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Alternate-Day Fasting Combined with Exercise: Effect on Sleep in Adults with Obesity and NAFLD.
Ezpeleta, M, Gabel, K, Cienfuegos, S, Kalam, F, Lin, S, Pavlou, V, Varady, KA
Nutrients. 2023;15(6)
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Non-alcoholic fatty liver disease (NAFLD) is defined as the presence of 5% or more fat in the liver, confirmed by hepatic imaging or biopsy. Poor sleep may adversely affect insulin sensitivity and inflammatory status, thereby contributing to the development and progression of NAFLD. The aim of this study was to investigate how intermittent fasting combined with exercise impacts body weight and sleep measures in adults with NAFLD. This study was a secondary analysis of a 3-month randomised, controlled, parallel-arm study. Participants were randomized to 1 of 4 intervention groups: alternate-day fasting (ADF) plus exercise, ADF alone, exercise alone, or a no-intervention control group. Results showed that intermittent fasting combined with exercise produced significant reductions in body weight and intrahepatic triglyceride content but no changes in sleep quality, duration, insomnia severity, or risk of obstructive sleep apnoea. Authors conclude that the weight loss induced by ADF combined with exercise does not improve sleep quality, duration, insomnia severity or risk of obstructive sleep apnea in individuals with obesity and NAFLD.
Abstract
Objective: This study investigated how alternate-day fasting (ADF) combined with aerobic exercise impacts body weight and sleep in adults with non-alcoholic fatty liver disease (NAFLD). Methods: Adults with obesity and NAFLD (n = 80) were randomized into one of four groups for 3 months: combination of ADF (600 kcal "fast day," alternated with an ad libitum intake "feast day") and moderate-intensity aerobic exercise (five sessions per week, 60 min/session); ADF alone; exercise alone; or a no-intervention control group. Results: By month 3, body weight and intrahepatic triglyceride content decreased (p < 0.001, group × time interaction) in the combination group versus the exercise group and control group, but not versus the ADF group. Sleep quality, measured by the Pittsburgh Sleep Quality Inventory (PSQI), did not change in the combination group (baseline: 6.0 ± 0.7; month 3: 5.6 ± 0.7), ADF group (baseline: 8.9 ± 1.0; month 3: 7.5 ± 0.8), or exercise group (baseline: 6.4 ± 0.6; month 3: 6.7 ± 0.6), versus controls (baseline: 5.5 ± 0.7; month 3: 4.6 ± 0.5). Wake time, bedtime, sleep duration, and insomnia severity did not change (no group x time interaction) over the course of the study in any group. Risk for obstructive sleep apnea was present in 30% of combination subjects, 75% of ADF subjects, 40% of exercise subjects, and 75% of controls, and did not change in the intervention groups, versus controls, by month 3. No associations were observed between changes in body weight, intrahepatic triglyceride content, and any sleep outcome. Conclusions: The weight loss induced by ADF combined with exercise does not improve sleep quality, duration, insomnia severity, or risk of obstructive sleep apnea in individuals with NAFLD.
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Insufficient sleep predicts poor weight loss maintenance after 1 year.
Bogh, AF, Jensen, SBK, Juhl, CR, Janus, C, Sandsdal, RM, Lundgren, JR, Noer, MH, Vu, NQ, Fiorenza, M, Stallknecht, BM, et al
Sleep. 2023;46(5)
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Short sleep duration, defined as less than 6 hours/night, is associated with all-cause mortality, cardiovascular diseases, hypertension, diabetes, and obesity. Sleep restriction causes metabolic and behavioural changes suggesting that short sleep duration may contribute to the development of obesity. The aim of this study was to investigate associations between short sleep duration or poor sleep quality and weight regain after weight loss. This study is based on data from the S-LiTE randomised, controlled trial. Participants followed a low-calorie diet (800 kcal/day) for eight weeks prior to randomisation. Those who lost at least 5% of initial weight were randomised to the control or intervention group. Results showed that participants with objectively measured short sleep duration after a diet-induced weight loss had less success during weight loss maintenance than those with longer sleep duration. Worse sleep quality was associated with less weight loss during a low-calorie diet and subsequent weight maintenance. Authors conclude that insufficient sleep predicts weight regain during interventional efforts to maintain weight loss. Exercise maintained low-calorie diet-induced improvements in sleep quality during 1 year of weight loss maintenance, and liraglutide transiently increased sleep duration.
