Awais Aftab, MD

Conversations in Critical Psychiatry is an interview series that explores critical and philosophical perspectives in psychiatry and engages with prominent commentators within and outside the profession who have made meaningful criticisms of the status quo..

Ronald W. Pies, MD, is Professor Emeritus of Psychiatry and Lecturer on Bioethics & Humanities at SUNY Upstate Medical Center, and Clinical Professor of Psychiatry at Tufts University School of Medicine. He is also Editor-in-Chief Emeritus (2007-2010) of 

. Dr Pies is the author or co-author of several psychiatric textbooks, including 

Clinical Manual of Psychiatric Diagnosis and Treatment: A Biopsychosocial Approach

 (2005). He is also the author of several books on comparative religion, philosophy, poetry and fiction

 need little introduction to Dr Pies. His articles and commentaries have been a staple feature of this publication for a long time, and he is well-known for his articulate defense of psychiatry in the face of various criticisms. I first became acquainted with his writings during my 

 into making sense of Thomas Szasz. This interview series naturally has been of great interest to him and has been the source of much mutual discussion. I have found him to be gracious, thoughtful, and warm in my interactions. I have great respect for him and consider him to be a wise friend. These interviews, for obvious reasons, tend to gravitate toward more contentious issues, and from certain perspectives we might be seen as being on opposite sides of the aisle but there are lot more commonalities than might be apparent.

For much of your career you have been a vocal critic of Thomas Szasz and his ideas. I am sure there were others, too, but I am aware of at least one exchange between you and Dr Szasz which happened in the 2004 book, 

. Dr Szasz’s response seemed dismissive; I don’t think he made a good faith effort to engage with what you or other critics were saying. Szasz never changed his mind. Does that tell us something about him as an individual or does it, more pessimistically, tell us something about humans in general . . . about our inability to change our minds when confronted with arguments to the contrary?

 I should say at the outset that it is difficult for me to be “objective” about Dr Szasz, who was one of my teachers during residency. It is fair to say that, over the course of more than 30 years, he and I had a “complicated” relationship! Tom (as most of us knew him) was a brilliant polemicist, and, on a one-to-one level, a charming and cordial man. I will always remember how, when I was still a medical student, he once poured tea for me in his office—an “old world” kindness I have never forgotten!

And, I would also credit Dr Szasz with forcing all of us in the profession to reexamine our most basic and cherished assumptions, regarding mental illness; the civil liberties of our patients; and the language we use to express and defend our positions. That said, I believe that Szasz’s deeply misguided views on psychiatric illness and the nature of “disease”; his personalized attacks on psychiatry; and his inflexible adherence to his own positions all did considerable damage to our profession and our patients. And, yes: I was deeply disappointed with his rejoinder to my chapter in 

My more recent critique of Szasz is found in the book, 

Science is a self-correcting enterprise. Progress relies on diversity of opinion, dissent, and criticism of the status quo from within the scientific discipline itself. Psychiatry has been under attack for so long now that many psychiatrists are quite weary of any critique. An abundance of popular criticism against psychiatry is hostile, ill-conceived, rhetorical, sentimental, and divorced from any meaningful science. Unfortunately that tends to drown out the legitimate, sincere, and well-intentioned criticisms that do need to be taken seriously. Part of my task through this series has been to invigorate that self-correcting function of scientific inquiry, and to separate the wheat from the chaff when it comes to meaningful discourse. I am certainly not alone in this. You have been more active in defending psychiatry against criticism and have developed a reputation for that role, but I don’t believe our motivations are that dissimilar. How do you see your own relationship with psychiatric critics?

I would distinguish between two quite different groups of “critics.” There are, on the one hand, sincere and well-intentioned critics of psychiatry—many of whom are psychiatrists—whose aim is to improve the profession’s concepts, methods, ethics, and treatments. Indeed, Dr Aftab, you have interviewed a number of such constructive critics in your ongoing series. On the other hand, there are “critics” whose hostile and vituperative rhetoric is clearly aimed at discrediting psychiatry as a medical discipline. These critics, in my view, fall under the rubric of “anti-psychiatry,” which I would define as,

“. . . that movement which denies the fundamental legitimacy of psychiatry as a medical specialty; consistently imputes malign or mendacious motives to the profession; and which denies the efficacy and legitimacy of psychiatric treatment, particularly its somatic treatments.” Dr Nassir Ghaemi, Sairah Thommi, and I described the dual nature and origin of the anti-psychiatry movement in an article that appeared in 

I have had fairly cordial relations with several representatives of the “critical psychiatry” school of thought, even though I often disagree with their claims. On the other hand, there are simply no excuses for the bogus arguments and hateful attacks leveled by the most extreme voices of anti-psychiatry. What strikes me about most of the latter critics is how little they understand of general medical nosology and praxis, or of the history of medicine—which leads them fallaciously to marginalize psychiatry from the other medical disciplines.

 I quite enjoyed your 2016 exchange with Professor Hannah Decker

 in which you defend the Alexandrian-Jasperian-Engelian (AJE) integrative tradition as the underappreciated “solid center” of psychiatry in contrast with the schism between biological and psychosocial approaches to mental illness. I think a more cynical view would be that the AJE tradition in psychiatry has been a long-standing but unrealized 

. I think you are right that the 1970s and 1980s—the period when psychiatrists of your generation were trained—were probably the “golden” years of AJE tradition, but I think the agenda was hijacked pretty quickly afterwards. The explosion of pharmaceutical development in the 1990s and early 2000s with the development of SSRIs and atypical antipsychotics resulted in the reductionistic, caricaturish portrayal of psychiatric disorders as “chemical imbalance” in the public imagination; there was a large influx of money into neuroscience research with an undelivered faith that neuroscience will soon revolutionize the field, and then managed care knocked out whatever wind was left in clinical practice. When I see bio-psycho-social thinking described as the “solid center,” I cannot help but think of the famous phrase from W.B. Yeats, “The center cannot hold.” Do you also share this sense that the solid center has somehow fallen apart?

