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If you Google, “how many macronutrients are there?”, article after article will say that there are 3: carbohydrates, proteins, and fats. However, as far as humans are concerned, there’s actually 4 macronutrients: carbohydrates, proteins, fats, and alcohol.
Their calorie contents are as follows: 4 calories per gram of carbohydrate, 4 calories per gram of protein, 9 calories per gram of fat, and last but not least, 7 calories per gram of alcohol.
This means since the US standard drink—12oz of 5% alcohol beer, 5oz of 12% alcohol wine, or 1.5oz of 40% alcohol spirit—which contains 14g of pure ethanol, all contain 98 calories from the alcohol molecule itself, before adding in the carbohydrates present within the drink as well.
Even a “pure” flavored White Claw has 100 calories.
This means that, even if you’re drinking hard alcohol, you should understand that you’re adding in about 100 calories into your diet per 1.5oz shot. Many cocktails contain as much as 3oz of hard alcohol—it all depends on the maker of the drink.
Let’s add it up with an “Old Fashioned” cocktail:
Total= 223 calories.
Having a good time? Did dinner turn into an evening of drinks with friends? If you sipped on 3 of these classics through the evening, you just consumed in excess of 750 calories just from your alcoholic beverages. If you had a 4th, that’s nearly 2 Big Macs—all in liquid form. That’s a lot of calories.
When people think about their liver, they typically think that its core function is to process toxins. After all, downing a bottle of acetaminophen will kill you through liver failure… and acetaminophen doesn’t contain any meaningful caloric value.
However, what many people fail to realize is that the liver is also very much a metabolic organ in the sense that it’s required to process all the calories and macronutrients that you put into your body.
It may sound controversial, but research has shown that the alcohol molecule itself isn’t as toxic to the liver as some of the effects that it causes, namely, it causes the buildup of fat in the liver—which is what then leads to swelling, scarring, and eventually cirrhosis.
When it comes to destroying your liver, alcohol isn’t directly causing the problem as much as you might think, rather it’s doing it indirectly through the buildup of liver fat. As we discuss at length in the article “Why Most Liver Disease Starts with Liver Fat”, people die from liver disease all the time without ever being consumers of alcohol. When it comes to liver disease, alcohol is only part of the problem, not the sole source for it.
Alcohol leads to the storage of fat within the liver by reducing the way the liver breaks down fatty acids through slowing down a process called “ß-oxidation”, and as the fat % within the liver increases, at some point it starts causing all kinds of problems… starting with swelling (steatohepatitis), which then leads to scarring over time (fibrosis), and then eventually, once enough scar tissue is present, prevents the liver from doing its core functions (as well as its ability to regenerate), and cirrhosis becomes present.¹
Once cirrhosis sets in, there’s basically no going back. Therefore, it’s critical to avoid liver disease progression, and all of this starts with doing everything you can to limit liver fat. Exercise is a great way to aid in this goal.
In the section above, we mentioned that alcohol packs a LOT of calories. Oftentimes, frequent drinkers are fatter than many non-drinkers. Why? Because they consume a normal amount of calories (2000–2500) a day through food… but then consume alcohol calories on top of that without moderating their diet or exercise habits accordingly.
In terms of alcohol consumption, the top 30% of drinkers consume an average of 30 drinks a week. This is an excess of roughly 3000 calories per week of alcohol—or about 430 excess calories a day from alcohol consumption alone. Generally speaking, every 3500 excess calories leads to a pound of body fat. This means that in theory, if you’re new to heavy drinking and consume about 30 drinks a week without changing your exercise or diet habits, you generally could expect to gain about a pound of body fat every 8 days or so until your basal metabolic rate (BMR) evens out with the excess weight gain. In practice, this generally isn’t so simple—as oftentimes alcohol begins to replace calories from other sources, but the point is very relevant—alcohol consumption leads to excess calories, which then leads to excess metabolic demand, which then leads to additional fat storage in the liver.
There’s only one problem with the above analysis: it doesn’t account for “peculiar manner in which the liver burns up alcohol.”
While excess calories find their way into the liver through liver fat… calories stemming from alcohol ends up being a twofer in the sense that they are a calorie that are more likely than other macronutrients, such as protein, to lead to the storage of liver fat.
