Predictive value of lung function measures for cardiovascular risk: a large prospective cohort study.

INTRODUCTION: Although lung function measures are associated with cardiovascular disease (CVD), the added predictive values of these measures remain unclear. METHODS: From the UK Biobank, 308 415 participants free of CVD with spirometry parameters were included. The CVD outcomes included were defined by QRISK3, the American College of Cardiology/American Heart Association (ACC/AHA) and the European Systematic Coronary Risk Evaluation (SCORE) prediction models, respectively. Cox proportional hazard models were used to estimate the associations of lung function measures with CVD outcomes. The predictive capability was determined by the decision curve analyses. RESULTS: Over a median follow-up of 12.5 years, 21 885 QRISK3 events, 12 843 ACC/AHA events and 2987 SCORE events were recorded. The associations of spirometry parameters with CVD outcomes were L-shaped. Restrictive and obstructive impairments were associated with adjusted HRs of 1.84 (95% CI: 1.65 to 2.06) and 1.72 (95% CI: 1.55 to 1.90) for SCORE CVD, respectively, compared with normal spirometry. Similar associations were seen for QRISK3 CVD (restrictive vs normal, adjusted HR: 1.30, 95% CI: 1.25 to 1.36; obstructive vs normal, adjusted HR: 1.20, 95% CI: 1.15 to 1.25) and ACC/AHA CVD (restrictive vs normal, adjusted HR: 1.39, 95% CI: 1.31 to 1.47; obstructive vs normal, adjusted HR: 1.26, 95% CI: 1.19 to 1.33). Using models that integrated non-linear forced expiratory volume in 1 s led to additional 10-year net benefits per 100 000 persons of 25, 43 and 5 for QRISK3 CVD at the threshold of 10%, ACC/AHA CVD at 7.5% and SCORE CVD at 5.0%, respectively. CONCLUSION: Clinicians could consider spirometry indicators in CVD risk assessment. Cost-effectiveness studies and clinical trials are needed to put new CVD risk assessment into practice.

An novel effective and safe model for the diagnosis of nonalcoholic fatty liver disease in China: gene excavations, clinical validations, and mechanism elucidation.

BACKGROUND: Non-alcoholic fatty liver disease (NAFLD) is one of the most common chronic liver diseases. NAFLD leads to liver fibrosis and hepatocellular carcinoma, and it also has systemic effects associated with metabolic diseases, cardiovascular diseases, chronic kidney disease, and malignant tumors. Therefore, it is important to diagnose NAFLD early to prevent these adverse effects. METHODS: The GSE89632 dataset was downloaded from the Gene Expression Omnibus database, and then the optimal genes were screened from the data cohort using lasso and Support Vector Machine Recursive Feature Elimination (SVM-RFE). The ROC values of the optimal genes for the diagnosis of NAFLD were calculated. The relationship between optimal genes and immune cells was determined using the DECONVOLUTION algorithm CIBERSORT. Finally, the specificity and sensitivity of the diagnostic genes were verified by detecting the expression of the diagnostic genes in blood samples from 320 NAFLD patients and liver samples from 12 mice. RESULTS: Through machine learning we identified FOSB, GPAT3, RGCC and RNF43 were the key diagnostic genes for NAFLD, and they were further demonstrated by a receiver operating characteristic curve analysis. We found that the combined diagnosis of the four genes identified NAFLD samples well from normal samples (AUC = 0.997). FOSB, GPAT3, RGCC and RNF43 were strongly associated with immune cell infiltration. We also experimentally examined the expression of these genes in NAFLD patients and NAFLD mice, and the results showed that these genes are highly specific and sensitive. CONCLUSIONS: Data from both clinical and animal studies demonstrate the high sensitivity, specificity and safety of FOSB, GPAT3, RGCC and RNF43 for the diagnosis of NAFLD. The relationship between diagnostic key genes and immune cell infiltration may help to understand the development of NAFLD. The study was reviewed and approved by Ethics Committee of Tianjin Second People's Hospital in 2021 (ChiCTR1900024415).

Association of plant-based diets with total and cause-specific mortality across socioeconomic deprivation level: a large prospective cohort.

