A Rebuttal to the A Priori Argument Against a Genetic Basis for Homosexuality

In recent years there has been a lot of hoopla as a seemingly endless list of genes "for" various things have been reported. We have heard that there are genes for obesity, genes for depression, genes for reading ability and all sorts of other behavioral traits. One of the more controversial claims has been claims that a gene for homosexuality has been discovered.

Much of the controversy is scientific. It is notoriously difficult to accurately map human behaviors to genetic components and there have been methodological challenges to this claim. This is, ultimately, an empirical question with a great many complicating factors and methodological hurdles. The scientific community has not reached a consensus on this claim and it is unlikely that any consensus will be reached in the near future.

It is not the purpose of this essay to address the scientific question. I will leave that to the experts. Many of the objections, however, are not scientific. One objection, in particular, attempts to make an a priori argument against the very possibility of a so-called "homosexual gene" using a spurious evolutionary argument. The argument can be aptly summarized by the claim that any homosexual gene would have disappeared from the population long ago since homosexuals don't reproduce.

On the face of it, the argument seems convincing. As far as genetics is concerned, there is no difference between dying in your crib and being a childless person who lives to the age of a hundred. So long as you fail to reproduce, your body is a genetic graveyard. Since homosexual sex does not result in offspring, it would seem logical, then, that homosexuality would have been bred out of the populace. I will demonstrate that there are several flaws with this argument.

The first problem is that homosexuality does not preclude the possibility of reproductive activity. In modern times, homosexual individuals can have children by utilizing a variety of technological solutions. Gay men can donate their sperm or find a surrogate mother. Lesbian women have a variety of in vitro and in utero options. Beyond that, there is nothing that physically prevents homosexuals from engaging in heterosexual acts. Indeed, in social climates where homosexuality is criminalized or where there is strong social pressure to conform to heterosexual norms, it is not at all uncommon for homosexuals to conform to heterosexual norms up to and including marriage and parenthood. In such a climate (which has been sadly common throughout history), even if the view of genetics that this argument projects were to obtain, any hypothetical genes for homosexuality would have few barriers to propagation. That said, the a priori argument does employ a naïve understanding of population genetics.

For the basis of this examination, let us consider a hypothesized homosexual gene to be reproductively deleterious (this isn't necessarily the case, but we'll return to that point later). It is critically important to stress that such an evaluation is not a moral judgment but, rather, a neutral statement that only pertains to the reproductive impact that such a hypothesized gene would have. In order to assist our efforts to think of this subject in morally neutral terms, I will not discuss how a gene for homosexuality could propagate itself in a population. I will, instead, discuss a hypothetical S gene that results in sterility. In point of fact, there are a variety of genetic conditions that lead to sterility but, for the purposes of this essay, they can all be subsumed under the common label.

How can a gene which compromises reproduction spread through a population? It would seem that the very first instance of the gene should eliminate itself through an act of genetic suicide. This would only be the case, however, if the presence of a gene invariably resulted in the physical expression of that gene. The technical terms for an organism's genetic structure is its "genotype". The term to describe an organism's physical structure is its "phenotype". Genotype does not equal phenotype. At best, an organism's genotype is an indicator of that organism's phenotype. Simply because I have the S gene, however, does not mean that I will necessarily be sterile.

How can this be? There are several reasons that this could be the case.

The first reason is that there are two different varieties of gene: dominant and recessive. A given gene will occupy a particular location on a chromosome called an allele. In humans (and most other organisms) each allele is occupied by a pair of genes with each half of the pair being inherited for each parent. A given gene will always have a phenotypic expression (meaning that it will be physically manifested) if it is dominant. A recessive gene, on the other hand, will only manifest if it is present in both slots of the allele.

To take a classic example, we'll use a gene for Brown eyes (designated with a capital B) and blue eyes (designated by a lower case b). Let us say that you have double-dominant set of genes for brown eyes (BB) and your partner has the double-recessive genes for blue eyes (bb). Let us further suppose that you have four children. Statistically, your children will receive the following gene combinations: Bb, Bb, bB, bB. Because brown is dominant, all four children will have brown eyes; however, each of them will carry a gene for blue eyes.

Let us suppose, now, that one of your children (Bb) marries a person who also have a dominant brown gene and a recessive blue gene (Bb). Statistically, your children will receive this combination: BB, Bb, bB, bb. Only the child with the bb gene combination will have blue eyes (although an additional two children will continue to carry the recessive genes for blue eyes.

If sterility were to be carried on a recessive gene, it could persist in the gene pool indefinitely in spite of the fact that it conferred a reproductive disadvantage. It is important to stress that, even though it would be allowed to persist, there would a critical population threshold above which an anti-reproductive gene would be selected against. Scandinavians are famed for having blue eyes. This is because their population has an abundance of the recessive genes that confer blue eyes. Since there is no reproductive disadvantage, such a bias in population is allowed. You would not, however, expect to find an equivalent population where an S gene had a majority representation in the populace.

There is, however, one way that an S recessive could positively leverage itself into future generations. This is via the mechanism of kin selection. The easiest way for a gene to get into the next generation is directly. This is why the sex instinct is so strong. When we have children, each child carries 50% of our genes into the next generation. So what happens if we can't have children? The solution is that we turn to our relatives. If you have brothers and sisters, each of them also has a 50% genetic relation to you. Any nephews or nieces you have will have a 25% relation. This isn't as high as your own children would be but, if you can't have children of your own, any additional assistance you could provide to your siblings to help them raise your nephews and nieces will be to your genetic advantage.

