Often, such grim descriptions are paired with an upbeat solution: better access to mental health care, including psychiatric drugs. Given the understanding of mental health that has been promoted to the public for the past 40 years, this advice makes sense. We have come to understand that depression and other mental problems are disorders of the brain. Psychiatric treatments fix this brain disorder, or at least induce changes in the brain that are helpful to the suffering person.

However, if the past is prologue to the future, this understanding will continue to make the problem worse. For the past 35 years, we have sought to spread “awareness” of depression and other mental health issues. This has led to a dramatic increase in the prescribing of antidepressants: in 1990, the CDC reported that fewer than 3% of adults had taken an antidepressant during the previous month — a number that rose to 13.2% in 2018 and 23.1% earlier this year. Yet the burden of depression in the United States and other Western countries has only risen during this time.

There is a fundamental reason why. We have organised our thinking, and care, around a narrative of medical progress — of effective drugs that fix chemical imbalances in the brain — that isn’t to be found in the scientific literature. And the chasm between what is told to the public and what is found in the scientific literature has led our societies astray.

Writers, philosophers, and doctors have long observed that melancholy — a time of sadness or grief — visits nearly everyone now and then. As the 17th-century physician Robert Burton advised in The Anatomy of Melancholy, “it is most absurd and ridiculous for any mortal man to look for a perpetual tenure of happiness in this life”. It was only when melancholy became a “habit” that it could be considered a “disease”.

This was the understanding that prevailed until the Eighties. People often suffered bouts of depression, particularly in response to setbacks in life, but such feelings were seen as normal. Depression was only a “disease” in cases where people stayed depressed for no apparent reason, and these were rare. Community surveys conducted in the Thirties and Forties in the United States found that fewer than one in a thousand adults suffered an episode of “clinical depression” each year. Among this group, most did not need to be hospitalised, and only a small minority became chronically ill.

These findings led experts at the National Institute of Mental Health (NIMH) in the Seventies to advise the public that depression was an episodic disorder, which would generally clear up on its own. Most depressive episodes, wrote Dean Schuyler, head of the depression section at the NIMH, “will run their course and terminate with virtually complete recovery without specific intervention”.

However, this understanding of depression was soon to disappear.

During the Seventies, leaders of the American Psychiatric Association (APA) worried that their field was in crisis. Critics argued that psychiatry functioned more as an agency of social control than as a medical discipline, that its diagnoses lacked validity, and that its brand of talk therapy, psychoanalysis, was no more effective than other therapies offered by psychologists and counsellors.

In response, American psychiatry decided to rebrand itself. The public needed to understand that psychiatrists were medical doctors who cared for patients with real diseases. Not only would this rebranding improve psychiatry’s public image, but it would also give psychiatrists a privileged place in the therapeutic marketplace. They had the power to prescribe drugs, while psychologists and counsellors did not.

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The APA, when it published the third edition of its Diagnostic and Statistical Manual in 1980, reconceptualised psychiatric disorders as diseases of the brain. The age-old distinction between ordinary depressive episodes and “clinical depression” was dropped, and both were lumped together as a single “disease”. Nancy Andreasen, future editor of the American Journal of Psychiatry, set forth tenets of this new psychiatry in her 1984 book, The Broken Brain. “The major psychiatric illnesses are diseases,” she wrote. “They should be considered medical illnesses just as diabetes, heart disease and cancer are.” With this understanding in mind, the APA quickly set out to market its new model of depression to the public.

It found an ally in pharmaceutical companies, who were also eager to change the narrative. Erasing the distinction between ordinary depression and clinical depression promised to create a huge market for antidepressants. Pharmaceutical companies gave money to the APA to develop its PR machinery in the early Eighties, and then, in 1988, they provided funds to support a NIMH campaign, called the Depression Awareness, Recognition and Treatment (DART) program, that was designed to sell the disease model to the public.

In anticipation of this campaign, the NIMH had conducted a survey of public attitudes about depression. Only 12% of Americans said they would take a pill — an antidepressant — to treat a depressive episode. And 78% said they “would live with it until it passed, confident that they could handle it with their own”. The purpose of DART was to relieve the public of this “misconception”. According to the NIMH, Americans needed to understand that depression was a “disorder” that regularly went “underdiagnosed and undertreated”. Absent treatment, it could become a “fatal disease”.

