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Late, but Not Early, Night Sleep Loss Compromises Neuroendocrine Appetite Regulation and the Desire for Food.
Meyhöfer, S, Chamorro, R, Hallschmid, M, Spyra, D, Klinsmann, N, Schultes, B, Lehnert, H, Meyhöfer, SM, Wilms, B
Nutrients. 2023;15(9)
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Sleep loss has become common in modern societies. In parallel, the prevalence of obesity and metabolic comorbidities, such as type 2 diabetes, are rising worldwide. The aim of this study was to investigate the impact of the specific timing of sleep loss compared to regular sleep on appetite regulation and desire for foods. This study was a randomised, balanced, crossover design on three conditions spaced at least three and at maximum five weeks apart. Fifteen healthy young male participants were included. All participants had a regular sleep–wake cycle during the last four weeks before the experiments, with a minimum of 7 hours sleep per night. Results showed that ‘late-night sleep loss’, but not ‘early-night sleep loss’, elevated ghrelin concentrations, as well as feelings of hunger and appetite, and desire for food during the subsequent morning. Leptin concentrations were not affected by acute sleep loss per se, nor timing of sleep loss. Authors conclude that their findings could be of clinical interest to healthcare practitioners working with sleep deprived individuals, regarding sleep hygiene and appropriate sleep recommendations.
Abstract
OBJECTIVE There is evidence that reduced sleep duration increases hunger, appetite, and food intake, leading to metabolic diseases, such as type 2 diabetes and obesity. However, the impact of sleep timing, irrespective of its duration and on the regulation of hunger and appetite, is less clear. We aimed to evaluate the impact of sleep loss during the late vs. early part of the night on the regulation of hunger, appetite, and desire for food. METHODS Fifteen normal-weight ([mean ± SEM] body-mass index: 23.3 ± 0.4 kg/m2) healthy men were studied in a randomized, balanced, crossover design, including two conditions of sleep loss, i.e., 4 h sleep during the first night-half ('late-night sleep loss'), 4 h sleep during the second night-half ('early-night sleep loss'), and a control condition with 8h sleep ('regular sleep'), respectively. Feelings of hunger and appetite were assessed through visual analogue scales, and plasma ghrelin and leptin were measured from blood samples taken before, during, and after night-time sleep. RESULTS Ghrelin and feelings of hunger and appetite, as well as the desire for food, were increased after 'late-night sleep loss', but not 'early-night sleep loss', whereas leptin remained unaffected by the timing of sleep loss. CONCLUSIONS Our data indicate that timing of sleep restriction modulates the effects of acute sleep loss on ghrelin and appetite regulation in healthy men. 'Late-night sleep loss' might be a risk factor for metabolic diseases, such as obesity and type 2 diabetes. Thereby, our findings highlight the metabolic relevance of chronobiological sleep timing.
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Improving perinatal sleep via a scalable cognitive behavioural intervention: findings from a randomised controlled trial from pregnancy to 2 years postpartum.
Bei, B, Pinnington, DM, Quin, N, Shen, L, Blumfield, M, Wiley, JF, Drummond, SPA, Newman, LK, Manber, R
Psychological medicine. 2023;53(2):513-523
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Sleep disturbance is a universal experience during the pregnancy and postpartum periods. Sleep disturbance is linked to a range of negative consequences. Literature shows that cognitive behavioural Therapy for Insomnia (CBT-I) is an effective treatment, with comparable short-term and superior long-term effects to sleep medication alone. The aim of this study was to evaluate the short-, medium-, and long-term efficacy of a non-pharmacological sleep intervention in the perinatal periods. The study was a longitudinal randomised controlled trial based on the SEED (Sleep Eat Emotions and Development) project which was a two-arm, parallel-group, single-blind, superiority randomised controlled trial. Participants were pregnant women enrolled in Childbirth Education and were randomised 1:1 to the intervention or a comparison condition. Results showed that compared to receiving an attention- and time-matched control, receiving a cognitive behavioural sleep intervention was associated with lower symptoms of insomnia, sleep disturbance, and sleep-related impairment during late pregnancy. Moreover, the intervention had long-term benefits to gestational parents’ sleep at 2-year postpartum. Authors conclude that a scalable cognitive behavioural sleep intervention, tailored for the perinatal periods, is feasible, acceptable, and efficacious in buffering against the natural increase in sleep complaints during the 3rd trimester.
