This Is MS Multiple Sclerosis Community: Knowledge & Support

[Nick]

Where Did MS Come From?

By Ashton Embry

As part of my MS literature research I have tried to answer big questions such as “what causes MS?” and “where did MS come from?”. It has always seemed to me that answers to such questions would be very helpful for developing effective therapies for both the prevention and treatment of MS. In this column I will summarize my answers to these important, yet rarely addressed, questions.

Most researchers agree that MS was probably very rare before 1800 and, previous to that time, there are only a very few records of a person having the rather distinctive symptoms and disabilities that we now label as MS. By the early 1800s MS seems to have affected enough people in France and Britain that many more records are available. By the mid part of the 19th century MS was recognized as a distinct disease and, as the population of the first world grew, MS prevalence grew with it and today it is estimated there are perhaps as many as two million people with MS.

So why did MS start to become so common about 200 years ago such that it was seen as a distinct disease? The answer to this lies in understanding the environmental factors that drive MS onset and progression and when and why such factors started to affect large parts of the population.

It is widely accepted that MS is an autoimmune disease which means the disease process is driven by one’s own immune system. Autoimmune disease involves the activation of immune cells that are sensitized to one or more self-proteins as well as the failure of the regulatory side of the immune system to suppress such potentially harmful reactions. In MS, the immune system becomes sensitized to and attacks proteins in the myelin sheath that protects the axons of the central nervous system. Such attacks on the myelin are not well controlled by immune suppression such that substantial damage often occurs and clinical symptoms become apparent. Given this understanding of the MS disease process, the obvious questions become “what environmental factors cause the activation of the myelin-sensitive immune cells?” and “which factors ensure that such attacks are not well controlled through immune suppression?”.

Research has revealed that fragments from foreign proteins derived from infectious agents and foods can activate myelin-sensitive immune cells through cross-reactions. Notably, many new foreign proteins were introduced into the human environment by the agricultural revolution, 10,000 to 5000 years ago. Such new proteins came from numerous infectious agents that crossed over to humans from domesticated animals (eg Epstein Barr virus) and from completely new food types such as dairy, grains and legumes. These new proteins had a great potential to cause autoimmune reactions because of the lack of any evolutionary experience with them.

However the introduction of these new proteins by agriculture apparently did not cause widespread MS and other autoimmune diseases because most people still had adequate immune regulation and were able to suppress any potentially harmful autoimmune reactions caused by the new proteins. Most people had adequate immune regulation because of an adequate supply of vitamin D and omega 3 EFA, established immune regulators, and also the occurrence of many chronic infections in childhood related to the unhygienic conditions of those times. Such infections result in well-educated immune system capable of optimal immune suppression.

Notably, in the early 1800s there was a substantial reduction of vitamin D supply due to the industrial revolution and there was also a major reduction in common childhood infections due to the establishment of hygienic conditions. These reductions resulted in many people no longer having an adequate capacity to suppress autoimmune reactions. This reduced suppression capacity within the population, combined with the already common presence of foreign proteins that could initiate autoimmune reactions, resulted in some of the people who were genetically susceptible to MS actually contracting it. Hence MS started to affect a large enough number of people that it was seen as a distinctive disease during this time.

The situation has gotten even worse over the last 100 years. Vitamin D intake has continued to decline due to more and more people having urban office jobs rather than outdoor, rural ones. The specter of skin cancer and the development of sunscreens have added to widespread vitamin D deficiency. Hygienic conditions have been improved such that most first world people live in an ultra-hygienic world. Children have only rare infections and consequently also have an undereducated immune system that has a greatly reduced capability for immune suppression. Finally, even omega 3 EFA intake has been greatly reduced due to a change from grass-fed domesticated animals to grain-fed ones.

In summary, the loss of immune regulation capacity over the past 200 years, in combination with the already present, cross-reactive antigens introduced earlier by agriculture, unleashed the MS monster in first world populations. This analysis leads to the insight that MS rates can be greatly reduced if first world societies either remove the problematic foreign proteins or substantially increase the immune suppression capacity of the population. It would be next to impossible to remove most of the foreign proteins so the obvious solution is to boost immune suppression capacity. Ensuring that all children receive adequate vitamin D and omega 3 EFA can readily do this and such a strategy would likely reduce MS to a very rare disease. For those with MS, the obvious strategies are to both remove the potentially cross-reactive food proteins and to boost immune regulation capacity through supplements of vitamin D and omega 3 EFA.


