Professor Ron Davis's response to Naviaux study, including Q and A with Dr Naviaux

[Ben H]

Ben, I have a question, but it´s for you rather than the researchers, as I´m sure you´ll know the answer:

Are OMI in communication with Lipkin and his group, or Montoya and his group? They seem to overlap to a certain extent in terms of their research areas. Is this a case of competition or collaboration (not saying either is better, just curious to know what the situation is)?

Hi @msf

I wish I knew the answer but I dont.

OMI is seperate from OMF (though some OMI researchers such as Kolgenik are working with OMF).

I have no idea if OMI is working with Lipkin or Montoya. My extent of knowledge goes only so far as OMF and the staff and researchers involved there.


B

 

[msf]

Hi @msf

I wish I knew the answer but I dont.

OMI is seperate from OMF (though some OMI researchers such as Kolgenik are working with OMF).

I have no idea if OMI is working with Lipkin or Montoya. My extent of knowledge goes only so far as OMF and the staff and researchers involved there.


B

I see. Thanks for the reply!

 

[boohealth]

Naviaux says: "In most cases, this strategy is effective and normal metabolism is restored after a few days or weeks of illness, and recovery is complete after a few weeks or months. For example, only a small percent of people who are acutely infected with Epstein-Barr virus (EBV) or human herpes virus 6 (HHV6), or Lyme disease go on to develop chronic symptoms."

Hello? Is one out of five (which is probably a low estimate) only a small percent of people? One out of five people who get lyme go on to have chronic symptoms, which is due to chronic infection, as demonstrated by Johns Hopkins research on persisters. So please take lyme out of the equation (and please do a literature search, researchers, before making such claims). Or else, put lyme in the equation and understand that chronic infection is part of the picture. Also, EBV and lyme should not be put into the same sentence. EBV is an almost universal infection, so we have learned to adapt to it--HOWEVER it is associated with increased risk of certain cancers. Indicating that, long term, it does potentially cause immune damage.

Lyme may be well on its way to becoming a serious epidemic, but it is not a universal infection, it is a vector-borne spirochetal illness. We have not, therefore, evolved to live with it.

So the thinking in that paragraph alone is so sloppy I am not impressed with the study and its claims. Probably a greater portion of those ill have ongoing infection. Hit & run is certainly possible, creating an ongoing maladapted information loop that feeds on itself (think of reflex sympathetic dystrophy as a model--a local, acute injury that gets misinterpreted by the brain, and turns into a systemic disorder of crippling, body-wide pain that often results in suicide). But imho or not so humble opinion, that will be the minority. The majority will have ongoing infection. Even HIV, when kept in check by ARVs, still burbles inside cells and creates ongoing inflammation that shortens lifespan by around ten years. The idea that the pathogens are just happily dormant, causing no problem for anybody, is completely belied by the scientific literature.

Lyme:

http://www.scientificamerican.com/a...e-with-how-wily-lyme-disease-prowls-the-body/

 

[JamBob]

@Ben Howell

Hi Ben - if you're still collecting questions.....

How do the metabolites found in the CFS/ME patients compare to the metabolites found in hypothyroid patients (hypothyroidism also being a state of hypometabolism). Is there a difference in the kind of metabolites found. I am curious as a lot of CFS/ME patients also have thyroid disease or thyroid antibodies.

 

[Cheesus]

@Ben Howell - I don't know if this is the appropriate thread for you to send questions to the OMF about this study (or to Dr. Naviaux, given that it wasn't an OMF study), but, going forward, I can see a lot of PWME being keen to have their blood analysed by Metabolon (or whoever else can do this stuff in our various countries).

It would make tons of sense and presumably speed research up considerably if we shared our data with the OMF/Naviaux. I can imagine people being willing to pay to get genetic testing, too.

Is anybody at OMF/Naviaux's lab thinking about this?

I'm currently doing testing with a company called MetabolomicDiscoveries. I have a xenobiotic in my urine that causes it to become very, very foamy. The only known cause of this is protein and is usually connected to kidney disease, however this is not the case with me. I contacted MetabolomicDiscoveries around a month ago to see if they could figure out what it was, and they seemed quite keen to help - even giving me a discount to make it affordable!

For me they are doing specialist urine analysis, however they are currently developing something called Kenkodo, which is a finger-prick test that is aimed at the general public. They're in beta testing at the moment, having previously launched the project on indiegogo, but once that is done it will be open to the general public.

This is a link to Kenkodo http://kenko.do

And this is a link to MetabolomicDiscoveries http://www.metabolomicdiscoveries.com

 

[Ben H]

Naviaux says: "In most cases, this strategy is effective and normal metabolism is restored after a few days or weeks of illness, and recovery is complete after a few weeks or months. For example, only a small percent of people who are acutely infected with Epstein-Barr virus (EBV) or human herpes virus 6 (HHV6), or Lyme disease go on to develop chronic symptoms."

