Sunday, January 19, 2014
A most remarkable study on ME/CFS was published January 15, 2014.
The study, by Dr. Carmen Scheibenbogen and her team at Berlin Charite, can be found here.
From the study:
“By comparing memory B- and T-cell responses of CFS patients with healthy EBV-infected subjects, we observed a profound deficiency in EBV-specific B- and T-cell memory response in the majority of CFS patients resembling the deficiency of EBV memory responses described in autoimmune diseases  and chronic HIV infection , , .”
The following comments are by anciendaze, who writes commentary on various forums, including Phoenix Rising, a forum that provides terrific information. Anciendaze writes with great knowledge, insight and clarity.
“This looks like the real thing. The highly specific immune impairment certainly looks like a virus defending itself. A complete lack of patient IFN-gamma response to the EBNA-1 challenge is striking. Latent replication allows the virus to benefit from clonal expansion of infected cells in response to immune challenges from unrelated pathogens. This is one feature I felt pretty sure about earlier, and only retroviruses seemed to have the required ability.”
“The parallels with HIV and HCV will make it much harder to ignore. Contrasts with SLE should illuminate the murky subject of autoimmune disease. We still don't know what initiates the process, since most ME/CFS patients were exposed to EBV long before the appearance of symptoms.”
I got the heads up on this research when I heard Dr. Scheibenbogen give a talk at the Invest in ME conference in London in May 2013
Three quarters through her half-hour talk I was struck by what she was saying. Dr. Scheibenbogen and her group looked at the normal EBV antibodies (IgG, IgM, EBNA) of their patients. In doing so they were surprised to find that 10% of these patients had low EBNA. The team took this to be another secondary indication of immune abnormality in a subset of CFS patients and they decided to look further at all the patients. They did not attach a particular meaning to this lower EBNA beyond that it was one more hint of immune abnormality in CFS patients (specifically in regard to EBV). She expressed her belief that this abnormality just represents the tip of an iceberg. Based on this finding, they developed a much more sensitive assay to access B cell antibody response, by looking for the response against more than 2000 peptide fragments of the whole EBV virus itself. From the almost 100 proteins of the EBV virus itself, they took the most relevant and cut the proteins in pieces and tested them. This sophisticated testing - looking for an abnormal response to EBV - found in the first round of assays that 2/3 of CFS patients had a different response than controls. They have continued to work with larger number including patients from Norway as well as using other diseases as controls. This altered EBV specific response is their basis for developing a diagnostic test for a subset of CFS patients. Her lab is collaborating with a company in Berlin in developing a diagnostic test for a subset of ME/CFS. (Patients in Germany are referred to as CFS).
In this talk Dr. Scheibenbogen indicated that her ideas about ME/CFS parallel those of Dr. Amolak Bansal, an immunologist in London, who also gave a lecture in 2013 at Invest in ME. She also gave a significant nod to the work of Dr. Oystein Fluge and Dr. Olav Mella.
Dr. Scheibenbogen and two of her colleagues attended a one-day pre-conference meeting of researchers on May 29, 2013. Thirty some researchers met to discuss a particular topic or focus for research. Last year the subject was Infections, Immunity and ME. The year before the research conference was on Autoimmunity. Of course getting researchers together to talk is a splendid idea. A good number of them come from outside the field of ME/CFS.
Invest in ME produces a modestly priced DVD of their annual conference. I suggest that those interested readers buy this DVD and view these lectures. The entire thrust of this conference and pre-conference private research discussions are quite extraordinary - and are driving towards a consolidation of research into this illness.
This conference is guided by Richard and Pia Simpson. Their nine or ten year struggle to focus research is really paying off with increasingly wide ranging connections with the sole intent of getting at this illness. I cannot say enough positive things about Invest in ME and urge American clinicians and researchers to attend this conference. I have witnessed myself the exchanges that happen at the pre-conference dinner, and on the conference day itself. This conference is the place to be if you want to encounter cutting edge research about this illness.
