Early Life Adversity Research Articles

Subtypes of childhood maltreatment and posttraumatic stress disorder symptoms in an adult trauma sample: The mechanistic role of sleep.

Childhood maltreatment is indisputably linked to adverse mental health outcomes, including an increased risk to develop posttraumatic stress disorder (PTSD) in adulthood. The role of childhood maltreatment in the context of recovery from a trauma later in adulthood is not well understood. A variable related to both childhood maltreatment and PTSD symptoms, and a potential link between the two, is sleep. The current study aimed to understand how sleep disturbances may play a mechanistic role in the effect of subtypes of childhood maltreatment on PTSD symptom severity in an adult trauma sample. 160 adults (90 women; Mage = 33.73, SD = 10.86) were recruited from the emergency department at a Level-1 trauma center in southeastern Wisconsin after experiencing a traumatic injury. Experiences of childhood maltreatment and sleep were self-reported at 2-week and 3-month posttrauma, respectively. PTSD symptoms were clinically assessed 6 months later. Sleep disturbances 3-month posttrauma mediated the effect of emotional abuse, physical neglect, and emotional neglect on PTSD symptom 6 months after the traumatic injury. The effect of sexual and physical abuse on PTSD symptoms was not significantly mediated by sleep disturbances. These findings highlight the differential impact of subtypes of childhood maltreatment on PTSD symptoms, the mechanistic role of sleep, and the need to consider early life adversity when assessing adult posttrauma experiences. These results also suggest that interventions aimed at improving sleep quality might improve PTSD symptoms in those who have experienced childhood maltreatment and a subsequent traumatic injury in adulthood. (PsycInfo Database Record (c) 2024 APA, all rights reserved).

Parvalbumin interneurons in human ventromedial prefrontal cortex: a comprehensive post-mortem study of myelination and perineuronal nets in neurotypical individuals and depressed suicides with and without a history of child abuse.

Cortical parvalbumin interneurons (PV+) are major regulators of excitatory/inhibitory information processing, and their maturation is associated with the opening of developmental critical periods (CP). Recent studies reveal that cortical PV+ axons are myelinated, and that myelination along with perineuronal net (PNN) maturation around PV+ cells is associated with the closures of CP. Although PV+ interneurons are susceptible to early-life stress, their relationship between their myelination and PNN coverage remains unexplored. This study compared the fine features of PV+ interneurons in well-characterized human post-mortem ventromedial prefrontal cortex samples (n = 31) from depressed suicides with or without a history of child abuse (CA) and matched controls. In healthy controls, 81% of all sampled PV+ interneurons displayed a myelinated axon, while a subset (66%) of these cells also displayed a PNN, proposing a relationship between both attributes. Intriguingly, a 3-fold increase in the proportion of unmyelinated PV+ interneurons with a PNN was observed in CA victims, along with greater PV-immunofluorescence intensity in myelinated PV+ cells with a PNN. This study, which is the first to provide normative data on myelination and PNNs around PV+ interneurons in human neocortex, sheds further light on the cellular and molecular consequences of early-life adversity on cortical PV+ interneurons.

40. Early Life Adversity in Mice Accelerates Age-Related Decline in Behavioral Pattern Separation

40. Early Life Adversity in Mice Accelerates Age-Related Decline in Behavioral Pattern Separation

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

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

Dimensions of early life adversity and their associations with functional brain organisation

Abstract Early life adversity is associated with differences in brain function and an elevated risk for poor mental health. Using data from children aged 10 (N = 5,798) from the Adolescent Brain Cognitive Development (ABCD) cohort, we investigated how adversity relates to functional brain organisation using a network neuroscience approach. We derived four data-driven categories of adversity by fitting a mixed graphical model: household/community instability, physical/sexual abuse, parental neglect, and financial difficulties. Analyses revealed that multiple forms of adversity were associated with reduced clustering and increased assortativity across the entire brain and that these local measures of organisation captured greater adversity-related variance than mesoscale measures like modularity. The most pronounced effects were in the somatosensory and subcortical networks. Financial difficulties showed the strongest and most widespread associations with brain organisation, with evidence of a mediating effect of assortativity on the association between financial difficulties and internalising symptoms. Adding race as a covariate attenuated most brain-adversity relationships, suggesting that experiences of adversity are strongly related to race/ethnicity in the ABCD sample. These results demonstrate that different forms of adversity are associated with both shared and unique variations in functional brain organisation, highlighting its potential significance for explaining individual differences in mental health outcomes following early life adversity.

