Scientist
links
iron imbalance
to Parkinson's Disease
October 12, 2004,
Newswise (TSN) — 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."