The alcohol flushing response: an unrecognized risk factor for esophageal cancer from alcohol consumption.
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ABSTRACT:
SUBMITTER: Brooks PJ
PROVIDER: S-EPMC2659709 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:Association between drinking and smoking has remained controversial since the association between two studies were influenced by various confounding. Thus, our study aimed to explore the causal effect of alcohol consumption and cigarette smoking using alcohol flushing as an instrument variable, which is free from confounders. We analyzed cross-sectional survey data from 2500 Korean young adults (1600 men and 900 women). Alcohol flushing was strongly associated with log transformed alcohol consumption (F = 272). In men, alcohol non-flushers were 1.41 times (95% CI 1.28-1.55) more likely to smoke 100 cigarettes in their lifetime in logistic regression analysis. Alcohol non-flushers were also 1.3 times (95% CI 1.21-1.40) more likely to become daily smokers and 1.39 times (95% CI 1.27-1.51) more likely to be current smokers than alcohol flushers. However, in an IV analysis, no causal relationships between alcohol consumption and smoking status were found. Alcohol consumption, on the other hand, was causally associated with lowering nicotine dependence and former smoking in men. Alcohol consumption determined by alcohol flushing status does not appear to be causally linked to the smoking behavior of young adults. The relationship between alcohol consumption and nicotine dependence and smoking cessation needs further study.
| S-EPMC8583641 | biostudies-literature
Project description:BackgroundAlcohol is a risk factor for cancer of the oral cavity, pharynx, oesophagus, colorectum, liver, larynx and female breast, whereas its impact on other cancers remains controversial.MethodsWe investigated the effect of alcohol on 23 cancer types through a meta-analytic approach. We used dose-response meta-regression models and investigated potential sources of heterogeneity.ResultsA total of 572 studies, including 486 538 cancer cases, were identified. Relative risks (RRs) for heavy drinkers compared with nondrinkers and occasional drinkers were 5.13 for oral and pharyngeal cancer, 4.95 for oesophageal squamous cell carcinoma, 1.44 for colorectal, 2.65 for laryngeal and 1.61 for breast cancer; for those neoplasms there was a clear dose-risk relationship. Heavy drinkers also had a significantly higher risk of cancer of the stomach (RR 1.21), liver (2.07), gallbladder (2.64), pancreas (1.19) and lung (1.15). There was indication of a positive association between alcohol consumption and risk of melanoma and prostate cancer. Alcohol consumption and risk of Hodgkin's and Non-Hodgkin's lymphomas were inversely associated.ConclusionsAlcohol increases risk of cancer of oral cavity and pharynx, oesophagus, colorectum, liver, larynx and female breast. There is accumulating evidence that alcohol drinking is associated with some other cancers such as pancreas and prostate cancer and melanoma.
