Lesions and SWI

[mrhodes40]

I bought decaffeinated ECGC personally........

Detailed referenced page on caffeine
http://www.benbest.com/health/caffeine.html

[Inge67]

Great stuff Cheerleader!

I had just emailed a request to my neurologist for a MRI or SWI based on the Haacke protocol. This site certainly helps. I will send it to him also.

Thanks also for the information on green tea extract: I will try and get he right pills here in The Netherlands.

I can't tell you enough how much all the information you all supply gives me hope and helps me in the debate with my doctor. I am really really happy that so many people pull together such relevant information.

I will keep yoy posted on my neurologist reply. Fingers crossed.

Inge

[NHE]

Thanks NHE. I got the gist of it all. Now I need to know how much, how often, and if there are extracts, what are the best ones? I bet I know someone who could help. Oh, Jimmylegs, are you around? I think we need you over here for a lesson on green tea...

I've been drinking green tea over the last several years since it is anti-inflammatory. Epigallocatechin gallate (EGCG) is known to inhibit the transcription factor NF-kB which, once activated, is involved in producing proinflammatory cytokines. Based on this information about the fluoride content in green tea, I try to limit myself to about 4 cups (or teabags) of green tea per day. My first cup of the day is usually caffeinated while the rest is decaf. Note that black tea also has fluoride as the tea plant accumulates it from the soil. However, black tea has less antioxidants in it since the leaves are allowed to ferment. Green tea is usually steamed or roasted to stop the fermentation process which consumes the antioxidants and converts the strong antioxidants into weaker ones.

NHE

[jimmylegs]

needled, i pm'd u back

beating the dead horse some more:
Zinc Deficiency-induced Iron Accumulation, a Consequence of Alterations in Iron Regulatory Protein-binding Activity, Iron Transporters, and Iron Storage Proteins*
Abstract
One consequence of zinc deficiency is an elevation in cell and tissue iron concentrations. To examine the mechanism(s) underlying this phenomenon, Swiss 3T3 cells were cultured in zinc-deficient (D, 0.5 μm zinc), zinc-supplemented (S, 50 μm zinc), or control (C, 4 μm zinc) media. After 24 h of culture, cells in the D group were characterized by a 50% decrease in intracellular zinc and a 35% increase in intracellular iron relative to cells in the S and C groups. The increase in cellular iron was associated with increased transferrin receptor 1 protein and mRNA levels and increased ferritin light chain expression. The divalent metal transporter 1(+)iron-responsive element isoform mRNA was decreased during zinc deficiency-induced iron accumulation. Examination of zinc-deficient cells revealed increased binding of iron regulatory protein 2 (IRP2) and decreased binding of IRP1 to a consensus iron-responsive element. The increased IRP2-binding activity in zinc-deficient cells coincided with an increased level of IRP2 protein. The accumulation of IRP2 protein was independent of zinc deficiency-induced intracellular nitric oxide production but was attenuated by the addition of the antioxidant N-acetylcysteine or ascorbate to the D medium. These data support the concept that zinc deficiency can result in alterations in iron transporter, storage, and regulatory proteins, which facilitate iron accumulation.

[msa]

The caffeine in green tea (extract) is also a vasoconstrictor though.

Isn't caffeine actually a vasodilator as it contains theobromine?

[Ernst]

About iron levels.. not in brain, but in urine --> found this article (2006, bbc news) and there was measured iron in urine with rr and sp/pp ms patients.

The study compared 10 MS patients with the relapsing-remitting form of the disease and 10 who had the more advanced secondary progressive form with 20 people who did not have MS.

They looked at iron levels because the metal has been linked with the facilitation and acceleration of oxygenated damage.

It was found that iron levels were significantly higher in people with MS, particularly so in those with the secondary progressive form of the disease.

link: http://news.bbc.co.uk/2/hi/health/4724414.stm

What do you think about this? Connection to CCSVI.. and how?[/i]

[LR1234]

Elevated urinary excretion of aluminium and iron in multiple sclerosis
Christopher Exley
Birchall Centre for Inorganic Chemistry and Materials Science, Lennard-Jones Laboratories, Keele University, Staffordshire, UK, c.exley@chem.keele.ac.uk

Godwin Mamutse

Department of Neurology, University Hospital of North Staffordshire Keele University, Staffordshire, UK

Olga Korchazhkina

Institute for Science and Technology in Medicine, Keele University, Staffordshire, UK

Eleanor Pye

Department of Neurology, University Hospital of North Staffordshire Keele University, Staffordshire, UK

Stanislav Strekopytov

Birchall Centre for Inorganic Chemistry and Materials Science, Lennard-Jones Laboratories, Keele University, Staffordshire, UK

