Critique 290 – Alcohol and cancer risk: what you need to know

Authors Pearson, H.

Citation Nature 2025 (639) 290-292. https://doi: 10.1038/d41586-025-00729-5.

Feature This feature article written by a senior editor of Nature is intended to explain at what level of drinking cancer risks start to rise.

Forum Summary

This brief feature article by Pearson (2025) is an elaboration of the 2025 US Surgeon General’s Advisory on Alcohol and Cancer Risk (U.S. Surgeon General, 2025). It describes the opinions of selected epidemiologists, all with a long track record of publishing on the adverse effects of alcohol consumption and human health. There are minimal references cited, and careful consideration of the text suggests that references and peer-reviewed evidence from earlier research are disregarded. The text is also emotive.

The feature article summarizes what the 2025 US Surgeon General’s Advisory has concluded, namely:

  • It emphasises the potential adverse effects of light to moderate alcohol consumption on the approximately seven alcohol-related cancers;
  • Conversely, it downplays alcohol’s potential beneficial health effects on, and decreased risk for other non-communicable diseases such as cardiovascular diseases (CVD) and diabetes mellitus type II, cognitive decline and dementias, as well as kidney cancer and non-Hodgkin lymphoma (Bagnardi et al., 2015);
  • Fails to discuss total mortality;
  • Fails to discuss a healthy lifestyle;
  • Incorrectly implies that cancer risk from alcohol is equivalent to tobacco smoking and asbestos exposure; and
  • Ill-considers references to calculating absolute risk estimates.

A more appropriate conclusion to Helen Pearson’s article is: ‘the whole evidence base for moderate drinking and improved health is scientifically sound’.

Forum critique

Background

This brief three-page feature article by Pearson (2025) is an elaboration of the US Surgeon General’s Advisory on Alcohol and Cancer Risk (U.S. Surgeon General, 2025) published earlier in January 2025[1], which is a public statement that calls Americans’ attention to an urgent public health issue and provides recommendations on how it should be addressed. Unlike the Surgeon General’s Report (2016)[2], the Surgeon General’s Advisory (2025) is a non-systematic review, which does not have to disclose search strategies or methods or inclusion criteria, and where evidence considered came from “resources suggested by a wide range of subject matter experts”, an approach that is neither comprehensive nor objective and has the potential of introducing bias.

The feature article describes the opinions of various alcohol epidemiologists, all with a long track record of publishing on the adverse effects of alcohol consumption and human health. There were minimal references cited, and careful consideration of the text suggests that references and peer-reviewed evidence from much earlier research were disregarded.

Also, instead of simply writing scientific fact, the language of this feature article is emotive and fear-mongering.

Critique

Emphasis on only the potential adverse health effects of any alcohol consumption

The feature article summarizes what the US Surgeon General’s Advisory on Alcohol and Cancer Risk (2025) has concluded, namely, it emphasises only the potential adverse effects of light to moderate alcohol consumption on the approximately seven alcohol-related cancers. Indeed, cancer is not a single disease and the other 100+ known cancers such as ovary, prostate, stomach, uterus, and bladder, appear not to be adversely affected by alcohol consumption.

Failure to acknowledge any positive health effects from light to moderate alcohol consumption

The feature downplays alcohol’s potential decreased risk for other non-communicable diseases. Despite being well documented for three or more decades, this feature disappointingly fails to acknowledge that there is a beneficial association between light to moderate alcohol consumption and CVD (Mostofsky et al., 2016). CVD is currently the leading cause of death globally and is projected from the Global Burden of Disease (GBD) Study 2019 to remain so into the 2050s (Chong et al. 2024).  Other beneficially associated diseases include diabetes mellitus type II (Li et al., 2025), cognitive decline and dementia (Zarezadeh et al., 2024), and renal disease including renal cancer (Song et al., 2012).  Evidence for a beneficial association comes from both epidemiology and sound experimental and clinical science of mechanisms for such beneficial associations.  The inclusion of only comments from Professors Jurgen Rehm and Timothy Naimi (of the Canadian Centre for Substance Abuse; CSA) who are authors of the controversial Canada’s Guidance on Alcohol and Health: Final Report (Paradis et al., 2023)  and the related recent Interagency Coordinating Committee on the Prevention of Underage Drinking (ICCPUD) Study on Alcohol Intake and Health (Shield et al., 2025), is also disappointing as is the unquestioning acceptance of repeatedly invalidated theories such as the sick quitter hypothesis, socio-economic bias and underestimation of alcohol consumption and cursory comment on the relevance of alcohol consumption patterns. Furthermore, the commentary omitted that Health Canada has not adopted CCSA’s recommendations to change the drinking guidelines.

Failure to discuss total mortality

The most glaring omission is failure to discuss total mortality, the overall outcome, or a summation of all the pros and cons of alcohol consumption. There is a continuum of convincing evidence available showing that total mortality is associated with alcohol consumption in a J-shaped way (Bryazka et al., 2022). This means that when one is drinking lightly to moderately one has a lower risk of dying whereas when one is not drinking or drinking more than moderately one has a higher risk of dying.

Consequently, the entire evidence base around moderate drinking is not ‘scientifically frail’, as stated by Naimi (2025), but it is a science-based reality as shown in The National Academies of Sciences, Engineering, and Medicine’s Review of Evidence on Alcohol and Health (National Academies of Sciences, Engineering, and Medicine, 2025); this review is a key resource for the U.S. Department of Health and Human Services (HHS) and U.S. Department of Agriculture (USDA) as they co-develop the Dietary Guidelines for Americans, 2025-2030.

Failure to discuss healthy lifestyle

The difference with modifiable lifestyle factors such as drinking alcohol is that it is a choice to drink, as it is for the other lifestyle factors listed; a voluntary rather than involuntary risk factor. Having a healthy lifestyle, however, does not guarantee that a person will not get a cancer, a CVD or another non-communicable disease, for example, but it reduces the overall risk of premature disability and death by improving general health. Furthermore, people do not drink for their health but choose to drink to relax and socialise. Relaxation and socialisation, inherent in a good quality of life, contribute positively to health and well-being as highlighted in the US Rancho Bernardo Study (Chan et al., 2009, Richard et al. 2019).

In conclusion, when the risk for one or more specific diseases/disorders marginally increases with light to moderate alcohol consumption, whereas that of others decreases to enable and enhance enjoyment of life, why would we treat drinking a light to moderate amount of alcohol as a generally unhealthy choice? The reason is, of course, that there is no scientific basis to do so.

