Kava and Shaivism

[SashaShiva]

I have been using Kava Kava since I was about 15 or 16 years old. I use Marihuana Religiously as a Hindu Shaivite, and if you don't know what that is the easiest way to understand it is like Ancient Rastafarianism from India, which is not just a comparison but a fact, Jamaica is the West Indies because Christopher Columbus thought he was in India. But that is another Subject.

Kava is related to Pepper, another Cousin of theirs' is Uziza Leaf, which contains Caryophyllene which is a Canna-Mimetic which is FDA approved as a food additive. There are Black Peppercorns, Green Peppercorns, White Peppercorns, Red Peppercorns, etc. A similar family is Mint, there is Pepper Mint, Spear Mint, Catnip, all in the same family and related to Motherworth/Marihuilla, Wild Dagga, and Clip Dagga. This overall family is an interesting one to look in to.

The first time I used Kava Kava a friend was telling me there were capsules we could buy at a Healthfood/Vitamin/Herb shop that would make Marihuana stronger. So we go in an buy an extract in capsules. The extracts is a shiny dark brown or black inside the capsules and I can't remember how we tried it first, but we eventually tried it all different ways, we ate the capsules, we broke them open aand made drinks, and we put it ontop of Marihuana and smoked it. And it definitely has Synergy with Marihuana. The best way in my mind to describe the taste is like a mix between chlorine like pool water boiled down (like Cuban coffee boiling) and dirt, even when smoked. So capsules is best.

After that I learned about Kavalactones. I got a lb or Kilo of raw root powder and had it for years using it with groups of Friends as Tea every once in a while, always warning them it tasted like Dirt Water.

Then learned about Yangonin. Yangonin is a Kavalactone that hardly anyone knows about, and it is a Canna-mimetic, which means it hits the Cannabinoid receptor but is not found in Cannabis. This is likely the Molecule that gives Kava Kava the great synergy with Marihuana. It is rarely isolated, but should be isolated more often a studied. You will not find a Yangonin product online yet, but that is probably the future of Kava Kava.

 

[SashaShiva]

Here is the only super pure Kava Extract I have ever seen

 

[Darcy Jay Strutt]

Interesting stuff

I wonder if Kavalactones,(and possibly the tiny amounts of other alkaloids found in kava) in their varying amounts exhibit an “Entourage Effect” similar to cannabis’s various cannabinoids and terpenes which in their varying amounts provide slightly different “highs”?


It may be that by isolating kavalactones that the experience becomes dull and without character as is often noted by those consuming pure THC.

 

[kasa_balavu]

You will not find a Yangonin product online yet, but that is probably the future of Kava Kava.

No.

 

[verticity]

I'm skeptical that yangonin's CB1 affinity contributes significantly to the pharmacology of kava. Yangonin has been experimentally shown by one research group to have an affinity for CB1 receptors that is quantitatively much weaker than THC, and whose qualitative nature is unknown (i.e. whether it is an agonist or has some other effect). That research is summarized here:

http://members.iif.hu/ujvary/Drugs/Ujvary2012-ICRS-kava-presentation.pdf

More recently others have done computational studies of it along with other CB ligands. I cannot discern any particular conclusion vis a vis yangonin from this work other then "our computer model is cool and sort of works!" For example:

http://bcc.bas.bg/BCC_Volumes/Volume_50_Special_B_2018/BCC-50-SI-B-2018-Sapundzhi3-44-48.pdf

So it might be that synthetic yangonin analogs with higher CB activity might in the future be useful medically, but, in my opinion, it's really only an odd and probably insignificant footnote in the richly complex psychopharmacology of the authentic, traditional kava drink.

 

[SashaShiva]

You all seem confused, CB1 Affinity is CB1 Affinity is CB1 Affinity, there is hardly a negligible activation of CB1 in existence

This is Yangonin
affinity for the cannabinoid receptor CB1 (Ki = 0.72 μM),

μM
1 uM = 1000 nM

Molar concentration - Wikipedia

en.m.wikipedia.org

The answer is 1000000000. We assume you are converting between nanomole and mole. You can view more details on each measurement unit: nanomoles or mole The SI base unit for amount of substance is the mole. 1 nanomoles is equal to 1.0E-9 mole.

It is similar to meters, US Measurements and Metric are different but all Metric are basically the same based on 10 fingers.

