Critique #293 – Commentary on Piano et al. (2025) and Marques-Vidal et al. (2025). 7th July 2025
Alcohol use and cardiovascular disease: A Scientific Statement from the American Heart Association
Mariann R. Piano, Gregory M. Marcus, Dawn M. Aycock, Jennifer Buckman, Chueh-Lung Hwang, Susanna C. Larsson, Kenneth J. Mukamal, and Michael Roerecke on behalf of the American Heart Association Council on Lifestyle and Cardiometabolic Health; Council on Cardiovascular and Stroke Nursing; Council on Clinical Cardiology; and Stroke Council. Circulation, 2025, https://doi.org/10.1161/CIR.0000000000001341
Diet and nutrition in cardiovascular disease prevention: a scientific statement of the European Association of Preventive Cardiology and the Association of Cardiovascular Nursing & Allied Professions of the European Society of Cardiology.
Pedro Marques-Vidal, Vasiliki Tsampasian, Aedin Cassidy, Giuseppe Biondi-Zoccai, Christina Chrysohoou, Konstantinos Koskinas, W M Monique Verschuren, Michał Czapla, Maryam Kavousi, Matina Kouvari, Vassilios S. Vassiliou and Demosthenes Panagiotakos. European Journal of Preventive Cardiology, 2025, https://doi.org/10.1093/eurjpc/zwaf310
Summary
ISFAR commends and endorses the two scientific statements from the American Heart Association (AHA) and the European Association of Preventive Cardiology, along with the Association of Cardiovascular Nursing & Allied Professions of the European Society of Cardiology. They are well-reasoned, detailed, and comprehensive scientific summaries. These statements update our understanding of the link between alcohol consumption and various cardiovascular diseases. ISFAR also emphasises the urgent need for randomised trials on light to moderate alcohol intake to produce more definitive conclusions. In the meantime, adopting a healthy diet and lifestyle, including regular physical activity, abstinence from tobacco, and maintaining a healthy body weight, is recommended in both statements.
Commentary
In June 2025, the American Heart Association (AHA) and the European Association of Preventive Cardiology, together with the Association of Cardiovascular Nursing & Allied Professions of the European Society of Cardiology, independently published scientific statements. These statements, which are essential guidance for healthcare professionals, patients, and the general public, provide important insights into the relationship between alcohol consumption and cardiovascular disease (CVD).
Given that both statements summarise the sound, peer-reviewed, published science generated over the past five or more decades, it is unsurprising that they are similar in content and conclusions and instil confidence in the statements’ reliability and research robustness. Although most of the results come from observational studies, those studies where there was potential bias from including former drinkers in the abstinent group were not considered as evidence.
Both acknowledge that alcohol is one of the most widely consumed beverages globally, but it also has complex associations with multiple aspects of cardiovascular health and disease. Consequently, its consumption remains a contentious issue in efforts to reduce the global burden of disease, with CVD ranking among the top five causes. Years of research have yielded inconsistent guidelines and conflicting messages regarding its consumption and its link to cardiovascular conditions such as hypertension, myocardial infarction (MI), stroke, heart failure (HF), and cardiac arrhythmias like atrial fibrillation (AF), as well as cardiomyopathy.
The J-shaped curve remains a valid concept; both statements both statements indicate that nil risk or the lowest risk of CVD mortality occurs at around 100 g of alcohol per week, or about one to two 10 to 14 g alcoholic drinks daily. This provides a more complete picture of the relationship between alcohol and cardiovascular health, as it involves not only the amount consumed but also the drinking pattern. The consensus recommended approach is to consume a light to moderate amount daily, since extensive research shows that heavy drinking, usually more than two drinks per day, and binge drinking are harmful to cardiovascular health. However, the risk linked to consuming one to two drinks daily and AF remains uncertain. The type of alcoholic beverage consumed may also influence its effects.
The association between alcohol consumption and health outcomes begins with initial observations that regular light-to-moderate drinking may be linked with positive health effects. This connection is essential because light-to-moderate drinking is the most common pattern in developed countries. Both statements later recognise that heavier drinking also leads to harmful health effects. The focus should then shift to separate analyses for binge and heavy drinkers. Adverse health effects are far more common in this latter group, and no medical professional would endorse such harmful drinking habits.
ISFAR commends and endorses the two statements, considering them to be well-reasoned, detailed, and comprehensive summaries prepared by a group of scientists selected by the American Heart Association and the European Heart Association. These statements update our understanding of the relationship between alcohol consumption and various diseases. ISFAR also highlights the urgent need for randomised trials on low to moderate alcohol consumption to yield more definitive conclusions. In the interim, adopting healthy diet and lifestyle practices, such as regular physical activity, abstaining from tobacco, and maintaining a healthy body weight, is recommended in both statements.
The authors of both statements conducted a thorough review process, examining publications that provided evidence from cross-sectional and cohort studies as well as experimental trials. Both positive and adverse health effects were considered. While the AHA and European Association of Preventive Cardiology statements are comprehensive, they differ slightly in their approach and conclusions, which enables a more nuanced understanding of the relationship between alcohol consumption and cardiovascular health.