Cheers
Nick

[LisaBee]

Hi Nick,

I've been giving the MS causation a lot of thought and have been following Ashton Embry's ideas. There are a couple of things I would contend with, one being that I don't know if improved hygiene really caught on until the latter 1900s, but maybe I'm wrong. Improved hygiene certainly was the culprit in the rise of polio epidemics through the early to mid 20th century, since in a cleaner world babies became less likely to encounter the polio virus while they were still breast-feeding and getting immunity from their mothers.

Since MS isn't all that common, and the symptoms are so variable among people with it, and it didn't generate epidemics, that it took a certain level of scientific sophistication to even spot and categorize it as an entity and then have a journal to report the results in. It might have been around a lot longer.

Given the assumption it did emerge, It is possible a new (and still unknown) infectious agent came along at about that time, perhaps a virus to which a certain segment of the population had an atypical response, producing MS. A virologist with insight into the historical emergence of disease might have some interesting thoughts. We have AIDS now, and that wasn't around earlier. The smallpox vaccine using cowpox got started in the late 1700s, but I don't know how widespread smallpox vaccination became.

I'm not an expert in diet history, but I wonder what dietary changes were localized around late 1700s early 1800s. People had been eating wheat, dairy etc for a long long time by then but maybe not larger quantities of refined sugar and maybe salt, I think those became more common at that time, but could be wrong. There may have been other diet shifts. I'm curious about European livestock practices - when in Europe did grain feeding animals become common practice? In the US, it wasn't until the 20th century, probably, that feedlots really got started, but maybe with space constraints in Europe it was sooner.

Vitamin D exposure probably did begin to drop in Europe in the early 1800s, with more people starting to work indoors in factories and getting less D.

There was the Faroe Island outbreak - apparently people in the Faroes didn't have MS until WWII or later, when soldiers came, and MS started showing up in the islanders. I've read that it could have been infection or diet changes, but reviews have been conflicting.

It's interesting stuff to go back historically. I'm amazed that the current research doesn't seem to get any closer to an answer after all this time.

Lisa

[Nick]

Hi Lisa

Thank you for your thought provoking comments. In particular, I would like to discuss a topic you've mentioned and one that is rather popular on this board. I am referring to a viral and bacterial cause of MS.

I find it credible that these antigens can and do play a role in MS but I contend they are not the main instigators of MS related autoimmunity.

Most prominently, why is there no recorded instance of MS contraction from one person with MS to a spouse? If it were transmissible than I would think this phenomena would be common. I can't fathom the notion that a virus would be contagious to only certain people or in which, as you put it, only applies to a certain segment of the population that had an atypical response, thus producing MS.

This would entail a new type of virus or bacteria which would have as a major trait, a self-limiting ability to replicate via specific contamination. This to me is not in a virus' best interest and would severely limit a life form's main goal, that being reproduction.

Its seems to me that a promotion of a yet-to be identified super virus or bacteria completely foreign to most life on earth smacks of trying to fit the solution to appeal to the MS community's collectively bruised ego rather than to fit the epidemiology of the disease. Just because decades of failed research hasn't identified the cause doesn't mean one needs to invoke an impossible to identify villain. See the Purloined Letter by EA Poe for a literary analogy.

Anyway, that's my take on the issue.

Cheers
Nick

[bromley]

Diet is a factor in many diseases and the UK (and I assume elsewhere) is experiencing an epidemic in disease such as diabetes (where obesity plays a role). However, I'm not convinced that it is the only factor in a disease such as MS. The US has the highest proportion of obese people in the world (Europe is catching up), but not every coke drinking, burger eating American is falling down with MS. I think there must be other factors:

- Viruses / bacteria are still a big unknown. The Antegren debacle showed that viruses such as JC lie dormant in the brain and can reactivate. EBV is also a good candidate for a trigger for MS.

