Cautionary optimism: caffeine and Parkinson’s disease risk
Identifieur interne : 000208 ( Pmc/Corpus ); précédent : 000207; suivant : 000209Cautionary optimism: caffeine and Parkinson’s disease risk
Auteurs : Leonard L. Sokol ; Michael J. Young ; Alberto J. Espay ; Ronald B. PostumaSource :
- Journal of Clinical Movement Disorders [ 2054-7072 ] ; 2016.
Abstract
Most Parkinson’s disease (PD) patients present without known family history and without a diagnosed prodromal phase, underscoring the difficulty of employing primary (neuroprevention) and secondary (neuroprotection) preventions. In cases of monogenic forms, however, potential gene-carrying family members of a proband could engage in neuroprevention, such as exercise or diet modifications, to attenuate the risk of, or delay, disease development. However, a historical lack of recognized disease-modifying interventions has limited clinicians’ ability to recommend reliable preventive measures in caring for at-risk populations. We briefly analyze the first retrospective study to examine caffeine consumption and PD risk in a LRRK2 R1628P cohort.
Url:
DOI: 10.1186/s40734-016-0037-8
PubMed: 27275394
PubMed Central: 4893836
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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Cautionary optimism: caffeine and Parkinson’s disease risk</title><author><name sortKey="Sokol, Leonard L" sort="Sokol, Leonard L" uniqKey="Sokol L" first="Leonard L." last="Sokol">Leonard L. Sokol</name><affiliation><nlm:aff id="Aff1">Department of Neurology, James J and Joan A. Gardner Center for Parkinson’s disease and Movement Disorders, University of Cincinnati, Cincinnati, OH USA</nlm:aff></affiliation></author><author><name sortKey="Young, Michael J" sort="Young, Michael J" uniqKey="Young M" first="Michael J." last="Young">Michael J. Young</name><affiliation><nlm:aff id="Aff2">Harvard Medical School, Boston, MA USA</nlm:aff></affiliation></author><author><name sortKey="Espay, Alberto J" sort="Espay, Alberto J" uniqKey="Espay A" first="Alberto J." last="Espay">Alberto J. Espay</name><affiliation><nlm:aff id="Aff1">Department of Neurology, James J and Joan A. Gardner Center for Parkinson’s disease and Movement Disorders, University of Cincinnati, Cincinnati, OH USA</nlm:aff></affiliation></author><author><name sortKey="Postuma, Ronald B" sort="Postuma, Ronald B" uniqKey="Postuma R" first="Ronald B." last="Postuma">Ronald B. Postuma</name><affiliation><nlm:aff id="Aff3">Department of Neurology, L7-305 Montreal General Hospital, 1650 Cedar Avenue, Montreal, QC H3G1A4 Canada</nlm:aff></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PMC</idno><idno type="pmid">27275394</idno><idno type="pmc">4893836</idno><idno type="url">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4893836</idno><idno type="RBID">PMC:4893836</idno><idno type="doi">10.1186/s40734-016-0037-8</idno><date when="2016">2016</date><idno type="wicri:Area/Pmc/Corpus">000208</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Corpus" wicri:corpus="PMC">000208</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">Cautionary optimism: caffeine and Parkinson’s disease risk</title><author><name sortKey="Sokol, Leonard L" sort="Sokol, Leonard L" uniqKey="Sokol L" first="Leonard L." last="Sokol">Leonard L. Sokol</name><affiliation><nlm:aff id="Aff1">Department of Neurology, James J and Joan A. Gardner Center for Parkinson’s disease and Movement Disorders, University of Cincinnati, Cincinnati, OH USA</nlm:aff></affiliation></author><author><name sortKey="Young, Michael J" sort="Young, Michael J" uniqKey="Young M" first="Michael J." last="Young">Michael J. Young</name><affiliation><nlm:aff id="Aff2">Harvard Medical School, Boston, MA USA</nlm:aff></affiliation></author><author><name sortKey="Espay, Alberto J" sort="Espay, Alberto J" uniqKey="Espay A" first="Alberto J." last="Espay">Alberto J. Espay</name><affiliation><nlm:aff id="Aff1">Department of Neurology, James J and Joan A. Gardner Center for Parkinson’s disease and Movement Disorders, University of Cincinnati, Cincinnati, OH USA</nlm:aff></affiliation></author><author><name sortKey="Postuma, Ronald B" sort="Postuma, Ronald B" uniqKey="Postuma R" first="Ronald B." last="Postuma">Ronald B. Postuma</name><affiliation><nlm:aff id="Aff3">Department of Neurology, L7-305 Montreal General Hospital, 1650 Cedar Avenue, Montreal, QC H3G1A4 Canada</nlm:aff></affiliation></author></analytic><series><title level="j">Journal of Clinical Movement Disorders</title><idno type="eISSN">2054-7072</idno><imprint><date