The Trouble with Testosterone Read online

  None of this strategizing has yet been shown to occur in male humans, but psychologist Jay Belsky and anthropologist Patricia Draper of Penn State and psychologist Laurence Steinberg of Temple University believe they have found something very much like it in human females. Their argument is actually the flip side of the delaying tactic used by antelopes and orangutans. In a nutshell, their premise is: When times are tough and life is unstable, hurry up, reach puberty, and start reproducing sooner.

  This thinking bears the mark of a certain style of ecology. One of the basic dichotomies made by ecologists is between “stable” and “opportunistic” species. Stable species live in unchanging, predictable environments. They live long lives in large populations, they are large-bodied, and they lavish a lot of parental attention on relatively few offspring. They opt for quality over quantity when it comes to reproduction; years later, members of these species are still doing the kids’ laundry and paying tuition for chirping lessons. Compared with closely related species that don’t have as many of these traits, stable species tend to reach puberty later. For them there is no rush: they can afford to grow big and healthy before starting to invest all that energy in a few pregnancies. Think of elephants, with their two-year pregnancies and sixty-five-year life spans. Or ancient redwood trees. Or humans, a classic stable species.

  In contrast are the opportunistic species, which live in ecosystems that are unstable and unpredictable, with long periods of severe weather, food shortages, and environments that are favorable only now and then. Animals that live near bodies of water that dry up seasonally or plants that grow best in soil just after a fire are opportunistic. They’re gamblers, living boom-or-bust existences. The population will be tiny for long periods. Then, when conditions suddenly become right, there’s tremendous pressure to take advantage of them fast, and, wham—everyone starts mating or pollinating. Quantity over quality, reproduce as much as possible, don’t bother taking care of the kids, just flood the market with offspring while the going is good. Opportunistic species tend to be small-bodied and short-lived, their population size fluctuates wildly, and once conditions are favorable, they reach puberty rapidly. Think of rabbits reproducing like rabbits and invading some new region, or of some kind of scrub weed that pops up overnight in the disturbed soil on the edge of a construction site.

  About a decade ago, Draper and her colleague Henry Harpending theorized that when girls are abandoned by their fathers during childhood, they grow up to become women who behave more like an opportunistic species. The girls have learned that males make unreliable parents, so they don’t bother searching for a reliable mate—they have sex at an earlier age, have more sexual partners, more kids, and are more likely to have rocky marriages.

  When Draper and Harpending proposed their theory, it was already well known that women who grow up in unstable homes are indeed more likely to behave this way—the novel thing about Draper and Harpending’s work was that they tried to explain this pattern from an ecological and evolutionary perspective rather than a psychological or socioeconomic one. Now Draper, Belsky, and Steinberg have built on this hypothesis by making the controversial suggestion that in unstable settings it’s not only the behavior of such girls that becomes more opportunistic, but their bodies as well, and so the girls reach puberty earlier.

  A handful of studies supports this idea. In two studies led by Belsky and one by Steinberg, girls who reported more strained relations with their parents, and girls raised in homes with persistent family conflict, reached puberty earlier than girls from more contented families. In a detailed 1990 study, Michele Surbey of Mount Allison University in Canada (who at the time proposed a theory quite close to that of Belsky and colleagues, but got no attention in the media for it) found that girls raised with the father absent because of divorce or abandonment also had earlier puberty. An Australian research group had found the same thing in 1972.

  The various authors wrestle a bit with potential physiological mechanisms for this effect (evolutionary theory is concerned with why puberty might be accelerated; physiological mechanisms, the nuts and bolts of hormones and the nervous system, explain how puberty might be accelerated). Surbey hypothesizes that biological fathers might release a puberty-delaying pheromone; take the father and his pheromones away and you’ve got earlier puberty. The problem here is how to explain Belsky’s results, in which the presumably pheromonally smelly father sticks around and constantly fights with the mother, with the same result of earlier puberty in the kid.