PURPOSE: Current evidence on the association between plant-based diet indices (PDIs) and mortality is inconsistent. We aimed to investigate the association of PDIs with all-cause and cause-specific mortality and to examine whether such associations were modified by socioeconomic deprivation level. METHODS: A total of 189,003 UK Biobank participants with at least one 24-h dietary assessment were included. All food items were categorised into three groups, including healthy plant foods, less healthy plant foods, and animal foods. Three PDIs, including the overall PDI (positive scores for all plant-based food intake and inverse scores for animal-based foods), the healthful PDI (hPDI) (positive scores only for healthy plant food intake and inverse scores for others), and the unhealthful PDI (uPDI) (positive scores only for less healthy plant food intake and inverse scores for others), were calculated according to the quantities of each food subgroup in three categories. The Townsend deprivation index was used as the indicator of socioeconomic deprivation level. Cox proportional hazard models were used to estimate the hazard ratios (HRs) of PDIs for all-cause and cause-specific mortality. The modification effects of socioeconomic deprivation levels on these associations were evaluated. RESULTS: During a median follow-up of 9.6 years, 9335 deaths were documented. Compared with the lowest quintile, the highest quintile of overall PDI was associated with adjusted HRs of 0.87 (95% CI 0.81-0.93) for all-cause mortality and 0.77 (0.66-0.91) for cardiovascular mortality. Compared with the lowest quintile, the highest quintile of hPDI was associated with lower risks of all-cause mortality (0.92, 0.86-0.98), and death caused by respiratory disease (0.63, 0.47-0.86), neurological disease (0.65, 0.48-0.88), and cancer (0.90, 0.82-0.99). Compared with the lowest quintile, the highest quintile of uPDI was associated with an HR of 1.29 (1.20-1.38) for all-cause mortality, 1.95 (1.40-2.73) for neurological mortality, 1.54 (1.13-2.09) for respiratory mortality, and 1.16 (1.06-1.27) for cancer mortality. The magnitudes of associations of hPDI and uPDI with mortality were larger in the most socioeconomically deprived participants (the highest tertile) than in the less deprived ones (p-values for interaction were 0.039 and 0.001, respectively). CONCLUSIONS: This study showed that having a high overall PDI and hPDI were related to a reduced risk of death, while the uPDI was linked to a higher risk of death. Sticking to a healthy plant-based diet may help decrease mortality risks across socioeconomic deprivation levels, especially for those who are the most socioeconomically deprived.

Starch intake, amylase gene copy number variation, plasma proteins, and risk of cardiovascular disease and mortality.

BACKGROUND: Salivary amylase, encoded by the AMY1 gene, initiate the digestion of starch. Whether starch intake or AMY1 copy number is related to disease risk is currently rather unknown. The aim was to investigate the association between starch intake and AMY1 copy number and risk of cardiovascular disease (CVD) and mortality and whether there is an interaction. In addition, we aim to identify CVD-related plasma proteins associated with starch intake and AMY1 copy number. METHODS: This prospective cohort study used data from 21,268 participants from the Malmö Diet and Cancer Study. Dietary data were collected through a modified diet history method and incident CVD and mortality were ascertained through registers. AMY1 gene copy number was determined by droplet digital polymerase chain reaction, a risk score of 10 genetic variants in AMY1 was measured, and a total of 88 selected CVD-related proteins were measured. Cox proportional hazards regression was used to analyze the associations of starch intake and AMY1 copy number with disease risk. Linear regression was used to identify plasma proteins associated with starch intake and AMY1 copy number. RESULTS: Over a median of 23 years' follow-up, 4443 individuals developed CVD event and 8125 died. After adjusting for potential confounders, a U-shape association between starch intake and risk of CVD (P-nonlinearity = 0.001) and all-cause mortality (P-nonlinearity = 0.03) was observed. No significant association was found between AMY1 copy number and risk of CVD and mortality, and there were no interactions between starch intake and AMY1 copy number (P interaction > 0.23). Among the 88 plasma proteins, adrenomedullin, interleukin-1 receptor antagonist protein, fatty acid-binding protein, leptin, and C-C motif chemokine 20 were associated with starch intake after adjusting for multiple testing. CONCLUSIONS: In this large prospective study among Swedish adults, a U-shaped association between starch intake and risk of CVD and all-cause mortality was found. Several plasma proteins were identified which might provide information on potential pathways for such association. AMY1 copy number was not associated with CVD risk or any of the plasma proteins, and there was no interaction between starch intake and AMY1 copy number on disease risk.

Associations of ultra-processed food consumption, circulating protein biomarkers, and risk of cardiovascular disease.

BACKGROUND: We aim to examine the association between ultra-processed foods (UPF) consumption and cardiovascular disease (CVD) risk and to identify plasma proteins associated with UPF. METHODS: This prospective cohort study included 26,369 participants from the Swedish Malmö Diet and Cancer Study, established in 1991-1996. Dietary intake was assessed using a modified diet history method, and UPF consumption was estimated using the NOVA classification system. A total of 88 selected CVD-related proteins were measured among 4475 subjects. Incident CVD (coronary heart disease and ischemic stroke) was defined as a hospital admission or death through registers. Cox proportional hazards regression models were performed to analyze the associations of UPF intake with risks of CVD. Linear regression models were used to identify the plasma proteins associated with UPF intake. RESULTS: During 24.6 years of median follow-up, 6236 participants developed CVD, of whom 3566 developed coronary heart disease and 3272 developed ischemic stroke. The adjusted hazard ratio (95% confidence interval) in the 4th versus 1st quartile of UPF was 1.18 (1.08, 1.29) for CVD, 1.20 (1.07, 1.35) for coronary heart disease, and 1.17 (1.03, 1.32) for ischemic stroke. Plasma proteins interleukin 18, tumor necrosis factor receptor 2, macrophage colony-stimulating factor 1, thrombomodulin, tumor necrosis factor receptor 1, hepatocyte growth factor, stem cell factor, resistin, C-C motif chemokine 3, and endothelial cell-specific molecule 1 were positively associated with UPF after correcting for multiple testing. CONCLUSIONS: Our study showed that high UPF intake increased the risk of CVD and was associated with several protein biomarkers. Future studies are warranted to validate these findings and assess the potential pathways between UPF intake and CVD.

