More on the origins of male homosexuality

Are there other theories on the origins of male homosexuality? Yes, quite a few. These theories generally fall into two categories: those that explain the relatively small variance due to genetic factors (30-45%) and those that explain the larger variance due to some environmental factor. Conceivably, we could be looking at an interaction between the two, i.e., an environmental factor (a pathogen, prenatal trauma, or perhaps environmental estrogens) interacting with a genetic predisposition (partly feminized male brains, as postulated by Ed Miller).

This week, we will look at another theory. Like Miller, Zietsch et al. (2008) postulate a genetic predisposition maintained by a balanced polymorphism. Unlike Miller, they believe this predisposition somehow increases mating success, rather than offspring survival.

Using twin data, they found that heterosexuals tend to have more sexual partners over a lifetime if they have a homosexual twin than if they have a heterosexual twin. This increased mating success, however, was significant only when the heterosexual was female. The authors attribute these findings to a genetically influenced behavioral trait.

Our hypothesis is that a number of pleiotropic (more than one effect) genes predispose to homosexuality but also contribute to reproductive fitness in heterosexuals. In the case of males, there are a number of alleles that promote femininity: if only a few of these alleles are inherited, reproductive success is enhanced via increased levels of attractive but typically feminine traits such as kindness, sensitivity, empathy, and tenderness. However, if a large number of alleles are inherited, even the feminine characteristic of attraction to males is produced. In females, the converse explanation could be used—a low dose could lead to advantageous typically masculine characteristics such as sexual assertiveness or competitiveness, and a large dose could further lead to attraction to females. (Zietsch et al., 2008)

The authors attribute this hypothesis to Ed Miller, although Miller’s theory has more to do with increased offspring survival (due to increased paternal investment) than to increased success on the mate market.

Does this hypothesis explain the authors' findings? Does it predict that hetero women with gay or lesbian siblings have more lifetime sexual partners? No. First, it doesn’t explain why such an effect is confined to female heterosexuals. Nor is it clear why this hypothesis should account equally well for hetero women with gay brothers and for hetero women with lesbian sisters. The authors seem to be arguing that these women have more lifetime partners than do other women because they’re more feminine in some cases and more masculine in others.

Hmm … Could we be looking at a shared family environment effect? Parental attitudes toward homosexuality in offspring tend to correlate with parental attitudes toward promiscuity in offspring, especially in daughters. This correlation is especially high if we compare religious families with non-religious ones. If a mother and father accept expression of homosexuality in their children, they would probably also accept their daughters having more sexual partners. On these grounds alone, a gay or lesbian child is likelier to have a sister who has more sexual partners on average. But this correlation would not be a cause-and-effect one. It would flow from a common cause: parental permissiveness.

One could shoot back: “Homosexuals are not made by permissive parents. They’re born that way.” True, but the participants in this study were asked to self-identify as heterosexual or homosexual (on a scale of 1 to 6). Even if family environment doesn’t determine latent sexual orientation, this factor would probably influence one’s willingness to affirm it, both to oneself and to others.

References

Zietsch, B.P., Morley, K.I., Shekar, S.N., Verweij, J.H., Keller, M.C., Macgregor, S. Wright, M.J., Bailey, J.M., & Martin, N.G. (2008). Genetic factors predisposing to homosexuality may increase mating success in heterosexuals. Evolution & Human Behavior, 29, 424-433.

Origins of male homosexuality - The germ theory

How does male homosexuality originate? More to the point, how does it perpetuate itself? According to Ed Miller, it results from a balanced polymorphism—a delicate balancing act where too much feminization of the male brain causes attraction to one’s own sex and too little causes indifference to one’s own children. This week, I will present an alternate explanation: Greg Cochran’s germ theory.

Greg has never published his theory in a peer-reviewed journal, although it is briefly summarized in Cochran et al. (2000). In itself, this is no shortcoming. Most journals seem uninterested nowadays in real debate. But sometimes I wish he would at least pretend he was writing for a journal. He tends to be polemical, as if only political correctness—or sheer stupidity—could motivate his detractors.

His starting point is the same as Miller’s. Male homosexuality makes no sense as a reproductive strategy. It should die out for the same reason that the Shakers did (the Shakers were a Protestant sect dedicated to lifelong celibacy). This point might seem obvious. Or maybe not. The following is an exchange between a germ theory critic and Greg Cochran:

Critic: Is it not likely that human sexuality is in fact a bell curve, with "strict homosexual" on one end and "strict heterosexual" on the other end, and the majority of the people falling somewhere in between? (With the caveat that sexual preference and sexual practice are not necessarily the same thing).

