Kids, Food, and Fatty Livers: Fructose vs the Med Diet

Antonella Mosca, MD; Andrea Vania, MD; Silvio Veraldi, MD; Valerio Nobili, MD


April 11, 2017

Diet and Fatty Liver Disease

Diet plays an important part in the pathogenesis of nonalcoholic fatty liver disease (NAFLD). The roles of potentially noxious nutrients (eg, fructose), potentially protective foods (eg, omega-3 fatty acids), and eating styles (eg, Mediterranean diet) in NAFLD have been described in previous research.

Over the past decade, studies have suggested that fructose intake increases the serum concentration of uric acid, and that both are increased in persons with type 2 diabetes, cardiovascular disease, and NAFLD.[1,2] NAFLD is now known to be the leading cause of liver disease in Western countries in both children and adults,[3] and its causes and prevention must be better recognized and appreciated.

It is estimated that 30% of the adult and up to 10% of the pediatric population is affected by NAFLD. In obese children, the proportion swells to over 70%.[4,5] Moreover, numerous studies have confirmed that the natural history of NAFLD involves the progression of liver damage to nonalcoholic steatohepatitis (NASH) with fibrosis and then, in some cases, to cirrhosis and hepatocellular carcinoma.[6]

Fructose and Uric Acid

A recent study[6] that we conducted at the Hospital Bambino Gesù enrolled 271 obese children with biopsy-proven NAFLD. All children completed a food frequency questionnaire, which assessed the quantity, quality, and frequency of specific foods consumed. The results showed that every day, 53% of children would skip breakfast, 47% would eat cereals, and 40% would consume vegetables and fruit. Moreover, almost 90% of children would drink sugary sodas and soft drinks at least once or several times weekly, and 95% of patients would consume at least one snack daily, consisting mainly of crackers, pizza, cookies, yogurt, or other sweet snacks.

According to the American Heart Association, daily consumption of added sugars (glucose, galactose, fructose, sucrose) for children aged 2-18 years should be ≤ 25 g. Most of the children in our study consumed more than 38 g of fructose daily. The average daily intake of added sugars in children with NASH was found to be about 70 g; higher fructose intake was associated with hyperuricemia (uric acid level ≥ 5.9 mg/dL) in 47% of these children compared with 29.7% of children without NASH (P = .003).

Both dietary fructose consumption (odds ratio [OR], 1.61; 95% confidence interval [CI], 1.25-1.86; P = .001) and serum uric acid level (OR, 2.48; 95% CI, 1.87-2.83; P = .004) were independently associated with NASH, and the consumption of fructose (OR, 2.02; 95% CI, 1.66-2.78; P = 0.01) was the only independent factor associated with uric acid concentration.[7]

It is well known that uric acid is one of the final products of hepatic fructose metabolism; thus, the more fructose that is ingested, the more uric acid is produced. This, in turn, will produce cellular oxidative stress, insulin resistance, and liver inflammatory processes.[8,9]


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