Page last updated: October 26, 2017

AWRI report - WineHealth 2017 - Navigating the health effects of alcohol consumption  

Dan Johnson, MSc, PhD, MBA and Creina Stockley, MSc, PhD, MBA

In February, the WineHealth 2017 international wine and health conference was held in Spain, the eighth in a series held since 1996. Approximately 200 delegates debated and discussed the latest data presented on the health effects of alcohol consumption, and considered future research directions. This article provides a summary of the trends discussed at that conference.

Consumers of light to moderate amounts of alcoholic beverages have lower risk of cardiovascular disease, type 2 diabetes, dementia and all-cause mortality than non-drinkers or heavy drinkers.

The relationship between alcohol consumption and risk of cancer is more complex. For some cancers, any alcohol consumption increases the risk. For other cancers, heavy drinking increases the risk and for some cancers there is a reduced risk or no association with alcohol consumption.

Polyphenolic compounds present in wine, fruits and vegetables have many positive effects in the human body and may act in synergy with other dietary components, including alcohol.

Consuming alcohol as part of a Mediterranean-style diet combined with other healthy behaviours (non-smoking, healthy weight, regular exercise) provides the greatest protection against the major non-communicable diseases.

The next WineHealth conference will be held in 2019 at UC Davis, California.

Effects of alcohol consumption on non-communicable diseases

Non-communicable diseases (NCD) such as cardiovascular disease (CVD), cancers, diabetes and dementia are major causes of death and disability across the world. The World Health Organization (WHO) suggests that CVD currently account for the most NCD deaths, or 17.7 million people annually, followed by cancers (8.8 million), respiratory diseases (3.9 million), and diabetes (1.6 million). As such there is considerable interest in understanding the risk factors for these diseases and any potential preventative measures that can be taken to reduce their incidence and severity. Modifiable behaviours, such as tobacco use, physical inactivity, unhealthy diet and the harmful use of alcohol, all increase the risk of NCDs.

Numerous population-based studies have investigated the effects of consuming alcoholic beverages on the risk of these NCDs. Heavy alcohol consumption has been consistently shown to be a risk factor for cardiovascular disease, cancers, diabetes and dementia, while the health effects of light to moderate alcohol consumption (approximately 10 to 20 g alcohol/day) on the risk of NCDs continue to be considered by public health authorities. In Australia, one standard drink is approximately 10 g alcohol (Food Standards Australia New Zealand 2017). Although the majority of population-level studies have not differentiated between wine, beer and spirit consumption, studies at the individual level have focused on the different beverages.

Clinical studies are also being conducted to examine the effects of consuming light to moderate amounts of alcohol, and test tube and animal studies are exploring plausible potential biological mechanisms of actions for the effects observed.

Cardiovascular disease

Cardiovascular disease includes high blood pressure, heart attacks, coronary heart disease, heart failure and stroke, and is currently the leading cause of death (33% of all deaths) in Australia. Of the 200 population-based studies conducted over the past 40 years, most have concluded that the relationship between the consumption of alcoholic beverages and the risk of CVD is J-shaped for both men and women. Light to moderate alcohol consumers have approximately a 30% lower risk of CVD compared to non-drinkers and heavier consumers (Di Castelnuovo et al. 2006, Rehm et al. 2010).

While the inclusion of ex-drinkers in the non-drinking reference groups in many of these early studies may have increased the risk of disease for ‘current abstainers’ (Stockwell et al. 2016), a J-shaped curve has almost always been seen in more recent studies when only lifetime abstainers comprised the non-drinking category (Klatsky and Udaltsova 2007, Midlov et al. 2016, Ronksley et al. 2011). As of 2017, the vast majority of population-based studies show a J-shaped curve for the relationship between alcohol consumption and CVD and mortality. Protection against CVD and mortality is not seen for drinking levels beyond 30 to 40 g alcohol/day or for binge drinking patterns.

