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The short answer is that science has proven at least in my opinion that moderate MDMA use does not cause any lasting harm. The long answer…is a very long answer indeed, but worth the read. To really appreciate the debate over MDMA neurotoxicity, it helps to understand a little bit about where these claims came from. It was still legal, and dealers were doing their best to capitalize on that fact. The Drug Enforcement Agency responded the way it always does when a drug becomes popular: It declared that MDMA was a terrible menace and had to be outlawed. There was just one problem: Federal law requires that a drug be inherently unsafe to use under any circumstances in order for the D. A to declare it illegal. They desperately needed a trump card to justify placing it in Schedule 1. Then, some bright fellow remembered that many drugs were neurotoxic causing damage to the brain at high doses; it was likely MDMA would be as well if the dose was pushed high enough. Ricaurte was a relatively young and inexperienced researcher, but his work had been very predictable: Ricaurte performed as expected: He got a grant, they got a paper declaring that MDMA was neurotoxic. And in fact, MDMA is neurotoxic if you give an animal too much under the wrong circumstances. 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. The real question, then, is not whether MDMA could cause permanent damage; at a high enough dose all drugs cause widespread damage and death. For interspecies scaling to work, the mechanism by which the drug is toxic must be a simple one. Throw more than one factor into the pot, and things tend to break down. The animal toxicity data is also based on injecting animals with the drug as much as Injecting a drug bypasses the digestive tract and delivers the drug into the bloodstream much more quickly than taking a drug orally would. As a result, an animal that gets an injection is exposed to much higher peak concentrations of the drug. His most recent claims are that 1. They got what they paid for: A scientist suggesting that human MDMA users were damaging their brains. It was all they needed. The entire legal record is available at MAPS. Given a large enough dose under the wrong circumstances, MDMA can cause the destruction of the axons of serotonin neurons. See Your Brain and The Neuron for more information on what serotonin neurons and axons are and do. The neuron itself cell body is not destroyed; only the axon is. These are before-and-after images of monkey brain frontal lobes. The bright lines are serotonin axons chemically treated to stand out. Given the selectivity of the damage, it seemed likely that something that was damaging to the axons was being concentrated within them. As more research was done, it became clear that the toxic chemical whatever it was was being actively pumped in by the serotonin transporters SERTs. Many researchers believed with a good deal of evidence to support the idea thatdopamine was the toxic chemical, which they thought might be getting in through the SERTs after the local serotonin supply was depleted by MDMA. In , an important new piece of research was done: Animals who had been given drugs that removed virtually all of the serotonin and dopamine in their brains were given what should have been a neurotoxic dose of MDMA. There was no damage. However, the scientists noticed that something else was different in these dopamine depleted animals: That was significant, because research has shown that body temperature is a critically important factor in MDMA neurotoxicity. Knowing this, the researchers took another group of dopamine depleted animals, gave them another overdose of MDMA, and warmed them with heating pads so that their temperature reached the same levels as normal control animals did when given the same amount of MDMA. The results were striking: The animals with essentially no dopamine in their brains suffered the same level of neurotoxic damage as the control animals did when their body temperatures were kept as high. Something else was at work; dopamine was not the toxic chemical in question. In the search for a toxic metabolite of MDMA, the best candidates were various forms of ether-ring cleaved N-demethylated MDMA, such as the glutathione adduct of 3,4-dihydroxyamphetamine which is indeed neurotoxic. Further research is needed. We do, however, have a lot of strange and interesting clues. How could it all be made to fit together? What did these things have in common? There is a common thread:. 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. Under this model, three things need to happen in order for you to suffer neurotoxicity. Neither steric hindrance nor the minor additional electron-donating effect of the alpha-methyl group provide an obvious barrier to oxidation by the heme group of MAO: What can an MDMA user do to protect themselves? The first defense is to keep doses within the realm of sanity nobody should be taking ten pills a night, period, and try to give yourself at least several days between uses. Second, be aware of the dangers of overheating. If you are going to be dancing or some other very physical activity stick to places that are reasonably cool and have good air flow. Visit Heatstroke for more information; too much water can be dangerous as well. And finally, take some antioxidants. Antioxidant use is actually good advice for any drug user, including smokers and drinkers. Visit Preloading for more information on antioxidants. SSRIs such as Prozac or Paxil can protect against neurotoxicity by preventing access to the inside of the axon. Lower levels of serotonin indicate neurotoxicity has occurred since serotonin is made by and stored in the serotonin axons. Although giving the rats Prozac fluoxetine up to six hours after the MDMA prevented some of the damage, it was only a partial solution. Even at three hours, significant damage appears to have occurred. In theory, Deprenyl is arguably the most potentially effective neuroprotective regimen, but more work needs to be done before any substantive statement on safety can be made. In order to use Deprenyl as a neuroprotectant, a moderate dose perhaps 5 mg should be taken before the MDMA. This combination may prove to be quite dangerous! 