-
1.
Association of meal timing with body composition and cardiometabolic risk factors in young adults.
Dote-Montero, M, Acosta, FM, Sanchez-Delgado, G, Merchan-Ramirez, E, Amaro-Gahete, FJ, Labayen, I, Ruiz, JR
European journal of nutrition. 2023;62(5):2303-2315
-
-
-
Free full text
-
Plain language summary
Despite the known consequences of excess body weight, the prevalence of obesity continues to rise. Body weight regulation and obesity are highly influenced by several factors such as genetics, physiology, and socioeconomic factors. The aim of this study was to elucidate the association of meal timing with anthropometry body composition and cardiometabolic risk factors in young adults. This study was a cross-sectional study of 118 young adults (n=82 women). Results showed that meal timing is not related to anthropometry or body composition parameters in young adults. Similarly, caloric midpoint, eating jetlag and the time from last food intake to midsleep point are not associated with cardiometabolic risk factors. However, a longer daily eating window and a shorter time from midsleep point to first food intake (i.e., earlier first food intake in a 24 h cycle) are associated with a healthier cardiometabolic profile in young men. Authors concluded that eating early in alignment with circadian rhythms may improve cardiometabolic health.
Abstract
PURPOSE To investigate the association of meal timing with body composition and cardiometabolic risk factors in young adults. METHODS In this cross-sectional study participated 118 young adults (82 women; 22 ± 2 years old; BMI: 25.1 ± 4.6 kg/m2). Meal timing was determined via three non-consecutive 24-h dietary recalls. Sleep outcomes were objectively assessed using accelerometry. The eating window (time between first and last caloric intake), caloric midpoint (local time at which ≥ 50% of daily calories are consumed), eating jetlag (variability of the eating midpoint between non-working and working days), time from the midsleep point to first food intake, and time from last food intake to midsleep point were calculated. Body composition was determined by DXA. Blood pressure and fasting cardiometabolic risk factors (i.e., triglycerides, total cholesterol, high-density lipoprotein-cholesterol, low-density lipoprotein-cholesterol, and insulin resistance) were measured. RESULTS Meal timing was not associated with body composition (p > 0.05). The eating window was negatively related to HOMA-IR and cardiometabolic risk score in men (R2 = 0.348, β = - 0.605; R2 = 0.234, β = - 0.508; all p ≤ 0.003). The time from midsleep point to first food intake was positively related to HOMA-IR and cardiometabolic risk score in men (R2 = 0.212, β = 0.485; R2 = 0.228, β = 0.502; all p = 0.003). These associations remained after adjusting for confounders and multiplicity (all p ≤ 0.011). CONCLUSIONS Meal timing seems unrelated to body composition in young adults. However, a longer daily eating window and a shorter time from midsleep point to first food intake (i.e., earlier first food intake in a 24 h cycle) are associated with better cardiometabolic health in young men. CLINICAL TRIAL REGISTRATION NCT02365129 ( https://www. CLINICALTRIALS gov/ct2/show/NCT02365129?term=ACTIBATE&draw=2&rank=1 ).
-
2.
Sleep disruption and activation of cellular inflammation mediate heightened pain sensitivity: a randomized clinical trial.
Irwin, MR, Olmstead, R, Bjurstrom, MF, Finan, PH, Smith, MT
Pain. 2023;164(5):1128-1137
-
-
-
Free full text
-
Plain language summary
Sleep disturbance is associated with elevated levels of inflammation. Experimental studies have found that even a modest amount of sleep loss activates inflammatory processes. Experimental sleep disruption also induces alterations in sleep architecture including loss of slow wave or N3 sleep and loss of rapid eye movement sleep. The aim of this study was to clarify whether changes in the amount of N3 sleep and cellular inflammation mediate thermal pain sensitivity (i.e., heat pain threshold) in response to experimental sleep disruption. This study was a secondary analysis (assessor-blind) of a randomised controlled trial. The enrolled participants were randomised to 1 of 2 groups: 2 nights of undisturbed sleep (US) and 2 nights of sleep disruption or forced awakening (FA). Participants underwent 2 consecutive nights of US (or FA), followed by a 2-week washout interval in their home environment, and then completed 2 consecutive nights of the opposing sleep condition FA (or US). Results showed that in healthy adults, experimental disruption of sleep due to the administration of FA induced a significant decrease in heat pain threshold, as compared with responses after US. Experimental manipulation of sleep with FA also led to disturbance in sleep continuity and changes in sleep architecture, including loss of N3 sleep. Moreover, in the morning after FA, there was a robust activation of cellular inflammation Authors conclude that the differential loss of N3 sleep and increases in cellular inflammation may be important drivers of pain sensitivity in response to sleep disruption.
