Chronic Cerebrospinal Venous Insufficiency (CCSVI)-

Artifishual · Post by **Artifishual** » Tue Mar 24, 2009 4:52 am

hey JL, I take paypal.....

,

sorry for the highjacking of this thread

Lyon · Post by **Lyon** » Tue Mar 24, 2009 5:23 am

Post by **jimmylegs** » Tue Mar 24, 2009 9:29 am

LOL!!! learned yer lesson didja?

Artifishual · Post by **Artifishual** » Tue Mar 24, 2009 10:13 am

not funny D

mrhodes40 · Post by **mrhodes40** » Tue Mar 24, 2009 10:58 am

Good heavens! let's take some calcium and get mg in balance.

I am repeating something I posted in the liver thread in case some of the researchers who are folowing this thread might be interested.

It is in regards to the fact that some people with MS have liver issues. Cheers husband was told he must have been drinking alcohol when he does not merely because he showed signs of trouble mimicing an alcohilic liver trouble . Quote from the other post:

PPMS is the pattern D of Zamboni's research. Pattern D includes lumbar vein issues and the azygous, which we already know is at issue drains the abdominal area in general, that's its main job, not draining the head
from wiki
one of a system of veins that drain the thoracic and abdominal walls; arises as a continuation of the right ascending lumbar vein and terminates in the superior vena cava
But the entire circulation of the liver is the main thing of the abdomen; the liver is the size of a football and all blood goes through there to be detoxified with every beat of the heart on its way to where it is going.

From wiki HERE

The hepatic portal vein (often simply portal vein) is a vein in the abdominal cavity that drains blood from the gastrointestinal tract and spleen. It is usually formed by the confluence of the superior mesenteric and splenic veins, and also receives blood from the inferior mesenteric, gastric, and cystic veins. The hepatic portal vein is a major component of the hepatic portal system, one of the main portal venous systems in the body.

Conditions involving the hepatic portal vein cause considerable illness and death globally. An important example of such a condition is elevated blood pressure in the hepatic portal vein. This condition, called portal hypertension, is a major complication of cirrhosis worldwide
The cause of cirrhosis is the portal hypertension, cirrhosis being "alcoholic liver".

I know actually a lot about that. The cirrhotic liver also backs things up behind it too, so that the esophogus ends up with gross vericosities...this can be a cause of death in the alcoholic person as when they rupture they can bleed all the way out.

What if there is a blockage in the azygous in just the right location so that it was backing up the liver circulation and causing venous hypertension there that is a mechanical cause of portal vein hypertension in SOME people with MS???

Could that cause a false "alcoholic liver"? Like Cheers husby?

The location of the blockage would have to be in JUST the right place...that would be why it would not get all MSers. Could men be more prone because of genes to a certain location??

THAT is a good question for Dr Zamboni.

In other words, Dr Anonymous, Dr Z or any of the other doctors:

Can a stricture in the azygous or lumbar veins mimic hepatic portal hypertension and cause cirrhosis like symptoms in some MS patients?

cheerleader · Post by **cheerleader** » Tue Mar 24, 2009 11:26 am

Can a stricture in the azygous or lumbar veins mimic hepatic portal hypertension and cause cirrhosis like symptoms in some MS patients?

Thank you for finding the connection, Marie.
This is what I was wondering when I posited about venous congestion affecting the liver. If there is venous blockage upriver from the liver, could it have caused the jaundice and elevated AST and ALTs??? Wow. More evidence?
Any doctors in the house, please comment!
AC

mrhodes40 · Post by **mrhodes40** » Tue Mar 24, 2009 2:05 pm

Yeah I am not sure. It'd have to be just right in my view location wise. The hepatic system drains into the mesenteric drains into the azygous, so if it was in the asygous it'd need to be near the mesenteric in a way that allowed that to back up all the way to the hepatic without any other way around, but the mesenteric is a large complex bunch of veins, so it seems like the possibliliies for a work around that would not be damaging would be possible, in other words branch A of the vein is congested and backed up so branch B takes more. I just don't know if a backup is possible to the degree it'd need to create hypertension....but if it DID

If the blockage CAN back up to the portal vein and cause pressure there then you would get the raised ALT etc. The pressure is a problem for the liver and is part of what makes it sick.

