It is a common joke among the party crowd and social drinkers to bemoan the plight of one’s liver and the suffering it endures as a consequence of imbibing alcohol. The morning after you have had a few drinks beyond your normal limit, everything can hurt. Your head, your achy muscles, your stomach. But your liver really does take the brunt of the damage because it is primarily responsible for breaking down the alcohol and getting rid of it. Here is what happens when your liver is exposed to alcohol. And yes, it’s sobering.
Alcohol Metabolism and the Liver
The interaction between alcohol and the liver begins when approximately 80% of the alcohol you ingest arrives at the liver where much of the alcohol dehydrogenase in the body is situated. This is the enzyme that converts ethanol to acetaldehyde. It is also present to a lesser extent in the kidneys, endocrine tissues, and the brain.
Acetaldehyde, the initial breakdown product of alcohol, is not directly toxic to the hepatocytes (liver cells), but it can bind with proteins in the cells and alter their structure, making liver cells more susceptible to damage. Acetaldehyde is also pro-inflammatory, acting as a catalyst for free radical production in the liver.
In addition to acetaldehyde byproducts, the alcohol itself elicits secretion of factors that cause inflammation. These changes, among others, create an accumulation of fatty acids in liver cells, referred to as “fatty liver” or steatosis.
What Causes Fatty Liver?
The liver itself does not normally store fat since fatty infiltration interferes with the health and functioning of liver cells. A normal, healthy liver converts excess carbohydrates and proteins derived from the food you have eaten into fatty acids and triglycerides. These are products that can be exported out into the blood and ultimately stored as fat in peripheral adipose tissue. When the liver is overtaxed by detoxifying harmful substances in alcohol and drugs, its ability to get rid of these fatty acids is compromised.
The exact mechanisms involved are not fully understood, but a number of possible causes have been proposed. One of the more complex pathways involves the ratio of the oxidized form of nicotinamide adenine dinucleotide (NAD+) to the reduced form (NADH) in the liver. The enzyme that metabolizes alcohol, alcohol dehydrogenase, removes a hydrogen atom from alcohol and transfers it to a molecule of NAD. NAD is converted (or “reduced” in chemical terminology) to NADH. NADH participates in numerous other reactions and passes on the hydrogen to other compounds.
These chemical interactions are called REDOX (reduction-oxidation) and in balance are essential for normal physiology and health. However, when NADH builds up in excess, the passing on of hydrogen to other compounds can create oxidative stress. The alcohol-related surplus of NADH causes alterations in fatty acid metabolism, such as slowing down the breakdown or oxidation of fatty acids.
Alcohol also stops the action of an enzyme that breaks down a backbone structure of triglycerides. When the supply of this backbone is in abundance, more triglycerides are made and put into circulation. So, alcohol works to both increase the amount of fatty acids and to limit the breakdown of fatty acids.
Fatty acids are broken down to generate NADH ultimately to create energy (ATP generation) via the Kreb’s cycle. The alcohol drinker has an excess of NADH as a result of metabolizing the alcohol that is consumed. In fact, the excess NADH tells the liver that conditions are just right for making fatty acids rather than breaking them down. As a result, when NADH is abundant as a result of alcohol consumption, fatty acids (in the form of triacylglycerols) accumulate in the liver. All of these mechanisms favor fatty liver.
How Do You Know if Your Alcohol Consumption Is Damaging Your Liver?
How do you know if your liver is affected by your level of alcohol consumption? A rise in liver enzymes is sometimes the indicator that liver health and functioning is compromised.
Liver enzymes are routinely measured in health screenings. Alanine-transferase (ALT) is an enzyme involved in amino acid metabolism and is uniquely derived from the liver. When the liver is damaged, the enzyme leaks into the blood, leading to a measurable increase above normal, healthy levels. However, 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 disease.
What science has shown is this: the amount of fatty acid in the liver depends on the balance between the processes of delivery and removal, but regardless of the mechanism, just about every individual who drinks four to five or more drinks a day, even for a short period of time, will develop fatty liver.
There is a great deal of ongoing research to reach a full understanding of all the metabolic shifts that result in fatty liver, especially since the obesity epidemic that plagues our nation has increased the percentage of people who suffer from fatty liver to at least 25% of the population. Fatty liver is strongly correlated with insulin resistance and usually progression to type 2 diabetes.
Early on, most people with fatty liver are asymptomatic, but if symptoms do occur, they may include fatigue, weakness, malaise, nausea, or discomfort localized to the right upper abdomen. The liver is encased in a sac and there will be pressure exerted as the liver becomes enlarged with fatty acids.
The condition can be improved and, in some cases, reversed, but how long that takes depends on many factors, such as the amount and duration of drinking, other diet and lifestyle factors, and individual susceptibility.
Nutrient therapies that benefit fatty acid metabolism in the liver include essential amino acids, caffeine, and omega-3 fatty acids along with a varied, nutrient-dense diet. Most importantly, honor the relationship between alcohol and the liver and give your liver a breather with mocktails every now and then.