The public was also presented with a new — apparently scientific — theory of depression: that it was caused by a lack of serotonin in the brain. Thankfully, scientists had discovered a medicine, selective-serotonin reuptake inhibitors (SSRIs), that fixed this chemical imbalance. Prozac and other SSRIs were heralded in the media as “breakthrough medications” that could not only fix depressed patients but make them feel “better than well”.

Untreated depression was now presented as a pressing public health concern. Most important, people were being trained to monitor their own emotions, and to treat sadness or emotional discomfort as symptoms of a disease requiring medical intervention.

The PR blitz worked. In a 2005 press release, the APA shared the “good news”: 75% of consumers now understood that “mental illnesses are usually caused by a chemical imbalance in the brain”.

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The low-serotonin theory of depression arose in the Sixties from the discovery of how the first generation of antidepressants, tricyclics and monoamine oxidase inhibitors, altered normal brain function. Both hindered the normal removal of serotonin (a monoamine) from the synaptic cleft between neurons.

Once this “mechanism of action” was discovered, researchers hypothesised that perhaps depression was due to too little serotonin. However, when researchers ran experiments to test whether people diagnosed with depression, prior to being medicated, suffered from low serotonin, the results were disappointing. As early as 1984, NIMH investigators concluded that “elevations or decrements in the functioning of serotonergic systems per se are not likely to be associated with depression”.

Investigations into the low-serotonin theory continued, but none provided convincing evidence to support it, and in 1999, the APA, in the third edition of its Textbook of Psychiatry, declared the theory dead, writing that decades of research “has not confirmed the monoamine depletion hypothesis”.

These conclusions were never promoted to the public, and so, this past June, when British investigators published a review of the history of this research and found there was no evidence to support the low-serotonin theory of depression, their conclusions were reported as shocking. In fact, we have known as much for two decades.

The real story, however, is even worse. Antidepressants block the normal reuptake of serotonin from the synaptic cleft. In response, the brain adapts to try to maintain its normal functioning. Since antidepressants raise serotonin, the brain responds by dialing down its own serotonergic machinery. In other words, antidepressants induce the very abnormality — a deficit in serotonergic function — hypothesised to cause depression in the first place.

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Antidepressants, then, do not fix any known disorder. But, their defenders might counter, could they nonetheless help depressed people?

Here, too, the evidence is thin. In the world of “evidence-based” medicine, placebo-controlled, double-blind randomised trials (RCTs) are the gold standard for assessing a drug’s effectiveness. A recent meta-analysis of such studies determined that 15% of depressed patients treated with an antidepressant experience a short-term benefit; the remaining 85% are exposed to the adverse effects of the drugs without any benefit beyond placebo.

Even those short-term results suggest a major problem with widespread use of antidepressants: six of seven patients experience the drugs’ side-effects without any corresponding benefit. The most common side-effect may be sexual dysfunction, which in some cases can last long after patients stop taking the drugs. But some patients can also suffer from a drug-induced worsening of their original symptoms.

There are two notable elements of this drug-induced worsening. First, antidepressants triple the risk that a depressed patient, within 10 months of initial treatment, will turn manic and be diagnosed as bipolar, which is a much more severe disorder than depression. Second, over the long-term, antidepressants increase the risk that a person will remain symptomatic and functionally impaired.

The latter worry showed up in the Seventies, not long after antidepressants were introduced. At that time, clinicians still had a memory of depressive episodes that regularly cleared up without the use of drugs, and several reported that patients treated with antidepressants were now relapsing more frequently than before. Epidemiological studies agreed. The third edition of the APA’s Textbook of Psychiatry, published in 1999, summed up the disappointing findings: Only about 15% of patients treated with antidepressants recover and are still well at the end of one year.

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Studies conducted since then suggest that even that 15% recovery rate may be too high. In the largest antidepressant trial ever conducted, the STAR*D study, only 108 of the 4041 patients who entered the trial remitted and remained well at the end of one year, a stay-well rate of 3%. The vast majority never remitted, remitted and then relapsed, or dropped out of the study. Meanwhile, a 2006 NIMH study of depressed patients who didn’t take antidepressants found that 85% recovered after one year, just like in the pre-antidepressant era.

