Muscle weakness / wasting linked to poor mitochondrial function

[haidut]

A study that once again illustrates the central principle of bioenergetics - structure and function cannot be separated. They are interdependent at every level. In this specific case, the "structural" pathology is muscle weakness and wasting (sarcopenia, cachexia, etc). Most doctors, when evaluating such condition, will look for structural problems such as genetic mutations, trauma, fibrosis, tumors, etc that may lead to this condition. If none such causes are found then the disorder will be declared "functional" and treated "supportively" by managing the symptoms so that the "quality of life" of the patient is maintained as much as possible. In other words, medicine would give up on trying to cure the condition because the issue is not "structural". Well, the study below demonstrates that this structural condition has a very functional origin. Namely, poor mitochondrial function, which led to decreases ATP levels and CO2 production, and decreased levels of mDNA synthesis (a hallmark of mitochondrial pathology). As such, it suggests that most such muscle wasting conditions may (and should?) be treated by simply improving the energetic flow through dietary and supplement interventions. Increased glucose, saturated fats (as they stimulate mitochondrial biogenesis), niacinamide, thiamine, methylene blue, CoQ10, progesterone, DHEA, T/DHT, etc.

Muscle atrophy induced by overexpression of ALAS2 is related to muscle mitochondrial dysfunction

Muscle Weakness Linked to Poorly Working Mitochondria in Porphyria...

The findings may provide new insights into the causes of porphyria, a team of researchers from China asserts.

porphyrianews.com

"...Upon close examination of pieces of tissue taken from the quadriceps, they found that transgenic mice had a high number of muscle fibers with centrally located nuclei. This particular feature is a clear sign of muscle disease. In contrast, in normal, wild-type muscle fibers, nuclei were located at the periphery and were distributed evenly. Moreover, in transgenic mice, the average diameter of single muscle fibers was almost half that of wild-type mice. In addition to being thinner, muscle fibers from transgenic also were damaged, as showcased in another experiment in which investigators used a special dye called Evans blue. This dye was able to enter into muscle fibers of transgenic animals — a clear sign of muscle tissue breakdown — but not those of wild-type mice. At the molecular level, transgenic mice had smaller amounts of certain muscle-specific proteins involved in the breakdown of proteins into smaller amino acids (protein building blocks). The researchers suggested this reduction may be “a protective attempt to reduce further muscle wasting.” To meet their energy demands, muscle fibers have multiple mitochondria. Researchers wondered if mitochondria damage could explain muscle weakness and wasting in transgenic mice. Using a transmission electron microscope to obtain highly magnified images of muscle fibers, they found that mitochondria of transgenic, but not of wild-type mice, were swollen. Mitochondrial swelling is a sign that mitochondria may not be working properly. More experiments revealed that mitochondria found in the muscles of transgenic animals produced less adenosine triphosphate (ATP) — the cell’s main energy source — than those found in the muscles of healthy mice. Overall, the researchers concluded that muscle weakness/atrophy in transgenic mice could be linked to poorly working mitochondria."

 

[Peatness]

Mitochondrial dysfunction in fibrotic diseases - Cell Death Discovery

Although fibrosis is a common pathological feature of most end-stage organ diseases, its pathogenesis remains unclear. There is growing evidence that mitochondrial dysfunction contributes to the development and progression of fibrosis. The heart, liver, kidney and lung are highly...

www.nature.com

 

[Lana]

A study that once again illustrates the central principle of bioenergetics - structure and function cannot be separated. They are interdependent at every level. In this specific case, the "structural" pathology is muscle weakness and wasting (sarcopenia, cachexia, etc). Most doctors, when evaluating such condition, will look for structural problems such as genetic mutations, trauma, fibrosis, tumors, etc that may lead to this condition. If none such causes are found then the disorder will be declared "functional" and treated "supportively" by managing the symptoms so that the "quality of life" of the patient is maintained as much as possible. In other words, medicine would give up on trying to cure the condition because the issue is not "structural". Well, the study below demonstrates that this structural condition has a very functional origin. Namely, poor mitochondrial function, which led to decreases ATP levels and CO2 production, and decreased levels of mDNA synthesis (a hallmark of mitochondrial pathology). As such, it suggests that most such muscle wasting conditions may (and should?) be treated by simply improving the energetic flow through dietary and supplement interventions. Increased glucose, saturated fats (as they stimulate mitochondrial biogenesis), niacinamide, thiamine, methylene blue, CoQ10, progesterone, DHEA, T/DHT, etc.

Muscle atrophy induced by overexpression of ALAS2 is related to muscle mitochondrial dysfunction

Muscle Weakness Linked to Poorly Working Mitochondria in Porphyria...

