Mitochondrial support supplementation

Cort

Founder of Health Rising and Phoenix Rising
Staff member
I found this hidden on my desktop. This is from my NP.. Sorry it's so small

View attachment 928
Interesting. I could read it OK

Just to relay something. I just talked to Ron Davis about his study. He thinks the data is pointing at the mitochondria right now...which are by the way INCREDIBLY complex - which is actually the kind of problem Ron love to take on. He loves on to take on big, complex problems...He's different that way.

;)
 

Who Me?

Well-Known Member
Interesting. I could read it OK

Just to relay something. I just talked to Ron Davis about his study. He thinks the data is pointing at the mitochondria right now...which are by the way INCREDIBLY complex - which is actually the kind of problem Ron love to take on. He loves on to take on big, complex problems...He's different that way.

;)
My last appointment with my NP she brought up mitochondria right at the end. About how they could mess us up but nothing more than that.

Another piece of the puzzle. I wish something was simple.
 

Strike me lucky

Well-Known Member
They look similar to supps i use although doses seem very high for some like carnitine or q10, although doses vary alot.
 

San Diego

Well-Known Member
I consulted a mitochondrial "specialist" several years back.

Mainstream medicine calls mito dz a ‘wastebasket diagnosis” if you don’t have muscle biopsy. It seems we’re in a transition phase of diagnosis as other less invasive techniques, including citrate synthase, are being developed and replicated/validated.

“Mitochondrial Disease Laboratory at SCHC” performed my citrate synthase test. $100 out of pocket and a buccal swab. I no longer have their contact information.

Attached are
1. my results
2. the lab’s statement regarding citrate synthase testing
3. the mito cocktail thusly prescribed. I took it for a year but stopped as it was costly. Looking back, I was better then, but I didn’t improve on the cocktail. I’ve gone downhill since, and can’t say it had anything to do with stopping the mito supplementation. I think it had more to do with me continuing to push.

Screen Shot 2016-02-12 at 2.11.32 PM.png Screen Shot 2016-02-12 at 2.11.51 PM.png Screen Shot 2016-02-12 at 2.12.37 PM.png
 

San Diego

Well-Known Member
Interesting. I could read it OK

Just to relay something. I just talked to Ron Davis about his study. He thinks the data is pointing at the mitochondria right now...which are by the way INCREDIBLY complex - which is actually the kind of problem Ron love to take on. He loves on to take on big, complex problems...He's different that way.

;)
Do you know what testing they are using? I can’t imagine doing a muscle biopsy on the severely ill. Apparently it’s much more invasive than it sounds.
 

IrisRV

Well-Known Member
I just talked to Ron Davis about his study. He thinks the data is pointing at the mitochondria right now...
Hah! I knew it! Okay, I didn't know, but I was pretty confident that's the way they were headed. It's my impression that Klimas thinks mitochondria are a big issue too.

High dose CoQ10 is a big help to me. So far the others on that list haven't done much, but if my CoQ10 was as low as it appears to have been, they might not have been able to help. I'll get around to trying them again sometime soon.

I didn't see PQQ on that list. My highly respected ME researcher/clinician (sorry, not comfortable using names yet) told me that PQQ is very important. It helps make more mitochondria (or something like that -- Blame brainfog for the lack of details).

I'm convinced mitochondrial dysfunction of some type is a major player in my variation of this illness. Looks like it might not be just me.
 

RuthAnn

Well-Known Member
Low CoQ10 caused by interference with the mevalonate pathway.
Why would this be common in ME, (and GWI and polymyositis)? I was trying to figure out what it could be about ME/CFS that would interfere with the mevalonate pathway because CoQ10 is a product of the mevalonate pathway and found this from selfhacked.com.
"When a viral infection becomes active it “hijacks” what’s known as the “mevalonate pathway.” Viruses use this pathway to make their protective outer coats.
In response, your body makes interferon, which suppresses the mevalonate pathway, which in turn suppresses the virus. However, inhibiting this pathway leads to a reduction in synthesis of pregnenolone and CoQ10."
 

RuthAnn

Well-Known Member
As for testing, here is a list of things they can look for in the blood. However, this list doesn't include aldolase, which I have seen is measured when looking for myopathies.
Muscle biopsies are common for some diseases such as polymiositis.

