Astounding Norwegian research breakthrough with Rituximab can solve CFS mystery!!!

[Freddd]

It can pay to remember that mb12 and Metafolin deficiencies can cause at least several autoimmune diseases as can cancer.

 

[ramakentesh]

Are you sure about that? Ive never heard of any and I know a lot about autoimmune diseases since Ive had one for eight years.

Autoimmunity is far more complex than simple deficiencies although low vitamin D levels have been linked speculatively to the development of autoimmunity in a genetically susceptible individual.

Autoimmunity centres around two very different branches of the immune system - some conditions appear to be chronic activation of the innate immune system through continual activation of pro-inflammatory cytokines like TNF alpha as an example.

Some theories include molecular mimicry where it is presumed that certain pathogens or bacteria are able to express proteins that the innate immune system cannot distinguish from self targets rich in the same histocompatibility. Infact certain histocompatibilities can be clearly associated with the potential to develop specific autoimmune disease - HLA -B27 the most obvious with Ankylosing SPondylitis and other histocompatibilities potentially in RA, m.gravis and perhaps Inflammatory bowel disease.

the recent analogy is that autoimmunity may be caused by an impaired immune response to particular pathogens based on histocompatibility which results in the innate immune system just destroying the whole area including mainly self targets because it lacks the capacity to launch an effective response to the actual pathogens.

the thing that always gets me about CFS is that if you go to a forum on Crohns disease, or Lupus, or Ankylosing Spondylitis or M.gravis, or RA and if you take out the actual descriptions of the pain based symptoms (the inflammated back, bowel, etc) and read the decriptions of their energy levels, autonomic symptoms and general feeling of wellness, you will see that they share much in common and you could be talking about the same illness.

 

[snowathlete]

the thing that always gets me about CFS is that if you go to a forum on Crohns disease, or Lupus, or Ankylosing Spondylitis or M.gravis, or RA and if you take out the actual descriptions of the pain based symptoms (the inflammated back, bowel, etc) and read the decriptions of their energy levels, autonomic symptoms and general feeling of wellness, you will see that they share much in common and you could be talking about the same illness.

Its interesting because my mum had crohns when she was young.

 

[Sing]

I'm really excited about the autoimmunity hypothesis and hope the Norwegians make rapid progress. I think that their not having the blinders of prejudice and presuppositions about ME to begin with is what has enabled them to go to the head of the pack. Also, as ramakentesh suggests, autoimmunity could involve so many different processes, as the immune system is so complex, science probably only knows a portion of what is possible. Having this is like a long jail sentence, but without knowing when we will be released. Thanks to everyone who contributes their intelligence to this effort!

 

[Freddd]

Are you sure about that? Ive never heard of any and I know a lot about autoimmune diseases since Ive had one for eight years.

Autoimmunity is far more complex than simple deficiencies although low vitamin D levels have been linked speculatively to the development of autoimmunity in a genetically susceptible individual.

Autoimmunity centres around two very different branches of the immune system - some conditions appear to be chronic activation of the innate immune system through continual activation of pro-inflammatory cytokines like TNF alpha as an example.

Some theories include molecular mimicry where it is presumed that certain pathogens or bacteria are able to express proteins that the innate immune system cannot distinguish from self targets rich in the same histocompatibility. Infact certain histocompatibilities can be clearly associated with the potential to develop specific autoimmune disease - HLA -B27 the most obvious with Ankylosing SPondylitis and other histocompatibilities potentially in RA, m.gravis and perhaps Inflammatory bowel disease.

the recent analogy is that autoimmunity may be caused by an impaired immune response to particular pathogens based on histocompatibility which results in the innate immune system just destroying the whole area including mainly self targets because it lacks the capacity to launch an effective response to the actual pathogens.

the thing that always gets me about CFS is that if you go to a forum on Crohns disease, or Lupus, or Ankylosing Spondylitis or M.gravis, or RA and if you take out the actual descriptions of the pain based symptoms (the inflammated back, bowel, etc) and read the decriptions of their energy levels, autonomic symptoms and general feeling of wellness, you will see that they share much in common and you could be talking about the same illness.

