Search

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. [ABSTRACT FROM AUTHOR]

Epidemiological studies of sugar-sweetened beverages (SSBs) and artificially sweetened beverages (ASBs) with Alzheimer's disease (AD) have provided controversial findings. Furthermore, little is known about the association between pure fruit/vegetable juices and AD. The present study aims to estimate the associations of SSBs, ASBs, and pure fruit/vegetable juices with AD, and to evaluate the theoretical effects of replacing SSBs and ASBs with the different consumption of pure fruit/vegetable juices on the risk of AD. This prospective cohort study of the UK Biobank included 206,606 participants aged 39–72 years free of dementia at baseline between 2006 and 2010. Dietary intake of SSBs, ASBs, and pure fruit/vegetable juices (naturally sweet juices) were collected using a 24-h dietary recall questionnaire completed between 2009 and 2012. Incident AD was identified by medical and mortality records. Cox proportional hazard models and substitution models were conducted to estimate hazard ratios (HRs) and 95% confidence intervals (CIs). A total of 699 cases of AD were identified over a median follow-up of 9.5 years. The consumption of SSBs and ASBs (> 2 units/d) were associated with a higher risk of AD. However, participants who drank > 1–2 units/d of pure fruit/vegetable juices were associated with a lower risk of AD. In substitution models, replacing SSBs with an equivalent consumption of pure fruit/vegetable juices could be associated with a risk reduction of AD. [ABSTRACT FROM AUTHOR]

Objectives: The detrimental association of mortality with sleep apnoea may increase with apnoea severity. To assess the association between life-course severe sleep apnoea and all-cause mortality and to investigate whether and to what extent the association was compensated by physical activity. Methods: The prospective cohort study included 407,128 individuals (mean age 56.26 years) from the UK Biobank. Severe sleep apnoea was defined as hospital admission. Moderate-to-vigorous physical activity (MVPA) was measured from frequency per week and duration per day via self-report. Cox proportional hazards regression models were performed to estimate hazard ratios (HRs) and 95% confidence intervals (CIs). Results: A total of 29,004 death (7.1%) events occurred (median of follow-up 12.7 years). The multi-adjusted HRs (95% CIs) of all-cause mortality were 1.57 (1.12–2.21) for early-life severe sleep apnoea, 1.30 (1.16–1.46) for mid-life severe sleep apnoea, and 2.75 (1.31–5.77) for early- to mid-life severe sleep apnoea, respectively. In joint effect analysis, compared to participants with an inactive level of physical activity and mid-life severe sleep apnoea, the HR (95% CI) of all-cause mortality was 0.57 (0.44–0.74) in those with sufficient physical activity and mid-life severe sleep apnoea. For physical activity intensity, a medium proportion of vigorous physical activity (VPA) per week buffered 56% impacts of mid-life severe sleep apnoea on all-cause mortality (HR = 0.44; 95% CI, 0.31–0.64). Conclusions: Not only mid-life severe sleep apnoea but also early-life severe sleep apnoea is positively associated with all-cause mortality. MVPA could compensate for the risk of all-cause mortality in relation to mid-life severe sleep apnoea. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM AUTHOR]

