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The Geschwind–Galaburda hypothesis proposes to..

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According to the Geschwind-Behan-Galaburda (GBG) hypothesis, ..

"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
centa. It is conceivable that some maternal genes not shared by the offspring have greater effects on females fetuses. Thus, the testosterone to which female fetuses are exposed comes predominantly from maternal tissues, whereas males produce it themselves in high quantities. In the study of Nichols and Chen (1981) sex hormones given to mothers were associated with a higher rate of hyperactivity in female offspring than in males." (Geschwind & Galaburda 1987: 133-134, Cerebral Lateralization)

Dyslexia and Neuroscience: The Geschwind-Galaburda Hypothesis, 30 Years Later.

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 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."
(Geschwind & Galaburda 1987: 135-6, Cerebral Lateralization)

"A corollary of our hypothesis is that hormonal effects on the brains of offspring may vary with the time of conception. The activity of the pineal gland changes seasonally with alterations in day length. As a general rule, during the dark winter months the pineal becomes active and suppresses both ovaries and testes, whereas in the summer it is inactive and sex hormone levels are higher. For this reason many animals bear young in the spring, an advantageous situation since temperature and food supplies are more suitable for survival. An example of such seasonal modulation of hormonal effects on the brain is observed in the HVc nucleus of the singing bird (Nottebohm 1981). This description of pineal physiology is, however, somewhat oversimplified. An animal's sensitivity to light may vary through the year. Gonadal hormones may thus become activated in the spring, but as a result of loss of sensitivity to light over the summer hormone levels may diminish as fall approaches. Despite these facts, day length is a powerful influence. Thus, steers increase their weight more rapidly in the winter when artificial light is supplied to lengthen the day. This light-enhanced growth of muscle mass does not take place if the bull is castrated, suggesting that the effect of light is mediated through a rise in testosterone effect (Tucker and Ringer 1982).....If pineal effects on sex hormone levels are important, then the birth months of lefthanders, and of those with learning disorders, might not be uniform throughout the year, since fetuses conceived at different seasons might be subjected to very different hormonal environments. These effects should differ in the Northern and Southern Hemispheres and at the equator, although other factors, such as variations in the ethnic composition of populations, would also have to be considered. Data are still very sparse. Badian (1983) found that in males born in each of the six months beginning in September, the rate of nonrighthandedness was higher than that found in any of the other six months, but no clear trend was observed for female births." (Geschwind & Galaburda 1987: 116-7, Cerebral Lateralization)

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According to the Geschwind-Behan-Galaburda (GBG) hypothesis, prenatal testosterone (T) causes a slowing in the development of the left brain with a consequent compensatory growth in the right brain, creating a reverse organisation of the cerebral lateralisation. That is, left- and right-handedness might be associated with high and low prenatal T levels, respectively. To test thishypothesis, the relations of T levels (umbilical cord blood) to grasp-reflex strengths were studied in human neonates. Handedness was assessed by measuringthe grasp-reflex strengths from the right and left hands in 10 trials from each hand alternatively. There were two handedness groups: right-handers (R-L significantlygreater than zero) and left-handers (significantly smaller than zero). Contrary to the GBG model, the mean free T concentration was found to be significantly higher inright-handers than left-handers for males and females. There was no significant difference in the total T levels between right- and left-handers. Free T concentrations positively correlated with R-L grasp-reflex strengths, i.e. right-handedness increased as T increased, and left-handedness increased as T decreased. Contrary to these positive correlations, T negatively correlated withthe grasp-reflex strengths from the right and left hands. These results partly supported the GBG hypothesis for this spinal-motor-asymmetry model. Total T did not significantly correlate with grasp-reflex strengths. The results suggest that prenatal T may at least play a role in prenatal determination of spinal motor lateralisation, with a possible consequent upward regulation of cerebrallateralisation.

"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)

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American behavioral neurologist Geschwind–Galaburda hypothesis , laterality hypothesis Wernicke–Geschwind model …
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