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From the Institute of Social Medicine (Dr. Hellenbrand, Dr. Robra), Faculty of Medicine, Otto-von-Guericke University, Magdeburg; the German Institute of Human Nutrition Potsdam-Rehbrucke (Dr. Boeing); the Department of Epidemiology and Social Medicine (Dr. Seidler, Dr. Nischan), Hannover Medical University, Hannover; the Department of Neurology (Dr. Vieregge), Lubeck Medical University, Lubeck; the Neurologic Clinic (Dr. Joerg), Barmen Hospital, Wuppertal; Department of Neurology (Dr. Oertel), Ludwig-Maximilians University, Munich; the Paracelsus-Elena-Clinic (Dr. Ulm), Kassel; and the Department of Neurology (Dr. Schneider), Hamburg-Harburg General Hospital. Drs. Joerg, Oertel, Schneider, and Ulm belong to the Medical Advisory Board of the German Parkinson's Disease Society.
Supported by the German Federal Ministry for Research and Technology (Grant No. 01K229012).
Received December 29, 1995. Accepted in final form March 5, 1996.
Address correspondence and reprint requests to Dr. Wiebke Hellenbrand, Institute of Social Medicine, Otto-von-Guericke Universitat Magdeburg, Leipziger Str. 44, D-39120 Magdeburg, Germany.
In a case-control study, we compared the past dietary habits of 342 Parkinson's disease (PD) patients recruited from nine German clinics with those of 342 controls from the same neighborhood or region. Data were gathered with a structured interview and a self-administered food-frequency questionnaire. Nutrient intakes were calculated from the reported food intakes through linkage with the German Federal Food Code and analyzed using multivariate conditional logistic regression to control for total energy intake, educational status, and cigarette smoking. At the macronutrient level, patients reported higher carbohydrate intake than controls after adjustment for total energy intake, smoking, and educational status (OR = 2.74, 95% confidence interval [CI]: 1.30-6.07, for the highest versus lowest quartile, p trend = 0.02). This was reflected in higher monosaccharide and disaccharide intakes at the nutrient level. There was no difference between patients and controls in protein and fat intake after adjustment for energy intake. We found an inverse association between the intakes of beta-carotene (OR = 0.67, 95% CI: 0.37-1.19, p trend = 0.06) and ascorbic acid (OR = 0.60, 95% CI: 0.33-1.09, p trend = 0.04) by patients, although only the trend for ascorbic acid intake reached statistical significance. There was no difference between groups for alpha-tocopherol intake after adjustment for energy intake. We also found that patients reported a significantly lower intake of niacin than controls (OR = 0.15, 95% CI: 0.07-0.33, p trend < 0.00005). Our results suggest that if antioxidants play a protective role in this disease, the amounts provided by diet alone are insufficient. Although the interpretation of the inverse association between niacin intake and PD is complicated by the high niacin content in coffee and alcoholic beverages, which were also inversely associated with PD in this study, the strength of this association and its biologic plausibility warrant further investigation.
NEUROLOGY 1996;47: 644-650
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