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How Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) Progresses: The Natural History of ME/CFS.
Nacul, L, O'Boyle, S, Palla, L, Nacul, FE, Mudie, K, Kingdon, CC, Cliff, JM, Clark, TG, Dockrell, HM, Lacerda, EM
Frontiers in neurology. 2020;11:826
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A good understanding of the disease course is vital not only for the design of preventative and intervention studies, but also to assess the timing and type of intervention that minimizes disease risk or optimizes prognosis. The aim of this review was to explore the long-term course of Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) and how presentation and pathophysiological abnormalities may vary with time. Literature shows that it is unknown how the initial host response to a stressor or insult compares in individuals who do or do not develop typical symptoms of ME/CFS. However, the return to good health, following exposure to mild or moderate levels of insult, seems to be impeded in ME/CFS when symptoms persist for longer than 3–6 months. Authors sought to provide a simple framework, similar to those of other chronic diseases, in an effort to extend the temporal perception of ME/CFS and better incorporate the less defined pre-illness stages of the disease. In fact, they conclude that by applying this framework to ME/CFS research efforts could better elucidate the pathophysiological mechanisms of the disease and identify potential therapeutic targets at distinct stages.
Abstract
We propose a framework for understanding and interpreting the pathophysiology of Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) that considers wider determinants of health and long-term temporal variation in pathophysiological features and disease phenotype throughout the natural history of the disease. As in other chronic diseases, ME/CFS evolves through different stages, from asymptomatic predisposition, progressing to a prodromal stage, and then to symptomatic disease. Disease incidence depends on genetic makeup and environment factors, the exposure to singular or repeated insults, and the nature of the host response. In people who develop ME/CFS, normal homeostatic processes in response to adverse insults may be replaced by aberrant responses leading to dysfunctional states. Thus, the predominantly neuro-immune manifestations, underlined by a hyper-metabolic state, that characterize early disease, may be followed by various processes leading to multi-systemic abnormalities and related symptoms. This abnormal state and the effects of a range of mediators such as products of oxidative and nitrosamine stress, may lead to progressive cell and metabolic dysfunction culminating in a hypometabolic state with low energy production. These processes do not seem to happen uniformly; although a spiraling of progressive inter-related and self-sustaining abnormalities may ensue, reversion to states of milder abnormalities is possible if the host is able to restate responses to improve homeostatic equilibrium. With time variation in disease presentation, no single ME/CFS case description, set of diagnostic criteria, or molecular feature is currently representative of all patients at different disease stages. While acknowledging its limitations due to the incomplete research evidence, we suggest the proposed framework may support future research design and health care interventions for people with ME/CFS.
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Intramyocellular Lipids, Insulin Resistance, and Functional Performance in Patients with Severe Obstructive Sleep Apnea.
Chien, MY, Lee, PL, Yu, CW, Wei, SY, Shih, TT
Nature and science of sleep. 2020;12:69-78
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Obstructive sleep apnoea syndrome (OSA) is characterized by repeated occlusion of the upper airway during sleep, resulting in periods of intermittent hypoxemia [low level of oxygen in blood]. The aim of this study was to (a) investigate the intramyocellular lipids (IMCL) and extramyocellular lipids (EMCL), biochemical data, and functional performance in patients with severe OSA versus controls, and (b) examine the correlations between intra-muscular lipid contents and biochemical and performance variables. This study is a clinical trial that recruited 20 patients with OSA and body mass index(BMI)-matched controls. Results demonstrate that patients with OSA had significantly lower IMCL and EMCL values when compared with their age-, and BMI-matched controls without OSA. Furthermore, compared with controls, patients with OSA had significantly reduced functional performance and exhibited abnormal biochemical data, including glucose and insulin levels and lipid profiles. Authors conclude that additional large-scale clinical trials are required to further explore the complex mechanism between OSA, muscle metabolism, and insulin action.
Abstract
PURPOSE An increasing number of studies have linked the severity of obstructive sleep apnea (OSA) with metabolic dysfunction. However, little is known about the lipid compartments (intramyocellular [IMCL] and extramyocellular [EMCL] lipids) inside the musculature in these patients. The present study was designed to investigate the IMCL and EMCL, biochemical data, and functional performance in patients with severe OSA, and to examine the correlations between intramuscular lipid contents and test variables. PARTICIPANTS AND METHODS Twenty patients with severe OSA (apnea-hypopnea index [AHI]: ≥30/h; body mass index [BMI]: 26.05±2.92) and 20 age- and BMI-matched controls (AHI <5/h) were enrolled. Proton magnetic resonance spectroscopy was used to measure the IMCL and EMCL of the right vastus lateralis muscle. Biochemical data, including levels of fasting plasma glucose, insulin, lipid profiles, and high-sensitivity C-reactive protein (hsCRP), were measured. Insulin resistance index (IR) was calculated using the homeostasis model assessment method. Performance tests included a cardiopulmonary exercise test and knee extension strength and endurance measurements. RESULTS Patients with severe OSA had significantly (P<0.05) lower values of IMCL (14.1±5.4 AU) and EMCL (10.3±5.8 AU) compared to the control group (25.2±17.6 AU and 14.3±11.1 AU, respectively). Patients with severe OSA had significantly higher hsCRP, IR, and dyslipidemia compared with controls (all P<0.05). Furthermore, IMCL was negatively correlated with AHI, cumulative time with nocturnal pulse oximetric saturation lower than 90% (TSpO2<90%) (ρ=-0.35, P<0.05), IR (ρ=-0.40, P<0.05), glucose (ρ=-0.33, P<0.05), and insulin (ρ=-0.36, P<0.05), and positively correlated with lowest oximetric saturation (ρ=0.33, P<0.01). CONCLUSION Skeletal muscle dysfunction and metabolic abnormalities were observed in patients with OSA that did not have obesity. IMCL was positively correlated with aerobic capacity and muscular performance, but negatively correlated with AHI and IR. Large-scale clinical trials are required to explore the complicated mechanism among OSA, intramuscular metabolism, and insulin action. CLINICAL TRIAL REGISTRATION ClinicalTrials.gov Identifier: NCT00813852.
