How Anecdotes Sell Drugs: On the 30th Anniversary Edition of Peter Kramer’s “Listening to Prozac”

Andrew Scull critiques the cultural influence of Peter Kramer’s 1993 book “Listening to Prozac.”

How Anecdotes Sell Drugs: On the 30th Anniversary Edition of Peter Kramer’s “Listening to Prozac”

Listening to Prozac: The Landmark Book About Antidepressants and the Remaking of the Self by Peter D. Kramer. Penguin Life. 480 pages.

THE STATISTICS ON antidepressant use in the United States are sobering. The proportion of those over age 12 taking antidepressants grew by an astonishing 400 percent between the periods 1988–94 and 2005–08. Women took antidepressants two and a half times as often as men, and 23 percent of women between the ages of 40 and 60 were taking the drugs. By 2019, more than 10 percent of female teenagers were taking them (twice the rate among their male equivalents), while at the other end of the age spectrum, almost a quarter of women over the age of 60 used them. And many of these patients had been taking these pills continuously for over a decade, despite there being no studies of the effects of taking these powerful drugs over such an extraordinarily long period. Peter D. Kramer’s 1993 bestseller Listening to Prozac can fairly claim to have played a key role in encouraging these developments. Last year, Kramer chose to issue a 30th anniversary edition of his book, whose appearance celebrates what he claims has been a major step forward in the treatment of depression and other forms of psychological distress.

The first antidepressant drugs, like the first antipsychotics, were discovered accidentally. At Seaview Hospital on Staten Island, New York, a treatment center for tuberculosis, Irving Selikoff and Edward Robitzek experimented in 1952 with a drug derived from leftover rocket fuel, iproniazid, thinking its antibacterial properties might prove therapeutically useful. They observed that one of the side effects of the drug was sharp improvement in a patient’s mood, appetite, and sleep patterns. Despite iproniazid’s development as a treatment for TB, three psychiatrists at Rockland State Hospital in Orangeburg, New York, five years later, tried administering iproniazid to hospitalized depressed patients and claimed spectacular results. Then, in 1958, the Swiss psychiatrist Roland Kuhn reported that a different drug, later called imipramine, which he had tested as an antipsychotic, had weak effects on schizophrenia but turned out to have antidepressant properties.

As was common at the time, these experiments were undertaken without the consent of the patients involved, and without any controls, but they sufficed to launch two different classes of drugs for the treatment of melancholia or psychotic depression, so-called monoamine oxidase inhibitors (MAOIs) and tricyclic antidepressants, the latter given that name because of the presence of three rings in their chemical structure. Both were moderately successful drugs but suffered from serious drawbacks: MAOIs could result in hypotension, nausea, diarrhea or constipation, and difficulty urinating. More seriously still, consuming cheese, cured meats, or certain red wines while taking these drugs could bring on a potentially fatal hypertensive crisis. As for tricyclics, along with producing such problems as gastrointestinal disturbances, mental confusion, and weight gain, they could be fatal if a patient overdosed. And the margins between a therapeutic dose and an overdose were not large, which was a problem in part because suicidal ideation might occur during the early stages of treatment.

These complications may help to explain why the explosion of antidepressant use came when it did. The year 1988 marks the introduction of a third class of antidepressant drugs, selective serotonin reuptake inhibitors, or SSRIs, the first and most famous of which, fluoxetine, was trademarked as Prozac. It is difficult to ingest a fatal overdose of Prozac, and its consumption does not entail dietary restrictions. And while MOAIs and tricyclics modify the biochemistry of the brain in opaque ways, Prozac, it was claimed, narrowly targets a particular neurotransmitter, serotonin.

When Eli Lilly brought Prozac to market, it asserted that this novel mode of action had created a new, more powerful, and more easily tolerated antidepressant. The sales of the previous generation of antidepressants had been modest—from January to August 1975, they brought in a mere $200 million. That changed rapidly. The cover of the March 26, 1990, issue of Newsweek featured a light-yellow-and-pale-green capsule. Prozac, its readers were informed, was “a breakthrough drug for depression.” And so it proved. As cases of depression soared, so did the market for the new pills. By 1998, Prozac’s annual sales were $2.8 billion. Inevitably, Prozac’s commercial success ensured that the marketplace would be flooded with a host of copycat drugs, the best known of which are Zoloft, Lexapro, and Paxil.

