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VDR alleles

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

  1. dbkita

    dbkita Senior Member

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    So I recently got my 23andMe results and used Genetic Genie to convert them to the Yasko panel.
    I will post my results in another thread at some point.

    My question though is as follows.

    For the VDR Taq SNP rs731236 I have the AA homozygote combination. According the Genetic Genie this is ++ in the Yasko notation.

    But when I look here:
    http://browser.1000genomes.org/Homo...7-48239257;v=rs731236;vdb=variation;vf=586368

    The reference is the A allele and the AA combination is greater than 50%!

    But according to Yasko this is the risk allele?

    I am confused. My questions is which allele leads to reduce dopamine production? The A or the G?

    Anyone have any thoughts?
  2. Sea

    Sea Senior Member

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    Hey I replied and then it disappeared, wonder how that happened. Anyway according to this link the risk allele is G

    http://www.snpedia.com/index.php/Yasko_Methylation

    I am AG so I can't help with which one is the mutated allele.

    The ++ is the one with lower dopamine, but on the positive side methyl groups should be tolerated
  3. dbkita

    dbkita Senior Member

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    Thanks. My confusion is Dr Yasko apparently thinks the AA combination is ++ with lower dopamine production. Is this simply an error on her part?
  4. Sea

    Sea Senior Member

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    Where are you seeing that Yasko thinks that AA is the risk allele?
  5. dbkita

    dbkita Senior Member

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    Ok to clarify, Genetic Genie shows my AA combination for VDR Taq as registering ++ in the Yasko Methylation panel.
    I interpreted that to mean A is considered the risk allele by Yasko.

    Here is a link that only adds to the confusion:
    http://geneticgenie.org/blog/2013/02/28/clearing-up-the-vdr-taq-confusion/

    Note how the VDR Taq is called a C (reverse complement of G) in the Yasko report and is shown as -/-.
    In the Genetic Genie conversion using the 23andme data, the base call is GG and is shown as -/-.
    Everyone else on the Internet has G as the risk allele. Honestly I just want to try to find out which one has the lower dopamine activity and the lower vitamin D activation.

    According to the link, and the author of Genetic Genie seems to be very clear they are correctly doing things in that blog, then AA = +/+ and GG = -/-, even though the frequency distribution is reversed (i.e. AA is the wild type in the population).

    Hence my confusion.

    Edit: gets even more confusing now ..

    Check out this thread:

    http://forums.phoenixrising.me/inde...tion-genetic-results.18309/page-4#post-325280

    from post #72 on.

    So Genetic Genie now considers A the risk allele to line up with Yasko's clinical observations. So now I am triply confused.
  6. Sea

    Sea Senior Member

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    It is very confusing and I can't really tell which one does what! Time for more digging. Just to add to the confusion I'm sure I read somewhere something Yasko wrote in March this year about changing how she reports Taq (different from kday's quote from January this year) I'll keep looking for that.

    I can say though that kday's explanation in the thread you linked with the A=T does not in this case apply. When Yasko calls the Taq mutation TT that is in comparison with tt, same as she uses FF and ff when reporting on Fok and BB or bb for Bsm. The T doesn't necessarily correspond to an A because she is not using T as an allele.
  7. Freddd

    Freddd Senior Member

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    Hi Dbkita,

    So Genetic Genie now considers A the risk allele to line up with Yasko's clinical observations. So now I am triply confused

    That confusion is usually where an armoured car of money or information disappears. For me, at least in the business i was in, and in solving the health problems at hand, things like this can be the money shots.
  8. dbkita

    dbkita Senior Member

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    Agreed but this link seems to confirm it:
    http://forums.phoenixrising.me/inde...ndme-yasko-methylation-genetic-results.18309/

    Note Gestalt's Yasko test results for VDR Taq: TT and the call is T (or reverse complement A).
  9. dbkita

    dbkita Senior Member

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    Agreed. I guess in reality the risk allele is the G since that can lead to excess dopamine production and possible mood swings for the general population.

