Can you have CFS without meeting the typical criteria?

[caledonia]

"often get severe stomach cramps and diarrhoea" - possible candida or other gut infection. See the 4R Gut Rebuilding program in my signature link.

"Blood tests over the 24 years have always been clear (eg: thyroid)" - typically they only test TSH and don't do a complete thyroid panel. This means you can have a thyroid issue which remains undiagnosed. Do you have other symptoms of low thyroid - fatigue (yes), cold temperature, gaining weight or trouble losing weight, dry hair, etc. etc.?

"I have this annoying problem, of 'waking up' later in the day, after being fatigued all day and being able to do more in the evening" - that plus fatigue - classic symptoms of adrenal fatigue

Here is a good link for some self tests for adrenal fatigue; the same website also has good thyroid info: http://www.stopthethyroidmadness.com/adrenal-info/

"possible rheumatoid arthritis" - sounds like an inflammatory process is underway. Might be a good idea to work on reducing inflammation via supplements and/or diet. A low starch diet sounds similar to the Zone diet which works because it keeps your blood sugar levels even and that helps inflammation. Candida and inflammation are also linked together. A lower starch diet is part of the 4R Gut Rebuilding Program.

The one thing in common with all of those is mercury toxicity. Do you have or have you had mercury amalgam fillings or other exposures to mercury? If you're not sure, you can do a hair metals and minerals test for under $100 - see my signature link for info about mercury toxicity and Andrew Cutler. There are many other sources of exposure which are not obvious such as acquiring part of your mother's body burden in the womb, air pollution from coal burning power plants, fish consumption and so on.

I would agree with Hip's assessment of what went wrong with the Modafinil. Your brain should adjust back to normal eventually. You were only on it 6 days, so I would think it would be sooner rather than later. If it impacted your adrenals, those should also go back to "your" normal at some point.

 

[Gingergrrl]

We do not actually know how many illnesses are under the ME/CFS umbrella, gingergrrl.

Agreed and I think there are many illnesses and many subtypes that are all under this one huge umbrella right now.

I think most physicians dealing with ME/CFS think that there will turn out to be several 'diseases' in there.

I agree on this as well.

If someone is very sick and is the only person int he world with their particular disease they are still very sick and need being taken seriously.

Absolutely and I couldn't have said it any better.

Totally agree. One day, PR might be left with no members because everyone will have been diagnosed with and treated for something other than that catch-all: ME/CFS.

@CCC, That would be a dream come true, that no one is left because we have all been diagnosed and treated for whatever is really going on in each of our individual cases.

 

[medfeb]

We do not actually know how many illnesses are under the ME/CFS umbrella, gingergrrl. The name is just a useful way of lumping together patients with what look like similar problems. I think most physicians dealing with ME/CFS think that there will turn out to be several 'diseases' in there. In my experience trying to make rigid classifications of disease just leads to bad medicine. The key thing is to recognise that there are a large number of people with illnesses that fall into the ME/CFS area and need their problems investigating and sorting out. If someone is very sick and is the only person int he world with their particular disease they are still very sick and need being taken seriously.

I agree that all patients need to be taken seriously, even if they have a rare disease that affects just a few people. And I also agree that its very likely that ME/CFS, even as defined by the CCC, will turn out to be more than one disease.

But the problem I see is that depending on who you talk to, the "ME/CFS" umbrella includes not only patients who satisfy the CCC, the ME-ICC, and the IOM criteria but also patients who don't satisfy those but do satisfy Fukuda, the 2005 Reeves criteria and the Oxford criteria and any of 15 or so additional criteria. Further, according to some of those definitions, patients can be suffering from primary mental illness and not have any physical impairment.

There's no doubt that there are sick patients in this broad umbrella who need care. But it seems like bad science and bad medicine to treat this full range of "ME/CFS" definitions and conditions as part of a single clinical entity to be studied and treated in the same way.

So to move forward, don't we need to have some level of agreement on what is included in the "ME/CFS" umbrella and what is not? For instance, the IOM, CCC and ME-ICC all require post-exertional malaise. Wouldn't that then be required?