Serotonin is a neurotransmitter and hormone that plays a vital role in a host of bodily functions. It has a particularly important role to play in digestion, helping to protect the gut and control bowel function as well as affecting appetite, but it is also important for healing wounds, regulating sleep and body temperature, controlling sexual health, causing feelings of nausea, and more. Excessive levels of serotonin in the gut may heighten a person’s susceptibility to osteoporosis and fractured bones. Reflecting its wide-ranging importance beyond its role as a neurotransmitter, over 90 percent of the serotonin in the body is found in the gut, which is also where it is manufactured as an amino acid from some of the foods we eat. As all this suggests, there is every reason to be concerned about the long-term bodily effects of tampering with serotonin levels, quite apart from its possible effects on mood regulation and the brain.

Eli Lilly cleverly suggested that it was a shortage of this substance that accounted for people’s depression. Inventing a fiction that was eagerly embraced by the public and many psychiatrists, Lilly declared depression a straightforward brain disorder that could be eliminated by adjusting the body’s biochemistry. In the words of one prominent patient, Al Gore’s then-wife Tipper: “What I learned […] is your brain needs a certain amount of serotonin and when you run out of that, it’s like running out of gas.”

No one did more to popularize this notion and proclaim Prozac’s extraordinary properties than Kramer, a hitherto obscure psychiatrist with a part-time appointment at Brown University. Listening to Prozac, his paean to the drug’s miraculous properties, was an international bestseller that brought its author both fame and fortune. In the months following the book’s publication, Kramer made a host of media appearances—on The Oprah Winfrey Show, Fresh Air, Good Morning America, The Charlie Rose Show, and even the national nightly news. Primed with juicy anecdotes about a handful of patients he had treated, Kramer garnered huge amounts of free publicity. Sales predictably followed. But two central assertions at the heart of his book were false: that Prozac was a safe and extraordinarily effective drug, with no major side effects; and that, even more remarkably, it could make you “better than well.” Kramer claimed that psychiatrists like him now possessed the tools to practice “cosmetic psychopharmacology”—they could reshape people’s personalities to order, just as cosmetic surgeons sculpt aging bodies into a simulacrum of permanent youth. These assertions proved irresistibly attractive to the media gatekeepers of Americans’ collective consciousness.


Listening to Prozac’s 30th anniversary edition is adorned with a new preface and afterword by its author. It constitutes a tribute of sorts to the power of celebrity and to the persistence of the myth that depression is a brain disorder that can be abolished by ingesting one of Big Pharma’s magic bullets. According to surveys, that belief is now held by over 80 percent of Americans—one of whom, it turns out, is still Peter Kramer. Those who don’t believe this fairy tale are, he alleges, simply ignorant anti-psychiatrists or members of the cult of Scientology, who are relying on “irrelevant, spurious, or zombie research.” They deny what, for Kramer, remains the reality even now, 30 years on from his infomercial for Prozac. We should, he tells us in his revised edition, celebrate “our own good fortune. Without further improvement, the antidepressants we’ve had access to for sixty years are miraculous.”

Kramer’s new introduction contains biographical detail about how he came to write the book. Trained at Yale in the mode of psychoanalysis that was, in the 1970s, about to lose its dominant position in American psychiatry, and specializing in public health, Kramer had little background in psychopharmacology. In the final year of his residency, in love with a woman who lived in Washington, DC (who subsequently became his wife), he proposed transferring the last stages of his training in community psychiatry to a university there. Instead, with unusual flexibility, Yale allowed him to spend his last months working under a member of their faculty who had been seconded to supervise the languishing federal community mental health centers. But before Kramer arrived, the program was canceled; federal agencies were moving toward the rigid biological reductionism that still dominates American psychiatry, and funding for social and community psychiatry was disappearing.

Kramer found himself working under Gerald Klerman, one of the most prominent proponents of psychopharmacology. Within months, despite having no background in the relevant science—“I had no leaning toward research, and certainly none toward neurobiology”—Kramer found himself acting supervisor of the grants program of the Department of Health and Human Services. Until he left to run the outpatient psychiatry services at Brown University, that administrative role would constitute his sole professional connection to the pharmacological revolution sweeping American psychiatry.

