The difference between MS and ME

[richvank]

I thought the following information was extremely interesting. It came from an article entitled, "Multiple Sclerosis: Overlooked Nutritional Research".

"So who does not get MS? This is perhaps the biggest clue to MS of them all. Generally, people with gout. According to one paper, a review of 20 million patient records found the ailments appear to be almost mutually exclusive.

If people with MS rarely develop gout, and those with gout rarely develop MS, then it would be logical to look at why these conditions may be close to mutually exclusive. First, let's look at what causes gout. It is high levels of uric acid.

Interestingly, studies in the U.S. and Hungary show that people with MS have low levels of uric acid."

This is a question for anyone who would like to help answer. If the cause of MS is the inability to break down proteins, how would this prevent gout?

Hi, Annesse.

Uric acid comes from the breakdown of purines. To make purines, the cells must use certain forms of folate. When B12 becomes deficient, whether an absolute or a functional deficiency, the methionine synthase reaction is inhibited for lack of the methyl B12 coenzyme it needs. The methyl trap mechanism then drains methylfolate from the cells. The cells continue to convert other forms of folate to methylfolate, which continues to drain out, so the cells go low in folates in general. This hinders their ability to make purines. Less purine means less uric acid, and bye-bye gout.

So if you can tie B12 deficiency to problems with protein digestion this should follow (which is plausible, because for example I know that if stomach acid is low, the conversion of pepsinogen to pepsin does not occur in the stomach, and protein digestion does not begin there, as it should. The B12 would thus remain tied up with the protein and not get bound to haptocorrin, and later to intrinsic factor, for absorption in the terminal ileum.)


I don't know if this is really what happens, but this sequence is logically self-consistent, and it conforms to known biochemistry.

Best regards,

Rich

 

[adreno]

What Annesse is saying sounds very similar to what is described in this thread:

http://forums.phoenixrising.me/showthread.php?15087-Dr.-Terry-Wahls-MS-recovery-plan

Terry Wahls is a clinical professor who recovered from MS on (basically) a paleo diet.

 

[Enid]

Thanks Annesse a lot going on here which is a pleasure to follow. Too late diagnosis of hyperthroidism - into full blown Me with osteoarthritis/porosis called reactive by my Neurologist. Still thought viral origins and immune suppression.

 

[aprilk1869]

RE: MS and gout. This is something that I've puzzled over and I know it has something to do with xanthine oxidase which involves molybdenum, zinc and iron. Copper inhibits it and many people have too much copper in relation to zinc. Purines are important too in producing uric acid. A number of people here have reported doing well with molybdenum.

So now I look up pesticide xanthine oxidase and see this:-

The significance of the measurement of serum xanthine oxidase and oxidation markers in patients with acute organophosphorus pesticide poisoning.
http://www.ncbi.nlm.nih.gov/pubmed/20515560

I've actually been working on a time line for my mum where I've tried to plot all the things I think may have contributed to her illness. I don't know if this fits in but when I was a baby (~13 years before my mum was diagnosed with MS) we had a problem with wet rot. This was treated with chemicals but then my mum thinks we re-entered the home too early and she developed allergic rhinitis (confirmed with skin testing). She also had some problems with losing the use of her arms temporarily. One time she even dropped me (luckily onto the bed). She got an xray for it but nothing showed up and then the problem went away on its own.

Fluoride and xanthine oxidase:-

Protective effects of selenium on fluoride induced alterations in certain enzymes in brain of mice.
http://www.ncbi.nlm.nih.gov/pubmed/20143719

 

[Annesse]

Thanks for applying your intelligence to the mystery of gout and MS Rich. Here is my knee jerk reaction to why MS sufferers do not get gout.

URIC ACID IS THE FINAL PRODUCT IN THE BREAK DOWN OF DIETARY PROTEINS. If you are unable to break them down, you will not have high levels of uric acid. The low levels of uric acid would be consistant with the low levels found in studies done in the U.S. and Hungary on patients with MS. This doesn't mean that low levels would not be found in these other diseases as well. They have just not looked.

Adreno, I read the thread. I am going to view the video also. So far, I agree with the basic premise of the diet. In autoimmune disease though, if you eat proteins you are unable to break down, these unbroken down protein fragments and DNA will end up in your bloodstream and cause many problems. This is what these NETs are comprised of in the following study. These NETs become lodged in the bodies organs and tissues leading to kidney failure etc. You could perhaps compare this to a celiac patient eating bread in order to recover from celiac disease. It would just make things much worse. Before you could implement such a diet, you would need to restore the ability of your body to digest proteins. http://www.sciencedaily.com/releases/2010/05/100503161423.htm

 

[Annesse]

Aprilk-Thank you also. Our posts crossed over. We are going to tackle magnesium deficiency next.

