How to Prevent or Promote Neurotoxicity

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        In spite of the seemingly inevitable neurotoxic effects that MDMA can have on the body there has been research with the aim of helping people protect themselves. The main focus of this research has been to find out what chemicals are causing serotonin axons to stop working and how to stop these chemicals from working their evil magic. The primary chemical which causes the inactivation is a neurotransmitter called dopamine. It is theorized that taking SSRIs, or using antioxidants, (specifically vitamin E) will inhibit the neurotoxic effects of Ecstasy (Johnson 2002 and Schmidt 1990). The anti-oxidants will stop the breakdown of dopamine inside the serotonin neuron and the dopamine blocker will make it so that dopamine does not enter back into the cell when it is inside the synapse. The SSRI will cause the serotonin reuptake center to be blocked, denying entrance to serotonin or dopamine. This is especially beneficial because, if prozac is taken within six hours after use of Ex, much of the nuerotoxic effects will by averted because dopamine will not be allowed to enter into the neuron and destroy it from the inside out.

        It is also a good idea to be aware of the contents of the drugs which are entering your body. A major problem with the MDMA on the street is that it is not purely MDMA but a combination of MDMA and one or more drugs. Since many people know that MDMA is thought to produce effects like the combination of hallucinogens and amphetamines, these are common among the "extras" included in the drug. Along with the variation in the amount of other drugs in street MDMA there is also varying quantities of MDMA itself. This means that one tablet could contain 80-90 mg of MDMA while others could have as little as half that much or they could contain much more. When the MDMA quantity is so variable it is difficult to judge what amount should be taken and could lead to harmful consequences if the tablets contain very different quantities of MDMA.




Prevention of Neurotoxicity


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