Lack of proteases (pancreatic enzymes) and the symptoms of CFS

[Valentijn]

Here is the source for the above information. http://www.metametrixinstitute.org/...with-Specific-Amino-Acid-Supplementation.aspx

I posted a study on the MS thread that identified the following amino acids lacking in fibromyalgia. Based on the spinal tap study results, I believe fibromyalgia and CFS are one and the same. The amino acids found missing were again: phenylalanine, taurine, valine, threonine, methionine, and tyrosine and alanine. Here is the study I posted.

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

These studies don't seem to support that FM and ME/CFS are one and the same. For example, in the ME/CFS study only 1 of the 25 participants had either low valine or threonine, but the FM study says lower levels of valine and threonine were significant. Also, only 5 of the 25 ME/CFS patients had low methionine, which would seem to suggest that a deficiency in that essential amino acid is not particularly telling.

I'm also curious as to how protease deficiency could cause low tryptophan in ME/CFS but (in my case at least) normal serotonin. There are also other studies ( http://jop.sagepub.com/content/19/4/385.short and http://submit.clinsci.org/cs/105/0213/cs1050213.htm ) that make the opposite finding as the one you listed, with high levels of tryptophan in ME/CFS patients.

Also my phenylethylamine and dopamine levels were normal and high-normal respectively, which would also not seem indicative of a problem with the digestion of phenylalanine.

The study you cited also shows that none of the ME/CFS patients had low levels of histidine, although this is also a essential amino acid. I guess I'm a bit confused as to whether you are saying that you think all proteases are lacking, or just specific ones cleaving certain amino acids?

 

[Annesse]

Hi Valentijn, I based my statement about CFS and fibromyalgia being one and the same on the Georgetown University study that detected an "IDENTICAL set of central nervous system, innate immune and amyloidogenic proteins in cerebrospinal fluids from two independent cohorts of subjects with overlapping CFS, PGI, and fibromyalgia." Here is what else the researchers stated, "Although syndrome names and definitions were different, the proteome and presumed pathological mechanisms may be shared."

Spinal fluid studies use very advanced technology;therefore, the results are extremely definitive.

You wouldn't really expect the amino acid studies to be identical. The ability to digest proteins would vary from person to person. What you are looking for is a pattern. The significant lack of phenylalanine is found in both studies. All of the above findings that I posted were based on amino acids that were found lacking in BOTH CFS AND FIBROMYALGIA. Do you know what your threonine levels were? Threonine is the precursor of serine. Serine is needed to produce tryptophan.
Both of the studies found a deficiency in threonine. Even though these percentages could vary from study to study, based on the variables of each person's biological differences, the fact remains, CFS and fibromyalgia sufferers lack essential amino acids that are derived from the break down of dietary proteins. These amino acids are critical and essential factors in the development of CFS itself.

I am not saying that CFS sufferers lack All proteases. The one that has been found lacking in lupus and what led me to every discovery I have made since then is DNase 1. Here is what the Department of Biochemistry states about DNase 1; "DNase 1 as a digestive enzyme that is physiologically regulated is poorly understood. DNase 1 is mainly responsible for the digestion of dietary DNA before it can be absorbed into the body."


Since we are talking about the amino acids that have been found lacking in CFS and fibromyalgia, this may be a good time to show why CFS sufferers are alcohol intolerant. If you are unable to digest proteins, you would not be able to produce the enzyme that is responsible for the metabolism of alcohol-alcohol dehydrogenase. You would also be missing another essential component of alcohol metabolism-zinc. Zinc is found primarily in high protein foods. Here is some information on where zinc is found. As the information states, " Zinc is very much associated with protein foods." http://www.nutritional-supplements-health-guide.com/zinc-food-sources.html

Here is a study that shows CFS sufferers lack zinc.

http://www.ncbi.nlm.nih.gov/pubmed/16338007


Here is a study that shows the role zinc deficiency plays in the ability to metabolize alcohol and it's effect on alcohol dehydrogenase. (Women, by the way, make about 25% less of alcohol dehydrogenase than men even under normal conditions)

http://www.ncbi.nlm.nih.gov/pubmed/21297347

And here is a clear explanation about how alcohol dehydrogenase is synthesized. The last sentence in the second paragraph shows how important these essential amino acids we have been discussing are for the synthesis alcohol dehydrogenase. Pay special attention also to the role that zinc has in the ability of alcohol dehydrogenase to function properly.

