It’s a common occurrence among the party crowd and social drinkers to joke about alcohol and the liver. Anyone who’s had a few too many or indulged in a little binge drinking has probably bemoaned the plight of their liver and the suffering it’s endured as a consequence of imbibing too many alcoholic beverages.
And the morning after you’ve had a few drinks beyond your normal limit, everything really can hurt. Your head, your muscles, your stomach. But it’s your liver that truly takes the brunt of the damage, as it’s the organ primarily responsible for breaking down the alcohol and getting rid of it.
Let’s now take a look at what really happens when alcohol and your liver get together. And in case you’re wondering, yes, it’s sobering.
Alcohol and the Liver: Let’s Talk Metabolism
Many people don’t realize that alcohol is actually considered a toxin. But if that’s true, why don’t we drop dead after too much alcohol—or any alcohol at all?
The reason for this is the enzyme known as alcohol dehydrogenase, which is found mostly in the liver and stomach (though it is also present to a lesser extent in the kidneys, endocrine tissues, and brain).
Alcohol dehydrogenase exists in the stomach as well as the liver because alcohol metabolism begins in the stomach. The approximately 80% of ingested alcohol that avoids getting broken down here is then absorbed into the bloodstream by the small intestine.
However, there's also a small percentage (about 2% to 5%) of alcohol that's excreted unchanged via respiration, sweat, and urine.
Once reaching the capillaries surrounding the small intestine, alcohol then goes directly to the liver. And it's here that the interaction between alcohol and the liver begins.
Here, alcohol mingles again with alcohol dehydrogenase and is broken down into acetaldehyde. Acetaldehyde is a highly toxic substance and known carcinogen. In fact, this is the chemical that results in hangover symptoms like nausea, headache, and discomfort.
In the second phase of metabolism, another enzyme known as acetaldehyde dehydrogenase breaks the toxic acetaldehyde down into a less active byproduct called acetate. This rather harmless substance is then further broken down into water and carbon dioxide, both of which can be easily eliminated by the body.
Interestingly, acetaldehyde is not directly toxic to the liver cells (hepatocytes). However, it can bind with the proteins in the cells and alter their structure, making them more susceptible to damage. It's also considered pro-inflammatory, as it acts as a catalyst for free radical production in the liver.
Free radicals result when oxygen molecules split into single atoms with unpaired electrons that then “scavenge” the body seeking other electrons to pair with. As these free radicals move about the body, stealing electrons from the nearest stable atom, they create yet more free radicals.
If this process continues to the point where more free radicals exist than there are antioxidants to neutralize them, it becomes known as oxidative stress. And this oxidative stress results in damage to cellular components, including proteins and DNA, and has been implicated in a number of medical conditions, including cirrhosis and liver cancer.
In addition to these toxic byproducts of acetaldehyde, the alcohol itself elicits secretion of factors that cause inflammation, including pro-inflammatory cytokines (special proteins that affect communication between cells).
These changes, among others, result in a defect in fatty acid metabolism and a subsequent accumulation of fatty acids in liver cells. This marks the earliest stage of alcoholic liver disease, known as fatty liver, or steatosis. Unchecked, alcohol-related liver disease can progress to alcoholic hepatitis (inflammation of the liver caused by drinking alcohol) and even cirrhosis.
What Causes Fatty Liver?
The liver itself does not normally store fat since the presence of too much fat, known as fatty infiltration, interferes with the health and functioning of liver cells.
A normal, healthy liver converts excess carbohydrates and proteins from the food you’ve eaten into fatty acids and triglycerides. These are substances that can be sent out into the blood and ultimately stored as fat in peripheral adipose (fat) tissue.
However, when the liver becomes overtaxed detoxifying the harmful substances found in alcohol and drugs, its ability to get rid of these fatty acids is compromised. The exact mechanisms involved in fatty infiltration are not fully understood, but a number of possible causes have been proposed.
One of these is the complex pathway involving the ratio of the oxidized form (meaning it’s been chemically combined with oxygen) of nicotinamide adenine dinucleotide (NAD+) to the reduced form (NADH) in the liver.
During this process that converts NAD into NADH, the enzyme that begins alcohol metabolism, alcohol dehydrogenase, removes a hydrogen atom from alcohol and transfers it to a molecule of NAD.
NAD is subsequently converted (or “reduced,” in chemical terminology) to NADH, which then participates in numerous other reactions and passes the hydrogen on to other compounds.
All of these chemical interactions are known as redox (reduction-oxidation) and are actually essential for normal physiology and health. However, when NADH builds up to excessive levels, the passing on of hydrogen to other compounds can create oxidative stress.
The alcohol-related surplus of NADH likewise causes alterations in fatty acid metabolism and can lead to a slowdown in the breakdown, or oxidation, of fatty acids. Alcohol also stops the action of an enzyme that breaks down the backbone structure of triglycerides.
