ME/CFS Research (Dr Amolak Bansal) and Management (Dr Charles Shepherd)

[TiredSam]

Splutter..

I share your spluttering. Can't work Dr Bansal out, here's a post about him I made in December last year:

Urgent help needed

Although he talks the immunologist talk, he also seems way too accepting of BPS/PACE bollocks for my liking.

 

[Valentijn]

Most people's lives are a series of challenges. But not everyone gets ME/CFS. So pointing to stress as a cause (as Dr Baranal does repeatedly) is not very helpful.

Especially when many of us were not stressed at all when becoming ill.

 

[Hutan]

Seriously though, when it comes to activity/energy management, one place where we could start is by looking at what strategies people have used (successfully and not successfully) in the very early stages of ME/CFS - i.e. in the days, weeks, months following the onset of their ME/CFS

I seem to be bashing on relentlessly here, sorry. Dr Shepherd, I have great respect for the work you do for PWME, especially given you too are sick.

So we've already covered three reasons why activity/energy management isn't a high priority for research dollars:
1. There are limited funds and it's more important to spend them on understanding the cause of the disease;
2. Without knowing the cause of the disease and having biomarkers, we can't know if any study population has the same disease and therefore will respond in the same way to rest or activity in the early stages; and
3. The whole activity/GET/rest question is politically fraught and quite likely to be hijacked by the BPS crowd.

Another one is that I rather doubt that activity levels in the early stages of the illness actually make all that much of a difference to the later outcomes. I know lots of people say 'if only I had rested' but we can't actually know. Again, it's the hindsight problem.

I've posted about my 4 data points on this before.

• I had ME/CFS when young. I mostly rested and I recovered in a year.
• I was well until my late 40's when I became ill again. I mostly stayed active and, although I'm better than I was, I am still quite affected.

So far the data points support the 'rest is best' camp. BUT

• My son got ME/CFS at the same time as my second bout. He mostly rested as his joint pain was quite severe. He is still sick.
• My daughter got ME/CFS at the same time too. She mostly kept active. She recovered to nearly 100% in two years.

So, even with similar genetics and the same illness, there is no recovery pattern related to whether we rested or remained active.

If you combine that sort of variability with a study population that may well include different diseases and certainly different subsets and throw in a researcher or two who has a preconceived idea of what the outcome should be; I think you have a recipe for unhelpful research.

 

[Seven7]

Huh. I tested positive for that one too, @lnester7... and muscle and joint pain is a problem, especially in the legs.

I also have the blood pooling type pain that one is more in big muscles and I know because when I put the compression stoking it goes away.

I guess I am saying the pain in CFS has to be deconstructed and I do not think is one type nor one reason.

 

[Dolphin]

J Intern Med. 2010 Sep;268(3):265-78. doi: 10.1111/j.1365-2796.2010.02228.x. Epub 2010 Mar 3.
Pain inhibition and postexertional malaise in myalgic encephalomyelitis/chronic fatigue syndrome: an experimental study.
Van Oosterwijck J1, Nijs J, Meeus M, Lefever I, Huybrechts L, Lambrecht L, Paul L.

RESULTS:
In patients with ME/CFS, pain thresholds decreased following both types of exercise, whereas they increased in healthy subjects.

http://www.ncbi.nlm.nih.gov/pubmed/20412374

 

[Dolphin]

Pain. 2004 Jun;109(3):497-9.
Exercise lowers pain threshold in chronic fatigue syndrome.
Whiteside A1, Hansen S, Chaudhuri A.

Pain thresholds, measured in the skin web between thumb and index finger, increased in control subjects with exercise while it decreased in the CFS subjects.

 

[Large Donner]

RE STRESS

With regard to stress, two points that Amolak was making were that:

1 Chronic on-going stress can disrupt the HPA axis and cortisol production. So when a significant acute stressor then appears - eg an infection - a past history of chronic stress could be creating fertile ground for an infection to trigger ME/CFS

On a personal basis, I was working one of these dreadful 1 in 2 rotas (ie working every day and every other night) that docs used to have to do in a very busy hospital

So I think that undue physical and mental stress (which I didn't actually have any obvious problem with at the time) may have acted as a co-factor when an episode of chickenpox (which I caught from a patient) tiggeed my own ME

So did all the doctors doing this rota get ME?

