Stress habituation, body shape and cardiovascular mortality. (September 2015)

• Record Type: Journal Article
• Authors: Peters, Achim; McEwen, Bruce S.
• Is Part Of: Neuroscience and biobehavioral reviews. Volume 56(2015:Sep.)
• Page Start: 139
• Page End: 150
• Publication Date: 2015-09
• Subjects: Allostasis -- Allostatic load -- Atherosclerosis -- Brain energy metabolism -- Cardiovascular mortality -- Selfish brain theory -- Stress -- Stress habituation -- Obesity -- Subcutaneous fat -- Turbulent blood flow -- Visceral fat; Psychophysiology -- Periodicals; Human behavior -- Periodicals; Animal behavior -- Periodicals; Neurology -- Periodicals; Behavior -- Periodicals; Ethology -- Periodicals; Neurology -- Periodicals; Psychophysiologie -- Périodiques; Comportement humain -- Périodiques; Animaux -- Mœurs et comportement -- Périodiques; Neurologie -- Périodiques; Animal behavior; Human behavior; Neurology; Psychophysiology; Periodicals; Electronic journals; 573.8
• DOI: 10.1016/j.neubiorev.2015.07.001
• Languages: English
• ISSNs: 0149-7634

Abstract

Highlights: Cardiovascular risk is associated with large visceral fat and lean body mass. High body mass and large subcutaneous fat is associated with low a mortality risk. During psychosocial stress the brain needs extra energy. Psychosocial stress causes visceral fat growth and cardiovascular complications. Stress habituation lowers cardiovascular risk, but its trade-off is body mass gain. Abstract: High cardiovascular mortality is well documented in lean phenotypes exhibiting visceral fat accumulation. In contrast, corpulent phenotypes with predominantly subcutaneous fat accumulation display a surprisingly low mortality. The term 'obesity paradox' reflects the difficulty in understanding the biological mechanisms underlying these clinical observations. The allostatic load model of chronic stress focuses on glucocorticoid dysregulation as part of a 'network of allostasis' involving autonomic, endocrine, metabolic, and immune mediators. Here, we expand upon the energetic demands of the brain and show that 'habituators' and 'non-habituators' develop divergent patterns of fat distribution. Central to this process is the recurrent rise in the cerebral energy need (arousal) that non-habituators experience during chronic stress. These neuroenergetic alterations promote visceral fat accumulation, subcutaneous fat loss, and atherogenesis with subsequent cardiovascular events. Habituators are more or less protected against such cardiovascular complications, but there is a metabolic trade-off that we shall discuss in the present paper.