Abstract
BACKGROUND Sleep disturbance is common in gestational parents during pregnancy and postpartum periods. This study evaluated the feasibility and efficacy of a scalable cognitive behavioural therapy (CBT) sleep intervention tailored for these periods. METHODS This is a two-arm, parallel-group, single-blind, superiority randomised controlled trial. Nulliparous females without severe medical/psychiatric conditions were randomised 1:1 to CBT or attention- and time-matched control. All participants received a 1 h telephone session and automated multimedia emails from the third trimester until 6 months postpartum. Outcomes were assessed with validated instruments at gestation weeks 30 (baseline) and 35 (pregnancy endpoint), and postpartum months 1.5, 3, 6 (postpartum endpoint), 12 and 24. RESULTS In total, 163 eligible participants (age M ± s.d. = 33.35 ± 3.42) were randomised. The CBT intervention was well accepted, with no reported adverse effect. Intention-to-treat analyses showed that compared to control, receiving CBT was associated with lower insomnia severity and sleep disturbance (two primary outcomes), and lower sleep-related impairment at the pregnancy endpoint (p values ⩽ 0.001), as well as at 24 months postpartum (p ranges 0.012-0.052). Group differences across the first postpartum year were non-significant. Participants with elevated insomnia symptoms at baseline benefitted substantially more from CBT (v. control), including having significantly lower insomnia symptoms throughout the first postpartum year. Group differences in symptoms of depression or anxiety were non-significant. CONCLUSIONS A scalable CBT sleep intervention is efficacious in buffering against sleep disturbance during pregnancy and benefitted sleep at 2-year postpartum, especially for individuals with insomnia symptoms during pregnancy. The intervention holds promise for implementation into routine perinatal care.
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Resistance Training Improves Sleep and Anti-Inflammatory Parameters in Sarcopenic Older Adults: A Randomized Controlled Trial.
de Sá Souza, H, de Melo, CM, Piovezan, RD, Miranda, REEPC, Carneiro-Junior, MA, Silva, BM, Thomatieli-Santos, RV, Tufik, S, Poyares, D, D'Almeida, V
International journal of environmental research and public health. 2022;19(23)
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Sleep is a behavioural state that is characterised by relative immobility and reduced responsiveness and can be distinguished from coma or anaesthesia by its rapid reversibility. Sleep has a number of functions, which include metabolism modulation and the repair of organic tissue. The aim of this study was to investigate the effects of a 12-week resistance exercise training (RET) protocol on subjective and objective sleep parameters in older individuals with sarcopenia and the possible role of inflammation status in this process. This study was a randomised, placebo-controlled, parallel-group study. Participants were randomly assigned to one of the two groups; RET group or control group. Results showed that a 12-week RET protocol simultaneously improved muscle strength. In addition to the increase in overall subjective sleep quality, there was also a reduction in sleep latency, apnoea-hypopnea index, and insomnia severity, as well as an increase in deeper stage 3 sleep (slow-wave sleep) in the RET group in comparison with the CTL group. Authors conclude that future studies are necessary to elucidate how different age groups and genders, with and without sarcopenia, can present specific muscle and sleep responses to potentially anti-inflammatory interventions, such as physical exercise.
Abstract
Sleep and exercise have an important role in the development of several inflammation-related diseases, including sarcopenia. Objective: To investigate the effects of 12 weeks of resistance exercise training on sleep and inflammatory status in sarcopenic patients. Methods: A randomized controlled trial comparing resistance exercise training (RET) with a control (CTL) was conducted. Outcomes were obtained by physical tests, polysomnography, questionnaires, isokinetic/isometric dynamometry tests, and biochemical analysis. Results: Time to sleep onset (sleep latency) was reduced in the RET group compared to the CTL group (16.09 ± 15.21 vs. 29.98 ± 16.09 min; p = 0.04) after the intervention. The percentage of slow-wave sleep (N3 sleep) was increased in the RET group (0.70%, CI: 7.27−16.16 vs. −4.90%, CI: 7.06−16.70; p = 0.04) in an intention to treat analysis. Apnea/hour was reduced in the RET group (16.82 ± 14.11 vs. 7.37 ± 7.55; p = 0.001) and subjective sleep quality was improved compared to the CTL (−1.50; CI: 2.76−6.14 vs. 0.00; CI: 1.67−3.84 p = 0.02) in an intention-to-treat analysis. Levels of interleukin-10 (IL-10) (2.13 ± 0.80 vs. 2.51 ± 0.99; p < 0.03) and interleukin-1 receptor antagonist (IL-1ra) (0.99 ± 0.10 vs. 0.99 ± 0.10 ng/mL; p < 0.04; delta variation) were increased in the RET group. Conclusions: RET improves sleep parameters linked to muscle performance, possibly due to an increase in anti-inflammatory markers in older sarcopenic patients.
