Most people with mood disorders—and people with other kinds of psychiatric illness too, I imagine—find it hard to put their subjective experience into words. Colors, metaphors, and visual images come to mind more readily than a precise verbal description. I’ve come to visualize depression as a series of gray tones deepening from pure white to pure black. For me, this image conveys the way depression moves subtly between darker and lighter as I feel worse and better and worse again over the passage of time. Put another way: if the healthy mind is a glass of clear water, depression is what happens if you add successive drops of ink and stir. Each addition darkens the consciousness within the mind, and the vision looking out from it.
Given my tendency to think of depression in shades of gray, I became curious about how it came to be called the blues. Long ago, when melancholia was thought to be caused by demonic possession, early Christian monks struggled against acedia, a state of apathy and despondence that the fourth-century monk Evagrius Ponticus called the noonday demon. By the eighteenth century, people were referring to their dark moods as the blue devils, or fits of the blues. And the descendants of slaves and sharecroppers in the Mississippi Delta who played and sang the blues transformed all kinds of trouble—drinking and gambling, heartbreak and sexual longing, poverty and racism, into one of the great musical art forms.
It’s a strange coincidence, then, one owing to science and not to art, that the color blue—a blue dye synthesized in 1876—was the first in a series of steps that led to the creation of a truly effective antidepressant. At that time, asylum psychiatrists could do nothing to cure those they treated because they didn’t understand what was causing the symptoms. Their task was to calm their anxious, agitated, or psychotic patients, to physically restrain those who were violent, to prevent suicides, and to confine patients whose families couldn’t take care of them. In the century before effective drugs for psychosis and depression arrived in the 1950s—by way of that blue dye—doctors sedated their asylum patients with opiates, digitalis, chloral, barbiturates, and bromides.
In the quest for effective antidepressant drugs, the two great challenges facing scientists have been learning the causes of disorder and finding ways to target and reverse those causes. Although one might think that the two go hand in hand, they haven’t. Instead, substances that affect the nervous system were discovered at a time when the nervous system was still poorly understood, and these substances then became the ground of further exploration and hypotheses. Since the mid-twentieth century we have had chemical agents that ease the symptoms of depression, but arriving at a clear understanding of what their effects mean within the complex neurophysiological disorder that seems to underlie the illness has been more difficult. Nevertheless, millions of Americans have come to rely on them.
The color that started it all, methylene blue, was created by a chemist called Herbert Caro at a time when chemists were creating dyes for the booming nineteenth-century textile industry. Trained as a calico printer in his native Germany, Caro later moved to Manchester, England, and worked in a chemical firm that made aniline-based dyes to meet the industry’s demand for new colors. As it turned out, methylene blue wasn’t well suited to the printing of cottons because it wasn’t colorfast, but its core compound, a three-ringed molecule called phenothiazine, was synthesized a few years later by Heinrich Bernthsen. Phenothiazine would prove important in drug research and in medicine as an anesthetic, an antipsychotic, an antihistamine, and an antimalarial.
In the late 1880s another German chemist, Paul Ehrlich, discovered that he could use methylene blue to stain cells. Under the microscope, he saw that the dye could isolate and deactivate certain live organisms, including plasmodium, the malaria parasite. (It was given to soldiers serving in the Pacific in World War II to prevent malaria; they were unhappy when their urine and the whites of their eyes turned blue.) It was phenothiazine, Ehrlich realized, that determined methylene blue’s affinity with nerve cells. When he injected a bit of the dye into a frog and then excised the tip of the frog’s tongue, he saw “the most subtle dark-blue ramifications of the nervous system of the tongue become visible . . . in a picture of impressive beauty.” In his address on winning 1908 Nobel Prize for his work on immune system antibodies, Ehrlich set out the hypotheses that there must be receptors in the nervous system, and that phenothiazine might be helpful in the treatment of psychoses. Decades later, he was proven correct. Pietro Bodoni, an asylum doctor in Genoa, usually goes unmentioned in this story, but in 1899 he wrote of his success in calming agitated and psychotic patients with methylene blue.
When reading about drug discoveries, one will almost certainly come upon the odd word “serendipity.” It comes from an ancient Persian fairy tale in which the three traveling princes of Serendip keep stumbling upon what they are not seeking. Penicillin for infections, warfarin for smallpox—these are two such fortunate accidents. The serendipitous discovery of a new chemical agent often sets off a process of finding what it might be useful for. This was the case with methylene blue and its active molecule, phenothiazine. Herbert Caro’s dye wasn’t useful in dyeing cottons, but Paul Ehrlich found it useful for staining cells. The road to relief from both psychosis and melancholic depression began with phenothiazine and Ehrlich’s hypothesis about receptors in the nervous system. Then nothing much happened for several decades.
