CFS is a metabolic condition!

[mellster]

MeSci,

I think there doesn't need to be a disagreement regarding the definition of infection. Out of the several types you cited, the opportunistic infection fits very well. Routine lab tests do not test for opportunistic bacteria, and even if they are detected, they are not mentioned in the reports. This may be different for patients who have a immune disease who will get screened for those because they may pose a serious threat to them. However, immune disease is a sliding scale and not a binary condition (IMO), so everybody with unexplained symptoms should be screened for opportunistic bacteria.(and viruses).The theory of bacteria found in mucosal membranes such as throat, mouth, etc. which becomes pathogenic through dissemination into surrounding tissue and gut is my favorite one right now simply because it makes most sense if you look at the majority of the symptoms and where they mostly occur.

 

[mellster]

Thank you for all the detailed responses to my question to @Elph68 and I wish I had a more scientific background so I could grasp it all. It sounds like you are saying the tests fail b/c most doctors either say "The antibodies are from a prior infection and found in 90% of the population blah, blah, blah" or someone's immune system is too compromised to even create the antibodies. Is that correct?

Almost, the first part is right, but if there are no to little antibodies they claim there is no infection

 

[MeSci]

I wish. It probably means a combination of circumstance and hard work.

Mostly the latter with me. The research was hard work, and the circumstance was having a little time available to do it! It was quite easy to put the findings into practice (leaky-gut diet).

 

[Elph68]

You might check out these posts on how various stealth viruses are able to evade the immune system through adaptation
http://forums.phoenixrising.me/inde...ted-by-bodys-immune-system.30744/#post-470493

http://forums.phoenixrising.me/inde...nic-fatigue-syndrome.27634/page-3#post-438264

In fact read through the entire thread how some of these viruses will send out enzymes to defeat the immune system

Deficient EBV-Specific B- and T-Cell Response in Patients with Chronic Fatigue Syndrome

EBV can subvert the human immune response, as we show that BPLF1 can remove ubiquitin tags from proteins in the TLR signaling cascade. This inhibits TLR signaling and decreases the expression of immune response genes.

Hi Eco,

you also might like to know 2 very basic scientific facts about bacteria:

1. Bacteria use Hydrogen sulfide to defeat the immune system
2. Bacteria use hydrogen sulfide against antibiotics, this is one of the major mechanisms of antibiotic resistance

Just thought you might like to know ....

 

[IreneF]

I recently met with head of immunology at major tertiary center. Due to severity of my muscle symptoms, specialist is referring me to NIH for muscle and mitochondrial genetic testing. We discussed possibility that some of us have genetic predisposition and the viral hit leads to metabolic dysfunction.

I suspect it may take a few months before I head to Bethesda but I will share results when available.

I was diagnosed at NIH, only because I lived nearby and didn't have a regular doc. They had a clinic. I was utterly flabbergasted when I got the diagnosis.

 

[Gingergrrl]

We discussed possibility that some of us have genetic predisposition and the viral hit leads to metabolic dysfunction.

@Dr.Patient Just curious but couldn't the above sentence summarize CFS? There is some kind of genetic predisposition and then the viral hit leads to metabolic dysfunction? I know it is just a theory but it makes so much sense.

 

[RYO]

@Dr.Patient Just curious but couldn't the above sentence summarize CFS? There is some kind of genetic predisposition and then the viral hit leads to metabolic dysfunction? I know it is just a theory but it makes so much sense.

It would be interesting to find out whether subset of CFS / ME patients have mitochondrial genetic defect. Unfortunately, if this was the case, I think treatment options would be limited.

However, if we identified genetic predisposition, it would be a significant milestone in understanding this disease.

 

[RYO]

I was diagnosed at NIH, only because I lived nearby and didn't have a regular doc. They had a clinic. I was utterly flabbergasted when I got the diagnosis.

We're you seen at NIH center for rare diseases? What was your diagnosis?

 

[IreneF]

We're you seen at NIH center for rare diseases? What was your diagnosis?