 

[Jonathan Edwards]

There's no doubt that there are sick patients in this broad umbrella who need care. But it seems like bad science and bad medicine to treat this full range of "ME/CFS" definitions and conditions as part of a single clinical entity to be studied and treated in the same way.

So to move forward, don't we need to have some level of agreement on what is included in the "ME/CFS" umbrella and what is not? For instance, the IOM, CCC and ME-ICC all require post-exertional malaise. Wouldn't that then be required?

But in a sense arguing about criteria is just arguing about what should be 'part of a single clinical entity' and in my experience in research you just don't get tied up in those knots. You look at the clinical problems and try and work out the possible mechanisms and treatments. You may have to divide patients up in lots of different ways to identify different parts of the mechanism and different treatment options because mechanisms involve lots of overlapping factors.

'Required\ criteria ring alarm bells for me. What about all the people I would see with early RA who had no swollen joints - that is the central criterion for RA but when the symptoms start there may just be swelling of tendon sheaths or carpal tunnel syndrome. Diagnostic criteria may seem tidy but they don't have much to do with either looking after people or research.

 

[lansbergen]

You may have to divide patients up in lots of different ways to identify different parts of the mechanism and different treatment options because mechanisms involve lots of overlapping factors.

Yep

 

[Gingergrrl]

But in a sense arguing about criteria is just arguing about what should be 'part of a single clinical entity' and in my experience in research you just don't get tied up in those knots.

It is so interesting because I used to completely disagree with you on this point (am just being honest!) and now I completely agree with you!

You may have to divide patients up in lots of different ways to identify different parts of the mechanism and different treatment options because mechanisms involve lots of overlapping factors.

I also agree with this and I think with treatments such as RTX, we need to be especially careful to try to identify which group or subgroup of patients might be the best responders. I could say this with any treatment from anti-virals, to antibiotics, to even supplements that appear benign. The more we know about the different sub-groups, or even distinct disease entities, the better treatment that can be provided.

Diagnostic criteria may seem tidy but they don't have much to do with either looking after people or research.

I agree and if someone has constant infections, fevers, sore throats, swollen lymph nodes, brain fog and flu-like symptoms than they are in a totally different subgroup than someone like me who has multiple auto-antibodies, severe dysautonomia and POTS, and MCAS and has not had a fever or flu in over three years. Yet we may overlap that we both continue to crank out IgM+ antibodies to EBV or other viruses so our immune systems are in chaos. We need to find the commonalities but also the differences.

 

[medfeb]

But in a sense arguing about criteria is just arguing about what should be 'part of a single clinical entity' and in my experience in research you just don't get tied up in those knots. You look at the clinical problems and try and work out the possible mechanisms and treatments. You may have to divide patients up in lots of different ways to identify different parts of the mechanism and different treatment options because mechanisms involve lots of overlapping factors.

'Required\ criteria ring alarm bells for me. What about all the people I would see with early RA who had no swollen joints - that is the central criterion for RA but when the symptoms start there may just be swelling of tendon sheaths or carpal tunnel syndrome. Diagnostic criteria may seem tidy but they don't have much to do with either looking after people or research.

I get that a good doctor will care for the patient as you suggest.

The issue that I see is two fold - and I am referring to clinical care not research although the clinical problem stems from what has been done in research...

For some doctors, a disease, especially one with the contested and psychologicalized history of this disease becomes a diagnosis of the leftovers, a convenient waste bin. While its somewhat better since the IOM, we are still fighting against the branding of patients as lazy, depressed, or disability seeking. And even for doctors who might be receptive, the "ME/CFS" broad umbrella as it exists in clinical guidelines today is so loose as to engender disbelief and suspicion in the disease.

The second issue is that "evidence based" guidelines for "ME/CFS" at least in the U.S. continue to include treatments recommendations and statements about psychological factors that are based on studies done with the Oxford and Reeves 2005 definition, even though each of these definitions have been called out as including people who do not have this disease. For instance, UpToDate, clinical guidelines, recommend IOM criteria for diagnosis and then recommend CBT and GET for treatment based on PACE and also state that patients who think they have a physical disease have a poorer prognosis - another Oxford gift.

