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In 2007 Finnish research indicated that regular coffee drinking may be connected with a reduced risk to have Parkinson’s disease (Hu et al. 2007). This risk relationship was dependent on the used amount of coffee each day. There was no significant difference between the genders. The findings were similar to those of another published study (Ascherio et al. 2001). The biological risk reducing mechanism behind this finding is still unclear but caffeine is considered to be the neuroprotective factor. Other possible elements may not be ruled out either, however. Caffeine is assumed to influence the strength of Parkinson medication by lengthening the effect of levodopa when it is consumed prior to taking the drug (Chand 2006). The amount was delimited to 3 or 4 cups of the drink daily. Those consuming at least 4 cups of coffee obtained slightly better results than those hardly using any coffee at all as reported in cross-sectional research on lung performance (Nettleton et al. 2009). Thus coffee appears to make lungs more effective. Parkinson postia has reported on some of the above stated studies in the past. Then, is caffeine good for all Parkinson patients? The last mentioned finding was applicable to non-smokers (or to those who discontinued smoking) only (Nettleton et al. 2009). In a follow-up study, an elderly woman’s memory deteriorated less when she consumed caffeine containing drinks or tea; caffeine consumption had no effect on memory of men (Ritchie et al. 2007). Genetic predisposition adds its own meaning: some people are fast caffeine metabolizers while others are slow caffeine metabolizers (Cornellis et al. 2006). Nonfatal myocardial infarction (MI) was noted as an interesting health factor. “Intake of coffee was associated with an increased risk of nonfatal MI only among individuals with slow caffeine metabolism, suggesting that caffeine plays a role in this association” (Cornellis et al. 2006). Three or more cups per day posed a problem. This would mean that slow caffeine metabolizers may need to delimit coffee drinking to 1-2 cups a day. Coffee is essentially considered a stimulant but it has also become a health food item. It may even enhance the outcome of Parkinson medication. For those PD patients who cannot tolerate medical preparations used to improve the quality of levadopa these findings may be of consequence. How then may coffee breaks be organized as part of every day activities when selection of food items, measurements of medicine in relation to nutrition, exercise breaks, and finding the right time to take a nap define the rhythm of the day? When would be the best time for coffee? Ascherio A et al. Prospective study of caffeine consumption and risk of Parkinson's disease in men and women. Annals of Neurology 2001; 50 (1): Chand, P. Effects of caffeine on levodopa pharmacokinetics and pharmacodynamics in Parkinson disease. Neurology 2006; 67: 897-89. Cornellis MC et al. Coffee, CYP1A2 Genotype, and Risk of Myocardial Hu G et al. Coffee and tea consumption and the risk of Parkinson’s disease. Movement Disorders 2007; 22 (15): 2242-2248. Nettleton JA et al. Coffee Intake, Smoking, and Pulmonary Function in the Atherosclerosis Risk in Communities Study. Am J Epidemiol 2009; 169 (12): Ritchie K et al. The neuroprotective effects of caffeine: A prospective population study (the Three City Study). Neurology 2007; 69: 536-545. Ross GW et al. Association of coffee and caffeine intake with the risk of Parkinson disease. JAMA 2000; 283 (20): 2674-2679.

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The Journal of Experimental Biology 205, 1843–1851 (2002)Printed in Great Britain © The Company of Biologists Limited 2002JEB3996 Delayed depolarization of the cog-wheel valve and pulmonary-to-systemic shunting in alligators Douglas A. Syme1,*, Kurt Gamperl2,† and David R. Jones2,‡1 Department of Biological Sciences, 2500 University Drive NW, University of Calgary, Calgary, Alberta,

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