White Wine Consumption Research Articles

Moderate alcohol consumption increases insulin sensitivity and ADIPOQ expression in postmenopausal women: a randomised, crossover trial

Aims/hypothesisTo determine whether 6 weeks of daily, moderate alcohol consumption increases expression of the gene encoding adiponectin (ADIPOQ) and plasma levels of the protein, and improves insulin sensitivity in postmenopausal women.MethodsIn a randomised, open-label, crossover trial conducted in the Netherlands, 36 apparently healthy postmenopausal women who were habitual alcohol consumers, received 250 ml white wine (∼25 g alcohol/day) or 250 ml of white grape juice (control) daily during dinner for 6 weeks. Randomisation to treatment allocation occurred according to BMI. Insulin sensitivity and ADIPOQ mRNA and plasma adiponectin levels were measured at the end of both periods. Insulin sensitivity was estimated using the homeostasis model assessment of insulin resistance (HOMA-IR). Levels of ADIPOQ mRNA in subcutaneous adipose tissue were determined by RT-PCR.ResultsAll subjects completed the study. Six weeks of white wine consumption reduced fasting insulin (mean ± SEM 40.0 ± 3.4 vs 46.5 ± 3.4 pmol/l; p < 0.01) and HOMA-IR (1.42 ± 0.13 vs 1.64 ± 0.13; p = 0.02) compared with 6 weeks of grape juice consumption. ADIPOQ mRNA levels (1.09 ± 0.15 vs 0.98 ± 0.15; p = 0.04) and plasma levels of total (13.1 ± 0.8 vs 12.0 ± 0.8 μg/ml; p < 0.001) and high molecular weight (HMW) adiponectin (9.9 ± 1.2 vs 8.8 ± 1.2 μg/ml; p = 0.02) significantly increased after alcohol compared with juice consumption. Changes in ADIPOQ mRNA levels correlated with changes in plasma levels of total adiponectin (ρ = 0.46; p < 0.01). Both fasting triacylglycerol (8.2%; p = 0.04) and LDL-cholesterol levels (7.8%; p < 0.0001) decreased, whereas HDL-cholesterol increased (7.0%; p < 0.0001) after prolonged moderate alcohol intake. No notable adverse effects were reported.Conclusions/interpretationModerate alcohol consumption for 6 weeks improves insulin sensitivity, adiponectin levels and lipid profile in postmenopausal women. Furthermore, these data suggest a transcriptional mechanism leading to the alcohol-induced increase in adiponectin plasma levels.Trial registration:ClinicalTrials.gov ID no.: NCT00285909Funding:Partly funded by the Dutch Foundation for Alcohol Research (SAR).

A prospective cohort study of red wine consumption and risk of prostate cancer

In light of recent, strong inverse findings between lifetime red wine consumption and prostate cancer among younger men, we revisited our previous cohort analysis to more thoroughly investigate red wine consumption and prostate cancer in the Health Professionals Follow-up Study (HPFS). In 1986, HPFS participants reported their average consumption of red wine, white wine, beer and liquor during the past year, and their change in alcohol consumption over the prior 10 years. Prostate cancer diagnoses were ascertained on each biennial questionnaire and confirmed by medical record review. Between 1986 and 2002, 3,348 cases of prostate cancer were diagnosed among 45,433 eligible participants. Using men who did not consume red wine as the reference, no linear trend was observed between red wine consumption and prostate cancer in the full analytic cohort (p-trend = 0.57). Among men with unchanged alcohol consumption in the prior 10 years, and those additionally <65 years of age, slightly lower risks were observed for men who consumed <or=4 glasses of red wine/week, whereas null or slight increased risks were observed for men who consumed >4 glasses/week, resulting in a lack of linear trend. These findings suggest that red wine does not contribute appreciably to the etiology of prostate cancer.

