Reduced glucose metabolism in the frontal cortex

A forum to discuss Chronic Cerebrospinal Venous Insufficiency and its relationship to Multiple Sclerosis.

Reduced glucose metabolism in the frontal cortex

Postby Cece » Sat Mar 31, 2012 7:40 pm

http://www.neurology.org/content/48/6/1566.short
Reduced glucose metabolism in the frontal cortex and basal ganglia of multiple sclerosis patients with fatigue

A 18F‐fluorodeoxyglucose positron emission tomography study

From the PET Program, Paul Scherrer Institute (Drs. Roelcke, Missimer, and Leenders, and R.P. Maguire), Villigen, Switzerland the Department of Neurology (Drs. Kappos, Lechner-Scott, Brunnschweiler, Huber, and Steck, Mr. Ammann, and Ms. Plohmann), Univ. Hospital, Basel, Switzerland; the Department of Neuroradiology (Drs. Dellas and Radü), Univ. Hospital, Basel, Switzerland; and the Department of Neurology (Dr. Leenders), Univ. Hospital, Zürich, Switzerland.

Abstract

To investigate the pathophysiology of fatigue in MS, we assessed cerebral glucose metabolism (CMR-Glu) in 47 MS patients using PET and 18F-fluorodeoxyglucose. Applying the Fatigue Seventy Scale (FSS), we first compared MS patients with severe fatigue (MS-FAT, n = 19, FSS > 4.9) and MS patients without fatigue (MS-NOF, n = 16, FSS < 3.7) on a pixel-by-pixel basis using Statistical Parametric Mapping (SPM95). Second, we compared FSS values of all 47 patients covering the whole range of this scale with CMRGlu using an analysis of covariance (SPM95). In addition, we determined global CMRGlu by region-of-interest analysis. Sixteen healthy subjects served as control subjects (CON). Global CMRGlu was significantly lower in both MS groups compared with CON (CON 43.3 ± 6.9 μmol/100 mL/min, MS-FAT 34.7 ± 4.4, MS-NOF 35.4 ± 4.5) but was not related to fatigue severity. Comparing the two MS groups, SPM95 analysis revealed predominant CMRGlu reductions bilaterally in a prefrontal area involving the lateral and medial prefrontal cortex and adjacent white matter, in the premotor cortex, putamen, and in the right supplementary motor area of MS-FAT. In addition, there were CMRGlu reductions in the white matter extending from the rostral putamen toward the lateral head of the caudate nucleus. FSS values were inversely related to CMRGlu in the right prefrontal cortex. CMRGlu in the cerebellar vermis and anterior cingulate was relatively higher in MS-FAT than in MS-NOF patients. CMRGlu of both regions showed positive correlations with FSS values. Our data suggest that fatigue in MS is associated with frontal cortex and basal ganglia dysfunction that could result from demyelination of the frontal white matter.

Can CCSVI explain these findings? Could the reduction in glucose metabolism be due to increased pressure or stasis in the capillaries of the brain leading to impaired glucose transfer and metabolization?

The data shows that the fatigue in MS is associated with frontal cortex and basal ganglia dysfunction. This could be a result of a demyelination of the frontal white matter, as suggested by the authors, or a result of CCSVI-related hypertension of the capillaries of the brain.
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Re: Reduced glucose metabolism in the frontal cortex

Postby cheerleader » Sat Mar 31, 2012 8:16 pm

Interesting....Reduced glucose metabolism found in normals exposed to high altitude exposure....or chronic hypoxia. It was high altitude that really slammed Jeff before venoplasty. Even after acclimation, the hypometabolism remained.

Positron emission tomography (PET) and [18F]-2-deoxy-2-fluro-D-glucose (FDG) imaging techniques were used to assess regional cerebral glucose metabolic rates (rCMRglc) in six US marines (Caucasian lineage) before and after a 63-day training program for operations at high altitudes ranging from 10,500 to 20,320 ft. Significant changes in rCMRglcwere found for 7 of 25 brain regions examined. Significant decreases in absolute cerebral glucose metabolism after high-altitude exposure were found in five regions: three frontal, the left occipital lobe, and the right thalamus. In contrast, for the right and left cerebellum significant increases in metabolism were found. The magnitudes of these differences, in terms of absolute metabolism, were large, ranging from 10 to 18%. Although the results may not be solely the result of lower oxygen levels at high altitude, these findings suggest that the brain of healthy human lowlanders responds to chronic hypoxia exposure with precise, region-specific fine tuning of rCMRglc.

