Discussion in 'Latest ME/CFS Research' started by slayadragon, Apr 11, 2013.
Curious how Brewer folks are dealing with bleeding?
The two papers are linked - the first paper is what was used to set the level that the second paper judged clinically significance and which also yielded what passed for the controls in the second paper. It was far from an ideal arrangement, not helped by a change in description in the second paper of the controls to 'healthy' when there was no apparent consistent testing of their health.
That's certainly true but we know very little about the effects of any kind of environmental element in MECFS, except perhaps that autoimmunity rather immunodeficiency appears the more active process in MECFS.
No, in the sense that the two amounts of 'tiny' are relative - we know the levels of acute toxicity of common mycotoxins, and we know the effects of chronic subacute exposure - organ damage etc, in a range of animals. These levels are greatly above the kind of levels that promote allergic responses in susceptible humans. When I first posted in this thread I made the point that allergic response was a far more probable reaction to mold elements - be they toxic or not - than a toxic response. There are arguments for genetic aspects in susceptibility to poisons - however if that were in play with mycotoxins one would expect susceptible individuals to show exceptional levels of organ disease rather than the amorphous symptomology of MECFS.
Species of fungus produce distinct mycotoxins - they're simply by-products of the fungus' metabolic processes. There are some toxins that are known to be produced by more than one fungal species but so far the total number of micro fungi species involved seems to be small. Things are different with the fungi that produce large fruiting bodies - mushrooms etc, where a few toxins are found across a large range of species.
If one were to argue for multiple mycosal infection, that still wouldn't increase the overall toxin load. The volumes of mycotoxins found in cereals and similar crops, which is probably the largest source of environmental exposure, comes from mass infection of crop - have a look at what this looks like on peanuts - http://services.leatherheadfood.com/eman/FactSheet.aspx?ID=78. That level of mould growth on a human, isn't going to be something you'd miss.
If the argument is that the test is for a biomarker for infection- then we return to the problem of excluding environmental confounders where the test sets clinical significance at an exceptionally low level.
I don't know about 'wrong' - I'd say that there isn't a falsifiable hypothesis shown to be robust in the face of adequate scientific rigour. In the case of the second Brewer paper the lack of an in trial control group means that no real conclusions can be made about treatment outcomes - basically where was the placebo ?
And the whole things seems to avoid confronting the obvious: there are people who belong to the larger ME patient population (in which allergy type symptoms are widely reported), who have symptoms of nasal congestion and facial sinus pain that are A1 typical of allergy. Yet some esotoric explantion involving mystery fungi doing things that fungi haven't been shown to do (i.e produce toxins in vivo without causing either major organ damage or surface tissue damage) is preferred to an explantion of allergy.
I think it is quite telling that there are people who identify mould affected buildings as a source of their ill health, who then get better by changing environments - this is typical of allergy and mystic toxic moulds aren't necessary to explain what has happened. Moulds may have been involved as an allergen but many other allergens share a mould favouring environment and could also have been involved or even wholly responsible for the ill health.
I am actually fine with the idea that Brewer has chosen a level of significance based on clinical experience with these patients. The patients he chose as controls who claim they feel healthy fall below that line and the patients who claim they feel ill are above it. Improvement in symptoms correlates with passing below that line. By biggest concern is lack of a placebo rather than choice of controls.
I think that it has already been shown that sinus infections can cause neuroinflammation, so I don't have a problem with relatively small levels causing harm. It may have something to do with the proximity of parts of the sinuses to the brain.
I think we know quite comprehensibly from Shoemaker's work the effect indoor environmental mold (or mold-associated toxins) has on patients with symptoms identical to those of MECFS.
I used allergy as an analogy, but my general point is that I don't see how you can claim that because some people are made ill by a certain level of a toxin that all people will be made ill by that level.
Shoemaker has already showed the effect of chronic exposure to mold or mold-related toxins is chronic innate immune activation which does indeed give rise to amorphous symptomology rather than exceptional levels of organ disease.
Wouldn't disagree with that
I agree it could be something associated with or interacting with the mold rather than the mycotoxins themselves.
Yeah no placebo is a problem, I suppose we will just have to wait.
I think the physicians treating these patients could recognise an allergy. I don't think the nasal congestion and post-nasal drip respond to anti-histamines.
Again, the work of Shoemaker is completely at odds with this, it is not an allergic response. The symptoms of MECFS (and those of CIRS) do not correlate with allergy and histamine release, there is no measurable allergic reaction but there is measurable innate activation and downstream consequencies (raised complement, tgf-beta, low VEGF, raised leptin etc etc).
When I first became involved with this subject I did so because I wanted to post Brewer's second paper. Later I realized that since we are a family of four all diagnosed with CFS and since we are all patients of Dr. Brewer I might be able to provide some helpful insight to others. I decided to continue to update our experience regardless of outcome. So whether we get a little better, a lot better or even if we get worse I plan to report it. We have had a spirited debate, but in the end it's all academic. We are at a very early stage. There are no blinded studies going on, and there won't be any for the foreseeable future, so anecdotal evidence is the best we will have for a while.
