Kristen L. Knutson

Self-reported and measured sleep duration: how similar are they?

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.Recent epidemiologic studies have found that sleep duration is associated with obesity, diabetes, hypertension and mortality. These studies have used self-reported habitual sleep duration, which has not been well validated. We model the extent to which self-reported habitual sleep reflects average objectively measured sleep. Eligible participants at the Chicago site of Coronary Artery Risk Development in Young Adults Study were invited to participate in a 2003-2004 ancillary sleep study; 82% (n=669) agreed. Sleep measurements collected in two waves included: 3-days of wrist actigraphy, a sleep log, and standard questions about usual sleep duration. Average measured sleep was 6 hours, and subjective reports averaged 0.80 hours longer than measured sleep. Subjective reports were not well calibrated, increasing on average by 31 minutes for each additional hour of measured sleep. Our model suggests that persons sleeping 5 and 7 hours over-reported, on average, by 1.3 and 0.3 hours respectively. Overall, there was a correlation of 0.45 between reported and measured sleep duration. The extent of overestimation, calibration and correlation varied by personal and sleep characteristics. Although asking about sleep duration seems uncomplicated, the correlation between self-reported and objectively-measured sleep in this population was moderate and systematically biased.

Associations between sleep loss and increased risk of obesity and diabetes.

During the past few decades, sleep curtailment has become a very common in industrialized countries. This trend for shorter sleep duration has developed over the same time period as the dramatic increase in the prevalence of obesity and diabetes. Evidence is rapidly accumulating to indicate that chronic partial sleep loss may increase the risk of obesity and diabetes. Laboratory studies in healthy volunteers have shown that experimental sleep restriction is associated with an adverse impact on glucose homeostasis. Insulin sensitivity decreases rapidly and markedly without adequate compensation in beta cell function, resulting in an elevated risk of diabetes. Prospective epidemiologic studies in both children and adults are consistent with a causative role of short sleep in the increased risk of diabetes. Sleep curtailment is also associated with a dysregulation of the neuroendocrine control of appetite, with a reduction of the satiety factor, leptin, and an increase in the hunger‐promoting hormone, ghrelin. Thus, sleep loss may alter the ability of leptin and ghrelin to accurately signal caloric need, acting in concert to produce an internal misperception of insufficient energy availability. The adverse impact of sleep deprivation on appetite regulation is likely to be driven by increased activity in neuronal populations expressing the excitatory peptides orexins that promote both waking and feeding. Consistent with the laboratory evidence, multiple epidemiologic studies have shown an association between short sleep and higher body mass index after controlling for a variety of possible confounders.

Sleep and the epidemic of obesity in children and adults

Sleep is an important modulator of neuroendocrine function and glucose metabolism in children as well as in adults. In recent years, sleep curtailment has become a hallmark of modern society with both children and adults having shorter bedtimes than a few decades ago. This trend for shorter sleep duration has developed over the same time period as the dramatic increase in the prevalence of obesity. There is rapidly accumulating evidence from both laboratory and epidemiological studies to indicate that chronic partial sleep loss may increase the risk of obesity and weight gain. The present article reviews laboratory evidence indicating that sleep curtailment in young adults results in a constellation of metabolic and endocrine alterations, including decreased glucose tolerance, decreased insulin sensitivity, elevated sympathovagal balance, increased evening concentrations of cortisol, increased levels of ghrelin, decreased levels of leptin, and increased hunger and appetite. We also review cross-sectional epidemiological studies associating short sleep with increased body mass index and prospective epidemiological studies that have shown an increased risk of weight gain and obesity in children and young adults who are short sleepers. Altogether, the evidence points to a possible role of decreased sleep duration in the current epidemic of obesity.

Sleep duration and cardiometabolic risk: a review of the epidemiologic evidence.

Laboratory studies have found that short-term sleep restriction is associated with impairments in glucose metabolism, appetite regulation and blood pressure regulation. This chapter reviews the epidemiologic evidence for an association between habitual sleep duration and quality and risk of cardiometabolic diseases including obesity, diabetes and hypertension. Multiple studies observed a cross-sectional association between short sleep duration (generally <6 h per night) and increased body mass index or obesity, prevalent diabetes and prevalent hypertension. Many studies also reported an association between self-reported long sleep duration (generally >8 h per night) and cardiometabolic disease. There have been a few prospective studies and several, but not all, have found an association between short sleep and incident diabetes, hypertension and markers of cardiovascular disease. Future prospective epidemiologic studies need to include objective measures of sleep, and intervention studies are needed in order to establish a causal link between impaired or insufficient sleep and cardiometabolic disease risk.

