I started off taking 1,200mg per day and then upped to 1,800 at one point. Perhaps I should cut that way down and try again…
Hi droit,
thanks for that summary/hard work, it’s clear to me now. This is something I’ve gotta keep an eye on for now for good.
Btw, This is the response from that Dutch lab:
So if I understood right, this test can actually be done at home + you send the sample to the laboratory. They did not answer specifically that how it is tested (blood, plasma, urine, spit, etc)… but it could be assumed that it is from blood (RCB etc). I haven’t asked about insurance/social security yet. I also haven’t asked whether this test can be done without doctor’s consent but I’ll assume that the answer for that is yes as well.
Does this look okay to you droit? IDK about all the folate components but it seems complete to me, yeah. EDIT Yeah, according to RVK’s paper, it’s all good. Yesssss.
Also, the elevated serum B12 could be a sign of eg. MTHFR (sp?) mutation, much like I suspected…
–
Anyways, as my general plan (also because of lack of money atm):
-
My first step is to fix my leaky gut + gut dysbiosis and possibly adrenal fatigue (easier said than done with leaky gut or possible methylation problems). With my current plan, it might not be too long in the future I’ll do it.
-
Next up or somewhere in-between, methylation pathway test along with 23andme seems like natural next step. Gut dysbiosis pretty much guarantees lack of B12 you know (Chris Kresser, GAPS)…
I had got done a Genova Diagnostic 3-time stool sample test. I have an hell of a infestation of Klebsiella Pneumoniae and I almost completely lack bifidobacterium and lactobacillus (should be like, pervasive/the most common bacteria in gut). The test could be an incorrect snapshot in a way, yes, but there’s no question about dysbiosis since I’ve indulged with heavy class - antibiotics for two months in total time… also hah hah, some embarrassing symptons re: faecal matter and certain foods…
It is most likely a 24 hour urinary panel where you will void your first AM flow and then your last one will be AM of the next day. The 23andMe is a saliva sample.
Btw, IF you do have methylation issues, you likely will not be able to adrenal (or gut dysbiosis) issues without addressing the methylation aspect alongside…
It’s a blood test. You have to take the kit to a place that does a blood draw. They measure red blood cell values amoung plasma values. Most hospital labs will do it.
Ok, thank you for the info Bryce and droit. Considering my really low folate (I’m going to post the full bloods later today I think) do you think this protocol would be beneficial? What significant improvements have any of you currently following it seen? (besides mario)
Got my 23andme results back already. I knew the B12 methylcobalamin and methylfolate made me feel a lot better and it turns out I do have 3 MTHFR heterozygous mutations. Also 3 homozygous BHMT mutations.
Gene & Variation rsID Alleles Result
COMT V158M rs4680 AG +/-
COMT H62H rs4633 CT +/-
COMT P199P rs769224 GG -/-
VDR Bsm rs1544410 CT +/-
VDR Taq rs731236 AG +/-
VDR Fok-I not found n/a n/a
MAO A R297R rs6323 T +
ACAT1-02 rs3741049 AG +/-
MTHFR C677T rs1801133 AG +/-
MTHFR 03 P39P rs2066470 AG +/-
MTHFR A1298C rs1801131 GT +/-
MTR A2756G rs1805087 AG +/-
MTRR A66G rs1801394 GG +/+
MTRR H595Y rs10380 CC -/-
MTRR K350A rs162036 AA -/-
MTRR R415T rs2287780 CC -/-
MTRR S257T not found n/a n/a
MTRR A664A rs1802059 AG +/-
BHMT-01 not found n/a n/a
BHMT-02 rs567754 TT +/+
BHMT-04 rs617219 CC +/+
BHMT-08 rs651852 TT +/+
AHCY-01 rs819147 TT -/-
AHCY-02 rs819134 AA -/-
AHCY-19 rs819171 TT -/-
CBS C699T rs234706 GG -/-
CBS A360A rs1801181 GG -/-
CBS N212N rs2298758 GG -/-
SUOX S370S not found n/a n/a
NOS3 D298E not found n/a n/a
SHMT1 C1420T rs1979277 AG +/-
bluejaysfan, thank you for posting your data. It is great to continue getting consistent data.
