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Muscular dystrophy

Category: Illness or disabilities



Introduction and description


Muscular dystrophy is also discussed in the context of the whole broad sprectrum of muscle diseases - see Muscle diseases.

Muscular dystrophy (MD) is a group of muscle diseases that weaken the musculoskeletal system. They are characterized by progressive skeletal muscle weakness, defects in muscle proteins, and the death of muscle cells and tissue.

Some cases may be mild and progress very slowly over a normal lifespan, while others produce severe muscle weakness, functional disability, and loss of the ability to walk. Some children with muscular dystrophy die in infancy while others live into adulthood with only moderate disability. The muscles affected vary. Muscular dystrophy can affect adults, but the more severe forms tend to occur in early childhood.


In the 1860s, descriptions of boys who grew progressively weaker, lost the ability to walk, and died at an early age became more prominent in medical journals.

In the following decade, French neurologist Guillaume Duchenne gave a comprehensive account of thirteen boys with the most common and severe form of the disease, which now carries his name—Duchenne muscular dystrophy.  It soon became evident that the disease had more than one form. These are shown in more detail in the table below.




Becker muscular dystrophy

Becker muscular dystrophy (BMD) is caused by the production of a truncated, but partially functional form of dystrophin.  Survival is usually into old age.  It affects only boys (with extremely rare exceptions)

Congenital muscular dystrophy

Age at onset: birth; symptoms include general muscle weakness and possible joint deformities; disease progresses slowly; shortened life span. 

Duchenne muscular dystrophy

Duchenne muscular dystrophy (DMD) is the most common childhood form of muscular dystrophy; it generally affects only boys. By age 10, the child may need braces for walking and by age 12, most patients are unable to walk. Life span ranges from 15 to 51.

Distal muscular dystrophy

Distal muscular dystrophies' age at onset: 20 to 60 years; symptoms include weakness and wasting of muscles of the hands, forearms, and lower legs; progress is slow and not life-threatening

Emery-Dreifuss muscular dystrophy

Emery-Dreifuss Muscular Dystrophy patients normally present in childhood and the early teenage years. Clinical signs include muscle weakness and wasting. Most patients also suffer from cardiac conduction defects and arrhythmias

Facioscapulohumeral muscular dystrophy

Facioscapulohumeral muscular dystrophy (FSHD) initially affects the muscles of the face, shoulders, and upper arms with progressive weakness. Symptoms usually develop in the teenage years. Some affected individuals become severely disabled.  It occurs both in males and females.

Limb-girdle muscular dystrophy

Limb-girdle muscular dystrophy affects both boys and girls. Muscle weakness affects both upper arms and legs. Though a person normally leads a normal life with some assistance, in some extreme cases, death from LGMD occurs due to cardiopulmonary complications.

Myotonic muscular dystrophy

Myotonic muscular dystrophy presents with delayed relaxation of muscles, as well as muscle wasting and weakness.  It affects many body systems in addition to skeletal muscles, including the heart, endocrine organs, eyes, and gastrointestinal tract.

Oculopharyngeal muscular dystrophy

Oculopharyngeal MD's age at onset: 40 to 70 years; symptoms affect muscles of eyelids, face, and throat followed by pelvic and shoulder muscle weakness



The symptoms by which muscular dystrophy is diagnosed are

  • Progressive muscular wasting
  • Poor balance
  • Drooping eyelids
  • Atrophy
  • Scoliosis (curvature of the spine and the back)
  • Inability to walk
  • Frequent falls
  • Waddling gait
  • Calf deformation
  • Limited range of movement
  • Respiratory difficulty
  • Joint contractures
  • Cardiomyopathy
  • Arrhythmias
  • Muscle spasms


The generally accepted medical view appears to be that the condition is generally inherited. In the early 1990s, researchers identified the gene for the protein dystrophin which, when absent, causes DMD. Dystrophin protein is found in muscle fibre membrane; its helical nature allows it to act like a spring or shock absorber.

