"Pathways to Prevention for ME/CFS"

I posted a comment on the CFIDS website regarding "Pathways to Prevention for ME/CFS":

Prevention? Prevention needs some sense of the cause(s), if I am not mistaken.

Yes, there are tentative, speculative causes. But all the so far presented "definitive" causes of ME/CFS share one thing in my eyes: complete lack of credibility. There is no trustworthy research pointing to an cause.

And would prevention look like?

For pathogens, it would be the prevention of the spreading of that pathogen. Problem is, there is no identified pathogen. Horning/Lipkin draw a blank. So against which pathogen do you want to prevent? Problem is, there are no known ones.

Sure, the psych*-doctors know that it is the patient who is to blame. Excuse my sarcasm, but to them it is the patient who is doing something wrong, in his/her wicked ways, as patients are – the patients simply "need" guidance by professional psych*-doctors. So their "prevention" would be some form of "education". Maybe teaching "resilience to fatigue"? Problem is, they think the disease exists in the minds of their patients, but their disease model exists only in the doctor's heads, not in reality.

Or do you want to somehow target groups at risk, and do something? Problem is, there are no identified risk groups. (Again pardon my sarcasm) Sure, the psych*-doctors will tell you it is crazy women who are at risk, but that is not reality – everybody is "at risk".

Did I miss some school of thought here? Oh, maybe the mainstream nutritional disciples will scare us of cholesterol, or saturated fat, or whatever they think is the current bogey man. Problem is, these things aren't the cause either.

So you need some preformed notions about ME/CFS to even consider "prevention". And the problem is that none of those preformed notions about ME/CFS are in any way backed up by robust studies.

It is noble to think about preventing ME/CFS, but unless we know more about the cause(s), any talk about "prevention" is pure fantasy, a waste of resources, and potentially quite harmful to the patient.

Try to find out affected pathways, try to find out cause(s) – and demand loud and clear that any prevention is based on clearly identified pathways and causes. I am afraid that any result of such a conference will be: "Doctors need to teach crazy women how to avoid tormenting their doctors with their problems." They might formulate it with more psych*-medical jargon, so it doesn't sound so offensive.

The CFIDS needs to be highly critical of this – otherwise this could have catastrophic effects on the people with ME/CFS.

Lipkin And Horning Draw A Blank

From the tweets from the 2014 "Stanford ME/CFS Symposium" I can see that Lipkin focuses on the "microbiome" (aka all the "good" and "bad" bacteria that live in your gut).

While he does not say it explicitly, he found no prevalent infections nor any prevalent immune system problems in people with ME/CFS. Granted, he found some leads with regards to IL-17 and eotoxins – but I am cautious and don't expect that anything will come from this.

And while I think that there is possibly a connection to the gut (and to nutrition!) in many diseases, I however think the reason that Lipkin looks in the gut is because he has exhausted the paths of inquiry that involve the body "proper".

Furthermore Lipkin appears to think that ME/CFS is one "monolithic" disease, so the only place where this one disease must hide (in his view) is in the microbiome in the gut.

I think he is wrong on two accounts:

1. I think there is good evidence that ME/CFS is not one monolithic disease, but instead a set of symptoms that can be caused by several diseases.

2. Lipkin is – as so many in medical research and the medical profession – unaware of the pathogenic potential of some the foods we eat (with dairy, cereal grains and seed oils/PUFA/TFA in my mind being probably the prime suspects).

For me, this is the disenchantment of Lipkin, as I had some hope that he might be able find at least one prevalent disease in people with ME/CFS.

(And BTW some of the things he said on "Autism and GI complains", on "Kawasaki syndrome and candida in the troposphere" and on "Chronic Lyme" are borderline woo. I do not think that Lipkin is a good ally. However if he investigates these things properly, and then clearly announces if he draws a blank, then I am OK with his lines of inquiry. The problem starts when he does not clearly say when he draws a blank…)

Personally I don't expect that Lipkin/Horning will find anything useful in the gut/microbiome – but it is good that they continue their inquiry, if only that they might spread more awareness of the disease or might find something by a lucky coincidence. One never knows…

[Postscript] One other thing is noteworthy: Lipkin found no evidence whatsoever that ME/CFS is caused by HHV-6 / HHV-6B. He found 3 or 4 patients – out of 586(!) – with HHV-6 or HHV-6B. This more or less invalidates the entire argument by the HHV proponents that ME/CFS is caused by an ongoing HHV infection. I think especially the attention given to Montoya (and others) in that regards is not warranted.

[Postscript 2] One more thing: As Lipkin didn't explicitly say it, let me put it in clear words:

Lipkin found no evidence for an ongoing infection in people with ME/CFS.

Clear enough for you?

If ME/CFS is caused* by pathogens (viruses or possibly bacteria), then they are long gone after the initial acute infection**. A case of "hit and run", if you want – the pathogen is gone, the damage stays.

No need to treat a pathogen that is gone, as that will usually do more harm than good. Or as they say at NASA:

Things are never so bad that they can't be made worse.

So the first order of business: Don't make things worse. Anti-viral and anti-bacterial and anti-whatnot medications have a high potential to make things worse – best to use them only if you are really really sure.

So, if there is no pathogen, what can you do? The best one could do is to identify the damage, and try to treat it (e.g. orthostatic intolerance with medication targeting the blood preasure – speak with your doctor!). If there is anything that alleviates symptoms, then doing it might be a good ides. Change nutrition, try a Paleo Diet, try an Eleminaion Diet. But please, stop claiming that phantom ME/CFS viruses, and phantom ME/CFS bacteria, and phantom ME/CFS fungi supposedly hide in the gut of people with ME/CFS, or in their tissues, or god knows where – you are hurting yourself and hurting other people.

