Genetic amplification versus G-E correlations

One curious aspect of IQ is that the heritability of it increases with age [3]. Given the nature of the increase, there are three plausible explanations. The increasing heritability is either a function of: 1) active GE correlations (rGE), 2) genetic amplification, or 3) novel gene expression through the developmental period. As it is, the current evidence suggests that the third possibility does not play a prominent role. Longitudinal studies show that genes contribute to the continuity of IQ across the development period [6,7]. Figure 3.4, graphically depicts the possible relations between genes and IQ continuity; model C corresponds to the data. Basically, the genes that lead IQ differences in infancy are the same genes that lead to differences in adulthood. Were novel genes to come into play, this would not be the case.

Environmentalists, naturally, have seized on the active rGE explanation. Accordingly, genetic differences in intelligence result from cognitive shaping environments, environments which individuals select on the basis of their genetically predisposed predilections [5]. By this model, the heritability of intelligence increases with age because with age individuals become freer to follow their dispositions and select their environments. Quasi-environmentalists are not the only ones that find this model appealing. For example, in the discussion section of their ground breaking study of 11,000 twin pairs across four counties, Haworth et al (2009) state [14]:

Why, despite life’s ‘slings and arrows of outrageous fortune’, do genetically driven differences increasingly account for differences in general cognitive ability during the school years? It is possible that heritability increases as more genes come into play as the brain undergoes its major transitions from infancy to childhood and again during adolescence. However, longitudinal genetic research indicates that genes largely contribute to continuity rather than change in g during the school years. We suggest that the developmental increase in the heritability of g lies with genotype–environment correlation: as children grow up, they increasingly select, modify and even create their own experiences in part on the basis of their genetic propensities. This leads to an active view of experiences relevant to cognitive development, including educational experiences, in which children make their own environments that not only reflect but also accentuate their genetic differences.

Oddly, they fail to mention the well known third alternative.

The reason that (the now gene-)environmentalists have embraced this model is fairly obvious: causally, it’s an environmental account of IQ differences; it just has a genetic veneer. For behavior geneticists, it offers more politically palatable interpretation to their findings.

Initially, the rGE explanation seems reasonable; when it comes to individuals differences, it doesn’t seem outlandish to suppose that naturally born intellectuals might increase their verbal IQ through bookish behavior. On the subpopulation level, likewise, it’s doesn’t seem implausible that a propensity for studiousness might lead to cognitive enhancement. Yet, there are a few bumps which preclude a simple rGE model. For one, it’s not merely this or that measure of intelligence that increases but, rather, the central factor and its numerous correlates [6]. In effect, rGE theorists are forced to maintain that g is created from the outside in. (See theoretical diagram below). Since g is structurally the same across individuals, cultures, sexes, and subpopulations, not only would the patterns of one’s environment have to construct g, the patterns of everyone’s environment would have to construct the same g.

Additionally, IQ g has numerous endophenotypic correlates, such as the volume of white and grey matter, the mass of the prefrontal lobe, and total brain size [1, 11, 13] and the overlap between IQ (g) and many of these endophenotypes is entirely due to genetic influences [1, 13]. To explain this genetic covariation, rGE theorists must maintain that genetics sets the parameters for environmental selection, which leads to the development of different cognitive phenotypes, which, in turn, molds the endophenotypic differences, thus creating the three way correlation. Since the Phenotypic/endophenotypic correlations have been found to be a function of differential rates of change during the development process [9] (see figure 2), rGE theorists must maintain that this environmentally induced endophenotypic molding occurs primarily during the developmental process and starts early on. If we kept in mind what we said above, that the genes that lead to slight genetic IQ differences in infancy are the same genes that lead to large genetic based differences in adulthood, and note that the heritability of many dispositions also increases with age [4], we can readily identify the problem with this conception. Somehow, dispositional differences, which are under heavy environmental influence early on, must set the phenotypic/endophenotypic molding (environmental) parameters in a way that happens to correspond to the genetic driven phenotype that the individual will later express.

