The relationship between inflammation and depression is becoming a crucial question
for psychiatry. In the early 1990s, Maes (
1
) first reported increased interleukin-6 (IL-6) production in depression and linked
that to immune irregularities in depression. Over the same period, depression was
firmly established as a risk for coronary artery disease (CAD) and inflammation was
recognized as an important step in the progression of CAD. By the late 1990s, investigators
began to ask if inflammatory abnormalities associated with depression might be a mechanism
explaining the increased risk of vascular disease in depressed patients. The observation
that 45% of malignant melanoma patients treated with high-dose alpha interferon developed
major depression raised questions about the role of inflammatory cytokines as a source
not only of vascular comorbidity but also of depressive symptoms and potentially depressive
episodes themselves (
2
,
3
).To read this article in full you will need to make a payment
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References
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© 2007 Society of Biological Psychiatry. Published by Elsevier Inc. All rights reserved.
