Muscular Dystrophy natural treatment
Feb 19 2014 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.
Suggestions to discuss with your doctor
It may be worthwhile to try small mounts of amino acid supplements and perhaps 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
Glutamine has been shown to acutely decrease whole-body protein degradation in Duchenne muscular dystrophy. To improve nutritional support, 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. Oral glutamine and amino acid supplementation inhibit whole-body protein degradation in children with Duchenne muscular dystrophy. Am J Clin Nutr. 2006.
Coenzyme Q10 and muscular dystrophy
CoQ10 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 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. Two successful double-blind trials with coenzyme Q10 on muscular dystrophies and neurogenic atrophies. Biochim Biophys Acta. 1995
Steinert's myotonic dystrophy is a genetic autosomal dominant disease and the most frequent muscular dystrophy in adulthood. It has been suggested that mitochondrial abnormalities can occur in this disease and deficiency of 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. Coenzyme Q10, exercise lactate and CTG trinucleotide expansion in myotonic dystrophy. Brain Res Bull. 2001.
Creatine and muscular dystrophy
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.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 for treating muscle disorders. Cochrane Database Syst Rev. 2007.
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. 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. Department of Medicine (Neurology and Rehabilitation), McMaster University, Hamilton, Canada.
Abnormal activation of nuclear factor kappa B (NF-kappaB) probably plays an important role in the pathogenesis of Duchenne's muscular dystrophy (DMD). In this report, we evaluated the efficacy of curcumin, a potent NF-kappaB inhibitor, in mdx mice, a mouse model of DMD. We found that it improved sarcolemmic integrity and enhanced muscle strength after intraperitoneal (i.p.) injection. Histological analysis revealed that the structural defects of myofibrils were reduced, and biochemical analysis showed that creatine kinase (CK) activity was decreased. We also found that levels of tumor necrosis factor alpha (TNF-alpha), interleukin-1 beta (IL-1beta) and inducible nitric oxide synthase (iNOS) in the mdx mice were decreased by curcumin administration. EMSA analysis showed that NF-kappaB activity was also inhibited. We thus conclude that curcumin is effective in the therapy of muscular dystrophy in mdx mice, and that the mechanism may involve inhibition of NF-kappaB activity. Since curcumin is a non-toxic compound derived from plants, we propose that it may be useful for DMD therapy. Curcumin alleviates dystrophic muscle pathology in mdx mice. Mol Cells. 2008.
Selenium and muscular dystrophy
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. Selenium metabolism and supplementation in patients with muscular dystrophy. Neurology. 1989 May. Muscle Research Centre, Department of Medicine, University of Liverpool, UK.
Limb-girdle muscular dystrophy or Erb's muscular
This is a class similar but distinct from Duchenne and Becker's muscular dystrophy. Limb-girdle muscular dystrophy encompasses a large number of rare disorders.
Ann Neurol. 2013 Sep. Therapeutic advances in muscular dystrophy. The muscular dystrophies comprise a heterogeneous group of genetic disorders that produce progressive skeletal muscle weakness and wasting. There has been rapid growth and change in our understanding of these disorders in recent years, and advances in basic science are being translated into increasing numbers of clinical trials. This review will discuss therapeutic developments in 3 of the most common forms of muscular dystrophy: Duchenne muscular dystrophy, facioscapulohumeral muscular dystrophy, and myotonic dystrophy. Each of these disorders represents a different class of genetic disease (monogenic, epigenetic, and repeat expansion disorders), and the approach to therapy addresses the diverse and complex molecular mechanisms involved in these diseases.
Would anabolic steroids be helpful for the treatment of a relatively benign muscular dystrophy in a 70 year old with muscular wasting and weakness?
This is not a topic I have studied.
I am the mother of two children, ages 4 and 7, who both have a rare form of Congenital Muscular Dystrophy, classified as Merosin Deficient. I am a strong believer in nutrition as a healing force, and a leading factor in my children’s health. Their daily diet consists of eggs, fermented porridge, kefir, raw milk, kale shakes, and protein/nutrient rich dinners. All food is organic, and sugar is extremely limited. They currently have cod liver butter oil and magnesium, each once daily. They are happy, generally in good health, and exceeding expectations in their capabilities. But, of course, they are still unable to walk, and suffer from muscle weakness. As a mother, I feel there is more that can be done for them. I have researched nutrition for muscular dystrophy, and while there is not a lot out there, I was able to find that some supplements are recommended: Coenzyme Q10, Vitamin E with Selenium, Taurine, and Green Tea Extract.