None of the above logically precludes a rGE explanation; the explanation would just have to be exceedingly complex. That said, there is a growing body of evidence against the active rGE model. According to it, as environmentally conditioned phenotypic differences cause endophenotypic differences, environments will correlate with endophenotyes [13]. This was found to not be the case by Posthuma et al. (2003), van Leeuwen et al (2009), and Betjeman (2009), disconfirming the model.

In addition to the above, Shikishima et al. (2009) found correlational evidence of a causal genetic g. This effectively rules out the possibility of a purely active rGE created g:

Accordingly, our findings could furnish an argument against the typical criticisms offered by those who are opposed to the concept of g; in other words, g is an “artifact” (Simon, 1969) of the statistical methods that psychologists apply to the data. Gould (1981) argued that g, as a factor extracted from the factor analysis, is neither a “thing with physical reality” nor a “causal entity”, but is a “mathematical abstraction”, maintaining that “we cannot reify g as a ‘thing’ unless we have convincing, independent information beyond the fact of correlation itself.” Although the present study also draws information from correlations, we were able to depict the structure of human intelligence beyond the fact of phenotypic and genetic correlations with an explicit comparison between the independent pathway and the common pathway model; and as a “causal entity”, as a highly genetically driven entity…

…Several recent reports have shown that g is also correlated with a variety of neural mechanisms, such as glucose metabolism (Haier, 2003), cortical development (Shaw et al., 2006), and biochemical activity (Jung et al., 2005), along with the identification of promising endophenotypes for intelligence such as working memory and processing speed (van Leeuwen, van den Berg, Hoekstra, & Boomsma, 2007). These studies allow us to assume that it is now reasonable to consider g to be a physiological or biological, genetic entity.

The alternative to the rGE model is the readily falsifiable genetic amplification model. Plomin (1987) summarizes it thusly:

Genes that affect IQ make only a small contribution to phenotypic variance at first, but their effects are amplified throughout development. Suppose, for example, that genetic differences among infants are responsible for differences among them in the formation of dendritic spines during the first few years of life and that the complexity of dendritic spines is related to information processing capabilities. At first, these structural differences do not have a chance to cause function differences because so little information has been processed at this point. Gradually, the functional differences are amplified as more and more information is processed by children. If we were to measure differences in categorizing ability early in childhood, the genetic differences among children due to the complexity of dendritic spines would contribute a negligible amount of variance to observed variability among children in categorization ability. The differences snowball as development proceeds, so that a study of the children when they are older will show more genetic variance. Yet the genetic correlation between the two ages is near unity because the genetic portion of observed variability at both ages originates with the same set of genes whose effect become amplified during development.

The model predicts that the genetic correlations from childhood to adulthood, as inferred by parental-offspring correlations and seen in longitude twin data, will continue to be high even as heritability increases [7]. As mentioned above, this has turned out to be the case. The model also predicts that genetic differences which cause small differences early on will cause larger differences latter on. Boomsma (1998) found confirmation of this: differences in intelligence between 5 and 7 year olds were due to the same genes; while at 5 those genetic differences resulted in minor IQ differences, at 7 they resulted in a much larger differences. Other studies have found that genetic amplification explains increased heritability in the samples studied [16].

In light of the evidence to date, a substantial gene-environmental explanation for the increasing heritability of general intelligence and with it individual differences is improbable; alternatively, a genetic amplification model is probable. When it comes to that oft discussed subpopulation difference, from a non-hereditarian standpoint, the improbability of the rGE explanation leaves one with an equally improbable environmental alternative.