BY 1950, RESEARCHERS at the French pharmaceutical firm Rhône-Poulenc were focused on the antihistamine characteristics of phenothiazine—particularly its sedative effect on the central nervous system. Scientists had realized that giving an antihistamine along with an anesthetic could lower the chances of surgical shock, a sudden and often fatal drop in blood pressure sometimes caused by anesthesia. Henri Laborit, a French army surgeon and anesthesiologist at the Val-de-Grâce military hospital in Paris, had been looking for something that would prevent shock by stabilizing the autonomic nervous systems of patients during surgery. In 1952, he tried a phenothiazine compound from Rhône-Poulenc called chlorpromazine, and found that it was not only effective in preventing surgical shock, but that it rapidly induced a state of calm indifference without loss of consciousness. Here was another confirmation that phenothiazine did something—it was unclear precisely what or how—to the central nervous system. Laborit suggested to the psychiatrists at Val-de-Grâce that it might be useful in treating agitated patients, and soon psychiatrists in Paris and beyond were carrying out trials with chlorpromazine. In the days before randomized clinical trials came to be the standard protocol, psychiatrists tested agents in this small-scale, ad hoc way, closely observing effects on their own patients, and sometimes on themselves.
At Sainte-Anne hospital in Paris, Jean Delay and Pierre Deniker gave small doses of the drug to thirty-eight patients with mania, and the calming effect was striking. With their psychotic patients, the results were even more impressive. In 1955, after Delay held an international conference and presented his results to psychiatrists from fifteen countries, the use of chlorpromazine spread rapidly. Heinz Lehmann, the director of a psychiatric hospital in Montreal, found that in his agitated schizophrenic and manic patients, many of whom had been delusional for years, chlorpromazine’s effects were extraordinary. “One has the impression that this drug promotes an attitude of sober resignation and of critical reflection, even in acutely disturbed patients,” Lehmann wrote. For people who at times had to be held in physical restraints, and for their caregivers, a breakthrough moment had arrived. The pharmaceutical company Smith, Kline & French, which gave it the brand name Thorazine for the U.S. market, was richer by seventy-five million dollars just a year after doctors began using it in American psychiatric hospitals. Troublesome side effects caused by prolonged use of chlorpromazine—neurological tics and weight gain, among others—were rarely mentioned amid all the buzz.
IN SWITZERLAND, before all the chlorpromazine excitement broke out, the Geigy Company had also been seeking to create an antihistamine useful for sedation. Geigy began as a dye manufacturer, and its chemists decided to look back through the warehoused company archive for molecules similar to phenothiazine. They chose a dye from 1898 called summer blue, with an active molecule called iminodibenzyl, in the hope of finding a useful sedative or hypnotic. After creating and testing several versions, in 1953 the researchers concentrated their efforts on the one whose structure was closest to that of chlorpromazine. Geigy labeled their chosen compound G22355, and sent it out to psychiatrists who had tested compounds for them in the past.
One of these doctors was Roland Kuhn, chief psychiatrist at the Münsterlingen Asylum on Lake Constance, which had about seven hundred inpatients. He was already dispensing chlorpromazine when Geigy asked him to test their new drug on the asylum’s schizophrenic patients. The results were not encouraging. Some became agitated, others became hypomanic, and those who had been taking chlorpromazine deteriorated. One man escaped from the grounds and rode a bicycle to town in his nightshirt, singing loudly all the way. The residents of Münsterlingen were not pleased, and Geigy brought the trial to an end.
After a time, Geigy asked Kuhn to try G22355 again, this time with his depressive patients. Like other psychiatrists of his day, Kuhn was accustomed to thinking of depressive patients in two categories: those with the melancholic type that he called vital or endogenous depression (an illness), and those with psychoreactive depression (a response to life events). Of the treatments available in the early 1950s, Kuhn felt that only two were effective. He used electroshock therapy for the worst cases in the first category, and psychotherapy for those in the second. Neither treatment was ideal. Prolonged shock therapy caused cognitive side effects and had to be managed carefully, while psychotherapy could take a long time to produce results. Stimulants like amphetamines were also used to treat depression at the time, but they were transient in their effects and could lead to addiction. Although he was a trained psychoanalyst, Kuhn was no purist. He hoped that his patients with severe depression might one day be treated with a drug as effective as chlorpromazine.
Kuhn began his trial of G22355 with a depressed and delusional patient called Paula F. on the twelfth of January, 1956. Six days later, a nurse reported that when Paula awoke that morning she appeared to be entirely well. Her “facial expression, her behavior, and her total being” were transformed. By April, Kuhn had tested the drug among broader groups of patients and was convinced that the compound had “markedly anti-depressive properties” and an “immense potential.” Kuhn wrote in his report for a Swiss medical journal that G22355 was most effective in patients with endogenous depression: “We mean by this a general retardation in thinking and action, associated with fatigue, heaviness, a feeling of oppression, and a melancholic or even despairing mood, all of these symptoms being aggravated in the morning and tending to improve in the afternoon and evening.” Such patients presented with “frequent depressive delusions and suicidal urges.” In the autumn of 1957, Kuhn presented his findings at the Second World Congress of Psychiatry in Geneva to an audience of only about a dozen psychiatrists. They were unimpressed, probably because of their psychoanalytic bias. Frank Ayd, an American who was present, later commented that those in the room were slow to realize “we were hearing the first announcement of a drug that was going to revolutionize the treatment of affective disorders.”
Six months later, Kuhn brought the news of his revolutionary discovery to the United States. He reported to doctors at the Galesburg State Hospital in Illinois that imipramine could bring about an extraordinary change within a short time, as patients’ tormenting fixed ideas, despondency, and despair all gave way to increased energy and renewed hope in the future. Such dramatic results, he said, would “not be achieved by intensive prolonged psychotherapy.” Kuhn admitted that for the present, imipramine’s mode of action remained “completely unknown.” Nonetheless, the implication was undeniable: imipramine could make hospitalization and electrotherapy unnecessary, and could also make obsolete the expenditure of time and effort that psychotherapy required of the patient with endogenous depression. A rapid drug response verified the ancient belief that endogenous depression—melancholia—was a disorder in the body.
