ME is not mould intolerance; mould intolerance is not ME

[JohntheJack]

If someone says they have ME-like symptoms from mould intolerance, I don't deny it. If someone says that they have ME and their symptoms are made worse by mould, again I don't deny it. If someone says they have ME caused by mould intolerance, again, again I don't deny it.

If someone's ME-like symptoms are relieved by mould avoidance, then they don't have ME, they have mould intolerance.

I think it's important that ME is not made a dustbin diagnosis or so broadened as to be meaningless.

I confess I have been disappointed by endorsement by some quite prominent patients with a good scientific background of a story of 'treating ME by avoiding mould'.

Mould intolerance is mould intolerance. ME is a discrete illness. ME is not treated by mould avoidance.

 

[Stukindawski]

I've read various interpretations of the meaning of the term 'Myalgic Encephalomyelitis' over the years.

The latter part of the term refers to an inflammation.

Inflammation can be brought about by agitation, when the source of the agitation is removed, the inflammation may have the chance to heal and abate.

By this interpretation, you could have an environmental, transient form of ME.

I think the greater distinction would borrow from the past.

I think Post Viral Myalgic Encephalomyelitis would be a much more helpful distinction, both clinically and in terms of research.

ME-Like Symptoms is all we have until there is a consensus on biomarkers. Though to be honest, I think the first biomarkers are likely to be complimentary to the symptom based diagnosis. rather than replace it altogether due to the heterogeneous nature of current diagnosis.

 

[Snowdrop]

I presume it's possible to have both ME and mould intolerance. I'm sure mold intolerance is a real thing. When things go wrong in the body we can start reacting to pretty much anything. It would be difficult to distinguish between where the symptoms of one begins and the other.

Many of us understand this experience from a host of co morbid conditions. Many of these conditions are also ill defined.

I suppose this is part of what makes diagnostic criteria tricky even with PEM to distinguish as people with mild ME (particularly the slow onset) don't always have clear and profound PEM episodes unless doing a great deal more than those more seriously affected meaning they might do some amount of exercise and be OK. This is of course how the PACE people managed to do what they did -- with mostly mild ME or even fatigue as most of their cohort.

 

[ash0787]

anything that aggravates the immune system is going to cause a flare in symptoms, but I don't know under what circumstances that would occur, you'd have to be exposed to an unnaturally high amount, and I would expect the levels of it in nature are quite high, so unless its certain strains which can only live in artificial environments ?
it would have to be on the level of mild hayfever to have an noticable effect though I imagine ...

 

[Jesse2233]

This is a question I've been struggling with

The most rigorous ME definition is Dr Hyde's who states that ME is acquired CNS damage from an enterovirus with sudden onset, there's a certain elegance and clarity to that idea

However Dr Klimas and others have found a common immunological signature that goes beyond Dr Hyde's strict definition

If we expand mold to mean any environmental contaminant problematic to an individual, then a strategy of attenuating one's body to detecting and avoiding that contaminat makes sense as a way to improve even if that wasn't the entire causal factor

Are there subtypes this works better for? Perhaps

Maybe they have fewer chronic infections or autoimmune processes. Or maybe removing environmental factors allows them to deal with other underlying factors more effectively

Will it work for everyone all the time? I don't know

At the end of the day I don't think we can make any conclusive statements because so little research has been done in this area

And for that reason, and the strong anecedotal reports, it's probably worth it for most ME patients to at least try once

 

[Hip]

Mould intolerance is mould intolerance. ME is a discrete illness. ME is not treated by mould avoidance.

I agree that these two illnesses, although symptomatically similar, should be differentiated, not least because an incorrect diagnosis can lead to the wrong treatment.

Just recently I read this article, in which Ryan explains how he had been misdiagnosed with ME/CFS and fibromyalgia for 10 years, when in fact he had chronic inflammatory response syndrome (CIRS) induced by mold. Once he had the correct diagnosis, and followed 3 aspects of Ritchie Shoemaker's protocol for treating mold-induced CIRS, he was back to near full health in just 5 months.

The Shoemaker protocol he followed included:

• Cholestyramine and Welchol to bind to the mycotoxins in the intestines, and pull them out of the body.
• The no amylose diet.
• The antibiotic BEG nasal spray to get rid of a MARCoN infection in the nasal and sinus mucous membranes (MARCoN = multiple antibiotic resistant coagulase negative staphylococci) infections.

The full 11 step Shoemaker protocol for mold and biotoxin induced illness (which Shoemaker calls chronic inflammatory response syndrome, or CIRS) is given here. The protocol is described in more detail here.



The difference between ME/CFS and mold-induced CIRS is that the former is typically triggered by viruses, and the latter is typically caused by the mycotoxins secreted by mold (or by other biotoxins like toxic blue-green algae, or ciguatera toxin).

