The Rise and Fall of Pragmatism in Psychiatry

Psychiatric TimesPsychiatric Times Vol 36, Issue 12
Volume 36
Issue 12

"Psychiatry has been frozen in time since the 80s, and hence the absence of progress since then is no surprise." So says, S. Nassir Ghaemi, MD, MPH, in the next installment of Conversations in Critical Psychiatry with Awais Aftab, MD.


S. Nassir Ghaemi, MD, MPH is a psychiatrist with clinical and research expertise in mood disorders and training in philosophy and public health. He is Professor of Psychiatry at Tufts University, Lecturer on Psychiatry at Harvard Medical School, and directs clinical drug discovery research in psychiatry at Novartis Institutes for Biomedical Research in Cambridge, Mass. He is the author of the new textbook Clinical Psychopharmacology (Oxford; 2019), and multiple other books including The Concepts of Psychiatry(Johns Hopkins; 2003), The Rise and Fall of the Biopsychosocial Model (Johns Hopkins; 2009), and the New York Times bestseller A First-Rate Madness: Uncovering the Links Between Leadership and Mental Illness (Penguin, 2011). He also shares his insights on his website

The aim of Conversations in Critical Psychiatry is to engage prominent individuals within and outside psychiatry who have made meaningful critiques of psychiatry and have offered constructive alternative perspectives to the current status quo.

conversations in critical psychiatry

Awais Aftab, MD

controversies, point-counterpoint

S. Nassir Ghaemi, MD, MPH

I first got exposed to Dr Ghaemi’s ideas about 7 years ago through his critical commentaries on DSM in Psychiatric Times, I subsequently discovered his wealth of writings on philosophical frameworks in psychiatry as well as how these conceptual issues have “real world” implications when it comes to the understanding, classification, and treatment of mood disorders.

A common refrain in Dr Ghaemi’s work has been that psychiatry has lost its way by pursuing a pragmatic, atheoretical framework of understanding mental illness (ie, progress requires going beyond pragmatism in search of truth). Over the years I have found his ideas to be highly thought provoking and engaging and his opinions have been instrumental in shaping my own views on psychiatry. Dr Ghaemi exemplifies the spirit of a maverick thinker and wields his nuanced understanding of history, philosophy, and research methodology to challenge conceptual errors rampant in the field.

Dr Aftab: In On Depression, you’ve argued that sometimes depression is a medical disease but often it is not. You write: “It has become de riguer to state that depression is a disease. I would say the opposite: most depression is not a disease. The part of it that is recurrent and episodic, or due to a specific medical cause, is disease. But the part that is not episodic, that is chronic and admixed with anxiety, becomes indistinguishable from personality.”1p14 From your perspective, what do you mean when you call something a “disease”? In cases when depression is not a disease, should it be considered a “disorder”?

Dr Ghaemi: The word “disorder” is meaningless. It is purposefully vague, introduced by DSM-III for every one of its 292 diagnoses in an attempt to be atheoretical about the causes or nature of those diagnoses. DSM-III leaders in 1980 wanted to reject psychoanalytic interpretations, and they did not want to commit to biological causes (diseases), so they replaced the earlier term “reaction” with the purposefully vague term “disorder.”

Disorder means nothing and everything; anyone can interpret it as they like. That kind of anarchic eclecticism is exactly what DSM-III intended, and psychiatry has inherited for 40 years. The term disease refers to a biological cause of a physical illness. Sometimes depressive states have such causation, as in manic-depressive disease; sometimes they do not. The term “major depressive disorder” vaguely combines many different depressive presentations, and thus, as a whole, means nothing scientifically.

Dr Aftab: It has been noted that the description of depression espoused by psychiatry has changed dramatically over the decades, from an acute, rare, self-limiting illness with favorable prognosis to a chronic, common illness in which only a minority of persons stay well. How do you make sense of this change in the conceptualization of depression’s history?

Dr Ghaemi: I wouldn’t say that characterization is correct. “Depression,” if by that term is meant “melancholia” in older usage, was seen as severe and episodic and common in Kraepelin’s work. The prognosis was not good in the sense that it was recurrent: each episode improved, but then recurred, and suicide was frequent. Neurasthenia reflected what was later termed neurotic depression. It was chronic and rampant in late 19th century America. I think American psychiatry simply is ignorant of the history of mental illnesses.

Dr Aftab: You have long crusaded against antidepressant use in bipolar disorder, arguing that these drugs lack efficacy and hinder recovery in patients with bipolar disorder. I think psychiatry’s official position has slowly shifted in that direction (at least for bipolar I), but antidepressants still remain widely prescribed for bipolar disorder, and it is common to hear clinicians say, “I know what the research says but antidepressants are clearly helping my bipolar patients.” What explains this persistent notion of anecdotal efficacy in clinical practice?