Despite the positive response of Kuhn’s patients, Geigy was slow to follow through in making Kuhn’s new antidepressant available to the public. They had set out to develop a rival to chlorpromazine, the powerful tranquilizer that was calming agitated and psychotic patients in asylums all through Europe and the United States. Geigy executives remained unconvinced that imipramine, so well suited to patients with melancholia, could result in anything like the profits that chlorpromazine was generating. There just weren’t all that many sufferers of melancholia. But it was not only melancholic patients who could benefit: Kuhn also reported excellent results in “several cases of apparently purely reactive depression.” In 1956, the company began consulting with outside experts to try and determine whether imipramine could command a wider market worth investing in. It wasn’t until a Geigy board member witnessed its extraordinary effect upon a relative with severe depression that the company decided to launch the drug in Switzerland. G22355 was now called imipramine hydrochloride, with the brand name Tofranil. It was the first in the family of tricyclic antidepressants, named for the three-ringed molecular structure they shared with methylene blue and chlorpromazine.
A scholarly looking ad for Tofranil published in a Swiss medical journal in 1956 offers a glimpse of how Geigy imagined the market for imipramine. It features an image of the mandrake plant from a fifteenth-century book of herbal medicine, and in small print refers to the earlier dependence on herbal remedies and magic in curing mood disorders. The juice of the mandrake plant, believed to have magical properties, was given as a soporific to people suffering from mania, melancholia, and other ailments from ancient times. It was also poisonous, and the large caption points to imipramine as a great step forward. Translated to English, it reads, “Tofranil, a milestone in the treatment of melancholia.”
Imipramine finally arrived on the U.S. market in 1959, also branded Tofranil, at a moment when lesser forms of depression and anxiety were already being addressed in a market saturated with stimulants and with minor tranquilizers like Miltown. It was marketed solely to doctors, with print ads appearing in medical journals like Mental Hospitals and the American Journal of Psychiatry. Compared with the bright optimism of antidepressant ads four decades later, which were targeted at the whole consumer market in Time, Newsweek, and other general interest magazines, these ads are somber and serious. Geigy didn’t change the tone of its advertising for the U.S. market, where ads for Tofranil conveyed the darkness of the illness it was meant to treat. In 1963, an eerie, alien-like face with sunken eye sockets appeared in the Archives of Internal Medicine, the image seeming to fade away much as the vibrant self does in melancholic depression. Two columns of small text alongside the image provided information a physician would need, and emphasized how Tofranil could halt a depressive disorder “before it becomes deeply entrenched, and will save the patient from hospitalization and electroshock.”
Today, when depression is a leading global cause of disability, it’s hard to imagine Geigy’s hesitation in bringing imipramine to the market. But at the time, far fewer people were hospitalized for depression than for mania and schizophrenia. People were brought to asylums only when they could no longer function, or when they were suicidal. Those who were less severely depressed, I assume, went without treatment and possibly without notice, since depression tends to make people feel ashamed and unwilling to talk about their state of mind. The creation of effective drugs brought the illness out of the shadows, but it was not until the late 1980s that this development really took hold.
Antidepressants and other psychiatric drugs were a major advance in treatment at a time when psychoanalytic theory remained the basis of training residents in psychiatry. At the time that I began taking imipramine, the treatment paradigm included both medication and psychotherapy, each representing different assumptions about depression’s cause and cure. Biological psychiatry assumed that illness resulted from physiological disorder, and that medication could address that disorder. Psychodynamic psychiatry assumed that depression was rooted in life experience, and sought to resolve problems by examining memories and bringing unconscious, unresolved conflicts to light. In the decades after my hospitalization, easy access to a whole array of drugs made the expensive and lengthy process of psychotherapy seem unnecessary. The decline in the cultural influence of Freud’s ideas was aided by drug makers who promised that simply by taking a pill, depressives could transform themselves into more cheerful, socially engaged, successful people.
EVEN AS BATTLE LINES were being drawn between psychodynamic and biological approaches to treatment, there was already a theory in place that supported both positions. According to the diathesis-stress model, some people inherit a genetic risk (the diathesis) that creates a predisposition, while stress or loss in early life experience can trigger the onset of the disorder. People in the same family may not share the same degree of genetic risk, but they do share the same environment. Some will become ill, and others will not; greater resilience and a happier disposition may provide protection. It has become increasingly clear to me that I not only inherited the risk, but that other factors—my gender, my temperament, my religious upbringing, and my parents’ stress—increased the possibility that risk would become disorder. My own history is an example of how a combination of genetic risk and psychological stressors can create the matrix out of which depressive illness may grow, and how its physiological and psychological components are best treated with both medication and psychotherapy.
As Roland Kuhn’s patient, Paula, was awaking one morning in January of 1956 to surprise her caretakers at the Münsterlingen asylum with her extraordinary recovery, I was in my mother’s womb. In April, my parents brought me home to a rowhouse in northeast Philadelphia. I was their second child, arriving seventeen months after my brother. By January of 1964 four more babies would arrive, and when we turned six each of us would go to the same parish school that my mother had attended, three blocks away.
