TH2 Immune System Dominance and Heterogeneity in ME/CFS

[Marco]

Apologies. This isn't news just some musings of my own and I didn't know where else to post it.

I've not been following ME/CFS research for many years. The XMRV thing brought me back in and I've been trying to get up to speed. One of the PR library papers (Broderick et al) got me doing a little reading on the TH1/TH2 immune imbalance theory which also got me doing a little thinking.

This is a beautiful paper. If anyone is interested in science for the sake of it this is a peach.

http://www.forums.aboutmecfs.org/showthread.php?4812-Broderick-2010-A-Formal-Analysis-of-Cytokine-Networks-in-CFS


I won't even try to explain the basic theory. Others are well versed, in fact its probably old hat to most people. For people like me, this provides a good accessible overview and critique of the limitations of the theory (can't unfortunately vouch for its accuracy) :

http://docs.google.com/viewer?a=v&q=cache:jE2nP3U1F6gJ:www.adltests.com/assets/files/pdf/Cytokines_Th1_Th2_Kidd.pdf+low+TH1+high+TH2&hl=en&gl=uk&pid=bl&srcid=ADGEESjglKiokexKb0qfb95NbDGM5EHSFmwnPGkq7_Jmetv_dPl7TGcXnw0IBPmnD83fzcMNMz_narNeWq9msAQTFQ1Yu1P1nZ34LMU0pRUlpQMrHPrOxO6c-45uhGKIP-_Z92X8eFih&sig=AHIEtbTOnIk8Qo3930pJJDJFMf-UcdcTCA


Anyway, we are all too painfully aware that ME/CFS is dogged by the issue of heterogeneity. On one hand there's the 'stating the bleedin' obvious' heterogeneity resulting from loose diagnostic criteria that allow anyone who is frequently tired to be labelled as CFS.

More substantively, we are all aware that those with 'true' ME/CFS often differ in many ways. Some have sudden onset, some gradual. Some can point to a viral onset, some not. Some cite vaccinations, heavy metals, organophosphates, (the gulf war?) as precipitating factors and some point to overexercise, diet, or stress. While viruses (and retroviruses) have long been proposed as pathogens, none to date have been found in all those diagnosed with ME/CFS. While XMRV may turn out to be the key, PWCs have already been tested negative and it is possible that many of those diagnosed with ME/CFS will be found not to have an active XMRV infection. Some people reportedly make a quick spontaneous recovery while others become chronically ill for many years and fluctuations/relapses are common. Some report that fatigue, the central and sometimes only symptom considered important in CFS, was not a factor in at least a stage of their illness. Finally, regardless of how we view 'therapies' such as CBT/GET or the Gupta Programme, they are reported to be of some help to some people (bear with me of the last point).

I would like to propose that ME/CFS, in ALL CASES, is caused by a dysregulation of the immune system leading to TH2 dominance. For want of a better title I'll call it Type 2 Immune Dysfunction Syndrome (syndrome to distinguish it from other specific illnesses caused by TH2 dominance).

Taking this approach I believe avoids the 'problem' of searching for a single etiology, improves diagnosis and clarifies the treatment options.

 

[Marco]

I said I wouldn't try to explain the theory but it helps to briefly set out my limited understanding and what I think it might imply. For those of you au fait with this stuff, my apologies. This is simplistic because (a) this is all I can remember and (b) others can explain it better and more fully. There is much more subtlety and upstream/downstream mechanisms than I've presented, but bear with me :

The human immune system is broadly hypothesised as comprising two arms that are activated as appropriate when confronted with specific pathogens. T helper 1 cells (TH1) lead the attack against intracellular pathogens such as viruses, bacteria and fight cancer cells. T helper 2 (TH2) cells protect against extracellular pathogens such as parasites and toxins.

TH0 the native unassigned immune cells stand ready to react to whatever pathogens are identified. Cytokines are the chemical messengers that send the appropriate signal for the production, from TH0 cells, of TH1 or TH2 cells depending on the pathogen identified. The cytokine IL12 signals that a TH1 response is required and IL10 signals that TH2 is required. When one system is up regulated the other tends to be down regulated.

Over-regulation or dominance of the TH1 arm can produce :

Organ specific autoimmune diseases such as rheumatoid arthritis, MS, type 1 diabetes, Crohn's, Graves Disease etc;

While over-regulation or dominance of the TH2 arm can produce :

Allergies and IgE-based disease, systemic autoimmune diseases including asthma and lupus.

