Excess fructose in kids linked to rise in liver disease
Work carried out in this latest study appears to show that dietary fructose consumption and serum uric acid (UA) concentrations are independently linked with the onset of non-alcoholic steatohepatitis (NASH), a less aggressive form of non-alcoholic fatty liver disease (NAFLD).
“The development of NASH may markedly affect life expectancy and quality of life in affected individuals,” said Dr Valerio Nobili, chief of the Hepatometabolic Unit Liver Diseases Laboratory, Bambino Gesù Hospital, IRCCS, Rome, Italy.
“It is crucial to understand the risk factors for NASH in children and adolescents in order to design effective interventions which can be used safely to treat this young group of patients," he added.
NASH is a condition that results in the accumulation of extra fat in the liver. Rising case numbers in both Western and developing countries coincide with the increase in numbers of overweight children.
Previous evidence has pointed to fructose, the type of sugar added to commercial cereals and soft drinks, as a cause of increased serum UA concentrations.
Study details
The research team looked at 271 obese children and adolescents with NAFLD. The sample consisted of 155 males with a mean age of 12.5 years.
These children answered questions on when specific foods were consumed throughout the day, their frequency throughout the week and portion size.
The team found 37.6% of patients had NASH. 47% of these patients also had high UA compared with 29.7% of patients who did not have NASH.
Statistical analysis confirmed that UA concentration and fructose consumption were independently associated with NASH, even after adjusting for variables.
Fructose consumption was also independently associated with an excess of UA in the blood (hyperuricemia).
“It is plausible that dietary fructose intake and uric acid concentrations are potential risk factors for liver disease progression in NAFLD,” said Dr Nobili.
“Numerous studies have shown that high uric acid levels are associated with metabolic syndrome and NAFLD, but to date, to the best of our knowledge, no studies have tested the independence of associations among uric acid concentrations, fructose consumption, and NASH confirmed by biopsy."
Liver disease in the West
Recent figures estimate up to 30% of the general population in Western countries and up to 9.6% of all children that include 38% of obese children exhibit a spectrum of liver disease, including NASH.
NASH’s progression from NAFLD has been the subject of a growing body of evidence that identifies fructose’s link to hyperuricemia.
One study showed that the increased consumption of fructose induces an upregulation of expression of genes essential in fructose absorption and metabolism.
Glut 5 and KHK were both upregulated by the concentration of fructose and by the intracellular production of UA.
The team acknowledged the limitations of the study that included the use of a dietary questionnaire to assess fructose consumption that they said may not truly reflect all dietary consumption of fructose.
“Any misclassification bias would tend to attenuate the strength of our findings, and would bias our results towards the null.”
Source: Journal of Hepatology
Published online ahead of print: doi.org/10.1016/j.jhep.2016.12.025
“Fructose consumption linked to the increase of liver disease among adolescents and children.”
Authors: Antonella Mosca, Valerio Nobili, Rita De Vito, Annalisa Crudele, Eleonora Scorletti, Alberto Villani, Anna Alisi, Christopher D. Byrne.
