From the original article on February 26, 2014. Author: JayMan.
In this post, I will review Gregory Cochran’s “gay germ” hypothesis. I wanted to make an index of Cochran’s posts from his and Henry Harpending’s blog West Hunter that discuss it. These posts don’t seem to all show up under the “Homosexuality” category there, and I wanted links to them to be all in one place. So here are the key posts, with a brief synopsis of each post’s major points. In reviewing this hypothesis, I cite an earlier paper co-authored by Cochran on the matter, one which discusses the role pathogens may play in all manner of human diseases and behaviors.
The “gay germ” hypothesis is very much Cochran’s, not mine (I haven’t contributed anything to it, except, perhaps, the name). I just believe that it is very likely correct, and promote it. Here is the list:
Depths of Madness – The first post in the series. Here Cochran lays out the basic case, and notes key facts that point to the pathogen (e.g., high rate of discordance between identical twins, the evolutionary maladaptiveness of obligate male homosexuality and the paradox of how it could have become so common, how pathogens can affect brain function)
Paternal Age and Homosexuality – Explains why genetic load (burden of accumulated deleterious mutation) can’t explain the existence of male homosexuality, especially at its relatively high prevalence. Notes that unlike afflictions that likely are caused by genetic load, there doesn’t seem to be increased incidence of homosexuality in the children of older fathers.
Group Selection (and homosexuality) – Why group selection (multi-level selection) of the type proposed by E.O. Wilson doesn’t work in general and why it certainly can’t explain male homosexuality. Debunks the “gay uncle” hypothesis.
Homosexuality, epigenetics, and zebras – Why developmental noise, including in-utero epigenetic modifications, cannot explain male homosexuality (in short, natural selection has a strong incentive to prevent low-fitness phenotypes from manifesting, so such congenital defects are all rare)
Heads exploding – The introspective post. Appropriately titled, Cochran invites discussion on the social and scientific consequences of nailing down the biological cause of homosexuality – any cause, regardless if that turned out to be the pathogen as he suspects. (As we’ve seen, public discussion of any biological determinant of homosexuality will have consequences, and as I’ve discussed, not necessarily good ones.)
Math is Hard – Rips on E.O. Wilson, and innumerate social scientists in general, who are largely unable to quantitatively evaluate their variously kooky hypotheses (as I’ve said elsewhere, “everything, and I mean everything, can be quantified”). Dishes on Wilson’s “gay uncle” hypothesis as example of these, one of many other nonsensical notions in social science.
Hamilton Rules OK! – Reviews the mathematics of kin altruism (Hamilton’s rule), and again notes why “gay uncle” type altruism doesn’t work.
Not Final! – Key post where Cochran reviews the case for the gay germ, demonstrating the unworkability of all the alternatives. Shows how processes of elimination (essentially, the reductio ad absurdum) can sometime be a useful method of getting at the truth. Excludes ideas such heterozygote advantage (requires very strong selective pressure for advantage – but nonetheless ruled out by GWAS), sexual antagonistic selection (i.e., benefit to females but costly to males – also ruled out by GWAS), group selection (impossible, and no evidence anyway). Explains the how immune complexes generated by molecular mimicry can cause damage to specific tissues not infected by the pathogen. Notes the ubiquitous impact of genes, but the often highly indirect nature of this impact, which may explain the low but non-zero heritability of homosexuality. And notes that pathogens are often responsible for common fitness-reducing syndromes.
Biological Determinism – Cochran references yours truly as he talks about the pervasiveness of heredity in all things (i.e., All Human Behavioral Traits are Heritable), with illustrative anecdotes about twins. Notes the role that genes play in infectious diseases, illustrating that they are often a necessary but not sufficient component of the outcome in question – i.e., you must invoke pathogens to explain something like tuberculosis. Such is the case with male homosexuality.
Evolution of Virulence – An in-depth discussion of the evolutionary pressures that lead to the insidiousness of pathogenic organisms. In particularly, notes that since pathogenic organisms’ populations are immensely large and their generation times are so short, they evolve far faster than their hosts could ever hope to. Discusses Trojan Horse pathogens, those that try to hide from their hosts’ defenses by mimicking host molecules, and why these selection on these types of infectious agents tend to favor late-appearing illnesses.
