Depressed patients have more blood clots and more heart attacks. They have elevated inflammatory markers in their blood. Antidepressants reduce these markers. This is interesting in terms of how depression is treated, but the bigger question is, what causes depression and what is the mechanism?
I came across an interesting article today in BMC Medicine:
“The identification of a number of potential factors that are known sources of inflammation, and their correlation to quality evidence linking those factors to increased risk of depression, provides mechanistic support for inflammation as one of the mediating pathways to both risk and neuroprogression in depression. The pivotal element is that most of these are plastic, and amenable to intervention, both therapeutic and preventative. While inflammation has suggested a number of very promising anti-inflammatory therapies, including statins, aspirin, pioglitazone and celecoxib, the latter preventative need is perhaps the more pressing [14,250,251]. Psychiatry largely lacks an integrated model for conceptualizing modifiable risk factors for depression. It has, therefore, lacked conceptually and pragmatically coherent primary prevention strategies, prioritizing the treatment of established disorders. Yet the rationale, targets and imperative to focus on prevention of depression at a population level is clear.”
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