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Brain-size grey matter and race Чfact or fiction.

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Brain-size, Grey Matter and Race Fact or Fiction?’
Department of Anatomy, University of the
Witwatersrand, Johannesburg
A critical review is given of those factors which may be accompanied
by variations in brain weight, viz. sex, body size, age of death, nutritional state in
early life, source of the sample, occupational group, cause of death, lapse of time
after death, temperature after death, anatomical level of severance, presence or
absence of cerebrospinal fluid, of meninges, and of blood-vessels. Valid comparisons
between the brain-weight of human populations should take all, or several, of these
variables into account; however, published studies have not done so, despite claims
to the contrary. The ideal sample is from subjects who have died suddenly without
prior disease: while three such samples are o n record for Europeans, none has been
recorded for Negroes. The brain-weight of healthy Negroes is not known. Most published interracial comparisons are invalid. The histological, chemical and functional
counterparts of big and small brains in modern man are not known. Published interracial comparisons of thickness of the cerebral cortex and, particularly, of its
supragranular layer, are technically invalid: there is no acceptable proof that the
cortex of Negroes is thinner i n whole, or in any layer, than that of Europeans. It
is concluded that vast claims have been based o n insubstantial evidence.
In this age of cellular and molecular
biology, ever more refined techniques are
being focussed on the central nervous system. Brains are being studied by electron
microscopy, autoradiography, ultraviolet
absorption spectromicrophotometry, biochemical analyses, cybernetic models, tissue culture and a host of other methods. In
the light of these developments, it is almost inconceivable that anything remains
to be said at all about so gross and crude
a measure as the overall size of the brain.
Yet, it is an astonishing fact that a great
deal remains to be said and, I am afraid,
much of it negative-for most that has
already been asserted does not stand up to
the cold light of scientific scrutiny.
The theme of this paper - “Brain-size,
Grey Matter and Rack - Fact or Fiction?”
- is based upon the oft-repeated claims
that the races of man have been shown to
differ in quantity of brain-substance and,
especially, of grey matter in the cerebral
cortex. More specifically, it is based upon
the claims that Negroes have smaller
brains than White or Caucasoid peoples
and upon the frequently drawn inference
that an apparently lesser intellectual performance by Negroes is based upon such
supposed differences of brain-size.
AM. J.
ANTHBOP.,32: 3-26.
It will be my aim to examine the evidence for such claims; to try to dissect
apart the facts from supposed facts. We
shall find that the evidence is inadequate
or, in some respects, totally lacking. Further, I shall try to examine the meaning
of brain-size differences in the light of
recent neurohistological and neurophysiological researches, as well as from an
evolutionary standpoint. We shall find that,
even were differences in brain-size validly
demonstrated among different populations,
they would be unable to explain adequately
variations in cerebral function and achievement among living human beings. Furthermore, we shall find that such variations, if
they do exist, are apparently not of much
importance in modern man. We shall see
that in this expanding universe, ours is
a world of contracting brains. Finally, we
shall be led to regard somewhat more critically the claims made about grey matter
in the men of today.
1Lecture delivered on 25 March 1969, on the first
anniversary of the departure from South Africa of
Dr. Raymond Hmenberg, formerly of the Department
of Medicine, University of Cape Town. This was the
1st Raymond Hoffenberg Lecture, delivered under the
auspices of the Department of Medicine, University of
Cape Town.
Some claims about race and
brain power
It has often been claimed that races
differ in intellectual capacity. For example, in 1961 and again in 1962, in a report on ‘The Biology of the Race Problem,” prepared by commission of the Governor of Alabama, George quotes I.&. test
performances, crime statistics, behaviour
and temperament traits, for all of which
differences are claimed to exist between
Whites and Negroes. These statements
by George have been quoted by Hofmeyr (’61), Swan (’64), Putnam (’63,
‘67) and others, Not being a psychologist,
a criminologist or a sociologist, I do not
feel competent to offer any authoritative
comment on the statistics, the objectiviy
with which they were obtained, the degree
to which such factors as economic and
educational background were considered
in the study of the crime statistics, nor the
validity of claims that the alleged differences are based upon racial factors, i.e.,
inherent or genetic differences.
However, 1 do feel better able to express
an opinion when George (’62), Swan (’64),
Putnam (’63, ’67) and others attribute
these differences to inherent anatomical
causes. The most important features cited
by these writers are the size of the brain,
the fissuration of the cortex and the thickness of the supragranular layer of the cortical grey matter. For example, we find
Putnam (‘67) stating.
tion of the degree to which these differences may be attributable to inherent morphological rather than to environmental
causes.” He goes on to add:
“Are there hereditary structural and
other biological differences between individuals and races that might serve to
explain the observed differences in intelligence and in behaviour in those
areas of activity that make western civilization? The presence of such differences is not only a reasonable expectation but is supported by evidence.” (Op.
cit., p. 25.)
The validity of the argument hinges on
two sets of premises: (i) the correctness
of the statements about the differences in
the anatomy of the brains; and (5)the
validity of the inference that these anatomical variations, if present, connote functional differences relevant to social behaviour, learning ability, ‘behaviour in
those areas of activity that make western
civilization,” and so on.
Perhaps the most important claimed
anatomical difference relates to brain size.
Thus, Swan (’64, p. 33) states: “Despite
sampling difficulties and variations in
methods, enough comparative racial studies of brain weight have been completed
to warrant a quantitative description of
the racid differences. The average cranial
capacity of European Whites is from 100
to 175 cm3 greater than that of African
Negroes, and their average brain weight
is some 8 to 12% greater.” (op. cit.,
p. 33).
‘We have enough studies of the Negro
What facts do we have about brain-size?
brain, under varied enough circumstances, to speak with assurance of its
First, what measure of brain-size should
relative weight. When this factor is
we use? If the actual brain is available,
combined with studies of its other feawe may weigh it or, less satisfactorily, detures, such as sulcification of the cortermine its volume. If the brain itself is
tex and thickness of the supragranular
layer, we can also speak with assurance
not available, we can still derive an apof its relative evolutionary status.” (Op.
proxima tion to brain-size by determining
cit., p. 103.)
the capacity of the cranium or brain-case.
These writers claim that this group of However, the brain-case accommodates a
supposed facts points to the Negro’s brain great deal more than simply brain. Thus,
being of lower evolutionary status, which, when we say that a skull has an endocranin turn, implies a lesser capacity to learn ial capacity of 1400 cm3, this includes not
(e.g., Putnam, ’67, p. 106).
only brain-tissue, but the roots and intraSimilarly, after detailing crime statistics cranial trunks of no fewer than 24 cranial
among Negro and White communities, nerves, the thick outer brain covering or
George (’62, p. 25) turns to consider the dura mater, the two thinner, inner coverbrains of Negroes and Whites with the ings, the arachnoid and pia mater, the
words, “We must now turn to a considera- subarachnoid space and its enlargements
called cisterns containing fluid, numerous
blood-vessels including special enlarged
venous channels called cranial venous
sinuses, blood, cerebrospinal fluid.
Thus, only a proportion of the cranial
capacity is made up of brain-tissue: estimates of this proportion vary from 10%
(Brandes, ’27) to 33.33% (Mettler, ’55).
Furthermore, the ratio is not a constant
figure within the adult lifetime of any one
individual, for the brain shrinks with age,
in certain illnesses and under some other
conditions, though the brain-case itself has
not been shown to diminish. Hence, as the
quality of life changes, the amount of nonneural cranial capacity increases and one’s
head may become progressively N e d more
and more with emptiness.
For these reasons, cranial capacity is a
less reliable indicator of brain-size than
brain-weight itself. When dealing with
fossil man, we are perforce obliged to consider cranial capacity, as our sole guide to
brain-size. But when speaking of living
man, we are able to determine brain-size
itself and thus eliminate at least some unnecessary sources of error. In this discussion on the brain-size of living man, attention will be confined largely to the actual
brain-weight. We shall see that even this
measure of brain-size is not as easy to determine as it may sound and that, even
though we avoid certain errors by not relying on cranial capacity, we nevertheless
remain with a large number of possible
sources of variance.
Some facts about brain-weight
For over 130 years, data have been accumulating on the weight and/or volume
of the human brain, or the cranial capacity, in samples drawn from different racial
groups. As long ago as 1849, S. G. Morton
published observations on the cranial capacity of skulls drawn from different populations: the mean capacity of a small
sample of Negro skulls was 91.3% of the
mean for a very small sample of Caucasoid
skulls, the values being 1360.1 cm3 and
1489.6 crn3 (converted to metric units by
Pearl, ’34). Other early studies on cranial
capacity gave similar results (Peacock,
1865 -88.4%
on 9 Negro skulls and
16 “European” skulls: Duckworth, ’04 92.5% ).