The elegant thing about this supposition is that we don't have to even suppose that the S gene would directly encourage you to devote your efforts to your sibling's children. So long as you have a general instinct to expend more effort on your closest relatives when you, yourself, are reproductively disadvantaged, such an instinct would be positively selected for. After all, genes aren't the only reasons one may be unable to reproduce. Circumstances alone (e.g., accidental castration) guarantees that a certain percentage of any given generation will be unable to reproduce regardless of genetics. As such, a kin assistance instinct would represent a good genetic strategy regardless. If humans do have such an instinct (and it must be stressed that this is speculative), any sort of recessive S gene would automatically result in efforts to assist non-manifesting copies of itself in near relatives even if the S gene were entirely deleterious for the individual who was carrying it.

Beyond this, the simple "pea pod" Mendelian model, where a single set of genes accounts for all of the genetic variance in a population, is, itself, typically an oversimplification. There is not, for instance, a single tall gene and a single short gene that determines whether one is short or tall. In reality, height is determined by a complex of different genes interacting in tandem (along with a variety of environmental factors, but let's not get ahead of ourselves). This is how things work in most cases of phenotypic expression. Instead of P = G (for every phenotype there is one and only one gene), P = G1, G2, G3… (for every phenotype there are multiple genes). Because of this, it is possible for certain combination of genes to result in anti-reproductive outcomes (e.g., sterility or premature death) while other gene combination are either neutral or reproductively advantagous.

Let us suppose, for the sake of argument, that sterility expresses itself only when four particular genes manifest. Let us further suppose that these four genes have reproductively beneficial manifestations when teamed up with most other alternative sets of genes. In such a schema, not only could these genes persist in spite of the occasional drawback of producing a non-reproducing individual but they could, in fact, be positively selected for because the majority of the time they would give a reproductive advantage to the person that they would find themselves in.

This is a bit like playing an odd game of poker where four aces result in a busted hand. Two aces or three aces would still make for a good hand (as would aces and kings or the aces in a full house, a straight or a flush). Even though four aces would be a "bad" hand, any other combination would be desirable and advantageous.

Beyond this, the path from gene to phenotype is not inevitable. The way that genes "build" bodies is through the production of proteins (with the help of RNA). Every gene encodes in the instructions for building a particular protein. Between the production of proteins and the production of bodies, there are a number of critical steps. During fetal development, various chemical cascades are turned on or off or modified according to the activation and deactivation of various chromosomes. This is a complex process that can often be very fuzzy. This is the reason that geneticists rarely say that gene X determines phenotype Y. Rather, they may say that particular genes result in a predilection for the presence of certain phenotypes. The predilection may be strong or weak but it is rarely absolute.

Take sex as an example. Most of us have been taught that boys have a Y chromosome and that girls don't. In the vast majority of cases, this is true. It is not, however, inevitable. Even discounting intersexual births (where a child is born with indeterminate genitalia) it is possible for a child with a Y chromosome to be born a female and, likewise, for a child who has two X chromosomes to be born a male. In most children, the Y chromosome signals the activation of testosterone production at a critical junction of fetal development. In some births, the signal either fails to go off (a false negative) or it goes off spuriously (a false positive).

If something as strong as sexual determination can only be considered a strong statistical likelihood, it should not surprise us that something as subtle as a behavioral gene could be present without manifesting itself. Even if the supposed S gene were dominant and even if it always resulted in an absence of reproduction when manifested, it would still be possible for non-sterile individuals to carry it forward into the next generation. If there was only a weak predilection, this would actually be the expected case.

Nor do potential environmental impacts end at the womb. Take left handedness as an example. Handedness is believed to have a strong genetic component. Never the less, for years left handedness was considered to represent a kind of moral failing (hence the word "sinister" which is a Latinate form of the word "left"). Because of this immoral reputation, children who exhibited left handed behavior were often sternly corrected (typically with a ruler) and encouraged to use their right hands. Such efforts did not always produce right handed behavior but the success rate (if we can use the word success in reference to such a practice) was sufficiently high that the practice remained in vogue for many years.

Environmental effects do not have to be coercive, either. Consider a predisposition to obesity. Even though an individual may have such a predisposition, it may not manifest itself unless they are exposed to certain foods or dietary conditions. A person with a predisposition to melanoma may not develop skin cancer unless they are exposed to greater than average amounts of UV radiation. Indeed, some genetic predispositions may only manifest spontaneously and at random. As such, perhaps only 25% of individuals with the S gene would actually become sterile (and, then, perhaps only the ones that have consumed high quantities of beta carotene or been exposed to high levels of environmental arsenic).

As we can see, even though it seems intuitive that a gene which would cause sterility would eliminate itself from the population in short order, the truth is that there are a multitude of avenues whereby it can find its way into further generations. Exchanging our S gene for a homosexual gene (or gene complex), we can see that a priori arguments that propose to establish the impossibility of such a gene are based on a fallacious understanding of both genetics as well as the sociological and medical realities.

As I stated earlier, the question or whether or not such genes exist is an empirical question. As such, the question can only be decided by a judicious application of scientific methodology. Philosophical and ideological objections are irrelevant to the question. Likewise, it must be cautioned that while science may be able to answer the empirical question, it is not capable of addressing the moral and theological questions that surround the issue of homosexuality. The absence of such a gene (or genes) can not logically be used to condemn homosexuality but neither can its existence be used to validate it. To do either would be to engage the Naturalistic Fallacy to the benefit of no one. We should be aware of the facts and realities of nature, of course, but what we do with those facts is a different question altogether.