Nutrition intervention in the management of multiple sclerosis

Christina S. Wozniak-Wowk

The National Multiple Sclerosis Society is the United States representative in the International Federation of Multiple Sclerosis Societies, which provides information based upon professional medical advice, published experience and expert opinion. Any additional information about MS may be obtained from the National Multiple Sclerosis Society (205 East 42nd Street, New York NY 10017-5706; MS Toll-Free Information Line: 1-800-227-3166).

Multiple sclerosis (MS) is the most common demyelinating disease of the central nervous system (CNS) in the United States and most temperate zones of the world. At the anatomical level, MS is characterized by the sporadic occurrence of multiple “plaques” or lesions of inflammation in the white matter of the brain, spinal cord, and optic nerves separated both in location and time, with a resultant loss of the myelin sheath.[1] This myelin sheath, which is synthesized by oligodendrocytes, serves as an insulation for axons, which are responsible for accelerating the transmission of nerve impulses in the brain and spinal cord.

Shortly after the formation of a new plaque, nerve impulse conduction through the affected area of the CNS is either slowed or blocked. This is variously referred to as an “exacerbation,” “attack,” “bout,” or “relapse.” As the inflammation in the new plaque subsides, nerve impulse conduction improves and remission occurs. These episodes of exacerbations and remissions may be entirely reversible and cause no permanent neurological deficits. However, if remyelination does not occur in plaques because of loss of competent oligodendrocytes and blockage by scar tissue, the ability to conduct nerve impulses is lost, and MS symptoms then become permanent. At the onset of MS, at least two-thirds of individuals have a course of clinical manifestations characterized by remissions and exacerbations; in another 15% of individuals, symptoms are slowly progressive from onset, and remissions never occur.[2] In those individuals with no clear exacerbations and remissions, MS symptoms slowly progress to chronic disability and ultimately paralysis, having a poor prognosis.

Since the course of MS is highly variable and unpredictable, both the number of plaques and the frequency of new ones vary widely from person to person, with some individuals having only a few and others having many. As a result, there exists in the individual a variety of types and levels of sensory, visual and motor dysfunction, largely depending upon the location and severity of the plaques. At one end of the spectrum, MS may present few clinical signs and symptoms such as mild disturbances in gait and dimness of vision–the so-called benign MS. In this situation, the diagnosis of MS is made only with an incidental magnetic resonance imaging (MRI) brain scan or at autopsy, when the individual has died of some other cause. At the other extreme MS exhibits a fulminating course of neurological impairment with early disability characterized by blurred vision or temporary blindness, slurred speech, vertigo, muscle weakness and spasticity, impaired coordination, numbness and tingling (paresthesias) in the extremities, tremors in hands and arms, severe fatigue, urinary urgency or incontinence, and loss of bladder function.[3] These common clinical manifestations may occur in any combination and can vary in severity, usually lasting days or weeks prior to improvement, which occurs conventionally 4 to 12 weeks after onset.

Besides being associated with a wide range of morbidity, such as complicating infections of the lungs, urinary tract, and skin, MS is also associated with mortality. Mortality rates among a large sample size (n = 1,543) of individuals attending MS clinics in Canada, who were followed prospectively up to 16 years, show that, of the 119 individuals for whom death was known, in 47.1% it was directly attributed to MS complications such as aspiration bronchopneumonia, pulmonary edema with choking, pulmonary embolism, respiratory failure, renal failure and pericarditis.[4] Of the remaining deaths, 15.1% were suicides with the proportion of suicides among MS deaths being 7.5 times that for the age-matched general population.


Currently there exists no specific, single laboratory test for the diagnosis of MS. The major clinical hallmark of a definitive diagnosis is the occurrence of two or more transient neurological deficits such as blurred vision, muscle weakness or impaired coordination occurring over time, which indicate abnormalities in more than one area of the CNS.[3] However, characteristic symptoms alone are never adequate to warrant a diagnosis of MS. Testing is performed to look for confirmatory signs on neurological examination (a detailed examination of the motor and sensory systems, vision and reflexes, etc.), that support the clinical impression. It also serves to exclude other possible causes of neurological deficits, i.e., strokes, compression of the brain by tumors or osteoarthritis of the spine, and damage to the spinal cord that may accompany diseases such as vitamin [B.sub.12] deficiency, pernicious anemia or diabetes.[2] Although a presumptive diagnosis of MS can often be made when an individual is first examined at the time of the initial attack, its confirmation usually requires several months and sometimes years.

The following battery of laboratory tests aid a neurologist in ascertaining a diagnosis of MS when considered in conjunction with relevant neurological findings and a documented neurological history of prior attacks:

* Cerebrospinal fluid examination for nonspecific oligoclonal bands (i.e., immunoglobulin G);

* Evoked potential testing of visual, auditory and somatosensory nerve tracts;

* MRI or computed tomographic (CT) scanning.

In particular, the MRI scan has proven to be very sensitive in the identification of multiple plaques of inflammation and demyelination in that it can detect clinically “silent” disease activity (Fig. 1). Since the MRI scan can demonstrate 5 to 10 times as many lesions as CT scanning, it is the best existing laboratory method for early diagnosis of MS. However, the MRI scan is not infallible since it is not positive in all, but identifies approximately 90% of individuals with MS.[2] Additionally, MRI scan reveals plaque-like abnormalities seen in other neurological disorders; therefore, it is not a disease-specific test.

The MRI scan has been used primarily to aid in MS diagnosis, but it may also play an important role in following the course of the disease and consequently, in monitoring the effect of therapy. Treatment that prevents the appearance of new plaques on the MRI scan in a substantial number of individuals over a period of time in a controlled therapeutic trial could suggest an efficacious form of therapy for MS.[5] Therefore, MRI monitoring could provide an objective, although costly, measure that can be used in future therapeutic trials.


