Sex‐specific Prenatal Programming
Identifieur interne : 001783 ( Istex/Corpus ); précédent : 001782; suivant : 001784Sex‐specific Prenatal Programming
Auteurs : P. O. Klingmann ; I. Kugler ; T. S. Steffke ; S. Bellingrath ; B. M. Kudielka ; D. H. HellhammerSource :
- Annals of the New York Academy of Sciences [ 0077-8923 ] ; 2008-12.
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Abstract
Women are four to eight times more likely to be affected by fibromyalgia syndrome (FMS). A lack of cortisol, potentially due to an adrenocortical deficit is postulated in FMS. The cause of such adrenal insufficiency is unknown. It could be assumed that stress exposure during critical periods contributes to vulnerability for FMS. These critical periods might include prenatal periods in which adversities may lead to an impaired development of the adrenal cortex, especially in females. More than 50% of FMS patients report major life events before the onset of the disease. Possibly due to adrenal insufficiency they may not be able to dampen their stress response by secreting sufficient glucocorticoids. Thus, stress mediators, such as catecholamines and pro‐inflammatory cytokines, may be disinhibited and affect brain function. This might result in an enhanced responsiveness to external and internal pain‐ and fatigue‐eliciting stimuli. In a study with female FMS patients (N= 93) those patients with a shorter gestational length (<38 weeks) showed a lower cortisol awakening response (CAR) than FMS subjects with a gestational length >38 weeks (F(3,31)= 2.94, P= 0.038). Additionally, more than 70% reported severe psychological stress alone or in combination with other factors at disease onset.
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DOI: 10.1196/annals.1410.020
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Steffke</name><affiliation><mods:affiliation>Center for Psychobiological and Psychosomatic Research (FPP), University of Trier, Trier, Germany</mods:affiliation></affiliation></author><author><name sortKey="Bellingrath, S" sort="Bellingrath, S" uniqKey="Bellingrath S" first="S." last="Bellingrath">S. Bellingrath</name><affiliation><mods:affiliation>Center for Psychobiological and Psychosomatic Research (FPP), University of Trier, Trier, Germany</mods:affiliation></affiliation></author><author><name sortKey="Kudielka, B M" sort="Kudielka, B M" uniqKey="Kudielka B" first="B. M." last="Kudielka">B. M. Kudielka</name><affiliation><mods:affiliation>Center for Psychobiological and Psychosomatic Research (FPP), University of Trier, Trier, Germany</mods:affiliation></affiliation></author><author><name sortKey="Hellhammer, D H" sort="Hellhammer, D H" uniqKey="Hellhammer D" first="D. H." last="Hellhammer">D. H. Hellhammer</name><affiliation><mods:affiliation>Center for Psychobiological and Psychosomatic Research (FPP), University of Trier, Trier, Germany</mods:affiliation></affiliation><affiliation><mods:affiliation>School of Psychology, Department of Clinical Psychology and Psychotherapy, University of Basel, Basel, Switzerland</mods:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:20F624E3F1A198B8FD811515529110F0AD39A2AD</idno><date when="2008" year="2008">2008</date><idno type="doi">10.1196/annals.1410.020</idno><idno type="url">https://api.istex.fr/document/20F624E3F1A198B8FD811515529110F0AD39A2AD/fulltext/pdf</idno><idno type="wicri:Area/Istex/Corpus">001783</idno><idno type="wicri:explorRef" wicri:stream="Istex" wicri:step="Corpus" wicri:corpus="ISTEX">001783</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a" type="main" xml:lang="en">Sex‐specific Prenatal Programming</title><author><name sortKey="Klingmann, P O" sort="Klingmann, P O" uniqKey="Klingmann P" first="P. O." last="Klingmann">P. O. Klingmann</name><affiliation><mods:affiliation>Center for Psychobiological and Psychosomatic Research (FPP), University of Trier, Trier, Germany</mods:affiliation></affiliation></author><author><name sortKey="Kugler, I" sort="Kugler, I" uniqKey="Kugler I" first="I." last="Kugler">I. Kugler</name><affiliation><mods:affiliation>School of Psychology, Department of Clinical Psychology and Psychotherapy, University of Basel, Basel, Switzerland</mods:affiliation></affiliation></author><author><name sortKey="Steffke, T S" sort="Steffke, T S" uniqKey="Steffke T" first="T. S." last="Steffke">T. S. Steffke</name><affiliation><mods:affiliation>Center for Psychobiological and Psychosomatic Research (FPP), University of Trier, Trier, Germany</mods:affiliation></affiliation></author><author><name