Targeted metabolomics-based understanding of the sleep disturbances in drug-naïve patients with schizophrenia.

BACKGROUND: Sleep disturbances are a common occurrence in patients with schizophrenia, yet the underlying pathogenesis remain poorly understood. Here, we performed a targeted metabolomics-based approach to explore the potential biological mechanisms contributing to sleep disturbances in schizophrenia. METHODS: Plasma samples from 59 drug-naïve patients with schizophrenia and 36 healthy controls were subjected to liquid chromatography-mass spectrometry (LC-MS) targeted metabolomics analysis, allowing for the quantification and profiling of 271 metabolites. Sleep quality and clinical symptoms were assessed using the Pittsburgh Sleep Quality Index (PSQI) and the Positive and Negative Symptom Scale (PANSS), respectively. Partial correlation analysis and orthogonal partial least squares discriminant analysis (OPLS-DA) model were used to identify metabolites specifically associated with sleep disturbances in drug-naïve schizophrenia. RESULTS: 16 characteristic metabolites were observed significantly associated with sleep disturbances in drug-naïve patients with schizophrenia. Furthermore, the glycerophospholipid metabolism (Impact: 0.138, p<0.001), the butanoate metabolism (Impact: 0.032, p=0.008), and the sphingolipid metabolism (Impact: 0.270, p=0.104) were identified as metabolic pathways associated with sleep disturbances in drug-naïve patients with schizophrenia. CONCLUSIONS: Our study identified 16 characteristic metabolites (mainly lipids) and 3 metabolic pathways related to sleep disturbances in drug-naïve schizophrenia. The detection of these distinct metabolites provide valuable insights into the underlying biological mechanisms associated with sleep disturbances in schizophrenia.

Association between sleep patterns and galectin-3 in a Chinese community population.

BACKGROUND: Irregular sleep patterns have been associated with inflammation. Galectin-3, a novel biomarker, plays an important role in inflammation. We investigated the relationship between sleep patterns and galectin-3 in a Chinese population. METHODS: A total of 1,058 participants from the Shenzhen-Hong Kong United Network on Cardiovascular Disease study were included in the analysis. Age and sex-adjusted linear regression models were employed to investigate the relationship between galectin-3 level and traditional metabolic biomarkers. Logistic regression models were used to estimate the association among sleep disturbance, nighttime sleep duration, and daytime napping duration and elevated galectin-3, with elevated galectin-3 defined as galectin-3 level > 65.1 ng/ml. RESULTS: Of study participants, the mean age was 45.3 years and 54.3% were women. Waist circumference, natural logarithm (ln)-transformed triglyceride, and ln-transformed high sensitivity C-reactive protein were positively associated with galectin-3 level (age and sex-adjusted standardized ß [95% confidence interval (CI)], 0.12 [0.04, 0.21], 0.11 [0.05, 0.17], and 0.08 [0.02, 0.14], respectively). Sleep disturbance was associated with elevated galectin-3 (odds ratio [95% CI], 1.68 [1.05, 2.68], compared to those without sleep disturbance) after adjusting for traditional metabolic biomarkers. No interaction was observed between galectin-3 and age, sex, obesity, hypertension, and diabetes on sleep disturbance. No association was found between nighttime sleep duration or daytime napping duration and elevated galectin-3. CONCLUSIONS: Our study provides evidence of a significant association between sleep disturbance and elevated galectin-3 level, independent of traditional metabolic biomarkers. Screening and interventions on galectin-3 could assist in preventing sleep disturbance-induced inflammatory disease.

Associations of sleep disorders with serum neurofilament light chain levels in Parkinson's disease.

