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Association between vitamin D and central precocious puberty in children: Threshold effects and mediation mechanisms
1Department of Clinical Laboratory, Renmin Hospital, Wuhan University, Wuhan, 430060, Hubei Province, P. R. China. lejuan0323@whu.edu.cn.
Insights
Lower vitamin D levels are linked to central precocious puberty (CPP) in children, with higher thresholds needed for protection in girls. Bone age acceleration and gonadotropin activation are key mediators in females, suggesting sex-specific supplementation.
Area of Science:
- Pediatric Endocrinology
- Nutritional Science
- Biostatistics
Background:
- Central precocious puberty (CPP) involves early onset of puberty, with potential links to environmental factors like vitamin D.
- Serum 25-hydroxyvitamin D (25(OH)D) is a key indicator of vitamin D status.
- Understanding sex-specific associations and mediation pathways is crucial for effective prevention and treatment strategies.
Purpose of the Study:
- To investigate the association between serum 25(OH)D levels and CPP in children.
- To analyze sex-specific threshold effects of 25(OH)D on CPP risk.
- To identify mediation pathways, including bone age acceleration and gonadotropin activation, linking 25(OH)D to CPP.
Main Methods:
- Cross-sectional study of 494 CPP patients and 2,259 controls.
- Quantification of serum 25(OH)D using liquid chromatography-tandem mass spectrometry (LC-MS/MS).
- Bone age assessment (Tanner-Whitehouse 3) and hormonal profiling.
- Restricted cubic splines (RCS) for dose-response analysis.
- Causal mediation analysis using structural equation models.
Main Results:
- CPP patients had significantly lower 25(OH)D levels and higher deficiency rates compared to controls, with sex-specific differences.
- RCS analysis identified inverse 25(OH)D-CPP associations with thresholds at 35.4 ng/mL (females) and 19.5 ng/mL (males).
- Lower 25(OH)D levels were associated with increased risk of advanced pubic hair maturation and CPP, particularly in vitamin D-insufficient/deficient individuals.
- Mediation analysis in females revealed bone age acceleration (64.6%) and gonadotropin activation (14.6%) as dominant pathways.
Conclusions:
- Vitamin D status shows sex-dimorphic associations with CPP risk, necessitating higher protective levels in females.
- Bone age acceleration and gonadotropin activation are primary mediators of CPP risk in females.
- Findings support the need for sex-specific vitamin D supplementation strategies for CPP prevention.
Purpose:
To investigate the association between serum 25-hydroxyvitamin D [25(OH)D] levels and central precocious puberty (CPP) in children, with emphasis on sex-specific threshold effects and mediation pathways.
Methods:
This cross-sectional study enrolled 494 CPP patients (female: 413; male: 81) and 2,259 age-matched healthy controls who underwent liquid chromatography-tandem mass spectrometry (LC-MS/MS) based 25(OH)D quantification, Tanner-Whitehouse 3 bone age assessment, and hormonal profiling. Dose-response relationships were analyzed via restricted cubic splines (RCS), and causal mediation analysis with 1,000 bootstrap resamples were quantified using structural equation models.
Results:
CPP patients exhibited significantly lower 25(OH)D levels than controls (median (IQR): females, 20.00 (14.00-24.20) vs. 23.40 (18.10-29.22) ng/mL, P < 0.001; males, 21.60 (16.00-27.10) vs. 23.30 (18.30-28.83) ng/mL, P = 0.033), with higher deficiency rates (females: 49.6% vs. 33.0%; males: 43.2% vs. 32.8%). RCS analysis revealed inverse 25(OH)D-CPP associations, with threshold concentrations at 35.4 ng/mL (females) and 19.5 ng/mL (males). Each 1 ng/mL increment in serum 25(OH)D was associated with 3.6% reduced risk of advanced pubic hair maturation (adjusted OR = 0.964, P = 0.009). Sex-stratified logistic regression showed elevated CPP risks in vitamin D-insufficient/deficient groups versus sufficient counterparts: females (OR = 2.13, P = 0.037; OR = 2.26, P = 0.030) and males (OR = 3.89, P = 0.059; OR = 4.71, P = 0.034). Mediation analysis identified bone age acceleration (64.6% mediation) and gonadotropin activation (14.6%) dominated pathways in females.
Conclusion:
Vitamin D demonstrated sex-dimorphic associations with CPP risk, requiring higher protective thresholds in females. Bone age acceleration and gonadotropin activation emerged as primary mediators in females. These findings advocated sex-specific vitamin D supplementation strategies for CPP prevention.
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