On the Origins of Homosexuality

As regulars of this blog might know, the biological origins of homosexuality* (and the evolutionary accounting for the same) are a popular topic in these parts.  My preferred hypothesis is a mix of neurological genes and prenatal hormones for the former and benevolent pleitropic and carrier effects for the latter, which also seems to be the dominant view of the relevant scientific community.  However, a post on the issue by Razib Khan and the comments therein got me following a mess of alternate biological explanations for the phenomenon, complete with their own discreet Darwinian explanations.  I did not emerge all too convinced by any, but I thought they were all interesting and deserving of wider circulation.

The first, which I had only encountered cursorily before, comes from Gregory Cochran, a biological anthropologist and former co-blogger with Razib when Gene Expression was over at Science Blogs.  One of Cochran’s preferred hypotheses is that many conditions we initially assumed to be genetic are in fact precipitated by viral infections, which are in turn made more likely by genetic factors.  He cites narcolepsy, which researchers suspect might be caused by an virally-triggered auto-immune disorder that attacks specific neuron involved in the production of hypocretins (a sleep-related neurotransmitter) and only seems to affect people with a specific HLA (a super locus of genes involved in self-recognition in cells).  The hypothesis is that homosexuality works similarly, with a viral infection and auto-immune irregularity wiping out, in a targeted fashion, neurons involved in proper orientation.  Cochran reasons this likely because its high prevalence does not resemble other deleterious genetic disorders:

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

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

 But what about homosexuality?   Well, from this biological perspective, it’s surely a disease. Disinterest in the opposite sex reduces reproduction quite a bit – around 80% in American conditions. Does it hit in early life?    Sure. Has it been around a long time?    Certainly.

It is an interesting hypothesis for sure, but I do not find the adaptionist rationale as compelling as Cochran does, largely because it has been amply established that defects with beneficial secondary effects on heterozygotes could stabilize in a population at percentages as high as five or ten percent, especially if thrust that high initially through drift.  What more, the additional evidence that Cochran musters to defend his claim are dubious at best.  Cochran implies that the pathogen jumped from sheep to humans during their domestication in Anatolia and spread throughout humanity from there, in a similar manner as pathogens like small pox.  Though this might account for the lamb-loving Greeks, it runs afoul of the prevalence of homosexuality found in many pre-agricultural societies.  Likewise, Cochran cites the differential between openly gay people in urban compared to rural environments, which he sees as reflective of a more conducive environment for a viral transfer, but to me seems to simply reflect differences in social mores.  Further, the auto-immune nature of the proposed disorder does not seem strong enough to account for the observed heritability of homosexuality.

The second explanation comes from an interested layman who became gradually disenchanted with Cochran’s hypothesis and groped about for a better explanation.  He seems to have settled on an explanation that hinges on chimerism as an explanation.  Chimeras are organisms who, during development, absorbed stem cell lines from a genetically distinct source, usually an undeveloped twin zygote or, occasionally, the mother.  This results in certain organs or parts of the body being genetically distinct from each other and could account, for instance, for people who have different colored eyes or ambiguous sexual organs.  This all seems quite esoteric and was assumed to be quite rare in humans (thought it is common in some species of mammals, like marmots).  However, recent research suggests that chimerism is far more common in humans than previously suspected.  The author suggests that this process could account for homosexuality as well:

 Some physiological differences have been found between heterosexual and homosexual men suggesting a slight, overall feminization of homosexual men, but the most compelling and obvious difference is behavior, which is neurologically determined. Humans are extraordinarily complex beings, and much of what we are is expressed by our minds. Our likes and dislikes, our tastes — both artistic and physical — are determined by our neurological makeup. Some of us are timid, some bold. Some are meticulous and some spontaneous. And, as it happens, some of us prefer women and others men. In most cases this can be determined by sex, i.e., most men prefer women and most women prefer men, but this obviously isn’t a hard-and-fast rule: some men clearly prefer men to women and some women prefer women to men…

It is likely that many stem cells, even from siblings, would eventually be rejected as foreign in a developing fetus, or would be weeded out when the child is born and begins to develop a mature immune system. However, certain tissues are exempt from this, including those in the brain. This means that stem cells that made their way into the incipient brain of an embryo could stay there safely, even if they are eliminated from other tissues. In fact, they could, and probably do, persist in the brain throughout the life of the organism. Female stem cells in a developing male infant’s brain could have profound implications for its ultimate form. Just as much of the rest of the body is shaped by our gender, so is the brain, and tests with rats have shown that hormones alone are not sufficient to masculinize the brain. The anatomical differences discovered in regards to homosexual brains, most of which show feminization, could be explained by pockets of genetically female cells, or even a few interspersed throughout areas critical to masculinization. Chimerism in the brain is probably more common than in other regions, and does not usually result in homosexuality, but can when cells colonize certain regions.

