Part III: Alcohol and breast cancer – The Case for Action by Erik Skovenborg, MD

Sir Austin Bradford Hill, an English epidemiologist and statistician, pioneered the randomised clinical trial and, together with Richard Doll, demonstrated the connection between cigarette smoking and lung cancer. To anyone involved in medical statistics, epidemiology or public health, Bradford Hill was simply the world’s leading medical statistician. Hill’s seminal 1965 Presidential Address to the Section of Occupational Medicine of the Royal Society of Medicine, where he presented what are now commonly called the “Bradford-Hill criteria”, offered a timeless insightful analysis about how to interpret our observations. His Presidential address closed with important observations about critical methodological and policy issues about how to interpret conclusions about causality in “real life” situations (Bradford Hill A. The Environment and Disease: Association or Causation? Proc R Soc Med 1965;58(5):295-300.):
“Finally, in passing from association to causation I believe in ‘real life’ we shall have to consider what flows from that decision. On scientific grounds we should do no such thing. The evidence is there to be judged on its merits and the judgment (in that sense) should be utterly independent of what hangs upon it – or who hangs because of it. But in another and more practical sense we may surely ask what is involved in our decision. In occupational medicine our object is usually-to take action. If this be operative cause and that be deleterious effect, then we shall wish to intervene to abolish or reduce death or disease.
While that is a commendable ambition it almost inevitably leads us to introduce differential standards before we convict. Thus on relatively slight evidence we might decide to restrict the use of a drug for early-morning sickness in pregnant women. If we are wrong in deducing causation from association no great harm will be done. The good lady and the pharmaceutical industry will doubtless survive.
On fair evidence we might take action on what appears to be an occupational hazard, e.g. we might change from a probably carcinogenic oil to a non-carcinogenic oil in a limited environment and without too much injustice if we are wrong. But we should need very strong evidence before we made people burn a fuel in their homes that they do not like or stop smoking the cigarettes and eating the fats and sugar that they do like. In asking for very strong evidence I would, however, repeat emphatically that this does not imply crossing every ‘t’, and swords with every critic, before we act.
All scientific work is incomplete – whether it be observational or experimental. All scientific work is liable to be upset or modified by advancing knowledge. That does not confer upon us a freedom to ignore the knowledge we already have, or to postpone the action that it appears to demand at a given time. Who knows, asked Robert Browning, but the world may end tonight? True, but on available evidence most of us make ready to commute on the 8.30 next day.”
Should women should fear breast cancer after enjoying one glass of wine?
The evidence for a causal association between a light to moderate alcohol consumption and risk of breast cancer was reviewed in Part I and II of “Alcohol and breast cancer – a study in weak associations”. Here we will focus attention on the evidence for a causal association between regular, light drinking, e.g. a glass of wine with your meal, and risk of breast cancer. “The association between alcohol and breast cancer is not strong and not necessarily causative, at least for moderate consumption.” (McPherson K. Moderate Alcohol Consumption and Cancer. Ann Epidemiol 2007;17:S46–S48.) Despite a dose-dependent association between alcohol and breast cancer risk, there is some uncertainty on the point of a possible threshold level of alcohol consumption above which the increased risk of breast cancer becomes clinically significant. ”But we should need very strong evidence before we made people burn a fuel in their homes that they do not like or stop smoking the cigarettes and eating the fats and sugar that they do like”, Sir Bradford Hill concluded in his seminal paper on association or causation. The question is: Do we have very strong evidence that women should fear breast cancer after enjoying one glass of wine?
Methodological problems with information on low level alcohol intake
• Underreporting (Part I): Underreporting of alcohol intake is a general and serious problem that has not been addressed in the reports from e.g. International Agency for Research on Cancer, World Health Organization, World Cancer Research Fund International and American Institute for Cancer Research. In a cohort study of cancer risk in participants reporting light–moderate drinking, the increased risk of cancer was concentrated in the stratum suspected of underreporting. (Klatsky et al. Moderate alcohol intake and cancer: the role of underreporting. Cancer Causes Control 2014;25(6):693-9.) In the important meta-analysis on alcohol, tobacco and breast cancer from 2002, the authors conclude: “Self-reported information on alcohol consumption is known to underestimate true consumption. Systematic under-reporting of consumption by both cases and controls would result in an overestimation of the relative risk of breast cancer for a given level of alcohol consumption. By contrast, random misclassification among both cases and controls would have the opposite effect, resulting in an underestimation of the relative risk. These two types of measurement error are inevitable, but counter-acting, and it is not possible to estimate their overall effect on the relative risks calculated here. Moreover, the shape of the dose-response relationship could be changed if, for example, heavy drinkers were more likely to under-report intake than moderate drinkers. Taken together, these reporting errors imply that some uncertainty remains about the true quantitative effect of an intake of a fixed amount of alcohol on the risk of developing breast cancer.” (Hamajima et al. Alcohol, tobacco and breast cancer – collaborative reanalysis of individual data from 53 epidemiological studies, including 58 515 women with breast cancer and 95 067 women without the disease. British Journal of Cancer 2002;87:1234-45.)