| S-EPMC4453639 | biostudies-literature
Project description:BackgroundThe alcohol-induced facial flushing phenotype (flushing) is common among East Asians. Despite a small intake of alcohol, they experience heightened levels of acetaldehyde, a group-1 carcinogen, which, in turn, causes unpleasant symptoms such as redness, acting as a robust protective mechanism against consuming alcohol. However, some individuals with this genetic trait exhibit weakened alcohol restraint, which increases the risk of developing alcohol-related cancers, such as esophageal and head or neck cancer, by several times. Although this flushing phenomenon is crucial for public health, there is a paucity of studies that have comprehensively investigated the effect of flushing or its genotype on alcohol consumption in a large group of East Asians while controlling for various sociodemographic and health-related variables at a country level.ObjectiveThis 2-year cross-sectional study aims to explore the effect of flushing on drinking behavior in Koreans and to examine whether the effect varies across sociodemographic and health-related factors.MethodsWe used data from the Korea National Health and Nutrition Examination Survey (KNHANES) for 2019 and 2020 conducted by the Korea Disease Control and Prevention Agency. Our sample comprised 10,660 Korean adults. The study investigated the association of 26 variables, including flushing, with drinking frequency and amount. The effect of flushing was examined with and without adjusting for the other 25 variables using multinomial logistic regression analysis. In addition, we tested the interaction effect with flushing and conducted a simple effect analysis. We used complex sample design elements, including strata, clusters, and weights, to obtain unbiased results for the Rao-Scott χ2 test, 2-tailed t test, and multinomial logistic regression analysis.ResultsThe suppressive effect of flushing was significant (P<.001) across all pronounced categories of alcohol consumption in 2019. The ranges of standardized regression slopes and odds ratios (ORs) were -6.70≥β≥-11.25 and 0.78≥OR≥0.50 for frequency and -5.37≥β≥-17.64 and 0.73≥OR≥0.36 for amount, respectively. The effect became somewhat stronger when adjusted for confounders. The effect also exhibited an overall stronger trend as the severity of alcohol consumption increased. The β values and ORs were consistently smaller in 2020 compared to the previous year. A simple effect analysis revealed a diminished alcohol-suppressive effect of flushing on alcohol consumption for specific groups (eg, those with low levels of education, limited family support, physical labor, or health-related issues).ConclusionsOur findings suggest that flushing suppresses drinking in Koreans overall but has little or no effect in certain susceptible populations. Therefore, health authorities should conduct targeted epidemiological studies to assess drinking patterns and disease profiles, particularly regarding alcohol-related cancers, and establish effective preventive measures tailored to this population.
| S-EPMC11325126 | biostudies-literature
Project description:ObjectivesThe purpose of this study was to determine the causal relationship between the genetically determined amount of alcohol consumption and the occurrence of major cancers.MethodsThe 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.ResultsFrom 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).ConclusionsThe 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.
| S-EPMC10728612 | biostudies-literature
Project description:ObjectiveTo investigate the relationship between alcohol consumption and the incidence of dementia.MethodWe will conduct a systematic search without language and year restrictions to identify all relevant published studies. The following electronic databases will be searched: PubMed, EMBASE, the Cochrane Library, Chinese BioMedical Literature Database (CBM) and China National Knowledge Infrastructure (CNKI), VIP, Wan-Fang. Cohort studies published in Chinese or English are considered for inclusion. Two authors will independently select studies base on inclusion criteria, extract data and assess the quality of included studies using the Newcastle-Ottawa Scale, the Grades of Recommendation, Assessment, Development, and Evaluation (GRADE) system will be used to quantify absolute effects and quality of evidence. Any disagreement will be resolved by consensus. We will use the hazard ratio (HR) as the effect indicator, piecewise linear regression model and restricted cubic spline model will be used for linear and nonlinear trend estimation, respectively.RegistrationThe dose-response meta-analysis is registered in the PROSPERO (CRD42019127367) international prospective register of systematic review.DiscussionIn the previous related dose-response meta-analysis studies, there were some limitations: on the 1 hand, the sex was not taken into account. On the other hand, relative risk (RR) is not the best effect indicator for time-to-event data, but compare with RR, HR is much better. This study intends to use HR as the effect indicator to explore the dose-response relationship and the sex difference between alcohol intake and dementia. Accurate alcohol drinking data can provide high-quality evidence for the prevention of dementia.
