Gender differences in sexuality are, among other things, a function of hormones and brain neurotransmitters. − Rakyat Biologi

First, lets review the evidence to the effect that hormones determine sexual identity in otherwise normal animals. I cover a lot of this terrain in chapter 6 because homosexuality and transsexualism are important fields of research in and of themselves, so I will skip that material here. At any rate, here is a summary of the relevant literature. Sexuality depends on five major things: 1) anatomy (one needs to have a penis, for example, to manifest and experience full male sexuality), 2) physiology (one needs the appropriate balance of hormones in brain and body to be capable of sexual function), 3) sexual identity (one will usually behave sexually more like a male or female if one feels like a male or female), 4) sexual orientation (independently of all the above, one will tend to manifest gender-specific sexual behavior if one is attracted sexually to the opposite sex), and 5) culture (for example, sexual behavior can be repressed or facilitated or oriented by cultural conditioning). Animal species vary a great deal with regard to how prenatal hormones can affect any of the five dimensions of sexuality I have just outlined. With regard to anatomy, the reader has already understood that sex hormones are the main determinant of the development of gender-specific anatomy in mammals in general and also in many other simpler animals as well. With regard to physiology, it is quite easy to render an animal impotent or sexually inactive with hormonal manipulations, and in some species, it is even possible to change the sexual behavioral profile with postpubertal manipulations. This is not observed in any radical manner in humans, though subtle such effects are observed. With regard to sexual identity and sexual orientation, it is very difficult to imagine how these two psychobehavioral dimensions could be dissociated in animals other than humans, but one thing is for sure, these two dimensions heavily depend on prenatal hormones in many species, including humans. Sheep resemble hormonal robots: a single well timed prenatal injection of a sex steroid of the opposite sex produces an ewe that sexually behaves more like a ram. Rats, whose natural sexuality is more androgynous than humans, also tip into the opposite gender’s sexual repertoire following a single hormonal injection before birth. There are many incidences of partial masculinization, demasculinization, feminization, or defeminization, by hormonal inflections, of animal sexual anatomy, physiology, and psychology. In rats, dogs and cows, there is the well-known "freemartin" effect: females that are exposed to androgens from male twins in utero are more ready to mount other females than females who did not have male co-twins. I have not found evidence of the existence or inexistence of this phenomenon in humans. I think that such research has simply not yet been carried out in humans. Animals and humans can be partly metamorphosed in their sexuality by a number of abnormal hormonal events: adrenal hyperplasy, androgen insensitivity, medical hormonal treatments of pregnant mothers, hormonal effects of maternal stress, hypogonadism, castration, etc.

The behavioral aspect of sexuality is less directly conditioned by sex hormones than is development of gender-typical anatomy. Sex hormones are unable to directly produce behavior. Only the brain directly produces behavior. How then can hormones modulate brain physiology responsible for behavior ? The main hormone-to-brain modulation would be expected to be via neurotransmitters. Neurotransmitters in fact resemble hormones molecularly. In mammals, steroidogenesis (particularly testosterone and estradiol) has been shown to alter neuronal firing patterns and the binding of neuronally released transmitters, either prenatally or postnatally. It is known (not by many people) that the hormone testosterone has an antagonistic relationship with the neurotransmitter serotonin, and an agonistic relationship with the neurotransmitter dopamine. In opposition to this, the hormone estrogen has an agonistic relationship with serotonin, and an antagonistic relationship with dopamine. In other words, estrogen favors the anabolism (synthesis) of serotonin and the catabolism (breakdown) of dopamine. One indicator of this is that when women are at their estrogen peak in the menstrual cycle, approximately 14 days before or after menstruation, brain serotonin is at its highest, and brain dopamine is at its lowest, as indexed by means of indirect indicators in the cerebrospinal fluid or in blood. The neurodynamic effects of sex hormones on the brain are not only developmental, not only structuring (trophic) or activational (affected by puberty), they are also physiologic. In other words, they have relatively immediate effects on brain function. A large number of behavioral fluctuations have been linked, for example, to the menstrual cycle. These modulations are quite subtle, and are technically quite difficult to measure. Modulations of cognitive abilities, behaviors and feelings in normal women have been and still are inconsistently replicated, and are therefore legitimately controversial. However, as I show in chapter 9, menstrual fluctuation of cognitive components of certain brain diseases or disorders help to clarify the link. One of the aspects of our experience and behavior which is conditioned by hormones is our sexuality.

