Sclerosis and Food Hypersensitivities
Ashton F. Embry
here to visit Dr. Embry's website
Sclerosis is an autoimmune disease in which the immune system causes damage to
tissues in the central nervous system. The disease results from both genetic and
environmental factors. Studies of identical twins demonstrate that MS develops
only in genetically susceptible individuals due to one or more environmental influences.
epidemiology of MS provides a number of important constraints for the interpretation
of the environmental factor which can be regarded as the main cause of MS. The
disease has a very uneven geographic extent and occurs mainly in USA, Canada,western
Europe, New Zealand and Australia where prevalences are generally greater than
50 per 100,000 population. In these areas there is a noticeable north/south gradient
with MS being more prevalent in higher latitude, temperate regions. Also within
individual countries there are significant differences in MS prevalence and incidence.
important constraints are the sudden increase in prevalence in the Faroe Islands
following World War II occupation by British troops and the fact that residency
in Hawaii increases the risk of MS for those of Japanese descent while simultaneously
decreasing the risk for Caucasians. Studies have also shown that MS cannot be
transmitted by person to person contact or by blood transfusion. Finally MS is
a modern disease which appeared about175 years ago. The prevalence has steadily
increased from that time.
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.
main disease processes in MS are breaches in the blood-brain barrier and the passage
of activated and inactivated immune cells into the CNS. These cells initiate a
variety of immune reactions which eventually destroy the myelin wraps on nerve
axons. Myelin loss results in various physical disabilities which increase with
progressive destruction of myelin.
diet factor which can result in such disease processes is the ingestion of hypersensitive
food. Food hypersensitivities reduce the effectiveness of the blood-brain barrier
through Type I (activation of basophils and mast cells) and Type III (deposition
of immune complexes) reactions. T-cells are activated against CNS proteins (Type
IV reaction) by both molecular mimicry of CNS self proteins by food proteins outside
the CNS and by exposure of autoreactive T-cells to previously sequestered CNS
proteins following passage of immune elements through a damaged blood-brain barrier.
anecdotal data indicate that many people have achieved either a permanent remission
or a significant slowdown in disease progress through diet revision involving
the elimination of hypersensitive food.
most common foods which result in immune reactions and eventual MS are dairy,
cereal grains, eggs, yeast and legumes. These are all foods which have been introduced
into the human diet relatively recently and are genetically difficult to tolerate
for some individuals.
approach to the problem of MS has been to try to find the most probable cause
of the disease by using published data on MS epidemiology (who gets and who doesn't),
MS pathogenesis (how the damage to the body happens) and MS recovery (who has
recovered from MS and how they did it). The relevant data on MS epidemiology are
presented in the first main section. In the next section all the proposed causes
are listed and each is tested against the established epidemiological constraints
to see if it is compatible with the data or can be rejected as a probable cause.
This has led to the identification of a single factor, diet, which satisfies the
basic disease process (pathogenesis) is presented in the next section. This is
followed by a discussion which demonstrates that dietary factors can result in
the known disease process. Finally a number of anecdotal accounts of recovery
are noted and it is shown that diet revision played a major role in each of these
is solid evidence that MS is an autoimmune disease which means it is the result
of the actions of one's own immune system on specific tissues in the body. For
example when the immune system attacks collagen in the joints the autoimmune disease
is called rheumatoid arthritis. There are almost 100 different autoimmune diseases
with each one being characterized by immune-mediated damage to specific tissues.
MS is characterized by chronic inflammation and damage to tissues in the central
nervous system (CNS) due to immune responses (Van Oosten et al., 1995). More details
of the disease process are presented in a later section.
ON INTERPRETATIONS OF THE CAUSE OF MULTIPLE SCLEROSIS
are two different aspects to a possible cause of multiple sclerosis. 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
20-30% 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). The fact that MS is more prevalent in women than men (~1.5/1) also
demonstrates the role of genes in MS. Thus there is little 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. This interpretation was recently
confirmed by Ebers et al. (1995). However, it appears that there is no one dominant
gene which determines genetic susceptibility and that many genes, each with a
small influence, are involved (Ebers, 1996). Not much more can be said about the
genetic factor and the best we can do is accept the fact that it exists.
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 "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.
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 Kurtzke, 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 more obvious
interpretation, that the adults do not experience the same environmental influences
as their children do in the new country, was seemingly ignored.
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 apparently 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.
area of research which yields important constraints for interpretation is the
global variance in MS prevalence (the number of people having MS which is usually
recorded as the number for each 100,000 population) and incidence (the number
of people who get MS per year, again recorded as the number for each 100,000 population).
