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A Little Poisoning Along the Road to ME/CFS
Looking at my symptoms, many of which are far less these days and some are gone, it would be easy to figure that I'd just been dealing with some heavy-duty menopausal issues.
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VDR alleles

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

  1. Sushi

    Sushi Moderator and Senior Member Albuquerque

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    dbkita

    Thanks for doing all this research on VDR SNPs. There has been a long-standing confusion between the results from Yasko and other labs. I'm afraid I don't know enough science to understand all that you have written, though I think I get the gist of it.

    I had my VDR SNPs tested at another lab. I'd be grateful if you could tell me how you would read them.

    Here is what it says:

    FOK1 polymorphism (ff)

    BSM1 polymorphism (BB)

    Thanks,
    Sushi
     
  2. dbkita

    dbkita Senior Member

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    I would agree with you except in the case of VDR, Dr Yasko was labeling the baT haplotype as "defective". While in her practice autistic children with baT may be able to tolerate more methyl donors the idea that the baT haplotype in the general population is defective and means less dopamine is plain wrong. It is the dominant haplotype. Especially in certain ethnic groups.

    Sorry but I have made so many posts. Try the search feature with "dbkita" and "immunne". Adreno has been on a lot of those threads as well. Good luck!
     
  3. dbkita

    dbkita Senior Member

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    Yasko and other labs NOW use the same notation I believe of b,B : t, T but what still differs is the interpretation of which is wild type and which is mutant. She relies on the fact the 95% of the time if a person is b then they are T OR if B then they are t. She ignores the Apo SNP which is weird since the Bsm-Apo-Taq is the haplotype triad often studied. So if you are B then I am guesssing (?) you are little t. But without seeing what Apo is I can't say much about what haplotype you are. I think there are a couple of haplotypes that are pretty functional (baT and BAt (?)). Not sure about Fok sorry.
     
  4. SonjaS.

    SonjaS.

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    Thank you. I really appreciate your opinion! You are clearly concerned and objective.

    I've read the research paper you've provided (Genetics and biology of the vitamin D receptor polymorphisms) and it was a well explained topic and very interesting research. I believe you when you say Yasko is plain wrong. It makes me wonder what else she may be wrong about...This is a serious mistake, because vitamin D is not something to supplement casually. Even though it is classified as a vitamin, it functions as a hormone, and together with PTH (parathyroid hormone) regulates calcium levels.Vitamin D can accumulate and its excess isn't good for anyone.

    I'll keep on reading...
    Sonja
     
  5. dbkita

    dbkita Senior Member

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    I don't think Dr Yasko was suggesting large supplementation of vitamin D. I think she was saying that those with the bT haplotype have defective VDR and hence lower dopamine and hence can tolerate more methyl donors and that those with the Bt haplotype would be the reverse with higher catecholamines and cannot tolerate methyl donors (i.e. use hb12 instead of mb12.

    I challenge the assertion that the bT haploptype is defective. Also I challenge that it leads to lower dopamine levels. I cannot say one way or the other how it impacts autistic children for their ability to tolerate methyl donors, that is the realm of the clinician. What I question is the reason given by Dr Yasko and her camp and then the extrapolations that come from there.
     
  6. greenshots

    greenshots Senior Member

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    I didn't read this whole thing but I can tell you this.......the VDR Taq borrows methylB12 from the MTR/MTRR enzyme in order to make dopamine. If its broken (++) then it isn't borrowing from the MTR/MTRR and nows there more methyls in the system. Rich, Yasko, James, and Deth have looked at the MTR quite a bit so it seems to fit. If the VDR Taq is not broke, its sorta like the COMT -/- because it just does its job and cleans all the little buggers out. Only in this case, the little buggers effect dopamine and methyl donors and if your sick, you're probably not making enough to begin with. Like my doc has told me in the past, not all defects are bad. Some are probably adaptive but in concert with others may spell trouble. The same could be true for no defects in one area in concert with a line of methyl depleting defects. If this coincides with how many methyls you'll tolerate, its probably worth noting. I don't know how others look at the VDR Taq but in this case, its more for predicting overall methyl status and dopamine, which may lead to some super duper mood shifts and neuro changes such as Parkinson's like syndromes. My doc says she has fine tuned just these two areas and seen drastic changes in dopamine deficiency like syndromes so it may be accurate.

