C2: PROXIMATE DIFFERENTIATION: ONTOGENETIC MASCULINIZATION AND DEFEMINIZATION

CHAPTER 2

PROXIMATE DIFFERENTIATION: ONTOGENETIC MASCULINIZATION AND DEFEMINIZATION

Why do men have nipples?

They have no functionality--men cannot lactate. Nipples should be a quintessentially, and exclusively, female morphological characteristic. Were it not for the fact all men have nipples protruding from their chests, imagine the chagrin a man would feel if he was the only male who possessed this female trait. The reason men have nipples may surprise you. Men have nipples because, in a sense, all men were once little girls.

The book of Genesis seems to have gotten it backwards. Rather than being created from males, females are the "generic" form--in humans, as well as in most other species. The basic trend of nature is to produce a female. To get a morphological male, some hormonal intervention must occur during early fetal development. Otherwise, a morphological female develops. Males, as we will learn in later chapters, are also a later evolutionary phenomenon--they evolved as a reproductively "parasitic" subspecies exploiting the greater reproductive and parental investment of females.

In this chapter we will examine the processes that must occur to transform the "generic" female morphology to arrive at the very different male morphology. By using a “proximate analysis” (focusing on immediate physical causes and mechanisms), we will learn how, during early development, males differentiated from the basic female form. There are two separate processes required: masculinization and defeminization.

Finally, we will examine how errors in either masculinization or defeminization, occurring at either the morphological or neural level, can affect morphology and behavior.

MASCULINIZATION AND DEFEMINIZATION

X AND Y CHROMOSOME

The biological sex of virtually all mammals is determined by sex chromosomes. Each individual inherits 23 chromosomes from each parent, for a total of 46, arranged as 23 pairs. Twenty-two of these pairs are matched, and are the same in males and females. This leaves 1 chromosome pair, the sex chromosomes, to determine the biological sex of an individual.

Females have two X chromosomes, one X from the mother and one X from the father, and are designated XX. Males have one X from the mother and one Y from the father, and are designated XY. Females, having XX are only able to pass X chromosomes to their offspring. Males, having both X and Y are able to pass either an X or Y chromosome to their offspring. If the male provides an X chromosome to the ovum at fertilization, then a genetic female, XX, will result. If, however, the male provides a Y chromosome to the ovum at fertilization, then a genetic male, XY, will result.

It is the presence of the Y chromosome that triggers the development of internal and external male sex organs. In the absence of a Y chromosome, external female sex organs will develop. (However, two X chromosomes are necessary to ensure the full development of both internal and external female sex organs.)

HORMONES AND GONADAL DIFFERENTIATION

Research demonstrates that a single gene on the Y chromosome, known as the sex-determining region of the Y chromosome, or SRY (Haqq, King, Ukiyama, Falsafi, Haqq, Donahoe & Weiss 1994). This single gene is part of the gene complex, which is the catalyst for the events that lead to formation of the male testes. This gene complex is referred to as TDF (Testes Determining Factor). The presence of TDF triggers the genetic blueprint for testes to activate, and hence male development ensues. In the absence of SRY and TDF, female development ensues.

All mammalian embryos have the potential to develop either male or female forms – that is they are sexually bipotential. If TDF is present and functioning, then male fetal gonads (testes) will develop. If TDF is not present, then female fetal gonads (ovaries) will develop.

Once the genetic blueprint for testes or ovaries is triggered through the presence or absence of TDF, the fetus’ own sex hormones become critical in the differentiation of the internal and external sex organs, and the brain. It is the gonads that produce and secrete these hormones into the bloodstream. Male gonads (testes) produce and secrete androgens, such as testosterone and mullerian inhibiting substance, or MIS, which influence male development. Female gonads (ovaries) produce and secrete estrogens, which influence female development.

Development of the internal and external male reproductive organs depends upon the secretion of the right amount of androgens, such as testosterone and MIS. MIS causes the Mullerian ducts to shrink, which results in the degeneration of internal female reproductive organs. At the same time, the testes’ production of testosterone stimulates the Wolffian ducts to develop into the male internal structures (vas deferens, seminal vesicles, ejaculatory ducts). Testosterone also stimulates the previously undifferentiated external tissue to develop into male external genitals.

In contrast, the presence of the right amount of a specific hormone is not needed for the development of the internal and external female reproductive organs. As we have mentioned earlier, the female is the generic, or default, sex. If testosterone and MIS is not secreted, the female structures continue to develop. Without MIS, the Mullerian ducts do not degenerate, and instead develop into the internal female structures (fallopian tubes, uterus, vagina). In the absence of testosterone, the Wolffian ducts naturally discintegrate. The absence of these androgens also allows for the previously undifferentiated external tissue to develop into female external genitals (clitoris, labia majora, labia minora).

At the twelfth week after conception, differentiation is complete. We have seen that without critical prenatal masculinizing secretions, the embryo naturally continues to develop as a female. To masculinize, the secretion of TDF, and subsequent secretion of testosterone and MIS, are necessary events to lead to male development. Masculinazation and defeminization are complex processes and are, as we will learn, more at risk to errors.

HORMONES AND NEURAL DIFFERENTIATION

I believe that all differences in behavior are based in differences in structure. Otherwise, you have to believe in ghosts and spirits in the brain. There’s no doubt, when you look closely, that there are structural differences between the brains of men and women. The whole question is, how does the brain respond to those differences? -- Mark Breedlove (quoted in Blum, 1997).

Most of us can agree that males and females not only look different, but they also behave tend to differently in certain situations. Research suggests that the same hormones affect the sexual differentiation of the reproductive organs also affects the organization of the fetal brain (Breedlove, 1992; Donovan, 1988; Gerall, Moltz & Ward, 1992). Just as critical hormone secretions are responsible for differentiation of the gonads, the brain is also dependent upon such secretions at critical periods for differentiation. As Barash and Lipton (1997) put it, “As the body goes, so goes the brain. And as the brain goes, so goes behavior.”

Most of our knowledge about neural differentiation relies upon the study of other mammals, such as rats. The rat’s brain is sexually undifferentiated at birth, much like the human brain at eight weeks after conception. Release of hormones at this time by the gonads determines whether the rat will have a brain with either a male or a female organization, and thus determines certain aspects of the rat’s behavior.

A nice example of the effect that hormones have on the brain and behavior comes from the manipulation of hormone exposure in lab rats. Since the rat’s brain is undifferentiated at birth, this gives the researcher a good opportunity to study the effects of hormones at critical periods in the rat’s neural development. If a newborn male rat is castrated, there is no opportunity for testosterone to be released into the bloodstream, and therefore the rat grows to look like a male, but tends to behave like a female. Since the masculinizing effects of specific hormones were absent at the critical time in the rat’s neural development, the brain develops according to its “default” setting –female. This castrated male rat will be much less aggressive than a normal male rat. If injected with female hormones later in life, he would likely welcome the sexual overtures of other male rats (Barash and Lipton, 1997).

