Dietary patterns and risk of ParkinsonÕs disease: a case–control study in Japan H. Okubo a,b , Y. Miyake c , S. Sasaki a,d , K. Murakami d , K. Tanaka c , W. Fukushima e , C. Kiyohara f , Y. Tsuboi g , T. Yamada g , T. Oeda h , H. Shimada i , N. Kawamura j , N. Sakae j , H. Fukuyama k , Y. Hirota e , M. Nagai l and the Fukuoka Kinki ParkinsonÕs Disease Study Group* a Department of Social and Preventive Epidemiology, Graduate School of Medicine, the University of Tokyo, Tokyo; b Research Fellow of the Japan Society for the Promotion of Science, Japan; c Department of Preventive Medicine and Public Health, Faculty of Medicine, Fukuoka University, Fukuoka; d Department of Social and Preventive Epidemiology, School of Public Health, the University of Tokyo, Tokyo; e Department of Public Health, Osaka City University Graduate School of Medicine, Osaka; f Department of Preventive Medicine, Graduate School of Medical Sciences, Kyushu University, Fukuoka; g Department of Neurology, Faculty of Medicine, Fukuoka University, Fukuoka; h Clinical Research Institute and Department of Neurology, Utano National Hospital, Kyoto; i Department of Geriatrics and Neurology, Osaka City University Graduate School of Medicine, Osaka; j Department of Neurology, Neurological Institute, Graduate School of Medical Sciences, Kyushu University, Fukuoka; k Human Brain Research Centre, Kyoto University Graduate School of Medicine, Kyoto; and l Department of Public Health, Saitama Medical Unviversity Faculty of Medicine, Saitama, Japan Keywords: case–control study, dietary patterns, factor analysis, Japan, ParkinsonÕs disease Received 4 July 2011 Accepted 20 October 2011 Background: Nearly all epidemiologic studies examining the association between the risk of ParkinsonÕs disease (PD) and diet have focused on single foods and specific nutrients. However, epidemiologic evidence for the association of dietary pattern with PD, namely the measurement of overall diet by considering the cumulative effects of nutrients is extremely limited. We conducted a hospital-based case–control study in Japan to examine the relationship between dietary patterns and the risk of PD. Methods: Patients with PD diagnosed using the UK PD Society Brain Bank criteria (n = 249) and controls without neurodegenerative diseases (n = 368) were recruited. At the time of recruitment, dietary intake during the preceding 1 month was assessed using a validated, self-administered diet history questionnaire. Dietary patterns from 33 predefined food groups (energy-adjusted food g/day) were extracted by factor analysis. Results: Three dietary patterns were identified: ÔHealthyÕ, ÔWesternÕ and ÔLight mealÕ patterns. After adjustment for potential non-dietary confounding factors, the Healthy pattern, characterized by a high intake of vegetables, seaweed, pulses, mushrooms, fruits and fish, was inversely associated with the risk of PD with a border-line sig- nificance (P for trend = 0.06). Multivariate Odds ratio (95% confidence intervals) for PD in the highest quartile of the Healthy pattern was 0.54 (0.32–0.92) compared with the lowest quartile. No associations with PD were detected for the other two dietary patterns. Conclusion: In this case–control study in Japan, a dietary pattern consisting of high intakes of vegetables, fruits and fish may be associated with a decreased risk of PD. Introduction Although the aetiology of ParkinsonÕs disease (PD) is unclear, epidemiologic evidence suggests that dietary components may contribute to the development of PD [1,2]. Several studies have suggested that oxidative stress may play a prominent role in the pathogenesis of PD, focusing attention on antioxidant vitamins, par- ticularly vitamins C and E, and carotenoids [3–5]. The association of other nutrients and dietary components, including B-vitamins (vitamin B 6 ,B 12 , folate) [6,7], dietary fats, including cholesterol [8–11], iron [12,13], caffeine [14,15] and dairy products [16,17], with the risk of PD has also been examined, but results have been inconsistent. One reason for the inconsistent findings Correspondence: H. Okubo, Department of Social and Preventive Epidemiology, Graduate School of Medicine, the University of Tokyo, Hongo 7-3-1, Bunkyo-Ku, Tokyo 113-0033, Japan (tel.: +81 3 5841 7872; fax: +81 3 5841 7873; e-mail: okubo@m.u-tokyo.ac.jp). *Other members of the study group are listed in the Appendix. Ó 2011 The Author(s) European Journal of Neurology Ó 2011 EFNS 681 European Journal of Neurology 2012, 19: 681–688 doi:10.1111/j.1468-1331.2011.03600.x