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The difference between MS and ME

alex3619

Senior Member
Messages
13,810
Location
Logan, Queensland, Australia
Hi Annesse, while I was studying biochem at uni I read a paper from India on type two diabetes. Using fish oil, B vitamins and traditional cooking oils, if I recall correctly, they reversed the diabetes in most patients. It was a small study, not very well reported on, I wish I remembered the details. I thought you might find it interesting to know that a return to traditional cooking (not the modern variant) plus some specific supplements could have an impact. Bye, Alex

Thank you Alex, that is really interesting. Something to think about for sure. Your vegetarian comment is interesting. The country with the most vegetarians in the world also leads the world in diabetes and heart disease. That country is India. The International Journal of Diabetes in Developing Countries calls India, "the diabetes capital of the world." Ninety- five percent of the diabetics in India have type 2 diabetes. In a study entitled: "Vitamin B12 Deficiency and Hyperhomocysteinemia in Rural and Urban Indians," even at an extremely low level tested (150 pg/mL) it was found that 81% of the urban middle class had low B12, and 79% had high homocysteine. Imagine what the deficiency would have been if they would have tested at a reasonable level? In India, they lack B12 and amino acids (insulin is made from amino acids) because they aren't eating animal proteins. We are eating these proteins, we just aren't breaking them down. The results, however, are the same.
 

Annesse

Senior Member
Messages
164
If we are right about all of these diseases being just symptoms really of the inabilty to break down proteins, then what we find in one, we should find in the other. Following is a study on the lack of zinc in CFS.

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

Mellster, I think I posted some information previously (I could be wrong) about the severe lack of B1 (thiamine) found in diabetes by researchers from Warwick University in England. The paper was published in Diabetologia. The researchers found that thiamine concentration in blood plasma was reduced 76% in type 1 diabetic patients and 75% in type 2 diabetic patients. This deficiency was not due to dietary imput of thiamine, but rather a PROFOUND increased rate of removal of thaimine from the blood into the urine they stated. Here is the thing, you can't absorb B1 if you lack B12. IT IS EXCRETED IN THE URINE. So, the lack of B12 does seem to play a significant role in the developement of diabetes. Here is a study from India that confirms this role.

http://www.ncbi.nlm.nih.gov/pubmed/19707742

If Indians lack B12, then they would not be able to make acetylcholine. Acetylcholine is one of the neurotransmitters that regulates the autonomic nervous system. The autonomic nervous system plays a part in insulin resistance. Also, the lack of acetylcholine would lead to diseases like Myasthenia Gravis. The rates of Myasthenia Gravis are very high in India.
 

Annesse

Senior Member
Messages
164
I did want to come back to this when I had time. I found this information on Livestrong.


"As proteins break down they form compounds called purines which in turn become uric acid, the final waste product of protein digestion, explains the University of Michigan Health System."

Read more: http://www.livestrong.com/article/369386-protein-diet-for-gout/#ixzz1gIBCPMJo

The inability to break down dietary proteins would solve the mystery of why MS patients don't get gout. Since uric acid is the final waste product of protein digestion, we would also expect to see low uric acid levels in the associated diseases, as we have in CFS.
 

Annesse

Senior Member
Messages
164
One of the main things that we would need to explain is the immune system attack on the bodies own tissues in autoimmune disease. We have already demonstrated that there is elevated tumor necrosis factor. Also, protein fragments and bits of DNA would end up in the bloodstream if you were unable to properly digest proteins. This would cause an immune response. There is another component though. What exactly is the immune system targeting in autoimmune disease?

