifted Children. and ed. 
Genetic Studies of Genius, Vol. I. Stanford U. Press, 
East, E. M. Insanity and Genius. J. of Hered., Aug. 738. 
Auxport, G. W. Personality. Holt. ’37. 

Dott, E. A. A Practical Method for the Measurement of Social Competence. Eug. 
Rev., Oct. °37. 

Morton, N. W. Personality Tendencies and Physique. J. Abnorm. Soc. Psychol. 
30:430. 36. 


Sexual Behavior 
Terman, L. M., and Mizzs, C. C. Sex and Personality. McGraw-Hill. 
WESTERMARCK, E. Chapter “Homosexual Love” in The Making of 
Man, edited by V. F. Calverton. Modern Library. °31. 
Henry, G. W. Psychogenic Factors in Overt Homosexuality. Amer. J. of Psychiatry. 

93:4. Jan. 737. ary : . 
— with GarsrairH, H. M. Constitutional Factors in Homosexuality. Amer. 

J. of Psychiatry, May °34. 
SanDERS, J. Homosexuelle Zwillinge. Genetica. 16:401. 734. 
Haynes, F. E. Criminology. McGraw-Hill. ’35. 
LancE, J. Crime and Destiny. A. & C. Boni. ’31. 
Report of Natl. Com. on Law Observance and Enforcement. U. S. 
Govt. Printing Office. ’31. 
HorrMan, F. L. The Homicide Record for 1936. Spectator, Apr. 29. 37. 
‘Rosanorr, A. J., et al. Criminality and Delinquency in Twins. J. Crim. Law and 
Criminology. 24:923. 734. 
Evolution | 
Hooton, E. A. Up from the Ape. Macmillan. 31. 
Hurst, C. C. Heredity and the Ascent of Man. Macmillan. ’35. 
MacCurpy, G. G. (Editor). Early Man. (A Symposium.) Lippin- 
cott. °37. 
Reiser, O. L. Cosmecology: A Theory of Evolution. J. of Hered., Nov. ’37. 
Barzun, Jacqurs. Race: A Study of Modern Superstition. (Includes 
an extensive critical bibliography.) Harcourt, Brace. 37. 
Boas, Franz. The Mind of Primitive Man. rev. ed. Macmillan. ’38.. 
Anthropology and Modern Life. rev. ed. Norton. ’32. 
Effect of American Environment on Immigrants and Their Descendants. 
Science; Dec. 11, ‘736. 
Hatpang, J. B. S. Heredity and Politics. Norton. ’38. 
Herskovits, M. J. The American Negro, A Study in Race Crossing. 
“Knopf. ’28. 
Huxzey, Jutian, and Happon, A. C. We Europeans. Harper. ’36. _ 
Reuter, E. B. Race Mixture: Studies in Intermarriage, etc. McGraw- 
Hill. ’31. 
(Editor). Race and Culture Contacts. McGraw-Hill. ’34. 
Hrouicka, Axes. Reflections Regarding Human Heredity. Amer. Philos. Scc.. 
Proceedings, 75, No. 4:295. 735 
Eugenic Problems 
Carr-Saunpgrs, A. M. World Populations. Oxford U. Press..’36. 
Hoimess, S. J. Human Genetics and Its Social Import. McGraw-Hill. 



Hountincton, Ettswortu. Tomorrow’s Children. Wiley. ’35. 
Lorimer, F., and Oszorn, F. Dynamics of Population. Macmillan. ’34, 
PopEnog, P., and Jonson, R. S. Applied Eugenics. 2d ed. Mae- 
millan. ’33. 
Myerson, A., et al. Eugenical Sterilization. (Report of Committee, 
Amer. Neurolog. Assn.) Macmillan. ’37. 
THompson, WarrEN. Population Problems. 2d ed. McGraw-Hill. ’35. 
A Eugenics Program for the U. S. Eug. Rev. 27:321. Jan. ’36. 
Pre-Marital Health Schedule. (As used in England, with notes for physicians.) 
Eug. Rev. 27:306. Jan. °36. 
Snyper, L. H. Present Trends in the Study of Human Inheritance. Eugenical 
News. 73:61. July-Aug, 38. 
Fertility and Sterility — 
CaTTELL, R. B. Sterility in Man. Oxford U. Press. ’37. 
Meaker, S. R. Human Sterility. Wood. ’34. 
WILHELM, S. F. Sterility in the Male. Oxford U. Press. ’37. 
Wacner-Manstau, W. The Inheritance of Fertility. Ann. Eugenics. 6:225. ’35. 
eso S. The Physiology of Fertility in Man and Monkey. Eug. Rev. 28:37. 
Apt ae 30. 
Genet Fi Domestic Plants and Animals 
Yearbooks, United States Dept. of Agriculture for 1936 and 1937. 
Superintendent of Documents, Washington, D. C. 

