Night Falls Fast Read online

  We have, then, within ourselves the capacity for extremes that will serve us well on occasion and badly on others. These extremes encompass not only rage and aggression but sadness and ecstasy, inertia and frenzied energy states, dullness and exploration. But why should the proclivity for suicide survive? Why do the genes and the volatile brain chemistry that underlie the suicidal potential remain in our genetic makeup? Is suicide a part of the price we pay for diversity? Are the reckless and impulsive behaviors associated with many acts of suicide also associated with capacities integral to the survival of the species? Or do these pathologies exist independent of any adaptive value? The fact that a condition is widespread does not necessarily mean that it is adaptive.

  The recently emerging field of evolutionary psychiatry has been looking at an important and closely related question: Why do the severe psychiatric illnesses—schizophrenia, manic-depression, and depression—persist in humans? The persistence of the genes for schizophrenia—a terrible, debilitating, and painful disease—is perplexing. It would seem that over tens of thousands of years, protection against or elimination of such a maladaptive genetic mutation should have occurred. Yet schizophrenia not only survives, it survives at a relatively high rate, in 1 percent of the population. Why? Some have argued that perhaps the same cognitive and social behaviors that, in their extreme forms, mark or destroy the lives of those with schizophrenia—bizarre and unpredictable thinking, strange or altered patterns of attention, paranoia, resistance to physical pain, acute sensory awareness, intense apprehension, isolation from others, resistance to certain inflammatory disorders or the infectious agents that precede them—may in their milder forms (watchfulness, novel thought, a heightened attentiveness to possible danger) have benefits not only to individuals but, if in an attenuated form, to their kin. Timothy Crow, a psychiatrist at the University of Oxford, creatively and controversially argues that language and psychosis have a common evolutionary origin and that schizophrenia may be the price that Homo sapiens pays for having language.

  It is easier to understand, and more vigorously argued by many, that mood disorders may give an advantage to both individuals and their societies. Depression, characterized as it is by a conservation of energy during times of scant resources, a reduction of activity at times of nonnegotiable threat, or a slowing or cessation of sexual behavior when environmental conditions are poor, is a not surprising biological reaction during times of change or stress. Its existence in mild forms may act as an alerting mechanism to other animals to act similarly and may, as some have argued, help to maintain a stable social hierarchy as well. (Less dominant animals, for example, may submit to more dominant ones in order to increase their own chances for survival and reproduction.) The discontents and darkness of the depressive mind may also create—through the arts and philosophy—a useful perspective in the collective social awareness.

  It is the temperamental, cognitive, and behavioral elements of manic-depressive illness that provide the strongest evidence for a possible link between the infrequent adaptive advantages of a severe illness, on the one hand, and suicide, on the other. American poet Anne Sexton, who committed suicide after a long struggle with manic-depression and alcoholism, wrote in one of her poems that high-flying Icarus

  … glances up and is caught, wondrously tunneling into that hot eye. Who cares that he fell back to the sea?

  The “wondrous tunneling” into the sun and subsequent falling back into the sea conjure an image of the dangerous relationship between exploration and recklessness. Mania, we know, is an aggressive and volatile state, but it is generative as well, an influential condition of contagious enthusiasms and energies. The elements that in part define mania—fearlessness, a fast and broad scattering of thoughts, an expansiveness of moods and ideas, utter certainty, the taking of inadvisable risks—often carry with them the power both to destroy and to create. When the high-voltage manic brain slows, as it must, and its mood seeps down into depression, the crackling together of manic impetuousness with a black mood can be lethal. Suicide is the not-uncommon end point of a short-lived, violent, and yet, on occasion, fertile time.