Hello? Is one out of five (which is probably a low estimate) only a small percent of people? One out of five people who get lyme go on to have chronic symptoms, which is due to chronic infection, as demonstrated by Johns Hopkins research on persisters. So please take lyme out of the equation (and please do a literature search, researchers, before making such claims). Or else, put lyme in the equation and understand that chronic infection is part of the picture. Also, EBV and lyme should not be put into the same sentence. EBV is an almost universal infection, so we have learned to adapt to it--HOWEVER it is associated with increased risk of certain cancers. Indicating that, long term, it does potentially cause immune damage.

Lyme may be well on its way to becoming a serious epidemic, but it is not a universal infection, it is a vector-borne spirochetal illness. We have not, therefore, evolved to live with it.

So the thinking in that paragraph alone is so sloppy I am not impressed with the study and its claims. Probably a greater portion of those ill have ongoing infection. Hit & run is certainly possible, creating an ongoing maladapted information loop that feeds on itself (think of reflex sympathetic dystrophy as a model--a local, acute injury that gets misinterpreted by the brain, and turns into a systemic disorder of crippling, body-wide pain that often results in suicide). But imho or not so humble opinion, that will be the minority. The majority will have ongoing infection. Even HIV, when kept in check by ARVs, still burbles inside cells and creates ongoing inflammation that shortens lifespan by around ten years. The idea that the pathogens are just happily dormant, causing no problem for anybody, is completely belied by the scientific literature.

Lyme:

http://www.scientificamerican.com/a...e-with-how-wily-lyme-disease-prowls-the-body/

Hi @boohealth

Have you read the study? Or have you ruled it out based on one comment? I am genuinely curious.

Thanks,


B

 

[Ben H]

@Ben Howell

Hi Ben - if you're still collecting questions.....

How do the metabolites found in the CFS/ME patients compare to the metabolites found in hypothyroid patients (hypothyroidism also being a state of hypometabolism). Is there a difference in the kind of metabolites found. I am curious as a lot of CFS/ME patients also have thyroid disease or thyroid antibodies.

Hi @JamBob

That has not been run yet-patients with hypothyroidism were not included in the cohort for the study for obvious reasons. Metabolomics is also absolutely cutting edge so I do not believe there has been a study run using this for hypothyroidism.

It would be interesting for sure. It may be a part of future research, when funded, that looks at chemical signatures in ME/CFS, vs other disease states.


B

 

[justy]

I am very interested in how the researchers view patients who have had long remissions only to become ill again - usually more severely. There are many of us around here who fit this profile. I was first ill late teens early twenties with M.E,. recovered spontaneously after a few years and then was almost normal functioning for around 8-9 years (some stamina issues and inability to get totally 'fit). A further viral infection, which then caused a bacterial infection put me down into the severe category, from which I have only had minor improvement over the past 8 years.

I have spoken with many other mainly middle aged women who have had the same illness trajectory. This makes me feel there is an immune deficiency somewhere that means we don't fight the precipitating infection(s) correctly and instead enter this 'stuck' mode.

 

[Tuha]

So the thinking in that paragraph alone is so sloppy I am not impressed with the study and its claims. Probably a greater portion of those ill have ongoing infection. Hit & run is certainly possible, creating an ongoing maladapted information loop that feeds on itself (think of reflex sympathetic dystrophy as a model--a local, acute injury that gets misinterpreted by the brain, and turns into a systemic disorder of crippling, body-wide pain that often results in suicide). But imho or not so humble opinion, that will be the minority. The majority will have ongoing infection. Even HIV, when kept in check by ARVs, still burbles inside cells and creates ongoing inflammation that shortens lifespan by around ten years. The idea that the pathogens are just happily dormant, causing no problem for anybody, is completely belied by the scientific literature.

Lyme:

http://www.scientificamerican.com/a...e-with-how-wily-lyme-disease-prowls-the-body/

I think we forget one thing. Maybe not everyone has to like the hypothesis which were proposed but what I think is the most important from this study that they found very strong evidence of metabolic problems. Of course we need replication but the results are very interesting. Now the researchers can work with their own hypothesis (and I am sure there will be a lot of them) and they will try to move us further.

 

[mermaid]

I am very interested in how the researchers view patients who have had long remissions only to become ill again - usually more severely. There are many of us around here who fit this profile. I was first ill late teens early twenties with M.E,. recovered spontaneously after a few years and then was almost normal functioning for around 8-9 years (some stamina issues and inability to get totally 'fit). A further viral infection, which then caused a bacterial infection put me down into the severe category, from which I have only had minor improvement over the past 8 years.

I have spoken with many other mainly middle aged women who have had the same illness trajectory. This makes me feel there is an immune deficiency somewhere that means we don't fight the precipitating infection(s) correctly and instead enter this 'stuck' mode.

