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April 15, 2011 (Orlando, Florida) — A genetic variant might predispose heavy beer drinkers to a higher risk for gastric cancer, according to the results of a new study.
The authors found that the consumption of 60 g of pure ethanol/alcohol carried a 65% increased risk for noncardia gastric cancer. However, they note that this association was largely confined to beer.
Further analysis showed that drinking 30 g of pure ethanol/alcohol or more a day derived from beer was associated with a 75% increased risk for gastric cancer. Notably, variants in the alcohol dehydrogenase gene cluster (ADH1) greatly exacerbated the risk for gastric malignancy.
The study results were presented here at the American Association for Cancer Research 102nd Annual Meeting, and represent the first time that this association of genetic variants, beer drinking, and gastric cancer has been noted in a European population.
Inconsistent Data
Alcohol consumption and the risk for gastric cancer have been evaluated in a number of epidemiologic studies, but the results have been inconsistent. There are a number of reasons for this inconsistency, said lead author Eric Duell, PhD, senior epidemiologist in the Cancer Epidemiology Research Program at the Catalan Institute of Oncology in Barcelona, Spain.
These include wide variations in beverage preferences and consumption patterns across populations, he noted during a press briefing. "Flaws in study design and methodology also might have contributed. There is also known genetic variation in alcohol metabolism within and across populations."
In their large prospective analysis, Dr. Duell and colleagues attempted to newly evaluate the association between alcohol consumption and gastric cancer.
They analyzed data from the European Prospective Investigation Into Cancer and Nutrition (EPIC), a prospective cohort of 521,000 adults 35 to 70 years of age who were recruited from 10 European countries from 1992 to 1998. The authors assessed the type and amount of alcohol consumed and associations by tumor location (cardia, noncardia), histology (diffuse, intestinal), and smoking status.
Beer Drinking Raises the Risk
In addition, they evaluated the possible effect of single-nucleotide polymorphisms (SNP) in ADH1 and its interactions with alcohol consumption in relation to gastric cancer risk in a case–control study (EurGast) nested in the EPIC cohort. Adjustment variables included age, center/country, sex, education, smoking, Helicobacter pylori infection, total energy, and dietary intake of fruits, vegetables, and red and processed meat.
The authors found that, compared with low ethanol consumption at baseline (0.1 to 4.9 g/day), heavy total consumption of alcoholic beverages (?60 g/day) and beer (?30 g/day) were statistically significantly associated with a higher risk for gastric cancer (total alcohol hazard ratio
, 1.65; 95% confidence interval [CI], 1.06 to 2.58; beer HR, 1.75, 95% CI, 1.13 to 2.73).
Consumption of wine and hard liquor was not associated with a risk for gastric cancer risk, Dr. Duell explained.
Strong Role of Genetic Variant
In the EurGast study nested within EPIC, 365 patients with gastric cancer were compared with 1284 control subjects. The authors found that 2 variants in the ADH1 locus were associated with gastric cancer risk.
Two variants in the ADH1 locus — rs283411 and rs1230025 — were statistically significantly associated with an increased risk for gastric cancer (P = .006 and P = .005, respectively). When looking at interactions between ADH1 locus SNPs and baseline alcohol consumption, the authors noted a statistically significant interaction between rs1230025 and beer consumption in relation to gastric cancer risk. People with the variant who were heavy consumers of beer had a relative risk for gastric cancer of 8.72 (P = .003 for trend).
The presence of SNP rs230025 was associated with a 30% increased risk for gastric cancer, said Dr. Duell. "When we looked at these 2 factors together — heavy beer drinking and having 2 copies of the variant — people had more than a 700% increased risk of gastric cancer."
"The results need to be replicated in other populations, as this is the first study to show a relationship between this SNP and gastric cancer risk," he added.
George Kim, MD, who was approached by Medscape Medical News for independent comment, noted that this "is not the first finding of an alcohol metabolic enzyme and some genetic alteration linked to cancer."
"The first studies were reported by Japanese researchers," said Dr. Kim, who is assistant professor of oncology at the Mayo Clinic College of Medicine and director of the gastrointestinal cancer group at the Mayo Clinic in Jacksonville, Florida. "This has been reported in the past. What is more relevant is the population — this is a European population and there are half a million people in the registry."
"It's an interesting finding but more work has to be done," he added.
American Association for Cancer Research (AACR) 102nd Annual Meeting: Abstract 3748. Presented April 4, 2011.