Many with ME/CFS develop a wide range of new allergies/sensitivities which might suggest an over active TH2 arm of the immune system. Additionally PWCs appear to be more prone to cancer, have a high viral load and low Natural Killer (NK) cell toxicity suggesting a complementary down regulation of the TH1 immune arm.

In addition, to the allergic/inflammatory symptoms associated with TH2 dominance, de Meirleir and others have suggested that many other of the ME/CFS symptoms are caused by a resulting channelopathy (see below).

Most viruses appear to have the ability to chemically mimic IL10 causing an inappropriate up regulation of the TH2 arm and suppression of the TH1 arm. The TH2 weapons (white cells and antibodies) are produced and TH1 weapons including NK cells are suppressed. With the TH1 arm suppressed previous infections can resurface and new opportunistic infections acquired.

With the TH1 arm ineffective, the immune system increases production of the anti-viral enzyme RNaseL which can't kill the virus but stops replication. In ME/CFS however the RNaseL produced is a low molecular weight type which is unable to kill infected cells and in fact causes damage to healthy cells. RNaseL fragments, according to de Meirleir, interfere with the functioning of ion channels (channelopathy) causing a range of symptoms. Continued RNaseL production, to provide some sort of anti-viral activity, no matter how ineffective, requires human growth hormone and over time the HGH supply becomes exhausted.

Low HGH levels have been associated with : Low energy, decreased lean muscle mass, increased abdominal fat, decreased strength and exercise tolerance, feelings or anxiety sadness and social avoidance, dry thin skin, sleep disturbances, decline in bone density, raised cholesterol, low blood sugar, irritability, night sweats etc.


So an imbalance of the immune system where the TH2 arm is dominant will quickly produce allergic symptoms and new sensitivities (to foods, chemicals, toxins etc) but may also produce a range of other symptoms due to channelopathy.

TH2 dominance also suppresses the TH1 arm leaving a compromised defence against new opportunistic virus infections, cancer etc. I have not discussed the possible symptoms of any viral infections as they are likely to be many and varied depending on the pathogen.

Over time, (maybe not that much time depending on the original levels of HGH) the need to replace (defective) RnaseL depletes the body of HGH leading to a range of familiar symptoms.


ASSUMING TH2 dominance holds true generally, how does this help?

 

[Marco]

Heterogeneity, diagnosis and treatment

TH2 dominance conditions have been shown to be caused by viruses, surgery, blood transfusion, pregnancy, emotional stress, athletic stress, academic stress, malnutrition, heavy metals, organophosphates, vaccinations etc. All frequently suggested triggers for ME/CFS.

There is no need to identify a single causal agent/factor in all cases to explain the onset of ME/CFS. ME/CFS is clearly identified as a disease of immune dysfunction. The only role for psychological or psychiatric treatments are if needed as an adjunct to treating the immune dysfunction. It also avoids the problem, if XMRV is found to be a major player, of those testing negative who would otherwise be relegated to Reevesville.

I would suggest that the investigation of all suspected cases of ME/CFS should include :

• A full medical history to narrow down potential triggers and perpetuating factors;
  
• Tests to indicate a TH2 dominant immune state;
  
• Tests to indicate total viral load.
  
• HGH status.

If the results suggest :

(a) Not TH2 dominant and no evidence of virus you do not have ME/CFS perhaps a course of antidepressants might help (in case anyone is offended by this I had severe clinical depression for a number of years and much prefer having ME/CFS in many ways thank you very much so I'm not disparaging the condition or afraid of the stigma!);

(b) High viral load but not TH2 dominant. By definition you do not have ME/CFS. Your immune system is reacting appropriately to a previously undiagnosed viral infection that should be treated appropriately. HGH supplementation has been shown to enhance the effects of HAART and may enhance the effects of any anti-viral where HGH is shown to be low.

(c) Low/no viral load but TH2 dominant. Likely to apply in cases with gradual onset, early cases and those with non-viral triggers. Therapy might consist of a period of recuperation (if still working or otherwise active), immune support (immune modulators), proper nutrition. HGH supplementation may be useful where levels are low. Light exercise (aimed at enhancing immune function) may be helpful if tolerated and psychological therapies may be appropriate as an adjunct where psychological issues are implicated in stressing the immune system. NOTE : There is no place for CBT or GET in this model. It is a disease of immune dysfunction. There are no illness beliefs to challenge and only exercise that doesn't further stress the immune system should be undertaken.