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 (Kurtzke,
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 (Kurtzke, 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 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.
are also lower order geographic trends in MS prevalence. One of the most oft quoted
trends is the occurrence of a north/south gradient within the areas of high prevalence.
For Canada and USA, prevalences are lowest in the southern USA, become higher
in the northern states and are highest in Canada (Kurtzke, 1980). In western Europe
the gradient is not as well expressed but prevalences are higher in the nordic
countries and Britain than in the more southerly Mediterranean countries (Rosati,
1994). The north/south gradient is well expressed in Australia and New Zealand
with the highest prevalences in the temperate, southern portions of these countries
(Sadovnick and Ebers, 1993). In all these cases genetics cannot explain the north/south
gradient and it is clear that the environmental factor is primarily responsible
for this general increase in MS in areas of higher latitude. Any interpretation
of the environmental factor must be compatible with the north/south gradient of
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). Similarly in Canada, MS is at least twice as prevalent in the Prairie provinces
(100-225) as it is on the island of Newfoundland (50) (Sadovnick and Ebers, 1993).
In these cases genetics has no bearing on this distribution (Newfoundland has
a higher percentage of Caucasians) and the environmental factor must be primarily
responsible for such drastic differences. This conclusion has been recently confirmed
by Rosati (1994) who states in his review of MS in Europe "variations in both
prevalence and incidence rates in ethnically homogeneous populations confirm the
importance of environmental factors". These macro and micro differences of MS
prevalence in the world must be explained by any interpretation of the environmental
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 (i.e. 6.5 Japanese with MS per 100,000 Japanese
in Hawaii) 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.
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.
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.
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).
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.
summary an acceptable interpretation of the environmental factor, which plays
a critical role in the onset and progression of MS, must explain the following
must be found throughout the world but be specific enough to affect only half
or less of the susceptible individuals.
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.
must be much more common or effective in northwestern Europe, Canada, United States,
Australia and New Zealand than in the rest of the world.
must be more common or effective in higher latitude areas so as to create a pronounced
north/south gradient of MS prevalence.
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.
must be transportable so as to explain the sudden increase in MS prevalence in
the Faroes following British troop occupation during World War II.
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.
MOST REASONABLE INTERPRETATION FOR THE ENVIRONMENTAL FACTOR WHICH CAUSES MULTIPLE
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:
factors: sunlight, altitude, climate, cosmic radiation, microwave radiation
- infections: specific
virus or bacteria, common virus or bacteria
non-infectious factors: heavy metals, pollution, sanitation, diet
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).
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:
constraints show that MS is not transmitted either person to person or through
a blood transfusion.
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.
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
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.
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
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.
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".
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.
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.
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.
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:
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
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.
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)".
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.
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.
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".
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.
the last section the epidemiological evidence for dietary factors as the main
cause of MS was presented. Of course, if diet is the main cause, it must be demonstrable
that specific dietary factors are capable of resulting in the various known disease
processes of MS. In this and the next sections the basic disease processes (pathogenesis)
of MS are reviewed and the theoretical basis for dietary factors resulting in
these processes are presented.
basic pathogenesis of MS involves the entry of immune cells (e.g. T-cells, B-cells,
macrophages) into the CNS through the walls of the capillaries and venules (Traugott,
1990; Poser, 1993). Immune reactions occur, a lesion is formed and myelin is eventually
destroyed. Myelin consists of fatty tissue which wraps around nerve axons. It
essentially acts as nerve insulation and is critical for proper nerve transmissions.
Loss of myelin results in degradation of nerve transmissions and a resultant multitude
of disabilities which gradually worsen over time as more myelin is destroyed.
is very important to note that in healthy individuals immune cells cannot pass
through the CNS capillaries and venules into the CNS tissue. This does not happen
because the walls of the capillaries in the CNS are different from those in the
rest of the body in that they have very closely packed cells which do not allow
the passage of immune cells. This special feature of the CNS vascular system is
referred to as the blood-brain barrier (BBB) (Traugott, 1990).
