The Toxic Truth

Too much fructose can damage your liver, just like too much alcohol

There is growing scientific consensus that one of the most common types of sugar, fructose, can be toxic to the liver, just like alcohol.1,2

Fructose is the sugar that makes fruit taste sweet. For most people, there's nothing wrong with eating fructose in its natural state, in fruit.

But today, manufacturers extract and concentrate the fructose from corn, beets and sugarcane, removing the fiber and nutrients in the process. Getting frequent, high doses of fructose throughout the day, without fiber to slow it down, is more than our bodies were designed to handle.

31%of American adults and13%of kids suffer from non-alcoholic fatty liver disease (NAFLD).

Nearly all added sugars contain significant amounts of fructose.3 Typical formulations of high-fructose corn syrup contain upwards of 50% fructose, depending on processing methods. Table sugar and even sweeteners that sound healthy, like organic cane sugar, are 50% fructose.

What's unique about fructose is that, unlike any other sugar, it's processed in the liver. Small amounts of fructose, meted out slowly, are not a problem for your liver. Think of eating an apple - its sweetness comes with a lot of chewing that takes time. The apple's fiber slows down its processing in the gut.

But when we consume large amounts of fructose in added sugar, particularly in liquid form on an empty stomach, it slams the liver with more than it can handle.

As with alcohol, a little added fructose, consumed with fiber-rich foods, is OK. It's only when we frequently consume large quantities, in concentrated form, that fructose becomes a health hazard.

Liver damage is a looming health issue

For a long time, doctors mainly worried about life-threatening liver disease in alcoholics. But since 1980, there has been growing concern about two new conditions linked to fructose consumption from added sugar, as well as to obesity and other unhealthy dietary additives, such as trans-fats:

- Non-alcoholic fatty liver disease (NAFLD): This is characterized by excess fat build-up in the liver.

- Non-alcoholic steatohepatitis (NASH): This is characterized by fatty liver, inflammation and "steatosis," which is essentially scarring as the liver tries to heal its injuries. That scarring gradually cuts off vital blood flow to the liver.

About one-quarter of NASH patients will progress on to non-alcoholic liver cirrhosis,4,5 which requires a liver transplant or else it can lead to death.

Since 1980, the incidence of NAFLD and NASH has doubled, along with the rise of fructose consumption. Approximately 6 million individuals in the United States are estimated to have progressed to NASH and some 600,000 to NASH-related cirrhosis. Eating a lot of trans-fats, being overweight and not exercising also can contribute to NASH. Most people with NASH also have Type II diabetes.

What is alarming is that NASH is now the third-leading reason for liver transplantation in America.6 And it will become the most common if recent trends continue. Rates of NASH have doubled in America during the past 20 years alongside a dramatic increase in sugar consumption.

Estimates vary, but conservatively, 31% of American adults and 13% of kids suffer from NAFLD.7,8,9,10

How do you know if you have a liver problem?

You should be concerned if you or your kids have a "sugar belly" or belly fat. If your waist is larger than your hips, you should ask your doctor for a blood test that checks for triglyceride levels.

A sugar belly occurs when the liver detects more fructose than can be used by the body for energy. That excess fructose is broken down by the liver and transformed into fat globules (triglycerides), some of which are exported into the bloodstream and selectively deposited around your midsection and internal organs. Just as people who drink too much get a "beer belly," those who eat or drink too much fructose can get a "sugar belly."

Fat cells that accumulate around your midsection send out disruptive hormonal messages that upset your body's normal chemical balance.11,12 Scientists are actively studying how these hormonal imbalances become implicated in a wide variety of diseases, including heart disease, stroke, diabetes, cancer and Alzheimer's disease.

Why am I only hearing about this now?

Scientific evidence on fructose and the liver is relatively new, but it is a major area of laboratory and clinical research in our best universities and medical centers.

The goal of SugarScience is to bring you the latest research, getting the most critical information out of universities and into public awareness as quickly as possible. Getting you the news on fructose toxicity could change your health and the health of your kids. It's a good example of why we're here.

[1] Leung, T.M., & Nieto, N. CYP2E1 and oxidant stress in alcoholic and non-alcoholic fatty liver disease. Journal of Hepatology , 58(2), 395-398.

[2] Lustig, R.H., Schmidt, L.A., & Brindis, C.D. Public health: The toxic truth about sugar. Nature , 487(5), 27-29. doi:10.1038/482027a. Retrieved from http://www.nature.com/nature/journal/v482/n7383/full/482027a.html

[3] Ng, S.W., Slining, M.M., & Popkin, B.M. Use of caloric and noncaloric sweeteners in US consumer packaged foods, 2005-2009. Journal of the Academy of Nutrition and Dietetics , 112(11), 1828-1834.e1821-1826.

[4] Powell, E.E., Cooksley, W.G., Hanson, R., Searle, J., Halliday, J.W., & Powell, L.W. The Natural History of Nonalcoholic Steatohepatitis: A Follow-up Study of Forty-two Patients for Up to 21 Years. Hepatology , 11(1).

[5] Farrell, G.C., & Larter, C.Z. Nonalcoholic fatty liver disease: from steatosis to cirrhosis. Hepatology , 43(2, Suppl 1), S99-S112.

[6] Charlton, M.R., Burns, J.M., Pedersen, R.A., Watt, K.D., Heimbach, J.K., & Dierkhising, R.A. Frequency and outcomes of liver transplantation for nonalcoholic steatohepatitis in the United States. Gastroenterology , 141(4), 1249-1253.

[7] Lazo, M., & Clark, J. The Epidemiology of Nonalcoholic Fatty Liver Disease: A Global Perspective.. Seminars in Liver Disease , 28(4), 339-50. doi:10.1055/s-0028-1091978

[8] Browning, J.D., Szczepaniak, L.S., Dobbins, R., Nuremberg, P., Horton, J.D., Cohen, J.C., & Hobbs, H.H. Prevalence of hepatic steatosis in an urban population in the United States: Impact of ethnicity. Hepatology , 40(6), 1387-1395. doi:10.1002/hep.20466. Retrieved from http://onlinelibrary.wiley.com/doi/10.1002/hep.20466/full

[9] Schwimmer, J.B., Deutsch, R., Kahen, T., Lavine, J.E., Stanley, C., & Behling, C. Prevalence of Fatty Liver in Children and Adolescents. Pediatrics , 118(4), 1388-1393. doi:10.1542/peds.2006-1212. Retrieved from http://pediatrics.aappublications.org/content/118/4/1388.long

[10] LindbÃ¤ck, S.M., Gabbert, C., Johnson, B.L., Smorodinsky, E., Sirlin, C.B., Garcia, N., & Schwimmer, J.B. Pediatric Nonalcoholic Fatty Liver Disease: A Comprehensive Review. Advances in Pediatrics , 57(1), 85-140. doi:10.1016/j.yapd.2010.08.006

[11] McGown, C., Birerdinc, A., & Younossi, Z.M. Host genetic variants in obesity-related nonalcoholic fatty liver disease. Clinics in liver disease , 18(1), 249-67. doi:10.1016/j.cld.2013.09.017. Retrieved from http://www.ncbi.nlm.nih.gov/pubmed/24274878

[12] Kershaw, E.E., & Flier, J.S. Adipose tissue as an endocrine organ. The Journal of clinical endocrinology and metabolism , 89(6), 2548-56.