PATHWAYS TO DEPRESSIVE SYMPTOMS AND INFLAMMATION FROM EARLY PSYCHOSOCIAL AND NUTRITIONAL ADVERSITY: A LONGITUDINAL STUDY OF CHILEAN YOUTH

Abstract

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.