05
Oct
Reading time - 12 mins
This will probably polarise a lot of people, as alcohol is not something that is traditionally mentioned in the realm of muscle gain or fat loss as a positive thing. And I am not about to claim alcohol offers benefits for muscle growth or fat loss either, however, the negative association alcohol has been given for years now is potentially unwarranted.
Now if you aren’t familiar of the famous asterisk in the world of nutritional or supplemental claims, essentially what it means is you need to either read the context of which the claim is being made or that the claim itself has not been supported or agreed upon by the necessary governing bodies.
In this instance, the asterisk is solely for context, as you will see the available literature does actually support the claim already made above.
So let's take a look at the proposed reasons as to why alcohol may affect fat loss and muscle gain and then discuss what the literature has found in order to come to a conclusion on whether or not alcohol is positive, negative or neutral in its effects on body composition and health.
If you’re unfamiliar with the term substrate, essentially all it refers to in biochemistry is the source or molecule in which the particular system or enzyme acts upon.
For example, when comparing fats, protein and carbs, the bodies preferred substrate for energy utilisation during high-intensity exercise, is glucose, whereas throughout the day or during in low-intensity exercise, the preferred substrate is a triglyceride from stored fat.
Outside of glucose and triglycerides, another substrate that can be used by the body is acetate, which is the by-product of ethanol/alcohol (1). Bear in mind, however, that this substrate is not a preferred fuel source but instead is one the body must remove preferentially over all other available substrates while its levels are still present in the blood due to its toxicity.
Which brings us to the first concern of alcohol and body composition…
Yes, it does*
Ahhh but the asterisk re-appears.
Knowing this, it has been theorised that due to the preferential substrate utilisation of acetate, the consumption of carbohydrates and fats in the presence of acetate leads to immediate fat storage or in the case of carbohydrates, lipogenesis, which is the conversion of a sugar into a storable triglyceride.
Which is somewhat true, acetate will be preferentially used and therefore the consumption of carbohydrates and dietary fats may result in them being stored, however, the theory fails to acknowledge 2 things:
In the presence of a calorically controlled diet, DNL does not appear to be a factor for fat storage (2) and similarly alcohol, or more specifically acetate, is not a substrate that is susceptible to fat storage either. To illustrate this even further, Siler et al (1999), found that while 2-3 standard drinks did not prevent glucose oxidation completely (they were still being used in the presence of acetate), and did inhibit lipolysis (fat breakdown), acetate itself only converted into 0.8g of triglyceride out of 24g ingested.
Pretty tiny!
The reality is simple, when a diet is calorically controlled, regardless of the presence of alcohol or not, fat storage will not occur above the net amount of fat burned once acetate has been removed.
Another theory that has been postulated is the ‘drastic’ effects alcohol consumption has on testosterone and estradiol/estrogen.
Let’s nip this one in the butt real quick.
Alcohol consumption does reduce testosterone, however, like above, the effect is so small it is not worth worrying about. At 30-40g of alcohol a day, which equates to 3 standard wines or beer resulted in a 6.8% reduction in testosterone and no increase in estradiol, with a simultaneous 11.7% increase in HDL cholesterol in both men and women (4).
Similarly, in another study, 1.5g of alcohol per kg of body weight over 3 hours caused a reduction in testosterone by 23% with no effect on Luteinising Hormone, alongside a 36% increase in cortisol at 11-14 hours post consumption.
So test levels go down, while cortisol simultaneously rises...BUT…
1.5g of alcohol per kilogram of body weight is nearly 4x that of the comparison study above and would equate to 150g of alcohol for a 100kg male, which is in the vicinity of 10 standardised beers in 3 hours.
Which is a great reference to the weekend binge drinkers reading this, as your cortisol levels will rise and test levels will drop at 14 hours after consumption, but not necessarily a great representation of the non-drinking community.
It is important to note, however, that no return to baseline blood work was taken or commented on in the post 14-hour phase, so it may just be that these levels return to normal 24 hours later, once the acetate is burned from the system.
Like the effect on lipolysis, the short-term reduction in testosterone after low to moderate alcohol intake is unlikely to cause any long-term adverse effects.
So here is the kicker, because it is always nice to finish on a positive note.
It’s not an uncommon thing to hear about the benefits of red wine consumed daily in the news, and a large majority of professionals, including myself, have hypothesised that the primary benefits are not from the alcohol itself but instead the accompanying antioxidants provided by the grapes.
However, after digging deeper, we can now comfortably say that ethanol itself has benefits for health as well. And not just any benefits, but ones that may aid in enhancing your body composition as opposed to hindering it.
Consuming between 15 and 50g of ethanol per day results in a reduction in circulatory triglycerides and facilitates an improved response to glucose consumption due to enhanced insulin sensitivity (5,6). In essence, having between 1 and 2 serves of pure alcohol daily, which would be of the spirit variety, may improve blood glucose regulation.
Pretty cool if you ask me!
Now before anyone voices his or her concerns about this being a pro-alcohol article, it is absolutely not. I am simply providing some interesting data on the perceived positives and negatives of alcohol consumption in relation to body composition changes.
Feinman, L., Lieber, C.S. (1999). Ethanol and lipid metabolism. American Journal of Clinical Nutrition, 70(5), pp791-792. WEB
Hellerstein, M. (1999). De novo lipogenesis in humans: metabolic and regulatory aspects. European Journal of Clinical Nutrition, 53(s1), pp.s53-s65.
Siler, S.Q., et al. (1999). De novo lipogenesis, lipid kinetics and whole-body lipid balances in humans after acute alcohol consumption. The American Journal of Clinical Nutrition, 70(5), pp 928-936. WEB
Sierksma, A., Sarkola, T., Eriksson, C., Gaag, M., Grobbee, D. and Hendriks, H. (2004). Effect of Moderate Alcohol Consumption on Plasma Dehydroepiandrosterone Sulfate, Testosterone, and Estradiol Levels in Middle-Aged Men and Postmenopausal Women: A Diet-Controlled Intervention Study. Alcoholism: Clinical and Experimental Research, 28(5), pp.780-785.
Valimaki, M., Tuominen, J., Huhtaniemi, I. and Ylikahri, R. (1990). The Pulsatile Secretion of Gonadotropins and Growth Hormone, and the Biological Activity of Luteinizing Hormone in Men Acutely Intoxicated with Ethanol. Alcoholism: Clinical and Experimental Research, 14(6), pp.928-931.
Davies, M., Baer, D., Judd, J., Brown, E., Campbell, W. and Taylor, P. (2002). Effects of Moderate Alcohol Intake on Fasting Insulin and Glucose Concentrations and Insulin Sensitivity in Postmenopausal Women. JAMA, 287(19), p.2559.
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