"Some people have reported Psychedelic effects from Mixing just Coffee, Almond, Cinnamon, Vanilla and Nutmeg" -Oilahuasca Forum, Herbpedia
The Concept behind this is based on known Science around MAOIs (Ayahuasca), and then Nutmeg unlocked the knowledge of Enzymes because it shows to only be effective when both Chemicals from Nutmeg are present. This is also similar to using Vanilla or Cinnamon to get more Drunk by depleting Glutithione (which works). This is also why some Meds say “DO NOT TAKE WITH GRAPEFRUIT” because of Enzyme activation and inhibition.
http://herbpedia.wikidot.com/oilahuasca-activators (http://herbpedia.wikidot.com/oilahuasca-activators)
Pepper (Pepperidine)
Anise Oil, B9, Valerian Root (Chinese Origin)
L-Lysine
Vanilla, Cinnamon
German Chamomile, Cayenne Pepper Capsule, Tangerine Skin extract/capsules
Almond Extract, Anise Oil, Cinnamon, Lemon Peel oil, Lime Peel oil, Cigarette/Nicotine Gum
CBD, Echinacea Purea, Pomegranate, Pummelo, Calamus Oil
Clove oil, Catechin, Dill Seed oil, Goldenseal
Apiole (Parsley)
Dillapiole (Dill Seed)
Sesamol (Sesame Seed)
Vanillin (Vanilla)
Ethyl Vanillin (Fake Vanilla)
Elemicin (Nutmeg)
y-Asarone (Acorus)
Myristicin (Nutmeg)
Sarisan (Piper affinis hispidinervum)
Croweacin (Crowea saligna)
Safrole (Sassafras)
Methyl Eugenol (Huon Pine)
Chavibetol (Piper betel)
Methyl Chavicol (Basil)
Eugenol (Clove)
Hydroxychavicol (Piper Betel)
Chavicol (Piper Betel)
Graviola- 5-HT1a Agonist
Black Cohosh- 5-HT1A, 5-HT1D & 5-HT7 Binding
C. Foetida L.- 5-HT1A Agonist
Yokukansan- 5-HT1A Agonist
DMT hits all of these, and can be found in tons of plants.
Black Cohosh- 5-HT1D maybe Rhodiola rosea, Albizia lebbeck & Albizia julibrissin.
5-HT1 Receptor Agonists: Turmeric, Ginger, Ginko Bilboa, Lemon Essential Oil, Rauwolfia, Valerian, Yohimbe
Estragole (in Sweet Basil)- 5-HT2A Agonist
Safrole (in Sassafras)- 5-HT2A Agonist
Cinnamon Bark- CYP2A6 & CYP2E1 Inhibitor (It will deplete your liver's Glutithione) Taken 1 Hour before Allybenzene,
Clove Leaf- CYP2C9, CYP3A4, CYP1A1 & CYP1B1 Inhibitor
German Chamomile- CYP1A2 Inhibitor (Caffeine may also do this) GoldenSseal & Echinacea purpurea very effectively do the same thing.
Black seed oil, 50% EGCG, Valerian root oil, Pomegranate, Vitamin B9, 40% Ellagic extract, Rooibos 20% Gallic acid extract, Rutin, B3 & Kudzu
AllylBenzenes
Anethole, Apiol, Asarone, Carpacin, Chavibetol, Chavicol, Dillapiole, Eugenol, Isoeugenol, Isosafrole, Methyl Eugenol, Methyl Isoeugenol, since Cinnamon is a Phenylpropanoid, and Phenylpropanoids are made from Phenelalamine, and people who took Phenelalamine claim to get better results. I decided to post a list of Phenylpropanoids also. Caffeyl Alcohol, Cinnamaldehyde, Cinnamyl alcohol, alpha-Cyno-4-hydroxycinnamic acid, Ethyl Cinnamate, Lignin, 2,4-Methlenedioxypropiophenone, Neoflavonoids, Nordihydroguaiaretic acid, Phenylpropanoic acid, Phloretic acid, Rhododendrin & Suberin.
Star Anise Extract or B9 for CYP2C9 Induction
NMDA Receptor Plants:
Uncaria Rhynchophyllia
Psychotria Colorata
Huperzia Serrata
Most important things:
CYP2C9 Induction Alcohol Dehydrogenase Induction
Aldehyde Dehydrogenase Inhibition
Piperidine and or Dimethylamine Supplementation
Methyl from foods
Exercise or compounds that produce effects like exercise
Less important, but still factors:
SSAO Inhibition (Caffeine, Phenethylamine, Phenelalamine, Tryptamine)
MAO-A Induction
MAO-B Induction
NDMA Antagonism
Prolactin Inhibition
Hungarian Parsley Seed is a better source of Myristicin than Nutmeg. The effects of it when activated properly are said to be like Mescaline and MDMA together. The P450 Enzymes CYP1A2 & CYP3A4 are what break this down and need to be inhibited. CYP2D6 could also play a big role.