Dr Ghaemi: Clinicians often base their opinions on their experience, not realizing that-as the old saying goes-half of what they see is false; they just don’t know which half. The same reasoning was the basis for the medical profession’s wide acceptance for two millennia of the four-humor theory and of bleeding.

What many clinicians don’t understand is the importance of confounding bias, that all their experience is confounded by the influence of other factors that they cannot know or control, foremost among these being natural history of recovery in an episodic illness. Each bipolar depressive episode resolves naturally, usually within months. Randomized placebo-controlled data show that antidepressants and placebo produce notable and equal improvement. Placebo is a stand-in for that natural history. Instead of giving nature the credit, as the randomized clinical trials prove, clinicians credit the drugs: a classic mistake of the unscientific practice of medicine.

Dr Aftab: Even outside of bipolar disorder, you are not a huge fan of antidepressants. Recently when the Cipriani and colleagues’2 meta-analysis was published, you wrote an editorial for Medscape commenting on how the results actually confirm what previous studies have shown, that over-all the benefit from antidepressants (over and above placebo) falls short of clinically meaningful.3 It is hard to imagine a group of medications whose efficacy has been as closely scrutinized as that of antidepressants, and yet despite the largest meta-analysis ever conducted, doubts about efficacy remain. Why is this issue so controversial and divisive?

Dr Ghaemi: The studies are replicated and clear: the effect size of benefit with antidepressants overall in MDD is small, and short of the cut-off for clinically meaningful benefit. On the other hand, the natural history of depressive episodes is that they resolve and so clinicians see improvement. They don’t realize that the benefit occurs almost equally with non-drug intervention (placebo). At root, the problem is an unwillingness to accept the verdict of science, as opposed to one’s wishes or beliefs.

The psychiatric profession appears to identify its medical legitimacy with the claimed efficacy of its drugs. There’s no reason to claim this equivalence. In fact, we hurt our legitimacy with the public and with our medical colleagues, when we cling to our treatments excessively. This process is no different now with drugs than it was half a century ago in American psychiatry with psychoanalytic extremism. The basic psychiatric attitude is the same, even though the treatments are different.

We need to change our basic philosophy and accept a self-critical attitude that submits to scientific judgment, with humanistic sensitivity. This basic philosophy is as old as Hippocrates, and reflects being a good doctor, period. It’s the right way to defend our medical and scientific legitimacy.

Dr Aftab: The long-term efficacy data for antidepressants in MDD are even weaker. What is your approach to antidepressant maintenance treatment in practice?

Dr Ghaemi: Antidepressants have modest short-term symptomatic benefit acutely, like aspirin for fever. They do not prevent depressive episodes in a definitive manner (ie, they are not disease-modifying). In my practice, I prefer to use them for the short-term, but routinely not long-term.

Other agents, especially lithium and possibly lamotrigine, have better evidence for depressive episodes, ie, have long-term disease-modifying effects.4 Antidepressants are analogous, in my view, to steroids in conditions such as multiple sclerosis: useful in an acute episode, but not preventive. Agents like lithium are disease-modifying, less relevant for active symptoms but indispensable for the underlying disease itself.

Dr Aftab: Given your clinical and research experience, what are your thoughts on the various approaches to new ideas such as mixed symptoms in depression?

Dr Ghaemi: The views here are strictly my own. There are five major players in these debates: clinicians, academics, the insurance industry, the FDA, and the pharmaceutical industry. Clinicians, the insurance industry, and the pharmaceutical industry are motivated by the profit motive, at least in part. The FDA is not so motivated but is affected by political influences (ie, the pharmaceutical lobby’s influence on Congress).

Academia’s motivations are complex-they believe what they want to believe with little outside influence. Such academic freedom is good and bad, since one is free to continue to believe untruths, instead of seeking the truth. With new ideas such as mixed states, the groups that are closest to economic influences seem to be the most pragmatic. This utilitarian attitude can be harmful, but it also is flexible, and open to new ideas.

In contrast, academia is often a major obstacle because there is no motivation to change established ideas. Some academics think they can outsmart the pharmaceutical industry, or the insurance industry, by supporting or opposing certain ideas. This is a fool’s errand. What academia needs to do is to seek the truth in as honest a way as possible, giving up one’s own favorite notions if needed. Only in this way can the other players be influenced in the right direction, converting a vicious cycle into a virtuous one.

