Interesting Junk Mail

Dear Mr. XXXXX,

A recent theory, put forth by Dr. Gregory M. Cochran, postulates that human male homosexuality results from a similar change in the brain, as does Narcolepsy. In the last ten years we have seen a substantial amount of empirical research and theory on the subject of sexually dimorphic brains and human homosexuality. Paradoxically, one of the most rational, well thought out theories has received little publicity.

In recent years, Gregory M. Cochran has gained recognition as the result of the Atlantic Monthly three part article, "A New Germ Theory" 1999, Click here, and other scientific papers authored by him. Dr. Cochran's research partners include: Paul W. Ewald and Henry C. Harpending. For those not familiar with Dr. Cochran, perhaps you have heard of the renowned WILLIAM D. HAMILTON who, prior to his untimely death, had concurred with Cochran on this theory which is meant in no way to hurt or bash gays. Previous studies on genetic causation have hinted at genetic diseases. "It's a very sensitive subject," Ewald admits, "and I don't want to be accused of gay-bashing. But I think the idea is viable. What scientists are supposed to do is evaluate an idea on the soundness of the logic and the testing of the predictions it can generate." Atlantic Monthly 1999. If you are interested, please read ahead:

An Evolutionary Look at Human Homosexuality

The first key idea is that evolution optimizes function. It makes things work. If there is a change in a gene that helps the organism, that change increases over the generations, becomes more common. If it causes trouble, as most changes do that make any difference at all, the change decreases over the generations, becomes rare. So although changes (mutations) happen, they don't happen very often, and natural selection tends to keep them rare. You could think of it as a filter, constantly removing changes that don't work. It magnifies the rare changes that improve things.

When we say that a mutation, a gene change, helps or hurts the organism, what we really mean is that it helps or hurts the organism reproduce. Reproduction is the currency of natural selection: a gene that made you long-lived, happy, and sterile would never become common. 'Good' means good at being passed into the next generation. Good genes are a recipe for all kinds of complex functions, and for good health - but from an evolutionary point of view, strength and health are just means, while babies are the end product.

So you don't expect defective genes to be the main cause of human disease, and they aren't. They do cause some genetic diseases which fall into two categories.

The first is simply the consequence of the fact that mutations happen: you might call it the noise in the system, the inevitable price of imperfect gene-Xeroxing. This means single-gene Mendelian disorders like classic dwarfism or muscular dystrophy, and I suppose I would include chromosomal disorders like Down's syndrome. Maybe 1% of the population (In Europeans say) has some Mendelian disorder, mostly mild ones, but no single disorder is at all common.

The second category consists of mutations that are surprisingly common - because, it turns out that they offer carriers some advantage, usually protection against some really unpleasant infectious disease. The most famous of these is the sickle-cell mutations, which protects carriers against the worst forms of malaria. We know of a number of others. Most are also malaria defenses (G6PD deficiency, alpha- and beta-thalassemia, etc.); some protect against other things. Cystic fibrosis probably protects against typhoid. We pay a lot of attention to them, because they are much more common than other genetic diseases, but they are atypical. They are common because they are actually useful in certain situations, rather than being an expression of the noise in the system. They are only important in populations whose ancestors have lived with malaria for many generations. For comparison, the most common disease of this sort in people of European ancestry is cystic fibrosis, which maybe hits one in 2500 kids, but sickle cell anemia can hit more than 1 in 100 kids in much of Africa, in some places one in 30.

How can we use this information to understand disease? Well, in the first place, if genetic problems were the only kind of problem we had, most of us would hardly get sick at all. The second point is that it gives us a new notion of what a disease is - anything that interferes with reproduction.

How could a serious disease be common, if evolution is always optimizing everything? Well, if it hit you at age 85, selection wouldn't be very good at filtering it away. People have already had their children by then ... So this optimizing process works less well at advanced ages. Which is the basic explanation for aging.

But how could a serious disease be common in early life? And think of it as we do - how could a condition that reduces or eliminates reproduction be common in early life?

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.

A disease caused by a malaria defense gene can exist in up to a few percent of people in a high-malaria region: but only there. No other disease has hit as many people as hard, no other disease evokes such high frequencies of expensive genetic defenses.

A common disease can be caused by something new in the world, something to which the human race has not had a chance to adjust. Most lung cancer is caused by cigarette smoking - but cigarettes just haven't been around for many generations.