(These two massive volumes present in elaborate detail genetic facts about al- 
most every important domesticated plant and animal.) 


The following are indispensable sources of information regarding 
the constant new developments in the field of genetics. Some of these 
are devoted chiefly to experimental genetics, but all carry many valu- 
able articles on human heredity. 

Annals of Eugenics. (A quarterly devoted to statistical studies in 
genetics and human inheritance.) Galton Laboratory, University 
College, Gower St., London, W.C. 1. 

Eugenical News. Eugenics Research Assn., Cold Spring Harbor, Long 
Island, N. Y. 

Eugenics Review. (Quarterly.) Published in London, Eng. Mac- 
millan & Co., Ltd., St. Martin’s St. W.C. 2. (Obtainable free with 
membership in the American Eugenics Society, 50 W. 5oth St., 
Ne we.C.) 

Genetics. Brooklyn Botanic Garden, Brooklyn, N. Y. 

Journal of Genetics. (British.) Cambridge U. Press, England. 

Journal of Heredity. Published by American Genetic Assn., Victor 
Bldg., Washington, D. C. 

‘ ve Py, ; 15 aye 
mi * 4 7 i ‘ é 4 
ne Pee 

a Pian ] hy als 


(Figures in bold face refer to illustrations.) 

Abnormalcy, 98 
Abortions, 36 
in U. S., 371 
sex ratio, 41 
Absolute pitch, 260, 261 
Achievement, 214 ff. 
Achondroplasia, 81, 99, 139, 195 
in animals, 145 
Acquired characteristics, 11, 19, 20, 
400, 402 
defined, 17 
disproof of inheritance, 327, 328 
experiments, 18 
skin color, 68 
Acromegaly, 140, 141, 145 
Addison’s disease, 69 
Adenoids, 227 
Adenoma, sebaceous, 189 (Rare 
cancers, etc., b.) 
Adrenals, 140 
Age of parents, effect on child, 23 
Albinism, 145, 147, 197, 198 
eyes, 56, 57 
hair, 63 
inheritance forecasts, 92 
Negroes (photo), 146 
effect on offspring, 20 
on embryo, 35 
on longevity, 170 
Allergic diseases, 129, 190 
Allport, Gordon W., 295 
Alopecia (juvenile hairlessness), 
148, 199 
Amaurotic idiocy, 162, 190 
Americans, 347, 348, 350 

Ancestry, 355 ff. 
blood concept (old), 355, 356 
significance, 357 ff. 
table of relationship, 358 
Anemia, 129, 189 
Angioneurotic oedema, 190 
Ape (see Primates) 
Appendicitis, 120 
deaths, 119 
Aptitudes, 279 ff., 401 
tests for, 281 
Aristocracy in man, 359 
Art, talent for, 280 
Artificial insemination, 43, 390, 
Aryan, Non-Aryan, 351 ff. 
Asthma, 129, 190 
Asthenic type, 84, 294 
Astigmatism, 192 
Ataxia, 149, 197 
Ateleotic dwarfs, 81, 139, 195 
Auer, Leopold, 277 « 
drawing of, 278 
Australoid peoples, 339, 340 
Aztecs, 340, 342, 349 

Bach, Johann Sebastian, 235 
Baldness, 134 ff., 199 
“cures, 138 
diseases causing, 137 
genes, 135, 136 
in eunuchs, 135 
inheritance, 136 
pattern, 134 
virility and, 137 


“Bastardy” actions, 205 ff. 
Baur, Ernest, et al., 343 
Beauty, 19 
inheritance, 96 
Behavior, 289, 290, 401 
(see also "Personality, Crime, 
Sexual behavior) 
Behaviorists, 20 
Bees, 175 
Bell, Alexander G., 382 
Birth, chances of, 27, 29, 31 
Birth control, 370, 375 
Birth rate, 367 ff. 
decline, 367, 368, 371 
differential, 368, 369, 370 
Birthmarks, 147, 197 
“Black” genes 
defined, 114 ff. 
elimination by 
376 ff. 
forecast tables, 202-204 
inheritance problems, 397 ff, 
“roll call,” 184 ff. 
Blakeslee, A. F., 293 
Blistering diseases, 148, 198 
Block, R. J., 229 
Blood cells, abnormal, 189 
Blood types, 206 ff. 
diagram, 207 
in paternity tests, 208, 210, 212 
Blue sclerotic (see Brittle bones) 
Blindness, 143, 191 ff. 
Boas, Franz, 82 
Body form, 80 ff. 
and behavior, 294 
inheritance forecasts, 95 
types, 84 
Bone fractures, multiple, 162 
Bonelli, Richard, 274 
Brachyphalangy (stub fingers), 
141, 142, 162 
as paternity proof, 211 
Brailowsky, Alexander, 237, 275 



Brain defects, 150 ff. 

