Maurizio Ponz de Leon. Letter to the Editor: What should we advise about alcohol consumption? Intern Emerg Med, DOI 10.1007/s11739-010-0487-1.
There has been quite a response to a Letter to the Editor by Ponz de Leon recently published in Internal & Emergency Medicine, which is copied below. Divergent opinions have been expressed in two follow-up Letters to the Editor in that journal, which are also given below. Further, we include a number of comments on the subject by members of our International Scientific Forum on Alcohol Research.
What should we advise about alcohol consumption?
Maurizio Ponz de Leon, Intern Emerg Med, DOI 10.1007/s11739-010-0487-1. Received: 18 September 2010 / Accepted: 30 October 2010
I read with interest, and with some concerns, the paper by Castelnuovo et al. , and the related commentary . The main message of the review is to present evidence for the protective effect of moderate alcohol intake against cardiovascular diseases. As a consequence, ‘‘low–moderate alcohol consumption may contribute to better health’’. I do not want to dispute the scientific background of this contention, which could also be well-grounded, though I remain unconvinced of such evidence. What I would like to argue is that the message seems to me hazardous and extremely dangerous to diffuse in the general population, at least for the following reasons:
1. Many people may be unable to distinguish between low–moderate and high consumption of wine, beer or spirits. Moreover, alcohol metabolism may differ remarkably from one subject to another. In current clinical practice, we observe severe liver or gastric damage associated with relatively low volumes of alcohol (especially in women), whereas other subjects may tolerate without any apparent explanation large amounts of alcohol;
2. Alcohol remains a frequent cause of car crash, and Governments (in almost all Western Countries) try to convince or force people to abstain from drinking before driving. The message of the present review does not help these efforts, since it offers a ‘‘moral’’ justification for drinking, even if in small-moderate amounts;
3. To consider alcohol as a medication whose consumption may contribute to improved health is another source of concern; for instance, the authors state ‘‘people who are already regular light-moderate alcohol consumers should be encouraged to continue’’, but, by the same token, we should encourage the abstemious to drink low–moderate amounts of alcohol, in order to lower HDL, to inhibit platelet aggregation and so on. Are we truly at the point of prescribing alcohol consumption in order to reduce the risk of stroke and coronary damage?
In conclusion, I do believe that more studies are needed before we can give sensible recommendations on alcohol consumption to the general population. Prospective, long-term, cohort investigations are particularly needed. Moreover, even when further evidence of a beneficial effort may be obtained, I would suggest that we use prudence, and even more prudence in dispensing indications for common drinks such as wine, beer or spirits, which are part of our culture, usually make for some joy in our lives, but can also contribute to causing much disease and suffering.
1. Di Castelnuovo A, Costanzo S, Donati MB, Iacoviello L, de Gaetano G (2010) Prevention of cardiovascular risk for moderate alcohol consumption: epidemiologic evidence and plausible mechanisms. Intern Emerg Med 5:291–297
2. Estruch R, Lamuela-Raventos RM (2010) Alcohol, wine and cardiovascular disease, two sides of the same coin. Intern Emerg Med 5:277–279
Conflicts of interest None.
CE – LETTER TO THE EDITOR
What should we advise about alcohol consumption? Reply letter by A. Di Castelnuovo
Augusto Di Castelnuovo, Simona Costanzo, Maria Benedetta Donati, Licia Iacoviello, Giovanni de Gaetano. Intern Emerg Med, DOI 10.1007/s11739-010-0502-6. Received: 21 October 2010 / Accepted: 24 November 2010
The main message of the letter by Ponz de Leon  is that any advice at a population level in favour of drinking alcohol in moderation, despite scientific evidence and prudence, is dangerous and must be avoided. We respect this opinion, but believe that progress in scientific knowledge should be to some extent independent of its potential application. The decision to implement a scientific upshot in guidelines and public health strategies is demanded from specific authorities and competencies, which have the appropriate capability to transfer specific scientific evidence into a global public health strategy. The assertion that at a population level, in any context, society and cultural environment and in respect to any specific subgroup of individuals, abstention is better than moderation is questionable and definitively not based on any scientific evidence . There are particular subgroups of individuals who can maximally benefit from the healthy effects of alcohol in moderation (e.g. adult men at high risk for cardiovascular disease ), as well as persons for whom abstention should be considered the right choice (e.g., young women at familial risk for breast cancer). To ask for global abstention is throwing out the baby with the bath water. Standing current scientific evidence, to ask for abstention is also ethically questionable, as well as less efficacious than to encourage the reduction of alcohol consumption. In our review  dealing with alcohol in moderation, that is two glasses of wine a day (or equivalent drinks) for men and one for women, we did not invite abstainers to start drinking, and strongly insisted that binge or excess drinking be avoided. What should we advise an adult who regularly drinks a glass of wine during meals: to stop drinking? Why? What is the scientific evidence to support such negative advice?
