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 Manganese madness I

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Nombre de messages : 1737
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Date d'inscription : 01/06/2005

MessageSujet: Manganese madness I   Mer 26 Avr - 19:17

By David Goodman, PhD

When Jonathon Ericson, environmental health scientist, began planning a two-day conference on toxic metals, his thoughts turned to the internal combustion engine. Day One he dedicated to lead of the tetraethyl variety added to silence engine knock. For fifty years, no-knock gasoline containing tetraethyl lead has spewed metallic wastes out of millions of tailpipes, tainting the soil and water�and the lungs and brains of little children.

For Day Two, Ericson planned to focus on MMT, an antiknock ingredient containing manganese. He issued invitations to speakers who could discuss the dangers of manganese to the brains of miners in Europe, Asia, South America and Australia who, after a few years on the job, run an increased risk for Parkinson's Disease. The manganese particles they inhale through the lungs then move to the brain with devastating effects.

Left with invitations for the final two conference speakers, Ericson turned away from internal combustion engines, tailpipes and toxic exhausts. Instead, he focussed on the dangers of a consumer product that has been on the market for about thirty years�the plastic bottle filled with soybean-based infant formula.

How a bottle of soy formula can be mentioned on the same program with a smoking exhaust pipe and brain damage in manganese miners is what kept the UC Irvine conference audience captivated. The soy story told by speakers Francis Crinella of the UC Irvine faculty and Trinh Tran from the UC Davis Department of Animal Studies unfolded like a Stephen King novel, complete with mindless villains, thickening plot and innocent victims too young to defend themselves.

Ericson's conference took place in September, 2000 at the University of California at Irvine. His two final speakers, Crinella and Tran, suggested that infants sucking on nipples of plastic bottles containing soy-based formula could absorb toxic amounts of manganese into their rapidly developing brains.

The melodrama�no, the tragedy�of toxic manganese in infant formula begins in 1980 when the Federal Government's Food and Nutrition Board established safe and acceptable values for manganese in adults, toddlers and infants. Permissible levels for the three age ranges were set at 2.5-3.0 mg/day in adults, 1.0 to 1.5 mg/day in toddlers and 0.5 to 1.0 mg/day in infants. The "safe" level for infants soon translated into soy formula products purchased by millions of mothers.

Despite government assurances, Phillip Collipp, a pediatric physician at Nassau County Medical Center in 1983 tested for the manganese in popular soy brands available locally, including Isomil, ProSoybee and Nursoy. They contained from 0.2 to 1.0 mg of manganese per quart of infant formula. Later that year, Bo L�nnerdal and Carl L. Keen, of the Department of Nutrition of UC Davis, tested baby formula taken from pharmacy shelves in eight countries. The manganese concentrations they found in soy formulas were higher, ranging from 0.4 to 2.2 mg; the mean value of 1.2 mg vastly exceeded the infinitesimal 0.005 mg found in human breast milk.

Nutritional scientists have reported how newborn babies absorb manganese from breast milk. Tiny amounts suckled daily a dozen times by the baby supply an adequate quantity of manganese to catalyze 50 biochemical reactions. The newborn's digestive system seems superbly attuned to absorb the scanty amounts of manganese it needs from its mother's milk.

However, soy formula, containing up to 200 times the manganese of breast milk, overloads the little body. The baby's immature liver cannot handle the load. With each swallow increasing the manganese content in its digestive track, what does the baby do to dispose of the excess? Bo L�nnerdal, a researcher from UC Davis, explained that in newborns, ingested manganese rises to high levels in the blood plasma and red blood cells and then permeates the liver, kidneys and other soft tissues of the body, including the brain. Only later, at the time of weaning, can the infant metabolize such large amounts of manganese.

Francis Crinella calculated that by eight months, an infant fed soy formula daily absorbs approximately 1.1 mg of manganese above metabolic need. "A significant amount, about 8 percent, is deposited in a brain region vulnerable to threat of manganese attack."

