Library of Excerpts
Testosterone, Estrogen, Related Hormones and Heterochronic Patterns
"The evolution of the relationship between cortisol and testicular androgens was verified on two teams of respectively 10 and 9 male subjects (average age 34) running 100 km races in an average time of 14 hours. When compared to a control population of the same age, these trained athletes exhibited reduced testicular androgen levels (T and DHT) and increased adrenal androgen (triangle 40 and cortisol levels with no significant alteration of LH. The period of recovery is characterized by rapid return to normal of the hormonal parameters whereas testosterone levels continue to increase in the following days. This hormonal picture, which reappears under certain pathological situations or when subjects are exposed to heavy stresses, seems to prove that the testicular androgens could be, both by their metabolic and psychic action, one of the limiting factors of physical aptitude to sustained effort." (Morville, R., Pesquies, P.C., Guezennec, C.Y., Serrurier, B.D., Guignard, M. (1979) Plasma variations in testicular and adrenal androgens during prolonged physical exercise in man. Annales D. Endocrinlogie (Paris) 40 (5): 501)
"Some authors actually describe an increase in the testosterone level after a short maximal exercise....Others, on the contrary, report a drop in plasma testosterone after less intense, but prolonged efforts..." (Morville, R., Pesquies, P.C., Guezennec, C.Y., Serrurier, B.D., Guignard, M. (1979) Plasma variations in testicular and adrenal androgens during prolonged physical exercise in man. Annales D. Endocrinlogie (Paris) 40 (5): 502)
"The drop is testicular androgen concentrations (dihydrotestosterone and especially testosterone) is not related at all to nycthemeral fluctuations (29.30). This drop is observed at km 50 but is more pronounced at the arrival. It confirms the results obtained in previous studies on prolonged efforts (19,21). This drop in testosterone levels is rapidly corrected, on the following day, and during the recovery phase and increase in testosteronemia is observed, as if the lower testicular reactivity to effort was followed by a phase of increased secretion, parallel to clinical recovery. ... Two mechanisms can account for a lower gland production of the hormone: -- a persisting significant rise in the levels of circulating epiniphrine could induce a drop in the plasma levels of testosterone by means of reduced testicular production, with unchanged global metabolic clearance (32); --- hypercortisolemia, under the condition that it is prolonged enough, would reduce the plasma levels of testosterone (33,34). This normal profile (hypercortisolemia, hypotestosteronemia) is described in other stress conditions (35,36) and in Cushings's syndrome (37,38,39).: (Morville, R., Pesquies, P.C., Guezennec, C.Y., Serrurier, B.D., Guignard, M. (1979) Plasma variations in testicular and adrenal androgens during prolonged physical exercise in man. Annales D. Endocrinlogie (Paris) 40 (5): 506) [note:If an inverse relatioship exists between T and sperm production, then a drop in T during prolonged excersise may mean the body is reving up to make more sperm.]
"Comings (1994) ranted Tourette Syndrome (TS) probands, their affected relatives, their unaffected relatives, and controls (in this order), to achieve ranking on assumed loadings for genes for TS. He found this ranking to yield highly significant correlations with responses to questions on (high) sex drive, and on inclinations to bisexuality, homosexuality, exhibitionism, pedophilia, fetishism, aversion to sex, and aversion to being touched. He concluded that "these studies suggest that genetic factors play a much greater role in a wide range of forms of sexual expression than previously thought." There are grounds for suspecting that one of these proposed genetic factors in hormonal, i.e., testosterone: 1) TS is 3-4 times more commonly diagnosed in men than in women (Shapiro et al., 1988); 2) Leckman and Scahill (1990) reported two male TS patients whose symptoms were exacerbated by anabolic steroids; and 3) Meikle et al., (1986,1988) have established that there is substantial heritability in men's levels of testosterone and other androgens. An unexplained curiosity of Comings' data is that TS patients report both high levels of sex drive and of aversion to sex. The point is reminiscent of data on patients with prostatic cancer, another condition suspected of being partially caused by androgens.: (James, W.H. (1995) Sexual expression, genetics, and testosterone in Tourette syndrome. American Journal Medical Genetics 60 (6): 593) (note: see Comings rebuttel of T theory in his 'response to letter by william h. james]
"We conclude that highly trained male athletes, like their female counterparts, may have a deficiency of hypothalamic gonadotropin-releasing hormone. This condition may be caused by the prolonged, repetitive elevations of gonadal steroids and other hormones known to suppress gonadotropin-releasing hormone secretion that are elicited by their daily exercise. [p. 411] Plasm testosterone concentrations increased to a similar extent in the runners and controls. There was no significant difference in either peak testosterone concentrations (12.5 + - 1.19 ng per milliliter in the runners vs. 12.0 + - 1.23 in the controls), area under the curve (576 + - 119 ng per mililiter times hours in the runners vs. 603 + - 92.4 in the controls), or the pattern of testosterone response.[p.413] Plasma testosterone increased significantly from a mean basal value of 5.4 + - 0.5 ng per milliliter to a peak of 8.76 + - 0.66 ng per mililiter 40 minutes after the start of the run, and it remained elevated for the duration of the run. The resting testosterone levels (4.55 + - 0.6 ng per mililiter) were reached by two hours after discontinuation of the exercise. The mean plasma gonadotropin concentrations did not change during or after the two-hour run. There was also no signigicant difference between the luteinizing hormone frequency or amplitude in the entire six-hour period before the run and that in the six-hour period after the run.[p. 413-414] Surprisingly, inspite of these abnormalities, the serum testosterone concentrations in the runners were normal. In contrast, female athletes with hypothalamic amenorrhea have low serum levels of estogen.[p. 414-415] However, profound suppression of testosterone production and of spermatogenesis may occur in men undergoing extremely intense physical training.[414] Similarly, short-term excercise in men not involved in physical training programs was followed by a decrease in levels of plasma gonadotropins and testosterone, thus confirming the suppression effects of exercise on the reproductive system.[p. 416]" (MacConnie, S.E., Barkan, A., Lampman, R.M., Schork, M.A. & Beitins, I.Z. (1986) Decreased hypothalamic gonadotrophin-releasing hormone secretion in male marathon runners. New England Journal of Medicine 315: pp. 411-417)
"Conjecturing as to physiological mechanisms, one hypothesis implicates testosterone and other sex hormones. Freeman (1934) found differences in the weight of the hypophysis (pituitary) with blacks having the heaviest (800 mg), whites being intermdiate (700 mg), and Orientals the lightest (600 mg). The pituitary is directly involved with the release of gonadotropins which stimulate the testicles and ovaries in their functions (the release of testosterone, estradiol, and progesterone on the one hand, and sperm and eggs on the other)." (Rushton, J.P. & Bogaert, A.F. (1987) Race differences in sexual behavior: Testing an evolutionary hypothesis. Journal Research in Personality 21(4): pp. 546)
"It is known that women who smoke have an earlier menopause than those who do not. (Whitley et al., 1981; Buchman et. al., 1978)" (MacMahon, B., Trichopoulos, D., Cole, P. & Brown, J. (1982) Cigarette smoking and urinary estrogens. New England Journal of Medicine 307: pp. 1062)
"As compared with nonsmokers and exsmokers, smokers had substantially and significantly lower levels of all three major estrogens in the luteal phase of the menstrual cycle. ... In follicular specimens estrogen concentrations for smokers did not differ significantly from those of nonsmokers. However, in the luteal specimens current smokers had levels about one third below those of nonsmokers or exsmokers for all three estrogens. The differences were significant for each estrogen and for the total." (MacMahon, B., Trichopoulos, D., Cole, P. & Brown, J. (1982) Cigarette smoking and urinary estrogens. New England Journal of Medicine 307: pp. 1063)
"The most intriguing question raised by these data is whether reduced estrogen levels in smokers are responsible for a possible reduced risk of breast cancer. The epidemiologic evidence linking high estrogen levels to a high risk of breast cancer has accumulated rapidly in recent years (Numoff et al., 1981; MacMahon et al., in press; MacMahon et al., 1982 in press), and the possiblity that a one-third reduction in luteal estrogen stimulus produces a 20 percent reduction in the risk of breast cancer is credible. ... An increased risk of osteoporosis or osteoporotic fractures has been reported among women who smoke. In view of the evidence that exogenous estrogens protect against such fractures, is is also possible that the mechanism whereby smoking increases the risk that they occur, if it does, is through a reduction in endogenous estrogens." (MacMahon, B., Trichopoulos, D., Cole, P. & Brown, J. (1982) Cigarette smoking and urinary estrogens. New England Journal of Medicine 307: pp. 1064)
