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CFI Spinal Fluid study from Lipkin and Hornig is out.

Research 1st

Severe ME, POTS & MCAS.
Messages
768
Unfortunately, it appears they aren't looking at ME, they're looking at a Chronic Fatigue Syndrome which is heterogeneous and has many causes and subsets. This is why in the blood and now CSF, they fail always, to find wide spread cytokine inflammation. (ME is inflammatory, it must be or its' CFS, the name must include inflammation).

Those with access to past CFS research, and those testing themselves privately, know full well Cytokines are chronically elevated in long term chronic ME not reduced, including IFN-y (Interferon Gamma). It's actually IFN-a that's reduced, hence the immune suppression (alongside RN-aseL deficiency aiding a poor defense against RNA viruses).

It's frustrating knowing this, that Dr Lipkin never finds anything in CFS infection related, but understandable It's all do to with who the 'samples' he uses are actually taken from. Certainly they aren't from long term severe ME patients at all (more likely) because they aren't having signs of ME, but meet fatigue based criteria only. Even CCC CFS is useless (as is SEID), I think it was shown recently that 36% or so of CCC CFS could be psych misdiagnosed and Newton et al, in the UK showed many who attend British CFS clinics, don't even have CFS! Well what a surprise.

Yet this anomaly when using stored blood samples, wrecks research if scientists are relying on such samples to determine what 'CFS' is or isn't. What you need is real speaking patients sitting in-front of you, people like Dr Montoya's patients, who, guess what? They do have elevated cytokines, and the more severe, the higher the levels. By complete fluke, his paper hasn't been since,from the announcement of it's imminent arrival in march 2014, it was meant to be out nearly a year ago, before the IOM report was rushed and finished early. What happened to the Montoya autoimmune inflammatory profile paper? It certainly shouldn't show the same findings as this low cytokine finding, teaming up with all people, with a psychiatrist and published in a journal of psychiatry - nice touch there and perhaps a nod to the future categorization as a neuroimmune psych disorder of non specific pathogen cause. Exactly what any government would want, in preference to a retrovirus or a novel bacteria such as a variant of Bartonella, which infects endothelial lining of blood vessels (endothelial dysfunction can happen in ME).

Sadly, as much as I welcome people with CFS feeling they are being 'saved' by a neuroimmune psych theory of CFS, this CSF fluid paper doesn't get my juices flowing. Those with experience of reading paper upon paper, and seeing all the twists and turns of 'CFS', know full well that the Dr Lipkin/Hornig paper refutes inflammatory ME and as this is an ME forum as well as CFS, I have an interest in inflammation in ME, not no inflammation!

One saving grace...

If you have severe relentless housebound ME to the point you aren't self caring, you can find the following cytokines are mostly (not all) off the charts 30 years after the disease, not ending after 3 years as we were told, which is incorrect. If you have ME, and measure your serum cytokines, spin/freeze them adequately and do this with RNA cytokines, as well as whole blood you'll see evidence of abnormal inflammatory immune activity:

IL-2, IL-4, IL-6, IL-8-, IL-10, IFN-gamma. MCP1, MIP1, can be very high.
In addition other inflammatory markers and Growth Factors, can also be very high: TGF-Beta 1, VEGF, and PGE2.

The worst offender,in my view, for 'flu feeling' is IFN-gamma, what we are told 'settles down' after 3 years. No it doesn't, in severe ME it's like this every day of your life, forever, hence we are severely affected and not able to travel to clinics as moderately affected patients as we feel so rotten. One day, someone will work out, it's worth testing the most sick FIRST, and the least sick LAST. (Basic logic). Currently, the most sick, never get researched. Totally dumb research policy, but helps push a behavioral management approach as the patients researched are not as sick, because those more sick are excluded from the research, because they have accepted reasons for chronic fatigue (caused by having ME).

These include pituitary dysfunction (Central drop out of HGH, Testosterone etc) and of course, cancers, cortisol failure, kidney disease, heart failure and hypothyroidism. These patients can't be used in 'CFS' research, how convenient for the CDC! Test these people for Cytokines though and see what you get. You'll find bed ridden and housebound CFS, or what many call call severe ME.

Clearly, severe ME is not Fukuda or CCC CFS, but we knew that anyway. ME is an inflammatory disease with evidence of such (such as eventual organ and tissue damage - brain atrophy, adrenal gland atrophy, empty sella - pituitary glad in the brain). These subsets of ME can be tested using Cytokines and Chemokines and other markers available now. Ironically, the only marker Dr Lipkin and the psychiatrist found, was Eotaxin, that perhaps awkwardly, can also elevated in XMRV+ CFS and HIV+.