| S-EPMC6617082 | biostudies-literature
Project description:In epidemiologic studies, alcohol consumption appears more strongly associated with risk of estrogen receptor (ER)-positive than ER-negative breast cancer. However, this association has not been assessed by other potentially relevant tumor markers, such as androgen receptor (AR) or insulin receptor (IR). In the prospective Nurses' Health Study cohort, we evaluated alcohol consumption and breast cancer risk by individual tumor marker expression (i.e., ER, progesterone receptor [PR], AR, and IR) while controlling for other markers and also assessed the joint effect of these receptors. During 26 years follow-up of 106,037 women, 2552 invasive breast cancers contributed to the analysis. When all four markers were considered simultaneously, no significant heterogeneity of the alcohol and breast cancer association was observed by any of the markers. However, each increment in one drink per day was associated with 10% (95% confidence interval [CI]?= 4%, 15%) and 9% (95% CI = 4%, 15%) increased risk of AR-positive and ER-positive breast cancer, respectively, while no increased risk was observed among AR-negative or ER-negative tumors. The association was independent of PR and IR expression. Assessment of the joint expression of hormone receptors revealed a significantly increased risk among AR+/ER+/PR+ (hazard ratio [HR] per drink/day = 1.11, 95% CI = 1.06, 1.17) but not in other subgroups (e.g. , AR-/ER-/PR-: HR = 0.99; 95% CI = 0.88, 1.12). Our data suggest that the alcohol and breast cancer association may be more pronounced among ER-positive and/or AR-positive breast tumors. However, our data do not support an important role of IR in the association.
| S-EPMC4631632 | biostudies-other
Project description:Existing evidence remains inconclusive as to how the association between inactive ALDH2 and esophageal cancer (EC) depends on alcohol consumption. The study is based on the China Kadoorie Biobank cohort, with 10 years follow-up of 0.5 million adults aged 30-79 years. ALDH2 activity was assessed by both self-reported flushing response and Glu504Lys (rs671 G?>?A) polymorphism. Among both male and female participants who consumed alcohol less than weekly (n?=?69,519; 211 EC cases), low active or inactive ALDH2 was not associated with increased EC risk [HRs (95% CIs): GA vs. GG 0.75 (0.54, 1.04); AA vs. GG 1.01 (0.46, 2.20)]. Among male weekly alcohol consumers, both flushing response [n?=?59,380; 501 EC cases; HRs (95% CIs): "soon after drinking" vs. "no" flushing response 1.45 (1.05, 2.01)] and rs671 [n?=?10,692; 94 EC cases; GA vs. GG 3.31 (1.94, 5.67)] were associated with EC risk. The increased EC risk associated with "soon" response or rs671 GA was apparent in men consuming alcohol ?30g/d. Among male daily consumers, the HRs (95% CIs) for EC associated with 15g/d of alcohol were 1.28 (1.15, 1.44) for "soon" response [vs. other responses: 1.12 (1.09, 1.15); pinteraction ?=?0.047; n?=?36,401, 425 EC cases] and 1.41 (1.08, 1.82) for rs671 GA [vs. GG: 1.16 (1.06, 1.27); pinteraction ?=?0.493; n?=?6,607, 80 EC cases]. Self-reported flushing response had low sensitivity (56.8%) and high specificity (88.4%) in identifying rs671 A allele among male weekly alcohol consumers. In conclusion, low-activity ALDH2 was associated with increased EC risk among male heavy alcohol consumers. More accurate measurement of alcohol-related EC risk allows better achievement of precision prevention.
| S-EPMC6175107 | biostudies-literature
Project description:BackgroundIt is still inconclusive whether alcohol consumption affects the risk of thyroid cancer. We conducted a meta-analysis of available epidemiological data to address this issue.ResultsCompared with nondrinkers, the pooled relative risks (RRs) and corresponding 95% confidential intervals (CIs) of thyroid cancer were 0.80 (95% CI 0.71-0.90) for any drinkers, 0.81 (95% CI 0.70-0.93) for light and 0.71 (95% CI 0.63-0.79) for moderate drinkers. The dose-response analysis suggested that there is no evidence of a dose-risk relationship between alcohol intaking and thyroid cancer risk (P = 0.112).MethodsEligible studies were identified by searching PubMed and EMbase databases. A total of 24 studies, included 9,990 cases with thyroid cancer, were included in this meta-analysis. We defined light alcohol intake as ≤ one drink/day and moderate as >one drink/day. The summary risk estimates were calculated by the random effects model. A dose-response analysis was also conducted for modeling the dose-risk relation.ConclusionThis meta-analysis confirmed an inverse association between alcohol consumption and thyroid cancer risk. Further studies are needed to better understand the potential mechanisms underlying this association.
