Saturday, April 20, 2013

The gay germ hypothesis


Incidence of chlamydia, a major cause of infertility. The high polygyny rate among the “female farming” peoples of sub-Saharan Africa may have favored the evolution of STDs. Is this where we should look for the precursor of the hypothetical “gay germ”? (source)

 

Heritability for male homosexuality is low to moderate (30 to 45%). There is thus some kind of genetic predisposition, but it’s weak and may simply be a low degree of pre-natal androgenization. All things being equal, such individuals would still develop a heterosexual orientation.

But all things aren’t equal. Something out there is tipping these individuals over the threshold that separates heterosexual from homosexual orientation. What is it? I suspect there are several causes, including the rising level of estrogens and estrogen-like substances in the environment over the past century (see previous post).

The cause may also be a pathogen that alters its host’s sexual orientation in order to enhance its chances of spreading to other hosts. This is the “gay germ” theory proposed by Greg Cochran (Cochran et al., 2000). It’s interesting, and there are certainly precedents for this kind of psychological manipulation … from zombie ants to rats losing their fear of cats.

But so far there’s no smoking gun. No candidate pathogens have been identified, although some STDs seem to have adapted to non-heterosexual modes of transmission, e.g., the bacterium responsible for bacterial vaginosis, particularly Gardnerella vaginalis, and some strains of vaginal yeast (see previous post).

Another objection is that natural selection should reduce host susceptibility. As Ron Unz (2013) has recently argued:

Cochran and others ridicule the gene model as absurd, arguing that strong selective pressure would have rapidly eliminated any such genes from the population, and this is not unreasonable. But similar criticism could applied to their own model, since genetic susceptibility to the germ would obviously be subject to equally powerful selective disadvantage.

A lot of pathogens seem undeterred by this argument. People die all the time from infections of one sort or another. One reason is that pathogens have shorter generation times and thus can evolve faster than their hosts can. An evolutionary equilibrium will eventually fall into place, but it will be heavily weighted in the pathogen’s favor. There are also limits to what a host can do. If the host’s defense system becomes too sensitive, it will attack not only possible pathogens but also host tissues.

Still, the most catastrophic epidemics tend to burn themselves out, largely because they destroy the pool of individuals they can most easily spread amongst. The Plague of Justinian of the 6th and 7th centuries may have wiped out half of Europe’s population. Then it disappeared. The Black Death of the 14th century killed between one and two thirds of all Europeans. It too disappeared, the last possible outbreaks being in the 18th century. This is not the case, however, with STDs, even in places where the consequences are dramatic, such as Africa’s “infertility belt”:

Africa shares the largest burden of infertility in the world. Estimates indicate that an average of 10.1% of couples experience infertility in Africa, with a high percentage of 32% in some countries and ethnic groups within Africa. An infertility belt” spreading through West Africa, through Central Africa to East Africa has been described. In some countries in this belt, up to one-third of women may be childless at the end of their reproductive lives. (Okonofu & Obi, 2009)

A pathogen would not sterilize one third of the population, generation after generation, unless it had something to gain, as Ron Unz notes. In sub-Saharan Africa, infertility can lead to abandonment of the wife, thus making her a better vehicle for pathogen transmission:

The high prevalence of untreated STD, resulting in increased infertility acts paradoxically to increase rather than decrease the fertility in Africa. Infertility is devastating for an African woman, resulting in divorce and diminished social status that often leads to prostitution. The fear of infertility results in refusal of contraception and early childbearing to demonstrate fertility. (O’Reilly, 1986)

Other separated women owe their status to infertility, which is a frequent reason for being driven from marriage and for being unable to marry […] Nadel […] identified such women as a major source of prostitutes: “Adultery and unchastity count less in her than other women. [The] paramount stigma [is] barrenness itself.” (Caldwell et al.,1989)

The existence of Africa’s infertility belt is generally attributed to a high prevalence of STDs, particularly gonorrhea and chlamydia (Collet et al., 1988), which in turn is related to a high polygyny rate (20 to 40% of all sexual unions throughout most of sub-Saharan Africa), which in turn is related to the low cost of maintaining a second or third wife, which in turn is related to year-round hoe farming and the ability of women to support themselves and their children with little male assistance.