 

[daisybell]

I find Dr Bansal's comments about exercise and endorphins interesting because my experience, which I think is shared (from reading the posts of others on various threads), is that we no longer feel any endorphin release from exercise. Maybe some is occurring but that endorphin rush I used to get on occasion when out running - when you feel on top of the world, and that you could run for ever - has COMPLETELY gone. My muscles never feel good for exercise, and I only ever feel tired and drained now.

I am still relatively active in that my lifestyle involves gardening and looking after animals, but I now have to go slow and pace myself very carefully. Aerobic type exercise is a big mistake. Also, I am very likely to get specific muscle soreness like I have pulled muscles if I do anything which requires more strength - I only need to do that movement once, and I feel as if I have pulled that muscle for several days.

So for me, reading that comment just makes me feel that Dr Bansal doesn't understand our disease.

 

[Research 1st]

Well, what you wrote that prompted my comment was:
So, that was specifically about increasing physical activity, not pacing or energy management.

I remain of the view that the most important research right now is understanding what causes the disease. Until then and until we can accurately identify people that actually have the same disease, any studies on whether rest or activity changes the outcome of the illness is severely compromised. How can you possibly know if the population you are studying all has the same disease?

I like your thinking, as its logical thinking.

We know the 'stress theory' as triggering the single disease ME isn't scientifically or medically accurate as the disease ME cannot be identified in its present state. This is because ME has become CFS (research wise), and CFS is not one illness but many involving Chronic Subjective Fatigue. Within subjective reports of fatigue have been found to be biological (NK dysfunction, POTS, Low Cortisol etc) and some psychological discoveries (Oxford CFS criteria where some find CBT helpful). As a consequence, what triggers or maintains CFS is thus wide open to researcher bias, one of these biases is 'stress theory'. (It's known stress weakens the immune system, as does lack of sleep etc, so hardly difficult for anyone to think of this as an idea).

If scientists can't accurately identify the patients they THINK they are researching in a study, then they don't KNOW they are looking at PWME at all. Ergo, their theory of 'stress' cannot be robust and will always remain experimental, because no objective markers are used to diagnose CFS and people with ME are excluded from influential research studies on CFS by sticking to weak diagnostic criteria, that shun the inclusion associated signs of Myaglic Encephalomyeltis(such as TILT demonstrated Autonomic Dysfunction). These 'effects' of presumed ME gets you REMOVED from CFS research. (POTS, for example, is an explained reason for many symptoms of CFS). The reality is PWME can develop POTS as a co-morbidty, as those with Diabetes and MS can also. Interestingly, if you have POTS but have MS, you aren't told you don't have MS and cannot be researcherd as MS- but within CFS research you are.

From all this we get studies that suggest (example here) that 56% of people with CFS report they were stressed at the onset of CFS and developed EBV. This actually means nothing as CFS 'patients' don't need to have anything wrong with them medically, to be diagnosed with CFS (other than meet a weak exclusion based criteria of self report symptoms). Thus no correlation can be made between not recovering from EBV, as we don't know the patient hasn't recovered, they just believe they haven't. Psychiatry knows this, psychiatry manipulate this to promote CFS as mind-body. Easy to do, and easy to suggest to Governments as cost effective (See UK NHS Socialized cost effective tax payer funded system).

Researchers then calling these people (E.g. post infectious EBV with CFS who benefit from CBT), 'ME' also means nothing, and doesn't medically associate CFS to ME, just with a name change (CFS into ME/CFS), as I see the NIH and others tend to do more recently. These are all just ideas of researchers, not science behind their claims, because the claim is based on the report of the patient being accurate -with no test, we don't have accuracy.

When these (theoretical) 56% of patients all carry the same autoimmune markers, share the same inflammatory profile etc, then we 're talking Science. Currently, it's all pseudo science as it's not very hard to promote 'stress' in people with fatigue as being associated to immunity and fatigue, as the two are inextricably linked. This doesn't mean there is any fact in the theory though.

