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Methylation, Blood pressure and B vitamins (TMG), Amino Acids

LINE

Senior Member
Messages
845
Location
USA
Overview:
Methylation is an important pathway.
Nutrients influence the Methylation pathway.
I measured methylation via blood pressure.

I use blood pressure to monitor my levels of inflammation, it is helpful to identify inflammatory events such as food sensitivity. It can also be used in testing my supplements such as antioxidants which bring down inflammation.

My blood pressure has been spiking lately regardless of the bp meds. The med is actually nitroglycerin (NG) works by helping the body to produce Nitric Oxide (NO). NO works in a variety of systems which includes vasodilation (hence, its ability to reduce blood pressure). It also works in immune response (and other systems). NO has been studied in a number of disease pathologies such as cardiovascular and Covid 19.

I have always able to control bp (sort of control) with a number of different attempts but could never isolate the substance. So, I decided to focus on methylation nutrients. Methylation is an important pathway that has been studied in ME and other diseases. There are a number of nutrients that play a role, the big ones are the sulfur containing amino acids (cysteine, taurine, methionine and I should not leave out NAC and SAMe which are derivatives of cysteine and methionine respectively).

B vitamins play a crucial role in methylation, I presume that all of them are participants, but I can say with confidence that individual needs may vary. For instance, I have more of a pronounced need for Vitamin B2 which happens to be supportive of immunity, nervous system and more. Choline is a good one for me as well, it is a strong methyl donor. As a side note, it is better to support all the b vitamins vs. supplementing heavily on a single one. This prevents the system from getting out of whack.

I did multiple isolation studies using the blood pressure machine (Omron). By isolation studies, I mean that I dose single nutrients to isolate what might be needed. I dosed with some strong amounts and would wait 1 hour and more to see if there was a change in blood pressure readings. I used taurine, cysteine, methionine at different intervals. I also tested all of the b vitamins individually.

I tried B1 (benfotiamine), B6, B12, Folic Acid, Choline/Inositol, B5 (pantothenic acid), B3, Biotin (as D-Biotin*) and so no significant drop.

I then isolated B2 and TMG - bam, I got significant results. At the moment, I suspect it was the TMG which has not been tested previously (new item). B2 has been tested in the past. TMG does play a role in the methylation cycle.

Conclusions:
  1. We can make a conclusion that if one is severely deficient, results should show up rapidly, while a moderate deficiency would be harder to identify.
  2. We could also make a conclusion that all nutrients work synergistically which is to say that TMG by itself, may not have worked as well without the other supportive nutrients.
  3. I think it is safe to say that methylation does influence the Nitric Oxide cycles.
  4. Nitric Oxide plays an important role in human health and keeping levels optimal should assist the body.
*D Biotin is different than biotin, it seems more bioactive for me. I noticed that by taking D-Biotin, my inflammation has been reduced. It is not always advertised as D Biotin on the label, I found Amazon Basics sells D version but listed as just biotin.; The Nutrition label will identify if questioned.)
 
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LINE

Senior Member
Messages
845
Location
USA
Other note is the role of arginine or citrulline which are precursors to Nitric Oxide. My past experiments with those were not favorable. Arginine is suspect for ME people since it can serve as a growth factor for viral replication. Citrulline may be a better choice but was no help.

I suspect that since ME people have altered metabolic pathways, there may be some abnormal conversions.
 

datadragon

Senior Member
Messages
407
Location
USA
B vitamins play a crucial role in methylation, I presume that all of them are participants, but I can say with confidence that individual needs may vary. For instance, I have more of a pronounced need for Vitamin B2 which happens to be supportive of immunity, nervous system and more.

Interesting. Vitamin B2 is needed for MTHFR. Riboflavin (vitamin B(2)) is the precursor for FAD, the cofactor for MTHFR and taking high dose helps to restore function in those with mutations as I mentioned in another post. Defective enzymes can be remedied or ameliorated by the administration of high doses of the vitamin component of the corresponding coenzyme, which at least partially restores enzymatic activity. https://forums.phoenixrising.me/thr...ons-disease-october-2-2023.90883/post-2445674

In recent years genome-wide association studies have identified a region near the gene MTHFR among eight loci associated with blood pressure. Epidemiological studies, which provide a separate line of evidence to link this gene with blood pressure, show that the 677C→T polymorphism in MTHFR increases the risk of hypertension by 24–87%. Targeted riboflavin supplementation in homozygous individuals (MTHFR 677TT genotype) lowers systolic blood pressure by 6 to 13 mmHg, independently of the effect of antihypertensive drugs. https://www.sciencedirect.com/science/article/abs/pii/S0098299716300589

Riboflavin (Vitamin B2) is also known as an inhibitor of NLRP3 - Riboflavin, vitamin B2, attenuates NLRP3, NLRC4, AIM2, and non-canonical inflammasomes by the inhibition of caspase-1 activity https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7645791/

Also a new study found a small protein cell glucagon-like peptide-1 (GLP-1) couples the body's control of both blood sugar and blood pressure. https://www.sciencedaily.com/releases/2022/02/220201074528.htm

However as I looked a bit more, I am finding that methylation is involved as part of the balance for inflammation in the body and not something separate to balance. Some of the genetics that are changed like MTHFR that impact methylation exist due to that balancing of inflammation levels, where certain groups among the population such as blood type As so far I believe are looking to be normal to have these mutations due to how they balance inflammation differently and should not by itself assume its bad and to fix it. For example high homocysteine raises ER Stress and activates the NLRP3 inflammasome while lowering the function of the PPAR anti inflammatory pathways also so this is a big finding. By the way, a deficient/unavailable zinc can create a methylation block, low glutathione leading to further b12 reduction, low b6 leading to further problems with homocysteine and nlrp3 inhibition. B6 is required for the conversion of methionine to SAMe and for the conversion of homocysteine to methionine as just two of its functions. zinc is needed for those ppars to function and also involved with BH4 needed for nitric oxide so its all linked as the body pivots like a see saw toward an inflammatory state. https://forums.phoenixrising.me/thr...s-chronic-fatigue-syndrome.90582/post-2443933


The active form of Vitamin B6 (P5p) prevents IL-1β production by inhibiting NLRP3 inflammasome activation and suggest its potential for preventing inflammatory diseases driven by the NLRP3 inflammasome. https://pubmed.ncbi.nlm.nih.gov/27733681/

Interferon-y (intensive exercise also is ifn-y), Interferon-α (IFN-a) and inflammatory cytokines IL-1β, IL-6 and TNF-a, have all been shown to induce metallothioneins which can reduce zinc availability and uptake. NLRP3 leads to IL-1 and IL-6, and IL-18. Interleukin-18 (IL-18) synergizes with IL-2 to enhance cytotoxicity, interferon-gamma (IFN-y) production, and expansion of natural killer cells
 
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LINE

Senior Member
Messages
845
Location
USA
Update: The appearing issue looks like methylation pathways. Methylation should be looked at a complete cycle with many players @datadragon suggests. TMG as a repeat did not work, but other methylation participants did (example taurine, cysteine, methionine and various b vitamins).

My blood pressure fell significantly following these methods.