A Woman Looking at Men Looking at Women

by Siri Hustvedt

  I think there is something wrong with this substitution because it leads the reader into a sense of false confidence about genes and their relation to our psyches. Pinker is hardly alone. He is one of many, but as the scientific mantra goes: correlation is not cause. Cause can be notoriously hard to prove in biology, but correlations pop up all the time. A study tells us that people who eat broccoli have lower incidences of cancer than people who never eat broccoli. Eating broccoli is correlated with being cancer free. The study does not show that eating broccoli prevents cancer or causes a noncancerous state in a person who might have been vulnerable to developing the illness without broccoli. Even smoking as a carcinogen has often been determined through correlations rather than direct causal factors. Scientists are researching the exact “mechanisms” for the connection, but many of them remain unknown or ambiguous. The correlation between smoking and any number of diseases, however, is so high that the relation has come to be understood as one of cause and effect rather than correlation. I remember watching a very old Bette Davis give an interview on television. She was in her eighties at the time. Wizened but elegant, she inhaled her cigarette from a long holder as she bemoaned the state of contemporary cinema. Davis puffed her way to the end. Dead at ninety-one, she was an exception to the correlation rule.

  Inside universities, numerous points of view coexist, but the conflicts among them are rarely aired in public because the arguments are not comprehensible to most people. This is not because the public is stupid but because the vocabulary of each of these internal languages is often impenetrable, not just to academic outsiders, but to professors in two different fields whose offices are just across campus from each other. Important case studies of individuals remain a part of science. Brenda Milner’s study over many years of the now famous patient H.M. remains a formidable example. After an operation to quell his continual seizures, during which H.M. lost a good part of the hippocampus in his brain, he was unable to hold on to new memories. Although he could recall his early life before the operation and was able to speak and interact with other people, he could not retain any memories of those encounters. As a routine part of science, however, case studies have receded from prominence. In contemporary psychiatry, recording the lives of individual patients has given way to statistical analyses and “evidence-based” science, which generally means the larger the study and the bigger the number of participants, the more accurate the results will be. Large studies and data have much to offer us, but disregarding the intimate view of the particular case has its costs. Ignoring the patient’s story rests on the assumption that an illness can be lifted out of a dynamic body in time and described as a list of symptoms that can be applied to any other body. Arguably, this is what diagnosis is—seeing similarities among many cases and giving those similarities a name. At the same time, every physician knows that the same drug, surgery, or treatment affects different people in different ways. Locating those differences is also of the essence.

  Vico’s critique of a fragmented academy has become only more true. Larry Summers seems to have accepted uncritically a particular scientific view advanced through the statistical research of behavioral genetics that asserts women are unsuited for higher mathematics and physics by nature. For Summers, the reason there are so few women in physics is caused by mental traits that have evolved in the female sex, traits that, despite the fact that sociological factors contribute to keeping women out of the field, are genetic and connected to variability.

  New and Old Adventures at Harvard, Testosterone, Placebo, False Pregnancies, and Wishes and Fears Coming True

  The name “Harvard” carries authority. Social policies in Norway have been swayed by Steven Pinker’s theories. A popular television show and book that telegraphed as its essential message “born that way” rehashed “facts” lifted from Pinker’s The Blank Slate for the Norwegian public as the truths of “hard” science and convinced many people of his views, including those in a position to make policy decisions. In other words, Pinker has become a representative for a discipline that has changed people’s minds about who we are, not only in the United States, but elsewhere. It is vital to stress that if his readers weren’t receptive to the message Steven Pinker and others like him bring to the public, it would drown in obscurity. Its popularity says as much about his readers as it does about him. The Blank Slate was published in 2002, but it lives on.

