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Does black seed oil potentiate dihydrocodeine and what other potentiaters do do people recommend?

Tifftifco2

Bluelighter
Joined
Oct 31, 2018
Messages
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Hi, my tolerance to dihydrocodeine is really getting high so I'm looking for good ways to potentiate it. I'm currently taking 8 30mg tablets + 900mg gabapentin + 6 30/500mg cocodamol 😪 not good I know. So I'm looking for a safer way to take less that actually works. How does the black seed oil work? Does anyone else have good potentiaters they could advise me off. I want to try kratom to replace the opiates for a break but I cant source any and I know I'm not allowed to ask here. But is that a good idea? I have fibromyalgia and inflammatory bowel disease so I do need to take a lot of painkillers but I'm taking my complete daily dose in a morning leaving myself with only nefopam for the night as I don't have the self control to split the dose most days. I only get 8 a day so if I go over I run out and I buy the cocodamol off a friend. Any advise would be appreciated please I need some relief!

Thanks everyone!
 
I guess you mean the nigella sativa oil with black seed oil. That oil seems to contain many different chemical compounds in similar amounts, and it's difficult to say which of them is responsible for the effects.

Some essential oils, including rosemary and lavender oil, have been claimed to have some effectiveness against opioid withdrawal and to potentiate the pain-relieving effect of opioids.


I have used rosemary and lavender EOs several times by inhalation with codeine to enhance the high, but I'm not sure if it only increases the intoxication and euphoria, or whether it also potentiates the analgesic effect. That combination sometimes actually gets me suddenly high enough to get me scared that I could have respiratory depression. Even natural products can have adverse effects if used in excessive amounts, though, so do this at your own risk.

There are also other natural products, including curcumin, which are claimed to prevent opiate tolerance:


Curcumin has a poor bioavailability unless it's taken with black pepper to inhibit the enzymes responsible for its metabolic breakdown.

Not sure if kratom can cause precipitated withdrawal (it's a partial mu agonist) if something like dihydrocodeine is replaced with it too quickly.
 
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I guess you mean the nigella sativa oil with black seed oil. That oil seems to contain many different chemical compounds in similar amounts, and it's difficult to say which of them is responsible for the effects.

Some essential oils, including rosemary and lavender oil, have been claimed to have some effectiveness against opioid withdrawal and to potentiate the pain-relieving effect of opioids.


I have used rosemary and lavender EOs several times by inhalation with codeine to enhance the high, but I'm not sure if it only increases the intoxication and euphoria, or whether it also potentiates the analgesic effect. That combination sometimes actually gets me suddenly high enough to get me scared that I could have respiratory depression. Even natural products can have adverse effects if used in excessive amounts, though, so do this at your own risk.

There are also other natural products, including curcumin, which are claimed to prevent opiate tolerance:


Curcumin has a poor bioavailability unless it's taken with black pepper to inhibit the enzymes responsible for its metabolic breakdown.

Not sure if kratom can cause precipitated withdrawal (it's a partial mu agonist) if something like dihydrocodeine is replaced with it too quickly.

Thankyou for your reply. So what would you do with the essential oils and at what stage ? Before, after gestation or something else? Do you inhale from the bottle or heat it up?
 
I'd put about 10 drops in a cup and inhale the vapors without heating. Usually about 10 to 20 minutes after the codeine dose. The lavender oil is probably less likely to have harmful side effects than the rm oil.

Here's my recent thread about those aromatherapy oils: https://www.bluelight.org/xf/threads/alpha-pinene-is-a-bzd-agonist.881325/

A more common way to potentiate opiates is to just take sedative antihistamines with them. Not sure if grapefruit juice would also lengthen the half-like of dihydrocodeine like it does with morphine.
 
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I'd put about 10 drops in a cup and inhale the vapors without heating. Usually about 10 to 20 minutes after the codeine dose. The lavender oil is probably less likely to have harmful side effects than the rm oil.

Here's my recent thread about those aromatherapy oils: https://www.bluelight.org/xf/threads/alpha-pinene-is-a-bzd-agonist.881325/

A more common way to potentiate opiates is to just take sedative antihistamines with them. Not sure if grapefruit juice would also lengthen the half-like of dihydrocodeine like it does with morphine.
Thank you I have ordered some lavender oil and will try this method. I will read your thread now also.Thanks again.
 
Just want to mention that using these essential oils did not show up in any way in liver function tests I had, but this does not mean that someone else couldn't have hepatotoxicity from excessive use, especially when it's the eucalyptol-containing oils.
 
Thanks, they didn't work for me but I will keep using it seen as i bought it. Who knows!
 
Thanks, they didn't work for me but I will keep using it seen as i bought it. Who knows!

Do you already use actual benzos, or alcohol, regularly? The oils probably don't have much effect if there's some tolerance to cns depressants. They did seem to lose effect if I used them too many days in a row. The lavender "trip reports" on Erowid gave an impression that some people experienced a lot of effect from it while someone else not that much.
 
No I'm not a drinker and can't get hold of benzodiazepines. Not much seems to work for me not even kratom!
 
Scopolamine-like anticholinergics can also potentiate the pain-relieving effect of morphine and other opiates, while making the opiate drug less addictive and tolerance-forming at the same time. This is probably because of the M5 receptor blockage that I mentioned in another thread, and which prevents some of the dopamine release caused by the opiate. I'm saying this assuming that that you're mainly using the drugs because of a medical need and not to "get high".

