As Thanksgiving nears, many of us anticipate a filling turkey dinner followed by a satisfying nap on the couch. The sleepiness that usually follows a Thanksgiving meal is often attributed to tryptophan, an amino acid found in turkey. This is just a myth as the acid only works on an empty stomach, according to the Stanford News Service. But this year, tryptophan may find a new claim to legitimate fame.

Researchers at Stanford Medical School’s Lawrence Steinman Neurology Lab have discovered that the tryptophan metabolites people form as their bodies break down amino acids may be used as a remedy for multiple sclerosis, an autoimmune disease that causes damage to the central nervous system.

Professor of Neurological Sciences Lawrence Steinman and a team of Stanford researchers recently showed that Tranilast, a drug with a chemical composition akin to trytophan metabolites, may reverse paralytic effects of multiple sclerosis. The exact effects of the drug, however, are not yet known. Steinman’s latest study will wrestle with the merits of this prospective treatment and will be published in the Nov. 4 issue of the journal Science.

“My prediction is that it will reduce relapses and block the progression of the disease,” Steinman says. He emphasizes that this is “just a prediction,” since the chemical has not yet undergone any human trials for effectiveness.

Steinman began his work when Michael Platten, a German postdoctoral researcher, proposed a study of Tranilast in conjunction with Steinman’s previous multiple sclerosis research. Steinman has spent the past 25 years at Stanford studying the disease.

The experiments were performed on mice who had the experimental autoimmune encephalomyelitis (EAE) model of multiple sclerosis. Peggy Ho, a Stanford postdoctoral scholar in neurology and the third research team member, says that, while other animals like rats and guinea pigs can also be used for testing, “it’s easiest to use mice.” In contrast with other experiment alternatives, mice are the most reliable option with the lowest amount of experimental error, she explains.

“The main focus is to develop novel therapeutics to treat the disease,” Ho says. The tests show that Tranilast helps the mice to regain the ability to walk. It is administered when signs of leg paralysis begin to appear. It also results in less frequent and less severe relapses, and in a reduction of inflammatory cells.

But Steinman says that it is much easier to cure multiple sclerosis in mice than in humans.

Tranilast has not yet been tested in human multiple sclerosis patients, but Steinman says that he has “very aggressive plans to move this ahead to begin clinical trial [in humans].”

Tranilast was developed in Japan as an anti-inflammatory agent, according to BioMed Central, an independent publishing house that provides access to peer-reviewed biomedical research. The drug is currently used clinically to treat asthma caused by allergies and keloids — overgrowths of skin tissue — but has not been tested on humans with multiple sclerosis.

“I have high hopes, but the proof is in testing it in humans,” Steinman says, and continues that the group needs both approval and money before these tests can begin. Steinman predicts that this could take a year, but says he is confident that they’ll eventually receive permission and funding for tests. While the researchers do not know exactly what this drug will do once tested in humans for multiple sclerosis, they say they do have high expectations that the human results will parallel those in mice. Steinman says he thinks that Tranilast could eventually be used for multiple sclerosis as well as for rheumatoid arthritis, Crohn’s disease and possibly even diabetes.

“I’m sure that this will be very exciting, not only in multiple sclerosis, but for other diseases,” Ho concurs. “Michael deserves all of the praise. This was his project, and I'm just thankful that he brought me on board.”