Vandaag is er weer een mythe bijgekomen: in de Vlaamse pers wordt gesuggereerd dat alleen mensen met een hoog verantwoordelijkheidsgevoel Parkinson krijgen.Welingelichte kringen neemt het weer over…
Van vooraanstaande neurologen krijgen we bericht dat het op geen enkele manier wetenschappelijk onderbouwd is: door Parkinson stop je met roken en koffie drinken. De ziekte van Parkinson is er al voor er verschijnselen zijn. Daar komt nog bij dat mensen die Parkinson hebben en roken of gerookt hebben eerder dement worden dan mensen met Parkinson die niet rookten.
En dan nog: Parkinson komt op alle leeftijden voor, maar vooral op oudere leeftijd. Als je flink gaat roken om Parkinson te voorkomen, heb je een grote kans al te zijn overleden (longkanker, hart en vaatziekten dus ook beroertes) voor je Parkinson an de beurt is .ga alsjeblieft niet roken als je Parkinson hebt, de kans op een beroerte wordt veel groter:
EDITORIAL Linda A. Hershey, MD, PhD Joel S. Perlmutter, MD Correspondence to Dr. Hershey: firstname.lastname@example.org Neurology® 2014;83:1392–1393 See page 1396 Smoking and Parkinson disease Where there is smoke there may not be fire
Several case-control studies have demonstrated an inverse relationship between the presence of Parkinson disease (PD) and smoking cigarettes.1,2 The risk of PD in someone who has ever smoked is about half of that of a nonsmoker.3,4 These observations prompted some to hypothesize that smoking could protect against the development of PD. The lay press popularized this notion, and the idea inspired studies to test whether nicotine can slow disease progression. Alternatively, the pharmacologic action of nicotine suggests a different mechanism of action. Nicotine, a rewarding drug, increases extracellular dopamine concentrations in the nucleus accumbens and produces stimulation of behavior in animals.5 Patients with PD have fewer available nicotinic acetylcholine receptors in the brain6 with reductions of up to 50% in the frontal and temporal areas involved in learning, memory, and execution of stimulusseeking behaviors. Thus, patients with PD may feel less nicotine-mediated “reward” from stimulusseeking behaviors or from cigarettes, which may make it easier for those with PD to quit smoking. This may explain an apparent neuroprotective effect of cigarettes in PD, whereas the actual underlying physiologic response may permit those with PD to quit smoking more easily than those without PD. In support of this reduced reward response, patients with PD compared to age-matched controls show fewer stimulus-seeking behaviors, such as less coffee drinking and less alcohol consumption.1,4,7 Clarification of the precise role of exposure to cigarette smoke for either progression of PD or nicotinic response in those with PD has important implications for development of therapeutic strategies. The report by Ritz et al.8 in this issue examines the possibility that quitting cigarettes might be a marker for PD onset, rather than smoking itself having a neuroprotective effect. The strengths of this study include (1) data acquisition from a large Danish registry (1,808 patients with PD and 1,876 controls); (2) a case-control study design, and (3) examination of nicotine substitute use, along with the use of cigarettes, caffeinated drinks, and alcohol. As previously reported, the authors found an inverse relationship between the diagnosis of PD and cigarette smoking.1,2 They also discovered that among former smokers who had quit, those who had extreme difficulty quitting had the lowest risk of PD. Reduced responsiveness to nicotine in patients with PD could account for this observation, as has been suggested by others.6 Therefore, ease of smoking cessation could be a nonmotor aspect of early PD that is similar to olfactory dysfunction, REM sleep disorder, or constipation, as described in the review by Chaudhuri et al.9 Alternatively, a lower lifelong risk of smoking in those with PD compared with controls (see table 1) could be an underlying mechanism accounting for differences in smoking behavior between patients with PD and controls. This latter hypothesis could not be tested in the study by Ritz et al.8 Nevertheless, this study suggests several important conclusions. One is that practicing neurologists should not recommend cigarette use or nicotine substitutes to delay onset of PD. No clinical study data support this, and the rationale may be faulty. Further development of nicotine agonist therapy for PD may not be justified. Finally, physicians, including neurologists, should encourage their patients to stop smoking, because cigarette smoking is a significant risk factor for stroke.10 All of the past smoke about PD may have been a misinterpretation of the data. Where there is smoke, there may not be fire. That is the key message from Ritz et al.8
STUDY FUNDING No targeted funding reported.
