Mono Sclerosis :: Stop MS in its tracks before it becomes Multiple

THE MOST REASONABLE INTERPRETATION FOR THE ENVIRONMENTAL FACTOR WHICH CAUSES MULTIPLE SCLEROSIS

The nine constraints listed are key to testing if a proposed cause of MS can be taken seriously or not. Clearly if a proposed cause is not compatible with one or more of these constraints then it must be rejected as the probable cause. Only factors which are compatible with all of these constraints can be considered as a probable cause of MS. All of the environmental factors proposed as a cause of MS have been compiled and these include specific virus or bacteria, common virus or bacteria, heavy metal poisoning, industrial pollution, sanitation, diet, sunlight, altitude, climate (temperature), microwave radiation and cosmic radiation. These factors can be placed into three main groups:

Indigenous factors: sunlight, altitude, climate, cosmic radiation, microwave radiation.

Infections: specific virus or bacteria, common virus or bacteria.

Transportable, non-infectious factors: heavy metals, pollution, sanitation, diet.

First of all, the indigenous factors can be readily eliminated on the basis of the Faroe Islands data. These data clearly demonstrated that the environmental factor is not indigenous but can be brought into an area (e.g. the Faroes).

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:

The constraints show that MS is not transmitted either person to person or through a blood transfusion.

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.

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".

It has also been postulated that common viral and bacterial infections cause MS through a phenomenon called molecular mimicry (Theofilopoulos, 1995b). For this to happen a part of the molecular structure of the infectious agent must closely resemble part of the molecular structure of one or more self-proteins in the CNS. Thus when the immune system is activated against the virus it may also attack the similar self-proteins in the CNS. In support of this it has been demonstrated that some viruses do have molecular sequences similar to those of CNS proteins (Wucherpfennig et al., 1995). Also Sibley et al. (1985) demonstrated a weak correlation between viral infections and MS exacerbations. However it must be mentioned that in Sibley et al's study many exacerbations occurred in the absence of infection and many viral infections did not trigger an exacerbation. Also, as shown by MRI studies (Lai et al., 1996), disease activity is essentially continuous in many cases and viral infections certainly are not.

A constraint which strongly indicates that common viral and/or bacterial infections are not the main cause of MS is the prevalence data for Japanese and Caucasians in Hawaii. The prevalence of common infections in Japan, Hawaii and California is very similar, being perhaps highest in Japan due to high population density. Thus, given that MS is three times more common in Japanese in Hawaii than in Japan, clearly demonstrates that common infectious agents are not the main cause of MS. Another constraint which demonstrates that common infections are not the main cause of MS is the north/south gradient of prevalence in many areas. The occurrence of common infections shows little variation within these areas and thus cannot explain such a pronounced gradient. Other constraints, such as the much higher prevalence of MS on the Canadian Prairies than in Newfoundland, also argue strongly against a common virus for the main cause.

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, I have looked at diet in the light of the nine constraints detailed earlier. I have found that diet fits all nine constraints and thus I currently believe the main environmental factor which is the prime cause of MS indeed is diet. In regard to the nine constraints:

Diet is obviously found throughout the world and it is specific enough to an individual with given dietary habits to result in MS affecting only half or less of genetically susceptible individuals.

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. Thus the immigration data are best interpreted in the light of immigrant children and immigrant parents experiencing different environmental factors in their new country.

This is not surprising because it is well known that immigrant children integrate much more than do immigrant adults. Identical 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 possibly have separate food sensitivities especially when they are older due to long term intestinal damage and increased permeability. Thus dietary and digestive system changes (and MS risk divergence) would occur in twins mainly after age 18. Thus diet and only diet explains this paradox.

The overall diets of the high prevalence areas have certain features in common including high dairy, cereal grain 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, cereal grains, high saturated fat) are more effective in causing MS as has been noted in various statistical studies (Shatin, 1964; Alter et al., 1974; Agranoff and Goldberg, 1974; Malosse et al., 1992; Lauer, 1994). Shatin (1964) found a good correspondence of MS prevalence with wheat consumption. Malosse et al. (1992) state "We have studied the relationship between MS prevalence and dairy product consumption in 27 countries and 29 populations all over the world. A good correlation (p=0.836) was found; this correlation was highly significant (p<0.001)". This echoed Agranoff and Goldberg (1974) who almost 20 years earlier had stated "a geographic predisposing factor in multiple sclerosis ... is directly related to milk consumption". Alter et al. (1974) found a significant correlation (0.7) between consumption of animal fats and MS prevalence. Furthermore on the basis of a recent multivariate analysis, Lauer (1994) concludes "The second MS-related bundle comprised characteristics ... with dietary variables (i.e. a diet low in fish and high in dairy products)".

