Association of healthy lifestyle factors and genetic liability with bipolar disorder: Findings from the UK Biobank.

BACKGROUND: The interplay between genetic and lifestyle factors in the development of bipolar disorder (BD) remains unclear. METHODS: A cohort study was carried out on 365,517 participants from the UK Biobank. Lifestyle scores, based on smoking, physical activity, diet, alcohol consumption, sedentary behavior, sleep duration, and social contact, were grouped as favorable (scores 6-7), intermediate (scores 4-5), or unfavorable (scores 0-3). The BD polygenic risk score (PRS) was also categorized into high, intermediate, and low-risk groups using PRS tertiles. Cox regression models determined hazard ratios (HRs) and 95 % confidence intervals (CIs) for BD. RESULTS: During the 12.9-year follow-up, 529 individuals developed BD. Comparing those with favorable lifestyles to those with unfavorable participants, the HR of developing BD was 3.28 (95 % CI, 2.76-3.89). Similarly, individuals with a high PRS had a risk of 3.20 (95 % CI, 2.83-3.63) compared to those with a low PRS. Notably, individuals with both a high PRS and an unfavorable lifestyle had a significantly higher risk of BD (HR = 6.31, 95 % CI, 4.14-9.63) compared to those with a low PRS and a favorable lifestyle. Additionally, the interaction between PRS and lifestyle contributed an additional risk, with a relative excess risk of 1.74 (95 % CI, 0.40-3.07) and an attributable proportion due to the interaction of 0.37 (95 % CI, 0.16-0.58). CONCLUSIONS: Our findings suggest that genetic liability for BD, measured as PRS, and lifestyle have an additive effect on the risk of developing BD. A favorable lifestyle was associated with a reduced risk of developing BD.

Dietary intake of potassium, vitamin E, and vitamin C emerges as the most significant predictors of cardiovascular disease risk in adults.

Prediction models were developed to assess the risk of cardiovascular disease (CVD) based on micronutrient intake, utilizing data from 90,167 UK Biobank participants. Four machine learning models were employed to predict CVD risk, with performance evaluation metrics including area under the receiver operating characteristic curve (AUC), accuracy, recall, specificity, and F1-score. The eXtreme Gradient Boosting (XGBoost) model was utilized to rank the importance of 11 micronutrients in cardiovascular health. Results indicated that vitamin E, calcium, vitamin C, and potassium intake were associated with a reduced risk of CVD. The XGBoost model demonstrated the highest performance with an AUC of 0.952, highlighting potassium, vitamin E, and vitamin C as key predictors of CVD risk. Subgroup analysis revealed a stronger correlation between calcium intake and CVD risk in older adults and those with higher BMI, while vitamin B6 intake showed a link to CVD risk in women. Overall, the XGBoost model emphasized the significance of potassium, vitamin E, and vitamin C intake as primary predictors of CVD risk in adults, with age, sex, and BMI potentially influencing the importance of micronutrient intake in predicting CVD risk.

miR-141-3p attenuates inflammation and oxidative stress-induced pulmonary fibrosis in ARDS via the Keap1/Nrf2/ARE signaling pathway.