PLEASE. STOP. IT.

Please?

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* There seems however to be evidence to indicate that acute infections can cause ME/CFS in some cases.

** Unless you are one of those rare 1 in a 100 ME/CFS cases were it is clearly established that there is an ongoing infection – and no, "Chronic Lyme" is not a ongoing infection, and neither is "Candida", nor "Chlamydophila pneumoniae" or any other somesuch woo terms being peddled by people who don't know better. These are makebelieve terms that only fool people (including those who doctors who use these terms).

Loose Ends And Chasing Ghosts

I might have made some progress, but some loose ends make me feel like I am chasing ghosts.

The good news is, I think I am making progress. In summer this year my health was tiny bit better then half a year before. Now it is again a tiny bit better than in summer. Alas, I do less, so maybe that is the reason why I feel better… And whenever I try to do something I still get worse. But my tolerance for doing stuff is slowly improving (I think, I have no real measure). I did some light work on Friday, and today (Saturday) I felt the work from yesterday, but could still do some more –  after that I felt awful.

One "trick" I found is that when I feel awful after doing some (light) work, I can feel better when I drink water – more water than I would normally drink (e.g. two glasses when I would drink only one). However when I drink too much, I feel sick… Fear not, I found another "trick": After drinking too much water, I need to take some sugar (a teaspoon or two, or a fruit) to feel better again. (and oh, I forgot to mention: I feel immediately better – within a couple of minutes – after I take a dump. I wish I knew if this is some blood pressure thing, or if this is some liver thing, or what.)

Another thing I noticed: When I take a bit of sugar, my nose "cleans up". Usually it feels a bit congested, but after taking a bit of sugar (which has to contain fructose – glucose alone does not do the trick!) my nose clears up and I can better breathe (BTW, funny thing, sometimes an orgasm clears up my nose as well…). However if I take to much sugar my nose "dries up" a bit. Something is wrong here, and I don't know what.

The improvement is so slow though, that it is painful (not literally painful, but every day seems like the last). And, whenever I do a bit more (maybe an hour or two a day), I get worse again.

And while I gained about one kilogram over the past month (or two), I am still eleven kilogram under my March weight. I have been carelessly eating stuff when I am not hungry, and that's the revenge for this.

What seems to unchanged is that my sleep is not a slightest bit restorative – on the contrary, I feel much better before sleep, than compared after a "good night's sleep". Shucks. In the morning my muscles hurt and they are stiff. My brain feels only half awake in the morning. I need to take a strong coffee, take a hot shower and about 2 to 3 hours to feel halfway like a human being.

Unfortunately there are still some loose ends. A couple of months ago I made an experiment of only eating fish, no more pork. During that time I developed some slight acne again. Which got slightly worse after I stopped fish and ate pork again. I even got some aphthous ulcers.

Now it took some time before the acne wound down again, during which time I removed olives, mustard, bananas and sausages from my nutrition.

Yesterday I ate a banana (not completely ripe), fish (smoked mackerel) and olives and got one slight ulcer.

So what did cause my acne/ulcers outbreak over the past months?

• Some weird fish protein / pork protein thingy
• Olives
• Mustard
• Sausages (or rather the casing of sausages)
• Bananas (possibly unripe?)
• Smoked meat/fish
• Food contaminations
• Toothpaste (certain brand)
• Something completely else
• All of the above
• Some of the above
• None of the above
• No external cause

Back to chasing ghosts…

And lest I forget: I have been occasionally eating some bread, and I do have the impression that I feel worse afterwards. The effect isn't too strong (and I could not swear that it is caused by bread), but I feel kind of "dehydrated" and "dry" for half a day to maybe one day.

The ME/CFS Zoo Hypothesis

A constant question regarding ME/CFS (and fibromyalgia) goes something like this:

Is it one disease, or is it a "spectrum", or is it multiple (distinct) diseases that look the same?

I that regard: I find the "Blind men and an elephant" parable helpful – and would like to expand it.

First of all, let me recount from the Wikipedia page a slightly modified summary of the parable:

In various versions of the tale, a group of blind men touch an elephant to learn what it is like. Each blind men feels a different part, but only one part, such as the trunk, or an foot, or the tusk.

A Jain version of the story says that six blind men were asked to determine what an elephant looked like by feeling different parts of the elephant's body. The blind man who feels a leg says the elephant is like a pillar; the one who feels the tail says the elephant is like a rope; the one who feels the trunk says the elephant is like a tree branch; the one who feels the ear says the elephant is like a hand fan; the one who feels the belly says the elephant is like a wall; and the one who feels the tusk says the elephant is like a solid pipe.

Afterwards the blind men talk to each other and learn that they are in complete disagreement. Some of the stories differ in how violent the conflict becomes, and how (or if) the conflict among the men and their perspectives is resolved.

In some versions, they stop talking, start listening and collaborate to "see" the full elephant. When a sighted man walks by and sees the entire elephant all at once, they also learn they are blind. While one's subjective experience is true, it may not be the totality of truth.

My impression is that many in the ME/CFS "community" think that most of the studies are equally "true" – I think that is the first mistake. To stay in the parable: Some of the blind men have never touched an elephant (or any other animal, for that matter) and simply make things up. Here you have blind men who describe not an elephant, but maybe an park bench, or an found umbrella, or maybe an object that exists only in their fantasy (and even describing that they suck). Yes Virginia, I'm talking about Lombardi, Mikovits and Ruscetti. There are others. Like those blind men trying to describe the color of the elephant. Somehow, now I have to think of the names Meirleir, Maes and Gerwyn.