"The H-Y antigen, determined by a gene on the Y chromosome is the principal determinant of maleness and hence of testosterone levels..."( McManus, I.C. & Bryden, M.P. (1991) Geschwind’s theory of cerebrel lateralization: developing a formal, causal model. Psychological Bulletin 110 (2): 240)
"In obese men and women abdominal body fat distribution is characterized by pronounced hyperinsulinemia. However, women with abdominal fat distribution may have increased percentage free testosterone fraction and reduced sex hormone-binding globulin (SHBG) concerntrations in periferal blood, and several lines of evidence support the hypothesis that hyperinsulinemia and sex hormone abnormalities may be causally related. In fact, a significantly positive correlation between the degree of hyperandrogenism and that of hyperinsulinemia has been found in hyperandrogenized obese and non-obese women. Moreover, in vitro studies have shown that insulin seems to act as an amplifier of luteinizing hormone (LH) effects by stimulating ovarian androgen synthesis. On the contrary, obesity in men may be characterized by reduced testosterone and SHBG concentrations with or without subnormal gonadotropin levels. The underlying mechanisms leading to these abnormalities have not been clarified, although it has been suggested that hyperestrogenemia due to increased aromatizaton of androgens in the adipose tissue may play a role by interacting with gonadotropin regulation." (Pasquali, R., Casimirri, F., Cantobelli, S., Melchionda, N., Labate, A.M.M., Fabbri, R., Capelli, M., and Burtoluzzi, L. (1991) Effect of obesity and body fat distribution on sex hormones and insulin in men. Metabolism 40: pp.101)
"Compared with controls, obese men presented significantly lower levels of total (357 + - 132 v 498 + - 142 ng/dl; p < .005) and free testosterone (14.2 + - 2.9 v 17.1 + - 2.6 pg/mL; p< .05) and sex hormone-binding globulin (SHBG; 41.7 +- 31.9 v 66.2 + - 18.6 nmol/L; p < .001) without any significant difference on the other sex steroid or on gonodrotropin concentrations." (Pasquali, R., Casimirri, F., Cantobelli, S., Melchionda, N., Labate, A.M.M., Fabbri, R., Capelli, M., and Burtoluzzi, L. (1991) Effect of obesity and body fat distribution on sex hormones and insulin in men. Metabolism 40: pp.101)
"Recently, it was reported that breast cancer may be associated with reversed cerebral asymmetry and hand preference. (Olsson and Ingvar 1991; Sandson et al. 1992; Hsieh et al. 1992). Independently, other researchers have suggested that increased levels of estrogens in pregnancy (Trichopoulos 1990), which are associated with higher birth weight (Gerhard et al. 1987; Petridou et al. 1990; Ekbom et al. 1992), may increase the risk of breast cancer in the offspring (Trichopoulos 1990)." (Petridou, E., Flytzani, V., Youroukos, S., Lee, I.M., Yen, Y.Y., Yong, D., Trichopoulos, D. (1994) Birth weight andhandedness in boys and girls. Human Biology 66 (6): 1094)
"Thin men have higher testosterone levels than do heavier men (10). Because the white men in this study were, on average, 11 pounds lighter than black men despite similar mean heights, we might expect white to have somewhat higher testosterone levels. In fact, simultaneous adjustment for weight and age exagerated slightly the differences in testosterone levels between the two groups.....Although alcohol intake is known to decrease circulating testosterone (13) when measured in close proximity to ingestion, there is no evidence of any long-lasting effect (10). .... Prostate cancer is reportedly much less common (4,17) and testosterone levels are reportedly substantially lower (18) in Africanblacks compared to U.S. blacks. (Ross, R., Bernstein, L., Judd, H., Hanisch, R., Pike, M., and Henderson, B.E. (1986) Serum testosterone levels is healthy young black and white men. Journal National Cancer Institute 76: pp. 47)
"Blacks in the United States have the highest prostate cancer rate in the world and nearly twice that of whites in the United States. The 2:1 black-to-white ratio in prostate cancer rates is already apparent at age 45 years, the age at which the earliest prostate cancer cases occur. This finding suggests that the factor(s) responsible for the difference in rates occurs, or first occurs, early in life. Testosterone has been hypothesized to play a role in the etiology of prostate cancer, because testosterone and its metabolite, dihydrotestosterone, are the principal trophic hormones that regulate growth and function of epithelial prostate tissue. This report gives the results of assays of circulating steroid hormone levels in white and black college students in Los Angeles, CA. Mean testosterone levels in blacks were 19% higher than in whites, and free testosterone levels were 21% higher. Both these differences were statistically significant. Adjustment by analysis of covariance for time of sampling, age, weight, alcohol use, cigarette smoking, and use of prescription drugs somewhat reduced the differences. After these adjustments were made, blacks had a 15% higher testosterone level and a 13% higher free testosterone level. A 15% difference in circulating testosterone levels could readily explain a twofold difference in prostate cancer risk. ... For this study we solicited 50 white and 50 black volunteers at two Los Angeles area universities: the University of Southern California (USC) and California State University of Los Angeles (CSLA)" (Ross, R., Bernstein, L., Judd, H., Hanisch, R., Pike, M., and Henderson, B.E. (1986) Serum testosterone levels is healthy young black and white men. Journal National Cancer Institute 76: pp. 45)
[abstract] "An antiestrogenic effect of cigarette smoking has been suggested, principally on the basis of data on premenopausal women. We examined the relation between cigarette smoking and endogenous sex-hormone levels in a population of 233 white, postmenopausal women 60 to 79 years of age. Current cigarette smokers had significantly higher mean plasma levels of the adrenal androgens dehydroepiandrosterone sulfate and androstenedione than nonsmokers. Mean levels for smokers and nonsmokers were 3.1 mumol per liter (116 micrograms per deciliter) and 2.3 mumol per liter (86 micrograms per deciliter), respectively (P less than 0.001), for dehydroepiandrosterone sulfate, and 27.8 nmol per liter (797 pg per milliliter) and 22.5 nmol per liter (643 pg per milliliter), respectively (P = 0.002), for androstenedione. A dose-response relation was apparent for these hormones; mean plasma levels increased concomitantly with cigarette consumption. The differences in hormone levels remained after adjustment for age and body-mass index. Mean levels of estrone, estradiol, testosterone, and sex-hormone-binding globulin did not differ between smokers and nonsmokers. These results suggest that the possible decreased risk of breast and endometrial cancer associated with cigarette smoking may not be mediated through lower levels of endogenous estrogen, at least in postmenopausal women, and they raise questions about the role of androgens in disease mechanisms in older populations." (Khaw KT, Tazuke S, Barrett-Connor E (1988) Cigarette smoking and levels of adrenal androgens in postmenopausal women. N Engl J Med 318(26):1705-1709)
[abstract]The clinical association between glucose intolerance, hyperinsulinaemia, insulin resistance and hyperandrogenism is well recognized in premenopausal women with polycystic ovarian disease. We examined the hypothesis that fasting plasma glucose levels might be related to endogenous androgen levels in postmenopausal women in the absence of overt clinical disease. 2. In a Southern Californian cohort of 848 nondiabetic postmenopausal women aged 50-79 years, fasting plasma glucose levels positively correlated with levels of the endogenous androgens dehydroepiandrosterone sulphate and free testosterone and negatively with sex-hormone-binding globulin across the whole range of glucose and hormone levels. Mean dihydroepiandrosterone sulphate and free testosterone levels were 16% and 46% higher, respectively, and mean sex-hormone-binding globulin levels 27% lower in the top compared with the bottom quartile of fasting plasma glucose levels. This relationship was independent of age, body mass index, cigarette smoking habit and exogenous oestrogen use. 3. These findings raise questions about the possible physiological role of androgens in the regulation of glucose metabolism and insulin resistance and, possibly, in the mediation of the some of the cardiovascular consequences of diabetes in women. (Khaw KT, Barrett-Connor E (1991) Fasting plasma glucose levels and endogenous androgens in non-diabetic postmenopausal women. Clin Sci (Colch) 80(3):199-203)
