This Is MS Multiple Sclerosis Knowledge & Support Community

Saturated Fat
https://healthyforgood.heart.org/eat-sm ... rated-fats
The American Heart Association recommends aiming for a dietary pattern that achieves 5% to 6% of calories from saturated fat. For example, if you need about 2,000 calories a day, no more than 120 of them should come from saturated fat. That's about 13 grams of saturated fat per day.

or is the min 75% of 5-6%?

Systematic Review of the Association between Dairy Product Consumption and Risk of Cardiovascular-Related Clinical Outcomes (2016)
fft: http://advances.nutrition.org/content/7/6/1026.full

Abstract
The objective of this systematic review was to determine if dairy product consumption is detrimental, neutral, or beneficial to cardiovascular health and if the recommendation to consume reduced-fat as opposed to regular-fat dairy is evidence-based.

A systematic review of meta-analyses of prospective population studies associating dairy consumption with cardiovascular disease (CVD), coronary artery disease (CAD), stroke, hypertension, metabolic syndrome (MetS), and type 2 diabetes (T2D) was conducted on the basis of the PRISMA (Preferred Reporting Items for Systematic Reviews and Meta-Analyses) statement. Quality of evidence was rated by using the Grading of Recommendations Assessment, Development, and Evaluation scale.

High-quality evidence supports favorable associations between total dairy intake and hypertension risk and between low-fat dairy and yogurt intake and the risk of T2D.

Moderate-quality evidence suggests favorable associations between intakes of total dairy, low-fat dairy, cheese, and fermented dairy and the risk of stroke; intakes of low-fat dairy and milk and the risk of hypertension; total dairy and milk consumption and the risk of MetS; and total dairy and cheese and the risk of T2D.

High- to moderate-quality evidence supports neutral associations between
the consumption of total dairy, cheese, and yogurt and CVD risk;
the consumption of any form of dairy, except for fermented, and CAD risk;
the consumption of regular-and high-fat dairy, milk, and yogurt and stroke risk;
the consumption of regular- and high-fat dairy, cheese, yogurt, and fermented dairy and hypertension risk; and
the consumption of regular- and high-fat dairy, milk, and fermented dairy and T2D risk.

Data from this systematic review indicate that the consumption of various forms of dairy products shows either favorable or neutral associations with cardiovascular-related clinical outcomes.

The review also emphasizes that further research is urgently needed to compare the impact of low-fat with regular- and high-fat dairy on cardiovascular-related clinical outcomes in light of current recommendations to consume low-fat dairy.

still not touching on cofactors, tsk tsk. maybe in the full text...

Influence of Diet in Multiple Sclerosis: A Systematic Review
http://advances.nutrition.org/content/8/3/463.short

Nutrition is considered to be a possible factor in the pathogenesis of the neurological disease multiple sclerosis (MS). Nutrition intervention studies suggest that diet may be considered as a complementary treatment to control the progression of the disease; a systematic review of the literature on the influence of diet on MS was therefore conducted. The literature search was conducted by using Medlars Online International Literature (MEDLINE) via PubMed and Scopus. Forty-seven articles met the inclusion criteria. The reviewed articles assessed the relations between macro- and micronutrient intakes and MS incidence. The patients involved used alternative therapies (homeopathy), protocolized diets that included particular foods (herbal products such as grape seed extract, ginseng, blueberries, green tea, etc.), or dietary supplements such as vitamin D, carnitine, melatonin, or coenzyme Q10. Current studies suggest that high serum concentrations of vitamin D, a potent immunomodulator, may decrease the risk of MS and the risk of relapse and new lesions, while improving brain lesions and timed tandem walking. Experimental evidence suggests that serum vitamin D concentration is lower during MS relapses than in remission and is associated with a greater degree of disability [Expanded Disability Status Scale (EDSS) score >3]. The findings suggest that circulating vitamin D concentrations can be considered a biomarker of MS and supplemental vitamin D can be used therapeutically. Other studies point to a negative correlation between serum vitamin B-12 concentrations and EDSS score. Vitamin B-12 has fundamental roles in central nervous system function, especially in the methionine synthase–mediated conversion of homocysteine to methionine, which is essential for DNA and RNA synthesis. Therefore, vitamin B-12 deficiency may lead to an increase in the concentration of homocysteine. Further research is clearly necessary to determine whether treatment with vitamin B-12 supplements delays MS progression.