Breasts, 85 

“Brittle bones,” 141, 143, 196 

Brode triplets, 105 

Bullosa connata, 
ing, d.) 

Bustabo, Guila, 260 

198 (Blister 

Cancer, 121 ff., 339, 400 
common, 121, 122 
deaths, 119 
intestinal, 123 
radium induced, 124 
rare types, 124, 188, 189 
skin, 123 
transmission, 124 

Carrel, Alexis, 170, 391 

Castle, W. E.,'53, 414 

Castration, effects 180 

Cataracts, 143, 191 
effect on eye color, 59 

Cat-dog mating, 26 

Cell, human 
differentiation, 47 
multiplication, 12 
number in body, 30 

Cerebral sclerosis, 191 

Chaliapin, Feodor, 254 

Chamlee, Mario, 276 

Chance, laws of, 88, 90 
diagram, 89 

Chess prodigies, 283 

Chicken or egg?, 325, 326 

“Child forecast” tables, 91-96 

Childhood rheumatism, 120, 121, 

188, 399 

Chin (and personality), 294 

Chinese, IQ’s, 229 
American boy reared among, 


in ancestry, 356 
as chain gangs, 44 ff. 
changes, 331 


Chromosomes (Cont.) 
combinations possible, 27, 28, 29 
definition, 6 
diagram 46 
in germ cells, 13 
in heredity process, 10 
incompatibility, 24 
under microscope, 7 
multiplication, 12 
arranged in pairs, 6 
sex. ( Xepand i) e59,, 10; 41, 

132 | 
in sperms, 5, 14 

Civilization, origin, 348 

Cleft palate, 141, 143, 195 

Coffee-colored spots, 147, 197 

Color-blindness, 131, 132, 133, 193 

Complexion, 66 

Conception (diagram), 32 

Congenital diseases, how differ 

from hereditary, 116f. 

Cornea defects, 193 

Cousin marriages, 381 ff. 

(see Inbreeding) 

Covadonga, Count of, 131 

Cranial soft spot, 143, 196 

Cretinism (idiocy), 117, 128, 141, 


Crime, 300 ff., 401 

“Criss-cross” inheritance, 132 

Cross-eyes, 144, 193 
in Dionnes, 111 

Dafoe, Allan, 107, 108 
Darwin, Chas., 11, 325 ff. 
theories, 332, 333 
Davenport, Charles B., 53, 414 
da Vinci, Leonardo, 281, 284 
Day blindness, 193 
Deafness, 144, 146, 195, 382 
inbreeding results, 382 
and intelligence, 227 
prenatal causes, 35 


causes—formerly, today, 160 
—principal causes, 119 
lethal genes, 161, 162 
(see also Longevity) 
Degeneracy, 361 
Delinquency, juvenile, 306 
Dementia precox, 294 
(see Schizophrenia) 
Diabetes, 125, 188, 398, 399 
death rate, 119 
Digestive diseases, 128 
Dionne quintuplets, 107 ff. 
birth of, 107 
differences, similarities, 108, 109, 
112 a 
handedness, 111 
how produced, 109, 110 
intelligence, 225, 226 
mirror-imaging, 111 
personality, 296, 297 
photograph of, 298 
webbed toes, 108 
Diseases, hereditary, 119 ff., 185 
cure of, 185 
inheritance forecasts, 201 ff. 
summary tables, 188 ff. 
(see also “Black” Genes) 
Dog-cat mating, 26 
“Dog” men (sweat gland defects) 
Dogs, studies of, 83 
Donkey-horse mating, 26 
Drosophila, 2, 52, 53, 87 
Drugs, effect on embryo, 35 
Drunkenness, inheritance, 20, 328 
- (see also Alcohol) 
Dublin, Louis I., 160, 163, 341 
Dugdale, R. L., 363 
Dwarfs, 81, 195 
inbreeding results, 382 
mating of, 139 
Dystrophica (see Blistering diseases) 


Ear defects, 144, 195 
outer ear, 194, 195 
Ear shapes, 74 
inheritance forecasts, 95 
Earthworm, 175 
Eczema, 129 
Egg, human, 33 
fertilized, 31 
formation, 39 
how produced, 15 
mother’s age effect, 20 
number in women, 6 
photograph, 4 
reduction division, 15 
variety possible, 27 
“weak,” “strong,” 36 
(see also Embryo) 
Elephant skin, 162 
Elman, Mischa, 278 
Embryo, human, 34 
effect of drugs, alcohol on, 35 
first stages, 31-33 
twelve-day-old, 33 
(see also Egg) 
English, formation of (map), 344 
Enesco, Georges, 254 
Environment and heredity, 20, 36, 
99 ff., 214 ff., 235 f., 402 ff. 
in degeneracy, 264 
in intelligence,’ 222, 223 
in talent, 281 
(see also Music talent) 
Epicanthic fold, 74, 194 
Epilepsy, 155, 156, 190 
genius and, 287 
Eskimos, 340, 342, 348 
Eugenics, 185, 366-403 
breeding of humans, 393 
conclusions regarding, 394, 395 
definition, 373 
early concepts, 373, 374 
mating problems, 397 ff. 
negative program, 373 ff. 
positive program, 385 ff. 