@justy - by middle aged, do you mean menopausal or maybe perimenopausal. My problems with energy levels (previously very good) began to develop at this time. So maybe hormone changes make women vulnerable, and if there are already genetic markers (is that a correct scientific term?) are there, then the body is weakened and doesn't recover so easily.
Conversely to your question though this was my first ME hit, and was mild to start with, but whooping cough some years in weakened me further. I have never quite got back to the previous state, though am much better this year (herbalism mostly). If the detached retina hadn't hit me I would have had a reasonable year!

 

[justy]

@justy - by middle aged, do you mean menopausal or maybe perimenopausal. My problems with energy levels (previously very good) began to develop at this time. So maybe hormone changes make women vulnerable, and if there are already genetic markers (is that a correct scientific term?) are there, then the body is weakened and doesn't recover so easily.
Conversely to your question though this was my first ME hit, and was mild to start with, but whooping cough some years in weakened me further. I have never quite got back to the previous state, though am much better this year (herbalism mostly). If the detached retina hadn't hit me I would have had a reasonable year!

no. I guess I don't specifically mean middle aged, just later than teens or twenties. I became ill the second time, or my remission ended age 38. I know of quite a few others on PR who had similar.

Is it genetics? it can tend to run in families - we have three generations of women in my family and we are particularly interesting because I wasn't brought up by my birth mother, who also has ME, so unless it was acquired in the womb I can only see genetics as being important.

 

[mermaid]

Yes, the genetics angle seems quite strong. Very interesting in your own case. Oddly there is nothing that I have that resonates with any of the rest of the family that I know of (I have autoimmune disease, and ME/CFS of course and know of no one else in the family with it).
However my mother had a lot of illness, diagnosed as mental illness, (and my father) but I listened to a Radio 4 prog the other day on some mental illness being recategorised, so she could have been wrongly labelled though it was OCD mostly. My son has schizophrenia and they are looking at that as a biological illness more now too as I understand it.

 

[lilpink]

"Metabolomics should be rolled out fairly soon for patients. I am working on this with the person involved-particulary the UK side of things. @Rose49 is well informed of all this." (Apols..not very good at inserting quotations!)

This interests me (for obvious reasons). Clearly there are a lot of questions apropos type of sample, time delay between sampling and arriving at Stanford/OMF, type of carrier etc etc. But... *if* there was an issue which could be overcome by having a personal courier from the Uk who could take samples from a central collection point in person to the US then my other half has volunteered himself.. fwiw.

 

[voner]

Hey @Ben Howell,

I'm curious about the sample collection process they used. It seems the only limitation they put on the blood draw was for it to be at least three hours after the last meal. Since they were measuring levels of metabolites, I would think that they would need to also limit exertion levels or something like that, but then again, i'm really quite clueless on this .... It would be nice to have this clarified.

 

[natasa778]

My best guess is its less stuck on than the off button is broken. We need to find that button.

According to Naviaux, the best chance of hitting that off button is by targeting and re-setting purinergic signalling system, at least as so far as autism is concerned. Hopefully we'll hear more on that in the next few months, paper pending...

 

[Ben H]

"Metabolomics should be rolled out fairly soon for patients. I am working on this with the person involved-particulary the UK side of things. @Rose49 is well informed of all this." (Apols..not very good at inserting quotations!)

This interests me (for obvious reasons). Clearly there are a lot of questions apropos type of sample, time delay between sampling and arriving at Stanford/OMF, type of carrier etc etc. But... *if* there was an issue which could be overcome by having a personal courier from the Uk who could take samples from a central collection point in person to the US then my other half has volunteered himself.. fwiw.

We are working on that specifically and should have it sorted-don't worry

Will keep you updated on this and there will most likely be a forum announcement. But its not ready just yet.


B

 

[adreno]

According to Naviaux, the best chance of hitting that off button is by targeting and re-setting purinergic signalling system, at least as so far as autism is concerned. Hopefully we'll hear more on that in the next few months, paper pending...

Well, in autism purigernic antagonists are used; we certainly don't need that on the basis of this paper. Do we need the opposite? To enhance purigernic signaling? Nucleotides perhaps?

 

[Biarritz13]

We are working on that specifically and should have it sorted-don't worry

Will keep you updated on this and there will most likely be a forum announcement. But its not ready yet.


B

Do you think there is a solution for whose who don't live in UK but still in Europe?

 

[Ben H]

Do you think there is a solution for whose who don't live in UK but still in Europe?

Yes


B

 

[alex3619]

Well, in autism purigernic antagonists are used; we certainly don't need that on the basis of this paper. Do we need the opposite? To enhance purigernic signaling? Nucleotides perhaps?

It would most likely be the target could turn out as a specific subset of purinergic signalling. Broad treatment is more likely to have unintended side effects.