MS Nutrition-summary pts 1st post, p.1

Tell us what you are using to treat your MS-- and how you are doing.

Re: MS Nutrition-summary pts 1st post, p.1

Postby jimmylegs » Wed Jul 04, 2012 6:56 am

can i just say THANK GOD that my doc is not a complete dickhead??!!! the crap other people have to deal with sometimes, seriously...
READ ME key info on nutrient targets - www.thisisms.com/ftopict-2489.html
my approach: no meds so far - just nutrient-dense anti-inflammatory whole foods, and supplements where needed
info: www.whfoods.com, www.nutritiondata.com
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Re: MS Nutrition-summary pts 1st post, p.1

Postby jimmylegs » Wed Jul 04, 2012 6:57 am

hahaha the forum censored me
READ ME key info on nutrient targets - www.thisisms.com/ftopict-2489.html
my approach: no meds so far - just nutrient-dense anti-inflammatory whole foods, and supplements where needed
info: www.whfoods.com, www.nutritiondata.com
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Re: MS Nutrition-summary pts 1st post, p.1

Postby jimmylegs » Wed Jul 04, 2012 9:56 am

wow, check out this 'normal' range for zinc, go japan! that's what you get for eating more rice and less bread i guess.

Zinc Deficiency and Clinical Practice
http://www.med.or.jp/english/pdf/2004_08/359_364.pdf

Table 4 Possible Conditions Suggested by Serum Zinc Levels and Countermeasures

Serum zinc level (ug/dl) 84–159 Normal range

which is... 12.85 - 24.33 umol/L. !!!

HOW did i not notice this before :S

AAAAND, the peak of that little bell curve, is 18.6 umol/L. snap!
READ ME key info on nutrient targets - www.thisisms.com/ftopict-2489.html
my approach: no meds so far - just nutrient-dense anti-inflammatory whole foods, and supplements where needed
info: www.whfoods.com, www.nutritiondata.com
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Re: MS Nutrition-summary pts 1st post, p.1

Postby jimmylegs » Sat Jul 07, 2012 2:17 pm

tried going a little above and beyond on the magnesium this week. no deal. making my legs weak. can't do it without adding some calcium too. going to back off again on the mag, and wait for my legs to perk up a little!
READ ME key info on nutrient targets - www.thisisms.com/ftopict-2489.html
my approach: no meds so far - just nutrient-dense anti-inflammatory whole foods, and supplements where needed
info: www.whfoods.com, www.nutritiondata.com
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Re: MS Nutrition-summary pts 1st post, p.1

Postby jimmylegs » Sun Jul 08, 2012 6:36 am

redistributed the magnesium in my dosette and even though i'm still feeling a little out of it, my legs already feel better. have a day off - going to make myself some vitamin d3 in this beautiful sunshine later today.

not feeling particularly sharp, just doing a lot of cooking while the day is still fairly cool. have some tomato-pesto sauce on the go, ready for future incorporation into a veggie-kale-cottage cheese lasagne.

half a baked potato diced is becoming hash browns in my cast iron pan, sauteed red onion, red pepper and spinach are sitting in 2 eggs sprinkled with a tiny bit of old cheddar, have most of the veg chopped up into a quinoa (mmm protein!) tabbouleh, chick peas and tahini are in the food processor waiting for final steps to complete hummous, and there's some locally raised goat meat thawing in the sink to make roti later :) have to get yellow split peas cooked next for that. going to make the wheat/split pea roti pastry from scratch too.

time to eat those eggs and potatoes :)
READ ME key info on nutrient targets - www.thisisms.com/ftopict-2489.html
my approach: no meds so far - just nutrient-dense anti-inflammatory whole foods, and supplements where needed
info: www.whfoods.com, www.nutritiondata.com
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Re: MS Nutrition-summary pts 1st post, p.1

Postby koopico » Mon Jul 09, 2012 11:55 am

Jimmylegs, GL with your "guinea-pigging!" Thanks as always for such sharing such incredibly informative...info! You're the best!
:)
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Re: MS Nutrition-summary pts 1st post, p.1

Postby jimmylegs » Tue Jul 10, 2012 4:50 am

thanks K! legs are all better, the verdict is in - i can't handle 3 magnesium pills a day. two's my limit: one mag glycinate, one mag citrate, done.
READ ME key info on nutrient targets - www.thisisms.com/ftopict-2489.html
my approach: no meds so far - just nutrient-dense anti-inflammatory whole foods, and supplements where needed
info: www.whfoods.com, www.nutritiondata.com
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Re: MS Nutrition-summary pts 1st post, p.1

Postby jimmylegs » Tue Jul 10, 2012 6:15 am

all right, on to my next thing..