Another interesting theory, but it too stumbles while trying to explain some observed phenomena with regards to male homosexuality.  To me, the biggest stumbling block is in the numbers.  The author seems to have misinterpreted the growing consensus of chimerism as common to mean essentially a widespread condition, afflicting a majority of humanity.  He assumes (without support) that chimerism occurs in between 50-70% of all pregnancies.  However, as the Cochrane article previously cited makes clear, when scientists and medical researchers use the word common, they are referring to something slightly different from the average person.  Cochrane defines it as anything occurring in a population at a rate greater than 1 in 1000.  The best I could tell, the current estimates for chimerism in humans as a whole run between 1% to 8%, with the latter number representing a clear upper bound of situations where chimeras could arise (multiple pregnancies resulting in a single birth).  However, remember that the author is arguing that one specific chimeric variant, which replaces set neurons in a certain hypothalmic nucleus, accounts for observed homosexual behavior.  Even given the most generous estimates, this variant cannot account for more than perhaps 1% of extant human chimeras (think of the numerous possibilities for just neurological replacements).  There is no way that this .01%-.08% of the population  can account for the roughly 3-8% of males that are gay. 

There are further problems with this hypothesis.  For instance, the author accounts for the observed hereditary element of homosexuality thusly:

 Homosexuality has high twin concordance, especially in monozygotic (identical) twins, where it approaches 50%. In fraternal twins it significantly lower, but still high, at 22%. Aside from genetic similarity, one of the factors that sets identical and fraternal twins apart is that most identical twin pregnancies are monochorionic, meaning that they share a placenta, whereas most fraternal twins are dichorionic, meaning that they each have their own placenta. Twins that share a placenta are naturally more likely to receive similar amounts of stem cells if any happen to be circulating through the placenta. Twins with separate placentas are still likely to be exposed to the cells, since they are both in the same uterus. However, each one has a distinct supply of nutrients and cells, so the ratio each twin receives would tend to vary more than in the case of identical twins.

Yes, “aside from genetic similarity.”  However, experience in other studies suggests that when two people with the same genes display the same behavior, the most parsimonious explanation is that the genes at least play a role.  I will also note that the presence of gay identical twins also offers a bit of a stumbling block for this theory as well, unless there was a third fraternal sister that was absorbed equally and similarly (i.e. replacing the same portion of the brain) by both twins, something that strikes me as highly unlikely.  His Darwinian logic is also a bit screwy too.  He argues that this arrangement would be evolutionarily advantageous because:

Fertility is obviously a genetically positive trait, and fertility is the result of eggs being both available and fertile. This means that more fertile eggs during ovulation would be genetically advantageous, but due to human child-rearing logistics the survival of only one fertilized embryo would also be advantageous. Therefore, women prone to having more than one egg fertilized, but whose pregnancies only resulted in only one live birth, would have the optimum level of fertility. A side effect of this could be an increased incidence of chimerism in human children, and in the case of multiple embryos with different genders, this could lead to physiological changes that result in homosexuality in a proportion of the population.

Generally speaking, for much of human history, higher child-per-mother rates period is considered the maximally effective strategy, since, given the vagaries of pre-industrial life, you never know which children will make it to reproduction and it is better to have more kids than to play the odds with fewer.  I certainly cannot conceive of a strategy that produces fewer children and does not provide them with any additional benefit in the process (instead saddling a few with some debilitating side effects) as being more effective than successful multiple pregnancies, when they do occur.  Instead, I would argue chimerism seems to simply be , from an evolutionary point of view, a neutral to mildly deleterious side effect of other processes, like the early elimination of unviable zygotes or the natural sloughing off of cells in the uterine environment.  This, especially when combined with the numerical issues involved in chimerical homosexuality, makes me somewhat dubious of this explanation.  However, since it does center on a little understood topic and is quite easily falsifiable, I would not dismiss it out of hand.  A quick experiment looking at slices of gay vs. straight hypothalmus neurons for double X’s or other signs of foreign female cells would settle the issue far better than supposition about numbers.

The final hypothesis comes from Gary Larden, who is, like Cochrane, a biological anthropologist.  He argues that early childhood stimuli and environment have a heavy influence in sexual orientation and gender, as much if not more so than prenatal or genetic factors.  This, he writes, leads to a wide spectrum of observed sexual orientations and genders:

If every single factor is thought of as a simple binary choice (and I use the word “choice” with no reference to human decision making) between two cannalized options, then the number of possible outcomes could be thought of as 2ⁿ where ‘n’ is the number of times a binary choice is encountered. So, if there are, say, three hormonal moments in utero, and one more after birth (puberty) and, say, three life stages that have major influences on gender (and I oversimplify) then the number of possible routes a person may take from conception to adulthood would be 2⁷. That is 128. If these different paths lead to mostly different outcomes, wouldn’t there be over 100 “genders” among humans?

Amongst other things, Larden seems to neglect that, in development, upstream inputs have a far more significant influence on outcomes than those further downstream.  Thus, his conjectural use of the Fundamental Counting Principle** is highly misleading: even if all seven of the hypothetical events have an effect on sexual orientation (which is questionable), the genetic makeup and prenatal environment would slant things disproportionately one way or another and later events would likely simply add fuzziness or ambiguity, rather than shunting it to another category.  Larden’s hypothesis also seems disconnected from the evidentiary support he cites.  He, for example, notes differences in how parents treat infants or how school-age girls and boys socialize and self-segregate differently, but does not demonstrate that these two phenomena are correlated (not to mention causal).  Instead, he seems to retreat to a more nuanced version of blank slate-ism, which cases like David Reimer’s do not seem to corroborate, which only reinforces Razib’s original point about the creeping convergence between the political correct left and the religious right on these issues.

*I should note that almost all mentions of homosexuality here and on the linked to articles refers to male homosexuality, which is better understood and seems less transient and more heritable than female homosexuality.

**See if you can guess which Lurer teaches math…