HYPOTHALAMIC-PITUITARY-ADRENAL AXIS DYSREGULATION, BODY MASS INDEX GROWTH TRAJECTORIES, AND OBESITY IN FEMALES WITH HISTORIES OF CHILDHOOD SEXUAL ABUSE AND NONABUSED COMPARISONS

Restricted (Penn State Only)
Author:
Li, Jacinda Changhui
Graduate Program:
Human Development and Family Studies
Degree:
Doctor of Philosophy
Document Type:
Dissertation
Date of Defense:
February 05, 2019
Committee Members:
  • Jennie G Noll, Dissertation Advisor
  • Jennie G Noll, Committee Chair
  • Chad Edward Shenk, Committee Member
  • Nilam Ram, Committee Member
  • Lori Anne Francis, Outside Member
  • Kathleen Loralee Keller, Special Member
Keywords:
  • obesity
  • childhood sexual abuse
  • stress physiology
  • hypothalamic-pituitary-adrenal axis
  • cortisol
  • female
  • adolescence
  • body mass index
  • stress
  • child maltreatment
  • multilevel modeling
Abstract:
Obesity disproportionately burdens females, thereby perpetuating intergenerational obesity and numerous other health problems in offspring. Thus, efforts to treat and prevent obesity in females is critical for combating the obesity epidemic. Effective intervention requires improving understanding about who is most vulnerable and what mechanisms explain their elevated risk. Childhood sexual abuse (CSA) has been established as a powerful risk factor for obesity in females, yet the potential mechanisms that explain the elevated risk remain unclear. Consistent with the literature on allostatic load, dysregulation of the stress response system through early-life traumatic stress—of which CSA is arguably one of the most severe forms—has been implicated in obesity. Specifically, hypothalamic-pituitary-adrenal (HPA) axis dysregulation, defined as initially-elevated cortisol levels followed by attenuated rates of growth in these levels over time, has been identified as a potential mechanism for excessive weight gain and obesity in individuals who were exposed to traumatic stress. The existing literature on the relationship between HPA axis dysregulation and obesity consists primarily of animal studies or short-term, laboratory-based human experiments. Thus, the role of long-term HPA axis dysregulation in obesity in humans remains inconclusive. Furthermore, there is a paucity of studies that formally test the extent to which HPA axis dysregulation accounts for excessive weight gain and obesity in females with objectively-confirmed CSA exposure, while taking into account potential confounding factors such as race/ethnicity, parity status, depression, and disordered eating. This dissertation addressed the existing gaps in the literature by investigating the long-term associations between HPA axis dysregulation, body mass index (BMI) growth trajectories, and obesity in sexually abused and nonabused females. It capitalized upon the unique cross-sequential cohort data of the Female Growth and Development Study (FGDS; PI: Noll), which prospectively followed a diverse sample of 173 females with court-substantiated CSA and demographically-matched nonabused comparisons from childhood into early adulthood. This dissertation examined (1) the associations between HPA axis dysregulation and BMI growth trajectories across development for females in general; (2) differential associations between HPA axis dysregulation and BMI growth trajectories for abused and nonabused females; and (3) the extent to which HPA axis dysregulation accounted for the effects of CSA on BMI growth rates and obesity status. Indicators of HPA axis dysregulation were derived by extracting the intercept and linear slope parameters from multilevel growth models of serum nonstress cortisol levels across development. A separate set of multilevel growth models estimated the effect of HPA axis dysregulation indicators on the intercept and linear slope parameters of BMI growth trajectories across development. In addition, growth models examined whether CSA group membership altered the effects of HPA axis dysregulation indicators on BMI growth trajectories. The extent to which HPA axis dysregulation indicators accounted for the effects of CSA on accelerated BMI growth rates was evaluated by the extent of reduction in the CSA effect on the linear slope parameter of BMI growth trajectories after accounting for HPA axis dysregulation indicators. Indirect effects analysis via Bootstrap Sobel Test examined the indirect paths of CSA on adulthood obesity through the average nonstress cortisol levels in childhood, adolescence, or in adulthood. All models controlled for potential confounds. Results of multilevel growth models showed that HPA axis dysregulation was associated with accelerated BMI growth rates across development, indicating a greater risk for excessive weight gain from childhood into early adulthood. The association between HPA axis dysregulation and BMI growth rates was stronger for the CSA group than for comparisons, indicating that abused females were more vulnerable to the effect of HPA axis dysregulation on excessive weight gain than were nonabused females. HPA axis dysregulation accounted for a significant portion of the effects of CSA on accelerated BMI growth rates. Results of indirect effects analyses showed that lower average levels of nonstress cortisol in adulthood accounted for a significant portion of the effect of CSA exposure on elevated obesity rates in adulthood. These findings provide evidence in support of theories that implicate HPA axis dysregulation as a potential mechanism for excessive weight gain and elevated risks for obesity for CSA females. Supplemental analyses examined the association between HPA axis dysregulation and BMI growth trajectories through alternative methods. Tests of the association between HPA axis dysregulation and BMI growth trajectories across time since abuse disclosure reinforced the findings from the primary analyses that had examined this association across development. Additionally, variability in nonstress cortisol levels was associated with accelerated BMI growth rates across development. Subsets of the CSA group that had abuse onset in late childhood/early-adolescence, abuse duration of single incident to one year, or abuse perpetrated by primary father figure showed the strongest association between HPA axis dysregulation and obesity-related outcomes. These findings help to identify the characteristics of high-risk CSA subgroups. This dissertation contributes to the growing body of work emerging from the FGDS to investigate the long-term consequences of CSA on female development across multiple levels of human functioning. By simultaneously examining the long-term trajectories of HPA axis dysregulation and of BMI while accounting for potential confounds, this dissertation also contributes to the literature on the putative role of HPA axis dysregulation in excessive weight gain and obesity. This dissertation also presented formal tests of the extent to which HPA axis dysregulation accounted for the effect of CSA exposure on excessive weight gain over time and elevated risk for obesity in adulthood. Findings help to advance trauma-informed obesity intervention models for females with histories of CSA as well as enhanced intervention and public health policy approaches for individuals in the general population who may also exhibit traumatic stress-related HPA axis dysregulation.