Prenatal and Early Life Exposure to Ambient Air Pollutants Is Associated with the Fecal Metabolome in the First Two Years of Life.

Prenatal and early life air pollution exposure has been linked with several adverse health outcomes. However, the mechanisms underlying these relationships are not yet fully understood. Therefore, this study utilizes fecal metabolomics to determine if pre- and postnatal exposure to ambient air pollutants (i.e., PM10, PM2.5, and NO2) is associated with the fecal metabolome in the first 2 years of life in a Latino cohort from Southern California. The aims of this analysis were to estimate associations between (1) prenatal air pollution exposure with fecal metabolic features at 1-month of age, (2) prior month postnatal air pollution exposure with fecal metabolites from 1-month to 2 years of age, and (3) how postnatal air pollution exposure impacts the change over time of fecal metabolites in the first 2 years of life. Prenatal exposure to air pollutants was associated with several Level-1 metabolites, including those involved in vitamin B6 and tyrosine metabolism. Prior month air pollution exposure in the postnatal period was associated with Level-1 metabolites involved in histidine metabolism. Lastly, we found that pre- and postnatal ambient air pollution exposure was associated with changes in metabolic features involved in metabolic pathways including amino acid metabolism, histidine metabolism, and fatty acid metabolism.

Development of systemic and mucosal immune responses against gut microbiota in early life and implications for the onset of allergies.

The early microbial colonization of human mucosal surfaces is essential for the development of the host immune system. Already during pregnancy, the unborn child is prepared for the postnatal influx of commensals and pathogens via maternal antibodies, and after birth this protection is continued with antibodies in breast milk. During this critical window of time, which extends from pregnancy to the first year of life, each encounter with a microorganism can influence children's immune response and can have a lifelong impact on their life. For example, there are numerous links between the development of allergies and an altered gut microbiome. However, the exact mechanisms behind microbial influences, also extending to how viruses influence host-microbe interactions, are incompletely understood. In this review, we address the impact of infants' first microbial encounters, how the immune system develops to interact with gut microbiota, and summarize how an altered immune response could be implied in allergies.

Defining and distinguishing early life stress, trauma, adversity, toxic and chronic stress and allostatic load: a descriptive review.

AIMS: Various concepts are used to study the impact of stress on childhood development. These concepts are often used inconsistently or interchangeably. Our main objectives were to determine how selected stress concepts (chronic stress, toxic stress, allostatic load, early life stress, childhood adversity, childhood trauma and adverse childhood experiences; ACEs) are defined, operationalized and described, and to provide a theoretical context to aid the choice for a preferred concept in public health research. METHODS: For this descriptive review, we systematically searched for literature published before 4 August 2021, on PubMed, Embase and PsycInfo. Two independent reviewers included studies. Exclusion criteria were: no systematic review, not peer reviewed, not published in English, selected stress concepts were no predetermined variable or a substantial topic in the discussion, full text was unobtainable or study described non-human or non-childhood populations. Data extraction forms were used. Descriptives were gathered, publication fields were identified through Journal Citation Reports categories, and verbatim descriptions were ordered in text and Venn diagrams. RESULTS: Of 264 screened studies, 124 were included. ACEs, childhood adversity and childhood trauma were used most. ACEs were the main concept used most frequently (47.6%). A total of 11 of 14 public and environmental health journals used ACEs. All concepts refer to prolonged, repeated, interpersonal stress from 0 to 18 years, that can alter physiological systems. Four concepts were stressor oriented, two concepts focused on stress response and effect and one on the state of challenged homeostasis. CONCLUSIONS: ACEs seem most fitting for public health setting, due to their operationalizability, large set of core experiences and widespread use.

Exploring perceptions of vulnerability among women facing psychosocial adversity before, during and after pregnancy: A qualitative interview-study using thematic analysis.

