|Volume 6 Issue 287 Published - 14:00 UTC 08:00 EST 13-Oct-2004 Next Update - 14:00 UTC 08:00 EST 14-Oct-2004||Editor: Susan K. Boyer, RN
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FSU scientist links iron imbalance to Parkinson's disease
You might want to toss those iron-fortified vitamins, because absent a diagnosed deficiency too much of a good thing can be bad.
Dietary iron imbalances either way spell trouble for healthy cells, triggering a chain of cellular events in the brain that increases the odds of developing Parkinson's disease, a degenerative condition affecting movement and balance in more than 1 million Americans each year. But excessive iron levels are worse -- much worse.
The findings from a study by Florida State University scientist Cathy Levenson are described in "The Role of Dietary Iron Restrictions in a Mouse Model of Parkinson's Disease" and will appear in an upcoming edition of Experimental Neurology. Levenson is an associate professor of nutrition, food and exercise sciences in FSU's College of Human Sciences and a faculty member in both the Program in Neuroscience and graduate program in molecular biophysics.
"We define our work here at the cellular level," said Levenson from her laboratory at FSU's Biomedical Research Facility. "Our primary research objective is to better understand how trace metal imbalances, which are associated with neuropsychiatric and neurodegenerative diseases, affect the molecular mechanisms that regulate gene expression."
Levenson performed the mouse model portion of the study in collaboration with Mark Mattson, Laboratory of Neurosciences chief at the National Institute on Aging in Bethesda, Md. Mice were fed varying amounts of iron to determine levels that precipitated onset or hastened the progression of Parkinson's-like symptoms such as tremors and balance problems, both in healthy rodents and where risk factors existed.
High levels of iron caused Parkinson's-like symptoms even in healthy mice without apparent risk factors for the illness, while accelerating the decline and death of those already diagnosed with the disease.
In contrast, low levels of iron delayed onset of Parkinson's in mice with risk factors and slowed progress of the disease in those already infected. But the low iron news was mixed.
Levenson also discovered that iron deficiencies in healthy risk-free rodents led to decreasing levels of dopamine, the neurotransmitter critical to relaying brain messages that control both balance and movement. Dopamine levels fall as the brain cells or "neurons" responsible for transporting it begin to "commit suicide" at higher-than normal-rates, triggering the chain of events that eventually precipitates the onset of Parkinson's disease.
The study confirms that both iron deficiency and toxicity are linked to the specific genes and neuronal suicide that lead to dopamine shortages responsible for development of Parkinson's.
Yet while low levels of iron then delay the onset of the disease once the neurological stage is set or slow the degenerative progress, iron toxicity both precipitates Parkinson's symptoms and hastens decline and death in existing victims.
Until further studies determine optimal levels of the essential nutrient, Levenson advises health-conscious consumers without doctors' orders to forego the mineral in tablet form in favor of natural dietary sources like red meats, dried fruits, dark leafy greens, tofu, cooked dried beans or wheat germ.
"I'd be nervous about just handing someone iron supplements and saying 'have at it," she said. "Self-medicating may have unintended consequences."
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