Long-term air pollutants exposure and respiratory mortality: A large prospective cohort study.

Ambient air pollution is a major global health concern. Yet, no study has thoroughly assessed its link to respiratory mortality. Our research evaluated the combined and individual effects of air pollutants on respiratory mortality risks based on the UK Biobank. A total of 366,478 participants were studied. A Cox proportional hazards model was used to estimate the respiratory mortality risk from combined long-term exposure to five pollutants, summarized as a weighted air pollution score. During a median of 13.6 years of follow-up, 6113 deaths due to respiratory diseases were recorded. The hazard ratios (HRs) and 95% confidence intervals (95% CIs) of respiratory diseases were 2.64 (2.05-3.39), 1.62 (1.23-2.12), 2.06 (1.73-2.45), 1.20 (1.16-1.25), and 1.07 (1.05-1.08) per 10 µg/m3 increase in PM2.5, PM2.5-10, PM10, NO2, and NOx, respectively. The air pollution score showed a dose-response association with an elevated respiratory mortality risk. The highest versus lowest quartile air pollution score was linked to a 44% increase in respiratory mortality risk (HR 1.44, 95% CI: 1.33-1.57), with consistent findings in subgroup and sensitivity analyses. Long-term individual and joint air-pollutant exposure showed a dose-response association with an increased respiratory mortality risk, highlighting the importance of a comprehensive air-pollutant assessment to protect public health.

Association between regular proton pump inhibitors use and cardiovascular outcomes: A large prospective cohort study.

BACKGROUND: Proton pump inhibitors (PPIs) are widely prescribed for gastroesophageal reflux disease and peptic ulcer disease. However, the association between the regular PPIs use and the risk of cardiovascular disease (CVD) outcomes remains unclear. We aimed to determine whether regular proton pump inhibitors (PPIs) use is associated with an altered incidence of cardiovascular disease (CVD) in the general population. METHODS: This prospective cohort study included 459,207 participants (mean [SD] age, 56.2 [8.1] years) from the UK Biobank study without prevalent CVD who enrolled between 2006 and 2010 and were followed until 2018. Hazard ratios (HRs) and 95% confidence intervals (CIs) for incident CVD and its components (coronary heart disease [CHD], stroke, heart failure, atrial fibrillation, and venous thromboembolism) were obtained using Cox proportional hazards models with adjustment for potential confounding factors, including demographic factors, lifestyle behaviors, prevalent comorbidities, and clinical indicators for PPIs use. RESULTS: During the follow-up period, we recorded 26,346 incident CVD events (including 13,749 CHD events, 4144 stroke events, 5812 atrial fibrillation events, 1159 heart failure events, and 4206 venous thromboembolism events). The fully adjusted HRs (and 95% CIs) associated with PPIs users compared to nonusers were 1.44 (95% CI 1.39-1.50) for incident CVD, 1.65 (95% CI 1.57-1.74) for CHD, 1.21 (95% CI 1.09-1.33) for stroke, 1.17 (95% CI 1.08-1.28) for atrial fibrillation, 1.61 (95% CI 1.37-1.89) for heart failure, and 1.36 (95% CI 1.24-1.50) for venous thromboembolism. CONCLUSIONS: Regular PPIs use was associated with higher risk of CVD outcomes. Clinicians should therefore exercise caution when prescribing PPIs.

Long-term air pollution exposure, habitual physical activity, and incident chronic kidney disease.

Both air pollution and physical inactivity contribute to the increased risk of incident chronic kidney disease (CKD). However, the detrimental effects of air pollution exposure could be augmented by an elevated intake of air pollutants during exercise. In the present study, we analyzed 367,978 participants who were CKD-free at baseline (2006-2010) based on the UK Biobank. Air pollutants included fine particulate matter (PM2.5 and PM10), nitrogen dioxide (NO2), and nitrogen oxides (NOX). Physical activity (PA) was obtained by the self-reported questionnaire. Using Cox proportional hazards models, hazard ratios (HRs) for incident CKD related to air pollution, PA, and incident CKD were evaluated. During a median of 12.4 years of follow-up, 14,191 incident CKD events were documented. High PM2.5, PM10, NO2, and NOX increased CKD risks by 11 %, 15 %, 14 %, and 12 %, respectively, while moderate and high PA reduced CKD risks by 18 % and 22 %, respectively. Participants with high PA and low air pollution exposure had 29 %, 31 %, 30 %, and 30 % risks of incident CKD than those with low PA and high air pollution exposure for the four air pollutants, with multivariable-adjusted HRs of 0.71 (95 % confidence intervals [CI]: 0.65-0.76) for PM2.5, 0.69 (95 % CI: 0.64-0.75) for PM10, 0.70 (95 % CI: 0.64-0.75) for NO2, and 0.70 (95 % CI: 0.64-0.75) for NOX. No clear interactions were observed between each air pollutant exposure and PA (all P for interaction > 0.05). The findings that reducing air pollution exposure and increasing PA were both independently correlated with a diminished risk of incident CKD suggest that PA could be targeted to prevent CKD generally regardless of air pollution levels. Further research is needed in areas polluted moderately and severely to examine our findings.

