This Is MS Multiple Sclerosis Community: Knowledge & Support

A new concept for MS

This sketch for a new concept for MS was last updated on 24 April 2013. It is my best assessment of what is MS. It is based on our learnings over the last two years, much of which can be found in the postings on this thread below.

Many years of venous obstruction in the drainage of the cerebro-spinal (CCSVI) will weaken the important tissue (endothelium) in the finest capillaries and the lymphatic system of the most affected areas in brain and spinal column (e.g. due to iron build-up). Nuclear receptors that control or activate important nutrition/transcription processes will be weakened (e.g. vitamin D receptors, RXR etc). Astrocytes / oligodendrocytes are not well maintained and will no longer sufficiently compete to maintain the nerves (but with these astrocytes and oligodendrocytes there is nothing intrinsically wrong). And the BBB will be compromised in affected areas...

A bacterial or virus infection may cause a further blocking of receptors. The Cpn bacteria and the EBV virus (which can be dormant for many years) are known for a sudden outbreak and their ability to block receptors. The Cpn bacteria may also affect the liver causing inadequate nutrition supply. If severe enough, the immune system will signal that there is something going wrong with the glucose metabolism, an acute inflammation will arise and a relapse is the result. Leukocytes will infiltrate the damaged region, removing the stimulus and repairing the tissue. And one is diagnosed with RR MS, or if you are lucky, you may escape at this stage. [The typical Time-constant of the phenomenon involved would seem to suggest an ion-pump related issue, possibly an impaired charging caused by short-term mitochondrial failure due to blocked receptors, and not to significant changes to the myeline or biological effects of toxidity on oligodendrocytes etc which are much more long-term and have typical Time-constants of months or years]

In the second progressive phase, MS is caused by a metabolic disorder/hormonal disregulation. As of mid-age (is age dependent phenomenon) the 'lining' of the gut breaks. The "leaky gut" will allow incompletely digested particles to be partially absorbed, including (very-) long chain fatty acids (V-LCFA) and other large molecules. These are targeted by antibodies, forming immune complexes that will pass through the intestinal walls and be carried by the bloodstream to distant site (but the substances are correctly seen by the immune system as foreign antigens).

After some time, the Carnitine production by the liver and possibly other metabolic regulation (e.g. Cortisol path) will be exhausted, large particles will not be sufficiently broken down anymore causing nutritional problems for the mitochondria. This then will stimulate the release of cytokines.

Problems spread through the body, other systems get affected like the parasympathetic nervous system with consequences on organs including the gut establishing a vicious circle. The gut working will further detoriate; nutritions and vitamins are insufficiently absorbed or produced in the gut; and T-cells are inadequately trained in the gut. Bad conditions (gut, compromised BBB) will lead to metabolic dysregulation, growing insulin/leptin resistance and further problems for the mitochondria.

Immune system (inter-)action will develop as inflammatory cytokines are released. More T/B-cells are drawn in and oxidative stress are created leading to a chronic hypoperfusion of the central nervous system, further induced mitochondrial energy failure, inflammation, a further neurodegeneration, oligodendrocyte apoptosis, myeline breakdown. SP/PP MS is the result.

The gut mechanism is the cause of many "auto" immune diseases, including diabetes and rheumatic disorder. Here MS will be intertwined with a diabetes related pheripheral neuropathy. In addition, typical RR effects caused by infectious agents that find an easy target in weakened cells followed by immune system repair will be superimposed on the steady progression course caused by mitochondrial failure.

Of course, the graph of the age of onset will show a double peak that is explained by the different underlying mechanisms taking their effect over time; where people who 'escaped' the MS diagnosis during the first phase because they had a fairly mild version can not escape anymore and get diagnosed after mid-age (if they developed a bad gut of course) ...


There are many aspects on the fringes, to mention some: neuro- and metabolic pathways that get excited as part of the regulatory system of the metabolism and that cause a multitude of reactions, e.g. the frequency to urinate is probably a perfectly healthy reaction of the body (kidney, brain) to reduce glucose levels in the blood as cells are too slow to open up, a badly functioning gut causing problems with the absorption of metals (copper, magnesium, zinc) and with the production/absorption of vitamin B(12), the lack of zinc to bind and store insulin thereby raising peaks and reducing insulin sensititity, the attempts at tissue repair (Weiss U. Nature 2008), besides bacteria and virus outbreaks like Cpn and EBV even a vaccination for Hepatitis may be suspect, the mind-body connection (stress, distress, prolactin), etc,

PwMS then may be affected in different ways depending on their genetic susceptibilities e.g. predisposition for diabetes type 2, the stress in their live and the Cortisol regulation/Adrenal fatigue, vitamin D / sun exposure during pregnancy of the mother and during adolecence that influences cell composition e.g. number of vit D gates, the vitamin D and the natural anti-biotics in the gut balancing the gut flora, environmental factors such as exposure to heavy metals (even of previous generations) and related genetic factors of veins (Boston document), the specific pattern of vascular insufficiencies of the draining neck veins, the hormonal balances (e.g the level of testosterone) and so forth.

