Improving health among disadvantaged girls to slow pubertal onset and reduce long-term health risks

University Of Washington, Seattle WA

Investigators

Linked publications, trials & patents

Abstract

Girls who experience puberty earlier than their same-age peers are at disproportionate risk for poor outcomes across domains of emotional, social, and physical health, setting the stage for life-long hardships. Just some of these outcomes include depression, self-harm, low self-esteem, poor body image, disordered eating, poor school performance, affiliation with delinquent peers, drug and alcohol use, earlier sexual debut, teenage motherhood, progressive weight gain and obesity, worsening cardiometabolic risk factor profiles, incident disease (e.g., type 2 diabetes, cardiovascular disease, cancer), and early mortality. At the same time, abundant research shows greater prepubertal body mass index (BMI) is a critical determinant of earlier pubertal onset. Integration of these research areas points to the novel focus of the proposed study which seeks to address whether weight loss and positive health behavior change in the prepubertal period may slow pubertal onset in girls at risk for accelerated pubertal development. The proposed study will conduct an RCT using an established treatment program to target childhood obesity (vs. control) in 240 prepubertal girls who are at risk for earlier pubertal onset based on BMI percentile ≥85th and low family income, both factors with strong prospective links to earlier pubertal onset. Pubertal onset will be indexed both by hormones and questionnaire-based pubertal staging methods to characterize the onset of the main pubertal development processes: 1) gonadarche (luteinizing hormone [LH], Tanner stage 2 breast development) and 2) adrenarche (dehydroepiandrosterone sulfate [DHEAS], Tanner stage 2 pubic hair development). It is hypothesized that the proportion of girls who experience pubertal onset at the 18-month and 30-month follow-up assessments will be lower in the intervention (vs. control) condition and that differences in pubertal onset will be partially attributable to mechanisms, including weight loss (reduced zBMI), improved health behaviors (diet quality, activity level, sleep duration), improved health status profiles (blood pressure, inflammation, and insulin resistance), and metabolic hormones (leptin, insulin-like growth factor 1 [IGF-1]). The clinical implications of this work are extensive. First, if slowing pubertal onset is possible, by extension, the numerous maladaptive outcomes associated with earlier pubertal onset could be reduced. Moreover, girls most in need may reap the most benefit as girls from disadvantage socioeconomic backgrounds are more likely to experience earlier pubertal onset. In this way, it is plausible that life course linkages between prepubertal obesity, earlier pubertal onset, and negative post-pubertal outcomes could be disrupted among those who are most vulnerable. Second, this work will inform new directions for existing obesity treatment programs in girls. Most obesity intervention and prevention efforts have not considered pubertal stage or the important intersections between obesity and pubertal onset. Findings will inform the value and optimal timing of conducting such interventions, including whether implementation in the prepubertal period may be most impactful due to the combined benefits of weight loss along with a reduction in risk for earlier pubertal onset and its sequelae.