General Nutrition/MS Research

[jimmylegs]

Vitamin and mineral needs during the oral contraceptive therapy: a systematic review
http://www.scopemed.org/?jft=89&ft=89-1385568410
Objectives: There is growing evidence that women using OCs change in serum trace elements and vitamins. Nowadays, in many cases, side effects associated with low levels of micronutrients are not considered during oral contraceptives (OCs) therapy. This review aims at checking the present literature in order to verify the evidences. Our purpose is to underline this aspect contributing to improve the therapeutic approach with OCs.
Methods: Systematic literature search was performed in electronic databases, covering the period from January 1967 to January 2012.
Results: Ninety-five articles were located; a cross sectional randomized and three RCTs studies were considered eligible.
Conclusions: A decrease in the serum concentrations of zinc, selenium, phosphorus and magnesium have been reported in OC users. Such reductions were proportional to the duration of contraceptive use. These reductions may imply a reduction in the probability of having a pregnancy and/or an increase of serious illness for the unborn. In this regard, a supplementation with the above compounds could be useful in OC users, namely for reducing side effects.

update: research indicates that OC users do better in terms of MS than non users. no need to avoid OCs, just be aware of the nutritional implications of hormone manipulation.

[jimmylegs]

The need to advance nutrition education in the training of health care professionals and recommended research to evaluate implementation and effectiveness (2014)
http://ajcn.nutrition.org/content/99/5/1153S.short

Nutrition education in medical school: a time of opportunity (2014)
http://ajcn.nutrition.org/content/99/5/1167S.short

Residency and specialties training in nutrition: a call for action (2014)
http://ajcn.nutrition.org/content/99/5/1174S.short

Implementation of a Dietitian-Led Enteral Nutrition Support Clinic Results in Quality Improvement, Reduced Readmissions, and Cost Savings (2014)
http://ncp.sagepub.com/content/early/20 ... 5.abstract

[jimmylegs]

The influence of nutritional factors on the prognosis of multiple sclerosis (2012)
http://www.nature.com/nrneurol/journal/ ... 2.194.html

The molecular basis of nutritional intervention in multiple sclerosis: A narrative review (2011)
http://www.sciencedirect.com/science/ar ... 9911000860

Multiple sclerosis and nutrition (2005)
http://msj.sagepub.com/content/11/1/24.short
Benefits from any particular diet in multiple sclerosis (MS) have not yet been proven. It is, however, frequent that malnutrition may potentially exacerbate the symptoms of MS. There is some evidence that a high intake of saturated fat increases the incidence of MS. Epidemiological studies imply that unsaturated fatty acids may have a positive effect on the course of MS. However, the results of controlled studies are ambiguous. A meta-analysis of three small controlled clinical trials suggests a benefit from linoleic acid. Intake of Vitamin D is associated with a lower incidence of MS. In MS, the risk of osteoporosis is high, and prophylactic vitamin D and calcium should be considered at an early stage. The role of minerals, trace elements, antioxidants, vitamins or fish oil is unclear. The possible relationships between diet and MS have not been subjected to adequate study. It seems possible that in the future, diets or dietary supplements may become recommended forms of treatment for MS.

[pawel96]

BTW, does anyone understand the discrepancy between high fat (Paleo, TW) and low fat (Swank, Jelinek) approach for managing MS? It is kind of annoying, these are 2 opposite approaches!

Pawel

[jimmylegs]

@ pawel - personally, i don't really follow these diets per se. i suspect the point is to find a healthy balance on a case by case basis. a daily fast food eater receiving an ms dx might do better on swank. for me as a 15 yr vegan (negligible fat) i probably would have been more likely to do better with paleo, although since going 'omni' i am not keen on the idea of excluding entire categories of whole food. swank recommendations would have made no sense to me either, since for example i had not eaten red meat in over a decade when i was diagnosed.
one dietary recommendation that i did follow early on was the 'high protein diet' eg '2-3 eggs for breakfast' recommended by klenner. i imagine the protein (and fat), as well as the high dose supplement regimen, had something to do with the dramatic improvements i experienced within days. i went with klenner because it made the most sense, given that i already knew some of the nutritional problems i could expect to cause problems while following a vegan lifestyle.

[jimmylegs]

Latitude is significantly associated with the prevalence of multiple sclerosis: a meta-analysis
http://jnnp.bmj.com/content/early/2011/ ... 0432.short
"This, the most comprehensive review of MS prevalence to date, has confirmed a statistically significant positive association between MS prevalence and latitude globally. Exceptions to the gradient in the Italian region and northern Scandinavia are likely a result of genetic and behavioural–cultural variations. The persistence of a positive gradient in Europe after adjustment for HLA-DRB1 allele frequencies strongly supports a role for environmental factors which vary with latitude, the most prominent candidates being ultraviolet radiation (UVR)/vitamin D."

