Mitochondria of Oligodendrocytes: CCSVI (hypoxia)+factor=MS

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

Postby 1eye » Fri Jun 03, 2011 4:23 pm

Four proteins in particular were responsible for distinguishing disease from control. Peptide fingerprint mapping unambiguously identified these differentially expressed proteins. Three proteins identified are involved in respiration including cytochrome c oxidase subunit 5b (COX5b), the brain specific isozyme of creatine kinase, and hemoglobin β-chain.

Proteins involved in respiration expressed differently than in non-'MS' mitochondria. Smells like hypoxia to me. Any way this can be tested?
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Postby MegansMom » Fri Jun 03, 2011 7:11 pm

Of course the proteins would be different. The body is being signaled that there is not enough oxygen and glucose so it tries to satisfy need with alternate methods.
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My 35 yo daughter is newly dx 8/19/10 (had 12 symptoms)
Dx with Type A CCSVI- 1 IJV & double "candy wrapper" appearance of her Azygos
Venoplasty done Sept 21, 2010
Doing extremely well-
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Postby 1eye » Sat Jun 04, 2011 5:02 am

Well, in this case we have some mitochondria of a dead person which have some apparently different proteins. It would be nice to show hypoxia and stenosis in the same group and not in the control group. Without blinding, using the catheter-based 'Clark' miniaturized polarographic oxygen electrode, with invasive testing, this can be done.

Blinding is not necessary. The instruments cannot be fooled. The testing is done in humans, in vivo, and distinguishes between people with CCSVI or 'MS' and not. Anybody want to put their money where their mouth is?

p.s. quoting from a posting of mine elsewhere:

-use an instrumented catheter such that blood in various vessels may be measured for oxygenation (pO2). use a 'Clark' miniaturized polarographic oxygen electrode.

-compare oxygenation with the same subject(s) having the same level of activity (as prescribed) and oxygen uptake (as collected and measured), between value(s) obtained in arterial flow and value(s) obtained in cerebral and spinal outflow.

You can of course also compare the cerebral and spinal outflow deoxygenated blood in subjects with CCSVI with that of subjects without.

-similar kinds of catheterized instruments may be used to measure things like pH and pCO2.


from Google scholar
Clinical evaluation of a multiparameter intra-arterial blood-gas sensor
E. Abraham, T. J. Gallagher and S. Fink
Intensive Care Medicine
Volume 22, Number 5, 507-513, DOI: 10.1007/BF01712177
"Try - Just A Little Bit Harder" - Janis Joplin
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Postby 1eye » Sat Jun 04, 2011 2:28 pm

I am not a physician or a scientist for a living or for a vocation. I would find the oxygen-blood experiment interesting, but welcome anyone who wants to convince me that it is a wrong idea.

Dr. MacDonald, or Sclafani, or Mehta, or Siskin, or any of the CCSVI doctors you have heard about here on this forum (see http://www.thisisms.com/ftopic-8778-day ... c-105.html - the whole thread) could perform this experiment. It could be done in Canada, US, UK, Poland, Italy, many, many places where there are, I'm sure, plenty of volunteers.

I know a guy at Carleton University in Ottawa who is expert in the ergometry and physiology. He knows how to do the gas collection and analysis.

Postures:

It may be impossible to perform the oxygen testing catheter work in any posture other than lying down. People perform work in various postures for fairly lengthy periods throughout their lives. I think it would be a good idea to collect this data at a predetermined interval after predetermined work loads (as well as after idleness) in sitting, standing, and prone positions. These things may not have an influence on the measurements in vivo, after the work is complete and the posture reverted to prone for the procedure, but then again, they may, so why take a chance?

On the other hand, since the test involves putting the catheter through the subject's heart, the testing physician may not want to do any exercise or postural manipulations at all.

Multiple procedures:

It is not a good idea to do multiple procedures of this type on the same individual. After an incision to the blood vessel involved, it would be a decision best left up to the patient and their own physician whether another such procedure were ever performed again. The business of healing the one(s) involved in the experiment is complex and must be dealt with by the attending doctor.
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Postby DrDiana » Sat Jun 04, 2011 3:03 pm

This is a topic I return to over and over.

Every patient I know of who was tested and/or treated for mitochondrial disorders (I was treated), had a negative test, and little or no result from treatment.

Are there any exceptions out there? I can't be the only one who is looking for people who HAVE responded...

It makes sense to me, not just the science, but how it translates to how we FEEL. Especially when we hit that "wall", usually mid-afternoon for me, when I can't even think. Exhaustion takes over. I can have caffeine, sugar and even Provigil -- no effect.

