Obesity and the pubertal transition in girls and boys

Abstract

Childhood obesity has become a major health concern in recent decades, especially with regard to metabolic abnormalities that impart a high risk for future cardiovascular disease. Recent data suggest that excess adiposity during childhood may influence pubertal development as well. In particular, excess adiposity during childhood may advance puberty in girls and delay puberty in boys. Obesity in peripubertal girls may also be associated with hyperandrogenemia and a high risk of adolescent polycystic ovary syndrome. How obesity may perturb various hormonal aspects of pubertal development remains unclear, but potential mechanisms are discussed herein. Insulin resistance and compensatory hyperinsulinemia may represent a common thread contributing to many of the pubertal changes reported to occur with childhood obesity. Our understanding of obesity's impact on pubertal development is in its infancy, and more research into pathophysiological mechanisms and longer-term sequelae is important.

Figure 1

Simplified schematic diagram of potential mechanisms by which increased adiposity could lead to early thelarche in girls. For the sake of clarity, separate diagrams highlight gonadotropin-independent (A) and gonadotropin-dependent (B) mechanisms. However, gonadotropin-independent and gonadotropin-dependent mechanisms may be involved concurrently.

Figure 2

Total testosterone, SHBG, and free testosterone concentrations in obese (BMI-for-age percentile ≥ 95; solid squares) and normal-weight girls (BMI-for-age percentile < 85; open squares) grouped by Tanner stage. Data are shown as mean ± SEM. Differences were assessed with Wilcoxon rank sum tests: *, P < 0.05; **, P ≤ 0.01; ***, P ≤ 0.001; ****, P ≤ 0.0001 before Bonferroni correction. Conversion from conventional to SI units: total testosterone × 3.47 (nanomoles per liter). Data from McCartney et al. 2007(used with permission).