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Open AccessJournal ArticleDOI

Exposure to violence during childhood is associated with telomere erosion from 5 to 10 years of age: a longitudinal study

TLDR
Support is provided for a mechanism linking cumulative childhood stress to telomere maintenance, observed already at a young age, with potential impact for life-long health.
Abstract
There is increasing interest in discovering mechanisms that mediate the effects of childhood stress on late-life disease morbidity and mortality. Previous studies have suggested one potential mechanism linking stress to cellular aging, disease and mortality in humans: telomere erosion. We examined telomere erosion in relation to children’s exposure to violence, a salient early-life stressor, which has known long-term consequences for well-being and is a major public-health and social-welfare problem. In the first prospective-longitudinal study with repeated telomere measurements in children while they experienced stress, we tested the hypothesis that childhood violence exposure would accelerate telomere erosion from age 5 to age 10 years. Violence was assessed as exposure to maternal domestic violence, frequent bullying victimization and physical maltreatment by an adult. Participants were 236 children (49% females; 42% with one or more violence exposures) recruited from the Environmental-Risk Longitudinal Twin Study, a nationally representative 1994 -- 1995 birth cohort. Each child’s mean relative telomere length was measured simultaneously in baseline and follow-up DNA samples, using the quantitative PCR method for T/S ratio (the ratio of telomere repeat copy numbers to single-copy gene numbers). Compared with their counterparts, the children who experienced two or more kinds of violence exposure showed significantly more telomere erosion between age-5 baseline and age-10 follow-up measurements, even after adjusting for sex, socioeconomic status and body mass index (B ¼� 0.052, s.e. ¼ 0.021, P ¼ 0.015). This finding provides support for a mechanism linking cumulative childhood stress to telomere maintenance, observed already at a young age, with potential impact for life-long health.

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Journal ArticleDOI

Adult psychiatric outcomes of bullying and being bullied by peers in childhood and adolescence.

TL;DR: The effects of being bullied are direct, pleiotropic, and long-lasting, with the worst effects for those who are both victims and bullies.
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Adult Health Outcomes of Childhood Bullying Victimization: Evidence From a Five-Decade Longitudinal British Birth Cohort

TL;DR: Midlife outcomes of childhood bullying victimization was associated with a lack of social relationships, economic hardship, and poor perceived quality of life at age 50, and interventions need to reduce bullying exposure in childhood and minimize long-term effects on victims' well-being.
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The Biological Effects of Childhood Trauma

TL;DR: This article focuses on peer-reviewed literature on the neurobiological sequelae of childhood trauma in children and in adults with histories of Childhood trauma.
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Paradise Lost: The Neurobiological and Clinical Consequences of Child Abuse and Neglect

TL;DR: This Review summarizes many of the persistent biological alterations associated with childhood maltreatment including changes in neuroendocrine and neurotransmitter systems and pro-inflammatory cytokines in addition to specific alterations in brain areas associated with mood regulation.
References
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Journal ArticleDOI

Relationship of childhood abuse and household dysfunction to many of the leading causes of death in adults. The Adverse Childhood Experiences (ACE) Study

TL;DR: For example, this article found a strong relationship between the breadth of exposure to abuse or household dysfunction during childhood and multiple risk factors for several of the leading causes of death in adults.
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The serial cultivation of human diploid cell strains.

TL;DR: A consideration of the cause of the eventual degeneration of these strains leads to the hypothesis that non-cumulative external factors are excluded and that the phenomenon is attributable to intrinsic factors which are expressed as senescence at the cellular level.
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Telomeres shorten during ageing of human fibroblasts.

TL;DR: The amount and length of telomeric DNA in human fibroblasts does in fact decrease as a function of serial passage during ageing in vitro and possibly in vivo.
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Telomere measurement by quantitative PCR

TL;DR: A primer pair is presented that eliminates the problem of presumed impossible to measure telomeres in vertebrate DNA by PCR amplification with oligonucleotide primers designed to hybridize to the TTAGGG and CCCTAA repeats, allowing simple and rapid measurement of telomere length in a closed tube, fluorescence-based assay.
Journal ArticleDOI

Accelerated telomere shortening in response to life stress

TL;DR: Evidence is provided that psychological stress--both perceived stress and chronicity of stress--is significantly associated with higher oxidative stress, lower telomerase activity, and shorter telomere length, in peripheral blood mononuclear cells from healthy premenopausal women.
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