No full-text available
To read the full-text of this research,
you can request a copy directly from the authors.
Spiegel K, Leproult R, Van CE. Impact of sleep debt on metabolic and endocrine function. Lancet 354, 1435-1439
Abstract
Chronic sleep debt is becoming increasingly common and affects millions of people in more-developed countries. Sleep debt is currently believed to have no adverse effect on health. We investigated the effect of sleep debt on metabolic and endocrine functions.
We assessed carbohydrate metabolism, thyrotropic function, activity of the hypothalamo-pituitary-adrenal axis, and sympathovagal balance in 11 young men after time in bed had been restricted to 4 h per night for 6 nights. We compared the sleep-debt condition with measurements taken at the end of a sleep-recovery period when participants were allowed 12 h in bed per night for 6 nights.
Glucose tolerance was lower in the sleep-debt condition than in the fully rested condition (p<0.02), as were thyrotropin concentrations (p<0.01). Evening cortisol concentrations were raised (p=0.0001) and activity of the sympathetic nervous system was increased in the sleep-debt condition (p<0.02).
Sleep debt has a harmful impact on carbohydrate metabolism and endocrine function. The effects are similar to those seen in normal ageing and, therefore, sleep debt may increase the severity of age-related chronic disorders.
... Adequate and regular sleep is crucial for the proper functioning of the body's metabolism, hormonal processes, and regulation of glucose metabolism. 5,6 Research has shown that short-term sleep restriction or sleep disturbances, 5,7 as well as chronic sleep deprivation, 5,8,9 are associated with glucose intolerance, insulin resistance, and metabolic and endocrine changes in healthy individuals. Additionally, there is a correlation between inadequate sleep (less than five hours) or excessive sleep (more than nine hours), difficulty initiating and maintaining sleep, and metabolic disorders such as type 2 diabetes and obesity. ...
... Adequate and regular sleep is crucial for the proper functioning of the body's metabolism, hormonal processes, and regulation of glucose metabolism. 5,6 Research has shown that short-term sleep restriction or sleep disturbances, 5,7 as well as chronic sleep deprivation, 5,8,9 are associated with glucose intolerance, insulin resistance, and metabolic and endocrine changes in healthy individuals. Additionally, there is a correlation between inadequate sleep (less than five hours) or excessive sleep (more than nine hours), difficulty initiating and maintaining sleep, and metabolic disorders such as type 2 diabetes and obesity. ...
... Adequate and regular sleep is crucial for the proper functioning of the body's metabolism, hormonal processes, and regulation of glucose metabolism. 5,6 Research has shown that short-term sleep restriction or sleep disturbances, 5,7 as well as chronic sleep deprivation, 5,8,9 are associated with glucose intolerance, insulin resistance, and metabolic and endocrine changes in healthy individuals. Additionally, there is a correlation between inadequate sleep (less than five hours) or excessive sleep (more than nine hours), difficulty initiating and maintaining sleep, and metabolic disorders such as type 2 diabetes and obesity. ...
... Considerando situações de privação de sono, veri ica-se um mecanismo de proteção das funções orgânicas a partir do aumento da glicose e insulina, constatando-se com isso, um importante prejuízo no metabolismo glicídico (SPIEGEL et al., 1999). ...
... Ao longo do dia, os níveis de glicose caem de forma importante em indivíduos que se encontram em jejum e repouso, e o contrário é observado durante o período de sono, quando os níveis de glicose se mantêm equilibrados (SPIEGEL et al., 1999;SPIEGEL et al., 2009). ...
... Tais dados conduzem à ideia de que a privação de sono, parcial ou total, possibilita a ocorrência de inúmeras consequências em adição aos prejuízos evidenciados no metabolismo orgânico, em especial no glicídico (SPIEGEL et al., 1999;BISSCHOP et al., 2001;PADILHA et al., 2011), tais como disfunção cognitiva, lapsos de atenção, memória reduzida e humor deprimido (BANKS;DINGES, 2007). ...
Considera-se importante marcador biológico o ritmo circadiano associado às características do estilo de vida e saúde. A privação de sono relaciona-se com alterações no metabolismo glicídico, possibilitando o desenvolvimento de patologias de ordem crônica, especialmente diabetes mellitus II. O objetivo do presente estudo foi identificar a relevância e consequências da deficiência de sono sobre o metabolismo glicídico. Para tal, utilizaram-se trabalhos publicados entre os anos 1990 e 2013 para compor a revisão, indexados nas bases de dados Medline, Lilacs e Scielo. Várias são as alterações evidenciadas no metabolismo glicídico decorrentes da privação de sono, que culminam no desenvolvimento de diabetes mellitus II. Verifica-se a necessidade de conscientização da população em relação à importância do período do sono com a finalidade de evitar a ocorrência de desequilíbrios metabólicos que envolvem o desenvolvimento de patologias, tais como a diabetes mellitus II, e, dessa forma, salvaguardar a saúde do organismo como um todo.
... Both decreased sleep quality and quantity result in varying states of disturbed sleep, situated along a spectrum of partial (< 5 h total sleep duration per night, continuous or fragmented) to total sleep deprivation (complete sleep abstinence for ≥ 24 h) (Keramidas and Botonis 2021). While periods of acute sleep deprivation or disturbance (e.g., < 1 week) have been shown to impair physiological function, including autonomic (blood pressure) dysregulation (Tochikubo et al. 1996), reduced glucose tolerance (Spiegel et al. 1999), and endurance performance (Roberts et al. 2019), even a single night of sleep deprivation can result in increased blood pressure (Carter et al. 2012) and muscular sympathetic drive (Kato et al. 2000), reduced heart rate variability (Schlagintweit et al. 2023), and cause considerable endothelial dysfunction (Sauvet et al. 2010;Vierra et al. 2022). These negative physiological and overall health effects associated with disturbed sleep are particularly concerning for individuals who are often physically active while in a sleep-deprived state, such as those working in occupations requiring day-long (10-12 h) and/or 24-h rotating shift work (Costa 2015), military personnel undergoing prolonged operations (Lindsay and Dyche 2012), or athletes experiencing pre-competition nervousness and/or jet lag Communicated by George Havenith. ...
... Of note, prior studies reporting sleep deprivation-related impairments in thermoregulation have employed exercise protocols fixed at an absolute work rate or relative to V O 2peak (Sawka et al. 1984;Kolka and Stephenson 1988;Dewasmes et al. 1993;Moore et al. 2013;Muginshtein-Simkovitch et al. 2015;Tokizawa et al. 2015). It is therefore possible that sleep deprivationrelated shifts toward a lower metabolic rate (Mullington et al. 2009;Spiegel et al. 1999) reduced the thermal stimulus for sweating and/or skin blood flow responses in sleepdeprived participants in the previous studies, perhaps partially explaining disparate results between our study and the significant findings reported in past literature. It is also important to acknowledge that there are numerous factors (e.g., V O 2peak, and body morphology) that could explain individual variation in thermoeffector response in our results. ...
Sleep deprivation has been associated with impaired thermoregulatory function. However, whether these impairments translate to changes in whole-body heat exchange during exercise-heat stress remains unknown. Therefore, following either a night of normal sleep or 24 h of sleep deprivation, 10 young men (mean (SD): 23 (3) years) completed three 30-min bouts of semi-recumbent cycling at increasing fixed rates of metabolic heat production (150, 200, 250 W/m²), each separated by a 15-min rest in dry heat (40 °C, ~ 13% relative humidity). Rates (W/m²) of whole-body total heat exchange (dry + evaporative) were measured continuously and expressed as peak responses [mean of the final 5-min of exercise at the highest metabolic heat production (250 W/m²)]. Body heat storage was quantified as the temporal summation of heat production and loss. Core temperature, indexed by rectal temperature, was measured continuously. Relative to normal sleep, sleep deprivation did not modify whole-body heat exchange (evaporative (−6 [−18, 5] W/m²; P = 0.245), or dry (7 [−5, 19] W/m²; P = 0.209; sleep deprivation—normal sleep mean difference [95%CIs]) and therefore total heat loss (1 [−14, 15] W/m²; P = 0.917). There were no differences in either the change in body heat storage (−9 [−67, 49] kJ; P = 0.732) or change in core temperature (0.1 [−0.1, 0.3] °C; P = 0.186) between conditions. Overall, we showed that 24-h sleep deprivation did not influence whole-body dry or evaporative heat exchange, resulting in no differences in total whole-body heat exchange or body heat storage in young adults during exercise under hot-dry conditions.
... The significant role of sleep in glycemic control and metabolism has been largely reported. Since the findings of Spiegel et al. [13] in 1999 regarding the negative impact of sleep debt on carbohydrate metabolism and endocrine function, many studies have reported a U-shaped relationship between sleep duration and type 2 diabetes [14][15][16]. Although the mechanisms underlying the relationship between total sleep duration and type 2 diabetes have not been fully elucidated, glucose tolerance and tryptophan concentration have been reported to decrease with sleep debt, whereas evening cortisol secretion increases, leading to increased insulin resistance [13]. ...
... Since the findings of Spiegel et al. [13] in 1999 regarding the negative impact of sleep debt on carbohydrate metabolism and endocrine function, many studies have reported a U-shaped relationship between sleep duration and type 2 diabetes [14][15][16]. Although the mechanisms underlying the relationship between total sleep duration and type 2 diabetes have not been fully elucidated, glucose tolerance and tryptophan concentration have been reported to decrease with sleep debt, whereas evening cortisol secretion increases, leading to increased insulin resistance [13]. Furthermore, sleep deprivation alters the metabolism of adipose tissue because sleep curtailment reduces Akt phosphorylation in adipocytes, indicating insulin resistance [17]. ...
BACKGROUND/OBJECTIVES
Sleep duration and diet quality are reportedly associated with the risk of diabetes. This study aimed to examine the risk of diabetes according to sleep duration and diet quality in middle-aged Koreans.
SUBJECTS/METHODS
Using the Korea National Health and Nutrition Examination Survey 2019–2020, raw data from 2,934 participants aged 40–64 yrs (1,090 men and 1,844 women) who were not diagnosed with type 2 diabetes were analyzed. With a sleep duration of 7–7.9 h per night as the referent category, diet quality was assessed using the Korean Healthy Eating Index (KHEI), which comprises adequacy, moderation, and energy balance.
RESULTS
The study results showed that individuals with a short sleep duration had significantly higher blood glucose (P = 0.034) and HbA1c levels (P < 0.001) than those had by individuals with a sleep duration of 7–7.9 h. Within the group with a sleep duration of 7–7.9 h, the lowest quintile of the KHEI score had a significantly higher risk of prediabetes than that had by the highest quintile of the KHEI score (Model 1: odds ratio [OR], 1.775; 95% confidence interval [CI], 1.072–2.939; P < 0.05 and Model 2: OR, 1.731; 95% CI, 1.040–2.882; P < 0.05).
CONCLUSION
Our findings suggest that achieving the sleep duration of 7–7.9 h and eating good diet are associated with the lowest risk of prediabetes. We recommend that the results of this study be used to educate adults aged 40–64 yrs on diet and lifestyle habits to prevent diabetes.
... When sleep is broken, then brain hormones and metabolism change in a manner to gain weight. Waking up repeatedly lowers the amount of GH, which is highly active during deep sleep and is lowered by decreased hypothalamic-pituitary-adrenal activity to prolong elevated evening and night levels of cortisol (Spiegel et al., 1999). When cortisol levels in the body go high, fat deposition occurs and insulin resistance occurs in particular the abdomen. ...
All over the globe, the occurrence of obesity has become a serious public health problem. While diet and physical activity have long been acknowledged as the primary culprits of childhood obesity, there is now convincing evidence to suggest that sleep patterns are also responsible. This article looks at how sleep timings, quality or duration relate to the threat of obesity in children and adolescents. We dive into the physiological and behavioral mechanisms that sleep disruption produces obesity. It includes hormonal imbalance, appetite regulation, and physical activity changes. We also analyze the influence of modern lifestyles like screen time, irregular school schedules, and socioeconomic factors on sleep and weight status in children. As per existing evidence, encouraging beneficial sleep patterns should be recognized as an essential part of preventing and managing obesity in children.
... The mechanism through which irregular sleep patterns increases risk of obesity could be explained under both theories [55]. Irregular sleep duration may adversely influence sleep quantity and sleep quality and is correlated with metabolically unhealthy sleep-related traits such as evening chronotype, which collectively lead to energy imbalance and weight gain [56][57][58][59]. Further, irregular sleep duration can disrupt the circadian timing system that regulates metabolic functions by interfering with external cues, such as light, which in turn affects glucose metabolism, insulin secretion, and appetite-regulating hormones, as well as causing misalignment between biological pathways driven by multiple peripheral and central clocks and external behaviors, adversely impacting metabolism [6,56]. ...
Background
Irregular sleep duration may disrupt circadian rhythms and contribute to metabolic, behavioral, and mood changes, potentially increasing the risk for obesity. However, quantitative data on the relationship between sleep duration irregularity and weight change are lacking.
Methods
In this prospective study, we analyzed data from 10,572 participants (mean age: 63 years) in the UK Biobank who wore accelerometers for a week between 2013 and 2015 and had two body mass index (BMI; kg/m²) measurements on average 2.5 years apart. Irregular sleep duration was assessed by the within-person standard deviation (SD) of 7-night accelerometer-measured sleep duration.
Results
Participants with sleep duration SD > 60 min versus ≤30 min had 0.24 kg/m² (95% CI: 0.08, 0.40) higher BMI change (kg/m²), standardized to three-year intervals, and 80% (95% CI: 1.28, 2.52) higher risk for incident obesity, after adjusting for sociodemographic factors, shift work, and baseline BMI or follow-up period (p-nonlinearity <0.02 for both). These associations remained consistent after adjusting for lifestyle, comorbidities, and other sleep factors, including sleep duration. Age, sex, baseline BMI, and genetic predisposition to higher BMI (measured with a polygenic risk score) did not appear to modify the association.
Conclusions
Since irregular sleep duration is common, trials of interventions targeting sleep irregularity might lead to new public health strategies that tackle obesity.
... Sleep is a dynamic, complex physiological process essential for homeostasis, recovery, and survival [1,2]. Disrupted or delayed sleep is associated with impaired immune function [3], increased susceptibility to infections and impaired wound healing [4,5], impaired metabolic and endocrine function [6], increased pain perception [7,8] and impairment of neurophysiologic organization and memory consolidation [9]. ...
Objective
Severe sleep disruption is common among intensive care unit (ICU) patients. However, the applicability of standard sleep scoring guidelines by the American Academy of Sleep Medicine (AASM) has been questioned, with most polysomnography (PSG) studies in critically ill patients reporting difficulties in setting up and processing and scoring the recordings. The present study explores human inter-rater agreement in sleep stage scoring following the AASM guidelines, within a heterogenous ICU patient cohort.
