mitochondrial peptide

[mlengineer]

In both Long Covid and ME/CFS, it is theorized that there is a strong mitochondrial component.
Has anyone here tried mitochondrial peptides?
I have some experience with taking peptides, such as TA1, TB4, GHK-CU etc, but none have helped me thus far.
However, mitochondrially derived peptides, like humanin, motilin (MOTS-c), and small humanin-like peptides (SHLPs), sound like they might be targeting the root cause of the issue. You may consult this review on mots-c in case you are interested in the details: mots-c. So, does anyone here have experience with taking any of them?

 

[Blazer95]

i took mots-c wich is also called exercise in a bottle. its funny because it caused PEM for me.

it seems SS31 is more suitable for this cases because a friend of mine had a similar pem reaction to mots-c but benefited from ss-31

how did ta-1 make you feel?

 

[mlengineer]

That's a neat name to remember its effects! Yeah, I thought it would be interesting to see what effect exercise-mimicry has on my body. Interestingly, mots-c levels are higher in people infected with Covid-19 (general population) vs a control group (mots-c in acute covid infections), whereas humanin levels are lower. Can we make anything of this? The authors argue that this a compensatory mechanism, but I am not convinced.

TA-1 did not change much about how I felt. However, I think I developed an allergy to the peptide, although I made sure to use an expensive but reliable supplier (accumulation of fluid at the injection site that took a day or two to drain and left blue spots).

I was also interested in trying SS-31. How has your friend benefited?

 

[Blazer95]

well he seemed to have overall more energy and more general wellbeing but nothing intense. i am talking about 10-15% here, but definitly noticable.

i am also considering ll-37 but it seems to be the strongest peptide ever so i am bit freaked out since i herxed from ta-1 very badly.

 

[Wishful]

I think it's more likely that there's a mitochondrial component for some people, but is not the core dysfunction of ME. Some of us don't seem to have any lack of ATP production. My feeling is that most of the studies with findings of (barely measurable) mitochondrial dysfunction are due to study politics and funding (easier to get funding, since "fatigue = low ATP" for those with little understanding) and are tailored to get the desired numbers. I haven't seen any convincing studies that ME has a strong mitochondrial component.

 

[mlengineer]

Thank you both for your input. After some consideration, I thought also about B7-33. I just scanned some keywords, but it promotes cardiovascular function and is a relaxin mimetic. As such, it interacts with receptors from the G-protein superfamily, which consititute 4% of the receptors in the body. From FDA-approved drugs, 34% target this family, so it seems to be quite important. From what is known about relaxin, it also promotes long-lasting suppression of some inflammatory pathways (see: https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0190935). Does this look interesting to you?

 

[mlengineer]

I think it's more likely that there's a mitochondrial component for some people, but is not the core dysfunction of ME. Some of us don't seem to have any lack of ATP production. My feeling is that most of the studies with findings of (barely measurable) mitochondrial dysfunction are due to study politics and funding (easier to get funding, since "fatigue = low ATP" for those with little understanding) and are tailored to get the desired numbers. I haven't seen any convincing studies that ME has a strong mitochondrial component.

It seems like it is the same with people throwing around the term "inflammation". From all the Long Covid studies I read, remarkably often there is no difference between PASC groups and control groups in terms of common inflammatory markers.

 

[Wishful]

I agree that ME and PASC probably don't have clear abnormalities of common inflammatory markers. The immune system is far more complex, and has far more potential for subtle dysfunction, than just a few common easy-to-measure serum markers.

 

[junkcrap50]

I have tried several peptides, but not yet SS31 or humanin. MOTS-C didn't seem to do very much for me. I had a great response to TA1 & TB4 - a lot less neuroinflammation, better mood, more energy.

I haven't heard of B7-33.

 

[Blazer95]

It seems like it is the same with people throwing around the term "inflammation". From all the Long Covid studies I read, remarkably often there is no difference between PASC groups and control groups in terms of common inflammatory markers.

I might want to disagree - atleast to some extent.

Maybe these studies are failing because of the criteria they let the long covid and ME patients participate. It has been often critizised that some researchers still use old criteria such as fukuda and oxford wich often doesn't even involve PEM.

I have read a study yesterday that shows a difference in Serum Amyloid A (SAA) between healthy individuals and the long covid group. The long covid group had it elevated. Serum Amyloid A or SAA is an inflammation marker and acute phase protein similar to CRP synthethized in the liver and very well studied in scholar medicine. The study: https://thorax.bmj.com/content/79/Suppl_2/A59.2

In case anyone doesnt believe its a well established diangostic marker: https://en.wikipedia.org/wiki/Serum_amyloid_A

It might be interesting that since coming down with ME my SAA is permanantly elevated.

 

[mlengineer]

Update:
I tried B7-33 and, although it does not completely address my movement-based PEM, I have a noticeably higher energy level than before. I wish I could properly quantify this and I hope it is not just a placebo effect.
In any case, I am quite satisfied with this peptide. I will try SS31 next.