Thanks! You've inspired me to start working on the update more consistently.
Interesting development regarding enzymes: some studies mention that CES1 is primarily (if not exclusively) found in the liver, while CES2 resides in the gastrointestinal tract. Why does that matter? I started to question how effective CES1 is at metabolizing salvinorin A, and wondered if maximizing absorption speed—even via the portal vein—would be effective. However, this development only further suggests that lymphatic absorption is key to avoiding metabolism. Inhibiting CES1 still seems impractical and/or unsafe, as it "is the most abundant drug-metabolizing enzyme in human livers." I'm no longer considering oils (like EVOO and C8) as effective ingredients for simpler formulations.
The logical route continues to be:
Phosphatidylcholine + water triggers the release of bile salts and forms an emulsification. This allows salvinorin A to rapidly incorporate into mixed micelles, which can then tranfer lipids + lipophilic compounds to entyerocytes before getting packaged into chylomicrons (lymphatic absorption to the bloodstream).
Adding a delay between lecithin (phosphatidylcholine) and Salvia divinorum powder—the current recommended method in "Crude" Salvine Tek V02.00—is important for maximizing absorption and improving consistency. A syrup likely won't be sufficient when compared to basic extract packaged in a specialized capsule system, so that is ultimately what must be done for "Pharma" Salvine Tek. Pill designs are now in the works.
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