How can we help accelerate Dr Naviaux's ME/CFS Suramin trial?

[pattismith]

Here's what we know so far about Suramin:

- it works on the purinergic pathway which Naviaux believes is central to core ME/CFS pathology

- it significantly improved the ability of Ron Davis' ME/CFS cells to pump out sodium in vitro

Thank you Jesse.

I have both low borderline plasma potassium and low borderline plasma sodium.

I wonder if the effect of suramin on sodium pumps is related to effect on purinergic pathway or not?

 

[wastwater]

It also kills parasites is that important
Think it’s anti fungal as well

 

[dreamydays]

@adamjfpickering Where are we at currently with the 3 potential trials?

 

[junkcrap50]

Additionally, As many maybe already aware a homeopathic version of Suramin has been created with promising results, and will be available in the coming weeks.

How and when did this happen? Who's made it? Can you buy it?

 

[RL_sparky]

Adam hasn't been around since Dec. 4th.

 

[junkcrap50]

Adam hasn't been around since Dec. 4th.

Ah, well does anyone have any answers to my questions?

 

[Learner1]

Suramin isn't a magic cure.

I had a lengthy chat with Dr. Naviaux at the August Symposium. The first of what I heard from him is the game is to remove all the cell dangers, then move all of one's pathways out of winter metabolism to summer metabolism, and then, and only tgen, would one use suramin if the body was still stuck in "sickness behavior" mode.

So, there's a lot of work to be done before most of us would be ready to use suramin.

 

[Tally]

Suramin isn't a magic cure.

I had a lengthy chat with Dr. Naviaux at the August Symposium. The first of what I heard from him is the game is to remove all the cell dangers, then move all of one's pathways out of winter metabolism to summer metabolism, and then, and only tgen, would one use suramin if the body was still stuck in "sickness behavior" mode.

So, there's a lot of work to be done before most of us would be ready to use suramin.

I didn't get that impression from his very detailed Q&A on suramin trial in ME/CFS.

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.

...

We have many state-of-the-art tools like PCR that allow this question to be answered with very high confidence.

...​

Suramin does not “switch off” the CDR. It just restores the CDR to normal balance so healing can start again. We tested if suramin had any affect on the frequency or severity of infections in the children with autism in the SAT1 study. Two of the placebo children came down with colds during the winter of the study, and two of the suramin children did too. There was no difference in the length or severity in symptoms between the two groups. People often forget that the immune system of patients with ME/CFS is not just down, it is unbalanced and dysregulated. We believe that suramin will restore balance between T-cells, B-cells, and NK cells. When balance is restored, the risk of “reactivation” of latent viruses should be less than during the normal course of untreated ME/CFS.

...

I believe that after a few months of treatment, the healing process can get started again and ME/CFS patients might improve enough to get back to more normal lives. In the beginning, once the first energy is restored, then a program of good food and activity will be possible. Just as a broken leg that has been in a cast for 6 weeks is a little deconditioned, so will the patients with ME/CFS. But soon, the gains will become self-sustaining, and chronic suramin will not be required.​

Both Dr. Davis and Dr. Naviaux said that so far it seems people with ME/CFS don't have active infections.

Someone correct me if I'm wrong but to me it sounds once infection is ruled out suramin trial can begin.

 

[pattismith]

Suramin isn't a magic cure.

I had a lengthy chat with Dr. Naviaux at the August Symposium. The first of what I heard from him is the game is to remove all the cell dangers, then move all of one's pathways out of winter metabolism to summer metabolism, and then, and only tgen, would one use suramin if the body was still stuck in "sickness behavior" mode.

So, there's a lot of work to be done before most of us would be ready to use suramin.

his protocol was brought on PR here:

http://forums.phoenixrising.me/inde...l-the-tank-flip-the-switch.51752/#post-854854

@Tally :
it seems Naviaux agree that a chronic intracellular infection can still play a role in the maintaining of the CFS/ME state in some cases.

 

[Learner1]

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

Most, if not all, patients will have toxicity. And many of us have infections, or the fallout from infections that should be treated first.

 

[Tally]

And many of us have infections

Could you please give me source for this? All the studies I read, Lipkin's microbe hunt, and what Dr. Davis has said so far indicate that most of us don't.

 

[Learner1]

Just look around on this site. There are a lot of us. There is research. There's this talk from 10/17 by one of the NIH working group members:

And I'm seeing a top ME/CFS specialist associated with one of the Centers of Excellence, shared by several on this site who has found treatable infections in many of us. Finding and treating my 7 infections, the ones that a dozen doctors missed or dismissed, has helped me quite a bit.

 

[Tally]

@Learner1 You can't use forum posts and internet chatter to judge how many ME/CFS patients have an active infection.

Could you please tell me which part of the talk mentions infections? It's over 1 hour long, I can't manage more than a few minutes.

 

[Learner1]

@Learner1 You can't use forum posts and internet chatter to judge how many ME/CFS patients have an active infection.

As you will note, I provided an authoritative resource who is familiar with the scope of current research, as well as the anecdotal info. As a patient, I have found it extremely useful to know what other patients are experiencing and it has helped me formulate questions and enriched the communication I have with my doctors.

Could you please tell me which part of the talk mentions infections? It's over 1 hour long, I can't manage more than a few minutes.

It's his very first topic. You can watch from 7:00 to 29:00.

