Rituximab: The Big Guns For ME/CFS

I appreciate all the good wishes I’ve received from readers. I want to assure everyone that the anonymous personal attacks don’t really bother me. It comes with the territory for hanging it out there as I have. I chose controversy consciously. This type of harassment is what happens when you step out of line and threaten the status quo. I actually kind of like the free-for-all in some ways. It lets us know what we are up against. Too much agreement makes for complacency. To people who have written that it makes you sick, please don’t internalize it. I don’t. I suspect the harassment is in fact a very few individuals. Don’t let it get you down. I do think things will calm down a bit now naturally, since I don’t foresee a great deal of retrovirology forthcoming on our behalf in the near future. I anticipate the discussion will now turn to treatment and how best to live with the disease. We should be on much more stable ground, since it is much harder to take pot shots at my medicine than my retrovirology. I’m sure someone will try though; wouldn’t it be wonderful if the criticism was considered rather than knee jerk?
The little mystery play we just witnessed, courtesy of Jason, exemplified the pitfalls of science as a religion unto itself. Operating under the guise of “science” creates a safety net for its practitioners, satisfying the need for self-aggrandizement, simultaneously providing excuses for not going the extra distance to look outside the box. Very much the same as the medical profession. The Health Director of Norway just apologized to patients for decades of neglect and abuse. I’d like to see a similar apology from the Surgeon General of the USA. An apology tied to some serious restitution. 
Personally, I was abused in every way possible due to CDC/NIH incompetence, from being unable to find adequate care to being denied entitlements, private disability to the SSDI system, all compounded by incompetent doctors, lawyers and now scientists. When I was first disabled in 1995, I had occupation specific disability insurance through Provident, meaning, if I couldn’t be an ER doctor, they had to pay, even if I could be some other kind of doctor, $6000/month for life. They harassed me with IME’s and other invasions into my life, literally forced me into psychiatric treatment I didn’t want, until I settled with them. For the sake of entertainment and telling the whole story, though it has no bearing on the discussion, my lawyer stole the money; he went to jail, after I spent a bunch more money to expose him, but I never recovered what he stole. When I was disabled the second time, I didn’t apply for SSDI right away, because I couldn’t believe I wasn’t going back to work. I applied after my first near death experience at our local Santa Fe hospital, with a thousand pages of records. But it turns out my last “date of insurability” was before that, so it was over before I knew I needed to build a case. Since I didn’t have a correct diagnosis for 15 years, I’m completely screwed, case sitting in appeal for 2 years as I write this. All because I didn’t have a diagnosis. And the new ICC wouldn’t have helped. It is coming to light now, that although I didn’t know what was wrong with me, Provident, in fact, did know. There is a class action suit about those policies, sold before so many yuppies were becoming disabled early in life, but since I settled, I can’t participate. A cluster fuck, as they say in the military. 
The observations that my behavior is not in line with what is considered “professional” has me thinking about what professionalism means to me now that I am reinventing myself yet again. According to Wikipedia, the criteria for a professional are: 
  • Expert and specialized knowledge in field which one is practicing professionally.
  • Excellent manual/practical and literary skills in relation to profession.
  • High quality work in (examples): creations, products, services, presentations, consultancy, primary/other research, administrative, marketing, photography or other work endeavors.
  • A high standard of professional ethics, behavior and work activities while carrying out one’s profession (as an employee, self-employed person, career, enterprise, business, company, or partnership/associate/colleague, etc.). The professional owes a higher duty to a client, often a privilege of confidentiality, as well as a duty not to abandon the client just because he or she may not be able to pay or remunerate the professional. Often the professional is required to put the interest of the client ahead of his own interests.
  • Participating for gain or livelihood in an activity or field of endeavor often engaged in by amateurs b : having a particular profession as a permanent career c : engaged in by persons receiving financial return.
  • Reasonable work morale and motivation. Having interest and desire to do a job well as holding positive attitude towards the profession are important elements in attaining a high level of professionalism.
  • Appropriate treatment of relationships with colleagues. Special respect should be demonstrated to special people and interns. An example must be set to perpetuate the attitude of one’s business without doing it harm.A professional is an expert who is master in a specific field.

I admit to difficulty with the last two at this point in my career. My disgust with most physicians and ‘the profession’ is profound and being ‘appropriate’ is low on my list of priorities. But I certainly can live by the rest of it. Personally, I would have been better off with a good village witch doctor than any of the so-called professionals who ‘took care’ of me for the first 15 years of my disease, all of whom did great harm to my mind, body and spirit. In fact, one of my goals in life is not to need a doctor or a lawyer:).

In general, CFS patients get better care if they don’t tell doctors what they have. Many patients have told me this. Have chest pain or a belly ache and need to go to the ER? You will get better care if you just talk about the chief complaint. Sad, but true. Maybe it is finally changing? XMRV, however it plays out, has brought us into the spotlight at last. We are finally worthy of study, not only because of numbers of affected people, but because maybe, just maybe, we are sick. And not because of our wrong thoughts. We don’t tolerate stress, because we have diffuse hormone receptor insensitivity and depletion, including stress hormones. The response to stress is abnormal, and not because of distorted thinking. Viruses hi-jack cellular machinery, and retroviruses do it on an evolutionary level, using the organism’s own DNA to replicate, either by reverse transcription and assembly of new viral particles or mitotically. Stress is an inevitable consequence of life, and some retroviruses have evolved a strategy to take advantage of this, hormone receptor elements that, when activated, turn on virus: Glucocorticoid Regulation of Murine Leukemia Virus Transcription Elements Is Specified by Determinants within the Viral Enhancer Region. Celander. Note interesting evidence that steroid responsiveness of MLV’s may be competitively inhibited by progesterone.

