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Neurosci Biobehav Rev. 2015 Sep;56:139-50. doi: 10.1016/j.neubiorev.2015.07.001. Epub 2015 Jul 3.

Stress habituation, body shape and cardiovascular mortality.

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Medical Clinic 1, University of Luebeck, Luebeck, Germany. Electronic address:
Harold and Margaret Milliken Hatch Laboratory of Neuroendocrinology, The Rockefeller University, New York, NY, USA.


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.


Allostasis; Allostatic load; Atherosclerosis; Brain energy metabolism; Cardiovascular mortality; Obesity; Selfish brain theory; Stress; Stress habituation; Subcutaneous fat; Turbulent blood flow; Visceral fat

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