Results
Two human experts independently scored a total of 51,454 epochs in 20 PSG recordings acquired at the ICU. Epoch-per-epoch comparison of scored stages revealed a Cohen’s κ coefficient of agreement of 0.36 for standard 5-stage scoring. Highest agreement occurred in Wake (κ = 0.46), while REM showed the lowest (κ = 0.12). Significant correlations were found between inter-rater agreement, and Simplified Acute Physiology Score (SAPS II, r = − 0.506, p = 0.038), and 12-month mortality (r = − 0.524, p = 0.031). Comparison with similar studies underscore challenges in applying AASM criteria to ICU patients. Despite accounting for artifacts, disparities persisted, emphasizing the need for a nuanced exploration of factors influencing scoring inconsistencies in critically ill patients.
Trial registration: Trial was registered as “Sleep and biorhythm in the ICU”, in the Centrale Commissie Mensgebonden Onderzoek register, with number NL-OMON43659 (https://onderzoekmetmensen.nl/nl/trial/43659), on registration date august 4th 2015.
... Comparable trends have also been observed in other regions, including China and Australia [25], underscoring that short sleep duration is a widespread global phenomenon. Research consistently indicated that short sleep could result in endocrine alterations [26], including reductions in leptin [27], glucose tolerance [28], and insulin sensitivity [29], as well as increased ghrelin levels, hunger, and appetite [30]. Additionally, various studies have established a link between short sleep and specific behavioral changes, such as decreased physical activity, lower fruit and vegetable consumption [31], and an increase in caloric intake that exceeds total daily energy needs [32]. ...
Background
Insufficient sleep is a widespread issue among children and adolescents, influenced by various factors, including dietary habits. This study aimed to examine the relationship between dietary habits and sleep insufficiency in children and adolescents aged 6 to 18 in Shandong Province, China.
Methods
Data were derived from a 2024 survey assessing sleep status among children and adolescents in Shandong Province. the prevalence of insufficient sleep was determined, and univariable Χ² test was used to explore associations between daily life behaviors and sleep duration. Multivariable logistic regression was employed to analyze the effect of specific dietary habits on sleep insufficiency, adjusting for potential confounding factors.
Results
The overall prevalence of insufficient sleep was 53.28%. After adjusting for confounders, the logistic regression model indicated that regular breakfast consumption 4 ~ 6 times per week (OR = 0.578, 95% CI 0.522 ~ 0.640) or every day (OR = 0.502, 95% CI: 0.450 ~ 0.561) was associated with significantly lower odds of insufficient sleep. Higher vegetable intake more than five times per week (OR = 0.376, 95% CI: 0.338 ~ 0.418) and fruit consumption 4 ~ 5 times per week (OR = 0.866, 95% CI: 0.816 ~ 0.918) or more than five times per week (OR = 0.446, 95% CI: 0.405 ~ 0.490) were also linked to reduced odds of insufficient sleep. Conversely, higher sugary beverage consumption 4 ~ 5 times per week (OR = 2.066, 95% CI: 1.903 ~ 2.243) or more than five times per week (OR = 2.021, 95% CI: 1.838 ~ 2.223) significantly increased the likelihood of insufficient sleep. Fast food consumption 2 ~ 3 times per week (OR = 1.025, 95% CI: 1.003 ~ 1.048) or more than three times per week (OR = 1.036, 95% CI: 1.002 ~ 1.071) was also associated with higher odds of insufficient sleep (P < 0.05).
Conclusion
Dietary habits significantly influence sleep duration among children and adolescents in Shandong Province. Regular breakfast consumption, increased intake of vegetable and fruit, and reduced consumption of sugary beverage and fast food were associated with improved sleep duration. These findings underscored the importance of promoting healthy eating behaviors as a key strategy for addressing sleep-related issues and improving overall well-being in young populations.
... Since the discovery of brain activities during sleep in the 1970s and 1980s, the importance of sleep has been progressively underscored, leading to the identification of numerous sleep disorders by 2005 [6]. As science and technology have advanced, the intricate interplay between sleep and health conditions has been rigorously explored, revealing links between sleep and various health conditions [7][8][9]. ...
Background
The increasing use of conventional cigarettes and e-cigarettes among young adults (18-35 years) in the US raises significant health concerns, including impacts on sleep. While smoking’s adverse health effects are well-documented, the combined effects of conventional cigarette and e-cigarette use on sleep remain under explored, particularly in young adults. This study investigates the association between dual cigarette and e-cigarette use and sleep outcomes in a nationally representative US sample.
Methods
We utilized self-reported data from the 2020 National Health Interview Survey (NHIS) on young adults (N = 6128, Unweighted). Descriptive statistics and chi-squared tests and t-tests, where appropriate, compared socio-demographic, clinical, behavioral, and sleep-related characteristics by conventional cigarette/e-cigarette use status. Multinomial logistic regression estimated the odds of reporting short (<7 hours) or long sleep ( ≥ 9 hours) compared to normal sleep (7-8 hours) across different smoking categories.
Result
Of the total sample, 51.0% were females, mean age: 26.6 years (SD = 4.8). Cigarette smokers were the oldest (mean age 29.2 years), while e-cigarette users were the youngest (mean age 24.7 years) (p < .0001). Poor or long sleep was reported by 72.8% of cigarette smokers, 69.4% of e-cigarette users, and 71.9% of dual users (p < 0.001). Trouble falling asleep daily, or most days was reported by 49.9% of cigarette smokers, 63.6% of e-cigarette users, and 58.5% of dual users (p < 0.001). Difficulty staying asleep daily for most days was reported by 38.0% of cigarette smokers, 45.0% of e-cigarette users, and 44.6% of dual users (p < 0.0001). Furthermore, 13.7% of cigarette smokers, 5.9% of e-cigarette users, and 12.3% of dual users reported never waking up well-rested (p < 0.001). Multinomial logistic regression revealed that cigarette-only users (aOR:1.40, 95%CI:1.06-1.85), e-cigarette users (aOR:1.32, 95%CI:1.06-1.66), and dual users (aOR:1.81, 95%CI:1.46-2.24) had 40%, 32%, and 81% higher odds, respectively, of having poor sleep compared to non-users.
Conclusion
Cigarette and e-cigarette use is associated with poor sleep patterns and quality, with dual users having the greatest odds of having poor sleep outcomes among young adults.
... This sleep phase has been significantly reduced by modern lifestyles [6]. In humans, Spiegel et al. [7] By adhering to a sleep-restriction protocol of four hours per night for six consecutive nights, he exhibited an increase in serum cortisol levels and sympathetic hyperactivity. Additional homeostatic disturbances, including hypothermia and reduced serum gonadal hormone levels, were observed in animals after paradoxical SD for 96 hours [8]. ...
Sleep deprivation (SD) is primarily defined as the quantitative or qualitative disruption of natural sleep. SD is responsible for a variety of adverse health consequences, including daytime sleepiness and an association with multiple chronic conditions. The goal of the investigation is to assess impact of SD on thyroid and pancreatic function in adult male albino rat. This study was conducted on 40 adult male albino rats of local strain. Rats were separated into four equal groups; Group (1): Control group was allowed to sleep normally, group (2): Intermittent SD group for 24 hours, and then rats were returned to home cage and allowed undisturbed for recovery for 12 hours, group (3): Intermittent SD group for 48 hours, and then rats were returned to home cage and allowed undisturbed for recovery for 12 hours, and group (4) was sleep deprived for 1 week (168 hours) continuously. Serum insulin level, fasting blood sugar (FBS), Oral glucose tolerance test (OGTT), and thyroid tissue were assessed. Serum insulin levels were significantly lower in group 2, 3, and 4 compared to group 1 (control group), while FBS levels were significantly higher in group 2, 3, and 4 compared to group 1 (control group) (P1, 2, and 3 <0.001). At 0, 30, 60, 90 and 120 minute, OGTT had significantly greater levels in group 3 and 4 compared to group 1 (control group) (P2, and P3 < 0.001). T3 and TSH levels were significantly greater in group 3 and 4 compared to group 1 (control group) (P2, and P3 < 0.001). T4 levels were insignificantly different among the fo ur studied groups. SD stress disturbed many metabolic functions on adult male albino rats.
... Additionally, sleep health is an essential factor in obesity prevention. However, epidemiological studies indicate that 36-50% of community-dwelling older adults experience trouble sleeping [25,26], which may contribute to obesity by affecting carbohydrate metabolism and endocrine function [3,27]. Despite growing recognition of sleep's role in obesity, high-quality empirical studies examining the association between trouble sleeping and obesity in older adults remain limited. ...
Background
As the global population ages, obesity among older adults has become an increasing public health concern. Lifestyle factors, including physical activity (PA) and sleep, play a critical role in obesity prevention. These behaviors occur within a 24-hour cycle, yet research on the impact of different PA patterns, trouble sleeping, and their combination on obesity in older adults remains limited. This study aimed to explore: (1) the relationship between PA patterns, trouble sleeping, and obesity among older Americans; and (2) the combined effect of PA patterns and trouble sleeping on obesity in this population.
Methods
A total of 10,891 participants aged 60 and older (55.0% female) from the National Health and Nutrition Examination Survey 2007–2018 were included. Trouble sleeping was assessed using the Sleep Disorder Questionnaire, and PA was measured using the Global Physical Activity Questionnaire. Body mass index (BMI) was calculated from objectively measured weight and height. Multivariate linear regression models were used to estimate the association between PA patterns, trouble sleeping, and BMI.
Results
Compared to the inactive group, participants in the insufficiently active group (β = -0.75; 95% CI = -1.27 to -0.23; P = 0.005), weekend warrior group (β = -1.08; 95% CI = -1.88 to -0.28; P = 0.009), and regularly active group (β = -1.58; 95% CI = -2.02 to -1.14; P < 0.001) had a significant negative association with BMI. Participants with trouble sleeping exhibited a positive association with BMI compared to those without trouble sleeping (β = 0.39; 95% CI = 0.02 to 0.75; P = 0.040). Conversely, among participants with trouble sleeping, those who were regularly active exhibited a negative association with BMI (β = -0.56; 95% CI = -1.05 to -0.07; P = 0.027). Additionally, compared to sufficiently active group, both the inactive and insufficiently active groups exhibited a positive association with BMI, regardless of the presence of trouble sleeping.
Conclusion
Insufficient PA and trouble sleeping in older adults are positively associated with obesity. Engaging in either a weekend warrior or regular PA lifestyle is negatively associated with obesity. Furthermore, adopting a regularly active lifestyle may mitigate the negative impact of trouble sleeping on obesity. However, regardless of the presence of trouble sleeping, insufficient PA remains positively associated with obesity in older adults.
... Some propose SSD acts as a stressor that resets sympathovagal balance causing enhanced activation of the sympathetic nervous system and hypothalamic-pituitary-adrenal axis. Accordingly, this results in increased circulation of adrenaline, noradrenaline, rennin, angiotensin, aldosterone, and cortisol, inducing blood vessel constriction that results in elevated BP [71][72][73]. The mechanisms of the LSD-associated elevation of BP are different. ...
Cardiology and sleep societies recommend 7–9 h sleep/night for adults (7–8 h for seniors) and more for youngsters; nonetheless, short sleep duration (SSD) of <7 h/night is epidemic. We searched PubMed for representative investigations, including those cited by meta-analyses, that reported association between SSD and long sleep duration (LSD) of >9 h/night and blood pressure (BP) levels to assess shortcomings of their methods. Studies indicate both SSD and LSD negatively impact BP despite major deficiencies, such as (i) reliance mainly on cross-sectional rather than longitudinal protocols, (ii) inclusion of participants diagnosed with hypertension (HTN) and/or taking antihypertension medications, (iii) assessment of BP and diagnosis of HTN performed by single wake-time office measurement rather than multiple measurements performed by 24 h ambulatory BP monitoring (ABPM), and (iv) determination of SD by subjective recall, single-night polysomnography, or diary recordings rather than objective wrist actigraphy of sufficient duration. The limited number of ABPM-based studies, despite evidencing major shortcomings, particularly (i) assessment for 24 h rather than preferred ≥48 h and (ii) inclusion of subjects diagnosed with HTN and/or taking antihypertension medications, also report association between abnormal SD and elevated 24 h ‘daytime’/wake-time diastolic and systolic (SBP) means plus ‘nighttime’/sleep-time SBP mean and dipping—the latter two indices, in combination, the strongest predictors of major adverse cardiovascular events.
... This dysregulation results in increased levels of glucocorticoid hormones such as cortisol, which can have significant adverse psychological effects, including anxiety (Hirotsu et al. 2015). One possible explanation for this is that SD is associated with hyperactivity of the HPA axis (Spiegel et al. 1999). Furthermore, short-term SD has been reported to increase glutamate concentrations in the basal ganglia (Korenic et al. 2020), and glutamatergic neurotransmission in this brain region has been implicated in mood disorders, including anxiety (Pagonabarraga et al. 2021). ...
Purpose
Insufficient sleep and insomnia are common issues associated with modern lifestyles that often contribute to the development of mental health disorders. 4‐aminopyridine (4‐AP), a voltage‐gated potassium (Kv) channel antagonist, is commonly used in the treatment of multiple sclerosis (MS). It has been shown to improve nerve conduction velocity, strengthen myelin, and increase axonal area after injury. In addition, 4‐AP has been reported to reduce behavioral disorders, including depression. The aim of this study was to investigate the effects of 4‐AP on anxiety‐like behavior in mice subjected to rapid eye movement (REM) sleep deprivation.
Methods
Fifty male mice were randomly divided into five groups: control, normal saline (NS) (receiving normal saline via gavage), AP‐0.25, AP‐0.5, and AP‐1 (receiving daily doses of 0.25, 0.5, and 1 mg/kg of 4‐AP, respectively by gavage). All groups except the control group underwent SD for five consecutive days. The animals' locomotion and anxiety‐like behavior were assessed using the open field and elevated plus maze tests. After behavioral testing, N‐methyl‐D‐aspartate receptor (NMDA‐R), α‐amino‐3‐hydroxy‐5‐methyl‐4‐isoxazolepropionic acid receptor (AMPA‐R), and tumor necrosis factor (TNF‐α) were measured by western blotting, and also malondialdehyde (MDA) and total antioxidant capacity (TAC) were analyzed by ELISA in the hippocampus.
Finding
AP‐1 significantly reduced the levels of anxiety‐like behavior compared to the NS group in both tests. In AP‐1, a significant decrease in the levels of NMDA‐R, AMPA‐R, TNF‐α, and MDA was observed. While these levels were increased in the NS group. In addition, AP‐1 showed a higher level of TAC compared to the NS group, indicating an increase in antioxidant levels.