: I agree with much of what you are arguing here, but I would suggest that a more nuanced analysis is in order. First, let’s distinguish between two related but distinct claims: first, that psychiatry has become predominantly, if not exclusively, “biological;” and second; that psychiatry endorses some form of a “chemical imbalance theory.”

Taking the second claim first: it is quite clear that the “chemical imbalance” trope has become deeply engrained among many in the general public. As you know, I have argued repeatedly that the so-called “chemical imbalance theory” was never a bona fide “theory” in the strict, scientific sense.

 Nor was it a model embraced by most academic psychiatrists or, importantly, by the pioneers of the biogenic amine hypothesis.

 Yes, our critics tirelessly quote this or that notable psychiatrist who used the phrase, “chemical imbalance,” but this doesn’t mean the psychiatric profession as a whole ever embraced the chemical imbalance theory. Nor was it ever a model espoused by academic psychiatrists, or the official position of our professional organizations.

Now, circling back to the first claim: I think it is incontestable that, since the heyday of psychoanalysis (ca. late 1950s-1960s), the field of psychiatry took a fairly sharp turn toward the “biological” in the period from roughly 1978 to 1998, which, to a considerable degree, persists to this day.

 But we were far from alone in taking this turn, as witnessed by U.S. President George H.W. Bush’s proclaiming the decade from 1990-1999, “The Decade of the Brain.” And there is no question that the movement toward the biological/biochemical has been heavily influenced by the pharmaceutical industry. Nonetheless, what I have called the “Alexandrian-Jasperian-Engelian (AJE) integrative tradition” has remained central to academic psychiatry, alongside Engel’s Biopsychosocial Model (BPSM). You and I and Dr Ghaemi have had a fruitful debate on the merits, demerits, and validity of the BPSM, and I won’t rehash that discussion.6-8 I will simply say that, while the AJE/BPSM framework has struggled to remain a central part of psychiatric practice—pushing back against powerful market forces that favor brief “med checks” and provision of psychotherapy by non-physicians—the “integrative impulse” is alive and well in our profession.

Indeed, since Engel’s 1977 paper on the BPSM first appeared, “. . . the flow of citations [of Engel’s model] did not appear to fade over the years and, indeed, it has increased in the last decade.”

department at SUNY Upstate Medical University

 emphasizes the integration of psychopharmacology and psychotherapy and explicitly endorses “the biopsychosocial approach.” This is also the case at the 

, where Engel taught and practiced. In short, I believe the AJE/BPSM center is still “holding,” but it is surrounded by powerful forces that threaten its integrity.

 I have followed the controversy surrounding “chemical imbalance” with some interest over the years, including the multiple articles you have written on this issue. Generally, I agree with you that the chemical imbalance was never accepted as the “truth” by academic psychiatry or by our professional organizations. It was likely an advertisement strategy by pharmaceutical companies that took on a life of its own. However, I am not sure I am ready to exonerate our profession. At best, it seems like we were silent spectators, watching as this misleading idea spread like wildfire in the society (including among our patients and patient advocacy groups), doing little to nothing to correct these public misperceptions. At worst, it seems like at least some of us were participants. Ken Kendler writes in a 2019 

 commentary, “I would commonly see patients who would say some version of ‘my psychiatrist said I have a chemical imbalance in my brain.’”

 I have had a very similar experience myself. Either way, surely as a profession, we could have done a better job of educating our patients and the public?

Yes, I agree that we—all of us—could have done a better job of counteracting the so-called “chemical imbalance” trope, which, as your comments imply, was more a creature of “Mad Men” than of men and women who study madness! I wish I had tackled the issue earlier than my 2011 article.

And, yes—we often hear anecdotes concerning patients who tell their current clinician some version of, “My psychiatrist said I have a chemical imbalance . . .” But where is the evidence that this is what patients were 

 told? Who has contacted the patient’s psychiatrist, or reviewed his/her case notes, to see if that was really what the patient was told? To my knowledge, there has never been a study examining the “other side of the story”—and, to be clear: patients are not infallible recorders of what their doctors tell them. So, we are really left to speculate, and with the knowledge that about 80% of antidepressant prescriptions are written not by psychiatrists, but by primary care physicians and family practitioners. Who knows what these doctors told their patients? So, I consider this really a fruitless debate, unless and until I see contemporaneous documentation of what patients were actually told by their psychiatrists; or, failing that, a large “N” of psychiatrists confirm that they regularly used the “chemical imbalance” trope to explain the nature of their patients’ problem. I will add that, in my own practice over 25 years or more, I did 

 a discussion of neurotransmitters in my explanations to patients, 

but always in the context of “bio-psycho-social” causes and risk factors.

 I understand that there is no conclusive evidence, but this is not a court of law or a Cochrane committee appraising research evidence. Philosophers talk of “epistemic injustice,” which occurs when someone is not believed because of who they are. The victims of epistemic injustice are typically underprivileged and marginalized members of the community such as women, racial and ethnic minorities, and pertinent to us, persons with mental illness. The latter group has historically been silenced and robbed of a voice. Foucault famously described psychiatry as a “

 of reason about madness” (my emphasis). So, my tendency is to take seriously what my patients tell me, unless I have good reason to think otherwise. You have already stated that you would need a high level of evidence to change your mind, so I'm not trying to convince you here. My fear is that many patients who will read what you have said will feel ignored and invalidated, and their trust in psychiatrists may be further eroded. I don't believe that is what you intend, so I want to give you an opportunity to reassure such readers who may find your words alarming.