- Vitamin D might be a factor but as I've noted before - is MS higher in nuns? And given that X million Brits take holidays to sunny places (often more than once a year) - the position on Vit D must be better than smog ridden London of 150 years ago.

- The biggies to me are car pollution and pesticides. I was born in the mid-60s and very few families down our road had cars. By the late 80's pretty much every household has a car and most two. There are 28 million cars in the UK. Every road is full of cars and kids walk to school breathing in the fumes. Urbanisation has been the big change over the last 150 years followed by car use. For those in the country, pesticides have increased in use to make farms more productive.

- The other dietary factor has got to be aspartamine which, I'm convinced, will be shown to be detrimental to health.

My conclusion - diet may play a role, but so do genes, viruses / bacteria, vit D, car pollution, pesticides, hormones etc etc. This could turn out to be many different diseases caused by a combination of different factors. This disease is, therefore, a researchers dream come true.

Bromley

[Nick]

Hi Bromley

Indeed genetics is the overwhelming determinant in MS. Once an individual is predisposed then it is a matter of environmental influence. For an environmental factor to be considered causal though, it must fit the pattern (epidemiology) of MS. Given that MS is autoimmune, the big question as to cause is what activates the immune system to attack self tissue in the CNS. Almost all researchers agree that the immune system is activated against self in the periphery, that is in the blood outside of the CNS. Furthermore the source of the activation almost assuredly must be a foreign protein.

Importantly the identical twin data convincingly shows that, in high prevalence areas, only about 50-60% of individuals (5 of 8 identical twins) who are genetically capable of getting MS, actually contract the disease. Thus almost half the people in high prevalence areas who are "genetically programmed" for MS don't get it. In low prevalence areas it would seem that less than 10% of susceptible individuals have MS. This demonstrates that there is at least one dominant environmental factor which results in a genetically susceptible individual being afflicted with MS. These are very important constraints on interpreting the environmental factor which can be regarded as the "ultimate cause of MS". It must be so common that it occurs over much of the world but it has to be very specific such that only half or less of susceptible people are affected by it. Furthermore this environmental factor must be much more prevalent or effective in certain areas of the world.

In summary an acceptable interpretation of the environmental factor, which plays a critical role in the onset and progression of MS, must explain the following constraining data.

1. It must be found throughout the world but be specific enough to affect only half or less of the susceptible individuals.
2. It must affect immigrant children more than it does immigrant adults. On the other hand it must affect susceptible identical twins mainly when they are adults rather than when they are children.
3. It must be much more common or effective in northwestern Europe, Canada, United States, Australia and New Zealand than in the rest of the world.
4. It must be more common or effective in higher latitude areas so as to create a pronounced north/south gradient of MS prevalence.
5. It must have enough variation so as to create significant MS prevalence and incidence differences within ethnically homogeneous populations over relatively short distances.
6. In Hawaii it must adversely affect those of Japanese origin whereas at the same time have a positive effect on Caucasians.
7. It must be transportable so as to explain the sudden increase in MS prevalence in the Faroes following British troop occupation during World War II.
8. It cannot be transmitted by either person to person contact or by a blood transfusion.
9. It must be increasingly more widespread and effective over the last 100 years.

The infectious causes seem to be the most commonly quoted explanation for the environmental factor. The reason for this appears to emanate from an a priori assumption that unexplained diseases are caused by an infectious agent with viruses preferred over bacteria due to their "difficult to detect" nature. The constraints listed above indicate that it is highly unlikely that either a specific virus or bacteria which infects the CNS is responsible for MS. The main reasons for rejecting a specific infectious agent are:

1. The constraints show that MS is not transmitted either person to person or through a blood transfusion.
2. The significant variation in MS prevalence and incidence in ethnically homogeneous populations over relatively small areas is hard to reconcile with a specific infectious cause of MS.
3. No physical evidence of a specific MS virus or bacteria has ever been found in the CNS of persons with MS despite a very long and concerted effort to find such material (Poser, 1993).