 

[Annesse]

I forgot the last link. Here it is.

http://people.mbi.ucla.edu/yeates/153AH_2009_project/siu.html

 

[Annesse]

Here is some more very good information on zinc and alcohol dehydrogenase. This information also lists the other enzymes that need zinc to function properly. The inability to digest proteins would affect our health in ways we can not even imagine.

http://www.netmedicos.com/?aiimsmdmsee2009nov/mcqs/Biochemistry/35/

 

[richvank]

Hi, Annesse.

It's true that serine is in the biosynthetic pathway for tryptophan, but this pathway is found only in bacteria and plants. Animals and humans require tryptophan in their diets, as one of the essential amino acids. Also, you have referred to Dnase1 as a protease, but it is actually a nuclease, i.e. it breaks down DNA, as you recently posted, not proteins.

Best regards,

Rich

 

[richvank]

Hi, Annesse.

It's true that on the average, people with ME/CFS are low in several of the amino acids, though in my experience of analyzing quite a few plasma and urine amino acids panels, this varies quite a bit. Some are even high in amino acids.

You have suggested that the reason for low amino acids levels is lack of enzymes needed to digest protein in the diet. This is certainly one possibility, especially since the exocrine pancreas is very sensitive to a methylation deficit, and we have shown in our clinical study that most PWMEs do have a methylation deficit.

However, there are other possible contributors to low amino acids levels. One is low stomach acid, which many PWMEs have verified for themselves using the baking soda--burp test. Low stomach acid prevents the conversion of pepsinogen to pepsin, which normally begins the digestion of proteins. In addition, low acid levels cause poor signalling of the pancreas to excrete digestive juice via the hormone secretin. I've suggested that the low stomach acid in ME/CFS is due to glutathione depletion in the parietal cells, which require a high rate of production of ATP to overcome the high concentration gradient faced by the proton pumps.

The other side of the amino acids equation involves the rates at which they are burned for fuel. Generally speaking, PWMEs are not able to burn carbs and fats at rates as high as normal, so that their cells burn amino acids at higher than normal rates. I have suggested that this results from a partial block of the enzyme aconitase in the mitochondria, due to glutathione depletion. The results of quite a few urine organic acids tests on PWMEs seem to support this explanation. The experience of weight gain that many PWMEs report after onset of the illness, if previous carb and fat intakes are continued, also seem to support this. The rate of burning of amino acids for fuel can be gauged by the rate of production of urea, and this appears to be elevated in many PWMEs.

Based on the above, I would say that there are other possible explanations for the low average amino acids levels in PWMEs than lack of protease digestive enzyme production capability.

As I've written before, I think you have a plausible mechanism for the autoimmune diseases, but as far as I know, there is no clear evidence that ME/CFS is autoimmune, other than the Hashimoto's component that is often present.

Best regards,

Rich

 

[Annesse]

Hi Rich, I posted the information from the Department of Biochemistry on DNase 1 to show that science is not really sure what it's role in the digestive process is. Based on the unbroken down bits of not only DNA, but also protein fragments in the lupus study, I think it is reasonable to assume it is also involved in the digestion of proteins. The lack of DNase 1 was determined to be a causitive factor of lupus. If we compare the findings in lupus, as we did in MS, you will find the same disease pattern. The overlap between all of these conditions would also indicate they originate from the same source.

I think we should clearly define what you think is taking place with the immune system in autoimmune disease. The information I posted on the lupus mice study done in Germany showed that the immune system is targeting the unbroken down bits of protein and DNA, not normal tissue.

