Logroscino G, Marder K, Graziano J, Freyer G, Slavkovich V, Lojacono N, Cote L, Mayeux R
The Gertrude H. Sergievsky Center, Department of Neurology, College of Physicians and Surgeons, Columbia University, New York, NY 10032, USA.
Mov Disord. 1998;13 Suppl 1:13-6.
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 the literature are available on the possible role of dietary iron in the development of PD.
In a population-based, case-control study, we addressed the hypothesis that high dietary iron intake was associated with PD. We assessed dietary iron intake with a semiquantitative food-frequency questionnaire in 104 PD patients and 352 control subjects, frequency matched for age and gender. We also studied the association of PD and dietary iron and animal fat intake in the presence of different iron stores measured by transferrin saturation.
No significant differences were observed between patients' and control subjects' dietary intake of iron from food or supplements (odds ratio [OR] for the highest quartile of intake, 0.9; 95% confidence interval [95% CI], 0.6, 1.3; p for trend = 0.60). Among those with low transferrin 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.
Dietary iron intake after caloric adjustment was not associated with an increased risk of PD. However, the previously described association between animal fat intake and PD was modified by iron level stores as measured by transferrin saturation. These observations suggest that dietary fat and a systemic defect in iron metabolism may act synergistically in the process of lipid peroxidation in PD.
近期研究提出饮食在帕金森病（PD）中可能发挥作用。PD的特征是黑质中铁沉积过多且铁蛋白浓度较低。关于饮食中铁在PD发病过程中的可能作用，文献中的数据较少。
在一项基于人群的病例对照研究中，我们探讨了高饮食铁摄入量与PD相关的假设。我们使用半定量食物频率问卷评估了104例PD患者和352例年龄和性别频率匹配的对照受试者的饮食铁摄入量。我们还研究了在通过转铁蛋白饱和度测量的不同铁储存情况下，PD与饮食铁和动物脂肪摄入量之间的关联。
患者和对照受试者从食物或补充剂中摄入的饮食铁量没有显著差异（摄入量最高四分位数的优势比[OR]为0.9；95%置信区间[95%CI]为0.6至1.3；趋势p值 = 0.60）。在转铁蛋白饱和度水平较低（低于50%）的人群中，与动物脂肪摄入量相关的PD优势比是低摄入量人群风险的九倍（OR为9.0；95%CI为2.7至29.9）。在转铁蛋白饱和度高的人群中，报告高动物脂肪摄入量的人患PD的风险比报告低摄入量的人高两倍（相对风险为1.9；95%CI为0.5至7.2）。
热量调整后的饮食铁摄入量与PD风险增加无关。然而，如通过转铁蛋白饱和度测量的那样，先前描述的动物脂肪摄入量与PD之间的关联因铁储存水平而有所改变。这些观察结果表明，饮食脂肪和铁代谢的全身缺陷可能在PD的脂质过氧化过程中协同作用。
