POLL: Which standard ME/CFS treatment protocols have you tried, and which led to major improvements?

[Stretched]

So you didn’t have any bad reaction to
Famciclovir? I can’t eat anything since I took it and I feel like I need to go to the hospital... how depressing

‘Sorry it’s not going good for you. Is there possibly a bad combo of medicines or especially foods which might be contrary to the Famvir? Also, how about state of physical health, e.g. a general malaise, stress, depression?

Try webMD review for ideas of contraindications, like milk or general dairy?

Maybe an analogue would work, i.e. another same level rx in this class of AV?

 

[heapsreal]

This occurrence, periodically leads me to think CFS has a direct brain/sleep component, especially considering that agressive rest otherwise lightens the ill load.

I think its why some cfs gurus consider cfs/me a neuroimmune disorder . I think the infections are possible neuro infections causing damage to the hypothalamus in the brain. Just look up hypothalamus function and many of them dont work too well in cfsers.

Many cfsers have crappy hormones from cortisol, dhea to the different sex hormones to aldosterone and other hormones that control fluid and electrolyte balance. All generally controlled by signalling from the hypothalamus or hpa axis. Its trial and error plus time to get on top of these issues plus infections.

 

[Stretched]

@heapsreal You know, seems there would be a cure imminent, just around the corner. The researchers have been onto this for some time now.
Maybe it’s a matter of hitting on the application of an existing drug. The brain chemistry is delicate and consequential but when you think about it there are
umpteen drugs routinely rxd for it: anti-depessants, sleep rx, tranquilizers, et al. Wouldn’t it be ironic if one of these ubiquitous neuro drugs rather than a virus
turns out to be implicated in CFS

 

[BadBadBear]

I think its why some cfs gurus consider cfs/me a neuroimmune disorder . I think the infections are possible neuro infections causing damage to the hypothalamus in the brain. Just look up hypothalamus function and many of them dont work too well in cfsers.

I have thought the same, that something happens to the hypothalamus. Not only did my HPA go off the rails, but my HPT (thyroid) does some whacky stuff. It all points to the hypothalamus.

 

[heapsreal]

@heapsreal You know, seems there would be a cure imminent, just around the corner. The researchers have been onto this for some time now.
Maybe it’s a matter of hitting on the application of an existing drug. The brain chemistry is delicate and consequential but when you think about it there are
umpteen drugs routinely rxd for it: anti-depessants, sleep rx, tranquilizers, et al. Wouldn’t it be ironic if one of these ubiquitous neuro drugs rather than a virus
turns out to be implicated in CFS

One reason i looked further into hormones was that prior to arvs for hiv patients, one treatment that improved their quality of life, reversed severe muscle wasting and to drs suprise increase immune function was the use of anabolic steroids. This was keeping hiv people alive longer and then later direct treatment with arvs put many into remission. I will say that doses used were within a normal range not mega high doses that bodybuilders use and they were regularly monitored.

I remember reading a document from the early 1990s. This dr explained that many chronic conditions as well as cfs, the patient is in a catabolic state ie the body is being broken down faster than its ability to repair itself. So the anabolic - catabolic ratio leans towards the catabolic state. In a catabolic state you have increased inflammation, increased oxidative stress a lowering of immune function. This dr wrote that treating patients with testosterone or deca durabolin reversed this catabolic state and cfsers started to improve.

Its much easier to treat a guy with these hormones as they are basically male hormones but many anabolic steroids were developed to minimize tge masculinizing effects of them. So there are a couple of steroids that are safe for females if properly monitored that can avoid masculinizing symptoms yet still reverse this catabolic state.

Many of these drugs have been around for over 50 years, its a shame the media has demonized them. When used properly and supervised by a doctor they are very safe drugs but can have profound improvements in people's health.

