mitodicure..promising or not?

[Carl]

Are there any such herbalists in the UK does anyone know?

I have been to a few herbalists in the UK, both TCM and traditional western and the western one despite having lots of certificates proclaiming her qualifications didn't really know much IMO. The TCM ones helped a little and it was what helped me find a very useful herb. However they could not really solve it despite TCM having herbs which could go some way to destroying the pathogens if used correctly with other things. It's the research which sucks, driven by false information propagated by drug companies attempting to preserve their drug sales. When someone else finally works it out it could have devastating consequences which is why there is so much false research to maintain the false information. Almost all the information on "leaky gut" is false and incorrect. I strongly disagree with the term "leaky gut" but even a perfect digestive system is leaky by nature. It is the degree of permeability which is crucial and permeability is affected by pathogens. I won't go into details about how and why but my ideas explain everything related to ME. The only research which gets closer than most other ME research is the research by Daniel Vipond where his research was funded by a ME charity. Sadly it didn't actually find where the pathogen(s) are located. I however did just after he began his research in Jan 2014. Unfortunately in 2015 I was bitten by a tick and developed lyme disease despite no positive lyme test and still no test for Bartonella which is causing me serious problems and could yet kill me.

A role for a leaky gut and the intestinal microbiota in the pathophysiology of Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) - Daniel T. Vipond
That largely guesses what the problem is but that is still substantially more advanced than most research on Increased Digestive Permeability. When the biofilm(s) have been eliminated the human digestive system will heal the digestive system without consuming Glutamine/glutamic acid etc. It heals fairly quickly within about 20 minutes, or did so in me when I destroy approx 2/3rds of the largest biofilm but not the one causing my ME which is very highly resistant. Without correcting that it is like sticking a plaster on a broken leg because it will not stop the damaging inflammation or the bodily control exerted by the hypothalamus and pituitary gland. I strongly believe that there is a cover up which is trying to make it seem like people can "think" their way out of ME. Thinking will not destroy pathogenic biofilm protected micro-organisms.

Everything adds up when you think correctly and approach it from the correct angle.

Of the four large biofilms, I am certain what the one that I partly destroy is, Staph sp. and the one which causes my ME I believe could be Klebsiella pneumoniae but the other two I have no clue as to what pathogens are responsible. All of these affect the permeability of my colon causing a massive amount of LPS absorption. I am now looking at Candida because that might be part of those other two biofilms, despite not really having any symptoms of Candida. They could potentially also be protozoa. Nothing I have ever taken has affected them to my knowledge, at least no symptoms. Whereas the other two have on many occasions to some degree.

 

[Dude]

**The Hypothesis of Wirth and Scheibenbogen:**

**ME/CFS is caused by a disturbed ion exchange in muscle cells, damaging the mitochondria. This leads to a negative spiral where mitochondria are further destroyed, explaining the symptoms of ME/CFS and Post-Exertional Malaise (PEM).**

1. **Circulatory Disturbance & Ion Exchange**

* Infections can damage the endothelium (cell layer on the inside of blood vessels), disrupting blood flow through the capillaries,
* leading to oxygen deficiency in muscles and organs.

2. **Response to Strain**

* During activity, muscles require more oxygen and nutrients, but due to circulatory disturbances, this need is not met.
* The body responds by increasing the pulse, further lowering blood pressure in the capillaries.

3. **Disturbance of the Sodium-Calcium Exchanger (NCX)**

* Normally, the NCX transports calcium out of the muscle cells and brings sodium in.
* In ME/CFS, sodium levels rise significantly due to circulatory disturbances and oxygen deficiency.
* If the sodium content exceeds a certain threshold, the NCX reverses its function, transporting calcium into the cells instead of pumping it out.

4. **Consequences**

* The overload of muscle cells with calcium damages the mitochondria, which are responsible for energy production in the cells.
* Damaged mitochondria release aggressive oxygen radicals, further lowering ATP levels (important for cellular energy) and additionally inhibiting the sodium-potassium ATPase (an ion pump).

5. **PEM & Vicious Circle**

* Upon renewed strain, the weakened mitochondria suffer further damage.
* This gradually reduces the number of functional mitochondria.
* When intracellular sodium reaches a critical level, the NCX switches and causes another calcium overload,
* leading to a marked worsening of symptoms (PEM).
* This endless spiral continuously worsens the health condition.

Mitodicure plans to begin the Phase 1 study for the ME/CFS drug candidate in autumn 2025, depending on securing investors/funding!