    But for Dr Yasko putting autistic kids and others on methylation treatments she segregates them in to two sub populations based on their VDR Taq (and COMT) status to determine who would be more susceptible to methyl donors and who in fact has more room to maneuver. So the risk allele gets switched to A even though >50% of the population (i.e. the wild type) is AA. Sigh from bioinformatics perspective that is just plain weird.
  10. Freddd

    Freddd Senior Member

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    "Just plain weird" says it well. So now, the question I would want to address concerning the dopamine is could that account to the hyper response to ATP in the limbic mitochondria as that appears to affect dopamine in some way causing wild uncontroallable emotional changes of a specific nature. Might that be connected then in some way? Or are we speaking a different set of moods?
  11. dbkita

    dbkita Senior Member

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    Possibly. Mood swings are associated with dysregulation of dopamine or serotonin or norepiphrine. Of course dopamine and NE are connected, one being a precursor catecholamine of the other. Dopamine and NE are associated with excited and anxiety states when too high. Inflammation also factors in. For example low inflammation and high norepinephrine = mania.

    For some people high dopamine inevitably leads to NE. But for others not so much as it depends on catecholamine metabolism. However, most people do not realize that NE can be made directly in the autonomic nervous system by specialized neuronal complexes that take in tyrosine and other building blocks and pump out NE in two steps but internal to the complex (the same is true for certain neuronal complexes in the brain / CNS that make GABA directly from glutamine in two internal steps). I only mention this since high NE does not necessarily suggest high dopamine as a precursor but instead due to a strong crisis response.

    So my bet would be on dopamine and / or NE. But in what proportion I cannot say. I am excluding serotonin only since its effects on mental state are typically different even when in excess. Glutamate is another possibility but if the action is in the limbic system my money would be on catecholamines.
  12. Freddd

    Freddd Senior Member

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    Hi Dbkita,


    I only mention this since high NE does not necessarily suggest high dopamine as a precursor but instead due to a strong crisis response

    People going through this response tend to get tied up into extreme psychological anxiety etc at the thought of almost anything (literally) which then causes more excitation and more anxiety in a vicious cycle. So it becomes a constant crisis response as anxiety about anxiety,anxiety about excitatory feelings and the ensuing anxiety starts. There is an interesting things that happens in some tantric sexual states. Some people get into anxiety and panic at the threshold of swirtching into a constant "orgasmic" state from a more normal excited state, the fear being voiced first a fear of death and then "help, what can I do, this could go on all night". I bet that is also in the limbic with it's FFF connection.
  13. dbkita

    dbkita Senior Member

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    So at this point I am going to have to conclude that there are oodles of people out there (many on these forums) who get their VDR Taq SNP tested and don't really know what it means. At this point I will have to rely on my theory that the risk allele is G for possible mania and mood swings, and somehow that got flipped by Dr Yasko to be the "good" allele, as maybe those autistic children hetero or homozygous in the G allele needed less methylation support. Meh whatever.

    The 52% of the population with AA is by definition the wild type. Maybe we make less dopamine than those with the G alleles, but it is what is. But as a someone who works in bioinformatics, for a medical professional to describe that as a dysfunctional VDR, is something I disagree with. I suspect methylation status and BH4 levels and presence of necessary cofactors or conversely CNS inflammation are bigger factors for dopamine levels. Yes there are seasonal correlations but then it is more a question of getting your vitamin D levels (active and inactive forms) right for you.

    Edit: Read the post below for the solution of the annotations though not the clinical interpretation.
    Sea likes this.
  14. dbkita

    dbkita Senior Member

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    Ok I would like to correct what I said earlier. I think I have been able to clarify some things. At least I know now what my SNP results mean for VDR Taq … why Dr Yasko considers her old ++ or new TT to be “defective” in terms of VDR expression and dopamine produciton is still beyond me. But working in bioinformatics I can at least live with my understanding my own results.

    The confusion seems to be regarding notation for VDR haplotypes, specifically BSM, Apa, and Taq.

    Here is an excellent paper with everything wanted (and did not want to know) about VDR polymorphisms:
    http://web.udl.es/usuaris/e4650869/Morella06/BB/Review_VDR_Polymorphism.pdf

    Pay particular attention to page 146 … that is the Rosetta stone.

