Needless to say, this would be especially mischievous given the presumed role of the testes as the biological wellspring of the hormonal essence of masculinity—that steroid tsunami that destroys all hopes of sex equality. As Wayne State University law professor Kingsley Browne recently put it:
Despite the frequent assertion that the gaps that favor men (although not those that favor women) are results of invidious social forces, the truth seems to be somewhat more basic. If the various workplace and non-workplace gaps could be distilled down to a single word, that word would not be “discrimination” but “testosterone.”2
In much the same way, economists who suggest that inherent sex differences in risk taking play a major role in economic and occupational inequalities sometimes finger testosterone as the biological culprit.3 And according to neuroscientist Joe Herbert, author of Testosterone: Sex, Power, and the Will to Win, “the testis is the source of most of what we term masculinity.”4 This is apparently because the testosterone it produces “prepares males for the rigorous and competitive events of reproduction.” Thus, he writes:
Testosterone has to do a great many things: it must influence physique; act on the brain; and inflame sexuality. But this hormone also makes males enjoy taking risks, resorting readily to competitiveness and aggression to obtain what they need, seeking domination over other males, resenting and repelling invasion of their territory.”5
That’s a big portfolio.
Science writer and behavioural endocrinologist Richard Francis coined the term “Testosterone Rex” to poke fun at the mistaken conception of testosterone as a “super-actor”—the “plenipotent executor of selection’s demands” that simply “takes care of everything.”6 Certainly, if the problem to be taken care of is how to create two kinds of individual, then testosterone as a plenipotent super-actor offers a neat and obvious solution. While scientific views on T’s role in social behaviour vary around the edges, they generally point to a link with competition as key.7 Most obviously, this refers to competition to acquire or defend social status, material resources, and sexual opportunities. However, it should also probably include a facet of parenting—protection of that most precious resource, offspring, argues University of Michigan social neuroendocrinologist Sari van Anders. Low T, by contrast, is linked with nurturance.8 So according to a T-Rex view, high-T individuals cluster at the competitive end of the continuum with the other aggressive, sexually inflamed risk takers, while low-T characters huddle at the duller but safer and more caring opposite pole.
Consider, for example, a cichlid fish known as Haplochromis burtoni that comes from the lakes of East Africa.9 In this species, only a small number of males secure a breeding territory, and they are not discreet about their privileged social status. In contrast to their drably beige non-territorial counterparts, territorial males sport bold splashes of red and orange, and intimidating black eye stripes. The typical day for a territorial male involves a busy schedule of unreconstructed masculinity: fighting off intruders, risking predation in order to woo a female into his territory, then, having inseminated her by ejaculating into her mouth, immediately setting off in pursuit of a new female. Add to this the fact that territorial males boast significantly larger testes and have higher circulating levels of testosterone than submissive non-territorial males, and a T-Rex view of the situation seems almost irresistible. These high-T fish are kings indeed, presumably thanks to the effects of all that testosterone on their bodies, brain, and behaviour. With a large dose of artistic license, we might even imagine the reaction were a group of feminist cichlid fish to start agitating for greater territorial equality between the sexes. It’s not discrimination, the feminist fish would be told, in tones of regret almost thick enough to hide the condescension, but testosterone.
But even in the cichlid fish, testosterone isn’t the omnipotent player it at first seems to be. If it were, then castrating a territorial fish would be a guaranteed method of bringing about his social downfall. Yet it isn’t. When a castrated territorial fish is put in a tank with an intact non-territorial male of a similar size, the castrated male continues to dominate (although less aggressively). Despite his flatlined T levels, the status quo persists.10 If you want to bring down a territorial male, no radical surgical operations are required. Instead, simply put him in a tank with a larger territorial male fish. Within a few days, the smaller male will lose his bold colours, neurons in a region of the brain involved in gonadal activity will reduce in size, and his testes will also correspondingly shrink. Exactly the opposite happens when a previously submissive, non-territorial male is experimentally manoeuvred into envied territorial status (by moving him into a new community with only females and smaller males): the neurons that direct gonadal growth expand, and his testes—the primary source of testosterone production—enlarge.11 In other words, the T-Rex scenario places the chain of events precisely the wrong way around. As Francis and his colleagues, who carried out these studies, conclude: “Social events regulate gonadal events.”12 Or to put it another way, just in case the significance of this sailed past unnoticed, cichlid testes are a social construction.
