54 replies to this topic

[ajnast4r]

..

why & how are you measuring doses of DMT low enough to give leave you still functioning and not hanging out here:

Edited by ajnast4r, 21 May 2010 - 05:45 PM.

[medievil]

My only reserve with DMT, is as it binds to the receptors (LD) it creates a very dreary depressant feeling(in me), until 4.5 hours comes along and all the natural serotonin built-up comes to swarm the receptors and then I'm super-happy, and plus, DMT has that switch that protects daily usage, right? That melatonergic or tryptaminergic switch or whatever it is that prevents daily dosing, can't remember the specifics, but know daily tryptaminergics usually don't work. Could be wrong, but, there's a stop-switch mechanism on DMT I know.

That isnt true, DMT is actually known for its lack of tolerance, altough tolerance barely (if ever) occurs to low doses of psychedelics.

[medievil]

..

why & how are you measuring doses of DMT low enough to give leave you still functioning and not hanging out here:

lol, i'm took like 1/10th of my mimosa hostilis extract this morning, now took 2/10th, slowly going up.

Never been in that place, but planning too .

[Guacamolium]

My only reserve with DMT, is as it binds to the receptors (LD) it creates a very dreary depressant feeling(in me), until 4.5 hours comes along and all the natural serotonin built-up comes to swarm the receptors and then I'm super-happy, and plus, DMT has that switch that protects daily usage, right? That melatonergic or tryptaminergic switch or whatever it is that prevents daily dosing, can't remember the specifics, but know daily tryptaminergics usually don't work. Could be wrong, but, there's a stop-switch mechanism on DMT I know.

That isnt true, DMT is actually known for its lack of tolerance, altough tolerance barely (if ever) occurs to low doses of psychedelics.

Possibly, but from my knowledge on DMT HD from my experiences in 2003; it has a mechanistic swithoff effect, and I commend you on your source! Mimosa Hostilis rootbark is probably the best source for it, but that is one I've LD'd and HD'd, and I'm telling you DMT has some negative perception qualities to it LD. (perhaps animal, or whoever can step in here and list the 5ht binding affinities?)

If it works for you though, nice bro, and if you ever decide to try the DOC path - I've got just the chickety to talk to, to help you on this quest.

Yes, I agree with the poster that wondering how in the living fuck are you taking DMT and still able to function normally? IN HD limits you are a vegetable, same with MD, but LD I was able to walk around fine but I was in a negative mood - same thing Shulgin experienced. Still, best of luck!

[John Barleycorn]

A few people here are clearly a lot better read in this area than I am, but here are some simplistic propositions that I have developed (ignoring downstream effects, nb):

1. 5HT2 agonism of some sort is a required feature of most of these substances.
2. Downregulation often occurs rapidly (ie, if someone is enough of a desperado to want to try for a second helping, the subsequent experience will be greatly attenuated). This presumably has implications for tolerance development.
3. Euphoria during the tryptamine experience is a bit of a hit and miss affair; however, day-after mood elevation seems to be better documented. PEAs, which started off as the topic of this thread, are obviously a completely different kettle of fish.
4. Some anti-depressants are specifically based upon 5HT2 antagonism, not agonism.
5. Kappa opioid antagonism can also result in an anti-depressant action. So, no get-out clause for salvinorin either.

Conclusion (highly simplistic, like I said): seeing things doesn't make anyone feel any better, but the aftermath might. Whether this has implications for chronic administration of stimulating PEAs is another matter.

[medievil]

A few people here are clearly a lot better read in this area than I am, but here are some simplistic propositions that I have developed (ignoring downstream effects, nb):

1. 5HT2 agonism of some sort is a required feature of most of these substances.
2. Downregulation often occurs rapidly (ie, if someone is enough of a desperado to want to try for a second helping, the subsequent experience will be greatly attenuated). This presumably has implications for tolerance development.
3. Euphoria during the tryptamine experience is a bit of a hit and miss affair; however, day-after mood elevation seems to be better documented. PEAs, which started off as the topic of this thread, are obviously a completely different kettle of fish.
4. Some anti-depressants are specifically based upon 5HT2 antagonism, not agonism.
5. Kappa opioid antagonism can also result in an anti-depressant action. So, no get-out clause for salvinorin either.

