HealthDay News — Recurring emotional stress may trigger a stronger biochemical response in overweight patients, possibly increasing their risk of chronic illnesses such as heart disease and type 2 diabetes, indicate the findings of a study published in Brain, Behavior, and Immunity.
“Overweight and obese individuals, who comprise approximately two-thirds of the U.S. population, are at increased risk for developing a range of diseases,” noted Christine McInnis, MS, a PhD student at Brandeis University in Waltham, Mass., and colleagues.
“This increased risk may be due in part to maladaptive stress responses within this group, including heightened low-grade inflammation and hypothalamic-pituitary-adrenal axis (HPA) non-habituation.”
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To study the relationship between adiposity, plasma interleukin-6 (IL-6), and HPA axis responses to repeated stress, the investigators placed study participants of various body sizes in stressful situations, including a very unfriendly job interview and a difficult oral math exercise. Saliva samples were taken to examine how stress affected patients’ body chemistry.
Overweight people repeatedly placed in a stressful situation exhibited increasing amounts of IL-6 in their saliva. Normal-weight people did not exhibit this escalation in IL-6 levels when exposed to repeated stress.
Lean participants started out with lower IL-6 levels than obese participants, but both lean and obese patients exhibited similar levels of biochemical response to stress on the first day. However, overweight or obese participants exhibited an IL-6 response on the second day nearly double that of their response the day before. Comparatively, the second-day response of lean people was the same as it was their first day.
“These findings point to maladaptive stress response patterns in overweight humans, which, through exposure to higher levels of inflammatory mediators, might partially explain diseases related with overweight and/or obesity,” concluded the researchers.
References
- McInnis C et al. Brain, Behavior, and Immunity. 2014; doi: 10.1016/j.bbi.2014.07.018