Hi Ramakentesh,



Are you sure about that? Ive never heard of any and I know a lot about autoimmune diseases since Ive had one for eight years.

A lack of mb12/metafolin causes immune impairment and hyper-reactivity. Parietal cell antibodies, intrinsic factor antibodies, Hashimoto's thyroiditis are known autoimmune responses caused by low b12/folate, many others are suspected.


Cancers can cause paraneoplastic syndrome
http://en.wikipedia.org/wiki/Paraneoplastic_syndrome

A paraneoplastic syndrome is a disease or symptom that is the consequence of the presence of cancer in the body, but is not due to the local presence of cancer cells.[1] These phenomena are mediated by humoral factors (by hormones or cytokines) excreted by tumor cells or by an immune response against the tumor.

It has a list of them in the article.

the thing that always gets me about CFS is that if you go to a forum on Crohns disease, or Lupus, or Ankylosing Spondylitis or M.gravis, or RA and if you take out the actual descriptions of the pain based symptoms (the inflammated back, bowel, etc) and read the decriptions of their energy levels, autonomic symptoms and general feeling of wellness, you will see that they share much in common and you could be talking about the same illness

B12/folate deficiencies cause massive amounts of inflammation throught the entire body and espcially the GI tract. They can cause 100% of the symptoms you are talking about that seem like the "same disease.

 

[heapsreal]

Fredd i think the excitement in finding what is actually causing this illness and now with the Norweigans on board may have a treatment. I thinks its about knowing whats coming then not knowing whats going on. How many of us think we have some type of cancer or some other possibly near inevitable fatal illness our doctors have missed, its the constant worry/paranoia of not knowing. I dont think anyone here really wants to have an auto-immune disorder but having justification of being ill, not being labelled one of wessely's psycho's.

cheers!!!

 

[lansbergen]

I think what they call autoimmunity is just the immunesystem trying to do its job. To get rid of infected cells they must be eliminated. Therefor these cells must be attacked in one way or another.

I am pretty sure the immunemodulator I use, helps my immunesystem to killl the infected cells and prefents the agent spreading to other cells. I can only fight the infection when the agent is active during flareups. I am convinced most of my cells are clean now but there are still some spots that are not cleared yet. It took a long time to get where I am now.

 

[Tia]

Fluge and Mella will speak at the London Invest in ME conference on June 1st 2012.

http://www.investinme.org/IiME Conference 2012/IIMEC7 Agenda.htm

Ooo, how exiting! :victory: Thanks for telling us!

I was at this big university hospital recently and the doctor there which I saw for my Graves disease, knew about CFS and said his patiens had talked about this new norweigan discovery. he even knew about the B-cell thing when I mentioned it was believed to be autoimmune. So: :victory:

 

[liquid sky]

Autoimmunity can be caused by other foreign substances than viruses/bacteria. Silicone is one example. If you have antibodies directed against your own cells with an elevated ANA, as some do in ME, autoimmunity may be an answer.

Being that this drug affects mostly on B cells, there is the possibility that a pathogen living in the B cells could cause a similar reaction. It will take time to work out which is true.

 

[Tia]

Liquid. I'm curious.. I have Graves disease, that sounds just like it. I was told graves is when your body stops recognising it's own cells and attacks it's own organs..?

 

[liquid sky]

It is similar. In Graves Disease, the autoantibodies are directed towards the thyroid specifically. An elevated ANA is autoantibodies directed towards the nucleus of your body's cells. It is not specific to any particular cell, tissue or organ. Rather, they can be directed towards any part of the body.

An elevated ANA is most closely linked to Lupus, but it is found in RA, Srogrens, Scleraderma (sp?), etc. There are so many autoimmune diseases that often overlap in symptoms. Check the Wikipedia on autoimmune diseases. It's unbelievable how many are listed. Even Schizophrenia is suspected of being autoimmune.