BACKGROUND: Sleep disorders are a prevalent non-motor symptom of Parkinson's disease (PD), although reliable biological markers are presently lacking. OBJECTIVES: To explore the associations between sleep disorders and serum neurofilament light chain (NfL) levels in individuals with prodromal and early PD. METHODS: The study contained 1113 participants, including 585 early PD individuals, 353 prodromal PD individuals, and 175 healthy controls (HCs). The correlations between sleep disorders (including rapid eye movement sleep behavior disorder (RBD) and excessive daytime sleepiness (EDS)) and serum NfL levels were researched using multiple linear regression models and linear mixed-effects models. We further investigated the correlations between the rates of changes in daytime sleepiness and serum NfL levels using multiple linear regression models. RESULTS: In baseline analysis, early and prodromal PD individuals who manifested specific behaviors of RBD showed significantly higher levels of serum NfL. Specifically, early PD individuals who experienced nocturnal dream behaviors (ß = 0.033; P = 0.042) and movements of arms or legs during sleep (ß = 0.027; P = 0.049) showed significantly higher serum NfL levels. For prodromal PD individuals, serum NfL levels were significantly higher in individuals suffering from disturbed sleep (ß = 0.038; P = 0.026). Our longitudinal findings support these baseline associations. Serum NfL levels showed an upward trend in early PD individuals who had a higher total RBDSQ score (ß = 0.002; P = 0.011) or who were considered as probable RBD (ß = 0.012; P = 0.009) or who exhibited behaviors on several sub-items of the RBDSQ. In addition, early PD individuals who had a high total ESS score (ß = 0.001; P = 0.012) or who were regarded to have EDS (ß = 0.013; P = 0.007) or who exhibited daytime sleepiness in several conditions had a trend toward higher serum NfL levels. CONCLUSION: Sleep disorders correlate with higher serum NfL, suggesting a link to PD neuronal damage. Early identification of sleep disorders and NfL monitoring are pivotal in detecting at-risk PD patients promptly, allowing for timely intervention. Regular monitoring of NfL levels holds promise for tracking both sleep disorders and disease progression, potentially emerging as a biomarker for evaluating treatment outcomes.

Association between vitamin C in serum and trouble sleeping based on NHANES 2017-2018.

Vitamin C is an important micronutrient for human. Association between vitamin C and trouble sleeping was less studied. Therefore, the purpose of this study was to investigate the possible link between vitamin C in serum and trouble sleeping. The cross-sectional data was derived from the National Health and Nutrition Examination Survey (NHANES, 2017-2018). Trouble sleeping was measured by asking participants: "Have you ever told doctor had trouble sleeping". Responses to this question was "yes" or "no". vitamin C in serum was obtained by measuring the serum samples. We used multivariable binary logistic regressions to examine the possible link between vitamin C in serum and trouble sleeping, and then a subgroup analysis was performed. Moreover, the non-linear relationship between vitamin C in serum and trouble sleeping was further detected using a restricted cubic spline (RCS) model. A total of 3227 participants were included in the study. After adjusting all potential confounders, the results of multivariable logistic regression showed the significant negative association between vitamin C in serum and trouble sleeping(OR = 0.816; 95% CI:0.669 ~ 0.995). The significant inverse association was also found in female(OR = 0.713; 95% CI:0.546 ~ 0.931), age ≤ 65 years(OR = 0.773; 95% CI:0.600 ~ 0.996), and in participants with high cholesterol level(OR = 0.738; 95% CI:0.548 ~ 0.994). In addition, the RCS model demonstrated the significant non-linear relationship between vitamin C in serum and trouble sleeping (P value of nonlinear = 0.010). Our study demonstrates the significant negative association between vitamin C in serum and trouble sleeping.

Variations in Sleep Characteristics and Glucose Regulation in Young Adults With Type 1 Diabetes.

CONTEXT: Short sleep duration and sleep disruptions are associated with impaired glucoregulation in type 1 diabetes (T1D). However, the mechanistic pathways between sleep and glucose variability remain unclear. OBJECTIVE: To determine within- and between-person associations between objective sleep-wake characteristics and glucose variability indices. METHODS: Multilevel models were used to analyze concurrent sleep and glucose patterns over 7 days in 42 young adults with T1D in their natural home environment. Young adults with T1D (mean age 22.2 ± 3.0 years, HbA1c 7.2%, 32.6% male) for at least 6 months with no other medical or major psychiatric comorbidity were included. Sleep-wake characteristics were measured via wrist actigraphy and glucose variability indices via a continuous glucose monitor (CGM). RESULTS: Lower sleep efficiency predicted higher glucose variability (less time in range ß = 0.011 and more time in hyperglycemia ß = -0.011) within-person. A longer wake after sleep onset and more sleep disruptions were associated with higher glucose variability between persons (ß = 0.28 and 0.31). Higher glucose variability predicted poorer sleep within-person (delayed bedtime, waketime, mid-sleep time, and lower sleep efficiency), while higher glucose variability was associated with poorer sleep and more sleep disruptions between persons (lower sleep efficiency, longer wake after sleep onset, and a higher sleep fragmentation index). CONCLUSION: Clinicians can address the reciprocal nature of the sleep-glucose relationship by optimizing sleep and targeting efforts toward a euglycemic range overnight. Sleep habits are a modifiable personal target in diabetes care.

