Journal
MOLECULAR PSYCHIATRY
Volume 11, Issue 10, Pages 892-902Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/sj.mp.4001873
Keywords
depression; obesity; HPA axis
Funding
- NCI NIH HHS [CA16042] Funding Source: Medline
- NCRR NIH HHS [RR000865, RR017365, RR16996] Funding Source: Medline
- NHGRI NIH HHS [HG002500] Funding Source: Medline
- NHLBI NIH HHS [HL04526] Funding Source: Medline
- NIDDK NIH HHS [DK063240, DK58851] Funding Source: Medline
- NIGMS NIH HHS [GM61394] Funding Source: Medline
- NIMH NIH HHS [MH062777] Funding Source: Medline
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Obesity and depression are serious public health problems and also constitute cardiovascular disease risk factors. Research organizations have called for efforts to explore the interrelationship between obesity and depression. A useful starting point is the fact that in both disorders there is dysregulation of stress systems. We review molecular and clinical evidence indicating that the mediators of the stress response are a key locus for gene environment interactions in the shared biology of depression and obesity. Scientific milestones include translational paradigms such as mice knockouts, imaging and pharmacogenomic approaches that can identify new therapeutic strategies for those burdened by these two afflictions of contemporary civilization. Perspectives for the future are promising. Our ability to dissect the underpinnings of common and complex diseases with shared substrates will be greatly enhanced by the Genes and Environment Initiative, the emerging Large Scale Studies of Genes and Environment in Common Disease, and the UK Biobank Project.
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