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Volume 15, Issue 1, Pages 47-52 (January 2009)


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Dietary fats, cholesterol and iron as risk factors for Parkinson's disease

Karen M. Powersa, Terri Smith-Wellera, Gary M. Franklinab, W.T. Longstreth Jr.bc, Phillip D. Swansonb, Harvey CheckowayacCorresponding Author Informationemail address

Received 19 November 2007; received in revised form 31 January 2008; accepted 3 March 2008.

Abstract 

Background

Epidemiologic findings suggest that dietary components may contribute to the etiology of Parkinson's disease (PD). This population-based case–control study evaluated PD risk and dietary intake of fats, cholesterol and iron.

Methods

Newly diagnosed case (n=420) and age/gender/ethnicity-matched unrelated controls (n=560) were identified between 1992 and 2006 from the Group Health Cooperative health maintenance organization in western Washington State, and the University of Washington Neurology Clinic. In-person interviews elicited data on food frequency habits during most of adult life. Nutritional intakes were calculated and analyzed, with adjustments made for total energy intake (the ‘nutrition density’ technique).

Results

Cholesterol intake in the highest quartile compared with the lowest quartile was associated with a decreased risk of PD in men (odds ratio (OR)=0.53, 95%CI: 0.33, 0.86). The highest versus the lowest quartile of dietary iron increased PD risk in men (OR=1.82, 95%CI: 1.11, 2.99). When the lowest quartile of cholesterol and the highest quartile for iron were compared to the highest quartile of cholesterol and the lowest quartile of iron, no association was seen in women, but for men PD risk was increased (OR=2.70, 95%CI: 1.26, 5.76). Saturated fat intake below the median in combination with iron intake above the median also increased the PD risk (OR=1.50, 95%CI: 1.07, 2.11) in both genders combined.

Conclusions

A low intake of cholesterol, particularly in the presence of high iron, may be associated with an increased risk for PD.

a Department of Environmental and Occupational Health Sciences, University of Washington, Seattle, WA, USA

b Department of Neurology, University of Washington School of Medicine, University of Washington, Seattle, WA, USA

c The Department of Epidemiology, University of Washington, Seattle, WA, USA

Corresponding Author InformationCorresponding author. Address: University of Washington, Department of Environmental Health, Box 357234, Seattle, WA 98195-7234, USA. Tel.: +1 206 543 2052; fax: +1 206 685 3990.

PII: S1353-8020(08)00097-7

doi:10.1016/j.parkreldis.2008.03.002


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