Muscular Dystrophy natural treatment options by Ray Sahelian, M.D.

Much has been said about the traditional medical approach to the treatment of muscular dystrophy. On this web page i try to include information on natural supplements that perhaps could be of help to those who have this difficult medical condition. We will update this site as more research is available. It may be worthwhile to try small mounts of amino acid supplements and perhaps 50 mg of CoQ10, but these are just suggestions and more research is needed to determine if they are effective and to determine whether additional supplement could be helpful in those with muscular dystrophy.

Glutamina or amino acid supplementation 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. 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 (0.5 g . kg(-1) . d(-1)) or an isonitrogenous, nonspecific amino acid mixture (0.8 g . kg(-1) . d(-1)) for 10 d. A significant effect of time was observed on estimates of whole-body protein degradation. A significant decrease in the rate of leucine appearance (an index of whole-body protein degradation) was observed after both glutamine and isonitrogenous amino acid supplementation. A significant decrease in endogenous glutamine due to protein breakdown was also observed. The decrease in the estimates of whole-body protein degradation did not differ significantly between the 2 supplemental groups. Oral glutamine or amino acid supplementation over 10 d equally inhibits whole-body protein degradation in Duchenne muscular dystrophy.

Coenzyme Q10 and muscular dystrophy
Two successful double-blind trials with coenzyme Q10 (vitamin Q10) on muscular dystrophies and neurogenic atrophies.
Biochim Biophys Acta. 1995 May 24;1271(1):281-6. Institute for Biomedical Research, University of Texas at Austin
Coenzyme Q10 is biosynthesized in the human body and is functional in bioenergetics, anti-oxidation reactions, and in growth control, etc. It is indispensable to health and survival. The first double-blind trial was with twelve patients, ranging from 7-69 years of age, having diseases including the Duchenne, Becker, and the limb-girdle dystrophies, myotonic dystrophy. Charcot-Marie-Tooth disease, and the Welander disease. The control coenzyme Q10 (CoQ10) blood level was low and ranged from 0.5-0.84 microgram/ml. They were treated for three months with 100 mg daily of CoQ10 and a matching placebo. The second double-blind trial was similar with fifteen patients having the same categories of disease. Since cardiac disease is established to be associated with these muscle diseases, cardiac function was blindly monitored, and not one mistake was made in assigning CoQ10 and placebo to the patients in both trials. Definitely improved physical performance was recorded. In retrospect, a dosage of 100 mg was too low although effective and safe. Patients suffering from these muscle dystrophies and the like, should be treated with vitamin Q10 indefinitely.

Coenzyme Q10, exercise lactate and CTG trinucleotide expansion in myotonic dystrophy.
Brain Res Bull. 2001 Oct-Nov 1;56(3-4):405-10. Department of Neuroscience, Neurological Clinics, University of Pisa, Pisa, Italy.
Steinert's myotonic dystrophy is a genetic autosomal dominant disease and the most frequent muscular dystrophy in adulthood. Although causative mutation is recognized as a CTG trinucleotide expansion on 19q13.3, pathogenic mechanisms of multisystem involvement of myotonic dystrophy are still under debate. It has been suggested that mitochondrial abnormalities can occur in this disease and deficiency of coenzyme Q 10 (CoQ10) has been considered one possible cause for this. The aim of this investigation was to evaluate, in 35 myotonic dystrophy patients, CoQ10 blood levels and relate them to the degree of CTG expansion as well as to the amount of lactate production in exercising muscle as indicator of mitochondrial dysfunction. Our data indicates the occurrence of reduced CoQ10 levels in myotonic dystrophy, possibly related to disease pathogenic mechanisms associated with abnormal CTG trinucleotide amplification.

Creatine and muscular dystrophy
Creatine for treating muscle disorders.
Cochrane Database Syst Rev. 2007 Jan 24;(1):CD004760. Kley R, Vorgerd M, Tarnopolsky M.
Progressive muscle weakness is a main symptom of most hereditary muscle diseases. Creatine is a popular nutritional supplement among athletes. It improves muscle performance in healthy individuals and might be helpful for treating myopathies. We evaluated the efficacy of oral creatine supplementation in muscle diseases. We searched the Cochrane Neuromuscular Disease Group Register in May 2004 for randomised trials using the search term 'creatine'. We also searched the Cochrane Central Register of Controlled Trials (The Cochrane Library, Issue 2, 2005) using the same search term. We adapted this strategy to search MEDLINE (PubMed, from January 1966 to September 2005) and EMBASE (from January 1980 to May 2004). Twelve trials, including 266 participants, met the selection criteria. Evidence from randomised controlled trials shows that short- and medium-term creatine treatment improves muscle strength in people with muscular dystrophies, and is well-tolerated. Evidence from randomised controlled trials does not show significant improvement in muscle strength in metabolic myopathies. High-dose creatine in glycogenosis type V increased muscle pain.

Creatine monohydrate supplementation does not increase muscle strength, lean body mass, or muscle phosphocreatine in patients with myotonic dystrophy type 1.
Muscle Nerve. 2004 Jan;29(1):51-8. Department of Medicine (Neurology and Rehabilitation), McMaster University, Hamilton, Canada.
Creatine monohydrate supplementation may increase strength in some types of muscular dystrophy. A recent study in myotonic muscular dystrophy type 1 did not find a significant treatment effect, but measurements of muscle phosphocreatine (PCr) were not performed. We completed a randomized, double-blind, cross-over trial using 34 genetically confirmed adult myotonic muscular dystrophy type 1 patients without significant cognitive impairment. Participants received creatine monohydrate (5 g, approximately 0.074 g/kg daily) and a placebo for each 4-month phase with a 6-week wash-out. Spirometry, manual muscle testing, quantitative isometric strength testing of handgrip, foot dorsiflexion, and knee extension, handgrip and foot dorsiflexion endurance, functional tasks, activity of daily living scales, body composition (total, bone, and fat-free mass), serum creatine kinase activity, serum creatinine concentration and clearance, and liver function tests were completed before and after each intervention, and muscle PCr/beta-adenosine triphosphate (ATP) ratios of the forearm flexor muscles were completed at the end of each phase. creatine supplementation did not increase any of the outcome measurements except for plasma creatinine concentration (but not creatinine clearance). Thus, creatine monohydrate supplementation at 5 g daily does not have any effects on muscle strength, body composition, or activities of daily living in patients with myotonic muscular dystrophy type 1, perhaps because of a failure of the supplementation to increase muscle PCr/beta-ATP content.

Selenium and muscular dystrophy
Selenium metabolism and supplementation in patients with muscular dystrophy.
Neurology. 1989 May;39(5):655-9. Muscle Research Centre, Department of Medicine, University of Liverpool, UK.
We studied selenium metabolism in patients with Duchenne muscular dystrophy and in contrast to previous reports found no significant abnormalities in these patients. Supplementation of muscular dystrophy patients and control subjects with sodium selenite (1 mg selenium/day) induced a variable rise in the activity of the selenium-dependent enzyme glutathione peroxidase in plasma and red cells, but no significant change in muscle glutathione peroxidase activities. There was no effect of selenium supplementation on disease activity in the patients with muscular dystrophy. Thiobarbituric acid-reacting substances (an index of free radical-mediated lipid peroxidation) were elevated in the muscle of patients with Duchenne muscular dystrophy in contrast to patients with other forms of muscular dystrophy and control subjects. This elevation was unaffected by selenium supplementation.

Muscular dystrophy questions
Q. Would anabolic steroids be helpful for the treatment of a relatively benign muscular dystrophy in a 70 year old with muscular wasting and weakness?
   A. This is not a topic I have studied.