Critique 263:Alcohol Drinking Patterns and Risk of Developing Acute and Chronic Pancreatitis
Becker U, Timmermann A, Ekholm O, Grønbæk M, Drewes AM, Novovic S, Nøjgaard C, Olesen SS, Tolstrup JS. 2023. Alcohol and Alcoholism Mar 1;agad012. doi: 10.1093/alcalc/agad012. Online ahead of print, 10pp.
Aim: The aim was to analyze the effects of drinking pattern and type of alcohol on risk of acute and chronic pancreatitis.
Methods: Prospective cohort study based on data from 316,751 men and women participating in the Danish National Health Surveys 2010 and 2013. Self-reported questionnaire-based alcohol parameters and information on pancreatitis was obtained from national health registers. Cox regression models were used adjusting for baseline year, gender, age, smoking, Body Mass Index, diet and education.
Results: Development of acute and chronic pancreatitis increased with alcohol intake with a significant increase among abstainers and those drinking >14 drinks per week compared with individuals drinking 1-7 drinks per week. Frequent binge drinking and frequent drinking (every day) was associated with increased development of acute and chronic pancreatitis compared with those drinking 2-4 days per week. Problematic alcohol use according to the CAGE-C questionnaire was associated with increased development of acute and chronic pancreatitis. Intake of more than 14 drinks of spirits per week was associated with increased development of acute and chronic pancreatitis, and more than 14 drinks of beer per week were associated with increased development of chronic pancreatitis, whereas drinking wine was not associated with development of pancreatitis.
Conclusion: This large prospective population study showed a J-shaped association between alcohol intake and development of pancreatitis. Drinking every day, frequent binge drinking and problematic alcohol use were associated with increased development of pancreatitis and drinking large amounts of beer and spirits might be more harmful than drinking wine.
Acute pancreatitis (AP) is a common clinical condition resulting from an acute injury to the pancreas usually causing pancreatic inflammation (1). It is self-limiting, meaning that it usually resolves on its own over time and approximately 90% of individuals recover without any complications. There are multiple aetiologies responsible for AP, with the two most common being gallstones, which account for up to 40% of cases, and alcohol, which is responsible for approximately 30% of cases. Other causes of AP include medications, infections, genetic predisposition, trauma and cancer and metabolic causes.
It is one of the most common gastrointestinal conditions that results in hospital admission in the USA, being estimated at 110 to 140 per 100,000 population, with an estimated more than 300,000 US emergency department visits per year. Admissions due to AP have increased from 9.48 cases per 1000 hospitalizations in 2002 to 12.19 in 2013, with a median hospital cost of nearly $7000 per hospitalization (2). The incidence of AP varies, however, across Europe. Gallstones are the dominant aetiology in southern Europe and alcohol in eastern Europe with intermediate ratios in northern and western Europe (3). The risk for a severe outcome was the highest in hypertriglyceridemia-induced AP followed by alcoholic AP, and biliary AP. Mortality rate was significantly greater in hyper-triglyceridemia-induced AP versus alcoholic AP or biliary AP. Pancreatic necrosis occurred more frequently in alcoholic AP than biliary AP patient. Overall, there is a potential association between aetiology and the development and course of AP (4).
Conversely, chronic pancreatitis (CP) is persistent long-standing inflammation of the pancreas that results in permanent structural damage marked by progressive fibrotic destruction of the pancreatic secretory parenchyma leading to an irreversible decrease in exocrine and endocrine pancreatic function. The reported prevalence of CP across the USA and Europe ranges from 0.2% to 0.6% and the incidence is about 7-10 per 100,000 (5). Its aetiology is also multifactorial, although the most common factors include chronic alcohol consumption, which accounts for over 50% of cases, and tobacco smoking. Studies show an independent dose-response relationship between both alcohol and smoking in the development of CP and it is likely that both risk factors exhibit a synergistic effect (6).
Not all people with risk factors, however, develop AP or CP suggesting that other cofactors are involved. For example, less than 10% of continuous heavy or excessive alcohol drinkers develop pancreatitis. This suggests that alcohol alone does not cause the condition. Other aetiologic factors include genetic predisposition, chronic obstructive causes, autoimmunity, hypercalcemia and hyperlipidaemia, while lifestyle factors such as cigarette smoking, diet, environmental stress and toxins, may also contribute to its development (30)(31). Since alcohol consumption is the second risk factor for AP, dose response relations were investigated and it was estimated that approximately 80 g of alcohol per day for a minimum of 6-12 years is required to produce symptomatic pancreatitis. The consumption of lesser quantities, however, may also lead to pancreatic injury and may have an impact on the progression of the disease (7). Other sources report that the risk of developing pancreatitis increases with increasing doses of alcohol (≥ 4 to 7 drinks/day in men and ≥ 3 drinks/day in women) (8)(9). Low or moderate levels of alcohol consumption are associated with progression from acute to chronic pancreatitis but less than 10% of patients with chronic alcohol consumption develop acute AP.