 

[aprilk1869]

Another thing, tyrosine can combine with nitric oxide to produce nitrotyrosine which is very bad. There seems to be a connection between this and xanthine oxidase.

Differential effects of NADPH oxidase and xanthine oxidase inhibition on sympathetic reinnervation in postinfarct rat hearts.
http://www.ncbi.nlm.nih.gov/pubmed/21295134

Superoxide Reacts with Nitric Oxide to Nitrate Tyrosine atPhysiological pH via Peroxynitrite*

In experiments using xanthine oxidase as a source of superoxide, tyrosine nitration was substantially
inhibited by urate formed from hypoxanthine oxidation, which was sufficient to account for the lack of tyrosine nitration previously reported. We conclude that peroxynitrite formed from the reaction of nitric oxide with superoxide at physiological pH remains an important species responsible for tyrosine nitration in vivo.
www.jbc.org/content/275/42/32460.full.pdf

I'm not the best person to make sense of any of this...

 

[adreno]

Adreno, I read the thread. I am going to view the video also. So far, I agree with the basic premise of the diet. In autoimmune disease though, if you eat proteins you are unable to break down, these unbroken down protein fragments and DNA will end up in your bloodstream and cause many problems. This is what these NETs are comprised of in the following study. These NETs become lodged in the bodies organs and tissues leading to kidney failure etc. You could perhaps compare this to a celiac patient eating bread in order to recover from celiac disease. It would just make things much worse. Before you could implement such a diet, you would need to restore the ability of your body to digest proteins. http://www.sciencedaily.com/releases/2010/05/100503161423.htm

I don't know much about this, but isn't the only way to handle indigestible proteins to avoid them? For instance, I have found that gluten and casein make my symptoms worse, so I avoid them. It hasn't cured me though. Or are there ways to boost enzyme reactions to make these proteins digestible? That is unheard of; AFAIK celiac (for example) is incurable. Or is it possible that by providing the building blocks for mitochondrial health to get the digestive system going again?

I am not a proponent of the Wahls diet, but since it is paleo based (avoiding grains and dairy), isn't it essentially avoiding ingestible proteins? Or is meat and fish equally indigestible?

 

[Annesse]

Here is some information on the magnesium deficiency found in MS. The author also makes reference to the other common deficiencies, B12 and vitamin D.

http://www.nhfw.info/magnesium.html

Here is some info on magnesium deficiency and CFS and Fibromyalgia.

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)

o 24% of CFS patients, 27% of FMS patients and 53% of patients with autonomic dysfunction had low magnesium levels (Wynants H & Moorkens, G. Magnesium and Vitamin D status in female patients with CFS, fibromyalgia or autonomic dysfunction. Abstract, AACFS, 2003

We know that homocysteine is elevated in CFS. In the study entitled, "Increased Plasma Homocysteine Levels in Patients with Multiple Sclerosis and Depression," it states in the results, "Homocysteine levels were SIGNIFICANTLY increased in MS patients compared to controls."

Homocysteine interferes with the metabolism of magnesium. In a study conducted at the Health Science Center in Brooklyn, it was determined that homocysteine causes a depletion of intracellular free magnesium. The study suggested the need for three B vitamins: B12, B6, and folic acid. Here is the title of the study. "Extracellular Magnesium Regulates Effects of Vitamin B6, B12, and Folate on Homocysteinemia-induced Depletion of intracellular Free Magnesium Ions in Canine Cerebral Vascular Smooth Muscle Cellsossible Relationship to Atherogenesis and Stroke"

 

[alex3619]

Many ME and CFS patients have high levels of uric acid and not low levels. Uric acid is an antioxidant, but the parent purines are needed for nucleotide synthesis including ATP, RNA, and DNA. Many of the purines are conserved, and reconverted back to nucleotides.

Purines are essentially components of RNA and DNA and their breakdown products. I do not understand why they are considered amino acid breakdown products - this seems wrong. Indeed foods high in nucleotides and not proteins are what gout patients are told to avoid. They attempted to diagnose me with gout but it didn't hold up on close examination, and I did not respond to therapy (allopurinol).

