Miles David Storfer (2000) Myopia, Intelligence, and the Expanding Human Neocortex. Psycoloquy: 11(083) Brain Intelligence (1)

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PSYCOLOQUY (ISSN 1055-0143) is sponsored by the American Psychological Association (APA).
Psycoloquy 11(083): Myopia, Intelligence, and the Expanding Human Neocortex

[International Journal of Neuroscience (1999), 98(3-4): 153-276]
Precis of Storfer on Brain-Intelligence

Miles David Storfer
The Foundation for Brain Research
46 Brittany A Drive
Delray Beach FL 33446


During the past century, a substantial increase has occurred in the size of the human brain, especially in 'association' areas of the neocortex heavily used to cope with a complex language-driven society. It is proposed that this neocortical expansion has made possible the large, gradual increase in IQ that has occurred across the developed world, and been responsible for the dramatic upsurge in the prevalence and severity of near-sightedness (myopia) usually found after societies urbanize. The impetus for these changes begins during prenatal development. Findings from studies of mammals reared in captivity suggest that there is a mechanism for adaptive epigenetic inheritance, one capable of modifying the timing and/or extent of gene expression prenatally, without altering the DNA sequences that comprise protein-coding and other structural genes. Mechanisms that appear capable of transporting such adaptive changes across the so-called 'germ-line barrier' -- without violating the basic precepts of Darwin's theory -- are proposed. The social and evolutionary ramifications of our apparent proclivity for rapid, progressive, adaptive neocortical change are discussed, as well as some ways of testing aspects of this theory are proposed.


allergy, brain size, development, evolution, gene expression regulation, genomic imprinting, gifted, intelligence, myopia, neocortex.

    Below is the Precis of "Brain Size, Intelligence and Myopia" by
    Miles David Storfer (970 lines). This monograph has been selected
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    Reviews of Storfer (1999), "Brain Size, Intelligence and
    Myopia," are invited on questions such as the following:

    (1) To what extent is the human brain growing intergenerationally,
    and why does the growth seem so specific to areas most heavily
    stressed by recent ancestral experience? (2) How does this brain
    growth relate to the gradual, substantial long-term rise in IQ
    scores? (3) How can the prevalence of myopia have risen so rapidly,
    yet continued to generate epidemiological data consistent with
    myopia as primarily an inherited condition? (4) Given the close
    correspondence between myopia and high IQ, and findings that relate
    neocortical size and IQ, does this imply a causal link between the
    secular increase in brain size and the upsurge in myopia? (5) Do
    recent post-mortem findings of a left-right asymmetry in a
    speech-analysis area of the neocortex of primates heavily exposed
    to (gestural + vocal) human speech, in contrast to the
    near-symmetry reported in much earlier studies, suggest a rapid,
    adaptive (intergenerational) biological response?

    The full text can be viewed and downloaded at no cost through the
    publisher's (Gordon and Breach) website: 
    In the US:
    {note: the letters IJN must be capitalized}. 
    Outside the US: may be required.


1. The extent to which the human brain has been growing intergenerationally is assessed in section 5 of the treatise, which focuses on four areas of association neocortex essential to solving conceptual problems that entail visual and/or language integration [NOTE 1]. These areas are: (1) the prefrontal cortex (which is conceptualized as the seat of thinking, judgment, planning, and conscious self- awareness); (2) the 'polysensory association' area of the parietal lobe (which is conceptualized as the place where the products of analyses performed in the various unisensory association areas are integrated); (3) the specialized visual association areas of the occipital lobe; and (4) the portions of the temporal lobe involved in visual or auditory components of language comprehension, or both.

2. At the heart of this analysis are MRI studies of healthy adults that permit comparisons of the amount of gray matter in these areas in young adulthood and at midlife (section 5.4). It is forcefully argued that the substantially greater amount of gray matter seen at age 20 than at age 45 does not mean that age-related atrophy occurs in these areas over this part of the lifespan. Among the many reasons for this conclusion are: (1) the per-decade change between age 20 and 45 is much faster than seen from age 45 to 60; (2) no major changes are found over this age span in the other key brain areas examined, including functionally related non-association areas of neocortex; and (3) the kinds of differences seen comparing young and middle-aged adults are not consistent with normal aging processes (e.g. the younger adults have many more large neurons in layer III, which interconnects distant association areas). With respect to how rapidly such a secular expansion might be occurring, two MRI studies suggest a growth of roughly 5% per decade in frontal association areas.

3. The sites at which this growth has been occurring mirror those viewed as the hallmarks of recent human evolution, based on comparisons of our brain with what one tends to find in primates of various sizes (see section 5.5).

4. The recent finding that the destinations of newly generated neurons in adult rhesus monkeys are these same association areas (Gould et al. 1999) suggests that (assuming our postnatally generated neurons migrate to cortical areas subserving environmentally stressed functions) this entire expansion might be accounted for by environmentally induced intergenerational changes in these migration patterns. However, the total amount of brain matter has also been undergoing rapid growth, as witnessed by: (1) the increase of a full standard deviation in the size and weight of U.S. children's brains between the 1920s and 1970s (see section 5.2); and (2) findings from very long-term post-mortem studies (see section 5.7 and especially the 'note added' after the appendix to section eight).