NEURAL MASCULINIZATION AND 'MOUNTING' BEHAVIORS

It seems reasonable to assume the behaviors required for successful copulation, in particular, would have a large genetic component, and that copulatory behavioral actions would be genetically "wired in" the brains of males and females. Copulatory behaviors are relatively specific, and complex, as noted by Weinrich (1987). To leave such essential reproductive behaviors to the vicissitudes of learning would be very reproductively risky. Indeed, copulatory behaviors are not learned behaviors, rather these behaviors are instinctive.

Masculine copulatory behavior consists of a sequence of actions referred to as mounting. Weinrich (1987) described mounting behavior in mammals as the following sequence:

Arousal, usually in the form of an erection, by the sight and/or smell of another, usually female animal, begins this process.

Positioning, generally so that the penis is near the female’s genitals.

Intromitting, inserting the penis into the vagina.

Thrusting, to stimulate the penis inside the vagina.

Orgasm, or ejaculation of semen into the vagina, is usually the culminating event for the male.

Mounting behavior by males must be conducted successfully in order to become a father and have descendants. Successful neural masculinization, by exposure to male hormones at the critical time, should “wire” into the brain mounting copulatory behaviors.

LACK OF DE-FEMINIZATION: 'MOUNT-RECEIVING' BEHAVIORS

Weinrich (1987) terms the complex and specific copulatory behavior in mammalian females as mount receiving behavior. We have seen that exposure to male hormones leads to masculine copulatory behaviors known as mounting. The absence of the male hormones leads to feminine copulatory behaviors known as mount receiving behavior.

Weinrich (1987) described mount receiving behavior in mammals as the following sequence:

Signaling, or demonstrating one’s willingness or sexual receptiveness, can be achieved behaviorally or chemically.

Positioning, generally so that the genetalia is accessable to the male.

Arching of the back, to further facilitate positioning.

Pelvic thrusting, coordinating with mate’s thrusts.

Orgasm, the function of which is still under investigation. There may be some adaptive value to the female orgasm, such as facilitating the entrance of sperm into the cervix. .

Mount-receiving behavior by females must be conducted successfully in order to become a mother and have descendants. Lack of defeminization should result in such mounting-receiving copulatory behaviors. Perhaps the above example with the castrated rat, having been deprived of male hormones at a critical period becomes clearer in light of this new information. Although, chromosomally he is male, through castration he lacks defeminization and therefore has the potential to display mount-receiving behaviors in later life.

THE SEXUALLY DIMORPHIC HYPOTHALAMUS

The hypothalamus, a brain structure just above the pituitary gland, monitors internal bodily conditions; its main function is the regulation of hormone production, hunger, thirst, body temperature, and sex drive. The hypothalamus serves as a link between the endocrine system (glands and hormones) to the nervous system (making us aware of our needs and drives). The hypothalamus plays a major role in fertility by directing the pituitary gland to release sex hormones.

Several researchers have reported a marked sex differentiation in the hypothalamus (Bloom et al., 1985; Breedlove, 1992; Crooks & Bauer, 1987). Once again, it is the prenatal circulation of testosterone that apparently causes this differentiation to occur. Certain specialized receptor cells in the hypothalamus are sensitive to the presence of estogens. If, in the case of a male, testosterone is present prenatally, the receptor cells are desensitized to estrogen. However, in the case of a female, the prenatal absence of testosterone allows these specialized cells to become very sensitive to the presence of estrogen.

At puberty, the female differentiated hypothalamus directs the pituitary gland to cyclically produce lutenizing hormone. This signals the ovaries to produce an egg, and the subsequent menstral cycle ensues. In contrast, the male differentiated hypothalamus directs the pituitary gland to steadily produce lutenizing hormone, resulting in the consistent production of testosterone. The sexually dimorphic hypothalamus results in cyclic fertility in females, and relatively consistent fertility in males (Breedlove, 1992).

THE SEXUALLY DIMORPHIC NUCLEUS (SDN)

The sexually dimorphic nucleus is a small (one cubic millimeter) section of the hypothalamus that is extremely sensitive to sex hormones. In rats, this area is five times as large in males than females; in humans, it is 2.5 times larger in males than females. This area may play an important role in male mounting behaviors and gender identity (Gibbons, 1991). Not surprisingly, it is suspected that prenatal levels of testosterone are related to this size difference in the SDN. If testosterone is injected into infant female rats, male-sized SDNs result. If male rats are injected with a testosterone-blocking agent, female sized SDNs result. The connection between the SDN and behavior is not yet completely understood, and is currently under investigation (see Blum, 1997; Breedlove, 1992; Swaab et al., 1989).

SEXUALLY DIMORPHIC CEREBRAL HEMISPHERES

Looking at the exterior of the brain, one can see that it is divided into two halves, right and left. These “halves” are the cerebral hemispheres, and appear to be mirror images of each other. Although the cerebral hemispheres appear to be very similar, each side is actually somewhat distinct in its organization and functions. In general, the left hemisphere is specialized for verbal processes (language), and the right hemisphere deals with spatial skills (recognizing shapes).

Diamond et al. (1981) reported finding that the cortex (outer layer of the brain) is thicker on the right side in male rats. Levels of testosterone are, again, associated with this difference, since male rats castrated at birth develop no such asymmetry. If human males exhibit this hemispheric difference, that might help explain the noted sex difference in spatial skills dependent on the right hemisphere (Geshwind & Galaburda, 1985).

One hypothesis that has received much attention recently suggests that males and females use their brains very differently. Males tend to be more “lateralized” than females – meaning that they rely more on one hemisphere than the other when performing a task. Females are more likely to use both hemispheres (Gazzaniga, 1992). This hypothesis was formed while observing stroke victims. Gazzaniga (1992) found that males were much more affected from damage to one side of the brain than were female stroke victims. That is, if a male and a female were to suffer identical strokes, the female would fare better, since she uses both hemispheres of her brain to perform a task (see Blum, 1997; Levy & Heller, 1992; Pool 1994).

SEXUALLY DIMORPHIC VERBAL AND SPATIAL SKILLS

Do females and males differ in their intellectual abilities? There is a large body of evidence that suggests that generally subtle perceptual and cognitive differences between males and females in fact do exist. The reason for these differences is debated in the scientific community, with social constructionists and biologists taking their usual polar stances. A sociological argument (oversimplified for the sake of example) could be that the difference in abilities stems from culturally influenced forces, such as curriculum choices (Wood Shop vs. Home Economics). Biologists could argue that sexually dimorphic brain organization (again, oversimplified), such as greater male lateralization or hemisphere dominance is responsible for the difference. Using the biosocial approach, we acknowledge that the differences are most likely due to a mixture of both cultural and biological forces, with small biological differences bolstering apparent cultural differences.

