Phlebotomy anyone?

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

Postby Merlyn » Thu Feb 10, 2011 6:01 pm

Hydrogen Peroxide (H2O2) - Posted by Larry Frieders, POPh - November 16, 2001

I received the following information from a doctor I know who offers this type of therapy. If you'd like more information contact me by email. I can forward his name and contact information.


General Information about Peroxide

There are lots of studies that demonstrate that peroxide does the following:

1. Peroxide stimulated the immune system.

2. Peroxide killed a dozen different pathogenic bacteria, killed many viruses, yeast and fungus too.

3. Peroxide even improved circulation and unblocked arteries, like chelation does.

4. It caused debris deep down in the lungs to be expelled.

5. It got rid of all kinds of chronic pains, but nobody was certain why.

6. It oxygenated the body, better than if you got into a $100,000 hyperbaric oxygen chamber.

7. Peroxide even destroyed some cancerous tumors.

There are many thousands of articles in the medical literature about peroxide. So if peroxide does so much good, why aren’t doctors using it more? The answer has to do with money and ignorance.

For example, drug companies would like doctors to prescribe a $75 antibiotic, not a few dollars worth of peroxide. You have to understand that the drug companies fill the medical journals with expensive and really slick advertising. Because of these ads, doctors perceive that drugs are the state of the art. Nobody advertises H202. Peroxide is not patentable. Who’s going to promote peroxide when anyone and any drug company can make it?

Then, some doctors are just plain stupid. They don’t even wash hands between examining patients, which was proven to reduce hospital infections by Dr. Semilweise a hundred years ago. It took doctors 40 years to accept the electrocardiogram as useful.

Well, it’s been over 60 years since peroxide was found to be miraculous. In 1929 there was a worldwide flu epidemic. There was no drug to kill the flu virus (and there still isn’t), so some people with poor immune systems died from it. Eighty-four percent (84%) of those that developed influenza pneumonia died.

In 1929 doctors took patients dying from influenza pneumonia, and for the first time in history gave them intravenous hydrogen peroxide, 48% of them lived! Yes, I’m telling you there has been an antiviral remedy for over 60 years, and doctors seem ignorant of it all.

Dr. Charles Farr, who is considered the foremost developer of H202 therapy, did a great clinical study on flu victims just a few years ago. He gave 44 patients with the flu a peroxide treatment, and told them to return the next day if they were no better. Seven returned (note: all seven that returned had a prior history of lung problems). He gave them a second peroxide treatment and told them to return if they were not any better. Two returned, and they required a third dose. How’s that for anti-viral action? You see, if you come early to the doctor with a virus, it can be helped rather easily.

Asthma, Emphysema, and Chronic Lung Disease

What about these diseases? It turns out that peroxide can do something special, something no other substance we know of can do. It can clean the lungs.

Ask a pathologist what color a baby’s lungs are. He’ll tell you they’re pink. At autopsy, 50 or more years later, those lungs are a gray-black…filled with pollution from the air we breath, which could not be eliminated by the body. It’s harder to transfer oxygen from the air you breath through soot-covered air sacks. Here’s the great news…intravenous peroxide burns the soot and debris and lifts it off the surface of the air sacks. Then you cough this gunk up, get it out of your body and then you can then breath easier. Nothing else in medicine has this action. This miracle isn’t always met with joy. All the patient knows is that they took a peroxide treatment and began coughing more than ever. They've got to understand that this coughing is good. The coughing can start as soon as the IV drip begins or after the IV is finished. This reaction to peroxide may occur for 3 to 6 treatments, after which it ceases. The job is done! The air sacks of the lungs have been cleaned.

The coughing doesn’t always occur. Instead of coughing, the loose debris is often brought up in the sputum (the mucous and phlegm in the throat), and then swallowed, without ever being aware of it.

How Many Treatments Are Needed For Lung Problems?

For asthma, emphysema, or chronic lung disease, peroxide treatments should be taken once per week for at least ten treatments. It takes some time for the changes to occur in chronic disease. You must realize that it will take more than 2 or 3 treatments to see results. And frankly, we really don’t want to start the peroxide unless you intend to finish a reasonable series. That’s because we don’t want people condemning peroxide therapy unless they’ve given it a proper chance to work. For asthma, emphysema, and chronic lung disease, this means taking at least ten treatments over 10 weeks.

How Many Treatments Are Needed For Most Problems?

Now maybe you’ve heard that peroxide could fix you up in just one or two treatments. That can be true…it really depends upon what disease we’re talking about. For example, a man came to us who was suffering with temporal arteritis. Temporal arteritis causes terrible, one-sided head pain around the eye and the temple. This man had been to dozens of doctors and top-notch pain centers. He was loaded with many different drugs. A smile came over this man’s face as the first IV was dripping. He could feel his pain going away. He took a second treatment, and the pain was gone! That was 6 months ago, and he hasn’t been back! So for some things it may take only a couple of treatments. Please give us a chance to meet with you personally and discuss approximately how many treatments are likely to be needed for your condition.

What Diagnosis Respond To Peroxide?

