The effect of acute sleep deprivation on cortisol level: a systematic review and meta-analysis.

Acute sleep deprivation has aroused widespread concern and the relationship between acute sleep deprivation and cortisol levels is inconsistent. This study aimed to explore additional evidence and details. The PubMed, Web of Science, EMBASE, CLINAHL and Cochrane databases were searched for eligible studies published up to June 7, 2023. All analyses were performed using Review Manager 5.4 and Stata/SE 14.0. A total of 24 studies contributed to this meta-analysis. There was no significant difference in cortisol levels between participants with acute sleep deprivation and normal sleep in 21 crossover-designed studies (SMD = 0.18; 95% CI: -0.11, 0.45; p = 0.208) or 3 RCTs (SMD = 0.26; 95% CI: -0.22, 0.73; p = 0.286). Subgroup analysis revealed that the pooled effects were significant for studies using serum as the sample (SMD = 0.46; 95%CI: 0.11, 0.81; p = 0.011). Studies reporting cortisol levels in the morning, in the afternoon and in the evening did not show significant difference (p > 0.05). The pooled effects were statistically significant for studies with multiple measurements (SMD = 0.28; 95%CI: 0.03, 0.53; p = 0.027) but not for studies with single cortisol assessments (p = 0.777). When the serum was used as the test sample, the cortisol levels of individuals after acute sleep deprivation were higher than those with normal sleep.

Accelerometer-measured physical activity and sedentary behaviour are associated with C-reactive protein in US adults who get insufficient sleep: A threshold and isotemporal substitution effect analysis.

This study aimed to investigate the association between physical activity, sedentary behaviour and chronic inflammation in short sleep adults. The study included 2,113 NHANES participants with self-reported insufficient sleep. C-reactive protein (CRP) was used as the inflammatory biomarker. Physical activity and sedentary behaviour were objectively measured by accelerometers. Weighted regression model, two - piecewise linear regression model, and restricted cubic splines were applied to evaluate associations mentioned above. An isotemporal substitution model was used to assess the modelled effects of replacing sedentary time (ST) with moderate-to-vigorous levels of physical activity (MVPA) or light physical activity (LPA). After adjusting for potential confounding factors, higher levels of ST and lower levels of LPA or MVPA were associated with higher CRP levels. Isotemporal substitution analysis indicated that replacing 30 minutes of ST with 30 minutes of MVPA was associated with a significant decrease in CRP levels. Saturation analysis suggested that the association between MVPA and CRP may plateau at over 20 minutes of MVPA per day. Findings of this study provides insight into the potential benefits of replacing ST with MVPA. This study also suggests that increasing MVPA beyond a certain point may not provide additional anti-inflammatory benefits in a short sleep population.

Effects of paradoxical sleep deprivation on oxidative parameters in the serum and brain of mice submitted to the animal model of hyperglycemia.

The present study aimed to investigate the effects of paradoxical sleep deprivation (PSD) on behavioral and oxidative stress parameters in the brain and serum of mice submitted to the animal model of hyperglycemia induced by alloxan, mimicking the main symptom of diabetes mellitus (DM). Adults C57BL/6 male and female mice received an injection of alloxan, and ten days later, the animals were submitted to the PSD for 36 h. The animals' behavioral parameters were evaluated in the open-field test. Oxidative stress parameters [Diacetyldichlorofluorescein (DCF), Thiobarbituric acid reactive substances (TBARS), Superoxide dismutase (SOD), and Glutathione] were assessed in the frontal cortex, hippocampus, striatum, and serum. The PSD increased the male and female mice locomotion, but the alloxan's pre-administration prevented the PSD-induced hyperactivity. In addition, the male mice receiving alloxan and submitted to the PSD had elevated latency time in the first quadrant and the number of fecal boli, demonstrating increased anxiety-like behavior. The HPA-axis was hyperactivating in male and female mice pre-administered alloxan and/or PSD-submitted animals. The oxidative stress parameters were also increased in the serum of the animals administered alloxan and/or sleep-deprived mice. Despite alloxan or PSD leading to behavioral or biochemical alterations, the one did not potentiate the other in mice. However, more studies are necessary to identify the link between sleep and hyperglycemia.

How BDNF affects working memory in acute sleep deprivation: The mediating role of spontaneous brain activity.

