Wonderful behavioral science writer Jonah Lehrer (Proust Was a Neuroscientist) writes for the New York Times Magazine on the idea that depression may be adaptive. It is not a new idea; I have followed the intriguing literature about possible evolutionary reasons for the persistence of depression ever since I was a psychiatric resident troubled by how readily we in the field want to obliterate any signs of the condition whenever our patients present with it. Some theories have focused on the advantages of resource preservation, given the social isolation, decreased motivation and lessened self-indulgence the depressed person displays. It has also been suggested that the depressive alteration in cognition, in the direction of impaired self-esteem, decreased sense of efficacy and control over one’s circumstances, and pessimism , may actually be more realistic, at least in some circulstances, than the rose-colored glasses with which we usually walk around.
But recent research adds neuropsychological evidence of increased brain activity in depressed patient in regions of the prefrontal cortex associated with problem-solving, proportional to the degree of depression. It is certainly not the whole explanation, as critics counter, because some of the maladaptive impact of depression, including poor self-care, impairment in childrearing, increased susceptibility to other illness, and last but not least suicide, will outweigh the problem-solving advantages it might confer. Furthermore, there are many different kids of depression both in terms of precipitant and symptomatology. At one extreme, a person may become depressed in response to an acute recent loss (or even a future anticipated one); on the other hand, some people can develop either a dense acute depression or a smouldering chronic one without substantial stresses or losses. The imprecisions in both the lay person’s use of the term depression and its more technical clincal utilization muddy the waters in this regard.
Still, it is worth asking why a condition that is so painful and takes such a heavy toll would persist if it were not at least some of the time of some use… and whether, at least some of the time, we do more harm than good in leaping to treat it. Except, of course, the unequivocal good done to the pockets of the shareholders and executives of the pharmaceutical companies, reaping the profits from the explosive growth in antidepressant sales of the last few decades. (New York Times Magazine)
FmH readers know of my preoccupation with psychiatric diagnosis, its follies and abuses, about which I am more likely to rant here than any other topic (other than George W. bush and his administration). Today, the American Psychiatric Association posted on the web the details fo the next proposed revision, version V, to the DSM (the Diagnostic and Statistical Manual), which is the ‘bible’ of accepted psychiatric diagnoses and their criteria. DSM-V is currently scheduled to come out in 2013 after a period of public comment on the revisions and several years of field trials. The release date has already been pushed back because of controversy about the proposals and the revision process, some of which is pointed to in this NYTimes.com piece.Several different things happen in these revisions. First, the universe of existing mental illnesses is reparsed and some of the afflicted end up going into different pigeonholes. By and large, this is a trend I welcome, as the new distinctions made, and the old distinctions collapsed and erased, appear to be generally in line with the clinical experience of frontline practitioners like myself who spend all our time actually treating the mentally ill. Some of my pet peeves, like the overdiagnosis of attention deficit disorder, of childhood bipolar disorder, and of posttraumatic stress disorder, may be improved. As Gregory Bateson defined it, information is a “difference that makes a difference”, and some of the refined distinctions here will of course be more useful to psychiatric research than to practice, but by and large I find them meaningful.
However, the other thing that goes on from revision to revision of the DSM is a proliferation of diagnoses, leading to a relentless expansion of the scope and incidence of mental disorders among the population. This is what has been referred to as the medicalization of ‘normal’ human variability and of personality differences. If a broader net is cast and more people are diagnosable with mental disorders, you can imagine some of the consequences, which include the increasing use of medications for more and more benign variations; changes in social stigmatization; insurance reimbursement for various states of distress; and various diminished responsibility defenses in criminal proceedings. More profoundly, we are rewriting the concepts of personal responsibility and autonomy and the balance between free will and determinism.
I already have far too much work to do to welcome such a broader net, but then again I don’t make a fortune on the basis of how many prescriptions are written. (Estimates are that anywhere from 50-70% of those working on the revisions derive substantial income or research funding from the pharmaceutical industry.)
Tonight, because one of their reporters has been a reader of FmH, I was interviewed by the BBC about my impressions about the DSM-V proposals. It remains to be seen whether I gave them any juicy quotes they can use.