As far as can be traced, the earliest references to the brain-weight of the Negro
were those of Soemmering (1788) who
weighed two brains, Tiedemann (1836)
who weighed one and Sir Astley Cooper
one (cited by Peacock, 1865). In 1865,
Peacock weighed another five brains of
Negroes; according to Pearl (’34), Peacock copied an additional two brain-weights
from tables compiled by John Reid. Five
of the seven individuals represented were
males, and three of them are reported to
have died of phthisis in a greatly emaciated
state. The mean weight for these five was
computed by Pearl (’34) as 1256.8 gm.
By 1885, Topinard could cull data for
29 male Negro brains from diverse sources
in the literature: the mean was 1234 gm.
In 1894, Waldeyer recorded a mean
brain-weight of as low as 1148 gm for 12
male African Negro brains, 11 of which
were weighed fresh. But, as Pearl pointed
out (’34, p. 432), two of these belonged
to 15-year-olds, while several had died of
wasting diseases and were severely emaciated. In 1909, Mall made the forthright
statement that the average brain-weight
of the Negro is about 100 gm less than that
of Whites. Bean, too, found a lower brainweight in Negro males than in White
males (’17).
Perhaps the most frequently quoted
study is that of Vint (’34) who found an
average brain-weight of 1276 gm in 389
adult male Kenya Africans. This is the
longest Negro series on record. Pearl (’34)
analysed brain-weights collected by Surgeon Ira Russell of the Eleventh Massachusetts Volunteers during the American
Civil War and published by S . B. Hunt in
London in 1869. The sample of brains of
enlisted soldiers had been broken down a
century ago into White, varying grades of
“mixtures”, and Black. It seems that the
various mixtures were determined by the
simple, though grossly misleading expedient, of examining skin colour. Pearl found
that the mean for 139 brains of Negroes
was 1354.8 gm, that is, 92.1% of the mean
for 24 brains of Whites (1470.6 gm).
Strangely enough, the mean for 240 brains
of people believed to be mixtures was
1333.6 gm i.e., lower than both the White
and Negro means! (table 1).
Pearl’s (‘34) analysis of brain weights of American Civil W a r dead. Measurements made originally by uncertain technique by surgeon Ira
Russell of the Eleventh Massachusetts Volunteers
brain weight
As I have recited them, these figures look
consistent and convincing. Indeed, they
have been immediately and uncritically accepted as indicating a lower average level
of intelligence of the Negro. As Putnam
has put it:
“The evidence is simply that, as a racial
average, the Negro brain is lighter t h a n
the White and that this, in turn, indicates a lower average level of intelligence.” (’63, p. 10)
We shall return later to the claim that
less brain-weight means less intelligence.
For the moment, let us examine the figures
on brain size more closely.
It is true that the studies just cited have
demonstrated a lower average brain weight,
or smaller average capacity of the braincase, in Negroes than in Whites. The biggest series of White or Caucasoid brains to
have been weighed was 2752 Americans:
their average weight was 1301 gm, or, if
672 diseased brains are excluded, the
average for the remaining 2080 brains was
1305 gm. (Appel and Appel, ’42). This is
only 29 gm heavier than the average for
the sample of Kenya African brains. On
the other hand, Davis (1868) recorded
capacitites from which Pakkenberg and
Voigt (’64) computed a mean brain-weight
in “Africans” of 1293 gm,whilst the average for 139 American Negro brains was
1355 gm (Pearl, ’34) - just 50 gm heavier
than the mean of the most comprehensive White series. Other Caucasoid series
range up to means of 1440 gm for 724
adult male Danes (Pakkenberg and Voigt,
’64), 1450 gm for 581 brains weighed at
the Institute for Forensic Medicine in
Prague (Matiegka, ’02) and 1455 for 372
brains of Bohemians (Pearl, ’05).
That is, the means for three fairly long
Negro series range from 1276-1355 gm,
while the means for some 11 White or
Caucasoid series range from 1301-1455
gm. It must be stressed that these are
ranges of averages; ranges of individual
values are much wider and overlap to
a greater extent. For comparison, means
for three Mongoloid series range from
1360-1375 gm (Kusumoto, ’34; Shibata,
’36 - cited by Bailey and von Bonin, ’51
and by Pakkenberg and Voigt, ’64). Bailey
and von Bonin (’51) have given an overall
average (weighted mean) of 1344 gm for
many modern human series irrespective of
race, i.e., for the living species Homo
sapiens at large (table 2).
Negro populations sampled have averages above and below the overall modern
human average. None the less, the overall
Negro average would seem to be somewhat
lower than the overall European average
in absolute terms, that is, when uncorrected for general bodily size and other related variables. However, a mere comparison of average figures may be misleading
unless allowance is made for these other
Average brain weight
Kenya Africans (389)
American Negroes (139)
Vint (’34)
Davis (1868)
Pearl (’34)
American Whites (2752)
11 White (Caucasoid) Series
Appel and
Appel (’42)
3 Mongoloid Series
1360- 1375
Kusumoto (’34)
Shibata (’36)
Bailey and
Von Bonin (’51)
Modern Homo sapiens
(weighted mean)
variables : we shall consider first the simple
notion that one might expect people with
bigger body sizes to have bigger brain
Brain size and body size
The size of the brain in relation to body
size has been employed chiefly in comparisons between species, in an effort to
show how predominant the brain has become in man. It was Cuvier who first introduced the concept of relative brainweight, that is, the weight of the brain expressed as a fraction of the weight of the
body (Krompecher and Lipak, '66). A picture given by Cobb of a small Asian woman
standing alongside a rhinoceros shows
graphically the difference in relative sizes
of brains. The woman may have a brainweight of 1200 gm in a body weighing,
say, 45 kg, whereas the rhinoceros has a
brain which may weigh 600 gm in a body
of about 2000 kg (Cobb, '65). The
brain: body ratio in the rhinoceros is 1:
3,000 in such a case, that of the woman
1:38. Even more revealing is a glance at
the Brontosaurus, one of the great dinosaurian ruling reptiles, perhaps 65 feet
long, that lived in the Jurassic period: its
brain constituted a mere 1/100,000 of its
35-ton bulk. A whale has a brain/body
weight ratio of 1:10,000; an elephant
1:600; a gorilla 1:200 and a man about
But it is sobering to see that while Man's
exalted brain constitutes just over 2%
of his body weight, this percentage is
surpassed by the lowly house mouse
(2.50% or 1:40), the porpoise with 1:38,
the marmoset with 1:19, and the attractive little squirrel monkey of tropical
America whose brain occupies 1/12 or
8.50% of its body weight (Cobb, '56)! Because Man, the sapient, did not come out
at the top, it is not surprising that Man,
the vainglorious and the arrogant, has been
searching ever since for an index which
would place him unequivocally and unassailably on the highest branch of the tree
of life. For example, when the length of
the hypothalamus is expressed as a fraction of the cerebrum, Man has the lowest
fraction and so comes out on top (Kummer, '61); when the weight of the spinal
cord is expressed as a fraction of the brainweight, Man has the lowest fraction and
so conies out on top (Latimer, '50; Krompecher and Lipak, '66); when the cranial
capacity is related to the area of the foramen magnum, Man has the highest value
and still ends up on top (Radinsky, '67) I
All the indices I have cited have a certain though limited usefulness when comparisons are made between one species
and another. However, few studies have
seriously addressed themselves to the problem within the species of man.
Matiegka ('02) and Pearl ('05) claimed
that, in Man, brain weight varies with body
weight and with body height. That is to
say, they claimed to find that taller people
and heavier people have larger brains.
However, more recent workers have questioned the correlation claimed to exist between brain weight and body weight within
the human species.
Pakkenberg and Voigt ('64) have made
a more refined statistical analysis on the
brains of European subjects. They showed
that the increasing brain weight with increasing body weight found by the earlier
workers is really owing to the fact that people with higher body weight are usually
taller than average (chart 1). The earlier
workers had failed to correct for body
height when evaluating the relation between brain weight and body weight. When
this correction was made (chart 2), it was
Pound that brain weight depends significantly on body height but not on body
weight (Pakkenberg and Voigt, '64, p.