The brain-derived neurotrophic factor (BDNF) mediates the plasticity associated with memory processing, and compensatorily increases after acute sleep deprivation (SD). However, whether the altered spontaneous brain activity mediates the association between BDNF and working memory in SD remains unknown. Here, we aimed to probe the mediating role of the spontaneous brain activity between plasma BDNF and WM function in SD. A total of 30 healthy subjects with regular sleep were enrolled in this study. Resting-sate functional magnetic resonance imaging (fMRI) scans and the peripheral blood were collected before and after 24 h SD. All participants also received n-back task assessing working memory (WM) performance. The amplitude of low-frequency fluctuation (ALFF) and fractional ALFF (fALFF) were calculated to reflect the intensity of regional spontaneous brain activity. Plasma BDNF was measured by sandwich ELISA. Our results revealed a significant decline in WM and increase in plasma BDNF level after SD, and negative association between the changed WM performance and plasma BDNF level. Specially, the ALFF of the left inferior parietal cortex and right inferior frontal cortex, and fALFF of the left anterior cingulate and medial prefrontal cortex and left posterior opercular cortex regulated the association between the BDNF and one-back reaction time respectively. Our results suggest that the association between BDNF and working memory may be mediated through regional spontaneous brain activity involving in the cerebral cortex, which may provide new sight into the interaction between neurotrophic factors and cognition, and potential targets for noninvasive brain stimulation on WM decline after acute SD.

Sex-specific association of sleep duration with subclinical indicators of metabolic diseases among asymptomatic adults.

BACKGROUND: Accumulating evidence suggests sleep duration may be involved in metabolic regulation. However, studies regarding the association with the early stage of the metabolic disease are limited, and the findings were inconsistent. METHODS: A study among 4922 asymptomatic adults was conducted based on a Chinese national survey in 2009. The early stage of metabolic diseases was evaluated using three proxies: triglyceride to high-density lipoprotein cholesterol ratio (TG/HDL-C), the product of triglyceride and fasting glucose (TyG), and lipid accumulation product (LAP). Multivariable linear and logistic regression models were used to explore the associations of sleep duration with the three indicators. RESULTS: The linear regression models revealed that, among females, sleep duration <7 h per day, compared with 7-9 h, was associated with an increased value of LAP and TyG by 25.232% (95%CI: 10.738%, 41.623%) and 0.104 (95%CI: 0.024, 0.185), respectively, in the crude model. The effects were attenuated but remained significant for LAP (11.405%; 95%CI: 1.613%, 22.262%). Similarly, the logistic regression models further found that sleep duration <7 h per day could increase the risk of elevated LAP (OR: 1.725, 95CI%:1.042, 2.856) after adjusting for multiple covariates. By contrast, no associations were found among males. CONCLUSIONS: Short sleep duration was associated with subclinical indicators of metabolic diseases, and females were more susceptible to the association.

Insulin resistance induced by long-term sleep deprivation in rhesus macaques can be attenuated by Bifidobacterium.

Long-term sleep deprivation (SD) is a bad lifestyle habit, especially among specific occupational practitioners, characterized by circadian rhythm misalignment and abnormal sleep/wake cycles. SD is closely associated with an increased risk of metabolic disturbance, particularly obesity and insulin resistance. The incretin hormone, glucagon-like peptide-1 (GLP-1), is a critical insulin release determinant secreted by the intestinal L-cell upon food intake. Besides, the gut microbiota participates in metabolic homeostasis and regulates GLP-1 release in a circadian rhythm manner. As a commonly recognized intestinal probiotic, Bifidobacterium has various clinical indications regarding its curative effect. However, few studies have investigated the effect of Bifidobacterium supplementation on sleep disorders. In the present study, we explored the impact of long-term SD on the endocrine metabolism of rhesus monkeys and determined the effect of Bifidobacterium supplementation on the SD-induced metabolic status. Lipid concentrations, body weight, fast blood glucose, and insulin levels increased after SD. Furthermore, after 2 mo of long-term SD, the intravenous glucose tolerance test showed that the glucose metabolism was impaired and the insulin sensitivity decreased. Moreover, 1 mo of Bifidobacterium oral administration significantly reduced blood glucose and attenuated insulin resistance in rhesus macaques. Overall, our results suggested that Bifidobacterium might be used to alleviate SD-induced aberrant glucose metabolism and improve insulin resistance. Also, it might help in better understanding the mechanisms governing the beneficial effects of Bifidobacterium.NEW & NOTEWORTHY Our findings demonstrated that long-term sleep deprivation is closely associated with metabolic syndromes. Bifidobacterium administration showed a superior effect on insulin resistance caused by sleep deprivation. Overall, we provide prevention and treatment methods for long-term sleep deprivation, a bad lifestyle habit among specific occupational practitioners, such as irregular shift workers.

