A new concept and treatment options for MS

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Postby jimmylegs » Wed Mar 16, 2011 9:59 am

no i don't think so 1h. calcium has to be balanced properly with magnesium intake. personally i consider things like muscle spasticity a sign that mine's out of balance. as in i don't have enough magnesium in the mix. hth!
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refractory hypokalemia

Postby tara97 » Wed Mar 16, 2011 11:32 am

everyone is different but i was reading about refractory hypokalemia and how you cannot correct a potassium deficiency without first replacing the magnesium. your kidneys will detect it and then dump it. magnesium will oppose the calcium so that potassium can enter I think. i would not replace calcium and D without first replacing this magnesium because with out magnesium and potasium the cells will become calcium loaded and for me the result was that my trapezius, neck muscles and my face started to freeze in the contracted possition.
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Postby jimmylegs » Wed Mar 16, 2011 1:20 pm

it's true tara, supplementing magnesium can also help address refractory potassium deficiency.
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Postby Leonard » Thu Mar 17, 2011 4:41 am

Cece wrote:Leonard, keep at it, you are doing great. Lots to read through and think about here.


Thank you. Of course I will keep at it. But what we really need is a concerted effort of the world of endocrinologists, people who really know about the issues. I just wish they were as brave as the SIRS.
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Postby Leonard » Sun Mar 20, 2011 2:21 am

When plotting the age of onset of MS of thousands of patients in a graph, this graph will show a double peak. One peak occurs between 25 and 30 years of age and another peak between 40 and 45.

If there would be a single mechanism underlying MS, you would expect a single peak with a curve that tapers off slowly towards the edges. The simple fact that there is such a second peak suggests that at one point in time another mechanism kicks in. The presumption on this whole thread is that this has something to do with the calcification/hardening of the cells at mid-age making the transport of essential nutrition to the cells more difficult.

The Vitamin D relationship in MS provides an indication in this same direction. High Vitamin D during pregnancy and childhood lowers intra-cellular calcium levels and thus the risk of developing MS (the lattitude relationship). And vice versa.

When studying calcification, there is an enormous amount of information that one can find on the net. Admittedly for a semi-literate like me it is difficult to absorb it all and get a good oversight. I got the following findings that I wanted to share with you on this forum.

The calcification can cause effects at least at three places:

1. the Red Blood Cells that do not release sufficient ATP. MS patients seem to have very high levels of ATP in their RBC (up to 300%). I guess this is the result of parts of the brain crying out for help because of undernourishment. The blood loads with ATP but somehow it can not get there. Metformin, a common drug for diabetes, could help the release from the RBC.

2. in addition to the iron deposits and, in a later stage, the inflammation caused by the MS, now the calcification of the veins makes the transport of ATP even more difficult. Restoring a good blood flow is the first and foremost important thing to do to improve the situation, offering better supply and taking deposits and inflammation away.

3. the main ion pump for motor functions is the K+ Na+ ion pump in the neurons. This is a complex of proteins embedded in the membrane that derives its energy from ATP to transport sodium and potassium across the membrane; to establish a membrane potential. The exchange pump is relatively slow in operation. If cells were initialized with equal concentration of sodium and potassium, it would take hours for the pump to establish a new equilibrium.

Relating this to my own experience: sometimes after (night)rest and/or sugar intake I walk very well, almost as normal. Perhaps the normal equilibrium in the neurons has been restored at that point. Then, after 30 - 15 min's or so, things go worse again, perhaps because insufficient energy/ATP is supplied to the ion pump to keep fully functional and maintain the right equilibrium (Na + K + ATPase).

The pump operates constantly. Besides the lack of energy supply to establish the equilibrium, the pump may also become progressively less efficient if the concentrations of sodium and potassium available for pumping are reduced. And this may be due to a calcification from the inside. What is the case? If the supply of energy/ATP is insufficient for the reasons we have seen, the normal sodium-potassium pump may be counteracted by an inward flow of sodium from the extra-cellular space while calcium is pumped outward of the intracellular space. The reason is that this process of "calcification of the cell membrane" does not require any energy source except the membrane voltage. It may therefore be precisely this lack of ATP energy that promotes the calcification process. At this point the net flow of charge is inward, and the pump runs "downhill". And our motor functions stop; we can not move anymore.

