Compilation of evidence based dietary advice in multiple sclerosis.
There are various reasons to suspect that diet could have a role in multiple sclerosis and that dietary intervention could be beneficial. For instance...
1) Only a small amount of the variability in risk of developing MS can be explained genetically, suggesting a role of environmental factors such as diet (68).
2) The prevalence of multiple sclerosis varies widely by region, possibly owing to differences in local diets. (53)
3) Migration to a region with higher MS prevalence early in life increases MS risk (55)
4) The incidence of MS risk appears to be rising in a genetically stable population and is linked to urbanization (86)
5) The gastrointestinal tract has abundant gut-associated lymphoid tissue with a known immunological role in humans (49).
6) Specific changes in the gut microbiome (content of microorganisms in the gastrointestinal tract) have been associated with multiple sclerosis and multiple sclerosis therapy (65, 66).
7) Some other autoimmune diseases have a known association with dietary factors.
8) Obesity itself may promote a low grade inflammatory response, and obesity is correlated with human leukocyte antigen gene alleles known to have a relationship to MS such as HLA-DRB1 (54)
9) There is a possible link between obesity and pediatric MS (67), although obesity has not consistently been linked to MS (i.e. 18).
10) There are anecdotal reports of MS relapses triggered by specific foods (45) and remission following dietary changes.
This is a list of dietary principles which may have significance in the treatment of multiple sclerosis. These principles have varying degrees of merit. None are proven. Speculative dietary ideas and comprehensive diet plans (i.e. the "swank" and "Terry Wahls" diets) are excluded from this list. The first list simply lists the dietary principles and brief information about how they can be implemented. The second list briefly reviews the evidence/theory behind the principle.
It is the opinion of this author that anecdotes regarding personal dietary implementation and subsequent results/symptoms are very likely to be misleading due to the placebo effect and the regression to the mean effect. This is particularly concerning for relapsing multiple sclerosis. I don’t mean to say that anecdotes should be disregarded but rather that principles should be subjected to serious scientific scrutiny. Unfortunately, it is often difficult to test diet as a treatment for human disease due to a) unblinding, b) poor patient compliance with diet, c) lack of funding (as there is no opportunity to profit from the study results), and d) poor methodology used by many investigators. Furthermore, different supplements may have a marginal and undetectable benefit individually but may have a clinically significant effects when combined with other strategies. For instance, if supplementation with riboflavin 100 mg daily had a 5% benefit in preventing disability progression in primary progressive multiple sclerosis, this would be extremely difficult to tease out in a clinical study.
List of dietary principles
1) Low saturated fat
Examples of foods containing high saturated fat: Animal fats (beef/fatty meats), milk products (butter, cheese, milk), certain oils [coconut, palm], eggs, chocolate, various processed foods.
2) Vitamin D supplementation
Natural sources of vitamin D from most concentrated to least concentrated: Cod liver oil, smoked eel, salmon, avocado, egg yolk, liver, butter, pork, milk
Supplementation of 100 IU D3 daily will increase 25(OH) vitamin D by 1ng/mL (2.5nmol/L) (5)
sun exposure to the entire body for an amount of time necessary to produce minimal redness of the skin is estimated to release 10,000-20,000 international units of vitamin D (6)
Optimal level of serum vitamin D [25(OH)VD] is unknown but estimated to be > 30ng/mL (75 nmol/L) by some experts (7). Others recommend higher levels.
4) Omega 3-and omega-6 fatty acids Various regimens of supplementation. One example is fish oil 6g/day (3.0g EPA, 1.8g DHA); Found in fatty fish such as mackerel, herring, sardines, albacore tuna, and salmon. Also found in plant sources such as soybeans, walnuts, sesame seeds.
