Longitudinal changes of telomere length and epigenetic age related to traumatic stress and post-traumatic stress disorder
Summary Several studies have reported an association between traumatic stress and telomere length suggesting that traumatic stress has an impact on ageing at the cellular level. A newly derived tool provides an additional means to investigate cellular ageing by estimating epigenetic age based on DNA...
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creator | Boks, Marco P Mierlo, Hans C. van Rutten, Bart P.F Radstake, Timothy R.D.J De Witte, Lot Geuze, Elbert Horvath, Steve Schalkwyk, Leonard C Vinkers, Christiaan H Broen, Jasper C.A Vermetten, Eric |
description | Summary Several studies have reported an association between traumatic stress and telomere length suggesting that traumatic stress has an impact on ageing at the cellular level. A newly derived tool provides an additional means to investigate cellular ageing by estimating epigenetic age based on DNA methylation profiles. We therefore hypothesise that in a longitudinal study of traumatic stress both indicators of cellular ageing will show increased ageing. We expect that particularly in individuals that developed symptoms of post-traumatic stress disorder (PTSD) increases in these ageing parameters would stand out. From an existing longitudinal cohort study, ninety-six male soldiers were selected based on trauma exposure and the presence of symptoms of PTSD. All military personnel were deployed in a combat zone in Afghanistan and assessed before and 6 months after deployment. The Self-Rating Inventory for PTSD was used to measure the presence of PTSD symptoms, while exposure to combat trauma during deployment was measured with a 19-item deployment experiences checklist. These groups did not differ for age, gender, alcohol consumption, cigarette smoking, military rank, length, weight, or medication use. In DNA from whole blood telomere length was measured and DNA methylation levels were assessed using the Illumina 450K DNA methylation arrays. Epigenetic ageing was estimated using the DNAm age estimator procedure. The association of trauma with telomere length was in the expected direction but not significant ( B = −10.2, p = 0.52). However, contrary to our expectations, development of PTSD symptoms was associated with the reverse process, telomere lengthening ( B = 1.91, p = 0.018). In concordance, trauma significantly accelerated epigenetic ageing ( B = 1.97, p = 0.032) and similar to the findings in telomeres, development of PTSD symptoms was inversely associated with epigenetic ageing ( B = −0.10, p = 0.044). Blood cell count, medication and premorbid early life trauma exposure did not confound the results. Overall, in this longitudinal study of military personnel deployed to Afghanistan we show an acceleration of ageing by trauma. However, development of PTSD symptoms was associated with telomere lengthening and reversed epigenetic ageing. These findings warrant further study of a perhaps dysfunctional compensatory cellular ageing reversal in PTSD. |
doi_str_mv | 10.1016/j.psyneuen.2014.07.011 |
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A newly derived tool provides an additional means to investigate cellular ageing by estimating epigenetic age based on DNA methylation profiles. We therefore hypothesise that in a longitudinal study of traumatic stress both indicators of cellular ageing will show increased ageing. We expect that particularly in individuals that developed symptoms of post-traumatic stress disorder (PTSD) increases in these ageing parameters would stand out. From an existing longitudinal cohort study, ninety-six male soldiers were selected based on trauma exposure and the presence of symptoms of PTSD. All military personnel were deployed in a combat zone in Afghanistan and assessed before and 6 months after deployment. The Self-Rating Inventory for PTSD was used to measure the presence of PTSD symptoms, while exposure to combat trauma during deployment was measured with a 19-item deployment experiences checklist. These groups did not differ for age, gender, alcohol consumption, cigarette smoking, military rank, length, weight, or medication use. In DNA from whole blood telomere length was measured and DNA methylation levels were assessed using the Illumina 450K DNA methylation arrays. Epigenetic ageing was estimated using the DNAm age estimator procedure. The association of trauma with telomere length was in the expected direction but not significant ( B = −10.2, p = 0.52). However, contrary to our expectations, development