Taller people tend to have bigger brains
Heavier people tend to be taller
Heavier people APPEAR to have bigger brains
Heavier people, adjusted for height, do NOT have
bigger brains
Taller people have bigger brains irrespective of
Brain-weight is positively correlated with body
height, but not with body-weight
ence to his “initial hypothesis” in this context is both seriously misleading and an
error of logic. The wording may eliminate
such sources of variance as different mean
body-weights from the hypothesis, but this
by no means eliminates these sources of
variance from the facts to which Putnam
tries to apply the hypothesis. By citing the
“initial hypothesis” as eliminating bodyweight and other variables, Putnam creates
the impression that the value he quotes of
8-12% lower brain-weight in the Negro
has been corrected for body size. He states
explicitly in another place (’67,p. 43),
“Brain weight or size comparisons were
never attempted without first allowing for
sex and body size, and when these adjustments were made the averages were both
consistent and clear.” But no height measurements were recorded for Vint’s Kenya
Africans nor for Pearl’s Civil War Negroes,
the two longest series of Negro data on record, nor for any of the earlier cited studies.
Where and by whom were the claimed adjustments made? Putnam’s statement is
totally erroneous: in none of the studies
cited, nor in Putnam’s own writings, has a
correction been made for the varying
heights of the subjects concerned, nor are
corrected or adjusted figures recorded. The
figures of 8-12% shortfall cited by him are
absolute figures as measured, not as corrected for body height differences.
In comparisons between different animals, Lashley (’49) suggested that the
“There is, I suppose, no dispute about
the fact that, other things being equal
total amount of brain material, expressed
(such as sex, body size, proportion of
as a fraction of total body size, “seems to
parts and sulcification), the weight of
represent the amount of brain tissue in exthe brain correlates with intelligence.”
cess of that required for transmitting im(Putnam, ’63, p. 10.)
pulses to and from the integrative centres”
Elsewhere, too, Putnam (’67,p. 53) states (op. cit., p. 33). Following up this notion,
“, .
constant efforts like Simmons’ oc- Jerison (’63) has demonstrated that brain
curred to confuse the issue by injecting size may be considered as two separate
variables which properly were eliminated components: one is directly related to the
in the initial hypothesis.” Putnam’s refer- size of the body, and it is bigger in Primates
with bigger body size, and vice versa. The
other component seems to vary independently of body size; it comprises the
Adult men have on the average 8.3gm of brain “surplus” nerve-cells which are present
for every centimetre of body height
over and above those required for the satisAdult women have on the average 8.0 gm of brain faction of immediate bodily needs. These
for every centimetre of body height
“surplus” nerve-cells, Jerison suggests, axe
available for response to the challenge of
the environment through a wider range
Exactly similar results were obtained by
Spann and Dustmann (’65) in a study of
1229 male and 632 female brains in the
medico-legal institute at the University of
Munich: brain weight rose with increasing
stature (chart 3), but no association could
be determined between brain-weight and
body-weight. In 1966,Schreider reanalysed
some old brain and body measurements
made in Paris in 1865-1870 by Paul Broca,
one of the great anatomists of the last century. Schreider found that between brainweight and body-height there was a positive correlation coefficient of 0.26 for 224
males and 0.31 for 111 females.
Clearly, if one does not allow for the
varying average body-sizes of different populations, one may be misled into making
false statements about the existence of
real differences in average brain size
among the populations compared.
With this in mind, one has reexamined
the main original sources on Negro brainweight in comparison with White brainweight. Neither Davis (1868) nor Vint
(’34),nor Pearl (’34),the three main students of Negro brain-weight, have taken
body height into account, nor made any
allowance for it. Yet, when it is pointed out
that many Negro groups have a lower average body size than many White groups,
Putnam’s reply is that such variables are
eliminated in the initial hypothesis, which
reads as follows:
of brain-behaviour mechanisms; that is, for
intelligent adjustment.
On the basis of cell-counts in a variety of
Primates and, given certain assumptions,
Jerison claims that it is possible to estimate
the number of cortical nerve-cells, not only
in the brain as a whole, but in each of the
two components. He has developed a series
of equations for the calculation of these
neuronal values, given the size of the
brain and the size of the body. By applying
these formulae, he has been able to compute the number of ‘extra’ neurones regarded as being available for brain:behaviour adaptive mechanisms. With this
second parameter, the number of “excess
neurones,” he has found it possible to distinguish the Primates and, especially, the
family of Man, on the basis of the relative
development of the extra neurones. Modern
man has f a r more excess neurones than,
say, the chimpanzee and gorilla. While the
African great apes can be shown by Jerison’s equations to possess 2.4-3.6 billion
excess neurones, modern man has over
eight billion.
The method involves many assumptions.
It does not adequately take into account
regional variations in the density of neurones, in the ratio between neuroglia and
neurones, in the size of nervecell bodies,
in the length and complexity of the dendritic processes of the neurones. None the
less, itprovides a novel, approximate gauge
of cortical development. Above all, the
method has been developed for comparisons between species, However, as an exercise, I have tentatively assumed that similar patterns of variation may occur between populations within a species, like
Homo sapiens, to those which occur between species. Purely to emphasize the
need for body-size to be taken into account
in discussions on human brain-sizes, I have
made some calculations, using Jerison’s
formulae, of the number of such “surplus”
nerve-cells in various races, for which
large samples of data on male brain size
and body size are available. The results are
given in table 3.
These results suggest that the differences
among various racial or population groups
are negligible, once allowance has been
made for body size. Further, it should be
noted that the figures quoted are averages
for each group: but individuals within
each group vary above and below the average, so that considerable overlap occurs.
It is stressed that this is only an exercise: it has yet to be shown whether Jerison’s method of analysis is valid in general,
and, more particularly, whether it can
validly be applied in this manner within a
We may conclude this section by stating
that no comparisons between the mean
brain-size of different populations or races
permit valid statements to be made on interracial differences, unless corrections
have been made for differences in body
height. On this basis alone, all comparisons
between Negro and White brain-sizes to
date are invalid.
It has long been known that the average weight of the human brain decreases
with advancing years (e.g. Pearl, ’05; Appel and Appel, ’42; Tiakahasi and Suzuki,
’61; Pakkenberg and Voigt, ’64; Spann and
Excess 7tezLrms in populatiolts of modem man
(Estimated by the method of Jerlson, ’63)
Average brain
Kenya Negro
American White
American Negro
Millions of
excess nervecells
mental animals may lead to permanent impairment of the brain, including diminution of brain-size. This effect occurs provided the period of undernutrition begins
before the cerebral cortex has reached its
adult state, or, at least, during the period
of maximum vulnerability of the brain to
stress. If the nutritional insults are administered within this critical post-natal period, or even if it is the pregnant mother
which is undernourished, the impairment
to the size, stature and chemistry of the
brain is not reversed by subsequent restoration of normal nutrition. These results
have been obtained on pigs, rats and mice
(Jackson and Stewart, '20; Dobbing and
Widdowson, '65; Davidson and Dobbing,
'65; Dickerson and Dobbing, '67; Dickerson
and McCance, '67; Dickerson and Walmsley, '67; Guthrie and Brown, '68; Zamenhof, van Marthens and Margolis, '68;
Chase, Lindsley and O'Brien, '69).
Is there any evidence for impaired brain
growth in man under conditions of malnutrition? The studies of Engel ('56), Nelson
('59, '63), Stoche and Smythe ('63, '67),
Cravioto and Robles ('65), Brown ('66),
Eichenwald and Fry ('69) and Baraitser
and Evans ('69) have all noted functional
impairments of the human brain following
early undernutrition. These workers have
studied electroencephalographic readings,
psychometric testing, rate of psychomotor
development, and head circumference, to
demonstrate abnormalities. It is still too
early to say whether the changes demonstrated are permanent; the analogy of animal experiments would suggest a permanent effect, while the recent study of Baraitser and Evans ('69) in the Department of Neurology at the Groote Schuur
Hospital, Cape Town, would tend to s u p
Evidence has accumulated, especially port the notion that the E.E.G. changes
in recent years, that undernutrition at outlast the acute stage of the nutritional
critical stages during ontogeny of experi- insult.
In their recent review, Nutrition and
Learning, Eichenwald and Fry ('69) summarise as follows:
Average brain weight : Decline with years
Dustman, '65; Schreider, '66), and that the
decline may begin as early as the twentieth
year. The drop in average brain weight
from young adulthood to about 80 years
of age varies from 95 gm in Swedes
(Pearl, '05, after Retzius, 1900) to 170 gm
in Danes (Pakkenberg and Voigt, '64).
