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Background Early-life adversity that increases the risk of growth stunting is hypothesized to increase the risk of obesity and, in girls, early-onset puberty. This hypothesis was tested in children adopted from orphanages. Methods Post-institutionalized (PI) youth were compared with youth reared in comparable families (non-adopted; NA) on height, weight, pubertal stage, and fat mass (127 PI, 80 female; 156 NA, 85 female, aged 7–14 years). Anthropometric findings at adoption were obtained from first US clinic visits. Results Overall, 25% of PI youth were height-stunted (<3rd percentile) at adoption. Years post adoption, PI youth had lower BMI-for-age ( P =0.004), height-for-age ( P <0.001), and less body fat ( P <0.001) than NA youth had, but they did not differ by sex. Pubertal status did not differ by group or sex. The anthropometric findings held when the stunted-at-adoption subset was examined; they were also less likely to be in central puberty than other PI youth. Conclusion Early deprived orphanage care increases the risk of growth stunting but not obesity in children adopted into US families, and it does not independently contribute to early-onset puberty for PI girls. The role of the environment following early adversity may modify the impact of early adverse care.

Early life stress (ELS) is linked to an elevated risk of poor health and early mortality, with emerging evidence pointing to the pivotal role of the immune system in long-term health outcomes. While recent research has focused on the impact of ELS on inflammation, this study examined the impact of ELS on immune function, including CMV seropositivity, inflammatory cytokines, and lymphocyte cell subsets in an adolescent cohort. This study used data from the Early Life Stress and Cardiometabolic Health in Adolescence Study (N = 191, aged 12 to 21 years, N = 95 exposed to ELS). We employed multiple regression to investigate the association between ELS, characterized by early institutional care, cytomegalovirus (CMV) seropositivity (determined by chemiluminescent immunoassay), inflammation (CRP, IL-6, and TNF-a determined by ELISA), and twenty-one immune cell subsets characterized by flow cytometry (sixteen T cell subsets and five B cell subsets). Results reveal a significant association between ELS and lymphocytes that was independent of the association between ELS and inflammation: ELS was associated with increased effector memory helper T cells, effector memory cytotoxic T cells, senescent T cells, senescent B cells, and IgD− memory B cells compared to non-adopted youth. ELS was also associated with reduced percentages of helper T cells and naive cytotoxic T cells. Exploratory analyses found that the association between ELS and fewer helper T cells and increased cytotoxic T cells remained even in cytomegalovirus (CMV) seronegative youth. These findings suggest that ELS is associated with cell subsets that are linked to early mortality risk in older populations and markers of replicative senescence, separate from inflammation, in adolescents.

Nonhuman animal models reveal that the hypothalamic–pituitary–adrenocortical (HPA) axis calibrates to the harshness of the environment during a sensitive period in infancy. Humans exposed to depriving institutional care in infancy show reduced HPA axis responsivity, even years after they are placed in supportive, well-resourced families. This study examined whether puberty opens a window of opportunity to recalibrate the HPA axis toward more typical reactivity when children shift from harsh deprived conditions in infancy into supportive conditions in childhood and adolescence. Participants (n = 129 postinstitutionalized, 68.2% female; n = 170 comparison, 52.4% female) completed 3 annual sessions beginning at ages 7 to 15 (M = 11.28, SD = 2.31). Each session assessed pubertal stage via nurse examination and cortisol reactivity to the Trier social stress test for children. The linear mixed-effects model controlling for sex and between-individual differences in pubertal stage showed a significant group by pubertal stage interaction: within-individual increases in pubertal stage were associated with increases in cortisol stress reactivity for postinstitutionalized youth but not nonadopted comparison youth. This study indicates that pubertal development reopens a window of opportunity for the HPA axis to recalibrate based on significant improvements in the supportiveness of the environment relative to that in infancy. The peripubertal period may be an important time in development where the caregiving environment has a substantial impact on the HPA axis and, perhaps, other stress-mediating systems. Future research is needed to examine the mechanisms of recalibration and whether HPA recalibration impacts physical and psychological health.