Impact of insufficient sleep on dysregulated blood glucose control under standardised meal conditions.

AIMS/HYPOTHESIS: Sleep, diet and exercise are fundamental to metabolic homeostasis. In this secondary analysis of a repeated measures, nutritional intervention study, we tested whether an individual's sleep quality, duration and timing impact glycaemic response to a breakfast meal the following morning. METHODS: Healthy adults' data (N = 953 [41% twins]) were analysed from the PREDICT dietary intervention trial. Participants consumed isoenergetic standardised meals over 2 weeks in the clinic and at home. Actigraphy was used to assess sleep variables (duration, efficiency, timing) and continuous glucose monitors were used to measure glycaemic variation (>8000 meals). RESULTS: Sleep variables were significantly associated with postprandial glycaemic control (2 h incremental AUC), at both between- and within-person levels. Sleep period time interacted with meal type, with a smaller effect of poor sleep on postprandial blood glucose levels when high-carbohydrate (low fat/protein) (pinteraction = 0.02) and high-fat (pinteraction = 0.03) breakfasts were consumed compared with a reference 75 g OGTT. Within-person sleep period time had a similar interaction (high carbohydrate: pinteraction = 0.001, high fat: pinteraction = 0.02). Within- and between-person sleep efficiency were significantly associated with lower postprandial blood glucose levels irrespective of meal type (both p < 0.03). Later sleep midpoint (time deviation from midnight) was found to be significantly associated with higher postprandial glucose, in both between-person and within-person comparisons (p = 0.035 and p = 0.051, respectively). CONCLUSIONS/INTERPRETATION: Poor sleep efficiency and later bedtime routines are associated with more pronounced postprandial glycaemic responses to breakfast the following morning. A person's deviation from their usual sleep pattern was also associated with poorer postprandial glycaemic control. These findings underscore sleep as a modifiable, non-pharmacological therapeutic target for the optimal regulation of human metabolic health. Trial registration ClinicalTrials.gov NCT03479866.

Pain sensitivity increases with sleep disturbance under predictable chronic mild stress in mice.

Even though it has been well documented that stress can lead to the development of sleep disorders and the intensification of pain, their relationships have not been fully understood. The present study was aimed at investigating the effects of predictable chronic mild stress (PCMS) on sleep-wake states and pain threshold, using the PCMS rearing conditions of mesh wire (MW) and water (W) for 21 days. Exposure to PCMS decreased the amount of non-rapid eye movement (NREM) sleep during the dark phase. Moreover, the chronicity of PCMS decreased slow-wave activity (SWA) during NREM sleep in the MW and W groups in both the light and dark phases. Mechanical and aversively hot thermal hyperalgesia were more intensified in the PCMS groups than the control. Higher plasma corticosterone levels were seen in mice subjected to PCMS, whereas TNF-α expression was found higher in the hypothalamus in the W and the trigeminal ganglion in the MW group. The W group had higher expression levels of IL-6 in the thalamus as well. The PCMS paradigm decreased SWA and may have intensified mechanical and thermal hyperalgesia. The current study also suggests that rearing under PCMS may cause impaired sleep quality and heightened pain sensation to painful mechanical and aversively hot thermal stimuli.

Differential effect of sleep deprivation on place cell representations, sleep architecture, and memory in young and old mice.

Poor sleep quality is associated with age-related cognitive decline, and whether reversal of these alterations is possible is unknown. In this study, we report how sleep deprivation (SD) affects hippocampal representations, sleep patterns, and memory in young and old mice. After training in a hippocampus-dependent object-place recognition (OPR) task, control animals sleep ad libitum, although experimental animals undergo 5 h of SD, followed by recovery sleep. Young controls and old SD mice exhibit successful OPR memory, whereas young SD and old control mice are impaired. Successful performance is associated with two cellular phenotypes: (1) "context" cells, which remain stable throughout training and testing, and (2) "object configuration" cells, which remap when objects are introduced to the context and during testing. Additionally, effective memory correlates with spindle counts during non-rapid eye movement (NREM)/rapid eye movement (REM) sigma transitions. These results suggest SD may serve to ameliorate age-related memory deficits and allow hippocampal representations to adapt to changing environments.