sortKey="Bellingrath, S" sort="Bellingrath, S" uniqKey="Bellingrath S" first="S." last="Bellingrath">S. Bellingrath</name><affiliation><mods:affiliation>Center for Psychobiological and Psychosomatic Research (FPP), University of Trier, Trier, Germany</mods:affiliation></affiliation></author><author><name sortKey="Kudielka, B M" sort="Kudielka, B M" uniqKey="Kudielka B" first="B. M." last="Kudielka">B. M. Kudielka</name><affiliation><mods:affiliation>Center for Psychobiological and Psychosomatic Research (FPP), University of Trier, Trier, Germany</mods:affiliation></affiliation></author><author><name sortKey="Hellhammer, D H" sort="Hellhammer, D H" uniqKey="Hellhammer D" first="D. H." last="Hellhammer">D. H. Hellhammer</name><affiliation><mods:affiliation>Center for Psychobiological and Psychosomatic Research (FPP), University of Trier, Trier, Germany</mods:affiliation></affiliation><affiliation><mods:affiliation>School of Psychology, Department of Clinical Psychology and Psychotherapy, University of Basel, Basel, Switzerland</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">Annals of the New York Academy of Sciences</title><idno type="ISSN">0077-8923</idno><idno type="eISSN">1749-6632</idno><imprint><publisher>Blackwell Publishing Inc</publisher><pubPlace>Malden, USA</pubPlace><date type="published" when="2008-12">2008-12</date><biblScope unit="volume">1148</biblScope><biblScope unit="issue">1</biblScope><biblScope unit="page" from="446">446</biblScope><biblScope unit="page" to="455">455</biblScope></imprint><idno type="ISSN">0077-8923</idno></series><idno type="istex">20F624E3F1A198B8FD811515529110F0AD39A2AD</idno><idno type="DOI">10.1196/annals.1410.020</idno><idno type="ArticleID">NYAS1148020</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0077-8923</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>adrenal insufficiency</term><term>cortisol awakening response (CAR)</term><term>fibromyalgia</term><term>prenatal programming</term><term>sex specific</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Women are four to eight times more likely to be affected by fibromyalgia syndrome (FMS). A lack of cortisol, potentially due to an adrenocortical deficit is postulated in FMS. The cause of such adrenal insufficiency is unknown. It could be assumed that stress exposure during critical periods contributes to vulnerability for FMS. These critical periods might include prenatal periods in which adversities may lead to an impaired development of the adrenal cortex, especially in females. More than 50% of FMS patients report major life events before the onset of the disease. Possibly due to adrenal insufficiency they may not be able to dampen their stress response by secreting sufficient glucocorticoids. Thus, stress mediators, such as catecholamines and pro‐inflammatory cytokines, may be disinhibited and affect brain function. This might result in an enhanced responsiveness to external and internal pain‐ and fatigue‐eliciting stimuli. In a study with female FMS patients (N= 93) those patients with a shorter gestational length (<38 weeks) showed a lower cortisol awakening response (CAR) than FMS subjects with a gestational length >38 weeks (F(3,31)= 2.94, P= 0.038). Additionally, more than 70% reported severe psychological stress alone or in combination with other factors at disease onset.</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>P. O. Klingmann</name><affiliations><json:string>Center for Psychobiological and Psychosomatic Research (FPP), University of Trier, Trier, Germany</json:string></affiliations></json:item><json:item><name>I. Kugler</name><affiliations><json:string>School of Psychology, Department of Clinical Psychology and Psychotherapy, University of Basel, Basel, Switzerland</json:string></affiliations></json:item><json:item><name>T. S. Steffke</name><affiliations><json:string>Center for Psychobiological and Psychosomatic Research (FPP), University of Trier, Trier, Germany</json:string></affiliations></json:item><json:item><name>S. Bellingrath</name><affiliations><json:string>Center for Psychobiological and Psychosomatic Research (FPP), University of Trier, Trier, Germany</json:string></affiliations></json:item><json:item><name>B. M. Kudielka</name><affiliations><json:string>Center for Psychobiological and Psychosomatic Research (FPP), University of Trier, Trier, Germany</json:string></affiliations></json:item><json:item><name>D. H. Hellhammer</name><affiliations><json:string>Center for