Naviaux et. al.: Metabolic features of chronic fatigue syndrome

[Mary]

The reality for some ME/CFS patients like my daughter is that a consequence of het autonomic dysfunction is drastically dysfunctional GI motility, both gastric emptying and large intestine motility are too slow. Food sits her stomach for too long and rarely digests as thoroughly as it should.

I don't know if this will be applicable to your daughter, but is probably worth checking out. One of the first things that went wrong with me was my digestion - it felt like food just sat in my stomach for hours and wasn't being digested. I could feel a heavy meal the next day just sitting there. It turns out I had low stomach acid. Most doctors won't check for this. I was fortunate enough to have a chiropractor who does muscle testing who helped me get my digestion on the right track. One of the first things he said to me was that he had to get my digestion working properly before taking other supplements; otherwise they wouldn't do any good. I do have to take betaine HCL with pepsin with heavy meals, but my digestion is soooo much better than before. Many many people with CFS have low stomach acid.

A simple test to check for low stomach acid is this:
On an empty stomach, drink a glass of water (about 8 oz.) into which you have mixed one-quarter teaspoon of baking soda (sodium bicarbonate). See how long it takes you to burp. If you haven't burped in two minutes, your stomach acid production is low.

And the supplements I take do make a difference now. I still have ME/CFS but am better than 10 years ago ...

You might want to look at this article also: http://healthyeating.sfgate.com/potassium-digestion-8978.html It talks about the role of potassium in gut motility and how low potassium can cause poor motility. I have trouble keeping my potassium levels up (despite low-normal results on blood work) and have to take potassium daily as well as drink low-sodium V8 which is high in potassium. Many on the board seem to have a problem with using potassium properly.

 

[osisposis]

I don't know if this will be applicable to your daughter, but is probably worth checking out. One of the first things that went wrong with me was my digestion - it felt like food just sat in my stomach for hours and wasn't being digested. I could feel a heavy meal the next day just sitting there. It turns out I had low stomach acid. Most doctors won't check for this. I was fortunate enough to have a chiropractor who does muscle testing who helped me get my digestion on the right track. One of the first things he said to me was that he had to get my digestion working properly before taking other supplements; otherwise they wouldn't do any good. I do have to take betaine HCL with pepsin with heavy meals, but my digestion is soooo much better than before. Many many people with CFS have low stomach acid.

A simple test to check for low stomach acid is this:
On an empty stomach, drink a glass of water (about 8 oz.) into which you have mixed one-quarter teaspoon of baking soda (sodium bicarbonate). See how long it takes you to burp. If you haven't burped in two minutes, your stomach acid production is low.

And the supplements I take do make a difference now. I still have ME/CFS but am better than 10 years ago ...

You might want to look at this article also: http://healthyeating.sfgate.com/potassium-digestion-8978.html It talks about the role of potassium in gut motility and how low potassium can cause poor motility. I have trouble keeping my potassium levels up (despite low-normal results on blood work) and have to take potassium daily as well as drink low-sodium V8 which is high in potassium. Many on the board seem to have a problem with using potassium properly.

this is interesting, I have dealt with diarrhea thoughout this, I rarely get constipated, I know I have low acid stomach, I also deal with bile back up, yuk, not as bad as it used to be, but once in awhile , I get horrible pain around the top of my stomach, because I don't tolerate corn/high froutose corn surup I found I can drink a little diet pepsi and burp and it relieves the pain, for real, and I know everyone thing aspartame, no, but that is what got me through this ordeal for all these years and I actually found a few articles that show that aspartame may be of benefit in this situation, and because of the lack of acid it's not harmful like it may be on a regular stomah PH or where some has high acid . goes a long way in playing attn. to what helps you and what doesn't. however I have to add that sence they took aspartame out of diet pepsi , it still makes me burp and that's is the main thing I need help with when I have these attacks, they are quit scary

 

