Human evolution theory utilizing concepts of neoteny & female sexual selection
An etiology of neuropsychological disorders such as autism and dyslexia, and the origin of left handedness.

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Hormones: bibliographical excerpts

"However, Couwenbergs et al. (1986) have reported that, when salivary T is related to serum T, this hormone ratio is clearly negatively correlated with serum T, in particular interindividually. This means that the share of free T in the total T is higher the lower the overall amount of T. An alternative explanation was given by Rey et al. (1988) who postulated that androgen metabolism is salivary glands modulates saliva testosterone levels both in men and women. In women, the "excess" of saliva testosterone cold be due to conversion of androstenedione in the salivary glands. (Hassler, M. (1991) Testosterone and artistic talents. International Journal Neuroscience 56 (1-4): p. 35)

"T exerts its influence together with other hormones and with neurotransmitters (Hutchinson & Steimer, 1984; Whalen, 1984), and it may act on the brain as T, or by its metabolites estradiol and dihydrotestosterone." (Hassler, M. (1992) Creative musical behavior and sex hormones: musical talent and spatial ability in the two sexes. Psychoneuroendocrinology 17 (1): pp. 66)

"Many environmental factors, such as food, temperature, photoperiod, and population density, affect the endocrine activity. Of these, nutrition is most fundamental, because the organs or cells that produce and release hormones must grow to be functional. These environmental factors induce production and/or release of hormones." (Matsuda, Ryuichi (1987) Animal Evolution in Changing Environments, with Special Reference to Abnormal Metamorphosis. N.Y.: Wiley Press pp. 7)

"If orthogenesis was the final expression of the spirit of American neo-Lamarckism, the alternative, less highly structured form of the theory continued to flourish into the twentieth century. The one point lacking was experimental proof of the inheritance of acquired characters, a deficiency that began to seem all the more important as the new trend toward experimental biology gained ground. The French physiologist C. E. Brown-Sequard reported positive results with the inheritance of epilepsy induced by brain mutilations in guinea pigs. This was widely discussed (e.g., Romanes, 1892-97), but it was not confirmed that the results were due to genetic inheritance. Possibly the mutilation produced a toxin transmitted from mother to offspring in the uterus." (Bowler PJ (1984) Evolution, The HIstory of an Idea. Univ of California Press: Berkeley p. 250)

"As early as 1918, Richard Godschmidt had spoken of "rate genes" (see Goldschmidt, 1923, and 1938, pp. 51-78, including discussion of Sewall Wright's {1916} studies of coat color in rabbits). He discovered that "genetic races" of the gypsy moth, Lymantria dispar, differed only in genes controlling the depositional rates of pigment in caterpillars. In some races, a pattern of light markings persists until pupation; in others, this pattern is gradually covered by a dark cuticular pigment deposited at definite rates. Goldschmidt found that those rates differed among races and were intermdiate in heterozygous hybrids of intermediate color. Ford and Huxley (1927) studied eye coloration in the amphipod Gammarus chevreuxi. Red and black are Mendelian alternatives. In this species, all colored eyes (some are uncolored) are red at first and change to black as melanin is deposited at definite rates during development. Ford and Huxley discovered a set of genes that produced a graded series of colors by altering both the rates and times of onset for deposition of melanin. Goldschmidt generalized this theme: 'The mutant gene produces its effects, the difference from the wild type, by changing the rates of partial processes of development. These might be rates of growth or defferentiation, rates of production of stuffs necessary for differentiation, rates of reactions leading to definite physical or chemical situations at definite times of development, rates of those processes which are responsible for segregating the embryonic potencies at definite times.' (1938, pp. 51-52) If genes produce enzymes and enzymes control rates of processes, what possible justification can be offered for universal acceleration in phylogeny? Acceleration, to be sure, does occur, but there is no reason to consider it any more fundamental, or even any more common, than retardation. The retardation of somatic characters usually results in paedomorphosis, while acceleration yields recapitulation. If both acceleration and retardation are equally valid in theory, then these results are equally orthodox. Paedomorphosis can no longer be cast aside as an exception to universal recapitulation. This new condition of "equal orthodoxy" is emphasized in J.B.S. Haldane's article on "The Time of Action of Genes, and Its Bearing On Some Evolutionary Problems": 'There has been a common tendency in evolution for development to accelerate, ie., for certain characters to appear progressively earlier in the life cycle...This presumably means that the time of first action of certain genes has tended to be pushed back...Another common tendency has been a retardation of certain characters relative to the life-cycle, so that originally embryonic characters persist in the adult. This is known as neoteny.' (1932, 00. 15-16; see also Huxley, 1923, p. 616) In writing his "critical restatement" of the biogenetic law, Garstang (1922) did not "discover" paedomorphosis or any of the other well-known exceptions to recapitulation. Instead, he recognized that they could no longer be dismissed as exceptional, for they were now the expectations of a new theory, and they demanded equal status with all the phenomena of recapitulation. Paedomorphosis is no "degenerative exception" to universal acceleration. Genogenesis is not the "secondary falsification" of an essentially palingenetic development. The facts that had lurked so long in limbo of exception were elevated to orthodoxy by the discoveries of mendelian genetics." (Gould, S.J. (1977) Ontegeny and Phylogeny. Cambridge: Belknap Press. p. 205-206)

