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Stress as a Common Risk Factor for Obesity and Addiction

  • Rajita Sinha
    Correspondence
    Address correspondence to Rajita Sinha, Ph.D., Yale Stress Center, Department of Psychiatry, Neurobiology and Child Study, Yale University School of Medicine, 2 Church Street South, Suite 209, New Haven, CT 06519
    Affiliations
    Department of Psychiatry, Yale Stress Center, New Haven, Connecticut

    Child Study Center, Yale University School of Medicine, New Haven, Connecticut

    Department of Neurobiology, Yale University School of Medicine, New Haven, Connecticut
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  • Ania M. Jastreboff
    Affiliations
    Department of Internal Medicine, Yale University School of Medicine, New Haven, Connecticut

    Department of Pediatrics, Section of Pediatric Endocrinology, Yale University School of Medicine, New Haven, Connecticut
    Search for articles by this author
      Stress is associated with obesity, and the neurobiology of stress overlaps significantly with that of appetite and energy regulation. This review will discuss stress, allostasis, the neurobiology of stress and its overlap with neural regulation of appetite, and energy homeostasis. Stress is a key risk factor in the development of addiction and in addiction relapse. High levels of stress changes eating patterns and augments consumption of highly palatable (HP) foods, which in turn increases incentive salience of HP foods and allostatic load. The neurobiological mechanisms by which stress affects reward pathways to potentiate motivation and consumption of HP foods as well as addictive drugs is discussed. With enhanced incentive salience of HP foods and overconsumption of these foods, there are adaptations in stress and reward circuits that promote stress-related and HP food-related motivation as well as concomitant metabolic adaptations, including alterations in glucose metabolism, insulin sensitivity, and other hormones related to energy homeostasis. These metabolic changes in turn might also affect dopaminergic activity to influence food motivation and intake of HP foods. An integrative heuristic model is proposed, wherein repeated high levels of stress alter the biology of stress and appetite/energy regulation, with both components directly affecting neural mechanisms contributing to stress-induced and food cue-induced HP food motivation and engagement in overeating of such foods to enhance risk of weight gain and obesity. Future directions in research are identified to increase understanding of the mechanisms by which stress might increase risk of weight gain and obesity.

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