MTHFR
You have compound heterozygous, which means you don’t have 2 mutations in anyone site on MTHFR, but you have 1 mutation in each. Here is a good interpretative guide which says having one 677CT and a 1298AC will give 50-60% reduced activity.
gdx.net/core/interpretive-gu … -Guide.pdf
I don’t know about MTHFR P39P, which is less researched. opensnp.org says only 19% of the population has a heterozygous mutation at that site and no one is homozygous. That means its under heavy selection.
Its no surprise that an expert would probably say you should take methylfolate even if this was discovered before PFS. I don’t know what dose.
@Bryce54, in your report with the methylation consultation did they mention what dose of methylfolate?
CBS
You are the first to not have a CBS mutation. There has been a high incidence of homozygous mutations in CBS in short term users. But you’ve said you were more long term.
BHMT
The thing you do have that everyone else has is a obliterated BHMT. All of the short term users have 1 or 2 mutations at all sites. You and moonman1 have homozygous mutations in all BHMT sites. This is a table of the frequency of mutations in the normal population (second to last column) vs. mutations in the 5 on this forum (last column) that have given their data. There is a 6th person I only have partial data for who says he only has 1 homozygous in BHMT so two of those frequencies are going to come down once his data is filled in.
BHMT-02 rs567754 36% 60%
BHMT-04 rs617219 39% 70%
BHMT-08 rs651852 49% 70%
These mutations are not clearly published on. I’ve read they they are upregulating, unlike the MTHFR mutations which slow down the enzyme. I’ve also read that BHMT mutations have the same effect as CBS. If anyone has any references on what these mutations do, please post.
For an information on the MTR check out the site Bryce54 posted:
Thanks for the post, Droit. I just saw it now.
Thinking I am seriously wacked out in methylation due to the various mutations. Been reading up and writing down some things I should eat and maybe missing vitamins. Sometimes I read that B6 is good and then I remember somewhere it said to avoid, based on a particular mutation.
Once I get a list figured out, I will add it in here. Going to try and dig BHMT info.
Has anyone here gotten there ammonia tested? Please post results if so.
where are you guys at? any improvements?
@bryce54:
I don’t have money for the tests or regiment for quite some time so don’t count on me for updates lol. If it was up to me tho i’d be all over this ASAP. I think the SNP testing could be that important in my case… I’m still going to be frequenting you guys/this topic for updates/progress.
@moonman1:
I think you are right (tho i don’t see your sources in regards to your claim):
I was thinking about improved hypothyroidism condition in RVK’s Methylation protocol study… I think I might have found a connection between thyroid metabolism and methylation/glutathione…
If this is true, then you would totally right: I would have to address all 3 at the same time to really get the best effect!
If the proposed mechanism by Dr. Brownstein & Dr.Abbrhams? behind oxidation of Iodide (to Iodine) within thyroid cells is true… then
- it means that Hydrogen peroxide is used in both oxidation of glutathione AND Iodide…
- …and Hydrogen peroxide is the byproduct of ATP production (Oxidative Phosporylation)…
- …which is in itself regulated critically by thyroid hormones and cortisol (by bringing glucose effectively to the cell)…
!. … which means that if either adrenal fatigue or hypothyroidism exists in person, the production of Hydrogen Peroxide is lowered…
!!. … which results in less oxidation of glutathione and Iodide, thus less glutathione activity and increasing hypothyroidism…
!!!. thus even less hydrogen peroxidase!
- Lack of selenium would also mean lack of glutathione peroxidase, which would that hydrogen peroxide would not get removed from system, resulting in damage to surrounding tissues -> autoimmune attack to the tissues.
I’m not sure if this could be true but in wikipedia article Glutathione Peroxidase, they call the term GSH “reduced monomeric glutathione”. GSH is the same term used in wikipedia of Glutathione.
It also mentions that the byproduct would be reduced back to glutathione by glutathione reductase… which goes by a name NADPH (which is what Dr.Brownstein called the oxidation of Iodide - “NADPH oxydation system”).
Wikipedia is not the best of sources, for sure, but I haven’t read in-depthly of chemistry of methylation either and I’d like to throw this idea out regardless.