Of the transported, non-infectious factors, heavy metals, industrial pollution and sanitation can also be rejected. The most convincing constraint for this conclusion again is the greatly increased prevalence of MS for Japanese living in Hawaii versus Japan where these factors are much more common than in Hawaii. The Faroe Islands data, as well as the much higher prevalence of MS on the Canadian Prairies than in the highly industrialized area of southern Ontario, also are not compatible with these factors.

This leaves us with one remaining factor which is DIET. Diet is certainly not a new interpretation for the key environmental factor responsible for MS although it tends to be arbitrarily dismissed by numerous authors. However a close reading of the arguments against diet leads to the conclusion that diet has not been rejected on scientific grounds, but rather on rhetorical ones (e.g. Sibley, 1992) . Statements like "diet has not been proven to affect the disease (McIlroy, pers. comm., 1993)" and "no controlled scientific study has proven without doubt that the course of MS can be modified by dietary changes (Girard, pers. comm., 1991)" are commonly quoted but, in effect, add nothing to the question of the role of diet. Such statements really mean "we have no idea if diet plays a role in MS". Notably no sound scientific argument has ever been presented against the possible effects of diet. For this analysis, diet in the light of the nine constraints detailed earlier fits all nine constraints and thus is most likely the main environmental factor which is the prime cause of MS.

Cheers
Nick

[bromley]

Nick thanks,

We'll have to agree to disagree. I think diet plays a role but I don't think it's the primary cause (although it wouldn't surprise me if they did prove that diet fizzy drinks trigger the process by screwing up the chemistry of the brain).

I'm still not convinced by the auto-immune argument i.e. the body attacking itself for no good reason. The immune system gets involved but it may be a reaction to something - the underlying disease process which has already started. We blame the immune system but perhaps it's doing what it is meant to - attacking death / disease. The myelin / nerves may be already dying off and the immune sytem is trying to help but makes things worse!

The best neuro I saw said that auto-immune diseases are diseases where the virus has yet to be identified [and bacteria]. He also noted that almost every sufferer he sees has had a run in with EBV.

EBV (or some other virus or bacteria) which infects those with the wrong genes, at the wrong time in life, remains dormant, and then starts this disease off at a later stage is my best bet. It would explain some of the so called outbreaks and, maybe, those families where there is many cases. George Ebers reported recently that one Canadian family had 14 members with MS. These individuals must have had the susceptibility gene so what triggered the disease? A virus to me would be a better explanation than the fact that they all ate too many cheese burgers or pizzas.

Bromley

[BioDocFL]

Why wasn't MS seen more in the past? Perhaps it has been there, we just haven't recognized it until the last 100-200 years.
Recognizing it as a separate disease is still difficult. Think how much harder that would be with the state of medical literature of 200 years ago not having published much if anything to define MS. How would a doctor know that he/she is seeing something separate from other established diseases? I still think we should bear in mind that the situation of MS suddenly appearing in an area may coincide with the arrival of a doctor who can recognize it as MS, i.e. better diagnosis. That could be an alternate explanation or an additional explanation for the sudden appearance. Since MRIs are used so much to make evaluations, did they have MRIs before in that area? Probably not.
Also MS was probably misdiagnosed more often than being recognized as something that had not been defined before. As an example of that problem, look at lupus in the early 20th century before it was recognized widely as a separate disease. Lupus can give a false positive result on a test for syphillis. That could really be a humiliating misdiagnosis.
If you look at how medicine is practiced in some countries still, that may reflect how it was handled in our country (US) in the past. For example, in some countries, the doctor does not tell the patient the problem (stomach cancer may be defined as an 'ulcer'). Perhaps the doctor would tell the family so they could make any decisions. Some tradition-based cultures hold the doctors in such high esteem that they don't dare question this approach. The patient then may not even know their own personal medical history very well.
Also, look at the life span of 200 years ago versus today. Since MS typically becomes a problem later than other diseases (measles, polio, whooping cough, etc.) and is not usually as sudden and obvious an attack as small pox, yellow fever, TB, or malaria, MS may have not become so obvious in a population when the average life span was only 40 years.
And something I always come back to: how do you explain the female/male ratio from an environmental agent or a viral or bacterial agent? I'm not saying there can't be a bias from an agent, I just want to hear how the bias would occur.