The present research aimed to investigate the effects and mechanisms of microRNA (miR)-141-3p on pulmonary fibrosis of acute respiratory distress syndrome (ARDS). A rat ARDS model was established by the intratracheal drip of 10 mg/kg lipopolysaccharide (LPS). miR-141-3p and Kelch-like ECH-associated protein 1 (Keap1) expression was detected using RT-qPCR assay. Inflammatory factors in bronchoalveolar lavage fluid (BALF) and lung tissues were measured with enzyme-linked immunosorbent assay (ELISA). Lung fibrosis was evaluated using Masson's trichrome staining and hydroxyproline assay kits. Tissue oxidative stress marker levels were assessed by a commercial kit. Protein variations in the EMT pathway and Keap1/nuclear factor-erythroid 2-related factor 2 (Nrf2)/antioxidant response element (ARE) pathway were investigated by Western blot analysis. Targeting relationship verified by dual-luciferase reporter assay. The expression of miR-141-3p was significantly upregulated in LPS-induced ARDS rats, while Keap1 was downregulated. Overexpression of miR-141-3p decreased the levels of tumor necrosis factor (TNF)-α, interleukin (IL)-1ß, IL-6, superoxide dismutase (SOD), and glutathione (GSH) while elevating malondialdehyde (MDA) expression in LPS-induced ARDS rats. Elevation of miR-141-3p reduced fibrosis scores, enhanced E-cadherin protein expression, and decreased vimentin and α-SMA protein expression in LPS-induced ARDS rats. This elevation of miR-141-3p also upregulated Nrf2, heme oxygenase-1 (HO-1), and NAD(P)H:quinone oxido-reductase-1 (NQO1) proteins levels. Moreover, Keap1 overexpression reversed the inhibitory effects of miR-141-3p on LPS-triggered inflammation, oxidative stress, and fibrosis. miR-141-3p may attenuate inflammation and oxidative stress-induced pulmonary fibrosis in ARDS via the Keap1/Nrf2/ARE signaling pathway. Our study provides new ideas for the treatment of ARDS.

Social contacts patterns relevant to the transmission of infectious diseases in Suzhou, China following the COVID-19 epidemic.

BACKGROUND: The COVID-19 pandemic has profoundly affected human social contact patterns, but there is limited understanding regarding the post-pandemic social contact patterns. Our objective is to quantitatively assess social contact patterns in Suzhou post-COVID-19. METHODS: We employed a diary design and conducted social contact surveys from June to October 2023, utilizing paper questionnaires. A generalized linear model was utilized to analyze the relationship between individual contacts and covariates. We examined the proportions of contact type, location, duration, and frequency. Additionally, age-related mixed matrices were established. RESULTS: The participants reported an average of 11.51 (SD 5.96) contact numbers and a total of 19.78 (SD 20.94) contact numbers per day, respectively. The number of contacts was significantly associated with age, household size, and the type of week. Compared to the 0-9 age group, those in the 10-19 age group reported a higher number of contacts (IRR = 1.12, CI: 1.01-1.24), while participants aged 20 and older reported fewer (IRR range: 0.54-0.67). Larger households (5 or more) reported more contacts (IRR = 1.09, CI: 1.01-1.18) and fewer contacts were reported on weekends (IRR = 0.95, CI: 0.90-0.99). School had the highest proportion of contact durations exceeding 4 h (49.5%) and daily frequencies (90.4%), followed by home and workplace. The contact patterns exhibited clear age-assortative mixing, with Q indices of 0.27 and 0.28. CONCLUSIONS: We assessed the characteristics of social contact patterns in Suzhou, which are essential for parameterizing models of infectious disease transmission. The high frequency and intensity of contacts among school-aged children should be given special attention, making school intervention policies a crucial component in controlling infectious disease transmission.

A machine learning algorithm based on circulating metabolic biomarkers offers improved predictions of neurological diseases.

BACKGROUND AND AIMS: A machine learning algorithm based on circulating metabolic biomarkers for the predictions of neurological diseases (NLDs) is lacking. To develop a machine learning algorithm to compare the performance of a metabolic biomarker-based model with that of a clinical model based on conventional risk factors for predicting three NLDs: dementia, Parkinson's disease (PD), and Alzheimer's disease (AD). MATERIALS AND METHODS: The eXtreme Gradient Boosting (XGBoost) algorithm was used to construct a metabolic biomarker-based model (metabolic model), a clinical risk factor-based model (clinical model), and a combined model for the prediction of the three NLDs. Risk discrimination (c-statistic), net reclassification improvement (NRI) index, and integrated discrimination improvement (IDI) index values were determined for each model. RESULTS: The results indicate that incorporation of metabolic biomarkers into the clinical model afforded a model with improved performance in the prediction of dementia, AD, and PD, as demonstrated by NRI values of 0.159 (0.039-0.279), 0.113 (0.005-0.176), and 0.201 (-0.021-0.423), respectively; and IDI values of 0.098 (0.073-0.122), 0.070 (0.049-0.090), and 0.085 (0.068-0.101), respectively. CONCLUSION: The performance of the model based on circulating NMR spectroscopy-detected metabolic biomarkers was better than that of the clinical model in the prediction of dementia, AD, and PD.

