Summary of wine and health articles on

A summary of the effect of alcohol and wine on diabetes

There is good clinical data to suggest that moderate consumption of wine can reduce the risk of diabetes. Animal studies are suggestive that the polyphenol in wine, resveratrol, may be helpful in preventing and treating some metabolic diseases, including diabetes.

Salas-Salvadó J review  in 2011 "The role of diet in the prevention of type 2 diabetes" stated that "The conclusion is that there is no universal dietary strategy to prevent diabetes or delay its onset. Together with the maintenance of ideal body weight, the promotion of the so-called prudent diet (characterized by a higher intake of food groups that are generally recommended for health promotion, particularly plant-based foods, and a lower intake of red meat, meat products, sweets, high-fat dairy and refined grains) or a Mediterranean dietary pattern rich in olive oil, fruits and vegetables, including whole grains, pulses and nuts, low-fat dairy, and moderate alcohol consumption (mainly red wine) appears as the best strategy to decrease diabetes risk, especially if dietary recommendations take into account individual preferences, thus enabling long-time adherence."

In the 2011 review by Tomasz Szkudelski and Katarzyna Szkudelska "Anti-diabetic effects of resveratrol" (*Note that resveratrol is present in wine) they stated that "In the last few years, rodent studies and experiments in vitro provided evidence that resveratrol (3,5,4′-trihydroxystilbene)—a naturally occurring phytoalexin present in numerous plant species—exerts beneficial effects in the organism and may be helpful in preventing and treating some metabolic diseases, including diabetes. In general, the management of diabetes involves three main aspects: reduction of blood glucose, preservation of β cells, and, in the case of type 2 diabetes, improvement in insulin action. Data from the literature indicate that the beneficial effects of resveratrol in relation to diabetes comprise all these aspects". 

In a 2014 review by Khemayanto H "Role of Mediterranean diet in prevention and management of type 2 diabetes" where the authors identified 451 articles with the key words: “Mediterranean diet” and “diabetes” up to 14 April 2014 the authors summarised:

"Daily moderate intake of alcohol (usually after a meal) in the form of red wine is one of the characteristic of Mediterranean diet. Moderate alcohol drinking is associated with 30% reduction of the risk of type 2 diabetes in both genders. The strongest inverse association was observed at 22–25 g/day. However, heavy consumption in both men and women (above 50 g/day for women and 60 g/day for men) were no longer provided protective effect but actually increased the risk for diabetes. Moderate alcohol consumption (40 g/day) for 17 days enhanced insulin sensitivity and plasma adiponectin levels, without any changes in the plasma tumor necrosis factor α (TNFα). Adiponectin stimulated glucose utilization and fatty acid oxidation. Adherence to the Mediterranean diet was associated with higher levels of adiponectin because of moderate consumption of red wine, which is inversely related to diabetes."

"Numerous studies on diabetic rats revealed the anti-hyperglycemic action of resveratrol. Among different beneficial effects of resveratrol found in diabetes, the ability of this compound to reduce hyperglycemia seems to be the best documented. The anti-hyperglycemic action of resveratrol was demonstrated in obese rodents and in two animal models of diabetes: in rats with streptozotocin- induced diabetes or with streptozotocin- nicotinamide-induced diabetes. Some studies also revealed that administration of resveratrol to diabetic rats resulted in diminished levels of glycosylated hemoglobin (HbA1C), which reflects the prolonged reduction of glycemia."

"The anti-hyperglycemic effect of resveratrol observed in diabetic animals is thought to result from its stimulatory action on intracellular glucose transport. Increased glucose uptake by different cells isolated from diabetic rats was found in the presence of resveratrol. Interestingly, in experiments on isolated cells, resveratrol was able to stimulate glucose uptake in the absence of insulin. The stimulation of glucose uptake induced by resveratrol seems to be due to increased action of glucose transporter in the plasma membrane. Studies on rats with experimentally induced diabetes demonstrated increased expression of the insulin-dependent glucose transporter, GLUT4, as a result of resveratrol ingestion, compared with diabetic animals not given resveratrol. It should be mentioned, however, that in some experiments on rats with streptozotocin-induced diabetes, resveratrol appeared to be ineffective and failed to decrease blood glucose."

A summary of the evidence of the effects of Alcohol on body weight

Smiling lady with glass of red wine

Does alcohol or wine cause you to put on weight?

Despite the calories in a glass of wine there is substantial clinical evidence that it does not cause the expected weight gain. The reason for this is unclear but animal studies have confirmed the theory that the body may process alcohol in a different way to certain foods meaning that excess calories are not automatically converted to fat. So headlines in the newspapers that a glass of wine contains the same calories as a slice of cake may be true, but the effect on the body is not the same as eating cake. 

The calorie was first defined by Nicolas Clément in 1824 as a unit of heat energy.The word comes from Latin calor meaning "heat" and is the approximate amount of energy needed to raise the temperature of one gram of water by one degree Celsius. Confusingly, the word calorie is very often used for what is actually a kilocalorie of nutritional energy. Sometimes, in an attempt to avoid confusion, it is written Calorie (with a capital "C") in an attempt to make the distinction, although this is not universal, and is not widely understood. So 1 Calorie  ≡ 1 kcal = 1000 cal.

The concept of Calories may be easy for nutritionists to explain to the obese but in the context of alcohol consumption further research is needed to explain the apparent anomalies. For example, sugar laden mixers in cocktails may be far worse for you than the alcohol itself. 

For Calorie and nutritional information by type of wine click below:

In 1991 Lieber CS in "Perspectives: do alcohol calories count?" wrote that "Chronic consumption of substantial amounts of alcohol is not associated with the expected effect on body weight. Isocaloric substitution of carbohydrates by ethanol results in weight loss, and addition of ethanol to an otherwise normal diet does not produce the expected weight gain. This energy deficit cannot be explained by maldigestion or malabsorption but has been attributed to induction of the microsomal ethanol oxidizing system (a metabolic pathway that oxidizes ethanol without associated chemical energy production), increased sympathetic tone and associated thermogenesis, and/or enhanced ATP breakdown (with increased purine catabolism) secondary to the acetate produced from ethanol. All these hypotheses do not fully explain the lack of weight deficit when alcohol is consumed with a very-low-fat diet, which suggests that an alteration in the energy utilization derived from fat plays a major role, possibly through uncoupling of oxidation with phosphorylation in mitochondria damaged by chronic ethanol consumption."

Liu S 1994 "A prospective study of alcohol intake and change in body weight among US adults", reported that "At baseline, women who reported at least one drink per day weighed 2.3 kg less than nondrinkers (95% confidence interval (CI) -0.4 to -4.2). Little relation was observed between body weight and alcohol intake cross-sectionally among men. Prospectively, both men and women drinkers tended to gain less weight than did nondrinkers (p = 0.006 for trend in women, p = 0.11 for trend in men). Drinkers also had more stable weight over the 10-year follow-up period. Drinkers were less likely to have majorweight gain or loss (gaining or losing > or = 10 kg) than were nondrinkers. Compared with nondrinkers, for those who consumed 1-6.9 drinks per week, women had an odds ratio (OR) = 0.7 (95% CI 0.5 to 0.9) for major weight gain and an OR = 0.7 (95% CI 0.5 to 1.1) for major weight loss, while men had an OR = 1.0 (95% CI 0.6 to 1.6) for major weight gain and an OR = 0.7 (95% CI 0.5 to 1.2) for major weight loss. For those who consumed > or = 2 drinks per day, women had an OR = 0.5 (95% CI 0.3 to 1.0) for major weight gain and an OR = 0.8 (95% CI 0.4 to 1.6) for major weight loss, while men had an OR = 0.9 (95% CI 0.5 to 1.6) for major weight gain and an OR = 1.0 (95% CI 0.6 to 1.7) for major weight loss. "

The authors concluded that "These data suggest that alcohol intake does not increase the risk of obesity."

Cordain L 1997, "Influence of moderate daily wine consumption on body weight regulation and metabolism in healthy free-living males" published that "Whether wine was imbibed or not, no significant differences (p > 0.05) were demonstrated for any of the following variables: body weight,body fat percentage, skinfold thickness, resting metabolic rate, respiratory quotient, caloric intake, dietary macronutrient content, or fasting insulin or glucose concentrations."

They concluded that "In free-living subjects over a 6-week period, the addition of two glasses of red wine to the evening meal does not appear to influence any measured variable which may adversely affect body weight or promote the development of obesity during this time period."

Wannamethee SG 2004 "Alcohol intake and 8-year weight gain in women: a prospective study" stated that "In cross-sectional analyses, there was a significant inverse relationship between alcohol and BMI even after adjustment for dietary factors and a wide range of confounders. In multivariate prospective analyses, a nonlinear relationship was seen between alcohol and weight gain (>or=5 kg) in all women. Compared with nondrinkers, the adjusted relative odds [95% confidence interval (CI)] of weight gain according to grams per day were 0.94 (0.89, 0.99) for those consuming 0.1 to 4.9 g/d, 0.92 (0.85,0.99) for 5 to 14.9 g/d, 0.86 (0.76, 0.78) for 15 to 29.9 g/d, and 1.07 (0.89,1.28) for those consuming 30+ g/d (p < 0.0001 for quadratic trend). Women who continued to drink heavily and those who became heavy drinkers showed similar increased odds of weight gain. The increased odds of weight gain associated with heavy drinking (30+ g/d) were most marked in the younger women (<35 years) (odds ratio 1.64; 5% CI 1.03 to 2.61). In African-American women, light drinking was associated with increased odds of weight gain compared with nondrinkers (odds ratio = 2.43; 95% CI 1.22 to 4.82)."

They concluded that "Our data suggest that light to moderate drinking (up to 30 g/d) is not associated with weight gain in women except possibly in African-American women. Heavier drinking may promote weight gain in women."

Tolstrup JS et al 2008  in "Alcohol drinking frequency in relation to subsequent changes in waist circumference" published that "Drinking frequency was inversely associated with changes in waist circumference in women and was unassociated with changes in waist circumference in men. Drinking frequency was unassociated with major waist loss but was inversely associated with major waist gain: odds ratios among men were 0.97 (95% CI: 0.73, 1.28), 0.95 (95% CI: 0.81, 1.12), 0.88 (95% CI: 0.77, 0.99), 0.82 (95% CI: 0.71, -0.95), and 0.79 (95% CI: 0.69, 0.9) for never drinking, drinking on 1, 2-4, 5-6, and 7 d/wk, respectively, compared with men who drank alcohol on <1 d/wk (P for trend < 0.0001). Results for women were similar. Adjustment for the amount of alcohol intake or total energy intake did not affect results considerably."

They concluded that "Drinking pattern may be associated with development of abdominal obesity; in this prospective study, drinking frequency was inversely associated with major waist gain and was unassociated with major waist loss."

In 2010 Wang et al in "Alcohol consumption, weight gain, and risk of becoming overweight in middle-aged and older women" reported that "There was an inverse association between amount of alcohol consumed at baseline and weight gained during 12.9 years of follow-up. A total of 7942 (41.3%) initially normal-weight women became overweight or obese (BMI > or =25) and 732 (3.8%) became obese (BMI > or =30). After adjusting for age, baseline BMI, smoking status, nonalcohol energy intake, physical activity level, and other lifestyle and dietary factors, the relative risks of becoming overweight or obese across total alcohol intake of 0, more than 0 to less than 5, 5 to less than 15, 15 to less than 30, and 30 g/d or more were 1.00, 0.96, 0.86, 0.70, and 0.73, respectively (P( )for trend( )<.001). The corresponding relative risks of becoming obese were 1.00, 0.75, 0.43, 0.39, and 0.29 (P( )for trend( )<.001). The associations were similar by subgroups of age, smoking status, physical activity level, and baseline BMI.

Wang concluded that "Compared with nondrinkers, initially normal-weight women who consumed a light to moderate amount of alcohol gained less weight and had a lower risk of becoming overweight and/or obese during 12.9 years of follow-up."

Alcohol, heart health and risk of dying (mortality) - A summary of clinical evidence

dead body.

The debate about alcohol and health benefits, the J-Shaped Curve and "Sick Quitter" Hypothesis

There has been consistent evidence in large scale clinical trials that moderate consumption of alcoholic drinks reduces the risk of dying prematurely versus being an abstainer - the so called J-shaped curve.

However, some have argued that the benefits are only applicable to a minority e.g. Knot et al 2015, BMJ "Compared with never drinkers, age stratified analyses suggest that beneficial dose-response relations between alcohol consumption and all cause mortality may be largely specific to women drinkers aged 65 years or more, with little to no protection present in other age-sex groups.". 

The paper says "The J-shaped relation is contentious, however, with some arguing that protective effects may be confounded by the common classification of heterogeneous non-drinking groups into a single referent category. Specifically, former drinkers have been found to exhibit poorer self reported health,higher levels of depression,and increased risk of mortality than never drinkers. As such, protective associations identified among light drinkers may be less a consequence of a beneficial biological mechanism and more a statistical artefact resulting from the application of a pooled non-drinking category. Indeed, when former drinkers were excluded from meta-analysis,the protective effect between alcohol consumption and total mortality was attenuated (P<0.01). Such a finding suggests that protective effects may have been over-estimated by existing studies."

Critics of the 2015 study point out that because the authors gathered data which clearly showed health benefits from moderate drinking and then divided it into so many subgroups that it was almost impossible for them to produce statistically significant results. In the end the only people who appeared to benefit from drinking were post-menopausal women.

The proponents of the "sick quitter" hypothesis that state that endorse the idea that teetotallers are more than those who do drink because they are chronically ill or because they are ex-alcohol drinkers and have damaged their bodies with alcohol. They argue that alcohol doesn't protect health its just that teetotallers are unusually sickly.

Rimm EB et al 2007, "Alcohol and Coronary Heart Disease: Drinking Patterns and Mediators of Effect" took on the "sick quitter" hypothesis saying "A recent meta-analysis raised questions about systematic misclassification error in observational studies because of inclusion among “non drinkers” of ex-drinkers and/or occasional drinkers. However, misclassification among a small percentage of non drinkers cannot fully explain the inverse relation, and there is substantial evidence to refute the “sick quitter” hypothesis. Furthermore, it has been shown that moderate alcohol consumption reduces CHD and mortality in individuals with hypertension, diabetes, and existing CHD. To address the issue of residual confounding by healthy lifestyle in drinkers, in a large prospective study we restricted analysis to only “healthy” men (who did not smoke, exercised, ate a good diet, and were not obese). Within this group, men who drank moderately had a relative risk for CHD of 0.38 (95% CI, 0.16–0.89) compared with abstainers, providing further evidence to support the hypothesis that the inverse association of alcohol to CHD is causal, and not confounded by healthy lifestyle behaviors."

There was further controversy when Stockwell et al published a new study in the March 2016 issue of the Journal of Studies on Alcohol and Drugs, "Do "Moderate" Drinkers Have Reduced Mortality Risk? A Systematic Review and Meta-Analysis of Alcohol Consumption and All-Cause Mortality."

The new study was a systematic review and meta-regression analysis of studies investigating alcohol use and mortality risk after controlling for quality-related study characteristics was conducted in a population of 3,998,626 individuals, among whom 367,103 deaths were recorded. A total of 87 studies were examined.

Tim Stockwell, Ph.D., the lead researcher on the analysis and director of the University of Victoria's Centre for Addictions Research in British Columbia, Canada said that "Most often, studies have compared moderate drinkers (people who have up to two drinks per day) with "current" abstainers. The problem is that this abstainer group can include people in poor health who've cut out alcohol. A fundamental question is, who are these moderate drinkers being compared against?"

The paper concluded that when his team corrected for those abstainer "biases" and certain other study-design issues, moderate drinkers no longer showed a longevity advantage. Further, only 13 of the 87 studies avoided biasing the abstainer comparison group--and these showed no health benefits. It stated that "Estimates of mortality risk from alcohol are significantly altered by study design and characteristics. Meta-analyses adjusting for these factors find that low-volume alcohol consumption has no net mortality benefit compared with lifetime abstention or occasional drinking. These findings have implications for public policy, the formulation of low-risk drinking guidelines, and future research on alcohol and health."