Generally, females score higher than males on tests of verbal ability. When spatial abilities are tested, males generally score higher than females (Blum 1997, Crooks & Bauer 1987, Kimura 1992).

SEXUAL DIMORPHIC CORPUS CALLOSUM

The corpus callosum, a bundle of nerves that connects the right and left cerebral hemispheres, is believed to be the chief path of communication between the two hemispheres. Studies show that the corpus callosum is generally proportionately thicker in females than in males (Gibbons, 1991). With age, the size of the corpus callosum decreases in males, but not in females. The larger female corpus callosum may explain why females seem to utilize both hemispheres for verbal and other tasks, while male neural function seems to be more lateralized (Gibbons, 1991). Many investigators also suggest the corpus callosum is prenatally influenced by hormones (e.g. de Lacoste, Holloway, & Woodward, 1986; Holloway, Anderson, Defendini & Harper, 1993; Johnson, Farnworth, Pinkston, Bigler, & Blatter, 1994).

Since male brains are larger (on average) than female brains (given that males are physically larger than females) it is important to note that the sex differences in size of the corpus callosum is relative to the average brain size of each sex. If one were simply to compare the size of the corpus callosum, without considering sex differences in relative size, no sex difference difference is found, leading some reviewers to erroneously conclude that this brain structure is not sexually dimorphic (e.g., Bishop & Wahlsten, 1985).

Sexually Dimorphic Hippocampus

Studies of both monogomous and polygynous animals suggest that the hippocampus, a neural structure deep in the brain, may be responsible, in part, for spatial memory (Gibbons, 1991). Spatial skills are required for roaming about, searching for mates and food, and remembering the way back home. These skills would come in quite handy for the male of a polygynous species in which males tend to roam in search of additional mates. For example, the male meadow vole is promiscuous, and can master a laboratory maze with ease. The female, who generally stays near to the nest, is not as proficient at negotiating the same maze. Not surprisingly, this promiscuous male maze master has a larger hippocampus than does the female (Blum, 1997; Gibbon, 1991).

In contrast, another species of voles, prairie voles, are monogamous, and both the males and the females do not stray far from the nest. Among this species, there is no significant difference in performance in laboratory mazes.

Work is being done to see if this area of the brain is also sexually dimorphic in humans (Gibbons, 1991). Some preliminary evidence suggests that it may be. Nass and Baker studied women who had been abnormally exposed to high levels of prenatal androgens. As would be expected from the animal research, these women demonstrated unusually high spatial abilities, presumably because the high levels of testosterone affected their hippocampus during development.

Hypothalamo-Pituitary-Adrenal Axis (HPA)

The hypothalamus and the pituitary are hormone secreting areas of the brain which are responsible for controlling some of our development and maintaining homeostasis. These two areas, along with the adrenal glands form a very important axis of hormonal control of the body. For example, this axis is the way that our bodies deal with stress. The normal stress response in most animals is a complex series of hormone releases that culminates in an increased level of corticosteriods into the blood. The corticosteriods allow the body to respond quickly to stress by freeing up glucose and raising the blood sugar and controlling inflammation. Unfortunately, excessive exposure to corticosteriods can negatively affect reproductive rates, which may be why high levels of stress have been correlated with infertility.

However there is evidence that the HPA is sexually dimorphic. Testosterone can inhibit HPA function, while estrogen can enhance it (Handa, et. al., 1994). This may be part of why men and women report experiences different levels of stress: In the face of the same stressor, women may actually physiologically have a more intense response than men. That stronger reaction to stress may in turn lead to development of vastly different ways of coping, and may even be the reason that women consistently report more feelings of fearfulness. Some researchers hypothesize that fear may have been an evolutionary advantage to females, because those that were more fearful weould be less likely to confront stressors and so more likely to stay alive to rear their children. Males, in contrast, have a less intense physiological stress response, tend to report less fear, and hypothetically have more to gain from confrontations because of the differential rate of reproduction.

Another consideration in the dimorphism of the HPA and the stress response is differential in parental investment. If a females is under high levels of stress, she may not be able to care for new infants (for example, if there is over-crowding), so the stress response negatively affecting her fertility may end up preventing the waste of energy and resource investment in offspring which have little chance of surviving. However, the male strategy involves far less investment. The possible benefits of copulating may outweigh the costs of wasted investments under stressful conditions. Thus the differences in stress response may in fact contribute to the opposite strategies of males and females.

Sexually Dimorphic Auditory System

Our sense of hearing involves the ear, the eardrum, the cochlea, the hair cells which are attuned to different frequencies of sound, the nerves that are activated by the hair cells and the area of temporal lobe of the brain called the primary auditory cortex, which is responsible for processing the input.

Men and women have been shown to have distinct differences in hearing function (McFadden, 1998). Males tend to be better at sound localization, while females have higher sensitivity to sounds and higher rates of a phenomenon known as Spontaneous Otoacoustic Emissions (SOAEs), which are small sounds made by the cochlea itself.

Again, this is interesting from a developmental perspective because it has been shown that the female twin from a dizygotic pair tends to have a pattern of SOAEs more similar to a male. Presumably this is because the higher levels of testosterone circulating in utero because of the male twin, so certain aspects of the female's neural development have been masculinized (McFadden, 1998).

Another way to view this difference is in the evolutionary advantage that each hearing specialization might impart on the two different sexes. Although it is difficult to empirically test such hypotheses, the existence of the different specialization implies that different environmental pressures shaped the evolution of hearing.

LOCALIZATION OF FUNCTION

There is some evidence that neural function in female brains is more widely distributed, while neural function in male brains is more localized or "modularized." For example, given the same amount of localized neural damage (e.g., stroke or trauma), males will usually show a larger functional deficit than females. Note in the graphic below that language function is dispersed in both the left and right hemispheres of the typical female brain (on the right), while it is limited to the left hemisphere in the typical male brain (on the left).

Language Function: Functional magnetic resonance

activation patterns of 19 men (left image) and 19 women

(right image) obtained while performing a rhyming task.

The men activated the left inferior frontal gryrus while

the women activated both the left and the right inferior frontal gyri.