1 nanometer = 0.001 micrometer
A nanometer is 1000 times smaller than a micrometer. 1 micrometer (μm) = 1000 nanometers.

IC50 - Wikipedia

en.m.wikipedia.org

Two agonists with similar binding affinity, different activity

Binding affinity data alone does not determine the overall potency of a drug.

Ki, the inhibitor constant

The inhibitor constant, Ki, is an indication of how potent an inhibitor is; it is the concentration required to produce half maximum inhibition.

Plotting 1/v against concentration of inhibitor at each concentration of substrate (the Dixon plot) gives a family of intersecting lines.

For a competitive inhibitor, the lines converge above the x axis, and the value of where they intersect is -Ki

For a non-competitive inhibitor, the lines converge on x axis, and the value of where they intersect is -Ki

This is NM-2201 a rather common cannabinoid, dose at about 5mg smoked, fairly potent. Definitely has a strong Marihuana like effect
binding affinity of 0.332 nM at CB1

This is JWH-018 which is stronger than THC, feels very much like THC. Less plastic feeling than all synthetics
reported binding affinity of 9.00 ± 5.00 nM at CB1

And just as an example, Yangonin is plenty strong. This is AB-FUBINACA

Ki values of 0.9 nM at CB1 and 23.2 nM at CB2and EC50 values of 1.8 nM at CB1 and 3.2 nM at CB2

It doses in Micrograms like LSD, and it kills people who take too much. I would never even ingest something like this, but all over Dallas this is now what people put in K2, called Thunderchicken in Dallas now. So Yangonin is plenty strong, I wouldn't want a Cannabinoid that was much stronger than Yangonin in any situation, outside of Religious Marihuana, anyway.

This is THC

the cannabinoid receptorCB1 (Ki = 10 nM), and the CB2 receptor (Ki = 24 nM)

These are Endocannabinoids which exist naturally in your brain

anandamide (AEA) by the Mechoulam group in 1992 confirmed its role as an endogenous ligand for the CB receptors, with a Ki of 61.0 nM at CB1 and 1,930 nM at CB2.

Sea Urchin Roe and Truffle Oil contain anandamide

Truffle oil - Wikipedia

en.m.wikipedia.org

Fine Points

The rich, gloriously weird sea urchin is a frontier even for adventurous omnivores.

www.forbes.com

2-arachidonoylglycerol (2-AG), with Ki values of 472 ± 55 nM at CB1 and 1,400 ± 172 nM for CB2, O-arachidonoyl ethanolamine, with Ki values of 1,900 nM at CB1 and 1,400 nM at CB2, and 2-arachidonoyl glycerol ether, with Ki values of 21.2 nM at CB1 and 480 nM at CB2

 

[verticity]

Ki, the inhibitor constant

The inhibitor constant, Ki, is an indication of how potent an inhibitor is; it is the concentration required to produce half maximum inhibition.

If you read that definition of the inhibitor constant, Ki, carefully It implies that Ki is inversely proportional to affinity. It refers to the concentration needed to have an inhibiting effect. A larger number means a higher concentration is needed. Nanomolar (like THC, etc.) is strong; micromolar, like yangonin, implies an orders-of-magnitude weaker affinity.

If you read the original paper (attached) that is made clear. In the conclusion they state: "...the binding affinity of this kavalactone [yangonin] to the CB1 receptor is measurable (Ki = 0.72 micromolar), being ~170-fold lower than that of THC..." and "...we identified yangonin as a unique and selective, though not very potent, CB1 receptor ligand..." They also point out in the paper that the type of activity (whether agonist, partial agonist, or antagonist) is unknown, and you correctly note that binding affinity alone cannot predict that. They do argue that despite it's weak affinity and unknown activity it might be pharmacologically relevant based on the fact that it's CB1 affinity at physiological concentrations might be similar to the GABAergic affinity of some of the KLs. That is the part that I'm skeptical of (and am also skeptical that the GABA effect is very significant), but it is still unknown. But it is definitely not true that yangonin is some kind of super potent cannabinoid, and that is a misconception that we need to dispel here because I see the claim made often.

