Browsing by Subject "Developmental Psychology"

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    Mitigating the Effects of Early Experience: Adolescent Social functioning as a predictor of adult health
    (2014-06) Puig, Jennifer
    Researchers examining the etiology of chronic illness in adulthood are increasingly looking back towards early life events to find risk factors for disease. To date, researchers have failed to account for the tremendous amount of social growth and development that takes place in the intervening years between infancy and adulthood. This prospective longitudinal study examines the influence of adolescent and young adult social functioning on adult physical outcomes above and beyond the influence of early life social functioning. This study also examines the relative influence of social functioning, socio-economic status (SES), and health history on adult health outcomes. Participants from this study are a subsample from the Minnesota Longitudinal Study of Parents and Children (N=167) who have been followed from birth to age 34 years. Social functioning was assessed in infancy as the continuity of attachment classifications between ages 12 and 18 months. Adolescent, young adult, and adult social functioning were assessed via qualitative codes of videotaped interactions and interviews. At age 32 and 34 years participants were asked about the presence of or treatment for any physical illness. Results indicated that infant social functioning predicted the likelihood of reporting a physical illness in adulthood above and beyond the effects of later social functioning, early and concurrent SES, physical health, concurrent body mass index, gender, and self-reported neuroticism. These findings indicate that attachment in infancy exerts a powerful influence on later physical health outcomes and suggests that it as a powerful point of intervention.
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    PATHWAYS TO DEPRESSIVE SYMPTOMS AND INFLAMMATION FROM EARLY PSYCHOSOCIAL AND NUTRITIONAL ADVERSITY: A LONGITUDINAL STUDY OF CHILEAN YOUTH
    (2020-06) Reid, Brie
    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.