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From Miller's paper:
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COHN, COHN, AND JENSEN ( 1988 ) reported evidence of a pleiotropic relationship between myopia and intelligence, and numerous other researchers (see Baldwin, 1981; Cohn et al., 1988; Curtin, 1985; Storfer, 1990 , pp. 383-386) have documented a correlation between intelligence and myopia. In the most striking, data on 157,748 Israeli Jewish males exhibited a strong positive association between myopia and intelligence, both verbal and nonverbal ( Rosner & Belkin, 1987). When extremely verbally precocious junior high school children (at the upper I in 10,000 level) were examined, 75% of them had myopia ( Benbow & Benbow, 1984 , p. 484:1986). The authors (1984, p. 484) commented, "We have as yet been unable to think of a plausible mechanism relating myopia to extreme intellectual precocity." The purpose of this article is to propose a possible mechanism, and to describe how it might be tested. Lubinski and Humphreys ( 1992 ) also reported a high incidence of vision defects among the mathematically gifted.
Both myopia and intelligence are considered to be subject to a large genetic influence. Karlsson ( 1978 , chap. 9 and 10:1991, pp. 39-45, 137-143) summarized in nontechnical language both the evidence for inheritance of myopia and for a correlation of myopia and intelligence. He ( 1978, p. 76; 1986) hypothesized that both myopia and intelligence might be affected by a single gene, which he estimated (from his data on California children) contributes about eight IQ points to intelligence. Teasdale, Fuchs, and Gold schmidt ( 1988 ) estimated the myopia effect to be seven IQ points in Danish draftees. The similarity in the magnitude of the effect is striking, because the data were collected from different populations and by different investigators. Plomin ( 1990 ) argues that no single major gene affecting intelligence has yet been isolated. This of course conflicts with Karlsson's claim.
Karlsson failed to exclude the possibility that the two genetic conditions might be correlated for some reason other than a pleiotropic relationship. Perhaps the myopes who left descendants were those who could compensate for the handicap of myopia through having sufficient intelligence to earn a living as craftsmen or clerks. Karlsson ( 1975 ) showed that high intelligence emerged by age 8 in students who were to become myopes, an age when very few students have yet developed myopia. This suggests the myopia was not producing greater learning by discouraging nonbookish activities and encouraging bookish activities.
Cohn et al. ( 1988 ) showed that not only was myopia more common among highly intelligent children but that myopia was more common among them than among their less talented siblings. A showing that myopia and intelligence were both heavily genetic and both often occurred in the same individuals might mean merely that certain families had more of the genes that caused these conditions. Either assortative mating (the myopic tending to marry the more intelligent for some reason) or ethnic stratification 1 could cause the genes for both IQ and myopia to be in the same family. If the effects were controlled by separate genes, there would be no tendency for the more intelligent sibling also to be the more myopic, but if one or more genes somehow lead to both intelligence and myopia (what is technically called a pleiotropic relationship), one would expect the more intelligent siblings also to be the more myopic, which is what was found by Cohn et al. A correlation caused by either assortative mating or ethnic stratification would not produce a correlation between myopia and intelligence in siblings.
Benbow ( 1986, 1988) showed that myopia was more common among her sample of extremely mathematically and/or verbally precocious students (top 1 in 10,000) than among the general population and that it was more common among these students than among their siblings, again suggesting that some genes affect both intelligence and myopia. The discovery of a pleiotropic relationship between myopia and intelligence raises the questions of how and why. On first glance, myopia and intelligence appear to be quite different phenomena. After all, the brain and the eye are different organs. Seeing and understanding are two different functions. However, the two organs are related in embryology. Most eye tissues originate as a brain outgrowth. Thus, some common genetic factors could affect both organs.
I hypothesized that a common genetic cause underlies the growth of both the brain and the eye. This could be a single gene coding for a single protein, but it could also be a substance affecting the growth of both the brain and the eyeball, whose quantity is affected by multiple genes. Large brains lead to high intelligences and large eyes to myopia. I was led to this hypothesis through research on the correlation between head size and intelligence and a statement in an encyclopedia that large eyes tended to be myopic. However, I have since discovered that Curtin ( 1985 , p. 12) has attributed to H. von Moers-Messmer, writing in 1940, a hypothesis that the intelligence-myopia correlation was "even ontogenic wherein the overdeveloped eye is part of the overdeveloped brain." The evidence for an eye size-myopia relationship and a brain size-intelligence relationship is briefly reviewed here.