• Drinking pattern: No information on the pattern of intake was collected by Hamajima et al. and information on drinking patterns is almost non-existent in the evidence base for the CUP Expert Report 2018 ‘Alcoholic drinks and risk of cancer’. There are three important aspects of drinking pattern regarding the association of alcohol intake and risk of breast cancer: 1) Regular drinking versus binge drinking; 2) Drinking a moderate amount of alcohol spread over most days/week versus a few days/week; and 3) Effect of fasting versus drinking with food on ethanol bioavailability.
1) Regular drinking versus binge drinking. After controlling for cumulative alcohol intake, binge drinking is associated with increased breast cancer risk (Part I).
2) Drinking a moderate amount of alcohol spread over most days of the week versus few days per week. Generally, there are two measures of alcohol exposure: the number of alcoholic drinks per time period, and ethanol intake in grams or millilitres per time period. In The Million Women Study, for example, women were categorized into five groups according to the total number of alcoholic drinks that contained about 10 g alcohol consumed per week, as reported in the recruitment questionnaire. The categories used were 0, less than or equal to 2, 3-6, 7-14, or greater than or equal to 15 drinks per week. In conclusion the study found regular consumption of low to moderate amounts of alcohol by women increases the risk of e.g. breast cancer. In the abstract the wording is: “for every additional drink regularly consumed per day…” although The Million Women Study had no data on drinking pattern regarding a consumption of ≥7 drinks per week.
3) Effect of fasting versus drinking with food on ethanol bioavailability. The decreased bioavailability of ethanol consumed with food versus drinking on an empty stomach is not addressed by the Continuous Update Project Expert Report 2018 for the simple reason that most studies do not collect information about drinking culture. An example of the important effect of drinking with food is the results of The Million Women Study (Simpson RF et al. Alcohol drinking patterns and liver cirrhosis risk: analysis of the prospective UK Million Women Study. Lancet Public Health 2019;4:e41–48.): At every level of alcohol consumption, cirrhosis incidence was lower in women who usually drank with meals compared with those who did not. After adjusting for the amount of alcohol consumed and potential confounding factors the relative risk for cirrhosis associated with usually drinking with meals compared with not drinking with meals was 0·69 (95% CI 0.62-0.77). An Italian case-control study of alcohol and breast cancer among women under the age of 75 (250 cases, 499 controls) was conducted in the Province of Vercelli, where wine drinking is widespread and wine is consumed mainly during meals. The alcohol questionnaire was structured by meals. In comparison with abstainers (30% of women in the study) and after adjustment for potential confounders, no appreciable breast cancer association was evident for alcohol consumptions below 30 g/day. (Toniolo P et al. Breast cancer and alcohol consumption: a case-control study in northern Italy. Cancer Res 1989;49:5203-06.)
The systemic availability of ethanol – effects of First Pass Metabolism (FPM)
Human Class I Alcohol Dehydrogenase (ADH) has a low Km = 0.05-0.1 g/L for ethanol as substrate. Km (Michaelis constant for the affinity of an enzyme for its substrate) is the concentration of substrate which permits the enzyme to achieve half the maximum rate of reaction (Vmax.). When BAC exceeds 2 x ADH Km (0.1-0.2 g/L), the enzyme is saturated with substrate and is working at maximum velocity. (Bosron WF et al. Relationship between kinetics of liver alcohol dehydrogenase and alcohol metabolism. Pharmacology Biochemistry and Behavior 1983;18 (Suppl 1):223-27.) The hepatic ADH enzyme therefore becomes saturated after ≥0.2 g alcohol/kg bodyweight = just a couple of drinks. When the ADK enzyme is saturated, the rate of disappearance of ethanol from blood becomes virtually independent of the prevailing blood-ethanol concentration (zero-order kinetics). Consequently, the rate at which ethanol molecules reach the hepatic ADH enzymes becomes a major determinant of systemic availability. The slower the rate of absorption of ethanol molecules from the stomach to the hepatic portal vein, the smaller the amount of ingested alcohol that escapes first pass hepatic metabolism and enter the systemic circulation = a small AUC (area under the curve) for a given dose. The swifter the rate of absorption of ethanol molecules from the stomach to the hepatic portal vein, the larger the amount of ingested alcohol that escapes first pass hepatic metabolism and enter the systemic circulation = a larger AUC for a given dose. (Levitt MD, Levitt DG. The critical role of the rate of ethanol absorption in the interpretation of studies purporting to demonstrate gastric metabolism of ethanol. J Pharmacol Exp Ther 1994;269:297-304.)
