The difference between MS and ME

[anniekim]

Annesse, your personal story of recovery and your hypothesis, albeit largely over my head, sounds very interesting. I hope you will continue to post. I don't think anyone was telling you not to, just the thread title was different to the main content of this thread. You could even start a new thread devoted to your work. I think there are many of us that would like to hear more

However, there is one point you made that I don't quite understand. You mention earlier in this thread that the fatigue between MS and ME is in your opinion the same. You provide a link on the nature of fatigue in MS. My understanding is there is a difference. Mainly fatigue in m.e is actually often not fatigue per se but post exertional malaise or the more recent phrase post exertional neuro immune exhaustion. Exertion makes us worse. My understanding is people with ms do not have this pem. Until their mobility becomes too restrictive they can exercise/undertake activity (say go out for a coffee with a friend) without an exacerbation of symptoms. They may feel fatigued but do not have to so carefully keep within their energy limits if they want to avoid a symptom flare.

Also I thought I read somewhere once (i may be wrong) that if people with ms are able to be as active as they can, it can help their fatigue. This is the deadly opposite in m.e. Have you any thoughts on this?

Also re Enid mentioning a trigger. My mum came down with m.e the same year as me. She was 52 I was 27. She was perfectly healthy until then. Does a trigger fit into your hypothesis? If so, how?

I had some vitamin testing done a few years back. I came up as low in zinc and magnesium and very low in B vitamins 1, 2 and 6 which I think fits in with what you say you found. I'd also be interested in your thoughts on LDn

Many thanks.

 

[Annesse]

You all have been here a lot longer than I have, so I will take my cues from you.

Anniekin, Here is some information on a study that shows the post exertional fatigue in ME is tied to autonomic dysfunction. All of these diseases have severe autonomic dysfunction. http://chronicfatigue.about.com/b/2...ional-malaise-in-chronic-fatigue-syndrome.htm

My thoughts on exercise and these diseases is that energy is what your body makes to allow you to exercise. You have lost the ability to make energy. I believe it is good to move as much as you can, and to do slow gentle walking if your body is up to it. When your energy starts to return is a sign that you are healing. Then and only then would I embark on any kind of a more strenuous routine. You asked about triggers. Too much exercise can be a trigger in itself. How many of us with these diseases were former athletes? Or worked in professions like nursing where you pushed yourself beyond your limits because you had no choice. Both strenuous exercise and stress of any kind rapidly depletes your body of enzymes and B12. You could liken it to running a marathon. As you run, you become more and more exhausted, but you keep pushing yourself, and then you give an extreme push to reach the finish line, using up all of your reserves. If you are going through something stressful, you call on your already depleted body to produce even more. Then, as you cross the finish line, you collapse.

Of course, there are other triggers as well. I think the first mass outbreak of CFS in Lake Tahoe is a good example of this. It was linked to excess fluoride in the water. Fluoride is a potent enzyme poison. Same with the exposure to pesticides that have been linked to these diseases. Pesticides are poisons and poisons work by 'specific inhibition of enzymes'.

Another example of a trigger for someone would be medications. The top 3 drugs that are known to induce lupus are all ENZYME BLOCKERS.

Bacteria and viruses can also trigger autoimmune disease. They wrap themselves in a 'protein shell' in order to disquise themselves from the immune system. It is the proteases job to remove this shell so your immune system will then target them for destruction. If you become infected with a virus or bacteria, and you are already low on these proteases, they would be even more depleted. This could lead to autoimmune disease.

Recovery is all about restoring the ability of your body to digest proteins. No drug or supplement (not even pancreatic enzymes in a bottle or LDN) will be able to do this. The specific enzyme that is missing (DNase 1) does not not come in a supplement. Even if it did, I wouldn't take it. Lots of things are not working. Enzymes are dependent on HCL for instance. This is a job for nature.

 

[Mij]

With all due respect Annesse, just from my experience with ME for the past 20yrs- being able to exercise more when you are "able" is NOT an indication or good sign of "healing" as you suggested so be careful with this advice.
NEVER embark on more strenuous exercise routine EVER with ME, it will cause further damage down the road.

ME causes cumulative effects on the body so stay within your limits- always! I also disagree with the comparisons made with ME and MS, btw.

ANNESSE wrote: My thoughts on exercise and these diseases is that energy is what your body makes to allow you to exercise. You have lost the ability to make energy. I believe it is good to move as much as you can, and to do slow gentle walking if your body is up to it. When your energy starts to return is a sign that you are healing. Then and only then would I embark on any kind of a more strenuous routine.

