Alcohol Intake and Pancreatic Cancer Risk: A Pooled Analysis of Fourteen Cohort Studies

Department of Oncology, Lombardi Cancer Center, Georgetown University Medical Center, Washington, DC, USA.
Cancer Epidemiology Biomarkers & Prevention (Impact Factor: 4.13). 03/2009; 18(3):765-76. DOI: 10.1158/1055-9965.EPI-08-0880
Source: PubMed


Few risk factors have been implicated in pancreatic cancer etiology. Alcohol has been theorized to promote carcinogenesis. However, epidemiologic studies have reported inconsistent results relating alcohol intake to pancreatic cancer risk.
We conducted a pooled analysis of the primary data from 14 prospective cohort studies. The study sample consisted of 862,664 individuals among whom 2,187 incident pancreatic cancer cases were identified. Study-specific relative risks and 95% confidence intervals were calculated using Cox proportional hazards models and then pooled using a random effects model.
A slight positive association with pancreatic cancer risk was observed for alcohol intake (pooled multivariate relative risk, 1.22; 95% confidence interval, 1.03-1.45 comparing >or=30 to 0 grams/day of alcohol; P value, test for between-studies heterogeneity=0.80). For this comparison, the positive association was only statistically significant among women although the difference in the results by gender was not statistically significant (P value, test for interaction=0.19). Slightly stronger results for alcohol intake were observed when we limited the analysis to cases with adenocarcinomas of the pancreas. No statistically significant associations were observed for alcohol from wine, beer, and spirits comparing intakes of >or=5 to 0 grams/day. A stronger positive association between alcohol consumption and pancreatic cancer risk was observed among normal weight individuals compared with overweight and obese individuals (P value, test for interaction=0.01).
Our findings are consistent with a modest increase in risk of pancreatic cancer with consumption of 30 or more grams of alcohol per day.

Download full-text


Available from: Graham G Giles,
17 Reads
  • Source
    • "Since therapeutic specimens have only little impact on patient survival, epidemiological studies and molecular research focus on identification and reduction of risk factors. Epidemiological data suggest a slight, but not significant increase in risk for pancreatic carcinoma for individuals consuming 30 or more grams alcohol per day [42]. However, there is an indirect relationship, since ethanol induces the development of chronic pancreatitis and this can lead to pancreatic carcinoma [43]. "
    [Show abstract] [Hide abstract]
    ABSTRACT: In this article we provide an overview of the newest data concerning the effect of non-alcoholic constituents of alcoholic beverages, especially of beer, on pancreatic secretion, and their possible role in alcoholic pancreatitis and pancreatic carcinoma. The data indicate that non-alcoholic constituents of beer stimulate pancreatic enzyme secretion in humans and rats, at least in part, by direct action on pancreatic acinar cells. Some non-alcoholic compounds of beer, such as quercetin, resveratrol, ellagic acid or catechins, have been shown to be protective against experimentally induced pancreatitis by inhibiting pancreatic secretion, stellate cell activation or by reducing oxidative stress. Quercetin, ellagic acid and resveratrol also show anti-carcinogenic potential in vitro and in vivo. However, beer contains many more non-alcoholic ingredients. Their relevance in beer-induced functional alterations of pancreatic cells leading to pancreatitis and pancreatic cancer in humans needs to be further evaluated.
    International Journal of Environmental Research and Public Health 03/2010; 7(3):1093-104. DOI:10.3390/ijerph7031093 · 2.06 Impact Factor
  • Source
    • "Results from smoking-stratified analyses that suggested a possible interaction between current smoking and heavy drinking should be interpreted with caution and require further validation in larger pooled studies, particularly given that the p-interactions for these analyses were >0.3. The association between alcohol consumption and pancreatic cancer in earlier studies has been discordant, with some hospital-based [24–28, 54–59] and population-based case–control [3, 5, 6, 8, 10, 11, 13, 14, 17, 19, 31, 60] and cohort studies [4, 7, 9, 32, 33, 38, 42, 61, 62] showing no association, and other hospital-based [29, 30] and population-based case–control [15, 16, 18] and cohort [20, 21, 34, 36, 37, 41, 63] studies suggesting increased risk. Discordant observations in the published literature may be due to small numbers of cases, residual confounding by risk factors associated with alcohol consumption such as smoking and chronic pancreatitis, unmeasured genetic factors, or absence of detailed data on alcohol exposure [16, 17, 23, 34, 39]. "
    [Show abstract] [Hide abstract]
    ABSTRACT: Alcohol consumption is postulated to be a risk factor for pancreatic cancer (PCA), but clarification of degree of risk related to consumption characteristics is lacking. We examined the association between alcohol consumption and PCA in a population-based case-control study (532 cases, 1,701 controls) in the San Francisco Bay Area. Population-based controls were frequency-matched by sex, age within 5-year categories and county of residence to cases identified by the cancer registry's rapid case ascertainment. Detailed alcohol consumption data, including binge drinking (>or=5 drinks/day), were collected during in-person interviews. Odds ratios (OR) and 95% confidence intervals (95% CI) were computed using adjusted unconditional logistic regression. Depending on dose, duration, and pattern of drinking, ORs were increased 1.5- to 6-fold among men but not women. In men, ORs increased with increasing overall alcohol consumption (22-35 drinks/week OR = 2.2, 95% CI = 1.1-4.0; >or=35 drinks/week OR = 2.6, 95% CI = 1.3-5.1, p-trend = 0.04). Most notable were effects with a history of binge drinking (OR = 3.5, 95% CI = 1.6-7.5) including increased number of drinks per day (p-trend = 0.002), and increased years of binge drinking (p-trend = 0.0006). In fully adjusted models that included smoking and other confounders, ORs for binge drinking in men were somewhat higher than in age-adjusted models. Results from our detailed analyses provide support for heavy alcohol consumption (including binge drinking) as a risk factor for PCA in men.
    Cancer Causes and Control 03/2010; 21(7):1047-59. DOI:10.1007/s10552-010-9533-6 · 2.74 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Pancreatic cancer (PDAC) is a deadly disease. It has an incidence ranging 8–12 per 100,000 per year, with a similar mortality, as more than 95% of patients diagnosed with PDAC will ultimately die. Prevention policies are therefore particularly important and they should be distinguished in: (1) Primary prevention, aimed at reducing risk factors for PDAC and possibly favouring protective habits. (2) Secondary prevention, aimed at the early diagnosis through appropriate screening tests in subjects with a particularly high risk. The most important risk factors for pancreatic cancer are family history of pancreatic cancer, smoking, obesity, diabetes, alcohol and chronic pancreatitis. Diabetes of recent onset should be considered a possible alarm symptom. In patients with defined genetic syndromes such as “familiar pancreatic cancer”, and Peutz–Jeghers syndrome screening for pancreatic cancer as a part of research protocols are performed in selected Centres. There are no sufficient data to suggest that vitamins or aspirin may have a role for PDAC chemoprevention.
    01/1970: pages 3-10;
Show more