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

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
A pre-existing defect in body temperature regulation may be a factor underlying some fatal reactions to MDMA (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, July 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, online December 2, 2009.

MDMA for PTSD
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.

Use of nutritional supplements
Acetyl-L-carnitine provides effective in vivo neuroprotection over 3,4-methylenedioximethamphetamine-induced mitochondrial neurotoxicity in the adolescent rat brain.
Neuroscience. 2009 Jan 23; Alves E, Binienda Z, Carvalho F, Alves CJ, Fernandes E, de Lourdes Bastos M, Tavares MA, Summavielle T. IBMC-Instituto de Biologia Molecular e Celular, Molecular Neurobiology, Neuroprotection Laboratory, Rua do Campo Alegre, 823, 4150-180 Porto, Portugal.
3,4-Methylenedioximethamphetamine (MDMA, ecstasy) 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.