We also learn of Kramer’s long-standing interest in writing, and more particularly in a certain kind of prose. He had always longed to write novels: “I had wanted to write fiction”; “I am happiest writing fiction.” Before entering medical school, he had spent two years in London studying literature supported by a Marshall Scholarship, and as a 40th birthday present, his wife Rachel had sent him to a weeklong program at the Iowa Writers’ Workshop. Vignettes about a handful of the patients he treated with the drug take up a great portion of Listening to Prozac, and Kramer acknowledges that his background in fiction played a significant role in how he crafted these portions of the book: “The fiction training showed most in the case vignettes. […] I wrote and rewrote vignettes, aiming to make them less medical, aiming for immediacy.”

Kramer is an avid admirer of Sigmund Freud and has written a brief biography of him; there are echoes in these passages of a confession Freud once made: “It still strikes me myself as strange that the case histories I write should read like short stories and that, as one might say, they lack the serious stamp of science.” Kramer is not in Freud’s league as a writer, of course, but just as the popular appeal of Freud’s work rests largely on his ability to turn case histories into compelling narratives, so too do Kramer’s sketches rely on his fiction-making skills. In fact, they are the only real evidence he offers in support of his claims. Titillating case histories are—obviously—far more likely to attract a mass audience than dry discussions of the efficacy and mode of action of a particular chemical. Anecdotes may not be data, but they do sell books—and drugs.

The vignettes are designed to show Kramer’s readers the many ways in which these pills can massage and modify the personalities of those lucky enough to take them. In his introduction to the original edition, Kramer recalls a successful and charming architect named Sam, who arrived feeling somewhat dejected after the death of both his parents. He had, it turned out, an obsession with hardcore pornography, which he forced his reluctant wife to view with him. On Prozac, his mood, his concentration, and his energy levels improved, and he declared himself “better than well.” But there was a fly in the ointment: he still, Kramer tells us, enjoyed sex but now shared his wife’s distaste for pornography. To save face, he continued to watch the videos even though it was now a chore.

Kramer insists in his new introduction that patient after patient whom he treated with the new drug promptly became better than well. Life’s troubles vanished. Some patients who had previously been cautious and inhibited promptly became “assertive and flexible.” Others improved in different ways.

Tess, for example, had been molested in childhood. Once grown, she was prone to abusive relationships. She commenced psychotherapy with Kramer while in the midst of an affair with a married man, and complained of weariness, insomnia, and general feelings of worthlessness. Kramer began a trial with an older antidepressant, imipramine. Tess improved slightly but was left struggling at work and plagued with side effects. Luckily, Prozac was released just then, and when Kramer switched her to that drug, she experienced a miraculous change. Almost immediately, she became relaxed, energetic, and full of laughter. She began a series of successful dates with a different class of men, gaining control of her personal and social life. At the same time, her confidence and performance at work improved markedly too, and soon she won both a promotion and a substantial pay raise. Prozac’s wondrous effects thus appeared to extend “to social popularity, business acumen, self-image, energy, flexibility, sexual appeal.” Even better, the drug “works like a switch,” and as a result, he reports, “I have seen case after case in which self-image changes overnight”—which is rather remarkable, given that patients taking SSRIs are routinely warned to expect no improvement for several weeks.

Tess is just one of a string of cases Kramer presents celebrating the rapid transformations Prozac brings about. Julia, for example, is obsessive-compulsive, making her husband’s and children’s lives miserable. She can only work part-time because of her insistence on keeping the house in perfect order. Then she ingests Prozac and voilà, a relaxed household and a new full-time career. Sketches of other patients are mobilized to assure us that Prozac can alleviate heightened sensitivity to criticism, emotional brittleness, shyness, hypersexuality, and a wide range of other deleterious traits. It’s a wonderful life on SSRIs, or so Kramer would have us believe.

Kramer informs us that, within two years of its introduction, “Prozac was shown to be useful in depression, OCD, panic anxiety, eating disorders, premenstrual syndrome, substance abuse, attention-deficit disorder, and a number of other conditions.” Even better, it “makes a person better loved, richer, and less constrained.” Perhaps it is surprising, under these circumstances, that only a quarter of middle-aged women and a smaller fraction of the rest of us are presently gobbling a daily dose of this wonder drug. “Before Prozac,” Kramer asserts, “drugs were dirty.” But Prozac “was clean,” blessed with a “lack of side effects.” And Kramer is not shy about telling us—or rather, as he occasionally confesses, “speculating”—about how Prozac comes to have such magical results.


If the reader makes it through the new 39-page introduction to the 30th anniversary edition and the 300-plus pages of the original text, he or she will find, buried in the closing paragraphs of the brief 2023 afterword, a couple of interesting concessions. Having spent most of the book that brought Kramer fame touting Prozac’s remarkable ability to transform the human personality in a host of desirable ways, we are belatedly informed that it isn’t quite so. Strange as it may seem, Kramer was “stretching the evidence.” It transpires that “we cannot yet tweak personality in a predictable fashion.”

