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[evol-psych] Raymond: Book review of Jensen on Intelligence-g-Factor

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  • Ian Pitchford
    psycoloquy.99.10.057.intelligence-g-factor.7.raymond Sat Dec 4 1999 ISSN 1055-0143 (10 paragraphs, 9 references, 235 lines) PSYCOLOQUY is
    Message 1 of 1 , Dec 4 1:43 PM
      psycoloquy.99.10.057.intelligence-g-factor.7.raymond Sat Dec 4 1999
      ISSN 1055-0143 (10 paragraphs, 9 references, 235 lines)
      PSYCOLOQUY is sponsored by the American Psychological Association (APA)
      Copyright 1999 B. Raymond

      BIOLOGICAL DETERMINISM UNWARRANTED
      Book review of Jensen on Intelligence-g-Factor

      B. Raymond
      Institute of Virology and Environmental Microbiology
      University of Oxford
      Mansfield Road
      Oxford OX1 3SR
      United Kingdom
      bdhr@...
      http://www.nerc-oxford.ac.uk

      ABSTRACT: Jensen (1998) does not present any evidence for the
      external validity of g other than through biological correlations
      with IQ. Hence it is impossible to assess the validity of g in
      comparison with competing theories from this book. The author's
      interpretation of heritability estimates of IQ and of racial
      differences in IQ adoption studies ignores any potential maternal
      effects on IQ. His insistence that the primary cause of variation
      in IQ within and between races is genetic does not seem warranted
      by the evidence presented.

      1. Jensen (1998, 1999) makes a wide ranging series of claims about the
      nature of intelligence, many of them controversial and potentially
      socially divisive. I would expect any treatment of sensitive issues
      such as the differences in IQ scores between races to be especially
      rigorous and objective. In this, the book under review is
      disappointing. I find examples of poor understanding of evolution,
      over-eager assumptions of causality, selective presentation and
      interpretation of data, and conclusions that are hard to warrant in the
      light of the evidence presented.

      2. It is difficult to extract any concise definition of g itself from
      the book. The best was "g is created from the correlations among second
      order factors, whose residual variance consists of whatever variance
      they do not have in common with each other". My understanding of g and
      factor analysis is that it is an attempt to reduce the
      multidimensionality of a battery of mental test results to one
      dimension which best represents the common variance shared between
      tests. As such, it is a mathematical abstraction, and it is not
      possible on theoretical grounds to dismiss other theories of
      intelligence (e.g., Thurstone's simple structure) which represent an
      equal amount of information from the data on more than one dimension.
      Spearman's original method of tetrad differences for testing for g was
      abandoned precisely because it often demonstrated that it was difficult
      to represent mental tests on one dimension (see p. 75). A hierarchical
      analysis which correlates these first order factors (e.g. spatial,
      verbal, and memory first order factors), avoids this problem only
      because these factors also tend to be correlated.

      3. Some inconsistencies also arise when g is used as a fundamental
      theory of intelligence; for example, the increase in IQ (a heavily g
      loaded parameter) over the last 50 years has been matched by a decrease
      in scholastic ability (another highly g loaded indicator; p. 322). Has
      g both increased and decreased simultaneously? Jensen blames this
      inconsistency on the use of different 'vehicles', yet there is no
      direct means of measuring g other than through 'vehicles' of one form
      or another. Jensen also indicates that g 'typically' accounts 'for a
      larger proportion of the total variance than any other factor and often
      accounts for more of the variance than all of the other factors
      combined' (p. 79). Exactly what 'typically' or 'often' represents is
      not discussed further, despite being fundamental to the justification
      of the method. Furthermore, in one cited African study on elementary
      cognitive tasks (p. 392) the largest common factor among tests is
      described as being possibly something other than g. How is it possible
      to make this distinction, unless the author is assuming an existence of
      g external to the test results?

