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gondal, did you read my post in which I said that fenugreek+tea or nutmeg help my joint pain? I suspect my joint pain is caused by inflammation from POIS. Although it could also be caused by anything that POIS does to inhibit tissue growth and repair.
Wow, romies, congratulations on finding something that works for you! Must be a big relief. I'm still searching for my own solution, because it turns out I don't respond to the same treatments you and kurtosis have had success with. I think my issue is that I am over-methylated, and combined with COMT and MAO-A mutations I quickly experience negative effects from methionine and other methyl donors. I suffer from psychosis unless I'm taking dopamine-blocking drugs, and I have terrible reactions to some meds that block the reuptake of dopamine or norepinephrine (Wellbutrin).My Genetic Genie results:I have 3 homozygous mutations on my AHCY gene. From my understanding this would increase methylation. What's confusing is I also have 3 homozygous mutations on my BHMT gene, which would reduce the conversion of homocystine to methionine, a decrease in methylation. I'm pretty sure that's right, correct me if I'm wrong! The CBS mutation should also decrease methylation, so I'm guessing that homocystine levels are not indicative of very much for me. My last check was very normal. Is the methylation problem (be it over or under) resulting in a normal homocystine level by having mutations that both increase and decrease methylation?I'm curious if I would respond to treatment that people with hypermethionemia have. http://wiki.medpedia.com/HypermethioninemiaI don't know exactly what that treatment is though, I havn't found a good resource on that.Besides the BH4/mast cell connection, I still have no idea how this would cause increased symptoms after orgasm!
The AHCY gene provides instructions for producing the enzyme S-adenosylhomocysteine hydrolase. This enzyme converts the AdoHcy into the compound homocysteine.
COMT (+/-) and VDR (+/+) behaves like COMT (-/-)
Lowest dopamine levelsPoor tolerance to toxins and microbesNeeds and tolerates dopamine precursors and methyl donorsLowest susceptibility to mood swings
Monoamine Oxidase A breaks down serotonin, a neurotransmitter that is generated from the dietary amino acid tryptophan, in a BH4 requiring reaction. Many anti-depressant drugs, including the SSRIs (Serotonin Selective Reuptake Inhibitors) work by blocking the breakdown of serotonin. Defects in serotonin metabolism have been associated with mood and neurological disorders. How best to address the MAO A R297R abnormality is not clear to me. As serotonin metabolism is adversely affected, individuals with the R297R defect should avoid large doses of high tryptophan foods (see appendix). High doses of St. John’s Wort, often taken to address depression, could lead to mood swings as serotonin levels fluctuate.
Phosphatidylcholine, or as a less expensive alternative, Phosphatidylserine 100 mg daily, to stimulate the BHMT reaction
S-Adenosyl Methionine (SAMe), the key methyl donor generated from methionine, is metabolized in to S-Adenosyl Methionine, and then on to homocysteine by AHCY. Individuals (+) for both AHCY and CBS often have low baseline urine sulfate levels, which then rise and fall in response to treatment. Early on the levels rise, as the “bottle neck” abnormal AHCY enzyme has been “limiting the supply” of homocysteine.
MTRR generates the methyl-B12 needed by MTR and many other methyl-B12 requiring enzymes. Blood B-12 levels may be normal, but if MTRR is (+/+) or (+/-), methyl-B12 formation will be compromised, homocysteine levels will be elevated, methylation in general will be compromised, and your physiology will be compromised.
Found this about hypermethioninemia: "Treatment of CBS deficiency usually begins with a trial of oral vitamin B6 (pyridoxine) supplementation, with daily measurement of plasma amino acids. CBS requires pyridoxine as a coenzyme for enzymatic activity. Overall, about 25% of patients respond to large doses of pyridoxine, although the percentage may be lower for patients identified through newborn screening. This pyridoxine response usually coincides with the presence of some residual enzyme activity. Dietary restriction of Methionine in conjunction with Cystine supplementation reverses the biochemical abnormalities to some extent and appears to reduce the clinical symptoms. Special formulas are available commercially, but the diet is difficult to maintain long term. In an attempt to decrease Homocysteine levels, folic acid, and betaine can be supplemented to induce recycling of this amino acid to Methionine for alternate metabolism. Vitamin B12 (cobalamin) may also be helpful.Because the diagnosis and therapy of Homocystinuria is complex, the pediatrician is advised to manage the patient in close collaboration with a consulting pediatric metabolic disease specialist. It is recommended that parents travel with a letter of treatment guidelines from the patient’s physician."http://www.perkinelmergenetics.com/Hypermethioninemia.htmI wonder if this is why B-complex improves my symptoms, but methionine seems to make me slightly worse.
