Reproductive factors, exogenous estrogen use, and risk of Parkinson's disease
Identifieur interne : 001734 ( Main/Corpus ); précédent : 001733; suivant : 001735Reproductive factors, exogenous estrogen use, and risk of Parkinson's disease
Auteurs : Kelly Claire Simon ; Honglei Chen ; Xiang Gao ; Michael A. Schwarzschild ; Alberto AscherioSource :
- Movement Disorders [ 0885-3185 ] ; 2009-07-15.
English descriptors
Abstract
To determine if reproductive factors or exogenous estrogen are associated with risk of Parkinson's disease (PD), we conducted a prospective study with 22 years of follow‐up among postmenopausal participants in the Nurses' Health Study. Relative risks (RRs) and 95% confidence intervals (CIs) of PD were estimated from a Cox proportional hazards model adjusting for potential confounders. Risk of PD was not significantly associated with any of the reproductive factors measured or exogenous estrogen use. Use of postmenopausal hormones, however, may modify the associations of smoking and caffeine intake with PD risk. The inverse relation between smoking and PD risk was attenuated among ever users of postmenopausal hormones (P for interaction = 0.05). Similar results were obtained for caffeine (P for interaction = 0.09). In exploratory analyses, women using progestin‐only hormones were found to have an increased PD risk, but this result was based on a very small number of cases (n = 4). In this large longitudinal study, we found no evidence of a beneficial effect of exogenous or endogenous estrogens on risk of PD. The use of postmenopausal hormone use may interact with other risk factors, but findings are preliminary and need confirmation in other populations. © 2009 Movement Disorder Society
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DOI: 10.1002/mds.22619
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ISTEX:ECC4CB54A6F0491BC5DD4D0BA6D19B3A770CBD9DLe document en format XML
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Relative risks (RRs) and 95% confidence intervals (CIs) of PD were estimated from a Cox proportional hazards model adjusting for potential confounders. Risk of PD was not significantly associated with any of the reproductive factors measured or exogenous estrogen use. Use of postmenopausal hormones, however, may modify the associations of smoking and caffeine intake with PD risk. The inverse relation between smoking and PD risk was attenuated among ever users of postmenopausal hormones (P for interaction = 0.05). Similar results were obtained for caffeine (P for interaction = 0.09). In exploratory analyses, women using progestin‐only hormones were found to have an increased PD risk, but this result was based on a very small number of cases (n = 4). In this large longitudinal study, we found no evidence of a beneficial effect of exogenous or endogenous estrogens on risk of PD. The use of postmenopausal hormone use may interact with other risk factors, but findings are preliminary and need confirmation in other populations. © 2009 Movement Disorder Society</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Kelly Claire Simon ScD</name><affiliations><json:string>Department of Nutrition, Harvard School of Public Health, Boston, Massachusetts, USA</json:string></affiliations></json:item><json:item><name>Honglei Chen MD, PhD</name><affiliations><json:string>Epidemiology Branch, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina, USA</json:string></affiliations></json:item><json:item><name>Xiang Gao PhD</name><affiliations><json:string>Department of Nutrition, Harvard School of Public Health, Boston, Massachusetts, USA</json:string></affiliations></json:item><json:item><name>Michael A. 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factors</keyword></keywordGroup><fundingInfo><fundingAgency>NIH/NINDS</fundingAgency><fundingNumber>R01 NS048517</fundingNumber><fundingNumber>T32 ES07069‐26</fundingNumber></fundingInfo><fundingInfo><fundingAgency>Intramural Research Program</fundingAgency></fundingInfo><fundingInfo><fundingAgency>National Institute of Environmental Health Sciences</fundingAgency></fundingInfo><fundingInfo><fundingAgency>National Institute of Health</fundingAgency><fundingNumber>Z01ES1019</fundingNumber><fundingNumber>W81XWH‐091‐0881</fundingNumber></fundingInfo><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><p>To determine if reproductive factors or exogenous estrogen are associated with risk of Parkinson's disease (PD), we conducted a prospective study with 22 years of follow‐up among postmenopausal participants in the Nurses' Health Study. Relative risks (RRs) and 95% confidence intervals (CIs) of PD were estimated from a Cox proportional hazards model adjusting for potential confounders. Risk of PD was not significantly associated with any of the reproductive factors measured or exogenous estrogen use. Use of postmenopausal hormones, however, may modify the associations of smoking and caffeine intake with PD risk. The inverse relation between smoking and PD risk was attenuated among ever users of postmenopausal hormones (<i>P</i> for interaction = 0.05). Similar results were obtained for caffeine (<i>P</i> for interaction = 0.09). In exploratory analyses, women using progestin‐only hormones were found to have an increased PD risk, but this result was based on a very small number of cases (n = 4). In this large longitudinal study, we found no evidence of a beneficial effect of exogenous or endogenous estrogens on risk of PD. The use of postmenopausal hormone use may interact with other risk factors, but findings are preliminary and need confirmation in other populations. © 2009 Movement Disorder Society</p></abstract></abstractGroup></contentMeta><noteGroup><note xml:id="fn1"><p>Potential conflict of interest: None reported.