Among the Danes, the drop from the age of
25 years to the age of 70 years is approximately 100 gm. These figures suggest a
drop in the average of 7 to 11% of the
maximum brain size (chart 4). Schreider
('66) showed negative correlation coefficients between brain weight and age as high
as -0.39 in males and -0.46 in females.
The cause of the fall with age need not
concern us here, but the relevance of this
finding is that if one series of brains includes a large proportion from old people,
the overall average would tend to be lower
than that of another series which includes
more young adult brains, even though both
series may stem from the same population. For many European series the ages
at death are known (e.g. Schreider, '66, on
Broca's material), but this is not true for
Negroid series, such as that of Vint ('34)
on Kenya African brains. We simply do
not know the ages of his Negroid subjects and cannot therefore decide to what
extent his relatively small average figure
of 1276 gm is attributable to age, and how
much to stature and to other variables in
that population. A valid comparison between two series of brains drawn from
different racial groups should take the
age composition of the sample into account.
It cannot be claimed that this has been
done for comparisons between the brainsizes of Caucasoids and Negroids.
Young adulthood
Drop of 95 gm
Drop of 170 gm
Drop in average
f 80 years
"Observations on animals and human
infants suggest that malnutrition during
a critical period of early life results in
short stature and may, in addition,
permanently and profoundly affect the
future intellectual and emotional development of the individual. In humans, it
is not known whether these results may
be caused by malnutrition alone or
whether such intimately related factors
as infection and an inadequate social
and emotional environment contribute
significantly to the problem. Field studies
to test these hypotheses are, at best, difEcult to design and to carry out; it seems
likely that it wiU prove impossible to
separate clearly the individual effects of
malnutrition, infection and social environment.”
In a subsequent editorial in Science,
Abelson (’69) summarised the results of
their study and of an International Conference on Malnutrition, Learning, and Behaviour (Scrimshaw and Gordon, eds., ’68)
as follows:
“Children reared in poverty tend to
do poorly on tests of intelligence. In part
this is due to psychological and cultural
factors. To an important extent it is a
result of malnutrition early in childIt seems likely that millions
of young children in developing countries are experiencing some degree of retardation in learning because of inadequate nutrition, and that this phenomenon may also occur in the United States
animal experiments suggest that (in
the human infant) good nutrition during the first three years of life is particu,”
larly important
Further follow-ups are obviously necessary
to confirm the hypothesis that malnutrition
at a critical age results in permanent braindamage, with permanent impairment of
intellect and emotions, and of brain
The substantial body of evidence for
such impairment leaves undecided the
question of whether changes have occurred
in the brain-size and structure. What direct
evidence do we have for such changes following early undernutrition? Several students have demonstrated that a smaller
brain-weight in man may result from early
undernutrition. Kerpel-Fronius (’61) found
a reduction of 10-20% in brain-weight of
the malnourished human infant. Brown
(’66),working on Uganda African children at Mulago Hospital, Kampala, found
a significant reduction in the brain weight
of malnourished children compared with
other Ugandan children. Even among
his control “non-malnourished children,”
Brown stressed, many, if not most, showed
suboptimal nutrition, though not rating the
autopsy diagnosis of kwashiorkor, marasmus or general undernourishment.
Recently, belated after-effects of starvation and other forms of maltreatment of
Second World War prisoners held in concentration camps have been investigated
in Norway (Strprm, ’68). Nearly 20 years
later, a number of survivors showed a reduction in the size of the brain, accompanied by signs of intellectual deterioration. Further, an article by W. Osler entitled “Belated scars of war prison,” which
appeared originally in the London “Sunday Times” and was quoted by the Johannesburg “Star” on November 11, 1968,
stated, “Research in Japanese camps had
shown that starvation causes the brain to
swell, and it is thought that on return to
normal conditions the brain then shrinks
to less than its original size.”
On the structural side, Eayrs and Horn
(’55) showed histologically that undernutrition impairs the elaboration of nervecell processes: this may be one of the
mechanisms behind both the reduced
brain-size and impaired brain-function.
Fishman, Prensky and Dodge (’69) have
recently shown changes in the brain lipids
of starved (or chronically malnourished)
human beings, resembling those found in
experimental animals. Not only is the total
lipid reduced, but most severely affected
are those classes of lipids of which myelin
is composed. Here, too we may have a
clue as to the mechanism, or one of the
mechanisms, responsible for the lower
brain-weight and the impaired function in
undernourished subjects.
One interesting point that emerges from
the studies on both men and experimental
animals is that the brain-weight reduction, though definite and significant, is not
as marked in degree as that of the body
as a whole, or as those of other organs,
such as muscles, spleen and liver (Platt
et al., ’65; Brown, ’66; Guthrie and Brown,
’68; Chase et al., ’69; etc.). In the study
of Kerpel-Fronius (’61), while the infant’s
body weight was 50% below the expected
value, the brain-weight was only 10-20%
reduced. Thus, although the absolute brainweight was depressed, the brain,/body
weight ratio is elevated in such caseswhich perhaps provides one further indica-
tion of the relative meaninglessness of the
brain/body weight ratio! It seems that
some protective mechanism may be operating which gives the brain priority in access
to nutrients during periods of undernutrition (Hammond, ’44; Kerpel-Fronius, ’61
Nevertheless, enough has been said to
show that in any population widely exposed
to varying degrees of undernutrition, it
would be reasonable to expect that heads
and brains would be signiikantly smaller,
on the average, than those of a population
on a good average level of nutrition. The
widespread incidence of varying degrees
of suboptimal nutrition in the African population is well-known (cf. Gillman and Gillman, ’51; Tobias, ’58; Brown, ’66; Smit,
’69). I am referring here not merely to an
extreme form, such as kwashiorkor, but
to lesser and subtler grades of undernutrition, such as have been uncovered by the
multidisciplinary study of Pretoria schoolchildren of African, Asian, Coloured and
European origin, by the National Nutrition
Research Institute of South Africa (Smit,
’69). The relevance of these malnutritional
effects for the interpretation of the mean
brain-weight of the Negro, and of other
poorly-nourished and emergent peoples, is
obvious: if lower mean brain-weights can
be validly demonstrated (and they have
not yet been validated), the degree to
which undernourishment is responsible for
the shortfall would have to be considered,
before such differences are lightly ascribed
to racial or genetic differences.
Is there a relationship between brainsize and structure on one hand, and the
degree of challenge, of enrichment, or of
impoverishment of the environment on the
other? Although there is little direct evidence for man, indirect evidence of several
kinds is available.
Marian Diamond and her co-workers at
Berkeley (’64, ’66) have studied the brains
of rats reared in an enriched, stimulating
environment and of their littermates reared
in an impoverished and isolated environment. Definite structural differences have
been demonstrated between the brains of
the two groups. Those from the enriched
milieu showed a significantly deeper visual
cortex and a higher glia-neuron ratio than
those from the isolated environment. Unforunately, I have not been able to trace
any reference to brain-size measurements
made in such experiments. At any rate, one
can say clearly that the “educational environment” of a growing rat influences the
fine internal structure of the cerebral cortex.
A second line of evidence is the demonstration that closely related animals may
differ in brain-size, according to the
amount of activity and the challenges, or
protective influences, emanating from their
environments. Thus, Poliakova (’60) has
shown that the agile, climbing, red fieldmouse possesses a larger brain-weight than
the relatively sluggish, grey field mouse, although both are classified as belonging to
the same species. Another series of studies
on dogs, pigs, rabbits, rats, guinea-pigs,
cats and ducks showed that domestication
causes a decrease of about 20%, in some
cases as high as 30%, in brain-weight
(Herre, ’58). Klatt (quoted by Herre, ’58)
showed that when wild animals are kept
in captivity from an early age, their brain
weight decreases markedly. Conversely,
asses which have been allowed to run wild
on the pampas of Argentina and Peru show
an increase in brain size of about 15%,
A similar figure obtains for cats which
have been allowed to run wild (Klatt). It
would seem that the docile life, in which
animals are fully protected from their enemies, provides a similar absence of environmental stimulation to the developing
brain of young animals, as obtains with
Marian Diamonds isolated rats reared in
an impoverished environment.
One cannot help thinking of the enriched
environment in which the ‘?laves” are
reared and the deprived and neglected
upbringing of the ‘3ave-nots.” There is
a distinct possibility that such differences
in the early home-upbringing and nursery
school facilities between members of different populations may contribute towards
structural and even size differences in their
brains. Here is one factor, which, as far
as I can determine, has not been examined in studies on human brain-size structure.
