https://www.goodreads.com/book/show/786753.Educability_And_Group_Differences
http://gen.lib.rus.ec/book/index.php?md5=501f355b6e474bdc0b7f3130dc3bf9c0&open=0
Why read a book from 1973? 41 years old? Well, it was a good read indeed! It is interesting how much of the evidence for racial differences were in place already in 1973, and it has more or less only become stronger since then. Basically, the book is a shorter and less technical (but not that much!) version of his major book The g Factor.
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This distinction between the individual and the particular gene pool from which the unique combination forming his genotype was derived extends beyond his family to the racial group with which he is identified and to the social status into which he is born. You are not your race; you are not your group. You are you. That is, if you are talking genetics. If you are talking sociology or politics, that may be another matter. You may be psychologically tied to and influenced by whatever groups you happen to identify with. If you are either elated or depressed about yourself because of such identification, don’t attribute this to genetics. It in fact contradicts this kind of typology which compels so many persons to identify with various groups as if the statistical attributes of the group determined their own characteristics. Racism and social elitism fundamentally arise from identification of individuals with their genetic ancestry; they ignore individuality in favor of group characteristics; they emphasize pride in group characteristics, not individual accomplishment; they are more concerned with who belongs to what, and with head-counting and percentages and
quotas than with respecting the characteristics of individuals in their own right. This kind of thinking is contradicted by genetics; it is anti-Mendelian. And even if you profess to abhor racism and social elitism and are joined in battle against them, you can only remain in a miserable quandary if at the same time you continue to think, explicitly or implicitly, in terms of non-genetic or anti-
genetic theories of human differences. Wrong theories exact their own penalties from those who believe them. Unfortunately, among many of my critics and among many students I repeatedly en
counter lines of argument which reveal disturbing thought-blocks to distinguishing individuals from statistical characteristics (usually the mean) of the groups with which they are historically or socially identified. I know professors, for example, who cannot bring themselves to discuss racial group differences when any persons from different racial groups are present, and the fact that I am
able to do so perhaps makes me appear insensitive in their eyes. I was once bothered by this too. I got over it as I studied more genetics and came more and more to appreciate its real implications.
Well written! I had the same idea, namely that what unites racists and ‘antiracists’ is their collectivism, their focus on the properties of groups instead of individuals.
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The important distinction between the individual and the
populationmust always be kept clearly in mind in any discussion
of racial differences in mental abilities or any behavioral charac
teristics. Whenever we select a person for some special educa
tional purpose, whether for special instruction in a grade-school
class for children with learning problems, or for a ‘gifted’ class
with an advanced curriculum, or for college attendance, or for
admission to graduate training or a professional school, we are
selecting an individual, and we are selecting him and dealing
with him as an individual for reasons of his individuality.
Similarly, when we employ someone, or promote someone in
his occupation, or give some special award or honor to someone
for his accomplishments, we are doing this to an individual.
The variables of social class, race, and national origin are
correlated so imperfectly with any of the valid criteria on which
the above decisions should depend, or, for that matter, with any
behavioral characteristic, that these background factors are irre
levant as a basis for dealing with individuals – as students, as
employees, as neighbors. Furthermore, since, as far as we know,
the full range of human talents is represented in all the major
races of man and in all socioeconomic levels, it is unjust to allow
the mere fact of an individual’s racial or social background to
affect the treatment accorded to him. All persons rightfully must
be regarded on the basis of their individual qualities and merits,
and all social, educational, and economic institutions must have
built into them the mechanisms for insuring and maximizing
the treatment of persons according to their individual behavior.
As written by a true racist, or something…
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A common misconception often arises in connection with standards
such as the following from an article by Dreeben (1969): ‘First,
genetic forces and environmental forces operate on two distinct
dimensions of time. Genetic effects are established when an ovum
is fertilized – at one moment in time; environmental effects extend
over time.’ This is often erroneously believed to mean that although
individuals may be endowed with different genotypes at the moment
of conception, all change and differentiation that take place
thereafter are the result of environmental forces. But this interpreta
tion overlooks the fact that the genes exert a continuing influence
on developmental processes. Many genetic effects are manifested
phenotypically only in later stages of development. As an obvious
example, patterns of baldness are genetically determined but do
not show up until middle age. Behavioral characteristics associated
with maturational processes, like mental development, variously
manifest genetic effects increasingly as the individual grows from
infant to adult. This is clearly seen in the gradually increasing
degree of correlation between the mental abilities of parents and
their biological children from infancy to late adolescence, which
occurs even when the children have never had contact with their
biological parents after infancy and have been reared by adoptive
or foster parents (e.g., Honzik, 1957). Under a normal range of
environmental conditions, an individual’s phenotypic IQ, from
infancy to maturity, converges toward its genotypic value.
