Impact Of Early Life Adversity Research Articles

Microglia: The Drunken Gardeners of Early Adversity.

Early life adversity (ELA) is a heterogeneous group of negative childhood experiences that can lead to abnormal brain development and more severe psychiatric, neurological, and medical conditions in adulthood. According to the immune hypothesis, ELA leads to an abnormal immune response characterized by high levels of inflammatory cytokines. This abnormal immune response contributes to more severe negative health outcomes and a refractory response to treatment in individuals with a history of ELA. Here, we examine this hypothesis in the context of recent rodent studies that focus on the impact of ELA on microglia, the resident immune cells in the brain. We review recent progress in our ability to mechanistically link molecular alterations in microglial function during a critical period of development with changes in synaptic connectivity, cognition, and stress reactivity later in life. We also examine recent research showing that ELA induces long-term alterations in microglial inflammatory response to "secondary hits" such as traumatic brain injury, substance use, and exposure to additional stress in adulthood. We conclude with a discussion on future directions and unresolved questions regarding the signals that modify microglial function and the clinical significance of rodent studies for humans.

291. Impact of Early Life Adversity on Reward Processing in Adolescents

291. Impact of Early Life Adversity on Reward Processing in Adolescents

Alterations in adolescent brain serotonin (5HT)1A, 5HT2A, and dopamine (D)2 receptor systems in a nonhuman primate model of early life adversity.

Stress affects brain serotonin (5HT) and dopamine (DA) function, and the effectiveness of 5HT and DA to regulate stress and emotional responses. However, our understanding of the long-term impact of early life adversity (ELA) on primate brain monoaminergic systems during adolescence is scarce and inconsistent. Filling this gap in the literature is critical, given that the emergence of psychopathology during adolescence has been related to deficits in these systems. Here, we use a translational nonhuman primate (NHP) model of ELA (infant maltreatment by the mother) to examine the long-term impact of ELA on adolescent 5HT1A, 5HT2A and D2 receptor systems. These receptor systems were chosen based on their involvement in stress/emotional control, as well as reward and reinforcement. Rates of maternal abuse, rejection, and infant's vocalizations were obtained during the first three postnatal months, and hair cortisol concentrations obtained at 6 months postnatal were examined as early predictors of binding potential (BP) values obtained during adolescence using positron emission tomography (PET) imaging. Maltreated animals demonstrated significantly lower 5HT1A receptor BP in prefrontal cortical areas as well as the amygdala and hippocampus, and lower 5HT2A receptor BP in striatal and prefrontal cortical areas. Maltreated animals also demonstrated significantly lower D2 BP in the amygdala. None of the behavioral and neuroendocrine measurements obtained early in life predicted any changes in BP data. Our findings suggest that early caregiving experiences regulate the development of brain 5HT and DA systems in primates, resulting in long-term effects evident during adolescence.

Impact of Early-Life Adversity on Cannabis Use: Exploring the Mediating and Moderating Effects of Chronic Pain.

Background: Although research suggests that early-life adversity (ELA) and cannabis use are linked, researchers have not established factors that mediate or modify this relationship. Identifying such factors could help in developing targeted interventions. We explored chronic pain as a potential mediator or moderator of this relationship. Methods: Using an online study, we collected cross-sectional data about ELA, cannabis use, and chronic pain to test whether ELA (adverse childhood experiences total score) is associated with cannabis use, and to examine pain as a potential mediator or moderator. Cannabis use was examined two ways: times used per day, and categorized as non-, some, or regular use. Chronic pain was measured as present/absent and as the number of painful body locations (0-8). Analyses used linear and multinomial regression. Results: ELA, chronic pain, and cannabis use were common among respondents. ELA was strongly associated with both measures of cannabis use. The number of painful body locations modestly mediated the association of ELA with cannabis use, reducing the magnitude of regression coefficients by about 1/7. The number of painful body locations modified the association between ELA and cannabis use (p≤0.006), while chronic pain presence/absence (a less-informative measure) had only a nonsignificant modification effect (p≥0.10). When either ELA or pain was high, the other was not associated with cannabis use; when either ELA or pain was low, more painful locations or higher ELA (respectively) was associated with more intense cannabis use. Conclusion: These exploratory findings suggest the importance of ELA and chronic pain as factors contributing to cannabis use, and of accounting for these factors in developing treatment and prevention strategies addressing cannabis use.