Because mycotoxins are non-living, they can be removed (detoxified from the body), which is something you cannot easily do with viruses. This makes CIRS from mold probably more treatable than ME/CFS.

Shoemaker believes that people with certain susceptible genetic predispositions (based on their HLA DR type), are unable to properly detoxify mycotoxins and other biotoxins from their body, so these biotoxins accumulate in the body, and cause CIRS. Shoemaker says that anyone with these susceptible HLA DR types will be prone to getting mold illness when exposed to mold, because their body cannot properly detoxify the mycotoxins. Shoemaker finds it requires cholestyramine to remove the biotoxins in such patients with susceptible HLA DR types who have developed CIRS from mold exposure.

Though the idea of people being genetically unable to detoxify biotoxins is controversial: this document is critical of doctors who use cholestyramine to detoxify mycotoxins and other biotoxins, saying that the short half lives of most mycotoxins do not support the theories of doctors like Shoemaker who say that mycotoxin get "stuck" in the bodies of individuals with certain susceptible HLA DR types.

By the way, if anyone wants to test whether they have high levels of mycotoxins or other biotoxins in their body, a free online visual contrast sensitivity test (VCS test) can give you a good indication. The online test takes about 5 minutes to complete.

This VCS test looks at your eye's ability to detect subtle differences in shades of gray. The retina has neurons in it which do the light sensing and information processing, and the VCS test checks the functioning of these neurons of the eye. This check of functioning is a way of gauging the health of these neurons — a health which may deteriorate if they are being affected by neurotoxins like mold toxins.



But in spite of the differences between ME/CFS and mold-induced CIRS, it is plausible that ME/CFS may involve both mold exposure and viruses in some cases. So it would be a good idea for ME/CFS patients to take the free VCS test linked to above, which will give some indication of whether they are currently affected by biotoxins such as mold toxins.

However, even if an ME/CFS patient is not currently affected by biotoxins, it is conceivable that during the time they first caught their ME/CFS-triggering virus, they could have been exposed to and affected by biotoxins, and these biotoxins may have modulated the immune system in such a way that it enabled the virus to trigger ME/CFS. Some mycotoxins have been shown to increase the Th2 immune response, which may thus make it harder for the body to fight viruses.

And if an ME/CFS patient is continually exposed to mold, possibly this Th2 response may worsen their viral infections. Note that you can be exposed to mold from your environment; but Dr Joesph Brewer theorizes that ME/CFS patients may have a chronic mold infection in their nasal and sinus mucous membranes, which would constantly be creating mycotoxins.

Also, if an ME/CFS patient's symptoms are relieved by mold avoidance, then that could simply be due to a mold allergy that they have. In this case, it does not mean the mold is causing the ME/CFS, but just making you feel worse, as allergies tend to do.

 

[Stukindawski]

(Note: I'm not wedded to any of this and very open minded/excited to read good rebuttals)

To put it another way, Myalgic Encephalomyelitis, describes Muscle Pain & Brain/Spinal Cord Inflammation.

As far as I know, Muscle Pain & Brain/Spinal Cord Inflammation hasn't been limited to only one possible cause. So temporary ME as a result of a Mould allergy isn't logically inconceivable.

If you're using ME in a historic sense and marrying it to a specific type of presentation (i.e Ramsay ME), then sure, that would be distinct.

 

[Jesse2233]

Just recently I read this article, in which Ryan explains how he had been misdiagnosed with ME/CFS and fibromyalgia for 10 years, when in fact he had chronic inflammatory response syndrome (CIRS) induced by mold

Interesting, Ryan said his onset was sudden and flu-like

 

[nasim marie jafry]

(Note: I'm not wedded to any of this and very open minded/excited to read good rebuttals)

To put it another way, Myalgic Encephalomyelitis, describes Muscle Pain & Brain/Spinal Cord Inflammation.

As far as I know, Muscle Pain & Brain/Spinal Cord Inflammation hasn't been limited to only one possible cause. So temporary ME as a result of a Mould allergy isn't logically inconceivable.

If you're using ME in a historic sense and marrying it to a specific type of presentation (i.e Ramsay ME), then sure, that would be distinct.

Hi, Stukinadawski, You said in an earlier comment that 'Post Viral Myalgic Encephalomyelitis would be a much more helpful distinction, both clinically and in terms of research'. Postviral Myalgic Myalgic Encephalomyelits is actually a tautology because the original description by Acheson/Ramsay *is* post viral. And I am personally married to this definition because this is the illness I was diagnosed with in early 1984, after a severe enterovirus - Coxsackie b4 - in late 1982. The consultant neurologist who diagnosed me worked with Ramsay and wrote the introduction to his 1986 book.

I remain ill with ME today. My history is RamsayME, I know no other version of ME.