And even if you sieve out all the blind men describing inanimate objects (or worse, make-believe objects), you get some who grabbed some random animal in the zoo and tried to described it. Now if they can describe two (or more) of those animals, and the differences between them, and if they do not try to make you believe that they describe the whole animal, I think they are much more trustworthy than those who want to make you believe they describe only an elephant, and that they know the entire elephant.

If you have someone who says "Here I found two animals with distinctly different tusk, one has leather like skin, the others is furry", well then we are on to something. Currently I have seen few people who would fit that bill: Alan Light (et al.), and maybe Julia Newton (come to my mind).

But one thing should be clear, all those harping about how we need better criteria to "sieve out all non-elephants" (to stay within the parable) should know that:
a) Your are an "blind men" yourself
b) You might be an "non-elephant" yourself
c) The studies you trust might describe non-elephants
d) The studies you trust might describe non-elephant animals that are different from you

Yes, better (and more stringent) criteria might be helpful, but what we need are ways to look at "a collection of zoo animals" (parable again), and learn to differentiate them properly, both in a research setting, and in a clinical setting.

A Cause of Chronic Immune System Activation

You want to know a secret? An overlooked cause of chronic immune system activation?

It's right there on your plate: Nutrition.

Forget about "gut flora disbalance" or somesuch BS. Forget about makebelieve "latent viruses" supposedly hiding somewhere in the tissue (hiding like commies during McCarthy's withhunt). If you want to know what has the potential to activate the immune system, you should look on your plate.

For decades I had acne (and other inflammation of the skin) and it only receded when I reduced dairy. When I increased dairy again, the acne came back. Over the past year  I had to learn that acne can be caused by other (ruminant) animal products like veal, lamb or sheep.

Got milk? Maybe that's the reason you got an activated immune system.

Connecting gut problems with nutrition should be easy, one thinks. So if one has known gut problems, why not think about nutritional causes? And from my experience, I can say that skin tissue (and oral mucosa) can be affected by nutrition – and the skin is probably (considering the path nutrients take through the bloodstream) the furthest away from the gut*. So it is only a small leap to consider that every tissue between the gut and the skin can be affected negatively by nutrition. Right?

There is only one way to find out: Do an elimination diet. (Almost) no doctor will help you that, no "multi-center microbiology deep-sequencing study" will help you with that, and certainly no virus-hunter (real or imaginary) will help you with that.



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* Unless of course you consider that mathematically the gut wall and the skin are part of the same surface. And that evolutionary the different epithelial tissues might be very closely related anyway.

Just When I Lose Interest in the ME/CFS Freak Show…

By now I am convinced that ME/CFS is not a monolithic disease, but a pool of superficially similar looking diseases. Take a large enough group of persons diagnosed with ME/CFS (regardless of which criteria used), then maybe 12% have "disease A", 10% have "disease B", 8% have disease C and so on. And I think that most people who research or write about ME/CFS are naive at best, and idiots at worst (with Light and Snell being the notable positive exceptions). And quite frankly I doubt that anything that comes with the "ME/CFS" label will help me regain my health.

But when an anonymous commenter* pointed me to some links, and I saw one about Lipkin I was intrigued. Lipkin may or may not be onto something – only time will tell. And it looks like some results from the Lipkin/Honig study are in. Unfortunately only one unreliable person has blogged about this (and as is typical for him he mumbles many things together, in order to spread optimism to those poor ME/CFS patients) – so I will have to wait until I find something more solid (like e.g. Research1st).

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* And to answer: I am not interested in some voodoo "gut treatment". I think the "methylation protocol" is at best wishful thinking, at worst quite expensive and possibly dangerous. I think the ME/CFS forums are cesspools. And no, I don't know who Gerwyn is. And quite frankly I try as best as I can not give a flying hoot about that idiot. Or the rest of the ME/CFS freak show.

Liver and Ammonia?

[Update 2013-10-14] I traced the ammonia smell to my use of artificial sweetener – talk about "first do no harm"…

Confusion and lethargy may occur if ammonia levels rise in the blood stream (ammonia is a waste product formed from protein metabolism and requires normal liver cells to remove it)
www.medicinenet.com/liver_disease/page4.htm

Is this the "weird" feeling I have? Increased ammonia in the blood stream? Because the metabolism of fructose (or other things like Ibuprofen) tax the liver too much, so it can no longer properly clear ammonia from the blood stream?

[Update] Now in the summer months I wake up in the morning a bit sweaty. And smelling slightly of ammonia – doh. So it is the liver that is part of the problem.

It seems like my liver has a problem metabolising protein, so I shall reduce the consumption of meat as well. Let's see what a potato, coconut-fat and coffee diet does for me…

Scheibenbogen, WTF?

Knops (from the Scheibenbogen/Charité group) wrote an promotion – thanks Dr. Speedy for pointing us to it. However, I am underwhelmed:

1. Any explanation involving "oxidative stress" or "nitrosative stress"("oxidativer und/oder nitrosativer Stress") makes me wary. This type of explanation is fashionable here in Germany for some people, but I would not bet my life on it.

2. While they are citing these cellular "stresses" very prominently, the Knops/Scheibenbogen group did *not* themselves test anything in that area. They have no own data whatsoever for this nitro/ROS stress. They cite works of other people – people that I find dubious (to put it mildly).

