Secular Trends in Adherence to Healthy Behaviors Among US Adults with Diabetes, 1999-2018.

Adherence to healthy lifestyle is essential for diabetes management in light of the plateaued metabolic control, diversifying causes of death, and continued excess mortality among people with diabetes (PWD). This study aims to assess the secular trend of adherence to healthy behaviors among PWD in NHANES, a nationally representative survey of Americans using a stratified, multistage probability design in 2-year cycles since 1999. Adherence to healthy lifestyle was estimated using never smoking, moderate drinking, adequate physical activity, and healthy diet, and the score ranged 0-4. Among 7410 participants, adherence to healthy behaviors across time slightly increased from 1.4 (95% CI, 1.3 to 1.5) in 1999-2002 to 1.6 (1.5 to 1.8) in 2015-2018 (Ptrend = 0.002). The non-Hispanic Blacks caught up with the non-Hispanic Whites in overall lifestyle score (1.7 vs. 1.6 in 2015-2018), while large socioeconomic disparities remained in that participants with higher income and education level, and covered by health insurance were more likely to have adherence to healthy behaviors. As the metabolic control plateaued and causes of death have diversified among PWD, our findings suggested a great potential of lifestyle modification in facilitating the long-term health of these patients.

Cardiovascular risk burden, dementia risk and brain structural imaging markers: a study from UK Biobank.

Background: Cardiovascular risk burden is associated with dementia risk and neurodegeneration-related brain structure, while the role of genetics and incident cardiovascular disease (CVD) remains unclear. Aims: To examine the association of overall cardiovascular risk burden with the risk of major dementia subtypes and volumes of related brain regions in a large sample, and to explore the role of genetics and CVD onset. Methods: A prospective study among 354 654 participants free of CVD and dementia (2006-2010, mean age 56.4 years) was conducted within the UK Biobank, with brain magnetic resonance imaging (MRI) measurement available for 15 104 participants since 2014. CVD risk burden was evaluated by the Framingham General Cardiovascular Risk Score (FGCRS). Dementia diagnosis was ascertained from inpatient and death register data. Results: Over a median 12.0-year follow-up, 3998 all-cause dementia cases were identified. Higher FGCRS was associated with increased all-cause dementia risk after adjusting for demographic, major lifestyle, clinical factors and the polygenic risk score (PRS) of Alzheimer's disease. Comparing the high versus low tertile of FGCRS, the odds ratios (ORs) and 95% confidence intervals (CIs) were 1.26 (1.12 to 1.41) for all-cause dementia, 1.67 (1.33 to 2.09) for Alzheimer's disease and 1.53 (1.07 to 2.16) for vascular dementia (all ptrend<0.05). Incident stroke and coronary heart disease accounted for 14% (95% CI: 9% to 21%) of the association between FGCRS and all-cause dementia. Interactions were not detected for FGCRS and PRS on the risk of any dementia subtype. We observed an 83% (95% CI: 47% to 128%) higher all-cause dementia risk comparing the high-high versus low-low FGCRS-PRS category. For brain volumes, higher FGCRS was associated with greater log-transformed white matter hyperintensities, smaller cortical volume and smaller grey matter volume. Conclusions: Our findings suggest that the positive association of cardiovascular risk burden with dementia risk also applies to major dementia subtypes. The association of cardiovascular risk burden with all-cause dementia is largely independent of CVD onset and genetic predisposition to dementia.

Denture use and risk for cardiometabolic disease: observational and Mendelian randomization analyses.