when="2016">2016</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p>Most Parkinson’s disease (PD) patients present without known family history and without a diagnosed prodromal phase, underscoring the difficulty of employing primary (neuroprevention) and secondary (neuroprotection) preventions. In cases of monogenic forms, however, potential gene-carrying family members of a proband could engage in neuroprevention, such as exercise or diet modifications, to attenuate the risk of, or delay, disease development. However, a historical lack of recognized disease-modifying interventions has limited clinicians’ ability to recommend reliable preventive measures in caring for at-risk populations. We briefly analyze the first retrospective study to examine caffeine consumption and PD risk in a LRRK2 R1628P cohort.</p></div></front><back><div1 type="bibliography"><listBibl><biblStruct><analytic><author><name sortKey="Costa, J" uniqKey="Costa J">J Costa</name></author><author><name sortKey="Lunet, N" uniqKey="Lunet N">N Lunet</name></author><author><name sortKey="Santos, C" uniqKey="Santos C">C Santos</name></author><author><name sortKey="Santos, J" uniqKey="Santos J">J Santos</name></author><author><name sortKey="Vaz Carneiro, A" uniqKey="Vaz Carneiro A">A Vaz-Carneiro</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Qi, H" uniqKey="Qi H">H Qi</name></author><author><name sortKey="Li, S" uniqKey="Li S">S Li</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Schwarzschild, Ma" uniqKey="Schwarzschild M">MA Schwarzschild</name></author><author><name sortKey="Xu, K" uniqKey="Xu K">K Xu</name></author><author><name 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<front><journal-meta><journal-id journal-id-type="nlm-ta">J Clin Mov Disord</journal-id><journal-id journal-id-type="iso-abbrev">J Clin Mov Disord</journal-id><journal-title-group><journal-title>Journal of Clinical Movement Disorders</journal-title></journal-title-group><issn pub-type="epub">2054-7072</issn><publisher><publisher-name>BioMed Central</publisher-name><publisher-loc>London</publisher-loc></publisher></journal-meta><article-meta><article-id pub-id-type="pmid">27275394</article-id><article-id pub-id-type="pmc">4893836</article-id><article-id pub-id-type="publisher-id">37</article-id><article-id pub-id-type="doi">10.1186/s40734-016-0037-8</article-id><article-categories><subj-group subj-group-type="heading"><subject>Letter to the Editor</subject></subj-group></article-categories><title-group><article-title>Cautionary optimism: caffeine and Parkinson’s disease risk</article-title></title-group><contrib-group><contrib contrib-type="author" equal-contrib="yes"><name><surname>Sokol</surname><given-names>Leonard L.</given-names></name><xref ref-type="aff" rid="Aff1"></xref></contrib><contrib contrib-type="author" equal-contrib="yes"><name><surname>Young</surname><given-names>Michael J.</given-names></name><xref ref-type="aff" rid="Aff2"></xref></contrib><contrib contrib-type="author"><name><surname>Espay</surname><given-names>Alberto J.</given-names></name><xref ref-type="aff" rid="Aff1"></xref></contrib><contrib contrib-type="author" corresp="yes"><name><surname>Postuma</surname><given-names>Ronald B.</given-names></name><address><email>ron.postuma@mcgill.ca</email></address><xref ref-type="aff" rid="Aff3"></xref></contrib><aff id="Aff1"><label></label>Department of Neurology, James J and Joan A. Gardner Center for Parkinson’s disease and Movement Disorders, University of Cincinnati, Cincinnati, OH USA</aff><aff id="Aff2"><label></label>Harvard Medical School, Boston, MA USA</aff><aff id="Aff3"><label></label>Department of Neurology, L7-305 Montreal General Hospital, 1650 Cedar Avenue, Montreal, QC H3G1A4 Canada</aff></contrib-group><pub-date pub-type="epub"><day>6</day><month>6</month><year>2016</year></pub-date><pub-date pub-type="pmc-release"><day>6</day><month>6</month><year>2016</year></pub-date><pub-date pub-type="collection"><year>2016</year></pub-date><volume>3</volume><elocation-id>7</elocation-id><history><date date-type="received"><day>26</day><month>2</month><year>2016</year></date><date date-type="accepted"><day>11</day><month>5</month><year>2016</year></date></history><permissions><copyright-statement>© Sokol et al. 2016</copyright-statement><license license-type="OpenAccess"><license-p><bold>Open Access</bold>This article is distributed under the terms of the Creative Commons Attribution 4.0 International License (<ext-link ext-link-type="uri" xlink:href="http://creativecommons.org/licenses/by/4.0/">http://creativecommons.org/licenses/by/4.0/</ext-link>), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (<ext-link ext-link-type="uri" xlink:href="http://creativecommons.org/publicdomain/zero/1.0/">http://creativecommons.org/publicdomain/zero/1.0/</ext-link>) applies to the data made available in this article, unless otherwise stated.