That's why pancreatitis ends up with liver problems; it has to do with the veins.

Ask your guy Cheer is there is any evidence of such a backup when he does venograms. This is an interesting possiblity.

And it seems like it adds to the overall Zamboni picture

gibbledygook · Post by **gibbledygook** » Wed Mar 25, 2009 5:56 am

This is the ingredient list of "Sure Fresh Cotton Roll", a common deodorant:

Aqua, Aluminum Chlorohydrate, Helianthus Annuus Seed Oil, Steareth-2, Parfum, Steareth-20, Silica, Propylene Glycol Dicaprylate/Dicaprate, Gossypium Herbaceum Fruit Extract, Citric Acid, Potassium Lactate, Benzyl Alcohol, Benzyl Benzoate, Benzyl Salicylate, Citronellol, Geraniol, Hexyl Cinnamal, Limonene, Linalool.

From wikipedia:

The variation most commonly used in deodorants and antiperspirants is Al2Cl(OH)5. There is no scientific evidence supporting widespread rumors that aluminium salts in deodorants can cause Alzheimer's disease or breast cancer. Amongst others, research published in the Journal of the National Cancer Institute[4] found no evidence whatsoever that these compounds increase the risk of breast cancer. However, aluminium is a neurotoxin that alters the function of the blood-brain barrier[5], and it is one of the few abundant elements that appears to have no beneficial function to living cells.

And from pubmed:

1: J Neuroimmune Pharmacol. 2008 Dec;3(4):286-95. Epub 2008 Oct 1. Links
Manufactured aluminum oxide nanoparticles decrease expression of tight junction proteins in brain vasculature.Chen L, Yokel RA, Hennig B, Toborek M.
Molecular Neuroscience and Vascular Biology Laboratory, Department of Neurosurgery, University of Kentucky Medical Center, 593 Wethington Bldg., 900 S Limestone, Lexington, KY 40536, USA.

Manufactured nanoparticles of aluminum oxide (nano-alumina) have been widely used in the environment; however, their potential toxicity provides a growing concern for human health. The present study focuses on the hypothesis that nano-alumina can affect the blood-brain barrier and induce endothelial toxicity. In the first series of experiments, human brain microvascular endothelial cells (HBMEC) were exposed to alumina and control nanoparticles in dose- and time-responsive manners. Treatment with nano-alumina markedly reduced HBMEC viability, altered mitochondrial potential, increased cellular oxidation, and decreased tight junction protein expression as compared to control nanoparticles. Alterations of tight junction protein levels were prevented by cellular enrichment with glutathione. In the second series of experiments, rats were infused with nano-alumina at the dose of 29 mg/kg and the brains were stained for expression of tight junction proteins. Treatment with nano-alumina resulted in a marked fragmentation and disruption of integrity of claudin-5 and occludin. These results indicate that cerebral vasculature can be affected by nano-alumina. In addition, our data indicate that alterations of mitochondrial functions may be the underlying mechanism of nano-alumina toxicity.

PMID: 18830698 [PubMed - indexed for MEDLINE]

link

1: Toxicol Lett. 2008 May 30;178(3):160-6. Epub 2008 Mar 27. Links
Alumina nanoparticles induce expression of endothelial cell adhesion molecules.Oesterling E, Chopra N, Gavalas V, Arzuaga X, Lim EJ, Sultana R, Butterfield DA, Bachas L, Hennig B.
Graduate Center for Toxicology, University of Kentucky, Lexington, KY 40536, USA.