Psychobiological and Psychosomatic Research (FPP), University of Trier, Trier, Germany</json:string><json:string>School of Psychology, Department of Clinical Psychology and Psychotherapy, University of Basel, Basel, Switzerland</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>fibromyalgia</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>prenatal programming</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>adrenal insufficiency</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>sex specific</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>cortisol awakening response (CAR)</value></json:item></subject><articleId><json:string>NYAS1148020</json:string></articleId><language><json:string>eng</json:string></language><originalGenre><json:string>article</json:string></originalGenre><abstract>Women are four to eight times more likely to be affected by fibromyalgia syndrome (FMS). A lack of cortisol, potentially due to an adrenocortical deficit is postulated in FMS. The cause of such adrenal insufficiency is unknown. It could be assumed that stress exposure during critical periods contributes to vulnerability for FMS. These critical periods might include prenatal periods in which adversities may lead to an impaired development of the adrenal cortex, especially in females. More than 50% of FMS patients report major life events before the onset of the disease. Possibly due to adrenal insufficiency they may not be able to dampen their stress response by secreting sufficient glucocorticoids. Thus, stress mediators, such as catecholamines and pro‐inflammatory cytokines, may be disinhibited and affect brain function. This might result in an enhanced responsiveness to external and internal pain‐ and fatigue‐eliciting stimuli. In a study with female FMS patients (N= 93) those patients with a shorter gestational length (>38 weeks) showed a lower cortisol awakening response (CAR) than FMS subjects with a gestational length >38 weeks (F(3,31)= 2.94, P= 0.038). Additionally, more than 70% reported severe psychological stress alone or in combination with other factors at disease onset.</abstract><qualityIndicators><score>7.407</score><pdfVersion>1.4</pdfVersion><pdfPageSize>504 x 720 pts</pdfPageSize><refBibsNative>true</refBibsNative><abstractCharCount>1304</abstractCharCount><pdfWordCount>4543</pdfWordCount><pdfCharCount>30024</pdfCharCount><pdfPageCount>10</pdfPageCount><abstractWordCount>197</abstractWordCount></qualityIndicators><title>Sex‐specific Prenatal Programming</title><refBibs><json:item><author><json:item><name>F. Wolfe</name></json:item><json:item><name>K. Ross</name></json:item><json:item><name>J. 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O.</forename><surname>Klingmann</surname></persName><affiliation>Center for Psychobiological and Psychosomatic Research (FPP), University of Trier, Trier, Germany</affiliation></author><author xml:id="author-2"><persName><forename type="first">I.</forename><surname>Kugler</surname></persName><affiliation>School of Psychology, Department of Clinical Psychology and Psychotherapy, University of Basel, Basel, Switzerland</affiliation></author><author xml:id="author-3"><persName><forename type="first">T. S.</forename><surname>Steffke</surname></persName><affiliation>Center for Psychobiological and Psychosomatic Research (FPP), University of Trier, Trier, Germany</affiliation></author><author xml:id="author-4"><persName><forename type="first">S.</forename><surname>Bellingrath</surname></persName><affiliation>Center for Psychobiological and Psychosomatic Research (FPP), University of Trier, Trier, Germany</affiliation></author><author xml:id="author-5"><persName><forename type="first">B. M.</forename><surname>Kudielka</surname></persName><affiliation>Center for Psychobiological and Psychosomatic Research (FPP), University of Trier, Trier, Germany</affiliation></author><author xml:id="author-6"><persName><forename type="first">D. H.