Nieuw concept voor MS
Geplaatst: 28 feb 2012, 10:55
Nieuw concept voor MS
update 21 June 2014
I would like to recap based on our learnings.
MS has many aetiologies. The picture is not black and white. MS is multifacetted with considerable variation among patients (the NO / OHNOO cycle interacts with distinct tissues to produce varying patterns of symptoms and signs) [url]http://www.allergyresearchgroup.com/Exp ... sp-35.html[/url] . Variation may also be seen in pattern/degree of ccsvi, immune system handling of EBV and gradations of ADMA generation by the kidney/renal system.
The pattern of thinking by most medical experts is too linear and singular rather than lateral and heterogeneous. [url]http://en.wikipedia.org/wiki/Paul_Feyerabend[/url] Everybody wants a magic bullet but for MS that does not work. Doctors should have a veterinarian look at things. As regards the therapy, it is the sum of all the things you do that makes a difference and it will take time to be effective.
In MS, the energy metabolism is disrupted with reduced absorption of essential nutrients. But most studies on MS get lost in the complexity at the back of the mechanism, a mechanism that does not even have to be fully understood. At the front we find the high EBV load, the vicious NO / OHNOO cycle, oxidative stress, peroxinitritie that jamps the cells etc. The approach should focus on the front, not on the back!
Ccsvi links the drainage of the dural nerve system, the dural sinuses, and meningeal inflammation. It provides a possible explanation for meningeal inflammation and subpial cortical lesions exclusively observed in MS patients. Environmental factors such as exposure to heavy metals (even of previous generations) and related genetic factors of veins may play their role here (Boston document, Texas study). Still apart from the whole amalgam discussion, PwMS also seem to have a worse than average dental health which may find its explanation here as well.
Quite a bit of research implicates EBV is central in the development of MS. One ingenious study looked at blood samples collected from 3 million US military personnel at their time of enlistment, and their subsequent development of MS. Those who had high anti-bodies to EBV at the time of enlistment, that is those who had a chronic viral infection, even up to 5 years before the onset of MS, had a 20-30 times higher risk of getting the disease than those with low antibody levels.
Researchers in Houston, Texas have speculated that some of the effects of interferons in MS might be due to their anti-viral properties (in fact as much as their effects on the immune system).
In susceptible people, or it is probably better to say people that have a certain predisposition, that is those with the 'right' genetic make-up, and the right sort of environmental triggers e.g. lack of sunshine, fish oil, infection with EBV may trigger the onset of the disease later in life. The kidney/renal system producing ADMA is a highly suspect factor predisposing people.
The mechanisms causing disability progression and the lesions are only loosely coupled: the EBV envelop protein vs EBV infected B cells inducing peroxynitrite nitrating the lipids. Studies also confirm that disability progression and lesions are not 1:1 correlated.
Autoimmunity is explained by chronic high concentration EBV immune complexes cross-coupling with epitodes of EBV remnants in transgenetic cells. About 8% of cells in our body is transgenetic, after about 120 million years of evolution.
In MS disability progression, because the effects of poor health of dendrocytes and a lack of energy come together, they appear one and the same process. But I think underlying are in fact two different processes: the EBV envelop protein causing the replenishment of new dendrocytes to stall vs peroxynitrite disabling glyceraldehyde-3-phosphate and ADP/ATP conversion causing mitochondrial energy / the pump to fail. In casu, I see my own disability progress but at the same time to migrate more and more towards an energy failure. And although there is a common causal factor, they are different processes. An explanation for the big temperature effects seen in Pw MS -who inevitably run more on the borderline- should probably be sought in this corner as well.
The count of mitochondria in our cells is important too. If you have more mitochondria and active membranes, you are less susceptible for developing MS, I think because it just takes longer for the system to get jammed. The number is proprotionate to the vitamin D level in the circulation of the mother from say the 2nd to the 6th month of pregnancy and of the adolecent during the main phase of cellular growth. Where the vitamin D level is influenced by cholesterol and sunlight. That is why I think that our modern low fat diet that may be good for mid-aged and elderly people and helps protect against heart disease etc is not necessarily good for young mothers and children.
Women are reported to produce more nitric oxide than men, possibly explaining the gender bias seen in MS. A similar gender bias is seen in autoimmune diseases characterized by excessive peroxynitrite (i.e. CFS, lupus, rheumatoid arthritis).
Nitric oxide is known to stimulate the nociceptors that initiate the perception of pain. I am sure nitric oxide is sky high in MS patients explaing the pain in limbs.
The cycle seems self-reinforcing: EBV infection gives ever weaker immune protection which aggravates EBV infection. Strengthening the immune function would seem central to any therapy.
I find the theory Beyond Avonex and Valtrex by Scott on regimens-f22/topic24019.html beautiful thinking and highly plausible as it connects all the things that I see in my own family. It is fully complementary to and reinforces the overall concept below. I cannot be naïve anymore and simply accept that this is all coincidence. It is just too good to be dismissed. I encourage you all to read Scott's theory.
Perverse drivers in the medical system and fear of stepping outside accepted practice hamper the exploration of new ideas. Fortunately, the collective cognition on the Internet leads to new concepts beyond old thinking in traditional quarters. Together with prof. Peter Finke [url]http://www.perlentaucher.de/buch/peter- ... ience.html[/url] , we can only hope that this citizen science that now thrives on social fora may find "ways out of the impasse of reality".
update 21 June 2014
I would like to recap based on our learnings.
MS has many aetiologies. The picture is not black and white. MS is multifacetted with considerable variation among patients (the NO / OHNOO cycle interacts with distinct tissues to produce varying patterns of symptoms and signs) [url]http://www.allergyresearchgroup.com/Exp ... sp-35.html[/url] . Variation may also be seen in pattern/degree of ccsvi, immune system handling of EBV and gradations of ADMA generation by the kidney/renal system.
The pattern of thinking by most medical experts is too linear and singular rather than lateral and heterogeneous. [url]http://en.wikipedia.org/wiki/Paul_Feyerabend[/url] Everybody wants a magic bullet but for MS that does not work. Doctors should have a veterinarian look at things. As regards the therapy, it is the sum of all the things you do that makes a difference and it will take time to be effective.
In MS, the energy metabolism is disrupted with reduced absorption of essential nutrients. But most studies on MS get lost in the complexity at the back of the mechanism, a mechanism that does not even have to be fully understood. At the front we find the high EBV load, the vicious NO / OHNOO cycle, oxidative stress, peroxinitritie that jamps the cells etc. The approach should focus on the front, not on the back!
Ccsvi links the drainage of the dural nerve system, the dural sinuses, and meningeal inflammation. It provides a possible explanation for meningeal inflammation and subpial cortical lesions exclusively observed in MS patients. Environmental factors such as exposure to heavy metals (even of previous generations) and related genetic factors of veins may play their role here (Boston document, Texas study). Still apart from the whole amalgam discussion, PwMS also seem to have a worse than average dental health which may find its explanation here as well.
Quite a bit of research implicates EBV is central in the development of MS. One ingenious study looked at blood samples collected from 3 million US military personnel at their time of enlistment, and their subsequent development of MS. Those who had high anti-bodies to EBV at the time of enlistment, that is those who had a chronic viral infection, even up to 5 years before the onset of MS, had a 20-30 times higher risk of getting the disease than those with low antibody levels.
Researchers in Houston, Texas have speculated that some of the effects of interferons in MS might be due to their anti-viral properties (in fact as much as their effects on the immune system).
In susceptible people, or it is probably better to say people that have a certain predisposition, that is those with the 'right' genetic make-up, and the right sort of environmental triggers e.g. lack of sunshine, fish oil, infection with EBV may trigger the onset of the disease later in life. The kidney/renal system producing ADMA is a highly suspect factor predisposing people.
The mechanisms causing disability progression and the lesions are only loosely coupled: the EBV envelop protein vs EBV infected B cells inducing peroxynitrite nitrating the lipids. Studies also confirm that disability progression and lesions are not 1:1 correlated.
Autoimmunity is explained by chronic high concentration EBV immune complexes cross-coupling with epitodes of EBV remnants in transgenetic cells. About 8% of cells in our body is transgenetic, after about 120 million years of evolution.
In MS disability progression, because the effects of poor health of dendrocytes and a lack of energy come together, they appear one and the same process. But I think underlying are in fact two different processes: the EBV envelop protein causing the replenishment of new dendrocytes to stall vs peroxynitrite disabling glyceraldehyde-3-phosphate and ADP/ATP conversion causing mitochondrial energy / the pump to fail. In casu, I see my own disability progress but at the same time to migrate more and more towards an energy failure. And although there is a common causal factor, they are different processes. An explanation for the big temperature effects seen in Pw MS -who inevitably run more on the borderline- should probably be sought in this corner as well.
The count of mitochondria in our cells is important too. If you have more mitochondria and active membranes, you are less susceptible for developing MS, I think because it just takes longer for the system to get jammed. The number is proprotionate to the vitamin D level in the circulation of the mother from say the 2nd to the 6th month of pregnancy and of the adolecent during the main phase of cellular growth. Where the vitamin D level is influenced by cholesterol and sunlight. That is why I think that our modern low fat diet that may be good for mid-aged and elderly people and helps protect against heart disease etc is not necessarily good for young mothers and children.
Women are reported to produce more nitric oxide than men, possibly explaining the gender bias seen in MS. A similar gender bias is seen in autoimmune diseases characterized by excessive peroxynitrite (i.e. CFS, lupus, rheumatoid arthritis).
Nitric oxide is known to stimulate the nociceptors that initiate the perception of pain. I am sure nitric oxide is sky high in MS patients explaing the pain in limbs.
The cycle seems self-reinforcing: EBV infection gives ever weaker immune protection which aggravates EBV infection. Strengthening the immune function would seem central to any therapy.
I find the theory Beyond Avonex and Valtrex by Scott on regimens-f22/topic24019.html beautiful thinking and highly plausible as it connects all the things that I see in my own family. It is fully complementary to and reinforces the overall concept below. I cannot be naïve anymore and simply accept that this is all coincidence. It is just too good to be dismissed. I encourage you all to read Scott's theory.
Perverse drivers in the medical system and fear of stepping outside accepted practice hamper the exploration of new ideas. Fortunately, the collective cognition on the Internet leads to new concepts beyond old thinking in traditional quarters. Together with prof. Peter Finke [url]http://www.perlentaucher.de/buch/peter- ... ience.html[/url] , we can only hope that this citizen science that now thrives on social fora may find "ways out of the impasse of reality".