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Association between Sleep Disturbances and Liver Status in Obese Subjects with Nonalcoholic Fatty Liver Disease: A Comparison with Healthy Controls.
Marin-Alejandre, BA, Abete, I, Cantero, I, Riezu-Boj, JI, Milagro, FI, Monreal, JI, Elorz, M, Herrero, JI, Benito-Boillos, A, Quiroga, J, et al
Nutrients. 2019;11(2)
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Inadequate sleep has been associated with poor health outcomes such as obesity and type 2 diabetes. The relevance of sleep patterns in the onset or progression of non-alcoholic fatty liver disease (NAFLD) is poorly understood. The aim of this cross-sectional study was to investigate the association between sleep characteristics and liver health in obese people with NAFLD compared to normal weight people without NAFLD. 94 overweight or obese patients with NAFLD and 40 normal weight people without NAFLD were enrolled in the study. Measures of liver health such as liver stiffness and levels of liver enzymes were assessed, along with sleep features evaluated using a Sleep Quality Index (SQI). A higher prevalence of short sleep duration and poor sleep quality were found in people with NAFLD. Sleep disturbance or sleep quality predicted up to 20.3% and 20.4% of the variability of liver stiffness, respectively, after adjusting for other factors. The authors of the study suggest that sleep disruption may be contributing to the development of NAFLD, and/or the alteration of the liver may be affecting sleep patterns. Consequently, sleep may be a modifiable behaviour to consider in the prevention and management of NAFLD.
Abstract
The relevance of sleep patterns in the onset or evolution of nonalcoholic fatty liver disease (NAFLD) is still poorly understood. Our aim was to investigate the association between sleep characteristics and hepatic status indicators in obese people with NAFLD compared to normal weight non-NAFLD controls. Ninety-four overweight or obese patients with NAFLD and 40 non-NAFLD normal weight controls assessed by abdominal ultrasonography were enrolled. Hepatic status evaluation considered liver stiffness determined by Acoustic Radiation Force Impulse elastography (ARFI) and transaminases. Additionally, anthropometric measurements, clinical characteristics, and biochemical profiles were determined. Sleep features were evaluated using the Pittsburgh Sleep Quality Index (PSQI). Hepatic status parameters, anthropometric measurements, and clinical and biochemical markers differed significantly in NAFLD subjects compared to controls, as well as sleep efficiency, sleep disturbance score, and sleep quality score. In the NAFLD group, a higher prevalence of short sleep duration (p = 0.005) and poor sleep quality (p = 0.041) were found. Multivariate-adjusted odds ratio (95% confidence interval) for NAFLD considering sleep disturbance was 1.59 (1.11⁻2.28). Regression models that included either sleep disturbance or sleep quality predicted up to 20.3% and 20.4% of the variability of liver stiffness, respectively, and after adjusting for potential confounders. Current findings suggest that sleep disruption may be contributing to the pathogenesis of NAFLD as well as the alteration of the liver may be affecting sleep patterns. Consequently, sleep characteristics may be added to the list of modifiable behaviors to consider in health promotion strategies and in the prevention and management of NAFLD.
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Bridging the Reciprocal Gap between Sleep and Fruit and Vegetable Consumption: A Review of the Evidence, Potential Mechanisms, Implications, and Directions for Future Work.
Noorwali, E, Hardie, L, Cade, J
Nutrients. 2019;11(6)
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Both sleep disruption and a low intake of fruit and vegetables (FV) are associated with higher rates of premature death and chronic disease. This review looked at previous studies in order to determine whether there is a link between sleep and FV consumption. A recent meta-analysis found that shorter sleep duration is consistently associated with low fruit and vegetable intake in children, but in adults the association is less clear. Studies looking at the effect of sleep on FV intake had variable results. Tart cherries and kiwi fruits were the most commonly studied fruits for their effect on sleep measures. Observational studies tended to find that both short- and long-sleepers tend to eat less FV than those that sleep for 7-8 hours. A lot of evidence shows that people who go to sleep later (‘owls’) tend to consume unhealthier diets with lower intakes of FV than people who go to bed earlier (‘larks’). The researchers also looked at potential mechanisms for the association between sleep and FV intake. Polyphenols in FV may influence sleep by increasing neurotransmitters via the gut-brain axis, improving energy metabolism and through alterations in circadian rhythms and the CLOCK genes. Ways in which disrupted sleep may affect FV consumption included changes in hunger hormones, emotional stress and impaired decision making. With further research, interactions between sleep measures and FV consumption may be clarified and potentially reduce the burden of chronic diseases and premature deaths.
