Lockwood, Kimberly G.
(2016)
ACUTE STRESSOR-EVOKED INFLAMMATORY RESPONSES:
PHYSIOLOGICAL ORIGINS AND RELATIONSHIP WITH CARDIOVASCULAR
DISEASE RISK.
Master's Thesis, University of Pittsburgh.
(Unpublished)
Abstract
Individuals differ appreciably and consistently in the magnitude of their inflammatory responses to acute stressors. These individual differences in acute stressor-evoked inflammatory responses may be one biological mechanism that contributes to heightened risk for cardiovascular disease (CVD) and other inflammatory diseases. Critically, the clinical implications and physiological origins of these responses remain relatively unexplored. This thesis addresses these questions by testing whether magnitude of stressor-evoked interleukin(IL)-6 responses relate to (1) markers of cardiovascular disease risk (i.e., systemic inflammation and atherosclerotic CVD risk) or (2) stressor-evoked parasympathetic nervous system responses. Participants were 91 healthy midlife adults (30-51 years; 33% female; 68% white) who completed a laboratory stress protocol consisting of two mental stress tasks: a multisource interference task and Stroop color word task. During the protocol, cardiovascular psychophysiological measures were assessed and blood samples were drawn after a 30-min baseline and 30-min after task completion. Systemic inflammation was indicated by basal levels of C-reactive protein (CRP) and preclinical atherosclerotic CVD risk was assessed with intima-media thickness. Parasympathetic nervous system activity was measured by high frequency heart rate variability (HF-HRV). Hierarchical linear regressions controlling for age, sex, race, and BMI tested whether stressor-evoked IL-6 responses were associated with basal CRP, intima media thickness, and stressor-evoked HF-HRV responses. Ancillary analyses assessed whether these relationships differed by sex. Primary analyses indicated that there were no significant associations between stressor-evoked IL-6 responses and CRP, intima-media thickness, or HF-HRV responses. However, ancillary analyses revealed that sex and stressor-evoked IL-6 responses interacted to predict CRP (ΔR2 = .08, B = -1.33, β = -.39, p = .02); in males, larger stressor-evoked IL-6 responses associated with higher CRP while in females, larger stressor-evoked IL-6 responses associated with lower CRP. These findings indicate that inflammatory responses to acute stressors associate with resting levels of CRP; however, this association differs by sex. Previous literature suggests that there are sex differences in stressor-evoked IL-6 responses, but this is the first study to show sex differences in the relationship between acute inflammatory responses and systemic inflammation. The contribution of these sex differences to inflammatory disease risk warrants further investigation.
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Details
Item Type: |
University of Pittsburgh ETD
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Status: |
Unpublished |
Creators/Authors: |
Creators | Email | Pitt Username | ORCID |
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Lockwood, Kimberly G. | kgl8@pitt.edu | KGL8 | |
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ETD Committee: |
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Date: |
27 January 2016 |
Date Type: |
Publication |
Defense Date: |
27 October 2015 |
Approval Date: |
27 January 2016 |
Submission Date: |
20 November 2015 |
Access Restriction: |
No restriction; Release the ETD for access worldwide immediately. |
Number of Pages: |
72 |
Institution: |
University of Pittsburgh |
Schools and Programs: |
Dietrich School of Arts and Sciences > Psychology |
Degree: |
MS - Master of Science |
Thesis Type: |
Master's Thesis |
Refereed: |
Yes |
Uncontrolled Keywords: |
Stress; Inflammation; Reactivity; Laboratory Stress; Cardiovascular Disease; Mechanisms; Acute Stress; Immune |
Date Deposited: |
27 Jan 2016 19:01 |
Last Modified: |
15 Nov 2016 14:30 |
URI: |
http://d-scholarship.pitt.edu/id/eprint/26343 |
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