XMRV doesn't exist, but there is an inflammatory profile that does, that doesn't equate to the 'CFS' they're describing here with low levels of cytokines, and that's important when many other researchers and CFS specialists also find elevated cytokines in patients, sick for decades and THAT is arguably why the IOM refused to let ME and CFS experts redefine 'CFS', and went for CFS+ PEM using no tests when they could have used Montoya's, De Meirleir's, and Mikovit's Cytokine Assays which as explained, can be off the chart, not reduced.

So far, everything in the nightmare of CFS is predictable, even when selecting who has CFS, and who doesn't have ME. I think the paper is OK, but it needs to be titled a 'subset of CFS', to be more accurate, as CFS is heterogenous. To his credit, Dr Montoya always does this, but Dr Lipkin and the psychiatrist Dr Hornig should also do this for reasons of accuracy and scientific integrity of which I am sure, they excel at, at all times.
 

Kati

Patient in training
Messages
5,497
Unfortunately, it appears they aren't looking at ME, they're looking at a Chronic Fatigue Syndrome which is heterogeneous and has many causes and subsets. This is why in the blood and now CSF, they fail always, to find wide spread cytokine inflammation. (ME is inflammatory, it must be or its' CFS, the name must include inflammation).

Those with access to past CFS research, and those testing themselves privately, know full well Cytokines are chronically elevated in long term chronic ME not reduced, including IFN-y (Interferon Gamma). It's actually IFN-a that's reduced, hence the immune suppression (alongside RN-aseL deficiency aiding a poor defense against RNA viruses).

It's frustrating knowing this, that Dr Lipkin never finds anything in CFS infection related, but understandable It's all do to with who the 'samples' he uses are actually taken from. Certainly they aren't from long term severe ME patients at all (more likely) because they aren't having signs of ME, but meet fatigue based criteria only. Even CCC CFS is useless (as is SEID), I think it was shown recently that 36% or so of CCC CFS could be psych misdiagnosed and Newton et al, in the UK showed many who attend British CFS clinics, don't even have CFS! Well what a surprise.

Yet this anomaly when using stored blood samples, wrecks research if scientists are relying on such samples to determine what 'CFS' is or isn't. What you need is real speaking patients sitting in-front of you, people like Dr Montoya's patients, who, guess what? They do have elevated cytokines, and the more severe, the higher the levels. By complete fluke, his paper hasn't been since,from the announcement of it's imminent arrival in march 2014, it was meant to be out nearly a year ago, before the IOM report was rushed and finished early. What happened to the Montoya autoimmune inflammatory profile paper? It certainly shouldn't show the same findings as this low cytokine finding, teaming up with all people, with a psychiatrist and published in a journal of psychiatry - nice touch there and perhaps a nod to the future categorization as a neuroimmune psych disorder of non specific pathogen cause. Exactly what any government would want, in preference to a retrovirus or a novel bacteria such as a variant of Bartonella, which infects endothelial lining of blood vessels (endothelial dysfunction can happen in ME).

Sadly, as much as I welcome people with CFS feeling they are being 'saved' by a neuroimmune psych theory of CFS, this CSF fluid paper doesn't get my juices flowing. Those with experience of reading paper upon paper, and seeing all the twists and turns of 'CFS', know full well that the Dr Lipkin/Hornig paper refutes inflammatory ME and as this is an ME forum as well as CFS, I have an interest in inflammation in ME, not no inflammation!

One saving grace...

If you have severe relentless housebound ME to the point you aren't self caring, you can find the following cytokines are mostly (not all) off the charts 30 years after the disease, not ending after 3 years as we were told, which is incorrect. If you have ME, and measure your serum cytokines, spin/freeze them adequately and do this with RNA cytokines, as well as whole blood you'll see evidence of abnormal inflammatory immune activity:

IL-2, IL-4, IL-6, IL-8-, IL-10, IFN-gamma. MCP1, MIP1, can be very high.
In addition other inflammatory markers and Growth Factors, can also be very high: TGF-Beta 1, VEGF, and PGE2.

The worst offender,in my view, for 'flu feeling' is IFN-gamma, what we are told 'settles down' after 3 years. No it doesn't, in severe ME it's like this every day of your life, forever, hence we are severely affected and not able to travel to clinics as moderately affected patients as we feel so rotten. One day, someone will work out, it's worth testing the most sick FIRST, and the least sick LAST. (Basic logic). Currently, the most sick, never get researched. Totally dumb research policy, but helps push a behavioral management approach as the patients researched are not as sick, because those more sick are excluded from the research, because they have accepted reasons for chronic fatigue (caused by having ME).

