Nonalcoholic fatty liver disease (NAFLD) is the most common chronic liver disease in children in the United States. Although changes in diet are often recommended to improve NAFLD, little is known regarding the influence of diet on histologic features of the disease.
This was a prospective, cross-sectional registry-based study. Children (n = 149) enrolled in the multicenter nonalcoholic steatohepatitis (NASH) Clinical Research Network had demographic, anthropometric, clinical, laboratory, and histology data obtained, including the Block Brief Food Questionnaire. Subjects were grouped by presence or absence of steatohepatitis and grades of histologic features according to NASH Clinical Research Network criteria.
No significant differences were found between children with steatosis compared with steatohepatitis for fraction of energy from fat, carbohydrates, and protein. Sugar-sweetened beverage consumption was low and did not correlate with histologic features, although uric acid, a surrogate marker for fructose intake, was significantly increased in those with definite NASH (P = 0.008). For all groups, vitamin E consumption was insufficient compared with the recommended daily allowance. Median consumption of vitamin E was lower in children with higher grade of steatosis (8.4 vs 6.1 vs 6.9 for grades I, II, and III, respectively, P = 0.05). Those consuming less vitamin C had increased ballooning degeneration (P = 0.05).
Children with NAFLD have a diet that is insufficient in vitamin E and this may contribute to the pathophysiology of NAFLD. In children with NAFLD, reported sugar-sweetened beverage consumption is low; however, uric acid, which may reflect total fructose consumption, was significantly associated with NASH and should be further evaluated.
*Pediatrics, Emory University, Atlanta, GA
†Epidemiology, Johns Hopkins University, Baltimore
‡NIDDK, National Institutes of Health, Bethesda, MD
§Pediatrics, Indiana University, Indianapolis, IN
||Pediatrics, University of Washington, Seattle, WA
¶Pediatrics, University of California, San Francisco
#Pediatrics, University of California, San Diego
**Pediatrics, Columbia University, New York, NY.
Address correspondence and reprint requests to Joel E. Lavine, MD, PhD, Morgan Stanley Children's Hospital of New York, Columbia University Medical Center, 3959 Broadway, CHN7-702, New York, NY 10032 (e-mail: email@example.com).
Received 31 January, 2011
Accepted 17 May, 2011
The NASH CRN is supported by the National Institute of Diabetes and Digestive Diseases (NIDDK) grants U01DK061732 (Case Western Reserve University), U01DK061713 (Duke University Medical Center), U01DK061737 (Indiana University), U01DK061718 (St Louis University), U01DK061734 (Columbia University), U01DK061738 (University of California, San Francisco), U01DK061728 (University of Washington), U01DK061731 (Virginia Commonwealth University), and U01DK061730 (Johns Hopkins University) and the National Institute of Child Health and Human Development (NICHD). Other grant support includes the following: National Institutes of Health General Clinical Research Centers or Clinical and Translational Science Awards: UL1RR024989, M01RR000750, RR02413101, M01RR000827, UL1RR02501401, M01RR000065, M01RR00188, M01RR020359. M.B. Vos is supported by NIH K23DK080953 and the Children's Digestive Health and Nutrition Foundation/Nestle Nutrition Award.
The authors report no conflicts of interest.