This radical idea — the scientists were suggesting that depressive disorder came with a net mental benefit — has a long intellectual history. Aristotle was there first, stating in the fourth century B.C. “that all men who have attained excellence in philosophy, in poetry, in art and in politics, even Socrates and Plato, had a melancholic habitus; indeed some suffered even from melancholic disease.” This belief was revived during the Renaissance, leading Milton to exclaim, in his poem “Il Penseroso”: “Hail divinest Melancholy/Whose saintly visage is too bright/To hit the sense of human sight.” The Romantic poets took the veneration of sadness to its logical extreme and described suffering as a prerequisite for the literary life. As Keats wrote, “Do you not see how necessary a World of Pains and troubles is to school an intelligence and make it a soul?”
But Andrews and Thomson weren’t interested in ancient aphorisms or poetic apologias. Their daunting challenge was to show how rumination might lead to improved outcomes, especially when it comes to solving life’s most difficult dilemmas. Their first speculations focused on the core features of depression, like the inability of depressed subjects to experience pleasure or their lack of interest in food, sex and social interactions. According to Andrews and Thomson, these awful symptoms came with a productive side effect, because they reduced the possibility of becoming distracted from the pressing problem.
The capacity for intense focus, they note, relies in large part on a brain area called the left ventrolateral prefrontal cortex (VLPFC), which is located a few inches behind the forehead. While this area has been associated with a wide variety of mental talents, like conceptual knowledge and verb conjugation, it seems to be especially important for maintaining attention. Experiments show that neurons in the VLPFC must fire continuously to keep us on task so that we don’t become sidetracked by irrelevant information. Furthermore, deficits in the VLPFC have been associated with attention-deficit disorder.
Several studies found an increase in brain activity (as measured indirectly by blood flow) in the VLPFC of depressed patients. Most recently, a paper to be published next month by neuroscientists in China found a spike in “functional connectivity” between the lateral prefrontal cortex and other parts of the brain in depressed patients, with more severe depressions leading to more prefrontal activity. One explanation for this finding is that the hyperactive VLPFC underlies rumination, allowing people to stay focused on their problem. (Andrews and Thomson argue that this relentless fixation also explains the cognitive deficits of depressed subjects, as they are too busy thinking about their real-life problems to bother with an artificial lab exercise; their VLPFC can’t be bothered to care.) Human attention is a scarce resource — the neural effects of depression make sure the resource is efficiently allocated.
But the reliance on the VLPFC doesn’t just lead us to fixate on our depressing situation; it also leads to an extremely analytical style of thinking. That’s because rumination is largely rooted in working memory, a kind of mental scratchpad that allows us to “work” with all the information stuck in consciousness. When people rely on working memory — and it doesn’t matter if they’re doing long division or contemplating a relationship gone wrong — they tend to think in a more deliberate fashion, breaking down their complex problems into their simpler parts.
The bad news is that this deliberate thought process is slow, tiresome and prone to distraction; the prefrontal cortex soon grows exhausted and gives out. Andrews and Thomson see depression as a way of bolstering our feeble analytical skills, making it easier to pay continuous attention to a difficult dilemma. The downcast mood and activation of the VLPFC are part of a “coordinated system” that, Andrews and Thomson say, exists “for the specific purpose of effectively analyzing the complex life problem that triggered the depression.” If depression didn’t exist — if we didn’t react to stress and trauma with endless ruminations — then we would be less likely to solve our predicaments. Wisdom isn’t cheap, and we pay for it with pain.
There is a caveat to this, though:
Andrews and Thomson respond to such criticisms by acknowledging that depression is a vast continuum, a catch-all term for a spectrum of symptoms. While the analytic-rumination hypothesis might explain those patients reacting to an “acute stressor,” it can’t account for those whose suffering has no discernible cause or whose sadness refuses to lift for years at a time. “To say that depression can be useful doesn’t mean it’s always going to be useful,” Thomson says. “Sometimes, the symptoms can spiral out of control. The problem, though, is that as a society, we’ve come to see depression as something that must always be avoided or medicated away. We’ve been so eager to remove the stigma from depression that we’ve ended up stigmatizing sadness.”
For Thomson, this new theory of depression has directly affected his medical practice. “That’s the litmus test for me,” he says. “Do these ideas help me treat my patients better?” In recent years, Thomson has cut back on antidepressant prescriptions, because, he says, he now believes that the drugs can sometimes interfere with genuine recovery, making it harder for people to resolve their social dilemmas. “I remember one patient who came in and said she needed to reduce her dosage,” he says. “I asked her if the antidepressants were working, and she said something I’ll never forget. ‘Yes, they’re working great,’ she told me. ‘I feel so much better. But I’m still married to the same alcoholic son of a bitch. It’s just now he’s tolerable.’ ”
The point is the woman was depressed for a reason; her pain was about something. While the drugs made her feel better, no real progress was ever made. Thomson’s skepticism about antidepressants is bolstered by recent studies questioning their benefits, at least for patients with moderate depression. Consider a 2005 paper led by Steven Hollon, a psychologist at Vanderbilt University: he found that people on antidepressants had a 76 percent chance of relapse within a year when the drugs were discontinued. In contrast, patients given a form of cognitive talk therapy had a relapse rate of 31 percent. And Hollon’s data aren’t unusual: several studies found that patients treated with medication were approximately twice as likely to relapse as patients treated with cognitive behavior therapy...