Unraveling the Meaning of Telomeres for Child Psychiatry

Drury, Stacy S.

doi:10.1016/j.jaac.2015.04.009

Cited by 5 publications

(5 citation statements)

References 15 publications

(12 reference statements)

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“…In females, the interaction between foster mother group and expected biological caregiving is consistent with the adaptive calibration model or mismatch theory (Del Giudice, Ellis, & Shirtcliff, 2011; Hostinar & Gunnar, 2013), which suggests ancestral experiences guide the developmental trajectory of the offspring (or even future generations) to match that expected environment. Postnatal environmental changes/mismatches with ancestral environment, either positive or negative, necessitate recalibration of physiological systems from the programmed pattern, that while adaptive, come at a biological cost, including increased oxidative stress and cellular metabolism, factors captured by telomere dynamics (Drury, 2015; Epel, 2009). In males, however, telomere attrition is more in line with a cumulative risk model.…”

Section: Discussionmentioning

confidence: 99%

Shaping long-term primate development: Telomere length trajectory as an indicator of early maternal maltreatment and predictor of future physiologic regulation

et al. 2017

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The molecular, neurobiological, and physical health impacts of child maltreatment are well established, yet mechanistic pathways remain inadequately defined. Telomere length (TL) decline is an emerging molecular indicator of stress exposure with definitive links to negative health outcomes in maltreated individuals. The multiple confounders endemic to human maltreatment research impede the identification of causal pathways. This study leverages a unique randomized, cross-foster, study design in a naturalistic translational nonhuman primate model of infant maltreatment. At birth, newborn macaques were randomly assigned to either a maltreating or a competent control mother, balancing for sex, biological mother parenting history, and social rank. Offspring TL was measured longitudinally across the first 6 months of life (infancy) from peripheral blood. Hair cortisol accumulation was also determined at 6, 12, and 18 months of age. TL decline was greater in animals randomized to maltreatment, but also interacted with biological mother group. Shorter TL at 6 months was associated with higher mean cortisol levels through 18 months (juvenile period) when controlling for relevant covariates. These results suggest that even under the equivalent social, nutritional, and environmental conditions feasible in naturalistic translational nonhuman primate models, early adverse caregiving results in lasting molecular scars that foreshadow elevated health risk and physiologic dysregulation.

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Section: Discussionmentioning

confidence: 99%

Shaping long-term primate development: Telomere length trajectory as an indicator of early maternal maltreatment and predictor of future physiologic regulation

et al. 2017

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“…The trajectory of TL change is likely a biological indicator of the lasting impact of early adversity and accelerated TL loss may foreshadow future health risks. Given that the strongest links to TL are found with cardiovascular disease and obesity, children exposed to early institutional care, similar to those exposed to maltreatment and chronic stress, should be carefully assessed not only for neurobehavioral and socio-emotional sequelae but also physical health parameters (Drury, 2015; Shonkoff and Garner, 2012). …”

Section: Discussionmentioning

confidence: 99%

Accelerated telomere shortening: Tracking the lasting impact of early institutional care at the cellular level

Humphreys

Esteves

Zeanah

et al. 2016

Psychiatry Research

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Studies examining the association between early adversity and longitudinal changes in telomere length within the same individual are rare, yet are likely to provide novel insight into the subsequent lasting effects of negative early experiences. We sought to examine the association between institutional care history and telomere shortening longitudinally across middle childhood and into adolescence. Buccal DNA was collected 2 to 4 times, between the ages of 6 and 15 years, in 79 children enrolled in the Bucharest Early Intervention Project (BEIP), a longitudinal study exploring the impact of early institutional rearing on child health and development. Children with a history of early institutional care (n=50) demonstrated significantly greater telomere shortening across middle childhood and adolescence compared to never institutionalized children (n=29). Among children with a history of institutional care, randomization to high quality foster care was not associated with differential telomere attrition across development. Cross-sectional analysis of children randomized to the care as usual group indicated shorter telomere length was associated with greater percent of the child’s life spent in institutional care up to age 8. These results suggest that early adverse care from severe psychosocial deprivation may be embedded at the molecular genetic level through accelerated telomere shortening.

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“…Besides several endogenous factors (e.g., inflammation, oxidative stress, and DNA damage), behavioral (e.g., smoking, physical activity, sleeping patterns, and meditation) and psychosocial factors (e.g., chronic and acute stress exposure, emotion regulatory processes, and social connections) have been described to either contribute to or protect against telomere attrition in PBMC (Jacobs et al, 2011;Puterman & Epel, 2012). To this end, TL has been suggested as a global sensor of changing cellular environments (Drury, 2015) and as a biomarker that integrates the cumulative effects of both adversity and resiliency factors on complex disease risk (Puterman & Epel, 2012). Tyrka et al (2010) provided first evidence for an association between CM and shortened PBMC TL decades later in life.…”

Section: Is Associated With Telomere Attritionmentioning

confidence: 99%

History of child maltreatment and telomere length in immune cell subsets: Associations with stress- and attachment-related hormones

Boeck¹,

Krause

Karabatsiakis³

et al. 2017

Dev Psychopathol

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Experiencing maltreatment during childhood can have long-lasting consequences for both mental and physical health. Immune cell telomere length (TL) shortening might be one link between child maltreatment (CM) experiences and adverse health outcomes later in life. While the stress hormone cortisol has been associated with TL attrition, the attachment-related hormone oxytocin may promote resilience. In 15 mothers with and 15 age- and body mass index-matched mothers without CM, we assessed TL in peripheral blood mononuclear cells and selected immune cell subsets (monocytes, naive, and memory cytotoxic T cells) by quantitative fluorescence in situ hybridization, as well as peripheral cortisol and oxytocin levels. Memory cytotoxic T cells showed significantly shorter TL in association with CM, whereas TL in monocytes and naive cytotoxic T cells did not significantly differ between the two groups. Across both groups, cortisol was negatively associated with TL, while oxytocin was positively associated with TL in memory cytotoxic T cells. These results indicate that long-lived memory cytotoxic T cells are most affected by the increased biological stress state associated with CM. Keeping in mind the correlational and preliminary nature of the results, the data suggest that cortisol may have a damaging and oxytocin a protective function on TL.

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Unraveling the Meaning of Telomeres for Child Psychiatry

Cited by 5 publications

References 15 publications

Shaping long-term primate development: Telomere length trajectory as an indicator of early maternal maltreatment and predictor of future physiologic regulation

Shaping long-term primate development: Telomere length trajectory as an indicator of early maternal maltreatment and predictor of future physiologic regulation

Accelerated telomere shortening: Tracking the lasting impact of early institutional care at the cellular level

History of child maltreatment and telomere length in immune cell subsets: Associations with stress- and attachment-related hormones

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