We are discovering a mechanism here that could well explain the weakening on exercise/recovery on rest and possibly the RR aspect of MS! The decrease of K+ conductance due to a lack of ATP energy to propel the ion pump is perhaps the fundamental underlying mechanism of MS This mechanism could be valid all MS patients, both for first as well as second peak patients, and as such not directly relate to the calcification/hardening at mid-age.

In a resting state, little ATP will be supplied again partly restoring the sodium-potassium membrane potential.
http://en.wikipedia.org/wiki/Membrane_potential

The importance of low intracellular calcium (and high Vit D?) seems confirmed by text books e.g. Discovering Biological Psychology by Laura Freberg pg 60 and further; and a huge number of related books in the field of cardiology that Google pushes forward.

Some more interesting information to think about:

The calcium ion pump and Vitamin D interact.
http://www.ncbi.nlm.nih.gov/pubmed/2426970

If the ion pumps are turned off by removing their energy source, the neurons can still fire hundreds of thousand of action potentials before their amplitudes begin to decay significantly.

A potassium deficiency inhibits the insulin response, suggesting a link with energy supply.

Metformin has an effect on the ATP release and in fact may have positive effects for MS. The same can be said for calcium channel blockers (e.g. Adalat see above postings). Now, it seems that these calcium channel blockers strengthen for instance the effect of Metformin, perhaps making 1 + 1 = 3. This leveraging would seem to point to interactions with the metabolism at the right places.

Magnesium may be a factor here too; I found reference to magnesium in several places. How diet influences the process (e.g. low sugar intake in diabetes, some old wise neurologist said to lower sugar intake on MS diagnosis) and more in particular the sodium / poitassium / calcium / magnesium balance may be relevant in this same context.

I would be very interested in your views.
Last edited by Leonard on Sun Mar 20, 2011 11:52 am, edited 3 times in total.
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Postby jimmylegs » Sun Mar 20, 2011 6:15 am

i just wrote a bunch of stuff but took it out because this says it exceedingly well with direct reference to calcification:

http://www.mgwater.com/agingcal.shtml

"Human Cell's Power Plant
The power plant of human cell is called the "mitochondrion." The mitochondrion is what generates energy for the cell to use. What everyone refers to as "energy" is derived from the oxidative reduction of the cellular respiration. This is done through the mitochondria.

But the problem arises when the cell is low in magnesium, relative to calcium. Adenosine triphosphate, the "energy currency" of the cell, is magnesium dependent. This means it is obvious that the calcium pump at the cell membrane is also magnesium dependent.

Without enough "biologically available" magnesium, the cellular calcium pump slows down. Thus a vicious cycle is established. The low levels of available magnesium inhibit the generation of energy, and the low levels of energy inhibit the calcium pump.

The end result? The mitochondrion, the powerhouse of the cell and the entire body, becomes calcified. This is the beginning of aging. It all starts in the cell. First the cells age. This leads to organ aging. And after the organs age, individual aging occurs. Since calcium is readily accumulated by mitochondria, this ion is potentially capable of antagonizing the activating influence of magnesium on many intramitochondrial enzyme reactions.

This means that every function of your body can be inhibited when the mitochondria calcify. It's like going through life with the emergency brakes on. Calcium is the brake. Magnesium is the accelerator. To be in optimal health, there must be a balance between the two."

this all reminds me of the wahls approach, restoring nutrient balance for proper mitochondrial function etc. here's a link to a review of her book:

http://alifesustained.blogspot.com/2010 ... ndria.html

going off on a diet recommendation tangent now...

i don't personally buy into dr wahls' gluten and dairy omission myself, which i suspect is a gleaning from best bet, but in general yes the nutritional approach is sound in my view.

i think the consumption of gluten, eggs, dairy, etc can be managed as long as you have net anti-inflammatory intakes overall, and ensure proper GI health, among other things.

for example zinc is low in ms patients, which can be the result of either gluten or phytates being excessive in the diet.

low zinc has myriad implications including leaky gut and the potential for poor gluten handling. in one study, zinc in serum increased in healthy controls on a gluten free diet. and as for phytates hampering zinc bioavailability, you just need to be careful in preparation methods for things like legumes, another food that are just written off in some ms diets. there's good nutrition in these foods as long as you process them properly!