Incorrectly implies cancer risk from alcohol is equivalent to tobacco smoking and asbestos exposure

As with the consumption of most foods, beverages, and drugs, including over-the-counter and prescription medications and recreational drugs, there is a dose-dependent relationship. Heavy alcohol consumption, whether regular or binging, and alcohol abuse are increasing the risks for alcohol-related cancers. Consequently, the IARC categorized alcoholic beverages (IARC, 1988) as carcinogenic, irrespective of dose, as the IARC has been doing with the majority of substances it has investigated.

For each of the seven alcohol-related cancers, the dose-response relationship is different, and is also influenced by an individual’s other risk factors for the cancer. The leading lifestyle risk factors for cancer include tobacco use, obesity, unhealthy diets, lack of physical activity and exposure to UV radiation, as well as alcohol consumption. The environmental risk factors include certain infections, chemical pollutants, and ionising radiation. Further, there are other non-modifiable risk factors for cancer such as age, genetics and hormones. IARC categories, however, do not provide information about the magnitude or level of risk.

Pearson (2025), however, incorrectly incorrectly implies that cancer risk from alcohol is equivalent to tobacco smoking and asbestos exposure. These risk factors only share the same IARC category, but the specific risks and levels of cancer they cause differ. Indeed, according to the IARC (2012) and WHO (2015), tobacco is the greatest modifiable risk factor and hence preventable cause of cancer worldwide, estimating that it causes up to 1.5 million cancer deaths each year. Tobacco is also a major modifiable risk factor for cardiovascular diseases (CVD)[3]. Conversely, light to moderate alcohol consumption is repeatedly reported in the medical and scientific literature as one of the five favourable or healthy lifestyle risk factors on healthy ageing and life expectancies (Li et al., 2018, Mahler et al., 2022).

Ill-considered reference to calculating absolute risk estimates

Pearson (2025) also refers to an Australian study from the Surgeon General’s Advisory as the source for calculating absolute risk estimates (Sarich et al., 2025), to suggest that other studies may not have appropriately accounted for potential confounding in their calculations. This is an ill-considered choice, particularly because the authors of this Australian study acknowledge that there is potential confounding or bias in their estimates, and that the relationship between alcohol consumption and cancer risk varies across regions, “due in part to regional variation in gene polymorphisms that relate to the metabolism of alcohol”.

This Australian study also had a low response rate of 19%. Furthermore, the analytical results showed that the risk of being diagnosed with an alcohol-related cancer did not increase until after 30 g/day, compared to those drinking to 3.5 drinks/week. There were a large number of analyses in the main paper and the supplement with this same result, which were explored in various models and sensitivity analyses.

Additional Comments

Forum Member Ursini considers that “rather than biased, but I believe the judgment of the feature article should be far more critical. While evidence-based medicine (EBM) aims to protect human health, it must not conflict with the solid foundation of basic scientific evidence, validated cultural and ethical traditions, and common sense.

The debate surrounding alcohol consumption has been raised many times, particularly regarding the type of drink and the manner of consumption. Drawing conclusions based solely on the average weekly ethanol intake from any source is an oversimplification and cannot be deemed scientifically sound.

From a mechanistic standpoint, there is no single experimental study demonstrating that ethanol itself causes cancer in animals. The actual mutagenic agent is acetaldehyde. While this is correct, it is also important to consider that Homo sapiens has a substantial aldehyde dehydrogenase (ALDH) activity, which dramatically increased nearly one million years ago in hominids. This mutation conferred a significant evolutionary advantage for obvious reasons. Additionally, aldehydes are naturally present in dairy products, fruits, and vegetables, contributing to their aroma. Should we then classify all aldehydes as mutagens and carcinogens at high doses only because the aldehydic group is chemically reactive?

Another significant bias (or deliberate omission?) in the article is its complete failure to acknowledge wine as part of a diet that is healthier when it includes moderate wine consumption. I prefer not to refer strictly to the Mediterranean diet but rather to a broader non-Western dietary approach. In my opinion, Ancel Keys did not discover a “magic diet”; rather, he revealed how poorly Americans were eating—and drinking.

For decades, basic scientific research has provided data on the pro-atherogenic modification of LDL and the protective role of wine when consumed with food. A more epistemologically correct approach to public health should prioritize confirming basic science through epidemiological research—not merely counting deaths and hypothesizing mechanisms of disease and mortality.

The scientific hierarchy must follow the logical progression:

1.         Basic Science →

2.         Mechanistic Insights →

3.         Epidemiological Studies & Meta-Analyses

Instead, we often see large-scale epidemiology applied to heterogeneous populations across different societies, increasing the risk of misleading conclusions. Do you recall the fluctuating and often contradictory conclusions drawn from studies on dietary fat, beta-carotene, red meat, eggs, coffee, sweeteners, Maillard reaction products, etc.?

The issue of the low or moderate dose is always open, and hormesis is not just a curiosity discovered by a toxicologist; it is a matter of life and health.

I am always open to further discussion on these issues and eager to contribute to a non-paternalistic approach to public communication regarding scientific matters.”

Forum Member Skovenborg suggests that “the feature by Helen Pearson incorporates many examples of ‘well-meaning’ anti-alcohol bias that are common in research and messaging around low-level drinking. The level of anti-alcohol bias seems to be growing and could contribute to the distrust of other, more objective, information that people need to prevent alcohol-related problems.

There are two apparent biases in the feature article as follows:

1.  The narrow and selective list of experts interviewed and quoted regarding the level of drinking at which cancer risks start to rise, suggests a bias or conflict of interest regarding alcohol research, for example,

  • Dr Timothy Naimi is an author of the Canadian Centre on Substance Use and Addiction (CCSA) recommendations Canada’s Guidance on Alcohol and Health: Final Report to inform the 2023 Canadian alcohol guidelines suggesting that “two alcoholic drinks per week equals low risk”. He is also quoted as stating “The bottom line is that alcohol is a generally unhealthy substance”.
  • Professor Emmanuela Gakidouis is one of the leading authors of The Global Burden of Disease (GBD) Study 2016. These authors “found that risk increases monotonically with dose and the minimal exposure to risk was zero drinks per day” (Griswold et al. 2019). Furthermore, in Hydes et al. (2019), the GBD Study 2016 is quoted as “robust evidence that low levels of alcohol intake do not provide any protective health benefits.”
  • Dr Helen Croker is Assistant Director of Research and Policy at the World Cancer Research Fund who endorses the current World Health Organization’s position of “no safe level of alcohol consumption”.
  • Professor Jürgen Rehm is an author of the Interagency Coordinating Committee on the Prevention of Underage Drinking (ICCPUD) Study on Alcohol Intake and Health (Shield et al., 2025) to inform the Dietary Guidelines for Americans 2025-2030, that concluded “among the U.S. population, the risk of dying from alcohol use begins at low levels of average use”.
  • Professor Nick Sheron is a hepatologist and an author of the controversial paper (Hydes et al., 2019) that compared wine and cigarettes related to cancer risk. These authors suggested that “one bottle of wine is associated with the same cancer risk as five cigarettes (men) or ten cigarettes (women) per week”.

