><p>MS - PROBABLE CAUSE AND BEST-BET TREATMENT 
by Ashton F. Embry, Ph.D. 
INTRODUCTION 

Last year my 18 year old son was diagnosed with MS with confirmation coming a month later with a MRI scan. Since that time I have been reading books, symposium volumes and journal articles on various aspects of this disease. For the past 28 years I have been a geological research scientist and this has served me well for analyzing the voluminous data and many interpretations and speculations for MS found in the literature. In geology I have dealt mainly with large, multifactorial problems (e.g. origin of the Arctic Ocean, geological history of the Canadian Arctic over a 200 million year time span) for which varied and mainly circumstantial evidence is available. I have spent much of my career synthesizing large, diverse and sometimes conflicting data sets into hypotheses and theories of earth history. In geology we are never absolutely sure we have the 'right' answer but we never shy away from making an interpretation. For this we choose the simplest hypothesis which fits the data. This hypothesis becomes the accepted right answer ('truth') until a better (simpler) hypothesis is proposed or new data require a modification or outright rejection of the currently accepted answer. I have provided this background because a geologist's approach to finding an answer to a large, multifactorial problem such as MS differs significantly from that of the medical scientist. In medical research there seems to be only a '100% sure interpretation' or a 'don't know' approach. 

I have written this essay to share with you some of my main findings and, more importantly, what my conclusions are regarding the probable cause of MS and how one can best fight back against the disease. I emphasize this is my best interpretation given all the data I have found and it is open to revision or rejection when more data are obtained. 

WHAT IS MS? 

There is solid evidence that MS is an autoimmune disease and is characterized by inflammation of the central nervous system due to the action of the immune system (van Oosten et al., 1995). It would appear that activated immune system cells cross the brain-blood barrier and attack one or more proteins associated with the myelin sheaths. This results in eventual loss of myelin, a degradation of nerve transmissions and a multitude of disabilities. The most important question concerning MS is 'what causes one's own immune system to malfunction such that it attacks the myelin proteins in the CNS'. 

CONSTRAINTS ON INTERPRETATIONS OF THE CAUSE OF IMMUNE SYSTEM MALFUNCTION 

There are two different aspects to a possible cause of a malfunction of the immune system. One is a genetic cause and the other is an environmental cause. The importance of both of these factors can be understood when one considers the research which has been done on identical twins. Current data from Europe and North America, which are both high risk areas for MS, indicate that, for identical twins with MS, about 25% of such twins both have MS (Ebers et al., 1986; Mumford et al., 1994). This compares with only 2% of affected fraternal twins both having MS (Ebers et al., 1986). Thus there is no doubt that there is a genetic factor in MS and it is likely that only genetically susceptible individuals have the possibility of getting the disease. Not much more can be said about the genetic factor and all we can do is accept the fact that it exists. 

Importantly the twin data also convincingly show 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 '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. 

Another important facet of MS research has been the investigation into the timing of the action of the environmental factor on the individual. Immigration data have been used to elucidate this question (Alter et al., 1966; Dean and Kurtze, 1971). It has been determined that adult immigrants retain the risk factor of their country of origin whereas their children tend towards the risk factor of the country they have immigrated to. This has been interpreted to indicate that the environmental factor only affects an individual before puberty (approx. age 15). 

The data on identical twins also provide insight into the question of timing. Twins share essentially the same environment until they leave home (16-21). Thus, the fact that only 25% of identical twins both have MS, is good evidence for the interpretation that the environmental factor comes into play mainly after age 18. Thus we have an apparent paradox. Immigration data indicate the environmental factor acts before age 15 whereas identical twin data indicate that it acts mainly after age 18. Any interpreted cause of MS must explain this paradox. 

