The damage that excessive alcohol consumption can cause to the liver is well understood. The ectopic stenosis that drives the liver damage associated with excessive alcohol consumption is caused by aberrations to the metabolism of fats and also to the direct production of fats from the acetate metabolite of ethanol. As fats accumulate in the liver, function is lost and gradually cirrhosis of the liver develops which leads eventually to death. However, fructose metabolism is surprisingly similar to that of ethanol, and the accumulation of ectopic fat in liver tissue is now associated with fructose consumption. While the hepatic fat accumulation (hepatic steatosis) is referred to as alcoholic fatty liver disease in the case of over consumption of ethanol, the over consumption of fructose instead leads to an identical pathology referred to as non-alcoholic fatty liver disease. Animal studies have investigated the effects of fructose overfeeding on liver damage, but often such studies also induce weight gain, and so fructose can not be isolated as the causative factor.
However, a recent paper published in the American Journal of Clinical Nutrition1 investigated the effects of dietary fructose on a group of monkeys (Macaca fasciculus) but without allowing the monkey to gain weight from their diets. Initially monkeys were fed an ad libitum (free access to food) low fat diet containing 24 % of energy as fructose. After only 3 months the monkey fed the high fructose diet had evidence of the accumulation of fatty acids in their livers. Over a 7 year period 15 % of the monkeys had developed type 2 diabetes, 3 times the normal incidence for monkeys of this variety. The high fructose diet monkeys also weighed considerably more than monkeys fed a low fat low fructose (0.5 % of energy) diet. The researchers then took another group of monkeys and fed then an energy controlled high fructose diet that did not allow the monkeys to gain weight. After just 6 weeks the fructose fed monkeys developed elevated liver enzymes, inflammation, and a trend towards increased cholesteryl ester synthesis.
Interestingly the authors of this study also noted the presence of endotoxemia caused by the translocation of gastrointestinal bacterial toxins to the liver, which may explain the inflammation. The authors presented evidence from other papers to show that this may be caused by a deterioration in gut wall integrity with fructose feeding. These results support other animal experiments in that in only a matter of weeks fructose ingestion can be shown to cause changes to liver tissue that are indicative of the development of non-alcoholic fatty liver. The prevention of weight gain through energy control appears to offer some protection against hepatic steatosis, but not to liver damage. This suggest that those who attempt to reduce energy intake, but who continue to eat a low quality diet containing fructose, will not be successful at reversing metabolic dysfunction that is the likely cause of their weight gain. Such a strategy is therefore destined to failure, which explains the high incidence of failure of calorie counting energy restrictive diets.
Dr Robert Barrington’s Nutritional Recommendation: Refined crystalline fructose is a metabolic poison. Refined sugar and fructose have no place in a healthy diet. Only sugars present in their natural plant material with their fibre present should be consumed.
RdB