If you are unable to digest proteins, you would not be able to form normal peptides. New research findings show that the immune system is also targeting these abnormal peptides in addition to the unbroken down bits of proteins and DNA. These amyloids are a key feature of the spinal fluid study findings in CFS. That is why I would classify CFS as being caused by PEDD (Pancreatic Enzyme Dificiency Disease) Another notable finding that would point directly to the lack of enzymes is the information I posted on these enzymes being necessary for the binding and transport of vitamin B12. I have also posted information on the pancreatic dysfunction found in CFS.

The dysregulated tumor necrosis factor found in CFS also points directly to serine proteases. This can not really be overlooked.
Also, the fact that these proteases regulate iron in the body. The lack of iron is another defining feature of these illnesses.

And last, but certainly not least, was that the No. 1 protein finding in the CFS cerebrospinal fluid study findings was a PROTEASE IMBALANCE.

I believe that low HCL would of course play a part, as would lack of beneficial bacteria. The entire GI tract needs to be addressed as I stated earlier.

Are you saying though, that for whatever reason, you believe that CFS could be caused by the body's inability to digest dietary proteins?

 

[November Girl]

Onions and the whole allium family are very toxic to cats. Our cat survived an occasional bite of onion (He loved pizza!) but the vet strongly cautioned us to not give him any at all when he heard about it. Any at all destroys some blood cells, and too much can lead to death.

-- Nonetheless, I can not think of anything else that would kill a rodent or other animal, such as a dog or a cat, that we should be taking into our bodies.

 

[Annesse]

Hi November Girl-So True! Grapes and chocolate for dogs. I will need to qualify that statement for sure. I should have said "kill a rodent or other animal in the same manner." Meaning it can affect humans in the same way as it does these other animals; through hypercalcemia which results in systemic calcification of soft tissue.

Hi Rich, you mentioned rapid weight gain in your last post. I was going to address that also. A lack of sleep due to a deficiency in melatonin (from the lack of the essential amino acid tryptophan) would lead to increased levels of leptin, cortisol and gremlin, which could cause weight gain.

The lack of phenylalanine (essential amino acid found in high protein foods) would lead to a lack of both of the thyroid hormones, since they are both derived from tyrosine. Tyrosine is derived from phenylalanine. A lack of the thyroid hormones could also lead to weight gain due to a metabolism slow down.


We have posted a study previously that shows CFS patients have autonomic dysfunction. As we have mentioned the autonomic nervous system is controlled by 2 neurotransmitters; adrenaline and acetylcholine. Adrenaline comes from dopamine. Dopamine comes from tyrosine. Tyrosine comes from phenylalanine. (essential amino acid found lacking in CFS) Acetylcholine come from choline. Choline comes from B12. Here is a chart that shows how autonomic dysfunction could lead to a condition called ROHHAD (Rapid-onset obesity with hypothalamic dysfunction, hypoventilation and autonomic dysregulation.)

http://www.childrensmemorial.org/depts/autonomic-medicine/images/rohhad-figure-large.gif

 

[xchocoholic]

Hi annesse,

Just wanted to congratulate you on healing yourself. I didn't realize that. I'm a self healer too
so I can appreciate your efforts. I started doing this myself in 2005, but without any medical background.
Fortunately , I see an integrrative doctor now who has the knowledge to know what tests to
run.

I wanted to let you know that I support using diet and nutrients for healing as
I've made quite a bit of progress this way. I'm just not as convinced
as you are that this is the answer to me. Cfs is too vague to know
what condition the patient really has.

I googled lupus gluten and found some matches. The same happened when I googled ms gluten.
And I found a match 5 years ago when I first googled cfs gluten. Turns out the nih knows that celiac
disease can be mistaken or lead to cfs. I don't know their position on gluten intolerance now but I think I started out with gluten intolerance
and it later turned into celiac disease.

Also, I don't know how long you've been aware of the terms cfs
and fibromyalgia, but when I was first diagnosed in 1992, fibromyalgia
only referred to the true definition of the term. Now they're using it
to refer to fm and cfs combined. Fwiw. I only have fm pain now from
eating bacon or tomatoes. I had it 24/7 for about 19 years.

