THERE can be no doubt that the prospect of hundreds of thousands of young people deliberately laying themselves open to Parkinson’s disease is truly frightening. So when a leading journal publishes evidence linking the illness to one of the most commonly used recreational drugs of our time, as Science did last week with ecstasy – it makes sense to sit up and take note.
Doubly so, when the study states that just a single night’s dabbling with the drug may be all it takes to trigger the type of brain damage that could in time give you Parkinson’s.
Triply so, when it bases that conclusion on the fact that monkeys and baboons exposed to “human-like” doses suffered “profound and severe brain injury”.
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As news of the research sped round the globe journalists had little need to hype it up to sell it to their editors. For once the typical headline – One night of ecstasy may bring on Parkinson’s – was an almost verbatim summary of the study’s own top line.
Even so, the evidence behind the Parkinson’s link is complicated and, being based on lab animals, indirect. It also hails from a lab, led by George Ricaurte at the Johns Hopkins University in Baltimore, whose previous findings have been the focus of an increasingly acrimonious debate about how science interprets ecstasy research for public consumption.
Put crudely, one school of thought says experts should paint the worst possible scenario to scare youngsters off the drug. The other camp says experts should scrupulously avoid raising false fears, since these could give youngsters an excuse to write-off everything they’re told about the drug as scaremongering. The latest animal findings are certainly the most alarming to date. But how relevant are they to human users of the drug? That’s the big question.
First the basic facts. The scientists gave up to three consecutive doses of MDMA to five squirrel monkeys and, in a follow-up experiment, five baboons. They gave the doses at three-hour intervals in a bid to mimic the way some all-night clubbers use the drug. Weeks later, the researchers examined the animals and found evidence of damage to dopamine-producing neurons in the brain’s striatum. These are the nerve cells lost in Parkinson’s disease – hence the alarm.
And the surprise, for the dopamine link overturns a 15-year assumption about the way MDMA interacts with the brain. Previous studies in monkeys and rats claimed the drug’s toxicity was strictly limited to serotonin-producing cells, a quite different nerve network.
But let’s be clear what the new study means by “brain damage”. The animals’ brains had abnormally low levels of both dopamine and certain “transporter” proteins that handle this neurotransmitter. There were also signs of inflammation. All of which suggests damage to the tips of the animals’ dopamine nerve fibres. Not good – but, just as you can prune a rose bush without killing it, you can damage nerve cell tips without destroying the cells, and there’s no evidence any nerve cells actually died. This distinction is important because dopamine cells certainly do die off in Parkinson’s.
Nevertheless, it’s not unreasonable to speculate that losing dopamine nerve endings as a youngster might put you at greater risk of developing Parkinson’s later in life – so it’s vital to ask whether similar dopamine effects are likely to afflict human users.
Here we run into two big problems. Surveys suggest that only about 50 per cent of pills sold as ecstasy actually contain MDMA. So many users of E may have never been exposed to the substance. The second problem is whether the MDMA doses in the study are equivalent to human doses.
You’d think this could readily be agreed upon from the animals’ sizes. Not so. Quirks in the way livers and body metabolisms function in different species could easily make an apparently low dose behave like a very high one. Ricaurte and his team claim their doses are equivalent to human ones, but other scientists doubt their calculation. The MDMA was injected rather than given orally and two of the 10 animals overheated so much that they died during the experiment. Overheating can strike down human users of the drug but not at this frequency.
And if the doses are comparable, where are the human victims of this dopamine effect? Some people already diagnosed with Parkinson’s disease may in fact be victims of MDMA, suggest the researchers – and their ranks may swell as users age. That view is backed by one or two doctors citing anecdotal cases. But with so many millions having used the drug, these could be just a coincidence. Britain’s Parkinson’s Disease Society, for one, is sceptical. It says there is no evidence that Parkinson’s disease is on the increase among people in their 30s, 40s and 50s. This despite the fact that the drug has been used on a massive scale since the early 1980s.
So far, scientists have also drawn a blank looking for dopamine damage in the brains of users without Parkinson’s. Two imaging studies that looked for such damage failed to find any. And two years ago Stephen Kish, at the Center for Addiction and Mental Health in Toronto, analysed the brain of a chronic ecstasy user after death. He remains the only neuroscientist to have published such a study. He found no evidence of dopamine depletion.