Regarding the publication of this paper yesterday one wonders what Dr. Ron Glaser will think of it? Are we going to have a confluence of ideas here - or the more typical disconnect that we associate with ME/CFS research? Certainly the researchers in Australia – Dr. Sonya Marshall-Gradisnik and Dr. Don Staines – will have their eye on this continuing research, as will Dr. Fluge and Mella. All of these researchers have made presentations at Invest in ME for the last few years and have participated in the pre-conference day discussions.
Further comments by anciendaze, to whom I am greatly indebted.
“This paper looks like the real thing. The immune impairment they describe is highly specific to EBV. One of the surprises in the main text is that none of the CFS patients they tested with a challenge involving a polypeptide from EBNA-1 produced an IFN-gamma response. This fits perfectly with the hypothesis of latent replication. Their results concerning deficits of polyfunctional immune cells with three different functions helps explain earlier mixed results concerning EBV. Researchers were looking for much less specific immune impairment.”
“Please note that the full text of the referenced paper describes tests for EBV infection which go a great deal beyond common clinical lab results. They also report that tests showed a great deal of latent replication must be taking place. Common assumptions in testing for EBV are based on active infections and antibody response to them. Few labs test for DNA of latent virus in immune cells. This paper specifically reports that certain evidence of RNA, produced by active infections, was absent or reduced. It also shows a crippled response via IFN-gamma. Under these circumstances it is unreasonable to say that it can't apply to you because you don't have unusual EBV results from standard clinical labs.”
“PCR testing, both qPCR and RTPCR, is part of the suite of tests used, but only part. They also used multiparameter flow cytometry to count immune cells with multiple markers. Even studies doing clinical flow cytometry have typically been limited to sorting cells by a single marker. (Note the disclaimer at the bottom of the page about the research instrument.) This would prevent them from detecting the specific deficits of polyfunctional immune cells found here. Beyond that they used ELISA and stimulated cell culture immunoassays. It's all there in the text.”
“This is the kind of battery of modern research techniques which has so often been absent in studies of ME/CFS. I'd say they really examined their early data and were guided by it in choosing that immune challenge with EBNA-1. This is not an example of confirmation bias behind a single favorite hypothesis.
A further comment from anciendaze:
"Normally, we think of a DNA virus like Epstein-Barr Virus (EBV) as being either active or latent, and assume it isn't doing much of anything while latent. EBV actually has several latent states. Latent phase 0 describes the least active state, which pretty well matches what we assume. There are also latent phases I, II, III. During these states it is possible for viral replication to take place. Active phase replication is typically lytic, with host cells being destroyed to release virions. Replication during latent phases need not destroy the host cell.
This has a major implication in the context of clonal expansion of immune cells. In this case stimulated immune cells divide by the normal process of mitosis, producing 2, 4, 8... daughter cells. This can lead to millions of cells producing a powerful response to an antigen detected by a small number of cells.
EBV infected cells have one or more episomes inserted inside the nuclear membrane. These are just plasmids, loops of DNA, floating around loose, not inserted in chromosomes. If clonal expansion just distributed a few episomes among many daughter cells, most of these cells would not be infected. However, if the virus is able to replicate viral DNA without destroying the host cell, it then has the ability to infect all cells resulting from clonal expansion. This has the potential to produce large numbers of infected cells without most of the indications of viral infection.
In order to exploit clonal expansion EBV doesn't even need to produce virions. It only needs to trigger replication of DNA strands, something host cell machinery does naturally during mitosis.
We know that retroviruses do exploit clonal expansion through passive replication of inserted provirus. (This has been a major problem in the fight against HIV.) We did not know this was often going on in a very common human virus which does not insert genes in chromosomes. What we did know was that most ME/CFS patients continue to show polyclonal expansion (of B cells in particular) while the disease state persists, but we could not find a single pathogen responsible. Immune response seems to be confused and often misdirected. Some patients do show autoantibodies (ANA, ATA, ACA); many do not, at least by current standards used for autoimmune diseases. Considering the limited understanding of those diseases, it may be time for a reevaluation.