It has been reported that pancreatic acinar cells are able to metabolize alcohol into toxic metabolites via both oxidative and nonoxidative pathways and exhibit effects that predispose the cells to autodigestive injury and predispose the pancreas to necrosis, inflammation, and cell death. These effects include increased enzyme content, destabilization of lysosomal and zymogen granules, sustained increase in calcium overload, and activation of pancreatic stellate cells. Another theory proposes that alcohol increases the propensity of formation of protein plugs within pancreatic ducts by altering the level of lithogenic proteins and increasing the viscosity of pancreatic secretions, causing obstruction, and, eventually, acinar atrophy.
Juliusson et al. 2018 (10) studied the alcohol consumption patterns and lifetime drinking history in patients with AP and patients with alcohol use disorder (AUD). They concluded that consumption pattern and lifetime drinking history were similar in these two patient groups. Males with AP had lower total amount of spirits and lower proportion of binge drinking than those with AUD, suggesting a distinctive and characteristic aetiology of AP.
Further, nutrition also plays an important role in liver and pancreatic diseases in addition to chronic alcoholism. Therefore, drinking habits and nutritional data of patients with alcoholic liver disease (ALD) and alcoholic pancreatitis (ALP) were compared. There was no difference in the age of starting alcohol consumption and mean amount of alcohol consumption per day between the groups. Patients with ALD were more likely to be daily drinkers with a longer duration of alcohol consumption. However, binge drinking and malnourishment was more common in the ALP group (11).
In a 2017 Swedish study, the potential relation between the incidence of (alcoholic and non-alcoholic) acute pancreatitis (AP) and alcohol consumption in the general population was evaluated. Seasonal variation, particularly in relation to periods with expected increased alcohol consumption, in the occurrence of AP was also assessed (12). This study in 1457 patients with only 17% having alcohol-induced AP showed that no clear relations between the sales and consumption of alcohol in the general population and the incidence of alcoholic or non-alcoholic AP could be observed. There were also no significant differences in the occurrence of AP among different seasons of the year or between holidays associated with higher alcohol consumption compared to periods before and after these holidays. Similarly, the trend in admissions for acute alcoholic pancreatitis ceased to show a connection with the national alcohol consumption during the past several years in a 2017 Finish study (13). This was also reported from a 2013 study in Iceland. Alcohol-induced pancreatitis did not increase despite increased alcohol consumption (14).
Research into acute and chronic pancreatitis and alcohol consumption patterns is uncommon, which makes the study of Becker et al. (2023) relevant and important. One 2016 study on moderate alcohol consumption showed that moderate alcohol consumption is protective against all types of pancreatitis in women and against recurrent AP and chronic hepatitis in men (15).
Two studies have looked into the effects of binge drinking and pancreatitis incidence. Binge drinking during Oktoberfest did not associate with increased hospital admissions for acute pancreatitis (16). On the other hand, in a Chinese retrospective study the association between binge drinking and severe first-attack AP was studied. The binge drinking group had higher triglyceride levels and differed in various other clinical parameters from the control group. Also, total mortality and complications incidences were higher in the binge drinking group than in the control groups. As such, binge drinking seemed to be a contributor to the aggravation of severe first-attack AP (17).
Study design and discussion comments
Forum member Hendriks shared that this is the second study of the Danish National Health Surveys group investigating the association between drinking pattern and pancreatitis. Previously, the same group analysed the association of drinking frequency and beverage type in a 2008 study (18), where the fully adjusted hazard ratios for monthly, weekly, almost daily, and daily alcohol drinking were not significantly different from never drinkers. In the fully adjusted model, amount of alcohol remained significantly associated with increased risk of pancreatitis (P < 0.001), indicating that amount of alcohol is more important than drinking frequency. So, no evidence was found that drinking frequency was associated with risk of pancreatitis. The researchers reported an adjusted hazard ratio for drinking more than 14 beers/week of 2.0 (95% CI: 1.3, 3.1). No association was observed regarding wine and spirits. There were, however, only a few participants in the highest categories of both wine and spirits.
In this most recent Danish prospective cohort study, surveys of the Danish Health Service issued either in 2010 or 2013 were used to evaluate the association between alcohol drinking patterns and the incidence of acute and chronic pancreatitis. The surveys were performed on randomly selected representative samples of the Danish population with a response rate of a little over 50%. Follow-up was until 2018 for both inpatient and outpatient diagnoses, whereas patient information for those solely treated in primary health care was not available. This means that with over 300,000 participants and a follow/up time of approximately seven years, some two million-person years were analysed.