References

[1] Betjemann, et al., 2009. Genetic Covariation Between Brain Volumes and IQ
[2] Boomsma, et al., 1998. Genetic influences on childhood IQ in 5- and 7-year-old Dutch twins
[3] Bouchard, 2009. Genetic influence on human intelligence (Spearman’s g): How much?
[4] Gardner, 2007. A meta-analysis of age-related changes in heritability of behavioral phenotypes over adolescence and young adulthood.
[5] Flynn, 2007. What is intelligence? Beyond the Flynn effect.
[6] Haworth, 2009. The heritability of general cognitive ability increases linearly from childhood to young adulthood
[7] Plomin, 1987. Development, genetics, and psychology.
[8] Posthuma, et al., 2003. Brain volumes and the WAIS-III dimensions of verbal comprehension, working memory, perceptual organization, and processing speed.
[9] Shaw et al., 2006. Intellectual ability and cortical development in children and adolescent
[10] Shikishima, et al., 2009. Is g an entity? A Japanese twin study using syllogisms and intelligence tests.
[11] Smit et al., 2010. Endophenotypes in a Dynamically Connected Brain.
[12] van Leeuwen, 2008. A twin-family study of general IQ
[13] van Leeuwen et al., 2009. A genetic analysis of brain volumes and IQ in children.
[14] Jensen, 1973, Educatability and group differences.
[15] Haworth, et al., 2009. The heritability of general cognitive ability increases linearly from childhood to young adulthood
[16] Soelen, 2011. Heritability of Verbal and Performance Intelligence in a Pediatric Longitudinal Sample

rénlèi běnxìng

Hans aren’t particularly tribal – it’s just that Western are unnaturally, and religiously so, universalistic.

RISE OF THE HANS

With China’s new prominence in global affairs, the Han race, which constitutes 90 percent of the Chinese population, is suddenly the most dominant cohesive ethnic group in the world — and it is seeking to remain that way through strategic alliances, aggressive trade policy, and attacks on racial minorities within the country’s boundaries. The less tribally cohesive, more fragmented West is, meanwhile, losing out….

…This represents a major shift in the identity of the Chinese tribe, a combination of political and economic power with a very homogeneous worldview. The best way to explain China’s economic and foreign policy is most accurately seen as a tribal expression of what Friedrich Nietzsche called a “will to power.” Essentially, the Han has become a tribal superpower that treats other groups — from China’s non-Han minority to much of the rest of the world — as a vast semi-colonial periphery. And with its growing economic and military might, Han China may soon be able to impose its will on some of these “lesser” cultures, should it desire..

homo natura

HOMO NATURA; to bring it about that man shall henceforth stand before man as he now, hardened by the discipline of science, stands before the OTHER forms of nature, with fearless Oedipus-eyes, and stopped Ulysses-ears, deaf to the enticements of old metaphysical bird-catchers, who have piped to him far too long: “Thou art more! thou art higher! thou hast a different origin!” — FN, beyond good and evil, 7, 233.

Religious, ethnic, and racial favoritism is natural, scientists say.

From: Bates and Lewis, 2010. Genetic Evidence for Multiple Biological Mechanisms Underlying In-Group Favoritism:

Abstract: In-group favoritism is ubiquitous and associated with intergroup conflict, yet is little understood from a biological perspective. A fundamental question regarding the structure of favoritism is whether it is inflexibly directed toward distinct, “essentialist” categories, such as ethnicity and race, or is deployed in a context-sensitive manner. In this article, we report the first study (to our knowledge) of the genetic and environmental structure of in-group favoritism in the religious, ethnic, and racial domains. We contrasted a model of favoritism based on a single domain-general central affiliation mechanism (CAM) with a model in which each domain was influencedby specific mechanisms. In a series of multivariate analyses, utilizing a large, representative sample of twins, models containing only the CAM or essentialist domains fit the data poorly. The best-fitting model revealed that a biological mechanism facilitates affiliation with arbitrary groups and exists alongside essentialist systems that evolved to process salient cues, such as shared beliefs and ancestry.

