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ORLANDO – Heavy long-term beer drinking is associated with an increased risk of gastric cancer, particularly in people with a variant in a cluster of genes that metabolize alcohol, according to findings from the European Prospective Investigation into Cancer and Nutrition study.
More than 521,000 people in 10 European studies were part of the observational cohort EPIC study. Total consumption of 60 g (vs. less than 5 g) of pure ethanol/alcohol per day from all beverage types over an average of about 8-10 years was associated with a 65% increase in the risk of gastric cancer.
The association was attributable to beer consumption, Eric J. Duell, Ph.D., reported at the annual meeting of the American Association for Cancer Research. That is, drinking 30 g of pure ethanol/alcohol per day strictly from beer (which equates to the alcohol level in about three beers) was associated with a 75% increase in risk. No significant increase in risk was seen with wine or liquor consumption.
Furthermore, an analysis of data from a nested case-control study within the EPIC cohort (the EurGast study) showed that in heavy beer drinkers with two copies of rs1230025 – an intergenic single nucleotide polymorphism (SNP) in the locus of the alcohol dehydrogenase gene cluster (ADH1) – the risk was increased by about 700%, compared with the risk in those who drank less and lacked the SNP (odds ratios, 8.72 and 1.29, respectively).
This interaction between the rs1230025 SNP (which itself confers a 30% increased risk of cancer) and beer consumption in relation to gastric cancer was statistically significant (P = .003), said Dr. Duell, senior epidemiologist in the cancer epidemiology research program at the Catalan Institute of Oncology in Barcelona.
The EPIC study enrolled adults aged 35-70 years from 1992 through 1998. Alcohol use and dietary factors were assessed by questionnaire. The current analysis included adjustment for age, center/country, sex, education level, smoking status, H. pylori infection (the main risk factor for gastric cancer, which is the second leading cause of death worldwide), diet, and total energy.
"This is the first study to see an association between this SNP and gastric cancer risk," Dr. Duell said, noting that although the findings need to be replicated in future studies, there are number of potential biological explanation for the associations.
For example, a build-up of acetaldehyde (a product of ethanol oxidation and a known carcinogen) in the stomach, excess nitrosamines (a known carcinogen found in beer), excess stomach bacteria resulting from atrophic gastritis (a known risk factor for gastric cancer), or a combination of these factors could be increasing risk, he said.
Dr. Duell had no relevant disclosures.
ORLANDO – Heavy long-term beer drinking is associated with an increased risk of gastric cancer, particularly in people with a variant in a cluster of genes that metabolize alcohol, according to findings from the European Prospective Investigation into Cancer and Nutrition study.
More than 521,000 people in 10 European studies were part of the observational cohort EPIC study. Total consumption of 60 g (vs. less than 5 g) of pure ethanol/alcohol per day from all beverage types over an average of about 8-10 years was associated with a 65% increase in the risk of gastric cancer.
The association was attributable to beer consumption, Eric J. Duell, Ph.D., reported at the annual meeting of the American Association for Cancer Research. That is, drinking 30 g of pure ethanol/alcohol per day strictly from beer (which equates to the alcohol level in about three beers) was associated with a 75% increase in risk. No significant increase in risk was seen with wine or liquor consumption.
Furthermore, an analysis of data from a nested case-control study within the EPIC cohort (the EurGast study) showed that in heavy beer drinkers with two copies of rs1230025 – an intergenic single nucleotide polymorphism (SNP) in the locus of the alcohol dehydrogenase gene cluster (ADH1) – the risk was increased by about 700%, compared with the risk in those who drank less and lacked the SNP (odds ratios, 8.72 and 1.29, respectively).
This interaction between the rs1230025 SNP (which itself confers a 30% increased risk of cancer) and beer consumption in relation to gastric cancer was statistically significant (P = .003), said Dr. Duell, senior epidemiologist in the cancer epidemiology research program at the Catalan Institute of Oncology in Barcelona.
The EPIC study enrolled adults aged 35-70 years from 1992 through 1998. Alcohol use and dietary factors were assessed by questionnaire. The current analysis included adjustment for age, center/country, sex, education level, smoking status, H. pylori infection (the main risk factor for gastric cancer, which is the second leading cause of death worldwide), diet, and total energy.
"This is the first study to see an association between this SNP and gastric cancer risk," Dr. Duell said, noting that although the findings need to be replicated in future studies, there are number of potential biological explanation for the associations.
For example, a build-up of acetaldehyde (a product of ethanol oxidation and a known carcinogen) in the stomach, excess nitrosamines (a known carcinogen found in beer), excess stomach bacteria resulting from atrophic gastritis (a known risk factor for gastric cancer), or a combination of these factors could be increasing risk, he said.
Dr. Duell had no relevant disclosures.
ORLANDO – Heavy long-term beer drinking is associated with an increased risk of gastric cancer, particularly in people with a variant in a cluster of genes that metabolize alcohol, according to findings from the European Prospective Investigation into Cancer and Nutrition study.
More than 521,000 people in 10 European studies were part of the observational cohort EPIC study. Total consumption of 60 g (vs. less than 5 g) of pure ethanol/alcohol per day from all beverage types over an average of about 8-10 years was associated with a 65% increase in the risk of gastric cancer.
The association was attributable to beer consumption, Eric J. Duell, Ph.D., reported at the annual meeting of the American Association for Cancer Research. That is, drinking 30 g of pure ethanol/alcohol per day strictly from beer (which equates to the alcohol level in about three beers) was associated with a 75% increase in risk. No significant increase in risk was seen with wine or liquor consumption.
Furthermore, an analysis of data from a nested case-control study within the EPIC cohort (the EurGast study) showed that in heavy beer drinkers with two copies of rs1230025 – an intergenic single nucleotide polymorphism (SNP) in the locus of the alcohol dehydrogenase gene cluster (ADH1) – the risk was increased by about 700%, compared with the risk in those who drank less and lacked the SNP (odds ratios, 8.72 and 1.29, respectively).
This interaction between the rs1230025 SNP (which itself confers a 30% increased risk of cancer) and beer consumption in relation to gastric cancer was statistically significant (P = .003), said Dr. Duell, senior epidemiologist in the cancer epidemiology research program at the Catalan Institute of Oncology in Barcelona.
The EPIC study enrolled adults aged 35-70 years from 1992 through 1998. Alcohol use and dietary factors were assessed by questionnaire. The current analysis included adjustment for age, center/country, sex, education level, smoking status, H. pylori infection (the main risk factor for gastric cancer, which is the second leading cause of death worldwide), diet, and total energy.
"This is the first study to see an association between this SNP and gastric cancer risk," Dr. Duell said, noting that although the findings need to be replicated in future studies, there are number of potential biological explanation for the associations.
For example, a build-up of acetaldehyde (a product of ethanol oxidation and a known carcinogen) in the stomach, excess nitrosamines (a known carcinogen found in beer), excess stomach bacteria resulting from atrophic gastritis (a known risk factor for gastric cancer), or a combination of these factors could be increasing risk, he said.
Dr. Duell had no relevant disclosures.
FROM THE ANNUAL MEETING OF THE AMERICAN ASSOCIATION FOR CANCER RESEARCH