The most striking epidemiological feature of MS is the geographical distribution of prevalence rates: the prevalence increases with latitude both north and south of the equator. Globally, the rate is highest in northern United States, Canada, Iceland, United Kingdom, northern continental Europe, Tasmania and southern New Zealand; it is relatively rare in the tropics and subtropics.[6,7] Interestingly, the place of birth is more important than later residence as a determinant of the risk of acquiring MS.

According to most recent statistics, the prevalence of MS in the United States ranges from 250,000 to 350,000 persons with physician-diagnosed clincally definite, probable or possible MS.[8] Canada reports a prevalence rate twice that of the United States. However, actual prevalence rates tend to be two to four times greater than the reported number, because persons with early symptoms may be underdiagnosed, and those in remission or with clinically silent forms of MS may escape detection.

Multiple sclerosis has occurred in all racial groups with the exception of Inuit (Eskimos); however, it is most common in Caucasians, especially those of northern European ancestry.[7] Even though the disease may become evident at virtually any age, it is rarely diagnosed before the age of 15 or after the age of 60 years. Its onset occurs primarily in young adults between the ages of 20 and 40 with a peak around the mid-20s.[9] Moreover, MS affects women more frequently than men with a ratio of 2:1.[2]


Although the etiology and pathogenesis of MS are elusive, it is speculated to be multifactorial in origin. Numerous hypotheses exist that relate to the causation and pathogenesis of MS, but most lack substantial, direct experimental support. Studies of the epidemiology, clinical features and immune status of individuals with MS have led to the most widely accepted hypothesis that an antigenic challenge by as yet unidentified environmental factor(s) such as a virus results in the development of the “MS trait.”[10] This trait or systemic condition may either never develop into the actual disease or may remain latent for a period of several years prior to the appearance of clinical signs and symptoms characteristic of the disease process. Most recent evidence indicates that 30 to 60% of new clinical attacks of MS occur shortly after a cold, influenza or other common viral illness.[2]

With the onset of disease, the MS trait manifests in genetically predisposed individuals as an aberration in the immune response resulting in an autoimmune (self) attack on one’s own myelin. This autoimmune demyelination may resolve either into partial myelin regeneration or into gliosis (scarring) of the white matter of the brain and spinal cord resulting in permanent disability. Therefore, current research on MS therapy is aimed at two forms of attack: 1) suppressing the autoimmune response, in order to prevent the disease, and 2) controlling the inflammation of myelin to prevent irreversible scarring.


Although MS has been recognized as a separate clinical entity since the mid-1800s, to date there is no definitive therapy that affects the ultimate course of the disease. This is a direct result of the present lack of understanding of the exact cause of or mechanisms of the disease process. Therefore, most proposed treatment modalities for MS are based on the hypotheses of causation.

Because of the variability of MS in different individuals and its tendency to show dramatic improvement without any therapy, it is important to exercise caution in attributing a cause-and-effect relationship to a particular form of treatment. Studies have shown that the use of any, including completely ineffective treatment, in persons with recent MS exacerbation is associated with improvement in 65 to 70% of individuals.[2] Thus, any proposed therapy for MS must produce sustained improvement in more than 70% of individuals, in order to deserve consideration as an effective form of treatment. Additionally, a completely efficacious treatment would arrest worsening in all cases, and probably produce improvement in the majority of afflicted persons. Only a double-blind study or prolonged observation over several years in each treated individual will differentiate a placebo effect or fluctuation in the natural course of MS from a true predictable treatment response.[2]

Currently the only acceptable therapy for MS approved by the Food and Drug Administration in the course of an acute exacerbation is a short-term, high-dose administration of corticosteroids (an immunosuppressive drug).[11] However, this form of treatment has been shown to have only a modest effect in reducing the frequency of acute attacks and slowing the progression rate of MS.[2] There is no documented evidence of a beneficial outcome from long-term corticosteroid use, which, on the contrary, is associated with significant serious side-effects including osteoporosis, fluid retention, hypertension and cataracts.[12]

Since there is no recognized curative or preventative therapy and because a pessimistic approach to MS management is prevalent, persons afflicted with the disease frequently seek unconventional therapeutic approaches, such as nutrition intervention, in order to arrest the downward course of the disease and improve their prognosis. Conflicting information about the various forms of dietary therapy for MS is disseminated in lay literature, commercial advertising and nonprofessional health services such as health food markets and self-help groups. Accordingly, the purpose of this article is to provide a brief overview of the role of nutrition intervention in the treatment and management of MS.


The role of nutritional factors as possible therapeutic agents for MS has been an area of considerable research interest for the last 50 years. Currently dietary regimens advertised as being beneficial or even curative for MS symptoms follow three basic hypotheses of the cause of MS: 1) excess of or deficiency in a food, 2) allergic reaction to a food and 3) toxic effects of a food. General management diets and miscellaneous empirical diets that have received most attention in scientific and/or lay literature to be discussed in this manuscript are as follows:

General Management Diets

* Swank’s Low-Fat Diet

* [omega]-6 and [omega]3 Polyunsaturated Fatty Acids (PUFAs)

Miscellaneous Empirical Diet Treatments

* Allergen-Free Diets –Gluten-Free Diet

–Pectin- and Fructose-Restricted Diet –Source- and Tobacco-Free Diet

* Raw Food, Evers Diet

* MacDougal Diet

* Cambridge Liquid Diet

* Vitamin Therapy

* Mineral Therapy


Swank’s Low-Fat Diet. The initial reports on the relationship of dietary fat intake to the prevalence of MS were based on epidemiological evidence.[6,7,13,14] A high geographical prevalence of MS was found in the northern, German-speaking part of Switzerland, a region in which large amounts of saturated fat of animal origin were consumed.[13] In the southern, Italian-speaking Swiss area where the diet was low in saturated fat, a very low prevalence of MS was observed. The French-speaking Swiss, who were thought to consume a diet somewhat intermediate between the German and Italian groups, had a prevalence of MS that fell in between that of the German and Italian speaking regions.

