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Eating behavior and stress: a pathway to obesity
Sominsky, Luba ; Spencer, Sarah J
Frontiers in psychology, 2014-05, Vol.5, p.434-434
[Periódico revisado por pares]
Switzerland: Frontiers Media S.A
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Título:
Eating behavior and stress: a pathway to obesity
Autor:
Sominsky, Luba
;
Spencer, Sarah J
Assuntos:
Corticotropin-Releasing Hormone (CRH)
;
Ghrelin
;
Glucocorticoids
;
hypothalamic-pituitary-adrenal (HPA) axis
;
Insulin
;
Leptin
;
Psychology
É parte de:
Frontiers in psychology, 2014-05, Vol.5, p.434-434
Notas:
ObjectType-Article-2
SourceType-Scholarly Journals-1
ObjectType-Feature-3
content type line 23
ObjectType-Review-1
Edited by: Tanya Zilberter, Infotonic Conseil, France
Reviewed by: Sabine Frank, University of Tübingen, Germany; Ulrich Schweiger, Lübeck University Medical School, Germany
This article was submitted to Eating Behavior, a section of the journal Frontiers in Psychology.
Descrição:
Stress causes or contributes to a huge variety of diseases and disorders. Recent evidence suggests obesity and other eating-related disorders may be among these. Immediately after a stressful event is experienced, there is a corticotropin-releasing-hormone (CRH)-mediated suppression of food intake. This diverts the body's resources away from the less pressing need to find and consume food, prioritizing fight, flight, or withdrawal behaviors so the stressful event can be dealt with. In the hours following this, however, there is a glucocorticoid-mediated stimulation of hunger and eating behavior. In the case of an acute stress that requires a physical response, such as a predator-prey interaction, this hypothalamic-pituitary-adrenal (HPA) axis modulation of food intake allows the stressful event to be dealt with and the energy used to be replaced afterward. In the case of ongoing psychological stress, however, chronically elevated glucocorticoids can lead to chronically stimulated eating behavior and excessive weight gain. In particular, stress can enhance the propensity to eat high calorie "palatable" food via its interaction with central reward pathways. Activation of this circuitry can also interact with the HPA axis to suppress its further activation, meaning not only can stress encourage eating behavior, but eating can suppress the HPA axis and the feeling of stress. In this review we will explore the theme of eating behavior and stress and how these can modulate one another. We will address the interactions between the HPA axis and eating, introducing a potential integrative role for the orexigenic hormone, ghrelin. We will also examine early life and epigenetic modulation of the HPA axis and how this can influence eating behavior. Finally, we will investigate the clinical implications of changes to HPA axis function and how this may be contributing to obesity in our society.
Editor:
Switzerland: Frontiers Media S.A
Idioma:
Inglês
Links
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