NEW YORK (Reuters Health) - People with cancer, AIDS (news - web sites) or other chronic illnesses often suffer wasting, a decay in muscle and fat tissue that cannot be treated with better nutrition. But a treatment for the condition may now be closer, according to researchers who have discovered a key component in disease-related muscle loss.

    While scientists have known about some of the links in the molecular chain that triggers muscle wasting, others have remained a mystery. Now researchers say that NF-kappa B, a natural substance that turns genes on and off, is a key missing link. They believe drugs that inhibit NF-kappa B may prevent the muscle-wasting syndrome known as cachexia.

    Denis C. Guttridge and his colleagues at the University of North Carolina at Chapel Hill report their findings in the September 29th issue of Science.

    This is an important basic finding with implications for (cachexia) therapy,'' co-author Dr. Albert S. Baldwin, Jr., told Reuters Health.

    It will, however, be ``a while'' before any new treatment is available, Baldwin said. Even though NF-kappa B inhibitors are under development, he noted, no one knows how they will behave in muscle.

    Baldwin and his colleagues used mouse muscle cells to uncover the role of NF-kappa B in muscle wasting. They already knew that a protein called tumor necrosis factor (TNF) was involved. Because TNF is a key immune defense protein, its levels rise in response to illness. The current experiments showed that elevated TNF activated NF-kappa B, which in turn suppressed a muscle-replenishing protein called MyoD. Without MyoD, muscle cells cannot develop normally.

    As many as one third of cancer patients die from cachexia, Baldwin noted. ``No matter how many calories they take in,'' he said, ``the body doesn't use them.'' The reason why this happens now seems clearer, according to Baldwin. ``We think we've figured out an important piece in the chain of command,'' he said.