Dietary protein sources, genetics, and cardiovascular disease incidence.

BACKGROUND: To explore the potential correlation between the amount and source of dietary protein and cardiovascular disease (CVD), as well as the potential impact of genetic susceptibility on these connections. METHODS: We performed a prospective analysis of 98,224 participants from the UK. We measured dietary protein intake using two 24-hour dietary recall interviews. To analyze the data, we used multivariable-adjusted Cox regression models and restricted cubic spline models. Additionally, we calculated weighted genetic risk scores. RESULTS: A total of 8818 new cases of CVD were documented, which included 4076 cases of coronary artery disease (CAD) and 1126 cases of stroke. The study found a J-shaped association (p nonlinearity = 0.005) between CVD risk and the percentage of energy obtained from consuming plant protein. Higher intake of plant protein and whole protein was associated with a decreased risk of CVD. On the other hand, larger intakes of animal protein was linked to a higher occurrence of CAD. Additionally, increased intake of plant protein was also linked to a lower incidence of stroke. Replacing 5 % of animal protein-based energy intake with plant protein-based energy intake resulted in a 5 % decrease in CVD risk. LIMITATIONS: There remains an effect of residual confounders. CONCLUSION: The consumption of larger amounts of plant protein, whole protein, and nut protein was found to be associated with a lower risk of CVD events. Conversely, higher intakes of animal protein was associated with an increased risk of CAD events. Furthermore, replacing 5 % of energy intake from animal protein with energy intake from plant protein was found to reduce the risk of CVD by 5 %.

Visceral adiposity associated with incidence and development trajectory of cardiometabolic diseases: A prospective cohort study.

BACKGROUND AND AIMS: There is a lack of literature concerning the effects of visceral adipose on the development of first cardiometabolic disease (FCMD) and its subsequent progression to cardiometabolic multimorbidity (CMM) and mortality. METHODS AND RESULTS: 423,934 participants from the UK Biobank with different baseline disease conditions were included in the analysis. CMM was defined as the simultaneous presence of coronary heart disease, T2D, and stroke. Visceral adiposity was estimated by calculating the visceral adiposity index (VAI). Multistate models were used to assess the effect of visceral adiposity on the development of CMM. During a median follow-up of 13.5 years, 50,589 patients had at least one CMD, 6131 were diagnosed with CMM, whereas 24,634 patients died. We observed distinct roles of VAI with respect to different disease transitions of CMM. HRs (95 % CIs) of high VAI were 2.35 (2.29-2.42) and 1.64 (1.50-1.79) for transitions from healthy to FCMD and from FCMD to CMM, and 0.97 (0.93-1.02) for all-cause mortality risk from healthy, FCMD and CMM, respectively. CONCLUSIONS: Our study provides the first evidence that visceral adipose may contribute to the development of FCMD and CMM in healthy participants. However, visceral adipose may confer resistance to all-cause mortality in participants with existing CMD or CMM. A better understanding of the relationship between visceral adipose and CMM can focalize further investigations on patients with CMD with high levels of visceral fat and help take targeted preventive measures to reduce the medical burden on individual patients and society.

Association of long-term exposure to various ambient air pollutants, lifestyle, and genetic predisposition with incident cognitive impairment and dementia.