"Smirnov published a paper in the Communist Academy Herald defending he concept of the inheritance of acquired characters. ... Smirnov devoted much of his presentation to the central idea of Mechanistic-Lamarckism n-- the assumption that changes in the somatic portions of the organism give rise to corresponding changes in the sex cells. Smirnov tried to find a hypothetical explanation for this correspondence. He favored the suggestion that the soma influenced the sex cells by means of hormones. " the result of a change in the environment, a particular organ is forced to exert itself, then this exertion will cause an unusual configuration in the hormones in the given organ. These hormones then enter into the sex cells and ... in the next generation, by virtue of their specificity, give rise to the same results in the parent generation. These conditions nicely explain induced inheritance." [quoted from Eugenni Sergeevich Smirnov's, New Data Concerning an Inherited Environmental Effect and Contemporary Lamarckism in Communications of the Communist Academy, 1928, Bk 25: p. 192] (Blacher, L. I. (1982) The Problem of the Inheritance of Acquired Characters. Amerind Publishing: New Delhi pp. 138-9)

"Among animal breeders there is a widespread belief that the high milk yield of cattle is due to the constant mechanical stimulation to the teats during milking and that the results of this action seem to effect not only the individuals experiencing the mechanical influence but their offspring as well. Since a physiological or genetic mechanism for such an effect through the teats on the germ cells and thereby on the milk production of the offspring was inconceivable, the breeders tried to think up some other explanation for the inheritance of a high milk yield. E. Dechambre advanced one such hypothesis. [footnote states that this was in E. Dechambre's Reflexions sur les caracteres acquis et sur leur transmissibilite in Rev. gen. Sci. pures et appl. et Bull Soc. philomat, 1949, 56: p. 182] He believed that the state of neoteny -- the absence of metamorphosis and the consequent occurence of sexual maturity in the larval stage as found with some salamanders, such as axolotl -- was linked to the underdevelopment of the thyroid gland. Since the larvae of the axolotl (Amblystoma mexicanum) live in nature under the same ecological conditions as the larvae of another species, A. tigrinum, which nonetheless undergoes metamorphosis, Dechambre considered neoteny inthe axolotl as a trait acquired under the influence of the environment and transmitted through inheritance. He concluded that this was an example of the environment acting on the soma which in turn affected the germ-plasm by means of hormones. In Dechambre's opinion, one could reason analogously that the intensified functioning of the milk glands during milking affected the production of hormones, which in turn acted upon the germ-plasm and caused a still more intensified development of the milk glands in the offspring. Of course, Dechambre could not cite any direct corroborating evidence for this hypothesis." (Blacher, L. I. (1982) The Problem of the Inheritance of Acquired Characters. Amerind Publishing: New Delhi pp. 188-9)

