Refined crystalline fructose has been compared to alcohol in terms of the metabolism it undergoes in the liver. In particular, both fructose and alcohol increase the synthesis and storage of fatty acids in the liver (steatosis). Excess alcohol can cause the formation of alcoholic fatty liver, a process whereby fatty acid accumulation in the liver becomes excessive and the liver tissue becomes engorged with fat, accounting for 5 to 10 % of the mass of the liver. The accumulation of fatty acids in the liver can cause the development of inflammatory responses and this can then subsequently cause the development of steatohepatitis and cirrhosis of the liver. A very similar pathogenesis occurs with fructose overconsumption causing the development of nonalcoholic fatty liver disease, but until relatively recently the association between fructose consumption and fatty liver disease was not recognised. The development of nonalcoholic fatty liver disease is often accompanied by the development of fructose induced insulin resistance.
Evidence for the association between high fructose intakes and nonalcoholic fatty liver disease have come mainly from animal studies and clinical human studies. However, epidemiological evidence is lacking. For example, researchers1 investigated the association between the a number of parameters including plasma triglyceride and gamma-glutamyl transferase levels, weight, waist circumference and body mass index and used it to estimate a score for nonalcoholic fatty liver disease. The habitual fructose intake of the subjects was then assessed using frequent food questionnaires The result of the study showed that those with the highest fructose intake actually had the lowest risk of nonalcoholic fatty liver. However the highest fructose intakes were associated with the highest fibre intakes which highlights the methodological flaw in the study. The researchers did not differentiate between fructose from fruit in its unrefined form, present with dietary fibre, and fructose in its refined crystalline form, such as is present in table sugar.
Fructose in fruit is present with fibre. This fibre encircles and contains the fructose. When consumed the fibre slows the digestion of the fructose because the main fibre in fruit, pectin, is water soluble. The resultant gel-like viscosity in the gut, slows the absorption of the sugars in the fruit and also has a positive effect on satiety. As a result fructose is much harder to overeat when present as whole fruit, when compared to fruit juice, or products containing refined crystalline sugars. Investigating the association between fructose intake and nonalcoholic fatty liver without differentiating between whole fruit and other sources of fructose is therefore disingenuous, and the results of this research should be treated with caution for this reason. Certain many other studies have firmly established the link between fructose and fatty liver disease. The fact that the researchers did not directly measure the presence of nonalcoholic fatty liver disease in the subjects is also a serious methodological flaw.
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