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.

A future food boom rescues the negative effects of early-life adversity on adult lifespan in a small mammal.

Early-life adversity, even when transient, can have lasting effects on individual phenotypes and reduce lifespan across species. If these effects can be mitigated by a high-quality later-life environment, then differences in future resources may explain variable resilience to early-life adversity. Using data from over 1000 wild North American red squirrels, we tested the hypothesis that the costs of early-life adversity for adult lifespan could be offset by later-life food abundance. We identified six adversities that reduced juvenile survival in the first year of life, though only one-birth date-had continued independent effects on adult lifespan. We then built a weighted early-life adversity (wELA) index integrating the sum of adversities and their effect sizes. Greater weighted early-life adversity predicted shorter adult lifespans in males and females, but a naturally occurring food boom in the second year of life ameliorated this effect. Experimental food supplementation did not replicate this pattern, despite increasing lifespan, indicating that the buffering effect of a future food boom may hinge on more than an increase in available calories. Our results suggest a non-deterministic role of early-life conditions for later-life phenotype, highlighting the importance of evaluating the consequences of early-life adversity in the context of an animal's entire life course.

Developmental epigenomic effects of maternal financial problems.

Early-life adversity as neglect or low socioeconomic status is associated with negative physical/mental health outcomes and plays an important role in health trajectories through life. The early-life environment has been shown to be encoded as changes in epigenetic markers that are retained for many years.We investigated the effect of maternal major financial problems (MFP) and material deprivation (MD) on their children's epigenome in the Avon Longitudinal Study of Parents and Children (ALSPAC) cohort. Epigenetic aging, measured with epigenetic clocks, was weakly accelerated with increased MFP. In subsequent EWAS, MFP, and MD showed strong, independent programing effects on children's genomes. MFP in the period from birth to age seven was associated with genome-wide epigenetic modifications on children's genome visible at age 7 and partially remaining at age 15.These results support the hypothesis that physiological processes at least partially explain associations between early-life adversity and health problems later in life. Both maternal stressors (MFP/MD) had similar effects on biological pathways, providing preliminary evidence for the mechanisms underlying the effects of low socioeconomic status in early life and disease outcomes later in life. Understanding these associations is essential to explain disease susceptibility, overall life trajectories and the transition from health to disease.

Early life adversity is associated with differential gene expression in immune cells: A cluster-based analysis across an acute psychosocial stressor

Elucidating mechanisms by which early-life adversity (ELA) contributes to increased disease risk is important for mitigating adverse health outcomes. Prior work has found differences in immune cell gene expression related to inflammation and mitochondrial activity. Using a within-person between-group experimental design, we investigated differences in gene expression clusters across acute psychosocial stress and no-stress conditions. Participants were young adults (N = 29, aged 18 – 25 years, 62 % female, 47 % with a history of ELA). Gene expression was assessed in peripheral blood mononuclear cells collected at 8 blood draws spanning two 5-hour sessions (stress vs. no-stress) separated by a week, 4 across each session (number of observations = 221). We applied two unsupervised gene clustering methods – latent profile analysis (LPA) and weighted gene co-expression analysis (WGCNA) – to cluster genes with similar expression patterns across participants. LPA identified 11 clusters, 7 of which were significantly associated with ELA-status. WGCNA identified 5 clusters, 3 of which were significantly associated with ELA-status. LPA- and WGCNA-identified clusters were correlated, and all clusters were highly preserved across sessions and time. There was no significant effect of acute stress on cluster gene expression, but there was a significant effect of time, and significant differences by ELA-status. ELA-associated clusters related to RNA splicing/processing, inflammation, leukocyte differentiation and division, and mitochondrial activity were differentially expressed across time: ELA-exposed individuals showed decreased expression of these clusters at 90-minutes while controls showed increased expression. Our findings replicate previous work in this area and highlight additional mechanisms by which ELA may contribute to disease risk.

