CIGARETTE SMOKING, ALCOHOL CONSUMPTION AND CAFFEINE INTAKE IN PD AND PD SUBTYPES: A COMMUNITY–BASED, INCIDENT COHORT WITH MATCHED CONTROLS
Identifieur interne : 002B74 ( Main/Corpus ); précédent : 002B73; suivant : 002B75CIGARETTE SMOKING, ALCOHOL CONSUMPTION AND CAFFEINE INTAKE IN PD AND PD SUBTYPES: A COMMUNITY–BASED, INCIDENT COHORT WITH MATCHED CONTROLS
Auteurs : Angus D. Macleod ; Carl E. CounsellSource :
- Journal of Neurology, Neurosurgery & Psychiatry [ 0022-3050 ] ; 2013-11.
Abstract
Background Previous studies have demonstrated negative associations between cigarette smoking, alcohol consumption and caffeine intake and Parkinson's disease (PD), but most data come from unrepresentative cohorts (1). One previous study suggested different associations with these exposures in different PD phenotypes (2). There are no data describing change in these exposures after diagnosis: a differential change between cases and controls would introduce bias to prevalence-based case-control studies. Methods We recruited a community-based, inception cohort of PD and matched controls and gathered data about previous duration and intensity of cigarette smoking and alcohol and caffeine intake with face-to-face questionnaires. We calculated odds ratios and adjusted odds ratios using logistic regression analysis to examine the associations between these exposures and PD and the tremor-dominant and postural instability and gait difficulty (PIGD) subtypes. We also assessed the change in exposures after recruitment in patients and controls with a linear mixed model. Results 201 patients with PD and 249 controls were analysed. Moderate and high cumulative levels of smoking, OR 0.42 (0.24–0.74) and 0.48 (0.28–0.82) respectively; high alcohol intake, OR 0.27 (0.13–0.56); and moderate and high caffeine consumption, ORs 0.48 (0.28–0.82) and 0.39 (0.22–0.68) respectively; were statistically significant negative associations with PD. There were statistically significant inverse trends between rising levels of consumption for each exposure and PD (P<0.001 for smoking, P=0.003 for alcohol and P<0.001 for caffeine). A similar pattern of associations with these exposures was seen in the PIGD and tremor-dominant patients as in the whole PD group. Smoking and alcohol consumption declined after diagnosis, but not at different rates between patients and controls. Conclusions Our study therefore provides further evidence for dose-dependent negative associations between these exposures and PD in a truly-representative inception cohort. We found no evidence of different associations with the tremor-dominant and PIGD PD subtypes. The lack of a differential reduction in exposure is important for interpretation of prevalent studies.
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DOI: 10.1136/jnnp-2013-306573.15
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<record><TEI wicri:istexFullTextTei="biblStruct"><teiHeader><fileDesc><titleStmt><title>CIGARETTE SMOKING, ALCOHOL CONSUMPTION AND CAFFEINE INTAKE IN PD AND PD SUBTYPES: A COMMUNITY–BASED, INCIDENT COHORT WITH MATCHED CONTROLS</title><author><name sortKey="Macleod, Angus D" sort="Macleod, Angus D" uniqKey="Macleod A" first="Angus D" last="Macleod">Angus D. Macleod</name></author><author><name sortKey="Counsell, Carl E" sort="Counsell, Carl E" uniqKey="Counsell C" first="Carl E" last="Counsell">Carl E. Counsell</name><affiliation><mods:affiliation>University of Aberdeen</mods:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:39C674605DA11E5EAB0495DD464D2BE04EDE18B3</idno><date when="2013" year="2013">2013</date><idno type="doi">10.1136/jnnp-2013-306573.15</idno><idno type="url">https://api.istex.fr/document/39C674605DA11E5EAB0495DD464D2BE04EDE18B3/fulltext/pdf</idno><idno type="wicri:Area/Main/Corpus">002B74</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a">CIGARETTE SMOKING, ALCOHOL CONSUMPTION AND CAFFEINE INTAKE IN PD AND PD SUBTYPES: A COMMUNITY–BASED, INCIDENT COHORT WITH MATCHED CONTROLS</title><author><name sortKey="Macleod, Angus D" sort="Macleod, Angus D" uniqKey="Macleod A" first="Angus D" last="Macleod">Angus D. Macleod</name></author><author><name sortKey="Counsell, Carl E" sort="Counsell, Carl E" uniqKey="Counsell C" first="Carl E" last="Counsell">Carl E. Counsell</name><affiliation><mods:affiliation>University of Aberdeen</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">Journal of Neurology, Neurosurgery & Psychiatry</title><title level="j" type="abbrev">J Neurol Neurosurg Psychiatry</title><idno type="ISSN">0022-3050</idno><idno type="eISSN">1468-330X</idno><imprint><publisher>BMJ Publishing Group Ltd</publisher><date type="published" when="2013-11">2013-11</date><biblScope unit="volume">84</biblScope><biblScope unit="issue">11</biblScope><biblScope unit="page" from="e2">e2</biblScope></imprint><idno type="ISSN">0022-3050</idno></series><idno type="istex">39C674605DA11E5EAB0495DD464D2BE04EDE18B3</idno><idno type="DOI">10.1136/jnnp-2013-306573.15</idno><idno type="href">jnnp-84-e2-57.pdf</idno><idno type="local">jnnp;84/11/e2-bd</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0022-3050</idno></seriesStmt></fileDesc><profileDesc><textClass></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract">Background Previous studies have demonstrated negative associations between cigarette smoking, alcohol consumption and caffeine intake and Parkinson's disease (PD), but most data come from unrepresentative cohorts (1). One previous study suggested different associations with these exposures in different PD phenotypes (2). There are no data describing change in these exposures after diagnosis: a differential change between cases and controls would introduce bias to prevalence-based case-control studies. Methods We recruited a community-based, inception cohort of PD and matched controls and gathered data about previous duration and intensity of cigarette smoking and alcohol and caffeine intake with face-to-face questionnaires. We calculated odds ratios and adjusted odds ratios using logistic regression analysis to examine the associations between these exposures and PD and the tremor-dominant and postural instability and gait difficulty (PIGD) subtypes. We also assessed the change in exposures after recruitment in patients and controls with a linear mixed model. Results 201 patients with PD and 249 controls were analysed. Moderate and high cumulative levels of smoking, OR 0.42 (0.24–0.74) and 0.48 (0.28–0.82) respectively; high alcohol intake, OR 0.27 (0.13–0.56); and moderate and high caffeine consumption, ORs 0.48 (0.28–0.82) and 0.39 (0.22–0.68) respectively; were statistically significant negative associations with PD. There were statistically significant inverse trends between rising levels of consumption for each exposure and PD (P<0.001 for smoking, P=0.003 for alcohol and P<0.001 for caffeine). A similar pattern of associations with these exposures was seen in the PIGD and tremor-dominant patients as in the whole PD group. Smoking and alcohol consumption declined after diagnosis, but not at different rates between patients and controls. Conclusions Our study therefore provides further evidence for dose-dependent negative associations between these exposures and PD in a truly-representative inception cohort. We found no evidence of different associations with the tremor-dominant and PIGD PD subtypes. The lack of a differential reduction in exposure is important for interpretation of prevalent studies.</div></front></TEI><istex><corpusName>bmj</corpusName><author><json:item><name>Angus D Macleod</name></json:item><json:item><name>Carl E Counsell</name><affiliations><json:string>University of Aberdeen</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>Association of British Neurologists (ABN) joint meeting with the Royal College of Physicians (RCP), London, 23–24 October 2013</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>PARKINSON'S DISEASE</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>STROKE</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>PARKINSON'S DISEASE</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>STROKE</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>PARKINSON'S DISEASE</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>STROKE</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>PARKINSON'S DISEASE</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>STROKE</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>PARKINSON'S DISEASE</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>STROKE</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>PARKINSON'S DISEASE</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>STROKE</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>PARKINSON'S DISEASE</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>STROKE</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>PARKINSON'S