Jacinda C Li1, Molly A Hall2, Idan Shalev3, Hannah M C Schreier4, Tomás González Zarzar5, Isabel Marcovici6, Frank W Putnam7, Jennie G Noll8. 1. College of Health and Human Development, Department of Human Development and Family Studies, The Pennsylvania State University, 325 Health and Human Development Building, University Park, PA, USA. Electronic address: jcl270@psu.edu. 2. College of Agricultural Sciences, Department of Veterinary and Biomedical Sciences, The Pennsylvania State University, 115 Henning Building, University Park, PA, USA. Electronic address: mah546@psu.edu. 3. College of Health and Human Development, Department of Biobehavioral Health, The Pennsylvania State University, 219 Biobehavioral Health Building, University Park, PA, USA. Electronic address: ius14@psu.edu. 4. College of Health and Human Development, Department of Biobehavioral Health, The Pennsylvania State University, 219 Biobehavioral Health Building, University Park, PA, USA. Electronic address: hms5427@psu.edu. 5. College of Agricultural Sciences, Department of Veterinary and Biomedical Sciences, The Pennsylvania State University, 115 Henning Building, University Park, PA, USA. Electronic address: tug156@psu.edu. 6. College of Health and Human Development, Department of Human Development and Family Studies, The Pennsylvania State University, 325 Health and Human Development Building, University Park, PA, USA. Electronic address: ixm5119@psu.edu. 7. Department of Psychiatry, University of North Carolina School of Medicine, 101 Manning Dr # 1, Chapel Hill, NC, USA. Electronic address: frank_putnam@med.unc.edu. 8. College of Health and Human Development, Department of Human Development and Family Studies, The Pennsylvania State University, 325 Health and Human Development Building, University Park, PA, USA. Electronic address: jgn3@psu.edu.
Abstract
BACKGROUND: Childhood sexual abuse (CSA) confers elevated risks for obesity in females. Mechanisms that explain this link remain unclear. This study tracked serum basal cortisol levels with body mass index (BMI) from childhood into adulthood to test whether hypothalamic-pituitary-adrenal (HPA) axis attenuation accounts for elevated obesity risks for sexually abused females. METHODS: Data drew from six timepoints of a longitudinal study of the impact of CSA on development. Participants were females aged 6-16 years at time of study enrollment with substantiated CSA and demographically matched non-abused peers. Analyses included only participants who did not have obesity at study enrollment. Main outcomes were BMI growth trajectories across ages 6-27 (n = 150; 66 abused, 84 comparisons) and early adulthood obesity status (ages 20-27; n = 133; 62 abused, 71 comparison). HPA axis functioning indicators were intercept and linear slope parameters extracted from multilevel growth trajectories of serum basal cortisol levels across development. Racial-ethnic minority status, parity, steroid medication use, depression history and disordered eating history were covaried. RESULTS: While controlling for covariates, multilevel modeling indicated that high initial serum basal cortisol levels in childhood and attenuated cortisol growth rate over time (i.e., HPA axis attenuation) were associated with accelerated BMI accumulation (p < .01). Attenuated cortisol growth rate mediated the effect of CSA on accelerated BMI accumulation and on elevated adulthood obesity rates (p < .05). CONCLUSION: This work establishes a mechanistic association between HPA axis attenuation and obesity, suggesting that trauma treatments for abuse survivors should include interventions that reduce health consequences associated with dysregulated stress physiology.
BACKGROUND: Childhood sexual abuse (CSA) confers elevated risks for obesity in females. Mechanisms that explain this link remain unclear. This study tracked serum basal cortisol levels with body mass index (BMI) from childhood into adulthood to test whether hypothalamic-pituitary-adrenal (HPA) axis attenuation accounts for elevated obesity risks for sexually abused females. METHODS: Data drew from six timepoints of a longitudinal study of the impact of CSA on development. Participants were females aged 6-16 years at time of study enrollment with substantiated CSA and demographically matched non-abused peers. Analyses included only participants who did not have obesity at study enrollment. Main outcomes were BMI growth trajectories across ages 6-27 (n = 150; 66 abused, 84 comparisons) and early adulthood obesity status (ages 20-27; n = 133; 62 abused, 71 comparison). HPA axis functioning indicators were intercept and linear slope parameters extracted from multilevel growth trajectories of serum basal cortisol levels across development. Racial-ethnic minority status, parity, steroid medication use, depression history and disordered eating history were covaried. RESULTS: While controlling for covariates, multilevel modeling indicated that high initial serum basal cortisol levels in childhood and attenuated cortisol growth rate over time (i.e., HPA axis attenuation) were associated with accelerated BMI accumulation (p < .01). Attenuated cortisol growth rate mediated the effect of CSA on accelerated BMI accumulation and on elevated adulthood obesity rates (p < .05). CONCLUSION: This work establishes a mechanistic association between HPA axis attenuation and obesity, suggesting that trauma treatments for abuse survivors should include interventions that reduce health consequences associated with dysregulated stress physiology.
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