Adversity during infancy can affect neurobehavioral development and perturb the maturation of physiological systems. Dysregulated immune and inflammatory responses contribute to many of the later effects on health. Whether normalization can occur following a transition to more nurturing, benevolent conditions is unclear. To assess the potential for recovery, blood samples were obtained from 45 adolescents adopted by supportive families after impoverished infancies in institutional settings (post-institutionalized, PI). Their immune profiles were compared to 39 age-matched controls raised by their biological parents (non-adopted, NA). Leukocytes were immunophenotyped, and this analysis focuses on natural killer (NK) cell populations in circulation. Cytomegalovirus (CMV) seropositivity was evaluated to determine if early infection contributed to the impact of an atypical rearing. Associations with tumor necrosis factor-alpha (TNF-α) and interferon-gamma (IFN-γ), two cytokines released by activated NK cells, were examined. Compared to the NA controls, PI adolescents had a lower percent of CD56bright NK cells in circulation, higher TNF-α levels, and were more likely to be infected with CMV. PI adolescents who were latent carriers of CMV expressed NKG2C and CD57 surface markers on more NK cells, including CD56dim lineages. The NK cell repertoire revealed lingering immune effects of early rearing while still maintaining an overall integrity and resilience.

This review presents evidence from animal and human studies demonstrating the possible connection and significant impact of poor iron status and psychological distress on neurocognitive development during pregnancy and the neonatal period, with implications for long-term cognition. Stress and iron deficiency are independently prevalent and thus are frequently comorbid. While iron deficiency and early-life stress independently contribute to long-term neurodevelopmental alterations, their combined effects remain underexplored. Psychological stress responses may engage similar pathways as infectious stress, which alters fundamental iron metabolism processes and cause functional tissue-level iron deficiency. Psychological stress, analogous to but to a lesser degree than infectious stress, activates the hypothalamic–pituitary–adrenocortical (HPA) axis and increases proinflammatory cytokines. Chronic or severe stress is associated with dysregulated HPA axis functioning and a proinflammatory state. This dysregulation may disrupt iron absorption and utilization, likely mediated by the IL-6 activation of hepcidin, a molecule that impedes iron absorption and redistributes total body iron. This narrative review highlights suggestive studies investigating the relationship between psychological stress and iron status and outlines hypothesized mechanistic pathways connecting psychological stress exposure and iron metabolism. We examine findings regarding the overlapping impacts of early stress exposure to iron deficiency and children’s neurocognitive development. We propose that studying the influence of psychological stress on iron metabolism is crucial for comprehending neurocognitive development in children exposed to prenatal and early postnatal stressors and for children at risk of early iron insufficiency. We recommend future directions for dual-exposure studies exploring iron as a potential mediating pathway between early stress and offspring neurodevelopment, offering opportunities for targeted interventions.

Guided by concepts from life history (LH) theory, a large human research literature has tested the hypothesis that exposures to extrinsic mortality (EM) promote the development of faster LH strategies (e.g., earlier/faster reproduction, higher offspring number). A competing model proposes that, because EM in the past was intimately linked to energetic constraints, such exposures specifically led to the development of slower LH strategies. We empirically address this debate by examining (1) LH variation among small-scale societies under different environmental conditions; (2) country-, regional-, and community-level correlations between ecological conditions, mortality, maturational timing, and fertility; (3) individual-level correlations between this same set of factors; and (4) natural experiments leveraging the impact of externally caused changes in mortality on LH traits. Partially supporting each model, we found that harsh conditions encompassing energetic stress and ambient cues to EM (external cues received through sensory systems) have countervailing effects on the development of LH strategies, both delaying pubertal maturation and promoting an accelerated pace of reproduction and higher offspring number. We conclude that, although energetics are fundamental to many developmental processes, providing a first tier of environmental influence, this first tier alone cannot explain these countervailing effects. An important second tier of environmental influence is afforded by ambient cues to EM. We advance a two-tiered model that delineates this second tier and its central role in regulating the development of LH strategies. Consideration of the first and second tier together is necessary to account for the observed countervailing shifts toward both slower and faster LH traits.