DISEASE</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>STROKE</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>PARKINSON'S DISEASE</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>STROKE</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>PARKINSON'S DISEASE</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>STROKE</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>PARKINSON'S DISEASE</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>STROKE</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>PARKINSON'S DISEASE</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>STROKE</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>PARKINSON'S DISEASE</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>STROKE</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>PARKINSON'S DISEASE</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>STROKE</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>PARKINSON'S DISEASE</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>STROKE</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>PARKINSON'S DISEASE</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>STROKE</value></json:item></subject><language><json:string>eng</json:string></language><abstract>Background Previous studies have demonstrated negative associations between cigarette smoking, alcohol consumption and caffeine intake and Parkinson's disease (PD), but most data come from unrepresentative cohorts (1). One previous study suggested different associations with these exposures in different PD phenotypes (2). There are no data describing change in these exposures after diagnosis: a differential change between cases and controls would introduce bias to prevalence-based case-control studies. Methods We recruited a community-based, inception cohort of PD and matched controls and gathered data about previous duration and intensity of cigarette smoking and alcohol and caffeine intake with face-to-face questionnaires. We calculated odds ratios and adjusted odds ratios using logistic regression analysis to examine the associations between these exposures and PD and the tremor-dominant and postural instability and gait difficulty (PIGD) subtypes. We also assessed the change in exposures after recruitment in patients and controls with a linear mixed model. Results 201 patients with PD and 249 controls were analysed. Moderate and high cumulative levels of smoking, OR 0.42 (0.24–0.74) and 0.48 (0.28–0.82) respectively; high alcohol intake, OR 0.27 (0.13–0.56); and moderate and high caffeine consumption, ORs 0.48 (0.28–0.82) and 0.39 (0.22–0.68) respectively; were statistically significant negative associations with PD. There were statistically significant inverse trends between rising levels of consumption for each exposure and PD (P>0.001 for smoking, P=0.003 for alcohol and P>0.001 for caffeine). A similar pattern of associations with these exposures was seen in the PIGD and tremor-dominant patients as in the whole PD group. Smoking and alcohol consumption declined after diagnosis, but not at different rates between patients and controls. Conclusions Our study therefore provides further evidence for dose-dependent negative associations between these exposures and PD in a truly-representative inception cohort. We found no evidence of different associations with the tremor-dominant and PIGD PD subtypes. The lack of a differential reduction in exposure is important for interpretation of prevalent studies.</abstract><qualityIndicators><score>4.856</score><pdfVersion>1.6</pdfVersion><pdfPageSize>595.276 x 793.701 pts</pdfPageSize><refBibsNative>true</refBibsNative><keywordCount>33</keywordCount><abstractCharCount>2245</abstractCharCount><pdfWordCount>356</pdfWordCount><pdfCharCount>2522</pdfCharCount><pdfPageCount>1</pdfPageCount><abstractWordCount>311</abstractWordCount></qualityIndicators><title>CIGARETTE SMOKING, ALCOHOL CONSUMPTION AND CAFFEINE INTAKE IN PD AND PD SUBTYPES: A COMMUNITY–BASED, INCIDENT COHORT WITH MATCHED CONTROLS</title><genre><json:string>abstract</json:string></genre><host><volume>84</volume><pages><first>e2</first></pages><issn><json:string>0022-3050</json:string></issn><issue>11</issue><genre></genre><language><json:string>unknown</json:string></language><eissn><json:string>1468-330X</json:string></eissn><title>Journal of Neurology, Neurosurgery & Psychiatry</title></host><publicationDate>2013</publicationDate><copyrightDate>2013</copyrightDate><doi><json:string>10.1136/jnnp-2013-306573.15</json:string></doi><id>39C674605DA11E5EAB0495DD464D2BE04EDE18B3</id><fulltext><json:item><original>true</original><mimetype>application/pdf</mimetype><extension>pdf</extension><uri>https://api.istex.fr/document/39C674605DA11E5EAB0495DD464D2BE04EDE18B3/fulltext/pdf</uri></json:item><json:item><original>false</original><mimetype>application/zip</mimetype><extension>zip</extension><uri>https://api.istex.fr/document/39C674605DA11E5EAB0495DD464D2BE04EDE18B3/fulltext/zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/document/39C674605DA11E5EAB0495DD464D2BE04EDE18B3/fulltext/tei"><teiHeader><fileDesc><titleStmt><title level="a">CIGARETTE SMOKING, ALCOHOL CONSUMPTION AND CAFFEINE INTAKE IN PD AND PD SUBTYPES: A COMMUNITY–BASED, INCIDENT COHORT WITH MATCHED CONTROLS</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher>BMJ Publishing Group Ltd</publisher><availability><p>BMJ</p></availability><date>2013</date></publicationStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a">CIGARETTE SMOKING, ALCOHOL CONSUMPTION AND CAFFEINE INTAKE IN PD AND PD SUBTYPES: A COMMUNITY–BASED, INCIDENT COHORT WITH MATCHED CONTROLS</title><author><persName><forename type="first">Angus D</forename><surname>Macleod</surname></persName></author><author><persName><forename type="first">Carl E</forename><surname>Counsell</surname></persName><affiliation>University of Aberdeen</affiliation></author></analytic><monogr><title level="j">Journal of Neurology, Neurosurgery & Psychiatry</title><title level="j" type="abbrev">J Neurol Neurosurg Psychiatry</title><idno type="pISSN">0022-3050</idno><idno type="eISSN">1468-330X</idno><imprint><publisher>BMJ Publishing Group Ltd</publisher><date type="published" when="2013-11"></date><biblScope unit="volume">84</biblScope><biblScope unit="issue">11</biblScope><biblScope unit="page" from="e2">e2</biblScope></imprint></monogr><idno type="istex">39C674605DA11E5EAB0495DD464D2BE04EDE18B3</idno><idno type="DOI">10.1136/jnnp-2013-306573.15</idno><idno type="href">jnnp-84-e2-57.pdf</idno><idno type="local">jnnp;84/11/e2-bd</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>2013</date></creation><langUsage><language ident="en">en</language></langUsage><abstract><p>Background Previous studies have demonstrated negative associations between cigarette smoking, alcohol consumption and caffeine intake and Parkinson's disease (PD), but most data come from unrepresentative cohorts (1). One previous study suggested different associations with these exposures in different PD phenotypes (2). There are no data describing change in these exposures after diagnosis: a differential change between cases and controls would introduce bias to prevalence-based case-control studies. Methods We recruited a community-based, inception cohort of PD and matched controls and gathered data about previous duration and intensity of cigarette smoking and alcohol and caffeine intake with face-to-face questionnaires. We calculated odds ratios and adjusted odds ratios using logistic regression analysis to examine the associations between these exposures and PD and the tremor-dominant and postural instability and gait difficulty (PIGD) subtypes. We also assessed the change in exposures after recruitment in patients and controls with a linear mixed model. Results 201 patients with PD and 249 controls were analysed. Moderate and high cumulative levels of smoking, OR 0.42 (0.24–0.74) and 0.48 (0.28–0.82) respectively; high alcohol intake, OR 0.27 (0.13–0.56); and moderate and high caffeine consumption, ORs 0.48 (0.28–0.82) and 0.39 (0.22–0.68) respectively; were statistically significant negative associations with PD. There were statistically significant inverse trends between rising levels of consumption for each exposure and PD (P<0.001 for smoking, P=0.003 for alcohol and P<0.001 for caffeine). A similar pattern of associations with these exposures was seen in the PIGD and tremor-dominant patients as in the whole PD group. Smoking and alcohol consumption declined after diagnosis, but not at different rates between patients and controls. Conclusions Our study therefore provides further evidence for dose-dependent negative associations between these exposures and PD in a truly-representative inception cohort. We found no evidence of different associations with the tremor-dominant and PIGD PD subtypes. The lack of a differential reduction in exposure is important for interpretation of prevalent studies.