Miller has no quarrel with my analysis of the myopia, intelligence, and brain-size data bases, but asserts that these statistical associations and trends can be easily explained within the framework of traditional genetics and evolutionary theory. I articulate features of a myopia inheritance model that would seem to be required for Miller's strong-inheritance + environmental- sensitivity view to explain myopia's upsurge, and discuss areas where, in the absence of a 'parental environment influences offspring myopia' effect, the body of evidence is inconsistent with such a construct.
2. Miller believes, however, that these statistical associations and trends can be "easily explained within the framework of traditional genetics and evolutionary theory." Regarding myopia's prevalence, he sees "no logical problem in a condition whose cross sectional variability indicates a strong genetic component changing over time for environmental reasons" and cites studies indicating the strong role that inheritance has continued to play in myopia: notably, one concerning the predictive power of refractions at 6-12 months of age (Pacella et al. 1999), long before reading can have an impact.
3. Such a construct implies that the set of genes one inherits governing the dimensions of the eye can confer an always, never, or maybe predisposition to myopia -- with differing 'maybe' genotypes conferring varying degrees of environmental sensitivity (i.e., in the amount of visual stimulation needed to actualize the myopia potential). For this model to fit observed trend data (a large multigenerational surge in myopia's prevalence in the Scandinavian and east-Asian studies cited), the proportion of individuals having a 'yes' or a highly sensitive 'maybe' predilection must have increased rapidly. But the literature lends no support to rapid changes in the gene pool occurring over the past century (no evidence for proportionately more myopes surviving childhood, having greater mate-finding success, or bearing more children). The dysgenesis argument (see #7 below) further develops this reasoning.
4. Miller states that there is very convincing evidence that myopia has a very high heritability, and I agree; but, if the pace at which gene frequencies change across generations is very slow, then the burden of explaining these trends falls on those 'maybe' genotypes that have a strong sensitivity to certain kinds of visual complexity. While we agree that near work (such as sewing or reading) can generate myopia, we are also cognizant that studies show that parental myopia is usually a far stronger factor than the amount of (early) visual stimulation. I also suggest that, while there is little doubt that the intense school + study regimen of (e.g.) Taipei children contributes to the epidemic of myopia, the same schoolwork regimen existed in their parents' generation, when myopia's prevalence (and severity) was far less. Indeed, a recent analysis by Mutti & Zadnik (2000) does not support the hypothesis that increasing environmental exposures to near work in recent decades has materially changed the prevalence of myopia.
5. These data are more easily explained if myopia is viewed as a quantitative trait that's alterable intergenerationally, and for an early predisposition for myopia to be expressed, a 'threshold of penetrance' must be surmounted: i.e., increased visual complexity in the grandparent's rearing environment induces a quantitative change which approaches but does not cross such a threshold, but which (assuming this increased complexity is maintained in the parents' generation) enables the grandchild to cross this threshold. In short, a large environmental change can engender progressive changes which unfold across several generations, even absent a further change in environment.
6. With respect to the high correlation between intelligence and myopia both within and between populations, Miller asserts that an obvious explanation is that high intelligence leads to more reading, and this leads to greater myopia. Yet, with respect to why myopia is so frequent among very intelligent people, he proposes 'a pleitropic genetic effect by which one gene promotes the growth of both the brain and the eyeball, with the eyeball growth leading to myopia, or a [greater] predisposition to myopia.' However, in the study Miller cites, where Myopia was twice as common among the extremely precocious students than among their siblings (whose IQs averaged 115), the non-gifted sib tended to spend about the same amount of time reading (Benbow 1986).