Similarly, the incidence of MS in Norway was found to be higher in the inland agricultural, dairy-eating regions than in coastal fishing communities.[15] A low incidence of MS was also observed among Eskimos and Laplanders, who consume large amounts of polyunsaturated fatty acids (PUFAs) in the form of blubber and cod liver oil.[16] However, the German and Italian Cantons in Switzerland, the groups studied in Norway and the Eskimos and Laplanders all differ in genetic backgrounds and dietary differences reflect cultural and ethnic influences, either or both of which may be the real cause for the variance in prevalence rates of MS. In contrast, white South Africans, who consume a diet very high in saturated animal fats, report a low incidence of MS.[2]

On the basis of accumulated epidemiological data from around the globe, Dr. Roy Swank of Portland, Oregon, a major proponent for both dietary etiology and dietary treatment of MS, hypothesized that the prevalence of MS was linked to a diet high in saturated animal fats and deficient in PUFAs.[14] According to Swank, persons afflicted with MS are with few exceptions, sensitive to or intolerant of saturated fats. He proposed that an abnormality in the metabolism of saturated fatty acids leads to the formation of microemboli at the circulatory level of the brain.[17] These microemboli are a direct consequence of an abnormal aggregation of formed blood elements (i.e., red blood cells and/or platelets) which results in small vessel occlusion and leads to the formation of perivascular plaques of demyelination.

In order to test his diet hypothesis, Swank conducted a 34-year longitudinal study in which he prescribed a diet low in saturated animal fats (less than 20 g/day) and supplemented with PUFAs in the form of cod liver oil (5 g/day) and vegetable oils (10 to 40 g/day) for a large series of patients with MS.[18] His data indicate that with a daily fat consumption of less than 20.1 g/day (average 17 g/day), average deterioration was slight and 31% of patients died. In contrast, a daily intake greater than 20 g/day (average 25 to 41 g/day) was attended by serious disability and death of 81% of patients.

The condition of minimally disabled patients who followed Swank’s dietary recommendations deteriorated little if at all, and only 5% of them failed to survive the 34th year of the study. On the contrary, 80% of the patients who failed to follow the prescribed diet did not survive the study period. The mild, moderately and severely disabled MS individuals who adhered strictly to Swank’s low-fat diet demonstrated less morbidity and a marked decrease in frequency of exacerbations and disability as well as 50% less mortality over time than those with higher levels of saturated fat intake. Finally, those individuals treated with the diet early in the disease did better than those in whom treatment was delayed.

It is important to note that Swank’s longitudinal study of MS patients treated with the prescribed low-fat diet and one relatively rich in PUFAs has four limitations. First, Swank’s low-fat diet was not tested or scientifically validated in a controlled double-blind trial and thus remains unproved. Second, reductions in deterioration and relapse rate were deduced from published accounts of the natural history of the disease or from the patient’s own previous history. Both of these methods are unacceptable, because of the differences in selection of patients, and because it is recognized that in the natural course of MS the relapse rate tends to decrease as the disease progresses and initial deterioration might well be more rapid than later change. Third, since there was an increase in PUFA intake associated with the lower saturated fat consumption, the specific dietary factor of benefit was not clearly identified. Fourth, in order to obtain maximum benefit from dietary treatment, Swank advocated the use of his prescribed diet as early as possible in the disease process, while symptoms were still transient and diagnosis unconfirmed. Thus, it is questionable whether some of his patients actually had MS in the first place.

Based on studies that have been conducted to date, the consensus approach of the medical experts and in particular the International Federation of Multiple Sclerosis Societies (IFMSS) Therapeutics Claims Committee is that Swank’s low-fat diet has not been proven to be effective in the treatment of MS.[2] More specifically, it plays little or no role in altering the natural history of MS by preventing exacerbations or progression of the disease. However, the possibility of a partial or incomplete effect has not been excluded. Accordingly, none of the National Multiple Sclerosis Society clinics located in the United States (clinics that counsel individuals with MS) endorse Swank’s low-fat diet as a form of therapy for MS.

On a positive note, as acknowledged by the IFMSS Therapeutic Claims Committee, Swank’s low-fat diet is a well-balanced diet that should be used universally. It is important to note that this type of diet, low in total fat, saturated fat and cholesterol, is in line with the Dietary Guidelines for Americans developed collaboratively by the U.S. Department of Agriculture and the Department of Health Education and Welfare. These guidelines are in close agreement with the dietary recommendations made by both the American Cancer Society and American Heart Association, which encourage Americans to eat lean meats and low-fat dairy products while adding more whole grains and fruits and vegetables (up to five servings per day) to their daily caloric intake. Thus, Swank’s low-fat diet is quite similar to diets now recommended for the prevention of coronary heart disease, certain cancers, obesity and gallbladder disease. It is important to note that this diet presents no nutritional risk for the MS patient and is healthier than the usual dietary patterns of most Americans who consume, on the average, 35 to 37% of total calories from fat.

[omega]-6 and [omega]-3 PUFAs. [omega]-6 (linoleic acid) and [omega]-3 ([alpha]-linolenic acid) PUFAs are essential fatty acids required for growth, development and maintenance of cell membranes, including those of the CNS where they are integral components of the myelin sheath. These PUFAs must be obtained from the diet because they cannot be synthesized de novo. In the body, they are metabolically elongated and desaturated to form a variety of highly unsaturated and biologically active PUFAs such as [gamma]-linoleic acid and arachidonic acid, which give rise to prostanoids of “2” series and eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), which give rise to prostanoids of “3” series and their subsequent derivatives (Fig. 2). As illustrated in Figure 3, [omega]-6 and [omega]-3 PUFAs have been shown to affect various aspects of the nervous, vascular and immune systems. Most importantly, they

* Comprise structural phospholipids of both cell membranes and myelin;

* Are used in the maintenance and repair of the CNS;

* Form peroxides that can affect the vascular system;

* Alter red blood cell and platelet aggregation and vessel permeability;

* Affect surface structure of immune cells and influence virus behavior; and

* Serve as source of prostaglandins and suppress cell-mediated immunity.

