Did you ever wonder if the food you eat has a direct effect on your health, well-being – and longevity? Well, I’m here to end that mystery. You ARE the foods you eat. Welcome to the Nutrition Facts podcast – I’m your host, Dr. Michael Greger.
Most diseases – aren’t known for their salubrious names. And Fatty liver disease is no exception. So, what is fatty liver disease – and how can we NOT get it?
Nonalcoholic fatty liver disease is now the most frequent chronic liver disease, thanks, in part, to our epidemic of obesity––now even seen in children. As many as nearly 70 to 80 percent of obese children may have fatty liver disease. Why do we care? Because a fatty liver can progress into fatty hepatitis, which can cause scarring and liver cirrhosis––which is bad enough without also causing you to develop liver cancer, too.
Okay, so what’s the source of the liver fat in fatty liver disease? There are three main sources: the excess sugar in our diet, excess fat in our diet, and the fat spilling over from your own excess body fat.
How do we know excess dietary sugar is bad? Because it’s been put to the test. If you randomize teens with fatty liver disease to a diet low in free sugars (meaning added sugar and sugary beverages), they experience a significant improvement within eight weeks. Given this new data, a liver journal editorial read, “[a] strong argument can be made that we are beyond any period of uncertainty about the harmful effects of excess sugar consumption and that we must now act … to inform the public of the health risks of eating too much sugar.”
How do we know excess dietary fat is bad? Because it’s been put to the test. Randomize people to the same low-calorie diet, but one that’s low-fat versus one that’s high-fat, and within just two weeks, the low-fat diet decreased liver fat by 20 percent, whereas the same number of calories on a high-fat diet increased liver fat by 35 percent!
On the low-fat diet, insulin levels went down about 15 percent, and on the high-fat diet, insulin levels went up about 15 percent. Low-carb and ketogenic diet advocates are always talking about how you have to eat more fat and less carbs to keep your insulin levels down, but the exact opposite happens when it’s actually put to the test. Even a single high-fat meal not only increases liver fat, but also insulin resistance. Within four hours, your whole-body insulin sensitivity can drop by 25 percent; so, your body has to pump out that much more insulin. As the accompanying editorial put it, a single fat dose packs a punch.
So, to help prevent or treat fatty liver disease, patients should limit or avoid eating fat-rich foods. While more long-term clinical trials are always needed, based on current evidence, we would recommend a diet low in fat, notably saturated fat––so, low in meat, dairy, and junk, and low in reﬁned carbs, notably soda.
Saturated fat is not only more metabolically harmful for the human liver than unsaturated fat; saturated fat is more harmful than straight sugar. If you overfeed people with 1,000 calories of saturated fat (like cheese and coconut oil), unsaturated fat (like nuts and olive oil), or sugar (like soda and candy), overeating 1,000 calories a day of anything isn’t good for you, but the saturated fat increased liver fat 55 percent, significantly more than the unsaturated fats, with the candy coming in between.
So, in terms of weight loss, although beneﬁcial, certain diets can actually cause or exacerbate this disease––such as very low-carbohydrate, high-fat diets––whereas those eating healthy plant-based diets may lower the risk of fatty liver disease. For example, the consumption of legumes (beans, split peas, chickpeas, and lentils) is associated with a lower risk of fatty liver––up to 65 percent lower odds eating more beans.
Now, in this study, they weren’t looking at people eating strictly plant-based diets, just more or less so. It’s harder to study those eating completely meat-free diets, since they currently represent just a small segment of the U.S. population. But what about Americans of Indian descent? Those originating from the Indian subcontinent are one of the fastest growing ethnic groups in the United States, and they appear to largely retain their diets, with about the same percentage of vegetarians as in India—nearly 40 percent. We know in India itself nonvegetarians (those who eat meat) are at significantly higher risk of fatty liver disease. In Taiwan, you see the same thing: vegetarians at significantly lower risk. And even the vegetarians who were affected had significantly less liver scarring. Their data suggests that replacing a single serving of soy with a serving of meat or fish was associated with 12 percent to 13 percent increased risk of fatty liver disease. But what about here in the United States?