Dr Aftab: It’s easy to forget the question of diagnostic validity in psychiatry. In the famous 1971 US-UK study that suggested that US psychiatrists diagnose schizophrenia far more liberally than British psychiatrists, the researchers comment: “though one may discuss whose concept of schizophrenia is more useful, or closer to Bleuler’s original description, one cannot meaningfully discuss which is right, for we have no external criterion . . . .”5

This is a problem that has plagued psychiatric classification. We can come up with non-DSM syndromic criteria and syndromic definitions (as you have done for bipolar spectrum disorder) but how can we demonstrate that one construct is more valid than another? Has our notion of validity made any progress since Robin and Guze6 presented their criteria in 1970?

Dr Ghaemi: This is a common claim in defense of the theory that underlies DSM-III through DSM-5. It’s a self-fulfilling prophecy: unscientific diagnostic constructs are used to claim that no definitive scientific validation can be made of them. In medicine, only psychiatry engages in this kind of epistemological solipsism. The brain can succumb to diseases, and these diseases can have psychological symptoms. Our job is to identify those diseases, not to create rationalizations why we shouldn’t search for them.

Robins and Guze had good perception: since we had no clear pathological basis for any psychiatric disease, we could use five lines of evidence (symptoms, course, genetics, biological markers, treatment), which, if they pointed in the same direction, would support the validity of a disease. This is the same rationale as Kraepelin’s emphasis on course of illness, not symptoms, as the basis of diagnosis. It’s also consistent with traditional medical science: symptoms vary among all medical illness, but combination with course and laboratory markers validates diagnosis.

There are many medical conditions in which no clear external cause or pathology is known, including seizure disorders, migraine, ulcerative colitis, rheumatoid arthritis. In psychiatry, this approach proved very successful with the carefully defined clinical syndrome of general paralysis of the insane, which was later found to correlate with the identification of treponema pallidum. Many DSM advocates claim that things are different now; current diseases are harder to define. Maybe so, maybe not. But we’ll never know if we keep using socially constructed DSM definitions, as opposed to making an effort to find the truth.

Dr Aftab: If Robert Spitzer had never created DSM-III, do you think the field of psychiatry would be in a better or a worse place today? In other words, do you see the legacy of DSM as largely beneficial or harmful?

Dr Ghaemi: I have no doubt psychiatry would have been better off without DSM-III and, more importantly, its successors DSM-IV and DSM-5. I know the usual mantra: DSM-III provided a common language in a time of Freudian babble-it allowed for reliability. This small advantage is far outweighed by what happened with DSM-IV and DSM-5: the dictionary of a common language became a fundamentalist Bible that we all have to believe and buy. Psychiatry has been frozen in 1980, hence the absence of progress since that time is no surprise. DSM’s legacy has been largely harmful.

Dr Aftab: Thank you!

Dr Aftab is a psychiatrist in Cleveland, Ohio. He completed his psychiatry residency from Case Western Reserve University/University Hospitals (2018) and trained in geriatric psychiatry at University of California San Diego (2019). He has been actively involved in initiatives to educate psychiatrists and trainees on the intersection of philosophy and psychiatry and is an executive council member of Association for the Advancement of Philosophy and Psychiatry. He is also on the Psychiatric Times’ Advisory Board. He can be reached at

The opinions expressed in the interviews are those of the participants and do not necessarily reflect the opinions of Psychiatric Times.

Previously in Conversations in Critical Psychiatry

Relentless Warrior for Mental Health: Allen Frances, MD

The Structure of Psychiatric Revolutions: Anne Harrington, DPhil

Skepticism of the Gentle Variety: Derek Bolton, PhD

Explanatory Methods in Psychiatry: The Importance of Perspectives: Paul R. McHugh, MD

Chaos Theory With a Human Face: Niall McLaren, MBBS, FRANZCP


This article was originally published on 12/3/19 and has since been updated.


Dr Aftab has no relevant disclosures or conflicts of interest. Dr Ghaemi discloses that he is an employee of Novartis Institutes for Biomedical Research. The views expressed here are his own and do not reflect those of his employers.


1. Ghaemi SN. On Depression: Drugs, Diagnosis, and Despair in the Modern World. Baltimore, MD: Johns Hopkins University Press; 2013.

2. Cipriani A, Furukawa TA, Salanti G, et al. Comparative efficacy and acceptability of 21 antidepressant drugs for the acute treatment of adults with major depressive disorder: a systematic review and network meta-analysis. Lancet. 2018;391:1357-1366.

3. Ghaemi SN. Antidepressants Work for Major Depression! Not so Fast. Medscape. June 13, 2018.

4. Ghaemi SN. Clinical Psychopharmacology: Principles and Practice. New York: Oxford University Press; 2019

5. Kendell RE, Cooper JE, Gourlay AJ, et al. Diagnostic criteria of American and British psychiatrists. Arch Gen Psychiatry. 1971;25:123-130.

6. Robins E, Guze SB. Establishment of diagnostic validity in psychiatric illness: Its application to schizophrenia. Am J Psychiatry. 1970;126:983-987.

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