While it has been postulated that fructose consumption could lead to non-alcoholic fatty liver disease, this is not supported by the totality of the scientific research.
Proponents of this theory argue that because fructose may be metabolized by de novo lipogenesis, that fructose could adversely affect the liver. However, de novo lipogenesis is a minor pathway in the overall human energy economy (Rippe & Etherton, 2012; Tappy & Le, 2010). Portion size and overall caloric consumption are more likely causes of non-alcoholic fatty liver disease. A double blind trial by Johnston et al. (2013), found that a high fructose diet did not cause any of the features of non-alcoholic fatty liver disease in participants. They concluded that, “…any advice on low fructose diets in NAFLD remains unjustified.” A ten week, randomized, prospective, partially blinded, parallel investigation by Bravo et al. (2013) showed that when fructose was consumed as part of the usual diet, there was no promotion of fat storage in the liver.