Further reading on the J-Curve debate
Eric Crampton "Moderate drinking and health"

Eric Crampton "he J-Curve: science vs politics"

Christopher Snowdon "Teetotallers die younger, don't let 'em fool you"

Key studies Alcohol,cardiovascular protection and mortality

Meta Analysis and summary studies

Rimm EB 1996, "Review of moderate alcohol consumption and reduced risk of coronary heart disease: is the effect due to beer, wine, or spirits" reporting "Most ecological studies suggested that wine was more effective in reducing risk of mortality from heart disease than beer or spirits. Taken together, the three case-control studies did not suggest that one type of drink was more cardioprotective than the others. Of the 10 prospective cohort studies, four found a significant inverse association between risk of heart disease and moderate wine drinking, four found an association for beer, and four for spirits.

Rimm concluded "Results from observational studies, where alcohol consumption can be linked directly to an individual's risk of coronary heart disease, provide strong evidence that all alcoholic drinks are linked with lower risk. Thus, a substantial portion of the benefit is from alcohol rather than other components of each type of drink."

Rimm EB et al 1999 in "Moderate alcohol intake and lower risk of coronary heart disease: meta-analysis of effects on lipids and haemostatic factors" reported that "61 data records were abstracted from 42 eligible studies with information on change in biological markers of risk of coronary heart disease. An experimental dose of 30 g of ethanol a day increased concentrations of high density lipoprotein cholesterol by 3.99 mg/dl (95% confidence interval 3.25 to 4.73), apolipoprotein A I by 8.82 mg/dl (7.79 to 9.86), and triglyceride by 5.69 mg/dl (2.49 to 8.89). Several haemostatic factors related to a thrombolytic profile were modestly affected by alcohol. On the basis of published associations between these biomarkers and risk of coronary heart disease 30 g of alcohol a day would cause an estimated reduction of 24.7% in risk of coronary heart disease." and they concluded that "Alcohol intake is causally related to lower risk of coronary heart disease through changes in lipids and haemostatic factors"

Iestra JA 2005 in "Effect size estimates of lifestyle and dietary changes on all-cause mortality in coronary artery disease patients: a systematic review" presented " A literature search was performed on the effect of lifestyle and dietary changes on mortality in CAD patients. Prospective cohort studies and randomized controlled trials of patients with established CAD were included if they reported all-causes mortality and had at least 6 months of follow-up. The effect estimates of smoking cessation (relative risk [RR], 0.64; 95% CI, 0.58 to 0.71), increased physical activity (RR, 0.76; 95% CI, 0.59 to 0.98), and moderate alcohol use (RR, 0.80; 95% CI, 0.78 to 0.83) were studied most extensively. For the 6 dietary goals, data were too limited to provide reliable effect size estimates. Combinations of dietary changes were associated with reduced mortality (RR, 0.56; 95% CI, 0.42 to 0.74)."

Di Castelnuovo et al 2006 "Alcohol dosing and total mortality in men and women: an updated meta-analysis of 34 prospective studies" used a meta analysis technique where the results of 34 studies were collated and reviewed. The study looked at the link between alcohol dose and mortality in both sexes in clinical trials conducted before the end of 2005 with over 1 million subjects. The scale of the overall analysis is therefore impressive.

The study reported that "A J-shaped relationship between alcohol and total mortality was confirmed in both men and women. Consumption of alcohol, up to 4 drinks per day in men and 2 drinks per day in women, was inversely associated with total mortality or the chance of dying, maximum protection being 18% in women and 17% in men Higher doses of alcohol were associated with increased chances of dying with women having a lower level than men before the chances of dying increased. ".

Concluding that "Low levels of alcohol intake (1-2 drinks per day for women and 2-4 drinks per day for men) are inversely associated with total mortality in both men and women. Our findings, while confirming the hazards of excess drinking, indicate potential windows of alcohol intake that may confer a net beneficial effect of moderate drinking, at least in terms of survival."

Patra J et al 2010 "Alcohol consumption and the risk of morbidity and mortality for different stroke types--a systematic review and meta-analysis" reported "The dose-response relationship for hemorrhagic stroke had monotonically increasing risk for increasing consumption, whereas ischemic stroke showed a curvilinear relationship, with a protective effect of alcohol for low to moderate consumption, and increased risk for higher exposure. For more than 3 drinks on average/day, in general women had higher risks than men, and the risks for mortality were higher compared to the risks for morbidity." and concluded that "These results indicate that heavy alcohol consumption increases the relative risk of any stroke while light or moderate alcohol consumption may be protective against ischemic stroke. Preventive measures that should be initiated are discussed."

Ronksley PE  2011 "Association of alcohol consumption with selected cardiovascular disease outcomes: a systematic review and meta-analysis" reported "The pooled adjusted relative risks for alcohol drinkers relative to non-drinkers in random effects models for the outcomes of interest were 0.75 (95% confidence interval 0.70 to 0.80) for cardiovascular disease mortality (21 studies), 0.71 (0.66 to 0.77) for incident coronary heart disease (29 studies), 0.75 (0.68 to 0.81) for coronary heart disease mortality (31 studies), 0.98 (0.91 to 1.06) for incident stroke (17 studies), and 1.06 (0.91 to 1.23) for stroke mortality (10 studies). Dose-response analysis revealed that the lowest risk of coronary heart disease mortality occurred with 1-2 drinks a day, but for stroke mortality it occurred with ≤1 drink per day. Secondary analysis of mortality from all causes showed lower risk for drinkers compared with non-drinkers (relative risk 0.87 (0.83 to 0.92))."

They concluded  "Light to moderate alcohol consumption is associated with a reduced risk of multiple cardiovascular outcomes."

Costanzo S 2011 "Wine, beer or spirit drinking in relation to fatal and non-fatal cardiovascular events: a meta-analysis" reported "previous studies evaluating whether different alcoholic beverages would protect against cardiovascular disease, a J-shaped relationship for increasing wine consumption and vascular risk was found; however a similar association for beer or spirits could not be established. An updated meta-analysis on the relationship between wine, beer or spirit consumption and vascular events was performed. Articles were retrieved through March2011 by PubMed and EMBASE search and a weighed least-squares regression analysis pooled data derived from studies that gave quantitative estimation of the vascular risk associated with the alcoholic beverages. From 16 studies, evidence confirms a J-shaped relationship between wineintake and vascular risk. A significant maximal protection-average 31% (95% confidence interval (CI): 19-42%) was observed at 21 g/day of alcohol. Similarly, from 13 studies a J-shaped relationship was apparent for beer (maximal protection: 42% (95% CI: 19-58%) at 43 g/day of alcohol). From 12 studies reporting separate data on wine or beer consumption, two closely overlapping dose-response curves were obtained (maximal protection of 33% at 25 g/day of alcohol). This meta-analysis confirms the J-shaped association between wine consumption and vascular risk and provides, for the first time, evidence for a similar relationship between beer and vascular risk. In the meta-analysis of 10 studies on spirit consumption and vascular risk, no J-shaped relationship could be found."

Krenz et al in the 2012 review, "Moderate ethanol ingestion and cardiovascular protection: From epidemiologic associations to cellular mechanisms" said the following:

"Abundant epidemiologic evidence and the results interventional mechanistic studies conducted in animal models and cell culture systems strongly support the notion that antecedent ethanol exposure at moderate levels confers protective cardiovascular effects."

"Given the well-established pathologic effects of heavy drinking, wine lovers world-wide no doubt rejoiced when large-scale epidemiological studies first emerged showing that regular consumption of light to moderate amounts of alcoholic beverages, in particular red wine, was associated with a cardio-protective effect. One of the first studies showing a significant negative association between alcohol consumption and the risk of a subsequent first myocardial infarction that was well-controlled for cigarette smoking and other risk factors was published in 1974 . Over the following 4 decades, numerous epidemiological studies including several meta-analyses have consistently reported that an average alcohol consumption in the range of 0.5 to 2 standard drinks per day reduces coronary heart disease-related risks and ischemic stroke compared to non-drinkers."

"Interestingly, initial work suggested that the protective effects associated with light to moderate intake of alcoholic beverages may be due to the polyphenols in grapes, wine, and dark beer. In particular, the stilbene resveratrol has been a major focus of research interest because this and other red wine constituent polyphenols exert powerful antioxidant actions, upregulate eNOS gene expression, enhance NO production and have been found to reduce morbidity and mortality due to cardiovascular disease. In the human diet, red wine is one of the richest sources of polyphenols and moderate red wine drinkers consume these compounds at levels well above the population average. Despite the demonstrated protective actions of resveratrol and flavonoids, discrimination between the effects of these red wine constituent polyphenols versus ethanol per se to induce protection associated with consumption of alcoholic beverages is controversial, in part owing to low levels of the former achieved in the blood following red wine ingestion. Indeed, flavonoids and other wine polyphenols are extensively metabolized during absorption, resulting in formation of glucuronidated, sulfated, and methylated derivatives of the parent polyphenol, which have not been extensively evaluated for their protective effects. As a consequence, the highest plasma concentrations achieved after ingestion of resveratrol-rich beverages by humans range between 1 and 10 μM. These concentrations are lower than those typically evaluated in cell culture models and in animal studies. To further complicate the distinction between ethanol- and resveratrol-specific effects, the downstream molecular mechanisms so far identified for the two compounds show substantial overlap."

"Some epidemiological studies have shown that consumption of red wine is more protective than other types of alcohol, whereas other studies failed to identify an additional advantage associated with red wine."

"The health effects of ethanol are dependent on the amount of alcohol consumed and the pattern of intake. Nearly all epidemiologic studies report a J-shaped curve, whereby light to moderate ethanol consumption (1-2 standard drinks per day) exhibit less risk for adverse cardiovascular events and overall mortality than abstainers, while heavy drinkers (3-4 or more drinks per day) demonstrate increased risk. As with liver injury induced by ethanol, this varies by sex, with women benefiting from 1 standard drink per day, whereas daily consumption of 1-2 drinks by males was associated with reduced total mortality. On the other hand, increased mortality occurs in females with daily intake of 2 or more alcohol beverages and in men consuming more than 3 drinks per day."

"The effects of light to moderate ethanol consumption appear to be most clearly related to cardiovascular benefits, with most studies reductions in risk for heart disease by 30-35% Regular alcohol consumption at low to moderate levels is associated with significant reductions in the incidence of myocardial infarction in both males and females, regardless of age in adults. Importantly, this effect was noted in higher risk populations, including individuals with diabetes, hypertension, hypercholesterolemia, known heart disease, or who are overweight, as well as in cigarette smokers."

"Cardiovascular disease risk is also lowered by moderate ethanol consumption in individuals adhering to healthy lifestyle behaviors. Indeed, it has been reported that men who exercised regularly for at least 30 min/day, abstained from smoking, adhered to a healthy diet, and maintained their body mass index at less than 25 kg/m2 derived a health benefit from regular alcohol intake at moderate levels, demonstrating a 40-50% reduction in risk for myocardial infarction. Moderate wine drinking also appears to strengthen the cardioprotective effects of fish consumption, an observation that links two important components of the Mediterranean diet, namely omega-3 fatty acids and wine."

In addition to reducing the incidence and severity of myocardial infarction, low to moderate alcohol consumption is also associated with lower risk for ischemic stroke, dementia, congestive heart failure, peripheral artery disease, intestinal and hepatic I/R injury, and frequency of Raynaud’s phenomenon."

"Although the concept that moderate intake of ethanol exerts protective effects in the cardiovascular system is now well accepted, important issues have been raised which challenge this premise. For example, it has been argued that uncontrolled confounding influences by lifestyle factors may play a role in the association between moderate alcohol intake and cardiovascular risk. Some work has led to the suggestion that individuals who regularly consume alcohol beverages exhibit healthier habits with regard to diet and/or exercise and enjoy superior sociodemographic factors, which could explain the reduced risk for ischemic myocardial disease . However, systematic review and meta-analysis of interventional studies directed at the association between alcohol consumption and disease markers associated with risk for cardiovascular disease in adults without known cardiovascular disease argues against this supposition, as do the results of studies designed to better control for confounding sociodemographic factors and differences in dietary patterns and exercise adherence.

"While the association between alcohol consumption and decreased cardiovascular risk is clear, it remains uncertain as to whether these correlative findings imply causation. However, a number of points regarding the aforementioned epidemiologic findings suggest that the association may indeed represent a cause-and-effect relationship. First, there is a temporal relation between alcohol use and prevention of cardiovascular disease. Second, greater protection is observed with increasing ethanol dose over the protective range of alcohol intake. Third, the protective association between ethanol consumption and adverse cardiovascular events has been consistently observed in diverse patient populations and in both men and women. Fourth, the reduction in risk remains significant even after the influences of potential confounders such as cigarette smoking, diet, and exercise are factored into the analysis. Fifth, the association is specific for lowering rates of cardiovascular disease but does correlate with protection in other conditions such as cancer. Finally, the coupling of the aforementioned epidemiologic associations with the interventional mechanistic studies discussed below, provides compelling support for the notion that ethanol intake may indeed confer protection against the deleterious effects of I/R."

Chiva-Blanch G 2013 "Effects of wine, alcohol and polyphenols on cardiovascular disease risk factors: evidences from human studies" stated "Heavy or binge alcohol consumption unquestionably leads to increased morbidity and mortality. Nevertheless, moderate alcohol consumption, especially alcoholic beverages rich in polyphenols, such as wine and beer, seems to confer cardiovascular protective effects in patients with documented CVD and even in healthy subjects." and " In conclusion, wine and beer (but especially red wine) seem to confer greater cardiovascular protection than spirits because of their polyphenolic content. However, caution should be taken when making recommendations related to alcohol consumption."

Knot et al 2015, "All cause mortality and the case for age specific alcohol consumption guidelines: pooled analyses of up to 10 population based cohorts" reported that "In unadjusted models, protective effects were identified across a broad range of alcohol usage in all age-sex groups. These effects were attenuated across most use categories on adjustment for a range of personal, socioeconomic, and lifestyle factors. After the exclusion of former drinkers, these effects were further attenuated. Compared with self reported never drinkers, significant protective associations were limited to younger men (50-64 years) and older women (≥65 years). Among younger men, the range of protective effects was minimal, with a significant reduction in hazards present only among those who reported consuming 15.1-20.0 units/average week (hazard ratio 0.49, 95% confidence interval 0.26 to 0.91) or 0.1-1.5 units on the heaviest day (0.43, 0.21 to 0.87). The range of protective effects was broader but lower among older women, with significant reductions in hazards present ≤10.0 units/average week and across all levels of heaviest day use. Supplementary analyses found that most protective effects disappeared where calculated in comparison with various definitions of occasional drinkers."

The authors concluded that "Beneficial associations between low intensity alcohol consumption and all cause mortality may in part be attributable to inappropriate selection of a referent group and weak adjustment for confounders. Compared with never drinkers, age stratified analyses suggest that beneficial dose-response relations between alcohol consumption and all cause mortality may be largely specific to women drinkers aged 65 years or more, with little to no protection present in other age-sex groups. These protective associations may, however, be explained by the effect of selection biases across age-sex strata."

 Stockwell et al published a new study in the March 2016 issue of the Journal of Studies on Alcohol and Drugs, "Do "Moderate" Drinkers Have Reduced Mortality Risk? A Systematic Review and Meta-Analysis of Alcohol Consumption and All-Cause Mortality."

The new study was a systematic review and meta-regression analysis of studies investigating alcohol use and mortality risk after controlling for quality-related study characteristics was conducted in a population of 3,998,626 individuals, among whom 367,103 deaths were recorded. A total of 87 studies were examined.

They reported that  "Without adjustment, meta-analysis of all 87 included studies replicated the classic J-shaped curve, with low-volume drinkers (1.3-24.9 gethanol per day) having reduced mortality risk (RR = 0.86, 95% CI [0.83, 0.90]). Occasional drinkers (<1.3 g per day) had similar mortality risk (RR = 0.84, 95% CI [0.79, 0.89]), and former drinkers had elevated risk (RR = 1.22, 95% CI [1.14, 1.31]). After adjustment for abstainer biases and quality-related study characteristics, no significant reduction in mortality risk was observed for low-volume drinkers (RR = 0.97, 95% CI [0.88, 1.07]). Analyses of higher-quality bias-free studies also failed to find reduced mortality risk for low-volume alcohol drinkers. Risk estimates for occasional drinkers were similar to those for low- and medium-volume drinkers."