Associations between an obesity-related dietary pattern and incidence of overall and site-specific cancers: a prospective cohort study.

BACKGROUND: A dietary pattern (DP) may impact on cancer incidence more strongly than individual foods, but this association remains uncertain. Here, we aimed to broadly explore the associations of an obesity-related DP with overall and 19 site-specific cancers. METHODS: This study included 114,289 cancer-free participants with at least two dietary assessments. A total of 210 food items were classified into 47 food groups, and the mean amount of each food group was used in reduced-rank regression to derive the obesity-related DP. Cox regressions were conducted to explore the associations of the obesity-related DP with overall and 19 site-specific cancers. The parallel mediation model was constructed to quantify the mediating roles of potential mediators. RESULTS: During a median follow-up period of 9.4 years, 10,145 (8.9%) incident cancer cases were documented. The derived-DP was characterized by a higher intake of beer and cider, processed meat, high sugar beverages, red meat, and artificial sweetener, and a lower intake of fresh vegetables, olive oil, tea, and high fiber breakfast cereals. Observational analysis showed that a higher obesity-related DP Z-score was linearly associated with an increased risk of overall cancer (adjusted hazard ratio (HR) = 1.02, 95% CI: 1.01, 1.04 per 1-SD increase, corrected P < 0.001). For site-specific cancer, positive linear associations for six cancer sites (oral, colorectal, liver, lung, endometrium, and thyroid) and nonlinear associations for six cancer sites (esophagus, malignant melanoma, prostate, kidney, bladder, and multiple myeloma) were observed. The paralleled mediation analysis suggested that the association between the obesity-related DP and overall cancer is mediated by the body mass index (BMI), the waist-to-hip ratio (WHR), C-reactive protein, high-density lipoproteins (HDLs), and triglycerides. CONCLUSIONS: The developed obesity-related DP is strongly associated with overall and multiple cancer sites. Our findings highlight the complicated and diverse associations between an obesity-related DP and cancers and provide clues for future research directions.

A low-inflammatory diet is associated with a lower incidence of diabetes: role of diabetes-related genetic risk.

BACKGROUND: Whether a low-inflammatory diet relates to type 2 diabetes risk remains unclear. We examined the association between a low-inflammatory diet and risk of type 2 diabetes among normoglycemic and prediabetic participants. We also explored whether a low-inflammatory diet modifies genetic risk for type 2 diabetes. METHODS: Among 142,271 diabetes-free UK Biobank participants (aged 39-72 years), 126,203 were normoglycemic and 16,068 were prediabetic at baseline. Participants were followed for up to 15 years to detect incident type 2 diabetes. At baseline, dietary intake was assessed with a 24-h dietary record. An inflammatory diet index (IDI) was generated based on high-sensitivity C-reactive protein levels and was a weighted sum of 34 food groups (16 anti-inflammatory and 18 pro-inflammatory). Participants were grouped into tertiles corresponding to inflammatory level (low, moderate, and high) based on IDI scores. Prediabetes at baseline was defined as HbA1c 5.7-6.4% in diabetes-free participants. Incident type 2 diabetes and age of onset were ascertained according to the earliest recorded date of type 2 diabetes in the Primary Care and Hospital inpatient data. A diabetes-related genetic risk score (GRS) was calculated using 424 single-nucleotide polymorphisms. Data were analyzed using Cox regression and Laplace regression. RESULTS: During follow-up (median 8.40 years, interquartile range 6.89 to 11.02 years), 3348 (2.4%) participants in the normoglycemia group and 2496 (15.5%) in the prediabetes group developed type 2 diabetes. Type 2 diabetes risk was lower in normoglycemic (hazard ratio [HR] = 0.71, 95% confidence interval [CI] 0.65, 0.78) and prediabetic (HR = 0.81, 95% CI 0.73, 0.89) participants with low IDI scores compared to those with high IDI scores. A low-inflammatory diet may prolong type 2 diabetes onset by 2.20 (95% CI 1.67, 2.72) years among participants with normoglycemia and 1.11 (95% CI 0.59, 1.63) years among participants with prediabetes. In joint effect analyses, normoglycemic or prediabetes participants with low genetic predisposition to type 2 diabetes and low IDI scores had a significant 74% (HR = 0.26, 95% CI 0.21, 0.32) or 51% (HR = 0.49, 95% CI 0.40, 0.59) reduction in type 2 diabetes risk compared to those with high genetic risk plus high IDI scores. There were significant additive and multiplicative interactions between IDI and GRS in relation to type 2 diabetes risk in the normoglycemia group. CONCLUSIONS: A low-inflammatory diet is associated with a decreased risk of type 2 diabetes and may delay type 2 diabetes onset among participants with normal blood glucose or prediabetes. A low-inflammatory diet might significantly mitigate the risk of genetic factors on type 2 diabetes development.