Conclusion
4‐AP may be effective in reducing anxiety‐like behavior in sleep‐deprived mice by modifying the levels of NMDA‐R, AMPA‐R, and TNF‐α, while simultaneously reducing oxidative stress induced by sleep deprivation in the hippocampus.
... Similarly, our large-scale analyses showed that a short sleep duration of less than 7 h is a significant risk factor for the development of obesity. An association between short sleep duration and obesity has been confirmed by the results of recent intervention studies on sleeping hours [27,28] and can also be partly explained by some physiological mechanisms [42,43]. About the physiological mechanisms, it was reported that short sleep duration was associated with reduction of anorexigenic hormone leptin and elevations of orexigenic factor ghrelin, which can lead to increased hunger and appetite [42]. ...
This multicenter study aimed to elucidate the association between sleep duration and various lifestyle-related disorders in healthy adults in Japan. A total of 62,056 healthy participants (age: 49.4 ± 10.9 years) who received medical checkups from 2010 to 2020 were analyzed cross-sectionally and longitudinally. The mean sleep duration was 6.2 ± 1.0 h in men and 6.1 ± 1.0 h in women. The distribution of sleep duration showed that older people tended to sleep longer, which was clearly observed in men but not in women. Univariate analyses showed that older age, lower body mass index (BMI), habitual drinking, and habitual exercise were significantly associated with longer sleep duration. Multivariate analyses in men showed that sleep duration was positively associated with age, habitual exercise, serum triglyceride (TG), systolic blood pressure (SBP), and habitual drinking and negatively associated with BMI and hemoglobin A1c (HbA1c). Alternatively, in women, sleep duration was positively associated with habitual exercise and TG and negatively associated with BMI, high-density lipoprotein-cholesterol, HbA1c, and current smoking. During the follow-up period, 3,360 of 31,004 individuals (10.8%) developed obesity. The Cox proportional hazards model showed that shorter sleep duration was a significantly higher risk of obesity, and longer sleep duration might be a lower risk of obesity. On the other hand, 1,732 of 39,048 participants (4.4%) developed impaired glucose tolerance, and 6,405 of 33,537 participants (19.1%) developed hypertriglyceridemia. However, the Cox proportional hazards model did not show significant association between sleep duration and impaired glucose tolerance or hypertriglyceridemia. In conclusion, our large-scale cross-sectional study showed that sleep duration was positively associated with habitual exercise and TG and negatively associated with BMI and HbA1c, regardless of sex. Longitudinal analysis revealed that shorter sleep duration is a significant risk factor for obesity.
... Elevated nighttime cortisol levels promote glucose production and reduce insulin sensitivity, thereby increasing the risk of developing type 2 diabetes and obesity. Sleep disorders exacerbate these metabolic risks by promoting chronic low-grade inflammation, driven by persistent HPA axis activation [40]. ...
The circadian rhythm of cortisol, a key hormone essential for maintaining metabolic balance and stress homeostasis, is profoundly disrupted by night-shift work. This narrative review examines the physiological mechanisms underlying cortisol regulation, the effects of shift work on its circadian rhythm, the associated health risks, and potential mitigation strategies. Night-shift work alters the natural secretion pattern of cortisol, leading to dysregulation of the hypothalamic–pituitary–adrenal axis, which in turn can contribute to metabolic disorders, cardiovascular diseases, and impaired cognitive function. Understanding the physiological pathways mediating these changes is crucial for developing targeted interventions to mitigate the adverse effects of circadian misalignment. Potential strategies, such as controlled light exposure, strategic napping, and personalized scheduling, may help to stabilize cortisol rhythms and improve health outcomes. This review aims to provide insights that can guide future research and inform occupational health policies for night-shift workers by addressing these challenges.
... The relationship between short sleep and MetS may involve multiple molecular mechanisms. Sleep deprivation is thought to activate the hypothalamic-pituitary-adrenal (HPA) axis, increasing glucocorticoid (especially cortisol) secretion, which leads to hepatic gluconeogenesis and reduced insulin sensitivity in adipocytes, thereby promoting insulin resis-tance and elevated blood glucose levels (Spiegel et al. 1999;Muniyappa et al. 2008). Furthermore, short sleep is associated with decreased leptin levels and increased ghrelin levels, which may lead to increased appetite and subsequently increased body weight and BMI (Spiegel et al. 2004;Taheri et al. 2004). ...
Metabolic syndrome (MetS) and short sleep are prevalent health concerns in the United States, yet the relationship between leisure-time physical activity (LTPA) and MetS among individuals with short sleep duration remains unclear. This cross-sectional study analyzed data from 8999 US adults aged 20 years and older in the National Health and Nutrition Examination Survey. Short sleep duration was defined as less than 7 h per night, and MetS was diagnosed based on criteria from the American Endocrine Society and the American Society of Clinical Endocrinology. Weighted regression analyses revealed a significant inverse association between LTPA and MetS, with higher LTPA levels linked to lower MetS (OR (95% CI): 0.990 (0.984, 0.997), p = 0.003). Participants who achieved the World Health Organization’s recommended LTPA levels had a substantially lower MetS compared to those with no LTPA (OR (95% CI): 0.624 (0.527, 0.738), p = 0.001). Stratified analyses showed that this protective effect varied across demographic subgroups, and a threshold effect was observed at 2000 MET-min/week, beyond which further LTPA did not significantly enhance protection against MetS. These findings highlight the importance of regular LTPA that is negatively associated with MetS among individuals with inadequate sleep, emphasizing the need for targeted health promotion efforts in this population.
... 2 Sleep deprivation may contribute to the development of cardiovascular disease, 3-5 type 2 diabetes, obesity, and premature mortality. [6][7][8][9][10] Furthermore, over 50% of adults had experienced sleep problems during the COVID-19 pandemic 11,12 with adverse consequences on overall health. 13 Within the United States, West Virginia (WV) is one of the most sleep-deprived states, with 42% of residents reporting less than 7 hours of sleep (Center for Disease Control [CDC]) as opposed to the F I G U R E 1 CDC Places: Age-adjusted prevalence of adults who reposted short sleep duration varied by country in 2018 (Reference 4 , CDC Places). ...
Introduction
Sleep is a key component of a healthy lifestyle and the Center for Disease Control (CDC) and prevention recommends that adults get at least 7 hours of sleep each night. Within the United States, West Virginia is among the most sleep-deprived states with 42% of the population reporting insufficient sleep per the CDC. Sleep insufficiency in rural populations is linked to disparities in health and accessibility to health care services. The study evaluated the impact of sleep hygiene (SH) education on sleep duration and quality.
Methods
A 12-week randomized controlled trial of participants residing in Harrison County, WV. Baseline data included the Pittsburgh Sleep Quality Index (PSQI), Epworth Sleepiness Scale, and sleep duration as recorded by a sleep wearable. The intervention included an SH video on weeks 3 and 5. The control arm did not receive intervention but were allowed to cross over and receive intervention at week 8.
Results
A total of 100 participants (61 females) were recruited from the community. No changes in sleep duration were observed in intention to treat analysis between Arm 1 and Arm 2 at 7 weeks. In the treatment analysis, the compliant cohort demonstrated a significant increase of 31 minutes mean sleep duration (P = .01) as well as an improvement in the PSQI (6.30 to 5.68 by week 12, P = .05).
Conclusion
The study demonstrates that the introduction of a modest SH intervention may have a beneficial effect on the duration and quality of sleep in a rural community. ClinicalTrials. gov Identifier: NCT04849572
... The SCN preserves peripheral clock synchrony through neuroendocrine mechanisms that directly influence metabolic processes. It communicates with the autonomic nervous system and regulates the secretion of cortisol, growth hormone, and melatonin, all of which play distinct roles in modulating insulin sensitivity [28]. Irregular sleep patterns, shift work, and exposure to artificial light at night can desynchronise peripheral and central circadian rhythms, leading to insulin resistance and hyperglycaemia [25]. ...
... Studies have shown that physiological changes linked to aging cause widespread sleep disturbances in the elderly [19]. Poor sleep quality or abnormal sleep duration not only disrupts the hypothalamic-pituitary-adrenal axis, resulting in hormonal imbalances [20], but also leads to elevated levels of inflammation [21,22]. Furthermore, substantial evidence shows that short sleep duration is linked to reduced mobility [23] and increased disability [24], whereas long sleep duration is associated with decreased walking speed [23]. ...
Objective
This study aimed to explore the relationship between adverse childhood experiences (ACEs), sleep, and lower extremity function in older adults using a nationally representative cohort.
Methods
This study included 4,439 participants aged 60 years or older (mean age: 67.2 ± 5.7 years) from the China Health and Retirement Longitudinal Study (CHARLS) 2015 national survey and the 2014 Life History Survey. ACEs, sleep duration, and sleep quality were assessed through self-report, and lower extremity function was measured using the Short physical performance battery (SPPB). The relationships between ACEs, sleep, and lower extremity function were analyzed using multivariate linear regression model and restricted cubic splines.
Results
After adjusting for covariates, older adults with four or more ACEs exhibited worse lower extremity function compared to those with no ACEs (β: -0.175). 6–8 h of sleep was associated with improved lower extremity function (β: 0.119), while good sleep quality was also associated with higher lower extremity function scores (β: 0.177). Age-related differences revealed that the association between four or more ACEs and reduced lower extremity function (β: -0.431) was significant only in individuals aged 70 years and older. In the 60–69 years age group, the sleep duration of 6–8 h was significantly related to better lower extremity function (β: 0.150), however, in those aged 70 years and older, more than 8 h of sleep was associated with poorer function (β: -0.378). Furthermore, good sleep quality was associated with better lower extremity function in individuals aged 70 years and older (β: 0.246).
Conclusion
ACEs, particularly household mental illness and parental disability, are associated with poorer lower extremity function in older adults. Normal sleep duration and good sleep quality are linked to better lower extremity function and may mitigate the negative effects of ACEs. However, these associations vary by age.
... Recent data have demonstrated that sleep disorder-induced dyslipidemia may be important in the increased risk of cardiovascular diseases among insomniacs. Theoretically, the quality and duration of sleep influence lipid metabolism in several ways, including altering the endocrine regulation of hormones [14], impacting genes responsible for cholesterol transportation [15], causing a proinflammatory condition, and triggering depression or other psychiatric disorders. However, evidence of an association between insomnia and dyslipidemia remains inconsistent. ...
Sleep is a fundamental phenomenon that helps maintain normal physiological processes. Conversely, sleep disorders, usually presented as insomnia, are a common public health problem that can lead to multiple pathophysiological changes in humans, including lipid metabolic abnormality. Interestingly, several previous studies have examined the potential relation of insomnia to metabolic syndrome and hyperlipidemia and found that insomnia was associated with elevated plasma cholesterol and triglyceride concentrations. This review summarizes evidence regarding the linkage between insomnia and lipid abnormalities. Moreover, the underlying physiologic mechanisms linking insomnia to lipid abnormalities are systemically discussed. Finally, issues with lipid-lowering drugs and the risk of insomnia are also presented. This knowledge can improve our understanding of the pathophysiological features of insomnia, which may help to prevent and treat insomnia-induced dyslipidemia clinically.
... In addition to physical obstacles to sleep, housing instability and material hardship contribute to psychological distress, which exacerbates poor sleep (101). Insufficient sleep increases the risk of mental health disorders, chronic physical conditions (e.g., cardiometabolic diseases, cancer, cognitive issues, dementia), and mortality (101,(111)(112)(113)(114)(115). Given that sleep is predictive of chronic conditions and is associated with physiological inflammation and accelerated epigenetic aging, sleep may be a critical health behavior linking HI with physiological and epigenetic markers of well-being among aging adults (116,117). ...
Introduction
Housing insecurity is a social determinant of health, as evidenced by its associations with mental, physical, and biological outcomes. The scientific understanding of the mechanisms by which housing insecurity is associated with health is still limited. This review adapts existing stress process models to propose a conceptual model illustrating potential pathways linking the specific stressor of housing insecurity to physiological and epigenetic manifestations of stress among aging adults.
Methods
This narrative review examines literature across multiple fields, including public health, psychology, and sociology. The literature selected for this review was identified through scientific databases including Web of Science, PubMed, JSTOR, and Google Scholar; primarily peer-reviewed empirical studies, literature reviews, and research reports published in English between 1981 and 2024; and principally based in the United States context. A synthesis of this literature is presented in a proposed conceptual model.
Results
The literature supports the existence of two main predictors of housing insecurity: sociodemographic characteristics and the historical/current context. The main mediating pathways between housing insecurity and manifestations of stress include health behaviors, psychosocial resources, and structural resources. Moderating factors affecting the associations between housing insecurity and manifestations of stress include government assistance, chronic discrimination/unfair treatment, and individual differences. These interdependent mediating and moderating mechanisms affect stressor reactivity, a proximal manifestation of stress, which contributes to the physiological and epigenetic distal manifestations of stress in aging adults.
Discussion and implications
The prevalence of housing insecurity among aging adults is growing in the United States, with significant implications for public health and health disparities, given the growing percentage of aging adults in the population. Further empirical testing of the mediating and moderating mechanisms proposed in the conceptual model will elucidate how housing insecurity is connected to health and provide insight into preventive strategies to ameliorate the adverse effects of housing insecurity on biological health among aging adults.
... 7,8 The non-food related lifestyle drivers, which are also very difficult to change include (i) increasing physical activity, 71,72 (ii) lowering stress, and (iii) improving sleep quality. 73 The good news is that the volume of research on what works has grown substantially over the last 10 years and the global health community that is focused on T2DM has enough high quality research to start putting together a way forward. An approach that uses lifestyle changes can include the following: ...
For over 50 years, health systems the world over have failed people with type 2 diabetes mellitus (T2DM). The WHO documents a quadrupling of people with diabetes in a 34-year period to 422 million in 2014, the overwhelming majority of whom were T2DM. This happened despite extensive scientific literature on the causes of, as well as proven treatments for, this disease. Using a health systems prism to review the extensive medical and nutritional T2DM published research, we identified three main shortcomings of health systems in T2DM: (i) failure in early detection; (ii) failure in understanding the actionable lifestyle drivers; and (iii) subsidizing the causes of the disease. Although small-scale success stories in T2DM control exist, the lack of documented evidence of any country-wide health system’s successful attempt to address this epidemic is alarming. The immense and ever-growing health and economic burdens of T2DM should provide all the motivation needed for national and global efforts to counteract the political-economy constraints standing in the way of successful whole-of-system approaches to T2DM.
... It has been reported that sleep deprivation induces hypertension, cardiovascular disease, and diabetes in humans because it increases sympathetic nervous system activity. It has been reported that sleep deprivation and intestinal bacteria are closely related to the onset of stress and disease in living organisms (Spiegel et al., 1999, Nagai et al., 2010. Although sleep duration in advanced nations such as the Netherlands, the United Kingdom, and New Zealand exceeds 7.5 hours per day, it is the longer in comparison to Japan and South Korea, at less than 6.5 hours per day (Tozer, 2018). ...