One important aspect of sexuality is « copulatory drive ». In most species, males have higher copulatory drive than females, and this is certainly the case for humans (Campbell, 1994; Ellis, 1991; Hessellund, 1976; Laumann, 1994). Sexual desire in women reaches its peak just after ovulation. Recent research has found that the peak of sexual desire in women is facilitated by naturally fluctuating testosterone and inhibited by naturally fluctuating progesterone. Androgen treatment in adult women not only slightly increases their libido (without changing their sexual orientation) but it specifically makes their clitoris more sensitive. In fact, androgen treatment increases women’s libido more than does estrogen treatment, which has on occasion been reported to actually lower the sex drive. It is now known that testosterone injections can alter the sex drive not only in adulthood, but even with prenatal treatment naissance (Adkins-Regan, 1988; Broere et al, 1985). Transsexuals who change from a male body to a female body, and who take the appropriate feminizing hormones, report a drop in their libido (sex drive). Women who become men report the opposite effect. One recent study found clear activating effects of sex hormones in humans. In a group of 35 female-to-male transsexuals and a group of 15 male-to-female transsexuals a large battery of tests on aggression, sexual motivation and cognitive functioning was administered twice: shortly before and three months after the start of cross-sex hormone treatment. The administration of androgens to females was clearly associated with an increase in aggression proneness, sexual arousability and spatial ability performance. In contrast, it had a deteriorating effect on verbal fluency tasks. The effects of cross-sex hormones were just as pronounced in the male-to-female group upon androgen deprivation: anger and aggression proneness, sexual arousability and spatial ability decreased, whereas verbal fluency improved. This study offers evidence that cross-sex hormones directly and quickly affect gender specific behaviours. The most radical natural effects of sex hormones on sexuality occur in relation to parturition, hysterectomy, and menopause. These situations produce huge and abrupt drops in estrogen in particular, and to a lesser extent of other sex hormones. One study found that sexual desire dropped to zero in 16% of women during the first twelve months after having given birth. Brain serotonin, as indexed in blood plasma, is believed to climb up during pregnancy, and to drop abruptly to a very low level at parturition. Another study found that a whopping 89% of normal women reported a major drop in sexual desire after menopause.

There are many interesting and relevant things that could be said about findings from investigations of the relations between individual differences in hormone physiology and in behavior, sexual in particular. More is known about effects of androgens, both because salivary assays have been problematic with estradiol and because of the difficulties of controlling for phase of the menstrual cycle. Elisabeth Cashdan recently looked at both estradiol and various androgens in serum, collected early in the follicular phase in women, and was surprised to find that estradiol and the androgens varied similarly with all the behaviors she looked at, including sexual "restrictedness". Levels of estradiol, total testosterone, free (unbound) testosterone, and androstenedione were all positively correlated with number of sexual partners within the last year, and negatively correlated with need for long-term commitment before engaging in sex. Unfortunately, Elisabeth did not collect data on libido. However, taste for sexual variety is necessarily related to libido one way or the other. Taste for sexual variety is, however, a stereotypically male trait, and it is interesting to find that it has direct hormonal correlates.

Of course, hormones are far from being the only important determinant of sexual behavior in humans. Social and genetic components are just as important. A researcher named Steve Gangestad has published evidence from twin studies that the disposition toward having casual sex is concordant enough in monozygotic twins and discordant enough in dizygotic twins to conclude to a moderate hereditary determination. It is not known whether the heredity of this trait depends on the sex chromosomes (X or Y), but that would be very unlikely. So in short, a large part of the variability of sexual behavior is driven by biology which is probably not, at outset, sex-specific.

High levels of serotonin in the female rat results in less frequent lordosis. In other words, she will less frequently adopt a receptive position for intercourse: immobility, raised rump, tail to the side. A high concentration of noradrenalin, a neurotransmitter molecularly very similar to an endocrine hormone secreted by the adrenal medulla, results in increased sexual receptivity in the female rat. Dopamine also stimulates the sexual response. Such effects are observed in the male and female rat (copulatory approach and execution) and in both sexes in humans (Wilson et al, 1982; Everitt, 1978). One study of rats found that injection of dopamine D1- and D5-receptor agonists favored lordosis in female rats, and injection of D1 and D5 antagonists reduced lordosis. The D1 receptor is so named because it was the first to be discovered, and more types are regularly being discovered. As has been remarked by certain commentators, neurochemical manipulations which reduce the sex drive should be interpreted with caution: any unpleasant effect of such a manipulation can in itself be the cause of reduction of sexual behavior. Likewise, manipulations which increase the sex drive could produce their effect by improving mood or energy level. So it will be important to carefully analyze such effects in humans while exhaustively controlling for relevant side effects. Psychopharmacology is progressing at a very rapid rate, such that antidepressive medication now carries fewer and fewer side effects. It is clear that certain serotonin agonists (reuptake blockers) frequently substantially improve mood, produce little unpleasant side effects, and severely curtail sexual desire. The opposite is never reported, namely the antidepressant effect and no side effects except increase in sexual desire. Also, Parkinson’s disease patients in the early stages of the disease often complain of anhedonia (loss of all forms of pleasure including sexual). One common treatment is L-DOPA a dopamine precursor (agonist). This medication has frequently been found to help lift the anhedonia, including the sexual part. Indeed, dopamine is believed to be the most important neurotransmitter involved in the experience of pleasure. Animals will administer themselves electrical current through electrodes implanted in their own brain. But they seek to so stimulate themselves (compulsively, I might add) most typically when the active part of the electrode is implanted in neurons which use dopamine as their neurotransmitter. One finding adds light to our very small baggage of knowledge about dopamine factors involved in the sex drive in humans -without the complications of drug administration to sick people. The geneticist Dean Hamer and his colleagues have observed a modest correlation between a dopamine D4 receptor gene polymorphism and lifelong number of sexual partners. This association appears to be mediated by the effect of the D4DR variation on the personality trait of Novelty Seeking. Obviously D4DR is not a "monagamy gene" per se, but it does illustrate, he says, how genes broadly involved in neurotransmission might contribute to rather specific aspects of behavior.