(d)High viral load and TH2 dominant. Likely to apply in many cases with a clear viral onset and in many long standing cases where immune dysfunction has allowed for many opportunistic infections. Therapies should include those mentioned in (c) above but excluding exercise until status improves. In addition a general antiviral should be used initially to reduce the overall viral load pending further investigation of specific pathogens. Tests may not be available for all potential pathogens, but reducing the overall viral load and rebalancing the immune system should provide some relief. HGH supplementation is again recommended where levels are found to be low.

 

[Marco]

I appreciate that, as set out, this is all very simplistic, but I feel that it represents a much more satisfactory paradigm than the current search for the 'magic bullet' and discussion of sub-sets and heterogeneity. All those with ME/CFS have an immune dysfunction. They only differ on the trigger and duration of illness. The Broderick et al paper, which states that the difference between the structure of cytokine expression in the CFS/ME group compared to the control group is ten times the magnitude of the variability within the groups certainly suggests that there may be a unique pattern of immune dysregulation.

What role for XMRV?

XMRV may turn out to be a causal factor in many cases of ME/CFS, may be another opportunistic infection or it may either be THE virus (and detection just needs to be improved) or THE factor which predisposes us to develop ME/CFS when presented with another triggering event. Certainly an explanation is needed as to why some people develop TH2 dominance and others don't when faced with vaccinations, viruses or other triggering events.

As for CBT/GET and the Gupta Programme and similar. Perhaps they have some benefit for those diagnosed as CFS but who are either no viral load and not TH2 dominant (i.e. they don't have ME:CFS) or those with no viral load but who are TH2 dominant (non viral onset) but at an early stage of illness and have neither acquired opportunistic infections nor HGH depletion. Both 'therapies' might help rebalance the immune system to some extent (or in the case of GET might exacerbate the problem) but neither will treat active virus infections.


CASE STUDY

Well what about me?

Although circumstances might suggest contact with an enterovirus, I have never been tested for viruses and have no evidence of any present or past viral infection.

Onset was sudden (full health to poor health) but not all of the symptoms were there at the start. My state of health has undergone three distinct step changes downwards over the course of coming up to 25 years.

I had developed GI problems and anxiety/depression and then collapsed while training. Since then I haven't been able to tolerate any aerobic exercise.

I then developed dizziness on standing, extreme sensitivity to cold, a wide range of food and chemical intolerances, joint and muscle pains, headaches etc but fatigue as such was not a major issue and I was able to even combine full time working and part time study so no cognitive issues.

Prior to the onset of illness though I was probably overactive physically, undernourished and under some personal and academic stress.

To fit it into my suggested schema; I was probably pushed to a TH2 dominant immune response but with no or a low viral load. TH2 dominance would explain the IBS, new intolerances and possible joint and muscle pains. PEM etc I don't know possibly de Meirleir's channelopathy.

Next step change I suddenly developed a whole raft of new symptoms in addition to those existing. These included rapid unexplained weight gain (abdominally for the first time) loss of strength and muscle tone, rapid greying of hair and apparent ageing, insomnia, anxiety, exacerbated fatigue, profuse sweating, dry skin etc. Strangely enough I have never again experienced real depression since this date. All very suggestive of exhausted HGH. Again circumstances might suggest another enterovirus effect (or vaccine?) as both step changes followed shortly after holidays abroad.

Finally, after seven years I had to leave work (for the afternoon I thought) and never went back. To the existing symptoms I added extreme fatigue (needing to sleep during the day) and severe cognitive problems. For the first number of months I couldn't walk, think, read or drive and still can't when I have a frequent bad spell.

I can't identify any specific triggers for the last step change. Perhaps this last stage was viral or perhaps I carried on too long with no relief? Perhaps the last stage was me developing full blown ME and not just part of it?

Any thoughts/criticisms would be much appreciated.

 

[slayadragon]

I really want to discuss this. It seems really important, and I've yet to figure out exactly how it fits in with the rest of how I personally am looking at this illness right now.

First, Th2 is supposed to "protect against extracellular pathogens and toxins."

Does this pertain to all toxins? Or just some of them?

In what way does Th2 protect us against those toxins? What are the immune system components that do this work?

Thanks, Lisa

 

[Countrygirl]

(b) High viral load but not TH2 dominant. By definition you do not have ME/CFS.