3. They did not use any healthy controls!!!! They compared the results of their patients against the lab reference ranges!!! Seriously, WTF???? And of course they did not compare it with other diseases. How do these results compare to those from MS patients? Or arthritis? A small group of controls from other diseases would have been interesting. What a wasted chance.

4. Personally (mildly) interesting is the MCHC value (page 31) on the high side of the reference value that they did find (which coincides with my MCHC values that are consistent somewhere around 35.5 to 36). But this is not a result that is in anyway a slam dunk for "us".

5. The values that they report are difficult to reconstruct. They should have used plots comparing results for CFS patients with results from healthy controls. By how much are the MCHC values increased in CFS patients? I don't know, as they don't report it. I would not have accepted a study that makes such important things not clear (but then again nobody cares about what I have to say).

6. The immunology results (CD8, IL2, CD57-/CD8-, CD4, IL5) seem interesting. Whether these results can be reproduced in another group of CFS patients, nobody knows.

7. The same goes for the IG subgroup deficits.

8. The correllation between MCHC and the CD*/IL* results seems *very* interesting. But then again, how does this look for healthy controls? Or other diseases?

Furthermore, I would have added "healthy sedentary controls" (if there is actually such a thing – if someone is sedentary, that person is not healthy IMHO) .

"Safety And Efficency"

For all those who think that the FDA will help solve ME/CFS, that the pharmaceutical industry will help solve ME/CFS, that "we, the patients" should lobby the FDA and doctors to help the pharmaceutical industry:
You are deluded.



BBC Panorama - "Paxil Study 329"


(Via 1 Boring Old Man)

Anecdote: Remove Dairy, Remove Brain Fog

Another one for the list:

I feel great. I actually feel as if there’s nothing wrong with me at this point in time. Nothing hurts, my brain is functioning adequately, my mood is euthymic, I’m never hungry, I have acceptable energy levels. Occasional mild anxiety/irritability but kava kava takes care of that (thank you Woo).

Was a stressful week at work. I was like “so what, let’s deal with this shit in a stepwise fashion” and handled it just fine.

This is a very unusual occurrence in the life of Sid, that nothing is hurting or broken. Is it possible I’ve been poisoning myself with dairy all these years? I haven’t felt this good since I first went VLC two years ago. In hindsight, I wasn’t eating that much dairy at the start because I wanted to lose weight as rapidly as possible and we all know cheese is stalling.

My brain works again. I don’t have horrible brain fog and the feeling that brain is functioning at 20% capacity.

(emphasis mine)

It's been only a week, so one will have to wait, I'll guess. But it looks promising.

Anecdote: Paleo helps for Fibromyalgia

Robb Wolf has the details.

When Patients Do Lobby-Work For Pharma

David Healy:

… Quite innocently some decades ago a network was set up by Silvio Garattini among others to investigate rare diseases. This later gave rise to Eurordis, an organization to speak on behalf of patients with rare diseases.

An organization of patients and by patients and for patients sounds like a wonderful thing but far from being a sanetocracy it has turned out to be an insanetocracy.

As it happens as of 2011 Eurordis took funds from 38 different pharmaceutical companies. These only amounted however to 22% of their income. Financial conflicts are not really the issue – they could survive without the money. It’s something else that keeps them tied to the Corporation. This is the patient group for whom pharmaceutical solutions are a lifeline. They are more committed to the interests of the pharmaceutical industry than are any of the employees of any of the pharmaceutical companies.

They can be absolutely depended upon to read the runes right and come out with a strong industry position, making it possible for industry representatives to sound relatively accommodating to others in contrast …

The ME/CFS community should take notice – especially those lobbying for Ampligen – not to become unpaid pharma shills.

Stephen Ralph on Psychiatry, Behçet's, ME/CFS and Misdiagnosis

The achilles heel of liaison psychiatry

Stephen Ralph DCR(D) Retired.

30th March 2013

Hello there,

In recent years I have been considering the reliability of the whole “CFS/ME” diagnostic process.

From personal experience I have encountered numerous doctors who failed to possess the detailed specialist knowledge they needed to make a diagnosis of Behçet’s disease at both GP and specialist level.

From personal experience I have learned that standard blood tests or even CT/MRI scans or indeed other diagnostic tests such as endoscopy can and do fail to detect a complex clinical disease present in a patient.

I have no doubt that there is a diagnostic black hole between the insufficient knowledge of the doctor and pathologies that are not detectable by the basic tests they choose to request which produce negative results they then choose to rely on.

The diagnoses of “CFS/ME” and now Somatic Symptom Disorder have in my view been deployed by liaison psychiatry to exploit that black hole.

Once a diagnosis has been made, that diagnosis is presumed to be accurate by subsequent doctors but in reality there is no standard of diagnosis from one doctor to another which means that the whole diagnostic system – especially for complex clinical presentations – is a total lottery.

The system to challenge a given diagnosis has not been changed in decades.

In the UK a patient has a right to ask for a 2nd opinion but there is no guarantee that the doctor who gives a 2nd opinion will have sufficient knowledge to correctly assess a complex clinical presentation where the usual round of simple tests come back negative.

And, having been given a first opinion of “CFS/ME”; the doctor who considers that patient for a 2nd opinion already has a subjective view of what could be wrong with that patient because they have been re-referred by a GP who will give a medical history that may lean towards a CFS/ME diagnosis because the GP has insufficient knowledge to write an accurate 2nd opinion referral listing all the relevant symptoms that could add up to a rare disease such as Behçet’s disease.

