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Muscular Dystrophy and Nutrition Therapy

Muscular Dystrophy


“At our son’s last visit to the pediatrician, the doctor was completely amazed at how well he is doing. He shows no signs of typical MD that she was expecting based on her experience with conventional medicine.” 

"I was diagnosed with the FSHD form of muscular dystrophy some years ago and given the typical 'there is no known cure' comment from the muscle specialist, neurosurgeon and my family doctor. I accepted the situation, but continued to hope for some development in the disease. I came across your web site, and read the article on M.D. For the first time in years I felt encouraged and began to try a combination of the items listed in the article. I noticed an immediate increase in my energy level, which felt good in itself, but the "amazing" happened just recently when both my wife and I noticed a increase in the size of my left leg's calf muscle (this is without exercising). It was very obvious. I am continuing with the vitamins and supplements with an eager, though cautious 'one day at a time,' expectation of further results."


Everybody knows what muscles are, and when they don’t work, the weakness, frailty and incapacity of a little child with muscular dystrophy makes for many a poignant poster and tearful telethon. "There is no treatment… there is no specific therapy," says the Merck Manual. The National Institutes of Heath says the same thing: "There is no specific treatment for any of the forms of MD." , accessed April 2004)

Such despairing, autocratic but research-friendly pronouncements must not be seen as the last word until we adequately weigh in maternal and fetal malnutrition as a fundamental cause of muscular dystrophy. The good news (to be considered further below) is that if nutrient deficiency can cause an illness, nutrient therapy may ameliorate, or even cure, that illness.

Malnutrition causes muscular dystrophy? The short answer is, Yes. "Dystrophy: 1. Defective nutrition. 2. Any disorder caused by defective nutrition." (American Heritage Dictionary of the English Language, p 407.) When we consider all this means, we are poised to head down a steep slope. Nothing gets you into the emotional soup faster than being perceived as blaming a baby’s birth defect on the mother’s diet. Truly, it is very difficult to know for sure if a birth defect is the result of genetics or environmental factors. The mother represents half of a developing baby’s heredity, but almost all of the developing baby’s environment. Every single cell in a baby is the product of inherited DNA instruction. But every single cell in a baby is also the product of the mother's diet.

"Dinner Table Heredity"

Ova (human eggs) are formed during the fetal stage of a female’s life. In other words, all of a woman’s own eggs are actually formed while she was developing inside her mother, before she herself was born. Wow. This means that what your grandmother ate significantly contributed to your anatomy. Think that one over: What looks to be purely a genetic problem may in fact be a largely a nutritional one. I call this "Dinner Table Heredity." Just because a problem comes out of the womb does not mean that that problem is genetic and only genetic. Science has known for decades that many a specific birth defect is a direct result of a specific vitamin deficiency. (1-3)

Spina bifida, now well-known to be caused by a lack of folic acid (folate), is an example. I personally was born with a slight degree of spina bifida. I do not blame my mother; I might blame those who wrongly advised her about her pregnancy diet. I most certainly blame the food processing industry for systematically milling away the B-complex vitamins from her daily bread, and I blame the government for letting them get away with it.

Unlike spina bifida, muscular dystrophy may be reversible. However, MD is almost certainly not a matter of simple malnutrition, for it often does not respond to low-dose nutrient therapy. But it may sometimes respond to high-dose nutrient therapy, and may therefore be what orthomolecular physicians call a "genetotrophic" disease.


The important interrelationship between food and the genes was first called the "genetotrophic concept" by Roger J. Williams, PhD. Dr. Williams, the discoverer of the B-vitamin pantothenic acid, has explained in his books and scientific papers how existing biochemical birth defects may be effectively overcome with optimum nutrition. ( Please consider (and note the publication date):

Williams RJ. (1953). Muscular dystrophy and individual metabolic patterns: The possibilities of a nutritional therapeutic approach. Proc. of the First and Second Medical Conferences [1951-1952] of the Muscular Dystrophy Assoc. of America, 118-22 (Additional references below, 4-7.)

In genetotrophic diseases, genetic abnormality leads to nutritional disability. To compensate, the body requires the availability of larger than normal quantities of one or more nutrients for the affected gene to successfully express itself. For that particular person, normal dietary vitamin intakes are quite inadequate for normal function. It is a bit like trying to take a hot bath with the drain open: it can be done, but you are going to need a lot more hot water.