Article: [RiffReporter](https://www.riffreporter.de/de/wissen/mecfs-long-covid-corona-pathomechanismus-mitochondrien-wirth-scheibenbogen-mitodicure)


The article is behind a paywall, but for those interested in detailed information, including studies, it is well worth the cost.

 

[tyson oberle]

**The Hypothesis of Wirth and Scheibenbogen:**

**ME/CFS is caused by a disturbed ion exchange in muscle cells, damaging the mitochondria. This leads to a negative spiral where mitochondria are further destroyed, explaining the symptoms of ME/CFS and Post-Exertional Malaise (PEM).**

1. **Circulatory Disturbance & Ion Exchange**

* Infections can damage the endothelium (cell layer on the inside of blood vessels), disrupting blood flow through the capillaries,
* leading to oxygen deficiency in muscles and organs.

2. **Response to Strain**

* During activity, muscles require more oxygen and nutrients, but due to circulatory disturbances, this need is not met.
* The body responds by increasing the pulse, further lowering blood pressure in the capillaries.

3. **Disturbance of the Sodium-Calcium Exchanger (NCX)**

* Normally, the NCX transports calcium out of the muscle cells and brings sodium in.
* In ME/CFS, sodium levels rise significantly due to circulatory disturbances and oxygen deficiency.
* If the sodium content exceeds a certain threshold, the NCX reverses its function, transporting calcium into the cells instead of pumping it out.

4. **Consequences**

* The overload of muscle cells with calcium damages the mitochondria, which are responsible for energy production in the cells.
* Damaged mitochondria release aggressive oxygen radicals, further lowering ATP levels (important for cellular energy) and additionally inhibiting the sodium-potassium ATPase (an ion pump).

5. **PEM & Vicious Circle**

* Upon renewed strain, the weakened mitochondria suffer further damage.
* This gradually reduces the number of functional mitochondria.
* When intracellular sodium reaches a critical level, the NCX switches and causes another calcium overload,
* leading to a marked worsening of symptoms (PEM).
* This endless spiral continuously worsens the health condition.

Mitodicure plans to begin the Phase 1 study for the ME/CFS drug candidate in autumn 2025, depending on securing investors/funding!

Article: [RiffReporter](https://www.riffreporter.de/de/wissen/mecfs-long-covid-corona-pathomechanismus-mitochondrien-wirth-scheibenbogen-mitodicure)


The article is behind a paywall, but for those interested in detailed information, including studies, it is well worth the cost.

I paid to read the article, but it doesn't say how to get a diagnosis regarding sodium-calcium in the muscle cells. Dude do you or anyone else know what tests that we can do to see if there's a problem with the sodium-calcium balance in the muscle cells?

 

[Dude]

@tyson oberle

This is part of the hypothesis. The article states that in an experimental study, it was found that the sodium content in the muscle cells of ME/CFS patients is elevated. Scheibenbogen referred to the disturbance of muscular ion transport as the "cause of PEM and muscular fatigue."

Therefore, it might not be so easy to test.
However, further down in the article, it is mentioned that initial experiments show that muscle fatigue can be halted by stimulating the sodium-potassium ATPase with the candidate drug.

 

[Wishful]

it was found that the sodium content in the muscle cells of ME/CFS patients is elevated.

Is this the usual "difference found between inactive patients and healthy, active controls?", meaning that the difference might not be due to ME itself? ATP stimulation might be working on changes due to inactivity.

 

[Dude]

Is this the usual "difference found between inactive patients and healthy, active controls?", meaning that the difference might not be due to ME itself? ATP stimulation might be working on changes due to inactivity.

This is the Study from the findings:
https://translational-medicine.biomedcentral.com/articles/10.1186/s12967-022-03616-z

The number of participants is very small and the procedure very complex, but the study shows that muscle sodium content before and after exercise was higher in ME/CFS patients than in healthy controls. Additionally, there was a correlation between muscle sodium content and handgrip strength.

In my opinion, this makes sense: the more severe the patient's condition, the less ATP energy is available for the sodium-potassium ATPase, leading to quicker muscle fatigue as the sodium content in the muscle increases.

Overall, this is a very intriguing hypothesis, especially since it could also explain the onset of the disease in non-viral events. The origin of the disease is suspected to lie in the blood vessels (endothelial damage, reduced blood volume). This reminds me of the athlete on this forum who developed ME/CFS after severe dehydration. The consequences there also include reduced blood volume.

 

[Wishful]

was higher in ME/CFS patients than in healthy controls.

