BackgroundEvidence suggests that short sleep duration may be a newly identified modifiable risk factor for obesity, yet there is a paucity of studies to investigate this.ObjectiveWe assessed the feasibility of a personalized sleep extension protocol in adults aged 18–64 y who are habitually short sleepers (5 to <7 h), with sleep primarily measured by wrist actigraphy. In addition, we collected pilot data to assess the effects of extended sleep on dietary intake and quality measured by 7-d food diaries, resting and total energy expenditure, physical activity, and markers of cardiometabolic health.DesignForty-two normal-weight healthy participants who were habitually short sleepers completed this free-living, 4-wk, parallel-design randomized controlled trial. The sleep extension group (n = 21) received a behavioral consultation session targeting sleep hygiene. The control group (n = 21) maintained habitual short sleep.ResultsRates of participation, attrition, and compliance were 100%, 6.5%, and 85.7%, respectively. The sleep extension group significantly increased time in bed [0:55 hours:minutes (h:mm); 95% CI: 0:37, 1:12 h:mm], sleep period (0:47 h:mm; 95% CI: 0:29, 1:05 h:mm), and sleep duration (0:21 h:mm; 95% CI: 0:06, 0:36 h:mm) compared with the control group. Sleep extension led to reduced intake of free sugars (–9.6 g; 95% CI: –16.0, –3.1 g) compared with control (0.7 g; 95% CI: –5.7, 7.2 g) (P = 0.042). A sensitivity analysis in plausible reporters showed that the sleep extension group reduced intakes of fat (percentage), carbohydrates (grams), and free sugars (grams) in comparison to the control group. There were no significant differences between groups in markers of energy balance or cardiometabolic health.ConclusionsWe showed the feasibility of extending sleep in adult short sleepers. Sleep extension led to reduced free sugar intakes and may be a viable strategy to facilitate limiting excessive consumption of free sugars in an obesity-promoting environment. This trial was registered at www.clinicaltrials.gov as NCT02787577.

The pooled effects of the studies with extractable data indicated that PSD resulted in increased EI with no effect on EE, leading to a net positive energy balance, which in the long term may contribute to weight gain.

The rise in the prevalence of obesity has been paralleled with a decline in sleep duration over the past century 1 . Disrupted sleeping patterns are emerging as a new and potentially important risk factor for obesity 2 . Short sleep duration and poor sleep quality have been associated with increased food intake and poorer diet quality 3 . However, the association between sleep and nutritional status remains underexplored. This study aimed to investigate the relationship between sleep duration and nutritional status in 2075 participants of the cross-sectional National Diet and Nutrition Survey Rolling Programme (NDNS-RP) (2008-2012) aged 18 years and over 4 . Sleep duration was categorized into short (⩽6 h), normal (7-8 h), and long (⩾9 h). Dietary intake was assessed using 4-day estimated food diaries and nutritional status was assessed using biomarkers in fasting blood samples and/or 24HR urine. Differences between the sleep categories were analysed using ANCOVA adjusting for sex, age and energy intake. Results showed that energy intake was significantly higher amongst normal sleepers (1742 ± 520kcal) compared to short (1677 ± 569kcal) or long sleepers (1583 ± 448kcal). Normal sleep was also associated with higher fibre intake (p < 0·001), higher vitamin C intake (p = 0·04) and higher iron intake (p < 0·001) compared to short or long sleep. Data from the nutritional biomarkers showed that normal sleepers tended to have higher total plasma carotenoids levels (p < 0·001), plasma selenium (p = 0·01) and urinary nitrogen levels (p = 0·03) compared to short or long sleepers. No associations were found for plasma ferritin (p = 0·59), vitamin B1 (p = 0·31), vitamin B2 (p = 0·95), vitamin B6 (p = 0·07), retinol (p = 0·42), 25-hydroxy-vitamin-D (p = 0·35), vitamin C (p = 0·09), alpha-tocopherol (p = 0·60), zinc (p = 0·15) nor urinary sodium (p = 0·19) or potassium (p = 0·15).In conclusion, normal sleepers tended to have a marginally different dietary intake pattern as well as some differences in nutritional status compared to short or long sleepers. Our group is currently undertaking more in-depth analysis of the NDNS sleep data and dietary intake.