    I'm not sure this helps clarify the whole thing but its what I know to be true.
     
  7. dbkita

    dbkita Senior Member

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    I am sorry that information for vdr is not entirely correct. The yasko ++ (now TT in her latest) is the dominant baT haplotype. Dr yasko and her camp are the only ones who consider the wild type defective. In some ethnic groups the baT haplotype is very dominant. Perhaps there is some clinical correlation to methyl donor tolerance for autistic children. But again unless we are talking about snps we do not about and do not currently measure the baT haplotype is NOT defective. Dr Yasko now labels the wild type as TT since there was significant confusion over labeling the baT haplotype as ++. In fact the baT haplotype is postulated to lead to more stable mRNA.

    COMT is a different matter and certainly mutations in COMT will affect dopamine catabolism and SAMe. So I have no concerns about those assertions.

    If you read my previous posts and follow the links it should be pretty clear. The key is haplotype notation which is easy to make a mistake in. Normally the wild type for a snp is lowercase and the mutation in the restriction site is capitalized. Not true for vdr taq since it is part of the bsm apo taq haplotype. Dr Yasko has said as much in a recent post linked above when she explains the recent shift to TT. So while a person with a GG homozygous taq may tolerate less methyl donors it hardly means the AA (TT) is defective. In fact quite the opposite. Hope that helps.
     
  8. greenshots

    greenshots Senior Member

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    Dbkita, I didn't say the VDR taq TT is defective, I just explained the reason Yasko considers that to be a problem. You wondered about it so I thought I'd mention it. Along the way you'll find that what scientists believe and what clinicians see is entirely different. Since this is all unchartered territory, I'm pretty sure we'll see alotta disagreement between anyone in the field. You can feel an utter certainty by science one day, only to know it was all BS the following week. As an ICU nurse, I see this all the time. They change the ACLS (advanced life support) guidelines all the time because the drugs we believed with 100% certainty would save your life turned out to be more damaging in the long run. It looked good on paper but the clinicians saw the outcomes, not the scientists. You just do the best you have with what you've got. I used to chase down every study and never really got any farther because everyone contradicted each other. Its a wild goose chase.
     
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  9. SonjaS.

    SonjaS.

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    Greenshots, I wish you had read this whole thing :)

    It doesn't help explaining what Dr. Yasko claims if her claim can't be supported by solid evidence. I've been reading Cohn & Roth on Metabolic Disease and Biochemistry and Disease, and I've been studying scientific papers available on line. While the classical genetics doesn't address DNA methylation as a functional problem, it does recognise MTHFR, MTR, MTRR and CBS defects. That's unqestionable. As for COMT and MAO-A variants, their effects are mostly measurable under conditions of stress, and they vary within a given population. Vitamin receptor polymorphisms (VDRs) do different things in different populations. If you google VDR Taq and methylation, you'll find no scientific articles on the subject. In fact, I couldn't find articles relating catecholamines and VDR, which makes me wonder where does Yasko take her information from? There is not one article mentioning relationship between VDR and methylcobalamin.

    If you had read my post, you would have known that I personally have nothing against Dr. Yasko, only trying to find out what's true or not. As a scientist, she has to share the discoveries in order to get them verified. That's just how it works. I agree with you on the wild goose chase and non-conclusive and confusing research. Yet unlike genetics, which is an unexplored area, biochemistry is a hard science; verifiable. It's easy for a biochemist to determine value of a study. I am not a biochemist, but do know how to read scientific studies. Some things are proven beyond doubt, others are uncertain. If I were to advise someone based on flimsy evidence, I'd be very apprehensive as I would hate to cause harm.

    I did find one very recent study on VDR and dopamine, and I'll post the abstract here.

    best,
    sonja
     
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  10. SonjaS.

    SonjaS.

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    Neuroscience. 2013 Apr 16;236:77-87. doi: 10.1016/j.neuroscience.2013.01.035. Epub 2013 Jan 25.
    The vitamin D receptor in dopamine neurons; its presence in human substantia nigra and its ontogenesis in rat midbrain.