Cece, you mentioned how the article said not to 'fast'. I agree, and I've been hesitant to say this for a long time, because it flies in the face of most everything we are working on with our diets. But here it is --

I do better (and I know others like me), who do better on a HIGH FAT diet. I know, sounds crazy. I'm not sure if it keeps the blood sugar steadier, or if it is more involved than that. Our brains are 60% fat (and fast is a big part of myelin), and we treat epilepsy with a VERY high fat diet ("ketogenic diets"). It is extremely effective.

I went on Axona to try to mimic the ketogenic diet, but within 12 hours, I was too acidic for my Diamox (takes pressure off of my brain) to work. But it gives the brain an alternative source of fuel (ketones) if we are unable to utilize glucose as well.

If someone is not taking Diamox, I'd highly recommend trying high fat (I stayed with the "healthier" fats, usually), and some Axona (my neurologist gave me samples). Axona is currently being tried for early Alzheimer's. Of course, you want to bring your doctor in on this with you, <disclaimer> as I can't practice medicine without a license over the internet without having seen you. But in the interest in sharing ideas that may or may not be helpful, I wanted you all to know...

OH-- this is also a HUGE reason why I have TONS of Fish Oil capsules (the fancy-pants ones that doctors take. ha). Lots of good fat there. BTY, my cholesterol is fine, and I'm a bit thin (no worries on those aspects).

If you try this, would you kindly let me know? I'm in a mood to do some more studies. :wink: 8O
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Postby 1eye » Sat Jun 04, 2011 4:17 pm

They did a thing with EAE on marmosets. They think maybe polunsaturated fats destabilize myelin...

Role of lipid interactions in autoimmune demyelination
Benjamin Ohler, Karlheinz Graf, Richard Bragg, Travis Lemons, Robert Coe, Claude Genain, Jacob Israelachvili, Cynthia Husted
Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease, Volume 1688, Issue 1, 20 January 2004, Pages 10-17, ISSN 0925-4439, DOI: 10.1016/j.bbadis.2003.10.001.
http://www.sciencedirect.com/science/ar ... 3903001650
Keywords: Experimental allergic encephalomyelitis; Myelin; Membrane lipid fluidity and packing; Multiple sclerosis

That's one reason I try to stick to olive oil. I think the type of fat molecules and hydrogenation and trans and all that can mess me up.
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Postby DrDiana » Sat Jun 04, 2011 4:39 pm

1eye wrote:That's one reason I try to stick to olive oil. I think the type of fat molecules and hydrogenation and trans and all that can mess me up.


Is this why many of us are reaching for the coconut oil now? I must confess, I will eat "bad" fats, too -- I may have cream cheese for lunch or a snack. Yikes, I know, but I FEEL better!

Interesting article. Thanks 1eye!

:)
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Postby monik_77 » Sun Jun 05, 2011 3:32 am

Other interesting paper:


Curr Alzheimer Res. 2011 May 18. [Epub ahead of print]
Effects of Coenzyme Q and Creatine Supplementation on Brain Energy Metabolism in Rats Exposed to Chronic Cerebral Hypoperfusion.
Horecky J, Gvozdjáková A, Kucharská J, Obrenovich ME, Palacios HH, Li Y, Vančová O, Aliev G.
Source
School of Health Science and Healthcare Administration, University of Atlanta, Atlanta, GA 30360 USA. GAliev@uofa.edu.
Abstract
It is known that oxidative stress and mitochondrial dysfunction both play an important role in animal models of brain ischemia. The present study was undertaken to test whether oral supplementation of coenzyme Q10 (ubiquinone) or creatine citrate could protect against brain ischemia-induced mitochondrial damage in the rats model. Brain ischemia was induced for 50 minutes with three-vessel occlusion (3-VO). Coenzyme Q10 was administered for 30 days before the ischemic event and coenzyme Q10 or creatine citrate for 30 days post-ischemia. Moreover, the concentrations of coenzyme Q10 and α-, γ- tocopherols as well as the formation of thiobarbituric acid reactive substances (TBARS) were measured in brain mitochondria and in plasma. Transient hypoperfusion revealed significant impairment in brain energy metabolism as detected by mitochondrial oxidative phosphorylation as well as decreased concentrations of brain and plasma endogenous antioxidants and increased formation of TBARS in plasma. When compared with the ischemic group, supplementation of coenzyme Q10 was ineffective as a preventive agent. However, the positive effect of therapeutic coenzyme Q10 supplementation was supported by the oxygen consumption values (p<0.05) and ATP production (p<0.05) in brain mitochondria, as well as by increased concentration of coenzyme Q9 (p<0.05) and concentration of α-tocopherol (p<0.05) in brain mitochondria and by increased concentration of α-tocopherol (p<0.05) and γ-tocopherol in plasma. This suggests that coenzyme Q10 therapy involves resistance to oxidative stress and improved brain bioenergetics, when supplemented during reperfusion after ischemic brain injury.

