Kathryn K Ridout1, Stephanie H Parade2, Hung-Teh Kao1, Stevie Magnan3, Ronald Seifer2, Barbara Porton1, Lawrence H Price4, Audrey R Tyrka5. 1. Department of Psychiatry and Human Behavior, Alpert Medical School of Brown University, Providence, RI, USA. 2. Department of Psychiatry and Human Behavior, Alpert Medical School of Brown University, Providence, RI, USA; Bradley/Hasbro Children's Research Center, E. P. Bradley Hospital, East Providence, RI, USA. 3. Mood Disorders Research Program and Laboratory for Clinical and Translational Neuroscience, Butler Hospital, Providence, RI, USA. 4. Mood Disorders Research Program and Laboratory for Clinical and Translational Neuroscience, Butler Hospital, Providence, RI, USA; Department of Psychiatry and Human Behavior, Alpert Medical School of Brown University, Providence, RI, USA. 5. Mood Disorders Research Program and Laboratory for Clinical and Translational Neuroscience, Butler Hospital, Providence, RI, USA; Department of Psychiatry and Human Behavior, Alpert Medical School of Brown University, Providence, RI, USA. Electronic address: Audrey_Tyrka@Brown.edu.
Abstract
OBJECTIVE: Childhood maltreatment is a major risk factor for the development of behavioral problems and poor physical and mental health. Accelerated cellular aging, through reduced telomere length and mitochondrial dysfunction, may be a mechanism underlying these associations. METHODS: Families with (n = 133) and without (n = 123) child welfare documentation of moderate-severe maltreatment in the past six months participated in this study. Children ranged in age from 3 to 5 years, were racially and ethnically diverse, and 91% qualified for public assistance. Structured record review and interviews were used to assess a history of maltreatment and other adversities. Telomere length and mitochondrial DNA copy number (mtDNAcn) were measured from saliva DNA using real-time PCR. Measures were repeated at a six-month follow-up assessment. Repeated measures general linear models were used to examine the effects of maltreatment and other adversities on telomere length and mtDNAcn over time. RESULTS: Maltreatment and other adverse experiences were significant positive predictors of both telomere length and mtDNAcn over time. Internalizing and externalizing behavior problems were also both significantly associated with telomere length, but only internalizing symptoms were associated with mtDNAcn. CONCLUSIONS: This is the first study to show that mtDNAcn is altered in children with stress and trauma, and the findings are consistent with recent studies of adults. Surprisingly, children who experienced moderate-severe levels of maltreatment in the prior six months had longer telomeres, possibly reflecting compensatory changes in response to recent trauma. Telomere length and mtDNAcn were also associated with behavioral problems, suggesting that these measures of cellular aging may be causally implicated in the pathophysiology of stress-related conditions.
OBJECTIVE: Childhood maltreatment is a major risk factor for the development of behavioral problems and poor physical and mental health. Accelerated cellular aging, through reduced telomere length and mitochondrial dysfunction, may be a mechanism underlying these associations. METHODS: Families with (n = 133) and without (n = 123) child welfare documentation of moderate-severe maltreatment in the past six months participated in this study. Children ranged in age from 3 to 5 years, were racially and ethnically diverse, and 91% qualified for public assistance. Structured record review and interviews were used to assess a history of maltreatment and other adversities. Telomere length and mitochondrial DNA copy number (mtDNAcn) were measured from saliva DNA using real-time PCR. Measures were repeated at a six-month follow-up assessment. Repeated measures general linear models were used to examine the effects of maltreatment and other adversities on telomere length and mtDNAcn over time. RESULTS: Maltreatment and other adverse experiences were significant positive predictors of both telomere length and mtDNAcn over time. Internalizing and externalizing behavior problems were also both significantly associated with telomere length, but only internalizing symptoms were associated with mtDNAcn. CONCLUSIONS: This is the first study to show that mtDNAcn is altered in children with stress and trauma, and the findings are consistent with recent studies of adults. Surprisingly, children who experienced moderate-severe levels of maltreatment in the prior six months had longer telomeres, possibly reflecting compensatory changes in response to recent trauma. Telomere length and mtDNAcn were also associated with behavioral problems, suggesting that these measures of cellular aging may be causally implicated in the pathophysiology of stress-related conditions.
Authors: Johan Fernström; Synthia H Mellon; Marlon A McGill; Martin Picard; Victor I Reus; Christina M Hough; Jue Lin; Elissa S Epel; Owen M Wolkowitz; Daniel Lindqvist Journal: Transl Psychiatry Date: 2021-11-17 Impact factor: 6.222
Authors: Jonatan A Mendoza-Ortega; Enrique Reyes-Muñoz; Sonia Nava-Salazar; Sandra Rodríguez-Martínez; Sandra B Parra-Hernández; Lourdes Schnaas; Blanca Vianey Suárez-Rico; Libni A Torres-Olascoaga; Andrea A Baccarelli; Rosalind J Wright; Robert O Wright; Guadalupe Estrada-Gutierrez; Marcela Tamayo-Ortiz Journal: Int J Environ Res Public Health Date: 2021-11-10 Impact factor: 3.390