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Emerging evidence links COVID-19 to the predisposition of Parkinson's disease (PD). However, the relationship between long COVID and prodromal PD-like features remains unclear, particularly in long COVID participants with dream-enactment behaviours (DEBs) that may be suggestive of possible REM sleep behaviour disorder. This study aimed to quantify the burden of prodromal PD-like features in long COVID. This online survey (May-Nov 2021) across 16 countries/regions included 11,261 participants. Data on demographics, COVID-19 diagnosis, long COVID symptoms, sleep features and other typical prodromal PD-like features were collected. The likelihood ratio (LR) of prodromal PD was calculated as a proxy for each participant's overall burden of prodromal PD-like features, based on the 2019 Movement Disorder Society research criteria. Participants with long COVID (n = 1155) exhibited more symptoms suggestive of prodromal PD-like features, including DEBs, olfactory dysfunctions, constipation, excessive daytime sleepiness, postural dizziness, depression with/without anxiety, urinary dysfunctions, cognitive impairment and a higher LR of prodromal PD when compared to non-COVID-19 participants and COVID-19 recoverees. Long COVID was associated with a 73% higher burden of potential prodromal PD-like features (adjusted odds ratio [aOR] = 1.73, 95% confidence interval [CI] = 1.57-1.90). Among those with long COVID, emergence or exacerbation of post-infection DEBs further increased this burden by 38% (aOR = 1.38, 95% CI = 1.19-1.60). Our study suggested that long COVID is associated with an increased burden of prodromal PD-like features, which appears to be further enhanced with DEBs.

Background: Identifying reliable predictors for dementia remains a critical unmet need. Light exposure plays a crucial role in regulating circadian rhythms, which influence cognitive function. However, the association between light exposure and dementia risk remains unclear. Aims: This study examined the associations of daytime and nighttime light exposure with dementia risk. Methods: A total of 87577 dementia-free participants (mean age 62.36 years; 56.98% female) were included. Daytime and nighttime light exposures were measured using 7-day free-living wrist-worn accelerometry. Incident dementia was identified from primary care, hospital inpatient admissions and death registry data. Cox proportional hazards models assessed associations, and mediation analyses evaluated circadian rest-activity rhythms, brain structures and vitamin D as potential mediators. Results: Over a median follow-up of 8.1 years, 741 participants developed dementia. Daytime light exposure above 1000 lux was associated with reduced dementia risk (HR 0.84, 95% CI 0.71-0.99). Longer exposure to brighter light was associated with further risk reduction. Circadian rhythms and brain structures partially mediated the association. Conclusions: High levels of daytime light exposure were significantly associated with lower dementia risk. Further research should explore its role in dementia screening and light-based interventions.

BACKGROUND: Obstructive sleep apnea is strongly linked to hypertension, yet most evidence derives from Western populations in whom obesity is common. Because East Asian adults frequently develop obstructive sleep apnea at lower body mass index, it remains unclear whether body mass index modifies the association between obstructive sleep apnea severity and morning blood pressure in this population.

METHODS: A total of 1849 adults aged 18-92 years underwent overnight, in-hospital polysomnography. Morning brachial blood pressure was measured twice in the seated position after 5 minutes of rest. Obstructive sleep apnea severity was quantified using the apnea-hypopnea index. Generalized linear models evaluated independent and interactive associations of body mass index and apnea-hypopnea index with systolic and diastolic blood pressure, adjusting for relevant covariates, including antihypertensive medication use.

RESULTS: A significant body mass index × apnea-hypopnea index interaction was observed for both systolic and diastolic blood pressure (p < .01), indicating that the association between obstructive sleep apnea severity and morning blood pressure varied across body mass index, for example, a 20-unit increase in apnea-hypopnea index was associated with larger increases in systolic/diastolic blood pressure at lower body mass index (∼3/1.5 mmHg at body mass index 20 kg/m²) than at higher body mass index (∼1.1/0.1 mmHg at body mass index 30 kg/m²). In sensitivity analyses using nocturnal hypoxemia (T <90%), a body mass index-dependent association was observed for systolic but not diastolic blood pressure.

CONCLUSION: These findings suggest that the association between obstructive sleep apnea severity and morning blood pressure differs across the body mass index spectrum, underscoring the importance of considering both obstructive sleep apnea burden and body weight in cardiovascular risk assessment, particularly in East Asian populations.

INTRODUCTION: Insufficient sleep increases the risk of weight gain and metabolic dysfunction, while obesity is linked to disrupted sleep and metabolic impairment. Although both conditions are tightly interconnected, it remains unclear whether body weight status determines how acute sleep loss alters metabolite levels. We aimed to assess whether acute sleep loss elicits different metabolic responses in individuals with and without obesity, and whether these responses are modified by sex.

METHODS: In a within-subject, randomized crossover study, 42 adults (mean age 24.9 years; 18 women, 24 men; 18 with obesity; 24 with normal weight) completed one night of total sleep deprivation (TSD) and one night of normal sleep (NS; 8 h). Morning fasted blood samples were analyzed using targeted metabolomics. Mixed-effects models were used to assess within-individual changes from NS to TSD, and to determine the magnitude and direction of these changes within each body weight group and sex.

RESULTS: In response to TSD compared with NS, tryptophan levels increased (+12%, FDR < 0.05) only in participants with obesity, while histidine, L-kynurenine, and creatinine levels decreased (4-21%, FDR < 0.05) only in normal-weight individuals. Notably, the kynurenine-to-tryptophan ratio decreased after TSD in both groups, and levels of circulating medium-chain acylcarnitines (+26-39%) increased within both weight groups - together indicating shared metabolic responses to acute sleep deprivation. Exploratory sensitivity analyses indicated that several of these responses were sex-specific. Polysomnography-based sleep architecture during NS, available in a subset of 36 participants, was largely comparable between body weight groups, suggesting that observed metabolic differences were not attributable to baseline differences in sleep structure.

