DIET AND PARKINSONS-DISEASE .2. A POSSIBLE ROLE FOR THE PAST INTAKE OF SPECIFIC NUTRIENTS - RESULTS FROM A SELF-ADMINISTERED FOOD-FREQUENCYQUESTIONNAIRE IN A CASE-CONTROL STUDY

Citation
W. Hellenbrand et al., DIET AND PARKINSONS-DISEASE .2. A POSSIBLE ROLE FOR THE PAST INTAKE OF SPECIFIC NUTRIENTS - RESULTS FROM A SELF-ADMINISTERED FOOD-FREQUENCYQUESTIONNAIRE IN A CASE-CONTROL STUDY, Neurology, 47(3), 1996, pp. 644-650
Citations number
44
Categorie Soggetti
Clinical Neurology
Journal title
ISSN journal
00283878
Volume
47
Issue
3
Year of publication
1996
Pages
644 - 650
Database
ISI
SICI code
0028-3878(1996)47:3<644:DAP.AP>2.0.ZU;2-3
Abstract
In a case-control study, we compared the past dietary habits of 342 Pa rkinson's disease (PD) patients recruited from nine German clinics wit h those of 342 controls from the same neighborhood or region. Data wer e gathered with a structured interview and a self-administered food-fr equency questionnaire. Nutrient intakes were calculated from the repor ted food intakes through linkage with the German Federal Food Code and analyzed using multivariate conditional logistic regression to contro l for total energy intake, educational status, and cigarette smoking. At the macronutrient level, patients reported higher carbohydrate inta ke than controls after adjustment for total energy intake, smoking, an d 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 nut rient 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% C I: 0.33-1.09, p trend = 0.04) by patients, although only the trend for ascorbic acid intake reached statistical significance. There was no d ifference between groups for alpha-tocopherol intake after adjustment for energy intake. We also found that patients reported a significantl y 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 pr otective role in this disease, the amounts provided by diet alone are insufficient. Although the interpretation of the inverse association b etween niacin intake and PD is complicated by the high niacin content in coffee and alcoholic beverages, which were also inversely associate d with PD in this study, the strength of this association and its biol ogic plausibility warrant further investigation.