Other sources for this idea/mechanism are Brownstein’s Iodine book, Paul Robinson’s RT3 book and STTM book.
–
I’ve also been thinking, this one is more imaginative/experimental… if this mechanism is true and if the role of boron in parathyroid holds up as well (the borax theory)… the parathyroid is connected to thyroid and for the oxidation to work/“boost”, it requires adequate intra-cellular levels of calcium. What would parathyroid/boron do? That’s right, it would act much like thyroid in concentrating calcium+boron to parathyroid - to ensure stabile, easily & carefully adjusted levels of calcium in eg. thyroid cells! Who would had thought, right… 
The lack of boron naturally would result to ineffective, uneven or even wrong distribution of calcium around the body. Tho if the boron thing is true then the body would produce… NBS?? (Natrium/Boron Symporter) in response to boron, and what signaling would indicate that? Surely not TSH like in Iodine’s case?? haha… Nevermind this tho, i just did this for fun.
gefinauser,
Thank you for spending some time on this angle. I will see if I can add a short summary of the generally accepted mechanism of the thyroid link to the glutathione-depletion/methylation-block theory, with references.
There is thyroid dysfunction and even hashimoto’s thyroiditis observed in the methylation-block communities. There are a couple of explanations generally excepted which roughly relate to, as you say, lack of glutathione allowing hydrogen peroxide to breed out of check. Here are the citations.
“Hydrogen peroxide-induced production of a 40kDa immunoreactive thyroglobulin fragment in human thyroid cells: the onset of thyroid autoimmunity?”
biochemj.org/bj/360/0557/bj3600557.htm
“Glutathione Peroxidase Degrades Intracellular Hydrogen Peroxide and Thereby Inhibits Intracellular Protein Iodination in Thyroid Epithelium”
endo.endojournals.org/content/138/7/2871.full
If you want a concise explanation, Dr. Van Konynenburg talks about this in his lecture that has been linked throughout this thread.
In terms of treatment, I think you just want to get the methylation cycle running again, replenish glutathione which will resume the protection of the thyroid.
@gefinauser, have you come across additional treatment plans?
droit,
Thanks a lot for that post. Looks like I was on the right track, though it suprised me that glutathione regulates the H202 somehow so yeah, maybe I should listen to that lecture. Those two papers are really good btw, thanks again.
What do you mean by “additional treatment plans”, droit? Do you mean supplemental to this protocol or my other plans in general? In general, I do have some ideas… lot of ideas actually.
I would like to clarify that I don’t mean to bump this topic out of maliciousness so sorry if the new posts got you guys hopes up. I think I’ll get to do the simple methylation protocol at the beginning of next Spring when I’m back to Finland and I have more money. 
Glutathione’s normal function in keeping hydrogen peroxide (H2O2) and other free radicals down is a core idea to this theory (of reduced glutathione) in explaining some of the PFS symptoms.
Radical oxygen is very damaging (oxidizing) to the cell. But Radical Oxygen creation is a normal part of healthy biochemistry. Free radicals are generated normally in both the thyroid (in production of thyroid hormone) and in the mitrochondrial electron transport chain.
However, it is necessary to have to have a normal level of glutathione (in the reduced form - GSH) in the cell to quench these free radicals.
isagenixhealth.net/wp-conten … -res-1.jpg
ep.physoc.org/content/94/3/305/F2.large.jpg
Otherwise you get damaged cells (lipids, DNA, etc - which would damage the thyroid and the mitochondria). Hence Moonman1’s high lipid peroxidaes I referred to in this post:
viewtopic.php?f=27&t=7178&start=120#p72048
I would also investigate whether the elevated bilburin we see in the lab results on the forum is related to oxidative stress getting the better of the liver cells because of depleted glutathione.
The range of impact depleted glutathione is vast. Hurting thyroid and energy production is just a couple of examples.
Guys,
Count me in on this one. If you followed my posts i do have subclinical hypothyroidism and i am receiving 62mcg T3 for more than 4 years. The endos i visited said : “Your thyroid for some reason got lazy and we don’t know why” and this was the only problem that i’ve found after my initial crash.
