Stewart and colleagues1 provided compelling evidence for the association between depressive symptoms and the progression of subclinical atherosclerosis. In a 3-year study, they found that higher levels of depressive symptoms (eg, anhedonia, fatigue, and sleep/appetite disturbance) at baseline were associated with a greater 3-year change in carotid intima-media thickness (IMT), and they suggested that depression may play a role in the earlier stages of the development of coronary artery disease. They acknowledged that it is unlikely that the symptoms per se are the pathobiological mechanism of atherosclerosis. A likely explanation for the observed association between depressive symptoms and atherosclerosis is that both are triggered and/or maintained by a common biological mechanism. The Stewart et al study1 included only healthy, older individuals, and the authors suspect that the association they observed may be specific to this population. A putative common mechanism that is affected by aging and may link depression and atherosclerosis has recently been discussed.2 This mechanism is the pathway of the inflammatory enzyme 5-lipoxygenase (5-LOX).
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