5. The increasing physical stature (height and breadth) of the human body over time suggests that enlargement of the brain could be a secondary outcome of this trend (i.e. reflecting a need to maintain an appropriate brain-size to body-size ratio). If true, this would imply a causal link to factors such as improving childhood nutrition, more exposure to sunlight and fewer or less-severe illnesses. However, studies suggest that neither the overall number of neurons in the brain nor IQ bear an appreciable relationship to height (see section 5.7).


6. A very large body of evidence indicates that, across the developed world, IQ scores have been rising gradually but substantially since the early part of the twentieth century (see section 4.6). The pace of this increase has averaged about a quarter of an IQ point a year on tests like the Stanford Binet that stress verbal and symbolic analytic reasoning, somewhat faster on the Wechsler (which contains equally weighted 'Performance' and 'Verbal' scales), and roughly 0.4 points a year on the Raven's Progressive Matrices test, a non-verbal test containing several series of 'pattern recognition and extension' problems.

7. The evidence suggests that this secular (i.e. long-term) increase in IQ scores denotes a real increase in intelligence (see reviews in Storfer 1990; Howard 1999), predicated on an increasing size of these key areas of association neocortex. Some researchers have proposed that improved nutrition has played a dominant role in this trend, but the studies cited in section 6.1 (see also Church & Katigbak 1991) would seem to sharply limit the extent to which differences in prenatal and early childhood nutrition could have affected later IQ.

8. MRI studies generally report moderate positive correlations between brain size and IQ (averaging approximately 0.4); where more detailed findings are available, the neocortex is found to be the chief source of this correlation (see section 5.2). Post-mortem examinations of people who've exhibited extraordinary gifts of intellect indicate that, in the neocortical areas viewed as strongly related to their exceptional acumen, very large neuropil (i.e. the space occupied by a cell body plus its dendrites) are found in the middle layers (the so- called receptive layers) of the neocortex (see section 3.3). Again, this parallels the differences observed when humans and other primates are compared (i.e. humans have a thicker neocortex attributable to larger neurons in our middle layers). Thus, both secular trends in, and the functional import of, individual differences in these association areas have followed and extended evolutionary pathways.

9. As this increase in IQ occurred, the data generated by the panoply of 'nature-nurture' settings examined suggest that: (1) on average, the heritability coefficient for IQ was 70%, with the remaining variance (30%) accounted for by (essentially) early environment; and (2) for most people, a very good or a very bad early home environment can exert a considerable impact on IQ (reviewed in Storfer, 1990, Part I).


10. As and after societies urbanize, a dramatic increase is usually found in the prevalence, severity and earliness of myopia (nearsightedness). This is documented in three fairly homogeneous populations: Scandinavian countries, Pacific Rim countries (where, in some large sub-samples, the use of corrective lenses for myopia approaches 90%), and Arctic villages (see section 1).

11. The moderate statistical association reported between myopia and intelligence strengthens greatly as one approaches the upper echelon of IQ performance (see section 2.1). For example, in a study by this author of 2,720 members of high-IQ organizations (mainly Mensa), 47% of the females and 33% of the males reported very early onset myopia (i.e. by age 10), compared with an 'expected' rate of roughly 5% among age cohorts with IQs in the normal range.

12. There is very strong evidence that myopia has been, and still is, mostly an inherited condition. This is not meant to imply that heavy exposure to 'near work' (such as reading or sewing) cannot induce myopia that requires the use of corrective lenses in people who have an underlying predisposition for it. Yet much of this rise is apparently due to a rapidly increasing proportion of urban/urbanizing populations being born with such a predisposition (see sections 4.1 to 4.3).

13. For inheritance to have continued its very predominant role in the face of so large a rise in myopia, it would seem that either: (1) myopes have recently begun procreating at much faster rates than non- myopes; or (2) in pre-urban societies, a very high rate of childhood mortality among myopes or a much lower rate of marriage had suppressed its prevalence, but myopes' survival or marriage rates have soared; or (3) a secular increase in the amount of parental exposure to near work is able to induce in their offspring a greatly increased prenatally appearing disposition for myopia. The available studies (see sections 4.4 and 4.5) would seem to rule out these first two possibilities.


14. A hallmark of myopia's progression is an elongation of the eye's axial length without corresponding size increases in its other dimensions. This increasing mismatch in size causes parallel rays from objects to unite further and further in front of the retina, and eyeglasses are then required to adjust this focal point accordingly.

15. It is proposed that the impetus for an enlargement in axial length emanates from the neurons of the brain that categorize and analyze visual inputs [NOTE 2], and the neurons that supply these visual association areas with focus-of-attention input (in essence, an increase in the size of the visual pathway). Extending from the eye to the primary visual-receptive fields in the back of the brain, inputs to and from the eye traveling along this pathway first pass through the lateral geniculate nucleus (LGN), which is the visual gateway to the thalamus, whose primary role is viewed as providing focus-of-attention input to and among very precise areas of neocortex. Since every 'neocortical column' is connected to a discrete area of thalamus (see Part II note 11), an enlargement of the cortical areas involved in analyzing stationary objects and written language would necessarily enlarge portions of thalamus subserved by the LGN. Significantly, the subtype-specific acetylcholine receptor present in the visual receptive fields is also found in, and affects only one part of the eye: axial length (see sections 3.1 and 3.2) [NOTE 3]. Thus, an increasing need for this chemical messenger is apt to effectuate this increase in axial length.

