Relation between Obesity and Precocious Puberty a Biochemical and Radiological Test
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Background: Obesity has also increasingly been recognized as a key player in the determination of pubertal timing, and there is compelling evidence associating excess adiposity with precocious puberty, most famously in girls. Precocious puberty, i.e., development of secondary sexual characteristics at less than 8 years in girls, has been associated with endocrine dysregulation, in the form of elevated leptin, insulin resistance, and increased estrogen secretion, all contributing to premature activation of the hypothalamic-pituitary-gonadal (HPG) axis.
Objective: The current study is intended to investigate the correlation between obesity and precocious puberty in biochemical markers (LH, FSH, estradiol, insulin, and leptin) and radiological assessment (assessment of bone age) in 8-9-year-old girls.
Methods: A retrospective cross-sectional study was conducted in Al-Khansa Hospital, where subjects were separated into obese and non-obese categories. Blood analyses were conducted for hormonal markers, and X-ray imaging was utilized to assess bone age advancement. Statistical analysis was conducted to analyze the association between obesity and the development of early puberty.
Results: Results indicate a significant correlation between precocious puberty with obesity, and 70% of the participants were found to have elevated LH, FSH, and estradiol levels, which supported premature activation of the HPG axis. Similarly, 70% had elevated fasting insulin, and 60% had elevated leptin, indicating a metabolic-hormonal association with the premature development of puberty. Radiological findings supported advanced bone age in obese children, further strengthening the hypothesis of premature pubertal development.
Conclusion Early screening, hormonal evaluation, and lifestyle interventions are crucial for delaying puberty onset and reducing long-term health risks in obese children at risk of precocious puberty.
Al-Beltagi, M., Bediwy, A.S. and Saeed, N.K. (2022) ‘Insulin-resistance in paediatric age: Its magnitude and implications’, World journal of diabetes, 13(4), p. 282.
Aydin, B.K. et al. (2022a) ‘High levels of FSH before puberty are associated with increased risk of metabolic syndrome during pubertal transition’, Pediatric Obesity, 17(8), p. e12906.
Aydin, B.K. et al. (2022b) ‘High levels of FSH before puberty are associated with increased risk of metabolic syndrome during pubertal transition’, Pediatric Obesity, 17(8), p. e12906.
Calcaterra, V. et al. (2025) ‘Impact of Obesity on Pubertal Timing and Male Fertility’, Journal of Clinical Medicine, 14(3), p. 783.
Chen, M. and Eugster, E.A. (2015) ‘Central precocious puberty: update on diagnosis and treatment’, Pediatric Drugs, 17, pp. 273–281.
Haymond, M. et al. (2013) ‘Early recognition of growth abnormalities permitting early intervention’, Acta Paediatrica, 102(8), pp. 787–796.
Koysombat, K., Dhillo, W.S. and Abbara, A. (2023) ‘Assessing hypothalamic pituitary gonadal function in reproductive disorders.’, Clinical science (London, England : 1979), 137(11), pp. 863–879. Available at: https://doi.org/10.1042/CS20220146.
Li, W. et al. (2017) ‘Association between Obesity and Puberty Timing: A Systematic Review and Meta-Analysis.’, International journal of environmental research and public health, 14(10). Available at: https://doi.org/10.3390/ijerph14101266.
Marcovecchio, M.L. and Chiarelli, F. (2013) ‘Obesity and growth during childhood and puberty.’, World review of nutrition and dietetics, 106, pp. 135–141.
Rose-John, S. and Schooltink, H. (2007) ‘Cytokines are a therapeutic target for the prevention of inflammation-induced cancers’, Cancer Prevention, pp. 57–66.
Shi, L., Jiang, Z. and Zhang, L. (2022) ‘Childhood obesity and central precocious puberty’, Frontiers in endocrinology, 13, p. 1056871.
Teo, Y.H. et al. (2022) ‘Enhancing the MEP coordination process with BIM technology and management strategies’, Sensors, 22(13), p. 4936.
Viner, R.M. et al. (2017) ‘Puberty, developmental processes, and health interventions’, Disease Control Priorities, 8.
