Fact: The medical community offers no cure, no effective treatment, and no chance for survival. But right here there is…

New Hope For Reversing Muscular Dystrophy

Imagine a child confined to a wheelchair from the age of 10. He can’t raise his arms to feed himself or breathe on his own. Chances are he won’t see his young adult years.

The downward spiral probably began around age three to seven. At first there was general weakness in the hips and shoulder muscles. Eventually all muscles enlarged, including the heart, even though the muscle tissue itself grows increasingly weak.

He waddles and falls much more frequently than other little boys his age. Sitting is difficult and he can’t climb stairs very well. Eventually, he may develop scoliosis. At age 10, when other boys are playing Little League, he watches from the sidelines in his wheelchair.

This progressive muscle-degenerating genetic disorder may kill him in a few short years.

But he and those who love him don’t have to sit around and wait for the “inevitable” end.

If you or someone you love are experiencing the same turmoil, what you’re about to read in this report can change your world and offer new hope.

Because:

Now there’s a breakthrough protocol that looks full of promise for reversing muscular dystrophy.

I understand that may go against everything you’ve been told about this crippling condition. The prognosis, in most cases, has been extremely poor. But if you read this report all the way through, allow yourself to keep an open mind, and try the recommended treatments, you could reverse this debilitating disorder and experience a whole new life.

Mattie Stepaneck, a gifted and courageous young boy, lost his life to muscular dystrophy just before his 14th birthday. In his short time here, he was a champion for raising awareness about MD and appeared on Oprah and several news programs. One of his favorite quotes was this: “If you want something bad enough, never give up trying to reach it, and you will succeed." Mattie never lost hope.

So in the spirit of Mattie:

I’m Offering You Hope

Mattie also said, “Remember to play after every storm.” That incredible attitude in the face of his daily reality allowed him to write a New York Times best seller when he was only 11 years old.

It is my hope you’ll “remember to play” after the current storm you’re weathering now. My intention is to give you fortitude and hope through this report.

The report will cover:

What happens on a cellular level with this condition

The cause of Muscular Dystrophy

How you can potentially reverse Multiple Dystrophy and live a full life

Understanding Muscular Dystrophy

Muscular dystrophy (MD) refers to a group of more than 30 genetic diseases that cause progressive weakness and degeneration of skeletal muscles used during voluntary movement. These disorders vary in age of onset, severity, and pattern of affected muscles. All forms of MD grow worse as muscles progressively degenerate and weaken. The majority of patients eventually lose the ability to walk.

Some types of MD also affect the heart, gastrointestinal system, endocrine glands, spine, eyes, brain, and other organs. Respiratory and cardiac diseases are common, and some patients may develop a swallowing disorder. MD is not contagious and cannot be brought on by injury or activity.

What Causes Muscular Dystrophy?

All of the muscular dystrophies are inherited and involve a mutation in one of the thousands of genes that program proteins critical to muscle integrity. The body's cells don't work properly when a protein is altered or produced in insufficient quantity (or sometimes missing completely). Many cases of MD occur from spontaneous mutations that are not found in the genes of either parent, and this defect can be passed to the next generation.

Genes are like blueprints: they contain coded messages that determine a person's characteristics or traits. They are arranged along 23 rod-like pairs of chromosomes, * with one half of each pair being inherited from each parent. Each half of a chromosome pair is similar to the other, except for one pair, which determines the sex of the individual. Muscular dystrophies can be inherited in three ways:

Autosomal dominant inheritance occurs when a child receives a normal gene from one parent and a defective gene from the other parent.

Autosomal recessive inheritance means that both parents must carry and pass on the faulty gene. The parents each have one defective gene but are not affected by the disorder.

X-linked (or sex-linked) recessive inheritance occurs when a mother carries the affected gene on one of her two X chromosomes and passes it to her son (males always inherit an X chromosome from their mother and a Y chromosome from their father, while daughters inherit an X chromosome from each parent).

Sons of carrier mothers have a 50 percent chance of inheriting the disorder. Daughters also have a 50 percent chance of inheriting the defective gene but usually are not affected, since the healthy X chromosome they receive from their father can offset the faulty one received from their mother. Affected fathers cannot pass an X-linked disorder to their sons but their daughters will be carriers of that disorder. Carrier females occasionally can exhibit milder symptoms of MD.