Abstract
A substantial burden of disease and mortality globally is attributable to both sleep disruption and low intakes of fruit and vegetable (FV) and there is increasing mechanistic and epidemiological evidence to support a reciprocal relationship between the two. This review provides an overview of experimental and observational studies assessing the relations between sleep and FV consumption from 52 human adult studies. Experimental studies are currently limited and show inconsistent results. Observational studies support a non-linear association with adults sleeping the recommended 7-9 hours/day having the highest intakes of FV. The potential mechanisms linking sleep and FV consumption are highlighted. Disrupted sleep influences FV consumption through homeostatic and non-homeostatic mechanisms. Conversely, FV consumption may influence sleep through polyphenol content via several potential pathways. Few human experimental studies have examined the effects of FV items and their polyphenols on sleep and there is a need for more studies to address this. An appreciation of the relationship between sleep and FV consumption may help optimize sleep and FV consumption and may reduce the burden of chronic diseases. This review provides implications for public health and directions for future work.
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A systematic review and meta-analysis of cognitive and behavioral interventions to improve sleep health in adults without sleep disorders.
Murawski, B, Wade, L, Plotnikoff, RC, Lubans, DR, Duncan, MJ
Sleep medicine reviews. 2018;40:160-169
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Sleep is important for good health but more than a quarter of the adult population reports poor quality sleep. This review and meta-analysis looked at cognitive and behavioural interventions in adults who report poor sleep but are not diagnosed with a clinical sleep disorder. The most commonly used interventions were stress management/relaxation, meditation, controlled breathing and stimulus control. A meta-analysis showed a medium improvement of overall sleep quality and a small but significant improvement of subjective sleep quality and duration with cognitive and behavioural interventions. The effects were bigger when sleep at baseline was worse. Effects of mode of delivery, study duration and the inclusion of a relaxation component were not assessed, due to insufficient numbers. The authors conclude that there is room for improvements of cognitive and behavioural interventions and call for more investigations into this.
Abstract
Many adults without a diagnosed sleep disorder report poor sleep health, which is defined by dissatisfactory levels of sleep duration, sleep quality, or the timing of sleep. No previous review has summarized and described interventions targeting poor sleep health in this population. This meta-analysis aimed to quantify the efficacy of behavioral and cognitive sleep interventions in adults with poor sleep health, who do not have a sleep disorder. Electronic databases (Medline, Embase, PsycInfo, Cinahl) were searched with restrictions for age (18-64 y) and English language full-text, resulting in 18,009 records being screened and 592 full-texts being assessed. Eleven studies met inclusion criteria, seven of which reported a measure of overall sleep health (Pittsburgh sleep quality index [PSQI]). Following appraisal for risk of bias, extracted data were meta-analyzed using random-effects models. Meta-analyses showed interventions had a medium effect on sleep quality (Hedge's g = -0.54, [95% confidence interval (CI)] -0.90 to -0.19, p < 0.01). Baseline sleep health was the only significant effect moderator (p = 0.01). The most frequently used intervention components were stress management and relaxation practice, stimulus control, sleep hygiene, and exercise. Interventions targeting cognitive and behavioral self-regulation improve sleep quality in adults without clinical sleep disorder.
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Sleep restriction increases the neuronal response to unhealthy food in normal-weight individuals.
St-Onge, MP, Wolfe, S, Sy, M, Shechter, A, Hirsch, J
International journal of obesity (2005). 2014;38(3):411-6
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Sleep patterns influence eating behaviour and the body’s response to food. Previous studies suggest that short sleep duration leads to increased caloric intake and a desire for high-fat foods, however the specific neural mechanisms explaining how sleep restriction modulates this response is unknown. The aim of this study was to determine whether a specific area of the brain is activated in response to unhealthy compared with healthy foods. 25 participants were included, all of which were normal weight and had normal sleeping patterns. Each participant was tested after five nights of either 4 or 9 hours in bed by functional magnetic resonance imaging (fMRI). The test was performed while the participant was shown healthy and unhealthy food photos in the fasted state. This study found that after a period of restricted sleep compared with habitual sleep, unhealthy foods led to greater activation in brain regions associated with reward compared with healthy foods. This finding provides a model of neuronal mechanisms relating short sleep duration to obesity and cardio-metabolic risk factors and warrants further investigation.