Effect of white wine consumption on oxidative stress markers and homocysteine levels

The aim of this study was to assess the influence of regular daily consumption of white wine on oxidative stress and cardiovascular risk markers. Forty-two healthy male volunteers consumed 375 ml of white wine daily. Each participant provided three venous blood samples (before wine consumption, following the wine consumption period and again a month later). Levels of superoxide dismutase, glutathione peroxidase, reduced glutathione, total antioxidant capacity, total cholesterol, HDL-cholesterol, apolipoprotein A I, apolipoprotein B, triglycerides, paraoxonase 1, C-reactive protein, homocysteine, thiobarbituric acid reactive substances (TBARS) and advanced oxidation protein products (AOPP) were measured. Immediately following the month of white wine consumption there was a significant increase in HDL-cholesterol (p<0.0001), paraoxonase 1 (p<0.001), glutathione peroxidase (p<0.001) and reduced glutathione (p<0.01) levels, a decrease in superoxide dismutase activities (p<0.0001), and a decrease in oxidation protein products (p<0.001) and TBARS (p<0.05) concentrations. However, there was also a clear increase in homocysteine (p<0.0001) after a month of white wine consumption. The results of our non-placebo controlled trial suggest that regular daily white wine consumption is associated not only with both antioxidative and antiatherogenic effects but also with a potentially proatherogenic increase of homocysteine concentrations.

Alcohol Use and the Risk of Prostate Cancer: Results From the VITAL Cohort Study

: An association between alcohol consumption and prostate cancer risk remains uncertain. Although some studies have found that heavy alcohol consumption is associated with increased risk, a recent study reported that red wine consumption is associated with reduced risk. We examined the association between alcohol use and prostate cancer among 34,565 men, 50–76 yr old, in the Vitamins and Lifestyle (VITAL) cohort in Washington State. Alcohol consumption was ascertained by baseline questionnaire between October 2000 and December 2002. Incident prostate cancers (n = 816) as of December 31, 2004, were identified through the Surveillance, Epidemiology, and End Results cancer registry. Men who consumed more than one drink per month had a small increased risk of prostate cancer (hazard ratio, HR = 1.20; 95% confidence interval, CI = 1.02–1.40) compared with men who drank no alcohol or less than one drink per month. White wine consumption was associated with increased risk (HR for any vs. no white wine consumption = 1.27; CI = 1.08–1.49). Red wine, liquor, and beer were not associated with prostate cancer nor was total alcohol consumed at ages 18, 30, and 45. Associations of alcohol use with prostate cancer are modest and complex. More detailed assessment of specific alcoholic beverages is warranted in future studies.

Lifestyle or Resveratrol? Comparison of White and Red Wine Consumption and Colorectal Neoplasia

Lifestyle or Resveratrol? Comparison of White and Red Wine Consumption and Colorectal Neoplasia

Effect of Moderate White Wine Consumption on Serum IgA and Plasma Insulin under Fasting Conditions

Background/Aims: The present study aims to investigate the contribution of alcohol toxicity to the development of malnutrition by assessing the effect of consuming a moderate amount of white wine on plasma insulin and serum IgA under fasting conditions. Methods: A total of 5 non-alcoholic males aged between 19 and 22 years participated in the current investigation. The experimental procedure required participants to undergo a 6-hour fast before ingesting 4 standard units of alcohol (40 g) in the form of white wine over a 120-min period. The level of blood alcohol, plasma insulin and serum IgA was assessed at 30-min intervals across the 120-min experimental period. Results: Consuming alcohol promotes a significant increase in serum IgA in the absence of any change in plasma insulin or ketone production in fasted individuals. Conclusion: White wine prior to a meal does not promote glucose metabolism and utilization and may increase the risk of developing a transient diabetic condition due to an alteration in energy metabolism.

Diagnostic Performance of Urinary Resveratrol Metabolites as a Biomarker of Moderate Wine Consumption

Nutritional biomarkers may be better measures of dietary exposure than self-reported dietary data. We evaluated resveratrol metabolites, potential biomarkers of wine consumption, in humans after moderate consumption of sparkling, white, or red wines. We performed 2 randomized, crossover trials and a cohort study. In the first study, 10 healthy men consumed 30 g of ethanol/day as sparkling wine or gin for 28 days. In the second trial, 10 healthy women consumed 20 g of ethanol/day as white or red wine for 28 days. We also evaluated 52 participants in a study on the effects of a Mediterranean diet on primary prevention of cardiovascular disease (the PREDIMED Study). We used liquid chromatography-tandem mass spectrometry to analyze urinary total resveratrol metabolites (TRMs) and predictive values and ROC curve analyses to assess the diagnostic accuracy. We observed significant increases in TRMs [72.4 (95% confidence interval, 48.5-96.2; P = 0.005), 211.5 (166.6-256.3; P = 0.005), and 560.5 nmol/g creatinine (244.9-876.1; P = 0.005)] after consumption of sparkling, white, or red wine, respectively, but no changes after the washout or gin periods. In the cohort study, the reported daily dose of wine consumption correlated directly with TRMs (r = 0.654; P < 0.001). Using a cutoff of 90 nmol/g, we were able to use TRMs to differentiate wine consumers from abstainers with a sensitivity of 72% (60%-84%); and a specificity of 94% (87%-100%). Resveratrol metabolites in urine may be useful biomarkers of wine intake in epidemiologic and intervention studies.