The challenge is now to subsume all the knowledge and expertise that is around in a new more advanced model of what MS is and rapidly progress this matter for our cause..

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The original first posting of 8 January 2011 starts here:

This is a copy of my posting on the thread on ccsvi:

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.

I see validity in this line of thinking with the mention of insulin resistance – insulin resistance is marked by an increase in the secretion of insulin, i.e., excess insulin.

By the way, I think a new peak has developed in pediatric patients. I believe six pediatric MS centers have been established across the US. I suspect this has happened because younger and younger children are consuming diets of more items that readily convert to glucose, thereby triggering more insulin production.

Old friends here are not surprised by my comments, right?

@ lindacarol: I think your comment that insulin resistance is marked by an increase in the secretion of insulin, i.e., excess insulin is more than valid, in particular if seen in connection with the high sugar consumption among MS patients!

It might well be that MS with an onset at mid age and diabetes type 2 are two sides of the same coin. In any event, the symptoms of both diseases show a remarkable similarity, which looks more than just a coincidence.
http://diabetes.niddk.nih.gov/dm/pubs/neuropathies/
http://care.diabetesjournals.org/conten ... 984.1.full


@ everyone who is interested, please have a look at

http://www.thisisms.com/ftopic-15083-da ... sc-15.html

The postings on this page explain how we got to the low glucose hypothesis.

thank you to all.

My husband has always been slightly cynical about CCSVI as he could not join the dots between it and MS. Your idea of diabetes has made a light switch come on in his head. He does consume a sickening amount of sugar on a daily basis,he was diagnosed in his late 30's but suffered the symptoms for a good dew years earlier.

I am tempted to get him some metformin from a friend of mine!

In the beginning of the 1980s, apparently there has been a discussion in the medical community of the connection of multiple sclerosis and diabetes. The discussion was inconclusive and eventually disappeared in the background.

I suppose that at that time, the vein insufficiency and the related low glucose condition were not part of the debate. But now with ccsvi, all this makes sense, and all the pieces of the puzzle come together. The low oxygen O2 also fits in quite nicely. http://www.thisisms.com/ftopict-15235.html

With the (hypo)thesis of this thread, I think we have come very close to unravel the MS mystery.

I believe that the main discussion on this forum should not concentrate exclusively on the vascular dimension (ref: http://www.thisisms.com/forum-40.html ). The reason why we have taken this discussion so far is that we have been able and willing to look outside the box, that is the box of the neurologists. Now we should not make the systemic failure of locking ourselves into the vascular box. Our primary goal must be to solve the mystery of MS, to find what causes MS and how to best treat it.

Therefore, we must keep our eyes open and continue to look broader, for instance into the low-glucose hypothesis. In fact, MS is a complex disease that to solve it, besides neurologists and vascular doctors, may need to involve other disciplines such as diabetics specialists.

In the beginning of the 1980's there has been a discussion about the links between MS and diabetes. But it was difficult to prove and the issue disappeared in the background. Now with this new ccsvi condition, perhaps the old discussion of the 1980s should be held again, in the right context and against this new background. For further information about the low glucose condition, see: http://www.thisisms.com/ftopict-15181.html

I think the medical world can not get around this low-glucose hypothesis. The explanation given for the double peak in the age of onset makes this highly plausible as a concept. For the rest of the posting, if you do google and bing searches, you will find many recent articles that can confirm every single sentence of the (hypo)thesis.

Therefore, I call on the medical world to investigate the low-glucose hypothesis as part of their efforts. They can deny, deter, defer, delay and try to destroy. But at the end of the day, that will not work because the evidences are there and the pieces of the puzzle just connect too neatly.

one thing that does not seem to be impaired in the MS brain is the analytical mind. I originally presented with MS for the first 8 years and then It started to go systemic into sjogrens and then down into lupus. I have spent time on all forums and no group is more intelligent than the MSer. our ability to analyze and delve into abstact thinking is second to none. we definately do not take anything at face value and there for use the persuit of self knowledge to explain everything behind the face. I love it!!!