Marco, Thank you for your excellent posts and I'm so glad that you have brought up this topic because it has been exercising my grey cell all this afternoon. I also understood that our immune system was Th2 dominant. However, I am really puzzling over a statement I heard Dr Judy Mikovits make at the 2009 IiME conference, which I have just heard on a DVD this afternoon. In her lecture, she says that it is always claimed that people with M.E. are TH2 dominant, but, she says, in those she has studied (and she would have been referring, I guess, to those in the Science study at that time). Dr Judy found that this is not true. Sadly, she does not elaborate her statement.

I am really puzzled by her finding. Can anyone comment on this please?

Thanks again Marco.

Warmest regards,

C.G.

 

[Marco]

C.G.

I can't comment on what Dr Mikovits said but everything Nancy Klimas has said about XMRV describes immune dysregulation and suppression (or at least ineffectiveness) of the TH1 side?

 

[Marco]

Slayadragon

I'd need to dig around to get a concise description of the TH2 components that 'protect us from toxins'.

In the meantime, I think the key point is that when the TH2 arm becomes overactivated, the immune system has a constant message that there is a toxin out there and actively searches out anything that is "not-self" or even in some cases starts attacking our own cells.

Things that were previously tolerated are now treated as toxic (e.g. food in the stomach and bowel is morphologically speaking 'outside the body' but if large food molecules escape into the body through a leaky gut they are toxic). I believe that this is how we develop new sensitivities/intolerances to common foods, chemicals, dental amalgam etc. We have previously been exposed to them and tolerated these substances, but the overactive TH2 arm is driven to identify the toxin it 'believes' is there and starts to identify previously innocuous substances as toxins.

 

[dannybex]

Marco, Thank you for your excellent posts and I'm so glad that you have brought up this topic because it has been exercising my grey cell all this afternoon. I also understood that our immune system was Th2 dominant. However, I am really puzzling over a statement I heard Dr Judy Mikovits make at the 2009 IiME conference, which I have just heard on a DVD this afternoon. In her lecture, she says that it is always claimed that people with M.E. are TH2 dominant, but, she says, in those she has studied (and she would have been referring, I guess, to those in the Science study at that time). Dr Judy found that this is not true. Sadly, she does not elaborate her statement.

I am really puzzled by her finding. Can anyone comment on this please?

Thanks again Marco.

Warmest regards,

C.G.

Hi CG,

I too am glad that Marco has brought this up -- very important, and very well studied over the years, but almost forgotten during the last year or so, and especially since the XMRV news. This is why some called it CFIDS, for Chronic Fatigue Immune Dysfunction Syndrome for a few years (they could leave out the "F-word" if you ask me, and it wouldn't be so bad.)

I don't know why she said it's TH2 dominant, but it's important to remember that Dr. Mikovits' expertise is retroviruses, not ME/CFS. Here's a quote from the doctor herself from earlier this year (Jan 22):

"Question: A lot of patients say they had a flu, a weird flu-like condition, a week or two before they got CFS. What you’re saying is that flu-like illness is a bug that came along and allowed the XMRV to create CFS?

Dr. Mikovits: Well, no. I know almost nothing about CFS, but what we think is happening is - remember the slide where I showed you with those little events? You know, what was the event that was the straw that broke the camel’s back? Where did the balance tip between here you’ve got your immune system working well and the virus and the immune system are co-existing just fine, then some other, that other bug, whether it be Lyme, a flu, anything, gets you."

I bolded "anything", because even though she may have meant some sort of 'bug', I personally believe perhaps that could include mold as Lisa is wondering, or pesticide or other chemical exposures -- things other than viruses, bacterial infections, etc.

I'm waaaaay late for bed, but thanks Marco for starting this thread. (Hey...I'm a poet!) :Retro smile:

d.

 

[guest]

Great post, Marco. I always wondered if there is anything good about a Th2 dominance, now it seems there is (lower incidence of MS, diabetes etc.). Thanks for posting it!

 

[Mark]

Then there are those handful of people with atypical MS and XMRV+ to fit in...

 

[Mark]

"Where did the balance tip between here you’ve got your immune system working well and the virus and the immune system are co-existing just fine, then some other, that other bug, whether it be Lyme, a flu, anything, gets you."

I bolded "anything", because even though she may have meant some sort of 'bug', I personally believe perhaps that could include mold as Lisa is wondering, or pesticide or other chemical exposures -- things other than viruses, bacterial infections, etc.

