Alcohol and Cardiovascular Disease

Note: For an archive of critiques, by topic, CLICK HERE.

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Critique 278 – A burden of proof study on alcohol consumption and ischemic heart disease – June 2024

Reference: A burden of proof study on alcohol consumption and ischemic heart disease. Carr S; Bryazka D; McLaughlin SA; Zheng P; Bahadursingh S; Aravkin AY; Hay SI; Lawlor HR; Mullany EC; Murray CJL; Nicholson SI; Rehm J; Roth GA; Sorensen RJD: Lewington S; Gakidou E. Nature Communications (2024) 15:4082. https://doi.org/10.1038/s41467-024-47632-7

A re-evaluation of existing study data using a relatively recent burden of proof meta-analytical framework suggests that different types of study are inconsistent on the alcohol-ischemic heart disease relationship. The authors conclude that Mendelian Randomization methodologies need to be developed further for more definitive answers from this study type and that more long-term randomized trials are needed

For the detailed critique of this paper by the International Scientific Forum on Alcohol Research, please click here.

Critique 276. Alcohol Consumption, High-Density Lipoprotein Particles and Subspecies, and Risk of Cardiovascular Disease: Findings from the PREVEND Prospective Study – May 2024

Reference:Alcohol Consumption, High-Density Lipoprotein Particles and Subspecies, and Risk of Cardiovascular Disease: Findings from the PREVEND Prospective Study. Kunutsor SK; Bhattacharjee A; Connelly MA; Bakker SJL; Dullaart RPF. Int J Mol Sci (2024), 25, 2290. https://doi.org/10.3390/ijms25042290

A protective effect of moderate alcohol consumption for CVD has been reported by numerous studies over decades.  This was a key finding of this study too. Further, it is also recognised that alcohol consumption increases high density lipoprotein cholesterol (HDL-C), and this was confirmed by this study too.  HDL-C has been considered for years the “good” cholesterol, as suggested by the inverse correlation between its plasma levels and cardiovascular (CVD) risk, as shown by the epidemiology. However, the relationship between HDL and atherosclerosis has been found to be much more complex. This study failed to find an association between alcohol consumption and HDL parameters, suggesting that the clinical relevance of HDL is more related to reverse cholesterol transport in which an inverse relationship has been detected with the prevalence of atherosclerosis, inflammation, and the promotion of plaque stability, as well as the incidence of CV events such as acute myocardial infarction. The ability of HDL to promote reverse cholesterol transport therefore appears to be more related to its size and composition in terms of proteins and lipids, than to HDL-C plasma levels, where identifying efficacy should move to HDL function measurement, that is, reverse cholesterol transport, instead of plasma levels.

For the detailed critique of this paper by the International Scientific Forum on Alcohol Research, please click here.

Critique 273 – Circulating metabolites may illustrate relationship of alcohol consumption with cardiovascular disease – January 2024

Two papers were recently published which consider the complexity of liver and gut-generated circulating metabolites of alcoholic beverages, such as wine, and their specific roles in human health (referred to as metabolomics). These papers collectively suggest that the 60 or more alcohol-associated metabolites following consumption, may be related to the risk of cardiovascular and other diseases.

For the detailed critique of this paper by the International Scientific Forum on Alcohol Research, please click here.

Critique 271 – Moderate alcohol consumption, types of beverages and drinking pattern with cardiometabolic biomarkers in three cohorts of US men and women

Cardiovascular diseases (CVDs) remain the leading cause of death globally, and leading risk factors for CHD and stroke include high blood pressure, high low-density lipoprotein (LDL) cholesterol, diabetes, smoking and second-hand smoke exposure, obesity, unhealthy diet, and physical inactivity.

Various randomized controlled trials have previously identified biomarkers that change with moderate alcohol consumption and which may explain its beneficial effects on CVDs. These biomarkers include HDL cholesterol, glycaemic control as HbA1c and adiponectin. Other relevant biomarkers changing with moderate alcohol consumption are fibrinogen, fibrinolysis, platelet aggregation, other lipoproteins, such as LDL cholesterol, HDL functionality, oxidative markers and triglycerides. This large epidemiological study provides further support for these beneficial effects but also highlights the beneficial effects on and inflammatory markers. The study also supports the importance of a regular and moderate pattern of alcohol consumption, not abstinence nor binge or heavy drinking, to maintain cardioprotection.