Rare variants in the CYP27B1 gene are associated with multiple sclerosis (2011)
http://onlinelibrary.wiley.com/doi/10.1 ... 8/abstract
Abstract
Objective:
Multiple sclerosis (MS) is a complex neurological disease. Genetic linkage analysis and genotyping of candidate genes in families with 4 or more affected individuals more heavily loaded for susceptibility genes has not fully explained familial disease clustering.
Methods:
We performed whole exome sequencing to further understand the heightened prevalence of MS in these families.
Results:
Forty-three individuals with MS (1 from each family) were sequenced to find rare variants in candidate MS susceptibility genes. On average, >58,000 variants were identified in each individual. A rare variant in the CYP27B1 gene causing complete loss of gene function was identified in 1 individual. Homozygosity for this mutation results in vitamin D-dependent rickets I (VDDR1), whereas heterozygosity results in lower calcitriol levels. This variant showed significant heterozygous association in 3,046 parent-affected child trios (p = 1 × 10−5). Further genotyping in >12,500 individuals showed that other rare loss of function CYP27B1 variants also conferred significant risk of MS, Peto odds ratio = 4.7 (95% confidence interval, 2.3–9.4; p = 5 × 10−7). Four known VDDR1 mutations were identified, all overtransmitted. Heterozygous parents transmitted these alleles to MS offspring 35 of 35× (p = 3 × 10−9).
Interpretation:
A causative role for CYP27B1 in MS is supported; the mutations identified are known to alter function having been shown in vivo to result in rickets when 2 copies are present. CYP27B1 encodes the vitamin D-activating 1-alpha hydroxylase enzyme, and thus a role for vitamin D in MS pathogenesis is strongly implicated.


background info...

Vitamin D: Production, Metabolism, and Mechanisms of Action
http://www.endotext.org/parathyroid/par ... frame3.htm
Vitamin D3 is produced in the skin from 7-dehydrocholesterol by UV irradiation, which breaks the B ring to form pre-D3. Pre-D3 isomerizes to D3 or with continued UV irradiation to tachysterol and lumisterol. D3 is preferentially removed from the skin, bound to DBP. The liver and other tissues metabolize vitamin D, whether from the skin or oral ingestion, to 25OHD, the principal circulating form of vitamin D, by the enzyme CYP27B1, the 25OHD-1αhydroxylase.


i am not sure if that last bit is exactly accurate...

Genetic evidence that the human CYP2R1 enzyme is a key vitamin D 25-hydroxylase (2004)
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC419671/
The synthesis of bioactive vitamin D requires hydroxylation at the 1α and 25 positions by cytochrome P450 enzymes in the kidney and liver, respectively. The mitochondrial enzyme CYP27B1 catalyzes 1α-hydroxylation in the kidney but the identity of the hepatic 25-hydroxylase has remained unclear for >30 years. We previously identified the microsomal CYP2R1 protein as a potential candidate for the liver vitamin D 25-hydroxylase based on the enzyme's biochemical properties, conservation, and expression pattern. Here, we report a molecular analysis of a patient with low circulating levels of 25-hydroxyvitamin D and classic symptoms of vitamin D deficiency. This individual was found to be homozygous for a transition mutation in exon 2 of the CYP2R1 gene on chromosome 11p15.2. The inherited mutation caused the substitution of a proline for an evolutionarily conserved leucine at amino acid 99 in the CYP2R1 protein and eliminated vitamin D 25-hydroxylase enzyme activity. These data identify CYP2R1 as a biologically relevant vitamin D 25-hydroxylase and reveal the molecular basis of a human genetic disease, selective 25-hydroxyvitamin D deficiency.