[jimmylegs]

Assessment of serum magnesium, copper, and zinc levels in multiple sclerosis (MS) patients
http://ijpbs.mazums.ac.ir/browse.php?a_ ... lc_lang=fa
"We found that serum level of magnesium, copper, and zinc is significantly decreased in patients inflicted with MS. This is shown in some other studies and may result in use of supplemental use of trace elements for MS patients to either decrease symptoms or complications"

[jimmylegs]

Kroushavi, M., Behrooz, M., Rashidkhani, B., Bahadori, N., & Hekmatdoost, A. (2015). Association between index of nutritional quality and multiple sclerosis. Journal of School of Public Health and Institute of Public Health Research, 12(3), 0-0. Chicago http://sjsph.tums.ac.ir/browse.php?a_id ... lc_lang=en

Background and Aim: The role of nutritional quality of the diet in the development and progression of multiple sclerosis (MS) is not yet well understood. The aim of the present study was to determine the association between index of nutritional quality (INQ) and MS.
Materials and Methods: In this case-control study, 70 patients with a definitive diagnosis of MS in the preceding year and 140 frequency-matched hospital controls were selected from among 20-50 year-old patients referred to Sina and Lolagar hospitals in Tehran. The subjects’ dietary intakes were assessed using a valid and reliable semi-quantitative food frequency questionnaire. INQs for all the nutrients were then calculated for every participant, and logistic regression analysis was used to calculate the odds ratios for having MS in relation to every nutrient’s INQ.
Results: After adjusting for potential confounders, it was seen that subjects who had higher INQs for alpha-linolenic acid, vitamins A, D, K, B1, B2, B5, B6, folate, B12, and C, and minerals calcium, phosphorus, zinc, and potassium were less likely (p<0.05) to have MS as compared to subjects with lower INQs for these nutrients.
Conclusion: The findings of the present study show inverse associations between the INQ of many nutrients and risk of having MS. Therefore, it seems that overall improvement of the nutritional quality of the diet might be an appropriate approach for prevention of this disease.

[jimmylegs]

lil OT but interesting.
free full text http://advances.nutrition.org/content/6/1/73.full.pdf
"A balanced and sufficient supply of macro- and micronutrients is important to support host immune defense and resistance against pathogens. The habitual diet is often not sufficient to meet the increased demands for micronutrients in infectious diseases. Dietary multimicronutrient supplements containing selenium up to 200 mg/d have potential as safe, inexpensive, and widely available adjuvant therapy in viral infections (e.g., HIV, IAV) as well as in coinfections by HIV and M. tuberculosis to support the chemotherapy and/or to improve fitness and quality of life of the patients (Table 1). Because many of these patients experience broad nutritional deficiencies, multimicronutrient supplementation appears to be a more promising approach than the use of selenium alone. Dietary supplementation with selenium-containing multimicronutrients might also be useful to improve supportive care and to strengthen the immune system of patients suffering from newly emerging viral diseases, such as in the current epidemic of Ebola fever in West Africa. Populations in several countries most afflicted by past and current outbreaks of Ebola fever (e.g., Liberia, Guinea, Democratic Republic of Congo) exhibit a high risk of selenium deficiency, and strikingly, the lowest dietary selenium supply in Africa was reported from Liberia, with a daily intake of only 23 mg Se (15)."

[jimmylegs]

Perspective: The Case for an Evidence-Based Reference Interval for Serum Magnesium: The Time Has Come (2016)
http://advances.nutrition.org/content/7/6/977.short
"The 2015 Dietary Guidelines Advisory Committee indicated that magnesium was a shortfall nutrient that was underconsumed relative to the Estimated Average Requirement (EAR) for many Americans. Approximately 50% of Americans consume less than the EAR for magnesium, and some age groups consume substantially less. A growing body of literature from animal, epidemiologic, and clinical studies has demonstrated a varied pathologic role for magnesium deficiency that includes electrolyte, neurologic, musculoskeletal, and inflammatory disorders; osteoporosis; hypertension; cardiovascular diseases; metabolic syndrome; and diabetes. Studies have also demonstrated that magnesium deficiency is associated with several chronic diseases and that a reduced risk of these diseases is observed with higher magnesium intake or supplementation. Subclinical magnesium deficiency can exist despite the presentation of a normal status as defined within the current serum magnesium reference interval of 0.75–0.95 mmol/L. This reference interval was derived from data from NHANES I (1974), which was based on the distribution of serum magnesium in a normal population rather than clinical outcomes. What is needed is an evidenced-based serum magnesium reference interval that reflects optimal health and the current food environment and population. We present herein data from an array of scientific studies to support the perspective that subclinical deficiencies in magnesium exist, that they contribute to several chronic diseases, and that adopting a revised serum magnesium reference interval would improve clinical care and public health."

