1. In this randomized controlled trial, a low free sugar diet resulted in reduced hepatic steatosis compared to a usual diet in adolescents males with Non-Alcoholic Fatty Liver Disease (NAFLD)
2. A low free sugar diet led to greater reduction in alanine aminotransferase, aspartate aminotransferase, and gamma-glutamyl transpeptidase levels.
Evidence Rating Level: 1 (Excellent)
Study Rundown: The prevalence of Non-Alcoholic Fatty Liver Disease (NAFLD) has increased among children, becoming one of the most common diseases in this population. While pediatric guidelines recommend lifestyle modification and exercise, there is no specific diet recommended. In this randomized controlled trial of adolescent boys with NAFLD, a low free sugar diet led to greater improvements in hepatic steatosis at 8 weeks compared to diet as usual. In addition, alanine aminotransferase, aspartate aminotransferase, and gamma-glutamyl transpeptidase levels were also reduced by a low free sugar diet.
While this study shows promising results for sugar restriction as treatment in adolescent NAFLD, the study has several limitations, including a small number of participants. Demographically, the study results are difficult to generalize due to exclusion of girls and a largely homogeneous Hispanic population. In addition, calorie-intake was lower in the low free sugar group, confounding whether sugar or calorie restriction was the main driver of results. Finally, it is unclear how the pathological and clinical endpoints in this study relate to morbidity and mortality.
In-Depth [randomized controlled trial]: 40 adolescent males aged 11 to 16 years old with a clinical-pathological diagnosis of NAFLD and evidence of active disease determined by MRI Proton Density Fat Fraction (PDFF) measurement of 10% or greater and ALT levels of over 45U/L were enrolled at 2 US academic centers. The low free sugar diet was set at a free sugar intake of less than 3% of daily calories for the intervention group with the control group eating a diet as usual. Study visits were conducted at baseline and at 4 and 8 weeks. The primary outcome was the change in percentage of hepatic steatosis as defined by MRI-PDFF at 8 weeks. Secondary outcomes included levels of alanine aminotransferase, aspartate aminotransferase, γ-glutamyl transpeptidase, fasting glucose, insulin, total cholesterol, low-density lipoprotein cholesterol, high-density lipoprotein cholesterol, and triglycerides. The mean decrease in hepatic steatosis from baseline to week 8 was greater for the intervention group (25% to 17%) compared with the control group (21% to 20%) and the adjusted week 8 mean difference was -6.23% (CI95 -9.45% to -3.02%). In addition, alanine aminotransferase, aspartate aminotransferase , gamma-glutamyl transpeptidase, and mean cholesterol levels were also reduced by a low free sugar diet (p < 0.05). No significant differences between groups were detected for insulin levels, homeostasis model assessment for insulin resistance, triglycerides, low-density lipoprotein cholesterol, high-density lipoprotein cholesterol, nor sweetness perception (p > 0.05). A low free sugar diet led to greater weight reduction than diet as usual (difference -2.00 kg; CI95 -3.30 to -0.79 kg).
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