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 » Mon Jun 11, 2012 8:23 am

linking up zinc status and allergic/inflammatory reactions (dairy in this case). note the reference to retarded height and weight in these patients, measures which are well known to be positively associated with zinc status.

Follow-up of nutritional status and dietary survey in children with cow's milk allergy
http://onlinelibrary.wiley.com/doi/10.1 ... x/abstract
The nutritional status of children with cow's milk allergy was followed during an elimination diet in 19 children (9 boys and 10 girls) beginning at the mean age of two years (range 0.6-4.1 years). The cow's milk allergy had been verified in hospital by a challenge test at a mean age of 0.9 years (range 0.2-1.9 years). Weight, height and laboratory indices to test protein, mineral and vitamin status were measured at three follow-up visits at three-month intervals. In addition to cow's milk allergy all these children had some other food allergies, and six of the 19 children were allergic to soy protein. Only two of the 19 children were given a soy-based formula. In the diets of the other children, cow's milk was replaced by increasing amounts of other foodstuffs and supplementary calcium. At the beginning of the study the relative heights of the children were slightly retarded (– 0.6 SD) and remained unchanged during follow-up (– 0.8 SD at the end of the study). The relative weights were found to be decreased during follow-up (p < 0.05). There was a significant reduction in serum prealbumin values; eight of the 19 children showed abnormally low values. Low serum zinc values were seen in 12 children. Serum iron concentration was low in two children and two had high serum alkaline phosphatase values. Seven-day food recording indicated that dietary intake of energy was below the recommendation in some children, but protein intake was high. Some children had low intakes of riboflavin. Correlations between dietary intake and nutritional status were not seen in the children with cow's milk allergy. Careful follow-up of children with cow's milk allergy is indicated and should include the monitoring of relative height and weight, serum prealbumin, serum trace elements and individual diet prescriptions.
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Re: MS Nutrition-summary pts 1st post, p.1

Postby jimmylegs » Mon Jun 11, 2012 8:38 am

think they might have this one backwards.... oh, science (shaking head)

Acrodermatitis enteropathica-like eruption and food allergy.
Abstract
"BACKGROUND: Acrodermatitis enteropathica-like eruption (AE) is a distinct rash associated with profound zinc deficiency. It is seen in a variety of conditions but has not been reported as a presentation of food allergy.
OBJECTIVE: To report AE as an unusual presentation of food allergy in infants.
METHODS: Acrodermatitis enteropathica-like eruption was diagnosed by a characteristic rash and a low serum zinc level. The diagnosis of food allergy was made by history, serum total IgE and food specific IgE levels, or oral challenge with suspected foods.
RESULTS: Two infants with AE, diarrhea, and low serum zinc levels were evaluated. Food allergy was found in both infants. The first infant had a serum IgE level of 4642 IU/mL. Specific IgE levels to milk, soybean, wheat, and peanut were 39.04, 10.14, 5.65, and 102.61 kU/L, respectively. Oral challenges to milk and peanut were positive and to soybean were negative. The second infant had a serum IgE level of 991 IU/mL; specific IgE levels to soybean and milk were 36.9 and 0.53 kU/L, respectively. Evaluation for other possible causes of diarrhea revealed homozygous delta F508 in the first infant, confirming the coexistence of cystic fibrosis; findings in the second infant were negative.
CONCLUSIONS: Undiagnosed food allergy can lead to profound zinc deficiency. Food allergy should be suspected in a child with acquired AE."

by this brilliant logic, we may also conclude that subacute combined degeneration of the spinal cord causes vit b12 deficiency, rickets causes d3 deficiency, and scurvy causes vit C deficiency. good to know :roll:
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Re: MS Nutrition-summary pts 1st post, p.1

Postby jimmylegs » Mon Jun 11, 2012 8:43 am

these posts above are exactly why i don't buy in to elimination of potentially allergenic foods as an ms treatment approach. it ignores the underlying problem. but if you address the zinc issue, the tendency of certain foods to promote inflammation is countered. and beyond that you get the other hundred or so benefits of having adequate zinc, that don't happen to be related to inflammatory reactions.
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Re: MS Nutrition-summary pts 1st post, p.1

