Unipolar depression and diabetes mellitus each account for a significant proportion of the global burden of disease. Epidemiological literature suggests a bi-directional relationship between these two common disorders, and evidence from the molecular sciences supports a role for inflammation in the pathogenesis and pathophysiology of each disorder individually. Recent advances in understanding the neurobiology of depression have implicated dysfunction of the hypothalamus-pituitary-adrenal axis, neurotrophins, and inflammatory mediators in the development of this disorder. Similarly, dysregulated facets of both the innate and adaptive immune system have been implicated in the onset of insulin resistance and type 2 diabetes. This review draws upon an emerging body of epidemiological and mechanistic evidence to support the hypothesis that shared inflammatory mechanisms may represent a key biological link in this co-morbidity. Given the shared mechanisms of this co-morbidity, these patients may be excellent candidates for novel immune targeted pharmacotherapy.
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