This statistical flaw is further worsened by patient bias, because we don't know WHO the patients are
for sure:

For example:
Some patients believe stress caused their ME as a trigger. Conversely, some patients say they weren't stressed at all had a stress free fantastic life, caught an infection/had a vaccine etc, and were never the same again. Both claim to have ME. Do they? No one knows. Maybe they do and 'stress' was just a by-stander, just as it is in all other diseases not lassoed by the BPS Lobby, allied to Government bodies who fund CFS research.

Both sides of the argument are only 'correct' about their theories, when in a prototype diagnosis. Sadly, that is what CFS and ME are:. Until the bi-polar opposite groups are tested for the pathogen/autommunity, this then proven to cause Myalgic Encephalomyelitis (on neuro-imaging and allied inflammatory panels), who presumably will have a diffuse autoimmune disease affecting Mitochondria and these findings proven to cause relapse from minor physical/mental exertion **with a delayed effect** due to various complex things we can only speculate about at this present moment in time.

Well, until then....People will always claim to have ME, but don't know they have it. This includes all of us, no matter how disabled we are. Until Science filters out ME from CFS, no one can prove to have 'it'. This is why psychiatry holds the ME community prisoner. Mind-Body-Immune theories are out of control, because this is what happens when lobbying is done, to prevent separation of severely neuro (autonomic/neuropathy) affected cohorts from mildly affected in research.

How did this happen? Well we should go back to the CDC, who caused all this to happen and observe:

The fundamental error in ME CFS research due to CDC Fukuda Criteria: Any ME patient with explained reasons for fatigue are removed from CFS research, because explained is not unexplained.

CFS should always be unexplained Chronic Fatigue, meaning the multiple co-morbidities of ME that develop over time, get your disease IGNORED A terrible tragedy, life destroying and life ending for some.

In medicine we have two current Epidemics, both denied by Government. Chronic Lyme & ME (CFS).
If people didn't know, I will remind them. Untreated Lyme Neuroborreolosis can lead to Encephalomyelitis. An additional feature of untreated (neurodamage) Lyme, is Myalgia. Lyme patients can thus develop a: Myalgia & Encephalomyeltiis. Sound familiar?

Myalgia & Encephalomyeltiis (effects of neuro Lyme said not to exist chronically).
Myalgic Encephalomyelitis. (said not to exist by the state and to be CFS).

Both have identical symptoms, identical inflamamtory cytokine profile, identical 'Flu that never went away' onset.
This relatively recent 'finding' that untreated Chronic Lyme possibly being ME, is why we have this huge fight on our hands (behind closed doors) in 2017-2020 when the autoimmune theories Vs HERV retroviruses will clash horns.

One group wants to prove Chronic untreated, but novel, Lyme = ME and associated to multiple HERV infections that go on to affect Heat Shock Proteins and Mitochondria leading to a metabolic disease (ATP) in which exercise is impossible.

Vs

The other (government groups) wants CFS to be an autoimmune disease of unknown cause leading to neuropsychiatric changes, in which CBT and GET are useful. Stress in that model can be the 'pathogen'
And anyone can have it, with a blood test to show these markers lead to FATIGUE.

To determine the logical (correct) research path for ME, we need to separate ME from CFS (this still hasn't been achieved due to lobbying by Psychiatry and the scarcity of state funded research focussing on Fatigue, not cardinal signs of ME - autonomic dysfunction, muscle inflammation/pain/weakness, chronic immune activation).

Even if we did do this tomorrow,(will never happen) we need to research the correct people (which still hasn't been achieved, but may start to occur with the likes of Ron Davis in America looking at the severely affected). However, they are still using the label 'ME/CFS' in their study,meaning any novel findings will not be associated to Myalgic Encephalomyleitis, but ME/CFS instead (ME/CFS doesn't exist other than conceptually). See: http://www.openmedicinefoundation.org/mecfs-severely-ill-big-data-study/

So even the 'good guys' forget If the word 'CFS' is associated to the severely affected study, then other studies (Psych CFS studies) won't find the same findings (due to heterogenous cohorts) and thus the findings of the severely affected in Ron Davis's study can be dismissed as a 'blip', as the NIH/ CDC would simply announce, that's only 25% of people (or less) are that sick, ergo 'ME/CFS' is not what ever Ron Davis's team find and CFS remains a mystery (as they have claimed since 1988). But that's another issue for the future.