Here are some other random cases, and how peroxide worked. First, let’s talk about shingles (also called herpes zoster). Just one or two treatments taken for a couple of days in a row and one more a week later generally does the trick! We had a patient with AIDS and shingles. It took about six treatments over the course of two weeks…not bad considering a battered immune system. Sometimes the pains that may linger after shingles (post herpetic neuralgia) responds to a peroxide series. I think it’s because there’s still live virus deep in the nerve root.

Some believe that Bell’s Palsy (of the face) is also from a virus similar to shingles, because the peroxide treatments have relieved the condition over a week or two.

For colds, or the flu, we’ve already told you that one or two treatments are generally sufficient.

A woman with malignant melanoma with metastasis to her lymph nodes was treated. She was in awful pain. She wanted one treatment every day. When she got it, she felt no pain, was active and busy. Without a daily treatment, she was miserable and could not function.

A lot of chronic painful conditions respond to peroxide. We believe that all chronic pain comes ultimately from insufficient oxygen getting into the effected area of the body. Peroxide gets the oxygen into the tissue and the pain leaves. Nevertheless, the official line is that we don’t understand why peroxide helps chronic pain. There’s no telling the best way to give the peroxide for chronic pain. One might need it once a week or once a day. We’ve recently learned that slowly infusing the peroxide all day long, using an infusion pump, can get rid of constant pain much better than just a short IV (our thanks to Dr. Jesse Stoff for that finding).

For disorders of blocked arteries, such as angina pectoris, or peripheral artery blockage in the legs, Dr. Charlie Farr says that one peroxide each week, plus two chelation treatments each week works the best. We think that’s a perfectly fine schedule, and about ten weeks of treatment should be considered minimal. Fifteen to twenty weeks would be really good.

If your immune system is down, and you get sick a lot, take one treatment a week for ten to twenty weeks, (you’ll need a variety of nutritional supplements too). Here the peroxide stimulates the production of T-helper cells and causes white cells to make interferon, and lots more.

Let’s talk about chronic fatigue syndrome. Chronic fatigue is not one disease. It more than likely is a name given to hundreds of not-yet-diagnosed problems in a person. What this means is that there may be someone with undiagnosed parasites, dragging their body around, exhausted. Well that’s chronic fatigue. And so is undiagnosed Epstein-Bar virus infection, and so is malabsorption with mineral deficiency. The point is there is no magic bullet remedy for what is called chronic fatigue, because the causes of chronic fatigue are varied. The underlying cause of each individual’s chronic fatigue needs to be determined and treated with the most suitable remedy or remedies. Peroxide is likely to help many chronic fatigue patients, because peroxide has so many actions.

For IBOM’s list of diagnoses for which peroxide has been found useful, please see the last page.

Is Peroxide The Magic Bullet?

Well if there were a magic bullet, it might well be IV peroxide, because peroxide has so many different actions. It can kill considerable numbers of viruses, bacteria, fungi, yeast, parasites, and even some tumor cells! It can boost the immune system by improving the number and quality of various blood cells. It can improve circulation, improve heart function, and provide oxygen to the brain. It can relieve pain. It can destroy toxic environmental chemicals inside your body and quiet allergies. Can you think of anything more likely to help an unknown, undiagnosed, hidden illness?

Mixing Other Substances In The Peroxide IV

It was once believed that the doctor could not add any other substance into the peroxide IV bottle. It was believed that either the peroxide would be destroyed, or that the added substance might be destroyed. Recently, however, studies have determined that certain vitamins and minerals can be added into a peroxide infusion. Sadly, vitamin C cannot be added. Fortunately, magnesium can be added.

Magnesium is one of our favorite minerals. That’s because magnesium lowers pressure, relaxes artery walls and this promotes increased circulation, reduces anginal chest pains, reduces irregular heart rhythms, relaxes muscles, alleviates muscle cramps, reduces anxiety levels, and increases energy production in every cell in you’re your body. Also, for reasons that we as of yet do not fully understand, but magnesium reduces the likelihood of pain at the infusion site. As far as we’re concerned, we will add magnesium to just about every peroxide IV we can.

Other trace minerals can be added to the peroxide IV also. And B-complex Vitamins and B-12 can be added when necessary. With one infusion treatment, the doctor may be able to accomplish more, by providing the body with needed nutrients as well as peroxide.

Isn’t Peroxide Harmful?

Peroxide is extremely well tolerated by the human body. This may come as a surprise to you. After all, if peroxide kills so many things, then why doesn’t it kill us? The answer is the enzyme CATALASE. Catalase found throughout the human body, causes hydrogen peroxide to change into harmless oxygen and water. Viruses don’t have catalase, so the peroxide destroys them. Humans have catalase in their cells, and are not destroyed by peroxide.

When you get an infection, your white blood cells surround the germs and kill them. Exactly HOW do the white blood cell kill germs? Let us tell you something that 9,995 out of 10,000 MD’s don’t know. Your white blood cells produce a little hydrogen peroxide, and they bathe the germs in the peroxide, and this kills the germs! It has always been peroxide that naturally cured infection in your body!

