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Infant Formula With High Iron Content Packs Brain Disorder

rons. 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
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