The difference between MS and ME

[Annesse]

Here is some additional information on the presence of white matter lesions in CFS. It states, "Pathological changes have been observed in CFS patients, including white matter lesions in the CNS and cerebral hypoperfusion. Other findings suggest CNS involvement include vestibular dysfunction and GAIT ABNORMALITIES."

http://www.chiro.org/nutrition/ABSTRACTS/Chronic_Fatigue_Syndrome.shtml

I think these diseases are all one and the same. I believe they have been given different names based on the progression and severity of symptoms.

 

[Annesse]

They can be found in lupus also.

http://www.na-mic.org/pages/DBP:Lupus

 

[mellster]

Hi Annesse, good info. I do believe though that - and that has been mentioned before - the reference ranges need to be adjusted for most lab tests as today hypothyroidism lies in the eye of the doctor. According to the conventional reference ranges I never had hypothyroidism, but the integrative doc thinks there is some at least temporary exhaustion. Also you mentioned low iron which not everybody has either, not sure whether the ferritin serum level test has similar shortcomings as it can be high in case of infection and maybe mask a deficiency? All in all so far I do believe that B12 is the most important to correct, followed by D3. cheers

 

[Annesse]

White matter lesions are present in Sjogren's also.
http://www.ncbi.nlm.nih.gov/pubmed/10381047

Hi Mellster, right, these are just common findings in all of these diseases. We are looking for a pattern. Not everyone will show the exact same symptomatology even if they have autonomic dysfunction or low iron for instance. These common findings will help us trace these diseases back to their source though.
When you look at findings such as pernicious anemia occuring 20 TIMES MORE FREQUENTLY in patients with hypothyroidism and hypothyroidism occuring in 85% of patients with CFS, I think we are being given some very strong clues as to the cause of these diseases.

 

[Annesse]

IBS and Celiac disease are also common findings in these associated diseases. White matter lesions are common in Celiac patients. Here is one study that states in the conclusion, " Ten patients had neurologic findings such as febrile seizuires, single generalized zeizures, mild ataxia, and muscular hypotonia with retarded motor development." Sounds a lot like MS symptoms to me.

http://pediatrics.aappublications.org/content/108/2/e21.full

Here is the connection. The little villi that are damaged in Celiac disease are repaired by vitamin B12. Also, here is a clue. Gluten is a protein.

 

[mellster]

Yeah makes, sense, IBS is most often involved. So what are you saying., proteins are bad or at least certain proteins are?

 

[Annesse]

LOL! Boy mellster, you sure picked up on that quick. I haven't said it yet, but I do intend to. Proteins are involved in the disease process of all of these diseases. What I think what will surprise you is why. I don't want to tackle this just yet. I have some more information to provide first. In the meantime, you could reflect on the fact that amyloids are found in all of these diseases. Amyloids are misshapen proteins. Proteins trigger cellular activity by locking together into each other like three dimensional keys. Since shape in a protein is everything, improper folding can cause a protein to be useless or even dangerous. Don't worry, in the end, everything will tie together.

Remember, amyloids were a key finding in the CFS/Fibro spinal tap studies.

 

[mellster]

OK, no problem here with waiting for how it all ties together, but I was asking because maybe in the meantime you might have a suggestion like "avoid protein rich diets" which would be controversial but appreciated if you truly thought so as many try to go the other way as in low carb high protein diets. I think protein is essential and can help a lot with malnutrition but I also noticed that people just chug down on protein bars these days as they were all athletes Btw. I have read about the misshapen proteins but I don't think many people are being tested for this and I don't know how prevalent they are.

 

[Lee Ann]

I had an MRI and the neurologist told me that a clinical test was done on people who did have MS. They gave them an MRI everyday for a year. Some days the MRI detected lesions and other days, it did not. I've only had one and the neurologist wanted me to have another one. I declined. If it is MS, there is no cure so life goes on

 

[alex3619]

Hi, misfolded proteins are not necessarily a problem. It depends. The issue is that conventional proteases, chemicals that break down proteins, also require specific shapes to break them down. A very wrong shape can severely restrict protein degradation, and so the protein accumulates.

KDM has repeatedly found abnormal proteins in CFS.

Protein folding requires all sorts of things, including sulphur based compounds such as glutathione. Since we are often glutathione deficient this can cause problems, though a lot of that will be unfolded proteins. I do wonder however what happens if these unfolded proteins are not degraded quickly.

