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YOU and
HERE DTT Y
by
AMRAM SCHEINFELD
assisted in the genetic sections by
MO RONG Deis GriW HIER) Ph.D:
RESEARCH GENETICIST, CORNELL UNIVERSITY
MEDICAL COLLEGE
PLEUS ERATE DEBBY. TinE AU THOR
With four color-plates and seventy-five draw-
ings, maps and diagrams
Including an original study of The Inheritance
of Musical Talent cite
ey
NENTS AY pat ge
Oo]
GARDEN CITY PUBLISHING CO, INC.
Garden City, New York Bp y |
a
fi}
CopPpyYRIGHT, 1939, BY AMRAM SCHEINFELD
All rights reserved. No part of this
work may be reproduced without the
written permission of the publishers.
H \/ JI3dO
S
we, |
To
MY FATHER
AND
THE MEMORY OF
MY MOTHER
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
/
PREFACE
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-
Vii
Vili PREFACE
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
genetics.
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
PREFACE ix
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
x PREFACE
“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
PREFACE xi
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.
AMRAM SCHEINFELD
New York City,
June 1, 1939.
Ristty!
n é a4 \
esas ¥
Se pach of
As . i}
Pie tate
wy
u?
CHAPTER
II.
III.
IV.
VI.
VII.
VIIl.
IX.
XI.
XII.
XIII.
XIV.
xv.
XVI.
XVII.
XVIII.
XIX.
XX.
XXI.
XXII.
XXIII.
XXIV.
XXV.
CONTENTS
PREFACE
- A NEW SCIENCE .
LIFE BEGINS AT ZERO
THE ETERNAL GERM-PLASM
WHAT WE “DON’T”? INHERIT
MYTHS OF MATING
THE MIRACLE OF “YOU” .
THE PERILOUS ROAD TO BIRTH
“BOY OR GIRL?”
SUPER CHAIN-GANGS .
PEAS, FLIES AND PEOPLE .
EYE COLOR . : n : *
HAIR COLOR
SKIN COLOR : é .
THE FEATURES
BODY FORM AND STRUCTURE
WHAT WILL YOUR CHILD LOOK LIKE?
WHAT MAKES US TICK
DUPLICATED HUMANS
THE DIONNES
THE “BLACK” GENES .
OUR PRINCIPAL ENEMIES .
FOR MEN ONLY .
STRUCTURAL DEFECTS
SICK MINDS
HOW LONG WILL YOU LIVE?
Xili
PAGE
Vil
II
17
22
27
3 I
37
44
49
55
62
70
80
97
oe
107
114
119g
130
130
150
158
XIV
CHAPTER
XXVI.
XXVII.
XXVIII.
XXIX.
XXX.
XXXI.
XXXII.
XXXIII.
XXXIV.
XXXV.
XXXVI.
XXXVII.
XXXVIII.
XXXIX.
XL.
STs
XLII.
XLIII.
CONTENTS
THE TWILIGHT SEXES
“BLACK” GENE ROLL-CALL
HOW DO YOU KNOW THE BABY’S YOURS?
ACHIEVEMENT: BIRTH OR LUCK?
THE BATTLE OF THE “IQ's”
MUSICAL TALENT: PART I
MUSICAL TALENT: PART II
FROM APTITUDE TO GENIUS
PERSONALITY) soe Iho sn ae
ENTER THE VILLAIN .
SEXUAL BEHAVIOR
EVOLUTION: CHICKEN OR EGGP
RACE (2s oR epee ask @ Bane Ver:
ANCESTRY) 5" ntect ited Reanim Pala eat in
THE ‘GIDDY (STORK its ae ee
EUGENICS: NEGATIVE APA Cg
PROGRAM FOR TOMORROW . ..
YOU ‘AND: HEREDITY 12 7) eee yk tee
APPENDIX eMedia stu sics kloan CM a een
INDEX . . . ° ° ¢ e e
PAGE
172
184
205
214
Stig
a
256
279
289
300
BEL
oa)
335
255,
366
373
396
409
423
LIST OF ILLUSTRATIONS
Parents and offspring (color plate). . . . . Frontispiece
The human egg and human sperms (from a photograph)
facing
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 .
Conception
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
PAGE
4
5
6
6
7
8
10
12
14
25
28
ay
32
33
34
40
46
50
56
56
62
68
72
2B
75
77
83
XVi LIST OF ILLUSTRATIONS
The laws of. chance
Homely parents: beautiful child. Eanes Parente Herel
child .
How twins are produced
Mirror-imaging
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
facing
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
facing
facing
PAGE
89
96
101
104
106
108
110
127
132
134
136
140
142
146
160
164
166
168
175
177
179
187
207
221
225
261
267
268
269
278
284
298
302
Lust OF TLEUS TRATIONS XV
PAGE
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
CHAPTER I
A NEW SCIENCE
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
another.
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
children.
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
I
2 YOU AND HEREDITY
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
principles.
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
beings.
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
A NEW SCIENCE 3
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.”
CHAPTER II
LIFE BEGINS AT ZERO
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
toothpaste!
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
4
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.
THE HUMAN EGG
HUMAN SPERMS
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
volume.
The black spot at
upper center is the
region of the nu-
cleus.
LIFE BEGINS AT ZERO 5
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
chromosomes.
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-
“CRANIAL
“UMBILICAL
CORD”
A)
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
father.
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
6 YOU AND HEREDITY
similar chromosomes—the contribution ofthe mother to the child’s
heredity.
eee @
=
> NUCLEUS
FERTILIZATION
(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-
somes.
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:
KARUCDALAVOHHOGREHD OM
ABCDEFGHIJKLMNOPQRSTUVWHH
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
LIFE BEGINS AT ZERO nile (7
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
HUMAN CHROMOSOMES
As they look under the
microscope.
8 YOU AND HEREDITY
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-
THE GENES
A. Section of a chromosome Cy
stretched out. The beads are &
the genes or contain the ‘SS
genes. ‘2
S
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 |
microscope.
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
true.
LIFE BEGINS AT ZERO 9
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.
THE HEREDITY PROCESS
EVERY MAN and EVERY WOMAN
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
CHAPTER III
THE ETERNAL GERM-PLASM
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,
If
12 YY O°U ASN(D2 EE REE Diletta
HOW A FERTILIZED EGC-CELL MULTIPLIES
)
oP
(1) Original cell. (Only four (2) Each chromosome splits in
chromosomes shown, for sim- half, lengthwise
plification )
»
ZO)\GO
(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
THE ETERNAL GERM-PLASM 13
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
virile.)
HOW SPERMS ARE PRODUCED
(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
them
(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
14
THE ETERNAL GERM-PLASM 15
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.
16 YOU AND HEREDITY
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.
CHAPTER IV
WHAT WE DON’T INHERIT
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-
17
18 _ YOU AND HEREDITY
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
WHAT WE “DON T’. INHERIT 19
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
queen.
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
Front.
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
20 - YOU AND HEREDITY
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
conclusions.
CHAPTER V
MYTHS OF MATING
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-
22
MYTHS OF MATING 23
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-
favorable.
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
24 YOU AND HEREDITY
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
attention:
“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
MATING
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
A HORSE A DONKEY
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
cells.
BUT All Varieties of Human Beings Are Fertile With One Another
Because
—All humans are of the
same species with the
same kind of chromo-
somes. Thus, the smallest
pygmy
—and the tallest Nordic
could mate and produce
a child perfectly normal
in the eyes of Nature.
26 YOU AND HEREDITY
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.
CHAPTER VI
THE MIRACLE OF YOU
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
27
28 YOU AND HEREDITY
Representing chromosomes Representing chromosomes
received from one's received from one's
MOTHER FATHER
ON
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
what?”
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
30 YOU AND HEREDITY
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.
CHAPTER VII
THE PERILOUS ROAD TO BIRTH
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—
31
CONCEPTION
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-
side.
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.
32
THE PERILOUS ROAD TO BIRTH 33
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
34 YOU AND HEREDITY
RELATIONSHIP BETWEEN MOTHER AND CHILD
MOTHERS OTHER'S
Hee & <— NERVES
RA
an, wy arse ferwne®. SO
> of . hte .
ReAP eno ee: UMBILICAL
: CORD
FLUID EMBRYO
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
them.)
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.
THE PERILOUS ROAD TO BIRTH 35
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-
thing.
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
36 YOU AND HEREDITY
then transmitted it to the child before or during the process of
birth.
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
survive.
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.
CHAPTER VIII
“BOY OR GIRL?”
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
wrong?
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-
ception.
. 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
37
38 YOU AND HEREDITY
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
SABIOY “OR GIRL?! 39
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
woman.
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
Y-bearers.)
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!
HOW SEX IS DETERMINED
This is what makes all the differences
there are between a woman and a man:
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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:
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the result is an individual with TWO "X"s
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the result is an "XY" individual, or
aT (<2) A BOY
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40
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
42 YOU AND HEREDITY
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-
ened.
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
DOBSO.YO Ba GRIN Pes 43
and then, by artificial insemination, producing boys and girls at
will?
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!”
