Which autoantibodies would you test for?

[erin]

Sorry to take your time @Jonathan Edwards, but what would be the sole purpose of measuring autoantibodies ? (in a nutshell if possible?) With the shopping basket example I had a rough idea but apart from that any other reason?

 

[Justy]

I cannot tolerate mcas medications as these all come along with some anticholinergic side effect

2nd egenration antihistamines dont have these effects. You could start with a low histamine diet, vitamin C daily in divided doses and quercetin

 

[Jonathan Edwards]

What confuses me a bit: I got the impression here that lab results aren't "central" in the sense that one cannot tell there's a problem by lab results. (Normally people with symptoms test their blood..)

How can you diagnose an autoimmune problem if you cannot rely on lab results or if lab results "don't tell it"?

I fear I wasn't able to communicate what I mean...

Your question is very clear @Inara
The answer is actually quite complicated but not too difficult to understand. The person who explained it best was a vet called David Bennett who had the nice touch of showing all his dog patients with the face blacked out for anonymity!

To make use of a test in explaining an illness one needs to have an abnormal test result PLUS a good reason for thinking it highly likely that the result shows the cause of the illness.

Imagine you have water coming through the kitchen ceiling. You look outside and see a tile missing on the roof. You get the roofer to fix it but the water keeps coming - it is caused by a faulty water cistern. If you then look down the road you will see that one in three houses has a tile missing, not so unusual. Also you realise that your missing tile is on the other side of the house from the kitchen.

So when we get an abnormal blood test result we have to establish the probability that it is causing the illness. If quite a few normal people have it (autoantibody) then we have to look hard for evidence. If the autoantibody does not seem the right one for the illness (on the wrong side of the house) we tend to ignore it.

At present we do not know of any autoantibodies that would clearly explain symptoms of ME/CFS. Some possible suggestions have been made but the antibodies are not much more common in ME than normal. SO at present we think they may just be missing tiles that do not matter.

 

[Inara]

Thank you, @Jonathan Edwards, a very clear reply that I understood! Just great

I think I got a wrong impression before.

So, can I summarize it as "lab results plus common sense and thinking"? (Which should be straightforward.)

But I think sometimes/often there's not an obvious connection found so that it's difficult to analyse the underlying problem. In that case, what may remain is "guessing" - or how would you do it? I think about maths problems, where guessing seldomly led to success. You had to find the connections and see the entire picture, but you also had to take small steps. But reality is not maths.

This makes bio-medical research - and diagnoses - quite difficult. I'd say unknown things can only be found by chance.

At present we do not know of any autoantibodies that would clearly explain symptoms of ME/CFS.

I daresay this is definitely correct. But there are some people with ME who have also autoimmune issues, no? Although I think this

SO at present we think they may just be missing tiles that do not matter.

is also correct.

 

[jpcv]

Very good explanation @Jonathan Edwards !
While discussing this subject elsewhere, you mentioned that some patients show up at reumathology clinic with a positiva ANA and fatigue but not with a specific disease or diagnosis. Can you expand your thoughts on this subject?

 

[Jonathan Edwards]

It is all a matter of what is likely.

One of the problems of 'guidelines' is that it is assumed that doctors 'make a diagnosis' and then treat.

In real life we do not act like that, and for very good reason. If there are dark clouds in the sky we do not say 'no diagnosis of raining because the ground is not wet' so not take a raincoat. We take the raincoat.

So we should not wait for 'a diagnosis of lupus' before asking questions about whether someone has symptoms related to high titre ANAs that might also produce more serious problems later. At least we should follow them in the clinic and check their blood tests. Unfortunately a lot of doctors do not transfer the common sense of real life into the clinic.

So in a rheumatology clinic a doctor should be following up a number of 'borderline cases' with autoantibodies and unexplained symptoms and in some cases treating them. When ANA is present with fatigue it may in some cases be helpful to use hydroxychloroquine, although over the years I became less and less convinced of this. Steroids are not very good for isolated fatigue and nor is rituximab as far as we can see at present.

So we are not looking for black and white answers but sensible strategies. The problem with immunological treatments for ME/CFS is that outside formal trials like RituxME they are very often ill thought out and poorly documented - which just makes everyone more confused.

