ME is not mould intolerance; mould intolerance is not ME

[Hip]

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.

I suspect that environmental exposure to toxic mold may be more common in the US, compared to the UK and Europe.

In the US, many homes are constructed from wood, which being a cellulose material, is idea for mold growth, especially after water damage. Whereas in Europe and the UK, I think most homes are brick built, with wood only being used for the windows, floors and roof. So this may be one factor behind why mold seems more of an issue in the US.

Also, I believe many US homes have air conditioning ducts circulating air (which can be subject to mold growth), whereas I have never seen a UK home with such air ducts.



But Dr Shoemaker does not consider CIRS to be the same as ME/CFS, and I think he is the leading mold researcher and clinician. So there is no conflation of CIRS and ME/CFS as far as he is concerned.

 

[Jesse2233]

This stuff is so hard to tease out

My onset came immediately after a likely Coxsackie B4 infection, but I'd also been sleeping in a room with prior mold issues for a year

 

[Snowdrop]

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.

I suspect that if the UK had a desert climate to move to as the US does then you'd get more people with mould illness submitting their symptoms under ME. As mould is pretty ubiquitous in the UK there is no cure for mould (nowhere to get away to domestically) therefore it gets 'lumped' as ME maybe.

I think I would like someone with a science background to explain to me how 'lumping' and 'splitting' works with regard to illness categories. I guess I come out as a splitter -- if someone is greatly improved by mould avoidance and I'm not then we don't have the same illness. But I lack any real knowledge on the subject.

 

[Hip]

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.

Did you not see Dr Joseph Brewer's 2013 paper, which found that 93% of ME/CFS patients tested positive for at least one mycotoxin, whereas none of the healthy controls tested positive.

That does not mean mold has to be answer in your particular case of course. At this present time, we don't have enough evidence to say whether mold might play a role in the triggering of ME/CFS in some cases, nor enough evidence to rule out that possibility.


I found it very interesting that Dr John Chia discovered that patients who catch enterovirus infections and are inadvertently given corticosteroids are at a higher risk of developing ME/CFS from the virus. Dr Chia says he sees hundreds of ME/CFS patients whose illness seems to be cause by a combination of enterovirus + corticosteroids. Corticosteroids of course are well-known immune suppressors.

So this shows that the immunological circumstances at the time of catching a virus can play a role in whether that virus triggers ME/CFS or not. And mold exposure can have immunological effects.


In the UK, there was an interest in pesticide exposure links to triggering ME/CFS.

 

[halcyon]

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.

The term ME is specifically meant to describe a persistent post-viral CNS disease with muscle involvement. Many diseases involve inflammation of the CNS, such as MS, ADEM, etc. ME and ADEM even present very similarly, but that doesn't mean they're the same disease.

The direction that research is taking now, with Davis and Naviaux, seems to be generic to all fatiguing illness. They're saying it doesn't matter what triggered your fatiguing illness, whether it be a virus, mold, or acute psychosocial stress, the end result is the same metabolic disease and you just need to flip the switch with suramin or some other drug and you'll be cured. I really doubt this approach is going to pan out.

As you mention, I think strict ME research should stick to sudden post-viral onset and stay as far upstream as possible. Similarly, I think research into mold related illness should proceed under the guise of CIRS-WDB and not overlap with ME research much if at all.

 

[halcyon]

I suspect that if the UK had a desert climate to move to as the US does then you'd get more people with mould illness submitting their symptoms under ME. As mould is pretty ubiquitous in the UK there is no cure for mould (nowhere to get away to domestically) therefore it gets 'lumped' as ME maybe.

The desert isn't a place to escape from mold.

 

[Jesse2233]

The direction that research is taking now, with Davis and Naviaux, seems to be generic to all fatiguing illness. They're saying it doesn't matter what triggered your fatiguing illness, whether it be a virus, mold, or acute psychosocial stress, the end result is the same metabolic disease and you just need to flip the switch with suramin or some other drug and you'll be cured. I really doubt this approach is going to pan out.

