A couple of months ago, one of my favorite genetic genealogy blogs linked a couple of blog posts from a blog that focuses on HBD, and a firestorm broke out in the comments. I made a mental note to write about the HBDosphere, but put it off for other things, till Rod Dreher’s post about race, genetics, and Nicholas Wade reminded me. So, here goes.
HBD is short for Human Biodiversity, which is described by its supporters as the investigation of human biological diversity, but which I would describe as the discussion of human biological variation by people who think that Steve Sailer has ideas on the topic worth hearing. Steve Sailer originated the term, and people who disagree with his views, even if they have an interest in the genetic history of hominids, don’t tend to self-label as people who are interested in Human Biodiversity. There’s a political slant to the label.
The other reason I describe the label in terms of people who like Steve Sailer is that it seems more accurate to me than the common liberal description of HBD as being all about thinking black people are stupid. While it does seem to be true that nearly all commenters in the HBDosphere think that black people are genetically predisposed to have a lower IQ than white people (apparently strongly so), and that much blogging effort is expended arguing that this is so, HBD extends beyond the IQ argument. It includes HBDchick, who rarely writes about IQ (though her politics align just fine with Steve Sailer’s), and Heartiste, whose main concern appears to be pickup artistry. It also includes some variation in attitudes on immigration, all the way from, say, Ron Unz to Steve Sailer. But it definitely doesn’t include Stephen Jay Gould, Jared Diamond, or Richard Lewontin.
I’ve encountered the HBDosphere, recently, mainly because of the intersection between HBDish interests and those of genetic genealogy. We all use, though for different purposes, Dienekes Pontikos’ nifty set of admixture calculators. We occasionally appreciate the same books (the link that caused the firestorm was to a series of maps of American regional origins, based in part on David Hackett Fischer’s in Albion’s Seed and Colin Woodard’s American Nations: A History of the Eleven Rival Regional Cultures of North America). General information about population migrations is of obvious interest to both genetic genealogists and HBD bloggers, though we do very different things with that information. And so, in my search for genetic genealogy information, I’ve encountered the HBDosphere, particularly through Razib Khan, source of all kinds of information about how to analyze your 23andme data, and of politics that don’t agree much at all with mine.
It’s an encounter that leaves me unsure how seriously to take this bunch of people. By which I mean, is HBD one of those fringe ideas that you really only encounter on the Internet? Am I spending more of my attention on it than it deserves? After all, I haven’t in the past twenty years had even one person in real life tell me that he or she believed that genetics are a significant driver of ethnic differences in test scores. And often the HBD bloggers themselves seem to describe themselves as an embattled minority, rejected by conservatives as well as liberals. Or is it my real world experience that’s the bubble, and do these views have more influence than I realize? Nicholas Wade’s book, I gather just about to be published so most of us can’t see it yet, has been getting many advance cheers in the HBDosphere for support it’s purportedly going to give their views. Nicholas Wade is a science writer for the New York Times, and the favorable review that Rod Dreher linked is in the Wall Street Journal, written by HBD friendly Charles Murray (who isn’t nearly as discredited in the conservative world as he is in the liberal world).
Mostly, the gulf is about race. But I want to start with a different topic, since it figured heavily in the firestorm at the genetic genealogy blog (which blog I won’t link, because I don’t want to plague the blogger, whom I admire, with controversy not much related to her blog). That topic is the “gay germ.” The blogger to whom she had linked, you see, is Jayman, a strong advocate of the Greg Cochran’s “gay germ” theory. Jayman has called the gay germ “by far the most likely explanation for male homosexuality,” writing that
If the “gay germ” is real – which it almost certainly is.
I think that “almost certainly” is, let’s say, a severe overestimate of the degree of evidence that this theory has been able to muster.
But I need to begin my story about the gay germ with a discussion of the theory that it’s meant to counter, the theory of the “gay gene.”
Though the “gay gene” and the “gay germ” are rival theories, it should be remembered that they aren’t, in principle, completely at odds. Dean Hamer, a leading advocate of the “gay gene” theory, says that he’s actually talking about many genes, not a single one, combined with environmental factors, that could include (his own example) something like getting measles as a child. (I don’t expect that he actually believes disease is a significant factor; he probably used measles just to show that “environment” doesn’t necessarily mean “social environment.” But in principle you could both have one or more “gay genes” and one or more “gay germs.”) Greg Cochran, the leading advocate of the “gay germ,” does acknowledge the possibility that genetic factors could influence response to that pathogen. Still, as theories of the main biological cause of sexual orientation, the theories are starkly opposed.
