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The Nutrigenomics of Selenium

Discussion in 'Genetic Testing and SNPs' started by ppodhajski, Aug 20, 2015.

  1. ppodhajski

    ppodhajski

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    If you want to investigate how your selenium metabolism is effected by your genes, this is a good place to start.

    Selenium and Chronic Diseases: A Nutritional Genomics Perspective

    http://www.mdpi.com/2072-6643/7/5/3621/htm
     
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  2. JaimeS

    JaimeS Senior Member

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    31 pages! :lol: I will read in a bit. Uh, in several sessions, probably. ;)

    Thanks for posting this! I've been wondering about selenium...

    -J
     
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  3. Gondwanaland

    Gondwanaland Senior Member

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    Would you please post a summary? :p:thumbsup:
     
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  4. JaimeS

    JaimeS Senior Member

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    Haha! @Gondwanaland , I have several that are in waiting for an energy-filled day... so we shall see. :)

    -J
     
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  5. ppodhajski

    ppodhajski

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    Ha, yeah, it's a big one.

    Basically, check these genes out in promethease:

    SEPP1
    SEPHS1 - I have a rare SNP here
    GPX1
    GPX2
    GPX3 - I have rare SNPs here
    GPX4 - I have one rare SNP here
    TXNRD1
    TXNRD2 - I have a very rare SNP here
    TXNRD3
    SEP15

    I take selenium and eat brazil nuts. It makes me feel better. I also take FMN (B2) since FAD is a cofactor for TXNRD2. FMN changed my life.
     
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  6. victoriana

    victoriana

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    Thank you for the link re selenium.

    Could you provide details re FMN (B2) ie brand; FAD as a cofactor for TXNRD2 (what is it?); and in particular how it has changed your life/health.

    Many thanks,

    A Canadian from Toronto
     
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  7. ppodhajski

    ppodhajski

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    I take Source Naturals Coenzymated B2 (FMN)
    http://www.iherb.com/Source-Natural...&lc=en-US&w=coenzymated b2&rc=52&sr=null&ic=3

    Here is a good chart of how riboflavin is transported and metabolized into FMN and FAD (both are cofactors and reduced forms of riboflavin)

    F5.large.jpg

    Here is a good brief explanation of FAD and FMN;
    http://sandwalk.blogspot.com/2007/04/riboflavin-vitamin-b2-fmn-and-fad.html

    If you are interested in the MTHFR gene you should look into riboflavin as well;
    http://www.ncbi.nlm.nih.gov/books/NBK6145/

    TXNRD2 is a thioredoxin Reducatse and helps with antioxidation in the mitocondria by recycling Thioredoixin. Thioredoixin is like glutathione.

    363_metabolism_10.gif

    When I first took FMN I had an immediate clarity and calmness that was so unusual it is indescribable. Now I notice it was a key to ending my IBS-D, fatigue, pain related to cartilage inflammation (costrocondritis). It also stops my heart palpitations 5 minutes after taking it. However, it is only part of my treatment. I found that taking FMN interacts with P5P, Zinc, and selenium.

    Also, I found that since taking FMN I cannot take (nor do I need to) magnesium. When I do now, instead of it making me calm it makes me very up and anxious and keeps me awake instead of helping me drift off to sleep.
     
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  8. minkeygirl

    minkeygirl But I Look So Good.

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    @ppodhajski i was just looking at this for adrenal support and for some other oddball symptoms I have.

    how does it react to the other things you mentioned, zinc and selenium?
     
  9. ppodhajski

    ppodhajski

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    @minkeygirl I would not say react, more like they are interdependant.

