Hassan, Doha

Objective: To examine changes in weight status after initiating zonisamide in children with epilepsy and elevated body mass index (BMI). Study Design: Retrospective chart review of children aged 2 to ≤18 years with epilepsy treated with zonisamide, assessing BMI changes over 2 years. Results: A total of 140 children were included; mean age (SD) at initiation was 9.60 years (3.93). BMI categories included 28 children with severe obesity, 28 with mild–moderate obesity, 28 with overweight, and 56 with healthy weight. Participants were 56.6% female, 91.4% non-Hispanic/Latino, and 88.6% White. At 2 years, BMI z score decreased significantly across all BMI groups: severe obesity −0.38 ( N = 13, 95% CI −0.64 to −0.13; p = 0.003), mild-moderate obesity −0.39 ( N = 15, 95% CI −0.62 to −0.16; p = 0.001), overweight −0.60 ( N = 14, 95% CI −0.84 to −0.36; p < 0.001), and healthy weight −0.46 ( N = 21, 95% CI −0.63 to −0.28; p < 0.001). Significant BMI z score reductions were also observed across age groups: 2–10 years −0.48 ( N = 40, 95% CI −0.62 to −0.34), >10–13 years −0.27 ( N = 15, 95% CI −0.50 to −0.04), and ≥13 years −0.63 ( N = 12, 95% CI 0.89 to −0.36). Conclusions: BMI reduction persisted up to 2 years following zonisamide initiation in children with epilepsy. Further prospective studies are needed to evaluate the weight loss effect and safety of zonisamide in children with epilepsy and elevated BMI.

Pediatric obesity represents an urgent public health concern, with rapidly increasing prevalence across all regions. While genetic susceptibility contributes significantly to interindividual variability in weight, the significant increase in obesity prevalence over the last 30 years is driven by shifts in environmental contributors. This narrative review will summarize evidence on the major environmental determinants of childhood obesity. Environmental contributors to obesity include the food environment, physical activity and built environments, socioeconomic and community context, home and family environments, digital exposures, early life and chemical obesogens and policy drivers. These environmental factors influence activity patterns, dietary habits, sleep, and stress. Additionally, many of these contributing factors cluster within communities that are disadvantaged, thereby increasing predisposition of specific racial, ethnic and socioeconomic groups to childhood obesity. We highlight research gaps and opportunities for multisectoral interventions aligned to impact the growing prevalence of childhood obesity.

ABSTRACT Objectives To evaluate the impact of semaglutide on body mass index (BMI) and cardiometabolic markers in adolescents with obesity and genetic variants associated with monogenic or syndromic obesity. Methods A retrospective chart review was conducted in adolescents with severe obesity who underwent multigene panel testing and were treated with semaglutide. Results Twenty‐seven adolescents (mean age 15 ± 1.9 years); BMI % of the 95th percentile 158 ± 29; (70% White) were treated with semaglutide for a mean of 10 ± 4.7 months. Participants were classified into three groups: (1) Dominant or Known Risk Variants ( n = 7); (2) Carriers of Rare Variants in Recessive Genes ( n = 10); and (3) Negative or Unmatched Genetic Findings ( n = 10). All groups showed reductions in BMI, which was not different between the groups. Adolescents with dominant or known risk variants experienced a significant decrease in BMI % of the 95th percentile (−17, (IQR −26 to −10) p = 0.022) and in BMI by −9.4% ± 7% ( p = 0.035). Significant improvements in median non‐HDL cholesterol (−16 mg/dL), total cholesterol (−15 mg/dL), and HbA1c (−0.3%) were noted in children with dominant or known risk variants ( p = 0.036). Conclusions Semaglutide was associated with significant reductions in BMI and cardiometabolic markers in adolescents (majority White) with dominant or known risk variants for monogenic obesity.