Dose effects vary for the different cardiovascular outcomes, with lowest risk of mortality from coronary heart disease and heart attacks occurring with 10 to 20 g alcohol/day, but the lowest risk of mortality from ischaemic stroke occurring with less than 10 g alcohol/day (Ronksley et al. 2011). When alcoholic beverages are broken down by type, no statistically significant association is found between spirits consumption and CVD risk. However, both wine and beer show a similar J-shaped curve to that for alcohol overall. This may be reasonably explained by a combined effect of the alcohol present in both and of the different but similarly beneficial phenolic compounds in the two beverages (Costanzo et al. 2010).

In addition to the established biomarkers for CVD risk such as cholesterol concentration, blood flow and blood pressure, low grade inflammation was recently recognised as another risk factor for CVD as well as for cancer and neurodegenerative diseases. Wine-derived phenolic compounds can act to reduce low grade inflammation (Bonaccio et al. 2017, Gresele et al. 2011) as well as positively influence the other key biomarkers for CVD risk.

Diabetes

Diabetes mellitus is a set of related diseases in which the body cannot regulate the amount of glucose in the blood. Diabetics either do not produce any or enough insulin to regulate their blood glucose level (type 1 diabetes) or their body is less sensitive to the effects of insulin and increasingly ineffective at regulating their blood glucose levels (type 2 diabetes). Type 2 diabetes accounts for more than 85% of all incidences of diabetes and is currently the fifth highest cause of death in Australia (Australian Bureau of Statistics 2016).  High blood glucose levels promote the development of atherosclerosis (build-up of lipid deposits inside the arteries), high blood pressure and high blood lipid levels, which increase the risk of a heart attack or stroke.

Similar to that for CVD, a J-shaped curve is seen for the relationship between the consumption of alcoholic beverages and risk of type 2 diabetes (Koppes et al. 2005, Tresserra-Rimbau et al. 2016). A 30% reduction in risk of type 2 diabetes occurs with light to moderate alcohol consumption, as well as for risk of heart attacks among type 2 diabetics. Reduced risk is also associated with a high intake of phenolic compounds, which are found in wine as well as in fruits and vegetables (Chiva-Blanch et al. 2013, Tresserra-Rimbau et al. 2013).

The primary protective effect of alcoholic beverages on the development of type 2 diabetes has been attributed to increasing insulin sensitivity, and reducing the spike in blood glucose (glycaemic response) that occurs after eating (Beulens et al. 2008, Joosten et al. 2008). Wine produces the greatest effect on blood glucose compared to beer and spirits, reflecting the fact that wine contains compounds other than alcohol that are physiologically relevant (Brand-Miller et al. 2007).

Light to moderate alcohol consumers, and particularly wine consumers, also appear to have a lower risk of developing metabolic syndrome which includes abdominal obesity, insulin resistance, low concentration of high density lipoprotein (HDL) cholesterol and high blood pressure (Tresserra-Rimbau et al. 2015). Metabolic syndrome is associated with an increased risk of developing both diabetes and CVD.

Cancers

The relationship between the consumption of alcoholic beverages and cancer is complex (Breslow et al. 2011, Cao and Giovannucci 2016). For example, the consumption of alcoholic beverages appears to linearly increase the risk of cancers of the upper aerodigestive tract (UADT; mouth, pharynx, larynx and oesophagus), colorectum and female breast, particularly when more than 25 to 30 g alcohol/day is consumed (Bagnardi et al. 2013, Bagnardi et al. 2015, Klarich et al. 2015). These cancers are specifically referred to as alcohol-related cancers. Food consumption at the time of drinking may lessen the risk (Dal Maso et al. 2002).

There appears to be a threshold (>50 g/day) above which alcohol consumption increases the risk of cancers of the stomach, liver, gallbladder, pancreas and lung. The consumption of wine (but not other alcoholic beverages) appears to be inversely associated with risk of kidney cancer, Hodgkin’s and non-Hodgkin’s lymphoma.

While the alcohol component of wine is carcinogenic, a Western Australian study suggests that a diet high in flavonoids sourced from tea, chocolate, fruit, vegetables and red wine may be associated with reduced risk of cancer, as well as that of CVD and overall mortality (Bo et al. 2016, Ivey et al. 2015). Wine-derived resveratrol as well as catechin, gallic acid and quercetin all appear to have potentially preventative effects, especially for colon cancer, which is the second most common cancer in Australia. With a grant from Cancer Australia, the AWRI is working in partnership with The Royal Melbourne Hospital to investigate the impact of daily consumption of resveratrol-enhanced wine on the risk of colorectal cancer. Potential mechanisms of action for this apparent anti-carcinogenic effect include protection of cells and DNA from damage leading to cancer, preventing damaged DNA replication and damaged cell growth, as well as initiating the death of damaged cells.

