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 » Fri Jun 21, 2013 10:14 am

OMG!!!!!!!!!! *super* lame but a step in the right direction for the canucks!!: http://www.bloodtestscanada.com/

update: LAME they have had to cancel operating in Canada - apparently too much red tape :S
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info: www.whfoods.com, www.nutritiondata.com
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Re: MS Nutrition-summary pts 1st post, p.1

Postby jimmylegs » Sat Jun 22, 2013 7:41 am

having an interesting little explore this morning.. I like stream of consciousness lit review :)

Heavy metals and living systems: An overview
http://www.ncbi.nlm.nih.gov/pmc/article ... 3373/#ref6
"Heavy metals are natural constituents of the earth's crust, but indiscriminate human activities have drastically altered their geochemical cycles and biochemical balance. This results in accumulation of metals in plant parts having secondary metabolites, which is responsible for a particular pharmacological activity. Prolonged exposure to heavy metals such as cadmium, copper, lead, nickel, and zinc can cause deleterious health effects in humans. Molecular understanding of plant metal accumulation has numerous biotechnological implications also, the long term effects of which might not be yet known."

very interesting and could obviously go both ways if you're measuring patient values...

Sedum alfredii H: A new Zn hyperaccumulating plant first found in China
http://www.researchgate.net/publication ... d_in_China
"The Zn concentration and accumulation in the shoots reached the highest at Zn supply level of 80 mg/L, with 19.67 g/kg and 19.83 mg/plant, respectively. All the results showed that Sedum alfredii Hance is a new Zn hyperaccumulating plant. This provides a new plant material to explore mechanism of plant to hyperaccumulate Zn, and a potent new plant species to phytoremediate Zn contaminated soils."

so interesting. potential for nutriceutical zinc harvest?? just have to watch what else this plant might be hyperaccumulating, and any byproducts of processing.

this is a bit of a non-sequitur.. searched on zinc ayurvedic for this result:

Ayurvedic Medicine Zinc Bhasma: Physicochemical Evaluation, Anti-Diabetic Activity and Safety Assessment
http://www.ingentaconnect.com/content/a ... 1/art00073
Bhasmas are unique Ayurvedic metallic preparations used for medicinal purposes since ancient times. With increasing knowledge of risk of nanomaterials, it becomes imperative to assess the safety of nanoparticulate Ayurvedic medicines using toxicity models. In this study, zinc bhasma was characterized using modern physicochemical techniques. In vitro toxicity test revealed no major cytotoxicity at all the dose levels tested. No behavioral abnormality, clinical signs and mortality was seen indicating no adverse effects. SGOT, SGPT and serum urea were also not significantly altered indicating no major organ toxicity. In the current study, zinc bhasma appears safe for human use.

so what is zinc bhasma, that took me down the yashada bhasma route

Pharmaceutical study of Yashadabhasma
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3530344/
"Yashadabhasma (Zinc calx) was prepared by subjecting it to Samanya shodhana (general purification method for all metals), Vishesha shodhana (specific putification method for Zinc), Jarana (roasting) and Marana (incineration) with Parada(Mercury) as a media under Gajaputa (classical heating system with 1000 cowdung cakes)."

I am sorely tempted to - nay, I cannot resist exclaiming: 'I shit you not!'