Elmicin is something you either need Chromotography type knowledge to get, or you have to buy it in small quantities. When activated properly it is like Mescaline, when activated wrong it is like Melatonin (sleepy). CYP1A1, CYP1B1, CYP1A2, CYP2A6, CYP2C9, CYP2A6, CYP2C9 & CYP2E1 are what are needed to be inhibited to activate this. CYP2D6 could also play an important role. Safrole is like MDMA when activated properly and like Melatonin when not. CYP2A6, CYP2C9, and CYP2E1 are most important for this. CYP2D6 could also be important. Methyl Chavicol when activated properly is like a light speedy LSD, when activated wrong it is said to be almost like Marijuana. CYP1A2 and CYP2A6 inhibit it, and CYP2D6 could also be important. If the CYP2D6 Enzyme is inhibited with all the others, these are possibly visually hallucinogenic Oilahuascas. And the Methyl Chavicol doesn't build a tolerance (the others do) it actually gets stronger for you every time you use it, or you can use less.
“Several allylbenzenes have been proven to form up to 3 alkaloid metabolites after ingestion by several animals.[2][3] They do not form amphetamines in vivo as has been speculated in the past. The alkaloids detected in animal urine are tertiary aminopropiophenones of 3 possible subtypes: dimethylamines, piperidines, and pyrrolidines.[1][2][3][4] The allylbenzene elemicin has been proven to form all 3 different alkaloid metabolites after ingestion in animals by analyzing urine using gas-liquid chromatography and chemical ionization mass spectrometry.[1] Safrole is also proven to form all three alkaloid metabolites after ingestion.[2] Myristicin appears to only form piperidines and pyrrolidines. Dimethylamines of myristicin have not been detected.[3] Allylbenzene, from which all allylbenzenes are derived, forms piperidine and dimethylamine alkaloids.[4] Propenylbenzene and its derivatives (asarone, anethole, etc.) do not form alkaloid metabolites.[4]”
CYP Enzymes (Drug Metabolism, etc)
(
)
Induction and Inhibition (Anti-Oxidants, etc)
(
)
All inhibitors of oxidative 17bHSD2 will prevent activation of allylbenzenes. This enzyme must be induced, not inhibited. It's the single most important enzyme to induce. If oxidative 17bHSD2 is not functioning, allylbenzenes cannot produce psychedelic activity. Naringenin also potently inhibits 17bHSD2. Grapefruit contains large amounts of naringenin, and also prevents the psychedelic action of allylbenzenes if taken before allylbenzenes. Inhibition lasts approximately 4-8 hours.
The Concept behind this is based on known Science around MAOIs (Ayahuasca), and then Nutmeg unlocked the knowledge of Enzymes because it shows to only be effective when both Chemicals from Nutmeg are present. This is also similar to using Vanilla or Cinnamon to get more Drunk by depleting Glutithione (which works). This is also why some Meds say “DO NOT TAKE WITH GRAPEFRUIT” because of Enzyme activation and inhibition.
http://herbpedia.wikidot.com/oilahuasca-activators (http://herbpedia.wikidot.com/oilahuasca-activators)
Pepper (Pepperidine)
Anise Oil, B9, Valerian Root (Chinese Origin)
L-Lysine
Vanilla, Cinnamon
German Chamomile, Cayenne Pepper Capsule, Tangerine Skin extract/capsules
Almond Extract, Anise Oil, Cinnamon, Lemon Peel oil, Lime Peel oil, Cigarette/Nicotine Gum
CBD, Echinacea Purea, Pomegranate, Pummelo, Calamus Oil
Clove oil, Catechin, Dill Seed oil, Goldenseal
Apiole (Parsley)
Dillapiole (Dill Seed)
Sesamol (Sesame Seed)
Vanillin (Vanilla)
Ethyl Vanillin (Fake Vanilla)
Elemicin (Nutmeg)
y-Asarone (Acorus)
Myristicin (Nutmeg)
Sarisan (Piper affinis hispidinervum)
Croweacin (Crowea saligna)
Safrole (Sassafras)
Methyl Eugenol (Huon Pine)
Chavibetol (Piper betel)
Methyl Chavicol (Basil)
Eugenol (Clove)
Hydroxychavicol (Piper Betel)
Chavicol (Piper Betel)
Graviola- 5-HT1a Agonist
Black Cohosh- 5-HT1A, 5-HT1D & 5-HT7 Binding
C. Foetida L.- 5-HT1A Agonist
Yokukansan- 5-HT1A Agonist
DMT hits all of these, and can be found in tons of plants.
Black Cohosh- 5-HT1D maybe Rhodiola rosea, Albizia lebbeck & Albizia julibrissin.