Stockwell concluded that "Estimates of mortality risk from alcohol are significantly altered by study design and characteristics. Meta-analyses adjusting for these factors find that low-volume alcohol consumption has no net mortality benefit compared with lifetime abstention or occasional drinking. These findings have implications for public policy, the formulation of low-risk drinking guidelines, and future research on alcohol and health."

Individual studies

Klatsky AL in 1992 "Alcohol and mortality" reported that "Heavier drinkers were at greater risk for death from noncardiovascular causes (relative risk at ≥ 6 drinks per day compared with no alcohol = 1.6, 95% Cl, 1.3 to 2.0) especially cirrhosis, unnatural death, and tobacco-related cancers. This alcohol-associated risk was higher in women (relative risk for death from all causes at ≥ 6 drinks per day = 2.2; Cl, 1.4 to 3.8) and younger persons (for persons < 50 years of age, relative risk for death from all causes at ≥ 6 drinks per day = 1.9; Cl, 1.3 to 2.9). Lighter drinkers were at lower risk for death from cardiovascular disease, especially coronary heart disease (relative risk at 1 to 2 drinks per day = 0.7; Cl, 0.6 to 0.9), independent of baseline risk, with the greatest reduction of risk in older persons. Lighter drinkers over 60 years of age also had a slightly lower risk for noncardiovascular death, but this finding was not independent of baseline coronary heart disease risk.

He concluded that  "Women and younger persons appear more susceptible to the increased mortality risk of heavy drinking. The reduced cardiovascular risk of lighter drinkers is more pronounced in older persons. Lower coronary disease prevalence may reduce the noncardiovascular mortality risk of lighter drinkers."

Doll R et al 1994, "Mortality in relation to consumption of alcohol: 13 years' observations on male British doctors" reported that "Men were divided on the basis of their response to the 1978 questionnaire into two groups according to whether or not they had ever had any type of vascular disease, diabetes, or "life threatening disease" and into seven groups according to the amount of alcohol they drank. By 1991 almost a third had died. All statistical analyses of mortality were standardised for age, calendar year, and smoking habit. There was a U shaped relation between all cause mortality and the average amount of alcohol reportedly drunk; those who reported drinking 8-14 units of alcohol a week (corresponding to an average of one to two units a day) had the lowest risks. The causes of death were grouped into three main categories: "alcohol augmented" causes (6% of all deaths: cirrhosis, liver cancer, upper aerodigestive (mouth, oesophagus, larynx, and pharynx) cancer, alcoholism, poisoning, or injury), ischaemic heart disease (33% of all deaths), and other causes. The few deaths from alcohol augmented causes showed, at least among regular drinkers, a progressive trend, with the risk increasing with dose. In contrast, the many deaths from ischaemic heart disease showed no significant trend among regular drinkers, but there were significantly lower rates in regular drinkers than in non-drinkers. The aggregate of all other causes showed a U shaped dose-response relation similar to that for all cause mortality. Similar differences persisted irrespective of a history of previous disease, age (under 75 or 75 and older), and period of follow up (first five and last eight years). Some, but apparently not much, of the excess mortality in non-drinkers could be attributed to the inclusion among them of a small proportion of former drinkers.

Doll concluded that "The consumption of alcohol appeared to reduce the risk of ischaemic heart disease, largely irrespective of amount. Among regular drinkers mortality from all causes combined increased progressively with amount drunk above 21 units a week. Among British men in middle or older age the consumption of an average of one or two units of alcohol a day is associated with significantly lower all cause mortality than is the consumption of no alcohol, or the consumption of substantial amounts. Above about three units (two American units) of alcohol a day, progressively greater levels of consumption are associated with progressively higher all cause mortality."

Grønbaek M et al 2005, "Mortality associated with moderate intakes of wine, beer, or spirits." reported that "The risk of dying steadily decreased with an increasing intake of wine--from a relative risk of 1.00 for the subjects who never drank wine to 0.51 (95% confidence interval 0.32 to 0.81) for those who drank three to five glasses a day. Intake of neither beer nor spirits, however, was associated with reduced risk. For spirits intake the relative risk of dying increased from 1.00 for those who never drank to 1.34 (1.05 to 1.71) for those with an intake of three to five drinks a day. The effects of the three types of alcoholic drinks seemed to be independent of each other, and no significant interactions existed with sex, age, education, income, smoking, or body mass index. Wine drinking showed the same relation to risk of death from cardiovascular and cerebrovascular disease as to risk of death from all causes. "

They concluded that "Low to moderate intake of wine is associated with lower mortality from cardiovascular and cerebrovascular disease and other causes. Similar intake of spirits implied an increased risk, while beer drinking did not affect mortality."

Thun et al 1997 "Alcohol consumption and mortality among middle-aged and elderly U.S. adults" reported "Causes of death associated with drinking were cirrhosis and alcoholism; cancers of the mouth, esophagus, pharynx, larynx, and liver combined; breast cancer in women; and injuries and other external causes in men. The mortality from breast cancer was 30 percent higher among women reporting at least one drink daily than among nondrinkers (relative risk, 1.3; 95 percent confidence interval, 1.1 to 1.6). The rates of death from all cardiovascular diseases were 30 to 40 percent lower among men (relative risk, 0.7; 95 percent confidence interval, 0.7 to 0.8) and women (relative risk, 0.6; 95 percent confidence interval, 0.6 to 0.7) reporting at least one drink daily than among nondrinkers, with little relation to the level of consumption. The overall death rates were lowest among men and women reporting about one drink daily. Mortality from all causes increased with heavier drinking, particularly among adults under age 60 with lower risk of cardiovascular disease. Alcohol consumption was associated with a small reduction in the overall risk of death in middle age (ages 35 to 69), whereas smoking approximately doubled this risk."

Thun concluded "In this middle-aged and elderly population, moderate alcohol consumption slightly reduced overall mortality. The benefit depended in part on age and background cardiovascular risk and was far smaller than the large increase in risk produced by tobacco."

Leong et al in 2014 "Patterns of Alcohol Consumption and Myocardial Infarction Risk: Observations from 52 Countries in the INTERHEART Case-Control Study" reported " We included 12,195 cases of first MI and 15,583 age- and sex-matched controls from 52 countries. Current alcohol use was associated with a reduced risk of MI (compared to non-users, adjusted odds ratio 0.87; 95% CI 0.80-0.94, p=0.001), however the strength of this assocation was not uniform across different regions (region-alcohol interaction p<0.001). Heavy episodic drinking (≥6 drinks) within the preceding 24 hours was associated with an increased risk of MI (odds ratio 1.4; 95% CI 1.1-1.9, p=0.01). This risk was particularly elevated in older individuals (for age >65 years, odds ratio 5.3; 95% CI 1.6-18, p=0.008).".

They concluded that "In most participants, low levels of alcohol use are associated with a moderate reduction in the risk of MI, however the strength of this association may not be uniform across different countries. An episode of heavy drinking is associated with an increased risk of acute MI in the subsequent 24 hours, particularly in older individuals."

Gaziano JM et al 2000 "Light-to-moderate alcohol consumption and mortality in the physicians’ health study enrollment cohort" reported that "There were 3,216 deaths over 5.5 years of follow-up. We observed a U-shaped relationship between alcohol consumption and total mortality. Compared with rarely/never drinkers, consumers of 1, 2 to 4 and 5 to 6 drinks per week and 1 drink per day had significant reductions in risk of death (multivariate relative risks [RRs] of 0.74, 0.77, 0.78 and 0.82, respectively) with no overall benefit or harm detected at the ≥2 drinks per day level (RR = 0.95; 95% confidence interval (CI), 0.79 to 1.14). The relationship with CVD mortality was inverse or L-shaped with apparent risk reductions even in the highest category of ≥2 drinks per day (RR = 0.76; 95% CI, 0.57 to 1.01). We found no clear harm or benefit for total or common site-specific cancers. For remaining other cancers, there was a non-significant 28% increased risk for those consuming ≥2 drinks per day."

The study concluded "These data support a U-shaped relation between alcohol and total mortality among light-to-moderate drinking men. The U-shaped curve may reflect an inverse association for CVD mortality, no association for common site-specific cancers and a possible positive association for less common cancers."

Grønbaek M 2000 "Type of alcohol consumed and mortality from all causes, coronary heart disease, and cancer" stated that "During 257 859 person-years of follow-up, 4833 participants died. J-shaped relations were found between total alcohol intake and mortality at various levels of wine intake. Compared with nondrinkers, light drinkers who avoided wine had a relative risk for death from all causes of 0.90 (95% CI, 0.82 to 0.99) and those who drank wine had a relative risk of 0.66 (CI, 0. 55 to 0.77). Heavy drinkers who avoided wine were at higher risk for death from all causes than were heavy drinkers who included wine in their alcohol intake. Wine drinkers had significantly lower mortality from both coronary heart disease and cancer than did non-wine drinkers (P = 0.007 and P = 0.004, respectively)."

The authors concluded "Wine intake may have a beneficial effect on all-cause mortality that is additive to that of alcohol. This effect may be attributable to a reduction in death from both coronary heart disease and cancer."

In 2004, Britton, "Different measures of alcohol consumption and risk of coronary heart disease and all-cause mortality: 11-year follow-up of the Whitehall II Cohort Study" reported "A U-shaped relationship was found between volume of alcohol consumed per week and outcome. Compared to those who drank moderately (10-80 g alcohol per week), non-drinkers and those drinking more than 248 g per week had approximately a twofold increased risk of mortality. The optimal frequency of drinking was between once or twice a week and daily, after adjustment for average volume consumed per week. Those drinking twice a day or more had an increased risk of mortality (male hazard ratio 2.44 95% CI 1.31-4.52) compared to those drinking once or twice a week. Drinking only once a month or only on special occasions had a 50% increased risk of mortality. The usual amount consumed per drinking session was not indicative of increased health risk in this cohort."

They concluded that "Epidemiological studies should collect information on frequency of drinking in addition to average volume consumed in order to inform sensible drinking advice."

Buelens JW 2007 "Alcohol consumption and risk for coronary heart disease among men with hypertension" reported that "During follow-up, 653 patients with MI were documented. Compared with patients abstaining from alcohol, the haz-
ard ratio for participants with MI consuming 0.1 to 4.9 grams of alcohol per day was 1.09 (95% CI, 0.86 to 1.37); consuming 5 to 9.9 grams of alcohol per day was 0.81 (CI, 0.60 to 1.08 g/d); consuming 10 to 14.9 grams of alcohol per day was 0.68 (CI, 0.51 to 0.91 g/d); consuming 15 to 29.9 grams of alcohol per day was 0.72 (CI, 0.54 to 0.97 g/d); consuming 30 to 49.9 grams of alcohol per day was 0.67 (CI, 0.48 to 0.94 g/d); and consuming 50 ormore grams of alcohol per day was 0.41 (CI, 0.22 to 0.77 g/d) (P0.001 for trend). Associations were similar for fatal and non-fatal MI. Alcohol consumption was not associated with total death or death due to CVD. Risks for total and ischemic stroke for patients consuming 10 to 29.9 g of alcohol per day were 1.40 (CI,0.93 to 2.12) and 1.55 (CI, 0.90 to 2.68) compared with that of
abstainers. When corrected for measurement error in alcohol consumption, dietary variables, and body mass index, the hazard ratio for participants with MI per 12.5 grams per day increment of alcohol intake was 0.68 (CI, 0.46 to 1.00).

They concluded that "In this population of men with hypertension, moderate alcohol consumption was associated with a decreased risk for MI but not with risks for total death or death due to CVD. As in the general population, men with hypertension who drink moderately and safely may not need to change their drinking habits."

Holahan CJ et al 2012, "Wine Consumption and 20-Year Mortality Among Late-Life Moderate Drinkers" reported "After adjusting for all covariates, both high-wine-consumption and low-wine-consumption moderate drinkers showed reduced mortality risks compared with abstainers. Further, compared with moderate drinkers for whom a high proportion of ethanol came from wine, those for whom a low proportion of ethanol came from wine were older, were more likely to be male, reported more health problems, were more likely to be tobacco smokers, scored lower on socioeconomic status, and (statistical trend) reported engaging in less physical activity. Controlling only for overall ethanol consumption, compared with moderate drinkers for whom a high proportion of ethanol came from wine, those for whom a low proportion of ethanol came from wine showed a substantially increased 20-year mortality risk of 85%. However, after controlling for all covariates, the initial mortality difference associated with wine consumption was no longer significant."

Holahan concluded "Among older adults who are moderate drinkers, the apparent unique effects of wine on longevity may be explained by confounding factors correlated with wine consumption."

Alcohol and Cancer - A summary of the clinical evidence

healthy living

Risk explained

Relative risk

Relative risk is the number that tells you how much changing something can change your risk compared to your risk of not doing anything at all. It is expressed as a percentage decrease or increase. If something you do or take doesn't change your risk, then the relative risk reduction is 0% (no difference). If something you do or take lowers your risk by 50% compared to someone who doesn't do the same, then that action reduces your relative risk by 50%. If something you do doubles your risk, then your relative risk increases 200%.

Absolute risk 

Absolute risk is the size of your own risk. Absolute risk reduction is the number of percentage points your own risk goes down if you do something protective, such as losing weight. The size of your absolute risk reduction depends on what your risk is to begin with.

Hazard Ratios

A hazard ratio considers your absolute risk to be 1. If something you do or take doesn't change your risk, then the hazard ratio is 1. If something you do or take lowers your risk by 25% compared to someone who doesn’t take the same step, then that action makes your hazard ratio 0.75, which means that the risk is 75% of what it was without taking the step (so your risk is 25% lower). If something you do doubles your risk, then your hazard ratio is 2.0.

Intrinsic and Extrinsic risk of developing cancer

A study published in Nature January 2016, "Substantial contribution of extrinsic risk factors to cancer development" by Song Wu et al appeared to confirmed that many cancers are caused by so called extrinsic or environmental factors. 

External factors like smoking, diet, sun, HPV (Human Papilloma Virus) and exposure to toxic chemicals cause more cancer than intrinsic factors like random cell mutations. Intrinsic factors accounted for just 10% to 30% of people’s lifetime risk of getting cancer, whilst extrinsic risks accounted for 70% to 90% for most common cancer types. 

The results are at odds with the results of a study in January 2015 published in Science which found that cell division and random mutations in DNA play the major role in the development of cancer.  "Variation in cancer risk among tissues can be explained by the number of stem cell divisions", Cristian Tomasetti. They concluded that "Why do some tissues give rise to cancer in humans a million times more frequently than others? Tomasetti and Vogelstein conclude that these differences can be explained by the number of stem cell divisions. By plotting the lifetime incidence of various cancers against the estimated number of normal stem cell divisions in the corresponding tissues over a lifetime, they found a strong correlation extending over five orders of magnitude. This suggests that random errors occurring during DNA replication in normal stem cells are a major contributing factor in cancer development. Remarkably, this “bad luck” component explains a far greater number of cancers than do hereditary and environmental factors."

So in summary, the situation is very confused!

Summary of evidence reviewing Cancer and Alcoholic drinks

Food, nutrition, physical activity and the prevention of cancer WCRF/AICR

In 2007 the World Cancer Research Fund (WCRF) and the American Institute for Cancer Research (AICR) published the results of an analysis of the effects of food, nutrition and physical activity based on a pooling of many hundreds of clinical trials.  The study was called "Food, Nutrition, Physical Activity, and the Prevention of Cancer: a Global Perspective. This has been described as the most comprehensive report ever produced on the links between lifestyle and cancer risk and is the most notable source of information on the link between alcohol and cancer. The WCRF/AICR analysis is ongoing and the next report is due 2017.

In 2015 Klatsky AL et al published "Alcohol Intake, Beverage Choice, and Cancer: A Cohort Study in a Large Kaiser Permanente Population" and reported that "With lifelong abstainers as referent, heavy drinking (≥ 3 drinks per day) was associated with increased risk of 5 cancer types: upper airway/digestive tract, lung, female breast, colorectal, and melanoma, with light-to-moderate drinking related to all but lung cancer. No significantly increased risk was seen for 12 other cancer sites: stomach, pancreas, liver, brain, thyroid, kidney, bladder, prostate, ovary, uterine body, cervix, and hematologic system. For all cancers combined there was a progressive relationship with all levels of alcohol drinking. These associations were largely independent of smoking, but among light-to-moderate drinkers there was evidence of confounding by inferred underreporting. Beverage choice played no major independent role."

