Association between childhood weight status and timing of puberty: a systematic review and meta-analysis

Childhood overweight and obesity have increased worldwide alongside a trend toward earlier pubertal onset, particularly in girls. Excess adiposity may affect pubertal timing through metabolic and endocrine pathways, but observational findings remain heterogeneous. This study systematically evaluated childhood weight status and pubertal timing, mapped the evidence, quantified early-puberty risk associated with overweight/obesity, and explored dose-response relationships and sex differences.

We systematically searched PubMed/MEDLINE, Embase, Web of Science, China National Knowledge Infrastructure (CNKI), and Wanfang databases from inception to January 2025. Observational studies using childhood weight/body mass index (BMI) as exposure variables and pubertal development indicators as outcomes were included. Two researchers independently screened literature, extracted data, and assessed study quality. The Newcastle-Ottawa Scale was used to evaluate risk of bias. Effect sizes were pooled using the DerSimonian-Laird random-effects model, with heterogeneity assessed via the I² statistic. Subgroup analyses were conducted by weight category and outcome type. An evidence map was constructed to describe the distribution and direction of evidence across different exposure and outcome types.

Forty-one studies were included in the systematic review, involving a total sample size of 416,789 participants. Studies were published between 2000 and 2025 and originated from 18 countries/regions. The evidence map indicated that quantifiable evidence primarily focused on BMI/weight classification and weight trajectory in relation to outcomes such as "onset/precipitation of puberty (including precocious puberty risk)" and "menarche/spermatogenesis onset time". Studies examining outcomes such as pubertal progression/duration and bone age were relatively scarce. From studies with consistent exposure grouping and extractable odds ratio (OR)/hazard ratio (HR)/relative risk (RR) and 95% confidence interval (CI), 24 effect size data points (from 3 studies) were extracted for meta-analysis. The random-effects model revealed that compared with normal-weight children, overweight/obese children had a significantly increased risk of early puberty onset (pooled OR/HR =1.56, 95% CI: 1.44-1.69, P<0.001; I²=96.0%). Subgroup analysis demonstrated a clear dose-response relationship: Overweight (OR/HR =1.46, 95% CI: 1.31-1.63), obesity (OR/HR =1.55, 95% CI: 1.36-1.77), and severe obesity (OR/HR =1.69, 95% CI: 1.37-2.07). Analysis by outcome type revealed the greatest impact on menarche timing (OR/HR =2.24, 95% CI: 1.82-2.75), followed by Tanner stage (OR/HR =2.06), breast development (OR/HR =1.47), pubic hair development (OR/HR =1.47), and testicular development (OR/HR =1.22).

Childhood overweight/obesity is significantly associated with increased risk of early puberty onset, exhibiting a dose-response relationship. Female pubertal markers, particularly menarche, exhibited greater sensitivity to weight status. These findings underscore the importance of childhood weight management in promoting normal pubertal development. Future studies should adopt standardized definitions of exposure and outcomes to enhance the comparability of evidence.