Another area of research which yields important constraints for interpretation is epidemiology which deals with the global variance in MS prevalence and incidence. As alluded to earlier the world can be divided into a high prevalence (risk) area which encompasses Europe, Canada, United States, Australia and New Zealand and a low prevalence (risk) area which encompasses the rest of the world (Kurtze, 1980). In the high risk area prevalences between 50 and 100 per hundred thousand people are common. In the low risk areas MS prevalences are an order of magnitude less (Kurtze, 1980). This distribution is in part due to the genetic factor because all the high risk areas are dominantly populated by individuals of European origin (Poser, 1994). However, the environmental factor is also responsible for the occurrence of these two very different risk regions. One line of evidence for this is the fact that blacks in United States have a far higher rate of MS than do blacks in Africa even after genetics are factored in (Poser, 1994). Immigration data also confirm the role of the environmental factor in this regard. For example immigrants to London, U.K. from areas of low risk (e.g. West Indies) have a low prevalence but their British-born children have the same high prevalence as British caucasians (Elian et al., 1990). An interpretation of the environmental factor must take into account these two different risk areas with the factor being much more common or active in the high risk area. 

Crucial data for constraining the nature of the environmental factor come from prevalences for both those of Japanese and Caucasian descent in Hawaii. Those of Japanese descent have a prevalence of 6.5 which is over three times that of Japan (2.1) (Kuroiwa et al., 1983; Alter et al., 1971). Conversely the Caucasians who were born and raised in Hawaii have a prevalence of 10.5 which is only one third that of the Caucasians of California (29.9) (Poser, 1994). Thus we have another paradox concerning the environmental factor. In Hawaii it acts such that it adversely affects those of Japanese descent whereas at the very same time it has a very beneficial effect on Caucasians. This puzzling paradox must be regarded as a critical constraint for an objective interpretation of the environmental factor. 

MS also shows large differences in prevalence within some individual countries in the high risk area. For example in Norway MS is up to five times more common in the inland farming areas than in the relatively nearby coastal fishing areas (Alter, 1977). In this case genetics has no bearing on this distribution and the environmental factor must be primarily responsible for such a drastic difference. These macro and micro differences of MS prevalence in the world must be explained by any interpretation of the environmental factor. 

Another aspect of MS is its common presentation as relapsing-remitting disease. Once again any interpretation of the environmental cause should be compatible with this aspect of MS. 

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 somehow directly or indirectly affect the immune system so as to result in harmful malfunction. 

2. It must be found throughout the world but be specific enough to affect only half or less of the susceptible individuals. 

3. 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. 

4. 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.

5. In Hawaii it must adversely affect those of Japanese origin whereas at the same time have a positive effect on Caucasians.

6. It must have enough variation so as to create significant MS prevalence differences within relatively small regions. 

7. Its action must vary in time so as to result in a relapsing-remitting character for the disease in many instances. 

THE BEST INTERPRETATION FOR THE ENVIRONMENTAL FACTOR WHICH CAUSES IMMUNE SYSTEM MALFUNCTION AND MYELIN DESTRUCTION 

The constraints listed above greatly limit the possible interpretations for the environmental factor. These constraints have been known for at least 20 years but the vast majority of medical researchers have either not considered the question of what the environmental factor is or have simply said they don't know what it is. Those who have been bold enough to offer an interpretation have tentatively suggested that an unknown and unidentified 'MS virus' may be the environmental factor. I considered this interpretation very closely because it does satisfy some of the constraints (e.g. the relapsing-remitting character of MS). However I have rejected this interpretation for the following reasons. 

1. It does not explain the paradox of the immigration data and the identical twin data. Clearly the concept of a viral agent acting early in life, and predisposing a susceptible individual to MS, is negated by the data for MS concordance in identical twins. 

2. The opposing effects of the environmental factor on Japanese and Caucasians of Hawaii clearly indicate the factor is not a virus. 

3. Data on MS prevalence in close, non-blood relatives of MS patients (spouses, step- brothers, etc.) show that these individuals do not have a increased risk of MS despite long and close contact with MS patients (McIlroy, pers. comm., 1995). 

4. The significant regional variation in MS prevalence in Norway is not compatible with a viral cause of MS. 

5. No physical evidence of a specific MS virus has even been found in MS patients despite a very long and concerted effort to find such material. 

