event merely prompts their curiosity about the cause behind this cause, and the cause behind that cause, and so on. After being beaten into submission by the barrage of questions, realizing that the child has a point and that the mysteries of the universe are often unknowable to children and adults alike, a parent may resort to the ambiguous, end-all answer: “Well, just because, dear….”
Subdisciplines of philosophy and psychology are devoted to how we determine causes—how we know what we know in
What is a cause? We may think of a cause as something that gives rise to an event or phenomenon. In other words, causes deal with the
Causes can also be distinguished by their level of analysis: micro versus macro.
Also, we can focus on causes at different spots along a very long timeline. Some causes are more immediate or proximal in nature; that is, closer in time to the event itself. Most causes offered up by biologists, psychologists, and sociologists are of this nature. Some causes are distal in nature—that is, further away in time from the event itself. Causes from a historical or evolutionary perspective can be distal in nature. Historical causes can be considered distal because they occurred in the distant past, perhaps many centuries ago. Evolutionary explanations are distal because they concentrate on why a phenomenon, such as asexuality within humans, may have evolved during a time in the natural history of the species, and/or why this phenomenon may have conferred an adaptive advantage (or at least not a disadvantage) across time. Some causes are so distal as to be construable as “ultimate.” Thus, one might argue that the Big Bang or God is the ultimate or first cause of everything, including human asexuality. Such ultimate causes may be correct in a broad sense, but they are often not particularly useful in the science of understanding current events or in understanding differences between people in the here and now.{Like micro and macro causes, distal and proximate causes are not necessarily incompatible, as they can also coexist at different points along a (potentially very long) causal stream or pathway for a given phenomenon. For example, an evolutionary cause of gender differences in sexuality is that during human evolution, men and women developed different mating strategies. Women developed a more cautious mating strategy to maximize their large parental/reproductive investment (relatively few eggs, nine months of gestation). Men developed a more risky and indiscriminate mating strategy to maximize their small parental/reproductive investment (cheap, replaceable sperm). A compatible proximate explanation is that these different mating strategies are caused by hormone levels affecting sex drive, with women exhibiting lower levels of testosterone and a lower sex drive than men. Sometimes evolutionary causes are construed as the
I have already mentioned two distal causes of asexuality. In chapter 3, I suggested that some historical eras—for example, the Victorian era in Britain—may have caused elevated rates of asexuality in certain individuals (e.g., upper-class women). One could expand on such distal explanations, if one were a historian (which I am not), and do an in-depth analysis of different eras and their roles in causing different prevalence rates of asexuality.{As mentioned, historical causes would also constitute more of a macro- than a microanalysis.}
Another relatively distal cause of asexuality is the evolutionary process. One of the great evolutionary puzzles of sexology, aside from why sex exists (see chapter 3), is why homosexuality exists, given that it is partly genetically based and has existed over time and across cultures. As I discussed in chapter 11, the answer may have to do with kin selection. If, for example, a “man-loving” gene is expressed not only in a gay man but also in his female relatives, it may confer a reproductive advantage on the latter, making his sisters particularly fertile and thus increasing the replication of the family’s genes. Alternatively, a gay gene (i.e., a genetic predisposition to same-sex attraction) may be of some advantage to an individual because, under certain environmental circumstances, it may be associated with helping relatives’ children (e.g., nephews and nieces) survive and reproduce. In both cases, then, “gay genes” may exist because they serve to replicate one’s broader gene pool (i.e., kin).
Asexuality may also be an evolutionary puzzle in need of a solution, assuming it also has a genetic basis across time. Perhaps asexuality “genes” are also conserved throughout evolutionary time because of kin-selection mechanisms. Thus, it would be interesting to examine in a research study if asexual people give, on average, elevated care for their siblings’ children, thus potentially offsetting their reduced sexual reproduction by such kin- enhancement strategies.{This is not to imply that this would be a “conscious” strategy.}
Speaking of genetics and asexuality, no studies thus far have tested for this linkage directly. Indirect evidence is all we can rely on at this point: no studies have ever examined asexuality as a trait and its “concordance” or similarity between identical (as compared to fraternal) twins, a common methodology used to determine if variation in a trait is partly genetically based. Moreover, no one has ever isolated a specific gene directly associated with asexuality.
But let’s discuss some plausible genetic candidates affecting asexuality. In chapter 6, we discussed the role of certain X-linked (female) or Y-linked (male) genes in sexual differentiation. Some of these genes may play a key role in the prenatal development of the brain. Some of these gene effects on prenatal development are also independent of hormonal effects. In other words, they may directly affect the structure or organization of brain cells associated with sexual attraction. These genes, however, are not well studied. Some other sex-linked genes are well studied and have been clearly shown to affect hormones and their impact on sexual differentiation. For example, the SRY gene allows for the development of the testes, which produce hormones during prenatal and postnatal development. There are also other “hormone-related” genes. For example, the androgen receptor (AR) gene is important in determining how hormones affect the body and the brain. As you may recall, receptors are specialized parts of the cell that receive and activate a hormone molecule, and androgens (testosterone in particular) affect sex drive and prenatally organize sites in the lower brain related to gender, sexuality, and attraction. Variation in the AR gene likely affects the person’s level of sensitivity to testosterone. Interestingly, variation in the AR gene has been implicated in male-to-female transsexualism (Hare et al., 2009), and there is evidence that asexuality is associated with elevated rates of atypical gender identity (see also chapter 6). There is also evidence that variation in the AR gene might influence the age at which puberty begins (Comings, Muhleman, Johnson, & MacMurray, 2002), and there is evidence that the age of first menstruation (menarche) is, on average, later in asexual women than in sexual women (Bogaert, 2004). Finally, one of the explanations for asexuality in animals is an alteration in the receptors for testosterone (see also chapter 3). In sum, this research suggests that variations in the AR gene may underlie (or least predispose someone to) asexuality.
Genes underlying receptors for other hormones, including estrogens (e.g., estradiol), may also be involved in the causes of asexuality. Estrogens, among other functions, help regulate women’s menstrual cycle,{Estrogens