Postby jimmylegs » Mon Jun 11, 2012 5:14 pm

on the use of interferon to treat ms:

http://en.wikipedia.org/wiki/Interferon
"Interferons (IFNs) are proteins made and released by host cells in response to the presence of pathogens such as viruses, bacteria, parasites or tumor cells. They allow for communication between cells to trigger the protective defenses of the immune system that eradicate pathogens or tumors.
IFNs belong to the large class of glycoproteins known as cytokines. Interferons are named after their ability to "interfere" with viral replication within host cells. IFNs have other functions: they activate immune cells, such as natural killer cells and macrophages; they increase recognition of infection or tumor cells by up-regulating antigen presentation to T lymphocytes; and they increase the ability of uninfected host cells to resist new infection by virus. Certain host symptoms, such as aching muscles and fever, are related to the production of IFNs during infection.
About ten distinct IFNs have been identified in mammals; seven of these have been described for humans. They are typically divided among three IFN classes: Type I IFN, Type II IFN, and Type III IFN. IFNs belonging to all IFN classes are very important for fighting viral infections.
Based on the type of receptor through which they signal, human interferons have been classified into three major types.
Interferon type I: All type I IFNs bind to a specific cell surface receptor complex known as the IFN-α receptor (IFNAR) that consists of IFNAR1 and IFNAR2 chains.[1] The type I interferons present in humans are IFN-α, IFN-β and IFN-ω.[2]"

http://en.wikipedia.org/wiki/IFNB1
"Interferon beta is a protein that in humans is encoded by the IFNB1 gene.[1]" one guess where i'm going with this...

Human interferons alpha, beta and omega.
http://www.ncbi.nlm.nih.gov/pubmed/15621727
"Type I interferons (IFNs), IFN-alpha, IFN-beta, IFN-omega, IFN-delta and IFN-tau are a family of structurally related, species-specific proteins found only in vertebrates. They exhibit a variety of biological functions, including antiviral, antiproliferative, immunomodulatory and developmental activities. Human Type I IFNs interact with the human IFN alpha receptor (IFNAR), which is composed of two identified subunits (IFNAR-1 and IFNAR-2). The interaction of IFN-alpha/beta with its receptor components results in the activation of a number of signaling pathways. The regulation of specific genes and proteins contributes to the numerous biological functions of Type I IFNs."

hmm interferon-beta synthesized from e.coli, tasty. would be interesting to read the full text and get a better handle on the nature of the 'several criteria'. makes the chinese hamster ovary option sound a bit more appealing...

Synthesis of human fibroblast interferon by E. coli.
http://www.ncbi.nlm.nih.gov/pmc/article ... =pmcentrez
"A cDNA library was constructed using mRNA from human fibroblasts induced with poly(I):poly(C). A bacterial clone containing fibroblast interferon [jl comment - as i understand it that's IFN-beta] cDNA sequences was identified by hybridization to a cDNA probe synthesized using deoxyoligonucleotide primers which hybridize to fibroblast interferon mRNA specifically. Expression plasmids were constructed which permitted the synthesis in E. coli of 8 x 10(7) units of human fibroblast interferon per liter of culture. The bacterially produced fibroblast interferon is indistinguishable from authentic human fibroblast interferon by several criteria."

The transcriptional code of humanIFN-β gene expression
http://www.sciencedirect.com/science/ar ... 9910000210
"Activation of interferon-β transcription is a highly ordered process beginning with the delivery of NF-κB to the IFN-β enhancer through a process involving stochastic interchromosomal interactions between the IFN-β enhancer and specialized Alu elements. NF-κB delivery is followed by the binding of ATF-2/c-Jun and IRF proteins in a highly cooperative fashion. The assembled “enhanceosome” then recruits PCAF/GCN5 which acetylates the histone tails of the adjacent nucleosomes. The transcriptional coactivator CBP, which binds in a complex with the RNA polymerase II holoenzyme is recruited by the enhanceosome replacing PCAF/GCN5. Next, SWI/SNF, which is part of the holoenzyme complex, induces a conformational change in a nucleosome positioned over the transcriptional start site allowing TFIID to bind, which promotes the sliding of this nucleosome to a new downstream position. At this point the full pre-initiation complex is assembled and transcription commences. This detailed picture of the IFN-β transcription program gathered through years of rigorous studies, now serves as a paradigm for understanding complex transcriptional switches in eukaryotic systems."

