The respectable position

Prior, I asked, “How did liberals establish the innate-equality dogma?” In part, they won the rhetorical agon through intellectual skullduggery. Through bombast, intimidation, scientific fraud, and specious arguments, they managed to establish their position as the dominant one. As a result, variants of the following discussion are commonplace:

Meneses. Science and the Myth of Biological Race. This side of heaven: race, ethnicity, and Christian faith. Ed. Priest 2007

Of course, we are well aware of what Scarr et al (1994) said (“it is exceedingly implausible that these differences are either entirely genetically based or entirely environmentally based”) and we are quite familiar with those ancestral studies. Moreover, we know that the size of the mean IQ gap increases with SES (Jensen, 1998), ruling out the deprivation explanation offered here.

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3 Responses to The respectable position

  1. JL says:

    What sort of study design do you think would be ideal for investigating the effect of white ancestry on African-American IQ? If a correlation between IQ and white ancestry in a representative sample of blacks was found when using contemporary ancestry estimation methods, it would pretty much clinch it, particularly if such variables as SES and skin color could also be controlled for.

    However, someone (perhaps it was you?) suggested a more powerful method: Study if white ancestry is associated with higher IQ within families by investigating if genetically whiter blacks are smarter than their genetically blacker siblings. This latter study design would probably require a huge sample size though, considering that the degree of white ancestry probably does not vary much between black siblings (unless one of their parents is white, which in turn would introduce further complications).

    • Chuck says:

      “What sort of study design do you think would be ideal for investigating the effect of white ancestry on African-American IQ?”

      Conducting the studies proposed by Jensen and Rushton would seem to be a good first step. If the genetic hypothesis was not falsified by findings thereof then more technical ones could be done to satisfy environmentalists.

      “The blood-group studies could be repeated with better sampling and methods of analysis, but probably never will be because a more powerful tool, DNA analysis, is now available for this purpose. In Section 8, we discussed the DNA methods that can ascertain degree of White ancestry in Black populations. Many other DNA markers identify Black–White differences regardless of how divergent the African ancestry. They have been recommended for evaluating admixture in genetic studies of disease (Collins-Schramm et al., 2002), and we recommend them for genetic studies of IQ.” (R&J, 2008. WANTED: MORE RACE REALISM,LESS MORALISTIC FALLACY)

      For a more sophisticated study, a variant of the following methodology could be used: Visscher, et al., 2005. Assumption-Free Estimation of Heritability from Genome-Wide Identity-by-Descent Sharing between Full Siblings.

      To note. Here was Reed’s comment on the Blood group studies and how new one could provide conclusive evidence for or against the genetic hypothesis:

      Reed, 1997. “The Genetic Hypothesis: It Was Not Tested but It Could Have Been

      I wish to comment on “The genetic hypothesis” (p. 95; for the Black-White difference in psychometric intelligence) in the Neisser et al. (February 1996) article, particularly the reference to two studies that used blood groups to estimate the degree of African ancestry in American Blacks in relation to their IQ scores (they found no relation). I have experience in such admixture estimation (e.g., Reed, 1969, 1973) and, as mentioned in the target article (Reed & Jensen, 1992, 1993), in studying biological factors in intelligence. My 1969 article gave the fast estimate of the proportion of White ancestry in American Blacks (Pw) with a standard error, 0.220 ± 0.0093 (using the Duffy blood group gene Fy~), and because it was based on large samples (more than 3,000 each of Blacks and Whites), it remains the best single estimate for non-Southern American Blacks. I contend that, because of their methodology, the two studies cited above—Loehlin, Vandenberg, and Osborne (1973) and Scarr, Pakstis, Katz, and Barker (1977)–did not adequately test the possible association of cognitive ability with Pw” Consequently, their negative results provide no evidence against the genetic hypothesis. I suggest a method that, had it been used with data of the second study and if the genetic hypothesis is true, probably would have confirmed the genetic hypothesis. The methodologies of these two studies share a basic misconception–that all blood (and serum) groups are useful in estimating P. This is plainly false, as I (Reed, 1969) showed. The P estimate in this population, w using the A and B genes of the ABO blood groups, was 0.200 ± 0.044; the above esti- mate with Fy’ provides (.044)V(.0093) 2 = 22 times more information than this ABO estimate. If I had estimated Pw using the MN blood groups (both the Loehlin and Scarr groups used them), the standard error would have been even much larger than for ABO and would have been worthless (see below). The racial informativeness of a gene used to estimate P (measured by the reciprocal of the variance of Pw) is a function of its relative frequencies in the two ancestral populations, African and White. A genetic Locus I is perfectly informative (an “ideal locus”; MacLean et al., 1974; Reed, 1973) when it has two codominant alleles (genes; say I and 12), with one allele being homozygous (i.e., PI ]) in all individuals of one ancestral population and the other allele being homozygnus (I 2I 2) in all individuals of the other ancestral population. Thus, when testing an American Black, every allele at this ideal locus derived from a White ancestor is recognized as such. The Gm serum group locus (testing for nine factors) closely approximates such an ideal locus, but with multiple alleles; three are White alleles and four are sub-Saharan African alleles (Roychoudhury & Nei, 1988). The Fy ~ allele alone, with a frequency of about .43 in Whites and about 01 in Africans, is not ideal. When present in. an American Black person, we are reason- ably sure that it came from a White ancestor, but other White matings could have contributed an Fy b allele (frequency about .57 in Whites and about .01 in Africans) and so would not be recognized (when testing only for Fy~). But contrast this with the situation using the MN blood groups: In both Whites and Africans, the M and N alleles each have frequencies close to .50. This locus provides essentially no information on the ancestry of American Blacks! The consequences of using all blood and serum groups available, without regard to their great differences in racial informativeness, as the Loehlin (Loehlin et al., 1973) and Scarr (Scarr et al., 1977) teams did, are severe.