</p></abstract><textClass><keywords scheme="keyword"><list><head>Keywords</head><item><term>PARKINSON'S DISEASE</term></item><item><term>STROKE</term></item><item><term>PARKINSON'S DISEASE</term></item><item><term>STROKE</term></item><item><term>PARKINSON'S DISEASE</term></item><item><term>STROKE</term></item><item><term>PARKINSON'S DISEASE</term></item><item><term>STROKE</term></item><item><term>PARKINSON'S DISEASE</term></item><item><term>STROKE</term></item><item><term>PARKINSON'S DISEASE</term></item><item><term>STROKE</term></item><item><term>PARKINSON'S DISEASE</term></item><item><term>STROKE</term></item><item><term>PARKINSON'S DISEASE</term></item><item><term>STROKE</term></item><item><term>PARKINSON'S DISEASE</term></item><item><term>STROKE</term></item><item><term>PARKINSON'S DISEASE</term></item><item><term>STROKE</term></item><item><term>PARKINSON'S DISEASE</term></item><item><term>STROKE</term></item><item><term>PARKINSON'S DISEASE</term></item><item><term>STROKE</term></item><item><term>PARKINSON'S DISEASE</term></item><item><term>STROKE</term></item><item><term>PARKINSON'S DISEASE</term></item><item><term>STROKE</term></item><item><term>PARKINSON'S DISEASE</term></item><item><term>STROKE</term></item><item><term>PARKINSON'S DISEASE</term></item><item><term>STROKE</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="2013-11">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/39C674605DA11E5EAB0495DD464D2BE04EDE18B3/fulltext/txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="corpus bmj" wicri:toSee="no header"><istex:xmlDeclaration>version="1.0" encoding="UTF-8" standalone="no"</istex:xmlDeclaration><istex:docType PUBLIC="-//NLM//DTD Journal Archiving and Interchange DTD v2.3 20070202//EN" URI="archivearticle.dtd" name="istex:docType"></istex:docType><istex:document><article article-type="abstract"><front><journal-meta><journal-id journal-id-type="hwp">jnnp</journal-id><journal-id journal-id-type="nlm-ta">J Neurol Neurosurg Psychiatry</journal-id><journal-id journal-id-type="publisher-id">jnnp</journal-id><journal-title>Journal of Neurology, Neurosurgery & Psychiatry</journal-title><abbrev-journal-title abbrev-type="publisher">J Neurol Neurosurg Psychiatry</abbrev-journal-title><abbrev-journal-title>J Neurol Neurosurg Psychiatry</abbrev-journal-title><issn pub-type="ppub">0022-3050</issn><issn pub-type="epub">1468-330X</issn><publisher><publisher-name>BMJ Publishing Group Ltd</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="doi">10.1136/jnnp-2013-306573.15</article-id><article-id pub-id-type="other">jnnp;84/11/e2-bd</article-id><article-id pub-id-type="other">jnnp;jnnp-2013-306573.15</article-id><article-id pub-id-type="other">e2.57</article-id><article-id pub-id-type="other">jnnp-2013-306573.15</article-id><article-categories><subj-group subj-group-type="heading"><subject>Association of British Neurologists (ABN) joint meeting with the Royal College of Physicians (RCP), London, 23–24 October 2013</subject></subj-group><series-title>015</series-title></article-categories><title-group><article-title>CIGARETTE SMOKING, ALCOHOL CONSUMPTION AND CAFFEINE INTAKE IN PD AND PD SUBTYPES: A COMMUNITY–BASED, INCIDENT COHORT WITH MATCHED CONTROLS</article-title></title-group><contrib-group><contrib contrib-type="author"><name><surname>Macleod</surname><given-names>Angus D</given-names></name><xref ref-type="corresp"></xref></contrib><contrib contrib-type="author"><name><surname>Counsell</surname><given-names>Carl E</given-names></name></contrib></contrib-group><aff><addr-line>University of Aberdeen</addr-line></aff><pub-date pub-type="ppub"><month>11</month><year>2013</year></pub-date><volume>84</volume><volume-id pub-id-type="other">84</volume-id><volume-id pub-id-type="other">84</volume-id><issue>11</issue><issue-id pub-id-type="other">jnnp;84/11</issue-id><issue-id pub-id-type="other">11</issue-id><issue-id pub-id-type="other">84/11</issue-id><fpage seq="57">e2</fpage><permissions><copyright-statement>Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://group.bmj.com/group/rights-licensing/permissions</copyright-statement><copyright-year>2013</copyright-year></permissions><self-uri content-type="pdf" xlink:role="full-text" xlink:href="jnnp-84-e2-57.pdf"></self-uri><abstract><sec><title>Background</title><p>Previous studies have demonstrated negative associations between cigarette smoking, alcohol consumption and caffeine intake and Parkinson's disease (PD), but most data come from unrepresentative cohorts (1). One previous study suggested different associations with these exposures in different PD phenotypes (2). There are no data describing change in these exposures after diagnosis: a differential change between cases and controls would introduce bias to prevalence-based case-control studies.