Iron metabolism panels should be a first
I think the difference between what we are looking at in the phlebotomy thread and classic hemochromatosis is that the majority of us doing the trials have only one gene for hemochromatosis, not the classic two. We generally have high transferrin saturation, not ferritin or serum-iron.
In classic hemochromatosis non-transferrin bound iron goes to the liver. No brain effect. But transferrin bound iron does cross the brain-blood barrier, I've even read that the brain produces it's own transferrin.
We are probably looking for another gene that fills in the C282Y/??
or H63D/?? gap. It's what we all have in common, the "??"
Cheers........
In classic hemochromatosis non-transferrin bound iron goes to the liver. No brain effect. But transferrin bound iron does cross the brain-blood barrier, I've even read that the brain produces it's own transferrin.
We are probably looking for another gene that fills in the C282Y/??
or H63D/?? gap. It's what we all have in common, the "??"
Cheers........
Are they going to be looking at the brains of the normal people? Because otherwise this whole study is poorly designed. And something else makes no sense to me. Zamboni said he did not find these narrow veins in any other neurological condition. BUT why not if 26% of the population has come, is it not rather odd that he did not find any. It be tested all of these other people with neurological conditions, you would expect to find a consistent number of people with it, in other words 25% of the people with other neurological conditions really should have stenosis. Otherwise it would seem like having stenosis would be almost protective because all of these other conditions feature iron in the brain also.Principal investigator Dr. Robert Zivadinov, an associate professor of neurology at the University of Buffalo, and his colleagues said Wednesday that 55 per cent of people with MS who were studied had narrowing of the veins that control blood flow from the brain, compared with 26 per cent of healthy control subjects, including some who were relatives of the MS patients.
Read more: http://www.cbc.ca/health/story/2010/02/ ... z0hhyNv6L7
Sorry, that last message was a mess. Dragon NaturallySpeaking takes a lot of proofreading, and I neglected to do it properly. But my point remains the same, why did Zamboni not find stenosis in all these other neurological conditions when 25% of healthy subjects have it. If he tested 60 people, you would expect to find at least 10 or 12 people with stenosis. Then NONE, it does not make any sense.
And I also want to put down a couple of thoughts concerning stenosis. If healthy subjects can have this problem, why are they not experiencing the same reflux back into the brain? Zamboni says that it is a mechanical problem, not a metabolic one. That improper drainage causes a backflow due to venous insufficiency. But if healthy controls are not experiencing this reflux, why not, they have the same mechanical problem and they should be. And before people maintain that that it is due to the extent of the stenosis, I have seen nothing that states this. I have seen no conclusions that the stenosis is more severe in MS, it is more that the veins are blocked by iron and plaque. But if 25% of controls have stenosis without the problematical blockage, why are they not accumulating iron at the same rate? Again, I think this points to higher levels of iron in the blood, which is a metabolic problem, not a mechanical one. I gather that there was a rather broad population tested, and some of these people with stenosis were older. So why aren't they developing the same kinds of blockages? It can't be simple luck.
Why are the healthy controls not experiencing that same backflow even though they have the same mechanical paradigm? In my opinion, there must be some other factor. Perhaps it is the viscosity of the blood? That thicker blood is harder to get through narrowed veins and eventually causes vascular plaques. So maybe people that have blood that is not so thick do not experience the same backflow because the blood is able to flow through the narrowing. I mean what other explanation is there? And if these people are experiencing a backflow that is depositing iron into the brains, why are they still healthy? I doubt 25% of the population is going to develop MS. How can healthy controls have the same stenosis without it causing neurological symptoms or disability?
Are they going to go back and study the healthy controls? Are they going to try to explain the rather obvious discrepancies between the healthy controls and the people with blocked veins/MS? I think it is the healthy controls that are going to reveal the real problem, and that it is more a problem with the blood than the veins.
And I also want to put down a couple of thoughts concerning stenosis. If healthy subjects can have this problem, why are they not experiencing the same reflux back into the brain? Zamboni says that it is a mechanical problem, not a metabolic one. That improper drainage causes a backflow due to venous insufficiency. But if healthy controls are not experiencing this reflux, why not, they have the same mechanical problem and they should be. And before people maintain that that it is due to the extent of the stenosis, I have seen nothing that states this. I have seen no conclusions that the stenosis is more severe in MS, it is more that the veins are blocked by iron and plaque. But if 25% of controls have stenosis without the problematical blockage, why are they not accumulating iron at the same rate? Again, I think this points to higher levels of iron in the blood, which is a metabolic problem, not a mechanical one. I gather that there was a rather broad population tested, and some of these people with stenosis were older. So why aren't they developing the same kinds of blockages? It can't be simple luck.
