No association between alcohol consumption and pancreatic cancer even among individuals genetically susceptible to the carcinogenicity of alcohol.
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ABSTRACT:
SUBMITTER: Shan YS
PROVIDER: S-EPMC8282609 | biostudies-literature |
REPOSITORIES: biostudies-literature
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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
Project description:OBJECTIVES:The objective of this study was to evaluate the association of genetically determined leptin with lipids. DESIGN:We conducted a Mendelian randomisation study to assess a potential causal relationship between serum leptin and lipid levels. We also evaluated whether alcohol drinking modified the associations of genetically determined leptin with blood lipids. SETTING AND PARTICIPANTS:3860 participants of the Framingham Heart Study third generation cohort. RESULTS:Both genetic risk scores (GRSs), the GRS generated using leptin loci independent of body mass index (BMI) and GRS generated using leptin loci dependent of BMI, were positively associated with log-transformed leptin (log-leptin). The BMI-independent leptin GRS was associated with log-transformed triglycerides (log-TG, β=-0.66, p=0.01), but not low-density lipoprotein cholesterol (LDL-C, p=0.99), high-density lipoprotein cholesterol (HDL-C, p=0.44) or total cholesterol (TC, p=0.49). Instrumental variable estimation showed that per unit increase in genetically determined log-leptin was associated with 0.55 (95% CI: 0.05 to 1.00) units decrease in log-TG. Besides significant association with log-TG (β=-0.59, p=0.009), the BMI-dependent GRS was nominally associated with HDL-C (β=-10.67, p=0.09) and TC (β=-28.05, p=0.08). When stratified by drinking status, the BMI-dependent GRS was associated with reduced levels of LDL-C (p=0.03), log-TG (p=0.004) and TC (p=0.003) among non-current drinkers only. Significant interactions between the BMI-dependent GRS and alcohol drinking were identified for LDL-C (p=0.03), log-TG (p=0.03) and TC (p=0.02). CONCLUSION:These findings together indicated that genetically determined leptin was negatively associated with lipid levels and the association may be modified by alcohol consumption.
| S-EPMC6858149 | biostudies-literature
Project description:Pancreatic cancer is one of the most fatal common cancers affecting both men and women, representing about 3% of all new cancer cases in the United States. In this study, we aimed to investigate the association of pancreatic cancer risk with alcohol consumption as well as folate intake. We performed a case-control study of 384 patients diagnosed with pancreatic cancer from May 2004 to December 2009 and 983 primary care healthy controls in a largely white population (>96%). Our findings showed no significant association between risk of pancreatic cancer and either overall alcohol consumption or type of alcohol consumed (drinks/day). Our study showed dietary folate intake had a modest effect size, but was significantly inversely associated with pancreatic cancer (odds ratio (OR) = 0.99, p < 0.0001). The current study supports the hypothesis that pancreatic cancer risk is reduced with higher food-based folate intake.
| S-EPMC5452178 | biostudies-other
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.
| S-EPMC9403779 | biostudies-literature
Project description:ObjectivesThe objective was to clarify the relationship between alcohol consumption/alcohol use disorders and patient complexity.DesignCross-sectional study.SettingA clinic located on a remote island in Okinawa, Japan, providing general outpatient practices and round-the-clock emergency services.ParticipantsPatients who lived on the island, visited Tarama Clinic from 1 April 2018 to 30 June 2018, were aged ≥20 years and had decision-making capacity were judged to be eligible for this study.Main outcome measuresAlcohol consumption/alcohol use disorders as measured by the Alcohol Use Disorders Identification Test (AUDIT) and patient complexity as scored by the Patient Centered Assessment Method (PCAM).ResultsDuring the 3-month study period, 355 patients (163 women and 192 men) with mean (SD) age of 66.4 (13.6) years were included. Multiple regression analysis of PCAM scores showed that, after adjusting for age, sex, education, occupation, physical activity, smoking, annual medical expenses and number of family members living with the patient, AUDIT scores classified as 'dependence likely' were associated with PCAM scores (p value=0.040).ConclusionsAlcohol consumption and alcohol use disorders classified as dependence likely are associated with patient complexity.
| S-EPMC7440824 | biostudies-literature
Project description:It is elusive why some heavy drinkers progress to severe alcohol-related liver disease (ALD) while others do not. This study aimed to investigate if the association between alcohol consumption and severe ALD is modified by diet. This prospective study included 303,269 UK Biobank participants. Alcohol consumption and diet were self-reported. The diet score was created from 4 items selected using LASSO. Cox proportional hazard model showed that the diet score was monotonically associated with severe ALD risk, adjusted for sociodemographics, lifestyle factors, and alcohol consumption. Relative excess risk due to interaction analysis indicated that having a higher ALD diet score and a higher alcohol consumption simultaneously confers to 2.44 times (95% CI: 1.06-3.83) higher risk than the sum of excess risk of each factor. In this work, we show that people who have a poor diet might be more susceptible to severe ALD due to alcohol consumption.