CHAPTER IX
SUPER CHAIN-GANGS
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.
A4
SUPER CHAIN-GANGS 45
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
OUR “CHAIN-GANGS”
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
Sculptor
Chemist
Engineer ete
Architect Colorist
e eae
oe ae y
Sa A Plumber
FROM
FATHER Carpenter
Mason
Engineer
Architect
CHAIN AY’
FROM
MOTHER
NOTE that in each of
these ''mated" chains,
the workers (“genes'|
at corresponding points, are ase«
signed to exactly the same type of |
work.
46
SUPER CHAIN-GANGS 47
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
48 YOU AND HEREDITY
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.
CHAPTER X
PEAS, FLIES AND PEOPLE
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
cultivates—fruit-flies.
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
49
ONE OF MENDEL’S EXPERIMENTS WITH PEAS
Asc
GENERATION &
RED 29 << WHITE
(A) vy (8)
PRODUCED
2 Nd
GENERATION
-But when any 4
of these offspring
were mated, they
PRODUCED
Zrd. “AW
GENERATION
3 in 4 RED LiIN4 WHITE
(Like Grandparent “A’) (Like Grandpt. B )
50
PEAS, FLIES AND PEOPLE 51
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-
flowered.
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 |
THe “MENDELIAN Laws”
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
52 YOU AND HEREDITY
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
PEAS, FLIES AND PEOPLE 53
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
54 YOU AND HEREDITY
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.
CHAPTER XI
EYE COLOR
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.
55
56 YOU AND-HEREDITY
(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.
WHAT MAKES YOUR EYE COLOR—
(Cross-section)
GENES
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
REAR
An optical illusion OF IRIS
(There is no blue pigment
(One alone is recessive to
all others except Albino)
in the eye)
—GREEN
—GRAY
(yellow ++ blue = green)
Effect
is due to
scattered yellow
pigment in
FRONT
OF IRIS
acting with the
blue reflection
Effect
is due to
scattered dark
pigment in
FRONT
OF IRIS
screening blue
reflection
from behind
(Gene action of green
and gray eyes not yet
clearly established)
Two brown-eye
—BROWN Effect genes
is due to
concentrated
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 -
pink
An Illusion
(The eye is really
colorless)
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
EYE COLOR a7
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
58 YOU AND HEREDITY
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
EYE COLOR 59
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,
60 YOU AND HEREDITY
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
prevalent.
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
EYE COLOR 61
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!”
CHAPTER XII
HAIR COLOR
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
factors.
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.
62
WHAT MAKES YOUR HAIR COLOR—
—WHITE
(Natural)
DUE TO
No
pigment
granules
among
hair cells
Yellow
effect
produced by
dilute
pigment
Effect
produced by
dissolved
red pigment
diffused with
the scattered
pigment granules
Effect
produced by
heavy deposit of
pigment granules
(The heavier the
déposit, the darker
the brown)
Intense
deposit of
pigment
granules
GENES YOU CARRY
(If white hair is
not due to age or
disease)
C@
(But all hair
color types may be
carrying one hidden
White-Hair Gene)
My
(
H
\
@+°?
(The "Red-Hair” Gene
is a special one
which shows its
effect if not
masked by
very "Dark-Hair”
Genes)
Red Gene may make
hair reddish-brown)
06: 0@
or Gene
for
ee1 |.
lighter
shade
NOTE: AN'Y GENE SYMBOL USED HERE MAY REFER TO MORE THAN ONE GENE
HAIR COLOR 63
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,
64 3 YOU AND HEREDITY
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
HAIR COLOR 65
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.
CHAPTER XIII
SKIN COLOR
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
bitterness.
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-
66
SKIN COLOR 67
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
68 YOU AND HEREDITY
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-
SKIN COLOR
IF A NEGRO MATES WITH A WHITE:
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
B
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
a
SKIN COLOR 69
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-
vader.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.
CHAPTER XIV
THE FEATURES
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
70
THE FEATURES 71
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
72 YOU AND HEREDITY
HOW THE “NOSE-BRIDGE” GENE WORKS
—lf a bit further
down, an average-
length nose; if much
further down, a
LONG
NOSE
@ If the "bridge"
gene in its
workings stops
short, result is a
SNUB
NOSE
—If it makes just
a small angle, re-
sult is a
CONCAVE
NOSE
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
"DOMINANCE" AND "RECESSIVENESS" IN NOSE-SHAPES
The gene DOMINATES The gene
for for
Prominent and Moderate and
Convex Straight
The gene The gene
SS fe DOMINATES Fs
-O On|
ae (_)
| High and Narrow Low and Broad Bridge
i Bridge (As in Negroes)
| The gene DOMINATES The gene
for for
1
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.
73
74 YOU AND HEREDITY
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
“EYE-SHAPE” GENES
The gene The gene
for— for—
© DOMINATES @e ie
STRAIGHT SLANT
(Not Chinese type)
LED DOMINATES Oe | ey.
MONGOLIAN FOLD EUROPEAN
(Chinese)
DOMINATES ©
On } | DOMINATES Oe a
LONG LASHES SHORT LASHES
©). via DOMINATES Oy Lo) x
(An abnormality)
75
76 YOU AND HEREDITY
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
THE FEATURES 77
THE “HAIRDRESSER” GENES
MAIR FORM: STRAIGHT WAVY CURLY KINKY
— = 2 @ea ee
2 IAS ic
\
s)
4
t
re
cow ee ow won
)
Me aucee by
genes shaping
HAIR FOLLICLE = . :
_ 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:
is
age gene “CURLY gee “WAVY “gene “STRAIGHT « gene
| Ominar? Q “omin ore? Q Comin ake? Q
A QA R
— a
78 YOU AND HEREDITY
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
genes.
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
THE FEATURES 79
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. :
CHAPTER XV
BODY FORM AND STRUCTURE
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
80
BODY FORM AND STRUCTURE 81
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
82 YOU AND HEREDITY
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
that:
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
BODY FORM AND STRUCTURE 83
HEAD SHAPES
ROUND HEAD LONG HEAD
(Brachycephalic) (Dolicocephalic)
a mr,
TOP y ( 0
VIEW
> an ia a
al v7
SIDE
VIEW
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
84 YOU AND HEREDITY
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.
~
BODY FORM AND STRUCTURE 85
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-
86 YOU AND HEREDITY
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.
CHAPTER XVI
WHAT WILL YOUR CHILD LOOK LIKE?
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
87
88 YOU AND HEREDITY
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
_ ONE’ TAILS” receive RECESSIVE
_ No matter how many times No matter how many children
THE LAWS OF CHANCE
IF YOU, TOSS A COIN WITH ~ SIMILARLY, IF YOU CARRY
TWO DIFFERENT SIDES, A MIXED PAIR OF ANY GENE,
ONE “HEAD” ONE “TAIL ”— ONE “DOMINANT, ONE “RECESSIVE"
The odds are exactly even When you mate, the odds
that it will ane are exactly even that
any child will receive
v \
o ©
p b e , THE DOMINANT THE RECESSIVE
HEADS TAILS GENE _ GENE
Lin 2 times Lin2times Lin2 times Lined times
IF YOU AND ANOTHER -SIMILARLY, IF YOU AND YOUR
PERSON EACH TOSS A COIN MATE EACH CARRY A MIXED
PAIR OF GENES FOR SOME TRAIT
You: Your Mate:
Rene © G © @
Every time you have a child
he Odds are exacty
Lin4 times
-The odds are exactly
1 in4times
BOTH
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
89
go YOU AND HEREDITY
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!
HOW TO USE THESE “‘CHILD FORECAST’’ TABLES
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.
EYE-COLOR FORECAST
IF EYES OF ONE
PARENT ARE:
BROWN (or BLACK)
Type r.
_ family were dark-eyed
Type 2. Where some in
this parent’s family have
lighter-colored eyes
(gray, green or blue)
GRAY or GREEN
BLUE
ALBINO (Colorless)
Ifallthisparent’s X
IF EYES OF OTHER
PARENT ARE:
No Matter
What Color
Brown, Type 2
Gray, Green
or Blue
Gray, Green
or Blue
Blue
Normal-eyed par-
ent of any eye-
color
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
brown)
Almost certainly blue.
(Rarely a darker shade,
the possibility being less
if parents’ eyes are light~
blue)
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
EYE-SHAPE FORECAST
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.
Q2
HAIR-COLOR FORECAST
IF ONE PARENT’S OTHER PARENT’S Child’ s Hair-Color
HAIR-COLOR IS: HAIR-COLOR: Will Be:
DARK (Brown or Black)
Type z. Where allinthis X No Matter What Almost certainly dark
parent’s family had dark
hair
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
occasionallylight-brown
or blond
x Blond Even chances, (a) red or
—(b) light-brown or blond
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
family)
#
Typez. Ifflaxenorwhite X Blond—Flaxen Certainly blond, but
: or white with shade of darker
parent apt to prevail
93
HAIR-FORM FORECAST
IF ONE PARENT'S
HAIR IS:
CURLY
Type xz. If all in this par-
ent’s family are curly-
haired
Type 2. If some wavy or
straight in this parent's
family
~«
WAVY
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
STRAIGHT
KINKY
Type z. Where all in this
parent’s family are kinky-
haired
Typez. Whereother hair-
forms appear in this par-
ent’s family
OTHER PARENT'S
HAIR:
Any Form, except
kinky or woolly
Curly, Type 2
Wavy
Straight
Wavy or Straight
Straight
Straight
No Matter What
Hair Form
Curly or Wavy
Straight
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
else).