Different types of screen time, physical activity, and incident dementia, Parkinson's disease, depression and multimorbidity status.

BACKGROUND: Several previous studies have shown that excessive screen time is associated with an increased prevalence of dementia, Parkinson's disease (PD), and depression. However, the results have been inconsistent. This study aimed to prospectively investigate the association between different types of screen time and brain structure, as well as the incidence of dementia, Parkinson's disease, depression, and their multimorbidity status. METHODS: We included 473,184 participants initially free of dementia, PD, and depression from UK Biobank, as well as 39,652 participants who had magnetic resonance imaging (MRI) data. Screen time exposure variables including TV viewing and computer using were self-reported by participants. Cox proportional hazards regression models were used to estimate the association between different types of screen time and the incidence of dementia, Parkinson's disease, depression, and their multimorbidity status. Multiple linear regression models were used to assess the linear relationship between different types of screen time and MRI biomarkers in a subgroup of participants. RESULTS: During the follow up, 6,096, 3,061, and 23,700 participants first incident cases of dementia, PD, and depression respectively. For moderate versus the lowest computer uses, the adjusted HRs (95% CIs) were 0.68 (0.64, 0.72) for dementia, 0.86 (0.79, 0.93) for PD, 0.85 (0.83, 0.88) for depression, 0.64 (0.55, 0.74) for dementia and depression multimorbidity, and 0.59 (0.47, 0.74) for PD and depression multimorbidity. The multivariable HRs (95% CIs) for the highest versus the lowest group of TV viewing time were 1.28 (1.17, 1.39) for dementia, 1.16 (1.03, 1.29) for PD, 1.35 (1.29, 1.40) for depression, 1.49 (1.21, 1.84) for dementia and depression multimorbidity, and 1.44 (1.05, 1.97) for PD and depression multimorbidity. Moderate computer using time was negatively associated with white matter hyperintensity volume (ß = -0.042; 95% CI -0.067, -0.017), and positively associated with hippocampal volume (ß = 0.059; 95% CI 0.034, 0.084). Participants with the highest TV viewing time were negatively associated with hippocampal volume (ß = -0.067; 95% CI -0.094, -0.041). In isotemporal substitution analyses, substitution of TV viewing or computer using by equal time of different types of PA was associated with a lower risk of all three diseases, with strenuous sports showing the strongest benefit. CONCLUSION: We found that moderate computer use was associated with a reduced risk of dementia, PD, depression and their multimorbidity status, while increased TV watching was associated with a higher risk of these disease. Notably, different screen time may affect the risk of developing diseases by influencing brain structures. Replacing different types of screen time with daily-life PA or structured exercise is associated with lower dementia, PD, and depression risk.

Impact of ultra-processed food intake on the risk of COVID-19: a prospective cohort study.

PURPOSE: Nutrition plays a key role in supporting the human immune system and reducing the risk of infections. However, there is limited evidence exploring the relationship between diet and the risk of COVID-19. This study aimed to assess the associations between consumption of ultra-processed foods (UPF) and COVID-19 risk. METHODS: In total, 41,012 participants from the UK Biobank study with at least 2 of up to 5 times 24-h dietary assessments were included in this study. Dietary intakes were collected using an online 24-h dietary recall questionnaire and food items were categorized according to their degree of processing by the NOVA classification. COVID-19 infection was defined as individuals tested COVID-19 positive or dead of COVID-19. Association between average UPF consumption (% daily gram intake) and COVID-19 infection was assessed by multivariable logistic regression adjusted for potential confounders. RESULTS: Compared to participants in the lowest quartile of UPF proportion (% daily gram intake) in the diet, participants in the 2nd, 3rd, and highest quartiles were associated with a higher risk of COVID-19 with the odds ratio (OR) value of 1.03 (95% CI: 0.94-1.13), 1.24 (95% CI: 1.13-1.36), and 1.22 (95% CI: 1.12-1.34), respectively (P for trend < 0.001), after adjusting for potential confounders. The results were robust in a series of sensitivity analyses. No interaction effect was identified between the UPF proportions and age groups, education level, body mass index, and comorbidity status. BMI mediated 13.2% of this association. CONCLUSION: Higher consumption of UPF was associated with an increased risk of COVID-19 infection. Further studies are needed to better understand the underlying mechanisms in such association.

The association of obesity-related dietary patterns and main food groups derived by reduced-rank regression with cardiovascular diseases incidence and all-cause mortality: findings from 116,711 adults.