BACKGROUND: Long-term exposure to air pollution has been found to contribute to the development of cognitive decline. Our study aimed to assess the association between various air pollutants and cognitive impairment and dementia. Additionally, explore the modification effects of lifestyle and genetic predisposition. METHODS: The exposure levels to various air pollutants, including particulate matter (PM) with diameters ≤ 2.5 (PM2.5), ≤ 10 (PM10), and between 2.5 and 10 µm (PM2.5-10) and nitrogen oxides (NO and NO2) were identified. An air pollution score (APS) was calculated to evaluate the combined exposure to these five air pollutants. A genetic risk estimate and healthy lifestyle score (HLS) were also generated. The Cox regression model adjusted by potential confounders was adopted to access the association between pollution exposure and cognitive decline, and several sensitivity analyses were additionally conducted to test the robustness. RESULTS: The combined exposure to air pollutants was associated with an increased risk of incident cognitive decline. Compared with the low exposure group, the hazard ratio (HR) and 95% confidence interval (CI) for all-cause dementia, Alzheimer's dementia, vascular dementia, and mild cognitive impairment (MCI) in those exposed to the highest levels of air pollutants were respectively 1.07 (95% CI: 1.04 to 1.09), 1.08 (95% CI: 1.04 to 1.12), 1.07 (95% CI: 1.02 to 1.13), and 1.19 (95% CI: 1.12 to 1.27). However, the modification effects from genetic predisposition were not widely observed, while on the contrary for the healthy lifestyle. Our findings were proven to be reliable and robust based on the results of sensitivity analyses. CONCLUSIONS: Exposure to air pollution was found to be a significant contributing factor to cognitive impairment and dementia, and this association was not easily modified by an individual's genetic predisposition. However, adopting a healthy lifestyle may help to manage the risk of cognitive decline related to air pollution.

Diagnostic and Predictive Significance of Serum MiR-141-3p in Acute Respiratory Distress Syndrome Patients with Pulmonary Fibrosis.

Pulmonary fibrosis (PF) is the major complication and death-related factor of acute respiratory distress syndrome (ARDS). This study evaluated the significance of miR-141-3p in ARDS and its complication of PF aiming to identify a potential biomarker for screening ARDS and predicting the occurrence of PF. A total of 137 ARDS patients and 69 healthy individuals were enrolled in this study and the serum samples were collected from all participants. The serum miR-141-3p levels were analyzed by polymerase chain reaction. The significance of miR-141-3p in the diagnosis and development of ARDS, and the occurrence of PF was evaluated by receiver operating curve, Chi-square test, and logistic regression analysis. MiR-141-3p was downregulated in ARDS patients and showed significant potential in its diagnosis. Reduced miR-141-3p was significantly associated with the increasing Murray and APACHEII score and the occurrence of PF in ARDS patients. MiR-141-3p, Murray score, and APACHEII score were identified as risk factors for the occurrence of PF in ARDS, and miR-141-3p was also found to be downregulated in ARDS patients with PF. Additionally, miR-141-3p could discriminate ARDS patients with PF and without PF, and was closely associated with the decreased total lung capacity, carbon monoxide diffusing capacity, and forced vital capacity of ARDS patients with PF. Downregulated miR-141-3p served as a biomarker for ARDS screening disease onset and indicating the severity. Reduced miR-141-3p was also identified as a risk factor for PF in ARDS patients and was associated with the severe progression of PF.

Association of spontaneous abortion with bipolar disorder and major depression based on inverse probability treatment weighting of multigroup propensity scores: Evidence from the UK Biobank.