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Short sleep duration and dietary intake: epidemiologic evidence, mechanisms, and health implications.
Dashti, HS, Scheer, FA, Jacques, PF, Lamon-Fava, S, Ordovás, JM
Advances in nutrition (Bethesda, Md.). 2015;6(6):648-59
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Short sleep duration is associated with various cardio-metabolic parameters that contribute to chronic disease. While the underlying mechanism is multifactorial, the link may be mediated through changes in dietary intake. This review provides an overview of the relationship between chronic short sleep duration and dietary intake. This review indicates that short sleep duration is associated with higher total caloric intake, higher fat intake and diets with relatively higher fat and lower protein composition. Further epidemiological studies are required to better establish the relationship between chronic short sleep and dietary patterns, and improvements in sleep should be an added factor in weight management programmes.
Abstract
Links between short sleep duration and obesity, type 2 diabetes, hypertension, and cardiovascular disease may be mediated through changes in dietary intake. This review provides an overview of recent epidemiologic studies on the relations between habitual short sleep duration and dietary intake in adults from 16 cross-sectional studies. The studies have observed consistent associations between short sleep duration and higher total energy intake and higher total fat intake, and limited evidence for lower fruit intake, and lower quality diets. Evidence also suggests that short sleepers may have irregular eating behavior deviating from the traditional 3 meals/d to fewer main meals and more frequent, smaller, energy-dense, and highly palatable snacks at night. Although the impact of short sleep duration on dietary intake tends to be small, if chronic, it may contribute to an increased risk of obesity and related chronic disease. Mechanisms mediating the associations between sleep duration and dietary intake are likely to be multifactorial and include differences in the appetite-related hormones leptin and ghrelin, hedonic pathways, extended hours for intake, and altered time of intake. Taking into account these epidemiologic relations and the evidence for causal relations between sleep loss and metabolism and cardiovascular function, health promotion strategies should emphasize improved sleep as an additional factor in health and weight management. Moreover, future sleep interventions in controlled studies and sleep extension trials in chronic short sleepers are imperative for establishing whether there is a causal relation between short sleep duration and changes in dietary intake.
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Nighttime snacking reduces whole body fat oxidation and increases LDL cholesterol in healthy young women.
Hibi, M, Masumoto, A, Naito, Y, Kiuchi, K, Yoshimoto, Y, Matsumoto, M, Katashima, M, Oka, J, Ikemoto, S
American journal of physiology. Regulatory, integrative and comparative physiology. 2013;304(2):R94-R101
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Night eating syndrome (NES) is defined by night time eating (25% or more of the total energy of the day is consumed after the evening meal or by waking up in the middle of the night to eat at least three times per week). Research suggests that it is associated with obesity and a higher BMI. Those with NES may have higher glucose and insulin levels, and lower levels of ghrelin during the night compared to those without NES. This randomised crossover study aimed to explore the impact of nighttime eating on energy, glucose and lipid metabolism in normal weight young women. Participants were asked to either complete a 2 week nighttime snacking intervention or a daytime snacking intervention. The snack represented 10% of the average energy requirement (1950 k/cal per day) with a protein:fat:carbohydrate ratio of 5:50:45. The study found no impact of nighttime snacking on body weight, energy expenditure or glucose metabolism compared to daytime snacking. However, it did find a decrease in fat oxidation and increases in total and LDL cholesterol. Hunger levels before lunch were also higher during the nighttime snacking intervention.