Did you know that hydrogen peroxide is made in the atmosphere, and that it comes down in our rainwater, and it kills off a certain amount of living organisms in the soil? If it were not for this peroxide, the earth’s surface would be putrid from bacterial overgrowth. What we’re trying to say is that peroxide is a wonderfully natural, beneficial molecule.

This is not to say that peroxide cannot be harmful. Humans can tolerate just so much of the stuff, and that’s why you should have peroxide treatments only from a well-trained physician.

Possible Side Effects

There are some POTENTIAL side effects to IV peroxide therapy. We say potential because, in truth, we hardly ever see undesirable side effects. But we want you to know about them. We may give you peroxide treatments, but we must follow all the rules and regulations for doing experimental medicine. Foremost is that you be fully informed about what we’re about to do, and that includes understanding potential side effects.

1. The most common side effect is vein inflammation, right where the IV is going in your arm. There can be pain, and if it occurs, there’s little to do except change the location of the needle. If you have a big vein, such as in the elbow crease that’s a great place to place the IV. The bigger the vein, the less likely any discomfort. Magnesium is added to the IV and this reduces the likelihood of any pain also.

2. You can get a red streak up your arm, starting right where the needle is inserted. There are two kinds of red streaks. One kind of streak is completely harmless and goes away within 20 minutes of finishing the IV. The other red streak means that the vein is getting inflamed, and we’ve got to change the needle insertion.

3. A few people get a chest sensation, with a shortness of breath feeling after the infusion has been running for a while. It was thought that this was oxygen bubbling off in the lungs… but that’s not so. We don’t know what causes this sensation, but we know that it’s okay to continue the infusion. We prefer to slow down the infusion, or discontinue it, if you’ve had most of the treatment.

4. Another side effect is chills. You can feel a little chilly because peroxide can throw off your body temperature regulation for a short while.

5. The next side effect is called a Herxheimer Reaction, also called a die-off reaction. Actually, it’s a good sign, but you don’t think so when it’s happening. If you’ve got a lot of candida (a yeast) or a lot of infection, when the peroxide kills the yeast, your body will react to the dead, disintegrating yeast until it is eliminated from the body. You can have chills, nausea, body aches, weakness and headaches during this time. It can happen following one, two, or three treatments, and then it ceases. You can’t predict in whom it will happen. If you get a Herxheimer Reaction, why not look on the bright side, your candida or infection is on the way out! You are about to feel better.

6. Finally, because peroxide intensifies the anti coagulant action of the drug Coumadin, the doctor has to reduce the Coumadin dose if you’re taking it.

That’s pretty much the downside of peroxide therapy.

Question: If there was nothing wrong with you, and you took peroxide therapy for no obvious disease or condition, would it be harmful? Absolutely not! It would act like a tune-up to your body.

Will insurance or Medicare pay? NO! Paying for large numbers of expensive surgeries and procedures has financially depleted most medical insurance companies, including Medicare.
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Postby Merlyn » Thu Feb 10, 2011 6:06 pm

I am continuing to use oral hydrogen peroxide, no real adverse effects, but I can't claim anything positive either. My Dr. is looking into nebulizing hydrogen peroxide but it is such a new therapy, there is not much info available. But she is going to talk to some pharmacists she knows and see whether she can come up with a safe amount if that is even possible because the lungs are very subject to free radical damage. There are people on the web doing this, but they seem to be doing it by themselves and I cannot find any references on PubMed or Google Scholar...
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Re: Hydrogen Peroxide

Postby NHE » Fri Feb 11, 2011 12:33 am

I originally wrote these statements on hyrogen peroxide back in Jan 2008, but I think they're important enough to repost them as they might be difficult to find after 3 years.

Hydrogen peroxide is so counter intuitive for anyone who knows anything about biochemistry that it's inconceivable that someone could recommend this type of treatment to anyone. Hydrogen peroxide is a strong oxidant. When it breaks down it forms free radicals. These free radicals will indiscriminately attack other molecules in the body, everything from DNA to lipids. It's the very thing that biology has evolved antioxidants to get rid of. For example, catalase is a naturally occurring antioxidant enzyme found in liver. It has the highest turnover number of any known enzyme. This means that it reduces dangerous hydrogen peroxide to harmless substances faster than any other known enzyme reaction in the body. This fact exemplifies the importance of getting rid of hydrogen peroxide. Moreover, a quick search through PubMed will yield many articles which report the involvement of various oxidants in MS. Several antioxidants actually have anti-inflammatory activity. These include curcumin, EGCG from green tea, r-lipoic acid and others. Clearly, oxidizing your body isn't a great idea especially for someone with MS.

