Vit D3>125nmol/L (50ng/ml) in blood. Goal for pwMS

[Squeakycat]

Seems very easy to assume when the blinkers are on, or when the past dialogue is the only source of input to brain storming.

Nigel,
I think it is suggested that one aim first and then shoot, not the other way around. :>)

I have only read this abstract, not the article, so I don't know the answers to your questions, but I think this marks considerable progress in that it notes that:

The assumption of a primary immunopathogenesis of the disease is seriously flawed and has failed to deliver an effective therapy for most patients . . . The primary pathology of multiple sclerosis is a process of neurodegeneration based on the integrity of the blood-brain barrier.

If the primary pathology of MS is a breakdown of the blood brain barrier, then the cause can be viral, bacterial, or problems with veins or some combination of these, NOT the immune system gone crazy and attacking the brain.

More relevant to the discussion here, vitamin D is the regulatory hormone which takes the leading role in maintaining the integrity of the blood brain barrier so whatever the prime mover in the process, if the problem is the breakdown of the BBB and vitamin D manages the integrity of the BBB, this is a useful paper for looking at MS in a new way.

[Squeakycat]

Ed I have seen articles that suggest that Vit D levels are responsible for the triggering of apoptosis and with that in mind these other findings in MS would require very thorough testing for bacterial involvement imo. It could be a classic assumption that Vit D is having an 'MS' effect when it is actually having an effect on a bacterial load instead.

Nigel,
Vitamin D is in fact the hormone that regulates apoptosis as a part of the cell replacement cycle. As I understand it, vitD is relatively agnostic. If something has gone wrong which requires a cell to be replaced, vitD initiates that process.

It doesn't matter what causes the cell to be defective: virus, bacteria, physical injury, genetic error. If it needs to be replaced, then that process is controlled by vitD.

This is one of many normal functions of vitD.

I'm not sure what you are suggesting. That the bacteria are responsible for apoptosis?

They could be responsible for the cell being defective, but the process of apoptosis is initiated by vitD.

[NZer1]

Thanks Ed,
A study I have always wanted to see would be with Vit D supplementing instead of using steroids.

And another study would be the assessment of body temperatures (infection clues) before and after a relapse.

The difference between RRMS and PPMS is where the Vit D theories get thin. To relapse and associate that with Vit D is a stretch and to consider Vit D levels in PPMS again is indicating that there is more likely an involvement of a pathogen and that Vit D has various effects on the life cycle of the pathogen plus the hosts ability to activate the immune system against infection, whether that be a low grade long term infection or a rapid infection such as EBV.

The other aspect that is interesting is how the timing of peoples latitude moves occurs and the development of the immune system and also the accumulation of infectious diseases and reactions to them. If the infections have the ability to modify the immune system such as what happens in Lyme and CPn where macrophages are desensitized to the pathogen and a slow low grade infection process occurs which includes other pathogens also, now that the immune system is deactivated. The biofilms that are building in the system can hide and protect the pathogen from testing and treatments.
When Vit D is involved the VDR system and the pathogen may have and often has modified the apoptosis of the host cells so that Vit D is not able to trigger processes for the immune system and the apoptosis system.
Bit confusing, my mind is fog personified and it may not be clear to folks who haven't followed my site for clues on the research into this line of thought over time.
https://www.facebook.com/pages/CCSVI-in ... 1636357984


Nigel

[NZer1]

Ed I have seen articles that suggest that Vit D levels are responsible for the triggering of apoptosis and with that in mind these other findings in MS would require very thorough testing for bacterial involvement imo. It could be a classic assumption that Vit D is having an 'MS' effect when it is actually having an effect on a bacterial load instead.

Nigel,
Vitamin D is in fact the hormone that regulates apoptosis as a part of the cell replacement cycle. As I understand it, vitD is relatively agnostic. If something has gone wrong which requires a cell to be replaced, vitD initiates that process.

It doesn't matter what causes the cell to be defective: virus, bacteria, physical injury, genetic error. If it needs to be replaced, then that process is controlled by vitD.

This is one of many normal functions of vitD.

I'm not sure what you are suggesting. That the bacteria are responsible for apoptosis?

They could be responsible for the cell being defective, but the process of apoptosis is initiated by vitD.

Ed,
bacteria such as CPn can halt host cell apoptosis even with mild/good Vit D levels. Apoptosis is 'stopped' by the bacteria modifying the host cells DNA.
The protection of self by the bacteria keeping the host cell alive beyond it's life cycle timing means that the bacteria is feed by the ATP from the host indefinitely.
The bacteria live only from the ATP of the host.
Only 'very high' dose Vit D supplementing can have an effect and sometimes it is no effect on resetting host apoptosis.
Bacteria have evolved far faster and further than immune cells.