Of all lifestyle factors related to cancer, the attributable risk for tobacco use is 20.1%, physical inactivity 5.6%, body mass 3.9%, and alcohol consumption 3.1% (Begg et al. 2007, Begg et al. 2008). Synergies are also observed between alcohol consumption and other lifestyle choices. Recent studies on alcohol consumption and the risk of cancers of the UADT suggest that tobacco use is the most important factor in the risk of these cancers, and that the risk is enhanced among those who also consume two or more alcoholic drinks per day. Alcohol consumption alone among non-smokers had little effect on the risk, except for oesophageal cancer (Anantharaman et al. 2011, Dal Maso et al. 2016, Hashibe et al. 2009, Szymanska et al. 2011).

For the relationship between alcohol consumption and breast cancer, consumption pattern may modify risk, with consumption of four to five drinks per session increasing risk by 50% compared to only one drink per session. Broadly speaking, increased risk of cancers appears most related to alcohol consumption above low to moderate levels.

Dementias

The collective scientific word for the mental processes of thinking, remembering, reasoning, judging and learning is ‘cognitive function’. Dementia is a form of cognitive change or impairment (dys-function) where a person loses the ability to think, remember and reason due to physical changes in the brain.

Cognitive decline and dementias such as Alzheimer’s disease appear to be triggered by a range of factors including depletion of antioxidants and inflammation. Risk factors for vascular dementia also include high blood pressure and coronary heart disease. In the later stages of dementia, the associated cognitive impairment creates total dependency, such that dementias are the single greatest cause of disability in Australians aged 65 years or older, and the third leading cause of disability burden overall. Dementias are also currently the second highest cause of death in Australia. As there is no cure, identification of factors associated with preservation of cognitive function could lead to substantial improvements in the quality of life in older Australians.

A J-shaped relationship between alcohol consumption and the risk of cognitive decline and development of dementias has been consistently observed (Ilomaki et al. 2015). Light to moderate alcohol consumption appears to reduce the risk of cognitive impairment, although heavy consumption is toxic. This relationship is observed for younger, middle-aged and older consumers. There is also a relationship between the effects of alcoholic beverages on the cardiovascular and neurological systems, given that reducing the risk of hardening and narrowing of the arteries and coronary heart disease also lowers the risk of cognitive impairment.

The amount of alcohol generally associated with protection against dementias appears to be up to 30 g alcohol daily, where wine may have a greater effect than beer or spirits, although this finding is based on a relatively small number of studies (Neafsey and Collins 2011, Xu et al. 2017). There are also multiple plausible biological mechanisms for wine-derived phenolic compounds to act on the accumulations of protein in the brain which are present in Alzheimer’s disease (Pasinetti 2012).

Mortality from all causes

The J-shaped relationship with the consumption of alcoholic beverages also applies to the risk of death from all causes, with an approximate 20% lower risk of death for light to moderate alcohol consumers compared with non-drinkers (Corrao et al. 2004, Costanzo et al. 2011). Risk increases, however, with consumption over approximately 40 to 60 g alcohol/day (Figure 1). This relationship is evident after controlling for known socio-demographic factors, genetic factors, lifestyle factors such as smoking, diet, and exercise, and diseases such as diabetes and previous coronary heart disease. That is, the observed effect of light to moderate alcohol consumption cannot be attributed to any of these other factors (Behrens et al. 2011, Dai et al. 2015, Midlov et al. 2016).

Figure 1. Relative risk of total mortality (95% confidence interval) and alcohol consumption extracted from 56 studies using fixed- and random-effects models (Di Castelnuovo et al. 2006).

