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Levodopa + EGCG + Quercetin = ?

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It seems I was overly enthusiastic about all this.. Anyway simply put, the initial theory was that perhaps a nutraceutical regimen could mimic the effects of Dr. A's COMT study. This would involve EGCG (decarboxylase inhibitor -> mimicking carbidopa), Quercetin (COMT inhibitor -> mimicking Tolcapone), and Mucuna Pruriens (contains L-DOPA.. enough said).

That theory lead me to uncover a model for treating HPPD, namely:

HPPD = Sensory Gating Deficits characterized by disinhibition of the visual apparatus (visual cortex/occipital lobe in particular), and inhibition of other cortical regions.
Sensory Gating Deficits and neuronal excitability can both be altered in various ways, leading to many possible ways of treating HPPD.
One of these would be NIBS (non-invasive brain stimulation), such as HD-tDCS (IMO the best option, as it exhibits the most precise targeting of regions of any NIBS method).

Yeah, those are the basics. Maybe most of you knew this already, but for me it took quite the time to extract this from all the scientific jargon.
Either way, thought I would come back here to simplify this for those of you who are just merely beginning to research HPPD, as a push in the right direction.

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