| S-EPMC11317484 | 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:IntroductionObservational studies have suggested that light-to-moderate alcohol consumption decreases the risk of Alzheimer's disease, but it is unclear if this association is causal.MethodsTwo-sample Mendelian randomization (MR) analysis was used to examine whether alcohol consumption, alcohol dependence, or Alcohol Use Disorder Identification Test (AUDIT) scores were causally associated with the risk of Late-Onset Alzheimer's disease (LOAD) or Alzheimer's disease age of onset survival (AAOS). Additionally, γ-glutamyltransferase levels were included as a positive control.ResultsThere was no evidence of a causal association between alcohol consumption, alcohol dependence, or AUDIT, and LOAD. Alcohol consumption was associated with an earlier AAOS and increased γ-glutamyltransferase blood concentrations. Alcohol dependence was associated with a delayed AAOS.DiscussionMR found robust evidence of a causal association between alcohol consumption and an earlier AAOS, but not alcohol intake and LOAD risk. The protective effect of alcohol dependence is potentially due to survivor bias.
| S-EPMC7057166 | biostudies-literature
Project description:ImportanceCardiovascular benefits of mild to moderate alcohol consumption need to be validated in the context of behavioral changes. The benefits of reduced alcohol consumption among people who drink heavily across different subtypes of cardiovascular disease (CVD) are unclear.ObjectiveTo investigate the association between reduced alcohol consumption and risk of major adverse cardiovascular events (MACEs) in individuals who drink heavily across different CVD subtypes.Design, setting, and participantsThis cohort study analyzed data from the Korean National Health Insurance Service-Health Screening database and self-reported questionnaires. The nationally representative cohort comprised Korean citizens aged 40 to 79 years who had national health insurance coverage on December 31, 2002, and were included in the 2002 to 2003 National Health Screening Program. People who drank heavily who underwent serial health examinations over 2 consecutive periods (first period: 2005-2008; second period: 2009-2012) were included and analyzed between February and May 2023. Heavy drinking was defined as more than 4 drinks (56 g) per day or more than 14 drinks (196 g) per week for males and more than 3 drinks (42 g) per day or more than 7 drinks (98 g) per week for females.ExposuresHabitual change in heavy alcohol consumption during the second health examination period. People who drank heavily at baseline were categorized into 2 groups according to changes in alcohol consumption during the second health examination period as sustained heavy drinking or reduced drinking.Main outcomes and measuresThe primary outcome was the occurrence of MACEs, a composite of nonfatal myocardial infarction or angina undergoing revascularization, any stroke accompanied by hospitalization, and all-cause death.ResultsOf the 21 011 participants with heavy alcohol consumption at baseline (18 963 males [90.3%]; mean [SD] age, 56.08 [6.16] years) included in the study, 14 220 (67.7%) sustained heavy drinking, whereas 6791 (32.2%) shifted to mild to moderate drinking. During the follow-up of 162 378 person-years, the sustained heavy drinking group experienced a significantly higher incidence of MACEs than the reduced drinking group (817 vs 675 per 100 000 person-years; log-rank P = .003). Reduced alcohol consumption was associated with a 23% lower risk of MACEs compared with sustained heavy drinking (propensity score matching hazard ratio [PSM HR], 0.77; 95% CI, 0.67-0.88). These benefits were mostly accounted for by a significant reduction in the incidence of angina (PSM HR, 0.70; 95% CI, 0.51-0.97) and ischemic stroke (PSM HR, 0.66; 95% CI, 0.51-0.86). The preventive attributes of reduced alcohol intake were consistently observed across various subgroups of participants.Conclusions and relevanceResults of this cohort study suggest that reducing alcohol consumption is associated with a decreased risk of future CVD, with the most pronounced benefits expected for angina and ischemic stroke.
| S-EPMC10979316 | biostudies-literature
Project description:BackgroundBoth positive expectancies regarding the effects of alcohol and internalizing problems, including negative emotionality and deficits in emotion regulation, are known risk factors for alcohol use disorder (AUD). The current study is the first to investigate how neural response to emotional stimuli may impact alcohol expectancies and risk for AUD.MethodsFunctional neuroimaging data was collected during an emotional word task from 168 emerging adults (M age = 19.65; 66% male). Activation to negative versus neutral words and positive versus neutral words was extracted for analyses. Participants also reported on their alcohol expectancies and information regarding alcohol use and problems was collected prospectively throughout adolescence and into adulthood (up to age 30).ResultsDecreased activation in the inferior frontal gyrus (IFG) to negative versus neutral words was associated with increased post-scan alcohol consumption, measured as average drinks per year. There was a significant indirect effect of positive alcohol expectancies on the association between IFG activation and post-scan alcohol consumption, even when controlling for quantity of alcohol consumption prior to the scan.ConclusionsThese results are the first to provide evidence that positive alcohol expectancies account for variance shared between brain regions associated with emotion processing and increased drinking behaviors. Alcohol expectancies may provide a modifiable target for treatments to decrease the link between deficits in emotion regulation and increased alcohol use.
| S-EPMC7357240 | biostudies-literature