As a result of epidemiological evidence indicating an association between essential fatty acids and prevalence rate of MS[14,19] and a series of reports of the biochemical deficiency of linoleic acid in the serum of patients with MS,[20] the therapeutic efficacy of [omega]-6 PUFAs was examined in three sizeable, scientifically controlled, double-blind, clinical trials.[21-23] Millar and co-workers[21] studied 75 patients with an acute remitting-relapsing course of MS, of whom 36 were treated with sunflower seed oil emulsion that contained 17.2 g of linoleic acid per day and 39 received 7.6 g/day of oleic acid (a nonessential PUFA) in the form of olive oil emulsion. After a 2-year supplementation period, clinical relapses tended to be less frequent and were significantly less severe (P [less than] 0.01) and of shorter duration in the linoleate-supplemented group than in the control group. However, no evidence for a reduction in overall clinical deterioration was observed. Unfortunately, since dietary records were not kept, intakes of other foods, including saturated animal fats, might have confounded the observed results.

Bates et al.[22] studied the effect of dietary supplementation with linoleic acid in patients with clinically definite, acute remitting MS and in those with chronic progressive disease for a period of 2 years. No therapeutic benefit was detected in the chronic progressive group, but in those with acute remitting MS, 29 patients who were treated with 23.0 g/day of linoleic acid had significantly shorter and less severe relapses (P [less than] 0.05) than the control group, which was given 16.0 g/day of oleic acid. Furthermore, as part of this study they observed the effect of dietary supplementation with [gamma]-linolenic acid. The premise that [gamma]-linolenic acid might provide a more efficient way of increasing the proportion of [omega]-6 fatty acids in the serum since it is incorporated into longer chain fatty acids more efficiently than linoleic acid provided the rationale for the study. Twenty-nine patients with acute remitting MS were given oil of evening primrose (Naudicelle) providing 360 mg of [gamma]-linolenic acid and 3.42 g of linoleic acid per day; a control group of 29 patients was given supplements of oleic acid. No statistically significant differences between the two groups were observed.

Paty and co-workers[23] observed the effect of dietary supplementation with linoleic acid in a mixed group of MS patients: those with acute remitting disease and those who had a chronic progressive course. The treatment group that consisted of 76 patients was given supplements of linoleic acid in the form of sunflower seed oil emulsion at a dose of 17 g/day and the control group received the same dose of oleic acid in the form of olive oil. In contrast to other studies, the results failed to show any benefit of therapy.

Since two of the trials found a statistically significant reduction in the severity and duration of relapses in patients receiving linoleic acid[21,22] and a third trial was not able to reproduce this result,[23] it has been proposed that the inconsistency in the results may be due to differences in the characteristics of individuals.[24] The patients in the two trials that found a beneficial effect of linoleic acid therapy, on the average, had less disability and a shorter duration of illness at entry to the trial than did those patients in the trial that found no statistically significant effect.

To further investigate the relationship between patient characteristics and the effectiveness of linoleic acid in the treatment of MS, Dworkin et al.[25] reanalyzed the data from the three double-blind trials discussed above. Since the methods used in all three trials were similar, the combined data were pooled and statistically reevaluated to determine if the effectiveness of linoleic acid varied as a function of disability and duration of illness at entry to the trial. The combined data consisted of neurological assessments over 2-1/2 years for 87 patients treated with linoleic acid and 85 patients who received the placebo emulsion of oleic acid. The groups were divided into those with mild MS (i.e., minimal or no disability), those with severe disease and those with a disease duration of less than 5, 6 to 10 and greater than 10 years.

The results indicate that patients with minimal or no disability at entry, who were treated with linoleic acid, had a significantly smaller increase (P [less than] 0.05) in disability over the course of the trial than did the control patients. Additional analyses indicate that patients with minimal or no disability, who were treated with linoleic acid, did not have a significant change in disability (P = 0.50) from the beginning of treatment to the end of the trial, whereas control patients had a significant increase in disability (P = 0.03). Furthermore, treatment with linoleic acid significantly reduced the severity and duration of relapses regardless of disability and duration of illness at entry (P [less than or equal to] 0.03). The reliability of this effect of linoleic acid on relapses was greatest in those patients with minimal or no disability and with a shorter duration of illness.

These data suggest that dietary supplementation with linoleic acid may have some beneficial effect not only on the severity and duration of relapses, but also on the progression of disability when patients are treated early in the course of the disease. However, since the characteristics of the MS patients studied in each trial differed, the analyses of the combined data must be interpreted cautiously and should not be considered as providing unequivocal evidence of the effectiveness of linoleic acid in the treatment of MS. Additional research is therefore necessary to systematically examine the extent to which a beneficial response to linoleic acid is related to patient characteristics.

On the basis of studies conducted to date, the IFMSS Therapeutic Claims Committee acknowledges that dietary supplementation with [omega]-6 PUFAs may have some efficacy, since it appears to slow MS progression and reduces the severity and duration of exacerbations without affecting their frequency rate.[2] However, this effect is apparently a very modest one, because it has been difficult to demonstrate consistently in scientific trials. Since the therapeutic evidence is conflicting in nature, [omega]-6 PUFAs therapy must be viewed as investigational.

The evidence that Eskimos who consume large amounts of fish oils (rich in [omega]-3 PUFAs) are resistant to MS and the fact that these PUFAs may exert their effect in MS via an immunological mechanism by inhibiting some key components of the inflammatory response, in particular the production and action of prostaglandins, thromboxane and leukotrienes, has led to the hypothesis that [omega]-3 PUFAs may have a different and a more beneficial effect in the treatment of MS than those derived from [omega]-6 PUFAs.[2,26,27] This hypothesis served as the impetus for a large multicenter controlled, double-blind trial of dietary supplementation with [omega]-3 PUFAs. Of the 312 individuals with MS studied, 155 received active treatment with 1.7 g/day of EPA and 1.1 g/day of DHA, whereas the 157 controls received 10 g/day of oleic acid in the form of olive oil for a period of 2 years.[26]