Insert table from Mike

ABNORMAL SEX CHROMOSOMES

So far we have discussed normal prenatal differentiation, beginning with the effects of chromosomes. As you recall, two sex chromosomes are paired to produce either a female (XX) or a male (XY). However, as in most natural processes, abnormalities may occur. Occasionally, an embryo develops with an extra chromosome, or a missing chromosome. The study of such phenomena has contributed greatly to our understanding of the roles that the sex chromosomes play in our development.

Turners Symdrome -- One X Chromosome

Turner’s Syndrome, an uncommon condition, results from the presence of only one sex chromosome, an X chromosome. This is caused when an abnormal ovum that contains no sex chromosome is fertilized by an X bearing sperm. In this case the zygote will develop with 45 chromosomes, rather than the typical 46. What would normally be an XX pair is an XO pair (Crooks & Bauer, 1987). An ovum that contains no sex chromosome that is fertilized by a Y bearing sperm will not survive – there are no YO individuals.

Individuals with the XO combination are classified as females, developing normal external female genetalia. However, the absence of fully developed internal reproductive structures results in sterility. At puberty, these individuals do not menstruate, nor do they develop breasts. Turner’s Syndrome females tend to appear short in stature and have short, thick necks (Crooks & Bauer, 1987). They also generally have difficulty with spatial skills (Garron, 1977; Rovet & Netley, 1982).

Behaviorally, Turner’s Syndrome females generally identify themselves as female, and do not differ significantly from females with XX chromosomal makeup. The fact that feminine gender identity can be formed without the internal sex structures and subsequent hormonal secretions again suggests that nature tends to default to female organization (Crooks & Bauer, 1987).

Klienfelter's Syndrome -- XXY Chromosomes

Another, more common, condition is Klienfelter’s Syndrome. This condition is due to a sex chromosome error through which an unfertilized ovum already containing two X chromosomes (XX), is then fertilized by a Y bearing sperm, resulting in an XXY individual. Since there exists a Y chromosome in the mix, the fetus with Klienfelter’s syndrome develops male sexual structures. But the extra X chromosome hampers complete defeminization, resulting in infertility, a more feminine appearance, and passive behavior (Crooks & Bauer, 1987). Some individuals with this syndrome may have problems with their sexual identity, and are proportionately over-represented in prisons and mental hospitals, and among transvestites, transsexuals, bisexuals, and homosexuals (Barash & Lipton, 1997).

XYY Males

Unlike the preceding syndromes caused by an abnormal ovum, a different chromosomal error can result from an abnormal sperm. An XYY (“super-male”) individual results from a normal ovum that is fertilized by an abnormal sperm bearing two Y chromosomes (YY). XYY individuals develop normal male internal and external sex organs, but are generally less fertile than XY males. They tend to be taller than most males, generally standing over 6 feet in height, and may sometimes have lower IQs (Crooks & Bauer, 1987).

For some time it was thought that “super-male” XYY individuals were more aggressive and violent, and were proportionately over-represented in prisons (Barash & Lipton, 1997; Crooks & Bauer, 1987). Further investigation, however, suggests that the XYY males who were in prison had actually committed less violent crimes than XY prisoners. It is thought that perhaps it is their lowered intelligence that causes the XYY criminal to be captured and convicted at a higher rate than their XY counterparts (Wilson & Hernstein, 1985).

ABNORMAL PRENATAL HORMONAL PROCESSES

Even if no chromosomal error occurs at conception (a normal ovum fertilized by a normal sperm), there is still a chance for hormonal errors. As you will recall, differentiation of the internal and external sex structures and of the brain depends greatly on the secretions of hormones at critical periods in development. It is easy to think of androgens as male hormones and estrogens as female hormones, but both males and females produce androgens and estrogens; the difference is in the proportions and subsequent metabolism. The female (ovaries) produce androgens, but most are converted to estrogens. The male (testes) produce testosterone, some of which are converted to estrogen. In both males and females, the adrenal glands also produce androgens.

With all of this hormonal production and conversion going on, and meeting the deadlines of critical periods, complications and errors can occur. Identifying resulting abnormalities can be particularly informative as they demonstrate the power of prenatal hormones, and their lasting effects on the body and mind.

NOTE: I am still working to complete this chapter. Some of the prose below is compiled from other authors.

FETALLY ANDROGENIZED FEMALES (FEMALES WHO HAVE BEEN ABNORMALLY MASCULINIZED)

From Mealey (1998):

A number of biological accidents may result in pseudohermaphroditism. One is the situation in which a chromosomally normal female (xx) is exposed to an excessive amount of androgens or androgen like substances during the critical period of prenatal sex differentiation. There are two possible sources of these androgens: They may be introduced as drugs the mother takes during pregnancy, or they may be produced by the fetus's own body. In the 1950s some pregnant women took a synthetic hormone drug to prevent miscarriage. Physicians who prescribed the drug (progestin) were unaware that it would have the same effect on the fetus as a dose of male hormones. Progestin and androgen have similar chemical structures, and as the drug circulated in the mother's bloodstream, the developing fetus was in effect exposed to a high dose of male hormones. Sometimes a female fetus's own adrenal glands malfunction and produce abnormally high amounts of androgen. This condition, known as adrenogenital syndrome (AGS), results from an inherited genetic defect. Regardless of the source of prenatal androgens, the effect at birth is similar. The internal reproductive structures of these chromosomal females do not appear to be affected. However, the external genitals are masculinized and resemble those of male infants to varying degrees. The clitoris is often enlarged and may be mistaken for a penis. The labia are frequently fused so they look like a scrotum. The masculinizing effects of AGS tend to be more pronounced than those of progestin-induced pseudohermaphroditism. Furthermore, if the problem of abnormal adrenal activity is not corrected after birth, excessive androgen secretions continue to masculinize AGS females throughout their developmental years. In contrast, the masculinizing effects of progestin are limited to the prenatal period.

In the not-too-distant past, the assignment of biological sex at birth was based solely on the appearance of a newborn's external genitals. Thus, in some cases of babies born with genital ambiguities, sex assignment was a toss-up, and the assigned sex may not have been consistent with the chromosomal sex. Today, however, physicians faced with such ambiguities obtain additional information about the composition of the chromosomes and the nature of the gonads, so most masculinized female infants are correctly identified and reared as females. Corrective surgery is performed to make the appearance of their external genitals consistent with their chromosomes and internal sex structures. In addition, females with AGS are given injections of synthetic cortisone from birth on, to reduce the abnormal output of androgen from the adrenal glands. Fetally androgenized females who are provided proper medical treatment, regardless of the source of prenatal androgens, undergo normal biological development through childhood and adolescence and become reproductively functional females.

Some years ago John Money and Anke Ehrhardt (1972) provided some fascinating data from their extensive study of 25 fetally androgenized females (10 progestin-induced and 15 with AGS). These 25, all of whom had received appropriate medical treatment and had been reared as girls from infancy, were matched by age, intelligence, race, and socioeconomic status with a group of nonadrogenized girls. There were marked differences in the behaviors of these two groups. Twenty of the 25 fetally androgenized girls identified themselves as "tomboys." Their parents and friends agreed with this label. These girls tended to be active and aggressive; they preferred to engage in traditionally male activities such as rough-and-tumble athletics and pushing trucks in dirt piles. They demonstrated little interest in bride and mother roles, disliked handling infants, and were uninterested in makeup, hairstyling, and jewelry. In contrast, only a small number of the girls in the matched sample claimed to be tomboys and then only to a limited extent. The fetally masculinized girls demonstrated a significantly greater amount of dissatisfaction with their gender identity than those in the matched sample, although none expressed a desire to actually change her sex.

ANDROGEN INSENSITIVITY SYNDROME (MALES WHO HAVE BEEN DE-FEMINIZED, BUT NOT MASCULINIZED)

The results of another study seem at odds with the observations we have just presented. Male children are occasionally afflicted with a biological anomaly known as androgen insensitivity syndrome (AIS). Individuals with this condition are chromosomally normal males (XY) whose gonads differentiate into testes that produce normal levels of prenatal androgens. However, as a result of a genetic defect, their body cells are insensitive to the action of testosterone and other androgens, and consequently their prenatal development is feminized. The Wolffian duct system is unable to respond to androgens, and therefore the normal internal male structures (the epididymis, vas deferens, seminal vesicles, and ejaculatory ducts) do not develop. Furthermore, the fetal testes produce Mullerian inhibiting substance, which acts in the normal way to prevent formation of internal female structures from the Mullerian ducts. Consequently, the AIS infant is born without a normal set of either male or female internal structures.

As a result of androgen insensitivity, the external genitals of the AIS fetus fail to differentiate into a penis and a scrotum and the testes do not descend. Instead, the newborn has normal-looking female external genitals and a shallow vagina. (The inner third of the vagina is normally formed from the Mullerian system. Minor surgery can lengthen the vaginal barrel, if necessary, so that it can accommodate a penis.) Nothing unusual is suspected, and such babies are classified as girls and reared accordingly. At puberty breast development and other signs of normal sexual maturation appear, the result of estrogen production from the undescended testes. (The body tissues remain insensitive to continued production of androgens.) The error may not be discovered until adolescence or later, usually as a result of medical consultation to determine why the person has not menstruated.

Money and his colleagues reported an in-depth study of 10 individuals with AIS (Money et al., 1968). All 10 had been reared as girls. Only one, a young girl with a very disturbed family background, showed any gender-identity confusion. The other nine were strongly identified as female by themselves and others. As a group they demonstrated strong preferences for the role of homemaker over an outside job, fantasies of becoming pregnant and raising a family, and inclinations to engage in typically female play with traditional girls' toys such as dolls. In a word, there was nothing that could be viewed as traditionally masculine in the way the girls behaved, despite their XY chromosomes and male gonads. In this example, unlike the first, social-learning factors seem to have played the decisive role.

From: Barash and Lipton p. 181 -182:

DHT-DEFICIENT MALES (DE-FEMINIZED BUT NOT MASCULINIZED)

Before we discuss the apparently contradictory findings of the first two studies, let us look at our third and final example of a hormone-based differentiation error. Some of the strongest evidence for a hormone-gender-identity relationship was provided by a team of Cornell University researchers who studied 18 boys raised in two rural communities in the Dominican Republic (Imperato-McGinley, et al., 1979). All these boys were afflicted with a genetic disorder that prevents the prenatal conversion of testosterone into DHT, which is necessary for the normal development of male external genitals. Their internal sex structures developed normally, and prenatal androgen levels were appropriate. However, at birth their testicles were undescended and their stunted penises were mistaken for clitorises. They also had partially formed vaginas and incompletely formed scrotums that looked like labia. These children were incorrectly identified as female, and all were apparently raised as girls. At the age of puberty, however, they showed no sign of breast development. When their as-yet-undescended testes began accelerated testosterone production, the most amazing things happened: Their voices deepened, their clitoris like organs enlarged and became penises, and their testes finally descended.

In response to these marked biological changes in their bodies, all but two of the 18 adopted the culturally mandated male gender roles, encompassing such things as occupational inclinations and patterns of sexual activity. Of the remaining two, one acknowledged that he was male but continued to dress as a woman, while the other maintained her female gender identity and gender role, married, and sought a sex-change operation to correct the inconsistencies in her body that had emerged at adolescence.

The Dominican study sparked considerable controversy in an already hotly debated area. Certain widely held assumptions of psychologists were seriously challenged by the findings of the Cornell researchers. Among them were the notions that gender identity is primarily learned and that once it is established during the critical early years of life it cannot be changed without creating severe emotional problems.

Certainly, this important research suggests that gender identity may be more malleable than previously thought. However, there are important questions that remain unanswered about the psychological environments of these Dominican youths. For example, because the study was conducted after the subjects had become adults, we cannot be sure that their early gender-identity socialization was unambiguously female. It is not clear whether all the subjects, as well as others who could report on their development, were personally interviewed and whether both parents were questioned in each case (Rubin et al., 1981). Furthermore, we must consider the possibility that these individuals converted to a male identity because of extreme social pressure (locals sometimes made the boys objects of ridicule and referred to them as "penis at 12" or "first woman, then man") or because the environment in this Caribbean country is so openly male-biased (Ehrhardt, 1985). (Some of the parents were proud to discover that their daughter was actually their son.)

Support for the sociocultural explanation of why the Dominican Republic youths were able to successfully change from a female to a male gender identity is provided by a recently reported investigation of DHT-deficient males among the Sambia society of Papua, New Guinea. The authors of this study, Gilbert Herdt and Julian Davidson, assert that sociocultural factors play a primary role in facilitating gender identity change in DHT-deficient males. They conclude that "cultural valuation of the male role makes gender-switching from female to male pragmatically adaptive" (1988, p. 33).

These studies of hormone-based differentiation errors in people reared as females have important implications. Chromosomal females, masculinized before birth from exposure to excessive androgens, tended to manifest typically masculine behavior despite having been raised as girls. In contrast, chromosomal males insensitive to androgens behaved in a typically feminine manner consistent with the way they were reared. Finally, chromosomal males whose biological maleness did not become known until puberty were able to successfully alter their gender identity to male, although they were apparently reared as girls. These findings seem to be at odds with the theory that social-learning factors are the primary or sole determinants of gender identity formation and gender-role behaviors. Proponents of this view argue that a person raised as a girl will acquire a female identity and behave in a feminine manner regardless of any biological anomalies that have arisen during prenatal development or at puberty. Although holding true for those with AIS, this prediction is not confirmed by the Dominican research or the studies of prenatally masculinized girls.

These apparent inconsistencies may not be contradictory at all when evaluated from a biological perspective. As we discussed earlier, there is mounting evidence that prenatal androgens may masculinize the human brain as well as the sex structures. This could explain the masculine behavior of fetally androgenized females. Furthermore, the same genetic defect that prevents masculinization of the genitals of individuals with AIS may also prevent the masculinization of their brains. Finally, the Dominican and Sambia boys may have been able to make the conversion from female to male identity so smoothly because their brains were already programmed along male lines by prenatal androgens. (Presumably, they had normal androgen levels during critical prenatal stages of development and were able to respond normally to these hormones; the lack of DHT affected only their external genital development.) Thus, it would appear that prenatal androgens, besides instigating proper differentiation of biological sex, may also masculinize the brain...

NEURAL MASCULINIZATION AND DEFEMINIZATION

As we have seen, fetal brain hormonalization also "masculinizes" brain structure and behavioral programming. Experiments with animals indicate that "mounting" behaviors are caused by fetal brain hormonalization (regardless of genetic sex); "mount-receiving" behaviors are caused by lack of fetal brain hormonalization (regardless of genetic sex).

It has been shown in animal studies that neural masculinization and defeminization occurs prenatally after morphological differentiation. This is a key point that some researchers make with respect to sexually "abnormal" individuals--homosexuals and bisexuals. (The term abnormal here is not meant in a moralistic sense, but rather in a biological sense. Clearly, genes that predispose individuals to exclusive homosexuality would be rapidly extinguished from the gene pool. However, there are some very speculative theories that such genes would be maintained in a small proportion of the population due to inclusive fitness--a concept that will be discussed later.)

Specifically, it is hypothesized that a predisposition to homo or bi-sexuality may be due to prenatal hormonal "errors," not during the critical period for morphological sexual differentiation, but later, during the critical period for neural sexual differentiation. In such instances one would see an indivudual with "normal" morphological sexual differentiation, but "abnormal" neural differentiation.

In the following sections we will examine Weinrich's (1987) theories regarding prenatally determined behavioral predispositions toward "normal" as well as homo- and bi-sexual behaviors. This theory should still be considered rather speculative, although there is some experimental support with animals and some supporting human evidence.

WEINRICH'S SEXUAL 'PERIODIC TABLE'

Weinrich (1987) proposes what he terms the “Sexual Periodic Table” to differentiate the various sexual types based on early sexual differentiation of the brain.

Low Masculinization

High Masculinization

High Defeminization

Asexuals

(Few mounting or mount-receiving behaviors, responsive limerance and lust. May include )

Heterosexual Males

(Mounting behaviors, Impulsive Lust, Responsive Limerance – may include some homosexual females)

Low Defeminization

Heterosexual Females

(Mount-receiving behaviors, Impulsive Limerance, Responsive Lust – may include some Homosexual Males)

Bi- or Homo-sexuals

((“hyper-sexual group” -- Both mounting and mount-receiving behaviors, impulsive limerance and lust)

OF LIMERANCE AND LUST

To better define Weinrich’s table, let’s define the terms “limerance” and “lust” as Weinrich uses them.

Weinrich (1987) suggests that males and females both experience lust and limerance, but whether they expereince them as an "impulse" or as a "response" may, on average, differ. Below is a brief summary of his theory. First a few definitions:

LIMERANCE / LIMERANT ATTRACTION: is an attraction to someone based on a particular idealized type of relationship, perhaps including attraction to a particular type of personality, character or way of affectionate relating. Specifically erotic attraction may develop later, but usually after the passage of time and the deepening of the relationship. To have a "crush" on someone you know fairly well is perhaps a very strong form of limerance.

LUST / LUSTY ATTRACTION: is based on a highly eroticised attraction to an idealized class of objects (appearances/forms/smells/feels, etc.), rather than to a particular idealized type of affectionate relationship. One can have a lusty attraction to a total stranger (who possesses many of the physical traits of one's idealized image). In fact, a relationship may even somewhat inhibit a lusty response.

Limerance and lustiness are both experienced as being "sexy." How do you know if what you are experiencing is limerance or lust? If you know ahead of time exactly what turns you on erotically in terms of shapes, smells, the feel of something, and it’s appearance, it's probably lust. If beforehand what is erotic to you is somewhat undefined, but later becomes more defined (or perhaps even changes) as the relationship with the other person develops, it is probably limerance. Weinrich (1987) suggests that males and females both experience limerance and lust, but generally differ in whether it is experienced as an "impulse" or as a "response," as defined below.

AN "IMPULSE": is a desire or readiness to engage in a behavior, and to actively seek out the opportunity to do so, without the prerequisite of special circumstances. Impulses have a low (or no) threshold for occurring. A craving might be considered an intense impulse.

A "RESPONSE": occurs only under particular circumstances, logically related to the behavior, and often is a reaction of the initiations of another person and/or special circumstances/situations that have been developing progressively over time. The threshold to elicit a response is higher than the threshold to initiate an impulse.

WEINRICH'S 3 HYPOTHESES:

1. Weinrich (1987) theorizes that, although males and females both experience limerance and lust, whether they generally experience it as an impulse or a response differs. He argues that females generally experience their impulsive sex drive primarily as limerance, while males generally experience their impulsive sex drive primarily as lust. Females generally experience lust as a response; males generally experience limerance as a response.

Sex Drive

	LIMERANCE	LUST
FEMALES	impulse	response
MALES	response	impulse

Thus, men should know that they have lusty impulses--and they may have to learn limerant responses. Women should know that they have limerant impulses--and they may have to learn lusty responses. Men may fall in lust quickly--and may take longer to fall in limerance; women may fall in limerance quickly, but may take longer to fall in lust.

2. Limerant attractions can be bisexual (in that relationships are not dependent per se on genitalia). Lusty attractions are less likely to be bisexual (since lusty attraction is likely to be object specific). Given this, and Hypothesis 1 above, we would expect more bisexual attraction in women than in men.

3. Early experience can "imprint" the objects of lusty attraction. For example, it is thought that sexual fetishes have their roots in some early experiences. Sexual fetishes may be considered extreme, even caricatured, examples of lusty impulses. However, rather than being lust directed toward certain appearances/smells/feels of certain people, a fetish is a lust toward an actual object with the desired appearance/smell/feel, e.g., perhaps boots, leather, or underwear. Given the hypotheses above, Weinrich (1987) would predict that males, since they experience their sexuality primarily as a lusty impulse, are more likely to "imprint" on incorrect objects than females. In fact, the vast majority of fetishists (perhaps 95% or more) are male.