The findings may provide new insights into the causes of porphyria, a team of researchers from China asserts.

porphyrianews.com

"...Upon close examination of pieces of tissue taken from the quadriceps, they found that transgenic mice had a high number of muscle fibers with centrally located nuclei. This particular feature is a clear sign of muscle disease. In contrast, in normal, wild-type muscle fibers, nuclei were located at the periphery and were distributed evenly. Moreover, in transgenic mice, the average diameter of single muscle fibers was almost half that of wild-type mice. In addition to being thinner, muscle fibers from transgenic also were damaged, as showcased in another experiment in which investigators used a special dye called Evans blue. This dye was able to enter into muscle fibers of transgenic animals — a clear sign of muscle tissue breakdown — but not those of wild-type mice. At the molecular level, transgenic mice had smaller amounts of certain muscle-specific proteins involved in the breakdown of proteins into smaller amino acids (protein building blocks). The researchers suggested this reduction may be “a protective attempt to reduce further muscle wasting.” To meet their energy demands, muscle fibers have multiple mitochondria. Researchers wondered if mitochondria damage could explain muscle weakness and wasting in transgenic mice. Using a transmission electron microscope to obtain highly magnified images of muscle fibers, they found that mitochondria of transgenic, but not of wild-type mice, were swollen. Mitochondrial swelling is a sign that mitochondria may not be working properly. More experiments revealed that mitochondria found in the muscles of transgenic animals produced less adenosine triphosphate (ATP) — the cell’s main energy source — than those found in the muscles of healthy mice. Overall, the researchers concluded that muscle weakness/atrophy in transgenic mice could be linked to poorly working mitochondria."

years ago I took metronidazole and nearly lost my life . I’m in the toxicity group where i learned to acquire thiamin and address the deficiencies it causes . It is a protozoal drug and inhibits protein synthesis. Which has caused changes to our bodies structure as I and other women in the group have gone from toned to soft and blubbery . A few women have reported their breasts have turned into water bags including mine !!! Does anyone have any idea how to address this ? Is it time that will just maybe possibly heal . What induces protein synthesis again to get the body back to shape

 

[Peatress]

years ago I took metronidazole and nearly lost my life . I’m in the toxicity group where i learned to acquire thiamin and address the deficiencies it causes . It is a protozoal drug and inhibits protein synthesis. Which has caused changes to our bodies structure as I and other women in the group have gone from toned to soft and blubbery . A few women have reported their breasts have turned into water bags including mine !!! Does anyone have any idea how to address this ? Is it time that will just maybe possibly heal . What induces protein synthesis again to get the body back to shape

Any update on your muscle weakness? Any improvement?

Nitrofurantoin also causes similar muscle weakness. I had a bad reaction to it a few years ago.

Nitrofurantoin Monograph for Professionals - Drugs.com

Nitrofurantoin reference guide for safe and effective use from the American Society of Health-System Pharmacists (AHFS DI).

www.drugs.com

"Peripheral neuropathy, which may be severe or irreversible, reported rarely; fatalities have occurred.

Initial symptoms include paresthesia and dysesthesia, usually of the lower extremities, which may progress to muscle weakness and muscle wasting. Severe neuropathy is characterized by edema of interstitial tissues, demyelination of peripheral nerve fibers, and secondary changes in the spinal cord and striated muscles.

Severity of symptoms and rate of recovery are not related to dosage or total amount of drug administered. Resolution varies inversely with severity of muscle weakness.

Risk of peripheral neuritis increased in patients with renal impairment (Clcr <60 mL/minute or clinically important Scr elevations), anemia, diabetes mellitus, electrolyte imbalance, vitamin B deficiency, and debilitating disease."

 

[yerrag]

I currently experience muscle weakness that coincides with having reduced breathing function (a result of using cinnamon bark oil orally in the wrong way).

Because I cannot breathe in oxygen and breathe out CO2 as freely as a result, I may be considered suffering from COPD (congestive obstructive pulmonary disease). And I now know how if feels o suffer from emphysema that smokers suffer from.

During this time when the mucous membranes have not fully recovered from inflammation caused by being exposed to cinnamon bark oil, I experience the downstream consequences of having less oxygen coming in and of CO2 going out from the lungs. Because of the respiratory acidosis (due to inability to exhale as much CO2 the body normally would exhale) I'm in, my blood and ecf is in a more acidic state. Because of this chronic acidic state, the the rate of relaxation of my muscles is slower, and I feel older. My left foot walks and lands differently, with less resolve and with slower reflexes, and I have fallen a few times because my left foot fails to execute what my mind wants it to. When I type, I miss making a few keys click, and miss a letter every now and then.

I cannot engage in a sport, be it in gaming or in physical games like tennis or basketball.


This illustrates the importance of having a perfect set of lungs to deliver oxygen and to excrete carbon dioxide out of the blood in our circulatory system.

When oxygen is lacking, or when CO2 is restricted from being released thru our lungs, there is less energy available to power our muscles, and there is also a slower reflex in the muscles. The motor nerves may give instructions, but the muscles cannot follow the command fully - in both voluntary peripheral muscles as well as in autonomic muscle movement. I can't walk with the gait I am used to, and I find myself drooling when I normally don't.

Is this a functional problem or is this structural? The problem is in the lungs, and as my lungs recover, the less and less I expect to see these problems.

Currently, my heart rate is in the 90s where it used to be in the high 60s, but I do not mistake this as improved metabolism, but a heart straining to make up for a slow relaxation time, a result of a suboptimal pH in the ecf, which is acidic, and which greatly affect the relaxation rate of muscles, the heart being a muscle itself.

Because of the slower muscle relaxation rate, my ECG QTc is longer than usual, but knowing this I don't see this as a primary hypothyroid problem, but as a primary lung problem where efficient gas exchange is impeded by mucous membranes that have undergone inflammation and breakdown and are recovering from the trauma induced by exposure to cinnamon bark oil.

It has been a month of learning from my mistake of using cinnamon bark oil wrongly and I'm glad it afforded me the opportunity of seeing how my body deteriorated as a result, and for me to understand the consequences. I hope my lungs recover fully so the muscular weakness issues would go away eventually.