How Many People Have MD?

MD occurs worldwide, affecting all races. Its incidence varies, as some forms are more common than others. Its most common forms in children, Duchenne and Becker muscular dystrophy, alone affect approximately 1 in every 3,500 to 5,000 boys, or between 400 and 600 live male births each year in the United States. **

Some types of MD are more prevalent in certain countries and regions of the world. Most muscular dystrophies are familial, meaning there is some family history of the disease.

• * Centers for Disease Control and Prevention, National Center on Birth Defects and Developmental Disabilities, July 27, 2005

Muscles are made up of thousands of muscle fibers. Each fiber is actually a number of individual cells that have joined together during development and are encased by an outer membrane. Muscle fibers that make up individual muscles are bound together by connective tissue.

Muscles are activated when an impulse, or signal, is sent from the brain along the peripheral nerves (nerves that connect the central nervous system to sensory organs and muscles) to the neuromuscular junction (the space between the nerve fiber and the muscle it activates). There, a release of the chemical acetylcholine triggers a series of events that cause the muscle to contract.

The muscle fiber membrane contains a group of proteins-called the dystrophin-glycoprotein complex-which prevents damage as muscle fibers contract and relax.

When this protective membrane is damaged, muscle fibers begin to leak the protein creatine kinase (needed for the chemical reactions that produce energy for muscle contractions) and take on excess calcium, which causes further harm. Affected muscle fibers eventually die from this damage, leading to progressive muscle degeneration.

Although MD can affect several body tissues and organs, it most prominently affects the integrity of muscle fibers. The disease causes muscle degeneration, progressive weakness, fiber death, fiber branching and splitting, phagocytosis (in which muscle fiber material is broken down and destroyed by scavenger cells), and, in some cases, chronic or permanent shortening of tendons and muscles. Also, overall muscle strength and tendon reflexes are usually lessened or lost due to replacement of muscle by connective tissue and fat.

How Do The Muscular Dystrophies Differ?

There are nine major groups of the muscular dystrophies. The disorders are classified by the extent and distribution of muscle weakness, age of onset, rate of progression, severity of symptoms, and family history (including any pattern of inheritance).

Although some forms of MD become apparent in infancy or childhood, others may not appear until middle age or later. Overall, incidence rates and severity vary, but each of the dystrophies causes progressive skeletal muscle deterioration, and some types affect cardiac muscle.

There are four forms of MD that begin in childhood

1. Duchenne MD is the most common childhood form of MD, as well as the most common of the muscular dystrophies overall, accounting for approximately 50 percent of all cases. It affects approximately one in 3,500 male births. Because inheritance is X-linked recessive (caused by a mutation on the X, or sex, chromosome), Duchenne MD primarily affects boys, although girls and women who carry the defective gene may show some symptoms. About one-third of the cases reflect new mutations and the rest run in families. Sisters of boys with Duchenne MD have a 50 percent chance of carrying the defective gene.

Duchenne MD usually becomes apparent when an affected child begins to walk.

Progressive weakness and muscle wasting (a decrease in muscle strength and size) caused by degenerating muscle fibers begins in the upper legs and pelvis before spreading into the upper arms.

Other symptoms include:

Loss of some reflexes, a waddling gait, frequent falls and clumsiness (especially when running),

Difficulty when rising from a sitting or lying position or when climbing stairs

Changes to overall posture, impaired breathing, lung weakness

And cardiomyopathy (heart muscle weakness that interferes with pumping ability).

Many children are unable to run or jump.

The wasting muscles, in particular the calf muscle (and, less commonly, muscles in the buttocks, shoulders, and arms), may be enlarged by an accumulation of fat and connective tissue, causing them to look larger and healthier than they actually are (called pseudohypertrophy). As the disease progresses, the muscles in the diaphragm that assist in breathing and coughing may weaken. Patients may experience breathing difficulties, respiratory infections, and swallowing problems. Bone thinning and scoliosis (curving of the spine) are common.

Some children are mildly mentally impaired. Between ages 3 and 6, children may show brief periods of physical improvement followed by progressive muscle degeneration. Children with Duchenne MD are typically wheelchair-bound by age 12 and usually die in their late teens or early twenties from progressive weakness of the heart muscle, respiratory complications, or infection.