Naturalistic studies in depressed patients regularly find that, over the long term, medicated patients are more likely to remain symptomatic and to become functionally impaired. These findings led Italian psychiatrist Giovanni Fava to propose, in a series of papers dating back to the Nineties, that antidepressants induce a biological change in the brain that makes patients more vulnerable to depression. As Rif El-Mallakh, an expert in mood disorders at the University of Louisville School of Medicine, put it in a 2011 paper: “A chronic and treatment-resistant depressive state is proposed to occur in individuals who are exposed to potent antagonist of serotonin reuptake pumps (i.e., SSRIs) for prolonged time periods.”

In other words, there is reason to believe that the mass prescription of antidepressants is making us, on the whole, more depressed. Indeed, the “economic burden” of depression — composed of workplace-related costs (absence from work), suicide-related costs, and direct-care costs — has steadily risen since the SSRIs came on the market. In 1990, it was calculated at $116 billion in inflation-adjusted terms. By 2020, it had nearly tripled to $326 billion.

Disability due to mood disorders has also risen. In community surveys conducted in 1991 and again in 2002, 30% of the adult population was found to suffer from an anxiety, mood, or substance disorder, based on DSM diagnostic criteria. However, while the prevalence of these disorders didn’t change, the percentage of people who got treated did, rising from 20% in 1991 to 33% in 2002. Over the same period, the number of American adults receiving a government disability payment due to a mood disorder rose from 292,000 to 940,000.

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Following the publication of DSM III in 1980, the public was told a story of a great advance in medicine. Research had found that depression was due to a chemical imbalance, which antidepressants fixed. We organised our thinking around that narrative: depression was a biological “disease” that required medical treatment. This false narrative is the root cause of our mental health crisis today.

The tragedy is that there is another, more optimistic narrative about depression that exists in the scientific literature. This narrative informs us that human beings are responsive to their environments, and that depressive episodes often arise in response to setbacks in life. Time, and finding ways to change one’s environment, regularly lead to a spontaneous remission of depressive feelings.

A society that wants to promote good “mental health” should strive first to create more nurturing environments — improving access to housing and childcare, and working toward a more equal distribution of financial resources. It should also favour, as a first response, holistic treatments for depression — diet, exercise, walks in nature, social engagements, and so forth — as these complement our natural capacity to recover.

Antidepressants could still serve as a useful tool. Their use would simply need to be informed by research that tells of their limited short-term efficacy and of their potential negative long-term effects. Doctors would also need to inform patients that these drugs do not fix a “chemical imbalance”. True informed consent would dramatically reduce the use of these drugs, and surely diminish prescribing habits that treat them as a go-to response.

Paradigm shifts do happen, and today’s mental health crisis is telling us that one is desperately needed. Forty years of the disease model of depression has left us sicker and unhappier than ever before. There is little reason to believe that more of the same will fix our problems, and plenty of reason to think it will continue to make them worse.

The Miserable Older White Woman emerges from the same blend of old-school misogyny and ageist ugh-mom-ism that brought us first the Wine Mom and then the Karen, in the summer of 2020. In theory, a Karen was a white woman who called the police on black people who were simply minding their own business. In practice, the term started getting used (and is indeed still used) in reference to any woman over the age of 25 who has spoken up, in any context. In the early pandemic days, I was once called “Karen” after asking some teenagers on public transit to put on masks. But anti-maskers also got labelled Karens too, so we can’t win (unless we stay silent).

Who has it in for these women? A significant number of the Twitter accounts piling hate on middle-aged women seem to be controlled by young men who give off incel vibes. They are also angry at young women for rejecting them, and their mothers for not sending their favourite meal down to them that evening in their proverbial basement. What is clear is that these women are an avatar for complaints that span, or defy, the ideological spectrum. The Miserable Older White Woman inspires an intense, if difficult to pin down, political fury. Both progressives and the Right seem to agree that “Liberal white women on antidepressants will be the end of our civilisation”, but the stereotype allows a range of people to channel a variety of frustrations. She’s the 53% of white women who supposedly (but not actually) voted for Donald Trump in 2016, but also the tear-strewn pussy-hat wearer at the Women’s March protesting that election’s outcome.