In the past we have frequently heard that evidence of EBV infection was inconsistent or absent in ME/CFS patients. This research shows that conventional lab results give a very misleading picture, and offers some reason why. Furthermore, the evidence available now paints a picture of cells with viral DNA and nuclear antigens, but reduced or absent RNA from lytic replication, cytokines and antibodies. It really appears that this virus is crippling specific immune response to itself.
This has implications for a wide range of clinical tests, and for a number of diseases besides ME/CFS."
Saturday, November 23, 2013
Various people, patients mostly, spoke positively to me of “the focus" of the conference and of the variety of information that it presented. Of course the packed room included many of Dr. Enlander’s patients - but there were also patients of Dr. Peterson and, I presume, of Dr. Klimas. One had the feeling that a number of the attendees had not previously attended a conference like this. At the end of the day it seemed as though many people did not want to leave.
A number of factors coalesced in this particular situation. Dr. Enlander, the sponsor and originator of this conference (aided mightily by Dwight Merriman, a major donor), is on the faculty of Mt. Sinai. This important medical center in NYC promotes the Mt. Sinai ME/CFS Center, which, in turn, is a huge platform upon which to operate a conference venue and to project information about this illness ME/CFS.
The speakers, limited to five, included clinicians and researchers.
The first speaker, perhaps the most dazzling (in the general sense), was Dr. Eric Schadt. If you want to be amazed, check out this talk from the last conference, recorded by my son Peter Cairns. Dr. Schadt has big plans for data assembly and manipulation. He works on various projects with various collaborators, all at the same time. Dr. Schadt, always dressed informally in his own private uniform, seems to be in a hurry. One wonders how much he knows about ME/CFS - and the feeling that I get is that he applies a schema from an allied chronic illness to ME/CFS. Nevertheless, he laid out various immensely complicated networks of disease, explaining the complexities and “perturbations” (a great word) along the way. It was all quite exciting. One wonders how much he works on our illness - and the big question is, how can we get him to do more work on ME/CFS? He seems propelled in a direction that would be extremely helpful. Certainly he is not lacking in enthusiasm, and is brimming with confidence.
Of particular note was his work with a technical collaborator, Dr. Joel Dudley, to find a drug for an existing illness (IBD), using their computational techniques. Through their elaborate process Joel Dudley identified Topiremate, an anti-seizure drug, to treat IBD in rats. No one previously had come close to thinking of using this drug for IBD. In another instance a previously unassociated tri-cyclite drug was found to be effective in a certain lung cancer with the results being published in Cancer Discovery.
The implication is that such a drug discovery process could be applied to ME/CFS. My suggestion would be to have Dr. Schadt and Dr. Dudley work on a drug-targeting project for ME/CFS, something that might be both quick and specific. For instance, imagine the possibilities if Dr. Schadt’s technology could interrogate particular cell lines from a tightly constructed cohort of ME/CFS patients.
Next up was Dr. Judy Mikovits, who gave another of her amazing “outside of the box” lectures. It was also a surprising lecture, at least to me, who was not expecting her to touch on this subject. But this is a wonderful thing about this researcher – she goes where she wants to go and always with the patients in mind. The reader might remember that Dr. Mikovits was jailed two years ago as she prepared to come to NY to give a presentation to the first Mt Sinai ME/CFS conference. At that time a great pall descended on this well-attended conference, as most conference attendees reacted with deep sadness to the very astonishing strangeness of the jailing of a researcher. At least for this second Mt. Sinai conference day, many participants were pleased to see Dr. Mikovits speak – and it was a triumph, another masterstroke of Dr. Enlander. In fact, many of the attendees had come exclusively to hear Dr. Mikovits’ talk. I was among them.