"The evolution of smaller- or larger-sized traits may vary dimorphically and result in a reduction in competition for resources between sexes. Dissociation of head growth from body growth has been recorded in species of North American garter snakes, such as Thamnophis sirtalis parietalis (Shine and Crews, 1988). Because of the action of testicular androgens early in development, inhibition in growth of the head occurs in males, resulting in smaller heads (shorter jaws) than in females. Body sizes are similar in males and females. Androgen administration occurs early in ontogeny and initiates different growth rates between males and females." (McKinney, M.L. & McNamara, K.J (1990) Heterochrony: The Evolution of Ontegeny: Plenum Press, New York p. 267)
"Cigarette smoking has been linked to thryoid disease, although studies of this problem have not shown consistent affects, with some studies linking smoking to increased thyroid hormone levels, and others to decreased thyroid hormone levels......Our findings suggest at least two distinct mechanisms for the effect of tobacco smoke on thyroid function; one related to higher levels of thyroxine-binding globulin and testosterone among smokers compared to non-smokers and another related to higher levels of thyrotoxins in tobacco smoke in heavy smokers compared to light and moderate smokers." (Fisher, C.L., Mannino, D.M., Hermann, W.H., Frumkin, H. (1997) Cigarette smoking and thyroid hormone levels in males. International Journal of Epidemiology 26 (5): 972) [ study of males]
"We found that current smokers have higher T4 level s and lower TSH levels than never smokers and former smokers. (Fisher, C.L., Mannino, D.M., Hermann, W.H., Frumkin, H. (1997) Cigarette smoking and thyroid hormone levels in males. International Journal of Epidemiology 26 (5): 974) [study of males]
"If males are signallying to females, then those signals are ripe for exploitation by a monstrous regiment of scavergers -- predators, parasites and competing males. ... And that is by no means the only kind of cost of being attractive. Sexual selection for increased body size in male birds invariably brings with it an increase in bill size, in some cases so great that males are forced to exploit suboptimal food niches (Selander 1972). The energetic costs of the males' display may be so high that they are pushed into abandoning safe foraging options for ones that possibly give higher energy returns but are more risky (Vehrencamp and Bradbury 1984). (Cronin, Helena (1992) The Ant and the Peacock: Cambridge Univ. Press, Cambridge p. 227)
"...primary hypogonadism, a condition resulting from the lack of increased production of androgen (testosterone) hormones in the interstitial Leydig cells in the testes at puberty. Because of this condition, emasculated singers may have been blessed with voices sweeter than a woman's, but burdened by an infantile penis, an underdeveloped prostate, "eunuchoid" (disproportionately long) arms and legs, beardlessness, pubic hair distributed in the female opposed to the male pattern, and fat deposits on the hips, buttocks, and breast area." (Margulis, L & Sagan, D. (1991) Mystery Dance, On the Evolution of Human Sexuality: Summit Books, New York pp. 67)
Definition Estradiol: The most potent naturally occurring estrogen in mammals. It is formed by the ovary, the placenta, the testis, and possibly the adrenal cortex. The theraputic indications for estradiol are those typical of as estrogen.
"Testosterone is one of a family of related hormones, collectively known as "androgens" or "anabolic steroids." They all are secreted from the testes or are the result of modification of testosterone, they all have a similar chemical structure, and they all do roughly similar things." He goes on to say androgens vary widely in important differenes] (Sapolsky 1997: 151, TheTrouble With Testosterone)
"The formation of sexually dimorphic nuclei in the hypothalamus and other structures is dependent on hormonal influences and especially on variations in testosterone level during development (Dorner 1980; Gorski et al. 1980; Pfaff 1966; Raisman and Field 1973; MacLusky and Naftolin 1981; McEwen 1981). Several authors have proposed a relationship between either sex chromosomes or hormones and patterns of cerebral dominance (Netley 1977; Hier and Crowley 1982)." (Geschwind & Galaburda 1987: 3, Cerebral Lateralization)
"There is probably some influence that slows the growth of parts of the left hemisphere so that, for reasons to be given, the corresponding regions on the right develop relatively more rapidly. On the basis of the higher frequency of lefthandedness and of learning disorders in males, it has been postulated that this influence is related to male sex, for instance, to testosterone or some factor related to it. H-Y antigen, to be discussed later, is normally present only in male fetuses, but this cannot be the exclusive male-related factor, since, if it were, the similar (although less marked) effects in females could not be accounted for. Both male and female fetuses are exposed to maternal and placental hormones. Once the male testes develop, the titer of testosterone rises to high levels. The formation of the testes and the secretion of testosterone are essential to the development of most of the features that differentiate males from females in most species. The female fetus is also exposed to testosterone, although in lower quantities. Factors that determine sensitivity to testosterone, or other male-related influences, will be important in both sexes. Both sexes are exposed to high levels of progesterone, which may have masculinizing effects on female fetuses at certain stages of development (Mayer-Bahlburg and Ehrhardt 1980)." (Geschwind & Galaburda 1987:11, Cerebral Lateralization)
"Testosterone also effects the growth of many other tissues. In particular, it retards the growth of structures involved in immunity, such as the bursa of Fabricius in the chick embryo (Warner, Szenberg, and Burnet 1962) and the thymus gland in the rat postnatally (Frey-Wettstein and Craddock 1970). Recent experiments in the rabbit by Behan (P. Behan, personal communication) are consistent with similar retarding effects on the fetal thymus. Thus, when testosterone effects of the brain are most marked, development of the immune system may be altered, heightening susceptibility to later immune disorders. It might be argued that this mechanism would lead to a higher rate of immune disorders in males, especially in the postpubertal period. Testosterone suppresses the thymus even in adult life (Frey-Wettstein and Craddock 1970; Wasi and Block 1961), so that thymic involution after puberty is more pronounced in males......We have also found that atopic disorders (for example, asthma, eczema, and hay fever) are more frequent in lefthanders. The fact that atopic disorders are more common in males in childhood (before the pubertal rise in testosterone) but more common in females after puberty (Crawford and Beldham 1976) is also compatible with this hypothesis." (Geschwind & Galaburda 1987: 13, Cerebral Lateralization)
"Second, estradiol has many of the same influences on neural and behavioral development, but not on physical development, that testosterone has. Although these masculinizing influences of estradiol were orginally considered paradoxical, they are now thought to parallel the process of masculinization that occurs in the normal male animal. The two major active metabolites of testosterone are dihydrotestosterone (DHT) and estradiol. DHT appears to be responsible for most aspects of neural masculinization. For example, administration of DHT to developing female rats masculinizes the genitalia, but not sexual behavior. In contrast, similar administration of estradiol or certain synthetic estrogens masculinizes sexual behavior and the volume of the SDN-POA, but not the genitalia. The hypothesis that testosterone is converted to estradiol before exerting many of its neural and behavioral influences is supported also by evidence tht behavioral masculinization can be prevented by exposing developing male rats to substances that block conversion of testosterone to estradiol or that block neural estrogen receptors." (Benson and Zaidel (Hines and Gorski) 1985: 77, The Dual Brain)
"Regardless of the complexity of sex differences in human neural asymmetries, the close relationship between gonadal hormones and neural sex differences in other species suggests the possibility of a relationship to the early hormonal environment. Data from at least one study support this suggestion. In this study, women who had been exposed to DES for at least 5 months of prenatal life, including the presumed critical period for hormonal influences on human development, were found to differ from their unexposed sisters in performance on a verbal dichotic task composed of consonant-vowel stimuli. As would be expected, given the masculinizing influences of DES on neural and behavioral development in other species (see the first section of this chapter for a discussion of some of these influences), their pattern of performance was shifted in the masculine direction (see Figure 2). Like men in a pilot study using the same dichotic task, as well as in other studies using similar tasks, they showed an enhanced right-ear advantage and a strong negative correlation between right- and left-ear scores. These differences did not seem to be due to other factors, such as age, birth order, pregancy complications, socioeconomic status, or educational background. Nor were they secondary to changes in personality, intelligence, or physical development, all of which were similar in the DES exposed women and their unexposed sisters. Rather, the most likely explanation for the differences between the two groups in performance on the dichotic task seemed to be the early hormonal environment." (Benson and Zaidel (Hines and Gorski)1985: 80, The Dual Brain)