</p></note></noteGroup></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Reproductive factors, exogenous estrogen use, and risk of Parkinson's disease</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>Reproductive Factors, Estrogens, and Risk of PD</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Reproductive factors, exogenous estrogen use, and risk of Parkinson's disease</title></titleInfo><name type="personal"><namePart type="given">Kelly Claire</namePart><namePart type="family">Simon</namePart><namePart type="termsOfAddress">ScD</namePart><affiliation>Department of Nutrition, Harvard School of Public Health, Boston, Massachusetts, USA</affiliation><description>Correspondence: Deptartment of Nutrition, Harvard School of Public Health, 665 Huntington Ave, Building 2, 3rd floor, Boston, MA</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Honglei</namePart><namePart type="family">Chen</namePart><namePart type="termsOfAddress">MD, PhD</namePart><affiliation>Epidemiology Branch, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Xiang</namePart><namePart type="family">Gao</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Department of Nutrition, Harvard School of Public Health, Boston, Massachusetts, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Michael A.</namePart><namePart type="family">Schwarzschild</namePart><namePart type="termsOfAddress">MD, PhD</namePart><affiliation>Department of Neurology, Massachusetts General Hospital, Boston, Massachusetts, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Alberto</namePart><namePart type="family">Ascherio</namePart><namePart type="termsOfAddress">MD, DrPH</namePart><affiliation>Department of Nutrition, Harvard School of Public Health, Boston, Massachusetts, USA</affiliation><affiliation>Department of Epidemiology, Harvard School of Public Health, Boston, Massachusetts, USA</affiliation><affiliation>Channing Laboratory, Department of Medicine, Brigham and Women's Hospital, and Harvard Medical School, Boston, Massachusetts, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="article" displayLabel="article"></genre><originInfo><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><place><placeTerm type="text">Hoboken</placeTerm></place><dateIssued encoding="w3cdtf">2009-07-15</dateIssued><dateCaptured encoding="w3cdtf">2008-10-01</dateCaptured><dateValid encoding="w3cdtf">2009-03-25</dateValid><copyrightDate encoding="w3cdtf">2009</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">1</extent><extent unit="tables">3</extent><extent unit="references">43</extent><extent unit="words">6206</extent></physicalDescription><abstract lang="en">To determine if reproductive factors or exogenous estrogen are associated with risk of Parkinson's disease (PD), we conducted a prospective study with 22 years of follow‐up among postmenopausal participants in the Nurses' Health Study. Relative risks (RRs) and 95% confidence intervals (CIs) of PD were estimated from a Cox proportional hazards model adjusting for potential confounders. Risk of PD was not significantly associated with any of the reproductive factors measured or exogenous estrogen use. Use of postmenopausal hormones, however, may modify the associations of smoking and caffeine intake with PD risk. The inverse relation between smoking and PD risk was attenuated among ever users of postmenopausal hormones (P for interaction = 0.05). Similar results were obtained for caffeine (P for interaction = 0.09). In exploratory analyses, women using progestin‐only hormones were found to have an increased PD risk, but this result was based on a very small number of cases (n = 4). In this large longitudinal study, we found no evidence of a beneficial effect of exogenous or endogenous estrogens on risk of PD. The use of postmenopausal hormone use may interact with other risk factors, but findings are preliminary and need confirmation in other populations. © 2009 Movement Disorder Society</abstract><note type="content">*Potential conflict of interest: None reported.</note><note type="funding">NIH/NINDS - No. R01 NS048517; No. T32 ES07069‐26; </note><note type="funding">Intramural Research Program</note><note type="funding">National Institute of Environmental Health Sciences</note><note type="funding">National Institute of Health - No. Z01ES1019; No. W81XWH‐091‐0881; </note><subject lang="en"><genre>Keywords</genre><topic>Parkinson's disease</topic><topic>estrogen</topic><topic>epidemiology</topic><topic>reproductive factors</topic></subject><relatedItem type="host"><titleInfo><title>Movement Disorders</title><subTitle>Official Journal of the Movement Disorder Society</subTitle></titleInfo><titleInfo type="abbreviated"><title>Mov. Disord.</title></titleInfo><genre type="Journal">journal</genre><subject><genre>article category</genre><topic>Research Article</topic></subject><identifier type="ISSN">0885-3185</identifier><identifier type="eISSN">1531-8257</identifier><identifier type="DOI">10.1002/(ISSN)1531-8257</identifier><identifier type="PublisherID">MDS</identifier><part><date>2009</date><detail type="volume"><caption>vol.</caption><number>24</number></detail><detail type="issue"><caption>no.</caption><number>9</number></detail><extent unit="pages"><start>1359</start><end>1365</end><total>7</total></extent></part></relatedItem><identifier type="istex">ECC4CB54A6F0491BC5DD4D0BA6D19B3A770CBD9D</identifier><identifier type="DOI">10.1002/mds.22619</identifier><identifier type="ArticleID">MDS22619</identifier><accessCondition type="use and reproduction" contentType="copyright">Copyright © 2009 Movement Disorder Society</accessCondition><recordInfo><recordContentSource>WILEY</recordContentSource><recordOrigin>Wiley Subscription Services, Inc., A Wiley Company</recordOrigin></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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