Short sleep, poor sleep: novel risk factors for type 2 diabetes

Abstract

Sleep curtailment has become a very common behavior in industrialized countries. The aging of the population is also associated with an increased prevalence of sleep disturbances. There is rapidly accumulating evidence to indicate that chronic partial sleep loss and decreased sleep quality may increase the risk of obesity and diabetes. Laboratory studies have shown that sleep restriction (4‐6 h bedtimes) is associated with a decrease in Insulin without adequate compensation in beta cell function, resulting in an elevated risk of diabetes. Reduced sleep quality, without change in sleep duration, is also associated with an increased risk of diabetes. Indeed, selective suppression of slow‐wave sleep rapidly results in a marked reduction in insulin sensitivity and disposition index. Prospective epidemiologic studies in both children and adults are consistent with a causative role of sleep disturbances in the increased risk of diabetes. Sleep curtailment is also associated with a dysregulation of the neuroendocrine control of appetite. Under conditions of controlled caloric intake and energy expenditure, there is a robust negative relationship between leptin levels and sleep duration. Ghrelin levels increase with short sleep. Thus, sleep loss may alter the ability of leptin and ghrelin to accurately signal caloric need. The adverse impact of sleep deprivation on appetite regulation is likely to be driven by increased activity orexinergic. Consistent with the laboratory evidence, multiple epidemiologic studies have shown an association between short sleep and higher BMI after controlling for a variety of possible confounders. Taken together, the current evidence suggest that chronic partial sleep curtailment, a novel behavior that appears to have developed with the advent of the 24‐h society, and reduced sleep quality may be involved in the current epidemic of obesity and diabetes.