Duchenne MD results from an absence of the muscle protein dystrophin. And blood tests of children with Duchenne MD show an abnormally high level of creatine kinase, which is apparent from birth.

2. Becker MD is less severe than but closely related to Duchenne MD. Persons with Becker MD have partial but insufficient function of the protein dystrophin. The disorder usually appears around age 11 but may occur as late as age 25, and patients generally live into middle age or later.

The rate of progressive, symmetric (on both sides of the body) muscle atrophy and weakness varies greatly among affected individuals.

Many patients are able to walk until they are in their mid-thirties or later, while others are unable to walk past their teens. Some affected individuals never need to use a wheelchair. As in Duchenne MD, muscle weakness in Becker MD is typically noticed first in the upper arms and shoulders, upper legs, and pelvis.

Early symptoms of Becker MD include:

Walking on one's toes

Frequent falls, and difficulty rising from the floor

Calf muscles may appear large and healthy as deteriorating muscle fibers are replaced by fat

Muscle activity may cause cramps in some people

Cardiac and mental impairments are not as severe as in Duchenne MD.

3. Congenital MD refers to a group of autosomal recessive muscular dystrophies that are either present at birth or become evident before age two. They affect both boys and girls. The degree and progression of muscle weakness and degeneration vary with the type of disorder.

Weakness may be first noted when children fail to meet landmarks in motor function and muscle control.

Muscle degeneration may be mild or severe and is restricted primarily to skeletal muscle. The majority of patients are unable to sit or stand without support, and some affected children may never learn to walk.

There are three groups of congenital MD:

Merosin-negative disorders, where the protein merosin (found in the connective tissue that surrounds muscle fibers) is missing;

Merosin-positive disorders, in which merosin is present but other needed proteins are missing; and

Neuronal migration disorders, in which very early in the development of the fetal nervous system the migration of nerve cells (neurons) to their proper location is disrupted.

Defects in the protein merosin cause nearly half of all cases of congenital MD.

Patients with congenital MD may develop contractures (chronic shortening of muscles or tendons around joints, which prevents the joints from moving freely), scoliosis, respiratory and swallowing difficulties, and foot deformities.

Some patients have normal intellectual development while others become severely impaired.

Weakness in diaphragm muscles may lead to respiratory failure.

Congenital MD may also affect the central nervous system, causing vision and speech problems, seizures, and structural changes in the brain. Some children with the disorders die in infancy while others may live into adulthood with only minimal disability.

4. Emery-Dreifuss MD primarily affects boys. The disorder has two forms: one is X-linked recessive and the other is autosomal dominant.

Onset of Emery-Dreifuss MD is usually apparent by age 10.

But symptoms can appear as late as the mid-twenties. This disease causes slow but progressive wasting of the upper arm and lower leg muscles and symmetric weakness. Contractures in the spine, ankles, knees, elbows, and back of the neck usually precede significant muscle weakness, which is less severe than in Duchenne MD.

Contractures may cause elbows to become locked in a flexed position. The entire spine may become rigid as the disease progresses.

Other symptoms include:

Shoulder deterioration

Toe-walking

Mild facial weakness

Serum creatine kinase levels may be moderately elevated

Nearly all Emery-Dreifuss MD patients have some form of heart problem by age 30, often requiring a pacemaker or other assistive device

Female carriers of the disorder often have cardiac complications without muscle weakness

Patients often die in mid-adulthood from progressive pulmonary or cardiac failure.

Youth/adolescent-onset muscular dystrophies are classified two ways:

1. Facioscapulohumeral MD (FSHD) initially affects muscles of the face (facio), shoulders (scapulo), and upper arms (humera) with progressive weakness. Also known as Landouzy-Dejerine disease, this third most common form of MD is an autosomal dominant disorder.

Life expectancy is normal, but some individuals become severely disabled. Disease progression is typically very slow, with intermittent spurts of rapid muscle deterioration. Onset is usually in the teenage years but may occur as late as age 40. Muscles around the eyes and mouth are often affected first, followed by weakness around the lower shoulders and chest. A particular pattern of muscle wasting causes the shoulders to appear to be slanted and the shoulder blades to appear winged. Muscles in the lower extremities may also become weakened. Reflexes are impaired only at the biceps and triceps.