Almost certainly straight
Almost certainly kinky
Even chance (a) kinky or
(b) curly or wavy; rarely
straight
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.
04
FORECAST OF FACIAL DETAILS
NOSE
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.
EARS
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.
MOUTH
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.
STATURE FORECAST
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.
BUILD
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.)
95
HOW TWO HOMELY PARENTS MAY
HAVE A BEAUTIFUL CHILD
FATHER MOTHER
Bald Black, straight
Murky-green us
eyes Dull-brown eyes
Long-lashes lost Drooping eyelids
rough disease Ba d skin
ty
‘(local disorder)
Beta
Misshapen mouth
due to bad teeth
Bad nose due to
accident
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
HOW TWO HANDSOME PARENTS MAY
HAVE A HOMELY CHILD
FATHER MOTHER
Curly, black hair ey Blond
Large, black tif
eyes, long Blue eyes
lashes Long lashes
Well-shaped aay Regular teeth «
mouth and
chin
Ws ; ( ee Pretty mouth
ar
Bx
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)
CHAPTER XVII
WHAT MAKES US TICK
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
97
98 YOU AND HEREDITY
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.
CHAPTER XVIII
DUPLICATED HUMANS
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:
99
100 YOU VA NID RE RIE Daal
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
SeX.
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
HOW TWINS ARE PRODUCED
IDENTICAL TWINS
Are products of
A single and
sperm
A single
egg
MAO oO
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
therefore
Always of the same sex — two boys
or two girls
IOI
FRATERNAL TWINS
Are products of TWO different eggs
fertilized by TWO different sperms
Oo
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
Both
of the
Two boys
102 YOU AND HEREDITY
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
them.
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-
DUPLICATED HUMANS 103
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-
104 YOU AND HEREDITY
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.
HOW “MIRROR-IMAGING” MAY BE
PRODUCED IN TWINS
Hair whorl —~4 ( AY Q)axyiar whorl coun
clockwise ter clocKwis€
nl
Ne
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
DUPLICATED HUMANS TO
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
often.
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-
106 YOU AND HEREDITY
HOW TRIPLETS MAY BE PRODUCED
Single sperm fertilizes Two separate sperms fertilize
single egg two separate eggs
Fertilized egg ~£ .)
(embryo)
divides
as in twins lf < she
eae The
other
as one sa
@ individual naa PY!
to form
One twins
remains
“set and
oes on
9 to Other
develop divides
again ]
oe
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.
RESULT: IDENTICAL TRIPLETS
(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.
CHAPTER XIX
THE DIONNES
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
THE DIONNE QUINTUPLETS :
(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)
YVONNE |ANNETTE} CECILE | EMILIE MARIE
HAIR WHORL
pe Nese dl
ane a Right
VISION ;:
+1. 25V
(Most far-
sighted)
v4 Stills sav
Cross -EYES
nel b=,
SVE Peau
Sli rar ai
ar-|
“sight ted)
Lingerin
trace oF
cross-EvyEeSsS
THE DIONNES 109
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
produced.
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:
II0 YOU AND HEREDITY
HOW THE DIONNE QUINTUPLETS WERE PRODUCED
(Theoretical probability)
1. Asingle sperm united
with a single egg. Se)
Ja RON
2. The embryo divided
to form “identical
twins."
rs 7a
3. The “twins" again di-
vided to form ‘quad-
ruplets.""
i '
4. But at this point, three ; ;
i t
' pane a !
!
Vv
went on, ‘'set,"' to de-
I
'
G
"
velop as individuals— '
i
!
!
!
!
t
§. The fourth again di- eo sts
vided. a, Ap
Identical
Quintuplets: YVONNE ANNETTE CECILE EMILIE MARIE
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
THE DIONNES it
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
right-handed.
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
fact:
1A photograph of the quintuplets, with their heights and weights as of August,
1938, is reproduced in Chapter XXXIV.
112 YOU AND HEREDITY
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.
THE DIONNES I13
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.
CHAPTER XX
THE “BLACK” GENES
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
II4
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
116 YOU AND HEREDITY
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,
THE “BLACK”? GENES 117
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
118 YOU AND HEREDITY
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.
CHAPTER XXI
OUR PRINCIPAL ENEMIES
Tue twelve diseases which take the largest toll of deaths in the
United States yearly are:
Deaths
_ per 100,000
(Approx.)
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
germ.
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.
119
120 Y OUGAN DGIDE RE Dicky
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-
OUR- PRINCIPAL ENEMIES tal
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
{22 YOU AND HEREDITY
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
OUR PRINCIPAL ENEMIES 123
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.
T24 YOU AND HEREDITY
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
diabetes.
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.
OUR PRINCIPAL ENEMIES 125
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
126 YOU AND HEREDITY
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
tuberculous.
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-
TUBERCULOSIS AND ENVIRONMENT
_ ECONOMIC STATUS IN DEATHS FROM
VARIOUS NEIGHBORHOODS TUBERCULOSIS
(As indicated by average (Approximate
monthly rentals) averages
per 1,000 pop.)
QU
(Based on figures compiled in Cleveland, O..,
for 1928-32, by Howard Whipple Green)
127
128 YOU AND HEREDITY
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.
OUR PRINCIPAL ENEMIES 129
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.
CHAPTER XXII
FOR MEN ONLY - «
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
130
FOR MEN ONLY 131
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.
“SEX-LINKED™ INHERITANCE
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,
(A) for COLOR-BLINDNESS
DAUGHTER SON
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
(B) ""CRISS-CROSS" TRANSMISSION
(1) WOMAN As in Hemophilia
Normal, but a carrier
‘Bleeding’ gene cov- (2) ONE-IN-TWO
ered by normal one. SONS
. A BLEEDER ©
oo
.
. All his sons receiving
only his "Y" are normal.
(3) Every one of
"'bleeder's'’
daughters is car-
rier, like grand-
mother. Vip cece eat repeated as from No. },
132
FOR MEN ONLY 133
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
134 YOU AND HEREDITY
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?
INHERITED PATTERN BALDNESS
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
FOR MEN ONLY 135
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
HOW BALDNESS
IS INHERITED
@ .. . "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).
MEN
Type
A
OO
TWO "BALDNESS" GENES
{All of this man’s sons will be bald,
and if wife is Type A, daughters also)
SINGLE "BALDNESS" GENE
(Same effect as two genes, but only
one-in-two sons of this man will be
bald)
ake
Oe
TWO-"NORMAL" GENES
No baldness in this man's sons unless
his wife is Type A or Type B
WOMEN
Type
A Q
LG
©
TWO "BALDNESS" GENES
Produces thin hair or partial bald-
ness in women. (All sons will be bald)
Type
SINGLE "BALDNESS" GENE
No effect on woman herself, but
one-in-two sons will be bald
TWO "NORMAL" GENES
No baldness in this woman's sons
unless her husband is bald
136
FOR MEN ONLY 137
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
138 YOU AND HEREDITY
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.
CHAPTER XXIII
STRUCTURAL DEFECTS
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,
139
THE DUCTLESS GLANDS
NORMAL IF DERANGED
FUNCTION: MAY PRODUCE:
Pituitary
—''Pacemaker." Reg- —Structural defects
ulates growth and de- such as gigantism, -
velopment; stimulates dwarfism, acromegaly
sex-functioning. and sexual disorders.
Thyroid
— "Thermostat." Reg- —Goitre, cretinism,
ulates metabolism. myxedema.
Parathyroids
—Govern bone- for- —Bone softening spasms
mation and "tone™ in children,
nervous system.
Pancreas
—''Sugar’’ gland.
Produces insulin, reg- —Diabetes.
ulating sugar-conver-
sion.
Adrenals
—''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.
acteristics.
Z 140
STRUCTURAL DEFECTS 14!
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
upset.)
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
children.
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
142 YOU AND HEREDITY
HAND ABNORMALITIES
(All inherited through dominant genes)
STUB FINGERS EXTRA FINGERS
NO MIDDLE i
<— JOINTS
seen
fe
"SPIDER" FINGERS SPLIT HAND
(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-
STRUCTURAL DEFECTS 143
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
later.
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
144 7 YOU AND HEREDITY
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
ODDITIES IN HUMANS WHICH ARE COMMON
TO OR BRED IN OTHER ANIMALS
IN HUMANS
Piebald
Spotting
Absence of
Sweat Glands
Woolly Hair
Albinism
White Blaze
Hairlessness
““Pin-Head”
(As in Microce-
phalic idiots)
~Dwarfism
(Ateleotic)
Extra Fingers
‘Achondroplasia
:
|
Pattern patches of white
skinagainstdarkerskin
Necessity to pant when
overheated
Found among Whites as
well as Negroes
Lack of pigment in eyes,
skin and hair
Patch of white hair over
forehead
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
145
IN OTHER ANIMALS
Cows, dogs, etc.