For the detailed critique of this paper by the International Scientific Forum on Alcohol Research, please click here.

Critique 268 – Alcohol intake including wine drinking is associated with decreased platelet reactivity in a large population sample – 1 August 2023

This study by Pashek et al. (2023) confirms previously observed associations between alcohol consumption and decreased platelet reactivity, but does not conclusively confirm differential beverage and gender effects.  

Our knowledge regarding the health effects of alcohol consumption might best be grouped into two complementary approaches. Observational studies, for example, have now reached epic proportions in sample size and duration, and feeding studies have assessed the immediate and short-term effects of alcohol on behaviour, biochemical pathways, and similar social or physiological endpoints. Clearly, neither of these approaches represents gold-standard evidence in biomedical research, that is, only a long-term randomized trial of clinical endpoints would meet that standard. Existing clinical trial and epidemiological evidence as well as confirmatory studies such as Pashek et al. (2023) provide useful insight into the endpoints that a clinical trial of moderate alcohol consumption might be best poised to tackle (Mukamal et al. 2016).

These observational data have demonstrated a differential effect of the alcoholic beverages on haemostatic cardioprotective mechanisms. More data are required, however, to establish the degree of differentiation between alcoholic beverages in conferring cardio-protection, cancer-protection and protection against other degenerative diseases.

For the detailed critique of this paper by the International Scientific Forum on Alcohol Research, please click here.

Critique 266: Reduced stress-related neural network activity mediates the effect of alcohol on cardiovascular risk – 3 July 2023

Well-known and studied causes of cardiovascular diseases include genetic, environmental, dietary and lifestyle components. Stress can be considered as a lifestyle component and risk factor for cardiovascular disease. The amygdala region of the brain is associated with stress responses via the sympathetic nervous system, and duly increases blood pressure and heart rate, and triggers the release of inflammatory cells to stressors. This study has focused on the role of alcohol in mitigating these adverse effects from stress on the cardiovascular system. The study showed that light to moderate alcohol consumption of 1 to 2 standard drinks daily compared to abstinence potentially lowers cardiovascular risk as it leads to long-term reductions in the brain’s stress signalling in the amygdala. The relationship is also j-shaped where heavier alcohol consumption, however, increases the risk of stress-related cardiovascular disease events.  This is a new plausible mechanism of action for alcohol on reducing cardiovascular risk which deserves further study.

For the detailed critique of this paper by the International Scientific Forum on Alcohol Research, please click here

Critique 222. A new analysis relating alcohol intake to coronary heart disease – 20 December 2018

In an attempt to judge the effects of alcohol on the risk of coronary heart disease (CHD), the authors have carried out analyses using a sample of subjects from the National Epidemiologic Survey on Alcohol and Related Conditions III (NESARC-III). They based their exposure to current alcohol use on a single assessment at baseline of self-reported consumption during the past year, when the subjects were an average of 38.9 years of age.  In addition they asked subjects if they had consumed larger amounts of alcohol when they were younger.

Their assessment of CHD was based on answers to questions at baseline as to having been told by a doctor that they had chest pain or CHD, apparently within the same 12-month period when they were asked about current alcohol consumption. Nothing in the paper indicates that the authors had data on the subsequent development of CHD during a follow-up period.  When relating reported alcohol intake to CHD, they excluded 1,671 who reported “previous CHD,” although for this relatively young group it is questionable how many actually had CHD, as no data on validation of the diagnosis was done.  For unclear reasons, for their comparison group they excluded any subjects with conditions that “may increase the risk of CHD (e.g., pneumonia, influenza, tuberculosis, liver disease, neurologic conditions, osteoporosis, arthritis, STD) and can be viewed as comorbid conditions related to alcohol consumption.”

Given that the exposure (alcohol) and outcome (CHD) were apparently from the same time period, there is reason to worry about reverse causation (i.e., subjects may have developed CHD and changed, either decreased or increased, their alcohol consumption during the same period).. As for using the self-reported amount of alcohol consumed at some time in the past as the exposure, there is a large chance of serious misclassification of exposure due to recall bias and bias according to current alcohol intake (as subjects currently reporting greater amounts of alcohol were more likely to report even higher intake in the past).