Independent effects of early life adversity on social cognitive function in patients with schizophrenia.

The aim of this study was to investigate the impact of early life adversity on cognitive function in patients with schizophrenia, with a focus on social cognition (SC). Two groups of patients with schizophrenia were recruited and matched on sociodemographic and clinical characteristics. One group consisted of 32 patients with a history of childhood trauma (SCZ-ct), and the other group consisted of 30 patients without a history of childhood trauma (SCZ-nct). In addition, 39 healthy controls without a history of childhood trauma (HC-nct) were also recruited. The intelligence of the three groups was assessed using the Wechsler Abbreviated Scale of Intelligence (WAIS-RC) short version. The cognitive function evaluation was conducted using the MATRICS Consensus Cognitive Battery (MCCB), and early life adversity was measured using the Childhood Trauma Questionnaire-Short Form (CTQ) and Bullying Scale for Adults (BSA). Patients with schizophrenia endosed significantly higher scores on the CTQ (F=67.61, p<0.001) and BSA (F=9.84, p<0.001) compared to the HC-nct. Analysis of covariance (ANCOVA) and post-hoc analyses revealed that SCZ-ct (F=11.20, p<0.001) exhibited the most pronounced cognitive impairment among the three groups, as indicated in MCCB total scores and in the domain score of SC. CTQ exhibited a negative correlation with MCCB (r=-0.405, p< 0.001); SC was negatively correlated with physical abuse (PA) of CTQ (r=-0.271, p=0.030) and emotional abuse (EA) of BSA (r=-0.265, p=0.034) in the whole patient sample. Higher SC performance was significantly predicted by CT_total (Beta =-0.582, p<0.001, 95% CI -0.96-0.46), and years of education (Beta=0.260, p =0.014, 95% CI 0.20-1.75) in schizophrenia. Besides familial trauma, schizophrenia patients appear to have a higher likelihood of experiencing bullying in their early life. These experiences seem to contribute significantly to their severe impairments in SC.

Effects of Maternal Separation on Effort-based Responding for Sucrose Are Associated with c-Fos Expression in the Nucleus Accumbens Core

In both people and animals, exposure to adverse experiences early in life can alter neurodevelopment and lead to long-term behavioral effects, including effects on reward processing. In the current study, we use a well-validated rodent model of maternal neglect, maternal separation (MS), to investigate the impact of early life adversity on reward learning and motivation and identify associated modifications in cellular activation in reward-relevant areas. Litters of Long-Evans rats were separated from the dam for either 15 min (brief) or 180 min (prolonged)/day from postnatal day (PND)2 to PND14. As adults, offspring were trained to lever press for a sucrose pellet using fixed ratio (FR) schedules and motivation was tested using a progressive ratio (PR) schedule over 10 daily sessions to assess sustained effects on effort-based responding. Immunohistochemical staining for c-Fos was conducted in a subset of animals that underwent an additional PR session. While there were no effects on reward learning, both MS180 males and females demonstrated increased effort-based responding on the first day of PR testing, while only MS180 males demonstrated a sustained increase in effort across all 10 days. MS180-induced changes in c-Fos expression in the dorsal and ventral striatum were observed, with subregion-specific effects along the rostrocaudal axis. Moreover, regression analyses suggest that motivated responding for a sucrose food reward in MS180-exposed, but not MS15-exposed animals, was associated with increased c-Fos expression in the rostral nucleus accumbens core. These findings implicate specific striatal regions in sex-specific modulation of sustained effort-based reward behavior following early life adversity.

Understanding the gaps in headache and migraine treatment with psychological and behavioral interventions: A narrative review.