Why are the healthy controls not experiencing that same backflow even though they have the same mechanical paradigm? In my opinion, there must be some other factor. Perhaps it is the viscosity of the blood? That thicker blood is harder to get through narrowed veins and eventually causes vascular plaques. So maybe people that have blood that is not so thick do not experience the same backflow because the blood is able to flow through the narrowing. I mean what other explanation is there? And if these people are experiencing a backflow that is depositing iron into the brains, why are they still healthy? I doubt 25% of the population is going to develop MS. How can healthy controls have the same stenosis without it causing neurological symptoms or disability?
Are they going to go back and study the healthy controls? Are they going to try to explain the rather obvious discrepancies between the healthy controls and the people with blocked veins/MS? I think it is the healthy controls that are going to reveal the real problem, and that it is more a problem with the blood than the veins.
hi Merlyn , lots of unknowns in CCSVI-MS. There was an argument here on TIMS regarding Dr. Zamboni's original diagnosis of CCSVI in MS people being nearly 100 %. Simply put ...Dr. Zamboni screened for definite MS people in his study. Key word ..definite. That makes perfect sense. It was a small sample study.
In Buffalo the people studied were more broad spectrum. And the research was double blinded ???? Correct me if I'm wrong..I can take it .
The results revealed 25 % of the study group --had stenosis' , but were labeled healthy controls . Once again I repeat that - I do not wish anything on anyone - but it has to be said that this could change.
I do hope Buffalo is keeping close watch on the HC-25% 'ers.
I think they hold the CCSVI key.
Mr. Success
In Buffalo the people studied were more broad spectrum. And the research was double blinded ???? Correct me if I'm wrong..I can take it .
The results revealed 25 % of the study group --had stenosis' , but were labeled healthy controls . Once again I repeat that - I do not wish anything on anyone - but it has to be said that this could change.
I do hope Buffalo is keeping close watch on the HC-25% 'ers.
I think they hold the CCSVI key.
Mr. Success
Until they test iron metabolism, they will not know whether CCSVI is the result of faulty iron metabolism. They've known for years the transferrin is the protein that deposits iron into the brain, I cannot think of a single valid reason for not testing this, to rule out whether it is implicated in the buildup of iron in the veins. I am disgusted by the whole thing, of course you can diagnose CCSVI without doing an iron metabolism panel, but what you cannot determine is whether the iron is there due to metabolic overload. You cannot determine whether what you are seeing is the result of faulty iron metabolism or whether it is simply mechanical. You know what I think? I think people are being snowed and people have died already because doctors are not doing a simple iron metabolism panel! MS really could not be that simple could it? Everybody is convinced that it is some alien disease that cannot be decoded , and it is abnormal iron metabolism. People had better wake up, they are spending thousands of dollars in subjecting themselves to risky surgery before running a simple iron metabolism panel. We have eight out of eight showing very abnormal iron levels, you cannot refute that, not that you are, not saying that, it is just that more people will die for lack of a simple blood test and I find that insane.
Lyon-the thing is, you don't have to guess! Just run the proper iron panel and join the growing group of people that are finding they are subclinical hemochromatosis, not detected by a ferritin test. Test total iron, TIBC (Total Iron Binding Capacity), ferritin and transferrin. Don't guess, prove it.
Well Merlyn . . . as Lyon points out, it's more complicated than it appears. 
I am one person here who has had those very tests run repeatedly and they do not at all reflect an iron overload.
I was intrigued by your hypothesis and I dug out all my tests and saw that every one of those tests have been run on me and every one of my tests is completely the opposite of what you say people with MS should have. I am severely iron deficient and anemic. Sorry! And I definitely have MS. And I have CCSVI.
Over the years I have encountered other people with MS who have discovered they had hemochromatosis. You're on to something important. But it is not the answer for everyone.