The author of the previous letter wrote that ‘‘Many people could be unable to distinguish between low-moderate and high doses of wine beer or spirits’’. While we are not convinced of this, and refute such a ‘‘paternalistic’’ approach (we know what you have to do), we cannot believe that this is a sufficient argument to disregard scientific evidence: besides alcohol, there are plenty of situations in which moderation is better that excess or abstention (e.g., the protective effect of low-dose aspirin in secondary cardiovascular risk prevention). The positive effect of many sleeping pills cannot be obscured by the fact that some use an excess of these pills and harm themselves.
The message of our review article was not that of drinking before driving, in a small-moderate amount. We reviewed the evidence about the role of moderate and regular alcohol intake in reducing the risk of cardiovascular disease and total mortality. It is obvious than in particular conditions drinking must be avoided at any dosage.
Dr. Ponz de Leon states that ‘‘more studies are needed before we can give sensible recommendations on alcohol consumption to the general population. Prospective, long-term, cohort investigations are particularly needed’’. Probably the author was alluding to ‘‘intervention clinical trials’’. In fact, the evidence of a positive role of alcohol in moderation derives from a very large number of ‘‘prospective, long-term, cohort investigations.’’ In our review of the literature, we identified, e.g., more than 30 large, prospective cohorts on alcohol and total or cardiovascular mortality, involving more than 1 million subjects . Randomized controlled intervention trials on alcohol might offer in the future a more solid answer than observational studies, but at the present moment, one has to rely upon the available observational studies, which clearly indicate a benefit at low doses that cannot be hidden by the scientific community.
In conclusion, we agree on the fact the great caution has to be taken when speaking about alcohol and health, but strongly believe that a scientific approach should always prevail over any ideological prejudice.
1. Ponz de Leon M (2010) What should we advise about alcohol consumption. Intern Emerg Med. doi:10.1007/s11739-010-0487-1
2. Rehm J, Mathers C, Popova S, Thavorncharoensap M, Teerawattananon Y, Patra J (2009) Global burden of disease and injury and economic cost attributable to alcohol use and alcohol-use disorders. Lancet 373:2223–2233
3. Costanzo S, Di Castelnuovo A, Donati MB, Iacoviello L, de Gaetano G (2010) Cardiovascular and overall mortality risk in relation to alcohol consumption in patients with cardiovascular disease. Circulation 121(17):1951–1959
4. Di Castelnuovo A, Costanzo S, Donati MB, Iacoviello L, de Gaetano G (2010) Prevention of cardiovascular risk for moderate alcohol consumption: epidemiologic evidence and plausible mechanisms. Intern Emerg Med 5:291–297
Conflict of interest None.
