Alcohol Consumption and Risk for Venous Thromboembolism: A Meta-Analysis of Prospective Studies

Mengyan Chen; Mingxia Ji; Tiejiang Chen; Xiaofei Hong; Yian Jia

doi:10.3389/fnut.2020.00032

April 2, 2020Frontiers in NutritionOpen Access

Alcohol Consumption and Risk for Venous Thromboembolism: A Meta-Analysis of Prospective Studies

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Why the study?

Observational studies investigating the association between alcohol consumption and venous thromboembolism risk have produced inconsistent results.

Does alcohol consumption reduce the risk of venous thromboembolism in the general population?

Structured PICO

Does alcohol consumption reduce the risk of venous thromboembolism in the general population?

P

Population

441,128 individuals pooled from 10 prospective studies (14 cohorts) with 10,221 venous thromboembolism (VTE) cases

I

Intervention

Highest consumption of alcohol

C

Comparator

Lowest consumption of alcohol

O

Outcome

Venous thromboembolism (VTE) riskhard clinical

This meta-analysis demonstrates that alcohol consumption is not significantly associated with the risk of venous thromboembolism, though a borderline protective association was observed in women.

Implication

Alcohol intake shows no overall VTE association; leaves open possible modest protection in women for prospective confirmation.

Abstract

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 (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, I2 = 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 non-linearity). 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.