... the impact of sleep duration and quality on insulin sensitivity in humans is both significant and direct [106,107]. extreme sleep conditions, whether characterized by excess sleep or deficient sleep, can lead to a decrease in leptin levels and an increase in ghrelin levels [108]. this hormonal imbalance can trigger heightened appetite, raising the risk of overeating [109], which may subsequently increase BMi and fat accumulation, thereby exacerbating insulin resistance [110,111]. ...
Objective
This study aimed to assess the associations between multidimensional sleep features and type 2 diabetes mellitus (T2DM).
Methods
We conducted a systematic search across the PubMed, Embase, Web of Science, and Scopus databases for observational studies examining the association between nighttime sleep duration, nighttime sleep quality, sleep chronotype, and daytime napping with type 2 diabetes mellitus (T2DM), up to October 1, 2024. If I² < 50%, a combined analysis was performed based on a fixed-effects model, and vice versa, using a random-effects model.
Results
Our analysis revealed that a nighttime sleep duration of less than 7 h (odds ratio [OR] = 1.18; 95% CI = 1.13, 1.23) or more than 8 h (OR = 1.13; 95% CI = 1.09, 1.18) significantly increased the risk of T2DM. Additionally, poor sleep quality (OR = 1.50; 95% CI = 1.30, 1.72) and evening chronotype (OR = 1.59; 95% CI = 1.18, 2.13) were associated with a notably greater risk of developing T2DM. Daytime napping lasting more than 30 min augments the risk of T2DM by 7-20%. Interactively, the incidence of T2DM was most significantly elevated among individuals with poor sleep quality and nighttime sleep duration of more than 8 h (OR = 2.15; 95% CI = 1.19, 3.91).
Conclusions
A U-shaped relationship was observed between sleep duration and type 2 diabetes mellitus (T2DM), with the lowest risk occurring at a sleep duration of 7 to 8 h. Additionally, poor sleep quality, evening chronotypes, and daytime napping exceeding 30 min emerged as potential risk factors for T2DM. These high-risk sleep characteristics interacted with one another, amplifying the overall risk of developing the disease.
... It should therefore not be surprising to unveil an effect of traumatic stressors when sleep is included as additional mediator since a bidirectional relationship between impaired sleep and PTSD has been extensively studied (Maher et al., 2006;Mellman et al., 2007;Lancel et al., 2021), as well as the role it plays in promoting resilience (Arora et al., 2022) and extinction of learned fear after traumatic events (Marshall et al., 2014;Genzel et al., 2015). Moreover, experimental evidence obtained through sleep deprivation protocols have shown that poor sleep quality can be considered as a stressor by itself (McEwen, 2006) that promotes high AL levels by increasing blood pressure, cortisol release, glucose resistance and inflammatory markers, among other effects (Spiegel et al., 1999;Knutson, 2007;Palagini et al., 2013;Dzierzewski et al., 2020;Li and Shang, 2021). ...
Objectives
We assessed the modulation of allostatic load (AL) by engagement in healthy habits and life stressors, mediated through resilience and the perceived influence of the stressors. Sleep was included as third mediator given extensive evidence associating to all the analysed factors.
Methods
Structural equation models to assess the modulation of AL by either traumatic or psychosocial stressors and healthy habits were generated with data from 620 mid-life adults (age 51.3 ± 5.48 years). Model 1 included self-reported life stressors, engagement in cognitive and physical activities, resilience and a pyramid score for diet. In Model 2, self-reported sleep quality was included in the mediation analysis between resilience and perceived stress on AL.
Results
Direct effects of sports and diet on AL, and on resilience by sports were found in all the evaluated models. The modulation of AL by both types of stressors was only revealed in model 2, through indirect effects of perceived influence via sleep quality. An effect of sport habits on AL via resilience was found to be mediated by sleep, and equivalent but opposed effects of perceived influence of stressors and resilience on sleep quality emerged as critical factor for AL modulation.
Conclusion
Our results suggest that sleep plays a pivotal role in the modulation of AL by both life stressors and sport habits, balancing the harmful and protective effects of perceived stress and resilience. The relative weight of one over the other to worsen or improve sleep quality will determine the resulting level of AL.
... During REM sleep, the body experiences significant fluctuations in heart rate and blood pressure, making this phase particularly susceptible to the deleterious effects of apnea, which can lead to systemic hypertension, arrhythmias, and other cardiovascular complication. 25 Additionally, REM-AHI is linked to the development of metabolic syndrome, affecting insulin sensitivity and glucose metabolism, thereby increasing the risk of diabetes 26 Regarding the nervous system, the absence of REM sleep is correlated with cognitive decline and emotional disorders. Poor sleep quality has been shown to impair attention, memory, and emotional stability 27 AI, similar to REM-AHI, higher AI values are indicative of increased sleep fragmentation. ...
Purpose
Obstructive sleep apnea (OSA) is a contributing factor to nonalcoholic fatty liver disease (NAFLD). This study aimed to investigate the clinical and polysomnographic characteristics of OSA patients with and without NAFLD, focusing on the relationships between sleep fragmentation, arousal and NAFLD.
Materials and Methods
We consecutively enrolled patients who underwent polysomnography, anthropometry, blood sampling, and abdominal ultrasonography. Patients were categorized into NAFLD and non-NAFLD groups. A comparative analysis of clinical and polysomnographic profiles was conducted, followed by multivariate binary logistic regression to explore the relationship between sleep disturbance indices and NAFLD.
Results
A total of 403 subjects were included, including 92 patients with NAFLD and 311 with non-NAFLD. NAFLD patients exhibited a greater apnea-hypopnea index (AHI) (51.19/h vs 33.60/h, p = 0.002) and oxygen desaturation index (ODI) (37.90/h vs 21.40/h, p=0.034) compared to non-NAFLD patients. Specifically, NAFLD patients had a higher rapid eye movement (REM)-AHI (53.70/h vs 43.60/h, p=0.001) and greater arousal index (AI) (32 vs 25, p = 0.009). Additionally, sleep latency (SL) was significantly lower in the NAFLD group (p < 0.05). Multivariate logistic regression analysis confirmed that REM-AHI (OR=1.023, p = 0.024), AI (OR=1.140, p = 0.01), and SL (OR=0.956, p = 0.035) were significantly associated with NAFLD in OSA patients.
Conclusion
This study revealed that sleep disturbance indices, especially AI, REM-AHI and SL, were closely related to NAFLD. When evaluating whether OSA patients are complicated with NAFLD, more attention should be given to sleep fragmentation and arousal.
... Similarly, there is an accumulating body of evidence from human experimental (Spiegel et al., 1999;Buxton et al., 2012), epidemiological (Kim et al., 2013;Bernsmeier et al., 2015;Morris et al., 2016;Wijarnpreecha et al., 2016;Marjot et al., 2021;Potter et al., 2016), and genetic (Sookoian et al., 2007) studies implicating an important role for the circadian clock and sleep cycle in the pathogenesis of the metabolic syndrome, specifically MASLD. Several observational studies based on self-reported sleep questionnaires have associated short sleep duration with MASLD (Hsieh et al., 2011;Kim et al., 2013;Bernsmeier et al., 2015;Imaizumi et al., 2015). ...
Metabolic dysfunction–associated steatotic liver disease (MASLD) is a multisystemic disease with a multifactorial pathogenesis involving dietary, environmental, and genetic factors. Previous mouse models suggested that circadian misalignment may additionally influence its development as it influences metabolism in diverse organs including the liver. Further, data from sleep questionnaires proved sleep-wake disruption in patients with MASLD. We objectively assessed sleep-wake rhythms in patients with biopsy-proven MASLD (n = 35) and healthy controls (HC, n = 16) using actigraphy 24/7 for 4 weeks. With the aim to re-align sleep rhythms a single standardized sleep hygiene education session was performed after 2 weeks. Actigraphy data revealed that MASLD patients had more awakenings per night (MASLD vs. HC 8.5 vs. 5.5, p = 0.0036), longer wakefulness after sleep onset (MASLD vs. HC 45.4 min vs. 21.3 min, p = 0.0004), and decreased sleep efficiency (MASLD vs. HC 86.5% vs. 92.8%, p = 0.0008) compared with HC despite comparable sleep duration. Patients with MASLD self-reported shorter sleep duration (MASLD vs. HC 6 h vs. 6 h 45 min, p = 0.01) and prolonged sleep latency contributing to poorer sleep quality. Standardized sleep hygiene education did not produce significant changes in sleep parameters. Our findings indicate fragmented nocturnal sleep in patients with MASLD, characterized by increased wakefulness and reduced sleep efficiency, perceived subjectively as shortened sleep duration and delayed onset. A single sleep hygiene education session did not improve sleep parameters.
... One possible explanation could be a sleep debt in late sleepers, which is associated with a decreased carbohydrate tolerance and increased sympathetic nervous system tonus [202], as well as increased caloric intake as there is more time and opportunities to eat and greater sensitivity to food reward [203]. Late sleeping results in higher exposure to ALAN. ...
Earth’s rotation around its axis has pressured its inhabitants to adapt to 24 h cycles of day and night. Humans adapted their own circadian rhythms to the Earth’s rhythms with a light-aligned awake–sleep cycle. As a consequence, metabolism undergoes drastic changes throughout the circadian cycle and needs plasticity to cope with opposing conditions in the day (when there is an increase in energy demands and food availability), and during the night (when prolonged fasting couples with cyclic changes in the energy demands across the sleep stages). In the last century, human behavior changed dramatically with a disregard for the natural circadian cycles. This misalignment in sleep and eating schedules strongly modulates the metabolism and energy homeostasis, favoring the development of obesity, metabolic syndrome, and metabolic dysfunction-associated steatotic liver disease (MASLD). This review summarizes the effects of circadian disruption, with a particular focus on the feeding and sleep cycles in the development of MASLD and hepatocellular carcinoma.
... The quality and quantity of sleep can be influenced by a variety of environmental, physiological, and chemical factors [2]. In addition, adequate sleep duration must be ensured to maintain homeostasis, cognitive function, and overall health [3]. ...
Background/Objectives: This study aims to investigate the effects of ethylene oxide (EO) exposure on sleep health, focusing on sleep duration and quality. Methods: The study analyzed data from the NHANES (National Health and Nutrition Examination Survey) 2015–2020 cycles, including 4268 participants aged 20 and older. EO exposure was measured using hemoglobin adducts of EO (HbEO), which serve as a reliable biomarker. Sleep health was assessed through self-reported questionnaires on sleep duration and quality. Participants were categorized based on sleep duration (<6 h, 6–9 h, >9 h) and symptoms of sleep disturbances. Statistical analyses employed survey-weighted logistic regression models to evaluate the associations between HbEO levels and sleep outcomes, adjusting for sociodemographic, health-related, and behavioral factors. Moreover, to examine whether the impact of ethylene oxide exposure on sleep quality and sleep duration varies by sociodemographic characteristics, stratified analyses were conducted based on gender, age, marital status, and employment type. Results: According to the results, higher EO exposure was associated with shorter sleep durations and increased likelihood of sleep disturbances. Moreover, according to sub-group analysis by sex, men with higher exposure to EO, were likely to have short sleep duration, and women with higher exposure to EO had higher risk of daytime sleepiness and sleep problems. Conclusions: The findings suggest that EO exposure may negatively impact sleep health, emphasizing the need for stricter EO exposure regulations and public health interventions to reduce associated risks.
... Recent research suggests that altering sleep architecture can influence glycemic control [35,36]. Spectral power, a measure of brain wave activity during sleep, can be increased to enhance the quality and duration of specific sleep stages, potentially leading to therapeutic benefits [37,38]. ...
Data on the relationship between sleep architecture and diabetes are limited. However, some evidence suggests that slow-wave sleep (SWS) plays a crucial role in maintaining normal glucose homeostasis and influences insulin secretion capacity. Diabetes is often associated with reduced SWS, even in the absence of sleep-disordered breathing. Notably, selective suppression of SWS—without reducing total sleep time—can lead to significant increases in insulin resistance, decreased glucose tolerance, and a higher risk of diabetes. Given the growing interest in non-pharmacological lifestyle interventions, such as modifying sleep architecture, it is important to understand how sleep patterns differ in individuals with diabetes and whether these alterations impact diabetes risk and glycemic control. This review aims to provide a concise overview of the current findings on sleep architecture changes in people with diabetes.
... The mechanism through which irregular sleep patterns increases risk of obesity could be explained under both theories (53). Irregular sleep duration may adversely influence sleep quantity and sleep quality and is correlated with metabolically unhealthy sleep-related traits such as evening chronotype, which collectively lead to energy imbalance and weight gain (54)(55)(56)(57). Further, irregular sleep duration can disrupt the circadian timing system that regulates metabolic functions by interfering with external cues, such as light, which in turn affects glucose metabolism, insulin secretion, and appetite-regulating hormones, as well as causing misalignment between biological pathways driven by multiple peripheral and central clocks and external behaviors, adversely impacting metabolism (6,54). ...
Irregular sleep duration may disrupt circadian rhythms and contribute to metabolic, behavioral, and mood changes, potentially increasing the risk for obesity. However, quantitative data on the relationship between sleep duration irregularity and weight change are lacking. In this prospective study, we analyzed data from 10,572 participants (mean age: 63 years) in the UK Biobank who wore accelerometers for a week between 2013-2015 and had two body mass index (BMI; kg/m ² ) measurements on average 2.5 years apart. Irregular sleep duration was assessed by the within-person standard deviation (SD) of 7-night accelerometer-measured sleep duration. Participants with sleep duration SD >60 minutes versus ≤30 minutes had 0.24 kg/m ² (95% CI: 0.08, 0.40) higher BMI change (kg/m ² ), standardized to three-year intervals, and 80% (95% CI: 1.28, 2.52) higher risk for incident obesity, after adjusting for sociodemographic factors, shift work, and baseline BMI or follow-up period (p-trend<0.02 for both). These associations remained consistent after adjusting for lifestyle, comorbidities, and other sleep factors, including sleep duration. Age, sex, baseline BMI, and genetic predisposition to higher BMI (measured with a polygenic risk score) did not appear to modify the association. Since irregular sleep duration is common, trials of interventions targeting sleep irregularity might lead to new public health strategies that tackle obesity.
Sleep disordered breathing, represented by sleep apnea syndrome, not only significantly reduces the quality of daily life but is also known to contribute to the development of various cardiovascular diseases. Since 2000, sleep apnea syndrome has become widely recognized by the general public. However, the number of suspected patients who seek medical consultation remains low, and even fewer receive a proper diagnosis and treatment. One reason for this is the lack of information that apnea is linked to cardiovascular disease, even among individuals experiencing typical sleep apnea syndrome symptoms such as daytime sleepiness and general fatigue. Additionally, healthcare providers may not be effectively guiding patients while providing sleep hygiene education. Furthermore, the limited number of medical facilities and technicians capable of conducting overnight polysomnography tests for diagnosing sleep disordered breathing is another factor preventing more patients from benefiting from treatment. This article explores the relationship between sleep disordered breathing and the onset of cardiovascular diseases, as well as the latest treatment approaches.