We know that the AIDS virus evolved in sub-Saharan Africa, and it may be that syphilis evolved out of yaws, likewise endemic to sub-Saharan Africa. It may be that this region favors the evolution of STDs; if so, we might best look for the precursor of the “gay germ” there as well, assuming of course that it does exist.
 

References

Caldwell, J.C., P. Caldwell, and P. Quiggin. (1989). The social context of AIDS in sub-Saharan Africa, Population and Development Review, 15, 185-234.
https://www.soc.umn.edu/~meierann/Teaching/Population/Readings/Feb%209%20Caldwell.pdf

Collet, M., J. Reniers, E. Frost, R. Gass, F. Yvert, A. Leclerc, C. Roth-Meyer, B. Ivanoff, and A. Meheus. (1988). Infertility in Central Africa: Infection is the cause, International Journal of Gynecology & Obstetrics, 26, 423–428 http://dx.doi.org/10.1016/0020-7292(88)90340-2

Cochran, G.M., Ewald, P.W., and Cochran, K.D. (2000). Infectious causation of disease: an evolutionary perspective, Perspectives in Biology and Medicine, 43, 406-448.

Okonofu, F.E. and H. Obi. (2009). Specialized Versus Conventional Treatment of infertility in Africa: Time for a Pragmatic Approach, African Journal of Reproductive Health, 13, 9-11.
http://www.ajrh.info/vol13_no1/13_1_editorial_english.php

O’Reilly, K.R. (1986). Sexual behaviour, perceptions of infertility and family planning in sub-Saharan Africa, African Journal of Sexually Transmitted Diseases, 2, 47-49.

Unz, R. (2013). “Gay gene” vs. “gay germ”, April 16, The American Conservative,
http://www.theamericanconservative.com/gay-gene-vs-gay-germ/

 

34 comments:

John Lilburne said...

The heredibility of homosexuality is about 20% not the 35-40% given(see Cohran at westhunter). Ther is a lot of PC nonscience in reported figures

Anonymous said...

I don't believe in either the gay germ or the group selection(gay uncles invest in nephews) theory...I believe it is a socialization/hormone/dopamine issue....

OKCupid took this chart down from their blog, but Very Short, Very Tall Men More Likely To Be Gay

http://www.akawilliam.com/study-very-short-very-tall-men-more-likely-to-be-gay

Anonymous said...

"OKCupid took this chart down from their blog, but Very Short, Very Tall Men More Likely To Be Gay"

I.E.... there are a lot of gay men(and women really) who are gay because they are(or were when they were being socialized) not sexually attractive to the opposite sex.

Anonymous said...

Didn't Jesse Jackson assure us that the CIA created AIDS?

Anonymous said...

Seems plausible that a unique environment - female provider - might lend itself to some unique bugs.

Peter Fros_ said...

John

Personally, I have no problem with a heritability of 20%, but many researchers would (like J. Michael Bailey). The Wikipedia entry for "Biology and sexual orientation" provides a good review of the topic:

"In men, genetic effects explained 0.34–0.39 of the variance, the shared environment 0.00, and the individual-specific environment 0.61–0.66 of the variance. Corresponding estimates among women were 0.18–0.19 for genetic factors, 0.16–0.17 for shared environmental, and 0.64–0.66 for unique environmental factors."

ted said...

You say that Cochran believes a pathogen alters the host's orientation in order to spread, but that is not what he's been saying ; this is not the first time I've heard you present his idea as such. He's said many times that the more likely scenario is that the damage to some critical cells is more likely a side effect of a common childhood pathogen, collateral damage, as it were, rather than a strategy of the bug to survive and spread.

Anonymous said...

I remember reading that the concordance of rheumatoid arthritis among MZ twins is 15-18 percent, an incidence not that different from that of MZ twins for homosexuality.

It's seems clear from studies on MZ twins that there is some enviromental trigger for RA, and it seems likely tye same is true for male homosex.

Mark said...