Sorry you are dealing with Graves. Not sure how they treat it except surgery and symptom relief. Not so sure B cell depletion would be effective, but I am no expert on that.

 

[ramakentesh]

Fredd there is no reputable evidence that Hashimoto's thyroiditis is caused be B12 or nutrient deficiencies. If you can find any article suggesting that a simple nutrient deficiency is the primary causal factor/etiology - and THAT has been published in a reputable, peer reviewed medical journal I would be interested. My mum has that condition and once again it is associated with particular genetic histocompatibility - this time the genetic markers being HLA-dr5 histocompatibility and some other associated genes. But that is ofcourse only part of the picture and there is so much to it.

Medical research is a funny thing. You can potentially find a medical paper that supports any conjectural theory. Publishing itself doesn't equate to fact.

What appears to occur in autoimmunity is that there is a genetic predisposition to loss of self tolerance or there is chronic activation of pro-inflammatory cytokines as in inflammatory arthritis. The immune system cannot recognise self targets as not being pathogenic or the innate immune system cannot turn off pro-inflammatory cytokines. To suggest that simple nutrient deficiencies are a primary CAUSE of specific autoimmune disease is too simplistic im afraid. Its like saying CFS is caused by Candida - it might fly in the early 90s in a naturopath's office but try and get that pear reviewed in a medical journal.

In a person with a predisposition to lack of tolerance to self, perhaps (as has been recently suggested) some deficiencies in their innate immune system, a trigger - usually a stressor such as pregnancy, infection, stress, emotional upheaval, heavy exercise or exposure to a toxin and occasionally immuno-modulation following vaccination - results in an autoimmune response. The target of that autoimmune response appears to be regulated either by the toxin in rare cases, perhaps the virus or infection but often it is just mediated by the histocompatibility of the patient:

HLA-b27 - ankylosing spondylitis
HLA-dr3 - graves disease
HLA-dr5 - Hashimoto's thyroiditis

And in M.gravis there may be histocompatibility issues and thymus tumours.

etc, etc.

So autoimmunity is not simply caused by nutrient deficiencies or by foreign substances - it is a highly complex process that they are only beginning to understand - it has received years and years of research focus and as yet the primary etiologies are still conjectural and only beginning to be understood. At any given time there are about 300 clinical trials ongoing for most major individual autoimmune diseases (compared to POTS which may have approx 20 and CFS which may have 30-40).

As for autoimmunity in cancer, yes that does occur quite frequently.

Personally what I think has happened in CFS is that for years doctors and serious research funding has been totally withheld from the CFS community. In response the patient group have had to for years actually run and lead the process of research for the primary etiology and push for their own treatment options.

But now I think that research is progressing rapidly and some impressive results - particularly the work of Stewart/Medows, the spinalfluid work and now this work in Norwey is starting to build a concept of CFS and related illnesses that is testable, repeatable, and most importantly stands up to peer-review for publishing in reputable and respected medical journals.

I think we need to be more discerning in what research we value and what we can see as being speculative, poorly researched or flim flam. Some patients need to have an answer so badly that they will actively attach themselves to that etiology like a faith. they will unwaveringly hold to that one etiology and try endlessly to bend new findings so that they can accommodate or support their 'faith etiology'.

Whereas often these speculative theories are supported on conjecture, incorrect or questionable assumptions and simplistic concepts of physiology. As an armchair speculator I am always attracted to the science that is well supported, has a strong evidence base, demonstrates clinical outcomes through therapy and interventions and gets published in reputable journals.

 

[ramakentesh]

Graves disease involves autoantibodies that can modulate TSH through activation of TSH receptors. The first line of treatment are medications that reduce the production of thyroid hormone, which diminishes the hypermetabolism caused by excessive release of thyroid hormone and its effects throughout the body.

Rarely their can be radioiodine treatment that effectively reduces the size and producing capability of the thyroid where medication is ineffectual.

Contrary to above, surgery to remove the thyroid is almost non existent now days as the efficacy of antithyroid medication is impressive and remission usually occurs.