The houses on our street were built just after World War II, and the front entrance jutted out from the stone façade to create a stoop and, on the inside, a vestibule. The strange word “vestibule” rolled around in my mind when I passed through it. Directly ahead as you came through, the stairway led up to three bedrooms, and the living room was to the right. This part of our house sets the stage for a strong memory. I was walking down the stairs and about to go outside to play, when just as I was about to enter the vestibule, a wave of sadness passed through me. It was such an unfamiliar feeling that I can still recall it. It was like walking through a cold atmosphere, or through a cloudbank. By the time I stepped out the front door into the sunshine, it had passed. Nothing that had just taken place had given me any reason to feel sad. I was so puzzled that I tried to make it happen again. I thought deliberately of the saddest things I could imagine. The death of my parents. My own death. I envisioned myself lying in a coffin, my family weeping. These thoughts brought tears to my eyes, but they didn’t bring back that unsettling feeling. I was perhaps seven or eight at the time. That sensation returned once or twice while we still lived in that house. I’ve sometimes wondered whether it was the shadow of the depressive illness that was coming for me, or that was perhaps already present.
Since I would eventually need the drug that Roland Kuhn discovered in the year of my birth, and for exactly the symptoms he described—the general retardation in thinking and action, the feeling of oppression, the melancholic, despairing mood, the depressive delusions and suicidal urges—it’s worth asking how this came about. When did my depression first set in, and how? There are no straightforward answers to such questions, as there would be for a disease like cancer or diabetes.
Scientists studying the genetics of mood disorder have found that in families where depression is present from generation to generation, more severe forms of the illness arise. Episodes appear earlier in life, and with greater frequency of later recurrence. While major depression is less strongly heritable than either schizophrenia or bipolar disorder, one study estimates the risk to siblings and children of a person whose first episode occurs before age twenty to be five times the risk in the general population. The risk decreases greatly in relatives of a person whose first episode occurred in middle age or later. There is also a strong correlation between depressive illness and stress, loss, neglect, or abuse in early life.
When I was first admitted to the hospital and a family history was taken, my parents told Dr. Young that each of their fathers had obvious periods of depression, and neither ever saw a psychiatrist or took medication. In that same meeting my father told him that he was on a tapering dose of imipramine, recovering from a period of serious depression brought on by a stressful time at work two years earlier. I hadn’t known about this at the time, though I was well aware that my sweet-natured father was always sensitive and often brooding. In his later years he took an antidepressant regularly. My mother’s father nearly attempted suicide with a razor blade when he was in his seventies and hospitalized for diabetes and Parkinson’s. I never heard about this until I read it in the family history taken from my parents. While it may seem odd that all of this went unmentioned, silence was my family’s default mode. We didn’t talk about how we were feeling; we simply made space for the moods and irritability of others. Feelings were private, and we kept them to ourselves while as far as possible pretending to be okay.
My family became the subject of a great deal of discussion in therapy sessions, although it felt like a betrayal to talk about them and to reflect critically on aspects of my upbringing. As I recalled scenes from my childhood, I realized that I had grown up in a household headed by young parents who were stressed to the edge of their endurance. My father went to work each day at an insurance company downtown, left at midday to attend courses at the University of Pennsylvania for his master’s degree, and then went back to work. He didn’t get home until ten on many evenings. The part-time coursework toward the master’s degree took six years, and his days were so long that he nearly gave it up more than once. In pictures of his Penn graduation, just days after his fifth child was born, he is holding my newborn sister in his arms. Next, he began to study after work to become a certified financial analyst. He often went to his parents’ house several blocks away for the evening, pacing with his book so as not to fall asleep, while my mother took charge of bath and bedtime duties as usual. All of this was necessary for him to earn enough money to send us all to college, as he was determined to do. On weekend nights he relaxed and listened to music. Lying in bed I would hear jazz and blues floating up the stairs: Billie Holiday, Art Pepper, Lee Wiley, Gerry Mulligan.
During these years my mother, often pregnant and often nursing, took care of everything else. She did all of the washing, including the cloth diapers, and everything was hung to dry on the clothesline until she was able to buy a dryer, around the time her fourth child was born. She did the cooking, the shopping, and the housecleaning. She did much of the ironing—which included my father’s shirts for work and the white cotton shirts of our school uniforms. Her mother often came by in the afternoons to lend a hand with the ironing. I can remember the warmth of my blouse on cold mornings when my mother did them as we were going out the door to school. It all seems extraordinary to me now, how difficult life was for both of my parents. But the burden fell heaviest on my mother. It’s easier to spend a day working in an office among adults than buried in housework, surrounded by demanding toddlers.
In my grandparents’ time, the large number of children in Irish families and the expectation that several would have to emigrate led in many instances to emotional distancing on the part of mothers. In my Irish-American family a version of this occurred as well, because my mother encouraged her older children to be independent, to soothe conflicts, to take ourselves out of the way. I responded by trying not to ask anything of her, and never seeking solace or support. When I discovered the work of child psychiatrists John Bowlby and D. W. Winnicott, who were both working in England during the 1950s and ’60s, I realized that they would have seen in my case a problem with attachment, and I would have to agree.
