Background: Recent epidemiologic studies have found that self-reported duration of sleep is associated with obesity, diabetes, hypertension, and mortality. The extent to which self reports of sleep duration are similar to objective measures and whether individual characteristics influence the degree of similarity are not known. Methods: Eligible participants at the Chicago site of the Coronary Artery Risk Development in Young Adults Study were invited to participate in a 2003–2005 ancillary sleep study; 82% (n = 669) agreed. Sleep measurements collected in 2 waves included 3 days each of wrist actigraphy, a sleep log, and questions about usual sleep duration. We estimate the average difference and correlation between subjectively and objectively measured sleep by using errors-in-variables regression models. Results: Average measured sleep was 6 hours, whereas the average from subjective reports was 6.8 hours. Subjective reports increased on average by 34 minutes for each additional hour of measured sleep. Overall, the correlation between reported and measured sleep duration was 0.47. Our model suggests that persons sleeping 5 hours over-reported their sleep duration by 1.2 hours, and those sleeping 7 hours over-reported by 0.4 hours. The correlations and average differences between self-reports and measured sleep varied by health, sociodemographic, and sleep characteristics. Conclusion: In a population-based sample of middle-aged adults, subjective reports of habitual sleep are moderately correlated with actigraph-measured sleep, but are biased by systematic over-reporting. The true associations between sleep duration and health may differ from previously reported associations between self-reported sleep and health.

Chronic sleep loss as a consequence of voluntary bedtime restriction is an endemic condition in modern society. Although sleep exerts marked modulatory effects on glucose metabolism, and molecular mechanisms for the interaction between sleeping and feeding have been documented, the potential impact of recurrent sleep curtailment on the risk for diabetes and obesity has only recently been investigated. In laboratory studies of healthy young adults submitted to recurrent partial sleep restriction, marked alterations in glucose metabolism including decreased glucose tolerance and insulin sensitivity have been demonstrated. The neuroendocrine regulation of appetite was also affected as the levels of the anorexigenic hormone leptin were decreased, whereas the levels of the orexigenic factor ghrelin were increased. Importantly, these neuroendocrine abnormalities were correlated with increased hunger and appetite, which may lead to overeating and weight gain. Consistent with these laboratory findings, a growing body of epidemiological evidence supports an association between short sleep duration and the risk for obesity and diabetes. Chronic sleep loss may also be the consequence of pathological conditions such as sleep-disordered breathing. In this increasingly prevalent syndrome, a feedforward cascade of negative events generated by sleep loss, sleep fragmentation, and hypoxia are likely to exacerbate the severity of metabolic disturbances. In conclusion, chronic sleep loss, behavioral or sleep disorder related, may represent a novel risk factor for weight gain, insulin resistance, and Type 2 diabetes.

Chronic partial sleep loss due to bedtime restriction and sleep complaints are increasingly prevalent in modern society. During the past few years, evidence from laboratory and epidemiologic studies has accumulated, suggesting that decreased sleep duration and/or quality may adversely effect glucose regulation and increase the risk of type 2 diabetes mellitus.

Despite mounting evidence that sleep duration is a risk factor across diverse health and functional domains, little is known about the distribution and determinants of sleep. In 2003–2004, the authors used wrist activity monitoring and sleep logs to measure time in bed, sleep latency (time required to fall asleep), sleep duration, and sleep efficiency (percentage of time in bed spent sleeping) over 3 days for 669 participants at one of the four sites of the Coronary Artery Risk Development in Young Adults (CARDIA) study (Chicago, Illinois). Participants were aged 38–50 years, 58% were women, and 44% were Black. For the entire sample, mean time in bed was 7.5 (standard deviation (SD), 1.2) hours, mean sleep latency was 21.9 (SD, 29.0) minutes, mean sleep duration was 6.1 (SD, 1.2) hours, and mean sleep efficiency was 80.9 (SD, 11.3)%. All four parameters varied by race-sex group. Average sleep duration was 6.7 hours for White women, 6.1 hours for White men, 5.9 hours for Black women, and 5.1 hours for Black men. Race-sex differences (p < 0.001) remained after adjustment for socioeconomic, employment, household, and lifestyle factors and for apnea risk. Income was independently associated with sleep latency and efficiency. Sleep duration and quality, which have consequences for health, are strongly associated with race, sex, and socioeconomic status.