[osisposis]

my mom was treated for hyperthyroidism for many years, than they desided she was hypo, made me so made, I tried telling her to quit having such blind faith in these doctors that don't know what the hell they are doing, I'm convienced she suffers from environmental exposures but she is old school and wont listen to me, she just thinks everything is part of getting old her basement smells mildew and I cant even stay the night there because it bothers me, this illness has tore my family apart in so many ways, when will the suffering end! 20 some years now that I've missed out of family stuff, I'm basicly a stranger now and no standard tests yet have showed I have hyper or hypothyroidism

 

[Research 1st]

It is interesting to hear talk about similarities with HIV/AIDS because AIDS patients are constantly fighting pathogens and they are helped with antiretrovirals - which is the opposite of what this study's authors are proposing. Being that they are constantly attacked, I would assume that HIV/AIDS patients are in a hypermetabolic state.

Some of us have retroviruses, but not like HIV, we have activated HERV's that, presumably, are associated to the autoimmunity , relatively recently discovered, in CFS + POTS and I've had the tests myself, which are also positive (I don't trust research claims blindly in a heterogenous diagnosis and test myself when possible). How this ties in with the Metabolic defect I have no idea..yet. I can only reference one paper at the moment, but the big one is meant to be coming out this year or next:

Here's a first (tiny) study with only 12 ME patients, positive at 66%, but interesting none the less considering the official line is we need to stop thinking about infections and do more exercise!

''In eight out of 12 individuals with ME, immunoreactivity to HERV proteins was observed in duodenal biopsies. In contrast, no immunoreactivity was detected in any of the eight controls''.

Source: In Vivo. 2013 Mar-Apr;27(2):177-87.
Plasmacytoid dendritic cells in the duodenum of individuals diagnosed with myalgic encephalomyelitis are uniquely immunoreactive to antibodies to human endogenous retroviral proteins.
De Meirleir KL1, Khaiboullina SF, Frémont M, Hulstaert J, Rizvanov AA, Palotás A, Lombardi VC.

Why am I mentioning infection on a Mitochondria test thread? Because of the endless amount of people you will find online with a diagnosis of ME, CFS, Chronic Lyme (3 disputed conditions), all reporting that when they test via LTT/Elispot, they have positive results for Chronic Intracellular Infection.

Why do I want to share this rambling of mine with you and others? Because not only does Cpn cause 'Chronic Fatigue', it can also be associated to worsening of Asthma, Heart Failure and Cancer etc, in it's chronic intracellular form where simple antibiotics won't work (like Lyme). The drugs won't work as it has no cell wall to target.

So yea, chronic infections are not only prevalent n ME CFS Lyme (whatever you want to call it) when not relying on serology (antibodies), they are also contributing to further ruining our lives. when we are already really ill to begin with. Hence it's critical we focus on pathogens, when we are riddled with chronic immune activation, ATP loss, inflammation and autoimmunity,

Check this out from the past (the past in Science is very important in research to find links to the present):

''Heatshock protein 60 (hsp60) in the matrix of mitochondria is essential for the folding and assembly of newly imported proteins''.

Source: Nature. 1990 Nov 29;348(6300):455-8.
The mitochondrial chaperonin hsp60 is required for its own assembly.
Cheng MY1, Hartl FU, Horwich AL.

''The heat-shock protein hsp60 is typically found in mitochondria''

Source: Mol Immunol. 1999 Jun;36(9):619-28.
A 60 kD heat-shock protein-like molecule interacts with the HIV transmembrane glycoprotein gp41.
Speth C1, Prohászka Z, Mair M, Stöckl G, Zhu X, Jöbstl B, Füst G, Dierich MP.

OK, so HSP is usually found inside Mitochondria. Which makes us remember this from 3 years ago.....