 

[SashaShiva]

If you read that definition of the inhibitor constant, Ki, carefully It implies that Ki is inversely proportional to affinity. It refers to the concentration needed to have an inhibiting effect. A larger number means a higher concentration is needed. Nanomolar (like THC, etc.) is strong; micromolar, like yangonin, implies an orders-of-magnitude weaker affinity.

If you read the original paper (attached) that is made clear. In the conclusion they state: "...the binding affinity of this kavalactone [yangonin] to the CB1 receptor is measurable (Ki = 0.72 micromolar), being ~170-fold lower than that of THC..." and "...we identified yangonin as a unique and selective, though not very potent, CB1 receptor ligand..." They also point out in the paper that the type of activity (whether agonist, partial agonist, or antagonist) is unknown, and you correctly note that binding affinity alone cannot predict that. They do argue that despite it's weak affinity and unknown activity it might be pharmacologically relevant based on the fact that it's CB1 affinity at physiological concentrations might be similar to the GABAergic affinity of some of the KLs. That is the part that I'm skeptical of (and am also skeptical that the GABA effect is very significant), but it is still unknown. But it is definitely not true that yangonin is some kind of super potent cannabinoid, and that is a misconception that we need to dispel here because I see the claim made often.

I am not confused about that, in my post it outlines that Ki affinity is also not potency necessarily. And if you read JWH018 compared to NM2201 you can see that they are reversed, but JWH is better and probably actually more potent.

But Yangonin is comparable to 2-AG and Anamadine.

You are basically trying to say that because Yangonin is not AB-FUBINICA it must be weak, when Cannabinoids like that are not examples of good Cannabinoids, but in fact abominations.

Did you also see at the bottom THC and Endocannabinoids. Both are higher than almost all other Cannabinoids.

Natural Cannabinoids are closer to Yangonin.

But, it still varies on selectivity, etc. But I don't see why anyone would want a super strong Cannabinoid, it is basically an abomination apart from Cancer therapy, those cannabinoids are used in Chemo now.

 

[verticity]

I am not confused about that, in my post it outlines that Ki affinity is also not potency necessarily. And if you read JWH018 compared to NM2201 you can see that they are reversed, but JWH is better and probably actually more potent.

But Yangonin is comparable to 2-AG and Anamadine.

You are basically trying to say that because Yangonin is not AB-FUBINICA it must be weak, when Cannabinoids like that are not examples of good Cannabinoids, but in fact abominations.

Did you also see at the bottom THC and Endocannabinoids. Both are higher than almost all other Cannabinoids.

Natural Cannabinoids are closer to Yangonin.

But, it still varies on selectivity, etc. But I don't see why anyone would want a super strong Cannabinoid, it is basically an abomination apart from Cancer therapy, those cannabinoids are used in Chemo now.

My point here is that while yangonin does have some modest interaction with CB1, yes it is much much weaker than the dangerous synthetic full agonists that you mention, and also very likely much weaker than the THC in cannabis itself. In other words, it's not really comparable to any synthetic or plant-origin cannabinoids that people use recreationally or medicinally with significant effect. Kava as a whole is just a different, much milder, category of thing. It is possible that yangonin's effect might be comparable to some of the endocannabinoids (whether as an agonist like 2-AG or antagonist like O-AEA we don't know), but we all have those in our bodies right now exerting their subtle regulatory effect and they don't make us "high" do they?

 

[SashaShiva]

My point here is that while yangonin does have some modest interaction with CB1 and CB2, yes it is much much weaker than the dangerous synthetic full agonists that you mention, and also very likely much weaker than the THC in cannabis itself. In other words, it's not really comparable to any synthetic or plant-origin cannabinoids that people use recreationally or medicinally with significant effect. Kava as a whole is just a different, much milder, category of thing. It is possible that yangonin's effect might be comparable to some of the endocannabinoids (whether as an agonist like 2-AG or antagonist like O-AEA we don't know), but we all have those in our bodies right now exerting their subtle regulatory effect and they don't make us "high" do they?

Yes they do get us "high" as you are calling it. Have you ever gotten hungry before? That's CB1, do you remember Health class? They made the very childish comparison that doing drugs makes you feel the same as you do from scoring a goal in soccer or a basket in basketball, then went on to suggest that it would diminish your ability to appreciate your success. Which is a very pop pop fizz fizz view of Human Nature, and things like Psychology and Criminology are soft science, you can not apply the Scientific method to populations of behavior and get an accurate output. You can get outputs and compare outputs, but you can't always repeat it.