5) probiotics: various regimens
6) Lipoic acid (i.e. 1200 mg daily)
7) Miscellaneous vitamins/minerals
8) Food allergies/intolerances (diary, gluten, grains, legumes, potatoes)
9) Reservatrol (50mg-250mg daily)
10) mitochondrial based supplements
11) B12 (often 1000 mcg subcutaneously or intramuscularly monthly; sublingual B12 also available (2,500 mcg weekly for maintenance or 2,500 mcg daily for deficiency); oral supplements may not be absorbed in some people)
12) Coenzyme Q10 (i.e. 600mg daily) or idebenone (synthetic analog of Coenzyme Q10) [eg idebenone 150mg daily]
13) acetyl-L-Carnitine (ALCAR) (i.e. 300mg-600mg daily)
14) L-Threonine (i.e. 500mg-1g daily)
15) dietary fiber (25 g/day for women and 38g/day for men recommended by one source)
16) folate (B9): (i.e. 500mg-1g daily)
17) riboflavin (vitamin B-2): 100-400mg daily (400mg daily is migraine prophylaxis dose)
18) niacin (B3): (i.e 500mg daily)
19) junk food
20) Low sodium diet (i.e < 2g sodium daily [or as low as 1.5g daily per some sources]; sodium is generally high in processed food and foods with added salt. Beets, celery, carrots, meat, and some other natural foods also contain high amounts of sodium).
Explanation of dietary principles and degree of evidence
1) Low Saturated fat:
There are many pre-clinical speculative reports suggesting that lipid metabolism may have an effect on the vascular endothelium in the blood brain barrier (8). One study suggests that individuals with multiple sclerosis have a different fatty acid composition of lecithin in the nervous system (9). A cross sectional study also suggested an association between oxidized low density lipoprotein (LDL) and higher disability (EDSS) in MS patients (10) . Liver consumption (liver is high in cholesterol and saturated fat) amongst individuals with MS has been associated with more severe disease (62)
Dr. Roy Swank (at Oregon Health Sciences University in Portland) was one of the early proponents of a low saturated fat diet in MS, basing his ideas on early epidemiologic studies suggesting a possible link. Various reports support this idea including a modern Iranian cross sectional study linking multiple sclerosis to saturated fat intake (83).
Examine the following data from 1934-1938 which demonstrated a marked variation in fat intake in different countries and a rough correlation with the prevalence of multiple sclerosis (94):
Aware of this, Dr. Swank placed 144 MS patients on a low-fat diet (< 20g fat/day). Those who adhered to the diet had less clinical deterioration and lower mortality (2). In fact, after 34 years, 95% of the those who adhered to the diet "survived and were physically active" (2). The mortality data comparing "good" and "poor" dieters is striking (94):
Of note, the fat intake of the "poor dieters" only averaged 38 grams per day which is very low compared to the typical American.
These patients also did well in comparison to reports of the natural history of multiple sclerosis. However, this study was only observational and did not have a blinded investigator. An evidence based cochrane review felt that the study's methodology was too poor to draw any serious conclusions (21). Of note, the famous nurses health cohort study from Harvard with 92,422 women and 14 years of follow-up did not find a link between total fat or saturated fat consumption and the risk of MS (69). Here are the results showing quintiles of total fat and animal fat consumption (quintile 1 on the left and quintile 5 on the right) .
There isn't the slightest hint of a correlation, but it should be noted that even the lowest quintile has much higher saturated fat consumption than recommended by Dr. Swank. Perhaps the variation among the general population is too low to detect an effect.
A recent study in 2014 was performed in 2014 at OHSU with a single blind methodology randomizing patients with relapsing remitting multiple sclerosis to either a low fat plant based diet or no dietary intervention. The patients receiving intervention had less fatigue, lost weight, and had more favorable lipid profiles, but there was no clear effect on MRI or disability outcomes (1).
