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NewAdventurer (guest) 18 Mar 2018 09:49
in discussion Hidden / Per page discussions » Oilahuasca Activators

I can't create a new thread, and I'm not sure the best place to put this. Apologies.

I just tried elemi oil for the first time earlier today with no effects at all. The oil I have shows 15.6% elemicin/elemol the GCMS shows them co-eluding. So I don't know exactly how much of each was in there. There was no iso-elemicin listed, and no eucalyptol with 98.42% recognition. I followed the diet for 2.5 days before consuming. This was on an empty stomach.

Here is a trip report by memory, next time I'll actually take notes.

@T-10 I took about 4 grams of Twinnings pure chamomile tea. I do not know for certain this is German chamomile, but the pictures used on the box and their website are of the German species, not roman. German chamomile flowers more rapidly and is more widely grown, so I would assume more chamomile teas are of the German variety, and it wasn't marketed as a "sleepy" tea, all leading me to believe it's German.

@T-9 I drank about half of the cup of black pepper tea made from about 4 grams of pepper strained well. Swallowed a teaspoon of coconut oil and a bit of milk.

@T-0 I took 1 gram of steviosides, with 500mg berberine, and 15 drops of whole elemi oil. Taken with coffee and some milk. I took one bite of a sandwich.

@T-5 I re-steeped the chamomile and drank it again.

@t-45 I dropped 3 drops Rosemary EO, 12 drops Elemi oil and two drops nutmeg oil, mixed with mineral oil and rubbed onto my thighs. I then wrapped my thighs with plastic wrap in an effort to get more absorption, not sure if this actually helped.

@t-50 I try vaporizing a few drops of elemi and a drop of nutmeg at a very low temperature (so I didn't choke myself), I put the oil on some cotton, stuck cotton in vape and inhaled directly.

Shortly after I vaped some Cannabis because at this point I was feeling nothing at all. Milk was occasionally drank throughout.

I have a very high tolerance to hallucinogens in general, but it doesn't seem to take extra to get me off baseline usually, it's just that the curve for me is much steeper once that's reached. This did not get me off baseline. It did get me thinking though. I started pouring over all the posts in my head and I started remembering mentions of iso-elemicin potentially making things stronger, and then I thought, what if it is only iso-elemicin that is at work. iso-elemicin gets extracted with elemicin, and it is even in the "pure" elemicin products. So I got up out of bed because I couldn't stop wondering about this and I started to do some research. I found this. I can't post links, but if you google leminger's scalines you should find it easily

Which is extremely interesting and strongly supports my theory. It's a short read and an extremely relevant one. The structure of iso-elemicin is very possibly psychedelic and very possibly and extremely potent psychedelic, it could potentially be the ONLY psychedelic compound in elemi oil. Elemicin could very possibly get turned into a psychedelic compound to some degree in some people as well, but I think that this theory deserves exploration.

The structure of iso-elemicin closely resembles the structure of other chemicals that give the feelings elemi oil can give, while elemicin's structure is less likely to be active in such a way.

I would love to hear feedback on the theory and if anyone has any advice on getting elemi/nutmeg to work for me. I plan to try again on wednesday with a much higher dose, niacinimide, and much mor chamomile, but I'd like to try transdermal, I didn't enjoy the burps. I saw mixed thoughts on icyhot and menthol. Besides DMSO, what delivery matrix might work best?

Imihuasca

sativar 30 Jul 2017 23:02
in discussion Hidden / Per page discussions » Imihuasca

Imihuasca is the creation of new molecules called imines, by combining an aldehyde and an amine/amide.

(More specifically, an aldimine is created, which is simply an imine which is derived from an aldehyde.)

Many aldehydes are highly reactive compounds. Some aldehydes are able to form adducts with amides or amines at room temperature without the need for a catalyst.

The word Imihuasca draws from the word ayahuasca which defines a mix of herbs in which DMT is made orally psychedelic by using enzyme inhibitors. The term Imihuasca was originally coined by the user 'Sativa' (the author)

Example reaction -

N-Benzylidene-N-phenethylamine is an aldimine (an imine which is derived from an aldehyde). It's found naturally in cocoa powders.