Yup, another pointless inactive ME patients vs healthy active controls. When will they learn that they need suitable inactive non-ME controls? That shouldn't be too difficult (although less convenient than finding normally active people). Convincing ME researchers to do this should be a critical task of the ME associations. Studies using active controls are resources effectively wasted.

 

[crussher]

Yup, another pointless inactive ME patients vs healthy active controls. When will they learn that they need suitable inactive non-

 

[crussher]

Yup, another pointless inactive ME patients vs healthy active controls. When will they learn that they need suitable inactive non-ME controls? That shouldn't be too difficult (although less convenient than finding normally active people). Convincing ME researchers to do this should be a critical task of the ME associations. Studies using active controls are resources effectively wasted.

Actually, they did that.

From subjects and study design section:

“The healthy controls in the study were required to have sedentary jobs and to perform less than three hours of physical activity per week.”

 

[Wishful]

I'm not sure that sedentary jobs as less than three hours of physical activity (actual exercise?) is a valid match for PWME. People might not do traditional exercises, but they might be fairly active doing housework or other such activities that PWME need to avoid doing. In their limitations, they did admit that they didn't know how much of a difference the activity levels made.

The study seems reasonable within its limitations. Hopefully the follow up will resolve some of the weaknesses they found with this one. Maybe they could match activity levels a bit better than just not doing traditional forms of exercise. Maybe compare against some people with other physically limiting diseases.

 

[godlovesatrier]

When polybio talk about t cells based therapies for long covid and potentially the same for ME I really don't think this has a chance in hell. Also I doubt we will ever see anything posted on x that isn't a medical intervention of breakthrough that's going to get us well. Even ampligen has a better chance than this.

 

[cfs since 1998]

When polybio talk about t cells based therapies for long covid and potentially the same for ME I really don't think this has a chance in hell. Also I doubt we will ever see anything posted on x that isn't a medical intervention of breakthrough that's going to get us well. Even ampligen has a better chance than this.

Isn't that for Long COVID though? If the persistent antigen in ME/CFS is something that cannot be cleared, like EBV, the same treatment isn't going to work. A recent trial of EBV-sensitive T-cell infusions in MS didn't work.

Mitodicure's idea behind MDC002 doesn't seem so far fetched, but I am not sure if this is something that can repair the damage or if it is something like Mestinon that treats it too far downstream to really make a difference in the long term?

I am critical of any theory that explains the ME/CFS disease process as a "vicious circle." I don't believe the body can get stuck in such a thing without some continuing external influence.

 

[Dude]

@cfs since 1998
When I look at the diagram, I have a little story to share. We have a local WhatsApp group for people affected by this condition in my state (I was surprised to find quite a few members). Among them is a guy who is a bit younger than me and has been affected for a few years as well. We get along very well. His condition is definitely on the milder side; although he is not able to work, he can drive and visits me from time to time. It's rare to find like-minded people to exchange experiences with.

A few years ago, he had his autoantibodies against the beta-2 adrenergic receptor (ß2AR) tested. According to research from Charite Berlin 【1】, these are elevated in about 30% of ME/CFS patients . However, we also know that this is not suitable as a diagnostic marker since it can be elevated in other diseases and sometimes even in healthy individuals. One of the consequences of these antibodies is circulatory disorders and reduced blood flow, which are also depicted in the diagram. Based on his results, he decided to undergo immunoadsorption in Germany, where antibodies are removed using a filter. After five sessions, his condition improved significantly, and he even started bouldering again. For a while, he thought he might be cured. The effect lasted a few months before he regressed to his previous baseline.

Why am I sharing this? The thing is, you hear and read a lot about people being cured by antiviral medications or supplements, but personally, I've never met anyone or seen anyone credible outside of the internet who has benefited to such an extent. I'm not saying these people are lying, but when you know someone personally, their stories are simply more believable. Similar stories are heard about the BC007 study (with phase 2 results being published in September).

Returning to the hypothesis of whether these antibodies are indeed the problem, remains to be seen. However, I do believe that blood flow and blood vessels play a significant role. There are countless studies on this, for example, this one【2】. I don't know about others, but I have abnormal sensations towards cold temperatures; my limbs are extremely sensitive. At the same time, I feel noticeably better after a hot shower, which also suggests that there might be an issue with blood vessels. I don't want to get my hopes up too much, but all these things make me believe that this hypothesis are on the right track.