</forename><surname>Hellhammer</surname></persName><affiliation>Center for Psychobiological and Psychosomatic Research (FPP), University of Trier, Trier, Germany</affiliation><affiliation>School of Psychology, Department of Clinical Psychology and Psychotherapy, University of Basel, Basel, Switzerland</affiliation></author></analytic><monogr><title level="j">Annals of the New York Academy of Sciences</title><idno type="pISSN">0077-8923</idno><idno type="eISSN">1749-6632</idno><idno type="DOI">10.1111/(ISSN)1749-6632</idno><imprint><publisher>Blackwell Publishing Inc</publisher><pubPlace>Malden, USA</pubPlace><date type="published" when="2008-12"></date><biblScope unit="volume">1148</biblScope><biblScope unit="issue">1</biblScope><biblScope unit="page" from="446">446</biblScope><biblScope unit="page" to="455">455</biblScope></imprint></monogr><idno type="istex">20F624E3F1A198B8FD811515529110F0AD39A2AD</idno><idno type="DOI">10.1196/annals.1410.020</idno><idno type="ArticleID">NYAS1148020</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>2008</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>Women are four to eight times more likely to be affected by fibromyalgia syndrome (FMS). A lack of cortisol, potentially due to an adrenocortical deficit is postulated in FMS. The cause of such adrenal insufficiency is unknown. It could be assumed that stress exposure during critical periods contributes to vulnerability for FMS. These critical periods might include prenatal periods in which adversities may lead to an impaired development of the adrenal cortex, especially in females. More than 50% of FMS patients report major life events before the onset of the disease. Possibly due to adrenal insufficiency they may not be able to dampen their stress response by secreting sufficient glucocorticoids. Thus, stress mediators, such as catecholamines and pro‐inflammatory cytokines, may be disinhibited and affect brain function. This might result in an enhanced responsiveness to external and internal pain‐ and fatigue‐eliciting stimuli. In a study with female FMS patients (N= 93) those patients with a shorter gestational length (<38 weeks) showed a lower cortisol awakening response (CAR) than FMS subjects with a gestational length >38 weeks (F(3,31)= 2.94, P= 0.038). Additionally, more than 70% reported severe psychological stress alone or in combination with other factors at disease onset.</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>keywords</head><item><term>fibromyalgia</term></item><item><term>prenatal programming</term></item><item><term>adrenal insufficiency</term></item><item><term>sex specific</term></item><item><term>cortisol awakening response (CAR)</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="2008-12">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><extension>txt</extension><original>false</original><mimetype>text/plain</mimetype><uri>https://api.istex.fr/document/20F624E3F1A198B8FD811515529110F0AD39A2AD/fulltext/txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Wiley, elements deleted: body"><istex:xmlDeclaration>version="1.0" encoding="UTF-8" standalone="yes"</istex:xmlDeclaration><istex:document><component version="2.0" type="serialArticle" xml:lang="en"><header><publicationMeta level="product"><publisherInfo><publisherName>Blackwell Publishing Inc</publisherName><publisherLoc>Malden, USA</publisherLoc></publisherInfo><doi origin="wiley" registered="yes">10.1111/(ISSN)1749-6632</doi><issn type="print">0077-8923</issn><issn type="electronic">1749-6632</issn><idGroup><id type="product" value="NYAS"></id><id type="publisherDivision" value="ST"></id></idGroup><titleGroup><title type="main" sort="ANNALS OF NEW YORK ACADEMY SCIENCES">Annals of the New York Academy of Sciences</title></titleGroup></publicationMeta><publicationMeta level="part" position="12001"><doi origin="wiley">10.1196/nyas.2008.1148.issue-1</doi><titleGroup><title type="main">Stress, Neurotransmitters, and Hormones Neuroendocrine and Genetic Mechanisms</title></titleGroup><numberingGroup><numbering type="journalVolume" number="1148">1148</numbering><numbering type="journalIssue">1</numbering></numberingGroup><coverDate startDate="2008-12">December 2008</coverDate></publicationMeta><publicationMeta level="unit" type="article" position="54" status="forIssue"><doi origin="wiley">10.1196/annals.1410.020</doi><idGroup><id type="unit" value="NYAS1148020"></id></idGroup><countGroup><count type="pageTotal" number="10"></count></countGroup><titleGroup><title type="tocHeading1">Part VIII. Stress and Development</title></titleGroup><copyright>© 2008 New York Academy of Sciences</copyright><eventGroup><event type="firstOnline" date="2008-12-11"></event><event type="publishedOnlineFinalForm" date="2008-12-11"></event><event type="xmlConverted" agent="Converter:BPG_TO_WML3G version:2.3.5 mode:FullText source:FullText result:FullText" date="2010-04-06"></event><event type="xmlConverted" agent="Converter:WILEY_ML3G_TO_WILEY_ML3GV2 version:4.0.1" date="2014-03-19"></event><event type="xmlConverted" agent="Converter:WML3G_To_WML3G version:4.1.7 