The view was based on an evaluation of some 41 articles in the literature predominantly published from 1995 onwards. In essence, the article suggested that the literature on any potential effects of wine-derived phenolic compounds in cardioprotection was inconclusive, as were, perhaps, certain clinical data relating to the role of ethanol per se in cardioprotection. The article concludes with a recommendation for a "large-scale, randomised, clinical end-point trial of wine intake", and that the AHA "maintains its recommendation that alcohol use should be an item of discussion between the physician and patient." The authors of the article are cautious both in their evaluation of the literature and their subsequent conclusions and recommendationsthis is proper and prudent, given the known adverse effects of alcoholic beverages and the propensity for misuse within certain communities. However, there are some statements, which are more grey rather than the stated black and white.

Risk factors for cardiovascular disease include: a high body mass index; a diet high in fats and low in fruits, grains and vegetables; a lack of exercise; cigarette smoking; an unbalanced plasma cholesterol concentration; and a high blood pressure. What is quite correct, as stated by the authors, is that the diet and lifestyle of consumers of wine is generally related to less risk factors for cardiovascular disease, than for example, consumers of beer and spirits. That is, consumers preferring beer usually consume more alcohol, smoke more, exercise less, and consume more fatty foods and less fish, fruit and vegetables than do abstainers or consumers of wine. Consumers of spirits have the least favourable patterns and practices. Furthermore, wine, in particular, is generally consumed with food, slowly or over a longer period of time and with regularitynot episodicwhich would attenuate a high blood alcohol concentration, prolong any acute plasma antioxidative and antithrombotic effects, promote any chronic effects and prevent any rebound effects of the ethanol and phenolic components of the beverage.

A high dietary intake of flavonoids, irrespective of the source of the flavonoids is associated with a reduced risk from cardiovascular disease, which is not attenuated by adjustment for dietary and non-dietary risk factors. However, while tea, fruit and vegetables provide a significant dietary source of flavonoids, wine, which is integral to the diet of the Mediterranean countries whose populations have the lowest risk for cardiovascular disease, contributes significantly to the daily combined dietary antioxidant capacity of blood plasma. Furthermore, comparing the character-istic diet of France with that of the Mediterranean countries, wine consumption appears to be extremely important in countries, which have a higher intake of saturated fats and a lower intake of polyunsaturated fats, such as France.

Most of the earlier evidence of a differential role for wine was based on in vitro data. In vitro studies have shown that the wine-derived phenolic compounds may prevent and even reverse the oxidation of LDL. They have also shown that under certain conditions, the wine-derived phenolic compounds increase the antioxidant capacity of blood plasma and serum, and are, collectively and individually, 1020 fold more anti-oxidative than endogenous vitamin E, where wine does confer protection against the oxidation of LDL by free radicals in blood plasma, in particular when the plasma concentration of vitamin E was being depleted.

A question of considerable concern, however, has been whether these in vitro data reflect accurately what is happening in the human body. While approximately 90% of the alcohol component is readily absorbed across the small intestine into the blood stream, it has only been relatively recently established from in vivo data that the wine-derived phenolic compounds are absorbed into the blood stream in sufficient quantity to act as effective anti-oxidants. Eight in vivo studies have been undertaken to date and the results of these data are less clear cut than that of the in vitro studies. Six of the eight studies conducted have shown that the wine-derived phenolic compounds are active antioxidants in vivo. Any inconsistencies in the study results may reflect differences in study design and duration as well as in the analyses used to assess antioxidant activity. Indeed, significant antioxidant activity may only be observed following the medium- to long-term consumption of wine, although the phenolic compounds are absorbed in significant amount after the acute or short-term consumption of wine. In addition, the eighth in vivo study showed that while LDL was significantly protected from oxidation following the consumption of de-alcoholised red wine, it was not protected following the consumption of red wine per se. This implies that any anti-oxidant effects of the wine-derived phenolic compounds may be counteracted by the pro-oxidant effects of ethanol, as the hepatic metabolism of ethanol has previously been postulated to induce the oxidation of lipids, such as LDL. Thus wine may have a positive role in protecting against ethanol induced damage and diseases.

In conclusion, the authors are indeed proper and prudent in their conclusions that the data are inconclusive as to whether wine is equally or more cardioprotective compared to the other alcoholic beverages. Research is, however, continuing to make the grey more black and white, including large-scale, randomised, clinical end-point trials of wine intake. It is also prudent of the authors to advise that alcohol consumers consult with their physician, as age, gender and genetics are all known to influence the effects of alcohol on human health.

Creina Stockley is Health and Regulatory Manager of the Autralian Wine Research Institute and member of the AIM Editorial Board