Continuous glucose monitoring as a growth-preserving strategy: Glycemic stability and GH–IGF-1 axis recovery in pediatric diabetes

Background: In pediatric type 1 diabetes (T1D), chronic dysglycemia disrupts hepatic GH receptor signaling and reduces IGF-1, impairing growth velocity and height SDS. Continuous glucose monitoring (CGM) and advanced hybrid closed-loop (AHCL) systems improve time-in-range (TIR) and reduce glycemic variability (GV), changes that may restore GH–IGF-1 physiology and preserve linear growth.

Objectives: To synthesize clinical and mechanistic evidence on the impact of CGM/AHCL on auxologic outcomes and the GH–IGF-1 axis in youth with diabetes, and to identify scenarios where early CGM adoption offers maximal growth preservation.

Methods: We reviewed randomized and observational pediatric studies reporting growth velocity, height SDS, IGF-1, or related endocrine measures alongside CGM metrics (HbA1c, TIR, GV). Risk of bias was assessed using RoB-2 (trials) and ROBINS-I (observational). Certainty of evidence was appraised with GRADE. Given heterogeneity of outcomes and follow-up, synthesis was narrative.

Results: Thirty-five studies met inclusion criteria: four pediatric AHCL randomized trials and 31 observational studies. Trials consistently demonstrated improved glycemia (HbA1c ↓ ~0.4–1.0%; TIR ↑ ~10–20%; GV ↓) with objective sensor-based endpoints. Although growth was not a prespecified endpoint in the trials, multiple cohorts linked higher TIR and lower GV with higher IGF-1 and more favorable growth velocity or stabilized height SDS, especially across puberty. Mechanistic data show rapid IGF-1 increases following metabolic stabilization, supporting reversal of functional GH resistance. Cross-sectional and longitudinal cohorts in the modern CGM era generally report near-normal mean height SDS, with subtle suppression concentrated among children with higher GV; this contrasts with the pre-CGM era, where conventional therapy was associated with delayed puberty and lower final height relative to target height. Nocturnal hypoglycemia fell and DKA did not increase in AHCL trials. By GRADE, certainty is high for glycemic outcomes, moderate for IGF-1 recovery, and low for definitive growth effects due to indirectness and confounding in observational designs.

Conclusions: CGM/AHCL reliably improves pediatric glycemia and is associated with IGF-1 recovery and stabilization of auxologic trajectories, particularly during puberty. While definitive growth effects require trials with prespecified auxologic endpoints, current evidence supports integrating structured growth surveillance with CGM metrics and adopting CGM early to optimize endocrine and growth outcomes in youth with diabetes.