LAUSR

The prevalence of childhood obesity has increased substantially over the past two decades with now approximately 18.5% of US youth between the ages of 2 and 19 years being classified as obese according the Centers for Disease Control. In addition, obesity has been shown in numerous studies to be associated with an early onset of puberty. The impact of adiposity on reproductive function has been long known. Dr. Rose Frisch in her manuscript in Science in 1974 demonstrated that a threshold of 17% body fat was required for menstruation in mature females. Adequate fat stores would indicate that sufficient food was available to provide support for a growing fetus as well as support health of the mother during pregnancy. Even before the earliest reports of the impact of body fat on menstruation, the association of obesity with early puberty have been investigated. Reports as early as 1970 demonstrated that menarche occurred earlier in obese girls as compared to their normal weight peers. In a combination of two larger studies, girls who matured early were more likely to be obese than those who matured later. Power and colleagues examined a British birth cohort finding a strong association between body mass index (BMI) and timing of puberty. These findings agree with more recent studies. Aris and colleagues examined the association of childhood BMI with pubertal timing in a cohort from the United States and Belarus and found a positive association between childhood BMI and advanced pubertal development. Lazzeri and colleagues in a nationally representative study of Italian youth found again that BMI was inversely associated with the age of menarche in females. Similarly in a Danish study of boys, testicular enlargement occurred significantly earlier in obese youth as compared to normal weight peers. From these studies and many more, it is evident that obesity confers an increased risk of early puberty in youth; however, whether such effect requires a chronic exposure to obesity throughout the preadolescent period is unclear. Specifically, if one is obese during childhood but regains normal adiposity prior to adolescence, is the timing of puberty now normal? Or, if the onset of obesity is delayed, are those individuals protected from early puberty? The study by Fan and colleagues in this issue begins to address these questions by the novel approach of evaluating pubertal timing as it relates to alterations in the BMI trajectory through childhood and early adolescence. The authors identified four patterns of BMI trajectories over time: normal BMI, rapid BMI growth, persistently overweight/obese, and early transient overweight/obese. The study defined these BMI trajectories using multiple statistical methods, which is a strength of this study. They found that obesity at any period was associated with a higher risk for early puberty as compared to peers with normal BMI throughout childhood; however, those who were persistently overweight carried the highest risk for early puberty. Also, 15% of the variance in timing for pubertal progression could be explained by a combined genetic score, sleep quality, and fat-free mass in the persistently overweight group. The body composition was measured by electrical impedance; while good for large population studies, it is not as sensitive as dual-energy X-ray absorptiometric measurements, which could be a limitation of these associations. As fat-free mass is the combination of lean mass and bone, the association of puberty progression with fat-free mass could also be a result of testosterone production, which was not assessed in the present study, as an anabolic hormone increasing lean mass. In addition, adipose tissue signaling modulating bone development may also play a role, but this did not appear to be included in the analysis. The authors found that girls who were consistently overweight/obese had the highest risk for early breast development; while girls that were transiently overweight/obese had the highest risk for early menarche. On examination of the BMI trajectories in these two groups, the girls who were transiently overweight had at least as high if not higher BMI than the girls in the consistently obese group at the earliest time point. One might assume from this that increased fat mass may be associated with early puberty specifically in the females; however, the authors did not appear to investigate this possible association in a sex-specific fashion. Males who had either a rapid rise BMI or were consistently overweight/obese were more likely to experience early testicular enlargement; however, the study was limited in that it used only participant recall for these findings rather than assessment by an experienced clinician. Their findings do suggest that the timing of the adiposity gain may exert differing effects on pubertal progression that may be tempered by sex. Studies of the impact of weight loss on pubertal progression have yielded differing results. Fan et al. found that, in females, those with a decline in BMI were at the highest risk for early menarche. However, Reinehr and colleagues found that a reduction in BMI standard deviation score (SDS) was associated with a decreased likelihood of puberty in girls but earlier onset of puberty in boys. While neither study investigates the mechanism by which weight loss might alter pubertal timing, Reinehr et al. postulated that the changes in weight would alter hormone levels. For example, weight loss could result in a decline in leptin reducing the signaling of pubertal onset and delaying puberty while an increase in weight may increase estrogen through