In my own case as an example, my GP had no appreciation that my episode of Epididymitis was relevant to a possible case of Behçet’s and so this issue was not referred to when I was sent to another out of area doctor who formed that 2nd opinion.

With regards to “CFS/ME” a GP or a psychiatrist or a general rheumatologist will give the patient a diagnosis based upon the repeated reporting of a set of “invisible” symptoms over a period of months.

At present, “invisible” symptoms are being ascribed as “medically unexplained” or as a sign of somatisation.

The doctors who make these diagnoses are not specialists in rare and complex diseases such as Behçet’s disease where there is a significant crossover of “invisible” symptoms.

In the case of Behçet’s disease the bulk of Behçet’s research is focused upon those who show all the physical signs yet the majority of those who have Behçet’s do not have to show those physical signs and indeed patients with Behçet’s may show few or no visible symptoms at an outpatient examination.

There is in fact a research black hole representing the majority of Behçet’s patients who do not have all the obvious signs of the disease which in turn misinforms those who rely upon such research to inform them about other potential cases.

In short, the diagnostic system presently in place is stacked heavily against the patient.

Having thought about this for a considerable period of time I have come to the conclusion that the pyramid built by liaison psychiatry that fuels their involvement in “CFS/ME” revolves around a simple foundation assumption that a “CFS/ME” diagnosis handed to a patient must be the correct diagnosis.

If a GP or a psychiatrist carries out tests in conjunction with an immunologist or a rheumatologist; a set of negative test results is all that GP/psychiatrist/rheumatologist needs to give a “CFS/ME” diagnosis.

If that diagnosis has been handed to a patient by doctors who have little or no knowledge of complex sero-negative clinical presentations relating to rare medical diseases then there is a significant risk that the diagnosis he or she is giving their patient is in fact the wrong diagnosis.

As people reading this will know, I was subjected to a medical misdiagnosis by a number of doctor’s including GP’s and specialists.

The number of doctors involved went into double figures over a period of 12 years in total.

Over that period, my many individual symptoms were wrongly ascribed to conditions other than Behçet’s disease but in the end when all those symptoms were put together and compared to the correct diagnostic criteria for Behçet’s disease; a doctor finally looked at the evidence and came to the conclusion that I had been misdiagnosed and that I did in fact have Behçet’s disease.

In recent months I have asked pretty well all the liaison psychiatrists in the UK if they have encountered cases of Behçet’s disease passing through their out-patient clinics and none of them has replied that they had.

Professor Sir Simon Wessely for example told me that he was no Behçet’s specialist and that he would have to phone a colleague who was. Professor Wessely did not know if he had seen cases of Behçet’s pass through his clinic wrongly diagnosed as “CFS/ME”.

I recently e.mailed Professor Wessely to ask him about the outcome of his enquiries that were aided by one of his medical students but in spite of a rapid reply to my previous sequence of e.mails; Professor Sir Simon Wessely has not replied to my query regarding his findings.

I sincerely believe that I have homed in upon the Achilles heel of liaison psychiatry and their dominance of “medically unexplained” CFS/ME or indeed their latest diagnosis of Somatic Symptom Disorder.

It is my view from the evidence that liaison psychiatry; by providing doctors with the diagnostic option of CFS/ME and SSD have been responsible for the dumbing down of the clinical diagnostic process within our NHS and indeed around the world.

It is my view from the evidence that liaison psychiatry has made the potential for medical misdiagnosis acceptable practice within the medical profession as a whole.

Instead of considering rare sero-negative auto-immune disease explanations for cases of what end up as CFS/ME, a doctor now has an easy pathway to give a benign diagnosis of CFS/ME on the grounds that their set of negative test results together with a certain set of “invisible” symptoms means that the condition they are looking at is “medically unexplained” or an example of somatised symptom disorder.

Once medically misdiagnosed, the patient is disqualified from being in receipt of medications and therapies that would have been prescribed had that patient been correctly diagnosed in the first instance.

Disqualification of access to treatment will lead to that patient suffering considerably yet the doctors concerned will not recognise the severity of that patients suffering because that suffering will be put into the wrong context by that medical misdiagnosis.

I have known a case of Behçet’s disease where a patient was wrongly diagnosed as having “CFS/ME” for more than a decade and only had that misdiagnosis overturned when they suffered ocular micro-embolisms that caused permanent blindness in one eye and partial blindness in the other eye.

Away from Behçet’s we know of patients who suffered “diagnostic overshadowing” that lead to the late diagnosis of cancer and a rare heart condition.

The symptoms of cancer and the complex heart pathology were fatal in both situations and in both examples, the symptoms of neurological cancer and the heart pathology were almost certainly wrongly ascribed to the “invisible” symptoms of “CFS/ME”.

As far as the medical profession is concerned, a medical misdiagnosis or a medically missed diagnosis are considered as being “unfortunate”.

For the patient, a medical misdiagnosis or a medically missed diagnosis have profound and serious consequences and outcomes.

None of the doctors involved in making or perpetuating a medical misdiagnosis are subsequently held to account for what they have done to those patients.

In my own case, once I had been re-diagnosed I was treated as though I had simply failed back to the bottom of the pack.

There was no process of clinical education in that no investigation took place and no doctor involved was alerted to their poor clinical opinions that lead to me being medically misdiagnosed.

In short, it is my view that the clinical diagnostic process is in fact seriously flawed.

Patient’s are at risk from the medical profession at GP and specialist level.

In particular patients are at risk from an insufficient level of expertise used to make a complex diagnosis based on negative test results and a history of “invisible” physical symptoms.