Effect of Hibiscus syriacus Linnaeus extract and its active constituent, saponarin, in animal models of stress-induced sleep disturbances and pentobarbital-induced sleep.

Treatment of sleep disorders promotes the long-term use of commercially available sleep inducers that have several adverse effects, including addiction, systemic fatigue, weakness, loss of concentration, headache, and digestive problems. Therefore, we aimed to limit these adverse effects by investigating a natural product, the extract of the Hibiscus syriacus Linnaeus flower (HSF), as an alternative treatment. In the electric footshock model, we measured anxiety and assessed the degree of sleep improvement after administering HSF extract. In the restraint model, we studied the sleep rate using PiezoSleep, a noninvasive assessment system. In the pentobarbital model, we measured sleep improvement and changes in sleep-related factors. Our first model confirmed the desirable effects of HSF extract and its active constituent, saponarin, on anxiolysis and Wake times. HSF extract also increased REM sleep time. Furthermore, HSF extract and saponarin increased the expression of cortical GABAA receptor α1 (GABAAR α1) and c-Fos in the ventrolateral preoptic nucleus (VLPO). In the second model, HSF extract and saponarin restored the sleep rate and the sleep bout duration. In the third model, HSF extract and saponarin increased sleep maintenance time. Moreover, HSF extract and saponarin increased cortical cholecystokinin (CCK) mRNA levels and the expression of VLPO c-Fos. HSF extract also increased GABAAR α1 mRNA level. Our results suggest that HSF extract and saponarin are effective in maintaining sleep and may be used as a novel treatment for sleep disorder. Eventually, we hope to introduce HSF and saponarin as a clinical treatment for sleep disorders in humans.

Serotonin variations and sleep disorders among shift workers. A cross-sectional study.

Sleep disorders are prevalent occupational health problems among shift workers, especially healthcare workers with long shifts. Serotonin is a neurotransmitter related to circadian variations accompanied by shift work. A cross-sectional study was performed on 73 nurses at a tertiary hospital in Cairo, Egypt, to assess sleep quality among shift work nurses (SWNs), to determine blood serotonin level, and its relation to shift work and sleep quality. A demographic and occupational history questionnaire, Pittsburgh Sleep Quality Index (PSQI) questionnaire, and measurement of blood serotonin were carried out to the studied group. The data were analyzed using SPSS 25, and descriptive statistics, unpaired t-test, ANOVA, Kruskal-Wallis Test, Chi-square, Spearman correlation, and multivariate regression analysis were utilized. The results showed that the mean PSQI global score was significantly higher among SWNs than non-shift work nurses (NSWNs) and was the highest (10.32 ± 3.56 and 10.22 ± 2.4, respectively) among rotatory and fixed night shift nurses. Blood serotonin showed highly significant differences between SWNs over NSWNs (p = 0.001), and mostly reduced among rotatory and fixed night shift nurses (66.7% and 65%, respectively). Moreover, there were highly significant differences in serotonin levels between poor and good sleep quality nurses (p < 0.001), and most of the poor sleep quality nurses (62.7%) had low serotonin levels. Abnormal serotonin level (odds = 246.5) and working years (odds = 1.2) were statistically significant predictors of poor sleep quality. In conclusion, SWNs, especially rotating and night shift nurses, suffer from poor sleep quality associated with abnormal levels of blood serotonin.

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

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

Impact of COVID-19 on serum melatonin levels and sleep parameters in children

Background/aim: This study aimed to analyze the serum melatonin levels and changes in sleep patterns in pediatric patients with coronavirus disease 2019 (COVID-19). Materials and methods: This study was designed as a descriptive, cross-sectional study. Serum melatonin levels and sleep parameters of children with the diagnosis of COVID-19 who had mild and moderate disease (i.e., COVID-19 group) were compared with those of children admitted with non-COVID-19 nonspecific upper respiratory tract infection (i.e., control group). The sleep disturbance scale for children (SDSC) questionnaire was applied to the participants> primary caregivers to analyze their sleep patterns at present and six months before symptom onset and to investigate the impact of COVID-19 on sleep patterns. Results: The entire study cohort consisted of 106 patients. The COVID-19 group included 80 patients, while the control group consisted of 26 patients. The mean serum melatonin levels were 136.72 pg/mL and 172.63 pg/mL in the COVID-19 and control groups, respectively (p = 0.16). There was no significant difference between the groups in terms of 6 subcategories of the SDSC questionnaire regarding the present time and 6 months before symptom onset. The total SDSC scores were also similar in two different evaluation time points described above (p = 0.99) Conclusions: We conclude that COVID-19 did not impact the sleep parameters of children. Serum melatonin levels of all patients were higher than the reference range; however, they were higher in the non-COVID-19 patient group than the COVID-19 group. Since serum melatonin levels were higher than the reference values in children with COVID-19, and this disease is significantly less morbid in children, melatonin may have protective effects against COVID-19.

