Stress and Body Mass Index Each Contributes Independently to Tumor Necrosis Factor-α Production in Prepubescent Latino Children

University of Miami Behavioral Medicine Research Center, c/o VA Medical Center, Miami, FL, USA.
Journal of pediatric nursing (Impact Factor: 1.01). 10/2009; 24(5):378-88. DOI: 10.1016/j.pedn.2008.02.034
Source: PubMed

ABSTRACT This investigation extended prior work by determining if stress and body mass index (BMI) contributed independently to tumor necrosis factor-alpha (TNF-alpha) levels among prepubescent Latino children and if sex and family history of type 2 diabetes mellitus (T2DM) modified these relationships. Data were collected in South Florida from 112 nondiabetic school-aged Hispanic children, of whom 43.8% were obese (BMI >/= 95th percentile) and 51.8% presented with a family history of T2DM. Stressful life events were assessed via parental report using a life events scale. Plasma TNF-alpha levels were determined with enzyme-linked immunosorbent assay. The relative contributions of stress and BMI with TNF-alpha levels and the potential interaction effects of sex and family history of T2DM were analyzed with multiple linear regression analyses. Stress and BMI each accounted for a significant proportion of the unique variance associated with TNF-alpha. The association between stress and TNF-alpha was not modified by sex or family history of T2DM. These findings implicate BMI and stress as independent determinants of TNF-alpha (an inflammatory cytokine and adipocytokine) among Latino children. Future investigations should examine the potential roles of exercise, nutritional status, age, and growth hormone in explicating the relationship between TNF-alpha production and psychosocial distress and risk for infection among obese children.

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Available from: Alan Delamater, Sep 28, 2015
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    • "Thus, it is unclear whether interpersonal stress of any form has consequences for inflammation or whether only particular relationship domains can get under the skin. Studies of biomarkers of low-grade inflammation (e.g., Dixon et al., 2009; Fuligni et al., 2009) also leave open the question of what underlying processes are taking place in the body that might contribute to inflammation. It may be that stress leads monocytes and macrophages to become overly aggressive towards pathogens, and secrete greater quantities of cytokines that eventually contribute to systemic inflammation. "
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    ABSTRACT: Researchers have identified cross-sectional links between interpersonal stress and inflammation. Little is known, however, about how these dynamics unfold over time, what underlying immune pathways might exist, or whether moderators such as race could alter the strength of the connection between interpersonal stress and inflammatory processes. We examined whether adolescent girls whose relationship trajectories were characterized by chronic stress would exhibit a proinflammatory phenotype marked by systemic inflammation, heightened cytokine responses to bacterial challenges, and resistance to the anti-inflammatory properties of cortisol. Significant Stress × Race interactions revealed that family stress trajectories predicted glucocorticoid sensitivity and peer stress trajectories predicted cytokine production for White but not Asian girls. Relationship stress trajectories were not associated with systemic inflammation, however. These findings suggest that particular subgroups of adolescent girls who face chronic and elevated stress in their close relationships may be at risk for disruptions to the immune system.
    Development and Psychopathology 04/2015; -1:1-12. DOI:10.1017/S0954579415000334 · 4.89 Impact Factor
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    • "Our study is unique in providing insight on the temporal relationship between adverse events in early and middle childhood, subsequent inflammation, and the persistence of inflammation. These results correspond with prior research indicating elevated levels of inflammation among children and adolescents (Murasko, 2008; Dixon et al., 2009; Fuligni et al., 2009a; Howe et al., 2010) and adults (Taylor et al., 2006; Danese et al., 2007; Pollitt et al., 2007; Taylor et al., 2011) who experienced adversity in early life. These findings may also explain some of the inconsistencies across earlier studies. "
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    ABSTRACT: Background: Retrospective studies show that childhood adversity is associated with systemic inflammation in adulthood. Few prospective studies have examined whether childhood adversity influences inflammation in an observable manner during childhood or adolescence and if these effects are sustained over time. Methods: Using longitudinal data from the Avon Longitudinal Study of Parents and Children, we examined associations between acute adverse events at seven time points prior to age 8 and inflammation at ages 10 and 15. Inflammatory markers at age 10 included interleukin-6 (IL-6; N=4655) and C-reactive protein (CRP; N=4647), and CRP was measured again at age 15 (N=3286). We further evaluated whether body mass index (BMI), depression, or cigarette smoking mediated associations between adverse events and inflammation. Results: Adverse events in middle childhood (occurring between ages 6 to 8), as well as cumulative adversity from birth to 8 years, were associated with higher levels of IL-6 and CRP at age 10. Adverse events reported in early childhood (1.5years) or middle childhood, and cumulative adversity from birth through 8years predicted increased levels of CRP at age 15, and these associations persisted after adjustment for CRP at age 10. Some, but not all, of these associations were mediated by BMI. Conclusions: This study documents that exposure to adverse events prior to age 8 is associated with elevated inflammation at age 10 and in mid-adolescence. These findings provide prospective evidence for a biological mechanism by which early experiences may shape long-term health. Future studies with earlier assessments of inflammation are necessary in order to elucidate potential sensitive periods and mechanisms that link childhood adversity to later disease vulnerability.
    Psychoneuroendocrinology 06/2012; 3(2). DOI:10.1016/j.psyneuen.2012.05.013 · 4.94 Impact Factor
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    ABSTRACT: Research suggests that adverse experiences in childhood affect the development of cardiovascular disease (CVD), and immune and inflammation dysregulation has been postulated to play role. However, it is unclear whether the effects of social adversity on immune-related biomarkers are evident in early life, and if these biomarkers may provide an early risk marker for targeting prevention and intervention. The purpose of this review is to evaluate research on the relationship between adversity and CVD-relevant immune biomarkers in youth, assess the consistency of the findings, and consider what additional research is needed. PubMed and PsycINFO searches were conducted through September 2011. Studies were selected using criteria related to the childhood exposure, biomarker outcome, age range, and sample selection. Twenty articles were identified, examining associations between childhood adversity and immune biomarkers (assessed during childhood) that are potential risk markers for CVD later in life. Although childhood adversity was not consistently related to youth levels of inflammatory and other immune markers relevant to CVD, a trend toward positive findings was observed. No detectable patterns were evident based on measure of adversity, biomarker, study design, or sample size. Overall, our findings suggest this avenue of research is worth continued investigation. We offer recommendations for future research related to (1) study design and sample, (2) definition and measurement of adversity, (3) statistical analysis, and (4) outcomes that will help distinguish whether there are immunologic alterations related to adversity and subsequent CVD risk that can be reliably detected in childhood.
    Brain Behavior and Immunity 11/2011; 26(2):239-50. DOI:10.1016/j.bbi.2011.11.003 · 5.89 Impact Factor
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