Prospective study of caffeine consumption and risk of Parkinson's disease in men and women
Identifieur interne : 001D14 ( Main/Corpus ); précédent : 001D13; suivant : 001D15Prospective study of caffeine consumption and risk of Parkinson's disease in men and women
Auteurs : Alberto Ascherio ; Shumin M. Zhang ; Miguel A. Hernán ; Ichiro Kawachi ; Graham A. Colditz ; Frank E. Speizer ; Walter C. WillettSource :
- Annals of Neurology [ 0364-5134 ] ; 2001-07.
Abstract
Results of case‐control studies and of a prospective investigation in men suggest that consumption of coffee could protect against the risk of Parkinson's disease, but the active constituent is not clear. To address the hypothesis that caffeine is protective against Parkinson's disease, we examined the relationship of coffee and caffeine consumption to the risk of this disease among participants in 2 ongoing cohorts, the Health Professionals' Follow‐Up Study (HPFS) and the Nurses' Health Study (NHS). The study population comprised 47,351 men and 88,565 women who were free of Parkinson's disease, stroke, or cancer at baseline. A comprehensive life style and dietary questionnaire was completed by the participants at baseline and updated every 2–4 years. During the follow‐up (10 years in men, 16 years in women), we documented a total of 288 incident cases of Parkinson's disease. Among men, after adjustment for age and smoking, the relative risk of Parkinson's disease was 0.42 (95% CI: 0.23–0.78; p for trend < 0.001) for men in the top one‐fifth of caffeine intake compared to those in the bottom one‐fifth. An inverse association was also observed with consumption of coffee (p for trend = 0.004), caffeine from noncoffee sources (p for trend < 0.001), and tea (p for trend = 0.02) but not decaffeinated coffee. Among women, the relationship between caffeine or coffee intake and risk of Parkinson's disease was U‐shaped, with the lowest risk observed at moderate intakes (1–3 cups of coffee/day, or the third quintile of caffeine consumption). These results support a possible protective effect of moderate doses of caffeine on risk of Parkinson's disease.
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DOI: 10.1002/ana.1052
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To address the hypothesis that caffeine is protective against Parkinson's disease, we examined the relationship of coffee and caffeine consumption to the risk of this disease among participants in 2 ongoing cohorts, the Health Professionals' Follow‐Up Study (HPFS) and the Nurses' Health Study (NHS). The study population comprised 47,351 men and 88,565 women who were free of Parkinson's disease, stroke, or cancer at baseline. A comprehensive life style and dietary questionnaire was completed by the participants at baseline and updated every 2–4 years. During the follow‐up (10 years in men, 16 years in women), we documented a total of 288 incident cases of Parkinson's disease. Among men, after adjustment for age and smoking, the relative risk of Parkinson's disease was 0.42 (95% CI: 0.23–0.78; p for trend < 0.001) for men in the top one‐fifth of caffeine intake compared to those in the bottom one‐fifth. An inverse association was also observed with consumption of coffee (p for trend = 0.004), caffeine from noncoffee sources (p for trend < 0.001), and tea (p for trend = 0.02) but not decaffeinated coffee. Among women, the relationship between caffeine or coffee intake and risk of Parkinson's disease was U‐shaped, with the lowest risk observed at moderate intakes (1–3 cups of coffee/day, or the third quintile of caffeine consumption). These results support a possible protective effect of moderate doses of caffeine on risk of Parkinson's disease.</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Alberto Ascherio MD, DrPH</name><affiliations><json:string>Department of Nutrition, Harvard School of Public Health, Boston, MA</json:string><json:string>Department of Epidemiology, Harvard School of Public Health, Boston, MA</json:string></affiliations></json:item><json:item><name>Shumin M. 