Creatine Won't Help Lou Gehrig's Disease
Researchers Continue Looking for Treatment Avenues
March 24, 2003 -- Despite promising early studies on mice, the supplement creatine monohydrate does not seem to help people with Lou Gehrig's disease. However, with so much research directed toward this effort, more promising results may soon develop.
The degenerative disease -- which is ultimately fatal and has no cure -- is known medically as amyotrophic lateral sclerosis (ALS). Named for a late baseball legend, Lou Gehrig's disease is a devastating disease that gradually deteriorates cells in the spinal cord, brainstem, and the brain, writes lead researcher Geert Jan Groeneveld, MD, with the University Medical Center Utrecht, in the Netherlands.
Because Lou Gehrig's disease affects nerve cells controlling motor function -- such as walking -- researchers believed creatine monohydrate could help improve muscle strength as it has done in prior studies an animal models. The supplement is used worldwide by patients with Lou Gehrig's disease.
A previous study involving mice had shown that creatine monohydrate -- which increases high-intensity power output, muscle strength, and lean body mass in healthy individuals -- might hold promise for people with Lou Gehrig's disease, writes Groeneveld in the April Annals of Neurology.
The 175 patients in his study all had symptoms of Lou Gehrig's disease. They randomly were given either creatine monohydrate or a placebo to take daily.
In their study, 87 received the placebo treatment and 88 received creatine. In tracking their progress for one year, researchers did not find any affect on survival or in rate of decline.
"Despite the high expectations for creatine monohydrate ... we were unable to find evidence of a beneficial effect," writes Groeneveld. "Spending money on this drug, which is relatively expensive and not covered by health insurance, is in our opinion unnecessary."
Hopefully, this "extensive" research will soon reveal better therapies for Lou Gehrig's patients, he writes.
SOURCE: April 2003 Annals of Neurology.