Associations between antipsychotics exposure and dementia risk: A prospective cohort study of 415,100 participants.

BACKGROUND: Antipsychotics (APs) are among the most widely prescribed medications, and have been shown to cause cognitive decline. But previous studies on their effects on dementia risk are controversial and scarce. We aimed to examine the relationships of APs exposure with the risk of dementia. METHODS: Data were obtained from a prospective cohort of 415,100 UK Biobank (UKB) participants. We investigated the effects of APs exposure and their various classes on dementia risk by using multivariable Cox proportional hazard models and further the dose-response effects of oral APs. RESULTS: After a mean follow-up of 8.64 years, 5235 (1.3 %) participants developed all-cause dementia (ACD), among whom 2313 (0.6 %) developed Alzheimer's disease (AD), and 1213 (0.3 %) developed vascular dementia (VaD). Exposure to any APs conferred increased risks of ACD (HR: 1.33, 95 % CI = 1.17-1.51, P < 0.001) and VaD (HR: 1.90, 95 % CI = 1.51-2.40, P < 0.001), but not AD (HR: 1.22, 95 % CI = 1.00-1.48, P = 0.051). Cumulative dose-response relationships of oral APs with the risks of ACD and VaD were observed (P for trend, P < 0.05). LIMITATIONS: Our study is observational and does not show evidence of causality. Since there are relatively few cases of dementia in the UKB, APs exposure may be higher than estimated in our study. CONCLUSIONS: APs exposure increased the risk of developing dementia. Dose-response relationships were found between oral APs and dementia risk. Efforts to raise awareness of doctors and patients about this potential drug-related risk are critical to reducing APs use.

Associations of dietary B vitamins intakes with depression in adults.

Background: The impact of the dietary B vitamins intakes on the development of depression has been scarcely investigated. Thus, this study aimed to examine the associations of dietary B vitamins intakes with the risk of depression in American adults. Methods: The data we used in this study were from the National Health and Nutrition Examination Survey (NHANES) 2007-2014. We used the Logistic regression models to analyze the associations of the dietary intakes of B vitamins with the risk of depression. Results: 17,732 individuals (8,623 males and 9,109 females) were enrolled in the study and they were all 18 or older. Compared to the lowest quartile of dietary intake, the ORs (95%CIs) of the highest quartile were 0.64 (0.50-0.82), 0.78 (0.62-0.97), 0.60 (0.47-0.78), 0.65 (0.50-0.84), and 0.71 (0.54-0.95) for vitamin B1, vitamin B2, niacin, vitamin B6, and vitamin B12, respectively. Compared to the people whose dietary intakes below the RDA in the model 2, those with intake meeting the RDA of vitamin B1 (OR: 0.68; 95%CI: 0.56-0.84), niacin (OR: 0.65; 95%CI: 0.51-0.81), B6 (OR: 0.65; 95%CI: 0.52-0.81), or B12 (OR: 0.65; 95%CI: 0.48-0.88) had a lower risk of depression, severally. We also found a nonlinear negative association between dietary vitamin B1, vitamin B2, niacin, vitamin B6, and vitamin B12 intakes and the risk of depression in the dose-response analyses, severally. Conclusions: Our results suggested that dietary vitamin B1, vitamin B2, niacin, vitamin B6, and vitamin B12 intakes may be inversely associated with the risk of depression.

Abdominal obesity increases the risk of reflux esophagitis: a systematic review and meta-analysis.

BACKGROUND AND OBJECTIVES: The association between abdominal obesity and reflux esophagitis (RE) has been extensively evaluated, but the current findings are mixed and more convincing epidemiological evidence urgently needs to be established. To thoroughly explore this relationship, we summarized the latest studies, performed an updated meta-analysis, and examined the dose-response relationship. METHODS: We performed a systematic search of PubMed, Web of Science, and Embase up to 28 March 2021, using prespecified terms to identify studies investigating the association between abdominal obesity and RE. Odds ratios (ORs) with 95% confidence intervals (CIs), mean differences (MDs) or standardized mean differences (SMDs) with 95% CIs were taken as effect-size estimates. RESULTS: Forty-two observational studies, including 11 cohort studies, were meta-analyzed. Overall, a statistically significant association was observed between abdominal obesity and RE, by both the pooled OR (adjusted OR = 1.51, 95% CI: 1.37-1.66, p < .001) and the pooled SMD (SMD = 0.36, 95% CI: 0.30-0.42, p < .001). Moreover, this significant relationship persisted with subgroup stratification. In subgroup analyses, we found that study design, abdominal obesity measurement, adjustment for covariates and sex were possible sources of between-study heterogeneity. For the dose-response analyses, the risk of RE increased with the degree of abdominal obesity, and the increasing trend accelerated when waist circumference (WC) reached 87.0 cm. CONCLUSION: This meta-analysis indicated a significant association between abdominal obesity and RE, and the risk of RE increased with abdominal obesity especially when the WC was over 87.0 cm.