The rosemary and lavender oils don't have as much effect for me anymore after using them several times a week for about two months. They probably have a robust effect only when someone hasn't taken any CNS depressants for weeks/months.

Ginger (the spice) is also said to slow down opiate tolerance, because it contains some kind of calcium channel blockers. I usually take a couple of grams of ginger with codeine.
 
Dihydrocodeine is a much better precursor than codeine. If you search the US patents for one David X. Wang you will see a HOST of different routes beginning with DHC. Unlike codeine, it cannot undergo allylic rearrangement and NaH2PO2 + KI yields HI but you do not need such harsh conditions to remove the 3 methyl ether. He carried out deprotection using HCl, HBr & HI and the key thing to note is that H3BO3 (boric acid) acts as a 'rate accelerant' (why it was not termed catalyst I don't know) so that deprotection proceeds x5 faster.
You do not want 58% HI. 34% seems to work best. The 6-hydroxy will also be reduced and some N-demethylation will occur but the key thing is that the majority (>80%) winds up as desomorphine & dihydromorphine. As you will see, the patent calls for an Xe2 atmosphere but dry N2 works just fine. Too much HI & 1-iododihydromorphine turns up in the product.


Once you have read 1 David X. Wang patents, I think you will read them all. An efficient codeine->hydrocodone route still eludes us (and metal catalysts break the ether bond so give poor yields) so that even the most effective route yields 66% and has a tricky work up.

I dunno know law where you are BUT I know that to import butorphanol as a PRECURSOR rather than as a medicine, no licence is required. Take a look at:

Butorphanol metabolites: Synthesis of cis- and trans3,14-dihydroxy-N-(3'-hydroxycyclobutylmethyl) morphinan.

Voila.
 
Once you have read 1 David X. Wang patents, I think you will read them all. An efficient codeine->hydrocodone route still eludes us (and metal catalysts break the ether bond so give poor yields) so that even the most effective route yields 66% and has a tricky work up.

You mean that the catalyst breaks the ether bond that is part of the 5-atom fused ring in codeine and morphine?
 
No, it demethylates the methyl-aryl ether on the A-ring of morphinan opioids. The A-ring is a protected phenol.


ll the refs are in here.

The KEY point is that H3BO3 & a few other salts act as 'rate accelerants' and you will note that 48% HBr isn't used. I seem to remember 32% HBr is used BUT HI works at about 17% Now, I would take a REALLY close look at the Krokodil synthesis. This uses 57% HI so N-demethylation & 1-iodination occur as side-reactions PLUS the 'cooks' cannot clean the product. I mean, forget I2 + P4 because even those with some skills were making HI from I2 & P4 in their homes with no ventilation so PH3 was an inevitable environmental toxin.
NaH2PO2 + KI yields HI with no PH3. By sufficiently diluting the HI & adding H3BO3 (other 'rate accelerants were tried, none were as good) and as the ref points out, H3BO3 makes the 3-demethylation occur 5 times as fast so MUCH less N-demethylated and 1-iodo impurities. The reaction spits out CH3I which isn't healthy so you need a fume cupboard BUT it avoids most of the real nasties.

If you want to remove the N-demethylated compound, forming an amide (i.e. non-basic ammonia) is simple and the less vigerous conditions means that the 1-iodo derivative isn't formed. Some 3-dehydroxylation may occur but that is easy to remove since it cannot form the calcinate salt. In short, you can produce clean desomorphine.

Now the KEY thing is that the Russians started from codeine thus allylic rearrangement occurs and forms a heap of products. Dihydrocodeine won't do this. The secondary -OH at 6 is reduced and the catallyzed 3-demethylation yields phenol & CH3I.

Now, my bad but it's Peter X. Wang - sorry about that. But real ALL the patents & use sci hub to read all of the papers..

I do not know where you are or the laws that apply where you live but please do not break the law.


Oh, and DO keep lab-notes. You will soon find optimum conditions and I am told that a yield of 76% is possible. If you want to go further, you will note that there are MANY routes to remove the N-methyl. Forming the amine oxide (mCPBA) and then reducing with FeCl2 yields the secondary amine which can readily have an appropriate 2-ethylaryl moiety added. https://www.unodc.org/unodc/en/data-and-analysis/bulletin/bulletin_1958-01-01_4_page007.html


All good fun but the reversed-ester of tilidine )the mu/DRI/NMDA) compound as potent as H, as euphoric as rock is just 2 steps from 1-phenylcyclopropene. I think I can safely post that as the 2 steps require some pretty ODD precursors which is not to say that it is hard.... but the stuff was just so MORISH that I was glad to run out.
 
Dihydrocodeine is a much better precursor than codeine. If you search the US patents for one David X. Wang you will see a HOST of different routes beginning with DHC.
K.W. Bentley and the orvinols and thevinols make me smile. 6,14-endoethenotetrahydrooripavine has got to be my favorite morphinan privileged scaffold.
 
K.W. Bentley and the orvinols and thevinols make me smile. 6,14-endoethenotetrahydrooripavine has got to be my favorite morphinan privileged scaffold.
Well, Thebaine is controlled, Oripravine is controlled, etorphine is controlled BUT the intermediate (formed by thebaine and the methyl vinyl ether) is NOT controlled. What is more, it's commercially available from India and China.

Check your own nations legal controls bu as far as I know, the intermediate (still x25 M) remains uncntrolled everywhere in the world. The KEY thinks is that with the UKs PsA, acompound intended as a precursor and is exempt.

II presume that it's because it's used to make buprenorphine but whatever the case, it's legal.
 
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