For the Left, the privileged lady wrangling a prescription for her non-problems can be blamed for all of society’s woes: racism, imperialism, the housing shortage, the cost of living, climate change, perhaps even monkeypox. Her antidepressant usage can be categorised as yet another indulgence she engages in while other people suffer, akin to a day at the spa: “White women live off of Starbucks and antidepressants.” The Left-produced caricature lives in a large suburban house with a rich husband and resents her perfect life: “Excess red wine, antidepressants, free time and money has truly done wonders to boomer white women.” This is a women whose problem is that she has it too good. If she had to deal with the same adversity as everyone else, this would build character, and she’d stop the whinging.

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For the Right, the Miserable Older White Woman is the opposition: “Democratic party supporters are self-hating college-educated white women. Basically if you live in an apartment in LA and own four cats, a massive ‘sex toy’ and consume a lot of antidepressants you are a Democratic party voter.” And she is getting her comeuppance for her decades of liberalism. She foolishly bought into the feminist myth that women have brains and should have high-powered careers and look at her now, all alone with her cats, pining for the life she could have had if she’d settled down when still turning heads. If she’d stayed a virgin until marrying Ward Cleaver at 22, she wouldn’t be popping pills of any kind. She’s sad because she’s alone, but don’t feel sorry for her, it’s a misery of her own making. A lesson for young women: get married before you’re middle-aged — and why not to one of the charming young men who spend their days online mocking older women?

And yet critics from the Right also have it in for the Miserable Older White Women who have settled down, but who fail to have either aged into traditionalist matrons or remained chipper 20-somethings. Pratt, of “Welcome to Hell”, more recently made the rounds for introducing Twitter’s cynical masses to the Peach Mom, a comic about the angst of an apparently well-off stay-at-home mom (albeit with side hustles) who despises her husband for doing less of the housework and childcare. The woman behind these evidently autobiographical comics then got widely ridiculed, in part because it is objectively ridiculous to post comics to the internet that bash your spouse, but also because she was a Miserable Older White Woman, unhappy with her lot, but for no good reason. Why wasn’t she grateful that she had a provider husband who also did some housework? (Much was made of the fact that he apparently does childcare when she goes out in the evening to teach yoga, as though the teaching of yoga is an indulgence and not a part-time job.) She should be grateful, was the gist.

But the common ground of why she’s demonised is that she represents liberal modernity, to people across the political spectrum who object to it. The Miserable Older White Woman is a normie, a Hillary not Bernie supporter. An AWFL (“affluent white female liberal”); a Twitter search for that very-online acronym paints a similar picture. Her reaction to Kamala is an enthusiastic yaaas. She posts milquetoast liberal messaging to her Instagram, about Black Lives Mattering and trans rights and abortion rights, but in a cringe way.

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There’s a perception, among her detractors, that liberal modernity has given women of this demographic too much ground, which has made them (as well as everyone else) worse off: “Affirmative action, war on poverty, and the modern feminist movement empowered white women. This newly empowered group remade society in a way that harmed men that couldn’t adapt. This new society is not so great and white women begin taking massive amounts of antidepressants.” Men’s rights activists agree with far-Left advocates for the true marginalised: white women are spoiled pseudo-victims. They are society’s actual most powerful, but imagine themselves oppressed.

Does it all come back to Hillary Clinton? Hillary — per her haters — the privileged complainer. Hillary, the embodiment of the dorky, stodgy mom who does not know how to relax. Unlike other ways of medicating away bad moods, antidepressants have exactly zero reputation for being edgy or fun. Much like you know who. Even Hillary’s supporters faulted her, during the 2016 US presidential campaign, for not appearing to have a good time. (Too young, too attractive, and too fun-loving is also a problem, as a certain Finnish prime minister could attest.) The people who wanted to vote Democrat in 2016 but just couldn’t stomach Hillary are, in their rhetoric, very like those who see a stat on older white women’s antidepressant usage and go: “makes sense.”

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There’s also cross-ideological consensus that older women have committed the crime of having aged out of hotness. A Reddit theorist suggests older white women are upset because “they’re the most protected and coddled class when they’re young. When their looks fade they stop getting preferential treatment which is hard for most to adjust to.” The thing where “when you’re accustomed to privilege, equality feels like oppression”, in other words. So, according to their critics, these women used to have too much and are now bitter over a normal existence.

