Effects of hormones on sexual motivation

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Sexual motivation is influenced by hormones such as testosterone, estrogen, progesterone, oxytocin, and vasopressin. In most mammalian species, sex hormones control the ability and motivation to engage in sexual behaviours.

Measuring sexual motivation

Sexual motivation can be measured using a variety of different techniques. Self-report measures, such as the Sexual Desire Inventory, are commonly used to detect levels of sexual motivation in humans. Self-report techniques such as the bogus pipeline can be used to ensure individuals do not falsify their answers to represent socially desirable results. Sexual motivation can also be implicitly examined through frequency of sexual behaviour, including masturbation.

Hormones

Testosterone

According to data from the Journal of Zhejiang University–Science, male testosterone levels exhibit a rhythm that corresponds to recent sexual activity.

sexual competition and may be particularly important motivating tools for low ranking males.[2]
It is important to note that elimination of testosterone in primates does not reduce the ability to copulate; rather, it reduces the motivation to copulate.

Testosterone levels in males have been shown to vary according to the ovulating state of females. Males who were exposed to scents of ovulating women recorded higher testosterone levels than males who were exposed to scents of nonovulating women.[3] Being exposed to female ovulating cues may increase testosterone, which in turn may increase males' motivation to engage in, and initiate, sexual behaviour. Ultimately, these higher levels of testosterone may increase the reproductive success of males exposed to female ovulation cues.

The relationship between testosterone and female sexual motivation is somewhat ambiguous. Research suggests

androgens, such as testosterone, are not sufficient by themselves to prompt sexual motivation in females. In particular, studies with rhesus macaques have observed testosterone was not significantly associated with variations in level of sexual motivation in females.[2] However, some research with nonhuman primates suggests a role for androgens in female sexual behaviour. Adrenalectomized female rhesus monkeys displayed diminished female sexual receptivity.[4] Later studies revealed this diminished sexual receptivity was specific to the elimination of androgens that can be converted to estrogen.[5]

It is also suggested that levels of testosterone are related to the type of relationship in which one is involved. Men involved in

polyamorous relationships display higher levels of testosterone than men involved in either a single partner relationship or single men.[6] Polyamorous women have both higher levels of testosterone and score higher on measures of sexual desire than women who are single or women who are in single-partner relationships.[6]

Estrogens and progesterone

periovulatory period of the female menstrual cycle is often associated with increased female receptivity and sexual motivation.[8] During this stage in the cycle, estrogens are elevated in the female and progesterone levels are low. At this time, mating is more likely to result in female pregnancy
.

Females at different stages of their menstrual cycle have been shown to display differences in

good genes hypothesis
).

Following natural or surgically induced menopause, many women experience declines in sexual motivation.[11] Menopause is associated with a rapid decline of estrogen, as well as a steady rate of decline of androgens.[12] The decline of estrogen and androgen levels is believed to account for the lowered levels of sexual desire and motivation in postmenopausal women, although the direct relationship is not well understood.

Oxytocin and vasopressin

The hormones oxytocin and vasopressin are implicated in regulating both male and female sexual motivation. Oxytocin is released at orgasm and is associated with both sexual pleasure and the formation of emotional bonds.[13] Based on the pleasure model of sexual motivation, the increased sexual pleasure that occurs following oxytocin release may encourage motivation to engage in future sexual activities. Emotional closeness can be an especially strong predictor of sexual motivation in females and insufficient oxytocin release may subsequently diminish sexual arousal and motivation in females.

High levels of vasopressin can lead to decreases in sexual motivation for females.

arousal phase. Vasopressin levels have been shown to increase during erectile response in male sexual arousal, and decrease back to baseline following ejaculation.[15] The increase of vasopressin during erectile response may be directly associated with increased motivation to engage in sexual behaviour.[13]

Nonprimate species

The hormonal influences of sexual motivation are much more clearly understood for nonprimate females. Suppression of estrogen receptors in the

ventromedial nucleus of the hypothalamus in female rats has been observed to reduce female proceptivity and receptivity.[16] Proceptivity and receptivity in the female rat are indicators of sexual motivation, thus indicating a direct relationship between estrogen levels and sexual motivation. In addition, female rats receiving doses of estrogen and progesterone were more likely to exert effort at gaining sexual attention from a male rat.[17]
The willingness of the female rats to access males was considered a direct measure of the females' levels of sexual motivation.

An increase in vasopressin has been observed in female rats which have just given birth. Vasopressin is associated with aggressive and hostile behaviours, and is postulated to decrease sexual motivation in females. Vasopressin administered in the female rat brain has been observed to result in an immediate decrease in sexual motivation.[13]

Sexual orientation

Little research has been conducted on the effect of hormones on sexual motivation for same-sex sexual contact. One study observed the relationship between sexual motivation in

bisexual women and period-related changes in circulating estrogen concentrations.[18] Lesbian women who were at the estrogen peak of their fertile cycle reported increased sexual motivation for sexual contact with women, whereas bisexual women reported only a slight increase in same-sex motivated sexual contact during peak estrogen levels.[citation needed
]