In a conference in 1976 in Munich, Dr. Thaler, a Viennan alcohol researcher discussed his findings in a presentation titled “Alcohol Consumption and Diseases of the Liver”. He stated:
“However, only recent experiences have shown that the main cause of alcoholic fatty liver should be sought in the rather peculiar manner in which the liver burns up alcohol. In the process of catabolism of ethanol to acetate, two NAD molecules are reduced to NADH. For this vital hydrogen acceptor there exists a steady state, i.e. O2 must be supplied at the same speed at which NAD is reduced to NADH, in order to oxidize NADH to NAD. For this reason, during the combustion of alcohol, 70% of the oxygen consumption of the liver is utilized for this special purpose alone. All other oxidative procedures must be considerably deferred. The citric acid cycle is thus also inhibited and the ß-oxidation of fatty acids is curbed. Therefore, the basic cause of alcohol fatty liver is reduced catabolism of fatty acids in the liver cell.”
According to Thaler, one of the original researchers in this field, alcohol causes the inhibition of metabolizing fatty acids in the liver cell, which then leads to the buildup of liver fat.
In a more recent research reviews, the authors of an article titled “Effect of Ethanol on Lipid Metabolism” state:
“Alcohol directly and indirectly impacts numerous aspects of hepatic lipid flux that ultimately lead to lipid accumulation. The simplest example is that alcohol metabolism itself directly causes steatosis (fatty liver).”
They further that:
“This metabolism robustly increases the ratio of NADH:NAD+ within the cell, which then favors the inhibition of fatty acid ß-oxidation in the liver … the net effect is to favor triglyceride accumulation in the hepatocytes.”
In other words, inhibition of fatty acid ß-oxidation in the liver causes liver cells (hepatocytes) to favor the accumulation of fat (triglycerides). Therefore, beyond the problem of alcohol being packed densely with excess calories, the way in which it is metabolized leads to the storage of fat within liver cells. Because liver fat is the first stage of many types of liver disease, and ß-oxidation is the means by which the liver clears liver fat, alcohol must be seen as a double metabolic problem when it comes to keeping a healthy liver.
One analogy that could be used in regard to keeping a healthy liver is that of the pedals in a car. The goal is for ß-oxidation to occur at a pace fast enough to prevent the accumulation of fat in the liver. The goal is catabolizing fats in the liver faster than they accumulate. Since alcohol inhibits the rate of ß-oxidation, alcohol must be seen as the “brakes” of fat metabolization in the liver.
This makes the point very clear: the more alcohol you drink, the more you’re pressing the brakes on liver fat metabolization, and the more liver fat you will gain.
This liver fat is one of the biggest stresses the alcohol puts on your liver. Besides working to consume less alcohol, what can be done to increase your rate of ß-oxidation?
To lose fat (and liver fat), generally speaking, you must burn more calories than you consume. Most people burn around 1600 calories a day through their BMR—that is, the number of calories that you burn just to exist while doing nothing. Exercise, whether it being from walking around at work, getting in and out of your car, or dedicated exercise sessions, all then piles on how many calories you can burn on top of that BMR.
If you burn more calories each week than you consume, you will on average lose weight. Generally speaking, for every 3500 calorie deficit that you run, you will lose around a pound of body fat. In the absence of extreme drinking habits, which will almost invariably lead to increased levels of liver fat regardless of weight loss through the reduction in ß-oxidation, weight loss in general should also lead to a reduction in liver fat. What’s interesting however, is that the liver both loses and gains fat quicker than the rest of the body. It’s sort of the canary in the coal mine for the rest of your body in the sense that fat buildup or loss occurs more rapidly to it.
In one review of the literature published in 2019, “Nonalcoholic Fatty Liver Disease and Obesity Treatment”, the authors summarize:
“The cornerstone of therapy [for FLD] is weight loss, as a reduction in body mass index (BMI) of 5% is associated with a 25% relative reduction in liver fat as measured by magnetic resonance imaging (MRI).”