I feel like Cochran's pathogen, if it exists, plus HIV make for a weird and tragic symmetry in the lives of many gay men. Or did, back when HIV was terminal.

Anonymous said...

Mark,

My understanding is new HIV infections continue among the gay male populations.

In other words, as son as retrovral meds improved, old behasviors returned. As long as the unpotected sex and promiscuity continue,you can look for the next bug to evolve to deadliness.

Ron Unz said...

The main argument against the naive Gay Gene model is that there would be strong selective pressure to weed out such genes, unless they provided some compensating benefits. And unless one can propose such a benefit (gay uncles not being very plausible), the whole argument is just hand-waving speculation.

But I would suggest that a similar problem may be found in the Gay Germ model. If the germ somehow strongly benefitted from inducing gayness in its hosts, the theory would make sense, but I haven't seen anyone provide a logical model for this.

The other possibility is that the orientation is an unintended side-effect of the germ's activity. But if the side-effect could be eliminated, there would be massive selective pressure on the host/germ system to do so, since the change would be very important to the host but totally unimportant to the germ. Therefore, the only reasonable model would be one in which the side-effect is inextricably linked to the germ's functioning. This is certainly possible, but requires us to posit some totally unknown explanatory factor, in exactly the same way that a Gay Gene supporter could hypothesize that the Gay Gene had some major positive compensating benefit, but without suggesting what it was or anything about it. Both of these cases are pure hand-waving speculation.

Until someone has proposed an evolutionary model explaining either the selective benefits of a Gay Gene or the selective benefits of the Gay Germ (to itself), we really don't have anything at all. And since the hypothethical Gay Germ doesn't really solve any of our evolutionary puzzles, Occam's Razor would seem to argue against it.

Anonymous said...

Ron Unz,

Can you explain how the lasting deleterious side effects of the measles, mumps, and rubella confer a selective advantage to each bug? I admit I don't understand what you're saying.

Sean said...

Gay men got less pre-natal testosteronisation; their fetal programming is maladaptive. If there was a bug that caused oestrogenisation then it could be reducing the reproductive fitness of men by making them less masculine, and sometime tipping them into homosexuality. But, in women it could spread through vertical transmission, and increasing reproductive fitness though making infected female fetuses more feminine. Do gay uncles have sexy sisters?

Anonymous said...

Can you explain how the lasting deleterious side effects of the measles, mumps, and rubella confer a selective advantage to each bug? I admit I don't understand what you're saying.

Something like rabies. The rabies virus makes the infected animals very aggressive and bite prone. The aggressive behavior and biting helps the virus spread to other animals.

Even something like sneezing or coughing, which we tend to associate strictly as a defensive or immune response, could be seen as something a bug causes and relies on to spread.

Anonymous said...

But I would suggest that a similar problem may be found in the Gay Germ model. If the germ somehow strongly benefited from inducing gayness in its hosts, the theory would make sense, but I haven't seen anyone provide a logical model for this.

The model proposed by one of Cochran's commentators is that it actually doesn't, but it does mimic the body in such a way that evolving a response to it would render the host sterile, because the immune system would end up targeting both the bug and the parts of the brain responsible for successful sexuality.

The pathogen does not benefit from the host being gay, but the host loses, so the pathogen is essentially pursuing a kind of mutually assured destruction policy (your victory, immune system... so pyrrhic!)

But then, still why is this only in humans?

The problem I am still having with the Gay Germ idea even after all the discussion at Cochran's blog, which convinced me a lot more than I was otherwise, under this theory:

The mechanism for choosing and successfully mating with humans must be very simple, assumed to be identical with other species, no different.

This is not really for any particular evidence based reason, but because more complex the mechanism becomes, the more vulnerable it is to load and sexually antagonistic selection, to the point where genetic hypotheses may begin to become possible. (Of course, it is arguably parsimonious as well)

However, if the mechanism is the same in humans, with no particular extra complexity, then why are humans the only ones to get the gay? And sheep? A Gay Germ should work everywhere right? If it's hard for humans to evolve a response, why would other species have an evolved response? Our herd sizes are pretty large, as one point, I suppose, but how would that link in.