I think muscular dystrophy may constitute a good example of a genetotrophic disease. This also goes a long way to answering the perennial parents' question as to how one child can be healthy while the sibling is afflicted with MD. . . when Mom ate pretty much the same diet during both pregnancies. There may be both a genetic component and a nutritional component. Rather than a nutrient deficiency, MD may more exactly be considered to be a genetically-influenced nutrient dependency.


To a family with a child with muscular dystrophy, it must seem like the worst form of Monday Morning Quarterbacking to say what might have caused the disease their child already has. Coulda, shoulda, woulda is poor compensation for the parents of a disabled child, and to discuss it is to invite after-the-fact feelings of guilt and helplessness. So the real question is, To what extent might individual nutrients enable the sufferer to overcome the existing condition? There is considerable good news, and all of it is nutritional.


By now, CoQ10 (umbiquinone) should probably be accepted as a vitamin. Many other vitamins are coenzymes. CoQ10 is found in very tiny quantities in foods. Most young people make CoQ10 in their bodies, but a youngster with muscular dystrophy may either make too little or have a bigger requirement because of the illness.

It has been established that heart muscle greatly benefits from CoQ10 supplementation, resulting in improvement in cases of congestive heart failure and even cardiomyopathy. Striated cardiac muscle and striated voluntary (skeletal) muscle are not that dissimilar. Furthermore, Folkers et all write that:

"Cardiac disease is commonly associated with virtually every form of muscular dystrophy and myopathy. . . The rationale of this trial was based on known mitochondrial myopathies, which involve respiratory enzymes, the known presence of CoQ10 in respiration, and prior clinical data on CoQ10 and dystrophy. These results indicate that the impaired myocardial function of such patients with muscular disease may have some association with impaired function of skeletal muscle, both of which may be improved by CoQ10 therapy. . . CoQ10 is the only known substance that offers a safe and improved quality of life for such patients having muscle disease." (8)

Because CoQ10 is so absolutely vital to muscle cells, involved with growth control, cellular energy production, and other essential life functions, it warrants special consideration for persons with muscular dystrophy.

In two placebo-controlled, double-blind trials, 100 mg CoQ10 daily resulted in "definitely improved physical performance" in patients with muscular dystrophies and atrophies. "In retrospect," the authors wrote, "a dosage of 100 mg was too low although effective and safe." But even at this low dose, their conclusion was emphatic: "Patients suffering from these muscle dystrophies and the like should be treated with vitamin Q10 indefinitely." (9)

I submit that 300-600 mg/day would be a more effective dose, especially for an older MD child. For most families, the limiting factors will be cost or medical disapproval. Even pricey supplements are cheaper than most drugs. And as there are no harmful side effects with CoQ10, it is inexcusable to NOT give it a serious therapeutic trial.

Let's be fair: If CoQ10 is important to rabbits, might it also be important to children? (Boler JB, Farley TM, Scholler J, Folkers K. Deficiency of coenzyme Q10 in the rabbit. Int Z Vitaminforsch. 1969;39(3):281-8.)


Like CoQ10, vitamin E is an antioxidant. There is a long history of scientific suspicion, to this day largely untested, that antioxidants are of unusual benefit to individuals with muscular dystrophy. Linus Pauling wrote about muscular dystrophy, both experimental and hereditary, in How to Live Longer and Feel Better. Dr. Pauling’s comments are here reprinted with permission of the Linus Pauling Institute, Oregon State University:

"It was recognized more than fifty years ago that a low intake of E leads to muscular dystrophy, a disorder of the skeletal muscles characterized by weakness similar to that caused by a deficiency of vitamin C (the studies of vitamin E and muscular dystrophy have been discussed by Pappenheimer; 1948). . . Several kinds of hereditary muscular dystrophies are known. For the most part their nature is not thoroughly understood, and there is no specific therapy recommended for them. Myasthenia gravis is treated by inhibitors of cholinesterase, corticosteroids, and surgical removal of the thymus gland. The medical authorities do not mention the possible value of vitamins in controlling muscular dystrophies. The evidence about the involvement of vitamin E and vitamin C as well as B6 and other vitamins in the functioning of muscles suggests that the optimum intakes of these nutrients should be of value to the patients. So far as I know, no careful study of an increased vitamin intake for patients with hereditary muscular dystrophy has been reported." (p 160)

