Too much iron and manganese in the diet may put people at increased risk for Parkinson’s disease, find researchers publishing in the June 2003 issue of Neurology.
Investigators from the University of Washington in Seattle believe the two minerals, common in foods such as spinach, beans, nuts, and whole grains, may impact Parkinson’s risk through their effect on the brain. Both iron and manganese are known to cause oxidative stress, which releases toxic substances known as free radicals and can cause degeneration of brain cells that produce dopamine. The loss of these brain cells plays a crucial role in the development of the disease.
The study involved 250 people with recently diagnosed Parkinson’s and 388 people without the disease. All were questioned extensively about their diets during their adult lives. Participants were then placed into categories depending on how much iron and manganese they consumed and also whether they were regular users of multivitamin or iron supplements.
Researchers found those in the top 25 percent of iron consumption were 1.7-times more likely to have Parkinson’s than those in the bottom 25 percent. Those with higher than average consumption of both minerals were 1.9 times more likely to have the disease. Participants with higher iron intake and a history of daily supplement use were 2.1-times more likely to have Parkinson’s. Those with higher manganese consumption and daily supplement use were 1.9-times more likely to have the disease.
However, the investigators do not suggest people limit their intake of foods rich in iron and manganese, noting the health benefits of eating these nutrient-rich foods probably outweigh the increased risk of Parkinson’s.
Harvey Checkoway, Ph.D., from the University of Washington in Seattle, says, “Our findings may improve understanding of how Parkinson’s disease develops. But there are most likely numerous environmental, lifestyle, and genetic factors that determine who will develop the disease. It’s too early to make any recommendations about potential dietary changes.”
SOURCE: Neurology, 2003;60:1761-1766