In this narrative review, we summarize relevant literature pertaining to psychosocial risk factors for headache and migraine progression, current behavioral and psychological treatments, and consider promising treatments. Headache and migraine are common and associated with significant burden and disability. Current treatments targeting psychosocial risk factors show modest outcomes and do not directly address the impact of early life adversity, including the development of maladaptive emotional processing. An intervention that could address these factors and include components of current evidence-based interventions may lead to improved outcomes. We searched PubMed and Google Scholar for articles through December 2022. Search terms included headache, migraine, psychological interventions, behavioral interventions, cognitive-behavioral therapy, mindfulness, psychiatric comorbidities, adverse childhood experiences, trauma, and emotional processing. Trauma and childhood adversity show a correlation with headache and migraine progression. Developmental adversity and trauma interfere with adaptive emotional processing, which may worsen headache and migraine symptoms, while adaptive ways of experiencing emotions are shown to improve symptoms. Current behavioral and psychological interventions, such as cognitive-behavioral and mindfulness therapies, are effective treatments for headache, but they produce small to medium effect sizes and do not directly address the impact of trauma and emotional conflicts-common factors that contribute to chronicity and disability, especially among certain subpopulations of headache patients such as those with migraine. Thus, there exists a gap in current treatment. There is a gap in headache and migraine treatment for those patients who have a history of trauma, childhood adversity, and maladaptive emotional processing. We suggest that an integrated psychological treatment that includes components of current evidence-based interventions and addresses gaps by focusing on processing trauma-related emotions may improve chronic and debilitating symptoms.

Loss of spines in the prelimbic cortex is detrimental to working memory in mice with early-life adversity

Adverse experiences in early life can shape neuronal structures and synaptic function in multiple brain regions, leading to deficits of distinct cognitive functions later in life. Focusing on the pyramidal cells of the prelimbic cortex (PrL), a main subregion of the medial prefrontal cortex, the impact of early-life adversity (ELA) was investigated in a well-established animal model generated by changing the rearing environment during postnatal days 2 to 9 (P2-P9), a sensitive developmental period. ELA has enduring detrimental impacts on the dendritic spines of PrL pyramidal cells, which is most apparent in a spatially circumscribed region. Specifically, ELA affects both thin and mushroom-type spines, and ELA-provoked loss of spines is observed on selective dendritic segments of PrL pyramidal cells in layers II-III and V-VI. Reduced postsynaptic puncta represented by postsynaptic density protein-95 (PSD-95), but not synaptophysin-labelled presynaptic puncta, in ELA mice supports the selective loss of spines in the PrL. Correlation analysis indicates that loss of spines and postsynaptic puncta in the PrL contributes to the poor spatial working memory of ELA mice, and thin spines may play a major role in working memory performance. To further understand whether loss of spines affects glutamatergic transmission, AMPA- and NMDA-receptor-mediated synaptic currents (EPSCs) were recorded in a group of Thy1-expressing PrL pyramidal cells. ELA mice exhibited a depressed glutamatergic transmission, which is accompanied with a decreased expression of GluR1 and NR1 subunits in the PrL. Finally, upregulating the activation of Thy1-expressing PrL pyramidal cells via excitatory DREADDs can efficiently improve the working memory performance of ELA mice in a T-maze-based task, indicating the potential of a chemogenetic approach in restoring ELA-provoked memory deficits.

Examining resting-state network connectivity in children exposed to perinatal maternal adversity using anatomically weighted functional connectivity (awFC) analyses; A preliminary report.