"A study reporting a relationship between rate of maturation and neural asymmetry might also be interpreted to suggest hormonal influences. This study reported that performance on a verbal dichotic task varied with maturation rate, as reflected in the development of secondary sexual characteristics. Individuals with late maturation (i.e., reduced secondary sexual characteristics for their age) showed an enhanced right-ear advantage in comparison to those with early maturation (i.e., enhanced secondary sexual characteristics for their age). This relationship is often interpreted to suggest causal relationship between the rate of neural maturation and the degree of lateralization. Because gonadal hormones determine the development of secondary sexual characteristics, however, the cause of the enhanced lateralization could be hormones rather than maturation rate. A third relationship that has been interpreted to suggest gonadal hormone influences on the development of neural asymmetries involves left-handedness, immune disease, migraine, and developmental learning disorders. Geschwind and Behan reported that individuals who were stongly left-handed were more likely to exhibit learning disorders (i.e., dyslexia and stuttering) and certain immune diseases (e.g., thyroid and bowel disorders) than those who were strongly right-handed. They also found that individuals who suffered from migraine or myasthenia gravis were more likely than controls to show some preference for use of the left hand. The authors suggest that the cause of the associations observed might be elevated testosterone levels during development. They speculate that high levels of testosterone produce left-handedness and learning disorders by delaying the growth of the left hemisphere in utero, and influence the maturation of the immune system by suppressing the thymus. Of interest to the present discussion is the suggestion that prenatal elevations in testosterone may be related to the development of left-handedness. This possibility is consistent with the increased incidence of left-handedness among men and boys (see discussion below), but not with the evidence available from studies of individuals exposed to high levels of testosterone or other gonadal hormones in utero. These individuals have been reported to show normal incidence of left-handedness. Larger samples may be needed to detect a hormonal influence on handedness, however, since the associations reported by Geschwind and Behan were small. Alternatively, the relationship among left-handedness, learning disorders, and immune diseases could be caused by other factors (e.g., the genome or developmental trauma). (Benson and Zaidel (Hines and Gorski) 1985: 82, The Dual Brain)
(In rats)"The period when gonadal steroids impair feminine-typical functions, such as gonadotropin regulation and lordosis, occurs a few days later than that when they enhance masculine-typical function, such as mounting. There is also some evidence that the left side of the mammalian brain develops earlier than the right. Nordeen and Yahr, therefore, suggest that the right and left sides of the hypothalamus, because they are developing at somewhat different rates, are undergoing sexual differentiation of different functions between 24 and 48 hours of age (the time when the animals received implants). Should this be the case, it would provide a potentially powerful mechanism for the development of asymmetries in sexually dimorphic functions. Because testosterone levels vary from day to day during the critical period comparable regions of the two sides of the brain could develop in appreciably different hormonal environments." (Benson and Zaidel (Hines and Gorski)1985: 89, The Dual Brain)
"There is also evidence of a functional asymmetry in the hypothalamus of the adult rat as reflected in control of gonadotropin release, and the direction of this asymmetry differs for the two sexes." (text continues with details) (Benson and Zaidel (Hines and Gorski) 1985: 90, The Dual Brain)
"It seems likely that gonadal hormones influence the development of neural symmetries in laboratory animals as well as in human beings. In people, the early hormonal environment is related to the degree of asymmetry shown in performance on verbal dichotic tasks. In rodents, a similar relationship exists between the early hormonal environment and the development of postural asymmetries. In both cases, the metabolite of testosterone responsible for the relationship appears to be estradiol." (Benson and Zaidel (Hines and Gorski) 1985: 90, The Dual Brain) (See additional information on same and next page.)
"As will be discussed in greater detail later, the neuronal migration and assembly may be modified by circulating sex hormones. Estrogens enhance cortical maturation and myelogenesis in the rat (Heim and Timiras 1963; Curry and Heim 1966), whereas androgens interfere with this estrogen effect (Toran-Allerand 1978) in vitro and in vivo." (Geschwind & Galaburda 1987: 18, 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 tht 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)
"In a later study Diamond (1984) found that removing the testes in newborn male rats also led to a reversal of the asymmetry pattern in several cortical regions." (Geschwind & Galaburda 1987: 49, Cerebral Lateralization)
"Although fewer females stutter, they have, on the average, more affected relatives, and they are more likely to have affected children than males who stutter (Kidd, Heimbuch, and Records 1981). It is easy to conceive of reasons for this pattern. If, for example, there were large differences in genetically transmitted sensitivity to testosterone, then females who stuttered would frequently have inherited high sensitivity, since in most cases females would not have exposure to very high levels of testoserone. Many of these females' relatives---and, in particular, many of their children---would share this high sensitivity. On the other hand, males with, on the average, higher levels of testosterone would not require as high a level of sensitivity to testosterone to be subjected to an excesive delaying effect. In particular, the female relatives of a male who stuttered, but did not have high testosterone sensitivity, would be expected to have low rates of the disability. Furthermore, since testosterone levels in male fetuses are sensitive to environmental effects (to be discussed in chapter 11), males could be affected more frequently by environmental causes. There are, of course, other possible explanations for the genetic findings; the above example only serves to illustrate that the greater frequency of learning disorders in males need not imply that affected males will have more affected relatives than affected females." (Geschwind & Galaburda 1987: 88, Cerebral Lateralization)
[Contrary to model] "Hier and Crowley (1982) found that congenitally hypogonadal males, who lack testosterone, typically had superior verbal scores and low scores on tests of spatial function, unlike normal males." (Geschwind & Galaburda 1987: 97, Cerebral Lateralization)
"Other data support a role for hormonal influences on laterality and associated skills. Famales with late menarche tend to have higher spatial scores than those with early menarche (Waber 1981) (Geschwind & Galaburda 1987: 98, Cerebral Lateralization) [late menarche suggests more neotony, later period may mean circle culture along with its features]
"The Y chromosome is unusual in bearing few genes; however, it carries a protein, the H-Y antigen (Haseltine and Ohno 1981), which is essential for development of the testes, which will later in fetal life secrete testosterone. This hormone is, in turn, essential for the deveopment of typically male structures in the body and brain. But H-Y antigen does not exert all its effects only indirectly through the formation of testes and the later production of testosterone; this antigen is expressed in other organs as well, among them the thymus gland, an essential component of the developing immune system (Ivanyi 1978). The ovaries appear to play a more limited role in prenatal development." (Geschwind & Galaburda 1987: 105-6, Cerebral Lateralization)
"Testosterone and its matabolites are essential not only for normal development of of genitalia and secondary sexual characteristics but also for the formation of the brain. Sex hormones affect the development of nervous structures involved in the control of reproduction, for instance, the cyclic release of gonadotropins, mating, and lactation." (Geschwind & Galaburda 1987: 106, Cerebral Lateralization)
The female zygote is also exposed to testosterone, little or none of which appears to come from the fetal ovaries, adrenals, and extragonadal structures such as fat. The fetus is protected from much of this maternal testosterone, because aromatase in the placenta converts it to estradiol, but the protection is not complete." (Geschwind & Galaburda 1987: 107, Cerebral Lateralization) [note: if fat influences the natal environment, could the excess of fat in neotenous mothers influence fetal development in a neotenous direction?]
