SIGNIFICANCE(?) OF THE FAROE ISLANDS

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Postby BioDocFL » Wed Aug 26, 2009 6:35 am

Along the lines of birds being involved, I remember hearing of a sudden increase in MS diagnoses on one of the Florida key islands when a new water reservoir was built. One possible cause mentioned was migratory birds using the water reservoir.
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Embry's take on an infectious agent as THE cause

Postby Nick » Fri Aug 28, 2009 12:41 pm

The following are excerpts from Ashton Embry’s article entitled Multiple Sclerosis and Food Hypersensitivities found here. It addresses very well the probability of an infectious agent being the cause of MS.

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One of the most interesting and widely quoted epidemiological studies of MS is that of the greatly increased prevalence of MS in the Faroe Islands (North Atlantic, west of Norway) following the occupation by 1500-2000 British troops between 1941 and 1944 (Kurtzke, 1977, 1980, 1995). Kurtzke has classified this increase as an epidemic although other authors have challenged this view (Benedikz et al., 1994, Poser et al. 1988). Regardless, there can be no doubt that MS prevalence substantially increased in the Faroes following the British occupation. Furthermore, the relationship between MS in the Faroe islanders and the presence of British soldiers is strongly supported by the fact the cases of MS all occurred in islanders who lived close to British bases (Kurtzke, 1980, fig. 15). This is an extremely important constraint because it demonstrates that the environmental factor is not solely indigenous and can transported from one area to another. Any interpretation of the cause of MS must satisfactorily explain the sudden increased prevalence in the Faroes and the mobility of the environmental factor.

Recently another very important epidemiological study was published by Ebers et al. (1995). These authors were able to demonstrate that children, who were raised in families in which non-blood relatives (step parents, step brothers and sisters, adoptees, etc.) had MS, had no increased risk of MS. This provided good evidence of the genetic factor in MS but more importantly demonstrated that MS is not transmitted by person to person contact. An earlier study which involved spouses of persons with MS also demonstrated this.

Another important piece of evidence for determining MS cause is the fact that there is no recorded case of MS having been transmitted to another person through a blood transfusion (Theofilopoulos, 1995a).
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).

Before leaving this topic it is important to note that the main evidence which is usually quoted by those advocating a specific viral cause of MS is the greatly increased incidence of MS in the Faroes following British troop occupation. The standard interpretation of these data follows Kurtzke (1977) and is that some of the British troops were infected with the MS virus and that they subsequently infected the Faroe islanders. At first glance such an interpretation seems plausible but a more penetrating analysis of the data, coupled with other constraints, makes the viral hypothesis of the Faroes increased prevalence very unlikely.

First of all, there were less than 2000 British troops in the Faroes and, given the 90/100,000 prevalence of MS in Britain, there were, at best, 2 troops with MS. Furthermore, given that any soldier exhibiting neurological disease would have likely been sent home, it is highly unlikely that there were enough troops to infect the islanders. Kurtzke (1995) has countered this argument by claiming that many people may be carriers of the MS virus but not have the disease themselves. There is certainly no evidence of such a phenomenon and Kurtzke's speculation is unsupportable.

Furthermore, as has been mentioned previously, there is no increased prevalence of MS in children with step brothers and sisters with MS or in individuals whose spouse has MS. These data clearly indicate that a specific viral cause of MS is highly unlikely and that any suggestion that one or two British troops transmitted a MS virus to the Faroe islanders is entirely unsupportable.

With the rejection of the Faroe Islands evidence for a viral cause, the interpretation of a specific virus being the main environmental factor which results in MS does not appear to be tenable. This conclusion was also reached by Poser (1993) who stated "the constant failure to confirm the role of a specific organism in the pathogenesis of MS has raised grave doubts about its existence".

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Postby BioDocFL » Fri Aug 28, 2009 12:56 pm

I would think that the British soldiers built new water systems and reservoirs that could have attracted migratory birds. Another possibility is that the water systems were dug into soil that had heavy metals. In other words, there could have been changes to the environment that introduced more risk without the soldiers having to be direct carriers of an infectious agent.

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Re: Embry's take on an infectious agent as THE cause

Postby notasperfectasyou » Fri Aug 28, 2009 1:08 pm

Ashton Embry’s article entitled Multiple Sclerosis and Food Hypersensitivities wrote:The various proposed environmental causes of MS can be tested against the epidemiological data base to see if they are compatible with the various constraints. All but one of the proposed causes,including a specific infectious agent (virus, bacteria) and common infectious agents (e.g. influenza virus), can be eliminated due to various incompatibilities with the established data. The only environmental factor which reasonably fits all the epidemiological constraints is diet.

There's a lot of references to that webpage, but none in the above paragraph. It's beyond comprehension how the author concludes that MS is caused by diet.

When I put up a post that says there is linkage to bacterial pathology in MS, I can back that up with peer reviewed articles.

Ken
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Postby Nick » Fri Aug 28, 2009 4:16 pm

Hi Ken

The paragragh you quote refers to the the nine constraining aspects of MS that were in my original post. These are unassailable facts of MS and Ashton's diet hypothesis honors these.

To suspect diet is not such an inconceivable proposal IMO. Certainly you're aware of another well know AI disease (Celiac) that is caused by a hypersensitivity to gluten (gliadin) in predisposed individuals.

If you are sweet on the bacterial cause, can you honestly say it satisfies all nine constraints?

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Postby Lyon » Fri Aug 28, 2009 6:38 pm

:lol: In this regard I feel a little like the bastards I work with who like to spread rumors and then sit back and be entertained by what happens after.

I started this thread so that I could sit back with interest to see what others think, but now that Nick has raised the issue, I've always appreciated Ashton's
Nick wrote:nine constraining aspects of MS
from a "loss of evolutionary normal" perspective and want to take my "crack" at it.

I don't present this with the presumption on my part that every sensible person should embrace it as "fact" but I do present it as an interesting and alternative for intelligent people to ponder.
Keep in mind that 150 years of disappointing MS research results point towards the need for factors requiring a different way of seeing things.

1. It must be found throughout the world but be specific enough to affect only half or less of the susceptible individuals.
The loss of the parasites commonly considered to have shared evolution with us is unique to the "developed" populations, which experienced the alarming increase in inflammatory immune dysfunctions, while those parasites continue to plague the "undeveloped" populations, which retain their historic low rates of incidence of inflammatory immune dysfunctions.

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.
While it doesn't necessarily constitute conclusive evidence, it's especially interesting that both the MS researchers and the "hygiene hypothesis" researchers separately and unknowing used different information to come to very similar conclusions. Most striking is that the age of 14/15 is an important turning point.

Hygiene hypothesis researchers came to the conclusion that experiencing "evolutionary normal" conditions to age 14/15 resulted in an immune system capable of behaving appropriately through adulthood, even in the absence of continued parasitism.

Independently by assimilating the available data, MS researchers came to the conclusion that someone migrating from an area of low MS incidence (which also are areas of high parasitism) to an area of high MS incidence after the age of 14/15 retains the lower risk of incidence, while someone migrating from low incidence to high incidence area before the age of 14/15 (NOT meeting minimal "evolutionary normal" requirement) will experience the higher risk of MS incidence, while people of any age migrating from an area of high MS incidence risk to an area of low MS incidence will retain the original high risk of MS incidence (people from "modern" populations go to great lengths to continue a civilized lifestyle, even when transferred to an "undeveloped" area. In other words, regardless of where we go, we insure that we retain sterile food and water and clean toilet habits).

On the other hand it must affect susceptible identical twins mainly when they are adults rather than when they are children.
It might not seem kosher for me to pick and choose what I do and don't want to answer but that one seems to fallen out of the sky and isn't a valid question. MS affects so few people that it's always been hard recruiting the necessary numbers to do valid studies. MS/Twin studies involve such low numbers that their results are below consideration. The attempt to reverse those results and arrive at reasonable conclusion is counter productive.

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.
As with anything in life, it's all a matter of perception. I honestly find it painful that possibly/probably the biggest failing in MS research was the early conclusions drawn from the "MS gradient of geographic incidence". That led researchers to the early (and continuing) conviction that because people living farther from the equator were lighter and more affected by MS that lighter skinned people must have a genetic predisposition to MS. In hindsight it's entirely possible and more likely that light skinned people who live farther from the equator were the "go getters" behind the industrial revolution which led to the creation and our being able to bankroll the world's first "developed" populations and lifestyles, part of which involved electricity, well water, flush toilets, sterile food and refrigerators to extend the life of food.

Another way of putting it is that, maybe there isn't a person on earth who doesn't have the "genetic predisposition to MS" when we are separated from the evolutionary normal conditions which was part of our evolutionary history/requirements.

4. It must be more common or effective in higher latitude areas so as to create a pronounced north/south gradient of MS prevalence.
Similarly, although a complicated situation, not only is it harder for parasites to survive in the harsh Northern climes but that is also where the "developed" lifestyle originated and increased.

5. It must have enough variation so as to create significant MS prevalence and incidence differences within ethnically homogeneous populations over relatively short distances.
Hygiene hypothesis is complicated but also very interesting. As mentioned earlier, higher latitudes make it increasingly hard for parasites to survive but it's also become obvious that the MS "exceptions to the rules" invariably involve "undeveloped" populations living in proximity to "developed" populations. Almost invariably involving aboriginal populations who live in closer quarters than "developed" populations, which is a necessity for continued parasite life cycle in hostile climes. Additionally aboriginal populations traditionally eat more wildlife and seafood (highly parasitized-zoonotic) and don't have what we would consider sanitary means of storing their food. In other words, the obvious difference between these genetically similar and latitudinally similar populations is their NOT sharing the "developed" lifestyle.

6. In Hawaii it must adversely affect those of Japanese origin whereas at the same time have a positive effect on Caucasians.
I wish we had better info on what studies Ashton used to arrive at this conclusion but what has long been obvious in my studies is that MS incidence is a continually evolving situation. Despite that, people aren't hesitant to compare study results from the 40's with results from the 80's etc....which leads to absolutely impertinent conclusions and I think that is what is going on here.

I think Ashton derived this from two studies, one regarding people from California having higher MS incidence than those in Hawaii and another showing that people from Japan experienced higher MS incidence in Hawaii. Both studies are too old for me to easily acquire. Truth be told, in the not too distant past (as late as the 1960's) it would have been correct to consider large parts of Hawaii as living under "undeveloped" conditions, but considering that MS information is totally derived from averages it really depends on the point in time in which the Hawaii averages were compared to the Japan averages in regards to which was more "developed" and had the higher MS rate at that particular point in time.

Another way of putting it is that both Japan and Hawaii lagged far behind the mainland US in meeting "developed" conditions and it's not hard to believe that at varying times Japan and Hawaii were neck and neck in their degree (percentage of population) of "development".

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.
Among the biggest reasons that the Hygiene Hypothesis/Loss of Evolutionary Normal Conditions is slow to be accepted is that it's not only complicated but it's the reverse of what everyone is looking for. Ashton didn't word it in a way that is easy to respond to but rather than the British bringing something with them to the Faroes it's possible, and I say likely/certain that the British presence changed the Faroese lifestyle/diet which eliminated their previously evolutionary normal lifestyle/living conditions.

8. It cannot be transmitted by either person to person contact or by a blood transfusion.
With the Hygiene Hypothesis/Loss of Evolutionary Normal Conditions in mind it's obvious that you can't transmit the absence of something via contact or a transfusion.

9. It must be increasingly more widespread and effective over the last 100 years.
"Developed" conditions and what it entails is more widespread and complete over the last 100 years. Regardless of a person's beliefs as to what "caused" the increasing MS incidence, that is a very good point because as we notice an increasingly global economy, the "MS gradient of geographic incidence" becomes more and more faint to the point that now some people attempt to make the argument that our strongest clue to the cause(s) never really existed at all.
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Postby notasperfectasyou » Fri Aug 28, 2009 9:01 pm

Nick wrote:Hi Ken

The paragragh you quote refers to the the nine constraining aspects of MS that were in my original post. These are unassailable facts of MS and Ashton's diet hypothesis honors these.

To suspect diet is not such an inconceivable proposal IMO. Certainly you're aware of another well know AI disease (Celiac) that is caused by a hypersensitivity to gluten (gliadin) in predisposed individuals.