http://ajpregu.physiology.org/content/277/1/R314.full
Husband dx RRMS 3/07
dx dual jugular vein stenosis (CCSVI) 4/09
http://ccsviinms.blogspot.com
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Re: Reduced glucose metabolism in the frontal cortex

Postby jackD » Sat Mar 31, 2012 8:43 pm

As I posted before there is 100 mg of this Shilajit in my CQ-10.

http://www.lef.org/Vitamins-Supplements ... &key=01426

http://en.wikipedia.org/wiki/Shilajit

There is a good version of this stuff ...

http://www.primavie.com/productinfo.html

jackD


Int J Ayurveda Res. 2010 Jan;1(1):37-40.

Shilajit: A panacea for high-altitude problems.

Meena H, Pandey HK, Arya MC, Ahmed Z.

SourceHerbal Medicine Division, Defence Research and Development Organization, DIBER, Field Station, Pithoragarh - 262 501, Uttarakhand, India.

Abstract
High altitude problems like hypoxia, acute mountain sickness, high altitude cerebral edema, pulmonary edema, insomnia, tiredness, lethargy, lack of appetite, body pain, dementia, and depression may occur when a person or a soldier residing in a lower altitude ascends to high-altitude areas. These problems arise due to low atmospheric pressure, severe cold, high intensity of solar radiation, high wind velocity, and very high fluctuation of day and night temperatures in these regions. These problems may escalate rapidly and may sometimes become life-threatening.

Shilajit is a herbomineral drug which is pale-brown to blackish-brown, is composed of a gummy exudate that oozes from the rocks of the Himalayas in the summer months. It contains humus, organic plant materials, and fulvic acid as the main carrier molecules.

It actively takes part in the transportation of nutrients into deep tissues and helps to overcome tiredness, lethargy, and chronic fatigue. Shilajit improves the ability to handle high altitudinal stresses and stimulates the immune system.

Thus, Shilajit can be given as a supplement to people ascending to high-altitude areas so that it can act as a "health rejuvenator" and help to overcome high-altitude related problems.

PMID:20532096[PubMed] PMCID:PMC2876922
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Re: Reduced glucose metabolism in the frontal cortex

Postby Cece » Sat Mar 31, 2012 10:30 pm

If Shilajit doesn't work, we could try pioglitazone.
http://www.jneuroinflammation.com/content/1/1/3

Pioglitazone worked like gangbusters for the SPMS patient in the article.

The beneficial effects of pioglitazone observed in this patient are somewhat unexpected as inflammation is less prominent in secondary progressive MS compared to relapsing remitting disease. However, improvements in upper body strength, coordination, dysphagia, and cognitive function, suggest neurological benefit associated with pioglitazone treatment. In addition to their anti-inflammatory actions, TZDs can also influence cell physiology in a receptor-independent manner, and we recently demonstrated that TZDs increase astrocyte glucose metabolism and lactate production [11]. It is therefore feasible that effects on brain metabolism, for example increased capacity of astrocytes to provide lactate to surrounding neurons, accounts in part for improved cognitive and motor function. However, the persistence of lower extremity paralysis appears a likely consequence of irreversible spinal cord atrophy.
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Re: Reduced glucose metabolism in the frontal cortex

Postby jackD » Sat Mar 31, 2012 10:57 pm

I am hoping that they will find Pterostilbene will have positive results when they get around to testing it on humans.

It is not toxic and I have just ordered my second batch of this stuff. I have recently found that I can walk without my cane. I still use the cane as a "walking stick" much of the time.

I take many supplements but I think this one is the one that is making the difference. I take this stuff for the HDL increase, the diabetic and anti-cancer effects.

I am going to get some blood tests soon to see if it really helps.

jackD
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Re: Reduced glucose metabolism in the frontal cortex

Postby cheerleader » Sun Apr 01, 2012 10:19 am

thanks for the info on supplements--some good stuff on aiding glucose metabolism.

