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Burnout and Risk of Type 2 Diabetes: A Prospective Study of Apparently Healthy Employed Persons

Melamed, Samuel PhD; Shirom, Arie PhD; Toker, Sharon MA; Shapira, Itzhak MD

doi: 10.1097/01.psy.0000242860.24009.f0
Original Articles

Objective: This prospective study was designed to test the extent to which the onset of type 2 diabetes in apparently healthy individuals was predicted by burnout, a unique affective response to combined exposure to chronic stressors.

Methods: The study participants were 677 employed men and women who were followed up for 3 to 5 years (mean = 3.6 years) for the onset of diagnosed type 2 diabetes. Burnout was assessed by the Shirom-Melamed Burnout Measure with its three subscales: emotional exhaustion, physical fatigue, and cognitive weariness.

Results: The burnout symptoms were remarkably consistent over the follow-up period irrespective of changes in place of work and in employment status. During the follow-up period, 17 workers developed type 2 diabetes. Logistic regression results indicated that burnout was associated with a 1.84-fold increased risk of diabetes (95% confidence interval [CI] = 1.19–2.85) even after adjusting for age, sex, body mass index, smoking, alcohol use, leisure time physical activity, initial job category, and follow-up duration. In a subsample of 507 workers, the relative risk of diabetes was found to be much higher after additional control for blood pressure levels (odds ratio = 4.32, 95% CI = 1.75–10.67), available only for this subsample.

Conclusions: These findings suggest that chronic burnout might be a risk factor for the onset of type 2 diabetes in apparently healthy individuals.

CI = confidence interval; CVD = cardiovascular disease; SMBM = Shirom-Melamed Burnout Measure; HbA1c = glycosylated hemoglobin A1c; VE = vital exhaustion; MI = myocardial infarction; MBI = Maslach Burnout Inventory; BMI = body mass index; SBP = systolic blood pressure; DBP = diastolic blood pressure; OR = odds ratio; APR = acute phase response; CRP = C-reactive protein; HDL = high-density lipoprotein; HPA = hypothalamic–pituitary–adrenal.

From the Department of Epidemiology and Preventive Medicine (S.M.), Sackler Faculty of Medicine (S.M., I.S.) and the Faculty of Management (A.S., S.T.), Tel Aviv University, Tel Aviv, Israel; and Tel Aviv Sourasky Medical Center (I.S.), Tel Aviv, Israel.

Address correspondence and reprint requests to Samuel Melamed, PhD, Associate Professor, Department of Epidemiology and Preventive Medicine, Sackler Faculty of Medicine, Tel Aviv University, Ramat Aviv, Tel Aviv, Israel. E-mail: smelamed@post.tau.ac.il

Received for publication May 11, 2006; revision received August 2, 2006.

Copyright © 2006 by American Psychosomatic Society
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