Sunday, September 20, 2009

Where the Problem Fixes You

Last month, Scientific American featured an article by two scientists contending that depression is not a mental disorder but rather an evolutionary adaptation designed to resolve the very issues responsible for depressive episodes in the first place. In contradiction to the conventional belief that depression is a deleterious malfunction, that the depressed mind needs “fixing” (often to the tune of heady prescription drugs), psychologists Andrews and Thomson argue that depression is fixing, that the depressed state of mind conduces to a productive style of analysis in which information is processed slowly, methodically, and with greater attention to detail — all in the service of self-preservation. It is suggested that the anatomy of the brain offers a biochemical complement to this, too, given that natural selection has preserved a specialized receptor that allows the energy-draining process of depressive rumination to “continue uninterrupted with minimal neuronal damage.” The emotional and behavioral traits associated with depression are therefore cast as evolved responses to the same types of complex dilemmas that humans have been facing since the dawn of the species. The Scientific American article raised a lot of questions for me, so I decided to chase down the primary source.

In "The Bright Side of Being Blue: Depression as an Adaptation for Analyzing Complex Problems," Andrews and Thomson note that depression (affecting some 121 million people on the planet) is the primary psychological condition for which help is sought. The DSM-IV (the standard reference manual for the diagnosis of mental disorders) names the presence of “clinically significant impairment or distress” among its general criteria for determining whether a psychological condition amounts to a biological dysfunction, inviting the psychologists to question whether a heightened capacity for analysis truly constitutes “impairment.” Andrews and Thomson make no distinction between clinical and subclinical depression. They maintain that clinical-significance criteria contribute to the overdiagnosis of depressive disorders and, further, that the threshold between minor episodic/situational depression and major chronic/intransitive depression is fairly arbitrary regardless. To them, depression is directive — at all points along the continuum, where there is illness, there is teleology.

The “analytical rumination hypothesis” put forward in the article holds that depression (1) activates neurological mechanisms that direct optimized focus toward problem-related analysis and (2) promotes bodily and behavioral changes in the interest of reducing exposure to stimuli that could disrupt the analytical reasoning requisite to resolving the “triggering problem.” (In short: Better thinking through misery.) The caveat, however, is that problem-solving processes are only improved insofar as they relate to the depressed person’s actual problem(s). Prior studies have shown that depressed people do very poorly on laboratory tasks (which typically have nothing to do with the subject of their ruminations). Even when lab tasks are designed to resemble real-life quandaries, the intensification of depressive symptoms may make it “progressively more difficult for depressed people to attend to anything but the specifics of their problems.” Contrary to the authors’ intentions in that point, though, I think it bears mentioning that the deeper the obsession with the problem, the wider the net of “specifics” relevant to it (and, likewise, the wake of associated skills). For example, depressed individuals generally outperform the nondepressed in low- or zero-contingency scenarios, i.e., when the participant’s action hardly changes, or does not change, the probability of the outcome. In such situations, nondepressed people are more likely to err in their judgment by overestimating their degree of control, whereas their depressed counterparts are more inclined to judge cause–effect patterns correctly. Along similar lines, depressed people are less likely to make the fundamental attribution error, a bias which Andrews and Thomson relate explicitly to the process of critical thinking:

For instance, people make the FAE when they attribute a pro-Castro stance to the writer of a pro-Castro essay even when they know that the writer wrote the essay as part of a class assignment and was assigned the pro-Castro stance by the course instructor. . . . Avoiding the FAE requires multiple processing steps in which an initial attribution is made based on the actor’s behavior (the pro-Castro stance), and then a correction is made based on the situational context (the assignment of the stance by the course instructor). This approach is cognitively effortful. People are less likely to use situational information and are more likely to make the FAE under conditions of cognitive load. Moreover, those who avoid the FAE take longer on the task.


It takes longer to read closely, analyze slowly, and process with care. These tasks demand patience, thoroughness, and resilience to brain burnout, all of which are allegedly abetted by depressive affect.

That depression should so resemble a learning experience is perhaps not surprising. You never learn so much about a system as when it breaks down, and illness certainly provides the opportunity to know oneself better. But its offerings are hard truths — knowledge of the kind most would prefer not to have. Avoidance responses to unwanted knowledge are a huge part of what is signified by the word “depression.” It goes without saying that avoidant action typically results in the production of avoidable stressors, posing an infinite loop of depressive potential. Perhaps avoidance is what allows Andrews and Thomson to make no distinction between clinical and subclinical depression, given that the “neurological orderliness” of the condition varies much less than an individual’s own strategies of escape (e.g., engagement in distractions, drug/alcohol use, somnolence, or the most avoidant behavior of all, suicide). What we may readily consider the symptoms of depression may in fact be avoidance-of-depression symptoms, that is, behaviors that address the traits — but not the causes — of the illness. It’s possible, too, that the environments that furnish the greatest number of opportunities to engage in avoidant behavior are also those in which depression is most common.