Abstract
Sleep loss heightens pain sensitivity, but the pathways underlying this association are not known. Given that experimental sleep disruption induces increases in cellular inflammation as well as selective loss of slow wave, N3 sleep, this study examined whether these mechanisms contribute to pain sensitivity following sleep loss in healthy adults. This assessor-blinded, cross-over sleep condition, single-site, randomized clinical trial enrolled 95 healthy adults (mean [SD] age, 27.8 [6.4]; female, 44 [53.7%]). The 2 sleep conditions were 2 nights of undisturbed sleep (US) and 2 nights of sleep disruption or forced awakening (FA, 8 pseudorandomly distributed awakenings and 200 minutes wake time during the 8-hour sleep opportunity), administered in a cross-over design after 2 weeks of washout and in a random order (FA-US; US-FA). Primary outcome was heat pain threshold (hPTH). Sleep architecture was assessed by polysomnography, and morning levels of cellular inflammation were evaluated by Toll-like receptor-4 stimulated monocyte intracellular proinflammatory cytokine production. As compared with US, FA was associated with decreases in the amount of slow wave or N3 sleep ( P < 0.001), increases in Toll-like receptor-4 stimulated production of interleukin-6 and tumor necrosis factor-α ( P = 0.03), and decreases in hPTH ( P = 0.02). A comprehensive causal mediation analysis found that FA had an indirect effect on hPTH by decreases in N3 sleep and subsequent increases in inflammation (estimate=-0.15; 95% confidence interval, -0.30 to -0.03; P < 0.05) with the proportion mediated 34.9%. Differential loss of slow wave, N3 sleep, and increases in cellular inflammation are important drivers of pain sensitivity after sleep disruption.Clinical Trials Registration: NCT01794689.
-
3.
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)
-
-
-
Free full text
Plain language summary
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.
-
4.
Sleep Disturbance Affects Immune Factors in Clinical Liver Cancer Patients.
Wang, Z, Wang, Y, Huang, J, Xu, J, Chen, F, Zhu, Z, Gao, L, Qin, J, Liu, B, Liang, C
Current oncology (Toronto, Ont.). 2022;29(10):7943-7952
-
-
-
Free full text
Plain language summary
Many studies have shown that sleep disorders promote tumor growth and can impair immunity at the cellular level. There is however a lack of research in patients with liver cancer. The aim of this study was the asses the quality of sleep and the prevalence of disturbed sleep in patients with liver cancer and to explore whether sleep quality influences immune factors. 210 patients with liver cancer were randomly divided into 2 groups: HBV (Hepatitis B virus) cirrhosis and non-HBV cirrhosis. Their sleep quality was evaluated using a questionnaire and then the patients were divided into 2 groups according to these scores. The association between sleep disturbances and immune factors was analysed by logistic regression models. Over half the patient experienced poor sleep quality. Sleep disturbances were higher in patients with liver cancer of non-HBV cirrhosis than with that coming from the HBV virus. A rise in CD3+ T cells and a reduction in NK cells are associated with sleep disturbances in patients with non-HBV cirrhosis liver cancer. Medicines that can promote sleep and therefore improve immune function might be beneficial. Non-pharmacological sleep interventions to improve sleep quality, should be a safer choice where there are complex drug side effects.
