Perhaps the street chemists’ most enduring achievements have to do with the simplification and refinement of methods used to manufacture Ecstasy, or MDMA. Ecstasy was first synthesized by the Merck Company in Germany in 1912, an unplanned byproduct of an attempt to synthesize Hydrastinin, a blood-clotting agent to which one of Merck’s competitors held the patent. Merck filed for a patent for its discovery but didn’t specify a purpose; the patent was issued in 1914. Though it’s common belief that MDMA was intended as an appetite suppressant, there seems to be no evidence that it was ever marketed or used as such. In any case, and not surprisingly in light of subsequent developments, Merck plays down the importance of the synthesis and the patenting of MDMA.
But that doesn’t stop the revisionists from romanticizing the history of the drug. Urban legend has it that MDMA was issued to German soldiers in World War I, and according to one tale, the “Christmas truce of 1914” – a brief and unofficial cessation of hostilities on the Western Front that saw German and British troops joining together for a little merrymaking – was fueled in part by Ecstasy. Though it almost seems a shame to put a damper on such a bohemian and almost decadent scenario, it wasn’t X that the soldiers brought to the party; it was good old ethyl alcohol.
In any event, MDMA did not fade to oblivion. Sixty years after the War to End All Wars, in the 1970s, it was actually thought to be an effective aid in psychotherapy, and within a decade it would become the drug of choice among Ravers in England. Ecstasy was popular there for a half-dozen years before wending its way through security at Florida airports in the mid-eighties. In South Florida it quickly became popular within the gay community in general and the dance clubs in particular. From there it made its way up the east coast, and then leapfrogged over the Heartland to California where it was immediately accepted and thought tremendously hip.
Statistics confirm that the drug’s popularity has hardly abated. In 1998 U.S. Customs officials confiscated a total of 750,000 doses of Ecstasy. The following year they seized three million. In 2000 the total exceeded six million – and these are only among the drugs that smugglers attempt to bring in from abroad, and that were subsequently confiscated. And a shocking reality lay just under the surface. By then Ecstasy, like methamphetamine, was easily and widely manufactured in domestic clandestine labs, and this is the source of the overwhelming majority of the Ecstasy used today. Surely one of Ecstasy’s greatest assets is the fact that young people are among its most ardent fans, a seemingly built-in trait that keeps it perennially popular. A federally sponsored survey of high school students indicated that Ecstasy use among high school seniors had increased fifty-five percent in the twelve months from 1998 to 1999.
Its recent history is peculiar indeed, and bespeaks the mercurial nature of the amphetamine molecule. Because Ecstasy’s molecular structure is slightly different from that of methamphetamine, the drug wasn’t technically illegal in the United States until 1985. The altered molecular structure, of course, produces a different psychological effect on the user, one quite different than methamphetamine. MDMA works by acting on the serotonin receptor sites in the brain, enabling them to take in large amounts of serotonin and other neurotransmitters, namely dopamine. Serotonin’s role is remarkably broad in scope. This is the chemical the brain employs to govern sleep, complex learning processes, and the integration of emotion. As would be expected, heavy use of Ecstasy causes the brain to produce less serotonin, which typically results in long-term depression and general anxiety when the user attempts to quit.
In recent years a peculiar debate has sprung up regarding the dangers inherent in the drug. During the 1970s a tiny corner of the psychiatric community believed small doses of MDMA (forty to sixty milligrams) to be safe and effective in treating depression. Some therapists actually took the drugs themselves, as they thought it helped them connect to and empathize with their patients, which, they argued, made them more effective therapists. Yet evidence of Ecstasy’s neurotoxicity is indisputable. The drug has been shown to produce hydrogen peroxide as the serotonin receptors attempt to break down dopamine. This hydrogen peroxide, researchers at the National Institute on Drug Abuse (NIDA) believe, causes long-term damage to the neurons in the brain that transmit serotonin. Because of its questionable medicinal value, MDMA was placed on Schedule I of the CSA.
The deaths that are blamed on Ecstasy use, however, are not a direct result of the drug’s meddling with brain chemistry. More often than not, death is a result of dehydration that comes from dancing for hours on end without rest. Of course Ecstasy is ultimately the cause, as it suppresses thirst and the need for sleep, while it compels users into repetitive motion – very much like its sister drug, methamphetamine. Dozens of deaths annually, however, have been attributed to a user overcompensating with water, and actually becoming overhydrated, which can also be fatal. A great many of those who have died do so on a crowded dance floor surrounded by strangers, whirling lights, and the mindless throb of techno-pop, all the while in the grip of a seizure that escorts them into the next world.
Methamphetamine would seem to be a most malleable clay. Indeed, one does not need to toy with its molecule much in order to drastically alter its effect on the user. The drug MDA (2-methylenedioxyamphetamine), for example, looks a lot like MDMA at the molecular level. Subtle differences in structure, however, make it more hallucinogenic than MDMA. In moderate doses, MDA produces effects much like that of LSD, while at higher doses the user behaves more like someone on high doses of amphetamine. The effect is similar enough that on the street it is still known as Ecstasy.
