It used to be that fatty liver disease was a serious medical condition primarily seen in alcoholics, but that all began to change over the past three decades as rising fructose consumption triggered a now widespread condition called non-alcoholic fatty liver disease.

This condition occurs when the human liver has difficulty breaking down fats and as a result, these fats accumulate in the liver causing a potentially life-threatening medical situation for the body. With this liver inflammation comes scarring of liver tissue and over time, liver failure can develop.

Quite often there are few severe symptoms indicating that non-alcoholic fatty liver disease (NAFLD) is developing. Some signs might include recurring pain in the upper right abdomen and chronic fatigue.

Because fructose is processed in the liver, which isn’t the case with other types of sugars, the liver is overwhelmed by the amounts of high fructose corn syrup and other types of fructose now found in Western diets. Small amounts of fructose can be handled by a healthy liver, yet the amounts coming from sweetened beverages and processed foods cannot be properly processed by even the healthiest of human livers. Nor can large amounts of fruit or their juices, including fructose rich carrot and beet juice.

Most consumers have no idea how much fructose they are consuming, much less how dangerous the fructose is to their health. This ignorance—and the health dangers that accompany it—has been intentionally perpetuated by the processed food and beverage industries.

A laboratory analysis of 23 popular sweetened beverages done in 2011 found that manufacturers consistently misled the public by listing a lower fructose and sugar content on labels than the products actually contained. Published in the medical journal Obesity, study authors discovered “that the total sugar content of the beverages ranged up to 128% of what was listed on the food label.”

A direct result of processed foods and beverages being laden with fructose is that 31% of American adults and 13% of children have now developed some degree of non-alcoholic fatty liver disease (NAFLD).

Severe cases of NAFLD progress into a condition called non-alcoholic steatohepatitis, in which vital blood flow into the liver is restricted. The non-profit medical science organization SugarScience estimates that up to 6 million people in the

U.S. now have this condition (the rates have doubled over just a few decades) and it has become one of the leading reasons for liver transplants.

An added health concern from fructose consumption is development of belly fat, sometimes called ‘sugar belly.’ As the fat cells accumulate around a person’s midsection, hormone imbalances are created in the body. These imbalances hasten the onset of many diseases, ranging from cancer and diabetes to heart disease and even Alzheimer’s disease.

 

More Evidence Linking Sweeteners & Non-Alcoholic Fatty Liver Disease

“We examined the cross-sectional association between intake of sugar-sweetened beverages and fatty liver disease in participants of the Framingham Offspring and Third General cohorts, 5908 participants. We observed that regular sugar-sweetened beverage consumption was associated with greater risk of fatty liver disease, particularly in overweight and obese individuals.”

Sugar-sweetened beverage, diet soda, and fatty liver disease in the Framingham Heart Study cohorts. Ma J. Et al. J Hepatol. 2015 May 29;SO168(15)00240–8.

 

“The objective of this study was to measure fructose absorption/metabolism in pediatric non-alcoholic fatty liver disease (NAFLD) compared with obese and lean controls. Children with histologically proven NAFLD and obese and lean controls received oral fructose.

Following fructose ingestion, NAFLD vs. lean controls had elevated serum glucose, insulin and uric acid but lower fructose excretion. Children with NAFLD absorb and metabolize fructose more effectively than lean subjects, associated with an exacerbated metabolic profile following fructose ingestion.”

Oral fructose absorption in obese children with non-alcoholic fatty liver disease. Sullivan JS. Et al. Pediatr Obes. 2014 Jun 24

 

 

Article by Brian Clement PhD LN

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