Do you think the initial viral trigger plays an ongoing role or that the type of damage it does, resulting pathology, and therefore potential treatment is specific to that virus?

 

[Esther12]

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 don't think that we have a good enough understanding of what 'ME' is to be able to be certain that, for some people, it cannot be treated by mould avoidance. I'm uncomfortable with the way some can make unfounded claims about the value of mould avoidance (to be fair to Rehmeyer she does often emphasise the lack of evidence and the fact that little can be drawn from her personal experience), but we also can't be certain that it isn't of some value for treating some people's ME.

My health problems started with a viral infection, but also... I'm sure being stuck in a damp property isn't too great for my health!

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.

We are lacking in a clear and objective way of defining ME, or saying with certainty who has it and who does not. That's a trouble, but that's the way it is. Generally, I'm not sure how much knowledge about ME can be gained from any individual's story. Has anyone told you that you should heed Julie's experience over your own? You're different people in different situations, maybe there are things that you can share and learn from each other, but it would be ridiculous to say that either one of you should try to conform to the experiences of the other.

The shared experience I most commonly relate to with other patients is the quackery and harm resulting from the misleading claims made about the value of CBT/GET. I've not read Julie's book, but her work on PACE has so far been really good, and I value that.

 

[halcyon]

Do you think the initial viral trigger plays an ongoing role or that the type of damage it does, resulting pathology, and therefore potential treatment is specific to that virus?

Yes, and I should clarify. Davis seems to think the trigger is gone in ME, Naviaux acknowledges that the trigger must first be removed, if present.

 

[aaron_c]

Davis seems to think the trigger is gone in ME

That's quite interesting because I think I read that Shoemaker is of the opinion that, at least for people with some HLA antigens, the trigger can also be gone while CIRS remains. Maybe this was only for people with the multi-susceptible haplotype? I think this was also the haplotype he linked with ME/CFS. Sorry that I'm being so vague, I think this is from Neil Nathan's book, and I'm not sure where.

Point being that if both viral-instigated and biotoxin-instigated ME/CFS (or whatever we call them) can self-perpetuate after the initial aggravation is gone then maybe they are the same disease.

As others have already said, there is so little we know. I agree that ideally we should differentiate CIRS patients from viral-onset ME/CFS patients...but I don't think we know how to do that, mostly because there is no yes/no lab test for CIRS or ME/CFS.

 

[MEMum]

Just for info @Stukindawski, or anyone else; diabetes refers to producing lots of urine.
For diabetes insipidus, "weak urine", this is due to inadequate production of ADH/vasopressin, - (hormone).
For diabetes mellitus, "sweet urine", the body is trying to get rid of high concentrations of glucose in the blood.
So yes, same symptom for different physiological reasons.
Same with Diabetes, Types 1 and 2. Same problem, high blood glucose. Type 1, autoimmune disease, insulin producing cells have been killed off. Type 2, insulin produced, but not working effectively,

 

[Valentijn]

Whereas in Europe and the UK, I think most homes are brick built, with wood only being used for the windows, floors and roof.

In the Netherlands they're built of concrete, though usually faced with brick on the outside. There's often no wood in the basic construction, beyond a wood frame which might be used for pouring concrete, and is removed after it sets. Only our stairs are constructed from wood. There's also a strip of wood on the wall in the stairwell, presumably to make the transition between the floors look nice and cover any gap or rough edges there.

Basically wood is mostly used in modern times for superficial finishes, and rarely buried where it can't be seen.

That's quite interesting because I think I read that Shoemaker is of the opinion that, at least for people with some HLA antigens, the trigger can also be gone while CIRS remains. Maybe this was only for people with the multi-susceptible haplotype? I think this was also the haplotype he linked with ME/CFS.

Shoemaker's haplotype research is completely meaningless. He compared the HLA types of his local patients to international rates. That is quite inappropriate due to the wide variation in HLA type based on ethnic origins.

