A new study has found that chronic drinkers with a specific gene are at an increased risk of developing colorectal cancer.
The researchers have found that individuals with a polymorphism of the alcohol dehydrogenase 1C (ADH1C) gene produce more acetaldehyde when they drink, which creates a higher risk for colorectal cancer.
The more acetaldehyde produced, the higher the risk of cellular DNA damage.
For people, who drink more than 30 grams of alcohol per day, ADH1C*1 is a significant genetic risk marker for colorectal tumours.
"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," said Mikko Salaspuro, professor at the University of Helsinki, and a specialist in internal medicine and in gastroenterology at the Helsinki University Central Hospital.
For this study, Helmut K. Seitz, professor of internal medicine, gastroenterology and alcohol research at the University of Heidelberg and his colleagues recruited 173 individuals (138 males, 35 females) with colorectal tumours diagnosed by total colonoscopies, and 788 "control" patients (523 males, 265 females) without colorectal tumours. Whole-blood genotyping was performed on all participants.
"Our results show that individuals who metabolize alcohol to acetaldehyde more rapidly produce more acetaldehyde, and therefore have an increased risk for cancer in the colorectum," said Seitz.
"This metabolism is modulated by the activity of an important enzyme called alcohol dehydrogenase, which is genetically controlled.
"Thus, acetaldehyde plays a major role in alcohol-mediated carcinogenesis, and may not only be a carcinogen for the large intestine, but also for the upper aero digestive tract and the breast, as shown by other studies," he added.
The study appears in Alcoholism: Clinical and Experimental Research (ACER).