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This study has been mentioned before---but I thought it might be valuable to have it on this thread dealing with looking for ferritin as opposed to hemosidrin in CSF--

Here is a study from 1988 which utilized autopsy tissue--remember what Dr. Zamboni discussed in his Big Idea paper regarding hemosiderin as a bio-marker for CHRONIC venous disease--vs. ferritin as a marker for a recent venous infarction.

Perivascular iron deposition and other vascular damage in multiple sclerosis.
Adams CW.

Division of Histopathology, United Medical School of Guy's Hospital, University of London, UK.
Abstract
Evidence of damage to cerebral vein walls was sought in 70 cases of multiple sclerosis. Seventy control cases were also examined. The multiple sclerosis cases showed venous intramural fibrinoid deposition (7%), recent haemorrhages (17%), old haemorrhages revealed by haemosiderin deposition (30%), thrombosis (6%) and thickened veins (19%). In all, 41% of all multiple sclerosis cases showed some evidence of vein damage.

Occasional control cases showed haemosiderin deposition in the brain but, unlike the multiple sclerosis cases, these were diffuse and almost entirely related to coexistent cardiovascular or cerebrovascular disease.

Haemosiderin deposition was common in the substantia nigra and other pigmented nuclei in all cases. It is concluded that the cerebral vein wall in multiple sclerosis is subject to chronic inflammatory damage, which promotes haemorrhage and increased permeability, and constitutes a form of vasculitis.

http://www.ncbi.nlm.nih.gov/pubmed/3346691

(I find it interesting that occasionally the control brains showed diffuse hemosiderin deposition and it was related to cardiovascular/cerebrovascular disease.)

Please note the area of the MS brains that showed the most iron deposition----it was seen in 1988 in this study, it is seen today in 2010 by Dr. Rohit Bakshi--
Substantia Nigra Pathology Predicts Disability in Multiple Sclerosis
Serial transcranial neurosonology in patients with MS reveals a possible link between substantia nigra pathology and progression of neurological disability.
— Rohit Bakshi, MD, FAAN
http://neurology.jwatch.org/cgi/content ... 2010/914/1

Dr. Bakshi has just returned from a visit to the University of Ferrara, where he addressed how his ten years of research and Dr. Zamboni's research are coming together.

cheer

bump--since Dr. Embry mentioned this as a "negative" study--
my point is that it's a moot study, because ferritin in CSF is not a correct biomarker for chronic venous disease.

Hemosiderin is.
cheer

What is wrong with the watch analogy is it assumes deceit. If I am buying a cheap watch on the street that might apply. I take these gaffers' word until it is proved wrong. I guess it depends on your view of human nature, but IMO the last place to look for deceit should be in scientific journals. I first read the abstracts assuming honesty.

Cheer,

I viewed the discussion article in the front of Neurology journal which features a brief commentary on the research paper.

Quite interesting - the doctor quoted believes many of his MS patients are in fact anemic - inflammation in the brain causes elevated CSF Ferritin levels which mask the low iron levels when CSF Ferritin levels are tested. He advocated other tests to identify anemia and believes all MS patients should be tested this way.

One could summise from this that as some have speculated CSF Ferritin levels in MS patients are not necessarily the best indicator of whats going on.

It may also be a cautionary note against trying to reduce ones iron levels to combat CCSVI....

Dreddk

cheerleader wrote:bump--since Dr. Embry mentioned this as a "negative" study--
my point is that it's a moot study, because ferritin in CSF is not a correct biomarker for chronic venous disease.

Hemosiderin is.
cheer

these are links I found:
http://truthseekerforum.com/?p=1381

http://www.communitycare.com/Practices/ ... ground.asp


http://www.kandmool.com/Multiple-Sclero ... rosis.html

dreddk wrote:From Neurology journal.

Normal CSF ferritin levels in MS suggest against etiologic role of chronic venous insufficiency

Objectives: Chronic cerebrospinal venous insufficiency (CCSVI) has been suggested to be a possible cause of multiple sclerosis (MS). If the presumed mechanism of venous stasis–related parenchymal iron deposition and neurodegeneration were true, then upregulation of intrathecal iron transport proteins may be expected.

Methods: This was a cross-sectional (n = 1,408) and longitudinal (n = 29) study on CSF ferritin levels in patients with MS and a range of neurologic disorders.

Results: Pathologic (>12 ng/mL) CSF ferritin levels were observed in 4% of the control patients (median 4 ng/mL), 91% of patients with superficial siderosis (75 ng/mL), 73% of patients with a subarachnoid hemorrhage (59 ng/mL), 10% of patients with relapsing-remitting MS (5 ng/mL), 11% of patients with primary progressive MS (6 ng/mL), 23% of patients with secondary progressive MS (5 ng/mL), and 23% of patients with meningoencephalitis (5 ng/mL). In MS, there was no significant change of CSF ferritin levels over the 3-year follow-up period.

