drugs prohibition kills

I wrote a feature about psychoactive drugs a few weeks ago, mainly inspired by the recent paper from David Nutt and colleagues who argued that the blanket ban of psychoactive drugs harms progress in neuroscience (apart from ruining the lives of millions of people with the unwinnable "war on drugs").

Since then, tragic events, including the death of a teenage girl here in Oxford, have highlighted the issue. There is a properly dangerous drug making the rounds in the UK right now, PMA (paramethoxyamphetamine) (probably called Dr Death for a reason), but as drugs are banned regardless of their harm, it's hard to know what is and what isn't dangerous. Plus, there is no quality control, and if kids buy an illegal pill, it could contain anything. In the Netherlands, by contrast, there are labs checking up on what is being traded, and they haven't had problems with PMA yet.

Essentially, my bottom line is, people always have used mind-altering drugs and always will do, and if there wasn't this blanket prohibition banning harmless and dangerous things alike, it would be much safer for them to do so. Hardline prohibitionists are just creating most of the problems they are pretending to solve.

Oh well. Don't get me started on this, it drives me up the wall in no time. Just read my feature:

Drugs prohibition is criminals’ gain, neuroscience’s loss

Current Biology, Volume 23, Issue 14, R585-R588, 22 July 2013 doi:10.1016/j.cub.2013.07.012

which is freely accessible (and legal, still!) as

HTML text

PDF file.

Cannabis sativa - picture credit: GW pharmaceuticals.

PS: couple of further links re. the recent deaths linked to PMA:

• Ian Birrell in The Guardian
• Excellent piece from Archie Bland in the Independent
• Martha Fernback post-mortem inconclusive (BBC news)

PPS only after publishing this blog entry I became aware of the organisation Transform Drug Policy Reform, which has published detailed suggestions for a drugs regulation based on actual scientific evidence and on policies that are feasible (borrowing bits and pieces from established frameworks such as the handling of prescription drugs). "After the War on Drugs: Blueprint for Regulation" is freely available as a PDF download, but if you would like to support the organisation, you can also order it as a book from them. You can also download the executive summary only, which is also available in several other languages including Spanish, Russian, and Italian.

a cap on addiction

I’ve often said that I am lacking the “gene for addiction,” as I can, for instance smoke or drink without risking excessive use. New research suggests that, at least in rats, the “I’ve had enough” factor is not a protein gene but a micro-RNA, i.e. a short piece of RNA that plays a role in gene regulation. As J. A. Hollander et al. report in last week’s issue of Nature (vol 466, page 197), expression of the micro-RNA miR-212 puts a cap on cocaine-seeking behaviour in rats that have free access to the drug.

So, rather than terrorising and criminalising people who get addicted to drugs, policy-makers should fund more research to find the equivalent mechanisms in humans that protect those like myself from addiction and work out a way to provide this protection to those people who don’t have it naturally. Shouldn’t be so terribly complicated, and the research would be a lot cheaper than current spendings on the “war on drugs” and all that. If somebody wants to check my genes for this research, I’ll be happy to provide a sample.

double life of nicotine

One intriguing thing I found in the current issue of Nature is that nicotine has very different effects on acetylcholine (ACh) receptors in the brain and in the muscles. As the CalTech researchers X. Xiu et al. put it on page 534:

"If nicotine activated ACh receptors found in muscle as potently as it does brain ACh receptors, smoking would cause intolerable and perhaps fatal muscle contractions."

The authors find that extremely subtle differences between these nearly identical receptors, which both respond the same way to their intended messenger, namely ACh, make that nicotine can mimic the non-covalent interactions of ACh with the brain receptor, but not with the muscular one. Specifically, it's one hydrogen bond and one interaction between pi electrons and a cation which are to blame for the difference.

While it is not yet clear why and how nicotine causes addiction, researchers believe this goes via such ACh receptors, and specifically via the receptor type that Xiu et al have studied.

Now what I find intriguing is that many people (like me, for instance) don't get addicted to nicotine. I rather enjoy the sensual experience of a good tobacco, but I can take it or leave it at any time, and as there is no place left in this world where one can enjoy it, I end up leaving it. It may be genetic, as my parents have similar experience.

So does this new research mean that I (and non-addicted people like me) have a more muscle-like ACh receptor in my brain ? In the post genome age this should be really easy to answer. And if this addiction effect depends on such extremely subtle and weak interactions, wouldn't it be easy to disrupt this and stop the addiction from happening (well, OK, I know we don't want to interfere with the ACh's natural interaction, so it may be tricky)? I tend to think that if people had really tried to solve this problem, rather than terrorising the people affected by it, it would have been sorted out by now.