I'm waaaaay late for bed, but thanks Marco for starting this thread. (Hey...I'm a poet!) :Retro smile:

d.

i agree, d.
ok, marco?

 

[helsbells]

Well what about me?

Onset was sudden (full health to poor health) but not all of the symptoms were there at the start. My state of health has undergone three distinct step changes downwards over the course of coming up to 25 years.

I had developed GI problems and anxiety/depression and then collapsed while training. Since then I haven't been able to tolerate any aerobic exercise.

I then developed dizziness on standing, extreme sensitivity to cold, a wide range of food and chemical intolerances, joint and muscle pains, headaches etc but fatigue as such was not a major issue and I was able to even combine full time working and part time study – so no cognitive issues.

Prior to the onset of illness though I was probably overactive physically, undernourished and under some personal and academic stress.

To fit it into my suggested schema; I was probably pushed to a TH2 dominant immune response but with no or a low viral load. TH2 dominance would explain the IBS, new intolerances and possible joint and muscle pains. PEM etc I don't know – possibly de Meirleir's channelopathy.

Next step change I suddenly developed a whole raft of new symptoms in addition to those existing. These included – rapid unexplained weight gain (abdominally for the first time) loss of strength and muscle tone, rapid greying of hair and apparent ageing, insomnia, anxiety, exacerbated fatigue, profuse sweating, dry skin etc. Strangely enough I have never again experienced real depression since this date. All very suggestive of exhausted HGH. Again circumstances might suggest another enterovirus effect (or vaccine?) as both step changes followed shortly after holidays abroad.

Finally, after seven years I had to leave work (for the afternoon I thought) and never went back. To the existing symptoms I added extreme fatigue (needing to sleep during the day) and severe cognitive problems. For the first number of months I couldn't walk, think, read or drive and still can't when I have a frequent bad spell.

I can't identify any specific triggers for the last step change. Perhaps this last stage was viral or perhaps I carried on too long with no relief? Perhaps the last stage was me developing full blown ME and not just part of it?

B]

I deffinately identify with your three distinct downward slides, this is completely what happened to me, also the first step where I developed massive anxiety literally out of no where and something the DR called malaise , actually I never fully returned to work but over time went back to study as at that a point I had no brain fog. But differ in that virus's, infections, sore throats et al came thick and fast until the point of the first down turn and when I became more or less housebound with brain fog (which I still have no reading, drawing etc or thinking or rememebring) BUT Viruss, colds stopped dead allergies flowered on the other hand. the third phase were I became so intolerant to food it was difficult to eat for a while and developed interstitial cystytis plus loads of other additional diagnosis's so my case history I think would fit in very well with what you are positing. What is HGH by the way - sorry if its obvious - I have said all along my immune system is dysfunctional because altho it rarely happenes I get any colds, virus's etc on the rare occasion I do the day before is the best I ever feel and even during feel better than normal in some ways and can deffinately get away with more foods and meds. MCS is now a massive problem for now too

 

[Marco]

I'm glad people are getting something out of my musings!

Mark - were you asking me a question??

Helsbells. HGH is human growth hormone - very important stuff to stop you feeling like - well what we do actually. Sorry to hear about your food intolerance problems - they sound horrendous. Food intolerances and GI problems/IBS have been my most long standing and consistent problems which is why I wouldn't be surprised if there was an enterovirus issue. I often think, if I could change one symptom, it would be to be able to eat without worrying about the consequences hours and days later. On the other hand I'd also like to be able to think straight for more than an hour at a time!


As I said - TH2 dominance is old news.

But it seems to me that ME/CFS researchers have identified a dysregulated immune system and have posited X,Y or Z virus as the pathogen. They typically test their patients and find A% have the virus an publish on the basis that virus X causes ME/CFS in a subset of patients.

Researcher B tries to replicate the results and finds low of no evidence of virus X and declares that virus X is not the cause of ME/CFS.

Researcher C then proposes that virus Y is the pathogen, or if they are a psych its bedwetting.

Perhaps I'm being unfair but the focus is always on the virus or other trigger. Did researcher A,B or C consider the possibility that the immune dysfunction IS the disease and the specific trigger of lesser importance (if you can call a potentially deadly retrovirus of lesser importance).

I was actually hoping that some scientifically minded bods could chip in and tell me why I'm obviously wrong??

