It is hypothesised that multiple sclerosis (MS) is caused by an insufficient glucose level in the brain or parts of the brain.
Patients with MS are consuming more sugar than the average person, to get it elevated in our blood streams, to try and meet the unmet needs of the brain. And the result of greater sugar consumption is a greater prevalence of chronic yeast infections and symptoms as candida . Also the faster recovery of motor functions of MS patients on the intake of sugar/glucose, in particular in the beginning, would seem to suggest a glucose link. Furthermore, it is an explanation for the fast recovery of some patients post- ccsvi liberation and a post-liberation increase in dreams and REM sleep, since REM has high glucose demands.
The blood flow delivers oxygen and glucose to the very hungry brain as well as other nutrients, and takes away waste products. A lack of glucose puts the neurons in a dormant state; they become under-nourished. The consequence is demyelination and, if seriously under-nourished for a longer period of time, myelin and neuronal death. When this happens, the microglia jump on this and clean up the mess. Once they get out of the BBB, the T-cells jump on them and we start see the scars and the inflammation. That is when MS shows up.
Why are the cells under-nourished? There are at least two reasons: iron deposits on the vessel walls that inhibit the transport of glucose across the BBB and; insulin resistance that inhibits this same transport of glucose. The iron deposition may develop at a young age as a result of problems with the drainage, its origin is probably pre-congenital. The insulin resistance may develop at a later age. MS is probably a consequence of both, in a wide variety of cases among the population. One effect may be a more important for an early age onset and the other for a later age onset. The double peak in the age of onset of MS would indeed suggest the possibility of such underlying mechanism
[there are two peaks on the age of onset graph at 25-30 and 40-45 http://newsgroups.derkeiler.com/Archive ... 01256.html
Stenoses in the veins draining the brain and spinal column (ccsvi, Zamboni) cause refluxes in the deep cerebral veins and will lead to iron deposition on the vessel walls (you can see this on 7T MRI) and this inhibits glucose transport through the affected parts of the BBB. Iron deposition is a normal phenomenon in organs and limbs in case of problems with the drainage that has been known for a long time. By opening up the blockages in the veins by angioplasty, the blood flow can restore to normal, and eventually as the iron is taken away the BBB function may restore to normal. The increased blood flow during pregnancy and stop of MS progression adds to the plausibility of the concept. The low fat/Swank diet and the use of blood thinners/anti-clotting (effect Copaxone?) may also help improve the blood flow with the same positive effects.
Some persons may already have a fairly weak glucose condition in their brain due to the low blood flow through the head and the iron depositions. At mid age then, the insulin resistance starts to develop and the glucose transport will be further weakened. The Vitamine D relationship, well known in MS, plays its role here.
As studies found, higher levels of Vitamine D (childhood and/or during pre-congenital phase) may delay the onset of MS a bit because of lower intra-cellular calcium levels where insulin resistance and problems with glucose transport will develop a bit later on. Conversely, lower levels of Vitamine D will elevate intra-cellular calcium levels where insulin resistance develops earlier on and thus impaired glucose transport across the BBB will develop earlier.
This may explain the differences found among MS patients and a control group that were screened for ccsvi: people who have stenoses and therefore a low blood flow but high Vitamine D will still provide enough glucose to their neurons and myeline, and therefore will not experience the MS symptoms, or at the very least not as quick as those with low Vitamine D. The prevalence of diabetes type 2 in MS patients would further suggest a link with the insulin resistance. It is also known that this insulin resistance develops long before the signs of diabetes become apparent and the diabetes type 2 is diagnosed, further adding to this part of the hypothesis.
Studies have also found that a low-glucose condition causes or at the very least it is likely to cause demyelination. The process of demyelination is already well underway before diabetes type 2 shows up.
Also it ties in with the effect of heat on glucose in the bloodstream (it fluctuates more wildly; diabetics have to account for this in the summer) and, if overheated, the brain will endure worse damage from this lack of glucose.
What lessons may we draw:
1. get the veins opened and restore the normal blood flow. This will increase the volume of blood, and improve the cerebral hypoxia side of the equation, and the cerebral hypoglycemia side. The iron deposits may be taken away (?)
2. if appropriate and confirmed, start taking (diabetes type 2?) medication early on to overcome insulin resistance and improve the glucose transport across the BBB. And also, get the blood sugar level back to normal.