With the current data base, the interpretation of a virus being the main environmental factor which results in MS does not appear to be tenable. However, as will be discussed later, common viruses (e.g. flu) likely have a role in MS exacerbations. 

Other possible environmental factors which have been mentioned in the literature include sunlight, altitude, temperature, microwave radiation, cosmic radiation, heavy metals, bacteria, and diet. With the exception of diet all of these can be rejected as the simplest and best interpretation because they are not compatible with many of the seven constraints. 

Diet is certainly not a new interpretation for the key environmental factor responsible for MS and has been 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 little sound scientific argument is ever presented against the possible effects of diet. Possible reasons for this approach will be explored later. 

Unlike the medical researchers who rejected diet out of hand rather than by scientific logic, I have looked at diet in the light of the seven constraints detailed earlier. I have found that diet fits all seven constraints and thus I currently believe the main environmental factor which is the prime cause of MS indeed is diet. As described below the evidence in favour of diet is all circumstantial but, until controlled scientific experiments are done to confirm or deny this interpretation, it must be regarded as the best interpretation. In regard to the seven constraints: 

1. Diet can readily affect the immune system through the ingestion of allergenic foods. By definition all allergenic foods cause an immune response. It is not unreasonable to think that daily irritation of the immune system over tens of years could eventually result in a malfunction of the system. A possible pathogenesis would involve the ingestion of a specific allergen which results in an immune response. Specific helper or killer T-cells are activated against a specific allergenic protein which happens to have a molecular structure very similar to a protein in the CNS (molecular mimicry). The activated T-cells then also have the potential to attack the CNS proteins. In most cases the brain-blood barrier remains intact and/or enough T-suppressor cells are activated to offset the action of the T-helper/killer cells so that no damage occurs in the CNS. The daily ingestion of the allergens eventually 'wears down' the immune system and in some instances not enough T-suppressor cells are activated. This results in a relatively high concentration of the T-helper/killer cells and they are able to pass through the brain-blood barrier and to inflame the CNS through their action against the 'allergenic' protein. Furthermore high intake of saturated fats has been related to an increase of the permeability of the blood vessels and a consequent increase in the chance of a breach of the brain-blood barrier (Swank and Dugan, 1987). 

2. Diet is obviously found throughout the world and it is specific enough to an individual to result in MS affecting only a proportion of genetically susceptible individuals. 

3. Diet also provides a reasonable explanation of the immigrant/twin paradox. Adults who immigrate have a strong tendency to maintain the diet of their homeland whereas their children are far more likely to consume more of the food of the country they live in (especially once they have left home). This results in a change of dietary habits and a consequent change of MS risk in the children but not the adults. Twins tend to have very similar diets when they live together at home but their dietary habits potentially diverge after they leave home and live apart. Furthermore identical twins can have separate food allergies especially when they are older. Thus dietary changes (and MS risk change) would occur in twins mainly after age 18. 

4. The overall diets of the high prevalence areas have certain features in common including high dairy, gluten and saturated fat consumptions. These are all much higher than in the low prevalence areas. The great differences in diet between the high prevalence areas and the low prevalence areas can readily account for the occurrence of two very different risk areas in the world. It would appear that the foods consumed in high prevalence areas (e.g. dairy, gluten, high saturated fat) are more effective in causing MS. 

5. Most importantly diet explains the paradox of the adversely affected Hawaiians of Japanese ancestry and the beneficially affected Hawaiians of Caucasian descent. Notably one of the world's experts on MS, Dr. Charles Poser of Harvard University, could only characterize these documented effects as puzzling (Poser, 1994). If Dr. Poser had considered diet as a possibility he would not have been so mystified. The diet of Japanese-Hawaiians includes many more elements of the high risk diets of Europe and North America (e.g. saturated fats, dairy products, gluten) than does the diet of native Japanese. Thus one would expect a significantly higher prevalence for Japanese in Hawaii. On the other hand the diet of Caucasians in Hawaii includes more elements of the low risk diets (e.g. fish, fresh vegetables and fruits) then does the diet of Caucasians of mainland North America. This of course would result in a lower prevalence for Caucasians in Hawaii. Thus it would appear that diet provides the solution for 'Poser's Puzzle'. 