So i think there are other drugsout there that could help many cfsers but i think too much of medicine is about making $$$ and treating symptomatically making you a patient for life. If there was one drug that could treat many issues and reduce the need for other drugs, this would be much better for the patient. But economically for many drs this would have a negative impact on buying their new Mercedes. Even if a doctor wanted to treat you a certain way, he is controlled by some much regulation that he is just stuck with cookie cutter type treatments eg cfs, antidepressants and exercise.

 

[heapsreal]

I have thought the same, that something happens to the hypothalamus. Not only did my HPA go off the rails, but my HPT (thyroid) does some whacky stuff. It all points to the hypothalamus.

Another interesting benefit i had from trt and helped me drop another drug i was taking was its effects on fluid and electrolyte balance . Previously I have had several blood work showing i was dehydrated even though my fluid intake was high but my output was very high, 10litres a day down the toilet. One hormone that can cause issues here is low aldosterone, and this can also impact pots/oi symptoms. Blood test i had showed normal levels but my 24hr urine collection showed theres a problem when one normally pees 1.5litres a day and i was pumping out 10 litres a day. But was put on desmopressin, a synthetic aldosterone drug. It helped but it obviously wasnt the issue until i treated my low testosterone and no longer need desmopressin and my urine output went back to normal.

I just mention this because there are so many functions hormones do that we dont realise, even many drs dont. Even things like thyroid are dependent on adequate cortisol levels.

One can go down a rabbit whole with all this but in simple terms one could get hormones tested and replace what needs replacing to an optimum level.

 

[Stretched]

So i think there are other drugsout there that could help many cfsers but i think too much of medicine is about making $$$ and treating symptomatically making you a patient for life. If there was one drug that could treat many issues and reduce the need for other drugs, this would be much better for the patient. But economically for many drs this would have a negative impact on buying their new Mercedes. Even if a doctor wanted to treat you a certain way, he is controlled by some much regulation that he is just stuck with cookie cutter type treatments eg cfs, antidepressants and exercise.

Here, here! Well said.

Damn shame GP Medicine has deteriorated; many doctors leaving profession.

BTW I remember using anabolics in my youth when I was seriously working out. We were all a little nervous about taking them, then (100 years ago,)

 

[Stretched]

Regarding this discussion, consider the anti viral theory of CFS.

I had a lightbulb which I posted elsewhere in PR today: Apply Biopsychosocial BPS abuse model to GWI, which Klimas parallels with CFS and you get a reasonable basis for examining non-viral causation. (“You live with constantly heightened cortisol levels. this has its effects on first gut, the immunesystem and so on. these are simple facts. That's the Bio part of BioPsychoSocial.” - @Sundancer, PR, 2/2/18.)

GWI fits the BPS abuse model, accelerated. IOW, look at the symptoms of BPS abuse over time and you indeed get similar symptoms to the otherwise accelerated symptoms of GWI and CFS.

I’m curious if she has thought along these lines in modeling her GWI and CFS similarities? It certainly seems to take the viral component out of the equation (which hasn’t solved anything as yet) and focuses on the immune system gone haywire, ergo the HPA axis dysfunction.

 

[JES]

Regarding this discussion, consider the anti viral theory of CFS.

I had a lightbulb which I posted elsewhere in PR today: Apply Biopsychosocial BPS abuse model to GWI, which Klimas parallels with CFS and you get a reasonable basis for examining non-viral causation. (“You live with constantly heightened cortisol levels. this has its effects on first gut, the immunesystem and so on. these are simple facts. That's the Bio part of BioPsychoSocial.” - @Sundancer, PR, 2/2/18.)

GWI fits the BPS abuse model, accelerated. IOW, look at the symptoms of BPS abuse over time and you indeed get similar symptoms to the otherwise accelerated symptoms of GWI and CFS.

I’m curious if she has thought along these lines in modeling her GWI and CFS similarities? It certainly seems to take the viral component out of the equation (which hasn’t solved anything as yet) and focuses on the immune system gone haywire, ergo the HPA axis dysfunction.

This model would perhaps fit GWI, but doesn't explain the typical case of CFS/ME, which often starts when a previously physically and mentally healthy person gets struck with an infection, which then triggers CFS/ME, sometimes within a matter of days. There is simply no place to fit the BPS model to explain all of this.

