Various other emotions serve various specific advantages. The male who harbors anger and hatred will compete more effectively against other males; he will attempt to destroy them and will therefore advantage his own reproductive tendencies. The male who is protective of his mate will also have an advantage; and the male who keeps other males away from his mate will maintain the chances for his genes to be passed along every time the female becomes fertile. The best shot at promoting genetic material, for animals who produce few young, is to combine a loving and attentive mother and a jealous and protective father (or vice versa). Passionate animals stand a good chance of reproducing more frequently. Animals who are energized by rage are likely to win in competitive circumstances. Love—eros, agape, friendship, filiality, maternity, and all the other forms of that ill-contained emotion—functions on a rewards and punishments model. We express love because the gratification of love is enormous, and we continue to express love and to act protectively because the loss of love is traumatic. If we did not experience pain on the demise of those we love, if we had the pleasure of love but felt nothing when the object of our love was destroyed, we would be considerably less protective than we are. Grief makes love self-protective: we will take care of those we love to avoid intolerable pain to ourselves.
This argument seems the most plausible to me: that depression itself serves little useful function, but that emotional range is invaluable enough to justify all the extremes we know.
The social evolution of depression and the biochemical evolution of it are linked but are not the same. Our genetic mapping is not sufficiently specific at this time for us to know the exact functions of the genes that may lead to depression, but it appears that the condition is linked to emotional sensitivity, which is a useful trait. It may also be that the very structure of consciousness opens the pathway to depression. Contemporary evolutionists work with the idea of the triune (or three-layer) brain. The innermost part of the brain, the reptilian, which is similar to that found in lower animals, is the seat of instinct. The middle layer, the limbic, which exists in more advanced animals, is the seat of emotion. The top layer, found only in higher mammals such as primates and people, is the cognitive and is involved in reasoning and advanced forms of thought, as well as in language. Most human acts involve all three layers of the brain. Depression, in the view of the prominent evolutionist Paul MacLean, is a distinctly human concern. It is the result of disjunctions of processing at these three levels: it is the inevitable consequence of having instinct, emotion, and cognition all going on simultaneously at all times. The triune brain sometimes fails to coordinate its response to social adversity. Ideally, when one feels instinctive withdrawal, one should experience emotional negativity and cognitive readjustment. If those three are in sync, one may experience a normal and nondepressive withdrawal from the activity or circumstance that is causing the deactivation of the instinctive brain. But sometimes the higher levels of the brain fight against the instinctive. One may, for example, have withdrawal at the instinctive level but feel emotionally activated and angry. This causes an agitated depression. Or one may feel withdrawn at the instinctive level but make a conscious decision to go on fighting for what one wants, so subjecting oneself to terrible stress. This kind of conflict is experientially familiar to us all and does indeed seem to result in depression or other disruptions. MacLean’s theory fits neatly with the idea that our brain is doing more than it evolved to do.
Timothy Crow at Oxford has moved beyond the principle of the triune brain. His theories are very much his own; whether they are true or not, they are calisthenically refreshing to minds worn out by the sometimes improbable claims made by mainstream evolutionary theorists of mind. He proposes a linguistic-evolutionary model in which speech is the origin of self-consciousness, and self-consciousness the origin of mental illness. Crow starts by rejecting modern classification systems and places the mental illnesses on a continuous spectrum. For him, the differences between ordinary unhappiness, depression, bipolar illness, and schizophrenia are all really differences of degree rather than of kind—dimensional differences rather than categorical ones. In his view, all mental illness springs from common causes.
Crow believes (while physiologists battle about it) that the primate brain is symmetrical, and that what makes humans human—the speciation point—is the asymmetrical brain (which, he proposes, on the basis of some rather complex genetic arguments, came about through a mutation of the X chromosome in males). While brain size was increasing relative to body size—in the evolution of the primates and then of man—a mutation allowed the two halves of the brain to develop with some measure of independence. So while the primate cannot, as it were, look from one part of his brain to the other, the human being can. This opened the way to self-consciousness, to an awareness of one’s own self as a self. A number of evolutionists have said that this could have been a simple mutation—one related to growth factors for each side of the brain—that over the course of evolution became a meaningful asymmetry.
The asymmetry of the brain is in turn the basis for language, which is the left-brain expression or processing of right-brain concepts and perceptions. This notion that language is located in the two sides of the brain seems to be borne out by evidence from stroke victims. Patients who have had limited strokes in the left brain can understand concepts and perceive objects, but they cannot name anything and they do not have access to language or to linguistic memory. This is not simply a vocal matter. Deaf people with left-hemisphere strokes can use emotional gesture and gesticulation (as all people and primates do), but they cannot use sign language nor understand the deep grammar we all use to assemble words into sentences and sentences into paragraphs. Patients with right-brain strokes, on the other hand, preserve intellectual abilities but lose the concepts and feelings those abilities may ordinarily express. They cannot process complex abstractions and their emotional capacities are very much compromised.
