How to Avoid Fatty Liver Disease

In the documentary Supersize 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. Most of their liver values started out normal, but, within just one week, most were out of whack, a profound pathological elevation in liver damage.

What’s happening is non-alcoholic fatty liver disease (NAFLD), the next global epidemic, as I discuss in my video How to Prevent Non-Alcoholic Fatty Liver Disease. Fatty deposits in the liver result in a disease spectrum from asymptomatic fat buildup to non-alcoholic steatohepatitis (NASH), which can lead to liver scarring and cirrhosis, and may result in liver cancer, liver failure, and death.

NAFLD is now the most common cause of chronic liver disease in the United States, affecting 70 million Americans, nearly one in three adults. Fast food consumption is a great way to bring it on, since it’s associated with the intake of soft drinks and meat. Drinking one can of soda a day may raise the odds of NAFLD by 45 percent, and those eating the equivalent of 14 chicken nuggets’ worth of meat a day have nearly triple the rates of fatty liver compared to those eating 7 nuggets or less.

It’s been characterized as a tale of fat and sugar, but evidently not all types of fat are culpable. Those with fatty hepatitis were found to have eaten more animal fat and cholesterol, and less plant fat, fiber, and antioxidants. This 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. It could also be related to the presence of specific phytonutrients, like the purple, red, and blue anthocyanin pigments found in berries, 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 successfully dampen liver inflammation.

A more plant-based diet may also improve our microbiome, the good bacteria in our gut. “‘We are what we eat’ is the old adage but the modern version might be ‘we are what our bacteria eat.’” 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 steatotic hepatocytes [fatty liver cells] to cause crystallization of the cholesterol.” This is one of several recent lines of evidence suggesting that dietary cholesterol plays an important role in the development of fatty hepatitis—that is, fatty liver inflammation.

In a study of 9,000 American adults followed for 13 years, researchers found a strong association between dietary 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. So, by measuring the non-HDL cholesterol in the blood, one can predict the onset of fatty liver disease. If we subtract HDL from total cholesterol, none of the hundreds of subjects 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 and…[its] needing continuous pharmacologic treatment,” but maybe avoiding it is as easy as changing our diet, avoiding sugary and cholesterol-laden foods.

“The unpalatable truth is that NAFLD could almost be considered the human equivalent of foie gras (loosely translated from French as ‘fat liver’). As we overeat and ‘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 hepatologists [liver doctors] in clinical practice!”


Like my video Preventing Gout Attacks with Diet, How to Prevent Non-Alcoholic Fatty Liver Disease covers an important topic worth the extensive coverage the video provides.

For more on how bad added sugars are for us, see:

For more on how bad cholesterol can be, see:

In health,
Michael Greger, M.D.

PS: If you haven’t yet, you can subscribe to my free videos here and watch my live, year-in-review presentations:

How to Counteract the Effects of Alcohol

More than a million new cases of skin cancer are diagnosed every year, affecting about one in three Americans in their lifetimes. As I discuss in my video Preventing Skin Cancer from the Inside Out, although the chief risk factor is UV exposure from the sun, alcohol consumption may also play a role. Most of the cancers associated with alcohol use are in the digestive tract, from mouth cancer, throat cancer, and stomach cancer down to cancers of the liver and colon. These involve tissues with which alcohol comes in more direct contact. But why skin cancer?

A study of 300,000 Americans found that excessive drinking was associated with higher rates of sunburn. It “may be that heavy and binge drinking are markers for an underlying willingness to disregard health risks” and pass out on the beach, but it also may be because breakdown products of alcohol in the body generate such massive numbers of free radicals that they eat up the antioxidants that protect our skin from the sun. Plants produce “their own built-in protection against the oxidative damage of the sun,” and we can expropriate these built-in protectors by eating those plants to function as cell protectors within our own bodies. One might say fruit and vegetables provide the best polypharmacy—the best drug store—against the development of cancer.

The ingestion of plant foods increases the antioxidant potential of our bloodstream, which can then be deposited in our tissues to protect us against the damaging effects of the sun’s rays, but only recently was it put to the test.

Researchers studied 20 women and burned their buttock skin with a UV lamp before and after half of them ate three tablespoons of tomato paste a day for three months. There was significantly less DNA damage in the derrieres of those who had been eating the tomatoes. So, three months or even just ten weeks before swimsuit season, if we eat lots of an antioxidant-rich food, such as tomato sauce, we may reduce the redness of a sunburn by 40 percent. It’s like we have built-in sunscreen in our skin. Now, this isn’t as good as a high SPF sunblock, but “[m]uch of the UV exposure over a life time occurs when the skin is not protected; thus, the use of dietary factors with sun-protecting properties might have a substantial beneficial effect.”

It works both ways, though. Alcohol consumption decreases the protection within our skin. If you have people drink about three shots of vodka, within eight minutes—not after ten weeks, but within just eight minutes––the level of carotenoid antioxidants in their skin drops dramatically. If, however, you drink the same amount of vodka in orange juice, there is still a drop in skin antioxidants compared with the initial value, but drinking a screwdriver cocktail is not as bad as drinking vodka neat. Is the difference enough to make a difference out in the sun, though?