They also, obviously, have a different emotional feel. Germs are icky, and if you find homosexuality icky, you may find it easier to believe in a gay germ. Genes are natural, and if your gay, lesbian, or bisexual orientation (or that of people dear to you) feels altogether natural, normal, and healthy, a gay gene has more appeal. But I’ll save the feeling side of the story for another post. For now, let’s pretend that I’m viewing this debate with Spock-like detachment, just looking at the evidence. I’m not, of course; I have feelings the same as everyone else. But you don’t have to care about my feelings to evaluate my argument.
I’ll start, though it’s a major oversimplification, by discussing a hypothetical single gay gene. If we have a gay gene, why hasn’t evolution bred it out of us, given the obvious reproductive disadvantage?
We know that having a larger number of older brothers increases the probability that a man will be gay, so perhaps we’re actually talking about new random mutations, which increase in children of older parents? It turns out that the answer is, no, we’re not. Paternal age, which is known to be associated with increased mutational load, is not associated with male homosexuality. (Though I myself, obviously, am not a gay man, but a married and faithful bisexual woman, I’m going to be forced to discuss mostly male homosexuality, because that’s what has been most researched. It’s also where most of the “gay gene” theories are; nobody worries much about how a “bisexual woman” gene could survive, if there is such a gene.)
So, if we’re talking about a gay gene, it has to have some reproductive advantage, to counter the obvious reproductive disadvantage, since, infrequent though homosexuality is, relative to heterosexuality, it obviously isn’t being bred out of us.
Perhaps the gay gene is, as E. O. Wilson suggested, a “good gay uncle” gene, which survives through kin selection. J.B.S. Haldane once said, “I would lay down my life for two brothers or eight cousins.” A gene that provides enough reproductive advantage to your close relatives can survive, even if it doesn’t supply you with any children directly. This effect is particularly evident among eusocial insects like bees, and so it’s no surprise that E. O. Wilson, researcher of eusocial insects, was one of the early proponents of kin selection theory. (Wilson has since shifted to arguing for a kind of multilevel selection that includes both individual selection and group selection, but as far as I know there isn’t a non-kin group selection theory explaining how a “gay gene” could work, so I’ll leave group selection alone till I run across it in my other series, where I make my way through blogging Jonathan Haidt’s book.)
Bees are supersisters, sharing more than the usual 50% of DNA that human siblings would share, so worker bees get more evolutionary bang for the buck when they lay down their lives for nephews and nieces than we do. A human good gay uncle has to be a very good gay uncle indeed for his kin selection advantage to outweigh his reproductive disadvantage (unless, I suppose, social pressure leads him to have enough less enthusiastic sex with his wife that he doesn’t suffer that much of a reproductive hit, in which case the gene only starts to get bred out of the population once GLBT relationships are socially accepted). But even a less impressively good gay uncle could find his avuncular virtue to be a partial offset to the evolutionary drawback of his gay gene, provided that the gene also has some other evolutionary advantage.
One such proposed advantage is the “fertile sister” gene, a sexually antagonistic gene that makes brothers gay and sisters more fertile. Maybe it just makes everyone who carries it, male or female, find sex with men really, really hot. Or maybe it has some other mechanism that we haven’t figured out. A 2004 study of 200 Italian families actually did show that sisters of gay men had more children, so maybe this version of the gay gene does exist. The study would need to be replicated in a larger population, though, for us to be sure.
Dizygotic advantage is another way that genes survive, despite a negative effect on survival or reproduction. If people with one copy of a gene have an advantage, while people with two copies have a disadvantage, the gene will reach equilibrium at some level of presence in a population. The most famous example is sickle cell anemia, where a single copy of the gene provides some resistance to malaria, while two copies cause anemia.
Another possibility is that the gay gene makes men prefer sex with men, but simultaneously in some way makes them more attractive to women. Evolution isn’t about making us happy; it’s about making us grandparents. And if, for much of our evolutionary history, a significant part of the male population has failed to reproduce because, despite really, really wanting sex with women, they couldn’t persuade women to have sex with them, then men who didn’t want sex with women all that much, but who were really good at persuading women to have sex with them, may actually have been rather good at producing grandchildren.
Part of the lesson of this exercise is that it’s possible to make up a Just So story for anything. The test is in whether you can produce evidence for your Just So story. Are gay men really more helpful uncles than straight men? Are their sisters really more fertile (can that Italian study be replicated)? Are they more attractive to women?
Proving that a “gay gene” couldn’t exist, though, is harder. Because you’d have to prove that none of the possible explanations for how a “gay gene” could work will hold true. And it gets worse. Because, in fact, nobody really thinks there’s just a single “gay gene.”