The reason I linked the altitude study was to show how it shares reduced glucose metabolism with MS fatigue in the frontal cortex.
and I've long said that Jeff's MS looked more like diffuse cerebral hypoxia than an errant immune system.
And now it's gone.

cheer
Husband dx RRMS 3/07
dx dual jugular vein stenosis (CCSVI) 4/09
http://ccsviinms.blogspot.com
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Re: Reduced glucose metabolism in the frontal cortex

Postby lyndacarol » Sun Apr 01, 2012 10:38 am

Cece wrote:If Shilajit doesn't work, we could try pioglitazone.
http://www.jneuroinflammation.com/content/1/1/3

Pioglitazone worked like gangbusters for the SPMS patient in the article.

The beneficial effects of pioglitazone observed in this patient are somewhat unexpected as inflammation is less prominent in secondary progressive MS compared to relapsing remitting disease. However, improvements in upper body strength, coordination, dysphagia, and cognitive function, suggest neurological benefit associated with pioglitazone treatment. In addition to their anti-inflammatory actions, TZDs can also influence cell physiology in a receptor-independent manner, and we recently demonstrated that TZDs increase astrocyte glucose metabolism and lactate production [11]. It is therefore feasible that effects on brain metabolism, for example increased capacity of astrocytes to provide lactate to surrounding neurons, accounts in part for improved cognitive and motor function. However, the persistence of lower extremity paralysis appears a likely consequence of irreversible spinal cord atrophy.


Currently, there is concern at FDA of a connection between bladder cancer and Actos (pioglitazone), there are even class-action lawsuits being developed.
The TZD family of diabetes drugs (including pioglitazone, rosiglitazone, and others) works by stimulating additional insulin production in the pancreas.
Be aware – this would lead to greater insulin resistance.
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Re: Reduced glucose metabolism in the frontal cortex

Postby Cece » Sun Apr 01, 2012 12:38 pm

cheerleader wrote:Interesting....Reduced glucose metabolism found in normals exposed to high altitude exposure....or chronic hypoxia. It was high altitude that really slammed Jeff before venoplasty. Even after acclimation, the hypometabolism remained.

Positron emission tomography (PET) and [18F]-2-deoxy-2-fluro-D-glucose (FDG) imaging techniques were used to assess regional cerebral glucose metabolic rates (rCMRglc) in six US marines (Caucasian lineage) before and after a 63-day training program for operations at high altitudes ranging from 10,500 to 20,320 ft. Significant changes in rCMRglcwere found for 7 of 25 brain regions examined. Significant decreases in absolute cerebral glucose metabolism after high-altitude exposure were found in five regions: three frontal, the left occipital lobe, and the right thalamus. In contrast, for the right and left cerebellum significant increases in metabolism were found. The magnitudes of these differences, in terms of absolute metabolism, were large, ranging from 10 to 18%. Although the results may not be solely the result of lower oxygen levels at high altitude, these findings suggest that the brain of healthy human lowlanders responds to chronic hypoxia exposure with precise, region-specific fine tuning of rCMRglc.

http://ajpregu.physiology.org/content/277/1/R314.full

It happened to me too. First optic neuritis attack after flying to Hawaii and hiking Mt. Haleakala on my honeymoon. Next attack that got me diagnosed was after childbirth. Next attack that led to first deterioration in five years was after a transatlantic flight two years ago. No attacks since CCSVI treatment but, if my pattern is an attack every five years, I'm not due for awhile. This is why reduction of relapses by DMDs isn't such a big deal to me (I'm not having relapses) but improvement in daily life and improvement of fatigue is.

It's unfortunate to have effects such as the reduction of glucose metabolism in specific areas of the brain written off as demyelination-related, when it could be a clue to what is going on with the hypoxia, and the research Cheer posted ties in well.

Here's a book that could be interesting, written by a trio of PhDs: Going Higher: Oxygen, Man, and Mountains, 2nd Edition
Flying—Flying is by far the most frequent cause of brief everyday hypoxia. Although they might reach altitudes of 30,000-45,000 feet, the cabins of commercial aircraft are kept at a pressure equivalent to an altitude of between 5,000 and 7,500 feet. For the average passenger flying for a few hours at this altitude, the effects are rather mild. A sensitive person may notice slight shortness of breath; occasional irregular breathing; periodic breathing; and some feeling of uneasiness or discomfort. Those who have a tendency to hyperthyroidism, or those with a mild anemia or a pulmonary-cardiac condition may notice the altitude more. Individuals who are at risk for or have a sickle trait, such as sickle cell anemia, should consult a doctor before flying, as lack of oxygen makes red blood cells more fragile.