Klatsky concluded "Heavy alcohol drinking is related to increased risk of some cancer types but not others. Because of probable confounding, the role of light-to-moderate drinking remains unclear."

Bowel cancer - increased risk at greater than 30g of alcohol per day but a mixed picture

The WCRF report states that "The evidence that consumption of alcohol of more than 30g/day of ethanol from alcoholic drinks is a cause of colorectal cancer in men is convincing, and probably also in women."

Cho et al in 2004 in their paper "Alcohol intake and colorectal cancer: a pooled analysis of 8 cohort studies" saw that "In categorical analyses, increased risk for colorectal cancer was limited to persons with an alcohol intake of 30 g/d or greater (approximately > or =2 drinks/d), a consumption level reported by 4% of women and 13% of men. "

In 2007, Ferrari et al reported on the link between rectal and colon cancers in Europe concluding that "In this large European cohort, both lifetime and baseline alcohol consumption increase colon and rectum cancer risk, with more apparent risk increases for alcohol intakes greater than 30 g/day."

The 2009 Park JY et al with participants from Norfolk concluded that "Total alcohol consumption was not associated with CRC risk before or after adjustment for age, sex, weight, height, and smoking status . No significant associations were observed between consumption of specific alcoholic beverages (beer, sherry, or spirits) and CRC risk when compared with non-drinkers after adjustment for lifestyle and dietary factors. Daily consumption of > or =1 unit of wine appeared inversely related to CRC risk (HR: 0.61, 95% CI: 0.40-0.94). No evidence was found for sex-specific relationships, and further exclusion of cases incident within 3 years of baseline did not change the associations observed. In this population-based UK cohort, we did not find any significant adverse effect of alcohol over the moderate range of intake on colorectal cancer risk.". So a 40% lower risk with daily consumption of wine!

In the 2010 UK study by Park et al, which looked at alcohol intake and risk of colorectal cancer (CRC) concluded that "No clear associations were observed between site-specific CRC risk and alcohol intake in either sex. " (up to 30g/day).

Hjartaker et al in 2013 looked at "subsite specific dietary risk factors for Colorectal cancer: A review of cohort studies" . The paper stated that "Ten articles were included in the review. Three analyses for both sexes combined consistently showed a higher risk of rectal cancer with increasing alcohol consumption and no significant associations for any of the colon subsites . In the EPIC studyan increased risk was reported both for rectal and distal colon cancer, whereas in the UK dietary cohort consortium (part of which is included in the EPIC study) a significantly increased risk was found for distal colon cancer only."

Breast cancer - contradictory in part but appears to be evidence that alcohol increases relative risk at levels over 30g of alcohol per day

The WCRF report confirms high heterogenicity (inconsistent findings) between studies, "Twelve cohort studies investigated ethanol intake and all-age breast cancer.Eight cohort studies showed increased risk for the highest intake group when compared to the lowest which was statistically significant in six.Four studies showed decreased risk which was statistically significant in one. Meta-analysis was possible on nine cohort studies, giving a summary effect estimate of 1.10 (95% CI 1.06–1.14) per 10 g/day, with high heterogeneity. Heterogeneity could be partly explained by differential adjustment for age and reproductive history."

Kuper et al in 2000 "Alcohol and breast cancer risk: the alcoholism paradox" reported that "A population-based cohort study of 36 856 women diagnosed with alcoholism in Sweden between 1965 and 1995 found that alcoholic women had only a small 15% increase in breast-cancer incidence compared to the general female population. It is therefore apparent, contrary to expectation, that alcoholism does not increase breast-cancer risk in proportion to presumed ethanol intake."

In 2006 Terry et al reported on lifetime alcohol intake and breast cancer risk, stating "Consumption of 15-30 grams/day (approximately one to two drinks) throughout life was associated with a modest 33% increase in risk (odds ratio [OR] = 1.33, 95% confidence interval (CI) = 1.01-1.74), but heavier consumption (> or = 30 grams per day) was not. Risk did not vary with alcohol type (beer, wine, or hard liquor) or by patterns of use, such as recent use, intake prior to age 20 years, or whether use began at an early age. The association with lifetime intake was limited to women with a BMI < 25 (OR = 2.13, 95% CI = 1.29-3.54).".

Mørch et al 2007 published "Alcoholic drinking, consumption patterns and breast cancer amongst Danish nurses:a cohort study" stated that "The relative risk of breast cancer was 2.30 [Confidence interval (CI): 1.56–3.39] for alcohol intake of 22–27 drinks per week, compared to 1–3 drinks per week. Among alcohol consumers, weekly alcohol intake increased the risk of breast cancer with 2% for each additional drink consumed. Weekend consumption increased the risk with 4% for each additional drink consumed friday through sunday. Binge drinking of 4–5 drinks the latest weekday increased risk with 55%, compared with consumption of one drink. A possible threshold in risk estimates was found for consumption above 27 drinks per week. Conclusions: For alcohol consumption above the intake most frequently reported, the risk of breast cancer is increased. The risk is minor for moderate levels but increases for each additional drink consumed during the week. Weekend consumption and binge drinking imply an additional increase in breast cancer risk." 

*However, nurses who drank small amounts of alcohol reduced breast cancer risk compared with abstainers, an effect which persisted to 24g per day. Between 24 and 36g per day, risk doubled and then fell back to +25% over 36g. 

In 2008 Barnett et al in the paper, "Risk factors for the incidence of breast cancer: do they affect survival from the disease?" said that "Improved prognosis was seen with increasing current alcohol consumption, with a 2% (95% CI, 1% to 3%) reduction in the risk of death per unit of alcohol consumed per week."

Bessaoud et al in 2008 published "Patterns of alcohol (especially wine) consumption and breast cancer risk: a case-control study among a population in Southern France" and reported that "Women who had an average consumption of less than 1.5 drinks per day had a lower risk (odds ratio [OR] = 0.58, 95% confidence interval [CI] = 0.34-0.97) when compared with nondrinkers. This protective effect was due substantially to wine consumption since the proportion of regular wine drinkers is predominant in our study population. Furthermore, women who consumed between 10 and 12 g/d of wine had a lower risk (OR = 0.51; 95% CI = 0.30-0.91) when compared with non-wine drinkers. Above 12 g per day of wine consumption, the risk of breast cancer increased, but the association was non-significant.

no association between the pattern of total alcohol consumption and breast cancer was found, the type of alcoholic beverage seemed to play an important role in this association. Our results support the hypothesis that there is a threshold effect that risk decreased or was not modified for consumption under a certain threshold. Above that threshold, risk increased, however. The drinking pattern of each type of specific beverage, especially wine, seems important in terms of alcohol-breast cancer association. Low and regular wine consumption does not increase breast cancer risk."

Chen et al in 2011 looked at moderate alcohol consumption and breast cancer risk reporting that " Increasing alcohol consumption was associated with increased breast cancer risk that was statistically significant at levels as low as 5.0 to 9.9 g per day, equivalent to 3 to 6 drinks per week (relative risk, 1.15; 95% CI, 1.06-1.24; 333 cases/100,000 person-years). Binge drinking, but not frequency of drinking, was associated with breast cancer risk after controlling for cumulative alcohol intake. Alcohol intake both earlier and later in adult life was independently associated with risk."

Chen also published in 2011, "Moderate alcohol consumption during adult life, drinking patterns, and breast cancer risk." and reported "During 2.4 million person-years of follow-up, 7690 cases of invasive breast cancer were diagnosed. Increasing alcohol consumption was associated with increased breast cancer risk that was statistically significant at levels as low as 5.0 to 9.9 g per day, equivalent to 3 to 6 drinks per week (relative risk, 1.15; 95% CI, 1.06-1.24; 333 cases/100,000 person-years). Binge drinking, but not frequency of drinking, was associated with breast cancer risk after controlling for cumulative alcohol intake. Alcohol intake both earlier and later in adult life was independently associated with risk." and "Low levels of alcohol consumption were associated with a small increase in breast cancer risk, with the most consistent measure being cumulative alcohol intake throughout adult life. Alcohol intake both earlier and later in adult life was independently associated with risk."

Schutze et al 2011 "Alcohol attributable burden of incidence of cancer in eight European countries based on results from prospective cohort study" reported that " If we assume causality, among men and women, 10% (95% confidence interval 7 to 13%) and 3% (1 to 5%) of the incidence of total cancer was attributable to former and current alcohol consumption in the selected European countries. For selected cancers the figures were 44% (31 to 56%) and 25% (5 to 46%) for upper aerodigestive tract, 33% (11 to 54%) and 18% (−3 to 38%) for liver, 17% (10 to 25%) and 4% (−1 to 10%) for colorectal cancer for men and women, respectively, and 5.0% (2 to 8%) for female breast cancer. A substantial part of the alcohol attributable fraction in 2008 was associated with alcohol consumption higher than the recommended upper limit: 33 037 of 178 578 alcohol related cancer cases in men and 17 470 of 397 043 alcohol related cases in women."

*Eight countries (France, Italy, Spain, United Kingdom, the Netherlands, Greece, Germany, Denmark) participating in the European Prospective Investigation into Cancer and Nutrition (EPIC) study.Participants 109 118 men and 254 870 women, mainly aged 37-70.

In 2013 McDonald et al published "Alcohol Intake and Breast Cancer Risk: Weighing the Overall Evidence" and concluded that "Moderate alcohol consumption has been linked to an approximate 30-50% increased risk in breast cancer. Case-control and cohort studies have consistently observed this modest increase. We highlight recent evidence from molecular epidemiologic studies and studies of intermediate markers like mammographic density that provide additional evidence that this association is real and not solely explained by factors/correlates of the exposure and outcome present in non-randomized studies. "

Liver Cancer - unclear as to the risks due to variable data but wine would appear to have little or no effect

The WCRF report states that there is "high heterogenicity" with a "dose response relationship apparent in case control but not cohort data".

"Data are available from 15 cohort studies. Eleven cohort studies showed increased risk for the highest intake group when compared to the lowest,which was statistically significant in two.Two studies showed non-significant decreased risk. Two studies stated that there was no significant difference but did not provide further data.. Heterogeneity is partially explained by differences in whether and how studies have adjusted for hepatitis virus status. Data are available from 33 case-control studies. Twenty-eight case-control studies showed increased risk for the highest intake group when compared to the lowest,which was statistically significant in 12 (one of these studies reported a non-significant decreased risk in women, but a statistically significant increased risk in men).Two studies showed non-significant decreased risk. Three studies stated that there was no significant effect on risk. Metaanalysis was possible on five studies, giving a summary effect estimate of 1.18 (95% CI 1.11–1.26) per drink/week, with high heterogeneity. A dose-response relationship is apparent from case-control but not cohort data."

"Three cohort studies and one case-control study reported separately on wine drinking. One cohort study showed non-significant increased risk with increased intake. Two studies stated that there was no significant effect on risk.The single case-control study showed non-significant increased risk."

Kidney (Renal) Cancer - evidence that alcohol reduces risk

The WCRF state state that "It is unlikely that alcohol increases the risk of kidney cancer, though a protective effect cannot be excluded".

Lee et al in 2007 reported on "Alcohol intake and renal cancer in a pooled analysis of 12 prospective studies" that in "A total of 1430 (711 women and 719 men) cases of incident renal cell cancer were identified. The study-standardized incidence rates of renal cell cancer were 23 per 100,000 person-years among nondrinkers and 15 per 100,000 person-years among those who drank 15 g/day or more of alcohol. Compared with nondrinking, alcohol consumption (> or = 15 g/day, equivalent to slightly more than one alcoholic drink per day) was associated with a decreased risk of renal cell cancer (pooled multivariable RR = 0.72, 95% confidence interval = 0.60 to 0.86; P(trend)<.001); statistically significant inverse trends with increasing intake were seen in both women and men. No difference by sex was observed (P(heterogeneity) = .89). Associations between alcohol intake and renal cell cancer were not statistically different across alcoholic beverage type (beer versus wine versus liquor) (P = .40)." and concluding  that "Moderate alcohol consumption was associated with a lower risk of renal cell cancer among both women and men in this pooled analysis."

Pelucchi C et al in 2008 in "Alcohol consumption and renal cell cancer risk in two Italian case control studies" reported "Compared with non-drinkers, the multivariate odds ratios (ORs) of RCC were 0.87 [95% confidence interval (CI) 0.73–1.04] for ≤4 drinks per day, 0.76 (95% CI 0.59–0.99) for >4 to ≤8 drinks per day and 0.70 (95% CI 0.50–0.97) for >8 drinks per day of alcoholic beverages, with a significant inverse trend in risk (P value = 0.01). The ORs were 0.85 (95% CI 0.71–1.02) for wine, 0.84 (95% CI 0.68–1.03) for beer and 0.86 (95% CI 0.70–1.05) for spirits consumption, as compared with abstainers. No trend in risk of RCC emerged with duration (P value = 0.94) and age at starting alcohol consumption (P value = 0.81). Results were consistent in men and women, as well as in strata of age, smoking and body mass index.". Pelucchi concluded that "This pooled analysis found an inverse association between alcohol drinking and RCC. Risks continued to decrease even above eight drinks per day (i.e. >100 g/day) of alcohol intake, with no apparent levelling in risk."

Stomach (Gastric) Cancer - evidence that moderate alcohol drinkers have lower incidence and particularly wine drinkers

Barstad B et al 2005 in "Intake of wine, beer and spirits and risk of gastric cancer" reported "The objective was to study prospectively the relation between quantity and type of alcohol and risk of gastric cancer. In a pooled database from three population studies conducted in 1964-1992, a total of 15,236 men and 13,227 women were followed for a total of 389,051 person-years. During follow-up 122 incident cases of gastric cancer were identified. Total alcohol intake itself was not associated with gastric cancer, but type of alcohol seemed to influence risk. Compared with non-wine drinkers, participants who drank 1-6 glasses of wine had a relative risk ratio of 0.76 (95% confidence interval (CI) 0.50-1.16), whereas those who drank >13 glasses of wine per week had a relative risk ratio of 0.16 (95% CI 0.02-1.18). Linear trend test showed a significant association with a relative risk ratio of 0.60 (95% CI 0.39-0.93) per glass of wine drunk per day. These relations persisted after adjustment for age, gender, educational level, body mass index, smoking habits, inhalation and physical activity. There was no association between beer or spirits drinking and gastric cancer." and  "In conclusion, the present study suggests that a daily intake of wine may prevent development of gastric cancer. "

Duell EJ et al 2011 "Alcohol consumption and gastric cancer risk in the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort" reported that "Heavy (compared with very light) alcohol consumption (≥60 compared with 0.1-4.9 g/d) at baseline was positively associated with GC risk (HR: 1.65; 95% CI: 1.06, 2.58), whereas lower consumption amounts (<60 g/d) were not. When we analyzed GC risk by type of alcoholic beverage, there was a positive association for beer (≥30 g/d; HR: 1.75; 95% CI: 1.13, 2.73) but not for wine or liquor. Associations were primarily observed at the highest amounts of drinking in men and limited to noncardia subsite and intestinal histology; no statistically significant linear dose-response trends with GC risk were observed.", and concluded that "Heavy (but not light or moderate) consumption of alcohol at baseline (mainly from beer) is associated with intestinal-type noncardia GC risk in men from the EPIC cohort."

Tramacere I et al published in 2012 "A meta analysis on alcohol drinking and gastric cancer risk" reported "Compared with nondrinkers, the pooled relative risk (RR) was 1.07 [95% confidence interval (CI) 1.01-1.13] for alcohol drinkers and 1.20 (95% CI 1.01-1.44) for heavy alcohol drinkers (≥4 drinks per day). The pooled estimates were apparently higher for gastric noncardia (RR for heavy drinkers=1.17, 95% CI 0.78-1.75) than for gastric cardia (RR=0.99, 95% CI 0.67-1.47) adenocarcinoma. The dose-risk model estimated a RR of 0.95 (95% CI 0.91-0.99) for 10 g/day and 1.14 (95% CI 1.08-1.21) for 50 g/day." and concluded that "This meta-analysis provides definite evidence of a lack of association between moderate alcohol drinking and gastric cancer risk. There was, however, a positive association with heavy alcohol drinking."