When evaluated with 61 other ME and 399 non-ME samples (331 BD, 20 Multiple Sclerosis and 48 Systemic Lupus Erythematosus patients), a peptide from Chlamydia pneumoniae HSP60 detected IgM in 15 of 61 (24%) of ME, and in 1 of 399 non-ME at a high cutoff (p<0.0001). IgM to specific cross-reactive epitopes of human and microbial HSP60 occurs in a subset of ME, compatible with infection-induced autoimmunity''.

Source:
PLoS One. 2013 Nov 28;8(11):e81155. doi: 10.1371/journal.pone.0081155. eCollection 2013.
Epitopes of microbial and human heat shock protein 60 and their recognition in myalgic encephalomyelitis.
Elfaitouri A1, Herrmann B, Bölin-Wiener A, Wang Y, Gottfries CG, Zachrisson O, Pipkorn R, Rönnblom L, Blomberg J.

Question we should all consider. As ME CFS doesn't have a test, when there is an evidence based test (potentially the Metabalon Metabolic one we are all discussing), does the percentage in the paper above, go up? And if so, by how much. It might stay level, it may soar up to 80%.

And the next question, what (if any) other infections (bacterial, viral, mycoplasmas, retroviral) can cause this proposed ''Infection Induced Autoimmunity' that Blomberg et al, discovered in 1 in 4 PWME, using no diagnostic test to confirm ME...as well?

If we start having a pathogen party, or should I say bacterial, I want to see the test results of patients with and without these chronic intracellular infections, and compare the differences to our 'scores' on the proposed Metabalon test, and the future Autoimmune tests, if any.

 

[mermaid]

t

@mermaid - has your friend who took a statin tried CoQ10? It might help with his recovery.

Thank you @Mary Yes, he's pretty clued up and has tried the best kind of CoQ10. Sadly it hasn't helped and he's done research which indicates that the damage can be permanent even so...

 

[Mary]

Thank you @Mary Yes, he's pretty clued up and has tried the best kind of CoQ10. Sadly it hasn't helped and he's done research which indicates that the damage can be permanent even so...

Wow - I'm really sorry to hear that. Maybe with all the research being done now on ME/CFS, something might turn up that could tangentially help your friend - there've got to be thousands more people like him unfortunately! :thumbdown:

 

[mermaid]

Thank you @Mary He's actually aged 70 now and in many ways seeing friends going downhill and sometimes dying of other things, and having spent many years researching his condition he is feeling pretty good - other than the mitochondrial issues that mean he is restricted energy wise. He has sorted out all the other symptoms!

Wow - I'm really sorry to hear that. Maybe with all the research being done now on ME/CFS, something might turn up that could tangentially help your friend - there've got to be thousands more people like him unfortunately! :thumbdown:

Edit: sorry I managed to put your quote under mine!

 

[Forbin]

Something that crossed my mind...

Could the "persistent environmental stress" that precipitates the hypometabolic dauer-state actually be the persistently elevated cytokines seen early in the illness by Drs. Hornig and Lipking at the CII?

This would push the chain of events back one step, making the question one of what is triggering and perpetuating the persistent cytokine elevation seen early in ME/CFS.

It certainly seems that the CII suspects the answer is in the microbiome.

 

[aimossy]

Am I the only one who is struggling through fog to find a list of the 612 metabolites that were tested in the paper. It should be in there somewhere shouldn't it - anyone know?
@Ben Howell Sorry - just tagging you, in case you can find out for sure.

If people missed it, in Dr. Maureen Hanson's Solve ME/CFS Initiative webinar she talks about findings in her metabolomics work and compares with the Naviaux paper and there seems to be some consistent findings. Dr Hanson says their paper is in the review process at the moment. I think the section on this starts about 18 minutes in.

 

[Forbin]

I haven't seen a list of all 612, but there is an appendix of supporting information here that lists the top 61 diagnostic metabolites for both males and females.

 

[knackers323]

Its probably far too early for it but is there any ideas on potential treatment options. Would the lipid therapy that garth nicolson and others used to talk about be any good?

Anyone tried these for an extended period?