Wine as part of daily diet and lifestyle

A series of large longitudinal studies looking at nutrition and healthy ageing in Australia (Dubbo Study of the Elderly), Italy (Moli-Sani) and Spain (PrediMed) have all shown that the inclusion of moderate alcohol consumption as part of a healthy diet and lifestyle reduces the risk of NCDs. Alcohol and phenolic compounds present in wine and beer may act in synergy with each other and with other dietary components, meaning that total diet may be more important than a single dietary component (Buil-Cosiales et al. 2016, Estruch et al. 2013).

Subjects in large population studies who are non-smokers, are not obese, eat a Mediterranean-style diet, and get regular exercise have much lower risk of NCDs and total mortality, whether or not they consume alcoholic beverages. Mukamal et al. (2006) observed, however, that regardless of other ‘healthy’ lifestyle factors, moderate consumption of alcoholic beverages provided greater reduction in risk of these diseases than was seen for the other factors in isolation (Mukamal et al. 2006).

A major new clinical study

The definitive experiment to determine any clinical association is a double-blind placebo-controlled clinical study. No long-term experimental study of the effects of alcohol consumption on risk of any chronic disease has, however, been performed. In September 2016, the US National Institute on Alcohol Abuse and Alcoholism received funding to conduct a large, international, randomised but unblinded clinical trial of the effects of alcoholic beverages on cardiovascular diseases and diabetes. Its aim is to better determine the strengths of relationships observed to date in population studies, the results of which will undoubtedly influence subsequent alcohol drinking guidelines (Mukamal et al. 2016). Australia is striving to participate in this study.

Looking at the big picture

The relationships between alcohol consumption and risk of CVD, dementias and diabetes are all J-shaped, with lower risk for low to moderate alcohol consumers than either abstainers or heavy drinkers. The relationship for alcohol-related cancers is different, with alcohol consumption linearly increasing risk. When all-cause mortality is considered, the J-shaped curve is seen again, with light to moderate alcohol consumers having reduced risk of death from all causes (Chiva-Blanch et al. 2013, Ferrari et al. 2014, Howie et al. 2011). This association is dependent, however, on both the amount and pattern of consumption, and may be modified by patterns such as binge drinking (Bobak et al. 2016, Graff-Iversen et al. 2013).

In addition to this population-based data, the accumulating experimental evidence continues to support an apparent role for light to moderate alcohol consumption in preventing many NCDs.

Acknowledgements

This work is supported by Australia’s grapegrowers and winemakers through their investment body Wine Australia and matching funds from the Australian Government. The AWRI is a member of the Wine Innovation Cluster in Adelaide. The authors would like to thank Prof. R. Curtis Ellison, MD, Professor of Medicine and Public Health, Boston University School of Medicine, for his comments on this paper. Ella Robinson is thanked for editorial assistance and Anne Lord is thanked for assistance with the references.

Reproduced with kind permission from the [Australian] Wine & Viticulture Journal.

References

Anantharaman, D., Marron, M., Lagiou, P., Samoli, E., Ahrens, W., Pohlabeln, H., Slamova, A., Schejbalova, M., Merletti, F., Richiardi, L., et al. 2011. Population attributable risk of tobacco and alcohol for upper aerodigestive tract cancer. Oral Oncol. 47(8): 725-731.

Australian Bureau of Statistics. 2016. 3303.0 - Causes of Death, Australia, 2014. http://www.abs.gov.au/ausstats/abs@.nsf/Lookup/by%20Subject/3303.0~2014~Main%20Features~Key%20Characteristics~10054

Begg, S., Vos, T., Barker, B., Stevenson, C., Stanley, L., Lopez, A.D. 2007. The burden of disease and injury in Australia 2003. Australian Institute of Health and Welfare: Canberra, ACT.

Begg, S.J., Vos, T., Barker, B., Stanley, L., Lopez, A.D. 2008. Burden of disease and injury in Australia in the new millennium: measuring health loss from diseases, injuries and risk factors. Med. J. Aust. 188(1): 36-40.

Behrens, G., Leitzmann, M.F., Sandin, S., Lof, M., Heid, I.M., Adami, H.O., Weiderpass, E. 2011. The association between alcohol consumption and mortality: the Swedish women’s lifestyle and health study. Eur. J. Epidemiol. 26(2): 81-90.