"The X chromosome plays an important role in effects of testosterone, since it contains the Tfm locus, one of the genes that controls sensitivity to this hormone (Bardin and Catterall 1981). Thus, although the female conceptus is usually exposed later in gestation to a lower level of testosterone than the male, it is probably more sensitive to maternally and placentally produced testosterone, especially in the earliest stages of embroyogenesis. At the time of lyonization one might expect the embryo to lose this higher sensitivity, but inactivation is not complete and the female retains a greater dosage of some X-linked products (Naftolin 1981). (Geschwind & Galaburda 1987: 106, Cerebral Lateralization)
"Another significant hormone is progesterone, which is also present in large amounts during fetal life and is known to have masculinizing effects in the female, at least at certain periods. Sensitivity perhaps differs in the two sexes. Many of the effects of testosterone may, of course, be mediated indirectly. Biegon and McEwen (1982) have found male-female differences in serotonin systems, which might play a special role in laterality. It is worth noting that infants of mothers who have taken LSD (a serotonin deriviative) in pregnancy may have missing fingers, especially on the right hand (Assemany, Neu, and Gardner 1970), which also suggests that serotonin may play a role in laterality." (Geschwind & Galaburda 1987: 107, Cerebral Lateralization)
[in the rat] "Dihydrotestosterone, the matabolite that affects many of the secondary male characteristics, does not act in some species in certain locations in the nervous system in which only testosterone may be effective. The actions of testosterone itself vary from location to location within the brain. Certain neurons within the rat preoptic nucleus and amygdala contain aromatase, the enzyme that converts testosterone to estradiol. The action of testosterone within the preoptic nucleus in the rat depends on this conversion. There are other locations in which aromatase is not found, even though the target organ contains testosterone receptors; one of these is the pituitary gland." (Geschwind & Galaburda 1987: 109, Cerebral Lateralization)
"In reviewing the literature, Karsch, Dierschke, and Knobil (1973) point out that in both nonhuman primates and humans administration of testosterone in pregnancy fails to alter normal ovarian cyclicity in female offspring, but that in these cases there is pronounced morphological and behavioral masculinization. Female mice with early exposure to androgens show permanent alterations in their responses to these substances; for example, when testosterone is administered again to them in adult life, they may show increased aggressiveness in contrast to normal adult females (Edwards 1964; Bronson and Desjardins 1968). Money and Ehrhardt (1972) have found that human females with congenital adrenal hypertrophy to show differences from other females later one, for instance, an increased tendency to participation in rough and tumble sports. Although many of these women marry and bear children, studies must still be carried out on large series to determine whether they suffer changes in menstrual function, fertility, and pregnancy." (Geschwind & Galaburda 1987: 111, Cerebral Lateralization)
"Although the majority of human females exposed to DES [diethylstilbestrol] resemble other women on the average, certain features are more common in this population; for example, DES has been shown to have masculinizing effects of the structure of the genitalia (Bongiovanni, Di George, and Grumbach 1959). DES daughters have been reported to have an elevated rate of menstrual difficulties, infertility, and problems during pregnancy, including premature and preterm births, prolonged labor, and higher rate of children with congenital anomalies (Herbst et al. 1980), though agreement on this is not universal. However, it should be noted that the mothers of these women also had some of these problems, which probably constituted the reason for their taking DES. It will be necessary to study a large number of DES daughters in order to ascertain whether they show an increased rate of the changes in the cortex that we have hypothesized would result from high intrauterine testosterone exposure. One might expect DES daughters to have an elevated frequency of lefthandedness, learning disabilities, high spatial talents, and the other associations hypothesized to be more frequent with elevated intrauterine male-related effects. Hines (1982) has reviewed the effects of DES. We have carried out a study on a group of 77 adults exposed to DES in utero, and our preliminary results show a markedly elevated rate of non-righthandedness in this population. Nichols and Chen (1981) have found that sex hormones administered to pregnant women lead to an elevated rate of hyperactivity in the offspring, especially the girls." (Geschwind & Galaburda 1987: 111-112, Cerebral Lateralization)
"Nottebohm (1981) has provided a dramatic example of the effects of testosterone on neuronal growth in the HVc nucleus, a structure critically involved in the control of bird song. Normally only the male sings, since testosterone is required for song production," (Geschwind & Galaburda 1987: 113, Cerebral Lateralization)
"Sex hormones administered during pregnancy increased the rate of hyperactivity in the offspring, the effects being greatest in black girls and white boys (Nichols and Chen 1981).
"Even if it is true that a male-related factor modulates intrauterine growth of certain cortical regions, it is obvious that cortical development will be susceptible to many other influences, some closely related to the hormonal effects, some more remote. Ward and Weisz (1980) showed that if a female rat is stressed during the course of pregnancy, the male offspring show demasculinization. After the stress there is a rapid rise of testosterone in male fetuses, followed by a fall to subnormal levels. It is not clear exactly how stress on the mother leads to this sequence of changes. It is interesting to note that the female offspring of such a stressed mother will also tend to have demasculinized male offspring, even though these famales are not themselves stressed in pregnancy. Phenobarbital administered during pregnancy has similar effects, and the male offspring have permanently low testosterone levels.This is an example of a phenomenon already mentioned, whereby chemical effects on the fetus may produce permanent alterations in metabolism. When present in the female they can lead to a mechanism of nongenetic transmission to the following generation. Sherman et al. (1980) have also demonstrated an environmental effect on lateralization. In studies carried out some years earlier it had been shown that brief periods of handling of newborn rats exerted permanent effects on emotionality and on other traits such as resistance to infection. In the more recent experiments it was shown that male rats who had been handled showed a greater right hemisphere lateralization in tests of emotionality and spatial performance than animals who had not been." (Geschwind & Galaburda 1987: 115, 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 th 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 shoudl 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)
"There is another locus found in the human on chromosome 15, which controls production of beta-2-microglobulin (B2M), a protein essential for immune responsiveness. Ohno (1977) has suggested that it is also necessary for the expression of the H-Y antigen, which is itself essential for the developnment of the male gonads. Smith et al. (1983) have reported, on the basis of large family studies, that dyslexia is linked to a locus on chromosome 15. It would not be surprising, from the point of view of our theory, if a locus that is involved in immune response and testicular development is also involved in the predisposition of dyslexia." (Geschwind & Galaburda 1987: 119, Cerebral Lateralization)
"The sex ratios for immune disorders may appear to present a problem, since the hypothesis implies that males should be at greater risk for immune disease. Indeed, before puberty the common immune disorders are the male-predominant allergies; after puberty the autoimmune disorders are generally, although not universally, female predominant. There is evidence, however, that testosterone in adult life acts to suppress autoimmunity, presumably by its effects on the thymus. The implication is therefore that the male is indeed more susceptible to autoimmune disorders but is protected by his own production of testosterone after puberty. High testosterone effect in utero increases susceptibility to immune disease, but after puberty it diminishes its expression. If this hypotheses is correct, then males subjected to high testosterone effect in utero, but who are hypogonadal after puberty, should have very high rates of autoimmune disease." (Geschwind & Galaburda 1987: 123, Cerebral Lateralization)
"One possibility, though a speculative one, is that antibodies binding to the hair follicles present a barrier to androgens. We have noted the lower rate of early male pattern baldness and sparse facial hair among the Japanese, resulting form insensitivity of the hair follicles to dihydrotestosterone. It would be interesting to know whether Europeans or Blacks with early gray hair also need to shave less frequently---that is, whether the immune protection against androgens also extends to facial hair." (Geschwind & Galaburda 1987: 163-4, Cerebral Lateralization) [more from this quote in Coloring section]
"Diethylstilbestrol (DES) was shown years ago to produce masculinizing effects on female offspring (Bongiovanni, Di George, and Grumbach 1959). The reasons for this have become clear in recent years with the discovery that testosterone masculizes the rat brain. Estradiol within certain nuclei of the hypothalamus is actually the final cause of this masculinization, but these nuclei are protected from the circulating estradiol that, in the rat, is bound to alphaafetoprotein (AFP). Testosteone is not bound by AFP and thus reaches these nuclei, where it is converted to estradiol by aromatase. DES also masculinizes; although it is an estrogen, it is not bound by AFP and thus reaches the brain sites within which it acts like estradiol to masculinize. It is not surprising that DES-exposed daughters have a high rate of gynecological difficulties and infertility and an elevated rate of children with congenital anomalies, all of which may reflect this masculinizing effect. We have seen several DES daughters with features such as facial hirsutism, acne, and unusual sensitivity to the masculinizing effects of phenytoin. A high rate of anomalous dominance might be expected in this group, and our preliminary findings of 77 DES daughters support this hypothesis. In psychological studies of a small sample of DES children Hines (1982) found some results that she interpreted as consistent with a masculinizing effect on the brain, but other data summarized in her review differ; the numbers were again small, however. Further study on larger numbers is obviously warranted." (Geschwind & Galaburda 1987: 172-3, Cerebral Lateralization)
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)
"Among the known causes, for instance, female athletes and those with anorexia aften fail to menstruate probably because of loss of estradiol producing body fat." (Geschwind & Galaburda 1987: 222, Cerebral Lateralization)
"Among lizards, repetitious behavior is perhaps best illustrated by the performance over and over again of the signature and challenge displays used by a male in trying to establish or maintain dominance over other males. In such situations, it is not always body size that is the deciding factor. Rather, it would almost seem that it was the rule of the game that the animal that perfomrs th greatest number of displays eventually wins out. There is a need for systematic studies relevant to this point. The presence of a reproductive female appears to have the effect of greatly increasing the number of displays by contesting males. The displays might be likened to a series of exclamation marks. Courtship presents another situation in which displays by the male and female may become repetitious and seem to carry the message of a series of exclamation marks. Speaking to this point in another context, Morris has remarked that the telephone often succeeds in attracting attention because of the number, rather than the loudness, of its rings." (MacLean 1990: 147, The Triune Brain in Evolution) [note: compulsive behavior in autism and tourette's may have its origin here. Is there evidence that female presence increases compulsive behavior in Tourette's in males?]