 

[Stretched]

This model would perhaps fit GWI, but doesn't explain the typical case of CFS/ME, which often starts when a previously physically and mentally healthy person gets struck with an infection, which then triggers CFS/ME, sometimes within a matter of days. There is simply no place to fit the BPS model to explain all of this.

But how do we know s/he gets struck with an ‘infection?’ Couldn’t that otherwise infection be e.g. a hypercortisol or other immune factor racing over a period of time,
with or without the concurrence of a ‘bug’?

FWIW, at the onset of my CFS, 30+ years ago I distinctly called the doctor’s attention to my feeling a ‘bug’ moving from throat to stomach areas and back again. All his testing could find no ‘bug’, infection... . Something hit hard because after that I was in decline from a super healthy state, albeit hyper stressed from work.

 

[JES]

But how do we know s/he gets struck with an ‘infection?’ Couldn’t that otherwise infection be e.g. a hypercortisol or other immune factor racing over a period of time,
with or without the concurrence of a ‘bug’?

FWIW, at the onset of my CFS, 30+ years ago I distinctly called the doctor’s attention to my feeling a ‘bug’ moving from throat to stomach areas and back again. All his testing could find no ‘bug’, infection... . Something hit hard because after that I was in decline from a super healthy state, albeit hyper stressed from work.

Infection being a trigger is generally accepted even among the BPS crowd. You are right that it hasn't necessarily been proven to be a virus, but what has been demonstrated is that typical acute "viral" symptoms often precede CFS, such as fever, swollen lymph nodes, etc. Now it could be something else than a bug causing it, but to me it sounds pretty far-fetched, because they are exactly the symptoms people get when they catch a cold/flu.

Regarding stressors, if this model was correct, one would furthermore think that people in stressful jobs (say the president of a country, or some shift worker) would more likely come down with CFS. But this doesn't seem to happen, even the war veterans who got it seems to be mostly from one specific war, which makes me think it probably was something environmental rather than stress alone.

 

[ljimbo423]

But how do we know s/he gets struck with an ‘infection?’ Couldn’t that otherwise infection be e.g. a hypercortisol or other immune factor racing over a period of time,
with or without the concurrence of a ‘bug’?

FWIW, at the onset of my CFS, 30+ years ago I distinctly called the doctor’s attention to my feeling a ‘bug’ moving from throat to stomach areas and back again. All his testing could find no ‘bug’, infection... . Something hit hard because after that I was in decline from a super healthy state, albeit hyper stressed from work.

One thing all of the triggers to CFS/ME have in common seems to be inflammation. Stress, infections of any kind, etc, all cause an increase in inflammation. An increase in inflammation can cause intestinal hyper-permeability or leaky gut.

Systemic inflammation results in an increased intestinal permeability. The increase in intestinal permeability is most likely caused by inflammation-induced paracellular permeability, rather than ischemia-mediated enterocyte damage.

LINK

Intestinal permeability is normal and happens to everyone, however-

Chris Armstrong/CFS researcher says-

"Well we all experience a bacteremia when we exercise. The type of bacteria that enter your bloodstream are usually quite controllable by your immune system but if your gut is further compromised they may release more bacteria into your blood or more pathogenic species or your immune system may already be depleted.

This is the concept for the chronic sepsis or SIRS and this is what I think may be behind PEM."

LINK

I think what happens to many people with CFS is that they already have some degree of dysbiosis and intestinal permeability.

The "triggers" are just enough to tip a person into CFS. Systemic inflammation can cause increased intestinal permeability and increased intestinal permeability, increases systemic inflammation.

Which I think might cause locked feedback loop, keeping the intestinal permeability, locked in place. The only "bugs" to be found would be in the gut.

It's the lipopolysaccharides (LPS) from the cell membranes of gram negative bacteria in the gut, that get into the bloodstream and are causing an immune system reaction, not the bacteria themselves.