Anthony Polwart

Life Sciences, Huxley Building, Keele University, Staffordshire, UK

Clive Hawkins

Department of Neurology, University Hospital of North Staffordshire Keele University, Staffordshire, UK

Multiple sclerosis (MS) is a chronic, immune-mediated, demyelinating disease of the central nervous system of as yet unknown aetiology. A consensus of opinion has suggested that the disorder is the result of an interplay between environmental factors and susceptibility genes. We have used a battery of analytical techniques to determine if the urinary excretion of i) markers of oxidative damage; ii) iron and iii) the environmental toxin aluminium and its antagonist, silicon, are altered in relapsing remitting (RRMS) and secondary progressive MS (SPMS). Urinary concentrations of oxidative biomarkers, MDA and TBARS, were not found to be useful indicators of inflammatory disease in MS. However, urinary concentrations of another potential marker for inflammation and oxidative stress, iron, were significantly increased in SPMS (P<0.01) and insignificantly increased in RRMS (P>0.05). Urinary concentrations of aluminium were also significantly increased in RRMS (P<0.001) and SPMS (P<0.05) such that the levels of aluminium excretion in the former were similar to those observed in individuals undergoing metal chelation therapy. The excretion of silicon was lower in MS and significantly so in SPMS (P<0.05). Increased excretion of iron in urine supported a role for iron dysmetabolism in MS. Levels of urinary aluminium excretion similar to those seen in aluminium intoxication suggested that aluminium may be a hitherto unrecognized environmental factor associated with the aetiology of MS. If aluminium is involved in MS then an increased dietary intake of its natural antagonist, silicon, might be a therapeutic option.

[mrhodes40]

Now this is fun!

One of the clues that MS is similar to chronic venous insufficiency is that we produce hemosiderin in the urine, it was a main point of "The Big Idea" (Zamboni, see research thread).

From Wikipedia:

Hemosiderin or haemosiderin is an iron-storage complex (ferritin being the other). It is always found within cells (as opposed to circulating in blood) and appears to be a complex of ferritin, denatured ferritin and other material. The iron within deposits of hemosiderin is very poorly available to supply iron when needed.

Several disease processes result in deposition of larger amounts of hemosiderin in tissues; although these deposits often cause no symptoms, they can lead to organ damage.

Hemosiderin is most commonly found in macrophages and is especially abundant in situations following hemorrhage, suggesting that its formation may be related to phagocytosis of red blood cells and hemoglobin. Hemosiderin can accumulate in different organs in various diseases.

Iron is required by many of the chemical reactions (i.e. oxidation-reduction reactions) in the body but is toxic when not properly contained. Thus, many methods of iron storage have developed.

The point is that the body is cleaning up iron somewhere in the body by devouring it with macrophages, an immune cell, which apparently forms this useless iron complex that has to be removed. In ordinary situations, let's say a red blood cell dies of old age, the iron is saved and reused on a new red blood cell. But iron in the form of hemosiderin is not bio available or useful anymore so it is chucked to the curb......... via the kidneys and urine.

Since hemosiderin is a form of iron seen when blood has gone where it does not belong and the immune system had to clean it up, that is a good support of what we are talking about with CCSVI.

[cheerleader]

Since hemosiderin is a form of iron seen when blood has gone where it does not belong and the immune system had to clean it up, that is a good support of what we are talking about with CCSVI.

Thanks for further explaining this, Marie- In Bologna, the night before the conference Dr. Z spoke about his testing for urine hemosiderin levels in MS patients during relapse, and he said the numbers were very high- as they were in patients with chronic venous insufficiency. Now I understand why!

And of course, this explains why Dr. Haacke was so excited at the conference, because CCSVI gives us a cause for all the iron deposition he was seeing in MS brains using SWI -you knew I had to bring this back OT

Dr. Haacke on his new website-

In fact, it (CCSVI) is a logical explanation as to why the entire brain is affected in MS, why the disease tracks backward along the venous drainage system, and why it emanates from the white matter near the ventricles in the drainage of territory of the medullary veins. If the thalamostriate system is affected with increased iron content along the venous system as I believe it is, then this all falls into place. CCSVI may just be the etiological source we have all been looking for. If so it provides great hope for MS patients worldwide and we cannot and should not wait years for funding to allow us to demonstrate this point.

cheer

[msa]

Has this recent study already been posted?:

Transcranial brain sonography findings predict disease progression in multiple sclerosis
U. Walter MD*, S. Wagner MD, S. Horowski , R. Benecke MD, and U. K. Zettl MD

From the Department of Neurology (U.W., S.H., R.B., U.K.Z.), Institute for Diagnostic and Interventional Radiology (S.W.), University of Rostock, Germany.

* To whom correspondence should be addressed. E-mail: uwe.walter@med.uni-rostock.de.