7. Miller argues that Jews tend to have much higher IQs and more frequent myopia because, under conditions of reproductive isolation, there was a strong impetus for natural selection to favor the survival of genotypes carrying alleles associated with high intelligence, and he cites MacDonald's perception that Rabbis had numerous children, while Priests were celibate. Yet, during the era when a tenfold increase in the number of Ashkenazi Jews is thought to have occurred (1800-1939), many Rabbis delayed childbearing until well after their youth -- i.e., after they completed their Yeshiva training and journeyed to distant villages (Shetels) for prolonged visits. Thus, like other members of the intellectually elite (who drifted toward urban centres, later marriages, smaller families, and secularism), Rabbis produced fewer generations of children per century. It is this aspect of population trends (four generations of children per century among families with below-average IQs and three generations among the top IQ quartile), that leaves proponents of dysgenesis at a loss to explain why there's been a gradual but profound rise in IQ, rather than a fall. Nor can this explain why, only 15 generations after Spain fostered the split between Ashkenazi and Sephardic Jews, the children of Ashkenazi Jewish immigrants to Israel outperformed the children of immigrants from Arab lands on IQ tests by a full standard deviation: even though rates of Jewish intermarriage approximated only 1% per generation.
8. Miller's focus is on the nucleotides comprising protein-coding genes, which he views as initiating all changes that affect the inheritance of traits; my focus is on the genomic landscape in functional proximity to the regulatory genes that govern the activity of a particular subset of protein-coding gene: namely, those inherited in a genomically-imprinted (gender-of-origin) manner, rather than a Mendelian (i.e., dominant-recessive) manner. I've proposed that the inheritance of the male input to such developmental landscapes is, at conception, likely to be embodied in the variations of (protamine-histone) bindings surrounding the sperm DNA, and is extracted by factors in the egg cytoplasm for incorporation into the uterine environment, where it governs the timing and extent of tissue-specific gene expression (by the methylation states at such cites during such critical periods). I see an environmentally-induced impetus generating changes in such methylation states, and I do not discount the idea that this process may involve 'selection' of emergent sperm having a favorable tandem-repeat number (which arise from unequal crossing over at sperm meiosis), or alternative ways of splicing a gene.
9. Miller makes the point that a genomically-imprinted gene that affects overall brain size is shown to express only the maternal allele, and that this goes against my conclusion that, with respect to the inherited aspects of IQ determination, the paternal influence exceeds the maternal influence. However, it is increasingly evident that the preponderance of imprinted genes occur as dyads, with the paternally-expressed dyad member usually controlling cell proliferation, and the female member setting a limit on such growth (so the head can pass through the birth canal). I view the discovery of a maternally expressed imprinted gene affecting overall brain size as portending the discovery of a paternally-expressed counterpart affecting the regional distribution of neuronal proliferation in association neocortex.
10. I don't disagree that a single structural gene might strongly influence both myopia and intelligence, but given the rapidity of change over the past century, I don't believe that the evidence which Miller presents justifies his assessment that: "the increase over time in myopia and intelligence, and ethnic group variations in intelligence and myopia are easily explained within the framework of traditional genetics and evolutionary theory."
Benbow, C.P. (1986). Physiological correlates of extreme intellectual precocity. Neuropsychologia, 24(5), 719-725.
MacDonald, Kevin (1994). A People That Shall Dwell Alone, Praeger.
Miller, E. M. (2000) Brain and eye size, myopia and intelligence PSYCOLOQUY 11(104) ftp://ftp.princeton.edu/pub/harnad/Psycoloquy/2000.volume.11/ psyc.00.11.104.brain-intelligence.4.miller http://www.cogsci.soton.ac.uk/cgi/psyc/newpsy?11.104
Mutti, D. O. & Zadnik, K. (2000). Age-related decreases in the prevalence of myopia: longitudinal change or cohort effect? Investigative Ophthalmology & Visual Science 41: 2103-2107.
Pacella R, McLellan J, Grice K, Del Bono EA, Wiggs JL, Gwiazda JE (1999). Role of genetic factors in the etiology of juvenile-onset myopia based on a longitudinal study of refractive error. Optom Vis SCI. 76(6):381-6.
Storfer, M. (2000) Precis of "Brain size, intelligence and myopia" PSYCOLOQUY 11(083) ftp://ftp.princeton.edu/pub/harnad/Psycoloquy/2000.volume.11/ psyc.00.11.083.brain-intelligence.1.storfer http://www.cogsci.soton.ac.uk/cgi/psyc/newpsy?11.083