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Where are we with Viruses...?

JBB

Senior Member
Messages
188
From Lipkin's so far uncompleted study:

"...high throughput sequencing...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.

...Lipkin said they also found Anelloviruses in 75% of those studied in plasma samples, but it was not specific for Chronic Fatigue Syndrome...“I really don’t know at this point what this finding means” said Lipkin.

They also found retroviruses in 85% of the sample pools."

So only 1.4% of CFS patients viruses like HHV, EBV, CMV according to this study (I know it's not complete yet but even so)?

I don't understand, I thought these viruses were pretty common in CFS so why are they not showing up?

Hasn't Dr De Meirleir done studies implicating these viruses are present?

No surprise about retroviruses (EDIT: got this wrong...enteroviruses is Chias research) given Dr Chia's work. I don't understand why they discovered such low % of other viruses which I thought were common in CFS. It seems like there are conflicting studies out there.

"The Dubbo studies (and others) have indicated that about 10% of patients with infectious mononucleosis come down with ME/CFS."

Am I missing something here?


Best wishes,

J
 
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JBB

Senior Member
Messages
188
Cleared up by Sushi...thanks :).

Essentially looks like I had I mis-interpreted the Lipkin study for being near completion / conclusion when it is in fact only in it's preliminary stages.

@wastwater Yes, HERVs I gather...
 

Firestormm

Senior Member
Messages
5,055
Location
Cornwall England
Cleared up by Sushi...thanks :).

Essentially looks like I had I mis-interpreted the Lipkin study for being near completion / conclusion when it is in fact only in it's preliminary stages.

@wastwater Yes, HERVs I gather...

We are expecting publication of Lipkin's teams work imminently, which suggests at least this aspect of the work is complete.

It will we understand detail the search within spinal fluid and blood samples for active pathogens that he talked about in his broadcast, to which you referred.

They didn't find active pathogens or the e.g. Lyme disease bacteria, and remember this was a search in one of the largest patient cohorts we have seen.

All work requires replication of course, and we haven't heard directly from those who submitted the samples e.g. Montoya, and who had previously been seen to propose a notion of active pathogen involvement.

I think you were quoting from our article and/or the transcript. Personally, I don't think we will ever see better than this work - but as I said science does require replication: though I think it will be some time (if ever) before we see the scale and quality of this work replicated especially when other efforts in the world of ME science never seem to be.

Other aspects of the team's work does remains to be reported - again it isn't clear what this area will involve exactly, though he was also talking about a search that had begun at least in some small way within the microbiome.

Others are I think hoping that some sort of virus will be involved in some way within tissue: though it wasn't clear - from what I can at this point recall - how Lipkin's team might be considering such theories and without the funding he said is needed.

Of course the lack of active pathogens that was the result of Lipkin's search, was countered by the work revealing cytokine involvement and the possible distinguishing feature surrounding the 3 year mark.

Personally, I find it very hard to think now of active viruses or the Lyme bacteria being involved in ME, other than for some people perhaps being a trigger or precipitating factor.

I have never been able to associate Lyme bacteria infection with ME, though I accept that in regard to Chronic Lyme Disease the symptoms are very hard to distinguish from ME, and that this is a field seemingly dogged by poor testing, false-positives and a propensity to treat widely with antibiotics.

I think for ME it is worth asking questions now why people who are tested for the presence of active pathogens are claiming their results endorse such a presence.

Could it be the efficacy of the test that is bring used? Could it be the results are being misinterpreted? Do active viruses or the signs thereof - above and beyond the subjective expression of symptoms - have any role within ME?

There is clearly an association between active viruses being a trigger in - perhaps - a large majority of patients who go on to be diagnosed with chronic ME and from that it is I think easy to see how the suggestion of continuing viral involvement began.

What needs to be considered more carefully are the reports from patients and experts that treatment with anti-virals has resulted - in some cases - in seeming improvement or recovery.

Because so long as doctors are willing to prescribe anti-virals to people who are thought to have an active virus, and whose ME symptoms are believed to stem from this virus, the association will ever continue at least in the psyche.

One further reason why I would personally like to hear from e.g. Peterson about these results to see if it will affect his treatment practices. Not that I can remember is he does treat with anti-virals, but you see what I mean.

Of course it is entirely possible - given we have no biomarkers for ME - that individuals who are treated with anti-virals are being treated as individuals and not for their ME. That they represent perhaps a sub-group: but again if this were so it wasn't something revealed by Lipkin's results. And that is a problem.

Thus far, we have little if no real evidence of continuing infection. Lots of small studies, and theories, but as Lipkin's work has demonstrated - and without seeing/reading the published papers - when pathogens were searched for they simply were not present.

N.B. The viruses found and to which you refer above, were also found don't forget in very similar quantities among the controls which tends to cancel out their relevancy.

@Simon I don't know if you perhaps have anything to add?
 
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JBB

Senior Member
Messages
188
@Firestormm Thanks for your detailed reply. Looks like there are different views about this study atm. Yes it could be that the search for viruses has really only just begun and that they are in fact hiding in tissues which are hard to access.

Could it be that the Lymes etc diagnosis were already out as these Drs (Montoya etc) had tested for that already and perhaps treated it along with all the common viruses?

It seems strange people respond well to anti virals if there are no viruses there. So maybe Lipkin just didn't hit the right spot looking in blood and spinal fluid?

If deep sequencing is what it claims to be then surely they would find some EBV, CMV etc if it was there. If these really arn't there then what do you test for in terms of infectious pathogens? I am skeptical that they arn't as so many people report positive labs for them. This is why I wonder if perhaps they were already treated as part of the protocol before being admitted for this study.

Anyone else have any ideas / info? This all seems quite confusing.o_O

Best wishes,

J
 

heapsreal

iherb 10% discount code OPA989,
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Location
australia (brisbane)
@Firestormm Thanks for your detailed reply. Looks like there are different views about this study atm. Yes it could be that the search for viruses has really only just begun and that they are in fact hiding in tissues which are hard to access.

Could it be that the Lymes etc diagnosis were already out as these Drs (Montoya etc) had tested for that already and perhaps treated it along with all the common viruses?

It seems strange people respond well to anti virals if there are no viruses there. So maybe Lipkin just didn't hit the right spot looking in blood and spinal fluid?

If deep sequencing is what it claims to be then surely they would find some EBV, CMV etc if it was there. If these really arn't there then what do you test for in terms of infectious pathogens? I am skeptical that they arn't as so many people report positive labs for them. This is why I wonder if perhaps they were already treated as part of the protocol before being admitted for this study.

Anyone else have any ideas / info? This all seems quite confusing.o_O

Best wishes,

J


I dont understand either, even in the healthy population u should find a high rate of herpes viruses, makes me wonder about the testing?

I wonder about any testing these days being accurate. I have heard many stories of someone being positive to something and then tested at another lab and being negative and this seems to happen in different countries as well???
 

Firestormm

Senior Member
Messages
5,055
Location
Cornwall England
@Firestormm Thanks for your detailed reply.

You are welcome. They are good questions/concerns to have I think and I share them too.

Looks like there are different views about this study atm.

Until such time as the paper(s) are published and even afterwards I suspect there will be different interpretations. The results are a slap in the face for many a theory - from patient and from various experts over the years.

Yes it could be that the search for viruses has really only just begun and that they are in fact hiding in tissues which are hard to access.

The 'hiding in tissue' is a theory, and something that remains to be proven. One of the great things about this study in relation thus far to active viruses was the means by which the search was done. Very thorough and a very large cohort. I feel like asking anyone really to 'beat that'. I think this marks the beginning of some high powered studies that ME has so desperately been in need for for decades.

We have had only small scale and insignificant studies up until now, but with independent financing as well as more focused government finance - perhaps we will see more on a similar scale. Stephen Holgate in the UK has already indicated he is also looking to conduct similar powered studies for example, and as more clinicians and researchers team up, I hope that we will see many an old theory put to the test and new pathways open up.

Could it be that the Lymes etc diagnosis were already out as these Drs (Montoya etc) had tested for that already and perhaps treated it along with all the common viruses?

No. These were patients with a diagnosis of ME/CFS and not Lyme's Disease, but the search included looking for the Lyme Disease bacteria - as well as a whole host of viruses and other pathogens. There are - as you can see from this forum - a lot of people who have or have been told they have the Lyme Bacteria and are being treated for it mainly with antibiotics as it is believed - or they are convinced - this bacteria is responsible for their state of poor health.

Some have ME as a diagnosis, some have Lyme Disease, some don't have either but have the symptoms which are very similar in the chronic state. What this study means is - to me - that people with a primary diagnosis of ME i.e. that meet the criteria, do not have the Lyme bacteria i.e. that the active bacteria cannot be responsible for their ME.

It seems strange people respond well to anti virals if there are no viruses there. So maybe Lipkin just didn't hit the right spot looking in blood and spinal fluid?

Yes it does. We hear a lot of anecdotal stories. We don't have firm data on very much in our little world. We have to consider the effect of being prescribed something, rather than nothing, of being told from having a test, that we have something, rather than nothing, etc. and as I said, some people may well be reacting positively to such treatment - understanding why is the key: but this study has shown that it cannot be because the drugs are fighting an active infection.

I am ever thinking to myself, "Well that only applies to those people they looked at in that study, how can it apply to everyone with a diagnosis of ME?" and I think in part it is because our trouble is at present we simply do not know beyond clinical opinion, use of criteria, elimination of alternate explanations, who actually has ME. We have no biomarker, not test, and until we find one we have to rely on these studies as a 'best we can do under the circumstances' but that doesn't mean this one should be dismissed.

However, if in the real world, someone with a diagnosis of ME, has been told by their doctor they have an active infection and are being treated as a result with an anti-viral medication, and they feel better during and after treatment - to such an extent that the symptoms they have associated with ME disappear and they can return to a much more normal existence: good for them. Wish it was me. Wish it had been proven to apply to ME as a disease - but it hasn't.

If deep sequencing is what it claims to be then surely they would find some EBV, CMV etc if it was there. If these really arn't there then what do you test for in terms of infectious pathogens? I am skeptical that they arn't as so many people report positive labs for them. This is why I wonder if perhaps they were already treated as part of the protocol before being admitted for this study.

I am no scientist so I don't understand the complexities of the actual testing employed by Lipkin's team here though as the article and transcript indicated, these tests had resulted previously in the discovery of over 500 viruses. I am more than happy for the results to be shown to be wrong, but I don't think we have seen such testing applied to ME patients before anywhere.

Not entirely sure I understand you here. They can only test for something they know about in the first place. So - as in the article and transcript - they had a list of things they set out to find, and couldn't. This was an active pathogen hunt and they found nothing of significance.

When we get the papers we will be able to see the nature of those included in the cohort perhaps. If I was to be included in research such as this and was fighting a cold or flu, I doubt they would take me on until I had gotten over it. Remember, this was trying to see if any of the likely candidates could be said to be involved with ME.

The importance would have been not in finding a few random infections in a few patients: but in finding pockets of infection or large numbers of infection in patients and little or no infection in controls of a similar type

A result that would have meant something tangible that could possibly indicate an association of active pathogen and ME disease.

The only one they did find, was - as you said above - in around 1.4% of patients and 1% controls. For there to be a firm association you might expect something - I don't know - around the region of 60% in patients and 1-2% controls.

Allenoviruses are very common across all populations - apparently - and the significance of them remains to be seen. Science is still pursuing the role they play (or don't play) in disease.

The retroviruses - while some have chosen to indicate this as a significant find or one that needs explanation - were played down by Lipkin in his presentation, and until we hear anything more about them I don't think we can consider them relevant to the results as a whole.

We got nothing, which is a shame and a disappointment perhaps, but the study was far from negative, was it? Quite exciting I would have said given what they were able to find. And I do hope to hear more as they pursue this larger project, about the cytokines and 3 year differential.

Personally, I think the microbiome will take a long long time to work through, but generally, science seems to be making a beeline now to this area in relation to several chronic diseases. For some reason it excites me far less than other aspects of the search, probably the association with it being a crap-shoot :)
 
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Snowdrop

Rebel without a biscuit
Messages
2,933
My two cents. I will be very glad when researchers start looking into hormones, cytokines and possibly electrolytes.
We know so little about them perhaps making a start of it more difficult, but I see this as a fruitful line of inquiry.
 

JBB

Senior Member
Messages
188
@Snowdrop

I think there are docs who specialize in hormone replacement such as Dr Hertoghe but KDM was very much apposed to treating in this way looking at one of his videos. Presumably he feels this is not addressing the underlying cause??

Some research in that area may yield some useful information!

Best wishes,

J
 

alex3619

Senior Member
Messages
13,810
Location
Logan, Queensland, Australia
I don't see anything inconsistent with Lipkin's findings. The problem is misinterpretations.

Doctors have looked for active virus in us, as in acute infection, for many decades. The result is zip, zero, nada, except for a small percentage.

Its also consistent with Lerner's and Chia's work. Lerner tends select patients with active herpes virus, and a small range of other things, and has found virus in many tissues. However Lerner looks not just at active virus but serology, at antibodies to virus. That tells you if their was an active virus recently, even if its gone.

Looking for viruses directly only tells you about active viruses. Looking at antibodies gives you a time window for active viral infection, and the strength of the antibodies numbers (titre etc.) give an indication of severity and how long ago it was, but its not very precise, and not always reliable.

Chia is looking at primarily gut enteroviruses, and not active infections. So Lipkin would not find this. So the results are consistent. This is not just a theory. It however has only been minimally replicated, and so far not in a very large formal study. The first studies of this kind were in the 80s. Chia replicated their work, though it was in muscle not gut. I forget who did that research though. If it turns out it was Chia, which I doubt, then his later work is not really a replication. This research also only applies to one broad family of viruses, the enteroviruses.

Both herpes viruses and enteroviruses lurk in tissues. This is a well known finding, and these viruses used to be called latent viruses before we discovered that they are active just not as active as in acute infection.

The retrovirus findings are interesting, and deserve a closer look.

I also wonder about mycotoxins. Why do so many of us have mold toxins?

As always though, we need the complete paper to be able to say anything with some conviction.

I find the change in longer term patients fascinating. Many of us have observed that. It might turn out to be a very useful finding in both diagnosis and treatment if its replicated and taken further.
 
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JBB

Senior Member
Messages
188
@Firestormm Thank you :).


Until such time as the paper(s) are published and even afterwards I suspect there will be different interpretations. The results are a slap in the face for many a theory - from patient and from various experts over the years.

Yes they are a bit but the 85% retroviruses may lead somewhere...also Lipkin did say the microbiome may hold some interesting finds. We will have to wait and see I guess.


I think this marks the beginning of some high powered studies that ME has so desperately been in need for for decades.

Couldn't agree more!


No. These were patients with a diagnosis of ME/CFS and not Lyme's Disease, but the search included looking for the Lyme Disease bacteria - as well as a whole host of viruses and other pathogens. There are - as you can see from this forum - a lot of people who have or have been told they have the Lyme Bacteria and are being treated for it mainly with antibiotics as it is believed - or they are convinced - this bacteria is responsible for their state of poor health.

Sorry I wasn't clear in what I meant. What I really meant was that this study used patients meeting "Fukuda and Canadian criteria". Doesn't the Canadian criteria rule out Lyme as a prerequisite for ME? I believe this is the Canadian criteria ( http://www.cfids-cab.org/MESA/ccpccd.pdf ) and it says on page 6-7 "exclusions...infectious diseases such as turberculosis, chronic hepatitis, Lyme disease". So these patients couldn't have had Lyme or they wouldn't fit the Canadian Criteria to be admitted for the study. Montoya et al must have ruled that out already. So for someone with CFS it is still reasonable to assume Lyme could be causing it.


What this study means is - to me - that people with a primary diagnosis of ME i.e. that meet the criteria, do not have the Lyme bacteria i.e. that the active bacteria cannot be responsible for their ME.

Exactly, because if you haven't been ruled out for Lyme you cannot be considered to fit the Canadian Criteria for ME. If any of these 400 or so patients had Lyme as a co infection I suspect Montoya et al have already treated it so it wouldn't appear in the study???


They can only test for something they know about in the first place.

Correct me if I'm wrong but I was under the impression that high throughput sequencing was able to find viruses which were previously unidentified. Therefore not only would it include the viruses listed but also any other active viruses which were "novel"...

Lipkin says:

"These same samples were studied using high throughput sequencing, which is a method that was really pioneered here – with which we have discovered over 500 viruses – so we feel fairly confident that to the extent of the technology’s capabilities at present; we would have detected everything that would have been present within these samples."


The only one they did find, was - as you said above - in around 1.4% of patients and 1% controls. For there to be a firm association you might expect something - I don't know - around the region of 60% in patients and 1-2% controls.

Indeed. I doubt that 1% vs 1.4% has any mathematical significance at all with 400 patients. I think that could easily be chance.


For some reason it excites me far less than other aspects of the search, probably the association with it being a crap-shoot :)

:lol:

Best wishes,

J
 

JBB

Senior Member
Messages
188
@alex3619 That does clear up quite a lot of my misunderstanding. Many thanks :).

Its also consistent with Lerner's and Chia's work. Lerner tends select patients with active herpes virus, and a small range of other things, and has found virus in many tissues. However Lerner looks not just at active virus but serology, at
antibodies to virus. That tells you if their was an active virus recently, even if its gone...

...Both herpes viruses and enteroviruses lurk in tissues. This is a well known finding, and these viruses used to be called latent viruses before we discovered that they are active just not as active as in acute infection.

So to clarify your saying that Lipkin only looked for active infections?

So EBV would show up on our blood labs but not in Lipkin's study as it is not strictly "active" which is what he was looking for? That seems strange so I'm not quite sure I completely understand. Or are you saying that these "lurking" viruses would not come up in blood labs or Lipkin's study? If they are latent and shouldn't come up in blood labs then why do they?

If Lipkin has just ruled out active viruses then I guess there is still a high possibility of viruses in tissues causing problems. But can we detect these with blood tests?


Chia replicated their work, though it was in muscle not gut. I forget who did that research though. If it turns out it was Chia, which I doubt, then his later work is not really a replication. This research also only applies to one broad family of viruses, the enteroviruses.

I believe Chia was replicating the work of some British scientists...on one of his videos he says he went to look back at the history of the disease and found exactly the same thing as they did. So I'm pretty sure his is a legitimate replication.


Best wishes,

J
 

alex3619

Senior Member
Messages
13,810
Location
Logan, Queensland, Australia
Any nucleic acid based testing from blood is basically looking at active infections. That includes high throughput sequencing. If you increase the sensitivity enough to find the odd speck of tissue-only infection, then I am guessing you will get massive cross reactivity and high error rates. I do not know this for certain though, my understanding of this technology is now more than a decade out of date.

Active viral infections follow the lytic lifecycle. Infect, replicate, lyse the cell to release millions of copies to infect more cells. Even in low grade active infections, there are millions of virus particles in the blood.

What used to be called latent infections use different lifecyles. Massive replication and cell lysis is rare. Basically they evade the immune system, which means staying out of the blood. Transfer of virus is often done by building bridges between adjacent cells. However this can change rapidly if the body is under attack, these viruses will often reactivate, travel via infecting B cells or similar, and lyse cells in inflammed areas to infect them ... though this might just be hypothesis, I am not aware of the scientific base for this claim, I have not had time to investigate it.

So essentially a "latent" infection is nearly always not present in blood. Its as though the viruses or other pathogens are hiding. Now in the case of Herpes family viruses I am aware there is work on secondary blood markers, based on how the virus alters cell function. I have not had time to investigate this. This would not be detected by any kind of nucleotide sequencing however, unless the marker is nucleotide based, such as an RNA strand.

The next stage of Lipkin's study will include looking at antibody responses. That is, trying to figure out what the immune system reacted to in the past. This may give very different results. What Lipkin has shown, and all that he has shown (presuming the results can be replicated) is that an active viral infection cannot cause ME or CFS. My understanding is that he has yet to really look at bacterial or fungal infections though.

Now an hypothesis I raised a long long time ago is that CFS could be caused by a bacteriophage infection of the gut bacteria. Nobody has even looked in detail. Maybe Lipkin will find something there.
 
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lansbergen

Senior Member
Messages
2,512
Now an hypothesis I raised a long long time ago is that CFS could be caused by a bacteriophage infection of the gut bacteria. Nobody has even looked in detail.

It would disturb the gut flora.
 

JBB

Senior Member
Messages
188
What used to be called latent infections use different lifecyles. Massive replication and cell lysis is rare. Basically they evade the immune system, which means staying out of the blood. Transfer of virus is often done by building bridges between adjacent cells. However this can change rapidly if the body is under attack, these viruses will often reactivate, travel via infecting B cells or similar, and lyse cells in inflammed areas to infect them ... though this might just be hypothesis, I am not aware of the scientific base for this claim, I have not had time to investigate it.

Very interesting stuff indeed!


So essentially a "latent" infection is nearly always not present in blood. Its as though the viruses or other pathogens are hiding. Now in the case of Herpes family viruses I am aware there is work on secondary blood markers, based on how the virus alters cell function.

Yes this is what I thought about "latent" infections such as Herpes family. So for Herpes family etc labs test for secondary blood markers rather than the viruses themselves? Thus enabling them to detect them even when they are hidden / not in the blood?


What Lipkin has shown, and all that he has shown (presuming the results can be replicated) is that an active viral infection cannot cause ME or CFS. My understanding is that he has yet to really look at bacterial or fungal infections though.

Understood :). Thank you! Well I guess that is good to rule out active viruses. So it does appear that this initial work still leaves a lot of investigation to be done.


Now an hypothesis I raised a long long time ago is that CFS could be caused by a bacteriophage infection of the gut bacteria.

Wiki: "A bacteriophage (informally, phage) is a virus that infects and replicates within bacteria" very interesting theory. That would certainly make the viruses hard to find.


Best wishes,

J
 

Snowdrop

Rebel without a biscuit
Messages
2,933
@Snowdrop

I think there are docs who specialize in hormone replacement such as Dr Hertoghe but KDM was very much apposed to treating in this way looking at one of his videos. Presumably he feels this is not addressing the underlying cause??

Some research in that area may yield some useful information!

Best wishes,

J

Sorry, I've been busy but to reply. Thanks for the suggestion but I wasn't thinking of just a lack of some of the more well know hormones.

I would like to see research into finding out more about the endocrine system. That is, I suspect that we have yet to discover all the hormones we harbour nor do we understand very well their function and interactions with each other and other systems and where things might break down other than being 'low' on a hormone.

It's kind of vague I guess and falls into the category of exploration because we don't know what we don't know.
This system certainly has some role to play.
 

knackers323

Senior Member
Messages
1,625
Any nucleic acid based testing from blood is basically looking at active infections. That includes high throughput sequencing. If you increase the sensitivity enough to find the odd speck of tissue-only infection, then I am guessing you will get massive cross reactivity and high error rates. I do not know this for certain though, my understanding of this technology is now more than a decade out of date.

Active viral infections follow the lytic lifecycle. Infect, replicate, lyse the cell to release millions of copies to infect more cells. Even in low grade active infections, there are millions of virus particles in the blood.

What used to be called latent infections use different lifecyles. Massive replication and cell lysis is rare. Basically they evade the immune system, which means staying out of the blood. Transfer of virus is often done by building bridges between adjacent cells. However this can change rapidly if the body is under attack, these viruses will often reactivate, travel via infecting B cells or similar, and lyse cells in inflammed areas to infect them ... though this might just be hypothesis, I am not aware of the scientific base for this claim, I have not had time to investigate it.

So essentially a "latent" infection is nearly always not present in blood. Its as though the viruses or other pathogens are hiding. Now in the case of Herpes family viruses I am aware there is work on secondary blood markers, based on how the virus alters cell function. I have not had time to investigate this. This would not be detected by any kind of nucleotide sequencing however, unless the marker is nucleotide based, such as an RNA strand.

The next stage of Lipkin's study will include looking at antibody responses. That is, trying to figure out what the immune system reacted to in the past. This may give very different results. What Lipkin has shown, and all that he has shown (presuming the results can be replicated) is that an active viral infection cannot cause ME or CFS. My understanding is that he has yet to really look at bacterial or fungal infections though.

Now an hypothesis I raised a long long time ago is that CFS could be caused by a bacteriophage infection of the gut bacteria. Nobody has even looked in detail. Maybe Lipkin will find something there.

This is an interesting idea. This could very well explain everything.
Do you know if looking will be looking at this phage idea?
Is anyone looking or planning to look into it?
Is there any testing available to the public for these types of infections?
What would the treatment be?

Alex, have you read the study buy Theophilis Hey? It may interest you
 
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alex3619

Senior Member
Messages
13,810
Location
Logan, Queensland, Australia
Sorry, I've been busy but to reply. Thanks for the suggestion but I wasn't thinking of just a lack of some of the more well know hormones.

I would like to see research into finding out more about the endocrine system. That is, I suspect that we have yet to discover all the hormones we harbour nor do we understand very well their function and interactions with each other and other systems and where things might break down other than being 'low' on a hormone.

It's kind of vague I guess and falls into the category of exploration because we don't know what we don't know.
This system certainly has some role to play.


Last time I looked we were still finding new hormones every year, though that was a while back. We are also still discovering new functions for many hormones, and new ways they interact. I don't think we are even close to really knowing what all the hormones are, and what they are doing. People usually don't appreciate that there are probably many hundreds of hormones. Even the average doctor could probably not name many.
 

alex3619

Senior Member
Messages
13,810
Location
Logan, Queensland, Australia
This is an interesting idea. This could very well explain everything.
Do you know if looking will be looking at this phage idea?
Is anyone looking or planning to look into it?
Is there any testing available to the public for these types of infections?
What would the treatment be?

Alex, have you read the study buy Theophilis Hey? It may interest you

When I run a search on Theophilis Hey about all I get is music lyrics.

Correcting gut function seems to induce either temporary or long term remission in a subset of patients. Research has been done on this for decades now, and includes things like the so-called "poop therapy", antibiotics, probiotics, glutamate, lactic acidosis, lipopolysaccharides and so on.

Lipkin might find clues in the gut microbiome analysis, which is why I mentioned it.

There is NO testing available that I am aware of. Despite that we know bacteria are subject to viral infection, and that we have large numbers of bacteria in the gut, and that the gut interacts with the immune system in complicated ways, there is very little research. As a result this is all very hypothetical, but plausible.