Facts About Fatty Liver

As our lifestyle in the past few decades has slipped further into the realm of processed foods and high fat eating, certain health disorders are becoming more common. One of these, NAFLD (non-alcoholic fatty liver disease or non-alcoholic steatohepatitis), is expected to become the next global epidemic. This is not a condition to be trifled with. Besides devastation of the liver, NAFLD is an independent risk factor for cardiovascular disease. NAFLD begins with the accumulation of fat in the liver. If this is allowed to continue the resulting severe inflammation initiates fibrosis (scar tissue) which will eventually worsen into cirrhosis and advanced liver disease including liver cancer, liver failure, need for a liver transplant and death (3,4).

In the past, excess consumption of alcohol was the cause of most fatty liver disease but overeating has overtaken alcohol as the most common cause. Fatty liver disease is now categorized as either alcoholic fatty liver disease (AFLD) or non-alcoholic fatty liver disease (NAFLD). Other causes are long-term feeding through parenteral nutrition, gastric bypass surgery and disorders of fatty acid metabolism. Fatty liver associated with overeating is a global health problem affecting both adults and children. In North America the prevalence of NAFLD in the general population ranges between 20% and 30% however it is present in up to 80 to 90% of obese people, 30 to 50% of diabetics and 90% of people with high blood lipids. The prevalence in children has risen from about 3% in 2000 to 5% in 2010. The cause of the increase in incidence of NAFLD in Western countries is undoubtedly poor lifestyle habits (2,3).

 

Influences on the Development of NAFLD

When food consumption far exceeds the need for calories, the unused energy is conserved in fat tissue in the form of triglycerides (fats) for use in times of hardship. Excess fat also deposits in the skeletal muscles, the liver and in other organs. The problem is that most people in the industrialized world no longer experience regular periods of famine and our storage tissues just keep filling up with little chance of ever emptying. At a certain point, high fat levels in tissues prevent insulin from having its desired effect and lock both glucose and fatty acids out of cells. This is insulin resistance.

Excess stored fat also leads to obesity and the development of metabolic syndrome, a cluster of events including insulin resistance and chronically elevated glucose, insulin, cholesterol and free fatty acid concentrations in the blood along with increased blood pressure and excess body fat around the waist. Metabolic syndrome is a strong predictor of fatty liver disease (1,3) and insulin resistance is present in most NAFLD patients including those who are not overweight (4). Non-HDL cholesterol (total cholesterol minus HDL-cholesterol) is another robust predictor of NAFLD and a stronger predictor than levels of other types of fat in the bloodstream (13). Part of the reason for this is that the liver takes up what it is served by the bloodstream. High lipids (fats) in the blood become high fats in the liver, an organ never meant to be a storage vessel for cholesterol, and it protects itself from the toxicity of cholesterol by dumping it back into the bloodstream.

With the increasing availability in our society of processed foods and beverages, convenience foods and fast foods, there has been a significant increase in sucrose and high-fructose corn syrup consumption. Excessive simple sugar intake is linked to increased prevalence of metabolic diseases and may contribute to the development and severity of NAFLD by boosting the deposition of fat into the liver, inflammation in the liver and development of fibrosis (14). The mechanism of this is the promotion by fructose of de novo lipogenesis (conversion of carbohydrates to fatty acids) as well as the effects of fructose on increasing insulin resistance, oxidative stress, bacterial overgrowth and inflammation (15). It must be emphasized that these problems do not apply to the fructose present in whole fruits. Sugar in fruit is packaged with fiber, antioxidants, vitamins and minerals that slow its absorption and protect against blood sugar spikes. Research has shown that even very high fruit consumption (up to twenty servings of fruit in a day) causes no increase in insulin resistance. In fact, fruit consumption actually improves sensitivity to insulin and decreases cholesterol blood levels (16,19,20,21).