With only a single assessment of current alcohol intake, an inadequate assessment of long-term alcohol intake, a lack of data during a follow-up period for the main outcome, CHD, and no validation of the outcome, Forum members considered that this was an unusual cohort to use when attempting to judge the relation of changes in alcohol consumption to the development of CHD. The necessary elements for a useful analysis were not available to these investigators using this population sample.

In any case, results from many well-done long-term cohort studies with repeated assessments of alcohol and validated CHD outcomes during follow up have already provided key data on this topic: they almost uniformly demonstrate that light-to-moderate drinkers who do not binge drink have significantly lower risk of developing CHD. The present analysis does not provide data that would question such findings.

Reference: Fan AZ, Ruan WJ, Chou SP.  Re-examining the relationship between alcohol consumption and coronary heart disease with a new lens.  Pre-publication.  Preventive Medicine 2019;118:336=343.

For the full critique of this paper by the International Scientific Forum on Alcohol Research, please click here.

Critique 173:  A Large Study of the Association of Alcohol with the Risk of Acute Myocardial Infarction  —  15 October 2015

This paper presents prospective data from a large population-based cohort from rural Norway, a region with typically light alcohol drinking and many abstainers who were not ex-heavy drinkers.  It relates reported alcohol intake, assessed on two occasions, with the risk of developing an acute myocardial infarction (AMI).  Its key findings are that, even in this very light-drinking population, drinkers had significantly lower risk (about 20% to 30%) of developing a MI than non-drinkers.  As the authors conclude: “Light-to-moderate alcohol consumption was linearly associated with a decreased risk of AMI in a population in which abstaining from alcohol is not socially stigmatized.  Our results suggest that frequent alcohol consumption is most cardioprotective and that this association is not driven by misclassification of former drinkers.”

As this was a rather homogeneous rural cohort without huge differences among subjects in socioeconomic status, it allows much better control of confounding.  The fact that these results show essentially a continuous inverse association (rather than the usually seen “J-shaped” curve) is not unexpected given the very few heavy drinking subjects in this cohort.   In addition to cardiovascular disease, the investigators also reported effects on total mortality, which showed a “J-shaped” curve.

Forum members considered this to be a very well-done study, and supports almost all previous research showing a protective effect of moderate drinking on the risk of coronary heart disease.  The authors had good data on alcohol exposure and the occurrence of AMI.  A key result from this study is that frequent light drinking, even less than an average of one drink/day, is associated with a significant decrease in the risk of coronary heart disease.  Based on this study and most previous research, the clear message to the public remains: if you have no contraindications to alcohol use and decide to consume an alcoholic beverage, the healthiest approach is to drink frequently but in small amounts.

Reference:  Gémes K, Janszky I, Laugsand LE, Lászlo KD, Ahnve S, Vatten LJ, Mukamal KJ.  Alcohol consumption is associated with a lower incidence of acute myocardial infarction: results from a large prospective population-based study in Norway. J Intern Med 2015; doi: 10.1111/joim.12428.

For the full critique of this paper by members of the International Scientific Forum on Alcohol Research, please click here.

Critique 167:  What determines a person’s belief that “alcohol is heart-healthy?”  –  22 July 2015

This paper, based on data from more than 5,000 adults participating in an internet-based survey, sought to determine what were the perceptions of subjects on the relation of alcohol to heart disease, and how these perceptions resulted in particular behaviors related to alcohol consumption.  Partricipants for the survey were recruited by a variety of methods, including announcements “in the lay press, promotional events, word of mouth, social media, e-mail, and clinic visits.”   While the goal of the study is commendable, the results of any such survey obviously depend on many social and cultural factors of  the people who respond to the survey; it was not a random sample of the population used in this analysis.  This is critical because an interpretation of the data requires an understanding of the population surveyed.

Forum members had other concerns about this paper, including the specific survey questions regarding the perceptions of alcohol effects.  For example, the key question asked in the survey was “Do you believe alcohol is good for your heart?”  Forum members pointed out that it is obvious to nearly everyone that this cannot be answered without quantifying the amount of alcohol or the pattern of drinking.  They consisdered that a more appropriate quesiton might be something such as “Do you believe that the moderate consumption of alcoholic beverages can benefit your heart?”