THE YEARS OF MY childhood coincided with the years in which Americans began to take drugs to help with the kinds of stresses my parents were under. My parents were exactly the sort of people—mothers stressed at home and fathers stressed at work—pictured in the ads for the mild tranquilizers that were popular in those years. Exhausted parents were also targeted in ads for uppers, like Dexedrine and Ritalin. Some of the images are scenes right out of my childhood. In an ad for Meprospan, a mother in skirt and blouse sits on the bathtub edge looking wearily at a naked little girl about to step into the tub, as if she can’t wait for her day to be over. The caption reads, “Her kind of pressures last all day. Shouldn’t her tranquilizer?” But in the early years of their marriage my parents would never have spoken to a doctor, much less a psychiatrist, about anxiety, depression, or exhaustion, and wouldn’t have thought of taking pills for relief. Growing up as the children of parents whose early lives had been harsher than their own, they never expected to have an easy life handed to them.
A 1956 ad for Dexedrine addresses doctors who might think of prescribing it for weary patients like the young woman pictured, who stands in her bathrobe holding a dishtowel and leaning on a kitchen counter piled with dirty dishes. “Why is this woman tired?” the caption asks. If she is a housewife and physically overworked, a physician should prescribe rest. If she is mentally exhausted, however, “crushed under a load of dull, routine duties,” the pill might renew “her energy and well-being,” her “interest in life and living.” The ad invites doctors to prescribe amphetamines for what sounds like depression, but it addresses the lack of fulfillment that Betty Friedan called “the problem that has no name”—a problem specific to women, and something neither amphetamines nor tranquilizers could cure.
My mother never moped in her bathrobe, but she was certainly tired. She was seventeen when she met my father at a New Year’s Eve dance, and she looks radiantly happy in the photograph taken that night. They married nearly five years later, after waiting out his Army service. When I was born, she was twenty-five. By the time I turned eight, she was thirty-three and the mother of six. She was still very beautiful but, like the woman the ad describes, crushed under dull, repetitive tasks. Because I was named after my mother and had the same dark hair and hazel eyes, I couldn’t help identifying with her. Her own mother had worked as a maid in the house of a wealthy family when she first came to this country. I hated the idea that this domestic servitude was the fate of women, and awaited me as well. I would have preferred to be a boy, since boys were clearly more valued and more privileged, and they didn’t do housework.
Just as I couldn’t help identifying with my mother, I couldn’t help absorbing her emotional force field. I noticed when her nerves were strained and when she seemed exhausted or exasperated. I helped in small ways—I ran to the store for milk, changed diapers, looked after the younger ones. We knew that to fight among ourselves was to put more strain on our parents. To this day my mother recalls, “I just wanted you all to be good.” But it wasn’t so simple. That word was huge, as huge as God. Being good meant being quiet, not making messes, not getting our clothes dirty, not arguing, doing well in school, and behaving well in front of the neighbors so as not to shame the family. We were always failing to be good in one way or another. One day a woman across the back alley complained to my mother about one of us, and she replied with great seriousness, “I am the one who is responsible to God Almighty for these children.” My mother and I laughed about this when she remembered it recently. It came up in the context of the fact that none of us go to church anymore.
If my mother was often angry as well as overwhelmed, the cultural perspective she inherited didn’t allow her to see anger as a justified response to her circumstances. She shared the assumptions of her own parents, who carried them to this country from the west of Ireland of their formative years, before 1925 or so. Instead of rebelling, she kept trying to meet the ideal of the self-sacrificing, subservient wife and mother, and she kept on performing the tasks required of her—cleaning, cooking, making sure her children were well dressed and polite—to the limit of her endurance. She had no choice. She had to meet the standards of my father’s mother, who had been sent to board at a convent school where she learned French and lace-making and fine embroidery, and who alone among my grandparents had attended school past the age of fourteen. She imposed her perfectionism upon my mother, who never received a word of praise or approval from her.
My own worries about not being good enough were present from the time I could read, if not before. When I was six, my mother gave me a book on the lives of the saints. I was astonished by the story of Joan of Arc, and stunned at how bravely the martyrs in Rome went to their deaths, first having to lie on beds of nails, or have their eyes plucked out, or some other unimaginable horror. I knew that if challenged to defend my faith I would cower and fail, like Judas. I just hoped I wouldn’t ever have to. It was a strange thing to be concerned about, given that in school we occasionally had to crouch under our desks for nuclear explosion drills. The political fears of those years—the Cuban missile crisis or that often-mentioned thing called the Iron Curtain, for instance—didn’t affect me at all. It was always the impossible challenges of faith that troubled me.
Another childhood memory: It was a summer night, and I was standing with a group of kids outside the house of a friend around the block. It was time to go home, and something in our conversation had started me thinking about time. The problem of Hell, introduced by the nun who taught my first-grade class, had provoked this bout of pondering. Eternity is time without end, and the suffering of hell has no limit in time. I kept trying to think further and further in time, the furthest out in time I could imagine, but I kept failing to grasp eternity. I walked home slowly, revolving these thoughts in my mind, feeling somehow pleased with the hard problem but also scared of its immensity, and trying not to imagine the pain of the fire that would burn me eternally.