Yet another variable which may influence the average brain weight is the source
from which the brains were obtained. As
Pakkenberg and Voigt (’64) have recently
pointed out, most of the series published
have been from hospitals, including mental
hospitals (as is the case with the largest
series, that of Appel and Appel (‘42)). This
implies that, with relatively few exceptions,
the brain weight of the normal or healthy
human being is not known! The only real
exceptions are brains which have been obtained through institutes of forensic medicine, i.e., following sudden death without
prior disease. Only three such series have
been traced in the literature, namely those
of Matiegka (’02) from the Forensic Institute in Prague, of Pakkenberg and Voigt
(’64) from the Neuropathological Laboratory of the Kommunehospitalet and the
University Institute of Forensic Medicine
in Copenhagen, and of Spann and Dustmann (’65) from the Institut fur Gerichtliche Medizin and Versicherungsmedizin
at the University in Munich. No Negro
series from such a source has been published: we do not know the brain weight of
the normal, healthy Negro! Vint (’34),
whose low average for the Negro brain
(1276 gm) has been most often quoted,
obtained his material from hospitals in
Nairobi, excluding the Mental Hospital.
His series therefore did not fulfill the
ideal requirement of sudden death without
prior disease.
Although many hospital patients may
suffer and die from diseases which probably do not affect brain weight (and even
on this point we lack precise information),
hospital populations as such are often
not a good cross-section of all levels of society. They tend to reflect the lower social
strata, while the upper strata tend to go to
private nursing homes or to receive medical care at home. Vint even says of his
Kenya African series, “These 100 brains
represent the average native population,
but do not include any of the so-called
educated class” (’34, p. 216).
Even bodies which are studied and dissected in Medical Schools are a far from
random sample. The law caters for two
main groups of subjects: those who die as
paupers in State Institutions - in South
Africa these tend to be largely Africans;
and those who bequeath their bodies to
the Medical Schools - and these people are commonly better educated and
often of the higher social strata. As
Burial Societies come more and more
within the reach of the poorest sections
of the community, fewer and fewer people
die as unclaimed paupers: and so gradually
the face of the dissecting room population
itself changes. This phenomenon is particularly vividly to be seen at present in
the Anatomy School of the Witwatersrand
T. Wingate Todd (’27) has recounted
how dramatic an effect an economic depression had on the dissection room population; all sorts of people took to dying as
unclaimed paupers who had previously
been numbered among the university’s
financial benefactors. The average brainsize of the cadaver population increased.
Todd entitled his address, “A liter and a
half of brains!”
We may conclude that no series of brainweights is available for healthy, normal
Negroes who have died a sudden death;
no Negro series can therefore be compared
validly with the best available European
series from Forensic Medical Institutes.
Brain-size and occupational groups
Closely related to the source from which
the brain was obtained is the question of
the occupational groups represented in the
sample (chart 5). Matiegka (’02) showed
an association between brain-weight and
occupation in his studies at the Forensic
Medical Institute in Prague. Results obtained in the recent study of Spann and
Dustmann (’65) tally remarkably closely
with those of Matiegka. Thus, in both
studies, unskilled workmen had a mean
brain-size of just over 1400 p, and the
academic, the professional and the senior
official group of just on 1500 gm. Spann
and Dustmann found some correlation
among women: three groups of skilled and
unskilled workers, handworkers, and lesser
officials all had mean brain-weights between 1300 and 1315 gm, while six female academics had the absurdly high
mean value of 1422 gm (just within the
Brain-size and occupation
Matiegka-Prague, '02;
Spann and Dustmann, Munich, '65
Average brain size
Unskilled workmen
Academics, professional men and senior officials
Paul Broca, Paris, 1865-70
Unskilled labourers
Semi-skilled and skilled workers
But the latter were taller than the former1
Question: Has there been a secular trend towards increased brain size, in parallel with the secular
trend towards increased stature?
lower end of the range of occupational
means among males!).
The tendency is apparently not a new
one: Broca's results from the late 1860's
yielded a mean brain-weight of 1365 gm
for 51 unskilled labourers and of 1420 gm
for 24 semi-skilled and skilled workers:
the difference is almost significant at the
5% level (Schreider, '66). Schreider comments, however, that the differences in
brain weight between the occupational
groups are probably related to differences
in body height, for the skilled and semiskilled group were on the average 1.34 cm
taller than the unskilled group.
The degree to which any sample of
brains represents, or departs from, a
cross-section of occupations may thus affect the validity of any comparisons between such a sample and any other.
Brain-size and cause of death
In a large hospital population, Appel and
Appel ('42) found that the mean weight
of the brain was highest (1374 gm) in
cases of violent and accidental deaths. On
the other hand, patients who died of
arteriosclerosis and cancer had average
brain weights of 100 gm less (1273 and
1275 gm respectively). For other categories
of causes of death, the average weights
lay between these two extremes. Of
the various disease groups, tuberculotics
showed the highest mean weight (1328),
that is, 55 gms above the mean for arteriosclerotics and 46 gms below the mean for
victims of accidental and violent deaths
(chart 6).
In the large Copenhagen medico-legal
series of Pakkenberg and Voigt ('64), the
highest mean brain weights were found
among those who had died from hanging,
poisoning (mainly by carbon monoxide or
barbiturates) and shock: similar results
were observed in the Munich series of
Spann and Dustmann. Low values, on the
other hand, were encountered in those who
had died following brain diseases, general
pathology, head trauma, drowning, asphyxiation, electrocution and protracted
Brain-size and cause of death
S t . Elizabeth's Hospital,
Washington, D. C .
(Male white data - after Appel and Appel '42)
Cause of death
Average brain
Urogenital diseases
Digestive diseases
Respiratory diseases
Circulatory disease
(incl. Arteriosclerosis1
Nervous diseases
ZIt is doubtful however whether this relatively
small difference in stature is adequate to explain all
the difference in brain-weight between the two groups.
On Spann and Dustmann's figure of 8.3 gm of brain
for e v e n centimeter of bodv heizht in men. the difference of'1.34 cm might account-for some i l . 0 g m 04
brain-weight difference: this would reduce the discrepancy to non-significant levels (with these small
samples), but there remains a shortfall of 44 gm be7
tween the two groups.
Again, in his study of Broca’s centuryold data, Schreider (’66) showed that
those who died from accidents had a mean
brain weight 60 gm greater than those
who had died of infectious diseases. It
seems that even 100 years ago, accidents
were common in the streets of Paristhough they were seemingly often owing to
horse kicks.
Thus, whether death is lingering or sudden, disease processes themselves may influence brain weight at death and, indirectly, the rate of increase in brain
weight with each passing hour after death.
It is well known that the patterns of fatal
diseases differ appreciably among M e r e n t
populations, especially where one group
lacks adequate medical and hospital facilities (as is the case with many African
Negro populations). Thus, two groups may
show differences in average brain-weight
simply because of a different pattern and
incidence of fatal diseases in the two
groups. Such a factor may account for
some of the discrepancy between, for instance, two Negro series, one in Africa
with an average brain-weight of 1276 gm
and one in America with an average of
1355 gm. Similarly, some of the differences
found in interracial comparisons may be
accounted for by such differential diseasepatterns.
Brain-size and the lapse of
time after death
Another source of variation in the average brain-size is the time that elapses between death and the removal of the brain
(chart 7 ) . Chemical changes go on in the
brain for several days after death, tending
towards an equilibrium that is appreciably
heavier than the original weight (Appel
and Appel, ’42). Thus, if left for 24 hours
after death, the brain weight is no less
than 40 gm heavier than if removed within
Time after death
Brain weight
g m
24 hours
48 hours
Maximum change
a few hours of death; 48 hours after death,
it weighs on the average 75 gm more. The
average maximum increase in weight is
90 gm, whilst the increase from the lowest
mean weight to the highest is no less than
117 gm,or 9% of the average weight for
the total array. Statistically and biologically, this is a significant and appreciable
increment. It is almost as great as the
decrease with age ( 1 1% ) and it is greater
than most of the recorded differences between the averages for various racial
groups, including Negroes and Whites.
Then, too, the temperature at which the
cadavers are kept between death and removal of the brains may affect the rate
of chemical change and, so, the increase
in weight after death.
