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  • Explaining Depression
  • James Phillips (bio)

The author has reviewed the history of biological theories of depression with a fascinating account of how researchers have argued backward, starting with the neurochemical effects of antidepressants on the monoamine system in the brain, and ending with etiological theories that place the biological cause of depression in disturbances of the monoamine system. He explains how further work in biological etiology (monoamine receptor theories and neuroplasticity theories) has followed the same backward path. In carrying out this task, he has done such an excellent job that I have little to offer as a critique of his work. The author uses a research model developed by Lakatos, and he points out that Lakatos's approach to philosophy of science has already been criticized by others.

My own interest is in pursuing the question of depression begins at the point where the author stops. He has clarified progress in the biology of depression, but his interest in depression does not extend beyond the biological dimension. Is there more to depression than its biology? I would say yes, that understanding depression does not begin and end with biology. Moving beyond biology, we encounter all the nonbiological factors that play a role in the etiology of depression. These include developmental factors such inadequate parenting, and environmental factors such as early sexual abuse. These factors might be called psychological, because they all work through the mind of the sufferer. In studying them, we leave psychopharmacology and the pharmacological bridge. If, for instance, we are studying the effects of childhood sexual abuse on depression, biology and the pharmacological bridge play no role in our research.

This does not mean that the nonbiological factors totally exclude biology and neuropathophysiology. In his review of biological theories of depression, the author writes that the original monoamine theories ended up in the 1990s in neuroplasticity theories of depression. Aside from direct biological effects on brain structure, neuroplasticity could be involved in the effects of mental phenomena on brain structure. One such path would involve epigenetics, in which an environmental factor creates a change in the individual's mental state, which in turn activates a genetic locus that plays a role in depression.

Let me now take a step further away from biology. I have pointed out that developmental and environmental etiological factors may elude the pharmacological bridge but still be connected to neuropathophysiology. This next step would involve phenomena such as mental conflict, severe enough to play a role in depression, but with no obvious link to pathophysiology. Hard-core reductionists would insist, of course, that everything is in one way or another biological, even if we do not understand the exact mechanism. Whatever is going on in my 'mind' is going on in my brain and can, even if not yet, be explained by specific brain changes. [End Page 303]

We are now entering on a long discussion of mind/brain reductionism, but I will try to abbreviate the discussion with reference to a recent article by philosopher Simon Critchley. Writing about his early mentor, philosopher Frank Cioffi, and the latter's attitude toward such reductionism, Critchley says:

This is the risk of what some call "scientism"–the belief that natural science can explain everything, right down to the detail of our subjective and social lives. All we need is a better form of science, a more complete theory, a theory of everything. Lord knows, there are even Oscar-winning Hollywood movies made about this topic. Frank's point, which is still hugely important, is that there is no theory of everything, nor should there be. There is a gap between nature and society. The mistake, for which scientism is the name, is the belief that this gap can or should be filled.

(Critchley, 2015, p. 10)

This is a rather dramatic statement that flies in the face of the reductionist tendencies of the biomedical model. In the context of the etiology of depression, Critchley and Cioffi are saying that the mental conflict involved in the etiology of depression may not map onto brain structure, and that more broadly, mind and brain may involve different, incommensurable discourses that cannot be subsumed under one...

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Additional Information

ISSN
1086-3303
Print ISSN
1071-6076
Pages
pp. 303-304
Launched on MUSE
2018-12-06
Open Access
No
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