Serum 25-hydroxyvitamin D concentrations and colorectal cancer incidence in adults with type 2 diabetes.

BACKGROUND: To examine the association of serum 25-hydroxyvitamin D (25[OH]D) with colorectal cancer (CRC) risk in adults with type 2 diabetes (T2D). METHODS: Using UK Biobank data, this study included 18,453 adults with T2D. Serum 25(OH)D concentrations were determined by the chemiluminescent immunoassay method. A Cox proportional hazards model was used to calculate hazard ratios (HRs) and 95% confidence intervals (CIs) for CRC outcomes. RESULTS: During a median follow-up of 8.8 years, there were 284 incident CRC cases. Compared with adults with serum 25(OH)D concentrations <25.0 nmol/L, the adjusted HRs (95% CIs) for lower to higher serum 25(OH)D concentrations (25.0 to <50.0, 50.0 to <75.0, and ≥75.0 nmol/L) were 0.61 (0.46-0.82), 0.50 (0.34-0.74), and 0.53 (0.30-0.94), respectively (Ptrend = 0.001). The risk of CRC decreased by 19.0% for per 1-SD increment in serum 25(OH)D concentrations. A nonlinear association of serum 25(OH)D concentrations with CRC risk was observed using a restricted cubic spline analysis (P nonlinearity = 0.002). CONCLUSIONS: Higher serum 25(OH)D concentrations were significantly and nonlinearly associated with a lower risk of CRC. These findings highlight the potential benefits of maintaining adequate vitamin D levels in CRC prevention among adults with T2D.

Associations of long-term joint exposure to various ambient air pollutants with all-cause and cause-specific mortality: evidence from a large population-based cohort study.

The association between long-term joint exposure to all kinds of ambient air pollutants and the risk of mortality is not known. Our study prospectively assessed the joint associations of various air pollutants with cause-specific and all-cause mortality risk and identified potential modifying factors affecting these associations. A total of 400,259 individuals aged 40-70 years were included in this study. Information on PM10, PM2.5-10, PM2.5, NO2, and NOx was collected. A weighted air pollution score was calculated to assess joint exposure to the above air pollutants. Hazard ratios (HRs) and 95% confidence intervals (CIs) were estimated using Cox proportional hazards models. During a median of 12.0 years (4,733,495 person-years) of follow-up, 21,612 deaths were recorded, including 7097 deaths from cardiovascular disease and 11,557 deaths from cancer. The adjusted HRs of all-cause mortality were 1.39 (95% CI: 1.29-1.50), 1.86 (95% CI: 1.63-2.13), 1.12 (95% CI: 1.10-1.14), and 1.04 (95% CI: 1.03-1.05) for every 10-ug/m3 increase in PM10, PM2.5, NO2, and NOx, respectively. The adjusted HRs associated with the air pollution score (the highest quintile versus the lowest quintile) were 1.24 (95% CI: 1.19-1.30) for all-cause mortality, 1.33 (95% CI: 1.23-1.43) for cardiovascular mortality, and 1.16 (95% CI: 1.09-1.23) for cancer mortality. Furthermore, we found that the air pollution score was associated with a linear dose-response increase in mortality risk (all P for linearity < 0.001). The findings highlight the importance of a comprehensive assessment of various air pollutants.

Association of Night Shifts and Lifestyle Risks With Incident Dementia.

