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Cross-Sectional and Longitudinal Associations of Chronic Posttraumatic Stress Disorder With Inflammatory and Endothelial Function Markers in Women
Posttraumatic stress disorder (PTSD) may contribute to heightened cardiovascular disease risk by promoting a proinflammatory state and impaired endothelial function. Previous research has demonstrated associations of PTSD with inflammatory and endothelial function biomarkers, but most work has been...
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Published in: | Biological psychiatry (1969) 2017-12, Vol.82 (12), p.875-884 |
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creator | Sumner, Jennifer A. Chen, Qixuan Roberts, Andrea L. Winning, Ashley Rimm, Eric B. Gilsanz, Paola Glymour, M. Maria Tworoger, Shelley S. Koenen, Karestan C. Kubzansky, Laura D. |
description | Posttraumatic stress disorder (PTSD) may contribute to heightened cardiovascular disease risk by promoting a proinflammatory state and impaired endothelial function. Previous research has demonstrated associations of PTSD with inflammatory and endothelial function biomarkers, but most work has been cross-sectional and does not separate the effects of trauma exposure from those of PTSD.
We investigated associations of trauma exposure and chronic PTSD with biomarkers of inflammation (C-reactive protein and tumor necrosis factor alpha receptor II) and endothelial function (intercellular adhesion molecule-1 and vascular cell adhesion molecule-1) in 524 middle-aged women in the Nurses’ Health Study II. Using linear mixed models, we examined associations of trauma/PTSD status with biomarkers measured twice, 10 to 16 years apart, in cardiovascular disease–free women, considering either average levels over time (cross-sectional) or change in levels over time (longitudinal). Biomarker levels were log-transformed. Trauma/PTSD status (based on structured diagnostic interviews) was defined as no trauma at either blood draw (n = 175), trauma at blood draw 1 but no PTSD at either draw (n = 175), and PTSD that persisted beyond blood draw 1 (chronic PTSD; n = 174). The reference group was women without trauma.
In models adjusted for known potential confounders, women with chronic PTSD had higher average C-reactive protein (B = 0.27, p < .05), tumor necrosis factor alpha receptor II (B = 0.07, p < .01), and intercellular adhesion molecule-1 (B = 0.04, p < .05) levels. Women with trauma but without PTSD had higher average tumor necrosis factor alpha receptor II levels (B = 0.05, p < .05). In addition, women with chronic PTSD had a greater increase in vascular cell adhesion molecule-1 over time (B = 0.003, p < .05).
Increased inflammation and impaired endothelial function may be pathways by which chronic PTSD increases cardiovascular disease risk. |
doi_str_mv | 10.1016/j.biopsych.2017.06.020 |
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We investigated associations of trauma exposure and chronic PTSD with biomarkers of inflammation (C-reactive protein and tumor necrosis factor alpha receptor II) and endothelial function (intercellular adhesion molecule-1 and vascular cell adhesion molecule-1) in 524 middle-aged women in the Nurses’ Health Study II. Using linear mixed models, we examined associations of trauma/PTSD status with biomarkers measured twice, 10 to 16 years apart, in cardiovascular disease–free women, considering either average levels over time (cross-sectional) or change in levels over time (longitudinal). Biomarker levels were log-transformed. Trauma/PTSD status (based on structured diagnostic interviews) was defined as no trauma at either blood draw (n = 175), trauma at blood draw 1 but no PTSD at either draw (n = 175), and PTSD that persisted beyond blood draw 1 (chronic PTSD; n = 174). The reference group was women without trauma.
In models adjusted for known potential confounders, women with chronic PTSD had higher average C-reactive protein (B = 0.27, p < .05), tumor necrosis factor alpha receptor II (B = 0.07, p < .01), and intercellular adhesion molecule-1 (B = 0.04, p < .05) levels. Women with trauma but without PTSD had higher average tumor necrosis factor alpha receptor II levels (B = 0.05, p < .05). In addition, women with chronic PTSD had a greater increase in vascular cell adhesion molecule-1 over time (B = 0.003, p < .05).
Increased inflammation and impaired endothelial function may be pathways by which chronic PTSD increases cardiovascular disease risk.</description><identifier>ISSN: 0006-3223</identifier><identifier>EISSN: 1873-2402</identifier><identifier>DOI: 10.1016/j.biopsych.2017.06.020</identifier><identifier>PMID: 28778657</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Adult ; Aged ; Biomarkers ; Biomarkers - blood ; C-Reactive Protein - metabolism ; Chronic Disease ; Cross-Sectional Studies ; Endothelial cell adhesion molecules ; Follow-Up Studies ; Humans ; Inflammation ; Inflammation - blood ; Inflammation - complications ; Intercellular Adhesion Molecule-1 - blood ; Least-Squares Analysis ; Longitudinal Studies ; Middle Aged ; Nurses ; Posttraumatic stress disorder ; Receptors, Tumor Necrosis Factor, Type II - blood ; Stress Disorders, Post-Traumatic - blood ; Stress Disorders, Post-Traumatic - complications ; Surveys and Questionnaires ; Trauma ; Vascular Cell Adhesion Molecule-1 - blood ; Women</subject><ispartof>Biological psychiatry (1969), 2017-12, Vol.82 (12), p.875-884</ispartof><rights>2017 Society of Biological Psychiatry</rights><rights>Copyright © 2017 Society of Biological Psychiatry. Published by Elsevier Inc. All rights reserved.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c504t-dae98cae5ee915885b44bde10fe3b5a089399eb6869a5be0d62e198c02767f303</citedby><cites>FETCH-LOGICAL-c504t-dae98cae5ee915885b44bde10fe3b5a089399eb6869a5be0d62e198c02767f303</cites><orcidid>0000-0002-4199-1766</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,776,780,881,27903,27904</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/28778657$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Sumner, Jennifer A.</creatorcontrib><creatorcontrib>Chen, Qixuan</creatorcontrib><creatorcontrib>Roberts, Andrea L.</creatorcontrib><creatorcontrib>Winning, Ashley</creatorcontrib><creatorcontrib>Rimm, Eric B.</creatorcontrib><creatorcontrib>Gilsanz, Paola</creatorcontrib><creatorcontrib>Glymour, M. Maria</creatorcontrib><creatorcontrib>Tworoger, Shelley S.</creatorcontrib><creatorcontrib>Koenen, Karestan C.</creatorcontrib><creatorcontrib>Kubzansky, Laura D.</creatorcontrib><title>Cross-Sectional and Longitudinal Associations of Chronic Posttraumatic Stress Disorder With Inflammatory and Endothelial Function Markers in Women</title><title>Biological psychiatry (1969)</title><addtitle>Biol Psychiatry</addtitle><description>Posttraumatic stress disorder (PTSD) may contribute to heightened cardiovascular disease risk by promoting a proinflammatory state and impaired endothelial function. Previous research has demonstrated associations of PTSD with inflammatory and endothelial function biomarkers, but most work has been cross-sectional and does not separate the effects of trauma exposure from those of PTSD.
We investigated associations of trauma exposure and chronic PTSD with biomarkers of inflammation (C-reactive protein and tumor necrosis factor alpha receptor II) and endothelial function (intercellular adhesion molecule-1 and vascular cell adhesion molecule-1) in 524 middle-aged women in the Nurses’ Health Study II. Using linear mixed models, we examined associations of trauma/PTSD status with biomarkers measured twice, 10 to 16 years apart, in cardiovascular disease–free women, considering either average levels over time (cross-sectional) or change in levels over time (longitudinal). Biomarker levels were log-transformed. Trauma/PTSD status (based on structured diagnostic interviews) was defined as no trauma at either blood draw (n = 175), trauma at blood draw 1 but no PTSD at either draw (n = 175), and PTSD that persisted beyond blood draw 1 (chronic PTSD; n = 174). The reference group was women without trauma.
In models adjusted for known potential confounders, women with chronic PTSD had higher average C-reactive protein (B = 0.27, p < .05), tumor necrosis factor alpha receptor II (B = 0.07, p < .01), and intercellular adhesion molecule-1 (B = 0.04, p < .05) levels. Women with trauma but without PTSD had higher average tumor necrosis factor alpha receptor II levels (B = 0.05, p < .05). In addition, women with chronic PTSD had a greater increase in vascular cell adhesion molecule-1 over time (B = 0.003, p < .05).
Increased inflammation and impaired endothelial function may be pathways by which chronic PTSD increases cardiovascular disease risk.</description><subject>Adult</subject><subject>Aged</subject><subject>Biomarkers</subject><subject>Biomarkers - blood</subject><subject>C-Reactive Protein - metabolism</subject><subject>Chronic Disease</subject><subject>Cross-Sectional Studies</subject><subject>Endothelial cell adhesion molecules</subject><subject>Follow-Up Studies</subject><subject>Humans</subject><subject>Inflammation</subject><subject>Inflammation - blood</subject><subject>Inflammation - complications</subject><subject>Intercellular Adhesion Molecule-1 - blood</subject><subject>Least-Squares Analysis</subject><subject>Longitudinal Studies</subject><subject>Middle Aged</subject><subject>Nurses</subject><subject>Posttraumatic stress disorder</subject><subject>Receptors, Tumor Necrosis Factor, Type II - blood</subject><subject>Stress Disorders, Post-Traumatic - blood</subject><subject>Stress