Beware of Excessive Alcoholic Beverages

Since ancient times, people have attributed a variety of health benefits to moderate consumption of fermented beverages such as wine and beer. Archaeological evidence suggests that the earliest known wine production occurred in Georgia (Eurasia) around 7,000 BC. There was domestication of grapevine during the Bronze Age sites including those from Egypt from around the third millennium BC. In Europe, it seemed to have started in Greece some 6,500 years. Traces of ancient wine dating back some 3,000 years have been discovered in China. In all these regions of the world, the same fermentation process by yeast caused the breakdown of mostly fructose (sugar) in grapes into alcohol. Taste may depend on types of grape used, length and method of fermentation. Ethanol (alcohol) is a component of many liquid medications too. For the non-Muslim who consume alcohol beverages, it’s no secret that excessive alcohol consumption is linked to increased risk of morbidity and mortality, as well as with home/work related, and traffic accidents.



Although many studies (Arranz et al. 2012; Brien et al. 2011) have demonstrated that light to moderate alcohol consumption is associated with reduced risk of cardiovascular disease (CVD), recent data suggest that the earlier findings of coronary protection by alcohol consumption may be due partly to misclassification of research data (Hansel et al. 2012). Neither are there current data available to directly support a causal relationship between alcohol intake and CVD. It remains, therefore, rather premature for health professionals to promote alcohol consumption as a basis for CV protection.

Western epidemiological studies are consistent in showing some protection from CVD at consumption levels of one to two drinks per day, while also showing a sharp increase in CVD associated with three or more drinks per day. Moderate alcohol may increase the good high density lipoprotein cholesterol (HDL-C) levels and favourably influences thrombotic factors, especially fibrinogen (a marker for blood thickness). Wine consumption may raise HDL-C by between 11 – 16% and may lower fasting fibrinogen by between 8 – 15% compared to not drinking wine (Hansen et al. 2005). It appears to exert additional beneficial effects on the heart by decreasing platelet aggregability (Llerena and Huerta 1998). However, studies also show an adverse effect of alcohol, particularly at higher doses, on blood pressure (leading to hypertension) and on the myocardium leading to arrhythmias (irregular heartbeat) and myocardiopathy.

The so-called French Paradox has led to speculation that wine is the only protective alcoholic beverage for CVD, or at least that it has a stronger effect. Multiple non-alcohol components of wine have been studied in the laboratory and have been shown to have antioxidant or anticoagulant effects. Although wine does appear to offer more protective in ecological studies, research demonstrates similar effects across alcoholic beverages (Criqui 1998). In general, maximal benefits and safety appear to be at the level of approximately 1 drink per day. Limited data suggest that the level for optimal benefit and safety may be slightly lower for women (Sesso 2001). The American Heart Association limits alcohol intake to no more than two drinks per day for men and 1 drink per day for women. Higher risk of death at heavy drinking levels is due to increased risk of cancer, liver diseases, cardiomyopathy, and stroke. (Gaziano and Buring 1998).

Nutritional therapists recommend the use of lifestyle modification such as regular exercise and the consumption of spices such as onion and mustard to raise one’s good HDL-C levels. If these natural approaches are insufficient to achieve the desired HDL-C levels, then moderate dose of niacin (vitamin B3) may be added to a supervised dietary programme. Elevated blood fibrinogen levels may be normalised by nutraceuticals such as EPA/DHA and vitamin E.



Acute or moderate use is associated with attenuated inflammatory responses, whereas heavy ethanol consumption linked with augmentation of inflammation (Goral et al. 2008). Fat accumulation, dysregulation of immunity, and impaired antiviral and autoimmune responses are three distinct pathophysiological mechanisms of alcoholic liver injury (Nath and Szabo 2009). Though subject to genetic variation (de Alwis and Day 2007), alcoholic liver injury may also take the form of liver cirrhosis (‘yellowish’) (Stickel and Hampe 2012) which may then progress to liver tumor or cancer (Seitz at al. 1998). It may surprise many that fructose (fruit sugar) metabolism in the liver is rather similar to its metabolism of alcohol, as they both lead to lipogenesis (excessive fat generation), insulin resistance (prediabetes), dyslipidemia (abnormal blood fats), and hepatic steatosis (fatty liver) (Lustig 2010).

Nutritional therapy can help control or even reverse alcoholic effects on carcinogenesis (cancer development) (Rogers and Conner 1986). Nutritional therapists widely use these nutraceuticals to treat and reverse liver damage: silybinin, dandelion, selenium, Schizandrae, alpha lipoic acid, magnesium, zinc citrate, HCA, EPA, and SOD.



The brain is one of the major target organs of alcoholic actions, and its chronic and acute intoxication results in significant alterations in brain structure and function, and in some cases to neurodegeneration (nerve damage) (Blanco and Guerri 2007). Nutrients useful in protecting our brain integrity include selenium, DHA, and d-alpha tocopherol.



The International Agency for Research for Cancer has classified alcohol consumption as carcinogenic for humans. Habitual consumption of alcoholic beverages can lead to cancers such as those of the oral cavity, pharynx, larynx, esophagus, colorectal, liver and female breast; and a link being suspected for cancers of the pancreas and lung (Boffetta and Hashibe 2006). The European Code Against Cancer recommends keeping daily consumption within two drinks for man and one drink for women since there are insufficient data to support the actually safe intake of alcohol. According to them, any level of alcohol consumption increase the risk of developing an alcohol related cancer. The level of risk increases in line with the level consumption (Testino 2011). Asians are known to have lower metabolic ability for alcohol compared to Caucasians. Consequently, our daily limits might be lower.