Effect of Acute and Chronic Moderate Red or White Wine Consumption on Fasted and Postprandial Lipemia in the Rat

The effects of acute and chronic (10 wk) red or white wine consumption on fasted and postprandial lipemia in the rat model are reported. Fasted rats, in the acute study, were loaded intragastrically with 5 ml of an olive oil emulsion (30% w/v) in the presence or absence of wine (8% v/v ethanol), and either mesenteric lymph or blood was collected 3 h postprandially. Animals in the chronic study received either red or white wine in drinking water for a period of 10 wk (3% v/v ethanol). Blood samples were collected from animals in either the fasted state or after fat–wine loading. Postprandially, wine delayed gastric emptying, reduced lymph triacylglycerol (TAG) secretion concomitantly with increased number and decreased chylomicron (CM) size, and increased plasma TAG and CM concentrations. Phospholipid and cholesterol contents of CM, but not very-low-density lipoprotein (VLDL), were increased, indicating enhanced liver bile secretion; however, a significant increase in plasma VLDL concentration was observed. In the chronic study, a wine–fat load resulted in increased high-density lipoprotein (HDL) cholesterol concentration and less pronounced postprandial hypertriglyceridemia and hyperchylomicronemia. In the fasted state, plasma TAG and total apolipoprotein B concentrations were not modified in these animals, and an increase in HDL and a decrease in low-density lipoprotein (LDL)/HDL cholesterol ratios were observed. No liver function or intestinal lipid absorption impairment was observed. In conclusion, unlike binge drinking, chronic moderate wine consumption appears to have a cardioprotective effect in the fasted state, an effect attenuated by the observed temporary postprandial hyperchylomicronemia and hypertriglyceridemia resulting from a direct effect of alcohol on CM size and number.

Roles of drinking pattern and type of alcohol consumed in coronary heart disease in men.

Although moderate drinking confers a decreased risk of myocardial infarction, the roles of the drinking pattern and type of beverage remain unclear. We studied the association of alcohol consumption with the risk of myocardial infarction among 38,077 male health professionals who were free of cardiovascular disease and cancer at base line. We assessed the consumption of beer, red wine, white wine, and liquor individually every four years using validated food-frequency questionnaires. We documented cases of nonfatal myocardial infarction and fatal coronary heart disease from 1986 to 1998. During 12 years of follow-up, there were 1418 cases of myocardial infarction. As compared with men who consumed alcohol less than once per week, men who consumed alcohol three to four or five to seven days per week had decreased risks of myocardial infarction (multivariate relative risk, 0.68 [95 percent confidence interval, 0.55 to 0.84] and 0.63 [95 percent confidence interval, 0.54 to 0.74], respectively). The risk was similar among men who consumed less than 10 g of alcohol per drinking day and those who consumed 30 g or more. No single type of beverage conferred additional benefit, nor did consumption with meals. A 12.5-g increase in daily alcohol consumption over a four-year follow-up period was associated with a relative risk of myocardial infarction of 0.78 (95 percent confidence interval, 0.62 to 0.99). Among men, consumption of alcohol at least three to four days per week was inversely associated with the risk of myocardial infarction. Neither the type of beverage nor the proportion consumed with meals substantially altered this association. Men who increased their alcohol consumption by a moderate amount during follow-up had a decreased risk of myocardial infarction.

The in vivo antithrombotic effect of wine consumption on human blood platelets and hemostatic factors.

We compared the in vivo effect of red vs. white wine consumption on platelet aggregation, responsiveness and membrane viscosity, plasma total antioxidant status, thromboxane B(2) levels, and fibrinolysis. Diet and red wine had a synergistic effect in decreasing platelet aggregation. Red wine did not have a significantly more favorable effect on the fibrinolytic factors than white wine. The reduction in platelet membrane viscosity after red wine, which could contribute to the protective antithrombotic role of red wine, needs further explanation.

The cardioprotective effect of wine on human blood chemistry.