http://www.mountaineersbooks.org/client ... ckness.cfm

lyndacarol, I remembered that you've done a lot of digging into glucose and MS. I think there's something to it. Thanks for the heads-up about pioglitazone. I'll have to cancel my order. :wink:

It is important to note that when hypoxia is discussed in terms of altitude, it is pressure altitude, not density altitude, that matters. There is always plenty of oxygen around — a whole atmosphere of it — but what controls the amount that reaches the brain is pressure differences across various membranes in the body. The process by which oxygen reaches the brain is affected by a great many factors that vary widely among individuals. By some definitions, normal people acclimatized to sea level begin to be hypoxic at 7,000 feet or so.

I bolded the part that I'd like to learn more about. Does it relate to what's discussed in CCSVI. http://www.flyingmag.com/technique/prof ... fingertips
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Q1 - Reduced glucose metabolism in the frontal cortex

Postby MarkW » Sun Apr 01, 2012 12:54 pm

The first question to ask and get a result for is:
-Does destenosis of all instances of CCSVI syndrome reverse this ???
I realise that speculating around this finding is more fun than the simple logical question but speculation is dangerous when seen by neurologists and CCSVI naysayers.
MarkW
Mark Walker - Oxfordshire, England. Registered Pharmacist (UK). 11 years of study around MS.
Mark's CCSVI Report 7-Mar-11:
http://www.telegraph.co.uk/health/8359854/MS-experts-in-Britain-have-to-open-their-minds.html
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Re: Reduced glucose metabolism in the frontal cortex

Postby cheerleader » Sun Apr 01, 2012 3:09 pm

Cece--great link. Yes, pressure differences make the difference in O2 utilization. And maybe venous congestion is contributing to that pressure difference in the CCSVI brain. Your link is also right on, it's not about the O2 in the atmosphere--it is the bioavailablity of that O2. The thought is that in CCSVI, the lack of O2 availability and glucose metabolism is due to slowed perfusion. Flying or being at high altitude then becomes the tipping point in an already stressed brain. The Haacke and Hubbard perfusion/BOLD studies will further elucidate this hypoperfusion, hypometabolism and low O2 availabilty.

Mark--it was all this "speculation" (as you call it) that got the doctors to look at hypoperfusion, low O2 and cerebral oxygenation levels in pwCCSVI before and after venoplasty. Researchers are now measuring it and finding a correlation. It is a BIOMARKER and it is important, even if you do not think it so.

Here is what Yulin Ge (from NYU) says about hypoxia and hypoperfusion in MS. This is his abstract from the ISNVD--

Technology Insights of Oxygen Metabolic Abnormalities in MS (Yulin Ge, USA)
The role of vascular pathology in multiple sclerosis (MS) was suggested long ago by Ribbert (1882) and Putnam (1933). With the invention and advances of imaging technology, now there is accumulating evidence in vivo of primary vascular pathogenesis and hemodynamic impairment in MS. In particular, there is cerebral blood perfusion changes in lesions and normal appearing brain tissues, suggesting there might be an ischemic and/or hypoxic origin of MS disease. In this presentation, I am going to discuss the hemodynamic perfusion changes and vascular abnormalities measured with several advanced MRI techniques and their pathophysiological significance in MS. First, the close perivenous relationship of MS lesions associated with the underlying vascular inflammatory changes can be evaluated with high resolution susceptibility-weighted imaging. Second, cerebral blood perfusion changes including cerebral blood volume (CBV) and flow (CBF) have been evaluated with dynamic susceptibility contrast-enhanced (DSC) and arterial spin labeling (ASL) MRI techniques. The lesions showed different patterns of perfusion change despite that hypoperfusion is a general feature seen in MS tissues. The perfusion changes in MS may provide additional information of microvascular abnormalities. Third, the recent promising vascular ischemic / hypoxic hypothesis can be evaluated in vivo with several techniques including perfusion- and diffusion- weighted imaging during the acute phase and oxygen metabolic measures as well as functional MRI techniques. In summary, there is increased awareness from both histopathologic and imaging studies of the role of microvascular and hemodynamic impairment in tissue injury in MS; therefore, targeting hypoxic injury may be indicated in the new therapeutic strategy.