Nanotechnology is a rapidly growing industry that has elicited much concern because of the lack of available toxicity data. Exposure to ultrafine particles may be a risk for the development of vascular diseases due to dysfunction of the vascular endothelium. Increased endothelial adhesiveness is a critical first step in the development of vascular diseases, such as atherosclerosis. The hypothesis that alumina nanoparticles increase inflammatory markers of the endothelium, measured by the induction of adhesion molecules as well as the adhesion of monocytes to the endothelial monolayer, was tested. Following characterization of alumina nanoparticles by transmission electron microscopy (TEM), electron diffraction, and particle size distribution analysis, endothelial cells were exposed to alumina at various concentrations and times. Both porcine pulmonary artery endothelial cells and human umbilical vein endothelial cells showed increased mRNA and protein expression of VCAM-1, ICAM-1, and ELAM-1. Furthermore, human endothelial cells treated with alumina particles showed increased adhesion of activated monocytes. The alumina particles tended to agglomerate at physiological pH in serum-containing media, which led to a range of particle sizes from nano to micron size during treatment conditions. These data show that alumina nanoparticles can elicit a proinflammatory response and thus present a cardiovascular disease risk.

PMID: 18456438 [PubMed - indexed for MEDLINE]

link[/url]

mrhodes40 · Post by **mrhodes40** » Wed Mar 25, 2009 7:02 am

GG thanks for those links, wow

Aluminum is really bad news it seems.
I think most antiperspirants in the US use aluminum cholrohydrate, but deodorants usually do not. It is the alu. chlo. that stops the sweating so you need to check the labels. We use deodorant that's alum. free

It pretty much looks like any metal that does not belong can do hurt the endothelium. Cheer's endothelium essay points the finger that way too.

gibbledygook · Post by **gibbledygook** » Wed Mar 25, 2009 7:43 am

When I was diagnosed I had a mineral check done which showed that I had high levels of aluminium. This was the only toxic metal I showed even though I used to smoke. I used to use those aluminium anti-perspirants a lot but not since diagnosis. I wonder if the aluminium needs to be removed from the system with silicon, another supplement to add to the list!
I was particularly interested to read of aluminium's interfering with elastin.

cheerleader · Post by **cheerleader** » Wed Mar 25, 2009 7:52 am

While aluminum is not a heavy metal, it has been found to be toxic. Because aluminum permeates our air,water, and soil, small amounts are present in our food. The average person consumes between three and ten milligrams of aluminum a day. Only recently has research revealed that aluminum is absorbed and accumulated in the body. Aluminum is a popular metal used to make cookware, cooking utensils, and foil. Excessive use of antacids is the most common cause of aluminum toxicity. Mylanta, Maalox, Glusil, Amphojel, and many others have a high aluminum hydroxide content. Many over-the-counter drugs used for inflammation and pain contain aluminum, including Arthritis Pain Formula, Ascriptin, Bufferin, and Vanquish. Several douche preparations, including Massengil and Summer's Eve, contain aluminum. It is also an additive in most baking powders and is sometimes evident in drinking water.

Many symptoms of aluminum toxicity are similar to those of Alzheimer's disease and osteoporosis. Aluminum toxicity can lead to colic, rickets, gastro-intestinal disturbances, poor calcium metabolism, extreme nervousness, anemia, headache, decreased liver and kidney function, forgetfulness, speech disturbances,and memory loss, softening of the bones, and weak, aching muscles. Research suggests that a chronic calcium deficiency may change the way in which the body uses minerals. Bone loss and increased intestinal absorption of aluminum and silicon combine to form compounds that accumulate in the cerebral cortex of the brain. These compounds prevent impulses from being carried to or from the brain.

An accumulation of aluminum salts in the brain has been implicated in seizures and reduced mental faculties. Autopsies performed on Alzheimer's victims revealed that four times the normal amount of aluminum had accumulated in the nerve cells in the brain. This suggests that long-term accumulation of aluminum in the brain may contribute to the development of Alzheimer's disease. In addition, an unidentified protein not found in normal brain tissue has been discovered in the the brain tissue of Alzheimer's victims.

link

Good chelators for aluminum include garlic, B12, magnesium, calcium, kelp and lecithin. Thanks, Gibs. Something else to consider-
AC

gibbledygook · Post by **gibbledygook** » Wed Mar 25, 2009 8:07 am

Does anyone think silicon is a good aluminium chelator? I saw that in the article which shows high levels in MS, the researchers suggest using silicon...any views? Silicon looks like it's good for bones.