mode:FullText,remove_FC" date="2014-10-14"></event></eventGroup><numberingGroup><numbering type="pageFirst" number="446">446</numbering><numbering type="pageLast" number="455">455</numbering></numberingGroup><correspondenceTo>Address for correspondence: Prof. Dr. D. H. Hellhammer, University of Trier ‐ Psychobiology, Johanniterufer 15, D‐54290 Trier, Germany. Voice: +49‐651‐201‐2928; fax: +49‐651‐201‐2934. <email>pk@pklingmann.de</email></correspondenceTo><linkGroup><link type="toTypesetVersion" href="file:NYAS.NYAS1148020.pdf"></link></linkGroup></publicationMeta><contentMeta><countGroup><count type="figureTotal" number="2"></count><count type="tableTotal" number="0"></count><count type="formulaTotal" number="0"></count><count type="referenceTotal" number="65"></count><count type="linksCrossRef" number="60"></count></countGroup><titleGroup><title type="main">Sex‐specific Prenatal Programming</title><title type="subtitle">A Risk for Fibromyalgia?</title></titleGroup><creators><creator creatorRole="author" xml:id="cr1" affiliationRef="#a1"><personName><givenNames>P. O.</givenNames><familyName>Klingmann</familyName></personName></creator><creator creatorRole="author" xml:id="cr2" affiliationRef="#a2"><personName><givenNames>I.</givenNames><familyName>Kugler</familyName></personName></creator><creator creatorRole="author" xml:id="cr3" affiliationRef="#a1"><personName><givenNames>T. S.</givenNames><familyName>Steffke</familyName></personName></creator><creator creatorRole="author" xml:id="cr4" affiliationRef="#a1"><personName><givenNames>S.</givenNames><familyName>Bellingrath</familyName></personName></creator><creator creatorRole="author" xml:id="cr5" affiliationRef="#a1"><personName><givenNames>B. M.</givenNames><familyName>Kudielka</familyName></personName></creator><creator creatorRole="author" xml:id="cr6" affiliationRef="#a1 #a2"><personName><givenNames>D. H.</givenNames><familyName>Hellhammer</familyName></personName></creator></creators><affiliationGroup><affiliation xml:id="a1" countryCode="DE"><unparsedAffiliation>Center for Psychobiological and Psychosomatic Research (FPP), University of Trier, Trier, Germany</unparsedAffiliation></affiliation><affiliation xml:id="a2" countryCode="CH"><unparsedAffiliation>School of Psychology, Department of Clinical Psychology and Psychotherapy, University of Basel, Basel, Switzerland</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en"><keyword xml:id="k1">fibromyalgia</keyword><keyword xml:id="k2">prenatal programming</keyword><keyword xml:id="k3">adrenal insufficiency</keyword><keyword xml:id="k4">sex specific</keyword><keyword xml:id="k5">cortisol awakening response (CAR)</keyword></keywordGroup><abstractGroup><abstract type="main" xml:lang="en"><p>Women are four to eight times more likely to be affected by fibromyalgia syndrome (FMS). A lack of cortisol, potentially due to an adrenocortical deficit is postulated in FMS. The cause of such adrenal insufficiency is unknown. It could be assumed that stress exposure during critical periods contributes to vulnerability for FMS. These critical periods might include prenatal periods in which adversities may lead to an impaired development of the adrenal cortex, especially in females. More than 50% of FMS patients report major life events before the onset of the disease. Possibly due to adrenal insufficiency they may not be able to dampen their stress response by secreting sufficient glucocorticoids. Thus, stress mediators, such as catecholamines and pro‐inflammatory cytokines, may be disinhibited and affect brain function. This might result in an enhanced responsiveness to external and internal pain‐ and fatigue‐eliciting stimuli. In a study with female FMS patients (<i>N</i>= 93) those patients with a shorter gestational length (<38 weeks) showed a lower cortisol awakening response (CAR) than FMS subjects with a gestational length >38 weeks (<i>F</i><sub>(3,31)</sub>= 2.94, <i>P</i>= 0.038). Additionally, more than 70% reported severe psychological stress alone or in combination with other factors at disease onset.</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Sex‐specific Prenatal Programming</title><subTitle>A Risk for Fibromyalgia?</subTitle></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Sex‐specific Prenatal Programming</title></titleInfo><name type="personal"><namePart type="given">P. O.</namePart><namePart type="family">Klingmann</namePart><affiliation>Center for Psychobiological and Psychosomatic Research (FPP), University of Trier, Trier, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">I.