If human sexuality (targeting and mating) is conversely, very complex and different from other animals, then....

Anonymous said...

The model proposed by one of Cochran's commentators is that it actually doesn't, but it does mimic the body in such a way that evolving a response to it would render the host sterile, because the immune system would end up targeting both the bug and the parts of the brain responsible for successful sexuality.

The pathogen does not benefit from the host being gay, but the host loses, so the pathogen is essentially pursuing a kind of mutually assured destruction policy (your victory, immune system... so pyrrhic!)


Same anon here.

Couple of other facets here which may be interesting:

If this were true, then one implication is that the gays would not be the carriers of the pathogen, the straights would.

This makes transmission to pre-gays very easy, because they would not actually have to come into contact with gays, in fact, the more they come into contact with straights, the better.

It would also make any intervention against any pathogen easier in a sense, as it would not be reliant on any consent by the gay community, because the bug is in the bodies of straight people (the straight people are the infected, while gays are those who are all clear, but whose sexuality was lost in the process).

Another facet might be that this might link up with testosterone levels - that is to say, if testosterone suppresses the immune system (somewhat skeptical of this but lets run with it) and homosexuality is an auto-immune response, then gays being somewhat low testosterone in some ways might make sense.

Gnome Seyin said...

Apart from its obvious scientific plausibility, I like this theory for the lulz. It is perhaps the Ultimate Un-PC Hate-Thought Ever Thunk, ever. All that self-importance, all that self-righteousness -- and it may all turn out to be a simple micro-organism. Parturiunt montes, nascetur ridiculus virus.

Anonymous said...

Anon at 1:54:

The crazed state of the rabies victim is not a "side effect"; it's an actual evolved strategy of transmission.

Deafness, testiular atrophy, encephalitis, ovarian inflammation, pancreatitis, etc. do not help MM&R spread, which is why they are termed "side effects."

Damaged heart valves are not strategies for transmitting bacterial infection in rheumatic fever or in endocarditis. They are side efects of the infections.

Anonymous said...

Ron unz, I'd say Occam Razor is an argument FOR the germ theory.

Anonymous said...

"The main argument against the naive Gay Gene model is that there would be strong selective pressure to weed out such genes."

I've never understood what was wrong with saying that social stigma against homosexuals historically forced them into marriages where they reproduced anyway. The stigma prevented the normal weeding processes from working. This kept the gene around despite its normally maladaptive consequences.

RS said...

> The pathogen does not benefit from the host being gay, but the host loses, so the pathogen is essentially pursuing a kind of mutually assured destruction policy

That kind of makes sense. You know, the eye, the gonad, and the brain are called 'immunopriveleged' because immune tone is low there. The reason it is low is because you are going to wind up pretty much 'darwinianly dead' if the immune system causes severe collateral damage to those sites -- even if you remain very much alive in a normal sense.

Some highly evolved and successful parasites therefore like to hang out in the brain, generally without ravaging it.

Well, it is conceivable that some areas of the brain, those most crucial to fitness, are more immunopriveleged than others. That would possibly be an even cooler place to hang out (than the brain in general), where you are even less apt to be eradicated by immunity.

How immunoprivelege works is understood, at least in part. The privileged tissues present special ligand molecules which bias certain white blood cells towards apoptosis (suicide) or anergy (lasting or permanent inactivity). Well, if the brain, eye, and gonad generally express such ligands at density x, some key parts of the brain might well express them at density 5x, or 4.23986x.

Skittles Man said...

Evolution made some men more masculine than others. Not just in terms of their bodies, but in terms of their brains. It is not ideal for all males to follow a super aggressive reproductive strategy, like Ghengis Khan. Alternative, more peaceful strategies evolved, such as faithfulness to a woman and investment in her children. We see these alternative mating strategies in many species.

As a quick and dirty solution to produce the second kind of males, their brains were somewhat feminized in the womb. Evolution is fine with quick and dirty solutions, as long as they work in the environment of that time.