Dogs, wolves
Sheep
Almost every animal from
mice to elephants
Horses (“‘Star’’ forehead)
Mexican hairless dog
Russian wolfhounds
‘““Toy’’ dogs
Cats, guinea-pigs
Dachshunds
146 YOU AND HEREDITY
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
causation.
“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.
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SONIPGTV OYDYN
STRUCTURAL DEFECTS 147
“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
neck.
“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
148 YOU AND HEREDITY
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
continually.
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
“beaded.”
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
STRUCTURAL DEFECTS 149
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.)
a
CHAPTER XXIV
SICK MINDS
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
known.
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,
150
SICK MINDS 151
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
chorea.
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.”
152 YOU AND HEREDITY
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.
SICK MINDS 153
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-
154 YOU AND HEREDITY
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
SICK MINDS 155
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
propagate.
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-
volved.
Epriepsy. The brain being part of the nervous system, there is a
popular cendency to confuse or link with defective mentality any
156 YOU AND HEREDITY
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
SICK MINDS 157
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.
CHAPTER XXV
HOW LONG WILL YOU LIVE?
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
always!
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
158
HOW LONG’ WILE YOU"LIVE? 159
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
life-span.
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
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HOW LONG WILL YOU LIVE? 161
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
maturity.
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
162 YOU AND HEREDITY
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
Tables.)
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-
HOW LONG WILL YOU LIVED? 163
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.
164 YOU AND HEREDITY
AS INCOMES DROP, DEATHS OF BABIES RISE
ECONOMIC INFANT
STATUS OF ° MORTALITY
FAMILY | PER
(As shown 1,000 BIRTHS
by monthly (Deaths under
rental paid) one year of age)
500 [20
MONTHLY ©
RENTAL ~*~.
*IQOM, os
x
75%
DEATHS
$5 ; “ZO
(OR LESS)
(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
HOW TONG WILE YoU ULLVE? 165
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-
viduals.
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
YOU AND HEREDITY
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
HOW LONG WILL YOU LIVEP 167
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,
168 | YOU AND HEREDITY
FEMALES LIVE LONGER!
AT BIRTH PROPORTIONATE
LwoPanl i). FEST BIRTH RATE
saa ek 6 vy, MORE BOYS
FEMALES THAN GIRLS
MALES
YOUTH a7’. ar. ae EQUAL
ae PROPORTION
OF BOTH SEXES
MATURITY i. Welt taceie a ee PROPORTION
I5%
MORE FEMALES
THAN MALES
RS Eh gb tee dace will Damaged a pt
ALMOST |
PEP oe TWICE AS MANY
FEMALES
AS MALES
SURVIVING
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-
HOW LONG WILL YOU LIVE?P 169
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.)
EXPECTATION OF LIFE
(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
170 b YOU AND HEREDITY
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-
zation.
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 .—
How LONG WILL VOoUCLIVED 171
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.
CHAPTER XXVI
THE TWILIGHT SEXES
399
“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-
tion?
172
THE TWILIGHT SEXES 173
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
174 YOU AND HEREDITY
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-
gans.
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-
ODDITIES IN SEX
THE TAPEWORM THE SNAIL AND THE EARTHWORM
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.
| AN OYSTER IN BEES
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.
IN POULTRY
® 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.
{75
176 YOU AND HEREDITY
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
HOW A GYNANDROMORPH
(Half-in-half creature)
MAY BE FORMED
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,]
gynandromorph.)
(After Morgan)
177
178 YOU AND HEREDITY
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-
THE TWILIGHT SEXES 179
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
AVERAGE INTERSEX AVERAGE
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
180 YOU AND HEREDITY
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
THE TWILIGHT SEXES 181
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.)
182 YOU AND HEREDLITY
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
THE TWILIGHT SEXES 183
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.
CHAPTER XXVII
“BLACK” GENE ROLL-CALL
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-
ments.
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
184
TRIACS (EIN BRO WI GA DT. 185
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
involved.
~ 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
186 YOU AND HEREDITY
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.”
KEEP THESE SYMBOLS IN MIND
KEY TO "BLACK" GENE TABLES
_
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
together.
DOMINANT QUALIFIED or RECESSIVE
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.
187
SUMMARY TABLES—“BLACK” GENES
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
INTERNAL AND GENERAL
Diabetes ‘Sugar Sickness’’. Due to pancreas defect.
False Diabetes
Childhood
Rheumatism
High Blood
Pressure ?
Kidney
Troubles
Cancer
(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-
hood.
Due to hardening of arteries. Late life.
Heredity uncertain.
a. Multiple cysts, serious in pregnant
women.
b. Urinary disorders. (Black, reddish, etc.)
(Stomach, breast, etc.) Inheritance doubt-
ful.
a. Malignant freckles. Dark, freckle-like
inflammations from sun, leading to cancer.
Infancy or childhood, usually fatal.
188
Genes
Required
@OR-
@ D(q)
@D
@@ R(q)
@@R
@@ R +}
SUMMARY TABLES—‘‘BLACK’’ GENES—CContinued)
Condition
Description
INTERNAL AND GENERAL (Continued)
Rare Cancers
and Tumors
(Continued)
Bleeding Diseases
- Anemia
Blood-Cell
Abnormalities
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
established:
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,
189
Genes
Required
@ D(q) Bh
?
@ D>}
@@R?
?
@ S-L
(Men only)
@ D(q)
@ S-LD
@D
?
ae
@ D
@D
SUMMARY TABLES—‘‘BLACK”? GENES—(Continued)
Condition
Description
INTERNAL AND GENERAL (Continued)
Jaundice
Stomach Ulcers 2
Reproductive
(Sexual)
Allergy
Migraine
Headaches
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.
Birth.
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
dispute.
BRAIN AND NERVE
Amaurotic Idiocy
Epilepsy ?
(Common
Type)
Epilepsy
(Myoclonus)
a Brain degeneration with blindness,
paralysis, idiocy. Infancy or childhood.
Fatal.
b. Juvenile and adult forms. Frequently
fatal.
c. Eye effect only. Brain normal. Puberty.
May be fatal.
Various spontaneous convulsive disorders.
Cause unknown. Heredity claimed but not
established.
(Rare. ) Consciousness not lost during seiz-
ures. Childhood.
190
Genes
Required
@@ R(q)
@ D(q)
?
@D
?
@ D
@D
@ D
@@ RG
@ D>
or S-L
@@R
SUMMARY TABLES—‘‘BLACK’’ GENES—(Continued)
Condition
BRAIN AND NERVE (Continued)
Mongolian
Idiocy ?
Microcephaly
Chorea
Insanity
Genes
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
_ EYES
i
i
| Cataract
Glaucoma
(Hereditary
Type)
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)
IQI
SUMMARY TABLES—‘‘BLACK’’ GENES—CContinued)
Genes
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 ?
t
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
192
SUMMARY TABLES—‘‘BLACK’’ GENES—(Continued))
Condition
EYES (Continued)
Color Blindness
(Partial)
Day Blindness
Night Blindness
(Complete)
Cross-Eyes
(Strabismus)
Oscillating Eyes
(Nystagmus)
Eye-Muscle
Paralysis
Drooping Eyelids
Defective Cornea
Genes
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
deficiency.)
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
193
SUMMARY TABLES—‘‘BLACK’’ GENES—(CContinued)
Condition
EYES (Continued)
Displaced Lens
Defective Iris
Inner Lid Fold
(Epicanthus)
Pink Eye Color
Mirror Reading
Unmatched Eyes
Double (Multiple)
Eyelashes
Genes
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?
EARS AND HEARING
Deafness
Outer Ear
Deformities
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,
p89.)
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)
|
194
SUMMARY TABLES—"*BLACK’’ GENES—(Continued)
Condition
EARS AND HEARING (Continued)
Outer Ear
' Deformities
(Continued)
Ear Fistula
Word Deafness
MOUTH AND TEETH
Cleft Palate
and Harelip
Defective Enamel
‘Teeth at Birth
: Missing Teeth
— Teeth
[Auxiliary Teeth
| Defects
SKELETAL
‘Dwarfism
)
Genes
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)
195
SUMMARY TABLES—‘*BLACK’’ GENES—(Continued)
Condition
Description
SKELETAL (Continued)
Hand and Foot
Abnormalities
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.
Birth.
MUSCLE AND NERVES
Muscular Atrophy
Muscle Disorders
Muscle Cramp
(Tonic)
Paralysis
Shriveling or degeneration of muscles:
a. Peroneal. Only hands and feet. Child-
hood.
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.
Maturity.
c. Soft-muscle. More common in males.
Youth.