BACKGROUND: Few studies have explored the association between the number of SAs and bipolar disorder and major depression (BDMD). This study aims to investigate the association between SA and BDMD, and the possible dose-response relationship between them. METHODS: We conducted a cross-sectional study of 13,200 female UK Biobank participants. Participants were classified into BDMD and no-BDMD groups based on their BDMD status. The number of SAs was grouped into non-SA, occasional SA (OSA), and recurrent SA (RSA). Baseline characteristics of the three groups were balanced using inverse probability treatment weighting (IPTW) based on propensity scores. The three-knots restricted cubic spline regression model was utilized to assess the dose-response relationship between the number of SAs and BDMD. RESULTS: The IPTW-adjusted multivariate logistic regression revealed that SA was an independent risk factor for BDMD, with adjusted OR of 1.12 (95 % CI: 1.07-1.19) and 1.32 (95 % CI: 1.25-1.40) in the OSA and RSA groups, respectively. The strength of this association amplified as the number of SAs (P for trend <0.001). There was a nonlinear relationship between the number of SAs and the risk of BDMD, with an approximately inverted L-shaped curve. LIMITATIONS: The information of the SA and BDMD status relied on self-reported by volunteers, and the study sample was mostly of European descent. CONCLUSIONS: Women who reported experiencing multiple SAs are more likely to have BDMD. Therefore, it is imperative to provide psychological care and interventions for women in the postpartum period.

No causal association between plasma cystatin C and cardiovascular diseases: Mendelian randomization analyses in UK biobank.

Background: We aimed to determine whether the plasma cystatin C is a causal risk factor for cardiovascular events, stroke, myocardial infarction (MI), and cardiovascular disease (CVD) mortality by conducting Mendelian randomization (MR) designs. Methods: Our study included 277,057 individuals free of CVDs or cancer at baseline in the UK Biobank. The genetic scores of plasma cystatin C comprising 67 single-nucleotide polymorphisms were calculated on the basis of data from a large genome-wide association study. By stratifying the genetic score, we conducted cox regression to assess the relationship between plasma cystatin C and CVDs. In this study, linear MR analysis was used to estimate the causal association between plasma cystatin C and CVDs. Results: Observational analyses showed that plasma cystatin C concentrations were associated with the risk of CVDs [hazard ratios (HR) per standard deviation (SD) 1.09, 95% confidence interval (CI); 1.07-1.10] and CVD mortality (1.14, 1.11-1.17). Among CVDs, plasma cystatin C were associated with stroke (1.10, 1.08-1.11) and MI (1.08, 1.07-1.10). Linear MR analysis did not provide evidence of a causal association between plasma cystatin C and the risk of CVDs [odds ratio (OR) per SD 0.96, 95% CI;0.90-1.03], stroke (0.96, 0.93-1.01), MI (0.97, 0.91-1.03), and CVD mortality (0.98, 0.96-1.01), with consistent estimates from sensitivity analyses. Conclusion: Observational findings indicated that higher plasma cystatin C is associated with a higher risk of CVDs; According to MR studies, there is no causal association between plasma cystatin C and the risk of CVDs and CVD mortality.

Feasibility Analysis of Polyurethane-Prepolymer-Modified Bitumen Used for Fully Reclaimed Asphalt Pavement (FRAP).

Asphalt pavement recycling technology with high reclaimed asphalt pavement (RAP) content has always been limited by unsatisfactory pavement performance and the rising cost of pavement materials. To address these challenges, polyurethane-prepolymer-modified bitumen (PPB) was proposed to be utilized as the asphalt binder of fully reclaimed asphalt pavement (FRAP) in this study. The proper formula of the PPB binder was determined based on a range of tests. The rheological behavior and tensile properties of the PPB binder were then investigated, and the economic cost of materials was discussed as well. Results revealed that the PPB system can be obtained through chemical synthesis using readily available raw materials. The reaction of polyurethane prepolymer and chain extender provides PPB with significant improvement in temperature susceptibility, rutting resistance, and tensile properties. It is also demonstrated in this study that the PPB mixture containing 100% RAP, on the whole, takes advantage of cost-saving especially compared to the epoxy asphalt mixture. Therefore, the PPB binder exhibits a favorable application prospect in FRAP.

Higher dietary intake of aromatic amino acids was associated with lower risk of cardiovascular disease mortality in adult participants in NHANES III.