6. Significant differences in diet can occur within a given country and these differences are sufficient to account for different prevalence rates. Notably much more fish is consumed in the low risk coastal areas of Norway than in the high risk farming areas. 

7. For any individual the ingestion of specific kinds and amounts of allergens which strongly affect the immune system and the brain-blood barrier will vary significantly with time. This fact, in concert with random infections by common viruses, results in a randomness of the timing and severity of exacerbations and a consequent relapsing-remitting character for MS. 

In summary the interpretation that diet is the main environmental factor for the cause of MS is well supported by our current data base. For those who would counter this interpretation I would ask them to provide either a better interpretation for the environmental factor (especially in regard to solving Poser's Puzzle) or to provide solid, well reasoned evidence of why diet cannot possibly be the main environmental factor in most cases. I am not saying that one specific food type (e.g. gluten) is responsible for MS but rather it is mainly the constant bombardment of the immune system by the food allergens which are specific to each individual and by a weakening of the brain-blood barrier by a high ratio of saturated to unsaturated fat intake. 

I realize this interpretation will be either ignored or hotly and vehemently denied by those with a vested interest in diet not being the cause (e.g. drug companies). However more rhetoric and supported statements won't help. Judgments must be based on data and logic. For anyone with MS it is their health which will suffer if they uncritically reject or ignore a reasonable interpretation on the basis of unsupported, highly subjective statements. 

When considering this entire debate it is essential to realize diet is basically outside the world of conventional medicine and is rarely even considered. Thus the subject is commonly either ignored or quickly brushed off. Furthermore there is not one dime of research money being spent to test the hypothesis of diet control for MS despite the obvious links between the two. I would urge anyone with MS to maintain an open mind on this subject and to consider the foregoing information objectively as possible. From my geological background I never forget that the theory of continental drift, which is now a fundamental concept of our science, was suppressed for 50 years (1912-1962) by the geological establishment. It was simply too threatening to too many careers of those in power.</p> 
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form#header_search input[type='button']:hover {
    background-color: #A5CE56;
    color: #fff;
}
form#header_search input[type="text"]:focus ~ input[type='button'] {
    background-color: #52AEDF;
    color: #fff;
}

</style>

<script>
function searchit(){
    
    // determine environment 
    var search_env 
    if (lycos_ad_www_server.indexOf(".pd.") > -1) {
       search_env = 'http://search51.pd.lycos.com/a/';
    } else if (lycos_ad_www_server.indexOf(".qa.") > -1) {
       search_env = 'http://search51.qa.lycos.com/a/';
    } else {
       search_env = 'http://search51.lycos.com/a/';
    }

var search_term = encodeURIComponent(document.search.search2.value)
var search_url = search_env+search_term;
window.open(search_url);

return false
}
</script-->
<style>
    .adCenterClass{margin:0 auto}
</style>
<div id="tb_ad" class="adCenterClass" style="display:block!important; overflow:hidden; width:916px;">

<div id="ad_container" style="display:block!important; float:left; width:728px ">
<script type="text/javascript">
if (typeof lycos_ad !== "undefined" && "leaderboard" in lycos_ad) {
  document.write(lycos_ad['leaderboard']);
}
</script>
</div>
</div>
</div>
<script type="text/javascript">
if (typeof lycos_ad !== "undefined" && "slider" in lycos_ad) {
  document.write(lycos_ad['slider']);
}
</script> <!-- added 7/22 -->
<div id="FooterAd" style="background:#DFDCCF; border-top:1px solid #393939; clear:both; display:none; width:100%!important; position:relative; z-index:999999!important; height:90px!important"> 
<div class="adCenterClass" style="display:block!important; overflow:hidden; width:916px;">
<div id="footerAd_container" style="display:block!important; float:left; width:728px">
<iframe id="lycosFooterAdiFrame" style="border:0; display:block; float:left; height:96px; overflow:hidden; padding:0; width:750px"></iframe>
</div>
</div>
</div>