 

[adreno]

Recovery is all about restoring the ability of your body to digest proteins. No drug or supplement (not even pancreatic enzymes in a bottle or LDN) will be able to do this. The specific enzyme that is missing (DNase 1) does not not come in a supplement. Even if it did, I wouldn't take it. Lots of things are not working. Enzymes are dependent on HCL for instance. This is a job for nature.

Ok, so what you're saying - if I understand you correctly - is that avoiding enzyme inhibitors (by adopting an organic paleo diet) is the best way to improve protein digestion?

A paleo diet, high in vegetables, is likely more alkalizing than the standard high grain/carb western diet. At the same time, as you said, enzymes need HCL to work. How does this tie together?

 

[alex3619]

There are certainly issues with energy production in ME, probably quite a few. Some of that is driven by mitochondrial function. However, on exercise, the worst complication is not lack of energy. Its either a cytokine storm or a profound dysregulation of cellular receptors, typically massive increase in some receptors. That is what may lie at the heart of PENE, as discovered by Alan and Kathleen Light.

Correcting mitochondrial function is only a step in the process. It remains to be seen if it is a sufficient step, it could be but it might not be.

It is also doubtful, though not impossible, that the heart problems are fully mitochondrial in nature. Some of them seem structural due to other things, but nobody really knows for sure.

Similarly a big problem with brain function is poor blood flow in the brain. Without sufficient oxygen mitochondria cannot function adequately, and if the brain cannot rapidly deal with toxins due to poor blood flow, toxicology could be important too.

Return of energy in ME is often a sign of change in chemistry, usually temporary. It does not usually mean healing, though it can. If you take that sign and increase activity you could be setting yourself up for a crash - caution is advised.

Bye
Alex

 

[Annesse]

I think my statements on exercise are being misinterpreted. First, there is no doubt that health and vitality (energy) are connected. Energy IS what your body makes to ALLOW you to excerise. That is why B12 is called the energy vitamin. It helps fat and protein to metabolize in the body. It also plays a major role in the conversion of carbhoydrates to gluscose-your bodies source of fuel. If you excerise if you don't have the "energy" then you would just further deplete your body of B12 and enzymes. I was not saying that at the first sign of a little energy, you should force yourself to excercise. I was saying the opposite. You should exercise if you have an abundance of energy. Energy to spare. And energy to spare is a sign of healing.

I said I thought it was a good idea to move as much as you can. If you are bedridden and you can get up to go to the bathroom, rather than use a bedpan, then I think the movement would be beneficial to your body.

Yesterday, I danced in the kitchen. I didn't do it because I was forcing myself to exercise. I did it because a good song came on and I felt like dancing.
It felt good- during and after. When I was at my sickest, bedridden and without the strength or energy to lift a telephone receiver at times, I don't think it would have been a good idea to dance in the kitchen. I don't think anyone should "dance" unless they have the energy.

 

[Mij]

I think my statements on exercise are being misinterpreted. First, there is no doubt that health and vitality (energy) are connected. Energy IS what your body makes to ALLOW you to excerise. That is why B12 is called the energy vitamin. It helps fat and protein to metabolize in the body. It also plays a major role in the conversion of carbhoydrates to gluscose-your bodies source of fuel. If you excerise if you don't have the "energy" then you would just further deplete your body of B12 and enzymes. I was not saying that at the first sign of a little energy, you should force yourself to excercise. I was saying the opposite. You should exercise if you have an abundance of energy. Energy to spare. And energy to spare is a sign of healing.

I said I thought it was a good idea to move as much as you can. If you are bedridden and you can get up to go to the bathroom, rather than use a bedpan, then I think the movement would be beneficial to your body.

Yesterday, I danced in the kitchen. I didn't do it because I was forcing myself to exercise. I did it because a good song came on and I felt like dancing.
It felt good- during and after. When I was at my sickest, bedridden and without the strength or energy to lift a telephone receiver at times, I don't think it would have been a good idea to dance in the kitchen. I don't think anyone should "dance" unless they have the energy.

Annesse, I don't know if you have ME but you clearly do not understand and I'm not misinterpreting your statements.