 

[Learner1]

Additionally, here are some articles relating various infections to ME/CFS. Some are reviews and clinician oriented, some are research articles. I can only upload 8 at a time here, but there are many more...

 

[halcyon]

Could you please give me source for this? All the studies I read, Lipkin's microbe hunt, and what Dr. Davis has said so far indicate that most of us don't.

Lipkin's microbe hunt is just beginning. If his prior study on leftover plasma was definitive at all I don't think he would have been granted 9.6 million to continue pathogen research in this disease.

As far as I've seen, Davis has only performed blood testing for something like 14 DNA viruses, the majority of which have never even been linked with or suspected of causing ME. The largest suspect of causing this disease, the RNA enterovirus, has not even been looked for yet in his study. They're not even performing serology for these viruses for reasons unexplained.

Keep in mind that in order to refute the past solid evidence for viral involvement in this disease, Davis and Lipkin are going to have to start slicing up brains.

 

[Tally]

@Learner1 I'll reply to you as soon as I can watch and read all that.

Lipkin's microbe hunt is just beginning. If his prior study on leftover plasma was definitive at all I don't think he would have been granted 9.6 million to continue pathogen research in this disease.

Maybe I'm putting too much ephasis on that one word and correct me if I'm wrong, but Lipkin didn't get that grant to search for current infections. He got it to search for infectious trigger (most researchers agree infections trigger ME/CFS, but the question is do they sustain it), metabolic research following exercise, and app development.


Columbia: In laboratory studies, the researchers will use state-of-the-art methods to analyze molecular footprints of potential bacterial, fungal, and viral triggers, together with corresponding immune responses, including autoantibodies. Other studies will analyze metabolites and gene expression in individuals with ME/CFS after physical activity, and mine databases for insights into clinical features, comorbidities, and sub-types that could refine laboratory analyses and enhance their care. ME/CFS scientists will also work with the ME/CFS community, including clinicians and people with ME/CFS, to design a mobile app called myME/CFS that will allow them to track symptoms in response to stressors and interventions. Aggregated data from the apps may yield insights into triggers that initiate or exacerbate disease, including links between infection and disease in a subset of patients.

They're not even performing serology for these viruses for reasons unexplained.

They will and it has been explained.

Keep in mind that in order to refute the past solid evidence for viral involvement in this disease, Davis and Lipkin are going to have to start slicing up brains.

There is no solid evidence. Just because a study exists that says something, doesn't mean it's solid evidence (remember the PACE trial?)

IOM panel looked at all ME/CFS research and concluded:

A few studies focused on the role of persistent enterovirus infection in ME/CFS (Chia et al., 2010; Galbraith et al., 1995; Lane et al., 2003). Chia and Chia (2008) showed that in a subset of ME/CFS patients who reported significant gastrointestinal complaints, the prevalence of enterovirus infection as demonstrated in stomach biopsy samples was significantly higher compared with control subjects. Other investigators failed to reproduce an increased incidence of enterovirus infection in ME/CFS patients (Lindh et al., 1996).

There is insufficient evidence for an association between ME/CFS and bacterial, fungal, parasitic, and other viral infections. These infectious agents may, however, be comorbidities, and their presence may reflect the presence of problems with immune function in these patients. Future research may clarify the role of these infections in this illness.​

As usual: There is not enough research in ME/CFS and more needs to be done. There is absolutely no "solid evidence".

 

[halcyon]

Maybe I'm putting too much ephasis on that one word and correct me if I'm wrong, but Lipkin didn't get that grant to search for current infections. He got it to search for infectious trigger (most researchers agree infections trigger ME/CFS, but the question is do they sustain it), metabolic research following exercise, and app development.

The description of the study is worded generically, but I take it to mean they will be looking directly for the presence of microbes: "molecular footprints of potential bacterial, fungal, and viral triggers"

They will and it has been explained.

That is discussing the digital PCR assay they are developing. This is not serology.

IOM panel looked at all ME/CFS research and concluded:

What's listed there is 4 papers out of over two dozen covering the role of persistent enterovirus in ME patients. What's missing there is the three autopsy case reports that prove enterovirus infection in the brains of ME patients. Again, it is impossible for blood based studies to refute this evidence.

 

[Tally]

@halcyon I agree it's not worded clearly, but still, as it stands now it doesn't sound like it. Footprints is what you look for when something has passed through and went away. Let's see, we don't really know what their grant proposal said, so I might be wrong.

Serology relies on your body reacting to a microbe. If there is no immune reaction there are no antibodies and you can still be infected. PCR looks for microbes directly, no matter if your body reacted to them or not.

IOM looked at all research pertaining to ME/CFS. They had to discard great majority of it because of too small sample size or bad quality, bad methodology or bad cohort definition. If you don't see research paper that you like there you can be almost certain there were serious issues with it.

 

[junkcrap50]

Serology relies on your body reacting to a microbe. If there is no immune reaction there are no antibodies and you can still be infected. PCR looks for microbes directly, no matter if your body reacted to them or not.

BOTH would be important to test for: serology and PCR. You could have tested positive for PCR microbes but your immune system isn't reacting to them (negative serology). Or, you could also have positive serology and not have any microbes in you (negative for PCR) , because you immune system is haywire and still producing antibodies.

+ PCR; - Serology = infected but not reacting
- PCR; + Serology = not infected no infection detected* but immune system reacting

EDIT: Changed not infected to "no infection detected." Often there is still infections present but are not found through testing. False negatives are frequently.