16. Supporting this proposed construct are findings that: (1) in rodents, exposure to an unusual amount of visual complexity (coupled with novelty) induces neuronal enlargement in the expected areas (and layers) of the neocortex, with these postmortem effects heightened with multigenerational exposure; and (2) intellectually gifted people have grossly enlarged neurons in the areas associated with their specific gift or talent (see section 3.3), especially in the cortical layers that interconnect distant association areas (III; V), and the layer between (IV), which connects cortex with thalamus.

17. The extremely high prevalence and greater average severity of myopia found among members of economically developed East-Asian cultures also supports this construct (see section 6.1), as: (1) the large number of diverse characters that comprise their written languages (pictographs and ideographs) would logically entail a more complex visual decoding apparatus (see section 6.2); and (2) the members of these cultures tend to excel at 'perceptual' problems (e.g., those where structural comparisons are used to derive similarity or causality). Yet, very early adoption of East-Asian children into European families did not alter the otherwise-expected 'shape' of their Wechsler IQ-test profile (see section 6.1).

18. It is further proposed that the markedly greater likelihood of females with high IQs having myopia compared with equivalent-IQ males (see section 2.1) reflects the smaller size of the female brain (males have roughly 15% more neocortical neurons, but, interestingly, only a 2% larger thalamus). Since females perform almost as well as males in the two-dimensional spatial-analysis components of IQ tests, it would seem to follow that, to cope with the visual complexity of a modern urban environment, a greater stress would be placed on the female's available neuronal resources. Thus, a proportionately larger visual pathway would be generated in females to accommodate the additional attentional strain.

19. An emergent hypothesis is that an intergenerational change in the (absolute or relative) size of an area of association neocortex can generate a medical condition generally thought to be rooted in an unrelated biological system. How this construct might explain the underlying cause of two related medical conditions whose prevalence has been increasing rapidly is discussed below.


20. Some areas of association neocortex have been getting appreciably smaller, both evolutionarily and in recent generations. In particular, the size of the area responsible for the analysis of odors (the olfactory cortex) is contracting rapidly (see section 6.4). Since having an effective immune system implies an ability to distinguish from among organisms that enter our nose those which are harmful and those which benign, and to react appropriately, it is proposed that the upsurge in the prevalence of allergy and asthma is an outgrowth of the shrinkage in this area's size. In essence, an allergic reaction to a particular pollen represents a failure of one's scent-analysis apparatus to distinguish a harmful from a benign inhalant.

21. Like myopia, the higher one's intelligence, the more likely one is to be allergic to inhaled substances and, thus, to have asthma. For example, in the study of 2,720 gifted people conducted by this author, more than 80% of those who reported having asthma also had allergies; here, the gifted females were also far more likely than the males to have these disorders, and myopes were nearly twice as likely as non- myopes to have severe or multiple allergies (see section 6.4).

22. Because the cortical destinations of postnally generated neurons reported for different mammals relate closely to their functional needs

 - in rodents, they migrate to the entorhinal, and hence olfactory,
cortex; in songbirds, in springtime, to the song-generating neurons of the frontal cortex (Nottebohm. 1981); and, in rhesus monkeys, to visual, language and frontal areas (Gould et al. 1999) - it is proposed that in humans their destinations would differ between children whose rearing stresses reading plus coping with a visually complex modern urban environment, and children reared in a community where farming, hunting and fishing are the primary occupations. It is also proposed that the greater the difference between the present environment and that of one's recent ancestors (in terms of the import of analyzing odors and objects in motion, as opposed to analyzing stationary visual objects plus language) the more likely that the biological changes that underlie an increase in IQ will also produce a greater susceptibility for asthma. This would explain the soaring rates of asthma found among lower- and middle-class Black children in the U.S.A., a country where the average performance of working-class Blacks on IQ tests now exceeds the average recorded for Caucasians in the 1920s [NOTE 4].


23. Taken together, the findings depicting the trends in, and factors influencing, myopia's prevalence and severity strongly suggest that neither heredity, nor environment, nor a single-generation interaction of changes in the two, can explain the rapidity of the changes observed, the patterns of intergenerational progressivity, or the continuing strength of inheritance as a given culture's rate of myopia soars. This is especially so in light of the earliness with which the predilection to develop myopia can be diagnosed. Instead, these data imply that: (a) the likelihood of a person acquiring myopia from a given rearing environment; (b) the age at which corrective lenses are first needed; and (c) the ultimate severity of that myopia are all also affected by the abundance, the nature, and the variety of visual complexity present in the rearing environments of that person's parents, grandparents, and great grandparents. The proposed model of myopia's inheritance is more fully described in the introduction to section 7.


