Sleep and Metabolic Fitness

The authors have indicated no financial conflicts of interest. WHO WOULD HAVE GUESSED IN 1988, WHEN REAVEN1 DESCRIBED THE CONCEPT OF SYNDROME X (SUBSEQUENTLY NAMED METABOLIC SYNDROME), THAT sleep would eventually be perceived as one of its main related environmental factors? Almost nobody, and this would have been understandable. Indeed, in a context where regular physical activity participation was already recognized as a key player in the prevention of the syndrome, it would have been difficult to anticipate that an increase of the most sedentary activity (i.e., sleep) would be a prerequisite to optimal metabolic fitness. The experimental evidence provided by Van Cauter's group2–4 can be viewed as a cornerstone in the global demonstration of a role of adequate sleep duration as a determinant of metabolic health. Specifically, partial sleep restriction tested in their laboratory decreased glucose tolerance, elevated cortisol concentrations, decreased the satiety hormone leptin, increased the appetite-stimulating hormone ghrelin, and increased hunger and appetite.2–4 In this issue of SLEEP, Gangwisch and colleagues5 contribute in an important manner to the proof of concept in this field. Their study, performed in a large sample of adolescents (n = 14,257) in the United States, showed that for each additional hour of sleep, a significant decrease is observed in the risk of being diagnosed with high cholesterol in young adulthood, particularly in females. In other words, short sleep durations in adolescence seem to leave a print that may increase the long-term predisposition to hypercholesterolemia. As mentioned by the authors, “interventions that lengthen sleep could potentially serve as treatments and as primary preventative measures for hypercholesterolemia.” This argument will however need to be supported by experimental evidence (the only method that can definitively prove causality), because the present observational study provides no insight into the putative underlying mechanistic relationship(s) between adolescent sleep duration and risk of hypercholesterolemia. Interestingly, a randomized clinical trial is currently under way to evaluate the efficacy of a behavioral intervention to extend sleep duration in obese short sleepers.6 Beyond the demonstration of the short sleep-hypercholesterolemia relationship, the study by Gangwisch et al.5 reminds us that there may be unintended consequences to our hectic lifestyle that values voluntary restriction of sleep. The National Sleep Foundation7 claims that sleep duration has decreased by more than one hour over the last few decades. Hopefully, the results of the Gangwisch et al.5 study could help in health education programs to promote a better sleep-related lifestyle in adolescents. After all, few would argue that the reduction of sleep time in adolescents is healthy, and therefore there is minimal risk in taking a pragmatic approach and encouraging a good night's sleep as an adjunct to other health promotion measures in teenagers.8–10

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