Dataset Information

Genetically determined alcohol consumption and cancer risk in Korea.

ABSTRACT:

Objectives

The purpose of this study was to determine the causal relationship between the genetically determined amount of alcohol consumption and the occurrence of major cancers.

Methods

The data used in this study were from 129,324 people selected from the Korean Cancer Prevention Study-II, the participants of which visited 18 health examination centers between 2004 and 2013. Cancer incidence was confirmed as of 2020 using data from the National Cancer Center. A genome-wide association study (GWAS) on alcohol consumption was performed using PLINK 2.0, and sex, age, chip type, and principal components were adjusted.

Results

From the GWAS, a genetic risk score for alcohol consumption was calculated and genetically determined alcohol consumption (GDAC) was estimated. GDAC was divided into quintile groups and showed significant causal relationships with rectal cancer and liver cancer, but not with other cancers. For liver cancer, an association was shown in the hepatitis B surface antigen (HBsAg)-negative group, and a particularly strong association was found in the over-60-year-old HBsAg-negative group, in which, compared to the GDAC Q1 group, the Q4 group had a 2.35 times higher risk (95% confidence interval [CI], 1.05 to 5.23), and the Q5 group had a 2.40 times higher risk (95% CI, 1.09 to 5.30).

Conclusions

The results of this study provided evidence that the amount of alcohol consumed is causally related to the occurrence of rectal cancer and liver cancer in HBsAg-negative individuals. Additional studies should be continued for other cancer types through long-term follow-up.

SUBMITTER: Jung KJ

PROVIDER: S-EPMC10728612 | biostudies-literature | 2023

REPOSITORIES: biostudies-literature

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Publications

Genetically determined alcohol consumption and cancer risk in Korea.

Jung Keum Ji KJ Baek Ji Woo JW Shin Sang Yop SY Jee Sun Ha SH

Epidemiology and health 20230823

<h4>Objectives</h4>The purpose of this study was to determine the causal relationship between the genetically determined amount of alcohol consumption and the occurrence of major cancers.<h4>Methods</h4>The data used in this study were from 129,324 people selected from the Korean Cancer Prevention Study-II, the participants of which visited 18 health examination centers between 2004 and 2013. Cancer incidence was confirmed as of 2020 using data from the National Cancer Center. A genome-wide asso ...[more]

PMID: 37641821

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Project description:Endometrial cancer (EC) is a common gynecological tumor in females with an increasing incidence over the past few decades. Alcohol consumption has been linked to the occurrence of various cancers; However, epidemiological studies have shown inconsistent associations between alcohol consumption and EC risk. In order to avoid the influence of potential confounding factors and reverse causality in traditional epidemiological studies, we used a method based on genetic principles-Mendelian randomization (MR) analysis to test whether there is a causal relationship between alcohol consumption and EC. MR analysis was conducted using publicly available summary-level data from genome-wide association studies (GWAS). Fifty-seven single nucleotide polymorphisms (SNPs) were extracted as instrumental variables for alcohol exposure from the GWAS and Sequencing Consortium of Alcohol and Nicotine GWAS summary data involving 941,287 participants of European ancestry. SNPs for EC were obtained from the Endometrial Cancer Association Consortium, the Endometrial Cancer Epidemiology Consortium, and the UK Biobank, involving 121,885 European participants. The inverse variance weighted (IVW) method was used as the primary method to estimate the causal effect, and the MR-Egger regression and weighted median method were used as supplementary methods. Sensitivity analyses were conducted using the Mendelian Randomization Pleiotropy RESidual Sum and Outlier global test, MR-Egger intercept test, and leave-one-out analysis to evaluate the impact of pleiotropy on causal estimates. An increase of 1 standard deviation of genetically predicted log-transformed alcoholic drinks per day was associated with a 43% reduction in EC risk [odds ratio (OR) = 0.57, 95% confidence interval (CI) 0.41-0.79, P < 0.001]. Subgroup analysis of EC revealed that alcohol consumption was a protective factor for endometrioid endometrial cancer (EEC) (OR = 0.56, 95% CI 0.38-0.83, P = 0.004) but not for non-endometrioid endometrial cancer (NEC) (OR = 1.36, 95% CI 0.40-4.66, P = 0.626). The MR-Egger regression and weighted median method yielded consistent causal effects with the IVW method. The consistent results of sensitivity analyses indicated the reliability of our causal estimates. Additionally, alcohol consumption was associated with decreased human chorionic gonadotropin (HCG) and insulin-like growth factor 1 (IGF1) levels. This MR study suggests that genetically predicted alcohol consumption is a protective factor for EC, particularly for EEC, and this protective effect may be mediated through the reduction of HCG and IGF1.

