Founder of Health Rising and Phoenix Rising
Naviaux does not believe what is happening in ME/CFS is your standard genetic mitochondrial dysfunction by the way; he believes the mitochondria are turned off - not damaged.Dr Goodman - neurologist and POTS doctor at Mayo, AZ has most of us doing a protocol for mitochondrial dysfunction. He says that the few test available to test for dysfunction are not enough. There is so much more that there aren't test for. CQ10 is one thing he has us take.
Also, I found it interesting that they mentioned an increase in peroxide. My having vitiligo and that possibly being because of higher peroxide levels and autoimmune issues - this is interesting. The body also ups peroxide to kill and eliminate pathogens. Probably a compensatory response that goes overactive.
I see. Dr Goodman always said he thought there was an issue with mitochondria. But had no way to know what was wrong. Would be interesting if the answer is they are turned off vs just not functioning properly. An ATP problem for sure.Naviaux does not believe what is happening in ME/CFS is your standard genetic mitochondrial dysfunction by the way; he believes the mitochondria are turned off - not damaged.
Also, the Mail online was perhaps the first (UK paper) posting this yesterday: http://www.dailymail.co.uk/health/article-3763433/Chronic-fatigue-real-condition-People-debilitating-illness-telltale-signs-blood.htmlSome media reports are out - no really major news outlets yet that I can see
Yeah, 'hibernation' seems to have been hit upon as a sparky aspect to relate to readerships, possibly making for plenty of misunderstanding that it's talking about a behavioral trait, or bizarrely inappropriate evolutionary throw-back. But of course, in the original instance, Naviaux is talking about a similarity between the cellular states as seen by looking at their metabolite levels. And the act of hibernation itself only being one potential source of metabolic stress that would trigger a cell to (independently) enter a 'dauer' like state. This kind of low-power-safe-mode being useful to avoid replicating local viruses or avoid various other pitfalls.the syndrome is like a state of hibernation
Yes ATP production is a core problem - but how to entice the mitocondria out of their slumber. Naviaux has ideas but there's no easy answer to that. That answer will take some time.I see. Dr Goodman always said he thought there was an issue with mitochondria. But had no way to know what was wrong. Would be interesting if the answer is they are turned off vs just not functioning properly. An ATP problem for sure.
Well said Zero Gravitas. I think it could be an evolutionary hijack though = one used for survival in the distant past which has gotten activated in ME/CFS somehow..Naviaux I think felt the media would jump on the hibernation idea and they have! It's more about low-metabolic states.Also, the Mail online was perhaps the first (UK paper) posting this yesterday: http://www.dailymail.co.uk/health/article-3763433/Chronic-fatigue-real-condition-People-debilitating-illness-telltale-signs-blood.html
Today the Telegraph chimed in (with what looks, in part, almost plagerised from the Times): http://www.telegraph.co.uk/news/2016/08/30/scientists-find-signature-of-chronic-fatigue-syndrome-in-blood-w/
And Me Ascossiation (UK) seem to have duplicated The Times article (possibly in full?), for those (like me) without access to the paper's paywall: http://www.meassociation.org.uk/2016/08/chronic-fatigue-syndrome-could-be-the-body-trying-to-hibernate-the-times-30-august-2016/
Yeah, 'hibernation' seems to have been hit upon as a sparky aspect to relate to readerships, possibly making for plenty of misunderstanding that it's talking about a behavioral trait, or bizarrely inappropriate evolutionary throw-back. But of course, in the original instance, Naviaux is talking about a similarity between the cellular states as seen by looking at their metabolite levels. And that only being one potential source of metabolic stress that would trigger a cell to (independently) trigger a 'dauer' like state. This kind of low-power-mode being useful to avoid replicating local viruses and avoiding other pitfalls.
So it's an important, protective, cellular mechanism, but in CFS it's widespread and just doesn't ever switch off (when it should have). Also, the observation of, on average, 75% of metabolic abnormalities unique to individual patients go beyond characterizing the dauer state, I think, and would surely go a long way to illustrating the basis of the great variety of patient symptoms (and how to address them). One also assumes that the hypometabilic state will amplify any existing problem areas of one's biology.
Where the heck is the New York Times. I wonder if they were put off by the 2-day early release of the paper.There was a very short blurb on the news on CBS this morning. Mentioned hibernation and new findings
If I did not have CFS I would have no idea what they were talking about. Hibernation does not describe my experience at all.
Adenosine is required for so metabolic factors _ ATP, ADP, FADP (?) and others = I was shown a list - that it could be at the core of all this apparently.I remembered a post I did years ago on the Health rising blogs. Dr Bateman had connected adenosine to CFS years ago. Here's part of a post I made.