of PTSD symptoms was associated with the reverse process, telomere lengthening ( B = 1.91, p = 0.018). In concordance, trauma significantly accelerated epigenetic ageing ( B = 1.97, p = 0.032) and similar to the findings in telomeres, development of PTSD symptoms was inversely associated with epigenetic ageing ( B = −0.10, p = 0.044). Blood cell count, medication and premorbid early life trauma exposure did not confound the results. Overall, in this longitudinal study of military personnel deployed to Afghanistan we show an acceleration of ageing by trauma. However, development of PTSD symptoms was associated with telomere lengthening and reversed epigenetic ageing. These findings warrant further study of a perhaps dysfunctional compensatory cellular ageing reversal in PTSD.</description><identifier>ISSN: 0306-4530</identifier><identifier>EISSN: 1873-3360</identifier><identifier>DOI: 10.1016/j.psyneuen.2014.07.011</identifier><identifier>PMID: 25129579</identifier><language>eng</language><publisher>England: Elsevier Ltd</publisher><subject>Adolescent ; Adult ; Afghan Campaign 2001 ; Age ; Cellular Senescence - genetics ; Combat Disorders - genetics ; Combat Disorders - psychology ; Combat trauma ; DNA methylation ; Endocrinology & Metabolism ; Epigenesis, Genetic ; Epigenetics ; Humans ; Male ; Military Personnel - psychology ; Post traumatic stress disorder ; Psychiatry ; PTSD ; Risk Factors ; Stress Disorders, Post-Traumatic - genetics ; Stress Disorders, Post-Traumatic - psychology ; Telomere ; Telomeres ; Traumatic stress ; Young Adult</subject><ispartof>Psychoneuroendocrinology, 2015-01, Vol.51, p.506-512</ispartof><rights>Elsevier Ltd</rights><rights>2014 Elsevier Ltd</rights><rights>Copyright © 2014 Elsevier Ltd. All rights reserved.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c627t-4007ba0601d980d25e72d86e12fe375f091bc6afa562b78fc23ea6fd59b6c7693</citedby><cites>FETCH-LOGICAL-c627t-4007ba0601d980d25e72d86e12fe375f091bc6afa562b78fc23ea6fd59b6c7693</cites><orcidid>0000-0003-3479-2379 ; 0000-0001-6163-7484</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0306453014002637$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3537,27901,27902,65306</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/25129579$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Boks, Marco P</creatorcontrib><creatorcontrib>Mierlo, Hans C. van</creatorcontrib><creatorcontrib>Rutten, Bart P.F</creatorcontrib><creatorcontrib>Radstake, Timothy R.D.J</creatorcontrib><creatorcontrib>De Witte, Lot</creatorcontrib><creatorcontrib>Geuze, Elbert</creatorcontrib><creatorcontrib>Horvath, Steve</creatorcontrib><creatorcontrib>Schalkwyk, Leonard C</creatorcontrib><creatorcontrib>Vinkers, Christiaan H</creatorcontrib><creatorcontrib>Broen, Jasper C.A</creatorcontrib><creatorcontrib>Vermetten, Eric</creatorcontrib><title>Longitudinal changes of telomere length and epigenetic age related to traumatic stress and post-traumatic stress disorder</title><title>Psychoneuroendocrinology</title><addtitle>Psychoneuroendocrinology</addtitle><description>Summary Several studies have reported an association between traumatic stress and telomere length suggesting that traumatic stress has an impact on ageing at the cellular level. A newly derived tool provides an additional means to investigate cellular ageing by estimating epigenetic age based on DNA methylation profiles. We therefore hypothesise that in a longitudinal study of traumatic stress both indicators of cellular ageing will show increased ageing. We expect that particularly in individuals that developed symptoms of post-traumatic stress disorder (PTSD) increases in these ageing parameters would stand out. From an existing longitudinal cohort study, ninety-six male soldiers were selected based on trauma exposure and the presence of symptoms of PTSD. All military personnel were deployed in a combat zone in Afghanistan and assessed before and 6 months after deployment. The Self-Rating Inventory for PTSD was used to measure the presence of PTSD symptoms, while exposure to combat trauma during deployment was measured with a 19-item deployment experiences checklist. These groups did not differ for age, gender, alcohol consumption, cigarette smoking, military rank, length, weight, or medication use. In DNA from whole blood telomere length was measured and DNA methylation levels were assessed using the Illumina 450K DNA methylation arrays. Epigenetic ageing was estimated using the DNAm age estimator procedure. The association of trauma with telomere length was in the expected direction but not significant ( B = −10.2, p = 0.52). However, contrary to our expectations, development of PTSD symptoms was associated with the reverse process, telomere lengthening ( B = 1.91, p = 0.018). In concordance, trauma significantly accelerated epigenetic ageing ( B = 1.97, p = 0.032) and similar to the findings in telomeres, development of PTSD symptoms was inversely associated with epigenetic ageing ( B = −0.10, p = 0.044). Blood cell count, medication and premorbid early life trauma exposure did not confound the results. Overall, in this longitudinal study of military personnel deployed to Afghanistan we show an acceleration of ageing by trauma. However, development of PTSD symptoms was associated with telomere lengthening and reversed epigenetic ageing. These findings warrant further study of a perhaps dysfunctional compensatory cellular ageing reversal in PTSD.</description><subject>Adolescent</subject><subject>Adult</subject><subject>Afghan Campaign 2001</subject><subject>Age</subject><subject>Cellular Senescence - genetics</subject><subject>Combat Disorders - genetics</subject><subject>Combat Disorders - psychology</subject><subject>Combat trauma</subject><subject>DNA methylation</subject><subject>Endocrinology & Metabolism</subject><subject>Epigenesis, Genetic</subject><subject>Epigenetics</subject><subject>Humans</subject><subject>Male</subject><subject>Military Personnel - psychology</subject><subject>Post traumatic stress disorder</subject><subject>Psychiatry</subject><subject>PTSD</subject><subject>Risk Factors</subject><subject>Stress Disorders, Post-Traumatic - genetics</subject><subject>Stress Disorders, Post-Traumatic - psychology</subject><subject>Telomere</subject><subject>Telomeres</subject><subject>Traumatic stress</subject><subject>Young Adult</subject><issn>0306-4530</issn><issn>1873-3360</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkT2P1DAQhi0E4paDv3BySZMwtjd20iDQiS9pJQqgthx7kvOS2IvtIO2_J2HvKKCgmmKemdE8LyE3DGoGTL461qd8DrhgqDmwfQ2qBsYekR1rlaiEkPCY7ECArPaNgCvyLOcjAMhW8qfkijeMd43qduR8iGH0ZXE-mInaOxNGzDQOtOAUZ0xIJwxjuaMmOIonP2LA4i01I9KEkynoaIm0JLPMZmvkkjDn3_gp5lL903E-x-QwPSdPBjNlfHFfr8m39---3n6sDp8_fLp9e6is5KpUewDVG5DAXNeC4w0q7lqJjA8oVDNAx3orzWAayXvVDpYLNHJwTddLq2QnrsnLy95Tij8WzEXPPlucJhMwLlkzKbp9J2SjVlReUJtizgkHfUp-NumsGehNuz7qB-16065B6VX7Onhzf2PpZ3R_xh48r8CbC4Drpz89Jp2tx2DR-YS2aBf9_2-8_muFnXzw1kzf8Yz5GJe0Rrj-ozPXoL9s4W_Zs9Ugl0KJX09prvM</recordid><startdate>20150101</startdate><enddate>20150101</enddate><creator>Boks, Marco P</creator><creator>Mierlo, Hans C. van</creator><creator>Rutten, Bart P.F</creator><creator>Radstake, Timothy R.D.J</creator><creator>De Witte, Lot</creator><creator>Geuze, Elbert</creator><creator>Horvath, Steve</creator><creator>Schalkwyk, Leonard C</creator><creator>Vinkers, Christiaan H</creator><creator>Broen, Jasper C.A</creator><creator>Vermetten, Eric</creator><general>Elsevier Ltd</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0003-3479-2379</orcidid><orcidid>https://orcid.org/0000-0001-6163-7484</orcidid></search><sort><creationdate>20150101</creationdate><title>Longitudinal changes of telomere length and epigenetic age related to traumatic stress and post-traumatic stress disorder</title><author>Boks, Marco P ; Mierlo, Hans C. van ; Rutten, Bart P.F ; Radstake, Timothy R.D.J ; De Witte, Lot ; Geuze, Elbert ; Horvath, Steve ; Schalkwyk, Leonard C ; Vinkers, Christiaan H ; Broen, Jasper C.A ; Vermetten, Eric</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c627t-4007ba0601d980d25e72d86e12fe375f091bc6afa562b78fc23ea6fd59b6c7693</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><topic>Adolescent</topic><topic>Adult</topic><topic>Afghan Campaign 2001</topic><topic>Age</topic><topic>Cellular Senescence - genetics</topic><topic>Combat Disorders - genetics</topic><topic>Combat Disorders - psychology</topic><topic>Combat trauma</topic><topic>DNA methylation</topic><topic>Endocrinology & Metabolism</topic><topic>Epigenesis, Genetic</topic><topic>Epigenetics</topic><topic>Humans</topic><topic>Male</topic><topic>Military Personnel - psychology</topic><topic>Post traumatic stress disorder</topic><topic>Psychiatry</topic><topic>PTSD</topic><topic>Risk Factors</topic><topic>Stress Disorders, Post-Traumatic - genetics</topic><topic>Stress Disorders, Post-Traumatic - psychology</topic><topic>Telomere</topic><topic>Telomeres</topic><topic>Traumatic stress</topic><topic>Young Adult</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Boks, Marco P</creatorcontrib><creatorcontrib>Mierlo, Hans C. van</creatorcontrib><creatorcontrib>Rutten, Bart P.F</creatorcontrib><creatorcontrib>Radstake, Timothy