And even OCD is now suspected to be autoimmune

 

[leela]

I'm not coming down on any side of the fence on the current discussion, but regarding medical theory, research, etc, when you say

Medical research is a funny thing. You can potentially find a medical paper that supports any conjectural theory. Publishing itself doesn't equate to fact.

I agree; and I also am reminded that every theory began as an outlier, unpublished or supported by other papers--until it was. Until it became the truth by consensus. That is the history of science and medicine--continually rewriting and upgrading itself, waiting for a collective agreement based on a set of accepted parameters. Sometimes the parameters themselves have to be rewritten as our understanding grows.

Let us not forget either, that medical (and industrial science in general) is no longer pure, especially since the patenting of organisms. Even before that, there are documented cases where treatments and inventions have been suppressed for financial reasons.

So I would personally not apply quite so much weight, or faith, to science/medicine as a Thing Unto Itself, and prefer to remain curious and open to those willing to be in the vanguard of investigative research. It is my opinion that through a cooperative, cross-platform approach between researchers, doctors, and patients (who are actually the most intimately knowledgeable about their illnesses) we have the best chance to solve these things. The scientific method could use a bit of an overhaul as well, IMO.

 

[Freddd]

Fredd there is no reputable evidence that Hashimoto's thyroiditis is caused be B12 or nutrient deficiencies. If you can find any article suggesting that a simple nutrient deficiency is the primary causal factor/etiology - and THAT has been published in a reputable, peer reviewed medical journal I would be interested. My mum has that condition and once again it is associated with particular genetic histocompatibility - this time the genetic markers being HLA-dr5 histocompatibility and some other associated genes. But that is ofcourse only part of the picture and there is so much to it.

Medical research is a funny thing. You can potentially find a medical paper that supports any conjectural theory. Publishing itself doesn't equate to fact.

What appears to occur in autoimmunity is that there is a genetic predisposition to loss of self tolerance or there is chronic activation of pro-inflammatory cytokines as in inflammatory arthritis. The immune system cannot recognise self targets as not being pathogenic or the innate immune system cannot turn off pro-inflammatory cytokines. To suggest that simple nutrient deficiencies are a primary CAUSE of specific autoimmune disease is too simplistic im afraid. Its like saying CFS is caused by Candida - it might fly in the early 90s in a naturopath's office but try and get that pear reviewed in a medical journal.

In a person with a predisposition to lack of tolerance to self, perhaps (as has been recently suggested) some deficiencies in their innate immune system, a trigger - usually a stressor such as pregnancy, infection, stress, emotional upheaval, heavy exercise or exposure to a toxin and occasionally immuno-modulation following vaccination - results in an autoimmune response. The target of that autoimmune response appears to be regulated either by the toxin in rare cases, perhaps the virus or infection but often it is just mediated by the histocompatibility of the patient:

HLA-b27 - ankylosing spondylitis
HLA-dr3 - graves disease
HLA-dr5 - Hashimoto's thyroiditis

And in M.gravis there may be histocompatibility issues and thymus tumours.

etc, etc.

So autoimmunity is not simply caused by nutrient deficiencies or by foreign substances - it is a highly complex process that they are only beginning to understand - it has received years and years of research focus and as yet the primary etiologies are still conjectural and only beginning to be understood. At any given time there are about 300 clinical trials ongoing for most major individual autoimmune diseases (compared to POTS which may have approx 20 and CFS which may have 30-40).

As for autoimmunity in cancer, yes that does occur quite frequently.

Personally what I think has happened in CFS is that for years doctors and serious research funding has been totally withheld from the CFS community. In response the patient group have had to for years actually run and lead the process of research for the primary etiology and push for their own treatment options.

But now I think that research is progressing rapidly and some impressive results - particularly the work of Stewart/Medows, the spinalfluid work and now this work in Norwey is starting to build a concept of CFS and related illnesses that is testable, repeatable, and most importantly stands up to peer-review for publishing in reputable and respected medical journals.

