The recent article in the Quarterly Review of Biology has some good points. It does not argue that homosexuality is adaptive, which would be silly. It does not argue for Lamarckian epigenetics, which would also be silly. I should also point out that they’ve given up on sexually antagonistic selection, since the GWAS surveys pretty much rule it out.
They note that variations in hormonal levels before birth don’t seem to cause much trouble, and conclude that humans adjust to those levels – homeostasis, basically. They suggest that this is implemented by epigenetic changes, and that sometimes those epigenetic changes are not properly reset in the next generation. Leaky epigenetics.
Of course, this hardly ever results in funny-looking genitalia – you’d think it would, but then natural selection has made that kind of error rare. Of course, it should have made epigenetic leakage that cause low-fitness behaviors like homosexuality equally rare. Which is the problem with this hypothesis: it rests on the assumption that natural selection in humans has been on a mysterious, all-expenses-paid vacation when it comes to mating. They suggest that maybe sexual behavior have changed since the human-chimp split and therefore there just hasn’t been enough time to thoroughly canalize sexual development in humans.
I guarantee that speech is newer than that. What fraction of people are unable to talk? Gee, being mute is far less frequent than homosexuality, even though speech sure seems more complicated. Why is speechlessness so rare? Speech is damn useful, and natural selection has made failure rare. But it’s not more useful than reproduction its own self.
Rice suggested sexually antagonistic genes, earlier. What fraction of known, common, fitness-reducing syndromes are known to be caused by that? Gee, none of them. What fraction are known to caused by leaky epigenetics? None.
What fraction are known to be caused by infectious organisms? Practically all of them. So you know it can’t be that, right? Life is really a vast murder mystery – it’s always the one you least suspect.
The Emmdees say that when you hear hoofbeats, think horses, not zebras. When explaining homosexuality, people think of pterodactyls and unicorns.
West Hunter 
But it’s not *that* maladaptive historically. Homosexuals still often have children, even today. Gay men often better at gaining access to females as well.
Suppression of homosexuality probably forced homosexuals to have children. Women were married off, men had kids to keep up appearances.
I guess a big test for genetic homosexuality would be whether the rates of it are actually lower in tolerant societies.
Some people just don’t know how to think quantitatively.
You know, I’d ask you to open a population genetics textbook, but I don’t think you could get past the introduction.
Sorry for the rudeness. I am mentally ill, and I harbor many viruses.
Well, like Greg said, the selective pressure against homosexuality is the sum total of all known Mendelian diseases. Even if it only resulted in a loss of fitness of 10%, on average, there’s no chance that it could drift to three percent of the population. None whatsoever.
You would think that finding women sexually attractive would have *something* to do with your ability to bear children. As for homophobia raising the fitness of gay men, people find all sorts of ways to shirk marital responsibilities when the occasion suits them. Gandhi found it quite easy, back when the British Empire made sodomy a criminal offense.
Again, it only has to diminish your fitness on average. There’s no point in sharing personal anecdotes about a gay friend who had five children. But the vast majority of people don’t think in terms of numbers. This is a problem.
I think the best clue must come from non-human species, where the arguments for tribal adaptiveness necessarily break down.
According to geneticist Simon Levay in 1996, “Although homosexual behavior is very common in the animal world, it seems to be very uncommon that individual animals have a long-lasting predisposition to engage in such behavior to the exclusion of heterosexual activities. Thus, a homosexual orientation, if one can speak of such thing in animals, seems to be a rarity.” There’s upwards of 1500 species where homosexuality is well-observed enough to be common, and in many cases, it’s far more common than among humans.
The extreme cases are the most interesting, imho. One species in which exclusive homosexual orientation occurs very frequently is that of domesticated sheep (Ovis aries); they’re very extensively treated upon in “Animal Homosexuality: A Biosocial Perspective” By Aldo Poiani.
“About 10% of rams (males) refuse to mate with ewes (females) but do readily mate with other rams.” Now, part of this might be imperfect observation from the study in question, but this is almost certainly an example of superhuman levels of gayness, and not unique. Can all of these be species-adapted toxoplasmosis emulators, infecting all of these species with the gay? Possible. But the pressure to counter-evolve a resistance to such an infection would be titanic.
I think the more parsimonious conclusion is that plasmosis-style infections may exist which exacerbate a common developmental risk; but this must be a risk which exists independently of infection, and which is too entrenched to eliminate via selection. An inherent and systemic risk like cancer, trisomy, and the scores of other developmental disorders which will never be selected out of existence.
Gandhi had four children. You seem to be implying that his spiritually-based celibacy was just a cover for homosexual preferences, and I think it is manifestly untrue to suggest that all spiritually-based celibacy is just a cover for homosexual preferences. (Though there is no doubt that in some cases it is.)
A couple of obvious problems with what you said. There are probably more. There’s no evidence that Gandhi was homosexual, which is what you implied. More significantly, he had four children. So your example actually illustrates the opposite of what you were intending.
You’re imposing a Christian, monogamous template of an agricultural society onto human hunter-gatherer prehistory, which was neither Christian nor monogamous. It’s unlikely that any man in your tribe would find fault with you for not competing with him over sexual access with the scarce number of reproductive age females available. And even within agricultural Christian society there were plenty of ways for gay men to escape marriage, such as the priesthood, the monastery, or the army and navy; about five to ten percent of men in medieval Europe did exactly that and never married.
NB: As misdreavus wrote, if homosexuality reduced the expected number of surviving descendants by only a mere ten percent (and it’s certainly much more than that) it’s unlikely it would be anywhere as common as it is.
“But it’s not *that* maladaptive historically.”
It is to a physicist that placed his bets a bit early and is now hissing like a cornered animal.
” It is to a physicist that placed his bets a bit early and is now hissing like a cornered animal.”
That a guy who named himself “Fruitcake” said this shouldn’t be surprising, but it is.
1) Why does it seem to you improbable or impossible that a physicist might know a great deal about something outside the typical parameters of his physics degree? Why would you conclude that a Ph.D. in another field, say anthropology or biology would make him more knowledgeable? Where is it written that such a degree would make his hypothesis more swallow-able for you? Do you believe it impossible in this age of modernity with its access to information from anywhere and anyone that a person so inclined could self-educate?
2) I don’t understand your conclusion that there’s any “hissing” from “a cornered animal.” Maybe you can enlighten us about any knowledge you have that his arguments are wrong?
Or are you so personally invested in something or other that you can’t see that you are the one who seems to be hissing…and maybe feel “cornered.” Why you feel that way, I can only guess.
New to the discussion and the topic, I see.
You may well be correct – it’s the best theory I have come across and it should become the main working hypothesis.
As an alternative (the ‘steady state’ theory to rival the ‘big bang’?), the second commonest cause of common, fitness-reducing syndromes is probably ‘toxic’ phenomena – poisoning, or endemic deficiency states (eg nutritional), especially things that damage the the brain.
Such damage may be relatively specific and focal (e.g. the way that alcohol picks out mamillary bodies in Korsakoff’s syndrome http://en.wikipedia.org/wiki/Korsakoff's_syndrome ).
(Rather like ideas for the cause of AIDS – the dominant HIV infective hypothesis, and Duesberg’s idea that the cause was toxic, perhaps a ‘recreational’ drug.)
I’d agree infection is more plausible. Is there evidence of epidemic-like spread? There is a normal way in which infections increase exponentially, plateuau, then decline (as they kill off the susceptible population) – and sometimes patterns of first increasing, then declining virulence with acute fatal infections evolving into chronic ones – eg syphilis. (Matt Ridley – Prediction: the future of disease).
Also see the role homophobia plays in all this, which I think supports the infection model:
A Gay Germ? Is Homophobia a Clue? « JayMan’s Blog
There are those who support the infection model for the rise and fall of heart attack rates from ca 1920 to present (that’s after correcting for the rise and fall of smoking). It would help if they could identify the infective agents, mind.
@dearieme – I support this – on the whole; since James Le Fanu pitched the idea to me 20 years ago. It would help if people actually *looked for* infectious agents, mind – but there is already quite a lot of evidence to support an infectious cause which is completely ignored. This is one of the areas where evidence does not really matter. After all, we know that dietary fat/ cholesterol definitely was NOT the cause of the coronary heart disease epidemic, but it doesn’t stop people believing it.
Oh quite.
1) In an r-type environment where the idea is to have as much sex with as many different women as possible without regard to who they are as you’re not going to stick around afterwards anyway would it make sense to have a lower threshold of sexual attaction i.e. men can be equally attracted to a 2/10 female as to an 8/10 female. If so wouldn’t that involve genes or a bug that tinkered with whatever filters sexual attraction? If so couldn’t that make women still preferred but men (or goats) less unattractive if there aren’t any women?
What might happen to a bug/gene like this if it moved into an environment of relatively strictly enforced anti-promiscuous monogamy – or one where female promiscuity was strictly controlled but male wasn’t? It could no longer spread heterosexually as easily as before and would have to adapt – in possibly more than one way e.g. homosexuality, reducing mate-guarding etc.
2) Can’t the logical possibilities be reverse-engineered from the twin study results i.e. if you had a list of postulated single causes then assume each was true in turn and think what the results of the twin studies *ought* to be if that cause was the correct single cause? Once you had those numbers and if none of them were a very close fit to the twin study results you could also play around with what combinations of two causes in what proportions would add up to the twin study results – seeing as you have *some* fixed points e.g. if womb hormones was a cause then it must be limited to near that percentage of twins who both turned out gay.