Nigel

[Squeakycat]

All I get from that is there is a relationship between vitamin d levels and relapse. Is there a perfect range? Can too high cause relapse? Is the vitamin d level related to fluctuating nature of ms or is ms related to fluctuating nature of vitamin d? Did you buy the paper?

Have not bought the paper yet.

Part of the answer to your question can be found here.

This is just the first page of the article, but it provides more information on their conclusion, but in a format that I can't copy.

[Squeakycat]

Thanks Ed,
A study I have always wanted to see would be with Vit D supplementing instead of using steroids.

Nigel,

Me too, with the addition of calcitriol which was found to be more effective than steroids.

I don't know why any neuro wouldn't want to give this a try if the patient asked. VitD3 is an over the counter medicine and calcitriol has been in widespread use in chronic kidney disease for over 20 years so the risks are both well known and very manageable.

It would be an easy trial to conduct since the whole point of steroids is to provide immediate relief from a relapse. You would know quite quickly whether vitD plus calcitriol was working or not.

Further, there is considerable evidence that steroids have no long term beneficial effect on MS so it seems tempting to try something that might not only bring a relapse to an end, but potentially have longer term positive benefit.

Perhaps we can persuade Professor Hutchinson to run a trial. :>)

But even without a trial, I would think that many neuros would be open to trying this if asked by their patients.

[NZer1]

Ed,
if the BBB is breached by CCSVI or the BBB/capillary beds are weaken by infections such as CPn and the CPn and any other bacteria cross into the WM and GM then there is a problem.
If the immune system has been modified by an infection such as CPn and deactivated from being alerted to certain pathogens in a biofilm then 'Houston we have a problem'.
The cascade of disease dx possibilities is 'HUGE'!
The ability of stealth bacteria and biofilms to hide and be undetectable to the immune system and to the medical system testing then we have an unknown cause and no tools to detect the pathways of such actions, imo.
Paul Thibault's paper on CPn involvement in CCSVI http://koti.mbnet.fi/hiihoo/ccsvi/thiba ... tkimus.pdf and the work of Stratton and also Wheldon http://davidwheldon.co.uk/ms-treatment.html have put together a very strong case and when the additional information on biofilm capabilities is added then it is hard not to believe, imo.

So after reading the data regarding the thought above, Vit D is definitely a factor in MS that needs to be monitored and using sunlight and diet and also if necessary supplements you 'may' improve symptoms but I doubt it is a key player in the incidence of MS.


Nigel

[Squeakycat]

And another study would be the assessment of body temperatures (infection clues) before and after a relapse.

Nigel,
That could be organized right here since it is simply information gathering. No drugs or prescriptions required.

If the infection is in an inactive phase, this wouldn't tell us very much, but it might be useful to see whether a relapse is a sign of an active infection.

You can organize that here. :>)

[Squeakycat]

The difference between RRMS and PPMS is where the Vit D theories get thin. To relapse and associate that with Vit D is a stretch and to consider Vit D levels in PPMS again is indicating that there is more likely an involvement of a pathogen and that Vit D has various effects on the life cycle of the pathogen plus the hosts ability to activate the immune system against infection, whether that be a low grade long term infection or a rapid infection such as EBV.

Nigel,
Not entirely sure I follow your point here.

The above study is suggesting that relapses in RRMS are brought on by the effects of steroids of which VitD is one. I don't think the author is suggesting that vitamin D levels a cause of relapses, high levels of low levels.

What I find useful is that he is noting that the root problem is the breakdown of the BBB. The root cause of that is not addressed. It could be low levels of vitD. It could be bacterial or viral. It could be the result of turbulent blood flow, all things that could cause a breakdown in the BBB or limit the body's ability to deal with a breakdown. What's important, at least to me, is that vitD as manager of the integrity of blood vessels is centrally implicated in the pathology.

Rather than speculating about the role of vitD on a pathogen, we know that if there is inadequate vitD, the body will not be able to repair damage to the BBB, whatever causes it: virus, bacteria, fungus, or mechanical damage from turbulent blood flow.

[grandsons4]

Having heretofore not heard of "Dawson’s fingers," I naturally had to research it, and just as naturally went off on a tangent. The tangent took me to causes of demyelination lesions, and specifically to those caused by focal compression. In a study with sheep (I know, sheep aren’t people), with compression, SEPs (electrical signals) were obliterated in all animals and failed to recover after 3 1/2 h following injury, irrespective of the duration of compression. These results show that reperfusion of the cord following a compressive insult is not accompanied with recovery of SEPs. Reperfusion injury is the tissue damage caused when blood supply returns to the tissue after a period of ischemia or lack of oxygen. The absence of oxygen and nutrients from blood during the ischemic period creates a condition in which the restoration of circulation results in inflammation and oxidative damage through the induction of oxidative stress rather than restoration of normal function. The inflammatory response is partially responsible for the damage of reperfusion injury. White blood cells, carried to the area by the newly returning blood, release a host of inflammatory factors such as interleukins as well as free radicals in response to tissue damage.
In Squeakycat’s post, the authors state, “The primary pathology of multiple sclerosis is a process of neurodegeneration based on the integrity of the blood-brain barrier.” My question to any with pertinent knowledge; If trauma to the spinal cord results in inflammation and oxidative damage through the induction of oxidative stress, can these “inflammatory factors” travel the spinal cord into the brain? P.S. My son has what was alternately described as a disk herniation and a disk protrusion at T4.

