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Dr. Ben Lynch - MTHFR Webinar 07/10/13

Discussion in 'Upcoming ME/CFS Events' started by roxie60, Jul 10, 2013.

  1. roxie60

    roxie60 Senior Member

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    Just got notified of this, starts in 15 mins. It appears it will also be archived.

    Today, Wednesday, July 10th, I am presenting via webinar on "Folate and Methylation Defects: Clinical Breakthroughs and Updates"

    For one hour, I will be discussing some of my latest findings which include:
    1. Clinical significance of nutrigenomics, introducing methylation and the importance of healthy diet, lifestyle and environment
    2. Pathways of folate metabolism, B12, transmethylation, transsulfuration, SAMe, mitochondrial function, detoxification pathways and cell membrane functions
    3. Common genetic polymorphisms along with their effects and interactions with diet, xenobiotics, nutrients and medications
    ​I am presenting some critical information which I've never presented before.

    ​The main webinar will be 45 minutes long followed by 15 minutes of Q and A.

    Bring your notepad!

    Register Now before you forget.

    Not able to make it? That's ok.

    Simply register now and you will be notified via email when it becomes available to watch on your own time.

    Respectfully,

    Dr Lynch

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  2. roxie60

    roxie60 Senior Member

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    I thought I was up to speed on this but I still learned new things. I had no idea that nitrous oxide was harmful and even more so if you have certain gene mutations. I have had a lot of dental work and I take nitrous oxide since I dont seem to get numb with the novocaine (slow to numb) and the gas helps me not focus on the pain. There is a lot more in Ben's latest presentation. It went very fast, he is promoting his upcoming MTHFR seminar for Drs. I know I have been sick and at times extremely sick for many years and I appreciate he admonishes Drs that they cant just tell sick patients like us to try this supplement, do this test and see me in 3 months. That has always been my complaint, there is no sense of urgency by so many Drs. Also mentions the methylation cycle has to be restarted/balaced carefully, depending on polymorphisms, otherwise patient can get more sick which is what has happened to me over the years and particularly last year. I am so worn out but I'm still trying not to give up but the medical people that are involved in my case just dont get how hard, how much energy I have used just trying to keep going.
    juniemarie likes this.
  3. roxie60

    roxie60 Senior Member

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    I think he said there were close to 1000 people listening to the webinar.
  4. roxie60

    roxie60 Senior Member

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    the webinar archive is suppose to be available tomorrow
  5. roxie60

    roxie60 Senior Member

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    I thnik I found a similar and longer version of the presentation
    Crux and juniemarie like this.
  6. roxie60

    roxie60 Senior Member

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    Looks like the recent webinar had over 2000 people so people are trying to understand SNPs and methylation, etc.
  7. juniemarie

    juniemarie Senior Member

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    Thanks for posting this. Would you be willing to post information here if you listened.
  8. roxie60

    roxie60 Senior Member

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    I wish I could but I have forgotten. I need to watch it again as I remember hearing him say some new things. Sorry
  9. roxie60

    roxie60 Senior Member

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    I think he had another one yesterday but I forgot to sign up. Have not had the energy to sit up at the computer that long to listen.
  10. taniaaust1

    taniaaust1 Senior Member

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    That's for sharing. I get very sick (extremely nauseus immediately if I have it) and actually collapse with nitrous oxide even when they turned it down, I still collapsed with it. Due to my very bad experiences with this over 20 years ago (before I had ME), I havent had it again nor wouldnt. I have a double copy of the Mthfr mutation.
  11. invisiblejungle

    invisiblejungle Senior Member

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    roxie60 likes this.
  12. roxie60

    roxie60 Senior Member

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    did not realize there might also be a connection t depression with MTHFR, the study linked under depresion only appears to study the 677 MTHFR not the 1298 (I could not see the entire article). I just wonder why are some gnes and SNPs studied more than others? A1298C is suggested often as not meaningful, why do people propogate such views when in actuality there has not been much study done for those with other MTHFR mutations. So to say the other MTHFR mutations are not meaningful seems short sighted and harmful to those who struggle with symptoms and they have no 677 mutation but their other MTHFRs do have mutations. I'm just frustrated, some times I feel as a group we perpetuate the harm when we make judgements with out proof...
  13. Valentijn