After the drinks, researchers exposed volunteers to a UV lamp and waited to see how long it would take them to burn, and the time span until they started turning red was significantly shorter after alcohol consumption than in the experiments in which either no alcohol was consumed or alcohol was consumed in combination with orange juice. It came out to be about an extra half hour out in the sun based solely on what you put in your mouth before heading to the beach. And, oranges are pretty wimpy––not as bad as bananas, but berries have the highest cellular antioxidant activity.

The researchers concluded that “[p]eople should be aware of the fact that the consumption of alcohol in combination with UV light [from sun exposure or a tanning booth] increases their risk of sunburn and therefore their risk of developing premature skin aging and even skin cancer.” If you are going to drink alcohol and be out in the sun, you should make sure you are using sunblock or, at the very least, drinking a strawberry daiquiri or something else to reduce oxidative damage.


Isn’t that wild? Antioxidant dynamics in the body change minute to minute so be sure to keep yourself topped off. See:

What else can tomatoes do? Check out Inhibiting Platelet Activation with Tomato Seeds.

Other videos on skin health include:

Alcohol doesn’t just raise the risk of skin cancer. See Breast Cancer and Alcohol: How Much Is Safe?. But, like the orange juice in a screwdriver cocktail, grape skin components may help mediate wine’s adverse effects. See Breast Cancer Risk: Red Wine vs. White Wine.

In health,
Michael Greger, M.D.

PS: If you haven’t yet, you can subscribe to my free videos here and watch my live, year-in-review presentations:

Change Your Diet; Change Your Microbiome

If whatever gut flora enterotype we are could play an important role in our risk of developing chronic diet-associated diseases (see What’s Your Gut Microbiome Enterotype?), can we alter our gut microbiome by altering our diet? Yes. Indeed, diet can rapidly and reproducibly alter the bacteria in our gut, as I discuss in my video How to Change Your Enterotype.

Concern has been growing that recent lifestyle trends––most notably the high-fat and high-sugar “Western diet”––have altered the composition and activity of our resident gut flora. “Such diet-induced changes to gut-associated microbial communities are now suspected of contributing to growing epidemics of chronic illness in the developed world,” yet it has remained unclear how quickly our gut bacteria could respond to dietary change. So, researchers prepared two diets: a “plant-based diet” rich in grains, beans, fruits, and vegetables, and an “animal-based diet” composed of meats, eggs, and cheeses. Neither diet contained refined sugars, as the researchers just wanted to test diets consisting of plant versus animal products. Within just one day of the animal-based diet hitting the gut, there was a significant shift.

What happens when you put a lifelong vegetarian on an animal-based diet? The vegetarian’s baseline microbiota was dominated by Prevotella, unlike everyone else eating a more standard American diet, who had large Bacteroides populations. Remarkably, the animal-based diet inverted the vegetarian’s Prevotella-to-Bacteroides ratio, causing the Bacteroides to outnumber the Prevotella within just four days on the animal-based diet. The entire gut flora got turned on its head and got completely reversed.

The fact that our gut can so rapidly switch between herbivorous and carnivorous functional profiles is probably a good thing in terms of evolution. If you bring down a mammoth and eat meat for a couple of days before switching back to plants, you want your gut to be able to deal with it. This flexibility is manifest in the diversity of human diets to this day, but what is the healthier state to be in most of the time?

Researchers looked at a number of different factors, such as the amount of short-chain fatty acids produced. Short-chain fatty acids, like acetate and butyrate, function to suppress inflammation and cancer, and our gut flora, when on plant-based diets, produce more of these than when on animal-based diets.

Other microbial metabolites, such as secondary bile acids, do the opposite, promoting the development of cancer. With a significant increase in bacterial enzyme activity to create these secondary bile acids on an animal-based diet, it’s no surprise there’s a significant increase in carcinogens like DCA, a secondary bile acid known to promote DNA damage and liver cancer. Microbial enzyme activity producing the rotten egg gas, hydrogen sulfide, also shoots up on an animal-based diet, which stinks because it’s stinky and also because it damages DNA and has been implicated in the development of inflammatory bowel diseases like ulcerative colitis. Hydrogen sulfide is made by pathogens such as Bilophila wadsworthia and is increased on the animal-based diet, again within just days of adopting it, supporting the link between diet and the outgrowth of microorganisms capable of triggering inflammatory bowel disease. Conversely, the only pathogen you see more of on a plant-based diet is just a virus that infects spinach.


Do you know What’s Your Gut Microbiome Enterotype?

See more about gut microbiomes:

I’ve produced a series about the epic fermentation battle in the gut between protein and carbs that offers lots of insight on why it matters who we have living down there:

And check out some other videos on inflammatory bowel disease:

In health,
Michael Greger, M.D.

PS: If you haven’t yet, you can subscribe to my free videos here and watch my live, year-in-review presentations: