What Causes (Male) Homosexuality?

My initial inspiration for starting this blog was a brief piece I had written about why Lady Gaga’s song, “Born This Way”, really got under my skin. The general premise of the song is, unless I’m badly mistaken, that homosexuality is genetic in nature, and, accordingly, should be socially accepted. The song is full of very selective logic and a poor grasp of the state of scientific knowledge, all of which is accepted in the service of furthering a political goal. For what it’s worth, I agree with that goal, but the means being used to achieve it in this case were misguided because:

“…I’m not so sure Lady Gaga – or any gay-rights supporter – wants to base their claims to equal rights on the supposition that homosexuality is a trait people are “born” with…If further research uncovers that people can come to develop a homosexual orientation for a number of reasons that have nothing to do with being “born like that”, I wouldn’t want to see the argument for equal rights slip away.”

Today, I’m going to be stepping back into that same political minefield that I did on the topic of race, and discuss a hypothesis regarding the cause of male homosexuality that some people may not like. People will not like this hypothesis for reasons extrinsic to the hypothesis itself, but do your best to contain any moral outrage you may be feeling. My first task in presenting this hypothesis will be to convince you that male homosexuality is not genetically determined – despite what an eccentric young pop-star might tell you – and is also not an adaptation.

Convincing critics is always such a pleasure.

For some, it might seem insulting that homosexuality requires an explanation, whereas heterosexuality does not. Aren’t both just different sides of a very bisexual coin? There’s a simple answer to that concern: heterosexual intercourse is the only means to achieve reproduction. An exclusive homosexual orientation is the evolutionary equivalent to sterility, and if three to five percent of the male population was consistently sterile – despite neither of anyone’s parents being sterile, by definition – that would raise some questions as to how sterility persists. There would be an intense selective pressure away from sterility, and any genes that actively promoted it would fail to reproduce themselves. That homosexuality seems to persist in the population, despite it being a reproductive dead-end, requires an explanation. Heterosexuality poses no such puzzle. 

The first candidate explanation for the persistence of homosexuality is that it’s part on an adaptation for assisting the reproduction of one’s kin. While homosexuals themselves may suffer a dramatic reduction in their lifetime reproduction, they activity assist other genetic relatives, delivering enough benefits to offset their lack of personal reproduction, similar to how ants or bees would assist the queen, forgoing reproduction themselves. This suggestion is implausible on three levels: first, it would require that homosexuals deliver enormous benefits to their relatives. For each one child a gay man wouldn’t have, they would need to ensure a brother or sister would have an additional two that they wouldn’t otherwise have without those benefits. This would require an intense amount of investment. Second, there’s no theoretical reason that’s ever been provided as to why homosexuals would develop a homosexual orientation, as opposed to, say, an asexual orientation. Seeking out intercourse with same-sex individuals doesn’t seem to add anything to the whole investment thing. Finally, this explanation doesn’t work because, as it turns out, homosexuals don’t invest anymore in their relatives than heterosexuals do (Rahman & Hull, 2005). So much for kin selection.

A second  potential explanation for homosexuality is that it’s the byproduct of sexually antagonist selection; a gene that damages the reproductive potential of males persists in the population because the same trait is beneficial when it’s expressed in female offspring (Ciani, Cermelli, & Zanzotto, 2008; Iemmola & Ciani, 2009). Another potential explanation is that a homosexual orientation is like sickle cell anemia: while it hurts the reproductive prospects of those who express it, it provides some unspecified benefit that outweighs that cost in some carriers, as sickle cell protects against malaria. Both explanations have a large issues to contend with but one of the most prominent shared issues is this: despite both hypotheses resting on rather strong genetic assumptions, half or more of the variance in male homosexual orientation can’t be attributed to genetic factors (Kirk et al., 2000; Kendler et al., 2000). Identical twins don’t seem to be concordant for their sexual orientation anymore than 30 to 50% of the time when one of the twins identifies as non-heterosexual. If homosexuality was determined solely by genes, there should be a near complete agreement. 

In fact, most of the variance appears to be due to our decadent Western lifestyle. Who knew, right?

Accordingly, any satisfying explanation for homosexuality needs to reference environmental factors, as all traits do; the picture is far from as crude as there being some genes “for” homosexuality. While there clearly are some genetically inherited components in the ontogeny of a homosexual orientation, it’s entirely unclear what those genetic factors are. It’s also far from clear how those genetic factors interact with their environment – or when, for that matter. They would seem to act sometime before puberty, but beyond that the door is open. What seems to have been established so far is that an exclusive homosexual orientation is detrimental to reproduction in a big way, and these costs are not known to be reliably offset.