BACKGROUND: Little is known about the combined relationship between night shifts and lifestyle risks with incident dementia or their potential interactions. To evaluate the association of night shifts and lifestyle risks with incident dementia and further analyze their interactions. METHODS: A total of 276 059 participants were included in this study from the UK Biobank cohort. Cox proportional hazards models were used to investigate the combined association of night shifts and lifestyle risks with incident dementia. RESULTS: Participants with always night shifts and 3 or 4 unhealthy lifestyle factors had the highest risk of incident all-cause dementia (hazard ratio: 3.15, 95% confidence interval [CI]: 1.74-5.69). An additive interaction was found between night shifts and lifestyle risks for incident all-cause dementia (p < .001), with a relative excess risk due to the interaction of 0.14 (95% CI: 0.11-0.45). The attributable proportions of the combined effect on the incidence of all-cause dementia were 22.6% (95% CI: 20.91%-26.75%) for night shift work, 65.0% (95% CI: 63.12%-69.80%) for unhealthy lifestyle factors, and 12.1% (95% CI: 8.67%-18.04%) for their interaction. CONCLUSIONS: Both night shifts and lifestyle risks were associated with a higher risk of incident dementia. The combined impact was higher than the increase in the risks related to each single factor. Our results indicated that most incident dementia cases might be prevented by a healthy lifestyle, and the benefits would be greater among night shift workers. Further studies are needed to confirm our results and explore the underlying mechanisms.

Dietary diversity and frailty among older Chinese people: evidence from the Chinese Longitudinal Healthy Longevity Study.

BACKGROUND: Dietary diversity is widely advocated as a means to promote health, but little is known regarding whether the beneficial effects still apply in older adults. OBJECTIVE: To examine the association between the dietary diversity score (DDS) and frailty among older Chinese adults. METHODS: A total of 13,721 adults aged ≥65 y without frailty at baseline were enrolled. The DDS at baseline was constructed based on 9 items of a food frequency questionnaire. We used 39 self-reported health items to construct a frailty index (FI), with FI ≥ 0.25 indicating frailty. Cox models with restricted cubic splines were used to evaluate the dose-response relationships of DDS (continuous) with frailty. In addition, Cox proportional hazard models were used to examine the association between DDS (categorized as scores ≤4, 5-6, 7, and ≥8) and frailty. RESULTS: During the mean follow-up of 5.94 y, 5250 participants met the criteria for frailty. Each 1-unit increase in DDS corresponded to a 5% lower risk of frailty (hazard ratio [HR]; 0.95; 95% CI: 0.94, 0.97]. Compared with participants with DDS ≤4 points, those with a DDS of 5-6, 7, and ≥8 points exhibited a lower frailty risk, with HRs of 0.79 (95% CI: 0.71, 0.87), 0.75 (95% CI: 0.68, 0.83), and 0.74 (95% CI: 0.67, 0.81), respectively (P-trend < 0.001). Protein-rich food items, such as meat; eggs; and beans, were associated with protective effects against frailty. In addition, a significant association was observed between higher consumption of 2 high-frequency foods, tea and fruits, and lower risk of frailty. CONCLUSIONS: A higher DDS was associated with a lower risk of frailty among older Chinese adults. This study highlights the importance of a diverse diet as a potential modifiable behavioral factor for preventing frailty in older Chinese adults.

Association of physical activity and air pollution exposure with the risk of type 2 diabetes: a large population-based prospective cohort study.

BACKGROUND: The interplay between physical activity (PA) and air pollution in relation to type 2 diabetes (T2D) remains largely unknown. Based on a large population-based cohort study, this study aimed to examine whether the benefits of PA with respect to the risk of T2D are moderated by exposure to air pollution. METHODS: UK Biobank participants (n = 359,153) without diabetes at baseline were included. Information on PA was obtained using the International Physical Activity Questionnaire short form. Exposure to air pollution, including PM2.5, PMcoarse (PM2.5-10), PM10, and NO2, was estimated from land use regression models. Cox regression models were used to estimate the hazard ratios (HRs) and 95% confidence intervals (95% CIs). RESULTS: During a median of 8.9 years of follow-up, 13,706 T2D events were recorded. Compared with a low PA level, the HRs for the risk of T2D among individuals with moderate and high PA were 0.82 (95% CI, 0.79-0.86) and 0.73 (95% CI, 0.70-0.77), respectively. Compared with low levels of air pollution, the HRs for risk of T2D for high levels of air pollution (PM2.5, PMcoarse, PM10, and NO2) were 1.19 (1.14-1.24), 1.06 (1.02-1.11), 1.13 (1.08-1.18), and 1.19 (1.14-1.24), respectively. There was no effect modification of the associations between PA and T2D by air pollution (all P-interactions > 0.05). The inverse associations between PA and T2D in each air pollution stratum were generally consistent (all P for trend < 0.05). CONCLUSION: A higher PA and lower air pollution level were independently associated with a lower risk of T2D. The beneficial effects of PA on T2D generally remained stable among participants exposed to different levels of air pollution. Further studies are needed to replicate our findings in moderately and severely polluted areas.