Levels of trace blood elements associated with severe sleep disturbance in maintenance hemodialysis patients.

PURPOSE: Sleep disturbance is frequently observed in patients on maintenance hemodialysis (MHD), and this population usually presents imbalances in trace elements. We investigated the association between blood trace element levels and sleep quality in patients on MHD. METHODS: This cross-sectional and single-center study was performed in September 2019. Patients regularly undergoing hemodialysis for > 3 months at our center were recruited, and demographic, clinical, and laboratory parameters were recorded. The Pittsburgh Sleep Quality Index (PSQI) was applied to define sleep disturbance. Blood trace element (zinc, manganese, copper, selenium, and lead) levels were measured using an inductively coupled plasma mass spectrometer. RESULTS: In total, 121 patients on MHD (male/female = 68:53) were enrolled in the study (mean age 63.7 ± 13.9 years, median dialysis vintage 38.0 [20.0, 60.0] months). According to PSQI, 56 (46%) patients experienced severe sleep disturbance. These patients were characterized by older age, higher serum parathyroid hormone levels, and lower blood selenium levels (all P < 0.05). No significant differences in blood zinc, manganese, copper, and lead levels were observed between groups. Univariate binary logistic regression showed that lower blood selenium levels were associated with severe sleep disturbance (odds ratio = 0.976, 95% confidence interval: 0.954-0.999, P = 0.038). Multivariate analyses also confirmed the results after adjusting for confounding factors. CONCLUSION: Our study indicated an association between lower blood selenium levels and the occurrence of severe sleep disturbances in patients on MHD. However, a prospective study with a larger sample size and assessing the importance of selenium supplementation are needed to confirm the results.

Sleep disturbance in adults with chronic pruritic dermatoses is associated with increased C-reactive protein levels.

BACKGROUND: Pruritus is a common symptom that can significantly reduce quality of life through sleep disruption. OBJECTIVE: To examine features of disturbed sleep in patients with chronic pruritic dermatoses and test the hypothesis that systemic inflammation may serve as a biomarker for impaired sleep in these patients. METHODS: Cross-sectional analysis of the National Health and Nutrition Examination Survey investigating systemic inflammation using C-reactive protein (CRP) levels. Logistic regression was used to compare patients with and without sleep disturbances, adjusting for demographics (model 1) and medical comorbidities (model 2). RESULTS: Chronic pruritic dermatoses were associated with multiple sleep disturbances, including nighttime awakenings (model 1: odds ratio [OR], 1.646; 95% confidence interval [CI], 1.031-2.627; model 2: OR, 1.329; 95% CI, 0.888-1.989) and early morning awakening (model 1: OR, 1.669, 95% CI, 1.118-2.493; model 2: OR, 1.582; 95% CI, 1.008-2.481). Mean CRP levels were 52.8% higher among patients with pruritic dermatoses reporting trouble sleeping compared with those who did not (0.663 vs 0.434 mg/dL; P = .034). Trouble sleeping was also positively correlated with CRP levels (ß = 0.142, P = .025). LIMITATIONS: Potential recall bias among participants. CONCLUSIONS: In addition to confirming sleep disturbances with pruritic dermatoses, we found these disturbances are more likely to present with elevated CRP levels. Clinicians should consider the potential risk for sleep-related and cardiac comorbidities in patients diagnosed with itchy skin conditions.

Symptom cluster profiles following traumatic orthopedic injuries: A protocol.