"One of the most curious results to come out of bird studies in recent years had been the discovery that "attractive" males make inattentive fathers." (Ridley 1993: 224, The Red Queen) [too much testosterone]
"In recent years more and more evidence has been found that testosterone affects not just ornaments and bodies but also brains. Testosterone is an ancient chemical, found in much the same form throughout the vertebrates. Its concentration determines aggressiveness so exactly tht in birds with reversed sex roles, such as phalaropes and in female-dominated hyena clans, it is the females that have higher levels of testosterone in the blood. Testosterone masculinizes the body; without it, the body remains female, whatever its genes. It also masculinizes the brain. Among birds it is usually only the male that sings. A zebra finch will not sing unless there is suffecient testosterone in its blood. With testosterone, the special song-producing part of its brain grows larger and the bird begins to sing. Even a female zebra finch will sing as long as she has been exposed to testosterone early in life and as an adult. In other words, testosterone primes the young zebra finch's brain to be responsive later in life to testosterone again and so develop the tendency to sing. Insofar as a zebra finch can be said to have a mind, the hormone is a mind-altering drug. Much the same applies to human beings. Here the evidence comes from a series of natural and unnatural experiments. Nature has left some men and women with abnormal hormonal doses, and in the 1950's doctors changed the hormonal conditions of some wombs by injecting some pregnant women with certain hormones. Women with a condition known as Turner's syndrome (they are born without ovaries) have even less testosterone in their blood than do women who have ovaries. (Ovaries produce some testosterone, though not as much as testicles do.) They are exaggeratedly feminine in their behavior, with typically a special interest in babies, clothes, housekeeping, and romantic stories. Men with less than usual testosterone in their blood as adults---eunuchs, for example---are noted for their femininity of appearance and attitude. Men exposed to less than usual testosterone as embryos---for example, the sons of diabetic women who took female hormones during pregnancy---are shy, unassertive, and effeminate. Men with too much testosterone are pugnacious. Women whose mothers were injected with progesterone in the 1950's (to avert miscarriage) later described themselves as having been tomboys when young; progesterone is not unlike testosterone in its effects. Girls who were born with an unusual condition called either adrenogenital syndrome or congenital adrenal hyperplasia are equally tomboyish. This order causes the adrenal gland, near the kidney, to produce a hormone that acts like testosterone instead of cortisol, its usual product. Somewhat like in the zebra finches, there is two periods when testosterone levels rise in male children: in the womb, from about six weeks after conception, and at puberty. As Anne Moir and David Jessel put it in a recent book, Brain Sex, the first pulse of hormone exposes the photographic negative; the second develops it. This is a crucial difference fro the way the hormone affects the body. The body is masculinized by testosterone from the testicles at puberty, whatever its womb experience. But not the mind. The mind is immune to testosterone unless it was exposed to a sufficient concentration (relative to female hormones) in the womb. It would be easy to engineer a society with no sex difference in attitude between men and women. Inject all pregnant women with the right dose of hormones, and the result would be men and women with normal bodies but identical feminine brains. War, rape, boxing, car racing, pronography, and hambergers and beer would soon be distant memories. A feminist paradise would have arrived. (Ridley 1993: 254-6, The Red Queen)
"Yet at five the testosterone levels in the average boy are identical to those of the average girl, and a fraction of what they were at birth." (Ridley 1993: 258, The Red Queen)
"He now [at puberty] has twenty times as much of it [testosterone] in his blood as a girl of the same age." (Ridley 1993: 258, The Red Queen)
"You need some testosterone around for normal aggressive behavior---zero levels after castration, and down it usually goes; quadruple it (the sort of range generated in weight lifters abusing anabolic steroids), and aggression typically increases. But anywhere from roughly 20 percent of normal to twice normal and it's all the same; the brain can't distinguish among this wide range of basically normal values." (Sapolsky 1997: 154, TheTrouble With Testosterone)
"This is critical: testosterone isn't causing aggression, it's exagerating the aggression that's already there." (Sapolsky 1997: 155, TheTrouble With Testosterone)
"There is indeed some evidence that females who are high and males who are low in the male sex hormone (androgen) score higher on spatial ability tests (see McGee, 1979). While this would support the idea of the need for an optimal (i.e. intermediate) level of hormones...." (Bradshaw & Nettleton 1983: 218, Human Cerebral Asymmetry)
"When gonadectomized males were treated with testosterone, however, they became more aggresive to subordinate males but not to more dominant males or females. Factors such as physical condition and previous social experience may be more important than gonadal hormones in influencing aggresive interactions in these captive groups of talapoins." (Dixon, A. & Herbert, J. (1977) Testosterone, Aggressive Behavior and Dominance Rank in Captive Adult Male Talapoin Monkeys Physiology and Behavior 18: pp. 539)
"All aggresion was directed towards lower ranking males, however, and no animal rose in rank after hormone therapy. All four males showed increased threats and three showed increased attacks towards subordinate males, whilst male 1017 showed small decrease in the frequency of his attack behavior. ... When gonadectomized males were treated with testosterone, they became more aggressive towards lower ranking males but not towards dominant males or females. No male rose in the hierarchy as a result of testosterone therapy. The high dose of testosterone produced supra normal levels of hormone in the plasma of gonadectomized males, but there were no further changes in their aggressive behavior." (Dixon, A. & Herbert, J. (1977) Testosterone, Aggressive Behavior and Dominance Rank in Captive Adult Male Talapoin Monkeys Physiology and Behavior 18: pp. 542)
"Androgens have a general anabolic effect. They reduce nitrogen excretion in many species. They promote growth of muscle. The uptake of glucose and glycogen sythesis in muscle is androgen-dependent. Men who have the genes for pattern baldness do not lose their head hair unless they have circulating androgens. Androgens increase sweat secretion rates. (Wagner and Hughes 1974). Carnivores in general have relatively large adrenal glands in terms of body weight; herbivores in general have thyroid glands relatively large in terms of body weight. The adrenals in adult women are about 70 percent larger relative to body weight than in adult female chimpanzees (Crile and Quiring 1940). Later studies of chimpanzees and rhesus monkeys confirm the relatively great size of the human adrenal glands (Bourne and Golarz de Bourne 1972; Bourne 1975; Graham 1970). Since there is no significant storage of androgens in the primate body, a fresh supply must be synthesized as it is used. The production rate of testosterone in nonpregnant adult human females is 0.29-0.35 mg/day and that of androstenedione 3.3-3.7 mg/day, the production of androgens by the adrenals being twice that of the ovaries (Reid, Ryan, and Benirschke 1972). Mean values of androgen excretion in the urine of normal women are 40 to 47 IU/day, or approximately two-thirds the amount excreted by males. Means of two adult female chimpanzees were 3.1 and 3.7 IU/day and those for ten adult female rhesus macaques ranged from 1.2 to 2.6 IU/day (Dorfman 1948: 501-502, 516). If we let 1 IU represent the biological activity of 0.1 mg. of adrosterone, the values in mg/kg/day are 0.7 for adult female chimpanzees and 8 for women. In a review of the literature, Graham (1970:203) noted that in chimpanzees male and female daily output of androgens was many times lower than the values obtained for man and close to values obtained for rhesus monkeys. Probably as a result of natural selection for endurance bipedal running, men and women have greatly larger thyroid glands, and signigicantly larger adrenal glands and consequently greater hormone output than do rhesus monkeys and chimpanzees. (Spuhler, J.N. (1979) Continuities and Discontinuities in Anthropoid-Hominid Behavior Evolution: Bipedal Locomotion and Sexual Receptivity In Evolutionary Biology and Human Social Behavior. N. Chagnon & W. Irons, eds. Pp. 458)
