By Jordan Feigenbaum MS, CSCS, HFS, USAW CC, Starting Strength Staff
One of the most common questions I get with regards to nutrition and/or training pertains to alcohol and how it effects potential performance, health, or aesthetic outcomes. I get asked this question so often that I’m dedicating an entire chapter of my book to the stuff. Instead of sharing part of the manuscript on here, I thought I’d post up a truncated version of my thoughts and findings on the subject, which will actually be broken up into three separate blog posts on this blog as well as my new website. Consider this advertising for what sort of cool things go on over on that site. You should join, methinks, to get some good information 🙂 Now, let’s talk about booze!
Let’s begin by defining alcohol as a dietary component. An average “drink” has approximately 14 grams of pure alcohol (ethanol) within it, which is in addition to all the other stuff in the drink, i.e. mixers, flavorings, etc. At any rate, a drink is defined by the volume of substance that has 14g of alcohol in it. This metric equates to the following serving sizes:
- 12-ounces of beer.
- 8-ounces of malt liquor.
- 5-ounces of wine.
- 1.5-ounces or a “shot” of 80-proof distilled spirits or liquor (e.g., gin, rum, vodka, or whiskey)
So now that we have defined our terms of what an actual drink is, what exactly happens to the good stuff when we’re out at happy hour? Orally ingested alcohol is transported through the proximal digestive tract intact, i.e. it is not broken down, metabolized, or otherwise changed until it gets into the stomach. The amount of alcohol that gets to the stomach is very high compared to other parts of the digestive system like the duodenum or other parts of the small intestine. Due to this high concentration, approximately 40% of alcohol is metabolized (broken down) in the stomach within the first hour following initiation of drinking. Within about 2 hours, up to73% of the total alcohol that was ingested has been metabolized in the stomach . Alcohol absorption, on the other hand, takes place in both the stomach (slow) and small intestine (rapid). The total amount of alcohol metabolized and absorbed in the stomach depends on the rate of emptying of the stomach, which is influenced by lots of things. At any rate, the stomach’s metabolism of alcohol in humans plays an important role in First Pass Metabolism.
Some of you science-minded folks might be thinking, Wait, the STOMACH metabolizes and absorbs alcohol? I thought that absorption occurred in the small intestine! Yes Virginia, this is normally correct. However, it has been shown that the stomach’s lining, more appropriately termed the gastric epithelium, contains a version of the enzyme alcohol dehydrogenase (ADH). This version, σ-ADH, is not present in the liver. breaks down ethanol into acetylaldehyde, which is the metabolite in the overall metabolism of ethanol. Different types of alcohol dehydrogenase (ADH isoforms) are present in the liver, but σ-ADH is only found in the gastric epithelium.
So how do we know that alcohol is actually metabolized and absorbed in the stomach and what sorts of things affect this? Blood alcohol levels, i.e. the amount of intact ethanol in the blood after ingestion, changes under certain conditions. When alcohol is ingested orally, lower blood alcohol levels are seen than when alcohol is given intravenously . This is due to the first pass metabolism occurring in both the stomach and liver, as both of these organs have high levels of alcohol dehydrogenase. Because the ethanol is metabolized and degraded into acetylaldehyde, as mentioned above, there is less of it that actually enters the blood stream and thus, less alcohol in the blood. These facts, however, do not tell us the importance of the stomach’s metabolism of ethanol. For that, we must dig deeper.
Aspirin and H-2 blockers (histamine receptor blockers) both decrease σ-ADH activity in the stomach, which results in less ethanol being metabolized to acetylaldehyde. These drugs also increase the rate at which the stomach’s contents are emptied into the small intestine. Both of these factors, i.e. less ADH activity and faster emptying, result in higher blood alcohol levels in humans. Interestingly, Japanese persons have lower σ-ADH activity naturally and thus, first pass metabolism is significantly compromised and blood alcohol levels are higher at a given dose than their non-Japanese counterparts .
You might be wondering what other sorts of things influence stomach emptying, you know, in case you wanted to see higher blood alcohol levels get drunk quickly. Fasting accelerates emptying, which results in less exposure of ethanol to the σ-ADH in the stomach and more rapid absorption of ethanol in the small intestine. On the other hand, consuming a high fat meal alongside alcohol significantly delays emptying and absorption of food. In general, the effect of food on alcohol metabolism and absorption, i.e. increasing metabolism and delaying absorption, is primarily due to the slowing down of gastric emptying. Alcohol content also influences rate of absorption, with maximum absorption occurring with consumption of a drink containing approximately 20-25% alcohol on an empty stomach. The absorption rate may be less when a 40% alcohol solution is consumed on an empty stomach. The rate may also slow down when high fluid volume/low alcohol content beverages, such as beer, are consumed.