And now we have the Rituxan study from Norway:

An unintended effect of treating a patient for cancer was remission of CFS symptoms and the patient’s doctor actually noticed. The entire CFS community owes the doctors who pursued and published their study a debt of gratitude. Whether Rituxan pans out for CFS or not, Drs. Fluge et al gave CFS patients big guns, and reported scientifically (though blinding doesn’t seem possible since the patients could probably mostly tell who got the drug).

Rituximab is not the only chemotherapeutic drug to result in temporary remission of CFS symptoms. The question is why and who might be helped by it enough to justify the risk. Given that it is possible to die from a trial of the drug, it isn’t an academic question, or mostly about money and politics, as with arv’s. If you want to look at the disease as an immune disorder of unknown etiology, rituximab, might help a subset of patients by depleting CD20 expressing B cells. However, even for rheumatoid arthritis patients, 40% or so don’t respond to B cell depletion, even though B cells are clearly involved in the pathogenesis of that disease. Rituximab also selectively depletes certain T cell and NK cell populations. Most cytokines/chemokines are made by T-cells, but under certain circumstances, B cells make proinflammatory cytokines also. Here are some hints:

And the argument against: The drug cripples immunologically on purpose and we may be more at risk than rheumatoid arthritis patients for the worst possible outcome:

Take a look at this paper, addressing the question of why some RA patients respond to B cell depletion and some don’t: New Insight in the Mechanism of Action of Rituximab: The Interferon Signature Towards Personalized Medicine. Verweij. It suggests that particular levels of gene expression, disease phenotype, low IFN signature, predicts response to treatment. This paper also talks about the effect of the drug on macrophages, shifting them to a more mature, less proinflammatory stage, possibly suggesting some mechanistic overlap with the positive clinical effect observed in some patients with GcMAF. Since a course of treatment, 2 infusions 2 weeks apart, costs $9000, generally needs to be repeated every 6 months, and includes significant risk of morbidity/mortality to the patient, it is important to predict response to treatment. There are over 8000 papers on PubMed about rituximab (a search for ‘chronic fatigue syndrome’ brings up 5430 papers). The arthritis literature seems to find the risk acceptable. The risk of hypotension, anaphylaxis from the infusion itself, can be ameliorated with skilled administration and/or concurrent treatment. The increased risk of infection, deemed mild to moderate, in the arthritis literature, is anecdotally significant, according to doctor friends of mine who have treated complications of the drug. There is a small risk of sepsis, fulminant hepatitis B reactivation and PML (progressive multifocal leukoencephalopathy). It does appear that the risks decrease for a particular patient with time, though the longest patients have only been followed for 5, to at most 10, years. Longterm Safety of Patients Receiving Rituximab in Rheumatoid Arthritis Clinical Trials. Vollenhoven.

Although I am enthusiastic that someone is talking about big guns for CFS, my initial reaction was, I’ll sit this one out until we know a lot more. It scares me. But when I answered Ali’s questions about why I’m not more interested, she said, “I’d take a small risk of death every 6 months for a complete remission.” So Russian Roulette. I have a patient with a high Rheumatoid Arthritis Factor, degenerative arthritic changes on MRI and clinical synovitis. She could probably get it covered, a problem for most CFS patients. Though I wouldn’t prescribe it at this time, this patient could seek treatment from any number of rheumatologists who have vast experience with the drug.

Dr. Michael Snyderman’s comments of this morning:

In my practice, rituximab at 375mg/m2 causes hypotension in most patients, about 60% need downward adjustment of their infusion rates and about 25% the hypotension is severe enough to be symptomatic. I would expect the hypotensive reactions to be more severe and frequent at the dose of 500mg/m2 used in the CFS protocol. If the patients signed a proper consent form they would have been warned that hypotension would be a risk, therefore most patients would be aware that they had received rituximab rather than placebo. The physicians who administered the rituximab would have to be adjusting the infusion rate in most patients and would also be aware that they had given the active drug rather than the placebo.

Therefore the statement that the study was double blinded is incorrect; it is not possible to double blind rituximab for the above reasons. Furthermore, the results are based on subjective, “how do I feel” criteria which could be influenced by the patients knowledge that they had received rituximab. We have not proven that there is an expansion or clonal component of B-lymphocytes in CFS. There may be but it has to be proved and we have just started looking on a small scale. I believe that the MLRVs (I know this is politically incorrect nomenclature) probably integrate into a number of cell types. I and other people with CFS and cancer have clonal gamma delta T-cell expansions. Gamma delta T-cells are a more likely source of the well-known and accepted elevation of cytokines/chemokines in CFS than B-cells. I could find very little about cytokine/chemokine production by B-cells, certainly with respect to those elevated in CFS. I did a search as to the origin of IL8 and could only find that neutrophils and “macrophages” which would be derived from monocytes could make IL8. I could not find any article saying that B- or T-lymphocytes made IL8 but maybe they do, the area needs more research.

With respect to the present preoccupation with B-cells in CFS all I have seen were nebulous references to autoantibodies. What are the autoantibodies that cause CFS? This is too much of a leap of faith for me. Finally, rituximab would have no activity against the T-cells that are responsible for elevated cytokines found in many patients with CFS.

It maybe that CFS patients have a veritable zoo of clonal cell lines that interact with each other. I would not be surprised at all if there was a clonal expansion of cells derived from monocytes in CFS. Monocytes are the source of macrophages and microglial cells. This would fit Dr. Sandra Ruscetti’s belief that microglial cells are part of the problem with CFS. So, MLRV would integrate into monocytes, increased levels of IL8 would be made and rogue microglial cells would cause problems in the CNS. Rituximab would have no activity against monocytes or microglial cells.