Like, you could raise a kid in a Bubble and make some Genius, and someone else could try it and make a Serial Killer.

Endocannabinoids effect happiness, hungryness, tiredness, bone growth, sperm cells, tumor cells, etc, etc, etc. And we have very very low doses in our brains. Kava is literally rich in substances that go to the brain.

THC isn't a super great Ki #, but people dose it higher. You don't take 5mg of THC, you take more, and 5mg is already more than you have of 2-AG and Anamadine.

I will have a Kava extract here tomorrow and we will get deeper into this.

 

[SashaShiva]

What we need, is someone who has access to Yangonin Isolate to explain their experience.

But I am not sure that exists yet, so we it needs to be Isolated commercially first.

Based on the articles posted here, which have no human experience commentary suggest this:

This image suggests Glutathione breaks these down, implying cinnamon or vanilla will make Kava hit harder and last longer. This also suggests FAAH Inhibiton, which. Drumroll... is the Endocannabinoid and Endorphin system, Kava uses 2-AG and Anandamide, that's how Kava works partially.

This is Ki Affinity, again not Human Experience. Yangonin is not highest or lowest on the list, but is on the low end.

Can someone explain why the CYP Enzyme info was removed? The people here are literally talking about Inhibitors, Inducers, Anti-Oxidants, and MAOIs, etc.

Once everyone starts to understand those concepts here, you will be able to make very intentional mixtures.

If Coffee has an effect, it is the Xanthine activity of Caffeine. People are even discussing Piperidine having an effect here, which is a base Molecule for many Psychoactive substances.

Why do you think Black Seed Oil works? Go read about how it effects your Enzymes.

Once Kava users understand Enzymes, they can make Ayahuasca type Kava mixtures.

This is Yangonin, all those O's are Oxygen. Highly reactive with Hydrogen, making H2O when they meet
View attachment 10604

This is Hydrochloric Acid found in your stomach
View attachment 10605



Black seed oil contains.

four saturated fatty acids (17.0%) and four unsaturated fatty acids (82.5%). Linoleic acid (55.6%), oleic acid (23.4%) and palmitic acid (12.5%) are its major components

anethole, p-cymene, limonene, carvone and thymoquinone

Thymoquinone
View attachment 10606

p-cymene, Hydrocarbons
View attachment 10607

CYP Enzymes (Drug Metabolism, etc)
Induction and Inhibition (Anti-Oxidants, etc)

 

[SashaShiva]

I'm skeptical that yangonin's CB1 affinity contributes significantly to the pharmacology of kava. Yangonin has been experimentally shown by one research group to have an affinity for CB1 receptors that is quantitatively much weaker than THC, and whose qualitative nature is unknown (i.e. whether it is an agonist or has some other effect). That research is summarized here:

http://members.iif.hu/ujvary/Drugs/Ujvary2012-ICRS-kava-presentation.pdf

More recently others have done computational studies of it along with other CB ligands. I cannot discern any particular conclusion vis a vis yangonin from this work other then "our computer model is cool and sort of works!" For example:

http://bcc.bas.bg/BCC_Volumes/Volume_50_Special_B_2018/BCC-50-SI-B-2018-Sapundzhi3-44-48.pdf

So it might be that synthetic yangonin analogs with higher CB activity might in the future be useful medically, but, in my opinion, it's really only an odd and probably insignificant footnote in the richly complex psychopharmacology of the authentic, traditional kava drink.

I wanted to expand on something in your PDFs you shared here. Because they have more information than you think.

These can be found in plants which are completely unregulated:

The CB2 receptor is Munchies, Immuno-activator, Anti-Epilepsy, kind of like Brain grease to oil the machine.

The CB1 receptor is pretty much everything else, Psychoactive, Tumor shrinking, etc.

FAAH is what breaks down Endorphines and Endocannabinoids. So an FAAH Inhibitor stops the breakdown.

