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Scientific Studies / Research Articles on ways to Reduce the Neurotoxicity of MDMA

enterjudas

Bluelighter
Joined
Jun 16, 2007
Messages
29
Hey guys,

I've got a friend who I have been trying to convince to try ecstasy with me, but she has forever been adamantly opposed. Recently, however, while logged into my college friend's computer, I stumbled on a psychology article about how antioxidants can greatly reduce the harmful effects of MDMA. After showing this to my friend, she immediately loosened up and said she would consider giving E a try if I could find more research to make sure we thoroughly prepared for the roll.

I already pretty much know what to take (Vitamins C, E, D, alpha-lipoic acid, etc.), but she won't believe Erowid trip reports or forum talk or even me; she wants to see peer-reviewed studies, medical jargon and all.

Unfortunately I can't find the article again because I'm not a member of the APA's PsycNET journal article database (my friend had access because he's a psych major). If anyone knows of any studies, articles, or research having to do with reducing the neurotoxicity of MDMA (or even meth or coke, for that matter), would you be kind enough to post a link so I can finally get this girl to have the greatest time of her life with me?



TL/DR -- I have a female friend who will take MDMA with me if I can find a bunch of scientific research and psychological articles about what supplements to take to reduce neurotoxicity.
 
You should research 5-HTP. It is over the counter, and sold in the vitamins section.

I think 5-HTP is a MUST if you want to reduce neurotoxicity. Your supposed to take a few before you roll, and take some after you have come down, and even the next following days.

If i remember correctly, Your brain goes through 4 or 5 stages to convert into new serotonin. 5-HTP is the chemical right before it turns into serotonin, so you skip 2 or 3 stages and serotonin is converted faster. Since MDMA floods your brain with serotonin, and exhausts your serotonin reserves, 5HTP is great to take before a roll and after you have come down from a roll. But never take 5HTP when you are rolling.. cause that can cause serotonin syndrome.

5HTP is a great tool to have, and greatly reduces negative side effects of X
 
Alves, E., Z. Binienda, et al. (2009). "Acetyl-L-carnitine provides effective in vivo neuroprotection over 3,4-methylenedioximethamphetamine-induced mitochondrial neurotoxicity in the adolescent rat brain." Neuroscience 158 (2): 514-523.

Shankaran, M., B. K. Yamamoto, et al. (2001). "Ascorbic acid prevents 3,4-methylenedioxymethamphetamine (MDMA)-induced hydroxyl radical formation and the behavioral and neurochemical consequences of the depletion of brain 5-HT." Synapse 40(1): 55-64.

Aguirre, N., M. Barrionuevo, et al. (1999). "Alpha-lipoic acid prevents 3,4-methylenedioxy-methamphetamine (MDMA)-induced neurotoxicity." Neuroreport 10(17): 3675-3680.

Tourino, C., A. Zimmer, et al. (2010). "THC Prevents MDMA Neurotoxicity in Mice." PLoS One 5(2): e9143.



Plus i know you said you already saw the erowid page but theres heaps of peer reviewed references at the bottom of the paper she can read.

http://www.erowid.org/chemicals/mdma/mdma_article3.shtml
 
THC Prevents MDMA Neurotoxicity in Mice.
http://www.ncbi.nlm.nih.gov/pubmed/20174577

The majority of MDMA (ecstasy) recreational users also consume cannabis. Despite the rewarding effects that both drugs have, they induce several opposite pharmacological responses. MDMA causes hyperthermia, oxidative stress and neuronal damage, especially at warm ambient temperature. However, THC, the main psychoactive compound of cannabis, produces hypothermic, anti-inflammatory and antioxidant effects. Therefore, THC may have a neuroprotective effect against MDMA-induced neurotoxicity. Mice receiving a neurotoxic regimen of MDMA (20 mg/kg x 4) were pretreated with THC (3 mg/kg x 4) at room (21 degrees C) and at warm (26 degrees C) temperature, and body temperature, striatal glial activation and DA terminal loss were assessed. To find out the mechanisms by which THC may prevent MDMA hyperthermia and neurotoxicity, the same procedure was carried out in animals pretreated with the CB(1) receptor antagonist AM251 and the CB(2) receptor antagonist AM630, as well as in CB(1), CB(2) and CB(1)/CB(2) deficient mice. THC prevented MDMA-induced-hyperthermia and glial activation in animals housed at both room and warm temperature. Surprisingly, MDMA-induced DA terminal loss was only observed in animals housed at warm but not at room temperature, and this neurotoxic effect was reversed by THC administration. However, THC did not prevent MDMA-induced hyperthermia, glial activation, and DA terminal loss in animals treated with the CB(1) receptor antagonist AM251, neither in CB(1) and CB(1)/CB(2) knockout mice. On the other hand, THC prevented MDMA-induced hyperthermia and DA terminal loss, but only partially suppressed glial activation in animals treated with the CB(2) cannabinoid antagonist and in CB(2) knockout animals. Our results indicate that THC protects against MDMA neurotoxicity, and suggest that these neuroprotective actions are primarily mediated by the reduction of hyperthermia through the activation of CB(1) receptor, although CB(2) receptors may also contribute to attenuate neuroinflammation in this process
 
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