A handful of studies[26,27,28] have documented the harmful effects of chronic alcohol consumption on sexual functioning but hardly any study found potential beneficial effects of alcohol on ED. We have demonstrated through meta-analysis the possible beneficial effects of alcohol on ED.
The relationship between alcohol and ED 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 less benefits.
Considering that ED 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 ED. 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 ED 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[9,16,18] have demonstrated progressively smaller ORs of ED for increasing levels of alcohol consumption.
We attempted to identify the cutoff 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 cutoff where the OR for ED 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 ED. The cross-sectional analysis of the HPFS data demonstrated a protective association of alcohol on ED, 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 ED. 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 ED 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.
A major limitation of previous population-based studies was their relatively small sample sizes, and we sought to overcome this sample size problem by pooling data across studies, although we suspected that the OR for '1–7 drinks/week' was not statistically significant due to inadequate sample size.
The meta-analyses had four limitations, (1) confounding, (2) definitions of ED and alcohol consumption, (3) weak causal inference and (4) heterogeneity.
Confounding can reduce the internal validity of a study, and since ED is a multifactorial disorder, the association between alcohol and ED as demonstrated could be confounded by some other factors not adjusted for. First, the effect size for alcohol consumption was not large, and the significant effect could be due to residual confounding. Second, we obtained pooled estimates based on ORs that were adjusted for different numbers of variables from different studies, and therefore each included study had a different level of confounding. Our minimum requirement for inclusion was that the ORs had to be age-adjusted, other than this if more variables were adjusted for the better. However referring to Figure 1, if confounding was a problem, one would find ORs that were adjusted for more variables to lie closer to unity (that is, no effect) and those that were only age-adjusted to be closer to zero (that is, protective association), but this did not appear to be the case.
Alcohol consumption was assessed in many ways, one by grams of alcohol, and most by the number of drinks/week, but the categories were different. We took a conservative approach in pooling the data, for example, if the categories in Millett et al.'s study were none/1–4/≥4 drinks/week, we excluded the OR for the 'open-ended' ≥4 drinks/week and only included the OR for 1–4 drinks/week into our final 1–7 drinks/week category, and likewise we only included the OR for 3–4 drinks/week from Cho et al.'s study in the 1–7 drinks/week category. We believe that this conservative approach in pooling the results should ensure the reliability of our results.
The included studies used two broad definitions of ED, one that was based on IIEF-5 or IIEF-15, and the other that was based on a single self-reporting question. Sensitivity analysis showed that the summary estimates based on each definition were different, and only the self-reported one was significant (OR = 0.73; 99% CI, 0.61–0.88; P<0.001) but not the IIEF one (OR = 0.95; 99% CI, 0.65–1.40; P = 0.739), and the latter was not statistically significant. This finding raises serious doubts to the use of single question self-reported composite measures of ED, which many studies worldwide used, since it appears that the summary estimate for each definition was different. However, since the estimates did not differ significantly (P = 0.1057), this difference could be due to chance.
Causal inference from the cross-sectional design is weak. The alternatives for better causal inference are either a cohort study or a randomized controlled trial, but in either case few studies have been done. We sought to support our meta-analysis results with the research findings from cohort studies (MMAS and HPFS), but the cohorts did not demonstrate any significant relationships between alcohol consumption and risk of ED. The cross-sectional HPFS supported our meta-analysis results of the cross-sectional studies in demonstrating a significant protective association, but the cohort HPFS did not, and this suggests that the protective association demonstrated in cross-sectional studies might have resulted from confounding. Another possible explanation was that men who developed ED opted not to drink alcohol, whereas men without ED continued to drink alcohol. As a result, an apparent 'harmful effect' of not drinking alcohol was found, which was the inverse of protective association of drinking alcohol in terms of ORs. Since the cohort study design has better causal inference, the results from the two cohort studies suggest that alcohol neither causes nor prevents ED from developing. Also, the statistical association was found after pooling a large number of studies, and may have limited biological significance for an individual drinker.
We found significant heterogeneity in two of the three meta-analysis estimates. In general, there can be many sources of heterogeneity in meta-analysis, and we can only surmise the sources in this study, which may include varying number of controlled confounders, different definitions of ED and alcohol consumption and the diverse populations included. We used the random effects model that is preferred to the fixed effects model when significant heterogeneity exists.
The geographical regions covered in this meta-analysis include South America (Brazil), Europe (Italy, Belgium), Africa (Egypt, Nigeria), Middle East (Turkey) and Asia-Pacific (Australia, China, Japan, Korea, Malaysia, Pakistan). Therefore our results have limited generalizability to other regions (for example, North America).
Two reasons might have propagated the myth that alcohol consumption is a risk factor for ED. First, that alcohol consumption enhanced sexual desire but impaired sexual performance is perhaps a short-lived effect of alcohol and will not cause ED permanently. Second, that severe alcoholism impairs sexual functions may be an extreme example and is confounded by underlying deterioration of general health, and unless it is excessive it is unlikely to cause ED permanently. More research has to be done to assess the association between acute (we did not investigate) and chronic (which we investigated) alcohol consumption and development of ED, particularly using large-scale cohorts since randomized controlled trials may be unethical.
This is the first study that systematically reviewed and meta-analyzed the association between alcohol consumption and ED. Our meta-analysis found a significant protective association of regular (chronic) alcohol consumption on ED in cross-sectional studies, in particular for the consumption of 8 or more drinks/week. Evidence from large cohort studies suggests that regular alcohol consumption is not significantly associated with ED development. Therefore this study has demonstrated, in the least, that chronic alcohol consumption is not a risk factor for ED. We hope to demonstrate with the results of this study that the association between alcohol consumption and development of ED might not be as straightforward as it seemed, and the undue popularity of alcohol being labeled as a risk factor for ED was probably unjustified since there was little research evidence to support it.
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Dr JYW Cheng, Department of Psychiatry, Li Ka Shing Faculty of Medicine, University of Hong Kong, Hong Kong, China. E-mail: email@example.com
Int J Impot Res. 2007;19(4):343-352. © 2007 Nature Publishing Group
Cite this: Alcohol Consumption and Erectile Dysfunction: Meta-Analysis of Population-Based Studies - Medscape - Jul 01, 2007.