Habitual fish oil supplementation and incident chronic obstructive pulmonary disease: Data from a prospective cohort study.

BACKGROUND: Fish oil is one of the most popular supplements in the UK and other developed countries. However, the relationship between fish oil use and chronic obstructive pulmonary disease (COPD) is unclear. OBJECTIVE: To prospectively examine the association of habitual fish oil supplementation with incident COPD risk and to evaluate potential effect modification by genetic predisposition. METHODS: This study included 484,414 participants (mean and standard deviation [SD] age: 56.5 [8.1] years) from the UK Biobank who completed a touchscreen questionnaire on habitual fish oil supplement use between 2006 and 2010 and were followed up through 2018. Cox regression models were used to estimate the hazard ratios (HRs) and 95% confidence intervals (95% CIs) with adjustment for sociodemographic and lifestyle behaviours, health conditions, and other potential confounding factors. A weighted genetic risk score (GRS) for COPD was derived from 112 validated single nucleotide polymorphisms. RESULTS: During a median follow-up of 9.0 years, 8860 incident COPD events were recorded. A total of 31.4% (152,230) of the study participants reported habitual fish oil supplementation at baseline. Habitual fish oil supplementation was significantly associated with a lower risk of incident COPD (adjusted HR: 0.88; 95% CI: 0.84-0.93). The association with COPD did not differ by GRS strata (P for interaction = 0.880). The results from subgroup and sensitivity analyses supported the robustness of our findings. CONCLUSIONS: Our findings suggest that habitual fish oil supplementation is associated with a lower risk of incident COPD, irrespective of genetic predisposition.

Association of Combined Lifestyle and Polygenetic Risk with Incidence of Venous Thromboembolism: A Large Population-Based Cohort Study.

As one of the fatal complications, venous thromboembolism (VTE) is associated with increased mortality. However, the combined effects of adopting multiple healthy lifestyles have not been firmly demonstrated. This study was to evaluate the association of combined healthy lifestyles and genetic risk factors with VTE and to investigate their interaction. A prospective cohort study from UK Biobank with a total of 442,963 men and women aged between 38 to 73 years were recruited from 2006 to 2010 and followed up through 2017 or 2018. A polygenic risk score was constructed and a weighted healthy lifestyle score, including no current smoking, regular physical exercises, healthy diet, and healthy body mass index, was categorized. During a median follow-up 9.0 years (3,912,396 person-years), there were 6,736 (172 per 100,000 person-years) incident VTE cases recorded. Among the participants with an unfavorable lifestyle, 1.80% developed VTE, versus 1.03% of the participants with a favorable lifestyle (hazard ratio [HR]: 1.58; 95% confidence interval [CI]: 1.48-1.68). Of the participants with high genetic risk, 2.42% developed VTE, versus 0.97% of the participants with low genetic risk (HR: 2.60; 95% CI: 2.39-2.81). Moreover, of the participants with high genetic risk and unfavorable lifestyle, 2.90% developed VTE, versus 0.66% of the participants with low genetic risk and favorable lifestyle (HR: 4.09; 95% CI: 3.48-4.79). No significant interaction between genetic risk and lifestyle factors was observed (p for interaction = 0.727). An unfavorable lifestyle was associated with a substantially higher risk of VTE, regardless of the genetic risk strata.

Association of Sugar-Sweetened, Artificially Sweetened, and Unsweetened Coffee Consumption With All-Cause and Cause-Specific Mortality : A Large Prospective Cohort Study.