Changes in facial appearance may include the development of a crooked smile, a pouting look, flattened facial features, or a mask-like appearance. Some patients cannot pucker their lips or whistle and may have difficulty swallowing, chewing, or speaking. Other symptoms may include hearing loss (particularly at high frequencies) and lordosis, an abnormal swayback curve in the spine.

Contractures are rare. Some FSHD patients feel severe pain in the affected limb. Cardiac muscles are not affected, and the pelvic girdle is rarely significantly involved. An infant-onset form of FSHD can also cause retinal disease and some hearing loss.

2. Limb-girdle MD refers to more than a dozen inherited conditions marked by progressive loss of muscle bulk and symmetrical weakening of voluntary muscles, primarily those in the shoulders and around the hips. At least three forms of autosomal dominant limb-girdle MD (known as type 1) and eight forms of autosomal recessive limb-girdle MD (known as type 2) have been identified. Some autosomal recessive forms of the disorder are now known to be due to a deficiency of any of four dystrophin-glycoprotein complex proteins called the sarcoglycans.

The recessive limb-girdle muscular dystrophies occur more frequently than the dominant forms, usually begin in childhood or the teenage years, and show dramatically increased levels of serum creatine kinase. The dominant limb-girdle muscular dystrophies usually begin in adulthood. In general, the earlier the clinical signs appear, the more rapid the rate of disease progression.

Limb-girdle MD affects both males and females.

Some forms of the disease progress rapidly, resulting in serious muscle damage and loss of the ability to walk, while others advance very slowly over many years and cause minimal disability, allowing a normal life expectancy. In some cases, the disorder appears to halt temporarily, but symptoms then resume.

Weakness is typically noticed first around the hips before spreading to the shoulders, legs, and neck. Patients develop a waddling gait and have difficulty when rising from chairs, climbing stairs, or carrying heavy objects. Patients fall frequently and are unable to run. Contractures at the elbows and knees are rare but patients may develop contractures in the back muscles, which gives them the appearance of a rigid spine.

Proximal reflexes (closest to the center of the body) are often impaired. Some patients also experience cardiomyopathy and respiratory complications. Intelligence remains normal. Most persons with limb-girdle MD become severely disabled within 20 years of disease onset.

There are three forms of MD that usually begin in adulthood.

1. Distal MD, also called distal myopathy, describes a group of at least six specific muscle diseases that primarily affect distal muscles (those farthest away from the shoulders and hips) in the forearms, hands, lower legs, and feet. Distal dystrophies are typically less severe, progress more slowly, and involve fewer muscles than other forms of MD, although they can spread to other muscles.

Distal MD can affect the heart and respiratory muscles.

Patients may eventually require the use of a ventilator. Patients may not be able to perform fine hand movement and have difficulty extending the fingers.

As leg muscles become affected, walking and climbing stairs become difficult and some patients may be unable to hop or stand on their heels. Onset of distal MD, which affects both men and women, is typically between the ages of 40 and 60 years. In one form of distal MD, a muscle membrane protein complex called dysferlin is known to be lacking.

Although distal MD is primarily an autosomal dominant disorder, autosomal recessive forms have been reported in young adults. Symptoms are similar to those of Duchenne MD but with a different pattern of muscle damage.

2. Myotonic MD, also known as Steinert's disease and dystrophia myotonica, may be the most common adult form of MD. Myotonia, or an inability to relax muscles following a sudden contraction, is found only in this form of MD. People with myotonic MD can live a long life, with variable but slowly progressive disability.

Typical disease onset is between ages 20 and 30, but it may develop earlier.

Myotonic MD affects the central nervous system and other body systems, including the heart, adrenal glands and thyroid, eyes, and gastrointestinal tract. Muscles in the face and the front of the neck are usually first to show weakness and may produce a haggard, "hatchet" face and a thin, swan-like neck. Wasting and weakness noticeably affect forearm muscles.

Other symptoms include:

Cardiac complications

Difficulty swallowing

Droopy eyelids (called ptosis)

Cataracts

Poor vision,

Early frontal baldness

Weight loss

Impotence

Testicular atrophy

Mild mental impairment

Increased sweating

Patients may also feel drowsy and have an excess need to sleep.