Oh, sorry. I don't remember which clinic it was. This was ten years ago; the clinic may no longer exist. I think I just called them and got an appointment. I was more or less in the 'hood, and the only doctor I had seen in years was a psychiatrist.

I was diagnosed with CFS. There wasn't any discussion of psychogenic causes, even though I was also being treated for depression.

 

[Dr.Patient]

It would be interesting to find out whether subset of CFS / ME patients have mitochondrial genetic defect. Unfortunately, if this was the case, I think treatment options would be limited.

However, if we identified genetic predisposition, it would be a significant milestone in understanding this disease.

My belief is there is no doubt a mitochondrial genetic defect in all patients. There are millions of people who have the infections listed in PR, but not all of them have ME. There are people who get ME slowly without acute infections.

The medical community needs to find this biomarker that will diagnose all patients, and they need to find specific ways of fixing the damages inflicted upon the mitochondria by either infectious/non-infectious agents. @justy

 

[shah78]

We already have the "specific ways of fixing the damages". An Ancestral based diet, methylation support, ATP support, phospholipids, Cold Thermogenesis. This will help every human being alive, CFS or not, young or old. The so called biomarker is a red herring. Name me one human being who couldn't benefit from"Just doing the right thing(s)".......Glad to have you asking these questions. And let's not forget the newest kid on the block. Prebiotics/probiotics.

 

[Gingergrrl]

We already have the "specific ways of fixing the damages". An Ancestral based diet, methylation support, ATP support, phospholipids, Cold Thermogenesis. This will help every human being alive, CFS or not, young or old. The so called biomarker is a red herring. Name me one human being who couldn't benefit from"Just doing the right thing(s)".......Glad to have you asking these questions. And let's not forget the newest kid on the block. Prebiotics/probiotics.

@shah78 why is the bio marker a red herring and what are phospholipids and cold thermogenesis?

 

[RYO]

I have tried various mitochondrial supplements without any improvement. I followed very healthy diet before, during and after my illness. There is no proven pharmacological therapy in primary mitochondrial disorders. However, CoQ10, creatine, and L-carnitine supplements are generally considered safe and some patients have responded in small studies. Certain drugs are to be avoided in mitochondrial disorders - valproic acid, barbiturates, tetracyclines, chloramphenicols, aminoglycosides and metformin. Hopefully, more progress will come from gene therapy. ( Sounds very attractive but likely a lot more complicated than we think... )

Personally, probiotics make me feel worse and I suspect contributed to my recent relapse. My suspicion is that the gut is either reservoir for latent virus or gut abnormalities trigger abnormal gut immune response (related to vagus nerve?) Sometimes I wonder whether my leg weakness and pain are partly due to nerve injury / pathology and or neurotoxicity from excess lactic acid.

 

[heapsreal]

@RYO
Sometimes I wonder whether my leg weakness and pain are partly due to nerve injury / pathology and or neurotoxicity from excess lactic acid.
Maybe not lactic acid but excess ammonia or possibly both??

 

[MeSci]

@RYO
Sometimes I wonder whether my leg weakness and pain are partly due to nerve injury / pathology and or neurotoxicity from excess lactic acid.
Maybe not lactic acid but excess ammonia or possibly both??

I suspected lactic acid/lactate initially, but more recently I have come to the belief that our adverse effects from exertion are largely due to inflammatory cytokines, and have done a blogpost on it, plus one on how it might be alleviated.

 

[MeSci]

My belief is there is no doubt a mitochondrial genetic defect in all patients. There are millions of people who have the infections listed in PR, but not all of them have ME. There are people who get ME slowly without acute infections.

The medical community needs to find this biomarker that will diagnose all patients, and they need to find specific ways of fixing the damages inflicted upon the mitochondria by either infectious/non-infectious agents. @justy

There is likely to be a multiplicity of biomarkers, which may identify different subgroups with different causes and remedies. This has been discussed quite a lot on PR, including here.

Being pedantic here, but I think it is important - the medical community doesn't do the research (as you probably know!) - it follows the rules and guidelines laid down by governing bodies (e.g. NICE) who draft the rules and guidelines after examining the evidence produced by scientific researchers.