Rituximab is very immunosuppressive and patients who receive it are at risk for opportunistic infections including the dreaded progressive multifocal leukoencephalopathy which is caused by the JC polyoma virus. I hope to soon prove that I have a unique MLRV (not “XMRV”) and it therefore doesn’t make sense to me to take an immunosuppressive drug. In conclusion, we need new treatment for CFS but for many reasons I don’t think that rituximab will be useful. 

Occam’s Razor, as applied to medicine, advocates looking for diagnostic parsimony, though patients may of course have more than one disease; the subsets of patients I think related, e.g. treatment refractory Lyme Disease and ME/CFS, may in fact have different diseases. In any case, it is a big step up to have an immune disorder rather than a psych disorder. But with respect to an explanation for all the manifestations of the disease, plus the epidemiology, I still think a retroviral hypothesis fits best. Clonality contributing to pathogenesis fits. MLV’s replicate mitotically, by clonal expansion, in addition to conventionally (as does HTLV). This is a likely explanation for the incomplete response to arv’s in people with advanced disease. The little bit of information that we have about this in CFS suggests that clonal expansion can happen with various cell lines, so B cells might be implicated in some patients, but T cell clonality more important in others. LabCorp has testing to look at both T cell and B cell clonality (southern blot and PCR).

Epigenetic factors are clearly a very important piece of the clinical picture, likely impacting who gets sick and who doesn’t. Here is an excellent article to start the discussion, illustrating where the environmental piece comes into play. As I’ve said before, I think environmental and retroviral illness are two peas in a pod, not in any way mutually exclusive hypotheses. Why Your DNA Isn’t Your Destiny. Cloud.

Silverman found that XMRV induces 30 genes in vitro within 24-48 post infection. This is the kind of quality work that isn’t being done on our behalf, because XMRV is dead. For posterity, please reread Lee/Silverman. Journal or Urology. Vol 185, No. 4S, Supplement, May 15, 2011 :

EPIGENETIC REGULATION IN INHIBITION OF PROSTATE-DERIVED ETS FACTOR, A TUMOR METASTASIS SUPPRESSOR, IN ADVANCED PROSTATE CANCER A TUMOR METASTASIS SUPPRESSOR, IN ADVANCED PROSTATE CANCER Joshua Steffan, Sweaty Koul, Randall B. Meacham, Hari Koul*, Aurora, CO INTRODUCTION AND OBJECTIVES: There is, at present, no effective treatment for intervention in metastatic prostate cancer. In our recent studies we demonstrated that Prostate-derived Ets factor (PDEF) expression is decreased, and even lost in high grade prostate cancer. Using in vitro assays we show that reintroduction of PDEF results in phenotypic reversal from aggressive to a less morbid pheno- type in prostate cancer cells. Since a common mechanism of tumor suppressor inactivation is by promoter hyper-methylation, the objective of this study was to determine if and how PDEF is regulated epigeneti- cally through promoter methylation. METHODS: LNCaP cells (Androgen dependent), LNCaP C4-2B (Androgen un-responsive) and PC3 (Androgen independent) prostate cancer cell lines were maintained in their respective growth media supplemented with 10% Fetal Bovine Serum and antibiotics. PDEF was over-expressed using bicistronic vectors and delivered by retroviral transfection. Where indicated cells were pretreated with 5-aza cytidine (5-azaC) for various time points prior to measurement of PDEF expression by RTPCR method. Cellular RNA was isolated, reverse- transcribed into cDNA, and PCR was performed using PDEF-specific primers. Migration (scratch assays and Boyden chambers without Matrigel) and invasion (Boyden chambers with Matrigel) were per- formed on cells treated with or without 5-azza-2’-deoxycytidine. RESULTS: We observed decreased PDEF expression in pros- tate cancer cell lines correlated with increased aggressive phenotype, and complete loss of PDEF protein in metastatic prostate cancer cell lines. Treatment of prostate cancer cells (PC3 cells) that do not show any PDEF expression with DNA methyl transferase inhibitor, 5-azaC, led to expression of PDEF in a time dependent fashion, suggesting epigenetic mechanisms in suppression of PDEF in advanced prostate cancer. Our studies suggest that treatment with 5-azaC results in decreased cell migration and invasion, concordant with an increase in PDEF expression. CONCLUSIONS: These studies demonstrate for the first time that inhibition of PDEF expression in aggressive prostate cancer cells is modulated by epigenetic mechanisms. Based on these exciting results, we propose that epigenetic regulations are critical for progres- sion of prostate cancer to aggressive phenotype and that demethylating agents like 5-azaC may serve as effective agents to prevent prostate cancer progression. 

Since XMRV is dead as a human pathogen it makes no sense for the Lipkin study to use precious specimens collected at a cost to the taxpayers of $450,000 ($1500/specimen to the doctors for each patient and control, 150 of each) to allow WPI to try to prove that they can do what they already proved they couldn’t do, and now without a chief scientist. It seems to me that the patient community should object to that vociferously. Rather, the rest of the money should be spent on deep sequencing, looking for the actual cause of the disease. Why not allow Dr. Lipkin to look? He said in Reno that if someone gave him a million dollars he’d look. Let the virus hunter hunt look for it, not Unevx. What if they don’t find it? Then it’s really dead. It is most definitely not in our best interest to give them another shot. They should sink or swim on their own, not spending the very few tax dollars earmarked for investigating causation in our disease. We should certainly not be willing to have the WPI be our last best hope at this point.

I thought this article particularly interesting while we consider where our disease came from: Canadian researcher traces AIDS to single bush hunter from 1921. The scientific community is showing a stunning lack of concern with respect to live vaccines and other medical technology known to be contaminated with animal retroviruses. The case is growing. Too many clues. The burden of proof is on the folks selling the stuff. A little humility, in short supply in the past, is certainly in order now. The band is playing on again.

