Victims of CSA may also be more likely to experience other forms of maltreatment thus confounding attempts to disentangle the specific effects of CSA ( Finkelhor et al., 2007 Mitchell et al., 2020). Underreporting may contribute to contamination of control groups in retrospective studies of abuse, a problem that can contribute to variability in reported associations between adult health outcomes and CSA exposure ( Shenk et al., 2016). (2016) found that 39.6% of adults with agency-notified CSA did not recall the abuse when asked about it as young adults. Comparing self-report in adulthood to agency-notified and substantiated CSA in a prospectively followed birth cohort, Mills et al. Prospective work in cohorts with substantiated CSA supports a tendency for non-disclosure in a portion of adult survivors. Additionally, many of these studies relied on retrospective, unsubstantiated reports of CSA. use of different questionnaires to assess abuse, level of sensitivity to abuse severity, length of time between abuse and TL assessment) between studies may contribute to divergent findings. Several studies testing the relationship between TL and child sexual abuse (CSA) found no association ( Glass et al., 2010 Jodczyk et al., 2014 Mason et al., 2015 Vincent et al., 2017). postnatal, pre-pubertal, adolescence) of exposure ( Ridout et al., 2018). abuse, neglect, all adversity) and timing (e.g. A recent meta-analysis on the impact of early adversity on TL demonstrates important differences in effect size depending on adversity type (e.g. (2013) found evidence of thinning in portions of the somatosensory cortex associated with the clitoris and genital area. In females with pre-pubertal sexual abuse history, Heim et al. For example, a review of the literature highlights maltreatment-type-specific differences in brain structure and connectivity of maltreated individuals ( Teicher et al., 2016). Extant studies attempting to disentangle the unique impact of different forms of child maltreatment point to intriguing differences in the biological embedding of each maltreatment type. (2010) found that a greater number of childhood adversities associated with shorter TL in adulthood. (2010) found that individuals reporting a history of child maltreatment had shorter telomeres than those without maltreatment history. Given the frequent co-occurrence of multiple abuse types ( Finkelhor et al., 2013 Vachon et al., 2015) and the difficulty in gathering large samples for abuse types with low population-level prevalence, treating all forms of child maltreatment as one category has been important in advancing our knowledge of the impact of early victimization. ‘toxic stressors’ or ‘adverse childhood experiences’). physical/sexual abuse, neglect) into one category (e.g. Research on the effects of child maltreatment often collapses various forms of maltreatment (e.g. TL, functioning as an indicator of cellular aging, may then represent a useful metric to quantify the impact psychological trauma has at the cellular level. Age-dependent shortening of telomeres, coupled with shortening observed due to stressor exposure, has given rise to the view of telomeres as cellular ‘clocks’ that can be used to distinguish biological age from chronological age ( Shalev et al., 2013a).
Similarly, children exposed to institutional care (orphanages) had faster rates of telomere shortening in a dose-response manner relative to those not exposed to institutional care ( Drury et al., 2012 Humphreys et al., 2016). (2013b) demonstrated that children exposed to multiple kinds of violence between age 5 and 10 years showed significantly more telomere erosion (i.e., by age 10) than peers. Experiencing trauma in childhood, for instance, has been linked to shorter TL cross-sectionally as well as to accelerated telomere shortening over time ( Pepper et al., 2018 Ridout et al., 2018). TL has been established as a hallmark of aging ( López-Otín et al., 2013) and thus, may serve as a useful indicator of accelerated aging due to trauma exposure ( Ridout et al., 2018 Shalev, 2012). Telomere length (TL), a measure of cellular aging, has been suggested as a link between traumatic childhood experiences and the disproportionate disease burden impacting survivors.
However, mechanisms conferring this risk at the biological level remain largely unknown. Exposure to trauma during childhood can lead to increased risk for poor health outcomes in adulthood ( Irish et al., 2010 Miller et al., 2011 Nusslock & Miller, 2016 Trickett et al., 2011).
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