Greg: No, it is not likely. Sheesh. That would make exactly as much sense as a bell curve of food preferences ranging from steak at the left to granite at the right, in which people in the middle liked steak and rocks equally well. Is an even split between a behavior that works and one that never does what you expect from biology? Do you expect half the geese to fly north for the winter? (source)

Since natural selection would tend to eliminate male homosexuality, it should be uncommon—like most genetic conditions that impair one’s ability to survive and reproduce.

First we have to say what ‘common’ means, in this context. Common means common compared to the noise in the system. So 1% is very common: no disease caused by random mutations is anywhere near that common. 1 in 10,000 is surprisingly common, but there are one or two mutation-caused diseases that are in that ballpark, like Duchenne’s muscular dystrophy. Turns out that the gene involved in muscular dystrophy is maybe 20 times longer than the typical gene — there are more opportunities for typos. So 1 in 7000 boys have Duchenne’s muscular dystrophy — that’s as common as a ‘system noise’ disease gets. (Cochran 2004?)

Since male homosexuality is not rare, it cannot have a genetic cause, at least not principally. There may be a genetic predisposition (with around 30-45% heritability, according to twin studies), but this predisposition is interacting with something in the environment. And this something cannot be a recent environmental change, since male homosexuality has been around for a long time.

The only remaining cause would be some kind of infectious agent that selectively alters certain parts of the brain while leaving the rest intact. There are precedents for this sort of thing.

Do we know of diseases in which there are very specific targets—in which certain cell types are damaged or destroyed while neighboring cells are left intact? Sure. In some cases, a pathogen targets a particular cell type and has little effect on anything else. Human parvovirus (also known as fifth disease) hits erythroid precursor cells (the cells that manufacture red cells) and temporarily inhibits red cell production. In type-I diabetes, it seems likely that Coxsackie virus infections (in people with a genetic predisposition, in which HLA type plays a major role) trigger an autoimmune disease that gradually (over a year or so) destroys the islet cells which produce insulin. Other cells are not much affected. (Cochran 2004?)

Such pathogens may be more common than we think. The ones that get our attention—that make us go and see a doctor—are the ones that cause discomfort. But those ones may be a small minority of all pathogens, with most of the others flying under the radar. After all, it is in the pathogen’s own interest to be discrete and not cause too much havoc. It needs a healthy home to live in, until it can spread to another host.

Greg also argues that male homosexuality should be less common in smaller communities than in larger ones—where pathogenic transmission is likelier.

We can deduce a few things about the hypothetical agent causing homosexuality. First, it has a small, but not incredibly small, critical community size. That is the size of the clump of people required to keep the agent going. Some agents, ones in which infection results in permanent immunity, need a _large_ number of people, big enough that there are new infected people showing up by the time it circles the community. Measles for example requires almost half a million people in close proximity. An agent that causes a persistent infection can have a very small community size: I'd guess that Epstein-Barr has a CCS under 50.

Since some communities seem to have no homosexuality at all (Bushmen, some hunter-gatherer groups in Indonesia and the Philippines, pre-contact Polynesians) we can be sure that this hypothetical agent has a critical community size larger than that of Epstein-Barr. More like chickenpox, which has a CCS of about 300 people. Not that I'm saying it _is_ chickenpox, mind you. (Cochran 2005)

Finally, this pathogen may selectively alter sexual orientation for reasons that go beyond those of not harming the host too much. There are, in fact, a number of pathogens that alter the host’s behavior in order to enhance their chances of transmission. The protozoan Toxoplasma gondii causes infected rats to lose their fear of cats, thus enabling it to enter a cat body and complete its life cycle (Wikipedia – Toxoplasmosis). The parasitic worm Euhaplorchis californiensis forms cysts in the brains of infected killifish that cause the fish to swim near the surface of the water and make tight turns that show off their glinting sides, thus enabling the worm to enter a bird’s body (Zimmer, 2008).

As a child, I remember being told that a chicken is an egg’s way of making another egg. If Greg Cochran is right, a gay man is a vehicle that a pathogen has constructed for its own survival and reproduction. Everything else is human-centered delusion.

This is an interesting argument, but it has a few holes. First, some genetic conditions do reach incidences that are comparable to that of male homosexuality (about 3-5% of all men). Abnormal hemoglobin variants can reach high incidences in sub-Saharan Africans and other populations (8% in the case of Hb AS among African Americans). These variants are typically maintained through balancing selection where the heterozygote state provides some protection against malaria. Greg acknowledges that such selection exists but sees it as being confined to malaria protection. Yet balancing selection can exist for many other reasons. For example, one in 200 Hopi is albino, apparently because cultural selection offsets the environmental disadvantages of albinism (Hedrick, 2003).

