What might lie behind these apparent correlations between sexual orientation and brain structure? Logically, three possibilities exist. One is that the structural differences were present early in life -perhaps even before birth- and helped to establish the men's sexual orientation. The second is that the differences arose in adult life as a result of the men's sexual feelings or behavior. The third possibility is that there is no causal connection, but both sexual orientation and the brain structures in question are linked to some third variable, such as a developmental event during uterine or early postnatal life.
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| Family trees of male sexual orientation show the rates of homosexuality (darker brown) in maternally related males. Rates in paternal relatives were not significantly above the average population rate of 2 percent. This finding raised the possibility of involvement of the X chromosome (shown below). Males have two sex chromosomes—a Y inherited from the father and an X from the mother. Thus, a trait inherited through the mother’s side might logically be influenced by a gene on one of her X chromosomes (indicated here in red ). In fact, further experiments showed that one small area at the tip of the X chromosome— Xq28—was shared by a large percentage of gay brothers. |
We cannot decide among these possibilities with any certainty. On the basis of animal research, however, we and the second scenario, that the structural differences came about in adulthood, unlikely. In rats, for example, the sexually dimorphic cell group in the medial preoptic area appears plastic in its response to androgens during early brain development but later is largely resistant to change. We favor the Þrst possibility, that the structural differences arose during the period of brain development and consequently contributed to sexual behavior. Because the medial preoptic region of the hypothalamus is implicated in sexual behavior in monkeys, the size of INAH3 in men may indeed influence sexual orientation. But such a causal connection is speculative at this point.
Assuming that some of the structural differences related to sexual orientation were present at birth in certain individuals, how did they arise? One candidate is the interaction between gonadal steroids and the developing brain; this interaction is responsible for differences in the structure of male and female brains. A number of scientists have speculated that atypical levels of circulating androgens in some fetuses cause them to grow into homosexual adults. Specifically, they suggest that androgen levels are unusually low in male fetuses that become gay and unusually high in female fetuses that become lesbian.
A more likely possibility is that there are intrinsic differences in the way individual brains respond to androgens during development, even when the hormone levels are themselves no different. This response requires a complex molecular machinery, starting with the androgen receptors but presumably including a variety of proteins and genes whose identity and roles are still unknown.
At first glance, the very notion of gay genes might seem absurd. How could genes that draw men or women to members of the same sex survive the Darwinian screening for reproductive fitness? Surely the parents of most gay men and lesbians are heterosexual? In view of such apparent incongruities, research focuses on genes that sway rather than determine sexual orientation. The two main approaches to seeking such genes are twin and family studies and DNA linkage analysis.
Next : Part 3
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