Phoenix Rising tells QMUL: release the PACE trial data
Mark Berry, Acting CEO of Phoenix Rising, presents the Board of Directors’ open letter to Queen Mary University of London (QMUL) urging them to release the PACE trial data, and hopes that other non-UK organisations will join British charities in the same request...
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Severe OCD

Discussion in 'Genetic Testing and SNPs' started by Lume, Apr 21, 2015.

  1. Lume

    Lume

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    Hi everyone! I hope someone can explain these SNP'S. Ive been diagnosed with OCD a year ago. Before that, I spent about 6 years lost in the medical system not knowing what was wrong with me, going from psychiatrist's to psychologist's and on different types of medication. It was about a year ago that I found this doctor that treats you with Nutrigenetics. I got my 23andme test and the SNP's that I had were impacting my methylation process. My doctor first put me on Hydroxy and on Thorne's methylguard plus. Now Im taking 2 continuous day the Hydroxy, the 3rd day a full dropper of B12 liquid formulated with methylcobalamin by pure encapsulations and everyday one capsule of methylguard plus.

    This combination seems to be working ok some days but then others not really. It almost feels like a fragile recovery, like im standing on the edge barely balancing myself but one little push will again bring the OCD back full throttle. The OCD get so bad that I get terrible anxiety and dont sleep at night.

    I read that if you have ACAT 102, BHMT and CBS snp's that these need to be treated first through detox and then the other mutations get treated. I have not received treatment for any of these so im starting to distrust my doctor. I also read that if your CBS is A3609 (+,-) like mine, that the detox might not be so important. Either way im confused as to what is going on and confused as to why my doctor did not mention the importance of these mutations and wondering if my SNP's are being treated correctly to correct my methylation process.
    Thank you so much!!! here is my 23andme results :)
    Also could anyone explain my detox profile? I have no idea as to what any of it means
    THANKS!
     

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    Last edited: Apr 21, 2015
  2. Sidereal

    Sidereal Senior Member

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    How so, if you don't mind me asking? Usually OCD is very obvious and diagnosis is easy. What are your symptoms?
     
  3. Lume

    Lume

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    Well I didnt have the typical OCD that has compulsions (germs, order) I have a lesser known form of OCD called "pure o" which is basically only obsessiveness and the compulsions happen in the mind. My main symptom is that I become lost in thought and worries for hours or days having one worry take over every minute of my day. This produces tons of anxiety...basically I cant stop thinking, worrying etcetera...
     
  4. Sidereal

    Sidereal Senior Member

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    Oh ok, fair enough. Sorry to hear about your troubles. Hopefully others who are well-versed on the SNPs can chime in.
     
  5. Lume

    Lume

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    Hopefully! Thanks! ;)
     
  6. ppodhajski

    ppodhajski

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    The same thing happened to me. It is not as easy to diagnose as people thing. I went from ADHD, to Bipolar, then finally OCD.
     
    Lume likes this.
  7. ppodhajski

    ppodhajski

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    Hey Lume, I had OCD/Anxiety, I do not anymore.

    Magnesium Citrate for that COMT is a certainty.

    I need to see your MAO-B SNPs which are not listed. You need to find them in 23andme.
    MAOB
    rs2283729
    rs1799836

    I am guessing the will be AA and GG respectively.

    Here is my sterlings report. Look familiar? :)

    I do not know how bad you were but I was in the Psyche ward twice in the early 2000's.

    Now I am on no meds and have zero symptoms. Looking for work, getting off of disability.


    Screen Shot 2015-04-21 at 6.22.13 PM.png
     
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  8. Lume

    Lume

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    Hi! Thanks for your answer it really made my day to know that you had the same and know are fine. I went from depression, bipolar, a bunch of alternative mumbo jumbo that just made me feel weak and guilty and then finally OCD. Youre right for the first Mao B

    rs2283729.- GG
    rs1799836.- CT

    What does this mean?

    I was also on Magnesium Citrate but my doctor had prescribed it so I would use the bathroom better. So where do I start with all this? How long until the OCD symptoms go away?

    THANK YOU SO MUCH!!!!!! :)
     
  9. ppodhajski

    ppodhajski

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    It means you do not break down dopamine, norepinepheine, and epinephrine that quickly and that expresses as anxiety/OCD symptoms.

    It is more complicated and simpler than that. Stay tuned.
     