You wrote: "When your energy starts to return is a sign that you are healing. Then and only then would I embark on any kind of a more strenuous routine. "

I am saying this is not true with ME, it is NOT a sign of healing. What exactly do you interpret "healing" to be? Read what I wrote to you, this illness is a cumulative stress on the body so the more you do(even if you think you are "healing") the WORSE off in the end you well be. got it? It can set you back when you think you are "healing", to use your language. You have to be careful with the words you use when addressing ME. The word "strenuous" should never even be in our vocabulary.

 

[Annesse]

Alex, you mentioned heart problems and ME. Part of the heart problems associated with ME could be due to mitral valve prolaspe. I know there are others and we can address those also. Here is some information I posted earlier.


o A study in Paris found a link between magnesium deficiency, chronic fatigue syndrome and mitral valve prolapse (MVP), an abnormality in which the valve between the hearts left atrium and ventricle malfunctions or is weakened and blood cannot circulate through the heart in the way it should. As many as 75 percent of those with fibromyalgia have MVP. (Durlach J, et al. Neurotic, neuromuscular and autonomic nervous form of magnesium imbalance. Magnes Res 1997 Jun;10(2):169-95

I think I posted some information earlier that stated 85% of CFS patients have mitral valve prolaspe. As many as 75% of fibromyalgia patients also have mitral MVP. We have posted information and studies that show homocysteine interferes with intracellular magnesium. All of these diseases also show the same lack of magnesium. MVP is a common disorder. It occurs mostly in women of childbearing age. (Just like autoimmue disease) I think this is a case much like the belief that white matter lesions were just found in MS. I myself thought this at first. Here is some information that shows how common it is. I know other heart conditions are connected to CFS and these can be explained as well.

http://www.nutritionalmagnesium.org...m-combats-mitral-valve-prolapse-syndrome.html

MVP is common in hypothryoidism. http://www.webmd.com/heart/news/19991130/heart-valve-defect-common-patients-thyroid-disease

Here is some info on lupus. Interesting that it wasn't discovered until they did an autopsy. http://www.ncbi.nlm.nih.gov/pubmed/3594966

 

[Annesse]

The increased risk of congestive heart failure in ME could also be linked to the elevated levels of homocysteine. The following study concludes: "An increased plasma homocysteine level independently predicts risk of the development of CHF." (congestive heart failure)

http://jama.ama-assn.org/content/289/10/1251.full

 

[Annesse]

Hi Rich- I was wondering what your thoughts might be on the inabilty to break down proteins leading to the lack of glutathione. The study I posted on fibromyalgia showed a lack of the amino acid methionine. Here is some infomation on methionine and where it is found.
http://www.livestrong.com/article/495492-methionine-deficiency-symptoms/


This study states methionine affects glutathione. http://jn.nutrition.org/content/127/11/2135.full

 

[richvank]

Hi Rich- I was wondering what your thoughts might be on the inabilty to break down proteins leading to the lack of glutathione. The study I posted on fibromyalgia showed a lack of the amino acid methionine. Here is some infomation on methionine and where it is found.
http://www.livestrong.com/article/495492-methionine-deficiency-symptoms/


This study states methionine affects glutathione. http://jn.nutrition.org/content/127/11/2135.full

Hi, Annesse.

I've been reading your book, which came today. Very interesting. As you know, I have proposed a different hypothesis for the pathogenesis and pathophysiology of ME/CFS from the one you have suggested. I'm still absorbing what you have written, and am not ready to get into the fine points with you yet.

So I'll respond to your question in principle, not saying whether I agree with your hypothesis: In principle, if a person were unable to digest proteins as well as normal, the amino acids in them would not be available in as high quantities as normal to be transported into the enterocytes, and from there into the blood. The plasma amino acid levels would be expected to be low, and that would negatively affect the synthesis of peptides and proteins by the cells.

Glutathione is a tripeptide, synthesized from cysteine, glycine and glutamic acid. Usually cysteine is the rate-limiting amino acid for the synthesis of glutathione. The average diet supplies only about half the cysteine that is needed by the body, and the other half is normally synthesized from methionine via part of the methylation cycle and the transsulfuration pathway. If methionine is depleted, it can be expected that cysteine will be low, also, and that can be expected to negatively affect the synthesis of glutathione.

Methionine is observed to be depleted in many cases of ME/CFS. According to the GD-MCB model, this occurs because of the partial block of methionine synthase, which causes more homocysteine than normal to flow into the transsulfuration pathway, and less to be converted back to methionine. Over time, the result of this can be depletion of methionine, unless the person's diet is able to replace it fast enough to make up for this, such as if the diet is high in meat. I have seen some cases where this appears to be true, and then methionine is not depleted, but glutathione usually still is.