Eating vegetarian was associated with being slimmer, having better blood sugars, better cholesterol, and less than half the odds of fatty liver disease. You don’t know if it’s cause-and-effect, though, until you put it to the test. In an effort to reverse a fatty liver patient’s inflammatory bowel disease with a plant-based diet, liver inflammation was dramatically improved. But, he also lost about 9 pounds in the first 11 days thanks to eating healthy; so, it’s hard to tease out the specific diet effects. In fact, you have to be careful about rapid weight loss, because all that extra fat being broken down can flood into the bloodstream and sometimes make things worse. So, for fatty liver disease patients, losing like three pounds a week might be safer.
Even though plant-based diets have yet to be properly put to the test in a randomized clinical trial for fatty liver disease, I would submit that they are still the best diet for fatty liver disease. Not based on a single case report, but based on the fact that cardiovascular disease is the most common cause of death among patients with fatty liver disease (not liver failure). And we do have randomized controlled trials proving a healthy plant-based diet and lifestyle programs can reverse heart disease––opening up arteries without drugs, without surgery, without stents. Yes, patients with fatty liver disease and fatty hepatitis may indeed eventually develop cirrhosis of the liver, but only if they don’t die of cardiovascular diseases first.
In our next story – we learn how whole grain consumption might have direct health benefit on fatty liver disease.
If oatmeal is so powerful that it can clear up some of the ravages of chemotherapy when just applied to the skin, what might it do if we actually ate it? The pharmacology of oatmeal. Oats are reported to possess varied drug-like activities like lowering of blood cholesterol and blood sugar, boosting our immune system, anti-cancer, antioxidant, anti-atherosclerosis, in addition to being a topical anti-inflammatory, and may also be useful in controlling childhood asthma, body weight, etc.
Whole grain intake in general is associated with lower risk of type 2 diabetes, cardiovascular disease, and weight gain. All the cohort studies on type 2 diabetes and heart disease show whole grain intake is associated with lower risk. They observed the same for obesity—consistently less weight gain for those who consumed a few servings of whole grains every day.
Yes, all the forward-looking population studies demonstrate that a higher intake of whole grains is associated with lower body mass index and body weight gain. However, these results do not clarify whether whole grain consumption is simply a marker of a healthier lifestyle, or a factor favoring “per se” lower body weight.
For example, high-whole grain consumers—those who eat whole wheat, brown rice, and have oatmeal for breakfast—tend to be more physically active, smoke less, and consume more fruit, vegetables, and dietary fiber than those who instead reach for Fruit Loops. Statistically, one can control these factors, effectively comparing only nonsmokers to nonsmokers with similar exercise and diet, as most of the studies did, and they still found whole grains to be protective, via a variety of mechanisms.
So, for example, in helping with weight control, the soluble fiber of oatmeal forms a gel in the stomach, delaying stomach emptying, making one feel full for a longer period, which helps with weight loss, and then there are other effects in the small and large intestine. So, it all seems plausible that whole grain intake does indeed offer direct benefits; however, only results from randomized controlled intervention studies can provide the evidence of cause and effect. In other words, the evidence is clear that oatmeal consumers have lower rates of disease, but that’s not the same as proving that if we start to eat more oatmeal, our risk will drop. To know that we need an interventional trial, ideally a blinded study where you give half the people oatmeal, and the other half fake placebo oatmeal that looks and tastes like oatmeal to see if it actually works. As you can imagine this has not been done, until now. Double-blinded randomized trial of overweight and obese men and women, and almost 90% of the real oatmeal-treated subjects had reduced body weight–compared to no weight loss in the control group–a slimmer waist on average, a 20-point drop in cholesterol, and an improvement in liver function.
Nonalcoholic fatty liver disease, meaning a fatty liver caused by excess food rather than excess drink, is now the most common cause of liver disease in the United States, found on autopsy in up to 90% of obese individuals, and can lead in rare cases to cirrhosis of the liver, cancer of the liver, and death. Theoretically, whole grains could help prevent and treat fatty liver disease, but this is the first time it had actually been put to the test like this. A follow-up study in 2014 confirmed these findings of a protective role of whole grains, but refined grains were associated with increased risk. So, one would not expect to get such wonderful results from Wonder Bread.
Finally today – we look at how to avoid sugary and cholesterol-laden foods to reduce the risk of our most common cause of chronic liver disease.
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 the 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 did find 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 just plain 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, fatty liver inflammation.
In a study of 9,000 American adults followed for 13 years, they 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. 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 nonalcoholic 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 nonalcoholic 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.
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