COMPONENTS OF GENDER IDENTITY AND GENDER ROLE

Weinrich (1987) provides us with some definitions of core gender identity, gender role, and sexual orientation (p. 20):

First, core gender identity. This is the innermost experience of oneself as male or female. Usually it goes along with the appearance of the genitals: most people who have a vagina and labia consider themselves female; most people with testicles and a penis consider themselves male. (This component is sometimes just called "gender identity.")

Next, gender role. This is the set of social roles that a particular society at a particular time prescribes for females and for males. Most societies, for example, expect that men and women will dress differently and perform different tasks-although what these differences will consist of varies quite a bit from society to society. (This component is sometimes called "sex role" or "social sex role.")

Finally, sexual orientation. This is the readiness particular people have to pair homosexually with a member of their own sex, or heterosexually with a member of the other sex. It includes the possibility that one might pair with members of either sex. Most people in our society expect to fall in love with, or be sexually attracted to, members of the sex whose genital shapes don't look like their own. (This component is sometimes called "sexual preference.")

Taken together, these three concepts are called gender identity.

NEURAL DIFFERENTIATION AND GENDER IDENTITY, GENDER ROLE, AND SEXUAL ORIENTATION

The masculinization of the brain is a gradual process, not an all-or-nothing, single event. Researchers have empirically tested this hypothesis with rats (Moir & Jesell, 1989). As we have seen, rat brains are undifferentiated at birth, but during the neo-natal period their exposure to gonadal hormones causes the differentiation. Thus rats provide us with an animal model that closely mirrors our own prenatal development.

The German researcher Dorner found that if young male rats are castrated, which prevents testosterone from masculinizing the brain, they develop typically female brains. However, he also found that the earlier the castration (and thus the less exposure to circulating testosterone) leads to a more typically female brain. If the castration occurs later, after the brain has been exposed to some testosterone, the rat is more likely to show some male characteristics.

Dorner hypothesizes that a similar process goes on with humans in the womb. He argues that different levels of hormones at different critical stages in neural development are related to gender role identity, sexual orientation and physical sexual characteristics. As we have seen previously, physical sexual traits are affected by prenatal exposure to hormones.

Dorner believes that the differentiation occurs in stages:

1. The Sex Center Development, in which the physical sexual characteristics develop.

2. The Mating Center Development, in which the hypothalamus is transformed by hormones and the control of later sexual orientation and desires is laid down.

3. Gender Role Center Development, in which the neural connections which are related to behaviors and traits are created. This stage is associated with behaviors like aggression/passivity, adventurousness/timidity.

The advantage of this explanation is that each of the three stages can experience abnormal levels of hormones and be affected in different ways. That is, according to Dorner, this theory explains a myriad of sexual identity and gender role situations. This theory can accommodate everything from effeminate heterosexual men (low levels of testosterone during the gender role center development) to masculine homosexual women (high levels of testosterone during the last two stages).

This theory also accounts for the higher rates of sexually deviant behavior like pedophilia and fetishism. Dorner’s theory assumes that the default setting of the brain is female. Therefore, men must go through a complex neural transformation, during which any number of factors may be abnormal and cause changes in the sexual centers of the brain.

The organizational effect of hormones on neural development shows how male homosexuals can have the same testosterone levels as heterosexual males, yet still be attracted to other men. Low levels of testosterone at certain prenatal stages is associated with attraction to men, while current testosterone levels are related to sexual drive, which is similar in homosexual and heterosexual men. Similarly, female homosexuals are different from females heterosexuals in the object of their attraction (prenatally predisposed) but not in their sexual drive (immediately determined).

GENDER TRANSPOSITIONS

Sexologists identify the gender transpositions as being comprised of five different groups: heterosexuals, homosexuals, bisexuals, cross-dressers, and transsexuals.

Weinrich (1987) provides us with some definitions (p. 20):

A gender transposition is a particular pattern of adherence to or differentiation from the typical patterns of gender identity; the differentiation consists of a transposition of masculine and feminine in comparison with the typical pattern. As seen below, transsexuals are fully transposed on core sexual identity, transvestites on gender role, and homosexuals on sexual orientation.

Sexual Transpositions
	Sexual Identity	Gender Role	Sexual Orientation
Heterosexuals	No transpositions
Bi-sexuals			Partially transposed
Homosexuals		Sometimes transposed	Fully transposed
Transvestites		Transposed
Transsexuals	Transposed	Transposed	?

ABNORMAL NEURAL DIFFERENTIATION

From Moir and Jessel, 1989:

EVIDENCE RELATED TO WEINRICH'S 'SEXUAL PERIODIC TABLE' MODEL

From Moir and Jessel, 1989, p. 120:

The book "Sexual Preference - Its Development in Men and Women" was the most exhaustive American survey of homosexual attitudes and behaviour. After interviewing 500 homosexuals, the authors found 'the role of parents in the development of their sons' sexual orientation to be grossly exaggerated'. They were also unconvinced by the notion of the unresolved Oedipus complex, the responsibility of cold, detached fathers, peer-group pressure, labelling as 'being a sissy' at an early age, or bad experiences with the opposite sex. Even among non-homosexuals, early same-sex experiences, interestingly enough, seemed not to play any role--'the popular stereotype that homosexuality results when a boy is "seduced" by an older male, or a girl by an older female, is not supported by our data.'

Single-sex boarding schools and prisons may be hotbeds of homosexuality, but they probably do not create the condition. At school, homosexuality may be part of adolescent curiosity, while in prison it may be a functional necessity. Both institutions may reveal, or bring out, the natural homosexuality in a boy or a man, but are unlikely to implant it.

What most clearly signalled whether or not a boy or a girl was going to be a homosexual was how they behaved as children - withdrawn, unathletic and shy boys; rowdy, active girls. For, although the hypothalamus hadn't yet been primed by the hormones of puberty, the general wiring of the brain had a 'wrong'-sex bias.

The biological explanation may even explain where some of the psychological explanations went wrong. For instance, it has long been thought that a hostile or indifferent father could be a cause of homosexuality - the boy reacting against the main male role-model of his early years, and rejecting traditional masculine attitudes and behaviour. Yet it is perfectly possible that the father became hostile for the very reason that the child was - naturally - unmasculine, and not 'the son I always hoped for'. Fathers who have looked forward to the day when they could go to the football match with their sons are likely to be disappointed, if not downright disapproving, when those sons, for whatever reasons, prefer more typically feminine pursuits.

So what is the original, biological cause of sexual deviation? If it's the hormones in the womb which so affect the sexuality of the child and adult, what happens to upset those hormones in the first place?

