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US time series evidence regarding alcohol-related risk of oral cancers and protection against stomach cancers: are higher concentration beverages different?

Article Excerpt
One aspect of beverage-specific alcohol consumption that generally receives little attention in research but may be important for particular outcomes is the concentration at which the alcohol is drunk. In the United States (US), popular beers range from 4% to 7% alcohol by volume (ABV), wines range from 8% to 15% ABV (17-22% for fortified wines) and spirits drinks are the most variable, with a range from below 5% to 50% or more, depending on the degree of dilution (Kerr, Greenfield, Tujague & Brown 2005). However, only spirits can be drunk at high concentrations when taken undiluted or with small amounts of mixer. In most studies, concentration differences are approximated by beverage type under the assumption that many spirits drinks have a higher percentage of ABV than wine or beer drinks. For some alcohol-related health problems the high concentration may accelerate or be an additional risk factor in the disease process.

Oral Cancers

The effect of high ethanol concentration has been demonstrated most clearly for oral cancers, where several studies have distinguished between beverage types. Huang and colleagues (2003) found in a sample of Puerto Rican males that only usual drinkers of undiluted liquor were at increased risk for oral cancers among non-smokers. Further, among moderate to heavy smokers for a given volume of alcohol consumption, risks from diluted spirits were higher than for beer or wine and risks from undiluted spirits were two to four times higher than for diluted. Although they did not distinguish drinkers of undiluted spirits, a Spanish study (Castellsague, Quintana, Martinez, et al. 2004) found that spirits drinkers had two to four times higher risks for a given level of alcohol intake and smoking.

Substantial individual-level research, mainly from case control studies, has established alcohol (of any type) as a risk factor for oral cancers, with an attributable fraction of 26% on a global basis (Boffetta, Hashibe, La Vecchia, Zatonski & Rehm 2006). Mechanisms of the potential effect of alcohol in oral cancer include the possibility that alcohol is converted to the carcinogen acetaldehyde in saliva and that alcohol acts as a co-carcinogen by increasing permeability of the mucosa, enhancing the effect of other carcinogens, particularly tobacco smoke (Castellsague et al. 2004). The main alternative risk factor is tobacco smoke, which also has a synergistic effect with alcohol. Estimated odds ratios as high as 50 have been reported for the heaviest smoking- and alcohol-volume groups relative to non-smoking abstainers (Castellsague et al. 2004; Huang et al. 2003). Since tobacco use and alcohol consumption are often found to co-occur in individuals (Kozlowski & Ferrence 1997) and in population trends and birth cohorts (Gillison 2008), this combined effect may be the major source of mortality.

Stomach Cancers

Stomach cancers are another area where alcohol concentration may potentially be related to disease risk. The main risk factors for stomach cancer are smoking, salt intake, nitrate intake, low fruit and vegetable intake, low socio-economic status, history of gastric ulcer and, most important, Helicobacter pylori infection (Engel, Chow, Vaughan, Gammon, Risch, Stanford et al. 2003; Kelley & Duggan 2003). Although a recent review of the literature regarding alcohol and stomach cancers (Kelley & Duggan 2003) concludes that the majority of studies have found no relationship with alcohol, there is evidence supporting an indirect protective effect of alcohol through suppression of H. pylori activity. Alcohol has been found to be associated with a lower risk of stomach cancer in some studies, including a Danish study that found reduced risk among wine drinkers (Barstad, Sorensen, Tjonneland, et al. 2005) and a Japanese study where a reduced risk among moderate--but not heavy--drinkers was found (Kikuchi, Nakajima, Kobayashi, et al. 2002). These studies suggest that the mechanism of protection is through inhibiting the growth of H. pylori, either through a direct effect of alcohol or through related effects of alcohol intake such as increased intra-gastric acidity.

Indeed, several studies have demonstrated an effect of alcohol on H. pylori infection. Two German studies evaluated H. pylori seroprevalence in relation to measures of alcohol consumption. The first found a graded reduction with increasing current alcohol intake, with a larger effect from wine consumption than from beer (spirits were...