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Sleep loss disrupts the neural signature of successful learning.
Guttesen, AÁV, Gaskell, MG, Madden, EV, Appleby, G, Cross, ZR, Cairney, SA
Cerebral cortex (New York, N.Y. : 1991). 2023;33(5):1610-1625
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Understanding how sleep disturbances impair learning and memory is increasingly important in modern society, where many people fail to regularly obtain an adequate amount of sleep. The aim of this study was to investigate the relationship between sleep-associated consolidation and next-day learning and how suppressing slow-wave activity (SWA) [during slow-wave sleep, electrical activity in the brain changes while the body relaxes into deep and restorative rest] contributes to this relationship. This study was a within-subjects (n = 30), crossover design which showed that sleep improved both memory retention and next-day learning however, there was no evidence of a relationship between these measures or with SWA. Furthermore, an absence of sleep disrupts the neural operations underpinning memory encoding, leading to suboptimal performance. Authors conclude that an extended lack of sleep might disrupt the ability to draw upon semantic knowledge when encoding novel associations, necessitating the use of more surface-based and ultimately suboptimal routes to learning.
Abstract
Sleep supports memory consolidation as well as next-day learning. The influential "Active Systems" account of offline consolidation suggests that sleep-associated memory processing paves the way for new learning, but empirical evidence in support of this idea is scarce. Using a within-subjects (n = 30), crossover design, we assessed behavioral and electrophysiological indices of episodic encoding after a night of sleep or total sleep deprivation in healthy adults (aged 18-25 years) and investigated whether behavioral performance was predicted by the overnight consolidation of episodic associations from the previous day. Sleep supported memory consolidation and next-day learning as compared to sleep deprivation. However, the magnitude of this sleep-associated consolidation benefit did not significantly predict the ability to form novel memories after sleep. Interestingly, sleep deprivation prompted a qualitative change in the neural signature of encoding: Whereas 12-20 Hz beta desynchronization-an established marker of successful encoding-was observed after sleep, sleep deprivation disrupted beta desynchrony during successful learning. Taken together, these findings suggest that effective learning depends on sleep but not necessarily on sleep-associated consolidation.
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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
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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 ).
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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
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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.
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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
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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.
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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.