Abstract
STUDY OBJECTIVES Insufficient sleep may attenuate weight loss, but the role of sleep in weight loss maintenance is unknown. Since weight regain after weight loss remains a major obstacle in obesity treatment, we investigated whether insufficient sleep predicts weight regain during weight loss maintenance. METHODS In a randomized, controlled, two-by-two factorial study, 195 adults with obesity completed an 8-week low-calorie diet and were randomly assigned to 1-year weight loss maintenance with or without exercise and liraglutide 3.0 mg/day or placebo. Sleep duration and quality were measured before and after the low-calorie diet and during weight maintenance using wrist-worn accelerometers (GENEActiv) and Pittsburgh Sleep Quality Index (PSQI). To test associations between insufficient sleep and weight regain, participants were stratified at randomization into subgroups according to sleep duration (≥6 h/night) or sleep quality (PSQI score ≤/>5). RESULTS After a diet-induced 13.1 kg weight loss, participants with short sleep duration at randomization regained 5.3 kg body weight (p = .0008) and had less reduction in body fat percentage compared with participants with normal sleep duration (p = .007) during the 1-year weight maintenance phase. Participants with poor sleep quality before the weight loss regained 3.5 kg body weight compared with good quality sleepers (p = .010). During the weight maintenance phase, participants undergoing liraglutide treatment displayed increased sleep duration compared with placebo after 26 weeks (5 vs. -15 min/night) but not after 1 year. Participants undergoing exercise treatment preserved the sleep quality improvements attained from the initial weight loss. CONCLUSIONS Short sleep duration or poor sleep quality was associated with weight regain after weight loss in adults with obesity.
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Changes in objectively measured sleep after a multidisciplinary lifestyle intervention in children with abdominal obesity: A randomized trial.
Catalán-Lambán, A, Ojeda-Rodríguez, A, Marti Del Moral, A, Azcona-Sanjulian, C
Sleep medicine. 2023;109:252-260
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The main factors that contribute to obesity are genetics, excessive energy intake, decreased physical activity, and sedentarism. Sleep duration, sleep timing and chronotype have also recently been recognised as possible risk factors for obesity in children. The aim of this study was to assess the effectiveness of an intervention (usual care vs. intervention group) on sleep quality and its relationship with changes in biochemical and metabolic syndrome related anthropometric parameters. This study was a randomised controlled trial. The multidisciplinary intervention consisted of a two-year program that comprised a 2-month intensive phase with individual and group sessions and a follow-up period at 12 and 24 months. Subjects were randomly assigned to the usual care or intervention group at a ratio of 1:3. Results showed that a lifestyle intervention improved most sleep parameters in children and adolescents with abdominal obesity. In fact, the lifestyle intervention showed a reduction in anthropometric indexes and several biochemical parameters, and improved sleep quality at 2, 12, and 24 months of follow-up. Decreasing sleep latency, awakenings duration and wakefulness after sleep onset (WASO) also accompanied improved sleep efficiency. Authors conclude that their findings add to the growing body of research on the relationship between sleep and metabolic health outcomes in children, emphasizing the need to consider multiple dimensions of sleep beyond just sleep duration.
Abstract
BACKGROUND/OBJECTIVE childhood obesity and sleep disorders have a well-established cross-sectional association, but lifestyle interventions' effects on sleep quality remain under-researched. This study aimed to evaluate the sleep quality of 122 participants (7-16 years) with abdominal obesity after a 2-year necessary lifestyle intervention. PATIENTS/METHODS participants were assigned to either the intervention group (moderate hypocaloric Mediterranean Diet) or the usual care group (standard recommendations on a healthy diet). Sleep was objectively assessed using triaxial accelerometry, and sleep parameters analyzed included latency, efficiency, wake after sleep onset, total time in bed, total sleep time, number of awakenings, and awakening duration. RESULTS AND CONCLUSIONS the results showed that the intervention group significantly improved sleep latency at 12 and 24 months and improved sleep efficiency at 2 and 12 months, compared to the usual care group. Wake after sleep onset and the number of awakenings were significantly reduced at 24 months in the intervention group. Wake after sleep onset and leptin levels were positively associated in all participants. Total time in bed was inversely associated with triglycerides and metabolic score, and total sleep time was inversely associated with leptin, triglycerides, and metabolic score after the 2-month intervention. Triglyceride levels were inversely associated with total time in bed and total sleep time at one year, while the metabolic score was directly associated with wake after sleep onset and the number of awakenings and inversely associated with efficiency. In conclusion, the multidisciplinary intervention in children and adolescents with abdominal obesity reduced anthropometric parameters and improved sleep habits.
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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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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.