Gullet, throat, mouth (oesophageal, mouth, larynx, pharynx) Cancer - link with alcohol but small compared with smoking and evidence that wine has no effect

The WCRF state "There is ample and consistent evidence, both from case-control and cohort studies, with a dose-response relationship. There is robust evidence for mechanisms operating in humans. The evidence that alcoholic drinks are a cause of mouth, pharynx, and larynx cancers is convincing. Alcohol and tobacco together increase the risk of these cancers more than either acting independently. No threshold was identified."

On  mouth, pharynx, and larynx cancers "Twenty-six case-control studies and four ecological studies reported separately on wine drinking. Most of the case-control studies showed increased risk with increased intake which was statistically significant in less than half. Five studies showed decreased risk,which was statistically significant in one. Meta-analysis was possible on 11 case-control studies, giving a summary effect estimate of 1.02 (95% CI 1.01–1.03), with high heterogeneity.All studies adjusted for smoking. All four ecological studies showed statistically significant increased risk."

On Oesophagus and wine "Ten case-control studies,one crosssectional study and five ecological studies reported separately on wine drinking. All but one of the case-control studies showed increased risk with increased intake,which was statistically significant in seven.About half of the studies adjusted for smoking. The single cross-sectional study showed non-significant increased risk. Most ecological."

Prostate Cancer - evidence of reduced risk with wine

Schoonen WM 2005, "Alcohol consumption and risk of prostate cancer in middle-aged men." reported that "No clear association with prostate cancer risk was seen for overall alcohol consumption. Each additional glass of red wine consumed per week showed a statistically significant 6% decrease in relative risk (OR = 0.94; 95% CI = 0.90-0.98), and there was evidence for a decline in risk estimates across increasing categories of red wine intake (trend p = 0.02). No clear associations were seen for consumption of beer or liquor. Our present study suggests that consumption of beer or liquor is not associated with prostate cancer. There may be, however, a reduced relative risk associated with increasing level of red wine consumption. Further research is needed to evaluate the potential negative association between red wine intake and prostate cancer risk."

Key clinical evidence for alcohol (wine) and health

The following is a list of key clinical studies which have examined the impact of alcohol and wine consumption on health and risk of dying prematurely. The list of studies is by no means exhaustive but includes many of the pivotal ones which have been highly influential over the last few decades.

Studies relating to alcohol addiction have not been included as the literature evidence linking abuse with alcohol is well documented and generally associated with other psychological or social problems except in special groups such as teenagers or the mentally ill.

Alcohol and cancer

For a full review of the evidence for the association between alcohol and wine and different cancers see below.

Heart disease, Mortality and Alcohol

For a full review of the clinical data click on the link below.

UK's new alcohol guidelines push prohibition agenda but with bias in scientific conclusions

Alcohol banned

UK alcohol guidance January 2016

When it comes to alcohol, it could be said that there's a definite case of Nanny State or Big Brother, following the UK Chief Medical Officer's new official guidelines on drinking.  Last week the number of units that UK citizens are recommended to drink  dropped from 21 to 14 units for Men and remained at 14 units for women. Yet the basis for this new prohibition on scientific grounds seems dubious at best. 

Note that has no links to the drinks industry and as a lover of wine the only vested interest is to explore the facts and communicate the truth. Wine, as an antidote to civilisation, is a pleasure that cannot be killed by public health bureaucrats.

The new guidance is the first full review of alcohol guidelines since 1995, although updated advice on drinking in pregnancy and for young people was published in 2007 and 2009, respectively. The advice is now that any amount of alcohol can increase the risk of cancer and pregnant women should not drink at all. But are the new guidelines too simplistic and based on the full range of clinical evidence?

See Alcohol Guidelines Review – Report from the Guidelines development group to the UK Chief Medical Officers. 

Differences in Blood Alcohol Concentration (BAC)

Despite differences in Body Mass Index (BMI), age and the ratio of fat/muscle and hence BAC (Blood Alcohol Concentration) males and females have been given the same maximum weekly limit in the new UK alcohol guidelines. 

Many experts around the world argue that applying a "one size fits all" alcohol limit is impossible as the way alcohol is metabolised varies significantly from person to person. Yet public health "experts" have attempted to apply a simplistic message to ease communication to the population.

The more your body can metabolise the alcohol, the less gets into the blood and the lower the Blood Alcohol Concentration. Those who metabolise the best are least affected and age as well as sex has a big impact.  An 85kg male who drinks two glasses of wine during a meal will have a much lower BAC than a women who drinks the equivalent amount with food, almost half as much, and as well as Body Mass Index effects there are also differences in certain enzyme levels between genders.

Drinking with food dramatically lowers blood alcohol levels as there is an enzyme in your stomach called alcohol dehydrogenase which helps break it down to acetaldehyde. The enzyme is also mainly found in the liver where it works to oxidise alcohol via the portal vein. Higher concentrations of alcohol depress the gastrointestinal (GI) tract to slow absorption and also mucus secretion is increased due to alcohol's irritant effect which further reduces its impact on the body.

The metabolite of alcohol, acetaldehyde, has been blamed by some for the rise in some cancers since it can alter DNA at higher concentrations but it is normally swiftly converted to safer molecules by an enzyme called acetaldehyde dehydrogenase and there are different versions including ALDH1 and ALDH2. 

 Some races have faulty versions of these enzymes e.g. about half of people from Han Chinese, Taiwanese and Japanese descent. This means that they become intoxicated even after drinking very small quantities of alcohol and get "Asian Flush", a characteristic reddening of the face.  Alcohol dehydrogenase levels are also lower in women than men and since alcohol is only distributed in the body in parts made of water not fat it it means that the BAC is also reduced as men have a higher water/fat ratio. As we age, levels of alcohol dehydrogenase also fall so a 65 year old will be intoxicated by alcohol by than a 21 year old.

Eating a high protein or fat meal will delay the release of alcohol from the stomach into the small intestine (where absorption is greatest). This has the effect of reducing BAC as the enzymes have a chance to break down more of the alcohol as the food/drink mixture is parked in the stomach for longer. So drinking wine with a meal or after it is the best way to keep blood steam levels low but eating after drinking has no effect as the alcohol has already reached the blood steam and therefore cannot sober you up.

Risks of alcohol consumption

The new guidelines highlight the increased risk of various cancers caused by alcohol, particularly breast cancer and bowel cancer at greater than 14 units. For example the risk of breast cancer in women is nearly 50% higher in drinkers consuming 14-35 units per week. The clinical evidence is strong that certain cancers and alcohol have a causal link. But alcohol confers significant positive benefits in reducing heart attack and stroke at moderate levels which which more than offset these negative effects in terms of total risk of dying and these were dismissed. Strange?

A counter view

The committee which developed the new guidelines seemed to be determined to focus on clinical research which supported their case but were dismissive of very large studies which showed the positive impact of moderate consumption of alcohol. The discarded data involved very large numbers grouping many individual studies. The message of the UK government is now that any level of drinking is unsafe. But having reviewed the evidence without a drink industry or public health committee agenda convinces me that this is not true. 

The positive effects of alcohol were dismissed by Dame Sally Davies and the committee as they concluded that drinking only had a protective effect for a small number of sub-groups. This may be because many of the members of the expert panel had a direct financial interest in painting a negative picture as they are involved in various anti-alcohol activities funded by academic research or other grants. Great emphasis has been placed on work done by the Sheffield group's statistical analyses, but very large population based studies which paint a much more positive picture have been dismissed.

Alcohol guidelines extracts

They state that:

"Meta-analyses have identified that for some conditions, notably ischaemic heart disease (IHD), drinking alcohol at low levels may have a protective effect (compared to not drinking), particularly for all-cause mortality.

However, the group noted that: any potential protective effect seems mainly relevant to older age groups; • unresolved confounding and health selection (for instance, the health of people who can afford to drink more in older age may be better than those who do not) may explain a substantial part of the protection observed; • mortality from IHD is continuing to decrease substantially; and • the peak of any protective effect is achieved at very low levels of consumption (around one unit a day).

"The group therefore concluded that the evidence supporting protective effects today is now weaker than it was at the time of the 1995 report and that there are substantial uncertainties around direct attribution to alcohol of the level of protection still observed. Taking this into account alongside all the known acute and chronic risks to health from drinking even at low levels, supports the conclusion of the group that there is no justification for recommending drinking on health grounds, nor for starting drinking for health reasons."

"Evidence for a net protective effect of alcohol from risk of death (which has been linked to possible reduced risks of heart disease late in life) is considered less strong than it was. A reduced risk still exists, but, in the UK, it now appears to matter overall in a significant way only for women aged 55 or older.13 The 1995 report for the current guidelines found this protective effect applied at that time to men over 40 and postmenopausal women. This change in understanding is consistent with changes in the profile of heart disease in the UK and a changing population. "

"The evidence about any protective effect of drinking small amounts (1 unit or less a day) of alcohol in reducing risks of death, mainly from ischaemic vascular disease such as heart disease, has been taken account of in framing the regular drinking guideline and was part of the research used to inform that.

The expert group concluded that people who do not drink any alcohol at all should not be recommended to start drinking in the interests of their health because such advice cannot be justified for a number of reasons:

  • (a) the evidence for a direct, protective, effect of alcohol on mortality is a subject of continuing scientific discussion;
  • (b) methodological limitations in the evidence base mean there is uncertainty on the extent of the effect;
  • (c) ischaemic vascular disease including heart disease, which is the key condition in the evidence of reduced risk, mainly affects older adults and particularly deaths in older age. Deaths from this type of disease have been falling in the UK population for some years, which means there is less risk for which low alcohol consumption might give protection;
  • (d) lifestyle changes, such as stopping smoking, increasing levels of physical activity, and eating a healthy diet, can help protect against heart disease, so any potential protective effects from alcohol could be achieved in other ways, which avoid the other health risks which come with any drinking of alcohol.

After accounting for these limitations in the evidence used within the Sheffield model, the best specific evidence available on protective effects suggests that the maximum net reductions in deaths are present in those regularly drinking only 1 unit or less a day.

Previous analyses suggested the protective effect was only likely to be relevant to men from age 40 onwards and for post-menopausal women. The Sheffield report commissioned for the expert group included a UK analysis, which has found that the net protective effect that may be attributable to drinking regularly at low levels appears now to be significant only for women aged 55+ (with men aged over 55+ showing such a protective effect only of negligible size).

The Sheffield report estimates that for females aged 55 and over, the greatest risk reductions occur in those drinking approximately five units per week (mean weekly consumption). 53. The impact of any such apparent protective effect would be expected to vary, for example, with differences in the risk of heart disease in the population over time, and so this recent finding is not necessarily inconsistent with previous evidence."

Disputing the official view

Christopher Snowdon (writer and researcher at the Institute of Economic Affairs) points out on his personal blog "Velvet Glove, Iron Fist" that, "The authors used a simple statistical trick. They gathered data which clearly showed health benefits from moderate drinking and then divided it into so many subgroups that it was almost impossible for them to produce statistically significant results. By the time the authors had sliced and diced the data, the only people who appeared to benefit from drinking were post-menopausal women. I wrote about it at the time, as did David Spiegelhalter. It was absolute junk."

See the full blog post at: 

The J-shaped curve

Many  studies have found a J-shaped relationship between drinking and heart disease & stroke/mortality. In other words, moderate drinkers have a reduced risk of cardiovascular disease and total mortality than total abstainers from alcohol. At higher levels of drinking these positive effects disappear. There have been numerous other clinical studies which have shown positive benefits of alcohol in Alzheimer's disease, diabetes and other conditions - all dismissed as irrelevant!

In 2006 Di Castelnuovo et al used a meta analysis technique where the results of 34 studies were collated and reviewed and published in the Archives of Internal Medicine (Arch Intern Med. 2006;166(22):2437-2445). The study looked at the link between the amount of alcohol drunk and death rates in men & women in clinical trials conducted before the end of 2005 with over 1 million subjects (1 015 835 subjects and 94 533 deaths). Yes over 1 million people!

A J-shaped relationship between alcohol and total mortality was confirmed in both men and women. Consumption of alcohol, up to 4 drinks per day in men and 2 drinks per day in women, was inversely associated with total mortality or the chance of dying, maximum protection being 18% in women and 17% in men. Higher consumption of alcohol was detrimental.

The J-curved relationship between alcohol consumption and coronary heart disease is particularly strong. It was summarised in a meta-analysis of 84 studies and can be illustrated with this graph from Corrao et al. (2000).

There is a lower rate of mortality  until drinkers consume 40 units of alcohol per week. Beyond this, risk increases above that of the teetotaller. A unit of alcohol is 8 grams so this works out at five standard drinks or more.

Yet this evidence is dismissed by the latest guidelines as apparently  "The evidence for a direct, protective, effect of alcohol on mortality is a subject of continuing scientific discussion. The committee says that "Evidence for a net protective effect of alcohol from risk of death (which has been linked to possible reduced risks of heart disease late in life) is considered less strong than it was. A reduced risk still exists, but, in the UK, it now appears to matter overall in a significant way only for women aged 55 or older.", "Previous analyses suggested the protective effect was only likely to be relevant to men from age 40 onwards and for post-menopausal women. "

There is a very large body of evidence that J-curve is real when it comes to alcohol and this clinical data is in fact larger and more consistent than the data linking alcohol with cancer. The committee even dismiss protection for heart disease saying "Deaths from this type of disease have been falling in the UK population for some years, which means there is less risk for which low alcohol consumption might give protection.", even though Ischaemic heart disease was the leading cause of death for males in 2013, which accounted for 15.4% of male deaths. The second leading cause of death in 2013 was lung cancer (malignant neoplasm of trachea, bronchus and lung) for males and ischaemic heart disease for females.


The committee state that "Lifestyle changes, such as stopping smoking, increasing levels of physical activity, and eating a healthy diet, can help protect against heart disease, so any potential protective effects from alcohol could be achieved in other ways, which avoid the other health risks which come with any drinking of alcohol."

Christopher Snowdon points out the following, "Imagine them saying this about anything else! Imagine them saying that people don't need to bother about eating too much salt because they can always reduce the risk of having a heart attack by losing weight. In any case, it's not true. A non-smoking teetotaller is as greater risk than a non-smoking moderate drinker.

This whataboutery is a blatant attempt to downplay the significance of alcohol's protective effect on heart disease to such an extent that they are even happy to downplay the significance of heart disease as a cause of death. The lengths these people will go to is extraordinary."


Should we worried that drinking a glass of wine is going the same way as smoking a cigarette? Some commentators are  now saying that the tide is turning against alcohol in public health circles with an excuse ultimately for governments to tax alcoholic drinks even more. In England and Wales, a bottle of wine is already taxed at £2 per 750ml plus 20% VAT ( tax on a packet of 20 cigarettes is £3.52 plus VAT). In Scotland, the minimum price per unit of alcohol has been set at 50p and despite resistance from the EU the public health zealots are pushing for this in the rest of the UK.

But unlike smoking tobacco which is proven without doubt to be very bad for your health, I do not agree with the conclusions of the "Report from the Guidelines development group to the UK Chief Medical Officers". 

Much is made of the evidence that alcohol causes cancer, but the positive effect of alcohol on stroke and heart attack risk as well as overall mortality for moderate drinkers has been erroneously dismissed out of hand. Ishaemic heart disease is the leading cause of premature death in England and Wales (38,000 male deaths, 25 female deaths in 2013).

Dame Sally Davies has been influenced by anti-alcohol zealots and let bad science get in the way of a good story. I continue to believe that drinking 2-3 glasses of wine a day has a negligible risk compared with many everyday activities such as travelling in a car, living in a city with any pollution, not eating healthily or doing no exercise. Everything in moderation......

Further articles and blog posts to read

The Sheffield study (Mortality and morbidity risks from alcohol consumption in the UK: Analyses using the Sheffield Alcohol Policy Model (v.2.7) to inform the UK Chief Medical Officers’ review of the UK lower risk drinking guidelines). 

Very good post from the blogger, the Stats Guy (Adam Jacobs, a medical statistician) called "New Alcohol Guidelines" and in it he says "Does any of this matter? After all, the guidelines are not compulsory. If my own reading of the evidence tells me I can quite safely drink 2 glasses of wine with my dinner most nights, I am completely free to do so.

Well, I think this does matter. If the government are going to publish guidelines on healthy behaviours, I think it is important that they be as accurate and evidence-based as possible. Otherwise the whole system of public health guidelines will fall into disrepute, and then it is far less likely that even sensible guidelines will be followed."

