POLL: Which ME/CFS researcher has the most compelling evidence for their theory?

[beatsmyth]

Enterovirus is a new one for me, one of the avenues I have yet to explore, but now I'm doing so. I'm guessing the same way to treat this though would be AV's

 

[MeSci]

Enterovirus is a new one for me, one of the avenues I have yet to explore, but now I'm doing so. I'm guessing the same way to treat this though would be AV's

Dr Davis says "it is plausible that the long-term antimicrobial treatments often used for ME/CFS patients are doing more harm than good." from the third para of the quote from http://forums.phoenixrising.me/inde...tudy-including-q-and-a-with-dr-naviaux.46520/

 

[Londinium]

(First post - so please be gentle!)

I've gone for Fluge & Mella but don't believe it's really an either/or between that group and the Naviaux & Davis cell danger response theory. The former have found responses to Rituximab and potentially Cyclosphosphamide that would be consistent with the presence of autoantibodies. The latter have found that patient serum in severe cases seems to provoke metabolic changes in healthy cells consistent with the cell danger response. I seem to recall reading somewhere that patient serum doesn't have this effect if it is filtered to remove large particles such as proteisn, including potentially autoantibodies. Thus it seems to me that the Fluge/Mella and Navaiux/Davis findings are entirely consistent with one another and shouldn't at this point be considered conflicting theories.

(It's this consistency from up-until-now separate research groups that gives me the most confidence that they are onto something and between them represent the most promising avenue of research).

 

[Basilico]

I don't believe any theory doesn't involve viruses. If viruses aren't the cause of ME/CFS then why can most of us trace our onset back to an acute viral illness?

I'm pretty sure I've seen posted here on PR that about 50% have gradual onset that is not linked to an acute viral illness. My husband had gradual onset, and I did, too. I've seen plenty of others in the same boat.

I think it's more likely that a viral infection is just one example of a trigger that can serve as a catalyst in someone with pre-existing issues (genetic, methylation, immune dysfunction, other). About 10-15 million people each year get infected with an enterovirus, yet very few go on to develop CFS/ME.

 

[alex3619]

Likewise, Fluge and Mella, have been very circumspect about whether their findings suggest antibodies, autoanitbodies or some other process that is somehow being moderated by Rituximab.

Yes, they are acting as responsible scientific investigators. We need to be careful with hypothesis and inference. If you recall the tale of the elephant and the blind philosophers, the guy who grabbed the trunk thought an elephant was a giant snake, and so on. With ME its worse in that we might have several different animals, not just a single elephant.

 

[Wonkmonk]

I voted for Lerner/Montoya.

(1) Lerner's studies report that a subset of patients had unnaturally high herpes virus AB titers and they greatly improved with antiviral therapy just as their titers went down. Coincidence?

(2) Lerner has a compelling theoretical rationale for the herpes virus hypothesis (abortive, non-lytic viral replication).

(3) As some have mentioned before, (viral) infection is often reported as a trigger of CFS. Especially Epstein-Barr virus has been suspected for decades.

(4) CFS symptoms resemble known morbidity of herpes virus infections, e.g. Infectious Mononucleosis or post-herpetic neuralgia after shingles.

So, I think it's safe to say that for some patients, herpetic infection that somehow got out of control is the culpritt.

That said, I believe that what we call "CFS" is a condition with similar symptoms but different causes. E.g., Lyme disease is known to produce long-term CFS-like symptoms in some cases, just like herpes virus infections. Although the symptoms are similar, the underlying cause, diagnostics and therapy would be very different.

So, several theories may be correct at the same time. There may be a bacterial-induced CFS, a viral-induced CFS, a cell-damage induced CFS and maybe others.


Btw. I think there is also a Neurological Channelopathy Hypothesis that might be missing in the list so far (or it's maybe included in the cell-damage point, not entirely sure):

http://onlinelibrary.wiley.com/doi/10.1002/(SICI)1099-1077(199901)14:1<7::AID-HUP64>3.0.CO;2-O/full

 

[halcyon]

My point is there are a load of non sudden onset people that don't fit the virus model and you can't ignore these people.

Gradual onset does not preclude viral onset. Infections can be subclinical and go unnoticed. The time period between my sudden viral onset and when I reached maximum symptoms and severity of illness was over 10 months. Without the obvious initial infection, I would have just noticed myself gradually getting worse in a stepwise fashion over this long time period. One of the enterovirus studies found the same evidence of chronic enterovirus infection in gradual onset cases.

 

[Gingergrrl]

(First post - so please be gentle!)

Excellent first post!

With ME its worse in that we might have several different animals, not just a single elephant.

Great analogy and I agree.

Btw. I think there is also a Neurological Channelopathy Hypothesis that might be missing in the list

My doctors and I feel that calcium channelopathy plays a role in my case but am not sure if it is more common than we know vs. I am a freak LOL.

 

[Wonkmonk]

I tried calcium channel blockers Nimodipine and Verapamil as suggested by Dr. Mason Brown for some weeks before starting antivirals and I can say that it definitely caused some degree of improvement.

