An article out tomorrow at 10am ET everyone
Naviaux et. al.: Metabolic features of chronic fatigue syndrome
- Thread starter A.B.
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My uneducated guess is that this chronically reduced metabolic rate at the cellular level is not simply a case of being stuck in the "low" position. Rather, it's driven by another chronic process that won't resolve, like an infection or autoimmunity, or an alteration in the microbiome (perhaps initiated by an infection), and one or more of those things is leading to chaos at the cellular level. Fix the problem upstream and, hopefully, the cellular metabolism will return to normal.
At the moment, at least, I think the real importance of this finding is in its diagnostic value as a biomarker. That in itself is HUGE.
At the moment, at least, I think the real importance of this finding is in its diagnostic value as a biomarker. That in itself is HUGE.
I hope so too!
Marilyn Black suggested a new name: Dauer Disease. Simple, describes the problem (assuming it is replicated) and is unlikely to be responded to with "Oh yes, well I'm in a dauer-like state all the time, and I just get on with things" or "my cousin's ex-wife's best friend's sister had that, and she just meditated and aligned her chi and that fixed her dauer-like state right up"
Marilyn Black suggested a new name: Dauer Disease. Simple, describes the problem (assuming it is replicated) and is unlikely to be responded to with "Oh yes, well I'm in a dauer-like state all the time, and I just get on with things" or "my cousin's ex-wife's best friend's sister had that, and she just meditated and aligned her chi and that fixed her dauer-like state right up"
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Yes! Yes I can! Wait for tomorrow's article!
In particular it will end false lines of research given a few years. It will also help narrow the range of research, give us much better targets to focus on, and far fewer potential therapeutic targets.
Yes... autoantibodies to sphingoglycolipids are mentioned. Or maybe that's one of the articles I read to assimilate this... 
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Sorry I am confused, is this article here on PR or somewhere else? I really want to understand how this study connects to autoantibodies and RTX.
Sorry, @Gingergrrl, on meaction.net
Autoimmune diseases can be reversed/cured by diet alone - look at Dr Terry Wahls and the folk with MS who are following her and taking part in the trials she is funding. A whole pile of folk with Hashimotos are doing the same, including me. Vast improvements on the autoimmune Paleo protocol. Not popular news here.
I REALLY WANT TO PUBLISH IT NOW, but I also really need to sleep.
We didn't get an advance copy: I'm still bitter. So your hard-working editor is up 'til all hours.
For more on WTF Naviaux is talking about re: 'lipid rafts', check out Morris et al's 2015 article, "The Deleterious Effects of Oxidative and Nitrosative Stress on Palmitoylation, Membrane Lipid Rafts, and Lipid-Based Cellular Signalling: New Drug Targets in Neuroimmune Disorders." Only reason I got as far as I did was because of having 'translated' that one awhile ago into my own language.
Whole section on lipid rafts and why they are important to immunity in that paper.
-J
We didn't get an advance copy: I'm still bitter.
So your hard-working editor is up 'til all hours. For more on WTF Naviaux is talking about re: 'lipid rafts', check out Morris et al's 2015 article, "The Deleterious Effects of Oxidative and Nitrosative Stress on Palmitoylation, Membrane Lipid Rafts, and Lipid-Based Cellular Signalling: New Drug Targets in Neuroimmune Disorders." Only reason I got as far as I did was because of having 'translated' that one awhile ago into my own language.
Whole section on lipid rafts and why they are important to immunity in that paper.
-J
Yeah sure, me too, I do great with more protein.
Unfortunately, 'great' means 'wow, better than before', rather than 'well'.
-J
Unfortunately, 'great' means 'wow, better than before', rather than 'well'.
-J
Just don't go marketing nematode pills! That's my idea!!!
