Zinc might be new weapon in war on Lou Gehrig's disease

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Zinc might be new weapon in war on Lou Gehrig's disease

By OSU News Service PORTLAND -

Researchers at Oregon State University may have gained ground in the battle

against Lou Gehrig's disease.

Growing evidence suggests that supplements of zinc and certain antioxidants may

slow disease progression in transgenic animal models of amyotrophic lateral

sclerosis, or Lou Gehrig's disease, researchers said at a national conference on

Diet and Optimum Health.

ph Beckman, director of the Environmental Health Sciences Center at Oregon

State University and a member of OSU's Linus ing Institute, said that zinc

has shown some value in studies done with mice that have a mutation that makes

them prone to ALS.

" Recently we've been asking whether you could treat Lou Gehrig's disease by

giving more zinc, and could the disease elevate more rapidly if you are

zinc-deficient? " Beckman said.

The research results have been promising. Studies indicate that mice that are

deficient in zinc develop the disease faster, Beckman said, and those that

receive supplements of zinc survive longer.

Zinc also improves immune function. And there appears to be a connection

between this nutrient and levels of the oxidant peroxynitrite, a natural

compound produced by cells that may cause motor neurons to die.

" These findings point to zinc as a possible factor in the treatment of ALS, "

Beckman said. " About 10 percent of the U.S. population is zinc deficient at

any given moment - vegetarians in particular. Moderate intake of zinc

supplements under 50 milligrams per day may be helpful in general, though higher

dosages can lead to copper deficiency and anemia. "

These and other studies about neurodegenerative disease, heart disease, cancer

and other major health problems were presented at a professional conference on

the role of diet in promoting optimal health, held in Portland and sponsored by

the Linus ing Institute.

Beckman has studied Lou Gehrig's disease for 10 years, exploring the underlying

biochemical causes of this fatal illness, which causes the death of motor

neurons through a period of about eight months to five years. The symptoms of

ALS can result from the progressive death of a surprisingly small number of

lower motor neurons controlling all voluntary muscles, leading to rapid muscle

degeneration, paralysis and eventually death.

ALS can develop quickly within the body, researchers say. People are born with

about a half-million motor neurons that send out messages and make contact with

the body's muscles. Upon development of ALS these neurons begin to shut off one

by one, causing loss of mobility in the body. The neurons cannot be

regenerated.

Beckman hopes to find a way to stop the disease before too much damage is done.

" My goal would be to turn this disease into something that resembles post-polio,

where the motor neuron damage is not progressive, " he said.

" People would still be able to continue to live and function with relatively

minor impairment. "

Related research of particular interest, Beckman says, points to the possible

role of peroxynitrite in ALS and perhaps other neurodegenerative diseases. This

inorganic oxidant is an essential component of the human immune system and

probably evolved to help fight infectious disease. But in some situations

excess levels of peroxynitrite appear to trigger a process that leads to motor

neuron degeneration and death.

In addition to zinc, a number of other antioxidants are under investigation to

help prevent motor neuron death in ALS, with promising results in vitro.

These studies are supported by the National Institutes of Health.

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