|Norman Geschwind & R. Galaburda
Cerebral Lateralization: Bibliographical Excerpts
|"The term anomalous dominance refers to those in whom the pattern differs from the standard form. There is no sharp cutoff point at which one can speak of a shift from standard to anomalous dominance. Our rough estimate is that anomalous dominance will be found in approximately 30% to 35% of individuals, roughly the percentage in whom the planum temporale is not larger on the left side. It is important to stress anomalous dominance rather than left-handedness. According to Annett's formulation, lefthanders comprise about half of those in whom handedness is random. She estimates that random handedness is present in 18% of the population, of whom about half, or 9%, will be lefthanded." (Geschwind & Galaburda 1987: 70, Cerebral Lateralization (930) The Genetical Theory of Natural Selection. Oxford. Clarendon Press pp. 145)
"Several homosexuals have written to us suggesting that there is a high rate of lefthandedness in this population, but no study of this claim has yet been reported. A high rate of nonrighthandedness in this population may seem at first to be difficult to explain in the light of some animal experiments. Ward and Weisz (1980) and Dorner, Gotz, and Docke (1983) have shown that, in rats, stress in midpregnancy causes the male offspring to have permanently low free testosterone levels and homosexual behavior. Dorner has reported low free testosterone in human homosexuals, but no other group has yet confirmed this. His group has also reported a higher rate of stress in pregnancy in mothers of homosexuals than in those of controls (Dorner et al. 1983). Low free testosterone has been found in male temporal lobe epileptics in whom altered sexual behavior, including hyposexuality, is frequently seen. The low testosterone level was independent of drug therapy (Toone et al. 1983). If the situation is the human is similar to that in the rat, then one would arrive at the apparently paradoxical conclusion that a group with low free testosterone levels in adult life should have a high rate of anamalous dominance. The answer is, we believe, given by the experiment of Ward and Weisz (1980) showing that when the pregnant rat is stressed, testosterone first rises to higher than normal levels in male fetuses and then drops to permanently low levels. Infants with Klinefelter syndrome may also have very high testosterone in cord blood, becoming hypogonadal only later on. Handedness would, of course, be determined by the level in fetal life, not by adult levels. Netley and Rovet (1982) have recently reported an elevated rate of lefthandedness in Klinefelter syndrome." (Geschwind & Galaburda 1987: 175, Cerebral Lateralization)
"The time of conception is another nongenetic random variable that may well significantly influence laterality. Seasonal effects have often been considered narrowly. The fact that schizophrenics are more likely to be born in January than July, a finding documented repeatedly has often been interpreted as a result of increased susceptibility of newborn infants to virus infection in the winter. There are many other possibilities, however. Consider, for example, changes in sex hormones with day length. The pineal gland, activated in the dark months, tends to suppress gonadal hormonal production. When it is suppressed, during periods of long days, sex hormones rise. We have already alluded to Badian's (1983) report of a higher rate of nonrighthandedness in males conceived from December through May (days being shortest on December 21 and increasing in length for the following six months). A pineal role in laterality has no direct experimental support, but it certainly deserves study."
It is possible that schizophrenia is more common in individuals who have spent the first six months of pregnancy under maximal hormonal influences. Mental defectives are also more likely to be born at the beginning of the year. On the other hand, many extensive studies of the birth months of eminent people have shown that they too tend to be born predominantly early in the year; even more consistently, the rate of such births is low in the midsummer months of July and August (Peterson 1979). (In all of these studies the data have been corrected for the normal yearly pattern of births.)" (Geschwind & Galaburda 1987: 219-20, Cerebral Lateralization)
"The fundamental pattern of the brain thus appears to be asymmetrical, with the same pattern of asymmetries found in most adults. There are, however, influences in pregnancy that tend to diminish the extent of left-sided predominance, at least in the regions involved in handedness and language, and thus secondarily to result in larger regions on the right side. As noted earlier, our hypothesis is that some factor related to male sex, perhaps testosterone or some closely related factor, is the most likely candidate. The net effect of these intrauterine influences is to produce a shift from left predominance to symmetry, and in a smaller number of cases to modest right predominance." (Geschwind & Galaburda 1987: 46, Cerebral Lateralization)
"Environmental factors can be an important source of nongenetic influences on laterality. Since the effect of a gene is to play a role in some form of chemical reaction, it is not surprising that genetic determination is not absolute. Every chemical reaction can be modified by alterations in pressure, temperature, pH, light, the presence of other substances, the availability of chemical precursors, and the rate at which products are removed. With growing sophistication of molecular genetics, it has become increasingly clear that nongenetic effects can play a powerful role; methylation, for example, has been shown to suppress expression of many genes. We will now consider some of the random effects that might modify lateralization. One implication of our hypothesis is that even if the genetic endowment of any particular fetus were known precisely, it would not be possible to make predictions concerning the distribution in a population basis. One of the reasons for this relative freedom from genetic determination is that if hormones do play a role in determining laterality, then the effects of testosterone or related substances on the developing brain will be modified by factors not under the control of the fetal genes. Androgens are produced not only by fetal testes and the placenta but also by the maternal ovaries, adrenals, and nonglandular tissues. The fetus can be influenced by the actions of many of the unshared maternal genes. It is reasonable to expect that if a fertilized ovum were transplanted into the uterus of an unrelated female, the final pattern of the brain would be quite different, because the brain would develop in an environment of hormones and other substances that would certainly differ in many respects. It might therefore be reasonable to take a different approach than usual to the genetics of many conditions. One should perhaps consider, not the genes carried by the offspring alone, but rather the genes of that organism existing or active only for the nine months of pregnancy; in other words, one should consider the mother and the fetus as a unit. This unit contains three groups of different genes: one paternal set present in the fetus, one maternal set present in the mother, and another maternal set present both in the mother and in the fetus. The situation is even more complex when dizygotic twins are involved, since the maternal-fetal unit will contain another group of paternal genes. The effects of substances produced by the mother will, however, be diminished by the capacity of the placenta to act as a barrier to some maternal hormones. The fetus is protected to a great extent form maternal testosterone, which is converted to estradiol by placental aromatase. Dihydrotestosterone, which is not aromatized and therefore crosses the placenta, is, however, usually present in the mother at much lower levels than testosterone. The protection from maternal testosterone is not complete, since offspring do show signs of masculinization when mothers are exposed to this hormone. In addition, progesterone administered to the mother may masculinize female fetuses. It is clear that the placental barrier is far from complete. Furthermore, it is likely that there are individual variations in the aromatizing capacity of the pla