I understand that your hypothesis suggests that amino acids are low in ME/CFS, as well as in several other disorders, because of lack of proteolytic enzymes from the pancreas that are needed to digest protein.

It's true that the digestion is not very good in many cases of ME/CFS. I think the first reason for that is that glutathione depletion in the parietal cells prevents them from supplying as much acid to the stomach as normal. This prevents the conversion of pepsinogen to pepsin in the stomach, thus interfering with the beginning of protein digestion there. (As you've written, this also prevents the separation of B12 from food proteins and the binding of B12 by R protein, also known as haptocorrin, which is produced in the stomach. Normally, the haptocorrin is digested in the gut, and then B12 is bound to intrinsic factor, also produced in the stomach, which transports it into the enterocytes in the terminal ileum, and thence to the blood, bound to transcobalamin.)

When the food moves into the duodenum from the stomach, the too low acid content causes a poor signal to be sent to the pancreas from cells in the wall of the duodenum via secretin, and not as much digestive juice (with bicarb and enzymes) as normal is excreted by the pancreas. That inhibits digestion. Also, there is competition from the dysbiotic bacteria and yeasts which overgrow in the small intestine because of the lower than normal motility. I frequently see elevations in the urine organic acids tests of people who have ME/CFS of bacterial metabolites of the amino acids. If the bugs are getting them, the people are not. So I agree that there is poor digestion after onset of ME/CFS, though I may not agree with you that that is the "first cause" of the disorder.

I think it's also true that people with ME/CFS burn amino acids for fuel in their mitochondria at higher rates than healthy, normal people do, because a partial block of aconitase in the Krebs cycle (which I believe is due to glutathione depletion) prevents them from burning carbs and fats at rates as high as normal. Many people with ME/CFS have found that they feel better and gain less unwanted weight on a high-protein diet, and I think that is the reason. Also, I often see high urea levels in urine test results, and this indicates a high rate of burning of amino acids. This higher rate of burning of amino acids for fuel could also be a cause of the low plasma amino acids levels.

Whenever a substance is found to be low or high in biochemistry, I have found that it's necessary to look both at the sources and at the sinks for the substance. In principle, abnormalities in either the sources or the sinks can be responsible for an abnormal level of the substance.

Best regards,

Rich

 

[Annesse]

Thanks Rich. Very informative as always. Low levels of glutathione can also be found throughout autoimmune disease. Also in the diseases that I can link back to the inability to digest proteins, such as COPD. Here is one on lupus that states in the conclusion, " A significant correlation between plasma glutathione and lupus severity exists..." http://www.ncbi.nlm.nih.gov/pubmed/18801305

If low levels of glutathione can be found in all of these diseases, does that not indicate they all share the same disease pathway? (Taking into consideration all of the other evidence of course.)

 

[alex3619]

Hi, just a quick thought to add to your comment Rich, although I mostly agree with you: sources, sinks and regulation. Too little is known about the altered functional genetics of ME, particularly post exercise.

Most might not be aware, but I have been in agreement with Rich on problems with aconitase, including a high utilization of aminos as fuel, for over a decade now, and that includes the importance of glutathione. Its not just about oxidative damage either. Proper folding of aconitase requires glutathione for the correct sulphur bonds. This may be true of other sulphur rich proteins as well. Bye, Alex

 

[Tristen]

IV Amino Acids get around this protein metabolism problem? Helped me improve.

 

[richvank]

Thanks Rich. Very informative as always. Low levels of glutathione can also be found throughout autoimmune disease. Also in the diseases that I can link back to the inability to digest proteins, such as COPD. Here is one on lupus that states in the conclusion, " A significant correlation between plasma glutathione and lupus severity exists..." http://www.ncbi.nlm.nih.gov/pubmed/18801305

If low levels of glutathione can be found in all of these diseases, does that not indicate they all share the same disease pathway? (Taking into consideration all of the other evidence of course.)

Hi, Annesse.

I appreciate learning about the status of glutathione in COPD, lupus and other disorders. My research has been rather narrowly focused on ME/CFS, and I don't know much about these other disorders.

