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Serotonin and Depression: A Disconnect between the Advertisements and the Scientific Literature

  • Jeffrey R Lacasse,
  • Jonathan Leo mail

    To whom correspondence should be addressed. E-mail: jleo1@tampabay.rr.com

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  • Published: November 08, 2005
  • DOI: 10.1371/journal.pmed.0020392

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A different type of mechanism?

Posted by plosmedicine on 31 Mar 2009 at 00:23 GMT

Author: Michael Hyland
Position: Professor of Health Psychology
Institution: University of Plymouth
E-mail: mhyland@plymouth.ac.uk
Submitted Date: March 06, 2008
Published Date: March 7, 2008
This comment was originally posted as a “Reader Response” on the publication date indicated above. All Reader Responses are now available as comments.

In a comment on the meta-analysis by Kirsch et al.[1], Blackburn points out that the there have been long standing doubts about serotonin imbalance explanation for the cause of depression (http://medicine.plosjourn...), see http://dx.doi.org/10.1371...) The present meta-analysis adds to these doubts, but what are the alternatives? To say that depression is a psychological not a physiological illness is dualist nonsense – minds do not exist independently of bodies. One alternative is to link depression with the body rather than the brain. Despite well established differences in immune function between depressives and normals, and the effect of psychological manipulations on immune function the immune theory of depression[2] has not yielded great therapeutic advances – though there is continuing support for omega-3 fatty acids (see comment by Sieswerda, http://medicine.plosjourn...) to which might be added exercise as well other lifestyle activities that improve well-being – there is a large industry of well-being enhancing techniques. Perhaps we should consider the possibility that depression (and some other problem diseases such as chronic fatigue syndrome, and irritable bowel syndrome) have a completely different kind of etiology to the assumption of specificity that has been so successful in other diseases. What this alternative might be is a matter of speculation, but one possibility is that it is some kind of informational error in a complex parallel processing psychoneuroimmunologicalendocrine system. If that is the case, we still have a long way to go.

1. Kirsch I, Deacon BJ, Huedo-Medina TB, Scoboria A, Moore TJ, Johnson BT. Initial severity and antidepressant benefits: a meta-analysis of data submitted to the food and drug administration. Plosmedicine 2008; 5:260 -267.
2. Maes M. Major depression and activation of the inflammatory response system. In: Dantzer R, Wollman EE, Virmiya R, editors. Cytokines, Stress, and Depression, pp 1 – 24. New York: Plenum; 1999.

No competing interests declared.