MCAS, COVID & Cancer: Advanced Genetics Part 2

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Summary
  • New genetic research updates in inflammatory conditions
  • Roles of RANTES, sCD40L, Thromboxane-A2, Veg-F, Nitric Oxide, Arachadonic Acid, PLA-2, histamine, IL-6
  • Research backed pathway supports
Transcript
Bob Miller, CTN

endothelial nitric oxide, and we have a substance called BH4, combined with oxygen, something called NADPH, and L-arginine to make nitric oxide. eNOS enzyme does that. And it’s also NADPH-dependent. This is what won the Nobel Prize in 1998 for circulation support from nitric oxide. However, here’s your eNOS enzyme. I’m sorry, your iNOS enzyme or NOS2, when we’re faced with bacteria, virus, fungus, or parasites, kicks in, makes a lot of nitric oxide to kill the pathogen. Good thing? Of course, unless it’s excessive. Tissue damage, organ dysfunction. Now, there’s also something called NOS uncoupling. BH4, tetrahydrobiopterin it’s a biopterin and four hydrogens, donates to make the nitric oxide. If this guy’s running too fast and too long, we run out of BH4. Now, when BH4 does its job, it turns into BH2, two hydrogens. Quite simply it has to be recycled. But there are genetic mutations QDPR, not enough NADPH. And we’re not gonna get into it today, but there’s two pathways that we make BH4. And we can actually have mutations along these paths here. It actually comes from the citric acid cycle. And then we need methyl folate, and we can have genetic mutations along here that we don’t make enough BH4. When we don’t have enough BH4, rather than making nitric oxide, we make superoxide free radical. Bad guy, combines with nitric oxide, makes something worse called peroxynitrite, further suppresses your BH4. And here is another pathway that feeds upon itself. Now, I’ve been talking about this for a while. It’s only in the last couple of months that we realized that histamine is one of the things that pushes this from the mast cells. 

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