Trait positive affect buffers the association between experimental sleep disruption and inflammation.

BACKGROUND: Sleep disturbances and insufficient sleep are highly prevalent. Both clinical sleep disorders and multiple forms of experimental sleep loss predict heightened inflammation. As such, it is necessary to investigate potential protective factors. Given that trait positive affect (PA) is associated with reduced inflammation, and buffers the proinflammatory effects of stress, it is possible that high trait positive affect might protect individuals from an inflammatory response to sleep disruption. The present study tested this hypothesis in an experimental sleep disruption paradigm with assessment of cellular inflammation. METHODS: Data were drawn from good sleeping adults (n = 79) who participated in a randomized, within-subjects crossover experiment comparing the effects of two nights of sleep disruption versus two nights of uninterrupted sleep. Stimulated monocytic production of intracellular proinflammatory cytokines tumor necrosis factor (TNF) and interleukin-6 (IL-6) were assayed using flow cytometric methods and indexed as the percentage of monocytes expressing TNF, IL-6, or co-expressing both. Hypotheses were evaluated using linear mixed effects models. RESULTS: Controlling for negative affect, body mass index, age, and sex, PA significantly moderated the associations between sleep condition and stimulated monocyte production of IL-6 (b = -1.03, t = -2.02, p = .048) and its co-expression with TNF (b = -0.93, t = -2.00, p = .049), such that inflammatory responses were blunted among those high in PA with increases principally among those low in PA. The effect on TNF was similar in terms of effect size, but marginally significant. CONCLUSIONS: Activation of cellular inflammation in response to sleep disruption is buffered by PA independent of negative affect. Interventions that promote PA might protect persons from the inflammatory activation following sleep loss, with the potential to mitigate the adverse health consequences of sleep disturbance.

Impairments in glycaemic control do not increase linearly with repeated nights of sleep restriction in healthy adults: a randomised controlled trial.

Evidence suggests reduced glycaemic control following sleep restriction in healthy individuals. However, it remains unknown if impairments in glycaemic control increase with each additional night of sleep restriction in a linear manner. This randomised crossover study aimed to determine if the impairment in glycaemic control increases with each additional night of sleep restriction. Ten healthy individuals underwent 4 nights of control sleep (8 hours in bed) and 4 nights of sleep restriction (4 hours in bed) in a sleep laboratory. An oral glucose tolerance test was conducted each morning. Serum glucose and insulin were measured. Glucose and insulin area under the curve were higher overall in the sleep restriction trial compared with control (p < 0.001 and p = 0.033); however, no effect of day (p = 0.620 and p = 0.863) or interaction effect (p = 0.152 and p = 0.285) were observed. This supports previous literature showing a detrimental impact of sleep restriction on glucose regulation. The present findings, however, suggest the impairment in glycaemic control does not increase in a linear manner with an increasing number of nights of sleep restriction. This may have implications for the design of future studies examining sleep restriction and glycaemic control. Novelty: Four nights of sleep restriction impaired glycaemic control in healthy individuals, but did not do so in a linear manner. No effect of number of nights of restriction was found for glucose or insulin, which may have implications for future studies.

Flowerpot method for rapid eye movement sleep deprivation does not induce stress as defined by elevated serum corticosterone level in rats.

Flowerpot method of rapid eye movement sleep (REMS) deprivation (REMSD) has been most extensively used in experiments to decipher the functions of REMS. The most common but serious criticism of this method has been presumed stress experienced by the experimental animals. The lack of systematic studies with appropriate controls to resolve this issue prompted this study. We have compared serum corticosterone levels as a marker of stress in male rats under REMSD by the flowerpot method and multiple types of control conditions. Additionally, to maintain consistency and uniformity of REMSD among groups, in the same rats, we estimated brain Na-K ATPase activity, which has been consistently reported to increase upon REMSD. The most effective method was one rat in single- or multiple-platforms set-up in a pool because it significantly increased Na-K ATPase activity without elevating serum corticosterone level. More than one rat in multiple platform set-up was ineffective and must be avoided. Also, large platform- and recovery-controls must be carried out simultaneously to rule out non-specific confounding effects.