"Blood Tests to Diagnose Myopathy
A serum enzyme test measures how much muscle protein is circulating in the blood. Usually, a serum enzyme test is helpful only at the early stages of the disease, when the sudden increase of protein level in the blood is conspicuous.
Types of muscle proteins include the following:

  • Creatine kinase (CK)
  • Lactic dehydrogenase (LDH)
  • Pyruvate kinase (PK)

As the disease progresses and muscle tissue wastes away, there is less and less protein to circulate and the amount in the blood drops to a normal level. The CK level is especially important in diagnosing Duchenne MD and the metabolic myopathies. The level of potassium in the blood helps diagnose periodic paralysis.
When an endocrine myopathy is suspected, appropriate blood tests are performed to detect hormone excesses or deficiencies. For example, thyroid function testing reveals hyper- or hypothyroidism.

Antibodies found in the blood might indicate an inflammatory myopathy. DNA may be collected from the blood to evaluate whether one of the known genetic defects is present
- See more at: http://www.healthcommunities.com/myopathies/diagnosis.shtml#sthash.REIhmkiU.dpuf"
 

RuthAnn

Well-Known Member
Here's an interesting twist from looking at it from a different direction,
Complex I and Complex IV being two pathways in the mitochondria.

"NO inhibits several enzymes including complexes I and IV of the mitochondrial electron transport chain, leading to ROS generation."
 

RuthAnn

Well-Known Member
Another way to look at mitochondrial disease.
Endoplasmic reticulum stress.

I don't know if the methodology of the experiment is valid, check and tell me what you think, somebody. But the last sentence is what I'm looking at.

http://www.sciencedirect.com/science/article/pii/S0898656808002994
Our results demonstrate that mitochondrial dysfunction is directly linked to the ER stress response, and together, cause aberrant insulin signaling and an abnormal increase of hepatic gluconeogenesis.
 

Strike me lucky

Well-Known Member
Another way to look at mitochondrial disease.
Endoplasmic reticulum stress.

I don't know if the methodology of the experiment is valid, check and tell me what you think, somebody. But the last sentence is what I'm looking at.

http://www.sciencedirect.com/science/article/pii/S0898656808002994
Our results demonstrate that mitochondrial dysfunction is directly linked to the ER stress response, and together, cause aberrant insulin signaling and an abnormal increase of hepatic gluconeogenesis.
May be related to leptin issues they found in cfsers?
 

Remy

Administrator
Another way to look at mitochondrial disease.
Endoplasmic reticulum stress.

I don't know if the methodology of the experiment is valid, check and tell me what you think, somebody. But the last sentence is what I'm looking at.

http://www.sciencedirect.com/science/article/pii/S0898656808002994
Our results demonstrate that mitochondrial dysfunction is directly linked to the ER stress response, and together, cause aberrant insulin signaling and an abnormal increase of hepatic gluconeogenesis.
Well, isn't this interesting.

There was a pretty long thread on PR about ER stress and protein folding a while back. One of the suggested supplements is TUDCA.

http://www.ncbi.nlm.nih.gov/pubmed/12198651

My hesitance with TUDCA is that is also is a CYP inducer which can put stress on the adrenals. But it might be a very mild inducer...hard to find info about this though. Time to try it, I think.
 
Last edited:

RuthAnn

Well-Known Member
Yes, tudca was the most popular supplement on that thread, but I never took it.

There are so many places where the mitochondria issues can take place, though, that I guess this one link to endoplasmic reticulum stress is most likely not all inclusive. Working on it can be a good place to start, though.
 
Last edited:

Who Me?

Well-Known Member
@Remy. I was just reading about TUDCA and cholesterol.

I remember you said you were trying it. How did it go? Did it cure you?

@Upgrayedd see Remys lonk (Or link if you prefer) above.
 

weyland

Well-Known Member
Just to relay something. I just talked to Ron Davis about his study. He thinks the data is pointing at the mitochondria right now...which are by the way INCREDIBLY complex
Not surprising since they just brought Dr. Naviaux on board.
 

Get Our Free ME/CFS and FM Blog!



Forum Tips

Support Our Work

DO IT MONTHLY

HEALTH RISING IS NOT A 501 (c) 3 NON-PROFIT

Shopping on Amazon.com For HR

Latest Resources

Top