would seem that an intact blood-brain barrier prevents CNS infiltration of immune
components and thus stops the possibility of MS occurring. As noted by Compston
(1991), one of Britain's leading MS researchers, "blood-brain barrier penetration
can be regarded as the primary disease process". This is especially true because
many people carry immune cells which are reactive with brain tissue but only a
few develop MS. As explained by Soll (1968) many years ago, "isolation (of the
CNS) begins to take place during fetal life, very likely before the so-called
immunologic "recognition of self" takes place. Thus, at least parts of our brain
may be capable of evoking an immune reaction... provided the immune mechanisms
were allowed direct access to the CNS". Thus almost 30 years ago it was recognized
that a critical disease process in MS is the breach of the BBB and the exposure
of the CNS to autoreactive immune cells. This concept is now widely accepted and
Theofilopoulos (1995b) notes in a recent, comprehensive review of autoimmune disease
"Induction of autoimmune disease, following contact with antigens of such so-called
"immunological privileged" sites, has been well documented".
concept has been supported by observations of MS lesions on MRI scans. On the
MRI scans it was observed that the CNS lesions could be enhanced by using gadolinium-DTPA
(Miller et al., 1988; Kermode et al., 1990). Passage of this substance through
the BBB clearly indicated that the MS lesions in the CNS occur where the BBB has
been damaged so that various substances, including gadolinium, could readily pass
through the damaged walls of the capillaries. Furthermore, Traugott (1990) notes
"that MS lesions are preferentially localized around postcapillary venules" which
have a "relatively low barrier function". This and other evidence led Poser (1987,
1992, 1993), in a series of watershed papers, to declare in no uncertain terms
"In order for MS to become a disease affecting the CNS, it is necessary for the
blood-brain barrier's impermeability to be altered" (Poser, 1993, p. 53). Recently,
this emphasis on the damage to the BBB as a key disease process in MS has been
confirmed by Lai et al. (1996). Based on a study of weekly MRI scans in patients,
these researchers state that "this finding suggests that breakdown of the blood-brain
barrier is an invariable and perhaps obligatory event in the development of new
second part of MS pathogenesis, which is more controversial, is the cause and
timing of the activation of the autoreactive T- helper cells (a type of immune
cell strongly implicated in MS pathogenesis [Traugott, 1990]) which react to the
CNS proteins. Two possibilities have been advanced. One hypothesis is that the
T- cells are activated in the blood outside of the CNS and these cells then cross
the BBB to attack the myelin or other CNS proteins. The other hypothesis, which
has been alluded to earlier, is that the autoreactive T-cells become activated
against CNS proteins after they have passed through a breach in the BBB and encounter
the previously sequestered CNS proteins.
me it is most likely that many of the pathogenic, autoreactive T-cells are activated
outside of the CNS. My reasoning for this conclusion is that MS is just one of
many autoimmune diseases and many of the others have only the presence of a normal
capillary wall between the blood and the tissue. These diseases require activation
of the T-cells outside the tissue and, thus, I believe such a requirement also
is the most reasonable assumption for MS.
cause of the activation of T-cells against CNS proteins outside the CNS is somewhat
problematic. The most widely accepted hypothesis (Theofilopoulos, 1995b) is that
peptides (fragments of proteins) from foreign antigens which are presented by
macrophages (another type of immune cell) to T-cells may resemble parts of CNS
self proteins from a molecular structure point of view. This is referred to as
molecular mimicry as was mentioned earlier. Experimental data have clearly shown
that such a mechanism by both food and viruses can result in the activation of
T-cells against various self proteins (Singh et al., 1989; Wucherpfennig et al.,
1995; Ostenstat et al., 1995). Thus molecular mimicry would indeed appear to be
a critical factor in the pathogenesis of MS.
summary, the evidence is strong that a key part of MS pathogenesis is the activation
of autoreactive T-cells both outside and within the CNS and that persons with
MS carry such CNS autoreactive T-cells. These activated T-cells set in motion
a series of immune reactions which results in myelin being destroyed by various
immune elements (e.g. macrophages) (Traugott, 1990).
related area regarding MS pathogenesis is that of the outward manifestation of
the disease. Most cases of MS start with a relapsing-remitting (RR) character
which refers to short periods when new symptoms appear or old ones increase (attack
or exacerbation) and long intervals when symptoms improve somewhat or stabilize
(remissions). On average it would appear a typical case involves about one attack
a year (Sibley, 1992). Notably it has been found through MRI studies that lesion
forming activity occurs even during remissions (Lai et al., 1996). Thus in many
cases it would appear as if disease activity is essentially continuous with a
waxing and waning character.
many instances RRMS evolves into secondary progressive (or chronic progressive)
MS where there are no clear relapses and remissions, only gradual deterioration.
some cases, MS does not present in a relapsing-remitting manner but rather gradual
deterioration begins at onset. This type of MS is known as primary progressive
untreated, RRMS can have a highly variable course in terms of disabilities although
an average rate of decline of one EDDS (a scale for assessing disability state)
level every six years has been documented (Swank and Dugan, 1987; Sibley, 1992).
proposed cause of MS should be able to explain the various types of MS and the
observed average decline rate.
