Key result
High cortisol reactivity combined with high life stress was associated with a greater incidence of verified upper respiratory infection compared to low reactivity or low life stress.
Why the study?
Does laboratory stress-elicited physiological reactivity moderate the relationship between life stress and upper respiratory infection in healthy subjects?
Cohort (n=115)
Does laboratory stress-elicited physiological reactivity moderate the relationship between life stress and upper respiratory infection in healthy subjects?
Acute HPA and immune responses to laboratory stressors serve as markers for vulnerability to stress-associated upper respiratory infections.
No takes yet. Share an insight, caveat, or question.
May flag high-reactors for elevated URI risk under stress; hypothesis-generating and requires prospective validation before practice change.
Cohen et al. (2002) conducted a cohort in Upper respiratory infection (n=115). High physiological reactivity to laboratory stress and high life stress vs. Low reactivity or low life stress was evaluated on Incidence of verified upper respiratory infection (URI). High cortisol reactivity combined with high life stress was associated with a greater incidence of verified upper respiratory infection compared to low reactivity or low life stress.
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