Impact of Sleep and Sleep Loss on Neuroendocrine and Metabolic Function

Background: Sleep exerts important modulatory effects on neuroendocrine function and glucose regulation. During the past few decades, sleep curtailment has become a very common behavior in industrialized countries. This trend toward shorter sleep times has occurred over the same time period as the dramatic increases in the prevalence of obesity and diabetes. Aims: This article will review rapidly accumulating laboratory and epidemiologic evidence indicating that chronic partial sleep loss could play a role in the current epidemics of obesity and diabetes. Conclusions: Laboratory studies in healthy young volunteers have shown that experimental sleep restriction is associated with a dysregulation of the neuroendocrine control of appetite consistent with increased hunger and with alterations in parameters of glucose tolerance suggestive of an increased risk of diabetes. Epidemiologic findings in both children and adults are consistent with the laboratory data.

Short sleep duration and incident coronary artery calcification

CONTEXT Coronary artery calcification is a subclinical predictor of coronary heart disease. Recent studies have found that sleep duration is correlated with established risk factors for calcification including glucose regulation, blood pressure, sex, age, education, and body mass index. OBJECTIVE To determine whether objective and subjective measures of sleep duration and quality are associated with incidence of calcification over 5 years and whether calcification risk factors mediate the association. DESIGN, SETTING, AND PARTICIPANTS Observational cohort of home monitoring in a healthy middle-aged population of 495 participants from the Coronary Artery Risk Development in Young Adults (CARDIA) cohort Chicago site (black and white men and women aged 35-47 years at year 15 of the study in 2000-2001 with follow-up data at year 20 in 2005-2006). Potential confounders (age, sex, race, education, apnea risk, smoking status) and mediators (lipids, blood pressure, body mass index, diabetes, inflammatory markers, alcohol consumption, depression, hostility, self-reported medical conditions) were measured at both baseline and follow-up. Sleep metrics (wrist actigraphy measured duration and fragmentation, daytime sleepiness, overall quality, self-reported duration) were examined for association with incident calcification. Participants had no detectable calcification at baseline. MAIN OUTCOME MEASURE Coronary artery calcification was measured by computed tomography in 2000-2001 and 2005-2006 and incidence of new calcification over that time was the primary outcome. RESULTS Five-year calcification incidence was 12.3% (n = 61). Longer measured sleep duration was significantly associated with reduced calcification incidence (adjusted odds ratio, 0.67 per hour [95% confidence interval, 0.49-0.91 per hour]; P = .01). No potential mediators appreciably altered the magnitude or significance of sleep (adjusted odds ratio estimates ranged from 0.64 to 0.68 per sleep hour; maximum P = .02). Alternative sleep metrics were not significantly associated with calcification. CONCLUSION Longer measured sleep is associated with lower calcification incidence independent of examined potential mediators and confounders.

Association between sleep and blood pressure in midlife: the CARDIA sleep study.

BACKGROUND Epidemiological studies have reported an association between self-reported short sleep duration and high blood pressure (BP). Our objective was to examine both cross-sectional and longitudinal associations between objectively measured sleep and BP. METHODS This study is ancillary to the Coronary Artery Risk Development in Young Adults (CARDIA) cohort study. Blood pressure was measured in 2000 and 2001 and in 2005 and 2006. Sleep was measured twice using wrist actigraphy for 3 consecutive days between 2003 and 2005. Sleep duration and sleep maintenance (a component of sleep quality) were calculated. Analyses included 578 African Americans and whites aged 33 to 45 years at baseline. Outcome measures were systolic BP (SBP) and diastolic BP (DBP) levels, 5-year change in BP, and incident hypertension. RESULTS After we excluded the patients who were taking antihypertensive medications and adjusted for age, race, and sex, shorter sleep duration and lower sleep maintenance predicted significantly higher SBP and DBP levels cross-sectionally as well as more adverse changes in SBP and DBP levels over 5 years (all P < .05). Short sleep duration also predicted significantly increased odds of incident hypertension (odds ratio, 1.37; 95% confidence interval, 1.05-1.78). Adjustment for 16 additional covariates, including snoring and daytime sleepiness, slightly attenuated the associations between sleep and BP. Sleep duration appeared to mediate the difference between African Americans and whites in DBP change over time (P = .02). CONCLUSION Reduced sleep duration and consolidation predicted higher BP levels and adverse changes in BP, suggesting the need for studies to investigate whether interventions to optimize sleep may reduce BP.