FACTORS, MS PATHOGENESIS AND MS TYPES
explained in the last section, MS is mainly the result of both the activation
of T-cells against CNS protein and damage to the blood-brain barrier which leads
to infiltration of immune cells into the CNS tissue and subsequent demyelinization.
There are two main components of diet which appear to be responsible for the activation
of T-cells and BBB damage.
first and perhaps most critical component is food antigens. Gell and Coombs (1975)
described four classes of hypersensitivity which is defined as "an increased state
of reactivity that involves a detrimental immune response" (Elgert, 1996). Each
of these types of hypersensitivity causes tissue damage through various types
of immune reactions (Elgert, 1996). Type I, III and IV hypersensitivity reactions
are relevant to this discussion of reactions involving food (Sampson, 1991).
I is the classic immediate, hypersensitivity immune reactions which involve the
increased production of IgE antibodies upon introduction of an offending food.
This is what is termed a food allergy and the reader is referred to Lichtenstein
(1993) for a comprehensive review of the immune response of allergens. Note that
only this specific reaction is termed allergy and all other reactions are referred
to as hypersensitivities. In brief, an allergen in the blood, through a complex
series of immune responses, stimulates mast cells and basophils (specific types
of immune cells) to secrete various chemicals and hormones such as histamine,
leukotrienes and tumor necrosis factor. It is well established that the chemicals
secreted by the activated basophils and mast cells can cause a significant increase
in the permeability of capillaries (Lichtenstein, 1993). As stated by Rozniecki
et al. (1995), "mast cells ... can participate in the regulation of blood- brain
permeability". Thus, food allergens are potentially capable of causing significant,
localized, increased permeabilities in the BBB. Activated mast cells may also
play a significant role in demyelinization (Johnson et al., 1988; Kruger et al.,
1990). Kruger and Nyland (1995) summarize these concepts: "multiple sclerosis
arises due to the effect of the various mediators (histamine and protease) released
from the perivascular mast cells after stimulation by some diet factor". Also
of significant importance is that IgG4 antibodies can also activate mast cells
and basophils (Shakib et al., 1986; Elgert, 1996). The role of IgG4 in pathogenic
immune reactions has been shown by Gerrard el al. (1976) and Rafei et al. (1989).
Rafei et al. (1989) found that only 29% of those with food allergies (as demonstrated
by food challenges) had positive IgE skin tests whereas 91% tested positive for
IgG4 and IgE. Furthermore one patient who demonstrated a delayed response to peanuts
had undetectable IgE but markedly elevated antipeanut IgG4. As recently shown
by Bengtsson et al. (1996), non-IgE immune reactions occur in adults due to the
ingestion of common foods such as eggs, milk and wheat. IgG4 may well be involved
in such reactions.
III hypersensitivity involves the production of immune complexes which are formed
by the combining of antigens and antibodies. This type of hypersensitivity is
likely responsible for many non-IgE reactions. It has been established that these
circulating immune complexes can have a pathogenic effect mainly by deposition
in blood vessel walls (Cochrane and Koffler, 1973). This causes inflammation of
the vessel walls and greatly increased permeability. Immune complexes can also
result in the activation of another part of the immune system, complement (plasma
proteins), which results in further damage (Elgert, 1996). Thus the increased
production of antibodies (mainly IgA, IgG, IgE and IgM), due to the introduction
of various food proteins into the circulatory system, can readily result in immune
complex formation, deposition in the vascular system of the CNS, activation of
complement and a resultant damage to the BBB.