Of course, there has since been a proliferation of definitions and criteria for ME, with the added and confusing conflation with 'CFS' in UK, especially. All of these illnesses are devastating, but it is extremely frustrating for someone like me whose life has been wholly diminished by RamsayME since I was 18 years old to see so many illnesses being subsumed now under ME label. Leonard Jason has done great work on case definitions and reports that Ramsay ME is considered to include the most severely physically impaired patients. In a sense, therefore, we have more to lose by conflation of non-ME with ME.

We seem rarely to be speaking of the same illness. I fully accept there is a mould-triggered illness that we should be exploring and researching but I am much, much more concerned about research that will bring understanding and treatments for the originally defined myalgic encephalomyelitis. I think that is understandable considering my 33 years of life with ME. A cluster of people got ill in the west of Scotland in early 1980s. We all lived in entirely different houses and geographic locations - what we had in common was Coxsackie, and for some reason we had an abnormal immune response. I doubt very much this is related to mould.

 

[Hip]

Interesting, Ryan said his onset was sudden and flu-like

I read that mold exposure can produce flu-like symptoms.

 

[Hip]

All of these illnesses are devastating, but it is extremely frustrating for someone like me whose life has been wholly diminished by RamsayME since I was 18 years old to see so many illnesses being subsumed now under ME label.

The fact that there are now several different sets of criteria used to define ME/CFS does not necessarily mean that there are several different illnesses.

My own ME/CFS seems to be driven by coxsackievirus B4, based on having CVB4 as an active infection in my blood tests; but whether such enterovirus ME/CFS is different to, for example, the ME/CFS that sometimes appears after mononucleosis / glandular fever is not known. They could be different diseases, or they could be the same. We don't know at this stage.

 

[Stukindawski]

Trying to see this from another point of view.

Ramsay's ME (Thus: ME) is inherently Postviral as it describes the symptoms of a specific disease presentation to which the use of the term ME was attached.

While it's impossible for a disease name to fully encompass its signs, symptoms and cause, attaching ME to that original, postviral presentation and excluding its use to all others is vital to the epidemiological process.

On that basis I assume it would be acceptable to have additional diseases such as AME (Allergic Myalgic Encephalomyelitis)

As a comparison, most people associate Diabetes with Blood sugar/Insulin problems. Diabetes Insipidus on the other hand is something quite different despite sharing urinary problems.

I think there's a difference between technically distinct and historically distinct. But given that new diseases require investigation over time, to fully understand their cause, processes and symptoms, the re-appropriation of terms however apt without a distinct qualification, creates confusion and can have deleterious effects on the epidemiological process.

 

[Esther12]

I think that there's so little really solid evidence here that it's best to be cautious in any of the claims we make.

It doesn't seem impossible to me that someon could fulfil all the criteria for ME and then find that their symptoms improve with something like mould avoidance. It can be difficult for them to talk of their experiences in a way that does not given an the impression that mould is an important factor in ME, but I do think that they have a responsibility to try to make this clear when there is no good evidence that mould is an important fact in ME. I also think that we all have a responsibility to treat people in a kindly manner when they discuss their personal experiences, and not pretend that there is good and clear evidence showing exactly what ME is an who should have the label. If someone improves with mould avoidance, then I don't think it's right to say that they cannot have had ME.

Personally, I've been uncomfortable with the way some coverage of Julie Rehmeyer's book has dwealt of the mould issue, but I also don't like the way some people have responded to this. There are so many clear-cut problems around ME that I think we're best of focussing on them, and not getting too caught up in arguing about areas where there's less clear-cut evidence to rely upon. I think that some people do assume that ME is a better understood, and more meaningful, diagnosis than it really is. I think that it is a bit of a dustbin diagnosis, for all of the major criteria used, and is likely to include people with a range of health problems. It will be good for everyone to get this sorted out, but also, there are many common problems that we all face and can try to support one another with.

 

[Cheesus]

If someone improves with mould avoidance, then I don't think it's right to say that they cannot have had ME.

I agree with this. I subscribe to the hypothesis that ME is an endpoint that possibly has multiple directions of arrival. Mould might be one direction by which people arrive at ME.

 

[JohntheJack]

I agree with this. I subscribe to the hypothesis that ME is an endpoint that possibly has multiple directions of arrival. Mould might be one direction by which people arrive at ME.

I am not saying if someone improves with mould avoidance they can't have ME. I am saying that ME cannot be treated with mould avoidance. So any improvement is not down to treating to ME but, possibly, a co-morbid mould intolerance.

Again, I am not saying that MI can trigger ME (I don't know whether it can or not), but if someone has MI-triggered ME, then that ME will still not be treated by mould avoidance, because ME is a discrete illness not treated by mould avoidance.

I agree it is good to avoid any nastiness, but ME cannot be broadened to include any illness with similar symptoms, whether due to mould or to psychological factors.