When we ingest a dietary protein, our bodies do not specifically use the protein, instead, following ingestion of the protein, enzymes within the digestive tract proceed to break the protein down into smaller peptide chains, in order to separate the amino acids. What if your body lacked the enzymes to properly break down dietary proteins into normal peptides? Could your body be in fact targeting abnormal proteins or peptides in autoimmune disease? Researchers at National Jewish Health and the University of Colorado Anschutz Medical Campus have identified the precise abnormal peptide that they believe is triggering diabetes. They state, the findings support "An emerging theory about the origins of autoimmunity." Here is an article about this discovery.

http://www.nationaljewish.org/about/mediacenter/pressreleases/2010/diabetes-tcells/
 

xrayspex

Senior Member
Messages
1,111
Location
u.s.a.
Hey, I read through page 5 here and will get to the rest, but wanted to jump into say I was dx with sjogrens this summer, after having had "cfs,fm" sort of stuff for over 20 years, and my doc ran a b12 check on me,(he works in mainstream clinic), and it came back high. how does that fit in? and whenever i tried to supplement with b12 in recent years it made me feel worse so stopped, even had injections.
 

richvank

Senior Member
Messages
2,732
I did want to come back to this when I had time. I found this information on Livestrong.


"As proteins break down they form compounds called purines which in turn become uric acid, the final waste product of protein digestion, explains the University of Michigan Health System."

Read more: http://www.livestrong.com/article/369386-protein-diet-for-gout/#ixzz1gIBCPMJo

The inability to break down dietary proteins would solve the mystery of why MS patients don't get gout. Since uric acid is the final waste product of protein digestion, we would also expect to see low uric acid levels in the associated diseases, as we have in CFS.

Hi, Annesse.

As far as I know, proteins themselves do not form purines. It's true that some foods that are high in proteins are also high in purines, but the proteins themselves are not converted into purines. The synthesis of purines uses a special pathway that requires ribose (not found in proteins), 10-formyl tetrahydrofolate, and some individual amino acids (glutamine, glycine and aspartate). It's true that amino acids do come from proteins, but they must be completely broken down to supply the amino acids, so I don't see how this would be associated with not being able to break down proteins properly. I suspect that the U. of Mich. Health System has not done their homework very well on purines. If you have better evidence than their unreferenced article, please let me know.

If you can tie poor protein digestion to a B12 deficiency, I can understand a connection to gout, as I wrote earlier, but I don't think it can happen by faulty protein breakdown producing excess purines.

Best regards,

Rich
 

mellster

Marco
Messages
805
Location
San Francisco
I have been wondering about the elevated TNF which increases apoptosis and whether it coulg be responsible for inflammation pain symptoms - here is an article that describes elevated TNF release by NK/immune cells in relation to dementia: http://www.ncbi.nlm.nih.gov/pubmed/11268360
That brings my train of thought to the next hypothesis that maybe, just maybe, the decreased number/activity (and maybe also function) of NK cells could be mediated by the body as a self-protecting mechanism from releasing too much TNF and attacking cells that might not need apoptosis (instead of thinking of an elusive pathogen as the causative factor). That ties in with he experience of some people that feel there immune system is on fire all the time - TNF is very important to kill bad cells, but if it goes overboard it can probably cause a wide range of issues, from pain in the body to - if acting within the brain - brain inflammation and dementia or even things like alzheimers. Maybe once the over-release of TNF and related cytokines is corrected, the immune cell numbers and their function/activity can normalize again. This is a great thread although it touches so many different topics ;) cheers

One of the main things that we would need to explain is the immune system attack on the bodies own tissues in autoimmune disease. We have already demonstrated that there is elevated tumor necrosis factor. Also, protein fragments and bits of DNA would end up in the bloodstream if you were unable to properly digest proteins. This would cause an immune response. There is another component though. What exactly is the immune system targeting in autoimmune disease?

When we ingest a dietary protein, our bodies do not specifically use the protein, instead, following ingestion of the protein, enzymes within the digestive tract proceed to break the protein down into smaller peptide chains, in order to separate the amino acids. What if your body lacked the enzymes to properly break down dietary proteins into normal peptides? Could your body be in fact targeting abnormal proteins or peptides in autoimmune disease? Researchers at National Jewish Health and the University of Colorado Anschutz Medical Campus have identified the precise abnormal peptide that they believe is triggering diabetes. They state, the findings support "An emerging theory about the origins of autoimmunity." Here is an article about this discovery.

http://www.nationaljewish.org/about/mediacenter/pressreleases/2010/diabetes-tcells/
 

Annesse

Senior Member
Messages
164
Hi Xray, I would need a little more info. Do you know what your actual B12 level is? Are you taking any other supplements?
The proper absorption of B12 is key. Your blood level is often not indicative of your cellular level.