      4. An assertion that g has validity beyond a mathematical abstraction
      requires that it be connected to biological reality, and moreover
      associated with biology in such a way that it has increased explanatory
      power relative to competing theories. This connection to basic biology
      is based on correlations with "stature, head size, brain size,
      frequency of alpha brain waves, latency of evoked potentials, rate of
      brain glucose metabolism, and general health" (p. 137). First,
      correlations themselves prove no causal link between g and biology, and
      the separation (p. 130-143) of correlations into intrinsic (causal) and
      extrinsic (spurious) is simply not valid. Correlation with body size is
      dismissed by Jensen himself as not causal (p. 146). EEG is correlated
      with IQ; but IQ, even if it is strongly correlated with g, is not g,
      and we cannot assess whether alternative theories of intelligence
      describe this relationship better (e.g., whether higher g-loaded
      measures of mental ability are better correlated with EEG results).
      Cerebral glucose metabolism, head size, and nerve conduction are also
      only correlated with IQ. Thus, Jensen presents no evidence of causal
      links, nor any evidence that g is better correlated with basic biology
      than multi-dimensional theories of intelligence.

      5. The study of brain size in relation to race has historically been
      controversial and riddled with error and bias (Gould, 1981). Figure
      12.4 does nothing to relieve my admittedly pre-conceived scepticism
      concerning this issue. The high correlation coefficient is cited but
      not the significance value (p = 0.037, which is just significant).
      Moreover, the plotted values of cranial capacity are not those
      corrected for body size; the correlation is not significant (p > 0.05)
      when the corrected values are used. The method of deriving IQ/race
      medians from means is obscure, and no reason for preferring means over
      medians is given. The black IQ of 80 is surprisingly low given the
      American mean of 85. There may well be evidence for racial difference
      in brain size, but the best study of adults cited is not described as
      controlling for obvious but potentially confounding environmental
      effects such as alcohol use (Ho et al., 1980). There are well
      established differences in brain size between males and females,
      without significant differences in IQ, and this is accounted for by
      differences in neuronal packing density (p. 438). Since this factor has
      not been studied in relation to racial differences, sweeping causal
      conclusions seem premature.

      6. Jensen's chapter on the heritability of g fails to address a recent
      meta-analysis of 212 IQ on this topic. That paper estimates that 20% of
      the covariance in twins IQ can be explained by maternal effects and
      that broad heritability is 48% (Devlin et al., 1997). Thus, the shared
      environment effects on twins reared apart are underestimated by Jensen
      to give inflated values of heritability. Furthermore, the meta-analysis
      supported a maternal effects model better than models which assume
      heritability increases with age. The types of maternal effects
      associated with IQ changes described in the literature include:
      dietary supplements (Harell et al., 1955) and PCBs (Jacobson &
      Jacobson, 1996). Moderate alcohol consumption of mothers can affect
      psychomotor development (Larroque et al., 1995); and polycyclic
      aromatic hydrocarbons are associated with reduced head circumference of
      newborns (Perera et al., 1999). It is not unreasonable to hypothesize
      that a more socially disadvantaged group will be subject to poorer
      diet, increased levels of environmental pollutants, as well as
      increased drug and alcohol use.

      7. This section also includes some fundamental errors in evolutionary
      understanding. The assertion that "traits that show genetic dominance
      provide evidence that they have been subjected to natural selection"
      (p. 170) is not correct. Recessive traits, and purely additive traits
      can also be subject to natural selection, and dominant alleles may be
      selectively neutral. The fact that a trait is heritable and variable
      means that it is potentially subject to natural selection, but even
      this does not mean we can infer selection; other evolutionary forces
      such as mutation and genetic drift can be responsible for changes in
      gene frequency. In this light, the discussion relating dominance to
      hybrid vigour and inbreeding depression is misguided (p. 189-197).

      8. Jensen's "default hypothesis" is that differences in white and black
      IQ scores are made up of genetic and environmental effects and that
      environmental effects are often small relative to genetic effects (e.g.
      pp. 177-175, 475, 476, 489). These conclusions seem best supported by
      estimates of heritability, discussed above, and from the Minnesota
      transracial adoption study. This adoption study has several flaws.
      Maternal effects were not considered as a serious possibility for the
      lower IQ of blacks relative to whites. The IQ of parents of adopted
      children was unknown. The mean age of adopted infants also differed
      between treatment groups. And most fundamentally, the parents of
      children were not selected randomly from the population. Infants of
      parents of varying socioeconomic status and race might give children up
      for adoption, or have them taken into care, for very different reasons.
      In contrast, Jensen dismisses data from a racial admixture study in
      Germany which found no significant or consistent differences in IQ with
      race, because parental IQ was unknown, and because white and black
      fathers were not randomly sampled, two faults shared with the Minnesota
      adoption study. The absence of differences in the German study is also
      consistent with a maternal effects hypothesis, since the mothers were
      all white.

