DIETARY IRON, ANIMAL FATS, AND RISK OF PARKINSONS-DISEASE

Citation
G. Logroscino et al., DIETARY IRON, ANIMAL FATS, AND RISK OF PARKINSONS-DISEASE, Movement disorders, 13, 1998, pp. 13-16
Citations number
21
Categorie Soggetti
Clinical Neurology
Journal title
ISSN journal
08853185
Volume
13
Year of publication
1998
Supplement
1
Pages
13 - 16
Database
ISI
SICI code
0885-3185(1998)13:<13:DIAFAR>2.0.ZU;2-O
Abstract
Background: Recent studies have proposed a role for diet in Parkinson' s disease (PD). PD is characterized by a high deposition of iron and a low concentration of ferritin in the substantia nigra. Few data in th e literature are available on the possible role of dietary iron in the development of PD. Methods: In a population-based, case-control study , we addressed the hypothesis that high dietary iron intake was associ ated with PD. We assessed dietary iron intake with a semi quantitative food-frequency questionnaire in 104 PD patients and 352 control subje cts, frequency matched for age and gender. We also studied the associa tion of PD acid dietary iron and animal fat intake in the presence of different iron stores measured by transferrin saturation. Results: No significant differences were observed between patients' and control su bjects' dietary intake of iron from food or supplements (odds ratio [O R] for the highest quartile of intake, 0.9; 95% confidence interval [9 5% CI], 0.6; 1.3; p for trend = 0,60). Among those with low transferri n saturation levels (lower 50%), the odds ratio for PD associated with animal fat intake was ninefold higher than the risk of those with low intake (OR, 9.0; 95% CI, 2.7-29.9). Among those with high transferrin saturation, risk of PD was two times higher (relative risk, 1.9; 95% CI, 0.5-7.2) for those who reported high intake of animal fat compared with those who reported low intake. Conclusion: Dietary iron intake a fter caloric adjustment was not associated with an increased risk of P D. However, the previously described association between animal fat in take and PD was modified by iron level stores as measured by transferr in saturation. These observations suggest that dietary fat and a syste mic defect in iron metabolism may act synergistically in the process o f lipid peroxidation in PD.