Eye Size and Myopia
This discussion is based on Curtin's standard textbook, The Myopias ( 1985 ). By definition, myopia is a defect of the eye such that rays of light from a distant object come to a focus in front of the retina, rather than on it. The most common cause of this appears to be an enlargement of the eye. The axial diameter, relative to the other optical components, increases by more than is required to offset changes elsewhere in the eye (such as the lens and cornea). Where light entering the eye comes to focus depends on multiple factors. These include the length of the optical axis and the curvature of the lens and cornea.
erent dimensions of the eye appear to be under genetic control and are approximately normally distributed, except for axial length. However, normal refraction appears to be more common than would result if these different optical features of the eye were randomly selected and combined. The different features of the eye appear to be correlated in such a way as to make normal refraction the most common outcome. In particular, the curvature of the cornea typically decreases as the eye becomes longer and larger (thus moving the retina farther from the lens). The mechanism by which this occurs is not known but appears to involve the extent to which the image is out of focus on the retina. Unusually large and long eyes tend to be myopic.
Myopia has traditionally been considered by ophthalmologists to be an inherited condition, although there are those (especially among the optometrists) who argue for environmental causes, notably near work ( Young, 1975). Undoubtedly, part of the belief in a genetic causation arises simply from the fact that the proximate cause is to be found in the dimensions of the eye, and body dimensions are generally considered to be under genetic control. However, twin studies and studies of family resemblance show myopia to act like other inherited conditions. Summaries of the relevant studies can be found in Curtin ( 1985 , pp. 63-72) and in Francois ( 1961 , chap. 19).
The most powerful evidence for inheritance comes from twin studies, where very high concordance rates (almost unity) are found for monozygotic twins and much lower rates for dizygotic twins. Karlsson ( 1974 ) (supplemented with a few pairs from his own research) was able to locate reports of 106 monozygotic twin pairs with myopia in at least one twin. Of these, 100 pairs were concordant. In contrast, out of 41 pairs of dizygotic twins reporting myopia, only 12 were concordant.
In probably the best twin study, Sorsby and Fraser ( 1964 ) examined correlations between various optical parameters in 78 pairs of uniovular twins, 40 pairs of binovular twins, and 48 control pairs. Their general finding was that "the coefficients approach the values expected on the hypothesis of quantitative inheritance due to a number of genes with additive effects and without dominance: unit for the uniovular twins, .5 for the binovular twins, and zero for the controls" (p.47). This applied to data for the cornea, depth of anterior chambers, lens, and axial length, with the axial length showing the largest (though still very limited) tendency to depart from that expected on the basis of quantitative inheritance. The twin and family data explain why myopia is usually considered a predominantly inherited condition.
It should be noted that the twin data could be reconciled with a large role for environmental conditions (notably the extent of near work) if what was inherited was not merely the dimensions of the eye under normal conditions but a tendency to seek out certain environments, such as those that involve near work. For example, those who inherited high intelligence might be led to do more studying, which could then lead to higher myopia. Indeed, Chen, Cohen, and Diamond ( 1985 ), in a study of 361 Taiwanese twins, found that monozygotic twins showed a highly significant tendency (p @ .001) to be more concordant in the amount of studying and reading done (72% concordant) than dizygotic twins (52.3%), suggesting substantial heritability in behavior. Considering only twins who were concordant in near work, the monozygotic twins were 83.6% concordant, whereas the dizygotic twins were only 59.5% concordant, showing substantial genetic influence after controlling for behavior (p @ .001). Statistically significant effects for the amount of near work were shown by considering only monozygotic twins, who of course have the same genes, and who were found to be 92.2% concordant for myopia when they were also concordant for the amount of near work, versus 79.3% concordant for myopia when they were discordant for the amount of near work.
Conceivably, if one believed that intelligence was predominantly determined by the amount of studying done, what was inherited could be a personality characteristic that led to extensive studying. This would then produce both intelligence and myopia. However, this sounds implausible, although possible. 3 Because there are monozygotic twins who are discordant for myopia (as well as correlations of less than unity in eye dimensions), there clearly are nongenetic conditions (possibly near work) that can contribute to myopia.
