This article was published in Scientific American’s former blog network and reflects the views of the author, not necessarily those of Scientific American
“I took X. I took X! We were out on the town, and it was wild,” so said an Australian acquaintance of mine after returning from a night on the town with her husband for an entertainment industry premiere. She spoke in hushed, giddy laughter, somehow as perfectly solemn as it was light. She had misbehaved, gone “wild” as a mother of two in her early 40s, felt as guilty as she did nostalgic. “I felt like I was a teenager again. We could have gotten arrested!”
My eyebrows knitted together. Ecstasy? E? Sure, ok, after all, this is New York, though from the way the tale was told the rave drug sounded almost trendy.
I didn’t think much of it until I read recent accounts of super-strength Ecstasy appearing in UK clubs and whispers of a Floridian teen murdering his parents while on, or because of, Ecstasy in late July.
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Are we at the scene of a '90s rave? Have we successfully rewound to the past?
Designer drugs, synthetic substances created to circumvent existing narcotics and drug laws, go in and out of fashion. The term was coined in the mid '80s when a fentanyl scare erupted in Congress. Usually these drugs piggyback on others like them and are far easier and cheaper to create. But silently, they slip in and out of public existence, arousing concern and panic on their danger factor but not always on their popularity. Many a time such deadly drugs are merely fringe substances. Because they're created to duck laws, designer drugs are often the subject of chemical identity crises, confusion and debate.
Ecstasy, E or X, waltzed onto the recreational drug scene in the late '70s and early '80s, perfectly legal. In the clubbing scene where pointy-toed heels, sickly saccharine Sex on the Beach cocktails, spandex pants and Duran Duran ruled, so did E. This new drug, appearing in a kaleidoscope of colors, shapes and sizes could be snorted, swallowed or injected. It allowed users to achieve a certain kind of high while remaining in possession of their motor skills, unlike LSD or other drug brethren. Once 1985 hit, however, “Hungry Like the Wolf” had passed its peak and E was as banned as heroin, and remains as such to this day: a schedule I classified substance.
Ecstasy is known for its compound known as MDMA, or 3,4-Methylenedioxymethamphetamine. In animal and human studies, MDMA seems to have a curious combination of hallucinogen and amphetamine effects. Though users don’t often experience the vivid and realistic false dreamscapes common of hallucinations, they often report heightened perceptions of the world around them. On top of it, users tend to become hyperactive, similar to those under amphetamine's hold.
MDMA doesn't fall neatly into a drug classification but it is cousin to two infamous classifications of drugs: amphetamines and hallucinogens. The drug uniquely alters behavior, yet it hasn't been proven to have similar addictive qualities. However, primates do take the drug voluntarily. Why? Basically, it dumps select neurotransmitters --mainly serotonin -- into the brain's synapses, creating an anxiety-diminished, pleasantly relaxed state for a few hours.
So, what, if anything, has changed about Ecstasy? Historically, the drug contained MDMA, but over the years its baser makeup changed along with laws and market availability. In the last decade or so, the street level drug could contain any varied amounts of MDMA or none at all, the ingredient instead substituted with caffeine, aspirin or other over-the-counter meds. If odiously unknown chemical makeup isn't frightening enough, the drug has been known to contain DXM (dextromethorphan), a cough suppressant, in enough quantity to cause hallucinations -- commonly in excess of 13 times the amount in a recommended cough syrup dosage. Now we may be flashing back to the '80s and '90s days of high MDMA-ridden Ecstasy so dealers can compete with stronger up-and-coming designer drugs like mephedrone. This means users taking Ecstasy may be synaptic surprised with a more potent concoction.
Evidence indicates that Ecstasy (containing MDMA) can damage serotonin receptors and cause as much as a 20-60% reduction in healthy neurotransmitter receptors.1 Short-term use damages neural axons and long-term use cripples and shortens the ropy body of the neural cell. Monkeys given Ecstasy were still found to suffer adverse effects in the brain seven years after exposure to the drug: the drug was shown to predominately affect the frontal lobe of the cerebral cortex (the thinking part of the brain) and the hippocampus (a memory sector of the brain). However, the most damage to cells occurs short term after Ecstasy use; long term, the brain might have the ability to repair itself.
Research shows that users have noticeably less serotonin activity in the brain in the first few weeks following drug use but that serotonin function bounces over time, in a period of a few months.2
Despite Ecstasy’s detrimental affects, is it reasonable to assume the drug encouraged a teen in Florida to bludgeon his parents to death with a hammer? Unlikely. But perhaps it is all interrelated: perhaps the teen’s chemical chalice contained a combination to inspire murder. We'll probably never know. However, it does bring to light the underlying issue: we’re still on square one of the effects of substance combination from a drug popular over 30 years ago and are equally befuddled on the individual and mixed drug's ramifications on mental illness. In this high stakes poker game, it looks like we're losing.
1 Hatzidimitriou, G., McCann, U.D. and Ricaurte, G.A. Altered serotonin innervation patterns in the forebrain of monkeys treated with (+/-)3,4-methylenedioxymethamphetamine seven years previously: factors influencing abnormal recovery. J. Neurosci., 19:5096-107, 1999.
2 Buchert, R., Thomasius, R., Nebeling, B., Petersen, K., Obrocki, J., Jenicke, L., Wilke, F., Wartberg, L., Zapletalova, P. and Clausen, M. Long-term effects of "ecstasy" use on serotonin transporters of the brain investigated by PET. J Nucl Med, 44:375-384, 2003.
Thanks to @Drug Monkey for the language correx on the Hatzidimitriou study.