24. The studies detailed in section 7.1 are used to demonstrate the existence of an adaptive, reversible inheritance mechanism in mammals. Among the environmental perpetuations shown to induce multigenerational effects in rodents are: (1) altering the ratio of oxygen to carbon dioxide in the rearing environment from a week before birth until weaning; (2) greatly altering the temperatures of the environment from that of recent ancestors; (3) inducing an increasingly early aversion to alcohol by early exposure to it in drinking water; (4) greatly improving the maze learning ability of offspring by maternal exposure to maze exploration; and (5) inducing a progressive thickening of visual association neocortex over four generations of exposure to visually and socially complex environments (see section 3.3.1, and Part IV note 13).

25. Exposing mice to an environment that differs greatly from that encountered in the wild (i.e. a laboratory cage), followed by stability for at least 50 years, is shown (in 10 strains of purebred, then inbred mice) to have induced complex rearrangements at various sites along the chromosomes, and often a maximal divergence from the founder stock (see section 7.1). The rates of divergence from ancestral lines are estimated to be 20 times faster than seen in wild mice.


26. Chimpanzees exposed to human language have recently been found to have a very substantial size difference favoring their left hemisphere in a cortical area associated with receptive language (see the research-recommendations section). Of special note are findings (Gannon et al. 1998) that, in 8 of 15 chimps autopsied, this left hemisphere area, the planum temporale, is more than twice the size of the right. An absence of a substantial hemispheric difference in pre-1975 studies implies that increasing and intergenerational exposure to human gestural or auditory language, or both, induced this rapid, essentially uni-hemispheric expansion. Two recent studies (Herndon et al. 1998; Herndon et al. 1999), which contrast life-span changes in the brain weights of chimpanzees and rhesus monkeys, strongly support this construct. Herndon et al. (1998) report that the brain weights of (400) rhesus monkeys are stable over the entire adult life span, even though these primates experience cognitive declines with age similar to humans. This research team (Herndon et al. 1999) also found, however, that chimpanzees (who, at the Yerkes Primate Research Center, often receive extensive cognitive training) display a pattern of age-related changes that's comparable to humans. Interestingly, the adolescent chimps had already achieved the same brain weights as the young adults (most of whom were of their parents' or grandparents' generations).


27. One might speculate that such (prenatal/early postnatal) perpetuations to the environment can induce these inheritable changes by altering a young female's womb, and thereby the intrauterine milieu that she'll eventually provide to her offspring. However, the cross-fostering studies in section 7.1 amply show that the impetus for such changes can be transmitted through the sperm.

28. Another field of research that supports the existence of a mechanism for transmitting development-altering stimuli across the male 'germ-line barrier' in mammals are the evaluations by A. C. Wilson and his co-workers of factors affecting the rates of chromosomal change in hundreds of diverse species (see section 7.2). Here, rapid rates of change seem to be evoked by social and sexual behaviors of a deme (i.e. a family, a group or a troop) that enhance the intergenerational stability of male-conferred genes and environments.

29. With respect to human intelligence, the nature/nurture database contains a statistical incongruity that requires explanation: how the parent's sex influences parent-child IQ correlations in adoptive versus biological families. Assuming one believes that early child-rearing practices can have a measurable, long-lasting impact on one's IQ score, one would expect to find that children's IQs would tend to bear a closer statistical relationship to their mothers' IQs than to their fathers' IQs for three reasons: (1) the large preponderance of the early caregiving was (in the middle third of the last century) almost always supplied by the mother; (2) the rate of fetal growth, which often influences IQ (reviewed in Storfer 1990), depends on the intrauterine environment; and (3) in instances of 'erroneous paternity,' the father-child IQ correspondence tends to be negligible. Indeed, a review of data from adoption studies, limited to early adoptions (see section 7.3), finds that IQ correlations between adoptive mothers and their adoptive children are consistently a good deal higher than between these children and their adoptive fathers (thus demonstrating an adoptive mother's greater ability to fashion her adoptive child's IQ after her own). Since the average adoptive father is apt to have a substantially greater involvement in his child's early development than the average biological father, and adoptive mothers supply no intrauterine environment, one would expect to find an even greater difference favoring mother-child IQ correlations in biological families than in adoptive families. However, a review of 111 high-quality studies found that, in biological families, father-offspring correlations and mother-offspring correlations were identical. Thus, if mothers make a greater contribution to the prenatal and postnatal environmental side of the nature/nurture equation then, for the parental influences to be equalized, fathers must make a greater biological contribution to intelligence at conception than mothers.


30. In mammals, it is believed that acquired traits cannot be inherited. This is not because the barrier to such inheritance is a fundamental characteristic of all living things, since organisms that reproduce by cloning have an inherent ability to evolve adaptively from exposure to a variety of specific stimuli; this includes mammalian cells grown in culture. In mammals the constraint on the inheritance of an environmentally induced developmental change is that, shortly after a mammal's germ line forms, its egg and precursors to its sperm are sequestered in a special chamber, where only radiation or random errors (e.g. in the process of sperm-cell division) are capable of altering nuclear DNA.

