A reader forwarded me a transcript of a conversation with Dr. Naviaux [Sep 13, 2017]. There are many points of interest raised so I thought that I would do a review.
For background on the Drs, see these MEpedia links
What is Suramin?
Suramin is a treatment for African sleeping sickness and river blindness. It is being tested for Zika virus.
What is Purinergic Sugnalling?
” form of extracellular signalling mediated by purine nucleotides and nucleosides such as adenosine and ATP.” [wikipedia]
What is adenosine is a mononucleoside consisting of adenine and D-ribose.[source]
Comments on Transcript
“A major misconception in medicine is that diseases that are “caused by different triggers are different diseases”. I believe this is wrong. The vast majority of chronic diseases are caused by the body’s response to stress or injury, and not the initial injury itself. In other words, over half of all chronic disease is caused by blocks in the healing process caused
by pathological persistence of the cell danger response (CDR). This is a categorically different way of thinking. It is different from the way doctors are trained to think about treating “acute” diseases like a strep infection, a broken leg, or a heart attack. “Chronic” disease needs to be analyzed and treated in a completely different way.”
- absolutely agreed, for one class of these diseases it is the persistence of a microbiome dysfunction which presents as a metabolic disorder with metabolic abnormalities. Why — the microbiome is the producer of many metabolites.
“The most important medical decision is to determine:
- if the person has an active infection or not. If yes, this must be treated.
- If there is not an active infection, then we also need to determine if they have a household or occupational exposure to toxins that is ongoing.
- If the answer to both investigations is “no”, then the patients would be eligible for the first pilot study.
- Since our hypothesis is that antipurinergic therapy with suramin will treat the root problem of ME/CFS that is common to all patients, then you could say that the hypothesis we are testing in the first small pilot study of 10 patients, is that purinergic signaling abnormalities are common to ALL patients with ME/CFS, regardless of any “subset” they might belong to.”
Absolutely agreed for the first steps — the key is confirms actual infections with reliable tests (most Lyme tests do not meet that criteria); the second item should include oral/dental issues.
D-Ribose is produced by Bacillus subtilis which according to DataPunk, clusters with (seen with), Lactococcus lactis, Bacillus clausii, Lactobacillys plantarum and others. The bacillus genus also produces: Norepinephrine, Dopamine and Vitamin B12
Adenine (once known as Vitamin B4) is produced by E.Coli 
- Evaluation of purine utilization by Lactobacillus gasseri strains with potential to decrease the absorption of food-derived purines in the human intestine.
- The effect of riboflavin analogues upon the utilization of riboflavin and flavin adenine dinucleotide by Lactobacillus casei.
In short: purinergic signaling abnormalities may be associated with microbiome changes.
The cost Aspects of doing CFS Studies..
“I estimate the CFS1 study of N = 10 patients will cost about $400,000…. so the cost of the clinical trials has nothing to do with the cost of the drug. Typically, it takes 15-30 people
on the clinical investigation team at each medical center to conduct a Phase III study. The main cost of the clinical trial is the salaries of the staff…the total cost of suramin drug development, from Phase I/II to Phase III trial is $20-$30 million.”
What do we know about how Suramin impacts the microbiome?
- Intratesticular multiplication of Mycobacterium leprae murium in normal and suramin-treated animals . many more studies of it’s impact on other mycobacterium
- Induced chain formation in Bacillus megaterium by suramin (Bayer 205) .
- Effect of suramin on the human pathogen Candida albicans: implications on the fungal development and virulence.
- “Firstly, it was demonstrated that suramin (500 microM) arrested its growth, showing a fungicidal action dependent on cell number. Suramin treatment caused profound changes in the yeast ultrastructure as shown by transmission electron microscopy.”
One of my frequent quotes is “They got the treatment right, but the theory behind may be incorrect”. The drug, suramin, that they are wishing to test based on their hypothesis/theory does not exclude the hypothesis of a persistence microbiome dysfunction if they are successful. While information is sparse on the microbiome impact of suramin, the fact that it impacts candida indicates that it very capable of microbiome changes.