Wesley

[LisaBee]

Wow, I had planned to respond earlier but had to work and there has been a lot of thoughts put out in the interim. So I'll take my own shot in the dark.

Working across the posts:

I agree with BioDocFL that one of the reasons that MS may not not have been seen more in the past was that it may not have been readily recognizable, and with the limitations of reporting and publishing case reports in the medical literature, it may be no surprise that MS didn't get "discovered" until the 1800s. Or, it may be possible that MS actually did become more common due the emergence of a risk factor, whether diet, infectious, or some other factor. It is difficult to say.

There are both genetic susceptibilities and environmental triggers that are needed - the twin studies show that. The genetics of MS does not indicate that if one has a certain genetic makeup, one is guaranteed to get the disease, but conversely, being an identical twin of an MS case puts one at greatly increase of MS compared to the population in general.

I also agree with Nick that with the evidence available, I don't think MS is necessarily due to the emergence of "special" infectious agent because MS doesn't appear to be transmissible in that sense. I didn't mean to imply that that MSers are infected with a unique organism. It could be due to an infectious agent that is relatively common in the population, but to which certain people with a genetic susceptibility have an atypical or more severe reaction to that results in MS. That agent may have been with humanity from the outset, or it may have emerged later. I don't know. I brought up AIDS as an example of a disease that is emerging in the human population only to show new diseases do emerge. I thought about another disease called neurobrucellosis, which has some interesting parallels to MS. I read somewhere that 5 percent of people infected with the brucellosis can develop neurobrucellosis, and it got me thinking about what factors may make 5 percent of people infected with an organism develop a neurological complication. What is it about those 5 percent? Do they have a more severe infection at the outset? Or do they have some susceptibility that sets them up for a neurological complication (including demyelination) to their illness? In other words, what makes neurobrucellosis cases occur as an uncommon complication of brucellosis? I don't know if anyone has looked into that, but it might provide some insight into MS.

In response to what BioDoc said about short life spans and MS not showing up against the backdrop of all the infectious illnesses and epidemics of the past, a random thought I had is that MSers might actually be survivors of a particular viral or bacterial illness, particularly in childhood, that in the past might have killed most people infected with it, and that MSers might have some susceptibility to developing a long term complication from that illness. I remember reading that back in the 1700s, getting visited by a physician was like the kiss of death, the standard treatment was to bleed sick people and make them vomit, which, regardless of their illness, was not really conducive to recovery. Nursemaids in the French aristocracy actually hid sick children from doctors, a scary thought. In the 1800s the standard of medical care began to change. In the early 1900s in the pre-antibiotic era, the standard of care was very supportive, with encouraging rest, fresh air, sunshine, and improved nutrition. My guess is that people, particularly children, began to survive certain illnesses in greater numbers than was seen in previous eras, and maybe MS started to show up in them as they got older. I'm totally guessing here.

As to BioDoc's question on the gender imbalance of MS incidence, I'll take a shot. Women could be more susceptible to developing MS due to hormonal differences directly related to sex hormone differences. However, one big enviromental confounder is that women, as a whole, may get less sunlight exposure and have lower Vitamin D levels than men, and girls get less than boys. There are cultural reasons for this, as well as differences in occupational trades - my guess is that men predominante in the current occupational trades that primarily work outdoors much of the day, Construction, utility repair, road construction crews, etc. are heavily male-dominated trades. My guess is that boys traditionally spent more time outdoors, playing sports, etc. although in the last few years I don't know if this is still true. If it is no longer true, it may be that MS incidence between the genders will approach parity. There have been some recent studies from the Middle East in which MS is more prevalent in women than in men, and in those societies differences in occupation, clothing, and outdoor exposure are more marked than in the US or Europe. I remember reading a recent Vitamin D report from Iran in which it was shown that Vitamin D deficiency based on 25-OD levels was more prevalent in girls (95%) than in boys= (45%) but even in boys was quite high. (Moussavi et al. 2005) I thought the numbers were alarming, but reports of Vitamin D deficiencies are cropping all over the world, even in places where people are presumed to have high sun exposure.