By the way, if you want to see the fastest known enzymatic reaction in action, then the next time you cook a chicken, save some of the liver, grind it up, and then add some hydrogen peroxide. It'll bubble and foam so put it in a container with adequate room.
Let's discuss a bit of chemistry. Hydrogen peroxide is a strong oxidizing agent. The H-O-O-H breaks down to the free radicals H-O• and H-O-O• which are the hydroxyl and peroxyl free radicals respectively. The single dot indicates that these molecules have a single unpaired electron. It is this unpaired electron which makes them free radicals. Free radicals are inherently unstable and they will attack other molecules stealing an electron and thereby turning that molecule into a free radical which goes on to attack other molecules. In contrast, antioxidants are molecules and enzymes that have the ability to donate an electron without becoming a free radical themselves. One of the examples that I used in my prior post was lipoic acid. This antioxidant has two sulfhydryl groups situated right next to each other. As such, each sulfhydryl group can donate an H• to a free radical and the two remaining sulfur atoms, R-S•, will bind to each other forming a disulfide bond, R-S-S-R (note that R symbolizes the rest of the molecule). In essence, lipoic acid can reduce two free radicals without becoming a free radical itself. A similar process occurs with ascorbic acid, except that here it is the R-OH bond located next to a carbon carbon double bond (C=C) which donates the H• and is converted to an R=O bond. This process is identical to what occurs with epigallocatechin gallate (EGCG) in green tea except that there are many more R-OH's available, 8 in EGCG versus 2 in ascorbic acid. This is what makes EGCG a more potent antioxidant.

So, now that we understand that hydrogen peroxide produces free radicals and thereby induces oxidative stress, it is important to note that oxidative stress is one of the means by which the immune system attacks foreign invaders such as cells infected by bacteria or viruses or cells which posses epitopes which the immune system mistakenly identifies as foreign such a myelin proteins in MS. In essence, oxidative stress can worsen MS. Injecting a substance such as hydrogen peroxide which increases oxidative stress is thus biochemically counterintuitive.

Another example of the dangers of oxidative stress is with an overdose of acetaminophen. The metabolites of acetaminophen are toxic and are rendered less harmful by the liver by using up some of its stores of glutathione (a naturally occurring antioxidant in the body). Under normal dosages, the body is able to compensate for this activity. However, an overdose of acetaminophen will use up a large percentage of the liver's available glutathione resulting in liver failure.

In summary, I would be very afraid of internal hydrogen peroxide.

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Postby Merlyn » Wed Feb 16, 2011 5:59 pm

I talked to a woman yesterday that is heavily involved in the Victoria MS chapter. She said she now knows about 11 people that have had CCSVI done in the United States and she had a couple very interesting observations on unexpected side effects... one woman was using a walker, still ambulatory with the aid of this device. She's had a couple of positive responses to the CCSVI, but directly after the procedure she developed full-blown diabetes. No previous symptoms, no thirst, no weight loss, no excessive urination etc. But the next day, developed all the signs of diabetes and testing shows she now is dealing with very high blood sugar.

The second concerns a man that has been wheelchair bound for about five years. He could not use his right hand whatsoever, and now he can. But he is also had another rather odd outcome from this procedure. He used to be able to drink his friends under the table so to speak. I gather he had an amazing capacity for alcohol. But since the CCSVI, two beers is his limit and he now gets quite drunk on two beer! He is pleased he did this operation, but finds his results totally inexplicable... just thought I would throw this out there because it makes me wonder about the diabetes link once again...
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Postby Merlyn » Fri Feb 18, 2011 1:09 pm

When magnesium levels fall, hyper secretion of adrenalin and insulin compensate. Their increased secretions help maintain the constancy of the levels in intracellular magnesium in the soft tissues. Plasma and intracellular magnesium concentrations are tightly regulated by insulin. But Dr. Ron Rosedale says that, “Extra insulin floating around in the blood causes plaque build-up. They didn’t know why, but we know that insulin causes endothelial proliferation. Every step of the way, insulin is causing cardiovascular disease. It fills the body with plaque, it constricts the arteries, it stimulates the sympathetic nervous system, and it increases platelet adhesiveness and coagulability of the blood.” So as we can see, when magnesium levels drop there is a cascade of physiological problems that corrupt the heart of our health.
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Postby PointsNorth » Sat Feb 19, 2011 5:45 pm

I thought that those considering/pusuing phlebotomies might like the following:

Iron and Neurodegeneration in Multiple Sclerosis

Michael Khalil,1,2 Charlotte Teunissen,2 and Christian Langkammer1

1Department of Neurology, Medical University of Graz, A-8036 Graz, Austria
2NUBIN, Department of Clinical Chemistry, VU University Medical Center, 1007MB Amsterdam, The Netherlands

Received 31 October 2010; Revised 26 December 2010; Accepted 2 January 2011

Academic Editor: Jeroen J. G. Geurts

Copyright © 2011 Michael Khalil et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Increased iron deposition might be implicated in multiple sclerosis (MS). Recent development of MRI enabled to determine brain iron levels in a quantitative manner, which has put more interest on studying the role of iron in MS. Evidence for abnormal iron homeostasis in MS comes also from analyses of iron and iron-related proteins in CSF and blood and postmortem MS brain sections. However, it is not yet clear if iron accumulation is implicated in MS pathology or merely reflects an epiphenomenon. Further interest has been generated by the idea of chronic cerebrospinal venous insufficiency that might be associated with brain iron accumulation due to a reduction in venous outflow, but its existence and etiologic role in MS are currently controversially debated. In future studies, combined approaches applying quantitative MRI together with CSF and serum analyses of iron and iron-related proteins in a clinical followup setting might help to elucidate the implication of iron accumulation in MS.
1. Introduction

Iron is essential for normal neuronal metabolism, including mitochondrial energy generation and myelination [1, 2]. However, excessive levels of brain iron may exert iron-induced oxidative stress and thus lead to neurodegeneration [3]. During the process of normal aging, various regions of the brain, predominantly the basal ganglia, tend to accumulate nonhemin iron, which is primarily stored in the form of ferritin [4]. Increased iron deposition has been observed in various chronic neurological disorders, including multiple sclerosis (MS) [5].