The data indicate a trend in favor of treatment with [omega]-3 PUFAs that did not, however, reach statistical significance (P = 0.07). Since both experimental and control groups were advised to increase their consumption of [omega]-6 PUFAs, it was assumed that the addition of [omega]-3 PUFAs provided a modest benefit in addition to that already observed with [omega]-6 PUFAs. Based on this evidence, it is the opinion of the IFMSS Therapeutic Claims Committee that EPA and DHA [omega]-3 PUFAs may have some efficacy in MS therapy, but the evidence is inconclusive and must be regarded as investigational.[2]


Allergen-Free Diets. Among the earliest diets proposed in the treatment of MS was the allergen-free diet, which was based on the rationale that the MS plaques might be due to an allergic reaction to common environmental allergens. This diet entailed the use of a regular diet from which foods known to produce hives, skin eruptions, hay fever and asthmatic attacks were eliminated.[2] These diets are also described as elimination diets. Examples of such diets include the gluten-free, the pectin- and fructose-restricted and the sucrose- and tobacco-free diets, which will be discussed below.

Gluten-Free Diet. A relationship between gluten sensitivity and MS was originally suggested by Shatin, who compared prevalence rates for MS in geographic areas where wheat, rye, barley, oats and other grains containing the protein gluten were grown with those in areas where the staple grain crops were low or lacking in gluten.[28] His results indicated that the prevalence of MS was high in the areas of the world that raised and consumed gluten-containing grains and low in areas that consumed rice and corn, which do not contain gluten. Therefore, he hypothesized that individuals with MS possess the homozygous recessive gene for glutten-induced enteropathy and proposed a diet excluding gluten-containing grains.

Hewson[29] used 7-day weighed food records to assess the efficacy of the gluten-free diet in a study of 17 individuals with MS. These individuals had been on the gluten-free diet from a few weeks to 10 years and had a wide range of neurological disability with an average disease duration of 14.4 years and a mean age of 40 years. Unfortunately, neurological assessment over a 3-year period was obtained for only six of the study subjects. Of these, the conditions of two subjects improved, two deteriorated, and two remained neurologically static. This inconclusive clinical evidence for the beneficial effect of a gluten-free diet in MS-afflicted individuals is confounded by three factors. First, a very small sample size of individuals with MS was used; second, the 3-year period is not a sufficient amount of time to study a chronic neurological disease of such a notoriously unpredictable nature; and third, individuals studied had a wide range of disability and disease duration.

However, Hewson’s findings do support the view in the literature that there is no overall evidence that gluten-free diets are universally beneficial in the management or treatment of MS. The lack of conclusive clinical evidence for the benefit of a gluten-free diet in MS is further supported by Hunter et al.,[30] who showed a lack of gluten antibodies in the plasma of 35 out of 36 individuals with MS. Based on the available data, the IFMSS Therapeutic Claims Committee has issued a recommendation that the gluten-free diet is ineffective in the management or treatment of MS.[2]

Although there is no scientific support for a beneficial effect of a gluten-free diet in the treatment of MS, such a diet is still used by some individuals solely on the basis of anecdotal evidence. Because a small number of individuals with MS, in particular those allergic to gluten, may benefit from a gluten-free diet, dietitians and nutritionists can help by giving practical advice on following a gluten-free diet while ensuring adequate nutrient intake.

Pectin- and Fructose-Restricted Diet. The pectin- and fructose-restricted diet is based on the hypothesis that methanol produced by the metabolism of pectins is converted to formaldehyde, which can bind to myelin components and as a result lead to an autoimmune response with consequent tissue damage.[2] As a result of this hypothesis, unripe fruits, fruit juices and other pectin-containing fruits and vegetables are eliminated from this diet. Since vitamin [K.sub.3] (menadione) promotes the formation of sphingomyelin, which may counteract the methanol effect, the diet is supplemented with vitamin [K.sub.3].

In a sizable, uncontrolled trial of patients on this diet, followed for more than a year, relapses and exacerbations occurred and a significant number of patients showed clinical deterioration.[2] Irrespective of this unfavorable outcome, the IFMSS Therapeutic Claims Committee does not recommend this diet because there is no generally accepted scientific basis for the methanol hypothesis. Moreover, this diet has never been tested in a properly controlled clinical trial.

Sucrose- and Tobacco-Free Diet. The rationale for the sucrose- and tobacco-free diet is based on the belief that MS occurs as a results of an allergic response to sucrose or tobacco, as well as to the food additive propylene glycol.[2] Therefore, the elimination of all food products containing sucrose in the form of cane, brown or maple sugars, molasses, sorghum or dates and also the avoidance of food products containing propylene glycol or shampoos with glycol searate is recommended. In addition, tobacco is not to be used in any form. Since this recommendation is based on personal experiences of eight individuals with MS and has not been properly tested in controlled double-blind trials, it has no generally accepted scientific basis for use.

Raw Food, Evers Diet. The raw food diet as originally prescribed by a German physician, Dr. Joseph Evers, is based on a rationale that many illnesses are due to unnatural methods of production and processing of foods.[2] As a result, Evers advocated the use of only raw (unprocessed) foods supplemented with a daily intake of germinated wheat. His diet promotes the use of raw root vegetables, whole wheat bread, cheese, raw milk, raw eggs, butter, honey and raw ham. Naturally processed wine and brandy are also permitted. However, some raw vegetables, especially leafy greens and stalks (e.g., salads, rhubarb, asparagus, cauliflower) are forbidden. Also forbidden are confections, condiments, sugar and salt. The original Evers diet has now been modified to include the use of PUFAs as supplements.[31]

Although the raw food diet has been used as therapy by some individuals with MS, the efficacy of this diet has never been tested in a properly controlled scientific trial. Since there is no scientific evidence that processed foods are chemically different from natural foods and none of the common food additives have been shown to produce lesions resembling those of MS, the IFMMS Therapeutic Claims Committee does not endorse the use of raw food diet in the treatment of MS. It important to note that the use of raw eggs, milk and ham places the individual with MS at a potential risk for food-borne infections.

