A brief overview of some hormonal effects on male and female sexual behaviors and thoughts
1998 by Rainer Stratkotter
For both males and females, various hormones can have "effects" on their sexual behaviors and thought
Among these hormones, androgenic hormones - such as testosterone (T) and dihydrotestosterone (DHT) - are especially noted for their ability to "increase the predisposition to engage in sexual behavior." (Udry, 1988, p. 710). This increased predisposition towards sexual behavior is believed to be linked with hormonally effected changes in the patterning (frequency, intensity, and duration) of sexual thoughts (e.g., sexual interests, motivations, attitudes, and fantasies).
The first section below deals with males, with its main focus on androgenic hormones' effects on sexual behaviors and thoughts (along with some mention of other hormones' effects). The second section deals with hormonal effects on females' sexual behavior and thoughts.
Hormonal effects on male sexual behaviors and thoughts
The view that there is a hormonal basis for sexual behaviors and thoughts is supported by "ample evidence" (Frayser, 1985, p. 12; see also Robbins, 1996), including evidence obtained from male adolescents (Udry, Billy, Morris, Groff, and Raj, 1985). Testosterone, which is an androgenic hormone, generally appears to be a dominant factor in male sexual libido and ejaculation, while erectile mechanisms can function despite abnormally low levels of T (Bancroft, 1984; Buvat, Lemaire, and Ratajczyk, 1996).
Although it is not certain what levels of the various androgens produce maximum effects on the various aspects of sexuality, studies which provide T to hypogonadal men suggest that above a certain threshold, increased T levels have no further effects (Sherwin, 1988). Since normal adult males' androgen levels are above the threshold, adult males are poor subjects for investigating the effects of androgens on sexuality (Udry, 1988, p. 711). In this regard, adolescent males are good subjects, as early adolescents can be considered to be analogous to hypogonadal adult males, except that normal pubertal development of the adolescents will remedy their androgen deficit (p. 711).
According to Udry, T is the "most behaviorally potent" androgen (Udry, 1990, p. 2; see also Udry, 1988, p. 713); although it is generally accepted that T's androgenic potency results from its conversion (by the 5a-reductase enzyme) to dihydrotestosterone (DHT) (Gower, 1995, p. 269; see also Norman and Litwack, 1987, p. 492; Demers, 1995, p. 28). Males with higher levels of T will generally also have higher levels of DHT.
[There are "intracellular receptors that bind testosterone and DHT with high affinity" (Winters, 1995, p. 1053), but "it has not been possible to unequivocally determine in which tissues which steroid [T or DHT] is the primary or sole initiator" (Norman and Litwack, 1987, p. 495). Hence, there is continued debate over whether T or DHT is the effectually most potent androgen, with support for either position dependent on the biological location in question (Mitchell, 1996, personal communication).]
Many of T's other actions depend on its metabolism, by an aromatase enzyme, to estradiol (Collaer and Hines, 1995, p. 57).
Of the total circulating T (Total-T) in normal men, "less than 4% is free (not protein bound), 1% to 2% is bound to cortisol binding globulin, about 40% is loosely bound to albumin, and the remainder is bound with high affinity to the b-globulin, SHBG" (Winters, 1995, p. 1050; this report conflicts with Udry's assertion that "Nine-tenths or more of T is so bound [to SHBG]", 1990, p. 3). Although "the function of SHBG remains controversial" (Winters, 1995, p. 1050), T effects should be interpreted in conjunction with SHBG effects, and should be the opposite of SHBG effects (Udry, 1988).
[Winters reports that "the finding of membrane binding sites for ABP (androgen binding protein) in the epididymis and for SHBG in testis ... suggests that these binding proteins" might be directly involved in androgen action (1995, p. 1050).]
The T that is unbound to SHBG is commonly termed Free-Testosterone (Free-T), and is believed to be the portion of the total amount of T able to act on receptor cites (directly or via T's metabolites, such as DHT and estradiol), thereby influencing behaviors and thoughts (Nieschlag, 1979; Udry, 1988). The Free-T level has been reported to be between about 1 and 2.5 or 3 percent of Total-T's level (Winters, 1995, p. 1051; see also Schurmeyer and Nieschlag, 1984); although higher percentages have been reported (e.g., Hammond, Nisker, Jones, and Siiteri, 1980, estimated that Free-T comprises 2 to 8 percent of Total-T).
There is a mixed use of the "Free-T" terminology in the literature. Some researchers make a clear distinction between "Free-T" and "bioavailable (non-SHBG bound) T" (e.g., Buvat, Lemaire, and Ratajczyk, 1996), while others do not (e.g., Udry, 1990; Christiansen and Winkler, 1992); and the term "Apparent Free Testosterone Concentration (AFTC)" also appears (e.g., Hjalmarsen, Aasebo, Aakvaag, and Jorde, 1996). The Free-T plus the albumin-bound T have been referred to as the non-SHBG-bound T (e.g., Gower, 1995, p. 337; Winters, 1995, p. 1051).
The albumin-bound T, because of the low-affinity binding constant, is thought to be as readily available to target tissues as is Free-T, hence "bioavailable testosterone is calculated by subtracting the SHBG bound testosterone from the total testosterone level" (Winters, 1995, p. 1051).
The Free-T index, which is calculated either as the Total-T / SHBG ratio, or as (Total-T)(SHBG) / (mean normal SHBG level), are ways "to correct the total testosterone value for variations in SHBG concentrations in plasma" (Winters, 1995, p. 1051). The Free-T index is believed to be a good indicator of measured Free-T; and is considered to be a better indicator of androgenicity than Total-T (Halpern, Udry, Campbell, Suchindran, and Mason, 1994, p. 221).
References and some suggested reading
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Christiansen, Kerrin; & Winkler, Eike-Meinrad (1992). Hormonal, anthropometrical, and behavioral correlates of physical aggression in !Kung San men of Namibia. Aggressive Behavior, 18: 271-280.
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Demers, Laurence M. (1995). Biochemistry and laboratory measurement of androgens in women. In G.P. Redmond (Ed.), Androgenic Disorders. New York: Raven Press. Pp. 21-34.
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Robbins, Ann (1996). The effects of hormones on male sexuality: Findings from clinical trials on male contraception. In Sondra Zeidenstein and Kirsten Moore (Eds.), Learning About Sexuality: A Practical Beginning. New York: The Population Council, Inc. Pp. 278-297.
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