Certain additives when consumed frequently can harm the body. Even within the ‘normal’ people (non-users) the top dot is actually over twenty times as far up as the bottom one. A less obvious problem in such human research is subject bias. [20] Bai F, Lau SS, Monks TJ “Glutathione and N-acetylcysteine conjugates of alpha-methyldopamine produce serotonergic neurotoxicity: possible role in methylenedioxyamphetamine-mediated neurotoxicity.” Chem Res Toxicol, 1999; 12(12):1150-7. People experimenting with it should be medically knowledgeable and have a support system in place to provide immediate emergency medical attention if a problem arises. After all, it’s not as if any of them actually read the research report. While dosages of such scale do (infrequently) occur in human users, it is likely that these users have reached such dosages in response to growing drug tolerance; with such progressive elevations of dosage over time, neurotoxic potential is reduced. Experiment 2: The first of the major studies in this field is from a team of scientists in the UK. Which drugs cause the most and least long lasting structural changes to the brain. Melody Ryan, in Clinical Neurotoxicology, 2009. However, the scientists noticed that something else was different in these dopamine depleted animals: When they gave them the overdose of MDMA, they didn’t overheat as expected. (Antioxidant use is actually good advice for any drug user, including smokers and drinkers.) Experiment 5: Beyond the above work finding no lasting harm from MDMA, the original ‘doom and destruction’ Ricaurte experiment has been replicated. In the meanwhile, when the minions of prohibition scurry about speaking of the ‘evils of ecstasy’, they will no doubt continue to refer to Ricaurte’s work as their ‘proof’, ignoring the newer, larger, more sophisticated, and much more numerous experiments suggesting that changes to the average ecstasy user’s brains from common patterns of use are, at worst, minor and temporary. A list of chemicals to be used in the development of an in vitro DNT testing method has been developed (Table 14.4), although never utilized, and strategies to improve such endeavor have been proposed (Kadereit et al., 2012). [19] The rats didn’t develop noticeable levels of neurotoxicity, which, combined with other clues, led some researchers to suggest that perhaps it was not MDMA itself that was toxic, but rather, that the MDMA was being metabolized (broken down) in the liver, converting into something that was toxic. [7] Simon NG, Mattick RP “The impact of regular ecstasy use on memory function”, Addiction, 2002; 97(12):1523-9. Abstract. Even at three hours, significant damage appears to have occurred. They studied 10 current ‘ecstasy’ users with an impressive average lifetime usage of about 650 ‘ecstasy’ tablets (one of the volunteers had taken nearly two thousand pills.) And finally, take some antioxidants. This phenomenon of your brain trying to compensate for unusual factors (such as drugs) is called neuroadaptation, and is one cause of drug tolerance (needing more to have the same effect) and physical dependence. [16] Hatzidimitriou G, McCann UD, Ricaurte GA “Altered serotonin innervation patterns in the forebrain of monkeys treated with MDMA seven years previously: Factors influencing abnormal recovery” J Neurosci 1999; 19(12):5096-107. Perturbations may appear and disappear rapidly, evolve slowly over days or weeks and regress over months or years, or cause permanent deficits. These monkeys were injected with 10 mg/kg of MDMA a day for four days straight by Ricaurte.[16]. Throw more than one factor into the pot, and things tend to break down. In the mid 1980s in the United States, MDMA was starting to be sold very openly and widely. For example, it has been shown that hepatotoxicity can be predicted by a few specific features (e.g., mitochondrial damage, oxidative stress, intracellular glutathione), which has allowed the development of potentially highly predictive screening approaches (Xu et al., 2008). • No drug mixing, including alcohol. This is particularly challenging for neurotoxicity, as multiple cell types and cellular mechanisms can be targeted by neurotoxicants. Further research is needed. It is not