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Background: Telomeres have been identified as a biomarker of cellular aging whereby shorter telomeres are linked to increased morbidity and earlier mortality (Entringer et al., 2015). Telomere erosion may be an important mechanism through which children faced with early life stress experience adverse biological and behavioral consequences (Drury et al., 2014). For instance, experiences of self-reported childhood trauma or abuse are associated with shorter telomeres in adulthood (Fagundes et al., 2013). The vast majority of research linking telomere length to adverse outcomes has been conducted with adults; however, we know much less about accelerated rates of telomere shortening in children. Therefore, the current study aims to explore risk factors for more rapid cellular aging in a sample of primarily low-income toddlers using a novel and simple method of collecting salivary DNA.
Methods: Participants were 66 preschoolers (6 to 45 months, M=23.95) and their mothers were recruited as part of a larger study to explore early biological mechanisms of resiliency in children experiencing early life stress. The participants were primarily from families experiencing financial stress, with 73.4% of families reporting family income at or below the poverty line. Lab members administered cheek swabs to participants to collect salivary DNA samples from children, and mothers independently provided saliva in test tubes. Relative telomere length values were determined using the quantitative polymerase chain reaction method (qPCR; Cawthon, 2002). Mothers completed the Life Events Checklist for children (LEC; Jackson et al., 2000), which captures stressful or traumatic events in the child’s life, as well as a questionnaire asking about participation in government-related services (e.g., Welfare, Food Stamps, WIC).
Results: Regression analyses indicated that more events endorsed in the LEC were linked to shorter child telomere length, controlling for child age and the mother’s telomere length, F(3, 41)=-.01, p<.05. That is, children’s telomere lengths were shorter over and above genetic predisposition to telomere length as a function of negative life events in the child’s lifetime. Additionally, among this primarily low-income sample greater use of government services was linked to longer telomere length in children, F(3, 60)=.01, p<.05, when controlling for child age and batch of analysis.
Conclusions: The current study supports studies with adults and older children linking shorter telomere length to greater exposure to traumatic and stressful experiences. Importantly, these results indicate that effects of early life stress may be seen as early as the first few years of life. Nevertheless, biological functioning of children in poverty also appears to be buffered from this stress via structured supports. This study also demonstrates that saliva samples for telomere length are methodologically feasible to collect in families facing adversity, and that telomere length may be a good candidate for an early biomarker of stress that can be collected in home or school environments. Ultimately, we hope to identify early interventions for positive parenting that can potentially buffer children from adverse consequences of early life stress via telomere lengthening, given some promising research of health-based interventions shown to slow the erosion of telomeres in children (Epel, 2012).
Amy Dominguez, University of Denver
Presenting Author
Lisa J. Schlueter, Children's Hospital Los Angeles, Sabin Research Institute
Non-Presenting Author
Marina Mendoza, Denver Preschool Program
Non-Presenting Author
Ariel Julian, University of Denver
Non-Presenting Author
Sarah Enos Watamura, UNIVERSITY OF DENVER
Non-Presenting Author