4 replies to this topic

[mitomutant]

Looking for clinical trials for mitochondrial myopathy, I stumbled upon this [1] clinical trial

 

Study Type: Interventional Study Design: Allocation: Randomized
Endpoint Classification: Safety/Efficacy Study
Intervention Model: Parallel Assignment
Masking: Double Blind (Subject, Caregiver, Investigator, Outcomes Assessor)
Primary Purpose: Basic Science Official Title: Effects of Low Level Carbon Monoxide Preconditioning on Human Mitochondrial Biogenesis in Aortic Valve Surgery Patients

 

Doing some searching, there are a few human studies on Carbon Monixide and mitochondrial biogenesis. This one [2] seems interesting

 

Carbon monoxide, skeletal muscle oxidative stress, and mitochondrial biogenesis in humans

Michael A. Rhodes , Martha Sue Carraway , Claude A. Piantadosi , Crystal M. Reynolds , Anne D. Cherry , T. E. Wester , Michael J. Natoli , E. Wayne Massey , Richard E. Moon , Hagir B. Suliman

American Journal of Physiology - Heart and Circulatory PhysiologyPublished 1 July 2009Vol. 297no. 1,H392-H399DOI: 10.1152/ajpheart.00164.2009

 

These findings provide evidence linking the HO/CO response involved in mitochondrial biogenesis in rodents to skeletal muscle in humans through a set of responses involving regulation of the mtDNA transcriptosome and mitochondrial fusion proteins autonomously of changes in exercise capacity.

 

I have seen dosages between 100 ppm and 200ppm during 1 hour for anything between 2 weeks to 4 weeks.

 

Worth trying ?

 

[1] http://clinicaltrial...how/NCT01727167

[2] http://ajpheart.phys...97/1/H392.short

[niner]

If your first response is WTF, the first paragraph of the text from mitomutant's link [2] lays out the basis for this:

 

 

Carbon monoxide (CO), as a toxic gas, causes tissue hypoxia (36), but direct cellular effects of CO also contribute to adaptive responses (24). Endogenous CO is detectable at nanomolar levels as a by-product of heme catabolism (8), which induces the expression of antioxidant enzymes, including heme oxygenase-1 (HO-1) and mitochondrial superoxide dismutase (SOD2). These responses depend on CO and protect against oxidative stress and thus raise the possibility that near-physiological concentrations of CO might be therapeutically useful (29).

 

I had no idea that we produced CO endogenously, but I guess it's not surprising, considering the role of NO, another molecule that took the biological world by surprise a couple decades ago.

[mitomutant]

material* LC50 ppm IDLH** cut-off***
carbon monoxide 3614 1200

 
 
Papers testing CO for therapeutic use are using 100-200 ppm during 1 hour; pretty safe.
 
[1] http://www.chem.purd...poisongases.htm

Edited by mitomutant, 13 October 2014 - 04:08 PM.

[Turnbuckle]

A cigar every once in a while, then?

 

Because of the long aging and fermentation process for cigar leaves, because of the larger size of cigars and because of the toxic way it burns due to cigars' nonporous wrappers, cigar smoke has 20 times more ammonia than cigarettes and 80 to 90 times the number of highly carcinogenic, tobacco-specific nitrosamines. Cigar smoke also contains 30 times more carbon monoxide than cigarette smoke.

 

http://www.quitsmoki....com/cigars.htm

 

 

 

 

[mitomutant]

A cigar every once in a while, then?
 

Because of the long aging and fermentation process for cigar leaves, because of the larger size of cigars and because of the toxic way it burns due to cigars' nonporous wrappers, cigar smoke has 20 times more ammonia than cigarettes and 80 to 90 times the number of highly carcinogenic, tobacco-specific nitrosamines. Cigar smoke also contains 30 times more carbon monoxide than cigarette smoke.
 
http://www.quitsmoki....com/cigars.htm

 

That´s what came to mind before posting. This has been already discussed here at Longecity. Too bad industrial tobacco contains so much shit nowadays.

 

Edited by mitomutant, 13 October 2014 - 06:21 PM.