</license-p></license></permissions><abstract id="Abs1"><p>Most Parkinson’s disease (PD) patients present without known family history and without a diagnosed prodromal phase, underscoring the difficulty of employing primary (neuroprevention) and secondary (neuroprotection) preventions. In cases of monogenic forms, however, potential gene-carrying family members of a proband could engage in neuroprevention, such as exercise or diet modifications, to attenuate the risk of, or delay, disease development. However, a historical lack of recognized disease-modifying interventions has limited clinicians’ ability to recommend reliable preventive measures in caring for at-risk populations. We briefly analyze the first retrospective study to examine caffeine consumption and PD risk in a LRRK2 R1628P cohort.</p></abstract><kwd-group xml:lang="en"><title>Keywords</title><kwd>Parkinson’s disease</kwd><kwd>LRRK2</kwd><kwd>Caffeine</kwd><kwd>Risk factors</kwd></kwd-group><custom-meta-group><custom-meta><meta-name>issue-copyright-statement</meta-name><meta-value>© The Author(s) 2016</meta-value></custom-meta></custom-meta-group></article-meta></front><body><sec id="Sec1"><title>Letter to the Editor</title><p>Caffeine is strongly associated with reduced risk of Parkinson’s disease (PD). Meta-analyses [<xref ref-type="bibr" rid="CR1">1</xref>, <xref ref-type="bibr" rid="CR2">2</xref>] suggest that non-users have a higher PD risk in a notably dose-dependent fashion [<xref ref-type="bibr" rid="CR2">2</xref>]. The underlying mechanism for this apparent effect is unclear. Potential explanations include a true neuroprotective benefit (supported by some animal models finding benefits of A<sub>2A</sub> antagonism [<xref ref-type="bibr" rid="CR3">3</xref>]), a symptomatic effect which delays diagnosis (supported by preliminary evidence of motor benefit of caffeine in small randomized controlled trials [<xref ref-type="bibr" rid="CR4">4</xref>]), reverse confounding (prodromal parkinsonism reduces caffeine intake via changes in tolerability or reward mechanisms such as has been suggested for smoking [<xref ref-type="bibr" rid="CR5">5</xref>]), or confounding by another unmeasured factor (e.g., the putative Parkinson personality [<xref ref-type="bibr" rid="CR6">6</xref>]).</p><p>Most recently, a new case–control study [<xref ref-type="bibr" rid="CR7">7</xref>] examined caffeine consumption and PD risk in a gene-carrier (LRRK2 R1628P) cohort of Chinese patients. LRRK2 R1628P is a low-penetrance variant that has been associated with increased PD risk in mainly Asian populations, with an odds ratio (OR) ranging from 1.20 to 2.83 [<xref ref-type="bibr" rid="CR8">8</xref>]. The study included 378 PD subjects and 434 healthy controls (PD median age: 66 years; controls: 60). For OR calculations, the authors defined the reference group (PD cases: 257; controls: 369) as those with the LRRK2 wildtype allele who had a reported history of caffeine consumption. Gene-carrier caffeine-abstainers had a 15.4 (95 % CI = 1.94,122.3, <italic>n</italic> = 11) OR of PD; by contrast, gene-carrier caffeine-consumers had a lower increased OR of 3.07 (2.02-4.66, <italic>n</italic> = 33). On the basis of these data, the study authors suggest that caffeine intake may be associated with reduced risk of PD development especially in those who are gene-carriers.</p><p>Some caveats should be considered when interpreting these results. First, the sample size was insufficient to provide an estimate of a true effect, as within the R1628P sample, there were too few PD cases (<italic>n</italic> = 28; 18 caffeine-consumers and 10 caffeine-abstainers) and controls (<italic>n</italic> = 16; 15 caffeine-consumers and 1 caffeine-abstainer), yielding an imprecise OR (1.94 to 122.3) that clearly overlapped with the OR for gene-carrier caffeine-consumers. Second, recall bias or other sources of measurement error may have influenced the interpretation of the PD environmental risk factor questionnaire. Third, it is unclear what number of multiple hypotheses were tested in this cohort; if dozens of potential gene-environment interactions were queried, the chances of a spurious result are high. It should be cautioned that many gene-environment findings based upon single cohort studies are not reproduced. Finally, the physiologic mechanism(s) governing the putative impact of caffeine in the PD neurodegenerative cascade remains unclear. Recognizing the excitement that the <italic>prima-facie</italic> favorable findings of this study may generate among patients and clinicians, these key caveats should be considered in the course of crafting an evidence-based and patient-centered approach to neuropreventive counseling and care.