got in this time. excerpts:

"Health implications of unbalanced diet
Nutritional imbalances might justify widespread vitamin deficiencies,101 reduced control of body weight,102,103 prevalence of atherosclerosis,104 hypertension,
hyperlipidemia, diabetes, and an increased risk of vascular comorbidities, observed in MS patients as compared to the general population.105 Emerging evidence of an increased risk of disease progression in MS patients with vascular and metabolic comorbidities makes it reasonable to assume the existence of a dangerous vicious circle.

Malnutrition
Malnutrition can be defined as a pathological state resulting from inadequate nutrition, including undernutrition, over-nutrition (overweight and obesity), and deficiency of one or more specific nutrients (such as vitamins or minerals). To date, its exact prevalence in MS patients is unknown, but some studies have demonstrated that malnutrition may occur more frequently in MS than in other chronic diseases, being more relevant in severely disabled patients. The detrimental consequences on functional abilities, mental activity, immune system, and muscle strength may contribute to worsen pre-existing MS symptoms,impacting negatively on patients’ quality of life.
...
Pressure ulcers and malnutrition
Pressure ulcers – which represent a major cause of hospitalization – occur more often in MS than in the general population, especially in the presence of mobility
decline (in advanced stages of the disease), older age, male sex, lower socio-economic status. Decreased albumin and hemoglobin levels, but also a low mid-arm circumference, seem to be related with pressure sores. An inadequate nutritional status characterized by a low intake of calories, iron, folate, vitamin D, zinc, arginine, and anti-oxidants,120 in combination with the use of medications, such as glucocorticoids, may contribute to delaying the healing process of pressure ulcers in MS patients, increasing costs for medical care and hospitalization.
...
Evaluation of nutritional status in MS
The evaluation of nutritional status in MS is a stepwise, time-consuming procedure, often neglected in clinical practice ...

*cough* YA DON'T SAY!! *cough*

... although the early identification of patients at risk of developing malnutrition or nutritional imbalances has important health implications. Many nutritional screening questionnaires are available: ... As suggested by Pasquinelli et al., the following steps should be observed:
• Evaluation of nutritional status through some key points. Nutrition ‘history’ (through diet diaries etc) assessing lifestyle and types/quantities of consumed food; ...
• Calculation of nutritional needs; ...
• Evaluation of dysphagia and potential interfering conditions with nutrition (through a multidisciplinary approach).
• Schedule of nutritional intake.
• Plan for the eventual occurrence of complications.
...
Dietary recommendation and specific nutrients in MS Until now, a specific dietary model has not been established for MS patients; therefore, balanced and healthy nutrition – as advised to the general population – is recommended.
...
In MS subjects, respecting the proportions between macro- (lipids, proteins, and carbohydrates) and micronutrients (vitamins and minerals), the diet
should increase plasma levels of essential fatty acids, unrefined carbohydrates (to alleviate symptoms such as fatigue and weakness), anti-oxidants, vitamin D and B12; it would also be appropriate to ensure an adequate supply of proteins, zinc (for tissue trophism), fibers, and fluids (to maintain regular gut function).
...
Vitamin D
... in case of demonstrated deficiency – a very common occurrence in MS population – oral supplements of vitamin D are strongly and unanimously recommended. ... a cumulative dose of 300 000–1 000 000 IU, over 1–4 weeks, is recommended, followed by a maintenance dose of 800–2000 IU/day (or weekly equivalent).

Minerals
Some authors have speculated about the relationship between the dysregulation of certain minerals and MS.176–178 It has been reported that selenium deficiency (contained in cereals, beef, white bread, pork, chicken, fish, and eggs), and that of zinc (in oysters, sardines, meat turkey, beef, lamb, poultry, pumpkin seeds, eggs, cereals, nuts, legumes, dark chocolate), magnesium (in green leafy vegetables, dried fruit, legumes, cereals, and bananas), and iron (in beef, pig, horse, poultry, and fish), probably associated with malnutrition and/or to an increased demand, may worsen some aspects of the disease (especially pressure sores and fatigue).109,179 Given their multiple biological roles and the lack of association between serum concentrations and homeostasis at tissue level, in the nutritional assessment of MS patients, it seems appropriate to evaluate the individual risk factors of mineral dysregulation and deficiencies, in order to promptly correct them according to the RDA.