Eunuchs, 181 
baldness in, 135 
Eurasiatics, 339, 342 
Europeans, formation of (maps), 
Eutelegenesis, 390 
(see Insemination, artificial) 
Evolution, 325 ff. 
of man (see Races) 
purposive, 333 
Eyebrows, 78 
Eye color, 55 ff., 56 
changing of, 61 
inheritance forecasts, 89 
patterns, 59 
unmatched eyes, 60 
Eye defects, 143, 144, 191 ff. 
“pop” eyes, 294 
Eyelashes, 92 
double, 194 
Eye shape, 74, 75 
inheritance forecasts, 92 
reasons for, 341 

Fallopian tube, 31, 32 
Far-sightedness, 144, 192 
Fatty skin growths (xanthoma), 
148, 198 
Features, 70 ff. 
environmental effects on, 79, 293 
inheritance forecasts, 87-96 
Feeble-mindedness, 152 ff., 191 
inbreeding results, 382 
IQ classifications, 154 
and musical aptitude, 257 
sterilization, 377 ff. 
Females, longevity of, 168 
(see Males and Females) 
in classes, 369 
inheritance, 182 
Fertilization, 6, 30, 32, 45 
Feuermann, Emanuel, 254 

Finger defects, 141, 142, 196 


Flagstad, Kirsten, musical pedi- 
gree, 261 
Freckles, 69 
(see also Malignant freckles) 
French, formation of (map), 344 
Friedreich’s ataxia, 149 

Galton, Francis, 373 
“Gemmule” theory, 11 
acquired effects on, 19 
action, 44 ff., 53, 67 
appearance, 8, 9 
composition, 44, 330 
inhibitors in eyes, 59 
intelligence, 231 
lethal, 131, 187 ff. 
Mendel’s concept, 51 
musical talent, 265 ff., 268 
mutations, 16, 328 ff. 
segregation in races, 342, 347 
size, 8 
—Morgan’s estimate, 415 
symbols, 187 
types of, diagram, 45 
(see also “Black” Genes, Chro- 
mosomes) i 
definition, 1 
future, 405 
in livestock, plants, 404 
Genius, 279 ff. 
286 f. 
gene hypothesis for, 285 
in women, 286 
Germans, 345, 351 ff. 
formation of (map), 345 
head shapes, 84 
Germ cells, 13 
Germ-plasm, 11 
Gibbs, F. A., 257 
Gieseking, Walter, 237 

insanity and, 


Glands (ductless), 97, 140 
behavior effects, 295 
homosexuality, influence in, 

319 £. 
sex, 180 

Glaucoma, 143, 191 

Glioma retina, 162, 192 

Gluck, Alma, 262 

Goddard, H. H., 360 

Goiter, 128 . 

Goldschmidt, Richard, 53, 320 

Gonads, 140 

Goossens, Eugene, 275 

Gray, James, 289 

Grayness, premature, 200 

Green, Howard W., 127, 164 

Gynandromorph, 174, 176, 177 

Habits, 293 

Hair, body, 78 

Hair color, 62 ff., 62 
environmental influences, 64 
inheritance forecasts, 93 
pubic, 65 

Hair defects, 148, 199, 200 
baldness, 134 ff., 136 
hairlessness, man, dog, 145 
premature grayness, 200 

Hair form, 76 ff. 
construction, gene action, 77 
inheritance forecasts, 94 
reasons for, 341 
woolly (non-Negroid), 200 

Hair whorl, 78, 103 
in Dionnes, 108 

Haldane, J. B. S., 350 

Hand abnormalities, 141, 142, 196 

Handedness, in Dionnes, 108 
in twins, 103 

Hapsburg lip, 76 
inheritance forecast, 95 

Hare-lip, 141, 195 

Hay fever, 129 
(see Allergic diseases, 190) 