Both lesbian and bisexual women showed decreases in sexual motivation for other-sex sexual contact at peak estrogen levels, with greater changes in the bisexual group than the lesbian group.[citation needed]

Clinical research

Men

  • Testosterone is critical for sexual desire, function, and arousal in men.
    3β-androstanediol may be involved in sexual function in men.[25][26][27]
  • Men experience
    medical castration causes profound sexual dysfunction in men.[29][30] Combined marked suppression of testicular testosterone production resulting in testosterone levels of just above the castrate/female range (70 to 80% decrease, to 100 ng/dL on average) and marked androgen receptor antagonism with high-dosage cyproterone acetate monotherapy causes profound sexual dysfunction in men.[29][31] Treatment of men with medical castration and add-back of multiple dosages of testosterone to restore testosterone levels (to a range of about 200 to 900 ng/dL) showed that testosterone dose-dependently restored sexual desire and erectile function in men.[32] High-dosage monotherapy with an androgen receptor antagonist such as bicalutamide or enzalutamide, which preserves testosterone and estradiol levels, has a minimal to moderate negative effect on sexual desire and erectile function in men in spite of strong blockade of the androgen receptor.[29][33][34][35]
  • Estradiol supplementation maintains greater sexual desire in men with surgical or medical castration.
    estrogen deficiency, appear to have normal sexual desire, function, and activity.[22][21] However, estradiol supplementation in some men with aromatase deficiency increased sexual desire and activity but not in other men with aromatase deficiency.[22][21][40] Treatment with the antiestrogenic selective estrogen receptor modulator (SERM) tamoxifen has been found to decrease sexual desire in men treated with it for male breast cancer.[41] However, other studies have not found or reported decreased sexual function in men treated with SERMs including tamoxifen, clomifene, raloxifene, and toremifene.[22][42]
  • 5α-Reductase inhibitors, which block the conversion of testosterone into DHT, result in a slightly increased risk of sexual dysfunction with an incidence of decreased libido and erectile dysfunction of about 3 to 16%.[43][44][24] Treatment of healthy men with multiple dosages of testosterone enanthate, with or without the 5α-reductase inhibitor dutasteride, showed that dutasteride did not significantly influence changes in sexual desire and function.[45][24] Treatment of men with high-dosage bicalutamide therapy, with or without the 5α-reductase inhibitor dutasteride, showed that dutasteride did not significantly influence sexual function.[46] Combined high-dosage bicalutamide therapy plus dutasteride showed less sexual dysfunction than medical castration similarly to high-dosage bicalutamide monotherapy.[47]
  • Treatment of men with very high-dosage DHT (a non-aromatizable androgen), which resulted in an increase in DHT levels by approximately 10-fold and complete suppression of testosterone and estradiol levels, showed that none of the measures of sexual function were significantly changed with the exception of a mild but significant decrease in sexual desire.[42][48][24] Treatment of hypogonadal men with the aromatizable testosterone undecanoate and the non-aromatizable mesterolone showed that testosterone undecanoate produced better improvements in mood, libido, erection, and ejaculation than did mesterolone.[21][42] However, the dosage of mesterolone could have been suboptimal.[42]

Women

Transgender individuals

See also

References

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  13. ^ a b c d Hiller, J. (2005). Gender differences in sexual motivation. The journal of men's health & gender, 2(3), 339-345.
  14. S2CID 2106719
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  37. . A favourable feature of flutamide therapy has been its lesser effect on libido and sexual potency; fewer than 20% of patients treated with flutamide alone reported such changes. In contrast, nearly all patients treated with oestrogens or estramustine phosphate reported loss of sexual potency. [...] In comparative therapeutic trials, loss of potency has occurred in all patients treated with stilboestrol or estramustine phosphate compared with 0 to 20% of those given flutamide alone (Johansson et al. 1987; Lund & Rasmussen 1988).
  38. .
  39. . Treatment of sexual offenders. Hormone therapy. [...] Oestrogens may cause breast hypertrophy, testicular atrophy, osteoporosis (oral ethinyl oestradiol 0.01-0.05 mg/day causes least nausea). Depot preparation: oestradiol [undecyleate] 50-100mg once every 3–4 weeks. Benperidol or butyrophenone and the antiandrogen cyproterone acetate also used.
  40. PMID 17824171. {{cite book}}: |journal= ignored (help
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  47. . Dutasteride and Bicalutamide is a regimen of non-inferior efficacy to LHRH agonist based regimens for prostate volume reduction prior to permanent implant prostate brachytherapy. D + B has less sexual toxicity compared to LHRH agonists prior to implant and for the first 6 months after implant. D + B is therefore an option to be considered for prostate volume reduction prior to PIPB.
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  63. . Among the slight and temporary adverse events [of flutamide], most frequently reported and not requesting treatment discontinuation were headache (7.8%), respiratory tract disorders (7.0%), nausea and/or vomiting (4.0%), diarrhea (4.0%), dry skin (9.5%), and reduction of libido (4.5%).
  64. . [...] changes in serum levels of the aminotransferases [11] or side effects (stomach pain, headache, dry skin, nausea, increased appetite, decrease of libido) are only occasionally seen [with flutamide] [10, 11].
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