N-Benzylidene-N-phenethylamine is a natural adduct created from the alkaloid phenylethylamine and the aldehyde benzaldehyde found in cocoa powder.[1]

1. Ziegleder G, Stojacic E, Stumpf B.;
Occurrence of beta-phenylethylamine and its derivatives in cocoa and cocoa products; Fraunhofer-Institut für Lebensmitteltechnologie und Verpackung, München, Bundesrepublik Deutschland.; Z Lebensm Unters Forsch. 1992 Sep;195(3):235-8.; PubMed PMID: 1413998]

Access to herbpedia wiki!

sativar 30 Jul 2017 22:38
in discussion Hidden / Per page discussions » CYP3A4

Hi - it's Sativa! (from the maxforum days) Please could I be allowed to join the herbpedia site so I can create new pages?

Thanks!

Access to herbpedia wiki!

sativar 30 Jul 2017 22:38
in discussion Hidden / Per page discussions » CYP3A4

Hi - it's Sativa! Please could I be allowed to join the herbpedia site so I can create new pages?

Thanks!

69ron 09 Oct 2016 20:49
in discussion Hidden / Per page discussions » CYP3A4

Hi TLT,

I did some research on Panax ginseng's effects in live human test subjects. According to the article below, it had no effects on CYP3A4 in humans test subjects, despite some promising in vitro effects. I run across this a lot where in vitro tests simply don't apply to live humans.

Clinical Assessment of Botanical Supplementation on Cytochrome P450 Phenotypes in the Elderly: St. John’s wort, Garlic oil, Panax ginseng, and Ginkgo biloba

69ron 09 Oct 2016 20:08
in discussion Hidden / Per page discussions » Oilahuasca Activators

Hi Bluegrass,

No, that post is not me. I always post as myself, not as a guest.

I'm currently working on researching activation formulas that are based on berberine. It has do date been the most powerful activator I am aware of. Formulas using berberine have activated elemicin at elemicin doses as small as 20 mg for some people.

Berberine has shed new light on activation theory. It very potently inhibits CYP2D6, and also inhibits CYP2C9 and to a lesser degree CYP3A4. This inhibition is proven in both live human test subjects, as well as in vitro lab tests. So it's rock solid reliable data. Tests also show it has no effect on CYP2E1, which is good.

It appears that major allylbenzene inactivation routes are O-demethylation (for compounds like elemicin and myristicin) and O-demethylenation (for compounds like safrole and myristicin). CYP2D6 is notorious for both O-demethylating and O-demethylenating hundreds of compounds. Once an allylbenzene is O-demethylated or O-demethylenated, it becomes extremely difficult for 1'-hydroxylation to take place. So we need to knock out all enzymes capable of O-demethylating or O-demethylenating allylbenzenes. Enzymes known to have these actions are CYP2C9, CYP2D6, CYP3A4 and some others. CYP2E1 doesn't appear to have this action on allylbenzenes. CYP2E1 is only known to 1'-hydroxylate allylbenzenes. That's why CYP2E1 appears to be so beneficial to induce.

One of the good things about using berberine is that it doesn't color up the experience. Most of the other inhibitors that have been shown to have some success such as black pepper, calamus oil, etc., have their own effects, and will color up the experience.

i find there is a very specific middle point between to much cayenne pepper and to little to help activation best.

As has been noted, cayenne pepper (which contains capsaicin) has been both beneficial and detrimental, depending on dosage. Unfortunately, I don't know of any reliable enzyme tests performed on human test subjects that give any real evidence on it's effects in humans. Perhaps some exist, but I haven't found them. All I know of are in vitro tests and some in vivo tests performed on animals, which may not at all apply to humans. Some tests in live rats show it inhibits CYP3A4 and also induces CYP2E1 and CYP3A4. CYP2E1 induction is good. CYP3A4 induction is not good. But humans are not rats. It may have very different effects in humans. If anyone knows of any enzyme effects proven in human test subjects please post about it. That could help us better understand how cayenne pepper works.

The proven stimulant effects that capsaicin has on the human central nervous system are definitely synergistic with psychedelics in general. Capsaicin can moderately boost the effects of most psychedelics if taken after the onset. So this might be one reason for cayenne pepper's perceived effectiveness as an activator. It may actually be more of a synergistic effect rather than an activation effect.