Analytical Study of Yashada bhasma (Zinc Based Ayurvedic Metallic Preparation) with reference to Ancient and Modern Parameters
www.omicsonline.org/scientific-reports/ ... SR-582.pdf
"Yashada bhasma, a Zinc based Ayurvedic metallic preparation, was prepared as per Rasa chandamshu text and it was tested with both ancient and modern analytical parameters to know how the basic metal was transformed into bio-absorbable bhasma form and also to know its physical nature as to in which form the final product is.
Results: The ancient bhasma parikshas revealed that the bhasma prepared after two gajaputas (heating system with 1000 dried cow dung cakes) passed all the tests and thus ascertaining it was properly formed and modern analytical techniques like XRD (X Ray Diffraction) identified the final product as Zinc oxide (ZnO)... ICPAES (Inductively Coupled Plasma Atomic Emission Spectroscopy) showed the presence of Zinc in major portion (95.08 ppm) and other elements like Sn (0.27), Pb (0.14), Fe (1.69), Ca (1.82), Mg (1.00), Cu, Co and Mn<0.5 ppm in the final product. ...
Methods adopted for the preparation of Yashada bhasma include Dhalana (a process where molten zinc was poured into specific liquids), Jarana (roasting purified Zinc with Achyranthes aspera powder) and Marana (adding roasted zinc with 1/4th mercury and sulphur and triturating with Aloe vera-Citrus limon juices and subjecting to Gajaputa).
Samanya shodhana (general purification) was done by the Dhalana (liquefying and pouring) method in Kanji (sour gruel), Takra (butter milk), Kulattha (Dolichus biflorus) kwatha (decoction), Gomutra (Cow’s urine), Tila (Sesamum indicum) and Taila (oil). Dhalana was carried out three times in each liquid media [2]. After samanya shodhana, Vishesha shodhana (specific purification) was carried out in Churnodaka (lime water) for seven times [3]. After shodhana, the metal became more brittle and was then subjected to Jarana (roasting) using Apamarga panchanga churna (powder of Achyranthes aspera) [4]. After Jarana, the metal was converted into a very fine grey shining powder which was deemed fit for Marana (incineration). The powder was then subjected to Marana by triturating it with Shuddha Parada (purified Mercury) and Shuddha Gandhaka (purified Sulphur), both
1/4th quantity of Yashada, to form a black powder, from which one bhavana (triturating in liquid media) each with Kumari swarasa (fresh juice of Aloe vera) and Nimbu swarasa (fresh juice of Citrus limon) was given and Chakrikas (pellets) prepared. After drying, they were kept in sharava (casseroles), sandhi bandhana (sealing) was done and subjected to Gajaputa (heating system with 1000 dried cow dung cakes). After two Gajaputas, Yashada bhasma of yellowish color was obtained (Figure 1) [5]."

how cool is that, seriously
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Re: MS Nutrition-summary pts 1st post, p.1

Postby jimmylegs » Tue Jun 25, 2013 9:32 am

on the variable gluten fractions found in wheat:

Characterization of Proteins from Grain of Different Bread and Durum Wheat Genotypes (2011)
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3189758/
"Wheat is unique among the edible grains because wheat flour has the protein complex called “gluten” that can be formed into dough with the rheological properties required for the production of leavened bread. The rheological properties of gluten are needed not only for bread production, but also in the wider range of foods that can only be made from wheat, viz., noodles, pasta, pocket breads, pastries, cookies, and other products. The gluten proteins consist of monomeric gliadins and polymeric glutenins. Glutenins and gliadins are recognized as the major wheat storage proteins, constituting about 75–85% of the total grain proteins with a ratio of about 1:1 in common or bread wheat and they tend to be rich in asparagine, glutamine, arginine or proline but very low in nutritionally important amino acids lysine, tryptophan and methionine. The gliadins constitute from 30 to 40% of total flour proteins and are polymorphic mixture of proteins soluble in 70% alcohol, and can be separated into α-, β-, γ-, and ω-gliadins with a molecular weight range of 30 to 80 kDa as determined by SDS-PAGE. The molecular weights of ω-gliadins are between 46 and 74 kDa, and the α-, β- and γ-gliadins have lower Mw, ranging from 30 to 45 kDa by SDS-PAGE and amino acid sequencing. The latter approach has shown that the α- and β-gliadins are closely related and thereby they are often referred to as α-type gliadins. α-Gliadins are thought to be responsible for gluten intolerance while γ-gliadins and glutenins are much less."

how to boost glutenins and suppress gliadins in wheat (also of note - zinc: not just for membrane integrity in humans!):

