CCSVI and CCVBP

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

Re: CCSVI and CCVBP

Postby Squeakycat » Wed Oct 23, 2013 2:31 am

uprightdoc wrote:Who says that genes in mice are relevent to study MS in humans?
Doc,

People who are MUCH smarter than I am. :>)

But seriously, the conversion of D3 to calcitriol is controlled by the CYP27B1 gene. Each of the immune cells that were the focus of the study, T-cells, are created by genes which are similar in mice and humans.

So with the study focused on these issues, the similarity between mice and humans as far as these genes seems to be very relevant, to me anyway.
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Re: CCSVI and CCVBP

Postby Squeakycat » Wed Oct 23, 2013 2:41 am

uprightdoc wrote:While the genes may be relevant for studying similar autoimmune reactions to EAE in mice and humans they are not necessarily genes possibly related to the cause of MS.
Doc,
Agree. No one is saying that these are the root cause of the cascade that ultimately results in damage to nerves that is characteristic of MS. It is addressing the second step in that cascade where likely, the immune response it self by being overly pro-inflammatory causes a failure in the process by which cells make calcitriol from D3. That leaves aggressive components of the immune system in an immortal state causing ongoing damage in the CNS.

Calcitriol is critical in this. As a regulatory hormone, it is what controls the local adaptive immune response to infection or injury. It activates it and it is supposed to also deactive it, but can't be there is insufficient calcitriol to manage the immune system.

As I said in an earlier post, these root causes still have to be addressed.
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Re: CCSVI and CCVBP

Postby Squeakycat » Wed Oct 23, 2013 2:53 am

uprightdoc wrote:For example, I suspect that genes related to structure, such as the design of the cranial vault, craniocervical junction and spine, as well as the design of the circulatory routes of the brain play a role in MS. In this regard, mice don't stand upright and walk around on two legs. They aren't even remotely similar to humans from a structural standpoint.
Doc,

And to a carpenter with a hammer, all problems are nails. :>)

I like a Grand Unified Theory of this based on Vitamin D. It is the hormone that directs angiogenesis so if the mother is vitamin D deficient at the right time during gestation, there will likely be venous malformations. That seems to be supported by the birth month effect in MS and the findings of the IRs doing CCSVI treatment.

But anything that causes a disruption in flow including bone structure that cause a flow impairment would likely contribute to the problem that triggers MS so I certainly wouldn't discount that as a factor.

The structure, however, doesn't cause the conversion of D3 to calcitriol to be blocked. It causes the problem that triggers an active immune response which in turn causes conversion to fail. So if you are looking at this at this stage, then mice probably are not a bad model, though human guinea pigs would be ideal, though hard to find. :>)
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Re: CCSVI and CCVBP

Postby Squeakycat » Wed Oct 23, 2013 3:07 am

uprightdoc wrote:As it is, humans show a great deal of variability in prevalence of MS according to race, gender and geographic location. Despite genetic similarity for autoimmune funcitons, MS affects females far more than males. It also affects Europeans far more than Asian or African races, as well as people living in more northern lattitudes. Thus, I don't see how EAE or mice with experimentally induced disruption of the blood brain barrier serve as good models for studying the cause of MS in humans.
Doc,

Would it surprise you if I suggest that a lot of the variations you are enumerating have a direct link to vitamin D? (Hammer and nail thing.) :>)

Prof Hayes has in fact looked at the variation between males and females in mice and is fairly certain that this has to do with an interaction between the female steroidal hormone estradiol and vitamin D which is a steroidal hormone. I believe this is something she is hoping to be able to study further.

As far as Europeans versus Asians and Africans, I think it is fairly well substantiated that this is most likely a latitude effect and that in turn results in fewer months of the year in which vitamin D can be naturally produced in the skin. Northern Europeans with high vitamin D diet from fish don't get MS. There are several good studies showing that the prevalence of MS increases with latitude in Scotland alone and the exceptions there turn out to all be because of altitude which also has an effect on the amount of UV-B radiation available with higher altitudes having lower incidence of MS and those at sea level having much higher rates.

Similarly, people with darker skins who move to northern latitudes are in fact more susceptible to MS because their skin pigmentation requires greater sun exposure to produce the same amount of vitamin D. While not MS, there are some interesting studies in the UK of how this is resulting in higher levels of Type 1 diabetes (another disease linked to vitamin D deficiencies and even ricketts in Asian populations in the UK.

So if the problems are caused by vitamin D deficiency or more specifically, the lack of calcitriol in the CNS, then mice aren't a bad model. If you were going to try to induce MS through "structural" problems in the bones of the head and spine, then they would certainly not be a good model. Putnam used dogs for what he was sure was a problem with veins and tied off their jugulars to induce a fairly good model of MS.
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Re: CCSVI and CCVBP

Postby Squeakycat » Wed Oct 23, 2013 3:32 am

uprightdoc wrote:According to the leaky blood brain barrier therory, lesions are a sign of breach or disruption of the blood brain and CSF barrier. In this regard, the classic lesions of MS are typically supratentorial (above the posterior fossa), periventricular and perivenular (Dawson's fingers). Many MS signs and symptoms, however, are often from infratorial structures (within the posterior fossa) such as the brainstem and cerebellum. The only lesions that I have found that clearly correlate with the signs and symptoms is optic neuritis and lesions in the optic nerve. It hard to explain arm and leg weakness according to classic lesions. Moreover, many patients have no lesions or obvious signs of disruption of the blood brain barrier. Some patients without lesions have more progressive conditons and greater disability.

Aside from optic neurtitis, do you know of any cases where the lesions correlate with the signs and symptoms?
Doc,
Happy to offer a possible explanation for this, just my speculation, nothing I've seen in the literature on it.

I think you are suggesting and I agree that what we are seeing on MRI is not necessarily the whole picture of what is going on.

With some imaging modes, we are probably seeing places where there BBB is injured and there is an active inflammatory state.

I would expect that there would also be relatively more damage in the CNS near these areas than farther away, but if the theory is correct that CD4+ T-cells are targeting myelin, I don't see any reason that if they cross into the CNS, they can't go almost anywhere in the CNS through the CNS circulatory system, CSF.

I know zip about this circulation, but it may also in some way be tied to the types of problems that are seen in CCSVI in which the left jugular almost always causes my flow disturbances than the right side and more issues with the left transverse sinus which sometimes isn't even there. Could the location of the problems associated with CCSVI explain the injury that occurs to the veins? I don't know. I'm not even suggesting this is the case as much as asking if it is and if so, does this help explain the geography of injury?

The other factor here may be that until fairly recently, we couldn't see lesions in gray matter so we assumed they were not there. Now that it is being examined, we are seeing both lesions and atrophy (presumably because nerves are dying) and has a much greater correlation with disability that white matter lesions which almost seem to have no relationship with disability.

Is "many" the right characterization of the number of people who show no lesions? I agree that white matter lesions tell us nothing about disability.

But, what if the process is as Prof Hayes found in her mice? A breach in the BBB allows immune cells that don't belong in the CNS to migrate there and cause damage to nerves through demyelination? Even after the BBB injury is healed, you've still got these immortal T-cells wrecking havoc because there is an insufficient amount of calcitriol to cause them to undergo programmed cell death.

RRMS then becomes a phase when there is ongoing or at least relapsing injury to the BBB which does show up nicely on MRI and SPMS and PPMS are states where the problem is solely the activity of the immune system in the CNS and the BBB is intact?

That works for me, but then there is way more about all this than my mind can get a handle on. :>)
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Re: CCSVI and CCVBP

Postby Squeakycat » Wed Oct 23, 2013 3:38 am

uprightdoc wrote:It is my contention that lesions are often a sign of what caused the problem. Dr. Schelling's theory regarding violent venous blood and CSF reflux (backjets) makes sense as a cause for the location of the supratentorial, periventricular and perivenular lesions.


That makes sense to me, but that doesn't explain damage to the nerves while the presence of CD4+ T-cells in the CNS does. I don't dispute the idea that turbulent blood flow causes damage to the BBB and that this sets of an aggressive immune response appropriate to such an injury.

To me, it fits then that some non-CNS immune cells migrate to the CNS side of the brain where they don't belong and they are what is causing the injury to the nerves, injury that only really shows up on MRI as atrophy.

I don't know enough about what is actually being seen on MRI to bet anything more than a dollar on that, however. :>)
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Re: CCSVI and CCVBP

Postby uprightdoc » Wed Oct 23, 2013 3:48 am

Squeakycat wrote:
And to a carpenter with a hammer, all problems are nails. :>)


And to a plumber, all problems are caused by leaks in the pipes.

Malformations and misalignments of the craniocervical junction, truamatic brain injuries, torn connective tissues, spondylosis, stenosis, scoliosis, Chiari malformations, tethered cords, as well as a host of other structural problems that can obstruct blood and CSF flow in the cranial vault and spinal canal, which can be demonstrated on MRI are not the consequence of calcitriol deficiency and plumbing problems.
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Re: CCSVI and CCVBP

Postby Squeakycat » Wed Oct 23, 2013 3:58 am

uprightdoc wrote:I don't see how calcitriol deficiency in CSF is related to my theory regarding the cause of neurodegenerative diseases. It does however, make a great deal of sense as a potential therapy in light of the glutamate cascade, as well as inflammation and their role in neurodegenerative processes. Among other things, excess calcium associated with the glutamate cascade leads to the formation of destructive enzymes. Calcitriol may help to restore proper calcium physiology and mitigate its potentially destructive effects.
Doc,
The deficiency of calcitriol in the CSF has no relationship to what causes a break down in the BBB. It is only relevant because you have rogue, immortal immune system cells in the CNS AND those cells are no longer capable of converting 25(OH)D3 to calcitriol which would allow them to undergo programmed cell death. They do die with Prof Hayes' high dose of calcitriol She directly measures this, it is not just a hypothesis.

Primary production of calcitriol is in the kidneys. It supplies it to the blood and in turn to the CSF.

But, because it is critical to the operation of the immune system, we have evolved to be able to make it in every cells as needed when it can't be obtained from the blood or CSF, AND there is sufficient 25(OH)D3, the main circulating form of vitamin D available.

Hayes can see amply supplies of 25(OH)D3 in the CSF but because rogue immune cells are not undergoing programmed cell death, knows that it is not being converted to calcitriol.

Adequate supplies of calcitriol would likely have a modulating effect on any problem involving calcium. Vitamin D does virtually everything it does by doing something with ionized calcium, Ca++. And since calcium is so critical to its operation, it controls the uptake of calcium in the gut and goes to great lengths to manage calcium homeostasis making sure there is just the right amount of Ca and Ca++ and that they are in the right place within cells.

Although the glutamate cascade is all about calcium, it is a part of the whole ischemic cascade which is a desired response to hypoxia. To the extent that this in fact the case because of say, impaired circulation, would you want to stop it? I have not looked at this with respect to what, if any role vitamin D plays in the cascade, but again, calcium and vitamin D are peas in a pod and you can't have one without the other, mostly so it may well have a moderating effect. Whether it does is way above my pay grade.
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Re: CCSVI and CCVBP

Postby uprightdoc » Wed Oct 23, 2013 4:08 am

Squeakycat wrote:...
Prof Hayes has in fact looked at the variation between males and females in mice and is fairly certain that this has to do with an interaction between the female steroidal hormone estradiol and vitamin D which is a steroidal hormone. I believe this is something she is hoping to be able to study further.

As far as Europeans versus Asians and Africans, I think it is fairly well substantiated that this is most likely a latitude effect and that in turn results in fewer months of the year in which vitamin D can be naturally produced in the skin. Northern Europeans with high vitamin D diet from fish don't get MS. There are several good studies showing that the prevalence of MS increases with latitude in Scotland alone and the exceptions there turn out to all be because of altitude which also has an effect on the amount of UV-B radiation available with higher altitudes having lower incidence of MS and those at sea level having much higher rates.

Similarly, people with darker skins who move to northern latitudes are in fact more susceptible to MS because their skin pigmentation requires greater sun exposure to produce the same amount of vitamin D. While not MS, there are some interesting studies in the UK of how this is resulting in higher levels of Type 1 diabetes (another disease linked to vitamin D deficiencies and even ricketts in Asian populations in the UK.

So if the problems are caused by vitamin D deficiency or more specifically, the lack of calcitriol in the CNS, then mice aren't a bad model. If you were going to try to induce MS through "structural" problems in the bones of the head and spine, then they would certainly not be a good model. Putnam used dogs for what he was sure was a problem with veins and tied off their jugulars to induce a fairly good model of MS.


I included Rickett's and Paget's disease in my forensic studies of pathological skulls. Interestingly, Paget's disease was associated with open sutures which suggests increased intracranial pressure. It seeems to me that according to the vitamen D theory then, patients with diabetes, Paget's and rickets, especially those living in northern climates who don't eat fish should have a higher incidence of MS. My sister in law is Hunan. Hunan Chinese live in northern climates and don't eat fish or beef. They eat a lot of chicken and pork. It so smoggy in Bejing that they get poor sunlight.

Scottish and other northern people eat alot of salmon and other fish and have a high incidence of MS. Eskimos don't get MS. No matter where they live. African-Americans have a very low incidence of MS. Instead they get a rare variant form of MS called Devic's disease. Asians get optic spinal MS. It is highly doubtful that the difference is due to with levels of calcitriol.

The EAE mice model is good for studying the reactions and affects of experimentally induced autoimmune-inflammatory encephalitis. Putnam's model of ligating the jugulars in dogs was good for studying the affects of obstruction to venous flow on cranial hydrodynamics. Neither study is a good model for studying MS.
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Re: CCSVI and CCVBP

Postby Squeakycat » Wed Oct 23, 2013 4:14 am

uprightdoc wrote:And to a plumber, all problems are caused by leaks in the pipes.

Malformations and misalignments of the craniocervical junction, truamatic brain injuries, torn connective tissues, spondylosis, stenosis, scoliosis, Chiari malformations, tethered cords, as well as a host of other structural problems that can obstruct blood and CSF flow in the cranial vault and spinal canal, which can be demonstrated on MRI are not the consequence of calcitriol deficiency and plumbing problems.
Doc,

Don't dispute this at all and didn't mean to suggest that calcitriol will do anything to address these problems.

I would say that to the extend that they involve bone, vitamin D had a role in the development of the problem.

To the extent they involve blood vessels, their development was managed by vitamin D.

But those are possible origins of problems that happened in utero, not something that is an active process that can be "fixed" with a shot of calcitriol.

Although I've heard that with the right dose of calcitriol, you can not only slice bread, you can toast it. :>)

What Hayes' treatment does is reset the immune system by making enough calcitriol available to get rid of rogue immune cells and return the system to its normal functional state.
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Re: CCSVI and CCVBP

Postby Squeakycat » Wed Oct 23, 2013 4:42 am

uprightdoc wrote:I included Rickett's and Paget's disease in my forensic studies of pathological skulls. Interestingly, Paget's disease was associated with open sutures which suggests increased intracranial pressure. It seems to me that according to the vitamen D theory then, patients with diabetes, Paget's and rickets, especially those living in northern climates who don't eat fish should have a higher incidence of MS. My sister in law is Hunan. Hunan Chinese live in northern climates and don't eat fish or beef. They eat a lot of chicken and pork. It so smoggy in Bejing that they get poor sunlight.

Scottish and other northern people eat alot of salmon and other fish and have a high incidence of MS. Eskimos don't get MS. No matter where they live. African-Americans have a very low incidence of MS. Instead they get a rare variant form of MS called Devic's disease. Asians get optic spinal MS. It is highly doubtful that the difference is due to with levels of calcitriol.

The EAE mice model is good for studying the reactions and affects of experimentally induced autoimmune-inflammatory encephalitis. Putnam's model of ligating the jugulars in dogs was good for studying the affects of obstruction to venous flow on cranial hydrodynamics. Neither study is a good model for studying MS.
Doc,

I think folks who know a lot more about this than I do would disagree that African-Americans (women in particular) have a very low incidence of MS:
Multiple sclerosis, long considered a disease of white females, has affected more black women in recent years, a new study finds. Hispanic and Asian women, who have previously seemed to be at less risk of MS, remain so, researchers report May 7 in Neurology. The findings bolster a theory that vitamin D deficiency, which is common in people with dark skin in northern latitudes, contributes to MS.


There have been a number of studies showing links between vitamin D related problems and diseases like diabetes which show that the origins of the problem are different, though still linked to vitamin D. In a recent study in the UK of early onset T1DM, they found that there were a string of genetic problem sin the metabolism of vitamin D that were common in the children with an inherited risk of T1DM who went on to develop it before the age of 5 and those who didn't develop it, didn't have those same genetic issues.

These same genetic variations are not found in pwMS, but it is known that there is both a birth month and latitude effect in MS that ties it to low vitamin D levels in mothers during the winter. Several Scandinavian studies show a difference in incidence at the same latitude linked solely to the quantity of fish consumption so I would think that Eskimos must be getting sufficient vitamin D in their diets and if they changed their diets would have similar incidence levels as others at the same latitude.

Interestingly, there is some research out of the Ebers group at Oxford that was investigating vitamin D and MS in some mice studies where they found that the grandchildren of grandmothers who were vitamin D deficient had vitamin D processing deficiencies similar to those found in children with early onset T1DM, but the children of these grandmothers did not have these defects. The skipped a generation.

MS incidence in Japan follows latitude with higher rates the further north. I don't have it in front of me, but I read a study that suggested the incidence of MS in China is unknown because it isn't monitored, not because it doesn't exist. I don't know that this study proves anything, but it may suggest that we really don't know the incidence and whether it follows latitude as it does in the rest of the world.

I think the literature showing birth month and latitude effect clearly ties MS to vitamin D deficiency. And the differences between diseases in which vitamin D is implicated is because the type of problem with vitamin D is different, ie, winter gestation births versus grandmothers who were D deficient during pregnance who cause an epigenetic change in the vitamin D metabolism genes in their grandchildren.

I'm not sure that the epidemiology of MS tells us much about what Hayes has found in EAE, but I do have a question for you on this.

Do you see any link between the birth month effect and the structural abnormalities that you see as linked to MS?
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Re: CCSVI and CCVBP

Postby uprightdoc » Wed Oct 23, 2013 1:10 pm

Squeakycat wrote:...The deficiency of calcitriol in the CSF has no relationship to what causes a break down in the BBB. It is only relevant because you have rogue, immortal immune system cells in the CNS AND those cells are no longer capable of converting 25(OH)D3 to calcitriol which would allow them to undergo programmed cell death. They do die with Prof Hayes' high dose of calcitriol She directly measures this, it is not just a hypothesis.


Ed,
I don't have the time to respond to all your statements or to tear into Dr. Hayes theory, nor do I want to spend alot of time on anatomy, physiology and pathology. I am not here to teach a course on neurodegenerative diseases, just to present my hypothesis and answer relevant questions. I will do my best to address the numerous controversial points you make. Regarding the statement above, I haven't seen cases or published studies showing clear evidence of rogue immune cells running amok and destroying the brain and cord, only isolated areas of degeneration, sometimes they never get worse. If the lesions continued to leak throughout life I would expect signs of increasing degeneration surrounding the lesions sites. Sometimes lesions heal and diappear with no intervention.

My theory can explain the common connections and causes seen in multiple sclerosis, Parkinson's, Alzheimer's, NPH, ALS, Huntington's disease, as well as other neurodegenerative conditions, many of which are variants of the above. It's hard to see calcitriol levels as a common cause with so many different manifestations and periods in life when these conditions show up tend to show up, as well as how they affect gender and race differently.
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Re: CCSVI and CCVBP

Postby uprightdoc » Wed Oct 23, 2013 1:28 pm

Squeakycat wrote:...Although the glutamate cascade is all about calcium, it is a part of the whole ischemic cascade which is a desired response to hypoxia. To the extent that this in fact the case because of say, impaired circulation, would you want to stop it? I have not looked at this with respect to what, if any role vitamin D plays in the cascade, but again, calcium and vitamin D are peas in a pod and you can't have one without the other, mostly so it may well have a moderating effect. Whether it does is way above my pay grade.


The glutamate cascade, which is also known as the ischemic cascade is not all about calcium. Moreover, it is not a desired response to hypoxia. It is a cascade of entirely destructive processes. The destructive enzymes formed by excess calcium is just one part of the problem. Eicosinoids, lipid peroxides and vasoconstriction are others. There is much more. It is a complicated process and there is nothing good about it. If calcitriol worked to arrest the process neurologists would be using it to treat stroke patients.

The relationship between vitamin D and calcium is pretty basic. I knew it when I was in high school. People with rickets were once treated with fresh air, sunshine and ground up egg shells.
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Re: CCSVI and CCVBP

Postby uprightdoc » Wed Oct 23, 2013 1:42 pm

Squeakycat wrote:
uprightdoc wrote:...I think folks who know a lot more about this than I do would disagree that African-Americans (women in particular) have a very low incidence of MS:
Multiple sclerosis, long considered a disease of white females, has affected more black women in recent years, a new study finds. Hispanic and Asian women, who have previously seemed to be at less risk of MS, remain so, researchers report May 7 in Neurology. The findings bolster a theory that vitamin D deficiency, which is common in people with dark skin in northern latitudes, contributes to MS.


There have been a number of studies showing links between vitamin D related problems and diseases like diabetes which show that the origins of the problem are different, though still linked to vitamin D. In a recent study in the UK of early onset T1DM, they found that there were a string of genetic problem sin the metabolism of vitamin D that were common in the children with an inherited risk of T1DM who went on to develop it before the age of 5 and those who didn't develop it, didn't have those same genetic issues.

These same genetic variations are not found in pwMS, but it is known that there is both a birth month and latitude effect in MS that ties it to low vitamin D levels in mothers during the winter. Several Scandinavian studies show a difference in incidence at the same latitude linked solely to the quantity of fish consumption so I would think that Eskimos must be getting sufficient vitamin D in their diets and if they changed their diets would have similar incidence levels as others at the same latitude.

Interestingly, there is some research out of the Ebers group at Oxford that was investigating vitamin D and MS in some mice studies where they found that the grandchildren of grandmothers who were vitamin D deficient had vitamin D processing deficiencies similar to those found in children with early onset T1DM, but the children of these grandmothers did not have these defects. The skipped a generation.

MS incidence in Japan follows latitude with higher rates the further north. I don't have it in front of me, but I read a study that suggested the incidence of MS in China is unknown because it isn't monitored, not because it doesn't exist. I don't know that this study proves anything, but it may suggest that we really don't know the incidence and whether it follows latitude as it does in the rest of the world.

I think the literature showing birth month and latitude effect clearly ties MS to vitamin D deficiency. And the differences between diseases in which vitamin D is implicated is because the type of problem with vitamin D is different, ie, winter gestation births versus grandmothers who were D deficient during pregnance who cause an epigenetic change in the vitamin D metabolism genes in their grandchildren.

I'm not sure that the epidemiology of MS tells us much about what Hayes has found in EAE, but I do have a question for you on this.

Do you see any link between the birth month effect and the structural abnormalities that you see as linked to MS?


I don't have time to address all these controversial points you make but will continue down this road a little further. I disagree that African-American women have shown a significant increase in the incidence of MS. While the incidence of MS in China needs further study, and Asians do get MS the incidence of Asians with MS living in Asia as well as western countries is still much lower than European races. I haven't looked into and fail to see any link that would cause me to regarding the birth month effect and structural abnormalities. I have enough on my plate. I will leave that one for others to look into.
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Re: CCSVI and CCVBP

Postby Squeakycat » Wed Oct 23, 2013 4:48 pm

uprightdoc wrote:I don't have time to address all these controversial points you make but will continue down this road a little further. I disagree that African-American women have shown a significant increase in the incidence of MS. While the incidence of MS in China needs further study, and Asians do get MS the incidence of Asians with MS living in Asia as well as western countries is still much lower than European races. I haven't looked into and fail to see any link that would cause me to regarding the birth month effect and structural abnormalities. I have enough on my plate. I will leave that one for others to look into.
Doc,

Appreciate this and don't want to waste your time.

But would like to explore how your theory of structurally induced neurodegeneration at least in MS is explained or not explained in light of the birth month and latitude effects which it seems to me are pretty well documented leaving out China for the moment and whether you see any relationship to vitamin D deficiency which is the conventional explanation for these factors.

I would also like to understand the theory itself in terms of whether you are saying that structure is what causes injury to blood vessels and that is what MS is? Or in your view, is MS something else that is caused by structural issues, not just damage to the plumbing?

Thanks for the time you have put into this discussion. I do understand that you have other things to do!
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