31. Thus, it's thought that each new generation must begin its journey into life at the same starting point as the last, except for random mutation, fitness for survival and the other well-articulated forces that comprise the evolutionary framework known as neo-Darwinism. Further, a neo-Darwinist would assert that, even if the parental environment could reshape an offspring's development, such an impetus for change could not 'flow backward' in time: i.e. it could not prepare the biology for certain kinds of expected experiences at an earlier stage of development (for Darwin's disquieting query about this, see section 7.4.2).

32. If differences in a mammalian species' form and function were tightly linked to DNA differences in its protein-coding and other structural genes, this would support the perceived immutability of this germ-line barrier. But with respect to the DNA sequences comprising structural genes, the differences between humans and our closest primate neighbors are slight (roughly 1%), while DNA differences among frogs that are similar in form and function can be enormous. In mammals there seems to be a disconnection between the slow, steady rate of change in the structure of protein-coding genes, and whatever processes have been enabling so rapid an evolution in form and function.

33. Thus, it is logical that mammals possess a mechanism for using their existing suites of genes to produce changes in development (i.e. changes in the timing and extent of gene expression in specific cell- types and tissues at specific stages of development). Although this would necessarily involve altering some aspect of the relationship (e.g. the distance) between a so-called regulatory gene (e.g. a 'promoter' or 'enhancer') and a structural gene whose behavior it affects, this is apparently accomplishable without altering the sequences of DNA that comprise such structural (or possibly these regulatory) genes themselves.


34. If such a candidate mechanism was to be proposed, it would seem appropriate to evaluate it on the following basis: (1) can it produce development-altering effects without altering the DNA of structural genes? (2) is it inherited in a manner that differs by sex? (3) is their a plausible way for it to affect the development-altering information transmitted by males at conception? and, ideally (4) can it provide a plausible explanation (in terms of an evolutionary benefit) for the overwhelming dominance in mammals of two-sex reproduction?

35. Such a mechanism is proposed. Called genomic imprinting, it is a gender-of-origin inheritance mechanism (rather than a dominant- recessive inheritance mechanism). It can produce tissue-specific, stage-specific changes in prenatal development (via the presence or absence of a 'silencer' over a stretch of DNA that can affect the activity of a regulatory gene). The template for the presence or absence of this silencer (the methylation state of cytosines) is not encoded on developing sperm until the middle of their (14-stage 72- day) development. A plausible way exists for the brain to 'inform' the only other non-dividing cells of the body (the Sertoli cells in the male that nurture the development of sperm, and their female counterpart, the Cumulus cells of the ovum). A highly variable and rapidly evolving 'landscape-influencing' counterpart to methylation state is found in mature sperm (locus-specific variations in protamine binding subtype, and locus-specific protamine-histone variation) [NOTE 5). Genomic imprinting underlies certain essential gender-specific contributions to embryonic development. Paternal and maternal imprints differentially affect neuronal proliferation in specific brain areas, including the neocortex, while variably imprinted genes are shown to affect intelligence and other behavioral traits and, assuming it permits certain survival-enhancing adaptive changes to be transmitted paternally and others maternally, it can confer an adaptive advantage that greatly exceeds the evolutionary costs of a second reproductive sex. The treatise's table of contents (sections 7.4-8.7) indicates where these topics and those articulated below are discussed.

36. Among the reasons why this gender-of-origin inheritance mechanism has been overlooked as a possible means of adaptively influencing a progeny's prenatal gene expression, are: (1) until recently, the number of genomically imprinted genes identified was rather small; (2) because tissue specific gene expression arising from different methylation-state patterns is limited to large-genomed animals, research on small-genomed animals does not evoke the same consequences; (3) knowledge of how aspects of the DNA landscape within or near an imprinted zone can effectuate quantitative differences in gene expression (see discussions of tandem repeats) has only recently emerged; (4) because: (a) a sperm's methylation-state template is erased prior to final sperm maturation, and (b) a generalized erasure of the fertilized egg's methylation-state template occurs at a very early stage (and is replaced soon after with a stage-specific template), it has been assumed that the functional significance of these methylation states are transitory and do not influence later development, as opposed to serving as a template that, in sperm, gets converted to protamine variations or, in preimplantation embryos, enables the extraction of developmental instructions for transmission to factors in the egg's cytoplasm; and (5) this gender-of-origin inheritance is assumed to be subject to the same intergenerational 'reset-button' constraint that applies to dominant-recessive inheritance. For a fine overview of imprinting's roles in mammalian development, see Latham 1999.


37. A possible alternative or complementary way of transporting development-altering information from the sperm to the egg at conception is proposed in the appendix to Part III. This involves the tiny number (50?) of male-derived mitochondria that enter the egg (but not its nucleus) at conception and are absorbed by factors in the egg cytoplasm, and is specific to the transformation of information about extremely active (hence mitochondrially active) areas of the paternal neocortex (and possibly grandparental neocortex) into a call to allocate more neuronal resources to these areas of his descendants' developing brains.