With the exception of the CoQ10 studies referenced above, Dr. Pauling's statement of 20 years ago, unfortunately, still pretty much stands. I found a couple of studies, one with 15 patients using vitamin E and selenium reporting "minimal" benefits (10) and another with 16 patients, showing "slight" benefit (11). I think they would have obtained far better results if they had used larger doses of selenium, much larger doses of vitamin E, and only the natural form of vitamin E.

Then there was this study, using 600 mg of vitamin E and a high amount of selenium (4,000 mcg Na2SeO3), which got very good results in all five patients studied. "All improved their grip strength. . ., two normalized their gait, another two can now sit down on their heels and stand up, one patient can now walk on his toes, one can now get up from lying on the floor without using a chair and two patients have improved their physical capacity. . . No side-effects were observed." (12)

This is, at the very least, genuinely encouraging.

Why no new, large-scale studies of high dose selenium-vitamin E therapy? Because drugless therapy is ignored by drug companies, and consequently remains unpromoted and unknown to physicians. There is no money in products that cannot be patented. Children learn at an early age that mud pies don't sell. No investment is made, no research is done where there is no money is to be recovered. Drug companies do not expect to find, nor do they want to find, a cure that does not involve a drug. A tragic example is modern medicine's approach to muscular dystrophy.

No doubt Jerry Lewis is a great guy and his heart is in the right place. But he may have unwittingly set the cause of health science back a generation. Telethons to raise cash for drug research for muscular dystrophy are expensive anachronisms. They are just re-inventing the wheel, and they're building it wrong to boot. Remember: "Dystrophy" means "malnutrition." There is no drug that corrects malnutrition, and never will be.

Agricultural scientists know this. You will have little trouble finding research studies on the role of selenium or vitamin E in preventing muscular dystrophies in chickens, cattle or calves, sheep or lambs. What works with calves should, in my opinion, be reasonably applied to people. (13,14)

Yet in spite of the long and expensive history of research on human muscular dystrophy, only a very small portion has involved vitamins, and was done quite some time ago. In the third edition of The Vitamins in Medicine, Bicknell and Prescott provide a thorough review of the literature on pages 612-619 and 635-641. There is considerable evidence that the disease is an inability of muscle tissue to efficiently utilize vitamin E. I give you the following quote:

"The peculiar muscular degeneration of muscular dystrophy may be produced in animals is caused and is only caused by lack of vitamin E. Human muscular dystrophy shows identically the same peculiar degeneration. The key to the cure of muscular dystrophy is vitamin E." (See: Rabinovitch R et al (1951) Neuromuscular disorders amenable to wheat germ oil therapy. J. Neurol. Neurosurg. Psychiat. 14:95-100.)

Synthetic vitamin E will not work. On pages 643-644 of The Vitamins in Medicine, DL alpha tocopherol (synthetic "vitamin E") is described as "valueless." It has to be the natural "D-alpha" form, specifically including the complete mix of natural tocopherols and tocotrienols, preferably from or with fresh stone ground whole wheat bread, wheat germ, or wheat germ oil. (p 645).

Muscular dystrophy is described as easier to cure in children, and easier still with added B vitamins and vitamin C (p 644).

Perhaps the most remarkable revelation of all is that this medical textbook was written in 1953. Has the human body changed in 55 years? Has muscular dystrophy changed in 55 years? No. Only our understanding of a disease can be said to have changed, and in this case, has changed for the worse. We have ignored the evidence, and doctors still tell patients that MD is incurable. If that angers you, read on.

The essential trace mineral selenium works closely with vitamin E and helps the body to get more out of less of the vitamin. This important biochemical partnership, or synergy, only works if both nutrients are present. It takes very little selenium, probably about 100 to 300 micrograms (mcg) a day to protect your cells and membranes from harmful oxidation via the protective selenium-containing enzyme, glutathione peroxidase, found in all body cells.