 Thank you for letting me clarify my comments, Dr Aftab. First, you are wise to take your patients’ reports and recollections seriously—and to treat such reports respectfully. Without mutual respect, the therapeutic alliance is doomed. My somewhat testy comments regarding, “Where is the evidence that this is what patients were 

 told?” were offered in the context of rebutting dubious claims by various antipsychiatry blogs, websites, and organizations. In the 

 context—sitting with my patients—I would 

challenge a report like, “My psychiatrist [family practitioner, general physician, etc.] said I have a chemical imbalance . . .” Rather, I would likely reply by asking the patient, “Can you tell me more about that meeting with your doctor, and how you felt when you heard what he/she said?” I would draw the patient out on what “message” he or she took from the encounter; eg, did apparent mention of a “chemical imbalance” leave the patient feeling relieved or anxious? More worried or less? etc. (Some patients react badly when given a purely “biochemical explanation” of their problem). Note that an interaction of this type 

does not prejudge the patient’s recollection

 or reach a final conclusion regarding what the patient was actually told by the psychiatrist or other physician. Remember: listening seriously and respectfully is not the same as listening 

As for Monsieur Foucault, that is a topic for another time! And keep in mind that while people with mental illness have indeed been marginalized and stigmatized, so have those of us who care for them. Among other factors, derogatory portrayals of psychiatry and psychiatrists in the media have contributed to stigma against psychiatrists and mental health professionals.

 When it comes to the AJE tradition, the biopsychosocial approach is surely the dominant player. There are many prominent psychiatrists—including Paul McHugh, Nassir Ghaemi, and Ken Kendler—who firmly remain embedded within the AJE tradition but have moved away from the BPS approach and have instead espoused other variants of pluralistic thinking. Are you heartened to see this flourishing of philosophical interest in pluralistic approaches?

 Yes, I am heartened, and I would add that I am not wedded to only one formulation of “pluralism,” such as the biopsychosocial model (or, as I prefer, 

), Kendler and Campbell,13 and our colleague, Dr Ghaemi,

 have all proffered pluralistic formulations of psychiatric diagnosis and treatment, some of which may well be improvements on Engel and Romano’s BPS model. We are all seeking comprehensive, holistic ways of understanding our patients and their afflictions, while hewing closely to evidence-based medicine.

In your discussions of the meaning of “disease” or “disorder,” you have focused on notions of suffering, impairment, and distress. When it comes to mental disorder, however, historically speaking its precursor concepts of “insanity” and “madness” have also included notions of social deviancy, irrationality, breakdown in meaningful connections, and harm to others. Do you think these notions still play an implicit role in our contemporary diagnostic manuals, and if so, is there a legitimate role for these notions in modern psychiatry?

 My short answer is, these features (social deviancy, irrationality, etc.) should not figure into our concept of disease, 

except in so far as they co-occur with states of severe or prolonged suffering and incapacity

. DSM-5 actually excludes “socially deviant behavior (eg, political, religious, or sexual)” and “conflicts that are primarily between the individual and society” from its definition of a mental disorder (p. 20 of the 

). The DSM-5 qualifies this somewhat by stating, “…unless the deviance of conflict results from a dysfunction in the individual” as described in the definition. That said, I would limit our concept of “disorder”—whether “mental” or “physical,” to raise that unfortunate Cartesian dichotomy—to states in which 

incapacity/dysfunction are present. The DSM-5, in contrast, specifies “distress 

disability” in its definition. I believe this is too broad a brush and would like to see a more stringent definition of “mental disorder”—and fewer DSM categories, too!

 In my more pessimistic moments, I feel that there has been an abdication of certain sorts of critical thinking in our profession. Let me give you a recent example to illustrate what I mean. In December 2019 FDA approved lumateperone for treatment of acute exacerbation of psychosis in schizophrenia. 

15 with an accompanying editorial. The article as well as the editorial however failed to respectively disclose and critically evaluate a crucial element of study design, that the participants had been rather abruptly withdrawn from their previous antipsychotic medications immediately prior to randomization. If you look at 

(this is not intended as a blanket endorsement of the commentary or 

), it becomes clear that the lumateperone phase 3 trial can instead be seen as a comparison of switching antipsychotics vs stopping antipsychotics in schizophrenia. Now one can take issue with the tone of the article or focus on the representation of this or that detail, but my major point is that we expect this sort of critical insight and evaluation to come from our premier research journals and our journals appear to have failed to do that repeatedly. What are we to make of this failure of critical scrutiny?

 This topic is far too complicated to deal with in a few paragraphs, but, in my view, there has been no lack of “critical thinking” about the risks and benefits of antipsychotics (for example, see the 

 for a comprehensive series of articles on this topic). Given space limitations, I will simply make a few general observations, rather than focusing on a single study or its critics:

I agree that we sorely need more long-term (> 2 years), randomized, double-blind, placebo-controlled studies of antipsychotics in the treatment of schizophrenia.

I believe that the evidence for the short-to-intermediate term efficacy (6 months to 2 years) of these agents in preventing relapse in schizophrenia is very compelling, based on numerous studies of varying methodologies.

 My colleague Dr Joseph Pierre and I in our review also concluded that considerable controlled evidence shows that antipsychotic treatment improves quality of life by various measures—at least within the first year of treatment, and perhaps for as long as 3 years.