Effects of zinc nutrition and high temperature on the growth, yield and grain quality of wheat (Triticum aestivum L.)
http://digital.library.adelaide.edu.au/ ... 2440/37982
Wheat production is the largest enterprise within the Australian grain industry, with an annual gross value of production of approximately $4 billion. However high temperature stress (>35°C) and zinc (Zn) deficiency in soils are a frequent occurrence across the Australian wheat belt and represent two of the most important environmental limitations to wheat production and grain quality. The work presented here has shown for the first time that Zn nutrition can provide wheat plants with a level of tolerance to high temperature stress. Field trials, along with controlled environment studies, showed that supplementary Zn nutrition improved photosynthetic activity during a high temperature event, by stabilising chlorophyll initial fluorescence, Fo. Since increases in Fo under heat stress are associated with an increase in lipid fluidity of the thylakoid membranes at high temperature, the results suggested that adequate Zn fertilisation could preserve membrane integrity during heat stress. Electron microscopy confirmed this hypothesis, and showed that adequate Zn nutrition could maintain the integrity of a number of cellular membranes during high temperature, including the tonoplast, chloroplast envelope and the thylakoid membranes. Measurements of canopy temperature depression showed an improvement in the evaporative cooling of the canopy with supplementary Zn nutrition in the Zn inefficient varieties, suggesting better soil water extraction under warm conditions. Supplementary Zn nutrition also increased the kernel weight of plants grown under warm conditions in the field, however this was unrelated to the improvement in photosynthetic ctivity. Nevertheless, results from both controlled environment and field experiments demonstrated that the detrimental effects of low Zn availability and high temperature on the yield of Zn inefficient or thermosensitive wheat varieties will be most damaging when these stresses occur in combination. Analysis of protein composition showed that supplementary Zn fertilisation increased the glutenin:gliadin ratio in the grain. This suggests that Zn fertilisation may improve the bread-making quality of wheat under conditions of Zn deficiency. The results also showed a negative association between grain Zn concentration and the number of days over 35°C during grain filling, which suggests that the negative effects of high temperature stress on grain protein composition will be compounded when plants are grown on soils of low Zn availability. This thesis represents a valuable contribution to the understanding of the relationships between micronutrient supply and environmental stress. Further studies should be undertaken to establish whether the protective effect of Zn on the photosynthetic apparatus will be maintained under consecutive heat stress events, to determine the ways in which Zn ions stabilise and protect bio- membranes under heat stress and to confirm the positive effects of Zn on grain protein composition and baking quality.
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Re: MS Nutrition-summary pts 1st post, p.1

Postby jimmylegs » Tue Jun 25, 2013 1:03 pm

just got home from a cranial mri w CONTRAST! last time I had a brain scan it was based on the neuro saying 'anything else'? as I was leaving a 2007 checkup. 2007!! and I said, sure - follow up MRI please. he didn't order contrast then, so this new scan (ordered by the family doc - haven't been to the neuro since that one appt in 07) will be the first one on my file with contrast since dx in 2006. will be verrrrry interesting to check out :D
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Re: MS Nutrition-summary pts 1st post, p.1

Postby jimmylegs » Thu Jun 27, 2013 1:01 pm

What Micronutrient Deficiencies Should Be Considered in Distinct Neurological Disorders?
http://link.springer.com/article/10.100 ... 013-0331-7
The expanding understanding of the biochemical and physiologic role of micronutrients, commonly referred to as vitamins and minerals, is driving the identification of their consequences in both deficiency and toxicity. Neural tissue is quite sensitive to physiologic changes, and as such, micronutrient deficiencies can have significant and profound effects on the functioning of both the central and peripheral nervous systems. Understanding which micronutrients can affect the nervous system can aid physician identification of these neurological symptoms and signs, leading to diagnostic testing and appropriate therapy.
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Re: MS Nutrition-summary pts 1st post, p.1

Postby jimmylegs » Tue Jul 02, 2013 9:59 am

THX1138 wrote:Thanks jimmylegs. When I was posting about my normal liver function test results, your writings about the frequent problems with "normal" results from tests came to mind and I thought, "LFT's had better not be another example of issues with tests!"
Here are my most recent test panel results:
Component Standard Range Your Value
ALBUMIN 3.5 - 5.0 g/dL 4.2
TOTAL BILIRUBIN 0.1 - 1.2 mg/dL 0.7
DIRECT BILIRUBIN 0.0 - 0.5 mg/dL 0.1
INDIRECT BILI 0.1 - 1.2 mg/dL 0.6
ALK PHOSPHATASE 25 - 125 IU/L 84
PROTEIN, TOTAL 6.0 - 8.0 g/dL 7.3
ALT(SGPT) 5 -40 IU/L 35
AST(SGOT) 10 - 40 IU/L 25


okay, my first look at selected liver enzymes in healthy controls:

Probiotics restore bowel flora and improve liver enzymes in human alcohol-induced liver injury: a pilot study (2008)
http://www.sciencedirect.com/science/ar ... 2908003017

alcoholic average
alanine aminotransferase (ALT) 104.1 U/L
aspartate aminotransferase (AST) 50.49

non-alcoholic average (which will have to pass for 'healthy' here)
alanine aminotransferase (ALT) 29.15 U/L
aspartate aminotransferase (AST), 22.96 U/

so clearly patients with alcoholic psychosis have levels elevated well above the range used at your lab. the averages for the non-alcoholic controls are interesting, but unfortunately no ranges were provided in the abstract and I don't have full text access. so, worth delving deeper into this one. more data replication from more specifically healthy controls is needed. liver enzymes in healthy people with low gluten intakes (ie less zinc binding) etc would be an interesting piece.

FYI the alcohol damage has a lot to do with zinc depletion.. pbx used in the above study are among the things that help protect the body from zinc depletion.. vit E is on the list too. at the end of the day the damage is from zinc depletion though.

Bifidobacterium animalis Protects Intestine from Damage Induced by Zinc Deficiency in Rats
http://jn.nutrition.org/content/129/12/2251.short

along this line, zinc supplementation repairs alcoholic liver damage (check it out, the subjects were 'normal' the whole duration of the study, but so much improvement recorded!)

Zinc Supplementation in Alcoholic Cirrhosis. A Double-Blind Clinical Trial (1979) - YES, 1979!!
http://onlinelibrary.wiley.com/doi/10.1 ... x/abstract
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
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Re: MS Nutrition-summary pts 1st post, p.1

Postby jimmylegs » Tue Jul 02, 2013 2:53 pm

another look at ALT and AST in healthy (non-typhoid) controls (look, ranges!!) I set it up similar to above for easier comparison

typhoid average
alanine aminotransferase (ALT) 20.89 ± 9.25 U/l
aspartate aminotransferase (AST) 41.56 ± 18.67 U/l,

non-typhoid average (which will have to pass for 'healthy' here)
alanine aminotransferase (ALT) 7.06 ± 3.54 U/l
aspartate aminotransferase (AST), 23.2 ± 13.07 U/l

Pattern of serum transaminases in enteric fever patients attending Ebonyi State University Teaching Hospital, Abakaliki
http://www.ajol.info/index.php/ijbcs/article/view/65536
"The result showed that the level of aspartate transaminases in the typhoid patients was 41.56 ± 18.67 U/l, and significantly higher (P<0.05) than that (23.2 ± 13.07 U/l) of the healthy controls, while the patient’s alanine transaminases activity was 20.89 ± 9.25 U/l and as well higher (P<0.05) than 7.06 ± 3.54 U/l for the controls."
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 THX1138 » Tue Jul 02, 2013 7:34 pm

Hey, are you suggesting that a result of "normal" on a lab test may not mean that all is well in the land? :lol:
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Re: MS Nutrition-summary pts 1st post, p.1

Postby jimmylegs » Tue Jul 02, 2013 8:06 pm

i screams it from the electronic rooftops :)
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Re: MS Nutrition-summary pts 1st post, p.1

Postby jimmylegs » Tue Jul 02, 2013 8:11 pm

maybe i'll just call my book NORMAL = BU||$H|T ;D no, maybe that can be a chapter. something.
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 » Thu Jul 04, 2013 5:37 am

thinking about prophylactic nutrition and ccsvi procedures..