In fact, even without looking at any data from behavioural endocrinology, suspicions about the T-Rex story should already be aroused. Recall the major conceptual and empirical shifts in sexual selection theory and research we met in the first part of the book. These have left the old assumptions that competition for mates, status, and resources are exclusively male pursuits in the fight for reproductive success gathering dust.13 By way of example from a different species of fish, Sarah Blaffer Hrdy described long ago how female coho salmon compete ferociously for nests in which to bury their eggs. These head-to-heads have such serious reproductive consequences that a third of the time a defeated female’s nest will be taken over and her eggs destroyed.14 So why wouldn’t some females also need a hormone to prepare them for the “rigorous and competitive events of reproduction”? As Cornell University neuroendocrinologist Elizabeth Adkins-Regan observes:
Many females are very aggressive, sometimes more so than males, aggression among females is an important dyadic level process driving the spacing patterns and social systems of many animals, and in mammals the fitness consequences of rank in a dominance hierarchy are better established for females than for males.15
Already, then, we should be sceptical that, as a general rule, T serves to polarize the competitive behaviour of the sexes. At the very least, the situation needs to be taken on a species-by-species basis. And when we turn to ourselves in light of what we’ve learned in the last few chapters, we immediately encounter a problem. The T-Rex view would work fine if men were like this and women were like that. When we make generic statements like “men are competitive, women are caring,” T differences seem like an obvious explanation. But can the T-Rex story explain the shape that sex differences actually take? How, for instance, does T-Rex make “boys be boys” when, as we saw in Chapter 4, there’s no essential masculine profile that simultaneously unites a boy or man with most other males, and cleanly separates him from females? How does the T-Rex story deal with the fact that gendered behaviour doesn’t, as was once thought, create a single dimension that runs from masculinity to femininity, or even two dimensions? Only when working from those simpler, outdated, one- or two-dimensional understandings of gender does it make sense to suppose that higher T could increase an individual’s masculinity, and/or decrease their femininity. But this just doesn’t work as an idea when masculinity and femininity are multidimensional, with most people possessing “a complicated array of masculine and feminine characteristics,” as Joel puts it.16 What particular attributes of masculinity should we expect a high-T man to show, or a low-T woman to lack? And in particular, how does T make males risk taking and competitive when, as we saw in the previous chapter, in some domains, contexts, and populations, female risk taking and competitiveness is equal to (or even surpasses) that of males? Or, to repeat the awkward question that chapter posed, given th
at risk taking is domain specific—the physical daredevil may well be socially or financially risk averse—what kind of risk taker should we expect our high-T guy to be?
Fortunately, we don’t have to answer difficult questions like these. This is because, in the evolution of scientific understanding of the relations between hormones and social behaviour, the notion of testosterone as the powerful hormonal essence of Testosterone Rex has not survived.
SPECULATION ABOUT TESTOSTERONE and behaviour has a long history. In his classic essay, The Trouble with Testosterone, celebrated neurobiologist and writer Robert Sapolsky hazards that “A dozen or so millennia ago, an adventurous soul managed to lop off a surly bull’s testicles and thus invented behavioral endocrinology” (that is, the study of the relations between hormones and behaviour). This inadvertent experiment
generated an influential finding—something or other comes out of the testes that helps to make males such aggressive pains in the ass.
That something or other is testosterone.17
However, it wasn’t until the mid-nineteenth century that the first formal experiments on testosterone-behaviour relations took place, in the busy hands of a German physiologist named Arnold Berthold.18 Berthold’s investigations began with the observation that when a cockerel is castrated, not only does its distinctively male comb go into retreat, but it also quits its roosterish lifestyle of fighting, mounting, and cock-a-doodle-doo-ing. Berthold then took the natural next step for an inquiring mind unbounded by squeamishness. He decided to see what happened when he either re-implanted the testes or, in other experiments (perhaps performed on days when he was in an especially macabre mood), when the testes were transplanted into the cockerel’s stomach. Berthold’s remarkable discovery was that both of these interventions restored the cockerel’s cockiness. Since the newly located testes were no longer connected to the nervous system, Berthold was able to infer the action of something secreted into the bloodstream—a hormone. As we now know, testosterone and other androgens (the class of steroid hormone to which T belongs) are secreted into the bloodstream by the gonads (both testes and ovaries produce both androgens and oestrogens) and the adrenal glands.
The classic “remove-and-replace” experiments, of which there are now hundreds, established that testosterone has important effects on both the body (as on the wattle and comb, if you happen to be a rooster) and mating behaviour. Pointing to the same conclusions are the experiments of nature that take place when animals shift between life-history stages, for example, from youth to adulthood (or in some species, from a small size to a more imposing stature), or in and out of a breeding season. In our own species, of course, the gonads start to produce both androgens and oestrogens with renewed vigour (following the prenatal flurry) in pubescence, helping to bring about the development of secondary sexual characteristics. Some species of fish can even pull off the remarkable hormonal trick of changing sex when the opportunity (such as the death or removal of the dominant male in the group) arises.