The effect of acute sleep deprivation on skeletal muscle protein synthesis and the hormonal environment.

Chronic sleep loss is a potent catabolic stressor, increasing the risk of metabolic dysfunction and loss of muscle mass and function. To provide mechanistic insight into these clinical outcomes, we sought to determine if acute sleep deprivation blunts skeletal muscle protein synthesis and promotes a catabolic environment. Healthy young adults (N = 13; seven male, six female) were subjected to one night of total sleep deprivation (DEP) and normal sleep (CON) in a randomized cross-over design. Anabolic and catabolic hormonal profiles were assessed across the following day. Postprandial muscle protein fractional synthesis rate (FSR) was assessed between 13:00 and 15:00 and gene markers of muscle protein degradation were assessed at 13:00. Acute sleep deprivation reduced muscle protein synthesis by 18% (CON: 0.072 ± 0.015% vs. DEP: 0.059 ± 0.014%·h-1 , p = .040). In addition, sleep deprivation increased plasma cortisol by 21% (p = .030) and decreased plasma testosterone by 24% (p = .029). No difference was found in the markers of protein degradation. A single night of total sleep deprivation is sufficient to induce anabolic resistance and a procatabolic environment. These acute changes may represent mechanistic precursors driving the metabolic dysfunction and body composition changes associated with chronic sleep deprivation.

Association of sleep quality and sleep duration with serum uric acid levels in adults.

OBJECTIVE: To date, the association between sleep duration or sleep quality and hyperuricemia has remained unclear. In addition, sleep duration and quality were not considered concomitantly in previous studies. Thus, this study was aimed toward an examination of the association of sleep duration and quality with uric acid level in a Taiwanese population. METHODS: A total of 4,555 patients aged ≥18 years were enrolled in this study. The sleep duration was classified into three groups: short (<7 h), normal (7-9 h), and long (≥9 h). The Pittsburgh Sleep Quality Index (PSQI) was used to evaluate sleep quality, and poor sleep quality was defined as a global PSQI score of >5. RESULTS: Poor sleepers were younger and had lower body mass index, blood pressure, uric acid, blood sugar, cholesterol, creatinine level, shorter sleep duration, and engaged in less exercise but had a higher white blood cell count and prevalence of smoking as compared to good sleepers. There were also differences in body mass index, blood pressure, uric acid, blood sugar, lipid profiles, and sleep quality among subjects with different sleep durations. After adjusting for other variables, poor sleep quality was associated with lower uric acid levels. In addition, short sleep duration was positively associated with higher uric acid levels. CONCLUSIONS: Poor sleep quality was related to lower uric acid levels, whereas short sleep duration was associated with higher uric acid levels.

Glucose control upon waking is unaffected by hourly sleep fragmentation during the night, but is impaired by morning caffeinated coffee.

Morning coffee is a common remedy following disrupted sleep, yet each factor can independently impair glucose tolerance and insulin sensitivity in healthy adults. Remarkably, the combined effects of sleep fragmentation and coffee on glucose control upon waking per se have never been investigated. In a randomised crossover design, twenty-nine adults (mean age: 21 (sd 1) years, BMI: 24·4 (sd 3·3) kg/m2) underwent three oral glucose tolerance tests (OGTT). One following a habitual night of sleep (Control; in bed, lights-off trying to sleep approximately 23.00-07.00 hours), the others following a night of sleep fragmentation (as Control but waking hourly for 5 min), with and without morning coffee approximately 1 h after waking (approximately 300 mg caffeine as black coffee 30 min prior to OGTT). Individualised peak plasma glucose and insulin concentrations were unaffected by sleep quality but were higher following coffee consumption (mean (normalised CI) for Control, Fragmented and Fragmented + Coffee, respectively; glucose: 8·20 (normalised CI 7·93, 8·47) mmol/l v. 8·23 (normalised CI 7·96, 8·50) mmol/l v. 8·96 (normalised CI 8·70, 9·22) mmol/l; insulin: 265 (normalised CI 247, 283) pmol/l; and 235 (normalised CI 218, 253) pmol/l; and 310 (normalised CI 284, 337) pmol/l). Likewise, incremental AUC for plasma glucose was higher in the Fragmented + Coffee trial compared with Fragmented. Whilst sleep fragmentation did not alter glycaemic or insulinaemic responses to morning glucose ingestion, if a strong caffeinated coffee is consumed, then a reduction in glucose tolerance can be expected.