  Regardless of what the mechanism might be, the mere idea that social instability leads to earlier puberty has upset a lot of people. Some investigators who have tried to duplicate these studies haven’t gotten the same results. Other critics note that measures of “parental strife” or “strain” in girls’ relations with parents rely largely on the girls’ own reports, so there’s plenty of room for bias and inconsistency.

  The biggest problem with the findings and the underlying theory is that they are exactly the opposite of much of what is known about the effect of stress on puberty. A lot of the research suggests that “when times are tough and life is unstable, hold off on reaching puberty—it’s a bad time to get pregnant and the kid won’t survive, so don’t waste energy ovulating.” And we’re not just talking about antelopes here. Girls who experience the stress of sustained physical exercise (for example, serious ballet dancers) reach puberty later than average, as do girls with anorexia nervosa. The workings of this effect are pretty well understood—your body has to have a certain amount of fat deposited before it does something as risky and expensive as starting to ovulate on a regular basis, and girls whose muscle/fat ratio falls below a certain critical set point delay the onset of puberty.

  Additional evidence that extreme physical stress suppresses reproductive physiology instead of stimulating it comes from studies of women who have already reached puberty. Consistently, physical stresses such as weight loss, heavy exercise, and illness delay or even block ovulation—again, muscle/fat ratios probably play an important role here. Moreover, psychological stresses can also inhibit ovulation. This is particularly relevant, given that the girls growing up in unstable home environments were probably being psychologically, but not physically, stressed.

  So most investigators find that unstable environments filled with physical or psychological stressors inhibit reproductive physiology. Yet these new reports suggest that instability accelerates puberty onset in girls.

  The authors of the new theory try to reconcile these differences. If Surbey is right that the girls reach puberty earlier because some puberty-delaying pheromone from their fathers is missing, then this is no longer a contradictory story about stress and maturation but instead a story about pheromones and maturation. Her data also suggest the broader theory might not be about “when life is unreliable, reach puberty earlier,” but merely about “when the primary male around you is unreliable, reach puberty earlier.” Surbey found that having a mother rather than a father absent didn’t accelerate puberty, yet growing up without a mother should be just as much of a lesson to a child that life is stressful.

  Belsky contends that there could be a difference between the effects of extreme, potentially life-threatening stress and milder forms of stress, such that a starving anorexic might delay puberty, while a stressed-out yet relatively healthy child of a broken home might reach it sooner. Yet experimental work shows that even milder stressors inhibit reproductive physiology (although to a lesser extent) rather than stimulate it. Another of Belsky’s speculations would sidestep a lot of the perceived problems with his findings—maybe the girls in the unstable environments become depressed, eat more, deposit more fat, and thus hit puberty earlier, tying into the muscle/fat ratio feature of puberty onset cited above.

  One other important factor may explain the effect, although it’s messy and complicated. The age of puberty onset is partially inherited—mothers who reach puberty early tend to have daughters who do so as well. Perhaps
early sexual maturation is somehow related to having unstable marital relationships later (since early sexual activity is). In that scenario, girls in unstable homes reach puberty earlier because they inherit that biological trait from their mother, not because the home environment is unstable. That would be a very different story, taking away a lot of the novelty of these findings. Surbey did find that the mothers of her early-maturing girls had indeed reached puberty early themselves. When the mother’s age of puberty onset was taken into account, the overall effect of home environment decreased.

  The ideas of Belsky, Surbey, and their colleagues may or may not turn out to be valid—now’s the time to trot out the cliché about more research being needed. In the meantime, it’s a perfect subject for a scientific disagreement, since there’s a lot of minutiae to squabble over. But there’s one problem that should have taken some of the pleasure out of the squabbling—the effect is tiny. When the various studies supporting this effect are averaged, they suggest that instability accelerates the onset of puberty in these girls by about five months. That’s nothing; these kids can’t even break in a new pair of jeans in that time. So why is it that not only are scientists bickering over this, but the lay press has picked up on this story?

