TABLE 1.

Short-term biological consequences of childhood sexual abuse (CSA) exposure.

Article	Age	Blood/Saliva/Buccal	Sample size	Biological function affected	Main results
Muller et al., 2014	7–12 years	Blood	11	HPA	↓	Children in institutional settings demonstrated an attenuated stress reactivity pattern, interpreted as an apparent lack of an appropriate HPA response when faced with a further stressor (e.g., forensic interview and medical examination).
Şimşek et al., 2016	9–17 years	Blood	38	HPA	↑	In children who developed a PTSD, oxidative stress was higher following multiple abuses and sexual abuses within the family.
Atabay and Arman, 2019	10–17 years	Blood	90	HPA	↑	CSA group showed high oxidative stress and low antioxidant process profile.
Muller et al., 2014	7–12 years	Blood	11	Immune system	↑	SA children in institutional setting had higher morning IL-6 concentrations during their clinic visit, which were inversely correlated with plasma cortisol concentrations.
Esteves et al., 2020	4, 12, 18 months	Buccal	155	Epigenetic and Chromatin	↓	Mothers’ high scores in the ACE questionnaire predicted shorter telomere length and emerging (mainly externalizing) behavioral problems in the offspring.
Shalev et al., 2013	5 and 10 years	Buccal	236	Epigenetic and Chromatin	↓	Accelerated telomere erosion was observed in children who were exposed to multiple forms of violence and the effects worsen over time.
Ridout et al., 2018	3–5 years	Saliva	250	Epigenetic and Chromatin	↑	Children who experienced moderate-severe levels of maltreatment within 6 months prior to the analysis, had longer telomeres and higher mtDNA, possibly reflecting compensatory changes in response to recent trauma.

HPA, hypothalamic-pituitary-adrenal axis; IL-6, Interleukin 6; ACE, adverse childhood experiences; mtDNA, mitochondrial DNA.