This autosomal dominant disease affects both men and women. Females may have irregular menstrual periods and may be infertile. The disease occurs earlier and is more severe in successive generations.

3. Oculopharyngeal MD (OPMD) generally begins in a person's forties or fifties and affects both men and women. In the United States, the disease is most common in families of French-Canadian descent and among Hispanic residents of northern New Mexico.

Patients first report drooping eyelids, followed by weakness in the facial muscles and pharyngeal muscles in the throat, causing difficulty swallowing. The tongue may atrophy and changes to the voice may occur.

Eyelids may droop so dramatically that some patients compensate by tilting back their heads. Patients may have double vision and problems with upper gaze, and others may have retinitis pigmentosa (progressive degeneration of the retina that affects night vision and peripheral vision) and cardiac irregularities.

Muscle weakness and wasting in the neck and shoulder region is common. Limb muscles may also be affected. Persons with OPMD may find it difficult to walk, climb stairs, kneel, or bend. Those persons most severely affected will eventually lose the ability to walk.

Diagnosing Muscular Dystrophy

Both the patient's medical history and a complete family history should be thoroughly reviewed to determine if the muscle disease is secondary to a disease affecting other tissues or organs or is an inherited condition.

It is also important to rule out any muscle weakness resulting from prior surgery, exposure to toxins, or current medications that may affect the patient's functional status. Thorough clinical and neurological exams can rule out disorders of the central and/or peripheral nervous systems, identify any patterns of muscle weakness and atrophy, test reflex responses and coordination, and look for contractions.

Laboratory Tests Confirm The Diagnosis Of MD.

Blood and urine tests can detect defective genes and help identify specific neuromuscular disorders. For example:

The level of serum aldolase, an enzyme involved in the breakdown of glucose, is measured to confirm a diagnosis of skeletal muscle disease. High levels of the enzyme, which is present in most body tissues, are noted in patients with MD and some forms of myopathy.

Creatine kinase is an enzyme that leaks out of damaged muscle. Elevated creatine kinase levels may indicate muscle damage, including some forms of MD, before physical symptoms become apparent. Levels are significantly increased in patients in the early stages of Duchenne and Becker MD. Testing can also determine if a young woman is a carrier of the disorder.

Myoglobin is measured when injury or disease in skeletal muscle is suspected. Myoglobin is an oxygen-binding protein found in cardiac and skeletal muscle cells. High blood levels of myoglobin are found in patients with MD.

Polymerase chain reaction (PCR) can detect mutations in the dystrophin gene. Also known as molecular diagnosis or genetic testing, PCR is a method for generating and analyzing multiple copies of a fragment of DNA.

Serum electrophoresis is a test to determine quantities of various proteins in a person's DNA. A blood sample is placed on specially treated paper and exposed to an electric current. The charge forces the different proteins to form bands that indicate the relative proportion of each protein fragment.

Electron Microscopy Identifies Changes In Sub-cellular

Components Of Muscle Fibers

Electron microscopy can also identify changes that characterize cell death, mutations in muscle cell mitochondria, and an increase in connective tissue seen in muscle diseases such as MD. Changes in muscle fibers that are evident in a rare form of distal MD can be seen using an electron microscope.

Exercise Tests Detect Chemical Elevations

Exercise tests can detect elevated rates of certain chemicals following exercise and are used to determine the nature of the MD or other muscle disorder.

Some exercise tests can be performed at the patient's bedside while others are done at clinics or other sites using sophisticated equipment. These tests also assess muscle strength. They are performed when the patient is relaxed and in the proper position to allow technicians to measure muscle function against gravity and detect even slight muscle weakness. If weakness in respiratory muscles is suspected, respiratory capacity may be measured by having the patient take a deep breath and count slowly while exhaling.

Genetic Testing Pinpoints Genes Associated With MD

Genetic testing looks for genes known to either cause or be associated with inherited muscle disease.

DNA analysis and enzyme assays can confirm the diagnosis of certain neuromuscular diseases, including MD. Genetic linkage studies can identify whether a specific genetic marker on a chromosome and a disease are inherited together. They are particularly useful in studying families with members in different generations who are affected. An exact molecular diagnosis is necessary for some of the treatment strategies that are currently being developed.