 

Strategies to Prevent and Treat NAFLD

There are no reliable medications for the treatment of NAFLD. However, obesity is strongly associated with the condition and so lifestyle modifications such as weight loss and increased physical activity are the mainstays of treatment. But advice to simply lose weight is pretty vague. Certain diets that induce weight loss actually contribute to the cause of NAFLD or make already existing disease worse, especially if they include foods rich in fatty acids such as animal-based foods, or high in refined carbohydrates, such as processed baked goods or soft drinks (17). Why not target the very foods that are spurring on the increased incidence of this disease?

Emerging evidence suggests that composition of the diet is very important in NAFLD. A Western-style diet, rich in animal proteins and refined foods, can cause low-grade disturbances in body glucose metabolism and acid/base balance. A large, ongoing study from the Netherlands published in April, 2017 shows that high animal protein intake in overweight people is associated with a 50% higher risk of NAFLD independent of other lifestyle and metabolic factors. This study also strengthened the observation that, although current guidelines suggest that fructose containing foods be avoided, the consumption of healthy sugar sources, such as antioxidant-rich fruit and vegetables, is not associated with development of NAFLD and in fact may have a beneficial effect. (16).
Patients are often advised to start a high fat/low carbohydrate diet when they are first diagnosed with NAFLD. Indeed such a diet can induce quick weight loss, at least at the start. However, diets high in fat and low in carbohydrate increase both insulin resistance and inflammatory risk. In addition, this type of diet increases the risk of type-2 diabetes, cardiovascular disease and premature death, especially when animal-based proteins and fats are consumed. (17)

Saturated fatty acids encourage inflammatory oxidation. On the other hand monounsaturated and polyunsaturated fatty acids reduce inflammation and insulin resistance. They also improve fat levels in the liver and the bloodstream thereby discouraging the development of NAFLD. Tellingly, these benefits occur even with no loss of body weight, suggesting that it is the modification of fat type itself rather than the weight loss that is improving NAFLD (17).
A randomized study showed that a diet low in fat decreases liver fat content by 20% and lowers fasting blood insulin levels while a high fat diet increases the fat in the liver by 35% along with increases in fasting blood insulin levels. (High fasting blood insulin indicates insulin resistance.) These results occurred within the short period of two weeks and without weight loss or change in intra-abdominal or subcutaneous fat mass, illustrating that the amount of fat in the diet is also a substantial factor in keeping the liver healthy (18).

 

The Best Diet for NAFLD

A comprehensive review of diets and their place in the prevention and treatment of NAFLD was completed in 2007. Many different diets were scrutinized including the official Dietary Guidelines for Americans; diets of the American Dietetic Association, the American Heart Association, the National Heart Lung and Blood Institute, and the American Diabetes Association; the National Cholesterol Education Program; the TLC (Therapeutic Lifestyle Changes) diet; the DASH (Dietary Approaches to Stop Hypertension) diet; the Mediterranean Diet; the Ornish Diet; the Atkins Diet; the Zone Diet; the South Beach Diet and the Weight Watchers Diet.

Although many of these nutrition plans showed some benefits for NAFLD, none of them were considered ideal. Their perceived drawbacks included not enough weight loss (Dietary Guidelines for Americans), not palatable enough (Ornish diet, DASH diet), too high in fat (American Heart Association, Therapeutic Lifestyle Changes diet), not enough effect on decreasing insulin resistance (American Dietetic Diet), too many simple carbohydrates (American Diabetes Diet) or too high in protein (Atkins Diet, Zone Diet, South Beach Diet). The conclusion of this review was the recommendation for a highly individualized approach when it comes to NAFLD (4).

Other research has shown that adherence to a Mediterranean-style diet is associated with less insulin resistance and less severe liver disease among patients with NAFLD but not with a lower likelihood of developing NAFLD (11).

 

Criteria to be considered for a diet and lifestyle that can prevent and treat NAFLD

1 A major goal is weight loss but this objective is best achieved through slow and consistent loss over time. For unknown reasons, sudden weight loss achieved through dietary modification may lead to worsening fibrosis and progression of liver failure. On the other hand, surgical weight loss methods such as gastric bypass bring about relatively quick results and have been successful in reducing progression of NAFLD (4,5).