On Palm Sunday in third grade I was kneeling next to my best friend Mary Kelly at Mass. We were following along in our missals as the priest read the story of Christ’s passion and, for a moment, tears came to my eyes. Mary looked at me with surprise. Walking home, she told me that she was impressed by my holiness. But I wasn’t holy. I was trying hard to overcome the distance between myself and Christ’s suffering. I was just trying to feel what I thought I should be feeling.
Something in my character made me take all those teachings very seriously. They were presented, of course, as deadly serious. But why did I accept the weight when other children in my family and among my friends appeared to be relatively unconcerned? All of this would dovetail with the illness that was to come, in which guilt and shame and a sense of never being good enough would sometimes expand to take up all the space in my consciousness. Surely this connection between childhood guilt and shame and depression is not a coincidence.
In a box of old photographs that included my third-grade class photo, I came across a little red booklet called “Stations of the Cross for Children” that might have been the source of my fervent wish to empathize with Jesus. Inside the cover, in shaky Palmer method script, I had written my name, address, and phone number. On the back, too, I had written my name. I’m amused now, but also horrified, to see this child’s thoroughgoing possession of the little book. Perhaps we were given these booklets in school, or perhaps I picked it up at church during Lent, when it was customary to meditate on Christ’s ordeal from his triumphant arrival in Jerusalem, through his trial and crucifixion, to his resurrection. Inside it, each station of the cross has a picture and a prayer, ending in a plea to “Teach me.” Here is the one for the second station, “Jesus Is Made to Carry His Cross”:
Dear Jesus, the cross which they are laying on Your shoulders is so heavy.
How it must hurt!
And You are all wounded and bleeding
how will You be able
to carry it up that steep hill?
Teach me to remember
That when I sin
It hurts You
Even more than that heavy cross.
The logic of all this was that children had to accept responsibility, just as adults did, for the death by torture of the son of God, because he died to redeem our sins. There was no such thing as an innocent child.
From my present perspective, this all seems a bizarre and certainly harmful approach to educating children. Since the Church’s priority in those days seems to have been indoctrination and discipline rather than education, children in themselves were unimportant and were not treated as individuals. Catholic homes and schools alike were places of surveillance and self-surveillance. We memorized the catechism, confessed our childish sins to the priest, and were told that God sees all. One pathetic memory proves just how pointedly I had taken this to heart. When a relative gave me a little red diary as a gift, I wrote on the first page, “To God, the only one who really understands me.” The very few entries that followed were addressed, “Dear God.” I was uncomfortable writing in it because despite its tiny lock and key, I felt sure that anyone in the house would read it if they could. In a house full of people, I enlisted God to be my friend and confidant.
I’ve wondered whether the aloneness I felt in the midst of my large family was an early manifestation of depression, although perhaps it’s a common thing for children to feel. I was conscious of things that were troubling and couldn’t be spoken of to any reassuring adult. The solitude of one’s own consciousness can be liberating, and reading was a joyful way—often the only way—for me to be alone. But there’s no doubt that an uncomfortable gap opened up around me early in life. I see myself standing apart, silent and observing, aware that I wasn’t as happy as I was expected to be. My trouble was invisible, and I sensed that I should keep it that way.
Despite my inwardly troubled state, I wasn’t outwardly a shy or anxious child. I felt more free when I was out of the house, playing games with the gang of kids who lived on our block. I liked bike races, stickball, climbing trees, and walking along the tops of fences. I was physically fearless, and found that being a tomboy was the best way of dealing with the problem of being a girl. I knew how to get along with people, so my inward separateness and my outward sociability ran parallel. I developed a double self, and was accomplished at appearing to be just fine.
When I was twelve my father took a new job in Manhattan, and we moved north to a larger house on rolling Pennsylvania farmland that was giving way to suburbs. I had my own room for the first time, and I started seventh grade in the brave new world of public school. My Catholic childhood had instilled the hyperactive conscience and the cruel self-critic, qualities that Dr. Young would later call “the most powerful superego he had ever seen,” and Dr. Waters would call a “lack of empathy” for myself. My attention to detail, my sense of orderliness, my desire to be as good, and as good at everything as I could be, came out of that particular home and school life. Along with a deeply internalized sense of shame—including the shame instilled about sex and the body—it all dovetailed perfectly with an incipient depressive disorder. There is a niche in me where shame will always live, no matter how far I’ve moved from the world of my parents and grandparents, and no matter what I’ve managed to achieve.
As time passed, the feeling of oppression became intolerable. Occasionally I rebelled. I was about sixteen when, one Sunday morning as we were all leaving for Mass, I announced that I wasn’t going. The sameness week after week—the priest’s droning of the liturgy, the congregation’s lifeless responses, the self-conscious parade to communion, the sermon of empty platitudes—it all drove me mad. I declared that I would walk to the nearby Quaker meetinghouse instead. My parents were livid, but I refused to get into the car, and we went our separate ways. Another weekend, I refused to clean the bathroom—something that my sisters and I were assigned in weekly rotation. It infuriated me to get down on my knees and scrub the floor around the toilet when my brothers didn’t have to. It was a beautiful day, and I went off on my bicycle to meet my friends. When I got home I learned that my mother had cleaned the bathroom. Rebellion inevitably boomeranged in this way, returning full force as guilt.