So we know that a varying amount of ethanol is metabolized in the stomach and a small amount is absorbed there as well. What happens to the ethanol that remains untouched and makes it to the small intestine? Ethanol in the small intestine, which is made up of the duodenum, jejunum, and ilieum from proximal to distal, is generally absorbed by diffusion from the inside of the GI tract’s lumen into the cells lining the tract, the enterocytes. Mechanistically, this likely occurs due to the high permeability of cells to pure alcohol/ethanol and it also appears that certain simple sugars (monosaccharides and disaccharides) like glucose, galactose, sucrose, etc. also increase the rate of absorption of ethanol in the small intestine. Carbohydrates are all eventually broken down into glucose, galactose, and fructose and are absorbed via sodium-dependent transport, i.e. sodium is concomitantly transported with the sugars. Carbohydrate absorption likely increases alcohol absorption through electrochemical gradient changes. This means the sugar containing margarita likely gets into your bloodstream faster than pure ethanol. Unfortunately, lactose, the main carbohydrate in milk, does not increase absorption rates .
Once into the enterocyte, ethanol diffuses into the veins suppying the enterocyte and is carried to the liver as part of the hepatic (liver) portal circulation. Once in the liver, ethanol diffuses from the venous blood into the liver cells, aka hepatocytes, where the majority of ethanol metabolism will finally occur. In the liver cell ethanol will encounter another isoform of alcohol dehydrogenase and get oxidized into acetylaldehyde. This enzyme, alcohol dehydrogenase, can become saturated at certain levels of ethanol ingestion and thus, extra ethanol will spillover into other metabolic pathways in order to be eliminated from circulation. While not particularly important to our discussion on the effects of booze on training, for the sake of completeness these other liver pathways include Microsomal Ethanol Oxidized System (MEOS)/Cyp2E1 (functions primarily during high levels of ethanol intake) and catalase (minor). An important take way from this is that ethanol must be metabolized or eliminated from the body, as it cannot be stored and serves no particular purpose. That should beg the question, why do we even have mechanisms and pathways in our body to eliminate ethanol anyway?
Alcohol dehydrogenase and the downstream pathways used to eliminate ethanol from circulation are believed to originate out of necessity due to the small amount, i.e. 3g or so, of ethanol produced daily by resident bacteria in the intestinal tract via fermentation and other biological processes . Similarly, only a small amount (2-10%) of ethanol is eliminated through the lungs and kidney, so the rest must be metabolized in the liver, stomach, etc. Maybe booze isn’t so Paleo after all? 🙂
So now, after all that rigamarole, we have two things that we’re dealing with that can cause potential downstream effects, ethanol and acetylaldehyde. Acetylaldehyde will eventually get metabolized acetate, which will get metabolized into acetyl-coA and contribute to one of the following pathways depending on what else is going on:
- Fatty acid synthesis (if insulin is elevated)
- Cholesterol synthesis (if insulin is elevated)
- Be used for fuel by the heart and skeletal muscle (and turned into co2 and water)
So, if you’re drinking alongside some carbohydrates or a mixed meal, the end products will be different than if you’re just boozing solo. Ethanol will, at some point, get metabolized as described before although while it’s floating around in the blood stream it will certainly exert some effects that will discuss during the rest of this article.
With all the background information out of the way now, we can get down to the business of actually talking about what drinking does performance and health-wise. To begin with, let’s talk about alcohol’s effect on metabolism, i.e. does it have a negative, positive, or neutral effect on you getting lean?
In general, ethanol carries about 7.1-7.5 kCal per gram. A “drink”, as defined by the 14g/ unit metric, therefore contains about 99kCal per “unit” just from alcohol. Remember how we talked about ethanol not being able to be stored and requiring almost immediate metabolism? Well, it turns out the ethanol becomes the “preferred fuel” of the liver and decreases liver fat oxidation by about 70% and protein oxidation by about 39%. It also almost completely abolishes carbohydrates being use for fuel even after an infusion. Normally, when carbohydrates reach the bloodstream their oxidation (metabolism) increases by about 2.5x. In the presence of ethanol, however, carbohydrate’s oxidation for fuel stays at baseline and storage of carbohydrates as fat increases .