Most common and serious diseases that have been around a long time and hit in early life are caused by germs - bacteria, viruses, parasitic worms, etc. Evolution doesn't necessarily make them rare, because evolution is playing on both sides in this struggle: they're evolving too. In much the same way, evolution doesn't just make zebras faster, it makes the lions faster too. Lions can continue to be a major problem for zebras over millions of years - and in the same way, malaria can continue to be a problem for humans indefinitely.

So, if a disease is common (> a tenth of one percent), hits in early life, has been around a long time (so we know it's not caused by some new industrial chemical or whatever), and it's not restricted to people from the malaria zone - it's probably caused by some bug.

But what about homosexuality? Well, from this biological perspective, it's surely a disease. Disinterest in the opposite sex reduces reproduction quite a bit - around 80% in American conditions. Does it hit in early life? Sure. Has it been around a long time? Certainly. Do you find it in non-African populations, people who never lived with malaria? Yes.

So it's a bug.

Now that we know that human male homosexuality looks like a disease caused by some infectious organism, the next question is how that could happen - how could some virus change sexual interest?

I don't think that anyone can be sure of the exact mechanism at this point. I think we can be fairly confident that it is caused by an infectious organism, from the information we have and general evolutionary considerations, but infectious organisms can cause harm in many different ways. Malaria colonizes and uses up red blood cells, diphtheria and cholera manufacture toxins, HIV slowly knocks out a key subpopulation of the immune system, leaving you defenseless against many other pathogens, while certain papillomavirus strains deregulates cell division and thus cause cervical cancer. And those are just samples: there are many pathogenic mechanisms involved in infectious disease, some not well understood.

What do we know? We have a lot of indications that there has been some change in the brain. After all, that's the most logical location for the cause of a change in behavior. Simon LeVay and others see differences in hypothalamic nuclei (similar to those seen in sheep). There are associated changes - the lisp, increased neuroticism and depression, etc. Somehow the cause is affecting the brain.

Just as important are all the things we don't see. We don't see IQ depression, we don't see epilepsy, we don't see convulsions, and we don't see aphasia. Clearly there is no gross trauma - somehow, the brain has been damaged, but in a very limited and focused way. A key function has been messed up, which gravely impacts reproductive fitness, but homosexual men can still hold down jobs, including very complex jobs. The overwhelming majority of mental functions are perfectly intact, or at most subtly changed. The damaged neural subsystem could be male-specific.

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.

We know of a similar, very specific damage pattern in the brain -

In Narcolepsy, most of the neurons that produce hypocretins (neurotransmitters) have somehow disappeared. There are only 30,000 of these neurons in the first place, all in a small hypothalamic nucleus. This loss leaves one pathologically sleepy, subject to cataplexy and in some cases hypnagogic hallucinations. Narcolepsy hits about 1 in 2000 people: identical twin concordance is around 25%. Almost all narcoleptics have a particular HLA type, one shared by about a third of the general population. Narcolepsy (almost always) is not present at birth but manifests in early adulthood.

Narcoleptics are pathologically sleepy, but most mental functions are unaffected.

There is at present a strong suspicion that narcolepsy is an autoimmune disease, possibly triggered by a viral infection. The HLA association points in this direction, but as yet the exact cause of the destruction of the neurons that make hypocretin is unknown. Narcolepsy does, however, show that there exists some mechanism that can destroy a particular hypothalamic neuron subpopulation without causing general brain trauma.

Narcolepsy can also be caused by a mutation in the gene for hypocretin or its receptor: so far, out of hundreds of narcoleptics examined, just one had such a mutation. Of course natural selection keeps such mutations rare. He had an unusual profile, being narcoleptic from birth.

Imagine a neurotransmitter that plays a key role in male sexual behavior, produced by a few specialized neurons, probably in another of the many known hypothalamic nuclei, quite possibly in the nucleus that LeVay studied... Obviously you can walk and talk without it - women probably don't have any at all, while children may not have much. You could live without it, think without it - just as eunuchs live and think without much testosterone. But this hypothetical neurotransmitter is more specialized than testosterone: instead of beginning a chemical cascade that has many effects on body and mind, like testosterone, this one mainly affects the choice of sexual partner: is involved in constructing a search image.

Occasionally a pathogen, in one of a few possible ways, causes the destruction of most or all of those specialized neurons. Maybe its molecular mimicry: maybe it has a tropism for those particular cells and kills them directly. But this kind of super-precise damage pattern can happen, because it does happen with narcolepsy. Maybe the HLA genes make a difference, maybe they don't. As in so many things in the male brain, the search image generator is by default female-type: doing nothing, failing to masculinize, results in sexual interest (testosterone is still being produced) but it's interest is in males, not females.