Abstract
CONTEXT Sleep restriction alters responses to food. However, the underlying neural mechanisms for this effect are not well understood. OBJECTIVE The purpose of this study was to determine whether there is a neural system that is preferentially activated in response to unhealthy compared with healthy foods. PARTICIPANTS Twenty-five normal-weight individuals, who normally slept 7-9 h per night, completed both phases of this randomized controlled study. INTERVENTION Each participant was tested after a period of five nights of either 4 or 9 h in bed. Functional magnetic resonance imaging (fMRI) was performed in the fasted state, presenting healthy and unhealthy food stimuli and objects in a block design. Neuronal responses to unhealthy, relative to healthy food stimuli after each sleep period were assessed and compared. RESULTS After a period of restricted sleep, viewing unhealthy foods led to greater activation in the superior and middle temporal gyri, middle and superior frontal gyri, left inferior parietal lobule, orbitofrontal cortex, and right insula compared with healthy foods. These same stimuli presented after a period of habitual sleep did not produce marked activity patterns specific to unhealthy foods. Further, food intake during restricted sleep increased in association with a relative decrease in brain oxygenation level-dependent (BOLD) activity observed in the right insula. CONCLUSION This inverse relationship between insula activity and food intake and enhanced activation in brain reward and food-sensitive centers in response to unhealthy foods provides a model of neuronal mechanisms relating short sleep duration to obesity.
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Sleep restriction for 1 week reduces insulin sensitivity in healthy men.
Buxton, OM, Pavlova, M, Reid, EW, Wang, W, Simonson, DC, Adler, GK
Diabetes. 2010;59(9):2126-33
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Short sleep duration is associated with an increased risk of many chronic diseases including diabetes, however the effects of sleep restriction on insulin sensitivity have not yet been established. The aim of study was to assess the effects of decreased sleep duration on insulin sensitivity in a controlled environment. This 12-day inpatient study included 20 healthy men who were randmoised to receive a wakefulness-promoting drug, modafinil, or placebo during the sleep restriction phase. This study showed that sleep restriction for one week significantly reduces insulin sensitivity. These findings raise concerns about chronic insufficient sleep on the development of metabolic diseases and promote further research into these effects.
Abstract
OBJECTIVE Short sleep duration is associated with impaired glucose tolerance and an increased risk of diabetes. The effects of sleep restriction on insulin sensitivity have not been established. This study tests the hypothesis that decreasing nighttime sleep duration reduces insulin sensitivity and assesses the effects of a drug, modafinil, that increases alertness during wakefulness. RESEARCH DESIGN AND METHODS This 12-day inpatient General Clinical Research Center study included 20 healthy men (age 20-35 years and BMI 20-30 kg/m(2)). Subjects spent 10 h/night in bed for >or=8 nights including three inpatient nights (sleep-replete condition), followed by 5 h/night in bed for 7 nights (sleep-restricted condition). Subjects received 300 mg/day modafinil or placebo during sleep restriction. Diet and activity were controlled. On the last 2 days of each condition, we assessed glucose metabolism by intravenous glucose tolerance test (IVGTT) and euglycemic-hyperinsulinemic clamp. Salivary cortisol, 24-h urinary catecholamines, and neurobehavioral performance were measured. RESULTS IVGTT-derived insulin sensitivity was reduced by (means +/- SD) 20 +/- 24% after sleep restriction (P = 0.001), without significant alterations in the insulin secretory response. Similarly, insulin sensitivity assessed by clamp was reduced by 11 +/- 5.5% (P < 0.04) after sleep restriction. Glucose tolerance and the disposition index were reduced by sleep restriction. These outcomes were not affected by modafinil treatment. Changes in insulin sensitivity did not correlate with changes in salivary cortisol (increase of 51 +/- 8% with sleep restriction, P < 0.02), urinary catecholamines, or slow wave sleep. CONCLUSIONS Sleep restriction (5 h/night) for 1 week significantly reduces insulin sensitivity, raising concerns about effects of chronic insufficient sleep on disease processes associated with insulin resistance.