Negative affective responses to a speech task predict changes in interleukin (IL)-6.

TitleNegative affective responses to a speech task predict changes in interleukin (IL)-6.
Publication TypeJournal Article
Year of Publication2011
AuthorsCarroll JE, Low CA, Prather AA, Cohen S, Fury JM, Ross DC, Marsland AL
JournalBrain Behav Immun
Volume25
Issue2
Pagination232-8
Date Published2011 Feb
ISSN1090-2139
KeywordsAffect, Anger, Anxiety, Blood Pressure, Female, Heart Rate, Hemodynamics, Humans, Interleukin-6, Male, Middle Aged, Neuropsychological Tests, Social Environment, Speech, Stress, Psychological, Sympathetic Nervous System
Abstract

Laboratory studies show that individuals differ appreciably in the magnitude of their inflammatory responses to acute psychological stress. These individual differences are poorly understood, yet may contribute to variation in stress-associated disease vulnerability. The present study examined the possibility that affective responses to acute stress contribute to these differences. For this purpose, 102 relatively-healthy community volunteers (mean age 50 years; 60% female; 91.2% white) performed an acute stress protocol and measures of affective state and serum levels of the proinflammatory cytokine, interleukin (IL)-6 were collected at the end of a 30-min resting baseline, a 5-min evaluative public speaking task, and a 30-min recovery period. Results of regression analyses, controlling for age, race, gender, menopausal status, and body mass index, revealed a positive association of task-related increases in anger and anxiety with increases in IL-6 (R² change = .08, p = .004; R² change = .08, p = .005, respectively). Further examination showed that these affective responses to the task were independent predictors of change in IL-6. Cardiovascular reactivity to the task did not explain the association. These results suggest that individuals who exhibit angry or anxious responses to acute challenge are more vulnerable to stress-related increases in markers of systemic inflammation, possibly rendering them more susceptible to inflammatory disease.

DOI10.1016/j.bbi.2010.09.024
Alternate JournalBrain Behav. Immun.
PubMed ID20888901
PubMed Central IDPMC3025042
Grant ListNR008237 / NR / NINR NIH HHS / United States
R01 NR008237 / NR / NINR NIH HHS / United States
R01 NR008237-01A1 / NR / NINR NIH HHS / United States
T32 HL007560 / HL / NHLBI NIH HHS / United States