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. Is MDMA neurotoxic at recreational doses? The Drug Enforcement Agency is absolutely adamant that they are, as are many politicians. Where there is a great lack of support for that idea, however, is from the people who should know: Biochemists and neurologists and psychiatrists. To date, I have only seen one group of researchers in the hard sciences biochem, neurochem, etc. Our good friend Ricaurte and his shifting little band of coconspirators. So what does science have to say about it? There are two basic kinds of research in this area: Studies that directly examine the brain, and studies of how well users are functioning. In the first case, brain scans that can detect SERTs are often used. If serotonin axons have been lost, then the number of SERTs will be lower as well, since they are part of the axons. In the latter case, users are given tests to check their memory, etc. The government of course hailed this as proof that the demon-drug ecstasy was destroying poor young minds. However, the study was far less clear-cut than it first appeared. The author Ricaurte failed to control for disruptions of sleep patterns long known to affect cognitive function, and likely to be an issue among stimulant users. They used more opiates, they used more amphetamines…and they smoked considerably more pot, long known to cause non-permanent memory problems. Indeed, there were numerous possible explanations for the modest differences in memory, including neuroadaptive responses to recent MDMA exposure. Marijuana in particular has proven to be a major factor is such test scores. They had slightly poorer memories because they were unrepentant potheads. It should be noted that minor memory problems in the days after use are common, due to disruption of the serotonin system and fatigue. Heavy users also often show some memory and concentration problems, similarly to marijuana and even alcohol users. This phenomenon appears to be the result of adaptive changes to the brain, not neurotoxicity. MDMA users have holes in their brains. The short version is that this is complete nonsense. Like most of the foolishness floating around the planet, this myth started on TV; the Oprah Show to be precise. This is some form of PET scan; the colors may indicate blood flow or sugar uptake or some more exotic measurement. Instead, the technician will choose which ranges of data are rendered. The result is that minor differences can be made to look very dramatic, as demonstrated in this rendering of another PET scan:. Perhaps we should start a campaign claiming cancer treatment makes your brain disappear? In fact, those two images could possibly have been generated from the same scan of the same person, merely rendered differently. As expected, there was a decrease in blood flow immediately after MDMA use, but it returned to normal within weeks. Further research has only confirmed their findings, so the answer is…yes and no. Yes, there is a modest change to your brain after using MDMA that seems to last for about three to four weeks, give or take. If you were really destroying parts of the serotonin system, blood flow should be more-or-less permanently altered. Human brain scans have proven neurotoxicity. The most colorful part of the ads in the literal and figurative sense was this image graphically showing SERT density:. Most people would agree that this looks pretty bad. Clearly, the Ecstasy user has done terrible damage to his brain. Likewise, the image on the left was selected because it was one of the ones with the fewest. The dots are the readings taken from different people. The higher up the dot of a person is, the more SERTs they had. Immediately some questions present themselves. What that means is that the data is actually spread out over a lot more space than it appears. Are we to believe that the range of normal for human brains has this much spread in it? The immediate conclusion is that there was something fundamentally flawed in the research. Maybe they did something wrong procedurally. Maybe they botched the calculations. Even if we assume that the brain scans were done properly, and that the data really is trustworthy, there are still some rather large questions. There is also the small problem of lack of reproducibility. So, we have a data spread that defies belief. And results that nobody else can reproduce. Beyond simply not being able to come up with results even remotely similar to what Ricaurte was claiming, the more recent brain scan work is well worth examining in its own right. To lay the groundwork for future human experiments with MDMA in psychotherapy, in a group of scientists in Switzerland gave a group of human volunteers sensitive brain scans to determine how many SERTs they had. They then gave them 1. A month after they had taken the MDMA, new brain scans were taken. They showed no signs whatsoever of neurotoxicity. The first of the major studies in this field is from a team of scientists in the UK. Further research has only confirmed what the Brits found. The next pair of experiments come from the Netherlands, conducted by the team of Reneman et al. This study is one of the largest, most sophisticated pieces of research of its type to date. This graphic represents SERT density in the different groups of women. Another view of the data, this time including the men:. As mentioned above, the moderate users were normal, the heavy male users were normal, the heavy current female users were below average, but former female users were again normal. So, how do you suppose the press reported this research? But perhaps I judge them too harshly. New research like this is brought to the attention of the press and through them, the public by press releases, which gives the people writing the press releases a great deal of influence over what the public thinks it meant. Only the research itself can be trusted to tell its story accurately, and even then not always. However, one might wonder, could this recovery of SERTs mean that neurotoxicity did occur destroying axons , but the axons regrew? This question has also been answered: When baboons were given a neurotoxic dose of MDMA destroying many of their serotonin axons , then given brain scans for SERT density a year later, axon regrowth was seen. 