38. As described in section 8.6, a link between IQ and an 'imprinted' gene that is only expressed when it is transmitted paternally has been discovered, with intellectually gifted people reported in two studies to be twice as likely to have one or two copies of a particular variant (allele) of this gene (IGF-2R), compared with people of near-average intellect. Interestingly, this gene is imprinted in some, but not all people, suggesting that a difference in allele (which affects the distance between a regulatory gene and the structural gene it regulates) can determine whether this gene's expression is inherited on a gender-of-origin basis or on a dominant-recessive basis [NOTE 6]. This variability in whether a gene-regulator combination is located within or outside an imprint zone suggests that such imprint zones confer opportunities for adjusting intergenerational regulatory controls in a manner that, in a new, fairly stable intergenerational environment, yield 'fast-track' adaptive evolution.


39. The term 'critical period' is generally used to indicate a time-limited stage of development during which the environment can profoundly influence the biological underpinnings to a given lifelong capacity. Storfer (1990) proposed that, with regard to skills requiring neocortical participation, a critical period's waning is demarked by the appearance of myelin sheathes encasing the axons that interconnect distant areas essential to that function. These patterns of human myelin-tract formation are summarized in section 8.8, and the so-called neonatal imprint period (which wanes as myelination occurs among axons connecting 'primary' visual and auditory areas with the thalamus) is discussed in section 6.3. Since connections between the frontal and parietal (polysensory) association areas don't myelinate appreciably until the second postnatal decade, some key tracts don't myelinate until we approach midlife, and some may never myelinate, certain aspects of the neuronal architecture retain their 'plasticity' throughout the childbearing years. A hypothesized relationship between programmed methylation-state changes in tandem repeats and the forces that control critical periods is discussed in section 8.3.2.

40. With respect to the question of when during embryonic development the overall size of the neocortex (and regional sizes?) might be affixed, an essential moment appears to be around the fortieth day of gestation, when the so-called progenitor cells (that 'beget' the various kinds of neurons that then become a neocortical column's lower and middle layers) are generated since, at that point, keeping the genetic machinery that produces a given area's progenitor cells turned on for a few extra hours could substantially enlarge that area (see section 8.2 and Rakic, 1988). The earliest that a neocortical area could begin functioning would seem to be when the connections are made that supply it with 'focus-of-attention' inputs from the thalamus; in the case of the frontal lobe area that's deemed essential to conscious self-awareness, no appreciable thalamic connections are apparently in place before the twenty-seventh prenatal week (Rakic, 1988).

41. Assuming the brain can (hormonally?) impart information about its present dendritic-architecture/cholinergic-use to the 'nursemaid' (Sertoli) cells of the testes, and thereby affect either: (1) the methylation-state that gets encoded on a developing sperm; or (2) the survival and success rates of sperm having different bindings (see, Palumbi 1999), would this theorized ability to transfer up-to-date information from the brain end at the onset of puberty, when the Sertoli cells reach full maturity, or can it continue indefinitely? The latter construct could explain why, independent of maternal age, older fathers reportedly beget disproportionately more highly intelligent children (see section 8.8).


42. An ideal way for mammals to reap the benefits of incorporating experience-derived changes into their offspring's development, while protecting against the deleterious effects of incorporating changes derived from unusual, temporary conditions, would be to have sex- specific domains of influence: 'hot spots' where the actualized phenotype of one sex can influence a specific aspect of its descendant's fetal growth, while the other sex provides a means of slowing or counterbalancing a change that could otherwise leave an altered phenotype unfit for survival should the 'normal' environment make an abrupt return.

43. For a species to have a way altering the timing and extent of gene expression in its descendants on a tissue-specific basis (as an ability to alter methylation states might impart) would constitute a powerful force for adapting rapidly to changing conditions. The closer the child-rearing and educational milieu comes to mirroring that provided to recent ancestors, the more completely an adaptive phenotype could then sweep through a population. This could explain why demes of 'barn mice' undergo substantially faster rates of chromosomal rearrangements than comparable strains of field mice, and why laboratory-reared rats 'evolve' faster than those in the wild. An intergenerationally stable environment thus induces a maximal divergence from ancestral lines.


44. It's proposed that a close repetition of ancestral child-rearing and educational practices can both induce and deepen adaptive responses in the prenatal brain development in a culture exposed to stability in its child-rearing regimen, and that under such stable conditions very substantial changes in quantitative and temporal aspects of gene expression can be evident within a few generations.

45. Storfer (1990) details how the members of various culturally isolated societies display marked differences in the 'shapes' of their intelligence, and how the areas in which members of these cultures tend to display cognitive acumen correspond closely to the nature of their ancestrally stressed child-rearing and educational practices. This includes two cultures having a high prevalence of myopia: the Japanese and Ashkenazi Jews (see Storfer, 1990, chapters 13, 14, and 20). Section 6.1 contrasts certain areas in which these two cultures tend to excel.


46. Whether adaptive changes in brain development in the proposed model of inheritance should be considered genetic or epigenetic alterations (the latter implying changes in the phenotype, but not the genotype) depends on which of the possible mechanisms described apply, and on whether a restoration of the rearing environment to its previous state would evoke a return to the previous developmental state and do so by the same biological pathway (see section 8.9). The possibility is also raised that the rearing environment can induce epigenetic changes in offspring, leading to genetic changes in grand-offspring.


