Duchenne Muscular Dystrophy by Ray Sahelian, M.D.

Duchenne muscular dystrophy is a frequent muscular disorder caused by mutations in the gene encoding dystrophin, a cytoskeletal protein that contributes to the stabilization of muscle fiber membrane during muscle activity. Affected individuals show progressive muscle wasting that generally causes death by age 30. Skeletal muscles become atrophied by muscular disorders such as muscular dystrophy, wasting and even aging. In addition to muscle atrophy, progressive muscle damage, inflammation and replacement of muscle fibers with fibrous and fatty tissues are observed in muscular dystrophy.
   Duchenne's muscular dystrophy is known to delay children's development of movement and coordination, but it may also slow language development.

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Glutamine and amino acid supplement for Duchenne muscular dystrophy
Oral glutamine and amino acid supplementation inhibit whole-body protein degradation in children with Duchenne muscular dystrophy.
Am J Clin Nutr. 2006 Apr;83(4):823-8. Mok E, Eleouet-Da Violante C, et al. Centre d'Investigation Clinique 9202 INSERM, Assistance Publique-Hopitaux de Paris, Hopital Robert Debre, Paris, France.
Glutamine has been shown to acutely decrease whole-body protein degradation in Duchenne muscular dystrophy (To improve nutritional support in Duchenne muscular dystrophy, we tested whether oral supplementation with glutamine for 10 d decreased whole-body protein degradation significantly more than did an isonitrogenous amino acid control mixture. Twenty-six boys with Duchenne muscular dystrophy were included in this randomized, double-blind parallel study; they received an oral supplement of either glutamine or an isonitrogenous, nonspecific amino acid mixture for 10 d. Oral glutamine or amino acid supplementation over 10 d equally inhibits whole-body protein degradation in DMD.

Creatine for muscular dystrophy
Creatine monohydrate as a therapeutic aid in muscular dystrophy.
Nutr Rev. 2006 Feb;64(2 Pt 1):80-8. Pearlman JP, Fielding RA. Nutrition, Exercise Physiology, and Sarcopenia Laboratory, Jean Mayer USDA Human Nutrition Research Center on Aging at Tufts University, Boston, Massachusetts, USA.
In recent years, dietary supplementation with creatine has been shown to enhance neuromuscular function in several diseases. Recent studies have suggested that creatine can be beneficial in patients with muscular dystrophy and other mitochondrial cytopathies, and may attenuate sarcopenia and facilitate rehabilitation of disuse atrophy. Though the mechanisms are still unknown, creatine has been shown to decrease cytoplasmic Ca2+ levels and increase intramuscular and cerebral phosphocreatine stores, providing potential musculoskeletal and neuroprotective effects.

Green tea, EGCG, and Duchenne muscular dystrophy
Green tea extract and its major polyphenol (-)-epigallocatechin gallate improve muscle function in a mouse model for Duchenne muscular dystrophy.
Am J Physiol Cell Physiol. 2006 Feb;290(2):C616-25. Laboratory of Pharmacology, Geneva-Lausanne School of Pharmaceutical Sciences, Univ. of Geneva, Switzerland.
In this study, the dystrophic mdx(5Cv) mouse model was used to investigate the effects of green tea extract, its major component (-)-epigallocatechin gallate, and pentoxifylline on dystrophic muscle quality and function. Three-week-old mdx(5Cv) mice were fed for either 1 or 5 wk a control chow or a chow containing the test substances. Histological examination showed a delay in necrosis of the extensor digitorum longus muscle in treated mice. Mechanical properties of triceps surae muscles were recorded while the mice were under deep anesthesia. Phasic and tetanic tensions of treated mice were increased, reaching values close to those of normal mice. The phasic-to-tetanic tension ratio was corrected. Finally, muscles from treated mice exhibited 30-50% more residual force in a fatigue assay. These results demonstrate that diet supplementation of dystrophic mdx(5Cv) mice with green tea extract or EGCG protected muscle against the first massive wave of necrosis and stimulated muscle adaptation toward a stronger and more resistant phenotype.