CE – LETTER TO THE EDITOR
What should we advise about alcohol consumption: reply letter by R. Estruch
Ramon Estruch • Rosa Ma Lamuela-Raventos. Intern Emerg Med; DOI 10.1007/s11739-010-0503-5. Received: 25 October 2010 / Accepted: 24 November 2010
We agree with the letter by Dr. Ponz de Leon  on concerns related to ‘‘alcohol use/misuse’’ in that high alcohol intake may be a cause of several chronic diseases, as well as social and labor problems. Thus, we must be cautious when recommending low-to-moderate alcohol consumption to the overall population. However, we cannot forget the scientific evidence supporting the beneficial effects of moderate alcohol/wine intake on cardiovascular disease , some type of cancer  and other degenerative diseases . Cardiovascular disease continues to be the main cause of death in developed and developing countries , and we have to fight against it with all the weapons available. Diet and exercise are the first step in the treatment of such disease. There is increasing evidence for a beneficial effect of Mediterranean diet on the prevention of cardiovascular disease, and wine is one of the traditional components of this food pattern. In our experience, most people are able to distinguish between low-to-moderate wine consumption (up to 2 glasses of wine a day for men and 1 glass of wine for women) and a high amount of alcohol intake. In his letter Dr. Ponz de Leon indicates that, in some cases, one may suspect liver disease related to alcohol intake in women who consume low doses of ethanol. However, it is well known that in some women it is often difficult to substantiate the veracity of a ‘‘low ethanol consumption’’, and some liver disease such as ‘‘non-alcoholic fatty liver disease’’ may be erroneously attributed to ‘‘low alcohol intake’’. In these cases, determination of serum and urine biomarkers of ethanol consumption may be a very useful tool to distinguish if ethanol is the main agent responsible for the disease.
On the other hand, we agree that people must abstain from drinking before driving or using heavy machinery at work. Nonetheless, the same subjects may consume a glass of wine together with a meal with family and friends. Fortunately, thanks to governmental campaigns against drinking and driving, most people who consume alcohol now abstain from driving their cars. Similarly, pregnant women must always abstain from having any alcoholic drink.
Currently, new prospective long-term investigations are ongoing to support the results from several ecological and cohort studies supporting the beneficial effect of moderate alcohol consumption on health. Ongoing studies also are investigating the possible effects of the different types of alcoholic beverages and the biochemical mechanisms to explain such beneficial effects. However, in the era of evidence-based medicine, nutritional recommendations should be based on large-scale randomized intervention studies in which clinically relevant (‘‘hard’’) end-points are evaluated. Up to now, no randomized controlled trial has ever been conducted to assess to what extent moderate alcohol consumption offers greater benefits than complete alcohol abstinence in the primary or secondary prevention of cardiovascular events. Without this level of evidence, we are not allowed to recommend moderate alcohol consumption to ‘‘teetotalers’’, and, as Dr. Ponz de Leon suggests, we have to be very cautious with our recommendations to the overall population.
1. Ponz de Leon M (2010) What should we advise about alcohol consumption. Intern Emerg Med doi:10.1007/s11739-010-0487-1
2. Di Castelnuovo A, Costanzo S, Donati MB, Iacoviello L, de Gaetano G (2010) Prevention of cardiovascular risk for moderate consumption: epidemiologic evidence and plausible mechanisms. Intern Emerg Med 5:291–297
3. Groenbaek M, Becker U, Johansen D et al (2000) Type of alcohol consumed and mortality from all causes, coronary heart disease and cancer. Ann Intern Med 133:411–419
4. Sherman FT (2006) The case for alcohol in the primary prevention of dementia: abstinence may be bad for your health! Geriatrics 61:10–12
5. Reddy KS (2004) Cardiovascular disease in non-Western countries. N Engl J Med 350:2438–2440
6. Cyr MG, McGarry KA (200 2) Alcohol use disorders in women. Screening methods and approaches to treatment. Postgrad Med 112:31–47
Conflict of interest None.
Additional comments by members of the International Scientific Forum on Alcohol Research
Comment from Francesco Orlandi, MD, Dept. of Gastroenterology, Università degli Studi di Ancona. Italy
To trust the patient is a crucial point of medical care and medical knowledge, and it becomes a pre-requisite for sustainable medical progress. Look at my next patient, an adult man at high risk for cardiovascular disease and no risk of addiction: the suggestion of moderate drinking is my ethical duty, otherwise I should adopt bad “defensive medicine.”