Coffee consumption and risk of bladder cancer: a pooled analysis of 501,604 participants from 12 cohort studies in the BLadder Cancer Epidemiology and Nutritional Determinants (BLEND) international study.

Recent epidemiological studies have shown varying associations between coffee consumption and bladder cancer (BC). This research aims to elucidate the association between coffee consumption and BC risk by bringing together worldwide cohort studies on this topic. Coffee consumption in relation to BC risk was examined by pooling individual data from 12 cohort studies, comprising of 2601 cases out of 501,604 participants. Pooled multivariate hazard ratios (HRs), with corresponding 95% confidence intervals (CIs), were obtained using multilevel Weibull regression models. Furthermore, dose-response relationships were examined using generalized least squares regression models. The association between coffee consumption and BC risk showed interaction with sex (P-interaction < 0.001) and smoking (P-interaction = 0.001). Therefore, analyses were stratified by sex and smoking. After adjustment for potential confounders, an increased BC risk was shown for high (> 500 ml/day, equivalent to > 4 cups/day) coffee consumption compared to never consumers among male smokers (current smokers: HR = 1.75, 95% CI 1.27-2.42, P-trend = 0.002; former smokers: HR = 1.44, 95% CI 1.12-1.85, P-trend = 0.001). In addition, dose-response analyses, in male smokers also showed an increased BC risk for coffee consumption of more than 500 ml/day (4 cups/day), with the risk of one cup (125 ml) increment as 1.07 (95% CI 1.06-1.08). This research suggests that positive associations between coffee consumption and BC among male smokers but not never smokers and females. The inconsistent results between sexes and the absence of an association in never smokers indicate that the associations found among male smokers is unlikely to be causal and is possibly caused by residual confounding of smoking.

The association between coffee consumption and bladder cancer in the bladder cancer epidemiology and nutritional determinants (BLEND) international pooled study.

BACKGROUND: Inconsistent results for coffee consumption and bladder cancer (BC) risk have been shown in epidemiological studies. This research aims to increase the understanding of the association between coffee consumption and BC risk by bringing together worldwide case-control studies on this topic. METHODS: Data were collected from 13 case-control comprising of 5,911 cases and 16,172 controls. Pooled multivariate odds ratios (ORs), with corresponding 95% confidence intervals (CIs), were obtained using multilevel logistic regression models. Furthermore, linear dose-response relationships were examined using fractional polynomial models. RESULTS: No association of BC risk was observed with coffee consumption among smokers. However, after adjustment for age, gender, and smoking, the risk was significantly increased for never smokers (ever vs. never coffee consumers: ORmodel2 1.30, 95% CI 1.06-1.59; heavy (> 4 cups/day) coffee consumers vs. never coffee consumers: ORmodel2 1.52, 95% CI 1.18-1.97, p trend = 0.23). In addition, dose-response analyses, in both the overall population and among never smokers, also showed a significant increased BC risk for coffee consumption of more than four cups per day. Among smokers, a significant increased BC risk was shown only after consumption of more than six cups per day. CONCLUSION: This research suggests that positive associations between coffee consumption and BC among never smokers but not smokers.

Quantified relations between exposure to tobacco smoking and bladder cancer risk: a meta-analysis of 89 observational studies.

BACKGROUND: Smoking is a major risk factor for bladder cancer (BC). This meta-analysis updates previous reviews on smoking characteristics and BC risk, and provides a more quantitative estimation of the dose-response relationship between smoking characteristics and BC risk. METHODS: In total, 89 studies comprising data from 57 145 BC cases were included and summary odds ratios (SORs) were calculated. Dose-response meta-analyses modelled relationships between smoking intensity, duration, pack-years and cessation and BC risk. Sources of heterogeneity were explored and sensitivity analyses were conducted to test the robustness of findings. RESULTS: Current smokers (SOR = 3.14, 95% CI = 2.53-3.75) and former smokers(SOR = 1.83, 95% CI = 1.52-2.14) had an increased risk of BC compared with never smokers. Age at first exposure was negatively associated with BC risk. BC risk increased gradually by smoking duration and a risk plateau at smoking 15 cigarettes a day and 50 pack-years was observed. Smoking cessation is most beneficial from 20 years before diagnosis. The population-attributable risk of BC for smokers has decreased from 50% to 43% in men and from 35% to 26% in women from Europe since estimated in 2000. Results were homogeneous between sources of heterogeneity, except for lower risk estimates found in studies of Asian populations. CONCLUSIONS: Active smokers are at an increased risk of BC. Dose-response meta-analyses showed a BC risk plateau for smoking intensity and indicate that even after long-term smoking cessation, an elevated risk of bladder cancer remains.