IV hypersensitivity refers to cell-mediated reactions and results in the activation
of T-cells which then induce an array of damaging immune reactions. These reactions,
like Type III reactions, are delayed and often occur days after the offending
foods are ingested. The mechanisms by which food antigens induce Type IV reactions
are currently poorly understood although such occurrences (e.g. celiac disease
in which cereal grain proteins cause cell-mediated reactions) are undoubted. As
mentioned earlier, one possible mechanism for foods to induce an activation of
T-cells against parts of the CNS is through molecular mimicry. Food proteins which
escape into the circulatory system are processed by macrophages which then present
peptides (protein fragments) derived from the food protein to T-cells. The molecular
sequencing in these peptides may be close enough to the sequencing of self-antigens
in the CNS (molecular mimicry) to induce T-cell activation against parts of the
CNS. For example it was recently shown that cereal proteins share amino acid homologies
with human joint tissue (procollagen) and that T-cells from the joints of arthritic
patients were activated by these cereal proteins. Thus molecular mimicry by cereal
proteins can result in arthritis (Ostenstad et al., 1995). It is readily conceivable
that various proteins found in dairy and grains as well as other foods (e.g. legumes,
yeast, eggs) have similar amino acid sequencing as proteins in the CNS.
summary it is clear that, from a theoretical point of view, hypersensitivity reactions
to foods can result in significant damage to and increased permeability of the
BBB and can also result in T-cell activation against the CNS. As discussed earlier,
such damage to the BBB and activation of T-cells initiates a cascade of immune
reactions to happen in the CNS which results in chronic inflammation, demyelination
and a diagnosis of MS. The interested reader is referred to the website www.webdirect.net/zeno for a comprehensive
discussion of the relationship of food hypersensitivities and disease.
factors as the main cause of MS also provides a reasonable explanation for the
different types of MS. For any individual the ingestion of specific kinds and
amounts of sensitive, which potentially affect the BBB and activate T-cells, will
vary significantly with time but can have a daily effect. This fact, in concert
with random infections by common viruses and bacteria which also affect the BBB
and activate T-cells, results in an ongoing disease process but a randomness in
the severity of disease activity and the effectiveness of suppressor reactions.
This would result in relapsing-remitting character for MS.
the BBB continues to degrade through time, by the daily irritation by dietary
factors and by gradual aging processes (weakening of suppressor reactions), a
point is often reached when ongoing disease activity maintains a relatively high
level and RRMS transforms into secondary progressive MS.
progressive MS is likely a reflection of an individual's extreme hypersensitivity
to various substances combined with high exposure and a relatively easy path for
the antigens to reach the circulatory system. In such a case almost continuous
BBB failure and T-cell activation might be expected such that suppressor recations
cannot modulate the disease process. Thus MS would progress with no periods of
it would appear as if dietary factors do provide a reasonable explanation for
the great variation in presentation and progression of MS.
final area of potential useful data is anecdotal evidence regarding recoveries
from MS or significant positive changes in the course of MS. Such data are quite
rightly regarded as "soft" and by themselves provide little, if any, good evidence
for interpreting the cause of MS. However, taken from another point of view, these
independent accounts of positive changes in MS progression can provide another
test of any proposed cause. For example, if dietary factors are the main cause
of MS, then it might be expected that diet revision, involving the avoidance of
hypersensitive fat food, was a critical factor in many of the documented anecdotal
test this I searched for all the accounts of "MS recovery" that I could find in
the literature, on the Internet, and through conversations with persons with MS.
On the basis of the results of this investigation it would indeed appear that
diet revision is a very critical treatment for achieving positive results in the
halting or significantly altering the progression of MS. Perhaps the most impressive
account of recovery is that of Roger MacDougall (1980) which is described in "My
Fight Against Multiple Sclerosis". Mr. MacDougall went from being near blind and
confined to a wheelchair to normal health and activity level (for over 35 years)
by faithfully adhering to a low fat, food sensitivity-free diet. Other published
"success" stories which used diet revision as the main therapy include those of
Rachelle Breslow, Alan Greer, Judy Graham, Bob Lawrence, John Pageler and Bryan
Forbes. Recently a number of accounts of recovery have been gathered on a website
(www.2cowherd.net/q) by an individual who himself has recovered from chronic progressive
MS (wheelchair confined) to a normal, healthy lifestyle through diet revision.
special interest is a scientific paper (Meyer et al., 1954) published over forty
years ago when "allergy" was seriously considered as a possible cause of MS. The
authors describe 17 case histories of persons with MS whose symptoms were greatly
alleviated by avoidance of identified food and inhalant "allergies" (non IgE-
mediated). Importantly the authors note that in cases where offending substances
were reintroduced that MS symptoms returned.
another well known study of diet revision, Swank and Dugan (1987) reported that
66 patients who reduced their daily saturated fat intake to less than 20 grams
experienced, on average, only very minor deterioration over 35 years. This result
contrasted with 31 patients who did not follow such a low fat diet and suffered
major deterioration during the same 35 year study. It should be noted that such
a low fat dietary regime also resulted in a greatly reduced consumption of the
foods which most commonly cause hypersensitivity reactions (dairy, grains, eggs).