“Cosmetic psychopharmacology” was, Kramer concedes, “the book’s best-known coinage,” and yet 30 years of experience has driven home, even to him, the fact that science has “not yet developed or happened upon drugs that allow doctors to sculpt personality.” It’s best not to read too much into this confession, however, for at the very beginning of the anniversary edition, in his new introduction, Kramer sings an altogether different song:

Rereading the book, I think: almost everything holds up. […] Where I address Prozac and similar drugs—the causes for excitement when they first came on the scene, the implications for medical practice, their influence on our sense of self—you can rely on those trains of thought. More or less, you can. Similarly for the speculation about antidepressants and their ability to modulate personality traits […]

Despite the intervening years and those three decades’ worth of new science, that story stands.

The contradiction between the assertions at the beginning of the book and at the end is passed over in complete silence.

What of Kramer’s other major original claim, the one that helped launch the market for SSRIs? Sadly, that too, it turns out, has largely fallen by the wayside. Kramer now acknowledges that “[t]he link between serotonin and depression remains speculative.” He hastens to add a qualifier: it remains “promising.” But it isn’t. In the words of a 2023 study published in the journal Molecular Psychiatry, a “comprehensive review of the major strands of research on serotonin shows there is no convincing evidence that depression is associated with, or caused by, lower serotonin concentrations or activity.”

Other psychiatrists who, like Kramer, once helped to sell the idea that depression was all about chemical imbalances have scrambled to dissociate themselves from this simplistic story, claiming that the “theory” was simply the invention of the marketing departments of the pharmaceutical industry. There is a kernel of truth to that, of course. Big Pharma did much to promulgate the myth. As Steven Hyman put it, “Undeterred by the lack of evidence, pharmaceutical companies popularized the impoverished idea of depression as a chemical imbalance among neurotransmitters to be rectified by their products.” Their advertising was replete with claims that a shortage of serotonin was the source of people’s chronic unhappiness.

To quote one of their early direct-to-consumer pamphlets, “Prozac doesn’t artificially alter your mood and it is not addictive. It can only make you feel more like yourself by treating the imbalance that causes depression.” Or, in the words of an advertisement for a rival pill, “[w]ith continued treatment, Paxil can help restore the balance of serotonin.” (It should be noted that we possess no means of measuring the levels of serotonin in people’s brains, let alone of determining what “normal” levels of this neurotransmitter might be.) Claims like this are reminiscent of the biobabble that fills Kramer’s book. See, for example, his wholly bogus claim that “the efficacy of medication is evidence that low self-esteem exists as a state of the neurons and neurotransmitters” or his assertion that “much of what has been called personality disorder is the final, behavioral expression of a variant state of the biogenic amines.”

The pharmaceutical industry found a particularly eager audience for the chemical imbalance theory among the ranks of patients told to “snap out of it.” If their troubles were biological, that meant that they were real. Groups such as the National Alliance on Mental Illness (NAMI), an organization primarily composed of parents and relatives of those with serious mental illness, were likewise vocal proponents of biological accounts of these afflictions and did much to promote the serotonin narrative. In return for this apparently “disinterested” endorsement of the theory, the pharmaceutical industry showered the organization with money, secretly providing as much as 75 percent of the funds NAMI raised. The group’s testimony proved particularly effective in the halls of Congress and in front of state legislators.

Apologists rely on historical amnesia when they attempt to dismiss the part played by the psychiatric profession in legitimizing the assertion that depression was the product of a shortage of serotonin. Benjamin Ang and his colleagues recently showed, via a careful analysis of major textbooks of psychiatry and of highly cited and influential research papers, that leading psychiatrists routinely addressed, and in many cases endorsed, the chemical imbalance theory, as some continue to do. Those professional endorsements may help to explain why journalists served as uncritical echo chambers for the pharmaceutical marketing operation that promoted adjustments to serotonin levels as the panacea for life’s emotional ups and downs.

