Alcoholic drinks contribute to obesity and should come with mandatory calorie countsBMJ 2015; 350 doi: https://doi.org/10.1136/bmj.h2047 (Published 28 April 2015) Cite this as: BMJ 2015;350:h2047
All rapid responses
There is no doubt that we have ongoing pandemics of both obesity and alcohol abuse. However, the link between them is not simply the energy content of alcohol. As stated by Dr Robert Lustig,1 ´a calorie is not a calorie´, meaning that the metabolic effect depends on the source of the energy and not simply related to the total amount of energy consumed. The hypothesis that obesity results from eating (and drinking) too much and exercising too little is therefore not true.
The metabolism of ethanol is described in detail in this excellent review.2 Ethanol taken in large quantities is a neurotoxin and taken chronically in large quantities is a hepatotoxin, and causes insulin resistance and metabolic syndrome in a dose-dependent manner. Ethanol is metabolised to acetaldehyde which generates reactive oxygen species (ROS) which have the potential to cause toxic damage. Acetaldehyde is then metabolised to acetic acid, and then acetyl-CoA, which in the presence of other energy substrates, participates in the synthesis of other fatty acids through de novo lipogenesis. Acetaldehyde stimulates the enzyme SREBP-1c which activates the enzymes of de novo lipogenesis,3 during which, the intermediate malonyl-CoA is formed in excess, which inhibits the mitocondrial enzyme, carnitine palmitoyl transferase-1, thus inhibiting the β-oxidation of fatty acids.4 Ethanol also blocks fatty acid β-oxidation through inhibiton of peroxisome proliferation-activated receptor-α and adenosine monophosphate-activated protein kinase. Therefore, increased de novo lipogenesis inhibits fatty acid β-oxidation in the liver, leading to accumulation of intrahepatic lipid.3
Export of VLDL is the principal means by which intrahepatic lipid is reduced and VLDL synthesis requires correct apoB100 protein folding prior to export which depends on microsomal triglyceride transfer protein (MTP). However, ethanol reduces hepatic peroxisome proliferation-activated receptor-α which downregulates MTP,5 resulting in alterations in VLDL particle size and subsequent rate of blood clearance, thus contributing to hypertriglyceridemia.
The metabolic effects of alcohol are similar to those of fructose,2 the consumption of which is ubiquitous as sucrose or ´sugar´ and high fructose corn syrup (HFCS) which is used in processed foods and sweet drinks. Consumption of both fructose and alcohol therefore lead to metabolic dysfunction, which is the cause of type 2 diabetes, hypertension, lipid problems, heart disease, fatty liver disease, polycystic ovarian syndrome, cancer and dementia,1,2 which together account for 75% of healthcare costs in the USA, and are a global problem related to ubiquitous consumption of modern processed food and alcohol.
Obesity is a marker for all of these diseases and It is widely believed that obesity is the main cause of these diseases, but this is untrue. It is important to note that 20% obese people have normal metabolic function, and in these persons, the obesity does not affect their health or lifespan.1
In the last 40 years, consumption of saturated fat has been drastically reduced globally as it was mistakenly thought to be linked with heart disease. This dietary fat was replaced by sugar. Coincidentally, the global incidence of metabolic disease increased dramatically.
In conclusion, metabolic dysfunction secondary to alcohol and fructose represents a global pandemic which has eroded the health of humanity. Statement of energy content, while well-meaning, is a distraction from the real mechanism of this ongoing catastrophe.
1. Lustig RH, Schmidt LA, Brindis CD. Public health: The toxic truth about sugar. Nature 2012 Feb 1;482(7383):27-9.
2. Lustig RH. Fructose: metabolic, hedonic, and societal parallels with ethanol. J Am Diet Assoc. 2010 Sep;110(9):1307-21.
3. You M, Crabb DW. Molecular mechanisms of alcoholic fatty liver: role of sterol regulatory element-binding proteins. Alcohol. 2004;34:39-43.
4. McGarry JD, Brown NF. The mitochondrial carnitine palmitoyltransferase system. From concept to molecular analysis. Eur J Biochem. 1997;244:1-14.
5. Nanji AA, Dannenberg AJ, Jokelainen K, Bass NM. Alcoholic liver injury in the rat is associated with reduced expression of peroxisome proliferator-alpha (PPARalpha)-regulated genes and is ameliorated by PPARalpha activation. J Pharmacol Exp Ther. 2004;310:417-424.
Competing interests: No competing interests
The addition of information regarding calorific content to alcohol packaging could afford the consumer greater awareness of the content, facilitate informed choice and hopefully promote appropriate behavioural change. Should the provision of such information become mandated it would be interesting to explore how consumer choice and drinking behaviours may be moderated.
Those in clinical practice should, as a matter of routine, ask questions about alcohol use in addition to diet and exercise, and from this the additional calories can be estimated (1 UK unit of alcohol contains 56 kcal), however the nature of the drink itself will add to the overall calorie counts (a 50ml measure of cream liqueur contains just under 1 unit of alcohol, but 121 kcal). Given that almost one in five junior doctors remain unaware of what a unit of alcohol actually is (1,2) there is a clear need to raise address these issues as part of the undergraduate medical school curriculum.
1. Das, AK , Corrado, OJ, Kyerematen, E, Smithson, JAJ & West, RM (2009) Do doctors understand alcohol units? Clinical Medicine, 9 (6): 525-527
2. Das, AK, Corrado, OJ, Sawicka, Z, Haque, S, Anathhanam, S, Das, L & West, R. Junior doctors' understanding of alcohol units remains poor. (2014). Clinical Medicine, 14 (2): 141-144
Competing interests: No competing interests