Lisa

[Nick]

Hey bromley

I think we agree on more than what you are willing to admit. I believe you are confused with the nature of autoimmunity. It is not the body attacking itself for no good reason. Through the process of molecular mimicry the immune system targets a perceived antigen and all other similar proteins in the body. It just so happens that certain novel food proteins from gluten (gliadin), dairy and legumes closely resemble self tissue. This process has been well identified in celiac disease & type 1 diabetes and I contend that MS shares the same disease process.

The Guggenmos et al study is exactly the evidence expected to be found in molecular mimicry (i.e. cross reactivity between antibodies to CNS tissue and a milk protein).

Unfortunately the tremendous significance of this research has gone unnoticed by the MS community and certainly this board's members. I feel that a response of 34% is quite remarkable because it was an observation of the response to only one of the hundreds of proteins found in dairy. Consider too that the study did not incorporate the other food proteins (e.g. gluten, legumes) known to have the capacity to precipitate autoimmunity.

Writing of which, it is well recognized that gluten and a hypersensitivity to it, are the cause of celiac disease. How can you disregard the association between an AI disease and a physiological response to a food protein in light of celiac disease? Worse yet, how can the best neuro you've seen state that auto-immune diseases are diseases where the virus has yet to be identified.

I would view this utterance, in light of celiac disease, as gross incompetence.

Further to a virus, a researcher recently found a very specific antibody in the spinal fluid of a number of PwMS. This antibody was found to be reactive with both a protein in myelin AND Epstein Barr virus. The odds of such an occurrence being by chance are astronomic. Thus we can feel relatively confident that MS is an autoimmune disease caused by molecular mimicry between myelin proteins and foreign proteins.

I believe this occurrence of an infection with one or more childhood illnesses(e.g. Epstein-Barr,HHV-6) which results in an autoimmune reaction against tissue in the CNS by molecular mimicry. Such autoimmune reactions are suppressed before any demyelination occurs. However memory cells against the infectious agent are produced and such memory cells can be seen as an autoimmune time bomb because they are also potentially autoaggressive.

MS does not occur as a result of a one time infection though. Repeated exposure to the causal element, in the absence of protective factors is required. Dietary proteins are the constant which provides this source.
How do you reconcile a bacterial/ viral cause with the Hawaii paradox? The cause must adversely affect those of Japanese origin whereas at the same time have a positive effect on Caucasians.

As for your comment about Ebbers, yes, I do agree with genetic susceptibility as a necessary component to MS but a family is most often chronically exposed to the same lifestyle influences as diet and vitamin D deficiency. You'll note Ebbers is an advocate of vitamin D playing a significant role in MS.

Please see my comments to his research posted at the ThisIsMS site
here.

BioDoc

Some of your comments ring true with respect to longevity and signs of MS. Consider though, Type 1 diabetes. It has been shown to have an identical disease process to MS aside from the self tissue which is targeted by the immune system. In diabetes the GAD proteins on the pancreas are targeted, thus impairing insulin production. Because there are so many fewer GAD proteins than CNS cells, it takes far fewer attacks on the pancreatic tissue than the CNS tissue to produce noticeable symptoms. Hence the alias of Type 1 diabetes being juvenile diabetes. It takes effect much sooner in life.

Were you aware that consumption of 2,000 IU per day vitamin D resulted in an 80% risk reduction of Type 1 diabetes in a study out of Finland?

I agree with Lisa on the exposure of females and males to sunshine. There's also the hormone card too, and the rounded hips and breasts and ………sigh.

Cheers
Nick

[kitkat2]

Nick,
Dare I ask about your opinion on the ax protocols? After all the compelling info regarding the supposed role of Vit D deficiency in ms, I wonder why my entire family[8 sibs] does not share my fate?
I am the only teetotaller in my extended family, and have never enjoyed coffee. It was always milk or water/juices for me.
I don't get it?

[nps999]

thanks nick...
my 2 cents on the topic a compromised BBB as a result of mercury usage.
symtoms were visible in crude gold production...before used as dental
amalgum. no such thing as autoimmune compleat and utter nonsence.
nps

[heyjude]

NPS touched on a subject I also found significant - Mercury. Prior to my diagnosis, I had been researching potential causes for trigeminal neuralgia. One thing led to another and eventually I crossed information regarding the mercury/MS link.