As I posted earlier in the CCSVI forum (although I think I feel more comfortable posting it here now):

Leonard – Please give me explanations for these two situations:

#1 Why is the glucose level lower in MS patients; that is, what lowers the glucose level?

Other than a diet low in glucose-making foods, the only answer I can suggest is a high level of insulin that sweeps the glucose out of the bloodstream.

#2 Several years ago there was successful treatment of children with seizures at Johns Hopkins. The treatment was a ketogenic diet (diet high in fats and protein) and did control the seizures. As I recall, the finding was that the brain could function just fine on ketones – that glucose was not necessary for brain function.

In the 1920s anthropologist-turned-Arctic-explorer, Vilhjalmur Stefansson, spent a decade among the Inuit, eating nothing but meat, no vegetables or fruit. His observation was that those who lived on this diet were among the healthiest imaginable. His observations contradicted conventional wisdom at that time that a varied diet was essential for good health. "It is a misconception that the brain and central nervous system require dietary glucose to function." See pages 319-325 of Good Calories Bad Calories by Gary Taubes.

Just today, 1-18-11, on the TV program, The Dr. Oz Show, Dr. Joseph Mercola stated that ketone bodies serve as an alternative fuel source to glucose: about 4:20 in the video at

http://www.doctoroz.com/videos/alternat ... versy-pt-2

I completely agree with you when you said:



I propose we start in the box of endocrinologists.

yes tara, you are right, I see that as well. I think it is 100 million years of evolution that has caused (and forced I might add) the people and their predecessors with a low glucose condition to think more strategic. (could also be that it is merely the evolution of the individual in one generation.) Conversely, those with a high glucose condition will think more of winning the 100 meters today.

I know this is all wild speculation, but it makes sense and supports the low glucose hypothesis, in fact it is another piece of the puzzle that fits in neatly.

thanks for your posting.

@ lyndacarol: The low glucose condition (not in the blood but in the cells of the cerebro-spinal) may have a number of causes where we see a large variability among the population: low blood flow, iron deposition, and increased insulin resistance. Also an impaired transport of oxygen may be a factor.

The first posting of this thread sets out the concept. I know, it may not be the perfect English (I am Dutch) and in the Internet age we are more used to scan rather than to read (I am no different). I would encourage everyone to really read and analyse the first posting of this thread. You will get the gist and get to understand what are the major pieces of the puzzle. [sorry about that ]

Your second point is very interesting: perhaps cells can be fed with other nutrition than glucose. but one thing is clear: they will have to be fed one way or the other as otherwise they will become under-nourished, go into a dormant mode and eventually die. so perhaps we should talk about low-nutrition condition of the brain? whow, we are making new connections here... notwithstanding, the glucose conditions will likely remain to be a main piece of the puzzle as it explains so neatly the double peak in the age of onset.

On your proposal to start in the box of endocrinologists: I did not know the word and looked it up at wikipedia. I agree, this is a discipline that should be part of the discussion, just like diabetes specialists. But I do not agree with some of the postings on some of the other threads that we should leave each group at its own platform. What this thing needs is a truly multidisciplinary effort to expeditiously solve this thing, forever. And we need to build on existing dynamics not to loose valuable time. We have been waiting for a solution for too many years.

i started writing this in response to the topic under CCSVI but have posted it here instead - sorry in advance for any non sequiturs as a result.

Okay, so, one potential cause of hypoglycemia: suboptimal trivalent chromium status.

LITERATURE
excerpts from a google scholar search on the terms hyperinsulinemia, chromium:

http://scholar.google.ca/scholar?hl=en& ... =&as_vis=0

Chromium supplementation for women with gestational diabetes mellitus
L Jovanovic, M Gutierrez… - The Journal of Trace …, 1999

Effect of chromium chloride supplementation on glucose tolerance and serum lipids including high-density lipoprotein of adult men
R Riales… - American Journal of Clinical Nutrition, 1981

Chromium action and glucose homeostasis
BW Morris - The Journal of Trace Elements in Experimental …, 1999 -

Chromium improves insulin response to glucose in rats
JS Striffler, JS Law, MM Polansky, SJ Bhathena… - Metabolism, 1995

and, an interesting abstract:
http://www.springerlink.com/content/u07857312h586124/
Chromium deficiency after long-term total parenteral nutrition


on the other hand... keeping in mind that chromium chloride is relatively poorly absorbed...:
The effects of chromium supplementation on serum glucose and lipids in patients with and without non-insulin-dependent diabetes