DISCLOSURE L. Hershey is a coinvestigator on NIH grant 8UL1TR0004 and is the site principal investigator for Baxter and Forum studies. She has received honoraria for educational presentations and online publications. J. Perlmutter is the principal investigator of NS41509, NS058714, and NS075321; coinvestigator on NS065701, R01 DK085575, NS075527, U10NS077384, NS077946, NS077959, ES02148, and MH092797; and is supported by the American Academy of Neurology, American Parkinson Disease Association (APDA) Center for Advanced PD Research at Washington University, Greater St. Louis Chapter of the APDA, McDonnell Center for Higher Brain Function, and Barnes-Jewish Hospital Foundation (Elliot Stein Family Fund and Parkinson Disease Research Fund). Go to Neurology.org for full disclosures. From the Department of Neurology (L.A.H.), University of Oklahoma Health Sciences Center, Oklahoma City; and Departments of Neurology, Radiology, and Neurobiology, and Programs of Physical Therapy and Occupational Therapy (J.S.P.), Washington University, St. Louis, MO. 1392 © 2014 American Academy of Neurology REFERENCES 1. Gorell JM, Rybicki BA, Johnson CC, Peterson EL. Smoking and Parkinson’s disease: a dose-response relationship. Neurology 1999;52:115–119. 2. Tanner CM, Goldman SM, Aston DA, et al. Smoking and Parkinson’s disease in twins. Neurology 2002;58: 581–588. 3. Sugita M, Izuno T, Tatemichi M, Otahara Y. Metaanalysis for epidemiologic studies on the relationship between smoking and Parkinson’s disease. J Epidemiol 2001;11:87–94. 4. Checkoway H, Powers K, Smith-Weller T, Franklin G, Longstreth WT, Swanson PD. Parkinson’s disease risks associated with cigarette smoking, alcohol consumption, and caffeine intake. Am J Epidemiol 2002;155:732–738. 5. Di Chiara G, Imperato A. Drugs abused by humans preferentially increase synaptic dopamine concentrations in the mesolimbic system of freely moving rats. Proc Natl Acad Sci USA 1988;85:5274–5278. 6. Quik M, Jeyarasasingam G. Nicotinic receptors and Parkinson’s disease. Eur J Pharmacol 2000;393:223–230. 7. Evans AH, Lawrence AD, Potts J, et al. Relationship between impulsive sensation seeking traits, smoking, alcohol and caffeine intake, and Parkinson’s disease. J Neurol Neurosurg Psychiatry 2006;77:317–321. 8. Ritz B, Lee PC, Lassen CF, Arah OA. Parkinson disease and smoking revisited: ease of quitting is an early sign of the disease. Neurology 2014;83:1396–1402. 9. Chaudhuri KR, Healy DG, Schapira AH. Non-motor symptoms of Parkinson’s disease: diagnosis and management. Lancet Neurol 2006;5:235–245. 10. Wolf PA, D’Agostino RB, Kannel WB, Bonita R, Belanger AJ. Cigarette smoking as a risk factor for stroke. JAMA 1988;259:1025–1029. Neurology 83 October 14, 2014 1393 DOI 10.1212/WNL.0000000000000896 Neurology 2014;83;1392-1393 Published Online before print September 12, 2014 Linda A. Hershey and Joel S. Perlmutter Smoking and Parkinson disease: Where there is smoke there may not be fire This information is current as of September 12, 2014 Services Updated Information & http://www.neurology.org/content/83/16/1392.full.html including high resolution figures, can be found at: References http://www.neurology.org/content/83/16/1392.full.html##ref-list-1 This article cites 10 articles, 5 of which you can access for free at: Subspecialty Collections http://www.neurology.org//cgi/collection/risk_factors_in_epidemiology Risk factors in epidemiology nism http://www.neurology.org//cgi/collection/parkinsons_disease_parkinso Parkinson’s disease/Parkinsonism http://www.neurology.org//cgi/collection/case_control_studies Case control studies following collection(s): This article, along with others on similar topics, appears in the Permissions & Licensing http://www.neurology.org/misc/about.xhtml#permissions its entirety can be found online at: Information about reproducing this article in parts (figures,tables) or in Reprints http://www.neurology.org/misc/addir.xhtml#reprintsus Information about ordering reprints can be found online: rights reserved. Print ISSN: 0028-3878. Online ISSN: 1526-632X. 1951, it is now a weekly with 48 issues per year. Copyright © 2014 American Academy of Neurology. All Neurology ® is the official journal of the American Academy of Neurology. Published continuously since