Dr. Mikovits, without a job and without money, has continued over the past several years to attend professional conferences (cancer, GcMAF, mitochondria, lipid, lyme, ME/CFS) and to unleash her immense curiosity in the direction of this illness. She makes unusual, dynamic and wide ranging observations. We need to have more minds like hers at work towards our betterment.
Speaking of curious and fine minds, it was just a year ago that my friend Rich van Konynenburg died. He gave a fine presentation at the last Mt. Sinai conference and his presence today was and always will be sorely missed. Two years ago, Dr. Enlander showed his stripes by inviting Rich to give his first, or one of his first, presentations at a major conference. For years, I had observed Rich get marginalized in various situations –and his important ideas relegated to the periphery of conferences - but he always persevered. He was a wonderfully gifted and intelligent man, and when I think of his absence I want to weep.
Dr. Mikovits chose this moment to revisit an old topic, a topic that for all intents and purposes was seen as having been put to bed. Dr. Mikovits’ lecture was an update on events since the Lipkin paper on XMRV. In today’s lecture, Dr. Mikovits presented various papers, some older, some newer that – and in a straight-line fashion - strung together the case that allowed the door to be reopened on a retroviral fingerprint in this illness. It was quite a talk, adjusted to the audience level, but still difficult to absorb.
Towards the end, Dr. Mikovits touched briefly on one of her recent investigations - aberrant mitochondrial workings at the genetic level. She is investigating genetic testing for indications of secondary mitochondrial dysfunction that has shown up in a few ME/CFS or ME-like patients. Courtagen is the company that does this testing. This test might very well identify an important part of this illness - with the possibility of immediate treatment. The medical director of Courtegan is Dr. Richard Boles, whom I had heard about several years ago from Dr. Joseph Brewer. Dr. Boles is an innovator. The hope is to form a collaboration with Courtagen, where they would run a small trial on severe ME/CFS patients.
To me, Dr. Mikovits has the most “out of the box” thought process in this illness world. In order to move this along, I think she needs to have more input into future conferences. Like Rich van Konynenburg, she has “a feel for this illness”, much of it springing from her work in cancer.
Dr. Mikovits and Dr. Schadt should have the opportunity to sit down for extended talks. Together, with the help of others, they might be able to crack a part of this illness.
By lunchtime, we had had two lectures – the amazing and the surprising. What could be a better start?
The remarkable Hillary Johnson, author of "My Mother Ruth", came to me in the middle of the conference and said that it reminded her of the Invest in ME conference in the UK, both in its ambience and its seriousness. Hillary was spot on. The Invest in ME conference is patient driven, which almost guarantees intensity and focus. These UK folks, primarily Richard and Pia Simpson, make things happen, without all the attendant crap of an ME/CFS Industry conference. If one wants to run an effective, hard-hitting conference, I would advise following the Invest in ME model.
Dr. Derek Enlander has done this. Perhaps it is inadvertent - but this Mt. Sinai conference had the same combination of clarity, variety, limited bullshit and consolidation of different aspects of research and treatment. Could the conference have been improved? - Yes, it could, but it was an amazing effort as a second conference - and this bodes well for any such future endeavors.
The lectures after lunch were directed towards clinical practice.
Dr. Dan Peterson gave the first presentation. Each time I hear him give this talk, he seems to reach a higher level of eloquence concerning an array of difficulties of this illness. Dr. Peterson appears to me to want to be as clear as possible regarding his treatment of virally reactivating patients. These patients, clearly identifiable, represent 15% of his patients. I believe that he is mindful of his legacy and wants his lifetime of work to be continued by others. Of course this is a noble sentiment. He touched on Ampligen, Vistide, and Valcyte, all heavy-duty anti-virals that sometimes bring near complete recovery to selected patients. Of course the drugs work extra magic in his hands, as he has such a feel for this. I have personally met patients undergoing these treatments who have returned to work. Towards the end, Dr. Peterson confessed that he and his colleagues at large (clinicians) have not given or not been able to give proper care to these very sick and disabled patients. There was a sense of humility in what he said, something that you do not hear expressed very often.