Back to the 'stress' debate (conjecture science):

Logic dictates:

You wouldn't search for HIV in a 1980's cohort of heterosexual males who have the common cold who became sick after an 'event', you would search for HIV in gay men with cancer, immune suppression and wasting disease to draw blood from. By doing this, it was concluded that untreated HIV leads to AIDS and then not a 'Gay Disease' (Gay Cancer) but an infection that could infect anyone once babies and pregnant women were found also to have HIV.

Until this happens with ME (breakthrough in Science studying people with signs of Myalgic Encephalomyleitis, not Fukuda CFS) researcher biased ideas about 'stress' (or any other reason) come to the forefront, often with the encouragement of patients, because some patients report they were stressed at work/school and ''came down with ME''. That's their experience, legitimate and to be researched. However, not all patents report this. More heterogenous cohorts once again, just what we don't need.

We have to look for other reasons then, other than 'stress' theory alone. ME also occurs immediately
after vaccines (we all have vaccines in the Western world as babies), and after infection where the patient is not mentally stressed, but the body is due to massive NF-Kappa B activation. Other patients report chemical exposure, such as walking next to a farmers field, or working on a farm where agricultural levels of pesticides are sprayed, and inhaled. (Nerve toxins). How do we even know these people have ME at all? We don't, but what we do know, is they all had vaccines.

Those with a keen eye for science will note decades AFTER the inducement of ME, people with ME still have raised
NF-Kappa B & Cytokines for decades, thus proving a chronically activated immune system (along with the massive cytokine expression). Lipkin and Hornig find the opposite, but they are studying CFS and calling it ME/CFS so I ignore them as I don't have their lack of inflammation but high levels of inflammation after 30 years, not 3 years.

So Lipkin's study patients, have a different disease presentation than mine. Unfortunately, the MRC (Fatigue based, pro PACE research) is going along the lines of Lipkin and shunning others who want Lyme and Retroviruses studied because if they didn't, they would lose their jobs. (Government health agencies study cancer, and thus they will be implicated in infecting the labs with mad made retroviruses - decades ago as well as now). These agencies fund CFS 'research' and will not study people with severe ME (had decades to do this)- you do the math.

Conclusion:

Problem 1: People with Ramsay ME want ME for themselves, as their disease is 'described' adequately for them.

Problem 2: Government researchers want to legitimize Organic CFS, by referring to Fukuda CFS criteria patients as 'ME', but these research do NOT want ME to be a Chronic Inflammatory disease allied to Lyme/Retroviruses as then we have a historical link back to VACCINES and Governments will have to pay COMPENSATION for Vaccine Injury, if the patients can PROVE they have man mad biologicals inside them, whose origins are in CONTAMINATED Cancer research labs. (NB: The patients and controls in the Lipkin study had antibodies to these man made retroviruses in which people with ME were all excluded from the study. (Organic diseases (that PWME develop) were exclusionary criteria ). Hence the failed study (of course) shows no difference between man made retroviral antibodies in healthy vs CFS . This is what the Government and Fauci wanted, so they got it with Mkovits's name on the negative paper, (despite her not being allowed to influence the study design as she was in jail at one point and forbidden to set foot on any government property or she would be arrested).

Both 'ideas' about ME cannot be right can they? And electronmicrographs of retroviruses isolated from CFS patients don't have bias, they are images taken from an microscope that sees rather than believes.

In time, it will be logical that maybe 10% or so of people with ME who believe they have ME (diagnosed by a doctor)
have ME, and 90% have something else. This is entirely predictable (predictable tragedy) if the CDC tell people
with multiple reasons for fatigue, (post viral and not post viral) they all have CFS and (CFS/ME = ME).

