Objective: Personality influences many aspects of the health process. It is unclear to what extent selfand informant-reports of the Big Five offer incremental validity for the prediction of inflammatory biomarkers and whether inflammation provides a unique pathway between personality and indicators of physical health, independent of health behaviors. Method: Using data from older adults (N = 1,630) enrolled in the St. Louis Personality and Aging Network study, we tested whether self-and informant-reported Big Five traits show unique associations with inflammation (IL-6, CRP, TNF-a). Further, we tested whether inflammation and health behaviors indirectly link personality to healthrelated quality of life, body mass index, and chronic disease burden using longitudinal mediation in a structural equation modeling framework. Results: Self-reports, informant-reports, and general trait factors of personality predicted future inflammatory biomarker levels (unstandardized regression coefficients ranged À.08 to .07 for self, À.13 to À.10 for informants, and À.16 to À.11 for general). Additionally, all assessment methods of personality were associated with the indicators of physical health through biomarker and health behavior pathways. Effects were primarily found for conscientiousness and neuroticism; IL-6 and CRP were the biomarkers with the most indirect effects; and indirect paths overall emerged more frequently through health behaviors, but this varied by outcome. Conclusions: Self-and informant-reports provided unique predictive validity of inflammatory biomarkers. Findings highlight the benefits of using of multiple assessments of personality and the importance of examining multiple, distinct pathways by which personality might influence health to understand the mechanisms underlying this relationship more fully.
Inflammation has been reliably associated with depression. However, the directionality of this association is poorly understood, with evidence that elevated inflammation may promote and precede the development of depression, as well as arise following its expression. Using data from older adults ( N = 1,072, ages 60–73) who participated in the ongoing longitudinal St. Louis Personality and Aging Network (SPAN) study, we examined whether inflammatory markers (interleukin-6: IL-6, C-reactive protein: CRP, and tumor necrosis factor α: TNFα) and depression were prospectively predictive of one another. Fasting serum samples and self-reports of depressive symptoms (Beck Depression Inventory-II) were obtained from participants at 2 sessions approximately 2 years apart. Structural equation models as well as regressions that accounted for a host of potentially confounding covariates and depression at baseline revealed that baseline IL-6 and CRP, but not baseline TNFα were associated with elevated depressive symptoms at the follow-up session (IL-6: β = 0.080, p = 0.036; CRP: β = 0.083, p = 0.03; TNFα: β = 0.039, p = 0.314). However, there was no association between baseline depressive symptoms and follow-up inflammatory markers (βs = −0.12 to −0.006, all p s > 0.05). Collectively, these data suggest that inflammation prospectively predicts depression, but depression does not predict inflammation in older age. These data add to a growing literature suggesting that inflammatory signaling may plausibly promote the development of depression.
Objective: Prenatal selective serotonin reuptake inhibitor (SSRI) exposure has been inconsistently linked to depression. Potential neural intermediaries remain understudied. We examined whether prenatal SSRI exposure is associated with depressive symptoms and brain structure during middle childhood. Methods: Prenatal SSRI exposure (retrospective caregiver-report), depressive symptoms (caregiver-reported Child Behavior Checklist) and brain structure (MRI-derived subcortical volume; cortical thickness and surface area) were assessed in children (analytic ns=5,420-7,528; 235 with prenatal SSRI exposure; 9-10 years old) who completed the baseline session of the Adolescent Brain and Cognitive DevelopmentSM Study. Covariates included familial (e.g., 1st degree relative depression density), pregnancy (e.g., planned pregnancy), and child (e.g., birthweight) variables. Matrix spectral decomposition was used to address multiple testing. Results: There was no evidence that prenatal SSRI exposure was associated with child depression after accounting for recent maternal depressive symptoms. Prenatal SSRI exposure was associated with greater left superior parietal surface area (b=145.3 mm2, p=0.00038) and lateral occipital cortical thickness (b=0.0272 mm, p=0.0000079), neither of which was associated with depressive symptoms. Conclusions: Our findings, combined with adverse associations of prenatal exposure to maternal depression and the utility of SSRIs for treating depression, suggest that risk for child depression during middle childhood should not discourage SSRI use during pregnancy. It will be important for future work to examine associations between prenatal SSRI exposure and depression through young adulthood, when risk for depression increases.
Leptin is involved in the endocrine control of energy expenditure and body weight regulation. Previous studies emphasize a relationship between hypoxic states and leptin concentrations. The aim of this study was to investigate the effects of acute hypoxia on leptin concentrations in healthy subjects. We examined 14 healthy men. Hypoxic conditions were induced by decreasing oxygen saturation to 75% for 30 minutes. Plasma leptin concentrations were determined at baseline, after 3 hours of euglycemic clamping, during hypoxia, and repeatedly the following 2.5 hours thereafter. Our results show an increase of plasma leptin concentrations in the course of 6 hours of hyperinsulinemic-euglycemic clamping which may reflect diurnal rhythmicity. Notwithstanding, there was no difference between levels of leptin in the hypoxic and the normoxic condition (P = .2). Since we did not find any significant changes in leptin responses upon hypoxia, plasma leptin levels do not seem to be affected by short hypoxic episodes of moderate degree.
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