OBJECTIVE: The term 'vulnerable' is often used to describe women facing psychosocial adversity during pregnancy, implying a heightened risk of experiencing suboptimal pregnancy outcomes. While this label might facilitate the pathway to appropriate care, it can be perceived as stigmatizing by the women it intends to help, which could deter their interaction with healthcare services. This study explores how women facing psychosocial adversity before, during and after pregnancy perceive the concept of vulnerability and experience being labeled as such. METHODS: We conducted a thematic analysis of semi-structured, in-depth interviews. Through purposive sampling targeting maximum variation, ten women of diverse backgrounds were included. RESULTS: Three central themes emerged: defining vulnerability, embracing vulnerability and the feeling of being stigmatized. Women perceived vulnerability as an inability to adequately care for themselves or their children, necessitating additional support alongside routine antenatal care. Acceptance of the 'vulnerable' label came when it also acknowledged their proactive efforts and strengths to improve their situation. Conversely, if discussions surrounding vulnerability failed to recognize women's agency - specifically, their personal journeys and the courage needed to seek support - the label was perceived as stigmatizing. CONCLUSIONS: Addressing vulnerability effectively in maternity care requires a nuanced, patient-centered approach, acknowledging both the challenges and strengths of women facing psychosocial adversities. Emphasizing personal narratives and their courage in seeking support can mitigate the stigmatizing effects of the 'vulnerable' label. Integrating these narratives into maternal healthcare practices can foster deeper connections with the women involved, enhancing the overall quality of care.

Strengths of fertilizer and litter effects on seedling recruitment and growth of grassland species differ depending on functional groups and seed size.

Agricultural grasslands play an important role in conserving the biodiversity of the European cultural landscape. Both, litter cover and soil nutrient availability, change with grassland management, but it is not well-studied how seedling recruitment and growth of multiple grassland species are influenced by their single or combined effects. Therefore, we studied the effects of nitrogen fertilization (100 kg N per year and ha) and litter cover (250 gdw per m2) on seedling recruitment and growth of 75 temperate grassland species (16 graminoid species, 51 forb species, 8 legume species) in a full factorial microcosm experiment. Overall, fertilizer reduced seedling emergence, while litter cover increased it even when combined with fertilization. Fertilization increased seedling height and biomass, and the combination of fertilizer and litter resulted in even stronger responses. Litter cover alone did not influence seedling biomass or seedling height. While the overall direction of treatment effects was similar across functional groups, their strengths were mostly weaker in graminoids than in non-legume forbs and legumes. Positive litter effects on seedling emergence were stronger in large-seeded species. Positive fertilization effects on seedling growth were stronger in small-seeded species, while their seedling biomass was negatively affected by litter cover. In summary, our results show for multiple grassland species that the combination of litter cover and fertilization modulates their single effects. The varying sensitivity of how grassland species representing different functional groups and seed sizes respond with their seedling emergence and growth to litter cover and nitrogen fertilization indicates that the consequences of land-use change on grassland diversity and composition already start to manifest in the earliest stages of the plant life cycle.

Individual longitudinal changes in DNA-methylome identify signatures of early-life adversity and correlate with later outcome.

Adverse early-life experiences (ELA) affect a majority of the world's children. Whereas the enduring impact of ELA on cognitive and emotional health is established, there are no tools to predict vulnerability to ELA consequences in an individual child. Epigenetic markers including peripheral-cell DNA-methylation profiles may encode ELA and provide predictive outcome markers, yet the interindividual variance of the human genome and rapid changes in DNA methylation in childhood pose significant challenges. Hoping to mitigate these challenges we examined the relation of several ELA dimensions to DNA methylation changes and outcome using a within-subject longitudinal design and a high methylation-change threshold. DNA methylation was analyzed in buccal swab/saliva samples collected twice (neonatally and at 12 months) in 110 infants. We identified CpGs differentially methylated across time for each child and determined whether they associated with ELA indicators and executive function at age 5. We assessed sex differences and derived a sex-dependent 'impact score' based on sites that most contributed to methylation changes. Changes in methylation between two samples of an individual child reflected age-related trends and correlated with executive function years later. Among tested ELA dimensions and life factors including income to needs ratios, maternal sensitivity, body mass index and infant sex, unpredictability of parental and household signals was the strongest predictor of executive function. In girls, high early-life unpredictability interacted with methylation changes to presage executive function. Thus, longitudinal, within-subject changes in methylation profiles may provide a signature of ELA and a potential predictive marker of individual outcome.

Threat, Emotion Dysregulation, and Parenting in a Clinical Sample of Children with Disruptive Behaviour.