The existence of a well-defined, antipsychotic “withdrawal syndrome” is very controversial, and the concept of “supersensitivity psychosis” owing to antipsychotic discontinuation remains largely speculative and theoretical. Moreover, as Emsley and colleagues

 have shown, relapses in schizophrenia following antipsychotic discontinuation are due to recurrence of the underlying disease, with no direct link to withdrawal phenomena.

There is a tendency among critics of antipsychotic medications to completely dismiss the therapeutic value of these medications. Those of us who have spent our professional lives treating “the sickest of the sick”—patients whose lives have been destroyed by schizophrenia—have little doubt that antipsychotic medication, judiciously prescribed, can literally be life-saving. Armchair critiques of the research literature are no substitute for working closely, year after year, with suffering patients and their families, as Dr Pierre and I have argued.

 Well, let me ask the question in a different way. Over the past 2 to 3 decades, the manner in which the research trials of new psychotropic medications (particularly those sponsored by pharmaceutical companies) have been published, editorialized, and commented upon in our leading psychiatry journals, would you consider that to be satisfactory? Given everything we now know about pharma misconduct in psychiatry, in retrospect do you think that our critical assessment of bias in the methodology of the trials, and our assessment of the efficacy and safety of the medications was wholly adequate?

The issue of bias, misrepresentation, and “conflict of interest” in the medical literature is very important—but the problem is not confined to psychiatry, and the blame cannot be laid entirely at the feet of the pharmaceutical industry. As one recent review by E.H. Turner noted, the responsibility for pervasive publication bias lies with various parties such as authors, journals, academia, industry, news media.

Turner suggests several possible remedies, including a requirement that “…results should be excluded from review until after a preliminary judgment of study scientific quality has been rendered, based on the original study protocol.”

 As a teacher of psychopharmacology, I think it is equally important to train our residents (and more senior clinicians) to recognize substantial biases in published papers, and to appreciate the critical importance of 

I have enjoyed your writings on “medicalization,” particularly your thoughtful essay in 

. I agree with you that medicalization is not an argument about empirically verifiable claims. You acknowledge that all states of suffering and incapacity are not disorders, so there does seem to be a vaguely defined sense in which it is appropriate to label some forms of suffering as disorders and some forms as not. In your view when is it inappropriate to characterize suffering as a disorder? Can there be legitimate disagreement about the characterization of something as a disorder, ie, disagreement that cannot be resolved by appealing to empirical facts and springs instead from conflicting value judgments?

: Indeed, I think the delineation of terms like “disorder,” “disease,” “illness,” “malady,” etc. is closely tied to very general values regarding “desirable” and “undesirable” states of mind and body; for example, witness the positive value we accord to being able to function in social and vocational roles. And this is true not only in psychiatry, but throughout general medicine—witness the intense debate over whether obesity is or is not a “disease.” (A 2008 commission of 

 concluded that the term “disease” is too complicated to be fully defined!)

This admission points us to the later work of the philosopher Ludwig Wittgenstein, regarding the pitfalls of “essential definitions”—for example, definitions of “disorder” or “disease” that specify 

 for these states. Wittgenstein famously argued (in his 

) that the search for such Platonic “essences” is misguided; and that, at most, we can identify certain “family resemblances” among entities and conditions that we would call “disorders” or “diseases.” That said, like Wittgenstein, I believe our “ordinary language” is as good a guide as any, with respect to defining these terms. In our ordinary parlance, when someone shows evidence of prolonged or severe suffering and incapacity that is not due to an obvious wound (eg, a bullet wound), we are perfectly justified in saying that the person is “ill”; has some kind of “disorder”; or is “diseased.” No labs or imaging needed! Indeed, the concept of disease (dis-ease) arose to explain just such instances of suffering and incapacity. In short, “disease” is a 

 instances of prolonged or severe suffering and incapacity are instantiations of “disease.” For example, someone might be tied to a chair by kidnappers or terrorists, then beaten and starved, and thereby experience profound suffering and incapacity—but we would not ordinarily attribute this to “disease.”

In the academic debate surrounding the bereavement exclusion from DSM-5, a pertinent aspect was that the issue was not just restricted to bereavement-related depression but had extended to all stress-triggered depressions. Jerome Wakefield and colleagues argued that episodes of uncomplicated depression triggered by bereavement and by other losses have similar symptom profiles and similar course, so 

 stress-related uncomplicated depressive episodes should be excluded from the category of major depressive disorder. Given that you played a prominent role in the debate surrounding bereavement exclusion, what was your assessment of this more radical proposal? How should stressful contexts be taken into consideration when it comes to the diagnosis of major depression?

 I was privileged to work with my colleagues Dr Sidney Zisook, Katherine Shear, and others, in arguing for removal of the “bereavement exclusion” in DSM-5. This was a long, complicated, passionate debate that went on for more than 5 years, and is nicely detailed in the paper by 

 Based in part on my experience as a specialist in mood disorders, I believe the conclusion of my colleagues in 2012 is still valid:

“The preponderance of data suggests that bereavement‐related depression is not different from MDE that presents in any other context; it is equally genetically influenced, most likely to occur in individuals with past personal and family histories of MDE, has similar personality characteristics and patterns of comorbidity, is as likely to be chronic and/or recurrent, and responds to antidepressant medications.”

Given space limitations, I won’t try to re-litigate the entire debate here. With respect to the argument that all stress-related, “uncomplicated” depressive episodes should be excluded from the category of major depressive disorder, I will simply say this: 

the issue boils down to the relevance of “context” to the presence or absence of “disorder.”