However, a German language study by Jancke and Holste ( 1941 ) was summarized by Curtin ( 1985 , p.65): "They studied MZ twins with significantly different patterns of near work and found that the volume of near work had little if any effect on the refraction. They also noted that discordance in MZ twins could not be attributed to near work." Curtin also summarized a Danish master's thesis (by Juel-Nielson): "The refractive states of MZ twins separated shortly after birth and having disparate near work habits did not display significant differences" (p. 65). Of 17 separately raised monozygotic twins in which a refractive error was recorded, 75% were concordant for refractive error ( Knobloch, Leavenworth, Bouchard, & Eckert, 1985). The pattern of concordance for refractive error was similar to that in the sample of twins raised together and studied by Sorsby and Fraser ( 1964 ). Thus, evidence supporting the theory that most cases of myopia have genetic causes, or a genetic predisposition, appears solid. 4 Of course, the evidence that the axial diameter of the eye is subject to genetic influence does not imply that environmental factors do not also affect it. Indeed there is evidence suggesting they can. 5
In a large longitudinal study of children in Ojai, California, Hirsch (1964) found that the refractive state of the eye at ages 5-6 predicted the refractive state at ages 13-14. The heavy close work of the school years is still in the future for children of ages 5-6. However, for both the brain and the eye, most of the growth in size has been completed by ages 5-6. For instance, the eye has reached a length of 21-22 millimeters by the age of 6 years versus about 24 millimeters for the eye in teenagers ( Grosvenor, 1991 , p. 143). And although differences in the small remaining eye growth that occurs during the school years (possibly influenced by differences in the extent of near work) probably contribute to causing some eyes to be myopic, the starting distribution of eye sizes also appears to play a major role. Thus, any factor that causes a correlation of brain size and eye size by this age could also lead to a correlation between myopia and intelligence at later ages.
Curtin divided myopias into categories partially by the degree of refractive error and partially using the associated complications. The eyes with the smallest degree of myopia are referred to as suffering from physiologic myopia, also known as low, simple, or school myopia. Of this Curtin stated (p. 171), "In physiologic myopia each component of refraction lies upon its normal distribution curve. The postnatal development of these eyes is normal; they are rendered myopic because of a correlation failure between the total refractive power (corneal and lens) and a normal axial diameter."
His next most serious type was called intermediate myopia or medium myopia, of which he stated (p. 173), "In intermediate myopia there is an expansion of the posterior segment of the globe that is in excess of normal ocular growth. This ocular elongation is also beyond the range within which neutralizing effects of reduced corneal and lens power can generally be expected to be effective. The precise manner in which this expansion occurs is unknown." Most critical, "Pathologic myopia is defined as that ocular disease in which a number of serious complications are associated with an excessive axial elongation of the eye" (Curtin, p. 237). This is usually found in the minority of eyes with unusually long axial diameters.
Curtin focused on the axial diameter because that is the dimension of the eye that is directly relevant to refractive power, with myopia correlated with higher axial diameters. The eyes with long axial diameters typically are myopic, since the other eye characteristics do not adjust sufficiently to compensate for the greater length. Eyes with long axial diameters appear to be both absolutely larger than other eyes and also more elongated. The greater size of the myopic eye is very apparent in his color Figure 13-1, which he labeled: "The normal eye compared with the distended, highly myopic eye." In his discussion of pathology (p. 247) he stated: "The highly myopic eye shows enlargement of all diameters but principally the anteroposterior." Very striking is a reproduction of "the classic illustration of Heine in which the highly myopic globe is superimposed in section upon the normal. The anterior segment appears identical, but the posterior segment, besides the obvious expansion, shows scleral thinning in the myopic specimens." This diagram, and others reproduced, shows the myopic eye being bigger because of an enlargement of the posterior part of the eye, causing its axis to get longer and the shape to become more elongated. Curtin goes on to argue against the widespread belief "that the anterior segment is normal in pathologic myopia," but his comments are not relevant to the discussion here.
