BACKGROUND: The associations between sleep patterns or behaviors and the risk of cirrhosis and the influence of genetic susceptibility on these associations among NAFLD participants remain inadequately elucidated.
METHODS: This study conducted a prospective follow-up of 112,196 NAFLD participants diagnosed at baseline from the UK Biobank cohort study. Five sleep behaviors were collected to measure a healthy sleep score. Five genetic variants were used to construct a polygenic risk score. We used Cox proportional hazard model to assess hazard ratios (HR) and 95% confidence intervals (CIs) for incidence of cirrhosis.
RESULTS: During the follow-up, 592 incident cirrhosis cases were documented. Healthy sleep pattern was associated with reduced risk of cirrhosis in a dose-response manner (ptrend < 0.001). Participants with favourable sleep score (versus unfavourable sleep score) had an HR of 0.55 for cirrhosis risk (95% CI 0.39-0.78). Multivariable-adjusted HRs (95% CIs) of cirrhosis incidence for NAFLDs with no frequent insomnia, sleeping for 7-8 h per day, and no excessive daytime dozing behaviors were 0.73 (0.61-0.87), 0.79 (0.66-0.93), and 0.69 (0.50-0.95), respectively. Compared with participants with favourable sleep pattern and low genetic risk, those with unfavourable sleep pattern and high genetic risk had higher risks of cirrhosis incidence (HR 3.16, 95% CI 1.88-5.33). In addition, a significant interaction between chronotype and genetic risk was detected for the incidence of cirrhosis (p for multiplicative interaction = 0.004).
CONCLUSIONS: An association was observed between healthy sleep pattern and decreased risk of cirrhosis among NAFLD participants, regardless of low or high genetic risk.

UNASSIGNED: The prevalence of obstructive sleep apnea (OSA) is high worldwide. This study aimed to quantify the relationship between the incidence of OSA and sleep patterns and genetic susceptibility.
UNASSIGNED: A total of 355,133 white British participants enrolled in the UK Biobank between 2006 and 2010 with follow-up data until September 2021 were recruited. We evaluated sleep patterns using a customized sleep scoring method based on the low-risk sleep phenotype, defined as follows: morning chronotype, 7-8 hours of sleep per day, never/rarely experience insomnia, no snoring, no frequent daytime sleepiness, never/rarely nap, and easily getting up early. The polygenic risk score was calculated to assess genetic susceptibility to OSA. Cox proportional hazard models were used to evaluate the associations between OSA and sleep patterns and genetic susceptibility.
UNASSIGNED: During a mean follow-up of 12.57 years, 4618 participants were diagnosed with OSA (age: 56.83 ± 7.69 years, women: 31.3%). Compared with those with a poor sleep pattern, participants with a normal (HR: 0.42, 95% CI: 0.38-0.46), ideal (HR: 0.21, 95% CI: 0.19-0.24), or optimal (HR: 0.15, 95% CI: 0.12-0.18) sleep pattern were significantly more likely to have OSA. The genetic susceptibility of 173,239 participants was calculated, and the results showed that poor (HR: 3.67, 95% CI: 2.95-4.57) and normal (HR: 1.89, 95% CI: 1.66-2.16) sleep patterns with high genetic susceptibility can increase the risk for OSA.
UNASSIGNED: This large-scale prospective study provides evidence suggesting that sleep patterns across seven low-risk sleep phenotypes may protect against OSA in individuals with varying degrees of genetic susceptibility.

OBJECTIVE: Evidence on the link between sleep patterns and cardiovascular diseases (CVDs) in the community essentially relies on studies that investigated one single sleep pattern at one point in time. This study examined the joint effect of five sleep patterns at two time points with incident CVD events.
METHODS: By combining the data from two prospective studies, the Paris Prospective Study III (Paris, France) and the CoLaus|PsyCoLaus study (Lausanne, Switzerland), a healthy sleep score (HSS, range 0-5) combining five sleep patterns (early chronotype, sleep duration of 7-8 h/day, never/rarely insomnia, no sleep apnoea, and no excessive daytime sleepiness) was calculated at baseline and follow-up.
RESULTS: The study sample included 11 347 CVD-free participants aged 53-64 years (44.6% women). During a median follow-up of 8.9 years [interquartile range (IQR): 8.0-10.0], 499 first CVD events occurred (339 coronary heart disease (CHD) and 175 stroke). In multivariate Cox analysis, the risk of CVD decreased by 18% [hazard ratio (HR) 0.82, 95% confidence interval (CI) 0.76-0.89] per one-point increment in the HSS. After a median follow-up of 6.0 years (IQR: 4.0-8.0) after the second follow-up, 262 first CVD events occurred including 194 CHD and 72 stroke. After adjusting for baseline HSS and covariates, the risk of CVD decreased by 16% (HR 0.84, 95% CI 0.73-0.97) per unit higher in the follow-up HSS over 2-5 years.
CONCLUSIONS: Higher HSS and HSS improvement over time are associated with a lower risk of CHD and stroke in the community.

To investigate whether a healthy sleep pattern would reduce the risk of cardiometabolic multimorbidity (CMM) among hypertensives.
This is a prospective cohort analysis from the UK Biobank. A total of 69 524 hypertensives without a history of diabetes mellitus, coronary heart disease, or stroke at baseline were enrolled. Five dimensions of healthy sleep at baseline including early chronotype, sleep 7-8 h/d, free of insomnia, no snoring, and no frequent excessive daytime sleepiness were used to generate a healthy sleep score ranging from 0 to 5 (one point was given for each dimension of healthy sleep). A higher score indicated a healthier sleep pattern. We set five groups corresponding to the healthy sleep score of 5, 4, 3, 2, and 0-1, respectively. The primary outcome was the incidence of overall CMM among enrolled hypertensives. We assessed the adjusted hazard ratios (HRs) and 95% confidence intervals (CIs) by Fine-Gray subdistribution hazard models.
We found the full-adjusted HR (95% CI) for overall CMM was 0.93 (0.91-0.95) for a 1-point increase in the healthy sleep score. Compared to hypertensives with a healthy sleep score of 0-1, those with a score of 5 had a 27% lower risk of overall CMM, and 37%, 23%, and 20% lower risks of diabetes mellitus, coronary heart disease, and stroke, respectively, after adjusting for sociodemographic characteristic, lifestyle, and clinical factors.
Our results indicated that a healthy sleep pattern was associated with lower risks of CMM outcomes among hypertensives.