Tc .. X

 

[Annesse]

Thanks xchocoholic, that is very kind of you to say. Your information on the connections you found to gluten intolerance and CFS, lupus and MS is interesting. I think they all share a common denominator-the inability to digest proteins. That is why they are so similar that it is hard, at times,to even tell them apart. On the MS thread, I don't think there was any disagreement that the findings and the symptoms are the same in MS as they are in CFS. I think someone may be given a diagnosis of MS if they have more severe myelin damage, or say an MRI is done and white matter lesions are detected. (versus not having an MRI done and no one realizing they are there)

I talked to a local pharmacist the other day that has a daughter with MS. I asked him if he was aware that white matter lesions could be found in CFS, lupus, Sjogren's, RA, and Celiac disease. He said he was not aware of that.

I think there is a lot of information that has been known about these diseases that is not shared with the patients or even doctors. For instance, the way I discovered that restless legs syndrome was connected to a lack of iron and dopamine was by talking to a girl that had RLS. She is a marathon runner, but had developed terrible RLS. She told me her doctor had given her a drug used for Parkinson's and that it was helping. I knew Parkinson's was caused by a lack of dopamine and so I asked her why the doctor thought a Parkinson's drug would help her RLS. She had no idea why. No one had even mentioned dopamine to her.

Another example of this would be tumor necrosis factor and Crohn's. The Crohn's drug, Humira, was designed to target tumor necrosis factor. If you go on the Humira website, it will tell you that TNF is elevated in Crohn's and that indeed the drug was designed to target TNF. Most Crohn's patients are not aware of this. The question to be asking is "WHY is my TNF elevated?" I have met Crohn's patients that developed such severe infections from taking Humira that the infections had to be literally cut out. TNF is controlled in the body by proteases. A targeted diet will restore these proteases. By retoring these enzymes, you will then be able to properly regulate TNF and heal your Crohn's.

I don't think we realize that what may perhaps be in our best interest may be, in fact, in direct conflict with the goals of the companies that control the flow of information. Here is a quote from a former New York Times reporter; "In this profit-driven world of medicine, I did not often hear the executives talk of cures. Instead, they focused like honeybees circling a picnic cake on products for what they called the chronic disorders. These were the drugs that did not cure, but 'managed' disease as patients took them once a day for the rest of their lives."

 

[aprilk1869]

Annesse what do you think of calcitonin gene-related peptide (CGRP)? I've just come across info about how it's elevated in complex regional pain syndrome (CRPS) which a friend has, her sister has ME and her sister's daughter has MS.

The important role of neuropeptides in complex regional pain syndrome.
http://www.ncbi.nlm.nih.gov/pubmed/11756594

It is also linked to migraines and lups, perhaps other conditions too.

The neuropeptide calcitonin gene-related peptide inhibits TNF-alpha but poorly induces IL-6 production by fetal rat osteoblasts.
http://www.ncbi.nlm.nih.gov/pubmed/9417811

Mechanism of action of calcitonin gene-related peptide in inhibiting pancreatic enzyme secretion in rats.
http://www.ncbi.nlm.nih.gov/pubmed/8099887

 

[Annesse]

Hi Aprilk1869, I would like to show first how Complex Regional Pain Syndrome and migraines would tie in with our discussion on the inability to break down proteins. We have done this with MS and lupus, but not CRPS and migraines. We can come back to CGRP if we need to.