The case for the gay germ is somewhat indirect, but very strong. Critics often level the charge that there is “no evidence” for Cochran’s hypothesis – i.e., that the offending pathogen has yet to be identified. But the claim that there is “no evidence” isn’t really true; there is in fact plenty of evidence. The facts are certainly consistent with a pathogenic explanation, even if we don’t have the pathogen itself nailed down. But, the most compelling evidence comes in the form of ruling out potential alternative explanations. This itself is a form of evidence. The Sherlock Holmes quote, “when you have eliminated the impossible, whatever remains, however improbable, must be the truth,” is an excellent guiding principle, and is certainly valid here. As I’ve said before, there is something to be said for explanations, that, while maybe not conclusively proven, have the virtue in that they lack meaningful competition. This perhaps one of the clearest examples.
Now, I honestly shouldn’t even have to say this, but let me state clearly that I have nothing against gays, I actually do have several gay friends. Quite often (not all the time, but more than a few times), when I discuss Cochran’s hypothesis, I’m accused of being homophobic. It’s very much a knee-jerk reaction. But, as a friend told me yesterday:
you can come across as harsh and I’m learning that to connect with the mainstream, you must tell them that 2+2=4 before you can tell them 4+2=6. If you don’t make the effort to tell them you’re not evil in each post you write, if it’s the first post they’ve read, they’re going to want to think you’re evil, because everyone wants to think that everyone else on the internet is 1) evil and 2) wrong.
…and then some – an unfortunate reality in these situation. This is especially interesting considering that one of the biggest proponents of the gay germ hypothesis, “misdreavus” (whose colorful commentary was featured in my previous post – and whose comments over at West Hunter have added invaluable insight to the gay germ model) is himself gay. How does that compute?
But biggest of all is that the gay germ model is suggestive of the poorly researched role that pathogens can have in some many other areas, both in illnesses and behaviors. Indeed, the of mode of action of Trojan Horse pathogens which rely on molecular mimicry could be responsible for many low-heritability, late-onset diseases, such as Alzheimer’s disease and cancer. Indeed, in the case of cancer, some are known to be caused by infectious agents, such as those caused by the human papilloma virus (HPV) (e.g., genitoanal cancers) and stomach cancer (apparently caused by Helicobacter pylori). As Paul Ewald (Cochran’s co-author on the paper on this matter) explains, as much as 80% of all cancers will turn out to be caused by infections. This would be revolutionary, if true, because it would suggest that there’s a way to fight the often highly unsuccessful war against cancer, as demonstrated by the success of the HPV vaccine.
Their paper discussed the under appreciated role of infectious agents in all manner of human diseases in great depth:
Infectious Causation of Disease: An Evolutionary Perspective (2000)
They note that infections have fallen out of favor as a possible cause of disease because infectious agents have been increasingly harder to identify – many of the easy-to-spot infectious agents have already been found. This leaves the harder to find pathogens to make up the bulk of those left to be discovered.
Indeed, their paper is very insightful, and quite chilling. They note that even many diseases with known genetic links may have infectious roots. Infectious agents may create a selective pressure favoring otherwise deleterious alleles to persist.
Their analysis breaks it down:
One useful tool for diagnosing infectious causation can be derived from the central principle of evolutionary biology: evolutionary fitness. Estimates of the fitness costs that are attributable to a particular disease (averaged over the entire population) can be used as an indicator for assessing whether the disease could reasonably be ascribed to genetic as opposed to infectious causation. For a genetic disease to be maintained at equilibrium in a population, the loss of the allele for the disease must equal the rate at which the allele is reintroduced. If the allele does not provide a fitness benefit, the loss due to the fitness costs of the disease would need to equal the rate at which the allele is generated through mutation. This reasoning leads to the conclusion that estimates of fitness costs can provide a sense of whether the disease is attributable to something other than simple genetic causation. Any human disease with a frequency that is too high to be maintained by the mutation rate is implicated as being caused by something other than just human genes. If the disease is inherited in Mendelian ratios and is too widespread to be accounted for by founder effects or genetic drift, and if the time has been sufficient for natural selection to drive the frequencies of deleterious alleles to low levels, the allele must have conferred some compensating fitness benefit. The only such compensating fitness benefit that has been documented for major human genetic diseases is resistance to infection
Cochran, Ewald, and Cochran note that most cancers – and even heart disease – probably have infectious origins/involvement. Indeed, they lambast the environmental insult (primarily “lifestyle”) explanation for such diseases, noting, (as I have done quite vocally), the failure to reliably establish such environmental causes.