Telegraph: Don’t let the public health zealots demonise us innocent drinkers, Charles Moore. 

The Guardian: The state needs to butt out of Britain’s drinking habits, Simon Jenkins. 

The Mail Online: Why those killjoy new alcohol rules are just plain wrong: A devastating critique by an award-winning writer on how alcohol affects our health, Tony Edwards. Some interesting extracts from the article:

  • Re. Dame Sally Davies "Her warning received huge publicity - but, having looked in detail at the research into alcohol and health, I'm afraid to say she's simply wrong. Her motivation may be admirable, but her knowledge of the scientific and medical evidence is decidedly not.
  • The irony is that if people who already drink within the old guidelines do follow her advice and completely stop drinking, their risk of disease and premature death will increase. Medical studies now running into many hundreds and published in the world's top journals say that, providing you don't go overboard on the booze, drinking will help you live a longer and healthier life."
  • "Yes, drinkers are at extra risk of liver disease - but the dangers are often exaggerated. For example, a recent official survey showed that, in the heavy-drinking South-East of England, only 6.7 in every 200,000 people die from alcohol-related liver diseases per year, not much more than the death rate from playing sport or doing exercise. And even that low figure is misleadingly high, with official figures for 'alcohol-related' deaths not quite what they might seem.
  • In detailed email exchanges with the UK Office for National Statistics last year, they told me that under the heading of 'alcohol-related' deaths, 'we include all deaths from liver cirrhosis except for (the rare) biliary cirrhosis . . . we are aware that liver cirrhosis can also be caused by drugs, exposure to chemicals, bile duct obstruction, diabetes, malnutrition, hepatitis C, other infective agents, and several other conditions.'"
  • "Another indication that the alcohol/liver problem is overblown is what happens to alcoholics. In 2003, researchers at Canada's prestigious Centre for Addiction and Mental Health surveyed the entire international evidence and found that only one in seven of the heaviest drinkers has any liver problems at all. 'Alcoholics drink an average of 160 grams of alcohol [i.e 20 units - more than half a bottle of scotch] per day,' they observed, but found only 'about 14 per cent of alcoholics will develop cirrhosis if they drink this quantity for a period of eight years'.
  • But what about sensible drinkers? Take a look at Finland, the country with Europe's highest rates of liver disease. Post-mortem studies by pathologists at Helsinki University show that 'in males, daily ingestion of alcohol below 40 grams for a period of 25 years does not increase the risk of alcohol-related liver disease'. What's 40g? Five units ie. half a bottle of wine, two to three pints of beer, or four measures of spirits.
  • But as you drink more, the liver does start to be affected and 'the incidence of liver cirrhosis increases significantly when daily alcohol intake exceeds 80 grams (ten units/day) - (but this occurs) in only 20 per cent of heavy consumers', the Finns reported in the journal Alcoholism: Clinical And Experimental Research."
  • "Utterly surprisingly, alcohol has been found to reduce the risk of about half a dozen cancers: kidney, thyroid and many of the blood cancers. That might explain the findings of a 2013 survey of the health of nearly half a million Europeans (part of the European Prospective Investigation into Cancer and Nutrition, one of the largest-ever studies) which showed a 21 per cent reduction in men's death rates from cancer after 'life-time alcohol consumption' of up to two-and-a-half units per day."

More articles on wine & health

Is drinking wine good or bad for you?

If you love to drink wine you are probably concerned when you read the endless negative headlines in the newspapers about alcohol and its effect on your health. Most governments, public health organisations and even charities advise not drinking or very limited drinking of alcohol. This review aims to discuss the balance of evidence to help you decide whether alcohol and wine is good or bad for you.

Background to the debate on alcohol, wine and health

The dangers of excessive drinking and the benefits of moderate amounts of alcohol have been part of a continued debate within the health community for decades. For example, a World Health Organisation (WHO) study published in October 2015 ranked ethanol in alcoholic beverages as definitely carcinogenic in common with processed meats like salami and bacon. In January 2016, the U.K.'s Chief Medical officer (CMO), Dame Sally Davies reduced "safe" drinking guidelines to 14 units a week for both men and women. See CMO Alcohol report.

In March 2016 Stockwell et al published a new study in the Journal of Studies on Alcohol and Drugs, "Do "Moderate" Drinkers Have Reduced Mortality Risk? A Systematic Review and Meta-Analysis of Alcohol Consumption and All-Cause Mortality."

The new study was a systematic review and meta-regression analysis of studies investigating alcohol use and mortality risk after controlling for quality-related study characteristics was conducted in a population of 3,998,626 individuals, among whom 367,103 deaths were recorded. A total of 87 studies were examined and the paper concluded that when his team corrected for abstainer "biases" and certain other study-design issues, moderate drinkers no longer showed a longevity advantage stating that "Estimates of mortality risk from alcohol are significantly altered by study design and characteristics. Meta-analyses adjusting for these factors find that low-volume alcohol consumption has no net mortality benefit compared with lifetime abstention or occasional drinking."

However other academics dispute Stockwell's analysis contesting strongly his assertion that abstainers were biased because many abstainer groups include people in poor health whod cut out alcohol and that his approach to dismiss many studies because of his group's reservations about design was over zealous.

Yet, whilst drinking too much wine is certainly not good for you and even with the debate about abstainer biases and "flawed design" raised by Stockwell and other academics, some major clinical studies with many hundreds of thousands of participants give strong evidence that moderate consumption (2-3 glasses of alcohol per day) has a beneficial impact on your overall health, reduce your risk of premature death and lower your chances of having a life threatening event like a heart attack. These studies were pioneered by scientists like Sir Richard Doll, noted for being one of the first to conclusively link smoking tobacco and lung cancer.

Clinical evidence in these large scale human studies is clear that total abstainers from alcohol are likely to die younger than those drinking a glass or two a day on average of alcohol. Conversely "binge drinking" or heavy daily consumption of any alcohol is not healthy, predominantly because of negative effects on the liver and increasing the risk of cancer. A moderate approach to wine consumption is therefore to be recommended for a happier, healthier and longer life!

In addition, certain types of wine may have a more beneficial effect on health than others. Laboratory studies confirm that red wines made from grapes with thick skins (e.g. Tannat & Malbec) have higher levels of a molecule called resveratrol which appears to have positive effects on the body. However some studies show an equal positive impact for both red and white wines leading some academics to suggest that it is alcohol itself which benefits health rather than any specific compound in wine or other drinks. 

Unpicking facts from fiction is a large task given the controversy and this review attempts to link the substantial human data relating to alcohol use and give a conclusion to the regular alcohol or wine drinker as to whether wine is good or bad for your health. 

Gene Ford in his 2003 book "The Science of Healthy Drinking" points out that antipathy to drinking became the norm in medicine when the American Medical Association passed a resolution in June 1917 which stated "alcohol as a beverage is detrimental to the human economy...or as a stimulant or as a food has no scientific basis...the use of alcohol as a therapeutic agent should be discouraged." This was followed by Prohibition in the United States between 1920 and 1933, a nationwide constitutional ban on the sale, production, importation, and transportation of alcoholic beverages.

Prohibition may have gone but temperance is a societal normal in many countries with a pattern of government sponsored bodies omitting drink positive research in disease articles and with a tendency to overstate the risks of abuse and addiction. Many highly regarded but conservative doctors still believe in a prohibitionary agenda despite the evidence that moderate consumption has a positive impact on health outcomes. Yet most doctors themselves are not abstainers!

Many drinkers worry about addiction but the evidence is substantial in the medical literature that only a very small percentage of alcohol drinkers will become addicted. Alcohol abusers tend to have underlying psychological or social problems which is linked to the addiction and certain genetic factors are key.

Positive studies associated with alcohol are explained away by some physicians by so called "confounding factors". They will argue that those who apparently had a lower risk of heart attacks or other negative health events may have been drinking more alcohol than abstainers but focus on the potential of better lifestyle in the alcohol drinking group. Others quote the 'sick quitter' hypothesis, an argument that the risks of not drinking were magnified as some people stop consuming alcohol because of problems with their health and therefore only lifelong abstainers should be studied.

Authors like Tony Edwards in "The Good news about Booze" summarise the picture that moderate drinking - or by today's puritanical standards, even relatively heavy drinking - reduces not only heart disease risk but overall mortality risk and the relationship is causal.

Dr Kari Poikolainen, a doctor of medical science and adjunct professor in public health (since 1983) at the University of Helsinki in Finland and Research Director at the Finnish Foundation for Alcohol Studies before he retired. In 2014 he published a very good book for those interested in alcohol and health called "Perfect Drinking and its enemies".

Dr Kari Poikolainen

Dr Kari Poikolainen

Poikolainen says "To sum up, the most likely estimate for increased health risk (from alcohol), compared with that of abstaining, is somewhat between 90 and 150g/day. Respectively, the optimal level might be 14-22g/day" (120 ml of wine, half a large glass = 12g of 100% alcohol). Furthermore he states that "Careful participant observations have found that many alcoholics consume much more, typically between 350 to 470g/day".

Those with a negative view of the alcohol benefit talk about "Even if moderate drinking does confer health benefits, which it probably does, they are rather modest - certainly not stronger than the effect of small daily doses of aspirin on heart health...the effect may be more in line with the apparent cardio-protective benefits of eating a modest portion of nuts each day" (Time magazine 2003). Yet clinical evidence from major studies indicates that drinking moderate amounts of alcohol has a more than "modest" benefit on risk of cardiovascular disease and overall mortality and in populations who are abstainers and are already eating healthily and perhaps using measures such as Aspirin the comparative benefit of drinking 2-3 glasses of alcoholic drinks are incrementally beneficial.

In 2006 Di Castelnuovo et al used a meta analysis technique where the results of 34 studies were collated and reviewed and published in the Archives of Internal Medicine. The study looked at the link between the amount of alcohol drunk and death rates in men & women in clinical trials conducted before the end of 2005 with over 1 million subjects. Yes over 1 million people!

A J-shaped relationship between alcohol and total mortality was confirmed in both men and women. Consumption of alcohol, up to 4 drinks per day in men and 2 drinks per day in women, was inversely associated with total mortality or the chance of dying, maximum protection being 18% in women and 17% in men. Higher consumption of alcohol was detrimental. The results were consistent with studies by other research including Sir Richard Doll's 1994 study "Mortality in relation to consumption of alcohol: 13 years' observations on male British doctors". 

Abigail Zuger wrote in the NYT in 2002 in the article "The case for drinking (All Together Now in Moderation), "Thirty years of research has convinced many experts of the health benefits of moderate drinking for some people. A drink or two of wine, beer or liquor is, experts say, often the single best non-prescription way to prevent heart attacks, better than a low fat diet or weight loss, better even than vigorous exercise. Moderate drinking can help prevent stokes, amputated limbs and dementia."

Zuger's view may be over eager but examples like the French Paradox (where despite a high fat diet and heavy smoking the people of several regions of France live a long life) show that moderate alcohol together with regular exercise, a good diet with olive oil/fish/nuts (in a regular, relaxed setting ideally non rushed eating) and not smoking is a key to long and healthy life. 

Do we need to drink wine - no! But life without wine would be a lot duller and wine is certainly an "antidote to civilisation". What do I mean by this? Well after a stressful or boring day at work, a rough day with the children, bad or good news, human beings sometimes need a reward. In earlier generations they may have smoked a few cigarettes to wind down and now in the modern world we need something else since we now know that the TAR in cigarettes isn't exactly positive (the risks certainly outweigh the benefits). The alclohol prohibitionists may say you don't need anything, "a glass of water will do", but we know that this suggestion isn't the same and the clinical evidence is there for all to see that less than half a bottle of wine a night is a lot better for you than smoking tobacco or cannabis or eating too much as comfort food - the benefits of moderate wine drinking certainly outweigh the risks. If you can do it with exercise and healthy eating even better! 

The evidence for Aspirin and Statins in reducing mortality plus risk of heart attack & stroke are substantial but given side effect concerns (e.g. gastrointestinal bleeds with Aspirin) the case for consuming 2-3 glasses of wine a day look equally compelling.

In the end it is all down to relative risk. Certain behaviours and environmental factors increase your risk of an event like cancer or heart attack. Although certain cancers such as Breast may rise in alcohol drinkers, the increase in risk is tiny compared with the absolute risk of dying in a car accident. Given the risk of dying prematurely in moderate drinkers seems convincingly lower, I for one am continuing my love of the fermented grape.

The debate and the controversy amongst academics will continue!

Negative effects of alcoholic drinks

  • Alcohol: high alcohol consumption (half a bottle of wine a day and over) results in a higher blood pressure and may cause hypertension at very high levels of drinking. It has a positive correlation with mouth, throat and gullet (oesophageal) cancer and under certain circumstances with liver cancer and liver cirrhosis. Some studies suggest a positive relationship between alcohol and breast & gastric cancer, though there is evidence that it may reduce the risk of kidney cancer. The relative risk of lung cancer for men who smoke is 2,300 percent higher than it is for men who don't smoke, whereas some studies show that alcohol may have a relative risk of around 100%, i.e. doubles your chance of getting cancer, which in many cases have a small absolute lifetime risk e.g. oesophageal (1 in 112) or liver (1 in 193). The most prevalent cancers are lung (most caused by smoking), prostate and breast.
  • Tannin: these compounds are plant polyphenols and may cause headaches. Tannins tend to bind starches while being digested. 
  • Sulfites / Sulphites: The term ‘sulfites’ is an inclusive term for sulphur dioxide (SO2). SO2 is a preservative and widely used in wine making because of its antioxidant and antibacterial properties. SO2 plays a very important role in preventing oxidisation and maintaining a wine’s freshness but some people seem to be sensitive to it and many higher quality wine makers are now trying to limit the addition of sulphite or eliminate it entirely.

Positive effects of alcoholic drinks

Risk of premature death

  • Risk of dying early up to 40% lower in drinkers than abstainers, with lower benefit for women and Asians
  • Moderate drinking increases longevity for all causes by about 3%

Reducing coronary heart disease

Epidemiological studies confirm that wine changes body fat levels with total cholesterol lower, bad LDL cholesterol and higher good high density lipoprotein (HDL) levels in drinkers than abstainers.

  • Alcohol significantly reduces incidence of cardiovascular disease, total mortality with lower incidence of angina pain and heart attacks
  • Daily alcohol intake reduces atherosclerotic plaque build up (arteriosclerosis), key in reducing the risk of strokes and heart attacks
  • Nearly a 50% reduction in heart attack risk amongst moderate daily alcohol drinkers has been reported with superior benefits to using daily Aspirin

High blood pressure

  • Light drinkers show favourable blood pressure profiles and less blood pressure induced strokes


  • Light alcohol consumption reduces risk of stroke, whilst lifelong abstention increases risk


  • Two to three alcoholic drinks per day reduce some cancer rates e.g. prostate and kidney

Alzheimer's disease and dementia

  • The Polyphenols in wine have an antioxidant and free radical scavenging action which may explain their positive benefit in reducing the risks of dementia. High doses of resveratrol which is found in wine has been shown to reduce the level of amyloid beta protein in blood (where it probably accumulates in the brain causing the classic symptoms of dementia). 


  • Detrimental metabolic factors are reduced in diabetics who consumer moderate amount of alcohol e.g. LDL cholesterol

Colds and Flu

  • Moderate daily drinking has been shown to reduce the risk of catching the common cold

Why is wine probably healthier than other alcoholic drinks?

In Arranz S 2011 "Wine, Beer, Alcohol and Polyphenols on Cardiovascular Disease and Cancer" they said that "The mechanisms responsible for the healthy effects of wine are extremely complex due to the many different pathways involved. Both alcohol and polyphenolic compounds have been extensively studied, despite the continued controversy as to which component is the most active. The underlying mechanisms to explain these protective effects against CHD include an increase in high-density lipoprotein (HDL) cholesterol, a decrease in platelet aggregation, a reduction in the levels of fibrinogen and an increase in insulin sensitivity, which have been attributed to the ethanol content in wine. Other studies have provided evidence that wine exhibits beneficial properties which are independent of the presence of alcohol, and should be attributed to their polyphenolic content.".

They conclude that "Wine consumption should not replace a healthy lifestyle. However, light-to-moderate wine drinkers, without medical complications, may be assured that their wine consumption is a healthy habit."

