Mental retardation or mental disability, is a generalized disorder characterized by impaired cognitive functioning. The affected individuals with mental retardation have an IQ below 70 (between 50 and 70 = mild mental retardation; Below 50 = moderate mental retardation).
The races differ in IQ (70 to Sub-Saharan Africans, 85 African Americans, 100 whites) but also in the prevalence of mental retardation, after correcting for socio-economic status. This is what Yeargin-Allsopp et al. (1995, pp. 326-327) have found : the prevalence of mild mental retardation among blacks was nearly twice (OR=1.7) as large as that among whites, controlling for SES and birthweight.
Their Table 3 shows that the Odd Ratio (adjusted for maternal age, sex, birth order, maternal education, and economic status) among children less than 6 years old is only 1.2, suggesting little difference between blacks and whites before the age of 6. Among the 6-7 and 8-10 year-old children, the difference is large (1.7 and 2.5, respectively). The authors speculate the reason could be that :
Black children may be at increased risk for mental retardation because they may be more likely than White children to be exposed to the cumulative effects of deleterious postnatal factors, such as ambient lead or anemia. Further, some maternal medical or biological conditions that are more common among Blacks may alter the in utero environment in such a way that the child’s risk of mild mental retardation is increased (these conditions include anemia, elevated lead levels, hypertension, diabetes, chronic renal disease due to hypertension or diabetes, and sickle cell anemia).
This does not explain, however, why the Black-White retardation difference increases when SES levels improve for Blacks. Their Table 4 shows that when the SES level increases, the OR increases as well. And it doubled, from 1.6 to 2.9.
This finding is fairly consistent with the conclusion that the IQ difference between blacks and whites increases with the level of SES (Jensen, 1973, p. 241; Herrnstein & Murray, 1994, pp. 287-288; Jensen, 1998, pp. 358, 469; Gottfredson, 2003, Table 2; See this blog article as well). However, individuals with low SES levels are more likely to be exposed to such environmental hazards. High-SES people live in a stable environment while low-SES people live in a chaotic environment. Therefore, if the environmental theory is correct, the IQ differences between blacks and whites should have decreased at higher levels of SES.
In addition, the regression to the mean (Rushton & Jensen, 2005, p. 263; 2010, p. 28; Murray, 1999, pp. 11-19) indicates that blacks and whites, matched for IQ level, have siblings whose IQ regressed halfway to their respective population means, regardless of IQ level. As Rushton & Jensen (2005, p. 263) explain :
Regression toward the mean is seen, on average, when individuals with high IQ scores mate and their children show lower scores than their parents. This is because the parents pass on some, but not all, of their genes to their offspring. The converse happens for low IQ parents; they have children with somewhat higher IQs. Although parents pass on a random half of their genes to their offspring, they cannot pass on the particular combinations of genes that cause their own exceptionality. This is analogous to rolling a pair of dice and having them come up two 6’s or two 1’s. The odds are that on the next roll, you will get some value that is not quite as high (or as low). Physical and psychological traits involving dominant and recessive genes show some regression effect. Genetic theory predicts the magnitude of the regression effect to be smaller the closer the degree of kinship between the individuals being compared (e.g., identical twin > full-sibling or parent–child > half-sibling). Culture-only theory makes no systematic or quantitative predictions.
Thus, with the effect of the regression, individuals at the lower half of the IQ distribution have siblings who have ‘gained’ some IQ points while individuals at the upper half of the IQ distribution have siblings who have ‘lost’ some IQ points. The regression lines showed no deviation from linearity (Murray, 1999, pp. 11-19) for siblings of blacks and whites over the full range of IQs, from 50 to 150 (Jensen, 1998, p. 471). If a cumulative effect is depressing black IQs, this will show up in a deviation from normality. The fact actually is that, the more an individual’s IQ is above (below) the average of his own population, the more the siblings will lose (gain) IQ points. This contradicts the theory of cumulative effects which posits that the lower social class will experience cumulative deficits regardless of their race. Although this looks strange, the IQ regression toward the mean does not appear to be a statistical artifact, having some genetic effect (Hu, April.19.2013; Fuerst, April.24.2013) since the regression effect is larger in the non-g dimension, as hypothesized by the hereditarians.
Returning to the cumulative effects theory, Jensen (1973, pp. 97-102) nicely countered it. The environment is not a major cause of IQ differences between white and black americans (neither is the best explanation for the B-W difference in mental retardation). It is noteworthy that cultural and biological environmental factors that have been studied with the method of correlated vectors are inversely related with g-loadings, while the performance on the Wechsler’s IQ test is poorer on the most g-loaded subtests (Spitz, 1988). The cognitive deficit of mentally retarded people is stronger on g, while the environmental influences are poorer on g.
Besides, some studies (Nichols, 1984; Drews et al., 1995) reported by Jensen (1998, p. 405) are clearly consistent with the hereditarian position :
21. Nichols (1984), reporting on the incidence of severe mental retardation (IQ < 50) in the white (N = 17,432) and black (N = 19,419) samples of the Collaborative Perinatal Project, states that at seven years of age 0.5 percent of the white sample and 0.7 percent of the black sample were diagnosed as severely retarded. However, 72 percent of the severely retarded whites showed central nervous system pathology (e.g., Down’s syndrome, posttraumatic deficit, Central Nervous System malformations, cerebral palsy, epilepsy, and sensory deficits), as compared with 54 percent of the blacks.