Because the exact mechanism by which the myopic eye gets larger is not known, one cannot be certain its growth in size is caused by a factor that might also affect the brain, but this interpretation appears plausible. Wildsoer and Pettigrew ( 1988 ) interpreted experiments using a putative neurotransmitter, kainic acid, as "supporting the hypothesis that growth of the anterior and posterior segments of the eye may be independently regulated." Kainic acid damage to the retina (which can be described as an extension of the brain tissue) appears to differentially affect the growth of the anterior and posterior segments of the eye in a complex way. This observation makes it more plausible that at some stage a common growth factor may affect the growth of both the brain and the eye.
Young ( 1975 , p. 23), in a paper arguing for an environmental explanation for myopia, reported an experiment in which monkeys were subjected to diets so low in protein "that the four- or five-year-old monkey looked as if it were an infant monkey. Yet the eyes had developed in a normal fashion. . . ." He argued that "these results support the suggestion that the nature of the nervous system is such that any protein available will be utilized by the brain and its units such as the eyes in preference to virtually any other system in the body." This supports the idea that there is a common mechanism controlling the growth of both the brain and the eye. According to Perkins ( 1981 , p. 121), "There are two main theories to account for the enlargement of the globe in myopia; the biological theory postulates that it is due to an overgrowth of the retina while the mechanical theory maintains that the eye enlarges as a result of an increased stress on the scleral envelope." In the scleral stress theory the growth of the eye during infancy and childhood is due to an increased production of the vitreous matter inside it, which can be accommodated only by an increase in volume, stressing the sclera. However, it is not known what determines the production of the vitreous matter or the extent to which the eyeball should be viewed as a container of fixed (or almost fixed size) under genetic control or as a more flexible container whose size adjusts to match the material put into it (as a balloon expands).
The pressure inside the myopic eye is typically higher than in nonmyopic eyes, and one could imagine a mechanism under which this greater pressure led to the expansion of the eye, with the expansion taking the form of expanding the posterior part simply because growth was induced along the equator of the eye. As Kelly ( 1981 , p. 110) (who himself argues for viewing myopia as being due to increased ocular pressure expanding the eye) put the latter theory, "The accepted cause for young myopia is overgrowth of the dominant tissue, the retina. So the choroid and sclera must go on growing until the retina stops." Because the retina is an extension of the nervous system, a common genetic factor affecting both is especially plausible in the latter case.
Curtin noted that "ocular growth most closely resembles the growth of the brain" (p. 97). By this he meant that the eye grows rapidly prenatally and in early infancy, and then slows greatly, very roughly paralleling that of the brain, especially that of the midbrain. "However, there is little doubt that there is a rapid early volumetric growth of the eye, which most closely resembles that of the spinal cord and midbrain. The cerebrum and cerebellum lag at first but later exhibit an accelerated growth pattern" (Curtin, p. 98). This makes it a little more plausible that the growth of the two organs could be under common genetic control.
From a purely geometric viewpoint, enlarging or shrinking all parts of the eye symmetrically would not cause an eye that was not myopic to become myopic. Thus, the increased-size hypothesis does require that the increased size of the eyeball not be accompanied by a proportionate increase in the dimensions of the lens, cornea, and so forth, at the front of the eye. The empirical data do show very strongly that eyes with unusually long axial diameters are typically myopic, implying that the enlargement of the eye was not proportionate in these extreme cases.
As an example of the empirical findings, Gernet ( 1981 ) reported a correlation of -.845 in 608 eyes between refraction and axial length and a slightly stronger one of -.870 between refraction and vitreous length. The correlation is negative because refraction in diopters is a negative number in myopia. The number of negative diopters grows larger as the eye becomes more myopic.
The explanation for the lack of proportionality may be related to the fact that the different parts of the eye arise from different embryonic tissues. The cornea and lens develop from the surface ectoderm of the embryo, whereas the retinal tissues develop from the neural ectoderm ( Barber, 1955). The retinal tissue in turn is an outgrowth of the brain. The embryonic brain develops two optical stalks that grow outward. The stalks become the optic nerves, and their ends, the retina. The skin under which the developing eyes lie becomes transparent, becoming the lens and cornea. These differences in embryonic development of parts of the eye make it plausible that the growth factor affecting the cornea and lens could be different from that which affects the eyeball proper and that the eyeball could respond to factors also affecting the brain.