Diet is readily compatible with the north/south gradient because diet varies directly with climate and thus latitude. The diets of cooler, more temperate regions include much more saturated fat, dairy and cereal grains which, as discussed above, are the most problematic foods.

Significant differences in diet can occur within a given country and these differences are sufficient to account for different prevalence rates. For example, the maritime Newfoundlanders consume much more fish and less dairy and cereal grains than do Canadians on the prairies and, as noted earlier, they have a far lower prevalence than do the land- locked, prairie dwellers.

Most importantly diet explains the paradox of the adversely affected Hawaiians of Japanese ancestry and the beneficially affected Hawaiians of Caucasian descent which Poser (1994) characterized as "puzzling". 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, cereal grains) 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 this puzzling paradox which is inexplicable by other postulated causes.

A critical question in this analysis is "Can diet explain the increased prevalence of MS in the Faroes following British troop occupation?" As has been discussed it is highly unlikely that the British brought with them a MS virus but it is clear that they did bring the environmental factor with them. The obvious interpretation is that they brought their own food supplies which would have of course included food high in saturated fat and the foods which most commonly cause hypersensitivity reactions (dairy, eggs, cereal grains, nuts, legumes). The islanders living near the bases (and working on them) would have had easy access to these "non-traditional" foods and added them to their diet. Thus such dietary changes in susceptible islanders can readily explain the sudden increase in MS. These imported foods likely became part of the standard diet of many of the islanders (especially the youth) and this accounts for the ongoing occurrence of MS in the Faroes. Thus diet does indeed provide a solid and reasonable explanation of one of the most specific and well controlled pieces of epidemiological evidence regarding the environmental factor.

Diet as the main factor is entirely compatible with the non- transmissible characteristic of MS as noted by Ebers (1996) who, on this basis, clearly stated "In sum these data strongly indicate that the environmental factor is affecting the population risk. Accordingly, factors which influence large populations such as diet ..... deserve careful reconsideration".

The diet of the high risk areas (western societies) has changed significantly over the last 100 years with substantial increase of saturated fat, a decrease in polyunsaturated fat and an increase in dairy and cereal grains (Swank and Dugan, 1987). This trend of a higher consumption of these foods has been significantly accelerated over the past fifty years with the rise and constant expansion of the "fast food" (e.g. hamburgers, pizza, donuts) industry. Thus the continued increase of consumption of these foods readily accounts for the steadily increasing prevalence of MS over the last 100 years.

OTHER ENVIRONMENTAL FACTORS
It would be naive to think that every single case of MS had the same cause and that most cases have only a single cause. MS is basically "an effect", a chronic inflammation and demyelination of the CNS, and it seems that a number of environmental factors can in combination, result in such a condition.

For example, it is known that a bacterial infection can cause chronic inflammation and demyelination but, because the cause is known, it is called Lyme Disease rather than MS. Furthermore, in rare cases, measles vaccination has also resulted in chronic demyelination and once again, because the cause is known, it is not referred to as MS but rather as chronic rubella encephalitis. Thus MS is basically a catch all term for chronic demyelination of unknown cause.

As discussed in the companion pages, dietary factors are most probably the main (but not the only) cause of most (but not all) cases of MS. Given this, it is essential to find out through testing if indeed your MS is caused mainly by food hypersensitivities and high saturated fat intake. If you avoid dairy, cereal grains, eggs, yeast, legumes and other hypersensitive food and follow a low fat diet with supplements and the progression of MS is not abated, then it is likely your MS is mainly caused by another environmental factor.