    Valentijn Activity Level: 3

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    Actually there have been studies about the effect of A1298C. And it doesn't do much by itself, but can exacerbate the folate problems of someone who is heterogeneous for C677T. It gets studied less because it's been proven not to have an effect by itself, thus is less interesting. Whereas C677T does have an effect, so researchers want to see how it effects whatever disease/etc that they're interested in.
  14. Sea

    Sea Senior Member

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    http://www.ncbi.nlm.nih.gov/pubmed/18580170

    This is one study about the dangerous elevation of homocysteine when Nitrous Oxide anesthesia is used in those who are homozygous for EITHER C677T or A1298C. I can only find the abstract which doesn't indicate whether the effect of one is greater than the other but both are important by themselves.

    The fact that A1298C has less or no effect by itself in some of the things that C677T has a large effect doesn't make it not worth studying.

    http://evidence.personalgenomes.org/?q=MTHFR E429A

    "OBJECTIVE: To determine associations of methotrexate (MTX) efficacy and toxicity with single-nucleotide polymorphisms (SNPs) in genes coding for folate pathway enzymes in patients with early rheumatoid arthritis (RA).

    METHODS: Patients (n=205)...
    The following SNPs were analyzed: methylenetetrahydrofolate reductase (MTHFR) 677C>T, MTHFR 1298A>C, dihydrofolate reductase (DHFR) -473G>A, DHFR 35289G>A, and reduced folate carrier 80G>A. In case of significant differences, odds ratios (ORs) were calculated.

    RESULTS: At 6 months, MTHFR 1298AA was associated with good improvement relative to 1298C (OR 2.3, 95% confidence interval [95% CI] 1.18-4.41), which increased with increased copies of the MTHFR 677CC haplotype. In contrast, MTHFR 1298C allele carriers developed more ADEs (OR 2.5, 95% CI 1.32-4.72).

    CONCLUSION: Patients with MTHFR 1298AA and MTHFR 677CC showed greater clinical improvement with MTX, whereas only the MTHFR 1298C allele was associated with toxicity. In the future, MTHFR genotypes may help determine which patients will benefit most from MTX treatment.
    roxie60 likes this.
  15. Valentijn

    Valentijn Activity Level: 3

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    Sea
    In the first one it's really a detox issue, not a methylation issue. Yes, it does have an impact, but only under extraordinary circumstances - being gassed. And even then there is no statistically significant impact upon folate levels, just a temporary increase of homocysteine. (full text is free at http://journals.lww.com/anesthesiol...of_Methylenetetrahydrofolate_Reductase.8.aspx )

    There's also a HUGE range of responses to the gassing, with the median far lower than the max - which suggests that a couple outliers dragged the average up. As they discuss in the paper, these results could be due to the small sample sizes in the wild-homozygous and homozygous-wild groups, and/or it seems likely that there is another unknown factor affecting results to a greater extent.

    The full text of the 2nd one is at http://onlinelibrary.wiley.com/doi/10.1002/art.21726/pdf
    That one is looking at the effect of drug treatments, so again is not looking at the standard functioning of the SNPs, but rather how they might impact the RA patients' reactions to a drug.

    I think this one is a bad study. To start with, it's being funded by insurance companies. It also uses subjective outcomes to determine improvement (sounds familiar), and is not talking about folate or even B12 or homocysteine status at all. It's also uncontrolled, so placebo effect could be a big factor. They report lab results from the beginning of the trial, but none from the end - did they not measure them at the end, or are they trying to hide objective data which contradicts the subjective outcome?

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