Suppose your new patient, Mr. Jones, tells you he is feeling “really down.” He meets all DSMIV symptomatic and duration criteria for a major depressive episode (MDE) after having lost his wife to cancer 2 weeks ago. Should you diagnose major depressive disorder?
I’m guessing most psychiatrists would be reluctant to do so. Indeed, DSM-IV permits a “bereavement exclusion” in such circumstances, provided the patient lacks “certain symptoms that are not characteristic of a ‘normal’ grief reaction.”
But, say, another week has gone by. Mr Jones tells you tearfully, “Doc, I caused my wife’s cancer. I’m thinking of driving my car into a tree. I’m just not worth keeping around.” He shows marked psychomotor retardation and has missed work this past week. Is this just “normal grief”? Maybe not so much, now that Mr Jones has those “certain symptoms” that would override the bereavement exclusion. These vexing issues are nicely discussed in a recent editorial by Maj.1
In the November issue of Psychiatric Times, we ran a commentary2 by Professors Alan V. Horwitz, PhD and Jerome C. Wakefield, PhD, authors of The Loss of Sadness: How Psychiatry Transformed Normal Sorrow into Depressive Disorder.3 Essentially, the Horwitz-Wakefield (H-W) thesis holds that the “decontextualized” criteria for MDE set forth in DSM-III (1980) and DSM-IV have created a “seeming epidemic of depression” and spuriously high depression prevalence rates. By “decontextualized,” Horwitz and Wakefield mean without considering the context of loss or bereavement that makes the person’s depressive symptoms “normal” or understandable. The second linchpin in the H-W thesis is the claim that psychiatrists can—and should— determine how “proportionate” the depressed person’s response is to the recent loss—based on so-called evolutionarily derived criteria.3(p221)
The Loss of Sadness is a thoughtful book with honorable intentions. But I believe the H-W thesis puts the conceptual “cart” many years before the evidentiary “horse,” and that its practical effect could be to undermine our care of some bereaved patients who also meet MDE criteria. I should note here that despite a collegial email exchange with Professor Wakefield, I remain deeply skeptical of the H-W thesis.
What is at issue here?
Let me be clear: after a major loss, many people experience intense sadness and isolated depressive symptoms (e.g., tearfulness, insomnia, poor appetite) that may not constitute “disease” or “mental disorder.” Many will feel better with simple support and “tincture of time,” after 1 to 2 months. As Maj notes, “Adepressive state is an expectable and culturally sanctioned response to the death of a loved one and . . . does not represent a mental disorder.” 1This much is not in dispute.
Rather, the controversies arising from the H-W thesis are these:
• Are there controlled, prospective data showing that recent loss or bereavement per se predicts a benign, self-limited course when the patient meets all symptomatic and duration criteria for an MDE?
• Are there controlled data showing that major depressive symptoms after recent loss or bereavement differ in fundamental ways, including treatment response, from typical depressive symptoms without loss or bereavement?
• Do we have any clinically validated instruments, based on “evolutionarily derived” criteria, by which to judge how “proportionate” a patient’s depressive reaction is to a putative stressor?
In our present state of very limited evidence, I believe the answer to these questions is no.1,4
Common sense or theoretical bias?
Horwitz and Wakefield make much of “common sense” in their book. Thus, they believe “a wealth of evidence supports the commonsense judgment that many people who develop symptoms of depression after a loss, even when they meet DSM criteria for a disorder, are not disordered, but are experiencing a biologically designed response.” 3(p51, italics added) First, we would do well to recall Einstein’s well-known dictum: “Common sense is the collection of prejudices acquired by age 18.” As for the supposed “wealth of evidence,” a careful search for controlled, prospective studies reveals only poverty.
Now consider the following “commonsense” view of depressive symptoms in the context of bereavement. Common sense tells us that bereavement- related depression (BRD) will abate on its own within a few weeks or months as the patient copes with the loss. Common sense tells us that BRD symptoms will more closely resemble those of “normal sadness” than those of nonbereaved (“standard”) major depression. And, because BRD is precipitated by a unique loss, common sense tells us the depression is not likely to recur, all other things being equal. Finally, common sense might tell us that BRD is a normal, “adaptive” response to loss, whose “biology” and response to antidepressants would differ considerably from that of standard major depression.
This is all quite commonsensical— and all quite without convincing controlled evidence. For example, Brent and colleagues5 studied depressive reactions in youths exposed to a friend’s suicide. The exposed subjects developed symptoms most consistent with major depressive episodes—not uncomplicated bereavement—on the basis of both course and risk of recurrence. The median duration of depression in the 37 subjects who became depressed was 8 months! Compared with controls, the exposed subjects also had a higher rate of depressive recurrence during the follow-up period, even after adjusting for previous history of depression and other risk factors.
Similarly, Karam and associates6 compared features of bereavementrelated and non–bereavement-related major depression in a prospective community study (N = 685). The global “symptom profile” of depressed persons and their risk for depressive recurrence was similar in bereaved and non-bereaved subjects. Moreover, the duration of illness was actually longer in the bereaved group. The authors concluded that “the descriptive and etiologically neutral approach the DSM presumes in reaching a diagnosis should be applied in the case of [major depression] until more convincing data point to the contrary.”
We have very limited data on the neurobiology of BRD versus “standard” major depression. However, Zisook and Kendler7 found that, in general, BRD has biological features that resemble those of “standard” major depression, including impaired immune function and excessive adrenocortical function. And it is far from clear that these abnormalities represent merely an “adaptive” response to loss.