As with Nasim, my illness is entirely viral.

 

[Hip]

I agree with this. I subscribe to the hypothesis that ME is an endpoint that possibly has multiple directions of arrival. Mould might be one direction by which people arrive at ME.

That's a possibility: ME/CFS and biotoxin illness / CIRS might share some, or even all, of the same pathophysiological mechanisms and pathways, so they could be pathophysiologically the same or similar diseases, but just with different triggering causes.

But from the diagnosis and treatment point of view, it makes very good sense to differentiate ME/CFS and biotoxin induced illness, because if you don't, you run the risk being labelled with ME/CFS, and then like Ryan, wasting 10 years of your life, when the correct treatment for biotoxin illness may fix you in a matter of months.

It's always bad when someone with a treatable illness gets misdiagnosed with ME/CFS.

 

[nasim marie jafry]

I think that there's so little really solid evidence here that it's best to be cautious in any of the claims we make.

It doesn't seem impossible to me that someon could fulfil all the criteria for ME and then find that their symptoms improve with something like mould avoidance. It can be difficult for them to talk of their experiences in a way that does not given an the impression that mould is an important factor in ME, but I do think that they have a responsibility to try to make this clear when there is no good evidence that mould is an important fact in ME. I also think that we all have a responsibility to treat people in a kindly manner when they discuss their personal experiences, and not pretend that there is good and clear evidence showing exactly what ME is an who should have the label. If someone improves with mould avoidance, then I don't think it's right to say that they cannot have had ME.

Personally, I've been uncomfortable with the way some coverage of Julie Rehmeyer's book has dwealt of the mould issue, but I also don't like the way some people have responded to this. There are so many clear-cut problems around ME that I think we're best of focussing on them, and not getting too caught up in arguing about areas where there's less clear-cut evidence to rely upon. I think that some people do assume that ME is a better understood, and more meaningful, diagnosis than it really is. I think that it is a bit of a dustbin diagnosis, for all of the major criteria used, and is likely to include people with a range of health problems. It will be good for everyone to get this sorted out, but also, there are many common problems that we all face and can try to support one another with.

Hi, Esther12, You say: 'If someone improves with mould avoidance, then I don't think it's right to say that they cannot have had ME'. The problem is the *proliferation* of definitions of ME, which I referred to above. Also, in a discussion on social media a while back, Julie told me she did not have RamsayME, so I am fairly clear we do not have the same illness, more from her descriptions of symptoms/dramatic recovery than anything else.

And I am not sure at all why we all have to suddenly be embracing 'mould as ME' - this recently published memoir - which I can see is garnering great reviews - the exploration of a personal, spiritual journey seems important too - will come and go, as all books do. And it is *one* person's experience. And why on earth would I heed that experience more than my own? While I am sure the book will resonate hugely for those who have had severe mould/environmental illness, it feels wholly irrelevant to my experience as far as the mould element goes. And I see no science anywhere jumping out to tell me that the reason I reacted abnormally to an enterovirus in 1982 is because of mould.

Dr Klimas - who I know Julie consulted - herself says that we must start with tight entry point criteria to get anywhere, we can't put everyone in the same pot. With that I very much agree.

 

[nasim marie jafry]

I am not saying if someone improves with mould avoidance they can't have ME. I am saying that ME cannot be treated with mould avoidance. So any improvement is not down to treating to ME but, possibly, a co-morbid mould intolerance.

Again, I am not saying that MI can trigger ME (I don't know whether it can or not), but if someone has MI-triggered ME, then that ME will still not be treated by mould avoidance, because ME is a discrete illness not treated by mould avoidance.

I agree it is good to avoid any nastiness, but ME cannot be broadened to include any illness with similar symptoms, whether due to mould or to psychological factors.

As with Nasim, my illness is entirely viral.

I feel I am banging my head against a wall, here, John, still I hope my comments have added to the debate.

 

[JohntheJack]

That's a possibility: ME/CFS and biotoxin illness / CIRS might share some, or even all, of the same pathophysiological mechanisms and pathways, so they could be pathophysiologically the same or similar diseases, but just with different triggering causes.

But from the diagnosis and treatment point of view, it makes very good sense to differentiate ME/CFS and biotoxin induced illness, because if you don't, you run the risk being labelled with ME/CFS, and then like Ryan wasting 10 years of your life, when the correct treatment for biotoxin illness may fix you in a matter of months.

It's always bad when someone with a treatable illness gets misdiagnosed with ME/CFS.

I think that's a really good point: bad for people with currently treatable MI to be told they have ME, which currently is not.

It benefits no one to conflate different illnesses.

 

[nasim marie jafry]

There is also I think more attachment to the mould hypothesis of ME in the USA than UK currently, although I could be wrong about that. Happy to be corrected.