  Lurking behind the scientific arguments is a big public policy conflict over what to do about teen pregnancies. The pregnancy rate for teens in the United States is astonishingly high for a Western country, twice that of Canada or England, for example. Teen mothers come disproportionately from poor inner-city populations rife with unstable, broken families. Children of such mothers are more likely to have health and learning problems, and thus to underachieve and place a burden on society for years to come.

  Belsky thinks the theory he’s helped formulate has something to say about this mess. In his view, the unstable early environment of many an inner-city teenage girl produces earlier puberty and the whole range of attendant opportunistic behavior that ends in an increased risk of pregnancy. “These teenagers aren’t necessarily carrying out bad behavior,” he says. “Their bodies are just responding to forces that have emerged over the course of evolution.”

  Belsky and Surbey’s critics, however, worry that the theory suggests that one can blame biology instead of society for the problem, and to some, blaming biology implies that we can’t do much about teen pregnancy. For a bloatedly wealthy country, they note, we expend very little effort to give a massive underclass any hope for jobs or education. Our mass media is permeated with a sexual hard sell that few adolescents have the means to respond to maturely. Our government wages war on sex education and access to contraceptives and makes it increasingly difficult for the young and the poor to have abortions. If these are the reasons why we have such an appallingly high rate of teen pregnancies among our poor, there is lots we can do about it. Or is it because early family conflict commands such girls to follow a biologically determined program of early pregnancy?

  Belsky doesn’t think the explanations are mutually exclusive. He believes that his theory is not about how biology can cause earlier pregnancy, but about how a biological drive can make the body of a young person from an unstable home more likely to respond to various societal pressures. This is what he calls a “nature-based theory of nurture.” If true, it predicts that the effects on puberty onset of growing up in an unstable home would be stronger among poor kids than among middle-class kids. And if he is right—if early stress and resulting biological changes do not form a direct link to more teen pregnancies but instead are one of the many factors influencing how teenagers respond to the seductive world around them—then perhaps the policy implications of his view are not so worrisome. Much of behavioral biology works through this sort of biology/environment interaction. These results are not an excuse for society to say, in effect, “There goes that darn biology again—nothing we can do about it,” and wash its hands of the mess. The findings are, if anything, a scientific rationale for why society has the responsibility to try to solve these social ills.

  EPILOGUE

  Surbey’s data were published in 1990; Belsky and colleagues published their more visible version of the same in 1991. What has happened since then? Have researchers been able to replicate the findings in their own study populations? Have the ideas contained in these papers influenced the thinking of other researchers?

  To date, I am aware of only a single study that has replicated the finding that growing up in an unstable home environment leads to slightly earlier puberty onset in girls. While this is nice, Belsky was one of the coauthors, and one hopes to see what is called “independent” replication of a finding. This is where someone completely unconnected to the discoverer of a new fact, someone with no stake in the matter—even better, someone who is skeptical about this new fact—comes forward and says, in effect, “I thought there was no way that things worked like this, but we tried it, and you know what, they’re right.” That hasn’t happened yet. That particular paper debunked Belsky’s speculative chain where unstable home environment leads to depressed kids leads to more eating leads to more fat deposition . . . and earlier puberty (and that chain was unlikely to work, as an unstable home setting doesn’t necessarily lead to depression, and depression is at least as likely to lead to undereating as to excessive eating). Note that that was Belsky as one of the coauthors reaching the conclusion that his earlier speculation wasn’t right—that’s a sign of an honorable scientist at work. The paper, instead, garnered support for Surbey’s notion that the early puberty/unstable home life link was an artifact, and that the real link was women with early puberty onset having daughters with earlier onset. I suspect that that is the explanation, which would reconcile this small effect with the extensive earlier literature showing the antireproductive effects of a stressful environment.

  What has been the influence of these studies on the thinking of others in the field? An interesting pattern has emerged. These studies have had some impact on the thinking of psychologists and evolutionary biologists about growth and development; the work has been cited about fifteen times by such scientists in recent years. In contrast, the papers have been entirely ignored by endocrinologists—in other words, scientists are often loath to pay attention to the work of individuals outside their immediate domain, even if it concerns work within their domain.