Abstract
BACKGROUND Sleep-wake disturbance is prevalent in patients with liver cancer, but there is no direct evidence of its association and related biological mechanisms. Our study was to assess quality of sleep and to describe prevalence of sleep disturbances in patients with different etiologies of liver cancer, especially to explore whether sleep quality influences immune factors. METHODS A total of 210 patients with liver cancer from August 2015 to December 2015 were randomly divided into two groups including HBV cirrhosis and non-HBV cirrhosis. The Pittsburgh Sleep Quality Index (PSQI) was used to evaluate their sleep quality, and then 202 patients enrolled in this study were divided into two groups according to their PSQI scores: PSQI ≤ 5 and PSQI > 5. The association between sleep disturbances and immune factors was analyzed by logistic regression models. RESULTS A total of 56.9% of liver cancer patients experienced poor sleep quality (PSQI > 5). The prevalence of sleep disturbances was significantly higher in patients with liver cancer of non-hepatitis B virus (HBV) cirrhosis than with that evolving from HBV cirrhosis (66.7% vs. 50%, p = 0.018). In non-HBV cirrhosis liver cancer patients, the PSQI > 5 group had a higher percentage of CD3+ T cells (71.06 ± 11.07 vs. 63.96 ± 14.18, p = 0.014) and lower natural killer (NK) cells (14.67 ± 9.65 vs. 20.5 ± 10.77, p = 0.014) compared with patients with PSQI ≤ 5. Logistic regression further confirmed that liver cancer patients without HBV cirrhosis are more prone to experience poor sleep with increased CD3+ T cells (OR = 1.07, 95% CI = 1.01-1.13, p = 0.030) and decreased NK cells (OR = 0.92, 95% CI = 0.85-0.98, p = 0.014). Our results indicate that increased CD3+ T cells and decreased NK cells are both associated with sleep disturbances in patients with liver cancer of non-HBV cirrhosis. CONCLUSIONS Most liver cancer patients suffer from sleep disturbances, especially evolving from non-HBV cirrhosis. A rise in CD3+ T cells and a reduction in NK cells are associated with sleep disturbances in patients with liver cancer of non-HBV cirrhosis.
-
5.
Partial sleep restriction-induced changes in stress, quality of life, and lipid metabolism in relation to cold hypersensitivity: A before-and-after intervention study.
Baek, Y, Jung, K, Kim, H, Lee, S
Medicine. 2022;101(46):e31933
-
-
-
Free full text
-
Plain language summary
Inadequate sleep has been associated with an increased risk of cardiovascular disease and has an adverse impact on quality of life (QOL), metabolism and the immune system. Furthermore, sleep is associated with the body’s thermoregulation ability, which is closely associated with distal and proximal skin temperature, as well as core body temperature. The hypothesis of this study was that the physiological and psychological changes caused by insufficient sleep will differ according to cold hypersensitivity (CH). This study was an uncontrolled, before-and-after study with 3 days of 4-hour sleep restriction (SR) as intervention. A total of 130 participants completed the study. Results showed that less-than-optimal sleep duration leads to worsened stress and QOL and reduced low-density lipoprotein cholesterol levels. These changes were significant in the CH group compared to the non-CH group. Authors conclude that their findings provide additional information for evaluating the clinical risks posed by sleep disturbances and assessing the usual sleep patterns according to CH.
Abstract
Sleep disturbances are associated with cold hypersensitivity (CH) and characterized by excessive cold sensation in specific body parts and cold thermal discomfort. This study investigated the effects of short-term sleep restriction followed by a recovery phase on subjective health status, inflammation, and lipid metabolism in different types of CH. A total of 118 healthy adults aged 35 to 44 years without sleep disturbances were enrolled. Participants underwent 4-hour sleep restrictions per day for 3 days at a hospital and then returned to their daily lives for 4 days of rest. CH was assessed using a structured questionnaire with eight characteristic symptoms. A questionnaire and blood tests were administered baseline, after sleep restriction, and follow-up to assess cortisol, lipid profiles, and self-reported stress and quality of life (QOL). Participants were divided into CH (44.1%) and non-CH (55.9%) groups. The CH group showed increased stress, impaired QOL, and decreased low-density lipoprotein-cholesterol (LDL-C) levels compared to the non-CH group after sleep restriction. The variance for QOL (effect size = 0.07), subjective stress (effect size = 0.053), and LDL-C (effect size = 0.029) among time points depended on the group. Short-term sleep restriction was associated with deterioration of subjective health and reduced lipid metabolism; such changes were more evident in the CH group. Our findings suggest the need to consider an individual's CH status to assess the clinical risk associated with insufficient sleep.
-
6.
The Role of Vitamin D in Sleep Disorders of Children and Adolescents: A Systematic Review.