The Other Tail of the Bell Curve

La Griffe has nice post on the Black-White familial mental retardation gap. As Steve Sailer notes, the MR gap is what led Jensen to begin investigating the race-IQ connection. Jensen makes a point of this gap in his infamous Harvard Educational Review paper:

Socioeconomic Level and Incidence of Mental Retardation. Since in no category of socioeconomic status (SES) are a majority of children found to be retarded in the technical sense of having an IQ below 75, it would be hard to claim that the degree of environmental deprivation typically associated with lower-class status could be responsible for this degree of mental retardation. An IQ less than 75 reflects more than a lack of cultural amenities. Heber (1968) has estimated on the basis of existing evidence that IQs below 75 have a much hither incidence among Negro than among white children at every level of socioeconomic status, as shown in Table 3. In the two highest SES categories the estimated proportions of Negro and white children with IQs below 75, are in the ratio of 13.6 to 1. If environmental factors were mainly responsible for producing such differences, one should expect a lesser Negro-white discrepancy at the upper SES levels. Other lines of evidence also show this not to be the case. A genetic hypothesis, on the other hand, would predict this effect, since the higher SES Negro offspring would be regressing to a lower population mean than their white counterparts in SES, and consequently a larger proportion of the lower tail of the distribution of genotypes for Negroes would fall below the value that generally results in phenotypic IQs below 75

Anyways, Statsquatch referred me to a paper [1] which provides ethnoracial rates of Mild MR for the state of Florida:

(The 8.8% to 39.6% is approximately .66 SD)

With regards to the paper, some of the authors’ comments are interesting:

Addressing all of these potential pathways related to maternal education may still not be enough to eliminate the large racial disparities found in mental retardation and among mild mental retardation placements in particular. Compared to White children, the prevalence of mild and moderate/severe mental retardation among Black children was 4.5 and 2.1 times higher. These racial disparities have persisted, even after controlling for sociodemographic factors (Yeargin-Allsopp et al., 1995). To fully address this problem, we may need to consider intergenerational risk factors, which involve the mother’s own developmental history. Maternal intergenerational factors clearly play a role in low birthweight (Emanuel, 1986; Emanuel, Filakti, Alberman, & Evans,1992), and it is likely that other aspects of development, including cognitive development, also have an intergenerational component (Chapman & Scott, 2001). Intergenerational factors may explain, in part, why race differences in mental retardation placements and risk factors associated with mental retardation, such as low birthweight, have persisted, even after controlling for maternal factors, such as age, education, SES, and prenatal care (G. Alexander, Kogan, Himes, Mor, & Goldenberg, 1999; Din-Dzietham & Hertz-Picciotto, 1998; Foster, Wu, Bracken, Semenya, & Thomas, 2000; Migone, Emanuel, Mueller, Daling, & Little, 1991; Starfield et al., 1991)

I have no doubt that a significant portion of the intergenerational factors are environmental or are due to g x e interactions. I did my time assisting with inner city Special Ed classes and have had the opportunity to meet quite of few of those parents; needless to say, some of the proclivities of the parents weren’t a recipe for normal intrauterine development. I also have no doubt that a significant portion is genetic but not directly related to the genetics of IQ. That is, a large portion of severe and moderate MR gap is due to medical genetic differences [3]. That said, given that a standard distribution of intelligence would necessitate that some individuals fall in the MR category based on intellectual differences alone, and given that there is a B-W g gap, it’s hard to see how some of the MR gap could not be a function of IQ differences. And, of course, to the extent that it is, we are confronted by Jensen’s point.

References

[1] Jensen, 1969. How much can we boost IQ and scholastic achievement?