To appear old is, in a sense, to look miserable. Society values women for youth, a fleeting quality, which is enough to make anyone miserable. But there’s also the specific fact that the changes to facial features that happen naturally with age read, on women, as anger. Women sick of being told they seem angry seek Botox — an anti-aging treatment — to remedy the situation. One wonders whether Miserable Older White Women are as miserable as all that, or just look that way, and are disproportionately prescribed antidepressants because their doctors — fallible humans like the rest of us — interpret their ordinary facial expressions as ones of distress. The medical establishment has made stupider mistakes.

Women, particularly housewives, have long been prescribed drugs at a much higher rate than men. One can look at this as society throwing drugs at women to distract them from their situational misery so that they don’t question the situation itself. But one might just as easily see this as a case of men not having access to proper mental health care, or indeed to the drugs that can be used relatively safely to make them less miserable. Are the men who sneer at antidepressant-using women just repulsed, or are they also, perhaps, envious? Do they wish they could be like the women who face somewhat less stigma for going ahead and making an appointment with their GP? Is the Miserable Older White Woman’s crime being miserable, or is it valuing herself enough to do something sensible about it?

When the first antidepressants were developed in the Fifties, the condition was considered so rare that the drug research seemed like a waste of money. But in a 2017 survey, 12.7% of Americans had taken antidepressants in the past month (and nearly twice as many women as men). It is not to deny the existence of catatonic states of despair to suggest that there may have been a definitional leak.

One might retort that “depression” was simply “under-diagnosed”, but equally present in every earlier stage of human history. Consider, though, the discovery of SSRIs, a class of drugs that combined lifetime use with a better safety profile than earlier antidepressants (just weight gain, sexual dysfunction, and the occasional suicide upon withdrawal). And consider the context of that discovery: a world where pharmaceutical companies fund much of the research used in their own regulation, and that research is easy to skew. In short, it is a truth universally acknowledged that a pharmaceutical company in possession of a new drug shall be in want of an endemic illness. As the GlaxoSmithKline slogan bluntly went: “Does your soul have a cold?”

Still, it would be sophomoric to think that depression was wholly and solely constructed by Big Pharma. Until recently, it was understood that “no man living is free, no stoic, none so wise, none so happy, none so patient, so generous, so godly, so divine, that can vindicate himself; so well composed, but more or less, some time or other he feels the smart of” melancholy. So wrote Robert Burton, a reclusive life-long fellow of Oxford, four centuries ago, in his freewheeling account of sadness, The Anatomy of Melancholy.

Burton was writing in one of the last periods where the role of the writer wasn’t to express an individual thesis, but instead to summarise everything. As such, his Anatomy has little in the way of synthetic thought. As Burton says, “I have read many Bookes, but to little purpose, for want of good method, I have confusedly tumbled over divers Authors in our Libraries, with small profit, for want of Art, Order, Memory, Judgment.” He can’t even settle on a definition of melancholy — “whether it be a cause or an effect, a disease or symptom … I will not contend about it” — but he does examine some potential causes. Black bread, melons, hot air, cold air, excessive exercise, defective exercise, the stars, God, hot baths, a hot brain, Calvinism, Catholicism, excessive studying, excessive merrymaking, excessive “chamber-making”.

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As for melancholy’s symptoms, “the tower of Babel never yielded such confusion of tongues, as the chaos of melancholy doth variety of symptoms”. Indeed, it’s sometimes difficult to separate cause from symptom, as in the glorious description “lascivious by reason of much wind”. Burton’s aim is to “adventure yet in such vast confusion and generality to bring them into some order; and so descend into particulars”. Many of these loopy excursions come to a familiar enough conclusion: melancholy’s cause is sin, and its cure is God: “We ought to fear our own fickle estates, remember our miseries and vanities, examine and humiliate ourselves, seek to God, and call to Him for mercy.”

But Burton does not deny the importance of strategies to combat melancholia. These include behavioural changes — drink a glass of water upon waking; seek hills or mountains; “be not solitary, be not idle” — and mental ones — avoid prolonging passionate thoughts; avoid believing in predestination; “be meek, merciful, and patient”. There is comfort here, for the post-modern reader. Thanks to the rapid rise of neuroscience and the branding of depression as a “brain disease”, many third-party carriers reimburse doctors for medication management only, and many depressed people are simply handed a prescription by a general practitioner and told to check in in six weeks. In Burton’s day, the old Galenic system of humours did emphasise the physical. But these days depression is treated like heartburn; in more exploring reaches, it’s treated by impersonal, one-size-fits-all cognitive behavioural therapy, now the province of therapy apps advertised by Instagram scroll.