so if we're talking CYP2B1, i think we're talking about hydroxylating 25(OH)D3 to 1,25(OH)2D3 in the kidney.

is zinc a limiting factor? here's one study suggesting this may be the case:

1,25(OH)2D response to combined zinc and phosphorus depletion in rats (1990).
http://www.cabdirect.org/abstracts/1992 ... 7E5BEACDA7
Vitamin D metabolites, parathyroid hormone (PTH) and mineral balance were studied during phosphorus depletion in rats with different zinc nutritional status. 66 male Lewis rats were pair fed on normal phosphorus, zinc-replete (+) or -deplete (-) diets for 2 weeks. Thereafter, half of each paired group underwent 1 week of P depletion. Zn-deplete rats had lower plasma Zn, and P-deplete rats had lower plasma P concentrations than replete controls. Plasma calcium PTH and 25-hydroxycholecalciferol concentrations were similar in all 4 groups at end of the experiment. Mean plasma 1,25(OH)2D concentration increased from 35±3 to 63±9 pg/ml (P<0.007) when values were compared before and after P restriction in Zn-replete rats. The increase from 35±4 to 38±4 pg/ml in 1,25(OH)2D concentration in rats with combined Zn and P depletion was not significant. External ca balance however, was maintained in the combined Zn- and P-deplete group. It is concluded that Zn depletion limits the increase in plasma 1,25(OH)2D concentration associated with P depletion. The mechanism is unknown but may involve an effect of Zn on renal 25(OH)D 1-α-hydroxylase synthetic activity.

not easy to find exactly what i'm looking for, all i know is zinc made a huge difference in my body's ability to hydroxylate to 25(OH)D3 in the liver. looks like it might help the kidney too. will have to keep digging. not sure if the research i'm really after has been done yet. if it has, i haven't figured out the right way to search for it yet!
READ ME key info on nutrient targets - www.thisisms.com/ftopict-2489.html
my approach: no meds so far - just nutrient-dense anti-inflammatory whole foods, and supplements where needed
info: www.whfoods.com, www.nutritiondata.com
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Re: MS Nutrition-summary pts 1st post, p.1

Postby jimmylegs » Tue Jul 10, 2012 8:13 am

let's see if i can get at it another way...

pulling these nutrigenomics abstracts into the mix, previously posted at diet-f9/topic17276-240.html#p192654

Nutrigenomics: the Rubicon of molecular nutrition (2003)
http://www.journals.elsevierhealth.com/ ... 02-8223(03)01380-4/abstract
The success of the Human Genome Project and the powerful tools of molecular biology have ushered in a new era of medicine and nutrition. The pharmaceutical industry expects to leverage data from the Human Genome Project to develop new drugs based on the genetic constitution of the patient; likewise, the food industry has an opportunity to position food and nutritional bioactives to promote health and prevent disease based on the genetic constitution of the consumer. This new era of molecular nutrition—that is, nutrient-gene interaction—can unfold in dichotomous directions. One could focus on the effects of nutrients or food bioactives on the regulation of gene expression (ie, nutrigenomics) or on the impact of variations in gene structure on one’s response to nutrients or food bioactives (ie, nutrigenetics). The challenge of the public health nutritionist will be to balance the needs of the community with those of the individual. In this regard, the excitement and promise of molecular nutrition should be tempered by the need to validate the scientific data emerging from the disciplines of nutrigenomics and nutrigenetics and the need to educate practitioners and communicate the value to consumers—and to do it all within a socially responsible bioethical framework.

Nutrigenomics: goals and strategies (2003)
http://nutrigene.4t.com/muller%20nrg1047.pdf
In the past decade, nutrition research has undergone an important shift in focus from epidemiology and physiology to molecular biology and genetics. This is mainly a result of three factors that have led to a growing realization that the effects of nutrition on health and disease cannot be understood without a profound understanding of how nutrients act at the molecular level. First, the completion of several large genome projects has markedly altered the research agenda by drawing attention to the importance of genes in human nutrition, and has provided a wealth of new genetic information to be explored1–3. Second, there has been a growing recognition that MICRONUTRIENTS and MACRONUTRIENTS can be potent dietary signals that influence the metabolic programming of cells and have an important role in the control of homeostasis. Third, nutrition researchers have increasingly started to recognize that genetic predisposition can be an important contributor to the main causes of mortality that are linked to diet, such as cardiovascular disease, diabetes type II and cancers.