The association of post-adoption experiences of discrimination with depressive symptoms was examined in 93 previously institutionalized (PI) youth (84% transracially adopted). Additionally, we explored whether sleep quality statistically moderated this association. Notably, we examined these associations after covarying a measure of autonomic balance (high/low frequency ratio in heart rate variability) affected by early institutional deprivation and a known risk factor for depression. PI youth exhibited more depressive symptoms and experiences of discrimination than 95 comparison youth (non-adopted, NA) raised in their biological families in the United States. In the final regression model, there was a significant interaction between sleep quality and discrimination, such that at higher levels of sleep quality, the association between discrimination and depression symptoms was non-significant. Despite being cross-sectional, the results suggest that the risk of depression in PI youth involves post-adoption experiences that appear unrelated to the impacts of early deprivation on neurobiological processes associated with depression risk. It may be crucial to examine methods of improving sleep quality and socializing PI youth to cope with discrimination as protection against discrimination and microaggressions.

Exposure to early-life adversity (ELA) and iron deficiency early in life are known risk factors for suboptimal brain and socioemotional development. Iron deficiency may arise from and co-occur with ELA, which could negatively affect development. In the present study, we investigated whether ELA is associated with iron deficiency in infants receiving no iron supplementation. This study is a secondary analysis of extant data collected in the 1990s; participants were healthy infants from working-class communities in Santiago, Chile ( N = 534, 45.5% female). We measured stressful life events, maternal depression, and low home support for child development during infancy and assessed iron status when the infant was 12 months old. Slightly more than half of the infants were iron-deficient (51%), and 25.8% were iron-deficient anemic at 12 months. Results indicated that ELA was associated with lower iron levels and iron deficiency at 12 months. The findings are consistent with animal and human prenatal models of stress and iron status and provide evidence of the association between postnatal ELA and iron status in humans. The findings also highlight a nutritional pathway by which ELA may impact development and present a nutritionally-focused avenue for future research on ELA and psychopathology.

BackgroundThe perseverative cognition hypothesis stipulates that rumination (repetitive, passive, uncontrollable negative thinking) prolongs the experience of a stressor which impacts stress physiology. In line with this hypothesis, we proposed that in response to real-life experiences of social rejection, adolescent girls who ruminate would show a blunted diurnal cortisol slope the next day relative to girls who do not ruminate. We also examined the effects of social rejection and rumination on waking cortisol levels and the cortisol awakening response.MethodParticipants were (n = 50) adolescent girls (mean age = 13.30, SD = 2.34) who varied on psychiatric risk and provided saliva samples 4 times a day for 3 days, as well as, daily diary reports of social rejection and rumination. A lagged multilevel model was utilized to examine the interactive effects of rejection and rumination on diurnal cortisol.ResultsThere was a significant interaction between social rejection and rumination. Specifically, rumination following social rejection was associated with a flatter diurnal cortisol slope. In the absence of rumination, social rejection was marginally associated with a steeper diurnal cortisol slope. The effects for waking cortisol levels and the cortisol awakening response were null.ConclusionFindings support the perseverative cognition hypothesis and suggest that cognitive mechanisms such as rumination can impact stress physiology.

Exposure to early life adversity (ELA) is thought to increase the risk of later psychopathology through alterations in immune system functioning, notably through increased inflammation. However, nutritional adversities such as iron deficiency may arise from and co-occur with ELA. Psychosocial adversity and nutritional adversities together may play a causal role in the development of psychosocial maladjustment via increases in circulating inflammatory factors. The present study investigates whether psychosocial ELA predicts iron status early in life and uses structural equation modeling to determine if ELA and iron status in infancy predict increased inflammation in adolescence and depressive symptoms in emerging adulthood. The study is a follow-up of infants from working-class communities in Santiago, Chile, who participated in a preventive trial of iron supplementation at six months of age. Anthropometrics, stressful life events, maternal depression, socioeconomic status, support for child development, and iron status were measured in the first year of life, five years, ten years, and adolescence. In adolescence, participants provided blood samples for inflammation assessments (CRP, WBC, neutrophil to lymphocyte ratio, and monocyte count). In emerging adulthood (21y), participants provided self-reported depressive symptoms. ELA in infancy predicted iron status in infancy and depressive symptoms in emerging adulthood. However, ELA did not directly predict increased inflammation in adolescence, and increased inflammation did not predict increased depressive symptoms. Iron status in infancy predicted increased monocyte count in adolescence, and ELA in infancy predicted higher levels of monocytes indirectly through iron status in infancy. These findings provide novel evidence of the association between postnatal ELA and iron status and suggest that ELA predicts depressive symptoms independent of inflammation in this population. These findings also provide evidence of a novel pathway by which early adversity and nutrition program the developing immune system.