Just my 2 cents worth.

Jim

 

[junkcrap50]

ARUP Lab, which uses the antibody micro-neutralization technique?

Can antibody microneutralization technique be done for other viruses, like EBV & CMV?

 

[Hip]

Can antibody microneutralization technique be done for other viruses, like EBV & CMV?

I believe so, but simpler antibody testing methods such as ELISA or IFA seem to be able to detect high titers to herpesvirus in ME/CFS patients, so neutralization may not offer any further advantages. Whereas for enterovirus, my understanding is that ELISA and IFA may struggle to detect the high titers / chronic infections found in ME/CFS, but neutralization has no trouble detecting these infections.

Antibody testing by neutralization takes more work at the lab, which is why I believe you don't get many labs offering it. But it's the gold standard of antibody testing.

 

[ebethc]

@Hip
This poll is from current PR readers, correct? (vs ppl who have left the forum for whatever reason, including improvement)

do you have any insight why valcyte is more successful than valtrex, etc.?

don't AV's have an anti-inflammatory effect? could that be the reason ppl improve? do blood test titers go down?

 

[Hip]

This poll is from current PR readers, correct? (vs ppl who have left the forum for whatever reason, including improvement)

The poll when it was conducted in 2018 was answered by people on this forum. You can actually see the member names of people who voted if you click on Votes, for example:

do you have any insight why valcyte is more successful than valtrex, etc.?

Not really, I was wondering myself why Valcyte seems much better than Valtrex. Maybe it is because Valcyte is a broader-spectrum antiviral for herpesviruses, so targets other herpesviruses in the patient that are active, but perhaps do not show up as high antibody levels (so the patient is not aware they have those herpesviruses as active infections).

don't AV's have an anti-inflammatory effect?

Not sure. It was originally thought that Valcyte might have an anti-inflammatory effect in the brain, by calming activated microglia. But then a later study refuted this.

 

[ebethc]

@Hip

Do you know if Valcyte causes titers to go down?

 

[Hip]

Do you know if Valcyte causes titers to go down?

I can't remember offhand, but it might be worth checking the studies, which are detailed in this post.

 

[gbells]

If you want to answer the poll, please see read the info below.

For a summary of the poll results, see here:




This poll asks which standard ME/CFS treatment protocols have resulted in major improvements in your overall ME/CFS symptoms, which treatments have resulted in minor improvements, and which treatments resulted in no improvements (if a treatment actually made you worse, then please choose the no improvement option).

Note that here we are using the terms "major" and "minor" with a precise definition:

A major improvement is defined as one where a patient moves up one level on the ME/CFS severity scale of very severe, severe, moderate, mild and remission. For example, if after treatment a patient moves up from severe to moderate, or moves up from mild to remission, those types of one-level improvements are classed as major.

So if you obtained such a major improvement from one of the treatment protocols in this poll, please vote accordingly.

If the health improvement you got from the treatment protocol was less than major, but is nevertheless definitely noticeable, that is defined as a minor improvement. If you had a minor improvement, please vote accordingly.

Minor is quite a broad category in this poll: from relatively small but clearly noticeable improvements, right up to significant improvements — but ones which are not quite large enough to be classed a major improvement.

In this poll, obviously only vote for treatments protocols that you have properly tried out. Do not vote for a treatment if you have never tried it, or have only half-heartedly tried it.



Rules for Voting in This Poll

To ensure that those who respond to this poll have properly tried the treatment they are voting for, please read the following rules before voting:

Voting for oxymatrine or Equilibrant: only vote if you tried this treatment for at least two to three months to ensure you gave it time to work. And only vote if you tested positive for a chronic active infection with coxsackievirus B or echovirus via the ARUP Lab antibody neutralization tests (titers of 1:320 or higher in the ARUP tests indicate active infection) or a similar antibody neutralization test, or if you tested positive for enterovirus via Dr John Chia's stomach biopsy VP1 stain test, and then used oxymatrine or Equilibrant to treat your CVB and echovirus infection. Oxymatrine / Equilibrant is normally ramped up to 6 x 200 mg pills per day.