  On January 1, 2015, in a letter to the editor, a man wrote to the New York Times in response to an article about the gap between men and women in technology fields. To bolster his argument that the problem is not an issue of discrimination but rather created by the fact that women simply don’t want to work in technology, he cites Pinker: “As discussed in Steven Pinker’s book ‘The Blank Slate,’ there is substantial scientific evidence to indicate that innate factors are a major cause of the tendency of men and women to be interested in different things. It is sheer political correctness to assume that this plays no role in why men and women tend to pursue careers in different fields.”94 I mention this letter because it illustrates how Pinker and “substantial scientific evidence” act as a seal of approval for the letter writer. Like M’s conviction that male entitlement or dominance is written in the genes, the writer to the Times refers to “innate factors” that keep women out of technology.

  What is this “substantial scientific evidence”? During his roundup of sex differences, Pinker writes, “Variation in the level of testosterone among different men, and in the same man in different seasons or at different times of day, correlates with libido, self-confidence, and the drive for dominance.”95 On the heels of this statement, Pinker quotes Andrew Sullivan, a journalist who had low testosterone levels, injected the stuff, and confessed, “I almost got in a public brawl for the first time in my life.”96 Because androgens, of which testosterone is one, are involved in masculinizing the fetus in utero and the secondary sexual characteristics that appear during male puberty, and men have up to ten times more circulating testosterone than women, it has long been a likely candidate for explaining the male psyche.

  In popular culture, testosterone is often seen as the “cause” of male aggression, touted as the explanation for fistfights, criminal gangs, the dog-eat-dog climate of Wall Street, and much more. Testosterone has been linked to both male and female libido, and its levels fluctuate in both sexes. Its role in human psychology remains blurry. Richard Lynn, a professor emeritus of psychology at the University of Ulster, has made an extremist career out of sex and race differences in intelligence. Lynn has been criticized by many scientists and was even chastised by the journal Nature. Pinker does not say men are more intelligent than women, and he is careful not to make a direct link between testosterone and aggression in men. He lets Sullivan’s testimony do that for him. Lynn has no such qualms about the evidence, but his ideas are not much different from the ones many evolutionary psychologists advance. The ideas don’t change all that much. The rhetoric does. In a provocative piece published in the Daily Mail, Lynn explains that men have “a natural advantage” over women. “Take, for example,” he writes, “the case of rutting stags or fighting chimps and you get the generally aggressive idea. Thanks to high levels of the male sex hormone testosterone, men are far more competitive and motivated for success than women.”97

  If you castrate male mice and rats, they lose their aggressive impulses. If you replace the lost testosterone, they will fight again. I am not contemptuous of rat and mice studies and their possible relation to people. We share traits with our mammalian cousins, which is why the epigenetic studies I mentioned earlier have been seen as potentially significant for human beings, not only for rats and mice. Estrogen has also been implicated in mouse aggression. Male mice that have been genetically altered to lack the enzyme that converts testosterone into estrogen also lose their aggressive and dominant behaviors. Hormones are complex. It is interesting, however, that after heroic efforts and hundreds of studies, scientists have been unable t
o make a definitive link between testosterone and aggressive behaviors in human beings.

  In a paper published in 2010, Scott H. Liening and Robert A. Josephs sum up the research: “Despite considerable evidence for testosterone’s connection to dominance, research on testosterone’s effect on human social behavior has been frustratingly inconsistent. Although many studies have found an association between testosterone and behavior, many others have found weak or nonexistent effects. These null findings range from competitive behaviors to aggression, both physical and non-physical.”98 A sampling of the findings: One study found that divorced men have higher levels of the hormone than men in stable marriages. Another found higher levels in women lawyers than women teachers and nurses, suggesting the hormone’s correlation with higher occupational status.99 Several studies have proposed that testosterone levels rise in response to a conflict or challenge; that is, this rise is not the cause of but perhaps the consequence of aggression. Some studies find this response only in males. Others have found it in both sexes for testosterone and estrogen: “These data . . . [provide] support for the notion that estrogen may play a significant role in the production of aggressive behavior in both sexes.”100 The author of a 2003 survey of the role of hormones in childhood and adolescence acknowledges that the studies on a relation between hormones and aggression are inconsistent. He suggests that hormones may act as “a cause, a consequence, or even as a mediator” of aggression.101