Conclusion (highly simplistic, like I said): seeing things doesn't make anyone feel any better, but the aftermath might. Whether this has implications for chronic administration of stimulating PEAs is another matter.

1. Yes but i dont think that is a problem, quite the opposite.
2. Rapid tolerance doesnt occur to the low doses, ive been taking 2CD allmost daily for the past 2 weeks without any form of tolerance developping.
3. Yeah, a psychedelic experience can produce a great afterglow, i do think this is also the case with PEA's.
4. Yes, because 5HT2A antagonism increases dopamine in the frontal cortex, HOWEVER i think that 5HT2A antagonism is a bad idea in many cases, 5HT2A agonism can be very interesting too when it comes to depression, 5HT2A can promote dopamine the mesolimbic area's.
5.

About the aftermatch, i havent notice any form of comedown or anything else.

[medievil]

My only reserve with DMT, is as it binds to the receptors (LD) it creates a very dreary depressant feeling(in me), until 4.5 hours comes along and all the natural serotonin built-up comes to swarm the receptors and then I'm super-happy, and plus, DMT has that switch that protects daily usage, right? That melatonergic or tryptaminergic switch or whatever it is that prevents daily dosing, can't remember the specifics, but know daily tryptaminergics usually don't work. Could be wrong, but, there's a stop-switch mechanism on DMT I know.

That isnt true, DMT is actually known for its lack of tolerance, altough tolerance barely (if ever) occurs to low doses of psychedelics.

Possibly, but from my knowledge on DMT HD from my experiences in 2003; it has a mechanistic swithoff effect, and I commend you on your source! Mimosa Hostilis rootbark is probably the best source for it, but that is one I've LD'd and HD'd, and I'm telling you DMT has some negative perception qualities to it LD. (perhaps animal, or whoever can step in here and list the 5ht binding affinities?)

If it works for you though, nice bro, and if you ever decide to try the DOC path - I've got just the chickety to talk to, to help you on this quest.

Yes, I agree with the poster that wondering how in the living fuck are you taking DMT and still able to function normally? IN HD limits you are a vegetable, same with MD, but LD I was able to walk around fine but I was in a negative mood - same thing Shulgin experienced. Still, best of luck!

These are DMT's affinities:

DMT: 4.00 5ht7, 3.97 5ht1d, 3.91 5ht2b, 3.53 Alpha2B, 3.53 Alpha2C, 3.51 D1, 3.42 5ht2c, 3.28 5ht1e, 3.25 5ht6, 3.16 5ht5a, 3.13 Imidazoline1, 2.95 Alpha1B, 2.75 Alpha2A, 2.70 Alpha1A, 2.58 5ht2a, 2.37 SERT, 2.23 Sigma1; 0.00: 5ht1a, D4, D5, Beta1, D2, D3, DAT, NET, 5ht1b, Beta2, Sigma2, CB2, KOR, Ca+Channel, M1, M2, M3, M4, M5, H2, CB1; ND: H1, DOR, MOR, NMDA

Hmm, in a low dose it increases the sharpness of the colors and boosts my mood a little, didnt notice any negative mood.

Edited by medievil, 25 May 2010 - 10:08 AM.

[medievil]

delete

Edited by medievil, 11 March 2013 - 11:40 AM.

[machete234]

So medievel how often did you do this in the last too years?
I have 2C-D and 2C-E and have used low dose D to turn a shitty day into a better one aswell as getting more motivation to learn.

Motivation seems to be my main problem and this is why it helped I guess.

[medievil]

Ill reply in the other thread later, main discussion was going on there i accidently bumped this one up by posting here.

[leftside]

Don't mix your psychedelics with your "normal" life.

[medievil]

Haha why the normal between quotes, wonder what you think my life looks like, but i can imagine knowing what shit i post here.

[leftside]

Because everyone's definition of what is a "normal" life is different

[medievil]

Ive allways found it interesting you can modulate your personality or personality threats, dont like this type tough as my personality threats are disconnected from my writing and sound more "professional"? while my humoristic self is disconnected havent tried modulating my personality this way much so dont know wheter it has benefits, perhaps for important meetings or writing papers, overall it makes me sound to cold and i become to boring haha, also its not disconnected from ocd wich defeats its purpose.

