Abstract

Moderate alcohol consumption has been observed to have a favourable effect on several diseases in numerous studies during the past 20 years. Individuals who consume small-to-moderate amounts of alcohol are at decreased risk for CVD, including myocardial infarction, peripheral arterial disease, angina pectoris and ischaemic stroke, and have a decreased risk of dying. The risk reduction is generally attributed to the beneficial effects of alcohol on lipids and haemostatic factors. The effect of alcohol has also been investigated for a variety of renal disorders. Moderate alcohol consumption has been shown to be protective in the formation of kidney stones. With respect to renal cell carcinoma, higher levels of alcohol intake seemed to offer protection in women, whereas no association between alcohol intake and renal cell carcinoma was observed in men. Beneficial effects of moderate alcohol consumption on renal function are plausible; because vascular diseases and chronic renal dysfunction are highly correlated, and because the pathogenic principles of nephrosclerosis and coronary atherosclerosis are similar, it is possible that moderate consumption of alcohol may also have a positive effect on the development of renal dysfunction. It is important to point out that alcohol might have different effects on future renal function in healthy individuals than in those with preexisting renal disease. Besides some antithrombotic properties, an alcohol-induced increase in HDL cholesterol subfractions has been discussed to be the major mechanism for the cardio- and renovascular benefit of moderate alcohol consumption. In addition, there is evidence that the consumption of light-to-moderate amounts of alcohol decreases the risk of type 2 diabetes mellitus and has preventive effects on the development of arteriosclerosis in patients with type 2 diabetes mellitus. It is important to emphasize that, as research questions on alcohol in humans cannot be analysed by randomized controlled trials, all research results are solely based on observational studies indicating associations only and no causal relationship. # S02.3 ALCOHOL AND THE RISK OF RENAL CELL CANCER {#article-title-2} Kidney cancer is the eighth most frequent common cancer in the European Union. Several risk factors, such as cigarette smoking, obesity, hypertension and use of antihypertensives, were consistently and positively associated with the risk of renal cell cancer (RCC), although risk ratios (RRs) were only moderately increased. In a pooled analysis of 12 prospective cohort studies, intake of alcohol was associated with a decreased risk of RCC. Compared with non-drinkers, alcohol consumption of >15 g/day was associated with a pooled RR of 0.72 (95% CI: 0.60–0.86). This result has been confirmed in two other large prospective cohort studies. The von Hippel Lindau (VHL) gene has been identified as a major player in RCC. VHL mutations occur in 42–82% of all sporadic cases of clear cell RCC (cc-RCC, the most frequent histological subtype of RCC). We investigated in the Netherlands Cohort Study whether alcohol intake is associated with mutations in the VHL gene in RCC. The RR of RCC for cohort members who consumed ≥30 g of alcohol per day was 0.69 compared with non-drinkers (95% CI: 0.44–1.07). RRs were not different for cc-RCC with and without VHL mutations, except for alcohol from beer, which was associated with an increased risk of cc-RCC without VHL mutations. The inverse association between alcohol consumption and RCC risk is remarkable, because alcohol consumption is associated with an increased risk of several cancers, like head-neck, esophageal, colon and breast cancer. Several explanations have been proposed for the inverse association between alcohol intake and RCC risk. Moderate alcohol intake is associated with a lower risk for type II diabetes and may be associated with increased insulin sensitivity, which might explain the observed inverse association. Another possible mechanism is the diuretic effect of alcohol, which may decrease the exposure of renal cells to carcinogens because of dilution and a shorter duration of exposure. Several studies did not observe an association between fluid intake and RCC risk. Besides alcohol, other nutrients like flavonoids might be responsible for the observed association. Most studies did not observe differences between different beverages like beer, wine or liquor and RCC risk. Further research is therefore needed to explain the inverse association between alcohol and RCC risk.

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