Vesicular monoamine transporter 2

In 2004, geneticist Dean Hamer popularized the idea of the God gene.

His hypothesis focused on the VMAT2, which is a gene involved in transporting neurotransmitters such as dopamine and serotonin within brain cells.

Now, Hamer proposed the genetic variations might influence how receptive someone is to mystical experiences or feelings of connection to something greater than themselves.

So his specific VMAT2 association was never convincingly established through independent replication.

And so if human brains have inherited, I guess, this biological characteristic that makes spiritual experiences possible or influence their frequency or or even a lot of what people say they experience today.

The question would be, is it reasonable to ask how those characteristics evolved? And the question is whether they were deliberately introduced to another or I guess not to, but by another intelligence.

The whole idea is these are all different weapons that we have to targeting this crappy disease.

So you could be on Botox and, uh, uh, and one of the VMAT2 inhibitors-

Yes

...

Well, it's one-

That's where we come in

... th- that is the good news, is that, number one, that there are things beyond that, because a lot of folks are dealing with people, they don't maybe have a new movement disorder specialist like yourself who is, um ... has that broad base of knowledge to be able to go ahead and, you know, maybe they're just dealing with their psychiatrist or neurologist who are just saying, "Well, we've tried the VMAT2 inhibitors.

For s- for whatever reason, it didn't, it didn't give you the results that we were hoping.

Sometimes the truth is upsetting, but the truth is the truth.

So here we have this article, Loss of Vesicular Monoamine Transporter 2 in Striatum of Long COVID and Relationship to Neuropsychiatric Symptoms, was published in eBioMedicine.

Um, so this is basically like COVID is, is causing Parkinson's disease, basically.

So this is a case control study, and it was done August 2022 through April 2025 in Toronto, Canada.

Two, first-generation drugs with higher D2 affinity cause more TD than lower affinity drugs.

Three, the VMAT2 inhibitors, which deplete presynaptic dopamine, treat it.

All three point at the same receptor.

Okay, but that model has a problem, doesn't it? It has a big problem.

The ones that show up at year 8, not year 1...

No cure exists.

VMAT2 inhibitors suppress.

They don't reverse.

Ibogaine and Norbogaine are non-competitive inhibitors of SIRT, the serotonin transporter, and DAT, the dopamine transporter.

They also exhibit submicromolar inhibition of VMAT2, which is the vesicular monoamine transporter, and OCT2, the organic cation transporter 2.

Finally, they show moderate to high binding affinity for sigma-2 receptors, which are highly associated with intracellular lipid and calcium signaling, and crucially are implicated in rapid neuronal repair.

I want to pause on VMAT2 for a second because I think it beautifully illustrates how deep this mechanism goes.

We talk about dopamine release, but when a neuron fires, it doesn't just blindly squirt out raw dopamine into the void.

No,

Right.

The dopamine has to be carefully, meticulously packaged into little cellular delivery trucks called vesicles.