[2] Chapman, et al., 2008. Public Health Approach to the Study of Mental Retardation

[3] Plomin and Spinath, 2004. Intelligence: Genetics, Genes, and Genomics

A second issue concerns the relationship between the normal and abnormal. For example, to what extent is mild mental retardation (MMR) genetically distinct from the rest of the distribution of intelligence? Surprisingly, no twin or adoption studies of MMR have been reported until recently (see the next paragraph). More than 200 rare single-gene disorders include mental retardation, often severe retardation, as a symptom (Zechner et al., 2001), and many chromosomal causes of mental retardation are also known (Plomin, DeFries, et al., 2001), including microdeletions of bits of chromosomes (Baker et al., 2002; Knight et al., 1999). In general, many of the single-gene mutations tend to be spontaneous in the affected individual as are most of the chromosomal anomalies. That is, these DNA causes of severe mental retardation are not usually inherited. Although no twin studies of severe mental retardation have been reported, an interesting sibling study shows no familial resemblance. In a study of over 17,000 children, 0.5% were moderately to severely retarded (Nichols, 1984). As shown in Figure 4 (dotted line), siblings of these retarded children were not retarded. The siblings’ average IQ was 103, with a range of 85 to 125. In other words, moderate to severe mental retardation showed no familial resemblance, a finding implying that mental retardation is not heritable. In contrast, siblings of mildly retarded children (1.2% of the sample) tend to have lower than average IQ scores (see Figure 4, solid line). The average IQ for these siblings of mildly retarded children was only 85. Similar findings—that MMR is familial but moderate and severe retardation are not familial—also emerged from the largest family study of MMR, which considered 80,000 relatives of 289 mentally retarded individuals (Reed & Reed, 1965).

Blood libeling the right

Krugman spearheads a new effort to blood libel the right…

It’s important to be clear here about the nature of our sickness. It’s not a general lack of “civility,” the favorite term of pundits who want to wish away fundamental policy disagreements. … The point is that there’s room in a democracy for people who ridicule and denounce those who disagree with them; there isn’t any place for eliminationist rhetoric, for suggestions that those on the other side of a debate must be removed from that debate by whatever means necessary. And it’s the saturation of our political discourse — and especially our airwaves — with eliminationist rhetoric that lies behind the rising tide of violence. … Of course, the likes of Mr. Beck and Mr. O’Reilly are responding to popular demand….

Where’s that toxic rhetoric coming from? Let’s not make a false pretense of balance: it’s coming, overwhelmingly, from the right. It’s hard to imagine a Democratic member of Congress urging constituents to be “armed and dangerous” without being ostracized; but Representative Michele Bachmann, who did just that, is a rising star in the G.O.P.

…and embraces an eliminationist strategy in the name of eliminating eliminationist rhetoric.

Well, what did you expect?

First They came for the Race realists — Chuck

First they came for the race realists on the ground that the realists were haters, and I didn’t speak out because I wasn’t a race realist.

Then they came for the paleoconservatives on the grounds that the paleos were haters and I didn’t speak out because I wasn’t a paleoconservative.

Then they came for the …

Occam’s butter knife

Let’s play a game. The game is called “radical environmentalism.” The goal is to create the most parsimonious environmental explanation for a given set of results. Ready?

Create the most parsimonious environmental explanation for the following set of data [4]:

Given the following:

1. The individuals identified as White (Europeans) and African Americans were done so on the basis of corresponding self and interviewer identification. The 116 individuals identified as mixed race individuals were done so on the basis of corresponding self identification and parental self-identification (102) or parental self identification (14). Mean age = 16.

2. The individuals identified as mixed race were judge by the interviewer as looking African-American.

3. The mean differences were uncorrelated or weakly correlated:

4. The SES adjusted Parental IQ means were equivalent to 103.2, 100.7, and 93.3.

5. IQ, sexual proclivity, and birth weight are moderately to highly heritable within populations [1,2].

My attempt below.

References

[1] Cherkas, et al., 2004. Genetic Influences on Female Infidelity and Number of Sexual Partners in Humans: A Linkage and Association Study of the Role of the Vasopressin Receptor Gene (AVPR1A). [Heritability of .4 for sexual proclivity in 1st word western nations]

[2] Magnusa, et al., 2001. Paternal contribution to birth weight. [heritability of .25 for birth weight in 1st world western nations.]

[3] Nettle, D. (2010). Dying young and living fast: Variation in life history across English neighbourhoods. Behavioral Ecology

[4] Rowe, 2002. IQ, birth weight, and number of sexual partners in White, African American, and mixed race adolescents.