 In brief, I believe that “context” is fundamentally irrelevant to the 

 as I have conceptualized it. However, context can be extremely important in working 

with patients. For example, therapy will differ when someone experiences a major depressive episode in the context of divorce, versus an episode that seems to arise “out of the blue.” But both people will be experiencing, in some degree and manner, suffering and incapacity.

By way of analogy: let’s imagine that an elderly man with known coronary artery disease is hiking along a woodland trail, when suddenly, a 9-foot grizzly bear appears in front of him. The man is gripped by terror and suffers a myocardial infarction. Would any physician exclude the diagnosis of myocardial infarction (MI) because it occurred in the context of “stress”? I don’t think so. Nor is the MI rendered a non-MI because it is “understandable” under such circumstances—I have called this, “

.” An MI is an MI, and a major depressive episode is a major depressive episode; ie, if you have all the signs, symptoms, distress and incapacity, you own the disorder! This, of course, is an entirely different matter than the presence of bereavement-related 

 which is normal, adaptive, and most certainly 

 I don’t think that the MI example does justice to this issue because the relevant pathological and clinical features of MI do not differ depending on context in a way that features of depression are alleged to. Wakefield, for instance, says that uncomplicated reactive depressions that emerge in the context of bereavement and other stressors have a markedly more benign profile and decreased frequency of “pathosuggestive” features (such as suicidality, psychosis, psychomotor retardation) relative to other instances of major depression, making it plausible to interpret them as “normal emotional reactions” rather than disorders.22 No such corresponding difference exists in the case of MI.

: You are raising an important issue, Awais. But let me say at the outset that the methods, interpretation, and clinical significance of the study you cite—and, indeed, of several bereavement-related papers from Wakefield and colleagues

—remain a source of intense debate and controversy, to this day. For the gory details, interested readers should consult the historical review by Zachar and colleagues.

Instead, let’s drill down into this concept of “relevant pathological and clinical features” and see how it applies to both myocardial infarction and clinically significant (“major”) depression. The cardiologists tell us that there are at least 

, including a primary coronary event, such as plaque rupture; coronary spasm, coronary embolism, and others. But all have in common the production of myocardial ischemia and myocardial-cell death. By the same token, with people who meet full DSM-5 symptom, severity, and duration criteria for a major depressive episode [MDE], we can again enumerate different etiologies and “contextual types”; for example, MDE arising in the context of a chronic medical illness, like cancer; in the context of a relationship breaking up; or after sudden job loss. Yet the “family resemblances” (I will resist the lure of a Platonic “essence”) that unite these diverse contextual types consist in what you rightly call the “relevant pathological and clinical features.” These are the well-known findings of 

depressed mood; changes in sleep and appetite; low energy; loss of interest or pleasure in usual activities; impaired concentration

accompany these features. Taken together, these features produce varying degrees of “suffering and incapacity.” 

It is this dyad that constitutes the “disorder-ness” that separates clinical depression from grief. 

, grief has experiential features that are readily distinguished from those of clinical depression, and which do not represent “disorder-ness.”

controlled, prospective, clinical studies

 of major depression that show substantive, qualitative differences in “disorder-ness”—understood in terms of suffering and incapacity—between contextually different types of major depression, including post-bereavement depression. By “controlled,” I mean that factors known to influence outcome of clinical depression, such as psychotic and melancholic features, must be “controlled for.” In my view, retrospective data obtained from community surveys carried out by lay interviewers, and subject to recall bias, cannot adequately assess the presence of “disorder-ness.”

: Allow me to present a thought experiment. Imagine an alternative world that is very similar to our own, except that in this alternative world there is a deeply held societal belief that depressive episodes emerging in the context of a major life stressor are “problems of living” and should not be considered disorders. The DSM in this alternative world 

 classify stress-related depressive episodes as disorders unless they are accompanied by symptoms such as suicidality, psychosis or psychomotor retardation. In this alternative world, individuals with stress-related depressive episodes do not routinely seek help from physicians, although they may seek counseling, family support, exercise, lifestyle changes, etc. Would you say that the alternative DSM gets it 

? Part of what I want to bring up in this thought experiment is the idea that disorder attribution serves pragmatic functions within a certain social context, and if that social context changes—as in this hypothetical scenario—the disorder attributions can change as well. Does it make sense to talk about the rightfulness or wrongfulness of disorder attributions independent of the social contexts?

 That’s a great question, Awais! My first impulse is to say that, indeed, our DSM gets it right, and the extraterrestrials have got it wrong, based on my own clinical experience as a mood disorder specialist. However, I think we’d agree that “right” and “wrong” are strongly evaluative terms, the foundation for which can always be questioned. I would prefer to say that the nosologists on your alternative world have made a “category mistake” (as per philosopher Gilbert Ryle), akin to calling a whale a fish. They are mistakenly classifying a bona fide depressive disorder as merely a “problem of living,” with no clear evidentiary justification, potentially to the detriment of their patients. Of course, it should be noted that while all “problems of living” are not disorders, all disorders present us with “problems of living,” to the extent they produce suffering and incapacity.

That said, I agree with you that disorder attribution “serves pragmatic functions within a social context,” which may vary from culture to culture—or planet to planet! This reminds us yet again that medical judgments are not “value-free,” even though they may draw on “objective,” clinical data. Zachar and Kendler note, for example, that a central controversy in the bereavement debate revolved around the question:

 which is more important when assessing depression: avoiding false positives or avoiding false negatives? 

Ultimately, this depends on which “pragmatic functions” a society wishes to promote and underwrite, and this is clearly a matter of societal values.

 What are your hopes for the future of psychiatry?