[hormonal distinction between progenesis and neoteny in insects] "Entomologists generally make a distinction between two types of juvenilization in adult insects. They speak of prothetely when the adult develops too "early" (perhaps at a precocious molt), leaving some characters in a larval state. When development proceeds at its normal pace, but certain characters retain their juvenile form in the imago, metathetely has occured (Singh-Pruthi, 1924; Wigglesworth, 1954; Novak, 1966; Matsuda, in press). This classification duplicates the distinction between progenesis (prothetely) and neoteny (metatheely). Before the elucidation of endocrine control for metamorphosis, entomologists often denied the validity of such a separation, arguing that protheely and metathetely merely represent the end points of a continuum (which, of course, they do) and that the distinction had no significance either in mechanism or adaptive meaning (just as students of other animal groups often denied a meaningful distinction between progenesis and neoteny). The demononstration of potentially different mechanisms for the two modes of juvenilization has verified the importance of separating prothetely and metathetely. Southwood (1961) has pointed out that brachyptery (short-wingedness) is often a juvenile trait, especially when it represents part of a polymorphism or spectrum of geographic variability within a species. It may arise in two distinct ways: by excessive influence of the juvenile hormone, leading to juvenile characters in the adult (metathetely); or by depression of juvenile hormone levels, leading to adult characters in the larva (prothetely), perhaps by suppression of a molt (prothoracic glands are often lost in the adult; if a pronounced drop in juvenile hormone induces the adult state at an early molt, later molts are usually suppressed). Southwood discusses ...'the problem of distinguishing between the former, production of an adult with larval characters, which could perhaps be called neoteny, and the latter, a larva with adult characters, which is a condition homologous with paedogenesis {=progenesis}...Such a differentiation may appear artificial, but it does have the important distinction, in the present theory, that the former results from a lengthening of the influence of the juvenile hormone and the latter from a reduction in this period.' (1961, pp. 63-64) (Gould, S.J. (1977) Ontegeny and Phylogeny. Cambridge: Belknap Press. p. 304)

"Numerous enviromental factors (carbon dioxide, tension, population density, temperature, photoperiod, etc.) have been known to influence the growth and sexuality in hydras (Loomis 1957, 1959, Burnett and Diehl 1964, Burnett 1968, Schulz and Lesh 1970, Gurkewitz et al. 1980, Shoskak 1981). These environmental factors affect the morphogenesis of hydras by influencing the activity of the four kinds of morphogens or hormones, which consist of an activator and inhibitor for head formation and an activator and inhibitor for foot formation; the two activators are peptides with molecular weights of about 1000, and the inhibitors are peptides with modecular weights (500) (Schaller et al. 1979). It is important to point out further that mutants known to affect morphogenesis of hydras (non-budding, aberrant, maxi, mini, discovered by Schaler el al. 1977a,b,c) control the quantity of localized hormones (morphogens). (Matsuda, Ryuichi (1987) Animal Evolution in Changing Environments, with Special Reference to Abnormal Metamorphosis. N.Y.: Wiley Press p. 62)

"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)

‘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)

"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)

"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)

"The GBG model is essentially a theory of sex-related differences because prenatal testosterone levels is the pivotal concept. If there is little or no prenatal testosterone available during the gestational stage when the genitals are being formed, the fetus will develop as a female, even if the chromosomal pattern is male. Thus, the effect of prenatal testosterone will depend on the amount available at different gestational ages and the sexual status of the fetus. Males necessarily are exposed to more prenatal testosterone than females because this hormone is produced by their own developing testes. The mother also provides smaller quantitites of masculinizing hormones via her adrenals and ovaries and from other structures such as body fat. Smoking and extreme stress can also increase testosterone production in pregnant women, which in turn increases the probability of left-handedness in offspring (Bakan, 1991). As predicted by the GBG model, males have a higher rate of left-handedness, superior visual-spatial skills, much higher incidences of dyslexia and stuttering, and a sex -differentiated pattern of immune disorders. (These data are reviewed in Coren & Halpern, 1991; Halpern & Coren, 1993; and Halpern, 1992.) (Halpern, D.F. (1994) Evaluating support for the Geschwind-Behan-Galaburda model: with a rubber ruler and a thumb on the scale. Brain and Cognition 26 (2): 186)

"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, N. & Galaburda, A.M. (1987) Cerebral Laterization. MIT Press: Cambridge p. 3)

"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)." (Worthman, Carol M. & Konner, Melvin, J. (1987) Testosterone levels change with subsistence hunting effort in !Kung San men. Psychoneuroendocrinology 12(6): pp. 450)

"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 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, N. & Galaburda, A.M. (1987) Cerebral Laterization. MIT Press: Cambridge pp. 116-117)

