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Mdma supplementation

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9 replies to this topic

#1 Nameiwillforget

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Posted 10 September 2018 - 01:21 AM


So I have read multiple guides to MDMA supplementation, and most advised precautions against neurotoxicity, like keeping your head cool, taking enough antioxidants, drinking grapefruit juice and so on. What I wanted to ask here is hom much residual neurotoxicity still exists if you do all these things. Asked differently: is it possible to get MDMA from very neurotoxic to not too neurotoxic?

#2 xEva

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Posted 10 September 2018 - 03:15 AM

you're aware of selegiline, right? 

 

 



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#3 Nameiwillforget

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Posted 10 September 2018 - 09:26 AM

I was not, thank you for mentioning it. So this should reduce damage caused by oxidation. But is that the only way MDMA exhibits neurotoxicity?

#4 xEva

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Posted 10 September 2018 - 05:27 PM

if you google MDMA and selegiline, the mechanism of MDMA neurotoxicity is explained pretty well, usually in the intro section of an article. I don't recall the details now, but the toxicity is not due to MDMA per se, but rather the monoamine oxidise B that breaks down the flood of neurotransmitters it induces, and selegiline (== L-deprenyl) inhibits this enzyme.

 

 

Here is one of the key old papers: 

The monoamine oxidase-B inhibitor L-deprenyl protects against 3,4-methylenedioxymethamphetamine-induced lipid peroxidation and long-term serotonergic deficits. 1995

 

I just saw the titles of the later articles, and it looks like with each passing year they go deeper and deeper into molecular pathways of both MDMA toxicity and how selegiline mediates it -- in case you want to know the details.

 

But, due to good luck and good intuition, long before these studies were available on the internet, I happened to  "rave" on X [-tasy], on some weekends,  while taking 5mg selegiline once a week, on Wednesdays. Never had any problems. Then I heard that taking X with a MAOI is a big no-no, coz it should lead to serotonin syndrome. So, once I took X while off selegiline for a long time and can attest that, without a steady low level of selegiline, the experience itself was not as nice and the aftereffects were nasty.  This was many years ago and the doses I took (once a month on average) were "regular rave doses". I'm not sure how to introduce selegiline while "supplementing" MDMA. It would be nice if you could find a way and told us about it  :)

 

 

 


Edited by xEva, 10 September 2018 - 05:40 PM.

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#5 Painkillerrr

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Posted 10 September 2018 - 10:11 PM

You risk a serotonin syndrome, and silimar syndrome for dopamine taking mao and mdma or similar.

https://en.m.wikiped...otonin_syndrome
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#6 mike_nyc

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Posted 11 September 2018 - 07:42 AM

Based on my own experiences, I like to take cooling, brain protective supplements at the start, middle (3 hours in) and end (6 hours).  These include:

 

skq1

j147
Liposomal Phosphatidylcholine

fisetin

ginger

curcumin

olive oil

r-ala

grape seed extract

bilberry

quercetin

msm

luteolin

rutin

bromelain

 

I also like magnesium to relieve jaw clenching

 


  • Pointless, Timewasting x 1

#7 Nameiwillforget

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Posted 11 September 2018 - 08:55 AM

if you google MDMA and selegiline, the mechanism of MDMA neurotoxicity is explained pretty well, usually in the intro section of an article. I don't recall the details now, but the toxicity is not due to MDMA per se, but rather the monoamine oxidise B that breaks down the flood of neurotransmitters it induces, and selegiline (== L-deprenyl) inhibits this enzyme.


Here is one of the key old papers:
The monoamine oxidase-B inhibitor L-deprenyl protects against 3,4-methylenedioxymethamphetamine-induced lipid peroxidation and long-term serotonergic deficits. 1995

I just saw the titles of the later articles, and it looks like with each passing year they go deeper and deeper into molecular pathways of both MDMA toxicity and how selegiline mediates it -- in case you want to know the details.

But, due to good luck and good intuition, long before these studies were available on the internet, I happened to "rave" on X [-tasy], on some weekends, while taking 5mg selegiline once a week, on Wednesdays. Never had any problems. Then I heard that taking X with a MAOI is a big no-no, coz it should lead to serotonin syndrome. So, once I took X while off selegiline for a long time and can attest that, without a steady low level of selegiline, the experience itself was not as nice and the aftereffects were nasty. This was many years ago and the doses I took (once a month on average) were "regular rave doses". I'm not sure how to introduce selegiline while "supplementing" MDMA. It would be nice if you could find a way and told us about it :)


I understand roughly the mechanism by which selegiline would help which is by interrupting a certain kind of oxidation process (“These data suggest that the deamination by monoamine oxidase-B of excessive dopamine within the 5-HT terminal generates hydrogen peroxide that may lead to membrane lipid peroxidation, and perhaps other oxidative insults, resulting in selective 5-HT terminal degeneration subsequent to MDMA treatment.“). I think this is great news, since normal antioxidants generally have a short half-live compared to MDMA, making effective supplementation difficult. But I am still not sure that this is the only mechanism through which MDMA exhibits neurotoxicity.

Edited by Nameiwillforget, 11 September 2018 - 08:57 AM.


#8 Nameiwillforget

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Posted 11 September 2018 - 09:08 AM

You risk a serotonin syndrome, and silimar syndrome for dopamine taking mao and mdma or similar.

https://en.m.wikiped...otonin_syndrome


What you say is true in general, however, one-time normal doses of selegiline inhibit almost exclusively MAO-B, making it safe in combination with MDMA. The idea behind it is also explained here:=“https://www.reddit.c...t_mdma_induced/.
  • Agree x 1

#9 Painkillerrr

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Posted 11 September 2018 - 09:44 AM

Mdma does not work only by serotonin. But do what you want.

#10 xEva

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Posted 11 September 2018 - 11:05 AM

I understand roughly the mechanism by which selegiline would help which is by interrupting a certain kind of oxidation process (“These data suggest that the deamination by monoamine oxidase-B of excessive dopamine within the 5-HT terminal generates hydrogen peroxide that may lead to membrane lipid peroxidation, and perhaps other oxidative insults, resulting in selective 5-HT terminal degeneration subsequent to MDMA treatment.“). I think this is great news, since normal antioxidants generally have a short half-live compared to MDMA, making effective supplementation difficult. But I am still not sure that this is the only mechanism through which MDMA exhibits neurotoxicity.

 

maybe if you look in the papers that reference the old one linked above, you could find studies that explain MDMA neurotoxicity in other ways -?

 

when considering antioxidants, the other question to ask is how well they penetrate through BBB, it at all. 


Edited by xEva, 11 September 2018 - 11:11 AM.






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