R.D.J</creatorcontrib><creatorcontrib>De Witte, Lot</creatorcontrib><creatorcontrib>Geuze, Elbert</creatorcontrib><creatorcontrib>Horvath, Steve</creatorcontrib><creatorcontrib>Schalkwyk, Leonard C</creatorcontrib><creatorcontrib>Vinkers, Christiaan H</creatorcontrib><creatorcontrib>Broen, Jasper C.A</creatorcontrib><creatorcontrib>Vermetten, Eric</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><jtitle>Psychoneuroendocrinology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Boks, Marco P</au><au>Mierlo, Hans C. van</au><au>Rutten, Bart P.F</au><au>Radstake, Timothy R.D.J</au><au>De Witte, Lot</au><au>Geuze, Elbert</au><au>Horvath, Steve</au><au>Schalkwyk, Leonard C</au><au>Vinkers, Christiaan H</au><au>Broen, Jasper C.A</au><au>Vermetten, Eric</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Longitudinal changes of telomere length and epigenetic age related to traumatic stress and post-traumatic stress disorder</atitle><jtitle>Psychoneuroendocrinology</jtitle><addtitle>Psychoneuroendocrinology</addtitle><date>2015-01-01</date><risdate>2015</risdate><volume>51</volume><spage>506</spage><epage>512</epage><pages>506-512</pages><issn>0306-4530</issn><eissn>1873-3360</eissn><abstract>Summary Several studies have reported an association between traumatic stress and telomere length suggesting that traumatic stress has an impact on ageing at the cellular level. A newly derived tool provides an additional means to investigate cellular ageing by estimating epigenetic age based on DNA methylation profiles. We therefore hypothesise that in a longitudinal study of traumatic stress both indicators of cellular ageing will show increased ageing. We expect that particularly in individuals that developed symptoms of post-traumatic stress disorder (PTSD) increases in these ageing parameters would stand out. From an existing longitudinal cohort study, ninety-six male soldiers were selected based on trauma exposure and the presence of symptoms of PTSD. All military personnel were deployed in a combat zone in Afghanistan and assessed before and 6 months after deployment. The Self-Rating Inventory for PTSD was used to measure the presence of PTSD symptoms, while exposure to combat trauma during deployment was measured with a 19-item deployment experiences checklist. These groups did not differ for age, gender, alcohol consumption, cigarette smoking, military rank, length, weight, or medication use. In DNA from whole blood telomere length was measured and DNA methylation levels were assessed using the Illumina 450K DNA methylation arrays. Epigenetic ageing was estimated using the DNAm age estimator procedure. The association of trauma with telomere length was in the expected direction but not significant ( B = −10.2, p = 0.52). However, contrary to our expectations, development of PTSD symptoms was associated with the reverse process, telomere lengthening ( B = 1.91, p = 0.018). In concordance, trauma significantly accelerated epigenetic ageing ( B = 1.97, p = 0.032) and similar to the findings in telomeres, development of PTSD symptoms was inversely associated with epigenetic ageing ( B = −0.10, p = 0.044). Blood cell count, medication and premorbid early life trauma exposure did not confound the results. Overall, in this longitudinal study of military personnel deployed to Afghanistan we show an acceleration of ageing by trauma. However, development of PTSD symptoms was associated with telomere lengthening and reversed epigenetic ageing. These findings warrant further study of a perhaps dysfunctional compensatory cellular ageing reversal in PTSD.</abstract><cop>England</cop><pub>Elsevier Ltd</pub><pmid>25129579</pmid><doi>10.1016/j.psyneuen.2014.07.011</doi><tpages>7</tpages><orcidid>https://orcid.org/0000-0003-3479-2379</orcidid><orcidid>https://orcid.org/0000-0001-6163-7484</orcidid><oa>free_for_read</oa></addata></record> |
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subjects | Adolescent Adult Afghan Campaign 2001 Age Cellular Senescence - genetics Combat Disorders - genetics Combat Disorders - psychology Combat trauma DNA methylation Endocrinology & Metabolism Epigenesis, Genetic Epigenetics Humans Male Military Personnel - psychology Post traumatic stress disorder Psychiatry PTSD Risk Factors Stress Disorders, Post-Traumatic - genetics Stress Disorders, Post-Traumatic - psychology Telomere Telomeres Traumatic stress Young Adult |
title | Longitudinal changes of telomere length and epigenetic age related to traumatic stress and post-traumatic stress disorder |
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