Another study found that low-fat dietary advice and omega-3 fatty acid supplementation was associated with lower relapse rate and lower disability (EDSS). The treated patients were found to have lower plasma n-e fatty acids and higher n-6 fatty acids (3). There was no control group in this study, and only 16 patients with early disease (mean disease duration 1.6 years) were followed, but annualized relapse rate (average rate of MS relapses per patient per year) was only 0.06 compared to 1.39 prior to the study:
Please note that “before-after” studies are methodologically limited due to a “regression to the mean” phenomenon seen in the placebo group of all multiple sclerosis studies.
In yet another study of 31 patients with relapsing remitting multiple sclerosis, a randomized trial was done with a low fat diet (15% calories from fat) and fish oil versus an American Heart Association step I diet (30% calories from fat) with olive oil supplementation (meant to be a placebo for fish oil). They were followed for an average of 11 months, and the lower fat diet with fish oil group had less fatigue and there was a weak trend towards a greater decrease in relapses compared to the pre-study period (15% fat group + fish oil group: -0.79 +/- SD 1.12 relapses/year (P = 0.021) vs. -0.69 +/- SD 1.11 (P = 0.044) in the 30% fat + olive oil group) (4)
Interestingly, some early multiple sclerosis reviews suggested a deficiency of fat as a possible cause of multiple sclerosis (45) based on reports of low fat intake in some MS patients. The overall data on this subject is somewhat murky.
2) Vitamin D:
Vitamin D reduces auto-reactive t-cells (15) and shifts inflammatory cytokines to a TH2 or cell mediated immune state (16). Vitamin D levels are correlated with regulatory t cell function (17). Gene expression of HLA-DRB1*1501 (known to be linked to MS) is modulated by vitamin D.
The correlation between low vitamin D and multiple sclerosis is well known. In fact, patients with multiple sclerosis have a slight lower bone mass than age-matched controls, likely due to low vitamin D levels (51). In a North American study with 79 pairs of identical twins, one with MS and the other without MS, the twin with MS on average reported less childhood sun exposure (57).
One study showed that lower vitamin D level in pregnant mothers is associated with higher risk of MS in their daughters (relative risk of 0.59 for mothers in the 5th quintile of vitamin D relative to mothers in the 1st quintile); (11). The risk to develop MS within 3 years for Canadian children with clinically isolated syndrome is linked to vitamin D blood levels (12). For individuals in the US military, high vitamin D predicted lower risk of developing MS (relative risk of 0.38 for the 5th quintile vs. the 1st quintile (13). Among those with clinically isolated syndrome (individual with a single demyelinating attack who do not yet meet the diagnostic criteria for multiple sclerosis), higher vitamin D levels were associated with a lower probability of developing MS and lower lesion accumulation (93).
In another study, supplementation of 400 IU of vitamin D in 200,000 US women was associated with a 33% lower incidence of future development of multiple sclerosis (13). Higher vitamin D level is also associated with a better clinical course (14, 95).
For instance higher vitamin D was related to relapse rate in a Tazmanian cohort (95):
This data is from a multivariate analysis, and larger bubbles represent greater precision. A survival curve for relapse free patients shows similar results (95):
This has been corroborated by various studies including a Finnish study (14). There are also some prospective randomized trials in multiple sclerosis patients, but many of them are open label trials, have other methodological problems, or present inconclusive data.
Various interventional trials with vitamin D in multiple sclerosis have been attempted. In 2013, a meta-analysis of 5 trials failed to demonstrage a benefit in relapse prevention (96):
Of course, the correlation between vitamin D and multiple sclerosis could be driven by sunlight exposure, an obvious potential confounder.
3) Fruits/ Vegetables
A retrospective study in Montreal revealed that controls had higher vegetable protein intake than patients with multiple sclerosis (odds ratio 0.38) (18). The same study found higher intake of juice in control patients (though not of fruits). The result are shown below comparing cases and controls, and correlations were found with various other factors including animal fat and various vitamins (18):
An old epidemiologic study in the United States found an inverse relationship between MS risk and fruit and vegetable consumption (along with fish) (50).