links to relevant khan academy videos (unfortunately nothing on magnesium as yet)

intro to cellular respiration
http://www.khanacademy.org/video/introd ... st=Biology

oxidation and reduction in cellular respiration
http://www.khanacademy.org/video/oxidat ... st=Biology

ATP
http://www.khanacademy.org/video/atp--a ... st=Biology

ooh, found a nice one re magnesium and calcium and muscles

http://www.ncbi.nlm.nih.gov/pubmed/7286246

Magnesium and the regulation of muscle contraction.
Potter JD, Robertson SP, Johnson JD.

Abstract
"There are a variety of Ca2+ binding sites in muscle (e.g., troponin, parvalbumin, myosin, and calmodulin) that may play a role in the regulation of muscle contraction and other enzymatic processes. since most of these proteins also bind Mg2+, it is important to consider the effect that the high free Mg2+ concentration (mM) found in muscle has on the Ca2+ binding properties of these sites. The major effect of Mg2+ is to greatly reduce the rate of Ca2+ binding to the sites that bind Mg2+ and Ca2+ competitively (Ca2+-Mg2+-type sites found in troponin, parvalbumin, and myosin, which would be essentially saturated with Mg2+ in a relaxed muscle) due to the slow dissociation of bound Mg2+. Thus during a transient increase in [Ca2+] similar to that which would occur during muscle activation, these sites would bind very little Ca2+ and, consequently, could not play a regulatory role. Even if Ca2+ were able to bind to these sites during muscle activation (e.g., if the free Mg2+ in muscle is lower than presumed), the dissociation of Ca2+ from these sites would be quite slow due to their very slow off rates for Ca2+, again making these sites unsuitable for participating in a rapid Ca2+-induced switching mechanisms. In contrast, the Ca2+-specific-type (regulatory) sites found in troponin and calmodulin do not have these restraints. The rate of Ca2+ binding to these sites is not affected by Mg2+ and the off rate of Ca2+ from these sites is very rapid due to their lower Ca2+ affinity. Thus, these sites are able to respond to rapid Ca2+ transients, an essential feature for any Ca2+ binding site that plays a regulator role."

that's it for now :)
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Postby jimmylegs » Sun Mar 20, 2011 7:27 am

as far as the RR thing goes, and sorry if this has previously been covered in this thread.. i haven't flipped back through...

anyway: one interesting observation in ms is that levels of a powerful antioxidant, uric acid, are low in relapse and high(er) in remission (still well below healthy ctrls). [note also that the ms relapse, average, remission AND healthy control levels for uric acid are ALL within the 'normal' range]

zinc is a big player in the urea cycle and low zinc goes with low uric acid. i used to have ms average uric acid status or lower, until i found and corrected my zinc deficiency. when i supplemented zinc, my uric acid shot up into near-healthy control levels. before that i had been eating high purine foods in hopes of elevating uric acid, but without understanding the zinc connection, i was just probably just overloading my system with ammonia.

zinc also modulates ATP activity. (rat study)
http://onlinelibrary.wiley.com/doi/10.1 ... 1/abstract
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Postby Bethr » Sun Mar 20, 2011 8:09 am

Just wanted to add in my thoughts about the ages ranges of onset you mention, and how there is a peak prior to 30 and then another after 40.

The peak age for childbirth is 30. I'm coming from the iron aspect.
Wouldn't childbirth lower iron levels for some period, creating a dip in the graph for those years in women, who of course dominate in MS and could skew the stats over men? Or do those ages apply to men as well?

Do we have any stats that are onset men vs women?
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Postby Leonard » Sun Mar 20, 2011 12:10 pm

The abstracts of the ISNVD Annual Meeting - Bologna, 14-15 marzo 2011 are on-line:

http://ccsvism.xoom.it/Convegno_ISNVD.html

and on this forum
http://www.thisisms.com/ftopict-15918.html Thank you cheer!!