CONCLUSIONS: Acute sleep loss elicits both shared and body-weight-specific changes in circulating metabolites in young adults. These findings indicate that body-weight status shapes which metabolic pathways respond to a single night of sleep loss, and in what direction, but larger studies are required to confirm the body weight- and sex-specific findings. Given that acute sleep loss is a common metabolic stressor that increases cardiometabolic risk, these differences may contribute to mechanistic hypotheses about the heightened vulnerability to metabolic dysregulation in individuals with obesity who are frequently exposed to sleep loss.

A rate-limiting step in the prevention and early intervention of osteoporosis is identifying its asymptomatic onset. Accumulating evidence shows that sleep disorders are associated with an increased risk of osteoporosis. Given their early detectable and modifiable nature, integrating sleep disorder management into osteoporosis prevention and care pathways offers a novel approach for enhancing skeletal health. This expert consensus represents a collaborative effort by specialists in sleep medicine and orthopedics from across the world, integrating epidemiological, mechanistic, and interventional evidence to provide general guidance for prevention and clinical practice, and to foster multidisciplinary collaboration in the management of sleep disorders and osteoporosis.

Daytime light exposure is essential for health, primarily by synchronizing tissue and cellular-level clocks with the external light/dark cycle. Insufficient exposure may disrupt circadian alignment and contribute to adverse outcomes, including cancer. Given the high prevalence of gastrointestinal cancer, we conducted a prospective cohort study of 89,069 participants with objectively measured daytime light intensity and duration. Cox proportional hazards models were used to evaluate associations with gastrointestinal cancer incidence and mortality. Over a median follow-up of 8.8 years (804,111 person-years), 1692 gastrointestinal cancer cases were recorded, of which 891 were fatal. Higher mean levels of daytime light (≥ 1916 lux between 7:30-20:30, based on the 80% cut-off) were associated with lower risk of gastrointestinal cancer incidence (Hazard Ratio [HR]: 0.87, 95% confidence interval [CI]: 0.76-0.99, p = 0.04) and mortality (HR = 0.76, 95% CI: 0.63-0.93, p = 0.008), particularly for pancreatic cancer incidence (HR = 0.58, 95% CI: 0.40-0.85, p = 0.005) and mortality (HR = 0.47, 95% CI: 0.30-0.73, p = 0.001). Daytime light exposure ≥ 2.4 h (≥ 5000 lux between 7:30 and 20:30, which is often used as a chronotherapeutic threshold) was associated with a lower risk of pancreatic cancer incidence and mortality. Predictive ability of daytime light metrics exceeded that of sleep quality, diet, depression, and alcohol consumption. Higher daytime light exposure was associated with lower risks of gastrointestinal cancer incidence and mortality, especially for pancreatic cancer, indicating a potential protective effect that warrants further investigation in prevention and prognostic contexts.

Night shift work can impair attention and increase biomarkers linked to neurodegenerative processes. Understanding factors that influence resilience to, or vulnerability under, sleep loss is therefore essential for identifying groups at particular risk. In this within-subjects study, we examined two potential modulators of vulnerability in 54 healthy, naturally cycling women aged 21-33 years: the ovarian hormone estradiol, known for its neuroprotective properties and the personality trait neuroticism, previously associated with stress sensitivity. Participants completed one night of habitual sleep followed by one night of overnight wakefulness, mimicking a transition from an off- to an on-night shift. Women with higher morning blood estradiol levels or lower neuroticism (indexed by higher emotional stability scores) exhibited non-significant tendencies towards faster reaction times during successful psychomotor vigilance test (PVT) trials, which assess sustained attention. Notably, lower neuroticism was also associated with significantly fewer attentional lapses (reaction times ≥ 500 ms) during the PVT, whereas estradiol levels were not. However, neither trait modulated the overall decline in attentional performance observed following the night-shift condition. In contrast, higher neuroticism-but not estradiol-predicted elevated morning levels of phosphorylated tau at threonine 181 (p-Tau181), a plasma biomarker associated with Alzheimer's disease-related neurodegenerative processes, after the night shift condition. These findings highlight neuroticism as a psychological factor linked to increased neurobiological sensitivity to overnight wakefulness among women.

Shift workers exhibit a higher incidence of coronary heart disease (CHD) than daytime workers. We examined whether this difference in CHD incidence between shift workers and daytime workers is associated with two dietary factors linked to lower CHD risk-daily fiber intake and meat avoidance-using UK Biobank data. The study included 222,801 participants (53.8% women; mean age 52.6 years), categorized as daytime workers, shift workers with no or occasional night shifts, or regular night shift workers. Dietary habits were assessed via touchscreen dietary questionnaires. During a median follow-up of 12.6 years, 12,265 fatal and non-fatal CHD events occurred. Compared with daytime workers, regular night shift work-but not shift work with no or occasional night shifts-was associated with higher CHD incidence (hazard ratio [HR] 1.10, 95% CI 1.01-1.20). HRs for CHD were higher (vs. daytime work) in both shift work groups among participants with lower daily fiber intake, whereas they were attenuated among those with higher fiber intake (p < 0.05 for interaction). Meat avoidance was associated with a 10.4% lower CHD HR compared with meat consumption (p = 0.020), although no significant interaction with work schedule was observed. In summary, while our finding that meat avoidance is associated with modestly lower CHD HR across work schedules aligns with established cardiovascular recommendations, our observation that higher fiber intake may reduce CHD differences specifically linked to night shift work highlights an additional, shift-specific dietary consideration that could complement the American Heart Association's Life's Essential 8.