Environmental perturbations during critical periods can have pervasive, organizational effects on neurodevelopment. To date, the literature examining the long-term impact of early life adversity has largely investigated structural and functional imaging data outcomes independently. However, emerging research points to a relationship between functional connectivity and the brain's underlying structural architecture. For instance, functional connectivity can be mediated by the presence of direct or indirect anatomical pathways. Such evidence warrants the use of structural and functional imaging in tandem to study network maturation. Accordingly, this study examines the impact of poor maternal mental health and socioeconomic context during the perinatal period on network connectivity in middle childhood using an anatomically weighted functional connectivity (awFC) approach. awFC is a statistical model that identifies neural networks by incorporating information from both structural and functional imaging data. Resting-state fMRI and DTI scans were acquired from children aged 7-9 years old. Our results indicate that maternal adversity during the perinatal period can affect offspring's resting-state network connectivity during middle childhood. Specifically, in comparison to controls, children of mothers who had poor perinatal maternal mental health and/or low socioeconomic status exhibited greater awFC in the ventral attention network. These group differences were discussed in terms of the role this network plays in attention processing and maturational changes that may accompany the consolidation of a more adult-like functional cortical organization. Furthermore, our results suggest that there is value in using an awFC approach as it may be more sensitive in highlighting connectivity differences in developmental networks associated with higher-order cognitive and emotional processing, as compared to stand-alone FC or SC analyses.

CHILDHOOD ADVERSITY IMPACTS PERSONALITY DEVELOPMENT ACROSS ADULTHOOD

Abstract Throughout adulthood, people’s personalities typically change favorably such that agreeableness and conscientiousness increase, and neuroticism decreases. However, the impact of early life adversity on these changes in personality has yet to be examined. We utilized data from 6,382 community dwelling adults (ages 25–75) that completed 3-waves of the Midlife Development in the U.S. Study (MIDUS) in 1995–96, 2005–06, and 2013–14. Early life adversity was computed using 16 retrospective items assessing emotional and physical abuse, socioeconomic disadvantage, familial instability, and early-life poor health. Personality was assessed with the Big 5 MIDI measure. Latent growth curves confirmed there was significant variability in change over the ~20 year follow-up (all RMSEAS &amp;lt; .06; and CFI/TLI &amp;gt; .96). More specifically, higher levels of early adversity predicted higher initial levels of neuroticism, and lower levels of conscientiousness and extraversion. Additionally, higher adversity predicted a steeper decrease in neuroticism across 20-years (all p’s &amp;lt; .05). Examination of specific adversity types revealed that emotional abuse and having poor health at a young age were especially detrimental to personality development. This research provides evidence that high levels of adverse experiences in childhood predict unfavorable personality development throughout adulthood. Moreover, this research demonstrates that early life adversity, especially certain types, can have lifelong detrimental effects on development. Interventions for those who have experienced adversity should be implemented as early in life as possible to prevent suboptimal psychological development trajectories. Such interventions could improve life outcomes if personality development is more normalized.

Fluoxetine treatment supports predictive validity of the three hit model of depression in male PACAP heterozygous mice and underpins the impact of early life adversity on therapeutic efficacy.

According to the three hit concept of depression, interaction of genetic predisposition altered epigenetic programming and environmental stress factors contribute to the disease. Earlier we demonstrated the construct and face validity of our three hit concept-based mouse model. In the present work, we aimed to examine the predictive validity of our model, the third willnerian criterion. Fluoxetine treatment was applied in chronic variable mild stress (CVMS)-exposed (environmental hit) CD1 mice carrying one mutated allele of pituitary adenylate cyclase-activating polypeptide gene (genetic hit) that were previously exposed to maternal deprivation (epigenetic hit) vs. controls. Fluoxetine reduced the anxiety level in CVMS-exposed mice in marble burying test, and decreased the depression level in tail suspension test if mice were not deprived maternally. History of maternal deprivation caused fundamental functional-morphological changes in response to CVMS and fluoxetine treatment in the corticotropin-releasing hormone-producing cells of the bed nucleus of the stria terminalis and central amygdala, in tyrosine-hydroxylase content of ventral tegmental area, in urocortin 1-expressing cells of the centrally projecting Edinger-Westphal nucleus, and serotonergic cells of the dorsal raphe nucleus. The epigenetic background of alterations was approved by altered acetylation of histone H3. Our findings further support the validity of both the three hit concept and that of our animal model. Reversal of behavioral and functional-morphological anomalies by fluoxetine treatment supports the predictive validity of the model. This study highlights that early life stress does not only interact with the genetic and environmental factors, but has strong influence also on therapeutic efficacy.

