Childhood Adversities and Salivary Cortisol Responses to the Trier Social Stress Test: A Systematic Review of Studies Using the Children Trauma Questionnaire (CTQ).

Chuk Ling Julian Lai,Monique On Yee Leung,Daryl Yu Heng Lee

doi:10.3390/ijerph18010029

Abstract

Alteration in cortisol response to acute social stressors has been hypothesized to mediate childhood adversities (CA) and increased morbidity in adulthood. However, the evidence supporting an association between CA and cortisol response to social stressors is inconclusive. The present review addressed this issue by reviewing the literature on CA and cortisol response to acute social stressors, with a focus on studies with adolescents or adults, using the Childhood Trauma Questionnaire (CTQ) to assess CA, and examining salivary cortisol response to the Trier Social Stress Test (TSST). Systematic searches of relevant articles in PsycINFO, PubMed, Web of Science and ScienceDirect in February and March 2020 identified 12 articles including 1196 participants with mean ages ranging from 15.3 to 52.3 yrs. across studies. CTQ scores were significantly associated with cortisol response in 2 studies. In addition, the physical abuse and emotional neglect subscales were associated with cortisol response respectively in 2 separate studies. The lack of association between CA and cortisol response calls for more longitudinal studies, and the use of formal records of maltreatment or informant reports in future research to complement information collected by retrospective measures. In addition, increased attention to biological mechanisms other than that associated with the regulation of cortisol in explaining the connection between CA and psychiatry morbidity is warranted.

Highlights

Received: 30 November 2020Accepted: 20 December 2020Published: 23 December 2020Publisher’s Note: MDPI stays neutral with regard to jurisdictional claims in published maps and institutional affiliations.license.Childhood adversities (CA), which refers to the abuse and neglect of children under the age of 18 in the physical, emotional, and/or sexual domain, has been shown to be a global phenomenon [1], and one of the important social environmental factors that may explain morbidity [2] and mortality [3] in adulthood
We arrived at eligible studies through a systematic search in PsycINFO, PubMed, Web of Science and ScienceDirect using a combination of specific keywords as illustrated in
The evidence showing an association between childhood adversities (CA) as measured retrospectively by the Childhood Trauma Questionnaire (CTQ) and cortisol response to the Trier Social Stress Test (TSST) is weak, this relationship is stronger in females with psychiatric conditions

Summary

Introduction

Received: 30 November 2020Accepted: 20 December 2020Published: 23 December 2020Publisher’s Note: MDPI stays neutral with regard to jurisdictional claims in published maps and institutional affiliations.license (https://creativecommons.org/licenses/by/4.0/).Childhood adversities (CA), which refers to the abuse and neglect of children under the age of 18 in the physical, emotional, and/or sexual domain, has been shown to be a global phenomenon [1], and one of the important social environmental factors that may explain morbidity [2] and mortality [3] in adulthood. The important health policy implication of the CA-morbidity association has triggered a surge of studies aiming at unravelling the mediating neurobiological mechanisms (e.g., [4]). There is evidence from both animal and human studies showing that exposure to maltreatments early in life or to childhood adversities (CA) contributes to pathological stress responses in adulthood (e.g., [5]). The altered stress responses, which are mediated by the hypothalamic-pituitary-adrenocortical axis (HPAA), are associated with chronic disease [6] and increased psychiatric morbidity in adulthood [7]. Because of the important role of the HPAA in mediating the stress response, studies examining the connection between CA and cortisol, the end product of the HPAA, have proliferated in the last two decades [6,8]. It is widely appreciated that the effect of CA on cortisol reactivity during critical periods of development interacts with specific genotypes to program longlasting changes in glucocorticoid signaling via epigenetic alteration of the sensitivity of the

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