Today’s song: I Won’t Back Down
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94 thoughts on “Rituximab: The Big Guns For ME/CFS

  1. >There is more.Coffin and Co actually defined the vp-62 sequence as being XMRV and anything other than the vp-62 sequence could not be xmrv.This is absurd.No MLV virus in history has been limited to one genetic sequence.They exist as families of related but genetically distinct viruss

  2. >Prior to about 150 years ago (when environmental toxins started to become prevalent), was autoimmune disease much of an issue for people? Or, as with CFS/ME, is this a new phenomenon?

    For instance, coeliac disease is now present in up to 1% of the population. According to Wikipedia:

    >Historically, coeliac disease was thought to be rare, with a prevalence of about 0.02%. Recent increases in the number of reported cases may be due to changes in diagnostic practice, but there is evidence that coeliac disease may be becoming more common in the United States.

    In general, I have serious doubts about any theory that suggests that people's bodies just go nuts for no reason. Everything that I ever have heard suggests to me that underestimating Mother Nature's design is a mistake, and that health issues that seem to be "internal" almost invariably turn out to have an external cause (toxin, pathogen, injury, nutritional deficiency).

    The same principle seems to apply to some of the high-profile theories of CFS/ME. Jay Levy, Rich van Konynenburg and Martin Pall are all brilliant, original thinkers whose work has contributed greatly to our understanding of the illness. But at least on occasion, they all have posed a "hit-and-run" theory that some not-too-extraordinary stressor has tipped our bodies off balance and caused us to be sick permanently.

    This does not sound right to me. Any system that were that fragile would not have survived natural selection, and the fact that CFS/ME appears to be a new disease makes me even more convinced that something more specific has happened.

    I certainly can imagine a toxin or pathogen that would be bad enough to cause permanent CFS/ME through a one-time hit. But I tend to think it would have to be a new one as well as a particularly bad one — and thus worth looking for.

    Obviously people have spent lots of effort and money looking for pathogens in this illness, and it never seems to get us anywhere.

    On the other hand, here's the entire literature on medical abnormalities in CFS/ME, with more than 600 articles summarized. Despite the facts that a) toxins are just as able to cause illness as pathogens and b) toxicity is almost universally recognized to be an issue in CFS/ME, there's basically _nothing_ looking at toxins.

    Isn't that weird?

    www dot tinyurl dot com /CFS-medical-abnormalities

  3. >I know we are getting a bit off-topic on toxins for this particular blog, which has focussed on xmrv, and on drugs.

    Nonetheless, I can't resist answering.

    I don't believe Jay Levy necessarily posits a hit-and-run toxin/pathogen. I think he has learned from studying HIV all this time, and in particular from studying the Berlin patient, as well as trying to understand what is happening in elite controllers, that he is looking at the immune system. The question is, what assaults once they get onboard, can derail the immune system?

    There was neurasthenia at one point. We don't really know what that entailed for sufferers, as we didn't have the internet back then—-we don't really have a good record.

    I hate to make it complex, but the truth is, it's really complex. There *can* be hit and run pathogens–ie a pathogen that sends the immune system off into a very destructive information loop, and its that repetitive loop that is damaging. Which is why you *can* cure aplastic anemia with chemo, by rebooting the immune system, so to speak.

    There may be new pathogens in circulation. Ian Lipkin in his speech to WPI pointed out that in this global world, not just travel, but agriculture etc (I'm paraphrasing totally from vague memory), more and more pathogens are common into common circulation. I think I recall foamy viruses as an example. There may be a whole new slew of exposures.

    Celiac is going up in part because wheat is so hybridized, so different than the original grain, so ubiquitous, and also has heavy metals to which you can form autoantibodies, and pesticides, and so on…I've seen doctors discussing this on private lists, it's interesting. It may also be going up because of a broken immune system, who knows. Toxins may also be related because both gliadin and cow's milk casein have 7-chain amino acid peptides that inhibit cysteine uptake and therefore lower glutathione…

    It is just astoundingly complex. The problem is, we look around and say, Oh yeah, cancer rates are going up. Fish are turning into hermaphrodites. Hmmm, there are drug residues in our water. Kids have diabetes, ADHD etc.

    And rather than look at our entire way of life, which would be far too painful, we go hunting for a retrovirus…

    What one *can* say is that a natural habitat, the way nature originally designed it, is likelier to heal than many other interventions, in many cases.

    But this blog is not about that…nor does it purport to be…so…


  4. >We know from past immunological research that the immune response in ME/CFS is shifted to Th2, which means overactivity of the B cells, producing antibodies, but also promoting inflammation.

    I suggest that in the Rituximab study, the drug lowered the inflammation by knocking out the B cells which were promoting it.

    Lowered inflammation means lowered oxidative stress, because inflammation involved production of oxidizing free radicals.

    Lowered oxidative stress means lowered demand on glutathione, which is the basis of the antioxidant enzyme system.

    I suggest that this allowed glutathione to rise enough to overcome the vicious circle mechanism that is at the heart of the pathophysiology of ME/CFS, involving a functional deficiency in B12, a partial block of the methylation cycle, and draining of folates from the cells.

    I suggest that in those who experienced long-term recovery, this was enough to allow the immune system to rebalance, and glutathione was able to stay up.

    In those who improved but then relapsed when the B cells came back, I suggest that the renewed inflammation overcame the glutathione resources and re-established the vicious circle mechanism.

    I suggest that in those who did not respond to the treatment at all, there were other factors depleting glutathione that were more important than inflammation in those cases, such as high body burdens of toxins.

    Perhaps a combination of methylation treatment together with something to knock down inflammation temporarily would allow more of the patients to recover.