Short sleep duration (⩽5-6 h/night) has been associated with an increased risk of weight gain (1,2) and non-communicable disease (3). Recently, through a systematic review and meta-analysis, we identified that short sleep duration may induce positive energy balance and have implications on weight gain over the long term (Al Khatib et al, unpublished data). Quality of sleep, opposed to its duration, has not been extensively reported in the context of the impact on disease risk. While self-reported measures of sleep quality have been linked to markers of adiposity and insulin resistance (4), there are no reports of objective measures of sleep quality in free-living conditions and cardio-metabolic disease risk. The Sleep-E Study is an on-going, cross-sectional study assessing associations between objective measures of sleep and cardio-metabolic risk factors in healthy adults, aged 18-55 years (N = 29; 12M/17 F). It is being conducted in accordance with the Declaration of Helsinki. Sleep parameters were assessed using the MotionWatch8 (CamNtech Ltd, Cambridge, UK) for six continuous nights, using sleep latency (time taken to transition from wakefulness to sleep) and sleep efficiency (actual sleep time expressed as a percentage of time in bed) as indicators of sleep quality. Fasting blood samples, blood pressure and anthropometric measurements were taken on study day 1. Correlations between sleep quality indicators and cardiometabolic risk factors, adjusted for age, sex and BMI, were investigated.These data show a strong negative correlation between sleep efficiency and TG concentrations and a moderate positive correlation with TC:HDL ratios. Similarly, sleep latency was moderately and positively correlated with both triglyceride concentrations and TC: HDL ratios. Sleep duration did not correlate with any risk factors. This cross-sectional data suggests that compromised sleep quality is linked to lipid metabolism. Sleep quality, independent of sleep duration, may be a potential, novel target for cardio-metabolic disease prevention. This cross-sectional study demonstrates the need for intervention studies assessing the relationship between sleep quality and cardio-metabolic risk.

Sleep is an unquestionable contributor to optimal health. The current guidelines for adults aged 18-64 years recommend 7-9 hours of sleep per night for physical and mental well-being (1) . Present patterns of sleep duration diverge from these recommendations due to lifestyle demands of the modern society (2) . The reduction in sleep duration has been paralleled by the increased prevalence in obesity and metabolic diseases over the past decades (3) . Intervention studies have demonstrated sleep deprivation may causally induce metabolic dysregulation (4) and positive energy balance (5) , driving the incidence of obesity and metabolic diseases. However, few studies have examined sleep's putative therapeutic impacts.To the best of our knowledge, this is one of the first randomised controlled trials (RCT) in healthy, free-living non-obese adults to attempt to lengthen sleep over an extended period, and uses objective measures of sleep to confirm compliance. In a parallel design, we investigated the feasibility of extending sleep using behavioural change techniques targeting sleep hygiene over a four week intervention period in habitually short sleepers (5−<7 hours/night) (Trial Registration: NCT02787577). The intervention group received a personalised sleep hygiene consultation session to extend their time in bed by 1-1·5 hours, and the control group were asked to resume their lifestyle as normal. Eligible participants were healthy men and women, aged 18-64 years, and were screened for sleep disorders and risk of low mood. The control and intervention groups were matched for age, sex, BMI and ethnicity by randomising with minimisation. Objective measures of sleep using 7-day wrist actigraphy (MotionWatch8, CamNtech Ltd, Cambridge, UK) were recorded at baseline and endpoint. We also collected pilot data to investigate possible effects on components of energy balance and metabolic risk indicators and to provide data for calculating the required sample size for a full trial in the future, including 7-day food diaries, energy expenditure, anthropometric measures, fasting blood samples, and blood pressure. A total of 43 participants (control n = 21, intervention n = 22) completed the study.All measures of sleep duration increased in the intervention group in comparison to the control group, confirming the efficacy of the behavioural change intervention strategy. We found no significant difference in all indicators of healthy lifestyle measures obtained. However, we found trends toward reduced carbohydrate (Mean Δ −19·5 g, 95 %CI 3·5, −42·0, P = 0·09) and free sugars intakes (Mean Δ −6·8 g, 95 %CI −14·9, 1·3, P = 0·06) in the intervention group compared to control. This feasibility study was likely to be statistically underpowered to detect differences in reported dietary intakes but data will be used to plan a larger fully powered trial using this behavioural sleep strategy to investigate the impact of sleep on free-living dietary intake. Current recommendations for weight and metabolic disease management may benefit from...