Brain-size and the treatment of
the brain after death
“To weigh the human brain is not as
easy as it sounds” (Bailey and von Bonin,
’51). Thus, the measured weight will depend upon where exactly one severs the
brain from the spinal cord. It is an agreed
definition that everything cranial to the
pyramidal decussation is “brain”; but the
decussation is not a point: it extends for
some little distance down the central nervous system. Different workers may sever
the brain from the cord at a systematically
higher or lower level (Bailey and von
Bonin, ’51).
Other technical points on which no standardization has been achieved include
whether and how one drains the cerebrospinal fluid from the brain; Brandes (’27)
stated that the complete drainage of the
cerebrospinal fluid from the fresh brain
may change its weight by as much as 50
gm. Again, there is the question: which of
the covering membranes (or meninges )
one removes from the surface of the brain
and which of them one includes; Brandes
(’27) determined the weight of the outer,
thick covering, the dura mater, as no less
than 50-60 gm. Should one strip the bloodvessels from the brain surface? Inconsistency between workers in every one of
these points may import additional variance in the results obtained by different
workers on different races or populations.
Some studies in the literature (e.g., Pakkenberg and Voigt, ’64; Spann and Dust-
mann, ’65) carefully define their methods;
in others, it is stated simply that the brains
were weighed.
As in other branches of science, standardization of technique and precise description of the methodology followed in
each study must obviously precede any
meaningful comparisons between any two
sets of data,
On the meaninglessness o f most studies
on brain-weight
For all these reasons, it is not surprising
that contradictory results appear in the scientific literature for the brain-sizes of
Negroes and Whites. We have seen that
brain-size may vary according to body size,
the age at death, the cause of death, the
selection of the sample, the sex, the early
environment, especially nutritional, the
lapse of time after death, the level at which
the brain is severed from the spinal cord,
the mode of drainage of the cerebrospinal
fluid and the treatment of the covering
membranes and blood-vessels; other factors
may intrude as well, such as the temperature at which the body is kept between the
time of death and the removal of the
brain (chart 8). These factors may cause
fluctuations in the measured brain-size up
to 9% too high if the brains are left for
several days after death, or 11% too low
if the sample of brains comes from elderly subjects. This order of variability,
stemming from only one or two of these
possible variables, is greater than most of
the supposed interracial differences which
have appeared in the literature. The ideal
sample is from subjects who have died
Measured brain size varies with:
1. Sex
2. Body size
3. Age at death
4. Nutritional state in early life
5. Non-nutritional environment in early Iife ( ? )
6. Source of sample
7. Occupational group
a. Cause of death
9. Lapse of time after death
10. Temperature after death
11. Anatomical level of severance
12. Presence or absence of C.S.F.
13. Presence or absence of meninges
14. Presence or absence of blood-vessels
suddenly without prior disease, as from vie
lence and accidents. No such study has
been recorded for Negro subjects.
It must be concluded that among the
widely varying estimates for Negro brainsize, none reflects the normal brain-size
of a healthy Negro group. W e do not know
the brain-size of healthy Negroes who have
died suddenly without prior disease. Few
of the published studies on any racial group
have been corrected for body size, age at
death and the lapse of time after death;
it is clearly difficult, if not impossible, to
correct for all the other factors enumerated.
These considerations largely invalidate
most interracial comparisons so far published. Certainly, it is invalid at this stage
in our knowledge to claim, as Swan (’64)
and Putnam (’63) have done, that the
average brain weight of European Whites
is some 8-12% greater than that of African Negroes. Equally misleading is the
bald statement of Gates (’46) that “Comparative weights are given as 1380 gm for
Caucasoids, 1300 gm for Mongoloids, 1280
gm for East Africans, 1240 gm for Negroes, and 1180 gm for Australian Aborigines.” These figures are meaningless without any attempt to consider the body size
of the various groups, let alone all the other
A fortiori, it is totally invalid at this
stage of our knowledge to cite the alleged
smaller brain-weight of Negroes as the
physical basis for differences in intelligence and behaviour tests.
W h a t do differences in
brain-size mean?
It has been known for long that in living
men, enormous variations in brain-size
may occur within the limits of normal
healthy functioning. Even well-known men
of high achievement may vary considerably (chart 9). Thus, the great French
writer, Anatole France, is reported to have
possessed a brain weight of as little as
1017 gm (or an endocranial capactiy of
about 1100 cm3); similar in size were the
brains of Franz Joseph Gall, the German
anatomist, physiologist and founder of the
pseudo-science of phrenology; and of the
French statesman, Ikon Gambetta (Dart,
Brain size and achievement.
A pot-pouri-i of big and small bTains
Brain weirrht
1000-1 100
Anatole France
Franz Joseph Gall
Leon Gambetta
Walt Whitman
Daniel Webster
Ivan Turgenev
Dean Swift
Otto Von Bismarck
Oliver Cromwell
George Gordon,
Lord Byron
’56); while only slightly larger was the
brain of the great American poet, Walt
Whitman (1282 gm) (Cobb, ’65).
At the other extreme, George Gordon,
Lord Byron, is said to have had a brainweight of 2,238 gm and Oliver Cromwell
of 2,231 gm (Keith, ’12, cited by Dart, ’56).
Brain-weights of about 1900 gm were
possessed by Daniel Webster, the American lawyer, statesman and orator; by Ivan
Turgenev, the Russian novelist; by Dean
Swift, the English satirist, and by Bismarck, the Prussian statesman and creator
of the German Reich (Dart, ’56).
Thus, considerable human achievement
is possible at very nearly both ends of the
scale of modern human brain-size. Further,
as Dart (’56) has pointed out, apparently
normal human beings have existed with
brain-sizes in the 700’s and 800’s.Schlaginhaufen (’50-’51) reported the skull of a
Melanesian woman from one of the Feni
Islands in the Bismarck Archipelago with
an endocranial capacity of only 790 cm3.
As far as Dart (’56) could trace in the
literature, this is the smallest capacity yet
attested for a normal human skull - for
it was not the skull of a pathological microcephalic! This capacity was found not in
an ape-man or a pre-man, but in an individual classifiable as a member of our
living species, Homo sapiens (Dart, ’56);
yet her capacity was a mere 38 cm3 greater
than the maximum capacity recorded for
an anthropoid ape, namely a gorilla with a
cranial capacity of 752 cm’ (Schultz, ’62).
Thus, normal human beings exist with
brain-sizes three times that of other human
beings. So fantastic a range would single
out brain-size as one of the most highly
variable parameters in modern man. Perhaps only body-weight exceeds brain-size
in the discrepancy between the top and
bottom of the range in normal healthy human beings.
What then do the W e r e n t brain-sizes
in normal men signify? Do people with bigger brains have more nerve-cells, or bigger nerve-cells, or more neurogkia (the
non-neural elements which lie between the
neurons), or more nerve-processes, or
longer nerve-processes, or tnicker nerveprocesses, or more highly-branched nerveprocesses? Or are larger brains larger
through a combination of any two or more
of these seven possible variables?
We simply do not know the answers to
these questions for modern human brains
within the range of normality. We shall see
in a moment that we have a little more information when it comes to comparisons
between different animals of different average brain-sizes. But within our species,
we do not know what the microscopic or
cellular basis is of varying brain-sizes.
If we do not know that simple physicophysical correlation, how can we hope to
make meaningful statements about the
correlation between gross brain-size and
cellular structure on one hand, and about
psychical and behavioural attributes on
the other? For the physico-physical correlation is basic to the physico-psychical
association. We do not have the requisite
information at either level.
No wonder that a leading neurologist,
Gerhardt von Bonin (’50), was led to remark, “The correlation between brain-size
and mental capacity is insignificant” and,
again, “Brain size as such is none too
meaningful.” Similarly, Holloway (’68),
moving outside the human species, has
concluded that “Gross size of the brain
alone does not explain differences of behaviour within the primate order.” He is
at pains to point out that “such correlations (as between brain-size and specific
behavioural traits like memory, insight,
forethought, symbolization) are not causal
analyses, and that a parameter such as
We are back at square one.
brain weight in grams, or volume in milliliters, or area in square millimeters, canWe must confess our ignorance of the
not explain the differences in behaviour functional meaning and value of different
which are observed.” (op. cit., p. 125) sized brains in modern human individuals.
