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
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.
A) PRENATAL EXPOSURE TO STEROID HORMONES
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).
COMPLICATIONS IN MALES:
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).
COMPLICATIONS IN FEMALES:
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"
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).
HORMONES THROUGHOUT LIFE
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
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).