A recent sociodemographic study by Drews et al. (1995) of ten-year-old mentally retarded children in Metropolitan Atlanta, Georgia, reported (Table 3) that among the mildly retarded (IQ fifty to seventy) without other neurological signs the percentages of blacks and whites were 73.6 and 26.4, respectively. Among the mildly retarded with other neurological conditions, the percentages were blacks = 54.4 and whites = 45.6. For the severely retarded (IQ < 50) without neurological signs the percentages were blacks = 81.4 and whites = 18.6, respectively; for the severely retarded with other neurological conditions the percentages were blacks = 50.6 and whites = 49.4.
Organic retardation comprises “over 350 identified etiologies, including specific chromosomal and genetic anomalies and environmental prenatal, perinatal, and postnatal brain damage due to disease or trauma that affects brain development” (Jensen, 1998, p. 368). The difference between familial and organic mental retardation is huge, insofar as the individuals with familial retardation score no lower in IQ “compared with their first-order relatives than gifted children (above +2σ) score higher than their first-order relatives” and that parent-child and sibling correlations for IQ “are the same (about +.50) in the families of familial retardates as in the general population” and that “the full siblings of familial retarded persons have an average IQ of about ninety, whereas the average IQ of the siblings of organic retardates is close to the general population mean of 100”. This leads Jensen to conclude that “the familial retarded are biologically normal individuals who deviate statistically from the population mean because of the same factors that cause IQ variation among all other biologically normal individuals in the population” (p. 368) because the other traits unrelated to IQ do not distinguish the familial retarded from other biologically normal people. Now, consider what Jensen (p. 369) notes here :
Statistical studies of mental retardation based on the white population find that among all persons with IQ below seventy, between one-quarter and one-half are diagnosed as organic, and between one-half and three-quarters are diagnosed as familial. As some 2 to 3 percent of the white population falls below IQ seventy, the population percentage of organic retardates is at most one-half of 3 percent, or 1.5 percent of the population. Studies of the percentage of organic types of retardation in the black population are less conclusive, but they suggest that the percentage of organic retardation is at most only slightly higher than in the white population, probably about 2 percent. [21] However, based on the normal-curve statistics of the distribution of IQ in the black population, about 16 percent fall below IQ seventy. Assuming that organic retardation has a 2 percent incidence in the entire black population, then in classes for the retarded (i.e., IQ < 70) about 2%/16% = 12.5 percent of blacks would be organic as compared to about 1.5%/3% = 50 percent of whites — a white/black ratio of four to one.
Strangely, at first glance this looks as if, for whites, an IQ of less than 70 is ‘pathological’, while for blacks, an IQ of less than 70 is ‘normal’. Blacks are normal in behavior and appearance, not whites (Jensen, 1998, p. 367). What is even more remarkable is that the prevalence of low birth weight infants is much higher among blacks and that blacks experience worst environments. Drews et al. (1995) noted that maternal age is correlated with organic mental retardation. However, as they showed, lower SES and maternal education also correlate with higher prevalence of organic mental retardation. Another mystery.
References :
Drews, C. D., Yeargin-Allsopp, M., Decouflé, P., & Murphy, C. C. (1995). Variation in the Influence of Selected Sociodemographic Risk Factors for Mental Retardation. American Journal of Public Health, 85(3), 329-334.
Gottfredson, L. S. (2005). Implications of cognitive differences for schooling within diverse societies. Comprehensive handbook of multicultural school psychology, 517-554.
Herrnstein, R. J., & Murray, C. (1994). The Bell Curve: Intelligence and Class Structure in American Life. NY: Free Press.
Jensen A. R., 1973, Educability and Group Differences. New York: Harper and Row.
Jensen A. R., 1998, The g Factor: The Science of Mental Ability. Westport, CT: Praeger.
Murray, C. (1999). The Secular Increase in IQ and Longitudinal Changes in the Magnitude of the Black-White Difference: Evidence from the NLSY. In Behavior Genetics Association Meeting.
Nichols, P. L. (1984). Familial Mental Retardation. Behavior genetics, 14(3), 161-170.
Rushton, J. P., & Jensen, A. R. (2005). Thirty Years of Research on Race Differences in Cognitive Ability. Psychology, public policy, and law, 11(2), 235-294.
Rushton, J. P., & Jensen, A. R. (2010). Race and IQ: A Theory-Based Review of the Research in Richard Nisbett’s Intelligence and How to Get It. The Open Psychology Journal, 3(1), 9-35.
Spitz, H. H. (1988). Wechsler Subtest Patterns of Mentally Retarded Groups: Relationship to g and to Estimates of Heritability. Intelligence, 12(3), 279-297.
Yeargin-Allsopp, M., Drews, C. D., Decouflé, P., & Murphy, C. C. (1995). Mild mental retardation in Black and White children in metropolitan Atlanta: A case-control study. American Journal of Public Health, 85(3), 324-328.