Myostatins myotonic dystrophy and bodybuilding

Protein is a vital part of your diet. Consisting of a variety of amino acids, proteins compound and fuse to regulate virtually every aspect of your body. Genetics play an important part in how and where those proteins are used – and how long they endure. Different proteins aid muscle development and use. They also help cellular growth. Over the last decade, researchers have isolated some proteins that can hinder and harm muscles and cells. Some may occur in birth others occur in your life span. Myostatin is a probable protein compound that does both. It is part of the roots of muscle diseases from dystrophies to recent diseases like DDX3X that affect many lives. Isolation of myostatin as having a role is a small part of a huge puzzle thwarting treatments and cures.

Myostatins are a group of micronutrients that bodybuilders use to control muscle growth. Most people have them naturally but, through aging process, there is muscle loss. Myostatins have this strange side-effect. They aid in the eventual wasting of muscle growth.

Myostatin inhibitors have been a rage in muscular and fitness. Some competitive athletes were disqualified for using supplements or gene-doping to produce enhanced performance effects. There are many muscle issues with natural aging and an entire list of neurological and muscle wasting diseases. Is it worth the excitement?

Myostatin is a secreted protein that acts as a negative regulator of skeletal muscle mass. During embryo-genesis (within the womb), myostatin is expressed by cells in the myotome (group of muscles that a single spinal nerve innervates) and in developing skeletal muscle and acts to regulate the final number of muscle fibers that are formed. The MSTN gene provides instructions for making a protein called myostatin. Myostatin is found almost exclusively in muscles used for movement (skeletal muscles), where it is active both before and after birth. This protein normally restrains muscle growth, ensuring that muscles do not grow too large.

The general theories to stop this myostatin-based muscle wasting is to inhibit this protein from infecting those muscles. Myostatin inhibitors are found in foods as phytonutrients – naturally occurring micronutrients:

Green tea
Chocolate (especially dark chocolate and raw cocoa powder)
Blackberries
Pomegranates
Broad beans (e.g. Fava Beans)

In the body, Myostatin is produced by the muscle tissue of the heart, and damage to the heart causes it to be released into the bloodstream. It is associated with potential muscle loss of heart tissue in people with heart disease. This may also be associated with producing naturally high LDL cholesterol levels within that group. It may also trigger low HDL and high triglyceride measurements within a cardiac lipid panel in repeated serum tests.

High myostatin levels are associated with muscle wasting and may be associated with many diseases. Research on animals indicate that Myostatin levels may be significantly higher in patients with diseases like amyotrophic lateral sclerosis (ALS), Duchenne muscular dystrophy, myotonic dystrophy and multiple sclerosis, among other neurological and muscle diseases. Disease diagnosis usually demonstrates a genetic cause. Those myostatin levels and muscular atrophy may be the result of this genetic impulse. Myostatin levels may show why drugs for Duchenne Muscular Dystrophy do not work.

So…it seems that myostatin inhibition might lead to helping people with muscle weakness but it isn’t easy. It’s very complicated. There are other proteins that have been influenced over time. For example, BP3 is a protein that may be involved in eliminating obesity. These proteins need co-factors to allow certain effects. Myostatin inhibition has to coincide with BP3 to trigger fat loss and muscle re-development.

One possible concern, according to Dr. Markus Schuelke, the pediatric neurologist at Charite University Medical Center in Berlin who discovered the myostatin mutation in the baby, is that blocking myostatin could interfere with satellite cells that help replace injured or dead muscle cells. It’s thought that myostatin helps keep the satellite cells at rest until they’re needed, and it’s possible that without myostatin the satellite cells could become depleted.

There are many conflicting opinions that myostatin blockers may be too targeted to boost muscle growth, as there are a variety of proteins similar to myostatin that also limit muscle growth.

There are several potential downsides to be aware of when using myostatin inhibitors for athletic enhancement.

One potential concern is that increased muscle growth will lead to an increased risk of injury due to increased stress on the muscle fibers. This is especially true for individuals using myostatin inhibitors as workout supplements instead of as part of a medical treatment for muscular dystrophy or other disorders. Muscle stress is linked with increased muscle atrophy among the various dystrophy illnesses.

It has been noted that drugs that induce myostatin inhibition may lead to higher probable risks of injury.

Other possible side effects of myostatin inhibitors include increased the chance of tendon rupture, heart failure due to inflamed cardiac muscle, and rhabdomyolysis, a breakdown of muscle fibers that often leads to kidney failure.

Meanwhile, vitamin supplement shelves have many products offering myostatin inhibitors in a bottle. They have many ingredients. Neither of these have been thoroughly tested by the FDA or European health organizations.

If myostatins and concordant protein compound interactions of the weaknesses of myotonia bring clues, treatments and cures are even more sophisticated as transport pathways may differ. Are transport pathways different because age or disease exist? Or were those pathways results from genetic instructions? Anyway, key muscles just do not work properly. That is myotonia.

Myostatin is a statin compound. Statins may irritate and amplify the effects of muscular dystrophy. Those with muscular dystrophies heart disease are told to avoid statins. The misuse of statins can produce some very insidious muscle effects without muscular dystrophy incidence.

According to WebMD, possible statin side effects among average people may be:
Headache
Difficulty sleeping
Flushing of the skin
Headache
Difficulty sleeping
Flushing of the skin
Muscle aches, tenderness, or weakness (myalgia)
Drowsiness
Dizziness
Nausea or vomiting
Abdominal cramping or pain
Bloating or gas
Diarrhea
Constipation
Rash
Drowsiness
Dizziness
Nausea or vomiting
Abdominal cramping or pain
Bloating or gas
Diarrhea
Constipation
Rash
Memory Loss

If muscle aches and weakness occur in people without muscular dystrophy, you might imagine how myostatin may effect those with muscular dystrophies.

The problems lie in the etiology or source among what makes muscles weak. For those with muscle wasting diseases – congenital and adult – the fantasy that myostatin inhibitors may work brings glimmers of hope. But will it heal the damages already done? There are research studies and results that are still clinically inconclusive. It may still be a long process ahead with many pathways. How myostatin works, how inhibitors work, and how dystrophic muscles vary are just a few of many questions that need thorough answers.

As I wrote this article, new DMD1 research is coming from UK using Tideglusib, as a pharmacological approach:

AMO-02 (tideglusib) is in development for the treatment of congenital myotonic dystrophy and has potential for use in additional CNS, neuromuscular and oncology indications. AM0-02 is positioned to enter clinical stage development for the treatment of the severe form of congenital myotonic dystrophy known as DM1 or Steinert disease. In cellular and animal models of DM1 and Duchenne muscular dystrophy, as well as in muscle biopsies from patients, activity of glycogen synthase kinase 3 beta (GSK3ß) has been shown to increase. Inhibitors of GSK3ß have been shown to correct the activity of regulatory proteins, such as CUGBP1 in animal models of DM1. AMO-02 is an inhibitor of GSK3ß that has demonstrated pre-clinical efficacy in transgenic models and reversal of muscle cell deficits in ex vivo tissue samples in patients with DM1.

I will follow this and see how it develops.

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