</p><p>While this study was neither definitive nor generalizable, it suggests the possibility that disease subtypes may have different environmental risk profiles. Of note, LRRK2 in PD is characterized by inconsistent deposition of synuclein, and a corresponding lower prevalence of non-motor manifestation such as REM sleep behavior disorder (RBD) and dementia [<xref ref-type="bibr" rid="CR9">9</xref>]. A recent case control study of patients with idiopathic RBD found that caffeine use did not protect against future development of PD; this is the only prospective study that has ever failed to find a caffeine effect [<xref ref-type="bibr" rid="CR10">10</xref>]. If there is an RBD subtype of PD that does not respond to caffeine, then might non-RBD subtypes respond even more?</p><p>If such a study is replicated in a larger series—which is critical for ascertainment of such gene-environmental interactions—it may have implications for other well-known LRRK2 variants, such as G2019S, which has a calculated disease penetrance of 26 % by age 80 [<xref ref-type="bibr" rid="CR11">11</xref>]. Might caffeine have a similar interaction? If so, might such patients benefit from using caffeine? Without better evidence, there remain dichotomous perspectives [<xref ref-type="bibr" rid="CR12">12</xref>, <xref ref-type="bibr" rid="CR13">13</xref>] on how to counsel carriers and their families. Research that examines how environmental behaviors might attenuate PD susceptibility is warranted [<xref ref-type="bibr" rid="CR11">11</xref>], as is further investigation on how to counsel such a vulnerable cohort [<xref ref-type="bibr" rid="CR14">14</xref>].</p></sec><sec id="Sec2"><title>Statement on ethics approval and consent to participate</title><p>Not applicable.</p></sec><sec id="Sec3"><title>Statement of consent for publication</title><p>Not applicable.</p></sec><sec id="Sec4" sec-type="materials|methods"><title>Availability of data and materials</title><p>Not applicable.</p></sec></body><back><glossary><title>Abbreviations</title><def-list><def-item><term>LRRK2</term><def><p>leucine-rich repeat kinase 2</p></def></def-item><def-item><term>OR</term><def><p>odds ratio</p></def></def-item><def-item><term>PD</term><def><p>parkinson’s disease</p></def></def-item><def-item><term>RBD</term><def><p>REM sleep behavior disorder</p></def></def-item></def-list></glossary><fn-group><fn><p><bold>Competing interests</bold></p><p>Financial disclosures related to research covered in this article: The authors report no conflicts of interest related to research covered in this article.</p></fn><fn><p><bold>Authors’ contributions</bold></p><p>All authors read and approved of the final manuscript. (1) Letter: A. Conception, B. Organization, C. Execution; (2) Manuscript: A. Writing of the First Draft, B. Review and Critique. LLS: 1A, 1B, 1C, 2A. MJY: 1B, 1C, 2A. AJE: 1B, 1C, 2B. RBP: 1B, 1C, 2B.</p></fn></fn-group><ack><title>Funding</title><p>Not applicable.</p><sec id="FPar1"><title>Full financial disclosures</title><p>L.L. Sokol has nothing to disclose. M.J. Young has nothing to disclose. A.J. Espay serves on scientific advisory boards for Solvay (now Abbvie), Chelsea Therapeutics, TEVA, Impax, Merz, Pfizer, Solstice Neurosciences, Eli Lilly, Acadia, and USWorldMeds; serves as an Associate Editor of the Journal of Clinical Movement Disorders and on the editorial boards of Parkinsonism and Related Disorders and The European Neurological Journal; receives publishing royalties from Lippincott Williams & Wilkins and Cambridge University Press; serves as a consultant for Chelsea Therapeutics, Cynapsus, Lundbeck, Abbvie, and Acadia; serves on speakers’ bureaus for UCB, TEVA, American Academy of Neurology, and the Movement Disorders Society; has received honoraria from UCB, TEVA, Acadia, the American Academy of Neurology, and the Movement Disorders Society; and receives research support from the NIH, CleveMed/Great Lakes Neurotechnologies, and the Michael J. Fox Foundation. R.B. 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