MAGL Inhibitors are kind of Esoteric. So, to understand these it is best to understand EndoCannabinoid Reuptake Inhibitors (eCRIs). This is like an FAAH Inhibitor, but specialized for the Endocannabinoids. Tylenol is the most common, it breaks down into AM404 which is an eCRI. And MAGL seems to work on another level similar to an eCRI. https://pubmed.ncbi.nlm.nih.gov/20047159/

Oleamide is apparently also a CB1 agonist https://pubchem.ncbi.nlm.nih.gov/compound/Oleamide

And it is what makes you tired when you are sleep deprived. It uses your inner Cannabinoids to make you tired.

More FAAH Inhibitors

Inhibition of fatty acid amide hydrolase by kaempferol and related naturally occurring flavonoids - PMC

Recent studies have demonstrated that the naturally occurring isoflavone compounds genistein and daidzein inhibit the hydrolysis of anandamide by fatty acid amide hydrolase (FAAH) in the low micromolar concentration range. The purpose of the present ...

www.ncbi.nlm.nih.gov

So what the MAGL Inhibitors do is a selective Inhibitor to keep 2-AG and other Cannabinoids and Endorphins in the brain, focusing on Cannabinoids

Monoacylglycerol lipase inhibitors: modulators for lipid metabolism in cancer malignancy, neurological and metabolic disorders

Monoacylglycerol lipase (MAGL) is a serine hydrolase that plays a crucial role catalysing the hydrolysis of monoglycerides into glycerol and fatty aci…

www.sciencedirect.com

Biochemical and pharmacological characterization of human α/β-hydrolase domain containing 6 (ABHD6) and 12 (ABHD12) - PMC

In the central nervous system, three enzymes belonging to the serine hydrolase family are thought to regulate the life time of the endocannabinoid 2-arachidonoylglycerol (C20:4) (2-AG). From these, monoacylglycerol lipase (MAGL) is well ...

www.ncbi.nlm.nih.gov

Inhibition of fatty acid amide hydrolase by kaempferol and related naturally occurring flavonoids - PMC

Recent studies have demonstrated that the naturally occurring isoflavone compounds genistein and daidzein inhibit the hydrolysis of anandamide by fatty acid amide hydrolase (FAAH) in the low micromolar concentration range. The purpose of the present ...

www.ncbi.nlm.nih.gov

Most MAGL Inhibitors are permanent, the one mentioned in the Kava study is not.

It seemed to suggest some Kavalactones are also MAGLs.

Other enzymes including ABHD6 and ABHD12 may also involve in the metabolism of 2-AG but to a much less extent compared to MAGL.

a previous study showed that MAGL is responsible for approximate 85% of the 2-AG-hydrolyzing activity in mouse brain

MJN110 is a MAGL used in research

Another strategy to reduce the central side effects is to use positive allosteric modulators (PAMs) of CB1Rs rather than typical orthosteric agonists. Allosteric modulators are substances that bind to a receptor and change the response of the receptor by either increasing its affinity to agonists or its ability to be activated by agonists.

I am pretty sure Oxytocin is a positive Activity Modulator, they just haven't researched it in those words yet. They also say Indoles are PAMs so probably any smell you would say is "your favorite smell" is probably a PAM.

Oxytocin Modulation of Neural Circuits - PMC

Oxytocin is a hypothalamic neuropeptide first recognized as a regulator of parturition and lactation which has recently gained attention for its ability to modulate social behaviors. In this chapter, we review several aspects of the oxytocinergic ...

www.ncbi.nlm.nih.gov

That logically leads to Mucuna Dopa https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3942911/

and Guarana

Guarana Provides Additional Stimulation over Caffeine Alone in the Planarian Model - PMC

The stimulant effect of energy drinks is primarily attributed to the caffeine they contain. Many energy drinks also contain other ingredients that might enhance the tonic effects of these caffeinated beverages. One of these additives is guarana. ...

www.ncbi.nlm.nih.gov

These will likely be great potentiators to Kava.

This is what eats away the Oxytocin in your brain

Mechanism of Action of Prolyl Oligopeptidase (PREP) in Degenerative Brain Diseases: Has Peptidase Activity Only a Modulatory Role on the Interactions of PREP with Proteins? - PMC

In the aging brain, the correct balance of neural transmission and its regulation is of particular significance, and neuropeptides have a significant role. Prolyl oligopeptidase (PREP) is a protein highly expressed in brain, and evidence indicates ...

www.ncbi.nlm.nih.gov

Oxytocin is not very Bioavailable, very short half life, breaks down within 10min in the system. Most of the Analogues are used to cause Labor and Birth. So it is more practical to use Inhibitors that protect peptides like Oxytocin from being cleaved by the PEP and PREP enzymes. Unless you can target Oxytocin this is not something to do daily, because Inhibiting PEP and PREP will cause build up of other Peptides too. Gingko Biloba does this.