As a result, doctors are left with faulty ideas about the nature of the disease and the role of patients' behavior and recommend inappropriate treatments that hurt patients.

Somehow, we need to reset clinicians' perception on the scope of the "ME/CFS" umbrella. Once we have biomarkers, that will be easy. But that won't happen tomorrow and in the meantime, patients are being harmed by evidence-based medicine that is inappropriately mixing and matching anything out of the "ME/CFS" evidence umbrella as though it all applies to the same group of patients. Short of being clear that there are hallmark criteria like PEM that define the disease and that evidence from Oxford and Reeves is not appropriate to the disease, I don't see how to reset that narrative and stop the medical harm in the short term.

Regarding the suggestion that some patients might not have hallmark symptoms like PEM early on... that then begs the question of what group of patients ME/CFS clinical guidelines will apply to. Will the same guidelines continue to be used for all patients with medically unexplained chronic fatigue? If so, I think we could well just end right back with the problems that we face today in clinical care.

 

[Jonathan Edwards]

The issue that I see is two fold - and I am referring to clinical care not research although the clinical problem stems from what has been done in research...

Yes, I totally agree that the current situation is ill-informed and muddled, and worse. It is not that I am against categorising and describing, but just that I think we need flexibility - we need the detail of understanding that a few physicians have had for a long time and to capitalise on that but not set things too much in stone.

I think there may be a bit of a red herring about PACE and Oxford. If PACE was accepted as showing benefit in at least some patients then criticising the recruitment would be fair. The reality, though, is that PACE shows no convincing evidence of CBT/GET helping anybody and the follow up paper pretty much proves they helped nobody. So the worry about Oxford becomes an irrelevance in a sense. Nevertheless, what is true is that the recruitment was in fact of 'people who conformed to Oxford and because they did not already know that exercise and CBT were a waste of time or worse agreed to enrol'. This sort of bias completely screws even use of Oxford. That has to be openly discussed by ME physicians and possible ways of mitigating such problems explored. At present we have the PACE authors still saying what a jolly good trial they did. Something has to give. I actually think the main thing that has to give is slipping out of the picture faster than we think, but there is more work to do.

 

[Denise]

Regarding the suggestion that some patients might not have hallmark symptoms like PEM early on... that then begs the question of what group of patients ME/CFS clinical guidelines will apply to. Will the same guidelines continue to be used for all patients with medically unexplained chronic fatigue? If so, I think we could well just end right back with the problems that we face today in clinical care.

It could also be that early on patients (and their clinicians) do not recognize PEM because neither is well-enough educated about what it is (and isn't), triggers, impact, etc.

 

[rosie26]

I personally suspect that the fatigue with Reiter's, which is one of those can be as bad as ME/CFS, or actually be a subset of ME/CFS.

Is POTS a symptom of Reiter's/Reactive Arthritis? I have looked at the symptoms and I can't remember seeing anything but then it's not really understood anyway. But from patients you have had over the years, did you hear them mention POTS-like symptoms?

 

[medfeb]

I think there may be a bit of a red herring about PACE and Oxford. If PACE was accepted as showing benefit in at least some patients then criticising the recruitment would be fair. The reality, though, is that PACE shows no convincing evidence of CBT/GET helping anybody and the follow up paper pretty much proves they helped nobody.

Yes, you make a good point about PACE failing to prove anything. And I think what's happening with PACE won't be turned back. But Oxford' nonspecificity could still be an issue because other Oxford studies are also being referenced in clinical guidelines to e.g. support claims that behavioral and psychological factors predispose and/or perpetuate the disease. And we also have the Reeves 2005 studies used to support the claim of child abuse as a risk factor and also claiming maladaptive personalities. And then there's the recent report of high prevalence in teens that was based on a cohort of parent reported chronic fatigue - not even CFS and not medically diagnosed. None of these studies are appropriate for ME/CFS clinical guidelines and yet they all showed up in a 2016 list of references provided by CDC as part of its med ed efforts.