MacDougal Diet. The proponent of this diet, Professor Roger MacDougal, a playwright and dramatist, devised the diet based on his personal experience with MS, which resulted in a complete and lasting remission. Through a process of inspiration, conjecture, research, and adaptation from other dietary regimens for MS, MacDougal a gluten-free diet but evolved to include four equally important components: 1) no gluten, 2) low sugar and no refined sugar, 3) a low-fat diet high in PUFAs and 4) megadose quantities of vitamins, minerals and trace element supplements.[32] Since the efficacy of the MacDougal diet has never been tested in any properly controlled clinical trials and there is no scientific evidence that this diet affects the natural course of MS, the IFMSS Therapeutic Claims Committee does not recommend the use of this diet for therapeutic purposes.[2]

Cambridge Liquid Diet. The Cambridge diet is a balanced, very low-calorie liquid diet (330 kcal/day), with suboptimal levels of protein (22 g/day) and extra potassium added. This diet is often used in the treatment of obesity.[2] Since studies have shown no acceptable rationale for use of this diet in individuals with MS, except to correct obesity, the Cambridge diet is not recommended by the IFMSS Therapeutic Claims Committee for treating MS. If used to treat obesity in individuals with MS, this diet should only be undertaken with medical or other health professional supervision.

Vitamin Therapy. Since the late 1920s, there have been numerous reports in the scientific literature in which vitamin supplementation was used as an effective form of therapy for MS. The rationale behind such an empirical diet treatment is the claim that MS can result from a deficiency in the uptake or utilization of one or more vitamins.[32] Interestingly, Reynolds et al.[33] reported an unusual vitamin [B.sub.12] deficiency in 10 patients who had MS. Only two of the patients had pernicious anemia; in the remaining patients, all of whom had hematological abnormalities, the vitamin [B.sub.12] deficiency was unexplained. The nature of the association of MS and vitamin [B.sub.12] deficiency is not clear at this time.

Even though there is no documented evidence in animal models that a vitamin deficiency can produce lesions resembling those of MS, various individual vitamins or combination of vitamins administered orally, parentally and intraspinally, in megadose quantities, have been used for treating MS. These include thiamin, niacin, vitamins A, [B.sub.6], [B.sub.12], C, D, E and [K.sub.32]. Although improvement in MS symptoms has been reported to occur up to 100% in some studies, none have been subjected to properly controlled scientific trials. In the opinion of IFMSS Therapeutics Claim Committee, there is no reliable evidence that megavitamin therapy influences the course of MS.[2] Therefore, a well-balanced diet containing all the essential nutrients ideally provides all the necessary vitamin requirements for individuals with MS.

It is important to note that consistent long-term use of megadose quantities of several vitamins may be associated with significant serious and undesirable side-effects. Indeed, in some individuals, very high doses of vitamin C (greater than 10 g/day) have been reported to produce diarrhea and an increase in urinary oxalate excretion which is associated with increased risk of kidney stones. Excessive chronic doses of vitamin A (greater than 20,000 [mu]g of retinol equivalents per day) have been associated with headaches, general weakness and fatigue, hypercalcemia, pain in bones and joints and many other symptoms that may vary with the individual. Furthermore, hypervitaminosis D (as little as 45 [mu]g/day) may result in anorexia, constipation, nausea, muscular weakness, joint pain, disorientation, hypercalcemia and irreversible calcification of the heart, lungs, kidneys and other soft tissues. Finally, high doses of vitamin [B.sub.6] (greater than 500 mg/day) may sometimes produce a disease of the peripheral nervous system (i.e., muscular weakness, fatigue and loss of balance) which mimics MS symptoms.

Mineral Therapy. Since the 1880s when Charcot, a French neurologist, tested the use of zinc phosphates, mineral salts in various forms and dosages have been used as a treatment modality for individuals with MS. Among the early therapies for MS, minerals such as potassium bromide or iodide, antimony, gold, silver, mercury, arsenic, thorium and metallic salts were used.[2] Currently, essential minerals, such as calcium, are being combined with various vitamin supplements.

This type of therapy has been advocated for over 20 years by Dr. Hans Nieper, who provides treatment for MS patients in his clinic at Silbersee Hospital in Hanover, Germany. Dr. Nieper’s very expensive treatment modality involves a life-long intake of massive quantities of “mineral transporters” such as calcium aminoethyl phosphate (AEP) and calcium orotate (calcium salts of synthetic organic compounds given intravenously and by mouth) in conjunction with daily doses of selenium and vitamins C, D and E, supplemented with a raw food diet.[39] Calcium orotate and AEP (also used in treatment of other autoimmune disorders) act as sealants of cell membranes against immune and toxin aggression without excluding nutritive substances from passing through the cell membranes.[34]

Interestingly, there have been numerous unsubstantiated claims of the success of Dr. Nieper’s therapeutic regimen by Americans with MS, who have visited the Nieper clinic in Germany and/or have obtained this therapeutic regimen through mail orders. According to Dr. Nieper, calcium AEP is said to have a very favorable effect on as many as 78% of his patients with MS (personal communication). Because Dr. Nieper’s therapeutic regimen has never been evaluated in a controlled, double-blind, clinical trial and involves many dietary components, and since objective, quantified data are not available, the IFMSS Therapeutic Claims Committee considers it an unacceptable form of therapy for MS.


As yet, there is no general agreement that any treatment exists to cure or retard the progress of MS. Nonetheless, nutrition intervention can successfully be incorporated as a treatment modality for some of the common symptoms and complications of MS, to optimize functional capacity and enhance the quality of life for those individuals afflicted with the disease. Symptoms and complications amenable to dietary intervention include 1) fatigue and physical disability, 2) dysphagia, 3) urinary incontinence, 4) constipation and 5) psychological and cognitive disturbances.