2. The eight references are mostly biased against even moderate alcohol consumption, for example,

  • The US Surgeon General’s Advisory on Alcohol and Cancer Risk (Office of the US Surgeon General, 2025).
  • The list of IARC Group 1 Carcinogens includes alcohol. Tobacco and asbestos are included as other group 1 carcinogens but not, for example, air pollution, wood dust or salted fish. This suggests an intention to frame alcohol as a particularly dangerous carcinogen on par with tobacco and asbestos.
  • The World Cancer Research Fund & American Institute for Cancer Research’s Alcoholic Drinks and the Risk of Cancer (WCRF, 2018). According to this report “Scientists expect that other cancer types will be added”, however, in the quote, there is no mention of cancer types associated with lower risk from consumption of alcohol, such as Non-Hodgkin lymphoma (UK cases in 2021: 13,512 cases), renal cancer (12,192 cases) and thyroid cancer (4,040 cases). In comparison, there were 11,090 cases of alcohol-associated Head and neck cancers.
  • Of the 19 authors of reference Sohi, et al. (2024), five are WHO staff members and three are WHO consultants.

In comparison to these references, the landmark report from the National Academies of Sciences, Engineering, and Medicine (2024) was not quoted nor even mentioned, which concluded:

  • Conclusion 5-1: The committee concludes that compared with never consuming alcohol, consuming a moderate amount of alcohol was associated with a higher risk of breast cancer (moderate certainty).
  • Conclusion 5-2: The committee concluded that, among moderate alcohol consumers, higher versus lower amounts of moderate alcohol consumption were associated with a higher risk of breast cancer (low certainty).
  • Conclusion 5-3: The committee determined that no conclusion could be drawn regarding the association between moderate alcohol consumption compared with lifetime non-consumers and risk of colorectal cancer.
  • Conclusion 5-4: The committee concluded that among moderate alcohol consumers higher versus lower amounts of moderate alcohol consumption were associated with a higher risk of colorectal cancer (low certainty).
  • Conclusion 5-5: The committee determined that no conclusion could be drawn regarding an association between moderate alcohol consumption and oral cavity, pharyngeal, oesophageal, or laryngeal cancers.

In addition, the feature article states that “another murky area is how risks change with age. The chances of developing cancer rise with age, as the body’s ability to metabolize alcohol drops, so it’s likely that alcohol would be having more of a risk as we get older, Croker says.” This statement is incorrect:  https://www.bmj.com/content/365/bmj.l4304/rr-16.  There are at least 14 references stating that the often-repeated assertion of diminished hepatic metabolic efficiency with increasing age is a myth. The landmark study by Vestal et al. was published in 1977. Thus, is this incorrect statement from Dr Croker a result of plain ignorance of the scientific literature on alcohol metabolism and age or is it an example of common ageism?”

Forum Member Ellison states that he is “always interested in articles by health writers when judged according to the “scientist” with whom they primarily communicated to reach their conclusions.  It is clear in the publication by Helen Pearson that there was very strong input by a Canadian-based ‘scientist’ who appears to spend his time seeking to ‘find holes’ in the massive amount of scientific data showing that moderate drinkers, especially those who consume an alcoholic beverage with their meals, have less heart disease, ischaemic stroke, diabetes, and dementia.  Further, such moderate drinkers have lower total mortality rates, in other words, more healthy years of life, than do people who are very similar in all of their lifestyle characteristics except that they abstain from any alcohol consumption. 

When considering the health effects of alcoholic beverages, I often think about the excellent, unbiased studies of the late clinical and research cardiologist and epidemiologist, Arthur L. Klatsky MD,[4] who based his work on the immense number of participants (>400,000) in the Californian Kaiser Permanente Research Bank.  In some of the most thoroughly examined and analysed datasets of people who reported that they consumed ‘1 or 2 drinks/day’, those also reporting alcohol misuse made up all of those who later developed cancer or hypertension.  Those whose extensive records revealed no such findings of alcohol misuse had the same risk as abstainers (Klatsky et al., 2006, Klatsky and Udaltsova, 2013, Klatsky et al., 2014).

Of course, the number of drinks over a week or other time period reported in epidemiologic studies is far from adequate to judge the health effects of alcohol consumption [although I do not know people who consume “alcohol”, but those who drink beverages containing alcohol]. We also know that the type of beverage, and especially the pattern of drinking, are as important as the number of drinks drunk.  Scientific studies continue to demonstrate that positive health effects occur mainly in drinkers who consume light-to-moderate amounts regularly, without binge drinking, and with food.  This is especially the case when the beverage consumed is wine.

Hundreds of scientists publish sound and unbiased articles on the positive and/or negative health effects of the consumption of alcohol-containing beverages.  Luckily, some of these scientists are members of our Forum and continue to provide accurate and balanced information on this topic.  We trust that journalists and science writers will take advantage of such reliable sources to assure that the information upon which they base their articles is scientifically accurate and unbiased.” 

Forum member Teissedre suggests that “regarding wine specifically, and cancers per se, it should also be emphasised that some synergistic habits, both good and bad, can be essential for the initiation and development of cancerous tumours. The effect of alcohol on cancer risk will depend, therefore. on the context, such as alcohol with or without a meal, the nature of the foods consumed (e.g., processed and red meats, the addition of aflatoxins and salt) as well as concomitant tobacco smoking. The average consumption of omega-6/omega-3 acids in habitual diets should also be considered. It is suggested that more than one-third of all cancers could be prevented by a healthy diet, regular physical activity, and no weight gain. Since cancer is a multifactorial disease, a person with a healthy diet, who exercises regularly, maintains a healthy body mass index (BMI), and who regularly and moderately consumes wine during a meal may be less likely to develop cancer than a person who does not drink alcohol but does not have a healthy diet, has a sedentary lifestyle and is overweight.

There is insufficient data, however, to affirm that moderate red wine consumption during meals in the frame of a healthy lifestyle is associated with an increased risk of cancer. Conversely, we know that this practice is beneficial for cardiovascular diseases, diabetes mellitus, and other chronic and degenerative diseases, and possibly for some cancers. For this reason, therefore, the relationship between alcohol consumption and cancer should continue to be explored. We should remember that it is easy to draw the wrong conclusion when a particular factor related to eating and drinking habits, such as wine consumption, is analysed out of context without taking cultural and culinary habits into account.

Only scientific evidence accumulated from an unbiased selection of epidemiological, extensive animal, cell culture, and human clinical studies will not promulgate misinformation. Indeed, all recent population studies show a significant and meaningful reduction in the risk of cardiovascular disease and total mortality from moderate consumption of alcoholic beverages such as wine (Teissedre et al., 2018, 2020).