Boosting decision-making in rat models of early-life adversity with environmental enrichment and intranasal oxytocin

Impaired decision-making constitutes a fundamental issue in numerous psychiatric disorders. Extensive research has established that early life adversity (ELA) increases vulnerability to psychiatric disorders later in life. ELA in human neonates is associated with changes in cognitive, emotional, as well as reward-related processing. Maternal separation (MS) is an established animal model of ELA and has been shown to be associated with decision-making deficits. On the other hand, enriched environment (EE) and intranasal oxytocin (OT) administration have been demonstrated to have beneficial effects on decision-making in humans or animals. Given these considerations, our investigation sought to explore the impact of brief exposure to EE and intranasal OT administration on the decision-making abilities of adolescent rats that had experienced MS during infancy.The experimental protocol involved subjecting rat pups to the MS regimen for 180 min per day from postnatal day (PND) 1 to PND 21. Then, from PND 22 to PND 34, the rats were exposed to EE and/or received intranasal OT (2 μg/μl) for seven days. The assessment of decision-making abilities, using a rat gambling task (RGT), commenced during adolescence. Our findings revealed that MS led to impaired decision-making and a decreased percentage of advantageous choices. However, exposure to brief EE or intranasal OT administration mitigated the deficits induced by MS and improved the decision-making skills of maternally-separated rats. Furthermore, combination of these treatments did not yield additional benefits. These results suggest that EE and OT may hold promise as therapeutic interventions to enhance certain aspects of cognitive performance.

Early adversity and sexual diversity: the importance of self-reported and neurobiological sexual reward sensitivity

Work shows that sexually-diverse individuals face high rates of early life adversity and in turn increased engagement in behavioral outcomes traditionally associated with adversity, such as sexual risk taking. Recent theoretical work suggests that these associations may be attributable to heightened sexual reward sensitivity among adversity-exposed women. We aimed to test these claims using a combination of self-report and EEG measures to test the relationship between early adversity, sexual reward sensitivity (both self-reported and EEG measured) and sexual risk taking in a sexually diverse sample of cis-gender women (N = 208) (Mage = 27.17, SD = 6.36). Results showed that childhood SES predicted self-reported sexual reward sensitivity which in turn predicted numbers of male and female sexual partners. In contrast we found that perceived childhood unpredictability predicted neurobiological sexual reward sensitivity as measured by EEG which in turn predicted male sexual partner number. The results presented here provide support for the notion that heightened sexual reward sensitivity may be a pathway through which early life adversity augments future sexual behavior, and underscores the importance of including greater attention to the dynamics of pleasure and reward in sexual health promotion.

Early life adversity is associated with greater similarity in neural representations of ambiguous and threatening stimuli.

Exposure to early life adversity (ELA) is hypothesized to sensitize threat-responsive neural circuitry. This may lead individuals to overestimate threat in the face of ambiguity, a cognitive-behavioral phenotype linked to poor mental health. The tendency to process ambiguity as threatening may stem from difficulty distinguishing between ambiguous and threatening stimuli. However, it is unknown how exposure to ELA relates to neural representations of ambiguous and threatening stimuli, or how processing of ambiguity following ELA relates to psychosocial functioning. The current fMRI study examined multivariate representations of threatening and ambiguous social cues in 41 emerging adults (aged 18 to 19 years). Using representational similarity analysis, we assessed neural representations of ambiguous and threatening images within affective neural circuitry and tested whether similarity in these representations varied by ELA exposure. Greater exposure to ELA was associated with greater similarity in neural representations of ambiguous and threatening images. Moreover, individual differences in processing ambiguity related to global functioning, an association that varied as a function of ELA. By evidencing reduced neural differentiation between ambiguous and threatening cues in ELA-exposed emerging adults and linking behavioral responses to ambiguity to psychosocial wellbeing, these findings have important implications for future intervention work in at-risk, ELA-exposed populations.

Associations Between Early-Life Adversity, Ambient Air Pollution, and Telomere Length in Children.

