Lipkin finds biomarkers not bugs

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The CDC PCOCA telephone broadcast on 10 September 2013, featured a lengthy presentation from Dr Ian Lipkin who revealed some stunning initial results from the study that is primarily hunting for pathogens in ME/CFS. Simon McGrath and Russell Fleming (Firestormm) review this exciting and possibly game-changing news...


Dr Ian Lipkin
Lead Researcher
Chronic Fatigue Initiative (CFI)
Pathogen Discovery and Pathogenesis Study

Read the full Lipkin Transcript: Here.

Dr Ian Lipkin has been a human whirlwind in ME/CFS research since he became involved a few years back, and he's just surprised us all by announcing the first results from the world's largest ever biomedical ME/CFS study in a public broadcast!

He started off by lowering expectations: their results thus far do not implicate a single infectious agent and they have not discovered the cause of CFS. But he then wowed the hundreds listening to the conference call by revealing they had found strong evidence for immune overstimulation, both in blood plasma and in cerebro spinal fluid; and that they were now hard at work trying to identify what could be causing these abnormalities.

The big pathogen hunt draws a blank thus far

This study is looking exhaustively for any pathogen: viral, bacterial, fungal or parasitic, to see if a chronic infection could explain ME/CFS. Many of the results are in, but so far there is no clear sign of viruses at least. It is every bit a collaborative effort, with patients provided by long-established physicians including Dr Dan Peterson and Professor Jose Montoya.

The Key Players

Lipkin began by thanking the clinicians who had provided the all-important samples. Effectively it was a roll call of America's top ME/CFS physicians:

Professors Jose Montoya, Anthony Komaroff and Nancy Klimas; and Drs Dan Peterson, Lucinda Bateman, Sue Levine and Donna Felsenstein.

The study itself was run by Dr Mady Hornig (CFI Principal Investigator) at the Centre for Infection and Immunity at Mailman School of Public Health; where Lipkin is also based.

He went on to acknowledged the very necessary support of the Chronic Fatigue Initiative, the Evans Foundation and an anonymous donor supporting Montoya's work.​

First the researchers looked at blood plasma for 285 CFS patients and 201 controls from Jose Montoya at Stanford (these are serious numbers). They searched for genetic evidence of infection using a panel that was able to detect 20 specific bacteria, viruses or parasites; including Epstein-Barr virus, Human Herpes Virus 6, enteroviruses, Influenza A and Borrelia bacteria.

Next they used high throughput sequencing, a method that was pioneered by Lipkin and colleagues that was used to discover over 500 viruses – so they felt fairly confident that if a virus was present, then they would have found it.

But they effectively drew a blank using both methods - only 1.4% of CFS patients were found to have HHV6 infection, but so did 1% of controls.

Other findings...

Lipkin said they also found Anelloviruses in 75% of those studied in plasma samples, but it was not specific for Chronic Fatigue Syndrome (we don't currently have separate figures for patients and controls). Anellovirus is believed to cause widespread chronic infection in the human population, but has not yet been associated to any specific disease. "I really don’t know at this point what this finding means" said Lipkin.

They also found retroviruses in 85% of the sample pools. However, Lipkin expressed caution:

"It is very difficult at this point to know whether or not this is clinically significant. And given the previous experience with retroviruses in Chronic Fatigue, I am going to be very clear in telling you – although I am reporting this at present – in Professor Montoya’s samples neither he nor we have concluded that there is a relationship to disease ...if I were to place bets and speculate, I would say that this is not going to pan out."

Window on the brain: Cerebrospinal fluid samples

Both Lipkin and Hornig were clearly excited to have had access to the 60 cerebrospinal fluid samples from Peterson, and kindly donated by his ME/CFS patients. Cerebrospinal fluid bathes our brain and spinal cord so it gives access to what goes on in the brain, a prime site of interest to researchers, but hard to access; so these spinal tap samples are precious.

However, using the same molecular techniques to track down pathogens as they had applied to Jose Montoya's samples, Lipkin's team again drew a blank.