Conclusions and future perspectives
...Furthermore, because diet-related comorbidities, such as malnutrition, metabolic syndrome, and cardiovascular disease, seem to be related to a decline in physical condition and quality of life in MS patients, an accurate nutritional counseling should be encouraged in clinical practice. Future studies, exploring the role of a healthy and specific diet on MS onset and/or evolution, should be strongly encouraged in order to move toward a holistic management of MS."

common sense FTW

glad to have seen this, finally. now i need the chicken/egg clarification.. i get the zinc finger connection where 1,25(OH)2vitamin d3 levels are concerned, but i'm still curious re zinc interactions with plain old 25(OH)vitamin d3.

The relationship of serum vitamin D and Zinc in a nationally representative sample of Iranian children and adolescents: The CASPIAN-III study (2016)
fft https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5307609/

Abstract
Background: Vitamin D (VitD) deficiency is a common worldwide problem. Some previous studies have shown that both Zinc (Zn) and VitD deficiency are prevalent in Iran. This study aimed to assess the relationship of serum Zn and vitamin D levels in a nationally representative sample of Iranian children and adolescents.

Methods: This case-control study was conducted as a sub-study of a school-based surveillance program entitled "the CASPIAN-III Study". An equal number of individuals with and without hypovitaminosis D including 330 participants aged 10 to 18 years were selected. The correlation of serum 25 hydroxy vitamin D (25(OH) D), cardiometabolic factors and Zn concentrations was determined. Statistical analysis was done using one-way analysis of variance (ANOVA), Pearson's correlation, linear regression, and logistic regression.

Results: The mean age was not significantly different in participants with and without hypovitaminosis D (14.74±2.52 vs. 14.74±2.66 years, respectively, p>0.05). The mean 25(OH) D level was 6.34±1.47ng/ml in the group with hypovitaminosis D and 39.27±6.42ng/ml in controls. The mean Zn level was significantly lower in the hypovitaminosis D group than in controls (1.15±0.26 vs. 1.43±0.32μg/ml, respectively, p<0.001). The Pearson's analysis showed a positive and significant correlation between Zn and 25(OH) D serum levels (p<0.0001). Odds ratios analysis for VitD level between various quartiles of serum zinc concentration for all participants showed that the odds of higher levels of VitD increased by higher levels of Zn.

Conclusion: We found significant associations between low serum concentrations of zinc and 25(OH) D. Food fortification or mineral supplementation should be considered in future health programs.

...

"Finally, conducting future studies to identify the factors affecting Vitamin D and Zinc deficiency in schoolchildren, their relationship and the real causes of simultaneous lack of VitD and Zinc is highly recommended."

yes pls. i still want to know for certain whether correcting my zn deficiency played a causative role in my tripled dose response to d3 supplementation. the timing is right but the lit i've found to date suggests greater impact resulting from the work i've done on magnesium status.

noting people's propensity for taking a moderation recommendation to outright omission extremes, i'll just leave this here for consideration

Can dietary saturated fat be beneficial in prevention of stroke risk? A meta-analysis
https://link.springer.com/article/10.10 ... 016-2548-3