There is one last hypothesis that may hold some potential, though, as I mentioned, I suspect many people won’t like it: the “gay germ” theory. The general idea is that some outside pathogen – be it a bacteria or a virus – manipulates development in some way, the end result being a homosexual orientation. This hypothesis seems to have potential for a number of reasons: first, it neatly deals with why homosexuality persists in the population, despite the massive reproductive costs. It could also account for why monozyogtic twins are often discordant for homosexual orientation, despite sharing genes and a prenatal environment. As of now, it remains an untested theory, but other lines of research suggest some preliminary success using the same basic idea to understand the persistence of disorders like schizophrenia and obsessive compulsive disorder, among many others. Of course, such a theory does come with some political baggage and questions.

Like: will two gay men ever be able to hold hands, post love-making, on top of an American flag, just like straight couples do?

The first set of questions concern the data speaking to the hypothesis: what pathogen(s) are responsible? When do they act in development? How do they alter development? Are those alterations an adaptation on the part of the pathogen or merely a byproduct? These are no simple questions to answer, especially because it won’t be clear which children will end up gay until they have matured. This makes narrowing the developmental window in which to be looking something of task. If concordance rates for monozyogtic twins are similar between adopted and reared together twins, that might point to something prenatal, depending on the age at which the twins were separated, but would not definitively rule out other possibilities. Further, this pathogen need not be specific to gay men; it could be a pathogen that much of the population carries, but, for whatever reason, only affects a sub-group of males in such a way that they end up developing a homosexual orientation.        

The second set of questions concern potential implications of this theory, were it to be confirmed. I’ll start by noting these concerns have zero, absolutely nothing, to do with whether or not the gay germ theory is true. That said, these concerns are probably where most of the resistance to the hypothesis would come from, as concerns for data (or lack thereof) are often secondary to debates. Yes, the hypothesis cries out for supporting data so it shouldn’t be accepted just yet, but I’m talking to those people who would reject it as a possibility out of hand because it sounds icky. In terms of gay rights and social acceptance, it shouldn’t matter whether homosexuality is 100% genetically determined, caused by a pathogen, or just a choice someone makes one day because they’re bored with all that vanilla heterosexual sex they’ve been having. That something may be, or is, caused by a pathogen should really have no bearing on it’s moral status. If we discovered tomorrow that it was a virus that caused men to have larger-than-average penises, I doubt many people would cheer for the potential to cure the “disease” of large-penis.         

References: Ciani, A.C., Cermilli, P., & Zanzotto, G. (2008). Sexually antagonistic selection in human male homosexuality. PLosone.org, 3, e,2282.

Iemmola, F. & Ciani, A.C. (2009). New evidence of genetic factors influencing sexual orientation in men: Female fecundity increase in the maternal line. Archives of Sexual Behavior, 38, 393-399

Kendler, K.S., Thornton, L.M., Gilman, S.E., & Kessler, R.C. (2000). Sexual orientation in a U.S. national sample of twins and nontwin sibling pairs. American Journal of Psychiatry, 157, 1843-1846

Kirk, K.M., Bailey, J.M., Dunne, M.P., & Martin, N.G. (2000). Measurement models for sexual orientation in a community twin sample. Behavior Genetics, 30, 345-356

Rahman, Q. & Hull, M.S. (2005). An empirical test of the kin selection hypothesis for male homosexuality. Archives of Sexual Behavior, 234, 461-467 

Do “Daddy Issues” Jumpstart Menstruation?

Like me, most of you probably come from the streets. On the streets, it’s common knowledge that “daddy issues” are the root cause of women developing interests in several activities. Daddy issues are believed to play a major role in becoming a stripper, developing a taste for bad boys, and getting  a series of tattoos containing butterflies, skulls, and/or quotes with at least one glaring spelling mistake. As pointed out by almost any group in the minority at one point or another, however, that knowledge is common does not imply it is also correct. For instance, I’ve recently learned that drive-bys are not a legitimate form of settling academic disagreements (or at least that’s what I’ve been told; I still think it made me the winner of that little debate). So, enterprising psychologist that I am, I’ve decided to question the following piece of folk wisdom: is father absence really a causal variable in determining a young girl’s life history strategy, specifically with regard to the onset of menstruation?

Watch carefully now; that young boy may start to menstruate at any moment… wait; which study is this?

First, a little background is order. Life history theory deals with the way an organism allocates its limited resources in an attempt to maximize its reproductive potential. Using resources to develop one trait precludes the use of those same resources for developing other traits, so there are always inherent trade-offs that organisms need to make during development. Different species have stumbled upon different answers as to how these trade-offs should be made: is it better to be small or large? Is it better to start reproducing as soon as possible or start reproducing later? Is it better to produce many offspring and invest little in each, or produce fewer offspring and invest more? These developmental and behavioral trade-offs all need to be made under a series of ecological constraints, such as the availability of resources or the likelihood of survival. For instance, it makes no sense for a convict to refuse a final cigarette before a firing squad executes him out of concerns for his health. There’s no point worrying about tomorrow if there won’t be one. On the other hand, if you have a secure future, maybe Russian roulette isn’t the best choice for a past time.