Head shape, 83 

environmental effects, 84 
and intelligence, 228 
Heart diseases, 120, 121 
deaths from, 119 
Heidelberg Man, 336, 337 
Heifetz, Jascha, 278 
Hemophilia, 130 ff., 132, 162, 189 
mutation, 329 
sterilization, 377 
in women, 131 
Henry, George W., 321 
Heredity and Environment (see 
Heredity process, 10 
Hermaphrodites, 176, 178 
lower animals, 175 
High blood pressure, 121, 188 
Hitler, Adolf, 354 
Hofmann, Josef, 254-258 
Hogben, Lancelot, 349, 365 
Hollingworth, Lita, 220 
Holmes, Justice O. W., 33 
Homeliness, inheritance, 96 
Homicides, U. S., other countries, 
(see Murder, Crime) 
Homo sapiens, 336-339 
Homosexuality, 317 ff. 
Homunculus, 4, 5 
Hooton, Ernest, 301 
Hormones (see Glands) 
Horny skin, 148, 198 
Horse-donkey mating, 26 
Hunchback, 141 
Hungarians, formation of (map), 
Huntington’s chorea, 150, 151, 191 
Hutcheson, Ernest, 251 
Hypospadias, 182, 190 (Reproduc- 
tive, a.) 
Hypotrichosis (complete. hairless- 
ness), 148 


Ibsen’s “Ghosts,” 35, 116 
Idiocy, 117, 154, 155, 190, 191 
(see also Feeble-mindedness) 
effect on child, 22 
effect on sex ratios, 42 
Immorality, 401 
Inbreeding, 381 ff. 
Incas, 340, 342, 349 
Incompatibility, genetic, 24, 26 
Indians, American, 340, 342, 349 
skin color, 67 
Infant mortality, 160 
and economic status, 164, 167 
(see also Longevity) 
Insanity, 150 ff., 190f., 399 
and body types, 294 
in genius, 287 
mating problems, 397 f. 
sterilization, 378 
Insemination, artificial, 390, 391 
Intelligence, IQ’s, 217 ff., 401 
children and parents, 221 f. 
Dionnes, 224 
and head shape, 228 
normal grades, table, 218 
race differences, 229 
subnormal grades, 154 
twins, 225 
women, men, 228 
Intersexes, 179 
Iris defects, 194 
Irish, formation of (map), 344 
Italians, formation of (map), 345 

Japanese, intelligence, 229 
Jaundice, familial, 129, 162, 190 
Java Man, 336, 337 
Jennings, H. S., 53, 296, 366 
Jews, 351 f. 

head shapes, 84 

stature, 82 

intelligence, 229 


Johannsen, W., 359, 414 
Juilliard Graduates, musical talent 
studies, 236, 251-254 
names, 253 
parents, 264 
summary table, 252 
Jukes family, 152, 360 ff. 

Kallikak family, 152, 360 ff., 362 

Kapterev, P. N., 170 

Kerap, Tage, 308 

Keys quadruplets, 105 

Kidneys, polycistic disease, 129, 

Kiepura, Jan, 276 

Klineberg, Otto, 223 

Kreisler, Fritz, 276 

Kretschmer, Ernst, 294 

Lamson, Edna, 223 
Lange, J., 301 
Latins, blond, 63 
Leber’s disease, 144, 192 (Optic 
atrophy, c.) 
Lehmann, Lotte, 276 
Leonardo da Vinci, 284 
Lethal genes, 131, 161, 162 
Light sensitivity, 148, 198 (Blister- 
ing, e.) 
Lipoidosis (fatty skin growths), 
Lips, 74, 95 
Lithauer, Donah B., 223 
Lobster claw (split hand), 142 
Lombroso, Cesare, 300 f. 
Lotka, A. J.,. 163, 341 
Longevity, 158 ff. 
alcohol effects, 170 
expectation of life, table, 169 
Females live longer!, 168 
infant mortality and economic 
status, 164 
occupational differences, 166 



Males and Females (comparisons) 
chances of survival, 41, 168 
expectation of life, table, 169 
intelligence, 228 f. 
ratios at conception, birth, later 

life, 41, 42, 168 
sex characteristics in limbs, 323 
talent (see Genius, Musical 
Malignant freckles, 124, 147, 162, 
(see also Rare Cancers, 188) 

Malthusian doctrines, 366 f. 