Early-life adversity is associated with the development of internalizing and externalizing problems in children. Despite this, there is a need to understand the mechanisms linking these experiences to psychopathology, especially in clinical samples. This cross-sectional study tested emotion dysregulation as a mechanism linking early-life threat to psychopathology in a clinical sample of children with disruptive behavior problems. We also explored parental positive reinforcement as a protective factor in these pathways. A clinical sample of 606 children aged 6-12 years, referred to a mental healthcare hospital, were included. Parent-reported child threat, and parent- and teacher-reported child emotion dysregulation and psychopathology, were collected. Path analysis was used to explore the mediating effect of emotion dysregulation in the relation between threat and psychopathology. The moderating effects of parental positive reinforcement were explored through moderated-mediation analyses. Emotion dysregulation partially mediated the association between threat and both internalizing (ß = .18, P = .006) and externalizing (ß = .19, P = .002) problems. Positive reinforcement did not buffer the association between threat and emotion dysregulation (ß = .09, P = .62) or the association between emotion dysregulation and internalizing (ß = - .003, P = .20) or externalizing (ß = - .002, P = .35). Poor emotion regulation may be a transdiagnostic mechanism linking early-threat with internalizing and externalizing problems in clinic-referred children with disruptive behaviors. Factors aside from parental positive reinforcement should be explored as protective factors in these pathways, including those directly implicated in the purported mechanisms linking these factors over time.

Macroscopic and microscopic morphological characteristics of gelatinous egg masses (egg veils) of yellow goosefish Lophius litulon (Lophiiformes; Lophiidae).

We recorded the morphological characteristics and effect of preservation methods on the structure of the egg veils of Lophius litulon found in field investigations. The egg veils were characterized as translucent sheet-shape with parallel opaque creases spaced approximately 2 cm apart. The egg veils were found to be composed of pentagonal or hexagonal chambers with rounded corners arranged in one layer, and each chamber enveloped one to three embryos. Cryopreservation is recommended to prevent structural changes in the egg veil rather than ethanol solution and neutral buffered formalin solution.

Exogenous glucocorticoids to improve extinction learning for post-traumatic stress disorder patients with hypothalamic-pituitary-adrenal-axis dysregulation: a study protocol description.

Background: Trauma-focused treatments for post-traumatic stress disorder (PTSD) are effective for many patients. However, relapse may occur when acquired extinction memories fail to generalize beyond treatment contexts. A subgroup of PTSD patients - potentially with substantial exposure to early-life adversity (ELA) - show dysregulation of the hypothalamic-pituitary-adrenal (HPA) axis, which results in lower cortisol levels. Glucocorticoids, including cortisol, appear to facilitate strength and generalization of emotional memories.Objective: We describe the protocol of an integrated PTSD study. We investigate (A) associations between HPA-axis dysregulation, ELA, epigenetic markers, and PTSD treatment outcome (observational study); and (B) effects of exogenous glucocorticoids on strength and generalization of extinction memories and associated neural mechanisms [pharmacological intervention study with functional magnetic resonance imaging (fMRI)]. The objective is to provide proof of concept that PTSD patients with HPA-axis dysregulation often experienced ELA and may show improved strength and generalization of extinction learning after glucocorticoid administration.Method: The observational study (n = 160 PTSD group, n = 30 control group) assesses ELA, follow-up PTSD symptoms, epigenetic markers, and HPA-axis characteristics (salivary cortisol levels during low-dose dexamethasone suppression test and socially evaluated cold-pressor test). The pharmacological intervention study (n = 80 PTSD group, with and without HPA-axis dysregulation) is a placebo-controlled fMRI study with a crossover design. To investigate strength and generalization of extinction memories, we use a differential fear acquisition, extinction, and extinction recall task with spatial contexts within a virtual environment. Prior to extinction learning, 20 mg hydrocortisone or placebo is administered. During next-day recall, strength of the extinction memory is determined by recovery of skin conductance and pupil dilation differential responding, whereas generalization is assessed by comparing responses between different spatial contexts.Conclusion: The integrated study described in the current protocol paper could inform a personalized treatment approach in which these PTSD patients may receive glucocorticoids as a treatment enhancer in trauma-focused therapies.Trial registration: The research project is registered in the European Union Drug Regulating Authorities Clinical Trials (EudraCT) database, https://eudract.ema.europa.eu/, EudraCT number 2020-000712-30.

This protocol reports a proof-of-concept study for glucocorticoids as an enhancer for PTSD treatment.The study examines whether glucocorticoids enhance the strength and generalization of extinction memory.A further aim is to identify HPA-axis-related PTSD subgroups that may particularly benefit.

Maternal gestational diabetes mellitus associates with altered gut microbiome composition and head circumference abnormalities in male offspring.

