Non-alcoholic Fatty Liver Disease and Carbohydrate-rich Diet: An Epidemic Involves Both Adults and Children.

Fatty liver disease, by its name, is a disease with excess fat accumulated inside the liver, and has been commonly observed in the cases related to alcohol use. However, there is another type of fatty liver disease, which is found in cases related to little or no alcohol use, thus, called non-alcoholic steatohepatitis (NASH.) NASH is a silent liver disease, characterized with accumulation of fat, inflammation and damage in the liver, which will become scarred and cirrhotic, even cancer, and will lose functions. Based on a report by the National Digestive Diseases Information Clearinghouse, NASH affects 2-5 % of the population. However, one out every five Americans has fat in their liver with no inflammation or damage. Unfortunately, no one can predict its long-term outcomes. When one’s blood tests and liver biopsy implicate accumulation of fat in the liver, it is called non-alcoholic fatty liver disease (NAFLD.)  [1]

In a report by the US Department of Veterans Affairs, updated on October 22, 2009, while the incidence of NAFLD was about one out of five Americans, the incidence of NAFLD significantly increased to four out of five diabetic Americans. Evidences showed that NAFLD could be eased with diabetic medications that implicated the disease is a result of hyperglycemia, not hyperlipidemia, from the diet. Interestingly, in a separate news inside this report, Dr. Brent Tetri and his colleagues fed mice with junk-food diet for 16 weeks, but were surprised that NAFLD was developed in just four weeks after the study started.  The Junk-food diet was high in fructose corn syrup, in addition to 40% of fats. [2] An article by Rochelle Collantes, “Non-alcoholic Fatty Liver Disease and the epidemic of Obesity”, cited that NAFLD is common in patients with metabolic syndrome and even more common with obesity, which is on the rise. [3] Studies have also reported that NAFLD is increasing among children who are obese. [4]

At this time, experts are scrambling in finding treatment(s) for NAFLD, and suggesting exercise and dietary regimens for weight loss and calorie reduction seem helpful. [5, 6] There is no definite prognosis on NAFLD in sight. Because of the increase in the cases of NAFLD in both adults and children, to stop its epidemic is very urgent. Having known the prevalence of NAFLD in other diseases, reversing the trends in obesity and diabetes mellitus is the top priority for preventive medicine.

Consuming excess calorie resulting in overweight or obesity has been the common thought. However, depending on the sources of the calories, the outcomes can be different. For instance, consuming carbohydrates raises the blood glucose level, which consequently triggers the secretion and release of insulin. Insulin helps cells take up glucose for producing energy, and put away the excess glucose in the storage inside the liver and muscles as glycogen and in the fatty tissue and organs as fats or triglycerides. In the situation of consuming excessive carbohydrate, insulin stops the breakdown of fats for producing energy. Consequently, the glucose-turned fats along with the dietary fats will be stored in the fatty tissues. To worsen the situation, the dietary fats will further increase the load in the fatty tissue. This is why a typical American Diet nowadays high in carbohydrate, fat, and calorie is so unhealthy. But, keep in mind that diets high in carbohydrate and calories with little or no fat will also reach the same outcome!

Having understood the links between diets and obesity, carbohydrates, not fats, play a major role in increasing both the production and storage of fats [7] and resulting obesity. Moreover, the increase in the postprandial blood glucose level, as a result of excess consumption of carbohydrate, increases the level of postprandial inflammation, which attacks the tissues and organs including the insulin-producing beta cells and paves the way of becoming diabetes mellitus when the mass of beta cells is reduced to about 40-60% of its normal size. [8] Thus, to restrict the consumption of carbohydrates for preventing obesity and diabetes mellitus does make sense. And, it should be logical to expect the trend in NAFLD could be halted or even reversed on the same track.

A study by Solga S, et al., “Dietary Composition and Nonalcoholic Fatty Liver Disease”, found a significant tie between higher consumption of carbohydrate and the level of inflammation, which exacerbates the pathology of NAFLD. Interestingly, the study also found higher intake of fat reduced the level of inflammation. [9] Other studies pointed out a strong, positive relationship between the consumption of fructose and the risk of NAFLD. Fructose is rich in some fruits. In addition, syrups and honey contain lots of fructose. [10, 11] Studies have shown fructose is metabolized in the liver to produce triglycerides and Very Low-Density Lipoprotein (VLDL) or to result in dyslipidemia.  [12]

While the Dietary Guidelines for Americans, 2010 is facing lots of questions about their soundness, avoiding diets high in carbohydrates especially fructose is the best way to reduce the risk of NAFLD.

Robert Su, Pharm.B., M.D.

References:

1. National Digestive Diseases Information Clearinghouse. “Non-alcoholic Steatohepatitis.”

2. US Department of Veterans Affairs. “Fatty Liver Disease: A New Epidemic?”

3. Collantes R. et al. “Nonalcoholic fatty liver disease and the epidemic of obesity.” CLEVELAND CLINIC JOURNAL OF MEDICINE VOLUME 71 • NUMBER 8 AUGUST 2004

4. Dunn W, Schwimmer JB. “The obesity epidemic and nonalcoholic fatty liver disease in children.” Current Gastroenterology Reports. 2008 Feb;10(1):67-72.

5. Valerio Nobili, Anna Alisi, and Massimiliano Raponi. “Pediatric non-alcoholic fatty liver disease: Preventive and therapeutic value of lifestyle intervention.” World J Gastroenterol. 2009 December 28; 15(48): 6017–6022

6. Sandra K Erickson. “NONALCOHOLIC FATTY LIVER DISEASE (NAFLD.)”

7. Hudgins LC, et al. “Human Fatty Acid Is Stimulated by a Eucaloric Low Fat, High Carbohydrate Diet.” Journal of Clinical Investigations, Volume 97, Number 9, Pages 2081–2091. May 1996.

8. Su, R. “Diabetes Mellitus: A Diagnosis Too Late.” Carbohydrates Can Kill. April 7, 14, 21, 2010.

9. Solga S, et al. “Dietary Composition and Nonalcoholic Fatty Liver Disease.” Digestive Diseases and Science. Volume 49, Number 10, Pages 1578-1583. October, 2004.

10. Ackerman, Z, et al.  ”Fructose-Induced Fatty Liver Disease: Hepatic Effects of Blood Pressure and Plasma Triglyceride Reduction.” Hypertension 2005;45;1012-1018

11. Ouyang X, et al. ”Fructose consumption as a risk factor for non-alcoholic fatty liver disease.” Journal of Hepatology. 2008 June; 48(6): 993–999.

12. Basciano H, Federico L, and Adeli K. “Fructose, insulin resistance, and metabolic dyslipidemia.” Nutrition & Metabolism, (Lond). 2005; Volume 2, Number 5, and online February 21. 2005.