The Organisation International de la Vigne et du Vin (OIV) has subsequently adopted the following resolution entitled Recommendation on the evaluation/ assessment and the communication of epidemiological studies concerning the consumption of grapes, wine and other vitivinicultural products (OIV-SECSAN 711-2022). The key points of this resolution adopted by its 51 member states has six key recommendations regarding such scientific communication as follows:

1.   Analysis and limits

A statistical analysis should be completed with biological interpretation. The data collected or obtained during an epidemiological study must be analysed in conformity with the study protocol. Nonetheless, data collected in a study may legitimately be analysed to evaluate hypotheses that were not explicitly formulated in the initial protocol, or for a secondary purpose different from that originally intended. Any significant change from the statistical methodology described in the study protocol must be expressly mentioned in any publication or presentation of the study results.

2.   Quality control for the study

The quality of the data collected, obtained, produced or published during or as part of an epidemiological study should be guaranteed.

3.    Scientific integrity

All study results regardless of whether the funders are public or private, are under the scientific supervision of the epidemiologist who is the principal investigator, and not of the funder, and the results should be published if their scientific validity is sufficient. Before submitting for publication any requests to hide the results or change or attenuate the content of a report or to delay publication must be categorically rejected.

As generally requested, the authors of epidemiological articles should report their possible conflicts of interest and inform who funded the research.

Furthermore, in order to ensure the above criteria, an assessment of the risk of bias in accordance with the well-acknowledged guidelines per study design should be conducted.

Therefore, any communication on epidemiological studies concerning the consumption of grapes, wine and other vitivinicultural products, should consider the following criteria:

4.      Impartiality

Users of published epidemiological studies should consider that results generally constitute only a small part of the information available, and some bias may affect the choice of data published, in selecting results that agree with the epidemiologist’s point of view and not mentioning those that contradict it. This type of partiality or bias must be avoided.

5.      Balance

Any communication must describe every aspect of the epidemiological study in an honest and balanced manner, without taking any other interests, especially non-scientific, into account.

6.      Good practices

All communication should use clear, precise, sincere, and confident information. It should be trustworthy, transparent, and impartial, and take into account that science is a process of collecting data and building strong evidence and must not contain speculations on what may be or may not be relevant in the future.”

Forum member Waterhouse strongly believes that “Helen Pearson’s opinion piece is another example of shoddy scholarship, accepted unquestioned by the complicit editors at Nature, because they are applying biased standards to the health effects of alcohol. Ultimately, this will only add fuel to the fire that is burning down respect for science and scientists.  Perhaps they have not noticed that science is losing respect among the public who feel the “experts” are telling them what they want them to believe, not the truth.  This is a prime example of misinformation from the experts who deliberately obscure decades of solid data showing that moderate alcohol consumption has a net health benefit and focus solely on relatively minor issues.  It is bad enough to be fighting TikTok ‘health experts’ these days, but it is very disheartening to find that respectable scientists are joining the misinformation train.  This arrogance by some has resulted in nearly the total loss of biomedical research funds in the USA right now, and we scientists everywhere must be honest with the public and demand that of each other or expect more of the same. “

Forum member Djousse states that “it is of great concern to see a misuse of absolute measures of effect such as the absolute risk or lifetime risk by a peer-reviewed journal such as Nature.  It is important to emphasize the importance of the two key qualities of an effect measure, namely the validity and the precision, in scientific inference.  Assuming that the authors addressed the validity issue via customary methods during the design, conduct, and data analyses, it is critically important to report the effect measure with its precision so that the reader can correctly interpret the results and draw a valid conclusion. Merely reporting the proportion of people with cancer in different groups is insufficient to interpret the data. For example, Pearson reported in the current editorial that “… This showed that around 17 out of 100 women who drink either nothing or less than one standard US drink per week (14 g ethanol) would develop such a cancer in their lifetime. This was taken as the baseline level of risk. This number rose to nearly 22 out of 100 women who have two drinks per day (28 g ethanol) on average. Therefore, five more women would develop cancer owing to the higher level of alcohol consumption.”  The absence of any measure of precision (i.e., standard deviation, 95% confidence interval -CI) around the proportions (17% or 22%) diminishes the utility of the reported proportions and provides no support for the conclusion of “… five more women would develop cancer owing to the higher level of alcohol consumption”.  While the crude difference between 17 percent and 22 percent is five, a measure of precision is required to know whether such a difference is statistically significant.

For example, using the approximation formula of the standard deviation [square root of [p*(1-p)/n)] where p is the proportion or risk and n is the sample size, 17 women out of 100 would have a 95% CI of 0.11 t0 0.26 while 22 women out of 100 would have a 95% CI of 0.15 to 0.31. Since these confidence limits overlap, one cannot conclude that there is a statistically significant difference between the two groups of women. In Contrast, 1700 cases of cancer out of 10,000 women (17%) and 2200 out of 10,000 (22%) would have non-overlapping 95% CIs [0.16 to 0.18 and 0.21 to 0.23, respectively] using the approximation formula above.  Unfortunately, such critical details that are necessary for the correct interpretation of the data are omitted in a peer-reviewed journal such as Nature.

I also agree with comments from our other colleagues.”

Forum member Goldfinger considers that “the cancer narrative seems to have overwhelmed the ‘literature’, as well as the ‘hearts and minds’ of those reporting on alcohol and health. Even as the NASEM report reinforces the j-shaped relationship between moderate beverage alcohol and total mortality and the salutary effect on cardiovascular disease, the position of the WHO and others spouting that any beverage alcohol is dangerous for human consumption, is gaining traction. If their concern is wholly correct on cancer, the simple question to the alcohol and cancer proponents is… what is best, to avoid cancer or live longer?

Cardiovascular disease is the leading cause of death worldwide, and the literature has been most consistent with a reduced incidence of cardiovascular events and death with moderate beverage alcohol consumption.

I strongly concur with the comments put forward by our other colleagues to date.”

Forum member Harding endorses the comments made by other Forum members and states that he has looked at all the references cited by Pearson (2025).  “It seems that the entire rationale for the assertion that alcohol consumption causes cancer is based on epidemiological associations.  Generally speaking, ‘relative risk’ is assumed to be ‘real risk’, without much, or indeed any, examination of supporting evidence.  Association and causation are assumed to be the same thing.  This is not the right way of going about things unless the objective is simply to present alcohol as a universal human carcinogen.