i don't plan to take the time to understand that whole abstract thoroughly, but i get this much:
"Activation of interferon-β transcription is a highly ordered process beginning with the delivery of NF-κB"

NF-kappa B, a potential therapeutic target for the treatment of multiple sclerosis.
http://www.ncbi.nlm.nih.gov/pubmed/19128210
"Multiple sclerosis (MS) is a chronic inflammatory autoimmune disease of the central nervous system (CNS) that afflicts over 2 million people worldwide. ... An increasing number of studies indicate that nuclear factor-kappaB plays an important role in controlling expression of genes relevant to the pathogenesis of autoimmunity. Genetic factors related to NF-kappaB may also be determinants of MS susceptibility, as polymorphisms in the molecules involved in regulation of the NF-kappaB signal transduction pathway differ between RR-MS and progressive MS. Herein, the role of NF-kappaB in MS will be reviewed and its potential as a new therapeutic target in MS will be considered and compared with existing treatments."

and we must have seen this abstract before...

Effects of zinc deficiency on immune functions
http://onlinelibrary.wiley.com/doi/10.1 ... 2/abstract
"Nutritional deficiency of zinc is widespread throughout the developing world. Zinc deficient subjects experience increased susceptibility to a variety of infections. Zinc deficiency in an experimental human model caused an imbalance between Th1 and Th2 functions. Production of IFN-γ and IL-2 (products of TH1) were decreased, whereas production of IL-4, IL-6 and IL-10 (products of Th2) were not affected due to zinc deficiency. Zinc deficiency decreased NK cell lytic activity and percentage of precursors of cytolytic T cells. In HUT-78, a Th0 cell line, zinc deficiency decreased gene expression of deoxythymidine kinase (TK), delayed cell cycle and decreased cell growth. Gene expression of IL-2 and IL-2 receptors (both α and β) and binding of NF-kB to DNA were decreased by zinc deficiency in HUT-78. In HL-60, a monocytic-macrophage cell line, zinc deficiency increased production and gene expression of TNF-α, IL-1β and IL-8. These cytotoxic cytokines are known to produce increased free radicals. Thus zinc may function as an important anti-oxidant. In conclusion, decreased production of IL-2 in zinc deficiency may be due to decreased activation of NF-kB and subsequent decreased gene expression of IL-2 and IL-2 receptor α. Our studies show that zinc deficiency affects cell-mediated immunity and leads to activation of monocytes-macrophages and may play an important role as an antioxidant."
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Re: MS Nutrition-summary pts 1st post, p.1

Postby jimmylegs » Wed Jun 13, 2012 12:01 pm

what a lovely day off. i have two in a row, amazing! today is sunny but not muggy. perfect. made some vitamin d3 out on the patio for an hour or so. at this time of day, will have to change my spot if i want to make any more :) a little front porch guitar sesh sounds like just the ticket :D
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Re: MS Nutrition-summary pts 1st post, p.1

Postby jimmylegs » Wed Jun 13, 2012 5:48 pm

well, turns out i was wrong, it's only one day off, but it was awesome.
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Re: MS Nutrition-summary pts 1st post, p.1

Postby NHE » Fri Jun 15, 2012 12:54 am

jimmylegs wrote:Gene expression of IL-2 and IL-2 receptors (both α and β) and binding of NF-kB to DNA were decreased by zinc deficiency in HUT-78.


Please correct me if I'm mistaken, but shouldn't this be a good thing for MS? NF-kB is a proinflammatory transcription factor. Antioxidants that are known to be beneficial for MS (or at least for MS models), e.g., r-lipoic acid, curcumin and EGCG, inhibit the NF-kB transcription factor. If memory serves me correctly, this is usually through inhibition of Ikk (a kinase which activates NF-kB).

NF-kB Pathway

Not all antioxidants are created equally. Some are proinflammatory while others are anti-inflammatory. For example, grape seed extract activates Ifn-gamma which is known to make MS worse.

N. Nair, et al., 2002. Grape seed extract activates Th1 cells in vitro.
Clinical and Diagnostic Laboratory Immunology, 9(2):470-476.