The impact of gestational diabetes mellitus (GDM) on maternal or infant microbiome trajectory remains poorly understood. Utilizing large-scale longitudinal fecal samples from 264 mother-baby dyads, we present the gut microbiome trajectory of the mothers throughout pregnancy and infants during the first year of life. GDM mothers had a distinct microbiome diversity and composition during the gestation period. GDM leaves fingerprints on the infant's gut microbiome, which are confounded by delivery mode. Further, Clostridium species positively correlate with a larger head circumference at month 12 in male offspring but not females. The gut microbiome of GDM mothers with male fetuses displays depleted gut-brain modules, including acetate synthesis I and degradation and glutamate synthesis II. The gut microbiome of female infants of GDM mothers has higher histamine degradation and dopamine degradation. Together, our integrative analysis indicates that GDM affects maternal and infant gut composition, which is associated with sexually dimorphic infant head growth.

The right educational environment: Oral tolerance in early life.

Oral tolerance promotes the suppression of immune responses to innocuous antigen and is primarily mediated by regulatory T cell (Tregs). The development of oral tolerance begins in early life during a "window of tolerance," which occurs around weaning and is mediated by components in breastmilk. Herein, we review the factors dictating this window and how Tregs are uniquely educated in early life. In early life, the translocation of luminal antigen for Treg induction is primarily dictated by goblet cell-associated antigen passages (GAPs). GAPs in the colon are negatively regulated by maternally-derived epidermal growth factor and the microbiota, restricting GAP formation to the "periweaning" period (postnatal day 11-21 in mice, 4-6 months in humans). The induction of solid food also promotes the diversification of the bacteria such that bacterially-derived metabolites known to promote Tregs-short-chain fatty acids, tryptophan metabolites, and bile acids-peak during the periweaning phase. Further, breastmilk immunoglobulins-IgA and IgG-regulate both microbial diversity and the interaction of microbes with the epithelium, further controlling which antigens are presented to T cells. Overall, these elements work in conjunction to induce a long-lived population of Tregs, around weaning, that are crucial for maintaining homeostasis in adults.

Effects of early social isolation and adolescent single prolonged stress on anxiety-like behaviors and voluntary ethanol consumption in female Long Evans rats.

BACKGROUND: Exposure to stress during childhood and adolescence is a risk factor for alcohol use disorder (AUD) and comorbid conditions, including posttraumatic stress disorder (PTSD). We previously established an adolescent social isolation (SI) model that leads to the emergence of a wide range of behavioral risk factors for AUD, including increased anxiety-like behavior, locomotor activity, and ethanol consumption in male and female rats. Here, we sought to test the hypothesis that SI may increase vulnerability to single prolonged stress (SPS), a rodent model of PTSD. METHODS: Female Long Evans rats (n = 8/group) were either single-housed or group-housed (GH) (4/cage) on postnatal day 21. One week later, rats underwent testing in the open field test (OFT), elevated plus-maze (EPM), and successive alleys test (SAT). Following initial behavioral testing, a subset of SI/GH rats were exposed to SPS. All rats were then tested on the novelty-suppressed feeding test (NSFT) followed by fear conditioning and home cage two-bottle choice to assess ethanol consumption. RESULTS: SI significantly increased activity in the OFT and anxiety-like behavior on the SAT, but not the EPM. While SI and SPS alone had no effect on the NSFT, exposure to both stressors significantly increased approach latency. Complex effects of stress history were observed across a 3-day fear conditioning paradigm and no group differences were observed with home cage ethanol consumption, regardless of prior ethanol exposure. CONCLUSIONS: The results from this study provide novel evidence that SI interacts with SPS in female rats to influence behavior in assays of unconditioned anxiety-like behavior (NSFT) and conditioned fear. Surprisingly, stress exposure had no effect on home cage ethanol consumption. Ultimately, these models provide useful avenues to examine the interaction between stressful experiences, alcohol exposure, biological sex, and the neurobiological adaptations underlying potential risk factors for psychiatric conditions.

Paternal absence and increased caregiving independently and interactively shape the development of male prairie voles at subadult and adult life stages.