Theobromine is in Chocolate

Exploring cocoa properties: is theobromine a cognitive modulator? - Psychopharmacology

Nutritional qualities of cocoa have been acknowledged by several authors; a particular focus has been placed on its high content of flavanols, known for their excellent antioxidant properties and subsequent protective effect on cardio- and cerebrovascular systems as well as for neuromodulatory...

link.springer.com

 

[SashaShiva]

Some people seem to think Medicine went straight from Earth, Wind, Water and Fire based healing and Bloodletting with holedrilling in heads to stop headaches, to Pills. As if Herbs were the bad medicine we got away from. But it was actually much more complicated than that and it didn't even really go in a straight line, and Herbs weren't the problem. Most of the bad medicine of the past we think of wasn't even invented until the Dark Ages or right before. For example, Hippocrates invented Chiropracty in Ancient Greece then his tables and devices were reimagined to create all the torture devices used by Kings and Queens. People seem to think Herbal remedies are random, but Herbs are the Pills. Once Herbal interaction in the Human body was understood (after lots of people died eating poison, or got rashes, etc) that is where Medicine started.

Imhotep was first, 5,000 years ago, around 3000 B.C. Imhotep invented Pyramids, Columns, Stairs, Surgery and Medicine. He stated that Medicine only works "with the proper incantation" which is to say that the Placebo Effect, which is real and there is no argument about if you can be healed by the Placebo effect (it works), must be activated for Medicine to work. An Incantation is a Poem or other set of words used to bring about a Magical action. He also removed Wood from people's bodies, and preformed other Surgeries. When he died his Temple was basically the first Hospital, where people would come from far and wide to find cures. One person brought his dying mother, and he claimed to see Imhotep's ghost who said he would show him how to heal his mother if he would write a book for him, and after she was healed he wrote the book which was at the Temple for a long time. Around 1000 B.C. and into A.D. Imhotep became an Egyptian God in his Temple.

Then there was Eshmun, who was the Phoenician Imhotep. When Imhotep became a God his image spread to other Cultures, people began to travel for healing, creating places of healing (Hospital type Temples), and found healing springs, etc.

Then as Imhotep reached Greece, they didn't want him to be Black, so they made Asclepius. Asclepius is Imhotep, and his Temple, the Asclepion, was the forerunner of the modern Hospital. The Caduceus was originally the Asclepius Rod with a Snake around it, the Hermes one is now used which is a symbol of Commerce. They would induce Dreqms and the goal was for Gods to give visions to the sick about how to heal them and if it didn't work they would give people Opium and put them under to perform surgery.

Then there were Socrates, Plato, Aristotle and Hippocrates. This is kind of where Earth, Wind, Water and Fire comes from. During the time of Socrates they had some idea of herbal medicines, they made Socrates drink poison and describe it for them as he died; and Hippocrates wrote the Hippocratic oath that is said today. But Hippocrates was really the main Medical one, and the other's Philosophies were translated into some of the Earth, Wind, Water and Fire.

Then Jesus and his healing and the people coming long distances to him. Then there was Galen, who wrote the first Pharmacoepedia of Herbal remedies. This was basically a Perscription guide for healers.

In India there is Ayurveda which is a type of Preventative Medicine "an apple a day keeps the Doctor away", you have 7 layers of Health including Food, Herbs, etc. Yoga is Ayurveda. It is basically Hindu Religious medicine, and they clearly had an understanding of Phytochemicals. India has been making dyes, and smells for thousands and thousands of years, it was a Center of Trade for Ancient Spices, and was a Center of Medical studies like that of the Chakras, which were developed by cutting open dead bodies and comparing that with Health.

In China there was Chinese Medicine being made, by Emporers and Healers seeking various things from Immortality to Pain relief. And you can see looking at their medicine that they had an understanding of the effects of the Molecules in the plants, even made Teas and other extracts. This is a Chinese herbal blend clearly targeting CYP and other Liver enzymes. But in 2020 we still hardly understand this form of medicine. Yet here is an ancient Potion that is clearly designed to effect enzymes.