Little is known about the associations between dietary aromatic amino acids (AAAs) intake and mortality from all causes and cardiovascular disease (CVD). Accordingly, we evaluated these associations in the adult population of the United States using data from the Third National Health and Nutrition Examination Survey. This was a cohort study. Dietary intake of AAAs (tyrosine, phenylalanine, and tryptophan) was determined from the total nutrient intake document. We hypothesized that higher dietary AAA intake would lower all-cause and CVD mortality in adults in the United States. First, we categorized participants into quintiles based on their dietary intakes of total AAAs, tyrosine, phenylalanine, and tryptophan. Then, we established 4 Cox proportional-hazards models (models 1-4) and calculated hazard ratios and 95% confidence intervals to estimate the associations between dietary intakes of total AAAs, tyrosine, phenylalanine, and tryptophan and all-cause and CVD mortality. Mortality status was primarily obtained from files linked to the National Death Index records up to December 31, 2015. After multivariate adjustment, the hazard ratios (95% confidence intervals) of CVD mortality in the highest quintiles of dietary total AAAs, tyrosine, phenylalanine, and tryptophan intake (reference: the lowest quintiles) were 0.66 (0.52-0.84), 0.65 (0.51-0.83), 0.66 (0.52-0.85) and 0.64 (0.50-0.82), respectively. In a nationally representative cohort, higher dietary intakes of total AAA and the 3 individual AAAs were independently associated with a lower risk of CVD mortality, and these associations were stronger in non-Hispanic White people than in other people.

Associations of dietary folate, vitamin B6 and B12 intake with cardiovascular outcomes in 115664 participants: a large UK population-based cohort.

BACKGROUND/OBJECTIVES: The evidence of relationship between dietary intake of folate, vitamin B6 and vitamin B12 and cardiovascular diseases (CVD) in UK populations is limited. We aimed to analyze the association of dietary intake of folate, vitamin B6, and vitamin B12 with CVD events [stroke, myocardial infarction (MI)] and CVD mortality. METHODS: We included 115,664 participants, aged 40-70 years, with no CVD events or cancer at baseline, enrolled between 2006 and 2010 and followed up to the end of 2018. Dietary intake was measured with an online 24-h dietary assessment. Multivariable Cox proportional hazards models were used to estimate hazard ratios (HR) and 95% confidence intervals (CI) for the associations. RESULTS: After multivariate adjustment, higher dietary folate intake was inversely associated with CVDs with hazard ratios of 0.99, 0.92, and 0.88 in groups 2-4 compared with group 1 (the lowest group); inversely associated with stroke with hazard ratios of 0.94, 0.90, and 0.86 groups 2-4 compared to group 1 (lowest group); inversely associated with MI with hazard ratios of 1.01, 0.90 and 0.86 groups 2-4 compared to group 1 (lowest group); inversely associated with CVD mortality with hazard ratios of 0.95, 0.80 and 0.74 Groups 2-4 compared to group 1 (lowest group). Each tablespoon/day higher intake of raw vegetable intake, pieces/day higher intake of fresh fruit intake bowls/week higher intake of cereal intake, and g/day higher intake of dietary fiber were associated with higher intakes of folate every 0.02,0.06,0.05, and 0.08 SD, respectively. E-value analysis suggested robustness to unmeasured confounding. CONCLUSIONS: Each increase in folate intakes was related to 5% lower risks of total CVD events and 10% lower risks of CVD mortality. Our findings support that strengthening dietary folate intake as a primary prevention strategy for CVD events and CVD mortality.

Corrigendum: No causal association between plasma cystatin C and cardiovascular diseases: Mendelian randomization analyses in UK biobank.

[This corrects the article DOI: 10.3389/fmed.2023.1191675.].

Association between dyslipidaemia and the risk of hyperuricaemia: a six-year longitudinal cohort study of elderly individuals in China.

