MS-Diet Support Group DIRECT-MS

BEST BET DIET BOOK Scientific Papers

"MS: Probable Cause and Best Bet Treatment" Dr. Ashton Embry © 1996
Section 5. The Most Reasonable Interpretation for the Environmental Factor Which Causes Multiple Sclerosis
The nine constraints listed above 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: 1. indigenous factors: sunlight, atlitude, climate, cosmic radiation, microwave radiation, 2. infections: specific virus or bacteria, common virus or bacteria , 3. 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: 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 homogenous 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". 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: 1. 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. 2. 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. 3. 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)". 4. 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. 5. 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. 6. 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. 7. 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. 8. 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". 9. 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.
End Section 5.