AIMS: Denture use may potentially increase the risk of cardiometabolic diseases (CMDs), but the casual relevance and strength of the associations are currently unknown. METHODS AND RESULTS: A total of 495 938 participants from the UK Biobank were included in the observational analyses. Linkage disequilibrium score (LDSC) regression and Mendelian randomization analyses were employed to estimate genetic correlation and the associations between the genetic liability for denture use with coronary artery disease, myocardial infarction, heart failure (HF), any stroke (AS), ischaemic stroke, haemorrhagic stroke, type 2 diabetes (T2D), and related clinical risk factors. In observational analysis, denture use was associated with 14-25% higher risks of various CMDs. The LDSC analysis found that denture use showed a positive genetic correlation with CMDs (rg 0.21-0.38). Genetic liability for denture use was associated with an elevated risk of HF [odds ratio: 1.49 (1.20-1.83)] and T2D [1.11 (1.01-1.24)]. By integrating genetic summary data of denture use with the sum of decayed, missing, and filled tooth surfaces (DMFS), a clinical measure of dental caries obtained from an independent source, genetically determined denture use/DMFS was also associated with an elevated risk of AS [1.21 (1.04-1.40)]. Furthermore, genetically predicted denture use/DMFS was significantly associated with established cardiometabolic risk factors, including HDL cholesterol, triglycerides, waist circumference, waist-to-hip ratio, and height. CONCLUSION: Our study supported potential causal associations between the genetic liability for denture use and risks for HF, AS, T2D, and related clinical risk factors. These findings may inform prevention and intervention strategies targeting dental diseases and CMDs.

This study examined the association of denture use with cardiometabolic diseases (CMDs) and related clinical risk factors through Mendelian randomization analyses using data from UK Biobank and published consortia. Genetic liability for denture use was associated with an 11­49% higher risk of heart failure, stroke, and type 2 diabetes.The potential causal relationship between denture use and CMDs was further strengthened by the associations of denture use with HDL cholesterol, triglycerides, waist circumference, waist-to-hip ratio, and height, which are among the major risk factors of CMDs.

Family History of AD/Dementia, Polygenic Risk Score for AD, and Parkinson's Disease.

Background: Co-occurrence of Alzheimer's disease (AD) and Parkinson's disease (PD) has been observed. However, there is limited knowledge on how family history of AD is associated with PD. Objectives: To prospectively examine the associations of family history of AD/dementia and polygenic risk score for AD (AD-PRS) with PD risk. Methods: The study included 477,190 participants from UK Biobank who were free of PD at baseline (2006-2010) and had complete data on the studied exposure variables, family history of AD and AD-PRS. Cox proportional hazards model was used to examine the hazard ratios (HRs) and their 95% confidence intervals (CIs) of family history of AD/dementia and AD-PRS for PD risk. We also conducted mediation analysis to examine the proportion of the association between family history of AD/dementia and PD risk that could be mediated by AD-PRS. Results: During a median follow-up of 12.5 years, we identified 2550 incidences of PD. Family history of AD/dementia (adjusted HR = 1.21; 95% CI 1.09-1.35) and AD-PRS (adjusted HR = 1.10 per 1 unit increment; 95% CI 1.05-1.14) were associated with PD risk, after adjustment for age, sex, lifestyle factors, and other potential confounders. The association between family history of AD/dementia and PD risk was mediated by 13.1% by the AD-PRS. As expected, we observed significant associations of family history of AD/dementia and AD-PRS with risks of dementia and AD (P < 0.001 for all). Conclusions: Family history of AD/dementia appeared to be associated with PD risk, and this association could be mediated partially by AD-related genetic factors.

Sleep Duration and Risks of Incident Cardiovascular Disease and Mortality Among People With Type 2 Diabetes.