Sir Austin Bradford-Hill (1965) knew that it was not the right way, too. This is why he identified seven criteria that should be applied to epidemiological data to assess causation.  The cited US Surgeon General’s Advisory, Alcohol and Cancer Risk (Office of the US Surgeon General, 2025) addressed this directly (page 7), with a general account of how the Bradford Hill criteria apply to the body of evidence on alcohol consumption and cancer risk overall. This is not right either, because it is known that alcohol has different effects, depending on the nature of the cancer.  So, what is needed is an analysis of how the Bradford Hill criteria apply to individual cancers.

For example, the body of evidence on the effect of alcohol consumption and breast cancer would certainly struggle to fulfill the criterion of consistency and of biological plausibility.  Indeed, the cited reference 6, which is specifically on breast cancer says, ‘the mechanisms underlying the alcohol-breast cancer association are not entirely clear’.  Nor is the actual relationship between alcohol and breast cancer ‘entirely clear’.  A 2019 study on about half a million Britons found no evidence of a causal association between alcohol consumption and breast cancer (Ingold et al. 2019).  A French study on wine consumption had already come to the same conclusion (Bessaoud and Daurès, 2008).  Further, wine appeared to offer a degree of protection as an intake of 15g/day reduced the risk of breast cancer by about 40%, and higher intakes did not increase risk at all.   A US study found zero risk of breast cancer among wine drinkers (Newcomb et al., 2009).

Further, alcohol consumption appears to convey a degree of protection for some cancers (e.g. kidney (Yuan et al. 2021, Lee et al. 2007), thyroid (Meinhold et al., 2009, Hong et al., 2017), blood cancers (Chiu et al., 1999, Morton et al., 2005, Gatspur et al., 2012, Ji et al., 2014) and multiple myeloma (Psaltopoulou et al., 2015), with wine seeming to be particularly beneficial (e.g. colorectal cancer (Crockett et al., 2011, Park et al., 2009), prostate (Schoonen et al., 2005), and even after the disease has been diagnosed (Downer et al., 2019), lung cancer (Chao et al., 2008, Brenner et al., 2019), and stomach cancer (Barstad et al., 2005). 

 All this demonstrates that the conclusions drawn by Pearson (2025) are deeply flawed.

Contrast this with the ‘biggest controversy’, which, according to Pearson (2025), ‘is whether low or moderate alcohol consumption has a protective effect against heart disease and stroke’, which has ‘not gone away completely’.  No, it hasn’t.  According to Jürgen Rehm (quoted on page 291 in Pearson’s article), ‘The Alcohol-Ischaemic Heart Disease relationship (meaning the protective effect of low to moderate consumption) fulfills all criteria for a causal association proposed by Hill’ (Roerecke and Rehm, 2014).

So, in my estimation, the central message of Helen Pearson’s article, ‘The bottom line is that alcohol is a generally unhealthy substance’, is just plain wrong.  It isn’t.”

Forum member McIntosh declares that The article by Helen Pearson examines a very narrow literature on the harms of alcohol use. It is narrow because the papers in this literature focus exclusively on cancer and mortality, leaving out mechanisms where alcohol use could have an impact on the longevity of respondents who do not die of cancer. It also ignores the possible effects of alcohol on the living who suffer from diseases other than cancer, like dementia, heart disease, diabetes, or stroke.  

Clearly, mortality is important, but this is an end-of-life event. Most people are not near the end of their lives and their concerns about the effects of drinking alcohol will be concentrated on how alcohol use affects their health. The important questions here are: does alcohol actually have an adverse effect on health?; and which diseases are most likely to become more or less prevalent in those who use alcohol?

There is not much research that focuses on these questions, and the paper being reviewed here certainly tells us nothing about them. However, these are easy issues to deal with because most countries collect high-quality sample survey data on the health of their population. In Canada, the Canadian Community Health Survey is administered every three or four years, and in the USA, the Behavioural Risk Factor Surveillance System (BRFSS) survey is carried out annually. This is the largest US survey and it is used here to show how alcohol affects diseases and health in the USA.

In the table below logistic regressions are carried out on cancer and three other diseases as well as self-reported health data from BRFSS survey for the year 2022. The survey asks respondents questions like “have you ever been told that you have cancer?” There are responses to the three other prominent diseases but no information on dementia, at least for the entire sample. Respondents are also asked to rate their health on a scale from 1 to 5. This variable is referred to as self-reported health and is widely collected by other countries. 

The alcohol variable is a quadratic function of the number of days per week that the respondent drank an alcoholic beverage. This is more reliable than the number of drinks consumed per day or week[5]; there is a much higher response rate for the frequency variable than the quantity, there is no disagreement about how much respondents consume, and there are likely to be fewer recall errors[6].

In Table 1 below, the odds of getting a disease are plotted against the number of respondent drinking days. For cancer, there is a significant decrease in the risk of getting cancer for days under five but a significant increase as drinking becomes more frequent relative to not drinking. On the other hand, for the other three diseases, there are major declines in risk as drinking becomes more frequent. Diabetes exhibits the largest response to alcohol; respondents who drink six days a week are one-third as likely to have diabetes as those who never drink. CVD is also much less likely among the more regular drinkers.

The survey also asks respondents about their health. It generates a five-category measure of self-reported health. Like many of the studies on all-cause mortality the response is a highly significant J-shaped curve with the largest benefits accruing to those who drink about four times a week. Moderate alcohol use unambiguously improves perceived health, and while it leads to slightly higher cancer probabilities, the detrimental effect of cancer on health is the smallest of the four diseases considered here. The real villains are diabetes and coronary heart disease, but these two diseases are the most likely to be prevented by regular drinking.

Table 1

Age and Gender Adjusted Odds For Cancer, Diabetes, Coronary Heart Disease, and Stroke For Males and Females over 50.

Days     Cancer      Diab.       CHD    Stroke

  0            1.00       1.00           1.00      1.00

  1            0.95       0.69          0.95      0.81

  2            0.94       0.49          0.92      0.69

  3            0.96       0.38          0.89      0.62

  4            0.98       0.34          0.88      0.60

  5            1.01       0.32          0.87      0.61

  6            1.06       0.33          0.86      0.67

  7            1.11       0.37          0.87      0.78

Table notes. Sample size = 221,561. The entries in the table are averages of pj(n)/pj(0) where pj(n) is the probability of having disease j given n days per week of alcohol consumption. Data source: BRFSS 2022.

These results are based on recent US data, however, similar results were obtained using the Canadian Community Health Survey for 2017-18. The only difference was that cancer responded positively to alcohol use. See McIntosh (2017).  In Table 1, both genders are pooled, however; there are no significant differences between males and females in their response to alcohol consumption. It should also be noted that within the literature on cancer mortality, two competing risk studies, Baer et al. (2011) and Bergmann et al. (2013), found beneficial effects due to moderate alcohol consumption.