PURPOSE: Research about using reduced-rank regression (RRR) to simultaneously study the effects of both individual and combined consumption of foods on cardiovascular diseases (CVD) is scarce. METHODS: This study included 116,711 CVD-free participants (a median of 11.8 year follow-up) with 2 or more 24-h online dietary assessments. A total of 210 food items were classified into 45 food groups, and the mean amount of each food group was used in RRR to derive dietary patterns (DPs) explaining the maximum shared variation in obesity-related indicators. The associations of DPs and its main food groups (|factor loading| [Formula: see text] 0.2) with the incident CVD and all-cause mortality were examined by Cox model. In cross-sectional analyses, the associations of DP scores with cardiometabolic risk factors (biomarkers) were examined by linear regression. RESULTS: The derived DP was characterized by higher intakes of beer and cider, high-sugar beverages, processed meat, red meat, artificial sweetener, and crisps, chips and savory snacks, and lower intakes of olive oil, high fiber breakfast cereals, tea, and vegetable. Compared to the lowest dietary score quintile, those in the highest were associated with higher risks of total CVD (adjusted-HR: 1.45, 95% CI 1.33-1.57) and all-cause mortality (adjusted-HR 1.31, 95% CI 1.18-1.45). We observed consumption alone of these food groups had a consistent but limited health effect on total CVD and all-cause death incidence. These associations were modified by age and sex. Higher DP scores were related to adverse biomarkers profiles. CONCLUSIONS: We developed obesity-related DPs prospectively associated with increased risks of CVD and all-cause mortality.

Application of the International Classification of Functioning, Disability and Health (ICF) in dementia research and practice: A scoping review.

OBJECTIVES: The International Classification of Functioning, Disability and Health (ICF) endorsed by the World Health Organization provides a conceptual framework for describing functioning and disability based on a biopsychosocial model. Although dementia is one of the leading causes of disability, yet little is known on the extent to how the ICF has been utilized in dementia research and practice. The study aimed to examine and map the current applications of the ICF with dementia from a body of earlier studies and to explore the potential use in person-centred dementia care. METHODS: The Arksey and O'Malley framework was used to guide the searching, selecting, and synthesizing process. The scoping review was reported following The Preferred Reporting Items for Systematic reviews and Meta-Analyses extension for Scoping Review (PRISMA-ScR) guidelines. RESULTS: A total of 34 studies were included. The applications of ICF were classified into 4 themes: (1) in clinical practice and the education of health professionals (n = 20); (2) community support services and income support (n = 3); (3) population-based, census, or survey data (n = 10); (4) advocacy and empowerment purposes (n = 1). CONCLUSION: The ICF has made a major impact on dementia in clinical settings. Findings strongly support applying the ICF to person-centered dementia care. In the future, more empirical studies are needed to expand the scope of ICF use in dementia research and practice.

A comprehensive genetic and epidemiological association analysis of vitamin D with common diseases/traits in the UK Biobank.

Vitamin D has been intensively studied for its association with human health, but the scope of such association and the causal role of vitamin D remain controversial. We aim to comprehensively investigate the links between vitamin D and human health through both epidemiological and Mendelian randomization (MR) analyses. We examined the epidemiological associations between serum 25-hydroxyvitamin D (25(OH)D) concentration and 90 diseases/traits in 326,409 UK Biobank (UKBB) Europeans. The causal relations between 25(OH)D and 106 diseases/traits were investigated by performing MR analysis using genome-wide significant 25(OH)D-associated variants (N = 143) from the largest UKBB GWAS to date. In epidemiological analysis, we found 25(OH)D was associated with 45 diseases/traits across cardiovascular/metabolic diseases, psychiatric/neurological diseases, autoimmune/inflammatory diseases, cancer, musculoskeletal diseases, and quantitative traits. In MR-analysis, we presented evidence suggesting potential causal role of 25(OH)D in increasing height (ß = .064, 95% confidence interval [CI] = 0.019-0.11) and preventing the risk of ovarian cancer (odds ratio [OR] = 0.96, 95% CI = 0.93-0.99), multiple sclerosis (OR = 0.96, 95% CI = 0.94-0.98), leg fracture (OR = 0.60, 95% CI = 0.45-0.80) and femur fracture (OR = 0.53, 95% CI = 0.32-0.84). These findings confirmed associations of vitamin D with a broad spectrum of diseases/traits and supported the potential causal role of vitamin D in promoting health.

Consumption of coffee and tea with all-cause and cause-specific mortality: a prospective cohort study.