To the extent that homosexuality is genetic, it is, like height, the effect of a number of different gay genes. We’re actually not talking about a gay gene, but a gay epistasis, a combination of genes that, if you get enough of them, will make you gay. This could explain why there have been mixed results in replicating Dean Hamer’s finding of an Xq28 gene that is associated with homosexuality. Perhaps Xq28 either is or isn’t a gay gene, depending on whether you’re surveying a population that does or doesn’t have a high frequency of the modifier genes needed to make Xq28 a gay gene.
Now, if we have a gay epistasis, rather than a single gay gene, then something similar to dizygotic advantage could operate at the epistatic level. Perhaps some of the genes involved in this epistasis have reproductive advantages (it needn’t be the same one for each gay gene) that show up even when you don’t have the full set, and the evolutionary disadvantage, homosexuality, only shows up if you have the genes in combination. You can see how it wouldn’t even take that large of a reproductive advantage per gene for the math to work, if you need fewer genes to get the evolutionary advantage than you do to get the evolutionary hit.
Finally, we have to consider the fact that, however many gay genes there may or may not be, they don’t work independently of the environment. Twin studies show a concordance rate of, well, actually twin studies turn out to show a variable concordance rate (I’ll get to that later), but none of them show a concordance rate of anything like 100%. So we’re actually talking about, not a flat out gay gene, but a gay gene expression.
“Environment” here could be either social environment (such as Daryl Bem’s “Exotic Becomes Erotic” theory of the origin of sexual orientation) or biological environment (such as hormonal exposure in the uterus).
One known environmental factor is the number of older brothers a man has. The more older brothers you have, the more likely you are to be gay. The study that showed this correlation reported that each older brother increases the odds of homosexuality by 33%. Father’s and mother’s age are no longer significant when siblings are controlled for (unlike some other traits that, due to the greater mutational load in aging parents, increase with age). It’s just older brothers. Not age. Not older sisters. The researchers who found this effect, Blanchard and Bogaert, theorize that the increase has something to do with a mother’s immune response being more likely to react to male specific proteins if the mother has carried previous male babies.
So, let’s suppose that we have a gay gene that only gets turned on under particular prenatal circumstances, ones likely to apply in women who have had previous pregnancies involving sons. But this gene might, hypothetically, convey some evolutionary advantage on everyone else. Our gay uncle has nephews and nieces, not only from his fertile sisters, but from his fertile older brothers. With enough siblings, enough nephews and nieces, and enough of an evolutionary advantage (of some kind or another) for the straight members of the family, the math could work. (Of course, it’s also possible, even, I suppose, likely, that the older brother effect isn’t mediated by any such gene at all. My point here is simply that whatever genetic influence is involved, there’s no particular reason to expect its “gay gene” effect to be activated in all environments.)
And here is where the case for the “gay germ” breaks down.
Now, the way the “gay germ” theory works is that Cochran takes each possible explanation for a “gay gene” in turn, and argues for why he thinks it won’t work. Here’s a round up, by Jayman, of Cochran’s various posts debunking various possible mechanisms by which a hypothetical gay gene could work.
And that’s it. That’s all the evidence for this “almost certainly” real gay germ.
I could imagine positive evidence that could point in the direction of a pathogen being a major factor. For instance, sexual orientation could have a prevalence that fit with some disease epidemiology. We could have a seasonal gay germ effect if, for instance, some seasonal virus, like the flu virus, altered sexual orientation if mothers catch the bug in a particular stage of pregnancy. Or if we had a gay germ that, like rubella, came in epidemics every seven years, we could trace its path. Perhaps a gay germ might show correlation with some disease vector. If it’s toxoplasmosis, for instance, you might be more likely to be gay if your mother changed the kitty litter herself. Perhaps children are more likely to be exposed if they live in crowded environments, such as cities. Or perhaps there’s a geographical “gay germ” belt, like the chlamydia related infertility belt in Central Africa. And of course, if we ever found actual antibodies that systematically differed between gay and straight people, that would be a big clue.
But no, we don’t have any positive evidence for a gay germ. It’s a germ of the gaps, a germ whose sole justification is that, well, we don’t know that anything else causes homosexuality.
It also seems a particularly improbable germ of the gaps, because, as Chris at The Lure points out, it would have to act like no pathogen we know.