Traumatic injuries affect millions of Americans annually, resulting in $671 billion in healthcare costs and lost productivity. Postinjury symptoms, like pain, sleep disturbance, anxiety, depression, and stressor-related disorders are highly prevalent following traumatic orthopedic injuries (TOI) and may contribute to negative long-term outcomes. Symptoms rarely present in isolation, but in clusters of two or more symptoms that co-occur to affect health in aggregate. Identifying symptom cluster profiles following TOI may identify those at highest risk for negative outcomes. Dysregulation of brain-derived neurotrophic factor (BDNF) is a potential biological mechanism responsible for symptom cluster profile membership after TOI and may be targeted in future precision-health applications. The purpose of this paper is to present the protocol of a cross-sectional study designed to identify symptom cluster profiles and measure the extent to which the BDNF val66met mutation and serum concentration of BDNF are associated with membership in symptom cluster profiles. We plan to recruit 150 TOI survivors within the first 72 h of injury. The study aims are to (1) describe TOI survivors' membership in symptom cluster profiles, indicated by pain, sleep disturbance, and symptoms of anxiety, depression, and stressor-related disorders, immediately following a TOI; (2) examine associations between demographic and clinical factors and symptom cluster profile membership among TOI survivors; (3) test the hypothesis that low serum concentrations of BDNF are associated with membership among symptom cluster profiles following TOI; and (4) test the hypothesis that the presence of the val66met mutation on one or both alleles of the BDNF gene is associated with membership among symptom cluster profiles following TOI.

Increased plasma orexin-A concentrations are associated with the non-motor symptoms in Parkinson's disease patients.

BACKGROUND: Orexin, a neuropeptide primarily secreted by neurons in the lateral hypothalamus, has been implicated in Parkinson's disease (PD). Studies on the relationship between plasma orexin-A levels and PD are rare. OBJECTIVES: This study aimed to assess levels of plasma orexin-A in the progression of PD and to evaluate the correlation between orexin-A levels and non-motor symptoms. METHODS: Enzyme-linked immunosorbent assay was used to determine plasma orexin-A levels in 117 healthy controls and 121 PD patients, including those with early (n = 68), medium (n = 40) and advanced (n = 13) stages of the disease. Evaluation of motor symptoms and non-motor symptoms in PD patients, such as sleep disorders, cognitive dysfunction, neuropsychiatric symptoms, autonomic nervous dysfunction, hyposmia and PD-related pain, were assessed by the associated scales. RESULTS: Plasma orexin-A levels were significantly higher in PD patients compared to healthy controls. Orexin-A levels were elevated in early-stage and medium-stage PD compared to healthy controls, but were decreased in advanced-stage PD. Orexin-A levels were negatively correlated with the Unified Parkinson's Disease Rating Scale Part III scores, disease duration, and dopamine receptor agonist doses, and were positively correlated with the Pittsburgh Sleep Quality Index, REM-sleep Behavior Disorder Questionnaire, 14-item Hamilton Anxiety Scale, Mini-Mental State Examination, and Non-motor Symptom Scale items 22-24 scores. CONCLUSIONS: We found for the first time that plasma orexin-A levels were increased in early-stage and medium-stage PD and were decreased in advanced-stage PD. Furthermore, orexin-A levels were correlated with the non-motor symptoms of insomnia, REM-sleep behavior disorder, anxiety, cognitive dysfunction, and renal dysfunction.

Sleeping disturbances and predictor risk factors among type 2 diabetic mellitus patients.

Background: Sleep disturbance is a major health issue among people with type 2 diabetes mellitus (T2DM). The Pittsburgh Sleep Quality Index (PSQI) has been the most widely used instrument to measure subjective sleep disturbance. Aim: The aim of this study was to determine the impact of sleeping factor structure of the PSQI as potential predictor for glycosylated hemoglobin A1c (HbA1C) among people living with T2DM in the Turkish community to facilitate its use in the clinical practice and research. Subjects and Methods: This is a cross-sectional study and participants were between the age group of 25 and 65 years old who visited the diabetes and endocrinology department of Mega Medipol University Teaching Hospital, Istanbul. The PSQI was conducted on 871 patients with T2DM. Good sleep quality was defined as PSQI score <5. Multivariate logistic regression analysis was used to estimate the associated risk factors for the T2DM. Results: The current study showed significant differences between male and female patients with respect to their age in years, body mass index (BMI) (kg/m2), physical activity, smoking habit, sheesha smoking, income, family history of metabolic syndrome, coronary heart disease (CHD), and PSQI. The results revealed significant differences between HbA1c ≤7 and females and HbA1c >7 T2DM patients with respect to gender, BMI (kg/m2), CHD, and PSQI. The study demonstrated significant differences between sleeping categories PSQI as good, average, and poor sleeping among T2DM patients with respect to age and gender. Meanwhile, significant differences were reported between sleeping categories among T2DM patients with respect to their: number of sleeping hours, wake-up time, sleeping time, HbA1c, fasting blood glucose, uric acid, and systolic and diastolic blood pressure. This study showed very strong statistically significant correlations between low HbA1c and poor sleep quality in patients with T2DM patients, including subjective sleep quality r = 0.763, sleep latency r = 0.327, sleep duration r = 0.472, habitual sleep efficiency r = 0.575, sleep disturbances r = 0.564, use of sleep medication r = 0.728, and daytime dysfunction r = 0.734. Multivariate stepwise logistic regression analysis revealed that Vitamin D (mmol/L) (P < 0.001), HbA1c (P < 0.001), duration of DM (P < 0.001), uric acid (mmol/L) (P < 0.001), systolic blood pressure mmHg (P = 0.006), diastolic blood pressure mmHg (P = 0.015), and BMI (P = 0.024) were considered at higher risk as the predictors for sleeping quality among T2DM patients. Conclusion: The results suggest a strong positive correlation between PSQI with HbA1c levels, systolic and diastolic blood pressure, age, BMI, among type 2 diabetic patients. This study ascertains that poor sleep quality may be due to elevated level of HbA1c, metabolic syndrome, diabetes, obesity, and/or hypertension.

