Prenatal substance exposure, early‐life adversity, and parenting: Associations with adolescent stress response

Abstract

We tested a conceptual model examining associations between prenatal substance exposure and adolescent cortisol reactivity profiles in response to an acute social evaluative stressor. We included cortisol reactivity in infancy, and direct and interactive effects of early-life adversity and parenting behaviors (sensitivity, harshness) from infancy to early school age on adolescent cortisol reactivity profiles in model testing.Participants were 216 families (51% female children; 116 cocaine-exposed) recruited at birth, oversampled for prenatal substance exposure, and assessed from infancy to early adolescence (EA). Majority of participants self-identified as Black (72% mothers, 57.2% adolescents), and caregivers were primarily from low-income families (76%), were single (86%), and had high school or below education (70%) at recruitment. Latent profile analyses identified three cortisol reactivity patterns including elevated (20.4%), moderate (63.1%), and blunted (16.5%) reactivity groups. Prenatal tobacco exposure was associated with higher likelihood of membership in the elevated reactivity compared to the moderate reactivity group. Higher caregiver sensitivity in early life was associated with lower likelihood of membership in the elevated reactivity group. Prenatal cocaine exposure was associated with higher maternal harshness. Interaction effects among early-life adversity and parenting indicated that caregiver sensitivity buffered, and harshness exacerbated, the likelihood that high early adversity would be associated with the elevated and blunted reactivity groups. Results highlight the potential importance of prenatal alcohol and tobacco exposure for cortisol reactivity and the role of parenting as exacerbating or buffering the impact of early-life adversity on adolescent stress response.

Prenatal Substance Exposure

“…Prenatal cocaine exposure is a marker of polysubstance exposure, and while studies discussed here include careful measurement of other substance use and statistical controls for these other exposures, it is difficult to understand cocaine-specific effects outside of the nested nature of multiple exposures (Eiden et al 2023). Results are mixed, with some studies reporting little evidence of associations with global measures of cognition (for a review, see Behnke et al 2013), while others report associations with specific cognitive domains.…”

“…Perhaps differences in results between the two studies were related to differences in the context of measurement and in how autonomic data were edited for artifacts (an automated process in the MLS versus manual editing in the MCHS). Studies examining associations with HPA reactivity are also limited, with some indication of greater reactivity among cocaine-exposed boys compared with girls in infancy (Eiden et al 2009), lower cortisol response (using a cortisol difference score from baseline to peak response) among cocaine-exposed early adolescents (Lester et al 2010), flatter or blunted patterns in response to acute stress among more heavily cocaine-exposed compared with non-cocaine-exposed older adolescents (Chaplin et al 2015), and no direct associations between cocaine exposure and early adolescent stress reactivity (Eiden et al 2023).…”

“…Little is known about cannabis effects on parent-child interactions, although a small literature indicates more robust associations between tobacco and cannabis co-use and maternal affective dysregulation and/or psychological distress in the prenatal-to-postpartum period (Godleski et al 2018), with prospective linkages with lower maternal sensitivity during mother-child interactions across the infant-toddler period compared with tobacco use alone (Eiden et al 2018a). There is a larger literature linking prenatal cocaine exposure to parenting difficulties (Eiden et al 2023), with human (Light et al 2004) and animal studies indicating cocaine effects on lower maternal postpartum oxytocin as a putative biological mechanism for this association, as noted above (McMurray et al 2008). Larger amounts of cocaine may also have an acute effect on increasing aggression, which may have cascading effects on parenting (Eiden et al 2011d).…”

“…In addition to continued substance exposure, other risk factors noted above often co-occur, and one approach for examining co-occurring risks may be to use a cumulative risk approach (Evans et al 2013). For instance, results from the MCHS indicate additive effects of prenatal cocaine exposure and cumulative early life adversity (composite of caregiver psychological distress, violence exposure, separations from caregivers, and nonoptimal caregiving routines) on externalizing problem trajectories from toddler to early school age (Molnar et al 2014); an interaction of adversity and caregiver sensitivity on blunted cortisol responses to social stress in adolescence such that in the context of adversity, sensitive caregiving was protective (Eiden et al 2023); and four profiles of varying levels of exposure to caregiver substance use, co-occurring family risks, and parenting from infancy to early school age, the majority of children experiencing substantial stability in these profile memberships, with consequences for adolescent well-being (Seay et al 2023). These examples highlight the importance of adversities and protective factors embedded in the postnatal environment that may have additive, protective, or mediating associations with outcomes across the life span.…”

“…At the same time, there have been recent calls for the investigation of prenatal stressors to be broader and include co-occurring risks and family processes and to address heterogeneity in outcomes (Huizink & de Rooij 2018). Alternate frameworks that consider genetic (e.g., Estabrook et al 2016) and environmental (e.g., Eiden et al 2023) influences, bidirectional associations between parent and child across time, and evocative child effects may be particularly helpful (e.g., Eiden et al 2018b). Careful consideration of the rearing environment including continued postnatal substance exposure, the role of co-occurring risk factors, and potential protective processes as significant predictors (as opposed to control variables) is critical to move the field forward.…”