The decrease of alcohol bioavailability via FPM is dependent on the rate of gastric emptying and the dose of alcohol. Liquids typically leave your stomach quickly; the half-time to gastric emptying (T1/2) after 300 ml black tea was 22.7 (95% CI 12.7-40.9) minutes. (Hillyard S et al. Does adding milk to tea delay gastric emptying? British Journal of Anaesthesia 2014;112 (1): 66-71.) After a steamed-rice with microwaved egg meal gastric emptying half time (T1/2) was 68.7 (95% CI 45.1-107.8) minutes. (Vasavid P et al. Normal Solid Gastric Emptying Values Measured by Scintigraphy Using Asian-style Meal: A Multicenter Study in Healthy Volunteers. J Neurogastroenterol Motil 2014;20:371-78) Increasing the energy content of the meal of fixed composition progressively delays the half time to gastric emptying: T1/2 = 57, 70, and 95 min. for 150 kcal, 300 kcal and 600 kcal, respectively. (Velchik MG at al. The effect of meal energy content on gastric emptying. J Nucl Med 1989;30(6):1106-10.) Intake of 400 ml beer (4.7 %vol), 200 ml red wine (13.7 %vol) or 100 ml whisky (43.5 %vol) or matching volumes of isotonic glucose solution after a solid 1485 kJ meal caused significant slowdown of gastric emptying (T1/2) in minutes: Beer 206 ±11 vs control 155 ±7; red wine 209 ±11 vs control 144±6; and whisky 248 ±16 vs control 144 ±8. (Kasicka-Jonderko A et al. Potent inhibitory effect of alcoholic beverages upon gastrointestinal passage of food and gallbladder emptying. J Gastroenterol 2013;48:1311-23.)
The FPM is increased after a substantial meal compared to a light meal. Forty-five ml of 95% alcohol, diluted to 150 ml with orange juice, was taken orally by six adult male volunteers under the following conditions: A (fasting), B (following a light breakfast) and C (following a heavy breakfast). Using treatment A (fasting) as a reference, the average area under the blood alcohol, time curve was reduced by 36% after a light breakfast and by 63% after a heavy breakfast. (Lin Y et al. Effects of solid food on blood levels of alcohol in man. Res Commun Chem Pathol Pharmacol 1976;13(4):713-22.) In a study with a low dose of alcohol (0.15 g alcohol/kg bodyweight = a 10 g dose for a woman weighing 66 kg) administered in a 5% dextrose solution (5 g/100 ml) perorally or intravenously 1 hour after a standard breakfast, FPM reduced the amount of ingested alcohol entering the systemic circulation (AUC) by 73%. (Fig. 1) When alcohol was given in the fasting state, there was no significant difference in blood ethanol level between the peroral and the intravenous dose. (DiPadova C et al. Effects of Fasting and Chronic Alcohol Consumption on the First-Pass Metabolism of Ethanol. Gastroenterology 1987;92:1169-73.)
Fig. 1. Reduced systemic bioavailability (AUC = area under the curve) of a low dose of alcohol taken with a meal (red line) vs alcohol intake on an empty stomach (black line). The figure is redrawn after DiPadova et al.’s data.
A mathematical model for calculating the systemic availability of alcohol was used by Levitt to illustrate the dramatic effect of a concomitant meal on the blood levels resulting from an oral intake. The figure shows the blood alcohol levels for an oral intake of 12 g of ethanol equivalent to one 12 ounce can of beer (red line); and 2 (green) or 3 (blue) times this dose, all ingested for a 20 minute time period either with (“fed”) or without (“fasted”) a meal. (Fig. 2) Ingestion of a coincident meal with the ethanol can reduce the peak blood level by about 4 fold at low doses. (Levitt DG. PKQuest: measurement of intestinal absorption and first pass metabolism – application to human ethanol pharmacokinetics. BMC Clinical Pharmacology 2002;2:4.)
