Embryology teaches that early embryos all start out as female. At some point in early gestation, if chromosomes destine the fetus to be male, this female embryo is altered by the genetically programmed addition of certain hormones, called androgens. These androgens, especially testosterone, instruct the embryo to develop male characteristics. In their absence, the embryo continues to develop into a female.
In a paper published almost a quarter of a century ago, a research psychologist at Villanova University was also puzzled about gender. Dr. Ingebog Ward…divided a group of pregnant rats into three groups. Suspecting that something special might be happening in the early stages of pregnancy, she subjected the first group to stress during the first ten days of gestation by irritating the mother rats to bright lights, noise and annoying vibrations. Ten days into a rat's pregnancy corresponds to the first trimester (3 months) of a human pregnancy. The second group was subjected to stress towards the end of their pregnancy, just before birth. The third group was comprised of male offspring from both prenatal stressed mothers and unstressed mothers. These babies were subjected to the same stress producing stimuli.
Dr. Ward then allowed all the males to grow to adulthood without further interference. She then placed each group of males in cages with healthy females to observe their ability and desire to mate with normal adult females. Here's what happened:
Abstract: "Male rats were exposed to prenatal (i.e. before they were born) or postnatal (after they were born) stress, or both. The prenatal stressed males showed low levels of male copulatory behavior and high rates of female lordotic responding. Postnatal stress had no effect. The modifications are attributed to stress-mediated alterations in the ratio of adrenal to gonadal androgens during critical stages of sexual differentiation. Specifically, it appears that stress causes an increase in the weak adrenal androgen, androstendione, from the maternal fetal adrenal cortices, or both, and a concurrent decrease in the potent gonadal androgen, testosterone."
- Parental Stress Feminizes & Demasculizes the Behavior of Males
Science pp. 83-84, January 7, 1972
Her findings showed that if a mother is stressed during the early stages of pregnancy, she will release an adrenaline related hormone into her own bloodstream and that of her unborn baby. This hormone, called androstendione, is structurally similar to testosterone, the male hormone. If the baby carries "XY" chromosomes and is destined to become a male, testosterone needs to be active when the Central Nervous System (including the hypothalamus) is being formed. This is the only way that the CNS "knows" to develop along male lines. Because the stress hormone seems to bind to the receptors that would normally be receiving testosterone, there is the delay or blockage of the effectiveness of testosterone, even if it is plentiful.
In 1972, Dr. Ward had no idea that androstendione in male pregnancies would prevent or inhibit the hypothalamus to develop into a healthy male brain, but this stress-related hormone now appears to do just that. The brain makes its gender commitment very early in development and, once committed to either male or female, it can not change. The interference with testosterone in the later stages of pregnancy, or after birth, does little or nothing to inhibit primary gender development of the other organs of the body.
In Doctor Ward's own words: "...The present data support the hypothesis that exposure of pregnant rats to environmental stressors modifies the normal process of sexual behavior differentiation in male fetuses by decreasing functional testosterone and elevating androstenedione levels during prenatal development. During stress conditions plasma testosterone emanating from the gonads decreases while adrenal androstenedione rises. The molecular structure of the two androgens, being very similar, it is postulated that the two hormones compete for the same receptor sites. Since androstenedione is a less potent androgen than testosterone, the decrease in male copulatory ability and increased lordotic potential seen in the prenatal stressed animals of the present study would be expected. The relative difference in potency between testosterone and androstendione has been repeatedly demonstrated."
It is therefore possible that while the body and organs of an animal can be a "male," the brain can coincidentally be "female." This extreme reaction to maternal stress has a very logical and natural purpose. Sensing that a population is under the stress of crowding or poor living conditions, nature provides this hormonal mechanism as a means to limit population growth and thereby reduce the cause of the stress. Homosexual behavior results in less offspring than heterosexual behavior.
Again, in Doctor Ward's own words: "The resulting alterations in sexual behavior provide the basis for an effective population control mechanism, since offspring so affected would not possess the behavioral repertoire necessary to contribute to population growth. Thus, the environment, by triggering an adrenal stress response, may control the reproductive capacity of successive generations of differentiating fetuses and, thereby, population size."
Prenatal stress in early pregnancy seems to be a rational and plausible explanation for male homosexuality and should be viewed as a natural population limiting phenomenon. Personal choice in homosexuality appears to be an insignificant factor in those offspring who are born with a female hypothalamus, encapsulated in an otherwise normal male body.