Short Sleep Duration Promoting Overconsumption of Food: A Reward-Driven Eating Behavior?

THE PROOF-OF-CONCEPT FOR SHORT SLEEP DURATION AS A POSSIBLE CAUSE OF OBESITY IS GROWING.^1,2 PROSPECTIVE COHORT STUDIES HAVE consistently shown that short sleep duration is associated with weight gain and incidence of obesity in children and adults. Intervention studies have provided a mechanistic explanation for the short sleep-obesity connection (i.e., that sleep restriction impacts hormonal regulation of appetite). Ongoing research is trying to determine whether sleep extension in sleep deprived obese individuals can influence appetite control and/or reduce body fat.³ Given the high prevalence of chronic sleep restriction, studies aiming to elucidate the possible causal association between short sleep duration and obesity are of utmost importance from a public health standpoint.

The potential mechanisms by which short sleep duration may influence body weight are under scrutiny. In order to produce weight gain, reduced sleep must either increase energy intake and/or reduce energy expenditure. Decreased energy expenditure as an explanation for why short sleep duration is associated with weight gain requires further research. The increased fatigue and tiredness associated with sleeping too little generally decreases people's motivation to follow exercise regimens. In particular, recent results have shown that short-term sleep restriction (2 nights of 4 h in bed) was accompanied by a decrease in daytime spontaneous physical activity in healthy men.⁴ Interestingly, the reduction in overall physical activity was explained by a shift toward less intense activities under free-living conditions. Reductions in involuntary physical activity (also called non-exercise activity thermogenesis, or NEAT) may be another mechanism by which lack of sleep influences energy expenditure. However, more research using objective physical activity monitoring to track NEAT levels in relation to lack of sleep is needed in order to improve our understanding of the contribution of this energy expenditure component.

On the other side of the energy balance equation, increased energy intake appears to be the most plausible explanation as to why short sleepers have a higher risk of becoming obese. Firstly, short sleep duration might increase the risk of weight gain by preventing the restoration of a hormonal profile facilitating appetite control (homeostatic regulation of feeding). Indeed, lack of sleep has been reported to decrease leptin levels, increase ghrelin levels, alter glucose homeostasis, and activate the orexin system.⁵ Secondly, lack of sleep could also lead to weight gain and obesity by increasing the time available for eating and by making the maintenance of a healthy lifestyle more difficult. In an environment where food is highly palatable and readily available, caloric intake may be directly proportional to the time spent awake, especially if most of waking hours are spent in sedentary activities, such as watching television, where snacking is common. This concept is supported by recent data showing that recurrent bedtime restriction under free-living conditions did not down-regulate the satiety hormone leptin nor up-regulate the appetite-stimulating hormone ghrelin, but increased intake of calories from snacks, which suggests hedonic rather than homeostatic mediators of the shift in food selection.⁶ Likewise, results from another study have shown that habitual short sleepers (average of 6 h/night) ate more often (i.e., > 3 meals/day, with more frequent nibbling) than did long sleepers.⁷ Hence, the hedonic value of food intake might play a crucial role in the short sleep-obesity link.

The cross-sectional study of Weiss and colleagues in this issue of SLEEP provides further evidence to support the theory of the hedonic value of food intake associated with short sleep duration.⁸ Indeed, the authors observe that shorter sleep duration in adolescents was associated with a relatively higher caloric intake derived from fat and a lower caloric intake from carbohydrates. Additionally, shorter sleep duration was associated with a 2-fold increased risk of consuming ≥ 475 kcal/day from snacks in unadjusted analyses. As highlighted by the authors, increased snacking and consumption of high energy foods may reflect effects of short sleep duration on stress responses and reward seeking behaviors. Strengths of this study include (i) the use of an objective measure of sleep duration (wrist actigraphy); (ii) the quantitative measures of macronutrient intake (multiple-pass 24-h food recalls); and (iii) the free-living environment.

An important target of future studies should be the non-homeostatic, reward-driven feeding behavior that could be affected by short sleep duration. Because bedtime restriction inevitably results in more extended exposure to readily available, energy-dense, palatable foods, the regulation of energy balance can be easily compromised in such circumstances. In particular, the advent of functional magnetic resonance imaging is likely to be instrumental in documenting food-related reward activation in the brain after sleep restriction.⁹ Interestingly, a recent study in adolescents reports that impaired sleep was associated with less reactivity of reward-related brain systems, suggesting that more exciting rewards are required to create the same level of neural activation.¹⁰ Because the orexin system is a critical regulator of sleep/wake states, and of feeding behavior and reward processes, it is a potentially important therapeutic target for the treatment of obesity.¹¹

Recent research and the mounting body of evidence regarding the health-related effects of short sleep duration remind us that sleep is not a waste of time and that voluntary sleep restriction can impact our health in various ways. Furthermore, the study of appetite control in our modern world reminds us that our quest for reward and pleasure is not finely tuned to our biology.^12,13 With modern sedentary activities (e.g., television viewing, video game playing, cognitive working, listening to music), promoting overconsumption of food “in the absence of hunger,”¹⁴ a better understanding of these environmental stimuli is needed if we are to develop behavioral strategies to cope with them effectively.

DISCLOSURE STATEMENT

Dr. Chaput has indicated no financial conflicts of interest.