I plan to revise my site based on two major issues, Vitamin D deficiency and Epstein Barr Virus
Dr. George Ebers has shown that there is a genetic marker in MS patients (HLA DRB1*15) which can lead to Vitamin D deficiency. This would explain the increased risk for MS in elevated Latitudes given the lack of sunlight during winter months since Vitamin D can only be synthesized when triggered by the sun’s ultraviolet rays (discovered 1974). Since adequate Vitamin D is the issue, theoretically supplementation during pregnancy and throughout life could put an end to MS once and for all, much like Vitamin C prevents scurvy (and Vitamin D can prevent rickets which leads to deformed bones).
While some have tried to fit this information into the Autoimmune theory of MS, I myself feel the Vitamin D deficit could deform the growing child’s vascular system as much as it does bones. Research is underway linking Vitamin D to the development of the endothelium, that is to say the walls of veins and arteries. If such deficiency can deform bones, why not veins? We still arrive at one origin of venous abnormalities and CCSVI. (There exists a large extent of variability in HumanLeukocyteAntigen (HLA) complex genes, and they do impact the immune mechanism. A very complicated picture I don’t pretend to understand. I’m mainly interested in finding a hands on, practical solution to my MS problem.)
Mononucleosis is caused by the Epstein-Barr virus which in turn is activated by an oxygen deficit in the brain. Poor blood/cerebrospinal fluid circulation in the central nervous system will diminish the oxygen supply. It may be the deformed vascular system in MSers leaves them open to this form of the EBV virus and to eventual active MS.
Leonard of Thisisms.com has been running a post since January 8, 2011 titled “A new concept and treatment options for MS” (updated May 19, 2014) He also has diabetes and I believe has reached the SPMS stage. He underwent Venoplasty in 2011. For a long time he dwelled on the “toxic gut” issue. On May 14, 2014 he wrote “I am sure the EBV virus causes my MS” since he has a very high load of the EBV antigens (Herpes simplex as well) and he does NOT have a “leaking gut”. He is taking an anti-viral medication to destroy the virus. (He provides an excellent overview of varied “natural” healing protocols as does Scott 1 on his post “Re: Beyond Avonex and Valtrex.” )
I believe that CCSVI poor blood circulation has reduced the Oxygen supply giving free rein to the activation of the latent EBV and that the root problem remains poor blood/brain fluid circulation. However, Leonard’s might be the best solution for him, especially if his blood circulation is seriously compromised and his MS has progressed to the point that Venoplasty won’t be effective.(?)
I believe an activated EBV virus is critical to developing Progressive MS. It is known that in the early Relapse/Remit phase (RRMS) lesions are visible on MRI scans. which are thought to be signs of inflammation in the brain’s white matter. As the disease develops lesions are less and less visible until they disappear entirely in the Progressive stage and serious handicap develops. What does this imply?
I believe the lesion inflammation signals a blood reflux caused by CCSVI venous obstructions – poor blood/fluid flow. It is in this early stage that venoplasty is the most successful. (True as well for ALL natural healing modalities.) Neurologists, believing that the lesions represent an auto-immune inflammation, also recommend launching into drug therapy immediately after diagnosis to stop the inflammation.
The weakness of the Disease Modifying Drug approach is that the drugs don’t nourish grey matter, and GREY MATTER ATROPHY IS THE KEY TO DISABILITY.
Once the disease develops, eventually the grey matter is progressively damaged. Is it possible that poor oxygen supply activates a dormant EBV virus and this virus itself damages the grey matter? When the blood stops flowing altogether (is that possible? Do the damaged, unused veins wither?), does the EBV virus take over triggering cell death? The lesions do not determine handicap, the damaged, atrophied grey matter does. What if the MS drugs weaken the immune system such that the EBV virus goes out of control? A second look at the Terry Wahl’s You Tube video “Minding Your Mitochondria” might be in order to re-focus the mind on how to nourish the brain’s grey matter and heal.
