Hormones acting prenatally (in males primarily) and at puberty cause the dimorphisms of the primary and secondary sexual characteristics. These hormones also act on the brain where they influence mood, behavior, and personality.

Males and females have specific internal and external genitalia that, for the most part, develop from the same tissues according to hormonal instructions. Testosterone governs the development of male duct patterns and the development of accessory sex glands (prostate, seminal vesicles, and bulbourethral glands) while the hormone DHT controls the development of male external genitalia. MIH, the Mullerian inhibitory hormone, causes the degeneration of the fetal structures which would otherwise develop into parts of the female reproductive system. The absence of these 3 hormones (testosterone, DHT, MIH) causes the female (Mullerian) duct system to develop and the degeneration of the male (Wolfian) ducts. Genitalia develop along a female specific pattern.

The fetal testes produce testosterone (which is subsequently converted to other forms such as dihydrotestosterone and estrogen) and this hormone mediates changes throughout the body in both reproductive structures and the brain. The actions of these hormones on the male brain prime it for male-pattern behavior (although this term is obviously easier to define in animals which lack culture). The fetal ovaries do not produce significant amounts of hormone.
Males may display a reduced response to androgens or be unable to convert testosterone to DHT. There are instances (ranging from physical disorders to maternal medications) in which females are exposed to androgens or estrogens prenatally and males are exposed to estrogens which affect development.

Fetal testes produce steroid hormones while fetal ovaries do not; there is no evidence of estrogen secretion by the fetal ovary (Ramirez, 2003). Not only does this expose the male fetal brain to testosterone (which can be converted to the androgen dihydrotestosterone), it also exposes the brain to estrogen (estradiol) since this is one of the conversion products of testosterone inside brain cells. The effects of these steroids both masculinize the male brain (allow the development of male behaviors) and defeminize the male brain (mediate the loss of the female behaviors which would otherwise develop). The masculinization of the male brain is accomplished by dihydrotestosterone and its interaction with the androgen receptor AR and female brains can be primed for masculine behavior by androgen receptors and their ligands. The defeminization of the male brain is accomplished through estradiol's interaction with the estrogen receptor ß (ERß) and males have higher expression of ERß genes in the hypothalamus during a period of late fetal development to early after birth (Kudwa, 2005; Auger, 2000; Sato, 2004).
Starting at six weeks, the male testes release testosterone at levels four times greater than the levels experienced prior to puberty. Primate studies have shown that introducing female fetuses to male hormones at specific developmental intervals can cause them to develop specific aspects of male behavior. In other words, the development of a brain in a male specific pattern occurs in discrete stages (Moir, 1991).

Male development apparently involves more than simply the differentiation of male genitalia and the male brain, given the developmental differences between male fetuses and infants. Infant males suffer from higher frequencies of certain birth defects (such as cardiac abnormalities), sudden infant death syndrome, and respiratory problems. Infant males are more likely to be born early and premature males have a greater chance of illness and death than premature girls. Newborn males sleep less and have more active sleep than girls (Elsmen, 2004). The gender of a fetus can affect the maternal levels of hCG. Male fetuses are more likely to have problems with the umbilical cord, undergo spontaneous abortion, have premature membrane rupture, be more neagatively affected by maternal response to the D antigen, and worse responses to the stress of birth (causing a higher frequency of Caesarian section). The gender ratio at conception is about 1.2 to 1 and most spontaneous abortions are male. Male fetuses are 100 to 200g larger at birth than females and have higher cord leptin levels (Elsmen, 2004).

After birth, girls will reach developmental milestones in their personality development (such as those involving moral judgment, aggression, and empathy) earlier than boys (Cohn 1991).

This male patterning of the brain that occurs before birth can supercede all aspects of nurture after birth in regards to the definition of gender roles. In one case, an infant whose penis was destroyed because of a burn and was subsequently raised female. This individual had sexual experiences with men and women, self-identified as bisexual, and claimed to fantasize exclusively about women (Bradley, 1998). Some children when born (especially in the past before modern molecular procedures) do not clearly have the genitalia of one gender or the other; these have been typically raised as females after an operation and hormone therapy. Many experiences indicate that the brains were male despite body image and upbringing. These observations include violent play atypical for females (other girls called one "the Neanderthal"), fantasies with women, problems or the complete lack of orgasm, and even the urge to urinate standing up.