We conducted a meta-analysis to summarize available evidence regarding the relation between saturated fatty acid (SFA) intake and stroke risk. We searched multiple electronic databases through February 2016. Log relative risks (RRs) with 95 % confidence intervals (CIs) of the highest versus the lowest for cohort studies were weighed by the inverse variance method to obtain combined RRs. 15 prospective studies including 476,569 individuals and 11,074 strokes were included. Higher SFA intake was associated with reduced overall stroke risk [RR = 0.89 (95 % CI 0.82–0.96)] and fatal stroke risk [RR = 0.75 (95 % CI 0.59–0.94)]. Subgroup analysis indicated that higher SFA intake was associated with reduced stroke risks for East-Asians [RR = 0.79 (95 % CI 0.69–0.90)], for dose <25 g/day [RR = 0.81 (95 % CI 0.71–0.92)], for males [RR = 0.85 (95 % CI 0.75–0.96)], and for individuals with body mass index (BMI) <24 [RR = 0.75 (95 % CI 0.65–0.87)], but not for non East-Asians, females, and individuals with dose ≥25 g/day and BMI ≥24. This meta-analysis reveals that higher SFA intake is inversely associated with risk of stroke morbidity and mortality with race, sex, and BMI as key factors influencing this risk. There seems to be a threshold of SFA intake for inverse relation of SFA intake with stroke. However, the stroke-reducing or -increasing effects for specific subtypes and specific food sources of SFA can be concealed. Functions of specific subtypes of SFA (e.g. lignoceric acid) and specific food sources of SFA (i.e. plant vs. animal) in relation to stroke need to be clarified in further studies.

have just been into an article on protein source vs fat source as something worth more consideration, but that will have to be for another time.

Food Sources of Saturated Fat and the Association With Mortality: A Meta-Analysis
http://ajph.aphapublications.org/doi/ab ... 013.301492

We summarized the data related to foods high in saturated fat and risk of mortality. We searched Cochrane Library, MEDLINE, EMBASE, and ProQuest for studies from January 1952 to May 2012. We identified 26 publications with individual dietary data and all-cause, total cancer, or cardiovascular mortality as endpoints.

Pooled relative risk estimates demonstrated that high intakes of milk, cheese, yogurt, and butter were not associated with a significantly increased risk of mortality compared with low intakes. High intakes of meat and processed meat were significantly associated with an increased risk of mortality but were associated with a decreased risk in a subanalysis of Asian studies. The overall quality of studies was variable.

Associations varied by food group and population. This may be because of factors outside saturated fat content of individual foods. There is an ongoing need for improvement in assessment tools and methods that investigate food sources of saturated fat and mortality to inform dietary guidelines.

inclusion criteria important!

The Misuse of Meta-analysis in Nutrition Research
https://jamanetwork.com/journals/jama/a ... irect=true

Controversial conclusions from meta-analyses in nutrition are of tremendous interest to the public and can influence policies on diet and health. When the results of meta-analyses are the product of faulty methods, they can be misleading and can also be exploited by economic interests seeking to counteract unflattering scientific findings about commercial products.

The term meta-analysis was coined by Glass in the mid-1970s for a set of techniques designed to characterize and combine the findings of prior studies in order to increase statistical power, provide quantitative summary estimates, and identify data gaps and biases. When applied to studies conducted with similar populations and methods, meta-analyses can be useful. However, many published meta-analyses have combined the findings of studies that differ in important ways, prompting Eysenck to complain that they have mixed apples and oranges—and sometimes “apples, lice, and killer whales”—yielding meaningless conclusions.

The effect of replacing saturated fat with mostly n-6 polyunsaturated fat on coronary heart disease: a meta-analysis of randomised controlled trials
https://nutritionj.biomedcentral.com/ar ... 017-0254-5

Abstract
Background
A cornerstone of conventional dietary advice is the recommendation to replace saturated fatty acids (SFA) with mostly n-6 polyunsaturated fatty acids (PUFA) to reduce the risk of coronary heart disease (CHD). Many clinical trials aimed to test this advice and have had their results pooled in several meta-analyses. However, earlier meta-analyses did not sufficiently account for major confounding variables that were present in some of those trials. Therefore, the aim of the study was to account for the major confounding variables in the diet heart trials, and emphasise the results from those trials that most accurately test the effect of replacing SFA with mostly n-6 PUFA.

Design
Clinical trials were identified from earlier meta-analyses. Relevant trials were categorised as ‘adequately controlled’ or ‘inadequately controlled’ depending on whether there were substantial dietary or non-dietary differences between the experimental and control groups that were not related to SFA or mostly n-6 PUFA intake, then were subject to different subgroup analyses.