"The concentrations of serum total and free testosterone were studied in 30 healthy, middle-aged men during a dietary intervention program. When men were transferred from their customary diet to an experimental diet, which contained less fat with a higher polyunsaturated/saturated ratio (P/S-ratio) and more fibre, there was a significant decrease in serum total testosterone concentrations (22.7 +/- 1.2 vs 19.3 +/- 1.1 nmol/l SEM, P less than 0.001). Furthermore, serum free, unbound testosterone fell from 0.23 +/- 0.01 to 0.20 +/- 0.01 nmol/l SEM (P less than 0.01). The hormonal changes were reversible. This observation suggests that testosterone activity in plasma can at least partly be modified by changing the composition of the diet." (Hamalainen EK, Adlercreutz H, Puska P, Pietinen P (1983) Decrease of serum total and free testosterone during a low-fat high-fibre diet. J Steroid Biochem18(3):369-70)

"The effect of acute activation of the ACTH-adrenal axis on circulating testosterone (T) levels was investigated. Elevation of circulating cortisol resulting from insulin-induced hypoglycemia or the administration of hydrocortisone was followed by a rapid decrease in serum T levels, without accompanying changes in LH or PRL. These findings suggest that hypercortisolism of endogenous or exogenous sources suppresses T secretion by a direct action on the testis. This adrenal-testicular axis may have biological implications on the reproductive adaptation to stress." (Cumming DC, Quigley ME, Yen SSC (1983) Acute suppression of circulating testosterone levels of cortisol in men. J Clinical Endocrinological Metabolism 57: 671)

“To determine whether ethanol per se affects testosterone metabolism, alcohol was administered to normal male volunteers for periods up to four weeks, resulting in an initial dampening of the episodic bursts of testosterone secretion followed by decreases in both the mean plasma concentration and the production rate of testosterone. The volunteers received adequate nutrition and none lost weight during the study, which tended to exclude a nutritional disturbance as the cause of the decreased testosterone levels. The changes in plasma luteinizing hormone suggested both a central (hypothalamus-pituitary) and gonadal effect of alcohol. In addition, alcohol consumption increased the metabolic clearance rate of testosterone in most subjects studied, probably owing to the combined effects of a decreased plasma binding capacity for the androgen and increased hepatic testosterone A-ring reductase activity. These results indicate that alcohol markedly affects testosterone metabolism independently of cirrhosis or nutritional factors.” (Gordon GG, Altman K, Southren AL, Rubin E, Lieber CS (1976) Effect of alcohol (ethanol) administration on sex-hormone metabolism in normal men. N Engl J Med 295 (15): 793)

"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)

"Reproductive hormonal dynamics were assessed in 10 massively obese men, 200-380% of ideal body weight (percentage ideal body weight) and 11 similarly-aged controls who were 85-135% of ideal body weight. The mean serum testosterone of the obese group was significantly lower than normal (223.1 + - 26.0 (sem) ng/dl vs. 599.2 + - 58.1 ng/dl, P < 0.001). Despite their reduced serum testosterone levels, the obese subjects had normal secondary sexual characteristics except for slightly decreased facial hair and normal sized testes. ... We conclude that, in massively obese men, 1) serum testosterone and sex-hormone-binding-globulin are low, 2) total serum testosterone and free testosterone correlate negatively with weight but do not correlate significantly with sex-horone-binding-globulin, 3) responses to LHRH, HCG, and clomiphene indicate substantial reproductive hormonal axis reserve, and 4) a subpopulation 2/10) of the most massively obese subjects may have a defect in the hypothalamic-pituitary axis as suggested by its low free testosterone in the absence of elevated gonadotropins or hyper-response to LRH." (Glass, A.R., Swerdloff, R.S., Bray, G.A., Dahms, W.T. & Atkinson, R.L. (1977) Low serum testosterone and sex-hormone-binding globulin in massively obese men. J Clinical Endocrinology and Metabolism 45 (6): pp. 1211)

"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)

"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)

"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)

"Current cigarette smokers generally showed higher levels of total, bioavailable, and free testosterone, DHT, SHBG, and higher DHT: testosterone ratios than did nonsmokers. This effect of smoking on total testosterone and SHBG levels was statistically significant for all ethnic groups combined (P< 0.05; Table 1)." (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)



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