Fig. 2. The BAC curves are redrawn after data from the PKQuest model study by Levitt.
“The mechanisms whereby alcohol may increase the risk of breast cancer remains uncertain” the CUP Update Report 2018 concludes. “The potential mechanisms affecting breast carcinogenesis are diverse. Alcohol can also be metabolized in breast tissue to acetaldehyde producing reactive oxygen species associated with DNA damage.” (World Cancer Research Fund/American Institute for Cancer Research, Continuous Update Project Expert Report 2018. Alcoholic drinks and the risk of cancer. Available at dietandcancerreport.org.) For alcohol metabolism in breast tissue to take place, systemic availability of alcohol is necessary. For a 170 cm height female weighing 66 kg the Widmark “r” factor would be 0.66 and her volume of distribution (body water) would be 66 x 0.66 = 43.56 litres. (Barbour A. Simplified estimation of Widmark “r” values by the method of Forrest. Science & Justice 2001;41(1):53-54.) Assuming a regular, moderate intake of alcohol an average alcohol elimination rate from blood would be 15 mg/100 ml/h. Consequently the woman would be able to metabolise 15 mg alcohol x 435.6 = 6534 mg (6.5 g) alcohol per hour.
When BAC exceeds 0.1-0.2 g/L (= 2 x Km), the hepatic ADH enzyme is saturated with substrate and at a higher BAC level some of the ethanol molecules that reach the hepatic ADH enzymes through the portal vein are not metabolized, and this fraction of ethanol molecules reaches the systemic circulation. The amount of alcohol leading to a BAC of 0.1-0.2 g ethanol/L is equivalent to 4.35-8.7 g ethanol in the female example mentioned above drunk within a few minutes on an empty stomach. When a 10 g dose of alcohol is taken during a meal (slowly, as small mouthfuls during 20-30 min.), BAC level will not exceed 0.1-0.2 g/L, the hepatic ADH enzyme will not be saturated, all ethanol molecules will undergo hepatic FPM and no (or very few) alcohol molecules will reach the breast tissue via systemic circulation.
Risk communication before and now
According to PubMed.gov, Albert J. Tuyns, a renowned French epidemiologist affiliated with the International Agency for Research on Cancer, Lyon, France, is the author of 27 papers on alcohol and cancer. In a chapter on cancer and alcoholic beverages in “Fermented Food Beverages in Nutrition” (Ed. Gastineau, Darby WJ, Turner TB. Academic Press, N.Y, 1979.) Tuyns in his summary considered what could be gained if a given population did not consume more alcohol and tobacco beyond a certain threshold. “In the case of Ille et Vilaine, if people kept within the reasonable limits of 10 cigarettes and half a liter wine (i.e. 40 gm of ethanol) per day, the incidence rate of esophageal cancer would be cut by 6/7 of what it is now.” In a 2006 review on alcohol and cancer Boffetta & Hashibe suggested that “given the linear dose-response relation between alcohol intake and risk of cancer, control of heavy drinking remains the main target for cancer control. For example, the most recent version of the European code against cancer recommends keeping daily consumption within two drinks (i.e., 20-30 g alcohol) for men and one drink for women. Total avoidance of alcohol, although optimum for cancer control, cannot be recommended in terms of a broad perspective of public health, in particular in countries with high incidence of cardiovascular disease.” (Boffetta P, Hashibe M. Alcohol and cancer. Lancet Oncol 2006;7:149-56.) Gerald Shaper presented a similar opinion: “The is no evidence that occasional or light drinking, i.e. 1-2 drinks per day in men and 1 drink per day in women, has any untoward effects and most would accept that this level of alcohol intake provides both individual and social pleasure.” (Shaper AG. New baseline needed for alcohol and mortality studies. Addiction Research and Theory 2007;15:26-28.)
Today’s warnings from Major International Health Organizations are presented without any reservations:
• “There is no safe level of alcohol – the cancer risk starts to increase even with low levels of alcohol consumption. For instance, drinking the amount of alcohol you would find in just a single glass of wine every day caused more than 4600 breast cancer cases in women in the WHO European Region in 2018” (Alcohol and cancer in the WHO European Region: an appeal for better prevention. Copenhagen: WHO Regional Office for Europe; 2020.)
Most of the studies presented by the International Agency for Research on cancer have no data on drinking pattern. The information about intake of alcohol is most often collected as number of drinks/grams of ethanol per week. The postulate of a certain definite breast cancer risk per glass of wine per day is a hypothesis without evidence and a furthermore a hypothesis that disregards methodological issues like underreporting and bioavailability of alcohol.