The more I researched, the more things started adding up. My doctor had been helping me deal with symptoms for quite some time. I just thought I was having an unusually difficult time with the change of life. We actually came in the back door when it came to MS. My MRI was to further investigate the source of the facial pain. When the neurologist ordered the spinal, I wasn't completely surprised to be diagnosed with MS. The symptoms had been there all along; we just didn't make the connection. In the meantime, I'd been suspicious of a rather large amalgam filling (50% mercury) since leaving the military in 99, which has only recently been removed.

I understand the ADA actually splintered over the use of amalgam in fillings in the early 1900s. Amalgams are a mixture of approximately 50% mercury (a known poison) and copper, silver, gold etc. Dentists who vocally express suspicions of mercury are pooh-poohed in the dental community. Still, a significant number of dentists are quietly removing amalgams and replacing them with bio-friendly materials at the customer's request. There's quite a big controversy over the subject. I read the Netherlands have banned the use of mercury in dentistry, but can't confirm whether this is true or not. Certainly another point to ponder...

Any thoughts?:wink:

[Nick]

Nick,
Dare I ask about your opinion on the ax protocols? After all the compelling info regarding the supposed role of Vit D deficiency in ms, I wonder why my entire family[8 sibs] does not share my fate?
I am the only teetotaller in my extended family, and have never enjoyed coffee. It was always milk or water/juices for me.
I don't get it?

Miss Kitty

Unless you were all genetically identical, I would suspect genetic variations are to account for you being the lucky stiff. Perhaps they have an other auoimmune disorder.

I would also speculate that drinking milk was/is your achilles heel. There are heaps of evidence implicating a hypersensitivity to milk as being a key component of the MS disease process in some individuals.

If you have an active bacterial infection and or a candida overgrowth then abx should help you out. However I don't think extended use is warranted for MS. Ensure you are getting plenty of acidophillus to keep you intestinal flora robust, ESPECIALLY when taking abx.

Cheers
Nick

[LisaBee]

Yeah, I've been wondering about the amalgam and mercury angle, having had a head full of it from age 10-12 until just a few years ago, when all my fillings started to fail and I had them replaced with the new white stuff, quadrant by quadrant. The thing is, the early MS-related symptoms I had were happening at the same time I had filling failures, a root canal, and some early stage periodontal problems.

Now, this all may have been totally a coincidence, except the big flare I had that put me a neurologist followed a couple of months after discovery of a major abscess in one of my back teeth (previously fixed with the new stuff) that required three rounds of antibiotics and a root canal. The tooth itself was okay, something got in around the gum and attacked the root. I've since wondered if MSers are more prone to have problems with their teeth and gums, and it may be this correlation is the important one, rather than the number of mercury fillings per se, as the fillings may just be a measure of an underlying problem.

There is a paper out there that shows, at least in the animal EAE model, the bacteria P. gingivalis (one of the main periodontal pathogens) exacerbates the EAE. There are also papers that show in humans, inflammatory cytokines in the blood are increased following dental procedures as a result of the transient bacteremia. Although there is no clinical study of periodontal problems and MS, one could argue that having a big bacterial load in the mouth and gum inflammation might be more of a detriment for MSers than the general population (although it is probably not good for anybody). It has made me much more vigilant about my teeth.

Lisa

[Nick]

One thing led to another and eventually I crossed information regarding the mercury/MS link.
Any thoughts?:wink:

Hey Jude, don't be a fool...

I think the relationship between MS and mercury is speculative at best. Certainly there are instances of neurological symptoms of mercury poisoning but the distinct epidemiology demonstrated by MS cannot, in my and others opinion, be satisfied by a reaction to mercury.

The most convincing constraint for this conclusion is the greatly increased prevalence of MS for Japanese living in Hawaii versus Japan where these factors are either the same or are much more common than in Hawaii. The Faroe Islands data, as well as the much higher prevalence of MS on the Canadian Prairies than in the highly industrialized area of southern Ontario, also are not compatible with these factors.

Cheers
Nick