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首页> 外文期刊>Pharmacogenetics and genomics >Association between caffeine intake and risk of Parkinson's disease among fast and slow metabolizers.
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Association between caffeine intake and risk of Parkinson's disease among fast and slow metabolizers.

机译：快速和慢速代谢者之间咖啡因摄入与帕金森氏病风险之间的关联。

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INTRODUCTION: Cytochrome P450 1A2 (CYP 1A2) is responsible for more than 90% of caffeine clearance. A polymorphic variant of CYP1A2 (-163C>A) (rs762551) is associated with high CYP1A2 inducibility. Both caffeine and its main metabolite, paraxanthine, may be neuroprotective. The association between caffeine intake and risk of Parkinson's disease (PD) in fast and slow caffeine metabolizers has not been compared. OBJECTIVE: In a case-control study, we analyzed the relationship between caffeine intake and risk of PD in both fast and slow caffeine metabolizers. METHODS: All the study participants were recruited prospectively, and interviewed for information on the amount and duration of caffeine intake. Genotyping of the CYP1A2 variant was carried out using the allelic discrimination method. RESULTS: Out of 1000 participants who were initially screened, 886 consisting of 418 PD and 468 race, sex and age matched controls were included. No evidence existed to suggest any association between CYP1A2 and the onset of PD (P=0.08). A significant association was seen between caffeine intake and the onset of PD (P=2.01x10(-5)), with the odds ratio for moderate and high drinkers at 0.71 [95% confidence interval (CI): 0.50-1.00] and 0.47 (95% CI: 0.34-0.65), respectively against the low drinkers. Multivariate analysis revealed no evidence of any interaction effects of caffeine with CYP1A2 (P=0.956). CONCLUSION: The association between caffeine intake and risk of PD was similarly observed in both fast and slow caffeine metabolizers, supporting experimental evidence in animal models that both caffeine and its major metabolite, paraxanthine, are neuroprotective.
机译：简介：细胞色素P450 1A2（CYP 1A2）负责90％以上的咖啡因清除。 CYP1A2（-163C> A）（rs762551）的多态性变异与高CYP1A2诱导能力有关。咖啡因及其主要代谢物对黄嘌呤都可能具有神经保护作用。咖啡因摄入量与快速和慢速咖啡因代谢物中帕金森氏病（PD）风险之间的关联尚未进行比较。目的：在一项病例对照研究中，我们分析了咖啡因摄入量与快速和慢速咖啡因代谢者中帕金森病风险之间的关系。方法：所有研究参与者均是前瞻性招募的，并接受了咖啡因摄入量和持续时间的采访。使用等位基因鉴别方法进行CYP1A2变异的基因分型。结果：在最初筛选的1000名参与者中，包括418名PD和468名种族，性别和年龄匹配的对照组组成的886名参与者。没有证据表明CYP1A2与PD的发作之间存在任何关联（P = 0.08）。咖啡因摄入量与PD发作之间存在显着相关性（P = 2.01x10（-5）），中度和高度饮酒者的比值比为0.71 [95％置信区间（CI）：0.50-1.00]和0.47 （95％CI：0.34-0.65），分别针对低饮者。多变量分析未显示咖啡因与CYP1A2有任何相互作用的证据（P = 0.956）。结论：在快速和缓慢的咖啡因代谢物中，咖啡因摄入与PD风险之间的相关性相似，这支持了动物模型中的咖啡因及其主要代谢物对黄嘌呤具有神经保护作用的实验证据。

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