  10. Valentijn

    Valentijn Senior Member

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    Is there some research supporting your claims, or is this merely your opinion? rs2283729 GG is the extremely common version, and I can't find any research implicating it in causing any problems.

    I also don't see anything saying that rs1799836 CT is a big issue. A 12% increase in risk of getting Parkinson's is only bringing that risk up from 0.3% to 0.336%. Not exactly earth-shattering, and I'm not sure how that is expected to implicate non-Parkinson's psychiatric symptoms. Or do you have another source?
     
  11. ppodhajski

    ppodhajski

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    If I say this to you again will you listen to me? I am not speaking about one gene when I mention how they effect people and how they cause disease.

    When looking at Lume's genes I am looking at the MAOA, MAOB and COMT together, as well as getting a hint from the CBS SNP. There are other SNPs I would like to see, like GAD1 and all the GABARA SNPs.

    And I am not taking about Parkinsons in this thread. People with Parkinsons's USUALLY have high activity MAOB genes, not low activity like Lume's. This is why they give MAOB Inhibitors to people with parkinsons. Lume has built in MAOB inhibitors.
    http://scholar.google.com/scholar?q...a=X&ei=Rxc5VbbyO8XmoATbrIDYCw&ved=0CB8QgQMwAA

    Single gene SNPs always have low risk. I am not doubting that. But put several together, along with environmental stressors, and that is where you increase risk. If you keep just looking at single genes and not step back to see there interactions you will not see how disease is created.

    If you want to be helpful help me write a program that pulls all these SNPs out of promethease so I can show you the pattern with out having to do all of them by hand.
     
  12. Valentijn

    Valentijn Senior Member

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    So the two SNPs Lume listed were completely irrelevant to your interpretation, despite that she was asking what they mean?
     
  13. ppodhajski

    ppodhajski

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    There were 100% relevant to my interpretation. Why do you think I was talking about them?

    I am saying her MAOA and MAOB and COMT SNPs are IN PART causing her anxiety issues. Why would you think that the lower rate of catecholamine degradation would NOT cause symptoms of anxiety?

    And everything I am saying is based on research. Just know that in the future and stop asking me. Google it and if you see I am wrong by the research point it out to me and we will discuss the research.

    If you think I am wrong explain chemically how you think I am wrong. Just point at a SNP and saying it is "low risk" does not prove what I am saying is wrong. Yes, I have a theory, but just saying my theory is wrong does nothing to help anyone. PROVE to me I am wrong.
     
    Last edited by a moderator: Apr 24, 2015
  14. Cheshire

    Cheshire Senior Member

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    Do you seriously believe that claim is enough for us to trust everything that you say?
    In case you're not aware of it, the vast majority of people here back up their posts with papers or videos, and when they don't, they are usually asked to do so!
     
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  15. ppodhajski

    ppodhajski

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    Ugh, I see how that could have been misinterpreted. I did not mean that I will not back up things with papers, it is just that the papers are out there and instead of just asking me to prove it do some work on your own. I do not just pull this stuff out of the air, I am reading the research.
     
  16. Cheshire

    Cheshire Senior Member

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    I'm not infering what you're saying is unscientific, I'm just saying your credibilty depends on your giving the links or tittle of these studies. The "do some work" response is not enough.
     
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  17. Valentijn

    Valentijn Senior Member

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    So which research is supporting your claims? I looked and I can't find it.
     
  18. ppodhajski

    ppodhajski

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    I am sorry, but most of this is common knowledge for those of us studying nutrigenomics. But I do provide studies (see above).

    But this same standard should be held to Val when she says thins like:
    "I also don't see anything saying that rs1799836 CT is a big issue. A 12% increase in risk of getting Parkinson's is only bringing that risk up from 0.3% to 0.336%. Not exactly earth-shattering, and I'm not sure how that is expected to implicate non-Parkinson's psychiatric symptoms. Or do you have another source?"