Fortunately, we have an excellent experimental animal model: sheep. Some rams, 6 percent in some herds, show sexual interest in males and no interest in females, ever. Breeding experiments, using artificial insemination, showed insignificant heritability. Studies of the sheep's brains show oddly differential hormonal activity in certain areas of the hypothalumus. OSU professor studies sexual preference in sheep.

Preferential homosexuality, sexual interest in males, rather than females, is very rare. The only two species known to exhibit this behavior, at the-few-percent level, are men and sheep. It may be worth noting that men and sheep have often been found in close association.

Another point worth mentioning is that the prevalence of homosexuality probably varies a lot. It seems to be considerably more common in young men who grew up in urban areas than in rural areas, something like a factor of three, which is also true of Schizophrenia. This is a much bigger effect than the birth order stuff. If you look out in the real sticks, say among the Kalahari Bushmen, there doesn't seem to be any at all. Typically, hunter-gatherers have trouble believing that homosexuality actually exists.

All this is speculative, of course: but the idea that male homosexuality is caused by a pathogen makes good evolutionary sense, unlike every other explanation ever proposed. This particular form of pathogen explanation of homosexuality, inspired by the recent breakthroughs in narcolepsy research, is consistent with the low identical twin concordance for homosexuality, with geographical variation in its incidence, with some observations of volume changes in a particular hypothalamic nucleus in homosexual men, and most importantly, with the dog that didn't bark - the fact that homosexual men do not suffer from general brain damage, do not show symptoms like IQ depression.

Gregory Cochran

Gregory M. Cochran, PhD

Gregory M. Cochran, physicist turned evolutionary biologist, is best known for his work with Dr. PAUL W. EWALD
using statistical analysis to make the case that many diseases long thought to be hereditary may in fact be caused by infectious agents.

What can we do with this information? Many respected biologists are in agreement that Cochran's theory is plausible, warranting scientific study. In fact, WILLIAM D. HAMILTON, possibly the greatest theoretical biologist of the twentieth century, reviewed Cochran's recent paper, "Infectious Causation of Disease: An Evolutionary Perspective" (published in Perspectives in Biology and Medicine, 2000). Click here which touched upon the possibility of infectious causation of male homosexuality. This was, sadly, Hamilton's final scientific review prior to his untimely death, at the age of 63. Of Cochran's theory, Hamilton said:

"This is an important reorienting review for scientific medicine and will be much cited...It is well our eyes to many quite weird possibilities about disease that most medical scientists, tending to be unaware of current evolutionary thought, don't think of. The idea about homosexuality, for example, while bound to be highly controversial is timely to be raised and is sensitively treated. What they suggest has certainly seemed to me a very real possibility: I had not, however, heard of the homosexual sheep and, as they say, that case immediately opens big possibilities for investigation."


We have sheep, an excellent animal model, and narcolepsy, an excellent disease model, if a pathogen is the cause of male homosexuality, then, someday, treatment might be an option, for ego dystonic homosexual men. Just recently, Dallas scientists reported that they are "closing in on a Narcolepsy cure." Click here.

Specifically, once brains of dud rams are in the laboratory, a microbiologist would look for signs, evidence and portents of infection. Then, gene chips would hopefully reveal specific differences in gene expression between the brains of dud and normal sheep. Differential PCR could look for DNA found in dud sheep but not in the others. (that's how they found the herpesvirus causing Karposi's sarcoma). Using RDA one would look for funny 16s rRNA and see if it's catching, in sheep. Identifying specific missing neurotransmitters in the brains of the dud rams, would also be a primary goal of the study. (same as in Narcolepsy). Click here Another option would be to clone a few homosexual rams. Cochran is willing to bet that clones of homosexual rams would usually be heterosexual.

In humans we could do the obvious: look, with the standard tools, for some known pathogen that exists in essentially all homosexual men. You might also use representational difference analysis (RDA) to look for DNA that exists in the homosexual twin of a discordant MZ pair.

Why am I contacting you? Due to the sensitive nature of this topic, government funding is unlikely. Research is only probable at a conservative university or if private money can be found. Setting up a ram experiment will cost some money, but not as much as you might think. We are simply looking for references of foundations and individuals who might be interested in funding something of this nature. Please contact me with your suggestions at For scientific inquiry, Gregory M. Cochran may be contacted at

Thank you for your consideration,

M E Howell
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