Sho-saiko-to

Sho-saiko-to

Sho-saiko-to or "Xiao Chai Hu Tang" is a mixture of 7 specific botanicals. The formulation is used in traditional Chinese and Japanese medicine to treat fever, gastrointestinal disorders, and some chronic liver diseases.

www.mskcc.org

Sho-saiko-to or “Xiao Chai Hu Tang” is a plant formula that is a mixture of 7 botanicals: Bupleurumroot (Chai hu), Pinellia tuber (Ban xia), Scutellaria root (Huang qin), Ginseng (Ren shen), Jujube (da zao), Licorice (Gan cao), and Ginger (Sheng jiang).

 

[SashaShiva]

Another part of how Pharmacology has gotten to where it is now. We think of Lab Rats as modern tools, but throughout history. For literally Thousands and Tens of Thousands of years as Homo Sapiens, even Neanderthals, Denisovans, maybe even so far back as Lucy, because this is basic. You don't have to see another Human being eat a berry and die to have questions about those berries. The Chukchi people who use Reindeer like Oxen, Horses and Donkeys, watch the Reindeer eat Amanita Muscaria mushrooms. The science behind it is that the Reindeer Decarboxylizes the Ibotenic Acid into Muscimol. The Chuckchi people didn't know what the word Decarboxylize meant, but they started collecting the urine of Reindeer who had eaten the Mushrooms and drinking it to avoid the negative side effects of Ibotenic Acid.

A crow can watch a person or animal do something and try to repeat it, they have a Neocortex and can actually think up procedures with tools and repeated steps to do things. Dogs and Cats have enhanced senses of smell, and cats have an obvious affection for cat nip. Birds are selective when picking sticks and grass for nests.

Throughout History, before Fire even existed, we have been watching other Animals to see how things work. We now have alienated ourselves, a way from Nature and as Humans consider nature to be "out there" but we got where we are by learning from Animals. The wheel may have been invented by the Dung Beetle tens of thousands of years ago, when we scaled it up, eventually thinned it out, and then made it spoked, and spoked wheels and the concept of those branches holding up the frame solidly became a metaphor and spread as a Religion as the spoked Wheel spread around 5,000-10,000 BC being compared to the planets, and cycles, eventually creating the Calandar and Time and Boat sails, Rudders and steering, and then Machinery. This all comes from watching Animals, and Nature. Science is not some Alien pursuit, it is simple observation and testing.

Even today the highest standard in Medicine available is to inject a rat until it dies to find the overdose range called EC50 and then test humans with the Medicine against the Placebo effect (defined as the body creating immune responses and cures due to belief one has been given to the person a.k.a. Magic). That is Science.

 

[SashaShiva]

The Kava Extract will be here today, it was delayed, so I am going to try a few things soon. I have Lemongrass Oil and dried Rosemary leaves, CBD Isolate, and have other things coming.

 

[SashaShiva]

People think that in the past people did not really have a method to what they were doing. But in this Spell, which supposedly turns the person who Casts it, into a Werewolf; Examples are given of various things. First, without the Placebo Effect, you would not Mentally become a Werewolf. Second, people wonder, "Why Parsley?" because Parsley has absolutely no Psychoactive Effect. And it doesn't have a Psychoactive effect, but it does have a Pharmaceutical Effect. Parsley effects your CYP Enzymes, which would alter the way other Substances broke down in your body, which means adding Parsley to the Brew, changes the effects of everything else in the Brew. Similarly to MAOIs in Ayahuasca.

The Greek writer Neuri wrote that people living north of the Black Sea, both Greeks and others, regularly turned into wolves for a few days each year. Neuri lived in the 5th century B.C.

To become a werewolf, one could wait until the night of the new moon, go to a lonely place, such as a desert or mountaintop, and, on a level spot, draw a chalk circle about seven feet in diameter. Then draw a smaller circle of about three feet inside the first circle. Build a fire in the center of the small circle, and hang an iron pot from an iron stand. These must be iron! Throw into the pot handfuls of three of the following: parsley, hemlock, henbane, saffron, aloe, poppyseed, opium, solanum, and asafetida. Then recite a Spell.