    Note haplotype 1 which is denoted as C-C-A on the gene diagrams (remember that C-C-A would not be the same as C-C-T since though usually A is equivalent to T on a reverse complement basis, we are talking about haplotype here, or combinations of polymorphisms). It is denoted as baT (even though C-C-A) is the most common haplotype across virtually all ethnicities and each individual bp read is for the reference allele (i.e. C/G for Bsm, C/G for Apa, and A/T for Taq). Haplotype 2 (also common) is A-A-T which is denoted as BAt.

    You see the confusion right? How would a scientist denote different haplotypes 1 and 2 even though the individual polymorphism for Taq is A on strand and T on the other, but its combination with Bsm and Apa on one strand is different! Usually a polymorphism that disrupts a restriction site is capitalized while a lower case one is wild type. But for the above haplotypes following a standard convention would not work since A and T are the same read on opposite strands.

    So what is the nomenclature?

    Check out table 1 of this article:
    http://www.cof.org.cn/pdf/2007/10/Vitamin D receptor haplotypes protect .pdf

    “TT” is wild type, “tT” is hetero and “tt” is the GG (=CC) mutant.

    Now Dr Yasko claims the VDR Bsm/Taq combination (which she assumes are always inverse in terms of notation bT or Bt because of haplotype frequency) has big effect on dopamine levels and methyl donor capacity. Ok fine. But according to her notation the ++ (or now TT, which is really the AA read from 23andme and the wild type as we established above) is the one with low dopamine levels … even though that is the wild type. So why the wild type is considered “defective” in terms of VDR expression is confusing.

    In fact my haplotype is baT (the most common one) and I have it on BOTH alleles (you always have two haplotypes though you may be heterozygote on the Taq or either of the other two SNPs).

    My baT/ baT haplotype has higher risk of osteoporosis and lower BMD. Uggh. Lower risk of cognitive decline with age. Yay! Much worse response to dengue fever (ok no trips to the tropics). Blah blah blah. The one thing that seems to be recurrent theme across papers is in vitro (for what it is worth) and some in vivo correlations, is the baT creates the more stable mRNA (though not all experiments agree) which should create healthy, active VDRs (though other SNPs may affect that which are not measured). Correlation is the best our civilization can do on these matters right now. So why the most common baT haplotype considered by Dr Yasko camp to be low dopamine and making for “defective” VDR? I don’t know.

    Thankfully I have 23andme results, can browse the raw data and see my results for all three SNPs not just the Taq shown on the Yasko panel. So now I know my haplotype and can go with that to research the significance (if any) in the literature. What this means for dopamine levels (mine are typically low) or methylation donor tolerance (which is also kind of low compared to many other on these forums) is anyone’s guess.

    My guess is the Yasko panel moved to the new notation because the +/+ or -/- was deemed eventually controversial by her scientific peers. So no they use “TT” and “tt” as per he industry. Why they feel the VDR Taq alone confers information on dopamine production and the effectiveness of the VDR is not clear. Perhaps they neglect the Apa SNP and assume the high “inverse” correlation seen between Bsm and Taq. Dunno. That is up to the world of clinical observations I suppose, but from what I have read there seems to be significantly more complexity from the many studies involving cancer, disease resistance, osteoporosis and everything else.

    Anyways when I see posts on the Internet where they say they are “TT” for VDR Taq and have a “defect” … I want to cringe now. That is so wrong ((.

    Welcome to the wonderful world of haplotypes.
    UM MAN likes this.
  15. Xara

    Xara Senior Member

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    Forgive me my boldness, but: why? I could be mistaken but I thought you said genes were not that important? Were you just curious, or are you now planning to make changes in your intake based on the outcome? BTW because I suppose you have informed yourself thoroughly about 23andme, as you always seem to do things thoroughly, do you think privacy is guaranteed and safe at 23andme?
  16. dbkita

    dbkita Senior Member

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    I don't think I said that genes are not important. I was simply trying to caution people that they are not the only thing and basing treatment solely on them was inadvisable given the role of epigenetics, other clinical factors, our incomplete knowledge of SNPs, and the nonlinear control problems posed by neurotransmitters and hormones.