Background
The etiology of type 2 diabetes mellitus (T2DM) is complex, with environmental factors playing a significant role in its pathophysiology. Nonsteroidal anti-inflammatory drugs usage and Helicobacter pylori infection are the two most frequent causes of peptic ulcer disease (PUD). The link between PUD and T2DM is unclear, and comprehensive analyses of anti-PUD medications’ impact on T2DM risk, especially in Asian populations, are lacking. This study aimed to determine the relationship between PUD, anti-PUD medications, and the likelihood of developing T2DM.
Objectives
Using a population-based cohort study conducted in Taiwan, we investigated the impact of PUD and anti-PUD medications on the risk of T2DM.
Design
This is a retrospective, population-based cohort study using the largest database used in Taiwan.
Methods
An 18-year follow-up period study was conducted on a cohort of patients with PUD diagnosed between 2001 and 2018 using the Taiwan National Health Insurance Research Database. The risk of PUD as well as anti-PUD medications use were examined using Cox proportional regression model.
Results
Based on multivariable Cox proportional hazards regression analysis, patients with PUD had a higher overall T2DM incidence (22.7 vs 21.3 per 1000 person-years) than patients without PUD. The adjusted hazard ratio was 1.12 (95% confidence interval = 1.10, 1.13). Patients with PUD have a higher risk of T2DM in both genders and age groups. Patients with anti-PUD medications, such as H2 receptor antagonists, proton-pump inhibitors, antibiotics, prostaglandin analogs, anticholinergics, and antacids usage, are associated with a lower risk of developing T2DM than those without. Patients with PUD who underwent surgery were found to have a higher risk of T2DM.
Conclusion
Patients with PUD are more likely to develop T2DM. Nevertheless, patients receiving anti-PUD medications have a lower incidence of T2DM.
Sportif performansının geliştirilmesi ve belirlenmesi, sporcuların
mevcut kapasitelerini en üst düzeye çıkararak başarıya ulaşmalarında kritik
bir rol oynamaktadır (Marković, ve ark., 2005; Taati ark., 2022). Spora özgü
biyomekanik talepleri karşılayabilmek, müsabaka ve santrenman süresince
dayanıklılık, hız, çeviklik gibi temel performans bileşenlerinde üstün bir
yetkinlik gerektirir (Bridge ve ark., 2014). Özellikle mücadele sporlarında,
başarı ile sonuçlanan performans bileşenleri, bu bileşenlerin ne ölçüde branşa
özgü ihtiyaçları karşılayabildiği ile yakından ilişkilidir. Taekwondo, yalnızca
fiziksel güç ve çeviklik değil, aynı zamanda yüksek teknik doğruluk ve
stratejik zeka gerektiren bir dövüş sporu olarak bu anlamda özgün
gereksinimler sunmaktadır. Ayrıca, nörolojik uyaranların sportif performansa
etkileri üzerine yapılan çalışmalar, müzik ve belirli aromaların, özellikle
yoğun egzersiz sonrası denge ve anaerobik performans üzerindeki olumlu
etkilerini vurgulamaktadır (Adanur ve ark., 2023).
Taekwondo branşında sporcuların teknik becerilerini ölçmek için
geleneksel laboratuvar testlerinin yanı sıra saha testleri de kullanılmaktadır.
Ancak laboratuvar testleri genellikle maliyetli ekipman ve uzman gereksinimi
nedeniyle her spor ortamında uygulanabilir olmamakla birlikte, genel fiziksel
uygunluk seviyelerini belirlemeye yönelik olduğu için branşa özgü
gereksinimleri karşılamada yetersiz kalabilmektedir (Chaabene, ve ark.,
2018). Bu bağlamda, özellikle taekwondo sporuna özgü gelişmiş çeviklik,
dayanıklılık ve teknik yeterliliğin değerlendirilmesine yönelik testlerin
geliştirilmesi gerekliliği ortaya çıkmaktadır. Taekwondo Spesifik Çeviklik
Testi (TSAT), Taekwondoya Özgü Aerobik-Anaerobik-Çeviklik Testi
(TAAA) ve Tekme Frekans Hızı Testi (FSKT) gibi testler, sporcunun dövüş
sırasında ihtiyaç duyduğu çeviklik, dayanıklılık ve teknik kapasiteyi detaylı
şekilde ölçerek performansın belirleyici yönlerini anlamaya olanak
tanımaktadır (Silva Santos, & Franchini, 2016). Bu testlerin her biri, antrenman ve müsabaka sürecine uyarlanabilir
olmalarıyla dikkat çekmektedir. Sporcuların gerçek dövüş ortamına özgü
becerilerini objektif bir şekilde değerlendirme imkanı sağlamaktadır.
Özellikle çeviklik, dövüş sırasındaki hızlı ve çok yönlü hareketlerin temel
unsuru olup, TSAT gibi branşa özgü testlerle ölçüldüğünde, sporcuların teknik
kapasitelerini doğrudan etkileyecek veriler sunmaktadır (Marković, ve ark.,
2005). TAAA ve FSKT testleri ise aerobik-anaerobik güç, dayanıklılık ve hız
gibi müsabaka performansını belirleyen unsurları değerlendirme fırsatı
tanıyarak, sporcuların yüksek yoğunluklu antrenman süreçlerinde performans
takibine yönelik uygun araçlar olarak ön plana çıkmaktadır (Taati ve ark.,
2022).
Otizm Spektrum Bozukluğu (OSB): Nörogelişimsel bir bozukluk olup
genetik ve çevresel faktörlerin etkisiyle erken yaşlarda ortaya çıkan baş
sallama, el çırpma, vücudunu sallama gibi streotip davranışlar ile birlikte
sınırlı sosyal iletişimin görüldüğü bir popülasyonu tanımlamaktadır. Bunların
yanı sıra genetik rahatsızlıklar, zihinsel işlev kaybı, dikkat eksikliği ve
hiperaktivite bozukluğu, kaygı ve duygudurum bozuklukları gibi bazı
yetersizliklerde görülebilir (Lord ve ark., 2018). Dünya genelinde ise görülme
sıklığının 1/68 olduğu düşünülmektedir. Küçük yaşlardan itibaren OSB’ li
bireylerde görülen sınırlılıklar, bireylerin günlük yaşam aktivitelerini olumsuz
etkilemekte ve fiziksel açıdan bireylerin motor deneyimini olumsuz
etkilemektedir. Denge, postüral stabilite ve kas gücünün geliştirilmesi, OSB’li
bireylerin motor deneyimini iyileştirmede önemli bir rol oynayabilir. Örneğin,
alt ekstremite kaslarını hedefleyen direnç egzersizleri, fiziksel performansı
artırmanın yanı sıra bireylerin günlük yaşam aktivitelerine daha etkin
katılımını destekleyebilir (Kurhan ve ark., 2024a). Bu durum OSB’ li
bireylerin fiziksel gelişimi sekteye uğratmaktadır (Monteiro ve ark., 2022).
Özellikle, OSB’ li bireyler, normal gelişim gösteren bireylerle
kıyaslandığında denge, postural stabilite, yürüme, eklem esnekliği, hareket
hızı (Manjoiviona & Prior, 1995) bilateral koordinasyon zayıf olup (David ve
ark., 2009) yürüme bozuklukları (Hardan ve ark., 2003) kaba (Armitano ve
ark., 2020) ve ince motor beceri (nesne kavrama, el yazısı) eksikliği
görülmektedir (McPhillips ve ark., 2014). Bunlara ek olarak, OSB tanılı
bireylerin sosyal etkileşim alanındaki sınırlılıklarından (Bahmani ve ark.,
2015) dolayı grupla yapılacak etkinliklere katılımı zor olabilir. Bu bireyler,
daha çok bireysel egzersiz müdahalelerinde gelişim sağlayabilir ve başarılı
olabilirler. OSB’ li bireylerin bazı seslerden ve kendisine dokunulmasından
hoşlanmaması gibi duyusal işlemleme farklılıkları fiziksel aktivitelere katılımı
zorlaştırabilir. Bireylerin bir kısmının bu anlamda hassasiyeti yüksek iken bir
diğer kısmı duyusal uyaranlara karşı ilgisiz kalabilir. OSB’ li bireylerin yaşadıkları güçlüklere karşın egzersiz müdahalelerinin, fiziksel gelişimin
yanısıra sosyal, bilişsel, dil ve iletişim hatta uyku gibi farklı gelişim alanlarını
destekleyen (Türkmen ve ark., 2024) ve invaziv olmayan bir yöntem olarak
ön plana çıktığı görülmektedir (Arslan ve ark., 2022). Bu nedenle OSB’ li
bireylerin genel sağlığını korumak ve sürdürmek açısından bireyselleştirilmiş
egzersiz reçeteleri ve erken müdahalelerin geliştirilmesi önem arz etmektedir.
Bu noktada, yüzme bireysel bir spor branşı olması nedeniyle, OSB’ li
bireylerin ihtiyaçlarına cevap veren önemli bir spor branşı olarak karşımıza
çıkmaktadır. Bireylerin fiziksel, sosyal, bilişsel ve psikolojik gelişimini pek
çok açıdan destekler. Yüzmenin otizmli bireylerin gelişimi üzerindeki olası
etkilerinin değerlendirilmesi bu popülasyona yönelik yapılacak egzersiz
reçetelerinin planlanması açısından önem arz etmektedir. Bu minvalde
otizmin karakteristik özellikleri ile yüzme branşının gereklilikleri üzerine
odaklanarak bir değerlendirme yapmak alana katkı sağlayacaktır.
Background
The cluster of cardiovascular risk factors, referred to as metabolic syndrome (MetS), represents a substantial risk factor for cardiovascular diseases and presents a significant public health challenge. However, previous epidemiological investigations exploring the link between sleep duration and MetS lack experimental evidence to establish a causal relationship. Hence, he objective of this study is to examine the association between sleep duration and MetS by employing the Mendelian randomization (MR) approach.
Methods
A cross-sectional study was conducted utilizing the Taiwan Biobank database, which comprised 33,270 predominantly Han Chinese individuals aged 30–70 years with no history of cancer and enrolled between 2008 and 2020. This study was conducted using Taiwan Biobank database. In MR analysis, we constructed weighted and unweighted genetic risk scores by calculating the SNP alleles significantly associated with sleep duration. Two-stage regression analysis was used to estimate odds ratio (OR) and 95% confidence interval (CI).
Results
In the observational epidemiologic study, after multivariate adjustment, the OR for sleep durations of < 5, 8–9 and > 9 h compared to those with a sleep duration of 7 h were 1.23 (95% CI: 1.07, 1.43), 1.15 (95% CI: 1.06, 1.24) and 1.84 (95% CI: 1.43, 2.36), respectively. In the MR analyses after multivariate adjustment, the ORs of MetS per 1 standard deviation increase in the estimated sleep duration and the probability of long and short sleep durations derived from weighted genetic risk scores were 0.64 (95% CI: 0.63, 0.66), 1.55 (95% CI: 1.51, 1.59), and 1.66 (95% CI: 1.62, 1.70), respectively.
Conclusions
Observational and MR analyses demonstrated that short and long sleep durations are potential causal risk factors for MetS. Therefore, long and short sleep durations should be considered as risk factors in MetS-prevention strategies.
Background
Hyperuricemia (HUA), marked by elevated serum urate levels, is increasingly prevalent worldwide. The relationship between lifestyle factors such as sleep duration, daytime napping, and HUA risk remains unclear. Although some studies suggest that sleep variables, including short or long sleep durations and napping, may influence serum uric acid levels, results are inconsistent.
Methods
A systematic review and meta‐analysis was performed according to the PRISMA guidelines. Databases such as PubMed, Embase, Web of Science, and Cochrane Library were searched until February 2024. The data were extracted, and the quality of the study was assessed independently by two reviewers.
Results
Ten studies involving a total of 231 978 participants were included. Short sleep duration was related to higher risk of HUA (odds ratio (OR) 1.10, 95% confidence interval (CI): 1.03–1.18), while long sleep duration had no significant effect (OR 0.98, 95% CI: 0.89–1.07). The risk of HUA and daytime napping was statistically significant(OR 1.34, 95% CI: 1.12–1.61).
Conclusions
Short sleep duration and prolonged daytime napping are associated with an increased risk of HUA. These findings suggest that sleep patterns should be considered in lifestyle interventions for HUA prevention. Further research is required to establish causal relationships.
Understanding and predicting individual responses to common stressors is essential for optimising performance in high-stress environments. This article outlines a protocol for a study to identify biomarkers that predict performance under heat, musculoskeletal, psychosocial and sleep stress, for future integration into a wearable sensor system. In Phase I, healthy adults aged between 18 and 45 years (n=104) will be recruited for an intervention trial that involves exposure to one of the four stressors: heat, musculoskeletal, psychosocial or sleep deprivation. Biomarkers will be identified from molecular markers in biological samples (eg, blood, saliva, sweat and stool), physiological measures and psychological assessments to predict cognitive and physical performance under stress. A within-subjects design will determine changes in molecular and non-molecular markers before and after stress exposure. In Phase II, we will use the biomarkers identified in Phase I to develop a wearable sensor to predict and monitor human performance under stress.
Understanding and predicting individual responses to common stressors is essential for optimising performance in high-stress environments. This article outlines a protocol for a study to identify biomarkers that predict performance under heat, musculoskeletal, psychosocial and sleep stress, for future integration into a wearable sensor system. In Phase I, healthy adults aged between 18 and 45 years (n=104) will be recruited for an intervention trial that involves exposure to one of the four stressors: heat, musculoskeletal, psychosocial or sleep deprivation. Biomarkers will be identified from molecular markers in biological samples (eg, blood, saliva, sweat and stool), physiological measures and psychological assessments to predict cognitive and physical performance under stress. A within-subjects design will determine changes in molecular and non-molecular markers before and after stress exposure. In Phase II, we will use the biomarkers identified in Phase I to develop a wearable sensor to predict and monitor human performance under stress.
Background
The pathophysiology of obstructive sleep apnea (OSA) and diabetes mellitus (DM) is still unknown, despite clinical reports linking the two conditions. After investigating potential roles for DM-related genes in the pathophysiology of OSA, our goal is to investigate the molecular significance of the condition. Machine learning is a useful approach to understanding complex gene expression data to find biomarkers for the diagnosis of OSA.