One of the most perceptive andheuristically useful comments about psychiatry that I have ever heard came from one of my residency mentors, Dr Robert Daly. Bob once said that in psychiatry, “You can do biology in the morning and theology in the afternoon.” That comment from nearly 40 years ago has always stuck with me. It speaks to the holistic and pluralistic nature of the psychiatric enterprise, which I wholeheartedly endorse, and which has radically shaped my entire career. So my chief hope for “the future of psychiatry” is that it recover its pluralistic “core”—what I earlier described as the AJE tradition. I say “recover” because, as I noted earlier, I believe that psychiatry’s “solid center” is besieged by market-driven forces that would like to reduce us to “writing scripts” and “turfing” psychosocial interventions to less costly non-physicians. We need to push back hard against those trends! At the same time, I would like to see psychiatry achieve much better integration with neurology and general medicine, in what has been called “

.” I also think psychiatry has to do a much better job of “public outreach,” whereby we go out into the community in a proactive way, so that the general public has a better understanding of who we are and what we do. We can’t afford to let antipsychiatry define us in the public mind. The stakes for our profession and the well-being of our patients are far too high.

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

Dr Aftab is a psychiatrist in Cleveland, Ohio, and Clinical Assistant Professor of Psychiatry at Case Western Reserve University. He is a member of the executive council of Association for the Advancement of Philosophy and Psychiatry and has been actively involved in initiatives to educate psychiatrists and trainees on the intersection of philosophy and psychiatry. He is also a member of the 

. Dr Aftab and Dr Pies have no relevant financial disclosures or conflicts of interest.

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

The Rise and Fall of Pragmatism in Psychiatry: S. Nassir Ghaemi, MD, MPH

Integrating Academic Inquiry and Reformist Activism in Psychiatry: Sandra Steingard, MD, and G. Scott Waterman, MD

Social Constructionism Meets Aging and Dementia: Peter Whitehouse, MD, PhD

50 Shades of Misdiagnosis: Susannah Cahalan

Institutional Corruption and Social Justice in Psychiatry: Lisa Cosgrove, PhD

The Impoverishment of Psychiatric Knowledge: Giovanni Fava, MD

Psychiatry and the Human Condition: Joanna Moncrieff, MD

Psychiatric Disorders as Imperfect Community: Peter Zachar, PhD

Weaving Conceptual and Empirical Work in Psychiatry: Kenneth S. Kendler, MD

1. Pies RW, Thommi S, Ghaemi SN. Getting it from both sides: foundational and antifoundational critiques of psychiatry. 

https://www.psychiatrictimes.com/view/getting-it-both-sides-foundational-and-antifoundational-critiques-psychiatry

2. Pies RW. Comments on “cyclical swings” by Professor Hannah Decker: The underappreciated “solid center” of psychiatry. 

3. Pies RW. Debunking the Two Chemical Imbalance Myths, Again. 

https://www.psychiatrictimes.com/view/debunking-two-chemical-imbalance-myths-again

4. Schildkraut JJ, Kety SS. Biogenic amines and emotion. 

5. Ruffalo M. The Psychoanalytic Tradition in American Psychiatry: The Basics. 

https://www.psychiatrictimes.com/view/psychoanalytic-tradition-american-psychiatry-basics

6. Pies RW. Can We Salvage the Biopsychosocial Model? 

https://www.psychiatrictimes.com/view/can-we-salvage-biopsychosocial-model

7. Ghaemi SN. The Postmodern Assumptions of the Biopsychosocial Approach. 

https://www.psychiatrictimes.com/view/postmodern-assumptions-biopsychosocial-approach

8. Aftab A. The Nine Lives of Biopsychosocial Framework. Psychiatric Times. January 23, 2020. 

https://www.psychiatrictimes.com/view/nine-lives-biopsychosocial-framework

9. Fava G, A, Sonino N. From the Lesson of George Engel to Current Knowledge: The Biopsychosocial Model 40 Years Later. 

10. Kendler KS. From many to one to many—the search for causes of psychiatric illness. 

11. Pies RW. Psychiatry’s new brain-mind and the legend of “chemical imbalance.” Psychiatric Times. July 11, 2011. 

https://www.psychiatrictimes.com/view/psychiatrys-new-brain-mind-and-legend-chemical-imbalance

12. Bhugra D, Sartorius N, Fiorillo A, et al. EPA guidance on how to improve the image of psychiatry and of the psychiatrist. 

13. Kendler KS, Campbell J. Interventionist causal models in psychiatry: repositioning the mind–body problem. 

14. Ghaemi SN. Existence and pluralism: the rediscovery of Karl Jaspers. 

15. Correll CU, Davis RE, Weingart M, et al. Efficacy and safety of lumateperone for treatment of schizophrenia: a randomized clinical trial. 

 2020. doi: 10.1001/jamapsychiatry.2019.4379.

16. Leucht S, Tardy M, Komossa K, et al. Maintenance treatment with antipsychotic drugs for schizophrenia. 

17. Pies RW, Pierre JM. Quality of Life and the Case for Antipsychotics. Psychiatric Times. September 5, 2016. 

https://www.psychiatrictimes.com/view/quality-life-and-case-antipsychotics

18. Emsley R, Nuamah I, Gopal S, et al. Relapse after antipsychotic discontinuation in schizophrenia as a withdrawal phenomenon vs illness recurrence: a post hoc analysis of a randomized placebo-controlled study. 

 2018;79(4):17m11874. doi: 10.4088/JCP.17m11874.