However, one study found that vegetarians with MS have comparable disease severity to those who eat meat (62)
4) Fatty acid supplementation
The putative importance of fatty acids is partly based on their function in the brain. For instance, DHA is a component of brain membrane phospholipids (24). ALA (alpha-linolenic acid) has a role in differentiation of cultured brain cells (24).
Various preclinical studies have suggested a possible importance of fatty acids in multiple sclerosis. For instance, fatty acid supplementation (EPA, DHA) was associated with lower metalloproteinase-9 levels which in turn may be associated with blood brain barrier destruction and t cell migration into the central nervous system (19). EPA is converted to prostaglandins I3 and E3 which have anti-inflammatory effects (20).
In a Cochrane analysis of 6 randomized controlled trials on supplementation with omega-6 fatty acids (linolenic acid 11-23g/day), there was no benefit in disease progression, but there was a trend toward fewer relapses. (21) . In a post hoc meta-analysis of 3 trials for linoleic acid, supplementation was felt to decrease relapses, especially at lower levels of disability (47). Blood levels of linoleic acid were not decreased in MS patients compared to controls according to one study with 33 patients (59), and a cross sectional study did not find a statistically significant link between linolenic acid consumption and MS (69; also 18).
In a randomized controlled trial on omega-3 fatty acids (1350mg of eicosapentaenoic acid and 850mg docosahexaenoic acid) in patients with MS, no beneficial effects on MRI disease activity, relapse rate, or disability progression were found (22). Shown below are the data from this study for new enhancing brain lesions on MRI (left) and new T1 dark lesions on MRI (right). Neither of these weak trends were statistically significant.
The data on cumulative relapses are even less impressive (22)...
An evidence based guideline from the American Academy of Neurology concluded that "fish oil is probably ineffective for relapses, disability, fatigue, MRI lesions, and quality of life" (48).
A study on omega-3 fatty acid supplementation listed in the "low saturated fat" diet section (above) did reveal a benefit, but this trial combined supplementation with dietary advice (23).
5) Probiotics (“live microorganisms which when administered in adequate amounts confer a health benefit on the host”)
Probiotics have been associated with generation of regulatory t-cells (25). In a study of the probiotics (L paracasei and
L. plantarum) in experimental autoimmune encephalitis (a multiple sclerosis-related disease in mice), disease activity decreased, and there were increases in interleukin 10 and TGF-beta which have anti-inflammatory properties (26).
The focus of probiotics research has generally been on gastrointestinal disorders, but there are numerous recent articles in relation to MS.
6) Lipoic acid
This is an antioxidant . It has been found to reduce serum metalloproteinase-9 which has a known association with multiple sclerosis (27). It also decreases soluble intercellular adhesion molecule-1 (sICAMP-1) which is a cell surface binding protein which may have a role in vascular endothelial injury. A recent randomized double blind study with 52 patients with relapsing remitting multiple sclerosis compared cytokine profiles in those who consumed 1,200mg lipoic acid daily versus placebo (97). The treatment group appeared to have a more favorable cytokine profile including low levers of pro-inflammatory cytokines such as IFN-gamma, ICAM-1, TGF-beta, and IL-4.
7) Miscellaneous vitamins/minerals
The Canadian study discussed in the fruits/vegetables section suggests an association of MS with lower intake of various vitamins: vitamin C, thiamine (B1), riboflavin, niacin (B3) along with the minerals potassium and calcium (18). Please see the chart above listed in the fruits/vegetables section.
See specific sections on riboflacin an niacin below.
8) Eliminating potential food allergies/intolerances (diary, gluten, grains, legumes, potatoes)
The possible connection between MS and food allergy has a long history. Some patients have reported experiencing multiple exacerbations after consuming specific food groups such as seafood or rye (45). One investigator documented a modest association between MS and atopy, an inappropriate immune reaction to a foreign substance (46).