Dr. Derek Enlander himself gave his usual polished, informative presentation, outlining his treatment protocol that has brought so much success to many patients. The room seemed to be full of his patients, in various stages of recovery. Dr. Enlander presented a brief view of his upcoming research into the limbic system and announced a Spect Scan collaboration with Dr. Byron Hyde. These isotope scans look like they could be a new insight into the limbic system. Do not be surprised to see Dr. Hyde on the next conference program.
The last speaker was Dr. Nancy Klimas. Earlier in the day, she had been at a CFI think tank discussion at Columbia - and thus missed most of the day’s presentations. She started her talk by promoting the new Neuroimmune Center at Nova University in Florida, which she heads up. Dr. Klimas has recruited various top-notch people from around the country including Gordon Broderick, one of my favorite researchers, and another, Mary Ann Fletcher, who had the guts to speak up in defense of our favorite advocate Eileen Holderman at the last CFSAC meeting. I have always appreciated Dr. Fletcher’s work, but my opinion of her rose sky-high in these few revelatory seconds.
This is some enterprise that Dr. Klimas has consolidated - and let us hope that she can move things along, particularly in terms of research. She has a knack of getting grants, particularly through piggybacking ME/CFS onto Gulf War illness research.
Further into her talk, Klimas spoke about various immunological aspects of this illness. I have seen variations of this presentation quite a few times now, but for many in the audience this was a new and exciting experience. Personally, I have never understood her cytokine profile - and the great difference between it and the separate efforts conducted by Dr. Montoya, Dr. Lipkin and Dr. Mikovits. For instance Klimas does not seem to pick up elevated IL-8 in her patient cohort. To me, elevated IL-8 is almost a signature in itself of this illness. Conversely, she routinely gets elevated IL-5, which is almost non-existent in other ME/CFS cytokine panel cohorts studied. This makes one wonder what she is seeing and in what patient group.
Lost in the shuffle of the last few years is the cytokine profile that came out of the WPI in 2011. In spite of its attachment to the defunct XMRV, this profile functions equally well if the letters XMRV are removed. This study certainly gave impetus to Dr. Jose Montoya in his search for a signature, and I am convinced that Dr. Ian Lipkin’s cytokine work is going to reflect a similar signature, or at least be something built on the WPI work. How could it not be?
Dr. Klimas went on to claim that we have, virtually, a biomarker in this illness right now. I found this somewhat disingenuous, and I do not think many people actually believe this. Certainly we can look forward to Dr. Jose Montoya’s studies in this regard, which will be presented in time. Dr. Montoya has told me that he continues working on this, is making progress, but that he “wants to get it right”. Also we can look forward to publication of Lipkin’s work on cytokines that should emerge soon. Most important to me is the work on NK cell and other immunological markers, a potential “fingerprint” of this illness, coming out of the work of Dr. Sonya Marshall-Gradisnik and Dr. Don Staines at Griffith University in Australia. I have written on some of this elsewhere.
Dr. Klimas went on to complain about replication and promoted the idea of “you replicate my work and I will replicate yours”. To me, not having replicating studies in ME/CFS is a big problem. In my opinion the first and foremost trial to try to replicate is Dr. John Chia’s 2007 study on enteroviral involvement. Not having an attempt to replicate Dr. Chia’s findings actually interferes with progress towards a solution of a significant part of this illness. It has great negative consequences for patients. Dr. Chia is left entirely to conduct this research on his own. Dr. Klimas should try to replicate Dr. Chia’s work - and then we can turn later to replicating something of her lab.