Being ocd makes me smart and productive with regards to my intrest, i can remove my ocd with certain supplements but sometimes i get completely disinterested in this all wich i consider something bad as my intrest in meds and pharmacology is a part of me, but offcourse a middle ground can be found. Im also not used to speaking like this so it probably sounds fucked up hahah, tried an old supplement, noticed on many ocasions how things modulate personality and behavor, within limits offcourse at the core there's still your own personality, i can act completley normal just noticed i started writing like this haha, i wonder wheter i really sound more "professional" haha. If your not like this but your brain is more balanced to it it comes out strange, like minocycline improves my decission making but sometimes i sound like im someones dad or completely strange as im not used to it. Haha i allways push it out can as well stay myself but my humor and extrovertism does seem more impaired.

Allright time to abort this and become myself again. Im completely bunk writing in a professional way, gonna sound funny when im back normal.

[SpawnMoreOverlords]

Have you guys read numerous studies on Ayahuasca using cultures ? Where they use this DMT/beta-carboline mixture for decades on regular basis, starting teenage years, 14-16 years old I believe, and yet these studies show absolutely healthy brain, even healthier than normal in terms of neurological disorders that plague the west ?

( I don't have time right now but if anyone doubts i can certainly link some studies in the future when I get enough time to dig in deeper into this topic )

Edited by SpawnMoreOverlords, 12 March 2013 - 10:34 PM.

[leftside]

I would love to try Ayahuasca. I can get the ingredients and have a few recipes. Just seems such a pain in the ass to make. I've never been able to get hold of DMT :(

[golden1]

Low dose DMT makes me incredibly happy and empathetic....

[Reformed-Redan]

Get ready for the "Broke my brain now you tell me how to fix it again" threads.

[SpawnMoreOverlords]

Get ready for the "Broke my brain now you tell me how to fix it again" threads.

Yeah I watched Reefer Madness movie back in school. That stuff gonna make you like devils music(Jazz) and push you to have interracial sex, besides making you think you can fly and other crazy stuff !!! Stay away it's gonna make you go insane !

Edited by SpawnMoreOverlords, 13 March 2013 - 11:19 PM.

[SpawnMoreOverlords]

I would love to try Ayahuasca. I can get the ingredients and have a few recipes. Just seems such a pain in the ass to make. I've never been able to get hold of DMT :(

It's pretty easy to make... just few hours boiling and reducing.

[Flex]

http://www.ncbi.nlm....pubmed/23638910
beta-phenethylamine--a phenylalanine derivative in brain--contributes to oxidative stress by inhibiting mitochondrial complexes and DT-diaphorase: an in silico study.
Mazumder MK¹, Paul R, Borah A. AIM:
Till date, the mode of action of ?-PEA on neurons is not well illustrated. We tested the hypothesis that ?-PEA has the ability to cause oxidative stress by inhibiting the antioxidant enzyme DT-diaphorase and mitochondrial complexes (Complex-I and complex-III).
METHODS:
Using molecular docking as a tool, we here studied and compared the inhibitory capacity of beta-PEA on DT-diaphorase and mitochondrial complexes. Three-dimensional structures of mitochondrial complexes and DT-diaphorase and their ligands were downloaded from the respective data banks, and free energy of binding (docking scores) were determined.
RESULTS:
The present finding demonstrated for the first time that ?-PEA potentiates reactive oxygen species generation by inhibiting the antioxidant enzyme DT-diaphorase, in addition to the mitochondrial complex-I and complex-III.
CONCLUSION:
As lowering of cellular antioxidant molecules is evident in many neurodegenerative disorders, beta-PEA-induced lowering of DT-diaphorase activity may have the capability to cause neurodegeneration, which may be potentiated by its ability to inhibit mitochondrial complexes. Thus, beta-PEA due to its cumulative actions may be more potent in causing neurodegeneration as compared to other endogenous neurotoxins.

