Caffeinated clues from epidemiology of Parkinson's disease.

Abstract

Although there is a growing interest in the genetic determinants of Parkinson’s disease (PD), the low concordance for clinical disease among monozygotic twins clearly indicates the etiologic importance of nongenetic factors.1 On top of the list of potential candidates is cigarette smoking. For many years, researchers have been intrigued by the strong inverse association between cigarette smoking and risk of PD, but despite extensive investigation it remains unclear whether nicotine or some other component of cigarette smoke reduces the risk of PD or whether people predisposed to PD have an early aversion to smoking.2 More recently, coffee and caffeine consumption have emerged as powerful predictors of risk of PD. Here we will review the epidemiologic evidence supporting this association and discuss the contribution of epidemiologic studies in clarifying the potential biologic mechanisms. Whereas the inverse association between cigarette smoking and risk of PD has been known for decades, relatively few early studies examined the potential role of coffee or caffeine consumption. Questions on coffee and tea consumption and risk of PD were included in some of the case-control studies on smoking3,4⇓ or environmental factors5 and risk of PD, but published results were not adjusted for smoking and thus were difficult to interpret. The first smoking-adjusted analysis of coffee consumption and PD was reported by Jimenez-Jimenez et al.,6 who studied 128 patients with PD (60 women) attending a movement disorder clinic in Madrid and 256 control subjects attending the emergency room of the same hospital for non-neurologic disorders. The data supported a 30% lower risk of PD among coffee drinkers (coffee drinking was reported as yes/no only) as compared with nondrinkers in men and women, but the results were not significant and received little attention. More detailed analyses of coffee consumption and risk of PD …