To regard depressive rumination as a conflict-resolution strategy has significant implications with regard to treatment, especially considering that more people seek help for depression than for any other psychological condition. If depression is truly engineered to resolve its own causes (as adaptationist hypotheses like Andrews and Thomson’s propose), then anything that circumvents the process of learning how to endure persistent painful feelings while negotiating possible solutions to them constitutes “avoidance.” This would include treatment with prescription drugs — or even sugar pills, according to the unpublished trials of pharmaceutical companies. The suggestion that a placebo can, in all but the most severe cases, match the effectiveness of prescription antidepressants does indeed imply that most human brains are pretty well equipped to deal with depression in one way or another. (Whether the mind agrees is another story, hence rumination.)

The idea that painful feelings draw attention to problems and motivate problem-solving behavior does not make those feelings any less painful, though. In an age when the interval between desire and gratification grows smaller by the day, our tolerance for struggle has probably shrunk accordingly. (Ideas to that end were the subject of an article in Scientific American last year.) Our modern lifestyles may predispose us toward the instant gratification that a temporary deferral of our problems can provide, but gratification, distraction, and deferral don’t really solve anything. Depression is a natural response to emotionally challenging pains and losses in life, and to “treat” it impatiently is tantamount to cheating oneself out of the potential for development that a formidable obstacle can supply.

Of the infinite number of possible problems generated by the human condition, not one of them is entirely unique. If life is hard, it’s because it should be. It takes a prodigious effort to turn rumination into a reward. Some might argue that certain problems (loss and trauma, especially) are so insoluble that no amount of mental activity can “resolve” them. At that point, I think we're talking about more profound sense of adaptation; specifically, the ability to earnestly ask near-unspeakable questions and candidly accept curious conclusions. And even then, "reconciling the insoluble" still isn't necessarily synonymous with "surviving your depression." But as the authors of “The Bright Side of Being Blue” conclude, “the extended nature of depressive pain is useful. Without it, people would not be motivated to engage in the extended effort required to solve complex problems. . . . [L]earning how to endure and utilize emotional pain may be part of the evolutionary heritage of depression, which may explain venerable philosophical traditions that view emotional pain as the impetus for growth and insight into oneself and the problems of life.”

One final note: Of particular interest to me, and also to self-professed neurotic and wonderful writer Maud Newton, is article’s pitch that expressive writing facilitates the resolution of depressive symptoms. Maud later updated her post to append the response of a reader who offered the cases of Virginia Woolf and David Foster Wallace as counterexamples to the analytical rumination/"writing cure" hypothesis. To that end, Woolf and Wallace are in considerable company.

More on that next time.

2 comments:

  1. This is fascinating, and it might shed some light on a question that's been bothering me for a while - why the incidence of depression seems to just rise and rise.

    "In the past 15 years, the number of people seeking treatment for depression in the U.S. has doubled; now 25 million a year. That’s bad news, but what is worse is that according to recent research, 90% of these people left their doctor’s offices with a prescription for antidepressants."
    --from http://depression.about.com/od/drugsalcohol/a/alcoholanddep.htm

    Obviously there's a certain amount of social reinforcement at work - the more people seek treatment for depression, the less stigma there can be about seeking it. But this hypothesis would explain another possible factor.

    If most depression is a case of the brain equipping itself to solve a problem, then treating depression (particularly if done chemically) may not only amount to treating the symptoms rather than the cause, but actually REMOVING THE ABILITY of the patient to resolve the cause. It's no surprise if the depression persists under such conditions.

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  2. Dan, thanks for your comment; you're absolutely on point. (But I should mention that your 25 million/year figure is from 2003, which despite being outdated is nonetheless poignant because it was in 2003 that the FDA first began issuing public health advisories about antidepressants and suicide. I'll say so at the end, too, but it's a much higher figure now.)

    That chemical treatment might remove the patient's ability to resolve the cause of the depression (or simultaneously increase the severity of the patient's symptoms) strikes me as a very real concern. In college, I took a seminar with psychologist/author Richard Gordon. When asked about the efficacy of chemical treatments for depression, he said (and I'm paraphrasing from memory here), "The funny thing about antidepressants is that there is no other class of drugs so widely prescribed about which so little is known."

    I avoided mentioning it in the post because I thought it too technical, but one of the hypotheses in The Bright Side of Being Blue is that the level of serotonin in the depressive brain is not too low (as is widely believed) but rather too high; and this has obvious implications with regard to treatment, especially in United States, where most (if not all) of the most commonly prescribed antidepressant medications are SSRIs. If depression really does entail above-average levels of serotonin, what good can there be in further inundating the brain with a neurotransmitter it already has in spades?

    In the Irving Kirsch interview I linked as "unpublished trials" above, he talks a little about the development and distribution of a class of drugs (called SSREs) that do the exact opposite of what Prozac, Zoloft, Paxil, and other SSRIs do. In line with the high-serotonin hypothesis put forth in Bright Side, Kirsch suggests that if depression were a state of low serotonin in the brain, then people who take SSREs would feel even more depressed, but they don't.

    As it turns out, the response rate for SSREs is about the same as it is for SSRIs and for other drugs, at 60 percent. And, as Kirsch says, "Look at these response rates: 60% of people don't have enough serotonin, 60% have too much serotonin, and 60% have just the right amount of serotonin but don't have enough of something else. My math teacher told me that there's something wrong when you've accounted for 180% of the population. So what do we do now?"

    The whole thing looks like neurotransmitter whack-a-mole to me. But the game grossed $9.6 billion last year, in the form of some 164 million prescriptions.

    I find that chilling.

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