I’ve received a few emails along this line:
“How does this new theory about depression enhancing problem-solving relate to all the studies that have shown cognitive deficits in people with depression?”
That’s a really good question. I tried to address this issue quickly in the article – I referenced the fact that the “cognitive deficits disappear when test subjects are first distracted from their depression and thus better able to focus on the exercise” – but I think it’s worth spending a little more time on the scientific literature. The key point here is that the deficits are “unstable,” which means they can be made to disappear when subjects are first distracted from their ruminations. (As Andrews told me, “Depressed subjects are trying to cope with a major life issue…It shouldn’t be too surprising that they have difficulty memorizing a string of random numbers.”) Look, for instance, at a 2002 study which compared clinically depressed subjects to non-depressed controls. In a test of executive function, the deficits of depressed subjects were erased when they were first distracted from their ruminations. Here’s their conclusion:
The aspects of executive function involved in random number generation are not fundamentally impaired in depressed patients. In depressed patients, the rumination induction seems to trigger the continued generation of ruminative stimulus independent thoughts, which interferes with concurrent executive processing.
In other words, the emotional pain of depressed subjects consumed scarce mental resources – the mind is a bounded machine – which meant they didn’t have enough attention left over to think about anything else, especially some artificial lab task. When we’re wracked with pain, everything but the pain is irrelevant.
I also think it’s worth pointing out that this latest hypothesis builds (as always in science) on numerous earlier conjectures. One important precursor for Andrews and Thomson’s idea was theoretical work done on “psychic pain,” by the evolutionary biologists Randy and Nancy Thornhill and by Randy Nesse, a psychiatrist at the University of Michigan. In essence, these scientists argued that emotional pain serves the same biological need as physical pain. When we break a bone in the foot, the discomfort keeps us from walking, which allows the bone to heal. The pain is also a learning signal, teaching us to avoid the dangerous behavior that caused the injury in the first place.
But there has been no shortage of clever conjectures on why depression exists. If you’d like an overview of the literature, I’d suggest reading this paper by Paul Watson, an evolutionary biologist at the University of New Mexico, whose work also influenced Andrews and Thomson. As I explicitly stated in the article, all of these theories remain just that: theoretical. There is very little direct evidence in support of any of them.
Finally, I think it’s worth repeating the obvious, which is that depression is an extremely varied mental illness. Although we only have one psychiatric diagnosis – major depressive disorder – that diagnosis covers a tremendous range of symptoms. (It’s also in constant flux, and will likely be altered yet again in the next DSM revision.) As I noted yesterday, one of the most cited papers in the field found that MDD exists on a spectrum of severity, ranging from mild (10.4 percent of patients) to very severe (12.9 percent), with the vast majority of patients somewhere in between. I tried to make this heterogeneity clear in the article, because I think it represents a real challenge for any theory that attempts to explain depression, either from an evolutionary perspective or from a neuroscientific perspective.
Although Nesse says he admires the analytic-rumination hypothesis, he adds that it fails to capture the heterogeneity of depressive disorder. Andrews and Thomson compare depression to a fever helping to fight off infection, but Nesse says a more accurate metaphor is chronic pain, which can arise for innumerable reasons. “Sometimes, the pain is going to have an organic source,” he says. “Maybe you’ve slipped a disc or pinched a nerve, in which case you’ve got to solve that underlying problem. But much of the time there is no origin for the pain. The pain itself is the dysfunction.”
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.
Personally, I think these are the two most important paragraphs in the article. One of the most challenging aspects of studying depression is the vast amount of contradiction in the literature. Virtually every claim comes with a contradictory claim, which is also supported by evidence. I tend to believe this confusion will persist until our definitions of depression become more precise, so that intense sadness and paralyzing, chronic, suicidal despair are no longer lumped together in the same psychiatric category.
Thank you again for all your comments and emails.