The authors make statements such as “Participants perceiving alcohol as heart healthy consumed 47% more alcohol.” This may sound alarming until it is revealed that the observed difference was from a baseline of 0-3 to 1-5 glasses of wine/week and from 1-7 to 2-8 total drinks/week.  These higher amounts are not ‘alarming’ at all, and in fact fall within usual guidelines for “sensible drinking.”

Forum members were particularly upset that the authors misquote a number of scientific papers to support their claim that even low levels of drinking increase the risk of certain diseases.  The authors also use such misrepresentations of data to justify their concerns that current guidelines for alcohol consumption may not be appropriate.  Forum reviewers found it especially disturbing that the peer review process by the journal failed to uncover such misrepresentations of data.

The authors repeatedly give the impression that they are against any amount of alcohol consumption.  They do not comment on the consistent findings in almost all well-done prospective studies indicating that moderate drinkers live longer than abstainers.   Further, statements by the authors that suggest that people who think that alcohol is heart healthy are misinformed does not stand up to scientific data, which indicate that moderate and responsible drinking is associated wtith better health and longevity.

It is interesting that the report indicates that older, higher-income, and more highly educated subjects are more likely to consider alcohol to be heart healthy than younger and less-educated subjects.  While a question was asked by the investigators as to whether or not the responder’s perception of the health effects of alcohol influences their decision to drink or to not drink, the specific responses to this question are not presented in the paper.  It remains unclear to what extent beliefs about alcohol’s potential health effects relate to alcohol use or, more importantly, to alcohol abuse.

Overall, Forum members thought that the idea behind this study was of interest, but emphasized that it is important to collect data based on a random and well described sample of the population if one is to provide significant and understandable results.  Further, the report is compromised by what appears to be a deliberate misrepresentation of the prior scientific literature to support the authors’ contention that alcohol is not healthy; there are a number of obvious errors that should have been detected during the review process by the journal.  In the opinion of the Forum, the most reliable result from these analyses relates to where people obtain their information regarding alcohol and health: it does not come from physicians or scientific publications, but primarily from the lay press.

Reference:  Whitman IR, Pletcher MJ, Vittinghoff E, Imburgia KE, Maguire C, Bettencourt L, Sinha T, Parsnick T, Tison GH, Mulvanny CG, Olgin JE, Marcus GM.  Perceptions, Information Sources, and Behavior Regarding Alcohol and Heart Health.  Am J Cardiol 2015; pre-publication.  http:// dx.doi.org./10-1016/j.amjcard/2015.05-029.

For the full critique of  this paper by members of the International Scientific Forum on Alcohol Research, please click here.

Critique 143: A Mendelian randomization assessment of alcohol and cardiovascular disease — 20 July 2014

Using a very large dataset from subjects of European descent, the authors have carried out a Mendelian randomization analysis to estimate the effects of alcohol consumption on cardiovascular disease (CVD), using as the instrumental variable an uncommon allele affecting alcohol metabolism, the ADH1B rs1229984 variant.  People with this variant are unusually sensitive to alcohol (developing flushing and other uncomfortable symptoms from alcohol) and it has been well demonstrated that they are less likely than people without this variant to consume alcohol, and are unlikely to be heavy drinkers.  The authors conclude that since the 7% of their subjects with the uncommon allele had less cardiovascular disease, this indicates that alcohol consumption is unrelated to CVD.

Forum members agree that the analyses were done correctly, but strongly disagree with the premise of the study and the conclusions of the authors, and consider the genetic factor chosen as inappropriate to use as the instrumental variable in Mendelian randomization.  The gene studied explains only a fraction of alcohol consumption in the population (not stated in the paper) and it may have effects on CVD beyond those explained by alcohol consumption.  Thus, this ADH1b allele violates the assumptions required for a variable for Mendelian randomization and would be inappropriate for judging the effects of alcohol on CVD.  Further, in the present study, the authors report little relation of their estimate of alcohol consumption with HDL-cholesterol, while essentially all observational studies, clinical trials, and experimental studies have shown that alcohol is an important determinant of HDL.  This further suggests that the use of the ADH1B allele provides an inadequate estimate of alcohol consumption.