Hazard ratios were estimated for various outcome parameters and adjusted for year, gender and age. Full adjustment additionally included smoking, BMI, diet and education. A separate further adjustment was performed for total alcohol consumption. Most of these covariates were derived from questionnaires and therefore self-reported. Self-report was mentioned as one of the limitations of the study, although evidence from this Danish cohort was in favour of the validity of the self-reported data. This is shown by referencing other work by this group on self-reported alcohol consumption (19), smoking (20) and weight (21), but a little less so for height (21).
However, there was no mention of the validity of the unhealthy diet question. Adjusting for diet is very important when looking at the effects of various beverages. We know that wine drinkers on average have more-healthy lifestyle than for instance beer drinkers, of which diet is one of the important contributing factors (22–24). Another Danish study into the dietary habits of wine drinkers (25) showed that wine, as compared with other alcoholic drinks, was associated with a higher intake of fruit, fish, cooked vegetables, salad, and the use of olive oil for cooking in both men and women. Men who preferred beer and spirits were less likely to have a high intake of salad compared with those who preferred wine. Even higher wine intake was associated with a higher intake of healthy food items compared with intake of < 2.5 glasses of wine/month. Also in this study, the results section starts by mentioning that the type of alcohol only had a minor influence on HRs of acute, chronic and total pancreatitis and concluded that after adjusting for total alcohol intake, drinking wine as not associated with any significant beneficial or harmful effects in relation to pancreatitis. Surprisingly though, the abstract states that drinking large amounts of beer and spirits might be more harmful than consuming (large amounts of) wine suggesting that the type of beverage would make a difference. The discussion section does elaborate on this issue by stating: Only few studies have evaluated the effect of preferred type of alcohol on risk of pancreatitis. In a previous study, we found an increased risk of pancreatitis when drinking more than 14 drinks of beer per week, whereas no association was observed for wine or spirits (18). In the present study, a large intake of spirits or beer was associated with increased risk of pancreatitis, whereas drinking more than 14 drinks of wine per week was seemingly less harmful. The results may reflect residual confounding as wine drinking is associated with a generally healthier lifestyle. It is unclear what the final conclusion is on this important aspect of the main topic of the paper. Further, in contrast Azodi et al. (2011) observed no association between consumption of wine or beer, frequency of alcoholic beverage consumption including spirits, or average total monthly consumption of alcohol (ethanol) and the risk of acute pancreatitis (32). They also observed, however, a dose–response association between the amount of spirits consumed on a single occasion and AP risk. After multivariable adjustments, there was a 52% increased AP risk for every increment of five standard drinks of spirits consumed on a single occasion, an association weakened slightly when those with gallstone-related pancreatitis were excluded. Forum members suggested that a faster rate of drinking, with a greater rise in BAC, for spirits drinkers may be an important factor in the observed higher risk of pancreatitis. In any case, the average total alcohol consumption did not affect the risk of pancreatitis; instead, it was the number of drinks consumed per occasion (of spirits, in this study) that was associated with an increase in risk. Although the response to the questionnaires were only about 50% and existing pancreatitis persons were excluded from the analysis, acute pancreatitis incidence was 1145 cases per 316,715 persons included, which corresponds to 361 cases per 100,000 over approximately seven years follow-up. This may correspond to an incidence of some 50 new cases per year. Looking at the global incidence of AP, Ianuzzi et al. (2022) (26) reported that in 1980, the incidence of AP in Denmark based on hospital registries was 18 per 100,000 persons. Despite fluctuations, this increased during two separate studies with an incidence of 36 cases per 100,000 persons in 1990 and 27 cases per 100,000 persons in 2012 (27). It seems that the incidence of AP is still on the rise in Denmark and that the response rate of 50% at least did not deselect for those at risk for AP.
The effect of binge drinking frequency was analysed on the risk of acute, chronic and total pancreatitis. Confounder adjusted risks for daily or almost daily binge drinking were elevated for all types of pancreatitis whereas further adjustment for alcohol intake resulted in a non-significantly increased risk for AP but a non-significantly decreased risk for CP. These results suggest that high alcohol consumption in combination with binge drinking may increase AP, whereas this may not be the case for CP. It is unfortunate that the low incidences of these diseases even in a large cohort study as the one discussed has insufficient power to derive at definite conclusions on the issue.