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Sorry, @Gingergrrl, on meaction.net
If I were a nematode, a bear, or a human, I would use hydrogen sulfide to enter this hypometabolic state. As a human though, I might also figure out a way how to reverse this hypometabolic state. A state where supraphysiological concentrations of hydrogen sulfide induce a reversal of flow in the electron transport chain as contrasted to physiologic concentrations of endogenous hydrogen sulfide that enhance metabolic function. This inhibitory mechanism on metabolism created by hydrogen sulfide can only be achieved at concentrations produced via exogenous synthesis. In other words this would represent a byproduct of sulfate and sulfur reducing bacteria. This hypometabolic state would protect the host against a redox imbalance as part of a highly conserved function of innate immunity and bioenergetic conservation mechanisms. These organisms evolved alongside the mitochondria as did their complex mechanisms of preserving host longevity even at the expense of host vitality.they also compete for that resource used in the synthesis of fatty acids, the precursor of those molecules found to be most significantly deranged in the present study,
Got a fix the GIT. B vitamins are not going to do this. It' can't be surprising that the organisms that do synthesize each and every one of these B vitamins might play a role here.
Got a fix the GIT. B vitamins are not going to do this. It' can't be surprising that the organisms that do synthesize each and every one of these B vitamins might play a role here.
IMO, it's the ones that don't that are important.
The whole idea behind this hypometabolic state is that it's protective. You're trying to starve the little buggers out. It's like a lord setting fire to his people's crops. We'll make it. We know the lay of the land. And the invaders will starve.
Multiple pathogens, including some of the ones most common in ME, rely on our B vitamins to survive. It's something I've looked up because I often feel great with high-dose Bs... for a little while, before I have a miserable crash. I was taking pretty high doses for awhile, but once I got a bit better I had to cut back to keep getting better, or I'd be encouraging them... sprinkling their favorite meal on the petri dish that is me.
-J
The whole idea behind this hypometabolic state is that it's protective. You're trying to starve the little buggers out. It's like a lord setting fire to his people's crops. We'll make it. We know the lay of the land. And the invaders will starve.
Multiple pathogens, including some of the ones most common in ME, rely on our B vitamins to survive. It's something I've looked up because I often feel great with high-dose Bs... for a little while, before I have a miserable crash. I was taking pretty high doses for awhile, but once I got a bit better I had to cut back to keep getting better, or I'd be encouraging them... sprinkling their favorite meal on the petri dish that is me.
-J
OK sleeeeep. Bye guys!
Bye guys!
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It explains everything potentially..
Without energy our immune systems won't work.
Effectively using this model, the more sick you get from damage from uncontrolled ATP derived inflammation, the more immune suppressed you get, but over time and a new form of immune suppression develops., this will likely damage your brain neurons via uncontrolled oxidative injury.
Very interestingly, if your brain ATP is ruined, your brain won't work - so expect cognitive dysfunction, and neuropsych symptoms without a doubt (neuropsych symptoms are common in neurological diseases). Also expect visual defects as neurons won't communicate efficiently, and also expect seizures (seizures are common in Mito disorders as well).
i am proposing this unchecked process, over time, will 'age' your cells, tissues (brain) and bones prematurely - precisely what a year 1 CFS diagnosed patient won't report, and what a 20 years CFS diagnosed patient does report. None of this will ever be detected if you focus on subjective FATIGUE in research. Hence we never got anywhere since 1988.
It would explain the huge variance in types of infection in CFS also (we never seem to share identical pathogens),but there must be a shared pathogen in their somewhere, driving the autoimmunity and we only all have that, due to the immune defect in the first place. The most obvious candidate after a HERV would be Lyme/Chlamydia pneumonia, or all 3 at once. Who knows at the moment, as we can't test ourselves yet.
Either way, from all this, subsets of disease damage (pathogens, autoimmunity, brain dysfunction) will be explained, and proven, once correct disease cohorts can be finally analysed, away from aforementioned FATIGUE only.
It is logical that it takes time to damage the immune system and a presentation of CFS at year 1, is not in the same league as CFS in year 20 (in terms of immune defense, inflammation, development of autoimmunity) and that is why (probably) many with CFS have CFS first....then go into POTS.....into Arthritis......into Cancer....(and some) .into fatal presentation. It also explains why people who recover fully, tend to in the first year.
The inflammation in ME will likely be a causative reaction to mitochondrial dysfunction, without chronic inflammation you won't have this disease (in its severe form at least), period.
