ABSTRACT
Childhood sexual abuse (CSA) not only compromises well-being in childhood but is also associated with a broad range of psychopathology and morbidity in adulthood [1], [2], [3], [4]. However, little is known about the biological mechanisms involved in mediating the long-term pathogenic effect of early-life trauma. One possible means for CSA to be biologically “embedded” in a manner that could lead to a latent pathologic consequence would be if it resulted in a change in the individual’s somatic cell DNA. Evidence shows childhood maltreatment predicts an increased
risk of clinically relevant levels of inflammation in adulthood [5],[6], and inflammation-associated reactive oxygen/nitrogen species are known to cause DNA damage/chromosomal changes. Stress-related inflammation also leads to perturbations in the regulation/expression of several genes, including (but not limited to) nuclear factor-kappa B (NF-kβ), interleukin1B, interleukin-6, and tumor necrosis factor-α [7], [8]. Additional evidence that early-life stress can lead to DNA-based alterations comes from reports of shortened telomeres in children exposed to adverse rearing settings [9], and in adults with a history of chronic or severe childhood illness [10] or childhood maltreatment [11], but the potential correlation between childhood maltreatment and telomere length is controversial [12].