The influence of maternal caregiving is a powerful force on offspring development. The absence of a father during early life in biparental species also has profound implications for offspring development, although it is far less studied than maternal influences. Moreover, we have limited understanding of the interactive forces that maternal and paternal caregiving impart on offspring. We investigated if behaviorally upregulating maternal care compensates for paternal absence on prairie vole (Microtus ochrogaster) pup development. We used an established handling manipulation to increase levels of caregiving in father-absent and biparental families, and later measured male offspring behavioral outcomes at sub-adulthood and adulthood. Male offspring raised without fathers were more prosocial (or possibly less socially anxious) than those raised biparentally. Defensive behavior and responses to contextual novelty were also influenced by the absence of fathers, but only in adulthood. Offensive aggression and movement in the open field test changed as a function of life-stage but not parental exposure. Notably, adult pair bonding was not impacted by our manipulations. Boosting parental care produced males that moved more in the open field test. Parental handling also increased oxytocin immunoreactive cells within the supraoptic nucleus of the hypothalamus (SON), and in the paraventricular nucleus (PVN) of biparentally-reared males. We found no differences in vasopressinergic cell groups. We conclude that male prairie voles are contextually sensitive to the absence of fathers and caregiving intensity. Our study highlights the importance of considering the ways early experiences synergistically shape offspring behavioral and neural phenotypes across the lifespan.

Antibiotic-driven dysbiosis in early life disrupts indole-3-propionic acid production and exacerbates allergic airway inflammation in adulthood.

Antibiotic use in early life disrupts microbial colonization and increases the risk of developing allergies and asthma. We report that mice given antibiotics in early life (EL-Abx), but not in adulthood, were more susceptible to house dust mite (HDM)-induced allergic airway inflammation. This susceptibility was maintained even after normalization of the gut microbiome. EL-Abx decreased systemic levels of indole-3-propionic acid (IPA), which induced long-term changes to cellular stress, metabolism, and mitochondrial respiration in the lung epithelium. IPA reduced mitochondrial respiration and superoxide production and altered chemokine and cytokine production. Consequently, early-life IPA supplementation protected EL-Abx mice against exacerbated HDM-induced allergic airway inflammation in adulthood. These results reveal a mechanism through which EL-Abx can predispose the lung to allergic airway inflammation and highlight a possible preventative approach to mitigate the detrimental consequences of EL-Abx.

Early life-history stages of the olive barb, Systomus sarana (Hamilton), and a key ontogenetic systematic character of Smiliogastrinae.

The current study aims to uncover the early life-history stages of Systomus sarana, a medium-sized smiliogastrin cyprinid important for aquaculture in South Asia. The fish were effectively bred in captivity by administering 0.25 mL of breeding hormone per kilogram of fish. The spawning occurred 8.54 ± 0.55 h after the injection, and the eggs were phyto-lithophilic with a pale yellow color and a diameter of 1.49 ± 0.04 mm. Hatching occurred 17 h after fertilization, and the yolk-sac larvae of 3.43 ± 0.08 mm total length (TL) were adhering to the plant parts and other substrata with the cement glands on the forehead. On the third day, with complete absorption of the yolk sac and the disappearance of the attachment organ, the pre-flexion larvae measured 5.3 ± 0.11 mm TL. On the eighth day, the flexion larvae measured 6 ± 0.4 mm TL with a well-inflated posterior swim bladder, and the post-flexion larvae, at 11 days post-hatching (dph), developed a two-chambered gas bladder. The juvenile stage, on day 21 post-hatching, was marked by the loss of the median finfolds and the appearance of black blotches on the caudal, subdorsal, and supra-anal regions. The commencement of squamation and the appearance of the rudiments of maxillary barbels distinguished the juvenile stage. The subadults measuring 4.6 ± 0.36 cm TL had finished squamation and completely lost the subdorsal and supra-anal blotches. We propose that the presence of subdorsal blotches is a distinctive ontogenetic and systematic feature of larval and juvenile forms of smiliogastrin barbs.

Early-Life Disease Exposure and Its Heterogeneous Effects on Mortality Throughout Life: Sweden, 1905-2016.

Exposure to infectious diseases in early life has been linked to increased mortality risk in later life in high-disease settings, such as eighteenth- and nineteenth-century Europe. Less is known about the long-term effects of early-life disease exposure in milder disease environments. This study estimates heterogeneous effects from disease exposure in infancy on later-life mortality in twentieth-century Sweden, by socioeconomic status at birth and sex. Using historical population data for southern Sweden, we study 11,515 individuals who were born in 1905-1929 from age 1 until age 85. We measure exposure to disease using the local post-early neonatal mortality rate in the first 12 months after birth and apply flexible parametric survival models. For females, we find a negative effect on life expectancy (scarring) at ages 1-85 following high disease exposure in infancy, particularly for those born to unskilled workers. For males, we find no negative effect on later-life survival, likely because stronger mortality selection in infancy outweighs scarring. Thus, even as the incidence of infectious diseases declined at the start of the twentieth century, early-life disease exposure generated long-lasting negative but heterogeneous population health effects.

