Pathology - Iron Content in Infant Formula

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Iron Content in Infant Formula

ironjustice@aol.com

2006-06-15, 4:26 pm

Source: Buck Institute for Age Research Released: Thu 08-Jun-2006,
15:40 ET
Embargo expired: Thu 15-Jun-2006, 00:05 ET
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Is It Time to Reexamine Iron Content in Infant Formula?
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Medical News Keywords
PARKINSON'S DISEASE, IRON, INFANT FORMULA, NEURODEGENERATION
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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.

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babawali@worldd.com

2006-06-15, 4:26 pm

Good, we find another place where adjustment in intake needs som possible
adjustment. It should be noted that in much of the world low iron for
infants is the number one health problem because the mother's milk doesn't
have enough, because she too is low iron. Using iron fortified milk
higher then human milk still makes sense. Good to see you take to the
reality of the concept of the minimal, optimal and maximal in biology,ie.
iron for infants too high or too low not good but in the middle just fine.