a comprehensive discussion of the totality of the research (although most brain scan work, pro and con, has been included.). [17] Buchert R, Thomasius R, Nebeling B, Petersen K, Obrocki J, Jenicke L, Wilke F, Wartberg L, Zapletalova P, Clausen M “Long-Term Effects of “Ecstasy” Use on Serotonin Transporters of the Brain Investigated by PET”, J Nucl Med 2003; 44: 375-84. It could also be that the oxidative strain placed on the axon by MDMA’s breakdown (if MDMA itself is indeed the culprit) is enough to increase the rate of SERT breakdown, causing levels of SERT to decline as ‘wear and tear’ on them exceeds the rate of replacement. Regardless of the mechanism, SERTs come back as long as the axon is still there…and there is good reason to believe the axons are still there in these people. 3. By contrast, only 30% of patients younger than 60 years developed neurotoxicity over 96 months of follow-up. ‘Severely damaged’ drug users who were actually normal. [26] Ricaurte GA, Yuan J, Hatzidimitriou G, Cord BJ, McCann UD “Severe Dopaminergic Neurotoxicity in Primates After a Common Recreational Dose Regimen of MDMA (“Ecstasy”)” Science, 2002; 297:2260-2263. However, approaches in this context have only recently started to be developed (Krug et al., 2013; Balmer and Leist, 2014). The ‘ecstasy’ users also smoked more pot, which other research has found also reduces the prolactin response to serotonin receptor activation.[36]. MDMA-related injuries and deaths are in most cases actually overheating injuries and deaths. Though there is still room for improvements and refinements, these in vivo tests have been shown, so far, to provide reliable indications on the potential neurotoxicity of chemical substances. [10] McCann UD, Szabo Z, Scheffel U, Dannals RF, Ricaurte GA “Positron emission tomographic evidence of toxic effect of MDMA (“Ecstasy”) on brain serotonin neurons in human beings”, Lancet 1998; 352(9138):1433-7. These Guidelines set forth principles and procedures to guide EPA scientists in evaluating environmental contaminants that may pose neurotoxic risks, and inform Agency decision makers and the public about these procedures. If serotonin axons have been lost, then the number of SERTs will be lower as well, since they are part of the axons. [10] While regrowth of serotonin axons could explain a recovery of total SERT density, the recovery seen in these heavy human users was uniform, precisely restoring normal SERT density in all regions of the brain studied, as contrasted with the patterns of serotonin axon regrowth seen in non-human primates given neurotoxic doses of MDMA (which produced hyperenervation of regions near the raphe nuclei but failed to restore enervation to less proximal regions.) They showed no signs whatsoever of neurotoxicity. There has been a popular belief that taking an SSRI like Prozac up to six hours after taking MDMA can prevent any neurotoxicity from occurring. So far, only 10–20 chemicals have been used in limited validation experiments. Managing oxaliplatin-induced neurotoxicity A fairly simple protocol of calcium and magnesium supplementation has been proposed to reduce the … By measuring levels of a ‘stress hormone’ called prolactin in the blood we can gauge the intensity of the animal’s reaction to serotonin receptor activating drugs, such as m-CPP (m-chlorophenylpiperazine.) Ricaurte’s great Ecstasy Parkinson’s Fraud: In the fall of 2002 George Ricaurte, the Dark Prince of suspect science, published an article in the prestigious journal Science that claimed that a “common recreational dose” of MDMA caused severe damage to the dopamine systems of monkeys. It was all they needed. However, the efficacy of platinum-based drugs is often compromised because of the substantial risk for severe toxicities, including neurotoxicity. [16] Hatzidimitriou G, McCann UD, Ricaurte GA “Altered serotonin innervation patterns in the forebrain of monkeys treated with MDMA seven years previously: Factors influencing abnormal recovery” J Neurosci 1999; 19(12):5096-107. [36] Gouzoulis-Mayfrank E, Becker S, Pelz S, Tuchtenhagen F, Daumann J “Neuroendocrine abnormalities in recreational ecstasy (MDMA) users: is it ecstasy or cannabis?” Biol Psychiatry, 2002; 51(9):766-769. As