Stress (Dec 2024)

Dimensions of childhood adversity differentially affect autonomic nervous system coordination in response to stress

  • Meredith A. Gruhn,
  • Rachel E. Siciliano,
  • Allegra S. Anderson,
  • Allison Vreeland,
  • Lauren M. Henry,
  • Kelly H. Watson,
  • George M. Slavich,
  • Jon Ebert,
  • Tarah Kuhn,
  • Bruce E. Compas

DOI
https://doi.org/10.1080/10253890.2024.2419668
Journal volume & issue
Vol. 27, no. 1

Abstract

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It is well-established that disrupted autonomic nervous system (ANS) reactivity exacerbates risk for long-term maladjustment following childhood adversity (CA). However, few studies have integrated measures of both the sympathetic (SNS) and parasympathetic (PNS) branches of the ANS, resulting in a unidimensional understanding of ANS functioning as a mechanism of risk. Further, past work has primarily measured CA only at the aggregate level (e.g. “total CA”), necessitating further research to accurately characterize this risk pathway. The present study examines how CA, measured cumulatively and dimensionally (i.e. CA characterized by threat versus deprivation), moderates the association between the SNS and PNS at rest and in response to acute social and nonsocial stressors. Participants included 97 adolescents ages 10-15 (Mage = 12.22, SDage = 1.68) experiencing a range of CA and one accompanying caregiver. Participants completed questionnaires assessing prior CA exposure. SNS and PNS responses were then continuously measured during rest and two stress tasks. First, results indicate a blunting effect of cumulative CA and CA characterized by threat (e.g. physical abuse) on resting SNS activity. Second, in moderation analyses assessing ANS coordination, threat exposure emerged as a significant moderator of the association between SNS and PNS reactivity to social stress. Results suggest that CA characterized by threat may specifically impact physiologic regulation by disrupting the coordination of the two branches of the ANS. Disentangling the independent and concurrent engagement of biological stress response systems following CA remains an important target for research to identify the etiology of aberrant stress reactivity patterns.

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