The HLA types he found in his patients were simply a normal representation of North American HLA types. Accordingly, based on his claims nearly all North Americans (around 90%) would be extra susceptible to different diseases.

 

[nasim marie jafry]

I don't think that we have a good enough understanding of what 'ME' is to be able to be certain that, for some people, it cannot be treated by mould avoidance. I'm uncomfortable with the way some can make unfounded claims about the value of mould avoidance (to be fair to Rehmeyer she does often emphasise the lack of evidence and the fact that little can be drawn from her personal experience), but we also can't be certain that it isn't of some value for treating some people's ME.

My health problems started with a viral infection, but also... I'm sure being stuck in a damp property isn't too great for my health!



We are lacking in a clear and objective way of defining ME, or saying with certainty who has it and who does not. That's a trouble, but that's the way it is. Generally, I'm not sure how much knowledge about ME can be gained from any individual's story. Has anyone told you that you should heed Julie's experience over your own? You're different people in different situations, maybe there are things that you can share and learn from each other, but it would be ridiculous to say that either one of you should try to conform to the experiences of the other.

The shared experience I most commonly relate to with other patients is the quackery and harm resulting from the misleading claims made about the value of CBT/GET. I've not read Julie's book, but her work on PACE has so far been really good, and I value that.

Hello, Esther12, You brought Julie's book and the coverage of that book into the mould conversation - that is why I mentioned it at all. I too have been a little concerned by headlines in USA. In UK we have endured 'Got ME, get out and exercise' for years - and if we were to start seeing 'ME and cured by Mould' headlines, that would be equally disappointing/misleading/harmful, IMO. There is absolutely nothing proven to link mould with ME. Yes, I respect Julie's work on PACE hugely, and say so often, but that doesn't mean I have to be convinced that her illness is ME. She has in her book expressed an urgency for research into mould and 'ME/CFS' - I don't agree with that specific urgency, when there has been such paucity of research into what I experience as ME, ie clearly virally triggered: RamsayME.

I should add for clarification that I very much welcome new writing on ME, fiction and non-fiction (my own book is almost a decade old) - we greatly need fresh, new works! I have read interviews and articles and extracts of Julie's book, but not the whole book, but I have a strong sense of the direction it takes. I do not think it likely we have the same illness.

 

[arewenearlythereyet]

I think there is quite a lot of speculation here. ME/CFS being post viral for one. I'm not sure that's been proven that this applies for everyone. In fact I belive 50% of people have gradual onset ....there is no doubt that viruses play a role as a trigger, but then to make the leap that they have a continuing effect is not proven. In fact what appears equally likely is that a dysfunctional immune system may be at play as a secondary symptom, making some folks susceptible to infection and overly sensitive to everyday things. Why mould might not be one of them or even a trigger that leads to a biochemical block is equally likely as a virus given the little we know.

Toxins are different to an allergic response to spores as I understand it so again conflating mould to toxins is another leap. One could equally be feeling drained by low level allergic response draining energy that can't be replenished.

I see a lot of people equating illness cause to some sort of attacking agent (toxin, virus, pathogens). This is persuasive since it often feels like you are under attack like the flu... Others say they feel like they are poisoned. I think this feeling is driving some to make leaps of logic in the debate on cause.

Personally I think the cause is clearly multifaceted since there wouldn't be so much debate from people's varying experience. On that basis I have an open mind about mould exposure.

 

[JohntheJack]

I don't think that we have a good enough understanding of what 'ME' is to be able to be certain that, for some people, it cannot be treated by mould avoidance. I'm uncomfortable with the way some can make unfounded claims about the value of mould avoidance (to be fair to Rehmeyer she does often emphasise the lack of evidence and the fact that little can be drawn from her personal experience), but we also can't be certain that it isn't of some value for treating some people's ME.

My health problems started with a viral infection, but also... I'm sure being stuck in a damp property isn't too great for my health!

