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Childhood Antecedents of Systemic Inflammation in Adolescence and Adulthood : Contributions of Childhood Family Environment and Socioeconomic Context.
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Childhood Antecedents of Systemic Inflammation in Adolescence and Adulthood : Contributions of Childhood Family Environment and Socioeconomic Context.
자료유형  
 학위논문
Control Number  
0017164332
International Standard Book Number  
9798346374398
Dewey Decimal Classification Number  
610
Main Entry-Personal Name  
Natale, Brianna Nicole.
Publication, Distribution, etc. (Imprint  
[S.l.] : University of Pittsburgh., 2024
Publication, Distribution, etc. (Imprint  
Ann Arbor : ProQuest Dissertations & Theses, 2024
Physical Description  
104 p.
General Note  
Source: Dissertations Abstracts International, Volume: 86-05, Section: A.
General Note  
Advisor: Reed, Rebecca;Hipwell, Alison;Hanson, Jamie;Shaw, Daniel;Marsland, Anna.
Dissertation Note  
Thesis (Ph.D.)--University of Pittsburgh, 2024.
Summary, Etc.  
요약The childhood family environment has been associated with lifelong health trajectories, including cardiometabolic disease morbidity and mortality. Systemic inflammation is one important preclinical marker of cardiometabolic risk, and prior studies have shown that early-life experiences, including family relationship quality and socioeconomic status, are related to circulating levels of inflammatory markers as early as adolescence. The current study utilized data from the Pittsburgh Girls Study to longitudinally investigate links between a childhood family environment latent variable-indicated by harsh punishment, caregiver-partner conflict, and caregiver depression-and inflammation in adolescence (n=429; M age=10.52) and early adulthood (n=1,362; Mage=23.57), while considering additional risk (financial strain) and protective (supportive parenting) factors. Structural equation models found that greater family adversity across ages 5-9 was prospectively associated with higher levels of interleukin (IL)-6 in both adolescence and adulthood, even when adjusting for covariates (e.g., child self-control, pubertal timing). Further adjustment for adolescent waist circumference attenuated the link between the childhood family environment and adult IL-6 to non-significance, and sensitivity analyses revealed that it was a significant mediator of this relationship. When adding financial strain into the models, the childhood family environment was no longer predictive of later inflammation, but there was evidence for associations between childhood financial strain and adult IL-6. Contrary to hypotheses, supportive parenting did not moderate associations between childhood family environment or financial strain and later inflammation. Together, these results suggest that the childhood family environment contributes to long-term systemic inflammation, although not independently of childhood socioeconomic context. The current study offers novel insights into links between childhood stressors and inflammatory profiles across developmental stages and highlights opportunities to further probe biopsychosocial mechanisms underlying these relationships.
Subject Added Entry-Topical Term  
Biomarkers.
Subject Added Entry-Topical Term  
Health behavior.
Subject Added Entry-Topical Term  
Socioeconomic factors.
Subject Added Entry-Topical Term  
Family income.
Subject Added Entry-Topical Term  
Scandals.
Subject Added Entry-Topical Term  
Adverse childhood experiences.
Subject Added Entry-Topical Term  
Teenagers.
Subject Added Entry-Topical Term  
Behavioral psychology.
Subject Added Entry-Topical Term  
Clinical psychology.
Subject Added Entry-Topical Term  
Home economics.
Subject Added Entry-Topical Term  
Health sciences.
Subject Added Entry-Topical Term  
Sociology.
Added Entry-Corporate Name  
University of Pittsburgh.
Host Item Entry  
Dissertations Abstracts International. 86-05A.
Electronic Location and Access  
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Control Number  
joongbu:657084
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