Interesting hypothesis about the “attracted-to-just-anything” bug. Wouldn’t it imply, then, that a good proportion of current homosexuals would be fine congregating with goats/sheep in the absence of other men? Somehow, I’m finding this questionable.
Well what i wonder is what would happen if an “attracted to anything” bug which worked well in a promiscuous environment was then transplanted to an environment where female promiscuity was almost completely curtailed. How could it adapt? One way – if the basic mechanism of the original bug involved interfering with the attractiveness filter – might be exclusive attraction to males?
Imagine an “attracted to everything bug” with multiple variations which included a lower threshold for attraction to men that then hits a new environment where attraction to any female is no longer helpful because the women are all culturally blocked off. Then the variations of the bug with the lowest threshold for attraction to men may be the ones that survive?
But by taking women out of equation, aren’t you removing a potentially significant mode of transmission (i.e. sexual)? Perhaps, the bug gets randomly transmitted in-utero via a mother breathing in the air emitted by homosexual males?
Theorizing a randy gene … like it!
Besides, to me, it would only explain the attraction of the mounter, but not the “mountee.”
Fair point. I’ve read in these kind of threads (but don’t know if true or not) that anal sex is or at least used to be rare among homosexuals so that may be moot (or not).
I think it’s pretty clear that most gays were gay before ever having gay sex, so that’s not a likely mode of transmission.
Homosexuality isn’t the only paraphilia around. ~549 other paraphilias have been diagnosed in humans. Paraphilias can be optional, preferred or exclusive. Preferred paraphilas are favored over normal sex. Exclusive paraphilias leave the sufferer unable to become aroused, except by the object of the paraphilia. Preferred and exclusive paraphlias are fitness reducing, as the fittest male is the one who is willing and able to have sex with a female at the drop of a hat, not the one who needs to convince the female to wear a certain outfit before he can become aroused.
Are paraphilias commonly found in hunter gatherers? I’m guessing not, but if anyone has data, feel free to share. Is it likely that a pathogen would somehow evolve to cause 550 different paraphilias?
Scientists have shown that it is quite possible to “hack” the partner preference of mammals in the lab, through classical conditioning, even inducing homosexual partner preference. The process of growing up in a society is essentially a form of conditioning.
For the vast majority of our history, humans evolved in an ancestral environment that was incredibly different from the one we live in today. The ancestral environment provided a certain type of stimuli (conditioning) to the people who were raised in it.
The people who would have been selected out in the ancestral environment were the ones who developed preferred/exclusive homosexuality/paraphilias, when they received the conditioning provided by the ancestral environment. Those people probably were successfully selected out, hence the lack of homosexuality and serious paraphilias in the few people still living in something close to the ancestral environments.
But the historical and modern environments are extremely different from the ancestral environment. The way that people are conditioned is extremely different from the way that they were conditioned in the ancestral environment. Some people who were perfectly well adapted for the ancestral environment are vulnerable to developing preferred/exclusive homosexuality/paraphilias when the conditioning from the ancestral environment is removed and the conditioning from the historical/modern environment is substituted. Those people are currently being selected out, but the process is not complete. Especially since the modern environment provides a set of stimuli (conditioning) that is very different from the stimuli (conditioning) that occurred in even the recent historical environment.
We’ve only had a few decades to select out the people who are vulnerable to developing preferred/exclusive homosexuality/paraphilias when they receive the stimuli (conditioning) that is provided by the modern environment. So currently a relatively high number of people are developing preferred/exclusive homosexuality/paraphilias and being selected out.
“Scientists have shown that it is quite possible to “hack” the partner preference of mammals in the lab, through classical conditioning, even inducing homosexual partner preference.”
You know, you have an inordinate fondness for making nonsensical posts. What the hell are you talking about?
Sixty years running, and somehow nobody has ever found a cure for homosexuality. Electroshock therapy won’t do it. Aversion therapy won’t do it. Hell, even a frontal lobe lobotomy won’t do it. If sexual orientation were as easy to re-orient as you presume, somebody would have discovered how to cure homosexuality by now through therapy. Nope.
As for paraphilias, we know precious little about them as it is, and the one that is the most heavily researched turns out to be exclusive only in a tiny minority of cases. None of these are as prevalent or as fitness-reducing as homosexuality.
Then again, I am, in all probability, arguing with a troll.
misdreavus said:
“You know, you have an inordinate fondness for making nonsensical posts. What the hell are you talking about?”
I said:
Here you go, full paper available at the link:
http://www.socioaffectiveneuroscipsychol.net/index.php/snp/article/view/17340
They took sexually naive male rats and gave them a shot of dopamine while they were hanging out with another male rat. They were able to generate homosexual partner preference towards that male rat.
It would not be ethical to try this experiment on sexually naive humans.
misdreavus said:
“Sixty years running, and somehow nobody has ever found a cure for homosexuality. Electroshock therapy won’t do it. Aversion therapy won’t do it. Hell, even a frontal lobe lobotomy won’t do it. If sexual orientation were as easy to re-orient as you presume, somebody would have discovered how to cure homosexuality by now through therapy. Nope.”
I said:
First of all, experiments of this sort are rarely done of sexually naive humans, like they were in the rat study. Preferences may be more difficult to change once they are set. Secondly, one would assume that it would be very difficult to reverse conditioning that had occurred over decades, especially while operating within the ethical limits of experiments on humans.
misdreavus said:
“As for paraphilias, we know precious little about them as it is, and the one that is the most heavily researched turns out to be exclusive only in a tiny minority of cases. None of these are as prevalent or as fitness-reducing as homosexuality.”
The effect of all 549 paraphilias combined is probably pretty significant though. Maybe not as significant as homosexuality, but worth factoring into your analysis.
Maybe someone has already linked this but–anyway–Heath did try this is the 1970s. A homosexual male had deep brain stimulation of the VgT while a prostitute (female) had sex with him. The end result was that a gay man had females added to his desires
Click to access Heath-Pleasure-and-brain-activity-in-man.pdf
Juan — I was going to try to write a long post of my own, but you’ve made many of my points, so I’m going to piggyback off of you.
The most important point is that it isn’t just homosexuality that needs to be explained, but paraphilias in general. I don’t see how you can do this with a model based on a single infectious agent. (Multiple agents seem implausible — a specific bug for S&M is just as bad as a specific gene for S&M).
My own idea is that since higher primates have lost the ancestral mammalian mechanism for determining sexual preferences, which is based on the sense of smell, they’ve had to replace it with something less reliable, involving learning. This is clearly something that can go wrong not just in one way, but in hundreds of ways.
What I think my theory would predict is that in “earthy” societies, where there is less effort to shield children from adult sexuality, there would also be less deviant sexuality of all sorts. Children would understand at an early age how things worked, and so would be less likely to get fixated on oddball ideas of their own. In more straitlaced societies the majority of children would still get end up figuring things out, but a much higher proportion would get confused and go off on tangents. It seems to me that this prediction fits the facts fairly well, and that the theory explains more than the infectious agent theory.
“Children would understand at an early age how things worked, and so would be less likely to get fixated on oddball ideas of their own.”
Evidently you are unaware of just how many children live in the same large room with their parents or the parent’s sexual partner. Go into a ghetto or into the hills and see how it works.
Then, find out if the percentage of man-on-man sex or the level of gender atypical kids is below that of affluent America.
Or can you figure it out w/out having to go to that trouble?
erica — Can you tell me what percentage of “ghetto” or “hill” children today grow up in a single room exposed to adult sexuality? I’d be interested in actual numbers, because I suspect it isn’t anywhere near as high as you are implying. Certainly it would be only the poorest of the poor, rather than everyone “below that of affluent America.” And even when families do live in a single room, they can still be straitlaced and prudish about sex, and do a pretty good job of keeping children in the dark about it. Do you think Ma and Pa ever talk freely with John-Boy about what goes on under the covers when they think he’s asleep? Or do they slap his mouth when he asks about it, and tell him never to bring that up again?
Farm children (as opposed to “hill” children, who might not live on farms) can of course learn a lot about sex by watching domestic animals, so it does seem my theory would suggest that they ought to have lower levels of deviant sexuality, and that would be a test. I’m not sure where to find those numbers though. Ghetto children, OTOH, risk exposure to all sorts of deviant behavior, sexual and otherwise, so I’m not sure what can be learned from them.
Also, what is your explanation for paraphilias? Is it something distinct from your explanation for homosexuality?
“It seems to me that this prediction fits the facts fairly well, and that the theory explains more than the infectious agent theory.”
Well, that might be because you don’t know any facts at all.
Homosexuality is _highly_ discordant among identical twins, whether they are raised in the same home, or in two different homes. Homosexuality is also curiously absent among Rwala bedouins, who are just about as socially conservative as they come.
I could go on and on about how stupid it is that sexual orientation can be derailed by an environmental stimulus as facile as insufficient exposure to sex during childhood. You would think evolution couldn’t be derailed by something so stupid.
@jb:
“Also, what is your explanation for paraphilias? Is it something distinct from your explanation for homosexuality?”
I have one:
IQ and Kink? « JayMan’s Blog
misdreavus — if my theory is right I would expect a discordance between identical twins! They might be genetically identical, but their life experiences are not, and it would hardly be remarkable if one of them saw something the other did not, or had other unique and unshared experiences that set them off on different paths.
And I absolutely would think that evolution can be derailed by the power of learning and ideas — this is something we see all around us every day! Really, is the idea that human sexuality might depend in some degree on learned experience — rather than being completely hard wired — that>/i> implausible to you?