106
Genes
Required
@ D(q)
—@ Dq)
@ D(q)
@ D(q)
@ D or
R or S-L
@@® RH
@ D(q)
@b
@@R
or @ D
f
@ D(q)
SUMMARY TABLES— ‘BLACK’? GENES—(Continued)
Condition
MUSCLE AND NERVES (Continued)
Friedreich’s
Ataxia
Tremor
(Hereditary)
Hypertrophic
Neuritis
Leg Swelling
SKIN
Birthmarks
a ores Spots
!
|
|
Malignant Freckles
|
Albinism
i
Genes
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
S1Ze.
d. Mongolian Spot—Slate-blue patch over
base of spine, characterizing Mongoloid
peopies. Disappears in childhood.
@ D
@®D
@@;R+?
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.
@@R
@ D(q)
197
SUMMARY TABLES—‘‘BLACK’’ GENES—(Continued)
Genes
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
198
SKIN (Continued)
SUMMARY TABLES—‘‘BLACK’’ GENES—(Continued)
Condition
Thick, or
Shedding Skin
Biireat-Gland Defects
i
i
]
Rubber Skin
! Scalp Cysts
i| ° 5
Defective Hair
|
Genes
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)
HAIR AND NAILS
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
men.
a. Infantile down remaining through life. @ D
_b. Beaded hair. May lead to baldness.
Infancy. @ D(q)
199
SUMMARY TABLES—‘‘BLACK’’ GENES—CContinued)
Condition
Description
HAIR AND NAILS (Continued)
Defective Hair
(Continued )
Woolly Hair
Premature
Grayness
White Forelock
Defective Nails
c. Excessive long, soft hair on face and
elsewhere. Other effects. C‘‘Dog-face’’.)
Childhood.
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-
fancy.
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.
200
Genes
Required
@ D(q)
@ D
@ D(q)
(or S-L)
@ D
@D
@@R
or @ D
@+D+?
@ D |
@ D(q)
@D
@D
THE FOLLOWING ‘‘FORECAST’’ TABLES
SHOULD INTEREST YOU IF—
—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.
WHEN USING THESE FORECAST TABLES, BE AS
CERTAIN AS POSSIBLE THAT—
—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 NO CASE CONSIDER YOUR ‘“‘FORECAST’’ CONCLUSIVE, OR
| TAKE ANY ACTION ON THE BASIS OF IT, WITHOUT CONSULTING
\COMPETENT MEDICAL AUTHORITY.
In All Cases It Is Best to Consult Your Family Doctor!
}
| ‘at
\
I. RECESSIVE GENE FORECASTS
@@R
(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
WHERE THE CONDITION IS RECESSIVE WILL INHERIT
IT:
1. IF BOTH PARENTS ARE AFFECTED * Almost certainly
2. IF ONE PARENT IS AFFECTED, THE OTHER
NOT BUT IF IN THE FAMILY OF THE ‘‘FREE”’
PARENT *—
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
chance
c. Some mote remote relative is affected: Possible, but not
probable
d. No one, near or far, has been known to have
the condition: Very unlikely
3. IF NEITHER PARENT IS AFFECTED *, BUT
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 |
ollowing:
io —
202
A
II. ““QUALIFIED’’ RECESSIVE FORECASTS
@@ 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.
III. ““RECESSIVE PLUS’? FORECASTS
@@+R+
The situations are about the same as in Table I, but with the probability
lessened in most cases.
IV. SEX-LINKED (RECESSIVE) FORECASTS
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.)
CHANCES CHILD
WILL INHERIT:
1. IF BOTH PARENTS ARE AFFECTED: Almost certainly in
all their children
2. IF MOTHER IS AFFECTED, BUT FATHER IS
FREE OF IT: Certainforeveryson,
, but no daughter
3. IF FATHER IS AFFECTED, AND MOTHER IS
wm FREE OF IT, BUI—
a. Her father, mother or a sister has or had the
condition: Even chance in any
child
b. One of her brothers is affected: One-in-four for any
child
c. One of her more remote relatives is affected: Extremely unlikely,
but yet possible
ad. No known case in her family: Virtually nil
_4. IF NEITHER PARENT IS AFFECTED, BUT IT No chance for any
' 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
203
V. DOMINANT GENE FORECASTS
@ 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.)
CHANCES CHILD
WILL INHERIT
THE CONDITION:
ts ed IF BOTH PARENTS ARE AFFECTED: Very probable
as ae PARENT IS AFFECTED, THE OTHER 4.0 chance
3. WHERE NEITHER PARENT IS AFFECTED, BUT
IT APPEARS IN THE FAMILY OF ONE OR
THE OTHER:
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
VI. ““QUALIFIED’’ DOMINANT FORECASTS
® 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.
VII. ““DOMINANT-PLUS” FORECASTS
@+ D+
(Rare, as in dwarfism and rare defective enamels.) Relative probabilities
are about as shown in Table V, but greatly reduced in most cases. :
VIII. SEX-LINKED DOMINANT FORECASTS
@ 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 |
CHAPTER XXVIII
HOW DO YOU KNOW THE BABY’S YOURS?
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.
vened.
“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-
205
206 YOU AND HEREDITY
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-
stances.
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
YOUR BLOOD EXPE
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
g
when brou
or '"B," does not function. Accordingly:
IF YOU
RECEIVED @+O
GENES: i
YOUR
BLOOD A
TYPE IS:
Containing
AN
substance
t together, work independently. But Gene ''O" is recessive; and if coupled with "A"
©+® @+®
@®+©
DWAR ©
©+O©
Containing Containing Containing
"B eat and "Bt only nc
substance substances substance
_ ALTHOUGH LOOKING ALIKE, THE BLOODS ARE NOT COMPATIBLE, SO IN
TRANSFUSIONS IT IS SAFEST TO MIX BLOODS OF THE SAME TYPE. BUT IN
EMERGENCIES:
—Containing both "A" and
B "B" substances, most easily
/ \ receives the others
w!
BLOOD
BLOOD
—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
clotting
—But can be transfused into
the others with the least clot-
ting
208 YOU AND HEREDITY
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
HOW DO YOU KNOW BABY’S YOURS? 209
of that child. So without further ado the judge dismissed the ac-
tion.
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
THE BABY IS NOT YOURS—
(Assuming that you’re a man and that its paternity is in doubt)
—I[F
THE BABY’S THE MOTHER’S —AND YOUR
BLOOD IS BLOOD IS BLOOD IS
OF GROUP ‘' OF GROUP OF GROUP
O No Matter Which AB
AB No Matter Which O
A O ot B O or B
B OorA OorA
OR, REGARDLESS OF THE ABOVE,
THE BABY IS NOT YOURS IF—
THE BABY HAS ‘ —AND YOUR
SUPPLEMENTARY THE MOTHER SUPPLEMENTARY
BLOOD TYPE TYPE IS
M No Matter What N
N No Matter What M
MN N N
MN M M
210
HOW DO YOU KNOW BABY’S YOURS? 2i!
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-
I. “‘PATERNITY’’ DECISION BASED ON A NOT UNCOM-
MON DEFECT, PLUS OTHER CHARACTERISTICS
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:
CHILD “‘A’’ HAS MOTHER HAS MAN “X"’ HAS
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.
II. DECISION BASED ON SIMILARITY OF COMMON
TRAITS WHEN “BLOOD” TESTS ARE NOT CONCLUSIVE
Child ‘‘B’’, about a year old. Two men, “‘Y’’ and “*Z’’ are equally under
suspicion of being the father.
CHILD MOTHER MAN “Y" MAN “Z”"
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.
212
HOW DO YOU KNOW BABY’'S YOURS? 213
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
decide.
CHAPTER XXIX
ACHIEVEMENT: BIRTH OR LUCK?
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
animals.
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-
214
ACHIEVEMENT: BIRTH OR LUCK? 2I5
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
216 YOU AND HEREDITY
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
exists.
So we frankly advise you that from now on in our book, with
regard to conclusions, you will be more and more “on your
own.”
CHAPTER XXX
THE BATTLE OF THE “IQ's”
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
workings.
217
218 YOU AND HEREDITY
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
predestined.
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
“geniuses.”
THE BARTUE, OFITHES =O 'sS 219
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
220 YOU AND HEREDITY
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
intelligence?
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»
parents?
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-
THE BATTLE OF THE “1Q’s” 221
tween adjacent groups of children are not radically great, the entire
range in IQ’s, from lowest to highest, averaging within twenty
points.
A criticism regarding the above data is that the comparison
HEREDITY?
Average
ID
of child
PROFES-
SIONAL
SEMI-PROFES-
SIONAL AND
MANAGERIAL
CLERICAL,
SKILLED
TRADES, RE-
TAIL BUSINESS
SEMI-SKILLED
MINOR CLERICAL
MINOR BUSINESS
pe SLIGHTLY
SKILLED
4
FATHERS ih DAY LABORERS
UPATIONS RURAL FARMERS,
(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
222 YOU AND HEREDITY
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
heredity?
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
THE BAT TLEcOFSTHE 10's” 223
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
points.
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.)
224 YOU AND HEREDITY
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;
AVERAGE DIFFERENCES IN IQ
BETWEEN
IDENTICAL TWINS REARED TOGETHER:
ORDINARY BROTHERS AND SISTERS
(a) Reared together:
UNRELATED ORPHAN PAIRS
(a) Reared together:
(b) Reared apart:
F\.} 17.72
(Based on tables from "Heredity and Environment,” by Gladys C. Schwesinger }
225
226 YOU AND HEREDITY
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
question:
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
development.