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Willett MD, DrPH</name><affiliations><json:string>Department of Nutrition, Harvard School of Public Health, Boston, MA</json:string><json:string>Department of Epidemiology, Harvard School of Public Health, Boston, MA</json:string><json:string>Channing Laboratory, Department of Medicine, Harvard Medical School and Brigham and Women's Hospital, Boston, MA</json:string></affiliations></json:item></author><articleId><json:string>ANA1052</json:string></articleId><language><json:string>eng</json:string></language><abstract>Results of case‐control studies and of a prospective investigation in men suggest that consumption of coffee could protect against the risk of Parkinson's disease, but the active constituent is not clear. To address the hypothesis that caffeine is protective against Parkinson's disease, we examined the relationship of coffee and caffeine consumption to the risk of this disease among participants in 2 ongoing cohorts, the Health Professionals' Follow‐Up Study (HPFS) and the Nurses' Health Study (NHS). The study population comprised 47,351 men and 88,565 women who were free of Parkinson's disease, stroke, or cancer at baseline. A comprehensive life style and dietary questionnaire was completed by the participants at baseline and updated every 2–4 years. During the follow‐up (10 years in men, 16 years in women), we documented a total of 288 incident cases of Parkinson's disease. Among men, after adjustment for age and smoking, the relative risk of Parkinson's disease was 0.42 (95% CI: 0.23–0.78; p for trend > 0.001) for men in the top one‐fifth of caffeine intake compared to those in the bottom one‐fifth. An inverse association was also observed with consumption of coffee (p for trend = 0.004), caffeine from noncoffee sources (p for trend > 0.001), and tea (p for trend = 0.02) but not decaffeinated coffee. Among women, the relationship between caffeine or coffee intake and risk of Parkinson's disease was U‐shaped, with the lowest risk observed at moderate intakes (1–3 cups of coffee/day, or the third quintile of caffeine consumption). 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To address the hypothesis that caffeine is protective against Parkinson's disease, we examined the relationship of coffee and caffeine consumption to the risk of this disease among participants in 2 ongoing cohorts, the Health Professionals' Follow‐Up Study (HPFS) and the Nurses' Health Study (NHS). The study population comprised 47,351 men and 88,565 women who were free of Parkinson's disease, stroke, or cancer at baseline. A comprehensive life style and dietary questionnaire was completed by the participants at baseline and updated every 2–4 years. During the follow‐up (10 years in men, 16 years in women), we documented a total of 288 incident cases of Parkinson's disease. Among men, after adjustment for age and smoking, the relative risk of Parkinson's disease was 0.42 (95% CI: 0.23–0.78; p for trend < 0.001) for men in the top one‐fifth of caffeine intake compared to those in the bottom one‐fifth. An inverse association was also observed with consumption of coffee (p for trend = 0.004), caffeine from noncoffee sources (p for trend < 0.001), and tea (p for trend = 0.02) but not decaffeinated coffee. Among women, the relationship between caffeine or coffee intake and risk of Parkinson's disease was U‐shaped, with the lowest risk observed at moderate intakes (1–3 cups of coffee/day, or the third quintile of caffeine consumption). 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xml:id="au1" creatorRole="author" affiliationRef="#af1 #af2" corresponding="yes"><personName><givenNames>Alberto</givenNames><familyName>Ascherio</familyName><degrees>MD, DrPH</degrees></personName><contactDetails><email>alberto.ascherio@channing.harvard.edu</email></contactDetails></creator><creator xml:id="au2" creatorRole="author" affiliationRef="#af1 #af3"><personName><givenNames>Shumin M.</givenNames><familyName>Zhang</familyName><degrees>MD, ScD</degrees></personName></creator><creator xml:id="au3" creatorRole="author" affiliationRef="#af2"><personName><givenNames>Miguel A.</givenNames><familyName>Hernán</familyName><degrees>MD, DrPH</degrees></personName></creator><creator xml:id="au4" creatorRole="author" affiliationRef="#af3 #af4"><personName><givenNames>Ichiro</givenNames><familyName>Kawachi</familyName><degrees>MD, PhD</degrees></personName></creator><creator xml:id="au5" creatorRole="author" affiliationRef="#af2 #af3"><personName><givenNames>Graham A.</givenNames><familyName>Colditz</familyName><degrees>MD, DrPH</degrees></personName></creator><creator xml:id="au6" creatorRole="author" affiliationRef="#af3 #af5"><personName><givenNames>Frank E.</givenNames><familyName>Speizer</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au7" creatorRole="author" affiliationRef="#af1 #af2 #af3"><personName><givenNames>Walter C.