Prono, F, Bernardi, K, Ferri, R, Bruni, O
International journal of molecular sciences. 2022;23(3)
-
-
-
-
Free full text
Plain language summary
Vitamin D deficiency or insufficiency is a global epidemic, estimated to affect over one billion people worldwide, including children. The main function of vitamin D is the regulation of bone homeostasis but it is also involved in many other conditions such as cardiovascular disease, cancer, diabetes mellitus and autoimmune disorders. Recent studies show that sufficient levels of vitamin D seem to be necessary to maintain sleep and low vitamin D levels have been associated with shorter sleep duration. This systematic review is the first to assess the association between Vitamin D and sleep disorders in children, 14 articles were included. Vitamin D deficiency in children is associated with decreased sleep duration and poorer sleep efficiency, as well as with delayed bedtimes. Children with reduced vitamin D serum levels have a higher risk of excessive daytime sleepiness (EDS). Since vitamin D levels influence sleep duration, sleep duration can also influence vitamin D serum concentration suggesting a bidirectional relationship. Evidence is scarce and so further high-quality prospective cohort studies and well-designed randomized controlled trials (RCTs) are needed to determine the effect of vitamin D supplementation in children with sleep disorders.
Expert Review
Conflicts of interest:
None
Take Home Message:
- Vitamin D plays an important role in the sleep quality of children. Healthcare practitioners may wish to establish vitamin D status in children presenting with sleep disturbances.
Evidence Category:
-
A: Meta-analyses, position-stands, randomized-controlled trials (RCTs)
-
X
B: Systematic reviews including RCTs of limited number
-
C: Non-randomized trials, observational studies, narrative reviews
-
D: Case-reports, evidence-based clinical findings
-
E: Opinion piece, other
Summary Review:
Introduction
Vitamin D levels have been associated with improved sleep in adults, but few studies have concentrated on the paediatric population. In order to identify if vitamin D plays a role regulating sleep in children and adolescents the paper reviewed studies, which looked at vitamin D in relation to sleep duration and quality of sleep. This included the following sleep disorders: obstructive sleep apnoea (OSA), restless leg syndrome (RLS) and insomnia.
Methods
- A broad systematic review following the PRISMA guidelines and using PubMed and Cochrane databases
- Search identified 748 papers. After exclusions for non-relevance, incorrect age group, or lack of data on sleep, 14 papers were included
- Due to the shortage of papers on this topic none of these papers were excluded, regardless of quality
- The participants in each study varied from 39 to 5289.
Results
The results highlighted:
- Plasma levels of vitamin D affect sleep duration and quality of sleep in children. Data taken from 5 studies
- Vitamin D cord blood levels were correlated to sleep in preschool children. Partly this was due to the mother’s vitamin D level during pregnancy affecting the level of vitamin D available to the foetus. Venous blood vitamin D level was linked to the sleep wake cycle of children. Data taken from 2 studies
- OSA was more likely to develop in children who had low vitamin D levels with a risk of 14.16% compared to a control group of 5.83% (1 study)
- Vitamin D supplementation was found to reduce neuron damage caused by hypoxia (1 study)
- An association exists between parental vitamin D insufficiency and their child’s vitamin D status (1 study). Data taken from 5 studies
- Vitamin D levels in specific diseases, such as coeliac disease (CD) showed a negative correlation with RLS
- For familial Mediterranean fever (FMF) vitamin D deficiency reduced sleep quality (36.5%). Data taken from 2 studies.
Conclusion
Notwithstanding the small number of studies, the review shows vitamin D deficiency, defined as <20 ng/mL, is associated with an increased risk for sleep disorders in children.
Clinical practice applications:
- Due to the role vitamin D plays in sleep in children, establishing vitamin D status may be useful for children presenting with sleep disturbances
- Adequate vitamin D levels during pregnancy are important to establish a vitamin D pool in the foetus
- Vitamin D supplementation is something to rule out in the case of OSA and associated hypoxia, metabolic dysfunction and systemic inflammation in children
- Due to the negative impact poor sleep has on the body, improving sleep quality at a young age could form an important part of preventative health care.
Considerations for future research:
- Additional studies are required to support the conclusion in this study
- Due to the low number of studies, any additional research should be of a high standard and include prospective cohort studies and randomised control trials.
Abstract
This review investigates the association between vitamin D and sleep disorders. Vitamin D is an essential nutrient known to play an important role in the growth and bone health of the human body, but it also appears to play a role in sleep. The goal of our review is to examine the association between vitamin D and sleep disorders in children and adolescents. We summarize the evidence about the role and the mechanism of action of vitamin D in children and adolescents with sleep disorders such as insomnia, obstructive sleep apnea (OSA), restless legs syndrome (RLS), and other sleep disorders. Systematic electronic database searches were conducted using Pubmed and Cochrane Library. The Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guideline was followed. The studies that met the established inclusion criteria were analyzed and compared. Results suggest a strict relationship between vitamin D deficiency in children and sleep disorders. There is evidence that vitamin D is implicated in the different neurochemical mechanisms involved in sleep regulation and mainly in the serotonergic and dopaminergic pathways. This might be responsible for the association of vitamin D deficiency and restless sleep, sleep hyperhidrosis, OSA, and RLS.