As we’ve seen in my posts on the topic (the whole category of my posts on health, particularly my posts Even George W. Bush Has Heart Disease and Trans Fat Hysteria and the Mystery of Heart Disease), the “lifestyle” causation model of most of these diseases is in pretty poor shape. Cochran et al even argue that even cancers with known environmental causes, like lung cancer, might have pathogenic involvement.
They point out the problem with the current understanding of heart disease:
At a practical level we need to understand the causes of disease to understand how best to decrease the suffering from disease. At a more basic level, as Nesse and Williams have emphasized, we need to understand the causes of disease, because the mix of superb engineering and seemingly underbuilt components in the human body is a mystery. Is a circulatory system prone to atherosclerosis, for example, really like a Mercedes Benz with the soda-straw fuel line? Or is a state-of-the art fuel line simply prone to microbial sabotage? The resolution of this question and the broader set to which it belongs is academic, but it also promises to reorient medical research and may improve fundamentally our states of health.
All these considered, it is rather shameful that researchers in the human sciences don’t take more of a serious interest in the “gay germ” hypothesis (and pathogenic models in general). Objection from non-scientists is somewhat understandable; no one (other than homophobes) wants to believe that gays are literally “diseased”, despite the fact that this is likely true. Here, that statement is merely an empirical one; it contains no value judgement attached to it. However, that scholars haven’t taken an interest in it is simply inexcusable. How patently ridiculous it is that serious thinkers could really believe at this point that any other explanation for male homosexuality is more likely.
As well, as I have noted before, the conventional dogma on homosexuality is an exercise in the purest of ironies. As Cochran put it in his post Against Biology, and as I said elsewhere:
Irony comes in because (obligate homosexual men, who what most are concerned with) were not “born that way” at all, since male homosexuality almost certainly is the result of a childhood infection.
Worse still, homophobia (or homoaversion, as it should properly called, according to Greg Cochran) is itself heritable, at least 54% so. Yes, homophobes were much more “born that way” than homosexuals themselves!
It doesn’t get much more ironic than that.
But the “born that way” meme does speak towards the prevailing attitude towards genetics. Nothing undesirable can be much heritable, for if it is so, it is seen as (not exactly accurately) being immutable. Hence, this is why sexual orientation can be inborn, but IQ, sex, or racial differences cannot.
This is an interesting statement on where we are, intellectually, as a society. Now, I have said that there will likely be some unpleasant consequences if knowledge of the gay germ were to become widespread. At least belief in a genetic cause leaves the promise of a “fix” way off in some uncertain point in the future (when we could say, screen embryos for whatever putative gay genes). However, an infectious origin offers better prospects, giving the hope (well-founded or not) of a more immediate fix, especially if the infectious agent is a virus; it may be prevented with a vaccine.
(As for the question of female same-sex attraction (SSA) – which is likely a completely separate phenomenon from male homosexuality – I will state that my current suspicion is that it likely a side effect of other useful functions. That is, otherwise beneficial genes carried by women sometimes lead to bisexuality. Female SSA appears to be significantly different from male homosexuality. For one, female SSA appears to be continuously distributed along the Kinsey scale, with the majority of non heterosexual women being bisexual. Male SSA, on the other hand, appears to be a more J-shaped distribution. Sexual fluidity seems to be common enough in women that it is a “normal” trait, so to speak. Indeed, I am beginning to suspect that true lesbians do not exist.)
But, even larger than the issue of homosexuality, the fact that pathogens can affect behavior means that they could be a big part of what it is that makes us different from one another – part of the “unexplained variance” – the difference seen identical twins raised together (see it’s not nature and nurture… | hbd* chick). This is an untapped avenue of research that remains to be explored. Now if we could only get that through to the “learned” people…
The diseases that afflict man, from homosexuality to cancer and heart disease, could be the result of nasty organisms that infiltrate our bodies and minds and attack from within. That pathogens could affect so much shouldn’t seem so bewildering, considering that our world is utterly awash in microorganisms. But no, researchers have been instead been generally wasting their time pursuing “lifestyle” as the main explanation for these illnesses (except in the case of homosexuality, as noted above). For some, mostly liberals, the belief that lifestyle is the root of our ills serves to give hope – hope that the things that ail us can be vanquished if we just get people to “eat better and exercise”. For others, mostly conservatives, the belief that the diseases of civilization are self-inflicted justifies haughtiness – giving one license to look down on the sick for their supposedly inferior lifestyles. It’s a tragic state of affairs.
Edit 6/12/14: See also the discussion in the comments here: Noli Irritare Leones » The Germ of the Gaps
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