5-HT1 Receptor Agonists: Turmeric, Ginger, Ginko Bilboa, Lemon Essential Oil, Rauwolfia, Valerian, Yohimbe
Estragole (in Sweet Basil)- 5-HT2A Agonist
Safrole (in Sassafras)- 5-HT2A Agonist
Cinnamon Bark- CYP2A6 & CYP2E1 Inhibitor (It will deplete your liver's Glutithione) Taken 1 Hour before Allybenzene,
Clove Leaf- CYP2C9, CYP3A4, CYP1A1 & CYP1B1 Inhibitor
German Chamomile- CYP1A2 Inhibitor (Caffeine may also do this) GoldenSseal & Echinacea purpurea very effectively do the same thing.
Black seed oil, 50% EGCG, Valerian root oil, Pomegranate, Vitamin B9, 40% Ellagic extract, Rooibos 20% Gallic acid extract, Rutin, B3 & Kudzu
AllylBenzenes
Anethole, Apiol, Asarone, Carpacin, Chavibetol, Chavicol, Dillapiole, Eugenol, Isoeugenol, Isosafrole, Methyl Eugenol, Methyl Isoeugenol, since Cinnamon is a Phenylpropanoid, and Phenylpropanoids are made from Phenelalamine, and people who took Phenelalamine claim to get better results. I decided to post a list of Phenylpropanoids also. Caffeyl Alcohol, Cinnamaldehyde, Cinnamyl alcohol, alpha-Cyno-4-hydroxycinnamic acid, Ethyl Cinnamate, Lignin, 2,4-Methlenedioxypropiophenone, Neoflavonoids, Nordihydroguaiaretic acid, Phenylpropanoic acid, Phloretic acid, Rhododendrin & Suberin.
Star Anise Extract or B9 for CYP2C9 Induction
NMDA Receptor Plants:
Uncaria Rhynchophyllia
Psychotria Colorata
Huperzia Serrata
Most important things:
CYP2C9 Induction Alcohol Dehydrogenase Induction
Aldehyde Dehydrogenase Inhibition
Piperidine and or Dimethylamine Supplementation
Methyl from foods
Exercise or compounds that produce effects like exercise
Less important, but still factors:
SSAO Inhibition (Caffeine, Phenethylamine, Phenelalamine, Tryptamine)
MAO-A Induction
MAO-B Induction
NDMA Antagonism
Prolactin Inhibition
Hungarian Parsley Seed is a better source of Myristicin than Nutmeg. The effects of it when activated properly are said to be like Mescaline and MDMA together. The P450 Enzymes CYP1A2 & CYP3A4 are what break this down and need to be inhibited. CYP2D6 could also play a big role.
Elmicin is something you either need Chromotography type knowledge to get, or you have to buy it in small quantities. When activated properly it is like Mescaline, when activated wrong it is like Melatonin (sleepy). CYP1A1, CYP1B1, CYP1A2, CYP2A6, CYP2C9, CYP2A6, CYP2C9 & CYP2E1 are what are needed to be inhibited to activate this. CYP2D6 could also play an important role. Safrole is like MDMA when activated properly and like Melatonin when not. CYP2A6, CYP2C9, and CYP2E1 are most important for this. CYP2D6 could also be important. Methyl Chavicol when activated properly is like a light speedy LSD, when activated wrong it is said to be almost like Marijuana. CYP1A2 and CYP2A6 inhibit it, and CYP2D6 could also be important. If the CYP2D6 Enzyme is inhibited with all the others, these are possibly visually hallucinogenic Oilahuascas. And the Methyl Chavicol doesn't build a tolerance (the others do) it actually gets stronger for you every time you use it, or you can use less.
“Several allylbenzenes have been proven to form up to 3 alkaloid metabolites after ingestion by several animals.[2][3] They do not form amphetamines in vivo as has been speculated in the past. The alkaloids detected in animal urine are tertiary aminopropiophenones of 3 possible subtypes: dimethylamines, piperidines, and pyrrolidines.[1][2][3][4] The allylbenzene elemicin has been proven to form all 3 different alkaloid metabolites after ingestion in animals by analyzing urine using gas-liquid chromatography and chemical ionization mass spectrometry.[1] Safrole is also proven to form all three alkaloid metabolites after ingestion.[2] Myristicin appears to only form piperidines and pyrrolidines. Dimethylamines of myristicin have not been detected.[3] Allylbenzene, from which all allylbenzenes are derived, forms piperidine and dimethylamine alkaloids.[4] Propenylbenzene and its derivatives (asarone, anethole, etc.) do not form alkaloid metabolites.[4]”
CYP Enzymes (Drug Metabolism, etc)
Induction and Inhibition (Anti-Oxidants, etc)
All inhibitors of oxidative 17bHSD2 will prevent activation of allylbenzenes. This enzyme must be induced, not inhibited. It's the single most important enzyme to induce. If oxidative 17bHSD2 is not functioning, allylbenzenes cannot produce psychedelic activity. Naringenin also potently inhibits 17bHSD2. Grapefruit contains large amounts of naringenin, and also prevents the psychedelic action of allylbenzenes if taken before allylbenzenes. Inhibition lasts approximately 4-8 hours.
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