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Biol Psychol. 2010 May;84(2):228-34. doi: 10.1016/j.biopsycho.2010.01.016. Epub 2010 Jan 29.

Neurohormonal and inflammatory hyper-responsiveness to acute mental stress in depression.

Author information

1
George Mason University, Center for the Study of Chronic Illness and Disability, 4400 University Drive, MSN 5B7, Fairfax, VA 22030, USA. aweinst2@gmu.edu

Abstract

Depression is associated with dysregulated hypothalamic-pituitary-adrenal (HPA) axis function, overactivity of the sympathoadrenal system, and increased levels of inflammation markers. It is not known whether these biological processes are disproportionately elevated in response to acute negative emotional arousal by mental stress (MS). The present study investigates responses of neurohormones and inflammatory markers to MS in 14 clinically depressed (age: 42+/-10 years; 50% female) and 14 non-depressed control (age: 39+/-6 years; 50% female) participants. Heightened acute MS reactivity was documented in depressed participants (adrenocorticotropic hormone, rho=0.001; norepinephrine, rho=0.042; epinephrine, rho=0.039), and a delayed increase in cortisol was observed (rho=0.002). Inflammation markers increased more strongly in depressed versus non-depressed participants (IL-6, rho=0.027; tumor necrosis factor-alpha, rho=0.050; and recovery C-reactive protein, rho=0.003). It is concluded that depressed individuals display hyper-reactivity of neuroimmunological markers in response to acute negative emotions. This hyper-reactivity may serve a pathologic role in the elevated morbidity and mortality risk associated with depression.

PMID:
20117167
PMCID:
PMC2875322
DOI:
10.1016/j.biopsycho.2010.01.016
[Indexed for MEDLINE]
Free PMC Article

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