Geographic distribution, MS and CCSVI

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

Postby mrhodes40 » Sat Nov 21, 2009 2:12 pm

Here's an abstract from another one found on pubmed

Effects of 1alpha,25 dihydroxyvitamin D3 on the expression of HO-1 and GFAP in glial cells of the photothrombotically lesioned cerebral cortex.
PMID 15531134
Abstract In ischemic cerebral injuries a cascade of degenerative mechanisms, all participating in the development of oxidative stress, influence the condition of the tissue. The survival of viable tissue affected by secondary injury largely depends on the balance between endogenous protective mechanisms and the ongoing degenerative processes. The inducible enzyme, heme oxygenase-1 metabolizes and thus detoxifies free heme to the powerful endogenous antioxidants biliverdin and bilirubin therefore enhancing neuroprotection. The secosteroid 1alpha,25-dihydroxyvitamin D3 (1,25-D3) is a modulator of the immune system and also exhibits a strong potential for neuroprotection as recently shown in the MCAO model of cerebral ischemia. We studied the effects of 1,25-D3 treatment on heme oxygenase-1 expression following focal cortical ischemia elicited by photothrombosis. Postlesional treatment with 1,25-D3 (4 microg/kg body weight) resulted in a transient, but significant upregulation of glial heme oxygenase-1 immunoreactivity concomitant with a reduction in glial fibrillary acidic protein immunoreactivity in remote cortical regions affected by a secondary spread of injury, whereas the size of the lesion's core remained unaffected. 1,25-D3 did not produce a temporal shift or extension of injury-related heme oxygenase-1 responses, indicating that 1,25-D3 did not prolong ischemia-related heme oxygenase-1 expression. In contrast to glial heme oxygenase-1 upregulation, glial fibrillary acidic protein, a sensitive marker for reactive gliosis, was significantly reduced. These findings support an additional protective action of 1,25-D3 at the cellular level in regions affected by secondary injury-related responses.
Authors Karl Zilles , Otto-W Witte , Hans-J Bidmon , Evelyn Oermann
Journal Title Journal of chemical neuroanatomy


This one says that the resulting damage is the sum of the inside the body (endogenous) protective mechanisms and the amount of degeneration caused by the damage...

They caused a type of blood clot to occur then watched the lesion that developed from it.

If they gave active vitamin d after the lesion was present the core of the lesion did not change but the secondary expansion of the lesion was reduced by reducing the gliosis which scarring to the nerve. In other words it didn't heal the initial brain lesion injury but it reduced the secondary injury.
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Postby ikulo » Sat Nov 21, 2009 3:36 pm

I remember reading a study that suggested that Vitamin D is integral in the formation of collagen, which is necessary for proper development of blood vessels, veins, etc. Also, there's an article out there that suggests that the most relevant measure of vitamin D is when the person is still in the womb or still very very young.. in fact I believe a larger number of MS'ers are born in the spring time, suggesting that the MSer did not get enough vitamin D in the womb because of the winter months. So, I suppose it would follow that in the womb an MS'er didn't get enough vitamin D, perhaps leading to lower levels of collagen??, and then maybe some type of event in the life that caused the jugulars, etc to collapse or become damaged because the collagen levels were low or the body didn't have a way to fix them?? Not sure if that make sense, what do you guys think?

ok, back to studying for finals.
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Postby mrhodes40 » Sat Nov 21, 2009 6:30 pm

Good thought!
From the Bologna conference finalized notes Cheer took saved on the research thread Dr Gabbiani said

By red staining for collagen and using unpolarized and polarized light, he saw that there is less collagen 1 type fibers in the MS jugular vein tissue, and more collagen III fibers in MS. This is the exact opposite of the controls.

Connective tissue in MS switches from collagen I to collagen III and this takes place in the IJVs. This switch also happens in fibromatosis, colloids and hypertrophied scars, and this remodeling may play a role in CCSVI disturbances


The problem is not that the viatmin d material disproves CCSVI--it is that no one has looked at vitamin D from this perspective. It is a rich area to find associations with CCSVI, there are many ways it may play in to this model.
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Postby ikulo » Sat Nov 21, 2009 7:58 pm

Mr.Rhodes - your note on Collagen I and III is echoed in this study:

Comparison of collagen subtype I and III presence in varicose and non-varicose vein walls.

Haviarova Z, Janega P, Durdik S, Kovac P, Mraz P, Stvrtinova V.