 

[helsbells]

Marco would TH2 dominance explain why I would feel relatively better just prior to getting a bug? I totally know I have immune dysfunction as you say is it chicken or egg? Problem being for me (and please bear in mind my biology/chem understanding was poor even prior to 12 years of virtual altzeimers) I have developed such sensitivity to anything that is chemically active (inc foods vits or seemingly oft times the air, in my case!!) if it was XMRV I don't know if I would survive treatement but equally if I have XMRV and do stem cells would the original problem, left untreated, take me down again (assuming SC therapy worked in the first place. )

 

[Marco]

Hi again Helsbels

I'm afraid I can't answer your questions -I don't have the science background either. I just pick up a basic understanding of things and then start piecing things together.

If is any comfort I don't personally think the sensitivities are particularly dangerous in themselves. Its think its just like the symptoms you get with a flu virus are not due to the virus itself but our immune reaction to it - all to do with neutralising and expelling the bug from the body before it can get inside the cells and multiply.

In the same way I think our reactions to food and chemicals are that our overactive T2 arm identifies them as toxins, produces flu like symptoms and tries to .. er .. expell them as quickly as possible - hence the IBS. The foods and chemicals themselves are usually pretty innocuous.

Please bear in mind I'm just a PWC trying to make sense of all of this :Retro redface:

 

[helsbells]

Trouble is Marco I have had some pretty bad reactions - it isn't like a standard allergy but I have lost consciousness and doxy left me with permanent Interstital cystitis so I am very very wary. Don't worry I appreciate you trying to make sense of this, I know I find some of the science actually pretty difficult to grasp although I am always grateful to the boffins for keeping tabs on things for us. As someone with ASD I like things to be black or white and the more I learn about medicine seems as if it is all a can of worms - you know something written clearly on a page becaming a three dimensional object and understanding that the perspective changes from all angles it is viewed, mind boggling for someone with very moderate brain

 

[Mark]

Whoops looks like I never posted this in the end, must have got sidetracked...

Marco I think the theory you've set out is really good, I think some categorisation very similar to yours is emerging.

I think if we talk about a "2-hit" condition, then we have to consider that multiple hits are possible, and also that people who've had one or the other half might have some but not all of the problems too.

Also that our histories might vary as we progress from 1-hit to 2-hit to 3-hit.

I see a big distinction between people who always catch colds and people who never do (there are two separate threads on that). Also between people sensitive to sunlight, sound etc, and those who are not. I thought the first was TH1 dominance vs TH2 dominance, so I'm wondering where that particular distinction fits in your analysis because I think I'm seeing what look like two quite distinct groups there. I suspect they are your (c) and (d), perhaps?

Marco as a quick guess fwiw, your own personal description sounds to me like, over the course of years, you battled as hard as you could to keep going and your body's strength and inertia kept you going for a while, then just sheer will-power, and then when you could do no more you were forced to stop, then got a massive version of the cold everyone overworked gets as soon as the first day of holiday relaxation starts. I also wonder if changes in environment circumstance, diet could have played a role. The biggest guess - and it is a guess - that I can make is: try different beds, bedding and sleeping arrangements. Experiment to find a way to sleep effectively (ie deeply) rather than for a long time. And different clothes, environmental control, diet etc are all always worth working on. Mold, of course...

btw there is masses on TH1 and TH2 in the archives, way over my head some of it, perhaps you've dug away through that a bit?

Anyway: thanks for a great thread Marco, really excellent stuff. I look forward to the forthcoming analysis.

 

[slayadragon]

"The Straw That Broke the Camel's Back"

Dr. Mikovits: Well, no. I know almost nothing about CFS, but what we think is happening is - remember the slide where I showed you with those little events? You know, what was the event that was the straw that broke the camel’s back? Where did the balance tip between here you’ve got your immune system working well and the virus and the immune system are co-existing just fine, then some other, that other bug, whether it be Lyme, a flu, anything, gets you."

I bolded "anything", because even though she may have meant some sort of 'bug', I personally believe perhaps that could include mold as Lisa is wondering, or pesticide or other chemical exposures -- things other than viruses, bacterial infections, etc.

From my mold-free "view from the rabbit hole," I have some observations that may or may not be relevant to this thread. I don't know enough about immunology to know. I thus am hoping that people here will tell me if any of what I'm thinking makes sense.

This is going to sound maybe like science fiction, but perhaps folks can bear with me to the point of telling me in a "what if" way how this might or might not fit into this theory....if indeed the observations I'm going to report are accurate rather than "mass hysteria."