April 15, 2011 (Orlando, Florida) — A genetic variant might predispose heavy beer drinkers to a higher risk for gastric cancer, according to the results of a new study.
The authors found that the consumption of 60 g of pure ethanol/alcohol carried a 65% increased risk for noncardia gastric cancer. However, they note that this association was largely confined to beer.
Further analysis showed that drinking 30 g of pure ethanol/alcohol or more a day derived from beer was associated with a 75% increased risk for gastric cancer. Notably, variants in the alcohol dehydrogenase gene cluster (ADH1) greatly exacerbated the risk for gastric malignancy.
The study results were presented here at the American Association for Cancer Research 102nd Annual Meeting, and represent the first time that this association of genetic variants, beer drinking, and gastric cancer has been noted in a European population.
Inconsistent Data
Alcohol consumption and the risk for gastric cancer have been evaluated in a number of epidemiologic studies, but the results have been inconsistent. There are a number of reasons for this inconsistency, said lead author Eric Duell, PhD, senior epidemiologist in the Cancer Epidemiology Research Program at the Catalan Institute of Oncology in Barcelona, Spain.
These include wide variations in beverage preferences and consumption patterns across populations, he noted during a press briefing. "Flaws in study design and methodology also might have contributed. There is also known genetic variation in alcohol metabolism within and across populations."
In their large prospective analysis, Dr. Duell and colleagues attempted to newly evaluate the association between alcohol consumption and gastric cancer.
They analyzed data from the European Prospective Investigation Into Cancer and Nutrition (EPIC), a prospective cohort of 521,000 adults 35 to 70 years of age who were recruited from 10 European countries from 1992 to 1998. The authors assessed the type and amount of alcohol consumed and associations by tumor location (cardia, noncardia), histology (diffuse, intestinal), and smoking status.
Beer Drinking Raises the Risk
In addition, they evaluated the possible effect of single-nucleotide polymorphisms (SNP) in ADH1 and its interactions with alcohol consumption in relation to gastric cancer risk in a case–control study (EurGast) nested in the EPIC cohort. Adjustment variables included age, center/country, sex, education, smoking, Helicobacter pylori infection, total energy, and dietary intake of fruits, vegetables, and red and processed meat.
The authors found that, compared with low ethanol consumption at baseline (0.1 to 4.9 g/day), heavy total consumption of alcoholic beverages (?60 g/day) and beer (?30 g/day) were statistically significantly associated with a higher risk for gastric cancer (total alcohol hazard ratio
, 1.65; 95% confidence interval [CI], 1.06 to 2.58; beer HR, 1.75, 95% CI, 1.13 to 2.73).
Consumption of wine and hard liquor was not associated with a risk for gastric cancer risk, Dr. Duell explained.
Strong Role of Genetic Variant
In the EurGast study nested within EPIC, 365 patients with gastric cancer were compared with 1284 control subjects. The authors found that 2 variants in the ADH1 locus were associated with gastric cancer risk.
Two variants in the ADH1 locus — rs283411 and rs1230025 — were statistically significantly associated with an increased risk for gastric cancer (P = .006 and P = .005, respectively). When looking at interactions between ADH1 locus SNPs and baseline alcohol consumption, the authors noted a statistically significant interaction between rs1230025 and beer consumption in relation to gastric cancer risk. People with the variant who were heavy consumers of beer had a relative risk for gastric cancer of 8.72 (P = .003 for trend).
The presence of SNP rs230025 was associated with a 30% increased risk for gastric cancer, said Dr. Duell. "When we looked at these 2 factors together — heavy beer drinking and having 2 copies of the variant — people had more than a 700% increased risk of gastric cancer."
"The results need to be replicated in other populations, as this is the first study to show a relationship between this SNP and gastric cancer risk," he added.
George Kim, MD, who was approached by Medscape Medical News for independent comment, noted that this "is not the first finding of an alcohol metabolic enzyme and some genetic alteration linked to cancer."
"The first studies were reported by Japanese researchers," said Dr. Kim, who is assistant professor of oncology at the Mayo Clinic College of Medicine and director of the gastrointestinal cancer group at the Mayo Clinic in Jacksonville, Florida. "This has been reported in the past. What is more relevant is the population — this is a European population and there are half a million people in the registry."
"It's an interesting finding but more work has to be done," he added.
American Association for Cancer Research (AACR) 102nd Annual Meeting: Abstract 3748. Presented April 4, 2011.
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)] If its not wine helping, no now the grapes, oh, now not really,,, now this. You really first must consider the flaws here:
