Timaca
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Created in 2008, Phoenix Rising is the largest and oldest forum dedicated to furthering the understanding of, and finding treatments for, complex chronic illnesses such as chronic fatigue syndrome (ME/CFS), fibromyalgia, long COVID, postural orthostatic tachycardia syndrome (POTS), mast cell activation syndrome (MCAS), and allied diseases.
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ahmo~ Thanks for your reply. The link does work when I click on it.....wonder why it didn't work for you......I have not heard about FMN. Thanks for the suggestion!!!@Timaca I got there w/ your blog address in signature; the one in your message didn't go anywhere.
Here's to the histamine journey. BTW, I had remarkable results in my histamine response when I started FMN form of B2. Possibly especially good for MAO snps. I wrote about it, in my signature.
I don't know......haven't been tested for copper. I will check into that......thanks for the suggestion!DAO is copper dependent ...maybe you are lacking in copper?
BTW, I had remarkable results in my histamine response when I started FMN form of B2.
DAO is copper dependent ...maybe you are lacking in copper?
I don't know the mechanism. it was suggested as an important co-factor for MAO, and as I reported in my blog, it's essentially eliminated my need for ongoing antihistamine and mast cell stabilizers, including Neuroprotek. I had no expectations for what I'd experience when I began it. It's significantly reduced my supps bill, as also my antioxidant needs decreased.@ahmo sorry if you have explained this before but how does FMN affect histamine and MCAS? Is it a certain brand or amount that you take? Do you take it prior to meals with other pre-food meds?
Well DAO .the enzyme that degrades histamine is copper dependent..partially & I am guessing I am copper deficient cos a supplement called proper copper has given me a big boost recently....it's Mitosynergy. They have a website by that name.
Copper.".bioavailable copper etc is big in certain circles right now.
I don't know the mechanism. it was suggested as an important co-factor for MAO, and as I reported in my blog, it's essentially eliminated my need for ongoing antihistamine and mast cell stabilizers, including Neuroprotek. I had no expectations for what I'd experience when I began it. It's significantly reduced my supps bill, as also my antioxidant needs decreased.
What is FMN?
Some people can't break down the co-factors. I am one of them and need to take a sublingual, co-enzymated type of B2 where the "job has already been done."Riboflavin (vitamin B2) is part of the vitamin B group. It is the central component of the cofactorsFAD and FMN...
http://forums.phoenixrising.me/index.php?threads/b2-i-love-you.15209/page-42#post-532708
aaron_c:I feel like I have not been thinking about b2 use as a cofactor in the right sense, so I wanted to share what I found.
The question I had recently is what Christine/DogPerson meant by B2 being “used up” by various other vitamins. Is it used up like ATP gets used up and becomes ADP? Or is it used up because there are more enzymes that require FMN (flavin mononucleotide, aka riboflavin-5-phosphate) as a prosthetic group--meaning it is more like a wrench that all flavoproteins (proteins using FMN or FAD) have to share.
At least in the case of recycling vitamin k via http://en.wikipedia.org/wiki/NADPH:quinone_reductase, and B6 by http://en.wikipedia.org/wiki/Pyridoxine_5'-phosphate_oxidase, the FMN is not “used up,” but is simply necessary for the enzyme to function. I also found an entry for a quinone oxidoreductase that did not mention NAD(P)H as a reactant...but looking around on biogps.org, all I could find was something that probably used NADPH...
What I take from all this is that the reason why B2 can take time to go from depleted to replete is that it is “stored” in the enzymes that use it. Obviously the picture is somewhat more complicated. It seems to me like b2 acts a little like something that is stored and a little like something that gets excreted fairly quickly.
http://forums.phoenixrising.me/inde...-histrelief-histame-daosin.10565/#post-186493
Rich VanK...links 2 research papers I’m guessing that you are referring to FMN. (There are two active coenzyme forms of vitamin B2, i.e. FMN and FAD. FAD is not available as a supplement in the U.S., but it is available in Japan as a prescription, and I think it’s also available in Scandanavia and in Russia.)
In rats (see below) and presumably also in humans, both the active forms of riboflavin are dephosphorylated in the gut before absorption, so if there is a deficiency in flavokinase, it would be a good idea to take sublingual FMN. If there is a deficiency in FAD synthetase (I have encountered one person with this, but it is pretty rare, I think) then prescription sublingual FAD would be the way to go.
1 pg thread re co-enzymated Bs, w/ links :http://forums.phoenixrising.me/index.php?threads/b2-i-love-you.15209/page-42#post-533072
If it helps, out of ALA, NAC, taurine, and denatured whey, only NAC, taurine, and denatured whey would contribute to ammonia, while all four would contribute sulfur. From what you quoted above, b2 should help convert toxic sulfites to helpful sulfates. However, I may have found the answer
As you probably know, sulfites and converted to sulfates by sulfite oxidase, which utilizes molybdenum. Some people (myself included) find that we need to take a relatively high amount of molybdenum, else we run into sulfur issues. But I have been wondering if sulfur was not the only drain on molybdenum, and your case might be indicating this.
Although sulfite oxidase is not a flavoprotein (it does not use B2), xanthine oxidase, which also uses molybdenum, is. Xanthine oxidase interconverts hypoxanthine, xanthine, and uric acid. Uric acid, according to wikipedia (citing a study I cannot immediately get access to) accounts for “over half the antioxidant capacity of blood plasma” in humans. Perhaps what happened is that when you added B2, your body increased the activity of xanthine oxidase in order to make more uric acid from xanthine and hypoxanthine, thus quenching some free radicals. In doing so, it also stole molybdenum from sulfite oxidase, making it unable to convert sulfites to sulfates. If this all is the case, it seems like taking extra molybdenum might fix the problem.
Of course, as with any attempt to find a new equilibrium after changing supplement doses, even if this is right, it might not prove to be the end of the story. But perhaps we can hope.
If you would like to visualize this (I know this helps me) check out http://biochemical-pathways.com/#/map/1 and type “xanthine” into the search box. Hypoxanthine is beneath it, and uric acid (they call it urate) is to the right.