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Comment from Fulvio Ursini, MD, Dept. of Biological Chemistry, University of Padova, Padova, Italy
I think that the comment of Dr Ponz de Leon is extremely useful, being a genuine and authentic example of the most common — and undesirable — mistakes we observe when scientific evidence needs to be translated into recommendations.
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Comment from R. Curtis Ellison, MD, Section of Preventive Medicine & Epidemiology, Boston University School of Medicine, Boston, MA, USA
Scientific data from epidemiologic studies, basic science, and limited clinical trials support a role for moderate alcohol consumption in the prevention of cardiovascular diseases. At the same time, we realize that this substance can be a “double-edged sword.”1 We have long known that excesses (in habits, foods, or alcohol) have problems that are inherent not in the activities or substances themselves, but in their inappropriate use. For example, in an address to a temperance society in 1842, Abraham Lincoln, later the 16th President of the United States, stated: “It has long been recognized that the problems with alcohol in this country relate not to the use of a bad thing, but to the abuse of a good thing.”2
There are no data showing than encouragement of moderate consumption increases abuse, and others have debunked the idea that people cannot tell the difference between moderate and heavy consumption. For example, Klatsky has stated: “ . . . most people know very well what the difference is between light to moderate drinking and binge or excessive drinking. While some patients may rationalize their heavy drinking because of its purported health effects, I have yet to find someone who had developed alcohol abuse because of messages about the health effects of moderate drinking.”3 Medical practitioners, in his view, “have a ‘solemn duty’ to tell the truth about alcohol consumption, as they understand it, to all of their patients.”3 And it is clear that advice about alcohol should vary according to the characteristics of the individual patient.
As described by Cole,4 the finest moral rationale for prevention-oriented public health activity should be informing people, and it should not be based on “paternalism” (“we know what is best for you and will tell you only what you need to know”). We have had examples of sound scientific information relating alcohol intake to coronary heart disease that has been sacrificed to be “politically correct.”5 It should be emphasized that there are certain people who should not drink at all (including former abusers of drugs or alcohol, people with certain medical conditions, children and adolescents, and people with religious or moral proscriptions against alcohol), and there can never be a general recommendation for everybody to consume alcohol. On the other hand, we should not withhold from our patients and the public scientifically sound and balanced data on alcohol and health. Whereas our current understanding suggests that moderate, sensible drinking can be potentially helpful for prevention of coronary heart disease in most adults (those without contraindications to alcohol use) as one component of a healthy lifestyle, individuals planning to change their drinking habits (e.g., teetotalers deciding to begin drinking) should always do this after consultation with their health care provider.6
1. O’Keefe JH, Bybee KA, Lavie CJ. Alcohol and cardiovascular health: the razor-sharp double-edged sword. J Am Coll Cardiol 2007;50:1009-1014.
2. Lincoln A: Talk to Washington Temperance Society of Springfield, Illinois, February 22, 1842, as published in http://www.druglibrary.org/schaffer/lincoln.htm.
3. Klatsky A. Panel Discussion V: The Message on Moderate Drinking, Ann Epidemiol 2007;17:S110–S111.
4. Cole P. The moral bases for public health interventions. Epidemiology 1995;6:78-83.
5. Seltzer CC. “Conflicts of interest” and “political science.” J Clin Epidemiol 1997;50:627-629.
6. These comments modified in part from the Conclusions in Ellison RC, Chapter 18: Effects of Alcohol on Cardiovascular Disease Risk, in Preventive Cardiology: Companion to Braunwald’s Heart Disease, Eds: Blumenthal R, Foody J, Wong ND. Elsevier, ISBN: 978-1-4377-1366-4, in press, February 2011.
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Comment from Arne Svilaas, MD, PhD, general practice and lipidology, Oslo University Hospital, Oslo, Norway
I find the Reply letter by A. Di Castelnuovo et al a reasonable comment and agree with other views expressed by Forum members. The statement of de Leon: “Many people may be unable to distinguish between low–moderate and high consumption of wine, beer or spirits” is hardly correct. For some people . . . maybe. Concerning accidents, etc., governments have to intensify their efforts to convince people to avoid drinking before driving. These two points of De Leon are not good arguments for abstention.
