How to Prevent Non-Alcoholic Fatty Liver Disease

How to Prevent Non-Alcoholic Fatty Liver Disease
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Avoid sugary and cholesterol-laden foods to reduce the risk of our most common cause of chronic liver disease.

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In the documentary Super Size Me, Morgan Spurlock eats exclusively at McDonald’s for a month, and predictably his weight, blood pressure, and cholesterol go up—but so do his liver enzymes, a sign his liver cells are dying and spilling their contents into the bloodstream. His one-man experiment was actually formally replicated. A group of men and women agreed to eat two fast food meals a day for a month, and most of their liver values started out normal—under 30 here for men. But within just one week, most were out of whack: a profound pathological elevation in liver damage.

What’s happening is NAFLD, non-alcoholic fatty liver disease, the next global epidemic. Fatty deposits in the liver can result in a disease spectrum—from asymptomatic fat buildup, to NASH, nonalcoholic steatohepatitis, which can lead to liver scarring, and cirrhosis, which can result in liver cancer, liver failure, and death.

It’s now the most common cause of chronic liver disease in the U.S., affecting 70 million Americans—that’s like one in three adults. And fast food is a great way to bring it on, since it’s associated with the intake of soft drinks and meat. One can of soda a day may raise the odds of fatty liver 45%, and those eating the equivalent of 14 chicken nuggets’ worth of meat a day have nearly triple the rates of fatty liver, compared to seven nuggets or less.

It’s been characterized as a tale of fat and sugar—but evidently, not all types of fat. Those with fatty hepatitis ate more animal fat and cholesterol, and less plant fat, fiber, and antioxidants, which may explain why adherence to a Mediterranean-style diet—characterized by high consumption of foods such as fruits, vegetables, whole grains, and beans—is associated with less severe non-alcoholic fatty liver disease, perhaps because of its anti-inflammatory and antioxidant effects. Maybe it is also because of specific phytonutrients, like the purple, red, blue anthocyanin pigments in berries, as well as in grapes, plums, red cabbage, red onions, and radicchio. These anthocyanin-rich foods may be promising for the prevention of fatty liver, but that’s mostly based on Petri dish experiments. There was one clinical trial that found that drinking a purple sweet potato beverage seemed to dampen liver inflammation.

A more plant-based diet may also improve our microbiome, the good bacteria in our gut. The old adage, “we are what we eat,” may be changing to “we are what our bacteria eat.” And when we eat fat, we may facilitate the growth of bad bacteria, which can release inflammatory molecules that increase the leakiness of our gut and contribute to fatty liver disease.

Fatty liver disease can also be caused by cholesterol overload. The thought is that dietary cholesterol, found in eggs, meat, and dairy, oxidizes and then upregulates liver X receptor alpha, which can upregulate something else called SREBP, which can increase the level of fat in the liver.

Cholesterol crystals alone cause human white blood cells to spill out inflammatory compounds, just like uric acid crystals in gout. That’s what may be triggering the progression of fatty liver into serious hepatitis, the accumulation of sufficient concentrations of free cholesterol within fatty liver cells to cause crystallization of the cholesterol—one of several recent lines of evidence suggesting that dietary cholesterol plays an important role in the development of fatty hepatitis.

In a study of 9,000 American adults followed for 13 years, they found a strong association between cholesterol intake and hospitalization, and death from cirrhosis and liver cancer, as dietary cholesterol can oxidize and cause toxic and carcinogenic effects. To limit the toxicity of excess cholesterol derived from the diet, the liver tries to rid itself of cholesterol by dumping it into the bloodstream. And so, by measuring the non-HDL cholesterol in the blood, one can predict the onset of fatty liver disease. If you subtract HDL from total cholesterol, none of the hundreds of people they followed with a value under 130 developed the disease. Drug companies view non-alcoholic fatty liver disease as a bonanza, as is the case of any disease of affluence, considering its already high and rising prevalence, needing continuous pharmacologic treatment. But maybe it’s as easy as changing our diet—avoiding sugary and cholesterol-laden foods.

The unpalatable truth is that non-alcoholic fatty liver disease could almost be considered the human equivalent of foie gras, as we “force-feed” ourselves foods that can result in serious health implications. However, having such a buttery texture in human livers is not a delicacy to be enjoyed by liver doctors in clinical practice, as it can have serious consequences.

To see any graphs, charts, graphics, images, and quotes to which Dr. Greger may be referring, watch the above video. This is just an approximation of the audio contributed by Katie Schloer.