It wasn't a substantial improvement and after several weeks I found it didn't improve further. But there definitely was a positive effect.

It should be noted however that Dr. Brown ascribed any improvement to vasodilation and flushing out of toxins and microbes rather than a channelopathy.

 

[Gingergrrl]

@Wonkmonk I am the opposite and reacted badly to a CCB in 2014 and then in 2016, I learned I have autoantibody that blocks the calcium channel and was told by Neuros not to take CCB's in the future. I do poorly w/vasodilators and do well w/Midodrine (vasoconstrictor) b/c I have hypotension.

 

[Wonkmonk]

Sigh...it seems with CFS everything can always go both ways.

 

[Sean]

Gradual onset does not preclude viral onset. Infections can be subclinical and go unnoticed.

I think this a very important point. Not specifically about viruses, but about whether the pathology underlying ME/CFS can exist as a subclinical entity for some time, possibly decades, before fully expressing itself for some reason or other, the 'onset'.

Before then patients may appear to be within statistically normal bounds on most measures, yet still have a problem that has not become serious or obvious enough to allow diagnosis, but which has a significant impact upon their function and lives.

 

[DaninCanada]

The doctor who had it from the begining.
Dr Byron Hyde Ottawa
Polio virus

 

[DaninCanada]

Milder form of polio explains it the best.

 

[msf]

Dr Davis says "it is plausible that the long-term antimicrobial treatments often used for ME/CFS patients are doing more harm than good." from the third para of the quote from http://forums.phoenixrising.me/index.php?threads/professor-ron-daviss-response-to-naviaux-study-including-q-and-a-with-dr-naviaux.46520/

I don´t think it´s going to be this simple.

 

[arewenearlythereyet]

Gradual onset does not preclude viral onset. Infections can be subclinical and go unnoticed. The time period between my sudden viral onset and when I reached maximum symptoms and severity of illness was over 10 months. Without the obvious initial infection, I would have just noticed myself gradually getting worse in a stepwise fashion over this long time period. One of the enterovirus studies found the same evidence of chronic enterovirus infection in gradual onset cases.

for me this was different. Infection was not the defining feature of my decline....chronic joint and muscle pain was with cognition problems. Infection played its part, but this wasn't defined by anything specific ....this was a series of different infections (skin, entero etc) that I slowly recovered from over the 9-12 months. In fact this is the same pattern I have now nearly 5 years later. This makes me believe that for some the immune system is involved at some level but not as a result of a specific viral infection.

One things for sure it will be fascinating to see what this looks like when all the threads are put together.

 

[GreyOwl]

When you say "type IV food sensitivity to oranges", do you mean stage four anaphylaxis or something different?

This is my lay explanation:
A type IV hypersensitivity is a form of "allergy" which is mediated by t-cells. An example of a t-cell allergy is a latex allergy which causes a rash. It's easy for a dermatologist or an allergist to test for a latex allergy resulting in dermatitis using patch testing, but an internal t-cell allergy is a very contested concept. There are no tests. Type IV sensitivities are often occupational diseases, which I'm sure does not help the need to research t-cell mediated food allergies.

I'm trying to think which molecule in an orange could cause the reaction...

 

[Wishful]

When you say "type IV food sensitivity to oranges", do you mean stage four anaphylaxis or something different?

Normal allergies are type I, involving IgE, histamine, etc. Type IV is a delayed hypersensitivity, involving T-cells. It really shouldn't be confused with allergies. BTW, none of the allergists I went to would even try to help me with a type IV sensitivity. Even the Canadian Society of Allergy and Clinical Immunology was unable to find a doctor who dealt with type IV sensitivity.

https://en.wikipedia.org/wiki/Type_IV_hypersensitivity has good information about the different types of immune system reactions.

 

[Gingergrrl]

@GreyOwl and @Wishful Thanks for explaining that although I am not certain still that I quite understand it! In the link you posted @Wishful, it lists Hashimoto's Disease as an example of a Type IV sensitivity (which I have) and had no idea! How would this compare to an IgE allergic response or to a mast cell response? What symptoms do you get when you eat an orange @Wishful and are they immediate or delayed?

 

[junkcrap50]

I don't believe any theory doesn't involve viruses. If viruses aren't the cause of ME/CFS then why can most of us trace our onset back to an acute viral illness?

I'm pretty sure I've seen posted here on PR that about 50% have gradual onset that is not linked to an acute viral illness. My husband had gradual onset, and I did, too. I've seen plenty of others in the same boat.

I think it's more likely that a viral infection is just one example of a trigger that can serve as a catalyst in someone with pre-existing issues (genetic, methylation, immune dysfunction, other). About 10-15 million people each year get infected with an enterovirus, yet very few go on to develop CFS/ME.

My CFS doctors has described to me several patients of his, who have textbook CFS presentation and meet several CFS diagnostic criteria, that had their CFS be triggered and started by physical trauma (broken legs, car accidents, whiplash, falling off ladders, etc). It's hard to believe but true. The only thing I can think of they share with typical cfs patients is that they likely have had various viruses and infection in the past, but from which they had recovered completely.