Here is what Dr. Zivadinov (from BNAC) says about it in his ISNVD abstract-
A hypoxia-like condition has been evidenced in patients with multiple sclerosis (MS). Perfusion MRI is particularly relevant to studying MS pathogenesis because it has been shown that hypoperfusion of the brain parenchyma in MS patients may precede disease onset. MS patients show abnormal blood flow perfusion patterns, such as increased mean transit time (MTT), and decreased cerebral blood flow (CBF) and cerebral blood volume (CBV) within normal appearing white matter (WM) and gray matter (GM). Perfusion MRI abnormalities are present from the earliest stages of the disease in normal appearing WM, while GM perfusion changes were evidenced at later disease stages. In fact progressive MS patients show more severe perfusion changes compared to relapsing MS. Chronic inflammatory events related to local blood congestion and secondary hyperemia of the brain parenchyma are proposed as a cause of these hemodynamic abnormalities detected on perfusion MRI in patients with MS. The hemodynamic abnormalities detected on perfusion MRI in patients with MS are currently interpreted as being a consequence of chronic inflammatory events related to local blood congestion and secondary hyperemia of the brain parenchyma. Furthermore, at this time it is not clear whether reduced perfusion of the brain parenchyma in MS patients is a sign of vascular pathology or decreased metabolic demand. Alternatively, it can be hypothesized as a disorder that involves the major vasoactive substances. Increased perfusion in the area of lesion formation could be a sign of vessel dilation mediated by pro-inflammatory cytokines. Chronic cerebrospinal venous insufficiency (CCSVI) is a vascular condition described in MS patients, characterized by multiple intra- and extra-luminal stenosing malformations of the principal pathways of extra-cranial venous drainage. An altered perfusion pattern may not only be a consequence of local circulatory disturbances due to inflammatory mechanisms in acute or chronic phases, but rather could result from an outflow blockage situated far away from the lesions. CCSVI may impact local hemodynamics at places distant from the location of the mechanical stenosis, as in any condition of venous obstruction of the major trunks. Such a mechanism may lead to capillary hypertension and leakage, consistently contributing to inflammation. Preliminary findings are presented from a pilot study investigating the relationship between the severity of CCSVI and hypoperfusion in the brain parenchyma.


and here's what Dr. Tucker says about it in his abstract---
This increase in blood pressure fluctuation at the venule end of the capillary bed, which would be equivalent to local hypertension, is predicted to reduce the pressure drop across the bed which, in turn, would reduce blood flow through the bed in accordance with Darcy’s Law. Such a reduction in blood flow through the bed would be accompanied by a reduction in the transfer of oxygen, glucose and other nutrients into the brain tissue in accordance with Fick’s Principle. The reduction in oxygen levels in the brain tissue (i.e. hypoxia), would, in turn, be associated with increased fatigue and decreased mental acuity in the subject patient. In addition, cerebral hypoxia may be associated with vasoconstriction of the endothelium and promotion of both leukocyte- endothelial adherence and angiogenesis (ie. growth of collateral veins). The deprivation of oxygen adjacent to the venules may also result in cell death, including endothelial, and oligodendrocyte cells.


http://www.isnvd.org/files/ISNVD%20Abstract%20Book.pdf
This is not "dangerous" or speculative, Mark....it's science, being done by top researchers.
cheer
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Re: Q1 - Reduced glucose metabolism in the frontal cortex

Postby Cece » Mon Apr 02, 2012 8:39 am

MarkW wrote:The first question to ask and get a result for is:
-Does destenosis of all instances of CCSVI syndrome reverse this ???

It could be different in different patients. 100% reversal, partial reversal, no reversal. If capillaries of the brain have thickened due to long-term effects of CCSVI-related outflow abnormalities, then the capillaries themselves might continue on the hypertension effect even after the CCSVI has been treated. And that hypertension would be what is causing the difficulty in glucose crossing over and being metabolized. I am not sure how the doctors would study this. Maybe PET.

CCSVI is complex. The treatment is comparatively simple (angioplasty of the neck veins and azygous vein) but there might also be the potential for adjunctive pharmaceutical treatments to be developed. It is worth discussing what effect diabetes drugs might have or drugs like diamox or hypertension drugs. Patients here have at times led the way, especially at bringing information to the IRs back in 2009 and 2010.