Hi Rich, I think I may put this on the back burner. I know that with the correct scientific data we will be able to come to a concensus. It is interesting though, and a great puzzle maybe yet to solve.

Hi mellster, no doubt we are not able to degrade TNF. I think you have come to the same conclusion I have. Here is what I wrote in my book. "It would seem to make more sense to simply fix the problem at the source, rather than risk such serious side-effects of various drugs. TNF would the get back to being a benefit to our bodies, rather than a painful disease promoter."


Here is another example of the immune system targeting abnormal peptides. This time it is in the autoimmune disease Rosacea. An article in U.S. News & World Report titled, "A New Front in the Fight Against Rosacea," discussed findings that Rosacea was associated with abnormal proteins. The lead researcher Dr. Richard Gallo of the University of California-San Diego stated, "In rosacea, PEPTIDES ARE MADE ABNORMALLY. One hundred percent of the rosacea patients we looked at made more antimicrobial peptides than normal. And the peptides were processed into an abnormal form that we found only in rosacea patients skin,not in normal skin. THIS ABNORMAL FORM TRIGGERS THE BODY'S INFLAMMATORY IMMUNE SYSTEM, WHICH NORMALLY ACTIVATES WHEN YOU HAVE A CUT OR AN INJURY."

Imagine this same response occurring 'inside' your body when it encounters a 'foreign' protein.
 

Annesse

Senior Member
Messages
164
The following information came from an article entitled, "Nutrients Found In Animal Protein Foods But Not In Plant Protein Foods."

"Although many plant-based foods such as cereals are fortified with vitamin B12, the best sources of vitamin B12 come from animal protein foods like meat, fish, chicken, clams, milk, eggs and other dairy products, according to the National Institutes of Health Office for Dietary Supplements. Although zinc is found in small amounts in some plant-based protein foods, such as beans, whole grains and nuts, the main source for zinc is animal-based protein foods, such as poultry, red meat, oysters, seafood and milk, according to the Office for Dietary Supplements. The form of iron that is best absorbed by the body is found in chicken liver, red meat, poultry, fish and seafood. Fish is an excellent source of omega-3 fatty acids."

The essential amino acid phenylalanine is also found in these same foods. We have shown that all of these diseases lack B12, iron and zinc.

If autoimmune sufferers are eating these proteins, why are they lacking these nutrients?

Time to talk about enzymes. We will need to look at the lupus NETs study again.
http://www.sciencedaily.com/releases/2010/05/100503161423.htm

In the last paragraph it states, "The scientists also discovered that NETs are degraded by the enzyme DNase 1, a protein which is normally found in the blood. Lupus patients, however, either lack this enzyme or their DNase 1 is blocked."

DNase 1 is found mostly in the pancreas where it is produced. The Department of Biochemistry states, "DNase 1 as a digestive enzyme is poorly understood."DNase 1 is mainly responsible for the DIGESTION OF DIETARY DNA before it can be absorbed into the body." So, it has another function besides breaking down the NETs and cleaning up cellular debris. The NETs were comprised of the very things that DNase 1 should have broken down before they entered the bloodstream. If DNase 1 is missing from the blood, then logically, it would be missing from the pancreas where it is produced. This missing enzyme leaves undigested DNA and proteins that should have been broken down during digestion, but were not.

DNase 1 is a protease. Protease break down proteins into smaller amino acids. Why do autoimmune sufferers lack B12 and the other nutrients found in proteins? Here is a study that states these same pancreatic enzymes are, "ESSENTIAL DETERMINING FACTORS FOR TRANSPORT AND ABSORPTION OF COBALAMIN (B12) IN MAN."

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC371670/
 

Annesse

Senior Member
Messages
164
The following information is from Phoenix Rising on the CFS spinal tap studies. Notice the first protein finding.