 

[Inara]

@Jonathan Edwards
I really do think you are the exception
I never met a doctor who acted and/or treated prospectively. Findings were only discredited as "meaningless"; connections are never looked for or understood. If you can't understand the problem, you can't solve it (unless you're lucky!).

It makes sense what you write.

 

[jpcv]

It is all a matter of what is likely.

One of the problems of 'guidelines' is that it is assumed that doctors 'make a diagnosis' and then treat.

In real life we do not act like that, and for very good reason. If there are dark clouds in the sky we do not say 'no diagnosis of raining because the ground is not wet' so not take a raincoat. We take the raincoat.

So we should not wait for 'a diagnosis of lupus' before asking questions about whether someone has symptoms related to high titre ANAs that might also produce more serious problems later. At least we should follow them in the clinic and check their blood tests. Unfortunately a lot of doctors do not transfer the common sense of real life into the clinic.

So in a rheumatology clinic a doctor should be following up a number of 'borderline cases' with autoantibodies and unexplained symptoms and in some cases treating them. When ANA is present with fatigue it may in some cases be helpful to use hydroxychloroquine, although over the years I became less and less convinced of this. Steroids are not very good for isolated fatigue and nor is rituximab as far as we can see at present.

So we are not looking for black and white answers but sensible strategies. The problem with immunological treatments for ME/CFS is that outside formal trials like RituxME they are very often ill thought out and poorly documented - which just makes everyone more confused.

Thank you, as a medical oncologist , I do agree with you in many aspects regarding guidelines, common sense and treating real life patients .
Bad quality data is worse than no data, it´s like navigating using a fake road map.
I tried a course of prednisone, 60 mg/day, with no improvment at all
is there any relation between rising ANA titers and worsening of symptoms? My titers are rising 1/320 and I´m not getting better...

 

[erin]

@Jonathan Edwards, thank you for the above post, it is very helpful.

 

[Josie]

2nd egenration antihistamines dont have these effects. You could start with a low histamine diet, vitamin C daily in divided doses and quercetin

Unfortunately they also have, not to such an extend as the first generation. But I get gastroparesis from the first generation anthihistamines too. I am low histamine for 15 years now, but that doesnt prevent my mastcells from misbehaving

 

[Samuel]

i hope the following is coherent and readable. i am not
able to do better at this time.

i think this thread raises highly interesting questions.

please consider the following symptom profile.

===

for some pwme, the symptoms that you see in the literature
are a miniscule subset of what they are dealing with.

is angioedema mentioned much? what about sleeping for 2w
straight as a child? anosmia and dysgeusia? prosopagnosia?
allodynia? urethritis? conjunctivitis? inability to plan?
autistic-like symptoms as a child? clear line of vascular
demarcation? unusual headache lasting for weeks after
0.75mg dose of scig? SEVERE hyperalgesia? intolerance to
effective pain medicine? anti-nausea useless?

expand. it is still a miniscule proportion of the number of
symptoms.

we do not see this massive symptom profile in the literature
afaik.

===

this profile has no specific name afaik. but it is possible
that this thread has 2-3 such people.

these people wonder whether they should even be in the
m.e. community, but:


1) they meet m.e. criteria
2) they often have rare symptoms (e.g. reversed phase
sleep) in the criteria, which bayes' theorem says
increases the posterior probability that they have m.e.
3) they usually have lots of the optional symptoms
mentioned in the criteria and lots of the symptoms
mentioned on m.e. forums


however, they still wonder whether they should instead be in
the fluoroquinolone, pesticide, mold, eds, mast, or lyme
communities -- and often HAVE many or even all of those.
(example: you take a fluoroquinolone and your finger joints
do not move. you stop and they get better. you start and
they get worse again.)

some of these pwme have several autoimmune diseases by lab
test. (examples below.)

now let's consider this subgroup of pwme.

i'll put myself forward as an example. feels risky.

===

my diagnostic story is 60 pages long. it has sentences like
"Restless legs, mostly left hip, deep. Usually at night."

my experience is that non-immunologist doctors are not going
to be both willing and able to take this list and find
tissues to look for antibodies in.

where do i find an immunologist to do this for people who
are bedridden?

===

now here's something.

excluding ana and crp, i have had 3 tests done.

here they are:

===

1) ds-dna was probably a stab in the dark. and positive.
2) intrinsic factor was probably a stab in the dark. and
positive.
3) igg subclasses was probably a stab in the dark. and
positive.