We do. We know that mould doesn't make a blind bit of difference to millions of patients with ME.

The question is whether if someone's symptoms are similar to those of ME, and they treat those symptoms by avoiding exposure to mould, whether that person's illness is/was ME. And there is absolutely no reason to say that it is. Mould intolerance is mould intolerance.

If ME is broadened to mean any not-very-well-understood illness with similar symptoms, then why not call it Chronic Fatigue and include psychological illnesses. Psychological illnesses are real.

ME is ME. It is a discrete illness. It cannot be treated by CBT or GET or mould avoidance. To conflate ME with MI or CF benefits no one and causes only harm.

(And on a personal level, I really don't understand why anyone with MI would want to claim they have ME.)

 

[JohntheJack]

I suspect that environmental exposure to toxic mold may be more common in the US, compared to the UK and Europe.

In the US, many homes are constructed from wood, which being a cellulose material, is idea for mold growth, especially after water damage. Whereas in Europe and the UK, I think most homes are brick built, with wood only being used for the windows, floors and roof. So this may be one factor behind why mold seems more of an issue in the US.

Also, I believe many US homes have air conditioning ducts circulating air (which can be subject to mold growth), whereas I have never seen a UK home with such air ducts.



But Dr Shoemaker does not consider CIRS to be the same as ME/CFS, and I think he is the leading mold researcher and clinician. So there is no conflation of CIRS and ME/CFS as far as he is concerned.

Mould is rife in parts of the UK, including this district of Swansea where I am currently living: an air trap beneath the hill, quite tightly packed terraced houses from the 19th century, many with extensions for kitchen and bathroom, mild, damp climate. Mould is everywhere.

 

[Stukindawski]

I think there is quite a lot of speculation here. ME/CFS being post viral for one. I'm not sure that's been proven that this applies for everyone. In fact I belive 50% of people have gradual onset ....there is no doubt that viruses play a role as a trigger, but then to make the leap that they have a continuing effect is not proven. In fact what appears equally likely is that a dysfunctional immune system may be at play as a secondary symptom, making some folks susceptible to infection and overly sensitive to everyday things. Why mould might not be one of them or even a trigger that leads to a biochemical block is equally likely as a virus given the little we know.

Toxins are different to an allergic response to spores as I understand it so again conflating mould to toxins is another leap. One could equally be feeling drained by low level allergic response draining energy that can't be replenished.

I see a lot of people equating illness cause to some sort of attacking agent (toxin, virus, pathogens). This is persuasive since it often feels like you are under attack like the flu... Others say they feel like they are poisoned. I think this feeling is driving some to make leaps of logic in the debate on cause.

Personally I think the cause is clearly multifaceted since there wouldn't be so much debate from people's varying experience. On that basis I have an open mind about mould exposure.

(Note: I'm basically using this thread to learn myself, so any arguments I form aren't sacred to me)

It has been argued is that ME is a postviral condition since the term was used for a specific, postviral condition, for decades prior to the invention of CFS.

Various CFS criteria have been used to 'classify' common symptoms among patients in recent years, creating a patchwork (often referred in research as 'heterogeneous') patient group, where the cause and nature of those symptoms has the potential to be much more diverse.

In most cases, ME isn't formally diagnosed as it has been clinically dumped into the CFS pile.

ME tends to get preferred over CFS because CFS is such an insulting name for the profound disablement patients endure.

But if you have CFS as the direct result of a mould allergy, then ME technically is no longer part of your diagnosis. In this case really, we need new names for various presentations.

It's all pretty complicated to be honest, which presents a challenge for advocacy as toes get inadvertently stepped on.