Second, male homosexuality is frequently reported in small communities, including bands of Amerindian hunter-gatherers. Known as ‘berdaches’, these male homosexuals were described by early European explorers and appear to have existed in pre-contact times, as indicated by origin myths (Desy, 1978). One witness was John Tanner, a white captive who lived among the Ottawa of Ontario and then the Ojibwa of Manitoba until 1828:

Some time in the course of this winter, there came to our lodge one of the sons of the celebrated Ojibbeway chief, called Wesh-ko-bug, (the sweet)... This man was one of those who make themselves women, and are called women by the Indians. There are several of this sort among most, if not all the Indian tribes. They are commonly called A-go-kwa, a word which is expressive of their condition. This creature, called Ozaw-wen-dib, (the yellow head), was now near fifty years old, and had lived with many husbands. I do not know whether she had seen me, or only heard of me, but she soon let me know she had come a long distance to see me, and with the hope of living with me. She often offered herself to me, but not being discouraged with one refusal, she repeated her disgusting advances until I was almost driven from the lodge. (Desy, 1978)

Of course, neither point disproves the germ theory of male homosexuality. An infectious agent may indeed be the cause or one of several causes. If we consider the developmental pathway for heterosexual orientation, there is probably a ‘default’ sequence that leads to sexual interest in men and an ‘override’ sequence that leads to sexual interest in women. The second sequence may be disrupted for many reasons: a psychological trauma, a chemical insult, or an infectious agent in combination with a pre-existing genetic predisposition for incomplete masculinization. As one comment noted:

Some of the disruptive factors implicated by empirical evidence are excess prenatal testosterone exposure (a major factor), prenatal stress, and exotic factors such as disruptive chemical agents. Infections proposed by Cochran may also disrupt development, but I do not know of any evidence that supports this assertion as of yet. (Cochran 2005)

References


Cochran, G.M. (2005). Cause of Homosexuality: Gene or Virus? Cochran Interview. Thrasymachus Online.

Cochran, G.M. (2004?). An evolutionary look at human homosexuality. World of Greg Cochran.

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

Désy, P.P. (1978). L'homme-femme. (Les berdaches en Amérique du Nord), Libre — politique, anthropologie, philosophie, 78(3), 57-102.

Hedrick, P.W. (2003). Hopi Indians, “cultural” selection, and albinism. American Journal of Physical Anthropology, 121, 151-156.

Zimmer, C. (2008). The Parasite Files. Discover. Dec. 16.

Origins of male homosexuality

Male homosexuality has always puzzled evolutionary biologists. It has 30-45% heritability, so there must be some genetic predisposition (Bailey et al., 2000). But how could such a predisposition get passed down from generation to generation? It ought to die out, by its very nature.

Well, not all predispositions are fully expressed. This observation led the economist and evolutionary psychologist Ed Miller to propose that male homosexuality has survived by means of a balanced polymorphism (Miller, 2000). In the human species, the male has to invest more in his offspring, particularly if the female is less able to feed herself and her offspring through food gathering, as in non-tropical environments. To change male behavior in this direction, the fastest way, with the least genetic change, is to partially feminize the male brain. This could be done through heterozygote advantage at some gene loci: if only one allele is changed, a man would become more child-oriented while still being heterosexual; if both alleles are changed, he would also become feminized in his sexual orientation.

But heterosis effects are absent at most loci. There is usually a simple dominant/recessive mode of action. Nonetheless, a balanced polymorphism is still possible through additive effects over many loci. If a certain proportion have alleles for mental feminization, a man will take more interest in his children without becoming feminized in his object of sexual interest. There may, however, be more than one ‘right’ mix of feminization/non-feminization alleles (the number of possible permutations being a function of the number of relevant genes). Even if all men in one generation have the right mix, reshuffling of genes from their generation to the next would produce some male offspring who are too feminized and others not enough.

Of course, this situation would be gradually corrected by natural selection. The ‘right’ mixes would not be exactly equal in their adaptive value. Natural selection would tend to favor some over others and eventually there would be fixation of one mix of alleles. But this would take a long time and paternal investment varies in importance even among the relatively young populations of Homo sapiens—itself a young species.