[Clint C]

http://www.ncbi.nlm....pubmed/23638910
beta-phenethylamine--a phenylalanine derivative in brain--contributes to oxidative stress by inhibiting mitochondrial complexes and DT-diaphorase: an in silico study.
Mazumder MK¹, Paul R, Borah A. AIM:
Till date, the mode of action of ?-PEA on neurons is not well illustrated. We tested the hypothesis that ?-PEA has the ability to cause oxidative stress by inhibiting the antioxidant enzyme DT-diaphorase and mitochondrial complexes (Complex-I and complex-III).
METHODS:
Using molecular docking as a tool, we here studied and compared the inhibitory capacity of beta-PEA on DT-diaphorase and mitochondrial complexes. Three-dimensional structures of mitochondrial complexes and DT-diaphorase and their ligands were downloaded from the respective data banks, and free energy of binding (docking scores) were determined.
RESULTS:
The present finding demonstrated for the first time that ?-PEA potentiates reactive oxygen species generation by inhibiting the antioxidant enzyme DT-diaphorase, in addition to the mitochondrial complex-I and complex-III.
CONCLUSION:
As lowering of cellular antioxidant molecules is evident in many neurodegenerative disorders, beta-PEA-induced lowering of DT-diaphorase activity may have the capability to cause neurodegeneration, which may be potentiated by its ability to inhibit mitochondrial complexes. Thus, beta-PEA due to its cumulative actions may be more potent in causing neurodegeneration as compared to other endogenous neurotoxins.

 

Oh yes. reactive oxygen species. this is stuff like molecular degeneration such as when mitochondria's electric transport chain is doing its thing such as metabolizing a hydoxal lipid for energy source and as a result a by product is created such as peroxide (H2O2). Now this peroxide is a free radical that has to be dealt with. more likely, it'll be dealt with by the mito's process of hydrolyzation. But for some reason, if the mito is to taxed out or its due to having some age on you, this hydrolyzation isn't gonna take place either at all or as effiencently as it should. What's gonna happen is this H2O2 will be food for reactive oxygen species to grow! The study I quoted above is saying that more than likely PEA interferes with things like H2O2 free radicals being dealt with, thus potentiating reactive oxygen species development. If this is the case, I will tell you that trimethylglycine (betaine) will help with peroxidation by products and another supplement by the name of PQQ will help combat against reactive oxygen species through the process of reducing Glutathione (when I say reducing, it doesn't mean diminish, its more of a meaning of restoring a already defeated/useless antioxidant that at one time was usefull before it was rendered of its benefits) so Glutathione may do its job by kicking some reactive oxygen species butt. So there you have it; on account of this articles study of PEA causing neurodegenerative disorders due to those bastard reactive oxygen species, just take ya one or both of the supplements I mentioned. Thats all.

 

[Flex]

Found this, its according to them far safer than amphetamines:

 

β-phenylethylamine, a small molecule with a large impact

PEA has been suggested as a ‘safe’ alternative to drugs, such as amphetamine or methylphenidate, which are accompanied by many undesirable side effects

http://www.ncbi.nlm....les/PMC3904499/

 

I just didnt know how problematic are the effects on the mitochondria.

[machete234]

PEA alone should be fairly inactive when taken orally because it is broken down quickly which is probably similar to taking DMT orally.

There should be hardly any effect from it. Is your article talking about endogenous phenetylamine?

 

Back to my microdose experiences which are from a while ago:

2C-D - I really really doubt this makes you smart. The only reason people think that is because a test person in Shulgin's book reported "I felt I could learn faster" or something to that effect.

What is possible with microdosing many psychedelics is in my oppinion getting into a flow state easier. With 2C-D this happens to be 5mg whereas a normal dose would be closer to 30mg (which makes you too altered for work) and getting a full trip with this is really hard dosage wise I would look elsewhere for that.

 

Some people mentioned using it as pre-workout on bluelight. I would say this makes running easier and the urge to stop excercise is reduced. So it can feel mildly stimulating and keep you in the flow easier (running trance or how you want to call it)

[Flex]

It looks to me that the supplemental form is discussed. Its brocken down to something active (opioids or something).

 

However it worked to me without any mao inhibitors: I was horny as fuck, anxious, high bloodpressure/vasoconstriction and pushed 

but the effect decreased after a while if I remember correctly. Got depressed in the meantime and since then, it doesnt work at all.