The history of MDA parallels that of amphetamine to a remarkable degree. MDA was first synthesized in Germany in 1910, and was later thought to have medicinal value in the treatment of Parkinson’s disease, and as an antidepressant. The pharmaceutical company of Smith, Kline, and French saw potential in MDA as an appetite suppressant (as many companies recognized amphetamine), and sold it for a time under the trade name Amphedoxamine. At the height of the Cold War the U.S. military thought it might prove useful as a truth serum, a kind of hallucinogenic Sodium Pentothal. Like all such substances with a recreational potential, it was discovered by the infinitely curious counterculture of the sixties. Once discovered, it would never be forgotten. Today it is sold illicitly in tablet form, and is one of the most popular designer drugs on the street.
Another amphetamine analogue is MDE, or 3,4-methylenedioxyethamphetamine. Known on the street as “Eve,” MDE’s effects are said to be very similar to those of MDA. Anecdotal accounts among users suggest that it’s generally less potent and the effects shorter in duration (two or three hours). They tend to report a less hallucinogenic effect than MDA, with many claiming MDE made them feel merely drunk or stoned. Like Ecstasy, a dozen or so users die every year as a result from taking the drug. Similarly, the cause of death is typically hyperthermia, or heat stroke.
Yet another analogue drug is a kind of crossbreed between methamphetamine and cathinone, called methcathinone. On the street it’s simply “Cat,” or sometimes “Star.” Cat is so new that it wasn’t strictly illegal in the United States until 1993, when it was placed on Schedule I of the CSA. The cathinone is derived from the Catha edulis shrub, a plant indigenous to east Africa and the Arabian Peninsula. For centuries people there have chewed the young leaves of the plant for its stimulant properties. Methcathinone, however, is a far more powerful hybrid, a blending of the ancient and modern methods of pharmacology. Cat is far more potent than its parent drug, and today is produced almost exclusively in clandestine labs that use ephedrine as its base. Like methamphetamine, Cat incites the brain’s neurotransmitters norepinephrine and dopamine to produce the same general sense of euphoria and well-being. It was first synthesized in 1928 and went on to be used as an antidepressant and appetite suppressant. Like meth, it increases the user’s energy and also inspires some remarkably erratic and violent behavior.
For reasons that are not entirely clear, the various amphetamine analogues are not equally toxic. Methamphetamine, for instance, appears to be far more detrimental than, say, Ecstasy. The longstanding conventional wisdom concerning the neurotoxicity of meth was that the drug damages but does not kill nerve cells in the brain. Research conducted on animals at NIDA indicates that damage occurred primarily to nerve endings of brain cells containing dopamine. Once exposure to methamphetamine stopped, the nerve endings were believed to recover, at least partially, within a few months. That is, the dopamine levels gradually came back, and brain function was more or less normal. Recent brain imaging studies on human beings, however, show a different picture.
Dr. Jean Lud Cadet, clinical director of the Intramural Research Program of the National Institute on Drug Abuse, has conducted groundbreaking research on the damage caused by heavy methamphetamine use. The conclusions he and his team arrived at go far beyond what was once conventional wisdom.
“People used to think that the most serious methamphetamine-induced damage was to dopamine nerve terminals because it put people at risk for developing Parkinson’s disease as they got older,” Dr. Cadet says. “It does not just destroy the endings of dopamine-containing nerve cells. It also kills other nerve cells that produce other neurotransmitters in additional brain pathways.” (Ironically, Hitler’s Dr. Morell treated his most notorious patient with a drug that is now thought not only to aggravate but to precipitate the very disease he was trying to treat.)
The damage inflicted on the brain is also believed to last longer than previously thought – for at least three years after the addict stops using. In some ways, the brain never recovers. Cadet’s research indicates that methamphetamine triggers a natural mechanism called apoptosis, a sort of cell suicide which results in widespread cell death in the striatum, hippocampus, and frontal cortex regions of the brain. Perhaps the most alarming aspect of this research has to do with the fact that these areas were previously believed to be untouched by heavy methamphetamine use. This is frightening for a very real reason. The damage appears to induce alterations in brain chemistry in long-term methamphetamine users similar to that found in people suffering from stroke or Alzheimer’s disease. The leading theory puts forth that by killing the nerve cells that produce other neurotransmitters, meth in effect chokes off the free electrical commerce of the brain.
On the face of it, premature onset of Alzheimer’s symptoms seems an ironic fate for the methamphetamine addict. The hyper-life they once pursued delivers them to a vacant and mindless world of premature elderliness. They all come to share an array of traits that lend an appearance of the failing senior citizen: the skullish eyes, the shedding of teeth, decaying fingernails, and ceaseless tremor running through the limbs – and all of it self-inflicted. The source is a lightning bolt that has made its way through their lives, searing the tender membranes through which they once apprehended a more subtle, complex and beautiful world.