Background: Earlier pubertal timing has been observed in many countries. We aimed to explore if prenatal exposure to maternal obesity, smoking, and alcohol intake was associated with timing of puberty by use of a novel marker of pubertal timing: 'the height difference in standard deviations' (HD:SDS).
Methods: HD:SDS is the difference between pubertal height in standard deviations and adult height in standard deviations, and it correlates well with age at peak height velocity. Pubertal height was measured by health care professionals at approximately 13 years in boys and 11 years in girls, and the children's adult height was predicted from parental height reported by the mothers during pregnancy. Information on HD:SDS was available for 42,849 of 56,641 eligible boys and girls from the Danish National Birth Cohort born 2000-2003. In a subsample, HD:SDS was validated against age at the following self-reported pubertal milestones: Tanner stages, menarche, first ejaculation, voice break, acne, and axillary hair. Prenatal exposures were reported by mothers during pregnancy.
Results: HD:SDS correlated moderately with the pubertal milestones considered (correlation coefficients: - 0.20 to - 0.53). With normal weight (body mass index (BMI): 18.5-24.9 kg/m) as the reference, maternal pre-pregnancy obesity (BMI: 30.0+ kg/m) was associated with earlier pubertal timing: 0.23 (95% confidence interval (CI): 0.18, 0.28) higher HD:SDS in boys and 0.19 (95% CI, 0.14, 0.24) higher HD:SDS in girls. Maternal smoking was not associated with pubertal timing. Compared to alcohol abstainers, maternal intake of > 3 units of alcohol weekly was associated with later puberty in boys only: 0.14 (95% CI, 0.05, 0.24) lower HD:SDS.
Conclusion: As correlations between HD:SDS and the considered pubertal milestones were comparable to those reported in the literature between age a peak height velocity and the considered pubertal milestones, the validity of HD:SDS seems acceptable. Maternal pre-pregnancy obesity was associated with earlier pubertal timing in both sexes, and maternal alcohol intake during pregnancy was associated with later pubertal timing in boys. Maternal smoking has been linked to earlier timing of puberty, but this was not replicated in our setting using HD:SDS as a marker of pubertal timing.
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http://dx.doi.org/10.1186/s12887-019-1715-0 | DOI Listing |
J Pediatr Endocrinol Metab
January 2025
Department of Pediatric Endocrinology, Kocaeli City Hospital, Kocaeli, Türkiye.
Objectives: This study aimed to identify clinical features of girls referred to a pediatric endocrinology clinic for suspected precocious puberty, differentiate true precocious puberty from other variants, evaluate treatment status, and identify distinguishing factors between patient groups.
Methods: We retrospectively evaluated the records of 275 consecutive girls aged 0-10 years referred for suspected precocious puberty.
Results: Among the patients, 30 (10.
HRB Open Res
January 2025
Department of Biobehavioral Health, The Pennsylvania State University - University Park Campus, University Park, Pennsylvania, PA 16802, USA.
Background: Puberty has been historically considered as a time of risk and vulnerability for young people. It is associated with rapid development in the hypothalamus, which is central in the production of both stress and sex steroids. While patterns of stress reactivity are calibrated in early life, this time of rapid development may provide a means for these patterns to change.
View Article and Find Full Text PDFArch Dis Child
January 2025
Pediatrics, Erasmus MC, Rotterdam, Netherlands
Objective: Impaired fetal and infant growth may cause alterations in developmental programming of the hypothalamic-pituitary-gonadal axis and subsequently pubertal development. We aimed to assess associations between fetal and infant growth and pubertal development.
Design: Population-based prospective birth cohort.
Children (Basel)
January 2025
Department of Pediatrics, Division of Pediatric Endocrinology, Demiroğlu Bilim University, 34394 Istanbul, Türkiye.
This review examines the inconsistent effects of endocrine-disrupting chemicals (EDCs) and pollutants on pubertal timing, emphasizing the methodological challenges contributing to variability in findings. Data from nine key studies reveal that chemicals such as BPA, phthalates, and PFAS impact pubertal onset differently based on exposure timing, dosage, and sex. For instance, BPA is linked to earlier puberty in girls but delayed onset in boys, while other EDCs show mixed effects across populations.
View Article and Find Full Text PDFRes Child Adolesc Psychopathol
January 2025
Department of Psychology, University of Illinois at Urbana-Champaign, Champaign, IL, USA.
Developmental changes in youth sleep preferences (chronotype) and pubertal development are consequential for youth risk for depression. Previous research has identified individual differences in chronotype in risk for psychopathology. However, little is known regarding how the timing of chronotype may confer risk in youth.
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