BACKGROUND: Previous observational studies have suggested an association between coffee intake and reduced risk for death, but these studies did not distinguish between coffee consumed with sugar or artificial sweeteners and coffee consumed without. OBJECTIVE: To evaluate the associations of consumption of sugar-sweetened, artificially sweetened, and unsweetened coffee with all-cause and cause-specific mortality. DESIGN: Prospective cohort study. SETTING: Data were extracted from the UK Biobank. PARTICIPANTS: A total of 171 616 participants (mean age, 55.6 years [SD, 7.9]) without cardiovascular disease (CVD) or cancer at baseline were eligible. Baseline demographic, lifestyle, and dietary data from the UK Biobank were used, with follow-up beginning in 2009 and ending in 2018. MEASUREMENTS: Dietary consumption of sugar-sweetened, artificially sweetened, and unsweetened coffee was self-reported. All-cause, cancer-related, and CVD-related mortality were estimated. RESULTS: During a median follow-up of 7.0 years, 3177 deaths were recorded (including 1725 cancer deaths and 628 CVD deaths). Cox models with penalized splines showed U-shaped associations of unsweetened coffee, sugar-sweetened coffee, and artificially sweetened coffee with mortality. Compared with nonconsumers, consumers of various amounts of unsweetened coffee (>0 to 1.5, >1.5 to 2.5, >2.5 to 3.5, >3.5 to 4.5, and >4.5 drinks/d) had lower risks for all-cause mortality after adjustment for lifestyle, sociodemographic, and clinical factors, with respective hazard ratios of 0.79 (95% CI, 0.70 to 0.90), 0.84 (CI, 0.74 to 0.95), 0.71 (CI, 0.62 to 0.82), 0.71 (CI, 0.60 to 0.84), and 0.77 (CI, 0.65 to 0.91); the respective estimates for consumption of sugar-sweetened coffee were 0.91 (CI, 0.78 to 1.07), 0.69 (CI, 0.57 to 0.84), 0.72 (CI, 0.57 to 0.91), 0.79 (CI, 0.60 to 1.06), and 1.05 (CI, 0.82 to 1.36). The association between artificially sweetened coffee and mortality was less consistent. The association of coffee drinking with mortality from cancer and CVD was largely consistent with that with all-cause mortality. U-shaped associations were also observed for instant, ground, and decaffeinated coffee. LIMITATION: Exposure assessed at baseline might not capture changes in intake over time. CONCLUSION: Moderate consumption of unsweetened and sugar-sweetened coffee was associated with lower risk for death. PRIMARY FUNDING SOURCE: National Natural Science Foundation of China, Young Elite Scientist Sponsorship Program by CAST, and Project Supported by Guangdong Basic and Applied Basic Research Foundation.

Non-Pharmaceutical Interventions Implemented to Control the COVID-19 Were Associated With Reduction of Influenza Incidence.

BACKGROUND: Non-pharmaceutical interventions were implemented in most countries to reduce the transmission of COVID-19. We aimed to describe the incidence of influenza in four countries in the 2019-2020 season and examined the effect of these non-pharmaceutical interventions on the incidence of influenza. METHODS: We used the network surveillance data from 2015 to 2020 to estimate the percentage increase in influenza cases to explore the effect of non-pharmaceutical interventions implemented to control the COVID-19 on the incidence of influenza in China, the United States, Japan, and Singapore. RESULTS: We found that the incidence of influenza has been almost zero and reached a persistent near-zero level for a continuous period of six months since epidemiologic week 14 of 2020 in the four countries. Influenza incidence decreased by 77.71% and 60.50% in the early days of COVID-19 in the 2019-2020 season compared to the same period in preceding years in Japan and Singapore, respectively. Furthermore, influenza incidence decreased by 60.50-99.48% during the period of compulsory interventions in the 2019-2020 season compared to the same period in preceding years in the four countries. CONCLUSION: These findings suggest that the application of non-pharmaceutical interventions, even everyday preventive action, was associated with a reduction of influenza incidence, which highlights that more traditional public health interventions need to be reasserted and universalized to reduce influenza incidence.

Association between Dietary Diversity Changes and Cognitive Impairment among Older People: Findings from a Nationwide Cohort Study.