One of the common denominators we have found throughout these diseases is autonomic dysfunction. If you are unable to digest proteins, you would not be able to make either of the neurotransmitters that regulate the autonomic nervous system. Autonomic dysfunction is also a well recognized feature of CRPS. Here is some information on this.

http://www.ninds.nih.gov/disorders/...rophy/detail_reflex_sympathetic_dystrophy.htm

Another common denominator is elevated tumor necrosis factor (TNF). TNF is regulated by proteases. (pancreatic enzymes that digest proteins)
Here is a study that demonstrates this.

http://www.ncbi.nlm.nih.gov/pubmed/19910617

Peripheral neuropathy is closely associated with CRPS. In fact, it is on the CRPS differential diagnostic list. Peripheral neuropathy is linked to vitamin B12 deficiency. Since acetylcholine is one of the neurotransmitters that regulates the autonomic nervous system, this would be expected. (Acetylcholine comes from choline, choline comes from B12) B12 is only found attached to dietary animal proteins, so this again would point to proteases. Here is some information on peripheral neuropathy and its close association to lack of B12.
http://peripheralneuropathycenter.uchicago.edu/learnaboutpn/typesofpn/systemic/nutrition.shtml

Lack of B12 would then lead to elevated homocysteine. Homocysteine induces "programmed cell death in human vascular endothelial cells." Here is the study.
http://www.jbc.org/content/276/38/35867.full

The damage to the endothelial cells would explain the link between migraines and CRPS. In Headache: The Journal of head and Face Pain, author Cris S. Constantinescu MD.,Ph.D., states, "Migraine and Raynaud phenomenon often coexist. Both have been associated with vascular endothelial cell dysfunction." (Constantinescu, 2002).

Here is a study that shows endothelial cell dysfunction in CRPS.

http://www.neurology.org/content/67/4/673.short

Certainly we can do some research on MTHFR. But, as you can see, every symptom of CRPS and its relationship to other diseases, such as lupus and migraines can be directly traced back to the inability to digest proteins.

 

[Annesse]

Hi again Aprilk1869, I tackled the calcitonin gene-related peptide question as to why it is elevated in the diseases you mentioned. Here is some information on its connection to lack of proteases.


"Regulation of the calcitonin gene related peptide (CGRP) gene is in part controlled by the expression of the mitogen-activated protein kinases (MAPK) signaling pathway,[8] cytokines such as TNF? [9] and iNOS.[10]"

So, first, its regulation is connected to TNF. (TNF is controlled by proteases) Also, it is in part controlled by mitogen-activated protein kinases. Here is where protein kinases are derived from.

"Mitogen-activated protein (MAP) kinases (EC 2.7.11.24) are serine/threonine-specific protein kinases that respond to extracellular stimuli (mitogens, osmotic stress, heat shock and proinflammatory cytokines) and regulate various cellular activities, such as gene expression, mitosis, differentiation, proliferation, and cell survival/apoptosis.[11]"

So, protein kinases are derived from the amino acids serine and threonine. Threonine is one of the amino acids found to be lacking in CFS and Fibromyalgia patients. It is found in high protein foods. Also, serine has been found lacking in studies on CFS.

This may be an example of what I was referring to when I talked about information being given to the public that may in effect be used as a distraction. I am pretty sure they know what regulates CGRP. If they can convince us that taking a drug to lower CGRP would be beneficial, then I believe that would be something they would probably do.

 

[xchocoholic]

Honey bees ? I was thinking fire ants ... Lol

I'm sure you know that gluten and casein act as opioids in people with leaky guts. Not all proteins
affect us that way. If you're not up on this, "Healing the 4's A's" is a good book. And unlike most
of us, you'll probably understand the whole book. Lol

I do have problems with digesting proteins tho. I need 5htp for sleep but chicken, turkey and tuna
make me so drowsy that all I want to do is sleep. I suspect it's the tryptophan in these. Beef is off the menu now because it just sits in my gut. I'm pretty sure mine is gut damage tho. I had significant damage 17 months post gf.

Functional or integrative doctors look at chronic illnesses as beginning in the gut. Cdsa's, nutritional
panels, hormone panels are their tools. I've really gotten an education on all this over the last 6 years.
I was a traditional doctor worshiper until I responded positively to a gfcfsf diet change within 24 hours.
When I started walking normally and saw after hours of googling that I'd had gluten ataxia, the
gloves came off .. I was po'd .. Lol ..