Now muscle uses purines to keep the citric acid cycle going. They are heavily dependent on purines to maintain mitochondrial metabolites. So low purines or high purines might also be linked to muscle mitochondrial problems - I am not saying they are, I am saying they might be, its something that could be worth considering.

I wish I were more up to date on this but I am very out of date on the science of this, it was something I knew a lot about one to two decades ago but I have not been tracking recent developments.

Uric acid is a final breakdown product of purines, and is excreted. Along the way it also provides much needed antioxidant defence.

Note that a high turnover of purines will put a huge demand on folate and other vitamins. So the problem might be that methylfolate etc is overutilized in patients with high uric acid levels. Vitamin reserves might be low.

Please correct me if I am mistaken.

Bye
Alex

PS In birds and reptiles uric acid is the final breakdown product of protein, but in mammals its urea. I just looked it up. Urea has different properties to uric acid.

 

[Annesse]

Adreno, I had to chuckle a little at your post. It was if you were saying, "No, we can't, wait maybe we can" over and over in your mind. My advice to you is to think positive. Yes, we can. I think the information we have been providing shows pretty clearly that the specific amino acids found in meat, fish, dairy etc. are lacking in all of these diseases. The lack of the essential amino acid phenylalaine alone would account for so many of the symptoms. If you lack phenylalanine, you would also lack dopamine, tyrosine, adrenal hormones and thyroid hormones. B12 is missing in all of these diseases, including Celiac disease. Another common feature and definite sign that you are unable to break down the proteins it is found in, namely meat, fish , eggs and dairy.

I will continue to provide evidence that it is the inabilty to digest proteins that leads to all of these diseases. In the end, we will be able to trace every symptom of every autoimmune disease directly back to this inability. We will also be able to trace the seemingly disparate but valid scientific findings such as the link to pesticide use or low magnesium back to this inability.

 

[Annesse]

Hi Alex, I think Cort wrote this.
How do CFS patients compare to metabolic syndrome patients? Given the heterogeneous findings for many of these tests in CFS its hard to definitively say. Some CFS patients in some studies have exhibited increased waist/hip ratios, increased sympathetic nervous system activity, low growth hormone levels, high lactic acid levels, higher c-reactive protein levels, altered electrolyte levels, increased fibrinogen, IL-6 and TNF-a. Other studies have shown differently with regard to SNS activity, growth hormone, lactic acid, fibrinogen, Il-6 and TNF-a. DR. CHENEY HAS STATED THAT HIS PATIENTS HAVE LOW, NOT HIGH URIC ACID LEVELS. Virtually all studies that I am aware of have indicated increased oxidative stress in CFS. At this point there do appear to be some broad similarities between the two syndromes.

 

[alex3619]

Hi Annesse, I am aware of other less known ME doctors who say that a subgroup of patients have high uric acid. I do not know if this corresponds to a real subgroup, or another type of disorder, or just a variation. One of the reasons its thought to occur is as an adaptive response to oxidative stress. Bye, Alex

PS I also had metabolic syndrome, but its now diabetes. This may mean that a subgroup of patients who are at risk of developing such complications might have high uric acid - but I am only guessing here.

PPS Another thought occured to me. While some patients might get problems due to issues with defects in folate metabolism, some might have issues due to high uric acid as a coping mechanism, draining the methylfolate reserves over time. My suspicion is that this might be more likely in slow onset patients like me. Folate reserves might start out normal, but eventually they become low. I am unsure whether or not B!2 reserves are similarly implicated, but the several years I spent as a vegetarian did severely worsen my ME.

 

[Annesse]

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.

 

[adreno]

Adreno, I had to chuckle a little at your post. It was if you were saying, "No, we can't, wait maybe we can" over and over in your mind. My advice to you is to think positive. Yes, we can. I think the information we have been providing shows pretty clearly that the specific amino acids found in meat, fish, dairy etc. are lacking in all of these diseases. The lack of the essential amino acid phenylalaine alone would account for so many of the symptoms. If you lack phenylalanine, you would also lack dopamine, tyrosine, adrenal hormones and thyroid hormones. B12 is missing in all of these diseases, including Celiac disease. Another common feature and definite sign that you are unable to break down the proteins it is found in, namely meat, fish , eggs and dairy.

I will continue to provide evidence that it is the inabilty to digest proteins that leads to all of these diseases. In the end, we will be able to trace every symptom of every autoimmune disease directly back to this inability. We will also be able to trace the seemingly disparate but valid scientific findings such as the link to pesticide use or low magnesium back to this inability.

