Stress resilience and the risk of inflammatory bowel disease: a cohort study of men living in Sweden. Issue 1 (27th January 2017)

• Record Type: Journal Article
• Authors: Melinder, Carren; Hiyoshi, Ayako; Fall, Katja; Halfvarson, Jonas; Montgomery, Scott
• Is Part Of: BMJ open. Volume 7:Issue 1(2017)
• Publication Date: 2017-01-27
• Subjects: EPIDEMIOLOGY -- GASTROENTEROLOGY; Medicine -- Research -- Periodicals; 610.72
• DOI: 10.1136/bmjopen-2016-014315
• Languages: English
• ISSNs: 2044-6055

Abstract

Abstract : Objective: To determine if low psychosocial stress resilience in adolescence (increasing chronic stress arousal throughout life) is associated with an increased inflammatory bowel disease (IBD) risk in adulthood. Subclinical Crohn's disease (CD) and ulcerative colitis (UC) can exist over many years and we hypothesise that psychosocial stress may result in conversion to symptomatic disease through its proinflammatory or barrier function effects. Design: National register-based cohort study of men followed from late adolescence to middle age. Setting: A general population cohort of men in Sweden. Participants: Swedish population-based registers provided information on all men born between 1952 and 1956 who underwent mandatory Swedish military conscription assessment (n=239 591). Men with any gastrointestinal diagnoses (except appendicitis) prior to follow-up were excluded. Primary outcome measures: An inpatient or outpatient diagnosis of CD or UC recorded in the Swedish Patient Register (1970–2009). Results: A total of 938 men received a diagnosis of CD and 1799 UC. Lower stress resilience in adolescence was associated with increased IBD risk, with unadjusted HRs (95% CIs) of 1.54 (1.26 to 1.88) and 1.24 (1.08 to 1.42), for CD and UC, respectively. After adjustment for potential confounding factors, including markers of subclinical disease activity in adolescence, they are 1.39 (1.13 to 1.71) and 1.19 (1.03 to 1.37). Conclusions: Lower stress resilience may increase the risk of diagnosis of IBD in adulthood, possibly through an influence on inflammation or barrier function.