Sleep disturbance in association with elevated pulse rate for prediction of mortality--consequences of mental strain?
OBJECTIVE
Sleep deprivation has experimentally been shown to adversely influence glucose metabolism, endocrine function and sympathovagal balance in young men without known serious disease. We investigated the impact of sleep problems and resting heart rate in a large sample of self-reported, healthy middle-aged men and women on long-term mortality.


METHODS
In all 22,444 men and 10,902 women participated in a population-based health screening (71% mean attendance), including blood sampling and examination of blood pressure (BP) and pulse rate after 10 min supine rest, as well as a self-administered questionnaire on sleep problems. Mortality was assessed from national death registers.


RESULTS
Sleep disturbances were related to increased cardiovascular risk factor levels at baseline in both sexes, and predicted total and cause-specific mortality after a mean of 12 years (women) and 17 years (men) of follow-up. In men, self-reported healthy at baseline, total mortality during follow-up was independently predicted by both sleep problems and increased resting heart rate, also after adjustment for smoking, body mass index (BMI), systolic BP, cholesterol, smoking and problematic alcohol drinking habits. A step-wise increased total mortality was shown in men reporting successively worse sleep problems and higher heart rate, highest hazard ratio 2.7 [95% confidence interval (CI) = 2.1-3.4] after adjustments, compared with men free from sleep problems and with normal heart rate.


CONCLUSIONS
Sleep disturbance is a predictor of total and cause-specific mortality in both sexes, but only interacts with increased resting heart rate for this prediction in healthy men. Sleep problems correlated cross-sectional with disturbances in lipid and glucose metabolism, even after adjustment for degree of obesity and smoking. Sleep disturbance is a symptom for a biological pathway that is correlated to premature mortality. One possible explanation would be that it acts in concert with sympathetic nervous activation (SNA), both being consequences of chronic stress exposure.
Nilsson
P M
PM
Department of Internal Medicine, University Hospital, Malmö, Sweden. peter.nilsson@medforsk.mas.lu.se
Nilsson
J A
JA
Hedblad
B
B
Berglund
G
G
D000704:Analysis of Variance; D002318:Cardiovascular Diseases / Q000209:etiology* / Q000401:mortality / Q000503:physiopathology; D005260:Female; D006339:Heart Rate / Q000502:physiology*; D006801:Humans; D008297:Male; D008875:Middle Aged; D009026:Mortality; D015995:Prevalence; D016016:Proportional Hazards Models; D012307:Risk Factors; D012893:Sleep Wake Disorders / Q000150:complications* / Q000453:epidemiology / Q000503:physiopathology; D013315:Stress, Psychological / Q000150:complications* / Q000503:physiopathology; D011795:Surveys and Questionnaires; D013548:Sweden / Q000453:epidemiology