That has to be openly discussed by ME physicians and possible ways of mitigating such problems explored. At present we have the PACE authors still saying what a jolly good trial they did. Something has to give. I actually think the main thing that has to give is slipping out of the picture faster than we think, but there is more work to do.

That would be excellent for ME physicians to think about ways of mitigating against/addressing how this broader "CFS" evidence is being used in ME/CFS evidence based guidelines today.

 

[Old Bones]

That sounds fine, but those views don't match the experience of my extended family . . . We're unlucky enough to have seen ME/CFS and HLA-B27 in various branches of the family . . .

One family member suffers badly, and the low (almost no) starch diet makes a huge difference to his life; breaking the diet also makes a huge and unpleasant difference. It doesn't matter to me (or the people Alan Ebringer's ideas have helped) that other experts don't agree.

My personal experience is also different from @Jonathan Edwards ' clinical observations. I have ME, positive HLA- B27, and a diagnosis of RA. My father had AS, and likely ME as well. Also my grandmother. A low (almost no) starch diet completely eliminated my joint pain and swelling. However, this diet caused insomnia, unhealthy weight loss and severe constipation. As a result, I was unable to continue. Soon after adding some starches back, the pain and stiffness returned. Several yeas ago, my rheumatologist disputed diet having any effect on inflammatory conditions. She has since acknowledged that she and her colleagues now realize their patients were correct -- diet does make a difference.

 

[Deltrus]

Dopamine from modafinil is very anti-inflammatory, perhaps it allowed a virus you were chronically fighting to gain a foothold. Perhaps this process was inevitable, and it only sped things up.

I have taken modafinil, and it gave poor results as well, when I normally am tired, it did nothing. After a few days, It also seemed to reactivate a virus in my trigeminal nerve in my cheek. I got symptoms similar to bell's palsy for a day or two but luckily no permanent damage.

I'm still using the modafinil in 50 mg doses every now and then when I need a little boost, just not 200 mg multiple days in a row.

It is important to note that modafinil acts on histamine receptors, which have not fully understood actions on the immune system, especially on astrocytes in the brain and nervous system. H1 blockers, normally used to reduce allergic reactions, can cause seizures because they mess with uptake of glutamate in brain astrocytes.

Insomnia is common in CFS.

It is sad that your partner isn't very supportive.

I had a hard time even understanding on my own the extent of my disability, I can imagine it is hard for other people to understand also. I always just blamed conventional things, like "being lazy, ADHD, being out of shape" etc until it got worse, and the change in perspective was a hard one.

When people are kids, they are told the normal reasons for being tired, failure to thrive etc, and slowly progressing un-testable disease is not mentioned at all! If I was in charge I'd make a whole class on this. A "life's roadblocks" class. It would not only prepare people for troubles ahead, but also increase empathy and understanding from those who are successful.

 

[Kenny Banya]

Here is a vague guess at what may have caused your increased fatigue after taking modafinil:

Modafinil is a dopamine reuptake inhibitor (DRI), meaning that it increases dopamine levels by inhibiting the dopamine transporter mechanisms which remove dopamine from the synaptic cleft. Cocaine also works by this mechanism.

Now low dopamine has been linked to fatigue, so what I am thinking it that you may have built up a tolerance to modafinil, such that your dopamine reuptake was up-regulated in order to compensate for the reduction of dopamine reuptake that modafinil produces.

So now you may have up-regulated dopamine reuptake, which will lower your dopamine levels, causing increased fatigue.

If this is indeed the problem, then it may that your dopamine reuptake mechanisms go back to normal eventually.



You could try taking some dietary supplements that boost dopamine, such as Q10 200 mg, DL-phenylalanine 2000 mg and alpha GPC 1000 mg.

If you want to try some dopaminergic pharmaceuticals, then very low dose amisulpride (say 12.5 mg daily), which increases activation of the dopamine D2 and D3 receptors (by an auto-receptor mechanism, which happily does not build up a tolerance over time), has been shown to reduce fatigue in ME/CFS. I have been taking amisulpride daily for several years now, with good effect for my ME/CFS (see my post here).