So where do family-related issues enter into the equation?  Within each species, different individuals have slightly different answers for those developmental question, and those answers are not fixed from conception. Like all traits, their expression is contingent on the interaction between genes and the environment those genes find themselves in. A human child that finds itself with severely limited access to relevant resources is thus expected to alter their developmental trajectory according to their constraints. This has been demonstrated to be the case for obvious variables like obtaining adequate nutrition: if a young girl does not have access to enough calories, her sexual maturation will be delayed, as her body would be unlikely to successfully support the required investment a child brings.

Another of these hypothesized resources is paternal investment. The suggestion put forth by some researchers (Ellis, 2004) is that a father’s presence or absence signals some useful information to daughters regarding the availability of future mating prospects. The theory that purports to explain this association states that when young girls experience a lack of paternal investment, their developmental path shifts towards one that expects future investment by male partners to be lacking and not vital to reproduction. This, in turn, results in more sexual precociousness. Basically, if dad wasn’t there for you growing up, then, according to this theory, other men probably won’t be either, so it’s better to not develop in a way that expects future investment. That father absence has been associated with a slightly earlier onset of menarche (first menstruation) in women has been taken as evidence supporting this theory.

The basic concept also spun off into a show on MTV.

The major problem with this suggestion is that no causal link has been demonstrated. The only thing that has been demonstrated is that father absence tends to correlate with an earlier age of menstruation, and the degree to which the two are correlated is rather small. According to some correlations reported by Ellis (2004), it looks as if one could predict between 1 to 4% of the variance in timing of pubertal development on the basis of father absence, depending on which parts of the sample is under discussion. Further, that already small correlation does not control for a wide swath of additional variables, such as almost any variables that are found outside the home environments. This entire social world that exists outside of a child’s family has been known to have been of some (major) importance in children’s development, while the research on the home environment seems to suggest that family environments and parenting styles don’t leave lasting marks on personality (Harris, 1998).

As the idea that outside the home environments matter a lot has been around for over a decade, it would seem the only sane things for researchers to do are more nearly identical studies, looking at basically the same parenting/home variables, and finding the same, very small to no effect, then making some lukewarm claim about how it might be causation, but then again might not be. This pattern of research is about as tedious as that last sentence is long, and it plagues psychological research in my opinion. In any case, towards achieving that worthwhile goal of breaking through some metaphorical brick wall by just running into it enough times, Tither and Ellis (2008) set out to examine whether the already small correlation between daughter’s development and father presence was due to a genetic confound.

To do this, Tither and Ellis examined sister-pairs that contained both an older and younger sister. The thinking here is that it’s (relatively) controlled for on a genetic level, but younger sisters would experience more years of father absence following the break-up of a marriage, relative to the older sisters, which would in turn accelerate sexual maturation of the younger one. Skipping to the conclusions, this effect was indeed found, with younger sisters reporting earlier menarche than older sisters in father absent homes (accounting for roughly 2% of the variance). Among those father absent homes, this effect was carried predominately by fathers with a high reported degree of anti-social, dysfunctional behavior, like drug use and suicide attempts (accounting for roughly 10% of the variance within this subset). The moral seems to be that “good-enough” fathers had no real effect, but seriously awful parenting on the father’s part, if experienced at a certain time in a daughter’s life, has some predictive value.

So you may want to hold off on your drug-fueled rampages until your daughter’s about eight or nine years old.

First, let me point out the rather major problem here on a theoretical level. If the theory here is that father presence or absence sends a reliable signal to daughters about the likelihood of future male investment, then one would expect that signal to at least be relatively uniform within a family. If the same father is capable of signaling to an older daughter that future male investment is likely, and also signaling to a younger daughter that future male investment isn’t likely, then that signal would hardly be reliable enough for selection to have seized on.

Second, while I agree with Tither and Ellis that these results are consistent with a casual account, they do not demonstrate that the father’s behavior was the causal variable in any way whatsoever. For one thing, Ellis (2004) notes that this effect of father presence vs absence doesn’t seem to exist in African American samples. Are we to assume that father presence or absence has only been used as a signal by girls in certain parts of the world? Further, as the authors note, there tend to be other changes that go along with divorce and paternal psychotic behavior that will have an effect on a child’s life outside of the home. To continue and beat what should be a long dead horse, researchers may want to actually start to look at variables outside of the family to account for more variation in a girl’s development. After all, it’s not the family life that a daughter is maturing sexually for; it’s her life with non-family members that’s of importance.

References: Ellis, B.J. (2004). Timing of pubertal maturation in girls: An integrated life history approach. Psychological Bulletin, 130, 920-958

Harris, J.R. (1998). The Nurture Assumption: Why Children Turn Out The Way They Do. New York: Free Press

Tither, J.M., & Ellis, B.J. (2008). Impact of fathers on daughters’ age at menarche: A genetically and environmentally controlled sibling study. Developmental Psychology, 44, 1409-1420/