Ethanol metabolism also requires a coenzyme, NAD+, that gets reduced to NADH when ethanol is converted to acetylaldehyde by alcohol dehydrogenase. NADH levels tend to rise during metabolism of ethanol and NAD+ levels tend to fall, thus increasing the NADH:NAD+ ratio. This increased ratio does a number of things metabolically, like increasing fat storage synthesis and causing damage to the mitochondria. Remember, mitochondria are the “energy powerhouses” of the cell and are very important . Some training protocols we use, like high intensity interval training and weight training increase “mitogenesis”, i.e. the creation of new mitochondria to burn fuel (carbohydrates and fat). Ethanol and acetylaldehyde exposure to mitochondria decreases mitochondria activity, increases reactive oxygen species creation (which can damage other tissues), and can eventually cause mitochondrial dysfunction and death.Decreased mitochondrial activity can have negative impacts on basal metabolic rate, as it will decrease in response to lower levels of mitochondrial density or functioning.
This isn’t meant to be a scare tactic, as with most things, the poison is in the dose. On the other hand, the level of alcohol intake required to become inebriated far exceeds the levels of ethanol and acetylaldehyde that were used experimentally to demonstrate deleterious changes in mitochondrial activity.
Actual metabolic rate based on measuring oxygen consumption will increases upon ingestion of alcohol, as it also does with food alone . Some people have taken this out of context and said that alcohol will increase metabolic rate to a greater degree than an isocaloric diet sans alcohol. Unfortunately, this has not been shown as of yet.
Another important metabolic issue as it pertains to ethanol, is that ethanol reduces the activity of muscle phosphorylase in human skeletal muscle . Muscle phosphorylase, i.e. glycogen phosphorylase that breaks down muscle glycogen into glucose, is an important enzyme needed for the muscles to use stored carbohydrates as fuel. A disease of this enzyme, McCardle’s Disease, presents with exercise intolerance, early fatigue, and excessive muscle breakdown products (myoglobinuria) that may lead to rhabdomyolosis. In any event, in addition to decreased muscle phosphorylase activity, ethanol exposure also decreases rates of muscle protein synthesis and whole body protein metabolism by 15-30% . The worst part is, these affects are primarily seen in type II fast-twitch fibers that we need for high level anaerobic performance!
To wrap up part 1 of this series, which was admittedly science-heavy (sorry), I’d like to state how I’d start to apply all these things practically. I do not believe it’s necessary to cut out all alcohol in the quest for ultimate performance and especially not for health, as we’ll discuss next time. On the other hand, I think many people are way too liberal with having a “few” drinks per day. That being said, I’m a proponent of counting the calories in liquor as carbohydrates, as they both demand preference for use as the primary metabolic substrate. What I mean by that is if ethanol is present, it will be metabolized first and foremost. Other calories and energy containing things will be stored so as not to compete with alcohol metabolism, in general. Carbohydrates are similar in that way, as they will be preferentially used by most tissues when the diet provides high levels of them. Additionally, both promote fat storage in the short term. Whether or not this leads to long term fat accumulation depends on the rest of the diet, i.e. total calories, macronutrients, etc.
So, yeah, count the alcohol as carbs and if it fits within your macronutrients and fiber goals for the day, it’s probably fine. On the other hand, I really like this soon-to-be-famous axiom:
“If you’re drinking enough to get drunk, you’re drinking enough to mess with your results.”
That’s it for part I. Sorry for the science primer, but it will pay off big time in parts II and III.
1) Cortot A, Jobin G, Fucrot F, et al. Gastric emptying and gastrointestinal absorption of al- cohol ingested with a meal. Dig Dis Sci 1986;31:343–8
2) Frezza M, Di Padova C, Pozzato G, et al. High blood alcohol levels in women. The role of decreased gastric alcohol dehydrogenase activity and first-pass metabolism. N Engl J Med 1990;322:95–9
3) Broitman SA, LS Gottlieb, JJ Vitale Augmentation of ethanol absorption by mono- and disaccharides Gastroenterology 1 June 1976 (volume 70 issue 6 Pages 1101-1107)
4) Lieber Charles S. Metabolism of Alcohol. Clinics in Liver Disease, Volume 2, Issue 4, Pages 673-702
5) Rosenberg Kathryn, Durnin J.V.G.A. The effect of alcohol on resting metabolic rate. British Journal of Nutrition (1978). Vol. 40. 293
6) Urbano-Marquez, A.; Fernandez-Sola, J. Effects of alcohol on skeletal and cardiac muscle. Muscle Nerve 2004, 30, 689-707.