【1】https://pubmed.ncbi.nlm.nih.gov/34441971/
【2】https://onlinelibrary.wiley.com/doi/10.1002/ehf2.12633

 

[Dude]

Video starts at 5:12:47. Klaus Wirt talk about his drug. As an english speaker you need subtitles.
https://www.youtube.com/live/q1T_dtgBqsk?si=5TWi-0A5ziMTooiL

 

[Dude]

In this video (the first of two), I talk to Professor Klaus Wirth about his latest research on mitochondrial dysfunction in ME/CFS and Long Covid.

Chapters:

0:00 Introduction
2:00 Professional background
3:12 Latest research
3:56 Cause of fatigue
6:10 Cause of PEM
6:49 PEM – permanent damage?
8:25 Unifying theory
10:58 Conclusion
12:09 Where was I...?

 

[Guwop2]

In this video (the first of two), I talk to Professor Klaus Wirth about his latest research on mitochondrial dysfunction in ME/CFS and Long Covid.

Chapters:

0:00 Introduction
2:00 Professional background
3:12 Latest research
3:56 Cause of fatigue
6:10 Cause of PEM
6:49 PEM – permanent damage?
8:25 Unifying theory
10:58 Conclusion
12:09 Where was I...?

Do you think it's possible to have LC and ME/CFS? I believe I have both. They're similar in description, but different enough in experience to make me believe they are different (and that you can have both)

 

[Dude]

@Guwop2
For me, Long Covid is merely an umbrella term that describes various scenarios in which the illness can manifest. For example, some people suffer actual organ damage to the lungs, which is then broadly classified as Long Covid. Others develop ME/CFS, but in that case, simply calling it Long Covid would be too unspecific. I believe many people don’t realize that they actually have ME/CFS—once fatigue and, most importantly, PEM are present, it’s no longer Long Covid but ME/CFS.

 

[Dude]

Things are moving forward:

Mitodicure GmbH is the only biotech startup worldwide pursuing a curative approach for Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) – a severe, currently untreatable disease that often occurs as a consequence of Long COVID. ME/CFS is driven by autoimmune processes and leads to severe fatigue, post-exertional malaise, and other symptoms comparable to those of multiple sclerosis (MS).

With an estimated prevalence of 1.3%, there are over 6 million potential patients in the largest Western markets and Japan. Due to its previous misclassification as a psychosomatic disorder, the disease was largely ignored by the pharmaceutical industry. However, recent research findings indicate that mitochondrial damage and cell necrosis in skeletal muscle are the underlying causes.

Mitodicure is developing the oral drug MDC002, which restores mitochondrial function and improves blood flow. The German regulatory authority BfArM considers the preclinical data sufficient to justify clinical trials. The company completed its pre-seed financing in 2024 and aims to finalize all IND-enabling studies within 18 months. MDC002 also holds potential for treating fibromyalgia, Lyme disease, Gulf War syndrome, and chronic fatigue associated with Ehlers-Danlos and Marfan syndromes.

https://informaconnect.com/bioeurop...it-hall-stage_next-generation-mitodicure-gmbh

 

[Guwop2]

The company completed its pre-seed financing in 2024 and aims to finalize all IND-enabling studies within 18 months. MDC002 also holds potential for treating fibromyalgia, Lyme disease, Gulf War syndrome, and chronic fatigue associated with Ehlers-Danlos and Marfan syndromes.

https://informaconnect.com/bioeurop...it-hall-stage_next-generation-mitodicure-gmbh

I didnt know what 'IND-enabling studies' meant, so i asked google gemini. "IND-enabling studies are conducted to evaluate potential toxicity risks prior to human studies and to estimate starting doses for clinical trials."
So i gather that within/after 18 months, after IND-Enabling studies have been done, clinical trials with humans can begin. I then gemini'd how long do clinical trials on average take before a drug is ready for market, and the answer was 10-15 years (on average). So, we'ere looking at around 17 years worst case scenario (and with ME/CFS i always embrace that metric), unless of course there are shortcuts that can be taken.

 

[Dude]

@Guwop2
Wirth mentioned in one of his lectures that he estimates 5–7 years for phases 1 and 2. If phase 2 yields very positive results, an application for emergency approval could be submitted to the federal government. Given the prevalence of the condition and the lack of available therapies, there would likely be a very good chance of success. Of course, that’s still a very long time. But what other options do we have? Off-label treatments have already been tried extensively. I find it highly unlikely that an existing drug will be found that could significantly improve our condition.

When you consider that much of Wirth’s hypothesis only recently gained solid scientific backing through studies like Rob Wüst’s muscle study, you realize how little progress has been made over the years. The study is extremely important and well-conducted, but it could just as well have been done 20 years ago—who knows where we would be today if it had?