What are the anatomical structures that make us prone to mood disorders? Crow has proposed that schizophrenic and affective disorders may be the price we pay for an asymmetrical brain—the same neurological development he credits with human sophistication, cognition, and language. He then proposes that all mental illness is the consequence of a disruption of normal interaction between the two halves of the brain. “It can be too much communication between them or too little; if what the hemispheres are doing is not in concert, the result will be a mental illness,” he explains. Crow suggests that asymmetry provides “increased flexibility of interaction” and “enhanced capacity for learning” and “an escalating capacity to communicate with members of the same species.” These developments, however, slow brain maturation, which takes longer in human beings than in other species. Human beings appear to retain greater brain plasticity as adults than do most other species—you can’t easily teach an old dog new tricks, but old men can learn whole new systems of motor activity as they accommodate later-life disabilities.
Our flexibility allows us to reach new insights and new understandings. It also means, however, that we can bend too far. For Crow, the same elasticity causes us to vary outside the normal range of personality and into psychosis. The change may well be triggered by external events. What evolution would have selected for, in this model, is not the particular expressions of the plasticity, but the plasticity itself.
The study of brain asymmetry is a hot topic at the moment, and the most impressive work in the United States is being done by the neuroscientist Richard J. Davidson at the University of Wisconsin at Madison. Davidson’s work has been made possible by increasingly good brain-scanning equipment. Scientists can now see all kinds of things in the brain that they couldn’t see five years ago, and it seems likely that in five years, they’ll be able to see a lot more. Using a combination of PET (positron-emission tomography) and MRI (magnetic resonance imaging), brain-imaging specialists can get a three-dimensional snapshot of the entire brain approximately every two and a
half seconds, with spatial information accurate only to within about three and a half millimeters. MRI has better time and spatial resolution; PET does a better job of mapping neurochemical reactions in the brain.
Davidson has begun by mapping neural and chemical activity in the brain in response to “normal” stimulus—what areas do what when a subject sees an erotic photograph or hears a scary noise. “We want to look at the parameters of emotional reactivity,” he says. Once you’ve figured out where in the brain the reaction to a particular kind of image takes place, you can measure how long the brain remains activated, and it turns out that this varies from person to person. Some people, exposed to a gruesome photo, will have a neurochemical rush that dies down fast; others will have the same chemical rush and it will take a long time to come back down. This matter is consistent for any given patient: some of us have snappy brains in this regard and some of us have slow ones. Davidson believes that people with a slow recovery time are much more vulnerable to mental illness than are those with a brisk recovery. Davidson’s group at Wisconsin have shown detectable changes in the speed of recovery in individual brains after six weeks of treatment with antidepressant medication.
These changes seem to be in the prefrontal cortex and they are not symmetrical—when someone is recovering from a depression, speed of activation and deactivation increases on the left side of the prefrontal cortex. It is known that antidepressants alter levels of neurotransmitters. It is possible that neurotransmitters control blood flow to various areas of the brain. Whatever the mechanisms, Davidson explains, “activation asymmetries”—differences in left-side and right-side activity—“in the prefrontal cortex are related to disposition, mood, and the symptoms of anxiety and depression. People with more right-side activation are more likely to have depression and anxiety.” And Davidson, like Crow, ultimately questions the categorical purity of depression as a condition. “One of the things that distinguishes human behavior from the behavior of other species is that we have a greater capacity to regulate our emotions. We also have the flip side, a greater capacity to disregulate our emotions. I think both mechanisms will prove to be very much associated with activity in the prefrontal cortex.” In other words, our troubles are a consequence of our strengths.
This kind of work, in addition to showing how the genetics of mood disorder may have developed, has enormous practical implications. If researchers can locate the exact area of altered activity in a depressed brain, they can develop the apparatus to stimulate or inhibit that area. Recent work suggests that abnormalities in serotonin metabolism occur in the prefrontal cortex in patients with depression. Asymmetrical stimulation of the brain may result from this; or there may be physical asymmetry—of capillary distribution and hence of blood flow, for example—in some brains.
Certain patterns of brain activity are set up early in life. Others change. We have now found that brain cells can and do reproduce in adult humans. It may be that we are gaining cells in some areas or depleting cells in others when we go through depression. New technologies may ultimately allow us to stimulate growth of or to lesion certain areas of the brain. Some early studies show that rTMS (repeated transcranial magnetic stimulation), which uses tightly focused magnetism to increase activity in a particular location, may, when directed at the left prefrontal cortex, cause amelioration of the symptoms of depression. It may be possible, through external intervention or through measured work oneself, to learn to activate the left brain. Resilience itself can be learned, especially in young people. It may be possible to scan brains and catch deactivated left frontal cortexes early and take preventative measures—“which might include meditation, for example,” Davidson says—to help people avoid falling into the pit of depression in the first place.