This is the fundamental problem in Science and Medicine today with ME + CFS. Maybe 10 or so different conditions using the same label, and wrecking research studies because of it, because:

Patient bias and Research bias can conjoin, to produce 'evidence' to claim Factor A, B, C is associated to 'ME/CFS' without knowing what ME/CFS actually is, and not stopping to think of the lunacy, of placing a forward slash infront of two acronyms. Sleep Apnea/Aspergillosis doesn't exist for a reason, and both involve respiratory function and Fatigue (the bizarre excuse fans of ME/CFS (to replace ME) is both ME and CFS involve Fatigue and reports of weakness) so it must be the same condition.

So in conclusion researchers and patients are entirely correct to claim ME is associated to stress, but they are also entirely wrong.

Catch 22.

 

[Seven7]

Parvovirus and ME/CFS - an interesting sub-group?

FYI, I am in the low NK cell subgroup (in my case activity and number), My primary virus is HH6V, that is the one that never gets under control. Parvo was secondary (since it comes and goes) successfully treated with equilibrant + Famvir. If the NK go way low random viruses reactivates, within them Parvo.

Funny enough the group of patients that started treatment about the same time as me, basically same story but usually the main virus (the one you have trouble to keep suppressed) does changes: EBV or HH6v or CMV. are the ones I have come acrossed (with the same immune testing I get). I did get EBV when my hh6v was way high but I suppress EBV ok (unless the NK goes way down). I have not been successful to raise NK because I do not tolerate the imunovir (immune modulator) at full dose.

Another patient that had EBV as primary, he is in CFS remission and successfully raised NK. Other than having to check NKs once a year, he is all normal. So I have hope if at least the NK sub group can keep the Nks level raised maybe we can be normal. I have had 3 remissions but very short lived (I struggle with POTs too).

Since I am feeling so much better these days, It will be interesting to see if my numbers are higher. Will keep posted here. I have my annual NK (activity and numbers) test coming up in a month. I added inosine to the imunovir.

Ahhh also when I was first tested (maybe 5 years into CFS) My B cells were very high and T cells low. Citokines all over the place: TNFI and II low, IL10 high, I always have IL1-b super low (apparently most of my Drs patients do)........., I can share the tests if you are interested in more details.

 

[charles shepherd]

So did all the doctors doing this rota get ME?

No - possibly because none of my nursing or medical colleagues at the time contracted a chickenpox encephalitis from the patient on the ward who had a nasty dose of shingles (= reactivation of chickenpox virus)

Professor Peter Behan (at the Institute of Neurological Sciences in Glasgow) and myself have always been interested in patients with ME/CFS where the viral trigger has been either chickenpox or shingles - because there appears to be a link with a more severe and persistent form of ME/CFS

 

[duncan]

Interesting claim, @charles shepherd . ME triggered by other viruses or bacteria is not as severe and not as persistent as ME/CFS brought about by herpes zoster?

 

[Large Donner]

No - possibly because none of my nursing or medical colleagues at the time contracted a chickenpox encephalitis from the patient on the ward who had a nasty dose of shingles (= reactivation of chickenpox virus)

Professor Peter Behan (at the Institute of Neurological Sciences in Glasgow) and myself have always been interested in patients with ME/CFS where the viral trigger has been either chickenpox or shingles - because there appears to be a link with a more severe and persistent form of ME/CFS

So they were all doing the same rota and none of them got chicken pox or ME? Does that include all the nurses that often do 12 hour shifts and nights that came into contact with the patient also, did they get ME?

Do you know if any of the other hospital staff, like porters or the meal service people who work long hours for little pay, who would have been around the chicken pox patient got the same virus or ME?

What about the patients family who would have been in direct contact with him, did they contract the virus or get ME?

Do you know if the student doctors who are now on strike to fight against the appallingly long difficult hours they work contract ME in any significant numbers as they are in constant contact with sick patients also?

 

[Sea]

• My son got ME/CFS at the same time as my second bout. He mostly rested as his joint pain was quite severe. He is still sick.
• My daughter got ME/CFS at the same time too. She mostly kept active. She recovered to nearly 100% in two years.

The Dubbo study showed us that those more severely ill with the virus that struck them down were the most likely to get ME/CFS. I think also those who recover in 2 years are less sick than those who don't recover. I think those who can remain active are less sick than those who cannot. I doubt it is the being active, rather the ability to remain active that is the difference.