Neurology textbooks identify manganese as a neurotoxic metal. In 1837, an English physician noted that some workers in a manganese mill appeared lethargic and their faces unexpressive. By the turn of the century, the disease of "manganism" had been described in medical journals. The disease struck miners exposed to toxic dust, and appeared to cause emotional lability, irrationality, hallucinations and impulsivity. Chronic exposure produced more severe symptoms, including muscular weakness, difficulty in walking, tremor, immobile facial expression, and speech disturbances�symptoms reminiscent of Parkinson's Disease. Sufferers of the Parkinson's-like neurological disease secondary to chronic poisoning accumulate large amounts of manganese in a circumscribed region of the brain.

The primary site of manganese toxicity regardless of the route of exposure�by mouth, inhalation or injection by intravenous tube�in humans, monkeys, rabbits and rats, is a mass of nervous tissue buried deep within the cerebral hemispheres. This is the basal ganglia, part of the extrapyramidal system controlling body movement. The neuronal damage caused by the manganese tends to be more extensive in young, immature animals than in adults.

Six years ago, tragic incidents in two London hospitals alerted the medical community to the vulnerability of sick babies to manganese attack. Suffering liver disease, the babies received nutrient solutions containing small amounts of manganese through intravenous tube feeding. Although the manganese concentration was no greater than that in soy formula, and considered safe by government standards, it caused brain damage after feeding periods lasting a few months to two years. Of 57 babies receiving "safe" amounts of manganese, two fell ill with movement disorders and six suffered damage to their basal ganglia.

John Donaldson, toxicologist and speaker on Day Two at the UC Irvine conference, described how manganese could cause a biochemical lesion in the basal ganglia. He reported how manganese overload can step up the brain's electric charge, increase its virulence tenfold, and attack vulnerable dopaminergic neurons.

Arvid Carlsson, last year's Nobel Prize winner in medicine, has shown that damage to these basal ganglia dopamine cells is symptomatic of Parkinson's Disease. At the conference, Donaldson warned that when "incredible" amounts of manganese are fed to infant mammals, the metal is capable of "running amok" in the basal ganglia dopamine nerve cells. "After chronic early exposure, they can be brain-damaged later in life," he said.

When Francis M. Crinella, Clinical Professor of Pediatrics at the University of California at Irvine, spoke, he described the effects of manganese overload in adolescents. His research had detected relatively high levels of manganese in the scalp hair of hyperactive children compared to matched controls. This replicated earlier studies by UC Irvine psychiatrist Louis Gottschalk, who detected elevated manganese in scalp hair of youths detained for felony crimes and incarcerated in four Southern California prisons. These findings, wholly unexpected, persuaded Crinella to launch inquiry into the most likely source of manganese in the hair, then to ask whether this had anything to do with hyperactivity in children, a syndrome attributed to a disturbance in the basal ganglia. To Crinella, the low levels of manganese in California soil, air and water meant the primary intake had to be through diet. Since adolescents are able to metabolize at least 97 percent of manganese ingested, exposure had to occur earlier in life, possibly during infancy. This hypothesis was first stated by Collipp in 1983 who had tested hair samples of babies fed soy-based infant formula and found them high in manganese. Crinella speculated that soy infant formula might provide one explanation for the current epidemic of adolescent violence sweeping the nation.

Crinella contacted his colleague Bo L�nnerdal at UC Davis to take a further look at the effects of manganese on the brain, particularly its toxicity to dopamine neurons in the basal ganglia. L�nnerdal and a graduate student Trinh Tran tested for behavioral and brain disorders in rat pups. For 18 days, four groups of rat pups suckled on the mother's breast and received by micropipette an additional dose of manganese salt dissolved in water. The doses corresponded to the amounts of manganese found in rat breast milk (0.05 mg) and several brands of soy-based infant formula (0.25 mg and 0.50 mg) found on pharmacy shelves today. The control group received just sugar water (0.0 mg). After 18 days of controlled feeding, the rat pups were returned to their cages and left undisturbed until 50 days of age. Then through Day 64 they were given behavior tests for evidence of disability. The animals given high amounts of manganese did less well on maze and shock avoidance than those given lesser amounts.
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