A number of people practicing Erik's "extreme avoidance" of mold have gotten to the point where we can tell right away if we have been exposed. Unfortunately, the spores and toxins stick to belongings, meaning that avoidance doesn't just mean walking away once we get hit. If we don't wash our clothes and ourselves, and attend to anything that the mold has stuck to, it continues to have an effect on us.

Even more unfortunately, there is one particularly bad kind of mold that causes a variety of especially damaging symptoms. These include heart palpitations/pain, chest pressure, excruciating migraine-like headaches, cognitive dysfunction that goes beyond brain fog (e.g. inability to read or do math, "white-outs" where brain goes blank), burning of skin/throat (sometimes severe burns), emotional responses (panic/anger/depression/suicidal inclinations), organ pain, severe chemical sensitivities, extremely deep skin "dents," seizures, convulsions, extreme sound/light sensitivity, shivering, diarrhea, vomiting, gait problems, and non-specific feelings of agony.

These are symptoms that many CFSers experience in low-grade form or on occasion. Note, however, that they are the "weird" ones that those with particularly severe CFS report. Osler's Web discusses them.

I met the Canadian Criteria, but only occasionally had this group of specific symptoms during my 12-year illness. (I'm from Chicago.)

After I had gotten to a relatively high degree of recovery through mold avoidance, I decided to pay a visit to Lake Tahoe on my own (without Erik's babysitting) to revisit a couple of buildings there. I figured that if I decontaminated (took a shower and changed clothes) afterwards, I would be okay.

The campground that I was at felt terrific for the first two nights. At about midnight on the third night, the barometer dropped. This is when mold of all sorts (toxic and non-toxic) lets loose with its dormant spores, since the possibility that water might follow makes it more likely that the "seeds" will be able to spring up into live mold.

The initial symptoms of the exposure weren't excruciating, so I waited until it was light before packing up my stuff and leaving. This was a mistake.

Over the next few days, my response continued to build to the point that I had all of the "weird" symptoms (above) at a far worse level than I'd ever experienced during my 14 year illness. And it just kept going on and on and on, both because of the big hit itself and then because re-exposure to my stuff brought the symptoms back.

For the first time in my life, I seriously prayed to die. Pain beyond endurance. Pain beyond imagining. And it doesn't seem wholly inconceivable that I actually could have died, based on what I was experiencing.

I made a big effort to clean all my stuff and to get rid of things that couldn't be cleaned or (like bedding) that I was in particular contact with. I came close to getting rid of the car too.

Toxic mold in general is immunosuppressive, and it seemed reasonable (especially in light of many of Erik's comments) that this particularly bad mold would be even more so. I thus decided to take some Famvir. My response to the items that had been contaminated with this mold got even worse for three days, then fell below baseline. That was a surprise!

So I thus managed to keep the car and most of my stuff. After several months, it all died down. (If it had been exposed for more than six hours, presumably it would have taken longer to die down.)

Other treatments (I give credit to Valcyte, continued detox with cholestyramine and neural therapy) helped me to decrease reactivity to toxic mold even further.

I'm now at the point where moderate amounts of "regular bad mold" (like the Stachy mix I had in my own house) don't have much of an effect on me. This "super mold" (or what I sometimes call "Tahoe mold") does still have an effect when I come into contact with it (I now can recognize it very fast!), but I can tolerate small amounts without as much harm.

Only after my own experience did Erik share his own experiences with and observations of this particularly bad mold. Others have reported their own experiences. They are consistent with mine in all respects.

One other thing that Erik told me is that he repeatedly has seen people unexpectedly drop dead of heart attacks when exposed to large amounts of this mold. The heart attacks are always blamed on something else. The fact that his own heart goes wild with palpitations at such moments makes him think that this is not just a coincidence.

This "super mold" is not (at least not yet) distributed evenly in the U.S. For instance, there is quite a large amount of it outside in the Tahoe/Truckee area (and to a lesser extent in Reno), but only in scattered places. Main sources include trees that have been treated with fire retardants, sewers and sewer ponds, and a compost farm. Those of us who are able to immediately identify it have found it outdoors in significant amounts in certain parts of Texas (e.g. Dallas), especially at certain times; in Telluride, Co.; and throughout the Bay Area. (Unfortunately, I don't have any reliable reports yet from most other countries or the eastern half of the U.S.)