We investigated the in vivo effects of regular consumption of red and white wine on the serum lipid profile, plasma plasminogen activator-1, homocysteine levels, and total antioxidant status. This study confirmed that moderate consumption of wine, red more than white, exerts cardioprotective effects through beneficial changes in lipid profiles and plasma total antioxidant status.

The effect of a moderate level of white wine consumption on the hypothalamic–pituitary–adrenal axis before and after a meal

The nutritional status of the individual at the time of alcohol consumption may mediate the rate of alcohol absorption and metabolism, thus influencing the systemic effect of alcohol on the body. The aim in the present investigation was to assess the effect of moderate white wine consumption on the hypothalamic–pituitary–adrenal (HPA) axis under variable nutritional conditions. Seven males aged between 19 and 22 years participated in all aspects of the current investigation. The experimental procedure for the fasting trial required participants to ingest either 4 standard units of alcohol (40 g) or the equivalent amount of placebo over a 135-min period before consuming food for 45 min. Alternatively, in the feeding trial, food was consumed for 45 min prior to participants ingesting either 4 standard units of alcohol (40 g) or the equivalent amount of placebo over a 135-min period. Blood alcohol, salivary cortisol, and salivary dehydroepiandrosterone sulfate (DHEAS) levels were assessed at 45-min intervals during the 180-min experimental periods. The results demonstrated a significant alcohol-induced decrease in salivary cortisol irrespective of nutritional status and a significant decrease in salivary DHEAS when alcohol is consumed alone under fasting conditions only. It was concluded that moderate white wine consumption may promote a transient alteration in the functioning of the HPA axis.

Red wine polyphenols, in the absence of alcohol, reduce lipid peroxidative stress in smoking subjects

Phenolic compounds in red wine can exert antioxidant effects on in vitro lipoprotein oxidation. This has led to speculation that red wine consumption mediates unique anti-atherosclerotic effects compared to other alcoholic beverages. However, studies assessing the effects of red wine consumption on lipoprotein oxidation ex vivo have not been conclusive. The recent identification of the F 2-isoprostanes as oxidative products of arachidonic acid has provided a reliable measure of in vivo lipid peroxidation. This randomized trial investigated changes in plasma and urinary F 2-isoprostane concentrations following red wine, white wine, or dealcoholized red wine consumption in humans. Eighteen male smokers consumed, in random order, red wine, white wine, or dealcoholized red wine, for two weeks with one week washout between beverages. Plasma and urinary F 2-isoprostane concentrations were measured before and after each beverage. Serum γ-glutamyl transpeptidase (γ-GT) and urinary 4-O -methylgallic acid were measured as markers of alcohol consumption and phenolic acid absorption, respectively. Plasma F 2-isoprostanes ( p < .05) decreased significantly with dealcoholized red wine but not with the alcohol-containing beverages. Urinary excretion of F 2-isoprostanes showed a similar trend. γ-GT decreased significantly with dealcoholized red wine and increased with both alcohol-containing beverages ( p < .01). Urinary excretion of 4-O-methylgallic acid increased significantly ( p < .001) in the 24 h urine samples following red wine or dealcoholized red wine ingestion, but not with white wine. Serum urate increased and β-carotene decreased with both alcoholic beverages relative to dealcoholized red wine. There was no change in the antioxidants α- and γ-tocopherol or vitamin C with any of the beverages. The results suggest that polyphenols in dealcoholized red wine can reduce in vivo lipid peroxidation as measured by F 2-isoprostanes in smoking subjects. However, no reduction in lipid peroxidation was observed following red or white wine consumption, suggesting that any protective effects of wine drinking on cardiovascular disease are unlikely to be related to inhibition of lipid oxidation.

Chromosomal damage rate, aging, and diet.

