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D.iet & H.ealth : C.hildren & W.omen Last Updated: Nov 12th, 2006 - 20:38:00


Iron in Infant Formula May Raise Adult Parkinson's Risk
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Jun 15, 2006, 21:26

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But the mouse study finding needs much more investigation, experts say

By Alan Mozes
HealthDay Reporter

THURSDAY, June 15 (HealthDay News) -- The high amount of iron consumed by babies reared on infant formula may increase their risk for developing Parkinson's disease as adults, suggests a study involving mice.

The study revealed that baby rodents weaned on a iron-fortified formula equivalent to that consumed by infants developed increasing amounts of Parkinson's-associated brain degeneration as they aged.

"Since this is a mouse and not a human study, it awaits epidemiological verification in human populations," cautioned study co-author Julie K. Andersen, a faculty member with the Buck Institute for Age Research in Novato, Calif.

"However," she added, "our data would suggest that this should be looked at to see if there is any correlation between infants receiving iron-fortified formula and later susceptibility for Parkinson's disease."

Andersen and her team note that an estimated 1.5 million Americans suffer from the mobility impairments -- such as slowness, rigidity, tremors and imbalance -- that stem from this incurable and progressive neurodegenerative disorder.

They also noted that Parkinson's patients have elevated levels of iron in the brain.

Such an overabundance of iron is thought to promote oxidative stress that, in turn, damages neurons in a part of the brain where a neurotransmitter called dopamine is produced. Parkinson's onset is associated with a decline in dopamine.

However, the research had failed to show links between adult diet and the risk for Parkinson's. That could be because the brains of older children and adults are shielded by what's known as the blood/brain barrier. So, the researchers wondered if excess iron might accumulate during the first two years of life -- before the blood/brain barrier has time to fully develop.

Reporting in the June 15 online issue of the Neurobiology of Aging, Andersen's team experimented with infant mice aged between 10 and 17 days.

The mouse pups were examined in that age range because their brain development is roughly equivalent to brain growth occurring in the first year of human life.

Because infant formula contains 40 times the daily iron intake of breast milk, the researchers gave the pups mouse milk with similar concentrations of the mineral.

The mice were then allowed to age to 2, 12, 16, or 24 months, before being dissected and assessed for neuron destruction in the substantia nigra (SN) portion of the brain responsible for dopamine production.

The result: by 2 months iron levels had increased significantly in the SN region, the researchers report. By the time the mice reached "middle age" (12 months) signs of neuron degeneration were evident, and by 16 to 24 months -- the equivalent of a 60-to-80-year-old human -- the mice had displayed a clear loss of neurons.

Andersen's team stressed that babies do need sufficient iron for healthy growth. But if excess iron in infancy does help cause Parkinson's in adulthood, that finding may support adjusting iron level in infant formulas accordingly.

However, more research is needed before any such move occurs, Andersen said. She noted, for example, that the current study focused on only one strain of mice. "In other words," said Andersen, "based on their genetic makeup, individuals may be more or less susceptible to the effects of early dietary iron."

Another expert was cautious about making the formula-Parkinson's link.

Francis M. Crinella, a clinical professor in the department of pediatrics at the University of California at Irvine, said infant formulas lack lactoferrin -- a key ingredient found in breast milk that promotes iron absorption.

Without lactoferrin, human infants are much less liable to iron overload because they aren't able to fully absorb large amounts of the nutrient.

"This is not to say that absorption of either too much or too little iron is not a problem," he stressed. "Like all essential minerals, higher or lower than optimal tissue stores can wreak havoc on the brain and other organ systems. I just don't think that this is going to occur through re-fortified infant formula."

Keith Keeney, a spokesman for the Atlanta-based International Formula Council (IFC), seconded the notion that neither the current study nor prior research has demonstrated any concrete link between Parkinson's and infant formula iron content.

"This is an iron study, not an infant formula study, and it is not relevant to infant feeding," said Keeney. "The extremely high doses of iron fed to the mice in this study are at least six times as much as that consumed in iron-fortified formulas on a weight-adjusted basis, and the form of iron is not the iron used in infant formula."

"Iron-fortified infant formula is considered a major U.S. public health policy success, having virtually wiped out the lifelong consequences of iron-deficiency anemia," he added.

"(Therefore) it is inappropriate to put this important public health advance and the normal development status of infants at risk on the basis of a rodent study using extremely high doses of iron in a model with unproven relevance to infant feeding practices," he stated. "Parents should not make feeding decisions based on the results of this report."

Keeney noted that iron content in infant formulas is regulated by the U.S. Food and Drug Administration (FDA), and that the IFC stands behind the American Academy of Pediatrics' recommendation that iron-fortified infant formula should be considered the only safe alternative to the preferred norm of breast-feeding.

More information

For more on Parkinson's disease, visit the U.S. National Institute of Neurological Disorders and Stroke.





SOURCES: Julie K. Andersen, Ph.D., faculty member, Buck Institute for Age Research, Novato, Calif.; Keith Keeney, spokesman, International Formula Council, Atlanta; Francis M. Crinella, Ph.D., clinical professor, pediatrics, University of California at Irvine; June 15, 2006, Neurobiology of Aging online

Last Updated: June 15, 2006

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