I believe the improvement we're noticing from NADH is increased energy and increased glutathione production. I also worry about fluctuating homocysteine levels that may contribute to the dull headache that some of us get. Just some thoughts. I realise that none of this is conclusive.I know NADH can be used to recycle bh4 and reduce ammonia levels. Another possibility is synthetic BH4. I think there's a product called Kuvan but I have not tried it. It's prescription only so, as usual, discuss it with your doctor. We both have CBS mutations. However, I think that some of our illness (and this may not apply to other POIS sufferers, just those that have A1298c and/or MTHFR C677T mutations) may be caused by low levels of glutathione. My skin and stomach problems improve very quickly when I add supplementary glutathione. I just don't think I'm making enough of this normally and need a helping hand.
Wow, romies, congratulations on finding something that works for you! Must be a big relief. I'm still searching for my own solution, because it turns out I don't respond to the same treatments you and kurtosis have had success with. I think my issue is that I am over-methylated, and combined with COMT and MAO-A mutations I quickly experience negative effects from methionine and other methyl donors. I suffer from psychosis unless I'm taking dopamine-blocking drugs, and I have terrible reactions to some meds that block the reuptake of dopamine or norepinephrine (Wellbutrin).My Genetic Genie results:I have 3 homozygous mutations on my AHCY gene. From my understanding this would increase methylation. What's confusing is I also have 3 homozygous mutations on my BHMT gene, which would reduce the conversion of homocystine to methionine, a decrease in methylation. I'm pretty sure that's right, correct me if I'm wrong! The CBS mutation should also decrease methylation, so I'm guessing that homocystine levels are not indicative of very much for me. My last check was very normal. Is the methylation problem (be it over or under) resulting in a normal homocystine level by having mutations that both increase and decrease methylation?I'm curious if I would respond to treatment that people with hypermethionemia have. http://wiki.medpedia.com/Hypermethioninemia [nofollow]I don't know exactly what that treatment is though, I havn't found a good resource on that.Besides the BH4/mast cell connection, I still have no idea how this would cause increased symptoms after orgasm!
"Increased CBS enzyme activity would act to convert homocysteine more efficiently to cysteine, thereby lowering homocysteine levels. Ultimately individuals with the CBS C699T upregulation of the CBS enzyme can generate more sulfur breakdown products with potential sulfur toxicity issues, enhanced ammonia production, and a lack of glutathione."
Freedenfeld s. [et al.], Biochemical effects of Ribose and nADH Therapy in children with Autism, 2011
I have the C699T up-regulation. I read Yasko's "Genetic Bypass" book and while I'm not 100% convinced that anybody knows 1) the exact interaction between all these genes2) that other genes are not involved that may complicate these interactions further. I think that the methylation pathyway diagrams make a lot of sense and seem somewhat, if not entirely, complete. Here's her quote on C699T from (page 48)Quote"Increased CBS enzyme activity would act to convert homocysteine more efficiently to cysteine, thereby lowering homocysteine levels. Ultimately individuals with the CBS C699T upregulation of the CBS enzyme can generate more sulfur breakdown products with potential sulfur toxicity issues, enhanced ammonia production, and a lack of glutathione."Yasko believes that ammonia and taurine are elevated in CBS up-regulations and that glutathione is decreased. Ammonia buildup is bad and the best way to clear it is with BH4, which can be recycled using NADH. NADH has also been shown to increase glutathione in one study I read. See QuoteFreedenfeld s. [et al.], Biochemical effects of Ribose and nADH Therapy in children with Autism, 2011I don't think there are enough studies to decide it's conclusive but it's worth thinking about.
Yes, Octave is pretty good as a MATLAB replacement. In your current routine, the blueberry extract is a replacement for Ginkgo Biloba extract, right? What's your daily dosage? any special dose before/after an O?Thanks!
Nightingale,I am not completely out of the woods yet.. The recipe is quite complex, so if I forget one or two ingredient, I sometimes still get some POIS symptoms, but for 12-18 hrs only, as opposed to 4-5 days before. Your COMT, VDR and MAO A profile is almost completely opposite from mine. so I guess your are more of the over-methylation type. Maybe taking Niacin before and after an O will help to mop up extra methyl and lessen the crash?I do think there are several sub-types of POIS. maybe there is a over-methylation type, where too much dopamine was generated. Dopamine response curve is U-shaped. too much DA does degrade cognitive and may also causes dopamine receptor to down-regulate, and causes a hang-over for 4-5 days after..
I'm having Phe, ammonia, Heavy metals, and maybe sulfur levels tested this weekend. I'm especially curious about ammonia, since after eating meat lately I'm getting this wave of brainfog and loss of concentration.EDIT: I wonder, too, if my having to take 1.5g of niacin to achieve a flush now has something to do with an excess of methyl? My first times trying niacin didn't require nearly as much, but early on I noticed I needed about 200mg to get a real flush were most were needing 100-150mg. It quickly climbed to where I had to buy 500mg niacin tablets. Actually, my flush isn't very strong anymore and I'm getting less reduction in symptoms, I might bump it up to 2g soon.
Yes, that's a good point. I believe that both blueberries and ginkgo can reduce inflammation. I like ginkgo but it sometimes makes me itchy whereas blueberries or pterostilbene (there's a patented extract in some supplements) seem to reduce POIS and I haven't noticed any side effects.