Infant iron deficiency, iron supplementation, and psychosocial stress as predictors of neurocognitive development in Chilean adolescents.

Objective: The aim of the current study was to examine the unique and joint contributions of iron deficiency, iron supplementation, and psychosocial stress in infancy and stress in adolescence to neurocognitive functioning in adolescence.Methods: The current study (N = 796; Mage = 14.4y) involved a prospective cohort of low- and middle-socioeconomic status adolescents in Santiago, Chile. As infants, they had participated in an iron supplementation trial. Infant iron status was assessed at 12-18 months, and mothers answered questions about family psychosocial stress at 6-12 months and in adolescence (maternal depressive symptoms, home support for child development, stressful life events, father absence, socioeconomic status, and parental education). Neurocognitive functioning was assessed in adolescence using the Balloon Analogue Risk Task, Stockings of Cambridge, Trail Making Test, Purdue Pegboard Test, and Wisconsin Card Sorting Test.Results: Greater psychosocial stress in infancy predicted less risk-taking, poorer planning abilities and fluid cognition, and slower processing speed in adolescence. Iron deficiency anemia in infancy predicted less risk-taking. Greater adolescent psychosocial stress predicted difficulties in set-shifting. There were no interactions between infant psychosocial stress and iron deficiency predicting adolescent neurocognitive functioning.Conclusion: These results suggest that interventions to reduce infant psychosocial stress may be more likely to prevent multiple neurocognitive deficits in adolescence than interventions to reduce infant iron deficiency.

Sensitive periods for psychosocial risk in childhood and adolescence and cardiometabolic outcomes in young adulthood.

Greater psychosocial risk in childhood and adolescence predicts poorer cardiometabolic outcomes in adulthood. We assessed whether the timing of psychosocial risk from infancy through adolescence predicts cardiometabolic outcomes in young adulthood. Young adults and their mothers participated in a longitudinal study beginning in infancy in Santiago, Chile (N = 1040). At infancy, 5 years, 10 years, and adolescence, mothers reported on depressive symptoms, stressful experiences, support for child development in the home, father absence, parental education, and socioeconomic status (SES) to create a psychosocial risk composite at each time point. Young adults (52.1% female; 21-27 years) provided fasting serum samples and participated in anthropometric and blood pressure (BP) assessments, including a dual-energy X-ray absorptiometry (DXA) scan for measuring body fat. Greater infant psychosocial risk was associated with a greater young adult metabolic syndrome score (ß = 0.07, 95% confidence intervals (CI): 0.01 to 0.13, p = 0.02), a higher body mass index and waist circumference composite (ß = 0.08, 95% CI: 0.03 to 0.13, p = 0.002), and a higher body fat (DXA) composite (ß = 0.07, 95% CI: 0.01 to 0.12, p = 0.02). No psychosocial risk measure from any time point was associated with BP. Infant psychosocial risk predicted cardiometabolic outcomes in young adulthood better than psychosocial risk at 5 years, 10 years, or adolescence, mean of psychosocial risk from infancy through adolescence, and maximum of psychosocial risk at any one time. Consistent with the Developmental Origins of Health and Disease model, findings suggest that infancy is a sensitive period for psychosocial risk leading to poorer cardiometabolic outcomes in young adulthood.

Pathways to inflammation in adolescence through early adversity, childhood depressive symptoms, and body mass index: A prospective longitudinal study of Chilean infants.

Early adversity, depression, and obesity are associated with increases in low-grade inflammation. However, there are few prospective and longitudinal studies to elucidate how these associations unfold in children. The present study used latent growth curve models to examine pathways between family adversity in infancy, depressive symptoms in childhood, body mass index (BMI) in childhood, and inflammation in adolescence (age = 16-18). The study is an adolescent follow-up of infants from working-class communities around Santiago, Chile, who participated in a preventive trial of iron supplementation at 6 months of age. Anthropometrics, stressful life events, maternal depression, socioeconomic status, and developmental assessments were measured at 12 months, 5 years, 10 years, and adolescence. In adolescence, participants provided blood samples for high-sensitivity C-reactive protein (hsCRP) assessment. Greater exposure to early adversity in the form of interpersonal conflict stress in infancy indirectly associated with increased hsCRP through its association to increased intercept and slope of childhood BMI. Depressive symptoms at any time were not directly or indirectly associated with increased hsCRP. These findings contribute to our understanding of how early family adversity and its associations with obesity and depressive symptoms across childhood are linked to low-grade, chronic inflammation in adolescence. The model identified as best capturing the data supported the pivotal role of childhood BMI in explaining how early-life adversity is associated with inflammation in adolescence.