There are many possible theoretical explanations for the relationship of human autoimmune disease to an immunological response to food. For instance, a foreign protein could enter the circulation in physiologic concentration and elicit an immunological reaction which coincidentally targets components of the myelin sheath. This could occur if the foreign protein structurally resembles a component of the myelin sheath, a phenomenon known as molecular mimickry. For instance, butyrophilin in cows milk has some homology to myelin oligodendryocyte glycoprotein (MOG) in the myelin sheath (84, 88). Take a look at the amino acid sequences in MOG and BTN (butyrophylin) and note the obvious similarities (88):
Butyrophilin has been reported to induce a mouse model of of MS (84), though another investigator found that it actually ameliorates this condition (85).
Reported food allergies in MS patients include egg, milk, cocoa, rye, oats, wheat, rice, orange, cabbage, fish, and onion-those with the highest incidence in MS were rye, oats, wheat, and orange (45). For example, in a blinded study, 26.2% of MS patients demonstrated an allergy to an ophthalmic ointment containing wheat compared to only 8% of controls (45). In the same data set, only 6.7% of patients on an allergen-free diet achieved a "full remission" after a 3 month period, and another 4.4% experienced a "clinically significant remission" (45)-The authors argue that these results are worse than random chance (page 12).
In a study with allergy testing performed on 49 patients with MS, 6 had pollen allergies and 8 had food allergies based on scratch skin tests (45).
Celiac disease (related to gluten intolerance) can cause neurological manifestations such as ataxia (incoordination) (28, 60). The MRI below shows an inflammatory lesion in a patient with neurological manifestations of celiac disease.
The lesion in the left middle cerebellar peduncle seen above is very typical of and indistinguishable from a multiple sclerosis lesion.
Celiac disease also has an association with polyneuropathy (peripheral nerve disease) (28) but was not associated with multiple sclerosis in this review. There have been individual case reports of multiple sclerosis and neuromyelitis optica with celiac disease, but there is no clear correlation. Various studies have revealed that the prevalence of antigliadin antibodies (associated with celiac disease) were similar between MS patients and controls (29). For instance, In one series, IgG anti-giladin antibody (which is associated with celiac disease) was found in 12% of MS patients and 13% of controls (58). It has been speculated that cases of neurological manifestations of Celiac’s disease have been misdiagnosed as multiple sclerosis.
Cow’s milk allergy has also been studied with respect to MS. It has been speculated that butyrate or viruses present in milk could contribute to MS risk (50). I mentioned the possible role of molecular mimicry and buryrophilin above (84). Children with demyelinating diseases have been found to have abnormal t-cell reactivity to cow's milk proteins (87). An old epidemiologic study in the United States reported an association between per capita milk consumption and higher rates of MS (50). Other studies recapitulate this result (90, 91). However, the nurses health study (at Harvard, 92,422 women with 14 years of followup) failed to find any correlation between dairy intake an MS (69). One study with 48 patients with MS and 48 control patients found no evidence of cow’s milk allergy determined by serum allergen specific IgE levels in any patient in either group (30). A similar study revealed no serum IgE specific to egg or fish in MS or control patients (31). Another study found no clear link between antibodies against casein (a milk protein) and MS (89). In one study, childhood cow’s milk allergy was not associated with future development of MS (32).
An in vitro study suggests that reservatrol may prevent EBV-immortalization of b-cell clones (33). B-lymphocyte auto-immunoglobin production and antigen presentation are believed to be important in the pathogenesis of MS. However, reservatrol was not helpful in a mouse model of MS (82).
10) Mitochondria based supplements
(Ubiquinone, iron, zinc, biotin, pantothenic acid, magnesium, manganese, pyridoxine, B12)
Research suggests a possible role of the involvement of mitochondrial malfunction, particularly in the progressive forms of multiple sclerosis (34). Mitochondria have various antioxidant enzymes, and reactive oxygen species may mediate damage to axons in MS (70, 75).