………..

Here’s what I came up with:

a) The three way trait difference between African-American/mixed and white kids results from the former picking up patters of behaviors from African-American culture (i.e. 3 patterns of cultural expectations). This explains why the differences are present in the tested population even though SES is controlled for. b) The African Americans cultural patterns result from a life history program that kicks in when individuals live in low SES conditions [ 3]. This explains why the differences exist and are uncorrelated in the tested population (i.e. there are three non-causally related cultural tendencies that result from a SES induced life history program). c) The differences between mixed race individuals and African-American individuals is due to a white parental cultural influence — which again results a different life history program. This explains the difference between African-Americans and Mixed-Americans even though the mixed race differences appeared African-American. d) While the parental-child IQ correlation is explained genetically, the between Black-White racial difference is explained by a) and a number (say 3) of additional cultural+ factors (such as stereotype threat (.2 SD), low motivation (.4 SD), and ?). This explains why cultural differences can cumulatively create an equivalent of 1.3 SD between group differences. (The SD of difference divided by the square root of the between-family environment and IQ correlation at age 16 (~.2) gives the amount of equivalent within group environmental difference, precluding g x e interactions and x- factors, needed to account for the difference; (.6/.45) = 1.3 SD. )

That’s an 8 factor model. See if you can beat that!

Immigrant Selection and Regression

So half of the mystery has been solved.

West African immigrants do better than indigenous US African-Americans because of immigration selection. In her exhaustive analysis, Suzanne Model shows that the relative West African success can be explained in total by selection and, moreover, that West Africans do no better than internally immigrating African Americans. From a condensed version of the book [1]:

To review, West Indian immigrants have long fared better economically than African Americans. This generalization holds even when immigrants and natives are assigned the same age, education, location, etc. Experts have proposed four distinct explanations for this state of affairs: West Indians are positively selected immigrants, Caribbean slavery taught West Indians valuable skills, socialization in an all-black society is psychologically beneficial for blacks, and white Americans discriminate less against West Indians than African Americans. When the four explanations are tested empirically, only positive selection receives support. This is not to say that growing up in an all-black society might not provide psychological benefits or that whites might not respond positively to blacks with a Caribbean accent. But even if these relationships hold (which has yet to be demonstrated), there is no empirical evidence that they enhance West Indian economic attainment. Rather, West Indian success can be attributed entirely to the greater talent and ambition of those who choose to move. Similarly, the subset of African Americans who are voluntary internal migrants are better off than their less venturesome counterparts. Once this point is clear, it is easy to see why West Indian success offers no lessons for African American improvement.

So, self selected African immigrants have a relatively higher IQ and take advantage of racial quotas. No surprises there. This leaves the other half of the mystery. Why do the offspring of West Indian Black immigrants — unlike those of some other immigrants — regress socioeconomically [2]…

…and perhaps otherwise?

[1] Model, 2008. The Secret of West Indian Success

[2] Sakamoto, et al., 2010. Does an Immigrant Background Ameliorate Racial Disadvantage? The Socioeconomic Attainments of Second‐Generation African Americans.

Pragmatic PC

I just came across this lovely piece by Eric Turkheimer (2007):

If I may address my fellow Jews for a moment, consider this. How would you feel about a line of research into the question of whether Jews have a genetic tendency to be more concerned with money than other groups? Nothing anti-semitic, mind you, just a rational investigation of the scientific evidence. It wouldn’t be difficult to measure interest in money and materialism, and it wouldn’t surprise me if as an empirical matter Jews scored a little higher on the resulting test than other groups. As a behavioral geneticist I can assure you without reservation that the trait would be heritable, and, if anyone bothered to take the time to find out, specific genes would have small associations with it. Of course, this research program has already been carried out, at least to the extent the relevant technology was available in 1939.

