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.

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.

Early Life Adversity with Height Stunting Is Associated with Cardiometabolic Risk in Adolescents Independent of Body Mass Index.

OBJECTIVE: To evaluate cardiovascular and metabolic function in youths adopted internationally from orphanages/institutions (postinstitutionalized) who were height-stunted at adoption. STUDY DESIGN: A total of 30 postinstitutionalized youths (age, 9-18 years; body mass index [BMI] percentile, 7.2-90.4) who were height-stunted at adoption were compared with age- and BMI percentile-matched youths (n = 90). Measurements included total body fat and visceral adipose tissue (dual radiograph absorptiometry), arterial stiffness (augmentation index and pulse wave velocity), cardiac autonomic function (heart rate variability), blood pressure, and fasting lipid, glucose, and insulin levels. Linear regression analyses were computed controlling for parent education, age, trunk tissue fat, height-for-age, sex, and race. RESULTS: Compared with controls of the same age, sex, and BMI, the postinstitutionalized children had higher systolic blood pressure (P = .018), augmentation index (P= .033), total cholesterol (P= .047), low-density lipoprotein cholesterol (P= .03), triglycerides (P= .048), insulin (P= .005), and HOMA-IR (P= .01) values. The postinstitutionalized children had a lower low-frequency to high-frequency ratio (P = .008), indicating lower sympathetic tone, as well as a lower total lean mass (P = .016), a lower gynoid lean mass (P = .039), and a higher proportion of trunk tissue fat (P = .017). The postinstitutionalized and control children did not differ in any other body composition measures. CONCLUSIONS: Early life stress, as represented by height-stunted growth in institutional care, may be associated with early pathways to cardiovascular and metabolic risk in youths even after moving into well-resourced homes early in life and in the absence of increased adiposity. These findings suggest that postinstitutionalized youths with a history of height stunting may need to be closely monitored for emergent cardiometabolic risk factors.