[jimmylegs]

From other sources, optimal serum cu:zn = 0.7-1.0

Serum copper zinc ratios

Healthy Controls (perfect, serum zinc is a little higher than serum copper)

per control group in an MS study...0.71 (see study dtls below. cu:zn basically perfect, if anything at the extreme end of optimal; this zinc level is unusually high esp in relation to copper)

Alzheimer's (bad, copper is high in relation to zinc)

Patient 1.......1.8
Patient 2.......1.6
Patient 3 n/a
Patient 4.......0.94
Patient 5.......1.2
Patient 6 n/a
Patient 7.......1.7

MS (very bad, copper very high, with even lower zinc)

RRMS mean....2.6
MS mean.......2.8
SPMS mean....5.5

not a huge data set, but wow that is *stark*

the long form info, from two recent studies:

Alzheimer's study

Patient 1: two-year history of cognitive decline... se cu 101mcg/dl, se zn 56mcg/dl serum Cu:Zn ratio 1.8.
Patient 2: word-finding difficulties, followed by difficulties with arithmetic... se cu 97mcg/dl, se zn 59mcg/dl, serum Cu:Zn ratio 1.6
Patient 3: didn't have enough data to conduct this analysis
Patient 4: treated with an antidepressant, [3yrs later trouble driving, then] executive, visuospatial, and memory deficits ... zinc 78mcg/dl, copper 73mcg/dl,
serum cu:zn ratio 0.94
Patient 5: began to have word-finding difficulty, disorientation, difficulty driving, difficulty following recipes and other instructions, and increased depression ... zinc 82mcg/l, copper 99mcg/l, serum cu:zn ratio 1.2
Patient 6: no bloodwork, can't assess.
Patient 7: headache, leg cramps, irritability, distractibility, and difficulty with memory, peripheral neuropathy and hyposmia. Neuro-psychological assessment revealed a high-functioning individual with mild reductions in spatial > verbal memory... serum copper 97mcg/dl, serum zinc 57mcg/dl, serum cu:zn ratio 1.7.

MS study

Table 1
..........................MS...:.................SPMS...:..........RRMS...:.........Controls
Zn level (µg/dL)...40.17 ±31.89a......23.12 ±10.59c.....42.06 ±32.94.....127.77 ±42.2
Cu level (µg/dL)..114.05 ±42b.......126.14 ±44.20.....111.22 ±39.45.......91.3 ±37

JL comments: note the basically inverted copper and zinc numbers for controls vs patients; bad for RRMS and TERRIBLE for SPMS
cu:zn
Controls......91.3 / 127.8 = 0.71
RRMS..........111.2 / 42.1 = 2.6
MS..............114.1 / 40.2 = 2.8
SPMS..........126.1 / 23.1 = 5.5

and on the flip side, ratios in copper deficiency, secondary to zinc excess, via high intake of denture cream:

Zinc toxicity (super low copper, very high zinc)

Patient 1.......0.05
Patient 2.......0.13
Patient 3.......0.16
Patient 4.......0.02

more info re zinc toxicity from overuse of denture cream:
http://www.thisisms.com/forum/natural-a ... ml#p245069

[ElliotB]

There are many similarities between MS and Alzheimers with the very basic difference being where the inflammation is in the brain (but obviously not the only difference).

From the article linked below
"Interestingly, both MS and Alzheimer’s disease are caused by chronic inflammation in the central nervous system.
In both diseases, cells called “microglia” are involved in the inflammation. Microglia are the main immune cells that are normally in the brain and spinal cord and those get over-activated in both Alzheimer’s disease and MS, leading to the formations of lesions, or scars.
However, in multiple sclerosis, the microglia are joined by other immune cells (including B cells and T cells) that have gotten across the blood brain barrier and attack the myelin. These “rogue” immune cells are not present in the central nervous system of people with Alzheimer’s disease."


BUT, the number of Alzheimers cases is staggering, over 5 million in the USA alone, with about 35 million affected worldwide. It is projected that these numbers may double in 20 or so years.