  The boldness and violence of the manic temperament may come at a cost, but there is strong evidence that manic-depression and its milder forms can provide advantages to the individual, his or her kin, and society at large. (An interviewer once asked me if a manic was not perhaps the first to throw a spear into the heart of a mastodon. The mastodon may have been brought down, but so too may have been the manic.) Several studies have shown that both manic-depressive patients and their relatives are uncommonly creative and academically successful. At least twenty studies have found that highly creative individuals are much more likely than the general population to suffer from depression and manic-depressive illness. Clearly, mood disorders are not required for great accomplishment, and most people who suffer from mood disorders are not particularly accomplished. But the evidence is compelling that the creative are disproportionately affected by these conditions.

  Suicide is also more common in highly creative or successful writers, artists, scientists, and businessmen than it is in the general population. Most are related to underlying depression, manic-depression, or alcoholism in combination with these mood disorders. Percy Bysshe Shelley, who attempted suicide when young, said, “But mark how beautiful an order has sprung from the dust and blood of this fierce chaos,” and this perhaps is true. Extremes in emotions and thinking, when tightly yoked with a disciplined mind and high imagination, certainly can advance the arts, sciences, and commerce. Suffering that may benefit a work of art or move the direction of a spiritual life—“Is the shipwrack then a harvest,” asked Gerard Manley Hopkins, “does tempest / carry the grain for thee?”—may not be of such benefit to the life of the artist. Immoderate thought, and behavior on the remotest ridges of experience, may end in death, yet some artists and explorers feel no choice but to go there. The pull between a life at the extremes and one in more moderate zones is fierce for many. “It isn’t possible to get values and color,” wrote Vincent van Gogh. “You can’t be at the pole and the equator at the same time. You must choose your own line, as I hope to do, and it will probably be color.”

  The toll of suicide on artists, writers, scientists, mathematicians, and others strongly influential on their societies is powerful. The rates of suicide in these groups have been examined in a series of studies conducted by researchers in the United States, Britain, Europe, and Asia. Eminent scientists, composers, and top businessmen were, in these investigations, five times more likely to kill themselves than the general population; writers, especially poets, showed considerably higher rates. Many of the artists, writers, and scientists who committed suicide are listed in the endnotes; the list is a long and disturbing one and gives credence to these lines from Dylan Thomas:

  The hand that whirls the water in the pool

  Stirs the quicksand; that ropes the blowing wind

  Hauls my shroud sail.

  CHAPTER 7

  Death–Blood

  —NEUROBIOLOGY AND NEUROPATHOLOGY—

  I have a violence in me that is hot as death-blood. I can kill myself or—I know it now—even kill another. I could kill a woman, or wound a man. I think I could. I gritted to control my hands, but had a flash of bloody stars in my head as I stared that sassy girl down, and a blood-longing to [rush] at her and tear her to bloody beating bits.

  —SYLVIA PLATH

  EVERYWHERE IN the snarl of tissue that is the brain, chemicals whip down fibers, tear across cell divides, and continue pell-mell on their Gordian rounds. One hundred billion individual nerve cells—each reaching out in turn to as many as 200,000 others—diverge, reverberate and converge into a webwork of staggering complexity. This three-pound thicket of gray, with its thousands of distinct cell types and estimated one hundred trillion synapses, somehow pulls out order from chaos, lays down the shivery tracks of memory, gives rise to desire or terror, arranges for sleep, propels movement
, imagines a symphony, or shapes a plan to annihilate itself.

  From its beginning in the DNA architecture twisted within a single cell, the brain owes its development not only to the tens of thousands of genes it inherits, but also to the constantly shifting environment within which it finds itself. While still in the womb, the brain’s evolution is beholden to a mother’s actions and experiences: if she drinks too much or smokes, eats poorly, or uses drugs, if she is infected by a damaging virus or bacterium, or if she is greatly stressed, the fetal brain registers the effects.