Genetic Counseling Reveals Parental Carriers

Genetic counseling can help parents who have a family history of MD determine if they are carrying one of the mutated genes that cause the disorder.

Two tests can be used to help expectant parents find out if their child is affected.

1. Amniocentesis, done usually at 14-16 weeks of pregnancy, tests a sample of the amniotic fluid in the womb for genetic defects (the fluid and the fetus have the same DNA). Under local anesthesia, a thin needle is inserted through the woman's abdomen and into the womb. About 20 milliliters of fluid (roughly 4 teaspoons) is withdrawn and sent to a lab for evaluation. Test results often take 1-2 weeks.

2. Chorionic villus sampling, or CVS, involves the removal and testing of a very small sample of the placenta during early pregnancy. The sample, which contains the same DNA as the fetus, is removed by catheter or a fine needle inserted through the cervix or by a fine needle inserted through the abdomen. The tissue is tested for genetic changes identified in an affected family member. Results are usually available within 2 weeks.

Testing Muscle Tissue Monitors Progression And Treatment Effectiveness

Magnetic resonance imaging (MRI) is used to examine muscle quality, any atrophy or abnormalities in size, and fatty replacement of muscle tissue, as well as to monitor disease progression. MRI scanning equipment creates a strong magnetic field around the body. Radio waves are then passed through the body to trigger a resonance signal that can be detected at different angles within the body. A computer processes this resonance into either a three-dimensional picture or a two-dimensional "slice" of the tissue being scanned. MRI is a noninvasive, painless procedure.

Muscle biopsies are used to monitor the course of disease and treatment effectiveness. Using a local anesthetic, a small sample of muscle is removed and studied under a microscope. The sample may be gathered either surgically, through a slit made in the skin, or by needle biopsy, in which a thin hollow needle is inserted through the skin and into the muscle. A small piece of muscle remains in the hollow needle when it is removed from the body. The muscle specimen is stained and examined to determine whether the patient has muscle disease, nerve disease (neuropathy), inflammation, or another myopathy.

Immunofluorescence testing can detect specific proteins such as dystrophin within muscle fibers. Following biopsy, fluorescent markers are used to stain the sample that has the protein of interest.

Neurophysiology Studies Identify Physical And/Or Chemical

Changes In The Nervous System

Electromyography (EMG) can record muscle fiber and motor unit activity. A tiny needle containing an electrode is inserted through the skin into the muscle. The electrical activity detected in the muscle can be displayed either in printout form or on a monitor, and can also be heard when played through a speaker. Results may reveal electrical activity characteristic of MD. Each electrode displays an average of that muscle's activity. Several electrodes may be needed to display activity in large skeletal muscles.

Nerve conduction velocity studies measure the speed with which an electrical signal travels along a nerve. A small electrode sends a signal to a receiving electrode placed elsewhere along the nerve. The length of the nerve between the electrodes is divided by the time needed for the signal to travel between them. The response can be used to determine any nerve damage.

Repetitive stimulation studies involve electrically stimulating a nerve 5 to 10 times, at a frequency of 2-3 shocks per second, to study muscle function. A mild shock is sent via electrodes that are taped to the skin on top of the muscle(s) to be tested and the response is displayed on an oscilloscope, an instrument used to examine electrical signals. A nerve is then stimulated at another site to evaluate electrical activity down the nerve, across the neuromuscular junction, and into the muscle.

Summary

The nine different forms of muscular dystrophy differ in the muscles affected, the age of onset, and its rate of progress. The prognosis varies according to the type of MD and the speed of progression. Some types are mild and progress very slowly, allowing normal life expectancy, while others are more severe and result in functional disability and loss of ambulation. Life expectancy may depend on the degree of muscle weakness and any respiratory and/or cardiac complications.

To make matters worse:

Conventional Treatments Can’t Stop Or Reverse

The Progression Of Any Form Of MD

All forms of MD are genetic and can’t be prevented.

Current treatment is aimed at keeping the patient independent for as long as possible and preventing complications that result from weakness, reduced mobility, and cardiac and respiratory difficulties. Treatment may involve a combination of approaches, including physical therapy, drug therapy, and surgery.

Assisted ventilation is often needed to treat respiratory muscle weakness that accompanies many forms of MD, especially in the later stages.

