It is well established that excessive energy intake can lead to adverse liver health outcomes including nonalcoholic fatty liver disease (NAFLD). However, recent scientific literature shows that there is no association between fructose consumption and the development of NAFLD. Participants that consumed more fructose had smaller waist circumferences, lower dietary fat intake, and higher fiber and vitamin E intake in one observational study. Thus, the researchers concluded that the potentially adverse effects of fructose intake are instead from excess caloric intake overall rather than sugar consumption alone. A meta-analysis of studies using energy-controlled protocols show fructose was not found to be associated with an increased prevalence of NAFLD. Some of the controversy regarding fructose is due to studies that were conducted by feeding individuals excessive fructose or implying a causal relationship from observational studies that are not designed for such outcomes.
It is now generally accepted that glucose, fructose, HFCS and sucrose consumption results in similar responses over the range of human exposure to each carbohydrate. Fructose consumption does not play a unique role in the development of adverse liver health outcomes.
Research Study Summaries
Effect of a Low Free Sugar Diet vs Usual Diet on Nonalcoholic Fatty Liver Disease in Adolescent Boys: A Randomized Clinical Trial
JAMA. 2019;321(3):256-265. doi:10.1001/jama.2018.20579 — Schwimmer JB, Ugalde-Nicalo P, Welsh JA, et al. Download Research Study PDF Objective To determine the effects of a diet low in free sugars in adolescent boys with NAFLD. Background From 1988 to 2010, the prevalence of nonalcoholic fatty liver disease (NAFLD) increased among children in the United States. Pediatric NAFLD […]
Download PDF Ribeiro A, Igual-Perez MJ, Santos Silva E and Sokal EM. Hepatology Communication 2019, 3:1; doi: 0.1002/hep4.1291 Objective To conduct a review to provide evidence of the negative effect of high fructose consumption in childhood on future liver health, with many similarities to alcohol, and to propose strategies for its reduction and to support […]
Nutrients 2019, 11, 522; doi:10.3390/nu11030522 — Cantoral A, Contreras-Manzano A, Luna-Villa L, et al. Download Research Study PDF Objective To assess the consumption of dietary fructose according to: 1) classification of hepatic steatosis by two indexes and 2) diagnosis of NAFLD by MRI. Background Previous studies have shown that consumption of fructose through soft drinks […]
Non-Alcoholic Fatty Liver Disease in Overweight Children: Role of Fructose Intake and Dietary Pattern
Nutrients 2018 Sept 19; 10(9):pii E1329. doi: 10.3390/nu10091329 — Nier A, Brandt A, Conzelmann IB, et al. — Download PDF Objective To determine if the dietary pattern and lifestyle of overweight children without NAFLD differs from overweight children showing early signs of NAFLD. Background Contrary to many other liver diseases, NAFLD is not a disease […]
J Hepatol. 2018 May;68(5):1063-1075. doi: 10.1016/j.jhep.2018.01.019 — Jensen T, Abdelmalek MF, Sullivan S, et al. — Download PDF — Objective To review the experimental and clinical evidence that fructose precipitates fat accumulation in the liver, due to both increased lipogenesis and impaired fat oxidation. Background Historically thought to result from over-nutrition and a sedentary lifestyle, […]
Habitual Fructose Intake Relates to Insulin Sensitivity and Fatty Liver Index in Recent-Onset Type 2 Diabetes Patients and Individuals without Diabetes
Nutrients 2018, 10(6), 774; //doi.org/10.3390/nu10060774 — Weber KS, Simon MC, Strassburger, et al. — Download PDF — Objective: To test the hypothesis that higher habitual intake of fructose from regular food sources (assessed as total fructose, fructose from fruits, fructose from juices, and fructose from sugar-sweetened beverages (SSB)) are associated with lower hepatic but not […]
A study entitled “Serum uric acid concentrations and fructose consumption are independently associated with NASH in children and adolescents,” was recently published in the Journal of Hepatology. The purpose of the study was to identify the factors associated with non-alcoholic steatohepatitis (NASH) in children and adolescents with confirmed cases of non-alcoholic fatty liver disease (NAFLD). More […]
Nonalcoholic fatty liver disease is associated with excessive calorie intake rather than a distinctive dietary pattern
A study published in Medicine sought to characterize the dietary patterns of patients with nonalcoholic fatty liver disease (NAFLD) and to assess the efficacy of dietary interventions on NAFLD related outcomes. Researchers collected a total of 55 NAFLD patients and 88 controls to complete the study in northern Germany. All participants were subjected to a […]
A new study of more than 1,600 people has concluded that fructose is not associated with the development of nonalcoholic fatty liver disease (NAFLD).
Available scientific evidence does not support a link between fructose consumption and risk of nonalcoholic fatty liver disease (NALFD), according to a recent review published in The American Journal of Clinical Health.
A systematic review and meta-analysis by Chiu et al found that fructose does not cause non-alcoholic fatty liver disease (NAFLD).
A recent article published in Harvard Heart Letter recommended that readers cut back on fructose.
Calorie-sweetened beverages and fructose: what have we learned 10 years later. Pediatr Obes 2013.
High rates of fructose malabsorption are associated with reduced liver fat in obese African Americans
The aim of this study was to investigate the frequency of fructose malabsorption between obese Hispanic and African American young adults.
Underpowered and unphysiologic design weakens fructose
In their recent article, Vos and McClain paint a grim picture of dietary fructose, likening its effect to alcohol-induced hepatic steatosis and liver injury and thereby ‘‘defining targets for therapeutic interventions.’’ The case for such interventions is unsupported, built as it is on inappropriate extrapolation of highly exaggerated diets to the human condition, and decidedly premature for two reasons.
Restraint urged in extrapolation of unphysiologic fructose experimentation to predictions of real-world outcomes
In their commentary accompanying the recent mechanistic paper from Peter Havel’s group, Hoffman & Tschöp (2) do not show the same restraint Havel does in extrapolating his admittedly unphysiologic results to typical human diets.