Using a longitudinal sample of girls followed from the ages of 5 to 9, results from this study illustrate that girls with higher weight status preceding puberty were at greater risk of earlier onset of puberty at 9 years. Specifically, girls with higher percent body fat at 5 years, and girls with higher percent body fat, higher BMI percentile, or larger waist circumference at 7 years were more likely to show more advanced pubertal development at 9 years. In addition, girls who showed greater increases in percent body fat from 5 to 9 years, or greater increases in waist circumference from 7 to 9 years, were more likely to experience earlier pubertal development at 9 years. Although earlier developers also exhibited accelerated growth from the ages of 5 to 9, results for weight status were still present after controlling for accelerated growth. The key contributions of this study are that it convincingly shows that weight status temporally precedes pubertal timing in a sample of white girls and that the association between weight status and pubertal timing is evident across multiple measures of weight status and pubertal timing.
Approximately 56% of girls in this study had begun breast development by 9 years. This figure differs somewhat from that reported by Herman-Giddens et al6
in which 32% of 9-year-old white girls had begun breast development. The discrepancy in these figures cannot be attributed to a lack of breast palpation in the current study because neither study used palpation to determine breast development. It is possible that the earlier onset of breast development in this sample is due to the high rate of overweight among the girls. Specifically, 30% of girls in this study were overweight at 9 years. However, this possibility is only speculative, as Herman-Giddens et al6
did not report the prevalence of overweight in their sample. Although the validity of visually assessing breast development is questionable, similar results were identified across all 3 measures of puberty. That is, no meaningful differences in the results were found when the 3 measures were combined to define earlier and later puberty, when only breast development was used to a make a similar classification, and when each measure was assessed individually as a continuous variable. Consequently, results from this study are generalizable across methods and are applicable to both clinical and academic settings, which generally have access to different resources to measure pubertal development.
There are at least 4 mechanisms that may explain the relationship between weight status during early and middle childhood and earlier onset of puberty among girls. First, a third parameter such as genetic influences may explain both early obesity and early onset of puberty. Obesity is known to have a genetic component.31
Obese mothers may have also had earlier onset of puberty, a trait that is passed on to their daughters. In this study, however, no differences were found in mothers’ age at menarche for girls with earlier and later puberty. Second, it is possible that both greater stores of body fat and earlier timing of puberty reflect a process of accelerated growth beginning early in development (ie, before 5 years). In this study, girls who experienced earlier puberty were taller at 5 years and showed acceleration in growth leading up to pubertal onset. However, results for each measure of weight status were still significant or marginally significant once height was taken into consideration. A third possibility is that excess estrogen produced by greater body fat may be a trigger for earlier onset of puberty. Research suggests that the central accumulation of body fat has an especially strong influence on levels of estradiol among pubertal-aged girls32
and may hasten the onset of puberty beyond that due to total body fat.23
This is consistent with our finding that waist circumference and change in waist circumference were positively associated with pubertal timing. Finally, obesity is associated with higher concentrations of leptin, which may have a permissive33,34
(ie, facilitative) or a direct18,35
effect on the onset of puberty in girls. Leptin is released from the adipocytes and may act as a metabolic signal to the hypothalamic pituitary gonadal axis for increased production of sex steroids.36
Although the genetic predisposition for earlier puberty can be ruled out as an explanation for findings in this study, additional longitudinal research is needed to disentangle the contributions of accelerated growth, estrogen, and leptin in explaining the association between body fat (including total body fat and body fat distribution) and change in body fat across middle childhood and earlier onset of puberty among white girls at 9 years. Ideally, such a study would begin at birth, would continue through to mid or late adolescence, and would incorporate repeated assessment of height, weight, body fat, body fat distribution, estrogen, leptin, and pubertal development. Additional research is also needed to determine if higher levels of body fat precede pubertal onset in girls from different racial and ethnic groups and whether differences in fat levels during early childhood can help to explain earlier onset of puberty in African American girls in comparison to white girls.6,12,13
Overweight and early timing of puberty among girls have both been linked to negative health and psychological outcomes. Overweight and obesity increase the risk of cardiovascular disease, diabetes, and cancer and psychosocial outcomes such as depression and low self-esteem.37
The finding that overweight is causally implicated in the onset of earlier pubertal development suggests that being overweight during middle childhood may also place girls at increased risk for negative outcomes associated with early puberty such as higher rates of delinquent behaviors,38,39
greater risk of reproductive cancers,40
and a greater likelihood of elevated weight status during adulthood.41
In the case of weight status during adulthood, the present research calls into question whether or not early puberty per se, or weight status preceding puberty, is a risk factor for overweight during adulthood and indicates a need for additional longitudinal studies to separate the influence of each factor in explaining obesity among adults. The practical implications of these findings emphasize the need for the implementation of early prevention and treatment programs for childhood overweight, beginning as early as the preschool period.