Besides the neurological and vascular dimensions, there is now for the first time a presentation on the nutritional aspect as the cause of MS:

http://ccsvism.xoom.it/ISNVD/Abstract-Trapp.pdf

And guess what, what we have been discovering here above is found in similar words in this abstract. I hope we are going to see a lot more on this in the near future, from the specialised micro-cellular doctors, that is the endocrinologists and the cardiologists. The latter because they seem to understand the Na/K and the Ca ion pumps better than anyone else.
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Postby Leonard » Sun Mar 20, 2011 12:20 pm

@jimmylegs thanks for all the information. I will study it in detail.

@ Bethr: thank you for your comment. You have a point that women who get children in their 30s may cause a dip in the graph. But in a statistical sense, you would expect the gap between the two peaks to be much shorter, years, not a decade. And they also get children in their 20s. Personally I do not think that this is enough to explain the two peaks. The calcification is more likely.
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Postby tara97 » Sun Mar 20, 2011 7:55 pm

I was thinking that the sodium potassium homeostasis is disrupted by prolonged elevation of cortisol also intertwined with the energy metabolism and later cortisol exhaustion or maybe that is why I went down into lupus. cortisol moves an equal number of sodium ions in /potassium out this alkalizing action supressed the immune system. my first attack I had hyperkalemia according to tests and hyper reflexia caused by this. my question is that arent my kidneys supposed to detect the potassium and then dump it to prevent alkalosis. if i have prolonged periods of elevated cortisol and become too alkaline then my immune system would be very compromised. I can either have hyperkalemia if for some reason my kidneys failed to do the job or I would start urinating alot, very clear waterlike urine dumping potassium and magnesium following. if this happens for too long cells become calcium loaded with a magnesium def. In my case the fourth time out of remission I had an adrenal crisis where I became cortisol exhausted I think when this happens I begin occilating between acidosis and alkalosis. at this point I had hypokalemia according to tests. but pH test strips indicated that I would swing between extemes.
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Postby jimmylegs » Mon Mar 21, 2011 1:07 pm

interesting re cortisol and energy. the klenner protocol for ms recommends high protein diet. as a vegan dx'd with ms, inadequate protein was highly likely. i followed the recommendations re eggs for breakfast and never looked back. i used to feel anxious or stressed all the time. since i got sorted out on the nutrition front, at least as sorted out as i am so far, i have been way WAY more relaxed.

found a study

Clin Exp Immunol. 1983 January; 51(1): 126–132.
Numerical and functional deficiency in T helper cells in protein energy malnutrition
Abstract
"Protein energy malnutrition decreased the number of rosette forming T lymphocytes, of T4 positive cells and their ability to provide help to B cells in antibody synthesis. There was a reduction in serum thymic hormone activity and an elevation of leucocyte terminal transferase and plasma cortisol levels. The numerical and functional deficiency of T4+ helper cells may be important in the pathogenesis of some of the clinical and immunological manifestations of protein energy malnutrition."

i used to be zinc deficient as well as low on protein. related article

ZINC AND IMMUNOCOMPETENCE IN PROTEIN-ENERGY MALNUTRITION
The Lancet, Volume 311, Issue 8076, Pages 1226-1228
"Malnourished children have thymic atrophy which is reversed by zinc supplementation. To see if their defect in cell-mediated immunity was also associated with zinc deficiency ten children were skin-tested with Candida antigen on both arms. One test site was covered with local zinc sulphate and the other with placebo ointment. There was a highly significant increase in the typical delayed-hypersensitivity reaction at the site covered with zinc. The magnitude of the difference between the supplemented and unsupplemented arms correlated negatively with the plasma-zinc concentration. These data show that zinc deficiency is a cause of the immunoincompetence seen in malnutrition. The normal reactions of the zinc-supplemented side indicate that, of the many nutritional deficits of malnourished children, zinc deficiency specifically impairs the cell-mediated immune system. Local skintesting with and without zinc may provide a measure of zinc status. Local application of zinc may enhance the reliability of tests to diagnose diseases such as tuberculosis in malnourished patients."
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It's the ion pump

Postby Leonard » Thu Mar 24, 2011 7:43 am

From a systems engineering point of view, a deficient Na+/K+ ion pump in the neurons due to a sustained shortage of energy (glucose) would explain so well the typical motor function response seen in MS patients:

- the pump operates constantly

- the exchange pump is relatively slow in operation. If cells were initialized with equal concentration of sodium and potassium, it would take hours for the pump to establish a new equilibrium.