My current research is moving away from supplements that are not proven inhibitors/inducers in human test subjects. So I'm not focusing on capsaicin, unless new data is available. There's just too many unknowns on it's effects in humans.

Piperine has been recently shown to inhibit CYP2E1 in human test subjects. This is probably the reason why whole black pepper is less effective for activation than filtered black pepper tea is. Piperine is a very potent inhibitor of CYP3A4. So a small amount is good, but as the dosage increases it starts inhibiting CYP2E1, which is not good. Filtered black pepper tea contains only a little bit of piperine because of it's very poor water solubility. At this time it's not known why filtered black pepper tea is better than whole black pepper. It's assume that there is another ingredient in black pepper that is a potent activator, and that piperine's presence is muddying the waters. However, it could be that piperine is the sole activator, and that by using filtered tea one simply limits the dosage of the piperine to a level small enough that it inhibits CYP3A4 without also inhibiting CYP2E1. More research needs to be done.

Berberine's inhibition of CYP3A4 is not that great. It needs an admixture to help knock out CYP3A4, but it needs to be one that doesn't also knock out CYP2E1. Small doses of piperine might do the trick. I will research combining small amounts of piperine with berberine, using piperine as a potent CYP3A4 inhibitor in very small doses, and berberine in large doses to inhibit CYP2D6 and CYP2C9. I also plan to research filtered black pepper tea in conjunction with berberine.

Re: Oilahuasca Experimentation Advice

69ron 09 Oct 2016 18:45
in discussion Hidden / Per page discussions » Oilahuasca Activators

Hi Corey,

First, my apologies for the very late response. I have extremely limited time these days so I don't visit forums like I used to. I work on this project periodically, and make updates to this site very infrequently when there's new important information available.

I'll address this question, as I believe it's the most important to answer, and I have very limited time at the moment.

Is the information on the Herbpedia pages up to date and thus credible?

The information is being updated slowly. I don't want to add anything new that's not been thoroughly tested or backed by solid facts.

There's ongoing sporadic research being done by various individuals, mostly from people wanting to remain anonymous. The vast majority of the people that contact me via Herbpedia don't post on public forums. In the early days of Oilahuasca, a lot of people were frustrated with the lack of results they had. Most people did not achieve any success whatsoever. Failures were probably in the 95% range. Because of that, the Oilahuasca subject became very controversial, so a lot of forums did not welcome Oilahuascatopic discussions. That's one of the reasons Herbpedia was created.

The single most important bit of recent research stems from tests done using berberine and steviosides. Berberine has greatly increased activation success rates, and reduced the amount of allylbenzenes needed for activation. To this date it's the most powerful activator I am aware of. Steviosides are great to use as UGT2B7 inhibitors. They are proven to be primary substrates of UGT2B7 in humans. Although not yet proven to act as inhibitors in human subjects, since they are proven primary substrates of UGT2B7 in humans, it stands to reason that they will work as competitive inhibitors. Both berberine and steviosides have received a lot of praise from various health organizations, because of their numerous health benefits. So it's great to see these become useful as Oilahuasca activator admixtures.

Another bit of information that has recently changed is that the P450 enzyme CYP2C9 is no longer considered beneficial. In addition to 1'-hydroxylating allylbenzenes it was shown to O-demethylate compounds, an action that is detrimental. Berberine is proven to fairly potently inhibit CYP2C9 in human test subjects, but has been shown to work really well as an activator. This data very clearly shows that CYP2C9 should be inhibited. Tests continue narrowing down the beneficial target P450 enzymes. The current tests I am aware of show that CYP2E1 is probably one of the most important P450 enzymes to induce. CYP2E1 can 1'-hydroxylate allylbenzenes and is not known to O-demethylate compounds. I have noted from hundreds of tests that anything that inhibits CYP2E1 will pull down Oilahuasca success rates.