The amount of dystrophin correlates with the severity of the disease (i.e., the less dystrophin present, the more severe the phenotype). Since the gene is on the X chromosome, this disorder affects primarily males, and females who are carriers have milder symptoms. Sporadic mutations in this gene occur frequently, accounting for a third of cases. The remaining two-thirds of cases are inherited in a recessive pattern.

However, other causes are starting to creep into the picture, including viruses. In effect, a virus is responsible for the absence and destruction or mutation of the gene. 

There have also been associations made with diseases like Ehlers-Danlos, another disease initially linked to genes, but now being linked more to viruses in particular.


Heart failure in children and adults is often the consequence of myocarditis associated with Coxsackievirus (CV) infection. Upon CV infection, enteroviral protease 2A cleaves a small number of host proteins including dystrophin, which links actin filaments to the plasma membrane of muscle fiber cells (sarcolemma). It is unknown whether protease 2A-mediated cleavage of dystrophin and subsequent disruption of the sarcolemma play a role in CV-mediated myocarditis. …..our findings indicate that protease 2A-mediated cleavage of dystrophin is critical for viral propagation, enteroviral-mediated cytopathic effects, and the development of cardiomyopathy. PMID:  24200690

Due to the number of variations of the disease, there may be more than one virus implicated.  There are also some complex variations on the virus theme, as certain forms of nutritional deprivation may also play a part.  Here we see how the Lassa virus is only able to exert its damage in the absence of Genistein - a natural chemical. 

The extracellular matrix (ECM) receptor dystroglycan (DG) serves as a cellular receptor for the highly pathogenic arenavirus Lassa virus (LASV) that causes a haemorrhagic fever with high mortality in human. In the host cell, DG provides a molecular link between the ECM and the actin cytoskeleton via the adapter proteins utrophin or dystrophin. Here we investigated post-translational modifications of DG in the context of LASV cell entry. Using the tyrosine kinase inhibitor genistein, we found that tyrosine kinases are required for efficient internalization of virus particles, but not virus-receptor binding. Engagement of cellular DG by LASV envelope glycoprotein (LASV GP) in human epithelial cells induced tyrosine phosphorylation of the cytoplasmic domain of DG. LASV GP binding to DG further resulted in dissociation of the adapter protein utrophin from virus-bound DG. This virus-induced dissociation of utrophin was affected by genistein treatment, suggesting a role of receptor tyrosine phosphorylation in the process. PMID: 23279385

The detail here becomes very complex, and the purpose is to provide an overview of the findings so far.


In some types of Muscular Dystrophy  there is also the suggestion that toxins are to blame. 

There is some interesting work being undertaken, for example, on the role of nanoparticles in the destruction of genes.  No doubt as one branch of the scientific community release nanoparticles, other branches of the scientific community will be employed in finding out which genes they destroy.

Mutations in the human dystrophin gene cause Duchenne muscular dystrophy, a common neuromuscular disease leading to a progressive necrosis of muscle cells. The etiology of this necrosis has not been clearly established, and the cellular function of the dystrophin protein is still unknown. We report here the identification of a dystrophin-like gene (named dys-1) in the nematode Caenorhabditis elegans. Loss-of-function mutations of the dys-1 gene make animals hyperactive and slightly hypercontracted. ….. the dys-1 mutants are hypersensitive to acetylcholine and to the acetylcholinesterase inhibitor aldicarb.  PMID:  9933302

Aldicarb is a carbamate insecticide which is the active substance in the pesticide Temik. It is effective against thrips, aphids, spider mites, lygus, fleahoppers, and leafminers, but is primarily used as a nematicide. Aldicarb is a cholinesterase inhibitor which prevents the breakdown of acetylcholine in the synapse. In case of severe poisoning, the victim dies of respiratory failure.

Aldicarb is used by farmers where resistance to organophosphate insecticides has developed, and is used by some farmers in potato production, in order to control  soil-borne nematodes and some foliar pests. Its high level of solubility restricts its use in certain areas where the water table is close to the surface.


We have often found in researching this site that the same pathogens eventually appear over and over again for apparently different diseases.  The diseases caused may differ only because the pathogen reached a certain organ before another - the heart rather than the liver, or a lung rather than the prostate.  And possibly in this case the fetus rather than the mother.  This is particularly true of parasites, where the point of entry can vary so much. 