Beulens, J.W., Rimm, E.B., Hu, F.B., Hendriks, H.F., Mukamal, K.J. 2008. Alcohol consumption, mediating biomarkers, and risk of type 2 diabetes among middle-aged women. Diabetes Care 31(10): 2050-2055.

Bo, Y., Sun, J., Wang, M., Ding, J., Lu, Q., Yuan, L. 2016. Dietary flavonoid intake and the risk of digestive tract cancers: a systematic review and meta-analysis. Sci. Rep. 6: 24836.

Bobak, M., Malyutina, S., Horvat, P., Pajak, A., Tamosiunas, A., Kubinova, R., Simonova, G., Topor-Madry, R., Peasey, A., Pikhart, H., et al. 2016. Alcohol, drinking pattern and all-cause, cardiovascular and alcohol-related mortality in Eastern Europe. Eur. J. Epidemiol. 31(1): 21-30.

Bonaccio, M., Pounis, G., Cerletti, C., Donati, M.B., Iacoviello, L., de Gaetano, G. 2017. Mediterranean diet, dietary polyphenols and low grade inflammation: results from the MOLI-SANI study. Brit. J. Clin. Pharmacol. 83(1): 107-113.

Brand-Miller, J.C., Fatema, K., Middlemiss, C., Bare, M., Liu, V., Atkinson, F., Petocz, P. 2007. Effect of alcoholic beverages on postprandial glycemia and insulinemia in lean, young, healthy adults. Am. J. Clin. Nutr. 85(6): 1545-1551.

Breslow, R.A., Chen, C.M., Graubard, B.I., Mukamal, K.J. 2011. Prospective study of alcohol consumption quantity and frequency and cancer-specific mortality in the US population Am. J. Epidemiol. 174(9): 1044-1053.

Buil-Cosiales, P., Toledo, E., Salas-Salvado, J., Zazpe, I., Farras, M., Basterra-Gortari, F.J., Diez-Espino, J., Estruch, R., Corella, D., Ros, E., et al. 2016. Association between dietary fibre intake and fruit, vegetable or whole-grain consumption and the risk of CVD: results from the PREvencion con DIeta MEDiterranea (PREDIMED) trial. Brit. J. Nutr. 116(3): 534-546.

Cao, Y., Giovannucci, E.L. 2016. Alcohol as a Risk Factor for Cancer. Semin. Oncol. Nurs. 32(3): 325-331.

Chiva-Blanch, G., Urpi-Sarda, M., Ros, E., Valderas-Martinez, P., Casas, R., Arranz, S., Guillen, M., Lamuela-Raventos, R.M., Llorach, R., Andres-Lacueva, C., et al. 2013. Effects of red wine polyphenols and alcohol on glucose metabolism and the lipid profile: a randomised clinical trial. Clin. Nutr. 32(2): 200-206.

Corrao, G., Bagnardi, V., Zambon, A., La Vecchia, C. 2004. A meta-analysis of alcohol consumption and the risk of 15 diseases. Prev. Med. 38(5): 613-619.

Costanzo, S., Di Castelnuovo, A., Donati, M.B., Iacoviello, L., de Gaetano, G. 2010. Cardiovascular and overall mortality risk in relation to alcohol consumption in patients with cardiovascular disease. Circulation 121(17): 1951-1959.

Costanzo, S., Di Castelnuovo, A., Donati, M.B., Iacoviello, L., de Gaetano, G. 2011. Wine, beer or spirit drinking in relation to fatal and non-fatal cardiovascular events:a meta-analysis. Eur. J. Epidemiol. 26(11): 833-850.

Dai, J., Mukamal, K.J., Krasnow, R.E., Swan, G.E., Reed, T. 2015. Higher usual alcohol consumption was associated with a lower 41-y mortality risk from coronary artery disease in men independent of genetic and common environmental factors: the prospective NHLBI Twin Study. Am. J. Clin. Nutr. 102(1): 31-39.

Dal Maso, L., Torelli, N., Biancotto, E., Di Maso, M., Gini, A., Franchin, G., Levi, F., La Vecchia, C., Serraino, D., Polesel, J. 2016. Combined effect of tobacco smoking and alcohol drinking in the risk of head and neck cancers: a re-analysis of case-control studies using bi-dimensional spline models. Eur. J. Epidemiol. 31(4): 385-393.

