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World J Clin Pediatr. Dec 9, 2025; 14(4): 110357
Published online Dec 9, 2025. doi: 10.5409/wjcp.v14.i4.110357
Uncovering hidden vitamin D deficiency in overweight children
Chandra Sekhar Devulapalli
Chandra Sekhar Devulapalli, Pediatric Outpatient Clinic, Department of Medicine, Helgeland Hospital, Alstahaug (Sandnessjøen) NO-8800, Nordland, Norway
Author contributions: Devulapalli CS conceptualized the study; curated the data; conducted the formal analyses and investigation; developed the methodology; gathered the resources; supervised the project; contributed to the validation of results and data visualization; and wrote, review, and edited the manuscript.
Conflict-of-interest statement: The authors have no conflicts of interest to declare.
Open Access: This article is an open-access article that was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution NonCommercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: https://creativecommons.org/Licenses/by-nc/4.0/
Corresponding author: Chandra Sekhar Devulapalli, MD, PhD, Consultant, Senior Researcher, Senior Scientist, Pediatric Outpatient Clinic, Department of Medicine, Helgeland Hospital, Prestmarkveien 1, Alstahaug (Sandnessjøen) NO-8800, Nordland, Norway. chandev@gmail.com
Received: June 5, 2025
Revised: June 13, 2025
Accepted: August 22, 2025
Published online: December 9, 2025
Processing time: 148 Days and 15.5 Hours
Abstract

Vitamin D deficiency is disproportionately prevalent among overweight and obese children, with conventional explanations such as poor dietary intake or reduced sun exposure offering only partial insight. Emerging evidence reveals a multifactorial pathophysiology, including sequestration of vitamin D in adipose tissue, altered hepatic metabolism, diminished bioavailability, and inflammation-induced resistance at the tissue level. These mechanisms contribute to a functional deficiency, wherein serum 25-hydroxyvitamin D levels may remain suboptimal despite adequate intake or sun exposure. Obesity-related alterations in vitamin D-binding proteins, receptor expression, and pro-inflammatory signaling further compromise biological activity. Current diagnostic criteria and supplementation guidelines do not fully reflect these physiological complexities, leading to underdiagnosis and insufficient treatment. Personalized approaches-incorporating higher, body composition-adjusted dosing and consideration of inflammatory status-are emerging as promising strategies to restore sufficiency and improve metabolic outcomes. While preliminary evidence supports the safety and efficacy of high-dose supplementation in this population, pediatric-specific clinical trials are lacking. This review synthesizes current understanding of the pathophysiological mechanisms underlying vitamin D deficiency in pediatric obesity and emphasizes the need for individualized, evidence-based interventions to optimize vitamin D status and overall health.

Keywords: Vitamin D deficiency; Pediatric obesity; Adipose sequestration; 25-hydroxyvitamin D; Bioavailability; Vitamin D metabolism; High-dose supplementation

Core Tip: This review challenges the conventional understanding of vitamin D deficiency in children with obesity by proposing a mechanistic framework that integrates adipose tissue dynamics, hepatic metabolism, and inflammatory signaling. It emphasizes that vitamin D status is not solely determined by intake or sun exposure, but rather results from complex physiological interactions. By highlighting the limitations of current diagnostic thresholds and supplementation strategies, the study advocates for a paradigm shift toward individualized, mechanism-based treatment approaches-an essential step to bridge the gap between biochemical adequacy and functional sufficiency in this vulnerable population.