The role of high BMI from infancy forward on clinician-rated pubertal timing in a large US sample.

Sadikova, Ekaterina; Deardorff, Julianna; Aris, Izzuddin M; Diemer, Elizabeth; Aghaee, Sara; Tiemeier, Henning; Kubo, Ai · J Clin Endocrinol Metab · 2026

retrospective_cohort · Level III

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Abstract

High childhood adiposity accelerates pubertal timing, particularly in females. However, it is unclear when in childhood intervention is most important. To disentangle the associations of body mass index (BMI) during infancy, early, mid-, and late childhood with pubertal timing. We studied 132,452 (46.6% female) full-term singletons born in Kaiser Permanente Northern California affiliated facilities between 01/01/2003 and 12/31/2011. A mediation analysis was used to disentangle how BMI during infancy (<2 years), early (2-<5 years), mid- (5-<9 years) and late (9+ years) childhood is associated with clinician-assessed Sexual Maturity Ratings (SMRs) for pubarche, thelarche, and gonadarche. Controlled direct effects isolated the impact of high BMI in earlier childhood periods only, while total effects included accumulating impact through subsequently high BMI. Risks for outcome onset (SMR≥2) were assessed for BMI 1 and 2 standard deviations above the population mean (+1SD and +2SD), respectively. Pubertal timing was not meaningfully associated with high BMI in infancy and early childhood (risk differences <0.001 to 0.007). High BMI in mid- and late childhood was associated with earlier pubertal onset, particularly in females. At median onset age, controlled direct effect risk differences for mid-childhood BMI +2SD ranged from 0.015, 95%CI (0.013,0.017) for male pubarche to 0.112, 95%CI (0.103,0.121) for female thelarche. Mid-childhood total effects exceeded controlled direct effects, indicating accumulation of impact due to persistence of high BMI into late childhood. Preventing high BMI in mid- and late childhood, but not in the first 4 years of life, may decelerate pubertal onset.