Disorders, Post-Traumatic - complications</subject><subject>Surveys and Questionnaires</subject><subject>Trauma</subject><subject>Vascular Cell Adhesion Molecule-1 - blood</subject><subject>Women</subject><issn>0006-3223</issn><issn>1873-2402</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><recordid>eNqFUctu1DAUtRCIDqW_UHnJJsF2EsfZIKqhLZUGgVSqLi3Hvmk8JPZgJ5XmN_jiOp22ghUryz6v63sQOqUkp4Tyj9u8tX4X97rPGaF1TnhOGHmFVlTURcZKwl6jFSGEZwVjxRF6F-M2XWvG6Ft0xERdC17VK_RnHXyM2TXoyXqnBqycwRvv7uw0G7s8nMXotVULHLHv8LoP3lmNf_g4TUHNY4I0vp4CxIi_2OiDgYBv7dTjK9cNakwEH_aPxufO-KmHwSbfi9k9ZuJvKvyCELF1-NaP4N6jN50aIpw8ncfo5uL85_prtvl-ebU-22S6IuWUGQWN0AoqgIZWQlRtWbYGKOmgaCtFRFM0DbRc8EZVLRDDGdCkIKzmdVeQ4hh9Ovju5nYEo8Gl7wxyF-yowl56ZeW_iLO9vPP3suKiaAhNBh-eDIL_PUOc5GijhmFQDvwcJW0Y56JmpUhUfqDqZd0BupcYSuRSqNzK50LlUqgkXKZCk_D07yFfZM8NJsLnAwHSqu4tBBm1BafB2JBKlcbb_2U8AB-rup4</recordid><startdate>20171215</startdate><enddate>20171215</enddate><creator>Sumner, Jennifer A.</creator><creator>Chen, Qixuan</creator><creator>Roberts, Andrea L.</creator><creator>Winning, Ashley</creator><creator>Rimm, Eric B.</creator><creator>Gilsanz, Paola</creator><creator>Glymour, M. 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Maria</creatorcontrib><creatorcontrib>Tworoger, Shelley S.</creatorcontrib><creatorcontrib>Koenen, Karestan C.</creatorcontrib><creatorcontrib>Kubzansky, Laura D.</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Biological psychiatry (1969)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Sumner, Jennifer A.</au><au>Chen, Qixuan</au><au>Roberts, Andrea L.</au><au>Winning, Ashley</au><au>Rimm, Eric B.</au><au>Gilsanz, Paola</au><au>Glymour, M. Maria</au><au>Tworoger, Shelley S.</au><au>Koenen, Karestan C.</au><au>Kubzansky, Laura D.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Cross-Sectional and Longitudinal Associations of Chronic Posttraumatic Stress Disorder With Inflammatory and Endothelial Function Markers in Women</atitle><jtitle>Biological psychiatry (1969)</jtitle><addtitle>Biol Psychiatry</addtitle><date>2017-12-15</date><risdate>2017</risdate><volume>82</volume><issue>12</issue><spage>875</spage><epage>884</epage><pages>875-884</pages><issn>0006-3223</issn><eissn>1873-2402</eissn><abstract>Posttraumatic stress disorder (PTSD) may contribute to heightened cardiovascular disease risk by promoting a proinflammatory state and impaired endothelial function. Previous research has demonstrated associations of PTSD with inflammatory and endothelial function biomarkers, but most work has been cross-sectional and does not separate the effects of trauma exposure from those of PTSD.
We investigated associations of trauma exposure and chronic PTSD with biomarkers of inflammation (C-reactive protein and tumor necrosis factor alpha receptor II) and endothelial function (intercellular adhesion molecule-1 and vascular cell adhesion molecule-1) in 524 middle-aged women in the Nurses’ Health Study II. Using linear mixed models, we examined associations of trauma/PTSD status with biomarkers measured twice, 10 to 16 years apart, in cardiovascular disease–free women, considering either average levels over time (cross-sectional) or change in levels over time (longitudinal). Biomarker levels were log-transformed. Trauma/PTSD status (based on structured diagnostic interviews) was defined as no trauma at either blood draw (n = 175), trauma at blood draw 1 but no PTSD at either draw (n = 175), and PTSD that persisted beyond blood draw 1 (chronic PTSD; n = 174). The reference group was women without trauma.
In models adjusted for known potential confounders, women with chronic PTSD had higher average C-reactive protein (B = 0.27, p < .05), tumor necrosis factor alpha receptor II (B = 0.07, p < .01), and intercellular adhesion molecule-1 (B = 0.04, p < .05) levels. Women with trauma but without PTSD had higher average tumor necrosis factor alpha receptor II levels (B = 0.05, p < .05). In addition, women with chronic PTSD had a greater increase in vascular cell adhesion molecule-1 over time (B = 0.003, p < .05).
Increased inflammation and impaired endothelial function may be pathways by which chronic PTSD increases cardiovascular disease risk.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>28778657</pmid><doi>10.1016/j.biopsych.2017.06.020</doi><tpages>10</tpages><orcidid>https://orcid.org/0000-0002-4199-1766</orcidid><oa>free_for_read</oa></addata></record> |
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subjects | Adult Aged Biomarkers Biomarkers - blood C-Reactive Protein - metabolism Chronic Disease Cross-Sectional Studies Endothelial cell adhesion molecules Follow-Up Studies Humans Inflammation Inflammation - blood Inflammation - complications Intercellular Adhesion Molecule-1 - blood Least-Squares Analysis Longitudinal Studies Middle Aged Nurses Posttraumatic stress disorder Receptors, Tumor Necrosis Factor, Type II - blood Stress Disorders, Post-Traumatic - blood Stress Disorders, Post-Traumatic - complications Surveys and Questionnaires Trauma Vascular Cell Adhesion Molecule-1 - blood Women |
title | Cross-Sectional and Longitudinal Associations of Chronic Posttraumatic Stress Disorder With Inflammatory and Endothelial Function Markers in Women |
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