Laura Etzel1, Waylon J Hastings1, Brooke C Mattern1, Monica L Oxford2, Christine Heim3, Frank W Putnam4, Jennie G Noll5, Idan Shalev6. 1. Department of Biobehavioral Health, The Pennsylvania State University, University Park, PA, USA. 2. Department of Family and Child Nursing, University of Washington, Seattle, WA, USA. 3. Department of Biobehavioral Health, The Pennsylvania State University, University Park, PA, USA; Charité - Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität zu Berlin, Berlin Institute of Health (BIH), Institute of Medical Psychology, Berlin, Germany. 4. Department of Psychiatry, University of North Carolina School of Medicine, Chapel Hill, NC, USA. 5. Department of Human Development and Family Studies, The Pennsylvania State University, University Park, PA, USA. 6. Department of Biobehavioral Health, The Pennsylvania State University, University Park, PA, USA. Electronic address: ius14@psu.edu.
Abstract
BACKGROUND: Exposure to maltreatment in childhood can lead to increased risk for poor health outcomes in adulthood. Child maltreatment and later poor health may be linked by premature biological aging. We tested whether childhood sexual abuse (CSA) was associated with telomere length (TL) in adult females. We further tested the hypothesis of intergenerational transmission of CSA-related effects by measuring TL in both CSA-exposed and non-exposed mothers and their children. METHODS: Participants were a subset of females and their children in a prospective-longitudinal cohort study of sexually abused females and a demographically comparable control group from the same Washington, D.C. area. TL was measured using qPCR in both leukocyte and buccal samples from females (N = 108, mean age 36.3 years) and buccal samples from their children (N = 124, mean age 10.5 years). Multilevel models were used to test associations between CSA-exposure and TL measured in leukocytes and buccal tissue in females and to test the intergenerational effect of maternal-CSA exposure on age-adjusted TL in their children. RESULTS: CSA-exposure was not associated with TL in adult females. Maternal TL and biological sex were significant predictors of child TL such that longer maternal TL predicted longer TL in children, and female children had longer TL than male children. However, maternal-CSA exposure did not predict TL in children. DISCUSSION: CSA-exposure was not associated with TL in this cohort of middle-aged females, nor was there evidence for an intergenerational effect of maternal-CSA exposure on child TL. This finding is in line with some previous results on CSA and adult TL. Previous significant results associating child maltreatment with shorter TL may be capturing a population of individuals exposed to either multiple types of maltreatment compared to controls with no childhood adversity, or maltreatment in childhood with concurrent TL measurements.
BACKGROUND: Exposure to maltreatment in childhood can lead to increased risk for poor health outcomes in adulthood. Child maltreatment and later poor health may be linked by premature biological aging. We tested whether childhood sexual abuse (CSA) was associated with telomere length (TL) in adult females. We further tested the hypothesis of intergenerational transmission of CSA-related effects by measuring TL in both CSA-exposed and non-exposed mothers and their children. METHODS:Participants were a subset of females and their children in a prospective-longitudinal cohort study of sexually abused females and a demographically comparable control group from the same Washington, D.C. area. TL was measured using qPCR in both leukocyte and buccal samples from females (N = 108, mean age 36.3 years) and buccal samples from their children (N = 124, mean age 10.5 years). Multilevel models were used to test associations between CSA-exposure and TL measured in leukocytes and buccal tissue in females and to test the intergenerational effect of maternal-CSA exposure on age-adjusted TL in their children. RESULTS:CSA-exposure was not associated with TL in adult females. Maternal TL and biological sex were significant predictors of child TL such that longer maternal TL predicted longer TL in children, and female children had longer TL than male children. However, maternal-CSA exposure did not predict TL in children. DISCUSSION: CSA-exposure was not associated with TL in this cohort of middle-aged females, nor was there evidence for an intergenerational effect of maternal-CSA exposure on child TL. This finding is in line with some previous results on CSA and adult TL. Previous significant results associating child maltreatment with shorter TL may be capturing a population of individuals exposed to either multiple types of maltreatment compared to controls with no childhood adversity, or maltreatment in childhood with concurrent TL measurements.
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