Even without the weakness of the allele chosen to reflect alcohol effects, conclusions derived from Mendelian randomization in general are heavily dependent on the assumption that the instrumental chosen is appropriate, of which you can rarely be confident.  Forum reviewers consider this method to be a very blunt instrument and subject to considerable bias for variables that are weakly correlated with exposure and not true instruments.

Some reviewers were concerned by the conclusion of the authors that this Mendelian randomization paper shows that all persons should drink less; this does not necessarily mean for people to completely avoid drinking.  The protection of moderate drinking against CVD that is generally observed shows a non-linear gradient: it is better manifested at a low alcohol consumption, while it is less strong as the consumption levels rise above optimum and finally disappears and is transformed into harm with heavy alcohol consumption.  This would be in agreement with the conclusions of most prospective studies and meta-analyses that drinking alcohol at low doses offers the best protection against CVD, as there is a J-shaped curve.

Reference: Holmes MV, Dale CE, Zuccolo L, et al (a total of 155 authors).  Association between alcohol and cardiovascular disease: Mendelian randomisation analysis based on individual participant data.  BMJ 2014;349:g4164 doi: 10.1136/bmj.g4164.

For the full critique of this study by members of the International Scientific Forum on Alcohol Research, please click here.

Critique 057:      Differences in effects on atherosclerosis of regular moderate drinking and binge drinking.   An experimental study in mice.    20 September 2011

An excellent study among experimental animals has reported very dramatic differences between the effects of alcohol administered in moderation on a daily basis and the same total weekly amount of alcohol administered on only two days of the week: binge drinking.  The mice used in the study that were given regular moderate amounts of alcohol showed no weight gain, improved lipid values, and much less development of atherosclerosis than did control animals.  However, those given alcohol in a binge-drinking pattern showed worse outcomes than control animals, and much worse outcomes than those given regular moderate alcohol.

This experimental study provides strong support for the frequent finding among humans in epidemiologic studies: benefits from regular moderate drinking, adverse effects from binge drinking.  It is especially important since, being an experimental study, the potential confounding effects of other lifestyle habits are not an issue, as is always the case for observational studies among humans.

Reference:  Liu W, Redmond EM, Morrow D, Cullen JP.  Differential effects of daily-moderate versus weekend-binge alcohol consumption on atherosclerotic plaque development in mice.  Atherosclerosis 2010, doi:10.1016/j.atherosclerosis.2011.08.034

For the full critique of this paper by members of the International Scientific Forum on Alcohol Research, please click here.

Critique 040.  Lower risk of coronary heart disease from alcohol, even with heavy drinking – 27 April 2011

Reference:  Le Strat Y, Gorwood P.  Hazardous drinking is associated with a lower risk of coronary heart disease: Results from a national representative sample.  Am J Addict 2011;20:257–263.

Using data from The 2001–2002 National Epidemiologic Survey on Alcohol and Related Conditions study (the NESARC study, n = 43,093), the authors of this paper conclude that alcohol may have cardioprotective effects not only in moderate drinkers, but also in individuals with patterns of use traditionally considered as “hazardous.”  While such a finding has been shown in some population studies, there were questions by Forum reviewers as to the adequacy of the method for diagnosing coronary artery disease: self-report, with most subjects listing angina pectoris, a “soft” criterion for coronary disease.

In addition, the categories of drinking used in this study were very broad: rare or only occasional drinkers were combined with regular drinkers up to 7 or 14 drinks per week in the “moderate” category; the “hazardous” category included a broad range of drinkers, from a minimal increase over the recommended limits to very heavy drinkers.  The pattern of drinking (especially the number of days per week that alcohol was consumed) was not reported, making it difficult to separate regular from heavy week-end drinkers.  The effects of heavier drinking on other conditions (such as alcohol-related liver disease, mortality, etc.) were not included in this analysis.

It is physiologically possible that even hazardous use of alcohol, like moderate use, may well lead to cleaner arteries and therefore lower rates of coronary artery disease.  If this is the case, an explanation for the increases in cardiovascular mortality reported for heavy drinkers in many studies may relate not directly to coronary artery disease, but to conditions such as cardiomyopathy or cardiac arrhythmias.  However, the rates of accidents, suicide and other morbidity associated with hazardous alcohol use may well overcome any protective effects on coronary disease.

