It’s estimated that between 80–100 million Americans have fatty liver disease. How could this number be so large?

Well, as we have pointed out in other articles—90% of problem drinkers (4-5 drinks per day) have fatty liver disease—even if they have not yet had it diagnosed yet. Furthermore, 75% of obese people have fatty liver disease. This means that if you are a heavy drinker and are overweight, you’re at a very high risk of having fatty liver disease.

As can be seen in the above picture, fatty liver disease is often the first stage in the liver’s march towards cirrhosis, which is an irreversible change to the liver that causes it to cease working properly and often leads to liver-related death thereafter—even though many people may extend their lifespan at this point through drastic measures such as stopping alcohol entirely and getting other liver-related treatments.

In this article we will discuss what fatty liver disease is, how it’s caused, why it matters, and what you can do to protect yourself.

FLD: NAFLD vs AFLD

When it comes to fatty liver disease (FLD), researchers often break it into 2 categories: 1) non-alcoholic fatty liver disease (NAFLD) and 2) alcoholic fatty liver disease (AFLD). The reason this is done is to signify what the main culprit behind a person’s fatty liver is. For most of history, the primary reason for fatty liver disease was due to alcohol. However, as obesity rates rose in the United States from under 10% in the 1950s to what’s projected to be near 50% by 2030, researchers found it helpful to break out NAFLD from AFLD. This was likely done to aid in NAFLD research—not AFLD research. The questions researchers were trying to get at was how non-alcohol factors led to liver fat, and thus it was necessary to make the distinction.

The fact of the matter is that both NAFLD and AFLD are the same thing: FLD.

The main difference is that NAFLD is primarily caused by non-alcohol reasons (such as poor diet and exercise) whereas AFLD is caused by alcohol. If you have FLD, the cause of it likely exists on a spectrum between alcohol on the one hand, and diet and exercise on the other. For some people, it may be an even contribution from both, but for others, it might primarily come from an overconsumption of alcohol or a bad diet with little to no exercise (untreated insulin resistance and diabetes can also contribute to FLD, independent of diet and exercise, but if you’re aware that you have these conditions, you should already be on a plan to manage them with your doctor; if you’re not, make an appointment ASAP). Therefore, when it comes to thinking about FLD, it’s important to know that the problem is the end result of liver fat, and your habits are merely the methods by which you can affect it.

What exactly is FLD?

Fatty liver disease can be described in visceral terms by comparing it to foie gras. Don’t know your french delicacies? Foie gras is a dish of fattened bird liver, usually from a goose or duck. Foie gras dates back at least 2500 years to Ancient Egypt, but is most famous in modern times as a dish in France, the largest producer of foie gras in the world.

It’s produced by force-feeding ducks to a point where the animal’s liver grows to as much as 10x its original size before the animal is slaughtered, the liver is packaged, and then used in fancy meals. It’s described as being “rich, buttery, and delicate, unlike that of an ordinary duck or goose liver.”

The reason that foie gras has this rich and buttery texture is because a large percentage of the liver is comprised of fat. This can easily be seen under a microscope.

Above is a liver histology showing a biopsy sample of a human child before (healthy liver—right side—labeled B) vs after building a large percentage of liver fat (FLD—left side—labeled A). As you can see in the side by side picture, the liver biopsy with FLD has enough fat globules where the liver image shows over 66% of the surface area being white rather than a healthy pink.

FLD is literally just the human equivalent of foie gras.

For those in America, where foie gras isn’t as common, another way to think about this would be the marbling of a beef steak.

When it comes to beef, the higher the degree of marbling (which is the term for evenly distributed fat deposits), the more valuable the cut of meat. These are then graded based on the amount of fat deposits by percentage.

However, unless your desire is to taste good to a cannibal, the goal is for your organs to not look like this. When it comes to your body, large amounts of stored fat is the enemy and is detrimental to your health—especially the health of the organs it’s stored in—such as your liver.