Chromosomal damage as measured by frequency of translocations, acentric fragments, telomere shortening, nondisjunction, chromosome loss, aneuploidy, and micronucleus formation has been shown to increase progressively with age. Using the cytokinesis-block micronucleus technique, which provides an efficient measure of chromosomal breakage and loss, we have been able to show that aging can explain at least 25% of the variation in chromosomal damage rate in lymphocytes from both males and females. We have also performed cross-sectional and placebo-controlled intervention studies to determine the relationship between the micronucleus (MN) frequency in lymphocytes and diet, and blood status for vitamins C, E, B12, and folic acid. Our studies have shown that MN frequency in the 41- to 60-year age group is significantly lower in vegetarians when compared to nonvegetarians, but the reverse was true in males aged between 20 and 40 years. This was accounted for by a deficient/low B12 status in vegetarian males; there was no difference in the MN frequency of vegetarian and nonvegetarian subjects aged between 61 and 90 years. Results from this study also showed significant negative correlations of MN frequency with folic acid and vitamin B12 but not with vitamin C or vitamin E. In separate studies on healthy men aged 50-70, we have verified the significant negative correlation between vitamin B12 status in plasma and MN frequency (r = -0.315, p = 0.013) in subjects who were not vitamin B12 deficient and observed a significant positive correlation between MN frequency and homocysteine status (r = 0.414, p = 0.0086) in those men who were not vitamin B12 and/or folate deficient. These data suggest that MN frequency is minimized when plasma B12 is above 300 pmol/L and plasma homocysteine is below 7.5 mumol/L. Double-blind placebo-controlled intervention studies conducted over four months have shown that above RDI intake of vitamin E (30 x RDI) or folic acid (10 x RDI) did not produce a significant reduction in MN frequency in men aged 50-70 years. In the latter case plasma homocysteine was reduced from a mean value of 9.33 mumol/L to 8.51 mumol/L, a level that does not correspond with minimization of MN frequency. We have also tested the hypothesis that moderate wine drinking can protect against the DNA-damaging effect of hydrogen peroxide and found that there was a strong ex vivo inhibition (> 70%) of hydrogen peroxide-induced MN frequency by plasma samples from blood collected one hour after consumption of red or white wine, as compared to plasma samples collected immediately before wine consumption (p = 0.0008). However, only samples following red wine consumption produced a significant reduction in baseline MN frequency. The above results suggest that chromosome damage can be modulated, under selected circumstances, by diverse dietary factors.

Moderate wine consumption protects against hydrogen peroxide-induced DNA damage.

We have tested the hypothesis that moderate wine drinking can protect somatic cells against the DNA-damaging effect of hydrogen peroxide which is an endogenous source of reactive oxygen metabolites. In this preliminary investigation, four male volunteers were placed on a plant-polyphenol-free (PPF) diet to ensure that the wine provided was the only main source of plant phenolic compounds. After 48 h on the PPF diet the volunteers were required to consume 300 ml of red or white wine and blood samples collected 1, 3, 8 and 24 h post-consumption while still on a PPF diet. Plasma was isolated from the blood samples and stored frozen for subsequent assays. In the subsequent assays, fresh lymphocytes from each donor were incubated in their corresponding plasma from the various intervention time-points for 30 min. The capacity of the plasma to prevent damage to DNA in lymphocytes by hydrogen peroxide was assessed using the cytokinesis-block micronucleus technique. The data from this preliminary investigation indicated that there was a strong inhibition (>70%) of hydrogen peroxide-induced micronucleated cells by the plasma samples from the blood collected 1 h after consumption of wine as compared to plasma samples from blood immediately before the consumption of wine. This protective effect was apparent for both red and white wine although statistical significance (P = 0.0068) was achieved only in the white wine intervention. A higher degree of statistical significance (P = 0.0008) was achieved when the data for samples following the consumption of red and white wine were combined. There was no difference in the hydrogen-peroxide-induced micronucleated cell frequency when comparing results immediately before starting on the PPF diet, before consumption of wine, 8 h after or 24 h after wine consumption. The hydrogen peroxide-induced micronucleated cell frequency in cells incubated with plasma from blood collected 3 h after wine consumption was intermediate to that observed for plasma after 1 and 8 h after wine intake. The protective effect of plasma against DNA damage cannot be readily explained by the red wine content of phenolic compounds because results for red wine were similar to those for white wine even though white wine had a much lower level of total polyphenols. A possible explanation could be that alcohol, glycerol and ascorbate in wine together with specific wine phenolic compounds that are also equally present in red and white wine (e.g. hydroxycinnamates) may have contributed to the observed protection of nuclear material from hydrogen peroxide-derived reactive oxygen metabolites. This explanation is supported by data from in vitro experiments showing that incubation of lymphocytes either with alcohol or wine stripped of phenolic compounds resulted in a statistically significant (P < 0.05) dose-related reduction (up to 87% reduction) in hydrogen peroxide-induced micronucleated cell frequency.