The overwhelming conclusion that can be drawn from this table is that alcohol consumption is beneficial to individual health. The Pearson message, representing the views of the anti-alcohol lobby, is that even low levels of alcohol consumption are, on balance, harmful. This is a gross distortion of the truth. Table 1 confirms this. Additionally, one of the papers she cites computes years of life lost to cancer deaths which are attributed to alcohol use but does not include years of life gained from the lower death rates from cardiovascular diseases due to alcohol consumption.[7]  This bad science and produces unreliable results. Readers of Nature deserve better than this.

References

Bagnardi, V., Rota, M., Botteri, E., Tramacere, I., Islami, F., Fedirko, V., Scotti, L., et al. (2015). Alcohol consumption and site-specific cancer risk: a comprehensive dose-response meta-analysis. Br J Cancer, 112(3), 580–593. https://doi.org/10.1038/bjc.2014.579

Baer, H.J., Glynn, R.J., Hu, F.B., Hankinson, S.E., Willett, W.C., Colditz, G.A., Stampfer, M., & Rosner, B. (2011) Risk factors for mortality in the nurses’ health study: a competing risks analysis. Am J Epidemiol, 173(3):319-29. https://doi.org/10.1093/aje/kwq368.

Barstad, B., Sørensen, T.I., Tjønneland, A., Johansen, D., Becker, U., Andersen, I.B., & Grønbaek M. (2005) Intake of wine, beer and spirits and risk of gastric cancer. Eur J Cancer Prev, 14(3), 239-43.

Bergmann, M.M., Rehm, J., Klipstein-Grobusch, K., Boeing, H., Schütze, M., Drogan, D., Overvad, K., et al. (2013) The association of pattern of lifetime alcohol use and cause of death in the European prospective investigation into cancer and nutrition (EPIC) study. Int J Epidemiol. 42(6):1772-90. https://doi.org/10.1093/ije/dyt154.

Bessaoud, F., & Daurès, J.P. (2008) Patterns of alcohol (especially wine) consumption and breast cancer risk: a case-control study among a population in Southern France. Ann Epidemiol, 18(6), 467-75.

Brenner, D.R., Fehringer, G., Zhang, Z.F., Lee, Y.A., Meyers, T., Matsuo, K., Ito, H., et al. (2019). Alcohol consumption and lung cancer risk: A pooled analysis from the International Lung Cancer Consortium and the SYNERGY study. Cancer Epidemiol, 58:25-32.

Breslow, R.A., Graubard, B.I. (2008) Prospective study of alcohol consumption in the United States: quantity, frequency, and cause-specific mortality. Alcohol Clin Exp Res, 32, 513-21

Bryazka, D., Reitsma, M. B., Griswold, M. G., Abate, K. H., Abbafati, C., Abbasi-Kangevari, M., Abbasi-Kangevari, Z., et al. (2022). Population-level risks of alcohol consumption by amount, geography, age, sex, and year: a systematic analysis for the Global Burden of Disease Study 2020. Lancet (London, England), 400(10347), 185–235. https://doi.org/10.1016/S0140-6736(22)00847-9

Center For Disease Control. (2022) Behavioural Risk Factor Surveillance System.

Chan, A.M., von Mühlen, D., Kritz-Silverstein, D., & Barrett-Connor, E. (2009) Regular alcohol consumption is associated with increasing quality of life and mood in older men and women: the Rancho Bernardo Study. Maturitas, 62(3):294-300. https://doi.org/10.1016/j.maturitas.2009.01.005.

Chao, C., Slezak, J.M., Caan, B.J, & Quinn, V.P. (2008) Alcoholic beverage intake and risk of lung cancer: the California Men’s Health Study. Cancer Epidemiol Biomarkers Prev, 17(10):2692-99.

Chiu, B.C., Cerhan, J.R., Gapstur, S.M., Sellers, T.A., Zheng, W., Lutz, C.T., Wallace, R.B., & Potter, J.D. (1999) Alcohol consumption and non-Hodgkin lymphoma in a cohort of older women. Br J Cancer, 80(9), 1476-82.

Chong, B., Jayabaskaran, J., Jauhari, S.M., Chan, S.P., Goh, R., Kueh, M.T.W., Li, H., et al. (2024) Global burden of cardiovascular diseases: projections from 2025 to 2050. Eur J Prev Cardiol. https://doi.org/10.1093/eurjpc/zwae281.

Crockett, S.D., Long, M.D., Dellon, E.S., Martin, C.F., Galanko, J.A., & Sandler, R.S. (2011) Inverse relationship between moderate alcohol intake and rectal cancer: analysis of the North Carolina Colon Cancer Study. Dis Colon Rectum, 54(7), 887-94.

Downer, M.K., Kenfield, S.A., Stampfer, M.J., Wilson, K.M., Dickerman, B.A., Giovannucci, E.L., Rimm, E.B., et al. (2019) Alcohol Intake and Risk of Lethal Prostate Cancer in the Health Professionals Follow-Up Study. J Clin Oncol, 37(17), 1499-1511.

Gapstur, S.M., Diver, W.R., McCullough, M.L., Teras, L.R., Thun, M.J., & Patel, A.V. (2012) Alcohol intake and the incidence of non-hodgkin lymphoid neoplasms in the cancer prevention study II nutrition cohort. Am J Epidemiol, 176(1), 60-69.

GBD 2016 Alcohol Collaborators (2018) Alcohol use and burden for 195 countries and territories, 1990–2016: a systematic analysis for the Global Burden of Disease Study 2016. Lancet, 392,1015-35.

Graff-Iversen, S., Jansen, M.D., Hoff, D.A., Høiseth, G., Knudsenm G.P., Magnus, P., Mørland, J., et al. (2013) Divergent associations of drinking frequency and binge consumption of alcohol with mortality within the same cohort. J Epidemiol Community Health, 67(4), 350-57.

Griswold, M., & Gakidou, E., GBD 2016 Alcohol Collaborators (2019) Alcohol and the global burden of disease – Authors’ reply. Lancet, 15393(10189):2391-92.

Hernandez, J.B.R., & Kim, P.Y. (2025) Epidemiology morbidity and mortality. [Updated 2022 Oct 3]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2025 Jan. https://www.ncbi.nlm.nih.gov/books/NBK547668/

Hill, A.S. (1965) The environment and disease: association and causation?  Proceedings of the Royal Society of Medicine, 58(5), 295-300.

Hong, S.H., Myung, S.K., Kim, H.S., Korean Meta-Analysis (KORMA) Study Group. (2017) Alcohol intake and risk of thyroid cancer: A meta-analysis of observational studies. Cancer Res Treat, 49(2), 534-47.