- if insufficient energy is supplied to the ion pumps to keep fully functional and maintain the right equilibrium, or the ion pumps are turned off by removing their energy source, the pumps run downhill and so does the action potential

- but the neurons that can still fire thousand of action potentials before their amplitudes begin to decay significantly

- on the short term the response/amplitude that decays after a period of exercise.

- in a resting state, little ATP will be recycled partly restoring the sodium-potassium membrane potential with motor functions back for a short while.

- on the short term the response after intake of extra glucose

- besides the lack of energy supply to establish the equilibrium, the pump may also become progressively less efficient over the years if the concentrations of sodium and potassium available for pumping are reduced

- over the years the (degrading) walking ability,

- this is possibly connected with a hysteresis in the pumps where an increasing amount of calcium (calcification) of the cell membrane replaces sodium/potassium permanently which then reduces the overall amplitude.

Against the background of MS being an auto-immune disease, I have never been able to understand the typical motor function response on exercise/rest and the typical eigen values of the metabolic system. The mechanism of the (failing) ion pump underlying MS would explain the whole system response so neatly. MS MUST BE RELATED TO THE ION PUMP!

Suppose it is the ion pump, the key question for us is: what should/could be done to restore the normal functioning of the ion pump?
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Postby jimmylegs » Thu Mar 24, 2011 11:23 am

one idea could be to make sure one does not have the low magnesium often seen in ms patients.

the sodium/potassium pump is ATP dependent. ATP is often Mg dependent.

normal range for magnesium is 0.70 mmol/L - 1.10 mmol/L however individuals can show signs of trouble at levels below 0.90 mmol/L.

low magnesium can manifest in various ways like shortness of breath, spasticity, dysphagia, anxiety/depression, fatigue, menstrual cramps, muscle tics, heart racing, etc etc etc etc etc.
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Postby gainsbourg » Sat Mar 26, 2011 1:12 pm

I've just read through this thread and I believe you are on the right track Leonard, as I believe Lynda Carol has been for some time - MS may be a disease of faulty metabolism within nerve tissue. However, I expect that you, like almost everyone else on TIMS and the medical community alike, are assuming that MS will eventually be explained purely in terms of physical disease.

When any part of the body, especially a main organ, becomes diseased (heart, kidney, skin for example) it is common sense to ask, what is the main function of this part of the body/organ? Is it being overused, misused, overstretched? After all, that's the first thing we ask if we are diagnosing faults in a machine.

So what is the white matter in the brain used for...and is it being overstretched? The glucose used by the brain and spine is used up providing cognition, sensory processing and communication between different regions of the brain. MS is a disease primarily of the white matter which is thought to mainly ferry information from one region of the brain to another.

Here's the crunch. Is the white matter somehow being overused? This would explain why it needs more oxygen/glucose - causing a strain on the vasculature which brings out inherent weaknesses.

I believe almost everyone in the modern, western world puts this extra strain on the brain - a strain it was not designed for - and for an unlucky tiny minority, MS develops as a result.

You'd think there would be studies investigating this hypothesis, but there are none. This is because it is considered taboo to discuss whether the way we use/misuse our brains in modern life could be causing any of the neurological problems that have blossomed in the last 150 years.

Interestingly women are known to use the white matter more than twice as much as men - this is almost certainly why they are better at multi-tasking. Studies by Haier (2004) and Jung (2005) reveal that genders really do think differently. Men use more grey matter, and women use significantly more white. The white matter has often been compared to a switchboard. Maybe if it is overused too often it gradually goes into meltdown!

MS lesions occur almost entirely in the white matter. Women are twice as likely as men to be affected by MS.

Could this be the reason why MS attacks so often follow episode of stress? In my own obsevations MS-rs are often great thinkers, analysers and stress prone people. Okay, you might say, so are the majority of westerners these days. I'm not saying that physical factors aren't part of the MS process (I suspect faulty metabolism of iron in nerve cells; autoimmune activity triggered by the presence of dormant herpes; and nutrient difficiency) but for me the mind is a huge and overlooked factor in the disease.


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