BACKGROUND: Despite abundant evidence linking dyslipidaemia to an increased risk of hyperuricaemia, the exact association between each component of dyslipidaemia and hyperuricaemia remains controversial. Thus, the objective of this research was to examine the correlation between dyslipidaemia and its components, as well as hyperuricaemia in Chinese people over the age of 60. METHODS: In this study, 4018 participants over 60 years without hyperuricaemia were investigated from 2014 to 2020. The association between each dyslipidaemia component and hyperuricaemia was evaluated employing Cox proportional hazards models. This research conducted further stratified and sensitivity analyses to assess the potential relationship. RESULTS: A total of 1155 participants suffered from hyperuricaemia (28.75%) at the time of the 6-year follow-up survey. In multivariable-adjusted analyses, compared to participants with normal lipid levels, those with dyslipidaemia had 1.28 times the risk (95% confidence interval 1.12 to 1.47) of experiencing hyperuricaemia. The hazard ratios (HR) (95% CI) comparing high TC, high TG, high LDL-C, and low HDL-C of dyslipidaemia with the regular group were 0.99 (0.72 to 1.37), 1.30 (1.07 to 1.57), 1.02 (0.70 to 1.50), and 1.20 (1.00 to 1.44), respectively. There was a nonlinear dose-response between TG, HDL-C, and serum uric acid (SUA). CONCLUSIONS: Dyslipidaemia and its two distinct types, high TG and low HDL-C, increased hyperuricaemia incidence in this prospective cohort. Further research should be undertaken to investigate the possible reverse causality between different components of dyslipidaemia and hyperuricaemia.

Association between the visceral adiposity index and risks of all-cause and cause-specific mortalities in a large cohort: Findings from the UK biobank.

BACKGROUND AND AIMS: The visceral adiposity index (VAI) has been recently established as a measure of visceral fat distribution and is shown to be associated with a wide range of adverse health events. However, the precise associations between the VAI score and all-cause and cause-specific mortalities in the general population remain undetermined. METHODS AND RESULTS: In this large-scale prospective epidemiological study, 357,457 participants (aged 38-73 years) were selected from the UK Biobank. We used Cox competing risk regression models to estimate the association between the VAI score and all-cause, cardiovascular disease (CVD), cancer, and other mortalities. The VAI score was significantly correlated with an increased risk of all-cause mortality (hazard ratio [HR], 1.200; 95% confidence interval [CI], 1.148-1.255; P < 0.0001), cancer mortality (HR, 1.224; 95% CI, 1.150-1.303; P < 0.0001), CVD mortality (HR, 1.459; 95% CI, 1.148-1.255; P < 0.0001), and other mortalities (HR, 1.200; 95% CI, 1.148-1.255; P < 0.0001) after adjusting for a series of confounders. In addition, the subgroup analyses showed that HRs were significantly higher in participants who were male, aged below 65 years, and body mass index less than 25. CONCLUSION: In summary, VAI was positively associated with an increased risk of all-cause and cause-specific mortalities in a nationwide, well-characterised population identified in a UK Biobank. The VAI score might be a complementary traditional predictive indicator for evaluating the risk of adverse health events in the population of Western adults aged 38 years and older.

Associations of Serum Biomarkers of Fruit and Vegetable Intake With the Risk of Cause-Specific Mortality and All-Cause Mortality: A National Prospective Cohort Study.

Objective: The purpose of this study was to evaluate the associations of serum biomarkers of fruit and vegetable intake (vitamin C and carotenoids) with cause-specific mortality and all-cause mortality in a nationally representative sample of US adults. Methods: We analyzed data from 12,530 participants from the National Health and Nutrition Examination Survey III (1988-1994). The Cox proportional hazards models with restricted cubic spline were used for the analysis. Results: During 246,027 person-years of follow-up, 4,511 deaths occurred, including 1,395 deaths from cardiovascular disease, 1,072 deaths from heart disease, 323 deaths from cerebral disease, and 954 deaths from cancer. The serum vitamin C was significantly associated with the cancer and all-cause mortality, with hazard ratios (HRs) (95% CIs) for each one SD of 0.80 (0.71-0.91) and 0.91 (0.86-0.96). The serum alpha-carotene was significantly associated with the cancer mortality, with HRs (95% CIs) of 0.70 (0.54-0.90), 0.68 (0.48-0.95), 0.64 (0.43-0.95), and 0.44 (0.33-0.60) for comparisons of groups 2-5 with group 1 in model 2, respectively. The change for each one SD in the composite biomarker score, equivalent to a 0.483 times/month difference in total fruits and vegetables intake, gave an HR of 0.79 (0.69-0.90) for cancer mortality. Conclusion: Inverse associations were found between serum vitamin C, carotenoids, and composite biomarker score and outcomes expect for cerebral disease, heart disease, and cardiovascular disease mortality. This finding supports an increase in dietary fruit and vegetable intake as a primary prevention strategy for cancer and all-cause mortality.