    Personally I wanted to answer the question if I had a CBS mutation. The answer is yes. 23andme and $99 seemed to be a good way to answer this. Yet despite a CBS homozygote I have a homocysteine >10 even while on methylation support. So something else is blocking the cycle.

    The MTRR cluster swarm of heterozygotes was a surprise as were the multiple BHMT homozygotes. The MAO + is not uncommon for men, just makes serotonin regulation a bit complicated. As I described ad nauseum the VDR Taq for me is wild type and in fact part of the dominant haplotype. The SHMT1 is more complicated since it is for the cytosol isozyme (thank God my mitochondrial one SHMT2 appears clean in 23andme). Still trying to get my head around its impact, though one obvious thing is it explains a glycine to serine imbalance that has been persistent over the years.

    So why? Information is always power. I would rather know than not know. Already this has helped answer a couple of questions I have had brewing for some time.

    And yes as far as I am concerned the 23andme privacy policy is ok. Is it absolutely guaranteed and safe? Impossible to know for certain. I don't worry too much about that anyways in my personal life.

    Take care Xara.
  17. Freddd

    Freddd Senior Member

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    HI Dbkita,


    There is a question bugging me and many of us here, whether recognized or not. As best we can know on limited studies, but also quite demonstrably pragmatically, that CFS/FMS along with Parkinson's, MS, Supranuclear palsy, Autism, Alzheimer's and some others all have low CSF cobalamin and some also checked and found MMA and/or Hcy in the CSF. The diabetic neuropathy study of intrathecal injection of 2.5mg of MeCbl showed that effectiveness and strongly elevated levels of cobalamin ended at the same time and in the study ranged from less than 3 months to 4 years and still counting.

    It also appears that there is a difficulty in getting sufficient MeCbl/AdoCbl to heal into the CSF of many people. There clearly are huge differences in loss rate.

    So what genes could be involved? It's something a lot of us would share. From what you have seen so far would you say that CSF/FMS/ME/etc appears to concentrate folate polymorphisms to what degrees?
    L'engle likes this.
  18. dbkita

    dbkita Senior Member

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    Hi Freddd,

    Warning long post incoming :)

    My thoughts: (wish they could be more upbeat and happier)

    Alzheimer's is unbelievably complicated and almost all of the old theories have been washed out (tau phosphorylation, beta secretase, etc.). No one knows. But ... too much of the population gets ALZ at some point (if they live long enough) for it to be one or two genes involved. I think the prevailing view is multiple points of failure + epigenetic stresses. Again it is highly controversial. So I would not go there attempting to explain by any theory. Quite frankly it will fail given the complexity. It is so bad that the current mindset is to focus on diagnosis and not treatment right now. I know these are things people don't want to here but it is what is going on right now. Our civilization is still behind the eight ball on that disorder. So while correlative risks may be teased out on early diagnostics, mechanism is highly uncertain. The fact that ALZ has low CSF b12 or issues with MMA or HCY, I fear doesn't really mean much. The CNS for an advanced ALZ patient is completely borked. Many measurements will be jacked. Do you know how much working brain matter a person with full blown ALZ has when the diagnosis was made in say the 1980s-1990s? 20-25%. Meaning if you cut open their skull and peaked inside, only 20-25% of cells were functional. Low biomarkers for the variables you mentioned I don't think mean much when 75% of brain matter has been turned into a wasteland.

    MS is a different story. The latest epidemiology studies and latest research really seems to point to a CNS autoimmune attack instigated by infection by a normally benign virus that prefers cold weather climates yet in some cases crosses the blood brain barrier. The result of being in the "wrong place" leads to microglia activation generating antibodies that attack white matter as per an autoimmune attack. You mention these other biomarkers, but inflammation is very central to MS. We just still do not know the antibody unfortunately. Some experts still disagree on this, but this virus to BBB crossing to CNS autoimmune link is becoming more and more crystallized. It is being forced onto the medical community based on careful diagnosis, patient history, and epidemiology analysis. There are a couple of genes that are considered risks for MS but I don't believe they have commonality to any of the other diseases you mentioned.