RésuméObjectif: Le but de cette étude était de déterminer l'impact de la structure du facteur de sommeil du PSQI en tant que prédicteur potentiel de l'HbA1C chez les personnes vivant avec le DT2 dans la communauté turque afin de faciliter son utilisation dans la pratique clinique et la recherche. Méthodes: Il s'agit d'une étude transversale et les participants étaient âgés de 25 à 65 ans et ont visité le service de diabète et d'endocrinologie du Mega Medipol University Teaching Hospital d'Istanbul. Le PSQI a été mené sur 871 patients atteints de DT2. Une bonne qualité de sommeil a été définie comme un score PSQI <5. Une analyse de régression logistique multivariée a été utilisée pour estimer les facteurs de risque associés au T2DM. Résultats: la présente étude a montré des différences significatives entre les hommes et les femmes en ce qui concerne leur âge en années, l'IMC (kg / m2), l'activité physique, le tabagisme, le tabagisme, le revenu, les antécédents familiaux de syndrome métabolique, les maladies coronariennes ( CHD) et PSQI. Les résultats ont révélé des différences significatives entre l'HbA1C≤7 et les femmes et l'HbA1C> 7 patients T2DM en termes de sexe, d'IMC (kg/m2), de maladie coronarienne (CHD) et de PSQI. L'étude a démontré des différences significatives entre les catégories de sommeil PSQI comme bon, moyen et mauvais sommeil chez les patients T2DM en ce qui concerne l'âge et le sexe.. Une analyse de régression logistique par étapes multivariée a révélé que la vitamine D (mmol / L) (P <0,001), l'HbA1c (P <0,001), la durée de la DM (P <0,001), l'acide urique (mmol / L) (P <0,001), la systolique La pression artérielle mmHg (P = 0,006), la pression artérielle diastolique mmHg (P = 0,015) et l'IMC (P = 0,024) étaient considérées comme présentant un risque plus élevé comme prédicteurs de la qualité du sommeil chez les patients atteints de DT2.Conclusion: Les résultats suggèrent une forte corrélation positive entre le PSQI avec les niveaux d'HbA1C, la pression artérielle systolique et diastolique, l'âge, l'IMC, chez les patients diabétiques de type 2. Cette étude établit qu'une mauvaise qualité de sommeil peut être due à un niveau élevé d'HbA1C, au syndrome métabolique, au diabète, à l'obésité et / ou à l'hypertension.

How do associations between sleep duration and metabolic health differ with age in the UK general population?

BACKGROUND: Despite a growing body of evidence suggesting that short sleep duration may be linked to adverse metabolic outcomes, how these associations differ between age groups remains unclear. We use eight years of data from the UK National Diet and Nutritional Survey (NDNS) (2008-2016) to analyse cross-sectional relationships between sleep duration and metabolic risk in participants aged 11-70 years. METHODS: Participants (n = 2008) who provided both metabolic risk and sleep duration data were included. Self-reported sleep duration was standardised by age, to account for differences in age-related sleep requirements. A standardised metabolic risk score was constructed, comprising: waist circumference, blood pressure, serum triglycerides, serum high-density lipoprotein cholesterol, and fasting plasma glucose. Regression models were constructed across four age groups from adolescents to older adults. RESULTS: Overall, decreased sleep duration (hrs) was associated with an increased metabolic risk (standard deviations) with significant quadratic (B:0.028 [95%CI: 0.007, 0.050]) and linear (B:-0.061 [95%CI: -0.111, -0.011]) sleep duration coefficients. When separated by age group, stronger associations were seen among mid-aged adults (36-50y) (quadratic coefficient: 0.038 [95%CI: 0.002, 0.074]) compared to other age groups (e.g. adolescents (11-18y), quadratic coefficient: -0.009 [95%CI: -0.042, 0.025]). An increased difference between weekend and weekday sleep was only associated with increased metabolic risk in adults aged 51-70 years (B:0.18 [95%CI: 0.005, 0.348]). CONCLUSIONS: Our results indicate that sleep duration is linked to adverse metabolic risk and suggest heterogeneity between age groups. Longitudinal studies with larger sample sizes are required to explore long-term effects of abnormal sleep and potential remedial benefits.