Partial sleep deprivation after an acute exercise session does not augment hepcidin levels the following day.

The purpose of the present study was to determine the effects of partial sleep deprivation (PSD) after an exercise session in the evening on the endurance exercise-induced hepcidin response the following morning. Ten recreationally trained males participated under two different conditions. Each condition consisted of 2 consecutive days of training (days 1 and 2). On day 1, participants ran for 60 min at 75% of maximal oxygen uptake ( V˙ O2max ) followed by 100 drop jumps. Sleep duration at night was manipulated, with a normal length of sleep (CON condition, 23:00-07:00 hr) or a shortened length of sleep (PSD condition). On the morning of day 2, the participants ran for 60 min at 65% of V˙ O2max . Sleep duration was significantly shorter under the PSD condition (141.2 ± 13.3 min) than under the CON condition (469.0 ± 2.3 min, p < .0001). Serum hepcidin, plasma interleukin (IL)-6, serum haptoglobin, iron, and myoglobin levels did not differ significantly between the conditions (p > .05) on the morning (before exercise) of day 2. Additionally, the 3-hr postexercise levels for the hematological variables were not significantly different between the two conditions (p > .05). In conclusion, the present study demonstrated that a single night of PSD after an exercise session in the evening did not affect baseline serum hepcidin level the following morning. Moreover, a 60 min run the following morning increased serum hepcidin and plasma IL-6 levels significantly, but the exercise-induced elevations were not affected by PSD.

Effect of sleep loss on executive function and plasma corticosterone levels in an arctic-breeding songbird, the Lapland longspur (Calcarius lapponicus).

Sleep is a fundamental component of vertebrate life, although its exact functions remain unclear. Animals deprived of sleep typically show reduced neurobiological performance, health, and in some cases, survival. However, a number of vertebrate taxa exhibit adaptations that permit normal activities even when sleep is reduced. Lapland longspurs (Calcarius lapponicus), arctic-breeding passerine birds, exhibit around-the-clock activity during their short breeding season, with an inactive period of ca. 4 h/day. Whether behavioral or physiological costs occur from sleep loss (SL) in this species is unknown. To assess the effects of SL, wild-caught male longspurs were placed in captivity (12L:12D) and trained for one month to successfully learn color association and spatial memory tasks. Birds were then placed in automated sleep fragmentation cages that utilize a moving wire to force movement every 1 min (60 arousals/h) during 12D (inactive period) or control conditions (during 12L; active period). After SL (or control) treatment, birds were presented with color association and spatial memory tasks a final time to assess executive function. Baseline plasma corticosterone concentration, body mass, and satiety were also measured. SL significantly elevated corticosterone levels and increased accuracy during color association recall but did not affect the overall time required to complete the task. SL had no effect upon spatial memory, body mass, or satiety. Taken together, these results suggest that Lapland longspurs exhibit a degree of behavioral, but not physiological, insensitivity to acute SL. Whether elevated plasma concentrations of corticosterone play a direct role in ameliorating cognitive deficits from SL require additional study.

Sleep Restriction With Circadian Disruption Negatively Alter Bone Turnover Markers in Women.

PURPOSE: The purpose of this work is to determine whether an uncoupling of bone turnover markers (BTMs) occurs in women exposed to the combination of sleep restriction with circadian disruption (SRCD), as previously reported in men. METHODS: Four bone biomarkers (N-terminal propeptide of type I procollagen [P1NP] and osteocalcin = bone formation; C-telopeptide [CTX] = bone resorption; sclerostin = bone formation inhibitor) were measured in bihourly samples over 24 hours at baseline and after approximately 3 weeks of sleep restriction (~5.6 hours of sleep/24 hours) with concurrent circadian disruption (SRCD, recurring 28-hour "day" in dim light). Maximum likelihood estimation in a repeated-measures model was used to assess the effects of SRCD and age on bone biomarkers. RESULTS: Five women were young (22 ±â€…2.8 years) and four were older (58 ±â€…1.8 years). Baseline bone biomarker levels did not differ by age (all P ≥ .07). Bone formation markers were lower after SRCD (estimate ±â€…SEE, ΔP1NP = -9.5 ±â€…2.8 µg/L, P = .01; Δosteocalcin = -2.3 ±â€…0.9 ng/mL, P = .04). The P1NP decline was greater in young women (ΔP1NP = -12.9 ±â€…3.7 µg/L, P = .01). After SRCD, CTX was significantly higher in young women (0.182 ±â€…0.069 ng/mL, P = .04) but did not change in older women. CONCLUSIONS: These pilot data are similar to previous findings in men and suggest that SRCD negatively altered bone metabolism in women by decreasing markers of bone formation and, in young women, increasing a marker of bone resorption. If sustained, this pattern of BTM uncoupling may lead to bone loss and lower bone mineral density.