Good luck with your book .. I may have to read it now. X

 

[aprilk1869]

Annesse, I'm trying to get my head around what you're written. You say that serine and threonin is often deficient and that these amino acids are needed for creating MAPK and that MAPK is needed for regulating CGRP.

But wouldn't that mean MAPK would be low? I've read that MAPK is elevated in migraines.

"It was determined in other experiments that nerve growth factor activated the CGRP promoter by stimulating mitogen-activated protein kinases (MAPKs)."
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3134175/

Or does it related to misfolded proteins?

Misfolded truncated protein ? induces innate immune response via MAPK pathway.
http://www.ncbi.nlm.nih.gov/pubmed/21813771

 

[adreno]

One thing we have to remember here is that correlation is not causation. A lot of different parameters can be found to be either lowered or elevated in ME, but that does not in any way enable us to conclude that these parameters are causative. In fact, they may indeed be compensatory.

One way to test a hypothesis like this would be to take a group of otherwise healthy animals and perform a pancreatectomy (or otherwise block the production or effects of pancreatic enzymes) and observe if they develop autoimmune diseases. Until then, we have no real evidence that this theory is valid.

Besides a handful of otherwise interesting anecdotes, we also have no evidence that diet can cure ME. And if a lack of pancreatic enzymes is the specific cause, I see no rational argument why supplementing them from a bottle wouldn't work. In fact, people who have had a pancreatectomy do exactly this.

 

[Annesse]

Hi xchocoholic, I will check that book out. It sounds very interesting. Thank you.

Hi Aprik1869, I think that the reason for the elevated CGRP would be most certainly related to either lack of, or improperly made, MAPK, due to lack of serine and threonine. The fact that it was so easily traced back to the inability to digest proteins is pretty noteworthy. Also, the study you provided is additional evidence that when the body lacks the proper building blocks (in this case serine and threonine) to make new proteins, it can and will then form misshapen proteins that will trigger an immune response. These amyloids will have far reaching and dramatic effects on our health.

Hi Adreno, I think that the spinal tap studies in CFS, along with everything else,, are pretty convincing evidence. Here is what an article in Medical News Today stated about these studies; "Taking advantage of previously unavailable methods for detailed analysis of spinal fluid, the investigators analyze the fluid by means of high powered mass spectrometry and special protein separation techniques.

Suzanne Vernon (director of the Chronic Fatigue and Immune Dysfunction Syndrome of America) stated about these studies, " They looked at a really important fluid using really advanced technology and they found clear differences. I'm very excited about this, you can't dispute these biological findings."

The No 1 finding was a protease imbalance.
No 2 was amyloids
The other findings were endothelial cell damage, cell suicide (apoptosis) and free radical production. These are all consistent with elevated homocysteine, which has been found in a previous spinal fluid study.

There are no inconsistencies here.

Many people take incredibly harmful drugs to find relief from the symptoms of these diseases. These drugs are designed to modify symptoms. In doing so, they will invariably cause more symptoms, some even more harmful than the ones they were designed to treat. None of them effectively address the cause. Doesn't it make sense that the answer would be diet? Our diet is the only source of the essential amino acids and nutrients that are found missing in CFS. I am not asking anyone to jump off a building without a parachute. I don't think anyone has anything to lose by trying to address this through diet. I do believe though that they have everything to gain. Hundreds of people have made full recoveries. All they are doing are eating the foods that should be in their diets anyway and avoiding things that have no business being in our environment, let alone our bodies. This approach has no side effects, just side benefits.

I don't think it is necessary to take someone's pancreas out to see if they would be able to recover from the inability to digest proteins. Here is a study that shows even Celiac patients can eat bread as long as the proteins( gluten) are properly broken down with enzymes and beneficial bacteria. In this study, they used fungal "proteases".

My computer is not allowing me to search at the moment so I will post the titles and then try and post some links later. Here is the title: "Highly efficient gluten degradation by lactobacilli and fungal proteases during food processing; new perspectives for celiac disease."

Here is the title of another study that found no toxic effects to celiac patients as long as the gluten was properly fermented the way nature intended.