  A 2010 paper by Christoph Eisenegger et al., “Prejudice and Truth About the Effect of Testosterone on Human Bargaining Behavior,” concluded that testosterone increased fair bargaining behavior in the women who took it. However, in a parallel study, if the women were told they were getting testosterone, even if they were given a placebo, they became self-serving and greedy.102 One of the researchers, Michael Naef, said, “It appears that it is not testosterone itself that induces aggressiveness but rather the myth surrounding the hormone.”103 Shall we conclude from this single study as the Telegraph did in its headline that “Testosterone Makes People More Friendly and Reasonable”?104 Perhaps rather than hardwire our way to happiness, we should inject our way there.

  If there were a direct relationship between testosterone and aggressive or even dominant behaviors, one might expect a flood of the hormone to increase both qualities. The case of a four-year-old boy with an androgen-producing tumor is instructive. The child displayed pubertal changes at his tender age—penis growth, pubic hair, erections, sweating, and a precocious interest in older girls and images of naked women. The authors of the paper note that there was absolutely no sign in the boy of either aggressive or dominating behavior. On the contrary, they describe him as “anxious and withdrawn.”105 If it happened to me, I would be anxious and withdrawn, too.

  Allan Mazur has studied the question of the hormonal relation to dominance and aggression in human beings for many years. At the end of his essay “Dominance, Violence, and the Neurohormonal Nexus,” he cites two of his own large-scale studies, one conducted on U.S. veterans, which found higher levels of testosterone among those veterans who were more likely to have been participants in “inner-city honor cultures” before their service than those who weren’t. The other study found no such relation. He concludes, “Like so many questions about neuroendocrinology and behavior, we do not have a clear answer.”106

  None of this means that there may not be some complex relation between both testosterone and estrogen and aggression, dominance, and cooperation in people, nor does it mean that hormones play no role in psychological sex differences. A much-publicized study found that men’s testosterone levels drop when they become fathers.107 Perhaps mothers’ levels do as well, but I have been unable to find any research on that. Estrogen levels drop in women after childbirth and during breast-feeding. Androgens have been related to women’s sexual functioning, but that link is unclear. So what does this all mean? Human beings and laboratory rats are not alike when it comes to testosterone and behavior. It seems to me that a one-to-one correspondence between a single hormone and aggression, dominance, and/or cooperation is unwarranted.

  In fact, the dynamic character of the human neuroendocrine system may not be well captured in any of these studies. The research further suggests that belief and the context for belief have profound effects on our bodily states, perceptions, and behaviors, a fact that turns us back to the fundamental mind-body question. Andrew Sullivan is not alone in proclaiming that infusions of testosterone made him feel brawny, tough, invigorated, and ready for battle. Nor do I doubt for one instant his veracity. There is scant evidence, however, that testosterone was responsible for those feelings. A woman I know who takes testosterone because her levels are low told me that she feels the hormone has helped her to feel less tired. Perhaps Sullivan interpreted a boost in energy through a macho perceptual lens. And yet, the question remains: If it’s not the hormone, what is it?