So, it was known that heritability increases already in 1957 (or 1973). I thought it entered common knowledge in 1994 with McGue M, Bouchard TJ, Jr, Iacono WG, Lykken DT. 1993. Behavior genetics of cognitive ability: A life-span perspective.
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Probably the best evidence for the threshold hypothesis would
be the finding of significantly higher heritability in groups that
are above average in SES and environmental advantages than in
groups of low SES.13 No one has ever done this systematically.
The gifted children in Terman’s study came mostly from the
higher SES levels and unquestionably had considerably better
than average environmental advantages for intellectual develop
ment. The mean IQ of their siblings was 123 and the correlation
between the IQs of the gifted and their siblings, estimated from
the sibling regression, is 0-44, which, when corrected for attenu
ation, is close to the genetically predicted sibling correlations of
0*5 (with random mating) or 0-6 (with an assortative mating
coefficient of 0-5), and does not differ much from sibling correla
tions reported in the general literature. The gifted group as adults
were, on the average, of higher SES than their own parents. Thus
the offspring of the gifted probably enjoyed even greater environ
mental advantages. The narrow heritability of IQ in this group,
estimated from the midparent-midchild regression, is 0-85. This
is significantly higher than the best estimate of narrow’ heritability
(0*71) given by Jinks and Fulker (1970, p. 342) on the basis of
Burt’s data, which includes a wride range of SES in the English
population. It is also higher than the midparent-midchild correla
tion (0-69 + 0-03) found in a largely rural population sample in
Vermont in 1920, with environmental advantages presumably
much below those provided by the Terman gifted and their
spouses (Jones, 1928, p. 69). These heritability findings, then, are
consistent with the threshold hypothesis. But the total evidence
for the hypothesis must still be regarded as quite ambiguous. A
clear finding of an appreciable difference between h2 in the Negro
and white populations, however, would be consistent with the
hypothesis depicted in Figures 7*5 and 7*6. It could mean, in
effect, that the scale of environmental effects differs for the bulk
of the two populations and not simply that the two populations are
distributed about different means on the same additive (i.e., equal
interval) scale of environments. So now we must examine what
meager evidence exists on the estimation of h2 in Negro populations.
With all the talk about h2 x SES interactions, Jensen was there 40 years ago too. :p
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A statistical test could be applied to determine if the lesser
variance of the Negro IQ distribution is an artifact of the scale or
a ‘fact of nature’. One would determine, for both Negro and white
population samples, separately and together, whether there is any
significant correlation (both linear and non-linear relationships
should be sought) between family means (based on fraternal twins
or siblings7) and within-family variances. Since the total variance
( V T) of a subpopulation is comprised of the between-families
variance ( VB) plus within-families variance ( V w), we should
determine if two subpopulations which differ in VT differ in VB
or Vw or in both. If they differ only in VB, this suggests a ‘fact of
nature’ rather than an artifact of scale, and this interpretation is
strengthened if it is found that there is no significant correlation
between family means and within-family variances. A correlation
between within-family variances and family means suggests a
scale artifact which might be eliminated by a transformation of
the scale. These tests, however, would not be worthwhile unless
performed on quite large and representative samples of the sub
populations in question. If it is found that the most adequate scale
from all these standpoints shows marked differences in IQ variance
for Negroes and whites, and if the heritabilities of IQ were either
closely comparable in both populations, or smaller in the Negro
population, the genetic uniformity hypothesis would be very
untenable. It would indicate less genetic variance in the Negro
population. (The results could, of course, go in the opposite
direction, but the evidence based on the existing scales of mental
ability indicates less variance in the Negro samples.) Smaller
variance, with the consequence of a lesser proportion of the
subpopulation having higher values on the intellectual ability
scale, even if the mean were the same as in the general population,
would have important social consequences for the subpopulation
with the lower variance in terms of the proportion of its members
who are able to compete successfully in those endeavors in which
proficiency is most highly correlated with intellectual ability.
J. B. S. Haldane (1965, pp. xcii-xciii) noted that ‘For cultural
achievements high variability may be more important than a high
average. . . . When we say the ancient Greeks were great mathe
maticians we are in fact thinking of about 20 men. We know
nothing about the average Greeks in this respect.’
Why should two populations have different genetic variances?