    If anyone wants more information on the rationale behind this model, please see the video and/or the PDF slides at this site:


    Best regards,

    Rich Van Konynenburg

  5. >The actual research shows that the cytokine profile produced in people with ME is actually a TH17 profile and not a TH2 profile.People seen in fatigue clinics display a TH2 profile consistant with immunosuppression caused by herpes virus infections or chronic elevation of stress hormones

    MLV viruses directly and indirectly deplete glutathione. but also raise NF-kappaB glutamate and by activating microglia produce TH17 cytokines

    Rituximab inhibits Nf-kappa B reduces Th17 cells and reduces numbers of B cells.Mlv viruses typically integrate into B cells

    Thus the effects of rituximab could be explained by the presence of HGRvs

  6. >What are the possible bad effects then of the B cells being "knocked out" by Rituximab? Surely this isn't without risk of getting diseases that the B cells would fight against.

    This doesn't even take into account that a lot of us with CFS/ME are chemically sensitive, and have enough problems with medications.

  7. >Also, isn't the prevalence of cancer reflecting lots of environmental toxins as well as genetic predispositions to them?

    There is a reason why our bodies have genetic mutations during our lives. Much of it must be responses to environmental toxins.

    It is known that certain chemicals cause cancer– dioxin, benzene, pvc's, all kinds of things, including the kind of plastic present in many bottles — which is why I now drink water out of a very soft plastic bottle (which I spill constantly), instead of the hard plastic.

  8. >I was diagnosed with ME/CFS 10 years ago by a CC doctor. Almost 10 years to the day I was diagnosed my doctor found monoclonal protein in my blood. (I'm only 35)

    So knowing in a decade I may be on Rituximab anyway if I develop MM, I'd like to see larger blinded clinical trials of Rituximab for ME/CFS.

    I don't care what this drugs side effects are, they aren't any worse than what a ME/CFS patient goes through daily. I'd take a cancer drug and a chance at life over what I go through any day of the week.

    But first I want the clinical trials to show it works.

  9. >I think the problem with taking Rituxan either for cfs or for RA is that you are suppressing the immune system. You may feel better for awhile because of the reduction in B cells, but you may also be opening the door to the secondary infections which can kill you. It's not the side effects of Rituxan that are worrisome but the chance that you will be overtaken entirely by one of these infections. Now if the scientists cannot find the true cause of cfs and we cannot find any other treatment, then maybe Rituxan would be worth the risk. For now, I would keep watching for further studies on the retrovirus(s) we may be infected with. Just my 2 cents.

  10. >What is monoclonal protein? What is MM?

    Yes, that is a big worry, what happens without B cells? What infections can one get? Can that be prevented?

    A lot to be concerned about. I guess we just have to wait for the further studies on Rituxan and the other studies going on now.

  11. >I like Paula's post. It makes a lot of sense to me about what could happen if one takes Rituxan, but to watch for further studies on the retrovirus(es) we may have.

    I'm just hoping that all of the virology studies and changes in genetic expression, brain matter, spinal fluid proteins, etc., will find something next year — as there is certainly a spurt in research, spurred somewhat by Judy Mikovits — whether she's proven right or wrong.

    She did set all of this interest off and motivated more research and media attention.

    All we can do is wait and push as hard as we can through words and action that we want the cause found and treatment that won't harm our immune systems.

  12. >@ Kathy D A monoclonal protein also known as an M-spike is an extra protein in the blood. It is a a precursor to blood cancers. MM stands for Multiple Myeloma. Many people who have M-spikes don't go on to die from the rare cancers associated with M-spikes because they usually don't show up in the blood until people are older. So they die of other things. Since I'm so young, the Monoclonal proteins have more time to become a rare cancer.

    Rituximab is one of the treatments for Multiple Myeloma. a rare cancer I never heard of until I had an M-spike.

  13. >Anon 3:56 AM,

    A monoclonal protein in a 20 year old is so rare I think it might be in error and would retest it. Rituximab has no activity against myeloma but does have activity against macroglobulinemia. A serum immunofixation would confirm the presence and the identity of the protein.

    Michael Snyderman, MD

  14. >Gerwyn–Thanks for the comment. I think it's possible that glutathione depletion can also be responsible for the shift to Th2, based on the work of Droge some years ago.


  15. >Agreeing with anon re how bizarre that Jamie is knocking this study. I, too, have continued to give her the benefit of the doubt but really it just seems she has an agenda. Just because someone went to med school does not mean they are unbiased or even best suited to treat patients. For all the people here who are adamant not to use a treatment until a cause is found, that is ludicrous. Cancers are treated all the time to improve the health of patients even though the cause is not known and relapse may happen. Are you saying people should not be treated until there is a CURE for something? Why not improve the quality of someones life as much as possible? At least that's what I'll be doing while others take their vitamins and wait for a cure.

  16. >Paula, you are functional, relatively speaking. Others including Klimas, and certainly Jamie on this blog, have pointed out that quality of life in some ME/CFS patients is horrendous, so poor. so torturous, that surely a drug that brings someone back from the living dead with global improvements should be seriously considered. As to PML and other infections, many patients with rheumatoid arthritis and other disabling conditions regularly take immunosuppressive drugs to gain quality of life–and many get symptomatically better without deadly PML etc ever occurring. PML and other infections are a risk with numerous of these drugs. Certainly a moderately or mostly functional person should not consider this, but for someone lying in a dark room in agony with earmuffs and eyemask, unable to bathe, read, etc…the idea of a drug like this is somewhat miraculous, imo. And myself, I'm a non-drug person, I barely can handle an antibiotic and have never considered all these drugs for myself.

    Nonetheless I think the study is fantastic and truly exciting, especially for the direction in which it points.

    Jill Neimark

  17. >Anon at 12 noon, not sure who you are challenging. As to trying Rituximab, I would try it if it was safe to use in a patient with multiple reactivated infections already. I don't think you want to suppress the immune system in a patient such as that, and most of us CFSers fit that category. I certainly do even though I never get colds or flu – just elevated titres of various infections from time to time.