Fatigue and Physical Disability. Persistent fatigue, loss of energy and restricted mobility (e.g., dependence on assistive devices such as crutches, braces or wheelchair) in persons with MS has a direct impact on the nutritional requirements and/or nutritional status of the individual.[12] When fatigue is problematic and mobility is restricted, the decrease in the individual’s activity level has nutritional implications. Many individuals with MS are likely to experience a significant reduction in the level of energy expenditure, which even in light of no increase in caloric intake, may result in a weight gain which further impairs mobility and exerts an additional strain on both the respiratory and circulatory systems. Therefore, it is important to control weight gain by encouraging healthy eating patterns, while concomitantly not imposing the stress of a very low-energy diet.

Although obesity can become problematic in the MS individual, nutritional wasting is also prevalent. As caloric intake declines it becomes increasingly important that the quality of the diet remains sufficient to provide adequate intakes of all nutrients. Fatigue, physical disability and altered emotional status adversely influence the individual’s food intake and may lead to:

* Dependence on low nutrient-dense convenience foods;

* Increased consumption of “comfort” foods;

* Loss of interest in food and decrease in appetite;

* Dependence on others for food shopping and preparation;

* Insufficient energy to eat a full meal at one sitting; and

* Need for assistance with feeding.

Those who live alone, those who are more disabled or those in long-term health care facilities comprise a group potentially more at nutritional risk.

Dysphagia. Dysphagia (i.e., difficulty in swallowing) is not frequently encountered in persons with MS but when present, it must be carefully assessed and managed on an individualized basis. Individuals may report intolerances of liquids, solids or both, with episodes of choking or recurrent aspirations.[35] These persons are at risk of cachexia from avoidance of foods and aspiration pneumonia from foodstuffs entering the respiratory passages. If swallowing cannot be improved, enteral tube feedings may be necessary to prevent slow dehydration and/or starvation.

Urinary Incontinence. Individuals with MS who develop a neurogenic bladder often experience urinary frequency, urgency and incontinence that indirectly affect their nutritional status.[35] In order to avoid the social embarrassment of urinary incontinence, these individuals may self-impose severe fluid restriction. This can result in a dry mouth, which may lead to loss of appetite, dysphagia and a decrease in solid food consumed. The ingestion of specific nutrients may be curtailed, due to a decrease in the intake of a specific fluid high in that nutrient (e.g., a decrease in calcium and vitamin C intake with a reduction in the use of milk and juices). In addition, fluid restriction results in a decrease in urine volume and in a relative increase in renal solute load, predisposing the individual to an increased risk of renal or bladder stone formation. Caffeine-containing beverages (used to manage fatigue) act as a diuretic and can further dehydrate the individual who is restricting fluid intake.

When frequent urinary incontinence is not controlled, there exists an increased risk of urinary tract infections (UTIs). Acidification of the urine through the use of cranberry or prune juice or large supplements of 2 to 4 g of vitamin C helps prevent infection by inhibiting bacterial growth and replication. By contrast, milk, dairy products, beverages containing sodium carbonate or sodium bicarbonate and citrus juices (e.g., orange, grapefruit, tomato) promote an alkaline urine, thereby increasing the risk of UTIs. In addition, adequate fluid intake in itself helps to avoid UTIs by preventing the formation of concentrated urine.

Constipation. Constipation is a common complaint among individuals with MS. It can be caused by decreased mobility, neurogenic sluggish bowel and self-imposed fluid restriction to control urinary incontinence.[35] Constipation can be prevented by increasing fluid intake to 2 to 3 quarts/day and a high-fiber diet.

Psychological and Cognitive Disturbances. Since MS is a chronic disorder of the CNS, it may present problems in psychological and cognitive domains, along with manifestations of physical disability. Characteristically, persons afflicted with MS may exhibit depression and anxiety as a result of the difficulty in adapting to the effects of the disease/disability and apprehension about the future. In approximately 25% of individuals with MS, cognitive dysfunction may proceed to forgetfulness, confusion, disorientation and memory loss.[36]

The concerns for dietitians and nutritionists counseling those individuals who experience cognitive impairments should be focused on areas of validity of dietary history and ability to follow through with plans of activity.[12] In such situations, formal evaluations by assessing the individual’s nutritional status and nutrient requirements, in order to make appropriate dietary recommendations, follow-up and monitoring for compliance, are essential.


Nutritional therapy for alleviating the symptoms of MS or altering the natural course of the disease is controversial. Even though there is no scientific evidence for nutrition as a specific etiologic agent in MS, a few scientists and physicians strongly believe that a key to MS treatment lies with nutrition. Therefore, these physicians prescribe dietary regimens to treat their MS patients. On the other hand, as noted by the IFMSS Therapeutic Claims Committee, most of the dietary regimens used for treating MS have not been subjected to controlled, randomized, double-blind trials and thus have not been proven to be of therapeutic significance.

Although testing the efficacy of dietary regimens for various diseases has always been difficult, both the remitting-relapsing nature of MS and the unpredictable reversibility of disability as part of the natural course of the disease make controlled dietary studies for this disease even more challenging. As a result, the majority of therapeutic claims made for dietary regimens are based on anecdotal evidence. For those dietary regimens subjected to scientifically controlled trials, none (with the possible exception of [omega]-6 PUFAs) have been demonstrated to be of significant therapeutic merit for MS; therefore, the IFMSS Therapeutics Claims Committee only endorses a well-balanced, nutrient-dense diet, restrictive in excessive caloric intake.[37]

As medical experts consistently note, many of the therapeutic, dietary regimens prescribed are expensive and restrictive in the variety of foods permitted. Consequently, some of these dietary regimens may potentially be harmful since they 1) eliminate certain foods from the diet and thereby reduce intakes of essential nutrients and 2) include megadose quantities of vitamins and/or minerals that substantially exceed the recommended daily allowances, increasing the risk of nutrient imbalance and possible toxic effects.

It is therefore essential, that we as nutritionists, dietitians and health care professionals, who are often called upon to counsel patients with MS, are knowledgeable about the disease process as well as the numerous therapeutic dietary regimens promoted in health food markets and/or through mail orders. Working in a team approach we must serve as allies to persons with MS, by educating them and supporting their efforts to regain some feeling of control over their destiny. Finally, we must appreciate that the uniqueness of each individual with MS will require individualized management; the nutritional requirements will not only be unique, but may change throughout the natural course of the disease.


