Fatty Liver Disease and Fructose

Chapter summary

Fatty liver disease (FLD) was once linked to heavy drinking. In 20 years incidence has skyrocketed, and an estimated one in three people now has it.
Prevalence is 80% to 90% in obese adults.
It may start mild but can lead to cirrhosis and liver cancer. It is reversible if caught early.
The author’s advice: stop fructose consumption, and treat it like alcohol.

Alcoholic: universal in heavy drinkers. Pathological changes appear at around 40g of alcohol a day.
Non-alcoholic (NAFLD): now the most common liver disease worldwide, affecting 20% to 30% of adults in Western countries. About 2% to 3% have the inflammatory form, NASH, which may progress to cirrhosis and liver cancer.
Most people have few symptoms. It is usually found through abnormal liver tests. It is linked to insulin resistance and metabolic syndrome.
Genetics plays a role. Some groups, such as Indian men, have higher rates.

Calories explanation: Earlier studies suggested fatty liver came from too many calories overall, with fructose playing no special role. The role of fructose is still described as controversial.
Fructose explanation: Kavanagh (Wake Forest) fed middle-aged, normal-weight monkeys a high-fructose diet with calories controlled to prevent weight gain. Liver damage more than doubled in six weeks, roughly three months in humans.
Caveat from the researcher: Kavanagh said the study cannot conclusively show fructose rather than glucose caused the damage. High added sugars let gut bacteria leak into the blood and injure the liver.
Fat versus sugar: High-fat diets produce obesity and some fat in the liver with little inflammation. A fast-food, high-sugar diet produced more inflammation and scarring. The author concludes high fat does not create NAFLD, but fructose does.
These are animal results. Human trials are smaller and shorter.

Detection is by routine blood tests. Treatment is weight loss (or, increasingly, drugs).
Livers are forgiving and can recover. Cut out sugary drinks and added fructose.
Limit alcohol, since liver damage from alcohol and fructose may be additive.
The author finds it puzzling that nutrition authorities do not warn more clearly about fructose.

Kavanagh, K. et al. (2013) Dietary fructose induces endotoxemia and hepatic injury in calorically controlled primates. Am J Clin Nutr. doi:10.3945/ajcn.112.057331
Bellentani, S., Scaglioni, F., Marino, M. and Bedogni, G. (2010) Epidemiology of non-alcoholic fatty liver disease. Dig Dis 28(1):155-161.
Basaranoglu, M., Basaranoglu, G., Sabuncu, T. and Senturk, H. (2013) Fructose as a key player in the development of fatty liver disease. World J Gastroenterol 19(8):1166-1172.
Fairbanks, K. (2014) Alcoholic liver disease. Cleveland Clinic Foundation.
Wikipedia. Non-alcoholic fatty liver disease.