temperatures rise, these enzymes become less effective, and eventually stop working altogether, leaving the reactive oxygen species to run wild and attack the axon. [38] Reneman L,, Endert E, de Bruin K, Lavalaye J, Feenstra MG, de Wolff F, Booij J “The acute and chronic effects of MDMA (“Ecstasy”) on cortical 5-HT 2A receptors in rat and human brain” Neuropsychopharmacology, 2002; 26:387–396. A chemical may cause a neuronopathy, an axonopathy or affect synaptic transmission; it may alter astrocyte or oligodendrocyte/Schwann cell functions, or act by other mechanisms that may lead to neuro-inflammation. Follow NIDA on Twitter and Fa Experiment 6: Neuroendocrine Challenge. His understanding of MDMA neurotoxicity has led him to believe that less than 1.3 mg/kg of MDMA in a human user would produce neurotoxic damage (a dose he arrived at by scaling from 5 mg/kg in non-human primates, which he reports as producing neurotoxicity. Abstract. [5] At the very least, producing a vast increase in toxicity by giving 2 mg/kg 3x instead of a single 5 mg/kg dose seems to demand some discussion; it suggests that at the least the authors have managed to come upon an atypically toxic dosing regimen. [8] Ricaurte GA, Yuan J, McCann UD “(+/-)3,4-Methylenedioxymethamphetamine (`Ecstasy’)-Induced Serotonin Neurotoxicity: Studies in Animals” Neuropsychobiology, 2000; 42(1):5-10. MRI abnormalities are consistent with cortical or white matter high‐signal changes with a predilection for the occipital lobes.120–124 One autopsy case of a patient who died from cyclosporine toxicity revealed diffuse patchy white matter edema and astrocytic injury without infectious/inflammatory process.122 Although the mechanism of cyclosporine neurotoxicity has not been fully elucidated, one theory suggests that hypocholesterolemia may result in upregulation of the low‐density lipoprotein receptors, which increases intracellular transport of cyclosporine. There’s been a news story claiming that ecstasy use causes depression. The male users didn’t show even temporary reductions in SERT this time, even among the “heavy” user group (which had an average lifetime use of 530 pills. Finally, a battery of alternative testing models for neurotoxicity is not expected to fully replace current in vivo animal testing, but would limit such testing only to those compounds for which, for different reasons, additional information on neurotoxicity is deemed important. Similarly, chemicals to be used as positive controls in validation studies should cover most, if not all, of these processes, and would thus need to be several dozens. • Antioxidants are chemicals that, when they run into an oxidizer like hydrogen peroxide or superoxide, will easily react with it, neutralizing it. Taking multiple full doses in an evening may not be safe. However, this argument falls short on several counts. “But I know people that are stupid/emotionally unstable from using ‘ecstasy’…doesn’t that mean they’ve been brain damaged?!”. ), Given a large enough dose under the wrong circumstances, MDMA can cause the destruction of the axons of serotonin neurons. ), But…it’s far from perfect. (MDMA does not appear to kill brain cells, even under this ‘neurotoxic’ scenario. How do we know that these people with below average but still normal levels of SERT weren’t simply more likely to take a serotonin releasing drug in the first place? In the case of coffee drinkers, your brain makes itself less sensitive to caffeine, creating tolerance (and in many cases, mild dependence.) Although many researchers have investigated the medical and cognitive consequences of drug abuse, the neurotoxicity induced by these drugs still requires comprehensive attention. [21] Colado MI, Green AR “The spin trap reagent alpha-phenyl-N-tert-butyl nitrone prevents ‘ecstasy’-induced neurodegeneration of 5-hydroxytryptamine neurones” Eur J Pharmacol, 1995; 280(3):343-6. [22] Bleh, ref has gone missing…try again in a month or two if you’re comitted. At the end of the day, I am wholly unmoved when Billy Bob the psychologist publishes an article claiming evidence of neurotoxicity because his ecstasy-using volunteers were not identical to his non-drug using volunteers. (‘Safe’ in the sense that driving a car