[1.] Matthews WB, Acheson ED, Batchelor JR, Weller RO. MacAlpine’s multiple sclerosis. New York: Churchill Livingstone, 1985:38-40.

[2.] Sibley WA, Therapeutics Claims Committee of the International Federation of Multiple Sclerosis Societies. Therapeutic claims in multiple sclerosis. New York: Demos Publications, 1992.

[3.] Miller AE. Clinical features. In: Cook CD, ed. Handbook of multiple sclerosis. New York: Marcel Dekker, 1990:169-87.

[4.] Sadovnick AD, Eisen K, Ebers GC, Paty DW. Cause of death in patients attending multiple sclerosis clinics. Neurology 1991;41:1193-6.

[5.] Miller DH, Barkhof F, Berry I, Kappos L, Scotti G, Thompson AJ. Magnetic resonance imaging in monitoring the treatment of MS: concerted action guidelines. J Neurol Neurosurg Psychiatry 1991;54(8):683-8.

[6.] Agranoff BWA, Goldberg D. Diet and the geographic distribution of multiple sclerosis. Lancet 1974;2:1061-1066.

[7.] Alter M, Yamoor M, Harshe M. Multiple sclerosis and nutrition. Arch Neurol 1974;31:267-272.

[8.] Anderson D. Revised estimate of the prevalence of MS in the United States. Ann Neurol 1992;52:781-93.

[9.] Acheson ED. Epidemiology of multiple sclerosis. Br Med Bull. 1977;33:9-14.

[10.] Booss J, Kim JH. Evidence for a viral etiology of multiple sclerosis. In: Cook CD, ed. Handbook of multiple sclerosis. New York: Marcel Dekker, 1990:41-61.

[11.] Troiano R, Cook SD, Dowling PC. Corticosteroid therapy in acute multiple sclerosis. In: Cook CD, ed. Handbook of multiple sclerosis. New York: Marcel Dekker, 1990:351-69.

[12.] Frankel DL. Multiple sclerosis. In: Gines DJ, ed. Nutrition management in rehabilitation. Rockville, MD: Aspen Publications, 1990:85-107.

[13.] Ackermann A. Die multiple sklerose in der schweiz. Schweiz Med Wochenschr. 1931; 61:1245.

[14.] Swank RL. Multiple sclerosis: a correlation of its incidence with dietary fat. Am J Med Sci 1950;220:421-30.

[15.] Swank RL, Lerstad O, Strom A, Backer J. Multiple sclerosis in rural Norway: its geographic and occupational incidence in relation to nutrition. N Engl J Med 1952;246:721-8.

[16.] Swank RL, Brewer-Dugan B. The multiple sclerosis diet book. Garden City, NY: Doubleday and Co, 1987.

[17.] Swank RL. Effects of high fat feedings on viscosity of the blood. Science 1954;120:427-8.

[18.] Swank RL. Multiple sclerosis: the fat and oil relationship. Nutrition 1991;7:368-76.

[19.] Sinclair HM. Deficiency of essential fatty acids and atherosclerosis. Lancet 1956; 1:381.

[20.] Thompson RHS. A biochemical approach to the problem of multiple sclerosis. Proc R Soc Med 1966;59:269-76.

[21.] Millar JHD, Zilkha KJ, Langman MJS, Payling-Wright H, Smith AD, Belin J, Thompson RHS. Double-blind trial of linoleate supplementation of the diet in multiple sclerosis. Br Med J 1973; 1:765-8.

[22.] Bates D, Fawcett PRW, Shaw DA, Weightman D. Polyunsaturated fatty acids in the treatment of acute remitting multiple sclerosis. Br Med J 1978;2:1390-1.

[23.] Paty DW, Cousin HK, Read S, Adlakha K. Linoleic acid in multiple sclerosis: failure to show any therapeutic benefit. Acta Neurol Scand 1978;58:53-8.

[24.] Dworkin RH. Linoleic acid and multiple sclerosis. Lancet 1981;1:1153-4.

[25.] Dworkin RH, Bates D, Millar JDH, Paty DW. Linoleic acid and multiple sclerosis: A reanalysis of three double blind trials. Neurology 1984;34:1441-5.

[26.] Bates D. Dietary lipids and multiple sclerosis. Uppsala J Med Sci 1990(Suppl);48:1973-87.

[27.] Lands WEM. Biochemistry and physiology of n-3 fatty acids. FASEB J 1992;6:2530-5.

[28.] Shatin R. Gluten and multiple sclerosis. Br Med J 1965;1:1433-4.

[29.] Hewson DC. Is there a role for gluten-free diets in multiple sclerosis? Hum Nutr Appl Nutr 1984;38(A):417-20.

[30.] Hunter AL, Rees BWG, Jones LT. Gluten antibodies in patients with multiple sclerosis. Hum Nutr Appl Nutr 1984;38(A):142-3.

[31.] Rosner LJ, Ross S. Multiple sclerosis: new hope and practical advice for people with MS and their families. Englewood Cliffs NJ: Prentice Hall, 1987.

[32.] Graham J. Multiple sclerosis: a self-help guide to its management. Rochester, VT: Healings Arts Press, 1988.

[33.] Reynolds EH, Linnell JC, Faludy JE. Multiple sclerosis associated with vitamin B12 deficiency. Arch Neurol 1991;48:808-11.

[34.] Neiper HA. Revolution in technology, medicine and society. Hanover, Germany: MIT Press, 1985.

[35.] Schapiro RT. Symptom management in multiple sclerosis. New York: Demos Publications, 1988.

[36.] Scheinberg LC. Multiple sclerosis: a guide for patients and their families. New York, Raven Press, 1983.

[37.] Giesser B. Positive nutrition. New York: National Multiple Sclerosis Society, 1990.

COPYRIGHT 1993 Lippincott/Williams & Wilkins

COPYRIGHT 2004 Gale Group

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