Alcohol consumption and gastric cancer risk: a meta-analysis of prospective cohort studies.
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ABSTRACT:
SUBMITTER: Han X
PROVIDER: S-EPMC5669963 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:Alcohol consumption is inconsistently associated with the risk of gastric cancer morbidity and mortality. The aim of this study was to systematically evaluate the association between alcohol consumption on gastric cancer risk. The PubMed, Embase, and Cochrane Library databases were searched from inception through April 2017. Prospective cohort studies evaluating the association between alcohol consumption and risk of gastric cancer which report its effect estimates with 95% confidence intervals (CIs) were included. The results summary was performed using the random-effect model. Twenty-two cohort studies involving 22,545 cases of gastric cancer and 5,820,431 participants were identified and included in our data analysis. Overall, drinking had little or no effect on gastric cancer as compared with non-drinkers. Furthermore, light and moderate alcohol consumption had no significant effect on gastric cancer risk when compared with non-drinkers. However, heavy alcohol consumption was associated with a greater risk of gastric cancer when compared with non-drinkers. The findings of the subgroup analyses indicated that light alcohol consumption was associated with a lower risk of gastric cancer in women, while heavy alcohol consumption was associated with an increased risk of gastric cancer regardless of country, gender, whether the study reported gastric cancer incidence, or whether the study adjusted for body mass index, educational attainment, or physical activity. The findings of this study suggest that light alcohol consumption might play a protective effect on gastric cancer in women, while heavy alcohol consumption is associated with a significantly increased risk of gastric cancer in all subgroups.
| S-EPMC5663611 | biostudies-literature
Project description:BackgroundControversial results of the association between alcohol consumption and risk of bladder cancer were reported by the previous meta-analyses.ObjectiveTo quantitatively investigate the association between alcohol consumption and risk of bladder cancer based on prospective cohort studies, and explore whether there is potential dose-response relation.MethodPubMed, EMBASE, the Cochrane Library databases, China Biology Medicine disc (CBM), and Chinese National Knowledge Infrastructure (CNKI) were searched for relevant studies. Categorical meta-analysis was performed for risk estimates of any alcohol consumers versus non-drinkers as well as different drinking degrees (light, moderate, and heavy) versus none. And two-stage generalized least-squares regression and restricted cubic spline, as well as fixed-effects dose-response models, were used for linear and nonlinear dose-response relation exploration.Results9 prospective cohort studies including 1,971,396 individuals were finally included. We did not observe a significant association between alcohol intake and the risk of bladder cancer in the entire population. Linear association was detected in those who consumed alcohol from liquor or spirits (P linear=0.02). One drink increment each day of alcohol could elevate the risk of bladder cancer by 9% (RR=1.09; 95%CI: 1.01-1.17). Alcohol was a risk factor of bladder cancer for male drinkers (RR=1.23; 95%CI: 1.13-1.35; I2=3.7%), while none linear or nonlinear relation was found.ConclusionNo significant association between alcohol consumption and bladder cancer risk was found in the entire population, but there was a linear dose-response relation in those who consume alcohol from liquor or spirits. Alcohol may elevate the risk of bladder cancer in males in a dose-independent way.Systematic review registrationhttps://www.crd.york.ac.uk/prospero/, PROSPERO (CRD42020216195).
| S-EPMC8479110 | biostudies-literature
Project description:The potential role of coffee consumption in the development of various types of cancer has been extensively investigated in epidemiologic studies. How coffee consumption may modulate risk of gastric cancer, however, remains a subject open for investigation. To better quantify this relation, we quantitatively summarized evidence from prospective studies. Eligible studies were identified on PubMed and Embase databases. The summary risk estimates were obtained using the random-effects model. Subgroup, sensitivity and dose-response analyses were conducted. The present meta-analysis included 12 prospective cohort studies. A pooled analysis of these studies suggested that coffee consumption (highest vs. lowest consumption) was not associated with risk of gastric cancer (RR = 1.12, 95% CI = 0.93-1.36). In the subgroup analysis, significant increased risk was detected in the U.S. studies (RR = 1.36, 95% CI = 1.06-1.74) and in the studies with <10 years of follow-up (RR = 1.24, 95% CI = 1.00-1.54), and the greatest increase in risk was observed in those studies without adjustment for smoking (RR = 1.48, 95% CI = 1.13-1.93). There was some evidence of publication bias (P for Egger's test = 0.03). Cumulative evidence from prospective studies suggests that coffee consumption is not associated with risk of gastric cancer. The observed positive results may be confounded by smoking and need further investigation.