My own healing approach at the moment means getting the blood/brain fluids to flow freely, and keeping the grey matter healthy by nourishing it with oxygen and nutrients which also should prevent an EBV relapse.
On March 21, 2013 it was announced that Professor George C. Ebers, MD, of University of Oxford in Ontario, Canada, had been chosen to receive the National MS Society/American Academy of Neurology’s 2013 John Dystel Prize for Multiple Sclerosis. The following quotes come from www.nationalmssociety.org site.
"His studies of twins have shown that susceptibility is partly genetic and partly environmental, indicating that MS is a complex genetic disease. These findings contribute to efforts to end MS through prevention. (Proceedings of the National Academy of Sciences U S A 2003;100:12877) This showed linkage to the Human leukocyte antigen (HLA) complex (genes related to the immune system) on chromosome 6. (Lancet 1982;2:88)…
Research is increasingly pointing to reduced levels of vitamin D in the blood as one factor that can increase the risk of developing MS. (Annals of Neurology 2011;70:881)
Delineating the natural history of MS: Dr. Ebers has performed detailed studies tracking over time the “natural history” of MS in London, Ontario, Canada, following more than 1,000 individuals since 1972. Natural history studies provide important knowledge, such as the average number of MS relapses a person may be expected to experience. This helps to appropriately design clinical trials and interpret their results. These studies have been published in a series of important papers on topics such as the predictive value of the early course of MS (Brain 1989;112:1419), and the features of primary progressive MS. (Brain 1999;122:625)…
Epidemiology of MS: Dr. Ebers’ studies have forged new paths our understanding of who gets MS, which is the goal of epidemiology. In a study of over 40,000 people from Canada, Sweden, Norway and the United Kingdom, Dr. Ebers showed that the relative risk of developing MS is higher if you are born in May (like me) and lower if you are born in November. The finding of a birth pattern suggests the possibility that the origins of the disease date to very early in life. (British Medical Journal 2005;330:120)" (My comment. The Sun related Vitamin D deficiency persists throughout growth. For example, people who moved to Sweden from Iran at an average age of 17 developed MS at the higher Scandinavian rate. (Ahlgren et al., 2010).
Dr. Ebers also has contributed to the study of gender differences in MS. Among other contributions, he documented in 2006 a significant increase in the number of women diagnosed with MS more than men, noting that the female to male ratio in the incidence of MS had increased progressively over the previous 50 years. (Lancet Neurology 2006;5:932) (My comment.. The FDA approved Birth Control Pills in 1960. I suspect use of hormonal therapy has triggered the striking increase in female susceptibility to MS, the original male/female ratio being 1:1.)
A series of studies on the relatives of people with MS including spouses, half-siblings, adoptees, and step-siblings suggested the idea that increases in the risk for developing MS come less from the familial environment than from factors operating at a general population level, such as climate and/or diet. These studies led to examination of role of Vitamin D in MS risk and the potential of vitamin D supplementation for MS patients and their families. (Lancet Neurology 2008;7:268)"
The Neurology Community was less pleased with Dr. Ebers when on 17 October 2013 he gave a lecture titled “Critical Review of outcomes used in MS clinical trials” which was posted on You Tube November 4, 2013 by the European Medicines Agency. (Thus far there have been only 803 views.) www.youtube.com/watch?v=OqY-_K1fYJY
Dr. Ebers basically said that current MS medications do NOT prevent descent into Progressive MS disability. See my blog (MS Drug/MRI Fallacy January 5, 2014) DMD’s treat the inflammation of the early RRMS. Once the Progressive stage sets in, they don’t work and decline sets in. Apparently the brain atrophies as do the veins draining the brain. It has been demonstrated that blood transit time in MS patients is one half that of normals. The question is one of perfusion i.e. blood flow, volume and mean transit time. ALL brain fluids contribute to adequate blood flow.
Dr. Ebers has engaged in debates denouncing (politely) the failure of Neurologists to face facts about DMD efficacy, arguing that the CCSVI controversy had revealed to what extent MS patients don’t trust their Doctors. If one obediently follows standard therapy only to finish in a wheelchair, by which time the CCSVI option and/or the “nourish the grey matter” option are less viable, one will have made a mistake. I believe current research delays owing to ideology and vested interests border on criminal.
Joan Beal (cheerleader on Thisisms.com), who oversees treatment for her husband Jeff, has combined the various options by 1) arranging the first Stanford CCSVI MS angioplasty (in his case the Jugulars were opened with stents) 2) using the MS drug Copaxone to prevent relapses and 3) "prescribing" optimal nutrition to nourish the brain's grey matter as well as the veins' epithelium.The Neurology community is still busy denying the viability of the CCSVI option, clinging to the observation that the benefits of Venoplasty disappear over time. So why not find out why and how to fix it?
Doctor Sclafani’s video “Causes of Non-Response to CCSVI” April 15, 2013 on the CCSVI Alliance website provides an expert analysis by an experienced Interventional Radiologist who has pioneered CCSVI Venoplasty. (Unfortunately the sound track is poor.)
“Causes of Non-Response to CCSVI”
Dr. George Ebers has shown that there is a genetic marker in MS patients (HLA DRB1*15) which can lead to Vitamin D deficiency. This would explain the increased risk for MS in elevated Latitudes given the lack of sunlight during winter months since Vitamin D can only be synthesized when triggered by the sun’s ultraviolet rays (discovered 1974). Since adequate Vitamin D is the issue, theoretically supplementation during pregnancy and throughout life could put an end to MS once and for all, much like Vitamin C prevents scurvy (and Vitamin D can prevent rickets which leads to deformed bones).
While some have tried to fit this information into the Autoimmune theory of MS, I myself feel the Vitamin D deficit could deform the growing child’s vascular system as much as it does bones. Research is underway linking Vitamin D to the development of the endothelium, that is to say the walls of veins and arteries. If such deficiency can deform bones, why not veins? We still arrive at one origin of venous abnormalities and CCSVI. (There exists a large extent of variability in HumanLeukocyteAntigen (HLA) complex genes, and they do impact the immune mechanism. A very complicated picture I don’t pretend to understand. I’m mainly interested in finding a hands on, practical solution to my MS problem.)
Mononucleosis is caused by the Epstein-Barr virus which in turn is activated by an oxygen deficit in the brain. Poor blood/cerebrospinal fluid circulation in the central nervous system will diminish the oxygen supply. It may be the deformed vascular system in MSers leaves them open to this form of the EBV virus and to eventual active MS.
Leonard of Thisisms.com has been running a post since January 8, 2011 titled “A new concept and treatment options for MS” (updated May 19, 2014) He also has diabetes and I believe has reached the SPMS stage. He underwent Venoplasty in 2011. For a long time he dwelled on the “toxic gut” issue. On May 14, 2014 he wrote “I am sure the EBV virus causes my MS” since he has a very high load of the EBV antigens (Herpes simplex as well) and he does NOT have a “leaking gut”. He is taking an anti-viral medication to destroy the virus. (He provides an excellent overview of varied “natural” healing protocols as does Scott 1 on his post “Re: Beyond Avonex and Valtrex.” )
I believe that CCSVI poor blood circulation has reduced the Oxygen supply giving free rein to the activation of the latent EBV and that the root problem remains poor blood/brain fluid circulation. However, Leonard’s might be the best solution for him, especially if his blood circulation is seriously compromised and his MS has progressed to the point that Venoplasty won’t be effective.(?)
I believe an activated EBV virus is critical to developing Progressive MS. It is known that in the early Relapse/Remit phase (RRMS) lesions are visible on MRI scans. which are thought to be signs of inflammation in the brain’s white matter. As the disease develops lesions are less and less visible until they disappear entirely in the Progressive stage and serious handicap develops. What does this imply?
I believe the lesion inflammation signals a blood reflux caused by CCSVI venous obstructions – poor blood/fluid flow. It is in this early stage that venoplasty is the most successful. (True as well for ALL natural healing modalities.) Neurologists, believing that the lesions represent an auto-immune inflammation, also recommend launching into drug therapy immediately after diagnosis to stop the inflammation.
The weakness of the Disease Modifying Drug approach is that the drugs don’t nourish grey matter, and GREY MATTER ATROPHY IS THE KEY TO DISABILITY.
Once the disease develops, eventually the grey matter is progressively damaged. Is it possible that poor oxygen supply activates a dormant EBV virus and this virus itself damages the grey matter? When the blood stops flowing altogether (is that possible? Do the damaged, unused veins wither?), does the EBV virus take over triggering cell death? The lesions do not determine handicap, the damaged, atrophied grey matter does. What if the MS drugs weaken the immune system such that the EBV virus goes out of control? A second look at the Terry Wahl’s You Tube video “Minding Your Mitochondria” might be in order to re-focus the mind on how to nourish the brain’s grey matter and heal.
My own healing approach at the moment means getting the blood/brain fluids to flow freely, and keeping the grey matter healthy by nourishing it with oxygen and nutrients which also should prevent an EBV relapse.
On March 21, 2013 it was announced that Professor George C. Ebers, MD, of University of Oxford in Ontario, Canada, had been chosen to receive the National MS Society/American Academy of Neurology’s 2013 John Dystel Prize for Multiple Sclerosis. The following quotes come from www.nationalmssociety.org site.
"His studies of twins have shown that susceptibility is partly genetic and partly environmental, indicating that MS is a complex genetic disease. These findings contribute to efforts to end MS through prevention. (Proceedings of the National Academy of Sciences U S A 2003;100:12877) This showed linkage to the Human leukocyte antigen (HLA) complex (genes related to the immune system) on chromosome 6. (Lancet 1982;2:88)…
Research is increasingly pointing to reduced levels of vitamin D in the blood as one factor that can increase the risk of developing MS. (Annals of Neurology 2011;70:881)
Delineating the natural history of MS: Dr. Ebers has performed detailed studies tracking over time the “natural history” of MS in London, Ontario, Canada, following more than 1,000 individuals since 1972. Natural history studies provide important knowledge, such as the average number of MS relapses a person may be expected to experience. This helps to appropriately design clinical trials and interpret their results. These studies have been published in a series of important papers on topics such as the predictive value of the early course of MS (Brain 1989;112:1419), and the features of primary progressive MS. (Brain 1999;122:625)…
Epidemiology of MS: Dr. Ebers’ studies have forged new paths our understanding of who gets MS, which is the goal of epidemiology. In a study of over 40,000 people from Canada, Sweden, Norway and the United Kingdom, Dr. Ebers showed that the relative risk of developing MS is higher if you are born in May (like me) and lower if you are born in November. The finding of a birth pattern suggests the possibility that the origins of the disease date to very early in life. (British Medical Journal 2005;330:120)" (My comment. The Sun related Vitamin D deficiency persists throughout growth. For example, people who moved to Sweden from Iran at an average age of 17 developed MS at the higher Scandinavian rate. (Ahlgren et al., 2010).
Dr. Ebers also has contributed to the study of gender differences in MS. Among other contributions, he documented in 2006 a significant increase in the number of women diagnosed with MS more than men, noting that the female to male ratio in the incidence of MS had increased progressively over the previous 50 years. (Lancet Neurology 2006;5:932) (My comment.. The FDA approved Birth Control Pills in 1960. I suspect use of hormonal therapy has triggered the striking increase in female susceptibility to MS, the original male/female ratio being 1:1.)
