Is Major Depression “Adaptive”? Clinical Data Say No
Is Major Depression “Adaptive”? Clinical Data Say No
The poet Denise Levertov was no stranger to sorrow and loss. In her poem, “Stepping Westward,”1 she writes of the aging process, as both a burden and a gift. The poem begins,
What is green in me/darkens, muscadine . . .
Muscadine is a woody vine that produces a musk-scented purple grape, used to make wine. Levertov’s image is one of growing darkness, but also of emotional growth and maturation. With old age comes “the fruit of the vine”—wisdom and awareness. Levertov’s poem goes on to observe,
If I bear burdens/they begin to be remembered/as gifts . . .
We all know that sorrow can bring insight, if it is properly and deeply understood. This “gift” may also emerge from the pensive reflection of ordinary grief and bereavement. I begin with Levertov’s poetic images because I want to distinguish what Thomas Kempis called “the proper sorrows of the soul” from what psychiatrists know as major depression. I would never argue against the claim that on some level, ordinary grief may be adaptive—in fact, in a series of articles, Dr Sidney Zisook and I have stated as much.2,3
But when the same claim is made with regard to major depressive disorder (MDD), as in the so-called analytical (or adaptive) rumination hypothesis (ARH),4-6 I am left shaking my head. In its simplest formulation, the ARH asserts that “. . . depression is nature’s way of telling you that you’ve got complex social problems that the mind is intent on solving” and that “depression is in fact an adaptation, a state of mind which brings real costs, but also brings real benefits.”4 In effect, the ARH asserts that the “analytical” and ruminative cognitive processes of the depressed person facilitate complex, social problem solving. A number of experimental manipulations are cited to support the ARH [eg, see Hertel and coworkers7], but few psychometric studies of clinically depressed patients (eg, meeting DSM-IV MDD criteria) are adduced as evidence. (Let’s leave aside the simplistic notion that depression arises from unresolved “social problems”—of course, this is sometimes so, but in many cases, interpersonal problems are the consequence of preexisting depression.8)
The basic claims of the ARH do not square with anything in my experience as a specialist in mood disorders for over 25 years, nor with the overwhelming majority of clinical studies of cognitive function in MDD, to be reviewed presently. But first, it is critical that we distinguish studies of clinical populations from experimental manipulations involving non-clinical test subjects—usually described as being “sad” or in a “depressed mood state”—who are asked to solve various artificial “problems” [eg, see Hertel and associates].7 These test subjects—eg, college student volunteers4—are usually “induced” to have very brief periods of depressed mood, using some experimental intervention. They have virtually nothing in common with the seriously depressed patients we treat, who have often been ill for weeks, months, or even years.
To be clear: I have many problems with the DSM-IV construct of MDD, such as its almost risible elasticity—MDD is a diagnosis that can be stretched around almost anyone with 2 weeks, or 2 years, of depressive symptoms.9 But when carefully applied to someone with a month or more of severe depression, 1 or more melancholic features, pronounced suffering, and substantial social-vocational incapacity, “MDD” describes a very real disease entity, with a suicide rate of about 4 in 100.10 The notion that such a condition is in any sense “adaptive” flies in the face of clinical experience, the reports of most severely depressed patients and, as I hope to show, most studies of cognitive and social function in depressed individuals.
As to “evolutionary” arguments for and against the ARH, I will leave those to authorities in the field of evolutionary biology,11 although I am deeply skeptical of some recent claims regarding the benefits of “analytical rumination.”6 My intention here, however, is to examine the published studies of cognitive function in patients with major depression and to pose the following questions:
1. Is there credible evidence showing that MDD (or clinically significant depression) enhances any specific types of cognitive skills or mental processes?
2. Is there credible evidence showing that rumination in MDD enhances any type of “problem-solving” skills?
3. Is there credible evidence showing that depressed individuals possess enhanced social or interpersonal skills, such that they might be at some kind of adaptive advantage?
These questions, of course, cannot address whether those who have endured an episode of severe MDD are or are not “wiser” for the experience, or whether they were able to find life-enhancing “meaning” or valuable perspectives in the course of their suffering. These are fundamentally philosophical and spiritual—not scientific—determinations. Finally, I will not address the controversial matter of antidepressant treatment, other than to note this: the claim that MDD is not “adaptive”—indeed, that it is pervasively maladaptive—is surely not to claim that all persons with MDD require, or benefit from, antidepressant treatment. Simply put, some do, and some probably do not.12 In any case, the issue of pharmacotherapy would take us far afield.