| S-EPMC4179186 | biostudies-literature
Project description:Results from observational epidemiologic studies on the relationship between coffee consumption and gastric cancer are inconsistent and inconclusive. To assess the association between coffee consumption and the risk of gastric cancer, we summarized evidence from prospective cohort studies.Relevant studies were retrieved through computer searches (PubMed, EmBase and the Cochrane Library) and a review of references up to December 2014. The quality of the included studies was evaluated by Newcastle-Ottawa quality assessment scale. We used a meta-analytic approach to estimate overall hazard ratios (HRs) and 95% confidence intervals (CIs) for regular coffee drinkers versus individuals who seldom drank coffee. Sensitivity analysis and subgroup analysis were performed to assess the reliability of our results. A dose-response analysis was performed to assess the risk of gastric cancer based on the level of coffee consumption.Nine prospective cohort studies involving 1,250,825 participants and 3027 gastric cancer cases were included in this meta-analysis. The pooled HR of gastric cancer for the study-specific regularly versus seldom coffee drinking categories was 1.05 (95% CI, 0.88 to 1.25) with significant heterogeneity across studies (I(2) = 74.0%, P = 0.000). After the sensitivity analysis, three studies were deleted; however the association remained insignificant (HR, 0.99; 95% CI, 0.91 to 1.08). Subgroup analysis by anatomic location showed a risk for coffee consumption associated with cardia cancer (HR, 1.23; 95% CI, 1.04 to 1.45; heterogeneity, I(2) = 36.4, P = 0.207). In the dose-response analysis, there was no significant association between coffee intake (in cups) and the risk of gastric cancer (P for linearity trend and non-linearity > 0.05).Our meta-analysis demonstrated that coffee consumption was not associated with overall gastric cancer risk; however, coffee consumption may be a risk factor for gastric cardia cancer.
| S-EPMC4449182 | biostudies-literature
Project description:The association between alcohol consumption and venous thromboembolism (VTE) risk has been investigated by various observational studies with inconsistent results. We examined this association by performing a meta-analysis of prospective studies. A comprehensive literature search was carried out in the PubMed, EMBASE, and Web of Science from its inception to February 2020. Pooled effect estimates were calculated using a random effect model. Ten prospective studies (14 cohorts) were included in this meta-analysis with a total of 441,128 individuals and 10,221 VTE cases. Overall, the highest consumption of alcohol was not associated with the VTE risk compared with the lowest group [relative risk (RR), 0.96 (95% CI, 0.89-1.04), P = 0.293]. No obvious heterogeneity of RRs was observed across these studies (P = 0.249 for heterogeneity, I 2 = 18.8%). Egger's and Begg's tests showed no evidence of publication bias (Egger, P = 0.443; Begg, P = 0.730). In the subgroup analysis by sex, a borderline significant association between alcohol consumption and VTE risk was observed in women [RR, 0.91 (95% CI, 0.82-1.00)]. In the dose-response analysis, we observed a linear decrease in VTE risk with increasing alcohol intake (P = 0.634 for nonlinearity). However, the reduced risk was not statistically significant. In conclusion, the results from this meta-analysis suggest that alcohol intake is not related with the risk of VTE. Further large well-designed cohort studies are warranted to investigate a potential protective role of alcohol against VTE in women.
| S-EPMC7145405 | biostudies-literature
Project description:Alcohol consumption remains inconsistently correlated with fracture risk, and a dose-response meta-analysis for specific outcomes is lacking. The objective of this study was to quantitatively integrate the data on the relationship between alcohol consumption and fracture risk. Pertinent articles were identified in PubMed, Web of Science, and Embase databases up to 20 February 2022. Combined RRs and 95% CIs were estimated by random- or fixed-effects models. Restricted cubic splines were used to model linear or nonlinear relationships. Forty-four articles covering 6,069,770 participants and 205,284 cases of fracture were included. The combined RRs and 95% CIs for highest compared with lowest alcohol consumption were 1.26 (1.17-1.37), 1.24 (1.13-1.35), and 1.20 (1.03-1.40) for total, osteoporotic, and hip fractures, respectively. A linear positive relationship between alcohol consumption and total fracture risk was detected (Pnonlinearity = 0.057); the risk was correlated with a 6% increase (RR, 1.06; 95% CI: 1.02, 1.10) per 14 g/d increment of alcohol consumption. J-shaped relationships of alcohol consumption with risk of osteoporotic fractures (Pnonlinearity < 0.001) and hip fractures (Pnonlinearity < 0.001) were found. Alcohol consumption of 0 to 22 g/d was linked to a reduced risk of osteoporotic fractures and hip fractures. Our findings show that any level of alcohol consumption is a risk factor for total fractures. Moreover, this dose-response meta-analysis shows that an alcohol consumption level of 0 to 22 g/d is related to a reduction in the risk of osteoporotic and hip fractures. The protocol was registered in the International Prospective Register of Systematic Reviews (CRD42022320623).
| S-EPMC10334160 | biostudies-literature
Project description:A meta-analysis was performed to assess the association of coffee consumption with colorectal cancer and to investigate the shape of the association. Relevant prospective cohort studies were identified by a comprehensive search of the PubMed, Embase and Web of Science databases from their inception through August 2015. Either a random-effects model or fixed-effects model was used to compute the pooled risk estimates when appropriate. Linear and nonlinear dose-response meta-analyses were also performed. Nineteen prospective cohort studies involving 2,046,575 participants and 22,629 patients with colorectal cancer were included. The risk of colon cancer was decreased by 7% for every 4 cups per day of coffee (RR=0.93, 95%CI, 0.88-0.99; P=0.199). There was a threshold approximately five cups of coffee per day, and the inverse association for colorectal cancer appeared to be stronger at a higher range of intake. However, a nonlinear association of rectal cancer with coffee consumption was not observed (P for nonlinearity = 0.214). In conclusion, coffee consumption is significantly associated with a decreased risk of colorectal cancer at ≥ 5 cups per day of coffee consumption. The findings support the recommendations of including coffee as a healthy beverage for the prevention of colorectal cancer.