      Loehlin Group

      Of the eight blood-group systems used, only Duffy (using Fy ~) has some utility in Loehlin et al.’s (1973) small sample of Black persons (42 twins). Assuming that they had the equivalent of 60 unrelated individuals (their sample contains monozygous and dizygous twins), one can calculate that a P for their sample would have a standard error of about .064 and, therefore, a large 95% confidence range (about .24). Other blood groups would have considerably larger standard errors and confidence intervals and, so, give little or no information. Yet Loehlin et al. performed rank-correlation between blood-group genes (arranged in descending order of the difference between frequencies in Whites and Blacks) and association with cognitive ability. The small sample size and non-informativeness of most blood groups mean that, except for Fy ~, they were usually dealing with noise, and their negative result was to be expected.

      Scarr Group

      Scarf et al. (1977) used Black twins from the Philadelphia area, and the number (181) was large enough, using both Fy ~ and Fy b of the Duffy group, to give a useful estimate ofP w. Gm serum groups were determined (testing for four factors) and could also have given a useful estimate of P,. Ten other groups were also tested. Scarr et al. attempted to obtain for each individual a measure of individual ancestry to associate with an estimate of cognitive ability, but this measure is deeply flawed. They used an “odds coefficient,” log[AtAzA3…/BtBzB3…], in which A was one ancestral population (e.g., African) and B was the other ancestral population, and the subscripts were the loci of the different blood and serum groups. A t was the frequency of an individual’s phenotype (group) at Locus 1 in Population A, Bt was the frequency of his or her phenotype in Population B at that locus, and so on. This coefficient was intended to give a rank ordering of individuals according to their degree of ancestry from one population, say A. Now consider the effect of one uninformative Locus X, for example the MN blood groups, on this coefficient. Because A/B x varies essentially at random, and Ax/B x multiplies all the other ratios, the odds coefficient acquires considerable randomness. Add the random effects of other only slightly informative loci, such as the ABO, and the coefficient will necessarily lose much of its potential for ancestry identification. Scarr et al.’s (1977) procedure for dealing with zero phenotype frequencies—replacement by .0001- further distorts the coefficient, particularly for the informative Duffy and Gm groups. This is because, with the usual sample sizes, absence of a phenotype at Locus Y does not mean that its true frequency is not of the order of.01 -.001. This procedure would often bias log(A/By) by about ± 1 to ±
      2. With the above problems, it is not surprising that the correlations between the odds coefficient and the measures of cognitive skills were nonsignificant; it would be surprising if they were otherwise. (Incidentally, although Scarf et al. thanked me and others for “consultation on the design and analysis of the study” [p. 86], I did not have any part in the design or analysis.)

      For a More Powerful Test of the Genetic Hypothesis MacLean et al. (1974) studied 372 adult Blacks in the Rochester, New York, area for possible correlation of diastolic blood pres- sure (DBP) with proportion of African ancestry (Pa = 1 -Pw). They used 10 blood and serum groups, including Duff), and Gm, and corrected the DBP readings for gender, age, and obesity. Although they recognized that accurate individual estimates of P were not a possible (Reed, 1973), such estimates were made anyway, and the corrected DBP values were regressed on them. A very significant (p < .001) positive linear regression was found: Increasing DBP accompanied increasing P. Evidently, the overall information on P was more than adequate, although individually inaccurate. But the point of this account is that DBP is a surprisingly good surrogate for IQ score: Both are quantitative traits, are moderately heritable (h: for DBP is estimated to be 0.37 by Cavalli-Sforza & Bodmer, 1971), and have similar relative changes going from 100% African ancestry to 100% White ancestry. Furthermore, the value (3.4) for their regression is still signifi-cant at the .001 level for 120 degrees of freedom. Therefore, ~fthe genetic hypothesis was true, I predict that the MacLean et al. methodology applied to the Scarr et al. (1977) data would show this.

      Scarr et al. (1977) knew of the MacLean et al. (1974) study (they referred to it), but they chose to use their own method. After expending so much effort in collecting their data, it is a pity not to analyze them properly.

      • JL says:

        Thanks. I wonder if the data from those 1970s studies are still available. They could be reanalyzed using Reed’s method.

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