BACKGROUND: Previous studies suggested that moderate coffee and tea consumption are associated with lower risk of mortality. However, the association between the combination of coffee and tea consumption with the risk of mortality remains unclear. This study aimed to evaluate the separate and combined associations of coffee and tea consumption with all-cause and cause-specific mortality. METHODS: This prospective cohort study included 498,158 participants (37-73 years) from the UK Biobank between 2006 and 2010. Coffee and tea consumption were assessed at baseline using a self-reported questionnaire. All-cause and cause-specific mortalities, including cardiovascular disease (CVD), respiratory disease, and digestive disease mortality, were obtained from the national death registries. Cox regression analyses were conducted to estimate hazard ratios (HRs) and 95% confidence intervals (CIs). RESULTS: After a median follow-up of 12.1 years, 34,699 deaths were identified. The associations of coffee and tea consumption with all-cause and cause-specific mortality attributable to CVD, respiratory disease, and digestive disease were nonlinear (all P nonlinear < 0.001). The association between separate coffee consumption and the risk of all-cause mortality was J-shaped, whereas that of separate tea consumption was reverse J-shaped. Drinking one cup of coffee or three cups of tea per day seemed to link with the lowest risk of mortality. In joint analyses, compared to neither coffee nor tea consumption, the combination of < 1-2 cups/day of coffee and 2-4 cups/day of tea had lower mortality risks for all-cause (HR, 0.78; 95% CI: 0.73-0.85), CVD (HR, 0.76; 95% CI: 0.64-0.91), and respiratory disease (HR, 0.69; 95% CI: 0.57-0.83) mortality. Nevertheless, the lowest HR (95% CI) of drinking both < 1-2 cup/day of coffee and ≥ 5 cups/day of tea for digestive disease mortality was 0.42 (0.34-0.53). CONCLUSIONS: In this large prospective study, separate and combined coffee and tea consumption were inversely associated with all-cause and cause-specific mortality.

Healthy lifestyle counteracts the risk effect of genetic factors on incident gout: a large population-based longitudinal study.

BACKGROUND: Risk genes linked to the development of gout have been identified, and lifestyle factors are related to gout risk. It remains unclear whether healthy lifestyle factors can mitigate the genetic risk of gout. Therefore, we aimed to explore whether and to what extent a healthy lifestyle can mitigate the risk of gout related to genetic factors. METHODS: Within the UK Biobank, 416,481 gout-free participants (aged 37-74) were identified at baseline. Polygenic risk for gout was assessed and categorized as low (lowest tertile), middle (tertile 2), and high (highest tertile). Healthy lifestyle factors included no/moderate alcohol consumption, no smoking, physical activity, and a healthy diet. Participants were categorized into three groups according to their number of healthy lifestyle factors: unfavorable (0 or 1), intermediate (any 2), and favorable (3 or 4). Data were analyzed using Cox proportional hazard models. RESULTS: Over the follow-up (median: 12.1 years), 6206 participants developed gout. Compared to low genetic risk, the hazard ratios (HRs) and 95% confidence intervals (CIs) of gout was 1.44 (1.35-1.54) for middle and 1.77 (1.66-1.89) for high genetic risk. The HRs (95% CIs) of gout were 0.63 (0.59-0.67) for a favorable lifestyle and 0.79 (0.75-0.85) for an intermediate lifestyle, compared to an unfavorable lifestyle. In joint effect analysis, compared to participants with low genetic predisposition and a favorable lifestyle, the HRs (95% CIs) of gout were 2.39 (2.12-2.70)/3.12 (2.79-3.52) in those with middle and high genetic predisposition plus unfavorable lifestyle profiles, and 1.53 (1.35-1.74)/1.98 (1.75-2.24) for those with middle and high genetic predisposition plus favorable lifestyle profiles, respectively. Moreover, compared to an unfavorable lifestyle, the HRs of gout related to a favorable lifestyle was 0.64 (95% CI, 0.56-0.73) for low genetic risk, 0.65 (95% CI, 0.58-0.72) for middle genetic risk, and 0.62 (95% CI, 0.57-0.69) for high genetic risk. There was a significant additive interaction between unfavorable lifestyle and high genetic risk on gout. CONCLUSIONS: Healthy lifestyle was associated with a lower risk of gout and may attenuate the risk of gout related to genetic factors by almost a third.

Association of impaired lung function with dementia, and brain magnetic resonance imaging indices: a large population-based longitudinal study.

OBJECTIVE: to examine the association between different patterns of impaired lung function with the incident risk of dementia and magnetic resonance imaging (MRI)-based brain structural features. METHODS: in UK Biobank, a total of 308,534 dementia-free participants with valid lung function measures (forced expiratory volume in 1 s [FEV1] and forced vital capacity [FVC]) were included. Association was assessed using Cox proportional hazards regression model. Furthermore, the association between impaired lung function and brain MRI biomarkers related to cognitive function was analysed among 30,159 participants. RESULTS: during a median follow-up of 12.6 years, 3,607 incident all-cause dementia cases were recorded. Restrictive impairment (hazard ratio [HR], 1.42; 95% confidence interval [CI], 1.27-1.60) and obstructive impairment (HR, 1.28; 95% CI, 1.15-1.42) were associated with higher risk of all-cause dementia. The restricted cubic splines indicated FEV1% predicted and FVC % predicted had reversed J-shaped associations with dementia. Participants with impaired lung function have higher risks of all-cause dementia across all apolipoprotein E (APOE) risk categories, whereas associations were stronger among those of low APOE risk (P for interaction = 0.034). In addition, restrictive and obstructive impairment were linked to lower total (ß: -0.075, SE: 0.021, Pfdr = 0.002; ß: -0.033, SE: 0.017, Pfdr = 0.069) and frontoparietal grey matter volumes, higher white matter hyperintensity, poorer white matter integrity, lower hippocampus (ß: -0.066, SE: 0.024, Pfdr = 0.017; ß: -0.051, SE: 0.019, Pfdr = 0.019) and other subcortical volumes. CONCLUSIONS: participants with restrictive and obstructive impairments had a higher risk of dementia. Brain MRI indices further supported adverse effects and provided insight into potential pathophysiology biomarkers.