Associations between Physical Activity Trajectories and Incident Hypertension.

Purpose: We aimed to characterize physical activity (PA) trajectories across adulthood and to estimate their association with incident hypertension risk. Methods: Data were obtained from the China Health and Nutrition Survey (CHNS) conducted during 2004-2011. Group-based trajectory modeling (GBTM) was used to identify distinct groups of PA trajectories. The Cox proportional hazards model was used to investigate the association. Results: A total of 11,162 participants whose PA was repeatedly estimated by self-report from questionnaires two to four times in the CHNS were included in our study. During the 5.4 years of follow-up, 3824 incident hypertension cases were identified. Five distinct PA trajectories were identified in men: light and slight decline, light and gradual decline then sharp rise, light to medium-heavy then decline, medium-heavy and gradual decline, and heavy and sharp decline. Two distinct PA trajectories were identified in women: light and stable, and medium and gradual decline. The PA trajectory of medium-heavy and gradual decline was significantly associated with decreased risk of hypertension in men, with the hazard ratios and 95% confidence intervals (CI) being 0.80 (0.63, 0.99), 0.74 (0.59, 0.93), 0.76 (0.60, 0.96), and 0.70 (0.55, 0.88) in models 1-4, respectively. Conclusions: Our study identified five distinct long-term PA trajectories in men and two distinct trajectories in women. The PA trajectory of medium-heavy PA in early adulthood followed by gradual decline was found to be significantly associated with a decreased risk of hypertension in later life in men.

Exploring the Bidirectional Associations Between Short or Long Sleep Duration and Lower Cognitive Function: A 7-Year Cohort Study in China.

Background: Sleep duration is linked to cognitive function, but whether short or prolonged sleep duration results from impaired cognition or vice versa has been controversial in previous studies. We aimed to investigate the bidirectional association between sleep duration and cognitive function in older Chinese participants. Methods: Data were obtained from a nationally representative study conducted in China. A total of 7984 participants aged 45 years or older were assessed at baseline between June 2011 and March 2012 (Wave 1), 2013 (Wave 2), 2015 (Wave 3), and 2018 (Wave 4). Nocturnal sleep duration was evaluated using interviews. Cognitive function was examined via assessments of global cognition, including episodic memory, visuospatial construction, calculation, orientation and attention capacity. Latent growth models and cross-lagged models were used to assess the bidirectional association between sleep duration and cognitive function. Results: Among the 7,984 participants who were followed in the four waves of the study, the baseline mean (SD) age was 64.7 (8.4) years, 3862 (48.4%) were male, and 6453 (80.7%) lived in rural areas. Latent growth models showed that both sleep duration and global cognition worsened over time. Cross-lagged models indicated that short or long sleep duration in the previous wave was associated with lower global cognition in the subsequent wave (standardized ß = -0.066; 95% CI: -0.073, -0.059; P < 0.001; Wave 1 to 2) and that lower global cognition in the previous wave was associated with short or long sleep duration in the subsequent wave (standardized ß = -0.106; 95% CI: -0.116, -0.096; P < 0.001; Wave 1 to 2). Conclusion: There was a bidirectional association between sleep duration and cognitive function, with lower cognitive function having a stronger association with long or short sleep duration than the reverse relationship. Global cognition was likely the major driver in these reciprocal associations.