Blood levels of selenium are reduced in muscular dystrophy. "Myotonic dystrophy and all its major symptoms (including muscle dystrophy) can be cured or prevented in animals by selenium supplementation." (Werbach M. (1988) Nutritional Influences on Illness, New Canaan, CT: Keats, p 310-311. A more recent version of this excellent book is reviewed at .)

The vitamin-E-friendly mineral selenium is found in nutritional (or brewer’s) yeast, seafood, legumes, whole grains, animal products, and vegetables. However, food can be an unreliable source of selenium, as selenium content of soils varies around the nation.

For normally healthy individuals, overdose of selenium is possible with chronic excessive dietary intake. But we need to bear in mind that in the Orndahl study cited above, muscular dystrophy patients showed improvement with a daily dose of up to 1,400 mcg elemental selenium over period of nearly two years. Toxicity is clearly not a major issue.


Lecithin has been shown to improve therapeutic response when included along with vitamin E supplementation. This is probably due to the fact that lecithin contains a great deal of both inositol and phosphatidvl choline, which appear to reduce creatinuria in those with muscular dystrophy. Daily dosage used is about 20 g, which is about three tablespoons per day (15-17).

A Medline search at the National Library of Medicine in Washington, D.C., will yield over 18,300 studies that in some way relate to muscular dystrophy. Yet I have seen no evidence whatsoever that current muscular dystrophy research includes megavitamin and mineral therapy. Every time I see "Jerry's kids" on a poster or on TV, it gets me right here. And every time I'm solicited for a donation to a medical charity, I tell the canvasser that I'll gladly contribute the moment their organization begins to sponsor clinical trials with lecithin, selenium, and vitamin E. It has already been shown that selenium, vitamin E and CoQ10 levels are decreased in people with muscular dystrophy. (Ihara Y, Mori A, Hayabara T, Namba R, Nobukuni K, Sato K, Miyata S, Edamatsu R, Liu J, Kawai M. Free radicals, lipid peroxides and antioxidants in blood of patients with myotonic dystrophy. J Neurol. 1995 Feb;242(3):119-22.) The Vitamins in Medicine was published over half a century ago. So was Dr. Williams' paper on treating MD with nutrition. What is taking so long to apply that knowledge to those suffering today?


A mother writes (January 14, 2008):


“My child will be two later this month. He was labeled with muscular dystrophy (MD) last year, quite by accident. He had an issue with breath holding: he held his breath at daycare too long, passed out, and they called an ambulance. He ended up in the hospital for seven days of testing, and at the end of those tests is when they tested for MD. 


“I was told by the muscular dystrophy doctor that his life expectancy will be a wheelchair by 10 years old, and death by 20 years old. As you can understand, it was quite a shock to our family. The following weeks later, when the DNA tests came back as positive for either Duchanes or Becker’s MD, I was totally confused. Our pediatrician told us that the medical world doesn’t really know with the DNA testing what type… that will be determined as he develops, but since he had been diagnosed so early, it was most likely Duchanes, and she was very sorry that there was nothing that could be done.


“The one thing that we did take away from the hospital experience as well as then the initial discussions with our pediatrician, was that once he had been given the MD label, people started treating him as a label, and not as a person. This experience has prompted us to not tell many people (unless it’s needed) of the label he has been given, as we want people to see the lad first as the person he is.


“My husband and I (with extended family support) decided this was not enough. We were not willing to accept that there is simply nothing we could do. Fortunately for us we found the DoctorYourself website by searching MD and nutrition on the internet.


“The following are the supplements that our child, age two, currently takes, and has been for the past year. He is now 33 inches tall and weighs 25 lbs.



Liquid children’s multivitamin (daily serving)

Liquid Calcium (600 mg)

Liquid Vitamin E (150 i.u.)

Cod Liver Oil (daily serving)

Soy Lecithin (1-2 tsp)

Flax seeds & wheat germ oil – when can get into foods, banana bread, yogurt, etc.


