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Need help Interpreting Genetic Genie, NutraHacker and Sterling Results

Discussion in 'Genetic Testing and SNPs' started by Darrin, Jan 25, 2015.

  1. Darrin

    Darrin

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    Please help me to understand this. I've been suffering from DEPRESSIVE RUMINATION(Family history of rumination, depression, bipolar, twitches and what not), anxiety, agoraphobia, blow my nose alot and hypoglycemia all my life. I have to eat every 1 1/2 to 2 hours. I have slow cognition and I find it hard to say what I mean and don't talk very much. I'm a male and 32 years old. I would have to say that the rumination is the worst thing and if I could fix anything...that would be it.

    In the mean time I'll be reading Caledonias SNPs Interpretation Guide and trying to make sense of all this. Any help would be appreated. There's also the chance that I may miss something important as well.
     

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  2. Critterina

    Critterina Senior Member

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    Have you ever had your cortisol levels checked? Just from my personal experience, the hypoglycemia makes me wonder.

    The SNPs in the methylation profile that bother most of us aren't there in yours. I wouldn't think that methylation supplements would make much of a difference for you. But with your depressive symptoms, well, who knows? I'm certainly no expert; I even had to look up what rumination means. I do wish you the best!
     
    Last edited: Jan 25, 2015
  3. Darrin

    Darrin

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    Thanks for replying :) . Growing up my mother told me that my family had blood sugar problems but I never really thought much of it cause I was a kid. I haven't had my cortisol tested but I always wondered about it. I've read that high and low cortisol can be confused with each other and it's hard to determine which it is sometimes. I tried licorice root and believe that I did feel better but I had to stop because it increases estradiol and lowers testosterone...and isn't something for long term use.

    NutraHacker had comments that said "Mutation associated with generalized glucocorticoid resistance, high cortisol, CFS" and that I should try phosphatidylserine. I'm planning on giving phosphatidylserine a long trial one of these days. I believe I read that norepinephrine can also cause problems with blood sugar as well and effect cortisol and I read that taurine can help with adrenaline problems but my NutraHacker report said that I should avoid it. So yeah it's all confusing...sheesh :) .
     
  4. Darrin

    Darrin

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    I'll post what the important looking NutraHacker cortisol stuff says...if it even matters :)

    NUTRAHACKER:

    *HPA axis / Endocrine rs1866388 NR3C1 G AA: 2/2 60.1431%
    Glucocorticoid receptor Mutation associated with generalized glucocorticoid resistance, high cortisol, CFS

    *HPA axis / Endocrine rs852977 NR3C1 G AA: 2/2 56.1304% Glucocorticoid receptor Mutation associated with
    generalized glucocorticoid resistance, high cortisol, CFS

    *HPA axis / Endocrine rs5522 NR3C2 A CC: 2/2 1.15040% Mineralocorticoid receptor, mediates aldosterone actions on salt and water balance Increased amygdala reactivity to stress, decreased cortisol binding
     
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  5. Darrin

    Darrin

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    I'm still looking into this but choline, cholinergics, tmg, dmg seem to make me irritated and makes it harder for me to think. For instance on dmg I would type and use the wrong words and miss a lot of errors. It may have to do with my blood sugar problems, insulin and too many methyl donors. I'm going to need a lot of research for this.
     
  6. Darrin

    Darrin

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    I'm now starting to believe my problems are caused by MAOA++, COMT+ and histamine. My neurotransmitters are being broken down slowly along with estradiol. My irritation from methyl donors is most likely caused by increased dopamine, norepinephrine and epinephrine.

    I have had a running nose most of my life and believe that histamine is playing a huge part in that. Adrenaline and cortisol counter histamine which could explain my hypoglycemia and anxiety.
     
  7. Leslieohan

    Leslieohan

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    Just got my daughter's report today and she has the same mutations (glucocorticoid receptor).I came across this article, http://annals.org/article.aspx?articleid=706919 and also http://www.biomedcentral.com/1741-7015/9/27 treatment is with something called Dexamethasone. I plan on looking into this further for my daughter, she also has hyperandrogenism and PCOS (polycystic ovarian syndrome). Both are related to the glucocorticoid receptor mutation and all have to do with HPA axis (hypothalamus pituitary adrenal axis) / endocrine.
     
  8. Darrin

    Darrin

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    I'm in a hurry but for PCOS you can try:

    *N-acetyl-cysteine (NAC): http://www.ncbi.nlm.nih.gov/pubmed/21831508
    "CONCLUSIONS:
    Metformin and NAC appear to have comparable effects on hyperandrogenism, hyperinsulinaemia and menstrual irregularity in women with PCOS. The effects of metformin and NAC on insulin sensitivity are not associated with TNF-α."