Institute of Anatomy, Faculty of Medicine, Comenius University, Bratislava, Slovakia. zora.haviarova@fmed.uniba.sk

STUDY OBJECTIVES: The connective tissue alterations in varicose vein wall are supposed to be one of the main causes of primary varicose vein (main sign of human lower limbs chronic venous insufficency). METHODS: 5 varicose vein samples from 5 patients undergoing stripping surgery of long saphenous vein were compared with 5 control samples of healthy (non-dilated) long saphenous veins from necroptic material (with no history of varicosis). They were fixed in a Baker solution, processed by use of light microscopic method, cut to ultra-thin sections (4-5 microm) and stained with PicroSirius Red for collagen. Sections were scanned with light microscope (Leica, Germany) and camera Canon S50 (Germany) and analysed by morphometric programme Image J v.1.38g (National Institute of Health, USA). RESULTS: In the group of healthy (non-dilated) veins the mean collagen I/III ratio value was 31.40 and in the group of varicose veins the mean collagen I/III ratio was 12.35; the difference is statistically significant: healthy veins contain significantly more of collagen subtype I and varicose veins contain significantly more of collagen subtype III in their walls. CONCLUSION: The statistically significant difference in the collagen I/III ratio between the groups of healthy (non-dilated) and varicose (dilated) vein walls is worthy of further following (Tab. 2, Fig. 7, Ref. 12). Full Text (Free, PDF) www.bmj.sk.
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Postby mrhodes40 » Sat Nov 21, 2009 9:42 pm

Now it is a chicken and egg question: does the collagen characteristic change in the face of venous pressure or does the collagen be different to begin with and result in the vericosities?

This is not answered conclusively in venous ulcer research yet so I assume will remain an unanswered thing for MS for a while anyway.

I am a lady, Marie Rhodes I have been 40 for 9 years now :wink:
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Postby ikulo » Sat Nov 21, 2009 11:33 pm

haha, sorry Marie! I saw Mrh... and I just thought Mr. :) Oh sure, blame the new guy! :lol:

As far as the question, I have no idea. I did try to find additional reports linking Vitamin D to venous malformation, etc. but nothing was coming up. Perhaps someone with some experience or knowledge in this topic could provide some clues.
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Postby ErikaSlovakia » Sun Nov 22, 2009 2:00 am

ikulo wrote:
Haviarova Z, Janega P, Durdik S, Kovac P, Mraz P, Stvrtinova V.

Institute of Anatomy, Faculty of Medicine, Comenius University, Bratislava, Slovakia. zora.haviarova@fmed.uniba.sk


Hi ikulo,
this lady: Stvrtinova V. is the prof. Dr. Viera Stvrtinova, PhD. who I visited at the beginning of my story - she is an Angiologist.
She knows Dr. Simka in person. They also met in Monaco during a conference of Phlebology this August. She was willing to help me with the health insurance but they made it so complicated that at the end it was not possible.
I am in contact with her. I would like to read this in Slovak. I will send an e-mail to Mrs. Haviarova to get the research.
Erika[/u]
Aug. 7, 09 Doppler Ultras. in Poland, left Jugul. valve problem, RRMS since 1996, now SPMS,
- Nov.3,09: one stent in the left jug. vein in Katowice, Poland, LDN, never on DMDs
- Jan. 19, 11: control venography in Katowice - negative but I feel worse
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Postby JSTCD » Sun Nov 22, 2009 10:35 am

I don't think vein formation is entirly genetic. It also has something do do with how you develop.

I would think that in a HOT climate, you would need to increase blood flow to the brain to cool it, and a child developing in that environment might develop wider veins.

In a cold Climate the opposite is true, so one would expect to develop smaller veins. Add some sort of genetic pre-disposition and voila CCSVI.

Once you finished growing, vein size would be fixed, hence the protection of latitude depending on where you grew up, not where you live as an adult.
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Postby mrhodes40 » Sun Nov 22, 2009 10:52 am

Now that is an interesting theory. When you start bending your head around the question "how might vit D and geographic location play a role in CCSVI" all kinds of things come up...researchers will have this happen too I think :D
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Postby radeck » Sun Nov 22, 2009 7:55 pm

Quick request for clarification, is the type of collagen change observed in CCSVI by Gabbiani and others of the same type as that in varicosed veins, or different?
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