</givenNames><familyName>Willett</familyName><degrees>MD, DrPH</degrees></personName></creator></creators><affiliationGroup><affiliation xml:id="af1" countryCode="US" type="organization"><unparsedAffiliation>Department of Nutrition, Harvard School of Public Health, Boston, MA</unparsedAffiliation></affiliation><affiliation xml:id="af2" countryCode="US" type="organization"><unparsedAffiliation>Department of Epidemiology, Harvard School of Public Health, Boston, MA</unparsedAffiliation></affiliation><affiliation xml:id="af3" countryCode="US" type="organization"><unparsedAffiliation>Channing Laboratory, Department of Medicine, Harvard Medical School and Brigham and Women's Hospital, Boston, MA</unparsedAffiliation></affiliation><affiliation xml:id="af4" countryCode="US" type="organization"><unparsedAffiliation>Department of Health and Social Behavior, Harvard School of Public Health, Boston, MA</unparsedAffiliation></affiliation><affiliation xml:id="af5" countryCode="US" type="organization"><unparsedAffiliation>Department of Environmental Health, Harvard School of Public Health, Boston, MA</unparsedAffiliation></affiliation></affiliationGroup><fundingInfo><fundingAgency>National Institutes of Health</fundingAgency><fundingNumber>NS 35624</fundingNumber></fundingInfo><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><p>Results of case‐control studies and of a prospective investigation in men suggest that consumption of coffee could protect against the risk of Parkinson's disease, but the active constituent is not clear. To address the hypothesis that caffeine is protective against Parkinson's disease, we examined the relationship of coffee and caffeine consumption to the risk of this disease among participants in 2 ongoing cohorts, the Health Professionals' Follow‐Up Study (HPFS) and the Nurses' Health Study (NHS). The study population comprised 47,351 men and 88,565 women who were free of Parkinson's disease, stroke, or cancer at baseline. A comprehensive life style and dietary questionnaire was completed by the participants at baseline and updated every 2–4 years. During the follow‐up (10 years in men, 16 years in women), we documented a total of 288 incident cases of Parkinson's disease. Among men, after adjustment for age and smoking, the relative risk of Parkinson's disease was 0.42 (95% CI: 0.23–0.78; <i>p</i> for trend < 0.001) for men in the top one‐fifth of caffeine intake compared to those in the bottom one‐fifth. An inverse association was also observed with consumption of coffee (<i>p</i> for trend = 0.004), caffeine from noncoffee sources (<i>p</i> for trend < 0.001), and tea (<i>p</i> for trend = 0.02) but not decaffeinated coffee. Among women, the relationship between caffeine or coffee intake and risk of Parkinson's disease was U‐shaped, with the lowest risk observed at moderate intakes (1–3 cups of coffee/day, or the third quintile of caffeine consumption). These results support a possible protective effect of moderate doses of caffeine on risk of Parkinson's disease.</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Prospective study of caffeine consumption and risk of Parkinson's disease in men and women</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>Caffeine and Parkinson's Disease</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Prospective study of caffeine consumption and risk of Parkinson's disease in men and women</title></titleInfo><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, MA</affiliation><affiliation>Department of Epidemiology, Harvard School of Public Health, Boston, MA</affiliation><description>Correspondence: Department of Nutrition, Harvard School of Public Health, 665 Huntington Avenue, Boston, MA 02115</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Shumin M.</namePart><namePart type="family">Zhang</namePart><namePart type="termsOfAddress">MD, ScD</namePart><affiliation>Department of Nutrition, Harvard School of Public Health, Boston, MA</affiliation><affiliation>Channing Laboratory, Department of Medicine, Harvard Medical School and Brigham and Women's Hospital, Boston, MA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Miguel A.</namePart><namePart type="family">Hernán</namePart><namePart type="termsOfAddress">MD, DrPH</namePart><affiliation>Department of Epidemiology, Harvard School of Public Health, Boston, MA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Ichiro</namePart><namePart type="family">Kawachi</namePart><namePart type="termsOfAddress">MD, PhD</namePart><affiliation>Channing Laboratory, Department of Medicine, Harvard Medical School and Brigham and Women's Hospital, Boston, MA</affiliation><affiliation>Department of Health and Social Behavior, Harvard School of Public Health, Boston, MA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Graham A.</namePart><namePart type="family">Colditz</namePart><namePart type="termsOfAddress">MD, DrPH</namePart><affiliation>Department of Epidemiology, Harvard School of Public Health, Boston, MA</affiliation><affiliation>Channing Laboratory, Department of Medicine, Harvard Medical School and Brigham and Women's Hospital, Boston, MA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Frank E.