I can't say whether the same vicious circle mechanism is involved in these other disorders as appears to be the case in ME/CFS. What would really be helpful would be to run the methylation pathways panel on some people with these disorders, to see how their SAMe, SAH, folates and reduced and oxidized glutathione levels compare. I think this would nail down whether the same vicious circle mechanism is involved. I guess I would doubt that they would be the same, because, though there is some overlap in symptoms, as you have written, there are also many differences between these various disorders. I have linked the symptoms in ME/CFS to the aspects of this vicious circle, so I doubt that the same vicious circle would produce different sets of symptoms, unless genomic variations between the people with the different disorders could explain this.
But for me, the first step would be to try to get some measured data with this panel in the different disorders. I realize that this would cost money. The panel costs $295 per person, and requires an order from a chiropractor or a physician.

As you know, I love to develop hypotheses myself, and it's fun to infer things, but there comes a point when the predictions of hypotheses must be compared to measurements in the real world, to see if they jibe. This is the essence of the scientific method, and it's really not possible to make progress toward determining the truth without doing this. So I hope something like this can happen.

Best regards,

Rich

 

[richvank]

Hi, just a quick thought to add to your comment Rich, although I mostly agree with you: sources, sinks and regulation. Too little is known about the altered functional genetics of ME, particularly post exercise.

Most might not be aware, but I have been in agreement with Rich on problems with aconitase, including a high utilization of aminos as fuel, for over a decade now, and that includes the importance of glutathione. Its not just about oxidative damage either. Proper folding of aconitase requires glutathione for the correct sulphur bonds. This may be true of other sulphur rich proteins as well. Bye, Alex

Hi, Alex.

Yes, you and I go back a long way! Good point about the regulation of enzyme activity via changes in gene expression. Also, good point about aconitase. I don't always see a drop between citric acid and the two following Krebs metabolites in the urine organic acids tests in ME/CFS. I think it gets obscured when citric acid is low itself for other reasons, such as deficiencies of the nutrients needed by the pyruvate dehydrogenase complex. But if citric acid is midrange or higher, I can usually see this drop.

Best regards,

Rich

 

[alex3619]

Hi Rich, that is interesting about the drop, and it fits with what we have been saying all these years. I wonder if the issues are in part circadian, and if a drop is more visible at varying stages of circadian energy production. How has the drop been measured? Are we talking blood serum measures? Bye, Alex

PS I have been interested in factors that could show this for a long time. The elevated urinary citrate data was late sleep cycle. This is a point of low energy production but high citrate release, which does not seem to fit offhand. Maybe the data is wrong, or maybe something happens that releases citrate (my third model). Citrate will certainly flush the cell of heavy metals, but also of important metals like magesium, zinc and calcium.

 

[Abha]

[QUOTE Citrate will certainly flush the cell of heavy metals, but also of important metals like magesium, zinc and calcium.[/QUOTE]
Hi alex3619,
I enjoy reading the postings on this thread even though i find a lot of it difficult to follow.At present I'm taking Magnesium Malate 1,250mg to help rid my body of high cadmium levels.I'm not sure how I obtained this as I'm a non smoker(maybe passively?)At one stage I had a bridge(?)fitted for my mouth(dentures)and I'm not sure what metals were used for that.I have also lived in areas of petrol pollutants(burn off)....not sure if it could come from that or water supplies.Alex you mentioned that "citrate will flush the cell of heavy metals,but also of important metals like magnesium,zinc and calcium.Are you saying that these metals(magnesium,zinc and calcium) are leached from the body too.I take calcium citrate daily(osteoporosis) too.Excuse me if this is off the point re MS/ME..(Heavy metals may be involved in these illnesses too?)

 

[richvank]

Hi Rich, that is interesting about the drop, and it fits with what we have been saying all these years. I wonder if the issues are in part circadian, and if a drop is more visible at varying stages of circadian energy production. How has the drop been measured? Are we talking blood serum measures? Bye, Alex

PS I have been interested in factors that could show this for a long time. The elevated urinary citrate data was late sleep cycle. This is a point of low energy production but high citrate release, which does not seem to fit offhand. Maybe the data is wrong, or maybe something happens that releases citrate (my third model). Citrate will certainly flush the cell of heavy metals, but also of important metals like magesium, zinc and calcium.

Hi, Alex.

I don't know about the circadian variation. My experience is with many urine organic acids tests, particularly the one offered by Genova Diagnostics, called the Metabolic Analysis Profile. There is also the Organix test offered by Metametrix, and the OAT offered by Great Plains Lab, and I have seen quite a few results of those, also.

