re-examine the practice of supplementing baby formula with iron

giving human infants milk with too much iron

Too much iron could lead to Parkinson's, Buck study indicates
Richard Halstead

A new study by the Buck Institute for Age Research in Novato suggests the need to re-examine the practice of supplementing baby formula with iron.
Baby formula, which is regulated by the Food and Drug Administration, is commonly supplemented with iron to prevent iron-deficiency anemia, which can lead to mental retardation. But a Buck study on mice indicates that giving human infants milk with too much iron may increase the chance of Parkinson's disease later in life. The study is published in today's online edition of the scientific journal Neurobiology of Aging.

"We recognize that this work is in mice, not humans," said molecular biologist Julie Andersen, the Buck Institute faculty member who led the study. "We're not saying not to supplement infant formula with iron, but perhaps the levels need to be adjusted."

Nevertheless, the Atlanta-based International Formula Council, an association of baby formula manufacturers, rejected the study's relevancy to human infant feeding. Council spokesman Keith Keeney said the doses of iron fed to the mice in the study were at least 60 times as much as that consumed in iron-fortified infant formulas on a weight-adjusted basis, and the form of iron used was not the iron used in infant formula.

Andersen responded that her study took into consideration the difference in iron absorption rates between humans and mice.

"There may be a difference in terms of the amount of iron given, but what we were looking at is the amount of iron absorbed," she said.

Most commercial baby formulas contain iron supplements, said Buck Institute spokeswoman Kris Rebillot. Before formulas contained iron, doctors advised mothers to give their infants separate iron supplements, Rebillot said.

Parkinson's is an incurable, progressive degenerative disorder that affects 1.5 million people in the United States. The disease's symptoms include tremor, slowness of movement, rigidity and problems with balance. Age is the largest risk factor for Parkinson's.

Patients with Parkinson's have elevated levels of iron in the brain. But epidemiologic studies have found no correlation between the dietary iron intake in adults and the incidence of the disease. The question Parkinson's researchers have sought to answer is: how does the iron enter the brain?

The Buck Institute's study suggests that the iron may collect in the brain during the first two years of life. The research involved feeding mouse pups daily doses of iron starting at 10 days of age, for one week. That stage in the mouse's life 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 - the area of the brain where dopamine, the neurotransmitter associated with Parkinson's disease, is made. Excess iron is believed to destroy the brain cells that produce dopamine.

Iron levels in the iron-fed mice were found to be significantly increased by two months of age. By 12 months of age - the equivalent of human middle age - the mice began to show signs of degeneration in the dopamine-producing area of their brains. Within 16 to 24 months - the same as 60 to 80 years of age in humans - the mice showed an actual loss of dopamine-producing brain cells.

"Early life exposure to iron does seem to set up a sequence of processes that leads to cell damage É later in life," said Dr. J. William Langston, chief executive of the Parkinson's Institute in Sunnyvale.

Andersen is continuing her research in this area, searching for a way to keep adults from contracting Parkinson's.




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