Journal of Sexual Medicine, 6(5): 1386-1394, 2009

Introduction. Alcohol consumption is a contentious social topic and is often assumed to have deleterious effects on sexual performance. There is a lack of consensus on whether alcohol consumption may in fact be beneficial to erectile function.

Aim. We examined the data from a population-based cross-sectional study of men’s health to assess the association between usual alcohol consumption and erectile dysfunction (ED).

Method. Reply-paid questionnaires were posted to a randomly selected age-stratified male population sample obtained from the Western Australian (WA) Electoral Roll.

Main Outcome Measures. The survey questionnaire included sociodemographic details, self-reported clinical

information, and drinking habits. The 5-item International Index of Erectile Function (IIEF-5) was used to assess erectile function.

Results. Most (87%) participants were current alcohol drinkers, with binge drinking, as defined by the Australian National Health and Medical Research Council (NHMRC), reported by 20% of drinkers. Compared with neverdrinkers, the age-adjusted odds of ED were lower among current, weekend, and binge drinkers and higher among ex-drinkers. Among current drinkers, the odds were lowest for consumption within the NHMRC guidelines of between 1 and 20 standard drinks a week. On further adjustment for cardiovascular disease (CVD) or for cigarette smoking, age-adjusted odds of ED were reduced by 25–30% among alcohol drinkers.

Conclusions. Our findings suggest a modest negative association between alcohol consumption and ED and confounding of the association by CVD and cigarette smoking. The Western Australia Men’s Health Study certainly provides no justification for advising men with ED whose drinking habits are consistent with NHMRC guidelines that they should cease or reduce their consumption of alcohol.

The serendipitous discovery that a drug, originally developed for cardiovascular use, restored erectile function has led to a burgeoning of research into the link between erectile function and cardiovascular health.

Our audit of the screening biochemistry of 1500 men presenting to the Keogh Institute with erectile dysfunction (ED) has shown that dyslipidaemia is by far the most prevalent abnormality, far more common than a low testosterone. Prevalence studies led by Dr Kim Chew in Western Australian general practice and in the community have confirmed that men with ED are at high odds of having cardiovascular disease and vice versa.

The big question has been whether ED by itself is an independent sign of underlying cardiovascular disease. Our clinical laboratory experiments, using measures of endothelial function in conduit and resistance arteries in the forearm, have suggested that this is so. Men with ED, without any known cardiovascular disease or any measurable cardiovascular risk factors were found to have demonstrable generalised vascular disease. This finding is consistent with the “artery size” hypothesis where endothelial dysfunction and disease presents first in small arteries, such as in the penis, causing ED, before being clinically evident in larger diameter arteries like the coronary circulation, causing angina or myocardial infarction. Presently, using data from our own clinic and the WA Morbidity and Mortality Database we are examining the time interval between those two events. We believe that this time interval represents a window of opportunity for cardiovascular risk reduction.

The prime focus of the management of ED has now moved from psychological counselling to identification and correction of cardiovascular risk factors.

ED is not the only men’s health issue moving from the psychological to the organic sphere of interest. Premature ejaculation (PE) is said to the most common male sexual complaint and is divisible into primary PE, which occurs and persists from the first sexual encounter, and secondary or acquired PE, which may be psychological but is commonly acquired in the older patient when erectile function begins to fail. Primary PE is now recognised to have an organic, probably genetic, basis although the exact mechanisms by which it occurs are yet to be fully elucidated. PE has been previously managed, rather unsuccessfully, by psychological and behavioural interventions. However, the recognition of the role of serotonin receptors in the control of ejaculation has led to the use of selective serotonin reuptake inhibitors and the development of newer SSRIs in the management of primary PE. However there is more to unravel in the complex imbalance in neurotransmitters and autonomic nervous control which leads to primary PE and, led by Dr Neil Palmer, the Keogh Institute is taking PE from the examination couch back to the clinical laboratory.