We need higher protein intake than healthy people, I think there is enough evidence to say that. However if the underlying problems can be resolved our protein requirements should go back to normal.

So if there is a problem it is not with proteins. It could be with protein regulation however.

This is not to say that specific proteins might not cause issues in specific people. It comes back to the proteases and other chemicals that interact with the proteins. Too many or too few of these chemicals will alter how the body handles a specific protein.

Bye
Alex

 

[Annesse]

I agree, Alex. The protein is not the problem. Just as in Celiac disease though, if you eat a protein you are unable to break down, it will lead to problems. Here is an actual picture of what happens in autoimmune disease when dietary proteins are not properly broken down.

http://www.sciencedaily.com/releases/2010/05/100503161423.htm

These NETS become lodged in the kidneys and other organs. The lack of the enzyme DNase 1 has been found to be a CAUSITIVE FACTOR in the developement of lupus. When this enzyme was removed in mice, the mice got lupus. When it was genetically modified, it lead to lupus.

This is one of the problems in autoimmune disease, you desperately need to eat animal proteins because that is the only place you will find B12. When you eat them though they will cause an immune reaction because they are not properly broken down. (I will provide additional evidence)

 

[Annesse]

I want to jump back to the hormones and neurotransmitters we have found missing in all of the diseases we have been discussing. If we can't account for why they are missing then we would need to keep searching for the cause of these diseases. We have found a lack of dopamine, adrenaline, noradrenaline, thyroxine, and triiodothyronine. The lack of these hormones and neurotransmitters does certainly explain many of the symptoms found in autoimmune and associated diseases. Our adrenals, our thyroid and our autonomic nervous system would not be able to function properly.

All of these missing neurotransmitters and hormones have something in common. They are all derived from the essential amino acid phenylalanine. Studies do show, in fact, that phenylalanine and other essential and nonessential amino acids are found lacking in these diseases. Here is one on fibromyalgia.

http://www.ncbi.nlm.nih.gov/pubmed/19281806

 

[Annesse]

Here is one on MS. Phenylalanine, tyrosine and tryptophan were found to be lacking in the cerebrospinal fluid of MS and degenerative diseases.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC490278/

 

[Annesse]

Here is some information on the lack of the amino acid serine in CFS. What is important to note is that threonine is the precursor to serine. Threonine was one of the amino acids found missing in the fibromyalgia study. Serine is needed to produce tryptophan. Tryptophan was found lacking in the MS study.

http://www.prohealth.com/library/showarticle.cfm?libid=428


And here is most likely some of the main reasons for the depression, insomnia, confusion, and anxiety found in all of these diseases.

Tryptophan is used to make serotonin, a mood-determining brain chemical. Both serontonin and tryptophan shortages have been linked to depression, confusion and anxiety. In addition, Serotonin then breaks down into melatonin. One important factor of a good night's rest is adequate production of the hormone melatonin.

These missing amino acids really do account for quite a bit.

 

[alex3619]

Hi Annesse, in about 1998 I was tested for serine and other issues by the people who discovered the problem. Their test showed that I was serine and glycine deficient I think, but I would have to recheck my records to be sure. I used to write about this stuff but that was over a decade ago and my memory is fubar compared to what it should be.

However, in 2000 a study came out from the UK, I don't recall the name/details. There were three things looked at (more?), and one showed the serine issue was probably an artifact. The case was closed and the world moved on. The same was true for glycine and a urinary marker and urinary citrate.

Now what they showed is that there was conversion of one chemical to another, I think this resulted in the urinary marker. They did not show why. I do not know if they were right, or wrong, and I suspect they were wrong about another study they did on CFS (about urinary citrate). In short the case isn't closed, but you will have a hard time convincing anyone of serine deficiency in CFS. It would require solid evidence.

One important question they did not answer was this: what if the conversion was in the patients and not the test? I would have to go back and reread the papers, but I dont recall which box in storage I put them in and dont have the energy to look. They had a real problem in how they conducted their tests. They presumed a constant marker, a constant chemical shift. Whereas the actual research showed the marker/shift was only present in the late stage of sleep. So everyone bought the UK study which had a dodgy protocol, and nobody went back and looked at the actual pattern.

This is not dissimilar to cytokine profiles in CFS. Its only post-exercise that you see the real shift. In the case of the urinary markers it is only post-sleep that the shift occurs. The rest of the day it is normal.