You read that right, it doesn’t take a large weight reduction change to lead to an even more significant reduction in liver fat. However, the inverse also appears to be true—a small amount of weight gain can lead to larger amounts of liver fat. The liver is both the fastest organ to shed and/or gain fat in relation to the rest of the body as a whole.
The authors further contend:
“The available evidence suggests that weight loss of at least 5% can improve NAFLD, with a weight loss of 7–10% having some impact on NASH and fibrosis.”
In other words, for overweight people, then at a weight loss of 5% (~8.5 pounds for the average 170 pound US female and 10 pounds for the average 200 pound US male), FLD can be improved. At a minimum of 7% (~12 pounds for the average female and ~14 pounds for the average male), the weight loss can actually lead to the improvement of liver swelling (NASH) and liver scarring (fibrosis).
It’s pretty simple… if you’re overweight, losing body fat can help reduce liver fat. And if you lose enough liver fat, your liver can start healing.
To lose weight (which should mostly consist of fat—not muscle), you have 3 choices: diet, exercise, or some combination thereof. In another article titled “Liver Fat and the Mediterranean Diet”, we discuss a liver friendly diet at length. However in this article, we will discuss the benefits of exercise on your liver.
We dealt with the first point above, but let’s now discuss exercise’s benefits on liver beyond that of creating a caloric deficit so as to lose weight.
In a study titled “Resistance exercise reduces liver fat and its mediators in non-alcoholic fatty liver disease independent of weight loss”, the researchers found that exercise (specifically strength training) led to the reduction of liver fat independent of weight loss.
In their conclusion, they state:
“An 8-week resistance exercise programme brought about an approximately 13% reduction in liver fat. This was accompanied by an approximately 12% increase in insulin sensitivity, and increased fat oxidation during submaximal exercise in the absence of any change in body weight.”
This is important because it shows that exercise’s beneficial effects on the liver are not limited to that of overall weight/fat loss. How is this possible? This study, among others, suggests that one of the main pathways is through increasing ß-oxidation (or fat oxidation in general).
As described above, the rate of ß-oxidation is the speed at which your liver can shed its fat. If alcohol is the “brake pedal” on this process, then exercise is the “gas pedal”. Therefore, if drinking alcohol is a common part of your life, then it must be matched with exercise.
In the above visualization, you can see a bunch of acronyms surrounded by yellow: TGs (triglycerides), FFAs (free fatty acids), and VLDL (Very-low-density lipoprotein). At the risk of being reductionistic, it can be understood that these are all “fats”. The other things you will see is DNL (de-novo lipogenesis) and ß-ox (ß-oxidation).
In this article we haven’t yet discussed de-novo lipogenesis, for the sake of simplicity. However, it’s worth quickly explaining. DNL is a way in which the liver can create fat from other sources, such as through sugar and carbohydrates. For the longest time, it was believed that you could have less fats in your blood by reducing the amount of fat in your diet. While this is true to a degree, depending on the source of carbs, in practice it often leads to something known as the “Eisenhower Paradox”. President Eisenhower, suffering a heart attack, worked with his doctor to decrease the fats in his blood by reducing his intake of dietary fat. The problem however is that it didn’t work, and he kept getting worse. How? De novo lipogenesis. The body needs fat, and thus has the ability to create it through other sources. The copious amounts of carbs he was eating from poor sources was simply converting into fat, thus defeating the purpose of limiting his fat intake.
Unfortunately for drinkers, alcohol not only decreases ß-oxidation, but it also increases de novo lipogenesis. Thus, alcohol both leads to 1) the creation of more fat through de novo lipogenesis, but then 2) slows down the reduction of this fat through decreasing ß-oxidation.¹
There is hope though. Beyond drinking less and eating a better diet, us drinkers do have a very important tool at our disposal to offset these negative effects of alcohol: exercise.
If you look at the illustration above again, you can see a number of arrows pointing to skeletal muscle. These arrows are showing fats being used up by your muscles as you exercise as well as while your muscles recover from it. As exercise occurs, not only does ß-oxidation increase—the way your burn off liver fat, but de novo lipogenesis also decreases—meaning that your liver is forming less fat from other sources.² As we discuss in an article called “Added sugar is almost gram for gram as hard on your liver as alcohol”, nearly 25% of liver fat often comes from DNL.³
Therefore, by decreasing DNL and increasing ß-oxidation, exercise can create a huge swing in fats in the body—but also liver fat in general.