Patients who present with a history of “invisible” symptoms and a set of negative routine test results are no longer referred to a super-specialist for the objective consideration of a set of relatively rare sero-negative medical diseases.

Instead, patients are given a benign diagnosis of “CFS/ME”; a diagnosis that by virtue of its own “somatisation” description – created by liaison psychiatry - is then incredibly hard or indeed impossible to overcome.

The present system seriously needs to be challenged and changed so that the patient has a fairer chance of being correctly diagnosed in the first instance and not medically misdiagnosed by inadequately qualified members of the medical profession.

The question is – how do we go about making a powerful effective challenge that effects such a change?

If we do nothing then nothing will change.

The medical profession have proven themselves happy to maintain the status quo.

As far as liaison psychiatry is concerned, it is imperative that the present system of a flawed diagnostic process stays exactly the same as it is today.

As far as immunology or rheumatology are concerned, they surely do not want their out-patient departments packed with patients who have discovered that they have been medically misdiagnosed.

A flawed diagnostic process fuels the creation of a base of “heterogeneous” patients who are subsequently involved in Cognitive Behavioural Therapy (CBT) or Graded Exercise Therapy (GET).

Those diagnosed as having “CFS/ME” are fodder for the exclusive “closed shop” self reinforcing research carried out by liaison psychiatry and no other parts of the medical profession.

One could argue that a totally unknown number of patients who are presently medically misdiagnosed with “CFS/ME” are in fact adding credence to the views of liaison psychiatry because a misdiagnosed patient will have a set of self perpetuating and untreated disabling symptoms (fueled by an unrecognised disease process) that the patient is unable to “cast off” or rid themselves of from a course of CBT or GET.

Those patients will reliably keep on reporting “somatised” “invisible” symptoms not because they have any mental impairment but because an auto-immune disease is producing those symptoms.

Such an unknown number of medically misdiagnosed patients can be accused by liaison psychiatry of being so neurotic or so somatised that they are unable to be “cured” by CBT.

Such misdiagnosed patients will be readily available year upon year for future “peer reviewed” research studies that go to reinforcing the validity of Somatised Symptom Disorder or “CFS/ME” using medically misdiagnosed patients to helpfully legitimise those artificial mental health labels.

Such misdiagnosed patients become – in the eyes of liaison psychiatry – desperately in need of even more psychiatric interventions and their sincere professional “help”.

Such patients become so firmly shunted into the somatisation cul-de-sac that they may never have their real diagnosis established unless they suffer a loss of sight or a pulmonary embolism or another “visible” crisis event such as a brain tumour or a fatal heart condition.

However, a pyramid can be reduced to rubble if the foundations are seen and recognised to be rotten.

Once it is realised that the pyramid is built on rotten foundations then when those foundations are condemned and removed, that pyramid will be reduced to rubble.

Sincerely,

Stephen Ralph DCR(D) Retired (diagnostic radiography)

See also…

http://www.meactionuk.org.uk/systemic-vasculitis-and-myalgic-encephalomyelitis.htm

Komaroff is an Idiot

I have to revise the high opinion I had of Anthony Komaroff. He jumbles all kind of definitions together and muddies the waters (when he should know better):

… What is fatigue? It's a sensation of sleepiness, muscle weakness, or a feeling that you don't have the energy to do something - either physical or mental. It's the brain that experiences fatigue; that means there are certain chemical changes in the brain that lead to fatigue - even though those chemical changes may be triggered by many different illnesses. …

Komaroff, what the heck????

No, no, no. Fatigue is not "sleepiness". Sleepiness is the urge to sleep – and you can be fatigued without being sleepy. Somnolence is "sleepiness". "Tiredeness" is maybe a combination of fatigue and "sleepiness". But one can be very well fatigued without being tired. Being chronicly "sleepy" and being chronicly "fatigued" are two different symptoms! Were you find one, it is not unusual to find the other, but they a separate sensations.

And fatigue is not the feeling of "muscle weakness". Yes, fatigue and the feeling of "muscle weakness" can go together (e.g. after doing way do much physical work) – but one can be very well fatigued without having the feeling of "muscle weakness".

Yes, one could say fatigue is the feeling that one is "lacking energy".

But for crying out loud, what is the problem with saying:
Fatigue is the feeling of EXHAUSTION.

Or you could bloody well say:
Fatigue is having the urge to rest.

And no, no, no. Fatigue (like for example the feeling of pain) is not simply "chemical changes in the brain". Both pain and fatigue are signals of the physical state of your body – if pain is the gauge of the engine temperature, then fatigue is the gauge of the petrol tank. If pain tells you "Mate, if you keep doing that, something is going end up on the fritz pretty soon", then fatigue tells you "Mate, you are running on reserve, take a rest and replenish your energy or you'll end up with power". Pain is (usually) alleviated by stopping the action that causes the pain, and fatigue is (usually) alleviated by resting. The cause is (usually) not in the brain, it is only registered in the brain.

Words fail me how someone like Komaroff, who is so seemingly methodical, can be so confused with elementary definitions of the diseases he deals with. And I find it shocking that he spreads this confusion.

PS: It is however interesting that he mentions both mental and physical fatigue, but alas, he does it not in a way that is helpful.

Will "THE" cause of ME/CFS ever be found?

Whenever I read someone writing that they are looking for "the" one cause of ME/CFS, or that even "the" one cause of ME/CFS might have been pinned down, I know that the person writing has no clue about ME/CFS.

If you take at random two persons with ME/CFS – regardless of how strict your diagnostic criteria are – chances are high that their similar diseases are caused by different things. One person's body might be tormented by an food-induced autoimmunity, the other person's body might fail to recuperate from an infection.

