Ecstasy use leads to feelings of euphoria, confidence, anxiety and an increased awareness of the senses. It also causes an increase in heart rate, sickness, dilated pupils, a clenching of the jaw and difficulty walking straight.

The high resulting from one or two ecstasy tablets lasts for 3-5 hrs and the “hangover”, characterised by muscle aches, fatigue and a depressed feeling, can last for several days.  Most people do not take ecstasy more than once a week as the effects become less ecstatic the more regularly it is taken.

The brain has a variety of messengers that its cells use to communicate with each other. Ecstasy works primarily by interfering with a messenger called 5-hydroxytryptamine which is abbreviated to 5-HT and is also known as Serotonin.  Scientists are still arguing about what sort of effects ecstasy has on other messengers in the brain.
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Epidemiology
The UK, along with Ireland and the Netherlands, boasts one of the worlds highest rates of ecstasy use, with more than a million people thought to have tried it.   Most of these people are 18-29 yrs of age.  It is very difficult to know exactly how many people have tried ecstasy because of the fact that it is illegal.
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The 5-HT System
A series of enzymes make 5-HT from Tryptophan, which we eat in things like cheese and chocolate.  The slowest of these enzymes is called Tryptophan hydroxylase.  This enzyme is particularly important because how fast we can make 5-HT depends on how fast our tryptophan hydroxylase is working.  Cells in the brain store most of the 5-HT they have made in little bubbles, called vesicles, which they spit out when they want to send a message to a neighbouring cell.  The rest of the 5-HT gets left in the cells internal fluid.   After a cell has spat out a few 5-HT vesicles, when it is sending a message, the 5-HT effectively flicks a switch on the neighbouring cell which tells this cell that it is receiving a message.  The 5-HT is then pumped by its own special pump back into the cell it came from, where it is either repackaged in more vesicles or broken down to form a waste product called 5-hydroxyindolacetic acid which is abbreviated as 5-HIAA.  Some people have measured 5-HIAA levels to try and determine how much damage ecstasy does, as we will see later.
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How MDMA Becomes Ecstasy
Ecstasy works by blocking the pump which pumps 5-HT back into the cell it came from after it has been released to send a message.  It also causes a lot of the 5-HT which was not packaged into vesicles (see above) to be forced out of the cell and into the gap between the cells.  This has the overall effect of leaving loads of 5-HT in the gap between the cells instead of inside the first cell where it belongs.   To send a message normally the 5-HT just has to flick the switch on the cell it is trying to communicate with once, when there is so much 5-HT outside the cell however it continues flicking the switch which leaves that cell rather confused.   There are many different types of switches, which can be on a cells surface and it is thought that as well as the aforementioned actions, ecstasy interferes directly with some of these switches.  Scientists do not all agree about which switches are affected by ecstasy and the situation is further complicated because, although ecstasy works mostly on the 5-HT system it probably also affects some of the switches which other messengers use and therefore also affects there actions.
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Animal Studies
The levels of 5-HT in the brains of rats show the same pattern of changes that peoples behaviour exhibits after taking ecstasy, supporting the idea that it is the levels of 5-HT outside the cells which make ecstasy work.  A dose of ecstasy also slows down the tryptophan hydroxlase  enzyme in rats brains. You may remember we earlier mentioned that how much 5-HT we can make depends on how fast our tryptophan hydoxylase is working.  It has been shown that ecstasy can kill off some of the nerve cells that it affects, however it would appear that to do this requires either a large dose or many smaller doses.  This damage has been shown to last for over a year in rats and over seven years in monkeys.  The doses shown to cause long term damage have been bigger than those normally taken by people but, because we have bigger brains, we are more susceptible than other animals to drugs which potentially damage the brain.
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Clinical Assessment
It is very difficult to assess the damage ecstasy does to people as it would not be allowed to do a controlled trial involving giving people ecstasy and measuring the effects.  Several studies have been done comparing ecstasy users to people who have never used it.  There is a big problem though, in that most ecstasy users have used other sorts of drugs as well so no one really knows which drug has done any damage that is found.  People have tried measuring levels of the waste product 5-HIAA (see above) and have shown that ecstasy users have less of it than other people, which supports the idea that ecstasy interferes with tryptophan hydroxlase (see above).

Other people have tried giving a legal drug called fenfluramine, which is similar to ecstasy, to ecstasy users and non ecstasy users and measuring the difference in responses.  The Ecstasy users showed less of a response and therefore can be considered to have developed some kind of tolerance to this type of drug.  This tolerance appears to be long lasting.
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Neuroimaging
Another approach to be tried is taking a variety of types of pictures of the brains of both ecstasy users and non users. These have, in my opinion, provided the best evidence so far that ecstasy damages the brain. They have shown decreased activity of several types of pump involved with the 5-HT system and an increased number of the switches which 5-HT uses to pass on messages, probably as a response to lower levels of 5-HT. Thy have even shown an overall decrease in the volume of the brain.
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The Parkinson Paradox
It is thought that the action of ecstasy on the 5-HT system indirectly interferes with another messenger called dopamine.  A shortage of dopamine in certain parts of the brain causes Parkinsons disease and therefore ecstasy should make parkinsons symptoms worse.  However the therapy for parkinsons, L-Dopa, causes serious side effects in that it makes previously underactive nerve cells activate themselves erratically causing jerky movements.   It has recently been reported that ecstasy when given with L-Dopa, relieves these side effects, probably by stopping the excessive activation of the nerves which control movement. Therefore a drug which should in theory make parkinsons disease worse has the potential to form a useful part of its therapy.
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Still in two minds?
It has been suggested that it is not direct damage to nerves which causes the long term effects sometimes reported to result from ecstasy use but rather the bad memory of a bad trip – sound like a theory dreamed up while on ecstasy? Perhaps, but then that’s the fun of science – if you can justify it you can believe it!
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In conclusion
This section is not accounted as it contains little jargon and is written in the best inglish wot I know guv!
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