It was great to hear the various clinician attitudes and nuances for treatment – the more the better as far as I am concerned. One longs to hear others - especially Drs. Cheney, Chia, Brewer, Gordon, and Horowitz. And then there are other outside of the box researchers - Richard Boles (mitochondria), Robert Naviaux (metabalome), Patricia Kane (lipid membranes), John McClaren Howard (mitochondria, lipids), Marco Ruggiero (GcMAF) and others.
There was a short question period at the end of the conference with the various presenters as well as Frank Ruscetti, Ashok Gupta, and Christian Becker. The panel ended with various questions to and statements or answers from the panelists.
Marian Lemle asked a question about her hypothesis that H2S plays a major role in ME/CFS and whether anyone made a connection with this. She must have been pleased that Dr. Enlander mentioned sulfur metabolism. From what I could see, Marian drew a blank from the rest of the panel. Her thesis is a good one and should be pursued.
Howard Bloom made an eloquent statement about being locked in a darkened room for five years with this illness – and the attendant emotional catastrophe of total isolation.
Dr. Frank Ruscetti, fielding a difficult question about government (NIH) support for this illness, gave a fine, partial answer (by necessity) that concluded with his belief that funding for this illness will have to come from private foundations. I could not have agreed more and what he said was very important - coming in the final minute of the day. So this was a great conference from the first minute - to the last.
It is my opinion that the question period could have been extended for another half hour. There were at least ten people with hands raised when the conference ended - and the interest to engage the panel was growing. Many patients husband their energy and resources to get to this conference, and for them it is a precious moment, a unique contact with individuals that are elevated in their minds. Patient questions are generally well articulated and diverse, polite and interactive. It is my belief that things –ideas, insights - come back the other way too and in unexpected fashion. I hate to say it, but panel members also need input - and some of these articulate patients might harbor insights that are useful to others, especially to medical practitioners. As far as I am concerned, they can never know enough about this disease and its peculiarities - and where else to get it but from the horse’s mouth.
Wednesday, November 13, 2013
There was another fantastic and interesting article on Dr. Alexander Khoruts today. It appears in City Pages, is entitled The Forgotten Organ (Mysteries of the Microbiome) and was written by Chris Parker. This fellow Dr. Khoruts, based right here in Minnesota, amazingly, is, along with Dr Thomas Borody, the most dynamic individual in this emerging field.
He took a 14th century idea, known as Yellow Soup, and updated it to the 21st century. Many people are standing back, wondering how such a "Progressive idea" could emerge in our own time. (This is a bit of a joke.)
I first read about Alexander Khoruts and his work a good number of years ago. He is right here in Minnesota at the University of Minnesota. He is a world leader in fecal transplantation and it is exciting to have him working so close by to where I live in Minnesota. Minnesota is not known to be a state that is aware of or gives legitimacy to ME/CFS (an understatement), so the possibility that a treatment for ME/CFS might emerge here is welcome news.
Here is an article on Dr. Alexander Khoruts, from the Guardian. As usual, the comments are interesting and informative.
A more immediate scientific observation regarding short term fatty acids in the gut can be found here.
Thursday, October 31, 2013
Dr. Derek Enlander is chairing an ME/CFS treatment conference at Mount Sinai in New York City on Wednesday, November 20, 2013. This one day conference will include presentations by Dr. Nancy Klimas, Dr. Dan Peterson, Dr. Judy Mikovits, Dr. Eric Schadt and Dr. Enlander himself. A panel discussion including the speakers as well as Dr. Frank Ruscetti and Christine Becker will occur at the end of the day. The emphasis will be on communication and interaction.
(The conference takes place in the Academy of Medicine, 1215 Fifth Avenue. Registration fee is $150 for physicians and $50 for patients. The conference runs from 11-4.)
It is my obervation that this conference is an outgrowth of a Simmaron research discussion held prior to the ME/CFS FDA meeting in May. At that time, Dr. Dan Peterson generously organized a pre-meeting open-format treatment discussion involving both Dr. Klimas and Dr. Enlander, along with a number of other clinicians, researchers and patients. The discussion was a lively one, and free-wheeling, just the kind of discussions necessary to push ideas along. Dr. Peterson's early morning meeting was the only item of real interest at this FDA conference and it is my feeling that this Mount Sinai conference is an attempt to build on that Simmaron discussion.