I must insist on re-stating that human sexual behavior is heavily socially conditioned. Nevertheless, several vestiges of primitive sexual brain circuits are operational in the human brain. Men’s erections and ejaculations are controlled (among other things) by opposed branches of the autonomic nervous system (ANS): the sympathetic and parasympathetic branches. The “purpose” of the sympathetic branch of the ANS is to activate the organism for an urgent response. Walter Cannon, a now deceased neurophysiologist, became famous, among other things, for his summary of sympathetic action. He called it the four “F” system (flight, fight, feeding, fornication). In opposition to this, the parasympathetic branch of the ANS is destined to activate vegetative function when the organism is in a relaxed state: digestion, micturition (number one), defecation (number two), etc. When a person is suddenly terrified, it sometimes happens that a massive surge of sympathetic activation is followed by an equally massive rebound of parasympathetic activation. When this happens, the person turns white (sympathetic overactivation) but then faints and micturates and defecates (parasympathetic overactivation), an experience which most people would rather avoid. This helps us to understand why the human male’s sexual function is subject to dysfunction: an imbalance in autonomic function may prevent either erection or ejaculation. Furthermore, penile tumescence (erection) consists of blood accumulating in sponge-like cisterns in the penis’s shaft. Obstruction or denervation (weakening of neural control) of the small blood vessels providing that surge of blood may also engender a problem of anerectility. Primitive brain circuits controlling aspects of sexuality in humans are not limited to the male sex. The sexuality of women is not angelic: for example, certain neurons in a woman’s brain stem, if pathologically uninhibited by rare neurological conditions, can lead her to manifest “lordosis”, sexual posturing seen usually in reflex form in lower mammals. A special type of tumor of the hypothalamus called “hamartoma” can produce sexual “mania” in girls as in boys. I have had the opportunity of studying in detail such a case. This seven year old patient was uncontrollably aggressive and made explicit sexual statements to anybody and everybody close enough to hear him. He had not yet developed precocious puberty, though this commonly happens in hypothalamic hamartoma. Surgery for such cases is not always effective, and when that happens, the prognosis (forecast) is very poor: the epilepsy gets worse and the patient has to be institutionalized.

Rhawn Joseph has contributed some interesting speculations about differences between men’s and women’s sexuality. He believes that men’s sexual response is far more “complicated” than women’s sexual response. This is an unusual point of view. Most commentators focusing on the psychological aspects of sexuality would, I think, come to the opposite conclusion. But please understand that Joseph is focusing here strictly on the actual reproductive act per se. Men, he states, must obtain erection, penetrate, thrust and ejaculate. Women, he states, are required to do none of these. Consequently, men’s sexual response must be more easily triggerable and guided by visual and tactile stimuli. Joseph even believes that men’s sexual behavior is “more easily disrupted” than women’s because of this. I am not convinced that this is entirely correct. Women are more at risk than men for inability to achieve orgasm (by about 20%), pain during intercourse (by about 22%), and lack of interest in sex (16%). The last of these should not be brushed off as trivial. It is the main cause of consultation to clinical sexologists. However, as I explain in chapter 6, men certainly are more at risk for paraphylias (reproductively ineffective sexual preferences).

I believe we must be very wary of ethological evolutionist speculation. Ethological evolutionist speculation consists of interpreting behavior in terms of it’s adaptiveness, and supposing that the genes underlying the behavior in question must have been favored by natural selection. Since very often, we know little about ecological niches (living environments) of species having existed in now extinct conditions, ethological evolutionist speculation about emergence of traits sometimes can be quite fanciful. And of course, we know virtually nothing about the genes underlying most behaviors. But here is one speculation about differences in sexual behavior between men and women (and animals in general) that seems sound to me. Because males must ejaculate for procreation to occur, nature arranged sex so that males would reach orgasm first. Better, nature arranged sex so that females would be very little enclined to interrupt sex before the male reached orgasm. If the female reached orgasm before the male, she might stop copulation and not be impregnated. Such females would have no progeny and would therefore fail the test of natural selection.