HUMAN SEXUALITY: HORMONES IN ADOLESCENCE:

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For humans as well as other mammals, the biologically active fraction of total testosterone is believed to be free testosterone, testosterone not bound to sex-hormone binding globulin, SHBG. Horst and others have shown in boys that the increase of total plasma testosterone levels in puberty is associated with a sharp decline of SHBG binding capacity (especially for ages nine to fifteen years) and of the percentage of bound testosterone, so that free testosterone is increasing at a relatively faster rate than total testosterone. The situation for girls is slightly different; although the SHBG binding capacity increases from prepubertal age to adulthood, free (unbound) estradiol rises from prepubertal age until stage 3 of puberty at which it plateaus. Thus, it is probably not even sufficient to measure total plasma concentrations; at least for certain key hormones, one may have to analyze the unbound fraction in order to arrive at valid relationships between hormones and behavior.

The mechanism by which the timing of puberty is regulated is not yet fully understood. Much available evidence points to the assumption that it is not primarily the peripheral glands nor the pituitary but the brain itself, especially the hypothalamus, which is responsible. The currently most widely shared theory is the one proposed originally by Hohlweg and Dohrn on the basis of rat experiments, according to which puberty is induced by a change in sensitivity to circulating sex steroids of a sexual center in the central nervous system which regulates gonadotropin secretion. In its present form, the theory states that the hypothalamic gonadotropin-regulating mechanism in the prepubertal individual is much more sensitive to the negative feedback effects of circulating androgens and estrogens than in the adult. Thus, the low levels of sex hormones in the prepubertal individual are sufficient to suppress the release of gonadotropin-releasing factor from the hypothalamus and thereby the secretion of FSH and LH. With the approach of puberty, the hypothalamic negative feedback receptors show a progressive decrease in sensitivity to the sex steroids. Consequently, the secretion of pituitary gonadotropins increases, stimulating an increased production of sex hormones which, in turn, leads to the development of the secondary sex characteristics. During mid- to late puberty, a second and positive feedback mechanism matures which provides the capacity for an estrogen-induced LH surge to effect ovulation in the female.

Another pubertal event is the establishment of an episodic or pulsatile secretion of gonadotropins which, during puberty only, is associated with an augmentation of secretion synchronous with sleep. When children approach and enter (physically visible) puberty, they show more and more consistently episodes of LH secretory bursts at night as compared to daytime, and the amplitudes of these bursts increase. With advancing puberty, the amplitude (not the number) of the secretory episodes increases further, and late in puberty, the daytime secretion is also elevated. Similar findings have been described for FSH. Since this phenomenon appears to be independent of gonadal activity, it underlines the active role of the central nervous system in the initiation of puberty.

A competing theory of the initiation of puberty has been proposed by Odell and Swerdloff, on the basis of extensive experiments in the rat and corroborating evidence from other animals. They believe that sexual maturation, at least in male rats, and probably in pigs and cattle, is predominantly due to maturation at the gonadal level as a result of FSH induction of LH receptors in the gonads, resulting in increasing gonadal steroid secretion. They conclude from certain endocrine data on children that this mechanism also may be a contributing factor in the onset of human puberty.

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