A series of studies on the relatives of people with MS including spouses, half-siblings, adoptees, and step-siblings suggested the idea that increases in the risk for developing MS come less from the familial environment than from factors operating at a general population level, such as climate and/or diet. These studies led to examination of role of Vitamin D in MS risk and the potential of vitamin D supplementation for MS patients and their families. (Lancet Neurology 2008;7:268)"
The Neurology Community was less pleased with Dr. Ebers when on 17 October 2013 he gave a lecture titled “Critical Review of outcomes used in MS clinical trials” which was posted on You Tube November 4, 2013 by the European Medicines Agency. (Thus far there have been only 803 views.) www.youtube.com/watch?v=OqY-_K1fYJY
Dr. Ebers basically said that current MS medications do NOT prevent descent into Progressive MS disability. See my blog (MS Drug/MRI Fallacy January 5, 2014) DMD’s treat the inflammation of the early RRMS. Once the Progressive stage sets in, they don’t work and decline sets in. Apparently the brain atrophies as do the veins draining the brain. It has been demonstrated that blood transit time in MS patients is one half that of normals. The question is one of perfusion i.e. blood flow, volume and mean transit time. ALL brain fluids contribute to adequate blood flow.
Dr. Ebers has engaged in debates denouncing (politely) the failure of Neurologists to face facts about DMD efficacy, arguing that the CCSVI controversy had revealed to what extent MS patients don’t trust their Doctors. If one obediently follows standard therapy only to finish in a wheelchair, by which time the CCSVI option and/or the “nourish the grey matter” option are less viable, one will have made a mistake. I believe current research delays owing to ideology and vested interests border on criminal.
Joan Beal (cheerleader on Thisisms.com), who oversees treatment for her husband Jeff, has combined the various options by 1) arranging the first Stanford CCSVI MS angioplasty (in his case the Jugulars were opened with stents) 2) using the MS drug Copaxone to prevent relapses and 3) "prescribing" optimal nutrition to nourish the brain's grey matter as well as the veins' epithelium.The Neurology community is still busy denying the viability of the CCSVI option, clinging to the observation that the benefits of Venoplasty disappear over time. So why not find out why and how to fix it?
Doctor Sclafani’s video “Causes of Non-Response to CCSVI” April 15, 2013 on the CCSVI Alliance website provides an expert analysis by an experienced Interventional Radiologist who has pioneered CCSVI Venoplasty. (Unfortunately the sound track is poor.)
“Causes of Non-Response to CCSVI”
- The neurons may be too damaged for renewed blood circulation to repair them.
- There has been too much de-myelination.
- Incomplete assessment of the vein, images misinterpreted
- Jugulars are not drained properly
- “Contrast too dense”, numerous reasons for a failed diagnosis
- Incomplete treatment if the catheter can’t get past the stenosis
- Patients fail follow-up care. A re-stenosis must be treated within 48 hours
- The vein is not dilated sufficiently. Dr. Sclafani insists that the Gold Standard for effective CCSVI treatment should be Venoplasty with the Intravenous Ultrasound (IVUS) in order to adequately measure the vein diameter as well as visualize the true condition of the valves and vein’s interior (webs, septums, stenosis).
- Dr. Zamboni uses the Doppler Ultrasound to diagnose CCSVI in the neck veins. However, Dr. Sclafani believes more veins need to be examined and opened, citing problems with the Azygos Valve stenosis and in particular the Renal Vein Compression Syndrome which 50% of MS patients exhibit. He remarks that it may be difficult for some to understand how a Kidney vein blockage can affect the brain, but it makes perfect sense to me, the entire circulatory system needs to be considered. (Just yesterday I couldn’t release my bladder so I asked my husband to massage my upper back. That sent me at once to the W.C. I’m convinced I have pelvic blood circulation congestion (CCSVI) which may have led to an entire complex of problems – urinary tract infections, menstrual cramps, ovarian problems, even endometriosis. Doctors separate these pathologies according to their respective specialties when in reality they should be treated as a CCSVI condition by an Interventional Radiologist. Interventional Radiology is a relatively new specialty which could probably have saved me much grief over the years. Neurologists assume as well that bladder problems originate in damage to the CNS. Maybe not.)
Dr. Sclafani will be participating in the Hubbard Foundation FDA Registry for MS CCSVI Treatment and Data Collection.
(Work in progress)
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