The AHA statement ignored or downplayed the numerous sound scientific papers published over more than five decades that have consistently supported a strong association between light-to-moderate alcohol consumption and a lower risk of most CVDs, diabetes, and other common diseases of ageing. Statements are included such as “Although excessive alcohol use is a leading preventable cause of chronic medical conditions, low to moderate alcohol consumption (e.g., no more than 1 to 2 drinks a day) has been hypothesised to confer a cardioprotective effect by reducing the risk of several forms of CVD. Data from recent studies using new methodologies (e.g., individual participant-level data meta-analysis and Mendelian Randomisation [MR]) have challenged the idea that any level of alcohol consumption has positive health effects.” This text does not recognise that many of the so-called ‘recent studies’ displayed confirmatory bias against the consumption of any alcohol and used inappropriate and limited analytical techniques like MR (Mukamal et al., 2020) and population modelling (Oliveira et al., 2023) to reach their conclusions. MR and Models depend on data and assumptions, and inaccuracies or oversimplifications can significantly affect the results. When scientifically evaluated by ISFAR, the data reported in these ‘recent papers’ (ISFAR critiques #076, 143, 278) generally support the previously demonstrated beneficial associations between light drinking and cardiovascular diseases, such as the Global Burden of Disease Study, which clearly shows the existence of a J-shaped curve.
The AHA statement is also based solely on the number of drinks consumed within a day or over a week. Analyses are, however, available on drinking patterns, which include the type of beverage consumed (since people do not drink ‘alcohol’ but rather a ‘beverage-containing alcohol’), the regularity of consumption, and whether the beverage is consumed with or without food. Therefore, it would have been more appropriate to source separate analyses based on whether the individual was following a ‘healthy’ or an ‘unhealthy’ drinking pattern. There are significant differences in the risk of adverse effects between these two groups. For example, in almost all research reports, the most favourable health outcomes attributed to alcohol are observed among individuals who regularly consume a beverage in moderation and with meals. Indeed, moderate alcohol consumption is associated with a lower rate of all-cause mortality as demonstrated across all 16 different cohorts of the MORGAM Project (Di Castelnuovo et al., 2023). Additionally, other components of alcoholic beverages, beyond the alcohol itself, might positively influence health.
Additional comments from ISFAR forum members
Forum member Ellison adds, “If a physician or agency is providing advice on drinking, it should never encourage anything other than a ‘healthy’ pattern of drinking. In other words, the public should be made aware of the benefits and risks usually associated with such a pattern of drinking, and then separately from the risks associated with binge, heavy, or other immoderate drinking. In the excellent work on this subject by the late Dr Arthur Klatsky and his colleagues (Klatsky et al., 2014), an attempt is made to evaluate separately any health effects that may indicate the subject consumed alcohol in a healthy or unhealthy manner. Then, an investigator can hope to identify and report any beneficial and adverse effects among those subjects strongly associated with their pattern of drinking. In the work of Klatsky et al., (2006), among subjects reporting that they consumed ‘1 to 2 drinks per day’, the investigators were able to use other data in their research files to find that some of these subjects had evidence of alcohol abuse. They found that those subjects were the ones who were more likely to have subsequent cancers and other diseases in comparison with subjects without such data. In other words, those without such evidence of abuse had much better future health outcomes. The better we become at obtaining an unbiased assessment of alcohol consumption and drinking patterns, the better we will be able to judge the risks and benefits associated with the consumption of alcohol-containing beverages.”
Forum member de Gaetano further states that “observational studies that reported a low/moderate alcohol benefit on several cardiovascular conditions consistently failed to show any low/moderate alcohol benefit on AF (Di Castelnuovo et al., 2017) or even reported an increased risk of AF (Csengeri et al., 2021). The methodology was consistent. Well-conducted analyses could, therefore, differentiate between various cardiovascular conditions. They are either all true or all false.”
Forum member Estruch argues that “the ‘recent studies’ using new statistical methods or Mendelian Randomisation (MR) cannot outweigh or obscure the consistent findings of hundreds of studies supporting a J- or U-shaped relationship between alcohol intake—particularly wine consumption—and the incidence of CVD or even all-cause mortality. Regarding MR studies, these have limited usefulness in assessing alcohol consumption and alcohol-related diseases due to several factors. Key genetic instruments (e.g., ALDH2, ADH1B) often exhibit pleiotropy, which breaches core assumptions of MR. Furthermore, the health effects of alcohol are often non-linear—something MR generally cannot capture. Genetic proxies may also fail to reflect actual drinking patterns (such as binge drinking or type of alcohol), and findings may lack generalisability due to population-specific genetic variation. Together, these limitations diminish the validity of MR in this context. Additionally, regarding statistical techniques, it appears that various groups are investigating different analytical arguments, particularly examining the characteristics of control groups (e.g., abstainers) to challenge the J- or U-shaped associations.