    As to Deckoff-Jones' ability to be objective, I have to say that I have known her for several years and she is about as objective and unbiased as they come. She is open to lots of ideas, does her homework and is willing to try treatments on patients knowing the treatments are not cures but may be helpful. She also is well aware of the risks for some patients of these treatments. Is she perfect? Of course not.

    Finally, for now, Deckoff-Jones and many others have been seriously harmed by some things that should have improved quality of life. SSRIs will make you crazy, not happy if your serotonin levels are normal to high. Quinolones will destroy your tendons and nerve cells, especially if you are chronically low in magnesium and glutathione as most of us are.

    So be careful, be very careful, what you choose to create a better life. Some of these roads lead to "hell". Buyer beware because most docs won't know this. Deckoff-Jones is the rare exception.

  18. >Based on comments, I sometimes wonder if we're all reading the same blog post. After a few deep breaths, I remind myself that we all see things through our own individual filters. Cut some slack accordingly.

    The *only* agenda I have ever seen here is a sick Mom with a sick child, a doctor with a big heart and big courage to put herself out here to share experiences and *thoughts*.

    In no way did I get a message that Jamie is drawing any line in the sand about this study. She simply shared her thoughts about it. My take away from the the post is that she has her opinion, and then she gets thrown a curve ball (as a Mom! not a doc) when her daughter has an "I'd try it" response.

    Again, as her patient, I cannot emphasize strongly enough that in my decades with this disease and the crappy docs and snake oil salesmen I've crossed paths with, her agenda is nothing but treating her patients as individuals, one size does not fit all, and lets collaborate to get the best quality of life possible. As a blogger, she's putting herself on the firing line just to share her experiences and thoughts.

    Many in our community are frustrated with the lack of info and sharing coming from the WPI. Then we've got folks accusing Jamie of having an agenda, because she shares everything. Which way do you want it?

    And really, what is that agenda? She hasn't opened a Fibro & Fatigue Center, for gawd's sakes. She's seeing patients on a very limited basis. She's not promising a damn thing to her patients, other than giving you her best. And I promise you, her best on a bad day is heads above any of the spectrum of docs I've seen on any day.

    I'm just not seeing any Kool Aid being served up here, folks.

  19. >Paula,

    I was not challenging you per se, just pointing out that your concern may not be warranted in severe cases.

    I signed my post btw.

    Re: "I don't think you want to suppress the immune system in a patient such as that, and most of us CFSers fit that category."

    Maybe you do. Maybe the infections are active because the innate immune system is not functioning properly while the adaptive immune system has gone haywire, generating cytokines and various stress hormones that actually stimulate viral reproduction. It's a complex picture. And this drug doesn't uniformly suppress immunity. Apparently NK cells actually go up…

    In addition, a good portion of autoimmune patients of any kind probably have reactivated infections, or inadequately cared for infections. They just aren't routinely tested or treated for that.

    Anyway not meaning to argue, just pointing out some stuff…


  20. >Jill,
    Thanks for your comments on this page – I feel that you have really contributed some great thoughts.

  21. >There has been good discussion here, certainly for me, the pros and cons of even considering taking Rituximab.

    However, given the good back-and-forth, I want to say that I halted at the criticisms of the very smart and kind blog writer here, and that stopped me from reading that entire post. It is out of place and like getting verbally assaulted. I can't read the messages associated with that. And it is not fair to those of us who are ill and have legitimate concerns about this "new miracle drug"!

    People have opinions. That is fine. Argue the opinions and ideas. (Just leave the animosity behind; it doesn't fit in a discussion as serious as this is.)

    I'm just learning (in the last few weeks as I've found more CFS/ME blogs to read) how absolutely disabled some people are who have this disease.

    We all may take different risks and make different choices, depending on our own levels of disability, other infections, etc.

    I think we have to all wait and see what comes of the further studies and what else all of the researches come up with.

    And I am assured that this blog will continue to provide information and sympathy and perhaps suggestions on how we can deal with this horrible illness.

    The points by Jill and Paula are very well-taken, and I am certainly pondering their points of view, and I appreciate both of them.

  22. >@ Mark said…
    "Sorry, but I'm going to quote Jason…


    Jamie, do you actually think there is only ONE cause of ME/CFS?

    Serious question.
    October 27, 2011 12:11 AM"

    Here's a serious question for you Mark.

    Are you under the impression that CFS and ME are the same illness?

    Last time I looked at the CDC website – who of course bequeathed CFS to us – they had stated unequivocally that they are not.

    Their CFS, which is broad enough to include a lingering flu or a depressive illness for example, could not possibly have only one cause. Its broadness has made it a dumping ground for any condition for which an immediate cause is not apparent. So no, of course CFS does not have one cause. No disagreement there.

    The neuroimmune disease ME on the other hand will undoubtedly have only one cause. The only reason we are discussing the one cause or many theory is because of the inclusion of CFS patients in the ME research since the mid 1980s. Prior to that there was no such theory. It was pretty clear that it was an infectious illness with epidemic outbreaks and sporadic cases, again with an infectious onset.

    This really isn't a question of semantics. The lumping together of these two entirely different entities muddied the waters to the extent that it has made a nonsense of the research. Which is why we are swimming in circles (still).

    The solving of the mystery of what causes this incredibly serious neuroimmune disease has not and will not be helped by renaming it "ME/CFS" and saying it has multiple causes. It just doesn't make good sense.

    Nor does it make for good science.

  23. >Anon @ 12:00

    After another quick skim of the post last night, I became even more puzzled at your comment.

    Dr. Jamie said, "Although I am enthusiastic that someone is talking about big guns for CFS, my initial reaction was, I'll sit this one out until we know a lot more. It scares me."

    I'm curious to know what you think her agenda is? I'm asking sincerely, not sarcastically.


