Chamomile alkaloids and their effects?

[Lightning-Nl]

So, in an attempt to help me sleep last night, I smoked two pretty big joints filled entirely with Chamomile Tea.

I've done this before and it's actually quite relaxing. It stop 90% if restless leg symptoms, seems to be an effective mold stabilizer, it's very anxiolytic and slightly euphoric. I would compare it to one hit of mild-moderate weed in terms of how it feels.

Anyways, that not what I'm making this thread about. The two chamomile joints I smoked was the most I've ever ingested at one time. I've tried eating 10 of the tea bags before, but that didn't do anything for me. Anyways, I did this roughly 8 hours ago and ever since 9AMish (4 and. 1/2 hours ago) I've been feeling incredibly shitty.

At first, when I tried smokig the first chamomile joint, I felt relaxed, sedated, and slightly euphoric. However it wasn't as powerful as I was hoping, so I tried smoking some more. It really didn't add anything in terms of positive effects, however it added a skyscraper amount of negative effects.

When I could no longer sleep at 9AM - my legs were so restless I could barely stand to sit still. I noticed, as I abruptly woke up, that I was "out of it" mentally. I had a headache, and felt dissociated. The mental impairment feels almost exactly like the day after a HUGE Dextromethorphan or Diphenhydramine dose. Meaning, the effects feel very anticholinergic or antiglutamatergic in nature and are very unpleasant.

Also, when I got out of bed and went into my bathroom to splash some water on my face, I noticed in the mirror that my pupils were huge. They were extremely dialated and I could see almost no Iris in my eye - it was all pupil (black). Also, I am having very mild hallucinations that are reminiscent of Dissociative Halluciogens. I have some pretty predominant closed-eye hallucinations at the moment, and I also have mild visual hallucinations that look nearly exactly the same as CEH's but in real life.

What compound that's in chamomile would chase the effects?

I know the primary, psychoactive constitute in Chamomile is Apigenin. But nothing about apigenin's pharmacology would lead me to believe it would produce these effects. So, most probably, it's another compound that's active in chamomile that's causing these effects, right? What compound would that be?

If no one can identify that compound for me, in your opinion, would you say that these effects are caused by antagonization of ACh of Glutamine? If you suspect nether, than what would cause effects so similar to that of DXM?

Thanks everyone! It's much appriciated!

 

[sekio]

If you suspect nether, than what would cause effects so similar to that of DXM?

Subjective experiences do not determine biological activity. Humans are too fallible. Why do you think people conduct affinity assays?

I know the primary, psychoactive constitute in Chamomile is Apigenin.

Is it? Aren't chlorogenic acids, coumarins etc also contributors?

By the way, "two pretty big joints" is almost totally useless as a measurement. The size and density of joints varies pretty widely.

Also, why alkaloids in particular?

 

[atara]

The flavonoids (not alkaloids) have as a class rather varied and weird pharmacology, catechin for example is a MAOI. They're related to the flavylium cation which is responsible for the color of flowers. Anywho, since we don't really know what it does, it's hard to say what's causing your issues. I don't even think the major active principal in chamomile is known, we just suspect apigenin.

 

[Lightning-Nl]

Yeah the word alkaloid in the title was a mistake. If you read through my post you can see that I referred to the substance or stabstances as compounds and not alkaloids. I though to myself while I was typing it "Well, a psychoactive substance doesn't have to have a Nitrogen bond in it to be active" so I said compound instead of alkaloid.

Anyways, I guess Sekio is right. One users experience isn't anywhere near enough information to narrow down a substances pharmacodynamics. I know that, but I keep making the assumption that everyone has my same thought process. So I should really explain what that is in order to clear up confusion.

I'm a curios person and because I that, I try to make sense of everything that happens to me with facts rather than assumptions. When there are no facts on something, you can only make assumptions, but that's not good enough for my subconscious so I try to make educated guesses using previous knowledge.

My previous knowledge in this situation was that Dextromethorphan wakes me up the next day feeling agitated, tired, with a headache, dialated pupils and very distinct "fuzziness". I've noticed that this very distinct and unpleasant "fuzzy" feeling is common of serotonergic drugs. For instance, Dextromethorphan makes me feel like this and it just so happens that it's a Serotonin reuptake inhibitor, but then the SSRI Paxil (especially Paxil CR; sustained release paroxetine) can also give me this feeling. Interestingly enough, Diphenhydramine has recently been found to have SERT inhibiting effects and DPH can also make me feel this way.

Knowing this, I made an educated guess that there must be a substance in Chamomile that also has serotonin reuptake inhibiting effects, due to the fact that all the substances that have made me feel this way before all have SERT inhibiting effects. I know I couldn't properly identify anything, however, my real question was if there were any known substances in Chamomile that are known to cause SERT inhibition, because that would be good enough answer for me - "Chamomile makes me feel like this, this and this and these substances have made me feel like that before, therefore, there must be some relation to how the substances work in Chamomile and how the substances that made me feel this way before work." Again, I made the mistake of thinking that everyone would interpret the question with my thought process.

Also, I know that I said anticholinergic and antiglutamatergic drugs, but SERT inhibition was my real question. I said the ladder because the SERT inhibiting effects of DPH have yet to be measured.

---

On a side note...

Could apigenin be used as a "Buprenorphine-like" substance except for Benzodiazepine withdrawal?

I thought of this while doing some mild research on Apigenin. According to Wikipedia, apigenin is a ligand for the benzodiazepine binding subsection of GABAa. It was found to be a competitive binding agent and therefore would stop another substance from binding to the receptor when it was present and it would also "knock-off" any substance that was already there. However, it was found to produce its own range of effects as it had some agonistic effects on the receptor. The effects are typical of GABAergic drugs. Meaning it produced sedation and anxiolysis. So knowing the psychopharmacological action of Buprenorphine, it's effects are similar in the fact that it's an agonist/antagonist like substance (I thought these kind of substances were called competative inverse-agonists, but I might be wrong)

So knowing that Buprenorphine is used for opiate withdrawal because it produces opioid-typical effects, but inhibited the binding of other opioids; and since Apigenin has a similar action, but on the Benzodiazepine subsection of GABAa, could apigenin be used like suboxone, but for benzo's?

 

[SeenSoFar]

Its funny, apigenin does indeed have some action at the SERT, but it is the opposite of the action of an SERT inhibitor. It actually increases the reuptake of 5-HT. This isn't really relevant or anything, just an interesting side note, since you were focusing on a serotonergic explanation.

SOURCE: http://www.sciencedirect.com/science/article/pii/S0197018609002794