| S-EPMC5386640 | biostudies-literature
Project description:This is a dose-response (DR) meta-analysis to evaluate the association of coffee consumption on endometrial cancer (EC) risk. A total 1,534,039 participants from 13 published articles were added in this meta-analysis. The RR of total coffee consumption and EC were 0.80 (95% CI: 0.74-0.86). A stronger association between coffee intake and EC incidence was found in patients who were never treated with hormones, 0.60 (95% CI: 0.50-0.72), and subjects with a BMI ≥25 kg/m(2), 0.57 (95% CI: 0.46-0.71). The overall RRs for caffeinated and decaffeinated coffee were 0.66 (95% CI: 0.52-0.84) and 0.77 (95% CI: 0.63-0.94), respectively. A linear DR relationship was seen in coffee, caffeinated coffee, decaffeinated coffee and caffeine intake. The EC risk decreased by 5% for every 1 cup per day of coffee intake, 7% for every 1 cup per day of caffeinated coffee intake, 4% for every 1 cup per day of decaffeinated intake of coffee, and 4% for every 100 mg of caffeine intake per day. In conclusion, coffee and intake of caffeine might significantly reduce the incidence of EC, and these effects may be modified by BMI and history of hormone therapy.
| S-EPMC4548216 | biostudies-literature
Project description:BackgroundThis study aimed to investigate the dose-response association between alcohol consumption and atrial fibrillation (AF) risk.MethodsPubMed, Embase, Cochrane Library, and Web of Science were systematically searched using keywords related to alcohol and AF from the establishment of databases up to 1 March 2021. Prospective studies examining the impact of alcohol on the risk of AF with hazard ratios (HRs) were included. Restricted cubic spline regression was performed to quantify the dose-response relationship between alcohol consumption and AF risk.ResultsThirteen eligible studies were included in the meta-analysis, with a total of 645,826 participants and 23,079 cases of AF. When compared with non-/seldom-drinkers, the pooled adjusted HRs of AF were 1.30 (95% confidence interval [CI]: 1.20-1.41) and 1.00 (95% CI: 0.96-1.05) for high and low alcohol consumption, respectively. Moderate alcohol intake significantly increased the risk of AF in males (HR, 1.21; 95% CI: 1.10-1.33) but not in females (HR, 1.02; 95% CI: 0.91-1.14). The cubic spline regression analysis illustrated that the risk of AF significantly increased with daily alcohol intake in a Non-linear manner (R2 = 0.64, P = 5.785 × 10-12).ConclusionThis study revealed a Non-linearly positive association between alcohol intake and the risk of AF. Low alcohol intake was not associated with the development of AF, whereas moderate alcohol intake significantly increased the risk of AF in males but not in females. Our meta-analysis highlighted that alcohol consumption should be restricted to a low level to reduce the risk of AF.
| S-EPMC8907587 | biostudies-literature
Project description:Many studies investigated the association between alcohol drinking and gastric cancer risk, but the results were controversial. We performed a meta-analysis of observational studies to explore the association.We searched PubMed to identify the relevant studies that reported the association between alcohol drinking and gastric cancer risk up to December 31, 2016. We pooled relative risks (RRs) in random effects model and performed dose-response analysis to quantify the association. Cochran Q test and I2 analyses were used to evaluate the heterogeneity. Meta-regression, subgroup, sensitivity and publication bias analyses were also performed.75 studies were included in our study. The pooled RR of high vs low total alcohol drinking was 1.25 (95% CI, 1.15-1.37, P < 0.001), and a nonlinear association was further observed. Subgroup analysis showed that alcohol drinking significantly associated with the risk of gastric noncardia cancer (RR, 1.19; 95% CI, 1.01-1.40, P = 0.033), but not with the risk of gastric cardia cancer (RR, 1.16; 95% CI, 0.98-1.39, P = 0.087). Notably, the pooled RRs of high vs low analyses were 1.13 (95% CI, 1.03-1.24, P = 0.012) for beer drinking, 1.22 (95% CI, 1.06-1.40, P = 0.005) for liquor drinking, and 0.99 (95% CI, 0.84-1.16, P = 0.857) for wine drinking.Our meta-analysis found a nonlinear association between alcohol drinking and gastric cancer risk, and heavy drinking level was strongly related to gastric cancer risk. Beer and liquor had significant positive associations with gastric cancer risk, while wine drinking would not increase gastric cancer risk. These results need to be verified in future research.
| S-EPMC5716786 | biostudies-literature