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Comment from Harvey Finkel, MD, Hematology/Oncology, Boston University Medical Center, Boston, MA, USA
Ponz de Leon’s attitude is unacceptably paternalistic. It comes from another era. Physicians must communicate fully with their patients, despite health-insurance companies’ and governments’ efforts to standardize the drive-through medical experience. That said, I would also have us consider that alcohol (I’m referring chiefly to wine) should be used to enrich life, not necessarily to medicate it.
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Comment from Andrew L. Waterhouse, PhD, Marvin Sands Professor, Department of Viticulture and Enology, University of California, Davis.
It is unfortunate that the editors have chosen to publish an editorial that castigates alcohol from an author with good scientific credentials, but little to no apparent research expertise in the subject of alcohol and health. Furthermore, his criticisms seem to stem from personal observations, and not research. While it might appear to be politically correct to facilitate uninformed criticism of alcohol, the same rigorous standards should apply in all areas of scholarship if the journal is to be successful in advancing knowledge.
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Comment from Erik Skovenborg, MD, Scandinavian Medical Alcohol Board, Practitioner, Aarhus, Denmark
Problems can arise when an editorial from an “expert” (de Leon) states that “he is unconvinced by the evidence” about the effects of alcohol when the author himself is not a real expert in the field of alcohol and health. “Paternalism” in setting alcohol policy has been alluded to by others. A notable occasion, mentioned above by Ellison, refers to an early report from the Framingham Heart Study. While the data after 24 years of follow up in that study strongly showed that abstinence from alcohol was a major risk factor for death from coronary heart disease, officials at the National Institute of Health (whose approval to publish was required) told the Framingham team to “remove all references to alcohol.” As described later by Seltzer(1), the NIH officials stated that “An article which openly invites the encouragement of undertaking drinking with the implication of preventing of CHD would be scientifically misleading and socially undesirable in view of the major health problem of alcoholism that already exists in the country.” The letter from NIH continued, “If you must say something about alcohol, say it has no effect.”(1) It seems that such a paternalistic approach continues to be voiced: scientifically sound evidence for the protective effect of moderate alcohol intake against cardiovascular diseases has been presented, but the message is too dangerous to diffuse in the general population.
The editorial by de Leon also indicates that the evidence is not sufficient. He and others seem to insist that randomized, prospective clinical studies of large cohorts are needed before sensible recommendations about alcohol consumptions can be made. However, such investigations have neither been done regarding exercise, diet, weight reduction, smoking, etc., because such studies would either be unethical, extremely costly, or extremely difficult to perform.
I would like to add another variation of the paternalism theme: data from the European Prospective Investigation Into Cancer and Nutrition-Potsdam Study were studied with end points including type 2 diabetes mellitus, myocardial infarction, stroke and cancer. The authors state that “We did not include moderate use of alcohol as a potentially beneficial behavior given the adverse health impact of excessive use”.(2).
1.. Seltzer CC. “Conflicts of Interest” and “Political Science.” J Clin Epidemiol 1997;50:627-629.
2.. Ford ES, Bergmann MM, Kröger J, Schienkiewitz A, Weikert C, Boeing H. Healthy living is the best revenge. Arch Intern Med 2009;169:1355-1362.
