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Abstract The connection between triglyceride-rich lipoproteins and cardiometabolic multimorbidity, characterized by the concurrence of at least two of type 2 diabetes, ischemic heart disease, and stroke, has not been definitively established. We aim to examine the prospective associations between serum remnant cholesterol, triglycerides, and the risks of progression from first cardiometabolic disease to multimorbidity via multistate modeling in the UK Biobank. We also evaluate the causality of these associations via Mendelian randomization using 13 biologically relevant SNPs as the genetic instruments. Here we show that elevated remnant cholesterol and triglycerides are significantly associated with gradually higher risks of cardiometabolic multimorbidity, particularly the progression of ischemic heart disease to the multimorbidity of ischemic heart disease and type 2 diabetes. These results advocate for effective management of remnant cholesterol and triglycerides as a potential strategy in mitigating the risks of cardiometabolic multimorbidity.

Abstract 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.

Abstract Previous studies have shown certain exposure factors (such as lifestyle and metabolism) are associated with colorectal cancer (CRC) events. However, the application of the exposome theoretical frame and the extent to which the exposome domain can modulate the risk of CRC remain unknown. Our study aimed to construct valid exposome measurements and examine the relationship between exposome counts and the risk of CRC. This study included 335,370 individuals in the UK Biobank. We used exploratory factor analysis to identify a valid construct of exposome factors. We then summed the exposome counts within each domain. Cox proportional hazard models were used to estimate the hazard ratios and 95% confidence intervals of CRC risk related to the exposome factors and counts. During an 8.69 year median follow-up, 10,702 CRC cases were identified. Five domains were extracted from 12 variables, including ecosystem, lifestyle, tobacco and alcohol use, social economics, and social support. The Cox model results showed that the ecosystem was positively related to the reduced CRC risk (HR = 0.970; 95% CI 0.952–0.989). Similar results were also found among the domains of healthy lifestyles (HR = 0. 889; 95% CI 0.871–0.907), and no tobacco and alcohol use (HR = 0.892; 95% CI 0.876–0.909). The disadvantageous social economic (HR = 1.081; 95% CI 1.058–1.105) and insufficient social support domains (HR = 1.036; 95% CI 1.017–1.056) were associated with an increased risk of CRC. Similar risk trends were also observed across the exposome count groups with CRC incidence. Our findings suggest that certain exposure domains are related to the incidence of CRC. Ecosystem, lifestyle, and social factors can be incorporated into prediction models to identify individuals at high risk of CRC.

Abstract Researchers have identified an association between lifestyle factors and colorectal cancer (CRC) risk. This study examined the relationship between sleep patterns and CRC events. 392,252 individuals were sampled from the UK Biobank. Chronotype, sleep duration, insomnia, snoring, and excessive daytime sleepiness were combined to measure a healthy sleep score. A number of healthy sleep factors were defined, along with factors for healthy lifestyle scores. Using Cox proportional hazards regression, computed hazard ratios (HRs) were used to examine the associations between sleep patterns, healthy lifestyles, and the incidence of CRC. Healthy sleep scores were inversely associated with CRC events. The HRs for CRC were 0.90 (95% CI, 0.88–0.92) and 0.95 (95% CI, 0.92–0.98) for a 1-point healthy sleep score increase among males and females. When analyzing sleep components, sleeping 7–8 h/day, no frequent insomnia, no snoring, and no frequent daytime sleepiness were independently associated with a 9%, 14%, 8%, and 14% lower risk of CRC, respectively, whilst healthy lifestyle scores were inversely associated with CRC incidence across all models. Sleep pattern and lifestyle are significantly correlated with CRC risk. The healthier the subject’s lifestyle and sleep pattern, the lower their CRC risk.

Abstract 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.