A sweetener used in fizzy drinks, biscuits, cakes and ice cream is causing an epidemic of liver disease among youngsters, warns new research.
Up to half of obese children are suffering a severe second stage of non-alcoholic fatty liver disease (NAFLD) that leads to inflammation of the liver and even cirrhosis.
If left untreated non-alcoholic steatohepatitis (NASH) leads to fibrosis, persistent inflammation which causes scar tissue around the liver.
Ultimately it causes cirrhosis where the liver shrinks and becomes scarred and lumpy.
This damage is permanent and can lead to liver failure and cancer.
The new study by UK and Italian scientists suggested fructose was to blame.
The sugar is found naturally in fruit but when eaten its effects are counteracted by the fibre and other compounds which slowly releases the energy.
But food manufacturers extract fructose removing the fibre and nutrients and use it as a sweetener which gives an instant sugar rush when eaten.
Recent research suggested dietary fructose may increase serum uric acid concentrations and that both uric acid concentration and fructose consumption may be increased in individuals with NAFLD.
The new study of obese teens established that both dietary fructose consumption and serum uric acid concentrations are independently associated with NASH.
NASH is estimated to affect up to five per cent of the UK population.
NAFLD is the term for a range of conditions caused by a build-up of fat in the liver and usually seen in people who are overweight or obese.
A healthy liver should contain little or no fat but it is estimated one in every three Britons has early stages of NAFLD where there are small amounts of fat in their liver.
The study suggested up to a tenth of children and two fifths of obese children have liver disease, including NASH.
Although NASH is a less aggressive form of NAFLD, it can progress to severe fibrosis and cirrhosis, with development of hepatocellular carcinoma in adults.
Senior investigator Dr Valerio Nobili said: “It is plausible that dietary fructose intake and uric acid concentrations are potential risk factors for liver disease progression in NAFLD.
“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.
The study involved 271 Italian obese children of which 155 were boys and all had a mean age of 12.5 years with NAFLD who underwent liver biopsy.
They filled out a questionnaire listing what they ate and drank, when and how often.
Their main source of fructose was fizzy and soft drinks with nine in ten drinking one or more times a week.
Almost all - 95 per cent - regularly consumed morning and afternoon snacks consisting of crackers, pizza and salty food, biscuits, yogurt, or other snacks.
Of the participants 37.6 per cent had NASH and 47 per cent with NASH had high uric acid compared with 29.7 per cent of patients who did not have NASH.
Fructose consumption was independently associated with high uric acid, which occurred more frequently in patients with NASH than in not-NASH patients.
Dr. Nobili concluded: “In this study, we show for the first time that uric acid concentrations and dietary fructose consumption are independently and positively associated with NASH.
“The development of NASH may markedly affect life expectancy and quality of life in affected individuals and therefore 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.
A recent study suggested fructose is the deadliest sugar you can eat because it boost harmful cholesterol raising the risk of diabetes, heart attacks and stroke.
The new study was published in the Journal of Hepatology.