[Squeakycat]

bacteria such as CPn can halt host cell apoptosis even with mild/good Vit D levels. Apoptosis is 'stopped' by the bacteria modifying the host cells DNA.
The protection of self by the bacteria keeping the host cell alive beyond it's life cycle timing means that the bacteria is feed by the ATP from the host indefinitely.
The bacteria live only from the ATP of the host.
Only 'very high' dose Vit D supplementing can have an effect and sometimes it is no effect on resetting host apoptosis.
Bacteria have evolved far faster and further than immune cells.

Nigel,
I'll accept for the sake of argument that CPn disrupts apoptosis.

How does that cause the symptoms of MS? Does CPn live happily within the immortal cell, or does it damage the blood brain barrier?

What is it doing that causes damage?

[Squeakycat]

My question to any with pertinent knowledge; If trauma to the spinal cord results in inflammation and oxidative damage through the induction of oxidative stress, can these “inflammatory factors” travel the spinal cord into the brain? P.S. My son has what was alternately described as a disk herniation and a disk protrusion at T4.

Grandsons4,
I do not have pertinent knowledge, but I can talk about the general subject of oxidative stress in MS.

If in fact, MS is the result of a breakdown in the blood brain barrier, vitD will set off an immune system response to that which involves the generation of reactive oxygen species (ROS) which is one of the ways the body cleans up damaged cells. This is typically a local response, but I can't see any reason that if this occurred in the spine, that it might not "spread" elsewhere in the brain via cerebrolspinal fluid.

The theory of MS that makes most sense to me is that it is the result of a breakdown of the blood brain barrier caused by any number of factors: low levels of vitamin D which prevents efficient maintenance of the BBB in the event of damage; bacterial infection of the BBB, viral infection of the BBB, or damage to the BBB from turbulent blood flow associated with CCSVI. And, it makes sense that it could also be caused by specific injury to the brain or spinal cord.

Not sure if that answers your question, but its the limit of my understanding of these things.

[Squeakycat]

The other aspect that is interesting is how the timing of peoples latitude moves occurs and the development of the immune system and also the accumulation of infectious diseases and reactions to them. If the infections have the ability to modify the immune system such as what happens in Lyme and CPn where macrophages are desensitized to the pathogen and a slow low grade infection process occurs which includes other pathogens also, now that the immune system is deactivated. The biofilms that are building in the system can hide and protect the pathogen from testing and treatments.
When Vit D is involved the VDR system and the pathogen may have and often has modified the apoptosis of the host cells so that Vit D is not able to trigger processes for the immune system and the apoptosis system.

Nigel,
My understanding of the way vitD manages the cell replacement cycle is that it sets off the process by expressing a gene (in the case of skin cells, but not necessarily all cells, the gene is ATP2C1). This expresses a protein that is a calcium (and manganese) receptor. Calcium enters the Golgi apparatus where it binds with a form of ATP and then makes its way to the cell nucleus where it tells the cell to divide.

When the cell divides, vitamin D expresses other genes to activate the immune system components needed to rid the body of the old cell.

All this gets started when the regulatory hormone vitamin D detects that the cell has been injured or is in some way defective. Probably because of some chemical imbalance such as too much or too little calcium or phosphorous, or the ionized forms which are isolated getting into places within the cell where they don't belong.

The process of cleaning up internal defects or pathogens is similar. A gene is expressed. It creates a protein that does something, usually involving causing something like calcium to bind with something else.

So there are lots of opportunities for a pathogen to disrupt some part of these complicated processes. For example, when calcium enters the Golgi apparatus as a part of the cell replacement cycle, the pathogen might be able to bind to the calcium rather than having it bind to the phosphorous in the ATP.

All well and good. Entirely plausible, even if unproven.

Biofilms are external to the cell, but you are suggesting that the bacteria lives within the cell. What's that all about? Different phases in the life cycle of the bacteria?

Rather than "desensitizing" the immune system, if a bacteria were able to disrupt the cell replication cycle, the immune system components necessary to remove the old cell would simply never be activated. The bacteria wouldn't need to modify the immune system, just block cell replication since that would effectively turn off the immune response to a defective cell.

All very interesting, but again, I don't see where this plays a role in disrupting the blood brain barrier which I think has to be at the heart of what is going on in MS.

Care to elaborate?