The first clues came from those rats again. It is known that high stress levels in mothers lower the level of male hormone in the womb. Experiments showed that when pregnant rats were subjected to severe stress, the resulting male offspring were attracted to other male rats - indeed that the rats were homosexual, apparently as a consequence of the stress endured by their mothers.

Dorner was intrigued by the news. Understandably, he could not put a laboratory-full of pregnant women under severe stress, but he could examine the results in the laboratory of history. He looked at the years of the Second World War - a time when the nhabitants of his country could be said to have been living under more than usually trying circumstances.

Dorner found that out of about 800 homosexual males, significantly more were born during the stressful war and early post-war period than in the years before and some time after the war. The highest number corresponded with the last months of the conflict.

Two-thirds of the homosexual men and their mothers reported experience of severe, or moderate, maternal stress during their pre-natal life - with factors such as bereavement, bombings, rape, or severe anxiety. On the other hand, none of the mothers of heterosexual men in a control sample had been the victims of severe stress, and only 10 per cent of moderate stress, during pregnancy.

Low pre-natal, male hormone levels can be affected by factors less drastic than major global conflict. Taking inappropriate medication is one of these. Barbiturates, one of the most widely prescribed and abused classes of drugs, are thought to have been prescribed in as many as 5 per cent of pregnancies between the 1950s and the I980s. In animal experiments involving exposure to barbiturates the drug acted directly on the neural tissue, and indirectly through the brain-sexing substances secreted by the foetus. Among the observed results was an 'alteration of behavioural and physiological sex differences'. In humans the predicted results would include 'psychosocial maladjustment, and demasculinisation of gender identity and sex role behaviour in males'.

The implication - and it is true of many drugs - is that pregnant women would be well advised to avoid barbiturates; it is comforting to know that they are no longer being prescribed as readily as they used to be.

Prenatal neural hormonalization may predispose one to a certain gender identity, gender role, and sexual orientation, respectively.   However, we need to keep in mind that a predisposition is simply a tendency.   Personal life experiences and socialization also have profound effects in shaping our sexuality, gender identity and gender role.

Donovan (1988, p. 252) notes:

The difficulties experienced in interpreting current information are neatly illustrated by reference to observations with twins. The vast majority of identical twins (arising from the division of a single fertilized egg and sharing a common set of genes) are concordant in their sexual preference, whether heterosexual or homosexual, so that sexual orientation may be taken to be biologically determined. On the other hand, in a few cases one identical twin is known to be heterosexual and the other homosexual, implying that some factor other than a common gene inheritance and development in the same uterus must be operative. There is even a family on record containing three pairs of identical twins in which two sets were homosexual and the third heterosexual (Heston and Shields, 1968; Zuger, 1976).

COMMUNICATION AND MISUNDERSTANDING BETWEEN THE VARIOUS SEXUAL 'TYPES'

From Weinrich (1987)

The most important thing to understand about the gender transpositions is that each has a particular pattern of core gender identity, gender role, and sexual orientation. Before these three components were understood, people commonly believed that they had to be interconnected: that is, that a lesbian really wanted to become a man, that someone who wanted to change sex really wanted to behave homosexually, that a man who wanted to put on a dress wanted to fall in love with a man, that a man who fell in love with men wanted to put on a dress. Not so! In fact, there is no necessary connection between any of these three components. Another generalization about gender-transposed people (including heterosexuals) is that they don't necessarily get along with each other. Remember that just because some people are atypical in one way doesn't mean they will understand people who are atypical in another. In this respect, alas, gender transpositions are no different than other traits on which humans differ. It is probably easier for someone atypical in one way to understand another's atypicality, but each still needs to be educated in the ways of the other. These conflicts and misunderstandings arise for several reasons. First, members of each kind of gender transposition view themselves in a particular way. Their emotions appear perfectly normal to themselves, and thus they find it easy to project these emotions onto others. Many heterosexuals think that penis and vagina fit together perfectly and cannot understand why someone wouldn't want to fit them together if they had the opportunity. Nor can such heterosexuals understand how someone could try fitting the two together and not find the experience delightful. Many heterosexual transvestites think that women's underclothes are inherently attractive and that any man would want to put them on. Many gay men presume that there must be something homosexual about the men who engage in the sort of nude horseplay common in locker rooms. Many lesbians believe that any woman could fall in love with a woman if given the social permission to do so. Second, members of the different gender transpositions don't talk very much with each other. This has to do with the sex taboo, of course, through which society makes some of the gender transpositions unspeakable. The result is that everyone falls back on his or her own experience, projects it onto everyone else, and gets puzzled or angry when people don't act the way they expect them to. Some heterosexuals, for example, remember their own anxiety when first encountering the other sex in bed and can only understand homosexuality (incorrectly) as a fear of the other sex. At this point, I could sit back and play the ultrascientist and tell you that these questions-who understands whom and so on-are social questions, not scientific ones. But besides getting me into hot water with sociologists (who are, after all, social scientists), such a statement is nonsense. These questions are a different kind of scientific question, but they are definitely scientific, and scientists ought to address them. The fact that group A doesn't get along with group B is an observation and itself has scientific significance (and social significance, too, of course), especially if we can figure out a pattern to the conflict.

From Moir and Jessel, 1989, p. 124

Our new understanding of the biology of sex raises profound questions about our attitude to, and treatment of, homosexuals. If biology - or nature - is at the root of it all, how can homosexuality be condemned as 'unnatural' - any more than, say, left-handedness? Or is the appropriate comparison some other biological manifestation, such as a congenital disability? Then again, is it right to label what is, in effect, a non-genetic 'race' of people as 'disabled'? Is the clinical correction of the syndrome all that far removed from the grotesque medical malpractices of the Third Reich which perverted medicine in its pursuit of racial purity - while, as we've seen, ironically provoking, in war, the very conditions in which homosexuals were more likely to develop?

We trust that the very knowledge of the natural and biological springs of sexual abnormality will bring about the recognition that the syndrome is natural, and may change our perceptions of what is normal. After all, the principal problem homosexuals face is not of their making; the problem derives from the rest of us, and our intolerance that they do not conform with what we decree is normal gender identity and sexual behaviour (though even that intolerance may be biologically wired into our brains, as a part of aggressive behaviour to the outsider).

Meanwhile, surely, it is time for an armistice in the battle between those who seek a biological, and those who look for a psychological, explanation for human behaviour. The terms of such a treaty were suggested decades ago, when a psychologist wrote to his colleagues that they should bear in mind that some day all our provisional formulations in psychology will have to be based on an organic foundation . . . It will then probably be seen that it is special chemical substances and processes which achieve the effects of sexuality . . .