Voting for Valtrex or Famvir: only vote if you tried this treatment for at least six months at a dose of around 1000 mg four times daily, which is Dr Lerner's protocol (or a slightly lower dose of 1000 mg x 3 daily which is Prof Montoya's protocol). And only vote if you tested positive for a chronic active infection with Epstein-Barr virus, which you used Valtrex or Famvir to treat. Dr Lerner says elevated antibodies in the EBV IgM VCA test and/or the EBV EA diffuse test by ELISA indicate active EBV infection.

Voting for Valcyte: only vote if you tried this treatment for at least six months at a dose of around 450 mg twice daily. And only vote if you tested positive for a chronic active infection with one or more of the following: Epstein-Barr virus, HHV-6 and/or cytomegalovirus, which you used Valcyte to treat. Dr Lerner says that antibody titers of 1:160 or higher are indicative of an active HHV-6 infection in the LabCorp HHV-6 IgM and IgG tests.

Voting for low-dose naltrexone: only vote if you tried this treatment for at least six months.

Voting for the methylation protocol: only vote if you tried this treatment for at least six months.

Voting for GcMAF: only vote if you tried this treatment for at least six months.


In this poll you are allowed to change your votes at a later date; so if you feel you made a mistake in your voting, you can alter it later.



Further Info on These ME/CFS Treatment Protocols

Note that the treatment protocols listed in this poll are standard ones used by the internationally renowned ME/CFS specialist doctors.

For further info on these ME/CFS treatments, you can search this forum for details, or consult the roadmap of chronic fatigue syndrome treatment which provides a basic overview of these treatments. A comprehensive list of ME/CFS treatments is found on MEpedia.


If you have experienced major improvements from some ME/CFS treatment not included in this poll, please post details in this thread.

I did 6 months of Goelic GcMAF. I suspect that the improvements are from high dose Vit D suppressing their immune system (like rituximab) and don't last. The protocol I did advocated 10,000 iu per day which is highly immunosuppressive. At the end of the treatment my blood level was 430 which was a big overdose. Luckily I wasn't on it long enough to have bone loss (tested by DEXA scan). However, I did develop systemic lupus erythematosis after the treatment was over and my doctor brought my vit D level back to normal after the treatment. If I had it to do over I would limit treatment to 4 months with vit D 1x/week in a normal range to see if this would avoid excess antibody generation and inducing SLE. On the bright side, I now have my dental infections under control (had 6 teeth pulled due to reinfections of previously successful root canals) which were previously a problem and have no problem generating antibodies. It didn't cure or improve the ME though.

 

[gbells]

I am not sure, but it's possible that Prof Montoya thinks that treating these bacterial co-infections usually does not lead to any improvements (eg, treating chronic Lyme with antibiotics often does not help).

I had a suspected co-infection from a flea bite from a feral cat. My Rocky Mountain spotted fever testing came back nonspecific positive 3x. Ruled out all the known pet diseases with Galaxy Labs PCRs. Differential diagnosis was unidentified bacterial infection vs false positive antibodies from lupus. I had daily severe headaches for 10 years and got the doctors to put me on the antibiotics just in case because I never tried a course of doxycycline. Headaches immediately improved on the drug. At two weeks headaches returned off drug but I found out people on lupus immunosuppressants (me) need longer treatment so had GP extend to 6 weeks (internal disease MD wouldn't do it and was skeptical thinking it was just anti-inflammatory effect of the medication). After six weeks of doxycycline no more headaches but still ME so successful treatment. Bacterial co-infections do need to be treated and it pays to be a pain when doctors are giving you the brush off but to do this you need to make a strong argument supported by research. To get the rx I had to argue that the only way to rule out bacterial infection was to do a course of drug treatment. ID MD only wanted to do 2 weeks to I got GP to extend to 6 weeks. If you make a good argument they really have to oblige and it's the easiest way to move on to the next patient.