  For centuries, physicians have been providing their patients with moral support in the form of pills, tonics, and other remedies they have regarded as medically useless. The placebo effect might be described as the beneficial effect of the nontreatment treatment. Some researchers have begun to regard placebo not as a minor irritant that interferes with the “real” effects of active drugs but as a powerful physiological reality, which may help us understand more about healing in general. Placebo has been correlated with the release of endogenous opioids (endorphins) in the brain, as well as other nonopioid changes that induce genuine therapeutic effects. Studies have documented the release of endogenous dopamine in Parkinson’s patients after placebo treatments and improvement among patients who underwent sham surgeries.108 In fact, in the study of patients given sham knee surgery, the surgery patients did no better than those who had “pretend” surgeries. One can also conclude, of course, that this particular kind of knee surgery may be a procedure due for reconsideration. A controversial but interesting study by Irving Kirsch and Guy Sapirstein found that a substantial effect of antidepressant medicines was the result, not of any active ingredient in the drug, but of the placebo effect.109 In 1996, Fabrizio Benedetti demonstrated that the release of endogenous opioids in the brain in response to placebo can be blocked by naloxone, an opioid antagonist, thereby preventing the analgesic effect.110 Sugar pills and other inert substances have also generated nausea, vomiting, headache, and other nasty “side” effects, a phenomenon known as nocebo. The question is: How does all this work and what does it tell us about the mind-body problem and the person-environment question?

  In a 2005 paper, Benedetti and his colleagues define the placebo effect as “the psychosocial context around the patient.” They then write that placebo is a model for understanding “how a complex mental activity, such as expectancy, interacts with different neuronal systems.”111 Look closely at their language. First, if placebo is the “psychosocial context around the patient,” one has to ask, how does it become the patient? Nothing short of this metamorphosis needs to be explained. I have often used context in the way the authors do, as a surrounding that affects the inside, so my critique is not meant to illustrate their shoddy thinking but rather to point out how what seems lucid when it is articulated can actually be murky when it is closely examined. Second, the idea of “interaction” implies that the psychological “complex mental activity” and “neuronal systems” are somehow distinct from each other and they cross paths in an unknown way. How does the thought or expectation I am going to get better, conscious or unconscious, “interact” with neurons?

  The authors’ notion of interaction doesn’t resolve mind-body dualism. In another paper, Benedetti refers explicitly to the mind-body unit. How are we meant to understand this? Does the term reinforce or undermine the mind-body division? The neuronal brain processes have a material reality, but the complex mental activity does not, or, if it does, we don’t know what or where it is and how it can interact with brain matter. It has no home in the model. Indeed, it begs the question Descartes, Princess Elis
abeth, Cavendish, and many others wrestled with long ago—how can mind stuff be separate from body stuff and, if the two are separate, how on earth would they interact? What exactly is “complex mental activity” and what is it made of? Surely the authors do not mean that complex mental activity is insubstantial, made of mysterious spirits or soul. Do they mean that this complex mental activity is somewhere inside a person but separate from the neurons in her brain? Is their argument dependent on the idea that brain and mind are indeed separable? I would repeat the question Margaret Cavendish posed in her Philosophical Letters of 1664: “I would fain ask them, I say, where their Immaterial Ideas reside, in what part or place of the Body?”112 If confronted, I suspect their answer would be the one often given by neuroscientists: we do not know how psychological factors relate to neurobiological factors. This is a missing link of enormous proportions. All references to “neural correlates, substrates, and underpinnings” for fear, love, memory, consciousness, or any other state imply this gaping hole in the understanding of mind-brain processes.

  I am not filling in the hole. I am pointing to what is known as the “explanatory gap” between mind and brain. Benedetti & Co. are in no way exceptional among neuroscientists in their description of two interacting levels. They are typical. The big problem is that even if we arrive at a moment when the whole brain—its synaptic connections, individual neurons, and chemistry—can be beautifully described, the gap remains. Is it reasonable to describe a person’s subjective thoughts, dreams, hopes, and wishes through neuronal processes? How do we know the two are the same thing? Could it ever be proven? Not only that, if thoughts, expectations, personality, desires, and suggestions are described as agents that change brain function, how does that work? If you are a dualist you will have to explain how these states work on neurons. If you are a monist and a materialist, you will feel deeply dissatisfied by this description. Isn’t the brain responsible for all of it? Luria regarded the immediate reduction from the psychological to the neurobiological as an error. Drawing a straight line between a person’s fear and the amygdala, for example, an almond-shaped part of the brain that is clearly implicated in fear experiences, is unwarranted. This may be true, but the gap doesn’t vanish.