Cordova AC 2009 in "Polyphenols are medicine: Is it time to prescribe red wine for our patients?" states that "The habit of having one or two drinks of red wine every day with meals may translate to a longer, healthier and better quality of life."

Are certain wines better for you than others?

Red wine polyphenols are a complex mixture of flavonoids (such as anthocyanins and flavan-3-ols) and nonflavonoids (such as resveratrol, cinnamates and gallic acid). Flavan-3-ols are the most abundant, with polymeric procyanidins (condensed tannins) composing up to 50% of the total phenolic constituents. These compounds act as potent antioxidants as they reduce low-density lipoprotein (LDL) cholesterol oxidation, modulate cell signaling pathways, and reduce platelet aggregation. Red wine contains more polyphenols than white wine (around 10-fold) because during the wine making process, red wine, unlike white wine, is macerated for weeks with the skin which is one of the parts of the grape with the highest concentrations of phenolic compounds. The concentrations in red wine range from around 1.2 to 3.0 g/L.

Certain wines seem to be more healthy than others and one theory is those with the healthiest credentials have the highest amount of procyanidins (proanthocyanidins) - proC, which is a polyphenol.  

The effects of proC include anti oxidant and free radical neutralisation, reducing blood fat, and inhibiting destruction of collagen, the most abundant protein in the body. They may also prevent cardiovascular disease by reducing the negative effects of high cholesterol on the blood vessels. These effects explain their apparent benefits in reducing the incidence of cardiovascular disorders. 

The amount of polyphenols varies from wine to wine, country to country and grape to grape.  The method of production can also significantly impact the amount of procyanidins.

In N Gall 2001 "Is wine good for your heart? A critical review" he says " Is there evidence to enable us to advise what to drink? Although the epidemiological evidence suggests not, there are at least theoretical reasons why red wines rich in flavonoids and resveratrol may hold extra benefit. Flavonoids, being found particularly in grape skins, occur in the highest concentrations in grape varieties with thick skins grown in hot climates.Cabernet sauvignon based wines from Australia, South America, and the southern Mediterranean are particularly rich sources. Syrah (shiraz) and merlot are good too. Fungal vine infection is more common in cooler, damper regions and occurs in significant quantities in pinot noir. Wines from this grape form Burgundy, Sancerre, New Zealand, and the north west United States are particularly rich in resveratrol. Merlot, gammay, syrah, zinfandel, and pinotage wines may also be too. May I advise: Nuits-St-Georges Premier Cru, Clos des Porrets, 1997, one nocte. As the French say, Salut."

What is Resveratrol and why is it important?


Other evidence points to the importance of the concentration of a stilbenoid, a type of natural phenol, called resveratrol in wine and some producers have sought to exploit higher concentrations of this chemical in their wines. 

Resveratrol is found in the skin of red grapes. For example, the Malbec grape, used extensively in Argentina and the Tannat grape found in Uruguay, have thick skins and contains high levels of resveratrol. Vine grapes grown in cooler climates have higher resveratrol levels than those from warmer climates such as Australia.

However, the science behind healthy wine is controversial with some scientists arguing that polyphenols are unimportant, and that factors such as the pips used or manufacturing process are more significant.For example,  see, "Red wine - what's behind its healthy reputation?"


Tannat - seemingly the grape with the highest health benefits

It is said that the tannat grape is the grape with the greatest health benefits. Tannat is used extensively in Madiran wine from SW France (not to be confused with Madeira Wine, a fortified Portuguese wine made in the Madeira Islands) and in Uruguay.

tannat grape vines

More recently wine makers in the Central Coast Region of California are beginning to grow the grape in larger quantities.

The other main factor in the health benefits of a Red Wine may be the method of duration of fermentation and maceration (which is the process of soaking crushed grapes, seeds, and stems in a wine must to extract coluor and aroma compounds as well as tannins). The long fermentation and maceration times that go into the production of Madiran Red Wine may be important factors in its apparent healthiness. The more mass produced Red Wines wines generally don’t conform to these criteria and usually have very low levels of procyanidins.

Procyanidin levels around the world (reds):

Dr. Roger Corder is an author of many scientific papers detailing his research into the flavonoids of foods, but wine in particular. He summarised his findings in "The Red Wine Diet, 2007". 


Among the important observations Corder makes is that regions of the world with the greatest longevity also correspond to regions with the highest procyanidin flavonoids in their wines. 

"Although differences in the amount of procyanidins in red wine clearly occur because of the grape variety and the vineyard environment, the winemaker holds the key to what ends up in the bottle. The most important aspect of the winemaking process for ensuring high procyanidins in red wines is the contact time between the liquid and the grape seeds during fermentation when the alcohol concentration reaches about 6 percent. Depending on the fermentation temperature, it may be two to three days or more before this extraction process starts. Grape skins float and seeds sink, so the number of times they are pushed down and stirred into the fermenting wine also increases extraction of procyanidins. Even so, extraction is a slow process and, after fermentation is complete, many red wines are left to macerate with their seeds and skins for days or even weeks in order to extract all the color, flavor, and tannins. Wines that have a contact time of less than seven days will have a relatively low level of procyanidins. Wines with a contact time of 10 to 14 days have decent levels, and those with contact times of three weeks or more have the highest."

He points out that deeply-coloured reds are more likely to be richer in procyanidins. Wines rich in procyanidins provide several-fold more, such that a single glass can provide the same purported health benefit as several glasses of a procyanidin-poor wine.

  • Australian: on average, low levels, except Cabernet Sauvignon which is moderate.
  • Argentine: Argentinian Malbec have some of the highest levels of procyanidins 
  • Californian: Those with the Tannat grape variety have the highest levels, but Cabernet Sauvignon has also a high content.
  • Chile: Cabernet Sauvignon stands out, then only moderate in content.
  • French: Bordeaux is moderate for procyanidins, Burgundy wines are low to moderate; Languedoc-Roussillon red wines moderate to high levels; Côtes du Rhône red Wines moderate to high. South-West France is a region with superior longevity of its residents. Wine of the Cahors appellation is mainly made from the Malbec grape. The wine with the highest procyanidin content is a wine grown in the Gers region of southwest France. The wines here are made with the tannat grape within the Madiran appellation; wines labeled "Madiran" must contain 40% or more tannat to be so labeled.
  • Italian:The southern Italian wines from Sicily, Sardinia, and the mainland have high levels of procyanidins while most northern varieties are moderate.
  • Spanish: Moderate levels 
  • United States: Cabernet Sauvignon is the standout for procyanidin content, with the Napa Valley a major production area.

Resveratrol concentrations in wine

Media coverage of wine health controversy

Prescription wine? - Horizon - Do I drink too much?

In this BBC documentary Dr William McCrea prescribes red wine to his patients in the Cardiac Ward of Scotland's Great Western Hospital.

The French Wine Paradox - CBS 60 Minutes

The ground breaking CBS feature on wine which changed the mindset of many an American when it comes to alcohol consumption and the impact on their health.

Click to watch video.

Eat well, Drink Wisely, Live Longer - Wine Spectator


Click for full article.

The French Paradox

The term "French paradox" was coined by Serge Renaud, a scientist from Bordeaux University in France, and has been in use since the early 1990s. His paper was published in 1992 "Wine, alcohol, platelets, and the French paradox for coronary heart disease".

Renaud et al based on the MONItoring system for CArdiovascular disease (MONICA) project which included seven million men and women between 35 and 64 years of age from 37 European, American and Asian populations, including the US, Canada, United Kingdom, France and China, among others. The World Health Organisation followed the subjects over a period of 10 years, from the mid-1980s to the mid-1990s. France presented a markedly lower annual mortality from CAD (coronary artery disease) compared with other industrialised nations, despite the fact that cardiovascular risk factors such as cigarette smoking, blood pressure, body mass index and serum cholesterol concentration were similar among these countries; furthermore, it had a three-fold higher intake of saturated fats than that of the US and the United Kingdom, which are not well known for their healthy eating .

Renaud's observations regarding the apparent disconnect between French patterns of high saturated fat consumption and their low rates of cardiovascular disease can be quantified using data from the Food and Agriculture Organisation of the United Nations. In 2002, the average French person consumed 108 grams per day of fat from animal sources, while the average American consumed only 72 grams. The French eat four times as much butter, 60 percent more cheese and nearly three times as much pork. Although the French consume only slightly more total fat (171 g/d vs 157 g/d), they consume much more saturated fat because Americans consume a much larger proportion of fat in the form of vegetable oil, with most of that being soybean oil. However, according to data from the British Heart Foundation, in 1999, rates of death from coronary heart disease among males aged 35–74 years were 115 per 100,000 people in the U.S. but only 83 per 100,000 in France.

Click to see video French Paradox - France

Possible explanations for the French Paradox:

  • High per capita consumption and appreciation of wine in France, particularly red table wine - Resveratrol, Procyanidins and polyphenols
  • Aspects of the French diet - The French diet is rich in vitamin K2, it is rich in short-chain saturated fatty acids and low in trans fats despite dishes like Fois Gras, Confit de Canard etc.  
  • Whole diet - Higher fruit and vegetable intake, more fish, Early life nutrition
  • Generally don't tend to over eat and don't eat quickly - quality over quantity, portion control and lack of over consumption
  • Limited processed and packaged ready meal type foods (many of which are high in sugar and salt)
  • Less snacking and more moderate exercise

American Heart Association - This shows rates of death from cardiovascular diseases (heart attack and strokes combined) for men in several countries, ranked from worst to best.

France stands out as a country with a high wine consumption but with a correspondingly low level of death caused by heart attacks and strokes.

Detailed clinical evidence - the health effects of alcohol consumption

For more detailed information on the health effects of alcohol and wine consumption on health outcomes such as heart disease and death with key clinical studies please see the link below:

Wine Spectator article 2001 - "Eat Well, Drink Wisely, Live Longer - The science behind a healthy life with wine"

Eat Well, Drink Wisely, Live Longer -The science behind a healthy life with wine, Per-Henrik Mansson

Posted: November 29, 2001

Danish researcher Morten Grønbaek has compared the health benefits of wine to those of beer and other forms of alcohol.

The Case for Red Wine        

The ambience of Les Prés d'Eugénie, a Michelin three-star restaurant in southwestern France, promises a rich meal in the grand tradition of haute cuisine. But the menu delivers something entirely different: all of the pleasure for your palate, with none of the peril to your health.

Chef and owner Michel Guérard has gathered all the elements for a great dining experience. Gascony is famous for gastronomic luxuries such as foie gras and duck confit. The restaurant's dining room, set in a 40-acre park amid lush gardens, features high ceilings, Persian carpets and valuable paintings. The wine list glitters with stars from Bordeaux, Burgundy and beyond.

Yet Guérard's special menu offers three delicious courses, plus one glass of wine, for a total of only 610 calories. Balance is the guiding principle of the chef's patented "cuisine minceur active," or active, healthy cuisine. There is no butter on the table or in the food. Cream has been eliminated. Sugar is replaced by natural fructose.

The meal is built on a trilogy of healthy eating principles. First, there is the wine, which can be selected from a list backed by a cellar containing thousands of fine bottles. Then there is the Mediterranean diet, which Guérard follows to the letter. Finally, he includes a dose of alpha-linolenic acid, an important component of the traditional diet of Crete, where old farmers in remote villages enjoy the longest life expectancy in the Western world.

Guérard is 68, but he has the energy of a much younger man as he directs and inspires his kitchen crew. He is living proof of the efficacy of his cuisine, and a committed member of a broadening movement seeking to maximize the benefits of wine and a healthy diet. He keeps on top of the latest scientific studies and works hand in hand with researchers of a major multinational food company, which he credits with helping him fine-tune the use of certain ingredients.

In the small countryside village of Eugénie-les-Bains, Guérard demonstrates that healthy living and living well are not mutually exclusive, but can be blended into a pleasurable lifestyle. "I believe that the future of cooking will be linked in some part to the science of food research," says the chef, who created his eating regimen four years ago. "It was designed to give protection against heart and arterial disease and hypertension. It's 'active' because it also provides vitality."

The scientific evidence

In recent years, research teams, many based in Europe, have provided fresh insights into the health benefits and unique characteristics of wine. As their results become better-known, these scientists are influencing European culture by inspiring chefs and wine lovers to apply their discoveries to a lifestyle that integrates healthier drinking, eating and living patterns.

The data have come from different sources: large population, or epidemiological, studies; laboratory work with test tubes and other in vitro experiments; in vivo work with rats, mice, rabbits, monkeys, dogs and hamsters; and experiments with human volunteers.

The research of French epidemiologist and nutritionist Serge Renaud has been particularly influential; he's widely credited with having proven the health benefits of wine and a strict Mediterranean-style diet. Renaud has influenced other European researchers, including Serenella Rotondo, an Italian researcher with central Italy's Consorzio Mario Negri Sud, where the biological impact of wine on health is studied. Renaud's most famous disciple is Morten Grønbaek, a Danish scientist who has gone even further than Renaud in demonstrating wine's health advantages over beer, spirits and abstinence from alcohol.

Renaud is now based in Bordeaux, which has become a center of research on wine and health. Also in Bordeaux is Jean-Marc Orgogozo, a professor at University Victor Segalen and an expert on wine's ability to help fight Alzheimer's disease and dementia in the elderly. Another professor there is Joseph Vercauteren, whose cutting-edge research focuses on the potential of certain wine components, especially polyphenols, to delay, prevent and even cure cancer and other diseases.

Vercauteren works with a network of scientists around Europe. Elias Castanas of Iráklion, on the Greek island of Crete, has used the polyphenols isolated by Vercauteren to demonstrate that wine might be able to delay or prevent the spread of breast and prostate cancer. "We are encouraged," says Jean-François Rossi, who is head of the Hematology-Oncology Department at the Lapeyronnie University Hospital in Montpellier, France, where some of these polyphenols are currently being tested in experiments with certain cancer cell lines, such as leukemia.

Wine has only gradually taken a starring role in this research. Until recently, most studies didn't differentiate between wine, beer and spirits, bundling them together as "alcoholic beverages." Over the last 30 years, hundreds of studies in America, Australia, Asia and western Europe involving more than 1 million people have confirmed that moderate drinkers of alcoholic beverages have a lower incidence of disease than nondrinkers. The results varied, but the studies were broadly in agreement that consumers of moderate amounts of alcohol -- two to four drinks a day -- had a rate of heart disease from 20 percent to 60 percent lower than that of teetotalers. This suggested that the ethanol in these drinks protected against heart and arterial disease.

In recent years, however, scientists have explored whether wine confers health benefits beyond those expected from its alcohol content. Several studies found that wine drinkers are better off than those who consume only beer and spirits. Renaud and Grønbaek's findings are particularly important in this respect. In separate studies in France and Denmark, they found that wine drinkers who consumed three to five glasses a day decreased their risk of heart disease by about one-third to two-thirds compared with beer or spirits drinkers.

The field of wine and health took another leap forward when researchers investigated links to cancer and other causes of death, not just heart disease. Wine drinkers enjoying up to three glasses a day reduced their risk of dying from cancer by about a fifth compared with nondrinkers', according to French and Danish studies. Even at five glasses a day, wine drinkers cut their cancer risk by 10 percent compared with teetotalers', Grønbaek found.

And wine drinkers have a lower risk of dying from causes other than cancer and heart disease. French and Danish studies found that wine drinkers enjoying two to five glasses a day lowered their all-cause mortality by 25 percent to 50 percent compared with nondrinkers' all-cause rates. Beer and spirits drinkers found no such significant protection.

Wine drinkers may owe their superior health partly to their general lifestyle. Epidemiological studies found that wine drinkers are better educated, eat more healthfully, smoke less and exercise more than people who prefer drinking beer and spirits. Such factors contribute to the generally longer lives of wine drinkers, some scientists say.

Another explanation for the superior protection enjoyed by wine drinkers, according to scientists, is linked to the special properties of red wine. Red wine contains antioxidant components known as polyphenols; they include flavonoids, anthocyanins and certain tannins. Research suggests that antioxidants may have anticarcinogenic properties, and may help prevent a number of diseases.