BACKGROUND: Little is known about the role of dietary diversity changes in affecting cognitive function among older people. Therefore, we aimed to evaluate the associations between dietary diversity scores (DDS) changes with cognitive impairment among older adults in a large prospective cohort. METHODS: Cognitive function was assessed using the Mini-Mental State Examination questionnaire at baseline and follow-up. A total of 9726 participants without Parkinson's disease, dementia, or cognitive impairment were enrolled at baseline. Nine food groups were collected using simplified FFQ at baseline and follow-up surveys. Then nine food groups change patterns and DDS change patterns (overall, plant-based and animal-based) were assessed. The associations of above DDS changes patterns with subsequent cognitive impairment were evaluated. A multivariable-adjusted Cox proportional hazards model was used to estimate HRs and 95%CIs. RESULTS: We documented 2805 cognitive impairments during 52,325 person-years of follow-up. Compared to high-to-high overall DDS change patterns, the multivariable adjusted HRs (95%CI) for high-to-medium, medium-to-medium, medium-to-low, low-to-medium and low-to-low DDS change patterns were 1.33 (1.12-1.57), 1.11 (0.94-1.32), 1.61 (1.39-1.86), 2.00 (1.66-2.40), 2.30 (1.90-2.78) and 2.80 (2.23-3.53), respectively. Compared with participants with stable DDS change pattern, those who in large improvement of DDS had a 13% lower risk of cognitive impairment (HRs, 0.87; 95%CI: 0.78-0.98). The associations of plant-based DDS, animal-based DDS, or nine food groups DDS change patterns with cognitive impairment were in a similar direction to the main result. CONCLUSIONS: Protective associations between maintaining high DDS and a reduced risk of cognitive impairment were observed. In contrast, lowering or maintaining a lower DDS increases the risk of cognitive impairment.

Associations Between High-Sensitivity C-Reactive Protein and All-Cause Mortality Among Oldest-Old in Chinese Longevity Areas: A Community-Based Cohort Study.

BACKGROUND: The association between high-sensitivity C-reactive protein (hsCRP) levels and all-cause mortality for the oldest-old (aged 80 years or older) remains unclear. We aimed to investigate the associations between hsCRP concentrations and the risks of all-cause mortality, and further identify the potential modifying factors affecting these associations among the oldest-old. METHODS: This prospective, community-based cohort study included 2,206 participants aged 80 years or older (median age 93.0 years) from the Healthy Aging and Biomarkers Cohort Study. Cox proportional hazards regression models were used to estimate hazard ratios (HRs) with 95% confidential intervals (95% CIs) for all-cause mortality according to hsCRP quartiles and recommendation for relative risk categories of hsCRP levels (< 1.0, 1.0-3.0, and > 3.0 mg/L), with adjustment for sociodemographic information, lifestyle, physical examination, medical history, and other potential confounders. RESULTS: During a median follow-up period of 3.1 years (IQR: 1.6-3.9 years), 1,106 deaths were verified. After full adjustment for potential confounders, a higher hsCRP concentration was positively associated with an increased risk of all-cause mortality (P for trend < 0.001). Compared with the lowest quartile, the fully adjusted HRs of the second, third, and fourth quartiles were 1.17 (95% CI: 0.94, 1.46), 1.28 (95% CI: 1.01, 1.61), and 1.49 (95% CI: 1.20, 1.87), respectively. The association of hsCRP with all-cause mortality was modified by smoking status (P for interaction = 0.011), an increased risk of hsCRP with all-cause mortality showed among non-current smokers (HR: 1.17; 95% CI: 1.07, 1.28), but no significance was observed in current smokers (HR: 0.83; 95% CI: 0.66, 1.18). CONCLUSIONS: Our study indicated that elevated hsCRP concentrations were associated with a higher risk of all-cause mortality among Chinese oldest-old. Future studies investigating additional factors of disease and aging processes are needed to obtain a better understanding of the mechanisms.

Association of smoking and polygenic risk with the incidence of lung cancer: a prospective cohort study.

BACKGROUND: Genetic variation increases the risk of lung cancer, but the extent to which smoking amplifies this effect remains unknown. Therefore, we aimed to investigate the risk of lung cancer in people with different genetic risks and smoking habits. METHODS: This prospective cohort study included 345,794 European ancestry participants from the UK Biobank and followed up for 7.2 [6.5-7.8] years. RESULTS: Overall, 26.2% of the participants were former smokers, and 9.8% were current smokers. During follow-up, 1687 (0.49%) participants developed lung cancer. High genetic risk and smoking were independently associated with an increased risk of incident lung cancer. Compared with never-smokers, HR per standard deviation of the PRS increase was 1.16 (95% CI, 1.11-1.22), and HR of heavy smokers (≥40 pack-years) was 17.89 (95% CI, 15.31-20.91). There were no significant interactions between the PRS and the smoking status or pack-years. Population-attributable fraction analysis showed that smoking cessation might prevent 76.4% of new lung cancers. CONCLUSIONS: Both high genetic risk and smoking were independently associated with higher lung cancer risk, but the increased risk of smoking was much more significant than heredity. The combination of traditional risk factors and additional PRS provides realistic application prospects for precise prevention.