| S-EPMC5342461 | biostudies-literature
Project description:This article has been corrected. The original version (PDF) is appended to this article as a Supplement. Background:Although consumption of tea at high temperatures has been suggested as a risk factor for esophageal cancer, an association has not been observed consistently, and whether any relationship is independent of alcohol and tobacco exposure has not been evaluated. Objective:To examine whether high-temperature tea drinking, along with the established risk factors of alcohol consumption and smoking, is associated with esophageal cancer risk. Design:China Kadoorie Biobank, a prospective cohort study established during 2004 to 2008. Setting:10 areas across China. Participants:456 155 persons aged 30 to 79 years. Those who had cancer at baseline or who reduced consumption of tea, alcohol, or tobacco before baseline were excluded. Measurements:The usual temperature at which tea was consumed, other tea consumption metrics, and lifestyle behaviors were self-reported once, at baseline. Outcome was esophageal cancer incidence up to 2015. Results:During a median follow-up of 9.2 years, 1731 incident esophageal cancer cases were documented. High-temperature tea drinking combined with either alcohol consumption or smoking was associated with a greater risk for esophageal cancer than hot tea drinking alone. Compared with participants who drank tea less than weekly and consumed fewer than 15 g of alcohol daily, those who drank burning-hot tea and 15 g or more of alcohol daily had the greatest risk for esophageal cancer (hazard ratio [HR], 5.00 [95% CI, 3.64 to 6.88]). Likewise, the HR for current smokers who drank burning-hot tea daily was 2.03 (CI, 1.55 to 2.67). Limitation:Tea consumption was self-reported once, at baseline, leading to potential nondifferential misclassification and attenuation of the association. Conclusion:Drinking tea at high temperatures is associated with an increased risk for esophageal cancer when combined with excessive alcohol or tobacco use. Primary Funding Source:National Natural Science Foundation of China and National Key Research and Development Program.
| S-EPMC6675598 | biostudies-literature
Project description:Evidence is inconsistent regarding alcohol and pancreatic cancer risk, although heavy drinking may increase risk.A population-based case-control study was conducted using 345 pancreas cancer cases diagnosed 2011-2012 and 1,285 frequency-matched controls from Ontario, Canada. Logistic regression was used to evaluate alcohol consumption and pancreatic cancer risk; data was also stratified by sex and smoking status to assess interaction.Alcohol consumption was not associated with pancreatic cancer risk (age-adjusted odds ratio=0.78, 95% CI: 0.58, 1.05 for 1 - 3 drinks/week; age-adjusted odds ratio=0.86, 95% CI: 0.63, 1.17 for 4 - 20 drinks/week), however there was a non-significant increased risk for heavy drinkers consuming ≥ 21 drinks/week (age-adjusted odds ratio=1.35, 95% CI: 0.81, 2.27). Cigarette smoking modified the alcohol-cancer relationship; among current smokers, heavy alcohol consumption was associated with a significantly increased pancreatic cancer risk (age-adjusted odds ratio=4.04, 95% CI: 1.58, 10.37), whereas this significant association with heavy drinking was not observed among non-smokers (age-adjusted odds ratio=2.01, 95% CI: 0.50, 8.18). Furthermore, light - moderate alcohol intake was associated with increased pancreas cancer risk among current smokers.While alcohol was not significantly associated with pancreatic cancer risk, smoking status modified this relationship such that among current smokers, alcohol intake was associated with a greater than two-fold increased risk of pancreatic cancer. The results should be interpreted with caution due to small sample sizes within subgroups and correction for multiple comparisons should be considered. These findings should be replicated in larger studies where more precise estimates of risk can be obtained.
| S-EPMC4391718 | biostudies-other