  If susceptible genes are exposed to one of these additional stresses, or “second hits,” from the prenatal environment, a lasting cost—certain forms of mental retardation or epilepsy, perhaps even autism or schizophrenia—may arise. Once a child is born, its exposure or lack of exposure to stimulation from its environment—through sounds, light, shapes, movement, nutrition, touch, and smell—determines which brain cells are pruned and which networks of nerve cells are put into place. The molding of the circuitry of the brain, the formation of its pathways and connections, will remain throughout an individual’s life a product of both inheritance and experiences derived from interactions with the world.

  The essence of the brain, its nerve cells (or neurons), communicate with one another electrochemically by sending information out across fibers called axons. These axons branch off into a number of small fibers that end in terminals; between terminals are the slight gaps known as synapses, across which messages are sent. Electrical stimulation of a nerve cell causes the release of neurotransmitters—such as norepinephrine, glutamate, acetylcholine, dopamine, and serotonin—from storage areas in vesicles located at the end of the neuron. The release of these neurotransmitters into the space between the nerve cells allows the transfer of information from cell to cell.

  Neurotransmitters are the lifeblood of the brain, governing the interactions from cell to cell, brain region to brain region, and brain to body. No one knows how many transmitters there are, nor does anyone fully understand the actions of the more than one hundred identified to date. We are only just learning about the profusion of transmitters that exist, and we have only the merest notion of their tangled relationships with one another. For scientists to focus on one or two substances at the expense of the others known or yet to be discovered, or to minimize the complexity of the chemical interactions within the brain or at the synapses, would be a damning mistake, a late-twentieth-century equivalent of earlier, primitive views that deranged minds were caused by satanic spells or an excess of phosphorous and vapors.

  Many neurotransmitters and hormones are critical to the regulation of mood and to the activation of the many behaviors involved in suicide. It is impossible to discuss or even mention all of them here. The primary focus here is on only one of the dozens of transmitters known to be involved in the complex activities of the brain, serotonin, but it is a central one and illustrative of the role of the brain’s chemistry in suicide and suicidal behaviors.

  Serotonin, a chemical found in plants as well as in ancient invertebrate nervous systems, is widespread in the bodies and brains of mammals, including humans. It acts in diverse ways: it controls the diameter of blood vessels, affects pain perception, influences the gut, plays a role in the body’s inflammatory responses, and causes platelets to clump. More significant from a psychiatric and psychological perspective, however, serotonin is deeply implicated in the roots of depression, sleep regulation, aggression, and suicide.

  Several lines of evidence link abnormalities in serotonin functioning to suicidal behavior. First, we have known for a long time that the neurotransmitters serotonin, norepinephrine, and dopamine are intricately involved with the origins of mood disorders, and we have also known that drugs that have an impact on these transmitters can precipitate or ameliorate depression or mania. Reserpine, a drug derived from the plant Rauwolfia serpentina, furnished an early illustration of this phenomenon. Used centuries ago in India as a remedy for insomnia and insanity and more recently in this century as a treatment for psychosis and high blood pressure, the drug had a disturbing effect on some patients who took it. A significant number became profoundly depressed; as it was subsequently shown, the depression was due to a dramatic depletion in the brain of serotonin, dopamine, and norepinephrine.

  In the mid-1950s a quite opposite clinical observation was made. Some patients who were being treated for tuberculosis with a drug called iproniazid became strangely cheerful and animated; despite their grim circumstances and prognoses, they were almost defiantly optimistic. A few were strikingly euphoric. It was not long before iproniazid, pinpointed by the clinicians and scientists who were studying it as the cause of the mood elevation, was in widespread use as an antidepressant. In short order the mechanism of its action was discovered: it worked because it inhibited the action of monoamine oxidase, an enzyme that inactivates norepinephrine, serotonin, and dopamine after they have been released at nerve synapses. This inhibition of monoamine oxidase in effect increased the availability of the neurotransmitter substances. It was becoming clear to researchers that the availability and distribution of neurotransmitters were critical to the expression and regulation of mood. This was underscored by Nobel laureate Julius Axelrod’s discovery that another antidepressant, imipramine (a tricyclic antidepressant, also known as Tofranil), worked by inhibiting the reuptake of neurotransmitters from the synaptic cleft back into the synapse that had first released them, thus increasing their availability.

