Depression as a Philosophical Problem: Rethinking the Meaning of Suffering in the Era of SSRIs

When I was sixteen, I was hospitalized for depression for six weeks and put on Prozac. At the time, I was taught that depression is, first and foremost, a medical problem. It was a sign that my brain was broken, and that I needed doctors to fix me through a combination of drugs and therapy. I’ve taken antidepressant drugs on and off throughout my adult life.

But over the last decade, I’ve come to think of depression as, primarily, a philosophical problem. Depression and its treatment engage some of the deepest questions philosophers ask, such as questions about agency, selfhood, and the good life.

To appreciate the philosophical dimension of depression, it’s helpful to take a step back and consider two contrasting paradigms of depression. This helps us see how each one involves distinct, implicit answers to those questions.

Two Paradigms of Depression

The first picture is the chemical imbalance view—or more generally, the brain dysfunction view. It holds that depression is a brain disease, kind of like epilepsy or Parkinson’s disease. The idea is that, with enough research, we’ll eventually find the underlying dysfunction—perhaps faulty serotonin transmission or an overactive amygdala.

Treatment in this paradigm tends to focus on medication or some combination of medication and therapy such as cognitive behavioral therapy, which seeks to heal depression by helping us understand the faulty reasoning process that underlies it. This is the dominant paradigm, despite there being little evidence that depression stems from a chemical imbalance or any known brain abnormality.

The second view can be called the “functional signal” view. The idea here is that depression is your brain’s well‑designed signal that some of your needs are not being met. It could be a career, a life goal, or something else in your life that is going wrong and needs to change. On this view, depression isn’t pathological; it’s purposeful. It performs an important function, just like physical pain does.

One school of thought that promotes this latter view of depression is evolutionary psychiatry. Evolutionary psychiatrists tend to consider mental health problems, like depression, anxiety, or even delusions, as designed by natural selection to serve a purpose. Yet you don’t have to accept evolutionary psychiatry to accept the idea that depression is a functional signal that something is wrong. This idea has long been part of the psychoanalytic tradition and is prominent in current approaches such as Internal Family Systems (which I discuss later on in this post).

One important question we must ask, of course, is: which paradigm is more likely to be true? In other words, which paradigm is more credible and consistent with the evidence? (My own view is that the evidence favors the “functional signal” idea, for reasons I point to here.) But we can ask a different question, one of equal importance from a therapeutic standpoint: which one of these views better promotes healing? If I come to believe that my depression is a chemical imbalance, rather than a functional signal—or vice versa—how does that affect my prospects for getting better?

Harms of the Brain Dysfunction Paradigm

Our beliefs about the causes of depression aren’t neutral. They shape prognosis in profound ways. In this respect, they’re somewhat different from, say, beliefs about the causes of multiple sclerosis (MS) or Alzheimer’s disease, where what I believe is unlikely to affect outcomes as much. Intriguingly, a large amount of research conducted over the last decade shows the same pattern: the idea—embodied in the chemical imbalance view—that depression is a brain dysfunction tends to harm patients in multiple ways. These harms include the following:

• Prognostic pessimism: the belief that mental health problems are due to brain dysfunctions tends to lead people to pessimism about healing. It leads people to think, “maybe depression is just how my brain works, so it’s probably not going to change.”
• Limiting treatment options: people who believe that their depression stems from a chemical imbalance are more likely to think that pills are necessary and that talk therapy is ineffective.
• Duration of antidepressant use: people who think their depression is a brain abnormality tend to stay on antidepressants for longer and are less likely to try to stop taking them.

What’s the harm in taking medications? The problem is that antidepressant drugs like selective serotonin reuptake inhibitors (SSRIs) give rise to negative side effects and withdrawal symptoms. A prominent side effect is some degree of sexual dysfunction—most often experienced as a dulling of genital sensation. For a small number of users, sexual dysfunction continues long after the pills are stopped. This is a poorly understood condition called “post-SSRI sexual dysfunction” (PSSD). Moreover, the longer a person takes antidepressants, the more likely they are to experience withdrawal symptoms when they try to stop, including fatigue, nausea, and “brain zaps.” Often, doctors mistake those withdrawal symptoms as the recurrence of depression itself, prompting a new cycle of antidepressant use.

In contrast, numerous studies (such as those I discuss here and here) suggest that seeing one’s depression either as a meaningful response to a life crisis or as the brain’s functional signal that one’s needs aren’t being met have the opposite effect. People who believe their depression is purposeful (rather than pathological) tend to be more optimistic about therapy, tend to feel less stigma about sharing their depression with other people, and tend to stay on antidepressants for shorter periods of time.

Depression as a Philosophical Problem

As I contemplated these results, I started to think that what was really helping people was, in the first place, a certain philosophical or conceptual shift they made about the meaning of their depression. This philosophical leap had to do with changing conceptions of agency, selfhood, and the good life.

First, consider selfhood. What are the boundaries of the self? Where does my “self” begin and end? The brain dysfunction view invites us to think of depression as something like an external affliction. It’s not part of who I am; rather, it’s a terrible accident that has befallen me, but that can potentially be reversed by medications or therapy. In contrast, the functional signal idea invites us to think of depression as a part of my very self. My “self” is wide enough to include my depression. Depression is like a part of my self trying to communicate with me.