Conclusion: These data do not support an etiologic role for CCSVI-related parenchymal iron deposition in MS.

Of course, another way of expressing these results is that RR MS patients were more than twice as likely to have pathologic CSF levels than normal, PP MS patients were almost three times as likely and SP MS were a whopping 8 times as likely. Also, these pathological levels persisted over a three year period. On the positive side, to counteract the sting likely to be felt by those pinning their hopes on Zamboni, these same researchers have graciously announced that chocolate rations have been increased to 20 grams a day!!!

Scorp--not sure what those links were in reference to. If you were linking to pages stating that ferritin is a good biomarker? Not sure. In any event...ferritin in CSF is a great biomarker for stroke and a one time infarction, but not for an ongoing, chronic venous disease. Here's why:

Fourteen patients with acute cerebrovascular stroke or transient ischemic attacks (one case) were followed by serial determinations of CSF-ferritin during 2 weeks or more from onset of symptoms. After cerebral stroke all patients exhibited an increase of CSF-ferritin with peak levels between 4 and 6 days from admission. Those three patients in whom computed tomography showed cerebral bleeding had the highest peak CSF-ferritin was 28 +/- 11 arb U/l in the patients who had cerebral infarction without signs of bleeding. In seven patients CSF-ferritin returned to the control range after 2 weeks.

http://www.ncbi.nlm.nih.gov/pubmed/7415809

It's the build up of ferritin over time that created the hemosiderin. Here's Dr. Zamboni explaining why--

"The origin of increased leg iron stores is extravasation of red blood cells (erythrocytes) in conditions of significant venous stasis. Erythrocytes are degraded by the interstitial macrophages, with the released iron incorporated into ferritin. Over time, with increasing overload of iron, the structure of ferritin changes to haemosiderin.4-9 In 1988, Ackermann found a twenty-fold higher average concentration of iron in lower limbs affected by venous ulcers as compared to the upper arm of the same subjects.8 The phenomenon of leg haemosiderin deposits seems to be significant for the entire body, since this protein has been demonstrated in the urine of patients affected by CVD.9"

Dr. Zamboni talked about this in Bologna...how hemosiderin was a terrific measure for iron deposition in chronic, ongoing venous disease. Not for a one time hit, like a stroke. He measured the hemosiderin in urine in chronic venous disease and in pwMS, and found the correlation.
hope this explains it better-
cheer

cheerleader wrote:...Dr. Bakshi has just returned from a visit to the University of Ferrara, where he addressed how his ten years of research and Dr. Zamboni's research are coming together.

cheer

Iron in Chronic Brain Disorders: Imaging and Neurotherapeutic Implications (... Rohit Bakshi)

http://www.neurotherapeutics.org/articl ... 6/abstract

...However, the link between observed iron deposition and pathological processes underlying various diseases of the brain is not well understood.

http://www.mssociety.org.uk/application ... 7&id=14320

From the Italian press---Professor Rohit Bakshi of Harvard University came to Ferrara University to discuss how his decade long study of iron deposition in MS brains has now intertwined with Dr. Zamboni's research:
...
its conclusions have been come to intertwine with the results of tests carried out by the researcher and neurologist Bologna Ferrara Fabrizio Salvi on Ccsvi, which have established a hypothetical link between stenosis of the venous vessels in the brain iron accumulation and the onset of multiple sclerosis.
...

hypothetical link:
link assumed by hypothesis; supposed; highly conjectural; not well supported by available evidence.

cah wrote:Sometimes I really feel sorry for those who do these pathetic attempts to disprove the CCSVI theory, being easily rebutted by laypersons with no other special skill than the ability to use google and read.

Right on!

cheerleader wrote:Scorp--not sure what those links were in reference to. If you were linking to pages stating that ferritin is a good biomarker? Not sure. In any event...ferritin in CSF is a great biomarker for stroke and a one time infarction, but not for an ongoing, chronic venous disease. Here's why:

Fourteen patients with acute cerebrovascular stroke or transient ischemic attacks (one case) were followed by serial determinations of CSF-ferritin during 2 weeks or more from onset of symptoms. After cerebral stroke all patients exhibited an increase of CSF-ferritin with peak levels between 4 and 6 days from admission. Those three patients in whom computed tomography showed cerebral bleeding had the highest peak CSF-ferritin was 28 +/- 11 arb U/l in the patients who had cerebral infarction without signs of bleeding. In seven patients CSF-ferritin returned to the control range after 2 weeks.

http://www.ncbi.nlm.nih.gov/pubmed/7415809

It's the build up of ferritin over time that created the hemosiderin. Here's Dr. Zamboni explaining why--