Some people have more highly activated left prefrontal cortexes and some people have more highly activated right prefrontal cortexes. (This has nothing to do with the question of hemispheric dominance that determines whether you are right-handed or left-handed, which occurs in other areas of the brain.) The majority of people have higher left-side activation. People with higher right-side activation tend to experience more negative emotion than people with higher left-side activation. Right-side activation also predicts how easily someone’s immune system will become depressed. The right-brain activation is also correlated with high baseline levels of cortisol, the stress hormone. Though the settled patterns of activation do not stabilize until adulthood, babies with greater right-side activation will become frantic when their mothers leave a room; babies with strong left-side activation will be more likely to explore the room without apparent distress. In babies, however, the balance is subject to change. “The likelihood,” Davidson says, “is that there’s more plasticity in the system in the early years of life, more opportunity for the environment to sculpt this circuitry.”
There are enormously interesting ideas to be adduced from putting together this thinking with some of Crow’s ideas about language. “One of the first things that you see when toddlers begin giving out single-word utterances is that they point,” Davidson says. “The utterance is a label for an object. And they point almost invariably, at first, with the right hand. The toddler is having a positive experience and is clearly interested in the object and is moving toward it. The initial use of language is very pleasurable to most toddlers. My intuition, which has not been studied in any systematic way, is that the left-hemisphere lateralization for language may actually be a byproduct of the left-hemisphere lateralization for positive emotion.”
This intuition is, it would seem, the basis for a neuroanatomy of catharsis. Speech is positive; it remains positive. Speech is one of life’s greatest pleasures, and the will to communicate is enormously powerful in all of us (including those who cannot produce coherent vocal sound and therefore use sign language, gesture, or writing to express themselves). People who are depressed lose interest in talking; people who are manic talk incessantly. Across broad cultural divides, the most consistent mood-enhancer is speech. Dwelling on negative events can be painful, but talking about current pain helps to alleviate it. When I am asked, as I am constantly, about how best to treat depression, I tell people to talk about it—not to work themselves up into hysteria about it, but simply to keep articulating their feelings. Talk about it with family if they’ll listen. Talk about it with friends. Talk about it with a therapist. It may well be that Davidson and Crow are onto the mechanisms through which talk helps: it may well be that certain kinds of talking activate the same areas of the left brain whose underperformance is implicated in mental illness. The idea of articulation as release is absolutely fundamental to our society. Hamlet weeps that he “must, like a whore, unpack my heart with words”—and yet what we have evolved, along with our capacity for mental illness, is that capacity to unpack our hearts (or, as the case may be, our left prefrontal cortexes) with words.
Though effective treatments exist even for diseases we do not begin to understand, knowing how the components of a disease are related helps us to discern its immediate precipitants and address them. It helps us to understand a constellation of symptoms and to see in what ways one system may influence another. Most of the systems of explanation for illness—the biochemical, the psychoanalytic, the behavioral, and the sociocultural—are fragmentary and leave many things unexplained, and they suggest that even the combinatory approaches now in vogue are highly irregular and unsystematic. Why do particular feelings and particular actions correlate in illness but not in health? “Psychiatry’s most pressing need,” McGuire and Troisi write, “is to embrace evolutionary theory and to begin the process of identifying its most important data and of testing novel explanations of disorders. Attempts to explain behavior, normal or otherwise, without having an in-depth understanding of the species one is studying invite misinterpretation.”
I am not persuaded that knowing the evolution of depression will be particularly useful in treating it. It is critical, however, to making decisions about t
reating it. We know that tonsils have a limited use; we understand what they are doing in the body; we know that fighting infection in tonsils is more trouble than removing them and that removing them does little harm to the body. We know that the appendix can be removed rather than healed. On the other hand, we know that an infection of the liver needs to be treated because if you remove someone’s liver, that person will die. We know that it’s necessary to snip off skin cancers but that pimples do not cause systemic inflammation. We understand the mechanisms of these different areas of the physical self, and by and large we know what kind and degree of intervention is appropriate in the event of dysfunction.
It is eminently clear that there is no consensus on when to treat depression. Should depression be removed like a tonsil, treated like liver disease, or ignored like a pimple? Does it matter whether the depression is mild or severe? To answer these questions correctly, we need to know why the depression is there at all. If depression served a useful function for hunter-gatherers but is irrelevant to modern life, then it should probably be removed. If depression is a misfunction of the brain that involves circuitry we need for other crucial brain functions, then it should be treated. If some milder depression is a self-regulating mechanism, then it should be ignored. Evolution may offer something of a unified field theory, revealing structural relationships among the other schools of thought that are used in studying depression; that will allow us to make decisions about whether, when, and how to treat the complaint.
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