Fetal damage can occur from parasites transitted sexually, but these are not the only parasites implicated

Previous studies have demonstrated loss/reduction of dystrophin in cardiomyocytes in both acute and chronic stages of experimental Trypanosoma cruzi (T. cruzi) infection in mice. The mechanisms responsible for dystrophin disruption in the hearts of mice acutely infected with T. cruzi are not completely understood. The present in vivo and in vitro studies were undertaken to evaluate the role of inflammation in dystrophin disruption and its correlation with the high mortality rate during acute infection. C57BL/6 mice were infected with T. cruzi and killed 14, 20 and 26 days post infection (dpi). The intensity of inflammation, cardiac expression of dystrophin, calpain-1, NF-κB, TNF-α, and sarcolemmal permeability were evaluated. Cultured neonatal murine cardiomyocytes were incubated with serum, collected at the peak of cytokine production and free of parasites, from T. cruzi-infected mice and dystrophin, calpain-1, and NF-κB expression analyzed. Dystrophin disruption occurs at the peak of mortality and inflammation and is associated with increased expression of calpain-1, TNF-α, NF-κB, and increased sarcolemmal permeability in the heart of T. cruzi-infected mice at 20 dpi confirmed by in vitro studies. The peak of mortality occurred only when significant loss of dystrophin in the hearts of infected animals occurred, highlighting the correlation between inflammation, dystrophin loss and mortality. PMID: 25102151


A number of illnesses on this site are linked to the live [attenuated] viruses in vaccines, but there are tentative links in a number of muscle and skeletal diseases with the adjuvant of the vaccine as opposed to the virus itself or the excipient [another cause].   The main culprit in the case of Muscular dystrophy appears to be the use of aluminium based adjuvants.

The following case study shows what can happen

A 62-year-old female patient experienced progressive muscular weakness over the last ten years, involving shoulder and pelvic girdle muscles, paraspinal and facial muscles. A biopsy was taken from the left deltoid muscle where hepatitis vaccination had taken place ...The specimen revealed macrophagic myofasciitis due to the injection of aluminium-bound vaccines. ...The pathomechanism is supposed to involve immune stimulation due to long term persistence of the adjuvant.  PMID: 14997943

and to show it happens in children as well

Macrophagic myofasciitis is a novel [sic], "inflammatory myopathy" described after a variety of vaccinations, almost exclusively in adults. We examined the relevance of histological findings of this myopathy to the clinical presentation in pediatric patients. Muscle biopsies from 8 children (7 months to 6 years old) with histological features of macrophagic myofasciitis were reviewed and correlated with the clinical manifestations.
Patients underwent quadriceps muscle biopsy for suspected mitochondrial disease (4 patients), spinal muscular atrophy (2 patients), myoglobinuria (1 patient), and hypotonia with motor delay (1 patient).
All biopsies showed identical granulomas composed of periodic acid-Schiff-positive and CD68-positive macrophages. Characteristic aluminum hydroxide crystals were identified by electron microscopy in 2 cases. The biopsy established diagnoses other than macrophagic myofasciitis in 5 patients: spinal muscular atrophy (2), Duchenne muscular dystrophy (1), phospho-glycerate kinase deficiency (1), and cytochrome c oxidase deficiency (1)....PMID: 18281624


We are certain that in due course there will be cases found to have been caused by bacteria and possibly even by fungi.



The main advice here is to get the cause investigated, as it is possible that if the disease was not inherited, that the pathogen can be halted and the disease progression stopped.

There are any number of tests that can be used from simple stool tests, to scans, blood tests to test for pathogens and for antibodies to them.

There is no known cure for muscular dystrophy.

Physical therapy, occupational therapy, orthotic intervention (e.g., ankle-foot orthosis), speech therapy and orthopaedic instruments (e.g., wheelchairs, standing frames and powered mobile arm supports) may be helpful. Inactivity and bodybuilding efforts can worsen the disease.

There may be mechanisms via food that can help in repair.  We will post all observations from PubMed that suggest efficacious methods in this area.


Related observations