My wife, youngest daughter and I have entered into the third month of the treatment. My oldest daughter has returned from college and is now in her second week of treatment. In an earlier post I provided environmental test results that would indicate we have been living in an excellent environment for about a year and a half or so. Despite this, none of the three of us living at home have experience any health benefits. My college daughter has been away from home most of the time for the past four years, yet her health is also no better .
I had been planning to update our status at the three month mark unless some bright line event happened in the meantime. It seems this has happened. I am close to 23 years of illness. During time, I have been able exercise minimally. Over the last couple of years I've lost this ability altogether. I have not exercised even a single day for the past year and for about two or three years prior to that only very rarely.
A few days ago I was able to exercise for the first time. Then, yesterday and today I was able to do it again. I was able to walk a couple of miles, about 30 minutes or so for three days in a row for the first time in years. I am not claiming victory. I now know I feel better and I have more energy than I did prior to the protocol. What happens going forward only time will tell. I will post it regardless.
For the last couple of weeks my wife has said she is "definately" better than before she started the protocol. She is not well by any means, but there is a clear and noticeable difference.
My youngest daughter is by far the sickest. She is 18 years old and had to quit school when in the 6th grade. She has not been well enough to even tutor at home for the last 3 1/2 years. Her excursions outside the home are very limited due to her neurological symptoms. The only thing I can say for certain is that she is feeling better than she did during worst of the die off. I am not sure if she is better or not than she was prior to the start of the protocol. She seems to feel and act a bit better than prior to the protocol but her energy level is still very low.
My older daughter is the least effected by the illness. She lives a fairly normal life, but has a great deal of fatigue and sleep issues and other symptoms. The start of the protocol has effected her similarly to the rest of us. She is definitely worse.
What really stands out about the treatment is how much is effects fatigue and malaise. During the die off I often slept 10 hours a night, sometime more, while barely moving a muscle. In order to get through it we had to pare down our activity level to the bare minimum. The good news for the three of us is that the worst seems to be over.
Sorry, he does not.
Thanks for letting me know! That's too bad.
Interesting that Dr. Shoemaker apparently treats for biofilms, but uses antibiotics instead of antifungals, at least according to ggingues at the bottom of this page:
Yes the BEG spray contains EDTA for breaking down biofilm, but this is for MARCoNS rather than fungal infections. See eg. http://www.survivingmold.com/docs/McMahon_11_Step_Biotoxin_Elimination_Pathway_Essay.pdf
Looks like Klinghardt has been talking about this for a while:
I have something anecdotal to add which I find interesting. On occasion, when I'm taking supplements which may be affecting "detox", such as methylation supplements, molybdenum, or modified citrus pectin, I will experience some mild, intermittent, sinus drainage. I experience no other symptoms related to my sinuses.
Occasionally, simultaneously with the sinus drainage, I will have an experience where I will distinctly remember a smell that I associate with mold exposure. It's as if I'm smelling the odor without its presence externally.
It is not my imagination, and I can think of several explanations for this happening, such as toxins being expelled from my sinuses during the drainage event.
Allergy can be quite difficult to exclude - http://www.waojournal.org/content/pdf/1939-4551-6-11.pdf . If the Rituximab studies show relevance to ME then allergy as an autoimmune function will need to be factored in to future thinking about the illness - http://www.nih.gov/news/health/jun2013/nci-02.htm and also http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3121058/ The fact that antihistamines don't work or are only of limited value doesn't rule out allergy just highlights the limits of current medication.
Shoemaker doesn't appear to have any peer reviewed published work, let alone replication studies supporting his hypothesis. The Shoemaker approach may look good on paper but really these lone operaters aren't contributing to meanigful research. If patients want to take a physician solley on trust that's their right, but it is not how the science of illness progresses.
Courtesy of Dr. Shoemaker's "Surviving Mold" newsletter from today, here is a link to the "Bulletproof radio broadcast, featuring Dr. Shoemaker:
I've no doubt allergy can be difficult to exclude, and no doubt there are links between many immune disorders.
I think Shoemaker does have peer-reviewed articles, and to me, his research is meaningful.
Playing the devil's advocate here. Is it possible that what is going on in Brewer's patients is that they are effectively indirectly treating MARCONs due to the fact that the spray prescribed contains EDTA? Did Brewer rule out MARCONs (or other biotoxin producing bacteria) in the patients presumably being treated for fungal infections?
Brewer does not test for this. Given that the treatment causes mycotoxin levels to drop and health to improve (at least in some patients) it seems unlikely.