This brings us to the important question of what hormones like T are for. In the first part of this book we met the idea that many animals only expend the biological costs of secondary sexual characteristics, and take the time, effort, and risk of courtship, when there’s a good chance of mating and fertilization taking place. Hormones can help coordinate this, by synchronizing the necessary changes in body and behaviour. But T can also help coordinate individuals’ behaviour on a shorter time scale. In a complicated and cruelly unpredictable world, it’s simply not the case that successful arrival at a particular life stage means that a single way of being in the world will suffice. Hormones “help adjust behavior to circumstances and contexts,” Adkins-Regan explains, “physical, social, and developmental.”19
One way T can do this is easily overlooked—via its effect on the body. T alters the body in more or less spectacular ways, depending on the species, and these masculinized features can then evoke particular responses in others. We met an example of this in Chapter 4: mother rats, attracted to the higher levels of testosterone in male pups’ urine, more intensively lick the anogenital region of their male offspring. This extra stimulation, we saw, ultimately contributes to sex differences in the brain and mating behaviour.20 A less subtle example, bypassing the brain altogether, is the “sword” of the male swordfish that develops when T increases during sexual maturation. Females are attracted to the sword, and so the male’s response to the female’s sexual interest is therefore in a sense “caused” by T, but in a rather indirect way.21 As for ourselves, there’s a case to be made that the pervasive and comprehensive gender socialization that penetrates just about every aspect of human culture is just another example of the indirect effects of sex hormones—via their effects on the body that identify us as female or male—on behaviour.
But testosterone does also affect the brain directly.22 In more lasting effects that take place at critical junctures in life—such as prenatally (in interaction with several other factors, as we saw in Chapter 4), in pubescence, or when spring is in the air—T helps to restructure neural pathways. T can also influence existing neural pathways in a more transient fashion (on the scale of minutes to weeks, depending on the mechanism), by either ramping up or down the electrical “excitability” of brain cells.23 The intricacies of how it does this show just how much goes on that expressions like it’s the testosterone overlook. In the fastest version of these short-term effects, T binds to the nerve cell membrane and, by altering chemical pathways, changes how readily a neuron fires.24 However, the best-known route by which T affects the brain is via hormone receptors. T binds to an androgen receptor, and is then “escorted” into the nucleus of the nerve cell. There, its next step is to “tickle the genome.”25 Then, in combination with what are called “cofactors,” a particular hormone-sensitive region of the gene is “turned on,” altering protein and peptide production (or gene “expression”). Sometimes though, with the assistance of a biological catalyst called aromatase, T converts from a “male” androgen to a “female” oestrogen, then binds to an oestrogen receptor. (Yes, even the “sex hormones” defy the gender binary.) Alternatively, the oestrogen might not originate from testosterone, or even from the gonads, since it turns out that the brain can synthesize its own oestrogens from scratch.26 Ultimately, this dance between steroid hormones and receptor can lead to a host of “behavior-impacting gene products,” as Adkins-Regan puts it, from enzymes involved in producing steroids, steroid receptors, and neurotransmitters to proteins that help build and repair neurons:
Through their intracellular receptors steroids alter neural activity now and in the future, alter their own production and reception and that of other steroids, and regulate some of the other neural signalling systems important for social behavior.27
In short, T certainly does stuff—important stuff. But now we get to the second reason for making you endure that dense last paragraph. Even though it barely begins to scratch the surface of the daunting complexities involved, it already makes clear that the amount of testosterone circulating in the bloodstream is just one part of a highly complicated system—the one that happens to be the easiest to measure.28 The many other factors in the system—the cofactors, the conversion to oestrogen, how much aromatase is around to make that happen, the amount of oestrogen produced by the brain itself, the number and nature of androgen and oestrogen receptors, where they are located, their sensitivity—mean that the absolute testosterone level in the blood or saliva is likely to be an extremely crude guide to testosterone’s effect on the brain.
This complexity may have made the preceding pages rough going, but it has a few useful consequences in the grander scheme of things. First of all, it means there’s scope for evolution to have moulded this multilayered system according to each species’ needs. T is ubiquitous among sexually reproducing species, but by tinkering with other factors, it’s possible for “the degree of association between hormones and behavior to vary.”29 And in fact, evolution se
ems to have done exactly that. The hypothetical neuroendocrinologist who clung to the Bateman-inspired hope that T will affect animals in similar ways across the sexually reproducing animal kingdom would be doomed to a life of repeated disappointments.30 This, in turn, means that just because testosterone has a particular effect on the behaviour of, say, elephant seals or bulls, doesn’t guarantee the same consequences in humans.
The complexity also helps to make the following problem less bewildering. How do humans achieve the feat of turning something rather large (average sex differences in circulating testosterone levels) into something usually rather small (average sex differences in behaviour)? No sex difference in basic behaviour comes close to the divergence between the sexes in circulating testosterone, for which there’s only about 10–15 per cent overlap between men’s and women’s levels.31 Potentially, this puzzle is solved by the important principle we met in Chapter 4: that sex effects in the brain don’t always serve to create different behaviour. Sometimes instead, one sex effect counteracts or compensates for another, enabling similarity of behaviour, despite dissimilarity of biology.32 Combine this principle with the considerable room for manoeuvre in the journey between T in the bloodstream and its action on the brain, and it becomes clear that there are potential ways for the relative testosterone-yness of males to be ramped down. One researcher, for instance, suggests that male exposure to the testosterone surge in utero somehow desensitizes the brain to testosterone’s effects later in life.33 This would be a smart way, maybe achieved through sex differences in neural sensitivity,34 of enabling males to tolerate the higher levels of testosterone their bodies need to develop and maintain male secondary sexual characteristics, without having an excessively large effect on behaviour.35
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