Humanity and Womanhood
Actual humanity in biological form is feminine. Biological femininity or womanhood is, in fact, actual humanity, it is claimed. It follows that women are the real human beings and men are the aberration to be tolerated as a price for continuance of humanity, that is, womanhood in the earth. An analysis:
“Our sex is ultimately laid down by our genes, which in humans are bundled together in each body cell in twenty-three pairs of microscopic packages called chromosomes. One member of each of our twenty-three pairs was acquired from our mother, and the other member from our father. The twenty-three human chromosome pairs can be numbered and distinguished from each other by consistent differences in appearance. In chromosome pairs 1 through 22, the two members of each pair appear identical when viewed through a microscope. Only in the case of chromosome pair 23, the so-called sex chromosomes, do the two representatives differ, and even that's true only in men, who have a big chromosome (termed an X chromosome) paired with a small one (a Y chromosome). Women instead have two paired X chromosomes.
What do the sex chromosomes do? Many X chromosome genes specify traits unrelated to sex, such as the ability to distinguish red and green colors. However, the Y chromosome contains genes specifying the development of testes. In the fifth week after fertilization human embryos of either sex develop a "bipotential" gonad that can become either a testis or an ovary. If a Y chromosome is present, that bet-hedging gonad begins to commit itself in the seventh week to becoming a testis, but if there's no Y chromosome, the go-nnd waits until the thirteenth week to develop as an ovary. That may seem surprising: one might have expected the second X chromosome of girls to make ovaries, and the Y chromosome of boys to make testes. In fact, though, people abnormally endowed with one Y and two X chromosomes turn out most like males, whereas people endowed with three or just one X chromosome turn out most like females. Thus, the natural tendency of our bet-hedging primordial gonad is to develop as an ovary if nothing intervenes; something extra, a Y chromosome, is required to change it into a testis.
It's tempting to restate this simple fact in emotionally loaded terms. As the endocrinologist Alfred Jost put it, "Becoming a male is a prolonged, uneasy, and risky venture; it is a kind of struggle against inherent trends towards femaleness." Chauvinists might go further and hail becoming a man as heroic, and becoming a woman as the easy fallback position. Conversely, one might regard womanhood as the natural state of humanity, with men just a pathological aberration that regrettably must be tolerated as the price for making more women. I prefer merely to acknowledge that a Y chromosome switches gonad development from the ovarian path to the testicular path, and to draw no metaphysical conclusions.
But there's more to a man than testes alone. A penis and prostate gland are among the many other obvious necessities of manhood, just as women need more than ovaries (for instance, it helps to have a vagina). It turns out that the embryo is endowed with other bipotential structures besides the primordial gonad. Unlike the primordial gonad, though, these other bipolar structures have a potential that is not directly specified by the Y chromosome. Instead, secretions produced by the testes themselves are what channel these other structures toward developing into male organs, while lack of testicular secretions channels them toward making female organs.
For example, already in the eighth week of gestation the testes begin producing the steroid hormone testosterone, some of which gets converted into the closely related steroid dihydrotestosterone. These steroids (known as an-drogens) convert some allpurpose embryonic structures into the glans penis, penis shaft, and scrotum; the same structures would otherwise develop into the clitoris, labia minora, and labia majora. Embryos also start out bet-hedging with two sets of ducts, known as the Mullerian ducts and Wolffian ducts. In the absence of testes, the Wolffian ducts atrophy, while the Mullerian ducts grow into a female fetus's uterus, fallopian tubes, and interior vagina. With testes present, the opposite happens: androgens stimulate the Wolffian ducts to grow into a male fetus's seminal vesicles, vas deferens, and epididymis. At the same time, a testicular protein called Mullerian inhibiting hormone does what its name implies: it prevents the Mullerian ducts from developing into the internal female organs.
Since a Y chromosome specifies testes, and since the presence or absence of the testes' secretions specifies the remaining male or female structures, it might seem as if there's no way that a developing human could end up with ambiguous sexual anatomy. Instead, you might think that a Y chromosome should guarantee 100 percent male organs, and that lack of a Y chromosome should guarantee 100 percent female organs.
In fact, a long series of biochemical steps is required to produce all those other structures besides ovaries or testes. Each step involves the synthesis of one molecular ingredient, termed an enzyme, specified by one gene. Any enzyme can be defective or absent if its underlying gene is altered by a mutation. Thus, an enzyme defect may result in a male pseudohermaphrodite, defined as someone possessing some female structures as well as testes. In a male pseudoher-maphrodite with an enzyme defect, there is normal development of the male structures dependent on enzymes that act at the steps of the metabolic pathway before the defective enzyme.
However, male structures dependent on the defective enzyme itself or on subsequent biochemical steps fail to develop and are replaced either by their female equivalent or by nothing at all. For example, one type of pseudohermaphrodite looks like a normal woman. Indeed, "she" conforms to the male ideal of female pulchritude even more closely than does the average real woman, because "her" breasts are well developed and "her" legs are long and graceful. Hence cases have turned up repeatedly of beautiful women fashion models not realizing that they are actually men with a single mutant gene until genetically tested as adults.
Since this type of pseudohermaphrodite looks like a normal girl baby at birth and undergoes externally normal development and puberty, the problem isn't even likely to be recognized until the adolescent "girl" consults a doctor over failure to begin menstruating. At that point, the doctor discovers a simple reason for that failure: the patient has no uterus, fallopian tubes, or upper vagina. Instead, the vagina ends blindly after two inches. Further examination reveals testes that secrete normal testosterone, are programmed by a normal Y chromosome, and are abnormal only for being buried in the groin or labia. In other words, the beautiful model is an otherwise normal male who happens to have a genetically determined biochemical block in his ability to respond to testosterone.
That block turns out to be in the cell receptor that would normally bind testosterone and dihydrotestos-terone, thereby enabling those androgens to trigger the further developmental steps of the normal male. Since the Y chromosome is normal, the testes themselves form normally and produce normal Mullerian inhibiting hormone, which acts as in any man to forestall development of the uterus and fallopian tubes.
However, development of the usual male machinery to respond to testosterone is interrupted. Hence development of the remaining bipotential embryonic sex organs follows the female channel by default: female rather than male external genitalia, and atrophy of the Wolffian ducts and hence of potential male internal genitalia. In fact, since the testes and adrenal glands secrete small amounts of estrogen that would normally be overridden by androgen receptors, the complete lack of those receptors in functional form (they are present in small numbers in normal women) makes the male pseudohermaphrodite appear externally superfeminine.
Thus, the overall genetic difference between men and women is modest, despite the big consequences of that modest difference. A small number of genes on chromosome 23, acting in concert with genes on other chromosomes, ultimately determine all differences between men and women. The differences, of course, include not just those in the reproductive organs themselves but also all other postadolescent sex-linked differences, such as the differences in beards, body hair, pitch of voice, and breast development.”
Jared Diamond, Why is Sex Fun? The Evolution of Human Sexuality, New York: Basic Books, 1997