Perhaps this is why i immediately felt better with NAC as this rises GSH.
Good info there, thanks.
As an update :
I am following the methylation protocol and receiving 1000 mg NAC and 850 mg Citrulline (to boost NO Production and remove ammonia). Previously i did not want to receive methylation supplements AND NAC at the same time but i am happy i tried to take everything. Recall that that even though with NAC i felt immediately normal (normal libido,sleeping / not depressed etc), there were still some neurological issues and neurodegeneration (“unconnected penis sensation”, arm numbness / pain at times in various places in my body). Now i feel much more complete although my memory is still not good.
My regimen is :
-Morning :
Methylcobalamin B12 in the upper lip for around 45 min
TMG 500 mg
Folate as Metafolin from Solgar 800mcg
L-Citrulline 850 mg
Vitamin C
NAC 600 mg
-Evening:
Methylcobalamin B12 in the upper lip for around 45 min
TMG 500 mg
-Night:
Selenium
Magnesium
Zinc
I dropped P-5-P, Phosphatidylserine as Droit suggested. Droit suggested also to take less TMG which i will do gradually.
I should probably explain why i believe i have neurodegeneration on a different post. The symptoms are very diverse and just to give you an example : Believe it or not 2 years ago I would feel the signal that my brain sends in my penis to create an erection. This has faded slowly away in intensity and now i barely feel anything. At the moment, it takes much more time to achieve an erection.
So if we want to consider just the erections, look at how many different levels there are problems : Neurological, Nitric Oxide (essential for Erection) Production and Hormonal.
Wow, that’s a mouthful mariovitali. I’m glad to hear that things are improving anyways with your supplement changes. The best way to improve glutathione peroxidase is just plain 200mcg of selenium (the regular dose). IDK which form though since from the top of my memor, RVK didn’t think selenomethione or amino acid forms were good… idk. 
Re: Hypothyroidism… lemme relate an experience in related to this:
I had pre-existing hypothyroidism prior to starting finasteride that I was treating with T4.
For no reason after 7d-14d I started using finasteride my hypothyroid symptons sudendly got worse.
They improved very quickly once I increased the T4 dosage to twice the amount by myself.
I got stuck on that dosage until crashing/the last year and now I’ve switched to T3 (partially, my adrenal fatigue makes it hard to use it properly).
Re: Brainsignaling:
I know that description of brain signaling… and I’m not always entirely convinced that it’s actual brain damage (well, in it’s entirity anyways!):
during Kos therapy, I had absolutely perfectly working brain-penis connection with immediate erection the day after the doctor started drenching the area where the nerves ran! I actually looked into idk Vogue and instead of looking at the models with an information that they were good looking, I immediately thought “wow she’s hot” and got a full erection. This lasted only for that day and after that, things returned back to normal more or less. Later on, blasé and others found inflammation in the pudental nerve and they made a topic about their findings…
Anyways, you can for sure heal the nerve damage with methylation over time but I’m also interested of how much of it is just plain localized inflammation and if there is a way to lower that or general inflammation in the body. Is Methylation the way to lower it, etc.
Mario, I read that vitamin C can interfere with the B12. Not sure of the dose or exact timing to your B12, but, I believe you want to max it at about 500mg. Also take it at least a half hour after b12.
OK Man, Thanks i will move Vit. C in the afternoon.
Another interesting tidbit… I have had great dreams every night for a solid week. Many times 2 or 3 a night that I remember. Hopefully that’s another good sign.
I’m not sure how that would tie in to methylation, but, it must some how
If I’m lucky I should have my hands on some sunflower lecithin in less than a week
I think it could help my methylation, as well.
bluejaysfan,
Thats good news. I also noticed the same effect a month into my protocol.
The methylation cycle is responsible for creating melatonin. There is a simple explanation here
lef.org/magazine/mag97/march97-report.htm.
Its likely that your protocol is now spinning the methylation cycle and consequently you’re creating more melatonin and able to go into a deeper sleep cycle.
Make sure to go slow with that lecithin and observe the effects it has on you. It made me so tired I had to sub out the lecithin for fish oils.