 

[charles shepherd]

I cannot recall anyone else in the hospital - staff or patients - catching chickenpox from this patient

Remember, chickenpox in adults is fairly uncommon - partly because many adults have caught it as a child (which I did not)

But when chickenpox does occur in adults it tends to be more severe than in children and can lead to more serious complications, including encephalitis

At the time, as I say, I was working a normal 35 - 40 hour week, as well as being on call every other night and weekend - which normally involved working late into the evening and then having to return to the ward or casualty several times during the night

Fortunately, this sort of crazy rota no longer happens but it was a form of physical and mental stress

Having seen a vast number of people with ME/CFS over the past 30+ years, and gone into their medical histories in considerable detail, my impression is that physical and/or mental stress can sometimes be a co-factor in the development of ME/CFS

Please note that I am not saying that stress causes ME/CFS - just that is in many other medical conditions stress can sometimes play a role in both triggering, exacerbating and maintaining an illness

As far as health workers today are concerned, I know a considerable number of doctors and nurses who have developed ME/CFS and whilst not backed up by any epidemiological evidence my gut feeling is that there is an increased incidence of ME/CFS amongst health workers (and teachers as well)

 

[BurnA]

We really do need to be adding research into this crucial aspect of very early management into the ME/CFS research portfoli

Sorry if it seems like I am nitpicking too.
We dont actually know it's a crucial aspect do we?
We don't even know if management plays any role in progression - there seem to be patients who push themselves continuously, suffer short term setbacks but get then going again, and then there are other patients who rest, stop work and still continue to decline ...

Having seen a vast number of people with ME/CFS over the past 30+ years, and gone into their medical histories in considerable detail, my impression is that physical and/or mental stress can sometimes be a co-factor in the development of ME/CFS

I feel like I am challenging you but Im just trying to understand this. How many non ME CFS people have you met who lead stressful lives ? I'd wager most people would say they are stressed and even more so when someone gets sick because it's only human to try to link it to something.

Given the history of linking stress to ulcers I'm very wary of any association with stress. I'd say most people beloved they were stressed before they got an ulcer when they were told that's what causes it.

Ask everyone you meet tomorrow if they are stressed and see what they say.

If stress played a role surely with the financial crises since 2008 we would have seen a surge in ME ?

 

[BurnA]

As far as health workers today are concerned, I know a considerable number of doctors and nurses who have developed ME/CFS and whilst not backed up by any epidemiological evidence my gut feeling is that there is an increased incidence of ME/CFS amongst health workers (and teachers as well)

Would you say that this is down to increased exposure to viral infections ?

 

[charles shepherd]

Would you say that this is down to increased exposure to viral infections ?

I think there are a number of reasons why health workers MAY be at increased risk of developing ME/CFS

First is the obvious fact that in some cases this involves dealing with people who have infections

Second is the increased use of vaccinations for occupational health reasons - I have collected a considerable number of health workers over the years who clearly predate the onset of their illness to a vaccination, hepatitis B in particular

Third is that health workers tend to be very conscientious and often continue working when ill - I certainly did and I believe that this made my condition considerably worse as a result………

Fourth (and I know some will disagree strongly) is the fact that some aspects of medical work are very stressful - both mentally and physically - and as already discussed, I believe that chronic stress (due to the effect on the HPA, cortisol and immune system function) can play a role in making some people more susceptible to developing ME/CFS when the right trigger factor (i.e. an infection) appears

 

[duncan]

Much the same can be said of parents, @charles shepherd . But parents are not more likely to develop ME/CFS - at least, not that I am aware.

 

[Large Donner]

I feel like I am challenging you but Im just trying to understand this. How many non ME CFS people have you met who lead stressful lives ? I'd wager most people would say they are stressed and even more so when someone gets sick because it's only human to try to link it to something.

Given the history of linking stress to ulcers I'm very wary of any association with stress. I'd say most people beloved they were stressed before they got an ulcer when they were told that's what causes it.

Ask everyone you meet tomorrow if they are stressed and see what they say.

If stress played a role surely with the financial crises since 2008 we would have seen a surge in ME ?

That is a great summary!!