Di Castelnuovo, A., Costanzo, S., Bagnardi, V., Donati, M.B., Iacoviello, L., de Gaetano, G. 2006. Alcohol dosing and total mortality in men and women: an updated meta-analysis of 34 prospective studies. Arch. Intern. Med. 166(22): 2437-2445.

Estruch, R., Ros, E., Salas-Salvado, J., Covas, M.I., Corella, D., Aros, F., Gomez-Gracia, E., Ruiz-Gutierrez, V., Fiol, M., Lapetra, J., et al. 2013. Primary prevention of cardiovascular disease with a Mediterranean diet. New Eng. J. Med. 368(14): 1279-1290.

Ferrari, P., Licaj, I., Muller, D.C., Andersen, P.K., Johansson, M., Boeing, H., Weiderpass, E., Dossus, L., Dartois, L., Fagherazzi, G., et al. 2014. Lifetime alcohol use and overall and cause-specific mortality in the European Prospective Investigation into Cancer and nutrition (EPIC) study. BMJ Open 4(7): 14.

Food Standards Australia New Zealand. 2017. Guide to labelling of alcoholic beverages.: Commonwealth of Australia: http://www.foodstandards.gov.au/code/userguide/pages/labellingofalcoholic4967.aspx 

Graff-Iversen, S., Jansen, M.D., Hoff, D.A., Hoiseth, G., Knudsen, G.P., Magnus, P., Morland, J., Normann, P.T., Naess, O.E., Tambs, K. 2013. Divergent associations of drinking frequency and binge consumption of alcohol with mortality within the same cohort. J. Epidemiol. Comm. Health 67(4): 350-357.

Gresele, P., Cerletti, C., Guglielmini, G., Pignatelli, P., de Gaetano, G., Violi, F. 2011. Effects of resveratrol and other wine polyphenols on vascular function: an update. J. Nutr. Biochem. 22(3): 201-211.

Hashibe, M., Brennan, P., Chuang, S.C., Boccia, S., Castellsague, X., Chen, C., Curado, M.P., Dal Maso, L., Daudt, A.W., Fabianova, E., et al. 2009. Interaction between tobacco and alcohol use and the risk of head and neck cancer: pooled analysis in the International Head and Neck Cancer Epidemiology Consortium. Cancer Epidemiology Biomarkers Prev. 18(2): 541-550.

Howie, E.K., Sui, X., Lee, D.C., Hooker, S.P., Hebert, J.R., Blair, S.N. 2011. Alcohol consumption and risk of all-cause and cardiovascular disease mortality in men. J. Aging Res. 2011: 805062.

Ilomaki, J., Jokanovic, N., Tan, E.C., Lonnroos, E. 2015. Alcohol Consumption, Dementia and Cognitive Decline: An Overview of Systematic Reviews. Curr. Clin. Pharmacol. 10(3): 204-212.

Ivey, K.L., Hodgson, J.M., Croft, K.D., Lewis, J.R., Prince, R.L. 2015. Flavonoid intake and all-cause mortality. Am. J. Clin. Nutr. 101(5): 1012-1020.

Joosten, M.M., Beulens, J.W., Kersten, S., Hendriks, H.F. 2008. Moderate alcohol consumption increases insulin sensitivity and ADIPOQ expression in postmenopausal women: a randomised, crossover trial. Diabetologia 51(8): 1375-1381.

Klatsky, A.L., Udaltsova, N. 2007. Alcohol drinking and total mortality risk. Annals Epidemiol. 17(5): S63-S67.

Koppes, L.L., Dekker, J.M., Hendriks, H.F., Bouter, L.M., Heine, R.J. 2005. Moderate alcohol consumption lowers the risk of type 2 diabetes: a meta-analysis of prospective observational studies. Diabetes Care 28(3): 719-725.

Midlov, P., Calling, S., Memon, A.A., Sundquist, J., Sundquist, K., Johansson, S.E. 2016. Women’s health in the Lund area (WHILA)--Alcohol consumption and all-cause mortality among women--a 17 year follow-up study. BMC Pub. Health 16: 22.

