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Biological aging in childhood and adolescence following experiences of threat and deprivation: A systematic review and meta-analysis.

ABSTRACT: Life history theory argues that exposure to early life adversity (ELA) accelerates development, although existing evidence for this varies. We present a meta-analysis and systematic review testing the hypothesis that ELA involving threat (e.g., violence exposure) will be associated with accelerated biological aging across multiple metrics, whereas exposure to deprivation (e.g., neglect, institutional rearing) and low-socioeconomic status (SES) will not. We meta-analyze 54 studies (n = 116,010) examining associations of ELA with pubertal timing and cellular aging (telomere length and DNA methylation age), systematically review 25 studies (n = 3,253) examining ELA and neural markers of accelerated development (cortical thickness and amygdala-prefrontal cortex functional connectivity) and evaluate whether associations of ELA with biological aging vary according to the nature of adversity experienced. ELA overall was associated with accelerated pubertal timing (d = -0.10) and cellular aging (d = -0.21), but these associations varied by adversity type. Moderator analysis revealed that ELA characterized by threat was associated with accelerated pubertal development (d = -0.26) and accelerated cellular aging (d = -0.43), but deprivation and SES were unrelated to accelerated development. Systematic review revealed associations between ELA and accelerated cortical thinning, with threat-related ELA consistently associated with thinning in ventromedial prefrontal cortex, and deprivation and SES associated with thinning in frontoparietal, default, and visual networks. There was no consistent association of ELA with amygdala-PFC connectivity. These findings suggest specificity in the types of early environmental experiences associated with accelerated biological aging and highlight the importance of evaluating how accelerated aging contributes to health disparities and whether this process can be mitigated through early intervention. (PsycInfo Database Record (c) 2020 APA, all rights reserved).

SUBMITTER: Colich NL

PROVIDER: S-EPMC7484378 | biostudies-literature | 2020 Sep

REPOSITORIES: biostudies-literature

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Biological aging in childhood and adolescence following experiences of threat and deprivation: A systematic review and meta-analysis.

Colich Natalie L NL Rosen Maya L ML Williams Eileen S ES McLaughlin Katie A KA

Psychological bulletin 20200803 9

Life history theory argues that exposure to early life adversity (ELA) accelerates development, although existing evidence for this varies. We present a meta-analysis and systematic review testing the hypothesis that ELA involving threat (e.g., violence exposure) will be associated with accelerated biological aging across multiple metrics, whereas exposure to deprivation (e.g., neglect, institutional rearing) and low-socioeconomic status (SES) will not. We meta-analyze 54 studies (<i>n</i> = 116 ...[more]

PMID: 32744840

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Project description:ImportanceMany studies have demonstrated an association between early-life adversity (ELA) and executive functioning in children and adolescents. However, the aggregate magnitude of this association is unknown in the context of threat and deprivation types of adversity and various executive functioning domains.ObjectiveTo test the hypothesis that experiences of deprivation are more strongly associated with reduced executive functioning compared with experiences of threat during childhood and adolescence.Data sourcesEmbase, ERIC, MEDLINE, and PsycInfo databases were searched from inception to December 31, 2020. Both forward and reverse snowball citation searches were performed to identify additional articles.Study selectionArticles were selected for inclusion if they (1) had a child and/or adolescent sample, (2) included measures of ELA, (3) measured executive functioning, (4) evaluated the association between adversity and executive functioning, (5) were published in a peer-reviewed journal, and (6) were published in the English language. No temporal or geographic limits were set. A 2-reviewer, blinded screening process was conducted.Data extraction and synthesisPRISMA guidelines were used to guide data extraction and article diagnostics (for heterogeneity, small study bias, and p-hacking). Article quality was assessed, and data extraction was performed by multiple independent observers. A 3-level meta-analytic model with a restricted maximum likelihood method was used. Moderator analyses were conducted to explore heterogeneity.Main outcomes and measuresPrimary outcomes included measures of the 3 domains of executive functioning: cognitive flexibility, inhibitory control, and working memory.ResultsA total of 91 articles were included, representing 82 unique cohorts and 31 188 unique individuals. Deprivation, compared with threat, was associated with significantly lower inhibitory control (F1,90 = 5.69; P = .02) and working memory (F1,54 = 5.78; P = .02). No significant difference was observed for cognitive flexibility (F1,36 = 2.38; P = .12). The pooled effect size of the association of inhibitory control with deprivation was stronger (Hedges g = -0.43; 95% CI, -0.57 to -0.29) compared with threat (Hedges g = -0.27; 95% CI, -0.46 to -0.08). The pooled effect size of the association of working memory with deprivation was stronger (Hedges g = -0.54; 95% CI, -0.75 to -0.33) compared with threat (Hedges g = -0.28; 95% CI, -0.51 to -0.05).Conclusions and relevanceExperiences of both threat and deprivation in childhood and adolescence were associated with reduced executive functioning, but the association was stronger for exposure to deprivation. Efforts to address the consequences of ELA for development should consider the associations between specific dimensions of adversity and specific developmental outcomes.