In the ancestral environment this brain feminization did not often produce homosexuals, because if it did it would have been selected out. With the hormone profiles that existed in the ancestral environment it quite reliably produced a more effeminate but still completely heterosexual provider male.

However, as civilization advanced, both male and female hormone profiles deteriorated because of environmental factors. For example, average testosterone levels dropped 17% between 1987 and 2004. They may have dropped a lot more than 17% between 1900 and 2013 (or whatever).

http://jcem.endojournals.org/content/92/1/196.abstract

In this new environment, old genes had new effects. Men became less masculine overall. The guys whose genes were coded for a Ghengis Khan strategy still came out relatively masculine, but the guys whose genes were coded for more feminized brains were at risk.

The effect that used to produce a slightly feminized brain following a provider strategy was no longer completely reliable in the era of degraded hormone profiles. It occasionally went too far and produced males with excessively feminized brains that had female-like sexual attraction mechanisms.

This flaw is currently being selected out of the population, but it has a long way to go because hormone profiles keep getting worse and worse, making new sets of formerly beneficial genes vulnerable to the problem. That's why young men are much more likely to be homosexual than older men.

Seems likely. Do I win something?

Anonymous said...

Skittleman

"As a quick and dirty solution to produce the second kind of males, their brains were somewhat feminized in the womb."

The trouble with game is all the nonsense around the word "beta."

Provider males evolved in environments where hunting was necessary to feed the children. There's no reason for those behaviors to evolve otherwise.

What game calls "alpha" behavior is male behavior from environments where the males were literally useless. It's because they were useless they evolved peacocking behaviors.

In the modern environment provider males have to a large extent lost the niche they had for thousands of years but there's nothing feminized about them.

Skittles Man said...

Providing for a woman and caring for her children is less masculine than crushing your enemies, seeing them driven before you and hearing the lamentations of the women (before you "embrace" them).

Recall that warfare used to be far more common in day to day life than it is in today's WEIRD societies. Hunter-gatherer life has been described as "constant warfare" and anthropologists have noticed that in at least some societies the violent tribesmen father the most children.

Our hunter gatherer ancestors were probably quite masculine and aggressive compared to us. It must have been quite the transition when society became more complex and elites started to be able to *EFFECTIVELY* prohibit unsanctioned violence. Previously adaptive genes for ultraviolence became maladaptive while previously maladaptive genes that produced less violent, more effeminate males became much, much more successful, leading to a dramatic increase in frequency in those genes.

Keep in mind, those guys still had far better hormone profiles than we do, on average, so they wouldn't seem effeminate to modern day people. Things only became problematic much later when environmental factors caused massive degradation of most people's hormone profiles.

http://www.gallup.com/poll/158066/special-report-adults-identify-lgbt.aspx

Per Gallup, only 1.9% of people age 65 and up are homosexual, while 6.4% of people ages 18-29 are homosexual (4.6% of men ages 18-29). Recall the study about the drop in testosterone levels. Expect the number of gay people to increase in the next generation as as average hormone profiles degrade further.

Skittles Man said...

Just so I'm not misunderstood, I'm not trying to claim that current adult testosterone levels are related to sexual orientation.

I suspect that the effect occurs in the womb. I'm merely using that study as an example of the well documented degradation of average hormone profiles.

Anonymous said...

"Providing for a woman and caring for her children is less masculine than crushing your enemies, seeing them driven before you and hearing the lamentations of the women (before you "embrace" them)."

It depends on the environment.

If you're living in a rainforest where the women can gather enough food to feed their children themselves then killing that man and taking his wife is viable because you're not the one feeding the resulting children.

If you're a steppe pastoralist then killing that man and taking his wife is viable because you're also taking his herd which can be used to feed two sets of children.

If you're an eskimo then killing that man and taking his wife is entirely pointless as you can only hunt enough to feed one family.

Seems to me, pre-agriculture, most people outside the tropics will have been living in the equivalent of the eskimo environment where one man can only feed one set of children.

Anonymous said...

Ron Unz

It seems to me the bug theory has to tick certain boxes based on the premises accepted.

1) If most male homosexuals are that way from an early age then that limits the possible forms of transmission.