  24. >Jill, sorry I missed your name. I have a lot of respect for your journalism. When I first studied Rituximab the research had just indicated it reduced RA symptoms for several months. I assumed, simplistically, that was because it reduced B cells and that RA was caused by mycoplasma which infects B cells. So I figured, again simplistically, that we should just take the antibiotics that control mycoplasma. It did work for me, probably about as well as Rituximab would have worked only, maybe safer.

    Yes, I am functioning at a somewhat higher level than many CFS patients. Yes, I have improved on longterm antibiotics. I have also been harmed by them. But I have a close friend with RA and FMS diagnosis who only gets progressively worse. She has been taking minocycline for years. Many women in the town where we lived are now sick. Most have an FMS label, but who knows what any of us have.

    The drug information on Rituxan states that viruses like herpes and hepatitis may worsen after treatment as the immune systems have been weakened. Jill, do you have elevated titres for any of the secondary infections found in CFS? EBV, HHV6, c. pneumonia, m. pneumonia etc.?
    I have all of these from time to time, yet I am able to get out and about to some extent. I never get flu or colds. I could be wrong, but I think I could take Rituxan without getting too damaged. I am not sure someone so sick they are in bed 24/7 could take Rituxan. It would be interesting to hear the details on the cases in the Norwegian research.

    I don't know what I would do in a case like that, probably try to take azithromycin for awhile and Garlicell. Maybe ImmunoPro. I do not own stock in any of these companies.

  25. >Gerwyn said:

    "Is there only one cause of multiple sclerosis Aids diabetes types 1 and 2

    yes there is"

    Oh god. My opinion of your "science" has gone even further downhill.

  26. >Why can't people just discuss the questions and responses without making cracks? Really. It isn't necessary. It does not help with anything, and it's unfair to those of us with questions about our health and possible help for us.

    Paula, what did you take that helped you?

    I'm sitting here thinking that when I was first diagnosed with this, my liver was enlarged and very tender, and I would get nauseous if it were examined.

    A year after that my liver enzymes went way up, and I got a "chemical hepatitis," as my doctor called it, but didn't name it as "A, B, or C," just a generalized hepatitis. But my skin yellowed, and I had to stop taking any medications or vitamins and eat a very simple diet. I got better, but years later when for another reason I had to take high iron supplements, right away my liver got inflamed and I got very nauseous, so I had to pull back on the iron.

    And now I have a Herpes virus, which I either never had or it was dormant or I wasn't tested for it.

    So perhaps Rituxan isn't in my future, but maybe something else will work.

    I'm taking Acyclovir for the Herpes. It's helping with that, but I have much less functioning time before crashing. It's down to a short time, and I'm much more homebound than ever except for the first year or post-surgery.

    I'm reading a book and following its subtleties is hard, even though reading fiction has been my salvation over the years.

  27. >@Mark L

    I see no explanation for you comment. Nice to know you skipped the science part.


    ME patients have a Th17 shift, Th2 is depression.

  28. >When is Science going to retract Paprotka et al?

    They have produced a study where there is not one assays with a proven analytical (synthetic virus) or diagnostic sensitivity (real virus).

    One of their self proclaimed (no evidence necessary) ERVs is still to be whole cloned from NU/NU and Hsd mice. And for some reason, they have still not screened 1 strain of wild mouse for XMRV, or the one proven ERV, PreXMRV-2. May as well have called it PostXMRV-2.

    All studies that used VP62, the synthetic clone, made in a lab, never once found in nature, should be retracted. It has no relevance to the HGRVs found in people with ME. Professor Racaniello and Dr Singh agree.

    “In my view the CDC paper should not have been published without a proper positive control, eg patient samples known to contain XMRV. If I had reviewed the CDC paper that's what I would have asked for.”


    "It’s just not sufficient to show that something can detect something in a plasmid template. It’s hard to know if it’s going to detect something in a matrix that’s as complicated as blood or cellular DNA. So I think that’s probably one of the biggest reasons for why people find different results.."
    'TWiV 94: XMRV with Dr. Ila Singh, 8 August 2010

    So VP62 studies are invalidated.

  29. >Paula, I forget what town you live in?

    I was thinking about this b-cell issue. It's fascinating. You know the recent research about lyme almost immediately going into the b-cells to evade immune system. And EBV is in there, too. If mycoplasma is also (from ticks, too?) you're going to have some pretty wacked out b-cells, and you really might get a hawyire immune response, auto antibodies, cytokines etc. The body tries to fix it, but that's a lot of infection in one cell type. Just wondering if wiping out a good portion of those infected b-cells, and then using antibiotics or antivirals, might work better? Not for me, of course. Just a thought experiment.

    I tested years ago for the HHV's (antibodies) and EBV. I never had elevated viral titers way back when. I theoretically could, who knows.

    The reason I think this experiment is so totally cool is that it does offer help/hope to some of the sickest, and moreover, points to a new direction for research/understanding the immune system in some chronic autoimmune diseases, of which much of CFS could be one (triggered by incompletely cleared infection, however).

    Why do some people live fine with those infections and others not? It's probably a very complex answer.

    Who knows….there is no easy answer, that's for sure. But the IRIS reaction is a concern with immune boosters, so, maybe a treatment like this that wipes out a lot of b-cell generating antibodies and the infected b-cells themselves, temporarily, would allow a temporary reset, and then some other treatments.


  30. >I should add, Paula, that actually I didn't even have measurable antibodies to the HHV's back then. My issue seems to be primarily fungal. I have insanely high antibodies to fungus (internal such as candida) and molds. This is one reason, along with lyme die-off, that antibiotics are tough on me.


  31. >There is no hypothesis for EBV, Lyme or HHV6 for ME. What would you be testing? How would a study be designed? They have been studied extensively and now there is suggestion of what you could test and for what reason.