      9. Within the "g factor" there is abundant evidence for various
      environmental correlates of IQ, and for effects which may be specific
      to the black population. On p. 385 a study that controlled for
      socio-economic status reduced the g factor difference between American
      blacks and whites by 12 IQ points. On p. 513, "stereotype threat", a
      form of test anxiety, could account for a 5 IQ point difference between
      black and white college students. 12 plus 5 is 17, and the mean
      difference between blacks and whites in the US is only 15 IQ points.
      There are also two strong patterns which are highly suggestive of
      environmental effects, namely, the steady increase in IQ scores of 3 IQ
      points per decade in the last half century (p. 307), and the strong
      geographical gradient in IQ among blacks from south to north. For
      example, a group of black schoolchildren in rural Georgia has a mean IQ
      of 71, and Jensen's comments are "we would be hard put to find a more
      socially disadvantaged black community... anywhere in the United
      States". Whereas the black mean in Minnesota is given as 90. The most
      poorly founded conclusion in the entire book also concerns
      environmental effects, namely that 'mother's education alone account[s]
      for 13% of the childrens' IQ variance, but this is most likely a
      genetic effect' (p. 502). Given these potentially numerous and powerful
      effects, Jensen's insistence on the primacy of genes is surprising.

      10. Overall, the book leaves an impression of biological determinism;
      the correlation between IQ and socioeconomic status is consistently
      presented as resulting from the causal effects of IQ. Jensen paints a
      picture of America as a country with perfect social mobility, where an
      absence of racial prejudice is effectively demonstrated by the
      overrepresentation of blacks in jobs of high socioeconomic status
      relative to their distribution of IQ (p. 568), despite the much lower
      correlation between IQ and socioeconomic status for blacks relative to
      whites (p. 358). This is not an impression that rings true.

      REFERENCES

      Devlin, D., Daniels, M., & Roeder K., 1997. The heritability of IQ.
      Nature 388: 468-471.

      Gould, S.J., 1981. The Mismeasure of Man. Penguin, London.

      Harrell, R.F., Woodyard, E., & Gates, A.I., 1955. The effects of
      mothers diet on the intelligence of offspring. Teacher's College, New
      York.

      Ho, K-c., Roessman, U., Stramfjord, J.V., & Monroe, G., 1980. Analysis
      of brain weight: II. Adult brain weight in relation to body height,
      weight , and surface area. Archives of Pathology and Laboratory
      Medicine 104:640-645.

      Jacobson, J.L., & Jacobson, S.W., 1996. Intellectual impairment in
      children exposed to polychlorinated biphenyls in utero. New England
      Journal of Medicine 335:783-789.

      Jensen, A. (1998) The g Factor: The Science of Mental Ability. Praeger

      Jensen, A. (1999) Precis of: "The g Factor: The Science of Mental
      Ability" PSYCOLOQUY 10 (23).
      ftp://ftp.princeton.edu/pub/harnad/Psycoloquy/1999.volume.10/
      psyc.99.10.023.intelligence-g-factor.1.jensen
      http://www.cogsci.soton.ac.uk/cgi/psyc/newpsy?10.23

      Larroque, B., Kaminski, M., Dehaene, P., Subtil, P., Delfosse, M.J., &
      Querleu, D., 1995. Moderate prenatal alcohol exposure and psychomotor
      development at preschool age. American Journal of Public Health 85:
      1654-1661.

      Perera, F.P., Jedrychowski, W., Rauh, V., & Whyatt, R.M., 1999.
      Molecular epidemiological research on the effects of environmental
      pollutants on the fetus. Environmental Health Perspectives 107:
      451-460.
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