Clinical studies of cognition in depression
Dr Charles DeBattista,13 in a recent review, concluded that “the types of executive deficits seen in depression include problems with planning, [as well as] initiating and completing goal-directed activities” and that such “executive dysfunction” tends to worsen in direct proportion to the severity of depression. Similarly, a review by French investigators concluded that “. . . executive deficits associated with frontal lobe dysfunction may be prominent in depression” and that “. . . unipolar depressed patients mainly exhibit cognitive inhibition deficits, problem-solving impairments, and planning deficits.”14 Furthermore, unipolar depressed patients tend to show “. . . difficulties in hypothesis testing with a loss of spontaneous and reactive cognitive flexibility,” attributable to dysfunction in the dorsolateral prefrontal cortex. (Ironically, proponents of the ARH suggest that prefrontal brain regions show enhanced activity in major depression, thus facilitating “analytical rumination”; in fact, the brain imaging evidence in MDD is complex and often conflicting, perhaps reflecting slightly differing subregions of the prefrontal cortex.15)
Cognitive problems may be especially pronounced in older depressed individuals, as Alexopoulos and colleagues16 have shown. They note that “depressed patients often have disturbances in attention, speed of processing, and executive function even in the absence of dementing disorders.” Moreover, “. . . executive dysfunction and related cognitive abnormalities confer significant disability and add to adversity experienced by the depressed elderly person [italics added].”16 Collectively, these findings do not suggest any salient adaptive advantages in the cognitive state of most clinically depressed patients. Quite the contrary: as Alexopoulos and colleagues note, citing the work of Nezu and Ronan, problem-solving therapy for geriatric depression actually “. . . originated from the observation that depressed patients use inadequate or inappropriate approaches in addressing their problems. . . . [italics added]”.
Rumination: friend or foe?
There is little disagreement with the observation that clinically depressed patients tend to ruminate; ie, to focus repetitively on the same issue, problem, or thought (the term comes from the Latin ruminari , “to chew cud”). In general, the research literature points to the deleterious effects of depressive rumination. As Rimes and Watkins17 observe, citing the work of Nolen-Hoeksema18 and others,
Increasing evidence suggests that rumination plays a role in the maintenance of depression. . . . Experimental studies have found that in dysphoric participants, compared to [use of] distraction, rumination increases depressed mood, cognitive distortions and . . . impairs problem-solving skills . . .
These findings are consistent with those of Donaldson and Lam,19 who found that patients with major depression who were made to ruminate experienced a deterioration in their mood and gave poorer problem solutions. Similarly, Park and associates20 found that experimentally induced rumination, as compared with distraction, increases depressed mood and negative memories in adolescents with a first episode of MDD.
Taken in total, these findings flatly contradict the central claim of the ARH; ie, that rumination is helpful and adaptive in addressing one’s problems, social or otherwise. But there is a complication we need to consider: rumination appears to be subdivided into analytical self-focus (ASF) and experiential self-focus (ESF). In essence, ASF involves thinking analytically ‘‘about’’ oneself and one’s symptoms; eg, “How did I get so depressed? Why do I feel so guilty?” In contrast, ESF involves a “here and now” focus on the direct experience of one’s thoughts, feelings, and sensations in the present moment; eg, “Right now, I’m feeling hurt and angry that John left me for someone else.”
Rimes and Watkins17 studied these 2 types of rumination in 30 depressed participants (MDD by DSM-IV critiera) and 30 never-depressed volunteers. Participants were randomly allocated to “analytical” (high analysis) or “experiential” (low analysis) self-focused manipulations. The study found that in depressed participants, ASF increased ratings of feeling “worthless” and “incompetent.” The ESF condition resulted in no significant change in such judgments. (Neither mode of rumination had a significant effect in the nondepressed controls). The authors concluded that “. . . an analytical mode of self-focused rumination may be particularly maladaptive in depression.”17
Once again, no support for the ARH is provided. Indeed, in direct contradiction of the ARH, Watkins and colleagues21 have shown that treating depressive rumination with cognitive-behavioral therapy “. . . appears to yield generalized improvement in depression and comorbidity.” If rumination were indeed adaptive and productive, we would expect the opposite result.