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. Somehow, MDMA use at least at heavy levels can cause temporary reductions in the number of SERTs on the axon, but the axons themselves appear to have been spared. This is your baboon on drugs: The image on the right is representative of the baboons that were given a neurotoxic dose of MDMA a year before the brain scans; the animal on the left was not given any drugs. 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. In , a group of German researchers working for the German version of the FDA published the results of a massive brain scan study on current and former ecstasy users. Where Ricaurte had 14 ecstasy users with an average use of tablets, the German group had 29 current users with an average of tablets and 29 former users with an average use of tablets. The results are shown in the graph below. 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? Maybe the gods smiled on him and brought him subjects that simply were not representative of the general population. Maybe he and his people screwed up somehow. We may never know for sure. One of the long-term effects of MDMA neurotoxicity in lab animals is that the animals become hyper-sensitive to drugs that activate serotonin receptors. This occurs because when levels of serotonin severely decrease, the brain increases the number of serotonin receptors to try to compensate. The graph below shows the difference in reaction to m-CPP in normal monkeys vs. Not only did they not have an exaggerated reaction to m-CPP, they actually had slightly less of a stress reaction than non-ecstasy users:. That they were actually somewhat less stressed by the drug seems surprising at first…but becomes less odd when you consider that, by definition, MDMA users are people who use and like drugs that activate serotonin receptors in the case of MDMA, by releasing serotonin. However, this argument falls short on several counts. Rats show complete re-setting of serotonin receptor densities within weeks of their last dose of MDMA. The press and politicians went mad. More than a year later, after scathing criticism from TheDEA. The monkeys had actually been given massive doses of methampetamine, not MDMA! Ricaurte claims the drug manufacturer switched the labels on two vials one of methamphetamine, one of MDMA causing the error. The manufacturer RTI has vigorously disputed the claim that a switch occurred at their facilities which are very tightly run under D. Somebody owes us a refund; I nominate Ricaurte. The pathology of this case delayed onset relative to drug use followed by rapid progression is inconsistent with all known research on the progression of MDMA neurotoxicity, which produces a maximization of damage shortly after exposure followed by slow partial recovery. If Ricaurte et al have additional information about this case that was unavailable to the doctors treating the patient, they have made no mention of it. 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. If only on the grounds of the sheer novelty of the results from this particular dosage regimen it seems presumptuous to declare equivalency to human users until some explanation can be offered for the sharp divergence of results between these two experiments. The principle author Ricaurte has long championed a minimalistic method of interspecies dosage scaling between non-human primates and humans. His understanding of MDMA neurotoxicity has led him to believe that less than 1. However, prospective human brain-scan experiments have failed to find even the slightest indication of neurotoxicity or even subject distress at 1. Given this pattern of recovery, there is every reason to believe that the minor temporary loss of available SERT proteins observed was not due to neurotoxic damage destruction of axons. Are we to believe that Ricaurte et al. In the final analysis, I must regard this recent product of Ricaurte et al. 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. The research this story is based on has apparently never been published, suggesting that it was of such low quality that even in an age of anti-drug hysteria no scientific publication felt it was worth printing. However, the basic finding that ecstasy users are more likely to have emotional problems does in fact appear to be true. In the case of coffee drinkers, your brain makes itself less sensitive to caffeine, creating tolerance and in many cases, mild dependence. 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. Neuroadaptation is not damage! It is a constant, normal, and entirely controlled process by which your brain tries to keep itself running smoothly. Sometimes neuroadaptation can be manipulated in useful ways: However, in the case of recreational drug use, this effect is almost always disruptive: You take a drug for a brief period, your brain tries to compensate, and then when the drug is gone your brain is off-balance again, now over-compensating. It will return to normal, but the process can take days, weeks, in some cases even months. In the case of MDMA, your brain makes itself less sensitive to serotonin to try to compensate for all the serotonin the drug releases. Fully re-setting its sensitivity levels after even a single use of MDMA can take weeks, even months from a very high dose. In extreme cases, this can apparently lead to users becoming seriously depressed, anxious, unmotivated, poor memories, etc. I absolutely believe that MDMA can be neurotoxic in humans. Taking multiple full doses in an evening may not be safe. MDMA-related injuries and deaths are in most cases actually overheating injuries and deaths. 