Results
When pooling results from only the adequately controlled trials there was no effect for major CHD events (RR = 1.06, CI = 0.86–1.31), total CHD events (RR = 1.02, CI = 0.84–1.23), CHD mortality (RR = 1.13, CI = 0.91–1.40) and total mortality (RR = 1.07, CI = 0.90–1.26). Whereas, the pooled results from all trials, including the inadequately controlled trials, suggested that replacing SFA with mostly n-6 PUFA would significantly reduce the risk of total CHD events (RR = 0.80, CI = 0.65–0.98, P = 0.03), but not major CHD events (RR = 0.87, CI = 0.70–1.07), CHD mortality (RR = 0.90, CI = 0.70–1.17) and total mortality (RR = 1.00, CI = 0.90–1.10).

Conclusion
Available evidence from adequately controlled randomised controlled trials suggest replacing SFA with mostly n-6 PUFA is unlikely to reduce CHD events, CHD mortality or total mortality. The suggestion of benefits reported in earlier meta-analyses is due to the inclusion of inadequately controlled trials. These findings have implications for current dietary recommendations.

moderation once again key.
makes sense to me that while plenty of people may need to dial certain things back, others can actually need more.
like i did... having been firmly in the 'no appreciable dietary fat' camp (nor protein, nor other key essentials) in the leadup to dx.
no one dietary strategy should be expected to make sense for all. from wherever you start, work towards the middle of the road - whatever that means in your individual case.

Diet and Breast Cancer: Evidence That Extremes in Diet Are Associated With Poor Survival
http://ascopubs.org/doi/abs/10.1200/JCO.2003.06.121

Purpose: Diet has been postulated to influence breast cancer prognosis; however, existing evidence is weak and inconsistent. Previous studies have sought evidence of a linear relationship between diet and breast cancer outcomes. Because of a U-shaped association of body mass index (BMI) with survival in breast cancer, we hypothesized that a nonlinear association also existed for dietary variables.

Patients and Methods: Four hundred seventy-seven women with surgically resected T1 to T3, N0/1, M0 breast cancer completed the Block Food Frequency Questionnaire 9.3 ± 4.6 weeks (mean ± standard deviation) after diagnosis, reporting intake over the preceding 12 months. Data on tumor-related factors, treatment, and outcomes were obtained prospectively from medical records. A series of Cox models was performed, modeling the association of dietary factors with breast cancer survival linearly and quadratically, adjusting for total energy intake, tumor- and treatment-related variables, and BMI.

Results: Significant nonlinear survival associations were found for protein, oleic acid, cholesterol, polyunsaturated-saturated fat ratio, and for percentage of calories from fat and percentage of calories from carbohydrates in multivariate models. The shape of the survival associations varied across nutrients. Hazard ratios for highest risk quintiles ranged from 2.1 to 6.5. For total fat, adjustment for BMI reduced the multivariate P value obtained from nonlinear Cox models from .05 to .10. No significant linear associations were identified.

Conclusion: The association of key dietary variables with breast cancer survival may be U-shaped rather than linear. Our data suggest that midrange intake of most major energy sources is associated with the most favorable outcomes, and extremes are associated with less favorable outcomes.

Variations in diet cause alterations in microbiota and metabolites that follow changes in disease severity in a multiple sclerosis model
https://www.wageningenacademic.com/doi/ ... M2017.0116

Multiple sclerosis (MS) is a metabolically demanding disease involving immune-mediated destruction of myelin in the central nervous system. We previously demonstrated a significant alteration in disease course in the experimental autoimmune encephalomyelitis (EAE) preclinical model of MS due to diet. Based on the established crosstalk between metabolism and gut microbiota, we took an unbiased sampling of microbiota, in the stool, and metabolites, in the serum and stool, from mice (Mus musculus) on the two different diets, the Teklad global soy protein-free extruded rodent diet (irradiated diet) and the Teklad sterilisable rodent diet (autoclaved diet). Within the microbiota, the genus Lactobacillus was found to be inversely correlated with EAE severity. Therapeutic treatment with Lactobacillus paracasei resulted in a significant reduction in the incidence of disease, clinical scores and the amount of weight loss in EAE mice. Within the metabolites, we identified shifts in glycolysis and the tricarboxylic acid cycle that may explain the differences in disease severity between the different diets in EAE. This work begins to elucidate the relationship between diet, microbiota and metabolism in the EAE preclinical model of MS and identifies targets for further study with the goal to more specifically probe the complex metabolic interaction at play in EAE that may have translational relevance to MS patients.