In a genetic study, some polymorphisms of complex I (involved in the electron transport chain) genes (haplotypes within NDUFS5 (1p34.2-p33), NDUFS7 (19p13) and NDUFA7 (19p13)) were found to be associated with MS.
Abnormalities in mitochondria have been reported in MS (71, 73) including oxidative damage to mitochondrial DNA in MS plaques (37). Gene therapy with the mitochondrial gene heat shock protein 70 (HSP70) appears to decrease the severity of a mouse model of multiple sclerosis (72). The development of oligodendroglia (myelin producing cells) is dependent on mitochondrial function (74). In rare cases, mitochondrial enzyme defects can cause relapsing central nervous system demyelination in humans, mimicking multiple sclerosis (56).
See notes on some specific supplements below.
There are mixed results with regards to vitamin B12 supplementation in multiple sclerosis as discussed in a review article (35). Based on one small randomized trial, B12 injections slightly improved the “Guy’s neurological disability scale” (GNDS) compared to placebo, though the results are confounded by use of other treatments in the study including lofepramine, l-phenylalanine (35).
One study suggested a possible link between lower median cerebrospinal fluid B12 concentration an multiple sclerosis (36).
Of note, B12 deficiency itself can cause other neurological diseases including subacute combined degeneration of the cervical spine, peripheral neuropathy, and dementia, which can mimic MS (76).
12) Coenzyme Q10
The possible role of mitochondrial failure in progressive forms of multiple sclerosis has sparked interest in mitochondrial based nutrient supplementation. Co Q10 is a coenzyme involved in the electron transport chain and has antioxidant functions.
One randomized study of CoQ10 500mg/day vs placebo in relapsing remitting multiple sclerosis suggested a reduction of oxidative stress in treated patients inferred based on a decrease in serum malondialdehyde and other serum markers, but no clinical effects were studied (39).
Idebenone (a synthetic analog of coenzyme Q10) was non-beneficial in a mouse EAE model (38)
At the time of this writing, there is a national institute of health sponsored study for idebenone in primary progressive multiple sclerosis.
13) Acetyl-L-carnitine (ALCAR)
L carnitine is involved in fatty acid transport. Its use in MS is mostly in treating MS related fatigue. Although, L-carnitine was found to attenuate nitrous oxide mediated injury in a mouse model of MS (78).
In one randomized, trial of amantadine 100mg twice daily (a drug used in MS fatigue) versus L-Carnitine 1g twice daily , 70% of L carnitine treated patients and 43% of amantadine treated patients reported improvement in fatigue (nonsignificant; p = 0.07) (40). However, a cochrane evidence based review concluded that there was insufficient evidence to advocate or reject the use of carnitine in MS fatigue (77).
ALCAR also has purported benefits as a nootropic (agent to improve memory/cognitive function), though high quality data is limited.
L-threonine has been proposed as a natural treatment for spasticity. The theoretical basis is that L-threonine crosses the blood brain barrier and is converted to glycine which is an inhibitory neurotransmitter. In one trial, L-threonine 6g/day was used in patients with spinal cord spasticity (not necessarily related to MS) suggesting a possible modest benefit (41).
15) Dietary fiber
A case control study suggests a relationship between decreased fiber consumption and multiple sclerosis (18), although the association was quite modest.
16) Folate/Methylated folate
Folate is most known for its involvement in the developing nervous system, and folate deficiency increases the risk of neural tube defects (42).
Folate is involved in DNA methylation.
A study on cerebrospinal fluid folate and B12 concentrations did not show an association between low CSF folate concentration and multiple sclerosis (43).
However, low folate (and low magnesium) consumption has been associated with MS related fatigue (79).
Riboflavin (vitamin B2) was studied along with various other nutrients in a case control study. The study suggests that increased riboflavin intake is inversely associated with MS, but review of the actual data suggests no difference (mean intake for cases [male/female] is 2.7mg/2.3mg and mean intake for control [male/female] is 2.5mg/2.4mg), so I am unsure of how they came to their conclusion. The text suggests analysis by “quartiles” (18)
Of note, high dose riboflavin can produce a benign side effect of bright yellow urine.