Publication bias, with a focus on psychiatry: causes and solutions

20. Zachar P, First MB, Kendler KS. The Bereavement Exclusion Debate in the DSM-5: A History. 

21. Zisook S, Corruble E, Duan N, et al. The Bereavement Exclusion and DSM‐5. 

22. Wakefield JC. The DSM-5 debate over the bereavement exclusion: Psychiatric diagnosis and the future of empirically supported treatment. 

23. Wakefield JC, Schmitz MF. Normal vs. disordered bereavement-related depression: are the differences real or tautological? 

Articles

In this interview, Dr Aftab and Dr Pies revisit several debates concerning various criticisms of psychiatry that Dr Pies has been involved in over the course of his career, and they discuss how to make sense of the profession’s relationship with its critics. 

The Battle for the Soul of Psychiatry: Ronald W. Pies, MD

Dr Kendler is a highly respected psychiatrist and genetics researcher, who has been further catapulted into fame over the past two decades through his widely read philosophical commentaries. In this interview with Dr Aftab, he discusses his philosophical and historical approach to psychiatry.

Kenneth S. Kendler, MD, is the Banks Distinguished Professor of Psychiatry and Professor of Human Genetics at 

, Virginia Commonwealth University. Dr Kendler received his medical and psychiatric training at Stanford and Yale University, respectively. Since 1983, he has been engaged in researching the genetics of psychiatric and substance use disorders, including schizophrenia, major depression, alcoholism, personality disorders and drug abuse and dependence. He has utilized methods ranging from family studies, to large-sample population-based twin and adoption studies to molecular genetic studies including linkage, genome wide association studies, and whole genome sequence aimed at identifying specific genes that influence the vulnerability to a variety of psychiatric disorders. Since 1996, he has served as Director of the Virginia Institute of Psychiatric and Behavioral Genetics. He has received numerous national and international awards for his work. He is a member of the National Academy of Medicine. He is one of the two editors of the journal 

. He played an active role in the development of DSM-III-R, DSM-IV, and DSM-5 (where he chaired the Scientific Review Committee), and he is currently the Vice-Chair of the APA DSM Steering Committee. He has published over 1200 articles. Dr Kendler is one of the highest cited researchers in psychiatry: according to Google Scholar, his academic work has been cited nearly 170,000 times, and his H-index is 196.

While Dr Kendler is internationally renowned and highly respected for his work in psychiatric genetics, he has been further catapulted into fame over the past two decades through his widely read commentaries on the philosophical foundations of psychiatry. I recently had the pleasure of reading the book 

Toward a Philosophical Approach to Psychiatry: The Writings of Kenneth Kendler 

(edited by Kenneth Kendler and Peter Zachar, Cambridge Scholars Publishing, 2019) and reviewing it for 

. The book is a selection of 21 of his most important philosophical and historical papers published over the course of his career. These articles address topics such as the classification and nature of mental disorders, mind-body relationship, causality and explanation in psychiatry, and historical studies in psychiatric nosology. My admiration of Dr Kendler is no secret at this point. As I write in the review, “Kendler is one of a kind among his psychiatric peers: I am hard-pressed to think of any other living psychiatrist who has the breadth of historical knowledge, rigor of scholarship, excellence in research, and depth of philosophical understanding that Kendler possess.” In the review I also offer a summary of major recurrent themes that are present in Kendler’s philosophical writings. For readers unfamiliar with Kendler’s philosophical work, this interview is best read in the context of the book review.

 I really like your description of how psychiatric nosology sits in a historically contingent developmental arc. In your opinion, how is this history relevant to on-going nosological debates in psychiatry, and how has ignorance of this history impeded our efforts at making progress?

 With respect to psychiatric nosology, there is quite a bit of truth to two worn maxims: i) if you don’t know where you have been it is hard to see where you are going and ii) if you don’t know your history you’re are at high risk to repeat your prior mistakes. So, I think history can provide a context and a background for what nosology can do and where it has taken wrong roads in the past.

I read with fascination that you collaborated with a translator to obtain English translations of Kraepelin’s previously untranslated works . . . will these translations be published or see the day of light in some manner?

 They are all sitting on my hard drive now and that of the translator, Ms Astrid Klee, but there is a lot more there than just Kraepelin. A very small percentage of the relevant German psychiatric literature of the late 19th and early 20th centuries have been translated. I have thought about trying to set up a website to make these widely available. That will take time, energy, and a bit of resources. If any of these readers want to help, be in touch.

 You have argued for a scientific pluralism where there are multiple explanatory perspectives available to us to understand psychiatric disorders and one perspective cannot be reduced to another perspective. You describe your pluralism as empirical and hard-nosed, by which you mean that risk factors have to earn their place at the table. It’s a little unfortunate that many discussions of pluralism in psychiatry tend to get stuck in debating the merits and demerits of the biopsychosocial model. For the most part, you’ve managed to stay away from those controversies and have successfully charted a course for pluralism independent of any baggage that the biopsychosocial model brings. Is it time for our field to abandon the biopsychosocial model?

 Its core idea was on target, but its implementation was so non-specific as to blunt any rigor it might have once had and its ultimate utility. I would not mourn its passing, but it did some important “historical work.”

 DSM-5 defines mental disorder as a syndrome that, among other things, “reflects a dysfunction in the psychological, biological, or developmental processes underlying mental functioning.” What is the intended meaning of the term “dysfunction” here? Did the members of the DSM committee tasked with this definition have any clarity or consensus regarding what it means?

 The hope that we could have a crisp set of inclusion and exclusion criteria for what constitutes a psychiatric “dysfunction” is a wonderful idea but (in my view, not for lack of trying) impossible. There are too many social and conceptual nuances. So, while there is a general idea of what dysfunction means, operationalizing in the way that would give substantial sharp precision to the definition has not proven possible.

