Sleep duration and metabolic syndrome

Extremes in duration of sleep have been associated with adverse health, specifically with the symptomatology characteristic of the metabolic syndrome. Body homeostasis and circadian rhythm are thought to interact and to influence energy metabolism. Environmental cues, such as time of year and amplitude of seasonal changes (changes in photoperiod length) influence both sleep behavior and energy metabolism, supporting a link between these two systems. However, little is known about the molecular mechanism underlying the relationships of sleep and the metabolic syndrome symptoms, or the sleep–circadian phenotypes per se. In genetic association studies on sleep duration (candidate clock genes approach and genome-wide association studies), we identified genes that are functionally involved in the development of the metabolic syndrome symptomatology. Although the relationship between sleep duration and body mass index may partly be caused by environmental influences such as voluntary sleep restriction and circadian misalignment, the association of sleep duration with genes related to metabolism indicates that genetic factors are central to it. In this article, the latest evidence of a gene–environment influence on the relationship of sleep duration with the metabolic syndrome symptomatology is discussed. Greater understanding of a common genetic pathway linking sleep duration to metabolic dysfunction, and the role of environment in the mediation of this relationship, will lead to the development of new guidelines for treatment of obesity, which is a major health issues in our society.