These impressive results are perhaps the best documented evidence of the beneficial
effects of diet revision on the course of MS.
AND SPECIFIC FOOD TYPES
appears that specific types of food are most commonly responsible for causing
various hypersensitivity reactions which lead to MS. Such foods are dairy, cereal
grains, eggs, yeast and legumes. The evidence supporting this comes from the previously-
quoted statistical studies of food consumption and MS prevalence (e.g. Malosse
et al., 1992) and the abundant anecdotal data (e.g. MacDougall, 1980). As noted
by Eaton and Konner (1985) these food types, as well as substantial saturated
fats have been added relatively recently to the human diet in terms of our two
million year evolutionary history. Our distant ancestors did not consume such
foods and did not suffer from most of the current lifestyle diseases, including
MS, which are now common in Western societies. It would seem that humans are genetically
less tolerant of these "recently" introduced foods which cause a great variety
of health problems (e.g. heart, stroke, cancer, autoimmune) for genetically susceptible
individuals in societies which consume large quantities of them (Eaton and Konner,
me the best explanation for the appearance and steady increase of MS in Western
societies is the continued increase over the last 150 years in the consumption
of the "late, genetically- hard-to-handle" foods such as dairy, cereal grains,
yeast, eggs, legumes and saturated fats. Thus, although these "late", potentially
problematic foods have been consumed for thousands of years, it is only recently
that large quantities have been ingested so as to exceed tolerance levels for
many genetically susceptible individuals. Later a suggested treatment for MS is
put forward and it is based on the final conclusion of Eaton and Konner (1985)
- The diet of our ancestors is perhaps the best defense against the diseases of
diverse data sets for MS are all compatible with the hypothesis that diet is the
main environmental factor in the cause of the disease. Only diet is compatible
with the extensive and varied epidemiological data base. It appears that the activation
of T-cells against the CNS by molecular mimicry initiated by food proteins and
the constant irritation and weakening of the blood- brain barrier by immune reactions
caused by food hypersensitivities eventually result in the onset and progression
of multiple sclerosis.
- Agranoff, B.W.
1974, Diet and the geographical distribution of multiple sclerosis. Lancet, p.
M., Leibowitz, U. and Spector, J., 1966, Risk of multiplesclerosis related to
age at immigration. Arch. Neurol., v. 15, p.234-237.
M., Okihiro, M., Rowley, W. and Morris, T., 1971, Multiplesclerosis among Orientals
and Caucasians in Hawaii. Neurology, v.21, p. 122-130.
M., Yamoor, M. and Harashe, M., 1974, Multiple Sclerosis andnutrition. Arch. Neur.,
v. 31, p. 267-272.
M., 1977, Clues to the cause based upon the epidemiology ofmultiple sclerosis.
in, Field, E.J. (ed.). Multiple Sclerosis: Acritical conspectus. Lancaster, MTP
Press Ltd., p. 35-81.
S., Cook, S.D. and Rohowsky-Kochan, C., 1995, MultipleSclerosis: immune mechanism
and update on current therapies. Annalsof Neurology, v. 37, p. S87-S101.
- Benedikz, J.,
Magnusson, H. and Guomundsson, G., 1994, MultipleSclerosis in Iceland with observations
on the alleged epidemic inthe Faroe Islands. Annals of Neurology, v. 36, supplement
C.G. and Koffler, D., 1973, Immune complex disease inexperimental animals and
man. Adv. Immunology, v. 16, p. 185.
A., 1991, Limiting and repairing the damage in multiplesclerosis. Jour. of Neurology,
Neurosurgery and Psychiatry, v. 54,p. 945-948.
G. and Kurtzke, J., 1971, On the risk of multiple sclerosisaccording to age at
immigration to South Africa. BMJ, v. 3, p. 725-729.
S.B. and Konner, M., 1985, Paleolithic Nutrition: Aconsideration of its nature
and current implications. New EnglandJournal of Medicine, v. 312, p. 283-289.
G.C., 1996, Genetic epidemiology of multiple sclerosis.Current Opinion in Neurology
G., Bulman, D., Sadovnick, A. et al., 1986, A population-based study of MS twins.
N. Engl. J. Med., v. 315, p. 1638-1642.
G., Sadovnick, A.D. and Risch, N.J., 1995, A genetic basisfor familial aggregation
in multiple sclerosis. Nature v. 377, p.150-151.