(italics mine). A more encompassing
Will a long-term evolutionary look at the
theory, Holloway states, should entail not problem throw any light on it?
merely the changes in brain weight which
Brain-size, evolution and survival
have occurred in evolution, but the internal reorganization of the cellular maWe showed above that, when allowance
terial of the brain. It is precisely at this is made for body size, the differences in the
level that we are most ignorant.
computed numbers of “excess” nerve-cells
If we compare different species of mam- in the cerebral cortex of various racial or
mals, many studies have demonstrated population groups are negligible - despite
that bigger brains are correlated with variations in the source, composition and
clearly defined cellular and chemical fea- treatment of the brains. Even if further
tures. For instance, the bigger the brain, studies did demonstrate that one group had
the lower is the density of nerve-cells in fewer surplus nerve-cells on the average
that brain (Nissl, 1898; von Bonin, ’48; than another, how valid would it be to
Tower and Elliott, ’52; Shad€, ’53; Tower, jump to the conclusion that fewer surplus
’54). Further, it has been claimed that nerve-cells automatically connote lesser
neurones are bigger and nerve-cell proc- cerebral development (cf. Vint) or lesser
esses longer and more complex in bigger evolutionary advancement (cf. Gates)?
brains. The glia-neurone ratio is likewise Putnam (’63) assumes that there is no dishigher. The claims and their validity have
been well summarised by Holloway (’68:). pute on this question, but his assumption
As he points out, an increase in dendritic is far from justified.
When one takes a long-term evolutionbranching means more synapses, more
connectivity, and with this goes more com- ary look at this problem, it seems clear that
increasing brain-size (and the organizaplex beh aviour.
On this kind of analysis of W e r e n t tion, fine structure and chemistry that went
species, increase in brain-size is coming with it) may once have been vitally imto be meaningfully analysed in terms of its portant in aiding survival - for instance
structural units and these, in turn, may in a world of wild animals and ape-men,
provide a more rational basis for under- bereft of fire. It seems, too, that the furstanding increasingly complex behaviour. ther development of man has placed less
But all this has been shown to apply in an and less of a premium on the size of brain,
assumed evolutionary progression from the numbers of nerve-cells and other inone form to another as one passes up the ternal organizational details. For during
scale. To a lesser extent, similar changes his evolution, culture and the benevolence
have been shown to apply to the ontoge- of social life have taken the place of nimnetic development of individuals within ble wits as an insurance policy against
a species. At the adult level, however, I extinction. Beyond a certain stage in the
reiterate the view expressed earlier: we do increase of brain-size, we have no evinot have any clear picture of the histologi- dence that further increase in any way imcal and chemical differences between big proved man’s adaptive abilities. For aught
and small brains among members of the we know, the slight preponderance of
same species. Therefore, we cannot pin- brain-size which is claimed for Caucasoid
point any cellular and chemical differences or White men of today may, if it exists as
between big and small brains which would a genetic feature at all, be a somewhat
indicate a basis for different behaviour. Are superfluous and gratuitous heritage from
there differences in behaviour between in- Stone Age ancestors, like Cro-Magnon and
dividuals with big brains and with small Neandertal men. For these ancestral men
brains? Evidence for such differences does had bigger brains on the average than
their present-day European descendants.
not seem to exist.
In fact, there is some evidence to suggest
that the trend towards increased brainsize, which marked the first two million
years of human evolution, has spent itself;
the wave of brain expansion has passed
its peak. This is true, as I have just said,
of early and modern Europeans; to a certain extent, it may be true of Africa as
well. Some of our Stone Age men had
carried the twin processes o€ reduction of
teeth and jaws, on the one hand, and expansion of brain, on the other, so far that
they seem to represent an ancient foreshadowing of the popular idea of the man
of the future. At any rate, that is the view
of them adopted by Professor Loren Eiseley
of Philadelphia, in his delightful and penetrating book of essays called “The Immense Journey” (’58). Listen to the way
in which he describes the man of the
future: “I have stared so much at death that
I can recognize the lingering personalities in the faces of skulls and feel accompanying affinities and repulsions
“One such skull lies in the lockers of
a great metopolitan museum. It is labelled simply: Strandloper, South Africa.
I have never looked longer into any human face than I have upon the features
of that skull. I come there often, drawn
in spite of myself. It is a face that
would lend reality to the fantastic tales
of our childhood. There is a hint of
Wells’s Time Machine folk in i t those pathetic, childlike people whom
Wells pictures as haunting earth’s autumnal cities in the far future of the
dying planet.
“Yet this skull has not been spirited
back to us through future eras by a
Time Machine. It is a thing, instead,
of the millennia1 past. It is a caricature
of modern man, not by reason of its
primitiveness but, startlingly, because
of a modernity outreaching his own. It
constitutes, in fact, a mysterious prophecy and warning. For at the very
moment in which students of humanity
have been sketching their concept of the
man of the future, that being has already come, and lived, and passed
away.” (Op. cit., pp. 127-128.)
‘Their voices,” says Eiseley, “‘ring
with youthful confidence, the c o d dence engendered by my persuasive colleagues and myself. At times I glow a
little with their reflected enthusiasm.
“I should like to regain that confidence, that warmth. I should like to
“There’s just one thing we haven’t
quite dared to mention. It’s this, and
you won’t believe it. It’s all happened
already. Back there in the past, ten thousand years ago. The man of the future,
with the big brain, the small teeth.
“Where did it get him? Nowhere.
Maybe there isn’t any future.Or, if there
is, maybe it’s only what you find in a
little heap of bones on a certain South
African beach.
“Many of you who read this belong to
the White race. We like to think about
this man o f the future as being White.
It flatters our ego. But the man of the
future in the past I’m talking about was
not White. He lived in Africa. His brain
was bigger than your brain. His face was
straight and small, almost a child’s face.
He was the end evolutionary product in
a direction quite similar to the one anthropologists tell us is the road down
which we are travelling.” (Op. cit.,
p. 129-130.)
. ..
In Africa, no less than in Europe, it
seems a corner has been turned, a peak has
been surmounted and something of a
downslope presents itself. Perhaps, we can
put it this way: the selective pressures
which once placed a considerable premium
on big brains have been somewhat relaxed.
Perhaps, we have reached a stage in human evolution, and I am convinced we
reached it thousands of years ago, where
100 people with smaller brains stand just
as good a chance of surviving to childbearing age as 100 with bigger brains, and
are likely to leave no fewer children than
the others. Brain-size is no longer a yardstick to survival as it may once have been.
We have used these very brains to develop
new mechanisms of adaptation, tools, shelters, clothing, fire, social institutions
and central heating, air-conditioning, refrigeration, disinfection, mink coats and
When Eiseley shows his students in sun shades. You can have these things with
Philadelphia a picture of what the man of a size 5.50 hat or with a size 8.50, just as
the future may be expected to look like, it makes no difference what size shoe you
they say, “It’s O.K. Somebody’s keeping an take.
eye on things. Our heads are getting bigBrain-size seems to make no difference
ger and our teeth are getting smaller. to your ability to avail yourself of the joys
of modern living. So, too, it seems that
publications mentioned, although the shortfall claimed by Vint for one other layer of
the cortex, the internal granular layer, is
Yet, when one goes back to the original
sources, one is left with serious doubts
about the validity of the data on which the
comparison was based. First, let us look
“Certainly, the weight of the brain is
at what Vint actually reported: he claimed
a very poor indicator of its functional
value” and, again, ‘Brain size as such
that the average total reduction of the
i s a very poor indicator of mental abilwhole cortex, as compared with that of the
European, is 14.8% in the cortical areas
A century earlier, James Hunt (1863) had examined.
His figures for the Negro were
stood before the Anthropological Society of
single study of Negro brains,
London and declared,
which, he states, did not include any of
. . we know that it is necessary to be
the “so-called educated class.” He did not
most cautious in accepting the capacity
study any European brains himself, alof the cranium as any absolute test of
the intellectual power of any race” (p.
though at least two of the references
quoted give the impression that Vint studIn the face of these individual variations ied European brains directly. Thus, Swan
of brain-size and achievement within a (’64) speaks of “Dr. F. W. Vint’s careful
single race, in the face of a decline in aver- comparative studies of the cortical histolage brain-size over the last tens of thou- ogy of the brains of European Whites and
sands of years, in the face of our knowl- African Negroes” (p. 27). Similarly, and
edge that a large part of man’s adaptabil- equally erroneously, Putnam (’67) states,
ity to new environments and to new ways “In 1934 F. W. Vint of the Medical Reof life is culturally determined,- who search Laboratory, Kenya, Africa, pubwould confidently assert that slightly lished the results of a Comparative study
smaller brains could be any deterrent what- of Negro and European brains in which he
ever to achievement, or set any brake upon found that the supragranular layer of the
mental capacity?
Negro cortex was about 15 per cent thinner
than the Whites” (p. 51) (italics mine).
