Today, the central questions at the intersection of psychiatry and culture seem to concern diagnosis. A number of books have appeared on the subject, each claiming that the medical professions have pathologized normality—making illnesses of unhappiness, shyness, and boyish impulsivity. To my mind, the most thoughtful of these efforts is The Loss of Sadness, by Allan V. Horwitz and Jerome C. Wakefield. It relies on a theory of mental disorder elaborated over decades. It is serious and scholarly. But I consider the book’s premises and conclusions to be profoundly, fundamentally wrong.

This week, I had the honor of debating Jerry Wakefield in a lecture-and-discussion session and an academic seminar at Rutgers University. On my website, I have posted the talk I prepared as the opening statement in that dialogue. What follows is a condensed account of key points.

To summarize the issue under debate: Wakefield (along with Horwitz) mistrusts the current standard diagnosis of depression, the one that says that if you have a cluster of symptoms for an interval of time, and if they cause sufficient impairment, then you are in an episode of illness. Wakefield complains that the method fails to take into account causation. He points to an exception recognized in the diagnostic manual: if the trigger for the depressive symptoms is the loss of a loved one, and if the syndrome is brief (less than two months) and only moderately severe, then the sufferer is considered to be bereaved, not depressed. Wakefield asks what is special about bereavement. If you are divorced or laid off from work, and you experience symptoms of moderate duration and severity, aren’t you are exhibiting an expectable response to loss? Shouldn’t you be called sad, and not depressed? Wakefield argues that the standard definition—the one that ignores the issue of cause—leads to over-diagnosis and over-treatment, especially with psychotherapeutic medication. Wakefield says that the definition of depression would be more valid if we extended the “bereavement exclusion” into a “major loss exclusion.”

In the talk I have posted, I say in detail why I consider this claim to be unproved and wrong-headed. In particular, I examine the major piece of research that Wakefield and Horwitz present in support of their proposal. They analyzed a survey of the general population and identified people with milder “caused” depressions. On certain measures these subjects do not look especially ill—therefore, they might better be called merely sad.

I looked at this same data. The survey has a glitch that caused a large group of patients to be misdiagnosed. If you apply the standard method (the one Wakefield considers too inclusive), few of the subjects Wakefield and Horwitz consider merely sad meet criteria for depression—so there is no over-diagnosis. Nor did doctors often offer prescriptions to these people. The subjects Wakefield and Horwitz picked out were much less likely than the average American ever to have received a medication for depression. And the psychological disruptions these “merely sad” subjects suffered were not all that mild. These less symptomatic subjects had experienced multiple episodes (whether of sadness or depression), and the average episode under study had lasted steadily for five months—more than twice as long as the “bereavement exclusion” permits.

Inadvertently, Wakefield and Horwitz seem to have highlighted evidence that the standard criteria do not label sadness as depression and that doctors in the period under study, the early 1990s, did not treat sadness with medication. Their book’s subtitle is “How Psychiatry Transformed Normal Sorrow into Depressive Disorder.” Their data says that psychiatry did no such thing.

My more general objections concern Horwitz and Wakefield’s theory. They mistrust a diagnostic system that determines depression by looking at the type, number, and severity of symptoms. Horwitz and Wakefield do accept that method when it comes to classifying depressions that arise out of the blue, “uncaused depressions,” but they want extra criteria added when despondency has a clear cause. To my mind, this distinction, “caused” versus “uncaused” episodes, mistakes the nature of depression. In behavioral genetics, the best model for the most common form of depression locates its basis in inborn differences, early childhood trauma, and then adversity—causes or triggers—in adult life.

People who are depressed almost always allude to recent causes. In the data set that Horwitz and Wakefield analyze, there are exceedingly few “uncaused” depressions or even uncaused intervals of more minor symptoms. Throughout history, it has been known that stressful events trigger episodes of depression; the problem is that, once under way, the episodes last too long and cause pain out of proportion to the causes. Decades of research attempting to dissect “endogenous,” or internally generated, from “exogenous,” or externally triggered, depression have found that that severity, more than causation, predicts the course of mood disorder. Horwitz and Wakefield propose their revision as mainstream and commonsensical; in fact it is strange and radical.

The current diagnostic method has permitted extraordinary research, studies that have led to findings in the genetics of mood disorder and that have identified abnormalities in the nervous, endocrine, cardiovascular, and skeletal systems of depressives. The method is flawed (on this point, Wakefield and I agree), but separating out “caused” depressions only seems to make matters worse.

Altogether, I mistrust Wakefield’s use of the words “loss” and “sadness.” Depression can be set off by a variety of stressors: sexual abuse, housing problems, illness in one’s child, and the other common problems you might imagine. To suggest that depression arises from loss is to skew the argument in the direction of the metaphor Wakefield prefers, the one that likens apparent depression to ordinary bereavement. Likewise, “sadness” does not capture the essence of depression, which is a marked disruption of brain and mind characterized by painful apathy. Not only in degree but also in quality, sadness and depression differ.

Whether the culture adequately respects sadness, pain, and suffering is a worthy question—but to my mind, Horwitz and Wakefield have failed to demonstrate that the standard diagnosis of depression has anything to do with the matter.

The lecture text gives a richer account of the context of the issues under debate and the reasoning that informs my viewpoint.

Additional note: The issue I engaged in my talk was the adequacy of the current diagnosis for depression and the benefit (or lack of benefit) that might result from “carving out” mild, caused syndromes and calling them sadness. I did not consider whether in their daily work doctors rely on the current criteria. Nor did I discuss the contention that now, more than a decade after the period covered by the survey data, antidepressants are overused. I believe that the question of over-prescribing demands detailed research of a sort that has so far been done only in limited populations.