A healthy liver is considered as having less than 5% fat in it (<5%). The medical definition of fatty liver disease is quite simple: it’s when a liver is comprised of 5% fat or greater. However, as can be seen in the chart above, there are different grades of FLD.

• Grade I FLD is between 5–33% liver fat and is considered “mild”.
• Grade II FLD is between 33–66% liver fat and is considered “moderate”.
• Grade III FLD is >66% liver fat and is considered “severe” or “marked”.

The medical name for FLD is “steatosis” (sometimes spelt “steotosis”) and comes from the Greek language. “Steo” literally means “fat” and “-osis” literally means “state” (conceptually meaning “state of being”). Therefore, together, steatosis translates as “fat state”. In the context of the liver (“hepa” in greek), “hepatic steatosis” literally means “liver that is in a fat state”.

The progression of liver disease.

In the chart above we can see that 15–30% of people with healthy livers go on to develop FLD. Recent estimates suggest that this number is most likely around 25%. As discussed above, FLD is simply the presence of larger than normal amounts of fat within the liver and has stages.

Once FLD sets in, 12–40% go on to develop steatohepatitis (or as labeled above: non-alcoholic steatohepatitis—”NASH”). Just like as we described above, the “non-alcoholic” portion is related to cause, as it can be caused by either alcohol-related reasons (such as drinking too much) or non-alcohol-related reasons (such as poor diet and exercise). Just like with FLD, steatohepatitis can be caused by a combination thereof on a spectrum between alcohol and non-alcohol reasons.

Steatohepatitis’ etymology is greek. It comes from “steato” (fat), “hepa” (liver), and “-itis” (literally “pertaining to”, but often used in the medical community as “inflammation” or “swelling”). All together, “steatohepatitis” means: “fatty liver swelling”.

There are many different charts showing the progression of liver disease. The above chart leaves out fibrosis, which is characterized by scarring of the liver.

Steatohepatitis is primarily characterized by inflammation within the liver caused by the accumulation of fat. As you might know from other experiences in your life, such as sports, the repeated inflammation of something leads to the deposits of fibers. For example, the tearing and re-tearing of one’s rotator cuff through repetitive motion sports (such as swimming, tennis, or baseball) often leads to large amounts of scar tissue within the shoulder joint. Or, a major cut on someone’s skin often leads to the deposits of scar tissue.

Scar tissue is the body’s way of protecting itself by accelerating the healing process through the depositing of collagen fibers and a fibrous matrix that leaves the new tissue different than the original. This is no different than what is occurring in the liver—albeit in a different organ. Repeated or continuous swelling of the liver through ongoing stress—such as through the heavy amounts of alcohol consumption or the overconsumption of unhealthy food, both of which can trigger large amounts of fat being stored in the liver—can over time begin “scarring” the organ. This scarring of the liver is called fibrosis.

Therefore, as the chart shows above, steatohepatitis can involve just swelling (inflammation). Or, if severe and frequent enough, can start leading to fibrosis. Of people with steatohepatitis, 15–25% go on to develop liver cirrhosis. The liver is an incredible organ in the sense that it is capable of regeneration, and thus even fibrosis is often considered reversible (albeit partially) if the right habits and treatments are put in place. Cirrhosis is characterized by so much scarring that the liver loses not only i) its remarkable ability to heal itself, but also ii) its ability to carry out its core function.

In the above microscopic images, you can see:

• 1) A normal liver. It is characterized by being comprised of primarily healthy red tissue.
• 2) A liver with FLD. It is characterized by being comprised of large amounts of fatty infiltration.
• 3) A liver with steatohepatitis and the onset of fibrosis. The blue areas are scarring that has began occurring to the liver’s structure. Scar tissue is replacing normal liver cells.
• 4) A liver with cirrhosis. The liver is comprised of so much scar tissue that it can no longer regenerate or function properly.

Once cirrhosis sets in, it can be managed, but it can no longer be reversed. At this point, quality of living and life expectancy will be significantly diminished. Roughly 50% of these people either die of the disease or receive a liver transplant.