Evidence for increased iron accumulation in MS is mainly derived from magnetic resonance imaging (MRI) and histopathologic studies; however, some information exists also from analyses of iron and iron-related proteins in cerebrospinal fluid (CSF) and blood. The following review summarizes current knowledge of increased brain iron accumulation in MS derived from (2) MRI, (3) histopathologic analyses, (4) studies on CSF and blood, and (5), finally, provides an outlook on potential therapeutic interventions.
2. Magnetic Resonance Imaging

In several studies, evidence for increased iron accumulation, preferentially in deep gray matter areas of the brain, was mainly derived from the signal reduction on T2-weighted MR images [5].

First reports on a regionally signal reduction on T2-weighted brain MRI images in MS indicative of increased iron deposition were published by Drayer et al. [6] and Grimaud et al. [7].

Several studies then followed with a focus on the clinical implication of increased iron accumulation in MS. Increased deep gray matter T2 hypointensities were found to be correlated with disease duration [8, 9], physical disability [9–13], and cognitive impairment [14]. Clinical followup studies in MS revealed that baseline gray matter T2 hypointensities were associated with disability progression over time [12, 15]. Another consistent finding is that deep gray matter T2 hypointensity, suggestive of increased iron content, is correlated with brain atrophy [8, 16]. While this was evidenced in patients with definite MS, there is only little information available regarding the extent and clinical significance of increased iron deposition in patients with a clinically isolated syndrome. Ceccarelli et al. found only minor changes of signal reductions on T2-weighted images compared to healthy controls, and the extent did not predict conversion to clinically definite MS [17]. The approaches used in the studies mentioned above suffered from the methodological drawback of deducing iron concentrations from a visual grading of the reduction of signal intensity on T2-weighted images even though more recent studies have determined the extent of T2 hypointensity in a semiquantitative manner [8, 10, 14, 16].

In recent years, methodical development of MRI enabled to assess brain iron concentrations quantitatively. In addition, quantitative iron mapping by MRI offers a more sensitive discrimination of iron levels and, therefore, is especially advantageous in longitudinal studies and monitoring of long-term disease progression.

The techniques utilized for quantitative iron mapping are mainly based on relaxation time mapping [18–20] (Figure 1) but also other approaches such as phase mapping [21, 22], magnetic field correlation [23], or direct saturation imaging [24] are applied.
Figure 1: R2* map of a 50-year-old female MS patient. Higher iron concentrations in basal ganglia structures are reflected by brighter signal intensities.

Susceptibility weighted imaging (SWI), a technique that takes advantage from the full complex MR signal by combining magnitude and phase images, has gained attention as a means to assess brain iron [25, 26]. However, the complexity of the postprocessing involved in SWI renders comparative studies challenging and remains an objective of research [27]. Quantitative susceptibility mapping (QSM) is an approach using solely phase images and produces susceptibility maps which are independent of the orientation of the tissue to the main magnetic field [28, 29]. Because paramagnetic iron is considered a main determinant of brain tissue susceptibility, QSM seems especially useful to assess brain iron.
2.1. Validation of MRI Methods

Several methods have been proposed for the measurement of brain iron concentration; however, the majority of them lack validation and, therefore, the specificity and sensitivity of these techniques are not reliably known.

From theoretical considerations based on susceptibility models for brain tissue, it can be concluded that iron is a main determinant of susceptibility-induced contrast in MRI [30]. Several studies have indirectly investigated the relation of MRI parameters with iron by using the age-dependency of iron accumulation in the basal ganglia as reported in [4, 31].

Recently, high-pass filtered SWI phase images were compared to regional iron concentrations in postmortem tissue determined by synchrotron X-ray fluorescence and revealed a correlation between phase shifts and iron [32].

Other recent work acquired quantitative MRI directly after death from seven human brains and subsequently determined brain iron concentrations by using inductively coupled plasma mass spectrometry [33]. This study showed that the relaxation rates R2 and R2* can be used as sensitive and linear measures for brain iron concentration.

These quantitative MRI techniques together with a better understanding of pathophysiologic concepts of increased iron levels [1–3] have put more interest on elucidating the role of iron in MS.

In recently performed studies on quantitative brain iron levels in MS, based on R2* relaxometry at 3 Tesla, increased iron levels have been found in patients with advancing MS compared to clinically isolated syndrome [20]. Using this validated quantitative technique, higher R2* levels in basal ganglia structures reflecting higher iron content were correlated with gray matter atrophy and also with T2-lesion volume [20]. These findings are supported by earlier studies where MRI T2 hypointensities suggestive of increased brain iron, preferentially located in deep gray matter areas, were linked to physical disability and gray mater atrophy in MS [8–10, 12, 34]. Further support comes from a followup study showing that MRI T2 shortenings in deep gray matter areas at baseline are predictive of the evolution of brain atrophy [16].