This notion of the self as a community of somewhat fragmented agents, rather than a simple, unified whole, has long been part of the psychoanalytic tradition. From very early in his career, Freud concluded that one couldn’t understand mental health problems without seeing the mind as consisting of somewhat disparate agents pursuing different goals. The idea of the self as a community is more explicit in Internal Family Systems, a therapeutic approach which encourages patients to give names to the different parts of their selves.

Second, consider the way notions of responsibility and agency differ between the two paradigms of depression. Is depression, at least to some extent, my responsibility? One alleged benefit of the brain dysfunction model is that it removes responsibility. I’m no more responsible for my depression than I would be for having Alzheimer’s disease or MS. In the 1980s and 1990s, doctors, journalists, and mental‑health advocacy groups held the optimistic view that the brain dysfunction paradigm would liberate depressed patients from shame and blame.

But the last decade of research on public messaging about mental health (e.g., here and here) has led to a far more nuanced picture. While the dysfunction paradigm can reduce the sense of blameworthiness, it can also give rise to pessimism about getting better, along with the other harms outlined above. If depression is the symptom of a broken brain, then it seems like there’s nothing I can do of my own accord to fix it. I need an expert to come along and heal me.

In contrast, the functional signal view puts agency and responsibility front and center. Depression is, in the first place, a call to action. It may be a call to end a relationship or transform it. It might be a call to change life goals or career paths. Although I might not be responsible for becoming depressed, I am responsible for the choices I make, choices which can impact the duration of depression.

Finally, these two paradigms involve different ideas about the good life, that is, what kind of life I ought to aspire to. The brain dysfunction view presents the good life as one in which, among other things, people don’t get depressed. It’s one in which people can pursue their life goals freed from this terrible affliction. (Incidentally, if you do a Google image search for “overcoming depression,” you’ll often see a stock photo of a man or woman outdoors with arms outstretched, apparently embracing the good life that comes with conquering depression.)

In the functional signal view, a good life isn’t one in which you never get depressed. It’s one in which depression serves its proper role—it does what it’s supposed to do. For an obvious analogy, consider physical pain. A child might think that a good life is one where nothing ever hurts. But adults recognize that a good life is one in which the pain response does what it is meant to do: namely, alert us to the fact that, say, we’ve stepped on a piece of glass or been stung by a bee, so that we can take appropriate corrective action. On the functional signal view, depression works a bit like physical pain: it alerts us that our lives have gone off track.

A Historical Puzzle

Several years ago, in considering these two paradigms, I arrived at a puzzle: If the brain dysfunction view of depression has such poor evidence behind it, and if it tends to do more harm than good in people’s lives, how did it become so prominent? (A large study in 2010 suggested that, at the time, about eighty percent of Americans believed that depression stemmed from a chemical imbalance in the brain. The chemical imbalance metaphor remains prominent among social workers, in YouTube videos, and even on medical websites.)

That question led me to become fascinated with the historical emergence of the biological paradigm, exemplified by the serotonin theory of depression, the dopamine theory of schizophrenia, and the noradrenaline theory of attention hyperactivity disorder (ADHD). How did we, as a society, come to be so taken with the idea that mental disorders are brain dysfunctions to be managed with pills?

A cynic might think the answer is obvious: it must have been a PR campaign devised by pharmaceutical companies to promote drugs. But the answer is far more nuanced. The push toward the biological paradigm came from several sources. True, there were pharmaceutical companies who wanted to sell drugs. But the push also came from patients and their families, who were tired of being told that their mental health problems represented unconscious conflicts or childhood trauma. And it came from psychiatrists themselves, who wanted to be taken more seriously as doctors by their colleagues in established fields like cardiology and urology.

The biological paradigm also emerged from scientific advances taking place in the 1970s suggesting that schizophrenia was primarily a disorder of dopamine. This was the famous dopamine hypothesis of schizophrenia, developed by the neuroscientist and psychiatrist Solomon Snyder. When I began studying Snyder’s life and times, I discovered that his dopamine hypothesis was a direct result of experiments he conducted in the 1960s and early 1970s with psychoactive drugs like LSD and amphetamines. He and his colleagues were fascinated with the question of whether these drugs could create psychosis in normal volunteers. He even ingested the drugs himself to see how they affected his mental states. His drug research led directly to his dopamine theory of schizophrenia, which became an important thread in psychiatry’s biological shift. I explore the history of the use of psychoactive drugs in medical research and how it helped give rise to the brain dysfunction model in my recent book, The Madness Pill: One Doctor’s Quest to Understand Schizophrenia (St. Martin’s Press, 2026).

In my view, moving away from the brain dysfunction model of depression requires developing and promoting humanistic and scientifically sound alternatives. But it’s equally about exposing the idiosyncratic historical forces that made the brain dysfunction view so prominent in the first place. If the dysfunction paradigm emerged from a blend of marketing strategists, outsized personalities, and patients frustrated with the status quo—rather than merely the cold march of scientific progress—then we’re free to envision better alternatives.