</p></sec><sec><title>Methods</title><p>We recruited a community-based, inception cohort of PD and matched controls and gathered data about previous duration and intensity of cigarette smoking and alcohol and caffeine intake with face-to-face questionnaires. We calculated odds ratios and adjusted odds ratios using logistic regression analysis to examine the associations between these exposures and PD and the tremor-dominant and postural instability and gait difficulty (PIGD) subtypes. We also assessed the change in exposures after recruitment in patients and controls with a linear mixed model.</p></sec><sec><title>Results</title><p>201 patients with PD and 249 controls were analysed. Moderate and high cumulative levels of smoking, OR 0.42 (0.24–0.74) and 0.48 (0.28–0.82) respectively; high alcohol intake, OR 0.27 (0.13–0.56); and moderate and high caffeine consumption, ORs 0.48 (0.28–0.82) and 0.39 (0.22–0.68) respectively; were statistically significant negative associations with PD. There were statistically significant inverse trends between rising levels of consumption for each exposure and PD (P<0.001 for smoking, P=0.003 for alcohol and P<0.001 for caffeine). A similar pattern of associations with these exposures was seen in the PIGD and tremor-dominant patients as in the whole PD group. Smoking and alcohol consumption declined after diagnosis, but not at different rates between patients and controls.</p></sec><sec><title>Conclusions</title><p>Our study therefore provides further evidence for dose-dependent negative associations between these exposures and PD in a truly-representative inception cohort. We found no evidence of different associations with the tremor-dominant and PIGD PD subtypes. The lack of a differential reduction in exposure is important for interpretation of prevalent studies.</p></sec></abstract><kwd-group><kwd>PARKINSON'S DISEASE</kwd><kwd>STROKE</kwd><kwd>PARKINSON'S DISEASE</kwd><kwd>STROKE</kwd><kwd>PARKINSON'S DISEASE</kwd><kwd>STROKE</kwd><kwd>PARKINSON'S DISEASE</kwd><kwd>STROKE</kwd><kwd>PARKINSON'S DISEASE</kwd><kwd>STROKE</kwd><kwd>PARKINSON'S DISEASE</kwd><kwd>STROKE</kwd><kwd>PARKINSON'S DISEASE</kwd><kwd>STROKE</kwd><kwd>PARKINSON'S DISEASE</kwd><kwd>STROKE</kwd><kwd>PARKINSON'S DISEASE</kwd><kwd>STROKE</kwd><kwd>PARKINSON'S DISEASE</kwd><kwd>STROKE</kwd><kwd>PARKINSON'S DISEASE</kwd><kwd>STROKE</kwd><kwd>PARKINSON'S DISEASE</kwd><kwd>STROKE</kwd><kwd>PARKINSON'S DISEASE</kwd><kwd>STROKE</kwd><kwd>PARKINSON'S DISEASE</kwd><kwd>STROKE</kwd><kwd>PARKINSON'S DISEASE</kwd><kwd>STROKE</kwd><kwd>PARKINSON'S DISEASE</kwd><kwd>STROKE</kwd></kwd-group></article-meta></front></article></istex:document></istex:metadataXml><mods version="3.6"><titleInfo><partName>015</partName><title>CIGARETTE SMOKING, ALCOHOL CONSUMPTION AND CAFFEINE INTAKE IN PD AND PD SUBTYPES: A COMMUNITY–BASED, INCIDENT COHORT WITH MATCHED CONTROLS</title></titleInfo><titleInfo type="alternative" contentType="CDATA"><partName>015</partName><title>CIGARETTE SMOKING, ALCOHOL CONSUMPTION AND CAFFEINE INTAKE IN PD AND PD SUBTYPES: A COMMUNITY–BASED, INCIDENT COHORT WITH MATCHED CONTROLS</title></titleInfo><name type="personal"><namePart type="given">Angus D</namePart><namePart type="family">Macleod</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Carl E</namePart><namePart type="family">Counsell</namePart><affiliation>University of Aberdeen</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="abstract" displayLabel="abstract"></genre><originInfo><publisher>BMJ Publishing Group Ltd</publisher><dateIssued encoding="w3cdtf">2013-11</dateIssued><copyrightDate encoding="w3cdtf">2013</copyrightDate></originInfo><language><languageTerm type="code" authority="iso639-2b">eng</languageTerm><languageTerm type="code" authority="rfc3066">en</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType></physicalDescription><abstract>Background Previous studies have demonstrated negative associations between