Project description:BackgroundNeighborhood deprivation adversely effects neurodevelopment and cognitive function; however, mechanisms remain unexplored. Neighborhood deprivation could be particularly impactful in late childhood/early adolescence, in neural regions with protracted developmental trajectories, e.g., prefrontal cortex (PFC).MethodsThe Adolescent Brain Cognitive Development (ABCD) study recruited 10,205 youth. Geocoded residential history was used to extract individual neighborhood characteristics. A general cognitive ability index and MRI scans were completed. Associations with neurocognition were examined. The relation of PFC surface area and cortical thickness to neighborhood deprivation was tested. PFC subregions and asymmetry, with putative differential environmental susceptibility during key developmental periods, were explored. Analyses tested PFC area as a possible mediating mechanism.ResultsNeighborhood deprivation predicted neurocognitive performance (β = -0.11), even after accounting for parental education and household income (β = -0.07). Higher neighborhood deprivation related to greater overall PFC surface area (ηp2 = 0.003), and differences in leftward asymmetry were observed for area (ηp2 = 0.001), and thickness (ηp2 = 0.003). Subregion analyses highlighted differences among critical areas that are actively developing in late childhood/early adolescence and are essential to modulating high order cognitive function. These included orbitofrontal, superior frontal, rostral middle frontal, and frontal pole regions (Cohen's d = 0.03-0.09). PFC surface area partially mediated the relation between neighborhood deprivation and neurocognition.DiscussionNeighborhood deprivation related to cognitive function (a foundational skill tied to a range of lifetime outcomes) and PFC morphology, with evidence found for partial mediation of PFC on neurocognitive function. Results inform public health conceptualizations of development and environmental vulnerability.

Project description:Epigenetic mechanisms are potential mediators of the physiological response to abuse by altering the genetic predisposition of the cellular response to the environment, leading to changes in the regulation of multiple organ systems. This study was established to review the epigenetic mechanisms associated with childhood abuse as well as the long-term determinants that these epigenetic changes may have on future illness. We retrospectively analysed the effect of exposure to adverse childhood experiences (ACEs, specifically those relating to childhood maltreatment) between the ages of 0 and 16 years on the human epigenome, as well as possible clinical associations. After meeting inclusion and exclusion criteria, 36 articles were included in this systematic review. Eight of these studies did not find a relationship between childhood maltreatment and DNA methylation. Of the remaining 28 studies, nine were genome-wide association studies, whereas the rest were candidate gene studies, mainly studying effects on neuroendocrine, serotoninergic and immunoregulatory systems. Meta-analysis of correlation coefficients from candidate gene studies estimated an association of childhood adversity and DNA methylation variation at r = 0.291 (P < 0.0001), and meta-analysis of two epigenome-wide association studies (EWASs) identified 44 differentially methylated CpG sites. In conclusion, childhood maltreatment may mediate epigenetic mechanisms through DNA methylation, thereby affecting physiological responses and conferring a predisposition to an increased risk for psychopathology and forensic repercussions. Similar evidence for somatic illnesses is not yet available. KEY POINTSAdverse childhood experiences are associated with increased mortality partly explained by acquired epigenetic changesThere is a positive correlation between childhood abuse and DNA methylation at specific gene sitesThe cumulative effect of different types of childhood abuse and neglect may lead to changes in DNA methylationEpigenome changes associated with childhood abuse appear to be involved in the development of psychiatric illness in adulthoodStudying epigenetic changes may have important public health and forensic applications in the future.

Project description:To quantify the tracking of apolipoprotein B (apoB) levels from childhood and adolescence and compare the tracking of apoB with low-density lipoprotein (LDL) cholesterol, a systematic search of MEDLINE, Embase, Web of Science, and Google Scholar was performed in October 2023 (PROSPERO protocol: CRD42022298663). Cohort studies that measured tracking of apoB from childhood/adolescence (< 19 years) with a minimum follow-up of 1 year, using tracking estimates such as correlation coefficients or tracking coefficients, were eligible. Pooled correlations were estimated using random-effects meta-analysis. Risk of bias was assessed with a review-specific tool. Ten studies of eight unique cohorts involving 4677 participants met the inclusion criteria. Tracking of apoB was observed (pooled r = 0.63; 95% confidence interval [CI] = 0.53-0.71; I2 = 96%) with no significant sources of heterogeneity identified. Data from five cohorts with tracking data for both lipids showed the degree of tracking was similar for apoB (pooled r = 0.59; 95% CI = 0.55-0.63) and LDL cholesterol (pooled r = 0.58; 95% CI = 0.47-0.68). Study risk of bias was moderate, mostly due to attrition and insufficient reporting.ConclusionApoB levels track strongly from childhood, but do not surpass LDL cholesterol in this regard. While there is strong evidence that apoB is more effective at predicting ASCVD risk than LDL cholesterol in adults, there is currently insufficient evidence to support its increased utility in pediatric settings. This also applies to tracking data, where more comprehensive data are required.What is known• Apolipoprotein B is a known cause of atherosclerotic cardiovascular disease. • Apolipoprotein B levels are not typically measured in pediatric settings, where low-density lipoprotein cholesterol remains the primary lipid screening measure.What is new• This meta-analysis of 10 studies showed apolipoprotein B levels tracked strongly from childhood but did not exceed low-density lipoprotein cholesterol in this regard. • More comprehensive tracking data are needed to provide sufficient evidence for increased utility of apolipoprotein B in pediatric settings.

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Biological aging in childhood and adolescence following experiences of threat and deprivation: A systematic review and meta-analysis.

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Biological aging in childhood and adolescence following experiences of threat and deprivation: A systematic review and meta-analysis.

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