OBJECTIVE: People with type 2 diabetes may have insufficient or prolonged sleep that could accelerate cardiovascular disease (CVD) onset, but existing evidence from prospective studies has been limited. We examined the association of sleep duration with CVD incidence and mortality in this high-risk population. RESEARCH DESIGN AND METHODS: This prospective study included 18,876 participants with type 2 diabetes in the UK Biobank who were free of CVD and cancer at baseline. Habitual sleep duration was obtained using a baseline questionnaire. Cox proportional hazards regression models were used to examine the association between sleep duration and CVD events. RESULTS: During an average follow-up of 11.0-12.0 years, we documented 2,570 incident cases of atherosclerotic cardiovascular disease (ASCVD) and 598 CVD deaths. Compared with sleeping for 7 h/day, the multivariable-adjusted hazard ratios of ≤5 and ≥10 h/day were 1.26 (95% CI 1.08, 1.48) and 1.41 (1.16, 1.70) for incident ASCVD, 1.22 (0.99, 1.50) and 1.16 (0.88, 1.52) for coronary artery disease, 1.70 (1.23, 2.35) and 2.08 (1.44, 3.01) for ischemic stroke, 1.02 (0.72, 1.44) and 1.45 (1.01, 2.10) for peripheral artery disease, and 1.42 (1.02, 1.97) and 1.85 (1.30, 2.64) for CVD mortality. Similar results were observed in most sensitivity analyses that aimed to address potential reverse causation and in the joint analyses of sleep duration and metabolic control or diabetes severity status. CONCLUSIONS: Short and long sleep durations were independently associated with increased risks of CVD onset and death among people with type 2 diabetes.

Association of a Healthy Lifestyle With All-Cause and Cause-Specific Mortality Among Individuals With Type 2 Diabetes: A Prospective Study in UK Biobank.

OBJECTIVE: To evaluate the association of a healthy lifestyle, involving seven low-risk factors mentioned in diabetes management guidelines (no current smoking, moderate alcohol consumption, regular physical activity, healthy diet, less sedentary behavior, adequate sleep duration, and appropriate social connection), with all-cause and cause-specific mortality among individuals with type 2 diabetes. RESEARCH DESIGN AND METHODS: This study included 13,366 participants with baseline type 2 diabetes from the UK Biobank free of cardiovascular disease (CVD) and cancer. Lifestyle information was collected through a baseline questionnaire. RESULTS: During a median follow-up of 11.7 years, 1,561 deaths were documented, with 625 from cancer, 370 from CVD, 115 from respiratory disease, 81 from digestive disease, and 74 from neurodegenerative disease. In multivariate-adjusted model, each lifestyle factor was significantly associated with all-cause mortality, and hazard ratios associated with the lifestyle score (scoring 6-7 vs. 0-2 unless specified) were 0.42 (95% CI 0.34, 0.52) for all-cause mortality, 0.57 (0.41, 0.80) for cancer mortality, 0.35 (0.22, 0.56) for CVD mortality, 0.26 (0.10, 0.63) for respiratory mortality, and 0.28 (0.14, 0.53) for digestive mortality (scoring 5-7 vs. 0-2). In the population-attributable risk analysis, 29.4% (95% CI 17.9%, 40.9%) of deaths were attributable to a poor lifestyle (scoring 0-5). The association between a healthy lifestyle and all-cause mortality was consistent, irrespective of factors reflecting diabetes severity (diabetes duration, glycemic control, diabetes-related microvascular disease, and diabetes medication). CONCLUSIONS: A healthy lifestyle was associated with a lower risk of all-cause mortality and mortality due to CVD, cancer, respiratory disease, and digestive disease among individuals with type 2 diabetes.

Association between Tea Consumption and Hypertension Risk among Middle-Aged and Older Chinese Adults.