Thanks for your reply. I have since been diagnosed with CFS (July last year)
At the time that I took Modafanil, no one had ever heard of this reaction. In hindsight, it wasn't dizziness as such, because that 'dizziness' has continued since - it is just significantly greater tiredness.

I am seeing Don Lewis at CFS Discovery next month & I will ask him for a prescription of Amisulpride, under the brand name Solian in Australia.
I have already tried fluoxetine (brand Lovan), with no effect, so hopefully I get the contrasted benefit as per your peer reviewed research study reference.

BTW, how do you go with Beta Blockers (Propanalol)?

 

[Hip]

BTW, how do you go with Beta Blockers (Propanalol)?

Propranolol triggered the return of some psychosis symptoms, so I could not use it.

 

[Kenny Banya]

Propranolol triggered the return of some psychosis symptoms, so I could not use it.

Are you also using low dose naltrexone?

 

[Hip]

Are you also using low dose naltrexone?

LDN only helps a small percentage of patients, and it did not help me. But for those it helps, LDN works well. Note that LDN may not work unless you also take vitamin D3.

 

[Alvin2]

Interesting, now that i read this thread i remember i once had a test done that came back positive (or is it elevated?) HLA-B27. I don't understand the implications because the replies to this thread are very confusing to me.

 

[CCC]

Interesting, now that i read this thread i remember i once had a test done that came back positive (or is it elevated?) HLA-B27. I don't understand the implications because the replies to this thread are very confusing to me.

HLA-B27 is a gene, well, three of them, that can do either or both of two things if you get the unlucky combination:

• retain too much iron (so monitor blood iron levels and give blood when the iron gets too high)
• get inflammation in the form of any combination of crippling IBS, ankylosing spondylitis or iritis. This version can be managed by diet, specifically limiting some starches (as with all things, it's trial and error, but there are guidelines), but diet won't cure it.

It is a problem only if you are homozygous for any of the three possible genes. My husband is, and he just gives blood once a year as it 'only' makes him accumulate iron. The offspring are all heterozygous, and they have no issues at all.

It's supposedly a far-northern hemisphere adaptation to a low-iron diet. I think the Celts have something to answer for here.

If you are homozygous for the gene, just keep an eye on your blood iron levels. If they get high, give blood. It will have to be a 'therapeutic' donation and they will throw it out. My husband is registered as a therapeutic donor. If you also have ankylosing spondylitis, then you might want to think about whether you feel better when you avoid white starches like grains and potatoes.

 

[Chrisb]

Feeling that it is time to enhance my reputation as being able to bore for Britain, I would quote this, which seems directly relevant to the thread title.

"Let us introduce two antithetical terms in order to avoid certain elementary confusions: To the question "How do you know that so-and -so is the case?" we sometimes reply by giving "criteria" and sometimes by giving "symptoms". If medical science calls angina an inflammation caused by a particular bacillus, and we ask in a particular case "Why do you say that this man has angina?" then the answer "I have found the bacillus so-and-so in his blood" gives us the criterion, or what we may call the defining criterion of angina.

If on the other hand the answer was "His throat is inflamed", this might give us a symptom of angina. I call "symptom" a phenomenon of which experience has taught us that it coincided in some way or other, with the phenomenon which is our defining criterion.

Then to say "A man has angina if this bacillus is found in him" is a tautology or it is a loose way of stating the definition of "angina". But to say , "A man has angina whenever he has an inflamed throat is to make a hypothesis.

In practice if you were asked which phenomenon is the defining criterion and which is a symptom, you would in most cases be unable to answer this question except by making an arbitrary decision ad hoc.....Doctors will use names of diseases without ever deciding which phenomena are to be taken as criteria and which as symptoms; and this need not be a deplorable lack of clarity. For remember that in general we don't use language according to strict rules...."

from Ludwig Wittgenstein, The Blue Book (The Blue and Brown Books, pub. Blackwell). I have introduced more paragraphs for convenience. Don't worry about the old use of angina. This was written in the early 1930's