So I do not think that one single cause of ME/CFS will ever be found, but instead the many different causes of ME/CFS in different people will be found – one by one.

Maybe Lipkin has a fast-track to finding the most prevalent causes of ME/CFS, but he will not find a silver-bullet to solve ME/CFS, once and for all.

Giving idle talk about "THE" cause of ME/CFS (and presenting it like a silver bullet) is not giving hope, it is spreading BS.

Someone giving the impression that there might be one single cause of ME/CFS is a either a charlatan, a quack or a idiotic know-nothing bullshitter.

Is POTS / OI / NMH another form of Deyhdration?

Dr. Briffa on dehydration:

I read a review paper recently about the assessment of dehydration. The authors conclude that we don’t have very good standardised tests for dehydration, but a reasonable test is to measure heart rate when sitting, and then again immediately on standing. During dehydration the blood volume tends to be lower and blood pressure too.

On standing, there is a tendency for blood to ‘pool’ in the lower body, causing blood pressure to drop further, which may induce a reflex increase in heart rate. If the pulse rate increases by 20 beats per minute or more on standing, this is generally taken as a sign of dehydration. However, as the authors concede, this test is not a particularly reliable way of assessing dehydration, even when blood volume is significantly depleted.

Low-dose naltrexone: Better than nothing?

Low-dose naltrexone for the treatment of fibromyalgia: Findings of a small, randomized, double-blind, placebo-controlled, counterbalanced, crossover trial assessing daily pain levels.
Younger J, Noor N, McCue R, Mackey S.

Stanford University School of Medicine, Palo Alto, California.

Abstract

OBJECTIVE:
To determine whether low dosages (4.5 mg/day) of naltrexone reduce fibromyalgia severity as compared with the nonspecific effects of placebo.

In this replication and extension study of a previous clinical trial, we tested the impact of low-dose naltrexone on daily self-reported pain.

Secondary outcomes included general satisfaction with life, positive mood, sleep quality, and fatigue.

METHODS:
Thirty-one women with fibromyalgia participated in the randomized, double-blind, placebo-controlled, counterbalanced, crossover study.

During the active drug phase, participants received 4.5 mg of oral naltrexone daily.

An intensive longitudinal design was used to measure daily levels of pain.

RESULTS:
When contrasting the condition end points, we observed a significantly greater reduction of baseline pain in those taking low-dose naltrexone than in those taking placebo (28.8% reduction versus 18.0% reduction; P = 0.016).

Low-dose naltrexone was also associated with improved general satisfaction with life (P = 0.045) and with improved mood (P = 0.039), but not improved fatigue or sleep.

Thirty-two percent of participants met the criteria for response (defined as a significant reduction in pain plus a significant reduction in either fatigue or sleep problems) during low-dose naltrexone therapy, as contrasted with an 11% response rate during placebo therapy (P = 0.05).

Low-dose naltrexone was rated equally tolerable as placebo, and no serious side effects were reported.

CONCLUSION:
The preliminary evidence continues to show that low-dose naltrexone has a specific and clinically beneficial impact on fibromyalgia pain.

The medication is widely available, inexpensive, safe, and well-tolerated.

Parallel-group randomized controlled trials are needed to fully determine the efficacy of the medication.

Color me unconvinced.

The results may be "significant" in the statistical sense – and then even barely, just look at the p-values and the small sample size. To me however they don't look significant in the common sense of the word.

LDN may help some patients, a bit – so I won't blame you if you do give it a try. A cure or significant help, LDN is not.

If the (small) benefits of LDN outweigh the side-effects, that can this study not answer.

ME/CFS? Don't spend money on tests.

I just recently read about a ME/CFS patient being robbed 2500 (!) British Pounds by one of our resident ME/CFS quacks. The patient went to Belgium for a short visit, and got one blood drawing for 2500 GBPs.

Oh my, oh my, oh my.

This is not how a proper differential diagnosis is done. A differential diagnosis rather follows a "rinse and repeat" pattern:

1. First, the doctor needs to get an overview of symptoms.
2. The she/he needs to consider the symptoms and think about what it might be, or might not be.
3. The doctor should then have list of a few diseases that could be it.
4. On that basis it may make sense to order one or the other test – it makes most definitely no sense to order tests for thousands of Dollars/Euros/Pounds
5. Taking into account the test-results and the symptoms, the doctor gets a preliminary diagnosis, based on which treatment can be chosen.
6. If there are signs that the diagnosis is not the correct one, some (or all) of the steps above need to be repeated.

A diagnosis based on a short consult and expensive tests is not worth the paper on which it is printed! Every symptom could be important.

I for an example did not put enough value into my skin symptoms. Turns out the aphthous ulcers I had (together with other skin symptoms) are a key sign for Behçet's – and there is no blood test (or otherwise) for Behçet's. The only thing a doctor can do is carefully make note of all the symptoms, and knowing to look up the diagnosis of Behçet's.

Blood tests alone are a waste of money, especially if a doctor orders lots of them.

If you have ME/CFS, don't spend large amounts of money on tests – you need the money, I'm certain.

If your doctor wants to extract $$$$$ from you for diagnosis, tests or treatments: Change your doctor. Even if he claims that the tests or the treatments are a bargain. Especially if he wants thousands of bucks from you for tests and claims it is a bargain. And especially if he does the tests in an lab that is closely associated with her/him.

My advise: If a doctor sees you as a walking ATM, then change this doctor, because she/he is bad for you and your health.