I’m not saying there is no biological component. But if there is also a learned component, then the weaker the signal the child receives from his surroundings, the more likely that he will be influenced and led astray by “noise” — which by its nature which will vary from one circumstance to another, and will be very difficult for researchers to isolate and analyze.
Also, I have been under the impression that if one identical twin was gay, then the odds that the other was also gay was 50%. However a number of comments here have been implying a lower number. Can someone tell me what that lower number is, and how well it is established?
@jb:
“Also, I have been under the impression that if one identical twin was gay, then the odds that the other was also gay was 50%. However a number of comments here have been implying a lower number. Can someone tell me what that lower number is, and how well it is established?”
It’s considerably lower. The heritability estimate of homosexuality in males 0.22. This was established from a large analysis of several twin registry studies.
JayMan — Thanks for the link! The author’s talk of “idiosyncratic factors” fits nicely with what I have been trying to say (“noise”) — although it fits the infectious agent theory also.
Can you tell me how the paper has been received? Are the findings widely accepted? Controversial? Widely ignored? Given that twin studies are the only hard scientific evidence I know of that argues that people are “born that way,” and that even at 50% the argument wasn’t all the strong, you would think people would be paying close attention to any new numbers.
No, strike that…, you wouldn’t think that at all, would you?
@jb:
“No, strike that…, you wouldn’t think that at all, would you?”
Nah…. 😉
Eh no. Humans dont have the same learning concept, and anyway, paraphilia sits on top of your underlying orientation. BTW the Dutch are very openly sexual in front of their children and there is a lot of homosexuality in the Netherlands. The Nordic countries have surprisingly little homosexuality, despite being just as accepting as the Dutch. That to me implies there is something different in Nordic haplogroups, or, a pathogen not found in the Scandinavian populations (or to which their genetics are resistant to).
“Preferred and exclusive paraphlias are fitness reducing, as the fittest male is the one who is willing and able to have sex with a female at the drop of a hat, not the one who needs to convince the female to wear a certain outfit before he can become aroused.”
I am not entirely sure of this. There is a risk to male promiscuity, at least in established cultures. The risk is that the male could be trapped with a woman who is either less fit or unfaithful. Finding a woman who is wiling to cooperate with (or at least tolerate) a paraphilia might be a way of ascertaining her suitability as a mate.
Men have often lamented the irrationality of women. A likely explanation for the irrationality is that a man who is willing to tolerate and even cooperate with the irrationality of his intended mate is perhaps more likely to be cooperative and supportive in other ways once they are married. To a lesser extent, this would apply even when it was the other way around, when it was the man who was particular.
For practical reasons we should stop debating homosexuality as a human issue, however interesting, and focus on animals such as sheep. Sheep is not affected by social, psychological, educational, etc. factors and they have a larger proportion of and more clearcut homosexual individuals than humans. I’d say that on the basis of prevalence of homosexuality in sheep we can dismiss all speculations that it is caused by specifically human conditions such as weak father figures or whatever psychological factors. It has to be something 100% biological.
BTW, we are talking of a serious economical problem for sheep husbandry. Anyone finding the cause and a remedy will make much money from in the sheep industry.
Very reasonable, except (I speculate) for the last bit. I can’t easily imagine that the industry suffers from a semen shortage due to the 8-10% of gay rams.
But there is a similar issue which I happen to know does have a fair deal of economic impact, and is very similar to Cochrans ideas on homosexuality being due to triggered developmental disorders: socalled “freemartins”, female sheep and cows which are exclusively homosexual in behavior, and often either infertile, or in need of artificial insemination. All due to hormonal disturbance during gestation. They fit Cochrans general hypothesis quite well, and are very closely studied, since they do indeed have a significant economic impact.
A freemartin or free-martin (sometimes martin heifer) is an infertile female mammal which has masculinized behavior and non-functioning ovaries.[1] Genetically the animal is chimeric: karyotyping of a sample of cells shows XX/XY chromosomes. [The animal originates as a female (XX), but acquires the male (XY) component in utero by exchange of some cellular material from a male twin, via vascular connections between placentas.] Externally, the animal appears female, but various aspects of female reproductive development are altered due to acquisition of anti-Müllerian hormone from the male twin.[2] Freemartinism is the normal outcome of mixed-sex twins in all cattle species that have been studied, and it also occurs occasionally in other mammals including sheep, goats and pigs.
http://en.wikipedia.org/wiki/Freemartin
Vanishing twin hypothesis — the idea that homosexuality may (in large part) be due to chimerism, or the absorption of a twin sibling while in the womb. The leftover opposite-sex cells from the vanished twin stick around, and if placed right, affect sexual preferences.
It seems like a viable hypothesis. Over 1 in 8 pregnancies seem to involve vanishing twins– and this number will probably grow as scanning techniques improve. Female neurons/brain hormones/etc in male brains could certainly affect sexual preferences.
Here’s the question, though: this seems like it’d be very easy to test. Why don’t we have a body of evidence supporting it? What would count as supporting vs contradicting evidence here, anyway?
Vanishing twins are estimated to be involved in 1 in 8 multifetus pregnancies, rather than 1 in 8 pregnancies. That being said… it’s impossible to estimate the rate of chimerism in “normal” births, they just would not be noticed. Since male cells outgrow female cells in this condition, the majority of male/female chimeras should be phenotypically male.
Freemartinism, resulting in homosexuality, is categorically a Developmental Disorder, and that’s the primary reason I mentioned it, it serves as an analogy for other DD’s also resulting in homosexuality. But while I doubt that most human homosexuals are chimeric, it would be incredibly interesting to discover human chimeras with the gay phenotype…
Above comment is me.
Prize-winning rams are expensive and buying one that fails to perform frustrates the owner as well the sheep. The economic loss can be significant. There is a demand for a solution. On the other hand, I wonder if human society is interested in a remedy. It is hard enough to get a girl as it is, so why increase the competition? It may be preferible to keep looking at those zebras.
@j: if it’s a common problem to buy a prize-winning stud without knowing anything about its ability to impregnate (confounded by homosexuality, but also infertility and the like), then farmers are less smart than I thought.
There is a fair argument that homosexuality reduces the pool of rams from which studs might be drawn. This doesn’t appear valued enough to attract the degree of research and investment that fx. Freemartinism does – perhaps in part be due to the sheep industry not being particularly focused on studs, as is the case with the cattle industry. In some countries, the majority of cattle are impregnated by superstud bull semen. A big part of this difference is likely historic – artificial insemination is much more difficult with sheep than with cattle, until recently – and a part is that value-per-animal is lower, meriting less investment.
A sheep doesn’t need to be sexually aroused to have semen collected from it. This is a solved problem.
PS. I’d not discard looking at ptherodactyls or at unicorns. The first may have been extinguished and the second never evolved as consequence of an epidemy of Toxoplasma gcochrani ver. arsenokoitai.
“erica — Can you tell me what percentage of “ghetto” or “hill” children today grow up in a single room exposed to adult sexuality? I’d be interested in actual numbers, because I suspect it isn’t anywhere near as high as you are implying.”
The point–I CAN tell you from having spent many years working with kids raised in this environment and having made many home visits that adult intimate behavior around kids was not confined to a room separated from their kids. Further, I can tell you that life was lived in in abodes that contained one kitchen sink + small fridge, a “dining area” with a living area that wouldn’t accomodate a standard sized 7 ft. sofa and one bedroom. Do I know the percentages of such homes. No, and don’t need to in order to know that a high percentage of kids saw mommy making whoopie, heard mommy making whoopie. And hey, they told you so.
It might also surprise you to know, from talking to middle class teens, just how much they see and hear from mom and dad or mom and boyfriend(s) or dad and girlfriend(s). Reading journals and talking to them is pretty revealing. You know, everyone grows up thinking his or her family behavior is pretty much the norm until they get a wider lens.
Jayman
“I think it’s pretty clear that most gays were gay before ever having gay sex, so that’s not a likely mode of transmission.”
If that was true and a bug is the single cause then they’d all have to have been infected in childhood?
“If that was true and a bug is the single cause then they’d all have to have been infected in childhood?”
I’d say mostly, considering that, assuming that a pathogen is the case, it apparently leads not just to sexual orientation being altered, but morphological changes such as the “gay face”.
I wasn’t neccessarily disagreeing with you. It just struck me as a logical follow-on and an interesting link to your post on homophobia being so child-centric.
I know you weren’t disagreeing with me, I was just expanding on the idea. 🙂
It’d be interesting to narrow down the time frame of infection in cases where homosexuality results. Presumably, it’s fairly early, likely before puberty, perhaps well before.
are the faces of discordant (for homosexuality) identical male twins different?
@anneallen3:
“are the faces of discordant (for homosexuality) identical male twins different?”
Very good question! The answer is I don’t know, but this would seem to be a highly significant point.
Writing off adaptive explanations as “silly” is a bit harsh. I’m not convinced that they’re overly likely, but there have been coherent hypotheses put forth for same-sex behaviour, especially in non-human animals (http://www.thestranger.com/images/blogimages/2009/09/14/1252958575-evolution_of_homosexuality.pdf).
Underly harsh. I was holding back.
Sorry, are you claiming that adaptive explanations are logically incoherent or that they’re unsupported/disproven? If the former, then I disagree; if the latter, then I’m willing to believe that, since this isn’t an area I’ve read deeply in.
(PS: loved the book! I’m planning to reference it in an outreach talk I’m giving in the next purple of months).
” purple of months” – synaesthesia?