These include pituitary dysfunction (Central drop out of HGH, Testosterone etc) and of course, cancers, cortisol failure, kidney disease, heart failure and hypothyroidism. These patients can't be used in 'CFS' research, how convenient for the CDC! Test these people for Cytokines though and see what you get. You'll find bed ridden and housebound CFS, or what many call call severe ME.

Clearly, severe ME is not Fukuda or CCC CFS, but we knew that anyway. ME is an inflammatory disease with evidence of such (such as eventual organ and tissue damage - brain atrophy, adrenal gland atrophy, empty sella - pituitary glad in the brain). These subsets of ME can be tested using Cytokines and Chemokines and other markers available now. Ironically, the only marker Dr Lipkin and the psychiatrist found, was Eotaxin, that perhaps awkwardly, can also elevated in XMRV+ CFS and HIV+.

XMRV doesn't exist, but there is an inflammatory profile that does, that doesn't equate to the 'CFS' they're describing here with low levels of cytokines, and that's important when many other researchers and CFS specialists also find elevated cytokines in patients, sick for decades and THAT is arguably why the IOM refused to let ME and CFS experts redefine 'CFS', and went for CFS+ PEM using no tests when they could have used Montoya's, De Meirleir's, and Mikovit's Cytokine Assays which as explained, can be off the chart, not reduced.

So far, everything in the nightmare of CFS is predictable, even when selecting who has CFS, and who doesn't have ME. I think the paper is OK, but it needs to be titled a 'subset of CFS', to be more accurate, as CFS is heterogenous. To his credit, Dr Montoya always does this, but Dr Lipkin and the psychiatrist Dr Hornig should also do this for reasons of accuracy and scientific integrity of which I am sure, they excel at, at all times.

Dude, these patients were handpicked by Dr Peterson, the godfather of ME. It doesn't get any better than this.
 

Gijs

Senior Member
Messages
690
''novel bacteria such as a variant of Bartonella, which infects endothelial lining of blood vessels (endothelial dysfunction can happen in ME).''

I know de Meirleir finds this variant. I hope he will publish his data.
 

lansbergen

Senior Member
Messages
2,512
Almost by definition a single cluster outbreak is a highly homogeneous group. There is some question as to whether or not that is the case once you merge cluster outbreak cohorts.

I agree but if Peterson can not spot ME nobody can.
 

msf

Senior Member
Messages
3,650
Research 1st, I agree with what you said in terms of the heterogeneous nature of the patient group for the cytokines in the blood study, but was this reflected in the results? If it was, you should see some (most) long-term patients with very low levels of cytokines, and a few with very high levels. Didn't Prof. Edwards say something about this info not being available?

Also, could you provide links for the studies you are talking about? I would be very interested to read them.
 

msf

Senior Member
Messages
3,650
Re: the Schutzer, study, I hope they don't replicate it because it was a pretty poorly controlled study in my opinion. The patient group was (according to the paper) tested to exclude Lyme, as well as other pathogens. They appear to have done this by testing for Bb immune complexes. This test was first invented in the 1990s, and yet it has never become the standard test for Lyme, which might be due to the debate about its sensitivity. If the test is 100 % sensitive, the conclusion of the paper is a tautology: 'none of these Lyme-free patients had Lyme.' If the test lacks sensitivity, then some patients with Lyme may have been included in the patient group. This would invalidate the methodology, since it would mean that it is not possible to differentiate Lyme patients from patients with other diseases,
 

msf

Senior Member
Messages
3,650
That is assuming that the point of the study was to see if they could differentiate 'CFS patients' (since they used the Fukuda criteria, another problem with the study) en masse from Lyme patients. If however, they were trying to differentiate those CFS patients who don't have Lyme from Lyme patients, then (assuming the screening was sensitive enough) the result itself doesn't really tell us anything, apart from the fact that people with different diseases have different cerebrospinal proteomes. As the paper says, the differences might allow some inferences to be drawn about the pathologies of these diseases, but that assumes that the CFS group you are left with is a heterogeneous group.

I think a more interesting study would be to see what proportion of patients in a particular ME patient group have some signs (counting borderline positives) of past or current Lyme infection, using the most sensitive tests available, and the comparing this to the proportion of controls (drawn from the same area) who show the same signs. Obviously, you would expect the first to be higher, but the proportions were say, 50%, and 5%, you could say that Lyme is likely to be involved in a significant proportion of ME cases, at least in that area. This study would ideally be a multi-center, international study, as then it would be less likely to reflect local differences in habitat, way of life, etc.
 

Jonathan Edwards

"Gibberish"
Messages
5,256
@Jonathan Edwards, what do you think?

Is the similarity to MS in figure 1 important?

I find this study much more difficult to interpret than the blood study, chiefly because of uncertainty over what the control population includes. This is a real problem for CSF studies and something that came up with the Australian study. I need to compare the results and have a think.
 

duncan

Senior Member
Messages
2,240
A possible problem, msf, is Lyme diagnostics for the most part suck.

If you are IgM positive, but it's, say, more than two months after your Lyme diagnosis, most clinicians would say you don't have Lyme. If you have only four bands IgG positive, or three, or two, or one, most clinicians would say you don't have Lyme - even though many knowledgeable Lyme insiders believe that a single band that is specific to Bb should be enough to diagnosis an active case.

So, this study you're suggesting could be identifying people as Lyme-free who simply aren't.
 

msf

Senior Member
Messages
3,650
Yes, that is a problem with the Shultzer, among others. That's why I suggested testing for any sign of either current or past infection, and then comparing the incidence with that of controls in the same area. It wouldn't tell you that they definitely had Lyme, but as I said, a difference of say 30% in the incidence of Lyme between the two groups would suggest that Lyme is likely to be involved in a significant proportion of ME cases.
 

A.B.

Senior Member
Messages
3,780
I find this study much more difficult to interpret than the blood study, chiefly because of uncertainty over what the control population includes. This is a real problem for CSF studies and something that came up with the Australian study. I need to compare the results and have a think.

Is the problem (as Sidereal pointed out) that 100% healthy people have little reason get a spinal tap?
 

msf

Senior Member
Messages
3,650
The only Lyme sufferers who wouldn't be picked up by my suggested study would be those who are completely seronegative - there might be some reason why these would be more common in an ME patient group, but I would still expect there to be a difference in the incidence rates between the two groups.
 

Antares in NYC

Senior Member
Messages
582
Location
USA
Yes, that is a problem with the Shultzer, among others. That's why I suggested testing for any sign of either current or past infection, and then comparing the incidence with that of controls in the same area. It wouldn't tell you that they definitely had Lyme, but as I said, a difference of say 30% in the incidence of Lyme between the two groups would suggest that Lyme is likely to be involved in a significant proportion of ME cases.
For many of us, that's quite true. A huge deal of folks here in Phoenix Rising have been diagnosed with Lyme at a point, in addition to ME/CFS. There may be many paths to the immune dysfunction at the core of ME/CFS, and Lyme may be just one of them. This may account for the difficulty in finding ONE pathogen to cause the illness. It may be a number of pathogens (viral, bacterial) that evolved immune evasion mechanisms.
 

snowathlete

Senior Member
Messages
5,374
Location
UK
Unfortunately, it appears they aren't looking at ME, they're looking at a Chronic Fatigue Syndrome which is heterogeneous and has many causes and subsets. This is why in the blood and now CSF, they fail always, to find wide spread cytokine inflammation. (ME is inflammatory, it must be or its' CFS, the name must include inflammation).

Those with access to past CFS research, and those testing themselves privately, know full well Cytokines are chronically elevated in long term chronic ME not reduced, including IFN-y (Interferon Gamma). It's actually IFN-a that's reduced, hence the immune suppression (alongside RN-aseL deficiency aiding a poor defense against RNA viruses).

It's frustrating knowing this, that Dr Lipkin never finds anything in CFS infection related, but understandable It's all do to with who the 'samples' he uses are actually taken from. Certainly they aren't from long term severe ME patients at all (more likely) because they aren't having signs of ME, but meet fatigue based criteria only. Even CCC CFS is useless (as is SEID), I think it was shown recently that 36% or so of CCC CFS could be psych misdiagnosed and Newton et al, in the UK showed many who attend British CFS clinics, don't even have CFS! Well what a surprise.

Yet this anomaly when using stored blood samples, wrecks research if scientists are relying on such samples to determine what 'CFS' is or isn't. What you need is real speaking patients sitting in-front of you, people like Dr Montoya's patients, who, guess what? They do have elevated cytokines, and the more severe, the higher the levels. By complete fluke, his paper hasn't been since,from the announcement of it's imminent arrival in march 2014, it was meant to be out nearly a year ago, before the IOM report was rushed and finished early. What happened to the Montoya autoimmune inflammatory profile paper? It certainly shouldn't show the same findings as this low cytokine finding, teaming up with all people, with a psychiatrist and published in a journal of psychiatry - nice touch there and perhaps a nod to the future categorization as a neuroimmune psych disorder of non specific pathogen cause. Exactly what any government would want, in preference to a retrovirus or a novel bacteria such as a variant of Bartonella, which infects endothelial lining of blood vessels (endothelial dysfunction can happen in ME).

Sadly, as much as I welcome people with CFS feeling they are being 'saved' by a neuroimmune psych theory of CFS, this CSF fluid paper doesn't get my juices flowing. Those with experience of reading paper upon paper, and seeing all the twists and turns of 'CFS', know full well that the Dr Lipkin/Hornig paper refutes inflammatory ME and as this is an ME forum as well as CFS, I have an interest in inflammation in ME, not no inflammation!

One saving grace...

If you have severe relentless housebound ME to the point you aren't self caring, you can find the following cytokines are mostly (not all) off the charts 30 years after the disease, not ending after 3 years as we were told, which is incorrect. If you have ME, and measure your serum cytokines, spin/freeze them adequately and do this with RNA cytokines, as well as whole blood you'll see evidence of abnormal inflammatory immune activity:

IL-2, IL-4, IL-6, IL-8-, IL-10, IFN-gamma. MCP1, MIP1, can be very high.
In addition other inflammatory markers and Growth Factors, can also be very high: TGF-Beta 1, VEGF, and PGE2.

The worst offender,in my view, for 'flu feeling' is IFN-gamma, what we are told 'settles down' after 3 years. No it doesn't, in severe ME it's like this every day of your life, forever, hence we are severely affected and not able to travel to clinics as moderately affected patients as we feel so rotten. One day, someone will work out, it's worth testing the most sick FIRST, and the least sick LAST. (Basic logic). Currently, the most sick, never get researched. Totally dumb research policy, but helps push a behavioral management approach as the patients researched are not as sick, because those more sick are excluded from the research, because they have accepted reasons for chronic fatigue (caused by having ME).

These include pituitary dysfunction (Central drop out of HGH, Testosterone etc) and of course, cancers, cortisol failure, kidney disease, heart failure and hypothyroidism. These patients can't be used in 'CFS' research, how convenient for the CDC! Test these people for Cytokines though and see what you get. You'll find bed ridden and housebound CFS, or what many call call severe ME.

Clearly, severe ME is not Fukuda or CCC CFS, but we knew that anyway. ME is an inflammatory disease with evidence of such (such as eventual organ and tissue damage - brain atrophy, adrenal gland atrophy, empty sella - pituitary glad in the brain). These subsets of ME can be tested using Cytokines and Chemokines and other markers available now. Ironically, the only marker Dr Lipkin and the psychiatrist found, was Eotaxin, that perhaps awkwardly, can also elevated in XMRV+ CFS and HIV+.

XMRV doesn't exist, but there is an inflammatory profile that does, that doesn't equate to the 'CFS' they're describing here with low levels of cytokines, and that's important when many other researchers and CFS specialists also find elevated cytokines in patients, sick for decades and THAT is arguably why the IOM refused to let ME and CFS experts redefine 'CFS', and went for CFS+ PEM using no tests when they could have used Montoya's, De Meirleir's, and Mikovit's Cytokine Assays which as explained, can be off the chart, not reduced.

So far, everything in the nightmare of CFS is predictable, even when selecting who has CFS, and who doesn't have ME. I think the paper is OK, but it needs to be titled a 'subset of CFS', to be more accurate, as CFS is heterogenous. To his credit, Dr Montoya always does this, but Dr Lipkin and the psychiatrist Dr Hornig should also do this for reasons of accuracy and scientific integrity of which I am sure, they excel at, at all times.

I think we all accept that a number of people with a CFS diagnosis may not have what many people call ME. I'm yet to be convinced though that the majority of patients with a CFS diagnosis don't have the same disease as those with an ME diagnosis.

I meet all the criteria definitions out there, and could potentially take part in any study using any of those criteria. But had I not seen KDM I would only have an ME/CFS diagnosis from my local NHS ME/CFS centre.

When you have experienced clinicians like Dr Peterson I just don't think there is much reason to think the samples that he uses in studies (or makes available to others to study) wont be as fully representative of what some people call ME.