T h e amount of grey matter
Thirty five years ago, Vint (’34) exam- In both quotations, the wording conveys
ined the grey matter of the cerebral cortex the impression that Vint had himself made
of Kenya Africans under the microscope a careful study of the cortex of European
and claimed that it was narrower on the brains, as well as of Negro brains, whereas
average than that of the European. This he had in fact studied only Negro cortices
work has often been quoted in publica- and compared his results with those obtions distributed by the Putnam Letters tained in one other study, by a different
Committee: e.g., by George (’62), by his worker, namely von Economo (’29) in
reviewer, Sanborn (n.d.), by Swan (’64) Europe.
In eight different regions of the cortex,
and by Putnam (’63, ’67), as well as by
Hofmeyr (’61). More particularly, this he measured the total cortical thickness
oup of writers has drawn attention to and the thickness of each of four layers
e supragranular layer of nerve-cells in comprising the total cortex, namely the
the cortex, which they claim Vint found to lamina zonalis, the supragranular zone,
be 14% (Sanborn, n.d.), more than 14% the internal granular zone and the infra(Putnam, ’63, p. 9), about 15% (Putnam, granular zone. Each of the five measure’67,p. 51), about 14% (George, ’62, p. ments in seven out of eight regions was
33) and 16% (Swan, ’64, p. 28) smaller then compared with a corresponding measthan that of Europeans. This layer is held urement as given in von Economo’s (’29)
by some to be the “most advanced” layer in book, and a percentage increase or dethe cortex; and that is presumably why crease recorded, as compared with “the
its supposed shortfall is stressed in all the European brain.”
brain-size does not limit your ability to
contribute to society, culture, science. Some
gifted people have had very small brains.
Others, also gifted, have had large brains.
And some very ordinary persons had
equally large brains. Small wonder that
Gerhardt von Bonin could say in 1963.
There are many possible sources of error in these comparisons. First, Vint himself points out that there is even some
doubt among different workers as to where
exactly to cut the little section of tissue
to measure the thickness of the layers whether from the tops of the convolutions
of grey matter, or from their sides, or from
the depths of the fissures between them.
Vint states that Bolton (’03, ’14) had recorded measurements which were the
average in each case between thickness
readings (i) on the flat external surface
of the convolution; (ii) at the lip of the adjacent sulcus or fissure; (iii) OR the side of
the fissure; and (iv) at the bottom of
the fissure.
Von Economo (’29) pointed out that the
thickness of the cortex on the summits of
the convolutions was twice as great as in
the floor of the fissures, but unfortunately
he did not make clear whether he had followed Bolton’s averaging method or some
other approach, Thus, Vint makes clear
that he is not exactly certain whether
von Economo’s measurements on European
brains were made in the same area as were
his (Vint’s) measurements on Negro
brains, namely only on the summit or
crown of the convolutions.
Secondly, the actual measuring of the
layers of the cortex is not as easy as it may
sound. Although the various layers are
fairly readily identified, the boundaries between them are not. The boundaries are
frequently wavy and exactly where to set
the termini for a particular measurement
may vary from worker to worker, even in
the same laboratory. It would be easy for
one worker consistently to measure from
a different part of such a wavy boundary,
compared with another, and so to introduce
a systematic error into his results. Vint had
received no specific training under von
Economo, as far as we know, and there is
no reason to believe that his technique of
making measurements would have been
precisely the same as that of von Economo.
Furthermore, Vint nowhere states how his
measurements were made, nor are the
boundaries of the layers marked in on his
photographs, in contrast, say, with the
illustrations on the human cortex by Bailey
and von Bonin (’51) .
A third most serious difficulty is the
technical procedures employed. To prepare
a brain for microscopical study requires a
number of chemical and staining procedures, a variety of which is available to
workers in most laboratories. Different
chemical treatments are known to produce
different degrees of shrinkage or swelling.
These influences readily affect measurements, especially when one is dealing with
a total cortical thickness as small as 1.886
to 3.006 mm (the range of average cortical
thicknesses found by Vint in 8 different
areas of the brain).
As an illustration, Diamond et al. (’64,
’66) measured the thickness of the rat’s
visual cortex by two different techniques:
frozen sections stained by thionin and elloidin sections stained by Windle’s modified
Nissl stain. The thickness measurements
by the second method were only 60.5%
of those by the former.
Even within one Laboratory, with the
use of only a single technique over and
over again, most variable results may be
obtained in the state of preservation (fucation) and staining of brains. As Carothers
(‘53,p. 82) has pointed out, “Comparative
assessments of cerebral histology are notoriously difficult and require special
knowledge of this type of work. .” Here,
then, we have the unsatisfactory position
of a series of h e measurements made on
brains treated in one laboratory by one
worker and derived from Negroes, being
compared with the results of another series
of fine measurements made by another
worker on European brains prepared in a
different laboratory, possibly under very
different conditions. And Vint’s are the
only data on record for Negro cortical
thickness1 If we left the matter there, anyone with a logical mind would realise that
no conclusions could validly be drawn
about alleged differences between races
culled from such unsatisfactory material.
To quote Carothers again, “Comparative
assessments of cerebral histology . . are
of little value d e s s the preparation of material and the techniques that are used
are virtually identical for the two groups.
These requirements were not convincingly
fulfilled (in Vint’s comparisons)” (op. cit.,
p. 82).
Vint himself points out a further serious
shortcoming. He states specifically, “Owing
to climatic and other conditions, it was impossible to fix the brain by injection of the
carotid arteries.”
If all these sources of variation apply
to the thickness of the entire cortex, how
much more strongly do they apply to the
supragranular layer alone, which Vint
found to vary in average thickness from
0.338 to 0.922 of a millimetre in six different parts of the cortex! (chart 10).
It is clear that Vint’s study, which has
been so widely quoted, permits only one
definite coriclusion about cortical thicknesses, namely that there is a need for
more carefully controlled studies. Yet, we
b d the alleged 15% difference in total
cortical thickness and the supposed 16%
shortfall in the supragranular layer being
quoted and re-quoted as established facts,
as further evidence of the supposed inferiority of the Negro’s brain. What is more,
the inferences drawn from these so-called
facts are used to Create the impression
that the Negro is a less highlyevolved
as for instance when Putnam
(’63, p. 9) states, ‘The thickness of the
supragranular layer of the cortex, which
is found to increase as we move up the
scale from animal to man, may thus be
said to be another measure of evolutionary
We are led to conclude that there is no
scientifically acceptable proof that the
cerebral cortex of Negroes is thinner in
whole, or in any layer, than that of Europeans.
I have singled out only two of the socalled well-established differences between
the brains of Negroes and of Whites,
namely brain-size and the thickness of the
Range of thickness measurements
(Vint, ’34)
cortex, and shown that they provide highly
unsatisfactory evidence of structural differences in the Negro’s brain, and of differences in intellectual capacity. Other
claims have been made, such as one about
the size of the frontal lobe and the degree
to which it is broken into convolutions,
claims which have been denied equally
strenuously by many other workers. From
my little venture into the study of the
brain, I have emerged with the conviction
that vast claims have been based on insubstantial evidence. I conclude that there is
no acceptable evidence for such structural
differencesin the brains of these two racial
groups; and certainly nothing which provides a satisfactory anatomical basis for
explaining any difference in I.&.or in other
mental and performance tests, in temperament or in behaviour.
The exploding of the myth about brainsize and grey matter differences leads to
the realisation that, in science, the truth
does not gain acceptance by mere repetition of a set of facts. Hypotheses are not
confirmed by statement and re-statement
of the hypotheses. Science requires rather
the patient testing of the facts, the repeating of early studies by more modern,
better controlled and better standardized
methods, the constant re-examination and
critical re-appraisal of premises and assumptions, the elasticity of mind which
permits, nay demands, old hypotheses to be
modaed when new facts emerge which
cannot be adequately explained by them,
resistance to the tendency to develop a
vested interest in a particular viewpoint,
avoidance of ascribing motives to scientists
of opposite viewpoint, in favour of the unbiassed examination of the evidence they
may advance, the eschewing of premature
hypotheses based on over-tenuous evidence.
It is to these stern and rigorous demands
of scientific method and to one who proved
himself a trenchant devotee of this philosophy that my address is dedicated.
Supragranular k y e r
I should like to express my gratitude to
Mrs. E. Hibbett, Mrs. E. Judd, Miss C.
Orkin and Mrs. S. Boles; and to Brian
Greis and Brian Hume.
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