The only species in that article that has a pattern like humans are the sheep. Do I think that either case has the slightest chance of being an adaptation? No. Let me be blunt about this: those ‘dud’ sheep will ignore a ewe in heat when she’s tied to the fence in front of them. Their minds are not right.
If things that make it harder to reproduce can’t possibly be part of the gene pool…
What about narrow hips? In the old days tons of women had trouble giving birth, lots dying in childbirth. Today many would die without cesarian.
It’s known that wider hips make it easier to give birth, yet lots of women have narrow hips, which aren’t adaptive for anything at all. Narrow hips impede reproduction way more than homosexuality, yet we still have millions of them. What’s selection doing here?
Narrow hips are adaptive for most leg-based athletic endeavors, which meant hunting, fighting, etc historically. Sexual dimorphism is hard to evolve. We’re still a work in progress on that point, or would be if not for modern medicine.
Forgot to mention that women select for narrow hips in men.
Surely the selection toward better men who run faster is not greater than for women able to survive childbirth. I’m no specialist I can’t do the math, but surely someone can.
Sexual dimorphism also sounds like a great deal. Why isn’t it stronger?
@spandrell well, yes, that’s why sexual dimorphism is hard to evolve. It selects for narrow-hipped men and wide-hipped women, which results in a mess in the short term
You know, Chinese women have those cute little asses … narrower than those of Western women. However, I know one small Chinese woman who gave birth to 8lb and 9lb babies pretty naturally.
We need data on ass-size/birthing ability.
You could help us collect some I’m sure.
My smaller than dress size zero/ring size three Chinese wife had no problems giving birth to a baby that size, with a head size in the 99+ percentile. I was pretty surprised
Narrow hips impede reproduction way more than homosexuality, yet we still have millions of them.
It may be nutritional. Like crowded, crooked teeth, the narrow hips of modern western women may be products of industrialized food.
Thanks for taking the time to link this.
The strength of the pathogen theory is that the pathogen can continue an arms race against the host, whereas other factors could not.
If it were simply “This pathogen exists, but does not really change” then evolutionary theory would dictate there would be pretty rapid selection for an immune response and it would be no better than any other theory.
But the pathogen can mutate and evolve.
But OTOH if “gay bugs” were difficult to evolve a “categorical” response to, wouldn’t they be very frequent outside humans? I.e. not “just sheep”.
Maybe it’s not the sheep’s fault? Apart from being physically shorter than cows.
I keep thinking of monagamy or even strictly controlled polygamy as a kind of guarantine so if sheep got it from humans then they couldn’t guarantine it.
(just a wild thought)
@ Greying : Don’t really quite understand your response… My query is, if it is a bug, why does it seem like it is only a bug for humans (and sheep) and not dogs, goats, cats etc.? And why do we not have an evolved response to it yet? This should hit fitness really hard, but humans haven’t evolved a response yet, while apparently the rest of the animal kingdom has (or why isn’t it there?).
Infectious diseases often infect a very limited number of species. Smallpox only infects humans. Measles only infects humans. Leprosy only infects humans and armadillos. Your question assumes that infectious diseases usually affect many species – but that’s not true.
The chimerism/vanishing twin and infectious disease hypotheses are not incompatible. Chimerism and homosexuality in both sheep and humans may be a side effect of a parasite. A parasite infecting the mother of offspring that will be Darwinianly handicapped by homosexuality. It need not have any other major Darwinian consequences for its hosts, positive or negative, since as Matt observed above, a pathogen can engage in an arms race with evolutionary adaptations by its hosts.
Nor are they incompatable with a genetic component: twins studies may be readily explained by genetic differences in resistance to the effects of chimerism in utero, whether or not a parasite is a necessary cause.
Domestic sheep and humans have something in common: our evolutionary environment has radically changed in a period so recent it can have been not so highly probable, versus what we would normally expect in wild animals, for a full defense to have evolved (especially if the cause is a pathogen which can, as Matt observed above, engage in an arms race with evolutionary responses).
One of those changes has been a great increase in crowding: sheep into pens and folds, humans into factories, offices, schools, and mass transit. We have also had the very recent Columbian exchange of parasites, with much resultant loss of Darwinian fitness in infected populations.
Chimerism as a side effect does suggest that something involving development or cell division is involved in the transmission vector: perhaps infection is abetted by greater shedding of skin, hair, or other dividing cells and a side effect is to cause more aggressive growth in other dividing cells, and thus in early stage fetuses, increasing the occurence of chimerism and thus homosexuality.
Another confounding factor for sheep (but not, AFAIK, humans) is that we have actually bred them for rapid cell division. In particular for rapid hair growth, but this could easily have a side effect of increaing the aggressiveness of other kinds of cell division, thus increasing vulnerability to chimerism. The selective pressure from breeding is quite strong here. I’m not sure it’s strong enough to explain by itself the high rate of chimeric homosexuality in domestic sheep, without the addition of an infectious agent that also increaases cell division in its hosts, but it would (besides the possible long odds of just having such a parasite appear among the species in the first place) explain why at least some breeds of domestic sheep have a far higher incidence of homosexuality than domestic animals bred for their non- or slowly-dividing cells (chicken, cattle, dogs, cats, etc.)
“Forgot to mention that women select for narrow hips in men.”
Which i think(?) implies selecting for men taller than them men due to the optical effect of perspective (and vice versa)
http://en.wikipedia.org/wiki/Perspective_(graphical)
Or just selecting directly for narrow hips, which, as I said, are useful for all sorts of essential activities, especially when you’re never going to be giving birth.
Also, you keep writing forms of the word “guarantine.” It’s not a word.
quarantine
Eli
“But by taking women out of equation, aren’t you removing a potentially significant mode of transmission (i.e. sexual)?”
Well if the bug originally caused promiscuity and then moved to an environment where female promiscuity was guarantined then it would restrict sexual transmission to male-male.
More generally i’m just thinking how different forms of transmission might provide clues and maybe it’s not sexually transmitted at all and therefore not connected to promiscuity at all.
Disappointed you weren’t a contributor to the edge.org’s annual question WHAT *SHOULD* WE BE WORRIED ABOUT?
On that note, I’d be interested in Cochran’s take on Geoffrey Miller’s response “Chinese Eugenics”. He writes:
“The BGI Cognitive Genomics Project is currently doing whole-genome sequencing of 1,000 very-high-IQ people around the world, hunting for sets of sets of IQ-predicting alleles. I know because I recently contributed my DNA to the project, not fully understanding the implications. These IQ gene-sets will be found eventually—but will probably be used mostly in China, for China. Potentially, the results would allow all Chinese couples to maximize the intelligence of their offspring by selecting among their own fertilized eggs for the one or two that include the highest likelihood of the highest intelligence. Given the Mendelian genetic lottery, the kids produced by any one couple typically differ by 5 to 15 IQ points. So this method of “preimplantation embryo selection” might allow IQ within every Chinese family to increase by 5 to 15 IQ points per generation. After a couple of generations, it would be game over for Western global competitiveness.”
I found it a little hyperbolic; do I have my head in the sand?
“I found it a little hyperbolic; do I have my head in the sand?”
I think there are likely to be some negative consequences of high IQ otherwise it would have happened already – although the negative consequences may not be as critical as in the past.
I think a smart fraction is only useful in a simple society with a lot of unskilled manual work which only requires a few shouters to function as the brain. I think a complex modern society requires *depth* in average IQ where the vast bulk of the population are 100+. If they just go for the smart fraction then i don’t think he’s right – well he is but for dysgenic reasons in the West not eugenic ones in the East – however if they go for a high average with low variance pattern then i think he’s right and they should make an all-Chinese version of Star Trek.
The best example of what i mean is military. If you take intelligent guys with initiative and then imagine how far down the ranks guys like that would extend for populations with varying average IQs then you can picture the kind of armies that would create. One army the intelligent guys might only extend down to the battalion commanders. Another they might extend down to the company commanders. In a third to the platoon commanders. In a fourth they might extend down not just to two junior NCOs per squad but with two spares as well. The latter cases would easily beat the cases above them.
“I think there are likely to be some negative consequences of high IQ otherwise it would have happened already – although the negative consequences may not be as critical as in the past.”
I think the desire to remove competition has been a significant factor in human evolution. All you have to do is say the word “Mensa” to see the hostility that can arise for high IQ. It is very easy to speculate that people would have taken direct action to remove intelligent competitors in the past. Unlike physical strength, intelligence does not always provide an immediate means for defense. Many intelligent people have found it necessary to conceal their intelligence.
@FredR: Not hyperbolic. See this talk by Steve Hsu (who is heavily involved with the project):
Genetics and Intelligence – YouTube
@Jayman Thanks for the link. I was referring more to Miller’s predicted scenario of how China would use this information, which I don’t think Steve Hsu really touches on either in his talk or on his blog, but maybe I missed it somewhere.
“I was referring more to Miller’s predicted scenario of how China would use this information, which I don’t think Steve Hsu really touches on either in his talk or on his blog, but maybe I missed it somewhere.”
Hsu does mention the “ethical” concerns involved, but it wouldn’t really be in his interest to go into the details on how the Chinese plan on using the information, owing to his own involvement in the research…
After reading Miller’s few paragraphs again I’ve changed my mind about what he’s saying; it looks like what he actually wants to do is use the bogeyman of a super-China to scare America into practicing eugenics.
Also, another random thought (apologies)
As well as thinking about the list of possible
– causes
– transmission methods for each possible
there’s also the list of possible purposes.