I think we need to be more discerning in what research we value and what we can see as being speculative, poorly researched or flim flam. Some patients need to have an answer so badly that they will actively attach themselves to that etiology like a faith. they will unwaveringly hold to that one etiology and try endlessly to bend new findings so that they can accommodate or support their 'faith etiology'.

Whereas often these speculative theories are supported on conjecture, incorrect or questionable assumptions and simplistic concepts of physiology. As an armchair speculator I am always attracted to the science that is well supported, has a strong evidence base, demonstrates clinical outcomes through therapy and interventions and gets published in reputable journals.

Hi Ramakentesh,

Medical research is a funny thing. You can potentially find a medical paper that supports any conjectural theory. Publishing itself doesn't equate to fact.

You can say that again. I have read a multitude of papers, co-authored a few and co-delivered at conferences. However, the topics were generally about how compensation mechanisms affected theraputic choices. Because of a complicated situatuation we were able to obtain all the claims data from insurers for multiple groups with various models of compensation ranging from full capitation to hybrid to full fee for service so we had the same docs with patients across multiple plans and compensation models. What we did not see were the uninsured and we all know how they get screwed by the system, there are plenty of studies on that. In any case, that is not relevent here except to say that we made a lot of people angry with what we found.

To take it to a different topic, opioids, I read a lot of papers for a project. I found that a mistake made in one early paper was endlessly repeated as fact in many others. The mistake was switching two data points on a serum level at 15 minute increments. This was in the graph. The original table wasn't avaialbe for examination, but the change in the curve was impossible to occur. For 15 minutes the 1/4 of the serum level disapppeared and then sudenly reappeared at the next increment. When the two points were switched the curve matched the calculated curve. In another the graph was manipulated to show an infamous "second release" of the medication when in fact there was none but the marketing deptment ran with it for several years until it disappeared from future versions of the graph, in 3 stages. In another paper for the same drug the serum peaks listed in the table was 40% lower in the graph, the AUC didn't match the table values, and on and on and on. Everything was manipulated to look like what the marketing wanted to show. These papers wouldn't have passed a high school chem lab for all the flaws.

In B12 papers, most of which were based on cyancbl or hycbl until recently, the unproven assumptions ran rampant and just don't match what happens with active mb12/adb12 despite being the basis of analysis of the newer mb12 research. Read 500 or 1000 papers and integrate them and the unvalidated assumptions, even myths, and problems will jump out. Then there are the outright conjectural papers labeled as such based on the same assumptions and myths and a collection of suspicious data. So now all the new findings are contradicting all the old ones so a person can choose to support whatever they want by how they want it to be. There are those who defend the old, "quantum physics theory advances one funeral at a time" and those who go with the newer papers.

To suggest that simple nutrient deficiencies are a primary CAUSE of specific autoimmune disease is too simplistic im afraid.


And there be your false and prejudicial assumptions. There is nothing simple about ACTIVE b12 and Methylfolate deficiencies. They are intimately tied together in a multitude of ways not yet defined but can be demonstrated repeatedly, predictably and reliably, but not with cyanocbl, hycbl and folic acid, and for some unfortunate percentage of the popuation, folinic acid found in vegetable source folates which can actually block the active methylfolate form leading to severe folate and b12 deficiency symptoms without lowering serum levels or affecting MMA or HCY becasue of the body's triage system. So the traditional tests are worthless for saying whether somebody has actual functional deficiencies or not. So every paper that counts on those tests for detecting b12 and folate deficiencies is invalid. So the need to "rule out" b12 deficiency for an MS diagnosis doesn't take into account the newer studies showing the CSF/CNS cobalamin deficiencies and elevated HCY in CSF in MS or the benefit of intrathecal injections of mb12. This is still very new and only a few papers out of Japan. However, it can be DEMONSTRATED very easily. So does a CNS/CSF deficiency of b12 rule out an MS diagnosis? You must be kidding. It is never mentioned. In this case the one death a time are thousands of patient deaths every year. Nobody dies of b12/folate deficiency these days, they die of the multitude named or unnamed disorders casued by these. If I had died 8 years ago my death certificate would have read "congestive heart failure" or something of the sort.