As we know, the governing bodies can be very wrong, as in our case. NICE get the definitions more-or-less right, then go on to recommend ridiculous treatments (CBT/GET).

 

[RYO]

I suspected lactic acid/lactate initially, but more recently I have come to the belief that our adverse effects from exertion are largely due to inflammatory cytokines, and have done a blogpost on it, plus one on how it might be alleviated.

There are several kinds of curcumin with varying levels of bioavailibilty. I have tried several with minimal effect other than yellowish stools. Also tried omega 3 fatty acids. I have only tried one brand of of resveratrol. It caused stomach cramps and vomiting. I have heard of anecdotal reports of curcumin helping psoriasis or RA. These are conditions where inflammatory markers such as sed rate or CRP are elevated. My inflammatory markers have always been stone cold normal.

 

[MeSci]

There are several kinds of curcumin with varying levels of bioavailibilty. I have tried several with minimal effect other than yellowish stools. Also tried omega 3 fatty acids. I have only tried one brand of of resveratrol. It caused stomach cramps and vomiting. I have heard of anecdotal reports of curcumin helping psoriasis or RA. These are conditions where inflammatory markers such as sed rate or CRP are elevated. My inflammatory markers have always been stone cold normal.

A bit O/T so will be brief - feel free to post comments/questions in my blog.

In the 2nd blogpost I cite evidence re curcumin bioavailability and something that can enhance absorption, otherwise it tends to go straight to the colon.

Do you recall what brand and dose of resveratrol you used?

Also, have you had tests for the specific inflammatory cytokines mentioned in the 1st blogpost that I cite?

Probably best to answer on the blog page to avoid keeping this thread off-topic!

 

[Sparrow]

I'm not up to reading everyone's replies here at the moment, but wanted to chime in that this fits some of my experience.

For me, I've learned (way too slowly) that I can keep my symptoms away if I do little enough. When I try to do things again, the symptoms reappear (and if I try to do too much, obviously, I get hit with the symptom truck that we all know so well). This can be as little as watching TV, or using the internet, or having conversations. If I were to lie in a room alone and bored, I can be almost symptom-free (in that my symptoms would involve limits on activity that I wasn't currently straining, but I no longer feel sick, painful, tired, etc.). It took me forever to realize that some of my constant symptoms were a cause and effect reaction from low levels of activity rather than an inevitable part of my daily existence. Very clearly for me (as with others), whatever the defect is in my health, it is tightly connected to activity.

When I crash, I feel very sick (among other things), so there's no doubt for me that the immune system is involved somehow. But it could be that it's involved by having been deprived of the necessary energy to keep it working at optimal levels (which allows infections to get out of control for a while). That has always been the explanation that felt the most "right" to me. Alternately, it could be that some energy defect is using up resources necessary for the immune system to function, or something like that. Or it could be that my immune system is so stretched in trying to keep invaders under control that the normal immune suppression that comes from exercise of any kind allows them to take over for a while. But my gut says that energy supplies are deeply involved. If I exert too much (either physically or mentally), my energy resources drain more and more until they literally give out. That shouldn't be possible.

The fact that some of the payback is delayed by around 24hrs has always been very interesting to me. It feels like surely that could help provide some direction for where to look as well.

 

[IreneF]

I'd like to know more about the role of natural killer (NK) cells. Some of us have had them tested and found them to be very low in cytotoxicity. (The test exposes them to tumor cells and counts how many are killed. Sort of like putting a cat in a room full of rats and counting the casualties.)

I wonder if whatever we've got is infecting or altering the NK cells--or their precursors in the bone marrow--and other cells respond by pumping out inflammatory cytokines in an attempt to activate the NKs. Dr. Kogelnik thinks something like this may be going on.

Since NK cells kill herpes viruses, I wonder if the high antibody titers we may have to EBV and/or HHV-6 is due to lack of suppression by the NKs. But then why don't we have more overt infections, such as shingles?