If you are sweet on the bacterial cause, can you honestly say it satisfies all nine constraints?

Cheers
Nick



Nick,
Like most articles that begin with the assumption that autoimmune theory is a requirement upon which the rest of the article is hinged, this article makes at least one critical assumption that I do not agree with and that is that MS is has a single cause.

So I disagree with the implied premise that a single cause must meet all nine criteria. In my writing, I do not tell people that MS is caused by bacteria. Nor to peer reviewed articles in the Journal of Neurology begin with the statement that MS is an autoimmune disease.

I'm certainly open to diet having an impact. I'm open to vascular abnormality being a key pathology. Heck, I'm even open to the tilted bed idea. But, for now, today, I'll say that Faroe does, in a simple and non-complicated way that doesn't require an hour to explain, link in with CPn infection quite well enough for me.

Respectfully agreeing to disagree, Ken
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Postby notasperfectasyou » Fri Aug 28, 2009 9:07 pm

Lyon,
You win. It's like the soft shell crabs that I can only stand to eat about twice a year. The words "Hygiene" and "hypothesis" being so close together causes some sort of inponderable loop in my head. (think Lewis Black and read that again). It keeps looping and looping and then it explodes and there's ear wax everywhere.
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Postby Lyon » Fri Aug 28, 2009 9:27 pm

notasperfectasyou wrote: The words "Hygiene" and "hypothesis" being so close together causes some sort of inponderable loop in my head. It keeps looping and looping and then it explodes and there's ear wax everywhere.
http://www.youtube.com/watch?v=HY-03vYYAjA Maybe things aren't quite that bad Ken. Just consider that human evolution dictates that you evolved not to be able to digest your food and survive without the aid of the bacteria in your gut.

Just as simply, but maybe not so obviously we evolved with parasites controlling aspects of our immune system. The beginning of our becoming "developed" in the late 1800's created the first instance in human history in which those parasites weren't able to adapt to the degree necessary to survive in our "developed" lifestyle. That time coincidentally?? matched the same populations and point in time with the beginning of the rise of inflammatory immune dysfunctions.

As mentioned, to each his own but it's something to consider and anyone wondering where my sick, sick mind lies.....that's it!
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Postby Terry » Sat Aug 29, 2009 6:01 am

Okay, how about Barium.

http://www.purdeyenvironment.com/barium%20MS.pdf

Can't copy and paste, so look at paragraph starting at line 168. Then 371.
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Postby lyndacarol » Sat Aug 29, 2009 7:41 am

Lyon --I read your postings with interest; but as you know, I subscribe to an insulin hypothesis rather than the hygiene hypothesis. When you write:
rather than the British bringing something with them to the Faroes it's possible, and I say likely/certain that the British presence changed the Faroese lifestyle/diet

I can wholeheartedly agree (because I am thinking a change in diet -- increased carbohydrates -- leads to increased insulin secretion).
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Postby Lyon » Sat Aug 29, 2009 8:05 am

lyndacarol wrote:
Lyon wrote:rather than the British bringing something with them to the Faroes it's possible, and I say likely/certain that the British presence changed the Faroese lifestyle/diet

I can wholeheartedly agree (because I am thinking a change in diet -- increased carbohydrates -- leads to increased insulin secretion).
You might find some of Ashton's information interesting then.

Despite the fact that the Faroese don't fit the mindset what most of us would call "natives" because they are light skinned whites, their original diet consisted largely of fulmers (sea birds) and sea food, both of which are largely parasitized and their method of food storage was drying, which doesn't do much of anything to eliminate parasites and their eggs.

That all seemed to fit my needs well but it remains to be seen how the changing Faroese diet would have affected insulin levels, although it's obvious that the British presence had an effect on the Faroese diet because they are still infatuated with British food.

This is kind of an interesting 1989 article I found in my bookmarks this morning http://findarticles.com/p/articles/mi_m ... i_8197281/
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Postby Nick » Sat Aug 29, 2009 11:26 am

Bob
Lyon wrote::lol: In this regard I feel a little like the bastards I work with who like to spread rumors and then sit back and be entertained by what happens after.


