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Intervening After Trauma to Improve Child Health: Child-Parent Psychotherapy Associates With Lower Pediatric Epigenetic Age

Sat, March 25, 8:15 to 9:45am, Salt Palace Convention Center, Floor: 3, Meeting Room 355 C

Abstract

BACKGROUND. Evidence indicates short- and long-term associations of early-life traumatic experiences on development and health (Nelson et al., 2020). One potential pathway may be biological embedding of these adversities into the molecular landscape reflected in epigenetics (Heim et al., 2019). Epigenetics, or modifications to the genome without affecting the underlying sequence, can be used to predict biological age, also known as epigenetic age (Aristizabal et al., 2020). Previous studies indicate epigenetic age is sensitive to stressors and predicts later life morbidity and mortality (Fransquet et al., 2019; Horvath, 2013). Specifically, those with a biological age older than their chronological age, thus experiencing faster epigenetic age acceleration (EAA), are at greater risk for health issues (Jones et al., 2015). Whereas mounting evidence suggests early-life adversity is associated with faster EAA in children (Wang & Zhou, 2021), it is unclear if demonstrably effective psychosocial interventions, such as Child-Parent Psychotherapy (CPP), may attenuate this acceleration.

OBJECTIVE. To examine the potential association of pediatric EAA with CPP participation by treatment-seekers when compared to a propensity-matched community sample.

APPROACH. Within a quasi-experimental repeated-measure study (N=155), we examined EAA of pediatric buccal epithelial cells (BEC) from cheek swabs in a treatment sample undergoing CPP for child trauma (n=45, 2-6 years old) and a community comparison sample (n=110, 3-6 yrs old) at baseline and post-intervention timepoints occuring roughly ten months apart. Treatment and control groups were successfully matched with full matching propensity weighting with caliper restriction using logistic regression (Austin & Stuart, 2017). Childhood adversity was measured by an abbreviated Traumatic Events Screen Inventory (Ford, 2002).

Epigenetic age was calculated using the pediatric buccal epigenetic (PedBE) clock (McEwen et al., 2020), which was highly correlated with chronological age (r = 0.89, 95% CI [0.85, 0.92], t(166) = 24.70, p < 2.2e-16). PedBE age was regressed onto chronological age, controlling for estimated BEC proportions. The residuals from this model constituted PedBE EAA. To estimate potential association of PedBE EAA and treatment, we employed a weighted ANCOVA, using propensity matching weights and controlling for all covariates (i.e., age, sex, ethnic identity, duration of time between samples, estimated BEC proportions, and baseline child adversity) matched on at both the baseline and post-intervention timepoints. At baseline, PedBE EAA was the same across the weighted groups of CPP treatment and propensity-matched control samples (F(1, 149) = 0.03, p = 0.854; Cohen’s f = 0.01, 95% CI [0.00, 1.00]). However, after the 20-session intervention, ~10 months after baseline, treatment group children had less PedBE EAA than matched controls (F(1, 149) = 6.39, p = 0.013; Cohen’s f = 0.21, 95% CI [4.90e-03, 1.00]).

SIGNIFICANCE. These findings indicate the potential of psychosocial intervention to ameliorate pediatric EAA in trauma-exposed children in the short-term. Findings also provide a critical foundation for future research into intervention effects on biological aging. While a small effect, the possible biological significance of slower EAA in early childhood is yet to be illuminated—these findings may indicate the potential for trauma-intervention related long-term differences in prospective health trajectories across childhood.

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