Apart from gray matter regions with known high iron levels (putamen, globus pallidus, caudate nucleus, substantia nigra, and red nucleus) efforts were made to investigate iron levels in white matter by MRI [22, 35, 36]. Using SWI, the phase values of MS lesions were investigated and compared to adjacent white matter [36]. However, compared with chemically determined iron concentrations of postmortem studies, the iron levels within MS lesions were not substantially altered than in reference white matter structures [4, 33]. Due to the confounding impacts of iron and myelin to MRI contrast generation, disease-induced alterations of iron levels in white matter need to be treated with caution and are an objective of ongoing research [37].

Further interest on iron deposition in MS has been generated by the idea of chronic cerebrospinal venous insufficiency (CCSVI) [38] that might be associated with the accumulation of iron in the brain due to a reduction in venous outflow [39, 40]. Following this hypothesis, CCSVI is postulated to be implicated in the etiology of MS. The underlying mechanism is believed to originate from increased iron accumulation in patients due to a reduced venous blood flow caused by constrictions of cerebral veins. This then leads to extravasation of erythrocytes with subsequent iron deposition [41], subsequently triggering inflammation-dependent tissue damage [42]. However, the existence of CCSVI as well as its etiologic role in MS are currently controversially debated [43], and there is an increasing amount of papers published now that challenge this hypothesis [44–47]. Furthermore, histopathologic studies do not provide clear evidence for extravasation of erythrocytes into lesions caused by increased intraluminal venous pressure [48–52].
3. Histopathology and Pathologic Significance of Increased Brain Iron

The normal anatomic and cellular age-dependent iron distribution within the brain, as described previously [4, 53, 54], should be considered when comparing with iron deposition in pathological conditions.

Craelius et al. described positive iron staining in MS brain sections surrounding demyelinated plaques, myelinated white matter near the lesions, and within blood vessels of gray matter near the lesion [55]. Iron deposits were also described in the putamen and the thalamus [6], in macrophages and reactive microglia [56] and in normal-appearing white matter tissue [57]. Mehindate et al. showed that heme oxygenase 1, which is involved in regulating iron metabolism, was upregulated in astrocytes of MS spinal cord tissue [58].

The exact underlying mechanism by which brain iron accumulates in MS is not fully understood. Iron transport across the blood-brain barrier is dependent on iron transport proteins, predominantly by transferring receptors expressed on brain epithelial cells [59]. Other transporters may also facilitate iron transport across the blood-brain barrier, such as the divalent metal transporter (DMT) and the lactoferrin receptor [60].

It is also not yet clear if increased brain iron deposition is implicated in MS pathology or merely reflects an epiphenomenon [3, 61]. Potential toxic iron products may arise when hydrogen peroxide is formed by superoxide dismutase, which then reacts with free or poorly liganded iron (Fenton reaction [62]). Superoxide may also react with ferric iron through the Haber-Weiss reaction, producing Fe2+, which then again affects the redox cycling [1, 2] (Figure 2).
Figure 2: Generation of reactive and damaging hydroxyl radicals (OH•). Free Iron (Fe2+) reacts trough the Fenton reaction with hydrogen peroxide, leading to the generation of very reactive and damaging hydroxyl radicals (OH•). Superoxide can also react with ferric iron in the Haber-Weiss reaction leading to the production of Fe2+, which then again affects redox cycling. The highly reactive hydroxyl radicals lead to oxidative stress-induced lipid peroxidation, mitochondrial dysfunction, and increase in intracellular free-calcium concentration, and finally causing neuronal death.

The resulting highly reactive free hydroxyl radicals (OH•) interact with molecules leading to the production of other free radicals [63]. This leads to oxidative stress-induced lipid peroxidation, mitochondrial dysfunction, increase in intracellular free-calcium concentration, and finally causing cell dysfunction and death [62–64]. Because neuronal membrane lipids are rich in highly polyunsaturated fatty acid, they are susceptible to damage caused by lipid peroxidation [62, 63]. Iron itself can initiate and amplify lipid peroxidation [62, 63]. Several naturally produced antioxidants, such as alphatocopherol, may help to reduce oxidative stress-induced tissue damage [62].
4. Cerebrospinal Fluid and Blood

Only a limited number of studies have analyzed iron and iron-related protein levels in CSF and peripheral blood of MS patients. CSF ferritin levels were shown to be elevated in patients with chronic progressive active MS [65] and in patients with SPMS compared to controls [46, 57]. Another study showed that CSF ferritin levels were lower but within normal limits in patients with optic neuritis compared to patients with other neurologic diseases [66]. Similar levels of CSF ferritin were detected in RRMS patients compared to controls [57, 67]. In a recently performed cross-sectional and longitudinal study, CSF ferritin levels did not significantly change over a time period of 3 years, which also may argue against an etiologic role for CCSVI-related parenchymal iron deposition in MS [46].