well, look who's decided to join us ;)

Diet in multiple sclerosis: Science takes a seat at the table
author info: https://www.ncbi.nlm.nih.gov/pubmed/29212826

Let food be your medicine and medicine be your food.
Attributed to Hippocrates

Editorial

Persons with multiple sclerosis (MS) are often proactive in their quest to delay or avoid disability. They frequently seek guidance from their physicians on modifiable lifestyle factors that may slow MS disease progression. Questions about exercise, dietary supplements, and various natural remedies are common, but dietary concerns are among the most common inquiries from patients. Low-fat, Paleolithic, gluten-free, vegan, Mediterranean, and ketogenic diets all have their advocates. Despite multiple self-help books and Internet sites advising specific diets for persons with MS, there is little high-level evidence in the scientific literature to inform clinical recommendations. Patients often ask for specific guidance that goes beyond “eat a healthy diet,” and, most importantly, information on whether or not dietary changes can reduce their risk of long-term disability. Thus far, we have had little basis for making any recommendations based on scientific data.
In this issue of Neurology®, Fitzgerald et al.1 provide epidemiologic evidence for an independent link between patient-reported healthier diets and lower disability. They describe self-reported data obtained from a questionnaire completed by 6,989 persons with MS registered in the North American Research Committee on MS (NARCOMS; a large registry of patient-reported disability and quality of life outcomes, health care utilization and comorbidities, and other health-related variables, such as diet, which is updated and expanded with biannual surveys). In their analysis, a healthy diet was quantified, in quintiles, as consumption of (1) more fruits, vegetables, legumes (fifth quintile = most), (2) more whole grains (fifth quintile = most), (3) less sugar from desserts and beverages (fifth quintile = least), and (4) less red and processed meats (fifth quintile = least). Persons with MS in the highest quintile for diet quality (sum of quintiles across the 4 food categories) vs lowest quintile were at 20% lower risk for severe vs mild self-reported physical disability, even after controlling for several other health-related factors (age, disease duration, body mass index, income, smoking). When examined separately, higher intake of whole grains was the only component of the diet score reliably linked to lower disability. These data from a large cohort of persons with MS provide a convincing observational link between diet and disability. The field of diet in MS has served up courses of a priori opinions garnished with anecdotes and small samples, to which Fitzgerald et al. add substantive and robust empirical data. This sets the table for subsequent work on mechanisms of action and causal relationships.
Fitzgerald et al. acknowledge limitations, including inability to draw causal inferences and to perform fine-grained dietary analyses (e.g., various fats) due to brevity of their diet survey. Fish intake, with the interesting link to vitamin D, is a potentially important dietary factor that was not investigated in this study. Like survey research generally, there was potential selection bias (68% response rate from an already active responder subgroup, one-third of the overall NARCOMS database: responders were older with longer disease duration and more likely to be Caucasian, married, and of higher income) and potential response bias may have occurred, since all variables were self-reported.
This study does not identify mechanisms of action. How might a healthy diet, as defined by Fitzgerald and colleagues, reduce disability among people with MS? It is unknown whether diet is linked to disability through relationships with inflammatory disease activity, disease-related degeneration, brain aging independent of MS disease, or interactions among these or other factors. Vascular disease risk factor comorbidities, such as hypercholesterolemia, may be a mechanism linking diet and MS disability,2 perhaps through increased disease activity 3 or cerebral atrophy.4 Another mechanism may relate to influences of diet on the gut microbiome, which is linked to inflammatory processes in MS.5 How much is it simply an issue of better symptom control, such as less fatigue or constipation? Might certain diets influence the absorption and metabolism of disease-modifying therapies, resulting in altered efficacy? Unrelated to MS, a Mediterranean diet is linked to lower risks for mortality,6 incident dementia,7 and cerebral atrophy 8 in non-neurologic cohorts, thereby also protecting patients against comorbidities that are associated with increased disability in MS. Consistent with the notion of brain reserve against disability in MS,9 lifestyle factors, such as diets, which contribute to preservation of brain health and structure could reduce risk for disability. Indeed, Fitzgerald et al. also reported that a composite healthy lifestyle (body mass index <25, physical activity, no smoking, better than average diet) was robustly related to lower risk for disability, ostensibly mediated through preserved brain health and maintenance of brain reserve.
The next important but challenging steps are to perform randomized controlled trials of diet to yield causal evidence for dietary interventions. Pilot studies have been completed 10 or are underway (e.g., NCT02986893, NCT02647502). Isolating specific dietary factors and mechanisms of action driving protective effects against disability and disease progression would help advance the field. Ideally such studies should be longitudinal, include patients with early disease, and involve multimodal objective assessments, including relapse rates, MRI, and postulated MS biomarkers.
Motivated by the current work of Fitzgerald and colleagues, future rigorous experiments and multidisciplinary collaborations on diet may someday yield empirically validated dietary recommendations for our patients. Until then, encouraging a healthy lifestyle (healthy eating, a normal weight, routine physical activity or exercise, and avoiding smoking) should be a fundamental message we give to all newly diagnosed patients with MS.

