Fructose and sugar: A major mediator of non-alcoholic fatty liver disease

Jensen, Thomas; Abdelmalek, Manal F.; Sullivan, Shelby; Nadeau, Kristen J.; Green, Melanie; Roncal, Carmen; Nakagawa, Takahiko; Kuwabara, Masanari; Sato, Yuka; Kang, Duk Hee; Tolan, Dean R.; Sánchez-Lozada, Laura G.; Rosen, Hugo R.; Lanaspa, Miguel A.; Diehl, Anna Mae; Johnson, Richard J.

doi:10.1016/j.jhep.2018.01.019

Cited by 639 publications

(474 citation statements)

References 159 publications

(186 reference statements)

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Section: Fructose As the Main Cause Of Nafldmentioning

confidence: 99%

“…Fructose is the major constituent of common sweeteners, such as sucrose (table sugar), high fructose corn syrup, and agave syrup, which consist of a mixture of fructose and glucose monosaccharides . Fructose consumption has risen uncontrollably over the past century, especially by ingestion of sugar‐sweetened beverages . It can also be found in fruits and honey, although with less noxious outcome than fructose in added sugar compounds due to its lower concentration and the presence of other constituents (primarily antioxidants and fibers) that alter its metabolic effect .…”

Section: Fructose As the Main Cause Of Nafldmentioning

confidence: 99%

“…This transient decrease of adenosine triphosphate does not occur with glucose metabolization and is the key to fructose‐mediated negative metabolic effects. One of those effects is intrahepatic lipid accumulation (steatosis) due to an increase in hepatic fatty acid (FA) synthesis from de novo lipogenesis (DNL), an increase in hepatic delivery of FAs, and a decrease in lipid clearance . Dietary sugars have been shown to enhance hepatic DNL, a metabolic pathway that affects lipid and glucose regulation and induces insulin resistance, cardiovascular disease, and hepatic steatosis .…”

Section: Fructose As the Main Cause Of Nafldmentioning

confidence: 99%

“…Fructose intake has a dose‐dependent correlation with NAFLD development and its progression to fibrosis in children and adolescents . A study including 271 obese adolescents with biopsy‐proven NAFLD showed that fructose consumption was significantly higher in patients with NASH compared with NAFLD, and patients from the first group had significantly higher uric acid levels .…”

Section: Fructose As the Main Cause Of Nafldmentioning

confidence: 99%

“…(29) Moreover, taking into account the ongoing rise of fructose consumption and childhood obesity and its role in NAFLD, a significative number of children might need liver transplantation and at earlier ages if no effective measures are assumed. (30,31) NASH recurrence in allograft with requirement of retransplantation is well recognized and can occur within a few months after transplantation if no solid lifestyle modification is attempted. (19,20,32,33) In adults, NAFDL is clearly associated with HCC even without the presence of significant fibrosis.…”

Section: Natural History Of Pediatric Nafldmentioning

confidence: 99%

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Childhood Fructoholism and Fructoholic Liver Disease

et al. 2018

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Nonalcoholic fatty liver disease (NAFLD) is an emerging entity, becoming the most prevalent pediatric chronic liver disease. Its broad spectrum of histological findings, comorbidities, and complications, including cirrhosis and liver failure, can occur in childhood, emphasizing the severity of pediatric NAFLD. Current lifestyle and diet modifications have been linked to the increasing prevalence of NAFLD, including the rise of fructose consumption, a monosaccharide present in foods that contain added sugar, such as sugar‐sweetened beverages. Excessive fructose consumption is believed to cause addiction like alcohol and other drugs. As such, the new term “fructoholism” refers to the consumption of a substance (fructose) that can cause psychological and physical damage and become a major public health concern, highlighting the seriousness of the excessive consumption of fructose in the pediatric age. Hepatic fructose metabolization leads to hepatic steatosis and progression to fibrosis through mechanisms comparable to alcoholic liver disease, hence the term “fructoholic liver disease.” Conclusion: The importance of implementing reliable global strategies, such as education campaigns to promote healthy diet, increasing taxes on foods that contain added sugars, subsidies to promote accessibility to fruit and vegetables, and strict food industry regulation to reduce sugar intake in children and adolescents, cannot be overemphasized.