So this is Miller’s theory: male homosexuality is the tail end of a balanced polymorphism due to selection for men who invest more in rearing their children and provisioning their families. Santtila et al. (2009) tried to test this theory, which they describe as follows:

Miller (2000) speculates that if a typical man inherits only a few of the alleles partially preventing androgenization, he would express more kindness, sensitivity, tendermindedness, and empathy. Only occasionally would a sufficient number of these alleles come together to produce homosexuality. Heterosexual carriers of these alleles would be better fathers and more attractive mates as men with such traits are less likely to harm their partner or children (Miller, 2000). These traits in men would help them to attract women and, thus, lead to greater reproductive success, ensuring the survival of the alleles in the gene pool. A heterosexual man without any of these alleles would exhibit traits such as ruthlessness, selfishness, insensitivity, and cruelty, making them unattractive to women.

This isn’t quite what Miller had in mind. Yes, a heterosexual carrier would be less likely to harm his partner and children, but a more critical factor would be his willingness to provide for them. Nor is it necessary to assume that such men are preferred as mates. Their greater reproductive success would come from the higher survival rate of their children. We’re talking natural selection here, not sexual selection.

This misunderstanding affected Santilla et al.’s experimental design. Heterosexual men with homosexual brothers were questioned on a wide range of behaviors: psychopathy, sexual aggression, sexual coercion, sexual activity, and number of children. No questions were asked about interest in children or willingness to care for them. Number of children might inversely correlate with paternal investment (some could die through neglect or insufficient care), but only if there are enough of them. Nowadays, family size is too small for this factor to be significant. Indeed, the heterosexual subjects had each fathered less than one child on average.

No significant differences were found between the heterosexual ‘carriers’ and a control heterosexual group. But it’s not clear to me that a difference should be expected, given the experimental design.

References

Bailey, J.M., M.P. Dunne, & N.G. Martin. (2000). Genetic and environmental influences on sexual orientation and its correlates in an Australian twin sample. Journal of Personality and Social Psychology, 78, 524-536.

Miller, E.M. (2000). Homosexuality, birth order and evolution: Toward an equilibrium reproductive economics of homosexuality. Archives of Sexual Behavior, 29, 1-34.

Santtila, P., A-L. Högbacka, P. Jern, A. Johansson, M. Varjonen, K. Witting, B. von der Pahlen, N. K. Sandnabba. (2009). Testing Miller’s theory of alleles preventing androgenization as an evolutionary explanation for the genetic predisposition for male homosexuality. Evolution and Human Behavior, 30, 58-65.

Bernard Arcand R.I.P.

The anthropologist Bernard Arcand passed away last Friday at the age of 63. He was one of my favorite professors at Laval, probably because he was among the least ideological ones. He avidly read the works of different Marxist writers but never considered himself to be one. In fact, he often criticized the unconscious Marxism that had seeped into much of anthropology, particularly the tendency to classify different populations by their mode of subsistence, notably hunter-gatherers versus agriculturalists. He would point out to us the artificiality of this distinction, and how there was just as much difference within these two categories as between them. In comparison to most agriculturalists, some hunter-gatherers were actually more sedentary, others more densely populated, and others still less egalitarian.

The Calusa of southern Florida formed a society divided into classes, lived in villages that could hold over 2,000 people, built temples, and kept an army that ensured the payment of tribute needed for a hierarchical system of local chiefdoms. This social complexity and these unequal social relations were supported by a hunting and gathering economy. (Arcand, 1988, p. 43)

According to Bernard, this unconscious Marxism reflected an economic determinism that was equally popular on the left and the right.

… an emergent industrial ideology ... succeeded, mainly in the 19th century, in postulating that the economy has an autonomous status and should be seen as the ultimate determinant of society and culture. The argument is already well known and need not be repeated. Industrial capitalism and its socialist critics affirmed the crucial determining role of the development of productive forces, which would ensure rising productivity and be a key condition for progress and happiness. Despite the radical contrast between their political programs and goals, capitalism and socialism wanted to take over the same producing machine. More humbly placed, the anthropology of hunter-gatherers could not easily claim that everyone was wrong and that this was all just secondary. So it went on pretending that the mode of subsistence was what mattered. (Arcand, 1988, p. 52)

Bernard was also a man of letters who wrote not only academic articles but also readable essays for the public at large, such as Abolissons l'hiver and an essay on pornography called Le jaguar et le tamanoir. His analysis was striking in its originality. To be sure, his works suffered from one shortcoming: very few of them have been translated into English.

He will be missed.

Reference

Arcand, B. (1988). Il n’y a jamais eu de société de chasseurs-cueilleurs. Anthropologie et Sociétés, 12, 39-58.