    Because when you look at the studies she refers to you will see they are in line to my way of thinking, that looking at only one dopamine pathway gene is silly and her microscopic view of genes and disease is hampering her ability to see what is going on. And also that MAOB rs1799836 ARE very important in regards to parkinson's. The reason why I do not post these studies is that it takes two seconds for anyone to google them.

    http://www.ncbi.nlm.nih.gov/pubmed/25805645?dopt=Abstract
    Patients were screened for variants of genes involved in dopamine metabolism: rs28363170 and rs3836790 polymorphisms in the SLC6A3 gene, rs921451 and rs3837091 in the DDC gene (encoding the aromatic L-amino acid decarboxylase involved in the synthesis of dopamine from l-DOPA), rs1799836 in the MAOB gene (coding for monoamine oxidase B) and rs4680 in the COMT gene (coding for catechol-O-methyltransferase).

    http://onlinelibrary.wiley.com/doi/10.1111/j.1469-1809.2007.00418.x/full
    We found similar interaction results between rs1721082 and rs1799836. In conclusion, variants in FGF20 and MAOB show evidence of statistical interactions, which emphasizes the importance of considering them jointly in genetic analysis of PD and illustrates potential patterns of biological interaction contributing to PD risk.

    http://europepmc.org/abstract/med/25636089
    The genotypic frequencies of COMT rs4680 AA, AG, GG were 8.9%, 42.0% and 49.1%. Those of rs4818 CC, CG, GG were 42.5%, 45.6% and 11.9%, respectively. The genotype frequencies of MAO-B rs1799836 A/AA, AG, G/GG were 74.4%, 14.1% and 11.5%, respectively. The haplotype formed by COMT rs4680 (GG) and MAO-B rs1799836 (A/AA) genotype has a frequency of 36.86%. CONCLUSION Polymorphisms of COMT and MAO-B genes has a unique characteristics among Chinese patients with Parkinson's disease. They may be related with differences in drug response in such patients.

    http://www.sciencedirect.com/science/article/pii/S0022510X14004626
    The relationships in the polymorphisms of rs1137070 C>T and rs1799836 A>G in the MAO gene with PD susceptibility observed in our meta-analyses support the view that the MAO gene may play an important role in the development of PD.

    I keep telling all of you that I know that single SNPs ALONE do not have an effect on disease but Val specifically keeps pointing at single genes.
     
  19. Valentijn

    Valentijn Senior Member

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    Well, I'm going with the science, rather than some personal theories that very common SNPs which have little impact are conspiring to make 100% of the population very ill. Because that is basically where your theories seem to lead, mathematically speaking.

    This one actually contradicts your claims. They studied it, and other SNPs, but only ones on a completely different gene were found to be relevant.
    Yup, that's the one I mentioned above which is associated with a tiny increase in risk of Parkinson's. No mention of OCD or anxiety.
    The abstract is merely stating the frequency of genotypes. With no comparison to non-Parkinson's controls, it lacks any context and is quite meaningless. There also isn't any full text article available for that. No conclusions can be drawn regarding the affect of alleles.
    This one says that the SNP isn't associated with disease risk for Caucasians, so would seem to be somewhat contradictory to your claims again. And even the Asian haplogroup model is only relevant if you know the status of the other necessary SNPs.

    And you still have not provided any source for your claims regarding rs2283729.
    If they cause disease as a group, that can also be determined via scientific research, such as by looking for haplogroups. Claiming that multiple common variations which have little or no impact are causing disease, with no research backing that claim, is just random nonsense. There are tens of thousands of such SNPs, and everyone has a boatload of them.
     
    Last edited by a moderator: Apr 24, 2015
  20. ppodhajski

    ppodhajski

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    So Val, are you saying that there is absolutely no relationship between Parkinson's and Monoamine Oxidase SNPs?


    Here is the full abstact:
    http://europepmc.org/abstract/med/25636089
    "OBJECTIVE To study polymorphisms of catechol-O-methyltransferase (COMT) and monoamine oxidase B (MAO-B) genes among Chinese patients with Parkinson's disease. METHODS Genotypes of the COMT and MAO-B genes of 1408 patients with Parkinson's disease was sequenced using Sanger method. And these patients were recruited by Chinese Parkinson Study Group from 29 research centers throughout the country. RESULTS The genotypic frequencies of COMT rs4680 AA, AG, GG were 8.9%, 42.0% and 49.1%. Those of rs4818 CC, CG, GG were 42.5%, 45.6% and 11.9%, respectively. The genotype frequencies of MAO-B rs1799836 A/AA, AG, G/GG were 74.4%, 14.1% and 11.5%, respectively. The haplotype formed by COMT rs4680 (GG) and MAO-B rs1799836 (A/AA) genotype has a frequency of 36.86%. CONCLUSION Polymorphisms of COMT and MAO-B genes has a unique characteristics among Chinese patients with Parkinson's disease. They may be related with differences in drug response in such patients."