Not that we don't have enough on our plates to deal with, but for those interested, you may find this article enlightening:

https://www.verywell.com/alzheimers-and ... es-2440709

[jimmylegs]

actually my points were

1. how easy it is to see this difference between alzheimer's, ms patients and healthy controls in this (small) sample, and

2. how hard is it (hint: not hard at all) to increase serum zinc, thereby improving the serum copper zinc ratio, and see where we get with these illnesses. noting in particular that the control group mean serum zinc is well outside the top end of what many labs consider the reference range for serum zinc (which by the way has been in decline societally, over the course of the decades in which these diseases have become more prevalent).

to your point on CNS inflammation:

Prasad, A. S. (2008). Clinical, immunological, anti-inflammatory and antioxidant roles of zinc. Experimental gerontology, 43(5), 370-377.
http://www.sciencedirect.com/science/ar ... 6507002458

The essentiality of zinc for humans was recognized only 40 years ago. Zinc deficiency was suspected to occur in Iranian patients with growth retardation, hypogonadism in males, hepato-splenomegaly, rough and dry skin, geophagia and severe iron deficiency anemia. Later we documented zinc deficiency in similar patients in Egypt. The diet of these patients consisted of mainly cereal proteins which contained high phytate and this led to decreased availability of iron and zinc. These patients had severe immune dysfunctions, inasmuch as they died of intercurrent infections by the time they were 25 years of age. In our studies in experimental human model of zinc deficiency, we documented decreased serum testosterone level, oligospermia, severe immune dysfunctions mainly affecting T helper cells, decreased serum thymulin activity hyperammonemia, [JL comment: wish i had known to test my ammonia levels when most zinc deficient, bc that was when i had the worst cognitive impairment - including trouble with driving like patients 4 and 5 above, resolved after zinc treatment] neuro-sensory disorders and decreased lean body mass.

The basic mechanisms of zinc action on immune cells have been reviewed in this paper. Our studies showed that the activation of many zinc dependent enzymes and transcription factors were affected adversely due to zinc deficiency. The gene expression and production of Th1 cytokines were affected adversely due to zinc deficiency.

Zinc is also an antioxidant and has anti-inflammatory actions. We have reported decreased plasma zinc, increased plasma oxidative stress markers and increased generation of inflammatory cytokines in the elderly subjects which were corrected by zinc supplementation. In cell culture studies, we have observed that zinc induces A20 which inhibits NF-κB activation resulting in decreased generation of inflammatory cytokines.

Dr. Prasad recognized by Congress for zinc studies (2011)

[jimmylegs]

re brain imaging

Alzheimer's
control:

patient:

"The top three images also show a routine T1-weighted MRI sequence, but from a patient with advanced Alzheimer's disease. In striking contrast to the normal subject, there is prominence of the CSF spaces both outside the brain (for example all the sulci are prominent) and within the ventricles. This increase is all caused by volume loss of the brain's white matter and grey matter.
The bottom 8 images are from an FDG-PET examination, which measures the brains metabolism. Using the colorized "heat" scale, where red shows the brain's normal high metabolism, and green-blue shows abnormally low metabolism, you can see a typical pattern of reduced metabolism in the bilateral parietal lobes, compatible with mid-stage Alzheimer's disease."

Multiple Sclerosis

can't get full text, but source is
Bermel, R. A., & Bakshi, R. (2006). The measurement and clinical relevance of brain atrophy in multiple sclerosis. The Lancet Neurology, 5(2), 158-170.
"Brain atrophy has emerged as a clinically relevant component of disease progression in multiple sclerosis. Progressive loss of brain tissue bulk can be detected in vivo in a sensitive and reproducible manner by MRI. Clinical studies have shown that brain atrophy begins early in the disease course. The increasing amount of data linking brain atrophy to clinical impairments suggest that irreversible tissue destruction is an important determinant of disease progression to a greater extent than can be explained by conventional lesion assessments."

[jimmylegs]

larger study. 308 subjects include 'probable' AD, confirmed and classified PD, and definite MS (most RRMS)

Alimonti, A., Ristori, G., Giubilei, F., Stazi, M. A., Pino, A., Visconti, A., ... & Bocca, B. (2007). Serum chemical elements and oxidative status in Alzheimer's disease, Parkinson disease and multiple sclerosis. Neurotoxicology, 28(3), 450-456.
http://www.sciencedirect.com/science/ar ... 3X06003020
Parameter... Controls................AD.......................PD..........................SM (sic)
Cu...............95.1 (808-1073).. 94.5 (799-1086)... 100.7 (797-1116).....94.0 (819-1031) (ug/dl)
Zn...............79.5 (703-897).... 69.1 (625-763).......72.0 (633-798).......65.0 (591-710) (ug/dl)

so, recalling optimal serum cu:zn is 0.7-1.0: AD group = 1.2, PD group = 1.4, MS group = 1.4

so, the differences are not as drastic here as above, but still showing up.