Serum soluble transferring-receptor levels were significantly increased in MS compared to controls [68, 69], while serum ferritin levels were elevated in patients with chronic active MS only [68]. Conversely, analyses of iron status in two children with recurrent episodes of tumefactive cerebral demyelination revealed decreased serum iron and ferritin and constant iron supplementation was needed to prevent an iron deficiency state in both children [70].
5. Therapeutic Implications

On basis of pathophysiologic concepts implicating iron-induced tissue damage in MS, potential therapeutic interventions, including iron chelators, and inhibitors of iron-related oxidative stress and lipid peroxidation may have beneficial effects [3, 71, 72]. Several chelators are of putative therapeutic value in neurodegenerative disorders [73].

Studies on experimental autoimmune encephalomyelitis (EAE), the animal model of MS, showed that treatment with the iron chelator desferrioxamine reduced clinical and pathologic signs of EAE [74]. Deferiprone, an orally delivered iron chelator, ameliorated signs of EAE, an inhibited T-cell function [75]. However, a clinical trial testing the iron chelating drug desferrioxamine in chronic progressive MS patients failed to demonstrate any effects on disease progression [76]. A recent observation revealed that supplementing nonanaemic iron deficiency in two children with recurrent episodes of tumefactive demyelination leads to sustained remission [70].

In the future large randomized double-blinded multicenter studies are needed to elucidate the potential use of therapies targeting oxidative stress and lipid peroxidation in patients with MS. Quantitative MRI techniques and detailed monitoring of body-fluid iron and iron-related proteins levels should be included in such study protocols.
6. Summary

In summary, increased iron deposition has been consistently reported to occur in MS, but its role in pathogenetic processes of this disease has not yet been completely clarified. Whether increased brain iron levels are also the cause or only the consequence of tissue destruction is still a matter of debate. Future longitudinal studies combining clinical disease status, quantitative MRI techniques sensitive for iron, and additional analyses of iron in CSF/serum and iron-related proteins (as well as iron regulator proteins), might help to unravel the implication of increased iron accumulation in MS. Quantitative MRI and histopathologic analyses of postmortem MS brains should complement these studies.

M. Khalil received research support from the Austrian Science Fund (FWF) [J2992-B09].

Hopefully, I will get phlebed this week. Best, PN
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Postby Bethr » Sun Feb 20, 2011 10:56 am

Thanks PN, and good luck with the phleb.
I just had my fourth one last Thursday. I had been feeling "normal" over Nov/Dec and the New Year, but started to get the fatigue back a few weeks ago. Did the phleb and I'm a box of birds again, better than ever :)

So that's two litres I've had out now, and funnily enough the nurse says to me when they did the finger prick test prior "you have great iron!". I had to stop myself pulling a face. My hemoglobin is back up to 156 again.
So not much chance of me becoming anemic I think. I told her I had donated four times in a year and she said it was most unusual that my Hb had stayed up so high in a women who still menstruates.
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Postby Bethr » Mon Feb 21, 2011 5:21 pm

Hemochromatosis (HFE) genotype and atherosclerosis: Increased susceptibility to iron-induced vascular damage in C282Y carriers

08/04/2010 Engberink MF et al. –

The authors found no association of HFE genotype with carotid IMT, despite higher iron status. Interestingly, C282Y carriers may be hyper responsive to vascular damage which needs to be confirmed in prospective cohort studies.
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Postby Merlyn » Sat Feb 26, 2011 7:33 pm

BethR-good find! I still can't do any more phlebotomy-so am looking into some HBOT treatment in my area. I keep reading good things about it, and Dr. Maxfield runs one of the clinics close to me. He is a known expert with HBOT and this dreaded disease...

hope the earthquake did not affect you or yours... terrible images/situations of devastation in Christchurch.
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Postby Bethr » Sun Feb 27, 2011 12:21 pm

Hi Merlyn, yes, it's bad, we are in a national emergency here in NZ.
I run an accommodation business and we have had evacuees stay. They are shell-shocked from the earthquake and many never want to go back to Christchurch. So many dead, it's just awful.

I am still feeling great and my hemoglobin/hematocrit has stayed way up.
I think my main problem from the start was a mild iron overload, this in turn triggered the brain lesion. I figure that so long as i keep my iron
levels under control I will not progress like my sister has. Time will tell. My head is so clear now, all the fog is gone. I look at the "Couch", my long time companion :lol: and just walk right past it during my busy day.

Good luck with the HBOT.
I think the research is moving fast now, and we will see major progress in the MS mystery, and all our observations will tie in somehow.
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Postby Bethr » Sun Feb 27, 2011 12:47 pm

I meant to say also, I came across another middle aged lady who had chronic fatigue and a DX of fybromyalgia, who found out she had hemochromatosis genes. Her transferrin saturation was 63%, ferritin not too bad at 75. Her Drs. did not want to do phlebotomy on her, so she went and donated blood. She felt a lot better, then went backwards again before the three months stand down was up. She just went back and did another donation and feels great again. Her Drs. are saying it's a "placebo" effect! Now where have I heard that one?

We are out here, us iron loaders and we need help.
Sooner rather than later.
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Postby Merlyn » Tue Mar 01, 2011 5:55 pm

I spoke to Humphrey today,

I think we would "click" because one of the things he immediately told me was to try to increase my glutathione... I have been nebulizing glutathione for a while, and I have been able to decrease my thyroid medication by one third!