 

[Mij]

Personally I think the cause is clearly multifaceted since there wouldn't be so much debate from people's varying experience. On that basis I have an open mind about mould exposure

Taken from Dr.Byron Hyde definition of ME:

Non-Infectious M.E. Type Disease: non infectious M.E.-type disease. Similar M.E. phenomena can occur due to diffuse CNS injuries from toxic chemical injury. I have seen this in police officers who have fallen into toxic chemical ponds in pursuit of those suspected of criminal activity. I have seen it in farmers repeatedly exposed to pesticides and herbicides, in hospital and industrial workers and in military personnel in contact with toxic chemicals, specifically toxic gases. I will discuss these at a later date as Secondary M.E. They do have one thing in common, and that is they also have a diffuse CNS injury as noted on brain SPECT scans. The diagnosis is made by history, as the actual cases are very difficult to diagnose due to the inability to assess brain levels of toxins in a live patient. Often these Secondary M.E. diseases are more severe than the infectious M.E. cases

 

[nasim marie jafry]

(Note: I'm basically using this thread to learn myself, so any arguments I form aren't sacred to me)

It has been argued is that ME is a postviral condition since the term was used for a specific, postviral condition, for decades prior to the invention of CFS.

Various CFS criteria have been used to 'classify' common symptoms among patients in recent years, creating a patchwork (often referred in research as 'heterogeneous') patient group, where the cause and nature of those symptoms has the potential to be much more diverse.

In most cases, ME isn't formally diagnosed as it has been clinically dumped into the CFS pile.

ME tends to get preferred over CFS because CFS is such an insulting name for the profound disablement patients endure.

But if you have CFS as the direct result of a mould allergy, then ME technically is no longer part of your diagnosis. In this case really, we need new names for various presentations.

It's all pretty complicated to be honest, which presents a challenge for advocacy as toes get inadvertently stepped on.

Hi, Stukindawski, As I said before my frame of reference is RamsayME, but not sure that there is really much awareness of his work in USA - where the current mould theory of CFS seems more prevalent - or how many have read his book, it is described here if you are interested: my neurologist wrote the preface (and I was dxd w ME 1984 after abnormal muscle biopsy and EMG and immune profiling, post Coxsackie):

http://www.meassociation.org.uk/201...port-heres-where-we-came-in-20-february-2015/

I also don't know where you are in world...

Yes, ME was hijacked by psychiatry in late 80s/early 90s in UK and criteria were diluted and broadened, CFS was used instead for any unexplained fatigue, you will no doubt have heard of the infamous Oxford Criteria. This has caused massive confusion all over, and in USA CFS is also used to describe actual ME, though I understand that the name ME is now being reclaimed in USA.

It is an unholy mess.

But I am 100% sure my illness has zero to do with mould.

If I have been ill since 1984 because of mould then I am screwed - there is no desert in UK I can go camping to.

 

[JohntheJack]

Taken from Dr.Byron Hyde definition of ME:

Non-Infectious M.E. Type Disease: non infectious M.E.-type disease. Similar M.E. phenomena can occur due to diffuse CNS injuries from toxic chemical injury. I have seen this in police officers who have fallen into toxic chemical ponds in pursuit of those suspected of criminal activity. I have seen it in farmers repeatedly exposed to pesticides and herbicides, in hospital and industrial workers and in military personnel in contact with toxic chemicals, specifically toxic gases. I will discuss these at a later date as Secondary M.E. They do have one thing in common, and that is they also have a diffuse CNS injury as noted on brain SPECT scans. The diagnosis is made by history, as the actual cases are very difficult to diagnose due to the inability to assess brain levels of toxins in a live patient. Often these Secondary M.E. diseases are more severe than the infectious M.E. cases

Maybe. But if there is CNS injury from mould exposure, then after mould avoidance that injury would persist. The injury is the ME, not the intolerance of mould. Avoidance of mould would presumably lead to some improvement but the illness would continue. The avoidance of mould would not treat the CNS injury deemed ME.

If exposure to pesticides causes a CNS injury, then of course it is necessary to avoid the pesticides, and once exposure has ended the body would have a better chance to recover. But pesticide avoidance in itself would not amount to treating the CNS injury.