2 Decrease total fat consumption.

3 Severely curtail intake of saturated fatty acids (animal-based foods and a few plant-based foods such as coconuts and cocoa butter) and replace with mono-unsaturated or poly-unsaturated fats. Saturated fatty acids have damaging effects on liver function (7) and also raise blood LDL concentrations (8).

4 Ensure sufficient intake of omega-3 fatty acids, specifically DHA and EPA. These healthy fatty acids improve blood lipid profiles and also decrease fat build-up in liver cells (steatosis).

5 Increase intake of plant-based foods for their high fiber content and their low rates of glucose uptake into the bloodstream. These foods decrease insulin resistance (4). Additionally they are good sources of vitamins and minerals. They also supply copious amounts of antioxidants such as anthocyanins that decrease fat accumulation in the liver and may counteract inflammation (12).

6 Reduce consumption of refined carbohydrates.

7 Avoid sugar-sweetened drinks because they cause higher triglyceride levels (through de novo lipogenesis) and increase insulin resistance (9,10).

8 Eat a diet moderate in protein and avoid animal protein (10).

9 Incorporate regular moderate exercise such as walking 3 to 4 kilometers three times a week (6).

 

What Does This Mean In Practical Terms?

For eating less total fat and saturated fat and more monounsaturated fatty acids and polyunsaturated fatty acids as well as decreasing animal protein: Avoid eggs, dairy products, red and white meat, fish and seafood and oils of any kind. Include moderate amounts of nuts and seeds in the daily diet. Avocados and whole olives can also be part of healthy nutrition.

For omega-3 fatty acids: Include moderate amounts of nuts and seeds. DHA and EPA supplements derived from algae can ensure that these omega-3s are being consumed.

For reducing insulin resistance and providing fiber and antioxidants: Eat all you want whenever you want of fruits, starchy and non-starchy vegetables, legumes (including beans, lentils and peas) and green leafy vegetables.

For their beneficial fiber: Eat intact whole grains.

For their high concentration of antioxidants: Add lots of herbs and spices

Eat foods in the non-processed state whenever possible.

Do not consume refined sugars such as pastries and sugar-sweetened beverages.

Eating this way reduces weight slowly and steadily without conscious effort or feelings of hunger.

This description fits the low-fat, whole-food plant-based diet to a “T”, adding yet one more health problem to the seemingly endless list of conditions for which it provides benefits. What are the side effects of this diet? Delicious satisfying meals. Eating to satisfaction. Effortless weight loss. No constipation. Better sleep. Energy in abundance.

 

SOURCES:

1 Hamaguchi, M., Koima, T., Takeda, N., Nakagawa, T. et al. The metabolic syndrome as a predictor of non-alcoholic fatty liver disease. Ann Intern Med. 2005 Nov 15; 143(10):722-728.

2 Bellentani, S., Scaglioni, F., Marino, M., Bedogni, G. Epidemiology of non-alcoholic fatty liver disease.
Dig Dis. 2010; 28(1):155-161.

3 Moore, J.B. Non-alcoholic fatty liver disease: the hepatic consequence of obesity and the metabolic syndrome. Proc Nutr Soc. 2010 May; 69(2):211-220.

4 Zivkovic, A.M., German, J.B., Sanyal, A.J. Comparative review of diets for the metabolic syndrome: implications for nonalcoholic fatty liver disease. Am J Clin Nutr August 2007 ; 86(2): 285-300.

5 Shaffer, E.A. Bariatric surgery: a promising solution for nonalcoholic steatohepatitis in the very obese.
J Clin Gastroenterol. 2006 Mar; 40 Suppl 1:S44-50.

6 Spate-Douglas, T., Keyser, R.E. Exercise intensity: its effect on the high-density lipoprotein profile. Arch Phys Med Rehabil. 1999 Jun; 80(6):691-695.

