Sleep and Biological Rhythms最新文献

Objectives: Social jetlag (SJL), the discrepancy between an individual’s inherent circadian rhythm and external social schedule, is associated with obesity. This study aimed to investigate whether SJL also influences body weight and body fat loss during dieting. Methods: This was an observational study from 2015 to 2018 with participants who had joined an exercise and nutrition program at a private personal training gym. Data from 11,829 individuals provided by the gym along with their sleep logs were analyzed. Differences in change in body mass index (BMI) and body fat percentage (%body fat) were compared by the degree of SJL. Regression was conducted for the change in BMI and %body fat on SJL, adjusted for gender, age, engagement duration in the program, initial BMI, initial %body fat, chronotype, and dietary intakes. Results: The subjects comprised 3,696 men and 8,133 women with a mean age of 40.4 years. Greater SJL was associated with a lower efficacy of BMI and %body fat reduction. The change in BMI (+ 0.56 / hour: SJL) and %body fat (+ 1.40 / hour: SJL) was associated with SJL after adjusting for each variable including dietary intake. Conclusion: SJL was associated with the effect of exercise and nutrition instruction on BMI and body fat reduction, even after adjustment for covariates related to dietary intake. Maintaining consistent sleep–wake rhythms may be crucial for enhancing the efficacy of weight loss programs.

This mini-meta-analysis evaluated the internal consistency of the Anxiety and Preoccupation about Sleep Questionnaire (APSQ) across existing studies to assess its potential as an orthosomnia (an obsessive preoccupation with achieving perfect sleep) screening tool. A systematic literature search identified four studies with 2,506 participants using English, Swedish, Turkish, and Arabic versions. Cronbach’s alpha ranged from 0.91 to 0.95 across studies. The APSQ demonstrated high overall internal consistency reliability (pooled Cronbach’s alpha of the entire ASPQ = 0.93, 95% CI 0.91–0.94), suggesting utility for screening orthosomnia symptoms. The pooled Cronbach’s alpha of the first and second factors of the ASPQ were: 0.91 (95% CI 0.89–0.93) and 0.87 (95% CI 0.84–0.89), respectively. APSQ demonstrated high overall internal consistency reliability; however, limited linguistic/cultural representation and significant heterogeneity across studies impact generalizability.

The study aimed to discuss the association between sleep duration and the risk of hyperhomocysteinemia (Hhcy). This cross-sectional study included 4173 adults (≥ 20 years) from the National Health and Nutrition Examination Survey 2005–2006. According to their sleep duration, participants were divided into five subgroups. Multivariate logistic regression analysis models and restrictive cubic spline regressions were used to explore the association between sleep duration and the risk of Hhcy. Compared with the participants who sleep 7 h, sleep deprivation (≤ 5 h) increased the risk of Hhcy, odds ratio (OR) 1.68 (95% confidence interval (CI) 1.06–2.68); Excessive sleep (≥ 9 h) also increased the risk of Hhcy, OR 1.86 (95% CI 1.09–3.14) after adjusting for a series of confounding factors in the entire population. The risk of Hhcy was distributed in a U-shape with sleep duration. Similar results were demonstrated in obese populations. The association between sleep duration and the risk of Hhcy is U-shaped. Both sleep deprivation and excessive sleep can increase the risk of Hhcy.

Sleep is integral to cognitive functioning, and disturbances in sleep patterns can impair cognition. This study investigated the relationships between executive functions, sleep problems, and negative pre-sleep cognitions, proposing a model for their interaction. We assessed 107 adults using the Bedtime Counterfactual Processing Questionnaire and the Glasgow Content of Thoughts Inventory for negative pre-sleep cognitions, the Insomnia Severity Index and the Pittsburgh Sleep Quality Index for sleep problems, and the Free Research Executive Evaluation test battery for executive functions. Regression and mediation analyses were conducted to examine both direct and indirect relationships between these variables. Higher executive functions were associated with fewer negative pre-sleep cognitions, which in turn predicted fewer sleep problems. However, the anticipated direct effect of sleep problems on executive functioning was not supported, indicating a more complex interplay. Notably, pre-sleep cognition mediated the relationship between executive functions and sleep problems, indirectly affecting sleep problems through its connection with executive functions. While the findings support the mediation model of executive functions, negative pre-sleep cognitions, and sleep problems, the proposed cyclical model was not fully substantiated. This suggests that additional factors may influence the dynamics of this relationship, offering potential avenues for future research and interventions targeting sleep disorders and cognitive well-being enhancement.

Stroke-related restless legs syndrome (sRLS) is an emerging clinical entity, with a clear relationship between stroke and the occurrence of restless legs syndrome (RLS). Dopamine dysregulation has been observed in sRLS of the lenticulostriate region with increased dopamine precursor and decreased dopamine transporter. The aim of this work is to explore an original case of regressive RLS following stroke. Anatomical (MRI) and functional (¹⁸F-FDG PET; ¹⁸F- FDOPA PET; ¹²³I-FP-CIT SPECT) brain imaging was performed in our patient. A 63 year-old woman experienced complete resolution of longstanding restless legs syndrome (RLS) after a right middle cerebral artery stroke (left faciobrachial sensorimotor deficit), efficiently treated with intravenous thrombolysis. Having had RLS for 14 years, she reported complete symptom relief within four days post-stroke. 2 year follow-up confirmed sustained improvement. In our patient, functional dopaminergic imaging revealed an overall normal dopaminergic tone. This case contradicts the more commonly reported scenario of sRLS where stroke leads to the onset or worsening of RLS. The pathophysiology of RLS remains unclear and in the absence of clear biomarkers for RLS, small lesion models in humans can provide valuable insights to a better understanding of this disease.

Chronic pain due to peripheral neuropathy can lead to sleep disorders that significantly worsen the patient's quality of life. Previously, we conducted brain wave measurements in a rat model of neuropathic pain and identified its potential as a model for sleep disorders associated with chronic pain (reported). In this study, we quantified melatonin secretion and assessed its circadian rhythm in a rat model of pain-induced sleep disorder. To create a model of chronic constriction injury (CCI), rats were loosely tied around the sciatic nerve, with approximately 1 mm spacing, 14 days before the experiment. Rats with no ties around the sciatic nerve were used as controls. Electroencephalograms and electromyograms were recorded for 3 days, and the episodes of waking, REM sleep, and non-REM sleep were compared between the groups. The samples for microanalysis were collected every 30 min and used for melatonin analysis. Compared to the control group, the CCI model group exhibited an increase in wake episodes and a decrease in non-REM sleep episodes. Analysis of the area under the curve of melatonin secretion revealed a significant increase in melatonin secretion and a loss of circadian rhythm in the CCI model group. Melatonin secretion markedly increased accompanied by loss of circadian rhythm in a rat model of CCI. Further studies investigating the causal relationship between neuropathic pain and melatonin secretion are warranted.