Inadequate sleep as a contributor to impaired glucose tolerance: A cross-sectional study in children, adolescents, and young adults with circadian rhythm sleep-wake disorder.

BACKGROUND: Sleep deprivation and circadian disruption are associated with decreased insulin sensitivity and hyperglycemia. It is uncertain whether circadian sleep-wake disorder (CRSWD), which relates to both the homeostatic sleep system and the circadian timing system, affects glycemic regulation and insulin secretion. We aimed to examine the associations among sleep duration, sleep architecture or circadian rhythm of the sleep-wake cycle, and glucose metabolism in children, adolescents, and young adults with CRSWD. METHODS: This cross-sectional observational study of 124 patients with CRSWD took place at Hyogo Children's Sleep and Development Medical Research Center in Hyogo, Japan. The patients underwent a 3-hour oral glucose tolerance test, anthropometric measurements, sleep-log analyses, and polysomnography. Analysis of covariance models were used to assess the association between sleep architecture or circadian rhythm of sleep-wake cycle and glucose/insulin homeostasis, adjusted for confounding variables such as age, gender, standardized body mass index, and sleep apnea index. RESULTS: Impaired glucose tolerance was detected in 25.8% of all patients with CRSWD. After adjustment for confounding variables, we found a negative association between total sleep time (TST) and the 2-hour plasma glucose level. Stage N1 (%TST) was also a significant predictor of 3-hour glucose level. However, we did not detect an association between circadian rhythm of the sleep-wake cycle and glucose/insulin measures. CONCLUSIONS: Decreased sleep duration and increased stage N1 (%TST) were associated with hyperglycemia in patients with CRSWD. Further research should elucidate how circadian misalignment in patients with CRSWD is associated with glucose and insulin homeostasis.

Effects of acute sleep loss on diurnal plasma dynamics of CNS health biomarkers in young men.

OBJECTIVE: Disrupted sleep increases CSF levels of tau and ß-amyloid (Aß) and is associated with an increased risk of Alzheimer disease (AD). Our aim was to determine whether acute sleep loss alters diurnal profiles of plasma-based AD-associated biomarkers. METHODS: In a 2-condition crossover study, 15 healthy young men participated in 2 standardized sedentary in-laboratory conditions in randomized order: normal sleep vs overnight sleep loss. Plasma levels of total tau (t-tau), Aß40, Aß42, neurofilament light chain (NfL), and glial fibrillary acidic protein (GFAP) were assessed using ultrasensitive single molecule array assays or ELISAs, in the fasted state in the evening prior to, and in the morning after, each intervention. RESULTS: In response to sleep loss (+17.2%), compared with normal sleep (+1.8%), the evening to morning ratio was increased for t-tau (p = 0.035). No changes between the sleep conditions were seen for levels of Aß40, Aß42, NfL, or GFAP (all p > 0.10). The AD risk genotype rs4420638 did not significantly interact with sleep loss-related diurnal changes in plasma levels of Aß40 or Aß42 (p > 0.10). Plasma levels of Aß42 (-17.1%) and GFAP (-12.1%) exhibited an evening to morning decrease across conditions (p < 0.05). CONCLUSIONS: Our exploratory study suggests that acute sleep loss results in increased blood levels of t-tau. These changes provide further evidence that sleep loss may have detrimental effects on brain health even in younger individuals. Larger cohorts are warranted to delineate sleep vs circadian mechanisms, implications for long-term recurrent conditions (e.g., in shift workers), as well as interactions with other lifestyle and genetic factors.