    Parkinson's is more murky. There are a couple of competing theories, though at least one of the classical ones is fading. Again an inflammatory condition that wrecks havoc in the substantia nigra part of the brain. This theory has come on strong of late since large scale studies of anti-inflammatories have showed a 15% or more (more for longer use) reduction in incidence of Parkinson's ... which is huge. Sorry I don't know more than that.

    Autism of course a broad spectrum disorder and while methylation seems to be an interesting means to help improve symptoms, the underlying cause and mechanism suggest defects in MANY genes + epigenetic factors during development in the womb. As an example of a totally different sort (and not autism, so people do not get all upset), Down's syndrome involves a massive deletion of a chromosome. My point is genetic defects do not have to be only point mutations. If only that were true it would make the world of bioinformatics a much simpler place.

    So to be perfectly honest on your question. I have no idea. I would bet my mortgage that it is not one or even a small number of genes. I would also further bet that most of the disorders you mentioned the genotype correlation is very low. I don't think we are looking for haplotypes with low linkage disequilbrium. Certainly not for ALZ. Not a chance. I think some of the disorders involve gene regulatory 'concert' defects while others involve breakdowns due to epigenetic factors (like a viral infection that gets into the CNS).

    My suspicion (and I know this may not be popular but what the hey) is there are multiple neurological disorders with many different causes that can end up producing low biomarkers related to methylation and folate cycles in the CSF. A similar analogy is there are many disorders that ultimately lead to hormonal dysregulation and adrenal fatigue. But the causes can be very different for each disorder that brought us to a similar place. Then again defects in genes that regulate the methylation and folate cycles won't help matters if "stress" is being put on those systems by virtue of epigenetic triggers that launch neurological disorders.

    I can't remember where it is now, but someone did a meta-analysis of fibromyalgia and determined a significant number of those diagnosed had hormonal problems. So which is the chicken and which is the egg? Some patients have high RT3 values, take Cytomel and they are in remission. Others that treatment does zilch. The reason I bring this up is I sadly feel CFS and Fibro are classifications that help doctors but with many diverse causes that lead to similar metastable (but bad) health states with certain similar symptoms. I think methylation and folate and ATP treatments have value because they try to get the body to heal itself and develop some sort of homeostasis. But I don't think that means their genes in those cycles doom them to CFS/ME.

    Heck personally I see a lot of people on here with bad health states but with honestly not that bad of genotypes (at least for SNPs we know of). Also though I am on these boards ... I don't have CFS. Rich and I arrived at that conclusion a couple years ago looking at a NutraEval from Genova and multiple other labs. Later I learned I have an autoimmune disease of the CNS (and periphery) and not a benign one. So why am I here? Because supplementing for the folate and methylation cycles helps me with some (I note SOME) of my symptoms. On the other hand if you took my glucocorticoids away from me, you might as well put a gun to my head. My point, as unsatisfying as it may be, is there may be MANY causes or triggers, but so many of us end up in similar places and treating some of the most fundamental biochemical cycles is one of only ways after years and years of damage to get the body to do some constructive rebuilding from the inside.

    Sorry if that was not the answer you were looking for. But it is what I think. I wish I could give a simpler and more empowering insight. I am almost positive that a simple straightforward genotype association does not exist across the spectrum of disorders you mentioned. Of course they have relevance but the outcomes are very nonlinear.

    For example in three generations my paternal family line has one case of SPS (me), one case of MS (aunt), and two cases of ALS (grandfather and his first cousin). I mention that to a neurologist and their eyes nearly bulge out of their head, then they relax, start to think, smile and I start to worry they are sizing me up for vivisection to get DNA samples (just kidding). On the other hand the same paternal family line but through my paternal grandmother had two cases of terminal ovarian cancer. Guess what all the other aunts did when all that went down? So in one case the genetics is probably important but unbelievably cloudy and complicated since we had three vastly different diseases for four people, in the other case the genetics is more straightforward since my grandmother and her daughter both had the same condition (though they responded to treatment very differently, one was known ahead of time and fought for a long time, the other was a shock and died almost instantly).

