Reference 9
NUTRITIONAL MEDICINE RESEARCH
UK

Selected sections from
Movement Disorders
Vol. 14, No. 1, 1999, pp. 21-27
Movement Disorder Society

Dietary Factors in Parkinson's Disease: The Role of Food Groups and Specific Foods
Cheryl Anderson, MPH, MS, Harvey Checkoway, PhD, $Gary M. Franklin, MD, *Shirley Beresford, PhD, Terri Smith-Weller, RN, MN, CORN-S, and Phillip D. Swanson, MD
University of Washington School of Public Health and Community Medicine, Department of Epidemiology; '?University of Washington School of Public Health and Community Medicine, Department of Environmental Health; and *University of Washington, Department of Neurology, Seattle, Washington, U.S.A

PURPOSE: The association between self-reported past food intake and Parkinson's disease (PD) was investigated in a case­ control study of men and women aged 40-89 years.
METHODS: Newly diagnosed idiopathic PD cases were as­certained from neurologists, and from outpatient and pharmacy computerized databases, at the Group Health Cooperative (GHC) clinics in the Puget Sound region of Washington state. Control subjects were chosen from the GHC patient roster and had no reported history of diagnosed neurodegenerative dis­ease. Dietary data were obtained from structured questionnaires.
RESULTS: An increase in PD risk with increasing intake was noted for foods that contain animal fat and foods contain­ing vitamin D. Intake of fruits, vegetables, meats, bread and cereals, or foods containing vitamins A, C, E, or iron was not significantly related to PD risk. Vitamin use, in general, was also not found to be related to PD risk, although a significant trend of increasing risk of PD was noted for intake of vitamin A supplements.
CONCLUSIONS: Although these data support previous findings of no association of past intake with most food groups and PD risk, they confirm an increased risk of PD associated with foods containing animal fat.
The etiology of Parkinson's disease (PD) is largely unknown. As the role of environmental factors in PD receives more attention, interest in the association be­tween diet and PD persists. Recent evidence has sug­gested that diet in early adult life may play an important role in PD pathogenesis. However, there is also con­flicting epidemiological evidence regarding the influence of past dietary habits on the development of PD. The consumption of antioxidants, in some studies, has been shown to have a seemingly pro­tective effect on PD, possibly by neutralizing free radicals that can injure neurons in the substantia nigra. Another focus of the diet-PD relationship has been on diets rich in lipids. High-lipid diets are thought to increase oxidative stress, and increased animal fat or carbohydrates have been associated with an increased risk of PD.
The complexity of diet as an environmental exposure creates special difficulties in studies of diet and disease. First, high error in assessing nutrient intakes resulting from imperfect, usually retrospective, measurement methods compromises the ability to identify any but the most powerful associations. Second, because food groups contain many nutrients, correlations among nutrients complicates identification of potentially causative or pre­ventive specific factors. Third, analyses based on nutrients alone may overlook the possible contribution to dis­ease risk from non-nutrient dietary components. Because the translation of food intake into nutrient intake is often imprecise, the associations between PD risk and indi­vidual food items or food groups are important. Asso­ciations of PD with foods rather than nutrients are presented in this article in an attempt to overcome some of these problems.
We conducted a retrospective assessment of past food intake as part of an ongoing case-control study investi­gating environmental influences on the development of PD. Data are presented both at the food and the food group level.
This study also found no significant association be­tween the group of foods containing antioxidants or use of the antioxidant vitamins C and E and PD risk. There is some evidence that oxidative stress and free-radical damage play a role in the pathogenesis of PD. yet whether antioxidant intake can be beneficial re­mains unknown.
An accumulation of iron in the substantia nigra in PD has been found previously. Jenner et al. measured levels of iron and ferritin in the substantia nigra in PD and found that the increased nigral iron load did not appear to be buffered by a compensatory rise in the nigral content of the iron-binding protein, ferritin.
Our most prominent finding was that consumption of foods containing high  animal fat was associated with an increased risk of PD. Although there was no apparent association with calories in these data this finding is supported by the findings from another population-based case-control study of the association between fat intake from animal sources and PD. A relationship with ani­mal fat consumption is biologically consistent with the hypothesis that oxidative reactions have a critical role in the pathogenesis of PD.
After adjustment, the significance of the asso­ciation remained, offering support for an unconfounded association between consumption of foods containing animal fats and the development of PD.
A particularly intriguing finding was the association between vitamin D and PD. However, the association with vitamin D-containing foods appears to be secondary to a relationship with animal fat consumption. Therefore, it seems premature to conclude that vitamin D is related to PD risk.

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