"Unique Protein Signature? - These proteins consisted of the following:

two proteins suggesting a protease antiprotease imbalance is present. This implicates increased production of elastase, an enzyme Dr. De Meirleir believes plays a role.
several proteins suggesting small amounts of bleeding in the brain could be caused by the aggregation of proteins (amyloids) in the blood vessesl.
Another protein suggests increased free radical production is present
Another suggests that problems with the vasoconstriction of the blood vessels and damage to the cells lining the blood vessels (the endothelial cells).
Another protein is associated with inflammation
One protein suggesting altered rates of cell suicide (apoptosis) are present."
 

aprilk1869

Senior Member
Messages
294
Location
Scotland, UK
Since reading up on health this year I felt that a lot of the problems we have in the west are because we've moved away from eating organ meats. In some countries eating organ meats is very important and that includes the pancreas. So this has led me to look up whether eating pancreas is used to treat illnesses.

Eat raw pork pancreas daily, live longer
http://www.philstar.com/article.aspx?articleid=508651&publicationsubcategoryid=448


"Exocrine pancreatic insufficiency (EPI) is the inability to properly digest food due to a lack of digestive enzymes made by the pancreas. This disease is found frequently in dogs. EPI is also found in humans afflicted with cystic fibrosis and Shwachman-Diamond Syndrome. EPI is caused by a progressive loss of the pancreatic cells that make digestive enzymes. Most commonly in dogs, this is caused by pancreatic acinar atrophy. The atrophy in turn can be caused by previous infections, a blocked pancreatic duct, or genetics. Chronic pancreatitis is the most common cause of EPI in humans and cats, but it is an uncommon cause in dogs.[1] Loss of digestive enzymes leads to maldigestion and malabsorption of nutrients.


Diagnosis and treatment


The most reliable test for EPI in dogs and cats is serum trypsin-like immunoreactivity (TLI).[9] A low value indicates EPI. Fecal elastase levels may also be used for diagnosis in dogs.[10]

In dogs, the best treatment is to supplement its food with dried pancreatic extracts. There are commercial preparations available, but chopped bovine pancreas from the butcher can also be used (pork pancreas should not be used because of the rare transmission of pseudorabies).[11] Symptoms usually improve within a few days, but lifelong treatment is required in most cases. A rare side effect of use of dried pancreatic extracts is oral ulceration and bleeding.[12]

Because of malabsorption, serum levels of cyanocobalamin (vitamin B12) and tocopherol (vitamin E) may be low. These may be supplemented, although since cyanocobalamin contains the toxic chemical cyanide, dogs which have serious cobalamin issues should instead be treated with hydroxocobalamin or methylcobalamin.[citation needed] Cyanocobalamin deficiency is very common in cats with EPI because about 99 percent of intrinsic factor (which is required for cyanocobalamin absorption from the intestine) is secreted by the pancreas. In dogs this figure is about 90 percent, and only about 50 percent of dogs have this deficiency.[11] Cats may suffer from Vitamin K deficiencies. If there is bacterial overgrowth in the intestine, antibiotics should be used, especially if treatment is not working. In dogs failing to gain weight or continuing to show symptoms, modifying the diet to make it low fiber and highly digestible may help. Despite previous belief that low fat diets are beneficial in dogs with EPI, more recent studies have shown that a high fat diet may increase absorption of nutrients and better manage the disease.[13] However, it has been shown that different dogs respond to different dietary modifications, so the best diet must be determined on a case by case basis.[14]

http://en.wikipedia.org/wiki/Exocrine_pancreatic_insufficiency
"

"Neurological Features and Enzyme Therapy in Patients With Endocrine and Exocrine Pancreas Dysfunction Due to CEL Mutations

OBJECTIVETo further define clinical features associated with the syndrome of diabetes and pancreatic exocrine dysfunction due to mutations in the carboxyl-ester lipase (CEL) gene and to assess the effects of pancreatic enzyme substitution therapy.

RESEARCH DESIGN AND METHODSNine patients with CEL gene mutation, exocrine deficiency, and diabetes were treated and followed for 30 months.