I am one person here who has had those very tests run repeatedly and they do not at all reflect an iron overload. I was intrigued by your hypothesis and I dug out all my tests and saw that every one of those tests have been run on me and every one of my tests is completely the opposite of what you say people with MS should have. I am severely iron deficient and anemic. Sorry! And I definitely have MS. And I have CCSVI.
Over the years I have encountered other people with MS who have discovered they had hemochromatosis. You're on to something important. But it is not the answer for everyone.
Bluesky63-Bluesky63-please, I apologize if I come across as obnoxious sometimes. I am just frustrated with the whole picture, that doctors are not first investigating iron metabolism. Yours is a case in point. Severe anemia is not normal iron metabolism! And I don't think doctors are recognizing what is called iron loading anemia. I beg you, if you could post some of your test results, it would clarify for a whole bunch of us what other forms of iron metabolism dysfunction is occurring. You see, iron loading anemia is treated the same way as hemochromatosis, the excess iron has to be removed! Has anyone ever mentioned this type of anemia to you, maybe they have, but if you could post your numbers, it would be very helpful. I have another guy on another forum that is just stunned to learn that his iron metabolism may be iron loading anemia. I would love to compare numbers!
http://www.annals.org/content/60/4/728.2
Iron-loading anemias are characterized by: (1) hypochromic microcytic red cells, (2) elevated serum iron with saturated TIBC, (3) siderosis of body tissues, and (4) sideroblasts in the bone marrow and circulating siderocytes. Two cases are presented which demonstrated a partial hematologic response after pyridoxine therapy. Iron59 studies revealed increased intestinal absorption and poor red cell utilization of iron before and after therapy. These findings explained the excessive siderosis of the liver and bone marrow which was seen in biopsy material from both cases. Energetic phlebotomy therapy was then instituted. Approximately 7 g of iron were removed from one patient during
http://lpi.oregonstate.edu/infocenter/minerals/iron/
Hereditary anemias
Iron overload may occur in individuals with severe hereditary anemias that are not caused by iron deficiency. Excessive dietary absorption of iron may occur in response to the body's continued efforts to form red blood cells. Anemic patients at risk of iron overload include those with sideroblastic anemia, pyruvate kinase deficiency, and thalassemia major, especially when they are treated with numerous transfusions. Patients with hereditary spherocytosis and thalassemia minor do not usually develop iron overload unless they are misdiagnosed as having iron deficiency and treated with large doses of iron over many years (7). The thalassemias (major and minor) are common in individuals of Mediterranean descent. It has been hypothesized that a Mediterranean form of iron overload, distinct from HH, also exists (43).
Lyon- The fact that there are so many different forms of iron loading anemias, hereditary hemochromatosis heterozygote iron loaders, etc. etc. means that it is absolutely insane to not test iron metabolism. How do they know that this CCSVI vein opening will last if people are continuing to accumulate iron in the wrong areas of the body.
Personally, I no longer believe that MS is all that complicated. I think we've been studying the wrong thing, which makes it seem complicated. It is sort of like ulcers. For years and years and years they told people not to eat spicy food etc., and then along comes someone that said it was bacteria that caused ulcers in the stomach. They were totally vilified until it was proved that he was right. Until you figure out what is root cause, therapies don't have the effects you want them to. What I have found from studying heavy metals for 10 years, is that they studied to death the effects of the heavy metals. But it doesn't really matter, you can study the toxic effects for years and years, but the cure/treatment is getting rid of the heavy metal. Nothing else works.
http://www.amazon.com/Mechanistic-Toxic ... 0849372720
What is complicated is what biological pathways heavy metals screw up. Iron is a heavy metal in excess.
Personally, I no longer believe that MS is all that complicated. I think we've been studying the wrong thing, which makes it seem complicated. It is sort of like ulcers. For years and years and years they told people not to eat spicy food etc., and then along comes someone that said it was bacteria that caused ulcers in the stomach. They were totally vilified until it was proved that he was right. Until you figure out what is root cause, therapies don't have the effects you want them to. What I have found from studying heavy metals for 10 years, is that they studied to death the effects of the heavy metals. But it doesn't really matter, you can study the toxic effects for years and years, but the cure/treatment is getting rid of the heavy metal. Nothing else works.
http://www.amazon.com/Mechanistic-Toxic ... 0849372720
What is complicated is what biological pathways heavy metals screw up. Iron is a heavy metal in excess.