Worldwide, rates of obesity have been steadily increasing, along with disorders commonly associated with obesity, such as cardiovascular disease and type II diabetes. Simultaneously, average sleep times have progressively decreased. Evidence from both laboratory and epidemiologic studies has consistently associated insufficient sleep or short sleep with increased risk of obesity. In the laboratory, it is now possible to control sleep behavior and study the link between sleep duration and alterations in circulating hormones involved in feeding behavior, hunger, and appetite. Carefully controlled laboratory studies of systematic sleep restriction in healthy adults have reported alterations in peripherally secreted hormones that modulate feeding. In these studies, participants also displayed increased subjective appetite and hunger ratings, greatest for high carbohydrate and high fat foods. Most importantly, recent studies have shown that short sleep duration is associated with increased actual consumption of snacks and high energy foods. These reported increases in hunger and food intake in a state of sleep debt exceed the energy demands of extended wakefulness therefore suggesting the involvement of hedonically driven eating, i.e. eating for pleasure rather than to fulfill a caloric need. We have recently examined the endocannabinoid system, known to facilitate hedonic eating, following normal and restricted sleep. Our studies show that under normal sleep conditions, blood levels of the most abundant endocannabinoid increase from mid-sleep to early afternoon. After sleep restriction, this increase in endocannabinoid concentration is amplified, coinciding with greater desire for palatable food. The identification of the endocannabinoid system as a mediator of increased hunger following sleep curtailment may help develop novel preventive strategies in the treatment of obesity.
18 - 21 May 2019
European Society of Endocrinology