</namePart><namePart type="family">Kugler</namePart><affiliation>School of Psychology, Department of Clinical Psychology and Psychotherapy, University of Basel, Basel, Switzerland</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">T. S.</namePart><namePart type="family">Steffke</namePart><affiliation>Center for Psychobiological and Psychosomatic Research (FPP), University of Trier, Trier, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">S.</namePart><namePart type="family">Bellingrath</namePart><affiliation>Center for Psychobiological and Psychosomatic Research (FPP), University of Trier, Trier, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">B. M.</namePart><namePart type="family">Kudielka</namePart><affiliation>Center for Psychobiological and Psychosomatic Research (FPP), University of Trier, Trier, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">D. H.</namePart><namePart type="family">Hellhammer</namePart><affiliation>Center for Psychobiological and Psychosomatic Research (FPP), University of Trier, Trier, Germany</affiliation><affiliation>School of Psychology, Department of Clinical Psychology and Psychotherapy, University of Basel, Basel, Switzerland</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="article" displayLabel="article"></genre><originInfo><publisher>Blackwell Publishing Inc</publisher><place><placeTerm type="text">Malden, USA</placeTerm></place><dateIssued encoding="w3cdtf">2008-12</dateIssued><copyrightDate encoding="w3cdtf">2008</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType><extent unit="figures">2</extent><extent unit="references">65</extent></physicalDescription><abstract lang="en">Women are four to eight times more likely to be affected by fibromyalgia syndrome (FMS). A lack of cortisol, potentially due to an adrenocortical deficit is postulated in FMS. The cause of such adrenal insufficiency is unknown. It could be assumed that stress exposure during critical periods contributes to vulnerability for FMS. These critical periods might include prenatal periods in which adversities may lead to an impaired development of the adrenal cortex, especially in females. More than 50% of FMS patients report major life events before the onset of the disease. Possibly due to adrenal insufficiency they may not be able to dampen their stress response by secreting sufficient glucocorticoids. Thus, stress mediators, such as catecholamines and pro‐inflammatory cytokines, may be disinhibited and affect brain function. This might result in an enhanced responsiveness to external and internal pain‐ and fatigue‐eliciting stimuli. In a study with female FMS patients (N= 93) those patients with a shorter gestational length (<38 weeks) showed a lower cortisol awakening response (CAR) than FMS subjects with a gestational length >38 weeks (F(3,31)= 2.94, P= 0.038). Additionally, more than 70% reported severe psychological stress alone or in combination with other factors at disease onset.</abstract><subject lang="en"><genre>keywords</genre><topic>fibromyalgia</topic><topic>prenatal programming</topic><topic>adrenal insufficiency</topic><topic>sex specific</topic><topic>cortisol awakening response (CAR)</topic></subject><relatedItem type="host"><titleInfo><title>Annals of the New York Academy of Sciences</title></titleInfo><genre type="journal">journal</genre><identifier type="ISSN">0077-8923</identifier><identifier type="eISSN">1749-6632</identifier><identifier type="DOI">10.1111/(ISSN)1749-6632</identifier><identifier type="PublisherID">NYAS</identifier><part><date>2008</date><detail type="title"><title>Stress, Neurotransmitters, and Hormones Neuroendocrine and Genetic Mechanisms</title></detail><detail type="volume"><caption>vol.</caption><number>1148</number></detail><detail type="issue"><caption>no.</caption><number>1</number></detail><extent unit="pages"><start>446</start><end>455</end><total>10</total></extent></part></relatedItem><identifier type="istex">20F624E3F1A198B8FD811515529110F0AD39A2AD</identifier><identifier type="DOI">10.1196/annals.1410.020</identifier><identifier type="ArticleID">NYAS1148020</identifier><accessCondition type="use and reproduction" contentType="copyright">© 2008 New York Academy of Sciences</accessCondition><recordInfo><recordContentSource>WILEY</recordContentSource><recordOrigin>Blackwell Publishing Inc</recordOrigin></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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