Mukamal, K.J., Chiuve, S.E., Rimm, E.B. 2006. Alcohol consumption and risk for coronary heart disease in men with healthy lifestyles. Arch. Intern. Med. 166(19): 2145-2150.

Mukamal, K.J., Clowry, C.M., Murray, M.M., Hendriks, H.F., Rimm, E.B., Sink, K.M., Adebamowo, C.A., Dragsted, L.O., Lapinski, P.S., Lazo, M., et al. 2016. Moderate Alcohol Consumption and Chronic Disease: The Case for a Long-Term Trial. Alcohol. Clin. Exp. Res. 40(11): 2283-2291.

Neafsey, E.J., Collins, M.A. 2011. Moderate alcohol consumption and cognitive risk. Neuropsych. Dis. Treat. 7: 465-484.

Pasinetti, G.M. 2012. Novel role of red wine-derived polyphenols in the prevention of Alzheimer’s disease dementia and brain pathology: experimental approaches and clinical implications. Planta medica 78(15): 1614-1619.

Rehm, J., Baliunas, D., Borges, G.L.G., Graham, K., Irving, H., Kehoe, T., Parry, C.D., Patra, J., Popova, S., Poznyak, V., et al. 2010. The relation between different dimensions of alcohol consumption and burden of disease: an overview. Addiction 105(5): 817-843.

Ronksley, P.E., Brien, S.E., Turner, B.J., Mukamal, K.J., Ghali, W.A. 2011. Association of alcohol consumption with selected cardiovascular disease outcomes: a systematic review and meta-analysis. BMJ 342: d671.

Stockwell, T., Zhao, J., Panwar, S., Roemer, A., Naimi, T., Chikritzhs, T. 2016. Do “Moderate” Drinkers Have Reduced Mortality Risk? A Systematic Review and Meta-Analysis of Alcohol Consumption and All-Cause Mortality J. Stud. Alc. Drugs 77(2): 185-198.

Szymanska, K., Hung, R.J., Wunsch-Filho, V., Eluf-Neto, J., Curado, M.P., Koifman, S., Matos, E., Menezes, A., Fernandez, L., Daudt, A.W., et al. 2011. Alcohol and tobacco, and the risk of cancers of the upper aerodigestive tract in Latin America: a case–control study. Cancer Causes Control 22(7): 1037-1046.

Tresserra-Rimbau, A., Guasch-Ferre, M., Salas-Salvado, J., Toledo, E., Corella, D., Castaner, O., Guo, X., Gomez-Gracia, E., Lapetra, J., Aros, F., et al. 2016. Intake of Total Polyphenols and Some Classes of Polyphenols Is Inversely Associated with Diabetes in Elderly People at High Cardiovascular Disease Risk. J. Nutr. doi: 10.3945/jn.115.223610.

Tresserra-Rimbau, A., Medina-Remon, A., Lamuela-Raventos, R.M., Bullo, M., Salas-Salvado, J., Corella, D., Fito, M., Gea, A., Gomez-Gracia, E., Lapetra, J., et al. 2015. Moderate red wine consumption is associated with a lower prevalence of the metabolic syndrome in the PREDIMED population. Brit. J. Nutr. 113 Suppl 2: S121-130.

Tresserra-Rimbau, A., Medina-Remon, A., Perez-Jimenez, J., Martinez-Gonzalez, M.A., Covas, M.I., Corella, D., Salas-Salvado, J., Gomez-Gracia, E., Lapetra, J., Aros, F., et al. 2013. Dietary intake and major food sources of polyphenols in a Spanish population at high cardiovascular risk: the PREDIMED study. Nutr. Metabol. Cardiovasc. Dis. 23(10): 953-959.

Xu, W., Wang, H., Wan, Y., Tan, C., Li, J., Tan, L., Yu, J.T. 2017. Alcohol consumption and dementia risk: a dose-response meta-analysis of prospective studies Eur. J. Epidemiol. 32(1): 31-42.

 

 

no website link
All text and images © 2003 Alcohol In Moderation.