Man, origin of, 333 £., 336 
(see also Homo sapiens) 

Manic-depressive insanity, 

191, 294 

aids to, 386 ff. 
postponement, 370 
school teachers’, 387 
(see also Eugenics, Mating) 

Martinelli, G., 251 
family of, 270 

Masculinity, Feminity, 179, 181, 

311 ff. 
age effects on, 316 
characteristics, 312, 316, 323 
gland effects on, 319 f. 
ink-blot tests for, 313 

scores, classifications, 315 


“Maternal impressions,” 34 

Mathematics, talent for, 282 
compatibility in humans, ani- 
mals, 25 
eugenic problems, 201, 397 ff. 
myths, 22, 23 
(see also Marriage) 
Mead, Margaret, 311 
Melchior, Lauritz, 276 
Mendel, Gregor, 49 ff. 
academic failings, 230 
experiment with peas, 49, 50 


Mendel, Gregor (Cont.) 
laws of, 51 f., 89 
“rediscovery,” 413 

Mental defects, 150 ff., 190 f. 
(see also Insanity, Feeble-mind- 

edness, Idiocy) 

Menuhin, Yehudi, 236 
background, 259 f., 270 
father’s opinion, 271 

Metropolitan Opera 

studies, 236, 245 
tables, 246-249 
voice types, table, 273 

Microcephalic idiots, 155, 191 

Midgets, 139, 195 
mating of, 81 
(see Dwarfs) 

Migraine headache, 129, 190 

Miles, Catherine C., 312 ff. 

Millichamp, D. A., 296 

Milstein, Nathan, 276 

Miosis (see “Pin-hole” pupil) 

Mirror-imaging, 104 
in Dionnes, 111 

Mirror-reading, 191 

“Missing Link,” 337 

Mjoen, J. A., 256, 261 

Mohr, Otto, 141 

Mongols, 339 ff. 
features, 341 
origin, migration, 340, 342 
skin color, 67 

Mongolian eye, 74, 75, 92 

Mongolian idiots, 117, 154, 191 

Mongolian spot, 69 
in paternity test, 211 

Monilithrix (defective hair), 199 3. 

Monsters, human, 35, 104 

Morgan, Thomas H., 1 
on acquired characters, 328 
on degeneracy, 365 
Drosophila experiments, 49, 52 f, 
gynandromorph, 177 



Morgan, Thomas H. (Cont.) 
proposes explanation of sex: 
linked inheritance, 414 
Moore, Grace, 276 
Morini, Erica, 272 
Morons, 155 
grading of, 154 
Mortality (see Longevity) 
Mother-child relationship, 33-36 
diagram, 34 
Holmes decision, 33 
Mouth shape, 74, 76, 95 
Mueller, Friedrich M., 351 
Mulattoes, 67, frontis. 
Mule, sterility in, 26 
Muller, H. J., 329, 391 
Murder, 301-307 
U. S., other countries, 302 
U. S. cities (map), 304 
attitude toward, 310 
Muscle defects, 148, 196 f. 
Muscle tone, 293 
Musical talent (original study), 
absolute pitch, 260 f. 
conclusions, 277 f. 
environment and heredity, roles, 
258, 272, 274-276 | 
feeble-mindedness and, 257 
genes, 265-269 
mathematics and, 281 
opinions on inheritance, 263 
requisites, 258 
results of various matings, 263, 
265, 269 
summary table, 259 
talent vs. training? (opinions), 
(Note: All musicians and sing- 
ers studied are listed alpha- 
betically in tables, pp. 238- 
241, 244, 246-249) 
Mutations, 16, 328 ff 
causes, 329 f. 


Mutations (Cont.) 
features, 341 
hemophilia, 329 
livestock, plants, 329 
X-ray effects, 330 
Muscular atrophy (peroneal), 196 
Mutism, 146, 194 
Myerson, Abraham, 380 
Myopia, 144 
Myxedema, 141 

Nail defects, 147, 199, 200 
Neanderthal Man, 336, 337 
Near-sightedness, 144, 192 

albinos, 146 

crime, 303, 306 

effects of sun on, 341 

hair form, 76 

“inferiority,” 350 

intelligence, 229 

origin, 340, 342 

primitiveness, 341 

red hair in, 63 

sex ratios, 42 

skin color, 66, 68 

tallest, 81 

-White problem in U. S., 68, 353 
Nephritis, 119 f. 
Nerves, 148, 196 f. 
Neuritis, hypertrophic, 197 
Neurofibromatosis (coffee-colored 

spots), 123, 197 
Nevus of Unna, 147 
Newman, H. H., 224, 298 
Night blindness, 144, 193 
Nipples, extra, 181, 190 (Repro- 
ductive, 0.) 

Nordic, 24, 26, 342 
“Normalcy” (defined), 98 
Norwegians, origin (map), 346 
Nose-bleed, 189 


Nose-shape, 70-73 
“bridge”-gene diagram, 72 
dominant-recessive shapes, 73 
inheritance forecasts, 95 
reasons for, 341 

Novaes, Guiomar, 245 

Nystagmus (oscillating eyeballs), 

144, 193 

Obesity, 85, 95 

Oddities in humans, 145 

O’Neill, Eugene (regarding 
“Strange Interlude”), 150 

Optic atrophy, 143, 192 

Organs, inheritance, 97 

Ormandy, Eugene, 260 

Orphans, intelligence studies, 222- 

Oscillating eyes, 144, 193 
Otosclerosis (middle-ear deafness), 
Ovaries, 15 
diagram, 32 
Ovum (see Egg) 
Oyster, sex in, 175 