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Section: Fructose As the Main Cause Of Nafldmentioning

confidence: 99%

Section: Fructose As the Main Cause Of Nafldmentioning

confidence: 99%

Section: Fructose As the Main Cause Of Nafldmentioning

confidence: 99%

Section: Fructose As the Main Cause Of Nafldmentioning

confidence: 99%

Section: Natural History Of Pediatric Nafldmentioning

confidence: 99%

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Childhood Fructoholism and Fructoholic Liver Disease

et al. 2018

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Sugar-Sweetened and Artificially Sweetened Beverages and Risk of Liver Cancer and Chronic Liver Disease Mortality

Zhao

Zhang

Coday

et al. 2023

JAMA

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ImportanceApproximately 65% of adults in the US consume sugar-sweetened beverages daily.ObjectiveTo study the associations between intake of sugar-sweetened beverages, artificially sweetened beverages, and incidence of liver cancer and chronic liver disease mortality.Design, Setting, and ParticipantsA prospective cohort with 98 786 postmenopausal women aged 50 to 79 years enrolled in the Women’s Health Initiative from 1993 to 1998 at 40 clinical centers in the US and were followed up to March 1, 2020.ExposuresSugar-sweetened beverage intake was assessed based on a food frequency questionnaire administered at baseline and defined as the sum of regular soft drinks and fruit drinks (not including fruit juice); artificially sweetened beverage intake was measured at 3-year follow-up.Main Outcomes and MeasuresThe primary outcomes were (1) liver cancer incidence, and (2) mortality due to chronic liver disease, defined as death from nonalcoholic fatty liver disease, liver fibrosis, cirrhosis, alcoholic liver diseases, and chronic hepatitis. Cox proportional hazards regression models were used to estimate multivariable hazard ratios (HRs) and 95% CIs for liver cancer incidence and for chronic liver disease mortality, adjusting for potential confounders including demographics and lifestyle factors.ResultsDuring a median follow-up of 20.9 years, 207 women developed liver cancer and 148 died from chronic liver disease. At baseline, 6.8% of women consumed 1 or more sugar-sweetened beverage servings per day, and 13.1% consumed 1 or more artificially sweetened beverage servings per day at 3-year follow-up. Compared with intake of 3 or fewer servings of sugar-sweetened beverages per month, those who consumed 1 or more servings per day had a significantly higher risk of liver cancer (18.0 vs 10.3 per 100 000 person-years [P value for trend = .02]; adjusted HR, 1.85 [95% CI, 1.16-2.96]; P = .01) and chronic liver disease mortality (17.7 vs 7.1 per 100 000 person-years [P value for trend &lt;.001]; adjusted HR, 1.68 [95% CI, 1.03-2.75]; P = .04). Compared with intake of 3 or fewer artificially sweetened beverages per month, individuals who consumed 1 or more artificially sweetened beverages per day did not have significantly increased incidence of liver cancer (11.8 vs 10.2 per 100 000 person-years [P value for trend = .70]; adjusted HR, 1.17 [95% CI, 0.70-1.94]; P = .55) or chronic liver disease mortality (7.1 vs 5.3 per 100 000 person-years [P value for trend = .32]; adjusted HR, 0.95 [95% CI, 0.49-1.84]; P = .88).Conclusions and RelevanceIn postmenopausal women, compared with consuming 3 or fewer servings of sugar-sweetened beverages per month, those who consumed 1 or more sugar-sweetened beverages per day had a higher incidence of liver cancer and death from chronic liver disease. Future studies should confirm these findings and identify the biological pathways of these associations.

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