This points to the biggest weakness of the gay germ theory: it fundamentally misunderstands why pathogens exists. When non-biologists consider pathogens (fun fact: most of the vocal gay-germ theorists are non-biologists), the temptation is to focus on the symptoms rather than on the pathogen itself. Thus viruses are simply bad things that happen to people. But pathogens are fairly indifferent to their host’s status. The only metric selection judges them on are their ability to reproduce and to find new hosts. The cost to the host comes as a service towards one of those two ends. For instance, the open sores and blisters caused by herpes are in part the result of the virus hijacking skin cells to produce so much protein components for future herpes viruses that the cell ruptures (the body’s own response to the infection also plays a role). These sores also aid the herpes virus in infecting new hosts, as the virus requires skin-to-skin contact with the sores to transmit. Indeed, there is a relationship between the parts of the body a pathogen typically infects and the mode of transmission: airborne pathogens typically infect the respiratory system, water-borne pathogens the GI tract, STDs genitalia and their related emissions. Biologists have also postulated a similar positive relationship between a germ’s virulence and its ease of transmission: the more a pathogen requires of its host to find a new host the less it can afford to impair its function. For instance, even though HIV and ebola viruses attack similar cells and transmit through contact with body fluid, Ebolaviruses transmit much much more easily (and produce copious bodily fluids externally) and thus can afford to kill their hosts within a matter of days rather than the years an HIV infection takes.
The hypothetical gay germ violates all of these principles. Rather than maximize its short-term viability, its plan seems to be:
1. Burrow down into the inner portion of the brain, probably the hardest place for an external pathogen to reach
2. Infect a small batch of neurons that control sexual orientation (but little, if anything, else), which, if the germs hits shortly after birth, will have no effect on the host’s behavior for at least a decade
It’s one thing to be a pathogen that manages to alter host behavior in a way that helps with your own replication. A sexually transmitted disease that makes the crickets it infects horny, or a toxoplasmosis induced loss of fear of cats that allows the Toxoplasma gondii parasite to get from its mouse host to the cat gut that is the only place where it can reproduce, both make sense. But a germ whose one effect is to change its host’s sexual behavior at least a decade in the future?
Gay genes, in contrast, almost certainly exist; the question is, how big of an effect do they have? The gold standard for determining how much a trait is genetic and how much it’s environmental, you see, is twin studies, in which you compare identical and fraternal twins. Twin studies seem to be all over the map in how large a genetic effect they report. At the high end, a 1991 study reported 52% concordance in identical twins and 22% in dizygotic cotwins, but other studies have reported lower concordance.
A 2005-2006 survey of all adult twins in Sweden found
Twin resemblance was moderate for the 3,826 studied monozygotic and dizygotic same-sex twin pairs. Biometric modeling revealed that, in men, genetic effects explained .34-.39 of the variance, the shared environment .00, and the individual-specific environment .61-.66 of the variance. Corresponding estimates among women were .18-.19 for genetic factors, .16-.17 for shared environmental, and 64-.66 for unique environmental factors. Although wide confidence intervals suggest cautious interpretation, the results are consistent with moderate, primarily genetic, familial effects, and moderate to large effects of the nonshared environment (social and biological) on same-sex sexual behavior.
So I figure maybe a third of the cause of sexual orientation is genetic, with would make sexual orientation pretty much on a par with many other traits (most personality traits and mental abilities seem to be at least 20% genetic). Some of the environmental cause is probably prenatal. Possible prenatal environmental influences include the immune reaction that Blanchard and Bogaert have proposed to explain the older brother effect, and variation in prenatal hormonal exposure, including epigenetic effects in which epi-marks from the opposite sex parent:
In this model, homosexuality occurs when stronger-than-average SA-epi-marks (influencing
sexual preference) from an opposite-sex parent escape erasure and are then paired with a weaker-thanaverage
de novo sex-specific epi-marks produced in opposite-sex offspring. Our model predicts that
homosexuality is part of a wider phenomenon in which recently evolved androgen-influenced traits
commonly display gonad-trait discordances at substantial frequency, and that the molecular feature
underlying most homosexuality is not DNA polymorphism(s), but epi-marks that evolved to canalize
sexual dimorphic development that sometimes carryover across generations and contribute to gonadtrait
discordances in opposite-sex descendants.
Even identical twins don’t have identical prenatal environments, so prenatal and well as postnatal environment could figure in twin non-concordance.
And there may be additional environmental effects after birth. Some of them may be quite large (given the large supply of identical twins with non-identical orientations), but no one’s figured out yet what they are.
I’m OK with that uncertainty. Given a choice between the gaps and an implausible germ of the gaps, I’ll stay with the gaps, and just figure we don’t fully know yet why some people are straight and some are gay.