Please consider volunteering to help out on the site.

In the documentary Super Size Me, Morgan Spurlock eats exclusively at McDonald’s for a month, and predictably his weight, blood pressure, and cholesterol go up—but so do his liver enzymes, a sign his liver cells are dying and spilling their contents into the bloodstream. His one-man experiment was actually formally replicated. A group of men and women agreed to eat two fast food meals a day for a month, and most of their liver values started out normal—under 30 here for men. But within just one week, most were out of whack: a profound pathological elevation in liver damage.

What’s happening is NAFLD, non-alcoholic fatty liver disease, the next global epidemic. Fatty deposits in the liver can result in a disease spectrum—from asymptomatic fat buildup, to NASH, nonalcoholic steatohepatitis, which can lead to liver scarring, and cirrhosis, which can result in liver cancer, liver failure, and death.

It’s now the most common cause of chronic liver disease in the U.S., affecting 70 million Americans—that’s like one in three adults. And fast food is a great way to bring it on, since it’s associated with the intake of soft drinks and meat. One can of soda a day may raise the odds of fatty liver 45%, and those eating the equivalent of 14 chicken nuggets’ worth of meat a day have nearly triple the rates of fatty liver, compared to seven nuggets or less.

It’s been characterized as a tale of fat and sugar—but evidently, not all types of fat. Those with fatty hepatitis ate more animal fat and cholesterol, and less plant fat, fiber, and antioxidants, which may explain why adherence to a Mediterranean-style diet—characterized by high consumption of foods such as fruits, vegetables, whole grains, and beans—is associated with less severe non-alcoholic fatty liver disease, perhaps because of its anti-inflammatory and antioxidant effects. Maybe it is also because of specific phytonutrients, like the purple, red, blue anthocyanin pigments in berries, as well as in grapes, plums, red cabbage, red onions, and radicchio. These anthocyanin-rich foods may be promising for the prevention of fatty liver, but that’s mostly based on Petri dish experiments. There was one clinical trial that found that drinking a purple sweet potato beverage seemed to dampen liver inflammation.

A more plant-based diet may also improve our microbiome, the good bacteria in our gut. The old adage, “we are what we eat,” may be changing to “we are what our bacteria eat.” And when we eat fat, we may facilitate the growth of bad bacteria, which can release inflammatory molecules that increase the leakiness of our gut and contribute to fatty liver disease.

Fatty liver disease can also be caused by cholesterol overload. The thought is that dietary cholesterol, found in eggs, meat, and dairy, oxidizes and then upregulates liver X receptor alpha, which can upregulate something else called SREBP, which can increase the level of fat in the liver.

Cholesterol crystals alone cause human white blood cells to spill out inflammatory compounds, just like uric acid crystals in gout. That’s what may be triggering the progression of fatty liver into serious hepatitis, the accumulation of sufficient concentrations of free cholesterol within fatty liver cells to cause crystallization of the cholesterol—one of several recent lines of evidence suggesting that dietary cholesterol plays an important role in the development of fatty hepatitis.

In a study of 9,000 American adults followed for 13 years, they found a strong association between cholesterol intake and hospitalization, and death from cirrhosis and liver cancer, as dietary cholesterol can oxidize and cause toxic and carcinogenic effects. To limit the toxicity of excess cholesterol derived from the diet, the liver tries to rid itself of cholesterol by dumping it into the bloodstream. And so, by measuring the non-HDL cholesterol in the blood, one can predict the onset of fatty liver disease. If you subtract HDL from total cholesterol, none of the hundreds of people they followed with a value under 130 developed the disease. Drug companies view non-alcoholic fatty liver disease as a bonanza, as is the case of any disease of affluence, considering its already high and rising prevalence, needing continuous pharmacologic treatment. But maybe it’s as easy as changing our diet—avoiding sugary and cholesterol-laden foods.

The unpalatable truth is that non-alcoholic fatty liver disease could almost be considered the human equivalent of foie gras, as we “force-feed” ourselves foods that can result in serious health implications. However, having such a buttery texture in human livers is not a delicacy to be enjoyed by liver doctors in clinical practice, as it can have serious consequences.

To see any graphs, charts, graphics, images, and quotes to which Dr. Greger may be referring, watch the above video. This is just an approximation of the audio contributed by Katie Schloer.

Please consider volunteering to help out on the site.

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