As these deficiencies can cause approximately 600 biochemical failures in the body (including CNS) according to another paper, sorry I can't give you the reference, I was doing the reading to save my life, not to pose an accademic question. I was in a hurry. These same deficiencies also lead to massive inflammation in every system of the body, system failure in every system, hyper reactivity of all kinds. They trash the immunce system. They rtrash the neurology leading to every variety of neuropathy known to mankind. Start trashing the autonomic nervous system and see what happens. These deficiencies trash the hormone systems, the neurotransmitter systems, the endothelium, the epithelial tissues, the muscles, the mitochondria, etc. I don't know of any tissue not affected potentially to the point of failure. So you call this SIMPLE? Tell me, how good are you at understanding and solving 1000 variable problems? What do you call complicated?

Its like saying CFS is caused by Candida - it might fly in the early 90s in a naturopath's office but try and get that pear reviewed in a medical journal.

Lots of nonsense gets hypothesized when nobody knows and nobody knows how to do an effective treatment. So a whole lot of specific viruses and other things have been hypothesized as a cause while ignoring that all of them are stressors that might trigger something else that goes on and on and on and that the original stressor could be almost anything if the person has certain genetic and/or aquired characteristics. The stressors include viruses, bacteria, physical trauma, chemicals, pregnacy, vaccines and who knows what else. In my own and family experience and those I have worked closely with, include all of those. In my 100 provider 20 year $200,000 search for a diagnosis and treatment I found a whole of ignorant male bovine excrement and that NOTHING worked and much of what was tried provoked horrendous side effects and hypersensitive responses despite the faith each provider had in their favored hypothesis. The MDs were no better than the naturopaths. The chiropractors actually helped with my back and neck problems but nothing else.



In a person with a predisposition to lack of tolerance to self, perhaps (as has been recently suggested) some deficiencies in their innate immune system, a trigger - usually a stressor such as pregnancy, infection, stress, emotional upheaval, heavy exercise or exposure to a toxin and occasionally immuno-modulation following vaccination - results in an autoimmune response. The target of that autoimmune response appears to be regulated either by the toxin in rare cases, perhaps the virus or infection but often it is just mediated by the histocompatibility of the patient:

Very good. This is exactly what I'm talking about.


So autoimmunity is not simply caused by nutrient deficiencies or by foreign substances - it is a highly complex process that they are only beginning to understand - it has received years and years of research focus and as yet the primary etiologies are still conjectural and only beginning to be understood.

Part of that long delay is the fault of research focusing on cyabocbl/hycbl and folic acid. I am suggesting that the tendency towards out of control hyperresponsive reactions are the result of cascading failures that exist as a result of the ACTICVE mb12/adb12/methylfoalte. Everything that uses understanding of what b12 doesn't do based on the study of cyanocbl and hydroxycbl is wrong. What failures result from people who can only utilize folate from meat and in whom vegetable folate blocks that meat folate and it happens their entire life. These kids also can't use the folic acid in formula and will usually have trouble casued by cyanocbl as well or at least can't utilize it becasue of the folic acid. What happens in utero to these kids?

Let's consider for a moment post partum depression and schizophrenia. In the late 40s and early 50s a couple of studies were done on the effect of concentrated liver extract on on these two disorders. They were targeting the "protein mystery factor" whcih they identifeid as cyanocbl (lab mistake) and was properly identified 10 years later as mb12 and adb12. In high probability it also included methylfolate. Becasue of the amount in liver in that period the doses may very well have been several hundred micrograms of each mb12/adb12 and methylfoalte. Women sufferring from post partum depression recovered in 3 days. Hospitalized schizophrenics were relaseable in 3 days of such treatment. So what happened? Two things. The results were not able to be duplicated with the "pure substances" which at that time was cyanocbl and folic acid and those studies were considered flukes. Also Thorazine and other drugs came on the market and everybody promptly forgot about these results that were not replicated with the inactive pseudo substances. I hope you can find them I came across a summary of these studies but never the studies themselves.