Nutrigenomics: From Molecular Nutrition to Prevention of Disease (2006)
http://www.ncbi.nlm.nih.gov/pubmed/16567153
"Until recently, nutrition research concentrated on nutrient deficiencies and impairment of health. The advent of genomics—interpreted broadly as a suite of high throughput technologies for the generation, processing, and application of scientific information about the composition and functions of genomes—has created unprecedented opportunities for increasing our understanding of how nutrients modulate gene and protein expression and ultimately influence cellular and organismal metabolism. Nutritional genomics (nutrigenomics), the junction between health, diet, and genomics, can be seen as the combination of molecular nutrition and genomics. The diverse tissue and organ-specific effects of bioactive dietary components include gene-expression patterns (transcriptome); organization of the chromatin (epigenome); protein-expression patterns, including posttranslational modifications (proteome); as well as metabolite profiles (metabolome). Nutrigenomics will promote an increased understanding of how nutrition influences metabolic pathways and homeostatic control, how this regulation is disturbed in the early phases of diet-related disease, and the extent to which individual sensitizing genotypes contribute to such diseases. Eventually, nutrigenomics will lead to evidence-based dietary intervention strategies for restoring health and fitness and for preventing diet-related disease. In this review, we provide a brief overview of nutrigenomics from our point of view by describing current strategies, future opportunities, and challenges."
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Re: MS Nutrition-summary pts 1st post, p.1

Postby jimmylegs » Tue Jul 10, 2012 9:08 am

ok so if we have a given that zinc regulates expression of certain genes, how far are we towards having a list? a few more abstracts...

A role for zinc in gene expression (1983) !!!
"Zinc deficiency in Euglena gracilis has been shown to affect growth, morphology, cell cycle and mitosis. These observations are best explained by a role for zinc in gene regulation possibly through zinc dependent enzymes. A similar role for zinc in man may exist with genetic and medical implications."

Regulation of Intestinal Gene Expression by Dietary Zinc: Induction of Uroguanylin mRNA by Zinc Deficiency (2000)
http://jn.nutrition.org/content/130/5/1393S.full
"The regulation of gene expression by nutrients plays an important role in the overall manifestations of nutritional deficiencies. Insufficient intakes of dietary micronutrients, such as zinc, produce profound effects in multiple organs and tissues. One of the major challenges, however, is to identify genes affected by changes in nutritional status."

A global view of the selectivity of zinc deprivation and excess on genes expressed in human THP-1 mononuclear cells (2003)
http://www.ncbi.nlm.nih.gov/pubmed/12756304
"Microarrays composed of approximately 22,000 elements were used to identify those genes responsive to either zinc depletion, zinc supplementation, or both conditions. Hierarchal clustering and ANOVA revealed that approximately 5% or 1,045 genes were zinc responsive. Further sorting based on this pattern of the zinc responsiveness of these genes into seven groups revealed that 104 genes were linearly zinc responsive in a positive mode (i.e., increased expression as cellular zinc increases) and 86 genes that were linearly zinc responsive in a negative mode (i.e., decreased expression as cellular zinc increases). Expression of some genes was responsive to only zinc depletion or supplementation."

Nutrient-gene interactions: a single nutrient and hundreds of target genes (2004)
http://www.ncbi.nlm.nih.gov/pubmed/15318805
"Zinc deficiency caused pleiotropic alterations in mRNA/protein levels of hundreds of genes"

Evidence for reprogramming global gene expression during zinc deficiency in the HUT-78 cell line (2006)
http://www.ncbi.nlm.nih.gov/pubmed/16979875
"gene expression for molecules that would increase T-lymphocyte response to signals from myeloid cells such as cytokine receptors and selected adhesion molecules were upregulated, whereas those associated with T-lymphocyte-directed immune functions, interleukin-2 and interleukin-6 receptors, the cytokine interleukin-4, and zinc finger transcription factors were downregulated"