</namePart><namePart type="family">Speizer</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Channing Laboratory, Department of Medicine, Harvard Medical School and Brigham and Women's Hospital, Boston, MA</affiliation><affiliation>Department of Environmental Health, Harvard School of Public Health, Boston, MA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Walter C.</namePart><namePart type="family">Willett</namePart><namePart type="termsOfAddress">MD, DrPH</namePart><affiliation>Department of Nutrition, Harvard School of Public Health, Boston, MA</affiliation><affiliation>Department of Epidemiology, Harvard School of Public Health, Boston, MA</affiliation><affiliation>Channing Laboratory, Department of Medicine, Harvard Medical School and Brigham and Women's Hospital, Boston, MA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="article" displayLabel="article"></genre><originInfo><publisher>John Wiley & Sons, Inc.</publisher><place><placeTerm type="text">New York</placeTerm></place><dateIssued encoding="w3cdtf">2001-07</dateIssued><dateCaptured encoding="w3cdtf">2000-11-20</dateCaptured><dateValid encoding="w3cdtf">2001-02-12</dateValid><copyrightDate encoding="w3cdtf">2001</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">3</extent><extent unit="tables">3</extent><extent unit="references">31</extent><extent unit="words">4852</extent></physicalDescription><abstract lang="en">Results of case‐control studies and of a prospective investigation in men suggest that consumption of coffee could protect against the risk of Parkinson's disease, but the active constituent is not clear. To address the hypothesis that caffeine is protective against Parkinson's disease, we examined the relationship of coffee and caffeine consumption to the risk of this disease among participants in 2 ongoing cohorts, the Health Professionals' Follow‐Up Study (HPFS) and the Nurses' Health Study (NHS). The study population comprised 47,351 men and 88,565 women who were free of Parkinson's disease, stroke, or cancer at baseline. A comprehensive life style and dietary questionnaire was completed by the participants at baseline and updated every 2–4 years. During the follow‐up (10 years in men, 16 years in women), we documented a total of 288 incident cases of Parkinson's disease. Among men, after adjustment for age and smoking, the relative risk of Parkinson's disease was 0.42 (95% CI: 0.23–0.78; p for trend < 0.001) for men in the top one‐fifth of caffeine intake compared to those in the bottom one‐fifth. An inverse association was also observed with consumption of coffee (p for trend = 0.004), caffeine from noncoffee sources (p for trend < 0.001), and tea (p for trend = 0.02) but not decaffeinated coffee. Among women, the relationship between caffeine or coffee intake and risk of Parkinson's disease was U‐shaped, with the lowest risk observed at moderate intakes (1–3 cups of coffee/day, or the third quintile of caffeine consumption). These results support a possible protective effect of moderate doses of caffeine on risk of Parkinson's disease.</abstract><note type="funding">National Institutes of Health - No. NS 35624; </note><relatedItem type="host"><titleInfo><title>Annals of Neurology</title><subTitle>Official Journal of the American Neurological Association and the Child Neurology Society</subTitle></titleInfo><titleInfo type="abbreviated"><title>Ann Neurol.</title></titleInfo><genre type="Journal">journal</genre><subject><genre>article category</genre><topic>Original Article</topic></subject><identifier type="ISSN">0364-5134</identifier><identifier type="eISSN">1531-8249</identifier><identifier type="DOI">10.1002/(ISSN)1531-8249</identifier><identifier type="PublisherID">ANA</identifier><part><date>2001</date><detail type="volume"><caption>vol.</caption><number>50</number></detail><detail type="issue"><caption>no.</caption><number>1</number></detail><extent unit="pages"><start>56</start><end>63</end><total>8</total></extent></part></relatedItem><identifier type="istex">33A39E66074D8FFE5E3013982575EC2E6E6785E6</identifier><identifier type="DOI">10.1002/ana.1052</identifier><identifier type="ArticleID">ANA1052</identifier><accessCondition type="use and reproduction" contentType="copyright">Copyright © 2001 Wiley‐Liss, Inc.</accessCondition><recordInfo><recordContentSource>WILEY</recordContentSource><recordOrigin>John Wiley & Sons, Inc.</recordOrigin></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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