J Sleep Res. (2016) 25, 379–380
Editorial
Sleep, rhythms and metabolism: too many links to be ignored One view of the sleep–wake cycle is that it represents an alternation between episodes of feeding and fasting. Indeed, we do not eat when we sleep; and when sleep is restricted, appetite increases and hormones such as ghrelin and leptin are altered (e.g. Van Cauter et al., 2008). Epidemiological studies have provided evidence for associations between selfreported sleep duration and obesity as well as the risk of type 2 diabetes (e.g. Fatima et al., 2015). Circadian rhythms can also be viewed as cycles of positive and negative energy balance. The circadian rhythm of ‘opening’ and ‘closing’ of the leaves of Mimos pudica, which persists in constant darkness as first described by JeanJacques de Mairan in 1729, parallels the cycle of photosynthesis and respiration in the light period and respiration only during darkness. Alterations in the genes generating circadian rhythmicity lead to metabolic phenotypes and circadian rhythms and metabolism are intertwined at the molecular level (Marcheva et al., 2013). Recent reports have emphasized that alteration of the timing of sleep relative to circadian rhythms is associated with metabolic risk factors (e.g. Wong et al., 2015). Several papers in the current issue of the Journal of Sleep Research provide new insights into the associations between sleep and aspects of metabolism. SLEEP AND DIETARY INTAKE IN ROTTERDAM One well-recognized limitation of the vast majority of epidemiological studies linking sleep and metabolic phenotypes is the reliance upon self-reported sleep duration. Another limitation of many epidemiological studies is that most do not collect information on diet and food intake, and it is therefore difficult to ascertain whether association between sleep and metabolic parameters are mediated by changes in energy intake or expenditure. The obvious remedy for these limitations is to collect objective measures of sleep and quantify diary intake (Dashti et al., 2016). In this study, data on actigraphically quantified sleep, subject reports on sleep duration and energy and macronutrients intake were collected from 439 participants with an average age of 56 [standard deviation (SD) 5.4] years. Several results of interest were reported. For example, the concordance between self-reported and actigraphically determined sleep duration was somewhat low. In accordance with previous reports, actigraphically recorded sleep duration was shorter than self-reported sleep duration, and very short sleep (
Editorial
Sleep, rhythms and metabolism: too many links to be ignored One view of the sleep–wake cycle is that it represents an alternation between episodes of feeding and fasting. Indeed, we do not eat when we sleep; and when sleep is restricted, appetite increases and hormones such as ghrelin and leptin are altered (e.g. Van Cauter et al., 2008). Epidemiological studies have provided evidence for associations between selfreported sleep duration and obesity as well as the risk of type 2 diabetes (e.g. Fatima et al., 2015). Circadian rhythms can also be viewed as cycles of positive and negative energy balance. The circadian rhythm of ‘opening’ and ‘closing’ of the leaves of Mimos pudica, which persists in constant darkness as first described by JeanJacques de Mairan in 1729, parallels the cycle of photosynthesis and respiration in the light period and respiration only during darkness. Alterations in the genes generating circadian rhythmicity lead to metabolic phenotypes and circadian rhythms and metabolism are intertwined at the molecular level (Marcheva et al., 2013). Recent reports have emphasized that alteration of the timing of sleep relative to circadian rhythms is associated with metabolic risk factors (e.g. Wong et al., 2015). Several papers in the current issue of the Journal of Sleep Research provide new insights into the associations between sleep and aspects of metabolism. SLEEP AND DIETARY INTAKE IN ROTTERDAM One well-recognized limitation of the vast majority of epidemiological studies linking sleep and metabolic phenotypes is the reliance upon self-reported sleep duration. Another limitation of many epidemiological studies is that most do not collect information on diet and food intake, and it is therefore difficult to ascertain whether association between sleep and metabolic parameters are mediated by changes in energy intake or expenditure. The obvious remedy for these limitations is to collect objective measures of sleep and quantify diary intake (Dashti et al., 2016). In this study, data on actigraphically quantified sleep, subject reports on sleep duration and energy and macronutrients intake were collected from 439 participants with an average age of 56 [standard deviation (SD) 5.4] years. Several results of interest were reported. For example, the concordance between self-reported and actigraphically determined sleep duration was somewhat low. In accordance with previous reports, actigraphically recorded sleep duration was shorter than self-reported sleep duration, and very short sleep (