Examine the independent associations and interaction between early-life adversity and residential ambient air pollution exposure on relative buccal telomere length (rBTL). Experiences of abuse, neglect, household challenges, and related life events were identified in a cross-sectional sample of children aged 1 to 11 years ( n = 197) using the 17-item Pediatric ACEs and Related Life Event Screener (PEARLS) tool. The PEARLS tool was analyzed both as a total score and across established domains (Maltreatment, Household Challenges, and Social Context). Ground-level fine particulate matter (PM 2.5 ) concentrations were matched to residential locations for the 1 and 12 months before biospecimen collection. We used multivariable linear regression models to examine for independent associations between continuous PM 2.5 exposure and PEARLS score/domains with rBTL. In addition, effect modification by PEARLS scores and domains on associations between PM 2.5 exposure and rBTL was examined. Study participants were 47% girls, with mean (standard deviation) age of 5.9 (3.4) years, median reported PEARLS score of 2 (interquartile range [IQR], 4), median 12-month prior PM 2.5 concentrations of 11.8 μg/m 3 (IQR, 2.7 μg/m 3 ), median 1-month prior PM 2.5 concentrations of 10.9 μg/m 3 (IQR, 5.8 μg/m 3 ), and rBTL of 0.1 (IQR, 0.03). Mean 12-month prior PM 2.5 exposure was inversely associated with rBTL ( β = -0.02, 95% confidence interval = -0.04 to -0.01). Although reported PEARLS scores and domains were not independently associated with rBTL, we observed a greater decrement in rBTL with increment of average annual PM 2.5 as reported Social Context domain items increased ( p -interaction < .05). Our results suggest that adverse Social Context factors may accelerate the association between chronic PM 2.5 exposure on telomere shortening during childhood.

Early-Life Adversities Are Associated With Lower Expected Value Signaling in the Adult Brain

BackgroundEarly adverse experiences are assumed to affect fundamental processes of reward learning and decision making. However, computational neuroimaging studies investigating these circuits in the context of adversity are sparse and limited to studies conducted in adolescent samples, leaving the long-term effects unexplored. MethodsUsing data from a longitudinal birth cohort study (n = 156; 87 female), we investigated associations between adversities and computational markers of reward learning (i.e., expected value, prediction errors). At age 33 years, all participants completed a functional magnetic resonance imaging–based passive avoidance task. Psychopathology measures were collected at the time of functional magnetic resonance imaging investigation and during the COVID-19 pandemic. We applied a principal component analysis to capture common variations across 7 adversity measures. The resulting adversity factors (factor 1: postnatal psychosocial adversities and prenatal maternal smoking; factor 2: prenatal maternal stress and obstetric adversity; factor 3: lower maternal stimulation) were linked with psychopathology and neural responses in the core reward network using multiple regression analysis. ResultsWe found that the adversity dimension primarily informed by lower maternal stimulation was linked to lower expected value representation in the right putamen, right nucleus accumbens, and anterior cingulate cortex. Expected value encoding in the right nucleus accumbens further mediated the relationship between this adversity dimension and psychopathology and predicted higher withdrawn symptoms during the COVID-19 pandemic. ConclusionsOur results suggested that early adverse experiences in caregiver context might have a long-term disruptive effect on reward learning in reward-related brain regions, which can be associated with suboptimal decision making and thereby may increase the vulnerability of developing psychopathology.

Problems in diagnosing pre-COPD (case report)

Cigarette smoke is a key risk factor for developing COPD (GOLD, 2024). One of the factors responsible for tissue damage and bronchial remodeling in the early stages of the disease is patients’ hypersensitivity to nicotine and components of cigarette smoke. Because of early life adversity combined with environmental and genetic interactions, pulmonary function measures alone may not be appropriate for the early recognition and diagnosis of COPD. It seems necessary to identify biomarkers of the risk of developing pre-COPD to identify the early stage of the disease. In the article we describe the clinical case of patient M., 21 years old, a smoker with a history of respiratory symptoms, who has signs of chronic obstructive pathology with the formation of bronchial hypersensitivity and persistent obstruction that does not reach the threshold for COPD, which reflects a common clinical problem. Сertainly, the formation of the concept of pre-COPD and the development of clinical and instrumental diagnostic criteria are necessary. Previously, we developed and tested a prick-prick test method with nicotine. We propose to use skin testing with a nicotine solution as one of the diagnostic biomarkers to identify hypersensitivity at the first stage of tissue damage.

