Greg has never published his theory in a peer-reviewed journal, although it is briefly summarized in Cochran et al. (2000). In itself, this is no shortcoming. Most journals seem uninterested nowadays in real debate. But sometimes I wish he would at least pretend he was writing for a journal. He tends to be polemical, as if only political correctness—or sheer stupidity—could motivate his detractors.
His starting point is the same as Miller’s. Male homosexuality makes no sense as a reproductive strategy. It should die out for the same reason that the Shakers did (the Shakers were a Protestant sect dedicated to lifelong celibacy). This point might seem obvious. Or maybe not. The following is an exchange between a germ theory critic and Greg Cochran:
Critic: Is it not likely that human sexuality is in fact a bell curve, with "strict homosexual" on one end and "strict heterosexual" on the other end, and the majority of the people falling somewhere in between? (With the caveat that sexual preference and sexual practice are not necessarily the same thing).
Greg: No, it is not likely. Sheesh. That would make exactly as much sense as a bell curve of food preferences ranging from steak at the left to granite at the right, in which people in the middle liked steak and rocks equally well. Is an even split between a behavior that works and one that never does what you expect from biology? Do you expect half the geese to fly north for the winter? (source)
Since natural selection would tend to eliminate male homosexuality, it should be uncommon—like most genetic conditions that impair one’s ability to survive and reproduce.
First we have to say what ‘common’ means, in this context. Common means common compared to the noise in the system. So 1% is very common: no disease caused by random mutations is anywhere near that common. 1 in 10,000 is surprisingly common, but there are one or two mutation-caused diseases that are in that ballpark, like Duchenne’s muscular dystrophy. Turns out that the gene involved in muscular dystrophy is maybe 20 times longer than the typical gene — there are more opportunities for typos. So 1 in 7000 boys have Duchenne’s muscular dystrophy — that’s as common as a ‘system noise’ disease gets. (Cochran 2004?)
Since male homosexuality is not rare, it cannot have a genetic cause, at least not principally. There may be a genetic predisposition (with around 30-45% heritability, according to twin studies), but this predisposition is interacting with something in the environment. And this something cannot be a recent environmental change, since male homosexuality has been around for a long time.
The only remaining cause would be some kind of infectious agent that selectively alters certain parts of the brain while leaving the rest intact. There are precedents for this sort of thing.
Do we know of diseases in which there are very specific targets—in which certain cell types are damaged or destroyed while neighboring cells are left intact? Sure. In some cases, a pathogen targets a particular cell type and has little effect on anything else. Human parvovirus (also known as fifth disease) hits erythroid precursor cells (the cells that manufacture red cells) and temporarily inhibits red cell production. In type-I diabetes, it seems likely that Coxsackie virus infections (in people with a genetic predisposition, in which HLA type plays a major role) trigger an autoimmune disease that gradually (over a year or so) destroys the islet cells which produce insulin. Other cells are not much affected. (Cochran 2004?)
Such pathogens may be more common than we think. The ones that get our attention—that make us go and see a doctor—are the ones that cause discomfort. But those ones may be a small minority of all pathogens, with most of the others flying under the radar. After all, it is in the pathogen’s own interest to be discrete and not cause too much havoc. It needs a healthy home to live in, until it can spread to another host.
Greg also argues that male homosexuality should be less common in smaller communities than in larger ones—where pathogenic transmission is likelier.
We can deduce a few things about the hypothetical agent causing homosexuality. First, it has a small, but not incredibly small, critical community size. That is the size of the clump of people required to keep the agent going. Some agents, ones in which infection results in permanent immunity, need a _large_ number of people, big enough that there are new infected people showing up by the time it circles the community. Measles for example requires almost half a million people in close proximity. An agent that causes a persistent infection can have a very small community size: I'd guess that Epstein-Barr has a CCS under 50.