Which reminded me of something Steve Sailer once said:

Unpleasant Fact #2: Far more subtle, although the Great and the Good ceaselessly sermonize us that racial conflicts are caused by the majority feeling superior to the minority, a quick global survey suggests the opposite. The doltish masses have frequently risen up against astute “middle-man minorities” that control trade.

Thus the truly unmentionable Unpleasant Fact today is not that blacks have mean IQs well below the white average. It’s that other groups have mean IQs well above it.

This censorship may be prudent. But it is crippling American intellectual discourse.

And, of course, that NYT editorial by Micheal Chabon (2010):

For we Jews are not, it turns out, entirely comfortable living with the consequences of this myth, as becomes clear from the squirming and throat-clearing that take place among us whenever some non-Jew pipes up with his own observations about how clever and smart we are in our yiddishe kops. These include people like the political scientist Charles Murray, author of an influential essay titled “Jewish Genius,” or Kevin B. MacDonald, a psychology professor at California State University at Long Beach who argues that Jews essentially undertook a centuries-long program of self-breeding, selecting for traits of intelligence, guile and skill at calculation, as a kind of evolutionary adaptation to the buffetings of history and exile.

Such claims, in mouths of gentiles, are a disturbing echo of the charges of the pogrom-stokers, the genocidalists, the Father Coughlins, who come to sharpen their knives against the same grindstone of generalization on which we Jews have long polished the magnifying lenses of our self-regard. The man who praises you for your history of accomplishment may someday seek therein the grounds for your destruction.

The sociologist’s first and second fallacies

The sociologist’s fallacy is the tendency to interpret a correlation between a social variable and a phenotype as causal, without considering that genetics could mediate the relationship. In Making sense of heritability, Neven Sesardic gives several good examples of this. A report from the Nuffielf Council on Bioethics (2002), for example, engages in the fallacy when it notes the following:

While it is often claimed that on average, black individuals score slightly lower on IQ tests than white individuals, who in turn score lower score lower than people from East Asia, there are also studies which show that, if black individuals and white individuals are closely matched on socioeconomic status, the differences in IQ are substantially reduced…The authors [of a study cited in the text] conclude that “socioeconomic differences are largely responsible for the usually reported differences in intellectual performance.

Apparently, it never crossed the authors’ mind that genetics could mediate the relation between SES and IQ. As it is, we might call this the sociologist’s first fallacy, since this fallacy has a corollary, which we can call the sociologist’s second fallacy. The sociologist’s second fallacy is the tendency to attribute any undesired “gap” found between a designated minority group and Whites after controlling for all know social variables to the mysterious effects of racism, without considering alternative possibilities. Here is a nice example of that:

Racism and Birth Weight

A large number of epidemiological studies have attempted to account for this disparity in terms of maternal age, education, lifestyle, and or socio-economical position. However, the results make it clear that these variables account for only a small proportion of the difference…Researchers involved with these studies argue that their findings “suggest that growing up as a woman of color in the US is somehow toxic to pregnancy, and imply a social etiology for racial/ethnic disparities in prematurity that is not solely explained by economics or education.

Apparently, it never crossed the author’s mind that genetics could contribute to the gap. After all, West SubSaharan Africans have a higher frequency than Europeans (80% to 30%) of the low-birth-weight-risk allele C825T on the GNB3 gene — not that those social constructs called ‘whites’ and ‘blacks’ are in any way related to Europeans and West Africans. When it comes to patterns of low-birth-weight one can see the following illuminating trend:

From: Rowe (2005)

This trend is just what hereditarians would predict. Magnusa, et al. (2001) estimates a .25 heritability for birth-weight with a .26 mother-child correlation and a .12 father-child correlation. Unsurprisingly, in the above sample the mixed children’s birth-weight falls between the population means and mixed children with White mothers have a higher mean birth-weight than mixed children with White fathers.

References

Magnusa, et al., 2001. Paternal contribution to birth weight

Rowe, 2005. Under the Skin : On the Impartial Treatment of Genetic and Environmental Hypotheses of Racial Differences