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
Testosterone appears to be a major contributing factor to sexual motivation in male primates, including humans. The elimination of testosterone in adulthood has been shown to reduce sexual motivation in both male humans and male primates. Male humans who had their testicular function suppressed with a GnRH antagonist displayed decreases in sexual desire and masturbation two weeks following the procedure. Research from male rhesus monkeys suggests testosterone functions to increase sexual motivation, thereby motivating males to compete for access to sexual partners. It is postulated that the motivating effects of testosterone in male rhesus monkeys promotes successful sexual competition and may be particularly important motivating tools for low ranking males. 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. 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. However, some research with nonhuman primates suggests a role for androgens in female sexual behaviour. Adrenalectomized female rhesus monkeys displayed diminished female sexual receptivity. Later studies revealed this diminished sexual receptivity was specific to the elimination of androgens that can be converted to estrogen.
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 a single partner relationship or single men. Polyamorous women both have 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.
Estrogens and progesterone Estrogens and progesterone typically regulate motivation to engage in sexual behaviour for females in mammalian species, though the relationship between hormones and female sexual motivation is not as well understood. In particular, estrogens have been shown to correlate positively with increases in female sexual motivation, and progesterone has been associated with decreases in female sexual motivation. The periovulatory period of the female menstrual cycle is often associated with increased female receptivity and sexual motivation. 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 sexual attraction. Heterosexual females not using birth control pills who are ovulating (high levels of estrogens) have a preference for the scent of males with low levels of fluctuating asymmetry. Ovulating heterosexual females also display preferences toward masculine faces and report greater sexual attraction to males other than their current partner. From an evolutionary perspective, increases in estrogens during fertile periods in females may direct sexual motivation toward males with preferential genes (the good genes hypothesis).
Following natural or surgically induced menopause, many women experience declines in sexual motivation. Menopause is associated with a rapid decline of estrogen, as well as a steady rate of decline of androgens. 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.Hiller, J. (2005). Gender differences in sexual motivation. The journal of men's health & gender, 2(3), 339-345. 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. A link between vasopressin release and aggression has been observed in females, which may impair female sexual arousal and sexual motivation by leading to feelings of neglect and hostility toward a sexual partner. In males, vasopressin is involved in the arousal phase. Vasopressin levels have been shown to increase during erectile response in male sexual arousal, and decrease back to baseline following ejaculation. The increase of vasopressin during erectile response may be directly associated with increased motivation to engage in sexual behaviour.
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. 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. 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.
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 lesbian and bisexual women and period-related changes in circulating estrogen concentrations. 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.
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.
Clinical research
Men Testosterone is critical for sexual desire, function, and arousal in men. Aromatization of testosterone into the estrogen estradiol appears to be partially responsible for the effects of testosterone on sexual desire and function in men. 5α-Reduction of testosterone into the more potent androgen dihydrotestosterone (DHT) may have a small contribution to the effects of testosterone on sexual desire and function in men. Based on animal research, metabolites of DHT, including the neurosteroids and weak estrogens 3α-androstanediol and 3β-androstanediol, may be involved in sexual function in men. Men experience sexual dysfunction at testosterone levels of below 300 ng/dL, with men that have levels of testosterone of approximately 200 ng/dL often experiencing such problems. Complete loss of testicular testosterone production resulting in testosterone levels within the castrate range (95% decrease, to 15 ng/dL on average) with surgical or medical castration causes profound sexual dysfunction in men. 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. 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. 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. Estradiol supplementation maintains greater sexual desire in men with surgical or medical castration. High-dose estrogen therapy, which results in marked or complete suppression of testicular testosterone production such that testosterone levels are within the castrate range (95% decrease, to less than 50 ng/dL), causes decreased sexual desire and function. It has also been used to suppress sex drive in men with paraphilias and sex offenders. However, sexual function and activity appear to be significantly better with high-dose estrogen therapy than with surgical castration. Treatment of men with medical castration and add-back testosterone to restore testosterone levels, with or without the aromatase inhibitor anastrozole, showed that prevention of the conversion of testosterone into estradiol partially prevented restoration of sexual desire and erectile dysfunction by testosterone in men. However, this was not the case in another study with a similar design that used the aromatase inhibitor testolactone. Men with aromatase deficiency and estrogen insensitivity syndrome, and hence estrogen deficiency, appear to have normal sexual desire, function, and activity. However, estradiol supplementation in some men with aromatase deficiency increased sexual desire and activity but not in other men with aromatase deficiency. 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. However, other studies have not found or reported decreased sexual function in men treated with SERMs including tamoxifen, clomifene, raloxifene, and toremifene.