A J-shaped associated was observed between the amount of alcohol consumed and the development of acute and chronic pancreatitis. This was illustrated in supplementary Figure 2 using the > 0-7 drinks/week as a reference group. It may have been interesting to also look at the results with the non-drinkers as a reference group, since this study both included the non-drinkers as well as the abstainers as potential references. The supplementary Figure 2 suggests that the only the hazard ratio for chronic pancreatitis increases as compared to the non-drinkers for those drinking > 14 drinks/week, which corresponds to 24 g/day.
Comments by specific Forum Members
Forum Member Ellison suggested that “while this paper on the relation of alcohol to pancreatitis mainly supports previous research on the topic, it is important due to its large number of subjects, apparently good ascertainment of disease, appropriate and well-described methodology, and the fact that data on the type of beverage were available. Further, it was carried out using data from subjects in a single country, thus is less likely to be confounded by mixing data from very divergent cultures.
The finding of an increased risk for daily drinkers might benefit by examining the characteristics of subjects in this group. It could relate to the category being a mix of regular moderate wine drinkers with meals (expected to have lower risk) and chronic heavy drinkers, who would be expected to be at increased risk of pancreatitis.
In any case, the key findings of this well-done study are that heavy drinking, especially of spirits and beer, are associated with increases in risk of pancreatitis, whereas drinking within recommended guidelines for any beverage appears to not increase the risk.”
Forum Member Erik Skovenborg adds that “underreporting in surveys that may be more serious than the authors suggest, for example, qualitative interviews have previously identified that having a non-routine drinking pattern, self-perception as a non-frequent drinker, and usually tracking drinking using experiential approaches as linked to more drinking being reported in the diary than the retrospective interview (28); and Danish wine drinkers have previously also been observed to have a healthier diet compared to Danish beer drinkers such that diet is a potential confounder (29).”
Altogether, an interesting study that shows that AP and CP risk increases at higher levels of alcohol consumption, at least well above the definitions for moderate alcohol consumption. Beverage type does not seem to be an important modulator of this risk, whereas problematic alcohol use was, even for the alcohol consumption adjusted hazard ratios.
Alcohol consumption has often been found to be a risk factor for acute pancreatitis (AP) and a number of biologic mechanisms for such an association have been suggested. Overall, however, the risk is rather low, as only 1-3% of heavy drinkers develop AP after 10-20 years of follow up.This is the second study of the Danish National Health Surveys group investigating the association between drinking pattern and pancreatitis. A prospective cohort study based on data from 316,751 men and women participating in the Danish National Health Surveys 2010 and 2013, it specifically assessed the effects of type of alcohol as well as drinking pattern on risk of acute and chronic pancreatitis. A J-shaped association between the consumption of alcohol and development of pancreatitis was observed particularly for beer and spirits where drinking frequency such as daily, frequent binge drinking and problematic alcohol use were associated with increased development of pancreatitis. The study is important because of its large number of subjects, apparently good ascertainment of disease, appropriate and well-described methodology, and the fact that data on the type of beverage were available. Further, it was carried out using data from subjects in a single country, thus is less likely to be confounded by mixing data from very divergent cultures. Placed in perspective, however, AP and CP risk was shown to increase at higher levels of alcohol consumption, at least well above the definitions for moderate alcohol consumption. Furthermore, beverage type does not seem to be an important modulator of this risk, whereas problematic alcohol use was, even for the alcohol consumption adjusted hazard ratios.
Comments on this paper by the International Scientific Forum on Alcohol Research were provided by the following members:
Henk Hendriks, PhD, The Netherlands
Creina Stockley, PhD, MSc Clinical Pharmacology, MBA; Principal, Stockley Health and Regulatory Solutions; Adjunct Senior Lecturer, The University of Adelaide, Adelaide, Australia
R. Curtis Ellison, MD, Professor of Medicine, Emeritus; Section of Preventive Medicine & Epidemiology, Boston University School of Medicine, Boston, MA, USA
Erik Skovenborg, MD, specialized in family medicine, member of the Scandinavian Medical Alcohol Board, Aarhus, Denmark
Pierre-Louis Teissedre, PhD, Faculty of Oenology–ISVV, University Victor Segalen Bordeaux 2, Bordeaux, France
Giovanni Gaetano, MD, PhD, Department of Epidemiology and Prevention, IRCCS Istituto Neurologico Mediterraneo NEUROMED, Pozzilli, Italy
Fulvio Ursini, MD, Dept. of Biological Chemistry, University of Padova, Padova, Italy
Mladen Boban, MD, PhD, Professor and Head of the Department of Pharmacology, University of Split School of Medicine, Croatia
Ramon Estruch, MD, PhD, Associate Professor of Medicine, University of Barcelona, Spain
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