MDMA danger, risk, safety, and benefits  protecting brain cells with nutritional supplements, vitamin
January 22 2016 by Ray Sahelian, M.D.

Deaths attributed to MDMA intoxication, which are fairly infrequent compared with the estimated number of recreational users, are often associated with a sharp increase of body temperature, also referred to as hyperthermia.

MDMA side effects, danger, safety, risk, harm and toxicity
A pre-existing defect in body temperature regulation may be a factor underlying some fatal reactions to 3,4-methylenedioxymethamphetamine. Thyroid hyperplasia (also called Graves' disease), is a thyroid disorder that makes patients less tolerant to heat. As the thyroid hormone is a major regulator of thermogenesis, hyperthyroidism may predispose some people to MDMA induced hyperthermia. Dr. Stephen J. Kish of the University of Toronto and the Centre for Addiction and Mental Health reports in the Journal of Forensic Sciences, 2007.
   Chronically hyperthyroid rats, compared with rats with normal thyroids, have much higher maximum body temperatures and rates of death following exposure to MDMA.

People who use the drug ecstasy may be raising their risk of the nighttime breathing disorder sleep apnea which causes a person's breathing to repeatedly stop and restart during the night -- leading to symptoms such as loud snoring and daytime drowsiness due to poor sleep. The answer may lie in the drug's toxic effects on serotonin-related brain cells, according to Dr. Una McCann, of the Johns Hopkins School of Medicine in Baltimore. Serotonin is a brain chemical with a range of vital functions, including roles in regulating mood, appetite and sleep. Dr. Una McCann thinks that damage to serotonin nerve cells explains the link between ecstasy and sleep apnea. Neurology, 2009.

MDMA may help people with posttraumatic stress disorder recover. Orjan Johansen of the Norwegian University of Science and Technology in Trondheim, reports that people with PTSD when given MDMA in addition to standard therapy have had good results. MDMA drug triggers the release of oxytocin, the so-called "cuddle chemical," which reduces fear while boosting trust. This could make it easier for PTSD victims to build a strong relationship with their therapist -- which is key to treatment success. MDMA could help re-balance the dysfunctional relationship between two brain regions seen in people with PTSD. These individuals show excessive activation of the amygdala and less activity in the ventro-medial prefrontal cortex. Journal of Psychopharmacology, online March 9, 2009.

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Acetyl-L-carnitine provides effective in vivo neuroprotection over 3,4-methylenedioximethamphetamine-induced mitochondrial neurotoxicity in the adolescent rat brain.
Neuroscience. 2009; Alves E, Binienda Z, Carvalho F, de Lourdes Bastos M, Tavares MA, Summavielle T. IBMC-Instituto de Biologia Molecular e Celular, Molecular Neurobiology, Neuroprotection Laboratory, Rua do Campo Alegre Porto, Portugal.
3,4-Methylenedioximethamphetamine is a worldwide abused stimulant drug, with persistent neurotoxic effects and high prevalence among adolescents. The massive release of 5-HT from pre-synaptic storage vesicles induced by MDMA followed by monoamine oxidase B (MAO-B) metabolism, significantly increases oxidative stress at the mitochondrial level. l-Carnitine and its ester, acetyl-l-carnitine (ALC), facilitate the transport of long chain free fatty acids across the mitochondrial membrane enhancing neuronal anti-oxidative defense. Here, we show the potential of ALC against the neurotoxic effects of MDMA exposure. Adolescent male Wistar rats were assigned to four groups: control saline solution, isovolumetric to the MDMA solution, administered i.p.; MDMA (4x10 mg/kg MDMA, i.p.); ALC/MDMA (100 mg/kg 30 min of ALC prior to MDMA, i.p.) and ALC (100 mg/kg, i.p.). Rats were killed 2 weeks after exposure and brains were analyzed for lipid peroxidation, carbonyl formation, mitochondrial DNA (mtDNA) deletion and altered expression of the DNA-encoded subunits of the mitochondrial complexes I (NADH dehydrogenase, NDII) and IV (cytochrome c oxidase, COXI) from the respiratory chain. Levels of 5-HT and 5-hydroxyindoleacetic acid (5-HIAA) were also assessed. The present work is the first to successfully demonstrate that pretreatment with ALC exerts effective neuroprotection against the MDMA-induced neurotoxicity at the mitochondrial level, reducing carbonyl formation, decreasing mtDNA deletion, improving the expression of the respiratory chain components and preventing the decrease of 5-HT levels in several regions of the rat brain. These results indicate potential benefits of ALC application in the prevention and treatment of neurodegenerative disorders.

Metabolic Brain Dis. 2013. Protective effects of N-acetylcysteine on 3, 4-methylenedioxymethamphetamine-induced neurotoxicity in male Sprague-Dawley rats. Exposure to 3, 4-methylenedioxymethamphetamine (MDMA) leads to spatial memory impairment and hippocampal cell death. In the present study we have examined the protective effects of N-acetyl-L-cysteine (NAC) on MDMA-induced neurotoxicity. A total of 56 male Sprague Dawley rats (200-250 g) received twice daily intraperitoneal (IP) injections of 5, 10 or 20 mg/kg MDMA plus NAC (100 mg/kg). Rectal temperatures were recorded before and after daily treatment. We used a Morris water maze (MWM) to assess spatial learning and memory. At the end of the study rats' brains were removed, cells were counted and the level of Bcl-2, Bax and caspase-3 expression in the hippocampi were measured. NAC pretreatment significantly reduced MDMA-induced hyperthermia. In the MWM, NAC significantly attenuated the MDMA-induced increase in distance traveled; however the observed increase in escape latency was not significant. The decrease in time spent in the target quadrant in MDMA animals was significantly attenuated (p < 0.001, all groups). NAC protected against MDMA-induced cell death and the up -regulation of Bax and Caspase-3, in addition to the down-regulation of Bcl-2. This data suggested a possible benefit of NAC in the treatment of neurotoxicity.