    If any other of you carefully look at the SNPs they are talking about you will find that all these high frequency SNPs in people with Parkinsons are the result of faster catecholamine depletion.


    As to anxiety and MAO and COMT SNPS:

    (Val, don't worry, I already know you will have a non paper backed up rebuttal on how these genes don't matter.)

    http://hmg.oxfordjournals.org/content/8/4/621.short
    One class of drugs effective in the treatment of panic disorder is represented by monoamine oxidase A inhibitors. Therefore, the monoamine oxidase A gene on chromosome X is a prime candidate gene. In the present study we investigated a novel repeat polymorphism in the promoter of the monoamine oxidase A gene for association with panic disorder in two independent samples (German sample, n = 80; Italian sample, n = 129). Two alleles (3 and 4 repeats) were most common and constituted >97% of the observed alleles. Functional characterization in a luciferase assay demonstrated that the longer alleles (3a, 4 and 5) were more active than allele 3. Among females of both the German and the Italian samples of panic disorder patients (combined, n = 209) the longer alleles (3a, 4 and 5) were significantly more frequent than among females of the corresponding control samples (combined, n = 190, χ2 = 10.27, df = 1, P = 0.001). Together with the observation that inhibition of monoamine oxidase A is clinically effective in the treatment of panic disorder these findings suggest that increased monoamine oxidase A activity is a risk factor for panic disorder in female patients.

    http://www.jbc.org/content/279/38/39645.short
    A spontaneous monoamine oxidase A (MAO A) mutation (A863T) in exon 8 introduced a premature stop codon, which produced MAO A/B double knock-out (KO) mice in a MAO B KO mouse colony. This mutation caused a nonsense-mediated mRNA decay and resulted in the absence of MAO A transcript, protein, and catalytic activity and abrogates a DraI restriction site. The MAO A/B KO mice showed reduced body weight compared with wild type mice. Brain levels of serotonin, norepinephrine, dopamine, and phenylethylamine increased, and serotonin metabolite 5-hydroxyindoleacetic acid levels decreased, to a much greater degree than in either MAO A or B single KO mice. Observed chase/escape and anxiety-like behavior in the MAO A/B KO mice, different from MAO A or B single KO mice, suggest that varying monoamine levels result in both a unique biochemical and behavioral phenotype. These mice will be useful models for studying the molecular basis of disorders associated with abnormal monoamine neurotransmitters.

    http://www.nature.com/tp/journal/v5/n1/abs/tp2014135a.html
    Elevated hippocampal and cortical tyrosine hydroxylase, downregulated cortical monoamine oxidase-A levels, as well as increased hippocampal brain-derived neurotrophic factor (BDNF) and pro-BDNF support the flavanol’s anxiolytic effects. In addition, elevated pAkt in hippocampus and cortex was observed. (−)Epicatechin ingestion did not facilitate touchscreen performance or DG neurogenesis, suggesting a non-neurogenic mechanism. The concurrent modulation of complementary neurotrophic and monoaminergic signaling pathways may contribute to beneficial mood-modulating effects of this flavanol.

    http://link.springer.com/article/10.1007/s10517-015-2826-8#page-1
    The development of behavioral disorders presented by low exploratory activity and high anxiety was associated with transformation of catalytic characteristics of cerebral monoamine oxidases, associated with the development of oxidative stress with predominant intensification of metal-catalyzed protein oxidation.

    http://www.sciencedirect.com/science/article/pii/S0191886915001749
    We examined associations of COMT rs4680 and personality in older adults.
    The COMT rs4680 GG genotype associated with lower Neuroticism scores.
    GG genotype also associated with higher Agreeableness and Conscientiousness score
    GG’s dopamine release might be optimal for a more adaptive personality profile.


    Here is a whole book on the subject:
    http://books.google.com/books?hl=en&lr=&id=pabKBwAAQBAJ&oi=fnd&pg=PA47&dq=COMT anxiety&ots=MjkADgccVz&sig=XCaPXH0FjzSn3AY8eWDVS32cIIY#v=onepage&q=COMT anxiety&f=false
     
    Last edited by a moderator: Apr 24, 2015

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