http://www.ncbi.nlm.nih.gov/pubmed/21592049


Any experience with supplements of CoQ10??
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Postby DrDiana » Mon Jun 06, 2011 2:43 pm

CoQ10 -- I DO take this, and although I can't get my hands on it right now, I read a study about how it seems to have neuroprotective effects, but here's the rub -- the amount that you had to take was A TON (if I remember correctly, it was about 5-6 of the big honking pills per day).

If I can find the article, I'll post it. I found a liquid CoQ10 and took that for a while, but am back down to 1 pill/day.

Doesn't it seem as if all we do is take supplements? (or who was it who said he now had more supplements than the Sunday paper?). ha.
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Postby Cece » Mon Jun 06, 2011 3:40 pm

Huh! I like coq10 but am taking a normal sized supplement.
Very interesting research posted. Makes you wonder what research would be done if pharma could make a profit off of vitamins.
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Postby 1eye » Tue Jun 07, 2011 11:12 am

1eye wrote:
-use an instrumented catheter such that blood in various vessels may be measured for oxygenation (pO2). use a 'Clark' miniaturized polarographic oxygen electrode.

-compare oxygenation with the same subject(s) having the same level of activity (as prescribed) and oxygen uptake (as collected and measured), between value(s) obtained in arterial flow and value(s) obtained in cerebral and spinal outflow.

You can of course also compare the cerebral and spinal outflow deoxygenated blood in subjects with CCSVI with that of subjects without.

-similar kinds of catheterized instruments may be used to measure things like pH and pCO2.


from Google scholar
Clinical evaluation of a multiparameter intra-arterial blood-gas sensor
E. Abraham, T. J. Gallagher and S. Fink
Intensive Care Medicine
Volume 22, Number 5, 507-513, DOI: 10.1007/BF01712177


I might add that if this instrument were used twice, before and after ballooning, it would certainly demonstrate the effect of the venoplasty on oxygenation. Were it to be used in any subsequent procedures a measurement of the patient's current status could be taken.
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Postby DrDiana » Tue Jun 07, 2011 11:58 am

Cool find, 1eye,

Could they get the instrument into the deeper parts of the brain, though?
I think many of our issues come from hypoxia deep in the hypothalamus, thalamus, periventricular areas, etc.

That's a tough cookie to crack!
Dr. Diana

Special interest in "brain drains" and how they affect numerous conditions, including MS, Ehlers-Danlos, Parkinson's, Alzheimer's, etc. I am a therapeutic optometrist on professional disability with EDS, POTS, CCSVI, mast cell disea
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Postby Cece » Tue Jun 07, 2011 12:12 pm

1eye wrote:I might add that if this instrument were used twice, before and after ballooning, it would certainly demonstrate the effect of the venoplasty on oxygenation.

I suggested something similiar to Dr. Sclafani last year, he did not jump on the idea with great enthusiasm. :)
www.thisisms.com/ftopicp-110957.html#110957
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Postby 1eye » Tue Jun 07, 2011 10:17 pm

In the case of a procedure where no ink is available (IVUS only) it would at least give some indication the procedure had succeeded.
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Postby MegansMom » Thu Jun 09, 2011 3:33 am

Cece wrote:
1eye wrote:I might add that if this instrument were used twice, before and after ballooning, it would certainly demonstrate the effect of the venoplasty on oxygenation.

I suggested something similiar to Dr. Sclafani last year, he did not jump on the idea with great enthusiasm. :)
www.thisisms.com/ftopicp-110957.html#110957


I know my daughters IR James Caridi (at Shands/Unversity Hospital at
Gainesville FL) measured the oxygen saturation above her blockages before ballooning and after PTA ballooning and there was a significant difference. In fact he had her on nasal cannula supplement oxygen in the recovery area.
I wonder if they all measure oxygen levels?
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My 35 yo daughter is newly dx 8/19/10 (had 12 symptoms)
Dx with Type A CCSVI- 1 IJV & double "candy wrapper" appearance of her Azygos
Venoplasty done Sept 21, 2010
Doing extremely well-
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