I will search for these UK papers and if I find them add some links later.

Bye
Alex

http://www.cfids-cab.org/cfs-inform/Hypotheses/jones.etal.05.pdf

The paper in this link was a publication of the earlier stuff, or a rehash I think, or I got my dates wrong. Please note this paper used the Oxford and CDC definitions, which makes it methodologically suspect anyway.

http://www.ncbi.nlm.nih.gov/pubmed/16095585
This is an abstract for the urinary metabolites, serine is being converted to another chemical in the testing procedure, or so it is claimed.

http://cfids-cab.org/cfs-inform/Hypotheses/hannestad.etal06.pdf
Here is another related paper, but I have not read it yet. After a brief examination it is clear this is a one day sample, whereas the original is from woken patients during late sleep.

 

[Annesse]

Thank you for your information Alex. I am going to spend some time printing it out and reading it tomarrow.

I think if the jury is out on serine that we are still OK. What I was trying to show was a lack of tryptophan. I just did a quick search and found this study. It states, " The two most commonly deficient amino acids seen in CFS subjects are PHENYLALANINE AND TRYPTOPHAN." Tryptophan is what is needed to make serotonin and melatonin. So this is what leads to the depression, anxiety, confusion and insomnia. This new infomation is actually more clear.

http://www.newtreatments.org/ga.php?linkid=357

 

[Firestormm]

Hi Fire, Here is one very recent study that shows the presence of white matter lesions in CFS. http://bjp.rcpsych.org/content/167/1/86.abstract

Of course, just as important as their presence is where they come from. Both MS and CFS patients lack B12. In the study entitledlasma Vitamin B12 Status and Cerebral White-matter Lesions it states in the conclusion, "These results indicate that vitamin B12 status in the NORMAL RANGE is associated with severity of white-matter lesions, especially periventricular lesions...it is hypothesised that the association is explained by effects on myelin integrity.." It also states, "Poorer vitamin B12 status was SIGNIFICANTLY associated with greater severity of white-matter lesions....

Morning,

I don't dispute the host of findings of 'lesions' in 'CFS/ME' patients. What I am saying is that these generalised 'lesions' do not equate with damage to myelin which is the determining factor in Multiple Sclerosis. I have not read anywhere that 'lesions' equate to myelin damage - indeed many of these studies that I have read are ambiguous in defining the nature of said 'lesions' and that is the crux of the problem.

The next issue is that these 'lesions' are (to take your first paper) found in non-'CFS/ME' patient samples too:

'White-matter lesions were found in a minority from all groups.' That is to say in the 'CFS/ME patient samples and in 'controls' and the patients also included those with depression (which may or may not have a bearing on this).

Here is some additional information on the presence of white matter lesions in CFS. It states, "Pathological changes have been observed in CFS patients, including white matter lesions in the CNS and cerebral hypoperfusion. Other findings suggest CNS involvement include vestibular dysfunction and GAIT ABNORMALITIES."

http://www.chiro.org/nutrition/ABSTRACTS/Chronic_Fatigue_Syndrome.shtml

I think these diseases are all one and the same. I believe they have been given different names based on the progression and severity of symptoms.

From that second paper the references to 'lesions' come from the following sources and I will try and have a read through them later to see if we can determine the exact nature and purpose of these 'lesions':

Buchwald D, Cheney PR, Peterson DL, et al. A
chronic illness characterized by fatigue,
neurologic and immunologic disorders, and
active human herpesvirus type 6 infection. Ann
Intern Med 1992;116:103-113.

Natelson BH, Cohen JM, Brassloff I, Lee HJ.
A controlled study of brain magnetic resonance
imaging in patients with the chronic
fatigue syndrome. J Neurol Sci 1993;120:213-
217.

Lange G, DeLuca J, Maldjian JA, et al. Brain
MRI abnormalities exist in a subset of patients
with chronic fatigue syndrome. J Neurol Sci
1999;171:3-7.

Until such time as we can make a clear connection between these 'lesions' and myelin damage (which I have to say I don't believe are the same thing), then we surely cannot draw conclusions.

As usual I suppose it depends on what the researchers are looking for in these studies. I have not heard of a study that looks at 'CFS/ME' patients specifically for myelin damage or even a decent explanation for these 'lesions' to be honest. It would be useful to find such things though I doubt if myelin damage has ever been observed - simply because that would mean a diagnosis of Multiple Sclerosis would it not?