What if the primary purpose of the bug isn’t to make the host organism homosexual – thus requiring an explanation for how that makes evolutionary sense. What if it’s primary purpose is to make *other* (competitor) males homosexual?
In the studies of sheep – if there have been any – were there rams who mated with both males (particularly when young?) and females but the rams they mated with became exclusively homosexual?
That’s a more interesting hypothesis, actually. And yet it still doesn’t explain (to me) how it’s possible that male twins can be born with one being a homosexual while the other one not being one. Obviously, if the father were either straight or bi, the advantage of having a son who is a homosexual is doubtful. But, yet, according to your thinking not only is the bug being transmitted by sex with another man (say, via rape), but also via having sex with a woman.
I’m not saying it’s implausible. It’s just takes a lot to wrap the mind around.
Technically, male-on-male rape exists and is probably rampant (in prisons for sure), but obviously under-reported. It’s highly doubtful that most men become gay after being raped. But can they become carriers of homosexuality? And if yes, why not all of their offspring, including (again) twins among whom only one is a homosexual?
It just seems that there’s something missing here…
“And yet it still doesn’t explain (to me) how it’s possible that male twins can be born with one being a homosexual while the other one not being one”
Well as far as i can see the argument is over the 4% (or whatever it is) figure being too high. There doesn’t seem to be a problem with 1% lesbians as a result of random stuff happening in the womb etc. So is it 4%? or is it actually 1% plus 3%? i.e. is there one cause for the unsurprising 1% (ish) and another cause for the difficult to explain 3%?
If so the 22% both homosexual rate from twin studies might relate to the first cause with a separate cause for the rest.
“Technically, male-on-male rape exists and is probably rampant (in prisons for sure), but obviously under-reported.”
And children’s homes.
And why the hell would the mode of transmission have to be anal intercourse? Jesus. I certainly don’t recall anyone buggering me when I was a child (I am a gay male).
You’re not thinking very hard about this. The purpose of the pathogen is to reproduce itself, nothing more. Any side effects are incidental.
The purpose of P. acnes is not to make its host disfigured or ugly – but that’s what it ends up doing.
Fair point.
“And why the hell would the mode of transmission have to be anal intercourse?”
I’m not saying it has to be. I’m considering various possible modes of transmission one at a time to see if any of them provide additional lines of inquiry – plus i wonder how the sodomy taboo came about.
Something to do with the don’t-touch-feces taboo?
true. i suppose having laws against sodomy (regardless of gender) is no different to all the laws around the world prohibiting people from eating food with faeces on it.
Note that “sodomy” traditionally refers to oral as well as anal intercourse. “French kissing” was also taboo in the past. Anal intercourse is “more taboo” than oral intercourse, which is why the term “sodomy” is still somewhat reserved for it. So where you find anal intercourse, you’re also going to find oral intercourse and French kissing being practiced. Anal intercourse tends to facilitate transmission generally since blood vessels are so close to the surface of the skin in the anus and colon. And obviously oral ingestion will facilitate transmission, directly through the gums or stomach. These activities will often be practiced at the same time or during the same session, creating all sorts of vectors.
Why first and secondary sexual characteristics are not affected?
In The Two Sexes: Growing Up Apart, Coming Together MacCoby points out that boys prefer to congregate in all-male groups and seriously dislike the company of girls until they reach puberty.
At that point they have to switch.
This suggests that we could be looking at a virus that affects the life-history control in males.
Has there been any long-term studies that look at the behavior of male homosexuals from birth to puberty?
(At one time I listened to those who suggested that male homosexuality was simply a developmental mistake, but given the efficacy of selection, that now seems unlikely. Also, contra my question, the one homosexual male I know who I watched growing up showed, in hindsight, seriously questionable behavior from a young age.)
The role of prenatal testosterone is the leading.But in SDN nucleus and stria terminalis has no difference between homosexual and heterosexual males.In mouse testosterone change SDN from male to female cell number and volume.Why this process has not confirmed in human brain research by D.Swaab.The epigenetic theory can not explain why primary and secondary sexual characteristics are not affected despite low sensivity of androgen pathway according to this theory.This theory can not explain structural differences in the brain.
1.) How likely is it that it could be more than one neurotropic virus/bug that could affects whatever part of the brain it is that controls mate choice?
2.) A similar question: might the same bug have different brain effects on different people?
I thought of this because of hearing a conversation recently in which my wife and her best friend, whose first born son is gay, were recollecting their pregnancies of many years ago.
It seems that both our friend and her sister-in-law were pregnant with their first children at the same time and were only a couple of weeks or so apart in gestation. When her sister-in-law came down with mono, our friend picked her up every morning since her husband was off to work, brought her to her house where she stayed put on the couch, slept all day and was nurse by our friend.
I asked how far along they were, and to the best of her recollection, they would have both been in the early second trimester.
As I said, our friend went on to have a son who turned out to be gay, but she said she felt no ill effects from having taken care of her mono-infected relative. Her sister-in-law went on to have a son who, from all we know was straight, but who committed suicide at 17. It was one of those things where only in hindsight people realized there must have been some serious depression. This woman’s second child, a female, is bi-polar, the mental illness having gotten so hard to control as she aged that she had to give up her job.
So, I got to thinking about the Epstein-Barr virus and homosexuality, depression, bi-polar, etc.
The connection is a loose one, I admit, with our friend saying that she showed no ill effects from having nursed her relative for weeks with a contagious illness, but it did get me to thinking about the bug theory. One pregnant woman with mono bears a kid who was so depressed he killed himself years later, later has another child who’s bi-polar, and the woman who cared for her when she was sick with mono and they were both pregnant has a gay kid from that pregnancy.
The connection is not just loose, it’s pretty non-existent, in this case.
“One pregnant woman with mono bears a kid who was so depressed he killed himself years later, later has another child who’s bi-polar”
While sample size is pretty small in this anecdote, the about points to heredity. How emotionally stable are the mom and dad?
” and the woman who cared for her when she was sick with mono and they were both pregnant has a gay kid from that pregnancy.”
Probably not related.
Or then again, maybe it is. Could Epstein-Barr be “the” virus?
“Sexual dimorphism also sounds like a great deal. Why isn’t it stronger?”
Well, for one, it has to ensure that the same set of genes would result in systematically different (and predictable) differences in phenotype if you switched from XX to XY, or vice versa. There are a wide variety of genes that influence every quantitative trait from height, to intelligence, to muscularity, and beyond — yet how many of them do totally different things in the presence of a Y chromosome? Selection for traits that are adaptive in males, but maladaptive in females (and vice versa) would have to preserve genetic variants that contribute to sexual dimorphism while junking all the rest. Epistasis is a tricky business.
Some 9 million years of natural selection and running, a whopping 15% of all female spotted hyenas die while giving birth for the first time. (The spotted hyena is one of the rare species in the mammal clade where the female is stronger and more physically robust than the male, and also has higher levels of testosterone.)
Life really sucks when you have to pass an object the size of a paperweight through a distended pseudo-penis. But what can you do.
“Some 9 million years of natural selection and running, a whopping 15% of all female spotted hyenas die while giving birth for the first time.”
Sexual dimorphism in solitary hunters will be constrained by the needs of hunting so i imagine there’s high rates for tigers, panthers, cheetahs etc but whats the rate for lionesses?
“so i imagine there’s high rates for”
meaning higher rates of death in childbirth for female tigers, cheetahs etc.
higher rates of dimorphism in lions.
Good point…
Hey Cochran, instead of sarcastically trashing every theory out there and speculating wildly in post after post, why don’t you put your own theory to the test and publish the results? That would save a lot of time and really help your credibility.
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Spandrell
“Sexual dimorphism also sounds like a great deal. Why isn’t it stronger?”
Maybe it was.
Don’t you need sexual selection for sexual dimorphism and since farming haven’t mating choices been mostly arranged familial choices rather than individual choices? If so there would be almost no direct sexual selection on the males – except maybe among the landless whose reproductive chances were handicapped by being landless – as it would be based on things like land and family connection and dowries. There might be some sexual selection on the female side as attractiveness (aka how fertile looking they were) would still apply but even then if the marriage form (h/t hbdchick) was mostly familial and the females had to come from a specific subset of cousins then sexual selection could only take place if there were multiple acceptable cousins – so in societies with that marriage form but with high pop. density (and therefore a higher likelihood of multiple acceptable cousins) you might get some sexual selection on the female side but societies with low pop. density there might only ever be one acceptable female cousin and no sexual selection.
If so then the populations with the most sexual selection then would be pre-farming and you might expect to see more sexual dimorphism in those populations. Also any population where individual choice had an unusually high significance relative to arranged familial marriages would have the possibility of more sexual selection but i think sexual dimorphism requires that females get to have a choice too with the most dimorphism where the choice is most 50/50? If so then i think that implies there should be more sexual dimophism in populations that spent the longest under the NW Euro marriage model?
(And as industrialization and urbanization has effectively spread that marriage model to various other parts of the world you might expect sexual dimorphism to increase in places like East Asia over time. Even under assortative mating – as long as the bulk of the choice is individual rather than familial – within each assortment you might start to see it happening.)
Just a thought.
;;;
misdreavus
“And why the hell would the mode of transmission have to be anal intercourse?”
Additional to earlier answer i was thinking of AIDS transmission and got a bit side-tracked by some youthful anecdata related to that but obviously promiscuity is its own form of transmission via STDs and doesn’t need a specific form of sex.
Ok. Why the hell would the mode of transmission have to be _any_ form of sexual contact?