“In the absence of definite proof, judgments about causation and public health recommendations are at least partially value laden, with both scientific and extrascientific values playing roles. Indeed, causal inference appears by this account to be more subjective than objective. Two recent examples are induced abortion in relation to breast cancer and alcohol in relation to breast cancer. In both cases, 2 different reviewers examined the same evidence at the same time using similar approaches to causal inferences and yet came to exactly opposite conclusions about causation and public health recommendations. These stark differences can best be explained by the different rules of inference assigned to the criteria (i.e., scientific values) and by extrascientific values such as wish bias, moral stances, or political positions regarding the acceptability or appropriateness of the exposure.” (Potischman N, Weed DL. Causal criteria in nutritional epidemiology. Am J Clin Nutr 1999;69(suppl):1309S–14S.). The “no safe level” message from WHO is an example of how generalized health risks lacking a clear evidence base can be officially promoted for the greater good of encouraging a healthier behaviour.
• “Current evidence does not identity a generally “safe” threshold for consumption of alcoholic drinks for breast cancer (pre and postmenopause)…” (World Cancer Research Fund/American Institute for Cancer Research, Continuous Update Project Expert Report 2018. Alcoholic drinks and the risk of cancer. Available at dietandcancerreport.org.)
The statement implies that it would be possible to establish a “safe threshold” for consumption of alcoholic drinks for breast cancer by scientific research. However, that is not possible, neither in theory nor in practice, to establish a “safe threshold” for activities that might involve a risk. As pointed out by Weinberg, transscientific questions are those that can be asked of science but cannot be answered by science, such as whether the amount of electromagnetic energy to which we are normally exposed increases the risk of cancer. In one of his examples, a study of the spontaneous mutation rate in mice exposed to 150 milirem of X-rays would require 8 billion mice in order to show an increase of one half percent (as extrapolated from much higher radiation doses, assuming a linear regression). In other words, a potentially answerable question is unanswerable in real life. (Weinberg AM. Science and transcience. Minerva 1972;10:207-222.)
An example from the outbreak of bovine spongiform encephalopathy (BSE or “mad cow disease) in Europe. Regarding risk of infection with the BSA Health Information for International Travel: 2007 (https://www.cdc.gov/prions/vcjd/risk-travelers.htlm) concluded: “The current risk for infection with the BSE agent among travelers to Europe is extremely small, if it exists at all.” Regarding prevention CDC suggested: “To reduce any risk of acquiring vCJD from food, concerned travelers to Europe or other areas with indigenous cases of BSE may consider either avoiding beef and beef products altogether or selecting beef or beef products, such as solid pieces of muscle meat (rather than brains or beef products like burgers and sausages) that might have a reduced opportunity for contamination with tissues that may harbor the BSE agent.” Please note that while the risk is “extremely small, if it exists at all”, no “safe threshold” for intake of burgers is suggested. An educated guess at that time compared the risk of eating a burger with the risk of riding 6 meters on a bicycle – a level of risk most people would find acceptable.
Another example: It has not been possible to identity a generally “safe” threshold for consumption of non-fermented milk products for breast cancer. In a prospective study of 33,780 women from the Swedish Mammography Cohort, high long-term non-fermented milk consumption was associated with increased ER+/PR+ breast cancer incidence, HR = 1.30 (95% CI:1.02 – 1.65) for the average of 1987 and 1997 intake of >2 vs. 0 servings/day and this increased risk was limited to women with BMI <25 kg/m2: HR = 1.55 (95%CI: 1.08 - 2.21). No significant associations with milk consumption were observed with ER-/PR- breast cancer. (Kaluza J et al. Long-term consumption of non-fermented and fermented dairy products and risk of breast cancer by estrogen receptor status − Population-based prospective cohort study. Clin Nutr 2021;40(4):1966-73.) Fraser et al. found similar results in a cohort study of 52 795 North American women. No clear associations were found between soy products and breast cancer, independently of dairy. However, higher intakes of dairy calories and dairy milk were associated with hazard ratios of 1.22 (95% CI: 1.05-1.40) and 1.50 (95% CI: 1.22-1.84), respectively, comparing 90th to 10th percentiles of intakes. Full fat and reduced fat milks produced similar results. Current guidelines for dairy milk consumption should be viewed with some caution. (Fraser GE et al. Dairy, soy, and risk of breast cancer: those confounded milks. Int J Epidemiol 2020;49(5):1526-37.)
