Insulin resistance, an unmasked culprit in depressive disorders: Promises for interventions

Kathleen Watson; Carla Nasca; Linn Aasly; Bruce McEwen; Natalie Rasgon

doi:10.1016/j.neuropharm.2017.11.038

Insulin resistance, an unmasked culprit in depressive disorders: Promises for interventions

Neuropharmacology. 2018 Jul 1;136(Pt B):327-334. doi: 10.1016/j.neuropharm.2017.11.038. Epub 2017 Nov 26.

Authors

Kathleen Watson¹, Carla Nasca², Linn Aasly³, Bruce McEwen⁴, Natalie Rasgon⁵

Affiliations

¹ Department of Psychiatry and Behavioral Sciences, Stanford University, 401 Quarry Road, Stanford, CA 94305, USA; Department of Health Research and Policy, Stanford School of Medicine, USA. Electronic address: [email protected].
² Harold and Margaret Milliken Hatch Laboratory of Neuroendocrinology, Rockefeller University, New York, NY 10065, USA. Electronic address: [email protected].
³ Department of Psychiatry and Behavioral Sciences, Stanford University, 401 Quarry Road, Stanford, CA 94305, USA. Electronic address: [email protected].
⁴ Harold and Margaret Milliken Hatch Laboratory of Neuroendocrinology, Rockefeller University, New York, NY 10065, USA. Electronic address: [email protected].
⁵ Department of Psychiatry and Behavioral Sciences, Stanford University, 401 Quarry Road, Stanford, CA 94305, USA. Electronic address: [email protected].

PMID: 29180223
DOI: 10.1016/j.neuropharm.2017.11.038

Abstract

Depressive disorders constitute a set of debilitating diseases with psychological, societal, economic and humanitarian consequences for millions of people worldwide. Scientists are beginning to understand the reciprocal communication between the brain and the rest of the body in the etiology of these diseases. In particular, scientists have noted a connection between depressive disorders, which are primarily seen as brain-based, and, insulin resistance (IR), a modifiable metabolic inflammatory state that is typically seen as peripheral. We highlight evidence showing how treating IR, with drugs or behavioral interventions, may ameliorate or possibly prevent, depressive disorders and their long-term consequences at various stages of the life course. This article is part of the Special Issue entitled 'Metabolic Impairment as Risk Factors for Neurodegenerative Disorders.'

Keywords: Acetyl-L-Carnitine; Allostatic load; Depression; Inflammation; Insulin resistance; Peroxisome proliferator-activated receptor.

Publication types

Research Support, Non-U.S. Gov't
Review

MeSH terms

Animals
Depressive Disorder / drug therapy
Depressive Disorder / metabolism*
Humans
Insulin Resistance*