K.D., 1996, Immunology. John Wiley and Sons, New York, 468p.
M., Nightingale, S. and Dean, G., 1990, Multiple sclerosisamong the United Kingdom-born
children of immigrants from theIndian subcontinent, Africa, and the West Indies.
J. NeurolNeurosurg Psychiatry, v. 53, p. 906-911.
P.G.H. and Coombs, R.R.A., 1975, Classification of allergicreactions responsible
for hypersensitivity and disease. InClinical Aspects of Immunology, P. Gell, R.
Coombs and P. Lachmann(eds.). New York, Blackwell, p. 761-781.
J.A. and Zaleski, A., 1976, Functional bladder capacitiesin children with enuresis
and recurrent urinary infections. InClinical Ecology, L. Dickey (ed.). Springfield,
Illinois, CharlesC. Thomas, p. 224-233.
P., Fleming, M.C. and Picard, E.H., 1986, Multiplesclerosis: decreased relapse
rate through dietary supplementationwith calcium, magnesium and vitamin D. Medical
Hypotheses, v. 21,p. 193-200.
D., Seeldrayers, P.A. and Weiner, H.L., 1988, The role ofmast cells in demyelination
1 myelin protein are degraded by mastcell proteases and myelin basic protein and
P2 can stimulate mastcell degranulation. Brain research, v. 444, p. 195-198.
- Kermode, A.G.,
Tofts, P.S., Thompson, A.J. et al., 1990,Heterogeneity of blood-brain barrier
changes in multiple sclerosis:an MRI study with gadolinium-DTPA enhancement. Neurology,
v. 40, p.229-235.
P.G., Bo, L., Myhr, K.M. et al., 1990. Mast cells andmultiple sclerosis: a light
and electron microscope study of mastcells in multiple sclerosis emphasizing staining
procedures. Acta.Neurol. Scand., v. 81, p. 31-36.
P.G. and Nyland, H.I., 1995, The role of mast cells anddiet in the onset and maintenance
of multiple sclerosis: ahypothesis. Medical Hypotheses, v. 44, p. 66-69.
- Kuroiwa, Y., Shibasaki,
H. and Ikeda, M., 1983, Prevalence of MSand north-south gradient in Japan. Neuroepidemiology,
v. 2, p. 62-69.
J.F., 1977, Multiple sclerosis from an epidemiologicalpoint of view in. Field,
E.J. (Ed.), Multiple Sclerosis: A criticalconspectus. MTP Press Inc., Lancaster,
J.F., 1980, Epidemiologic contributions to multiplesclerosis: an overview. Neurology,
v. 30, p. 61-79.
J.F., 1995, MS epidemiology worldwide. One view of currentstatus. Acta. Neurol.
Scandin., Supplement 161, p. 23-33.
M. et al., 1996, A preliminary study into the sensitivity ofdisease activity detection
by serial weekly magnetic resonanceimaging in multiple sclerosis. Journal of Neurology,
Neurosurgeryand Psychiatry, v. 60, p. 339-341.
K., 1994, The risk of multiple sclerosis in the USA inrelation to sociogeographic
features: a factor analytic study. J.Clin. Epidemiology, v. 47, p. 43-48.
L.M., 1993, Allergy and the immune system. ScientificAmerican, v. 269, p. 117-124.
R., 1980, My fight against multiple sclerosis. RegenicsInc., Mansfield, Ohio.
D., Perron, H. and Seigneurin, J.M., 1992, Correlationbetween milk and dairy product
consumption and multiple sclerosisprevalence, a worldwide study. Neuroepidemiology,
v. 11, p. 304-312.
M.G., Johnston, A. and Coca, A.F., 1954, Is MultipleSclerosis a manifestation
of idioblaptic allergy? The PsychiatricQuarterly, Jan. p. 1-15.
D.H., Rudge, P.Johnson, G. et al., 1988, Serial gadoliniumenhanced magnetic resonance
imaging in multiple sclerosis. Brain,v. 111, p. 927-939.
C., Wood, N., Kellar-Wood, H. et al., 1994, The BritishIsles Survey of multiple
sclerosis in twins. Neurology, v. 44, p.11-15.
B., Dybwad, A., Lea, T., Forre, O., Vinje, O. and Sioud,M., 1995, Evidence for
monoclonal expansion of synovial T cellsbearing V2.1/V5.5 gene segments and recognizing
a synthetic peptidethat shares homology with a number of putative autoantigens.
Immunology, v. 86, p. 168-175.