    First, riboflavin kinase (RFK) uses Riboflavin, ATP, Zinc, and Magnesium to turn riboflavin into FMN.
    http://www.uniprot.org/uniprot/Q969G6

    Also, for example, since Glutathione Perioxidase (GPX) is a selenium based enzyme when you take Selenium GPX activity will increase. That oxidizes the glutathione getting rid of H2O2. But now we have oxidized glutathione that we need to recycle and that is done by Glutathione Reductase which uses FAD as a cofactor and that will use up more FAD and therefor more B2 and FMN. So by taking selenium we could cause a greater riboflavin deficiency. Note it will also increase need for NADH, a reduced form of niacin.

    riboflavin_figure1_v3.png

    As for zinc and magnesium, I will point you to this pathway of B6 metabolism:

    B6 Pathway.png
     
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  10. ppodhajski

    ppodhajski

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    Also, if you are looking at the adrenals, COMT is more highly expressed there than MAOA or MAOB, which points to magnesium and increasing SAMe production as well. (I also have slow COMT SNPs)

    http://www.proteinatlas.org/ENSG00000093010-COMT/tissue
    http://www.proteinatlas.org/ENSG00000069535-MAOA/tissue
    http://www.proteinatlas.org/ENSG00000069535-MAOB/tissue
     
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  11. ahmo

    ahmo Senior Member

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    How are you determining this? Are you researching each snp?
     
  12. ppodhajski

    ppodhajski

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    First I search and sort for the gene in Promethease based on frequency:

    gpx3.png

    Then I look to see what the distribution of the SNPs look like in SNPedia

    snpedia.png

    CT is at 18% and we can see a homozygous SNP there is nearly on average 2%. That to me is important evolutionarily since it seems the C allele is not favorable and is not passed on frequently. the alleles which are more evenly spread seem less important to me.

    http://www.biomedcentral.com/1755-8794/3/57
    "However, disease-associated alleles were more likely to be low frequency derived alleles relative to null expectations. "

    Then I research to if that SNP is associated with increased or decrease enzyme activity.
    http://www.arcmedres.com/article/S0188-4409(14)00076-9/abstract
    http://www.arcmedres.com/article/S0188-4409(14)00076-9/abstract

    So this is me hypothesizing...
    It looks like it is an increase in gene activity, and therefor I will use up more selenium and recycle glutithione very well. Which makes me think I have a heightened immune response, which would be true since I have several autoimmune issues. If I am exposed to mercury this could be a problem since mercury binds to selenium as well. So I am more sensitive to mercury exposure and a lab test would show that I have higher than average mercury levels then the general population.

    Just based on intuition I feel that any SNP under 20% will show some difference from the general population, either increased or decreased activity which would make us outliers.
     
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  13. Valentijn

    Valentijn Senior Member

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    You can't assume a SNP is relevant just because it is rare. Everyone has hundreds or thousands of rare SNPs, yet this does not mean they are all walking around with a ton of "unfavorable" variations. The vast majority of those rare variations have no appreciable impact, and we can't guess that they are problematic simply based upon rarity.

    And even if we could assume that rare SNPs have an impact (we can't), it's impossible to guess what that impact would be. But since rs8177404 and rs8177406 aren't even on GPX3, it's even more unlikely that they are capable of having an impact GPX3. They're actually located on uncharacterized LOC105378228.
     
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  14. ppodhajski

    ppodhajski

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    I am not assuming it is relevant only because it is rare. I would never! That would be foolish! I also look at the research and I also look at it's function in relation to metabolism of nutrients and the creation of neurotransmitters and antioxidants. I am not looking at the whole geneome for rare SNPs, just the subset that have to do with nutrigenomics.

    And hey, what can I say, it works. I am a 100% different man than I was a year ago. Would love you to help me figure out why it works.

    First, if you could post references I would appreciate it, because I do not understand what you are saying here. When I look up in 23andme, promethease and in the research for rs8177404 and rs8177406 they are clearly SNPs in GPX3. The only thing I found for LOC105378228 was an RNA gene. Am I missing something?

    rs8177404 at chr5:150399584 in GPX3
    https://www.pharmgkb.org/rsid/rs8177404

    rs8177406 at chr5:150399634 in GPX3
    https://www.pharmgkb.org/rsid/rs8177406
     
  15. Valentijn

    Valentijn Senior Member

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    http://www.ncbi.nlm.nih.gov/pubmed/24819036 says that they have no impact regarding metabolic syndrome. I don't see any other research regarding those SNPs. Being "polymorphic" simply means that they each have more than one observed allele, which is quite common - every SNP tested by 23andMe is polymorphic, with two possible alleles. And "tight linkage disequilibrium" means that the SNPs discussed (including rs8177404 and rs8177406) are almost always inherited together, which each one taking the same form (homozygous for the major allele, heterozygous, or homozygous for the minor allele).
    Yes, http://www.ncbi.nlm.nih.gov/projects/SNP/snp_ref.cgi?rs= is a better source if you want to see exactly where the SNP is. It's the most up to date. 23andMe data, such as SNP location on a chromosome or a gene, can be years out of date.
     
