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.
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.
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.