Riboflavin consumption was actually positively associated with MS risk on one epidemiologic study (50)
The importance of NAD (nicotinamide adenine dinucleotide) in multiple sclerosis is suspected based on the idea of energy failure of neurons, particularly in progressive multiple sclerosis. Theoretically, supplementation could involve niacin or niacinamide. NAD is a cofactor in a large number of reduction oxidation reactions. Various theoretical associations between NAD and MS have been described (44)
a) An association between wallerian degeneration in mice and the relationship between a nicotinamide mononucleotide andylyltransferase1 (NMNAT1) gene mutation.
b) Increased NAD in the CNS in EAE models (possibly due to immune infiltration)
c) Mice with the mutation described in a had better prognosis in MOG induced EAE (a mouse model of MS)
There is a case report of a Mongolian with MS who also had various micronutrient deficiencies including niacin deficiency (80)
19) Junk food
A case control study suggested that consumption of pork/hot dogs (odds ratio 1.24) and sweets/candy (odds ratio 1.29) was positively associated with the risk of developing multiple sclerosis (18). Sweets were associated with MS in an Israeli case control study (51). An older epidemiologic study found an association of margarine and smoked meat with multiple sclerosis. However, a Polish study found that MS patients had lower cake consumption (50)
One author argues that multiple sclerosis became more prevalent in the Faroe Islands due to smoking fish, forming the generation of potentially toxic nitrophenols (63)
20) Low sodium diet
There is some preclinical evidence to suggest that a high salt diet may promote an inflammatory response. For instance, high salt intake has been linked to elevated monocyte (a type of white blood cell) activity and elevated proinflammatory cytokines such as IL-6 and IL-23 (81)
On 4/25/2013, three papers were published in nature with the following 3 findings
a) Sodium regulates, TH17 cells, a subset of t helper cells implicated in the pathogenesis of multiple sclerosis
b) Sodium upregulates serum glucocorticoid kinase 1 (SGK1) gene expression which enhances TH17 differentiation in vitro and in vivo
c) High sodium levels worsen experimental autoimmune encephalomyelitis, an animal model of multiple sclerosis.
Recently in an Argentinian study, high sodium intake was correlated with higher relapse rate and higher MRI lesion accumulation in multiple sclerosis (61). In an observational study, higher sodium intake was linked to a higher relapse rated (92).
A low sodium diet is generally achieved by minimizing processed foods and avoiding added salt. The general cutoff would be less than 2 grams of sodium daily (the cutoff for low sodium used in the Argentinian study, 61).
An old epidemiologic study reported an inverse relationship between fish consumption and rates of multiple sclerosis in different countries (50). The same study found that animal fat and butter fat was positively correlated with rates of MS (50). Fish consumption was found to be inversely related to the risk of MS in Belgium (64). Fish consumption is correlated with higher vitamin D levels in MS patients because it is generally rich in vitamin D, but fish consumption was not associated with MS disease severity in the same study (62)
As you can see, there is a lot of conflicting and low-quality evidence with regards to diet and multiple sclerosis. No dietary recommendations can be made with a high level of confidence, but the following rough recommendations can be made with a low level of confidence:
Eat a diet abundant in fruits and vegetables, particularly vegetables with a higher protein and fiber content such as legumes, nuts, and leafy greens. Avoid processed foods, junk food, added salt, and excess saturated fat. Fish may be preferred to other meats, particularly fatty meats. Supplement with vitamin D if your serum level is low (below 50 nmol/L) or get more sunlight exposure. Take a multivitamin which has adequate amounts of vitamin C, thiamine (B1), riboflavin (B2), niacin (B3), and calcium. Make sure that your potassium intake is adequate with frutis such as bananas/grapes or with other sources.. Avoid known personal food allergies/intolerances, particularly those to wheat, rye, and milk.
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