Abstract
The increase in obesity and lipid disorders in industrialized countries may be due to irregular eating patterns. Few studies have investigated the effects of nighttime snacking on energy metabolism. We examined the effects of nighttime snacking for 13 days on energy metabolism. Eleven healthy women (means ± SD; age: 23 ± 1 yr; body mass index: 20.6 ± 2.6 kg/m(2)) participated in this randomized crossover trial for a 13-day intervention period. Subjects consumed a specified snack (192.4 ± 18.3 kcal) either during the daytime (10:00) or the night time (23:00) for 13 days. On day 14, energy metabolism was measured in a respiratory chamber without snack consumption. An oral glucose tolerance test was performed on day 15. Relative to daytime snacking, nighttime snacking significantly decreased fat oxidation (daytime snacking: 52.0 ± 13.6 g/day; nighttime snacking: 45.8 ± 14.0 g/day; P = 0.02) and tended to increase the respiratory quotient (daytime snacking: 0.878 ± 0.022; nighttime snacking: 0.888 ± 0.021; P = 0.09). The frequency of snack intake and energy intake, body weight, and energy expenditure were not affected. Total and low-density lipoprotein (LDL) cholesterol significantly increased after nighttime snacking (152 ± 26 mg/dl and 161 ± 29 mg/dl; P = 0.03 and 76 ± 20 mg/dl and 83 ± 24 mg/dl; P = 0.01, respectively), but glucose and insulin levels after the glucose load were not affected. Nighttime snacking increased total and LDL cholesterol and reduced fat oxidation, suggesting that eating at night changes fat metabolism and increases the risk of obesity.
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Impact of five nights of sleep restriction on glucose metabolism, leptin and testosterone in young adult men.
Reynolds, AC, Dorrian, J, Liu, PY, Van Dongen, HP, Wittert, GA, Harmer, LJ, Banks, S
PloS one. 2012;7(7):e41218
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Chronic sleep deprivation is a feature of modern life. It may be due to social, lifestyle and/or occupational demands. It has been associated with metabolic disorders such as type 2 diabetes, metabolic syndrome, insulin resistance and obesity. This study aimed to examine the impact of sleep restriction on glucose metabolism, triglycerides and to explore the impact on testosterone, leptin and cortisol in healthy young men. The sample were 16 men aged between 22 and 36, who did not have any acute or chronic medical or psychological conditions. Subjects were studied in groups of 3 or 4 for 9 consecutive days, and had two baseline nights of 10 hours sleep followed by five nights of 4 hours sleep. Food intake was controlled during the laboratory phase. The study found evidence of impaired glucose metabolism following sleep restriction (elevated glucose and insulin). Researchers suggested this may be due to a rise in afternoon cortisol reflecting adrenal axis activation. Leptin levels also increased, but did not lead to appetite changes. Testosterone levels did not change but SHBG did decrease, possibly due to increases in insulin that could have down-regulated SHBG. There were also alterations in cortisol levels, with elevated levels in the afternoon and evening. The researchers concluded that short term sleep restriction may lead to an increased risk of type 2 diabetes.
Abstract
BACKGROUND Sleep restriction is associated with development of metabolic ill-health, and hormonal mechanisms may underlie these effects. The aim of this study was to determine the impact of short term sleep restriction on male health, particularly glucose metabolism, by examining adrenocorticotropic hormone (ACTH), cortisol, glucose, insulin, triglycerides, leptin, testosterone, and sex hormone binding globulin (SHBG). METHODOLOGY/PRINCIPAL FINDINGS N = 14 healthy men (aged 27.4±3.8, BMI 23.5±2.9) underwent a laboratory-based sleep restriction protocol consisting of 2 baseline nights of 10 h time in bed (TIB) (B1, B2; 22:00-08:00), followed by 5 nights of 4 h TIB (SR1-SR5; 04:00-08:00) and a recovery night of 10 h TIB (R1; 22:00-08:00). Subjects were allowed to move freely inside the laboratory; no strenuous activity was permitted during the study. Food intake was controlled, with subjects consuming an average 2000 kcal/day. Blood was sampled through an indwelling catheter on B1 and SR5, at 09:00 (fasting) and then every 2 hours from 10:00-20:00. On SR5 relative to B1, glucose (F(1,168) = 25.3, p<0.001) and insulin (F(1,168) = 12.2, p<0.001) were increased, triglycerides (F(1,168) = 7.5, p = 0.007) fell and there was no significant change in fasting homeostatic model assessment (HOMA) determined insulin resistance (F(1,168) = 1.3, p = 0.18). Also, cortisol (F(1,168) = 10.2, p = 0.002) and leptin (F(1,168) = 10.7, p = 0.001) increased, sex hormone binding globulin (F(1,167) = 12.1, p<0.001) fell and there were no significant changes in ACTH (F(1,168) = 0.3, p = 0.59) or total testosterone (F(1,168) = 2.8, p = 0.089). CONCLUSIONS/SIGNIFICANCE Sleep restriction impaired glucose, but improved lipid metabolism. This was associated with an increase in afternoon cortisol, without significant changes in ACTH, suggesting enhanced adrenal reactivity. Increased cortisol and reduced sex hormone binding globulin (SHBG) are both consistent with development of insulin resistance, although hepatic insulin resistance calculated from fasting HOMA did not change significantly. Short term sleep curtailment leads to changes in glucose metabolism and adrenal reactivity, which when experienced repeatedly may increase the risk for type 2 diabetes.