gibbledygook · Post by **gibbledygook** » Wed Mar 25, 2009 8:23 am

here's something:

1: J Toxicol Environ Health. 1996 Aug 30;48(6):667-83.Links
Prevention and treatment of aluminum toxicity including chelation therapy: status and research needs.Yokel RA, Ackrill P, Burgess E, Day JP, Domingo JL, Flaten TP, Savory J.
College of Pharmacy, University of Kentucky Medical Center, Lexington 40536-0082, USA. ryokel1@pop.uky.edu

The prevention and treatment of aluminum (Al) accumulation and toxicity are reviewed. Recommendations to further our understanding of desferrioxamine (deferoxamine, DFO) treatment and to develop more effective chelation approaches are provided. Reduction of Al accumulation and toxicity may benefit end-stage renal disease (ESRD) patients and perhaps those suffering from specific neurodegenerative disorders as well as workers with Al-induced neurocognitive disorders. The clearance of Al may be increased by extracorporeal chelation, renal transplantation, perhaps complexation with simple ligands such as silicon (Si), and systemic chelation therapy. The abilities of extracorporeal chelation and Si to reduce Al accumulation require further evaluation. Although it may not be possible to design Al-specific chelators, chelators with greater Al selectivity are desired. Aluminum-selective chelation might be achieved by targeted chelator distribution or by the use of adjuvants with the chelator. The ability of carboxylic acids to facilitate Al elimination, under specific conditions, warrants further study. Desferrioxamine does not produce significant biliary Al excretion. A chelator with this property may be useful in ESRD patients. The necessity for an Al chelator to distribute extravascularly to be effective is unknown and should be determined to guide the selection of alternatives to DFO. The lack of oral efficacy and occasional side effects of DFO encourage identification of orally effective, safer Al chelators. The bidentate 3-hydroxypyridin-4-ones are currently the most encouraging alternatives to DFO. They have been shown to increase urinary Al excretion in rats and rabbits, but to have toxicity comparable to, or greater than, DFO. Their toxicity may relate to incomplete metal complexation. The ability of orally effective chelators to increase absorption of chelated metal from the gastrointestinal (Gl) tract needs to be evaluated. Orally effective, safe Al chelators would be of benefit to peritoneal dialysis patients and those with neurodegenerative disorders, if Al chelation therapy is indicated. The reduction of Alzheimer's disease (AD) progression and the reversal of Al-induced behavioral deficits and neurofibrillary tangles by DFO encourage further study of Al chelation therapy for selected neurodegenerative disorders.

PMID: 8772805 [PubMed - indexed for MEDLINE]

link

mrhodes40 · Post by **mrhodes40** » Wed Mar 25, 2009 11:38 am

I said

In other words, Dr Anonymous, Dr Z or any of the other doctors:

Can a stricture in the azygous or lumbar veins mimic hepatic portal hypertension and cause cirrhosis like symptoms in some MS patients?

I got an answer

.

Anatomically, there is NO (direct or indirect) connection between azygous vein and portal or hepatic veins. Portal vein collect blood from splenic and superior mesenteric veins. Then blood passes through hepatic sinuses, and drains via hepatic veins into the inferior caval vein. Azygous vein drain into the superior caval vein, yet there are interconnections of the veins in the azygous territory with the inferior caval vein (still, they have nothing to do with hepatic veins or veins of the portal system). Thus, a stricture in the azygous vein cannot affect liver function.
It cannot be completely ruled out, though, that a similar structure to that of azygous vein could arise in a hepatic vein, yet it is highly unlikely and very rarely described; moreover, there are at least three hepatic veins, and simultaneous strictures are even less likely. Injury of the liver could be more likely a consequence of legion of factors, anti-MS drugs in particular.

SO there we go, not likely at all;

Wow, Thank You doctor!!

Lyon · Post by **Lyon** » Wed Mar 25, 2009 12:37 pm