Pace Kramer, those taking issue with his Panglossian portrait of SSRIs are not confined to the ranks of the Scientologists and anti-psychiatrists enamored of “zombie research,” unless we are supposed to assimilate people like Steven Hyman to their ranks. From 1996 to 2001, Hyman directed the National Institute of Mental Health, where he did much to redirect research toward neuroscience and genetics. He is a past president of the Society for Neuroscience and of the American College of Neuropsychopharmacology, and now heads the Stanley Center for Psychiatric Research at Harvard and MIT. He remains a staunch defender of biological psychiatry and cannot plausibly be described as a hostile witness. Yet he is blunt in his assessment of SSRIs: they are, as he told the journalist Daniel Bergner, “mediocre” drugs. Though the older antidepressants were “more toxic, and less tolerable,” he emphasizes that SSRIs have “offered no advance in efficacy or speed of onset.”

And Hyman is not an outlier here. Published research comparing antidepressants to placebos show that the drugs routinely outperform sugar pills, and this difference is statistically (but often not clinically) significant. Yet there are significant problems with such findings. In the first place, antidepressants rather quickly create noticeable side effects, so patients may soon guess whether they are receiving active treatment, undermining the double-blind nature of the clinical trial. Second, the vast majority of drug trials are funded by the pharmaceutical industry, which owns and controls the resulting data—a fact that has introduced a serious degree of bias into the published literature, since those studies that produced results those companies did not like were prone to disappearing, their data never seeing the light of day. As much as 30 percent of trials of antidepressants simply weren’t published, and those unpublished studies routinely involved negative assessments of the drugs under review. As a 2008 report in The New England Journal of Medicine concluded, “Selective publication of clinical trials—and the outcomes within those trials—can lead to unrealistic estimates of drug effectiveness,” with the result that “the true magnitude of each drug’s superiority to placebo was less than a diligent literature review would indicate.” [1]

Most recently, a study published in The British Medical Journal in 2022 has suggested that the clinical picture is more complicated than these average findings suggest. The authors were able to examine the patient-level data for individuals with major depressive disorder who were treated with an antidepressant “in randomized, placebo controlled trials submitted to the US Food and Drug Administration from 1979 to 2016,” a total of 73,388 participants, including those in both published and unpublished studies. The authors note that existing “[m]eta-analyses have shown small mean differences between drug and placebo arms,” but they rightly question whether “the drug effect might not be a uniform small, and hence clinically unimportant, benefit across patients […] Rather, it could occur as a large, and thus clinically important, difference for a small subpopulation.” Their data allowed them to provide a provisional answer to this question and to further specify whether, if there was a group that experienced a more powerful response, it differed by age, gender, or the severity of the depression.

This particular study found that, overall, those given the drug improved by 9.8 points on the Hamilton scale widely used to assess depression, while those on placebo improved by 8.0 points, just as previous studies had found, with little difference between men and women. As the severity of the depression increased, however, the difference between the drug and placebo groups grew, though the mean increase was only 2.5 points among even the most severely ill. But the hypothesis that the average response masked within-group differences was born out. A small minority, approximately 15 percent of the total, experienced significant improvement in their emotional lives, 16 points or more on the Hamilton scale, which occurred twice as often among those taking an antidepressant rather than a placebo. Somewhat more than 20 percent of patients experienced “little or no improvement” whether they were taking a drug or a placebo, and the remainder, listed by the authors as nonspecific responders, showed a range of improvement over the timescale covered by the trials but the “distinctly broad range and similar likelihood [of improvement] for drug and placebo groups” explains why the gross numbers show only a small and clinically nonsignificant difference between antidepressant and placebo. As they emphasize in their concluding remarks, their study reinforces what others have shown: “[T]he mean effect of antidepressants is only a small improvement over placebo.”

These are intriguing findings, but a major problem is that psychiatrists do not know in advance which of these outcomes will materialize when they prescribe antidepressants for any given patient. As this study’s authors conclude, for depressed patients, particularly those with “mild to moderate acute depression,” we need to bear in mind “the modest absolute likelihood of substantial benefit over placebo.” Beyond that, “[w]e cannot fully exclude the possibility that the effects of the drugs are accounted for by functional unblinding. This possibility could result in biased assessments by unblinded raters or an increased placebo effect in unblinded participants.” Given the risks and side effects associated with taking antidepressants, there’s much to be said for beginning with lower-risk treatments.


In Listening to Prozac, Kramer assures us that the drug (and, by extension, other SSRIs) have essentially no side effects. That is simply false. All drugs have side effects. Prescribing psychiatric drugs is ethically and practically thorny for four basic reasons: many patients fail to respond to either antipsychotics or antidepressants; it’s difficult or impossible to determine in advance which patients are likely to respond; improvement can be minimal; and side effects can compromise health in other ways, and can be irreversible.