Finally, I imagine ME will be validated more rapidly now because other diseases which have brain damage, have similar findings to ME (Organic CFS)- thus further validating it. e.g. an out of control CDR or feature that Ron Davis/Navieux found may well progress into Parkinson's, and never be diagnosed as CFS, but yet they share a similar link. This is all my speculation, but it seems plausible as we know for a fact Mitochondria in areas of Parkinson's patients brains aren't working correctly. The next question - what about our brains?!
Once a test is out, so many people will find out they have 'it', but in a presentation unique to them, which also fits in with findings in research and clinical practice.
Most of the above was observed by Dr Cheney ages ago, specifically that he observed there are phases in 'CFS', with the brain getting affected first, then the heart, and finally the immune system gives up,
With a future test, Dr Cheney and others can prove this observation as present or not, by testing CFS patients diagnosed for: 1, 5, 10, 15, 25, 40 years and then see who has what, and at what stage of their illness. Then we're really talking as you can demonstrate that the disease has consequence by not being appropriately funded.
Then NIH/CDC/HSS will have to fund massively, as if not, you can prove the patient will develop incurable or highly debilitating co-morbidities.
Without energy our immune systems won't work.
Effectively using this model, the more sick you get from damage from uncontrolled ATP derived inflammation, the more immune suppressed you get, but over time and a new form of immune suppression develops., this will likely damage your brain neurons via uncontrolled oxidative injury.
Very interestingly, if your brain ATP is ruined, your brain won't work - so expect cognitive dysfunction, and neuropsych symptoms without a doubt (neuropsych symptoms are common in neurological diseases). Also expect visual defects as neurons won't communicate efficiently, and also expect seizures (seizures are common in Mito disorders as well).
i am proposing this unchecked process, over time, will 'age' your cells, tissues (brain) and bones prematurely - precisely what a year 1 CFS diagnosed patient won't report, and what a 20 years CFS diagnosed patient does report. None of this will ever be detected if you focus on subjective FATIGUE in research. Hence we never got anywhere since 1988.
It would explain the huge variance in types of infection in CFS also (we never seem to share identical pathogens),but there must be a shared pathogen in their somewhere, driving the autoimmunity and we only all have that, due to the immune defect in the first place. The most obvious candidate after a HERV would be Lyme/Chlamydia pneumonia, or all 3 at once. Who knows at the moment, as we can't test ourselves yet.
Either way, from all this, subsets of disease damage (pathogens, autoimmunity, brain dysfunction) will be explained, and proven, once correct disease cohorts can be finally analysed, away from aforementioned FATIGUE only.
It is logical that it takes time to damage the immune system and a presentation of CFS at year 1, is not in the same league as CFS in year 20 (in terms of immune defense, inflammation, development of autoimmunity) and that is why (probably) many with CFS have CFS first....then go into POTS.....into Arthritis......into Cancer....(and some) .into fatal presentation. It also explains why people who recover fully, tend to in the first year.
The inflammation in ME will likely be a causative reaction to mitochondrial dysfunction, without chronic inflammation you won't have this disease (in its severe form at least), period.
Finally, I imagine ME will be validated more rapidly now because other diseases which have brain damage, have similar findings to ME (Organic CFS)- thus further validating it. e.g. an out of control CDR or feature that Ron Davis/Navieux found may well progress into Parkinson's, and never be diagnosed as CFS, but yet they share a similar link. This is all my speculation, but it seems plausible as we know for a fact Mitochondria in areas of Parkinson's patients brains aren't working correctly. The next question - what about our brains?!
Once a test is out, so many people will find out they have 'it', but in a presentation unique to them, which also fits in with findings in research and clinical practice.
Most of the above was observed by Dr Cheney ages ago, specifically that he observed there are phases in 'CFS', with the brain getting affected first, then the heart, and finally the immune system gives up,
With a future test, Dr Cheney and others can prove this observation as present or not, by testing CFS patients diagnosed for: 1, 5, 10, 15, 25, 40 years and then see who has what, and at what stage of their illness. Then we're really talking as you can demonstrate that the disease has consequence by not being appropriately funded.
Then NIH/CDC/HSS will have to fund massively, as if not, you can prove the patient will develop incurable or highly debilitating co-morbidities.