Format

Send to

Choose Destination
Trends Pharmacol Sci. 2008 Sep;29(9):433-6. doi: 10.1016/j.tips.2008.05.004.

Serotonin and depression: pathophysiological mechanism or marketing myth?

Author information

1
Neurosciences Building, Warneford Hospital, Old Road, Headington, Oxford OX3 7JX, UK. phil.cowen@psych.ox.ac.uk

Abstract

The notion that impaired serotonin (5-HT) function can lead to clinical depression has a long history but is still controversial. Some have argued that the 5-HT hypothesis has been misused by the pharmaceutical industry to promote a simplistic biological model of depression to market selective serotonin reuptake inhibitors (SSRIs) to medical practitioners and the public. By contrast, there is now substantial evidence that unmedicated depressed patients have abnormalities in brain 5-HT function; however, the relation of these abnormalities to the clinical syndrome is unclear. The best evidence that 5-HT contributes to the pathophysiology of depression comes from studies of tryptophan depletion, which show that lowering brain 5-HT levels can induce acute symptomatic relapse in recovered depressed patients. Clarification of the mechanism of this effect will enable an understanding of how impaired 5-HT activity contributes to the subjective experience of depression.

PMID:
18585794
DOI:
10.1016/j.tips.2008.05.004
[Indexed for MEDLINE]

Supplemental Content

Full text links

Icon for Elsevier Science
Loading ...
Support Center