Adolescent Internalizing, Externalizing, and Social Problems Following Iron Deficiency at 12-18 Months: The Role of Maternal Responsiveness.

This study tested whether maternal responsiveness moderated or mediated pathways from iron deficiency (ID) at 12-18 months to adolescent behavior problems. Participants were part of a large Chilean cohort (N = 933). Iron status was assessed at 12 and 18 months. Maternal responsiveness was assessed at 9 months and 5 years. Parents reported their child's symptomology at 5 years, 10 years, and adolescence (11-17 years; M = 14.4). Structural equation modeling identified a previously unrecognized pathway by which child externalizing problems and negative maternal responsiveness at 5 years mediated associations between ID at 12-18 months and adolescent internalizing, externalizing, and social problems. Positive maternal responsiveness in infancy did not buffer those with ID anemia from developing 5-year internalizing problems.

Infant Psychosocial Environment Predicts Adolescent Cardiometabolic Risk: A Prospective Study.

OBJECTIVE: To prospectively assess whether the infant psychosocial environment was associated with cardiometabolic risk as early as adolescence. STUDY DESIGN: Participants were recruited in Santiago, Chile, and have been followed from infancy. Inclusion criteria included healthy infants with birth weight ≥3 kg and a stable caregiver. The psychosocial environment, including depressive symptoms, stressful life events, poor support for child development, father absence, and socioeconomic status, was reported by mothers at 6-12 months. Body mass index (BMI) z score was assessed at 5 and 10 years. BMI z score, waist-to-hip ratio, systolic and diastolic blood pressure, fat mass and body fat percentage, fasting glucose, total and high-density lipoprotein cholesterol, and homeostatic model of insulin resistance were tested in adolescence. RESULTS: Adolescents ranged from 16 to 18 years of age (n = 588; 48.1% female). A poorer infant psychosocial environment was associated with BMI z score at 10 years (ß = 0.10, 95% CI = 0.00-0.19) and in adolescence (ß = 0.15, 95% CI = 0.06-0.24) but not at 5 years. A poorer infant psychosocial environment was associated with higher blood pressure (ß = 0.15, 95% CI = 0.05-0.24), greater anthropometric risk (ß = 0.13, 95% CI = 0.03-0.22), greater biomarker (triglycerides, homeostatic model assessment of insulin resistance, total cholesterol) risk (ß = 0.12, 95% CI = 0.02-0.22), and a higher likelihood of metabolic syndrome in adolescence (aOR = 1.50; 95% CI = 1.06-2.12). CONCLUSIONS: These findings demonstrate that a poorer infant psychosocial environment was associated with greater adolescent cardiometabolic risk. The results support screening for infants' psychosocial environments and further research into causality, mechanisms, prevention, and intervention.

Infant Iron Deficiency and Iron Supplementation Predict Adolescent Internalizing, Externalizing, and Social Problems.

OBJECTIVE: To evaluate associations between iron supplementation and iron deficiency in infancy and internalizing, externalizing, and social problems in adolescence. STUDY DESIGN: The study is a follow-up of infants as adolescents from working-class communities around Santiago, Chile who participated in a preventive trial of iron supplementation at 6 months of age. Inclusionary criteria included birth weight ≥3.0 kg, healthy singleton term birth, vaginal delivery, and a stable caregiver. Iron status was assessed at 12 and 18 months of age. At 11-17 years of age, internalizing, externalizing, and social problems were reported by 1018 adolescents with the Youth Self Report and by parents with the Child Behavior Checklist. RESULTS: Adolescents who received iron supplementation in infancy had greater self-reported attention-deficit/hyperactivity disorder but lower parent-reported conduct disorder symptoms than those who did not (Ps < .05). Iron deficiency with or without anemia at 12 or 18 months of age predicted greater adolescent behavior problems compared with iron sufficiency: more adolescent-reported anxiety and social problems, and parent-reported social, post-traumatic stress disorder, attention-deficit/hyperactivity disorder, oppositional defiant, conduct, aggression, and rule breaking problems (Ps < .05). The threshold was iron deficiency with or without anemia for each of these outcomes. CONCLUSIONS: Iron deficiency with or without anemia in infancy was associated with increased internalizing, externalizing, and social problems in adolescence.