7 Wei, Y., Wang, D., Topczewski, F., Pagliassotti, M.J. Saturated fatty acids induce endoplasmic reticulum stress and apoptosis independently of ceramide in liver cells. Am J Physiol Endocrinol Metab 2006; 291:E275–281.

8 Musso, G., Gambino, R., De Michieli, F., Cassader, M. et al. Dietary habits and their relations to insulin resistance and postprandial lipemia in nonalcoholic steatohepatitis. Hepatology. 2003 Apr; 37(4):909-916.

9 Basciano, H., Federico, L., Adeli, K. Fructose, insulin resistance, and metabolic dyslipidemia.
Nutr Metab (Lond). 2005 Feb 21; 2(1):5.

10 Zelber-Sagi, S., Nitzan-Kaluski, D., Goldsmith, R., Webb, M., Blendis, L., Halpern, Z., Oren, R. Long term nutritional intake and the risk for non-alcoholic fatty liver disease (NAFLD): a population based study. J Hepatol. 2007 Nov; 47(5):711

11 Kontogianni, M.D., Tileli, N., Margariti, A., Georgoulis, M. et al. Adherence to the Mediterranean diet is associated with the severity of non-alcoholic fatty liver disease. Clin Nutr. 2014 Aug; 33(4):678-683.

12 Valenti, L., Riso, P., Mazzocchi, A., Porrini, M., Fargion, S., Agostoni, C. Dietary anthocyanins as nutritional therapy for nonalcoholic fatty liver disease. Oxid Med Cell Longev. 2013;2013:145421.

13 Zelber-Sagi, S., Salomone, F., Yeshua, H., Lotan, R. et al. Non-high-density lipoprotein cholesterol independently predicts new onset of non-alcoholic fatty liver disease. Liver Int. 2014 Jul; 34(6):e128-35.

14 Vos, M.B., Lavine, J.E. Dietary fructose in nonalcoholic fatty liver disease. Hepatology. 2013 Jun; 57(6):2525-2531.

15 Lim, J.S., Mietus-Snyder, M., Valente ,A., Schwartz, J.M., Lustic, R.H. The role of fructose in the pathogenesis of NAFLD and the metabolic syndrome. Nat Rev Gastroenterol Hepatol. 2010 May; 7(5):251-264.

16 Alferink, L., Kiefte-deJong, J.C., Veldt, B., Schoufour, J.D. et al. Animal protein is the most important macronutrient associated with non-alcoholic fatty liver disease in overweight participants: The Rotterdam Study . Journal of Hepatology 2017 ; 66(1): Supplement, p S50.

17 Asrih, M., Jornayvaz, F.R. Diets and nonalcoholic fatty liver disease: The good and the bad.
Clinical Nutrition 2014; 33 : 186e190

18 Westerbacka, J., Lammi, K., Häkkinen, A-M., Rissanen, A., Salminen, I., Aro, A., Yki-Järvinen, H. Dietary Fat Content Modifies Liver Fat in Overweight Nondiabetic Subjects. The Journal of Clinical Endocrinology & Metabolism May 2005; 90(4): 2804–2809.

19 Wallace, I.R., McEvoy, C.T., Hunter, S.J., Hamill, L.L., Ennis, C.N. et al. Dose-Response Effect of Fruit and Vegetables on Insulin Resistance in People at High Risk of Cardiovascular Disease – A randomized controlled trial. Diabetes Care. 2013 Dec; 36(12): 3888–3896.

20 Meyer, B.J., de Bruin, E.J.P., du Plessis, D.G., van der Merwe, M., Meyer, A.C. Some biochemical effects of a mainly fruit diet in man. South African Medical Journal 1971 ; 45: 253-261.

21 Jenkins, D.J., Kendall, C.W., Popovich, D.G., Vidgen, E., Mehling, C.C., Vuksan, V. et al. Effect of a very-high-fiber vegetable, fruit, and nut diet on serum lipids and colonic function. Metabolism. 2001 Apr; 50(4):494-503.