Many of these healthy components merge in what has become known as the Mediterranean diet. Traditional foods enjoyed in the region include fruit and raw vegetables, onions, garlic and olives -- all of which are important sources of polyphenols. Traditional Mediterranean patterns of wine drinking -- moderate quantities taken regularly with meals -- also seem to confer the most benefits. In one study, men who drank wine three to four days a week were 30 percent less likely to get heart disease than were those men who drank wine one day per week or less.

Public interest in the health benefits of wine exploded a decade ago, when the CBS television show 60 Minutes broadcast a segment on the so-called French Paradox. In the television program, Renaud described how the French had an unexpectedly low rate of fatal heart attacks given the amount of animal fat they ate, and he explained that it was due to the large amounts of alcohol the French consumed in the form of wine.

Since the virtues of drinking wine in moderation were extolled in that broadcast on Nov. 17, 1991, the science of wine and health has gone mainstream. Interest in the health benefits of wine and the Mediterranean diet has intensified across Europe at universities, medical laboratories, hospitals, enology schools and pharmaceutical and food companies. And Renaud became known as the "father of the French Paradox."

For the complete article, please see the Dec. 15, 2001, issue of Wine Spectator magazine, page 32. Click here.

Clinical study in type 2 diabetics shows that moderate red wine intake modestly decreases cardiometabolic risk

A new clinical study published this month in the Annals of Internal Medicine which assessed the impact of randomly assigning alcohol abstaining patients with type 2 diabetes mellitus 150 mL of mineral water, white wine, or red wine with dinner for 2 years. 224 individuals started the study and 87% completed the 2 year review.

In addition to the changes in the water group (Mediterranean diet only), red wine significantly increased good cholesterol (HDL high-density lipoprotein cholesterol) and decreased the total cholesterol ratio. Only slow ethanol metabolisers significantly benefited from the effect of both wines on blood glucose control. Across the 3 groups, no material differences were identified in blood pressure, adiposity, liver function, drug therapy, symptoms, or quality of life, except that sleep quality improved in both wine groups compared with the water group. Overall, compared with the changes in the water group, red wine further reduced the number of components of the metabolic syndrome.

So those using wine appeared not to have any negative effects and there were clear metabolic benefits. 

The details of the paper are included below:

Published online 13 October 2015

Two-Year Moderate Alcohol Intervention in Adults With Type 2 Diabetes
Yftach Gepner, MPH; Rachel Golan, RD, PhD; Ilana Harman-Boehm, MD; Yaakov Henkin, MD; Dan Schwarzfuchs, MD; Ilan Shelef, MD; Ronen Durst, MD; Julia Kovsan, MSc; Arkady Bolotin, PhD; Eran Leitersdorf, MD; Shoshana Shpitzen, MA; Shai Balag, MD; Elad Shemesh, MD; Shula Witkow, RD, MPH; Osnat Tangi-Rosental, BA; Yoash Chassidim, PhD; Idit F. Liberty, MD; Benjamin Sarusi, MSc; Sivan Ben-Avraham, RD, MPH; Anders Helander, PhD; Uta Ceglarek, PhD; Michael Stumvoll, MD; Matthias Blüher, MD; Joachim Thiery, MD; Assaf Rudich, MD, PhD; Meir J. Stampfer, MD, DrPH; Iris Shai, RD, PhD

Ann Intern Med. 13 October 2015,():  doi:10.7326/M14-1650

Background: Recommendations for moderate alcohol consumption remain controversial, particularly in type 2 diabetes mellitus (T2DM). Long-term randomized, controlled trials (RCTs) are lacking.

Objective: To assess cardiometabolic effects of initiating moderate alcohol intake in persons with T2DM and whether the type of wine matters.

Design: 2-year RCT (CASCADE [CArdiovaSCulAr Diabetes & Ethanol] trial). 

Setting: Ben-Gurion University of the Negev–Soroka Medical Center and Nuclear Research Center Negev, Israel.

Patients: Alcohol-abstaining adults with well-controlled T2DM.

Intervention: Patients were randomly assigned to 150 mL of mineral water, white wine, or red wine with dinner for 2 years. Wines and mineral water were provided. All groups followed a Mediterranean diet without caloric restriction.

Measurements: Primary outcomes were lipid and glycemic control profiles. Genetic measurements were done, and patients were followed for blood pressure, liver biomarkers, medication use, symptoms, and quality of life.

Results: Of the 224 patients who were randomly assigned, 94% had follow-up data at 1 year and 87% at 2 years. In addition to the changes in the water group (Mediterranean diet only), red wine significantly increased high-density lipoprotein cholesterol (HDL-C) level by 0.05 mmol/L (2.0 mg/dL) (95% CI, 0.04 to 0.06 mmol/L [1.6 to 2.2 mg/dL]; P < 0.001) and apolipoprotein(a)1 level by 0.03 g/L (CI, 0.01 to 0.06 g/L; P = 0.05) and decreased the total cholesterol–HDL-C ratio by 0.27 (CI, −0.52 to −0.01; P = 0.039). Only slow ethanol metabolizers (alcohol dehydrogenase alleles [ADH1B*1] carriers) significantly benefited from the effect of both wines on glycemic control (fasting plasma glucose, homeostatic model assessment of insulin resistance, and hemoglobin A1c) compared with fast ethanol metabolizers (persons homozygous for ADH1B*2). Across the 3 groups, no material differences were identified in blood pressure, adiposity, liver function, drug therapy, symptoms, or quality of life, except that sleep quality improved in both wine groups compared with the water group (P = 0.040). Overall, compared with the changes in the water group, red wine further reduced the number of components of the metabolic syndrome by 0.34 (CI, −0.68 to −0.001; P = 0.049).

Limitation: Participants were not blinded to treatment allocation.

Conclusion: This long-term RCT suggests that initiating moderate wine intake, especially red wine, among well-controlled diabetics as part of a healthy diet is apparently safe and modestly decreases cardiometabolic risk. The genetic interactions suggest that ethanol plays an important role in glucose metabolism, and red wine's effects also involve nonalcoholic constituents.

Is Milk Thistle beneficial to your liver if you drink too much alcohol?

About Milk Thistle

Milk thistle (silymarin) is a dietary supplement traditionally used to treat and prevent damage to the liver. There has been some research of mixed quality to assess the potential of Milk Thistle in treating and preventing liver damage from alcohol and from other causes which has shown a potential benefit. However it is clear more robust, placebo controlled clinical studies are needed.

What is Milk Thistle?

Silybum marianum (milk thistle) is an annual or biannual plant of the Asteraceae family. This fairly typical thistle has red to purple flowers and shiny pale green leaves with white veins. Originally a native of Southern Europe through to Asia, it is now found throughout the world. The medicinal parts of the plant are the ripe seeds.

Other common names for this species include Blessed Milk Thistle, Marian Thistle, Mary Thistle, Saint Mary's Thistle, Mediterranean milk thistle, Variegated Thistle and Scotch thistle.

Milk Thistle gets its name from the milky sap that comes out of the leaves when they are broken. The leaves also have unique white markings that, according to legend, were the Virgin Mary’s milk. Milk thistle shouldn't be confused with Blessed Thistle (Cnicus benedictus).

Traditional milk thistle extract is made from the seeds, which contain approximately 4–6% silymarin. The extract consists of about 65–80% silymarin (a flavonolignan complex) and 20–35% fatty acids, including linoleic acid.

Silymarin is a complex mixture of polyphenolic molecules, including seven closely related flavonolignans (silybin A, silybin B, isosilybin A, isosilybin B, silychristin, isosilychristin, silydianin) and one flavonoid (taxifolin). 

In clinical trials silymarin has typically been administered in amounts ranging from 420–480 mg per day in two to three divided doses. However higher doses have been studied, such as 600 mg daily in the treatment of type II diabetes and 600 or 1200 mg daily in patients chronically infected with hepatitis C virus.

An optimal dosage for milk thistle preparations has not been established. 

Clinical efficacy of Milk Thistle - does Milk Thistle work and is it safe?

A thorough review of the literature on milk thistle current to the year 2000 can be found at Milk Thistle: Effects on Liver Disease and Cirrhosis and Clinical Adverse Effects which is located here. This review finds that the evidence to date is strongly suggestive that milk thistle helps heal or cleanese the liver, although studies to date are not yet conclusive.

A more recent review of the literature can be found in Saller (2008) which concluded, "Based on the available clinical evidence it can be concluded - concerning possible risks /probable benefits - that it is reasonable to employ silymarin as a supportive element in the therapy of Amanita phalloides poisoning but also (alcoholic and grade Child 'A') liver cirrhosis. A consistent research programme, consolidating existing evidence and exploring new potential uses,would be very welcome."

Side effects of Milk Thistle

On the available evidence, which is not exhaustive, Milk Thistle (Silymarin) is likely to be safe for most adults. However, it sometimes causes a laxative effect. Other less common side effects are nausea, diarrhoea, indigestion, intestinal gas, bloating, fullness or pain, and loss of appetite.

Special Precautions & Warnings:

Pregnancy and breast-feeding: Not enough is known about the use of milk thistle during pregnancy and breast-feeding. Stay on the safe side and avoid use.

Allergy to ragweed and related plants: Milk thistle may cause an allergic reaction in people who are sensitive to the Asteraceae/Compositae plant family. Members of this family include ragweed, chrysanthemums, marigolds, daisies, and many others. If you have allergies, be sure to check with your doctor or pharmacist before taking milk thistle.

Hormone-sensitive conditions such as breast cancer, uterine cancer, ovarian cancer, endometriosis, or uterine fibroids: Extracts from Milk Thistle plant might act like oestrogen. If you have any condition that might be made worse by exposure to estrogen, don’t use these extracts. In contrast, the more commonly used milk thistle seed extracts do not seem to act like oestrogen.

Milk Thistle Products

You can buy Milk Thistle in the form of tablets, capsules and drops either as a single ingredient in different strengths or as a combination with other liver cleansing herbs. Popular brands include Vogel, Solgar and Schwabe.

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Should I take Milk Thistle supplements regularly?

The jury is still out on whether it really works, but Milk Thistle appears to have low toxicity and studies are suggestive of a positive effect on the liver and have a protective effect against alcohol consumption. The benefits therefore appear to outweigh any risks. But do your own research before taking this supplement and this is not a recommendation to use Milk Thistle. 


Lawrence V, Jacobs B, Dennehy C, et al. (2000) Milk thistle: effects on liver disease and cirrhosis and clinical adverse effects. Evidence Report/Technology Assessment No. 21. AHRQ Publication No. 01-E025. Rockville, MD. 

Rainone F. (2005).Milk thistle. Am Fam Physician. 72(7), 1285-8. 

Saller R, Brignoli R, Melzer J, Meier R. (2008). An updated systematic review with meta-analysis for the clinical evidence of silymarin. Forsch Komplementmed. 15(1), 9-20. 

Tamayo C, Diamond S. (2007). Review of clinical trials evaluating safety and efficacy of milk thistle (Silybum marianum [L.] Gaertn.). Integr Cancer Ther. 6(2), 146-57. 

Further clinical evidence points to benefits of resveratrol (found in wine) in preventing Alzheimer's disease

old man drinking wine

There is always so much bad publicity and hype about the dangers of drinking alcohol (liver disease, premature death) that the benefits of moderate drinking (2-3 glasses of wine a day) on reducing your risk of death (mortality) is often forgotten by the media. Red wine from certain regions of the world, grapes with thick skins, appear to have clear health benefits despite what the press have to say.

So it was good to come across another positive study in relation to a chemical found in wine and its potential benefits in preventing dementia and Alzheimer's disease. Prescription wine, here we come!

The blog has written about the potential health benefits of resveratrol in wine and a new study published recently in Neurology gave further evidence of the potential effects of polyphenols in Alzheimer's disease. See earlier article here.

The accumulation of amyloid plaques in the brain is often used as a biomarker for Alzheimer’s disease. But there is still plenty of debate amongst Alzheimer's experts on the role of amyloid plaques and whether they cause the disease or are just a result of other more destructive mechanisms. However, for now amyloid levels in the brain are a good indicator for progression.

The latest Resveratrol and Alzheimer's disease study Georgetown University, Washington

Scientists at Georgetown University Medical Centre in Washington DC  gave 119 participants with mild to moderate symptoms of Alzheimer's either one gram of synthesised resveratrol twice a day in oral form for 12 months, or a placebo containing no active ingredient. Note that the resveratrol was synthesised since the dose was many magnitudes higher than that found in wine or foods.

The study published on September 11th in 119 participants concluded that it " provides Class II evidence that for patients with AD resveratrol is safe, well-tolerated, and alters some AD biomarker trajectories."  Over the 12 months of the study, those in the placebo group showed signs that their Alzheimer’s was progressing, including reductions in in the level of amyloid beta protein in their blood (where it probably accumulates in the brain causing the classic symptoms of dementia). Those taking resveratrol, showed little or no change in amyloid beta levels in their blood and by implication had less accumulation of amyloid in the brain tissues where it can cause damage.

What is resveratrol?

Resveratrol is found in the skin of red grapes as well as in dark chocolate and in certain fruits and vegetables such as raspberries. For example, the Malbec grape, used extensively in Argentina and the Tannat grape found in Uruguay, have thick skins and contains high levels of resveratrol. Vine grapes grown in cooler climates have higher resveratrol levels than those from warmer climates such as Australia.

What does this new study mean - can red wine really prevent you from getting Alzheimer’s disease?

The jury is still out but the evidence continues to mount that resveratrol appears to have a positive impact, without any major side effects even at the very high doses used in this latest study. Doses many times higher than found in wine or raspberries! The good news is that even at high doses, there does not seem to be any negative impact.

The question many scientists are asking themselves is what is the mechanism by which resveratrol might protect against dementia and Alzeheimer's.

 In laboratory experiments, extreme low calorie diets have reduced age-related diseases and it is has been postulated that this might occur because of the activation of enzymes called sirtuins, which may alter gene expression and protect against the effects of stress, including a poor diet.

Resveratrol may activate sirtuins just like these extreme low calorie diets but the evidence is not conclusive.

Summary of the implications

This latest study published this month on the potential effect of resveratrol adds fuel to the fire about the health benefits of chemicals like this found in fruit, wine and even dark chocolate at relatively low levels. Other small clinical studies have also demonstrated benefits of resveratol on human health measures and overall drinking wine has a definite benefit in reducing mortality compared with teetotalers (in  moderation). For many years, scientists have proposed that the very high life expectancy in certain parts of France despite high saturated fat diets, the so called French Paradox, is related to daily consumption of wine in the population. 

The Washington study adds yet more positive data to the debate about resveratrol and hopefully a large scale study will confirm these initial promising findings.

More details on the Washington clinical are below:

A randomized, double-blind, placebo-controlled trial of resveratrol for Alzheimer diseaseR. Scott Turner, MD, PhD,  Ronald G. Thomas, PhD, Suzanne Craft, PhD,  et al
September 11th 2015
For the Alzheimer's Disease Cooperative Study


Objective: A randomized, placebo-controlled, double-blind, multicenter 52-week phase 2 trial of resveratrol in individuals with mild to moderate Alzheimer disease (AD) examined its safety and tolerability and effects on biomarker (plasma Aβ40 and Aβ42, CSF Aβ40, Aβ42, tau, and phospho-tau 181) and volumetric MRI outcomes (primary outcomes) and clinical outcomes (secondary outcomes).

Methods: Participants (n = 119) were randomized to placebo or resveratrol 500 mg orally once daily (with dose escalation by 500-mg increments every 13 weeks, ending with 1,000 mg twice daily). Brain MRI and CSF collection were performed at baseline and after completion of treatment. Detailed pharmacokinetics were performed on a subset (n = 15) at baseline and weeks 13, 26, 39, and 52.

Results: Resveratrol and its major metabolites were measurable in plasma and CSF. The most common adverse events were nausea, diarrhea, and weight loss. CSF Aβ40 and plasma Aβ40 levels declined more in the placebo group than the resveratrol-treated group, resulting in a significant difference at week 52. Brain volume loss was increased by resveratrol treatment compared to placebo.

Conclusions: Resveratrol was safe and well-tolerated. Resveratrol and its major metabolites penetrated the blood–brain barrier to have CNS effects. Further studies are required to interpret the biomarker changes associated with resveratrol treatment.

Classification of evidence: This study provides Class II evidence that for patients with AD resveratrol is safe, well-tolerated, and alters some AD biomarker trajectories. The study is rated Class II because more than 2 primary outcomes were designated. © 2015 American Academy of Neurology