Methods
Differentially expressed analysis for OSA and DM data sets obtained from GEO were carried out firstly. Then four machine algorithms were used to screen candidate biomarkers. The diagnostic model was constructed based on key genes, and the accuracy was verified by ROC curve, calibration curve and decision curve. Finally, the CIBERSORT algorithm was used to explore immune cell infiltration in OSA.
Results
There were 32 important genes that were considered to be related both in OSA and DM datasets by differentially expressed analysis. Through enrichment analysis, the majority of these genes are enriched in immunological regulation, oxidative stress response, and nervous system control. When consensus characteristics from all four approaches were used to predict OSA diagnosis, STK17A was thought to have a high degree of accuracy. In addition, the diagnostic model demonstrated strong performance and predictive value. Finally, we explored the immune cells signatures of OSA, and STK17A was strongly linked to invasive immune cells.
Conclusion
STK17A has been discovered as a gene that can differentiate between individuals with OSA and DM based on four machine learning methods. In addition to offering possible treatment targets for DM-induced OSA, this diagnostic approach can identify high-risk DM patients who also have OSA.
Importance
Short sleep duration during pregnancy and the perimenopausal period has been associated with adverse cardiometabolic outcomes. However, it remains unclear how sleep duration changes after delivery and whether such changes are associated with the cardiometabolic health of birthing people.
Objective
To investigate whether persistently short sleep during pregnancy and after delivery is associated with incident hypertension and metabolic syndrome.
Design, Setting, and Participants
This secondary analysis of the Nulliparous Pregnancy Outcomes Study: Monitoring Mothers-to-Be Heart Health Study (NuMoM2b-HHS), an ongoing prospective cohort study, was conducted between September 5, 2023, and March 1, 2024, in 8 US academic medical centers. Participants were aged 18 years or older at NuMoM2b enrollment; recruited during their first pregnancy between October 1, 2010, and September 30, 2013; and followed up for a mean (SD) of 3.1 (0.9) years after delivery.
Exposures
Self-reported short sleep duration (<7 hours) during pregnancy and 2 to 7 years after delivery was defined as persistent short sleep.
Main Outcomes and Measures
Incident hypertension and metabolic syndrome (MetS) at follow-up. Regression models were used to estimate relative risks of incident hypertension and MetS by sleep duration pattern. Hypertension analyses excluded participants with hypertension at baseline, and MetS analyses excluded participants with MetS at baseline. Multivariable models included a priori covariates of baseline age and time from delivery to follow-up. Incident hypertension analyses included an additional covariate of body mass index at baseline.
Results
Among 3922 participants (mean [SD] age, 27.3 [5.4] years; 598 Hispanic [15.2%], 485 non-Hispanic Black [12.4%], and 2542 non-Hispanic White [64.8%]), 565 individuals (14.4%) experienced persistent short sleep. Non-Hispanic Black (adjusted odds ratio [aOR], 2.17; 95% CI, 1.59-2.97) and unmarried (aOR, 1.68, 95% CI, 1.29-2.19) participants were significantly more likely to experience persistent short sleep compared with non-Hispanic White and married participants, respectively. Persistent short sleep was associated with higher odds of incident MetS (aOR, 1.60; 95% CI, 1.21-2.11) but not incident hypertension (aOR, 0.91; 95% CI, 0.69-1.19).
Conclusions and Relevance
In this study, short sleep duration that persisted from pregnancy to 2 to 7 years after delivery was associated with a greater risk for adverse cardiometabolic outcomes. Future studies should explore whether sleep-targeted interventions during and after pregnancy are associated with improved cardiometabolic health outcomes, particularly among populations at increased risk.
A circadian disruption, manifested by disturbed sleep and low-grade inflammation, is commonly seen in noncommunicable diseases (NCDs). Cardiovascular, respiratory and renal disorders, diabetes and the metabolic syndrome, cancer, and neurodegenerative diseases are among the most common NCDs prevalent in today’s 24-h/7 days Society. The decline in plasma melatonin, which is a conserved phylogenetic molecule across all known aerobic creatures, is a constant feature in NCDs. The daily evening melatonin surge synchronizes both the central pacemaker located in the hypothalamic suprachiasmatic nuclei (SCN) and myriads of cellular clocks in the periphery (“chronobiotic effect”). Melatonin is the prototypical endogenous chronobiotic agent. Several meta-analyses and consensus studies support the use of melatonin to treat sleep/wake cycle disturbances associated with NCDs. Melatonin also has cytoprotective properties, acting primarily not only as an antioxidant by buffering free radicals, but also by regulating inflammation, down-regulating pro-inflammatory cytokines, suppressing low-grade inflammation, and preventing insulin resistance, among other effects. Melatonin’s phylogenetic conservation is explained by its versatility of effects. In animal models of NCDs, melatonin treatment prevents a wide range of low-inflammation-linked alterations. As a result, the therapeutic efficacy of melatonin as a chronobiotic/cytoprotective drug has been proposed. Sirtuins 1 and 3 are at the heart of melatonin’s chronobiotic and cytoprotective function, acting as accessory components or downstream elements of circadian oscillators and exhibiting properties such as mitochondrial protection. Allometric calculations based on animal research show that melatonin’s cytoprotective benefits may require high doses in humans (in the 100 mg/day range). If melatonin is expected to improve health in NCDs, the low doses currently used in clinical trials (i.e., 2–10 mg) are unlikely to be beneficial. Multicentre double-blind studies are required to determine the potential utility of melatonin in health promotion. Moreover, melatonin dosage and levels used should be re-evaluated based on preclinical research information.
Sleep is a vital restorative process that plays a pivotal role in maintaining the delicate equilibrium of mental and physical well-being. Both short and long sleep duration are associated with a range of adverse health outcomes. Numerous studies have consistently demonstrated a robust association between sleep duration and liver disease. In this study, we conducted statistical tests and performed subgroup analyses to explore potential variations in this association across different contexts, aiming to elucidate the correlation between ALT, AST, and TB with sleep duration. This cross-sectional investigation utilized datasets from the National Health and Nutrition Examination Survey 2005 to 2010. Multivariate linear regression models were used to examine the linear association between ALT, AST, and TB with sleep duration. Test for interaction is commonly conducted using multivariabte models to assess statistically significant subgroup disparities. Fitted smoothied curves and threshold effect analyses were employed to depict nonlinear relationships. The study enrolled 17,491 participants aged 16 to 85 years who met the inclusion and exclusion criteria, with a mean age of the participants was 45.58 ± 19.94 years. Multivariate linear regression analysis showed a significant positive association between sleep duration and ALT [−0.23 (−0.45, −0.00) 0.0455] and AST[−0.20 (−0.38, −0.01) 0.0338] in Model 3. Using a two-segment linear regression model, we found an U-shaped relationship and significant inflection point between between ALT and AST with sleep duration. The present study unveiled a significant inverse correlation between sleep duration and levels of ALT and AST, while no significant association was observed with TB levels. Furthermore, variations in the optimal sleep duration for liver function recovery were identified across diverse populations, thereby offering valuable healthcare recommendations to public.
Background
Sleep, cognition, and mortality may be interdependent.
Objective
We explored paths between sleep, cognition and mortality and potential interactions.
Methods
The study examines the relationship among sleep, global mental status, and mortality risk using data from 1364 participants from the Healthy Aging in Neighborhood of Diversity across the Life Span (HANDLS) study. We used Cox proportional hazards models and four-way decomposition models to analyze sleep patterns and global mental status.
Results
After a median time at risk of 8.2 years, 172 deaths occurred, with rate of 16 per 1000 person-years. A 1-unit increase in the Pittsburgh Sleep Quality Index (PSQI) global score was linked to a 7% increase in mortality risk in the reduced model, but this effect was attenuated in the full model. In both reduced and fully adjusted models, the PSQI global score and sleep quality domains interacted with global mental status, with poor sleep generally associated with mortality risk in the group with better global mental status at first-visit. In four-way decomposition models, total effects (TE) of PSQI scores on mortality risk were positive and statistically significant, while being mostly controlled direct effects. However, among women, the inverse TE of global mental status on mortality risk was partially mediated by PSQI sleep latency and the PSQI global.
Conclusions
Poor global mental status is associated with greater mortality risk at better sleep quality levels and vice versa. Further longitudinal studies with multiple sleep and cognitive performance repeats are needed to corroborate these findings.
Data from rodent studies indicate that cumulative stress exposure may accelerate senescence and offer a theory to explain differences in the rate of aging. Cumulative exposure to glucocorticoids causes hippocampal defects, resulting in an impairment of the ability to terminate glucocorticoid secretion at the end of stress and, therefore, in increased exposure to glucocorticoids which, in turn, further decreases the ability of the hypothalamo-pituitary-adrenal axis to recover from a challenge. However, the consensus emerging from reviews of human studies is that basal corticotropic function is unaffected by aging, suggesting that the negative interaction of stress and aging does not occur in man. In the present study, a total of 177 temporal profiles of plasma cortisol from 90 normal men and 87 women, aged 18-83 yr, were collected from 7 laboratories and reanalyzed. Twelve parameters quantifying mean levels, value and timing of morning maximum and nocturnal nadir, circadian rhythm amplitude, and start and end of quiescent period were calculated for each individual profile. In both men and women, mean cortisol levels increased by 20-50% between 20-80 yr of age. Premenopausal women had slightly lower mean levels than men in the same age range, primarily because of lower morning maxima. The level of the nocturnal nadir increased progressively with aging in both sexes. An age-related elevation in the morning acrophase occurred in women, but not in men. The diurnal rhythmicity of cortisol secretion was preserved in old age, but the relative amplitude was dampened, and the timing of the circadian elevation was advanced. We conclude that there are marked gender-specific effects of aging on the levels and diurnal variation of human adrenocorticotropic activity, consistent with the hypothesis of the "wear and tear" of lifelong exposure to stress. The alterations in circadian amplitude and phase could be involved in the etiology of sleep disorders in the elderly.
Long-term gradual sleep reduction effects were investigated on 4 young adult collegiate couples. The battery of assessment tools included a sleep log, Stanford Sleepiness Scale, Profile of Mood States, Feeling Tone Checklist, a measure of circadian oral temperature, Williams Word Memory test, Digit Span test, Wilkinson Auditory Vigilance task, Wilkinson Addition task, Minnesota Multiphasic Personality Inventory, Rapid Alternation task, psychiatric and medical examinations, and a subjective effects questionnnaire. It was concluded that 6–8 months of gradual sleep restriction, down to 4.5–5.5 hrs per night, does not result in behavioral effects measurable by the instruments used. Subjective fatigue appears to be the limiting factor in determining tolerability of gradual sleep restriction. At the end of an additional 12-month follow-up period, total sleep time was still 1–2.5 hrs below baseline, but measures of well-being had returned to baseline levels.
One current hypothesis of biological aging proposes that aging results from the deterioration of neuroendocrine functions. Sleep dependent growth hormone (GH) secretion is diminished in elderly people. However, the time course of this decrease from puberty to senescence is still unknown. Cortisol secretion is also related to sleep processes with the 24 hr nadir occurring, like the sleep dependent GH secretory surge, during the first half of nocturnal sleep. Whether age also affects the sleep-associated nadir of cortisol secretion has yet to be clarified. This study investigated changes in GH and cortisol secretion during sleep in 30 male volunteers age 20 to 92 yr.
After an adaptation night, each subject spent another night in the sleep laboratory for polygraphic sleep recording and determination of GH and cortisol levels every 15 min.
GH peak values exponentially decreased with age (r = -.80, p < .001), while the cortisol nadir increased linearly as a function of age (r = .79, p < .001). Age-related changes in sleep-dependent secretion of GH and cortisol correlated significantly (r = .47, r = -.55, respectively; p < .05) with an age-dependent decrease in slow wave sleep.
Alterations of GH peak amplitude and basal cortisol secretion are not restricted to senescence. These changes develop gradually during adult life with different time courses. Both changes in GH and cortisol secretion may act together to reduce anabolic functions of sleep in the aged.
Data from rodent studies indicate that cumulative stress exposure may accelerate senescence and offer a theory to explain differences in the rate of aging. Cumulative exposure to glucocorticoids causes hippocampal defects, resulting in an impairment of the ability to terminate glucocorticoid secretion at the end of stress and, therefore, in increased exposure to glucocorticoids which, in turn, further decreases the ability of the hypothalamo-pituitary-adrenal axis to recover from a challenge. However, the consensus emerging from reviews of human studies is that basal corticotropic function is unaffected by aging, suggesting that the negative interaction of stress and aging does not occur in man. In the present study, a total of 177 temporal profiles of plasma cortisol from 90 normal men and 87 women, aged 18-83 yr, were collected from 7 laboratories and reanalyzed. Twelve parameters quantifying mean levels, value and timing of morning maximum and nocturnal nadir, circadian rhythm amplitude, and start and end of quiescent period were calculated for each individual profile. In both men and women, mean cortisol levels increased by 20-50% between 20-80 yr of age. Premenopausal women had slightly lower mean levels than men in the same age range, primarily because of lower morning maxima. The level of the nocturnal nadir increased progressively with aging in both sexes. An age-related elevation in the morning acrophase occurred in women, but not in men. The diurnal rhythmicity of cortisol secretion was preserved in old age, but the relative amplitude was dampened, and the timing of the circadian elevation was advanced. We conclude that there are marked gender-specific effects of aging on the levels and diurnal variation of human adrenocorticotropic activity, consistent with the hypothesis of the "wear and tear" of lifelong exposure to stress. The alterations in circadian amplitude and phase could be involved in the etiology of sleep disorders in the elderly.
Sleep curtailment constitutes an increasingly common condition in industrialized societies and is thought to affect mood and performance rather than physiological functions. There is no evidence for prolonged or delayed effects of sleep loss on the hypothalamo-pituitary-adrenal (HPA) axis. We evaluated the effects of acute partial or total sleep deprivation on the nighttime and daytime profile of cortisol levels. Plasma cortisol profiles were determined during a 32-hour period (from 1800 hours on day 1 until 0200 hours on day 3) in normal young men submitted to three different protocols: normal sleep schedule (2300-0700 hours), partial sleep deprivation (0400-0800 hours), and total sleep deprivation. Alterations in cortisol levels could only be demonstrated in the evening following the night of sleep deprivation. After normal sleep, plasma cortisol levels over the 1800-2300-hour period were similar on days 1 and 2. After partial and total sleep deprivation, plasma cortisol levels over the 1800-2300-hour period were higher on day 2 than on day 1 (37 and 45% increases, p = 0.03 and 0.003, respectively), and the onset of the quiescent period of cortisol secretion was delayed by at least 1 hour. We conclude that even partial acute sleep loss delays the recovery of the HPA from early morning circadian stimulation and is thus likely to involve an alteration in negative glucocorticoid feedback regulation. Sleep loss could thus affect the resiliency of the stress response and may accelerate the development of metabolic and cognitive consequences of glucocorticoid excess.