As for the rest of your post, I think we have a textbook case of the Dunning-Kruger effect in action.
“Ok. Why the hell would the mode of transmission have to be _any_ form of sexual contact?”
It doesn’t have to be. I’m just assuming a premise to see if it leads to testable ideas which can be used to discard the premise e.g. if the anomalous form was related to promiscuity (i’m assuming two forms with the anomalous percentage attached to the larger second form) then the link might not be a gay dad or uncle but a promiscuous dad or uncle.
;;;
“As for the rest of your post, I think we have a textbook case of the Dunning-Kruger effect in action.”
I must be missing something as i’d have thought sexual dimorphism required sexual selection? If there was limited sexual selection then dimophism couldn’t happen?
Admittedly i’m a dabbler rather than an expert but aren’t paleolithic skeletons more sexually dimorphic?
“If there was limited sexual selection then dimophism couldn’t happen?”
Why on Earth would you think that? males don’t have to be attracted to women with wider birth canals for those women to survive childbirth better. Females don’t have to be attracted to good hunters for them both to survive hunger when the good hunter hunts successfully.
“then the link might not be a gay dad or uncle but a promiscuous dad or uncle.”
Just to finish this line of thought based on the assumed initial premise of it being somehow connected to promiscuity and tying it in with the idea that if it’s a pathogen and if most homosexual men are gay before adulthood then they must get infected young (pre-puberty even?) then i think that implies a pathogen which causes promiscuity among adults but can cause homosexuality in pre-pubescent boys (caused by the promiscuity pathogen operating on the sexual discrimination part of the brain)(possibly in a similar way to the mice research erica mentioned).
If form of transmission was primarily sexual then how could it easily be passed from promiscuous father to pre-pubescent son without that? How does sexual contact work? How many fathers patch up bleeding pre-pubescent sons after they fell out of trees or had their brother hit them on the head with a rock? How many of them wear surgical gloves when they do it?
Again, just a logical exercise – not saying it’s right.
I’m going to take a stab and say that the mode of transmission is probably not body fluid. This is a wild guess, so I could easily be very wrong.
Yeah. It’s just a thought. It could be any kind of contact.
If it’s father to son or father to mother to son then it might tie in with the r-type population versus K-type population idea i.e. if it was somehow connected to a promiscuity bug that was common among r-type populations then you’d expect those populations to have a higher level of exclusive homosexuality but if transmission to pre-pubescent boys required the fathers to be around to transmit it then that wouldn’t happen.
Also when i say this
“(caused by the promiscuity pathogen operating on the sexual discrimination part of the brain)(possibly in a similar way to the mice research erica mentioned).”
i mean things like, if female attractiveness is related to fertility and secondary sexual cues and the promiscuity bug worked by lowering discrimination then it might make men *relatively* more attractive as well
e.g.
– if it reduced the relative attractiveness of breast size then men with the bug would be relatively more attracted to women with flat chests (or men) than the average man
– if it reduced the relative attractiveness of a 0.7 waist-hip ratio then men with the bug would be relatively more attracted to women who had no hips (or men) than the average man
– if it *didn’t* affect attraction to youth as a fertility cue then it the the discrimination changes would only affect their attitude to boys and young men
It could be indirect sexual transmission. If you have a population that practices anal and oral intercourse, oral-anal contact, etc., and is passing around bodily fluids and fecal matter, then that stuff can be transmitted via non-sexual contact when people shake hands, sneeze, hang out in crowded public areas, etc.
Reminds me of a scene in a mafia movie where one of the mafioso discussing having a mistress says
“My wife kisses my children with that mouth.”
It’s well-established that male public restrooms can be areas for anonymous homosexual activity (cf. Larry Craig). These areas are often not very sanitary. They’re heavily trafficked and used, including by young children, and people often don’t wash their hands there.
“Occurrence of bacteria and biochemical markers on public surfaces.”
http://www.ncbi.nlm.nih.gov/pubmed/16134485?dopt=Abstract
Indeed. Most of these germs come from other children, however… Kid-to-kid transmission is probably not the trick.
Many people that take public transportation have fecal matter on their hands. Kids taking public transportation could pick it up, or their parents that take public transit could bring it home.
“Faecal bacteria join the commute
More than one in four commuters has bacteria from faeces on their hands, an investigation suggests.”
http://news.bbc.co.uk/2/hi/health/7667499.stm
>Kid-to kid transmission is probably not the trick.
You know how you are born with a coke bottle, and about ten years or eighty pounds later you grow a turtleneck? Unless circumcised. If circumcision isn’t about staying cute for pedophiles, I don’t know what is. And if the local droit du signor involves an elder respected throughout the community sucking the blood out of the wound, we have a vector.
“Many people that take public transportation have fecal matter on their hands. Kids taking public transportation could pick it up, or their parents that take public transit could bring it home.”
No doubt. It’s a nasty world out there, in more ways than one…
http://usatoday30.usatoday.com/yourlife/health/2011-03-02-grocerycarts_N.htm
Kids of course often sit inside these things while their parents push them around in the grocery store.
http://usatoday30.usatoday.com/news/health/2010-05-20-swimming-pool_N.htm
You know, shooting wildly in the dark is never a wise or particularly helpful strategy.
Then again, some of the more prolific commenters here don’t even own a pistol, have never seen a goddamn pistol, and would probably shoot themselves in the foot if they ever saw one.
Does sexual dimorphism require sexual selection and would it be proportional to the amount of sexual selection?
How much sexual selection is involved in arranged marriages? Where it exists is it equally male and female or disproportionately female?
Over the 10,000 years of agricuture what proportion of mating was arranged between families for reasons unrelated to sexual selection and what proportion individual choice including sexual selection?
Is the practise of “bundling” effectively an arranged form of sexual selection?
Are paleolithic skeletons (or those of earlier hominids) more sexually dimorphic?
Do lionesses have lower rates of death in childbirth than cheetahs?
etc
Do lionesses have lower rates of death in childbirth than cheetahs?
What on earth have you been smoking? As far as I am aware, neither Lions nor Cheetahs have difficulty during birth, since they have small cubs (although several.)
Even chimps do not have difficulty during birth.
I mentioned spotted hyenas because their unusual evolutionary history mandates that the female give birth through a narrow, distended pseudo-penis that ruptures open during intercourse. Hence the high mortality rate for first time mothers. Evolution has a hard time finding a solution to this phenomenon because those genes serve a totally different purpose in males of the species. You moron.
It could have taken you all of two minutes to look this up on Wikipedia. Then again, you appear to take a perverse delight in spamming this blog with reams of cringe-worthy, unreadable verbiage… Why should I stop you?
Are there any known infectious diseases that strike disproportionately at younger brothers? Wasn’t there a finding some years back that homosexual men were disproportionately younger brothers?
Greg, I can’t remember you ever commenting on Welmer’s chimerism explanation of homosexuality (http://www.welmer.org/2008/07/14/the-chimera-hypothesis-homosexuality-and-plural-pregnancy/)
Do you care to comment on it? It would be most interesting to hear. Thanks!
@nanonymous: in GC’s ‘Depths of Madness” post (last february), Steve Sailer asked GC to comment on the chimera hypothesis. GC responded: “I think it’s silly”
BTW – reading through the Depths of Madness post would save lots of commentors from asking questions that GC has already answered
Nanonymous, you’re losing your memory. (I understand.) From that “Madness” thread”:
________________________________
Nanonymous says:
February 16, 2012 at 9:24 pm
Why do you think it is silly?
Is homosexuality indeed virtually unknown among hunter-gatherers? Weber cites Koniagas of Kodiak Island and the Aleuts to the contrary, references to North American Indians homosexuality are quite common, and I thought that homosexuality was known among some Australian Aborigines? Is there any systematic study/review on this subject?
_________________________________
gcochran9 says:
February 17, 2012 at 10:17 am
A couple of reasons. I look at the odds. Think of syndromes that are Darwinian diseases: that is, they substantially dinged fitness in typical past environments. Now consider the common ones, that affect more than 1 in 100 of the population. The great majority of such syndromes have been shown to be caused by some microorganism. Suppose we have a syndrome of that sort that is not yet explained, like homosexuality. The default explanation is that it too is caused by some microorganism. Since no diseases has ever been definitely shown to be caused by microchimerism, it ranks really low on my list. Moreover, imagine that microchimerism did cause a problem: selection would tend to reduce it over time, and there would be no countervailing tendency, since the foreign cells (as far as we know) do not propagate further and hence do not evolve.
Greg – Do you think that both male and female homosexuality have the same infectious agent as cause?
you may be a different Jim but this same question was asked and snswered in ‘Depths of Madness’
Jim says:
February 16, 2012 at 10:10 am
Cochran – Do you think that male and female homosexuality are both caused by the same infectious agents? Also are the behavioral changes in the host an accidental side effect or could they be advantageous to the virus (or whatever)? Male homosexuals
have generally many more sexual partners than most male heterosexuals which might be advantageous to a sexually transmitted agent. Also the modes of intercourse among male homosexuals are more likely to result in transmission of an infectious agent.
Reply
gcochran says:
February 16, 2012 at 1:06 pm
No, probably not the same thing with lesbians. Side effect or strategy? Unclear: probably side effect.
ps- It would be nice if simeone would ask an intelligent question that GC has not already taken his valuable time to answer in previous threads. If readers and commentors would take time to read what GC has said over and over again then maybe this thread would be more productive.
Sorry. I forgot that I had asked that question a year ago.