Amala and Kamala - Wikipedia

en.m.wikipedia.org

Werewolves of Ossory - Wikipedia

en.m.wikipedia.org

https://ryanfb.github.io/loebolus-data/L071.pdf?fbclid=IwAR28pfw6q8JurLDgXuUqSHffVo2DuY6-JoRih-0loGFQLnXrrYqmv2Ve6zo

http://sites.middlebury.edu/feastsandfestivals/files/2015/09/Galen-introduction-on-the-humors.pdf?fbclid=IwAR2UuRHqG7SQkHuh8VpsIlPF_q_p_LqjCZyy6IxZs2d8hQlcyxekXQ_zIF8

Saul and the Medium at Endor
3 Now Samuel was dead, and all Israel had mourned for him and buried him in his own town of Ramah. Saul had expelled the mediums and spiritists from the land.

4 The Philistines assembled and came and set up camp at Shunem, while Saul gathered all Israel and set up camp at Gilboa. 5 When Saul saw the Philistine army, he was afraid; terror filled his heart. 6 He inquired of the Lord, but the Lord did not answer him by dreams or Urim or prophets. 7 Saul then said to his attendants, “Find me a woman who is a medium, so I may go and inquire of her.”

“There is one in Endor,” they said.

8 So Saul disguised himself, putting on other clothes, and at night he and two men went to the woman. “Consult a spirit for me,” he said, “and bring up for me the one I name.”

9 But the woman said to him, “Surely you know what Saul has done. He has cut off the mediums and spiritists from the land. Why have you set a trap for my life to bring about my death?”

10 Saul swore to her by the Lord, “As surely as the Lord lives, you will not be punished for this.”

11 Then the woman asked, “Whom shall I bring up for you?”

“Bring up Samuel,” he said.

12 When the woman saw Samuel, she cried out at the top of her voice and said to Saul, “Why have you deceived me? You are Saul!”

13 The king said to her, “Don’t be afraid. What do you see?”

The woman said, “I see a ghostly figure[a] coming up out of the earth.”

14 “What does he look like?” he asked.

“An old man wearing a robe is coming up,” she said.

Then Saul knew it was Samuel, and he bowed down and prostrated himself with his face to the ground.

15 Samuel said to Saul, “Why have you disturbed me by bringing me up?”

“I am in great distress,” Saul said. “The Philistines are fighting against me, and God has departed from me. He no longer answers me, either by prophets or by dreams. So I have called on you to tell me what to do.”

16 Samuel said, “Why do you consult me, now that the Lord has departed from you and become your enemy? 17 The Lord has done what he predicted through me. The Lord has torn the kingdom out of your hands and given it to one of your neighbors—to David. 18 Because you did not obey the Lord or carry out his fierce wrath against the Amalekites, the Lord has done this to you today. 19 The Lord will deliver both Israel and you into the hands of the Philistines, and tomorrow you and your sons will be with me. The Lord will also give the army of Israel into the hands of the Philistines.”

20 Immediately Saul fell full length on the ground, filled with fear because of Samuel’s words. His strength was gone, for he had eaten nothing all that day and all that night.

21 When the woman came to Saul and saw that he was greatly shaken, she said, “Look, your servant has obeyed you. I took my life in my hands and did what you told me to do. 22 Now please listen to your servant and let me give you some food so you may eat and have the strength to go on your way.”

23 He refused and said, “I will not eat.”

But his men joined the woman in urging him, and he listened to them. He got up from the ground and sat on the couch.

24 The woman had a fattened calf at the house, which she butchered at once. She took some flour, kneaded it and baked bread without yeast. 25 Then she set it before Saul and his men, and they ate. That same night they got up and left.

 

[Darcy Jay Strutt]

I can’t lie, this is getting a bit intense

 

[SashaShiva]

I can’t lie, this is getting a bit intense

We are creating the future with this research. People are going to be using the things being learned here and the Potentiates thread for years to come.

 

[SashaShiva]

Sasha Shulgin clearly states that he was working for us. His research was not a dormant textbook, but an Alchemical Spellbook for Posterity, meaning Future Generations. He says there is a silence being imposed on them by an unsympathetic Authority, and that in the Future someone (Me) will have a particular view of him that will put his tools to use.

 

[kavakarma]

Terence Mckenna.

Hey SashaShiva when can we have a shell together? Let's make it sooner rather than later.