Social and interpersonal skills in depression
Does being clinically depressed somehow make one more empathic, or improve one’s ability to “read” the social cues of others? Might depression enhance social bonding in a way that could be “adaptive”—if not on an “evolutionary” time scale, at least in the here and now?
Some preliminary answers have emerged from studies of the ability to recognize facial expression. What does facial expression have to do with social and interpersonal skills? A good deal, according to Yoon and colleagues.22 They note that “biases in the processing of subtle facial expressions of positive affect may . . . contribute to the interpersonal difficulties that maintain [depression].” Put in more colloquial terms: if you can’t tell that someone is smiling at you, the two of you are not likely to hit it off. Indeed, in their study of subjects with MDD, Yoon and coworkers found that major depression interferes with “reading” subtle expressions of positive affect, such as the famous “Mona Lisa smile.” It is hard to see any adaptive advantage in this perceptual bias.
A core argument of the ARH is that unresolved “social problems” precede clinical depression, which is said to be an adaptive response to these problems. But as Segrin8 observes in his review,
Three different theoretical relationships between disrupted social skills and depression [have been] described . . . [namely] poor social skills as a cause of depression, depression as a cause of poor social skills, and poor social skills as a vulnerability factor in the development of depression. Currently, there is some evidence to support each of these conceptualizations.
Despite this ambiguity, there is little doubt that clinically depressed individuals show a variety of social and interpersonal deficits, including, according to Segrin,8
. . . inhibition in initiating new relationships and interactions with others; problems in expressing themselves clearly to others; inappropriately and excessively self-disclosing information, especially if it is negatively toned, to others; and sometimes being overly negative and perhaps even hostile around other people.
Once again, it is hard to imagine any short-term, adaptive advantage emerging from these widespread interpersonal difficulties in depression, much less an enhanced “evolutionary” advantage that would favor attracting a mate, engaging in sexual activity, reproducing, etc. But these are matters of debate for the evolutionary biologists.
I would wager that the great Renaissance artist Albrecht Durer understood clinical depression far better than some modern-day proponents of the ARH. In his 1514 depiction of “Melencolia I” (“Melancholy”—see Figure), Durer shows the pensive goddess sitting amidst an array of unused analytical tools and instruments, staring somberly into space. As one commentator observes,
. . . her fixed state is one of intent though fruitless searching. She is inactive not because she is too lazy to work but because work has become meaningless to her; her energy is paralyzed not by sleep but by thought.”23
A psychiatrist could hardly have described severe depression more accurately, or refuted the ARH more succinctly.
I do not doubt that for some patients with MDD, there are indeed “remembered gifts” that are appreciated on recovery from their depression. But this is not to say that MDD itself is “adaptive” during the course of the patient’s illness. Virtually all the evidence I have reviewed leads to precisely the opposite conclusion. Nonetheless, the final word has not been written on this controversy. It would be instructive to do a carefully designed, empirical study that examined the question of depression’s “upside” from the patient’s point of view—controlling for possible confounds, such as the type of depression; whether or not the patient is hospitalized; how much support the patient is receiving from significant others; when in the course of illness the patient is asked the question, etc.
I’m not aware of such studies, whereas I have countless experiences hearing about the hellish suffering brought on by major depression. I remain open to the possibility that brief periods of mild depression may sometimes permit useful reflection on one’s problems, and perhaps even lead to some solutions. But in my experience, it is usually despite—not because of—serious depression that solutions to life’s problems are found. We owe our patients more than specious theories regarding the “upside” of their depression; we owe them safe, effective, and readily available treatment.12
Acknowledgments: I would like to express my appreciation to Drs Katharine Rimes and Rebecca Park for their helpful comments and references; and to Drs George Alexopoulos and Emily Becker-Weidman for providing their papers. I also want to acknowledge the seminal research of Dr Helen Mayberg in studying regional brain imaging in MDD. However, this commentary represents solely my own analysis and conclusions.
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23. Melencolia by Albrecht Durer, 1514. Back to Classics.com. Virtual art gallery. http://www.backtoclassics.com/gallery/albrechtdurer/melencolia. Accessed October 17, 2010.