Why FLD matters.

For the longest time, FLD wasn’t as frequently studied in comparison to its later evolutions such as fibrosis and cirrhosis, as that’s when things actually become problematic. One temptation of medicine is that there’s often an overemphasis on fixing problems rather than preventing them in the first place.

However, in recent decades, this tendency has reversed itself—likely due to the increase of obesity and the accelerating growth of NAFLD. The graph on the left shows academic articles written on FLD by country over a span of 20 years. It shows that there was almost no research around FLD prior to the 2000s—but also thankfully that research into the topic has exploded in recent years. My experience is that it hasn’t slowed down at all since 2014 when this graph was created.

While we also study steatohepatitis and fibrosis, our main focus at Cheers is finding ways to help reduce FLD and its tendency to develop into steatohepatitis. Thus, most of our focus is on techniques to reduce liver fat.

Our rationale for focusing on FLD is quite simple: i) this is what most people have, and ii) this is the first stage of the disease. Without fatty liver, it’s likely impossible to develop into later stages of alcohol or fat related liver disease.

In an article published in The Journal of Hepatology in 2019 titled “Effect of ethanol on lipid metabolism”, the authors state:

“Although transient steatosis is largely an inert pathology, the chronicity of alcohol-related liver disease seems to require steatosis.”

While this might seem basic based on the above charts about liver disease progression, the authors of the above study find it important to point out to other liver disease researchers that they cannot find examples of liver disease progressing without first involving the accumulation of liver fat. And thus, by implication, that working to reduce FLD is important in terms of preventing the progression of later, more harmful, and often irreversible forms of liver disease. They explain this directly when they state:

“Therefore, a full understanding of how alcohol induces steatosis could be key in preventing progression to later stages of [alcoholic liver disease].”

The logic is quite simple… prevent and/or reduce steatosis and likely prevent the disease from progressing further.

For the longest time, it was believed that FLD (or steatosis) was irrelevant in the sense that it was clinically silent and didn’t have any negative effects in and of itself. The authors’ argument is that this understanding of FLD is misguided. In the words of the authors:

“Steatosis can also be clinically ‘silent,’ and can exist in the absence of increases in any other index of liver damage, such as plasma aminotransferases, for example. For these reasons, steatosis was originally viewed as an inert pathology in ALD (and in other fatty liver diseases). However, more recent studies have suggested that blunting or preventing steatosis could help attenuate the progression of ALD; in fact, the degree of steatosis is an early predictor of overall disease severity. These facts challenge the assumption that steatosis is an inert pathology. Hepatic fat accumulation can invoke metabolic changes that sensitize the liver to further injury (see below). Therefore, a full understanding of how alcohol induces steatosis could be key in preventing progression to later stages of ALD.”

In other words, if you can understand how to reduce or manage steatosis, especially that caused by alcohol, you could potentially understand how to prevent its progression into later stages of alcoholic liver disease.

Combatting FLD through better habits.

At Cheers, we’re drinkers — and so are our customers. Therefore, similar to the authors of the above study, our focus is on the health of people that consume alcohol (“drinkers”).

One of the best ways we can do this is to give people best practices in regards to ways they can reduce liver fat. Our Liver Habits Score currently targets at least 10 different categorical ways in which people can work to improve their liver health—specifically in regards to liver fat. These strategies range from alcohol consumption habits, to dietary habits, to exercise habits.

As you can see in the chart above, the better you do in each category, the better your overall score, and the better your liver fat percentage is likely to be.

By working to reduce FLD among drinkers, our hope is to prevent the progression of liver disease for many people across the nation so that they may enjoy alcohol throughout a long, healthy, and happy life.

You can read about our motivation for creating the Liver Habits Score here.

To get started in adopting best practices for liver health, take our Liver Habits Score to see how you’re currently doing and how you can begin improving!

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¡Salud!

Brooks, Founder of Cheers

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