As many of my readers know, I like to pull a lot of breaking science news from Eurekalert. One particular article today has drawn my attention, and I’d like to point out to the very disingenuous manner in which it was presented to the lay audience, who may lack the time, educational background, or simply a healthy amount of skepticism to see the spin.
Montreal, December 17, 2009 – Canadian teenagers are among the largest consumers of cannabis worldwide. The damaging effects of this illicit drug on young brains are worse than originally thought, according to new research by Dr. Gabriella Gobbi, a psychiatric researcher from the Research Institute of the McGill University Health Centre. The new study, published in Neurobiology of Disease, suggests that daily consumption of cannabis in teens can cause depression and anxiety, and have an irreversible long-term effect on the brain. […]
“Teenagers who are exposed to cannabis have decreased serotonin transmission, which leads to mood disorders, as well as increased norepinephrine transmission, which leads to greater long-term susceptibility to stress,” Dr. Gobbi stated. […]
It is also the first study to demonstrate that cannabis consumption causes more serious damage during adolescence than adulthood.
Fair enough. Cannabis effects some neurotransmitters and stuff, and affects the development of the brain. It sounds plausible…
…except the actual study was neither performed on humans nor even involved any actual compounds present in marijuana.
This study (actual pubmed link) used adolescent rats and a compound known as WIN 55,212-2. WIN 55,212-2 is known to both be stronger in its affinity for CB1 receptors than marijuana, and beside that structurally quite different.
Mentioned in the actual paper, but not in the “press release” was that the study did not find that exposure to WIN55,212-2 influenced anxiety-related behaviors, at least not in all of the assays. The elevated plus maze test results did not show an increase in basal level anxiety. In other words, the adolescent exposure to this highly-cb1-agonizing drug did not effect the rats propensity to visit an “open arm” at all. Nor was chronic, daily exposure to WIN 55,212-2 found to effect the rats behavior in the open field test. Both of these tests are considered extremely important in assessing a rats propensity towards anxiety/depressive-like behavior.
The rats did show a reduced tendency to feed in new environments after high exposure to the marijuana-analogue, in a task known as the novelty suppressed feeding task.
However, what about DOSING?
Lets take a look at the dosage.”the adolescent exposure group received for 20 days once-a-day i.p. injections of a low dose (0.2 mg/kg) or a high dose (1 mg/kg) of WIN55,212-2 or the vehicle.” Lets take an average human weighing 80kg. And an average rat weighing .5kg2mg dose to a human, divided by 80kg is .025 mg/kg the LOW dose to the rat was .1mg/kg intravenous injection. that’s 4 times the human oral ingestion to get high. the high dose was .5 mg/kg thats 20 times the human oral ingestion to get high.
Injection should be using A LOT less than an oral ingestion, correct?
Something seems off with the dosages, but I’m not a scientist. Is there anything wrong with my reasoning?
No, sir, the dosing does sound a wee bit high to correlate too strongly to adolescent smoking.
Now, to be fair:
Animal model systems are an essential component to research, as are chemical analogues, and inferences can be made using these. The fact that these techniques were used doesn’t in and of itself invalidate the underlying premise that habitual use of any drug can change human behavior. Nor should data be completely be disregarded simply because one aspect lacks in robustness, but given the actual content of the paper I’ve got to wonder — did the P.R. department even read the paper before typing up their blurb? At what point does over-simplification become deception and misdirection?
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