Abstract
Neurobiological models of depression aim to explain its conditions through a description of the underlying neurocircuitry. The present paper analyses the skeptical doubts that may be raised in response to neurobiological accounts of depression and the conditions under which these models may shed some light on the corresponding phenomena. Far from excluding other kinds of enquiries, neurobiological models may greatly benefit from a philosophical enquiry on our affective life, and especially from closer attention paid to ill-defined phenomena like moods. I suggest that what is crucial to depression is defective affective regulation, and that it is with this perspective that we may make sense of neurophysiological data.
I would like to thank Jerome Wakefield and Steeves Demazeux for their feedback on the draft of this paper, Samuel Lepine for his comments on an earlier version, and Larry Dewaële for his careful reading of the final version.
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Notes
- 1.
To say that depression should not be confused with experiences of intense sadness (due for instance, to a loss) does not mean that the fact that MDD is usually adversity-triggered is ignored. As Jerome Wakefield has convincingly shown (Wakefield 2015), in no way does the “bereavement exclusion” necessitate that grieving people cannot be diagnosed with depression . But to define tests in order to draw the line correctly between normal sadness and depression may be problematic: for instance, impairment in role functioning or even a feeling of worthlessness, if temporary, may not be a clear sign of a depressive, pathological state. This is why, to define depression , we may focus on the recurrence of the symptoms rather than on their specificity.
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Forest, D. (2016). Is an Anatomy of Melancholia Possible? Brain Processes, Depression, and Mood Regulation. In: Wakefield, J., Demazeux, S. (eds) Sadness or Depression?. History, Philosophy and Theory of the Life Sciences, vol 15. Springer, Dordrecht. https://doi.org/10.1007/978-94-017-7423-9_7
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