    Although flavonoids manifest a diverse range of biological activities, including antitumor and antiviral effects, the molecular mechanisms underlying these activities await elucidation. We hypothesize that the flavonoid constituents of a proprietary grape seed extract (GSE) that contains procyandins exert significant antiviral and antitumor effects, by inducing production of the Th1-derived cytokine gamma interferon (IFN-gamma) by peripheral blood mononuclear cells) from healthy donors. Our results show that GSE significantly induced the transcription of IFN-gamma mRNA as demonstrated by reverse transcription-PCR but had no effect on the Th2-derived cytokine interleukin-6. The enhancing effect of GSE on IFN-gamma expression was further supported by a concomitant increase in the number of cells with intracytoplasmic IFN-gamma as well as the synthesis and secretion of IFN-gamma. Our results demonstrate that the potentially beneficial immunostimulatory effects of GSE may be mediated through the induction of IFN-gamma.

    Free full text is available.


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

Postby jimmylegs » Sat Jun 16, 2012 7:34 pm

heya NHE! will have to investigate further. the various functions probably have a wide array of pros and cons. searched accordingly and found this so far. have not spent any time on it really. just throwing this into the mix:

NF-kappaB signaling: pros and cons of altering NF-kappaB as a therapeutic approach
http://www.ncbi.nlm.nih.gov/pubmed/17057194
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Re: MS Nutrition-summary pts 1st post, p.1

Postby jimmylegs » Sat Jun 16, 2012 7:40 pm

only read the first couple pages - all the same....

The NF-kB Family of Transcription Factors and Its Regulation
http://cshperspectives.cshlp.org/conten ... 4.full.pdf

sample article info:
The NF-kB Family of Transcription Factors and Its Regulation
Andrea Oeckinghaus1,2 and Sankar Ghosh1,2
1Department of Immunobiology and Department of Molecular Biophysics and Biochemistry, Yale University School of Medicine, New Haven, Connecticut 06520
2Department of Microbiology and Immunology, Columbia University, College of Physicians and Surgeons, New York 10032
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Re: MS Nutrition-summary pts 1st post, p.1

Postby jimmylegs » Sun Jun 17, 2012 4:07 pm

if you met me today and are reading this now, here's a link for you:
regimens-f22/topic2489-375.html#p193260

nb as noted above, i make the opposite conclusion to the study authors, based on their observations!

next, you can read the zinc item in the bloodwork section here:
regimens-f22/topic2489.html#p15460

there you go, good luck :)
READ ME key info on nutrient targets - www.thisisms.com/ftopict-2489.html
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Re: MS Nutrition-summary pts 1st post, p.1

Postby jimmylegs » Fri Jun 22, 2012 2:04 pm

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

Postby jimmylegs » Tue Jun 26, 2012 7:56 pm

interesting...

Regulation of Zinc Metabolism and Genomic Outcomes
http://jn.nutrition.org/content/133/5/1521S.full
Abstract
Differential mRNA display and cDNA array analysis have identified zinc-regulated genes in small intestine, thymus and monocytes. The vast majority of the transcriptome is not influenced by dietary zinc intake, high or low. Of the genes that are zinc regulated, most are involved in signal transduction (particularly influencing the immune response), responses to stress and redox, growth and energy utilization. Among the genes identified are uroguanylin (UG), cholecystokinin, lymphocyte-specific protein tyrosine kinase (LCK), T-cell cytokine receptor, heat shock proteins and the DNA damage repair and recombination protein-23B. Zinc transporters (ZnT) help regulate the supply of this micronutrient to maintain cellular functions. Expression of ZnT-1 and -2 is regulated by dietary zinc in many organs including small intestine and kidney. ZnT-4 is ubiquitously expressed but is refractory to zinc intake. Expression of ZnT-1, -2 and -4 changes markedly during gestation and lactation from highly abundant to undetectable. Each ZnT has an endosomal-like appearance in the tissues examined. Upregulation of ZnT-1 and ZnT-2 by dietary zinc strongly implicates these transporters in zinc acquisition and/or storage for subsequent systemic needs. THP-1 cells were used as a model to examine the response of human cells to changes in zinc status. Based on mRNA quantities, Zip1 and ZnT-5 were the most highly expressed. Zinc depletion of these cells decreased expression of all transporters except Zip2, where expression increased markedly. Collectively, these findings provide a genomic footprint upon which to address the biological and clinical significance of zinc and new avenues for status assessment.
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Re: MS Nutrition-summary pts 1st post, p.1

