CHAPTER 2
PROXIMATE DIFFERENTIATION: ONTOGENETIC MASCULINIZATION AND DEFEMINIZATION
© Copyright 2004 Michael E. Mills
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).
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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. |
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.
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
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
Support for the sociocultural explanation of why the
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 "I