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Xenoestrogen reduction through diet and supplements

Discussion in 'Detox: Methylation; B12; Glutathione; Chelation' started by Journeyman, Oct 11, 2013.

  1. Violeta

    Violeta Senior Member

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    I'm glad to hear it's working out for you. www.sensiblehealth.com has the best Chinese herbs for the liver because Julia Chang knows Chinese Medicine but also makes sure that her formulas don't contain estrogenic herbs.
  2. BFG

    BFG

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    I'm not sure what you mean by doing things by halves. I thought that having the +/+ at a gene meant almost zero activity of that enzyme? I've never heard of the D'Adamo theory and genes. I'll have to look that up. Also, I tried to enter the GSTT1 snp into my 23andme raw data, but it all came out as "no call".
  3. Valentijn

    Valentijn Activity Level: 3

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    +/+ usually means just slight reduction in gene activity. It almost never means that there's no activity or almost no activity.

    The reference to "doing things by halves" might be because heterozygous SNPs often have no impact, or a much milder one compared to homozygous. However, there certainly are exceptions to this, especially in the case of compound heterozygous mutations. Hence while most +/- results are about the same as -/- results, you have exceptions, such as with MTHFR C677T +/- reducing methylfolate production to 65%, which then gets even worse when combined with MTHFR A1298C -/+ on the opposite strand.
  4. Journeyman

    Journeyman

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    It's a cute way of saying 'when you have a mutation you do the whole thing'. It seems you're absent GSTT1. This should be in its own separate section at the bottom of your detox panel results which are not viewable in many peoples screenshot of their panel....
  5. BFG

    BFG

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    THanks for the explanations. I think I get it now.

    23andme says no call, which means: "No call: Occasionally, a user's data may not allow us to determine his or her genotype confidently at a particular SNP. It is possible that future review will allow us to call the genotype, but until that time, the data does not appear"

    and I ran my rawdata through genetic genie and it says absent, but I don't know for certain if it is really absent due to the no call on 23andme.

    If this gene is absent what sort of implications does it have, if any?
  6. Valentijn

    Valentijn Activity Level: 3

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    It probably really is absent. GSTT1 is missing in 15% of Europeans, so it isn't that uncommon. And most of the normal no-call results are just one or two SNPs missing in a gene, not all 20 SNPs missing from a gene.

    It indicates problems with detoxing certain pollutants and toxins. Amitriptyline and rituximab are known to be problematic, and some other drugs probably are as well.
    Journeyman likes this.
  7. Journeyman

    Journeyman

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    I think I've found an extremely useful journal article here http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2784188/ which not only explains how cruficerous vegetables affect CYP1A2 enzyme activity, but how geneotype variations on the GST strand alter the effectiveness of these vegetables in promoting the increased CYP1A2 activity. I find these articles quite testing to read and want to confirm my existing understandings as being correct. Based on this article is it fair to say (1) for GSTT1 null individuals (such as myself) the 1C diet promoted a slight upregulation of CYP1A2 enzyme activity and that the 2C diet (7gm/kg of body weight crucifers) caused a statistically significant upregulation in the order of about 15% ? Have I interpreted this correctly?

    Furthermore, when they speak of the 2C diet being 7gm/kg body weight are we to assume this is the daily intake of the crucifers? Meaning that if I weight 70kg I would be eating 490gm of the crucifers per day? or are they referring to the total intake spread over the 12 days they performed the study over? This last point is hugely important because in my mind it will make it clear whether diet is worth pursuing to achieve a therapeutically significant effect. ie: if I have to eat 500gm of crucifers per day then its not really practical to achieve a mere 15% upregulation in enzyme activity and thus (presumably) xenoestrogen excretion...
  8. Valentijn

    Valentijn Activity Level: 3

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    It's hard to guess exactly, because they don't have a GSTT1-null group which is GSTM1+. But in table 3, the "basal fold change" after eating the veggies is 1.35. So it sounds like CYP1A2 activity is increasing by 35%. Because there doesn't seem to be any significant variation based on the version of CYP1A2 rs762551, GSTT1, or GSTM1, all of the effect seems to come from the food, regardless of genotype.

    So essentially they're saying that eating the 2C diet results in a 24-35% increase of CYP1A2 activity for everyone. While there is a small difference between the GSTT1 positive/null and GSTM1 positive/null groups, it probably isn't significant, due to the small sample size.
    Yes, it's the daily intake. They clarify that a bit here:
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  9. Journeyman

    Journeyman

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    Thanks so much Valentijn - I just need my attention brought to the part you quoted re: the 307-662gm for men etc..
    Having read back over it with a fresh set of eyes I also note that the vegetables they used were a mix of frozen cauliflower/brocolli and fresh red/green cabbage. The quantities involved to maintain a 1C style diet are almost doable for me, but 2C is just impractical. Having said that, using the knowledge gained from another article ( http://lpi.oregonstate.edu/infocenter/phytochemicals/i3c/ ) I understand that Brussell sprouts supply a far higher amount of I3C which ends up going to DIM where it exerts strong anti estrogen effects. The difference between glucosinolate content (of which 10% is I3C) between cabbage and brussel sprouts is 0.8mg/gm vs 2.4mg/gm. so it makes adherence to the 1C diet not that difficult to achieve after all... Of course nobody wants to be eating the brussel sprouts more than once or twice a day but I can achieve the bottom end of the 1C diet by eating just 105gm of Brussel sprouts per day and thus gain a 15% enzymatic improvement for my mutated CYP1A2 gene. Not to mention all the secondary benefits the other Isothiocyanates provide in preventing carcinogens and providing I3C.

    It may seem that I've gone into an awful lot of detail to get real world values but its by doing this that I have made the research worthwhile, and by leaving it here for posterity others who have similar interests or gene polymorphisms can get the benefit of my research in a much shorter time.
    cigana likes this.

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