Mechanisms of mammalian zinc-regulated gene expression (2008)
http://www.ncbi.nlm.nih.gov/pubmed/19021537
"evidence for the involvement of zinc dyshomoeostasis in the aetiology of diseases, including Type 2 diabetes, Alzheimer's disease and cancer, highlights the importance of zinc-regulated gene expression"

arg i need a translation on this one. i recognize all the words, just not how they are put together ;) all i get is, MS, genes, predict outcome, related to zinc:

Zinc-ion binding and cytokine activity regulation pathways predicts outcome in relapsing–remitting multiple sclerosis (2007)
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1941964/
"Using complementary-DNA microarrays we studied peripheral-blood gene expression patterns in 53 relapsing–remitting MS patients... An optimal set of 29 genes was depicted as a clinical outcome predictive gene expression signature and classified appropriately 88·9% of patients. This predictive signature was enriched by genes related biologically to zinc-ion binding and cytokine activity regulation pathways involved in inflammation and apoptosis...
Biological regulation of the predictive clinical outcome gene expression signature
Functional annotation of the 34 predictive genes demonstrated that this group of genes was enriched significantly by zinc-ion binding protein genes (S100B, KLF4, CAII) and by genes with cytokine activity (CCL17, MUC4, PTN VEGFB), P = 0·02 and P = 0·005, respectively (Fig. 3b). The Genomica software confirmed enrichment by the zinc-ion binding gene family and by cytokine activity genes using all the 431 differentiating gene expression signature data (Fig. 3c). Using these enriched gene-families, regulatory pathways were reconstructed (Fig. 3d,e). These pathways suggest that apoptosis regulation through zinc-ion binding and cytokine activity is responsible for Th1/Th2 shift and may play a role in the clinical outcome of RRMS."
READ ME key info on nutrient targets - www.thisisms.com/ftopict-2489.html
my approach: no meds so far - just nutrient-dense anti-inflammatory whole foods, and supplements where needed
info: www.whfoods.com, www.nutritiondata.com
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Re: MS Nutrition-summary pts 1st post, p.1

Postby jimmylegs » Tue Jul 10, 2012 10:11 am

not sure what this means to the overall picture, just throwing it into the record:

Relationships among element contents in the internal jugular vein similar to the arteries
http://www.springerlink.com/content/d040068866862414/
" the authors investigated the relationships among element contents in the internal jugular veins, in which a higher accumulation of calcium and phosphorus occurred with aging... It was found that there were extremely significant direct correlations among the contents of calcium, phosphorus, magnesium, and sodium in the internal jugular vein. In addition, very significant direct correlations were also found both between zinc and either iron or silicon contents and between sulfur and iron contents in the vein. As calcium and phosphorus increased in the internal jugular vein, the mass ratios of Mg/Ca and Mg/P decreased gradually in the vein, whereas the mass ratio of Ca/P hardly decreased. These results indicated that with regard to both the relationships among the contents of calcium, phosphorus, and magnesium and the changes of the mass ratios of Mg/Ca and Mg/P, the internal jugular vein was very similar to the arteries."
READ ME key info on nutrient targets - www.thisisms.com/ftopict-2489.html
my approach: no meds so far - just nutrient-dense anti-inflammatory whole foods, and supplements where needed
info: www.whfoods.com, www.nutritiondata.com
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Re: MS Nutrition-summary pts 1st post, p.1

Postby jimmylegs » Tue Jul 10, 2012 10:31 am

whew! just logged two 20 minute d3 sessions outside. HOT! shower time.
READ ME key info on nutrient targets - www.thisisms.com/ftopict-2489.html
my approach: no meds so far - just nutrient-dense anti-inflammatory whole foods, and supplements where needed
info: www.whfoods.com, www.nutritiondata.com
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Re: MS Nutrition-summary pts 1st post, p.1

Postby jimmylegs » Tue Jul 10, 2012 1:45 pm

went to the doc. time for some more labs! had my blood pressure taken. 98/60. dehydrated. easy fix on that one at least!
READ ME key info on nutrient targets - www.thisisms.com/ftopict-2489.html
my approach: no meds so far - just nutrient-dense anti-inflammatory whole foods, and supplements where needed
info: www.whfoods.com, www.nutritiondata.com
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Re: MS Nutrition-summary pts 1st post, p.1