At the Invest in ME conference in May, Hornig said they had tentative findings that there might just be a novel pathogen or pathogen candidate in these samples - but it was too early to say for sure. In reply to a question yesterday, Lipkin said there is no more to report:

"we do not yet have a novel pathogen nor do we have a pathogen candidate in which I would have any confidence. So at this point we have no plans to publish anything."
Nonetheless, he also said they hadn't finished all the DNA sequencing work on these samples, so this is not yet a dead end.

Immune stimulation and biomarkers

Up to this point we'd heard a lot of very impressive negative findings, based on large, well-defined samples of patients and controls, and using powerful research techniques. But what we most wanted to hear about was positive leads - and Ian Lipkin duly obliged:


Plasma is the clear fluid left when blood is separated

They took plasma from the CFI cohort of 200 very well-defined ME/CFS cases and 200 controls collected by clinicians (See 'Key Players' above). Then they searched for cytokines and chemokines, which are regulators and controllers of the immune system.

The big finding was a decrease in levels of Interleukin's IL-17, IL-2, IL-8 and in TNF-alpha - all of which have a role in pro-inflammatory responses. Lipkin believes these significant differences are worth follow-up in larger cohorts to better understand what they mean.

Professor Jonathan Edwards (who is an adviser to the planned UK Rituximab trial) commented on this forum yesterday, that it was a surprise to see TNF-alpha levels decrease, and suggested it could mean that 'inflammation' is too crude a concept for the process.

Lipkin and colleagues also found upregulation in Leptin, a hormone that plays a key role in regulating energy uptake and use, and Serpin, a protein family with multiple roles. More obscure cytokines, and and their cousins chemokines, were also affected but Lipkin didn't give any further detail.

Two new patient types revealed

Ian Lipkin said they found something very surprising in their data: there appear to be substantial differences in profiles between those people who have had the disease for 3 years or less and those who have had the disease for more than 3 years. And that this is important because, "it could have implications for therapy as well as for diagnosis".

In the ‘early group’, who have been ill for less than 3 years, there seem to be a number of markers suggestive of some sort of allergy aspect. For example there are often increased numbers of eosinophils in blood, with more differences in cytokines. But while this is tentative, he was more confident in the finding the IL-17 was elevated in these 'early' patients, compared with reduced levels in patients ill for over three years.

Lipkin said that he thought this 3-year division could be very important and that it hadn't been something they were looking for; but would be looked at in any future work they did.

Cerebrospinal fluid: different differences

Lipkin's team also found differences in cerebrospinal fluid biomarkers between patients and controls. I'm not sure from what he said if there were significant differences between the 'early' group and patients who had been ill for more than three years. However, they did find that patients had elevated levels of the TH-2 type cytokines IL-10 and IL-13 and elevated levels of four TH-1 cytokine: IL-1 beta, TNF-alpha, IL-5, and IL-17. Lipkin said this is compatible with a profile of some particular types of response that may provide insights into immunological dysregulation in Chronic Fatigue Syndrome.

So, overall they found clear differences between patients and controls in both plasma and spinal fluid. Many immune differences have been detected before, but findings are not very consistent and none had used such a large and robustly-defined patient cohort (meeting Fukuda and Canadian criteria), or with such carefully matched controls.

HEALTH WARNING

Dr Ian Lipkin again was very clear that he did NOT recommend anyone act on these provisional findings: he doesn't want anyone to get a spinal tap, or measure the cytokine levels and hope to modulate them with drugs based on this research: it's too early for that.​

The lost years...
Back in 1999 Ian Lipkin published his first paper on CFS, which ruled out a connection between the illness and Borna Disease Virus (one of the many viruses he's discovered). But crucially they found evidence of polyclonal B-cell reactivity. He commented that back then:

"there was a very strong sentiment in some portions of the scientific and clinical communities – not always and not everywhere – but in some portions of the community, that this was a psychological illness. What I said was that based on our findings we had very strong evidence that people with Chronic Fatigue Syndrome were truly ill with a physical illness and they deserved a "Deep Dive" to find out why they were ill."
He noted that was a long time ago and dryly added "I am pleased to see that people are now paying much more attention to this disorder and what we can do about it".
What next?

"I still believe the primary cause is likely to be an infectious agent."
Having found clear signs of cytokine abnormalities, Lipkin wants to find out what is causing these changes; he currently thinks that an ongoing stimulus is causing immune system activation which might be resulting in the symptoms we associate with the disease. And interestingly, he still believes that infection lies at the root of it all - despite not yet finding any infections.

The team - working closely with the clinicians he's already mentioned - plan even more extensive work on a cohort of 200 CFI patients and controls. They will further test for viruses and crucially they will also look for bacteria and fungi by sequencing ribosomal RNA (which should detect unknown bacteria and fungi, as well as known ones).

Previous infection detection

The group has looked for current pathogens in the blood and spinal fluid samples they have - and has so far drawn a blank, though there is more work underway. However, what if the trigger for ME/CFS is an earlier infection that has since been cleared: the 'hit and run' scenario Hornig has described? Lipkin says they are looking for "shadows" of previous infections by searching for antibodies against specific infections, rather than the infections themselves (the body will continue to produce low levels of specific antibodies years after an infection has been cleared (the basis of much immunity)).

They will use a technique called LIPS to look for antibodies against particular known infection. In addition, as in their viral sequencing work, they will use an 'unbiased' system (using peptide arrays) that should detect all potential viruses - or rather antibodies against them. They don't currently have an 'unbiased' system that works on bacteria or fungi.

Fecal future?

What excites Ian Lipkin most is the gut microbiome, the community of micro-organisms that live in our gut - which might seem odd given his focus so far on pathogens and the immune system. However, it turns out that the microbiome can have a profound influence on the immune system and may be important in many diseases. Hornig and Lipkin have already developed techniques to study the microbiome, and have shown it could be a factor in autism and even in the severity of colon cancer.

It turns out the best way to find out what lives in the microbiome is to measure what comes out of the gut: fecal matter, or 'poop' to you and me. Their ME/CFS microbiome project has started, but Lipkin felt there wasn't enough material in the first attempt at gathering samples, so things have been delayed as they switch to a new technique (the 'special' collection cups).

The Big Ask: "we can't do this without you"

Microbiome research is very expensive (analysis, not sample collection), and they currently only have the funds to do 10% of what's needed. In fact, throughout the call, Lipkin was stressing the need for more funds, because good research costs and ME/CFS is woefully underfunded: there just isn't enough money to do the work needed. The current science budget cuts (Sequestration) in the US makes the climate even harder.

"It is probably inappropriate for me to be passing the hat, but that’s precisely what I am doing."

He urged patients to contact their representatives in Congress, demanding more funding for ME/CFS research - pointing out that in the early days of HIV, there was little funding until patients demanded it. He also said that if patients were able to afford it, they should invest in research themselves.

Conclusion

ME/CFS research is coming of age. Ian Lipkin has reported these early - and soon-to-be published results - from a huge study, using 285 of Jose Montoya's patients, the 200 patients from the Chronic Fatigue Initiative, plus the 60 'gold-dust' spinal fluid samples from Dan Peterson's patients. Using state-of-the-art techniques, they have largely ruled out a role for a specific pathogen - though that work is incomplete. And they have strong evidence of ongoing immune stimulation in ME/CFS patients, with abnormalities found in both the blood and spinal fluid. The next stage involves deeper searching for bacteria and fungi, looking for 'shadows' of previous infections and investigating the gut microbiome. These are exciting times!

Thanks to the CDC for organizing the presentation and to Firestormm for providing a transcript of this talk, and above all to Dr Ian Lipkin for taking time out to talk to patients.

If you would like to donate to Ian Lipkin's research, click here. In the comments box, put "for M.E/C.F.S Study" to make sure it goes to the right place.


Simon McGrath tweets on ME/CFS research:



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Comments

Does anyone know where we can donate money for the Lipkin's microbiome research?
He wasn't asking specifically for funds - unless (my impression) you have access to a large trust fund - although the CFI is a registered charity: so I suppose you could ask them about establishing a means to donate smaller sums from the community perhaps - that might be a good idea.

Mainly he was talking about applying pressure to your political representatives. He said that Facui and (I forget) - the CDC and NIH - were receptive to his ideas and to ME research being pursued - but the implication was that of the funds that were available: we just don't have enough of a profile to gain access to what is needed.

This sequestration that is being applied globally isn't helping: but if we can somehow raise the profile of ME in terms of solid research direction e.g. the kind of collaborative efforts on large scale that CFI is pursuing - and for things like (not my own preference) the microbiome - with some more background from Lipkin himself perhaps: you could try and pressure the government to increase funding for ME.

I think it needs to be specific. More specific than campaigns in the past. And personal - from you to your own Congressman etc. but it could be planned as part of a PR campaign or an even larger effort. We have - preliminary - biomarkers now: we'd need I think to wait for publication - but that's more credible now than ever before: so it gives us, well, some credibility and we'd not just be demanding funds as before.

We might also have more background detail from the publication of Lipkin's paper (whenever that will be). Be nice to hear something more solid (excuse the pun) about the microbiome and crap-shoot that he appeared so energised by. I think it could be an expensive waste: but I admit to knowing very little about the direction he wishes to take here.

In the transcript - and review - I provided a link I think to the Autism and microbiome paper he co-authored. Might be worth taking a look. I will when I get round to it.

Here's a general piece from Carl Zimmer (also there was another one (NYT I think) linked to in the transcript). You might find it interesting to read more about the possibilities:

A Living Drug Cocktail

by Carl Zimmer
And another recent one from Nat Geo:

I think the Microbiome is fascinating, don't get me wrong, but I also think it can be a wild goose chase: unless you know what you are looking for it's very easy to get lost.

There are a hell of a lot of theories out there, and remedies for things that nobody can yet prove: but it would be good to get some hard science on the table in relation to PwME at last.

In a very mean spirited way, I am pleased that Lipkin and CFI are taking this challenge on. It is very expensive - as he said - and there's obviously no guarantees.

But I guess it has to be done by somebody - and I'd rather it was him and the incredible team he has assembled within CFI and elsewhere in collaboration.
 
New study: http://www.ncbi.nlm.nih.gov/pubmed/24027260 "Cytokines do not change after exercise or sleep deprivation in chronic fatigue syndrome" Thread here. Made me wonder the circumstances under which the samples in Lipkin's study were taken. Of course we don't know them yet - but it might be prove interesting when we do.

------------

Returning to the pathogen hunt, Lipkin said:


So then. Borrelia species bacteria. We hear an awful lot about people being told they have Lyme Disease and receiving treatment for it - or not; but it looks like there is not a role for this at least in this study.

Much more is said on the forums about various doctors testing folk for the bacteria and determining that this is the source of the CFS-like symptoms - how then can Borrelia not be a factor in Lipkin's results when those patients taking part were diagnosed using Fukuda and CCC?

Any thoughts? Or is this the beginning of the end for people with CFS being misdiagnosed with Lyme disease and receiving inappropriate treatments based on spurious testing?
One possible explaination for the zero cases in this study might be that anyone with Lyme disease did not make it into the study in the first place, as the people picking the partisipants are good ME/CFS docs who can spot the difference and if I remember correctly Borrelia is in the CCC under conditions that should be excluded before diagnosis.

Which is why there are still plenty of people with Lyme disease who get misdiagnosed with ME/CFS without Lyme having been ruled out by their non-expert doctors, and subsequently ME/CFS docs find a fair number of patients that come to them with diagnosed ME/CFS actually have Lyme.
 
From MECFS Forums:

Re: CDC Conference Call Tues. Sept.10 3:00pm

« Reply #43 on: Today at 09:44:32 PM »
Wildaisy said:
I asked Dr. Lipkin about the retroviral sequences and this was his reply:

Quote
"The sequences were not specific for CFS. We find them in many people with and without disease."​
I don't believe the forthcoming paper will provide any further detail about these sequences. Not sure when we might discover more.
 
I'm not too surprised about the differences in the disease after 3 years.

I can't say if it was exactly 3 years, but in the beginning I had horrible sore throats and didn't have muscle pain. Now, at fourth year I never get sore throat and pain is constantly present.
Same here. I can't say when it happened exactly, but I was ill for quite a while with sore throats etc, still working etc. trying to find out what was wrong. Then BAM, something changed, the sore throats disappeared but I got much more ill.
 
Great article Simon, thank you!
And thanks Russ for your work on all this too!

Some really interesting stuff there. Lots of questions spring to mind! But I agree that one of the reasons why there is so much value to these studies is the large and robust cohort.

A nice surprise to hear about some of these results up front before publication. I guess that helps speed the process up of getting the funding he needs to keep things going, else it might take even longer.

So if I understand correctly, the sequencing for bacteria and fungi is yet to be completed. Would it be a surprise if he found something here? I'd have thought not as bacterias can be just as nasty as viruses and cause cytokine changes. Perhaps though, they have started and not found anything yet, so although they can't confirm it's not bacteria at this stage, they are fairly confident that it's not going to be?

If anything, it seems to me that Lipkin is even more convinced now of an infectious agent being involved, with these immune results, than he was before.

Regarding cytokine results not matching other studies, as I understood it, processing has a major impact on the result, so the important thing would be consistancy within Lipkin's tests (which I am sure will be the case) and any subsequent validation tests by someone else.
 
Has anyone ever done research looking for pathogens in ear/nose/throat tissue? It seems that many people that have a post-viral onset do so from mono or a mono-like illness where the symptoms concentrate in those areas. I'm under the impression that viruses that park in those areas don't always infect the blood or spinal fluid.

For me personally, one of my first symptoms was tinnitus. It just popped up one day, and progressively got worse, and then I crashed a few weeks later and developed the rest of my symptoms. Along with that I developed excessive earwax and get ear infections that come and go. I think the microbiome is interesting and important, but I'd love for someone to virus-hunt in my ears.
 
One possible explaination for the zero cases in this study might be that anyone with Lyme disease did not make it into the study in the first place, as the people picking the partisipants are good ME/CFS docs who can spot the difference and if I remember correctly Borrelia is in the CCC under conditions that should be excluded before diagnosis.

Which is why there are still plenty of people with Lyme disease who get misdiagnosed with ME/CFS without Lyme having been ruled out by their non-expert doctors, and subsequently ME/CFS docs find a fair number of patients that come to them with diagnosed ME/CFS actually have Lyme.
I tend to agree and Lyme Disease is an exclusion under CCC. This result though does rule out Borellia as am infectious agent involved in CFS it would seem which would endorse the view that CFS is a distinct disease.

I'd be pretty darn careful who tested me for Borellia before being ruled out and treated - because there's a lot of uncertainty surrounding some of the tests and treatments - but we needn't get into any of that here.

There was one virus that was omitted which I did think about: Q Fever. I think from my early days with ME is was one of those that was considered a trigger at least. I guess it could show up for some people as a 'shadow'.

Made me wonder how Mady and Lipkin might have arrived at their choice of pathogens?

And finally, here is someone who is evidently not impressed with Lipkin's work:
Dr J Deckoff-Jones and her Bats in the Belfry :zippit:
 
Firestormm , Q fever would be part of the bacterial studies, not viral studies. As a result we have yet to hear the verdict on that. Q fever can lead to Post Q Fever, and some of those become indistinguishable from ME. There are parts of the world where outbreaks of this are still common, including in Europe.

Let me reiterate again, the current results from Lipkin are about acute viral infection and immune markers. Viruses are still not ruled out, just acute viral infection of likely viral pathogens.
 
Just to clarify what I think Lipkin found (or did not find): he did not find evidence of acute viral infection, but did find immune markers. HHV-6 etc. do not always present as acute viral infections, and are not ruled out except as acute viral infections. In other words, the classic viral model, the one doctors learn in med school, does not fit ME. Is that somehow a surprise?
 
Firestormm , Q fever would be part of the bacterial studies, not viral studies. As a result we have yet to hear the verdict on that. Q fever can lead to Post Q Fever, and some of those become indistinguishable from ME. There are parts of the world where outbreaks of this are still common, including in Europe.

Let me reiterate again, the current results from Lipkin are about acute viral infection and immune markers. Viruses are still not ruled out, just acute viral infection of likely viral pathogens.
Thanks Alex. Isn't Borellia a bacteria? This was what he said, prior to listing the agents he could test for:

Let me begin first by talking about the work that we have done with Jose Montoya of Stanford. Now, our role here was to try to look specifically for infectious agents and as many of you will know, Dr Montoya is a rigorous clinician who has been working in this field now for a decade or more; and he sent us plasma samples [that] we characterised using a method that allows us to detect genetic evidence of infection [from] a wide variety of bacteria, viruses and parasites.
I know he later - when talking about what they are also doing at present - he says:

In addition we specifically look for bacteria using a method called 16S ribosomal RNA sequencing, which is a method that allows us to amplify by polymerase chain reaction (PCR) a region that we can then sequence and look for variability in the presence of specific bacteria. We do the same thing by using a method called 18S ribosomal RNA to look at fungi and I know that many people are interested in not only viruses but also bacteria and fungi.
And it's that part that obviously hasn't been reported on. But the results he did talk about were for active infections as per the list I cited above.

Not sure if these bacteria and fungi searches will be part of the microbiome and poo-hunt or not: I'd presume so - what do you think?
 
Do you have links Alex to the Leptin info you reference? TIA
You might find this abstract interesting. Be warned its only an abstract. Many of us have circadian issues, particularly long term patients, which I have noted before I start to see after year 3 ... which matches the timing of the shift in cytokines Lipkin observed.

http://jap.physiology.org/content/early/2013/07/16/japplphysiol.00630.2013.abstract
Diminished leptin signaling can alter circadian rhythm of metabolic activity and feeding

Leptin, a hormone mainly produced by fat cells, shows cell-specific effects to regulate feeding and metabolic activities. We propose that an important feature of metabolic dysregulation resulting in obesity is the loss of the circadian rhythm of biopotentials.

Then there is this:

http://onlinelibrary.wiley.com/doi/10.1111/cpf.12030/abstract
The associations between peak O2 consumption and leptin in 10- to 12-year-old boys

We can conclude that leptin first of all correlated negatively with relative peak O2 consumption. Absolute VO2peak correlated with leptin only in total group.
I wonder if our leptin goes up on day two of a repeat CPET test? It would be interesting to find out.
 
Has anyone ever done research looking for pathogens in ear/nose/throat tissue? It seems that many people that have a post-viral onset do so from mono or a mono-like illness where the symptoms concentrate in those areas. I'm under the impression that viruses that park in those areas don't always infect the blood or spinal fluid.

For me personally, one of my first symptoms was tinnitus. It just popped up one day, and progressively got worse, and then I crashed a few weeks later and developed the rest of my symptoms. Along with that I developed excessive earwax and get ear infections that come and go. I think the microbiome is interesting and important, but I'd love for someone to virus-hunt in my ears.
PDXhausted. Some time ago, Newcastle University (Australia) did a study on the bacteria Staph in the nose and found that those who have ME/CFS tend to carry a toxin producing kind of Staph there (25% of healthies carry Staph there but not the kind we tend to do).

This of cause isnt causing our ME/CFS but seems to be one of those things which can go with it and just one added thing knocking at our health. (So you may want to consider having a nasal swab done and then treating Staph if found there).
 
For anyone interested in the Anellovirus finding.

"Anellovirus infections are highly prevalent in the general population. A study in Japan found that 75–100% of patients tested were infected with at least one of the three human anelloviruses, and many were infected with multiple species "

So it seems that finding of the percentage found in us has no meaning at all (unless of cause the tiers were far higher then normal??).
 
I think the issue with sequencing blood and CSF is that some of these agents don't really inhabit either. For example, Lyme testing via PCR in blood and in CSF is specific, but has very low yield. Its mainly a tissue based infection. Some other pathogens might be the opposite. Its really hard to make hard conclusions as to what extent a pathogen is involved unless you know where it primarily lives and those tissues are sampled. So its important that they also look for the antibodies as well.
 
Mainly he was talking about applying pressure to your political representatives. He said that Facui and (I forget) - the CDC and NIH - were receptive to his ideas and to ME research being pursued - but the implication was that of the funds that were available: we just don't have enough of a profile to gain access to what is needed.

This sequestration that is being applied globally isn't helping: but if we can somehow raise the profile of ME in terms of solid research direction e.g. the kind of collaborative efforts on large scale that CFI is pursuing - and for things like (not my own preference) the microbiome - with some more background from Lipkin himself perhaps: you could try and pressure the government to increase funding for ME.

I think it needs to be specific. More specific than campaigns in the past. And personal - from you to your own Congressman etc. but it could be planned as part of a PR campaign or an even larger effort.
Thank you for the elaborate reply.

Unfortunately I'm not from the US, so there's nothing I can do about the government. The best I can do is donate a bit every month.
 
Lipkin's team might have benefited from consulting the HHV-6 Foundation about HHV-6 testing [re problems detecting in blood]
Isn't Montoya connected with them? And Lipkin used Montoya's samples, I think.
Interesting point. Montoya is an HHV6 expert, and the HHV6 foundation are funding his pilot study:
Valganciclovir shows promise during first randomized clinical trial for treatment of HHV-6 & EBV in CFS patients | HHV-6 Foundation
So would be interesting to hear what Montoya would say on that issue (and yes, he did supply the samples for this study)
 
The news is that there is no news. Lipkin did find nothing special. Only the CSF findings are interesting as a marker because they are consistent. This need to be validated in a larger population. This can proof 'infection' in the nervous system. Which is the cause of this disease, i believe.
 
I think we might find leptin can be used as a treatment biomarker, but will be useless diagnostically. In other words, leptin might tell a doctor if a treatment is more likely to be helping than harming.

Leptin cannot be used diagnostically for two reasons: its found to be high in many conditions including obesity, diabetes and the metabolic syndrome; and its individually variable. However as a treatment biomarker the comparison will always be your own leptin levels.
 
The news is that there is no news. Lipkin did find nothing special. Only the CSF findings are interesting as a marker because they are consistent. This need to be validated in a larger population. This can proof 'infection' in the nervous system. Which is the cause of this disease, i believe.

I'd argue the point that CSF markers serve as proof of an infection, viral or otherwise, of the nervous system. They certainly hint at a form of immune dysregulation within the brain and perhaps entire central nervous system but are not even close to showing an infectious causation, certainly that could be one cause of such a dysregulation but there are numerous others to further explore too.
 
I'd argue the point that CSF markers serve as proof of an infection, viral or otherwise, of the nervous system. They certainly hint at a form of immune dysregulation within the brain and perhaps entire central nervous system but are not even close to showing an infectious causation, certainly that could be one cause of such a dysregulation but there are numerous others to further explore too.
Many viruses like the nervous system, so its possible that those markers found in csf are from viruses. Meningittis is one that comes to find and a recent study i read somewhere and dont have a link, maybe someone can help out, but with some type of new testing ebv was found to be a major cause of viral meningittis where the older testing methods couldnt detect which infection was the issue. chickenpox/shingles loves the nervous system.

All comes down to which types of tests are the best for which viruses.

I still cant get past many of us not having chronic viral infections when most of us have low nk function, who's job it is to kill viruses. if its herpes virus or some other virus, if they cant find them then they probably havent looked in the right places or dont have the right tests.

A quick search of other auto immune illnesses too show viral infections play apart in some of them. There is even some with MS who have improved on valtrex. Maybe when all this is sorted they will possibly find viral infections implicated in other illnesses that they dont have the final answer in like many auto immune illnesses.

Thats my opinion anyway.