Chronic stress and comfort foods: self-medication and abdominal obesity

Abstract

Central corticotropin-releasing factor (CRF) networks are recruited by chronic stressors and elevated glucocorticoids (GCs) that initiate recruitment of central CRF activity in the amygdala. Increased central activity of the CRF network stimulates all monoaminergic cell groups, as well as premotor autonomic and other limbic structures resulting in the typical arousal, behavioral changes, autonomic, and neuroendocrine changes that accompany the chronic imposition of a stressor. By contrast, elevated GCs appear, through a variety of means to counteract the effects of central CRF, which they have initiated. Together with insulin, the GCs stimulate drive for and ingestion of "comfort foods" that may directly result in reduction of the negative effects of the chronic stressor in the nucleus Accumbens, through stimulation of the anterior, more pleasure-associated part of this cell group, thus reducing the weight of the stress-stimulated posterior, more defensive part. Furthermore, the shift in caloric intake from chow to preference for "comfort foods," together with elevated GCs and insulin, reorganize energy stores from a peripheral to a central distribution, primarily as abdominal fat. A signal associated with this fat depot appears, as with eating "comfort foods," to reduce the influence of the chronic stress network on behaviors, autonomic, and neuroendocrine outflow.