These are run on first morning urine samples, so they reflect the metabolism that occurs during sleeping. The labs have reference ranges for the Krebs cycle metabolites, shown on the reports. What I'm referring to is the levels of these metabolites relative to their normal reference ranges. If citric acid is high relative to its normal mean value, while one or both of the following two are low relative to theirs, I interpret this as a partial block of aconitase. Of course, in doing this, I am relying on the labs to have accurate reference ranges for these metabolites, and one could question that, because these specialty labs often just base these ranges on a collection of samples people have sent them, and of course, most who send in samples to them are probably ill with some disorder, or they would not to testing. Nevertheless, I think this does work.

Best regards,

Rich

 

[Annesse]

Low glutathione is another common factor that all of these diseases share; just like low iron, zinc, vitamin D, B12, dopamine, phenylalanine, adrenaline, noradrenaline, high homcysteine, dysautonomia, spinal cord changes, elevated tumor necrosis factor and abnormal calcium metabolism. They also share the same symptoms due to the lack of the same hormones, neurotransmitters, lack of nutrients and conditions, such as the abnormal calcium metabolism. All of the scientific findings, including every symptom, every missing nutrient, and every dysruption that results, such as elevated tumor necrosis factor and dysautonomia can be traced directly back to one thing. And only one thing. The lack of proteases. Science has proven this. The evidence is overwhelming. Low glutathione does not explain the lack of hormones and neurotransmitters. It does not explain dysautonmia or the lack of vitamin D. The same thing that explains low glutathione explains low vitamin D and the lack of hormones and neurotransmitters.

I believe I have shown conclusively by using scientific data that these diseases originate with the lack of proteases. So when does a hypotheses that is based on proven science become truth? The questions you ask, such as how SAMe and folates compare to lack of glutathione, have already been answered. Glutathione is also low in MS. Here is one study that addresses B12, folate and homocysteine in MS. You can find additional studies in all of the autoimmune diseases.

http://www.ncbi.nlm.nih.gov/pubmed/19153046

Vitamin B12 acts as a coenzyme in the transformation of homocysteine to methionine. This reaction is essential to make S-adenosylmethionine (SAMe). If all of these diseases lack B12, then they would of course not be able to produce SAMe. This is science and logic. You don't have to draw blood to prove this. Although you certainly could.

These diseases have been named after their primary symptoms, i.e., lupus "marks of a wolf", rosacea "flushed blood vessels", myasthenia gravis "heavy muscles". I think they should be named after their cause, "Pancreatic Enzyme Deficiency Disease " (PEDD).

The lack of these proteases explains the most definitive evidence we have in ME/CFS-The spinal tap studies.
Suzanne Vernon, the scientific director of the Chronic Fatigue and Immune Dysfunction Syndrome Association of America stated, "You can't dispute these biological findings." The No. 1 finding was a protease imbalance. All of the other findings are also directly related to this lack of protease.

I don't expect that most researchers, pharmaceutical executives, or even medical professionals will acknowledge this evidence. There would be no monetary benefit. This information would devastate the economy of the richest most powerful people in the world. It would put untold numbers of researchers and medical personnel out of work. Their jobs and their livelihoods depend on not finding the answer. The evidence will be ignored, but it cannot be denied.

Rich,I think our research is compatible. We have much common ground. And if the people that are supposed to be helping are not, then we most certainly should. I don't expect autonomic agreement. I know you will weigh the facts and give thoughtful consideration to the evidence presented.

I have talked a great deal about the immune system and its involvement in these diseases. Science has shown that the immune system is targeting abnormal peptides. It is also targeting unbroken down DNA and proteins, such as in the lupus NETs. The third component is elevated tumor necrosis factor (TNF). TNF is a cytokine. It is a normal necessary part of the immune system. I previously posted a study entitled: "Dysregulated expression of tumor necrosis factor in chronic fatigue syndrome.." The immune system is not broken. It is just not being regulated properly and it is just doing it's job by targeting abnormal proteins. What is responsible in the body for regulating TNF? As the following study states, " proteases are key regulators of the inflammtory response." It goes on to state, "proteases specifically process and release CYTOKINES." Is this a hypothesis? No, it is fact.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2440796/

Speaking of hypothesis and fact, I haven't posted anything concerning the disease process that isn't fact. I hope this information helps you question what you have been told. I hope it brings you closer to the answers you have searched for. The moderators and I have decided today that this thread is off-topic. This is my last post on this thread. I have publishing deadlines I need to attend to, but I hope when I am able to start posting again under a new thread.