BACKGROUND: Current evidence on tea consumption and hypertension is inconclusive, and prospective studies among habitual tea drinkers remain limited. OBJECTIVE: We investigated the associations of habitual tea consumption with hypertension risk and longitudinal blood pressure changes in 2 large cohorts. METHODS: This study included participants aged 40-75 y from the Shanghai Women's Health Study (n = 31,351) and the Shanghai Men's Health Study (n = 28,342), without hypertension, diabetes, cardiovascular disease, or cancer at baseline. Information on tea consumption was assessed during in-person interviews at enrollment and follow-up visits. Incident hypertension was identified by self-reported diagnosis, medication use, or blood pressure measurements. RESULTS: Current tea drinkers had a 7% higher risk than the non-current tea drinker group [HRs (95% CIs): women, 1.07 (1.01, 1.14); men, 1.07 (1.02, 1.12)]. The amount of tea drinking showed significant dose-response associations with hypertension: compared with the non-current group, HRs (95% CIs) for women and men were 1.01 (0.90, 1.14) and 1.02 (0.96, 1.08) for low (women/men: <100/200 g/mo), 1.07 (1.01, 1.15) and 1.05 (0.99, 1.12) for medium (women/men: 100-250/200-250 g/mo), and 1.18 (1.01, 1.39) and 1.10 (1.03, 1.17) for the high-amount group (women/men: >250 g/mo). Among participants without hypertension, compared with non-current tea drinkers, least-squares means of 3-y changes in blood pressure were 0.3-0.4 mm Hg higher for women and men as current drinkers and 0.7-0.9 mm Hg higher for men in the high-consumption group. Compared with those who never drank tea, women who drank tea consistently had 0.5 (0.2, 0.7) mm Hg higher diastolic blood pressure (DBP), whereas men had 0.5 (0.04, 0.9) mm Hg higher systolic blood pressure and 0.3 (0.04, 0.6) mm Hg higher DBP, respectively. CONCLUSIONS: Our findings suggest that habitual tea drinking is associated with a slightly higher risk of hypertension and a minor increase in blood pressure among middle-aged and older Chinese adults, which warrants confirmation by long-term intervention studies.

MRG15 orchestrates rhythmic epigenomic remodelling and controls hepatic lipid metabolism.

The rhythmic regulation of transcriptional processes is intimately linked to lipid homeostasis, to anticipate daily changes in energy access. The Rev-erbα-HDAC3 complex was previously discovered to execute the rhythmic repression of lipid genes; however, the epigenetic switch that turns on these genes is less clear. Here, we show that genomic recruitment of MRG15, which is encoded by the mortality factor on chromosome 4 (MORF4)-related gene on chromosome 15, displays a significant diurnal rhythm and activates lipid genes in the mouse liver. RNA polymerase II (Pol II) recruitment and histone acetylation correspond to MRG15 binding, and the rhythm is impaired upon MRG15 depletion, establishing MRG15 as a key modulator in global rhythmic transcriptional regulation. MRG15 interacts with the nuclear receptor LRH-1, rather than with known core clock proteins, and is recruited to genomic loci near lipid genes via LRH-1. Blocking of MRG15 by CRISPR targeting or by the FDA-approved drug argatroban, which is an antagonist to MRG15, attenuates liver steatosis. This work highlights MRG15 as a targetable master regulator in the rhythmic regulation of hepatic lipid metabolism.

[Evolution and transition of source of Patrinia Herba and Patrinia Radix].

Both Patrinia Herba and Patrinia Radix are traditional Chinese herbal medicines. The herbal source and medicinal part of them are confusing in the herbal medicine market of China. To explore the evolution and transition of the herbal source and medicinal part of Patrinia Herba and Patrinia Radix, this paper systematically summarizes the record of the herbal source and medicinal part of them in ancient classics of herbal medicine in China. According to the findings, before Ming Dynasty, Patrinia Herba originated from the radix of the plants with yellow flowers of Patrinia. In Ming and Qing Dynasty, Patrinia Herba originates from the whole plant (including the radix)of the plant with white flowers of Patrinia. In Ming Dynasty, Patrinia Radix, stemming from the radix of the plants with yellow flowers of Patrinia, started to be used as a traditional Chinese herbal medicine, which had the same herbal source with that of Patrinia Herba before Ming Dynasty. Therefore, Patrinia Herba and Patrinia Radix can be seen as the same traditional Chinese herbal medicine, and the genuine of Patrinia Herba should be the radix and the whole herba of P. scabiosaefolia and P. heterophylla.