Postby jimmylegs » Fri Jun 29, 2012 3:51 pm

just added a couple updates to post 1 on page 1. highlighted the date in red.
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Re: MS Nutrition-summary pts 1st post, p.1

Postby jimmylegs » Tue Jul 03, 2012 7:41 am

well this has been an odd morning's work. it started with a gentleman in the park yesterday, who had double thumbs on each hand. so this morning i learned that this is called polydactyly, and being clearly a birth defect i thought, why not hunt for a zinc link, since it's known that zinc is so critical to foetal development.

anyway. i came across a possible connection between neural tube defects, and polydactyly. so searching on neural tube defects and serum zinc, i found this:

Serum zinc, selenium, copper, and lead levels in women with second-trimester induced abortion resulting from neural tube defects. A preliminary study (2004)
http://www.springerlink.com/content/j942g31512j56xk0/

...Cases had significantly low serum zinc and selenium levels (62.48±15.9 vs 102.6±23.7 and 55.16±11.3 vs 77.4±5.5, respectively, p<0.001). Serum Cu and whole-blood Pb levels were significantly high when compared to controls. ...an interaction among environmental, genetic, and nutritional factors such as trace elements and vitamins would explain these anomalies. If folic acid supplementation is given, additional Zn supplementation should be considered for the further decrease in the recurrence and occurrence of NTDs.


i'd say those zinc levels were low! that works out to 9.6 umol/L average. still need more info on the polydactyly factor though... searched etiology polydactyly and found this one (fyi "VACTERL is a non-random association of birth defects. ... while the complications are not pathogenetically related they tend to occur together more frequently than expected by chance"):

A Population Study of the VACTERL Association: Evidence for Its Etiologic Heterogeneity

"...There were 76 cases with three or more defects, whereas less than one case was expected. Of these 76 cases, seven had recognized causes (five chromosomal anomalies, two single-gene disorders); another 19 had recognized clinical phenotypes or syndromes of unknown etiology. In the remaining 50 cases ... Their most common limb defects were reduction deformities (34%) and polydactyly (20%). This study confirms the clinically recognized nonrandom occurrence of the VACTERL association. ... A common denominator of the VACTERL association is suggested to be a defective mesodermal development during embryogenesis, due to a variety of causes and leading to overlapping manifestations."


so then i latched onto defective mesoderm development and searched with polydactyly, which came up with this hit:

A novel acropectoral syndrome maps to chromosome 7q36 ...
jmg.bmj.com/content/38/5/304.full
" ...of the gene Sonic hedgehog(Shh) in limb buds and lateral plate mesoderm during development causes preaxial polydactylyand sternal defects respectively..."


now i've heard of sonic hedgehog before, but now i'm wondering about the zinc-dependence of Shh expression.. so i searched "sonic hedgehog" "serum zinc" and got this:

"The Plausibility of Maternal Nutritional Status Being a Contributing Factor to the Risk for Fetal Alcohol Spectrum Disorders: The Potential Influence of Zinc Status as an Example"

article excerpt, starting generally with alcohol, zinc depletion and links to birth defects...

"From work with experimental animals, it is well documented that deficiencies of certain nutrients, including folate, vitamin B12, Zn, Fe and Cu, during pregnancy can result in abnormal CNS development, and deficiencies of these nutrients are commonly noted in alcoholics [18–23]. With respect to the above nutrients, the hypothesis that maternal Zn status is an important predictor of the risk for FASD has received particular attention. Over 25 years ago, Flynn et al reported that maternal plasma Zn and fetal cord plasma Zn were lower in pregnant women who consumed alcohol versus non-alcohol drinking women [24]. Importantly, these investigators reported that there were negative correlations between maternal plasma Zn concentrations and the severity and frequency of birth defects in the infants, suggesting an etiologic role for Zn deficiency in human FASD."