-
7.
Essential Hypertension and Oxidative Stress: Novel Future Perspectives.
Franco, C, Sciatti, E, Favero, G, Bonomini, F, Vizzardi, E, Rezzani, R
International journal of molecular sciences. 2022;23(22)
-
-
-
Free full text
Plain language summary
High blood pressure is one of the main risk factors for cardiovascular disease and a significant contributor to the development of strokes, heart attacks, and heart and kidney failure leading to early disability and reduced life expectancy. Essential or primary hypotension makes up 95% of high blood pressure cases, which is abnormally elevated blood pressure that is not a result of any other medical condition. Essential hypertension arises from various factors such as diet, lifestyle, environmental and genetic influences. Despite many available medications, not all patients attain well-managed blood pressure levels. Unmanaged high blood pressure can, over time, lead to narrowing and stiffening of the blood vessels and ultimately to structural and functional changes in the blood tissues. In part, this is mediated by oxidative stress, changes in antioxidant capacity and chronic low-grade inflammation, which damage the blood vessels' endothelial tissue and result in vascular stiffness. Melatonin is one of the most potent antioxidants found in nature and has been studied in short-term trials for its blood pressure lowering, antioxidant and vascular protective effects. This small open-label randomised study sought to get a better understanding of the long-term use of melatonin. Initially, the study assessed endothelial tissue damage, oxidative status and vascular stiffness in patients with high blood pressure. Subsequently, some of the participants received a low-dose melatonin supplement (1 mg/day) for one year, whilst being monitored for clinical and structural vascular changes. The study included 23 patients and 14 in the final analysis. After one year, the results showed a significant improvement in arterial stiffness in the melatonin group (11) and an improvement in endothelial tissue function, though the latter was not at statistically significant levels. Improvement in arterial stiffness seemed to be linked to a reduction in total antioxidant capacity (TAC). These findings suggest that melatonin can contribute to restoring oxidative balance in blood plasma, which reflects improved arterial stiffness. The study also demonstrated that besides being a well-tolerated intervention, melatonin also has clinical benefits even when administered at lower doses than normal.
Abstract
Among cardiovascular diseases, hypertension is one of the main risk factors predisposing to fatal complications. Oxidative stress and chronic inflammation have been identified as potentially responsible for the development of endothelial damage and vascular stiffness, two of the primum movens of hypertension and cardiovascular diseases. Based on these data, we conducted an open-label randomized study, first, to evaluate the endothelial damage and vascular stiffness in hypertense patients; second, to test the effect of supplementation with a physiological antioxidant (melatonin 1 mg/day for 1 year) in patients with essential hypertension vs. hypertensive controls. Twenty-three patients of either gender were enrolled and randomized 1:1 in two groups (control and supplemented group). The plasmatic total antioxidant capacity (as a marker of oxidative stress), blood pressure, arterial stiffness, and peripheral endothelial function were evaluated at the beginning of the study and after 1 year in both groups. Our results showed that arterial stiffness improved significantly (p = 0.022) in supplemented patients. The endothelial function increased too, even if not significantly (p = 0.688), after 1 year of melatonin administration. Moreover, the supplemented group showed a significative reduction in TAC levels (p = 0.041) correlated with the improvement of arterial stiffness. These data suggest that melatonin may play an important role in reducing the serum levels of TAC and, consequently, in improving arterial stiffness.
-
8.
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)
-
-
-
Free full text
Plain language summary
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.
-
9.
Melatonin Supplementation Lowers Oxidative Stress and Regulates Adipokines in Obese Patients on a Calorie-Restricted Diet.