[Squeakycat]

Ed,
if the BBB is breached by CCSVI or the BBB/capillary beds are weaken by infections such as CPn and the CPn and any other bacteria cross into the WM and GM then there is a problem.
If the immune system has been modified by an infection such as CPn and deactivated from being alerted to certain pathogens in a biofilm then 'Houston we have a problem'.
The cascade of disease dx possibilities is 'HUGE'!
The ability of stealth bacteria and biofilms to hide and be undetectable to the immune system and to the medical system testing then we have an unknown cause and no tools to detect the pathways of such actions, imo.

So after reading the data regarding the thought above, Vit D is definitely a factor in MS that needs to be monitored and using sunlight and diet and also if necessary supplements you 'may' improve symptoms but I doubt it is a key player in the incidence of MS.

Nigel,
I buy this, partially.

We know the immune system is very active in MS so it doesn't fall together that CPn is shutting down the immune system.

I can accept the notion that the BBB could be damaged by a bacterial infection. Why not?

It might block the action of vitamin D in repairing this damage at least as far as the cell replacement cycle.

But it doesn't make sense that it is shutting down the immune system in MS when we know full well that it is very active.

As far as whether vitD is central in MS, I would argue that if, as seems logical, MS is the result of a breakdown in the BBB, then vitD is very central since its role is to maintain the integrity of the BBB.

That doesn't mean that something like CPn might not block vitD in carrying out its function, but it is still central in the sense that it has been unable to do its job.

[NZer1]

Ed,
sorry I used the wrong term shutting down.
The bacteria such as CPn are able to adapt into their DNA sections with host cell DNA to enable them to alter their identity so they are seen as self or non threatening and they are able to alter the DNA of the host cells such as cytokine and macrophage cells once they have established entering the cells.
So they have made themselves immune to the immune detection as well as making the immune cells dysfunctional to a degree.

The immune cells are still very active and when there is natural CPn die off or induced die off from diet such as herbs or from some other form, like stress or antibiotics, that causes the endo toxins as the CPn cells die and are recycled by the immune cells normal clean up process around the body, the immune system becomes activated but not against CPn directly, rather against the toxins and then the cytokine over response and over production of cytokines gives the symptomatic issues seen in many 'auto-immune' type diseases.

The vascular involvement of bacterial infections in endothelial cells is common as the endothelial cells have easy access and prime food supply (ATP). By weakening the endothelial cells and also creating infections they can establish biofilms and collect other bacteria for their protection and dispersion.

There are other knowns with some bacteria like CPn such as they are not oxygen dependant or iron dependant. They use magnesium in their cycle and when we are often low on magnesium it can be a clue and it adds to the lack of magnesium in our diets and the symptoms causes which are hand in glove with 'MS' and 'autoimmune' type symptoms. The imbalances created in the CPn use of some other minerals and nutrients by both using up ATP and creating by products in host cells, gives the immune system and Western Medicine false clues and enables a stealth bacteria to mildly continue a 'low grade infection' for decades.

The fluctuations in symptoms and disease flairs and progression induced by stealth bacterial infections are related to the changes in host environment due to things such as diet, exercise, stresses and general health which are compounded because of the low level of general health and responses from the stressed immune system and over producing cytokine cell volume. The immune system is essentially in full gear all the type and not finding the target.

** Regarding CCSVI it is common to find CPn and CCSVI. Which comes first or second is indistinguishable. The two are symbiotic in a way and the opportunistic co-infections are clouding the picture as well. Diseases such as Lyme, mycoplasma's and Borrelia or any of the Stealth Bacteria are also implicated in the symptom group of causes that create the outcome of a dx 'MS' at a stage in the development of symptoms and that may be related more because of the biofilm status rather than being a factor in CCSVI directly. The other co-factors in 'MS' such as injury and spinal alignment are also main factors in MS occurring and progressing through CCSVI breaches of the BBB. There are probably 3 main 'causes' required to develop a dx of MS and other multiples required for dx's such as Fibro, Alzhiemer's and Parkinson's and so on. **

CPn is commonly found in blood vessel plaques in atherosclerosis and some believe it is the primary cause for that disease. It is another place that the bacterial stealth methods make it very difficult to determine the cause or effect processing of the infection leading to Heart diseases and Strokes in that group of outcomes.

These findings have just begun crossing the Medical Specialists awareness because patients are doing lots of Internet searching and communication in the same way that CCSVI awareness has become available because of the Internet and Social Groups.

I think that because Neuro's are 'lazy' when they assess a patient and are not skilled in the way a Psyhio's or Chiro's such as Dr Flanagan are, the dx of neuro-degenerative diseases and 'auto-immune diseases have become purely a 'money spinner' by stealth of the Drug Manufacturers and their lobby groups. imo

First day of spring down here today, or MS treatment by UV,
;)
Nigel