4. Discussion
glucose tolerance, cardiometabolic disease, sugar reduction, cardiometabolic, chronic disease
DISEASE, SECONDARY, TYPE 2 DIABETES, INSULIN SENSITIVITY, CHRONIC DISEASE
A dietitian-led intervention with the goal of reducing free sugar intake to Given that we saw sugar reductions in both our intervention and control groups, we also conducted an exploratory analysis that more specifically looked at the impact of sugar reduction on our outcomes of interest by comparing participants with and without total sugar reduction, independent of randomization. Our exploratory results indicate that reducing sugar intake as an intervention strategy may still hold promise for improving cardiometabolic health for at-risk Latino youth. Specifically, we found that participants who successfully reduced their sugar intake saw improvements in their oral-DI as compared to participants who did not reduce their sugar intake, indicating that they had improvements in their beta-cell function. Specifically, those with sugar reduction improved their oral-DI by 23% as compared to only a 9% improvement in those without sugar reduction. Oral-DI is a sensitive measure of the beta-cell function that measures beta-cell output while adjusting for insulin sensitivity. Oral-DI is a significant biomarker of disease risk and has been indicated to be more important in predicting the future development of type 2 diabetes as compared to fasting and 2-h glucose levels [In addition to our findings relevant for the risk of type 2 diabetes, our exploratory analysis revealed that participants without sugar reduction had some differences in fasting serum lipids and inflammatory markers as compared to those with sugar reduction. Specifically, we report that those without sugar reduction had a 6.5% increase in triglycerides. This outcome aligns with previous pediatric cohort studies which found that increased sugar intake is positively associated with triglycerides [There is one key factor which likely explains the difference in outcomes reported between our primary and exploratory results. As mentioned above, the difference in total sugar intake between the intervention and control groups after 12-weeks was significant but was relatively small at 3% of total calories, and we observed participants with sugar reduction in both groups. In contrast, in the exploratory analysis, the difference in total sugar intake between those who reduced their total sugar intake compared to those who did not was approximately 7% of total calories. Therefore, we conclude that the benefits of a real-world dietary intervention focused on sugar reduction, where participants met with a registered dietitian monthly and receive deliveries of bottled water, does not confer additional improvements in cardiometabolic risk factors compared to participants receiving general diet advice. However, our exploratory results confirm our hypothesis that sugar reduction in at-risk Latino adolescents results in improvements in biomarkers of cardiometabolic risk; specifically, beta-cell function, fasting serum lipids, and the inflammatory marker TNF-While we did report some findings from our exploratory analysis, many of the hypothesized changes in cardiometabolic risk factors for glucose tolerance and its determinants, serum lipids, blood pressure, and inflammatory markers were not statistically significant with non-clinically meaningful effect sizes. There are a few potential explanations for these null findings. One is that while there was a 7% difference in sugar intake as a percentage of total calories in our exploratory analysis, this difference may have still been too small to result in hypothesized shifts in these biomarkers. Additionally, while our population was overweight, they may have been too metabolically healthy at baseline to observe statistically significant improvements in some of our outcomes of interest. Further, our study was originally powered based on the study’s primary aim of liver fat, so we may have been underpowered to detect significant changes in some of our secondary and exploratory outcomes of interest. Finally, the study was not blinded, so it may be that participants in the intervention group inaccurately reported their sugar intake to be less than their actual intake, which would have biased results toward the null.Our study has some important strengths which increase our confidence in our results. First, it assessed glucose tolerance through dynamic testing. Second, we had good participant compliance, with 81.6% of intervention participants reducing their free sugar intake and 71.4% meeting the goal of a free sugar intake maximum of 10% of total calories. In addition, we controlled for changes in fat mass statistically, which provided us with greater certainty that any observed outcomes were due to dietary changes and not changes in body weight or composition. Some limitations of this study include that approximately 35% of participants included in this analysis already met the intervention free sugar intake target of ≤10% of total calories prior to study enrollment. While this decreased our ability to ascertain whether reducing sugar intake through our intervention effects our outcomes of interest, our study still provides key insight into the impact of sugar reduction on our outcomes of interest through our exploratory analysis. Also, given our 12-week study period, we are unable to capture the impact of long-term sustained sugar reduction beyond 3-months. While our study had generally good compliance, following and sustaining a low sugar diet is challenging especially in pediatric populations [In conclusion, our results help fill a critical gap in the literature by further exploring the effects of sugar reduction interventions to improve biomarkers of cardiometabolic disease risk in pediatric populations. Our outcomes indicate that dietary sugar reduction interventions have the potential to reduce the risk of chronic disease development through improvements in beta-cell function, fasting serum triglycerides, and inflammatory markers such as TNF-