Emotion Regulation as a Pathway Connecting Early Life Adversity and Inflammation in Adulthood: a Conceptual Framework.

Chronic inflammation is implicated in a variety of diseases (e.g., cardiovascular disease and cancer). Much evidence suggests that early life adversity (ELA), such as maltreatment or neglect, can increase risk for inflammation in adulthood. ELA may program proinflammatory activity via its effects on brain areas involved in emotion regulation. Of multiple emotion regulation strategies, some are considered maladaptive (e.g., expressive suppression), while others are generally adaptive (e.g., cognitive reappraisal). We propose a conceptual framework for how emotion regulation tendencies may affect vulnerability or resilience to inflammation in adults who experienced adversity in childhood and/or adolescence. In support of this framework, we summarize evidence for the relationships between emotion dysregulation and higher inflammation (i.e., vulnerability), as well as between cognitive reappraisal and lower inflammation (i.e., resilience), in healthy adults with a history of ELA. Plausible neurobiological, physiological, psychosocial, and ELA-specific factors, as well as interventions, contributing to these associations are discussed. Strengths and limitations of the extant research, in addition to ideas for future directions, are presented.

Hypothalamic-pituitary-adrenal axis attenuation and obesity risk in sexually abused females.

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.

Childhood Sexual Abuse and Early Timing of Puberty.

PURPOSE: The purpose was to examine whether the timing of puberty, indexed by breast development and pubic hair development, was earlier for sexually abused females compared with a matched comparison group of nonabused females, controlling for key alternative confounds. METHODS: A cohort of sexually abused females and matched comparisons was followed longitudinally at mean ages 11 through 20 years. Sexually abused participants (N = 84) were referred by protective services. Comparison participants (N = 89) were recruited to be comparable in terms of age, ethnicity, income level, family constellation, zip codes, and nonsexual trauma histories. Stage of puberty was indexed at each assessment by nurse and participant ratings of breast and pubic hair development using Tanner staging-the gold standard for assessing pubertal onset and development. Cumulative logit mixed models were used to estimate the association between sexual abuse status and the likelihood of transitioning from earlier to later Tanner stage categories controlling for covariates and potential confounds. RESULTS: Sexual abuse was associated with earlier pubertal onset: 8 months earlier for breasts (odds ratio: 3.06, 95% CI: 1.11-8.49) and 12 months earlier for pubic hair (odds ratio: 3.49, 95% CI: 1.34-9.12). Alternative explanations including ethnicity, obesity, and biological father absence did not eradicate these findings. CONCLUSIONS: This study confirms an association between exposure to childhood sexual abuse and earlier pubertal onset. Results highlight the possibility that, due to this early onset, sexual abuse survivors may be at increased risk for psychosocial difficulties, menstrual and fertility problems, and even reproductive cancers due to prolonged exposure to sex hormones.