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
>
228 YOU AND HEREDITY
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
THE BATTLE OR THE TO” §°” 229
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
mentality?
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.
230 YOU AND HEREDITY
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,
because:
“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,
232 YOU AND HEREDITY
genes for intelligence inferior to those of parents in the professional
class.
“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
group.
“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-
THE RAT TE EY ORCEH EaeLO. Ss. 233
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.
CHAPTER XXXI
MUSICAL TALENT: Paar I
(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-
234
MUSICAL TALENT 235
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.
236 YOU AND HEREDITY
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
field.
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
ours.
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-
MUSICAL TALENT 237
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
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242 YOU AND HEREDITY
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
talented?
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
itself.
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
talent.
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
MUSICAL TALENT 243
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
Busch.
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
}
ft
MUSIC TABLE II
CHILDREN OF INSTRUMENTAL ARTISTS
MUSICIAN WIFE
He,
Musical? Family?
ARTUR BODANZEY Yes Yes
ADOLF BUSCH Yes ey ane
| Grandf.*
WALTER DAMROSCH No No
WALTER GIESEKING Yes Yes
EUGENE GOOSSENS Yes No
JASCHA HEIFETZ Yes Grandf.*
(Florence
Vidor)
ERNEST HUTCHESON Yes Yes
(many)
JOSE ITURBI ? ae
JOSEF LHEVINNE Yes* No
(Pianist) »
SERGE PROKOFIEFF Yes* Yes (both
(Singer) parents)
SERGEI RACHMANINOFF Yes No
ARTUR RODZINSKI No
ARTUR RUBINSTEIN Yes f.; cond s*
ARTUR SCHNABEL Yes* Yes
| (Singer) (many)
RUDOLF SERKIN Yes Yes
(A. Busch)
JOSEPH SZIGETI No No
ARTURO TOSCANINI Yes Some
EFREM ZIMBALIST Yes* No
CA. Gluck)
TOTALS—Wives: Talented, 14; Not, 3; ?, 1.
Children: Of 37, 27 Talented.
244
Number
2.
I
P Rp A
eed
CHILDREN
Musical?
Both, to a degree
Yes
All 4
Both
1 yes,* 3 no
Both
Both
Talented
Daughter, yes;
son, no
Both talented but
not trained
Both
No
(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
No
MUSICAL TALENT 245
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
difficulties.
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.
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250 YOU AND HEREDITY
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
ranks.
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.
MUSICAL TALENT 251
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.
252 YOU AND HEREDITY
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.
MUSIC TABLE IV
MEMBERS OF GRADUATE SCHOOL OF
JUILLIARD INSTITUTE
Average Age
Talent Expressed:
Talent in Mothers:
(a) Definitely Yes
(b) Some Talent or
Musicality
(c) Totals of Both
Talent in Fathers:
(a) Definitely Yes
(b) Some Talent or
Musicality
(c) Totals of Both
Brothers and Sisters:
Number in Families
(a) Definitely Tal-
ented
(b) Some Talent or
Musicality
(c) Totals of Both
Talent in Other Kin:
(a) Those reporting
talent in one
or more grand-
parents
- (b) Those reporting
talent in near
kin of any
kind, includ-
ing grand-
parents
INSTRUMENTALISTS
Ge)
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%)
253
VOCALISTS
G4)
Females
(8)
5)
5(63%)
5(63 7%)
338%)
338%)
6
4(67%)
1
5(83%)
5(63 %)
675%)
Males
()
81,
4(677%)
1
5(83 %)
3(50%)
1
4(6770)
5
3(60%)
3(60%)
5(83 %)
5(83%)
TOTALS
(50)
534 yrs.
32(64%)}
2
37(74%)
24(48%)
5
29(587%)
72
41(57%)
10
51¢71%)
26(652%)
37(747%)
254 YOU AND HEREDITY
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,
MUSICAL TALENT 255
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?”
CHAPTER XXXII
MUSICAL TALENT: Parr II
(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
256
.
MUSICAL TALENT 257
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.
258 YOU AND HEREDITY
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
MUSICAL TALENT 259
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
Janeiro.
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—
MUSIC TABLE V
SUMMARY—ALL THREE GROUPS
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%),
260 YOU AND HEREDITY
“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.
MUSICAL TALENT 261
KIRSTEN FLAGSTAD’S MUSICAL PEDIGREE
Maternal Maternal Maternal Paternal Paternal
GRANDMOTHER GRANDFATHER GRAND-UNCLE GRANDMOTHER GRANDFATHER
Singer Violinist Cellist (not musical)
Absolute
: Pitch
| a
MOTHER FATHER
‘Pianist, Op- Violinist,
| tratic Coach Conductor
‘KIRSTEN
| aed ene
SISTER BROTHER BROTHER
\ 1ER
Absclute Singer Cellist, Pianist
Conductor
| ‘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
262 YOU AND HEREDITY
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,”
MUSIC TABLE VI
OPINIONS AS TO THE INHERITANCE
OF MUSICAL TALENT
(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
MUSICAL TALENT 263
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
musicality.)
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.
264 YOU AND HEREDITY
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-
tion.
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.
MUSICAL TALENT
265
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-
MUSIC TABLE VII
“TALENT’ RESULTS QF: DIFFERENT MATINGS
(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
Virtuosi
(26 families)
Bros. & Sisters
of Metropolitan
Singers
(26 families)
Bros. & Sisters
| of Juilliard
| Graduates
| Gz families)
Totals for All
_ Three Groups
Where Both
Parents
Had Talent
Number Number
of Other With
Children* Talent
31 22
(71%)
42 26
(62%)
21 19
(907)
94 67
(71%)
*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
Parent
Had Talent
Number Number
of Other With
Children* Talent
35 21
(60%)
16 8
(50%)
20 14
(70%)
71 43
(60%)
Where Neither
Parent
Had Talent **
Number Number
of Other With
Children * Talent
a7, &
(15%)
ys Z
(8%)
14 4
(29%)
(66 10
(15%)
266 YOU AND HEREDITY
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.
MUSICAL TALENT 267
| - THE TOSCANINI FAMILY
SYMBOLS & A) Eyer)
PRONOUNCED SOME DEGRE
MUSICAL TALENT OF TALENT BLANKS -NO TALENT
The Maestros The Maestro's
Father Mother
ARTURO MRS. ARTURO
“TOSCANINI TOSCANINI
(mildly musical
but not
talented)
ing diab VLADIMIR
ve HOROWITZ
WAILLY WALTER WANIDA \y
ie MARRIED ne MARRIED Gy ¢) MARRIED G|
‘ASTELBARCO Lote ,
~GRANDAUGHTER GRANDSON RAND-DAUGHTER
(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
HOW MUSICAL TALENT MAY BE INHERITED
(An hypothesis)
Granted that a person has the ordinary "aptitude" genes (see text), the additional -
"something" required for musical talent may be produced by
TWO SPECIAL dominant "TALENT" GENES:
TALENT TALENT
GENE GENE
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
COMBINATIONS PRODUCING TALENT:
(All have the same effect.)
COMBINATIONS PRODUCING NO TALENT:
~2
eee
OR
9
(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.) |
268
OR
tT |
HT
[Pe eB,
ah
Ih
aI
AI
I
AWA
SOME POSSIBLE MUSICAL TALENT RESULTS
FROM VARIOUS MATINGS
| {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
TALENTED CHILDREN WITHOUT TALENT
! 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:
genes:
» Clearer:
HT
|
Jay ee
BUT ALL CHILDREN TALENTED WOULD RESULT
FROM ANY OF THE FOLLOWING MATINGS:
3. BOTH PARENTS TALENTED 4. ONLY ONE PARENT TALENTED
| of these types —of this rata
type
bee oe
G2 as } 6 a gh
5. BOTH PARENTS WITHOUT - # a7 am
| TALENT “XW
—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.
269
270 YOU AND HEREDITY
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
P MUSICAL TALENT 271
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
272 YOU AND HEREDITY ‘
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
SINGING VOICES—PARENTS AND OFFSPRING
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.’’)
: PARENTS CHILDREN
New" FATHERS MOTHERS DAUGHTERS SONS
| 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)
273
274 YOU AND HEREDITY
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
cords,
“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-
ment?
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
MUSICAL TALENT 275
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.” |
MUSIC TABLE VIII
WHICH IS MORE IMPORTANT IN MUSICAL
ACHIEVEMENT ..INHERITED TALENT OR TRAINING?
(Opinions of the artists)
Instrumental — Metropolitan
Virtuosi Singers Totals
Both Equally Important.......... 16 12 (10 women 28
zemen\))
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?
276 YOU AND HEREDITY
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.
MUSICAL TALENT 277
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-
278 YOU AND HEREDITY
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.”
as
pepe cr
*
ee
(a is We C Reta, je yf YG
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PROFESSOR AUER
As sketched by the author on the occasion mentioned in the text.