With CFS – there are few things other than symptoms that can be shown with science. There are some markers like adenosine levels, (Here’s a thread with a link of a really cool slide show on this that has a link you can go to on adenosine. It’s a bit of a round about way to get to it – but, I think you will like it.http://forums.dinet.org/index.php?/topic/21517-cfs-fms-ms-studies-being-conducted-and-showing-genes-involved-in-connection-with-exercise-intolerance-maybe-this-would-apply-to-us-potsies-too/?hl=adenosine ) T-cell and B-cell abnormalities with CFS.
Here is a study done by Lucinda Bateman in SLC shows that she is finding OI and POTS with her CFS patients. (This is my sister’s doctor. There is a genetic component in our family – as all three of her kids have what they think is either POTS or OI. My sister has OI/CFS/FMS and I have POTS/EDS/MCAS/FMS and some autoimmune problems.)
I wrote about adenosine inducing a hibernation like syndrome a couple of years ago.Adenosine is required for so metabolic factors _ ATP, ADP, FADP (?) and others = I was shown a list - that it could be at the core of all this apparently.
I wrote about adenosine inducing a hibernation like syndrome a couple of years ago.
Cool Remy!I wrote about adenosine inducing a hibernation like syndrome a couple of years ago.
Note that that is the same Dr Sid Baker that is now pioneering the HDC treatment I also posted on recently.Whoa - check this out from Remy
I believe at this time that my chronic infections have induced a sort of hibernation syndrome caused by a high level of adenosine without a sufficient amount of adenosine deaminase enzyme to break it down. This high level of adenosine causes a vicious cycle that is devastating to the immune system and allows the infections to continue to gain ground.
This study has shown that adenosine is the "switch" that turns on hibernation.
Turns out, the hibernation switch in squirrels is a receptor on brain cells for the ‘drowsiness’ neurotransmitter adenosine, which sends us to sleep by building up gradually in the brain during the day, New Scientist explains.
By blocking it using a chemical called cyclopentyltheophylline, the researchers could wake hibernating squirrels up; stimulating it using a chemical called cyclohexyladenosine sent them back to sleep.
Finally, I also found a pilot study that contends that Valtrex modulates adenosine levels.
Dr. Sid Baker, in cooperation with Jill James Ph.D., conducted a pilot study of 10 children with autism. Nine children were treated with acyclovir and one child was not treated.
Note: Valtex is quickly converted to acyclovir in the intestines and the liver5. From a viral treatment perspective many viruses that Valtrex can affect can also take up residence in the liver. Valtrex is also more bioavailable than oral acyclovir6 (more similar to IV acyclovir) and has what seems to be a safer side-effect profile.
In all the 9 children adenosine levels were seemingly improved. Some children had higher levels of adenosine and they were lowered. Some children had lower levels and they were raised. The untreated child’s level remained unchanged. This striking normalizing effect is not very common in medicine.
I wonder if this is actually why antivirals seem to help - they may not only be stopping the viral replication, but they are modulating adenosine levels. I know that I have found improvement from high doses of AVs.
But, if it's a compensatory response and has a good reason for being that way......if we try to activate it when it's a protection to us for whatever reason-----we may create much worse issues.Well said Zero Gravitas. I think it could be an evolutionary hijack though = one used for survival in the distant past which has gotten activated in ME/CFS somehow..Naviaux I think felt the media would jump on the hibernation idea and they have! It's more about low-metabolic states.
If I'm understanding it correctly - I think they mean - the mitochondria, energy part of the cells is not working. Not just dysfunctional - but asleep - like in hibernation. They kept referring to pathogens and virus as a possible connection/cause. But appears the immune system is flat not working along with the mitochondria. The ATP or energy factor of the cell. Adenosine is not there or is there and not working. Same with leptin. It's there but not working. Now whether there is a genetic factor at play here, a kindling or issues with protein folding - I guess they still need to figure that out. Also channelopathys maybe. (I am reading into this based on what I've read over the years.) I think maybe the science is catching up with what we thought was the issues. We are now starting to get proof.So energy production is reduced probably related to mitochondria etc. The hibernation reference doesnt make sense at all as most mecfsers i know ate insomniacs and its mostly only in tbe very early stages of the illness peopletend to sleep alot.
So what are they preposing to fix this issue that hasnt been tried already in cfs?
From what i have read in reguards to other genetic mito disorders the only real treatments arent that effective and are supplements like q10, carnitine etc. I cant call the name of the treatment protocol but involved ritalin and mito supps for cfs, it seemed somewhat effective but not a cure or treatment for other symptoms like sleep disorders, pain etc? So didnt really seem to be getting at the issue.
I am sounding negative but just would like to see what type of treatments they will use.
Is it another subgroup? I suggest this as the 2 treatments rituximab and ampligen, which currently seem to have the most success, appear to work on the immune dysfunction .
Time will tell i guess.