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Comment from Maritha J. Kotze, PhD, Human Genetics, Dept of Pathology, and David Van Velden, MD, Dept. of Pathology, University of Stellenbosch, South Africa
Genes determine how individuals respond to modifiable risk factors such as diet, exercise, smoking, as well as the metabolism of alcohol and drugs. Apo E genotyping may be useful in the assessment of the impact of alcohol consumption on healthy aging. In this context, Anttila et al1 have shown that the risk of dementia increased with increasing alcohol consumption only in those individuals carrying the Apo E4 allele. When LDL-cholesterol levels are compared among Apo E subgroups on the basis of drinking status, these levels are significantly higher in male drinkers with the Apo E4 allele than in non-drinkers.2 In women, the expected effect of Apo E alleles on LDL-C levels was present in both drinkers and non-drinkers. In a model with adjustment for age, sex, body mass index, smoking, exercise, waist-hip ratio, TV viewing, and study site, the increase in HDL-cholesterol associated with alcohol was significantly higher in subjects without the Apo E4 allele than in those with this allele.3 These findings suggest that subjects carrying the Apo E4 allele may not benefit from moderate alcohol drinking as part of the dietary measures to lower CHD risk as do subjects with other alleles. As an example of yet another gene related to the effects of alcohol, cancer risk appears to be increased with high alcohol intake when folate status is low in mutation carriers of methyltetrahydrofolate reductase (MTHFR) gene.4 Decreased MTHFR activity is of special concern in individuals with high alcohol intake since this may lead to impaired folate status due to malabsorption, increased excretion, or abnormal folate metabolism.5
Long-term intervention strategies for health promotion including lifestyle modification and safer daily drinking habits may therefore be more effective when guided from the genetic background. Genetic testing forms an important component of continuous efforts to optimize disease diagnosis and lifestyle intervention for CVD risk reductions. In order to prevent misinterpretation of genetic data when performing a multi-gene CVD assay developed in South Africa,6,7 information on non-genetic risk factors, biochemical parameters, family history, and known gene-gene or gene-environment interactions are taken into account and explained when the genetic results are reported (www.gknowmix.com). The formulation of individualized risk reduction strategies and health monitoring programs implemented by referring health professionals are based on conventional risk factors integrated with the genetic test results.8
Therefore, the debate on the health benefits of low to moderate alcohol consumption must take into consideration genetic predisposition for certain diseases. Molecular biology has made it possible for us to identify certain individuals that may not benefit from alcohol consumption. It is not possible to formulate general guidelines without recognizing the fact that people react differently to drugs. Some medications meant to treat disease are also toxic to people if their bodies cannot metabolize the drug, and alcohol is no different. Science has made great strides since molecular biology has been shown to partially explain the concept of diet-gene interactions. These interactions are strongly influenced by many environmental, socioeconomic and behavioral factors, and therefore it is unlikely that any single gene or risk factor will have the predictive power needed to confirm a predisposition for a particular chronic condition, as we have shown for other interactions.9
1. Anttila T, Helkala EL, Viitanen M, et al. Alcohol drinking in middle age and subsequent risk of mild cognitive impairment and dementia in old age: a prospective population based study. BMJ 2004; 329:539.
2. Corella D, Tucker K, Lahoz C, et al. Alcohol drinking determines the effect of the APOE locus on LDL-cholesterol concentrations in men: the Framingham Offspring Study. Am J Clin Nutr 2001; 73:736-45.
3. Djousse L, Pankow JS, Arnett DK, Eckfeldt JH, Myers RH, Ellison RC. Apolipoprotein E polymorphism modifies the alcohol-HDL association observed in the National Heart, Lung, and Blood Institute Family Heart Study. Am J Clin Nutr 2004; 80:1639-44.
4. Bailey LB. Folate, methyl-related nutrients, alcohol, and the MTHFR 677C-T polymorphism affect cancer risk: Intake recommendations. J Nutr 2003; 133: 3748S-3753S.
5. Halsted CH, Villanueva JA, Devlin AM, et al. Metabolic interactions of alcohol and folate. J Nutr 2002; 132: 2367S-2372S.
6. Kotze MJ, Kriegshäuser G, Thiart R, de Villiers JNP, Scholtz CL, Kury F, Moritz A, Oberkanins C. Simultaneous detection of multiple familial hypercholesterolaemia mutations facilitates an improved diagnostic service in South African patients at high risk of cardiovascular disease. Mol Diagn 2003;7:169-174.
7. Kotze MJ, Thiart R, de Villiers JNP, Scholtz CL, Joffe Y. Cardiovascular genetics: practical applications and gene-based intervention. Cardiovasc J S Afr 2003;14:269-270.
8. Kotze MJ, Badenhorst H. Chronic disease risk management: Combining genetic testing with medical and nutrition therapy. SA Fam Pract 2005; 47: 40-42.