You have shown some correlation between different diseases and symptoms, but I haven't seen any evidence yet that these are caused by an inability to break down proteins.

 

[Annesse]

If MS patients and CFS/FM patients lack magnesium and we have associated this deficiency with homocysteine, then we should find this same lack of magnesium associated with elevated homocysteine in hypothyroidism. We have already shown that hypothyroid patients have a severe lack of vitamin B12, so logically, they would also have elevated levels of homocysteine. Here is some in information on the magnesium deficiency found in hypothyrodism. It states, " LIPID ABNORMALITIES IN HYPOTHYROIDISM contribute to the the disproportionate increase in cardiovascular risk....The results showed a SIGNIFICANT DECREASE ....in total and ionized Mg (magnesium) in hypothyroid patients in comparing with control group."

http://www.jlponline.org/article.as...e=2;spage=49;epage=52;aulast=Al-Hakeim;type=0

In the following study, researchers concluded that homocysteine levels are elevated in hypothyroidism and the "THE ASSOCIATION OF HYPERHOMOCYSTINEMIA AND LIPID ABNORMALITIES occuring in hypothyroidism may represent a dynamic atherogenic state.

http://www.ncbi.nlm.nih.gov/pubmed/10646653

So in conclusion, magnesium deficiency is found in CFS/FM, MS and hypothyroidism. Elevated homocysteine is also found and is most likely the cause of the shared magnesium deficiency. This of course could be directly traced back to lack of B12.

 

[mellster]

That's not really a fair comparison with regards to a vegetarian lifestyle. I suppose (can't prove though) that the number of diabetes and heart disease increased with the influx of western "food and culture", i.e. fast and processed food. I like and eat meat and think it is harder to have a balanced vegetarian (even moreso vegan) diet, but I think it is possible. Likely though a vegetarian lifestyle makes maintaining adequate B12 levels harder.

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]

Hi Mellster, I think the comparison is being made in India. Commenting on why Indians are more at risk for heart disease, Dr, Shashank Shah, author of a new research report presented at a World Congress event for Obesity and Metabolic Diseases in Los Angeles, stated, "We found that Indians are grossly deficient in vitamin B12, which is a crucial cardio-protective factor in the body. Vitamin B12 is usually found in food that comes from animals, like fish, meat, poultry, milk and milk products. However, since a lot of Indians are vegetarians, they do not get adequate amount of vitamin B12 in their diet. When vitamin B12 levels fall, homocysteine levels increase. The latter is known to cause atherosclerosis as well as an increased risk of heart attacks, strokes, and blood clot formation."

The following excerpt came from The Times of India. "Widespread deficiency of vitamin B12 among vegetarians is leading to a growing incidence of stroke and heart attacks among young people, warn doctors. Deficiency of vitamin B12 increases the concentration of a chemical called homocysteine in the blood, which causes blocks in arteries and veins. These blocks, in turn, are responsible for heart attacks and strokes. "

Sudhir Kothari, neurologist at Poona Hospital stated, "More and more young people are having heart attacks and falling prey to strokes. Invariably, it is a vitamin B12 deficiency caused by a pure vegetarian diet that is leading to this condition."

Rustom S. Wadia, neurologist at Ruby Hall Clinic, agrees, saying, " There is no doubt that it is a huge phenomenon. Nearly 70 percent of vegetarians have a vitamin B12 deficiency. And 70 percent of the cases of strokes that I have come across are due to this deficiency."

 

[mellster]

Thanks Annesse, well but they are supposed to have excellently low rates of other diseases (stomach etc.). I think the B12 deficiency makes sense but I am wondering whether heart disease and diabetes have always been high over there - I can see that mainly for heart disease but doubt that diabetes was a problem in earlier times.

 

[Annesse]

We can also find the same lack of magnesium in RA as in the other associated diseases. Here is a study that shows RA patients lack magnesium.

http://www.ncbi.nlm.nih.gov/pubmed/8782128

We have posted a study previously that shows homocysteine is dysregulated in RA. In the conclusion it stated, " Elevated homocysteine levels occur commonly in patients with RA..."

The first study also shows a lack of zinc in RA. Here are some of the foods zinc in found in. http://www.livestrong.com/article/233086-which-foods-contain-zinc/

The natural sources for are meat, fish and high levels in oysters. B12 is found more abundantly in oysters than in almost any other food.