C.M., 1986, Pathogenesis of multiple sclerosis. ActaNeuropathol., v. 71, p. 1-10.
C., 1987, Trauma and multiple sclerosis. J. Neurol. v. 254,p. 155-159.
- Poser, C., 1992,
Multiple sclerosis. Observations and reflections -a personal memoir, J. Neuro.
Sci., v. 107, p. 127-140.
C., 1993, The pathogenesis of multiple sclerosis. Additionalconsiderations. J.
Neuro. Sci., v. 115 (suppl.) p. S3-S15.
C.M., 1994, The epidemiology of multiple sclerosis: ageneral overview. Ann. Neurology,
v. 36, p. S181-S193.
C. et al., 1988, An analysis of the "epidemic" of MS in theFaroe Islands. I. Clinical
and epidemiological aspects.Neuroepidemiology, v. 7 , p. 168-180.
A.E., Peters, S.M., Harris, N. et al., 1989, Diagnosticvalue of IgG4 measurements
in patients with food allergy. Ann.Allergy, v. 62, p. 94-99.
G., 1994, Descriptive epidemiology of multiple sclerosis inEurope in the 1980s:
a critical overview. Annals of Neurology, v.36, p. S164-S174.
J.J., Hanser, S.L., Stein, M. et al., 1995, Elevatedmast cell tryptase in cerebrospinal
fluid of multiple sclerosispatients. Ann. of Neurology, v. 37, p. 63-66.
- Sadovnick, A.D.
and Ebers, G., 1993, Epidemiology of multiplesclerosis: a critical overview. Can.
Jour. Neur. Sci., v. 20, p.17-29.
H.A., 1991, Immunologic mechanisms in adverse reactions tofoods. Immunology and
Allergy Clinics of North America, v. 11, p.701-716.
F., Brown, H.M., Phelps, A. and Redhead, R., 1986, Study ofIgG sub-class antibodies
in patients with milk intolerance. Clin.Allergy, v. 16, p. 451-458.
R., 1964, Multiple Sclerosis and geography. Neurology, v.14, p. 338-344.
- Shoab, B.O. and
Patten, B.M., 1996, Human adjuvant disease:presentation as a multiple sclerosis
- like syndrome. South. Med.J., v. 89, p. 179-188.
W.A., Bamfield, C.R. and Clark, K., 1985, Clinical viralinfections and multiple
sclerosis. Lancet, p. 1313-1315.
W.A., 1992. Therapeutic claims in multiple sclerosis. DemosPublications, New York,
New York, 202 p.
V.K., Yamaki, K., Donoso, L. and Shinohara, T., 1989, Yeasthistone H3-induced
experimental autoimmune uveitis. Journal ofImmunology, v. 142, p. 1512-1517.
- Soll, R.W., 1968,
Delayed hypersensitivity: a possible mechanism inthe etiology of multiple sclerosis
in Alter, M. and Kurtzke, J.(eds.). The epidemiology of multiple sclerosis. C.C.
Thomas,Springfield, Illinois, p. 110-128.
L., 1993, Autoimmune Disease. Scientific American, v.269, p. 107-114.
- Swank, R.L. and
Dugan, B.B., 1987, The Multiple Sclerosis dietbook, Doubleday, Garden City, New
R.L. and Dugan, B.B., 1990, Effect of low saturated fat dietin early and late
cases of multiple sclerosis. Lancet, v. 336, p.37-39.
A.N., 1995a, The basis of autoimmunity: Part IIGenetic predisposition. Immunology
Today, v. 16, p. 150-158.
A.N., 1995b, The basis of autoimmunity: Part IMechanisms of aberrant self-recognition.
Immunology Today, v. 16,p. 90-98.
U., 1990, Evidence for Immunopathogenesis. in, Handbookof Multiple Sclerosis,
S.D. Cook (ed.). Marcel Dekker Inc., NewYork, p. 101-127.
Oosten, B.W., Truyen, L., Barkhof, F. and Polman, C.H., 1995,Multiple sclerosis
therapy, a practical guide. Drugs, v. 49, p.200-212.
K.W., 1995, Molecular mimicry in T cell-mediatedautoimmunity: viral peptides activate
human T cell clones specificfor myelin basic protein. Cell, v. 80, p. 695-705.
Throughout this entire website, statements are made pertaining to
the properties and/or functions of food and/or nutritional products.
These statements have not been evaluated by the Food and Drug Administration
and these materials and products are not intended to diagnose, treat,
cure or prevent any disease.