is safe; relative, not absolute safety. Maybe…maybe not. [18] Lieb R, Schuetz CG, Pfister H, von Sydow K, Wittchen H “Mental disorders in ecstasy users: a prospective-longitudinal investigation.” Drug Alcohol Depend 2002; 68: 195-207. The patient developed memory failure, gait ataxia, and incontinence in the postradiation setting. Close. Or has he? Abstract. [15] Scheffel U, Szabo Z, Mathews WB, Finley PA, Dannals RF, Ravert HT, Szabo K, Yuan J, Ricaurte GA “In Vivo Detection of Short- and Long-Term MDMA Neurotoxicity–A Positron Emission Tomography Study in the Living Baboon Brain”, Synapse 1998; 29(2):183-92. Tissue necrosis and atherosclerosis of large cerebral vessels have also been identified, suggesting vascular injury and subsequent tissue infarction and necrosis as potential mechanisms of WBRT-related neurotoxicity [81]. The ‘ecstasy’ users were also all amphetamine users; a practice which should increase the risk of neurotoxicity. METH can also damage the heart and lungs, leading to ischemic and hypoxic injury to the brain. There is difficulty in establishing causality in many of these cases, mainly because of the possibility of nervous system infection or fevers as additionally potentially causative factors. Now…would you care to take a guess as to what miscreant produced this bit of scientifically suspect but loved-by-the-government ‘research’? [1] Ricaurte GA, DeLanney LE, Irwin I, Langston JW “Toxic effects of MDMA on central serotonergic neurons in the primate: importance of route and frequency of drug administration” Brain Res , 1988; 446(1):165-8. It may not be possible to avoid all the sources, but at least if known, a person can try to reduce its exposure as much as possible. I don’t buy it. MDMA does not normally cause significant increases in body temperature in humans; a significant increase in body temp is abnormal and should be treated immediately. • Treatments that block an enzyme in the brain called MAO (MonoAmine Oxidase) can completely prevent neurotoxicity. [9] Vollenweider FX, Gucker P, Schönbächler R, Kamber E, Vollenweider-Scherpenhuyzen MFI, Schubiger G, Hell D “Effects of MDMA on 5-HT uptake sites using PET and [11C]-McN5652 in humans” Conference of the German Society for Psychiatry, Psychotherapy and Neuromedicine, 2000. In one of the earlier experiments with MDMA neurotoxicity, MDMA was directly injected into a small part of some rat’s brains. The eyes do not appear in the other image, suggesting that different settings have been used–settings that would hide more of the scan’s data. Can MDMA (Molly, ecstasy) damage your brain? Information on reproducibility and interlaboratory variability are also needed. . Where things get tricky is that these renderings don’t show all the data. Ravers (attendees of all-night dance parties) are usually the recruitment pool for volunteers, which brings a rather unlikely assumption of otherwise equivalent lifestyles between ecstasy users and non-users. In vivo testing guidelines for neurotoxicity and developmental neurotoxicity have been developed, implemented and validated. What about brain scans done on real world heavy users, who frequently push nightly doses to 3 mg/kg and higher? Drugs.com provides accurate and independent information on more than 24,000 prescription drugs, over-the-counter medicines and natural products. • MAPS coverage of the scandal (including links to the original article, the retraction, and reactions from the research community.). However, the study was far less clear-cut than it first appeared. But…1.5 mg/kg isn’t all that much higher than the 1.28 mg/kg Ricaurte swore would cause detectable damage. These alternative tests should serve as Tier 1 tests to allow the screening of compounds whose potential neurotoxicity is unknown. As a result, parts of the brain near the raphe nuclei (the clusters of serotonin neurons in the base of the brain) had much higher levels of serotonin axons than the brains of normal baboons, but the more distant parts of their brain remained depleted of serotonin axons. CSF shunting may be partially beneficial in a subset of patients. A more radical approach is the use of the MAOI L-Deprenyl (Selegiline), which has proven to be extremely effective in preventing