Project description:ImportanceAlthough numerous studies have shown an association between alcohol consumption and cancer, how changes in drinking behavior increase or decrease the incidence of cancer is not well understood.ObjectiveTo investigate the association between the reduction, cessation, or increase of alcohol consumption and the development of alcohol-related cancers and all cancers.Design, setting, and participantsThis population-based cohort study analyzed adult beneficiaries in the Korean National Health Insurance Service. Participants (aged ≥40 years) included those who underwent a national health screening in both 2009 and 2011 and had available data on their drinking status. Data were analyzed from April 16 to July 6, 2020.ExposuresAlcohol consumption level, which was self-reported by participants in health screening questionnaires, was categorized into none (0 g/d), mild (<15 g/d), moderate (15-29.9 g/d), and heavy (≥30 g/d) drinking. Based on changes in alcohol consumption level from 2009 to 2011, participants were categorized into the following groups: nondrinker, sustainer, increaser, quitter, and reducer.Main outcomes and measuresThe primary outcome was newly diagnosed alcohol-related cancers (including cancers of the head and neck, esophagus, colorectum, liver, larynx, and female breast), and the secondary outcome was all newly diagnosed cancers (except for thyroid cancer).ResultsAmong the 4 513 746 participants (mean [SD] age, 53.6 [9.6] years; 2 324 172 [51.5%] men), the incidence rate of cancer was 7.7 per 1000 person-years during a median (IQR) follow-up of 6.4 (6.1-6.6) years. Compared with the sustainer groups at each drinking level, the increaser groups had a higher risk of alcohol-related cancers and all cancers. The increased alcohol-related cancer incidence was associated with dose; those who changed from nondrinking to mild (adjusted hazard ratio [aHR], 1.03; 95% CI, 1.00-1.06), moderate (aHR, 1.10; 95% CI, 1.02-1.18), or heavy (aHR, 1.34; 95% CI, 1.23-1.45) drinking levels had an associated higher risk than those who did not drink. Those with mild drinking levels who quit drinking had a lower risk of alcohol-related cancer (aHR, 0.96; 95% CI, 0.92-0.99) than those who sustained their drinking levels. Those with moderate (aHR, 1.07; 95% CI, 1.03-1.12) or heavy (aHR, 1.07; 95% CI, 1.02-1.12) drinking levels who quit drinking had a higher all cancer incidence than those who sustained their levels, but when quitting was sustained, this increase in risk disappeared. Compared with sustained heavy drinking, reduced heavy drinking levels to moderate levels (alcohol-related cancer: aHR, 0.91 [95% CI, 0.86-0.97]; all cancers: aHR, 0.96 [95% CI, 0.92-0.99]) or mild levels (alcohol-related cancer: aHR, 0.92 [95% CI, 0.86-0.98]; all cancers: aHR, 0.92 [95% CI, 0.89-0.96]) were associated with decreased cancer risk.Conclusions and relevanceResults of this study showed that increased alcohol consumption was associated with higher risks for alcohol-related and all cancers, whereas sustained quitting and reduced drinking were associated with lower risks of alcohol-related and all cancers. Alcohol cessation and reduction should be reinforced for the prevention of cancer.

Dataset Information

Genetically determined alcohol consumption and cancer risk in Korea.

Objectives

Methods

Results

Conclusions

Publications

Genetically determined alcohol consumption and cancer risk in Korea.

Similar Datasets

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