There are lots of people severely ill with the disease who have a CFS diagnosis too (especially in countries where an ME label often isnt a diagnostic option). The reason why severe patients are excluded from research is obvious: It is because you have to take the test to them as they cant come to clinic. That costs more and is more logistically complex. I hope we see more severe patient research, but that is why it hasn't happened yet.

Regarding Dr Hornig being a psychiatrist I don't see that as a problem at all, and I dont think anyone should either. For me, it is not about their label, it is about their stated belief regarding the disease. Dr Hornig has been abundantly clear that she considers it a physical not a pyschological disease and a brief look at her track record shows she doesnt spend time psychologicalizing (real word? doubt it, but you probably get the point) the biological diseases she works on. It is a huge mistake to see someone as an enemy because of their title, or qualifications, when it is their actions that matter.

I think it is disrespectful and unnecesary to refer to her as "the psychiatrist" when you bothered to put Dr Lipkin's name before saying that. Why be derogatory like that?

I think it was a smart move putting it in a journal of psychiatry. It challenges the nonsense that gets published about us in these journals and has the potential to influence people working in pyschiatry who so far have been told it is a pyschological disease. It shows guile in my opinion and we need that. I think it is an absolute worst nightmare for psychiatrists who promote the psychological view as it challenges them in their own territory where they are used to having full control of the narrative.
 

cigana

Senior Member
Messages
1,095
Location
UK
That is assuming that the point of the study was to see if they could differentiate 'CFS patients' (since they used the Fukuda criteria, another problem with the study) en masse from Lyme patients. If however, they were trying to differentiate those CFS patients who don't have Lyme from Lyme patients, then (assuming the screening was sensitive enough) the result itself doesn't really tell us anything, apart from the fact that people with different diseases have different cerebrospinal proteomes. As the paper says, the differences might allow some inferences to be drawn about the pathologies of these diseases, but that assumes that the CFS group you are left with is a heterogeneous group.

I think a more interesting study would be to see what proportion of patients in a particular ME patient group have some signs (counting borderline positives) of past or current Lyme infection, using the most sensitive tests available, and the comparing this to the proportion of controls (drawn from the same area) who show the same signs. Obviously, you would expect the first to be higher, but the proportions were say, 50%, and 5%, you could say that Lyme is likely to be involved in a significant proportion of ME cases, at least in that area. This study would ideally be a multi-center, international study, as then it would be less likely to reflect local differences in habitat, way of life, etc.
The problem with the Schutzer study is they put the word "Lyme" in the title.
If instead they'd said "we found lots of unique markers for people diagnosed with Fukuda CFS and Lyme that were not found in healthy controls" then I think there'd be less debate.

I can't think of anything better than a large number of unique markers to further explore...at lot better than some vague inconsistent cytokine meaurements. At this stage I don't care where Fukuda CFS and Chronic Lyme happen to fall on the venn diagram, or whether ME falls within the Fukuda set or in it's own set....the point is the sets are different to controls. Far better to be diagnosed and treated for something now than wait another 15 years to find a unique marker for a particular subset we can't even define properly (and assume a priori it will even have it's own marker).
 

Helen

Senior Member
Messages
2,243
For many of us, that's quite true. A huge deal of folks here in Phoenix Rising have been diagnosed with Lyme at a point, in addition to ME/CFS. There may be many paths to the immune dysfunction at the core of ME/CFS, and Lyme may be just one of them. This may account for the difficulty in finding ONE pathogen to cause the illness. It may be a number of pathogens (viral, bacterial) that evolved immune evasion mechanisms.
Or the other way around? Something, probably genetic, affecting the immune systeme that makes us vulnerable to many kinds of infections? Still waiting for results from genome studies.
 

Antares in NYC

Senior Member
Messages
582
Location
USA
Or the other way around? Something, probably genetic, affecting the immune systeme that makes us vulnerable to many kinds of infections? Still waiting for results from genome studies.
Indeed, Helen. That too!
I think the recent genome studies on the HLA-DR4 gene allele point in that direction. Apparently they have discovered that the 20% of folks that get treated with ABX for Lyme but never recover have that very specific gene allele (same one responsible for rheumatoid arthritis), and when infected by pathogens like Lyme it produces tons of cytokines like Interferon Gamma, but not the killer cells that should fight the infection off. People who recovered quickly from Lyme after treatment had a different gene allele, HLA-DR11, which led to the production of natural killer cells instead of Interferon Gamma.

It wouldn't surprise me if the research aimed to solve ME/CFS ends up solving chronic Lyme.
 
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