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. The role of overheating in MDMA neurotoxicity can hardly be exaggerated; no animal experiment has ever produced neurotoxicity at any dose of MDMA at normal human body temperature. Although the exact mechanisms of MDMA neurotoxicity are at best imperfectly understood, damage is clearly a result of the combination of the unusual strain placed on the neurons by drug exposure being greatly amplified by overheating. I do not anticipate human neurotoxicity at any likely voluntarily taken dose of MDMA in the absence of significant and prolonged hyperthermic response. Origin of the Species. The research leading to this final document involved a comprehensive review of English-language MDMA research from the s to present; well over a thousand journal articles detailing numerous animal and human experiments, field reports from doctors, opinions of experts, etc. I compiled my notes, discussed and argued with other academics, contacted researchers for more information in some cases, etc. 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. It is not a comprehensive discussion of the totality of the research although most brain scan work, pro and con, has been included. This was not done as a way to avoid evidence against my position; rather it is because the quality of such research has been so consistently poor as to not merit detailed examination. The typical work in this category makes the following chain of assumptions:. There are no differences in sleep patterns, sub-clinical psychiatric disturbances or any other environmental factors that could affect test performance. Any differences that are found must be due to permanent damage. Neuroadaptation such as the brain scan research amply demonstrates the existence of will not be considered. 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. Assumption 2 cannot easily be disproven, but is unlikely to be true. Assumption 3 is disproven by the unremarkable fact that when concurrent use of marijuana is controlled for, differences in cognitive performance such as word recall mostly or entirely vanish. 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. That MDMA causes transient disruptions of memory is well established anecdotally, and should be inferred from research identifying neuroadaptive changes in available serotonin receptor densities in both experimental animals and humans following recent MDMA exposure. Those that do make some effort to control this effect usually do no more than ask volunteers not to use for two weeks and give urine test for drugs the day of testing. However, all research indicates that MDMA can subtly affect the mind for at least weeks, and urine drug tests only detect use within the past few days. A less obvious problem in such human research is subject bias. Any sort of expectation of what the results will be by the test subjects will throw off those same results. For instance, just about anybody you recruit for an MDMA study knows that they are expected to have memory problems. How can you control for this sort of bias? It takes balls of steel to deliberately shape experimental results like that, but not everybody working in this field has a high sense of scientific integrity. In the end, I hold a dim view of the genre. Besides, why try to guess at serotonergic damage from behavior when we have perfectly capable brain-scanning technology to directly examine the serotonin system? For these reasons of both quality and directness of the measurement technique this page almost exclusively examines brain scan work. 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. The quality of retrospective human research has, however, been increasing over the years; with luck, the future may bring more substantive work. In the Beginning… To really appreciate the debate over MDMA neurotoxicity, it helps to understand a little bit about where these claims came from. Mechanisms of neurotoxicity Given a large enough dose under the wrong circumstances, MDMA can cause the destruction of the axons of serotonin neurons. How it causes this strangely precise damage has been the subject of a lot of speculation and debate. There is a common thread: The result is that minor differences can be made to look very dramatic, as demonstrated in this rendering of another PET scan: The most colorful part of the ads in the literal and figurative sense was this image graphically showing SERT density: The other brain scan work: The data shown was collected from part of the cingulate cortex. Another view of the data, this time including the men: 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: Not only did they not have an exaggerated reaction to m-CPP, they actually had slightly less of a stress reaction than non-ecstasy users: And of course, there is my own not-so-little contribution to the shit-storm: Ecstasy use and mental health. Origin of the Species The research leading to this final document involved a comprehensive review of English-language MDMA research from the s to present; well over a thousand journal articles detailing numerous animal and human experiments, field reports from doctors, opinions of experts, etc. The typical work in this category makes the following chain of assumptions: The people we recruit are representative of the larger user population. No other drugs that the volunteers use will affect results.

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Mdma molly

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How to take MDMA (Molly/Ecstasy)

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How to take MDMA (Molly/Ecstasy)

How to take MDMA (Molly/Ecstasy)

How to take MDMA (Molly/Ecstasy)

mdma molly

How to take MDMA (Molly/Ecstasy)

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