The metabolism of alcohol leads to the generation of acetaldehyde (AA) and free radicals (ageing chemicals). Research evidence suggests that AA is predominantly responsible for alcohol-linked carcinogenesis. AA can also be produced by oral (mouth) and faecal (stool) bacteria. Smoking, which changes the oral bacterial flora, and poor oral hygiene also increase AA. Neutralising the damaging free radicals generated by AA is a key to this cancer prevention. Additionally, an alcohol-mediated increase in estradiol (estrogen) may be partly responsible for increased breast cancer risk (Poschl and Seitz 2004). Consult only a MoH-licensed nutritional therapist for adjunct therapy on estrogen or alcohol-related cancer prevention.

Cigarette smoking, heavy alcohol consumption and hepatitis B antigen seem to be independently linked to increased risk of mortality from liver cancer but they do not interact synergistically (Jee et al. 2004).



Arranz S, Chiva-Blanch G, Valderas-Martínez P et al. Wine, beer, alcohol and polyphenols on cardiovascular disease and cancer. Nutrients. 2012 Jul;4(7):759-81.

Blanco AM, Guerri C. Ethanol intake enhances inflammatory mediators in brain: role of glial cells and TLR4/IL-1RI receptors. Front Biosci. 2007 Jan 1;12:2616-30.

Boffetta P, Hashibe M. Alcohol and cancer. Lancet Oncol. 2006 Feb;7(2):149-56.

Brien SE, Ronksley PE, Turner BJ et al. Effect of alcohol consumption on biological markers associated with risk of coronary heart disease: systematic review and meta-analysis of interventional studies. BMJ. 2011 Feb 22;342:d636.

Criqui MH. Do known cardiovascular risk factors mediate the effect of alcohol on cardiovascular disease? Novartis Found Symp. 1998;216:159-67.

de Alwis WNM and Day CP. Genetics of alcoholic liver disease and nonalcoholic fatty liver disease. Semin Liver Dis. 2007 Feb;27(1):44-54.

Gaziano JM, Buring JE. Alcohol intake, lipids and risks of myocardial infarction. Novartis Found Symp. 1998;216:86-95.

Goral J, Karavitis J and Kovacs EJ. Exposure – dependent effects of ethanol on the innate immune system. Alcohol. 2008 June; 42(4):237-47.

Hansel B, Kontush A, Bruckert E. Is a cardioprotective action of alcohol a myth? Curr Opin Cardiol. 2012 Sep;27(5):550-5.

Hansen AS, Marckmann P, Dragsted LO et al. Effect of red wine and red grape extract on blood lipids, haemostatic factors, and other risk factors for cardiovascular disease. Eur J Clin Nutr. 2005 Mar;59(3):449-55.

Jee SH, Ohrr H, Sull JW, Samet JM. Cigarette smoking, alcohol drinking, hepatitis B, and risk for hepatocellular carcinoma in Korea. J Natl Cancer Inst. 2004 Dec 15;96(24):1851-6.

Llerena RI, Huerta ME. Wine and heart. Rev Esp Cardiol. 1998 Jun;51(6):435-49. [Spanish].

Lustig RH. Fructose: metabolic, hedonic, and societal parallels with ethanol. J Am Diet Assoc. 2010 Sep;110(9):1307-21.

Nath B and Szabo G. Alcohol-induced modulation of signaling pathways in liver parenchymal and nonparenchymal cells: implications for immunity. Semin Liver Dis. 2009 May;29(2):166-77.

Poschl G, Seitz HK. Alcohol and cancer. Alcohol 2004 May-Jun;39(3):155-65.

Rogers AE, Conner MW. Alcohol and cancer. Adv Exp Med Biol. 1986;206:473-95.

Seitz HK, Poschl G, Simanowski UA. Alcohol and cancer. Recent Dev Alcohol. 1998;14:67-95.

Sesso HD. Alcohol and cardiovascular health: recent findings. Am J Cardiovasc Drugs. 2001;1(3):167-72.

Stickel F, Hampe J. Genetic determinants of alcoholic liver disease. Gut. 2012 Jan;61(1):150-9.

Testino G. The burden of cancer attributable to alcohol consumption. Maedica (Buchar). 2011 Oct;6(4):313-20.

Share this article

About Author

Dato’ Steve Yap

Masters’ in Metabolic & Nutritional Medicine (USF Med Sch);

Advanced Fellow, Anti-Aging Regenerative Functional Medicine (USA);

Fellow, Integrative Cancer Therapies (USA);

Nutritional Therapy Council Certified Practitioner (UK);

President, Federation of Complementary & Natural Medical Associations M’sia;

Complementary Medicine Director, DSY Wellness Longevity Center (

Login to post comments

Contact Us

Greenpower Empire Sdn Bhd (1010678-A)


Registered Address: 33-1-5, Mutiara Court, Lorong Delima 20, Green Lane, 11700 Jelutong, Pulau Pinang, Malaysia.


Email: [email protected]

Last Posts