Hydes, T.J., Burton, R., Inskip, H., Bellis, M.A., & Sheron, N. (2019) A comparison of gender-linked population cancer risks between alcohol and tobacco: how many cigarettes are there in a bottle of wine? BMC Public Health, https://doi.org/10.1186/s12889-019-6576-9

International Agency for Research on Cancer. (2012) Personal habits and indoor combustions. Volume 100E. IARC monographs on the evaluation of carcinogenic risks to humans. Lyon: IARC, 2012.

International Agency for Research on Cancer (1988) Alcohol Drinking IARC Monographs on the Evaluation of the Carcinogenic Risks to Humans. Lyon: IARC, 2012

Ingold, N., Amin, A., Drenos, F. (2019) Alcohol causes an increased risk of head and neck but not breast cancer in individuals from the UK Biobank study. medRxiv, https://doi.org/10.1101/19002832

Ji, J., Sundquist, J., & Sundquist, K. (2014) Alcohol consumption has a protective effect against hematological malignancies: a population-based study in Sweden including 420,489 individuals with alcohol use disorders. Neoplasia, 16(3), 229-34, 234.e1. https://doi.org/10.1016/j.neo.2014.03.003.

Klatsky, AL. (2002) Alcohol and cardiovascular disease. A historical overview. Ann NY Acad Sci, 957, 7-15.

Klatsky, A.L., Gunderson, E.P., Kipp, H., Udaltsova, N., & Friedman, G.D. (2006) Higher prevalence of systemic hypertension among moderate alcohol drinkers: An exploration of the role of underreporting. J Studies Alcohol, 67(3), 421-28. https://doi.org/10.15288/jsa.2006.67.421

Klatsky, A.L. & Udaltsova, N. (2013) Commentaries. Addiction, 108: 1549-52. https://doi.org/10.1111/add.12157

Klatsky, A.L., Udaltsova, N., Li, Y., Baer, D., Tran, N.H., & Friedman, G.D. (2014) Moderate alcohol intake and cancer: the role of underreporting. Cancer Causes Control, 25(6), 693-9. https://doi.org/10.1007/s10552-014-0372-8.

Lee, J.E., Hunter, D.J., Spiegelman, D., Adami, H.O., Albanes, D., Bernstein, L., van den Brandt, P.A., et al. (2007). Alcohol intake and renal cell cancer in a pooled analysis of 12 prospective studies. J Natl Cancer Inst, 99(10), 801-10.

Li, X., Hur, J., Smith-Warner, S. A., Song, M., Liang, L., Mukamal, K. J., Rimm, E. B., & Giovannucci, E. L. (2025). Alcohol intake, drinking pattern, and risk of type 2 diabetes in three prospective cohorts of US women and men. Diabetes Care. https://doi.org/10.2337/dc24-1902

Li, Y., Pan, A., Wang, D.D., Liu, X., Dhana, K., Franco, O.H., Kaptoge, S., et al. (2018) Impact of Healthy Lifestyle Factors on Life Expectancies in the US Population. Circulation, 138(4), 345-55.

Mahler, L., Sebo, P., Favrod-Coune, T., Moussa, A., Cohidon, C., & Broers, B. (2022) The prevalence of five lifestyle risk factors in primary care physicians: A cross-sectional study in Switzerland. Prev Med Rep, 26, 101740.

McIntosh, J.  (2017) Alcohol and Canadian health. Global J Health Sci, 9(5). https://doi.org/10.5539/gjhs.v9n5p96

Meinhold, C.L., Park, Y., Stolzenberg-Solomon, R.Z., Hollenbeck, A.R., Schatzkin, A., Berrington, de., & Gonzalez, A. (2009) Alcohol intake and risk of thyroid cancer in the NIH-AARP Diet and Health Study. Br J Cancer, 101(9), 1630-34.

Morton, LM., Zheng, T., Holford, T.R., Holly, E.A., Chiu, B.C., Costantini, A.S., Stagnaro, E., … & InterLymph Consortium. (2005) Alcohol consumption and risk of non-Hodgkin lymphoma: a pooled analysis. Lancet Oncol, 6(7):469-76.

Mostofsky, E., Chahal, H. S., Mukamal, K. J., Rimm, E. B., & Mittleman, M. A. (2016). Alcohol and immediate risk of cardiovascular events: a systematic review and dose-response meta-analysis. Circulation, 133(10), 979–987. https://doi.org/10.1161/circulationaha.115.019743

National Academies of Sciences, Engineering, and M. (NASEM). (2025). Review of Evidence on Alcohol and Health. The National Academies Press. Washington, DC., 1–254.

Newcomb, P.A., Nichols, H.B., Beasley, J.M., Egan, K., Titus-Ernstoff, L., Hampton, J.M., & Trentham-Dietz, A. (2009) No difference between red wine or white wine consumption and breast cancer risk. Cancer Epidemiol Biomarkers Prev, 18(3), 1007-10. https://doi.org/10.1158/1055-9965.EPI-08-0801. Erratum in: Cancer Epidemiol Biomarkers Prev. 2009 May;18(5):1667.

Paradis, C., Butt, P., Shield, K., Poole, N., Wells, S., Naimi, T., Sherk, A., & the Low-Risk Alcohol Drinking Guidelines Scientific Expert Panels. (2023). Canada’s Guidance on Alcohol and Health: Final Report. Ottawa, Ont.: Canadian Centre on Substance Use and Addiction.

Park, J.Y., Mitrou, P.N., Dahm, C.C., Luben, R.N., Wareham, N.J., Khaw, K.T., & Rodwell, S.A. (2009) Baseline alcohol consumption, type of alcoholic beverage and risk of colorectal cancer in the European Prospective Investigation into Cancer and Nutrition-Norfolk study. Cancer Epidemiol, 33(5), 347-54.

Pearson, H. (2025). Alcohol and cancer risk: what you need to know. In Nature (Vol. 639, Issue 8054, pp. 290–292). https://doi.org/10.1038/d41586-025-00729-5

Plunk, A.D., Syed-Mohammed, H., Cavazos-Rehg, P., Bierut, L.J., Grucza, R.A. (2014) Alcohol consumption, heavy drinking, and mortality: rethinking the j-shaped curve Alcohol Clin Exp Res, 38, 471-78.

Psaltopoulou, T., Sergentanis, T.N., Sergentanis, I.N., Karadimitris, A., Terpos, E., & Dimopoulos, M.A. (2015)  Alcohol intake, alcoholic beverage type and multiple myeloma risk: a meta-analysis of 26 observational studies. Leuk Lymphoma, 56(5), 1484-501.

Richard, E.L., Kritz-Silverstein, D., Laughlin, G.A., Fung, T.T., Barrett-Connor, E., & McEvoy, L.K. (2017) Alcohol intake and cognitively healthy longevity in community-dwelling adults: The Rancho Bernardo Study. J Alzheimer’s Dis, 59(3), 803-14. https://doi.org/10.3233/JAD-161153.