One problem in the past was that a lot of herbs and supplement inhibitor/inducer data was taken from in vitro tests. For the most part in vitro tests are nearly worthless. Many potent in vitro enzyme inhibitors/inducers turned out to have no effects when tested in humans. So a lot of the previously recommended inhibitors/inducers where either ineffective, or only slightly so. I have since concentrated my research focusing on inhibitors and inducers that have been proven to work in human test subjects. I still use some in vitro test data as a guide to potentially useful inhibitors/inducers, when real human test case data is not available, but I try not to rely on it.

69ron 26 Sep 2016 00:08
in discussion Hidden / Per page discussions » CYP2C9

Thanks. I've updated the page to include information on EPA with a reference to a study showing that it inhibits CYP2C9. The study shows several other polyunsaturated fatty acids also have this action. In addition it shows inhibition for CYP1A2, CYP2E1 and CYP3A4.

TLT (guest) 18 Dec 2014 06:08
in discussion Hidden / Per page discussions » Glucuronosyltransferase (UGT)

Recently ive found egcg also inhibits 1a6 & 1a9

TLT (guest) 10 Dec 2014 22:28
in discussion Hidden / Per page discussions » Glucuronosyltransferase (UGT)

Rifampin is a known potent broad inducer of drug-metabolizing enzymes including UGT1A1

TLT (guest) 09 Dec 2014 00:48
in discussion Hidden / Per page discussions » CYP3A4

Panax ginseng was the ginseng in the study saying its known to inhibit 3a4 in vivo

TLT (guest) 09 Dec 2014 00:41
in discussion Hidden / Per page discussions » CYP3A4

In vivo, ginseng is known to inhibit CYP3A4, the primary enzyme involved in the metabolism of imatinib

TLT (guest) 09 Dec 2014 00:38
in discussion Hidden / Per page discussions » CYP3A4

The Journal of Clinical Pharmacology, 06/20/2011

Malati CY et al. – Fexofenadine pharmacokinetics were unaltered by P ginseng administration. Based on these results, P ginseng appeared to induce CYP3A activity in the liver and possibly the gastrointestinal tract. Patients taking P ginseng in combination with CYP3A substrates with narrow therapeutic ranges should be monitored closely for adequate therapeutic response to the substrate medication.

TLT (guest) 05 Dec 2014 05:16
in discussion Hidden / Per page discussions » Oilahuasca Activation

^ other psychedelic oil that was suggested is valerian root with high valerenic acid content

TLT (guest) 03 Dec 2014 06:13
in discussion Hidden / Per page discussions » CYP2C9

Eicosapentaenoic acid on wikipedia says:EPA has an inhibitory effect on CYP2C9 and CYP2C19 hepatic enzymes. At high dose, it may also inhibit the activity of CYP2D6 and CYP3A4, important enzymes involved in drug metabolism.

TLT (guest) 03 Dec 2014 02:49
in discussion Hidden / Per page discussions » Sulfotransferase (SULT)

ABSTRACT Safrole, present in mace and its essential oils, causes liver tumours in rodents at high dose levels due to formation of DNA reactive 1'-sulfooxysafrole. The present study identifies malabaricone C as a mace constituent able to inhibit safrole DNA adduct formation at the level of sulfotransferasemediated bioactivation. This inhibition was incorporated into physiologically based biokinetic rat and human models. Dosing safrole at 50 mg/kg body weight and malabaricone C-containing mace extract at a ratio reflecting the relative presence in mace, and assuming 100 or 1% uptake of malabaricone Ccontaining mace extract, the model predicted inhibition of 1'-sulfooxysafrole formation for rats and humans by 90 and 100% or 61 and 91%, respectively. To validate the model, mace extract and safrole were co-administered orally to Sprague-Dawley rats. LC-ECI-MS/MS based quantification of DNA adduct levels revealed a significant (p<0.01) 55% reduction of safrole DNA adduct formation by malabaricone C-containing mace extract in the liver of rats exposed to safrole. The data obtained were used to perform a refined risk assessment of safrole. Overall, the results suggest a lower tumour incidence when safrole would be tested within a relevant food matrix containing sulfotransferase inhibitors compared to dosing pure safrole.