Tooth Loss, Denture Use, and Cognitive Impairment in Chinese Older Adults: A Community Cohort Study.

BACKGROUND: Evidence regarding the associations of tooth loss and denture use with incident cognitive impairment is inconclusive in older adults, and few prospective studies have examined the potential interaction between tooth loss and denture use in these specific populations. METHODS: Data were assessed from 17 079 cognitively normal older adults aged ≥65 years, participating in the Chinese Longitudinal Healthy Longevity Survey. The outcome of interest was cognitive impairment (assessed by the Chinese version of Mini-Mental State Examination). The number of natural teeth and status of denture use were collected by a structural questionnaire. RESULTS: A total of 6456 cases of cognitive impairment were recorded during 88 627 person-years of follow-up. We found that compared with participants with 20+ teeth, those with 10-19, 1-9, and 0 teeth had increased risks of incident cognitive impairment (p-trend < .001). Participants without dentures also had a higher risk of incident cognitive impairment, compared with those who wore dentures. Effect modification by denture use was observed (p-interaction = .010). Specifically, among those without dentures, the adjusted hazard ratio (95% confidence interval) for participants with 10-19, 1-9, and 0 teeth were 1.19 (1.08, 1.30), 1.28 (1.17, 1.39), and 1.28 (1.16, 1.41), respectively, as compared to those with 20+ teeth. In contrary, among denture users, detrimental effect was only observed among those with 0 teeth (hazard ratio 1.14, 95% confidence interval: 1.16, 1.41). CONCLUSIONS: In Chinese older adults, maintaining 20+ teeth is important for cognitive health; denture use would attenuate the detrimental effects of tooth loss, especially for partial tooth loss, on cognitive impairment.

Glucosamine use, smoking and risk of incident chronic obstructive pulmonary disease: a large prospective cohort study.

Chronic inflammation exerts pleiotropic effects in the aetiology and progression of chronic obstructive pulmonary disease (COPD). Glucosamine is widely used in many countries and may have anti-inflammatory properties. We aimed to prospectively evaluate the association of regular glucosamine use with incident COPD risk and explore whether such association could be modified by smoking in the UK Biobank cohort, which recruited more than half a million participants aged 40-69 years from across the UK between 2006 and 2010. Cox proportional hazards models with adjustment for potential confounding factors were used to calculate hazard ratios (HR) as well as 95 % CI for the risk of incident COPD. During a median follow-up of 8·96 years (interquartile range 8·29-9·53 years), 9016 new-onset events of COPD were documented. We found that the regular use of glucosamine was associated with a significantly lower risk of incident COPD with multivariable adjusted HR of 0·80 (95 % CI, 0·75, 0·85; P < 0·001). When subgroup analyses were performed by smoking status, the adjusted HR for the association of regular glucosamine use with incident COPD were 0·84 (0·73, 0·96), 0·84 (0·77, 0·92) and 0·71 (0·62, 0·80) among never smokers, former smokers and current smokers, respectively. No significant interaction was observed between glucosamine use and smoking status (Pfor interaction = 0·078). Incident COPD could be reduced by 14 % to 84 % through a combination of regular glucosamine use and smoking cessation.

Healthy Sleep Associated With Lower Risk of Hypertension Regardless of Genetic Risk: A Population-Based Cohort Study.

Background: Hypertension is a leading contributor to the global burden of disease and to mortality. The combined effects of sleep factors on the risk of hypertension are unclear. We aimed to evaluate the effect of combined sleep factors on the risk of hypertension and to explore whether this association is independent of genetic risk. Methods: This population-based prospective cohort study included 170,378 participants from the UK Biobank study. We conducted a healthy sleep score based on a combination of major five sleep factors and a genetic risk score based on 118 risk variants. Cox proportional hazard regression models were used to estimate hazard ratios (HRs) and 95% confidence intervals (CIs). Results: A total of 170,378 participants were included. Compared to participants with a healthy sleep score of 0-1, those with healthy sleep scores of 2 (HR, 0.90; 95% CI, 0.83-0.98), 3 (HR, 0.81; 95% CI, 0.75-0.88), 4 (HR, 0.74; 95% CI, 0.68-0.81), or 5 (HR, 0.67; 95% CI, 0.59-0.77) had increasingly lower risks of hypertension (P for trend <0.001). Participants with high genetic risk and an unfavorable sleep pattern had a 1.80-fold greater risk of hypertension than participants with low genetic risk and a favorable sleep pattern. The association between sleep patterns and hypertension persisted in subgroup analysis, stratified by the genetic risk. Nearly 18.2% of hypertension events in this cohort could be attributed to unfavorable sleep pattern. Conclusions: Favorable sleep pattern was associated with a low risk of hypertension, regardless of genetic risk. These findings highlight the potential of sleep interventions to reduce risk of hypertension across entire populations.