Depending to some extent on the particular antidepressant taken, side effects can include weight gain, nausea, sleep disturbance, diarrhea or constipation, and disturbances of sexual desire and performance—for men, premature ejaculation or loss of erections; for both sexes, a loss of libido, numbing of the genitals, and an inability to achieve orgasm. The many reports of decreased emotional responsiveness, a flattening of feelings, suggest that numbness extends from people’s genitals to their emotional lives. Sometimes these noxious side effects diminish or disappear after some weeks when the drugs are discontinued, but for the unlucky, they persist and may never go away. [2]

For a not inconsiderable fraction of those taking SSRIs, discontinuing the drugs turns out to be highly problematic, which may account for their long-term use. Those prescribed SSRIs are given stern warnings about not stopping them abruptly and not without medical supervision, not least because of the emotional turmoil and suicidal ideation that such action often produces. But while, for some patients, tapering the dosage results in mild and transient symptoms as they transition off the drug, others experience persistent and serious difficulties, in effect finding themselves trapped in an endless cycle of antidepressant usage—a major iatrogenic problem. [3] So much for Kramer’s continued insistence that Prozac is a drug free of major side effects.

Two other issues raised by this history deserve attention. Suicidal thoughts are not confined to patients who abruptly discontinue their medications. On the contrary, they have surfaced as a major problem among children and adolescents who take SSRIs. A lawsuit against GlaxoSmithKline revealed that while their published papers claimed that Paxil was safe and effective, the actual data showed that it was associated with a threefold increase in suicidal ideation; since they owned the data, however, the company simply suppressed these findings. The heightened risks here of increased suicidal thoughts, interpersonal violence, and actual attempts at suicide have prompted the FDA and its British counterpart to issue black box warnings of the dangers SSRIs pose for this group, the most drastic step that can be taken short of ordering the drugs off the market. Unfortunately, those warnings have not had much effect on prescribing practices.

Reading Listening to Prozac also serves to remind us how remarkably few of the patients whose stories Kramer presents for our entertainment, and as “proof” of his favorite drug’s effectiveness, suffer from what we would ordinarily think of as serious depression. They are instead “people with mild degrees of impairment: minor depression, minor compulsiveness, sensitivity to loss, personality styles fallen from favor.” Though the book played an important role in persuading the public of the value of treating depression with SSRIs, Kramer acknowledges that “Listening to Prozac focuses on mild ailments and conditions that doctors might not diagnose at all.” Aggressive direct-to-consumer marketing of SSRIs, a practice only New Zealand and the United States permit, has meant that Kramer, and the profession at large, can prescribe Prozac to just about anyone with impunity, and without resistance.

Anniversaries are usually occasions for celebration. This one is not.



[1] See also Joel Lexchin et al., “Pharmaceutical Industry Sponsorship and Research Outcome and Quality: Systematic Review”; Hans Melander et al., “Evidence B[i]ased Medicine—Selective Reporting from Studies Sponsored by the Pharmaceutical Industry: Review of Studies in New Drug Applications”; Catherine DeAngelis and Phil Fontanarosa, “Impugning the Integrity of Medical Science: The Adverse Effects of Industry Influence.”

[2] See James Ferguson, “SSRI Antidepressant Medications: Adverse Effects and Tolerability”; Raymond Rosen, Roger Lane, and Matthew Menza, “Effects of SSRIs on Sexual Function: A Critical Review”; Audrey S. Bahrick, “Persistence of Sexual Dysfunction Side Effects After Discontinuation of Antidepressant Medications: Emerging Evidence”; Sidney H. Kennedy and Sakina Rizvi, “Sexual Dysfunction, Depression, and the Impact of Antidepressants.”

[3] See James Davies and John Read, “A Systematic Review into the Incidence, Severity and Duration of Antidepressant Withdrawal Effects: Are Guidelines Evidence-Based?”; Giovanni A. Fava et al., “Withdrawal Symptoms After Selective Serotonin Reuptake Inhibitor Discontinuation: A Systematic Review.”


Featured image: Birger Carlstedt, Nightmare, 1945, is licensed under CC BY-SA 4.0 by Amos Rex.

LARB Contributor

Andrew Scull’s most recent book, Desperate Remedies: Psychiatry’s Turbulent Quest to Cure Mental Illness (Harvard University Press), has just been published in paperback.


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