If it makes us less likely to eat or dance or drink or screw, and sometimes makes us kill ourselves, then why do people get depressed?
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”…
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.