From researchgate

TLT (guest) 02 Dec 2014 03:28
in discussion Hidden / Per page discussions » CYP2E1

Catechins, major polyphenol constituents of green tea, are potent chemopreventive agents against cancers caused by chemical carcinogens in rodents. The effects of four epicatechin derivatives, epigallocatechin gallate (EGCG), epicatechin gallate (ECG), epigallocatechin (EGC) and epicatechin (EC), on the metabolic activation of benzo[a]pyrene (B[a]P), 2-amino-1-methyl-6-phenylimidazo-[4,5-b]pyridine (PhIP) and aflatoxin B(1) (AFB(1)) by human cytochrome P450 (CYP) were examined. B[a]P, PhIP and AFB(1) were activated by respective human CYP1A1, CYP1A2 and CYP3A4 expressed in the membrane fraction of genetically engineered Salmonella typhimurium (S. typhimurium) TA1538 cells harboring the human CYP and human NADPH-CYP reductase (OR), when the membrane fraction was added to S. typhimurium TA98. Galloylated catechins, ECG and EGCG inhibited the mutagenic activation potently, while EGC and EC showed relatively weak inhibitory effects. Catechins also inhibited the oxidations of typical substrates catalyzed by human CYPs, namely ethoxycoumarin O-deethylation by CYP1A1, ethoxyresorufin O-deethylation by CYP1A2 and midazolam 1'-hydroxylation by CYP3A4. The IC(50) values of catechins for the inhibition of human CYP were roughly the same as those seen in the mutagenic activation. EGCG inhibited other forms of human CYP such as CYP2A6, CYP2C19 and CYP2E1, indicating the non-specific inhibitory effects of EGCG toward human CYPs. Furthermore, EGCG inhibited human NADPH-cytochrome CYP reductase (OR) with a K(i) value of 2.5 microM. These results suggest that the inhibition of the enzyme activity of CYP is accounted for partially by the inhibition of OR.

TLT (guest) 02 Dec 2014 03:25
in discussion Hidden / Per page discussions » CYP2E1

Copy and paste these on google to see the full report and if they are worth being on your site. Hope I helped!

TLT (guest) 02 Dec 2014 03:20
in discussion Hidden / Per page discussions » CYP2E1

EGCG inhibited other forms of human CYP such as CYP2A6, CYP2C19 and CYP2E1, indicating the non-specific inhibitory effects of EGCG toward human CYPs.
From pubmed

TLT (guest) 27 Nov 2014 23:15
in discussion Hidden / Per page discussions » Glucuronosyltransferase (UGT)

Aims: The only FDA approved medication for colorectal cancer (CRC) prevention is celecoxib. Its adverse effects underline the need for safer drugs. Polyphenols like resveratrol are in clinical trials for this purpose. This study aimed at examining effects of resveratrol alone and in combination with curcumin or chrysin on UGT induction in Caco-2 cells. Phytochemical combinations were selected using drug combination analyses of various anti-proliferation ratios of resveratrol + curcumin and resveratrol + chrysin. Main methods: Cell proliferation and UGT1A1 induction assays were carried out with individual polyphenols and combinations. Cell viability was determined with AlamarBlue assays. UGT1A1 mRNA was quantified via real time RT-PCR. UGT activity was determined with 4-methylumbelliferone (4MU) glucuronidation. Key findings: Cell proliferation IC50 estimates (± SE) for resveratrol, curcumin and chrysin were 20.8 ± 1.2, 20.1 ± 1.1 and 16.3 ± 1.3 μM respectively. Combination of anti-proliferative effects showed additivity for resveratrol + chrysin and resveratrol + curcumin. Resveratrol at its IC 50 mediated a four-fold induction of UGT1A1 mRNA in a concentration independent manner. Chrysin at its IC50 induced UGT1A1 expression seven-fold while Curcumin at its IC90 mediated a two-fold induction. The 20 μM:40 μM resveratrol + curcumin and 20 μM :32 μM resveratrol + chrysin combinations mediated the greatest increases in mRNA expression (12 and 22 folds respectively). Significant increase in 4-MU glucuronidation was observed with combinations exhibiting maximal mRNA induction. Significance: Phytochemical combinations can offer greater chemoprevention than single agents. These chemicals might offer safer options than present synthetic therapeutics for CRC prevention. © 2011 Elsevier Inc. All rights reserved.

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