The factors discussed below are other likely contributors to MS and, although in most cases they are subsidiary to hypersensitive foods, they may be major factors in some cases.Finally it is important to note that MS is a relatively new disease with the first recorded case being from the beginning of the nineteenth century (Swank and Dugan, 1987). As argued by Swank and Dugan (1987), MS is basically a "disease of modern times" although it is possible a few cases occurred earlier than 1800.

There is no doubt that incidence and prevalence of the disease has been increasing over the last century. Thus the cause of the disease must be due to an environmental factor(s) which is progressively having more effect over the last 100 years.

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.

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

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.

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.

It must be more common or effective in higher latitude areas so as to create a pronounced north/south gradient of MS prevalence.

It must have enough variation so as to create significant MS prevalence and incidence differences within ethnically homogeneous populations over relatively short distances.

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

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.

It cannot be transmitted by either person to person contact or by a blood transfusion.

It must be increasingly more widespread and effective over the last 100 years.

Inhalants
Another possible cause of immune reactions which damage the BBB and possibly activate T-cells are hypersensitivities (type I, III, IV) to inhalants. IgE, immediate sensitivity reactions to inhalants seem relatively rare in persons with MS (Oro et al., 1996) but IgG reactions may be more common and problematic. Once again a blood-allergy ELISA or RAST test which measures IgE and IgG4 production on antigen challenge for a variety of inhalants is a reasonable way of determining if this is a major contributing factor to your MS. If the test is positive for a number of inhalants then once again it is essential to avoid or greatly lower the exposure to these substances. This maybe more difficult than for foods but allergists should be able to advise on various methods of avoidance and reduction. Extreme measures such as moving to another part of the country may be necessary in rare cases.

Viruses and Bacteria
Common viral and bacterial infections undoubtedly can affect the BBB and activate T-cells against the CNS through molecular mimicry. It is very doubtful if common viral and bacterial infections are the main cause of MS onset and progression as revealed by the epidemiological data but, in a few cases, such occurrences may play a major role in progression. Strong antibiotics are useful in cases where bacteria play a significant role in MS. In general, strategies to avoid infections should be adopted and any common bacterial infection should be treated with standard antibiotics as soon as possible.

Heavy Metals
Heavy metals can be very toxic to the CNS and thus, in some cases, may play a significant role in MS onset and progression. One of the most obvious sources of heavy metal toxicity is mercury in dental fillings. Currently there is considerable debate on this point and it is difficult to separate the data from the hype. Current scientific data do not support the concept of mercury amalgams being a major cause of MS. Such data include (1) PwMS do not have abnormal amounts of mercury in the CNS. (2) Many persons with MS have no fillings. (3) Professions which are exposed to abnormal amounts of mercury do not have abnormal rates of MS.

Furthermore, replacement of mercury amalgams is very expensive and may itself cause problems. However there is enough theoretical and anecdotal data available to indicate that mercury fillings may possibly contribute to MS progression. If diet revision does not result in an effective halt of MS progression then it may well be worth the trouble and expense to have the fillings replaced.

An interesting and insightful study of the effect of toxins on the CNS concerns the response of 26 women with failed, silicone breast implants (Shoab and Patten, 1996). "All patients had evidence of disseminated CNS lesions" and 80% had oligoclonal bands (IgG antibodies) in their spinal fluid. All the women had "systemic, inflammatory, autoimmune disease with CNS involvement" which was "triggered by the foreign material (silicone) in their body". This example clearly indicates that foreign, "antigenic" material can cause BBB failure and demyelinating immune reactions.

It is worth having a blood test and perhaps even a hair analysis for levels of heavy metals (see appendix). Chelation therapy can be valuable for detoxifying when anomalously high levels of heavy metals are detected.

Vaccinations
Poser (1986, 1993) has stated that vaccinations may be an important factor in MS onset and progression. Given the fact that vaccinations cause immune reactions it is clear that they may well affect the BBB and cause CNS inflammation (not necessarily an exacerbation). Poser (1986) provides references for a number of incidences where vaccinations resulted in MS. The most reasonable explanation of such occurrences is that the vaccination provided the final stress on an already embattled immune system. Also the hepatitis B virus has similar molecular structures to myelin basin protein and thus could cause molecular mimicry. Overall I would suggest that vaccinations (including the flu shot) be avoided unless they are absolutely necessary.