    Last edited: Aug 22, 2015
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  16. ppodhajski

    ppodhajski

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    So I still do not understand. From that web site you gave me it still says they are both GPX3 SNPs. Can you point out to me exactly what you are talking about? Plus, I am pulling the data from promethease, which is very up to date and run by geneticists.

    Screenshot.png

    Screenshot-1.png
     
  17. Valentijn

    Valentijn Senior Member

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    Hover over the gene on the map view (thick horizontal bar), or zoom out until you can see the gene labels. They aren't on GPX3.

    And what research into those SNPs makes you think they're relevant?
     
  18. ppodhajski

    ppodhajski

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    Look at the images I pasted above, it clearly says "Gene: GPX3". How can you say they are not in the GPX3 gene? You are wrong.

    I am not going to get into proving to you that any single SNP is significant. I have told you before that I use several gene SNPs and any evidence I show you just seem to say it is not good enough. I will let the several people who benefited from my ideas, like how FMN helps those with MAOA and MAOB SNPs, speak to what I see. If you want to help you can help me find out why I am better.

    To everyone else: I am not responding to Valentijn's posts anymore. Do not let my silence let you think that what she says is correct to me, that is the only reason I responded to her in the past. I know what I am saying is mostly theory and speculative, but I am better and that is all the proof I need. No more anxiety, OCD, IBS, CFS, depression, paresthesia, inflammatory skin issues, costrocondritis, high blood pressure...that is my proof.
     
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  19. Valentijn

    Valentijn Senior Member

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    In those images, two genes are listed for each. SNPs are rarely on two genes at the same time, so it's a good indication that you need to look closer. And in this case, the SNPs are at best "near GPX3". Even dbSNP will say "GPX3" in one field and later clarify "nearGene" elsewhere. But currently the best evidence is that rs8177404 and rs8177406 are on an uncharacterized locus (suspected gene) close to GPX3.

    The most recent assembly used by dbSNP shows that GPX3 is on chromosome 5 from positions 151,020,438 to 151,028,993. On that same assembly, rs8177404 is at position 151,020,023 on chromosome 5, and rs8177406 is on position 151,020,073 on chromosome 5. Thus rs8177404 is 415 SNPs away from being on the GPX3 gene, and rs8177406 is 365 SNPs away from GPX3.

    Here's the dbSNP screen shot from http://www.ncbi.nlm.nih.gov/projects/SNP/snp_ref.cgi?rs=rs8177406 . The blue-purple horizontal bar is the locus on which rs8177404 and rs8177406 are located. The green horizontal bar on the right side is GPX3. The thin green vertical line is the the exact location of rs8177406, with rs8177404 being 50 SNPs to the left of it, even further away from GPX3. Also note "nearGene-5" in the "Function" field of the "Gene Models" section directly above the map view.
    rs8177406.jpg

    They are obviously not on GPX3. They are near it. And they are located with a different group of SNPs which is suspected of being an entirely different gene.

    Your method seems to be assuming that any rare-ish SNP on an interesting gene must be having a specific impact which you are arbitrarily assigning to it. But the vast majority of rare SNPs do not have an impact, and in the absence of research into those specific SNPs it is irrational to decide that they must be misbehaving. And it is even more irrational to randomly decide that the hypothetical misbehavior is in the form of an upregulation versus a downregulation, or vice versa.

    There are billions of SNPs. We could spend many life times randomly picking ones that we label as doing this or that. That is not science. That is divining, right up there with astrology and tarot cards.
     
    Last edited: Aug 23, 2015
  20. mariovitali

    mariovitali Senior Member

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    Just to give my two cents :


    Selenium is important for Endoplasmic Reticulum stress control :



    also Selenium is very important for proper protein folding :



    However too much of it should be avoided :


     

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