 Could you articulate what that general idea of dysfunction is? I am also interested in whether “dysfunction” necessarily implies that the locus of the problem is primarily 

 the individual and not in interpersonal relations and social context? And if there is such an implication, does this relegate interpersonal and social causal risk factors to a more secondary status?

The general idea of dysfunction is common-sensical – that the relevant psychobiological system is not doing what it is supposed to do. Examples might include providing your higher centers with an approximately veridical sense of the world around you, keeping levels of anxiety roughly appropriate to the real dangers being confronted, producing mood states approximately congruent to the environmental situation, etc. DSMs have traditionally seen disorders as existing within individuals and, for example, avoided providing diagnoses for dysfunctional marriages or families. So, in that sense, the underlying disturbance is seen to exist within individuals. I do not see that definition having much of anything to do with the causes. Environmental experiences like severe 

 can clearly cause dysfunctional mood-modulation systems as well as a high genetic vulnerability.

 To what extent is the “dappled” distribution of causal risk factors of psychiatric disorders a result of the heterogeneity of constructs… for example, a discussion of the distribution of causal risk factors of “chronic fever disorder” is not likely to be very meaningful. Furthermore, it is true for major depressive disorder

 that no single causal risk factor has dominant explanatory power, but it may be the case for 

 that there are causal risk factors of large explanatory power. What are your thoughts?

 I don’t buy it. Most psychiatric disorders are, I think, multifactorial “all the way down.” I also think that for a few affected individuals they do suffer from disorders largely as a result of one major cause. I sometimes call your model the “mental handicap model.” Imagine you were a physician in the mid-19

 century caring for what would then have been called idiots or imbeciles. If you could apply modern diagnostic methods to that group, a fair proportion would have a range of specific causes: Down syndrome, fragile X, a host of autosomal recessive disorders impacting on all kinds of brain-relevant genes which when mutated produce widespread CNS dysfunction, a range of small deletions, and a whole bunch would be non-specific multifactorial. That is, a lot of your cases (but far from all) would have largely monocausal conditions. This has been long postulated for psychiatric illness. It has, in my judgment, been largely a pipedream. I think that lesson applies more broadly.

 You are widely respected in the field and that has afforded you a certain privilege to advocate for the need to take philosophy of psychiatry seriously. Your philosophical writings are published and featured prominently in leading American psychiatric journals, which don’t usually publish articles related to philosophy of psychiatry. I have wondered if one of the reasons why mainstream journals are so receptive to your philosophical work – aside from the undisputed academic quality and rigor – is that your conclusions don’t threaten or destabilize the status quo in a way that conclusions of some of the other philosophical commentators do. It was interesting to me that one of your more controversial articles – on the dopamine hypothesis of schizophrenia – was also the one that had a difficult time getting accepted. What are your thoughts on why leading American psychiatry journals publish so few philosophical articles, are so afraid of controversy, and whether this needs to change?

 I have made a deliberate attempt over the last 15+ years to try to “crack open” the leading psychiatric journals for articles with a primary philosophical and/or historical content. I have, in the process, been substantially aided by some of the key editors. Nancy Andreasen (prior editor in chief of AJP) was quite supportive of a number of my early efforts and Bob Freedman who succeeded her and Julio Licinio (editor of 

) have also been sympathetic. Not every paper was accepted by a long shot, but they listened, were willing to send them out for review and accept a fair proportion.

I agree with you that my ability to do that has been, in part, a result of the fact that I have achieved some standing in empirical areas of psychiatric research. To be vernacular, I have accumulated some “street cred.” I also think the papers were written in a way the audience could understand and that spoke to their concerns. I did not consciously “edit” the papers to make them less controversial. I still think that non-scholarly issues impacted on the problems we had with the dopamine hypothesis paper – that was perhaps a special case. I don’t want to blow up psychiatry. I believe quite deeply in our clinical and research mission. But we surely can think more clearly about a number of issues in our clinical work, nosology and research.

 Some critics hold the view that if a classification can be misused, it will be misused. To what extent should the concern for misuse constrain classification decisions? Do the creators of DSM have a responsibility to make academic as well as public educational efforts to reduce the ways in which the diagnostic manual is misunderstood and misused?

 Our primary responsibility on DSM is to the patients we care for and the research community that we assist. But possible misuse does, appropriately, arise in nosologic debates. For example, it played a key role in the opposition to the late-luteal-phase dysphoric debate in DSM-IV – that the diagnoses would be used in ways prejudicial to women. So, it would be unrealistic for DSM to ignore completely the possible misuse of the document. But, if the chips are down, I think serving our patients and research is the more important mission. It is impossible to control all the possible misuses of DSM and if you took that concern too far, it would be paralyzing.

Awais Aftab, MD, interviews this highly respected psychiatrist and genetics researcher, who has been further catapulted into fame over the past two decades through his widely read philosophical commentaries.

Author | Awais Aftab, MD

Articles

The Battle for the Soul of Psychiatry: Ronald W. Pies, MD

Weaving Conceptual and Empirical Work in Psychiatry: Kenneth S. Kendler, MD

Psychiatric Disorders as an Imperfect Community: Peter Zachar, PhD

Psychiatry and the Human Condition: Joanna Moncrieff, MD

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

The Impoverishment of Psychiatric Knowledge

Institutional Corruption and Social Justice in Psychiatry

50 Shades of Misdiagnosis

Reading Linehan in the Age of Critical Psychiatry

Social Constructionism Meets Aging and Dementia