Association of sleep and circadian patterns and genetic risk with incident type 2 diabetes: a large prospective population-based cohort study.

OBJECTIVE: To examine the association of incident type 2 diabetes (T2D) risk with sleep factors, genetic risk, and their combination effects. DESIGN: Large prospective population-based cohort study. METHODS: This population-based prospective cohort study included 360 403 (mean (s.d.) age: 56.6 (8.0) years) participants without T2D at baseline from the UK Biobank. Genetic risk was categorised as high (highest quintile), intermediate (quintiles: 2-4), and low (lowest quintile) based on a polygenic risk score for T2D. Sleep scores, including long or short sleep duration, insomnia, snoring, late chronotype, and excessive daytime sleepiness, were categorized as an unfavourable, intermediate, or favourable sleep and circadian pattern. RESULTS: During a median follow-up of 9.0 years, 13 120 incident T2D cases were recorded. Among the participants with an unfavourable sleep and circadian pattern, 6.96% (95% CI: 6.68-7.24%) developed T2D vs 2.37% (95% CI: 2.28-2.46%) of participants with a favourable sleep and circadian pattern (adjusted hazard ratio (HR): 1.53, 95% CI: 1.45-1.62). Of participants with a high genetic risk, 5.53% (95% CI: 5.36-5.69%) developed T2D vs 2.01% (95% CI: 1.91-2.11%) of participants with a low genetic risk (adjusted HR: 2.89, 95% CI: 2.72-3.07). The association with sleep and circadian patterns was independent of genetic risk strata. Participants in the lowest quintile with an unfavourable sleep and circadian pattern were 3.97-fold more likely to develop T2D than those in the lowest quintile with a favourable sleep and circadian pattern. CONCLUSIONS: Sleep and circadian patterns and genetic risk were independently associated with incident T2D. These results indicate the benefits of adhering to a healthy sleep and circadian pattern in entire populations, independent of genetic risk.

Association of dietary diversity changes and mortality among older people: A prospective cohort study.

BACKGROUND & AIMS: The association between dietary diversity (DD) changes and mortality remains unclear. We aimed to investigate the association between DD changes and all-cause mortality among older people. METHODS: A total of 17,959 participants with a mean age of 84.8 years old were enrolled at baseline. Food groups were collected at baseline and follow-up using simplified food frequency questionnaire (FFQ), and then overall, plant-based and animal-based dietary diversity score (DDS) were calculated. DDS changes were calculated using DDS at baseline and the first follow-up. The association between three DDS changes (overall, plant-based and animal-based DDS) and subsequent all-cause mortality were evaluated. Nonparametrically restricted cubic splines and a multivariable-adjusted Cox proportional hazards model were used to estimate HRs and 95% CIs. RESULTS: We documented 12,974 deaths over a 129,590 person-years of follow up. Compared with high-to-high DDS pattern, participants with lower overall DDS patterns had increased mortality risk with HRs (95%CI) of 1.39 (1.29-1.49), 1.53 (1.37-1.70), 1.38 (1.18-1.60) and 1.55 (1.31-1.83) for medium-to-medium, low-to-low, low-to-high and high-to-low patterns, respectively. And compared with high-to-high DDS pattern, the estimates were 1.34 (1.23-1.46), 1.49 (1.35-1.65), 1.43 (1.23-1.67) and 1.62 (1.40-1.88) for plant-based DDS, and 1.23 (1.15-1.31), 1.29 (1.20-1.40), 1.24 (1.12-1.37) and 1.28 (1.15-1.44) for animal-based DDS for medium-to-medium, low-to-low, low-to-high and high-to-low patterns, respectively. There was a U-shaped association between DDS change scores and mortality, and compared with participants with whose DDS remained stable, those with extreme declines and extreme improvements had higher risks of mortality with HRs (95% CI) of 1.15 (1.09-1.22) and 1.11 (1.04-1.17). CONCLUSIONS: Maintaining a lower DDS, extreme declines and extreme improvements in DDS were all associated with an increased risk of all-cause mortality.