Just to keep this thread as complete as possible, this is a copy of an earlier posting on:
From dr. Haacke's paper:
Back in the 1980s, Swank et al. found that past the age of 40 years, MS patients had markedly reduced blood flow compared with normal individuals .
http://www.expert-reviews.com/doi/pdf/1 ... ern.10.174
The same text is now proliferating through other channels e.g. http://www.medscape.com/viewarticle/734517_3
But the actual publication suggests something more than what is mentioned in dr. Haacke's paper, namely that it is not just the blood flow, but also the RBC delivery
: Swank RL, Roth JG, Woody DC Jr. Cerebral blood flow and red cell delivery in normal subjects and in multiple sclerosis. Neurol. Res. 5(1), 37–59 (1983).
In the patients with multiple sclerosis there occurred a progressive generalized decrease in CBF and in RCD with age which was significantly greater than observed in normal subjects. The rate of decrease in CBF and RCD correlated directly with the rate of progress of the disease. (RCD = Red Cell Delivery)
This ties in with an earlier posting on TIMS on the increased ATP level in MS patients (300%). The high level is probably best explained by signallers in the body calling out loudly for help (Endothelin1?) and the fact that the RBC (Red Blood Cells) do not release the ATP, at least not enough.
This may well be related to the hardening/calcification starting at mid age (but not necessarily exclusively). Traditionally, this hardening was understood as a hardening of the arteries, we know now that also the veins are subject to hardening. But I found several references that, besides the hardening of the vessel walls, also the release of the nutrition (= the release of ATP from the RBC) is now understood to be an issue.
In this same context of hardening/calcification, this is potentially of greatest importance: http://en.wikipedia.org/wiki/Ischemic_cascade
4.The ion pumps can no longer transport calcium out of the cell, and intracellular calcium levels get too high.
Hence the inflammation of the BBB may be a very important factor adding further to the hardening/calcification of the BBB and causing a vicious circle, making nutrition even more difficult etc.
I read the material on ATP on Wikipedia. The ATP is the main supplier of energy to the body. It is a phosphor something that contains the mixture of the glucose with the oxygen. In fact, it is not just the glucose or oxygen that passes through the veins to the cells; that is done through a more sophisticated mechanism involving the ATP and is called the "aerobic glycolysis". My attention that that was drawn on this thread (which shows the value of these fora) http://www.thisisms.com/ftopic-15188-da ... sc-45.html
Just to demonstrate the scale of the issue which gives a feeling for the size of the problem: the total volume of ATP that is recycled every day (that is ATP taking on glucose and oxygen and releasing that in the destined cells) is as big as the total mass of the body. You can see that if there is a problem with the RBC release of ATP, the body will have a problem. If in addition to the locking of the ATP in the RBC, you already have a low flow because of the stenoses, you have a serious problem. The concept that is described here is no different from my hypothesis on the above thread.
Last month, I have done a lot of searching on ATP, glucose and insulin. And I believe that I can tell from the search engine (if you understand how Google works), that people - probably including many professionals- are massively searching on this topic. And there are some names, mainly in the US, who are in fact on top of this.
In this same context of ATP, this hypothesis is interesting
It concludes quote … greatly expanding the list of tangible hypotheses for the etiology and treatment of non-insulin-dependent diabetes mellitus unquote to which I would add … and for the etiology and treatment of MS.