Red wine consumption does not affect oxidizability of low-density lipoproteins in volunteers

Phenolic compounds in red wine may protect low-density lipoproteins (LDL) against oxidative modification, thereby reducing the risk of cardiovascular morbidity. However, in vivo data are scarce. We gave 13 healthy volunteers 550 mL red wine and another 11 volunteers white wine for 4 wk in a randomized double-blind trial. Interference by alcoholic components of wine was eliminated by reducing the alcohol content to 3.5% Red wine did not affect the susceptibility of LDL to Cu2+ -mediated oxidative modification [lag time before and after red wine drinking (chi +/- SD) 61.8 +/- 7.7 and 62.7 +/- 11.8 min, respectively; lag time before and after white wine drinking: 64.5 +/- 10.4 and 63.3 +/- 10.8 min, respectively]. Concentrations of the antioxidants urate, vitamin C, and glutathione in plasma and of vitamin E and ubiquinol-10 in LDL were also unchanged after either red or white wine consumption. The results of this study do not show a beneficial effect of red wine consumption on LDL oxidation.

Consumption of red wine with meals reduces the susceptibility of human plasma and low-density lipoprotein to lipid peroxidation

The effect of consumption of red or white wine (11% alcohol) with meals on the propensity of plasma and low-density lipoprotein (LDL) to undergo lipid peroxidation was studied in 17 healthy men who were divided into two groups: 8 received 400 mL red wine/d for 2 wk, and 9 received a similar amount of white wine. Red wine consumption for 2 wk resulted in a 20% reduction in the propensity of plasma to undergo lipid peroxidation (in the presence of a free-radical-generating system) as determined by the thiobarbituric acid reactive substances (TBARS) assay. In parallel, red wine consumption reduced the propensity of the volunteers' LDL to undergo lipid peroxidation (in response to copper ions) as determined by a 46%, 72%, and 54% decrease in the content of TBARS, lipid peroxides, and conjugated dienes in LDL, respectively, as well as by a substantial prolongation of the lag phase required for the initiation of LDL oxidation. On the contrary, dietary consumption of white wine for 2 wk resulted in a 34% increase in plasma's propensity to undergo lipid peroxidation and also in a 41% increased propensity of the LDL to undergo lipid peroxidation. The antioxidant effect of dietary red wine on plasma lipid peroxidation was not secondary to changes in the plasma vitamin E or beta-carotene content but could be related to the elevation of polyphenol concentration in plasma and LDL. Thus, some phenolic substances that exist in red wine, but not in white wine, are absorbed, bind to plasma LDL, and may be responsible for the antioxidant properties of red wine.

Lifetime consumption of alcoholic beverages, tea and coffee and exocrine carcinoma of the pancreas: a population-based case-control study in The Netherlands.

From 1984 to 1988 a population-based case-control study was carried out in the Netherlands, in collaboration with the International Agency for Research on Cancer, to examine the possible relationship between the habitual lifetime consumption of alcohol, coffee and tea and exocrine pancreatic carcinoma in 176 cases and 487 controls. An interviewer-administered questionnaire was used to ascertain major life events and obtain estimates of consumption (ever-never) and frequency of consumption throughout life. Logistic regression analyses yielded odds ratios adjusted for age, sex, response status, smoking, dietary intake of energy and vegetables and of alcoholic or non-alcoholic drinks. When compared with data from non-drinkers, the cumulative lifetime consumption of all types of alcohol in grams of ethanol (ORs 1.00, 0.97, 0.93, 1.25, p trend 0.55), beer, spirits, red wine and fortified wine was not related to risk. The consumption of white wine was inversely associated with risk (OR 0.41, 95% CI 0.24-0.70). The uniformly reduced risk estimates for the lifetime number of drinks of white wine were based on small numbers (ORs 1.00, 0.44, 0.25, 0.40, p trend 0.001). When compared with data from non-drinkers, our findings suggest an inverse dose-response relationship for the lifetime consumption of coffee (ORs 1.00, 0.72, 0.37, 0.58, p trend 0.06), whereas lifetime consumption of tea and of ground, instant and decaffeinated coffee was not associated with risk. The absence of an effect of lifetime consumption of decaffeinated coffee may be due to the small numbers of subjects. These results further strengthen existing evidence against a positive association between consumption as well as lifetime consumption of (sources of) alcohol, tea or coffee and the development of exocrine pancreatic cancer.