CHAPTER XXXIII
FROM APTITUDE TO GENIUS
Ir there is a hereditary basis for musical talent, a logical inference
would be that heredity plays a part in other specialized talents and
aptitudes.
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
performers.
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
79
280 YOU AND HEREDITY
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-
FROMVAPIFIFUDE-TO GENIUS 2d.
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-
sions.
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
282 YOU AND HEREDITY
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
inherited.
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
FROM APTITUDE TO GENEIUS 283
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
284 - YOU AND HEREDITY
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
history?
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
HEREDITY OR TRAINING?
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
simultaneously.
FROM APTITUDE TO GENIUS 285
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.
286 YOU AND HEREDITY
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
physically?
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
wrote,
“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
FROM APTITUDE TO GENIUS 287
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
sane?
Because the records of great men were carefully kept, and their
lives subjected to close scrutiny, it should be expected that their
288 YOU AND HEREDITY
“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.
CHAPTER XXXIV
PERSONALITY
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
villains.
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
289
290 YOU AND HEREDITY
¢
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
PERSONALITY 291
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
serious.
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
292 YOU AND HEREDITY
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
PERSONALITY 293
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
hereditary.*
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.
294 YOU AND HEREDITY.
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-
eans.
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
PERSONALITY 295
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
296 YOU AND HEREDITY
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
differences.
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
PERSONALITY 297
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.
298 YOU AND HEREDITY
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
environment.
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-
ity.”
“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,
etc.
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.
THE DIONNE QUINTUPLETS
YVONNE MARIE CECILE ANNETTE EMILIE
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.
PERSONALITY 299
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.
CHAPTER XXXV
ENTER THE VILLAIN
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
300
ENTER THE VILLAIN 301
lay the thought that one could be born predestined to a life of
crime.
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 |
302 YOU AND HEREDITY ;
HOMICIDES*—UNITED STATES AND OTHER COUNTRIES
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 |
ENTER THE VILLAIN 303
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?”
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ENTER THE VILLAIN 305
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-
noying.
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-
306 YOU AND HEREDITY
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,
ENTER THE VILLAIN 307
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
existence.
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.
308 YOU AND HEREDITY
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-
ENTER THE VILLAIN 309
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
310 YOU AND HEREDITY
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
development.
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.
CHAPTER XXXVI
SEXUAL BEHAVIOR
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
subject.
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
311
312 YOU AND HEREDITY
| | Whether You Are a Man or a Woman
—YOU ARE CONSIDERED
"MASCULINE"
IN THE DEGREE THAT
YOU ARE INTERESTED IN:
Exploit and adventure
Outdoor activity and physi-
cally strenuous occupations
Machinery and tools
Science, physical phenomena
and inventions
Business and commerce
—AND TO THE EXTENT
THAT YOU ARE:
Self-assertive
Aggressive
Hardy
Fearless
Rugged
Blunt of manner and speech
—YOU ARE CONSIDERED
“FEMININE”
IN THE DEGREE THAT
YOU ARE INTERESTED IN:
Domestic affairs
Art, literature, music
Sedentary and indoor occu-
pations
Ministering to the helpless
and distressed
“Moral" activities
—AND TO THE EXTENT
THAT YOU ARE:
Compassionate
Timid
Sympathetic
Fastidious
Emotional
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.”
THe "INK-BLOT" TESTS for "MASCULINITY" and "FEMININITY"*
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
ww
. boat J I. couch
. door . 2. cow
. hat 3. deer
. stump 4. horse
HERE IS HOW THE ANSWERS ARE SCORED:
| PICTURE: A B G D E F SG H 1 J
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
313
| Masculine:
Feminine:
314 YOU AND HEREDITY
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’
clothing!
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
“MASCULINITY” AND “FEMININITY”
(How various classifications of men and women rank according to average scores int
the ''M-F"' tests)
_ MASCULINITY FEMININITY
(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
Nurses
Lawyers, Salesmen, ;
Bankers, Executives -60
Women College
Dentists, Teachers Students (Avirags) | -~50
Doctors
— Mechanical Occupations r ip
OW Clerks and Merchants. Who's Who
Women
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")
315
316 YOU AND HEREDITY
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.
SEXUAL BEHAVIOR 317
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.)
318 YOU AND HEREDITY
{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
factors.
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
SEXUAL BEHAVIOR 319
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
320 YOU AND HEREDITY
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.”
SEXUAL BEHAVIOR 321
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
322 YOU AND HEREDITY
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
SEXUAL BEHAVIOR 323
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
results.
All this is predicated on the assumption that homosexuality
SEX CHARACTERISTICS IN LIMBS
ARMS LOWER LIMBS
FEMALES MALES FEMALES MALES
Angle, corresponding Straight Slightly knock-kneed Straight
to knock-knees
i
|
I
|
|
|
|
4)
|
|
i
|
|
1
|
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.
324 YOU AND HEREDITY
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.
CHAPTER XXXVII
EVOLUTION: CHICKEN OR EGG?
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
down.
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
man.
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?
325
WHICH CAME FIRST...?
ACCORDING TO DARWIN:
. First there was a I.
certain kind of
bird,
. It laid and hatched
eggs,
. 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
PASSED ON THROUGH Ca
THEIR EGGS
. Until, with many |
such changes in
successive gen-
erations added
together, even-
tually there re-
sulted
THE CHICKEN
. Which then produced the
characteristic |
CHICKEN EGG
So by this reasoning
THE CHICKEN CAME FIRST.
y
—BUT ACCORDING TO
MODERN GENETICS:
First there was a cer-
tain kind of egg,
iy . Which produced a
©
3.
Sa
. Which produced
characteristic kind of
bird,
But in some of these
birds something hap-
pened to produce
MUTATIONS
Which resulted in their
laying eggs with certain Pot 9
y=
=
Y
TOL
Me
CHANGED GENES
birds differing from
their parents. And as
mutations continued,
In the course of ages
there resulted A NEW
KIND OF EGG WITH
NEW GENES
Which produced
THE CHICKEN
Thus, as science
now indicates,
THE EGG CAME
FIRST.
“eo
ce
©
Vi
poe:
EVOLUTION, ACHICKEN (OR EGG? 327
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-
cestors.
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.
328 YOU AND HEREDITY
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
them.)
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 to.live 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.
EVOLUTION: CHICKEN OR EGG? 329
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
330 YOU AND HEREDITY
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!
EVOLUTION: “CHICKEN OR EGG? 331
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-
ferentiated.
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-
332 YOU AND HEREDITY
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,
EVOLUTION: CHICKEN OR EGGP 333
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
334 YOU AND HEREDITY
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.
CHAPTER XXXVIII
RACE
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.
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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
word.
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
338 YOU AND HEREDITY
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
species.
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
RACE She
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,
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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)
342 YOU AND HEREDITY
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
party.
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
THE MELTING POTS OF EUROPE
These were the primary sources of your ancestry if your descent is—
IRISH: ENGLISH:
: . 7
Scandinavians,’
/
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
FRENCH:
; \\
English \\ aK \\
1200 -!500% NAY
Cy
SNS \
Norsemen en
ay 7
Iberians | pe an 4/0
from N.Africa_-~ Lit 18
GR eOOOR Co ety a(S
344
SERMAN:
Vikings ©)>
9 and tothe, <
Gérman-Swabians
(Fred'kK Barbaross«
1154 AD.
*»
~
— ee ee ee
EtruscansS)
800 B.C.
SPANISH:
Germanic
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.)
345
RUSSIAN:
_---@) Finns (from Siberia)
eee
Vikings BAS hom
1300 A.D. Vu ete tamcnoaans Huns
Bese a5
ooh
>
——
mae
Turk-Tartaric
peoples ~T50 AD.
NORWEGIAN AND ge Qe U
SWEDISH ait Mie TSS)
coe ae om aa
tay 100 A.D
Vy Also 9OO-1000 AD
@) Finns
(8.C)
rir!
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 [ -
22
S
f
\
re
o
=
5
o
=
ae
=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. |
346
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
348 YOU AND HEREDITY
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
a-seal?”
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
Schmeling.
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
350 YOU AND HEREDITY
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.”
352 YOU AND HEREDITY
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
features.)
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
apart.
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?”
354 YOU AND HEREDITY
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.
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CHAPTER XXXIX
ANCESTRY
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
355
356 YOU AND HEREDITY
OLD CONCEPT OF ANCESTRY
BLOOD OF GREAT-GRANDPARENTS
-Paternal: -Maternal:
GTlVGlWSC (VF \o
|
A
Grandparents’
blood poured h
into
Parents’ blood
poured into the
INDIVIDUAL
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
ANCESTRY ; 357
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.
YOU AND YOUR ANCESTORS
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.
Generation
Back
First
(Your parents)
Second
(Grandparents)
Third
(Great g.ps.)
Fourth
(Great-great g.ps.)
Fifth
(Great-great-
great-g.ps.)
Sixth
Seventh
Eighth
Ninth
Tenth
Eleventh
Twelfth
Thirteenth
Fourteenth
Fifteenth
No. of
**Potential”’
Approx. Year and Generation Ancestors
2
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
(Columbus)
No. of Chromosomes
from
Each (Av.)