Over 60 years ago, Selye1 recognized the paradox that the physiologic systems activated by stress can not only protect and restore but also damage the body. What links these seemingly contradictory roles? How does stress influence the pathogenesis of disease, and what accounts for the variation in vulnerability to stress-related diseases among people with similar life experiences? How can stress-induced damage be quantified? These and many other questions still challenge investigators. This article reviews the long-term effect of the physiologic response to stress, which I refer to as allostatic load.2 Allostasis — the ability to achieve stability through change3 — . . .
TSH levels in human, which normally peak in the late evening, are augmented by sleep deprivation. Based on prior research, we postulated that TSH secretion is governed by both sleep and circadian processes. However, environmental and behavioral factors known to affect each of those processes were not controlled in prior investigations. Therefore, we evaluated TSH secretory patterns in three different conditions: 1) entrainment to the 24-h day, 2) a constant routine designed to unmask the endogenous component of circadian rhythmicity, and 3) before and after a light-induced phase shift of the circadian timing system. We found that TSH levels rose over the 4-5 h preceding sleep during entrainment, followed by a precipitous drop at sleep onset. When subjects remained awake on a constant routine, TSH levels remained elevated throughout the nighttime hours. Subjects kept awake for 2 consecutive nights on constant routine showed two distinct cycles of nocturnal TSH secretion, despite increasing sleep deprivation. Both the TSH and body temperature rhythms were substantially shifted, by an equivalent amount, in response to three consecutive nightly exposures to bright light. These data demonstrate that both the output of the human circadian pacemaker and the inhibitory effect of sleep contribute to the regulation of TSH secretion. Under normal conditions, the inhibitory effect of sleep on TSH secretion opposes the nocturnal peak in the circadian TSH drive.
To determine whether a cumulative sleep debt (in a range commonly experienced) would result in cumulative changes in measures of waking neurobehavioral alertness, 16 healthy young adults had their sleep restricted to an average 4.98 hrs per night for 7 consecutive nights. Ss slept in the laboratory, and sleep and waking were monitored. Three times each day, Ss were assessed for subjective sleepiness and mood and were evaluated on a brief performance battery that included psychomotor vigilance (PVT), probed memory (PRM), and serial-addition testing. Once each day they completed a series of visual analog scales (VASs) and reported sleepiness and somatic and cognitive/emotional problems. Sleep restriction resulted in statistically robust cumulative effects on waking functions. Subjective sleepiness ratings, subscale scores for fatigue, confusion, tension, and total mood disturbance from the mood and VAS ratings of mental exhaustion and stress were elevated across days of restricted sleep. PVT performance parameters were also significantly increased by restriction. Significant time-of-day effects were evident in subjective sleepiness and PVT data. Findings suggest that cumulative nocturnal sleep debt had a dynamic and escalating analog in cumulative daytime sleepiness and that asymptotic or steady-state sleepiness was not achieved in response to sleep restriction. (PsycINFO Database Record (c) 2012 APA, all rights reserved)
This book is not meant to be a comprehensive text on sleep, but a selective and personal account giving several hypotheses about a variety of aspects of sleep. (PsycINFO Database Record (c) 2012 APA, all rights reserved)
The plasma C-peptide immunoreactivity (CPR) in 10 normal subjects varied considerably when measured with different antisera in parallel assays. The CPR level correlated with the blank “CPR” value measured in plasma devoid of C-peptide and to a lesser degree with the sensitivity of the standard curves obtained with the individual antisera.
Storage of plasma samples at different temperatures and for different lengths of time before the analyses were carried out resulted In further variation in the CPR results. This was caused by a time- and temperature-dependent fall in CPR, which was more pronounced with some antisera than with others. This sensitivity to storage of plasma did not correlate with the antigenk characteristics of the antisera as determined by their reactivity with 11 specific fragments of the C-peptide molecule.
The contribution of human proinsulin to the CPR concentration in normal subjects was considered to be negligible even though the relative immunoreactivity of human proinsulin and C-peptide ranged from 11 to 143 per cent among these antisera.
These results suggest that differences in C-peptide antisera are a major reason for the variation in the concentration of circulating CPR as measured in different, C-peptide immunoassays.
Insulin secretion rates can be accurately estimated from plasma C-peptide levels with a two-compartment model for C-peptide distribution and degradation. In previous studies, the kinetic parameters of C-peptide clearance were derived in each subject from the decay curve observed after bolus intravenous injection of biosynthetic human C-peptide. To determine whether standard parameters for C-peptide clearance could be defined and used to calculate insulin secretion without obtaining a decay curve in each subject, we analyzed 200 decay curves of biosynthetic human C-peptide obtained in normal, obese, and non-insulin-dependent diabetes mellitus subjects studied in our laboratory. This analysis showed that the volume of distribution and kinetic parameters of C-peptide distribution and metabolism vary by less than 30% in a population highly heterogeneous in terms of age, sex, degree of obesity, and degree of glucose tolerance. The volume of distribution correlated with the degree of obesity as quantified by body surface area (BSA). This dependence of C-peptide distribution volume on BSA was more marked in men than in women. The long half-life was slightly longer in elderly subjects than in younger adults. When effects of BSA, sex, and age were taken into account, the parameters of C-peptide kinetics were very similar in normal, obese, and diabetic subjects. Based on these findings, a simple procedure to derive standard parameters for C-peptide clearance taking into account degree of obesity, sex, and age was defined. These standard parameters resulted in estimations of mean insulin secretion rates, which differed in each subject by only 10-12% from those obtained with individual parameters. The approach of using standard rather than individual parameters did not systematically underestimate or overestimate insulin secretion so that group values for the fasting secretion rate, the mean 24-h secretion rate, and the number and the amplitude of secretory pulses obtained with standard parameters differed by only 1-2% from the values obtained with individual parameters. Furthermore, the accuracy of measurements based on standard parameters was not different from that associated with replicate determinations of the parameters of C-peptide clearance in the same subject. We conclude that it is possible to estimate insulin secretion rates from plasma C-peptide levels with standard parameters for C-peptide clearance rather than individually derived parameters without significant loss of accuracy.
Aging is associated with hyperinsulinemia, but reports vary on the contributions of altered insulin clearance versus insulin secretion to this phenomenon. To elucidate the role of insulin secretion in the hyperinsulinemia of aging, 10 elderly (age 66 +/- 4 yr, body mass index 25 +/- kg/m2) and 8 young (age 30 +/- 5 yr, body mass index 24 +/- 3 kg/m2) subjects were studied to determine rates of insulin secretion in response to fasting, mixed meals, and intravenous glucose administration. Insulin secretion was determined with a two-compartment model based on individual C-peptide kinetic parameters derived after bolus injection of biosynthetic human C-peptide. Basal insulin secretion rates were increased in elderly subjects (82.5 +/- 9.0 vs. 62.8 +/- 6.1 pmol.min-1.m-2; P less than .05). This was reflected in elevated serum insulin levels in elderly subjects (62.8 +/- 10.1 vs. 41.1 +/- 5.0 pM, P less than .05). During a 24-h mixed-meal profile, elderly subjects had an increase in their glucose response (P less than .01 by analysis of variance [ANOVA]) and total insulin secretion (261 +/- 28 vs. 195 +/- 22 nmol.24 h-1.m-2; P less than .05) compared with young subjects. However, the relative total increases in both glycemia and insulin secretion, calculated as a function of basal levels, were similar between the groups (both NS). To experimentally control for differences in glycemia, both groups underwent a 16.8-mM hyperglycemic clamp and a stepped intravenous glucose infusion to match glycemia. Under these steady-state and dynamic conditions, insulin secretion profiles were nearly identical (NS by ANOVA).(ABSTRACT TRUNCATED AT 250 WORDS)
Glucose tolerance depends on a complex interaction among insulin secretion from the beta-cells, clearance of the hormone, and the actions of insulin to accelerate glucose disappearance and inhibit endogenous glucose production. An additional factor, less well recognized, is the ability of glucose per se, independent of changes in insulin, to increase glucose uptake and suppress endogenous output (glucose effectiveness). These factors can be measured in the intact organism with physiologically based minimal models of glucose utilization and insulin kinetics. With the glucose minimal model, insulin sensitivity (SI) and glucose effectiveness (SG) are measured by computer analysis of the frequently sampled intravenous glucose tolerance test. The test involves intravenous injection of glucose followed by tolbutamide or insulin and frequent blood sampling. SI varied from a high of 7.6 x 10(-4) min-1.microU-1.ml-1 in young Whites to 2.3 x 10(-4) min-1.microU-1.ml-1 in obese nondiabetic subjects; in all of the nondiabetic subjects, SG was normal. In subjects with non-insulin-dependent diabetes mellitus (NIDDM), not only was SI reduced 90% below normal (0.61 +/- 0.16 x 10(-4) min-1.microU-1.ml-1), but in this group alone, SG was reduced (from 0.026 +/- 0.008 to 0.014 +/- 0.002 min-1); thus, defects in SI and SG are synergistic in causing glucose intolerance in NIDDM. One assumption of the minimal model is that the time delay in insulin action on glucose utilization in vivo is due to sluggish insulin transport across the capillary endothelium. This was tested by comparing insulin concentrations in plasma with those in lymph (representing interstitial fluid) during euglycemic-hyperinsulinemic glucose clamps. Lymph insulin was lower than plasma insulin at basal (12 vs. 18 microU/ml) and at steady state, indicating significant loss of insulin from the interstitial space, presumably due to cellular uptake of the insulin-receptor complex. Additionally, during clamps, lymph insulin changed more slowly than plasma insulin, but the rate of glucose utilization followed a time course identical with that of lymph (r = .96) rather than plasma (r = .71). Thus, lymph insulin, which may be reflective of interstitial fluid, is the signal to which insulin-sensitive tissues are responding. These studies support the concept that, at physiological insulin levels, the time for insulin to cross the capillary endothelium is the process that determines the rate of insulin action in vivo.(ABSTRACT TRUNCATED AT 400 WORDS)
To determine the relative contributions of changes in glucose effectiveness, B-cell function, and insulin sensitivity to changes in glucose tolerance upon exercise cessation in regularly exercising individuals, we studied seven young subjects who were performing aerobic exercise on a regular schedule. Each subject was studied 12 and 84 hours after the last bout of exercise with an intravenous glucose tolerance test (IVGTT) to quantify insulin sensitivity and glucose effectiveness at zero insulin (GEZI) using the minimal model of glucose kinetics. Additionally, B-cell function was quantified as the acute insulin response to glucose (AIRglucose), and intravenous glucose tolerance as the glucose disappearance constant (Kg). Twelve hours after the last bout of exercise, SI was 8.47 +/- 1.12 x 10(-5) min-1/pmol/L, as compared with 6.98 +/- 1.17 x 10(-5) min-1/pmol/L 84 hours after exercise (mean +/- SE, P = .005). No changes was observed in GEZI (0.020 +/- 0.004 min-1 at 12 hours v 0.019 +/- 0.002 min-1 at 84 hours, P = NS) or AIRglucose (588 +/- 213 pmol/L at 12 hours v 687 +/- 271 pmol/L at 84 hours, P = NS). Thus, the difference in intravenous glucose tolerance observed 12 hours after exercise as compared with 84 hours after the last bout of exercise (Kg, 2.91 +/- 0.70%/min at 12 hours v 2.23 +/- 0.60%/min at 84 hours, P < .05) would appear to be entirely related to a difference in SI and not to differences in glucose effectiveness or B-cell function.
To determine the magnitude and direction of phase shifts of human circadian rhythms occurring within 1 day after a single exposure to bright light, plasma thyrotropin, melatonin, and cortisol levels and body temperature were monitored for 38 h in 17 men who were each studied two times, once during continuous dim light conditions and once with light exposure. After a period of entrainment to a fixed sleep-wake cycle, a 3-h light pulse (5,000 lux) was presented under constant routine conditions, and the resultant phase shifts were measured, also under constant routine conditions, on the 1st day after pulse presentation. The phase shifts in response to light occurred within 24 h and were in the delaying direction for most of the nocturnal period, with the crossover to phase advances occurring approximately 1 h after the temperature minimum. Phase shifts averaged 1 h, with delays being larger than advances, and were achieved without significant changes in rhythm amplitude. The immediate response of the human circadian clock to a single 3-h light pulse is thus characteristic of "type 1" resetting.
TSH levels in human, which normally peak in the late evening, are augmented by sleep deprivation. Based on prior research, we postulated that TSH secretion is governed by both sleep and circadian processes. However, environmental and behavioral factors known to affect each of those processes were not controlled in prior investigations. Therefore, we evaluated TSH secretory patterns in three different conditions: 1) entrainment to the 24-h day, 2) a constant routine designed to unmask the endogenous component of circadian rhythmicity, and 3) before and after a light-induced phase shift of the circadian timing system. We found that TSH levels rose over the 4-5 h preceding sleep during entrainment, followed by a precipitous drop at sleep onset. When subjects remained awake on a constant routine, TSH levels remained elevated throughout the nighttime hours. Subjects kept awake for 2 consecutive nights on constant routine showed two distinct cycles of nocturnal TSH secretion, despite increasing sleep deprivation. Both the TSH and body temperature rhythms were substantially shifted, by an equivalent amount, in response to three consecutive nightly exposures to bright light. These data demonstrate that both the output of the human circadian pacemaker and the inhibitory effect of sleep contribute to the regulation of TSH secretion. Under normal conditions, the inhibitory effect of sleep on TSH secretion opposes the nocturnal peak in the circadian TSH drive.
In animals, circadian pacemakers respond to seasonal changes in day length by making corresponding adjustments in the durations of diurnal and nocturnal periods of circadian rhythms; these adjustments mediate effects of photoperiod on breeding and other seasonally recurring phenomena. Little is known about photoperiod responses of human circadian pacemakers. To investigate this question, we recorded and compared circadian rhythm profiles of 15 individuals after chronic exposures to short (8 h) and long (14 h) nights. As occurs in animals, durations of nocturnal periods of active melatonin secretion (11.9 +/- 1.6 vs. 10.3 +/- 1.3 h, df = 14, t = 4.583, P < 0.0005, paired t test), high prolactin secretion (12.9 +/- 2.1 vs. 9.9 +/- 2.2 h, df = 11, t = 2.917, P < 0.01), and sleep (10.6 +/- 0.8 vs. 7.6 +/- 0.4 h, df = 14, t = 17.122, P < 0.0005) were longer after exposure to long nights than after short ones. Durations of nocturnal periods of low rectal temperature (11.6 +/- 2.3 vs. 9.5 +/- 1.6 h, df = 12, t = 3.912, P < 0.001) and rising cortisol secretion (10.8 +/- 1.6 vs. 9.3 +/- 1.9 h, df = 14, t = 3.130, P < 0.005) were also longer. Some of these differences persisted during 24-h periods of enforced wakefulness in constant dim light, indicating that prior exposure to the two regimes induced abiding changes in the timing of internal processes, such as circadian pacemaker oscillations, that control the durations of nocturnal and diurnal periods of the rhythms.