    Cui X, Pelekanos M, Liu PY, Burne TH, McGrath JJ, Eyles DW.
    Source

    Queensland Brain Institute, The University of Queensland, Qld 4072, Australia.
    Abstract

    There is growing evidence that vitamin D is a neuroactive steroid capable of regulating multiple pathways important for both brain development and mature brain function. In particular, there is evidence from rodent models that prenatal vitamin D deficiency alters the development of dopaminergic pathways and this disruption is associated with altered behavior and neurochemistry in the adult brain. Although the presence of the vitamin D receptor (VDR) has been noted in the human substantia nigra, there is a lack of direct evidence showing that VDR is present in dopaminergic cells. Here we confirm that the VDR is present in the nucleus of tyrosine hydroxylase (TH)-positive neurons in both the human and rat substantia nigra, and it emerges early in development in the rat, between embryonic day 12 (E12) and E15. Consistent evidence based on immunohistochemistry, real-time PCR and western blot confirmed a pattern of increasing VDR expression in the rat midbrain until weaning. The nuclear expression of VDR in TH-positive neurons during critical periods of brain development suggests that alterations in early life vitamin D status may influence the orderly development of dopaminergic neurons.
    Crown Copyright © 2013. Published by Elsevier Ltd. All rights reserved.
    PMID:
    23352937
    [PubMed - in process]
     
  11. dbkita

    dbkita Senior Member

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    I understand that you did not call the TT defective but Dr Yasko and heartfixer did suggesting it led low dopamine levels. The baT haplotype makes the more stable mRNA. There is a lot of corroborating evidence to this. The bsm-apo-taq haplotypes are a very hot area of interest. Of recent time Dr Yasko and others have backed off the "defective" label. My point is simple. Regardless of what is seen in the clinic for autistic children, a person who gets their dna tested and is told they have a deleterious homozygote mutation in vdr taq when in fact they have the dominant haplotype is just plain wrong. It is not a good thing to see something clinically and stretch for a gentic pattern that is then used to extrapolate to the general population. After 20 years in bioinformatics and biocomputation I see this rwpeatedly and it is not imo the right way to do things. Another classic exampme is the cbs c699t mutaion 10x snafu I discussed in my other thread "couple of questions".

    I do agree there is much we do not know and there is going to be lots of revisions to our understanding going forward but there is a reason the scientific method exists. We can only make conclusions on what we measure or can observe reproducibly. Maybe autistic children who are TT have more mood issues because they have other snps or epigentic factors so the suspect is less dopamine. But extrapolating that to the dominant world haplotype especially one that is really dominant in some large ethnic groups is not good science imo. Also the extrapolations of heterozygotes with high population frequencies really raises the hackles on my bioinformatics neck. Looking at individual snps is really misleading. Haplotypes are the standard of knowledge in this area.
     
  12. greenshots

    greenshots Senior Member

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    I agree with you SonjaS, I wish I hadn't chimed in on this one either. You are rehashing stuff I have long since learned about and walked away from so I didn't have my sources all lined up to withstand scrutiny. Two issues here, firstly, I mistook the role of VDR and methyl b 12 since it appears to be more of an indirect role with MTR. It looks like MTR/MTRR leads to what we all know about.....Methionine, SAM, and SAMe and its really about methyl donors and dopamine levels.

    Second, you have more faith in science then I do. I used to believe all that too but then I had a friend who worked in the industry "cleaning" up study findings and as an ICU nurse, I got to see all the patients they dumped out of our studies when they suddenly didn't "fit the criteria" when it was really about not falling in line with what the researchers wanted. Not to mention the fact that way too many peer reviewed nutritional studies are never printed because the medical bodies won't do it. Don't get me wrong, I'm the first person to jump on a study that supports something I already believe. I LOVE quoting "scientific data" that supports my position.

    But in reality, it takes alotta $$$ and precious, precious time to conduct a study and even more to include more then a few variables so the idea about it being a scientist's duty to get their results in print is sorta laughable. In fact, it was this very point that saved my life.....indirectly. My doc met Rich at a UC Davis MIND meeting because she called out Jill James on such a bogus statement. When she was finished, Rich said he wanted her to have a standing ovation but he settled for talking to her half the night about science and medicine. This was how my doc learned about Yasko. Anyway, I love your enthusiasm and idealism.....if only it translated to the medical and scientific field (when there aren't billion dollar drugs on the line). As for biochem being hard science, well, it is and it isn't. Take glutathione. Up until Rich's passing (God bless that man!) he and Yasko and Pall all agreed that this was a problem but which comes first and why? And everyone used to think you had to replace glutathione but no matter how much they did, people didn't stay better. The basic tenets may be somewhat predictable but all the rest isn't. And all the rest is where healing people comes into play. This is where the clinician plays such a big part because they see how patients respond even while the scientists are tellng them it should work. This is usually mocked as "soft science" or "empirical" data but it is what it is. I know the answer isn't to throw the scientist's observations out so I guess we need both. But maybe we need to respect the outcomes as much as the test results?