(Note: Exercise are not only opposites when it comes to DNL, ß-ox, and calorie totals… but also other important pathways such as SIRT and AMPK. For the sake of simplicity, we will not introduce SIRT and AMPK in this article, but instead will discuss it in a future article.)
As we have discussed in another article, most forms of liver disease start with liver fat. There are a number of ways that you can target liver fat: drinking less (quantity), drinking less (frequency), eating better, reducing sugar intake, having a better BMI, and dietary additions. However, one of the most powerful that us drinkers have at our disposal is exercise.
Why? Because alcohol and exercise are opposites on almost all pathways that lead to liver fat. In this article we focused on ß-oxidation, as it’s the most studied and easiest to understand. However, it also goes for DNL, SIRT, AMPK, and other important pathways.
In the above screenshot from a page of a study called “Fitness Versus Fatness: Moving Beyond Weight Loss in Nonalcoholic Fatty Liver Disease”, you can see how much diet and exercise can lead to positive results in liver health on a number of important biomarkers: AST, ALT, hepatic steatosis, FLD stage, NASH score, hepatic triglycerides, liver fatness, insulin resistance, and more (seen in later pages of the study).
One of the questions we often get asked is how much exercise, what type, and how often. Generally, the answer is quite simple: the more (quantity) and harder (intensity) that you exercise, the better the results will be.
One of the studies examined in the above article helps explain this:
“The largest study to examine for possible independent effects of PA in NAFLD showed that 3 months of a behavior change–based intervention signiﬁcantly improved liver enzymes independent of weight loss. In this study, participants who achieved low (60–119 minutes/week) and moderate (120–239 minutes/week) volumes of incidental PA experienced a hepatic beneﬁt, with the greatest improvement in those who increased their PA levels to >150 minutes/week and had improved VO2 max.”
These researchers found that even “low volumes” of physical activity (PA), at between 1–2 hours a week, experienced liver health increases (hepatic benefit). The greatest improvements occurred when people did at least 150+ minutes of exercise, and at a high enough intensity to increase their VO2 max (which is a key measure of fitness as it examines the amount of oxygen that you can utilize during exercise).
Therefore, while the answer is that more is typically better, 2.5 hours of good exercise a week can have significant benefits on your liver. If you’re going to drink, one of the ways you can “earn it” is through exercise!
¡Salud! (The act of saying “cheers” in Spanish. It literally means “to health”.)
This blog provides general information and discussions about health and related subjects. The information and other content provided in this blog, website, or in any linked materials are not intended and should not be considered, or used as a substitute for, medical advice, diagnosis or treatment. This blog does not constitute the practice of any medical, nursing or other professional health care advice, diagnosis or treatment. We cannot diagnose conditions, provide second opinions or make specific treatment recommendations through this blog or website.
If you or any other person has a medical concern, you should consult with your health care provider or seek other professional medical treatment immediately. Never disregard professional medical advice or delay in seeking it because of something that you have read on this blog, website or in any linked materials. If you are experiencing a medical emergency, please call 911 or call for emergency medical help on the nearest telephone immediately.
¹You, M., & Arteel, G. E. (2019). Effect of ethanol on lipid metabolism. Journal of hepatology, 70(2), 237–248. https://doi.org/10.1016/j.jhep.2018.10.037
²Rabol, R., Petersen, K. F., Dufour, S., Flannery, C., & Shulman, G. I. (2011). Reversal of muscle insulin resistance with exercise reduces postprandial hepatic de novo lipogenesis in insulin resistant individuals. Proceedings of the National Academy of Sciences, 108(33), 13705–13709. https://doi.org/10.1073/pnas.1110105108
³Sanders, F. W., & Griffin, J. L. (2016). De novo lipogenesis in the liver in health and disease: more than just a shunting yard for glucose. Biological reviews of the Cambridge Philosophical Society, 91(2), 452–468. https://doi.org/10.1111/brv.12178
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