“In addition, over a two day span, in a powdered form mixed together and put into milk (I try to do it in equal amounts over each day)


1,000 mg Taurine

400 mcg folic acid

60 mg CoQ10

50 mcg selenium

1,000 mcg Vitamin B12

1,000 mg Vitamin C

120 mg Gingko

4,000 mg MSM

20 g whey protein

8000 mg L-Glutamine

1,500 mg L-Arginine

800 mg Creatine


“Additionally, we try to ensure a healthy diet, including organic milk products, fruit and vegetables, and limit refined sugar in his diet (but certainly do no limit it completely – just try to use info from Dr. Saul’s website on healthy eating for children). We do other non-nutritional things too, including seeing a physical therapist twice a month.


“At our son’s last visit to the pediatrician in early December, 2007, the doctor was completely amazed at how well he is doing. He shows no signs of typical MD that she was expecting based on her experience with conventional medicine.” 



While this is admittedly a long way from cure, I think it is very encouraging. There is little if any downside to trying nutritional therapy. Bad nutrition has never improved anything, and good nutrition frequently has.



1. Hillemann HH. (1956) "Maternal Malnutrition and Fetal Prenatal Development Malformation" (Address at Oregon State College, November 9)

2. Hillemann HH. (1958) "Maternal Malnutrition and Congenital Deformity" ( Grants Pass Oregon Address, March 17)

3. Hillemann HH. (1961) "The Spectrum of Congenital Defect, Experimental and Clinical" Journal of Applied Nutrition 14:1,2.)

4. Williams RJ. Beerstecher E, Jr, and Berry, LJ. "The Concept of Genetotrophic Disease," Lancet, February 18, 1950, 287-90.

5. Williams RJ. "Concept of Genetotrophic Disease," Nut. Rev, 8, 257-60 (1950).

6. Williams RJ. "The Unexplored Field of Genetotrophic Disease," MD, 6, 123-4, 136 (1951).

7. Williams RJ. and Rogers, LL. "The Formulation of a Genetotrophic Supplement for the Experimental Treatment of Diseases of Obscure Etiology," Texas Reports Biol. Med., 11, 573-81 (1953).

8. Folkers K, Wolaniuk J, Simonsen R, Morishita M, Vadhanavikit S. Biochemical rationale and the cardiac response of patients with muscle disease to therapy with coenzyme Q10. Proc Natl Acad Sci U S A. 1985 Jul;82(13):4513-6.

9. Folkers K, Simonsen R (1995) Two successful double-blind trials with coenzyme Q10 (vitamin Q10) on muscular dystrophies and neurogenic atrophies. Biochim Biophys Acta 1271(1):281-6. May 24.

10. Backman E, Henriksson KG. Effect of sodium selenite and vitamin E treatment in myotonic dystrophy. J Intern Med. 1990 Dec;228(6):577-81.

11. Gamstorp I, Gustavson KH, Hellstrom O, Nordgren B. J Child Neurol. 1986 Jul;1(3):211-4. A trial of selenium and vitamin E in boys with muscular dystrophy.

12. Orndahl G, Sellden U, Hallin S, Wetterqvist H, Rindby A, Selin E. Myotonic dystrophy treated with selenium and vitamin E. Acta Med Scand. 1986;219(4):407-14.)

13. Orndahl G et al. (1983) Selenium therapy of myotonic dystrophy. Acta. Med. Scand. 213:237.

14. Hidiroglou M, Jenkins K, Carson RB, Brossard GA. Selenium and coenzyme Q10 levels in the tissues of dystrophic and healthy calves. Can J Physiol Pharmacol. 1967 May;45(3):568-9.

15. Jackson MJ, Jones DA, Edwards RH. Vitamin E and muscle diseases. J Inherit Metab Dis. 1985;8 Suppl 1:84-7. (This review explains how vitamin E, and the phospholipids in lecithin, benefit the muscles.)

16. Milhorat AT and Bartels WE. (1945) The defect in utilization of tocopherol in progressive muscular dystrophy. Science 101:93-4.

17. Milhorat AT et al. (1945). Effect of wheat germ on creatinuria in dermatomyositis and progressive muscular dystrophy. Proc. Soc. Exp. Biol. Med. 58:40-1.

Copyright 2008, 2007 and prior years by Andrew W. Saul,

Andrew Saul is the author of the books FIRE YOUR DOCTOR! How to be Independently Healthy (reader reviews at ) and DOCTOR YOURSELF: Natural Healing that Works. (reviewed at )

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Andrew W. Saul


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