    The stuff below is an old esoteric snippet from some of Yasko's earliest comments. I'm sure some stuff has changed but I thought I should provide what she said and not my memory of it.



    MTR : methionine synthase MTRR : methionine synthase reductase

    Methionine synthase is responsible for the conversion of homocysteine back to methionine. A number of mutations that actually decrease the activity of this enzyme have been well characterized. Mutations that increase the activity have also been described for this gene. The A2756G mutation in the methionine synthase gene (MTR) has been reported to increase the activity of this enzyme.

    MTR A2756G

    As is the case for the CBS C699T up regulation, the ultimate result of a number of these mutations that increase rather than decrease enzymatic activity is to deplete the methylation cycle of key intermediates that are needed for this pathway to function properly. In the case of the MTR A2756G, the net result of this upregulation may be to use up B12 at an even faster rate than normal, causing a depletion of methyl B12 from the cycle.

    Decreased function of the MTR or a lack of B12 will diminish the level of conversion of homocysteine to methionine via this enzymatic route. A secondary route exists to convert homocysteine to methionine, utilizing the BHMT enzyme. Rather than using 5 methyl tetrahydrofolate and methyl B12 for this conversion, the BHMT enzyme utilizes TMG (betaine) as starting material for this alternative reaction. As described in the PDR (Physicians Desk Reference) "Betaine or trimethylglycine is a quarternary ammonium compound that was first discovered in the juice of sugar beets

    (Beta vulgaris). Betaine is a metabolite of choline and is a substrate in one of the two recycling pathways that convert homocysteine to L-methionine. The other and principal recycling reaction is catalyzed by the enzyme methionine synthase and uses methylcobalamin as a cofactor and 5- methyltetrahydrofolate as a cosubstrate.”

    Methionine synthase reductase (MTRR) acts in concert with methionine synthase enzyme to recycle homocysteine back to methionine. The function of methionine synthase reductase (MTRR) is to regenerate methyl B12 for methionine synthase to utilize. Mutations that impair the function of MTRR will have secondary consequences on the activity of the methionine synthase gene. Even if there are no mutations in the methionine synthase gene, the inability of MTRR to regenerate sufficient methyl B12 will impact upon MTR activity in the methylation cycle.
    The combination of a mutation in MTRR that compromises it’s ability to regenerate B12, in concert with a MTR upregulation that is utilizing B12 at an accelerated rate would result in severely depleted levels of methyl B12 in the body. This would also create a roadblock in the methylation pathway between methionine and homocysteine that would require nutritional bypass for restored pathway function.





    COMT : catechol O methyl transferase VDR : vitamin D receptor

    If an individual has a COMT variation it means that they have a change in one of the amino acids of the enzyme. In the case of COMT one of the frequent amino acid changes is from a valine to a methionine. This is what is being tested for when the COMT V158M SNP test is run. The lab is able to look at the DNA to determine the information for which of these two amino acids that your copy of COMT contains. If you have the version with the information for a methionine in the sequence, it is written as COMT + meaning that you are positive for the methionine version. If you are COMT- it means that you do
    not have methionine in that spot of the enzyme and you have valine there instead. Since the valine in that spot is considered the “norm” the methionine represents the variation, so it is + for a variation being present.

    The form of the COMT with the variation (the methionine in it at a particular location) is a less efficient form of the enzyme. When the methionine is present it does not do as good a job of breaking down the dopamine. Therefore an individual who is COMT+ will not break dopamine down as easily. An individual who is COMT- (with the valine in that spot) will break dopamine down more efficiently.