Chromium picolinate increases membrane fluidity and rate of insulin internalization


Effect of Chromium Supplementation on Glucose Metabolism and Lipids
http://care.diabetesjournals.org/content/30/8/2154.full


REVIEW ARTICLE
Chromium Research from a Distance: From 1959 to 1980
Walter Mertz, MD
http://www.jacn.org/cgi/reprint/17/6/544.pdf (full text)


TESTING
http://www.muschealth.com/lab/content.aspx?id=150241

Chromium measurement

What is this test?
This test measures the amount of chromium in blood. It is used to evaluate and manage chromium exposure or poisoning, and chromium deficiency.

What are related tests?
-Chromium measurement, urine
-Glucose tolerance test
-Insulin measurement

SUPPLEMENTATION
A study. regrettably small n. but a starting point:

Effects of supplemental chromium on patients with symptoms of reactive hypoglycemia.
Anderson RA, Polansky MM, Bryden NA, Bhathena SJ, Canary JJ.
Metabolism. 1987 Apr;36(4):351-5.
Abstract
"To determine if chromium (Cr) is involved in hypoglycemia, eight female patients with symptoms of hypoglycemia were supplemented with 200 micrograms of Cr as chromic chloride for three months in a double-blind crossover experimental design study. Chromium supplementation alleviated the hypoglycemic symptoms and significantly raised the minimum serum glucose values observed two to four hours following a glucose load. Insulin binding to red blood cells and insulin receptor number also improved significantly during Cr supplementation. These data suggest that impaired Cr nutrition and/or metabolism may be a factor in the etiology of hypoglycemia."

Chromium treatment does not appear to affect glucose levels in kwarshiokor, a protein-energy deficiency disease in which, in this study at least, the patients had 'normal' chromium levels:

Chromium(III) in Hypoglycemia and in Impaired Glucose Utilization in Kwashiorkor
http://www.ajcn.org/content/21/3/195.abstract
"...The diabetic glucose tolerance curves returned to normal following treatment with a high-protein, high caloric diet for 1-2 weeks. Chromium deficiency did not appear to be responsible for the rapidly reversible impaired glucose utilization seen in patients with kwashiorkor in Cairo, Egypt, United Arab Republic."

Therefore, it would seem a chromium test would be useful before deciding whether chromium might be implicated in a particular individual's hypoglycemia.

OPTIMAL CHROMIUM VALUES
Biological Trace Element Research
Volume 79, Number 3, 205-219, DOI: 10.1385/BTER:79:3:205
Concentrations of seven trace elements in different hematological matrices in patients with type 2 diabetes as compared to healthy controls
"This study aimed to compare the trace element status of patients with type 2 diabetes (n=53) with those of nondiabetic healthy controls (n=50). The concentrations of seven trace elements were determined in the whole blood, blood plasma, erythrocytes, and lymphocytes of the study subjects. Vanadium and iron levels in lymphocytes were significantly higher in diabetic patients as compared to controls (p<0.05 for iron and p<0.01 for vanadium). In contrast, lower manganese (p<0.01) and selenium (p<0.01) concentrations were detected in lymphocytes derived from patients with type 2 diabetes versus healthy subjects. Furthermore, significantly lower chromium levels (p<0.05) were found in the plasma of diabetic individuals as compared to controls. Trace element concentrations were not dependent on the degree of glucose control as determined by correlation analysis between HBA1c versus metal levels in the four blood fractions. In summary, this study primarily demonstrated that trace element levels in lymphocytes of patients with type 2 diabetes could deviate significantly from controls, whereas, in general, no considerable differences could be found when comparing the other fractions between both patient groups. Therefore, it seems reasonable to analyze metal levels in leukocytes to determine trace element status in patients with type 2 diabetes and perhaps in other diseases."

Ooh.. here's one with values/units!:

"Our results indicate that the chromium concentration ranges of serum and urine for diabetics are 0.22–0.36 and 4.54–5.90 μg/L, respectively, significantly lower than 0.66–0.84 and 7.80–9.68 μg/L for the normal (P<0.001), which implies that the elderly diabetics probably lack chromium."

So, these patients had a third of the chromium in their systems compared to healthy controls? Yikes.

Too bad I can't find anything on chromium levels in MS patients... grr.