"In Homo Sapiens, erotic imagery, sensations, and actions are influenced in both males and females by androgens; in males the androgens are influenced in both males and females by androgens; in males the androgens are of both testicular and adrenal origin, in females mostly of adrenal secretion." (Spuhler, J.N. (1979) Continuities and Discontinuities in Anthropoid-Hominid Behavior Evolution: Bipedal Locomotion and Sexual Receptivity In Evolutionary Biology and Human Social Behavior. N. Chagnon & W. Irons, eds. Pp. 460)
"Hominids responded to the selective challenge of endurance walking and running in order to take large game animals by developing hypertrophied thyroid and relatively larger adrenal glands. A side effect was the higher degree of continual sexual receptivity in hominid females." (Spuhler, J.N. (1979) Continuities and Discontinuities in Anthropoid-Hominid Behavior Evolution: Bipedal Locomotion and Sexual Receptivity In Evolutionary Biology and Human Social Behavior. N. Chagnon & W. Irons, eds. Pp. 461)
"The male contribution to fertility is also affected by starvation. In young American men who volunteered to undergo experimental starvation, sperm were fewer, less motile, and shorter-lived than normal (Klatskin et al. 1947, cited in Stein and Sausser 1975). High temperatures and high altitudes also tend to produce aspermia (Cowgill 1969). (Bernds, W.P. & Barash, D.P. (1979) Early Termination of Parental Investment in Mammals, Including Humans In Evolutionary Biology and Human Social Behavior. N. Chagnon & W. Irons, eds. Pp. 495)
"It is also now clear that high plasma levels of testosterone are immunosuppressive (fig 2). This may have first arisen as a mechanism to suppress actions of the immune system within the testes, because as developing spermatozoa become haploid, they develop surface proteins that are recognized as foreign by cells of the immune system. Thus, suppression of immune responses within the testes enhances fertility. Problems arise when testosterone is secreted into the blood and then has the potential to inhibit the immnune system throughout the organism." (Wingfield, J.C., Jacobs, J. & Hillgarth, N. (1997) Ecological constraints and the evolution of hormone-behavior interrelationships. Annals of the N. Y. Academy of Science 807: pp. 25)
"Conflict with parental care: In many avian species, males provide significant parental care, resulting in marked increases in reproductive success. Evidence is mounting that high plasma levels of testosterone interfere with expression of parental care in males, resulting in reduced reproductive success. (Wingfield, J.C., Jacobs, J. & Hillgarth, N. (1997) Ecological constraints and the evolution of hormone-behavior interrelationships. Annals of the N. Y. Academy of Science 807: pp. 34)
"Masculinised females, who by our hypothesis, should have a high rate of personal and familial anomalous dominance, have elevated levels of luteinizing hormone. Since their offspring may have greater exposure to masculinizing effects in utero, they may have an elevated rate of LH. This hypothesis is in conformity with the higher rate of LH in mothers of twins and in the twins themselves." (Geschwind, N. & Galaburda, A.M. (1985) Cerebral Lateralization. Biological mechanisms, associations, and pathology: II. A hypothesis and a progam for research. Archives of Neurology 42(6): pp. 535)
Sas & Szollosi (1980) reported that men with low sperm counts who were given methyltestosterone therapy (10 mg per day orally) sired 45 boys and 17 girls during treatment and up to 3 months after." (James, W. H. (1986) Hormonal control of the sex ratio. Journal of Theoretical Biology 118: 434.)
"Lastly it is clear that stress reduces testosterone levels in men (Kreuz et al., 1972). And Leedy & Wilson (1985) concluded that male hormone levels may be affected by the stressors of routine military flight. So the reportedly low sex ratios of children born to men in stressful occupations e.g. aircraft pilots (Goerres & Gerbert, 1976; Synder, 1961) and abalone divers (Lyster, 1982) may have hormonal---perhaps androgenic---determinates." (James, W. H. (1986) Hormonal control of the sex ratio. Journal of Theoretical Biology 118: 435)
"Now gonadotrophin levels are lowered by anxiety (La Ferla it al., 1978; Peyser et al., 1973) and operative procedures (Soules et al., 1980). It seems likely too that the disruption of menstrual patterns by other stressful events has a similar cause." (James, W. H. (1986) Hormonal control of the sex ratio. Journal of Theoretical Biology 118: 435)
"Women who are smokers are known to have low levels of estrogen on the average (MacMahon et al., 1982). And in an unpublished brief review of the literature, I have noted a slight but significant (P<0.05) excess of females born to women who smoke." (James, W. H. (1986) Hormonal control of the sex ratio. Journal of Theoretical Biology 118: 436)
"It has been noted that stress reduces testosterone levels in men and gonadotrophin levels in women. And it has been suggested accordingly that men under stress are more likely to produce girls, while women under stress are more likely to produce boys." (James, W. H. (1986) Hormonal control of the sex ratio. Journal of Theoretical Biology 118: 438)
"I have suggested that the sex of a zygote is somehow associated with maternal gonadotrophin levels at conception, and I have argued that this hypothesis is supported by a seasonal variation in sex ratio in U.S. White births synchronous with the seasonality in gonadotrophin levels (as evidenced by seasonality in twinning and in births of boys with undescended testes)." (James, W. H. (1980) Race, season, gonadotrophin, and sex ratio. Lancet 2: pp.1032)
Discussion of thyroid glands, metamorphosis, and goitrogen-treated larvae in relation to TRH and TSH. (Yamaguchi, M., Tanaka, S., & Wakahara, M. (1996) Immunohisto- and immunocytochemical studies on the dynamics of TSH and GTH cells in normally metamorphosing, metamorphosed, and metamorphosis-arrested Hynobius retardatus. General Comparative Endocrinology 104(3): pp. 273-83)
"They showed in Table I and II and Figs. 1 and 2. Alcohol patients showed significantly lower testosterone levels than controls. The circadian rhythm was lost after withdrawal but it recurred on third day and progressively increased until full recovery, i.e. the difference between hormone levels at 9 and 21 h increased slowly, reaching nearly the level of signification on day 15. FSH and LH levels were signifantly higher in alcoholics at day 1, and the levels did not vary significantly during the 15 days of the study. A strong relationship existed between levels of FSH and LH (r = 0.56, P< 0.0001), but not between these hormones and testosterone. Prolactin levels significantly increased during the 15 days of observation, being in the interior limit of the normal range at the beginning." (Castilla-Garcia, A., Santolaria-Fernandez, F.J., Gonzalez-Reimers, C.E., Bastita-Lopez, N., Gonzalez-Garcia, C., Jorge-Hernandez, J.A., & Hernandez-Nieto, L. (1987) Alcohol-induced hypogonadism: reversal after ethanol withdrawal. Drug and Alcohol Dependence 20(3): pp. 257)
"In our study, testosterone levels progressively returned to normal along the 15 days of the observation period. In addition, the circadian rhythm, lost at the beginning of the study --- a feature also reported by Gordon (2) and Bertello(22) --- became evident again in the last days of the observation period. These data suggest that hypogonadism seems to be functional in nature. .... Prolactin has been found to be elevated in alcholics after a week of abstinence (13,23), and decreased during the hangover phase, with blockade of the prolactin response to TRH (24). In this connection it has been argued that ethanol withdrawel may lead to an excessive dopaminergic activity, and, as a consequence, to a low release of prolactin (24). In our study, serum prolactin levels-especially those obtained at 21 h --- recovered progressively from the low limit of the normal range observed in the first days to the higher levels at the end of the observational period." (Castilla-Garcia, A., Santolaria-Fernandez, F.J., Gonzalez-Reimers, C.E., Bastita-Lopez, N., Gonzalez-Garcia, C., Jorge-Hernandez, J.A., & Hernandez-Nieto, L. (1987) Alcohol-induced hypogonadism: reversal after ethanol withdrawal. Drug and Alcohol Dependence 20(3): pp. 259)
Chart (book wall) comparing testosterone levels of Chinese, Japanese, African and Whites, all USA. Whites had lowest level of the four, contradicting shift theory expectations. Actually, since Africans have lower T than African-Americans, this makes more sense. (Wu, A.H., Whittemore, A.S., Kolonel, L.N., John, E.M., Gallagher, R.P., West, D.W., Hankin, J., Teh, C.Z., Dreon, D.M., & Paffenbarger, R.S.Jr. (1995) Serem androgens and sex hormone-binding globulins in relation to lifestyle factors in older African-American, white, and Asian men in the United States and Canada. Cancer Epidemiology, Biomarkers & Prevention 4(7): pp. 738)