Objective: In multiple sclerosis (MS), an early neurodegenerative affection of subcortical gray matter has been suggested. Transcranial sonography (TCS) shows hyperechogenic lesions of substantia nigra (SN) and basal ganglia, thought to reflect iron accumulation, in a number of primary neurodegenerative diseases. The present study deals with the question of whether TCS can also display deep gray matter lesions in patients with MS and whether sonographic findings relate to severity and progression of MS.

Methods: We prospectively studied 75 patients with different courses of MS and 55 age-matched healthy subjects clinically and with TCS. Twenty-three patients additionally had 1.5-T MRI at the time of TCS. Disease progression was assessed clinically 2 years after TCS.

Results: Abnormal hyperechogenicity of SN, lenticular nucleus (LN), caudate nucleus, and thalamus was found in 41%, 54%, 40%, and 8% of the patients with MS, with similar frequency in patients with relapsing-remitting and primary or secondary progressive MS if corrected for disease duration, but only in 13%, 13%, 5% (each, p < 0.001), and none (p = 0.028) of the control subjects. Hyperechogenicity of SN and LN correlated with more pronounced MRI T2 hypointensity, thought to reflect iron deposition. Larger bilateral SN echogenic area was related to higher rate of disease progression, whereas small SN echogenic area (SN hypoechogenicity) predicted a disease course without further progression within 2 years.

Conclusions: Neurodegenerative disease–like deep gray matter lesions can be frequently detected by transcranial sonography (TCS) in patients with multiple sclerosis (MS). Findings suggest that TCS shows changes of brain iron metabolism which correlate with future progress of MS.

[LR1234]

What I can't work out is if we should lower our iron intake or should we increase it? The only reason I say this is because weirdly I seem to feel better when I increase my iron levels and increase vitamin C (maybe it encourages the body to metabolise it better or something)

The Swank diet suggests lower iron intake would be better as it excludes red meat.

[radeck]

What I can't work out is if we should lower our iron intake or should we increase it? The only reason I say this is because weirdly I seem to feel better when I increase my iron levels and increase vitamin C (maybe it encourages the body to metabolise it better or something)

The Swank diet suggests lower iron intake would be better as it excludes red meat.

Perhaps a new thread on this topic should be started so those who have researched this can put it all there and those who are experimenting with iron intakes can say what they've experienced?

I've been taking 2g/day of IP6 (extract of rice bran) which is allegedly to be a good iron chelator. I tried to verify that it has that effect, but unfortunately couldn't find anything of substance, so I just went with the believe. Have had no problems with it so far and if anything am feeling a bit more mentally clear. That could have other reasons as well though. One thing I noticed is that I had more muscle twitching in the first couple of days. I thought maybe it also chelates magnesium so started suplpementing Mg, which completely resolved the problem.

[mrhodes40]

My take on it is that you should not alter iron intake. The iron is in your blood. Fact. You could not get oxygen to your tissues if it was not there. Iron forms hemoglobin and that is what carries oxygen around in your body. All red blood cells have iron on them in the form of hemoglobin.

CCSVI results in a leaking of red cells into the brain parenchyma. As long as red blood cells leak there will be some iron getting in where it does not belong.

Reducing iron may help the issue as rat studies on EAE showed that iron deficient mice did better. BUT MS is NOT EAE. it never was and never will be, and if MS is CCSVI it is even more different than we thought than EAE. Not even autoimmune proponents at this point in time is recommending keeping people anemic to address MS.

SO my personal thought on that is that if your doctor thinks you are anemic and need iron, then take it. If not don't mess about with adding it or denying it. Iron overload can be a problem, and anemia can be a problem. Iron is not like, say, a b-vitimain that just goes out in the urine if you get too much. It accumulates. Minerals like that should be monitored and supplemented only if the need is there, not just based on how a person thinks they feel.

If the CCSVI model is correct, being iron deficient is not likely going to help because blood will still leak and it will still have some iron in it...and SWI will continue to detect it...........

[Sharon]

Marie wrote

If not don't mess about with adding it or denying it. Iron overload can be a problem, and anemia can be a problem. Iron is not like, say, a b-vitimain that just goes out in the urine if you get too much. It accumulates.

Important for everyone to understand - iron overload (also known as haemochromatosis) indicates accumulation of iron in the body due to any cause. This can be genetic. My husband had it -- his body stored the iron in his organs -- this is dangerous. Extra iron should only be taken when ordered by a doctor.

Sharon

[jimmylegs]

It was found that iron levels were significantly higher in people with MS, particularly so in those with the secondary progressive form of the disease.

interestingly, ms patients are also lower in zinc, that pesky iron regulator. i can't find a study that compares zinc in spms and other forms of ms though.