Alcohol Consumption and Erectile Dysfunction

Alcohol is long regarded as a risk factor for erectile dysfunction (ED), whether in textbooks, review articles or clinical teachings. It was a long-held empirical observation that acute alcohol intoxication increases sexual desire but inhibits sexual performance. The scientific explanation is that alcohol is a central nervous system depressant, but it also leads to disinhibition and increases sexual desire.

Epidemiological studies have demonstrated numerous risk factors for erectile dysfunction, such as age, variables related to diabetes, depression, hypertension and smoking. With more accumulating evidence, the risk of alcohol consumption in ED seemed more equivocal. Erectile dysfunction has also been said to be the harbinger of cardiovascular events. Endothelial dysfunction has been hypothesized to result from cardiovascular risk factors such as hypertension or diabetes, which in turn leads to ED, myocardial infarction and stroke. As evidence accumulates to support the similarity in cardiovascular risk factor profiles of erectile dysfunction and cardiovascular diseases, it was fair to hypothesize that alcohol may demonstrate a J-shaped (or inverse) relationship with ED, with moderate alcohol consumption conferring the lowest risk of erectile dysfunction. Furthermore, considering the scale of the studies done on cardiovascular diseases and that of erectile dysfunction, it was not surprising that perhaps erectile dysfunction studies were simply not large enough to delineate the risk of erectile dysfunction associated with alcohol consumption.

It was the aim of this paper to use meta-analysis to pool the risk of regular alcohol consumption associated with erectile dysfunction.

A handful of studies have documented the harmful effects of chronic alcohol consumption on sexual functioning but hardly any study found potential beneficial effects of alcohol on erectile dysfunction. We have demonstrated through meta-analysis the possible beneficial effects of alcohol on erectile dysfunction.

The relationship between alcohol and erectile dysfunction was complex from the data: consuming 1–7 drinks/week appeared to confer the lowest risk (OR = 0.73; P = 0.101) but it was not statistically significant, and only 8 or more drinks/week was significant (OR = 0.85; P = 0.007). It appears that alcohol consumption, much similar to its relationship with cardiac survival, is related to sexual function in a J-shaped manner, with moderate consumption conferring highest protection and higher consumption conferring fewer benefits.

Considering that erectile dysfunction and heart diseases share similar cardiovascular risk factors, and the well-known chronic cytotoxic effects of alcohol on general health, hepatic function and immune function, general health might be a mediator between the association of high alcohol consumption and erectile dysfunction. This J-shaped relationship finding might explain why studies have shown harmful effects of heavy alcoholism on sexual function, that is alcoholism entails excessive drinking and carries the increased risk of erectile dysfunction at the tail of the J curve. However, caution has to be exercised in the extrapolation, as our results did not show a statistically significant OR for consuming 1–7 drinks/week, and did not demonstrate any harmful effects of alcohol on sexual function. In fact, three large studies have demonstrated progressively smaller ORs of erectile dysfunction for increasing levels of alcohol consumption.

We attempted to identify the cut-off level of alcohol consumption where risks outweigh benefits, by identifying the 'number of drinks/week' that has an OR closest to 1. To our surprise, the category '8 or more drinks/week' generated an OR that barely missed the unity and was statistically significant. Although we were unable to pinpoint the level of alcohol consumption where risks (OR>1) outweigh benefits (OR<1), we were at least able to say that '8 or more drinks/week' is likely to be a cut-off where the OR for erectile dysfunction becomes less than 1. Whether consuming more or less alcohol would yield a smaller OR was indeterminate.

The results from the two cohort studies complicated the picture even further: they did not show any significant effects of alcohol consumption on erectile dysfunction. The cross-sectional analysis of the HPFS data demonstrated a protective association of alcohol on erectile dysfunction, much in a J-shaped manner, but after follow-up of the subjects the cohort analysis did not find any significant associations between alcohol consumption and erectile dysfunction. Since the level of evidence from a cohort study is generally higher than from a cross-sectional study, due to less confounding and recall bias, the evidence from the HPFS cohort should weigh more heavily in our analysis. This suggests that the apparent protective association of alcohol consumption on erectile dysfunction was probably due to confounding (since recall, selection, observer and volunteer biases were less likely in the selected population-based cross-sectional studies). However, the sensitivity analysis demonstrated a significant protective association of alcohol consumption with higher level of statistical adjustments (less confounding), not with age adjustment alone (more confounding), and suggests that with better statistical adjustments (reduction of confounding) the demonstration of protective association might be possible. The sensitivity analysis on study sample size found that smaller studies demonstrated larger effects than larger studies, and might suggest that the estimate obtained from larger studies would be more reliable (effect towards null), although their estimates did not differ significantly. The relative importance of each study with regard to their sample sizes was taken care of by the differential weighting of the random effects model.

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