47. This proposed inheritance model holds that a person's actualized intelligence is a product of their genes, their rearing environment, and the cumulative effects of the early environments of their male ancestors on their progeny's prenatally unfolding neuronal growth trajectory, as modified by a maternally supplied impetus for accommodation or stasis. Here, the term 'male ancestors' is chosen to incorporate the idea that a grandfather's environment can induce an epigenetic change in a descendant's early development that occurs before its germline differentiates, and thereby induce a genotypic change in his grandchildren (see sections 7.4, 8.8, and 8 note 10). Since the early rearing environment is, in the main, maternally supplied (and is strongly influenced by the parenting approach and the various skills imparted to her by her lineage), the maternal and paternal contributions to developed intelligence are equalized.

48. Thus, for neocortically based quantitative traits (such as intelligence and myopia are hypothesized to be), whose effects seemingly depend on the number and dendritic complexity of neurons that receive transmissions of acetylcholine, a model of inheritance is proposed in which a paternal contribution to embryonic development acts (via a paternally expressed imprinted site) as an impetus for change, and if a maternal contribution to this trait exists (acting via a maternally expressed imprinted site), it provides a receptive or a supportive environment, or serves as a force for stasis (see section 9 note 3).


49. Section 9.3 assesses the effects of this proposed inheritance model on some key features of the prevailing evolutionary framework. It strengthens two of Darwin's basic evolutionary concepts: natural selection and descent with modification. Nevertheless, it suggests some major revisions to the orthodox evolutionary framework (the so- called Modern Synthesis, or neo-Darwinism).

50. Charles Darwin articulated the concept of evolution as representing descent with modification (meaning that a gradual development of all life forms occurs as a series of small changes that ultimately converts one species into another), fueled by natural selection (survival of the fittest), acting on spontaneously arising variations (a term eventually replaced with random mutations, and then applied solely to accidental mistranscriptions of the genetic code that in a mammal occurs when its germ cells are generated).

51. The feedback mechanism proposed here (i.e. that environmentally induced changes in gene expression during a mammal's early development become an inherited feature of its future offspring's earlier development) materially strengthens the power of natural selection. Environmental adaptation promotes survival and, if a postnatal opportunity for inducing inheritable changes exists, the inheritance of adaptively beneficial changes in form and function could occur at an extremely rapid pace. Further, if many individuals can adapt to an altered environment in the same way, and then transmit key aspects of that adaptive expression to their progeny, then survival-promoting changes can sweep through a reproductive population fast enough for descent with modification to have accomplished what some detractors say could not have occurred within the time periods involved.

52. The principle of descent with modification is not injured by a rapid means of accomplishing this end. It means that Darwin's idea of gradualism needs to incorporate possibilities like: (1) changes in quantitative traits occur at a rate of one or two turns of a 'volume- control' knob per generation; (2) for some traits, a 'threshold of penetrance' exists, beyond which the expression of an alternative coping mechanism (e.g. a different way of splicing a gene) can be induced (see section 7.1); and (3) it is possible for such events to occur simultaneously (and automatically) in all predisposed members of a reproductive population.

53. With respect to the idea that random mutation is the sole source of altered mammalian inheritance, the exceedingly rapid changes that seem to occur in mammalian form and function pose a dilemma for biologists who equate evolution with molecular evolution. Since, at the molecular level, frogs have been evolving at about the same rate per million years as mammals, and may differ from one another (in this way) to the same extent as do such mammals as bats and whales, while chimpanzees and human beings are roughly 99% the same at the molecular level, but differ radically in neocortical size and abilities, either molecular evolution is of minor importance as an explanation for mammalian evolution, or mammals have evolved a new way to incorporate beneficial mutations into their inheritable developmental program for gene expression. The basis of this proposed inheritance model, developmental changes in the timetables for the unfolding of changes in gene expression at variably methylated sites, suggests a rationale for rapid changes in mammals: stage-specific or tissue-specific alterations that affect the 'terrain' in which regulatory genes reside. Since tissue- and cell-type variations in methylation patterns are a basic feature of complex genomes, but are rarely seen in small- genomed species, one would expect the potential for such changes to grow exponentially as organisms have gotten more complex. Thus, the certainty that random mutations constitute the sole, or even the primary source of inherited changes in mammals is greatly lessened by this construct.

54. Among the social implications of humankind's apparent proclivity for rapid, adaptive neocortical change are the possible long-term deleterious consequences of working mothers' decisions to re-enter the labor force when their children are infants, coupled with the inadequate training given to most surrogate caregivers.


[1] Association areas of the neocortex are distinguished from primary sensory areas in that they do not receive sensory inputs or execute motor-output tasks, but perform the mental processing and planning tasks between.

[2] The cortical region responsible for the classification of visual objects is organized into an average of perhaps 30 centers, each of which is thought to perform a specialized kind of feature analysis (see section 8.2.1). An increase in the number of such centers is thought to have accompanied human brain evolution, and it is believed that the environment can influence both the total number of centers and their specialties; an analogous example, applicable to language-related areas, is that people who are fluent in several languages are found to use different cortical areas to access each language's vocabulary.