Early-life adversity predicts performance and fitness in a wild social carnivore.

Studies on humans indicate that encountering multiple sources of adversity in childhood increases the risk of poor long-term health and premature death. Far less is known about cumulative effects of adversity during early life in wildlife. Focusing on the spotted hyena Crocuta crocuta, a social mammal with small litters, extensive maternal care, slow development and access to resources determined by social rank, we determined the contribution of ecological, maternal, social and demographic factors during early life on performance and fitness, and tested whether the impact of early-life adversity is cumulative. Using longitudinal data from 666 female hyenas in the Serengeti National Park, we determined the early growth rate, survival to adulthood, age at first reproduction (AFR), lifetime reproductive success (LRS) and longevity. We fitted multivariate models in which we tested the effects of environmental factors on these performance measures. We then constructed a cumulative adversity index and fitted models to test the effect of this index on each performance measure. Finally, the value of cumulative adversity models was tested by comparing them to multivariate and single-effect models in which the effect of each environmental factor was considered separately. High maternal rank decreased the AFR of daughters. Singleton and dominant cubs had higher growth rate than subordinate cubs, and singletons also had a higher survival chance to adulthood than subordinates. Daughters of prime age mothers had a higher growth rate, longevity and LRS. Little and heavy rainfall decreased survival to adulthood. Increasing numbers of lactating female clan members decreased growth rate, survival to adulthood and LRS. Cumulative adversity negatively affected short-term performance and LRS. Multivariate models outperformed cumulative adversity and single-effect models for all measures except for AFR and longevity, for which single-effect models performed better. Our results suggest that in some wildlife populations the combination of specific conditions in early life may matter more than the accumulation of adverse conditions as such.

Early life social instability stress causes lasting cognitive decrement and elevated hippocampal stress-related gene expression

BackgroundEarly life stress may have profound effects on brain health, yielding both short- and long-term cognitive or psychiatric impairment. Early life Social Instability Stress (SIS) in rodents has been used to model the effects of early chronic human stress. While many studies have assessed acute and short-term responses to this stressor, less attention has been paid to the lasting effects of early life stress in rodents. MethodsThe current study utilized SIS in young mice to assess the impact of early life adversity over the lifespan. Mice were assessed in adulthood between the ages of 18 to 66 weeks for changes in behaviors associated with anxiety, affect, sociability, aggression, motivation, and recognition memory. Additionally, mice were assessed for changes in glucocorticoid level and hippocampal mRNA expression in a subset of genes that display alterations in humans following exposure to stress (CRHR1, CRHR2, FKBP5, SLC6A4). ResultsMice exposed to early SIS showed disrupted memory and increased hippocampal expression of FKBP5, CRHR2 and SLC6A4 mRNA compared to non-stressed mice. Importantly, there was a significant association between increased FKBP5 and CRHR2 with reduced recognition memory. Additionally, mice exposed to SIS showed increased responding on a progressive ratio schedule of reinforcement, indicating that reduction in memory performance was not mediated by decreased effort. ConclusionsEcologically-relevant social stress in mice causes long-term decrements in recognition memory, possibly mediated by persistent changes in moderators of the stress cascade. Additionally, animals exposed to early life stress showed increased motivation for reward, which may contribute to a host of hedonic seeking behaviors throughout life. These data suggest that SIS can be used to evaluate therapeutic interventions to attenuate or reverse lasting effects of early life adversity.

