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Background: A vast literature links childhood adversity to poor adult outcomes (Hughes et al., 2017), with prominent impacts on intermediary health risk behavior like substance use (SU; Dube et al., 2003), along with more distal outcomes like parenting stress (PS; Lange, Callinan, & Smith, 2019). HPA-axis dysregulation is one pathway thought to mediate adverse outcomes. For example, elevated cortisol levels have been associated with heavy drinking (Boschloo et al., 2011; Dube et al., 2003) and smoking (Badrick, Kirschbaum, & Kumari, 2007). In turn, SU has been associated with elevated PS (Rutherford & Mayes, 2019). Interrupting this cascade of outcomes linking ACEs to SU and PS is critically important in parenting interventions. Parenting sense of competence (PSOC), or parenting efficacy, is one mechanism indicated as mediating parenting intervention outcomes (Deković et al., 2010). This study expands on previous work by testing whether PSOC can interrupt links between ACEs, SU, and PS.
Methods: Data were collected from caregivers (n=119), who were 80% Latina mothers, ages 18-49 (M=31.5) with an average net income of $27,186 (Range=$0-135,000). On average, caregivers reported 2.2 ACEs (Felitti et al., 1998; Range=0-8), a PSOC score of 39.4 (Gibaud-Wallson & Wandersman, 1978; Range=10-48), a Parenting Stress Index score of 70.7 (PSI; Abidin, 1990; Range=36-122), and average bedtime cortisol values across two days of 0.48 ug (0-.29). A composite SU score was created using dichotomously rated current smoking, ≥2 daily alcoholic drinks, and SU treatment in the previous year. (M= .19, Range = 0-2). In step 1: a mediation model examined bedtime cortisol as a mediating ACEs on SU. In step 2: a regression examined the effect of SU on PS. In step 3: PSOC was examined as a moderator for (1) the relationships between bedtime cortisol and SU and (2) between SU and PS.
Results: In step one, a mediation model (n=119) found that ACEs predicted elevated bedtime cortisol, b=.0087, t=3.14, p<.05, and SU, b=.054, t=2.79, p=.006, and bedtime cortisol predicted elevated SU, b=1.57, t=2.52, p=.01. Bedtime cortisol partially mediated the relationship between ACEs and SU, d=0.14 [95% CI, 0.0008, 0.0412]. In step two, a linear regression demonstrated that SU predicted elevated parenting stress, b=9.36, t=3.5, p=.009. In step three, PSOC was tested as a moderator. First, PSOC was found to marginally moderate the effects of bedtime cortisol on SU, b=.23, t=1.81, p=.07, such that higher levels of PSOC moderated substance use only when bedtime cortisol levels were lower, ΔR2 = .10, ΔF(3, 115) =5.23, p= .002 (Figure 1). Second, PSOC moderated the effects of SU on PS, b=1.65, t=2.77, p=.01, such that higher PSOC reduced PS only when SU was also lower, ΔR2 = .13, ΔF(3, 115) =6.96, p<.001 (Figure 2).
Implications: These findings demonstrate a pathway by which early adversity may be intergenerationally transmitted through the adoption of health risk behaviors and PS. While PSOC buffered these relationships, effects were lowered in the context of higher bedtime cortisol and SU. Caregivers facing elevated stress and SU may need additional supports to interrupt the consequences of early adversity.