The hypothesis proposed in this review is that normal diurnal rhythms in the hypothalamic-pituitary-adrenal (HPA) axis are highly regulated by activity in medial hypothalamic nuclei to effect an interaction between corticosteroids and insulin such that optimal metabolism results in response to changes in the fed or fasted state of the animal. There are marked diurnal rhythms in function of the HPA axis under both basal and stress conditions. The HPA axis controls corticosteroid output from the adrenal and, in turn, forward elements of this axis are inhibited by feedback from circulating plasma corticosteroid levels. Basal activity in the HPA axis of mammals fed ad lib peaks about 2 h before the peak of the diurnal feeding rhythm, and is controlled by input from the suprachiasmatic nuclei. The rhythm in stress responsiveness is lowest at the time of the basal peak and highest at the time of the basal trough in the HPA axis activity. There are also diurnal rhythms in corticosteroid feedback sensitivity of basal and stress-induced ACTH secretion which peak at the time of the basal trough. These rhythms are all overridden when feeding, and thus insulin secretion, is disrupted. Corticosteroids interact with insulin on food intake and body composition, and corticosteroids also increase insulin secretion. Corticosteroids stimulate feeding at low doses but inhibit it at high doses; however, it is the high levels of insulin, induced by high levels of corticosteroids, that may inhibit feeding. The effects of corticosteroids on liver, fat, and muscle cell metabolism, with emphasis on their interactions with insulin, are briefly reviewed. Corticosteroids both synergize with and antagonize the effects of insulin. The effects of stress hormones, and their interactions with insulin on lipid and protein metabolism, followed by some of the metabolic effects of injury stress, with or without nutritional support, are evaluated. In the presence of elevated insulin stimulated by glucocorticoids and nutrition, stress causes less severe catabolic effects. In the central nervous system, regulation of function in the HPA axis is clearly affected by the activity of medial hypothalamic nuclei that also alter feeding, metabolism, and obesity in rats. Lesions of the arcuate (ARC) and ventromedial (VMN) paraventricular (PVN) nuclei result in obesity and hyperactivity in the HPA axis. Moreover, adrenalectomy inhibits or prevents development of the lesion-induced obesity. There are interactions among these nuclei; one mode of communication is via inputs of neuropeptide Y (NPY) cells in the ARC to the VMN, dorsomedial nuclei, and PVN.(ABSTRACT TRUNCATED AT 400 WORDS)
To determine the relationship between insulin sensitivity and beta-cell function, we quantified the insulin sensitivity index using the minimal model in 93 relatively young, apparently healthy human subjects of varying degrees of obesity (55 male, 38 female; 18-44 yr of age; body mass index 19.5-52.2 kg/m2) and with fasting glucose levels < 6.4 mM. SI was compared with measures of body adiposity and beta-cell function. Although lean individuals showed a wide range of SI, body mass index and SI were related in a curvilinear manner (P < 0.0001) so that on average, an increase in body mass index was associated generally with a lower value for SI. The relationship between the SI and the beta-cell measures was more clearly curvilinear and reciprocal for fasting insulin (P < 0.0001), first-phase insulin response (AIRglucose; P < 0.0001), glucose potentiation slope (n = 56; P < 0.005), and beta-cell secretory capacity (AIRmax; n = 43; P < 0.0001). The curvilinear relationship between SI and the beta-cell measures could not be distinguished from a hyperbola, i.e., SI x beta-cell function = constant. This hyperbolic relationship described the data significantly better than a linear function (P < 0.05). The nature of this relationship is consistent with a regulated feedback loop control system such that for any difference in SI, a proportionate reciprocal difference occurs in insulin levels and responses in subjects with similar carbohydrate tolerance. We conclude that in human subjects with normal glucose tolerance and varying degrees of obesity, beta-cell function varies quantitatively with differences in insulin sensitivity.(ABSTRACT TRUNCATED AT 250 WORDS)
The purpose of this study was to characterize carbohydrate metabolism associated with the development of gestational diabetes. Six control (Ctl) and ten women with gestational diabetes mellitus (GDM) were evaluated using an intravenous glucose tolerance test and hyperinsulinemic-euglycemic clamp with [6,6-2H2]glucose prior to conception (P) and at 12-14 (E), and 34-36 wk of gestation (L). There was an increase (P = 0.0001) in first-phase insulin response in Ctl (P 174 +/- 133, E 388 +/- 120, and L 587 +/- 303 microU/ml) and GDM (P 197 +/- 94, E 267 +/- 77, and L 376 +/- 162 microU/ml) but a significant (P = 0.02) lag in change in GDM with advancing gestation. Basal endogenous glucose production increased during gestation [Ctl: P 2.74 +/- 0.23, E 2.62 +/- 0.38, and L 3.14 +/- 0.36; GDM: P 2.68 +/- 0.51, E 2.78 +/- 0.45, and L 2.98 +/- 0.48 mg.kg fat-free mass (FFM)-1 x min-1; P = 0.02], but there was resistance to suppression by insulin infusion (P = 0.03) in late gestation (GDM: 0.61 +/- 0.44 vs. Ctl: 0.16 +/- 0.17 mg.kg FFM-1 x min-1). Insulin sensitivity decreased during gestation (Ctl: P 10.78 +/- 2.78, E 8.34 +/- 2.36, and L 4.75 +/- 1.22; GDM: P 7.49 +/- 2.13, E 7.40 +/- 1.45, and L 4.21 +/- 1.01 mg.kg FFM-1 x min-1; P = 0.0001) and was primarily decreased (P = 0.04) in GDM compared with Ctl from P through E. These findings closely resemble those of non-insulin-dependent, predominantly insulin-resistant diabetes, which is often a sequel of GDM.
This article has no abstract; the first 100 words appear below.
Abnormalities of glucose, insulin, and lipoprotein metabolism are common in patients with hypertension. These changes can also be discerned in normotensive first-degree relatives of hypertensive patients. They are not present in patients with secondary forms of hypertension, do not necessarily improve when blood pressure is lowered pharmacologically, and may even be made worse by some forms of antihypertensive treatment. These metabolic abnormalities may play a part in both the pathogenesis and the complications of hypertension in many patients. We hypothesize that the metabolic abnormalities are linked to the hypertension by a pathophysiologic process that involves the sympathoadrenal system and exerts . . .
Source Information
From Stanford University, Palo Alto, Calif. (G.M.R.); Uppsala University, Uppsala, Sweden (H.L.); and Northwestern University, Chicago (L.L.).
Address reprint requests to Dr. Landsberg at the Department of Medicine, Northwestern University Medical School and Northwestern Memorial Hospital, Wesley Pavilion 296, 250 E. Superior St., Chicago, IL 60611.
A questionnaire was sent out to a randomly selected, age (20-34, 35-49, and 50-64 years) and sex stratified sample of 600 adult inhabitants in Uppsala County, Sweden. Overall response rate was 68%. The questionnaire comprised questions about sleep and sleep complaints. Subjects were also asked to rate the degree of a number of proposed causes and consequences of insufficient sleep, in accordance with how they had perceived them when they had experienced insufficient sleep. Results showed that twelve percent of the total sample fulfilled the criteria for persistent insufficient sleep (PIS), an operationally defined condition of considerable chronic sleep loss. One-half of these subjects also reported concomitant sleeping difficulties. In subjects with PIS without sleeping difficulties, the most conspicuous causes of insufficient sleep were work-related factors and simply too little time for sleep. As for the effects of insufficient sleep in subjects with PIS with concomitant sleep complaints, factors relating to somatic symptoms, dysphoric mood and impaired cognition were the most prominent, while dysphoric mood was most noticeable in subjects with PIS without sleep complaints.
Population-based data suggesting that contemporary society does not value sleep are difficult to obtain. In this report, historical change in item endorsements relevant for disturbed sleep and daytime fatigue from the Minnesota Multiphasic Personality Inventory (MMPI) generated from normative, upper Midwestern adult populations was analyzed. Response rates from the 1930s and 1980 were compared. The data indicated that, relative to individuals in the post-Great Depression/pre-World War II era, contemporary men were more likely to report fatigue and tiredness, although they were no more likely to report disturbed nocturnal sleep. The results are compatible with the voluntary curtailment of sleep typical in modern society described in the report of the National Commission on Sleep Disorders Research.
This study was undertaken to understand the dynamics of glucose metabolism in healthy non-diabetic subjects older than age 80 (old-old) compared with subjects aged 61 to 79 (young-old), as well as to compare healthy older subjects with impaired glucose tolerance (IGT) with older subjects with normal glucose tolerance (NGT).
A cross sectional, observational study.
A university hospital clinical research center.
There were 28 community-dwelling adults, 10 older than age 80 and 18 aged 61 to 79. Thirteen of these people had NGT and 15 had IGT. Subjects were not taking any medication that interfered with glucose tolerance.
Status of glucose tolerance was determined by an oral glucose tolerance test categorized as NGT or IGT according to WHO criteria. Insulin sensitivity (SI) and glucose effectiveness (SG) were assessed using a tolbutamide-assisted intravenous glucose tolerance test (IVGTT). The data were analyzed using the Minmod modeling program. Glucose tolerance (K(g)) and the acute insulin response to glucose (AIRg) were calculated from the IVGTT.
There were no significant differences between the young-old and old-old in body mass index or in plasma glucose, insulin, or C-peptide levels in the fasting state or during the OGTT. Values for K(g), SI, SG, and AIRg from the IVGTT were similar in the two age groups. When the subjects were classified by glucose tolerance status, the subjects with NGT had age, gender, and body mass index similar to the subjects with IGT. Older people with IGT had a lower K(g) and tended to have higher fasting glucose and similar fasting insulin compared with people with NGT. IGT subjects had lower SI and tended to have lower SG. The AIRg in IGT subjects tended to be low rather than high when compared with older people with NGT.
Otherwise healthy adults more than 80 years of age have measures of glucose metabolism similar to people aged 61 to 79. The presence of IGT in older adults is associated with insulin resistance, regardless of patient age. We hypothesize that the lack of pancreatic islet compensation for insulin resistance may contribute to impaired glucose tolerance in older adults.
We have recently demonstrated that the overnight profiles of cardiac interbeat autocorrelation coefficient of R-R intervals (rRR) calculated at 1-min intervals are related to the changes in sleep electroencephalographic (EEG) mean frequency, which reflect depth of sleep. Other quantitative measures of the Poincaré plots, i.e., the standard deviation of normal R-R intervals (SDNN) and the root mean square difference among successive R-R normal intervals (RMSSD), are commonly used to evaluate heart rate variability. The present study was designed to compare the nocturnal profiles of rRR, SDNN, and RMSSD with the R-R spectral power components: high-frequency (HF) power, reflecting parasympathetic activity; low-frequency (LF) power, reflecting a predominance of sympathetic activity with a parasympathetic component; and the LF-to-HF ratio (LF/HF), regarded as an index of sympathovagal balance. rRR, SDNN, RMSSD, and the spectral power components were calculated every 5 min during sleep in 15 healthy subjects. The overnight profiles of rRR and LF/HF showed coordinate variations with highly significant correlation coefficients (P < 0.001 in all subjects). SDNN correlated with LF power (P < 0.001), and RMSSD correlated with HF power (P < 0.001). The overnight profiles of rRR and EEG mean frequency were found to be closely related with highly cross-correlated coefficients (P < 0. 001). SDNN and EEG mean frequency were also highly cross correlated (P < 0.001 in all subjects but 1). No systematic relationship was found between RMSSD and EEG mean frequency. In conclusion, rRR appears to be a new tool for evaluating the dynamic beat-to-beat interval behavior and the sympathovagal balance continuously during sleep. This nonlinear method may provide new insight into autonomic disorders.
Etiology and pathogenesis of type II diabetes mellitus and related disorders
- C R Kahn
Kahn CR. Etiology and pathogenesis of type II diabetes mellitus and
related disorders. In: Becker K, ed. Principles and practice of
endocrinology and metabolism. Philadelphia: JB Lippincott, 1995:
1210-16.
The autonomic nervous system in sleep Principles and practice of sleep medicine
- Parmeggiani
10 Parmeggiani P. The autonomic nervous system in sleep. In: Kryger MH, Roth T, Dement WC, eds. Principles and practice of sleep medicine. Philadelphia: WB Saunders, 1994: 194–203.
Sleep deprivation Principles and practice of sleep medicine
- Bonnet
- Mh
12 Bonnet, MH. Sleep deprivation. In: Kryger MH, Roth T, Dement WC, eds. Principles and practice of sleep medicine. Philadelphia: WB Saunders, 1994: 50–67.
Carbohydrate metabolism during pregnancy in control subjects and women with gestational diabetes
- P M Catalano
- E D Tyzbit
- R R Wolfe
Catalano PM, Tyzbit ED, Wolfe RR, et al. Carbohydrate metabolism
during pregnancy in control subjects and women with gestational
diabetes. Am J Physiol 1993; 264: E60-67.
Sleep science: integrating basic research and clinical practice
- E Van Cauter
- K Spiegel
Van Cauter E, Spiegel K. Hormones and metabolism during sleep. In:
Schwartz WJ, ed. Sleep science: integrating basic research and clinical
practice. Monogr Clin Neurosci 1997: 15: 144-74.
Principles and practice of endocrinology and metabolism
- C R Kahn
Kahn CR. Glucose homeostasis and insulin action. In: Becker KL, ed.
Principles and practice of endocrinology and metabolism, 2nd edn.
Philadelphia: JB Lippincott, 1995: 1198-02.
Restoration of brain energy metabolism as the function of sleep
- Benington
11 Benington JH, Heller HC. Restoration of brain energy metabolism as
the function of sleep. Prog Neurobiol 1995, 45: 347–60.
Principles and practice of sleep medicine
- P Parmeggiani
Parmeggiani P. The autonomic nervous system in sleep. In: Kryger
MH, Roth T, Dement WC, eds. Principles and practice of sleep
medicine. Philadelphia: WB Saunders, 1994: 194-203.
Principles and practice of sleep medicine
- M H Bonnet
Bonnet, MH. Sleep deprivation. In: Kryger MH, Roth T,
Dement WC, eds. Principles and practice of sleep medicine.
Philadelphia: WB Saunders, 1994: 50-67.
Glucose homeostasis and insulin action
- Kahn
Hormones and metabolism during sleep. Schwartz WJ. Sleep science: integrating basic research and clinical practice
- Van Cauter
Quantification of the relationship between insulin sensitivity and B-cell function in human subjects: evidence for a hyperbolic function
- Kahn
Effects of aging on insulin secretion
- Gumbiner