A couple of colleagues recently presented some interesting information on a topic called the Aryl Hydrocarbon Receptor, and think it may be a major player in chronic illness, and the world of Long Haul and CFS. Interestingly enough its directly connected to a few other pathways and mechanisms, importantly, the NMDA receptors, and Robert Phaire's metabolic trap. For those of you, who have issues related to Glutamate Excitotoxicity and or over activation of NMDA receptors, you will want to dive in here.
The Aryl Hydrocarbon receptor can stimulate the NMDA receptors, and also interestingly enough gets stimulated itself by some of the following:
LPS - From Gram Negative Bacteria (um, hello C Diff)
Arachadonic Acid (Hello PLA2, TNFA, and platelet activation)
High homocysteine (hello low B6, sulfur issues)
Polycystic Aromatic Hydrocarbons (Air Pollution)
Excess quinolinic acid, due to a block in converting quinolinic acid into picolinate acid (hello zinc picolinate).
But wait, there is more, AHR can stimulate IDO1 (oh wait, isn't that related to Robert Phaire's metabolic trap theory...?, yep, that is right).
What calms down the the NMDA receptors ? Zinc.
Also interestingly enough the AHR receptor, is connected to :
Mast Cells and the KIT genes
Ooooh, AHR is connected to mast cells. That is interesting!.
How do we calm all this down!?
There are several known compounds that inhibit the AHR receptor, and I will b trialing some combinations of different things that also help out the metabolic trap. Dang, that sounds interesting!
What else calms down the AHR receptor? Methyl B12 and Methyl Folate. And guess what patterns i see in folks who struggle here? Mutations on the folate receptors, and mutations on the B12 transport genes (TCN1, TCN2, TCN3) in addition to additional demand for Methyl B12 (MTR, MTRR). Even better, these folks tend to also have issues with B2 transport, and transport of one or more of the following: Selenium, Iodine, and Molybdenum. Uh, oh. And based on the work of Dr. Greg Jones, selenium, iodine, and molybdenum are needed to enable B2, while Methyl B12 needs B2 to become functional. There seems to be a whole stack of things that get lined up related to the AHR receptor.