Background: Serum uric acid (SUA) had been associated with incident hypertension, but it is uncertain whether and to what extent the effect of SUA is mediated by other metabolic factors.Methods: Data from the China Health and Retirement Longitudinal Study (CHARLS) during 2011 to 2015 was employed for this study. A total of 7639 participants aged between 35 and 96 years without hypertension was included. Cox proportional hazards model was used to investigate the association between elevated SUA and hypertension. A mediation model was used to separately explore mediating effects (MEs) of metabolic factors on the association between SUA and incident hypertension.Results: During a median 4.0 years of follow-up, 2348 individuals were diagnosed with hypertension. After adjustment for metabolic confounders, participants with the highest SUA quartile had a hazard ratio of 1.16 (1.02-1.33) compared with the lowest category for incident hypertension. The association between SUA and incident hypertension were partially mediated by waist circumference (WC; ME = 0.034), body mass index (BMI; ME = 0.016), triglycerides (TG; ME = 0.024), total cholesterol (TC; ME = 0.009), high density lipoprotein cholesterol (HDL-C; ME = 0.009), fasting plasma glucose (FPG; ME = 0.005), and glycated hemoglobin (HbA1c; ME = - 0.002). Additionally, proportional mediation was 32.7% by WC and 15.4% by BMI for obesity indicators; 23.1% by TG, 8.7% by TC, and 8.7% by HDL-C for blood lipid; and 4.8% by FPG and - 1.9% by HbA1c for blood glucose.Conclusions: The positive association between elevated SUA concentration and hypertension was reconfirmed in a Chinese population. Obesity indicators, blood lipids, and blood glucose may play important mediating roles in the pathways. [ABSTRACT FROM AUTHOR]

Accumulated evidence confirmed depression was positively associated with coronary heart disease (CHD). But evidence of the association between depression and premature CHD is still unknown. To explore the association between depression and premature CHD, and to investigate whether and to what extent the association is mediated by metabolic factors and systemic immune–inflammation index (SII). In this large population–based cohort study based on the UK Biobank, 176,428 CHD–free (mean age: 52.70) adults were followed up for 15 years to detect incident premature CHD. Depression and premature CHD (mean age: female, 54.53; male, 48.13) were ascertained from self–report data and linked hospital–based clinical diagnosis. Metabolic factors included central obesity, hypertension, dyslipidemia, hypertriglyceridemia, hyperglycemia, and hyperuricemia. Systemic inflammation was evaluated by calculating SII, which equals platelet count (/L) × neutrophil count (/L) / lymphocyte count (/L). Data were analyzed using Cox proportional hazards models and generalized structural equation model (GSEM). During follow–up (median: 8.0 years, interquartile range: 4.0 to 14.0 years), 2990 participants developed premature CHD (1.7 %). The adjusted hazard ratio (HR) and 95 % confidence interval (CI) of premature CHD related to depression were 1.72 (1.44–2.05). The association between depression and premature CHD was 32.9 % mediated by comprehensive metabolic factors (β = 0.24, 95 % CI: 0.17–0.32) and 2.7 % by SII (β = 0.02, 95 % CI = 0.01–0.04), respectively. Concerning metabolic factors, the strongest indirect association was for central obesity, accounting for 11.0 % of the association between depression and premature CHD (β = 0.08, 95 % CI: 0.05–0.11). Depression was associated with an increased risk of premature CHD. Our study provided evidence that metabolic and inflammatory factors might play a mediating role in the association between depression and premature CHD, especially central obesity. • Study on the relationship between depression and the risk of premature coronary heart disease (CHD) is scarce. • Central obesity mediated the highest proportion (11.0%) of the depression–premature CHD association. • Systemic immune–inflammation index (SII) mediated 2.7% of the depression–premature CHD association. • The combination of higher SII and metabolic mediators might play more positive mediating roles in the given association. [ABSTRACT FROM AUTHOR]

To investigate the associations of recreational screen time with risks of brain-related disorders (dementia, stroke, and Parkinson's disease) and neuroimaging features. Prospective cohort study. A total of 407,792 participants from the UK Biobank who were free of dementia, stroke, or Parkinson's disease at enrollment (2006–2010). TV viewing and time spent using the computer were self-reported at baseline. Among a subsample of 40,692 participants, neuroimaging features were measured by magnetic resonance imaging in 2014. Data were analyzed using Cox proportional hazard models, restricted cubic spline models, and general linear regression models. During a median follow-up of 12.6 years, 5227 incident dementia, 6822 stroke, and 2308 Parkinson's disease cases were identified. Compared with TV viewing >0–1 h/day, watching TV ≥5 h/day was associated with higher risks of dementia [hazard ratio (HR), 1.44; 95% confidence interval (CI), 1.28–1.62], stroke (HR, 1.12; 95% CI, 1.01–1.25), and Parkinson's disease (HR, 1.28; 95% CI, 1.06–1.54). Moreover, we observed inverse associations between TV viewing time and both gray matter volume and hippocampus volume (P trend <.001). However, we did not observe the significant associations between discretional computer use and brain-related disorders or neuroimaging features. Our findings suggest that high TV viewing time is associated with increased risk of various brain-related disorders, highlighting recreational TV viewing could have an important impact on brain-related health. [ABSTRACT FROM AUTHOR]

