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