So let's reproduce that in an experimental model. Take some subjects (we used 10 volunteers) who have had a year or more of excellent healing from CFS/FMS with mb12/adb12 and Metafolin. Take your base blood tests. Give them sufficient glutathione and/or precursors NAC/l-glutamine. Observe, if they have sufficienct b12 in their bodies by dose, that their urine becomes MUCH pinker or redder or red-orange-brown if lots of yellow color within hours of the glutathione. Continue until the increasing symptoms become too much. Take blood tests every week. Stop before neurological damage becomes evident, no more than 6 weeks, and record ALL symptoms, major and minor, day by day. The early symptoms will duplicate those of Cerefolin-NAC side effects. Deplin does not have those.

Then, using normal 1mg injected doses of cyanocbl and of folic acid, dose doesn't appear important, more might be worse, attempt to reverse the symptoms in group A. In group B give 15mg of metafolin per day in divided doses with each meal and 10mg iSC injections of mb12 or 50mg of Jarrow sublingual held for 3 hours or more under upper lip. Also 50mg of Adb12 (Source naturals). Repeat each day until back to all induced symptoms reversed in group B. If the dose is insufficient, increase, doubling or tripling. Compare to group A. Then do the same for group A to heal that which cyanocbl and folic acid can't do.

Six weeks should be enough to cause profound inflammation all over the body, the start of hyper-reactivity but not much as that takes longer return of folate deficiency symptoms starting in hours to days and mb12 deficiency symptoms starting up in 3-7 days and adb12 deficiency sypmtoms starting with 14-28 days. Mood and personality changes should be apparent withn 28 days and worsening. By worsening I mean depression and the appearance of irratiblity and so on in a shift that might be called Dr Jeckyll to Mr Hyde. These will usually start before actual neurological damage becomes apparant. These induced deficiencies will give you a lot of blood test information of what goes wrong.


and THAT has been published in a reputable, peer reviewed medical journal I would be interested. My mum has that condition and once again it is associated with particular genetic histocompatibility - this time the genetic markers being HLA-dr5 histocompatibility and some other associated genes. But that is ofcourse only part of the picture and there is so much to it.

The reference may be on the former wrongdiagnosis b12 thread. That was where the Hashimoto's discussion came up and I think a number of references and/or links posted. Do a search on the board for it if it's not on the thread. I was diagnosed hypothyroid in 1956 or 57 I think it was at about the age of 8. One or more persons on the board who were still in the active phase of Hashimoto's had their thyroid function restored and verified by tests.


As an armchair speculator I am always attracted to the science that is well supported, has a strong evidence base, demonstrates clinical outcomes through therapy and interventions and gets published in reputable journals.

I was dying. I couldn't afford to wait for my hypothetical great grandchildren to benefit. I prefer that too. However, the entire body of b12 and folate research needs to be redone with mb12 without asking only the questions established by cyanocbl and folic acid. In fact ALL research using those things as a base need to be redone those pseud vitamins are such poor replacements for the real thing. I changed my standards. There has to be some (several items) research in reputable journals that have the information reading beteween the lines if not in the conclusions. There has to be widespread actual success on the internet in a form without too many confounding factors, all the things must pass the "sniff" test and lack the component of male bovine excrement and all of it has to INTEGRATE across hundreds of separate examples. That was what didn't match up on my only severe mistake, glutathione precursors. I took the peer reviewed journals word for things and the internet HYPE but no results that passed the sniff test and it didn't integrate. I broke my own standards and knew I was doing it. I also knew I was missing an important factor and suspected that might be it. It wasn't. It was a disaster. However, it lead me to the missing factor, paradoxical folate deficiency.