===

do the brits call that a hat trick? it seems like a red
flag for something. dunno what.

what does this mean? i don't know. my doctor doesn't know.

1) is my m.e. autoimmune? i am too ignorant to conclude
that.
2) does it mean i want to know more about autoimmunity in
my case? YES! here are examples:
- which symptoms if any are related to sle? which if
any are related to pernicious anemia?
- could i have some unusual antibody that underlies
stuff?
- do i have m.e. because i have immune issues?
vice-versa? coincidence? common underlying cause?
this could inform treatment.
- where does my angioedema come from?
- c1-inh normal, c4 low normal, but a trial of 4x
dose of antihistamines ineffective. i could die
within a few minutes.
- random hypotheses
- maybe this is my current mold exposure? i was
previously mold-injured and am being mold-injured
right now.
- mcas? mast cell site mentions in passing. and
mentions autoimmune comorbidities.
- am i crazy to wonder if it is autoimmune? my
doctor is busy. uptodate mentions sle in
passing.

===

we are listening closely!

but many pwme need immune science to offer a comprehensive
or systematic algorithm FROM THE TESTING SIDE that a
non-immunologist can use for bedridden and housebound.

regardless of m.e. etiology.

===

i know i am asking for jet packs and flying cars. but pwme
are known for being vexatious. so that is my excuse.

i'd like epitope chips, analogous to gene chips, that can
test for every known human autoantibody. or a better
understanding of the immune system that leads to a
non-symptom-based algorithm for finding tests to run. and i
want more treatments for special cases.

===

@jonathanedwards said:

> it would help to have a clear idea what to look for

that's exactly what i want!

 

[Jonathan Edwards]

You raise some interesting questions, @Samuel.

The problem lies in the nature of the way we have to calculate probabilities - Bayes theorem and all that, as you know.

So the question is why does it seem that doctors are less likely to take interest and look for autoantibodies, the more symptoms they are presented with. The reason is that the doctor's first task is to try to deduce the most likely causal links underlying symptoms. The second task is of course to address the symptoms themselves but very often to do that efficiently they have to have an idea of the likely cause. And doctors deduce causal links from specific clinical patterns. So swollen joints and pericarditis makes them think rheumatoid arthritis very likely.But swollen joints, conjunctivitis and pericarditis makes rheumatoid arthritis much less likely.

The bottom line is that if a doctor is given a long list of symptoms they have no way of making any sense of them in terms of a recognised syndrome for which they can find evidence in the books for a cause. So the usual practice is to try to make sense of four or five major symptoms and assume that the others may be coincidental.

It might seem that we should be looking for causes for more complex patterns shown by individuals - maybe with a dozen symptoms. But if we can only deduce causal links from reliable correlations between symptom patterns and lab tests we need at least ten cases with the same pattern and the same lab tests to have any reason to think they go together.

We then have the problem that the more autoantibodies we look for the more spurious associations we will find. About 40% of normal people will have one of the common autoantibodies. If you tested for forty autoantibodies I suspect almost all normal people would come up positive on some. So we have the same problem we have with the research papers we have seen recently where nothing can be concluded because so many things have been looked for.

I also have a strong feeling that the cases of ME most likely to be autoimmune will not be those with lots of different symptoms but ones with fatigue/malaise and not much else. In known diseases where patients have several types of symptom you are pretty guaranteed that at least one will be based up by objective pathology or radiology tests. So a patient with lupus with five symptoms is almost bound to show an abnormal ESR or blood count or chest x-ray or a skin biopsy. On the other hand a patient with a lupus-like illness that might get diagnosed as ME is likely just to feel ill and have maybe one or two other symptoms.

Similarly for the T cell based auto inflammatory diseases, the ones that might get diagnosed as ME are the ones with very few specific features. The ones with joint swelling, rash, urethritis and bowel problems have objective clinical pathology.

The priority for me is to try to find something on a lab test that tells us something about the cause of the central symptoms of ME/CFS - the malaise and intolerance of external stimuli for instance. Until we have some progress on that I see no point in chasing symptoms that a small minority might have. I can see that we might want to find one explanation for a core set of features that varied from case to case. In RA we pinned down a causal mechanism for nine core features. We tested 50 tissues and found nine positive and forty one negative so we felt we were on the right track. But we had decided in advance exactly what single molecule we were going to test for. Looking for lots of answers, each to explain a different symptom is just not practical.