2) It has to effect the mechanism of sexual attraction.

3) It has to have a way of not being successfully selected against.

"If the germ somehow strongly benefitted from inducing gayness in its hosts, the theory would make sense, but I haven't seen anyone provide a logical model for this."

"The other possibility is that the orientation is an unintended side-effect of the germ's activity. But if the side-effect could be eliminated, there would be massive selective pressure on the host/germ system to do so, since the change would be very important to the host but totally unimportant to the germ. Therefore, the only reasonable model would be one in which the side-effect is inextricably linked to the germ's functioning."

I'm not sure if this idea is entirely plausible but

If the original bug evolved in a promiscuous environment as a promiscuity increasing STD that worked by manipulating the visual part of the attraction mechanism e.g. making a person equally visually attracted to flat hips as to a 0.7 waist-hip ratio, then in that environment it has a good way to spread itself.

If as a side-effect the sons of mothers with the bug had a chance of turning out with some maladjustment to their visual attraction mechanism - including exclusive homosexuality - then the people in that environment might develop an immunity to that side-effect.

If the bug then travels *outside* the original environment the people outside might not have the same immunity.

A second possibility might be the the bug doesn't cause homosexuality in the first environment but some difference between the old and new environments makes the bug mutate and it's the mutated version that can cause infected mothers to have homosexual sons (and possibly other maladjustments to visual attraction like visual ttraction to pre-pubescent children or post-menopausal women).

In the first case the second population would just not have developed an immunity *yet* because of limited exposure e.g. if it was a tropical west african virus then northern europeans would have had some exposure through sailors and merchants from the 16th century or so but only large scale exposure since mass immigration.

If so this might imply a test i.e. that populations with the most exposure e.g. American Southerners and White South Africans ought to have lower rates of homosexuality?

In the second case where the premise is the bug mutated then the original population wouldn't have the immunity and so you might expect higher rates of homosexuality among members of the original population who had moved to the new enviroment than those who had stayed behind i.e. if it was a tropical west african virus and the original didn't cause homosexuality but a version that mutated in northern europe *did* then you might expect west africans who moved to northern europe to have higher rates of homosexuality than those who stayed in west africa.

There may be a fatal flaw in there somewhere but it seems to me dual environments could possibly square the circle.

Anonymous said...

addendum
Obviously the above doesn't cover sheep so there's something missing somewhere.

Anonymous said...

Skittles - That's a slightly odd argument.

What you seem to be saying is that declining sex hormone levels are responsible, but it's following a provider strategy that left humans on the knife edge of being vulnerable. But the latter proposition seems basically unnecessary - humans could've just been "on the knife" because why would nature masculinize a brain more than it is necessary to anyway, given the environment of evolutionary adaptedness?

One thing here is that the groups we would expect to be more providerish (e.g. Whites and Asians) have a lower percentage of male homosexuals (in the GSS, the Gallup Survey and the ADD Health Youth specific survey) than West Africans or Latin Americans.

Anonymous said...

Over on Greg Cochran's blog it was pointed out that there have been individuals who suffered damage to the brain (after and accident, say) who became homosexual afterwards. While only a small number of individuals, it suggests that the target is a small part of the brain that when damaged causes males to be attracted to other males.

There was also an article about a man with a brain tumor who became highly sex seeking and could not control himself.

Anonymous said...

"Over on Greg Cochran's blog it was pointed out that there have been individuals who suffered damage to the brain (after and accident, say) who became homosexual afterwards....There was also an article about a man with a brain tumor who became highly sex seeking and could not control himself."

It does seem to me an obvious place to start looking for the cause - bug or otherwise - would be the *mechanism* of sexual attraction.

There must be a piece of the brain that controls whether men get turned on by pictures of men or of women?

Michael Hester said...

I don't think that polls on homosexuality are a good indicator of increasing homosexuality. These polls rely entirely on self reporting of homosexuality. Given the change in cultural attitudes, older people are far more likely to either outright lie about their sexuality or even refuse to admit it to themselves. Therefore it is not surprising that a much higher number of young people admit to being gay than old people.

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