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Tufts OpenCourseware
Author: Ross S. Feldberg

1. Background: Is There a Biological Basis for Homosexuality?

Because almost all the biological research has been on male homosexuality, we will deal only with this aspect of homosexual behavior. We begin by looking at homosexuality in history to understand first that our very perception of an issue is determined by the society we live in. Indeed for most of history, homosexual behavior was recognized, but the idea that individuals might form a group (homosexuals) was not. Once the idea that an individual might be attracted only to members of their same sex was recognized, a number of ideas as to why this might occur have been suggested.

1.1. Psychological Explanations (Freud and the distant father)

The view that dominated most of the last century was proposed by Freud. Homosexuals were made, not born, and homosexuality was the result of a distorted family life involving a distant father and an overwhelming mother. This view led to homosexuality being classified as a deviance for most of the 20th century. It wasn’t until 1957 that Karen Hooker administered a variety of psychological tests to hetero and homosexual men and found no significant difference between them. It still took until 1973 for the American Psychiatric Association to remove homosexuality as a disorder from its Diagnostic and Statistical Manual of Psychological Disorders (DSM). It took another 20 years for the APA to finally state, "...homosexuality is neither a mental illness nor a moral depravity.  It is the way a portion of the population expresses human love and sexuality."

1.2. Biological Explanations

It is the case that sexuality seems to be an essential component of personality, so intrinsic to our nature that it is hard to imagine ourselves having a different orientation. It is interesting that homosexuality seems to occur at a frequency of 4-6% or so no matter what culture we examine. This has led many scientists to search for the biological explanation of sexual preference (preference is really too weak a word to express this).

  1. Male birth order: For each additional brother that precedes him, a boy’s chance of growing up to be gay increases by 30% ( Am J. Psychiatry 153: 27-31 (1996) – but note, be suspicious of "percent increases." If an event only occurs 2% of the time, a 30% increase means it will occur 2.6%, and one has to ask is this difference real or meaningful). Indeed, it has been noted that this factor may account for only 14% of all gay men and it only seems to occur if the boy is right-handed (even though left-handed boys are more likely to be gay than right-handed boys). One explanation has been the “Maternal Immunization Hypothesis” (see J . Am. Acad. Child Psychiatry 24: 363 (1985)) – but we will not cover this in this class.

  2. Prenatal Exposure to Hormones: In animals that have litters of young, there is good evidence that position of the fetus can influence its eventual sexual behavior (i.e., a female fetus developing between two male fetuses has more male-typical behavior than expected). This suggested that prenatal exposure to hormones could affect the developing brain. Again, we will not cover this topic in class.

  3. Twin Studies: The classical way to demonstrate that something is biological is to demonstrate that it has a genetic origin (although I will show you in a moment that is probably not a valid assumption). Many twin studies are very poorly done, but some have generated useful data. Initial studies reported in 1991 indicated that in identical twins, if one twin was gay, the other had about a 50 percent chance of also being gay while for fraternal twins, the rate was about 20 percent, and for unrelated individuals the chance is that of occurrence in the general population, estimated at about 4-6%. A later and larger study conducted in Australia found that for identical twins the concordance value was 38% rather than 50%. So here we have our first bit of confusing data. Identical twins share 100% of their genes, so if homosexuality was purely genetic in origin, we might expect the concordance should be higher than 38%. Fraternal twins share only 50% of their genetic information, so you might predict if this was due to genes alone, the concordance rate should be 8-12% (twice that of the general population. So these data seem to suggest both genetic and environmental components (and perhaps a component of chance).

  4. The Homosexual Brain: Scientists love to measure the brain and there is a long and disreputable history of scientists using brain measurements to explain a variety of social inequalities. In the 1980s, several scientists reported finding gender differences in the size of four neuron rich areas in the hypothalamus (the Interstitial nuclei of the anterior hypothalamus (INAH-1 to 4)). In 1991 LeVay extended this to the brains of homosexual men who had died of AIDS. However, he found a statistically significant difference between men and women only for the INAH-3 but not in the INAH -1, -2 or -4. We will read and discuss this paper in detail.

  5. Homosexuality as an X-linked Trait: (Was Freud right? Is your mother to blame?) Dean Hamer at NIH is a geneticist who specializes in behavioral genetics – the search for the genetic basis for a variety of human traits. On many levels, the efforts in this field have been a great disappointment. People have been looking for the genetic basis for schizophrenia, criminal behavior, manic-depressive disorder, and a variety of other pathologies for 30 years with very limited success.
    The problem here is that it is nearly impossible to identify a gene for a trait among the 23 different human chromosomes. There is simply too much genetic material to scan. But if you could narrow your search down to a single chromosome, you might have a chance. Hamer decided to look for male homosexuals who inherited this trait via their X-chromosome. He did this in a very clever way by only analyzing gay men who had a gay brother and one or more gay maternal uncles (this would suggest an X-linked trait).

We will discuss this paper in detail in class, but let me point out one major problem with this approach. This view assumes a single gene with a strong effect is responsible for the condition. But consider schizophrenia. People have been searching for a gene responsible for schizophrenia for years and still haven’t found any clear candidate, but might it not be the case that schizophrenia isn’t a single condition but rather many different conditions that we lump together under a single name? And why assume it is caused by a single gene exerting a strong effect rather than a combination of gene alleles each making a weak contribution to an overall final state? Finally, this approach totally neglects the contribution of chance or environmental factors in prenatal and postnatal development.