Matt
“Don’t really quite understand your response… My query is, if it is a bug, why does it seem like it is only a bug for humans (and sheep) and not dogs, goats, cats etc.?”
Well it just struck me – as a logical option, no idea how likely it is – that sheep might have got it from humans. If so sheep being the odd one out rather than cows or chickens might have a simple ergonomic explanation. I don’t really want to be more detailed than that as it’s probably a dumb idea anyway 🙂
“And why do we not have an evolved response to it yet? This should hit fitness really hard, but humans haven’t evolved a response yet,”
Well that’s why i wonder about it being a side-effect or a mutation of something that had advantages in a different environment e.g. a promiscuity bug that developed in a promiscuous polygamous environment, or something along those lines. Also cultural taboos as quarantine outside the areas where it was beneficial could be one response that worked fine until the taboos broke down.
“while apparently the rest of the animal kingdom has (or why isn’t it there?).”
Yes tis odd – hard to see why it should be so different between cattle and sheep. Although if it is a bug in sheep then separate from the rest i’d wonder if it worked by messing up the discrimination filter – in this case messing with their sense of smell?
Please stop posting.
Also, you still have no flippin’ clue what “quarantine” means.
1) “Please stop posting.”
Do lionesses have lower rates of death in childbirth than cheetahs? What level of sexual selection is there in marriages arranged between families solely on the basis of relatedness? Is there likely to be much sexual dimorphism without sexual selection?
You mean like that?
2) “Also, you still have no flippin’ clue what “quarantine” means.”
It’s close enough to get the idea across. Strict – especially virginal – monogamy is a kind of quarantine for anything sexually transmitted.
3) The argument is that the rate of male homosexuality is too high to make genetic sense and therefore it’s more likely to be a bug. A lot of the responses to that revolve around trying to think up some possible adaptive benefit that outweighs the disbenefit most of which seem to have one flaw or other. However if you accept for the sake of argument it’s a bug – and so deleterious – then don’t similar arguments apply? Why does it effect so few? Why aren’t people immune? How does it spread? Is it connected to the bug’s strategy or a side-effect? etc
I find that interesting.
“And why do we not have an evolved response to it yet? This should hit fitness really hard, but humans haven’t evolved a response yet,”
For the same reason we haven’t evolved a response to a whole hell of a lot of viruses–because they evolve faster than we can against them. All they have to do is alter the pattern of their surface proteins and, voila, they have become unrecognizable to our defenders. Or have you only had ONE cold or ONE respiratory infection in your life and everlasting immunity to them after that? Why do kids get RSV more than once, sometimes many times in childhood, even as dangerous as it can be?
As for why it shows its effect in this way in only a certain small percentage of the population? As GC has written, why does the polio virus, which lives seemingly peacefully in the gut of about a third of the world’s population, manage to wander elsewhere and do great damage in some people?
As for cross-species transmission: Check this out: http://mmbr.asm.org/content/72/3/457.abstract
why do we not have an evolved response to it yet? This should hit fitness really hard, but humans haven’t evolved a response yet
Maybe it crossed the species barrier relatively recently. If it only hits humans and sheep, we can look to a possible neolithic origin. Sheep and humans came into close association only 11kya with domestication. But since it reproductively disables both species, neither can be a coevolved source for the other.. so where is it from?
Goats were also domesticated at the same time or soon after sheep It could well be a goat virus, harmless to them, which jumped the species barrier to sheep after the 2 species were kept together unnaturally by man. And during our long and continued association, a mutant version jumped from either goat or sheep, to humans.
And maybe we HAVE evolved a response. Maybe the rate of homoconversion was 50… 70… 95%… when it first jumped the species barrier 10ky ago. And in both sheep and mankind, a few resistant males could easily polygynously tup the females… quite gladly in fact… and keep the lineage going.
“Maybe the rate of homoconversion was 50… 70… 95%… when it first jumped the species barrier 10ky ago. And in both sheep and mankind, a few resistant males could easily polygynously tup the females”
“8,000 Years Ago, 17 Women Reproduced for Every One Man”
http://www.psmag.com/nature-and-technology/17-to-1-reproductive-success
The money quote:
“Like was there some sort of weird virus that only affected males across the whole globe, 8,000 years ago?”
Greg,
Roissy may have some insight.
http://heartiste.wordpress.com/2013/01/15/the-manjaw-ification-of-american-women-science/
fourth doorman
“Do lionesses have lower rates of death in childbirth than cheetahs?
What on earth have you been smoking? As far as I am aware, neither Lions nor Cheetahs have difficulty during birth, since they have small cubs (although several.)”
It’s related to an earlier side-argument over sexual dimorphism and sexual selection. I was just guessing there was probably *some* differential between lionesses on one hand and tigers, cheetahs etc on the other on the basis that in a hierarchy of need hunting speed – narrow hips – would come before birthing – wider hips – in solitary hunters.
However, as I pointed out, even chimps, members of a highly related genus to Homo, do not have problem with birth. Also, in looking at dogs, it is the smallest breeds that have problems with birth, not the larger ones, because head sizes do not scale down so well.
I must be being really unclear about my point – which was related to sexual dimorphism and *solitary* hunting animals (like cheetahs) having less potential for sexual dimorphism in hip size than group animals (like lions)(or dogs and chimps).
In a similar way the potential for sexual dimorphism in humans depends on the proportion of sexual selection in the mating decisions (and how opposing they are i.e. to what extent are both male and female selecting on different characteristics). Over a long enough time period a population where the mating decisions are 80% sexual selection and mutually opposing (which is where the cheetah point comes in) should display more sexual dimorphism than one which is 80% arranged marriages.
I don’t see how either of those two things are complicated.
It seems like we might learn something from looking at social patterns of gayness.
Suppose gayness is mainly caused by social environment–not seeing your parents f-cking, weak fathers and domineering mothers, reading “Heather has two mommies” at an impressionable age, whatever. We have a really nice parallel example of a fitness reducing social environment change–alcohol. People whose ancestors didn’t have alcohol tend to get really clobbered by it, in both personal and fitness terms, probably because the social environment change led to a genetic change to make populations that have had lots of generations of exposure less susceptible. If social environment is driving gayness, then we ought to see a similar pattern. People from societies that have a long history of whatever exposure makes people gay will have less of a fitness hit than people from societies that are just recently being so exposed.
China might turn out to be a test-case for this.
Assuming a pathogen is at least part of the explanation and assuming just for the sake of generating testable propositions that it’s connected to a promiscuity bug commonly found in tropical west africa which then adapts when it’s transplanted to a more monogamous population then the effects should start to show up in China because of the number of Chinese working there. I was thinking it would probably be impossible in their case to separate any measurable effect from possible cultural causes but maybe not if they got a very big hit very suddenly as you suggest.
“Of course, this hardly ever results in funny-looking genitalia – you’d think it would, but then natural selection has made that kind of error rare. Of course, it should have made epigenetic leakage that cause low-fitness behaviors like homosexuality equally rare.”
Did you miss this part:
Cochran please explain me how histones passes between cell generation after mitosis?Is this possible?
> they’ve given up on sexually antagonistic selection, since the GWAS surveys pretty much rule it out
Which surveys are you referring to?
It isn’t stats, but there are plenty of gays who marry and have kids: http://www.reddit.com/r/AskReddit/comments/1musrq/closeted_spouses_of_reddit_how_did_you_have_sex/
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Eusociality, the highest level of organization of animal sociality, is defined by the following characteristics: cooperative brood care (including brood care of offspring from other individuals), overlapping generations within a colony of adults, and a division of labor into reproductive and non-reproductive groups.
The reason for homosexuality is the high level of meat eating during the pregnancy.Vitamin A in meat diminish androgen synthesys by fetal Leydig cells in the testicles.
http://www.bbc.co.uk/news/magazine-26089486?utm_source=dlvr.it&utm_medium=twitter this is the BBC today, struggling with why homosexuality is not “genetic”.
Omg stop whit this unproven theories.Masculinization is associated only with the action of testosterone and testosterone is responsible for the control of neuronal apoptosis.Just pick the brains of corpses and compare the neuronal number.This is elementary!!!!!!!!!!!!This is a good indicator because the number of neurons does not restores.According to Byne inah-3 is masculinized in the homosexual group.Just look at the Ventromedial Nucleus.
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What about youthful erectile dysfunction? At first blush it would seem that this condition is as maladaptive as homosexuality. Is its percentage of the (say, 20 year old) population as high as that of homosexuality (3%) and thus unlikely to be the result of genetic drift? “A study in the July 2013 Journal of Sexual Medicine suggests that ED is more common among younger men than previously thought. Researchers found that ED affected 26 percent of adult men under 40. Almost half of these men suffered from severe ED.” [http://www.healthline.com/health-slideshow/erectile-dysfunction-young-men#3]. Perhaps in most affected men this condition is simply periodic (or due to environmental factors such as alcohol or drugs) and not constant? But what about the half said to have “severe ED?”
Further research tells me youthful ED (as opposed to ED brought on with age) is commonly thought to be psychological in nature. That is, these are men who naturally have a very high level of anxiety, which is enhanced when trying to have sex. A high level of anxiety produces too much adrenaline, which in turn suppresses erection functionality. Of course, this is really a guess since I doubt adrenaline levels have really been measured. And why wouldn’t some alcohol (but not too much) alleviate the anxiety? Perhaps it’s not that these men have high anxiety levels (who doesn’t that first time?), but rather that they either secrete very high levels of adrenaline in response to anxiety. Or perhaps their sexual response system is hypersensitive to adrenaline? Regardless of why, it seems reasonable that an initial failed attempt at having sex would lead to even more anxiety thereafter.