    *D-Chiro-inositol: http://www.ncbi.nlm.nih.gov/pubmed/21831508
    "Clinical, endocrine and metabolic effects of metformin vs N-acetyl-cysteine in women with polycystic ovary syndrome."

    I also believe licorice root helps with cortisol and increasing estradiol.

    I'm starting to question the validity of these tests lately.

    As for Dexamethasone it seems hard core I wish you good luck if you use it. If it was me I would be worried about long term use of such things. Anyway gotta bail have a good day.

     
  9. Darrin

    Darrin

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    Well I think I've discovered my problems. I have a genetic mutation of g6pc2 Rs560887 and I believe it's causing hyperinsulinism, hypoglycemia, high cortisol(Evening and night - I had it tested), acidosis, high lactic acid and ect.
    I have to eat every hour and a half and I think this explains it. But what is strange is that this mutation says I would have high fasting blood glucose. Maybe it's too high and insulin reduces it or the information on the gene is wrong. I'm thinking of trying out Benagene to fix my nad/nadh ratio and l-cysteine to inactivate insulin release. I'll have to do more research into this.
     
  10. Valentijn

    Valentijn Senior Member

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    rs560887 only has a tiny impact. I'd be pretty surprised if it's capable of causing problems.
     
  11. Darrin

    Darrin

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    I know these are only mice studies below and could mean nothing or could mean something. I wonder if it's possible that my gp6c2 mutation isn't opposing pancreas Glucokinase and giving me low blood sugar and so forth. If you don't think it's probable could I ask what you would think it is if it's genetic and I have to eat every hour and a half. No one in my family is diabetic. When I'm out driving or haven't eaten in a hour and a half I start feeling that low blood sugar, sick, anxiety feeling I'll eat something and right away feel so much better.

    http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3636628/
    "We provide evidence that G6pc2 acts as a novel, negative regulator of basal GSIS by hydrolyzing G6P and thereby opposing the action of the glucose sensor, glucokinase (15,16). This glucokinase/G6pc2 futile substrate cycle is predicted to reduce glycolytic flux and hence insulin secretion. Consistent with this model and human GWAS data, we show that a reduction in G6pc2 expression results in a leftward shift in the dose-response curve for GSIS such that under fasting conditions, blood glucose levels are reduced."

    http://grantome.com/grant/NIH/R01-DK092589-03
    "Based on these data our first hypothesis is that the glucose-6-phosphatase activity of G6PC2 opposes the action of glucokinase (GCK), which catalyses the conversion of glucose to G6P. Glycolytic flux has been shown to determine the S {0.5} of glucose-stimulated insulin secretion (GSIS) and the existing paradigm in the islet field proposes that GCK alone is the beta cell glucose sensor."
     
  12. Valentijn

    Valentijn Senior Member

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    It's one SNP on the gene. There are hundreds of other SNPs on the same gene, a great many of which would have far, far more impact that that SNP.

    Hence it doesn't really matter what the gene can do, when it comes to assessing the impact of that single SNP. What matters is what that one SNP does, and that one does almost nothing.
     
  13. Darrin

    Darrin

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    Thanks for explaining it. I was really hoping that I found something.
     
  14. Sea

    Sea Senior Member

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    According to this page the average difference in fasting blood glucose for this snp is 2 mg/dl. That tiny difference is only of interest to researchers, not relevant for any clinical issues.
    http://www.snpedia.com/index.php/Rs560887

    Have you had any testing to uncover the basis of your need to eat frequently? Possible answers can be found in blood glucose regulation disorders, lipid metabolism disorders, carbohydrate metabolism disorders, protein metabolism disorders. These are often referred to collectively as inborn errors of metabolism.

    A good place to start is to research the symptoms of some of these disorders and see where you may fit and get some testing done. Some forms are deadly and make their presence known soon after birth, but others are milder and can go unnoticed for many years showing up in adolescence or adulthood or only having an effect when a person is otherwise sick with something else. So don't be put off by the serious ones, you'll be looking more at the later onset ones.

    A home glucose monitor is probably a good a good way to rule in or out a problem with glucose metabolism.
     
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  15. Darrin

    Darrin

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    Thanks very much for your help :) . When I was younger I had a bad experience at a hospital when they took my blood. I turned white and almost passed out. The doctor wanted me out and I couldn't move. It really made me feel like they cared. Anyway I've avoided hospitals ever since.

    I'll definitely look into those things you've mentioned and try to get some tests.
     

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