Angelman syndrome and melatonin: What can they teach us about sleep regulation.

In 1965, Dr Harry Angelman reported a neurodevelopmental disorder affecting three unrelated children who had similar symptoms: brachycephaly, mental retardation, ataxia, seizures, protruding tongues, and remarkable paroxysms of laughter. Over the past 50 years, the disorder became Angelman's namesake and symptomology was expanded to include hyper-activity, stereotypies, and severe sleep disturbances. The sleep disorders in many Angelman syndrome (AS) patients are broadly characterized by difficulty falling and staying asleep at night. Some of these patients sleep less than 4 hours a night and, in most cases, do not make up this lost sleep during the day-leading to the speculation that AS patients may "need" less sleep. Most AS patients also have severely reduced levels of melatonin, a hormone produced by the pineal gland exclusively at night. This nightly pattern of melatonin production is thought to help synchronize internal circadian rhythms and promote nighttime sleep in humans and other diurnal species. It has been proposed that reduced melatonin levels contribute to the sleep problems in AS patients. Indeed, emerging evidence suggests melatonin replacement therapy can improve sleep in many AS patients. However, AS mice show sleep problems that are arguably similar to those in humans despite being on genetic backgrounds that do not make melatonin. This suggests the hypothesis that the change in nighttime melatonin may be a secondary factor rather than the root cause of the sleeping disorder. The goals of this review article are to revisit the sleep and melatonin findings in both AS patients and animal models of AS and discuss what AS may tell us about the underlying mechanisms of, and interplay between, melatonin and sleep.

[Association between sleep and serum hemoglobin A1c in nondiabetic population in Beijing].

Objective: To understand the status quo of sleep and its associations with serum hemoglobin A1c (HbA1c) among nondiabetic people of 18-79 years old in Beijing. Methods: Data was gathered from the 2017 Beijing Non-communicable and Chronic Disease Surveillance Program. Multiple classified clusters sampling method was used while the 18-79 years old were sampled from the 16 districts of Beijing. Questionnaires would include information on demographic characteristics, chronic diseases and related risk factors, sleep duration and related problems (snore/asphyxia, difficult to get to sleep, waking often during the night, waking up early or taking sleeping pills) within the last 30 days. Complex sampling logistic regression models were established to analyze the association between sleep-related problems and serum HbA1c. Results: A total of 11 608 non-diabetic participants were involved in this study, with average age, reported sleep duration and median of serum HbA1c level as (43.36±15.27) years old, (7.49±1.29) h/d and 5.30%, respectively. 47.38% of them reported having sleep problems within the last 30 days. With the increasing time of sleep, serum HbA1c level was fluctuating significantly (F=413.06, P<0.01). Significant differences appeared in serum HbA1c levels among different age groups (t=358.3, P<0.01). Among participants with several kinds of sleep problems, the serum HbA1c levels were significantly higher than those without, through the single factor analysis (U=15.11, P<0.01). After adjusting for potential confounding factors, the combination of one sleep-related problem (OR=1.21, 95%CI: 1.03-1.41) and snore/asphyxia were associated with higher serum HbA1c levels (HbA1c≥5.7%) (OR=1.37, 95%CI: 1.16-1.61). People under 60 years of age were with higher risk of having higher serum HbA1c levels. Conclusion: Duration and sleep-related problems might affect the serum HbA1c levels, especially among those younger than 60 years of age.

Baseline Vitamin D Status, Sleep Patterns, and the Risk of Incident Type 2 Diabetes in Data From the UK Biobank Study.