"Sourdough bread made from wheat and nontoxic flours and started with selected lactobacilli is tolerated in celiac sprue patients"

The evidence is overwhelming that CFS patients are unable to digest proteins. It is an amazing and remarkable thing that we are able to correct this through diet.

 

[adreno]

Hi Adreno, I think that the spinal tap studies in CFS, along with everything else,, are pretty convincing evidence. Here is what an article in Medical News Today stated about these studies; "Taking advantage of previously unavailable methods for detailed analysis of spinal fluid, the investigators analyze the fluid by means of high powered mass spectrometry and special protein separation techniques.

Suzanne Vernon (director of the Chronic Fatigue and Immune Dysfunction Syndrome of America) stated about these studies, " They looked at a really important fluid using really advanced technology and they found clear differences. I'm very excited about this, you can't dispute these biological findings."

The No 1 finding was a protease imbalance.
No 2 was amyloids
The other findings were endothelial cell damage, cell suicide (apoptosis) and free radical production. These are all consistent with elevated homocysteine, which has been found in a previous spinal fluid study.

There are no inconsistencies here.

You did not include any references, but a recent study on the CSF of patients with Post-Treatment Lyme Disease and Chronic Fatigue Syndrome found the following:

PLoS One. 2011 Feb 23;6(2):e17287.
Distinct cerebrospinal fluid proteomes differentiate post-treatment lyme disease from chronic fatigue syndrome.
Schutzer SE, Angel TE, Liu T, Schepmoes AA, Clauss TR, Adkins JN, Camp DG, Holland BK, Bergquist J, Coyle PK, Smith RD, Fallon BA, Natelson BH.
Source
Department of Medicine, University of Medicine and Dentistry of New Jersey-New Jersey Medical School, Newark, New Jersey, United States of America. schutzer@umdnj.edu
Abstract
BACKGROUND:
Neurologic Post Treatment Lyme disease (nPTLS) and Chronic Fatigue (CFS) are syndromes of unknown etiology. They share features of fatigue and cognitive dysfunction, making it difficult to differentiate them. Unresolved is whether nPTLS is a subset of CFS.
METHODS AND PRINCIPAL FINDINGS:
Pooled cerebrospinal fluid (CSF) samples from nPTLS patients, CFS patients, and healthy volunteers were comprehensively analyzed using high-resolution mass spectrometry (MS), coupled with immunoaffinity depletion methods to reduce protein-masking by abundant proteins. Individual patient and healthy control CSF samples were analyzed directly employing a MS-based label-free quantitative proteomics approach. We found that both groups, and individuals within the groups, could be distinguished from each other and normals based on their specific CSF proteins (p<0.01). CFS (n?=?43) had 2,783 non-redundant proteins, nPTLS (n?=?25) contained 2,768 proteins, and healthy normals had 2,630 proteins. Preliminary pathway analysis demonstrated that the data could be useful for hypothesis generation on the pathogenetic mechanisms underlying these two related syndromes.
CONCLUSIONS:
nPTLS and CFS have distinguishing CSF protein complements. Each condition has a number of CSF proteins that can be useful in providing candidates for future validation studies and insights on the respective mechanisms of pathogenesis. Distinguishing nPTLS and CFS permits more focused study of each condition, and can lead to novel diagnostics and therapeutic interventions.
PMID: 21383843.

The researchers did not conclude that the different protein signatures are the cause of these syndromes, and neither can we. From the full text:

Our results represent the most comprehensive analysis of the whole CSF proteome to date for both CFS and nPTLS. These two disorders have similar symptoms that have created diagnostic dilemmas. It has been speculated that one (nPTLS) is a subset of the other, but our results do not support that notion. Our findings alone do not describe why CFS or nPTLS occur, but are provided to illustrate that CSF proteome analysis may provide important and meaningful insights into the biological processes modulated as a function of disease and facilitate the identification of protein candidates for further investigation.