Roerecke, M., & Rehm, J. (2014) Alcohol consumption, drinking patterns, and ischaemic heart disease: a narrative review of meta-analyses and a systematic review and meta-analysis of the impact of heavy drinking occasions on risk for moderate drinkers, BMC Medicine, 12, 182.

 Sarich, P., Canfell, K., Egger, S., Banks, E., Joshy, G., Grogan, P., & Weber, M. F. (2021). Alcohol consumption, drinking patterns and cancer incidence in an Australian cohort of 226,162 participants aged 45 years and over. Br J Cancer, 124(2), 513–23. https://doi.org/10.1038/s41416-020-01101-2

Schoonen, W.M., Salinas, C.A., Kiemeney, L.A., & Stanford, J.L. (2005) Alcohol consumption and risk of prostate cancer in middle-aged men. Int J Cancer, 113(1), 133-40.

Song, D. Y., Song, S., Song, Y., & Lee, J. E. (2012). Alcohol intake and renal cell cancer risk: a meta-analysis. British Journal of Cancer, 106(11), 1881–90. https://doi.org/10.1038/bjc.2012.136

Substance Abuse and Mental Health Services Administration (US); Office of the Surgeon General (US). Facing Addiction in America: The Surgeon General’s Report on Alcohol, Drugs, and Health [Internet]. Washington (DC): US Department of Health and Human Services; 2016 Nov.

Teissedre, P.-L., Rasines-Perea, Z., Ruf, J.-C., Stockley, C., Antoce, A.O., Romano, R., Fradera, U., & Kosti, R.I. (2020) Effects of alcohol consumption in general, and wine in particular, on the risk of cancer development: a review. OENO One, 4, 813-32. https://doi.org/10.20870/oeno-one.2020.54.4.3569

Teissedre, P.-L., Stockley, C., Boban, M., Gambert, P., Alba, M.O., Flesh, M., & Ruf, J.-C. (2018) The effects of wine consumption on cardiovascular disease and associated risk factors: a narrative review. OENO One, 52, 2, 67-79. https://doi.org/10.20870/oeno-one.2018.52.1.2129

U.S. Surgeon General. (2025). Alcohol and cancer risk. https://www.hhs.gov/surgeongeneral/reports-and-publications/alcohol-cancer/index.html

World Health Organization (2015) Cancer Prevention. https://www.who.int/cancer/prevention/en/

Yuan, H.C., Yu, Q.T., Bai, H., Xu, H.Z., Gu, P., & Chen, L.Y. (2021) Alcohol intake and the risk of chronic kidney disease: results from a systematic review and dose-response meta-analysis. Eur J Clin Nutr, 75(11), 1555-67.

Zarezadeh, M., Mahmoudinezhad, M., Faghfouri, A. H., Mohammadzadeh Honarvar, N., Regestein, Q. R., Papatheodorou, S. I., Mekary, R. A., & Willett, W. C. (2024). Alcohol consumption in relation to cognitive dysfunction and dementia: A systematic review and dose-response meta-analysis of comparative longitudinal studies. Ageing Res Rev, 100, 102419. https://doi.org/10.1016/j.arr.2024.102419

Comments on this critique by the International Scientific Forum on Alcohol Research were provided by the following members:

Henk Hendriks, PhD, The Netherlands

Creina Stockley, PhD, MBA, Independent consultant and Adjunct Senior Lecturer in the School of Agriculture, Food and Wine at the University of Adelaide, Australia

Fulvio Ursini, Emeritus Professor of Biochemistry, University of Padova, Padova, Italy

Erik Skovenborg, MD, specialized in family medicine, member of the Scandinavian Medical Alcohol Board, Aarhus, Denmark

R. Curtis Ellison, MD, Section of Preventive Medicine/Epidemiology, Boston University School of Medicine, Boston, MA, USA

Pierre-Louis Teissedre, PhD, Faculty of Oenology–ISVV, University Victor Segalen Bordeaux 2, Bordeaux, France

Andrew Waterhouse, PhD, Department of Viticulture and Enology, University of California, Davis.

Luc Djoussé, MD, DSc, Dept. of Medicine, Division of Aging, Brigham & Women’s Hospital and Harvard Medical School, Boston, MA, USA

Tedd Goldfinger, DO, FACC, Desert Cardiology of Tucson Heart Center, University of Arizona School of Medicine, Tucson, AZ, USA

Richard Harding, PhD, Formerly Head of Consumer Choice, Food Standards and Special Projects Division, Food Standards Agency, UK

James McIntosh, PhD, Retired Professor of Economics, Concordia University, Montreal, Canada

Matilda Parente, MD, consultant in molecular pathology/genetics and emerging technologies, San Diego, CA, USA

Fulvio Mattivi, MSc, Scientific Advisor, Research and Innovation Centre, Fondazione Edmund Mach, in San Michele all’Adige, Italy

Ramon Estruch, MD, PhD.  Associate Professor of Medicine, University of Barcelona, Spain

Giovanni de Gaetano, MD, PhD, Department of Epidemiology and Prevention, IRCCS Istituto Neurologico Mediterraneo NEUROMED, Pozzilli, Italy


[1] https://www.hhs.gov/surgeongeneral/reports-and-publications/alcohol-cancer/index.html;

[2] https://library.samhsa.gov/sites/default/files/surgeon-generals-report.pdf

[3] https://www.tobaccoinaustralia.org.au/chapter-3-health-effects/3-1-smoking-and-cardiovascular-disease#:~:text=Premature%20CVD%20is%20highly%20preventable,at%20harmful%20levels%20and%20diabetes.

[4] Arthur Klatsky and colleagues at Kaiser-Permanente in Oakland, CA were the first to show in healthy populations the J-shaped relationship of alcohol consumption to coronary heart disease (CHD) events and have most thoroughly pursued the possible causal nature of the association through major population studies. They consistently found, since the late 1960s, lower CHD and ischemic stroke risk in moderate drinkers than in abstainers and heavy drinkers. They found sufficiently plausible mechanisms in HDL raising, anti-clotting, anti-inflammatory, and insulin sensitivity effects of alcohol to bolster the causal hypothesis for alcohol effects on risk. They also found the association highly significant, greater in men than women, in younger than older, and independent of but influenced by body mass, blood pressure, and particularly smoking. https://www.youtube.com/watch?v=GrpLg_UVOYQ

[5] There is some reliable information on the quantity of alcohol consumed. One question asked whether the respondent drank more than two drinks a day. Only 7.1 % said yes to this question.

[6] It was used by Li et al (2025) on three American surveys in the analysis of type 2 diabetes.

[7] This is done in  Paradis et al (2023).

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