For the full critique of this paper by members of the International Scientific Forum on Alcohol Research, please click here.

Critique 035.  A review of the association of alcohol consumption with cardiovascular disease outcomes – 5 March 2011

Reference:  Ronksley PE, Brien SE, Turner BJ, Mukamal KJ, Ghali WA.  Association of alcohol consumption with selected cardiovascular disease outcomes: a systematic review and meta-analysis.  BMJ 2011;342:d671; doi:10.1136/bmj.d671.

In an excellent summary, the authors of this paper have synthesized results from longitudinal cohort studies comparing alcohol drinkers with non-drinkers for the outcomes of overall mortality and mortality from cardiovascular disease (CVD), incident coronary heart disease (CHD), mortality from CHD, incident stroke, and mortality from stroke.  They conclude that light to moderate alcohol consumption is associated with a reduced risk of multiple cardiovascular outcomes.  Further, they suggest that current scientific data satisfy Hill criteria indicating causality, that alcohol intake is the cause of the lower risk of cardiovascular disease among moderate drinkers.

Forum members thought that this was a very well-done, comprehensive summary of a large number of studies on alcohol and cardiovascular disease.  Some believed that two topics were not adequately discussed: (1) greater benefits from wine than from other beverages, a result seen in many studies, and (2) the importance of the pattern of drinking on the health effects of alcohol.  However, Forum members welcomed the discussion in the paper as to causality and regarding future directions in research, with more emphasis into how physicians and individual patients might respond to encouragement to consume alcohol for its potentially beneficial effects on cardiovascular disease.  Most believe that there is no substitute for balanced judgment by a knowledgeable, objective health professional when discussing alcohol intake, and this requires is a synthesis of common sense and the best available scientific facts as they apply to the individual.

For the full critique of this paper by members of the International Scientific Forum on Alcohol Research, please click here.

Critique 034. A review of interventional studies in humans showing effects of alcohol on risk factors for cardiovascular disease – 5 March 2011

Reference:  Brien SE, Ronksley PE,Turner BJ, Mukamal KJ, Ghali WA.  Effect of alcohol consumption on biological markers associated with risk of coronary heart disease: systematic review and meta-analysis of interventional studies.  BMJ 2011;342:d636; doi:10.1136/bmj.d636.

A summary paper on the effects of alcohol consumption on biologic mechanisms associated with coronary heart disease provides an excellent review of a large number of intervention studies in humans.  Appropriate analyses were done and the results are presented in a very clear fashion, although there was little discussion of the separate, independent effects of alcohol and polyphenols on risk factors.

The trials the authors reviewed have demonstrated that the moderate intake of alcoholic beverages leads to increases in HDL-cholesterol, apolipoprotein A1, and adiponectin and decreases in fibrinogen, all factors associated with a lower risk of heart disease.  The findings described in this paper strengthen the case for a causal link between alcohol intake and a reduced risk of coronary heart disease, suggesting that the lower risk of heart disease observed among moderate drinkers is caused by the alcoholic beverage itself, and not by other associated lifestyle factors.

For the full critique of this paper by members of the International Scientific Forum on Alcohol Research, please click here.

Critique 033. Moderate-to-heavy alcohol intake may increase risk of atrial fibrillation. 12 February 2011

Reference:  Kodama S, Saito K, Tanaka S, Horikawa C, Saito A, Heianza Y, Anasako Y, Nishigaki Y, Yachi Y, Iida KT, Ohashi Y, Yamada N, Sone H.  Alcohol consumption and risk of atrial fibrillation.  A meta-analysis.  J Am Coll Cardiol 2011;57:427–436.

A number of well-done studies have shown an increase in the risk of atrial fibrillation to be associated with heavy alcohol intake or with alcoholism.  Most previous studies suggest little if any increase in risk from light-to-moderate drinking.  The present study was a meta-analysis based on 14 studies from Europe or North America.  It showed an increase in risk with alcohol, but there were limited dose-response data to determine if there was a threshold above which the risk was increased.  Overall, the scientific evidence from many studies suggests that at least heavy drinking may increase the risk of atrial fibrillation, although whether light-to-moderate intake increases the risk seems unlikely.  Previous basic scientific data of mechanisms of atrial fibrillation have suggested that alcohol has little effect on this arrhythmia.

For the full critique of this paper by members of the International Scientific Forum on Alcohol Research, please click here.

Critique026. Chinese study suggests that alcohol increases angiographically significant   coronary artery disease. 8 December 2010

Reference:  Zhou X, Li C, Xu W, Hong X, Chen J.  Relation of alcohol consumption to angiographically proved coronary artery disease in Chinese men.  Am J Cardiol 2010;106:1101–1103.

Among a large number of Chinese men presenting with chest pain or EKG changes, sequential subjects undergoing cardiac angiography were evaluated for obstructive coronary artery disease (CAD) lesions according to their reported recent alcohol intake.  The study population consisted of 1,476 consecutive men 36 to 84 years of age; participants were categorized as nondrinkers, light drinkers, moderate drinkers, or heavy drinkers.  Adjusted odds ratios for angiographically proved CAD for light, moderate, and heavy drinking were 1.16 (95% confidence interval 0.68 to 1.94), 1.78 (1.35 to 2.27), and 2.18 (1.46 to 3.25).  Compared to non-drinking, adjusted odds ratios were 1.03 (0.54 to 1.87) for drinking 0 to 15 years, 1.61 (1.28 to 2.14) for 16 to 30 years, and 1.98 (1.23 to 3.05) for >30 years.  The authors concluded that moderate-to-heavy alcohol consumption increased the risk of CAD in Chinese men.  CAD risk tended to increase with an increase in frequency and duration of drinking.

This was a very select group of patients (those presenting with chest pain or EKG changes), and not typical of the Chinese population.  No information was available on drinking patterns or on previous alcohol intake.  Further, a recent large population-based study from mainland China showed that consumers of alcohol were less likely to develop coronary disease, results similar to those in most Western populations.  It is not possible from the present study to say that the association of alcohol intake with CAD is different between Chinese and Western populations, as the present study gives results only for a very select group of patients.

The most important outcome regarding CAD is the occurrence of clinical events (myocardial infarction, cardiac death, etc.).  The detection of such events requires long-term follow-up studies to be able to judge the overall effects of alcohol drinking on CAD.

For the full critique of this paper by members of the International Scientific Forum on Alcohol Research, please click here.

Critique 025.  Pattern of drinking and type of beverage affect the relation of alcohol intake to coronary heart disease 1 December 2010

Reference: Ruidavets J-B, Ducimetièere P, Evans A, Montaye M, Haas B, Bingham A, Yarnell J, Amouyel P, Arveiler D, Kee F, Bongard V, Ferrières J.  Patterns of alcohol consumption and ischaemic heart disease in culturally divergent countries: the Prospective Epidemiological Study of Myocardial Infarction (PRIME).  BMJ 2010;341:c6077 doi:10.1136/bmj.c6077.

Using cohort data from Belfast and France, investigators related weekly alcohol consumption, incidence of binge drinking (alcohol >50 g on at least one day a week), incidence of regular drinking (at least one day a week, and alcohol <50 g if on only one occasion), volume of alcohol intake, frequency of consumption, and types of beverage consumed to risk of coronary heart disease (CHD) events over a 10 year follow-up period.  Overall, 60.5% of subjects from N. Ireland and 90.6% of French reported drinking alcohol at least once a week.  Among drinkers, 12% of men in Belfast drank alcohol every day compared with 75% of men in France.  Mean alcohol consumption was 22.1 g/ day in Belfast and 32.8 g/day in France.  Binge drinkers comprised 9.4% and 0.5% of the Belfast and France samples, respectively.

Results showed that, after multivariate adjustment, the hazard ratio for hard coronary events compared with regular drinkers was 1.97 (95% CI 1.21 – 3.22) for binge drinkers, 2.03 (95% CI 1.41 – 2.94) for never drinkers, and 1.57 (95% CI 1.11 – 2.21) for former drinkers.  The hazard ratio for hard coronary events in Belfast compared with in France was 1.76 (95% CI 1.37 to 2.67) before adjustment, and 1.09 (95% CI 0.79 to 1.50) after adjustment for alcohol patterns and wine drinking.  Only wine drinking was associated with a lower risk of hard coronary events, irrespective of the country.