Objective: Few studies have investigated the associations of sleep duration and sleep quality with incident cardiovascular diseases (CVDs), cancer, and mortality in the same large population. This study aimed at estimating the independent risk factors of long or short sleep durations and several typical characteristics of poor sleep quality for incident CVDs, cancer, and mortality.Methods: In this prospective cohort study, 407 500 individuals were enrolled. Cox proportional hazards models were used to calculate the adjusted hazard ratios and 95% confidence intervals (HR, 95%CI) of associations of sleep duration and quality with incident CVDs, cancer, and mortality.Results: Compared with the sleep duration of 7 h, sleep duration of ≤5 h and ≥9 h were both associated with higher risk of all-cause mortality (HR = 1.25, 95% CI: 1.16-1.34 and HR = 1.30, 95% CI: 1.22-1.38, respectively), CVD mortality (HR = 1.27, 95% CI: 1.09-1.49 and HR = 1.32, 95% CI: 1.16-1.50, respectively), and CVD incidence (HR = 1.23, 95% CI: 1.16-1.31 and HR = 1.08, 95% CI: 1.02-1.15, respectively). Additionally, long sleep duration (≥9 h) was associated with a higher risk of cancer mortality (HR = 1.19, 95% CI: 1.10-1.30) and cancer incidence (HR = 1.08, 95% CI: 1.04-1.12). Moreover, CVD incidence was significantly associated with snoring, insomnia and narcolepsy, increasing the risk by 7%, 26%, and 20%, respectively.Conclusion: Long sleep durations may substantially increase the risk of mortality and morbidity. Snoring, insomnia, and narcolepsy were independent risk factors for incident CVD. [ABSTRACT FROM AUTHOR]

This study aimed to examine the relationship between sleep duration and all-cause mortality, and to assess the role of cognitive impairment, physical disability, and chronic conditions on this association among very old adults. A prospective cohort study. Within the Chinese Longitudinal Healthy Longevity Surveys, 17,637 oldest-old aged 80-105 years were followed up to 10 years (2005- 2014). Data on sleep duration at baseline were based on self-report and were categorized as short (<7 hour), moderate (7-9 hours), and long sleep (>9 hours). Information on cognitive function using the Mini-Mental State Examination (MMSE), physical disability using Activities of Daily Living (ADL), and chronic conditions including diabetes, heart disease, stroke, asthma, and cancer were collected at baseline based on a structured questionnaire. Information about vital status was ascertained and confirmed by a close family member or village doctor of the participant during the follow-up. Data were analyzed using Cox proportional hazards models, with adjustment for potential confounders. During the follow-up of 10 years, 11,067 (62.7%) participants died. The multivariate-adjusted hazard ratios (HRs) with 95% confidence interval (CI) for mortality were 1.03 (0.98-1.09) for short sleep and 1.13 (1.08-1.18) for long sleep compared with moderate sleep duration. In stratified analysis by cognitive impairment, physical disability, and chronic conditions, the risk of morality was present only among people with MMSE scores ≤24 but did not differ much when stratified by physical disability and chronic conditions. There was a statistically significant interaction between long sleep and cognitive impairment on mortality (P for interaction =.002). Long sleep duration is associated with higher risk of mortality in very old adults independently of health conditions. Cognitive impairment may enhance this association. These findings suggest that health practitioners and families should be aware of the potential adverse prognosis associated with long sleep. [ABSTRACT FROM AUTHOR]