“For more than a generation now, we in the West have aggressively spread our modern knowledge of mental illness around the world. We have done this in the name of science, believing that our approaches reveal the biological basis of psychic suffering and dispel prescientific myths and harmful stigma. There is now good evidence to suggest that in the process of teaching the rest of the world to think like us, we’ve been exporting our Western “symptom repertoire” as well. That is, we’ve been changing not only the treatments but also the expression of mental illness in other cultures. Indeed, a handful of mental-health disorders — depression, post-traumatic stress disorder and anorexia among them — now appear to be spreading across cultures with the speed of contagious diseases. These symptom clusters are becoming the lingua franca of human suffering, replacing indigenous forms of mental illness.” (New York Times Magazine)
“Despite the scientific implausibility of the same disease—addiction—underlying both damaging heroin use and overenthusiasm for World of Warcraft, the concept has run wild in the popular imagination. Our enthusiasm for labeling new forms of addictions seems to have arisen from a perfect storm of pop medicine, pseudo-neuroscience, and misplaced sympathy for the miserable.” — Vaughan Bell (Slate)
“Two scientists suggest that depression is not a malfunction, but a mental adaptation that brings certain cognitive advantages”. (Scientific American) Evolutionary explanations are appealing, for if depression were not adaptive then why would it be so prevalent across cultures and epochs? Estimates are that between one quarter and one half of the public are clinically depressed at some point in their life.
The suggestion here is that the depressive state, with ruminative thinking, social isolation, and loss of interest in usually pleasurable activities, etc. promotes periods of uninterrupted analytical thinking. This turns some of the therapeutic approaches to depression on their head. Interventions which discourage ruminative thinking might prolong the resolution of a depressive episode. Patients encouraged to amplify on their ruminating, such as journalling, might do better. Perhaps even antidepressant medications might interfere in constructive problem-solving?
I have thought there might be a different evolutionary advantage to depression. After a loss or setback, the depressed person’s lack of energy, motivation and activity act to conserve resources. Their way of thinking about the world, with pessimism and a helpless sense of lack of control over what befalls one, might be more realistic, at least at such a time.
Monoamine Oxidase A and Catechol-O-Methyltransferase Functional Polymorphisms and the Placebo Response in Major Depressive Disorder: “The placebo response shows pronounced interindividual variability. Placebos are postulated to act through central reward pathways that are modulated by monoamines. Because monoaminergic signaling is under strong genetic control, we hypothesized that common functional polymorphisms modulating monoaminergic tone would be related to degree of improvement during placebo treatment of subjects with major depressive disorder. We examined polymorphisms in genes encoding the catabolic enzymes catechol-O-methyltransferase and monoamine oxidase A. Subjects with monoamine oxidase A G/T polymorphisms (rs6323) coding for the highest activity form of the enzyme (G or G/G) had a significantly lower magnitude of placebo response than those with other genotypes. Subjects with Val158Met catechol-O-methyltransferase polymorphisms coding for a lower-activity form of the enzyme (2 Met alleles) showed a statistical trend toward a lower magnitude of placebo response. These findings support the hypothesis that genetic polymorphisms modulating monoaminergic tone are related to degree of placebo responsiveness in major depressive disorder.” (Journal of Clinical Psychopharmacology)
Some behavioral scientists consider the placebo response to be a nuisance that confounds psychopharmacological research; patients get better even when they do not get the active drug. Some of us, however, feel that the placebo response is a good friend of clinical psychiatry. Some meta-analyses of antidepressant efficacy studies suggest that the medications may not be that effective and that much of the therapeutic response to antidepressants may in fact be ascribable to the placebo response. (The psychiatrist’s role, as a corollary, may be not the art of picking a drug to prescribe but enlisting the individual into a mindset that mobilizes their self-healing capacities.) We already know that depression is related to the reward circuitry in the brain and that genetic susceptibility to depressive disorders relates to polymorphism in the catecholamine system. If the placebo response as well varies with differences in that circuitry, could it be that those patients with lower capacity for the placebo response could also be those patients prone to become depressed int he first place? If we cannot as effectively mobilize their placebo response when they are in the placebo wing of a drug study, perhaps they cannot as effectively bring self-suggestion, affirmation and other coping strategies to bear on the distressing situations in their lives?