I began to realize that I was “sensitive” when I wanted to spend more and more time alone in my room, reading or listening to music. I assumed that being sensitive was a good thing, connected with my interest in poetry and books. In my junior year I dropped the mask of sociability, that part of my double self that appeared to be happy, popular, even enviable. I stopped seeing my friends and stopped going out with boys. High school—all of it—was stupid and boring and meaningless, and I couldn’t get away to college soon enough. This, I later recognized, was my first definite and prolonged depressive episode. I remember lying awake in the middle of the night as surges of anxiety tightened my chest and made it hard to breathe. I was intensely irritable, but also aware that I couldn’t feel anything—no love, no enthusiasm, no pleasure. I refused to go to the senior prom or even to my graduation. I took a road trip with my sister instead, down through the Blue Ridge mountains and east to the beaches of the Outer Banks. Outdoors, I could always breathe more easily. During these long stretches of gloom, I never thought of confiding in my parents. And it wouldn’t have occurred to them that they could have me see a psychiatrist, or that medication was available for what must have looked to them like a period of ordinary teenage angst.
I’ve sketched the early period of my life and its particular familial and cultural setting to show how I responded to my family’s stressful circumstances. There was nothing unusual about our situation, with parents too overwhelmed to focus on nurturing and bolstering the confidence of each of their children. “Emotional intelligence” was not yet a thing; “parenting” was not yet a word. We had two parents who were assuring that their six children would go to college, and they didn’t spare themselves. In this we were truly fortunate. My father had lived at home and worked in a supermarket during his college years, and my mother, having taken the business track in high school, had gone to work as a bookkeeper when she graduated from high school.
It’s clear at this point that challenging circumstances leave physiological marks upon children, changing the developing neural pathways. Over the past few decades, so many persuasive studies have linked early stress and early loss with depression that we can accept that relationship as a reality. Recent research also indicates that prenatal exposure to prolonged maternal stress can cause lifelong hyperactivation of the hypothalamic-pituitary-adrenal (HPA) axis in the developing child, resulting in greater vulnerability to depression and other disorders. The HPA axis is the part of the neuroendocrine system activated in response to stress, and the source of uncontrolled surges of cortisol in melancholia. Given how permeable and defenseless children are, their parents’ emotions pass through them like lightning through water. Any sort of early loss—the loss of a parent or of a parent’s love—is felt by a child as a nearly unbearable stress. If depression is an illness closely associated with something as pervasive and universal as stress, it’s no wonder that depressive disorders are so common.
Guilt and shame are also felt as stress by a child, and my longstanding hunch that my childhood experience was linked more than coincidentally to my later illness was justified recently with the publication of new research. A team at Washington University found that the anterior insula, a part of the brain involved in emotion and perception, was smaller in depressed children who expressed excessive guilt than in children who were not depressed. These children were more likely to have chronic and relapsing depression as they got older. Andrew Belden, the lead author of the study, said that while excessive guilt has long been recognized as a predictor of depression, “our findings would suggest that guilt early in life predicts insula shrinkage,” and that depression in early life may predict changes in the brain. MRI scans increasingly point to evidence that locates depression in several areas of the brain’s anatomy. Whether these anatomical features are the causes or effects of the illness is not always clear, but, as in this study, they can help to identify children who need early treatment.
WHEN I LEFT THE HOSPITAL, both of my doctors seemed to believe that my immediate problems were psychological ones. Dr. Waters, my new outpatient psychiatrist, met me in the aftermath of a single episode of melancholic depression that had apparently been triggered by a postpartum bereavement. The prominent psychoanalyst who was the director of the hospital sent her a copy of my discharge report, which included Dr. Young’s notes on the family history taken from Jake and my parents the morning after I was admitted. I wasn’t present in that meeting, so when I first read through the report years later, it was strange to see myself through their eyes.
PERSONAL HISTORY:
The patient’s past history is most remarkable for the apparent lack of significant problems at any time in the past. She has consistently maintained a very good level of function and has demonstrated a quite stable ego-resourcefulness over time. She is a magna cum laude, Phi Beta Kappa graduate of a prestigious New England college and has worked as a book designer in Manhattan since graduation.
PREMORBID PERSONALITY:
The patient seems to have always had a constricted range of interpersonal relatedness, maintaining a small group of personal friends and relying predominantly on family. Her capacity to relate to others is in fact quite good but a shy, quiet complacency has kept her quite constricted.
PREVIOUS ILLNESS:
The patient has no prior formal psychiatric contacts nor history of sustained alterations of mood and affect beyond what may properly fall in a normal/neurotic spectrum. This current episode represents a first episode of psychological difficulty requiring professional attention.
RECOMMENDATIONS FOR FUTURE TREATMENT:
Long-term intensive individual treatment with an insight-oriented approach is essential for this patient. It is recommended that she continue on nortriptyline.
Given that Jake and my parents described me in the family meeting as a person who had always seemed well-adjusted and performed well in school and at work, not only my suicidal depression but my later admission of deep unhappiness came as a complete surprise to them. This suggests, again, the presence of a double self: I presented to others the person they expected to see—going along, doing fine—while acquiescing to my circumstances and trying to manage my misery privately. But under “premorbid personality,” they’ve also described me as a shy, complacent, constricted person—a person who sounds to me like she is already at least mildly depressed. If this was the façade of happiness I was presenting, I wasn’t doing it very well. Nonetheless, it seems that this muted, placid, “constricted” affect was what they were used to in me.