    What I do think is that low biomarkers for methylation and folate cycles, means those cycles are in jeopardy in the CNS and the best we can do is try to fortify them. And hey for many of us that is very helpful. You and I each in our ways have beat (or I should say are defying) odds that were stacked against us. Doesn't mean a cure but can mean a really significant improvement that holds back the red tide.

    Take care.
  19. adreno

    adreno 3% neanderthal

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    I agree with dbkita. Neurodegenerative disorders are incredibly complex and cannot be reduced to nutritional deficiencies (B12, folate or whatever). In disease you will find many biological readings that are off, but that doesn't mean we can conclude they are causes. Alternative doctors often jump on this; if vitamin D is found to be low, then that must be a cause of the disease and so on.
  20. SonjaS.

    SonjaS.

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    Dbkita,
    thank you for airing these suspicions and discussing the validity og SNP interpretation by Yasko. Very interesting.

    I've been around for half a century. I have no background from informatics or genetics (linguistics and anthropology) as the informatics came too late for me, but I'm a systems thinker by nature. I've suffered series of collapses throughout life and recently rehabilitated myself from dysautonomia. I came into this forum backwards; only after finding help through supplements that worked, did I start to question the genetic underpinnings of DNA methylation.

    Mine is a long and complex story. I am self diagnosed and self treated for the past 16 years. I came to this forum through recently discovering Richard van Konynenburg's methylation hypothesis on Dr. Sarah Myhill's website. I only learned of Amy Yasko through this forum, and of Genetic Genie through a rare haplotype group I share with 18 people that may or may not cause lowered tetrahydrobiopterin. It's been a very steep learning curve!

    While I in general consider Amy Yasko a credible pioneer, trying to help primarily children with autism and their parents, I wonder if she has taken too much upon herself, and therefore simplified the whole approach, contrary to her proclaimed intentions of individualised interpretation. She does state that the genetic profile is just one of the many factors in multifactorial disease. However, her methylation and detox profile seem to contradict that, as one predictive value seems to be given to all SNPs. I don't know if that's her fault, or if the people using her data misinterpret.

    I read your posts here on the topic of VDR Taq with great interest, as I share your confusion and suspicion (without intending to diminish her work). Based on what little I have grasped about polymorphism variation, I find it simplicistic to assign a +/- value to variation that may be differently distributed in different populations, gender, age or in correlation with other SNPs. Both the COMT 158 Val/ Met and the VDR Taq seem to be population specific, according to scientific studies. However, even the scientific studies on genetic polymorphisms are not a measure of anything. The work on the COMT 158 Val/Met polymorphism reads like a horoscope (you're either 'a warrior' or 'a worrier'), but that SNP itself is significant. I prefer to focus on the biochemistry of its function, rather than on the personality traits.

    I cringe when I read "being positive for a mutation". Genotyping is not like testing positive for a viral or a bacterial infection, but in most peoples' minds it may sound like that! Although the genetic variation technically is a mutation - a mutation that many people carry - it is not a mutation in the sense of the gene defect. From the established genetics point of view, ie current knowledge about the inborn errors of metabolism, only the proven defects are caused by gene mutation. What a single polynucleotide variation does in any individual, is to be discovered, not simply charted.

    The SNP variation does not cause anything directly, but indirectly, by affecting a synthesis of an important vitamin or coenzyme, or by inability to metabolise common drugs and environmental toxins. Here I'm in agreement with Yasko.

    The only thing I can think of, in her defence, is that autism may be a differently organised system altogether. I am on the opposite side of that spectrum (gifted and not a trace of developmental problems). I too am a fast oxidiser and despite having genotypes that enable me to deal with stress more successfully than most people, my HPA axis broke down. I've experienced first hand dysautonomia (a total neuro-endocrine-immune derangement) so I know how a deranged metabolism is not like a normal metabolism. That's why I wonder if maybe Yasko's interpretation of methylation in autists is based on her clinical experience that won't be matched by the usual genetic studies.

    Just thinking out loud. If you'd care to comment, I'd appreciate it very much.

    If you do reply, could you also point me to the posts you wrote about immune dysfunction, as I find that the most difficult area of all I had to deal with. Thanks in advance.

    Sonja

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