Immune cell dynamics in response to an acute laboratory stressor: a within-person between-group analysis of the biological impact of early life adversity

Early life adversity (ELA) is a risk factor for early onset morbidities and mortality, a relationship that may be driven in part by immune system dysregulation. One mechanism of dysregulation that has yet to be fully examined in the context of ELA is alterations to immune cell dynamics in response to acute stress. Using a within-person between-group experimental design, we investigated stress-induced changes in immune cell populations, and how these changes may be altered in individuals with a history of ELA. Participants were young adults (N = 34, aged 18–25 years, 53% female, 47% with a history of ELA). Complete immune cell counts were measured at four time-points over a 5-hour window across two sessions (Trier Social Stress Test [TSST] vs. no-stress) separated by a week. Across all participants, total white blood cells increased over time (F(3,84)=38.97, p < .001) with a greater increase in response to the TSST compared to the no-stress condition at 240 minutes post-test (b = 0.43±.19; t(179)=2.22, p = .027). This pattern was mirrored by neutrophil counts. Lymphocyte counts were initially depressed by TSST exposure (b =−205±.67; t(184)=−3.07, p = .002) but recovered above baseline. ELA status was associated with higher stress-induced immune cell counts, a difference likely driven by increases in neutrophils (F(1,22)=4.45, p = .046). Overall, these results indicate differential immune cell dynamics in response to acute stress in individuals with a history of ELA. This points to altered immune system functioning in the context of stress, a finding that may be driving increased morbidity and mortality risk for ELA-exposed individuals.

Neural correlates of attentional control in social anxiety disorder: the impact of early-life adversity and DNA methylation.

Background:Social anxiety disorder is characterized by intense fear and avoidance of social interactions and scrutiny by others. Although alterations in attentional control seem to play a central role in the psychopathology of social anxiety disorder, the neural underpinnings in prefrontal brain regions have not yet been fully clarified.Methods:The present study used functional MRI in participants (age 18–50 yr) with social anxiety disorder (n = 42, 31 female) and without (n = 58, 33 female). It investigated the interrelation of the effects of social anxiety disorder and early-life adversity (a main environmental risk factor of social anxiety disorder) on brain activity during an attentional control task. We applied DNA methylation analysis to determine whether epigenetic modulation in the gene encoding the glucocorticoid receptor, NR3C1, might play a mediating role in this process.Results:We identified 2 brain regions in the left and medial prefrontal cortex that exhibited an interaction effect of social anxiety disorder and early-life adversity. In participants with low levels of early-life adversity, neural activity in response to disorder-related stimuli was increased in association with social anxiety disorder. In participants with high levels of early-life adversity, neural activity was increased only in participants without social anxiety disorder. NR3C1 DNA methylation partly mediated the effect of social anxiety disorder on brain activity as a function of early-life adversity.Limitations:The absence of behavioural correlates associated with social anxiety disorder limited functional interpretation of the results.Conclusion:These findings demonstrate that the neurobiological processes that underlie social anxiety disorder might be fundamentally different depending on experiences of early-life adversity. Long-lasting effects of early-life adversity might be encoded in NR3C1 DNA methylation and entail alterations in social anxiety disorder–related activity patterns in the neural network of attentional control.

Amygdala Allostasis and Early Life Adversity: Considering Excitotoxicity and Inescapability in the Sequelae of Stress.

Early life adversity (ELA), such as child maltreatment or child poverty, engenders problems with emotional and behavioral regulation. In the quest to understand the neurobiological sequelae and mechanisms of risk, the amygdala has been of major focus. While the basic functions of this region make it a strong candidate for understanding the multiple mental health issues common after ELA, extant literature is marked by profound inconsistencies, with reports of larger, smaller, and no differences in regional volumes of this area. We believe integrative models of stress neurodevelopment, grounded in “allostatic load,” will help resolve inconsistencies in the impact of ELA on the amygdala. In this review, we attempt to connect past research studies to new findings with animal models of cellular and neurotransmitter mediators of stress buffering to extreme fear generalization onto testable research and clinical concepts. Drawing on the greater impact of inescapability over unpredictability in animal models, we propose a mechanism by which ELA aggravates an exhaustive cycle of amygdala expansion and subsequent toxic-metabolic damage. We connect this neurobiological sequela to psychosocial mal/adaptation after ELA, bridging to behavioral studies of attachment, emotion processing, and social functioning. Lastly, we conclude this review by proposing a multitude of future directions in preclinical work and studies of humans that suffered ELA.

Impulsivity mediates the impact of early life adversity on high risk behaviors among Tunisian adolescents.