Erik encountered it in small amounts in Truckee High School (where he was a student) in the early 1970s, and then in Germany in 1976. He found it in the Bay Area in 1980, and then outdoors in Incline Village immediately prior to the epidemic there in 1984.

It's also present in scattered buildings. This tends to be especially the case in places where it's growing outside (presumably because the spores that the colonies let loose settle on building materials and then spring to life when they get some water), but in other places too.

Erik has encountered this mold growing (e.g. in his trailer) on various occasions and apparently has a sample collection. We believe that it's a particular strain of Stachy, one that is capable of growing in places that have been treated with chemicals and perhaps that uses the chemicals as "food" to create particularly strong toxins.

He says that he's talked in depth about this "super mold" to Judy Mikovits, and that she has introduced him to various researchers at the University of Nevada about studying this mold and discussed the possibility of WPI funding such studies.

I don't believe in hiding information and so have decided to share what I know about this stuff freely.

Just about everything about CFS makes sense to me now. (I'm not saying that I'm RIGHT about everything.....just that it fits into a coherent theory.)

The one thing that's perplexed me is the Th1/Th2 issue. I've yet to find any doctors/researchers who have been able to answer my questions on it, or to figure them out to my own satisfaction. Perhaps folks here will be able to help.

I believe that this mold is so damaging that it has the possibility of killing people who are susceptible to it. It thus would be a functional response of the system to do everything that it thinks it has to in order to protect itself from this mold, short of having the protective measures result in death themselves.

A question is why it would be that certain people are so affected by this mold while others are not affected (or affected only to a relatively lower extent even by large quantities). Here are a few possibilities.

1. Dr. Shoemaker is right and the genes that he believes to be "mold susceptible" or "multi susceptible" prevent us from processing and eliminating this super mold from our systems in an efficient and effective way.

2. Insofar as their "toxic tank" is already full, people may be less able to tolerate this mold.

This is not inconsistent with how Dr. Bill Rea and others have described sensitivities to other toxins working. For instance, people who have had a huge exposure to pesticides tend to have big reactions to new exposures of even tiny amounts.

Those who have spent a lot of time exposed to "regular bad molds" in sick buildings conceivably may be especially susceptible to this particularly bad mold. But those with other toxic exposures (e.g. mercury, pesticides) that they have not been able to effectively eliminate from their systems also may be affected more strongly than the average person.

3. Whatever the pathogen is that "defines" CFS and caused the Tahoe Flu may cause people to be more affected by this mold.

This is consistent with what Erik observed during the epidemic in Incline Village. He reports that he and others showed symptoms to exposures to the "super mold" (even though the other people always blamed it on something else) even before the "flu" went through. After the flu, exposures to it went from having a minor effect in relatively large quantities to a horrific effect in even tiny quantities.

Why it would be that this "funny little flu bug" would cause people to be more susceptible to this mold, I don't know. It seems to me that we're missing a "shield" that's supposed to protect us from it. My initial layman's guess, based on my own experiences with it, is that perhaps it destroys our ability to make a particular enzyme that breaks it down before it gets into the system. It also could be affecting the system's ability to detoxify it, though the effects of it happen so fast (through a few breaths, probably hitting the vanilloid receptors and going right to the brain rather than acting through the bloodstream) that the "protective" mechanism of an enzyme or first level immune system barrier (e.g. macrophages) to keep it out seems more likely to be me to be the problem.

(Note that I'm way out of my league here, in terms of understanding the likely physiology. That's why I need help.)

Something else could be going on to make some of us really affected by this stuff as well.

*

Okay. So here's the question.

If indeed what I'm saying is true (you'll have to give me the benefit of the doubt for the purposes of this discussion), would it be functional for the Th1/Th2 response to be occurring?

It seems to me that if the system got one big hit of this stuff and survived, it might say to itself, "Close call, that stuff is BAD. Let's go on full alert to make sure it doesn't do us in the next time."

(This conceivably would be consistent with the stories of the many people who say that they have gotten sick with CFS following visits to Incline Village, btw.)

Would this sort of "full alert" ongoing response be consistent with the Th1/Th2 shift?

I don't know yet. That's why I want to know "What kind of toxins?" and what parts of the immune system might be involved in protecting us from them.

I would appreciate your thoughts.

Best, Lisa

 

[HopingSince88]

How does this all jive with the folks that have Crohn's and/or Interstitial Cystitis, which I thought were common in ME/CFS?