• “Do as I do, think about cancer before you have a glass of wine.” (Dame Sally Davies, CMO)
New British guidelines were introduced in 2016 which said that men and women should drink no more than 14 units a week – equivalent to six pints of beer or seven glasses of wine – and some days should be free of alcohol altogether. The UK’s chief medical officers’ advice was based on research which showed that any amount of alcohol can increase the risk of cancer. The new guidelines were criticized for sending a message that miscommunicates the risks of drinking to the public. “Except for the strong willed minority who will quit drinking entirely, the warning that “no alcohol is safe” will probably be counterproductive, as people might be happy to cut down but not to eliminate alcohol completely. In addition, why should people try to adhere to the new limits rather than the old ones if they are being told that the new recommended levels are not safe?” (Shaw DM. Drunk on risk: how the chief medical officers’ alcohol guidelines are demonising drink. BMJ 2016;352:i1175.) The letter in BMJ went on the accuse the chief medical officers to be “drunk on risk”: “Good guidelines give balanced information on risk and let people make their own choices. It is scaremongering to say that there’s no safe amount when having a small or moderate amount increases risk only marginally. Sally Davies has even suggested that we should think about cancer every time we consider having a glass of wine; the chief medical officers seem to be drunk on risk and demonising drink.” (Donnelly L. Do as I do, think about cancer before you have a glass of wine, says chief medical office. Telegraph 2016. https://www.telegraph.co.uk/news/health/12136938/Doas-I-do-think-about-cancer-before-you-have-a-glass-of-wine-says-chief-medical-officer.html.)
Suggestions for future risk communication
A survey of 942 women in a screening mammography cohort sought to identify factors associated with women’s unwillingness to decrease their alcohol intake to decrease their breast cancer risk. Levels of unwillingness to decrease alcohol intake differed by age − women who were 60 years and older were twice as unwilling to decrease their alcohol intake compared to the younger women, and household income − women who had an annual household income of >$200,000 were 1.75 times more unwilling to decrease their alcohol intake compared to the less affluent women. (Matin J et al. Factors Associated with Women’s Unwillingness to Decrease Alcohol Intake to Decrease Breast Cancer Risk. J Prim Care Community Health 2021;12:21501327211000211.) The risk communication of the health agencies builds on the logic of ‘a will to health’, and some drinkers tend to prefer other rationales, associating alcohol use with socialisation, pleasure and relaxation. Understanding individual attitudes toward alcohol drinking and the influence of cultural and social factors will improve our assessment of the impact of alcohol drinking to tailor public health messages toward most susceptible population subgroups. (Scoccianti C et al. Female Breast Cancer and Alcohol Consumption. Am J Prev Med 2014;46(3S1):S16–S25.)
In an editorial with comments on a case-control study by Ferranoni et al., Klim McPherson observed that alcohol is clearly an integral part of many peoples civilized life. The advice given by Ferraroni et. al. was for pre-menopausal women who consume more than two drinks a day to consider a reduction in consumption. “Such a strategy would seem wise by any criterion, not least because of the known causative effects of alcohol on liver disease and digestive cancers.” McPherson wrote, adding: ”Clearly the notion, which is implicit in the 12% attributable risk figure, that all women should abstain from this prime cause of breast cancer, is neither sensible, achievable nor remotely justifiable on health grounds. The ACS study, for example, suggests that all cause mortality is a full 20% lower among middle aged women who drink one drink per day compared with women who abstain.” (McPherson K. Alcohol and breast cancer. Eur J Cancer 1998;34(9):1307-8.) A strategy for future risk communication about alcohol and breast cancer might underline the low risk of light drinking – especially light drinking with a meal − like a glass of wine or beer sipped slowly during the meal as opposed to drinking alcoholic beverages on an empty stomach.
Erik Skovenborg is a Danish physician with a special interest in the health benefits of moderate alcohol consumption. His published work includes In Vino Sanitas, 1990; Lead in Wine throughout the Ages, 1994; Wine and Health – Myths and Facts, 2000. Member of the Social, Scientific and Medical Council of AIM (Alcohol in Moderation) from 1992 and co-founder of the Scandinavian Medical Alcohol Board (SMAB) in 1994. Chairman of the 1996 Copenhagen “Health and Alcohol Symposium” and the 1998 Stockholm “Women and Alcohol Symposium”. For many years Erik Skovenborg has lectured extensively on alcohol and health to medical professionals and the general public and he is currently researching the effects of a moderate consumption of beer, wine and spirits.