Dr. Young strongly recommended long-term psychotherapy; the continuation of nortriptyline seemed less important by comparison. He offered in the report his insight into my object relations (the unequal power dynamics of the marriage), but we hadn’t explored the question of whether I remembered having previous depressive episodes, whose presence would suggest that an endogenous disorder was already present and recurrent. My prognosis appeared to depend on how I resolved my marital troubles, and the discharge report underscores the psychodynamic emphasis of the hospital’s approach to treatment.
My own impression at the time was that therapy was the more critical element of my post-hospital treatment, and that the medication would serve to keep relapse at bay in my transition back to the world. Like Dr. Young, Dr. Waters was trained psychoanalytically, and we never talked about what a melancholic episode with psychosis might portend. Dr. Waters continued to prescribe my antidepressant medication as our work together moved beyond my marriage and into my earlier life, to dredge up what had prepared the ground for my current situation. I began to recognize that the sadness and feeling of separateness I experienced as a child had returned at intervals through my teenage years and into my young adulthood. When I wanted to know whether someday I would no longer need to take medication, she would reply that she really couldn’t say, but that it was certainly possible.
Over the next few years, as episodes kept recurring, it became more and more obvious that what I had begun to voice to myself in high school—there’s something wrong with me—was true, and not just the common malaise of being a teenager. The something wrong was a mood disorder I had lived with unawares for a long time, and which was indistinguishable from the inward, pessimistic, and self-critical aspects of my character. Elements of my upbringing—the silence and self-suppression, the habit of yielding to others that looks like complacency but is driven by guilt—certainly led to some of my difficulties. Given the power of inheritance and conditioning, it’s a lot to ask of either psychotherapy or medication to change what is so deeply marked in habits of thinking and feeling by the time someone reaches adulthood, and it was very late for me when I began to try to change those habits.
The slow awakening to the knowledge that one has been living with a depressive disorder, which allows one’s past experience to click into focus through this new lens, is something that countless sufferers have commented upon. David Karp, a sociologist who has interviewed hundreds of people with depression, offers the framework of the “career” for this dawning recognition, which in turn requires accepting the necessity of medication and adjusting one’s expectations to the limits imposed by the illness. When I read his book Speaking of Sadness, I recognized my experience in all four stages of this awakening. He writes, “Every person I interviewed moved through these identity turning points in their view of themselves and their problem with depression”:
1.A period of inchoate feelings during which they lacked the vocabulary to label their experience as depression.
2.A phase during which they conclude that something is really wrong with me.
3.A crisis stage that thrusts them into a world of therapeutic experts.
4.A stage of coming to grips with an illness identity during which they theorize about the cause(s) for their difficulty and evaluate the prospects for getting beyond depression.
“Each of these career moments,” Karp writes, “assumes and requires redefinitions of self.” The slowness of this process may explain why so many people don’t get professional help until their illness is well established. The first two steps above align with my vague awareness of sadness in childhood and my deepening malaise in high school; the third aligns with the crisis that followed Anna’s death. But step four—coming to grips with an illness identity, which meant acknowledging the necessity of medication—took a very long time.
Imipramine, the drug that Roland Kuhn discovered the year I was born, was the first medication prescribed for me. It didn’t save me from hospitalization and electroshock, as the ads claimed it would, but I’m fairly confident that it would have if I had started taking it a month or two earlier. The tricyclics can take several weeks to reach a therapeutic level in the blood, and I was already desperately ill and suicidal when I began to take it just two weeks before my first suicide attempt. Suicidal patients need to be closely watched in the first few weeks on antidepressants because as the medication begins to take effect, people who had been immobilized by illness begin to be capable of taking action. If energy increases before mood improves, this renewed energy may provide just enough motivation to attempt the act of suicide. This is what seems to have happened with me. And this was why, once I was in the supposed safety of the hospital, they decided to continue the imipramine and give it more time to take effect. This plan ended with my second suicide attempt.
The second drug I was given, a couple of weeks after ECT was over, was nortriptyline, another tricyclic, and like imipramine, it wasn’t trouble free. Once out of the hospital, I tried to go running several times a week in an effort to regain some energy and to lose the weight I had gained since beginning to take it. But even at a slow easy pace, my heart pounded at an alarming speed, over 180 beats per minute. Given my youth and relative fitness, I should only have reached this heart rate at a much higher level of exertion. I would stop and walk, then jog again slowly. In bed in the morning, my resting heart rate was also much higher than normal. Dr. Waters sent me for an EKG, which confirmed the tachycardia, a common effect of the tricyclics. Since my mood was just getting stabilized, she didn’t want to change my meds. She suggested I forget about running and walk for exercise instead.
In addition to increasing levels of norepinephrine and serotonin, the tricyclics affect other neurotransmitters as well. Two of these, histamine and acetylcholine, account for the sedation and the drying of mucus membranes. The side effects reminded me daily that I was a person with a psychiatric disorder, and I would stop taking them as soon as I was feeling better for a month or two. Then I would slide gradually into a trough of despair, start the meds again, feel better for several months, stop again, get depressed, go back on. Because I was seeing a psychiatrist regularly, this was safer than it might have been otherwise. Therapy provided support and insight, but it couldn’t reverse the underlying physiological disorder. It would take another suicidal phase, eight years after the first, to make me realize that medication was absolutely necessary to arrest the freefall of my moods.