24
12
6
Leor:2¢)
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
42tol
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.
358
ANCESTRY 359
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
360 YOU AND - HEREDITY
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
ANCESTRY 361
“bad”) and after long research into the pedigrees, produced this ex-
planation:
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.,
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ANCESTRY 363
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
name).
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-
364 YOU AND HEREDITY
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
ANCESTRY 365
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.”
CHAPTER XL
THE GIDDY STORK
“We hold these truths to be self-evident, that all men are created
EQUAL Is
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,
366
THE GIDDY STORK 367
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
368 YOU AND HEREDITY
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
THE GIDDY STORK 369
THE BIRTH-RATE "DIFFERENTIAL"
(As Viewed by a Population Expert) *
CROSS-SECTION OF
U. S$. POPULATION
x 6% Professional and most-favored
oy Soke o ee = be | groups
rs
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 %
2
Nef be o
e
Ey
sk
=
.
pe
ae
«,
30% Unstable, shiftless, indifferent, unin-
telligent, unsocially-minded, most un-
Highest productive
Birth.
fates
Here
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.
370 YOU AND HEREDITY
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
years.
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
THE GIDDY STORK 371
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
children.
Apart from the social factors cited (which by no means constitute
372 YOU AND HEREDITY
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?
CHAPTER XLI
EUGENICS: NEGATIVE
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
373
*
374 YOU AND HEREDITY
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,
£
EUGENICS: NEGATIVE 375
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
376 YOU AND HEREDITY
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
sterilization?
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
different.
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
EUGENICS: NEGATIVE 377
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-
378 YOU AND HEREDITY
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
percent.
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
Present
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RECESSIVE "BLACK" GENES
(Where a pair of the genes produce a
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genes in carriers would still be |
passed on, thus...
Next generation: Proportion of these
defectives only slightly reduced
SEX-LINKED "BLACK" GENES
(Single gene producing serious defect
in male, two genes required for female.)
By sterilizing all the defectives,
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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.
380 YOU AND HEREDITY
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
community.”
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
EUGENICS: NEGATIVE 381
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
382 YOU AND HEREDITY
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
godmother!
It is incorrect to assume that there is a deep-rooted or instinctive
EUGENICS: NEGATIVE 383
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
384 YOU AND HEREDITY
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.
CHAPTER XLII
PROGRAM FOR TOMORROW
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
strains).
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
help:
385
386 YOU AND HEREDITY
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
abroad.)
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
attention.
These measures may relieve the Smiths of some of their wor-
ries. But suppose Mrs. Smith can’t afford to risk losing her job?
Hence:
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:
PROGRAM FOR TOMORROW 387
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
families.
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
“catches”!
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
388 YOU AND HEREDITY
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
men.
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
PROGRAM FOR TOMORROW 389
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
390 YOU AND HEREDITY
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
PROGRAM FOR TOMORROW 391
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
produced.
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
392 YOU AND HEREDITY
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
states.
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?”
PROGRAM FOR TOMORROW 393
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
animals.
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-
temporaries.
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,
394 YOU AND HEREDITY
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.
DESIRABLE TRAITS IN WOMEN
SOCIALLY: EUGENICALLY:
Beauty unimportant
Beauty first
Delicate features Strong features
No “deep” intellect High intelligence
Vivaciousness
Seriousness
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
PROGRAM FOR TOMORROW 395
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.
CHAPTER XLIII
YOU AND HEREDITY
Tuis book began, as you may recall, with “Stop and think about
yourself.”
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?
306
YOU AND HEREDITY 397
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
succession.
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
398 YOU AND HEREDITY
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-
YOU AND HEREDITY 399
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
past:
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
400 YOU AND HEREDITY
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-
ports:
. 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
YOU AND HEREDITY 401
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-
402 YOU AND HEREDITY
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,
YOU AND HEREDITY 403
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
404 YOU AND HEREDITY
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
genes.”
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
animals.
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.
YOU AND HEREDITY 405
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
406 YOU AND HEREDITY
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
grandchildren.
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
YOU AND HEREDITY 407
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.
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HIGHLIGHTS IN THE HISTORY OF GENETICS
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.
EARLY BACKGROUND
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
believed.
1849 (1) Sir Richard Owen (England) enunciates principle of
the continuity of the germ-plasm. This idea culminated in
the:modern gene theory.
Ali
412 APPENDIX
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-
tion.
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
1887
1888
1890
1892
1898
1899
1900
1902
APPENDIX 413
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-
herited.
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.
~ MODERN GENETICS
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).
4u4
APPENDIX
1902-3 W. W. Sutton (United States) shows that body chromo-
1903
1904
1905
1906
1907
1908
1909
1910
1911
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-
up.
(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”
chromosomes.
(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
inheritance.
(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.
APPENDIX 415
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-
velopment.
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
States).
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.)
~
SUGGESTIONS FOR FURTHER READING
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.
GENERAL
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.
Conx.in, 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.
416
APPENDIX 417
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.)
SPECIAL TOPICS
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.
Genes
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.)
Featurcs
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
GENERAL. )
Twins
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.
418 APPENDIX
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.
Longevity
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.,
Sept..377.
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,
36.
LevINE, Puitip. Application of Blood Groups in Forensic Medicine. Am. J. Politi-
cal Science. 3:157. 732.
APPENDIX _ 419
WIENER, A. S. Blood Grouping Tests in the N. Y. Courts. U. S. Law Rev., Dec.
eee Parentage. Scientific Monthly, Apr. ’35.
Intelligence
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.,
bie
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.
Genius
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.
Personality
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.
G20 APPENDIX
Sexual Behavior
Terman, L. M., and Mizzs, C. C. Sex and Personality. McGraw-Hill.
26.
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.
Crime
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.
Race
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.
26.
APPENDIX 428
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.
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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.)
rT LEADING PUBLICATIONS DEALING WITH HEREDITY
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
FANT
INDEX
(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
Alcohol,
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,
391
Aryan, Non-Aryan, 351 ff.
Asthma, 129, 190
Asthenic type, 84, 294
Astigmatism, 192
Ataxia, 149, 197
Ateleotic dwarfs, 81, 139, 195
(Lilliputians)
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
424
“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
Blatz,aWakac27o
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
sterilization,
INDEX
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,
354
Chromosomes
in ancestry, 356
as chain gangs, 44 ff.
changes, 331
INDEX
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,
155
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
425
Death
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)
199
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)
426
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.
INDEX
Eunuchs, 181
baldness in, 135
Eurasiatics, 339, 342
Europeans, formation of (maps),
344-346
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)
Fertility
in classes, 369
inheritance, 182
Fertilization, 6, 30, 32, 45
Feuermann, Emanuel, 254
Finger defects, 141, 142, 196
INDEX
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
Genes
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
Genetics
definition, 1
future, 405
in livestock, plants, 404
Genius, 279 ff.
abnormalities,
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,
427
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)
428
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
Environment)
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,
302
(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),
346
Huntington’s chorea, 150, 151, 191
Hutcheson, Ernest, 251
Hypospadias, 182, 190 (Reproduc-
tive, a.)
Hypotrichosis (complete. hairless-
ness), 148
INDEX
Ibsen’s “Ghosts,” 35, 116
Idiocy, 117, 154, 155, 190, 191
(see also Feeble-mindedness)
Illegitimacy
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
INDEX
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,
188
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),
198
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
4
429
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
talent)
Malignant freckles, 124, 147, 162,
197
(see also Rare Cancers, 188)
Malthusian doctrines, 366 f.
Man, origin of, 333 £., 336
(see also Homo sapiens)
Manic-depressive insanity,
191, 294
Marriage
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
15;
“Maternal impressions,” 34
Mathematics, talent for, 282
Mating,
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
430
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
Company
INDEX
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),
234-279
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),
275
(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.
INDEX
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
Negro
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
431
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-
225
Oscillating eyes, 144, 193
Otosclerosis (middle-ear deafness),
194
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-
213
Peas, Mendel’s experiment, 49 ff,
50
Pearl, Raymond, 163
Pekin Man, 336, 337
Personality, 289 ff.
beauty and, 291 f.
conclusions on inheritance, 298 f.
defectives’, 296
Dionnes’, 296 f.
432
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,
407
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
. INDEX
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
(see
Scalp cysts, 199
Scaly skin, 147, 198
Schizophrenia, 152 f., 191
(see also Insanity)
Schnabel, Artur, 243
Schola Cantorum (Voice types),
273
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)
Sex
abnormalities, 172 ff., 178, 182,
309
characteristics, 174, 179 ff.
—in limbs, 323
chromosomes, 132, 133
differences in longevity, 167, 168
INDEX
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
433
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.
betes)
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
434
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
EASOATa.a)
_ 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),
196
Thrombasthenia,
disease, c.)
Thyroid, 140
defects, 128
effect on behavior, 294
Toscanini, Arturo, 184, 236, 242,
258
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
INDEX
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
Women,
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
growths)
Young, Hugh H., 178
Zimbalist, Efrem, 262, 270
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