cigarette smoking, alcohol consumption and caffeine intake and Parkinson's disease (PD), but most data come from unrepresentative cohorts (1). One previous study suggested different associations with these exposures in different PD phenotypes (2). There are no data describing change in these exposures after diagnosis: a differential change between cases and controls would introduce bias to prevalence-based case-control studies. Methods We recruited a community-based, inception cohort of PD and matched controls and gathered data about previous duration and intensity of cigarette smoking and alcohol and caffeine intake with face-to-face questionnaires. We calculated odds ratios and adjusted odds ratios using logistic regression analysis to examine the associations between these exposures and PD and the tremor-dominant and postural instability and gait difficulty (PIGD) subtypes. We also assessed the change in exposures after recruitment in patients and controls with a linear mixed model. Results 201 patients with PD and 249 controls were analysed. Moderate and high cumulative levels of smoking, OR 0.42 (0.24–0.74) and 0.48 (0.28–0.82) respectively; high alcohol intake, OR 0.27 (0.13–0.56); and moderate and high caffeine consumption, ORs 0.48 (0.28–0.82) and 0.39 (0.22–0.68) respectively; were statistically significant negative associations with PD. There were statistically significant inverse trends between rising levels of consumption for each exposure and PD (P<0.001 for smoking, P=0.003 for alcohol and P<0.001 for caffeine). A similar pattern of associations with these exposures was seen in the PIGD and tremor-dominant patients as in the whole PD group. Smoking and alcohol consumption declined after diagnosis, but not at different rates between patients and controls. Conclusions Our study therefore provides further evidence for dose-dependent negative associations between these exposures and PD in a truly-representative inception cohort. We found no evidence of different associations with the tremor-dominant and PIGD PD subtypes. The lack of a differential reduction in exposure is important for interpretation of prevalent studies.</abstract><subject><genre>Keywords</genre><topic>PARKINSON'S DISEASE</topic><topic>STROKE</topic><topic>PARKINSON'S DISEASE</topic><topic>STROKE</topic><topic>PARKINSON'S DISEASE</topic><topic>STROKE</topic><topic>PARKINSON'S DISEASE</topic><topic>STROKE</topic><topic>PARKINSON'S DISEASE</topic><topic>STROKE</topic><topic>PARKINSON'S DISEASE</topic><topic>STROKE</topic><topic>PARKINSON'S DISEASE</topic><topic>STROKE</topic><topic>PARKINSON'S DISEASE</topic><topic>STROKE</topic><topic>PARKINSON'S DISEASE</topic><topic>STROKE</topic><topic>PARKINSON'S DISEASE</topic><topic>STROKE</topic><topic>PARKINSON'S DISEASE</topic><topic>STROKE</topic><topic>PARKINSON'S DISEASE</topic><topic>STROKE</topic><topic>PARKINSON'S DISEASE</topic><topic>STROKE</topic><topic>PARKINSON'S DISEASE</topic><topic>STROKE</topic><topic>PARKINSON'S DISEASE</topic><topic>STROKE</topic><topic>PARKINSON'S DISEASE</topic><topic>STROKE</topic></subject><relatedItem type="host"><titleInfo><title>Journal of Neurology, Neurosurgery & Psychiatry</title></titleInfo><titleInfo type="abbreviated"><title>J Neurol Neurosurg Psychiatry</title></titleInfo><genre type="Journal">journal</genre><identifier type="ISSN">0022-3050</identifier><identifier type="eISSN">1468-330X</identifier><identifier type="PublisherID">jnnp</identifier><identifier type="PublisherID-hwp">jnnp</identifier><identifier type="PublisherID-nlm-ta">J Neurol Neurosurg Psychiatry</identifier><part><date>2013</date><detail type="volume"><caption>vol.</caption><number>84</number></detail><detail type="issue"><caption>no.</caption><number>11</number></detail><extent unit="pages"><start>e2</start></extent></part></relatedItem><identifier type="istex">39C674605DA11E5EAB0495DD464D2BE04EDE18B3</identifier><identifier type="DOI">10.1136/jnnp-2013-306573.15</identifier><identifier type="href">jnnp-84-e2-57.pdf</identifier><identifier type="local">jnnp;84/11/e2-bd</identifier><accessCondition type="use and reproduction" contentType="copyright">Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://group.bmj.com/group/rights-licensing/permissions</accessCondition><recordInfo><recordContentSource>BMJ</recordContentSource></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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