OBJECTIVE: Circulating vitamin D concentrations have been associated with the risk of type 2 diabetes (T2D), but the results are inconsistent. Emerging evidence suggests that vitamin D metabolism is linked to sleep behaviors. We investigated the prospective association between serum 25-hydroxyvitamin D (25OHD) and the risk of incident T2D and whether such association was modified by sleep behaviors. RESEARCH DESIGN AND METHODS: The study included 350,211 individuals free of diabetes in the UK Biobank. Serum 25OHD (nmol/L) concentrations were measured. Five sleep behaviors including sleep duration, insomnia, snoring, chronotype, and daytime sleepiness were included to generate overall sleep patterns, defined by healthy sleep scores. We also calculated genetic risk scores of sleep patterns. RESULTS: During a median follow-up of 8.1 years, we documented 6,940 case subjects with incident T2D. We found that serum 25OHD was significantly associated with a lower risk of incident T2D, and the multivariate adjusted hazard ratio (HR) (95% CI) per 10 nmol/L increase was 0.88 (0.87-0.90). We found a significant interaction between 25OHD and overall sleep patterns on the risk of incident T2D (P for interaction = 0.002). The inverse association between high 25OHD and T2D was more prominent among participants with healthier sleep patterns. Among the individual sleep behaviors, daytime sleepiness showed the strongest interaction with 25OHD (P for interaction = 0.0006). The reduced HR of T2D associated with high 25OHD appeared to be more evident among participants with no frequent daytime sleepiness compared with those with excessive daytime sleepiness. The genetic variations of the sleep patterns did not modify the relation between 25OHD and T2D. CONCLUSIONS: Our study indicates that higher serum 25OHD concentrations are associated with a lower risk of incident T2D, and such relations are modified by overall sleep patterns, with daytime sleepiness being the major contributor.

Effect of melatonin administration on the PER1 and BMAL1 clock genes in patients with Parkinson's disease.

Sleep disorders are a widespread condition in patients with Parkinson's disease (PD), which has been linked to a deregulation of the circadian cycle and therefore of the clock genes. The aim of this study was to evaluate the effect of melatonin (MEL) on the PER1 and BMAL1 clock genes in patients with PD. A double-blind, cross-over, placebo-controlled randomized clinical trial pilot study was conducted in 26 patients with stage 1-3 PD according to the Hoehn & Yahr scale, who received either 25 mg of MEL or a placebo at noon and 30 min before bedtime for three months. The relative expression of the PER1 and BMAL1 genes was measured, as well as the presence of daytime, nocturnal, and global sleepiness, and the progression of PD. The levels of the PER1 and BMAL1 genes at baseline were 0.9 (0.1-3) vs. 0.56 (0.1-2.5), respectively; while after the intervention with MEL or placebo the BMAL1 levels increased to 2.5 (0-3.70) vs. 2.2 (0.10-3.30), respectively (d = 0.387). Fifty percent (50 %) of patients had daytime sleepiness and sixty-five percent (65 %) had abnormal nighttime sleepiness, yet neither group showed changes after the intervention. Patients with PD exhibited an alteration in the levels of the clock genes: MEL increased the levels of BMAL1, but the PER1 levels remained unchanged.

Sleep disorders and vascular responsiveness in patients with rheumatoid arthritis.

BACKGROUND: Rheumatoid arthritis (RA) is the most common systemic autoimmune disease characterized by chronic systemic inflammation. Half of the deaths of patients with RA are due to cardiovascular diseases (CVD), considered to be 1.5 to -2.0-fold that in the general population. Patients with RA also experience poor sleep, which by itself is associated with endothelial dysfunction, CVD events and sudden death. Our aim was to study the mechanistic pathways and the correlations between sleep efficiency and vascular reactivity of patients with RA. METHODS AND RESULTS: A prospective study that evaluated quality of sleep using ACTi Graphs, vascular inflammation and endothelial function of 18 patients with RA. Inflammation was studied by levels of E-selectin, intercellular adhesion molecule 1 (ICAM-1) and NO in serum. Endothelial function was studied using the brachial artery plethysmography method. Eighteen RA patients (aged 57.56 ± 13.55 years; 16 women) with a long-standing active RA: Eight patients had impaired sleep efficiency and 10 had a good sleep efficiency. Those who had an impaired sleep had larger baseline diameters of the brachial artery (0.39 ± 0.08 cm vs. 0.32 ± 0.04 cm; P = 0.02). Negative correlations were found between baseline brachial artery diameter and sleep efficiency (P = 0.01), and with NO level (P = 0.04). Stepwise regression found that brachial artery diameter at baseline and NO level could predict sleep efficiency (r2  = 0.543, P = 0.01). CONCLUSION: Vascular reactivity could predict quality of sleep in patients with RA. Quality of sleep may serve as an independent CVD risk factor in patients with RA.