Vitamin Treats Muscular Dystrophy

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A form of the vitamin, niacin, could help treat Duchenne muscular dystrophy, the most common and severe form of the disease. Patients suffering from Duchenne muscular dystrophy (DMD) are unable to produce dystrophin. This protein is responsible for connecting the various parts of muscle cells. Without dystrophin, the cells do not function correctly and this triggers an inflammatory response, which gradually destroys the muscle. In addition, this process also triggers a decrease in the fuel, called NAD+, that powers cells. Muscles weaken, inflammation escalates, and more muscle is lost. Researchers at the Ecole Polytechnique Federale of Lausanne in Switzerland investigated the possibility of reducing this muscle inflammation by providing the worn out powerhouses of muscle cells with more access to fuel. They tested their theory on mice genetically modified to develop the disease. They supplemented the diet of these animals with nicotinamide riboside (NR), the vitamin precursor of NAD+ and a special form of the B vitamin, niacin. The results were remarkable. Large doses of NR significantly lowered muscle lesions associated with the disease. “We have good reason to think that humans will also respond to this treatment and that we will be able to reduce inflammation,” the researchers conclude.

Animals fed diets supplemented with NR showed enhanced cellular activity and increased lifespan in a study from the same Swiss researchers.

Elizabeth Somer, M.A.,R.D.

In Perspective: NR is a vitamin precursor of NAD+. As a supplement it appears to be much more potent at enhancing cells’ energy cycle, presents no known toxicity even in high doses, and excesses appear to be easily excreted in urine.

Ryu D, Zhang H, Ropelle E, et al: NAD repletion improves muscle function in muscular dystrophy and counters global Prylation. Science Translational Medicine 2016; October 19th.

Zhang H, Ryu D, Wu Y, et al: NAD+ repletion improves mitochondrial and stem cell function and enhances life span in mice. Science 2016; 352:1436-1443.

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