There are males whose reduced ability to respond to testosterone prevents this prenatal differentiation from occurring normally. Males with Androgen Insensitivity Syndrome often lack both sets of ducts (male and female) since they produce the Mullerian Inhibitory Hormone which causes the regression of the female ducts but lack the response to the androgens needed for the Wolfian ducts. In complete androgen insensitivity/testicular feminization, the testes form (although they may be located in the labia or in the inguinal canal) and MIH causes female ducts to degenerate. A vagina may form, although it ends blindly. Male external genitalia do not form, the individual is raised as female and often doesn't identify the problem until she cannot conceive or doesn't menstruate. Castration may be chosen after sexual maturity. The results of incomplete testicular feminization are similar to those given above but some virilization (fusing of labia, clitoromegaly) occurs. Castration after diagnosis prevents further disfiguring virilization. The effects of Reifenstein's syndrome may vary (even in a family) from infertile men with some feminization to phenotypic women with pseudovaginas and is caused by a decreased ability/inability of the androgen receptor to bind DNA (Gast, 1995). Males with androgen insensitivity may develop female fat deposition patterns and breasts through the estrogen produced from testosterone (Hines, 2004).
Some individuals possess a mutation in the enzyme 5 alpha reductase which converts testoterone to DHT. Because DHT is responsible for the prenatal development of male external genitalia, the infant appears female externally although testes form and normal male duct growth occurs. Individuals are typically recognized and raised as girls. When puberty occurs, the testes make testosterone which cause the external genitalia to develop normally. They become normal (or relatively) pubescent boys, often very little problem adjusting to new gender roles.

Estrogens given to pregnant diabetic women have been linked to atypical behavior in their male offspring (Moir, 1991).

Rodent and primate studies indicate that androgen exposure during female brain development increase the "male-like" activity patterns and aggression while reduction of androgen exposure in male development decreases male-specific behavior (Berebaum, 1995; Giammanco, 2005). Female fetuses can be exposed to higher than normal levels of androgens prenatally; this has caused masculinization of genitalia (in which the clitoris enlarges and may resemble a small penis; the labia enlarge and partially fuse). Behavioral changes have also been described including higher energy expenditure in play, preference for male playmates, fewer motherhood fantasies, more fighting, less interest in dolls, and a higher aversion to infant care.
How could a female fetus be exposed to androgens during fetal development? Some women take anabolic steroids that mimic androgens while they are pregnant or before they realize that they are pregnant. CAH women (congenital adrenal hyperplasia) secrete higher than normal amounts of androgens from their adrenal glands (which secrete androgens in both sexes). Fraternal twins of opposite sexes share a portion of their extraembryonic membranes; males are unaffected but females undergo some masculinization. In domestic animals, such an individual is sometimes called a "free martin" (Dabbs, 2000).
Androgens were once given to expecting mothers to treat toxaemia which were associated with atypical behavior in their daughters (Moir, 1991). A synthetic estrogen called DES was once prescribed to pregnant women who were diabetic. Since estrogen is produced in developing male brains but not female brains because of the relative inactivity of the fetal ovary, there is some masculinization of girls born to women who took DES while pregnant (Hines, 2004).

The “feminine”/“masculine” behavior of young girls has been linked in some studies to both non-biological phenomena (such as the existence of older male siblings) and to levels of testosterone. Maternal testosterone levels may increase later in life (or at least the ratio of testosterone to estrogen can increase) and this may have an effect on fetal development (Ramirez, 2003).

In the disorder Congenital Adrenal Hyperplasia, individuals secrete high amounts of androgen from their adrenal glands. Although there seems to be little effect on males, this disorder can cause the masculinization of females in both physical features and behavior. CAH females can be born with indeterminate genitalia and, upon being raised as females (their genetic gender), display considerable dissatisfaction with typical gender roles. In some cases, the adrenal glands release so much androgen that the individual (genetically female) is born looking like a normal boy, is raised as a boy, and only discovers the situation at puberty upon failing to develop further (Moir, 1991). CAH women perform better on tests involving spatial ability and showed less verbal expression than normal women. (Resnick, 1986). In human CAH females, childhood activities and toys were similar to those preferred by boys rather than other girls (Berebaum, 1995). CAH and DES women are more likely than control women to be homosexual or bisexual (Hines, 2004).

Estrogen is a conversion product of testosterone which helps the male brain to develop in a male-specific way. Women with Turner syndrome lack functional ovaries and there is evidence that the lack of estrogen influences their behavior so that female behaviors are more evident than in normal females. Turner syndrome females often display exaggerated levels of behaviors associated with girls (such as doll play, interest in babies, interest in clothing) (Moir, 1991).


Although hormones mediate most of the differences between males and females, apparently there are also mechanisms of gender differentiation which are independent of hormonal action. Gender differences between embryos (such as size and characteristics of brain cells) exist before the gonads differentiate. This suggests that some gender differences result from differential gene activity in males and females rather than hormonal influence (Arnold, 2003).