MDMA neurotoxicity in lab animals and does not interfere with MDMA’s desired activity. How could it all be made to fit together? Researchers in the ‘ecstasy users have worse memories’ field tend to ignore this problem. For instance, only one of the ‘ecstasy’ users was actually below the normal range of the non-users, and he was one of the lighter users. Abstract. [7] Reneman L, Booij J, Lavalaye J, de Bruin K, Reitsma JB, Gunning B, den Heeten GJ, van Den Brink W “Use of amphetamine by recreational users of ecstasy (MDMA) is associated with reduced striatal dopamine transporter densities: a [123I]beta-CIT SPECT study– preliminary report” Psychopharmacology (Berl), 2002; 159(3):335-340. Abstract. Some of the effects of neurotoxicity may appear immediately, while others can take months or years to manifest.The effects of neurotoxicity depends on various different factors such as the characteristics of the neurotoxin, the dose a person has been exposed to, ability to metabolise and excrete the toxin, the ability of affected mechanism and structures to recover and how vulnerable a cellular target is.Some of the symptoms of neurotoxicity include: 1. Key elements of the validation process are the choice of neurotoxic compounds (which ones and how many) and their concentrations to be used in in vitro tests. We conclude the chapter with a discussion of addicted patients who might benefit from such interventions. There was no damage. [25] Lim HK, Foltz RL “In vivo and in vitro metabolism of 3,4-(methylenedioxy)methamphetamine in the rat: identification of metabolites using an ion trap detector” Chem Res Toxicol, 1988; 1(6):370-8. [33]) It’s also possible that the axons make fewer SERTs available on their surface as a response to over-activation during MDMA exposure. [31] Liechti ME, Vollenweider FX “Acute psychological and physiological effects of MDMA (“Ecstasy”) after haloperidol pretreatment in healthy humans” Eur Neuropsychopharmacol 2000; 10(4):289-95. May 17, 2018. They needed a ‘scientist’ to do the research, and they knew just who to call: George Ricaurte. Neurotoxicity, Immunotoxicity and Drug Toxicity – A Review. If there were reason to believe that somebody was beginning to suffer neurotoxic damage (high dose, heatstroke) an SSRI might be an effective ‘rescue’ medication to limit the extent of the damage. The scan on the left side was selected from the ‘non-user’ group because it had a high number of SERTs. Here is another, more recent look at MDMA supplements. In one study, 100% of patients older than 60 years who were treated with WBRT-containing regimens for PCNSL experienced clinical neurotoxicity manifesting as dementia, ataxia, and incontinence, with a median time to onset of 13.2 months [80]. To lay the groundwork for future human experiments with MDMA in psychotherapy, in 2000 a group of scientists in Switzerland gave a group of human volunteers sensitive brain scans to determine how many SERTs they had. Hence, there is a great need to develop alternative models, utilizing mammalian cell preparations of different complexity and/or nonmammalian animal system, as indicated earlier. Any differences that are found must be due to permanent damage. There is an ocean of confounds that must be bridged to make such conclusions credible, especially in light of the strong evidence of no permanent structural changes in user’s brains. The quality of retrospective human research has, however, been increasing over the years; with luck, the future may bring more substantive work. Some disrupt neural function, others induce maldevelopment or damage to the adult nervous system. Neurotoxicity is a potentially devastating complication that can occur in response to antineoplastic therapies including WBRT and chemotherapy. This is your baboon on drugs: SERT density measured by PET scan. For alternatives for different types of pain, see our charts, Pharmacotherapy of … It clears out alcohol, drugs, and chemicals from your blood. This document expresses and makes the case for the final opinion that my research brought me to: That moderate recreational use of MDMA does not present a credible risk for neurotoxicity. These patients had reduced concentrations of nerve growth factor and brain-derived