"The origin of increased leg iron stores is extravasation of red blood cells (erythrocytes) in conditions of significant venous stasis. Erythrocytes are degraded by the interstitial macrophages, with the released iron incorporated into ferritin. Over time, with increasing overload of iron, the structure of ferritin changes to haemosiderin.4-9 In 1988, Ackermann found a twenty-fold higher average concentration of iron in lower limbs affected by venous ulcers as compared to the upper arm of the same subjects.8 The phenomenon of leg haemosiderin deposits seems to be significant for the entire body, since this protein has been demonstrated in the urine of patients affected by CVD.9"

Dr. Zamboni talked about this in Bologna...how hemosiderin was a terrific measure for iron deposition in chronic, ongoing venous disease. Not for a one time hit, like a stroke. He measured the hemosiderin in urine in chronic venous disease and in pwMS, and found the correlation.
hope this explains it better-
cheer

Sorry Cheer it was getting late for me when I posted those links. I researched comments made by proponenets of Zamboni's study and it looked to me as if they were saying that ferritin levels were one way to measure iron in the body and high levels would help confirm Zambonio's hypotethsis. I do not see where Zamboni has ever said ferretin levels in the CSF is not a good biomarker for ongoing chronic venuous disease. I do see where he states hemosiderin is an important biomarker but I can not see where he stated that ferretin levels are generally irrelevant.

.

Lyon wrote: But I guess that's the point of this whole thing....questioning whether Zamboni is causing all this misinformation by NOT making the necessary information needed to replicate his findings easier to come by. Every other researcher historically has put that information in their initial study articles specifically to make replication attempts easier. Zamboni charges for lessons.

Lyon, as far as I can judge this, Zamboni always wanted and was open to work with the neurologists. (See, for example, his interview with ccsvi.nl.) Wouldn't it be a good, sensible approach to seek the in-depth dialogue, learn each others point of view, and THEN question each others methodology? This just seems reasonable to me. I can't understand why they don't even want to talk to him before trying to replicate his research. Even if it wasn't more than some sort of "know your enemies".

Lyon wrote: But I guess that's the point of this whole thing....questioning whether Zamboni is causing all this misinformation by NOT making the necessary information needed to replicate his findings easier to come by. Every other researcher historically has put that information in their initial study articles specifically to make replication attempts easier. Zamboni charges for lessons.

What's wrong with Zamboni charging money for his ultrasound detection method if he invented it? Like any other inventor, isn't he entitled to the fruits of his ingenuity? He might have been more clear, however, that using an ultrasound as a detection tool without proper training could lead to mixed results. He should have recommended a venogram or at least an MRV as detection tools for any replication studies. The margin of error associated with different methods of Doppler detection vs. venogram should have been established before it's use could be advised in replication studies.

Just stumbled over the study in the MSIF e-mail news of this evening and was wondering about the authors behind it. Great you already discussed it.

Below how the MS International Federation presented it in their e-mail news (and funny that this "interesting examination" was followed by an article of potential increased risk of cardiovascular disease - "but data are limited" they say). As we know the scientific committees in the MS associations are mainly composed of neurologists that choose the type and style of research summaries to be published... I have no other words for this "interesting examination" while there are far more other interesting ones related to the topic that could be mentioned!!

>>Normal CSF ferritin levels in MS suggest against etiologic role of chronic venous insufficiency

The authors conducted an interesting examination of CSF ferritin levels in patients with all sub-types types of MS and a range of other neurological disorders to investigate the role of venous stasis related parenchymal iron deposition in pathogenesis of MS. In MS patients, there was no significant change of CSF ferritin levels over the 3-year follow-up period. The data from this study therefore does not support an etiologic role for CCSVI-related parenchymal iron deposition in MS.
authors: Worthington V, Killestein J, Eikelenboom MJ, Teunissen CE, Barkhof F, Polman CH, Uitdehaag BM, Petzold A.
source: Neurology. 2010 Sep 29. [Epub ahead of print]<<

>>Risk of Arterial Cardiovascular Diseases in Patients with Multiple Sclerosis: A Population-Based Cohort Study

Patients with multiple sclerosis (MS) may have a higher risk of cardiovascular diseases (CVD) than the general population, but data are limited. Researchers from Denmark conducted a population-based cohort study involving Danish citizens diagnosed with MS (n = 13,963) from 1977 to 2006 and an age- and sex-matched population cohort (n = 66,407) and calculated the risk of arterial cardiovascular disease (CVD) for all subjects.

Adjusted incidence rate ratios at 1yr follow up and subsequent 2-30 year follow up for myocardial infarction (MI), overall stroke rate, heart failure and atrial fibrillation/flutter were calculated. In this Danish cohort, the risk of CVD among MS patients was low, but greater than that in the general population, particularly in the short term.
authors: Christiansen CF, Christensen S, Farkas DK, Miret M, Sørensen HT, Pedersen L.
source: Neuroepidemiology. 2010 Sep 24;35(4):267-274. [Epub ahead of print]<<