Drug therapy may be prescribed to delay muscle degeneration, though they have dangers of their own.

Physical therapy can help prevent deformities, improve movement, and keep muscles as flexible and strong as possible.

Support aids such as wheelchairs, splints and braces, other orthopedic appliances, and overhead bed bars (trapezes) can help maintain mobility.

Repeated low-frequency bursts of electrical stimulation to the thigh muscles can produce a slight increase in strength in boys with Duchenne MD.

Speech therapy may help patients whose facial and throat muscles have weakened.

Special exercises, or a special diet and feeding techniques, can help MD patients who have a swallowing disorder.

Dietary changes have not been shown to slow the progression of MD.

Occupational therapy may help some patients deal with progressive weakness and loss of mobility.

And corrective surgery is often performed to ease complications from MD.

Despite these efforts, the prognosis is almost always ill-fated, if not fatal.

But finally, there is an exciting new possibility available for children and adults living with muscular dystrophy.

How To Reverse Muscular Dystrophy, Naturally

We’re thrilled to announce now there is a safe and effective supplement with tremendous potential to improve or even reverse MD. The protocol I strongly recommend is relatively new. However, we are strongly convinced the chance of seeing remarkable improvement in many areas of your health, including return of muscle strength and ambulation, is very promising.

I’m sure you’re wondering why your doctor hasn’t told you about this supplement. Frankly, the reason is because he doesn’t know about it. Most doctors are only comfortable with pharmaceutical drugs on the market and often don’t look outside the conventional protocol. However, that doesn’t change the fact that these supplements have the potential to restore and transform your life.

There are so many reasons to be optimistic. Over the years we have learned about supplements with an astonishing ability to reawaken, revitalize, and strengthen the function of cells. As a matter of fact, our number one supplement suggestion may actually revolutionize the treatment and consequent reversal of muscular dystrophy.

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We now know this life-renewing supplements show promising results in reviving dystrophic cells.

The remainder of this report is dedicated to explaining how Rejuvin works and how to use it.

Rejuvin Protocol For Muscular Dystrophy

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As you may not be familiar with frequency enhanced water, let me explain a bit more about how it works. As modern physics has shown, everything has an energetic frequency specific to it and constantly emits this subtle vibratory frequency. Water has the property of being able to pick up vibrations it is exposed to and capture them in the water. Water has even been considered for possible use as computer memory for this very reason.

For 200 years homeopathy has made use of this ability of water. The water in homeopathic drops is transmitting to your body the frequency of the substance to which it was exposed. In the 1990s, French biochemist, Jacques Benveniste showed that molecules of other substances use water for communication, and that water acts as a transmitter of stored physical and vibrational energy. He is a respected scientist whose experiments observed quantifiable effects on living cells using accepted scientific methodology. His experiments showed that water does retain and transfer information, and its molecular structure allows it to act as a transmitter and receptor of vibrational information.

Rejuvin Transmits Revitalizing Molecular Messages To Cells

Just like a radio transmission, water has the ability to allow molecules to communicate with touching each other, via their specific vibrations. So water has the ability to allow molecules to interact within a cell, and to conduct molecular messages so that they reach different parts of the body via the watery fluids between the cells.

Cells pick up information from frequency enhanced water because they too communicate via vibrations. Cells could be described as a bioelectronic factory and radio receiver, vibrating at specific frequencies. Healthy cells have their own frequency.

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With Rejuvin, water is used to capture the frequencies that took two years to develop. When you drink small amounts of this water these frequencies are transferred to the watery fluids in your body, and literally send messages to the cells. The instructions from Rejuvin stimulates the rejuvenation of the cells including the cells in the muscles. After about three months of drinking Rejuvin your cells are made strong enough to even resist the flu and cold viruses, the SARS virus, or even herpes virus.

You will need to use 3 liters of Rejuvin a month. In 2 to 3 months you’ll see improvement. It will take 5 to 9 months of taking three ounces of Rejuvin a day to reverse muscular dystrophy.

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Disclaimer: These statements have not been evaluated by the Food and Drug Administration. The products and information contained herein are not intended to diagnose, treat, cure, or prevent any diseases or medical problems. It is not intended to replace your doctor's recommendations. The information is provided for educational purposes only. Nutritional benefits may vary from one person to another.