Chronic drinking is a risk factor for colorectal cancer, possibly through the effects of acetaldehyde, which is created by the alcohol dehydrogenase (ADH) enzyme.
This study investigated if a polymorphism of the ADH1C gene that is found in Caucasians may effect acetaldehyde concentrations. Findings confirm ADH1C*1 as a genetic risk marker for colorectal tumors among people who drink more than 30 grams of alcohol per day.
Results will be published in the March issue of Alcoholism: Clinical & Experimental Research and are currently available at Early View.
"In 2007, the International Agency for Research on Cancer clearly stated that chronic alcohol consumption increases the risk for colorectal cancer," said Helmut K. Seitz, professor of internal medicine, gastroenterology and alcohol research at the University of Heidelberg. "This has enormous practical implications since, in many countries, alcohol consumption is high and the prevalence of colorectal cancer is increasing. In other words, one of the leading types of cancers worldwide is further stimulated by alcohol drinking." Seitz is also the study's corresponding author.
"Regular alcohol consumption of about 50 grams or approximately four drinks per day results in a 1.4-fold risk for colorectal cancer compared to non-drinkers," added Mikko Salaspuro, professor at the University of Helsinki, and a specialist in internal medicine and in gastroenterology at the Helsinki University Central Hospital.
Acetaldehyde is the first metabolite of alcohol, both researchers explained. The more acetaldehyde produced, the higher the risk of cellular DNA damage, leading to cancer. While studies of upper digestive tract cancers have strongly implicated exposure to acetaldehyde in saliva, both direct and indirect evidence also implicate the role of acetaldehyde in the cells of the colonic mucosa and cancer development in the colorectum.