  32. >Jill, I lived near Charlotte, NC when I got sick. But I already had joint pains in 1972 while living in Chattanooga. I had several chigger and flea bites that summer. Around 1985 I developed Hashimotos. In 1994 I had a classic bull's eye rash after working in my garden in SC. I was not diagnosed but did have lupus like symptoms with sun sensitivity. In 1995 I crashed. Fortunately, I started going to Dr. Jorge Flechas who was involved with a mycoplasma study being done by Dr. Aristo Vojdani. I tested positive for mycoplasma incognitus and started on minocycline. I could not tolerate minocycline at that time, so I was switched to Zithromax at 500 mg a day and began an amazing recovery. (I suspect I had/have babesia which would respond to Zithromax but not cure it.) Curiously, I can now eat minocycline like candy and have no reaction. I suspect the original sensitivity was die-off of something?

    I was finally diagnosed with borrelia in 2003 but did not improve at all and was severely harmed by the several months of quinolones I was prescribed.

    I have been helped by taking ImmunoPro non-denatured whey protein. I have also responded to GarliCell taking 4-6 capsules at bedtime. By the next morning you do not smell garlicy – amazing. My son swears by it. He had a severe onset of Lyme and who knows what else in 2004 and had fully recovered. So has my husband. But it looks like men may have a recovery more likely. This is true in Dr. D-J's family as well – both men well, both women still sick.

    As to measurable antibodies, I think they flare up only from time to time. I don't always have the same ones and have never had another positive for m. incognitus. But I do know of one patient in the past who tested positive in his bone marrow – not good.

    I think Dr. D-J has some amazing ideas on way to treat us – not a cure. She is good at putting the puzzle together. Maybe we will find out what all is going on in the next couple of years.

  33. >Paula, I could be wrong, but I'm of the understanding from other interactions that you a) are fairly toxic mold "aware" and b) currently live in Las Vegas (a city that some of us have found to be pretty good in terms of the "Locations Effect").

    I thus would like to at least float the idea that one reason that you are doing relatively well (compared to a lot of people with CFS/ME) in general, and that you now can take antibiotics without excessive die-off, could be because your environment is reasonably good.

    Does that seem possible to you?

    In general, the IRIS response seems to be a real impediment with regard to allowing people to make improvements in this disease. Using something like Rituximab conceivably may be one option to get around that.

    But insofar as people can decrease their inflammatory response — and thus benefit from the drugs — as a result of controlling their own environments, that seems like it's at least worth considering as an alternative. That's a really scary (not to mention expensive) drug, in my opinion.

  34. >Paula, thanks for the info. I'll have to look up garlicell. I take a very strong allicin extract. I don't know if there *is* an actual gender divide but if so, it would strengthen the case for CFS/ME/Lyme having a strong autoimmune component, since women generally are more vulnerable to autoimmune for various reasons, including the delicate choreography of hormones.


  35. >Posted for "rendere":

    31 October 2011

    Today's program on Democracy Now (www.democracynow.org) hosts medical ethicist, Harriet Washington, who discusses her book, "Deadly Monopolies". Washington talks at length about how corporations go to unethical lengths to obtain patents and put profits before patients.

    You cannot watch this program without reflecting on what's happening with MLV's/HGRV patents and research.

  36. >I think the gender difference is more that certain hormones feed the infections. I think Dr. D-J wrote about this.

    Lisa, yes, I live in Las Vegas and my home is not mold toxic. However, I got much worse while living here at first due to severe emotional stress, not mold or lack thereof. I recovered to about 90% while living in moldy, humid South Carolina.

    That said, the airport here was refurbished and cleaned around 2001 due to stachybotrus contamination, and I have walked in buildings where I got very sick in a few minutes due to mold contamination. I am a sort of mold dog now due to Erik telling us to be aware of how we responded to moldy buildings up at Reno. My husband isn't bothered at all, but I am. The casinos full of cigarette smoke and carpet are perfectly horrible. I can't say Las Vegas is better than anywhere else. AND we do have ticks out in the desert. Oh well…

    I used to follow the stock market thinking that some biotech could make a lot of money off us CFIDSers. Over time, I have become very cynical. The few biotechs that seem to be doing good studies are those were the head CEO's spouse or child has some severe illness. Go figure.

  37. >Thanks for the suggestion to watch Harriet Washington on Democracy Now. Good program. She is an amazing and knowledgeable person, and nearly everything she said is about horrible developments. And I agree with her.

    The issue of medications for profits is very true. Pharmaceutical companies make enormous profits.

    Even now this situation with shortages of about 200 medications, many for life-threatening diseases. Many are deliberately kept from the market to keep prices high, and companies make a small amount also to keep prices high. A news story on google news tells of a drug that usually sells for $26 now being sold for $1200.
    The whole situation is absurd and dangerous to many people.

    Even if Rituximab turns out to help a substantial number of CFIDS sufferers — and I have a wait-and-see attitude, and examine the side effects view — it may never be available to many of us because of cost. I'm not pushing for this, as there are so many problems with it, but I'm for seeing the future studies.

    I just experienced two medications I take soar in price, putting them out of reach for me.

  38. >Rich (re: methylation block)

    I have watched the presentation you gave in Sweden twice and plan to watch it a third time and take notes.

    I hope everyone gets a chance to watch it.


    As you said, your theory doesn't rule out a retroviral infection, but I think it certainly explains mechanisms for how a retroviral infection or sustained toxic assault could wreak so much havoc on the body.

    You recommendations for treating a methylation/glutathione block have helped me, especially the most recent ones.

  39. >Hey Dr. JDJ,

    Not sure if you received my last email, but I am chomping at the bits–especially since you posted the Democracy Now piece. Please feel free to contact me any time. Looking forward to further dialogue!

    Kyle McNease

  40. >When is the multi lab study going to be pulled? No one taking part is using a validated assay.

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