Nutritional Intake Correlates with Function in Persons with Mild-to-Moderate Multiple Sclerosis (2018)
http://www.ijmsc.org/doi/abs/10.7224/15 ... =cmsc-site

Abstract
Background: To assess the association between nutrition, ambulation, daily activity, quality of life (QOL) and fatigue in individuals with mild-to-moderate disability with multiple sclerosis (MS).

Methods: Cross-sectional pilot study that included twenty ambulatory volunteers with MS (14 F/6 M, 57.9±10.2 years, EDSS = 4.1±1.8). Primary outcome variables included dietary assessment (3-day dietary consumption and the Food Frequency Questionnaire), and 6-Minute Walk Test (6MWT). Secondary measures included the Timed 25-Foot Walk test (TW-25), Timed Up and Go test, daily activity and 3 self-report questionnaires; 12-Item Multiple Sclerosis Walking Scale (MSWS-12), Short Form (SF)-36, and the Modified Fatigue Impact Scale (MFIS).

Results: Significant correlations were seen between the percent of diet comprised from fats and the 6MWT (r = 0.51, P = .02) and the physical functioning (PF) component of the SF-36 (r = 0.47, P = .03). The percent of carbohydrates was significantly correlated with the 6MWT (r = −0.43, P = .05), daily activity (r= −0.59, P = .005) and the PF component of the SF-36 (r = −0.47, P = .03). Cholesterol, folate, iron, and magnesium were significantly positively correlated with the PF component of the SF-36 and the 6MWT.

Conclusions: These findings indicate better ambulation and daily function as well as QOL with increased fat intake, decreased carbohydrate intake, and increased intake of the micronutrients cholesterol, folate, iron, and magnesium. This pilot study highlights the potential impact that diet may have on function and QOL in MS.

The conclusion of the study:

These findings indicate better ambulation and daily function as well as QOL with increased fat intake, decreased carbohydrate intake, and increased intake of the micronutrients cholesterol, folate, iron, and magnesium


OMG, imagine that contrary to what most believe and have been told by so called experts, increased fat (I assume they are referring to good Omega 3 fats) and reduced carbs is a good thing! The Dr. Swank people and others who are advocates of low fat/no fat MS diets will not be happy!!! Although I would imagine they will just ignore this.

I happen to agree with this finding as that the general diet they recommend (too bad they don't give details) is basically the type of diet I follow and have been for 4 years and I am doing very well. But of course there are many (most) who follow a diet low in fat and high in carbs that are also doing well. The bottom lines is nobody is certain at this time as to what is the best diet to follow.

all such studies would do far better to measure dietary impacts on internal macro and micronutrient status as well as on function. would help explain contradictory study results, why a given diet worked for subject a and didn't for subject b, etc.

i had a next to no fat diet at dx. i had done things like take nutrient laden nuts out of my vegan diet, because of the fat content. idiotic.

for the far greater proportion of the population for whom a high fat diet is status quo leading up to dx, certainly one could expect benefits from a lower fat approach.

extremes in either direction are the danger.