The authors conclude that regular and moderate alcohol intake throughout the week, the typical pattern in middle-aged men in France, is associated with a low risk of ischemic heart disease, whereas the binge drinking pattern more prevalent in Belfast confers a higher risk.  While a strong inverse association between moderate alcohol consumption and cardiovascular disease has been demonstrated for decades, more recent research has emphasized the importance of the pattern of drinking (regular moderate versus episodic or binge drinking).  Further, there continues to be debate about the potential greater effect of wine versus other beverages containing alcohol.  This study shows that regular moderate drinking (especially of wine) is associated with lower risk of MI, but episodic or binge drinking (especially of beer or whiskey) increases the risk.  Lifetime abstinence has a similar adverse relation to CHD as does episodic or binge drinking.

For the full critique of this paper by members of the International Scientific Forum on Alcohol Research, please click here.

Critique 010. Should moderate alcohol consumption be advised following a heart attack? 30 June 2010

Reference:  Carter MD, Lee JH, Buchanan DM, Peterson ED, Tang F, Reid KJ, Spertus JA, Valtos J, O’Keefe JH.  Comparison of outcomes among moderate alcohol drinkers before acute myocardial infarction to effect of continued versus discontinuing alcohol intake after the infarct.  Am J Cardiol 2010 (Published early online).

There has been considerable recent interest in the effects of alcohol consumption following an acute myocardial infarction (AMI).  In an observational study among 325 subjects who were moderate drinkers prior to an AMI, 84% continued to drink and 16% quit.  While most of the outcome measures showed no statistically significant effects between the two groups of patients, all outcomes showed a tendency towards better physical and mental health outcomes for persistent drinkers in comparison with those who quit drinking.

A key problem with this analysis, and with all observational epidemiologic studies on this topic, is that the reason that some subjects stopped drinking after having an AMI, while others continued to drink, is not known.  Even though adjustments were made for many known related factors, there is always the possibility that subjects who stopped drinking were “sicker” in many ways than those who persisted in their alcohol consumption.

It may well require a randomized trial, in which some subjects having an AMI are randomly advised to continue to drink and others advised to stop drinking, to be able to determine reliably the effects on the clinical course of the persistence of alcohol intake following an AMI.

For the full critique of this paper by members of the International Scientific Forum on Alcohol Research, please click here.

Critique 006. For patients who already have cardiovascular disease, continued moderate alcohol consumption may reduce their risk of death 2 June 2010

Reference:  Costanzo S, Di Castelnuovo A, Donati MB, Iacoviello L, de Gaetano G.  Contemporary Reviews in Cardiovascular Medicine.   Cardiovascular and overall mortality risk in relation to alcohol consumption in patients with cardiovascular disease.  Circulation 2010;121;1951-1959.

This review paper in Circuation summarizes data from 8 epidemiologic studies of subjects with cardiovascular disease (CVD) as to their subsequent mortality (both CV and total-mortality) according to their alcohol consumption.  Most studies showed significantly lower risk of both CV and total mortality for patients with CVD who were consumers of alcohol.

Despite these clear-cut findings, the authors were very cautious in their conclusions, focusing on the dangers of excessive drinking and not encouraging cardiovascular patients who do not drink to start regular drinking.   They state that moderate consumers of alcohol who have CV disease should not be advised to stop drinking, but should be advised to not consume alcohol more heavily.

It is interesting that these authors published the meta-analysis upon which this review is largely based in the Journal of the American College of Cardiology earlier in 2010.  In that paper, their conclusions were less restrained: “Cardiologists should be aware that regular, moderate alcohol consumption, in the context of a healthy lifestyle (increased physical activity, no smoking), dietary habits (decreased dietary fat intake, high consumption of fruit and vegetables), and adequate drug therapy, would put their patients at a level of cardiovascular or mortality risk substantially lower than either abstainers or heavy or binge drinkers.”

For the full critique of this paper by members of the International Scientific Forum on Alcohol Research, please click here.