Fear of predators reduces body and physiological condition affecting offspring survival and the ‘quality’ of the survivors

Abstract Predators affect the survival of developing young by eating them. More recently, the fear of being eaten has been uncovered as a powerful driver of offspring survival reducing recruited offspring numbers by 53%, but the mechanisms driving these effects are not well understood. We exposed song sparrows to predator or non‐predator playbacks throughout three breeding seasons. We followed offspring as eggs through development and into maturity. We quantified the repercussions of being reared in a fearful environment on body (fat, mass, size) and physiological condition using 12 different measures categorized into six systems (oxygen carrying capacity, energy reserves, immune function, antioxidant protection, oxidative stress/damage, glucocorticoids). We further tracked offspring survival in the nest to maturity and determined which measures of condition significantly predicted survival. We report that fear of predators affected offspring condition at all stages of life, with survival consequences. Predator‐playback offspring hatched from heavier eggs (8%) but quickly lost this advantage and never regained it. Nestlings reared by ‘frightened’ parents were as heavy and much leaner than non‐predator playback nestlings. This pattern extended throughout development into maturity where offspring reared by frightened parents were up to 31% leaner and 5% lighter. Predator‐playback nestlings also were evidently in poorer physiological condition, having shorter telomeres, while late dependency stage fledglings carried relatively less uric acid and more haptoglobin perhaps indicative of chronic susceptibility to infection. Only body condition (mass and fat) predicted survival during peak mortality periods (nestling and early fledging), with the leanest lightest offspring from the predator‐playback treatment being least likely to survive. Thereafter, mass predicted survival irrespective of playback treatment. Similarly, at this later stage, offspring with less telomere loss and high uric acid levels survived best regardless of playback group. Our findings reveal that fear of predators is a potent form of early life adversity which persistently alters the condition of offspring affecting early stage survival and the ‘quality’ of the survivors throughout their life. Development is fuelled by food and fear‐induced reductions in parental provisioning at the earliest stages likely instigated these effects, with consequences on the population growth rate. Read the free Plain Language Summary for this article on the Journal blog.

Neural foundation of the diathesis-stress model: longitudinal gray matter volume changes in response to stressful life events in major depressive disorder and healthy controls.

Recurrences of depressive episodes in major depressive disorder (MDD) can be explained by the diathesis-stress model, suggesting that stressful life events (SLEs) can trigger MDD episodes in individuals with pre-existing vulnerabilities. However, the longitudinal neurobiological impact of SLEs on gray matter volume (GMV) in MDD and its interaction with early-life adversity remains unresolved. In 754 participants aged 18-65 years (362 MDD patients; 392 healthy controls; HCs), we assessed longitudinal associations between SLEs (Life Events Questionnaire) and whole-brain GMV changes (3 Tesla MRI) during a 2-year interval, using voxel-based morphometry in SPM12/CAT12. We also explored the potential moderating role of childhood maltreatment (Childhood Trauma Questionnaire) on these associations. Over the 2-year interval, HCs demonstrated significant GMV reductions in the middle frontal, precentral, and postcentral gyri in response to higher levels of SLEs, while MDD patients showed no such GMV changes. Childhood maltreatment did not moderate these associations in either group. However, MDD patients who had at least one depressive episode during the 2-year interval, compared to those who did not, or HCs, showed GMV increases in the middle frontal, precentral, and postcentral gyri associated with an increase in SLEs and childhood maltreatment. Our findings indicate distinct GMV changes in response to SLEs between MDD patients and HCs. GMV decreases in HCs may represent adaptive responses to stress, whereas GMV increases in MDD patients with both childhood maltreatment and a depressive episode during the 2-year interval may indicate maladaptive changes, suggesting a neural foundation for the diathesis-stress model in MDD recurrences.