neurotrophic factor, both of which are postulated to influence the survival of neurons, suggesting that they may have a role in neurotoxicity associated with heroin use. 4. They used more opiates, they used more amphetamines…and they smoked considerably more pot, long known to cause (non-permanent) memory problems. Don’t mix MDMA with drugs that could increase the risk of overheating, such as amphetamines. Archived. In one study from the Australian government, it was found that, although people who used ‘ecstasy’ and pot did have slightly worse memories than people who didn’t use any drugs, the deficits were in the same places and of the same magnitude as those seen in the group of people that used similar amounts of pot but no ‘ecstasy’. After all, MDMA is an amine, MAO attacks amines, and MDMA is clearly being attacked at the amine by something in brain tissue. Current ecstasy users had slightly lower SERT density than non-users, but the former ecstasy users were indistinguishable from people who had never used the drug: So, how it possible that the original piece of Ricaurte research, so vaunted by the US government, trumpeted from every news outlet, and chronically referred to in prohibitionist literature as proof of the evils of MDMA was so badly off? [32] Schmidt CJ “Neurotoxicity of the psychedelic amphetamine, methylenedioxymethamphetamine” J Pharmacol Exp Ther, 1987; 240(1):1-7. (See the User’s Guide for more information on dosages. Visit Preloading for more information on antioxidants. Further research has only confirmed their findings, so the answer is…yes and no. The prescribing information for Adderall published by the U.S. Food and Drug Administration(FDA) states that the medication is not recommended to be taken long term. In their final report, the researchers concluded that “Low-dose recreational MDMA use does not cause detectable persistent rCBF (regional cerebral blood flow) changes in humans.”. These interventions involve various targets such as dopaminergic system, mitochondria, cell death signaling, and NMDA receptors, among others. That suggests there wasn’t any actual loss of axons…just a temporary reduction in the SERTs on them. Just as many other drugs are, such as that Adderall you were given for your attention-deficit disorder, as well as a number of other fairly safe FDA-approved drugs. Elderly patients with PCNSL are especially vulnerable to treatment-related neurotoxicity. [37] Scheffel U, Lever JR, Stathis M, Ricaurte GA “Repeated administration of MDMA causes transient down-regulation of serotonin 5-HT2 receptors” Neuropharmacology, 1992; 31(9):881-93. Drugs account for 2- [14] Reneman L, Booij J, de Bruin K, Reitsma JB, de Wolff FA, Gunning WB, den Heeten GJ, van den Brink W “Effects of dose, sex, and long-term abstention from use on toxic effects of MDMA (ecstasy) on brain serotonin neurons” Lancet 2001; 358(9296):1864-1869. Abstract. Oxaliplatin is an integral part of chemotherapy for colorectal cancer (CRC) in the adjuvant and metastatic setting. (See MDMA At Work. If you’re going to be dancing or otherwise physically very active for a prolonged period, pay some attention to staying hydrated. What did these things have in common? Shame on the authors for the incomplete, misleading and sensationalistic nature of this research report, and shame on the editors of Science for publishing it. Neurotoxicity. Assumption 1 has been disproven; pre drug-use rates of mental illness in ecstasy users are higher than those of non-drug users as well as users of other categories of drugs. One patient developed decreasing visual sensitivity in one eye after the 5th dose of liposomal cytarabine 50 mg; the condition improved upon discontinuation of liposomal cytarabine [27c]. Theories about why and how MDMA might be neurotoxic are fine and good, but we haven’t really answered the most important question of all yet: Are ‘ecstasy’ users damaging their brains? Drugs with least and most neurotoxicity/long term changes to the brain. Visual disturbances were developed by 8 patients; furthermore, 6 of those patients developed double vision and papilledema. His ‘ non-users ’ were ( prior to their drug use ) just non-drug... 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