There are some tests that might be called for, e.g. tests for hypothyroidism, BUT THE WORTHWHILE TESTS ARE PAID FOR BY THE INSURANCE. There are some test that might be "interesting" (like the NK-cell function test), but they do nothing to help you get "more legit" as a patient, or to choose a better therapy.

And just because someone is "Anti-CBT" or "Anti-GET", that does not mean he knows what he does.

Behçet's Disease can look like CFS

Info Video by the American Behçet's Disease Association

It all sounds so familiar. Crippling chronic fatigue, friends saying "you are faking", doctors don't now what's wrong. So people are relieved and almost happy when they finally – after years in most cases – get a proper diagnose that explains their symptoms.

Differential between Behçet's and ME/CFS is needed

Some of the symptoms of Behçet’s:

• Unpredictability: impossible to predict onset or clearing-up of symptoms, onset of symptoms sudden, difficulties in keeping to arrangements, appointments, working, affairs, managing household, family, social activities, hobbies
• Arthritis: reduced mobility or complete immobility, pain.
• Oral ulcers: pain,diet restricted to soft or liquid food, inability to eat at all, inability to talk, dribbling, dehydration, malnutrition.
• Genital ulcers: immobility, sex-life affected, embarrassment, suspicion, urinary retention, pain.
• Visual level: fear of onset of blindness, handicapping according to level of impairment and ability to adapt, pain.
• Skin: disfiguring and embarrassing skin lesions, easy bruising, poor slow healing, pain.
• Gastro-intestinal: wind, diarrhoea (with blood and mucus) or constipation, severe abdominal pain. Mimics inflammatory bowel diseases, irritable bowel syndrome. Stomach ulcers, ulcers in gullet. Risk of perforated ulcer. Dehydration, malnutrition
• Thrombophlebitis: immobility, pain.
• Thrombosis: immobility, pain. Risk of embolism.
• Ears: hearing loss, tinnitus, vertigo
• Chest: wheezing, breathlessness, haemorrhages, haemoptysis, pleurisy, pain.
• Cardio-vascular: breathlessness, haemorrhages, dysrhythmias, pericarditis, valve problems, pain. Risk of ruptured aneurysms.
• Neurological: paralysis, strokes (CVAs), transient ischemic attacks (TIAs), memory & concentration impairment, seizures, migraine-type or meningitis-type headaches, double vision, incontinence, impotence, strange sensations, motor impairment ranging from mild clumsiness to vegetative states, personality changes, psychoses.
• Fatigue: profound persistent exhaustion affecting all activity.
• Feverishness: effects like having ‘flu, night sweats, bizarre sense of feeling cold or warm.

(Remember no patient has all symptoms! See below for the diagnostic criteria for Behçet’s.)

I marked those who I think are the most prominent overlap with ME/CFS. One can see that there is some kind of overlap (not including some of the neurological and gastro-intestinal symptoms that doubtlessly some of the ME/CFS patients have as well)

If some of primary symptoms of Behçet’s (oral ulcers, eye inflammation) are not pronounced (or in rare cases even oral ulcers can be absent), then it is easy to misdiagnose Behçet’s as ME/CFS.

Again, this shows how utterly important a proper differential diagnosis is in cases of suspected ME/CFS. There are many known diseases out there that can look to the untrained eye like another case of ME/CFS.

Of course there are newer and older diagnostic criteria. These are the newer (and probably better) 2006 ICBD criteria:

Add points for every symptom:

• Oral aphthosis ("mouth ulcers"): 1 point
• Skin lesions (e.g. acne): 1 point
• Vascular lesions: 1 point
• Positive pathergy test: 1 point
• Genital aphthosis ("genital ulcers"): 2 points
• Eye lesions: 2 point

3 points or more? It is most likely Behçet's.

And what are the older diagnostic guidelines for Behçet's?

1. International Study Group strict research level guidelines for diagnosis

Must have:

• mouth ulcers (any shape,size or number at least 3 times in any 12 months)

Along with 2 out of the next 4 ‘hallmark’ symptoms:

• genital ulcers (including anal ulcers and spots in the genital region and swollen testicles or epididymitis in men)
• skin lesions (papulo-pustules, folliculitis, erythema nodosum, acne in post-adolescents not on corticosteroids)
• eye inflammation (iritis, uveitis, retinal vasculitis, cells in the vitreous)
• pathergy reaction (papule >2 mm diameter, 24-48 hrs or more after needle-prick)

2. Practical clinical guidelines for patients not included in research cohorts

Must have:

• mouth ulcers

Along with 1 out of the 4 ‘hallmark’ symptoms above

Along with 2 of the following symptoms:

• arthritis/arthralgia
• nervous system symptoms
• stomach and/or bowel inflammation
• deep vein thrombosis
• superficial thrombophlebitis
• cardiovascular problems
• inflammatory problems in chest and lungs
• problems with hearing and/or balance
• extreme exhaustion
• changes of personality, psychoses
• any other member of the family with a diagnosis of Behçet’s disease

3. 'Suspected' or 'possible' diagnosis

Usually given when someone does not have mouth ulcers or has mouth ulcers but does not have 1 of the 4 'hallmark' symptoms but has other symptoms and signs of inflammation and other causes for these have been ruled out.

Care must be taken for a differential between ME/CFS and Behçet's. As with all diagnostic criteria:

• someone who meets some set of diagnostic criteria for a disease, does not necessarily have the disease – and could have another disease instead
• and someone who barely meets the criteria may actually have the disease (see "suspected diagnosis" above)

regardless of whether it is Behçet's, ME/CFS or any other disease.