 

[Milo]

My OI started after hip replacement surgery. I’d had mecfs for many years before that, with low normal blood pressures, but whatever happened in this major surgery resulted in a disabling problem with hypotension. I imagine it was the anaesthesia’s effect on the nervous system, which I have heard can result in some permanent damage

Hello @Sing It is also my experience that my OI / POTS started during my gallbladder surgery recovery, some 5 months following my EBV onset disease. After that it really felt like my symptoms kept adding up. OI, depth perception issues (this lasted about 2weeks), sound and light sensitivity, chest pain and shortness of breath, etc.

is there any relation between rising ANA titers and worsening of symptoms? My titers are rising 1/320 and I´m not getting better

My ANA titers have been straight 1:1280 for at least 25 years now (I have had ME for 9 years now) and i have not been diagnosed with a specific illness despite the ANA. Doctors simply decided to stop testing that. Same with my ESR=25-38. If drs stop checking all of that, then they don’t get worried. As for me, it took a while, but i had not much choice to also let go of measuring my ESR, besides my health care system does not cover it unless it is ordered by a specialist.

The question remains, is it meaningful or relevant? On one side, we the patients feel sick and too often we lack recognition on how bad we feel. We seek out proof on paper that indeed we are sick. Things would get much easier if we had proof on paper amd if we could quantify how sick we are.

We need biomarkers!

 

[Inara]

The bottom line is that if a doctor is given a long list of symptoms they have no way of making any sense of them in terms of a recognised syndrome for which they can find evidence in the books for a cause. So the usual practice is to try to make sense of four or five major symptoms and assume that the others may be coincidental.

I imagine if I were presented with the long list of symptoms I have I would feel overstrained. Additionally, if I had no experience with multi-systems and how they interact - if I would expect only ONE underlying cause - I couldn't solve the problem.

There is a high probability that if one system is affected (e.g. endocrinal), another will be (e.g. neurological), and others will follow.

There is also some probability that an autoimmune illness is accompanied by another or even several others.

Some days ago I spoke with a genetist. I mentioned two main symptoms (which will leave you riddled). She said instead of picking certain genes she feels it's more reasonable to look at the exome.

In retrospect, I wish that some people had looked at a bigger picture than just use a selection "strategy". Overall it would have been even cheaper.

Please correct me wherever needed.

Edit: In fact, what I missed to say, there are possibly several illnesses that cause that many symptoms.

 

[Jonathan Edwards]

She said instead of picking certain genes she feels it's more reasonable to look at the exome.

Not sure I follow that. The exam seems to be a fashionable buzz word for 'everything'. It seems a bit like saying don't try climbing the Matterhorn, climb the world. Tough to know how to do that.

 

[Inara]

In fact, that's what she meant: Instead of trying to find which illness and symptom go together, she will take "the entire picture" (of course, exome is not everything, but very much). She had made the experience that with their "picking" they missed illnesses. And after that she might be able to allocate symptom to illness.

The question is simple: Might there be a genetic cause? If everything's fine, for her the question is answered. They won't search every detail I suppose. So it doesn't necessarily mean there is nothing. But I think this course is reasonable for this kind of question.

Of course, this is quite different from ME. And after our discussion here and in other threads, I see that really understanding ME is quite difficult. You maybe won't get around allocating symptoms to illness in this case - but to me, it seems to be arbitrarily complex. Much thinking will be needed.

But maybe, I wonder now, this is not so dumb after all: See what deviates from normal and then try to find connections and then underlying causes. That's how I understood my problem with vitamin B6.

 

[Bluesky]

i am not sure of the answers. i do know that you seem to have dx factors of b12 deficiency. that in itself can cause a whole host of symptoms. its very often missed and dx as m.e. also there does seem to be benefit from many pwme from taking b12 injections. this is covered on dr myhills site. i think that anit biotic is known for causing those symptoms and problems with ligaments. believe i may have read it has black box warnings.

one thing i do know is that we do as we get so very badly ill that we cannot leave our beds let alone prep food and shop cook so we will prob get vitamin deficiencies.

as with sun exposure and getting vit d which in itself cause a whole string of problems including more weakness.

have you been treated correctly for b12 pa? there is a very good video by a usa nurse who is taking the system on re this misdiagnosis level and non treatment of pa correctly.