RESULTSTreatment improved symptoms in seven of nine patients. Exocrine and endocrine function assessed by fecal elastase and A1C were not affected, although fecal lipid excretion was reduced. Vitamin E was low in all patients but increased with treatment (P < 0.001 at 30 months) and improved in five subjects. A predominantly demyelinating neuropathy was seen in a majority of patients, and carpal tunnel syndrome was common.

CONCLUSIONSPancreatic enzyme substitution alleviated symptoms and malabsorption and normalized vitamin E levels. Glycemic control was not significantly affected. The CEL syndrome seems associated with a demyelinating neuropathology.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2518335/
"

As I mentioned in a previous post, health problems in the female line of my family include diabetes and carpal tunnel syndrome.


"PANCREAZE may cause serious side effects, including:

A rare bowel disorder called fibrosing colonopathy
Irritation of the inside of your mouth. This can happen if PANCREAZE is not swallowed completely
Increase in blood uric acid levels. This may cause worsening of swollen, painful joints (gout) caused by an increase in your blood uric acid levels
Allergic reactions including trouble with breathing, skin rashes, or swollen lips
http://www.pancreaze.net/epi
"


"THE INFLUENCE OF THE INGESTION OF RAW PANCREAS UPON THE BLOOD LIPIDS OF COMPLETELY DEPANCREATIZED DOGS MAINTAINED WITH INSULIN*

The results of the present investigation show that the level of the blood lipids of the completely depancreatized dog maintained with insulin can be strikingly influenced by the presence and absence of raw pancreas in the diet. When such animals are fed a diet containing none of the glandular tissue, a drop in the lipid concentration of the blood sets in soon after pancreatectomy. The time of onset of these changes in blood lipids was found to vary among the animals studied. A drop below the normal or prc-operative level occurred as early as 12 days after pancreatectomy. In eight dogs cholesterol esters were reduced to between 0 and 3 mg. per cent at intervals of 20 to 122 days following pancreatectomy, while in three others 7 to 14 mg. per cent were still found in whole blood as late as 96 to 202 days after pancreatectomy.

http://www.jbc.org/content/112/1/155.full.pdf
"

Severe impaired deambulation in a patient with vitamin D and mineral deficiency due to exocrine pancreatic insufficiency.
http://www.ncbi.nlm.nih.gov/pubmed/21904076

Zinc metabolism in patients with exocrine pancreatic insufficiency.
http://www.ncbi.nlm.nih.gov/pubmed/9853534

Bone mineral metabolism, bone mineral density, and body composition in patients with chronic pancreatitis and pancreatic exocrine insufficiency.
http://www.ncbi.nlm.nih.gov/pubmed/10811020

Treatment Failure in Celiac Disease Due to Coexistent Exocrine Pancreatic Insufficiency
http://pediatrics.aappublications.org/content/80/6/924

Is exocrine pancreatic insufficiency in adult coeliac disease a cause of persisting symptoms?
http://www.ncbi.nlm.nih.gov/pubmed/17269988
 

Abha

Abha
Messages
267
Location
UK
In Dr Jadin's book(S.Africa/Belgium) "A disease called Fatigue"(2002)she writes "Why do certain human races not develop tick -bite fever?
Why is multiple sclerosis not usually found amongst the African racial groups?
Is this a matter of secular immunity?"

An Indian surgeon (born UK?)that I know doesn't seem to believe in ME/CFS.His wife is/was a psychiatrist.He states that it doesn't exist in India and that Ayurvedic medicine there is very good(for such things as viruses/bacteria etc)Perhaps that race(indian) are not so suscetible to this illness(like Africans?).However,I think i read recently an ME /CFS Group was being set up in India.This may be for those richer(mixed race) Indians(better educated).From my own experience in these countries I know that the majority of people are very poor and die at a very young age.Their medical histories are never known/checked.