At the extremes, the “chemical imbalance” theory raises troubling questions about human character; and its Brave New World-style treatment can make the human being feel like an unruly dog. No matter how many analogies one can make to infectious disease or broken legs, depression is experienced at a complicated level inextricable from one’s most virtuous traits — sensitivity, self-criticism, ambition — and to think of oneself as merely a malfunctioning machine or a bundle of “trauma reactions” can impoverish the self.

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The experience of The Anatomy is one of overload, and perhaps it is best to read it with the desperation and joy of Samuel Johnson, who “frequently resorted to [The Anatomy] for the purpose of exhilaration” while running his tiny, failing school at Edial Hall. Its very eclecticism and capaciousness is its virtue. Perhaps reading anecdotes about ancient kings won’t cure you: but given that depression rarely is “curable” at all, there’s something beautiful about feeling this continuity of human experience, across time and space, to feel one’s sadness as part of a world history full of delight and variety. Compare the experience of the sad person today, asking their doctor for Prozac or maybe playing with an adult colouring book, to the experience of a Samuel Johnson. The first is made to feel small and simple; the second is made to feel himself more intelligent, more dignified, more ambitious. Moreover, as any reader of Shakespeare’s tragedies will know, the early Moderns had a way of laughing about despair, solitude, even suicide — a kind of manic sad clowning found absent from the way most people talk about mental health now, both infantilising and deadly serious. Burton, after all, wrote The Anatomy under the name Democritus Junior: the laughing philosopher.

I read The Anatomy the winter after my first law school exams, ambivalent about a course of study that was beginning, nonetheless, to gel into inevitability. I was staying on the couch of a family member in Florida, in a condo surrounded by red and orange tropical plants and buzzing constantly with the exertions of a leaking air conditioner. Through the screen door, at any hour of the day or night, I could see the recently discharged woman next door swaying silently in front of a blue-fuzz TV. Against her state, obviously, The Anatomy is of little use. But for the sort of low-grade malaise I found myself in — the sense that my fears would never disappear but my possibilities, one by one, would — The Anatomy made me feel a little bit better. I read it on the beach, I read it over diner milkshakes, I read it on hot and sleepless nights, on that orange leather sofa that congealed to my skin.

The Anatomy clocks in at 1,392 pages — my paperback quickly broke in half — and any paragraph swims through a dizzying array of references, Homeric through Renaissance; medical, theological, and philosophical. On the one hand, its difficulty made me feel accomplished; and on the other hand, it made me feel, basically, that it was fine to be scared, to still be doubting. I could try cabbage one day, clear water another, oranges, opening windows, perfume, walking in fields, sweet-scented baths, confessing to a friend, faith in God, eating earlier, fasting, seeing sunlight upon waking, reading Herodotus, reading Elizabethans. And above all, as Burton’s last section of course requires, truly and steadfastly resisting despair.

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Small consolations, it’s true, but ones that fit into a life well lived — unlike antidepressants, with their dubious efficacy and their near-certain, unpleasant side effects; and unlike so much of self-help, with its individualism, and its transactional focus on convenience and utility. Burton’s salves are enriching, not subtracting. They make the reader feel, in some small way, in control of their condition, an active agent. As the habit makes the monk, the medicine makes the patient, and against the pop psychology and medical cocktails more commonly on offer, there’s something to be said for the demanding and delightful sublimations of The Anatomy. That the book is often baffling only further recommends it. It feels good to do something difficult; and it feels good to get out of one’s own time, to defamiliarise one’s own condition: though people may have always felt sad, they felt differently about feeling sad.

The Anatomy of Melancholy won’t cure depression. But there’s something comforting about this futility: if sadness has always existed and always will, even for those, like Burton, of exemplary learning and unparalleled discipline, even in the most foreign reaches of time and place, even after 13,000 pieces of advice and 400 years, then we might try to make something generative of some of the pain, to “write of melancholy, by being busy to avoid melancholy”.