i have certainly found treating vitamin deficiencies to help ie vit d. i am one who finds the mitochondrial function test was very poor indeed and i found the vitamin q10 very helpful. i still use it today.

b12info uk i think is the site i use to check symptoms and find the links to nice guidelines in uk as to how to dx treat etc. hopefully you will find it useful

this is the nurse Nurse Sally Pacholok this is conversational but very imformative with case studies which makes it easier to watch if you are neurological severe range

there are tests that can show some genetic markers for problems with mtfhr and also upcoming with b12

Full Feature Film starring Annet Mahendru as Nurse Sally Pacholok
https://www.youtube.com/watch?v=OvMxJ6GRBNQ
i guess i am working wth my dr on fixing a bit at a time not working for a cure but to be the best i can be. i am starting with this diet. it certaininly does bring reaction whe i eat food left to rest which was ok to eat when first served. this results in pain etc so i as i have found diet to help and vitamins very important to consider in diet. i messed up yesterday staying with friend and ate out of politeness the christmas dinner which had thoughtfully been made with wheat free sauces and products. though it had been left to rest. am suffering today. so i do believe that there is somethinng in this low histamine diet.

tough though when its so complicated and you are pretty severe mostly, people see those good days hours and make assumptions.

half the battle would be won if we had more of the advocacy like 25% ME group so rights of equity to health care would be fought for quite rightly.

on the others issues johnathon edwards has a much more educated reply than i could ever do

 

[Samuel]

You raise some interesting questions, @Samuel.

...

Looking for lots of answers, each to explain a different symptom is just not practical.

thank you for taking the time. i think i understand a
little better. but that last sentence ... i want a small number of answers to explain most of them.

i'm not sure if your post addresses the symptom profile i am talking
about.

> The problem lies in the nature of the way we have to
calculate probabilities - Bayes theorem and all that, as you
know.

ok.

> So the question is why does it seem that doctors are less
likely to take interest and look for autoantibodies, the
more symptoms they are presented with. The reason is that
the doctor's first task is to try to deduce the most likely
causal links underlying symptoms. The second task is of
course to address the symptoms themselves but very often to
do that efficiently they have to have an idea of the likely
cause.

the unusualness of the cases i am talking about (outrageous
number of symptoms but also obvious m.e.) seems to call for
a doctor who will think about biology.

because i have no clue.

> And doctors deduce causal links from specific clinical
patterns. So swollen joints and pericarditis makes them
think rheumatoid arthritis very likely.But swollen joints,
conjunctivitis and pericarditis makes rheumatoid arthritis
much less likely.

so /adding/ a symptom makes a diagnosis /less/ likely in
your example.

i /think/ i understand, but i find it troubling.

i can see the value of algorithms and checklists to keep
things sane.

however, this feels like case-based reasoning. a set of
templates. each person has one disease, unless
complications are mentioned in the disease that fits. if a
fit isn't good enough, then press harder. confidently
prescribe a drug that fails. send the bill. or something?

that's kind of my experience with doctors.

===

by around 1999 i had dozens of "probably correct as far as
they go" diagnoses like conjunctivitis and interstitial
cystitis, but NO UNDERLYING DIAGNOSIS after more than 30
years.

they kept testing for hiv and asked me if i was gay, and
confirmed the interstitial cystitis or reversed phase sleep
disorder or whatever by doing absolutely nothing, and then
sent the bill.

so i bought medical books.

===

Amazon says Harrison's internal has 2,784 pages. It is set
in small print, multicolumn. Lange's Internal is also huge.

i went through EVERY DISEASE IN BOTH BOOKS to find out which
one i had. the closest i found by symptoms was wegener's
granulomatosis, but that seemed wrong.

there was a "cfs" but they said something like
"characterized by fatigue, treatment reassurance".

===

i kept getting stuck on "and other symptoms". ANYTHING fits
that! there's a laying on of hands in medicine that i was
not part of. i could not pierce those three words.

WHICH OF THOSE "AND OTHER SYMPTOMS" DISEASES WAS MINE? i
had no idea. maybe it was hidden deep in the chapters on
osmolality vs. osmolarity. (joke -- NOOOOOOOT.)

so case-based reasoning didn't work. i needed somebody to
think about biology. or at least to translate "and other
symptoms" into laymanese.