On another point re proteins/illness...Tim Hunt(Sir)spoke very well about his work on Radio Four today.His mother died of cancer and he stated that if he had it he would just be in the same position as anyone else!
Hunt was awarded the 2001 Nobel Prize in Physiology or Medicine with Paul Nurse and Leland H. Hartwell for their discoveries of protein molecules that control the division (duplication) of cells.[1]
 

maddietod

Senior Member
Messages
2,860
From what I have read, the symptoms of MS and ME are very similar. The triggers for both MS and ME can be the same also. Also, an MRI always doesn't show lesion of a person w/MS. I am very confused only because not any doctor has been able to give me a diagnosis. The fatigue was the last symptom that hit and technically, according to the CDC and my doc the fatigue pre dates the other symptoms. Has this been the case for any of you where you had other symptoms prior to the fatigue? I am really at the end of my rope. I would just like to know. I have children and I think it is important for them.

Symptoms

muscle twitching, tingling and numbness..... First set of symptoms
Few months later...... Dizziness, Nystagmus low blood pressure
And then about 4 months later, the crushing dibilating fatigue and brain fog

I do appreciate you're feedback. I have had improvement, but and a big but, All is not well

This thread seems to be way off track from this original question.

One of my sisters has MS, and her symptoms have always been completely different from mine. She has no fatigue or cognitive issues, had no PEM when she could still exercise, and has no trouble sleeping. Unlike me, she has increasingly severe loss of use of her arms and legs, and this is unrelated to OI (which neither of us has).

I hope you find a doctor who can give you a diagnosis. I thought it was pretty easy to rule out MS.

Madie
 

richvank

Senior Member
Messages
2,732
Hi Rich, I think I may put this on the back burner. I know that with the correct scientific data we will be able to come to a concensus. It is interesting though, and a great puzzle maybe yet to solve.

O.K., Annesse. I'm still tracking with you, and am looking forward to reading your book, which was supposedly shipped yesterday. After I've had a chance to get my brain around your whole hypothesis, I may have some questions or comments to offer. I don't think I have the whole picture yet, but maybe you have explained it all in your book.


I gather that you prefer a "cliff hanger" approach to explaining it, i.e. "tune in tomorrow for more!" :D:D


Your experiences with herbal treatments certainly sound impressive.

Best regards,

Rich
 

Annesse

Senior Member
Messages
164
If you are still wondering if the inability to digest proteins could lead to the same symptoms in the diseases we have been discussing, (MS, CFS, etc.) then we need to look no further than the autoimmune disease lupus. The lack of the protease DNase 1 has been determined to be a causative factor of lupus. When this enzyme is removed in mice, the mice developed lupus. When it was genetically modified, lupus was the result. Does lupus have the same symptoms as CFS and MS? Does lupus have the same lack of nutrients found in high protein foods, such as zinc? Does it lack the same neurotransmitters? Do lupus patients lack vitamin D and have high homocysteine? What are we looking for? Autonomic dysfunction, spinal cord changes, white matter lesions, endothelial cell damage etc.

Here is a study that confirms that not only lupus patients, but also RA patients have "SEVERE AUTONOMIC DYSFUNCTION." http://www.ncbi.nlm.nih.gov/pubmed/20422909

According to the Lupus Foundation Of America, in about half of those with lupus, the disease attacks the brain and spinal cord. They also state, "Science has not yet been able to provide an explanation for this."

Here is a study that confirms lupus patients lack zinc, iron, and magnesium.
http://www.ncbi.nlm.nih.gov/pubmed/15583971

A 2001 study published in "Lupus" shows that most patients have a vitamin D deficiency.

A 2004 study published in "Rheumatology International" looked at the incidences of anemia and serum vitamin B12 deficiencies in patients with RA and systemic lupus and found that anemia was much higher in patients suffering from these diseases and that such patients should be monitored for vitamin B12 deficiency."

An article on lupus entitled: "Nutritional Influences on Illness" by Melvyn Werbach, MD states, " The amino acids phenylalanine and tyrosine appear to aggravate the disease, apparently due to a specific intermediary block in their metabolism. Findings from both animal and human studies have confirmed the efficacy of removing these amino acids from the diet." The inabilty to digest proteins would account for the inability to metabolize the components of a protein.