    The COMT enzyme uses methyl groups to help to inactivate dopamine. “COMT” stands for catechol O methyl transferase. So that when the COMT is working to inactivate dopamine and nor epinephrine it does so by using methyl groups that you have available in your system. These methyl groups are donated by SAMe that is generated via the methylation pathway. Individuals who have the less efficient form of COMT (the COMT+ +) will be using less methyl groups because they are not inactivating dopamine as rapidly. Relative to the COMT - - individual they will have more methyl groups available for other reactions in the body.
    Clinically, I have found that both the COMT status, as well as the VDR Taq genes act in concert to have an impact upon overall need for methyl donors and dopamine support. In general individuals who are COMT - - will have lower levels of dopamine due to enhanced COMT activity and will need and are able to tolerate higher doses of methyl donors. Conversely individuals who are COMT + + will have increased levels of dopamine, due to less efficient breakdown, and need and tolerate lower amounts of methyl donors.

    In addition, two of the three vitamin D receptor mutations also appear to play a role in dopamine levels and methyl donor tolerance. I believe that this is due to the relationship between vitamin D receptor and dopamine levels. Vitamin D increases the level of the enzyme involved in synthesizing dopamine. Increased levels of vitamin D would be expected to lead to increases in dopamine, norepinephrine and epinephrine. The VDR/Taq – genetic status results in higher levels of vitamin D. Therefore, individuals who are negative for the VDR Taq polymorphisms (VDR /Taq - -) may have higher levels of dopamine due to enhanced levels of vitamin D. As would be expected if this were the case, I have found that these individuals are more sensitive to nutritional supplementation with methyl donors and nutrients that enhance dopamine levels than individuals who are homozygous (have both copies) for the VDR /Taq + + variation.

    Increased levels of dopamine appear to aid in
    protecting cells from arsenic toxicity under conditions of low glutathione. This would suggest that supporting healthy dopamine levels for COMT – and VDR /Taq + individuals who also have glutathione mutations and/or CBS up regulations (which lead to decreased glutathione) may be helpful in reducing the effects of arsenic toxicity. Animal models indicate that chronic arsenic exposure leads to decreases in dopamine. Therefore low dopamine levels (in conjunction with reduced glutathione) create a “catch 22” whereby the toxicity of arsenic is increased, leading to further reductions in dopamine.


    COMT-- VDR/Taq-- • MTR+or++
    • MTRR +or++

    There is also a mutation in the methionine synthase reductase gene (MS_MTRR or MSR), as well as a mutation in the methionine synthase gene (MS or MTR). The function of MSR is to regenerate B12 for the MS to utilize. The methionine synthase mutation is an up regulation mutation that enhances the activity of the enzyme. This should cause the enzyme to use up added B12 at an even faster rate than normal. What this means in practical terms is that he/she may be severely deficient in methyl B12. The supplementation of B12 is therefore very important for him/her. Due to his/her COMT and VDR /Taq status he/she should need and will tolerate the addition of methyl containing supplements. Supplementation with methyl B12 should be beneficial for him/her. This will both help to support the MTR mutation as well as to add methyl groups to his/her system.
     
  13. dbkita

    dbkita Senior Member

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    greenshots:

    The reason why a person who has what Dr Yasko labels as VDR Taq -/- (now tt) most likely have higher serum levels of vitamin D (note this assertion itself is controversial as different authors have arrived at different conclusions, she is choosing one side of the argument) is the individual VDR receptors are strongly suspected to be less stable due to the SNPs in the regulatory domain (however Taq alone does not determine this is really based on the Bsm-Apo-Taq haplotype).

    Ergo the body tries to respond with higher levels of vitamin D produce to get the same effective VDR results. There are many parallels to this effect in other receptors with stability problems. This does not imply that the person with the mutant VDR haplotypes has increased net VDR activity and then further extrapolation to higher dopamine. The body is compensating through other mechanisms to deal with less stable, less active VDR enzymes. Again this not uncommon when the expressed products of a mutant haplotype are less active or less stable at a mRNA or an enzyme level.

    If this correlates somehow to something she sees in her clinical practice with regards to neurotransmitters and/or methylation then great and I do not dispute that ... but then there is something else going on with regards to why it is happening. Note however, in an alternate theory, people who have high levels of active vitamin D often have high levels of TH1 inflammation as the active form is produced in macrophages (not even talking about sarcoidosis). This production of active vitamin D has zilch to do with their genetics. This is common for people with autoimmune disease, Lyme's, and other chronic infections. The increased NE levels are due to the inflammation and not the vitamin D directly.

