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  • Writer's pictureRyan Allen

A prevention-based approach to NAFLD

In my last post on the concerning epidemic of non-alcoholic fatty liver disease (NAFLD), I introduced the detrimental impacts of dietary fructose on hepatic (liver) fat production. I had mentioned that this de novo lipogenesis (DNL; meaning creation of fat anew in the liver) from fructose is just one input in the “net liver fat equation” to consider. You may recall that there are two key inputs (dietary fat consumption and de novo lipogenesis) and two key outputs (fat oxidation, or burning, and export to other parts of the body). The equation should then look something like this:

total liver fat = dietary fat + DNL - oxidation - export

In this post, I want to lay out a framework for preventing this disease by addressing each factor in this equation.

1. Exogenous (dietary) fat intake

While this is an input to consider and therefore limit whenever possible, I tend not to worry too much about dietary fat consumption as it doesn’t seem to contribute as much as DNL to liver fat stores. For starters, throughout the development of the NAFLD epidemic, our societal dietary fat intake has actually decreased. This decrease has accompanied a substantial increase in carbohydrate and, regrettably, refined carbohydrate consumption in the United States. As we have seen with fructose and will continue to emphasize, the fat produced de novo from these excessive carbohydrates has actually proved far more unsettling than fat that just comes from ingestion. Of course, limiting caloric intake would generally be a good idea for limiting liver fat. One’s calories have to come from somewhere, though. For the purpose of liver fat, it appears that dietary fat may actually be a sort of “lesser of two evils” as a fuel source compared to carbohydrates.

2. De novo lipogenesis (DNL)

We’ve already established the dangers of fructose metabolism and ramping up DNL in the last post, so I won’t spend too much time on this factor in the equation. The primary strategy to prevent this input would be to limit fructose consumption, and especially avoid fructose in liquid form (regular sodas, juice, some sport drinks, etc.). Personally, I would draw a hard line with a strict limit on fructose intake, particularly with the knowledge that it can actually increase your hunger for it. Through the ATP depletion mechanism previously discussed, the body adopts an anabolic state to build up fuel stores. In an unregulated fashion, fructose metabolism signals its desire for you to consume even more and produce more fat. Be very cautious any time you think about tipping over the first domino in this process by consuming fructose.

3. Fat oxidation (“fat-burning”)

Whereas we want to limit our inputs into the equation, we of course want to stimulate the outputs to decrease our liver fat. The first way to do this is to utilize the fat as fuel. There are various ways to “burn fat,” but the best may be to exercise in your physiological Zone 2. As a reminder, this is the highest level of exertion you can sustain while limiting your energy metabolism to the mitochondria. This way, you maximize the efficient use of fatty acids with aerobic metabolism, rather than rely on less efficient glycolytic mechanisms that burn glucose in the cytoplasm. Using this higher-efficiency system implies low-to-moderate intensity exercise that doesn’t demand energy that rapidly. This means keeping your heart rate at roughly 60-70% of your max, and being just comfortable enough to sustain a conversation. Zone 2 exercise has several metabolic benefits that make those who consistently do it, like endurance athletes, so healthy. A considerable portion of these benefits are derived from their efficiency of fat metabolism, and their resulting ability to clear liver fat with ease and avoid downstream problems.

Figure 1: Generic depiction of a lipoprotein particle, which transports lipids (fats) in the circulation. Phosphatidylcholine is an essential phospholipid component of these particles, therefore suggesting a role in lipid export and potential impact of choline consumption on liver fat clearance. (Image: Maric et al., 2019)

4. Lipid export

Lastly, our liver can clear fat by exporting it to the rest of the body. Lipids (which can be thought of as synonymous with “fat”) are key components of cells, forming membranes and other structures. These molecules can enter circulation in particles called lipoproteins. A key, limiting component of the lipoprotein particle is phosphatidylcholine. There is some evidence, therefore, that insufficient choline consumption may result in fatty liver. Choline is an essential nutrient, meaning that our bodies do not produce it. Rather, we rely on exogenous supplies from our diet to form these lipoprotein particles and export liver fat. To ensure you have enough, it’s best to consume a balanced diet that includes foods like eggs, nuts, meats, and cruciferous vegetables that contain choline. Now, fat export to the rest of the body can cause other problems such as atherosclerosis in cardiovascular disease. Though it’s probably preferable to have this fat exported out of the liver, it’s worth noting that choline consumption does not simply negate poor dietary habits on the “input” side. For optimal liver health, one should focus on moving each of these metrics in the right direction, rather than lacking on certain components and overcompensating in others.


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