[3] For discussions of the roles that acetylcholine and neurons that receive cholinergic inputs are proposed to play in myopia, intelligence, and the inheritance of intelligence through the male germ line, see sections 3.2 (first paragraph and note 7), 6.4 (second paragraph), 8.4 (third paragraph from the end, and notes 10 and 19) and, in the appendix, the sections titled 'Mitochondria, Acetylcholine, Neocortex and Testes' and 'A Cholinergic Connection.'

[4] Black and Caucasian children in the U. S. underwent roughly equivalent size increases in head circumference since that time. Although (within race) head-circumference/IQ correlations are about half those reported for brain-size/IQ, their significance may be inferred from the following analysis of findings from a longitudinal study of 38,000 children born in 12 U.S. urban areas (Broman et al. 1987, table #8-19). Here, the average circumference of those Black and the White children whose IQ scores (on the Wechsler at age 7) were 120 or higher were identical (52.1 cm); similarly, among children having IQs between 90 and 119, the head circumferences averages were 51.5 cm for the White children and 51.4 cm for the Black children; and for those with IQs between 70 and 89, the averages were 50.9 cm and 51.0 cm, respectively. In this study, both the IQ difference (a full standard deviation) and within-race correlations between head circumference and IQ at three ages (at birth, at age 3, and at age 7) were consistent with the literature (Lynn 1990). For an analysis of intelligence and brain size by race, see Rushton & Ankney 1996.

[5] For some new findings pertaining to these points, see Gardiner- Garden et al. 1998, Heath & Hilbish 1998, and Rooney & Zhang 1999.

[6] A 'methylation-regulated chromatin boundary' model for this gene's imprinting has recently been proposed (see Schmidt, Levorse & Tilghman 1999). Another behavior-influencing gene (affecting the serotonin receptor gene locus) has also been found to be imprinted in some, but not all people (see the 'note added in proof' after the appendix to section 8); but in this case, when it's imprinted, only the maternally transmitted gene is expressed.


Broman, S. H., Nichols, P. L., Shaughnessy, P. & Kennedy, W. (1987) Retardation in Young Children. Erlbaum.

Church, A. T. & Katigbak, M. S. (1991) Home environment, nutritional status, and maternal intelligence as determinants of intellectual development in rural Philippine preschool children. Intelligence 15: 49-78.

Gannon, P. J., Holloway, R. L., Broadfield, D. C. & Braun, A. R. (1998) Asymmetry of chimpanzee planum temporale: Humankind pattern of Wernicke's brain language area homolog. Science 279: 220-222.

Gardiner-Garden, M., Ballesteros, M., Gordon, M. & Tam, P. P. (1998) Histone- and protamine-DNA association: conservation of different patterns within the beta-globin domain in human sperm. Molecular & Cellular Biology 18: 3350-3356.

Gould, E., Reeves, A. J., Graziano, M. S. & Gross, C. G. (1999) Neurogenesis in the neocortex of adult primates. Science 286: 548-552.

Heath, D. D. & Hilbish, T. J. (1998) Mytilus protamine-like sperm- specific protein genes are multicopy, dispersed, and closely associated with hypervariable RFLP regions. Genome 41: 587-596.

Herndon, J. G., Tigges, J., Klumpp, S. A. & Anderson. D. C. (1998). Brain weight does not decrease in adult rhesus monkeys. Neurobiology of Aging 19: 267-272.

Herndon, J. G., Tigges, J., Anderson. D. C., Klumpp, S. A. & McClure, H. M. (1999) Brain weight throughout the life span of the chimpanzee. Journal of Comparative Neurology 409: 567-572.

Howard, R. W. (1999) Preliminary real-world evidence that average human intelligence really is rising. Intelligence 27: 235-250.

Latham, K. E. (1999) Epigenetic modification and imprinting of the mammalian genome during development. Current Topics in Developmental Biology 43: 1-49.

Lynn, R. (1990) The role of nutrition in secular increases in intelligence. Personality and Individual Differences 11: 273-285.

Nottebohm, F. (1981) A brain for all seasons. Science 214: 1368-1370.

Palumbi, S. R. (1999) All males are not created equal: Fertility differences depend on gamete recognition polymorphisms in sea urchins. Proceedings of the National Academy of Science 96: 12632- 12637.

Rakic, P. (1988) Specification of cerebral cortical areas. Science 241: 170-176.

Rooney, A. P. & Zhang, J. (1999) Rapid evolution of a primate sperm protein: Relaxation of functional constraint or positive Darwinian selection? Molecular Biology & Evolution 16: 706-710.

Rushton, J. P. & Ankney, C. D. (1996) Brain size and cognitive ability: Correlations with age, sex, social class, and race. Psychonomic Bulletin & Review 8: 21-36.

Schmidt, J. V., Levorse, J. M. & Tilghman, S. M. (1999) Enhancer competition between H19 and IGF2 does not mediate their imprinting. Proceedings of the National Academy of Science 96: 9733-9738.

Storfer, M. (1990) Intelligence and giftedness: the contributions of heredity and early environment. Jossey-Bass.

Storfer, M. (1999) Myopia, intelligence and expanding human neocortex: Behavioral influences and evolutionary implications. International Journal of Neuroscience 98(3-4): 153-276.

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