Sleep has been associated with aging and relevant health outcomes, but the causal relationship remains inconclusive. In this study, we investigated the associations of sleep behaviors with biological ages (BAs) among 363,886 middle and elderly adults from UK Biobank. Sleep index (0 [worst]–6 [best]) of each participant was retrieved from the following six sleep behaviors: snoring, chronotype, daytime sleepiness, sleep duration, insomnia, and difficulties in getting up. Two BAs, the KDM‐biological age and PhenoAge, were estimated by corresponding algorithms based on clinical traits, and their residual discrepancies with chronological age were defined as the age accelerations (AAs). We first observed negative associations between the sleep index and the two AAs, and demonstrated that the change of AAs could be the consequence of sleep quality using Mendelian randomization with genetic risk scores of sleep index and BAs. Particularly, a one‐unit increase in sleep index was associated with 0.104‐ and 0.119‐year decreases in KDM‐biological AA and PhenoAge acceleration, respectively. Air pollution is another key driver of aging. We further observed significant independent and joint effects of sleep and air pollution (PM2.5 and NO2) on AAs. Sleep quality also showed a modifying effect on the associations of elevated PM2.5 and NO2 levels with accelerated AAs. For instance, an interquartile range increase in PM2.5 level was associated with 0.009‐, 0.044‐, and 0.074‐year increase in PhenoAge acceleration among people with high (5–6), medium (3–4), and low (0–2) sleep index, respectively. Our findings elucidate that better sleep quality could lessen accelerated biological aging resulting from air pollution.

Theory predicts that biological processes of aging may contribute to poor mental health in late life. To test this hypothesis, we evaluated prospective associations between biological age and incident depression and anxiety in 424,299 UK Biobank participants. We measured biological age from clinical traits using the KDM-BA and PhenoAge algorithms. At baseline, participants who were biologically older more often experienced depression/anxiety. During a median of 8.7 years of follow-up, participants with older biological age were at increased risk of incident depression/anxiety (5.9% increase per standard deviation [SD] of KDM-BA acceleration, 95% confidence intervals [CI]: 3.3%–8.5%; 11.3% increase per SD of PhenoAge acceleration, 95% CI: 9.%–13.0%). Biological-aging-associated risk of depression/anxiety was independent of and additive to genetic risk measured by genome-wide-association-study-based polygenic scores. Advanced biological aging may represent a potential risk factor for incident depression/anxiety in midlife and older adults and a potential target for risk assessment and intervention.

Background: Depression and anxiety are two mental disorders that are often comorbid. However, the associations of long-term air pollution exposure with depression and anxiety remain inconclusive. Objective: We conducted a cross-sectional and prospective study to examine the associations of ambient exposure to particulate matter (PM) with a diameter of ( ), ( ), and ( ), nitrogen oxides ( ), and nitrogen dioxide ( ) with the risk of depression and anxiety in the UK Biobank. Methods: This study included 398,241 participants from the UK Biobank, 128,456 of whom participated the 7-y online mental health survey. A total of 345,876 individuals were free of depression and anxiety at baseline; of those, 16,185 developed incident mental disorders during a median of 8.7 y of follow-up. Depression and anxiety were assessed using hospital admission records and mental health questionnaires. Associations of air pollution with prevalent and incident mental disorders were examined using logistic regression and Cox regression models, respectively. Results: Elevated levels of the five air pollutants were associated with higher odds of mental disorders at baseline. Levels of four pollutants but not were also associated with higher odds and risks of mental disorders during follow-up; specifically, hazard ratios [HR, 95% confidence interval (CI)] of an interquartile range increase in , , , and for incident mental disorders were 1.03 (95% CI: 1.01, 1.05), 1.06 (95% CI: 1.04, 1.08), 1.03 (95% CI: 1.01, 1.05), and 1.06 (95% CI: 1.04, 1.09), respectively. An air pollution index reflecting combined effects of pollutants also demonstrated a positive association with the risk of mental disorders. HR (95% CI) of incident mental disorders were 1.11 (95% CI: 1.05, 1.18) in the highest quintile group in comparison with the lowest quintile of the air pollution index. We further observed that the associations between air pollution and mental disorders differed by a genetic risk score based on single nucleotide polymorphisms previously associated with genetic susceptibility to mental disorders in the UK Biobank cohort. Discussion: To our knowledge, this research is one of the largest cohort studies that demonstrates an association between mental health disorders and exposure to long-term air pollution, which could be further enhanced by genetic predisposition. https://doi.org/10.1289/EHP10391

Background Evidence is limited regarding the association of healthy lifestyle including sleep pattern with the risk of complicated type 2 diabetes mellitus (T2DM) among patients with hypertension. We aimed to investigate the associations of an overall healthy lifestyle including a healthy sleep pattern with subsequent development of T2DM among participants with hypertension compared to normotension, and to estimate how much of that risk could be prevented. Methods This study examined six lifestyle factors with T2DM cases among hypertension (227,966) and normotension (203,005) and their interaction in the UK Biobank. Low-risk lifestyle factors were defined as standard body mass index (BMI), drinking alcohol in moderation, nonsmoking, engaging in moderate- to vigorous-intensity physical activity, eating a high-quality diet, and maintaining a healthy sleep pattern. Results There were 12,403 incident T2DM cases during an average of 8.63 years of follow-up. Compared to those with 0 low-risk lifestyle factors, HRs for those with 5–6 were 0.14 (95% CI 0.10 to 0.19) for hypertensive participants, 0.13 (95% CI 0.08 to 0.19) for normotensive participants, respectively (ptrend < 0.001). 76.93% of hypertensive participants were considerably less likely to develop T2DM if they adhered to five healthy lifestyle practices, increased to 81.14% if they followed 6-factors (with a healthy sleep pattern). Compared with hypertension adults, normotensive people gain more benefits if they stick to six healthy lifestyles [Population attributable risk (PAR%) 83.66%, 95% CI 79.45 to 87.00%, p for interaction = 0.0011]. Conclusions Adherence to a healthy lifestyle pattern including a healthy sleep pattern is associated with lower risk of T2DM in hypertensives, and this benefit is even further in normotensives.

Cardiac injury is a common complication of the coronavirus disease 2019 (COVID-19), and is associated with adverse clinical outcomes. In this study, we aimed to reveal the association of cardiac injury with coagulation dysfunction. We enrolled 181 consecutive patients who were hospitalized with COVID-19, and studied the clinical characteristics and outcome of these patients. Cardiac biomarkers high-sensitivity troponin I (hs-cTnI), myohemoglobin and creatine kinase-myocardial band (CK-MB) were assessed in all patients. The clinical outcomes were defined as hospital discharge or death. The median age of the study cohort was 55 (IQR, 46–65) years, and 102 (56.4%) were males. Forty-two of the 181 patients (23.2%) had cardiac injury. Old age, high leukocyte count, and high levels of aspartate transaminase (AST), D-dimer and serum ferritin were significantly associated with cardiac injury. Multivariate regression analysis revealed old age and elevated D-dimer levels as being strong risk predictors of in-hospital mortality. Interleukin 6 (IL6) levels were comparable in patients with or without cardiac injury. Serial observations of coagulation parameters demonstrated highly synchronous alterations of D-dimer along with progression to cardiac injury. Cardiac injury is a common complication of COVID-19 and is an independent risk factor for in-hospital mortality. Old age, high leukocyte count, and high levels of AST, D-dimer and serum ferritin are significantly associated with cardiac injury, whereas IL6 are not. Therefore, the pathogenesis of cardiac injury in COVID-19 may be primarily due to coagulation dysfunction along with microvascular injury.