| Summary: | In Western populations, the lifetime-documented prevalence of clinical depression (DE) is currently 10%, with a significant burden on general physical health and, most importantly, cardiovascular burden. As for lipid elements, mounting evidence indicates that various exogenous factors, such as unhealthy diet, restricted exercise, and co-occurring anxiety, appear to contribute to the increase in lipid profile abnormalities in depressed patients. To note that in patients with DE, selected biological links are disrupted, resulting in lipid abnormalities, even if the well-established exogenous mediating factors have been controlled. In this review, we explore the possible direct biological links between DE and lipid abnormalities namely serotonin, inflammatory, and stress processes a matter which has not yet been clarified. Serotonin alterations probably play an essential role in lipid and DE association; low lipid levels coexist with decreased serotonergic activity, while low serotonin concentrations have been detected in depressed individuals. Stress - induced lipolysis model may also play an important role; free fatty acids produced by activating lipoprotein lipase derived by stress hormones are available in liver and circulation to elevate lipoproteins. DE appears to be both an internal triggering factor (stressor) but also a consequence of the stress system dysregulation (allostasis), resulting in both emotional burden and dyslipidemia driven in a circular causality. Furthermore, altered immunological profile in depressed subjects is considered to be another factor which probably mediates this connection. Conclusively, although many studies provide reliable data on the presence of the above mechanisms apart from the influences of unhealthy lifestyle attitudes, the presence of a direct biological association between DE and lipid alterations, cannot yet be supported by consistency.
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