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Context Epidemiologic studies have demonstrated that overweight/obese girls (OW/OB) undergo thelarche and menarche earlier than normal weight girls (NW). There have been no longitudinal studies to specifically investigate how body weight/fat affects both clinical and biochemical pubertal markers in girls. Objective To investigate the effect of total body fat on reproductive hormones and on the maturation of estrogen-sensitive tissues during puberty in girls. Methods Ninety girls (36 OW/OB, 54 NW), aged 8.2 to 14.7 years, completed 2.8 ± 1.7 study visits over 4 years. Visits included dual-energy x-ray absorptiometry to calculate total body fat (TBF), Tanner staging, breast ultrasound for morphological staging (BMORPH; A-E), pelvic ultrasound, hormone tests, and assessment of menarchal status. The effect of TBF on pubertal markers was determined using a mixed, multistate, or Cox proportional hazards model, controlling for baseline BMORPH. Results NW were older than OW/OB (11.3 vs 10.2 years, P Conclusion In late puberty, girls with higher TBF demonstrate differences in standard hormonal and clinical markers of puberty. Investigation of the underlying causes and clinical consequences of these differences in girls with higher TBF deserves further study.

Background Girls who are overweight/obese (OB) develop breast tissue but do not undergo menarche (the first menstrual period) significantly earlier than girls of normal weight (NW). It has been proposed that estrogen synthesized by adipose tissue may be contributory, yet OB do not have higher serum estrogen levels than NW matched on breast stage. We hypothesized that estrogen synthesized locally, in mammary fat, may contribute to breast development. This hypothesis would predict that breast development would be more advanced than other estrogen-sensitive tissues as a function of obesity and body fat. Methods 80 pre-menarchal girls (26 OB, 54 NW), aged 8.2–14.7 yrs, underwent dual-energy x-ray absorptiometry to calculate percent body fat (%BF), Tanner staging of the breast, breast ultrasound for morphological staging, trans-abdominal pelvic ultrasound, hand x-ray (bone age), a blood test for reproductive hormones, and urine collection to determine the vaginal maturation index (VMI), an index of estrogen exposure in urogenital epithelial cells. Results When controlling for breast morphological stage determined by ultrasound, %BF was not associated with serum estrogen or gonadotropin (LH and FSH) levels or on indices of systemic estrogen action (uterine volume, endometrial thickness, bone age advancement, and VMI). Tanner breast stage did not correlate with breast morphological stage and led to misclassification of chest fatty tissue as breast tissue in some OB. Conclusions These studies do not support the hypothesis that estrogen derived from total body fat or local (mammary) fat contributes to breast development in overweight/obese girls.

Overweight/obese girls (OB) undergo thelarche but not menarche significantly earlier than normal weight girls (NW). It has been proposed that estrogen synthesized by adipose tissue may be contributory, yet OB do not have higher serum estrogen levels than NW matched on breast stage. We hypothesized that in OB, adipose tissue overlying the breast bud may be a ready source of estrogen that is sufficient to initiate thelarche because the primitive breast bud is intimately associated with the mammary fat pad during development (Anbazhagan Am J Anat ’91, Neville J Mammary Gland Biol Neoplasia ’98). Estrogen derived from mammary fat could act locally to induce thelarche but would not be detected in the circulation and therefore would not act systemically to induce uterine maturation/menses. To address this hypothesis, we measured reproductive hormones and imaged the breast, uterus, and ovaries in 80 pubertal, pre-menarchal girls (26 OB, 54 NW) aged 8.2-14.7 yrs. We used total percent body fat (%BF), determined by DXA, as a proxy for mammary fat, taking advantage of the positive correlation between these two measures (Novotny Am J Hum Biol ’11, Schautz Eur J Clin Nutr ’11, Zhu Eur Radiol ’16). We predicted that if estrogen derived from mammary fat contributes to breast maturation, then girls with higher %BF (and thus more mammary fat) would demonstrate immaturity of other estrogen-sensitive tissues (e.g. uterus, endometrial lining, vaginal epithelium) compared with girls of the same breast morphological stage (stages A-E based on Bruni et al. Adolesc Pediatr Gynecol ‘90) with lower %BF. OB were younger than NW (10.1 ± 1.1 vs. 11.3 ± 1.3 yrs, p