FOOD SOURCES

http://www.whfoods.com/genpage.php?tnam ... nt&dbid=51
"Romaine lettuce is an excellent source of chromium while onions and tomatoes are very good sources of this mineral. Other food sources of chromium include brewer's yeast, oysters, liver, whole grains, bran cereals, and potatoes. Many people do not get enough chromium in their diet due to food processing methods that remove the naturally occuring chromium in commonly consumed foods."

Hope that sheds a bit of extra light.

PS ON SUGAR CRAVINGS
Long-term safety evaluation of a novel oxygen-coordinated niacin-bound chromium (III) complexM Shara, AE Kincaid, AL Limpach… - Journal of inorganic …, 2007
http://www.ncbi.nlm.nih.gov/pubmed/17555823
"... A significant volume of research studies have demonstrated that chromium (III) complexes play a significant role in regulating appetite, reducing sugar cravings and increasing lean body mass."

_________________
my approach: no meds so far - just balanced whole foods (partial 'paleo', much less outright elimination), science, supplements, & bloodwork
my regimen - www.thisisms.com/ftopict-2489.html
www.whfoods.com, www.nutritiondata.com

JL – good information. I thought I had read somewhere some time ago that peanuts were a good source of chromium so I was surprised NOT to find it listed in the information. I don't think I'll give them up (I like peanuts.), but I will add more romaine lettuce to my diet. Thanks for the info.

np LC

i can't find info on the amount of chromium in peanuts. the food source info above comes from 'world's healthiest foods' web site so maybe they don't consider peanuts the healthiest choice compared to lettuce, tomato and onion?

also on the detailed peanut info page at nutritiondata.com, there is nothing on chromium content:
http://nutritiondata.self.com/facts/leg ... cts/4357/2

i have seen 'nuts' mentioned generically as sources of chromium but the actual sources seem to be brazil nuts and hazelnuts.

so looks like, enjoy the peanuts lol just don't rely on them, not for chromium anyway!

couple more tidbits:

"Chromium Foods
The Institute of Medicine recommends a daily intake of 25 to 45 mcg for adolescents and adults. Meeting these recommendations is relatively easy when eating an overall balanced diet. Romaine lettuce, an excellent source of chromium, contains 16 mcg per two cups. Onions contain 25 mcg per cup and tomatoes contain 9 mcg of chromium; both are very good sources of chromium."

_________________
my approach: no meds so far - just balanced whole foods (partial 'paleo', much less outright elimination), science, supplements, & bloodwork
my regimen - www.thisisms.com/ftopict-2489.html
www.whfoods.com, www.nutritiondata.com

MS Made Simple:

Many years before we get to see symptoms of MS, a process has already started inside our body caused by under-nourished myelin and neurons. However we do not notice it yet. The cause is vein constriction in the neck (causing a poor circulation of blood through the cerebro-spinal, origin from birth) and on top of that the formation of iron depositions in the draining veins (which will make glucose transport across that part of the blood brain barrier more difficult).

For some people then who already have a low glucose condition (due to the venous strictures but no MS), by mid age insulin resistance will develop and this will further deteriorate glucose transport (the second peak in the age of onset).

Initially, under-nourished neurons will go in sleep mode. If there is serious malnutrition, the myelin and neurons will die. Microglia then clean up the mess. T-cells can not enter through the BBB. At the time that microglia come out, T cells jump on them and do their job.

If after years that process has advanced sufficiently, we see inflammation of the BBB and eventually scars. And a little later one is diagnosed with MS typically when the neurological symptoms start to occur.

Nothing autoimmune therefore, the T cells are just doing their job.

People with MS generally have need for sugar, also have high glucose in their blood in an attempt to meet the needs of the hungry brain. But over time this also attracts a greater insulin resistance, so when that happens, the high consumption of sugar starts to work counterproductive and the situation will deteriorate further.

what to do:
1. ensure the veins are open to ensure a good blood flow and possibly that the iron depositions are taken away.
2. bring the blood sugar back to normal and if necessary take medication to overcome the insulin resistance (step 2 especially important for those people diagnosed after 35; to note as well that due to the high sugar consumption in our modern society increasingly young people develop insulin resistance)

For myself, I am sure that this MS. And also that this line of thought will prevail.

here is further evidence for the low-glucose hypothesis: http://www.ncbi.nlm.nih.gov/pubmed/12938635

ccsvi is part, in fact it causes a low glucose condition that sets off a whole cascade of events with MS as the final neurological outcome.