Postby jimmylegs » Sun Jul 15, 2012 2:50 pm

interesting, another range for zinc, given as optimal, and again the peak is mid-18. wish this was referenced.

http://www.diabetesexplained.com/zinc-d ... -test.html

3. Plasma Zinc
This is the main lab test done to establish zinc deficiency. Although it is very good at picking up major deficiencies it is quite insensitive to marginal deficiency because a change in plasma zinc does not occur until zinc intake is extremely low. So a patient with `normal' results may still be deficient.

Plasma levels of zinc can be influenced by hypo or hyperproteinemia, acute infections, stress, time of sampling (how long after a meal), pregnancy, liver disease, malignancies and pernicious anaemia.

Zinc supplements will affect the results of plasma tests so one needs to avoid taking these for at least 24 hours prior to the test.

The optimal range of plasma zinc is 13.8 - 22.9µmol/L (90-150µg/dl).

Clinical signs of zinc deficiency may occur when plasma zinc concentrations drop below 9.9µmol/L (65 µg/dl).

Values less than 5µmol/L (33 µg/dl) are particularly associated with loss of the senses of taste and smell, abdominal pain, diarrhoea, skin rash, and loss of appetite.


also interesting..

Reference ranges of copper and zinc and the prevalence of their deficiencies in an Arab population aged 15-80 years.
http://www.ncbi.nlm.nih.gov/pubmed/12713027
Serum concentrations of copper and zinc were measured by flame atomic absorption spectrophotometry in 560 Kuwaitis aged from 15 to 80 yr who were in apparent good health to establish reference ranges and determine the prevalence of the deficiency of the trace metals. ... zinc (17.0 +/- 3.5 [males] vs 15.5 +/- 3.4 [females]) and zinc/copper ratios (0.87 +/- 0.28 [males] vs 0.67 +/- 0.27 [females]), gender-specific reference ranges were established in addition to reference ranges for the total population.
READ ME key info on nutrient targets - www.thisisms.com/ftopict-2489.html
my approach: no meds so far - just nutrient-dense anti-inflammatory whole foods, and supplements where needed
info: www.whfoods.com, www.nutritiondata.com
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Re: MS Nutrition-summary pts 1st post, p.1

Postby jimmylegs » Mon Jul 16, 2012 7:45 am

Dietary patterns in clinical subtypes of multiple sclerosis: an exploratory study
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2731789/ (free full text)
Background
Multiple sclerosis is a neurodegenerative disorder with a wide range in disease course severity. Many factors seem to be implicated in multiple sclerosis disease course, and diet has been suggested to play a role. Because limited data is present in the literature it was investigated whether variations in dietary intake may be related to the severity of the disease course in multiple sclerosis.
Methods
Using a food diary during 14 days, the dietary intake of 23 nutrients and vitamins was measured in patients with primary progressive (n = 21), secondary progressive (n = 32), and benign multiple sclerosis (n = 27) and compared to each other. The intake measured was also compared to the intake of the Dutch population and to the recommended daily allowance.
Results
Compared to the other MS groups, the secondary progressive MS patients had a lower intake of magnesium, calcium and iron. The total group of MS patients had, compared to the Dutch population, a lower intake of folate, magnesium and copper and a lower energy intake. Compared to the daily recommended allowance, the MS patients had a lower than recommended intake of folic acid, magnesium, zinc and selenium.
Conclusion
Magnesium, calcium and iron intake may possibly be related to MS disease progression, and should receive further attention. This is important because no effective neuroprotective treatment for MS patients is available.


the full text includes a link to additional file 1 "Total daily nutritional intake (mean ± SD) in the MS study groups and Dutch population, including Recommended Daily Allowance"

pretty interesting, for example, although the difference did not achieve statistical significance, benign ms patients have higher total fat intake than the other patient groups
READ ME key info on nutrient targets - www.thisisms.com/ftopict-2489.html
my approach: no meds so far - just nutrient-dense anti-inflammatory whole foods, and supplements where needed
info: www.whfoods.com, www.nutritiondata.com
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