Detecting month and year of birth effects on reproduction and marriage patterns in two long-term data sets.

This study examines the effects of birth month on reproduction and mating behavior using historical and contemporary census data from 1820 to 1970. The research examines the effect of birth month on the number of children for women and their male spouses, finding a monthly cycle for both men and women. In addition, the study examines whether birth month influences whether a person has ever been married. In support of previous research, we find clear birth month effects on the number of children for both women and their spouses, while the time series of ever being married shows a 60-month and a 10-year cycle, the latter possibly related to the solar cycle. Although the effects are small, both results, based on a large and representative dataset, indicate the importance of early life factors on mating and reproduction.

Early-life risk factors for depression among young adults in the United States general population: Attributable risks and gender differences.

BACKGROUND: This study adopts individual and societal-level approaches to examine the contribution of childhood risk factors to major depressive episodes (MDE) in 2526 American young adults. METHODS: Nationally representative data from the 2017 U.S. Panel Study of Income Dynamics - Transition into Adulthood Supplement (PSID-TAS) were analyzed using multivariate methods to assess the impact of parental mental illness, childhood adversities, childhood mental disorders, and childhood physical conditions. Adjusted odds ratios and population attributable risk proportions (PARPs) are calculated to estimate the proportion of MDE cases related to risk factors. RESULTS: The 12-month prevalence of positive screens for MDE was 25.4 %. Approximately 34 % of these were attributable to childhood mental disorders, 24 % to childhood physical conditions, 21 % to childhood adversities, and 16 % to parental mental illness. Childhood and parental depression were critical risk factors, both at the individual (odds ratio exceeding 2) and societal (PARP approximately 24 %) levels. Gender-specific risk factors were identified, with childhood physical abuse and childhood anxiety disorders constituting risk factors for females, and childhood externalizing disorders and childhood headaches as risk factors for males. Approximately 60 % of U.S. young adult MDE cases are attributable to risk factors before age 18. LIMITATIONS: Possible over reporting of MDE may have biased the associations between predictors and depression. CONCLUSIONS: Exposure to depression at a young age-one's own or parental depression-is a robust risk factor for both genders. Policies and interventions focused at alleviating the societal burden of depression should value its generational transmission.

Childhood trauma is linked to epigenetic age deceleration in young adults with previous youth residential care placements.

Background: Early adversity increases the risk for mental and physical disorders as well as premature death. Epigenetic processes, and altered epigenetic aging in particular, might mediate these effects. While the literature that examined links between early adversity and epigenetic aging is growing, results have been heterogeneous.Objective: In the current work, we explored the link between early adversity and epigenetic aging in a sample of formerly out-of-home placed young adults.Method: A total of N = 117 young adults (32% women, age mean = 26.3 years, SD = 3.6 years) with previous youth residential care placements completed the Childhood Trauma Questionnaire (CTQ) and the Life Events Checklist (LEC-R) and provided blood samples for the analysis of DNA methylation using the Illumina Infinium MethylationEPIC BeadChip Microarray. Epigenetic age was estimated using Hovarth's and Hannum's epigenetic clocks. Furthermore, Hovarth's and Hannum's epigenetic age residuals were calculated as a proxy of epigenetic aging by regressing epigenetic age on chronological age. The statistical analysis plan was preregistered (https://osf.io/b9ev8).Results: Childhood trauma (CTQ) was negatively associated with Hannum's epigenetic age residuals, ß = -.23, p = .004 when controlling for sex, BMI, smoking status and proportional white blood cell type estimates. This association was driven by experiences of physical neglect, ß = -.25, p = .001. Lifetime trauma exposure (LEC-R) was not a significant predictor of epigenetic age residuals.Conclusion: Childhood trauma, and physical neglect in particular, was associated with decelerated epigenetic aging in our sample. More studies focusing on formerly institutionalized at-risk populations are needed to better understand which factors affect stress-related adaptations following traumatic experiences.

Growing literature links early adversity to altered epigenetic aging, yet results have been heterogeneous.We assessed childhood and lifetime trauma exposure using the Childhood Trauma Questionnaire and the Life Events Checklist and estimated epigenetic aging by obtaining Horvath's and Hannum's epigenetic age residuals in a sample of formerly out-of-home placed young adults.In this high-risk sample, childhood trauma, physical neglect in particular, but not lifetime trauma was negatively related to epigenetic aging.