Does anyone know if 'inflammation' = 'lesions' by any chance? I mean it is another general term I know but one that keeps cropping up and I have never really gotten my head around how they identify 'inflammation' let alone determine it as a defining characteristic.

Fire

 

[Jenny]

Thank you for your information Alex. I am going to spend some time printing it out and reading it tomarrow.

I think if the jury is out on serine that we are still OK. What I was trying to show was a lack of tryptophan. I just did a quick search and found this study. It states, " The two most commonly deficient amino acids seen in CFS subjects are PHENYLALANINE AND TRYPTOPHAN." Tryptophan is what is needed to make serotonin and melatonin. So this is what leads to the depression, anxiety, confusion and insomnia. This new infomation is actually more clear.

http://www.newtreatments.org/ga.php?linkid=357

Thanks for this Annesse. I think tryptophan is interesting. Researchers at the University of Sunderland have been looking at how it is metabolised in autism and ME. They think that something goes wrong with its metabolism.

Here is a post of mine from a year or so ago on this:

Ive just had the results of a urine test done by autism researchers at the University of Sunderland.

It showed high levels of indolyl-3-acryloylglycine ((IAcrGly), indole lactic acid, and two types of casein peptides. No gluten peptides.

Apparently many ME patients have high IAcrGly. Its produced from tryptophan. The researchers say:

The precise route by which IAcrGly is formed from tryptophan is still under research although it is thought that (it) represents the detoxified version of a very unpleasant acidic precursor, indole-3-acrylic acid (IAcrA). IAcrA could well find its way into many of the membranes of the body and hence make them more permeable to other biologically active produces such as peptides. Many membranes would be affected but of particular interest to us are those lining the gut wall and the blood brain barrier.

It also seems that when tryptophan is metabolised in this way less serotonin is produced.



Jenny

 

[xchocoholic]

Hi all,

Sorry to butt in, but have you seen Dr.Terry Wahls info on her recovery from ms ? She
went from being in a wheelchair to riding a biking ..

After becoming aware of her info, I looked on the web and found similiar stories. If you look at theglutenfile you'll find a section near the bottom left on ms.

Fwiw. I had lesions on my brain that disappeared after going on a gfcf, etc diet. Not to
mention that I was able to give up using motorized cart because my ataxia went away.

What an exciting time to be in healthcare .. tc . X

 

[aprilk1869]

Hi all,

Sorry to butt in, but have you seen Dr.Terry Wahls info on her recovery from ms ? She
went from being a wheelchair to riding biking ..

After becoming aware of her info, I looked o the web and found similiar stories. If you look at theglutenfile you'll find a section near the bottom left on ms.

Fwiw. I had lesions on my brain that disappeared after going on a gfcf, etc diet. Not to
mention that I was able to give up using motorized cart because my ataxia went away.

What an exciting time to be in healthcare .. tc . X

Earlier in the year I saw a documentary about dystonia where people's muscles would go into spasm. There was one woman whose life was totally ruined because of it and she had trouble speaking. It was painful just to watch her.

I was curious to know more about the condition and it seems that it's recommended that people with dystonia go on a gluten free diet. There are a number of reports on the internet of people whose dystonia has either reduced or gone away completely because of a gluten free diet.

Paroxysmal nonkinesigenic dystonia and celiac disease

Keywords:

paroxysmal nonkinesigenic dyskinesia;
dystonia;
celiac disease;
gluten free diet;
pediatric movement disorder

Abstract

Celiac disease has been associated with ataxia and other neurological signs but has not been associated with paroxysmal nonkinesigenic dyskinesias (PNKD) to date. We present a child with biopsy-proven celiac disease and a movement disorder resembling PNKD since the age of 6 months. She had complete resolution of her neurological symptoms with introduction of a gluten-free diet. Because a susceptibility locus for celiac disease has been reported on 2q33 and studies in PNKD show linkage to 2q, this report suggests further genetic investigations around this locus may be useful. We also review the literature regarding the genetic susceptibility to PNKD and celiac disease.
http://onlinelibrary.wiley.com/doi/10.1002/mds.21148/abstract

I know that my mum feels better when she cuts out bread but she keeps returning to it like a junkie returning to cocaine.