9. Van Velden DP, van der Merwe S, Fourie E, Kidd M, Blackhurst DM, Kotze MJ, Mansvelt EPG. The acute influence of a Mediterranean-like diet with and without red wine on patients with the metabolic syndrome. S Afr J Enol Vitic 2007;44-49.
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Comment from Ulrich Keil, MD, PhD, Institute of Epidemiology and Social Medicine, University of Münster, Münster, Germany
I think that one of the first convincing papers on the protective effect of light to moderate alcohol consumption on myocardial infarction was the deductive meta-analysis by M. Maclure published in Epidemiologic Reviews1 . . . in 1993! Maclure analyzed no fewer than 30 prospective cohort studies performed between 1968-1993 on the topic of light to moderate alcohol consumption and fatal and non fatal myocardial infarction. In his so called deductive meta-analysis he took into account that he was dealing with observational studies and not with randomized clinical trials. He concluded that there was clear evidence for a protective effect.
When I was submitting the first paper with German data on alcohol consumption and its relation to CHD and total mortality in a beer drinking population of southern Germany to Epidemiology in 1996, I was afraid that it would not be accepted because the protective effect of alcohol on CHD was already clear. I argued in this paper that the protective effect of alcohol on CHD was nearly as evident as the negative effect of smoking on CHD. The paper was published in 1997.2
In the same year a paper by Thun, Peto, Lopez, et al,3 based on 490,000 men and women of the huge prospective cohort study from the American Cancer Society, appeared in the NEJM. It clearly showed that men and women who did not drink any alcohol but smoked had the highest all-cause mortality, while men and women who did not smoke but consumed alcohol had the lowest all-cause mortality. The other groupings were in between.
These studies appeared more than a decade ago, but the old arguments of ” I do not believe” are repeated again and again by certain groups or individuals, some because of “conflicts of interest,” “political science,” or ” paternalism,” others by colleagues who are afraid of the “devil alcohol.”
As large-scale randomized controlled trials on the topic of alcohol and cardiovascular disease will never happen, because of ethical and other reasons, we have to live with these politically tainted arguments. But to our relief, at least in central and southern Europe, most people do not drink alcohol in light to moderate amounts for protecting their health, but because they want to enjoy a delicious meal or simply enjoy life.
1. Maclure M. Demonstration of deductive meta-analysis: ethanol intake and risk of myocardial infarction. Epidemiol Rev 1993;15:328-351.
2. Keil U, Chambless LE, Döring A, Filipiak B, Stieber J. The relation of alcohol intake to coronary heart disease and all-cause mortality in a beer-drinking population. Epidemiology 1997;8:150-156.
3. Thun MJ, Peto R, Lopez AD, Monaco JH, Henley SJ, Heath CW Jr, Doll R. Alcohol consumption and mortality among middle-aged and elderly U.S. adults. N Engl J Med 1997;337:1705-1714.
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Comment from Tedd Goldfinger, DO, FACC, Desert Cardiology of Tucson Heart Center, Dept. of Cardiology, University of Arizona School of Medicine, Tucson, Arizona
I reject the notion Ponz de Leon projects that we consider, or not consider, alcohol as a medication. As clinicians, we not only prescribe medications, but also discuss healthy lifestyle choices with our patients so as to promote better health and longevity. Would he consider as “medications” fresh fish, green vegetables, and fruit & nuts, all of which contribute to a healthy and longer life?
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Comment from Dee Blackhurst, PhD, Lipid Laboratory, University of Cape Town Health Sciences Faculty, Cape Town, South Africa
In medical practice, the physician has a duty to deliver clear advice against harmful lifestyle, and should be careful about being too prescriptive about lifestyle issues that do not have very powerful effects. Definitely, potentially beneficial lifestyle matters should be discussed in an informed way for the citizen to make a decision based on, for example, economy, preferences and culture. Amounts of alcohol can be clearly stipulated to enable citizens to distinguish between low, moderate, and high consumption of alcohol.