    Also the COMT -/- is the wild type. Its behavior is not enhanced. The other COMT variants have reduced catecholamine metabolism. That does translate directly into higher levels of dopamine and norepinephrine.

    Hope this helps.
     
  14. greenshots

    greenshots Senior Member

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    Actualy, I don't think I mentioned that the COMT -/- was defective since it would be the COMT +\+ so not sure why the last reference was made. We seem to be having a miscommunication issue and I honestly regret having chimed in on this one. We have two different view points that can't be easily reconciled. Thats ok, everyone gets there their own way. After years of searching, now that I'm healthy and back to work, I feel I've found the right one. But I know its not that way for everybody. Even though I don't agree with all of Yasko's stuff, I can't really debate her clinical observations. She has experience using this on so many people and I just don't have that kind of experience.

    Best to you in your search
     
  15. dbkita

    dbkita Senior Member

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    Yeah my bad I misread one of Dr Yasko's statements in the stuff you posted. Word flip.

    Glad you are feeling better. I guess I am failing to clarify that while I am sure Dr Yasko's clinical findings are quite useful and help many people ... however, some of the ideas tying it to genomic SNP data are not correct or at best have questionable support.

    I do not believe that a person can be diagnosed properly merely by there genomic information. I am sure that when Dr Yasko or someone similar would have ALL the information involved then they could develop a treatment that will be effective for many people. But a lot of people on here are using the genomic information for some 30 odd SNPs to determine how they should treat themselves. And there are a couple of clear errors in this process that are purely due to misunderstanding or misinterpretation of bioinformatic data on the part of Dr Yasko and her camp.

    An even more classic example is the the assertion that CBS +/+ is a 10 x up regulation. As I showed in my other thread, that was a clear misinterpretation of an artificial mutation deleting the entire c-terminal regulatory domain. Probably just a simple oversight like the statement that alpha keto glutarate is produced in the trans-sulfuration pathway when it is in fact alpha keto butyrate. That has since been corrected, but these faulty memes live on for a long time and can be misleading to someone especially if they are not being guided by the right doctor.

    Good luck and God bless!
     
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  16. Lotus97

    Lotus97 Senior Member

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    Viral and bacterial infections were mentioned earlier in this thread. My memory is a bit foggy, but somehow I remember there was mention of certain SNPs making a person more susceptible to viruses/infections. Does anyone know anything about this?
     
  17. greenshots

    greenshots Senior Member

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    My knowledge is limited here but I know that the MTHFR A1298C, MTHFR C677t, SHMT, ACAT, and AHCY increase bacterial issues. The MTHFR C677T seems to increase H. Pylori more and the SHMT and AHCY seem to increase strep and staph infections.

    Gut problems and infections seem to be big with the ACAT, SHMT, BHMT, MTR/MTRR and MTHFR A1298C. Where the CBS is more likely to cause viral and yeast problems. The Pancreas seems to be heavily hit by virus, especially measles and rubella but I'm not sure that having a VDR Fok upregulation will increase this risk or not. There are probably more associations but this is what I've retained.
     
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  18. Lotus97

    Lotus97 Senior Member

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    I don't care if you don't have CFS/ME, but recent research on neuroinflammatory diseases and Human Endogenous Retrovirus (HERV) expression seems to suggest an autoimmune nature to CFS/ME:
    http://phoenixrising.me/archives/16017
     
  19. dbkita

    dbkita Senior Member

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    Huh ???? Sorry but I do care !!!!

    For those others may be confused by you cutting out a snippet out of context, here is my original paragraph:

    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.

    People have been chasing autoimmune and viral links for CFS / ME for awhile. XRMV for example was pushed for years but is a total bust. We will see if HERV pans out. Anything is possible.

    The problem is CFS is not likely from one source anyways. People arrive at the same place for different reasons. That is what makes it multifactorial and so complicated. That being said now that it is an accepted disorder I am sure headway will be made and I would not put it past a micro-organism root cause for many CFS patients.
     
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  20. adreno

    adreno 3% neanderthal

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    Maybe this is considered heresy, but I do not believe ME/CFS to be a singular disease. Like dbkita, I believe ME/CFS to be sort of a biochemical endpoint configuration, with lots of different roads leading to this. A single uniform cause of ME/CFS will never be found IMO. But whatever the causes, getting the background biochemistry running properly is a very important (and necessary) step in the healing process.
     
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