Axonal death could relate to iron deposition with phagocytosis being a subsequent action related to the clean up of the apoptosis of axons, etc.
It still doesn't necessarily mean a faulty immune system. Genes can and do mutate through repeated reproductions, it doesn't mean we are born with faulty genes. If their normal expression is interrupted or interfered with, sister generations result in mutations. The mutations don't have to play a role in MS, they could be as a consequence of repeated immune expressions that are strengthened by newer gene replications because of being triggered more often than in a healthy person.
MS is not considered an inherited illness so I don't think gene anomalies mean we started with a faulty immune system or gene mutations. I think immune participation occurs as a result of whatever process is going on, be it iron deposition or whatever else is found to be a potential trigger.
I honestly am not a believer that a dysfunctional immune system is a part of the whole pathogenesis of MS. I don't think evidence strongly points to immune dysregulation as an originating or contributing factor. I would have thought if that were so, MS or signs of immune weakness would show up much earlier in people.
Is RRMS misunderstood?
Maybe... or as some believers say "May that turn out as you say...". I had certain symptoms plus fatigue before CCSVI, then after the liberation procedure I was actually functioning almost like a normal person, and now 3 levels down once more. (On a scale from 1-10, post-CCSVI I was 9.5, pre-CCSVI 7.5-8, and now 7). Veins working perfectly, more open than ever... so, I would say that we are still quite a bit in the dark with MS and I agree that we've at least moved a step further from CRABs.seems related to how much underlying damage has already occurred. But after that Christmas miracle thread, it seems like there is hope even for the worst cases.
Still, just as being aware of MS can totally ravage, being in the dark can have the same effect.
There is no doubt that CCSVI is a critical part of the MS disease process and I am confident that restoring normal blood flow in persons newly diagnosed will prove to be a means of halting further disease activity for most.
Unfortunately I suspect most neurologists and certainly drug company scientists see the same likely scenario which is an obvious financial disaster for both parties. Hence they will fight tooth and nail to prevent CCSVI treatment becoming standard practice, especially for the newly diagnosed. They basically couldn't give a damn about those with SPMS who generate little cash for the MS machine.
I wish I could agree that persons with MS have normal immune systems but the genetic, immunological and epidemiological data say otherwise.
Another big question in all this is why adequate vitamin D in childhood prevents MS. If the concept that MS cause does not involve abnormalities the immune system is correct, then clearly adequate vitamin D must prevent CCSVI from occurring. This is not unreasonable but we need some empirical data to support this. Theoretical reasoning that vitamin D affects the vascular system is a start but is not enough given vitamin D affects almost every system in the body.
What we need are data regarding CCSVI in people without MS. A huge question is whether or not CCSVI is relatively common in the general population as the Buffalo data (note majority of HCs were NOT relatives of PwMS) indicated. If it is, then clearly MS must involve an immune component and we can also then test if CCSVI exhibits a strong N-S gradient in the normal population. If not, then vitamin D is doing its magic in MS some other way (most likely through the immune system). If so, then we know how to easily prevent CCSVI and MS.
The bottom line still remains if you have MS then get tested and treated for CCSVI ASAP. Furthermore, to cover your bases, use the recommended nutritional strategies to offset MS disease processes (immune reactions, oxidation etc) already established.
Unfortunately I suspect most neurologists and certainly drug company scientists see the same likely scenario which is an obvious financial disaster for both parties. Hence they will fight tooth and nail to prevent CCSVI treatment becoming standard practice, especially for the newly diagnosed. They basically couldn't give a damn about those with SPMS who generate little cash for the MS machine.
I wish I could agree that persons with MS have normal immune systems but the genetic, immunological and epidemiological data say otherwise.
Another big question in all this is why adequate vitamin D in childhood prevents MS. If the concept that MS cause does not involve abnormalities the immune system is correct, then clearly adequate vitamin D must prevent CCSVI from occurring. This is not unreasonable but we need some empirical data to support this. Theoretical reasoning that vitamin D affects the vascular system is a start but is not enough given vitamin D affects almost every system in the body.
What we need are data regarding CCSVI in people without MS. A huge question is whether or not CCSVI is relatively common in the general population as the Buffalo data (note majority of HCs were NOT relatives of PwMS) indicated. If it is, then clearly MS must involve an immune component and we can also then test if CCSVI exhibits a strong N-S gradient in the normal population. If not, then vitamin D is doing its magic in MS some other way (most likely through the immune system). If so, then we know how to easily prevent CCSVI and MS.
The bottom line still remains if you have MS then get tested and treated for CCSVI ASAP. Furthermore, to cover your bases, use the recommended nutritional strategies to offset MS disease processes (immune reactions, oxidation etc) already established.
I think that Ashton is correct in the thinking with what we know so far. The key thing that will unearth more knowledge is understanding what is the mechanism when disability returns, and why it is over such a relatively short time.Nasti wrote:Maybe... or as some believers say "May that turn out as you say...". I had certain symptoms plus fatigue before CCSVI, then after the liberation procedure I was actually functioning almost like a normal person, and now 3 levels down once more. (On a scale from 1-10, post-CCSVI I was 9.5, pre-CCSVI 7.5-8, and now 7). Veins working perfectly, more open than ever... so, I would say that we are still quite a bit in the dark with MS and I agree that we've at least moved a step further from CRABs.seems related to how much underlying damage has already occurred. But after that Christmas miracle thread, it seems like there is hope even for the worst cases.
Still, just as being aware of MS can totally ravage, being in the dark can have the same effect.
The example above sends out messages. What is happening that creates a return, is the flow change, or something about flow itself that is the critical issue. Do the damaged areas benefit from flow alone or is it stopping reflux and oxygen starvation?
I think that Vit D helps delay the disability process, but I doubt it will be in itself enough benefit once the disease has begun. The prevention of MS from conception is still a long shot, the population that does not become effected by low Vit D, family members, neighbors, relatives, other ethnicities and the like challenge the Vit D theory too much. The difference in Afro-American and Asian people with similar disease forms to MS e.g Devics Disease rattles the Vit D theory as well. There is something to be learnt here and I believe the skull and spine structure (as Dr. Flanagan has shown) has some part to play is this jigsaw.
The study of people treated for CCSVI will be so important, that data needs to capture so much, I hope that is being done!
The responsibility lies with the current practitioners to get that data base working for PwMS.
Actually there is no good challenge (ie empirical data or theoretical concepts) to the interpretation that adequate vitamin D from birth onwards will prevent MS. Notably there are robust and diverse data that says it will.
The twin studies show that genetics plays a substantial role in MS, that is, one has to be genetically susceptible to MS to get it. This fundamantal requirement discounts all of the objections that Nigel raised to vitamin D perhaps not preventing MS. If you don't have the genetic susceptibilty, you won't get MS no matter what environmental factors, including low vitamin D during childhood, you encounter.
I again repeat there are no data which suggest that the concept vitamin D prevents MS is wrong. That does not mean it is correct. However, given all the data that do say it will prevent MS, we have to go with that until we have data which might cause us to seriously doubt it.
Finally it is worthwhile to consider the important role of genetics which is without question given the twin data. If CCSVI is the sole cause of MS, then clearly the genetic component must be tied mainly to the susceptibility to getting CCSVI due to various environmental factors. So far no one has identified any genes in MS that are related to the development of the vascular system but I expect they haven't been looking. The dominance of immune-related genes in MS cannot be ignored in any objective analysis.
Bottom line is anyone with MS should ensure all first degree relatives are on adequate vitamin D, especially babies (1000 Iu) and children (2000-4000 IU). We are not sure how it prevents MS but here is little doubt that it does. My bet is on how vitamin D regulates both the immune and vascular systems.
The twin studies show that genetics plays a substantial role in MS, that is, one has to be genetically susceptible to MS to get it. This fundamantal requirement discounts all of the objections that Nigel raised to vitamin D perhaps not preventing MS. If you don't have the genetic susceptibilty, you won't get MS no matter what environmental factors, including low vitamin D during childhood, you encounter.
I again repeat there are no data which suggest that the concept vitamin D prevents MS is wrong. That does not mean it is correct. However, given all the data that do say it will prevent MS, we have to go with that until we have data which might cause us to seriously doubt it.
Finally it is worthwhile to consider the important role of genetics which is without question given the twin data. If CCSVI is the sole cause of MS, then clearly the genetic component must be tied mainly to the susceptibility to getting CCSVI due to various environmental factors. So far no one has identified any genes in MS that are related to the development of the vascular system but I expect they haven't been looking. The dominance of immune-related genes in MS cannot be ignored in any objective analysis.
Bottom line is anyone with MS should ensure all first degree relatives are on adequate vitamin D, especially babies (1000 Iu) and children (2000-4000 IU). We are not sure how it prevents MS but here is little doubt that it does. My bet is on how vitamin D regulates both the immune and vascular systems.
The challenge with Vit D is the ethnic and equator distances where the patient can move country in early age and be dx'ed with MS. You can be born and live near the equator up to age 15-16 I believe and move out to a problem latitude and have a MS dx, with no family history of MS only European decent.Direct-MS wrote:Actually there is no good challenge (ie empirical data or theoretical concepts) to the interpretation that adequate vitamin D from birth onwards will prevent MS. Notably there are robust and diverse data that says it will.
The twin studies show that genetics plays a substantial role in MS, that is, one has to be genetically susceptible to MS to get it. This fundamantal requirement discounts all of the objections that Nigel raised to vitamin D perhaps not preventing MS. If you don't have the genetic susceptibilty, you won't get MS no matter what environmental factors, including low vitamin D during childhood, you encounter.
I again repeat there are no data which suggest that the concept vitamin D prevents MS is wrong. That does not mean it is correct. However, given all the data that do say it will prevent MS, we have to go with that until we have data which might cause us to seriously doubt it.
Finally it is worthwhile to consider the important role of genetics which is without question given the twin data. If CCSVI is the sole cause of MS, then clearly the genetic component must be tied mainly to the susceptibility to getting CCSVI due to various environmental factors. So far no one has identified any genes in MS that are related to the development of the vascular system but I expect they haven't been looking. The dominance of immune-related genes in MS cannot be ignored in any objective analysis.
Bottom line is anyone with MS should ensure all first degree relatives are on adequate vitamin D, especially babies (1000 Iu) and children (2000-4000 IU). We are not sure how it prevents MS but here is little doubt that it does. My bet is on how vitamin D regulates both the immune and vascular systems.
I would like to see the Twin Studies that have been done through time revisited and the CCSVI testing done on the couples to investigate the incidence. I would personally only trust the skills of a Zamboni picked team to do the testing though.
I am a little concerned that people are believing that Dr. Zamboni's CCSVI findings are the only type of Vascular issue that is seen in MS and other diseases.
Transverse Myelitis has vascular restriction problems within the spinal cord that create disability as well.
There was a paper or two about the involvement of Vit D in development of the Vasculiture indicating a need for adequate Vit D for growth, but it did not indicate any connection to malformation in the study type.
CCSVI in New Zealand
The news we have been waiting for;
Scientists are closer to solving one of the many mysteries of multiple sclerosis and other demyelinating diseases, thanks to a recent study conducted at the Salk Institute for Biological Studies
http://www.sciencedaily.com/releases/20 ... 152258.htm
"If the sodium level drops, an accompanying drop in the leak current will maintain the signal, whereas if the sodium drops but the leak current doesn't, signal transmission may fail. Conversely, if the sodium level is too high and the leak current doesn't increase, a patient may experience twitching. The "safe" zone lies between the two limits.
"Trying to influence the balance between the two ion channels is a completely new approach, and drugs that target leak currents could be as important as those targeting the sodium current," adds Sejnowski. "I think we have a good chance at some point to help MS patients. The first step is to understand what's going on."
"Our model offers a novel explanation for many of the peculiar and intermittent symptoms that MS patients experience," says first author Jay S. Coggan, who had studied leak channels in previous work. "The injured axon is continually struggling to maintain order within a functional range. There is danger to the right and left. A variety of perturbations can nudge the axon one way or the other. It makes sense that leak channels might participate in these changes."
In some instances, for example, their symptoms worsen if they are too warm, but improve if they are cooled off-a phenomenon that correlates to the fact that these channels are temperature-dependent. "If a patient is near one of the boundaries and only marginally 'safe,' heating up could cause him or her to cross into the failure zone," Coggan adds. Temperature, therefore, hints at which boundary the patient is approaching.
Beyond MS and demyelinating diseases, insights into the sodium/leak current have applications to intractable pain-a field that Sejnowski's group will be investigating next."
This is in my view a positive step in the understanding of the effect within the damaged areas of CNS early on in the process prior to the lesion forming, the cause is the next step. What causes the imbalance and what causes the lack of sodium or potassium will be the key.
The news we have been waiting for;
Scientists are closer to solving one of the many mysteries of multiple sclerosis and other demyelinating diseases, thanks to a recent study conducted at the Salk Institute for Biological Studies
http://www.sciencedaily.com/releases/20 ... 152258.htm
"If the sodium level drops, an accompanying drop in the leak current will maintain the signal, whereas if the sodium drops but the leak current doesn't, signal transmission may fail. Conversely, if the sodium level is too high and the leak current doesn't increase, a patient may experience twitching. The "safe" zone lies between the two limits.
"Trying to influence the balance between the two ion channels is a completely new approach, and drugs that target leak currents could be as important as those targeting the sodium current," adds Sejnowski. "I think we have a good chance at some point to help MS patients. The first step is to understand what's going on."
"Our model offers a novel explanation for many of the peculiar and intermittent symptoms that MS patients experience," says first author Jay S. Coggan, who had studied leak channels in previous work. "The injured axon is continually struggling to maintain order within a functional range. There is danger to the right and left. A variety of perturbations can nudge the axon one way or the other. It makes sense that leak channels might participate in these changes."
In some instances, for example, their symptoms worsen if they are too warm, but improve if they are cooled off-a phenomenon that correlates to the fact that these channels are temperature-dependent. "If a patient is near one of the boundaries and only marginally 'safe,' heating up could cause him or her to cross into the failure zone," Coggan adds. Temperature, therefore, hints at which boundary the patient is approaching.
Beyond MS and demyelinating diseases, insights into the sodium/leak current have applications to intractable pain-a field that Sejnowski's group will be investigating next."
This is in my view a positive step in the understanding of the effect within the damaged areas of CNS early on in the process prior to the lesion forming, the cause is the next step. What causes the imbalance and what causes the lack of sodium or potassium will be the key.