Cytokines, Neuropeptides, and Reperfusion Injury during Magnesium Deficiency
http://onlinelibrary.wiley.com/doi/10.1 ... x/abstract

Protective effects of magnesium against ischaemia-reperfusion injury through inhibition of P-selectin in rats.
http://www.ncbi.nlm.nih.gov/pubmed/17973860

The effects of magnesium pretreatment on reperfusion injury during living donor liver transplantation
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3121087/
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 06, 2013 1:31 pm

had a blast with food and music today :)

also, i updated my daily supplement regimen on page one yesterday. it was quite out of date.
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
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Re: MS Nutrition-summary pts 1st post, p.1

Postby jimmylegs » Sun Jul 07, 2013 5:34 pm

off topic.

i have 5 guitars piled around me, and am thoroughly enjoying an acoustic in open C right now.
chris cornell is singing along via youtube ;) he has no idea how much fun we're having :D
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 08, 2013 4:37 am

interesting:

The plasma zinc/serum copper ratio as a biomarker in children with autism spectrum disorders (2009)
http://informahealthcare.com/doi/abs/10 ... 0902783747
"The frequency of zinc deficiency, copper toxicity and low zinc/copper in children with autism spectrum disorders (ASDs) may indicate decrement in metallothionein system functioning. A retrospective review of plasma zinc, serum copper and zinc/copper was performed on data from 230 children with autistic disorder, pervasive developmental disorder-NOS and Asperger’s syndrome. The entire cohort’s mean zinc level was 77.2 μg dl−1, mean copper level was 131.5 μg dl−1, and mean Zn/Cu was 0.608, which was below the 0.7 cut-off of the lowest 2.5% of healthy children. The plasma zinc/serum copper ratio may be a biomarker of heavy metal, particularly mercury, toxicity in children with ASDs."

Interference by toxic metal ions with zinc-dependent proteins involved in maintaining genomic stability
http://www.sciencedirect.com/science/ar ... 1502000431
Metal ions are essential components of biological systems; nevertheless, even essential elements may have toxic or carcinogenic properties. Thus, besides As(III) and Cd(II), also Ni(II) and Co(II) have been shown previously to disturb different types of DNA repair systems at low, non-cytotoxic concentrations. Since some metals exert high affinities for SH groups, we investigated whether zinc finger structures in DNA-binding motifs of DNA repair proteins are potential targets for toxic metal ions. The bacterial formamidopyrimidine-DNA glycosylase (Fpg protein) involved in base excision repair was inhibited by Cd(II), Cu(II) and Hg(II) with increasing efficiencies, whereas Co(II), As(III), Pb(II) and Ni(II) had no effect. Furthermore, Cd(II) still disturbed enzyme function when bound to metallothionein. Strong inhibition was also observed in the presence of phenylselenyl chloride, followed by selenocystine, while selenomethionine was not inhibitory. Regarding the mammalian XPA protein involved in the recognition of DNA lesions during nucleotide excision repair, its DNA-binding capacity was diminished by Cd(II), Cu(II), Ni(II) and Co(II), while Hg(II), Pb(II) and As(III) were ineffective. Finally, the H2O2-induced activation of the poly(ADP-ribose)polymerase (PARP) involved in DNA strand break detection and apoptosis was greatly reduced by Cd(II), Co(II), Ni(II) and As(III). Similarly, the disruption of correct p53 folding and DNA binding by Cd(II), Ni(II) and Co(II) has been shown by other authors. Therefore, zinc-dependent proteins involved in DNA repair and cell-cycle control may represent sensitive targets for some toxic metals such as Cd(II), Ni(II), Co(II) and Cu(II), as well as for some selenium compounds. Relevant mechanisms of inhibition appear to be the displacement of zinc by other transition metals as well as redox reactions leading to thiol/disulfide interchange.

because of that I went looking for research connections between mercury and fragile X.. google threw me this:

A Prospective Study of Mercury Toxicity Biomarkers in Autistic Spectrum Disorders (2007)
http://www.tandfonline.com/doi/abs/10.1 ... dqq88zD_q4
"Porphyrins are derivatives formed in the heme synthesis pathway and porphyrins afford a measure of xenobiotic exposure. The steps in the heme pathway most vulnerable to heavy metal inhibition are uroporphyrin decarboxylase (UROD) and coproporphyrinogen oxidase (CPOX) reactions. Mercury toxicity was associated with elevations in urinary coproporphyrin (cP), pentacarboxyporphyrin (5cxP), and precoproporphyrin (prcP) (also known as keto-isocoproporphyrin) levels. Two cohorts of autistic patients in the United States and France had urine porphyrin levels associated with mercury toxicity. A prospective study of urinary porphyrin testing at LabCorp (United States) and the Laboratoire Philippe Auguste (France) involving 71 autism spectrum disorder (ASD) patients, neurotypical sibling controls, and general population controls was undertaken. ASD patients had significant elevations in urinary levels of cP, 5cxP, and prcP relative to controls, and > 50% of ASD patients had urinary cP levels more than 2 standard deviations above the mean values for neurotypical sibling controls. Significant reductions in urinary 5cxP and cP levels were observed in ASD patients following chelation. A significant correlation was found between urinary porphyrins measured at LabCorp and those measured at the Laboratoire Philippe Auguste on individual ASD patients. The established developmental neurotoxicity attributed to mercury and biochemical/genomic evidence for mercury susceptibility/toxicity in ASDs indicates a causal role for mercury. Urinary porphyrin testing is clinically available, relatively inexpensive, and noninvasive. Porphyrins need to be routinely measured in ASDs to establish if mercury toxicity is a causative factor and to evaluate the effectiveness of chelation therapy."

so then I thought I had better refresh my memory re porphyrin and porphyria and found this:

Zinc in Porphyria
http://ajcn.nutrition.org/content/22/10 ... l.pdf+html
Very few data are available for the excretion of zinc in urine and zinc levels in serum and plasma in human subjects, as reliable methods have been developed only recently. These results have been tabulated for normal persons and show that the normal zinc excretion is of the order of 100-900 µg Zn/24 hr, but that this may be affected by food intake and is increased in a number of diseases, being highest in periarteritis nodosa, followed by organic brain syndrome, and then alcoholism. The excretion in porphyrics is very high in patients with acute intermittent porphyria but may be below normal in some forms of cutaneous porphyria.
The normal serum and plasma levels of zinc are approximately the same and of the order of 100 µg Zn/100 ml. This level again can show physiological variations due to food intake and pregnancy and varies considerably in neonates and young children. Liver disease, especially alcoholic cirrhosis, lowers the serum zinc, whereas in porphyrics with cutanea tarda and who are alcoholics serum zinc levels are high. Serum zinc levels are also very high in patients severely ill with acute intermittent porphyria and both the serum and urinary zinc levels increase with the severity of the disease. In no other disease have such high serum or plasma zinc levels been reported.
Though zinc is not etiologically connected with porphyria, there is a secondary link. Some symptoms seen in porphyrics are possibly due to local zinc deficiency in particular tissues caused by the complexing of zinc required for some metalloenzymes by excess porphyrins present.

so would that also connect to the high serum zinc then? released from tissue and racing around in serum working on the porphyrin excess? hmmm..

back to fragile x - http://en.wikipedia.org/wiki/Fragile_X_syndrome
"Fragile X syndrome is associated with the expansion of the CGG trinucleotide repeat affecting the Fragile X mental retardation 1 (FMR1) gene on the X chromosome, resulting in a failure to express the fragile X mental retardation protein (FMRP), which is required for normal neural development. Depending on the length of the CGG repeat, an allele may be classified as normal (unaffected by the syndrome), a premutation (at risk of fragile X associated disorders), or full mutation (usually affected by the syndrome).[1] A definitive diagnosis of fragile X syndrome is made through genetic testing to determine the number of CGG repeats. Testing for premutation carriers can also be carried out to allow for genetic counseling. The first complete DNA sequence of the repeat expansion in someone with the full mutation was generated by scientists in 2012 using SMRT sequencing.[2]"

cutting edge, nice. okay enlighten me re trinucleotide repeats.

https://en.wikipedia.org/wiki/Trinucleo ... t_disorder
Trinucleotide repeat disorders (also known as trinucleotide repeat expansion disorders, triplet repeat expansion disorders or codon reiteration disorders) are a set of genetic disorders caused by trinucleotide repeat expansion, a kind of mutation where trinucleotide repeats in certain genes exceed the normal, stable threshold, which differs per gene.