From this we can conclude that these biomarkers are primarily of diagnostic value. We can also see that the study suggest that the two syndromes are dissimilar, which would indicate different etiologies.

Many biomarkers have been described as abnormal in CFS. But biomarkers are indications, not necessarily causes. For instance, cortisol is found to be be low in CFS. Does this mean that low cortisol is the cause of CFS? No, it doesn't. Similarly, vitamin D levels are found to be low, does this mean that CFS is caused by vitamin D deficiency? No. Abnormal biomarkers are most likely effects, not causes.

Many people take incredibly harmful drugs to find relief from the symptoms of these diseases. These drugs are designed to modify symptoms. In doing so, they will invariably cause more symptoms, some even more harmful than the ones they were designed to treat. None of them effectively address the cause.

This idea that all drugs are poisonous and only treating symptoms is simply not true. The reason why most drugs for chronic illnesses are only palliative is simply because the etiologies are poorly understood, and cannot be properly addressed at this point.

Doesn't it make sense that the answer would be diet? Our diet is the only source of the essential amino acids and nutrients that are found missing in CFS. I am not asking anyone to jump off a building without a parachute. I don't think anyone has anything to lose by trying to address this through diet. I do believe though that they have everything to gain. Hundreds of people have made full recoveries. All they are doing are eating the foods that should be in their diets anyway and avoiding things that have no business being in our environment, let alone our bodies. This approach has no side effects, just side benefits.

It is possible that diet changes can cure CFS, but it is far from an automatic given. As has been said before in this thread, many PWCs have tried dieting already, without success. Without controlled, reproducible studies, we simply do not know. To claim that diet is the cure of all autoimmune diseases and/or CFS is simply premature at this point, and I find it unethical to suggest treatment that is not evidence-based.

I don't think it is necessary to take someone's pancreas out to see if they would be able to recover from the inability to digest proteins. Here is a study that shows even Celiac patients can eat bread as long as the proteins( gluten) are properly broken down with enzymes and beneficial bacteria. In this study, they used fungal "proteases".

My computer is not allowing me to search at the moment so I will post the titles and then try and post some links later. Here is the title: "Highly efficient gluten degradation by lactobacilli and fungal proteases during food processing; new perspectives for celiac disease."

Here is the title of another study that found no toxic effects to celiac patients as long as the gluten was properly fermented the way nature intended.

"Sourdough bread made from wheat and nontoxic flours and started with selected lactobacilli is tolerated in celiac sprue patients"

This is interesting, but I fail to see the relevance between a celiac patient study and CFS. It's a strong argument that gluten can be properly digested if fermented, but it adds no support to your hypothesis that CFS is caused by a defiency of pancreatic enzymes.

The evidence is overwhelming that CFS patients are unable to digest proteins. It is an amazing and remarkable thing that we are able to correct this through diet.

In fact, the evidence you have presented is very underwhelming.

 

[Annesse]

Hi Adreno, Well, we obviously disagree and that is OK. I can think of a few very strong arguments that weren't readily accepted by everyone in the beginning. The earth versus the sun being the center of the universe for one. The information is available for each person to decide for themselves what their choice will be.When I was sick, I would have given anything to have had someone share this information with me.

You say you fail to see the revelance between a celiac patient and CFS. I believe both celiac disease and CFS are caused by a lack of protease. There is no disagreement that celiac patients are unable to digest gluten, which is a protein. The researchers used fungal protease to make the protein digestible for the celiac patients. Celiac patients also lack B12. This is significant because this shows they are also not digesting other proteins in addition to gluten. Here are the diseases and disorders associated with celiac disease.

http://www.celiac.com/categories/Celiac-Disease-Research:-Associated-Diseases-and-Disorders/

CFS is on this list. These are also the same diseases and disorders associated with CFS. Ask yourself, how would celiac disease cause CFS? Remember, we KNOW what causes celiac disease. So, the answer is it doesn't. Why then is CFS linked to celiac disease? And why are all of the other conditions and diseases we have been able to link directly to the inability to digest proteins on the list also?