This is one of the best videos I’ve ever seen on the physiological roots of depression. This guy (Robert Sapolsky) really goes in-depth and connects the dots between scientific facts and common philosophy & anecdote. 52 minutes — not for the faint of heart.
The scientists, including collaborators at the University of Colorado at Boulder and the University of Maryland, studied 20 adolescent boys. On average they had been on probation 139 of the last 180 days; 19 of the 20 had the psychiatric diagnosis of conduct disorder, and all had diagnoses of substance use disorder. They had been abstinent, however, an average of about five weeks when studied. They were compared with 20 other boys who did not have serious antisocial or drug problems, but who were of similar age, ethnicity, and home neighborhoods.
All played a computerized risk-taking game that repeatedly presented a choice between a cautious and a risky behavior: press the left button and always win one cent, or press the right button and either win five cents or lose ten cents. The scientists examined brain activation with functional magnetic resonance imaging (fMRI) as the boys decided to press right or left, and then as they experienced wins or losses after right presses.
Brain activation differed dramatically in the two groups. The anterior cingulate cortex monitors changing rewards and punishments, and then sends that information to another brain region (dorsolateral prefrontal cortex), which regulates one’s choices among possible behaviors. During decision-making, antisocial boys had significantly less brain activity than normals in both of those regions, and also in other decision-making areas (orbitofrontal cortex, amygdala, insula).
Cocaine addicts take cocaine vaccine, then go broke – “After the vaccine, doing cocaine was a very disappointing experience for them,” said Kosten, a professor of psychiatry and neuroscience at Baylor College of Medicine in Houston.
Nobody overdosed, but some of them had 10 times more cocaine coursing through their systems than researchers had encountered before, according to Kosten. He said some of the addicts reported to researchers that they had gone broke buying cocaine from multiple drug dealers, hoping to find a variety that would get them high. “
I’m way more entertained than I probably should be.
Alcohol substitute that avoids drunkenness and hangovers in development – Telegraph – “An alcohol substitute that mimics its pleasant buzz without leading to drunkenness and hangovers is being developed by scientists. The new substance could have the added bonus of being “switched off” instantaneously with a pill, to allow drinkers to drive home or return to work. The synthetic alcohol, being developed from chemicals related to Valium, works like alcohol on nerves in the brain that provide a feeling of wellbeing and relaxation.”
Sounds all well and good, but, as a rule I’m skeptical of pharmaceuticals. I can just imagine something like this becoming the norm, and then ten years down the road we find out it causes some yet-unheard-of form of bodily damage. (Vioxx, anyone?)
BusinessWeek, among others, published a new press release of the same McGill University “marijuana” study which, while at least mentioning that it was done on animals, still failed to mention several points — one of them being that the study itself did not even use marijuana, and in this case has the particularly large blight of outright stating that the rats were given cannabis, when in fact, they were given WIN 55212-2, a synthetic compound that is a stronger agonist of CB1 receptorsÂ than tetrahydrocannabinol, the main active ingredient of marijuana (though there are a few others).
If any of you recall, I made a post entitled “An unsurprisingly disingenuous look at marijuana” criticizing NOT the study itself, but the strong misrepresentation it was given on multiple popular science websites.
Most of the ORIGINAL press this study got fell short in mentioning:
- The study was in animals.
- That the anxiety-like/depressive behavioral symptoms were not demonstrated in all of the results, and the study failed to demonstrate the same effects in the “open field test.”
- That even the “low” dose may have been somewhat high, and thus not a good comparison for smoked marijuana, had it even been marijuana they tested in the first place.
- And finally… That the study didn’t use marijuana, but instead a synthetic compound calledÂ WIN 55212-2, which has demonstrated both a stronger affinity for CB1 receptors than THC, and is structurally different. (which the news press release has done no better at)
While I was quite pleasantly surprised that BusinessWeek (and the others hosting this new, updated press release), took the opportunity to mention that the study wasn’t done in humans:
Although the finding stems solely from work conducted with adolescent and adult lab rats — not yet replicated among humans
They still fell short in all other respects mentioned earlier, and in fact, explicitly and incorrectly stated that the rats were given cannabis, as shown:
To assess the role cannabis may play on adolescent brain development, for 20 days — a period characterized as “prolonged exposure” — adolescent rats were given daily injections of either a low-dose (0.2 milligrams/kilograms) or high-dose (1.0 milligrams/kilograms) of cannabis.
Round 2, still can’t get it right? Fire your PR department, McGill! Honestly.Â A little proofreading, or a little honest (choose your slant) can go a long way.