Perhaps this is an evolutionary response to cull from the population those genomes which produce high levels of anxiety, levels that might result in individuals not having sufficient courage to protect the tribe.
But to say that 26% of adult men under 40 suffer from ED and half of these (13%) have “severe ED” still seems like way too high a number. It seems the culling should have reduced that number significantly. I wonder if the cited stat is anywhere near correct.
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The problems with Cochrane’s argument is that it ignores the fact that there are plenty of variations in humans that are seemingly contra-survival and which persist at about the same level in the population. Homosexuality isn’t at all like being mute, rather it is much more like having a serious degree of speech pathology which, BTW, affects between 2-3% of the population. A far more extreme defect than homosexuality is asexuality, which Kinsey measured as at about 1.5% of the population. How is it that a trait that renders the subject completely “unable” to reproduce persists at about 1.5% of the population?
Cochrane’s article is sneering and obviously biased. I think the comment that he was a physicist had relevance. Biology is very different from physics in that the systems under study are enormously complex, non-ideal, and notoriously difficult to quantify. Few if any physics experiments incorporate such a plethora of unknowns and so much noise.
A point not made is that domesticated rams have an awful lot in common with humans in that both were created by and exist in a zone of radically altered and reduced natural selection. Human social structure and the use of reason and technology that enable it has driven evolution very powerfully in ways that are radically different from what is seen in species that did not develop language and technology. That changes the rules of the game. For one thing, it removes humans from straight-up wild type natural selection because humans no longer exist solely in that environment. If they did they would have nowhere near the burden of unfitness that they now experience. Absent technological civilization what beneficent selection genie hands out eyeglasses for presbyopia or myopia? Who gives the insulin injections to the Type I diabetics in the wild?
As to the fixation on infectious agents causing homosexuality that has to reckon with the fact that each successive male pregnancy greatly increases the odds that the resulting offspring will be homosexual. This pertains only to males, not females. How does that jibe with an infectious agent? It also assumes a naive and binary view of homosexuality which is certainly wrong. Gay men tend to see all MSM as gay. This isn’t so. As Kinsey demonstrated decades ago, homosexuality exists on a spectrum which includes varying degrees of bisexuality. An observant person who frequents the baths and sex clubs will see this pretty quickly because these venues select for bisexual and especially married bisexual men.
The vast majority of these men are NOT closeted gays, rather they are men who, to varying degrees, like to have sex with women, as well as men. An infectious agent isn’t precluded in this situation, but it is made much more difficult and unlikely. In the male population as a whole there is a spectrum of masculinity and this probably has powerful survival advantage for the species as a whole. Men are not all alpha male, head butting reindeer and it would be hard to imagine humanity existing in such a rigid framework. Rather, we exist in a world of leaders and followers, soldiers, priests and peasants. That argues for gradations of masculine and feminine imprinting. Obligate homosexuality is probably best seen as part of that process and perhaps part of the price that was paid for nuanced, gender specific behavior.
I think we should probably take care to avoid oversimplification. I suspect that the condition of homosexual inclinations is due to multiple factors. The effeminate homosexual who identifies as a woman, who sees himself as a woman trapped in a man’s body, has little in common with the hyper-masculine homosexual who’s able to conceal his proclivities from the world at large.
There are other kinds of conditions that have a spectrum. Schizophrenia is not a monolithic condition. It’s an umbrella term that encompasses a variety of conditions. The four classical types of schizophrenia is a good starting point for seeing that variety.
Yep, I agree. Like schizophrenia and autism the category of homosexuality is probably a ragbag of many different brain malfunctions and errors of development that produce similar symptoms. As Greg likes to point out, all happy families are alike but every unhappy family is unhappy in its own way.
There must be many different causes of these errors and malfunctions. Certain genes may make them more likely, but only partly for obvious Darwinian reasons. Conditions in the womb such as hormone levels, and maybe certain pathogens can do it too.
The bigger question here is why are humans susceptible to these kinds of developmental errors at all?
Probably not. We’ve found a number of variants linked to autism, some to schizophrenia: none to homosexuality.
What about the variants I gave? Effeminate and hyper-masculine?
I read this today over at Medical Express. Seems like an excellent candidate mechanism for infection induced homosexuality as well:
https://medicalxpress.com/news/2018-05-uk-scientist-reveals-childhood-leukaemia.html?utm_source=nwletter&utm_medium=email&utm_campaign=weekly-nwletter
excerpts:
“His research concludes that the disease is caused through a two-step process of genetic mutation and exposure to infection that means it may be preventable with treatments to stimulate or ‘prime’ the immune system in infancy.
The first step involves a genetic mutation that occurs before birth in the foetus and predisposes children to leukaemia—but only 1 per cent of children born with this genetic change go on to develop the disease.
The second step is also crucial. The disease is triggered later, in childhood, by exposure to one or more common infections, but primarily in children who experienced ‘clean’ childhoods in the first year of life, without much interaction with other infants or older children.”
“Professor Greaves suggests childhood ALL is a paradox of progress in modern societies—with lack of microbial exposure early in life resulting in immune system malfunction.
In a landmark paper published in Nature Reviews Cancer today, Professor Greaves compiled more than 30 years of research—his own and from colleagues around the world—into the genetics, cell biology, immunology, epidemiology and animal modelling of childhood leukaemia. The research in his lab at The Institute of Cancer Research (ICR) was largely funded by the charities Bloodwise and The Kay Kendall Leukaemia Fund.
Professor Greaves challenged previous reports of possible environmental causes, such as ionising radiation, electricity cables, electromagnetic waves or man-made chemicals—arguing that none are supported by robust evidence as major causes.
Instead, he presented strong evidence for a ‘delayed infection’ theory for the cause of ALL, in which early infection is beneficial to prime the immune system, but later infection in the absence of earlier priming can trigger leukaemia.
Professor Greaves suggests that childhood leukaemia, in common with type I diabetes, other autoimmune diseases and allergies, might be preventable if a child’s immune system is properly ‘primed’ in the first year of life—potentially sparing children the trauma and life-long consequences of chemotherapy.
His studies of identical twins with ALL showed that two ‘hits’ or mutations were required. The first arises in one twin in the womb but produces a population of pre-malignant cells that spread to the other twin via their shared blood supply. The second mutation arises after birth and is different in the two twins.
Population studies in people together with animal experiments suggest this second genetic ‘hit’ can be triggered by infection—probably by a range of common viruses and bacteria. In one unique cluster of cases investigated by Professor Greaves and colleagues in Milan, all cases were infected with flu virus.
Researchers also engineered mice with an active leukaemia-initiating gene, and found that when they moved them from an ultra-clean, germ-free environment to one that had common microbes, the mice developed ALL.
Population studies have found that early exposure to infection in infancy such as day care attendance and breast feeding can protect against ALL, most probably by priming the immune system. This suggests that childhood ALL may be preventable.
Professor Greaves is now investigating whether earlier exposure to harmless ‘bugs’ could prevent leukaemia in mice—with the possibility that it could be prevented in children through measures to expose them to common but benign microbes.
Professor Greaves emphasises two caveats. Firstly, while patterns of exposure to common infections appear to be critical, the risk of childhood leukaemia, like that of most common cancers, is also influenced by inherited genetic susceptibility and chance. Secondly, infection as a cause applies to ALL specifically—other rarer types including infant leukaemia and acute myeloid leukaemia probably have different causal mechanisms.
Professor Mel Greaves, Director of the Centre for Evolution and Cancer at The Institute of Cancer Research, London, said:
“I have spent more than 40 years researching childhood leukaemia, and over that time there has been huge progress in our understanding of its biology and its treatment—so that today around 90 per cent of cases are cured. But it has always struck me that something big was missing, a gap in our knowledge—why or how otherwise healthy children develop leukaemia and whether this cancer is preventable.
“This body of research is a culmination of decades of work, and at last provides a credible explanation for how the major type of childhood leukaemia develops. The research strongly suggests that ALL has a clear biological cause, and is triggered by a variety of infections in predisposed children whose immune systems have not been properly primed. It also busts some persistent myths about the causes of leukaemia, such as the damaging but unsubstantiated claims that the disease is commonly caused by exposure to electro-magnetic waves or pollution.
“I hope this research will have a real impact on the lives of children. The most important implication is that most cases of childhood leukaemia are likely to be preventable. It might be done in the same way that is currently under consideration for autoimmune disease or allergies—perhaps with simple and safe interventions to expose infants to a variety of common and harmless ‘bugs’.” Professor Paul Workman, Chief Executive of The Institute of Cancer Research, London, said:
“This research has been something of a personal, 30-year quest for Professor Mel Greaves—who is one of the UK’s most influential and iconic cancer researchers. His work has cut through the myths about childhood leukaemia and for the first time set out a single unified theory for how most cases are caused.
“It’s exciting to think that, in future, childhood leukaemia could become a preventable disease as a result of this work. Preventing childhood leukaemia would have a huge impact on the lives of children and their families in the UK and across the globe.”
30 year quest to nail down childhood leukemia. Probably take that long to prove the same for homosexuality too. Or maybe not. After six or seven other diseases are proven to have similar etiology the bar will perhaps be a bit lower.
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“Of course, this hardly ever results in funny-looking genitalia”
evo_homo is arguing that cryptorchordism actually is prevalent enough to occur in roughly 2% of male births.