 

[Snow Leopard]

I haven't seen a list of all 612, but there is an appendix of supporting information here that lists the top 61 diagnostic metabolites for both males and females.

The key is that we want to know which ones were ruled-out as normal!

 

[Sasha]

Its probably far too early for it but is there any ideas on potential treatment options. Would the lipid therapy that garth nicolson and others used to talk about be any good?

Anyone tried these for an extended period?

I tried it for a few months at a high dose and it did nothing.

 

[mermaid]

Its probably far too early for it but is there any ideas on potential treatment options. Would the lipid therapy that garth nicolson and others used to talk about be any good?

Anyone tried these for an extended period?

@knackers323 There's another thread on treatment implications after the study here
http://forums.phoenixrising.me/inde...udy-pnas-august-2016.46524/page-2#post-758949

 

[aimossy]

I haven't seen a list of all 612, but there is an appendix of supporting information here that lists the top 61 diagnostic metabolites for both males and females.

Thanks took me a while to find that section as well. Someone is going to find your link here to that useful. I should've asked earlier instead of frying my brain. Was trying to find list to see all the metabolites that were covered so we can cross compare with other studies as they come.

 

[Simon]

If people missed it, in Dr. Maureen Hanson's Solve ME/CFS Initiative webinar she talks about findings in her metabolomics work and compares with the Naviaux paper and there seems to be some consistent findings. Dr Hanson says their paper is in the review process at the moment. I think the section on this starts about 18 minutes in.

Well worth a watch (starts at 18' 15", here).

This is the relevant slide, comparing Naviaux's study on the left with Hanson's new study (submitted for publication) on the right. The Hanson study is smaller (17 patients v 15 controls), and female only, so this slide compares females from Naviaux with the whole Hanson cohort.

The key finding is that Maureen Hanson's study also found a hypometabolomic state, with most significant differences with controls showing lower metabolite levels in patients. They found some of the same differences (central panel. "common", but found differences Nav did not (eg energy metabolism) and didn't find others (eg sphingolipids).

Though both studies used Mass Spectrometry there were differences in the methods (Hanson's study only detected 361 metabolites), which might account for some of the differences. Plus both studies are small, so you would expect some differences anyway due to random variation.

 

[Marco]

@Simon

Quite generous significance levels there!

 

[Tuha]

@Simon

Ok, I am very bad in reading scientific articles. If we compare Naviaux and Hanson´s study what can we say? Are the results consistent or there are again a lot of differences? Or can we say that Hanson replicated at least part of Naviaux´s study?

 

[A.B.]

The key finding is that Maureen Hanson's study also found a hypometabolomic state, with most significant differences with controls showing lower metabolite levels in patients. They found some of the same differences (central panel. "common", but found differences Nav did not (eg energy metabolism) and didn't find others (eg sphingolipids).

Though both studies used Mass Spectrometry there were differences in the methods (Hanson's study only detected 361 metabolites), which might account for some of the differences. Plus both studies are small, so you would expect some differences anyway due to random variation.

Did the Hanson team test for sphingolipids?

She also said (paraphrasing) that there were differences in the testing procedure which might account for the differences, which is a little worrying, but probably doesn't invalidate the broader conclusion of a hypometabolic state.

Ok, I am very bad in reading scientific articles. If we compare Naviaux and Hanson´s study what can we say? Are the results consistent or there are again a lot of differences? Or can we say that Hanson replicated at least part of Naviaux´s study?

The finding of hypometabolism is confirmed.

 

[Simon]

@Simon

Quite generous significance levels there!

Not necessarily. I'm a bit hazy on this, but I think Q<0.15 means a false discovery rate of 15% i.e. 15% (1 in 7) of the reported "abnormalities" would be expected to be a false positive (that's NOT the same as p<0.15, which would be much slacker and bring in a lot of false positives). The previous slide showed Q<0.10 was used by Naviaux in his study. I need to spend more fun time on these stats.