August59
Daughters High School Graduation
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For me, replicating the Schutzer study is an absolute priority.
Absolutely!
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Created in 2008, Phoenix Rising is the largest and oldest forum dedicated to furthering the understanding of and finding treatments for complex chronic illnesses such as chronic fatigue syndrome (ME/CFS), fibromyalgia (FM), long COVID, postural orthostatic tachycardia syndrome (POTS), mast cell activation syndrome (MCAS), and allied diseases.
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For me, replicating the Schutzer study is an absolute priority.
Yep.@cigana
Is this the study you're referring to: http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0017287
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.
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 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.
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.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.
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.
The problem with the Schutzer study is they put the word "Lyme" in the title.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.
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.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.
Indeed, Helen. That too!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.