Association between childhood trauma and accelerated telomere erosion in adulthood: A meta-analytic study

Li, Zongchang; Hé, Ying; Wang, Dong; Tang, Jian; Chen, Xiaogang

doi:10.1016/j.jpsychires.2017.06.002

Cited by 69 publications

(58 citation statements)

References 60 publications

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“…Some other large-scale studies have not found effects of childhood adversity on TL (e.g., van Ockenburg et al, 2015;Verhoeven et al, 2015), which, again, may be due to differences in stress measurement (e.g., limited assessment of chronic childhood stressors). Nevertheless, the critical role of cumulative childhood adversity on LTL is consistent with mostly cross-sectional descriptive and meta-analytic findings (Coimbra et al, 2017;Hanssen et al, 2017;Li et al, 2017;Price et al, 2013;Ridout et al, 2017;Shalev et al, 2013a), as well as with prospective evidence (Shalev et al, 2013b). Our posthoc results also suggest that the early developmental years may be particularly important for shaping LTL attrition in adulthood, though replication is needed in samples with greater stress exposure in early and middle childhood as well as adolescence.…”

Section: Discussionsupporting

confidence: 85%

“…Tyrka et al (Tyrka et al, 2010) provided the first evidence for shortened TL in adults with a history of childhood maltreatment. Three meta-analyses have since demonstrated a dosedependent relationship between various types of childhood adversity and shorter telomeres (Hanssen et al, 2017;Li et al, 2017;Ridout et al, 2017). However, the vast majority of studies have assessed TL cross-sectionally (e.g., Puterman et al, 2016), limiting our understanding of how early adversity affects adult telomere shortening over time (i.e., "telomere attrition").…”

Section: Introductionmentioning

confidence: 99%

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Cumulative lifetime stress exposure and leukocyte telomere length attrition: The unique role of stressor duration and exposure timing

Mayer

Prather

Puterman

et al. 2019

Psychoneuroendocrinology

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Background: Stress exposure occurring across the lifespan increases risk for disease, potentially involving telomere length shortening. Stress exposure during childhood and adulthood has been cross-sectionally linked with shorter telomere length. However, few longitudinal studies have examined telomere length attrition over time, and none have investigated how stressor duration (acute life events vs. chronic difficulties), timing (childhood vs. adulthood), and perceived severity may be uniquely related to telomere length shortening. Methods: To address these issues, we administered a standardized instrument for assessing cumulative lifetime stress exposure (Stress and Adversity Inventory; STRAIN) to 175 mothers of children with Autism Spectrum Disorder or neurotypical children and measured their leukocyte telomere length (LTL) at baseline and 2 years later. Results: Greater count of lifetime stressors was associated with shorter LTL at baseline and greater LTL attrition over time. When separating lifetime stressors into acute life events and chronic difficulties, only greater count of chronic difficulties significantly predicted shorter baseline LTL and greater LTL attrition. Similarly, when examining timing of stressor exposure, only greater count of chronic childhood difficulties (age < 18) significantly predicted shorter baseline LTL and greater LTL attrition over the 2-year period in mid-life. Importantly, these results *

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Section: Discussionsupporting

confidence: 85%

Section: Introductionmentioning

confidence: 99%

Cumulative lifetime stress exposure and leukocyte telomere length attrition: The unique role of stressor duration and exposure timing

Mayer

Prather

Puterman

et al. 2019

Psychoneuroendocrinology

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“…A recent study by Mitchell et al (264) also found a significant association between father loss and children's telomere length, with the death of father showing the greatest effect, and a 90% greater effect in the children with the most reactive alleles of the 5-HTTLPR gene. Finally, two current meta-analytic studies, confirmed the significant association between ELS/CT and accelerated telomere erosion in adulthood (265,266). ELS/CT could, thus, possibly partly mediate their long-term biological impact also through shorter telomere length, representing another biomarker of increased cacostatic load (51,256).…”

Section: Telomere Lengthsupporting

confidence: 71%

Developmental Trajectories of Early Life Stress and Trauma: A Narrative Review on Neurobiological Aspects Beyond Stress System Dysregulation

et al. 2019

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Early life stressors display a high universal prevalence and constitute a major public health problem. Prolonged psychoneurobiological alterations as sequelae of early life stress (ELS) could represent a developmental risk factor and mediate risk for disease, leading to higher physical and mental morbidity rates in later life. ELS could exert a programming effect on sensitive neuronal brain networks related to the stress response during critical periods of development and thus lead to enduring hyper- or hypo-activation of the stress system and altered glucocorticoid signaling. In addition, alterations in emotional and autonomic reactivity, circadian rhythm disruption, functional and structural changes in the brain, as well as immune and metabolic dysregulation have been lately identified as important risk factors for a chronically impaired homeostatic balance after ELS. Furthermore, human genetic background and epigenetic modifications through stress-related gene expression could interact with these alterations and explain inter-individual variation in vulnerability or resilience to stress. This narrative review presents relevant evidence from mainly human research on the ten most acknowledged neurobiological allostatic pathways exerting enduring adverse effects of ELS even decades later (hypothalamic-pituitary-adrenal axis, autonomic nervous system, immune system and inflammation, oxidative stress, cardiovascular system, gut microbiome, sleep and circadian system, genetics, epigenetics, structural, and functional brain correlates). Although most findings back a causal relation between ELS and psychobiological maladjustment in later life, the precise developmental trajectories and their temporal coincidence has not been elucidated as yet. Future studies should prospectively investigate putative mediators and their temporal sequence, while considering the potentially delayed time-frame for their phenotypical expression. Better screening strategies for ELS are needed for a better individual prevention and treatment.

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“…Advanced biological aging (i.e an increased biological clock) has been associated to poor somatic health, including the onset of aging-related somatic diseases such as cardiovascular disease, diabetes and cognitive decline 3 . Advanced biological aging has also been correlated to mental health: childhood trauma 5 , psychological stress and psychiatric disorders 6,7 .…”

Section: Introductionmentioning

confidence: 99%

An integrative study of five biological clocks in somatic and mental health

Jansen

Verhoeven

Han

et al. 2020

Preprint

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1 5 15 20 ABSTRACT Biological clocks have been developed at different molecular levels and were found to be more advanced in the presence of somatic illnesses and mental disorders. However, it is unclear whether different biological clocks reflect similar aging processes and determinants. In ~3000 subjects, we examined whether 5 biological clocks (telomere length, epigenetic, transcriptomic, proteomic and metabolomic clocks) were interrelated and associated to somatic and mental health determinants.Correlations between biological clocks were small (all r<0.2), indicating little overlap. The most consistent associations with the advanced biological clocks were found for male sex, higher BMI, metabolic syndrome, smoking and depression. As compared to the individual clocks, a composite index of all five clocks showed most pronounced associations with health determinants. The large effect sizes of the composite index and the low correlation between biological clocks, indicate that one's biological age is best reflected by combining aging measures from multiple cellular levels. 2 30 35 40 45

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Association between childhood trauma and accelerated telomere erosion in adulthood: A meta-analytic study

Cited by 69 publications

References 60 publications

Cumulative lifetime stress exposure and leukocyte telomere length attrition: The unique role of stressor duration and exposure timing

Cumulative lifetime stress exposure and leukocyte telomere length attrition: The unique role of stressor duration and exposure timing

Developmental Trajectories of Early Life Stress and Trauma: A Narrative Review on Neurobiological Aspects Beyond Stress System Dysregulation

An integrative study of five biological clocks in somatic and mental health

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