"It is important to note that mechanistically, one would predict multiple synergistic interactions between an alcohol insult and a condition of marginal Zn deficiency. As an example of the above, it is well documented that Zn contributes to the oxidant defense system through multiple means, including through its ability to: (1) regulate Cu-Zn superoxide dismutase (CuZn SOD) activity; (2) regulate metallothionein levels; (3) protect sulfhydryl groups from oxidation; (4) modulate intracellular thiol groups; and (5) inhibit the binding of redox active metals, such as Fe and Cu, to intracellular sites where they can generate free radical reactions (e.g., Fenton-type reactions). Given the above, it is evident that one functional consequence of Zn deficiency is an increased susceptibility to exogenous oxidative stressors, such as smoking, endotoxin challenge, and, particularly germane to this paper, alcohol [27,39,41] The consequences of excessive tissue oxidative stress in the embryo can include lipid, protein and DNA oxidative damage, and an increase in apoptosis, all of which can trigger abnormal development. It is important to note that all of the above are common findings in animal models for FASD [23]."

and getting down to the sonic hedgehog connection,
"Another potential point of interaction between Zn deficiency and an alcohol challenge involves sonic hedgehog (Shh) signaling. Shh signaling is critical for polarizing activity, and Shh null fetuses are characterized by a postaxial forelimb ectrodactyly in mouse models [42]. Shh is a Zn-dependent developmental trigger[43], and reduced Shh expression has been implicated in ethanol-induced postaxial forelimb ectrodactyly in the mouse [44]. Schreiner and co-workers [45] have suggested that a state of embryonic Zn deficiency secondary to an alcohol-induced acute-phase response (see below; [46–48]) in the mother results in reduced Shh signaling with subsequent dysmorphology [45]. This is an interesting hypothesis that merits further investigation. Importantly, if it is shown to be correct, there are numerous other Zn-dependent developmental proteins, many in the hedgehog signaling pathway (e.g., Gli Zn finger transcription regulators), that might also be affected through the mechanism described above."


Sonic hedgehog
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1187306/
"Several polydactyly syndromes are thought to result from mutations in GLI3... It has been postulated that preaxial polydactyly in humans could result from ectopic expression of Shh in the anterior limb bud. Mutations in GLI3, a downstream target of SHH, can be seen in Grieg syndrome (craniofacial anomalies with postaxial polydactyly of hands"


a cited article of interest which i'm not having much luck finding, except as a citation:

Goldberg YP. Extending hand to GLI3: functionally different GLI3 mutations in postaxial polydactyly, Greig’s cephalopolysyndactyly syndrome and Pallister-Hall syndrome. Clin Genet 1998;53:334–6.

last of all, since i can't find a direct study of polydactyly and human zinc status, here's one on cadmium toxicity and birth defects in mice:

Characteristics of the limb malformations induced by maternal exposure to cadmium in the mouse
http://www.sciencedirect.com/science/ar ... 389090041S
"Single doses of 2,3,4,6,8,10, and 15 mg/kg of cadmium chloride were administered (SC) to groups of MF1 mice on one of day to 12 of gestation. Fetuses collected on day 18 were observed for limb malformations, and alizarin red-S stained skeletons were examined for their skeletal bases. ... Ectrodactyly, postaxial polydactyly, syndactyly, brachydactyly, adactyly, phocomelia, meromelia, and malrotation of the limbs were detected in a significant number of fetuses."


Cadmium causes zinc depletion by sitting in zinc receptors - for more info review this:
regimens-f22/topic6318-105.html#p52191

a little academic backing for the previously unreferenced content in the above post:

Cadmium-Zinc Interactions: Implications for Health
http://naldc.nal.usda.gov/download/44821/PDF
"Cadmium and zinc are chemically similar.. they therefore compete with one another for a variety of ligands... because cadmium is considered to have only adverse effects in biological systems... and zinc is an essential nutrient, the significance of their competitive interactions for health merits investigation.
...Cadmium enters man from several sources.. these include air, cigarette smoke, drinking water, and food... the availability of dietary zinc for absorption is also influenced by the diet composition. The digestibility of food is a crucial factor. Hence zinc in meat, sea food, or milk products ... is considerably more available than zinc in grains, legumes and other vegetables, which contain phytate or other ligands that can complex with zinc to form insoluble chelates in the alkaline environment of the small intestine.
...A recent autopsy study ... revealed a positive corelation between renal cortical cadmium:zinc ratio and the severity of atherosclerosis."
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 03, 2012 1:12 pm

new updates (dates highlighted in red) made to page 1 post 1 today: regimens-f22/topic2489.html#p15460
READ ME key info on nutrient targets - www.thisisms.com/ftopict-2489.html
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