Association of coffee and genetic risk with incident dementia in middle-aged and elderly adults.

BACKGROUND: Prior evidence suggests that coffee might be related to dementia, however, little is known about coffee and dementia in individuals with elevated genetic susceptibility for dementia. Additionally, most previous studies have focused on total coffee instead of examining coffee types separately. METHODS: This study included 203,776 participants (60-73 years old) from the UK Biobank who were initially free of dementia. Polygenic risk scores for dementia were divided into quintile to stratify individuals into low (lowest quintile), intermediate (quintile 2-4), and high (highest quintile) genetic risk categories. Coffee intake was assessed at baseline and included total, instant, ground, and decaffeinated coffee. RESULTS: During a median follow-up of 11.4 years, 4405 cases of dementia occurred (1856 Alzheimer's disease [AD], 1105 vascular dementia). Compared to non-coffee drinking, heavy instant coffee drinking (> 6 cups/day) and moderate decaffeinated coffee drinking (1-3 cups/day) were associated with a higher risk of dementia (hazard ratio [HR] 1.19-1.34) and AD (HR 1.41-1.51), while moderate ground coffee drinking was associated with a lower risk of dementia (HR, 0.78; P = 0.001) and vascular dementia (HR, 0.58; P < 0.001). Among participants at high genetic risk, heavy coffee drinking was associated with a 95% (HR; 1.95, 95% CI, 1.21-3.16) higher risk of AD than non-coffee drinking. We found an interaction between coffee and genetic risk in relation to AD (P = 0.038). CONCLUSION: The association of dementia and coffee varied by coffee types. Heavy coffee consumption was associated with a higher risk of AD in individuals with high genetic risk for dementia.

Risk of Accidents or Chronic Disorders From Improper Use of Mobile Phones: A Systematic Review and Meta-analysis.

BACKGROUND: Mobile phone use has brought convenience, but the long or improper use of mobile phones can cause harm to the human body. OBJECTIVE: We aimed to assess the impact of improper mobile phone use on the risks of accidents and chronic disorders. METHODS: We systematically searched in PubMed, EMBASE, Cochrane, and Web of Science databases for studies published prior to April 5, 2019; relevant reviews were also searched to identify additional studies. A random-effects model was used to calculate the overall pooled estimates. RESULTS: Mobile phone users had a higher risk of accidents (relative risk [RR] 1.37, 95% CI 1.22 to 1.55). Long-term use of mobile phones increased accident risk relative to nonuse or short-term use (RR 2.10, 95% CI 1.63 to 2.70). Compared with nonuse, mobile phone use resulted in a higher risk for neoplasms (RR 1.07, 95% CI 1.01 to 1.14), eye diseases (RR 2.03, 95% CI 1.27 to 3.23), mental health disorders (RR 1.16, 95% CI 1.02 to 1.32), and headaches (RR 1.25, 95% CI 1.18 to 1.32); the pooled risk of other chronic disorders was 1.20 (95% CI 0.90 to 1.59). Subgroup analyses also confirmed the increased risk of accidents and chronic disorders. CONCLUSIONS: Improper use of mobile phones can harm the human body. While enjoying the convenience brought by mobile phones, people have to use mobile phones properly and reasonably.

Consumption of coffee and tea and risk of developing stroke, dementia, and poststroke dementia: A cohort study in the UK Biobank.

