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Against Depression (the disease, and the image of the "heroic melancholy")

Liz S's picture

Against Depression Critique


What if van Gogh had taken Prozac? This is the central question of Against Depression, or at least the question that led Peter Kramer to write this book. After the publication of his book Listening to Prozac, Kramer noticed that at every stop along the book tour someone would inevitably ask this question. At first he brushes it off, annoyed, but eventually he comes to a realization—people do not have a full understanding of depression as a disease.

What if Dinesen had taken penicillin? This is the question that Kramer asks, in jest, inadvertently explaining our culture’s misunderstanding of depression. Isak Dinesen was a short story writer, diarist and Danish icon who died of syphilis. We do not think of withholding penicillin from a person who has contracted syphilis. We do not think of withholding antibiotics from people afflicted with disease. The problem is that not everyone sees depression for what it really is—a disease. Depression, Kramer argues, is no different from any other medical condition or disease. But the van Gogh question illustrates that depression has some sort of intrigue. People mistake symptoms of depression for personality traits. We believe that depression gives us depth. We, in essence, romanticize a disease.

Kramer believes that part of the problem is the tradition of the heroic melancholy. Hippocrates believed that a moderate amount of black bile (an excess of black bile was thought to cause melancholy at the time) created men that were “superior to the rest of the world in many ways.” Another example is Hamlet—the underlying message of the play, Kramer argues, is that melancholy bestows depth. It is hard to argue with Kramer, because there is much evidence that we as a culture have long romanticized depressive traits. In 1896, Maurice Maeterlinck wrote that the “value of ourselves is but the value of our melancholy and our disquiet" (2).

But despite what we think of depression, an overwhelming amount of research has recently demonstrated that depression is a disease just like any other. Just the fact that Prozac and other anti-depressants work shows that our brain chemistry plays a role in the course of depression. Moreover, Robert Sapolsky has experimented on rats in order to better understand the effects of aging and chronic exposure to stress hormones on hippocampal atrophy. Sapolsky’s research suggests that excess stress hormones, while not directly destroying cells, bring neurons to the “brink of death” (Kramer 117). This over-expression of stress hormones and the subsequent destruction of the hippocampus may be a central factor in the development and course of depression. Too much stress can trigger an episode of depression, and depression itself leads to chronic stress. Therefore, Kramer contends, stress hormones may play a causal role in the development of depression, or at least a significant role in the course of the disorder.

Another biological dynamic to depression appears to be BDNF, brain-derived neurotropic factor. BDNF, a growth promoter, acts as a resilience factor for the brain—a protector against atrophy and neuronal death. And research has shown that decreasing an animal’s BDNF levels leads to depressive symptoms. Moreover, Grazyna Rajkowska found that in deceased humans who had suffered from depression, the patients had a deficit in BDNF (in addition to hippocampal atrophy) (1). Clearly, then, the biological evidence paints a very un-romantic picture of depression.

Other factors come into play in the development of depression—genetics, prenatal issues, environment, etc. Twin studies and other research have demonstrated that major depression is heritable—35-40% (Kramer 116). In terms of prenatal environment, researchers have found that maternal stress during pregnancy correlates with depression in offspring in monkeys. The environment also plays a large part in the development of depression, interacting with genetic and biological factors that create vulnerability for the disease. Stressful events in life, especially humiliating losses, increase the likelihood for developing major depression. And creating an even more complex picture is the finding that genetically vulnerable people also put themselves into “high-risk environments” (Kramer 139).

Considering, therefore, all the complex factors involved in the development and course of depression, it seems all the more shocking that people would continue to ask the van Gogh question. It is equally hard to imagine asking such a question after reading the arguments and evidence that Kramer provides during the course of the book. Someone in the forum commented that the image of the “suffering artist” is popular in today’s culture. But, clearly, this image has been with us for much longer. If anything, that viewpoint is less powerful today than in previous generations because we are actually beginning to see and understand the biological aspects to the disease. We are finally able to see what depression really is—a disease.

Whether we are willing to accept this fact is perhaps a different story. The fact that Peter Kramer is consistently asked the van Gogh question suggests that our society is not quite ready to let go of the image of the suffering artist, of the belief that melancholy provides us with a deeper understanding of life. But perhaps we are now better able to separate the catchall of melancholy from the disease, the reality of major depression. It may be easy to romanticize the paintings and life of a depressed artist, but it sounds absurd to romanticize a disease that costs you friends, jobs, years off your life, and at the same time atrophies your brain. One can hope, then, that Kramer’s optimism about a future in which we are free from depression will actually come to fruition. Who would argue with that? Probably not van Gogh, and certainly not me.



1. Against Depression -

2. Romanticzing depression