Authors: Andrew Solomon
The capacity to make commitments is to the evolutionary advantage of one’s genes; it is the basis of the stable family unit that provides the ideal environment for the young. But once we have that capacity, which serves an evolutionary advantage, we can use it in any way we choose; and in these choices lies the moral compass of the human animal. “People’s reductive notions of science have caused us to see relationships mostly as mutual manipulations and mutual exploitations,” says Nesse, “but in fact feelings of love and hate often extend to the impractical. They don’t fit with our rationalistic system at all. The capacity for love may serve an evolutionary advantage, but how we act in the face of love is a process of our own. The superego pushes us to do things that give benefit to others at the cost of our own pleasure.” It invites us into the realm of moral alternatives, a realm that loses its meaning if we try to eliminate grief and its milder sad cousin, regret.
Some insects are born from untended egg sacs with a lifetime food supply intact; they need sexual impulse, but not love. The precursors of attachment, however, exist even in the world of reptiles and birds. The instinct to sit on an egg and keep it warm—in contrast to laying an egg and then sauntering off and leaving it to get cold, be crushed, or be devoured by passing animals—clearly enhances reproductivity. In most postreptilian species, mothers who feed their young, as good birds do, have more young who survive, and this enhances their success in producing little chicks who will grow into big birds and procreate. The first emotion, and one for which selection would most significantly occur, is a version of what we call love between a mother and her young. It seems likely that love emerged among the first mammals and that it motivated these creatures to care for the relatively helpless young born without an eggshell into the threatening world. A mother who associates strongly with her offspring, who protects them from marauders and who readily nurses and feeds them, has a much better chance of passing on her genetic material than does a mother who leaves her young to be attacked and eaten up by predators. The offspring of protective mothers stand a far greater chance of reaching maturity than do the offspring of indifferent mothers. Selection would favor the loving mother.
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.