  More recently, the “third-generation antidepressants,” drugs that act much more specifically on individual neurotransmitters, have not only radically altered clinical practice by their widespread popularity and use but have also provided further evidence for the role of neurotransmitters in the origins or perpetuation of depression. Classified as selective serotonin reuptake inhibitors, they act primarily by blocking the removal of the serotonin at the synapses. This in turn increases the availability of serotonin in the brain.

  In addition to the link between neurotransmitters and depression, there is another line of evidence implicating serotonin in suicidal behavior; this is its entanglement with impulsive behavior, aggression, and violence. We know from studies of rodents and nonhuman primates that if the availability of serotonin is curtailed or its transmission impeded, animals become more aggressive and impulsive. Rats with low serotonin levels attack and kill other rodents, and “knockout” mice—mice that are lacking a gene necessary for normal serotonin functioning—attack faster, acquire addictions more quickly, and press levers more rapidly and erratically. Rats and other animals selectively bred for docility, on the other hand, have higher levels of serotonin.

  Monkeys with low levels of serotonin’s breakdown product, 5-hydroxyindoleacetic acid (5-HIAA)—a metabolite that is presumed to reflect serotonin functioning in the central nervous system—are far more likely than those with higher levels to assault other monkeys, increase their alcohol intake, and engage in highly risky behaviors such as leaping long distances at perilous heights. If serotonin levels in monkeys or other animals are artificially elevated by drugs or by adding tryptophan (a precursor of serotonin) to their diets, their aggressive and impulsive behaviors sharply decrease.

  Psychologist J. Dee Higley and his colleagues at the National Institute on Alcohol Abuse and Alcoholism followed the lives of forty-nine free-ranging rhesus monkeys on a South Carolina sea island. When the monkeys were two years old, the scientists measured their 5-HIAA levels by drawing samples of cerebrospinal fluid (CSF). The animals were ranked from lowest to highest in their levels of aggression, and a record was made of all existing scars and wounds. Four years later, the scientists recaptured and reassessed the animals. Eleven of the monkeys were dead or presumed missing; the correlation between the primates’ survival and their 5-HIAA levels was stunning. Nearly half of the monkeys with low CSF 5-HIAA concentrations, as determined at the initial assessment when the monkeys were two years old, had died as a result of violence. N
one of the monkeys with high concentrations had died or was missing. Low levels of serotonin were predictive not only of premature death but of excessive aggression and risk taking as well.

  Studies of serotonin levels and violence are of direct relevance to humans, who share with other group-living primates most of the genes that are involved in violent, aggressive, and impulsive behavior. And as Higley and other primatologists point out, nonhuman primates and humans share many critical infant-rearing patterns, relatively stable personality traits, and similar serotonin pathways and chemistries. Serotonin functioning in the central nervous system, as measured by CSF 5-HIAA, appears to be an enduring trait in individual animals and humans, and it correlates well with impulsive and aggressive behavior. Interestingly, however, Higley and his collaborators conclude from their primate studies that low CSF 5-HIAA concentrations are not correlated with rates of aggression in a simple way. They are correlated only with aggression that is impulsive and unrestrained. High rates of impulsive behavior, the scientists believed, were associated with “severe, unrestrained aggression, but not with competitive, restrained aggression used to maintain social status or aggression that seldom escalated out of control.”

  Primates with low CSF 5-HIAA levels are not only more likely to be inappropriately aggressive, they are not well accepted by their peers and they are less likely to breed. Often forced to live apart from their natural social groups, many end up living in isolation. The impact of serotonin functioning on aggression and social behavior is powerful and potentially life-threatening. An animal’s biology, behavior, and physical and social environments link together and influence one another in complex and subtle ways we are just beginning to understand.