Nevertheless, one issue that requires further investigation is the connection between alcohol consumption and the development of AF, as evidence suggests that the harmful effects of alcohol may begin with the very first drink. In the PREDIMED study, we observed that participants in the Mediterranean diet group, supplemented with extra-virgin olive oil—an intervention that included moderate wine intake—had a significantly lower incidence of AF compared to the control group. This leads me to believe that the impact of wine consumption within the Mediterranean diet may differ from the same amount of wine consumed outside of meals or outside of that dietary pattern. This hypothesis also warrants additional investigation.”
A suggestion from Forum member Goldfinger is that “as expected, recommendations are given with great caution, recognising the lack of randomised controlled trials on alcohol (beer, wine, and spirits) and health outcomes. Both statements note that most research is observational and, therefore, susceptible to bias and confounding. They specifically describe the relationship with CVD as complex and controversial, leading to inconsistent advice and mixed messages.
While randomised controlled trials are regarded as the gold standard for establishing causality, they are not always practical, ethical, or feasible, especially for long-term exposures such as diet, physical activity, or environmental factors. In such cases, observational data become not just valuable but essential. When a substantial body of observational evidence consistently points in the same direction across different populations, methodologies, and settings—such as the link between moderate alcohol consumption, particularly red wine, and CVD—it provides a strong indication that the association is genuine and not caused by chance or bias. This consistency, especially when supported by biological plausibility — i.e., a credible mechanistic explanation based on physiology or biochemistry — enhances the inference.
When observational findings are strong, reproducible, and biologically coherent, they form a scientifically sound basis for public health advice, particularly in areas where waiting for perfect evidence could lead to preventable harm. In general, the recommendations are not anti-alcohol, but, in my opinion, fail to fully recognise the potential of the observational data available to date.”
Forum member Harding suggests that, since the title ofthe AHA statement is ‘Alcohol use and cardiovascular disease: A scientific statement’, and the EAPC’s title is similar, that should be the focus of the statement. The first paragraph of the AHA statement includes the sentence, ‘Although excessive alcohol use is a leading preventable cause of chronic medical conditions, low to moderate alcohol consumption has been hypothesised to confer a cardioprotective effect by reducing the risk of several forms of CVD.’ From this sentence, no one would realise that there is a vast amount of remarkably consistent evidence accumulated over decades indicating that moderate, regular alcohol consumption significantly reduces mortality from all forms of CVD in both men and women. This represents by far the greatest impact of any dietary intervention on CVD — nothing else comes close. No drug can achieve this either. Given this evidence linking moderate alcohol consumption with reduced mortality, the next straightforward question for research is whether it is causal. Does alcohol actually cause the reduction in mortality from CVD? Furthermore, because of the apparent magnitude of this effect, it remains a compelling question.
So, this should be the question that these ‘scientific statements’ address. However, these statements are primarily focused on epidemiology, and epidemiology of any sort cannot address the question of causality. Other approaches are needed. The Bradford-Hill criteria for causality have been in use since 1965. Why are those criteria not applied here? The section ‘Physiological mechanisms and other mediating factors associated with alcohol consumption’ in the AHA statement begins to address this, but not in sufficient depth. The important review by Brien et al. (2011) on the effect of alcohol consumption on biological markers associated with the risk of coronary heart disease is not even cited in either statement. The lengthy section on obesity defaults to epidemiology and does not explain how alcohol might affect obesity, such as how it is converted to fat. Further, at the end of this section, it states ‘…the way in which alcohol affects vascular, myocardial, and brain function…..is beyond the scope of this scientific statement’. I disagree. It is precisely what the paper should address.
References
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This ISFAR commentary on Piano et al. (2025) and Marques-Vidal et al. (2025) was prepared and endorsed by:
Creina Stockley, Co-director ISFAR, PhD, MBA, Independent consultant and Adjunct Senior Lecturer in the School of Agriculture, Food and Wine at the University of Adelaide, Australia
R. Curtis Ellison, Chair ISFAR, MD, Section of Preventive Medicine/Epidemiology, Boston University School of Medicine, Boston, MA, USA
Henk Hendriks, Co-director ISFAR, PhD, Independent consultant and partner of the Nutrition Consultants Cooperative, Netherlands
Giovanni de Gaetano, MD, PhD, Department of Epidemiology and Prevention, IRCCS Istituto Neurologico Mediterraneo NEUROMED, Pozzilli, Italy
Ramon Estruch, MD, PhD. Associate Professor of Medicine, University of Barcelona, Spain
Tedd Goldfinger, DO, FACC, Desert Cardiology of Tucson Heart Center, University of Arizona School of Medicine, Tucson, AZ, USA
Mladen Boban, MD, PhD, Professor and Head of the Department of Pharmacology, University of Split School of Medicine, Croatia
Luc Djoussé, MD, DSc, Dept. of Medicine, Division of Aging, Brigham & Women’s Hospital and Harvard Medical School, Boston, MA, USA
Lynda H. Powell, MEd, PhD, Chair, Dept. of Preventive Medicine, Rush University Medical School, Chicago, IL, USA
Dominique Lanzmann-Petithory, MD, PhD, Nutrition/Cardiology, Praticien Hospitalier, Hôpital Emile Roux, Paris, France
Richard Harding, PhD, Formerly Head of Consumer Choice, Food Standards and Special Projects Division, Food Standards Agency, UK
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