Cited by 1,073Regulation of Appetite and ObesityEating Disorders and BehaviorsAdipokines, Inflammation, and Metabolic Diseases

Depression and obesity: evidence of shared biological mechanisms

Open access
Milaneschi, Yuri, Simmons, W. Kyle, van Rossum, Elisabeth F. C., Penninx, Brenda WJH·2019·Molecular Psychiatry

Abstract

Depression and obesity are common conditions with major public health implications that tend to co-occur within individuals. The relationship between these conditions is bidirectional: the presence of one increases the risk for developing the other. It has thus become crucial to gain a better understanding of the mechanisms responsible for the intertwined downward physiological spirals associated with both conditions. The present review focuses specifically on shared biological pathways that may mechanistically explain the depression-obesity link, including genetics, alterations in systems involved in homeostatic adjustments (HPA axis, immuno-inflammatory activation, neuroendocrine regulators of energy metabolism including leptin and insulin, and microbiome) and brain circuitries integrating homeostatic and mood regulatory responses. Furthermore, the review addresses interventional opportunities and questions to be answered by future research that will enable a comprehensive characterization and targeting of the biological links between depression and obesity.

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Crossref · 10.1038/s41380-018-0017-5

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Research works printed but not linked: 3

  1. Major Depressive Disorder Working Group of the Psychiatric Genomics Consortium. Identification of 44 genetic associations for major depressive disorder. bioRxiv [Internet]. 2017. http://www.biorxiv.org/content/early/2017/07/24/167577
  2. Cani PD, Bibiloni R, Knauf C, Waget A, Neyrinck AM, Delzenne NM, et al. Changes in gut microbiota control metabolic endotoxemia-induced inflammation in high-fat diet-induced obesity and diabetes in mice. Diabetes. 2008;57:1470–81. http://diabetes.diabetesjournals.org/cgi/doi/10.2337/db07-1403 [cited 5 Sep 2017] · DOI · Paper page
  3. Wong BC, Chau CK, So H Genetic overlap of depression with cardiometabolic diseases and implications for drug repurposing for comorbidities. 2017;1–28. https://www.biorxiv.org/content/early/2017/08/23/140590

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Authors
Milaneschi, Y., Simmons, W. K., van Rossum, E. F. C., & Penninx, B. W.
Affiliations
  • Amsterdam Neuroscience (NL)
  • Laureate Institute for Brain Research (US)
Corresponding author
Penninx, Brenda WJH
Venue
Molecular Psychiatry
Published
2018-02-16
Volume
24
Issue
1
Pages
18-33
ISSN
  • 1359-4184 (ISSN-L)
  • 1476-5578
OpenAlex
W2793219717
Cited by
1,073
References
209
Citations by year
2026: 128 · 2025: 216 · 2024: 180 · 2023: 181 · 2022: 147 · 2021: 108 · 2020: 59 · 2019: 44 · 2018: 9
FWCI
7.69
Type
journal article
Language
en
Open access
Locations
  • Molecular Psychiatry (publishedVersion)
  • PubMed (publishedVersion)
  • Pure Amsterdam UMC (publishedVersion, other-oa)
  • EUR Research Repository (Erasmus University Rotterdam) (publishedVersion)
  • EUR Research Repository (Erasmus University Rotterdam) (submittedVersion)
  • Amsterdam UMC (VU Amsterdam) - Institutional Repository (submittedVersion)
  • Data Archiving and Networked Services (DANS) (submittedVersion)
Funders
Nederlandse Organisatie voor Wetenschappelijk Onderzoek
Topics
  • Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Regulation of Appetite and Obesity
  • Social Sciences › Psychology › Clinical Psychology › Eating Disorders and Behaviors
  • Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
Keywords
depression, obesity, bidirectional comorbidity, hypothalamic-pituitary-adrenal axis, inflammation, leptin, insulin, gut microbiota, energy metabolism, neuroendocrine regulation, brain circuits, genetic risk factors
MeSH terms
Brain, Depression, Major Depressive Disorder, Depressive Disorder, Energy Metabolism, Female, Homeostasis, Humans, Hypothalamo-Hypophyseal System, Inflammation, Insulin, Male, Obesity, Pituitary-Adrenal System, Leptin, Melanocortins, Microbiota

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