You can read all the journals you want and nowhere will you find about the variablity of neurological effects of mb12 at the crystal level or about the practical meaning of mb12s photolytic breakdown nor the effects of metafolin on retention of mb12/adb12 or the differences of mb12 brands on neurological and other systems nor the effects of sublingual time on absorbtion percentage of mb12/adb12 dose and how it relates to injections or what amount of injected and/or sublingual mb12/adb12 it takes to consistantly deliver cobalamin to the CNS/CSF. These are all original work by me.

Doctors and researchers ASSuME folate deficiency is a thing of the past since folic acid. Paradoxical folate deficiency is not recognized but is easliy demonstrable as more and more people are doing on this board. The 70 year clock is just starting on this understanding. Mb12/adb12 became commercoially available in 1998, so another 55 years to possible understanding based on history.

ankylosing spondylitis

I and my son, with the same b12/folate situation as I have, have both had that suggested to us as a problem. With the mb12 my CRP went to < 1.0 and stayed there. There has been no further problem since mb12 for either of us and the pain was almost entirely relieved. Hard to say since I have so much damage from being broken in half sideways by a red light runner.


"Science is the art of making the obvious so to everybody"
John W. Campbell Jr.

"Sufficiently advanced technology looks like magic"
Arthur C. Clarke


Be in good health.

 

[crmfghtr]

So the question is, do we have to wait a year or two as they say or is there a way to get this treatment, maybe Mexico? I know its got risk, but at this point, I would do anything.

 

[ramakentesh]

Interesting. Time will tell but thanks for your detailed response.

 

[Freddd]

Interesting. Time will tell but thanks for your detailed response.

Hi Ramakentesh,

I am always interested in anything that can expand my knowledge and understanding. The b12 deficiency thread over at WD looked like the hypothyroid threads as that was possibly the number one "hard" damage. Lack of methylation isn't damage, but function. The lack, when maintained over time causes untold damage as so many hthings get broken down and not repaired. It was Rich's methyaltion hypothesis that brought me to Phoenix. I had my own "depleted methyaltor" hypothesis as I described it, since almost 9 years ago. It's very difficult not to notice that. It is universal in this whole set of disorders. Our only significant disagreement is over the CAUSE of such, and even that may not be different, just a different view and entry point into a chicken and egg cycle. Becasue of the difference in cause we view the corrrective measures slightly differently. Also, I look more at symptoms and he looks more at biochemistry, another chicken and egg cycle.

 

[ramakentesh]

Interesting, although time will tell and you must admit that clinical research in the area of methylation in relation to autoimmunity isnt exactly booming. Personally I keep my eyes open to everything. That is why I like Cort - he doesnt dismiss any possibility and that is the way to go in my opinion.
because of my background however I am perpetually drawn to the research that is well supported in peer reviewed medical journals.

 

[Freddd]

Interesting, although time will tell and you must admit that clinical research in the area of methylation in relation to autoimmunity isnt exactly booming. Personally I keep my eyes open to everything. That is why I like Cort - he doesnt dismiss any possibility and that is the way to go in my opinion.
because of my background however I am perpetually drawn to the research that is well supported in peer reviewed medical journals.

Hi Ramakentesh,

Just consider that methylation is a fractional part of what the active b12s and methylfoalte do. In any case the hyper response is casued by the deficiencies in some way and the autoimmune appears to be hyperresponsivenss in the immune area when it is triggerred inappropriately. Of course I might not be correct on that and that doesn't matter. The autoimmune is a result of underlying things going wrong, not the cause except for the results at the next step in the cascade of multi system failure in the body. Consider the possibility that as there are hundreds or maybe thousands of such secondary, tertiary, quadnary etc failures it has tens of thousands of researcher years spent chasing their tails looking for a cause in an effect and blinded to the deepest cause because they KNOW WITH CERTAINTY that it can't be cyanocbl or folic acid (and they are right about that) because the 50 years of mistaken research that is well supported in peer reviewed medical journals on a lab mistake tells them so and they confuse those things with the REAL B12s and the REAL FOLATE with 100 to 10,000 times more and different effectiveness. Now this is just specualtion on my part and/or maybe it just tickles my funny bone. Wouldn't that be one hell of a joke?