Article - Potential genetic association between coffee/caffeine consumption and erectile dysfunction: a Mendelian randomization study and meta-analysis.

Plain Language Summary

Coffee is widely consumed and has been linked to benefits for various chronic diseases, but whether it affects erectile dysfunction (ED) risk is unclear. This study explores the potential link between coffee and caffeine consumption and the risk of ED, a condition where men have difficulty achieving or maintaining an erection.

The findings showed no association between genetically predicted coffee or caffeine consumption and the risk of ED.

It was concluded that there was no association between coffee/caffeine consumption and the risk of ED in European populations. However, this does not rule out a relationship entirely, as genetic instruments can only capture part of a person's lifetime exposure, and the exact nature of this relationship remains complex and may benefit from further exploration using larger datasets.This study could be used by healthcare professionals to understand that, based on current genetic evidence, there is no indication that coffee or caffeine consumption increases or reduces a person's risk of developing ED.

Expert Review

Reviewer: Sarah Cassar

20th Aug 2026

Conflict of interest

None

Take home message

There is currently no strong genetic evidence to show that coffee/caffeine intake may increase or reduce the risk of ED.

Evidence category

A: Meta-analyses, position-stands, randomized-controlled trials (RCTs)

Summary review

Introduction

This study used Mendelian randomisation (MR) to investigate the possible associations between coffee/caffeine consumption and erectile dysfunction (ED).

Method

This was a two-sample MR study in predominantly European-ancestry populations.

Genetic variants associated with coffee consumption were obtained from a genome-wide meta-analysis (GWMA: n=91,462) and a genome-wide association study (GWAS: n=375,833). A further GWAS (n=407,072) assessed caffeine consumption from tea.
ED data were obtained from two independent European datasets: Bovijn et al. (n=223,805 men) and FinnGen (n=95,178 participants).
The inverse variance-weighted (IVW) method was the primary approach, supported by MR-Egger, weighted median and mode-based analyses.
The results from the two ED datasets were pooled using fixed-effect meta-analysis.

Results

Bovijn et al. study dataset: MR analysis did not find a significant causal association between coffee consumption (GWMA: IVW OR=1.021; 95% CI:0.843–1.238; p=0.829; GWAS: IVW OR=1.314; 95% CI: 0.754–2.289; p=0.335) and caffeine from tea (IVW OR=1.107; 95% CI: 0.690–1.776; p=0.673) on ED.
FinnGen study dataset: MR analysis did not find a significant causal association between coffee consumption (GWMA: IVW OR=0.908; 95% CI: 0.478–1.725; p=0.768; GWAS: IVW OR=0.531; 95% CI: 0.134–2.101; p=0.367) and caffeine from tea (IVW OR=0.792; 95% CI: 0.229–2.747; p=0.531) on ED.
The meta-analysis of the two datasets did not find a causal relationship between coffee/caffeine consumption and ED

(GWMA: OR: 1.011, 95% CI 0.841–1.216, p=0.906; GWAS: OR: 1.049, 95% CI 0.487–2.260, p=0.903; caffeine from tea: OR: 1.061, 95% CI 0.682–1.651, p=0.793).

Conclusion

These findings provide no strong evidence of a causal association between coffee/caffeine consumption and ED in European-ancestry populations. However, further studies are needed to validate these findings and investigate the underlying mechanisms.

Clinical practice applications

Current genetic evidence does not suggest a causal association between coffee/caffeine consumption and ED. Therefore, this key consideration should be kept in mind when providing personalised nutrition advice.
If patients ask, healthcare practitioners can explain that current genetic-based research has found no strong evidence of a causal link between coffee/caffeine intake and ED.

Considerations for future research

Studies with larger samples are needed to address the relatively low ED case rate across the datasets used.
Both exposure and outcome data were derived from European populations, thus, future research should validate these findings in more diverse populations.
Future studies should investigate potential physiological mechanisms linking coffee/caffeine consumption to the risk of ED.

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Abstract

BACKGROUND

Coffee is a widely consumed beverage with potential benefits for various chronic diseases. Its effect on reducing erectile dysfunction (ED) risk is unclear. This Mendelian randomization (MR) study investigates the impact of coffee/caffeine consumption on ED.

METHODS

Two sets of coffee consumption-associated genetic variants at the genome-wide significance level were obtained from recent studies of coffee consumption. Taking into account other sources of caffeine, genetic variants associated with caffeine consumption from tea were also obtained. The inverse variance weighted (IVW) method was utilized as the primary analysis. Sensitivity analysis methods and meta-analysis methods were performed to confirm the robustness of the results, while the genetic variants associated with confounders, e.g., diabetes and hypertension, were excluded.

RESULTS

Genetically predicted coffee/caffeine consumption was unlikely to be associated with the risk of ED in the Bovijn datasets, with similar directional associations observed in the FinnGen datasets. The combined odds ratio for ED was 1.011 (95% CI 0.841-1.216, =0.906) for coffee consumption from the genome-wide meta-analysis, 1.049 (95% CI 0.487-2.260, =0.903) for coffee consumption from the genome-wide association study, and 1.061 (95% CI 0.682-1.651, =0.793) for caffeine from tea.

CONCLUSION

Using genetic data, this study found no association between coffee/caffeine consumption and the risk of ED.