Adverse Childhood Experiences Run Deep: Toxic Early Life Stress, Telomeres, and Mitochondrial DNA Copy Number, the Biological Markers of Cumulative Stress

Ridout, Kathryn K.; Khan, Mariam; Ridout, Samuel J.

doi:10.1002/bies.201800077

Cited by 89 publications

(61 citation statements)

References 125 publications

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“…All three markers investigated in this study have been shown to be influenced by stress exposure, which may be acting as a mediator in BD's accelerated aging process. Oxidative stress, which is characterized by an imbalance between oxidants and antioxidants in favor of the oxidants, is known to disrupt the redox signaling and control and accelerate aging processes by leading to accumulation of cellular damage .…”

Section: Discussionmentioning

confidence: 89%

Accelerated hippocampal biological aging in bipolar disorder

et al. 2019

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Objectives Evidence suggests accelerated aging mechanisms in bipolar disorder (BD), including DNA methylation (DNAm) aging in blood. However, it is unknown whether such mechanisms are also evident in the brain, in particular in association with other biological clocks. To investigate this, we interrogated genome‐wide DNAm in postmortem hippocampus from 32 BD‐I patients and 32 non‐psychiatric controls group‐matched for age and sex from the NIMH Human Brain Collection Core. Methods DNAm age and epigenetic aging acceleration were estimated using the Horvath method. Telomere length (TL) and mitochondrial DNA (mtDNA) copy number were quantified by real‐time PCR. Between‐group differences were assessed by linear regression and univariate general linear models with age, sex, race, postmortem interval, tissue pH, smoking, and body mass index included as co‐variates. Results Groups did not differ for epigenetic aging acceleration when considering the entire sample. However, after splitting the sample by the median age, an epigenetic aging acceleration was detected in patients compared to controls among older subjects (P = .042). While TL did not differ between groups, a reduction in mtDNA copy number was observed in patients compared to controls (P = .047). In addition, significant correlations were observed between epigenetic aging acceleration and TL (r = −.337, P = .006), as well as between TL and mtDNA copy number (r = .274, P = .028). Conclusions Hippocampal aging may underlie neurocognitive dysfunctions observed in BD patients. Moreover, our results suggest a complex cross‐talk between biological clocks in hippocampus that may underlie clinical manifestations of premature aging in BD.

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Section: Discussionmentioning

confidence: 89%

Accelerated hippocampal biological aging in bipolar disorder

et al. 2019

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“…However, one must not get 11 carried away with how this is framed. While, on the one hand there is evidence for 'biological marks of stress' (Ridout et al, 2018), this is quite simply a sign of normal functioning. If we were able to examine all of our molecular and physiological structures, we would find biological marks for many other of our experiences, and some of these would probably affect our health.…”

Section: Adverse Childhood Experiences Emerge In Social Epidemiologymentioning

confidence: 99%

A Critique of the Adverse Childhood Experiences Framework in Epidemiology and Public Health: Uses and Misuses

Kelly-Irving¹,

Delpierre²

2019

Preprint

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Adverse childhood experiences (ACEs) have emerged as a major research theme. They make reference to an array of potentially harmful exposures occurring from birth to 18 years of age and may be involved in the construction of health inequalities over the lifecourse. As with many simplified concepts, ACEs present limitations. They include diverse types of exposures, are often considered cumulatively, can be identified using prospective and retrospective approaches, and their multidimensional nature may lead to greater measurement error. From a public health perspective, ACEs are useful for describing the need to act upon complex social environments to prevent health inequalities at a population level. As the ACEs concept becomes popular in the context of policy interventions, concerns have emerged. As a probabilistic and population-level tool, they are not adapted to diagnose individual-level vulnerabilities, an approach which could ultimately exacerbate inequalities. Here, we present a critique of the ACEs framework, discussing its strengths and limits.

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“…Childhood trauma also increases the risk of respiratory, heart, and metabolic diseases [ 13 ]. Childhood trauma deteriorates health through various mechanisms such as systemic inflammation [ 14 ], reducing telomere length [ 15 , 16 , 17 , 18 ], and DNA methylation [ 19 , 20 , 21 ]. Exposure to childhood trauma also impacts the developing brain [ 22 ].…”

Section: Introductionmentioning

confidence: 99%

Family Socioeconomic Status and Exposure to Childhood Trauma: Racial Differences

Assari

2020

Children

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Background: Minorities’ diminished returns (MDRs) refer to weaker effects of socioeconomic status (SES) indicators such as parental educational attainment and family income in generating tangible childhood outcomes for racial and ethnic minorities compared to the majority group, a pattern prevalent in the US. Our existing knowledge is minimal, however, about diminished returns of family SES on reducing exposure to childhood trauma. Aim: To determine if there was a difference between non-Hispanic whites (NHW) and non-Hispanic blacks (NHB) in the effect of SES on exposure to childhood trauma among children ages 8–11 years old. Materials and methods: In this cross-sectional study, we analyzed data from 4696 NHW or NHB American 8–11-year-old children who were participants in the Adolescent Brain Cognitive Development (ABCD) Study. The independent variables were parental educational attainment and family income. The primary outcome was exposure to 1 or 2+ childhood traumas, measured by the Kiddie Schedule for Affective Disorders and Schizophrenia (K-SADS) semi-structured interview. Polynomial regression was used for data analysis. Results: Parental education and family income had statistically significant protective (negative) effects on childhood trauma, indicating children from high income and highly educated families were exposed to a lower level of childhood trauma. However, race/ethnicity showed statistically significant interactions with parental education and family income on exposure to childhood trauma, indicating weaker protective effects of parental education and family income on reducing exposure to trauma for NHB compared to NHW children. Race-specific models showed protective effects of parental education and family income on exposure to childhood trauma for NHW but not NHB children. Conclusion: The protective effects of parental education and family income against exposure to childhood trauma are systematically diminished for NHBs compared to NHWs. To minimize the racial/ethnic health gaps, diminished returns of parental education and family income should be addressed. There is a need for programs and interventions that equalize not only SES but also the marginal returns of SES for ethnic groups. Such efforts require addressing structural and societal barriers that hinder NHB families from translating their SES resources into tangible outcomes. There is a need for studies that can minimize MDRs for NHB families, such that SES can similarly secure tangible outcomes in the presence of SES resources.

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Adverse Childhood Experiences Run Deep: Toxic Early Life Stress, Telomeres, and Mitochondrial DNA Copy Number, the Biological Markers of Cumulative Stress

Cited by 89 publications

References 125 publications

Accelerated hippocampal biological aging in bipolar disorder

Accelerated hippocampal biological aging in bipolar disorder

A Critique of the Adverse Childhood Experiences Framework in Epidemiology and Public Health: Uses and Misuses

Family Socioeconomic Status and Exposure to Childhood Trauma: Racial Differences

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