What do we mean by “backbone”?
When we’re talking about triglycerides, we’re actually discussing the type of lipid we commonly refer to as fat. And each of these fat molecules is made up of two parts: a glycerol backbone and three fatty acid tails. In fact, it’s these three fatty acid tails that put the “tri” in triglycerides.
When the enzyme that breaks down this glycerol backbone is not allowed to do its job, the supply of backbones becomes more abundant. And this leads to more triglycerides being made and put into circulation.
So, alcohol creates a vicious cycle in which more fatty acids are made and fewer are broken down.
Fatty acids are broken down in order to generate NADH and create adenosine triphosphate (ATP)—the major form of chemical energy in the body—via the Krebs cycle. However, when you drink alcohol, the process of metabolizing that alcohol results in an excess of NADH.
Instead of breaking down fatty acids, the excess NADH actually tells the liver that conditions are perfect for making even more. As discussed earlier, this results in more and more fatty acids accumulating in the liver in a process that may eventually lead to fatty liver and, if unchecked, liver damage.
In fact, according to the National Institute on Alcohol Abuse and Alcoholism (NIAAA), more than 90% of heavy drinkers will eventually develop fatty liver.
How Do You Know if Your Alcohol Consumption Is Damaging Your Liver?
If you’re concerned about how your alcohol intake is affecting your liver, you should know that in the early stages of liver damage, a rise in liver enzymes may be the only indicator that anything’s wrong.
If you’ve ever had a health screening, you’ve probably undergone blood tests, of which liver enzymes are a routine part. And one of these enzymes, alanine aminotransferase (ALT), is involved in amino acid metabolism.
When the liver is damaged, ALT leaks into the blood and may show up as elevated on a blood test. Yet tests of liver function are often normal despite the presence of fatty liver disease.
More sophisticated tools like magnetic resonance spectroscopy or ultrasonography can directly measure liver fat, but these techniques are usually reserved for research purposes or patients with advanced liver problems.
However, what science has shown us is this: the amount of fatty acids in the liver depends on the balance between the processes of delivery and removal.
Regardless of the mechanism, people who engage in heavy drinking—classified by the NIAAA as more than 4 drinks a day or 14 per week for men and more than 3 drinks a day or 7 per week for women—for even a short period of time will most likely develop fatty liver.
Research into the metabolic shifts that result in fatty liver is ongoing, especially in light of the obesity epidemic among Americans today.
In fact, the rise of nonalcoholic fatty liver disease as a result of obesity has increased the total percentage of the population suffering from fatty liver to at least 25%!
In addition to obesity, other risk factors for this condition include:
- Insulin resistance
- Type 2 diabetes
- High blood pressure
- Hepatitis C
- Elevated lipids
- Corticosteroid use
Symptoms of Alcoholic Liver Disease
Most people in the fatty liver stage of alcohol-related liver disease have no symptoms of liver disease. However, if symptoms do occur, they may include:
- Discomfort in the middle or right upper abdomen
If excessive drinking continues, inflammation of the liver (alcoholic hepatitis) will progress, and more serious damage to the liver may result.
The most severe form of alcohol-related liver disease is alcoholic cirrhosis, which is a condition in which scar tissue gradually replaces normal liver tissue.
While cirrhosis often has no symptoms until severe liver damage has already occurred, when symptoms do occur, they may include:
- Loss of appetite
- Weight loss
- Abdominal pain
- Lower extremity swelling
If cirrhosis progresses far enough, liver function can become compromised to the point of liver failure and liver transplant may be necessary.
Treatment of Alcoholic Liver Disease
If you or someone you care about is suffering from the effects of liver disease, please know that the condition can be improved and, in some cases, reversed. However, how long this takes will depend on many factors, including:
- How much alcohol is consumed
- How long alcohol use has occurred
- Other diet and lifestyle factors
- Individual susceptibility
There are also various nutrient-based therapies that have been shown to benefit fatty acid metabolism in the liver. These include:
EAAs for Liver Health
Adhering to behavioral and lifestyle modifications is extremely difficult for individuals with alcohol use disorder, with only 7% ever seeking professional help. Supplementation with a targeted high-dose of essential amino acids can help reduce excessive accumulation of lipids in the liver and offset the harmful effects of alcohol even when no other nutritional changes occur and alcohol consumption stays the same.
According to a study published in the journal Nutrients, a 13-gram dose of essential amino acids taken twice a day can lower intrahepatic lipid content in people with alcohol use disorder even when alcohol consumption remains unchanged.
If you'd like to give a little extra support to your liver, click here to learn more about our essential amino acid blends.
Most importantly, be sure to honor the relationship between alcohol and the liver and think about giving your liver a breather with some mocktails every now and then.