[PHNUTR-L] Iron in infant formula? Mice develop Parkinson-like symptoms

[Kathrynne Holden, MS, RD]

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Source: Buck Institute for Age Research 	  	
Released: Thu 08-Jun-2006, 15:40 ET
Embargo expired: Thu 15-Jun-2006, 00:05 ET
http://www.newswise.com/articles/view/521148/?sc=dwhp

Is It Time to Reexamine Iron Content in Infant Formula?

Neonatal mice fed the equivalent amount of iron used in human infant 
formula develop Parkinson’s-like neurodegeneration as they age.

Newswise — A Buck Institute study suggests a need to reexamine iron 
supplementation in human infant formula, most of which results in the 
absorption of twelve times the amount of iron versus that absorbed from 
human breast milk. The suggestion is based on research that shows 
neonatal mice fed the human equivalent of iron supplementation in human 
formula developed neurodegeneration akin to that observed in Parkinson’s 
disease (PD) as they aged. Age is the largest risk factor for PD in 
humans. The study appears in the June 15 on-line edition of the journal 
Neurobiology of Aging.

Patients with PD have long been shown to have elevated levels of iron in 
the brain, compared to those without the incurable, progressive 
neurodegenerative disorder which affects 1.5 million people in this 
country. The symptoms of PD include tremor, slowness of movement, 
rigidity and problems with balance. Epidemiologic studies suggest that 
there is not a clear correlation between dietary iron intake in adults 
and the incidence of PD. The question remains, how does the iron get 
into the brain? Research led by Buck Institute faculty member Julie 
Andersen, PhD, suggests that the iron can collect in the brain during 
the first two years of life, before the human blood/brain barrier is 
fully closed.

The research involved delivering iron orally to mouse pups on a daily 
basis starting at ten days of age for one week. That time period is 
equivalent to the first year of human life; the dosage was equivalent to 
the amount of iron in fortified infant formula. The mice were then 
allowed to age normally to two, 12, 16 and 24 months of age. Iron levels 
were measured in the substantia nigra (SN), an area of the brain where 
dopamine, the neurotransmitter associated with Parkinson’s disease, is 
made. Excess iron is believed to cause oxidative stress which eventually 
destroys the neurons which produce dopamine.

Iron levels in the iron-fed pups were found to be significantly 
increased in the SN by two months of age; by 12 months of age (the human 
equivalent of middle-age) the mice began to show signs of SN 
neurodegeneration. Within 16 -24 months (60 to 80 years of age in 
humans) the mice showed an actual loss of dopamine-producing neurons. 
All of the mice, bred from the same genetic strain, showed signs of damage.

“We recognize that this work is in mice, not humans,” said Andersen, 
“We’re not saying not to supplement infant formula with iron, but 
perhaps the levels need to be adjusted.” Human infant formula, which is 
regulated by the FDA, is supplemented with iron to prevent 
iron-deficiency anemia, which can lead to mental retardation. Although 
iron supplementation in humans shows no discernable adverse effects up 
to six years of age, its affects later in life have yet to be assessed, 
according to the American Academy of Pediatrics.

“We really have very few models to study early exposure to toxins as a 
risk factor for a late-life disease such as PD,” said J. William 
Langston, MD, CEO and Scientific Director of the Parkinson’s Institute. 
“We haven’t had good proof of principle; Julie’s work really is one of 
the few examples where that seems to be the case in an experimental 
model. Early life exposure to iron does seem to set up a sequence of 
processes that leads to cell damage in the substania nigra later in 
life.” Langston added, “That’s a really important principle known as 
‘long-latency neurotoxicity’ that scientists have been trying to prove 
for many, many years. Her work could be groundbreaking, moving this 
field forward. And of course this research has obvious public health 
implications.”

Studies involving the mice continue in the Andersen lab; efforts are 
aimed at determining whether the oxidative damage is reversible, and at 
what point that could be accomplished. Once the blood/brain barrier is 
closed, the iron cannot be removed from the brain. An earlier study by 
Andersen showed that “tying up” excess iron in mice by using a metal 
chelator (derived from the Greek word for claw) prevented damage to the 
dopamine-producing neurons of the SN.
“Extensive elimination of iron from the brain is not desirable,” said 
Andersen. “It is an essential trace metal needed for many biological 
reactions including the synthesis and release of neurotransmitters. 
However, we think the results of this study warrant further 
epidemiological studies in humans, especially as it impacts on 
neurological function in older individuals.” Andersen added, “It would 
also be interesting to assess the value of iron chelation as a possible 
therapeutic in regards to the progression of age-related 
neurodegeneration as a consequence of high iron intake in infants.”

Joining Andersen in the study include Deepinder Kaur, lead author on the 
publication as well as Subramanian Ragajolan and Shankar Chinta from the 
Buck Institute and Dino Dimonte at the Parkinson’s Institute in 
Sunnyvale, California. This work was funded as part of a collaborative 
center grant on the role of the environment in Parkinson’s disease 
funded by the National Institute of Environmental Health (NIEH).

The Buck Institute is the only freestanding institute in the United 
States that is devoted solely to basic research on aging and 
age-associated disease. The Institute is an independent nonprofit 
organization dedicated to extending the healthspan, the healthy years of 
each individual’s life. The National Institute of Aging designated the 
Buck a “Nathan Shock Center of Excellence in the Biology of Aging,” one 
of just five centers in the country. Buck Institute scientists work in 
an innovative, interdisciplinary setting to understand the mechanisms of 
aging and to discover new ways of detecting, preventing and treating 
conditions such as Alzheimer’s and Parkinson’s disease, cancer and 
stroke. Collaborative research at the Institute is supported by new 
developments in genomics, proteomics and bioinformatics technology. For 
more information: http://www.buckinstitute.org.
-- 
Kathrynne Holden, MS, RD < fivestar at nutritionucanlivewith.com >
"Ask the Parkinson Dietitian"  http://www.parkinson.org/
"Eat well, stay well with Parkinson's disease"
"Parkinson's disease: Guidelines for Medical Nutrition Therapy"
http://www.nutritionucanlivewith.com/