===

> The bottom line is that if a doctor is given a long list
of symptoms they have no way of making any sense of them in
terms of a recognised syndrome for which they can find
evidence in the books for a cause. So the usual practice is
to try to make sense of four or five major symptoms and
assume that the others may be coincidental.

it seems extraordinary that my huge number of diseases and
symptoms are all coincidental except a few. something
something occam.

so i am confused.

===

but maybe we are talking at cross purposes?

are you referring to what's needed for (1) TREATMENT of an
individual with a non-textbook symptom profile, or (2)
SCIENCE on a relatively narrowly defined disease, m.e.?

my question is (1).

i want to have diagnosis and treatment.

> It might seem that we should be looking for causes for
more complex patterns shown by individuals - maybe with a
dozen symptoms. But if we can only deduce causal links from
reliable correlations between symptom patterns and lab tests
we need at least ten cases with the same pattern and the
same lab tests to have any reason to think they go together.

perhaps you are referring to (2) scientists trying to find
the cause of m.e.?

that sounds reasonable for science.

that's not my concern here. i need diagnosis and treatment.

> We then have the problem that the more autoantibodies we
look for the more spurious associations we will find. About
40% of normal people will have one of the common
autoantibodies. If you tested for forty autoantibodies I
suspect almost all normal people would come up positive on
some. So we have the same problem we have with the research
papers we have seen recently where nothing can be concluded
because so many things have been looked for.

i get this. will those normal people be healthy? still, i
get this.

but does this mean that an individual with a large symptom
list -- who has tested positive for ds-dna and intrinsic
factor and hypogammaglobulinemia -- shouldn't get tested for
anything autoimmune?

if the answer is "no no, go ahead and test for the four
biggest things", i don't even know what four symptoms are
most relevant, and my doctor is lost in all this and busy.

> I also have a strong feeling that the cases of ME most
likely to be autoimmune will not be those with lots of
different symptoms but ones with fatigue/malaise and not
much else. In known diseases where patients have several
types of symptom you are pretty guaranteed that at least one
will be based up by objective pathology or radiology
tests. So a patient with lupus with five symptoms is almost
bound to show an abnormal ESR or blood count or chest x-ray
or a skin biopsy. On the other hand a patient with a
lupus-like illness that might get diagnosed as ME is likely
just to feel ill and have maybe one or two other symptoms.

ok for those people, but this misses the symptom profile i
am talking about. where does it fit?

where do i (and others who are similar) belong? i am
starting to think i do not technically belong in the
m.e. community at all.

i have m.e. by strict definitions. i resonate with
m.e. descriptions. i have m.e.

but i recently sense that NOBODY in the m.e. community
(including scientists) is thinking about symptom profiles
like mine, which means it is much more rare than i thought.

so i am definitely alienated here.

do i have an underlying disease that is causing m.e. as part
of it? what disease is that?

> Similarly for the T cell based auto inflammatory diseases,
the ones that might get diagnosed as ME are the ones with
very few specific features. The ones with joint swelling,
rash, urethritis and bowel problems have objective clinical
pathology.

a little confused. do you mean diagnosed or misdiagnosed?

but again i sense not relevant to the symptom profile i am
describing.

> The priority for me is to try to find something on a lab
test that tells us something about the cause of the central
symptoms of ME/CFS - the malaise and intolerance of external
stimuli for instance. Until we have some progress on that I
see no point in chasing symptoms that a small minority might
have.

i'm ok with being cast aside by m.e. researchers if that is
the best thing to do. i will rot and die in the gutter
having never really known what health is like, but more
normal m.e. people will be saved.

but i'd like at least some doctor or researcher, anywhere in
the world, to figure out what is wrong with me, even if only
roughly.

> I can see that we might want to find one explanation for a
core set of features that varied from case to case. In RA we
pinned down a causal mechanism for nine core features. We
tested 50 tissues and found nine positive and forty one
negative so we felt we were on the right track. But we had
decided in advance exactly what single molecule we were
going to test for. Looking for lots of answers, each to
explain a different symptom is just not practical.

back to the last sentence again. i get this, but somebody with the symptom profile i am describing has SOME REASON for having it. am i right?

if it's a different disease, then fine -- where is the
science for THAT disease? m.e. is just a tiny subset.

i have wanted a name for my disease my whole life and i no longer think m.e. is the underlying disease -- if you are right about the small number of symptoms thing as i understand it from your post.