Differences in gene frequencies and in the degree of assortative
mating are the chief causes.8 A difference in gene frequencies for
a given characteristic will cause different means and variances,
although if the number of gene loci is large, the difference in
variances will be relatively less than the difference in means. If
the genetic means in both populations are equal, the most likely
explanation of unequal genetic variances is differences in degree
of assortative mating. That is, the tendency for like to mate with
like with respect to a particular trait. It is known that there is a
high degree of assortative mating for intelligence in the white
population. (There are no published studies of assortative mating
for intelligence in non-white populations.) Assortative mating
increases the total genetic variance in the population; it also
increases the between-families variance relative to within-families
variance. Some 15 to 20 percent of the total variance in the white
population is attributable to assortative mating for intelligence.
Assortative mating per se has no effect on the mean, so if both the
genetic means andvariances differ between two populations, we
can suspect differences in gene frequencies as well as differences
in assortative mating.
This is interesting. Especially if the assortative mating might be increased due to internet dating. This could have big social implications. With IQ 100, SD 15, 2.3% are >130. But if we increased variance 10% cuz of stronger assortative mating, it wud be 3.45% above. The effects are huge when we get farther out. Ofc, on the other hand, it will also give me imbeciles. Im willing to take the trade. :p
As for the unequal variances between races with africans having less. This seems implausible in the light of the fact that africans have higher variance in all genes. So, it wud be odd if they had lower variance in the g-genes.
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Since variation in skin pigmentation, because of its social-
environmental consequences, is controlled in this research design,
any direct biochemical connection between degree of skin pig
mentation and intelligence must be either ruled out or, if such a
relationship is established, its consequences for the present design
must be assessed. The possibility of a biochemical connection
between skin pigmentation and intelligence is not totally unlikely
in view of the biochemical relation between melanins, which are
responsible for pigmentation, and some of the neural transmitter
substances in the brain. The skin and the cerebral cortex both arise
from the ectoderm in the development of the embryo and share
some of the same biochemical processes.
And it now makes sense that Jensen later wrote his comment in: Jensen, Arthur R. “Comments on correlations of IQ with skin color and geographic–demographic variables.” Intelligence 34.2 (2006): 128-131.
Templer and Arikawa emphasize that they regard skin color only as a climatic variable, a multigenerational reflection of climatic history. And this may well be theoretically adequate for their present purpose. But we should not let it mislead us to dismiss completely other possible, and presently causal, connections between skin color and IQ—an idea the authors, perhaps too cautiously, called “absurd.” This stance overlooks the probability of the genetic phenomenon of pleiotropy acting as at least a partial cause of the IQ × skin color correlation in present day populations. (Pleiotropy is the condition of a single gene having two or more phenotypically quite different effects. For example a single gene could affect both IQ and skin color.)
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But the whole notion of equating for SES, in the first place,
involves what has been called the ‘sociologist’s fallacy’. This fallacy
is seen in full bloom in one sociologist’s criticism of studies of
Negro-white IQ differences which equated the groups for SES
or other environmental factors: ‘Actually in most of the studies he
[Jensen, 1969a] reports on, the most important environmental
variable, the IQ of the parent, has not been equated at all’
(Stinchcombe, 1969, p. 516). Apart from the strictly environmental
effect of parental IQ ,1 it is obvious that, since IQ variance contains
a large genetic component, equating groups for parental IQ means
equating them for genetic factors more than for environmental
factors. The same is true, though to a lesser degree, when we
equate for SES. When typical Negro children are equated with
white children on some index of SES, one is comparing a majority
of the Negro population with some lower fraction of the white
population.2 The white comparison group, therefore, is not
genetically representative of the entire white population but is
genotypically (as well as environmentally) lower by some sub
stantial degree. Thus, if one supposes one is equating only for
environmental influences, equating on SES equates too much.The
method would be a proper control of environmental factors if all
children had been placed in their SES categories completely at
random, in the nature of a true experiment. But as it is, SES
classification is more a result than a cause of IQ variance.
quite possibly the first formulation of the sociologists fallacy.
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Data on two white populations show that fetal loss (Fx genera
tion) in matings of the parental generation ( P J increases
cumulatively by approximately 2-5 percent to 3 percent with
each additional country of birth in the great-grandparental
generation (Px). A dependent relation shows that increased fetal
loss is also related to greater distances between birthplaces of
mates within the Px generation. Conversely, low fetal loss is
encountered with a small number of countries in the background
and shorter distance between birthplaces. It is suggested that a
large number of countries of birth represents a larger number
of Mendelian gene pools and that with increased mixture of
these gene pools, fetal loss increases proportionately. An animal
model is cited in support of this contention, (p. 24)
Never heard of this effect! It somewhat offsets hybrid vigor.