Paderewski, Ignace, 254 
Pancreas, 140 
Paralysis, 149, 196 
eye muscle, 144, 193 
Parathyroids, 140 
Paternity (doubtful), 205 ff. 
blood tests, 206, 207, 210 
decision by various traits, 211- 
Peas, Mendel’s experiment, 49 ff, 
Pearl, Raymond, 163 
Pekin Man, 336, 337 
Personality, 289 ff. 
beauty and, 291 f. 
conclusions on inheritance, 298 f. 
defectives’, 296 
Dionnes’, 296 f. 


Personality (Cont.) 
genes for, 290, 292, 299 
physical traits and, 291-293 
sexual, 316 
twin studies, 298 
(see also Crime, Intelligence, 
Sexual behavior) 
Philiptschenko, J., 256, 271 
Piebald skin, 145, 198 (Albin- 
ism, d.) 
Pigmies, 24, 26, 81, 141 
Piltdown Man, 336, 337 
“Pin-hole” pupil, 144, 192 
~ Pink eye-color, 194 
Pituitary, 140 
Placenta, 31-35, 34 
Pneumonia, 119, 120 
Polyposis of colon, 189 (Rare can- 
cers, ‘etc.,f/)5 399 
Pons, Lily, 276 
Population problems, 366 ff. 
Porphyrinuria congenita, 148, 198 
(Blistering, e.) 
Poultry (sex reversal), 175, 180 
Predestination, 214, 218, 301, 305, 
Pre-Marital Health Schedules, 383, 
Bibliog. 421 
Pre-natal influences, 34 
on sex, 38 
Primates, 335, 336 
Prodigies, 283 f. 
chess, 283 
musical, 234 
Prostitution, 308-310 
Psoriasis, 198 (Scaly skin, d.) 
Puberty, 182 
Pyknic body type, 84, 294 

Quadruplets, 105 
Quintuplets (see Dionne) 

Races, 335 ff. 
characteristics, 374 ff. 
concepts of, 343 


Races (Cont.) 
crime, 305 
differentiation (maps), 344-336 
formation of, 339, 340, 342 f. 
intelligence, 229 
“purity,” 347, 353 
sexuality, 317 
Race-crossing, 24, 26, 353 £. 
Negro-White, 68 
Rachmaninoff, Sergei, 275 
Reflexes, 290, 328 
Renal glycosuria, 126, 188 (False 
diabetes ) 
Reshevsky, Samuel, 283 f., 284 
Retinitis pigmentosa, 143, 192 
Rheumatic heart disease 
Childhood rheumatism) 
Rhythm theory (in women), 32 . 
Rodzinski, Artur, 237, 276 
“Rubber-skin,” 147, 199 
Rubinstein, Artur, 260 
Russians, formation of (map), 346 


Scalp cysts, 199 
Scaly skin, 147, 198 
Schizophrenia, 152 f., 191 
(see also Insanity) 
Schnabel, Artur, 243 
Schola Cantorum (Voice types), 
Schwesinger, Gladys C., 225 
Seashore, Carl E., 256 f. 
Harold G., 258 
Seborrhea (Baldness, d.), 199 
Seidel, Toscha, 260, 278 
Selection, pre-natal, 36 
Semitic, 351 
(see also Jews) 
abnormalities, 172 ff., 178, 182, 
characteristics, 174, 179 ff. 
—in limbs, 323 
chromosomes, 132, 133 

differences in longevity, 167, 168 


Sex (Cont.) 
factors in eye color, 60 
glands, 180 
impulse, 316 f. 
oddities (lower animals), 175 
Sex-determination, 37 ff. 
diagram, 40 
false ideas about, 37 f. 
influencing, 38 
irregularities, 173 
Sex-limited inheritance, 134 
Sex-linked inheritance, 130 ff. 
diagram, 132 
eye defects, 144 
longevity, 168 
sweat-gland defects, 147, 199 
Sex-ratio, 37, 41-43 
control by artificial insemina- 
tion, 391 
Sex reversal, 174, 175, 178, 180 
Sexual behavior, 311 ff. 
gland effects on, 319 f. 
Shakespeare, William, 285 
Sickle-shaped blood cells, 189 
Skeletal defects, 141, 195 f. 
Skin, 78 
Skin color, 66 ff., 68 
environmental effects, 68 f. 
reasons for, 341 
Skin defects, 146, 148, 197-199 
Skull form, 82, 83 
Small eyes, 96, 143, 192 
Smeterlin, Jan, 237, 276 
Snail, sex in, 175 
Snyder, L. H., 293 
“Social genes,” 402 ff. 
Spanish, formation of (map), 345 
“Spectacle” eyes; 193 
Sperms, human, 4, 40 
age effect on, 13, 19 
artificial insemination, 390 f. 
contents, 5 
defective, 388 
early concepts, 4, 5 

haw produced, 11, 13, 14 


Sperms, human (Cont.) 
number in individual, 13 
sex-determining, 38-43 
size, 4 
variety possible, 27 