The study entitled: "U-M study: High heart disease risk for lupus patients may be linked to rapid death of blood vessel lining cells" states, "Mass suicide by protective cells that line every blood vessel in the body may be to blame for the increased risk of heart and vascular disease faced by patients with the autoimmune disease lupus, new research suggests." In the conclusion it states, " We hypothesized that rapid apoptosis could exist at the level of the ENDOTHELIAL CELLS, that they might commit suicide and thereby affect vascular function." A study entitled, "Homocysteine Induces Programmed Cell Death in Human Vascular Endothelial Cells..." shows the connection to lupus and homocysteine.

A high association to hypothyroidism is also found just as in the other diseases. The Johns Hopkins Lupus Center states, "Autoimmune thyroid disease is common in lupus." This would indicate the same lack of hormones and neurotransmitters as does the autonomic nervous system dysfunction.

Severe white matter lesions are also found in lupus. http://www.ncbi.nlm.nih.gov/pubmed/9050960

There are more connections to be made, but I think we have shown that the lack of proteases does in fact lead to the same symptoms and biological findings that we find in all of the diseases we have been discussing.

This will be my last post on this thread unless the moderators feel it is appropriate to continue. I am not offended in any way, I just do not want to overstep any boundaries.
 

xrayspex

Senior Member
Messages
1,111
Location
u.s.a.
Annesse
I will look for my test results on the b12 level, was done in sept. Doc didnt mention it, he is savvy enough that he probly took the level cus he knows its associated with CFS/Fm AI stuff but not involved enough to explore if a high level means anything. Maybe it doesnt merit exploring unless you're in the ER with other in your face stuff but I did my own digging around and learned:

"Conditions that can increase B12 levels include liver disease (such as cirrhosis or hepatitis)
and myeloproliferative disorders (for example, polycythemia vera and chronic myelocytic leukemia)."

So I wish he would have then ruled out the myeloproliferative disorders and done at least a test for gene mutation JAK2V617F, but maybe they arent allowed to in the mainstream system? if someone has an obscure issue how in the heck does it ever get discovered before you get to the dangerous irrersible stage!?
 

paddygirl

Senior Member
Messages
163
This thread is brilliant, don't stop! A lot is over my head but makes so much sense.

When my alarm went at 5 am this morning my arms and hands were so dead that i couldn't turn on the light and was late for work. Worst it's ever been.

Like trying to throw a switch with a lamb chop. :headache:

My diagnosis is FM, but since my medical carers are pig ignorant in every sense of the word, i could have anything. I'll be sending for your book too Annesse.

Is it accessible for non-science types like me? Like many I'm my own doctor and need my instructions laid out like a recipe. :D

Paddy

By the way, what do you think of LDN? Does it fit in with your theories?
 

aprilk1869

Senior Member
Messages
294
Location
Scotland, UK
This will be my last post on this thread unless the moderators feel it is appropriate to continue. I am not offended in any way, I just do not want to overstep any boundaries.

Technically things have gone off topic however since researching health this year I have believed that these illnesses have the same root cause and are simply being divided up into separate illnesses based on symptoms.

I think there is a lot to gain from this thread and it should keep going.
 

adreno

PR activist
Messages
4,841
If you are still wondering if the inability to digest proteins could lead to the same symptoms in the diseases we have been discussing, (MS, CFS, etc.) then we need to look no further than the autoimmune disease lupus. The lack of the protease DNase 1 has been determined to be a causative factor of lupus. When this enzyme is removed in mice, the mice developed lupus. When it was genetically modified, lupus was the result. Does lupus have the same symptoms as CFS and MS? Does lupus have the same lack of nutrients found in high protein foods, such as zinc? Does it lack the same neurotransmitters? Do lupus patients lack vitamin D and have high homocysteine? What are we looking for? Autonomic dysfunction, spinal cord changes, white matter lesions, endothelial cell damage etc.

Annesse, it is an interesting theory you have. Do you have any thoughts of enhancing the activity of DNase 1? I believe many CFS sufferers (including me) have already tried supplementing pancreatic enzymes without success.