Cross-sectional and Longitudinal Associations Between Objectively Measured Sleep Duration and Body Mass Index The CARDIA Sleep Study

Numerous studies have found an association between shorter sleep duration and higher body mass index (BMI) in adults. Most previous studies have been cross-sectional and relied on self-reported sleep duration, which may not be very accurate. In the Coronary Artery Risk Development in Young Adults (CARDIA) Sleep Study (2000-2006), the authors examine whether objectively measured sleep is associated with BMI and change in BMI. They use several nights of wrist actigraphy to measure sleep among participants in an ongoing cohort of middle-aged adults. By use of linear regression, the authors examine whether average sleep duration or fragmentation is associated with BMI and 5-year change in BMI, adjusting for confounders. Among 612 participants, sleep duration averaged 6.1 hours and was grouped into 4 categories. Both shorter sleep and greater fragmentation were strongly associated with higher BMI in unadjusted cross-sectional analysis. After adjustment, BMI decreased by 0.78 kg/m(2) (95% confidence interval: -1.6, -0.002) for each increasing sleep category. The association was very strong in persons who reported snoring and weak in those who did not. There were no longitudinal associations between sleep measurements and change in BMI. The authors confirmed a cross-sectional association between sleep duration and BMI using objective sleep measures, but they did not find that sleep predicted change in BMI. The mechanism underlying the cross-sectional association is not clear.

Cross-Sectional Associations Between Measures of Sleep and Markers of Glucose Metabolism Among Subjects With and Without Diabetes: The Coronary Artery Risk Development in Young Adults (CARDIA) Sleep Study

OBJECTIVE To examine whether sleep duration and quality are associated with fasting glucose, fasting insulin, or estimated insulin resistance in a community-based sample of early middle-aged adults. RESEARCH DESIGN AND METHODS This was an ancillary study to the Coronary Artery Risk Development in Young Adults (CARDIA) Study. Habitual sleep duration and fragmentation were estimated from 6 days of wrist actigraphy collected in 2003–2005. Insomnia was defined as self-reported difficulty falling asleep or waking up in the night three or more times per week plus average sleep efficiency of <80% based on actigraphy. Fasting blood samples to measure glucose and insulin were collected after the sleep measures during the CARDIA clinical examination in 2005–2006. Insulin resistance was estimated using the homeostatic model assessment (HOMA) method. Analyses were cross-sectional and stratified by the presence of diabetes. RESULTS There was no association between sleep measures and fasting glucose, insulin, or HOMA in the 115 subjects without diabetes. Among the 40 subjects with diabetes, after adjustment for covariates, 10% higher sleep fragmentation was associated with a 9% higher fasting glucose level, a 30% higher fasting insulin level, and a 43% higher HOMA level. Insomnia was associated with a 23% higher fasting glucose level, a 48% higher fasting insulin level, and an 82% higher HOMA level. CONCLUSIONS The observed association between poor sleep quality and higher glucose, insulin, and estimated insulin resistance among subjects with diabetes warrants further examination of the effect of sleep disturbances on glucose control in type 2 diabetes.

Does inadequate sleep play a role in vulnerability to obesity

The prevalence of obesity is increasing rapidly worldwide, which is cause for concern because obesity increases the risk of cardiovascular disease and diabetes, reduces life expectancy, and impairs quality of life. A better understanding of the risk factors for obesity is therefore a critical global health concern, and human biologists can play an important role in identifying these risk factors in various populations. The objective of this review is to present the evidence that inadequate sleep may be a novel risk factor associated with increased vulnerability to obesity and associated cardiometabolic disease. Experimental studies have found that short‐term sleep restriction is associated with impaired glucose metabolism, dysregulation of appetite, and increased blood pressure. Observational studies have observed cross‐sectional associations between short sleep duration (generally <6 h per night) and increased body mass index or obesity, prevalent diabetes, and prevalent hypertension. Some studies also reported an association between self‐reported long sleep duration (generally >8 h per night) and cardiometabolic disease. A few prospective studies have found a significant increased risk of weight gain, incident diabetes, and incident hypertension associated with inadequate sleep. Given the potential link between inadequate sleep and obesity, a critical next step is to identify the social, cultural, and environmental determinants of sleep, which would help to identify vulnerable populations. Future human biology research should consider variation in sleep characteristics among different populations and determine whether the associations between sleep and obesity observed in Western populations persist elsewhere.