  And naturally, as we speak, teen pregnancies continue unabated in the United States, untouched by this particular academic hiccup.

  Final note: I kind of liked the title of this piece until someone canvassed a bunch of friends and discovered that they thought the title was male-biased. I was thoroughly puzzled by this. While males’ first nocturnal emissions are certainly likely to occur nocturnally, it seems obvious that the onset of one’s menses can occur while in pj’s as well (in humans, for example, there is a strong bias toward women giving birth at night, a pattern seen among most primates, who would just as well not give birth midday in the middle of a savannah filled with hungry predators). Time for some quantitative data. Does anyone know of any study concerning time of day of menses onset? Operators are standing by for your call.

  FURTHER READING

  The original reports can be found in M. Surbey, “Family Composition, Stress, and the Timing of Human Menarche,” in T. Ziegler and F. Bercovitch, eds., Socioendocrinology of Primate Reproduction (New York: Wiley-Liss, 1990), 11; and in J. Belsky, L. Steinberg, and P. Draper, “Childhood Experience, Interpersonal Development, and Reproductive Strategy: An Evolutionary Theory of Socialization,” Child Development 62 (1991): 647.

  The follow-up study noted in the epilogue is T. Moffitt, A. Caspi, J. Belsky, and P. Silva, “Childhood Experience and the Onset of Menarche: A Test of a Sociobiological Model,” Child Development 63 (1992): 47.

  An introduction to stable and unstable species (known for agonizingly obscure reasons having to do with mathematical formulas as “K” and “r” species—the reasons even including the stricture of the “K” being capitalized and the “r” not) can be foun
d in the classic E. O. Wilson, Sociobiology: The New Synthesis (Cambridge, Mass.: Harvard University Press, 1975). This is also the best book for an introduction to thinking about behavior having evolved strategically (i.e., the sort of issues discussed early on in the piece, such as when does an animal “decide” that it’s a good time to carry out some behavior).

  Work concerning unstable home environments and earlier onset of sexual behavior is summarized in P. Draper and H. Harpending, “Father Absence and Reproductive Strategy: An Evolutionary Perspective,” Journal of Anthropological Research 38 (1982): 255.

  A review of the Vandenbergh effect can be found in K. Darney, J. Goldman, and J. Vandenbergh, “Neuroendocrine Responses to Social Regulation of Puberty in the Female House Mouse,” Neuroendocrinology 55 (1992): 534. The particular cloverleaf study is described in A. Massey and J. Vandenbergh, “Puberty Delay by a Urinary Cue from Female House Mice in Feral Populations,” Science 209 (1980): 821.

  A review of how stress generally inhibits reproductive physiology and behavior can be found in chapter 7 of R. Sapolsky, Why Zebras Don’t Get Ulcers: A Guide to Stress, Stress-Related Diseases, and Coping (New York: W. H. Freeman, 1994). For a review of what fat deposition has to do with puberty onset, see R. Frisch, “Body Weight, Body Fat and Ovulation,” Trends in Endocrinology and Metabolism 2 (1991): 191.

  Measures of Life

  Francisco José de Goya, The Third of May, 1808, 1814; Prado, Madrid, Alinari/Art Resource, New York

  It is one of the most riveting paintings ever made. In 1808 the populace of Madrid rose up against an occupying French army, an uprising that was soon crushed; the painting depicts the mass executions of insurgent Spaniards that began before dawn on the third day of May. Goya captures the appalling, machinelike process of the slaughter, implied by the piled-up bodies and the waiting line—those men in the light, seconds away from death, who have time only for a single burst of emotion: mute terror, fervent prayer to an indifferent god, or a final bellow affirming life and existence. And then they too are dead. It is impossible not to think of their dying and impossible not to imagine oneself in that circumstance. One wonders: How would I react? Would I be brave? Again and again one’s eyes return to the men in that circle of final light.