"After adjustment for age, Quetelet's index, and physical activity, levels of testosterone (total, free, and bioavailable) were higher for Asians born in Asia versus for those Asians born in North America, whereas levels of SHBG and DHT were similar in both groups (Table 4). On the other hand, the DHT: testosterone ratio was lower in Asians born in Asia compared to those born in North America. However, none of the differences between Asians born in North America and those born in Asia were statistically significant." (Wu, A.H., Whittemore, A.S., Kolonel, L.N., John, E.M., Gallagher, R.P., West, D.W., Hankin, J., Teh, C.Z., Dreon, D.M., & Paffenbarger, R.S.Jr. (1995) Serem androgens and sex hormone-binding globulins in relation to lifestyle factors in older African-American, white, and Asian men in the United States and Canada. Cancer Epidemiology, Biomarkers & Prevention 4(7): pp. 739)
"Stenuous physical activity may result in lower levels of testosterone (26-28). Smoking may inhibit production of estrogens in women (29) but data on its effect in men are not consistent (30,31). In a study of Caucasian upper middle class men in a California retirement community, smokers showed significantly higher serum estrogen levels than did nonsmokers (30). However, in the Multiple Risk Factor Intervention Trial, serum estrogen levels in men were not associated with total amount of cigarettes smoked (31). Levels of testosterone were higher among men who smoked compared withmen who did not in both studies (30,31). Heavy alcohol use may increase estrone production and, thus, increase conversion of androgens to estrogens (32, 33). The present findings suggest higher total testosterone levels in smokers compared to nonsmokers, but there were few consistent associations between physical activity, alcohol use, and androgen levels. In this study, men with a self-reported history of a benign prostate condition showed a signigicantly higher DHT: testosterone ratio, a marker of 5a-reductase activity (34), compared to men without such history. This observation is compatible withthe hypothesis that the development of benign prostate (35). .... The present study of older men, most of whom were 60 years or older, found lower testosterone levels in whites compared to African-Americans, similar to studies conducted in young college men and Vietnam veterans aged 31-50 years. However, there is little evidence from this and other studies that testosterone levels in Asians residing in Asia or in North America are lower than those in whites. On the other hand, the strongest support for ethnic differences in androgen levels in this study was bsed on the DHT:testosterone ratio, which was highest in African-Americans, intermdiate in whites, and lowest in Asian-Americans, reflecting the prostate cancer incidence rates in these groups." (Wu, A.H., Whittemore, A.S., Kolonel, L.N., John, E.M., Gallagher, R.P., West, D.W., Hankin, J., Teh, C.Z., Dreon, D.M., & Paffenbarger, R.S.Jr. (1995) Serem androgens and sex hormone-binding globulins in relation to lifestyle factors in older African-American, white, and Asian men in the United States and Canada. Cancer Epidemiology, Biomarkers & Prevention 4(7): pp. 739-40)
"First, both physical and psychological stress have been consistently found to depress T (Mason, 1968; Kreuz et al., 1972; Opstad & Aakvaag, 1982). Second, aggressive or competitive/dominance encounters generally raise T levels, which also reflect the outcome of the encounter: T levels are elevated in winners and relatively repressed in losers (Rose et al., 1975; Elias, 1981). ... Generally, sustained moderate-to-intense exercise appears to elevate T, although data from studies have been equivocal (Kuoppanalmi et al., 1980)." (Worthman, Carol M. & Konner, Melvin, J. (1987) Testosterone levels change with subsistence hunting effort in !Kung San men. Psychoneuroendocrinology 12(6): pp. 450)
"In Western clinical populations, a marked diurnal variation in serum T levels has been reported, with evening values averaging around 30% lower than morning values (Nieschlag, 1974). Baseline values of !Kung hunters show similar diurnal variation." (Worthman, Carol M. & Konner, Melvin, J. (1987) Testosterone levels change with subsistence hunting effort in !Kung San men. Psychoneuroendocrinology 12(6): pp. 452)
"Evolutionary arguments for the importance of hunting in shaping foundations of men's behavior have tended to focus on its aggressive, competitive and stressful components. Its basic nature as a form of effort, or work, has been less frequently considered. The data suggest that !Kung men do not experience subsistence hunting as mere stress, which depresses T levels, for its main effect was an increase in evening values. On the other hand, no interaction of hunt outcome and T levels were observed, in contrast to reports that T reflects success and failure in certain aggressive and dominance interactions. Rather, these data are most congruent with reported effects of moderate prolonged excercise." (Worthman, Carol M. & Konner, Melvin, J. (1987) Testosterone levels change with subsistence hunting effort in !Kung San men. Psychoneuroendocrinology 12(6): pp. 456)
"We conclude that subsistence hunting was associated with significant changes in testosterone patterns in !Kung hunters, due primarily to the maintenance of T concentrations during hunting days that is reflected in elevation of evening values. Diurnal variation in circulating T was hence markedly attenuated. It is also notable that shifts in T level were a consequence, not a primary cause, of the behaviors observed here; hormone changes followed and supported, not preceded, hunting activity. Studies of human behavioral biology might consider the ways in which the dominant context of human evolution, the hunting-gathering niche, may have selected for efficient, appropriate responses to subsistence-related effort." (Worthman, Carol M. & Konner, Melvin, J. (1987) Testosterone levels change with subsistence hunting effort in !Kung San men. Psychoneuroendocrinology 12(6): pp. 456)
"Nevertheless, castrated tomcats live longer than their intact male counterparts, and so do human castrates. Detailed comparisons standardized for age, intelligence, and category of mental deficiency among castrated and intact inmates of a mental institutution in Kansas demonstrated that the median age at death of intact men was 55.7 years, as compared to 69.3 years of castrates, and that the earlier the castration was performed, the more life expectancy was increased." (Badcock, C. (1991) Evolution and Individual Behavior: An Introduction to Human Sociobiology Oxford: Blackwell. pp. 14)
"For instance, one known effect of testosterone is to raise the resting metabolic rate of males by approximately 5 percent as compared to females. Effectively, this means tht the male biochemical "engine" is running about one-twentieth faster all the time than is that of a woman, perhaps explaining why it wears out sooner." (Badcock, C. (1991) Evolution and Individual Behavior: An Introduction to Human Sociobiology Oxford: Blackwell. pp. 15)
"...whereas women have about one quarter of their body weight in the form of fat, men on average have only about half that amount. In other words, although women on average have about twice as much fat as men, they nevertheless weigh on average almost a quarter less than men.....When we observe that in women the degree of fat deposits is critical to reproductive success in primal condiditions, but that in men muscle, bone, and height are critical in aggressive encounters with other men..." (Badcock, C. (1991) Evolution and Individual Behavior: An Introduction to Human Sociobiology Oxford: Blackwell. pp. 144)
"...human testis size falls right in the middle of the range for ground-dwelling polygynous primates such as gelada and hamadryas baboons, which suggests thatm like them and like gorillas, human males arenot as adapted for easygoing promiscuity as ome earlier enthusiasts for the chimpanzee model of human adaptations may have wished." (Badcock, C. (1991) Evolution and Individual Behavior: An Introduction to Human Sociobiology Oxford: Blackwell. pp. 149)
Sandor and Mehdi (1979) postulated that steroids are very ancient biomolecules which evolved prior to the origin of eukaryotes and were even synthesized abiotically." (Matsuda, Ryuichi (1987) Animal Evolution in Changing Environments, with Special Reference to Abnormal Metamorphosis. N.Y.: Wiley Press pp.9)
"We found that although all salivary T concentrations fell within the normal physiological range in both males and females, non-RH of both sexes had significantly lower average T concentrations than did RH." (Hampson, E. & Moffat, S.D. (1994) Is testosterone related to spatial cognition and hand preference in humans? Brain and Cognition 26: 262)
"In our sample, LH or ambidextrous individuals tended to have lower, not higher, T concentrations. However, this does suggest that some relationship between T and hand preference may in fact be present, and it will be important to work out the mechanisms that account for the difference in free T, as these may eventually shed light on the ontogeny or correlates of hand preference." (Hampson, E. & Moffat, S.D. (1994) Is testosterone related to spatial cognition and hand preference in humans? Brain and Cognition 26: 262)
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