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Parkinsonism Relat Disord. 2014 Jan;20(1):82-7. doi: 10.1016/j.parkreldis.2013.09.023. Epub 2013 Oct 1.

Dietary fat intake, pesticide use, and Parkinson's disease.

Author information

1
Epidemiology Branch, National Institute of Environmental Health Sciences, National Institutes of Health (NIH), Department of Health and Human Services (DHHS), Research Triangle Park, NC, USA. Electronic address: kamel@niehs.nih.gov.
2
The Parkinson's Institute, Sunnyvale, CA, USA.
3
Biostatistics Branch, National Institute of Environmental Health Sciences, NIH, DHHS, Research Triangle Park, NC, USA.
4
Epidemiology Branch, National Institute of Environmental Health Sciences, National Institutes of Health (NIH), Department of Health and Human Services (DHHS), Research Triangle Park, NC, USA.
5
Westat Inc, Durham, NC, USA.
6
Toronto Western Hospital, University of Toronto, Toronto, Ontario, Canada.
7
Department of Neurology, University of Lübeck, Lübeck, Germany; Department of Clinical and Molecular Neurogenetics, University of Lübeck, Lübeck, Germany.
8
Institute of Cognitive Neurology, Institute of Neuroscience, Favaloro University, Buenos Aires, Argentina.
9
Occupational and Environmental Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, NIH, DHHS, Rockville, MD, USA.
10
Veterans Affairs Pacific Islands Health Care System, Honolulu, HI, USA.

Abstract

BACKGROUND:

Dietary fat intake may modify Parkinson's disease (PD) risk directly or by altering the response to environmental neurotoxicants including pesticides.

METHODS:

We conducted a case-control study of PD nested in the Agricultural Health Study (AHS), a cohort of pesticide applicators and spouses. We evaluated diet and pesticide use before diagnosis in 89 PD cases, confirmed by movement disorder specialists, or a corresponding date in 336 frequency-matched controls. Associations were evaluated using multivariate logistic regression to estimate odds ratios (ORs) and 95% confidence intervals (CIs).

RESULTS:

In the AHS, PD was inversely associated with N-3 polyunsaturated fatty acids (PUFAs) (OR 0.4, 95% CI 0.2-0.8 for highest vs. lowest tertile) and the N-3 precursor α-linolenic acid (0.4, 0.2-0.8). In a meta-analysis of nine studies, including the present one, PD was inversely associated with α-linolenic acid (0.81, 0.68-0.96). In the AHS, associations of PD with the pesticides paraquat and rotenone were modified by fat intake. The OR for paraquat was 4.2 (1.5-12) in individuals with PUFA intake below the median but 1.2 (0.4-3.4) in those with higher intake (p-interaction = 0.10). The OR for rotenone was 5.8 (2.3-15) in those with saturated fat intake above the median but 1.5 (0.5-4.2) in those with lower intake (p-interaction = 0.02).

CONCLUSIONS:

PUFA intake was consistently associated with lower PD risk, and dietary fats modified the association of PD risk with pesticide exposure. If confirmed, these findings suggest that a diet high in PUFAs and low in saturated fats might reduce risk of PD.

KEYWORDS:

Dietary fat; Parkinson's disease; Pesticides; Polyunsaturated fatty acids

PMID:
24120951
PMCID:
PMC3936597
DOI:
10.1016/j.parkreldis.2013.09.023
[Indexed for MEDLINE]
Free PMC Article
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