Szewczyk-Golec, K, Rajewski, P, Gackowski, M, Mila-Kierzenkowska, C, Wesołowski, R, Sutkowy, P, Pawłowska, M, Woźniak, A
Oxidative medicine and cellular longevity. 2017;2017:8494107
-
-
-
Free full text
Plain language summary
Obesity is one of the major global health problems. Melatonin is a hormone which regulates wakefulness, functions as an antioxidant and plays a role in the immune system. Previous research suggests that melatonin deficiency is associated with obesity. The aim of this study was to estimate the effect of melatonin on oxidative stress and levels of cell signalling proteins released by fat cells (adipokines) in obese patients on a calorie-restricted diet. Thirty obese patients were supplemented with a daily dose of 10 mg of melatonin or placebo for 30 days with a calorie-restricted diet. Blood levels of melatonin, adipokines and markers of oxidative stress were measured at baseline and after supplementation. Significant body weight reduction (7%) was observed only in the melatonin group. After melatonin supplementation, the adiponectin and omentin-1 levels and glutathione peroxidase activities statistically increased, whereas the malondialdehyde concentrations were reduced. In the placebo group, a significant rise in 4-hydroxynonenal and a drop in the melatonin concentrations were found. The results show evidence of increased oxidative stress accompanying calorie restriction. The authors concluded that melatonin supplementation facilitated body weight reduction, improved the antioxidant defence, and regulated adipokine secretion. The findings suggest that melatonin should be considered in the management of obesity.
Abstract
Obesity is one of the major global health problems. Melatonin deficiency has been demonstrated to correlate with obesity. The aim of the study was to estimate the effect of melatonin on oxidative stress and adipokine levels in obese patients on a calorie-restricted diet. Thirty obese patients were supplemented with a daily dose of 10 mg of melatonin (n = 15) or placebo (n = 15) for 30 days with a calorie-restricted diet. Serum levels of melatonin, 4-hydroxynonenal (HNE), adiponectin, omentin-1, leptin, and resistin, as well as erythrocytic malondialdehyde (MDA) concentration and Zn/Cu-superoxide dismutase, catalase, and glutathione peroxidase (GPx) activities, were measured at baseline and after supplementation. Significant body weight reduction was observed only in the melatonin group. After melatonin supplementation, the adiponectin and omentin-1 levels and GPx activities statistically increased, whereas the MDA concentrations were reduced. In the placebo group, a significant rise in the HNE and a drop in the melatonin concentrations were found. The results show evidence of increased oxidative stress accompanying calorie restriction. Melatonin supplementation facilitated body weight reduction, improved the antioxidant defense, and regulated adipokine secretion. The findings strongly suggest that melatonin should be considered in obesity management. This trial is registered with CTRI/2017/07/009093.
-
10.
The microbiome: A key regulator of stress and neuroinflammation.
Rea, K, Dinan, TG, Cryan, JF
Neurobiology of stress. 2016;4:23-33
-
-
-
Free full text
Plain language summary
This study discusses the concept of intestinal microbiota as the key regulator involved in energy regulation, gut barrier function, protection from pathogens, and immune system function amongst others. The gut microbiota is the complex community of microorganisms that lives in the digestive tracts of humans. The main aim of this study is to summarise the role of gastrointestinal microbiota in fundamental physiological and pathophysiological processes and thereafter to understand and treat a range of stress and immune-related disorders. This review outlines the numerous complex relationships between gastrointestinal microbiota, stress and immune responses at the three critical stages of life The authors concluded that the evidence from this study suggests that resilience to stress and immune-related disorders and dysfunction of stress and immune systems may be dependent on the diversity and complexity of gastrointestinal microbiota. However, gut microbiota mediated relationship to stress and neuro-inflammation is still unconfirmed as previous studies mostly, have largely been, preclinical and further studies are warranted.
Abstract
There is a growing emphasis on the relationship between the complexity and diversity of the microorganisms that inhabit our gut (human gastrointestinal microbiota) and health/disease, including brain health and disorders of the central nervous system. The microbiota-gut-brain axis is a dynamic matrix of tissues and organs including the brain, glands, gut, immune cells and gastrointestinal microbiota that communicate in a complex multidirectional manner to maintain homeostasis. Changes in this environment can lead to a broad spectrum of physiological and behavioural effects including hypothalamic-pituitary-adrenal (HPA) axis activation, and altered activity of neurotransmitter systems and immune function. While an appropriate, co-ordinated physiological response, such as an immune or stress response are necessary for survival, a dysfunctional response can be detrimental to the host contributing to the development of a number of CNS disorders. In this review, the involvement of the gastrointestinal microbiota in stress-mediated and immune-mediated modulation of neuroendocrine, immune and neurotransmitter systems and the consequential behaviour is considered. We also focus on the mechanisms by which commensal gut microbiota can regulate neuroinflammation and further aim to exploit our understanding of their role in stress-related disorders as a consequence of neuroinflammatory processes.