Spider hand, 141, 142 

Spinal deformities, 141, 196 

Spinal muscular atrophy, 162, 19€ 

Split hand, 142, 196 | 

Stanton, Hazel M., 256 

Stature, 80 ff. 
genes for, 82 
gland effects, 84 
inheritance forecast, 95 

Steatopygia, 85 

Sterility, 372, 388-391 
causes, 389 
inheritance, 182 
in mules, 26 
social, 371, 388 
treatments for, 389, 391 

Sterilization, 375 ff. 
history, 375 f. 
in Kansas, 380 
operation, nature of, 375 
possibilities, 376 ff., 379 - 

Still births, 36 
sex-ratio, 41 

Stockard, Charles R., 53 
dog studies, 83 

Strabismus (cross-eyes), 193 

“Strawberry” marks, 34 

Structural defects, 139 ff., 195 

Stub fingers, 141, 142, 196 

St. Vitus dance (chorea), 191 

Sugar urine, 126, 188 (False dia. 


Suicide, 309 f. 

Sunburn, 68 

Sweat-gland defects, 145, 147, 199 

Sydenham’s chorea, 191 

Symmetry, facial, 79 

Syphilis, 143 
congenital, 35, 115 
deaths, 119 

Syphilis (Cont.) 

“inheritance,” 114 
and intelligence, 227. 

Talent inheritance, 280 ff., 401 
(see also Musical talent) 
Tapeworm, 175 
Taste, sense of, 293 
Taussig, Frederick, 372 
Teeth, 76 
Teeth defects, 141 f., 195 
sex-linked, 133 
Telangiectasis, 189 (Bleeding dis 
_ Telegony, 23 
Temperament (see Personality) 
‘Lerman, L. M., 221,°226, 312 iff: 
Testes, 13 
Theft, 308-310 
Tibbett, Lawrence, 276 
Thomsen’s disease (muscle cramp), 
disease, c.) 
Thyroid, 140 
defects, 128 
effect on behavior, 294 
Toscanini, Arturo, 184, 236, 242, 
family, 259, 262, 267, 270 
Tremor, hereditary, 197 
Triplets, 105, 106 
Trophoedema (leg swelling), 197 
Tuberculosis, 126 
deaths, 119 
environment and, 127 
Tumors, 162, 192 
(see also Cancer) 
Twinning, 104-105 
Twins, 99-106 
crime studies, 301 
homosexuality in, 319 [102 
identical, fraternal, 100, 101, 
intelligence studies, 224, 225 

189 (Bleeding 


Twins (Cont.) 
mirror-imaging, 103, 104 
personality, 298 
Siamese, 104 

Ulcers, stomach, 129, 190 

Unmatched eyes, 194 

U. S. Department of Agriculture 
Yearbooks on genetics, 404 

Victoria, Queen, 131, 329 
Virtuosi (instrumental musicians) 
studies, 236 ff. 
tables, .238-241 
children of, 244 
Vocal talent, 250 ff. 
Voice type inheritance (original 

study), 273 

Waddington, C. H., 33 
Wallenstein, Alfred, 260 
War instinct, 307 
Webbed fingers, toes, 141, 196 
(hand, foot abnormalities) 
in Dionnes;, 108 
sex-linked, 133 
Weismann, August, 327, 413 
Wellman, Beth, 224 
Wells, H. G., 330 
White blaze (or forelock), 145,: 
197 (Albinism, c.) 
Wilson’s disease (chorea), 191 
desirable traits, 393, 394 
talent suppression, 272 
(see also Males and Females, 
Masculinity-Feminity, Sex) 
“Word deafness,’ 146, 194 f. 

X-ray, mutations through, 330 
Xanthoma (see Fatty 

Young, Hugh H., 178 
Zimbalist, Efrem, 262, 270 


HV2330 Cel 

Scheinfelf, Amram 
You and heredity. 

HV2330 | Gel 

Scheinfelf, Amram 


You and heredity. 

fi DATE J 

Pale el le 


pals toh Et tlth: 
ee ee 
ririatoh Bt lelete 


Patel ; cnt 
hn oy at = 
petal etsy Cate rettat: 
he TelSetetyis 2 i 

Seca ees 

eee | 

fences Sauna = 
pots rats 




ihe tet pe: 


wi ner x 

a tae 



pe serees