I believe that this discussion should not concentrate exclusively on the vascular dimension. 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.
tara97 wrote: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!!!
lyndacarol wrote: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.
I completely agree with you when you said:I believe that this discussion should not concentrate exclusively on the vascular dimension. 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.
I propose we start in the box of endocrinologists.
A 63-year-old female developed unexplained hyperglycemia and glycosuria during administration of a total parenteral nutrition regimen on which she had been stable for several months. Because the patient had no history of diabetes or evidence of an infection, chromium deficiency was considered. Plasma chromium level was 0.1 g/dl (laboratory reference interval: 1.8–3.8 g/dl). Fourteen days of supplemental intravenous chromium chloride (200 g/day) allowed complete withdrawal of exogenous insulin with no further hyperglycemia or glycosuria. Correction of unexplained glucose intolerance following vigorous chromium supplementation indicates that the patient had chromium deficiency. Subsequent plasma chromium levels remained unchanged, possibly reflecting the sensitivity limits of the assay that was used, the uncertainty that exists regarding appropriate reference intervals for this element, and the fact that plasma levels do not always correlate with total body stores.
Seventy-six patients with established atherosclerotic disease were treated daily with either 250 μg of chromium orally as chromium chloride or a placebo for a period of 7 to 16 months (mean, 11.1 months). Serum chromium increased from 2.69 ± 0.09 to 12.12 ± 0.77 nmol/L (mean ± SE, P < .005). Serum triglycerides were lower (1.68 ± 0.11 and 2.10 ± 0.14 mmol/L, respectively; P < .02) in the chromium-treated patients than in the patients who received placebo, and serum high-density lipoprotein (HDL) increased (from 0.94 ± 0.05 to 1.14 ± 0.07 mmol/L, P < .005) in the patients who received chromium. There was no change in serum cholesterol or blood glucose during the study.
The effects of chromium chloride, chromium nicotinate, and chromium picolinate on insulin internalization in cultured rat skeletal muscle cells was examined. Insulin internalization was markedly increased in cells cultured in a medium that contained chromium picolinate and the increased internalization rate was accompanied by a marked increase in the uptake of both glucose and leucine. The effect was specific for chromium picolinate since neither zinc picolinate nor any of the other forms of chromium tested was effective. The increased insulin internalization rate may result from an increase in membrane fluidity since chromium picolinate and to a lesser extent, chromium nicotinate, increased the membrane fluidity of synthetic liposomal membranes
No significant effect of chromium on lipid or glucose metabolism was found in people without diabetes. Chromium supplementation significantly improved glycemia among patients with diabetes. However, future studies that address the limitations in the current evidence are needed before definitive claims can be made about the effect of chromium supplementation.
Key teaching points:
• Chromium is recognized as an essential element.
• Chromium potentiates insulin action.
• A major challenge in chromium research is the development of practical methods for diagnosing chromium deficiency.
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