I have had two thorough CCSVI procedures by one of the best and, even though I have had nice improvements, I am not 100% better. I still have symptoms that I would classify as CCSVI symptoms, from what I know of CCSVI. There are those who get the procedure and then declare that they no longer feel any MS symptoms! That was never me.

If neurologists are observing, then they are welcome to join in. I believe we would have something to learn from the neurologists, as long as all sides were able to be respectful. And speaking of respect, or lack thereof, we have not had the problem with naysayers that we used to have.

I have to keep reading what Dr. Tucker, Dr. Ge, and Dr. Zivadinov have to say on this. So much to learn.
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Re: Reduced glucose metabolism in the frontal cortex

Postby Taurus » Mon Apr 02, 2012 10:21 am

Please see that Sillajit is high in iron content which may be bad for persons with CCSVI. Anybody with MS who has tried Sillajit, please comment.
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Re: Reduced glucose metabolism in the frontal cortex

Postby jackD » Mon Apr 02, 2012 11:09 am

Taurus wrote:Please see that Sillajit is high in iron content which may be bad for persons with CCSVI. Anybody with MS who has tried Sillajit, please comment.



Could you please share with me how you found the Iron content.

The RAW form of this Sillajit stuff is POSION ie heavy metals, but it is removed and the final version I take with my LEF CQ-10 is...

http://www.primavie.com/product_technicaldata.html


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Re: Reduced glucose metabolism in the frontal cortex

Postby Cece » Mon Apr 02, 2012 2:07 pm

http://neuroscience.uth.tmc.edu/s4/chapter11.html

an informative link about the blood-brain barrier (aka the endothelium of brain capillaries) with some discussion of glucose transport
Gases. Gases such as CO2, O2 and volatile anesthetics diffuse rapidly into the brain. As a consequence, the rate at which their concentration in the brain comes into equilibrium with plasma is limited primarily by the cerebral blood flow rate.
The brain is metabolically one of the most actice of all organs in the body. The brain does not store excess energy and derives almost all of its energy needs from aerobic oxidation of glucose. Therefore, it requires a continuous supply of glucose and oxygen to meet its energy requirements.
Figure 11.10 shows there is an excellent correlation between the amount of glucose uses and local cerebral blood flow. Regulation of blood flow to a brain area is achieved by control of dilation of cerebral vessels.
If CCSVI is resulting in congestion and slowed flow, then the brain cannot self-regulate blood flow as effectively.

Estrogen augments glucose transporter and IGF1 expression in primate cerebral cortex: http://www.fasebj.org/content/15/6/907.full

other articles: http://www.google.com/url?sa=t&rct=j&q= ... _eCsH-7oKA

http://physiologyonline.physiology.org/ ... /2/71.full

Considering
the earliest legion of MS is microvascular and
considering the ease with which microvessels may
be isolated from MS human autopsy brain plaque
tissue (Pardridge et al, 1987; Washington et al,
1994), it is somewhat surprising that there are so
few studies on the immunology and biochemistry of
capillaries isolated from MS plaque tissue.

http://www.jneurovirol.com/pdf/5(6)/556-569.pdf
If this would be easy autopsy research to do, then someone ought to do the research! For all the research on the glucose transfer mechanisms of the endothelium of the capillaries of the brain, I am finding nothing on how reflux and stasis of the blood flow would affect the situation. Dr. Zivadinov's research on the reduction in parenchyma in MS patients allows us to infer that reflux and stasis causes capillary die-off.

Dick et al.4 estimated that capillary endothelial cells in the brain transport about 10 times their weight of glucose per minute to support the glucose requirements of the brain
Normally, the transport of glucose across the blood–brain barrier is not rate-limiting, and about 50 percent of the glucose transported diffuses back into the blood. The intracellular phosphorylation of glucose to glucose-6-phosphate is the rate-limiting event for cerebral glycolysis.
http://www.nejm.org/doi/full/10.1056/NE ... 9053251006

ketogenic diet: http://en.wikipedia.org/wiki/Ketogenic_diet
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Re: Reduced glucose metabolism in the frontal cortex

Postby Taurus » Mon Apr 02, 2012 6:29 pm

jackD
Perhaps processed form of Salajjit is safe for pwMS but commercial raw form needs to be taken with care http://health.indiamart.com/ayurveda/ay ... -herb.html

How has been your experience
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