Electroencephalography-Guided Anesthetic Administration and Postoperative Delirium.

Abstract

In Reply Messrs Tang and Gao raise 2 questions regarding our study of dietary sugar in pediatric nonalcoholic fatty liver disease.1 They suggest that the effect observed in our trial may have been solely a function of weight loss. The study was not designed to promote weight loss; participants ate without calorie or macronutrient restriction. In support of the argument for a weight loss effect, Tang and Gao reference practice guidelines that were written primarily for adults with nonalcoholic fatty liver disease and recommend weight loss of 5% to 10% of body weight.2 However, rather than focusing on weight loss, pediatric guidelines focus on lifestyle modifications to improve dietary quality.3 We did observe an incidental weight loss of 1.6% in the intervention group, which is well below the level thought to produce a meaningful change in hepatic fat content in patients with nonalcoholic fatty liver disease. Notably, the correlation between change in weight and change in hepatic steatosis measured by magnetic resonance imaging was moderate (r= 0.42; 95% CI, 0.12-0.65), and when controlling for weight change, the between-group difference for change in hepatic steatosis was only slightly attenuated. Thus, the small weight loss observed is unlikely to be the sole explanation for the significant change in hepatic fat and liver enzymes. Tang and Gao also question whether the outcome could be the result of other differences in the diets of the 2 groups, such as protein, energy, or nutrients. Although weight loss suggests a decrease in caloric intake, in contrast, the intervention group reported increased calories and the usual diet group reported decreased total energy intake compared with baseline. In the intervention group, changes to macronutrient composition were small and an expected result of sugar reduction. We acknowledge the complexity of modifying the target element in an individual’s diet without modifying nontarget components. Clinical trials focused on the role of dietary sugar in the treatment of nonalcoholic fatty liver disease are of clinical importance. The most common recommendation made by pediatric gastroenterologists in the United States is to decrease sugar consumption.4 We demonstrated that reducing free sugar intake to less than 3% of total daily calories was associated with a 30% reduction in hepatic fat content and a 40% reduction in alanine aminotransferase. As opposed to long-term caloric deficits, avoidance of free sugars is a viable long-term strategy, particularly for children. Sugars may influence nonalcoholic fatty liver disease via direct or indirect mechanisms. To disentangle the relative contribution of these mechanisms would require studies designed with that specific objective.