One week in and I feel better. I also started gastrocrom for mast cell activation and it will calm down cytokines. Maybe I need more time into this or we are hitting different bugs and not ones carrying mycos. I am having a lot of bloody mucous, though. Not too bad, but not scanty either.
Good to hear that you are better. Can you elaborate on what your doctor said about mast cell activation and gastrocrom? My daughter will see Brewer in a few weeks and I want to ask him about mast cell activation.
I see an immunologist and am being treated for mast cell activation. I started with the basics of the protocol which would be h1-h2 blockers twice a day (zyrtec/zantac or claritin/pepcid are generally used though we use allegra for my daughter because the others make her sleepy). I felt improvement on those. My daughter's standing pulse (POTS) went from 120 -130 down to maybe 100-110. This helped me most with reactivity, not my POTS. Then I added ketotifen (mast cell stabilizer) which is compounded through Clark's Pharmacy in WA state. I take 2 mg twice a day. This does make many people sleepy, most adjust but some don't. My daughter does not take this. My livedo reticulitis disappeared, maybe a shadow of what it was. My daughter has worked up to 8 vials of gastrocrom a day 2X4, every 6 hours is the goal and I am on 3 vials a day and ramping up to 4 next week. Some of us have to ramp up slowly on this. Goal is 8-16 vials a day, but many can settle on 8. I am catching her standing pulse in the 80s rarely and 90s often. We also take Neuroprotek which was developed by Dr Theoharides (Tufts University: www.mastcellmaster.com ). I am supposed to take the max dose, but I can get away with 4 a day now. My daughter takes 4 a day. I am not sure how much this is helping her and will be ramping down once she has been on 8 vials of gastrocrom (sodium cromolyn) for a while (takes about 6 months to have full effect). I was able to replace midodrine with NP and additional benefit is that NP is anti inflammatory which I have benefited from.
I know one of the mold doctors prescribes the nebulized form of sodium cromolyn. Gastrocrom comes in vials to squeeze into water. This comes in vials to put in nebulizer. I think this is to help patients deal with exposures. I have not heard a patient say that they were told this was for mast cell activation. I have heard of some mast cell patients benefiting from the nebulized form, though.
Some people have to take gastrocrom and ketotifen and quercetin (quercetin and luteolin are in neuroprotek along with some rutin). It seems that the different mast cell stabilizers have different specialties. I know some that do fine with quercetin and some other natural supports but they control their diet as well. Most everyone cannot get away with not controlling diet to some extent. The meds all have an accumulative effect, so it can take time to see effects though h1 and h2s clearly immediately helped with the histamine related symptoms and for some reason NP (I also successfully used Querca Max from Clark's Pharmacy) at least within days also work very quickly to help with my POTS venous pooling and inflammation in legs.
Gastrocrom may work well alone, but often these other interventions are needed. I hope to taper down on the h1-h2s if possibly using gastrocrom and possibly ketotifen as main line of defense but it is also good to have h1-h2s around for "attacks". I use benadryl when I have "breakthrough" symptoms and I use atarax at night to replace zyrtec as my pm h1 blocker. It crosses the BBB and does not have the tolerance issues benadryl has. I also have hyper activity at night. Histamine is it's highest around 3 am or so.
We have MCAS with systemic issues. If you are dealing with mast cell reactions to the fungus but do not have MCAS, you may just need gastrocrom (or nebulized sodium cromolyn) or an allergy formula like Querca Max or D Hist might be helpful. H1 and possibly h2 blockers, if histamine is an issue. People with MCAS are advised to use both h1-h2 blockers to close a loop.. histamine will trigger more mast cells to activate. Nasalcrom might be something to look into as well. It is sodium cromolyn in a nasal spray. This can be purchased "over the counter" as well.
In the Grant interview linked in this thread, she mentioned that hyphae can trigger mast cells. I think this would beneficial for Brewer to look into. Fungi trigger mast cells. Some of his patients may have developed mast cell activation syndrome or may be dealing with some form of mast cell activation.
I was already working on this angle before I started the sinus protocol. There are a subset of us as well that present with POTS/OI, Ehlers Danlos or another CTD and MCAS. I am in that subset. But I don't think one has to have this trio presentation to have MCAS or simply a mast cell issue comorbid with a fungal infection.
I've crashed today.. really tired. Little sleep night before and huge appointment with an EDS specialist that took all day. So not feeling so good today. Don't want it to sound like I think this will be a piece of cake. It was just interesting that my legs for days and soon after starting the sinus protocol and adding in gastrocrom felt better than they have in almost a decade. Today.. they are heavy.
Didn't want to say anything when you were feeling better, but I think if the protocol is going to work some suffering is inevitable. It took me eight weeks to turn the corner and now I've been better for five days. On the other hand my daughter is still not better after nine weeks. If she is to fall in the 2 to 12 week range Brewer talked about she'll have to hurry up.
I appreciate the detailed mast cell information. I plan to bring it up with Brewer.
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