BACKGROUND: Previous studies have revealed the involvement of coffee and tea in the development of stroke and dementia. However, little is known about the association between the combination of coffee and tea and the risk of stroke, dementia, and poststroke dementia. Therefore, we aimed to investigate the associations of coffee and tea separately and in combination with the risk of developing stroke and dementia. METHODS AND FINDINGS: This prospective cohort study included 365,682 participants (50 to 74 years old) from the UK Biobank. Participants joined the study from 2006 to 2010 and were followed up until 2020. We used Cox proportional hazards models to estimate the associations between coffee/tea consumption and incident stroke and dementia, adjusting for sex, age, ethnicity, qualification, income, body mass index (BMI), physical activity, alcohol status, smoking status, diet pattern, consumption of sugar-sweetened beverages, high-density lipoprotein (HDL), low-density lipoprotein (LDL), history of cancer, history of diabetes, history of cardiovascular arterial disease (CAD), and hypertension. Coffee and tea consumption was assessed at baseline. During a median follow-up of 11.4 years for new onset disease, 5,079 participants developed dementia, and 10,053 participants developed stroke. The associations of coffee and tea with stroke and dementia were nonlinear (P for nonlinear <0.01), and coffee intake of 2 to 3 cups/d or tea intake of 3 to 5 cups/d or their combination intake of 4 to 6 cups/d were linked with the lowest hazard ratio (HR) of incident stroke and dementia. Compared with those who did not drink tea and coffee, drinking 2 to 3 cups of coffee and 2 to 3 cups of tea per day was associated with a 32% (HR 0.68, 95% CI, 0.59 to 0.79; P < 0.001) lower risk of stroke and a 28% (HR, 0.72, 95% CI, 0.59 to 0.89; P = 0.002) lower risk of dementia. Moreover, the combination of coffee and tea consumption was associated with lower risk of ischemic stroke and vascular dementia. Additionally, the combination of tea and coffee was associated with a lower risk of poststroke dementia, with the lowest risk of incident poststroke dementia at a daily consumption level of 3 to 6 cups of coffee and tea (HR, 0.52, 95% CI, 0.32 to 0.83; P = 0.007). The main limitations were that coffee and tea intake was self-reported at baseline and may not reflect long-term consumption patterns, unmeasured confounders in observational studies may result in biased effect estimates, and UK Biobank participants are not representative of the whole United Kingdom population. CONCLUSIONS: We found that drinking coffee and tea separately or in combination were associated with lower risk of stroke and dementia. Intake of coffee alone or in combination with tea was associated with lower risk of poststroke dementia.

A network analysis framework of genetic and nongenetic risks for type 2 diabetes.

Both genetic and nongenetic factors have been found to be associated with type 2 diabetes, however, the correlation between them is still unclear. In the present study, we aimed to fully decipher the nongenetic and genetic factor association network for type 2 diabetes. We identified risk factors for type 2 diabetes by systematically searching for related meta-analyses and genome-wide association studies (GWAS) database. Among a total of 27,822 studies screened, 202 articles were eligible, from which 174 nongenetic factors and 210 genetic factors associated with type 2 diabetes were identified. Then, we obtained 584 associations between the nongenetic and genetic factors of type 2 diabetes, based on which a risk factor association network was conducted. The nongenetic factors could be classified into seven categories according to the Global Burden of Diseases (GBD). Of these seven categories of nongenetic factors, five were found to be correlated with genes associated with type 2 diabetes, including environmental risks, behavioral risks, metabolic risks, related disease of type 2 diabetes, and treatments. Specifically, air pollutants of environmental risks, alcohol using of behavioral risks, obesity of metabolic risks, rheumatoid arthritis of related disease risk, and simvastatin of treatment was correlated with the largest number of genes. In summary, the correlation between genetic factors and nongenetic factors identified in this study indicates that there is a common phenotype-genotype association in type 2 diabetes, with the combinations of genotypes ("genetic signature") clustering in phenotypes related to type 2 diabetes. Thus, we should take a systematic approach to explore the relationship of various factors for type 2 diabetes, as well as other noncommunicable diseases.

Consumption of Preserved Egg Is Associated with Modestly Increased Risk of Nonalcoholic Fatty Liver Disease in Chinese Adults.

BACKGROUND: Although preserved egg is a traditional Chinese delicacy widely consumed in China and Southeast Asian countries, whether habitual preserved egg consumption is associated with nonalcoholic fatty liver disease (NAFLD) remains unknown. OBJECTIVES: This study aimed to examine the association between preserved egg consumption and risk of NAFLD in a cohort of Chinese adults. METHODS: This prospective cohort study included 15,883 participants aged 19-88 y (58% women) from the TCLSIH (Tianjin Chronic Low-grade Systemic Inflammation and Health) cohort study who were free of liver diseases, cancer, and cardiovascular disease at baseline. Preserved egg consumption was assessed using an FFQ at baseline. NAFLD was diagnosed by transabdominal sonography during an annual health examination. Multivariable Cox proportional hazards regression models were used to calculate HRs and 95% CIs across categories of preserved egg consumption. RESULTS: During 56,002 person-years of follow-up, 3683 first incident cases of NAFLD were recorded. After adjustment for sociodemographic characteristics, lifestyle risk factors, total energy intake, egg intake, and eating patterns, the multivariable HRs (95% CIs) of incident NAFLD according to categories of preserved egg consumption were 1.00 (reference) for never, 1.05 (0.98, 1.14) for <1 time/wk, 1.09 (0.96, 1.24) for 1 time/wk, and 1.26 (1.09, 1.46) for ≥2 times/wk (P-trend < 0.01). The results were robust to a series of sensitivity analyses. CONCLUSIONS: Habitual preserved egg consumption is associated with a modestly higher risk of NAFLD among the Chinese adult population. The mechanism underlying this association warrants further research.This trial was registered at www.umin.ac.jp/ctr/ as UMIN000027174.