The theory that the expansion of the eyeball is due to an increase in the amount of the vitreous matter contained within it could explain a divergence between the axial diameter and the properties of the front of the eye. There is no apparent reason why an expansion of the eyeball caused by an increase in the quantity of vitreous matter should produce a proportionate enlargement of the front of the eye. In contrast, if the eye was thought of as an organ that grew proportionately in all its components (perhaps each component grew at the same rate as long as a growth factor was present), there would be no reason for the refractive properties to depend on the size of the eye.
Curtin might put this theory of the origins of certain myopias under the category of ectodermal -- mesodermal growth disparity (discussed on p. 63). He rejected earlier versions of such theories of the etiology of myopia but went on to say that "this theory could be revised to postulate the formation by the retina of an excess of vitreous or vitreouslike substance that expands the posterior sclera. Such expansion might take place at the oraequatorial zone where normal postnatal expansion is seen to occur; it may conceivably affect the entire posterior sclera, or, in the presence of a localized weakness in the sclera, a posterior staphyloma could ensue. In laboratory studies involving the lid-sutured animal, myopia genesis may take place in this way."
The lid-sutured animal experiments referred to show that when animal eyelids are sewn shut, myopia develops. This myopia appears to be due to an increase in the axial diameter rather than to changes in other optical parameters ( Smith, 1991; Wallman, 1991). Particularly striking is a diagram provided by Raviola and Wiesel ( 1985 ) showing the eye of a monkey whose eyelids had been sewn shut superimposed on the normal monkey eye. The front parts of the eye are the same, but the eyeball is much larger in the lidsutured eye Other experimental procedures that produce myopia also appear to operate by causing an increase in axial diameter. This provides some of the strongest evidence that axial diameter increase can be regarded as a cause of myopia. They also support the idea that there is a feedback mechanism in the eye, by which the quality of the image affects the growth of the eye. This is consistent with the hypothesis that near work plays a role in the etiology of at least some myopia.
So far it has been argued that there is a correlation between intelligence and axial length of the eye. The argument has been indirect, depending on the correlation between intelligence and myopia and the correlation between myopia and the axial length of the eye. The argument has had to take this form because most studies correlated the extent of myopia (easily measured) with intelligence without making the more difficult axial length measurements. However, one study of Japanese school children (Otsuka, cited by Baldwin, 1981 , p. 520) reported "the result that a person with a better scholastic record has a longer axial length and a smaller refractive power of the lens than a person having a poor scholastic record. The refractive power of the cornea was virtually the same for both groups. Furthermore, the school records had a significant, but not so intimate correlation to the refractive states as compared to axial length." The results of this study increase the probability that the myopia/intelligence correlation is indeed due to a correlation of intelligence with eye size (as measured by axial length).
Some indirect evidence for the plausibility of a growth factor playing a role in the etiology of myopia is provided by a number of studies that show a height/myopia correlation (see Baldwin 1981 , p. 521, for citations). For example, Teikari ( 1987 , p. 674) found that, among twins, not only were the male myopic subjects taller but, among the twins discordant for myopia, "the partners with myopia were found to be taller than their non-myopic co-twins at the ages of 10, 15, and 20 years in males. Among females there was no difference." The correlation could be caused by a growth factor adding to both the size of the body and the size of the eye. 6
Rates of growth and myopic change have been found to be correlated, a finding consistent with a growth factor directly affecting the rate of growth in eye size as well as the rate of growth in height. Goss, Cox, Herrin-Lawson, Nielsen, & Dolton ( 1990 ) found, in a cross-sectional study, that the axial axis of the eye kept growing in myopic children beyond the age at which ocular growth stopped in nonmyopic children. They stated, "One interpretation of the data from the present study is that ocular axial elongation in childhood myopia progression continues to about the same time as the cessation of general body growth" and that "a number of investigators have suggested that
release of biochemical growth factors is responsible for increases in axial length in childhood myopia progression. If these growth-regulating substances are synergistic with human growth hormone or somatomedin, childhood myopia progression would be expected to stop or slow down when the adolescent growth spurt stops."
Gardiner ( 1955 ) found that the rate of growth in children is greater for active myopes (i.e., those whose myopia is increasing) than for stationary myopes. This again suggests that whatever causes growth of the eye also has effects on nonocular parts of the body.
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Miller, E. (1992) On the Correlation of Myopia and Intelligence. Genetic, Social, and General Psychology Monographs, 118: 361-383.
-GFA
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05-21-2003, 10:03 PM
Re: Myopia and g