Your workplace sounds interesting ;-)

I do like to ponder about such possible causes and admittedly the causal antigen theory is tempting so I couldn’t resist contributing my two cents to your original baited post. I believe that for very few individuals the cause of their MS is attributable to an intestinal antigen. Just as food proteins resembles self tissue and offers the immune system of a predisposed person a target that resembles self tissue so too can an intestinal bacteria or viral antigen serve as a mimic to self tissue and thus confound the immune system.

Lyon wrote:while people of any age migrating from an area of high MS incidence risk to an area of low MS incidence will retain the original high risk of MS incidence (people from "modern" populations go to great lengths to continue a civilized lifestyle, even when transferred to an "undeveloped" area. In other words, regardless of where we go, we insure that we retain sterile food and water and clean toilet habits).


This pattern is not so. MS prevalence in Irish and English migrants to Australia display a remarkable gradient from north to south. Those that settled in the Hobart region had roughly the same high prevalence as their homeland ancestors. Those that wound up in Queensland had eighty percent less MS than the mother country. While this gradient doesn’t endorse the diet protein cause, it doesn’t disprove it either. According to the hygiene theory then folks in Queensland must be a whole lot more unsanitary than those in Tasmania.

It is however a ringing endorsement for how the influence of vitamin D can trump the cause of food proteins. The regulatory influence vitamin D has on the autoimmune process has been well documented. The parasite/bacteria/viral cause has to reconcile vitamin D and this is where such a purported cause falls short.

Not only that but then you have to reconcile the well remarkable similarity of type 1 diabetes to MS. Taking this further, a p/b/v cause has to address how Banwell et al demonstrated that diabetics and MS’ers had antibodies to their respective targeted organs, pancreatic and MOG respectively, AND how the antibodies were cross reactive to eachother as well as cow milk proteins. Though into the mix the over representation of MS and type 1 diabetes in celiac sufferers and you now have a major conspiracy theory that is needed to account for a whole raft of AI conditions caused by the all so elusive p/b/v culprit. Not only that but you have to then disprove celiac disease as being autoimmune in addition to not being caused by a hypersensitivity to gluten. Good luck with that mate.

On the other hand it must affect susceptible identical twins mainly when they are adults rather than when they are children. It might not seem kosher for me to pick and choose what I do and don't want to answer but that one seems to fallen out of the sky and isn't a valid question. MS affects so few people that it's always been hard recruiting the necessary numbers to do valid studies. MS/Twin studies involve such low numbers that their results are below consideration.


Granted the number of identical twins, one of which is with MS is rare, but it provides for excellent insights into the role of genetic influence and an environmental factor. If you dismiss the twins data as not statistically worthy of consideration I believe you’re cherry picking here Bob because there were less than 2000 British troops in the Faroes and, given the 90/100,000 prevalence of MS in Britain, there were, at best, 2 troops with MS. Furthermore, given that any soldier exhibiting neurological disease would have likely been sent home, it is highly unlikely that there were enough troops to infect the islanders.

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Postby Lyon » Sat Aug 29, 2009 1:03 pm

Hi Nick,
Minimally, this thread has been a learning experience. EyeDoc mentioned a little cluster in the Keys so I looked up that and other purported MS "clusters" and it seems that most "clusters" end up being MS incidence within statistical probability or don't end up being MS at all and I started questioning whether the Faroes really involves MS clusters but Dr Kurtzke is a WAY better statician than I am and goes to great lengths to insure that the cases really are MS.

Nick wrote: there were less than 2000 British troops in the Faroes and, given the 90/100,000 prevalence of MS in Britain, there were, at best, 2 troops with MS. Furthermore, given that any soldier exhibiting neurological disease would have likely been sent home, it is highly unlikely that there were enough troops to infect the islanders.

I agree that there probably would have been darned few infected British to spread an "unidentified" infection, although my contention is that the British presence didn't spread anything more than well water, choice of food and refrigeration among the Faroese.
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Postby Nick » Sat Aug 29, 2009 2:17 pm

Lyon wrote:I agree that there probably would have been darned few infected British to spread an "unidentified" infection, although my contention is that the British presence didn't spread anything more than well water, choice of food and refrigeration among the Faroese.


Gotcha.
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