Adverse childhood experience (ACE) has become an alarming phenomenon exposing youth at a great risk of developing mental health issues. Several studies have examined the mechanism by which ACE affects adolescent's engagement in risky behaviors. However, little is known about these associations in the Tunisian/African context. We investigated the role of impulsivity in the link between ACE and health risk behaviors among schooled adolescents in Tunisia. We performed a cross sectional study among 1940 schooled adolescents in the city of Mahdia (Tunisia) from January to February 2020. To measure ACE, we used the validated Arabic version of the World Health Organization ACE questionnaire. The Barratt Impulsivity Scale and the Internet Addiction Test were used as screening tools for impulsivity and internet addiction. A total of 2520 adolescents were recruited. Of those, 1940 returned the questionnaires with an overall response rate of 77%. The majority (97.5%) reported experiencing at least one ACE. Emotional neglect (83.2%) and witnessing community violence (73.5%) were the most reported intra-familial ACEs. Males had higher rates of exposure to social violence than females. The most common risky behavior was internet addiction (50%, 95%CI=[47.9-52.3%]). Our survey revealed that ACEs score predict problematic behaviors through impulsiveness (% mediated=16.7%). Specifically, we found a major mediating role of impulsivity between the exposure to ACE and the risk of internet addiction (% mediated=37.5%). Our results indicate the role of impulsivity in translating the risk associated with ACE leading to engagement in high risk behaviors.

Early life adversity and health inequality: a dual interaction model

This article examines the impact of early life adversity on health inequality from a life course perspective. We develop a dual interaction model that considers how both the frequency as well as the duration of early life adversity might shape an individual's health. Analyzing data from the China Health and Retirement Longitudinal Study (CHARLS, 2011-2014), we show that not only does early life adversity have a direct effect on an individual's health, but throughout the life course it also produces cumulative disadvantages through worsening the individual's life conditions such as less education, lower social-economic status, and less job security. The combination of the frequency of adversity experience and the length of exposure creates an exponential effect on poor health, contributing to the persistence of health inequality in contemporary Chinese society.

Emotion regulation strategies modulate the effect of adverse childhood experiences on perceived chronicstress with implications for cognitive flexibility.

Exposure to early life adversity is associated with chronic stress and a range of stress-related health problems in adulthood. Since chronic stress debilitates activity in the prefrontal cortex (pFC), maladaptive regulatory strategies in response to stress have been proposed as one explanation for the impact of early life adversity on health outcomes in adulthood. We conducted a study to examine the impact of adverse childhood experiences (ACEs) on cognitive flexibility, a key executive function implicated in activity in the pFC, in a sample of adults (N = 486). Additionally, we investigated whether perceptions of chronic stress in adulthood would mediate the influence of ACEs on cognitive flexibility. However, stress is a subjective experience, and emotion regulation strategies can attenuate the stress response. So, we also examined if individual differences in emotion regulation strategies would modulate the relationship between ACEs and chronic stress. Our results demonstrate that early life adversity, as characterized by ACEs, is associated with decreased cognitive flexibility in adulthood. Additionally, number of ACEs was positively correlated with perceived stress, which in turn was negatively correlated with cognitive flexibility. But, individual differences in the habitual use of emotion regulation strategies moderated the influence of ACEs on chronic stress. Specifically, habitual use of cognitive reappraisal attenuated the stress levels whereas habitual use of expressive suppression exacerbated stress levels. Overall, our study highlights the importance of examining emotion regulation in individuals who have experienced early life adversity.

A review and update of the potential impact of early life adversity on telomere length

Early life adversity is a risk factor for many diseases, but the related mechanism is not clear. Some research clues suggest that early life adversity is related to biological aging, and at present, the more recognized biological aging index is telomere length. Therefore, exploring the relationship between early life adversity and telomere length is of great significance to reveal the related mechanism of adversity. Through a review of previous literature, this paper discusses the possible effects of different adversity types, exposure time and research design on the relationship between early life adversity and telomere length, so as to provide a basis for the intervention of early life adversity.