Since some communities seem to have no homosexuality at all (Bushmen, some hunter-gatherer groups in Indonesia and the Philippines, pre-contact Polynesians) we can be sure that this hypothetical agent has a critical community size larger than that of Epstein-Barr. More like chickenpox, which has a CCS of about 300 people. Not that I'm saying it _is_ chickenpox, mind you. (Cochran 2005)
Finally, this pathogen may selectively alter sexual orientation for reasons that go beyond those of not harming the host too much. There are, in fact, a number of pathogens that alter the host’s behavior in order to enhance their chances of transmission. The protozoan Toxoplasma gondii causes infected rats to lose their fear of cats, thus enabling it to enter a cat body and complete its life cycle (Wikipedia – Toxoplasmosis). The parasitic worm Euhaplorchis californiensis forms cysts in the brains of infected killifish that cause the fish to swim near the surface of the water and make tight turns that show off their glinting sides, thus enabling the worm to enter a bird’s body (Zimmer, 2008).
As a child, I remember being told that a chicken is an egg’s way of making another egg. If Greg Cochran is right, a gay man is a vehicle that a pathogen has constructed for its own survival and reproduction. Everything else is human-centered delusion.
This is an interesting argument, but it has a few holes. First, some genetic conditions do reach incidences that are comparable to that of male homosexuality (about 3-5% of all men). Abnormal hemoglobin variants can reach high incidences in sub-Saharan Africans and other populations (8% in the case of Hb AS among African Americans). These variants are typically maintained through balancing selection where the heterozygote state provides some protection against malaria. Greg acknowledges that such selection exists but sees it as being confined to malaria protection. Yet balancing selection can exist for many other reasons. For example, one in 200 Hopi is albino, apparently because cultural selection offsets the environmental disadvantages of albinism (Hedrick, 2003).
Second, male homosexuality is frequently reported in small communities, including bands of Amerindian hunter-gatherers. Known as ‘berdaches’, these male homosexuals were described by early European explorers and appear to have existed in pre-contact times, as indicated by origin myths (Desy, 1978). One witness was John Tanner, a white captive who lived among the Ottawa of Ontario and then the Ojibwa of Manitoba until 1828:
Some time in the course of this winter, there came to our lodge one of the sons of the celebrated Ojibbeway chief, called Wesh-ko-bug, (the sweet)... This man was one of those who make themselves women, and are called women by the Indians. There are several of this sort among most, if not all the Indian tribes. They are commonly called A-go-kwa, a word which is expressive of their condition. This creature, called Ozaw-wen-dib, (the yellow head), was now near fifty years old, and had lived with many husbands. I do not know whether she had seen me, or only heard of me, but she soon let me know she had come a long distance to see me, and with the hope of living with me. She often offered herself to me, but not being discouraged with one refusal, she repeated her disgusting advances until I was almost driven from the lodge. (Desy, 1978)
Of course, neither point disproves the germ theory of male homosexuality. An infectious agent may indeed be the cause or one of several causes. If we consider the developmental pathway for heterosexual orientation, there is probably a ‘default’ sequence that leads to sexual interest in men and an ‘override’ sequence that leads to sexual interest in women. The second sequence may be disrupted for many reasons: a psychological trauma, a chemical insult, or an infectious agent in combination with a pre-existing genetic predisposition for incomplete masculinization. As one comment noted:
Some of the disruptive factors implicated by empirical evidence are excess prenatal testosterone exposure (a major factor), prenatal stress, and exotic factors such as disruptive chemical agents. Infections proposed by Cochran may also disrupt development, but I do not know of any evidence that supports this assertion as of yet. (Cochran 2005)
Cochran, G.M. (2005). Cause of Homosexuality: Gene or Virus? Cochran Interview. Thrasymachus Online.
Cochran, G.M. (2004?). An evolutionary look at human homosexuality. World of Greg Cochran.
Cochran, G.M., Ewald, P.W., & Cochran, K.D. (2000). Infectious causation of disease: an evolutionary perspective. Perspectives in Biology and Medicine, 43, 406-448.
Désy, P.P. (1978). L'homme-femme. (Les berdaches en Amérique du Nord), Libre — politique, anthropologie, philosophie, 78(3), 57-102.
Hedrick, P.W. (2003). Hopi Indians, “cultural” selection, and albinism. American Journal of Physical Anthropology, 121, 151-156.
Zimmer, C. (2008). The Parasite Files. Discover. Dec. 16.