Limited bedding and nesting increases ethanol drinking in female rats

Prenatal opioid exposure (POE) and postnatal adverse experiences are early life adversities (ELA) that often co-occur and increase problematic alcohol (EtOH) drinking during adolescence. We investigated the relationship between POE, postnatal adversity, and adolescent EtOH drinking in rats. We also sought to determine whether ELAs affect alpha-adrenoceptor density in the brain because the noradrenergic system is involved in problematic alcohol drinking and its treatment. We hypothesized that the combination of POE and postnatal adversity will increase alcohol drinking in rats compared to rats with exposure to either adversity alone or to control. We also predicted that POE and postnatal adversity would increase α1-adrenoceptor density and decrease α2-adrenoceptor density in brain to confer a stress-responsive phenotype. Pregnant rats received morphine (15 mg/kg/day) or saline via subcutaneous minipumps from gestational day 9 until birth. Limited bedding and nesting (LBN) procedures were introduced from postnatal day (PD) 3-11 to mimic early life adversity-scarcity. Offspring rats (PD 31-33) were given opportunities to drink EtOH (20 %, v/v) using intermittent-access, two-bottle choice (with water) procedures. Rats given access to EtOH were assigned into sub-groups that were injected with either yohimbine (1 mg/kg, ip) or vehicle (2 % DMSO, ip) 30 min prior to each EtOH access session to determine the effects of α2-adrenoceptor inhibition on alcohol drinking. We harvested cortices, brainstems, and hypothalami from EtOH-naïve littermates on either PD 30 or PD 70 and conducted radioligand receptor binding assays to quantify α1- and α2-adrenoceptor densities. Contrary to our hypothesis, only LBN alone increased EtOH intake in female adolescent rats compared to female rats with POE. Neither POE nor LBN affected α1- or α2-adrenoceptor densities in the cortex, brainstem, or hypothalamus of early- or late-aged adolescent rats. These results suggest a complex interaction between ELA type and sex on alcohol drinking.

Fight Injustice with Darkness: The Effect of Early Life Adversity on Malevolent Creativity Behavior

ABSTRACTTwo studies were conducted to investigate the relationship between Early Life Adversity and Malevolent Creativity as well as its underlying mechanism. Study 1 established a moderated mediation model to explore the mediating role of Belief in a Just World (BJW) and the moderating role of Dark Triad. A total of 353 college students (Mage = 21.25, SDage = 2.21, 58.9% women) were recruited to fill out questionnaires. The results showed that Early Life Adversity positively predicted Malevolent Creativity behavior and indirectly predicted Malevolent Creativity behavior through BJW. Dark Triad reduced the effects of Early Life Adversity on BJW and intensified the effects of Early Life Adversity on Malevolent Creativity behavior. Study 2 explored the effect of threatening BJW on Malevolent Creativity potential. A total of 180 participants (Mage = 20.53, SDage = 1.7, 64.4% women) were investigated with questionnaires and a Malevolent Creativity Problem‐Solving Task. Study 2 validated study 1 and illustrated that the Malevolent Creativity potential (including fluency, originality, and malevolence) was enhanced when Belief in a Just World was threatened. However, greater fluency was only observed in men. As a whole, these finding emphasizes the important linking role of BJW between Early Life Adversity and Malevolent Creativity, and Dark Triad and gender influence the expression of Malevolent Creativity as well.

The effect of cognitive reappraisal and early-life maternal care on neuroendocrine stress responses

Early-life adversity (ELA) is related to profound dysregulation of the hypothalamic–pituitary–adrenal (HPA) axis, reflected in both, blunted or exaggerated cortisol stress responses in adulthood. Emotion regulation strategies such as cognitive reappraisal might contribute to this inconsistent finding. Here, we investigate an interaction of early-life maternal care (MC), where low MC represents a form of ELA, and instructed emotion regulation on cortisol responses to acute stress. Ninety-three healthy young women were assigned to a low (n = 33) or high (n = 60) MC group, based on self-reported early-life MC. In the laboratory, participants received regulation instructions, asking to cognitively reappraise (reappraisal group, n = 45) or to focus on senses (control group, n = 48) during subsequent stress exposure, induced by the Trier Social Stress Test. Salivary cortisol and subjective stress levels were measured repeatedly throughout the experiment. Multilevel model analyses confirmed a MC by emotion regulation interaction effect on cortisol trajectories, while controlling for hormonal status. Individuals with low MC in the control compared with the reappraisal group showed increased cortisol responses; individuals with high MC did not differ. These results highlight the significance of emotion regulation for HPA axis stress regulation following ELA exposure. They provide methodological and health implications, indicating emotion regulation as a promising target of treatment interventions for individuals with a history of ELA.