This is the second conference arranged by Dr. Enlander and the ME/CFS Center at Mount Sinai. Dr. Enlander is one of a very few physicians who is attached to a major university hospital doing research on this difficult illness. The last Mount Sinai ME/CFS Center conference was held two years ago and featured several very powerful and important lectures. Foremost was a talk by Dr. Eric Schadt that can be found here. Additonally Rich van Konenynberg gave a fine presentation on his mehtylation blockage/glutathione depletion ideas. Rich, who died a year later, is sorely missed by the patient community and many others who experienced the very rare character of this man. Rich's fully articulated three-hour lecture in Sweden can be found here. Dr. Kenny De Meirleir's often referenced talk on GcMAF can be found here. Dr. Enlander himself gave a fine presentation of his treatment strategy.
It is well known that Mount Sinai received a generous research gift from one of Dr. Enlander's patients, thus fueling the ongoing ME/CFS research at this center. It is less well known that these conferences at Mount Sinai, with all their very great importance, are constructed on a shoe string. It is time for someone else to step forward and help with this conference, especially considering the reality that very few of these kinds of discussions are ongoing in the field of ME/CFS treatment. This conference has very great potential to expand and ignite substantial treatment discussions - but someone is going to have to help Dr. Enlander in order for this conference format to reach its full potential.
For those readers who are not familiar with Dr. Enlander, here is a short radio interview with him.
Saturday, October 19, 2013
Dr. Joseph Brewer gave a smashing talk on Mycotoxins and ME/CFS. Dr. Brewer is an Infectious Disease physician from Kansas City, MO, who has a longstanding interest in chronic illness. Dr. Brewer should be included in any serious discussion of these complex illnesses. He has great curiosity - which he backs up with science.
Dr. Brewer began by giving a general overview about mold, presenting a 2011 study of mold in water damaged buildings, a 2009 study of water damaged buildings after Katrina and a recent study out of Texas Tech. He illustrated stachybotrus chartarum, one of the most notorious forms of mold.
He presented mycotoxins as extremely toxic, secondary metabolites. The three big ones, measured at Real Time Lab, are Aflatoxin, Ochratoxin A and Trichohothecene.
Dr. Brewer and Dr. Hooper published a very important paper in April, 2013 on “Mycotoxins and ME/CFS”. Amazingly, they found 93% of 104 patients tested positive for one or more mycotoxins, compared to 0% in 52 controls. Some have all three - the mycotoxins trifecta.
The clinical associations with mycotoxins poisoning are dysregulation of the immune system and especially dysregulation of mitochondria. Mycotoxins are potent mitochondrial poisons. Mycotoxins produced the same symptoms as ME/CFS - and also as Lyme.
It is Dr. Brewer’s supposition that mold takes up residence in the body, particularly in the sinuses. He cited scientific studies that led him to this conclusion. This exposure can be current - or it can be longstanding from living or working in a moldy environment, ten, twenty or twenty-five years ago.
Dr. Brewer presented his treatment strategy for getting at the mold and getting rid of it. The first step is to reduce input. The second step is to enhance output. This can be through improving glutathione, increasing sweating, using binders like Cholestyramine or activated charcoal (his particular favorite) - and developing an antifungal strategy.
The main approach that he uses is a mist delivery of Ampho B. The instrument of delivery is a Nasa Touch .
I asked Dr. Brewer about nasal colloidal silver. He said that he thought that colloidal silver was a promising treatment.
It was wonderful to see Dr. Brewer drop the mold bomb on this Lyme conference. He walks into a room and, when he is finished his delivery, things have changed. Dr. Brewer needs to be heard in more places. Meanwhile he goes about his work of helping patients. This clinician/researcher is among the very best.