Maltreatment timing, HPA axis functioning, multigenic risk, and depressive symptoms in African American youth: Differential associations without moderated mediation.

Adrienne A Vanzomeren,Timothy Piehler,Meredith Gunlicks-Stoessel,Jingchen Zhang,Sun-Kyung Lee,Dante Cicchetti

doi:10.1017/s0954579420000589

Abstract

Utilizing a large (N = 739), ancestrally homogenous sample, the current study aimed to better understand biological risk processes involved in the development of depressive symptoms in maltreated, African American children age 8-12 years. Maltreatment was independently coded from Child Protective Services records and maternal report. Self-reported depressive symptoms were attained in the context of a week-long, summer research camp. DNA was acquired from buccal cell or saliva samples and genotyped for nine polymorphisms in four hypothalamic-pituitary-adrenal (HPA)-axis-related genes: FKBP5, NR3C1, NR3C2, and CRHR1. Salivary cortisol samples were collected each morning (9 a.m.) and late afternoon (4 p.m.) throughout the week to assess HPA functioning. Results revealed that experiences of maltreatment beginning prior to age 5 were most predictive of depressive symptoms, whereas maltreatment onset after age 5 was most predictive of HPA axis dysregulation (blunted daytime cortisol patterns). Multigenic risk did not relate to HPA functioning, nor did it moderate the relationship between maltreatment and HPA activity. There was no mediation of the relationship between maltreatment and depressive symptoms by HPA dysfunction. Results are interpreted through a developmental psychopathology lens, emphasizing the principle of equifinality while carefully appraising racial differences. Implications for future research, particularly the need for longitudinal studies, and important methodological considerations are discussed.

Highlights

Child maltreatment is a potent relational pathogen whereby caregivers deprive children of basic emotional, physical, and/or psychological needs by inflicting harm and/or omitting essential care (Cicchetti & Lynch, 1995)
Childhood depressive symptoms are costly to both individuals and society because they interfere with the completion of salient developmental tasks (Rice & Miller, 1995; Wulsin & Singal, 2003) and increase risk for chronic, recurrent psychopathology (Fombonne, Wostear, Cooper, Harrington, & Rutter, 2001) and disability (González et al, 2010) throughout the lifespan
Findings from several lines of research over the past few decades have been used to support the theory that maltreatment uniquely predisposes for depressive symptoms through its dysregulating impact on HPA axis functioning

Summary

Introduction

Child maltreatment is a potent relational pathogen whereby caregivers deprive children of basic emotional, physical, and/or psychological needs by inflicting harm and/or omitting essential care (Cicchetti & Lynch, 1995). Maltreatment timing, HPA axis functioning, multigenic risk, and depressive symptoms in African American youth: Differential associations without moderated mediation. Childhood depressive symptoms are costly to both individuals and society because they interfere with the completion of salient developmental tasks (Rice & Miller, 1995; Wulsin & Singal, 2003) and increase risk for chronic, recurrent psychopathology (Fombonne, Wostear, Cooper, Harrington, & Rutter, 2001) and disability (González et al, 2010) throughout the lifespan. It is important to understand the ways that maltreatment increases risk for depression in children to help identify early intervention targets and alleviate the tremendous impact on personal and public health. Findings from several lines of research over the past few decades have been used to support the theory that maltreatment uniquely predisposes for depressive symptoms through its dysregulating impact on HPA axis functioning. But are not limited to, the following: (a) various forms of HPA dysfunction are present in depressed individuals (Lopez-Duran, Kovacs, & George, 2009; Nestler et al, 2002) and prospectively predict depressive symptoms (e.g., Halligan, Herbert, Goodyer, & Murray, 2004, 2007; Heim & Binder, 2012; Koss, Cummings, Davies, & Cicchetti, 2017; Saridjan et al, 2014; VrshekSchallhorn et al, 2013), but are not present in all depressed individuals (Adam et al, 2010; Birmaher et al, 1996; Feder et al, 2004), (b) reversal of both HPA dysfunction and depressive behavior in maltreated rodents can be accomplished via pharmacologic manipulation of HPA axis regulators (Weaver et al, 2004), and (c) HPA dysfunction has been observed in maltreated individuals as early as infancy (Cicchetti, Rogosch, Toth, & Sturge-Apple, 2011b), but is most evident in depressed, maltreated individuals—both children and adults—when directly compared to depressed, nonmaltreated; maltreated, nondepressed; and non-depressed, nonmaltreated individuals (e.g., Cicchetti, Rogosch, Gunnar, & Toth, 2010; Hart, Gunnar, & Cicchetti, 1996; Heim et al, 2000, 2001, 2008)

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