ooh, this looks good

How environmental and genetic factors combine to cause autism: A redox/methylation hypothesis
http://www.sciencedirect.com/science/ar ... 3X0700215X

ran into this work again:
A Prospective Study of Mercury Toxicity Biomarkers in Autistic Spectrum Disorders (2007)
http://www.tandfonline.com/doi/abs/10.1 ... dqq88zD_q4
Adams et al. (2007) evaluated baby teeth as a measure of cumulative exposure to toxic metals during fetal development and early infancy in autistic children relative to matched controls. The reported mean mercury level in baby teeth from autistic children (mean = 0.15 ± 0.11 ppm) was 2.1-fold higher than the mean for the controls (mean = 0.07 ± 0.06 ppm) whereas lead and zinc levels were similar in both groups. These investigators concluded that, on mean, autistic children had a higher body burden of mercury during fetal/infant development than neurotypical children.

I will have to go find this adams work, and look at the data

Mercury, Lead, and Zinc in Baby Teeth of Children with Autism Versus Controls
http://www.tandfonline.com/doi/abs/10.1 ... dqz4czD_q4
This study determined the level of mercury, lead, and zinc in baby teeth of children with autism spectrum disorder (n = 15, age 6.1 ± 2.2 yr) and typically developing children (n = 11, age = 7 ± 1.7 yr). Children with autism had significantly (2.1-fold) higher levels of mercury but similar levels of lead and similar levels of zinc. Children with autism also had significantly higher usage of oral antibiotics during their first 12 mo of life, and possibly higher usage of oral antibiotics during their first 36 mo of life. Baby teeth are a good measure of cumulative exposure to toxic metals during fetal development and early infancy, so this study suggests that children with autism had a higher body burden of mercury during fetal/infant development. Antibiotic use is known to almost completely inhibit excretion of mercury in rats due to alteration of gut flora. Thus, higher use of oral antiobiotics in the children with autism may have reduced their ability to excrete mercury, and hence may partially explain the higher level in baby teeth. Higher usage of oral antibiotics in infancy may also partially explain the high incidence of chronic gastrointestinal problems in individuals with autism.

well I couldn't find raw data (YET) but oh boy.. I didn't know abx reduced mercury excretion. that's rough. low zinc and high mercury in fetal development, or low maternal/fetal zinc leading to impaired mercury excretion... higher infection rates, more antibiotics, disturbed gut flora, more mercury accumulation...

ouch. need a break but will come back to the triple repeat aspect..
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 08, 2013 6:18 am

ok for now looking at zinc and cgg repeats

Altered zinc transport disrupts mitochondrial protein processing/import in fragile X-associated tremor/ataxia syndrome
http://hmg.oxfordjournals.org/content/20/15/3079.short
Fragile X-associated tremor/ataxia syndrome (FXTAS) is a late-onset neurodegenerative disorder that affects individuals who are carriers of small CGG premutation expansions in the fragile X mental retardation 1 (FMR1) gene. Mitochondrial dysfunction was observed as an incipient pathological process occurring in individuals who do not display overt features of FXTAS ( 1). Fibroblasts from premutation carriers had lower oxidative phosphorylation capacity (35% of controls) and Complex IV activity (45%), and higher precursor-to-mature ratios (P:M) of nDNA-encoded mitochondrial proteins (3.1-fold). However, fibroblasts from carriers with FXTAS symptoms presented higher FMR1 mRNA expression (3-fold) and lower Complex V (38%) and aconitase activities (43%). Higher P:M of ATPase β-subunit (ATPB) and frataxin were also observed in cortex from patients that died with FXTAS symptoms. Biochemical findings observed in FXTAS cells (lower mature frataxin, lower Complex IV and aconitase activities) along with common phenotypic traits shared by Friedreich's ataxia and FXTAS carriers (e.g. gait ataxia, loss of coordination) are consistent with a defective iron homeostasis in both diseases. Higher P:M, and lower ZnT6 and mature frataxin protein expression suggested defective zinc and iron metabolism arising from altered ZnT protein expression, which in turn impairs the activity of mitochondrial Zn-dependent proteases, critical for the import and processing of cytosolic precursors, such as frataxin. In support of this hypothesis, Zn-treated fibroblasts showed a significant recovery of ATPB P:M, ATPase activity and doubling time, whereas Zn and desferrioxamine extended these recoveries and rescued Complex IV activity.
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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jimmylegs
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