Treatments are still $100, and I will have to transfer from wheelchair to a bench... I am so spastic, this will take some planning. I asked him if I could store a Hoyer lift at the clinic, but he did not know what a Hoyer lift entails, so we will have to see if there is storage space. But this is the only way I can figure out how to transfer without endangering those helping me or me myself... cannot use a transfer bench, I totally hyperextend and lock up.

You do not need a prescription which is fortunate, because as Humphrey said doctors don't know anything about it anyway. Yesterday I joined a Yahoo newsgroup to ask a couple questions about HBOT. This treatment is far more accepted and utilized in the UK. I am going to try a few treatments, but financially I am not sure I could keep doing treatment after treatment... it is much cheaper in the UK I gather. I am going to reprint a response I got from the Yahoo group... one good thing, the clinic in Victoria is open until 530 or 6 PM and up for me is critical because by the time I get there it will surely be later in the afternoon. Humphrey says he has gotten people out of wheelchairs, and he has a vibrating machine and other healing devices on site... here is the promised response from Yahoo:

Dear Marilyn

I have had MS for 29 years since 1982 aged 42. I have used HBOT weekly with benefit for more than 25 years. Your doctors will know nothing about HBOT. Why? Because HBOT is still not taught in the medical schools and it is not included in their training. But they can never admit their ignorance. Knowledge is power. They often try to give the impression they know all about it by simply dismissing it as of no value. So of course most patients will accept their doctor or neurologist must know what they are talking about.

In the UK many hundreds of people with MS use HBOT every week. Over the last 30 years there have been in excess of two-million HBO treatments involving in excess of 19,000 people with MS.

HBOT cannot repair your existing damage but it can help in the management of symptoms. Long-term HBOT is shown to slow down the progression and obviously, as with any disease, the earlier one starts the better. You should have benefit from where you start. You will certainly be no worse off.

Oxygen, Inflammation and Hypoxia Inducible Factor Protein

It has been known for many years that breathing more oxygen causes blood vessels to constrict reducing blood flow. Oxygen controls blood flow by involving another gas which has been thought for many years to be just a poison - nitric oxide. But there is even more than this to the oxygen story and it is of direct relevance to the disease underlying 'MS'. Even those doctors who are convinced that the auto immune theory is correct admit that the affected areas of the brain and spinal cord in MS are inflamed.

A review in a top scientific journal 'Nature' entitled 'Oxygen and inflammation' (Carl Nathan, Weill Medical College, Cornell University, USA) gives the detailed information. Inflammation causes the level of oxygen in the tissues to fall and this, in turn, activates a protein system - the Hypoxia Inducible Factor proteins (HIF). One protein, HIF 1 alpha, not only controls the migration of white blood cells into the tissues to control infection, it is also responsible for the growth of new capillaries in wounds. This master protein regulates over 300 genes. So giving a high level of oxygen even has genetic consequences and it is little wonder that one hour of oxygen in a chamber has effects that last.

All those of us who have used oxygen as a treatment for their MS for many years are shown to be correct and it is time for all neurologists, General Practitioners and all the MS Societies to listen to their expert patients and members.



(Information source Emeritus Professor Philip James, University of Dundee, Scotland.)
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Postby Bethr » Wed Mar 02, 2011 1:07 pm

For those following this thread and our journeys with phlebotomy to reduce iron levels, I really need to stress the importance of checking your iron levels.

This journey has come full circle for me, and I am normal again.
Full of energy, no pain, no fatigue other than the precious kind you get when you do a hard days work.

When people have classic hemochromatosis, their ferritin rises, and this is often when it is picked up on a blood test (it can rise for other reasons, so is not definitive), but the test people need to get done is their Transferrin Saturation. This test is not standard in many countries.

I urge everyone to get tested in the off-chance that their transferrin saturation is raised (women >45%, Men >50%). Many women seem to get this problem, with normal ferritin and serum iron levels.

A transferrin saturation of 62% in men is 98% predictive of Iron Overload from the latest studies I have read. In women it is lower.

Therapeutic phlebotomy is very safe and cheap. I only needed four draws to reverse all my symptoms, and believe me they were wrecking my life. The brain lesion and loss of my right hand for a while was the least annoying. The fatigue and pain made life very hard.

I'm sure this is just a small part of the picture, and but may apply to some. I was early in my journey which may be why I was able to reverse the damage.
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Postby Merlyn » Thu Mar 03, 2011 6:21 pm

I was given a big container of this yesterday, looks interesting...
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Postby Bethr » Sun Mar 06, 2011 2:57 pm

Great news. My sister with MS is visiting a Dr. today who does therapeutic phlebotomy. I'm going with her and we are crossing our fingers that he will go ahead with treatment. This will be the real test to see if it works on her fatigue and other symptoms, like it has on mine. We both carry the C282Y hemochromatosis gene, and both have brain lesions.

If it works for her too, then I think we are really on to something here for those of us with high iron levels or a particular genetic makeup.

Will update as this progresses. Wish us luck!
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