Monday, December 21, 2009

The Adolescent Brain And Cannabis

Hi folks (well, those of you who have persevered over the past 6 months of nothing).

I am back online for a little while and have been moved to comment about the not so latest headlines warning of adolescent brain damage from chronic cannabis use.

Well DUH! 

ANY  abuse of a mind altering substance will adversely affect a developing brain. 
Alcohol will. 
Morphine will.
LSD will.
Anti-depressants will.

Should I list the hundreds of drugs that will affect a growing brain?
Now, let's look at the abstract of the study, courtesy of

Chronic exposure to cannabinoids during adolescence but not during adulthood impairs emotional behaviour and monoaminergic neurotransmission

Francis Rodriguez Bambicoa, Nhu-Tram Nguyena, Noam Katza and Gabriella GobbiCorresponding Author Contact Information, a, E-mail The Corresponding Author
a Neurobiological Psychiatry Unit, Department of Psychiatry, McGill University, 1033 Pine Avenue West, Montreal, Canada H3A1A1

Received 9 October 2009; 
revised 21 November 2009; 
accepted 26 November 2009. 
Available online 5 December 2009.


The pathophysiological neural mechanism underlying the depressogenic and anxiogenic effects of chronic adolescent cannabinoid use may be linked to perturbations in monoaminergic neurotransmission. We tested this hypothesis by administering the CB1 receptor agonist WIN55,212-2, once daily for 20 days to adolescent and adult rats, subsequently subjecting them to tests for emotional reactivity paralleled by the in vivo extracellular recordings of serotonergic and noradrenergic neurons. Chronic adolescent exposure but not adult exposure to low (0.2 mg/kg) and high (1.0 mg/kg) doses led to depression-like behaviour in the forced swim and sucrose preference test, while the high dose also induced anxiety-like consequences in the novelty-suppressed feeding test. Electrophysiological recordings revealed both doses to have attenuated serotonergic activity, while the high dose also led to a hyperactivity of noradrenergic neurons only after adolescent exposure. These suggest that long-term exposure to cannabinoids during adolescence induces anxiety-like and depression-like behaviours in adulthood and that this may be instigated by serotonergic hypoactivity and noradrenergic hyperactivity.
Keywords: Cannabinoids; Adolescence; Serotonin; Norepinephrine; Anxiety; Depression

 OK, that study was conducted on rats. The study linked below was conducted on real humans, not rats:

Delta-9-THC in the Treatment of Spasticity Associated with Multiple Sclerosis

Here is the abstract:

Marijuana is reported to decrease spasticity in patients with multiple sclerosis. This is a double blind, placebo controlled, crossover clinical trial of delta-9-THC in 13 subjects with clinical multiple sclerosis and spasticity. Subjects received escalating doses of THC in the range of 2.5-15 mg, five days of THC and five days of placebo in randomized order, divided by a two-day washout period. Subjective ratings of spasticity and side effects were completed and semiquantitative neurological examinations were performed. At doses greater than 7.5 mg there was significant improvement in patient ratings of spasticity compared to placebo. These positive findings in a treatment failure population suggest a role for THC in the treatment of spasticity in multiple sclerosis.

While I agree that abuse of phycoactives is bad for a growing brain, I cannot understand why we are using animals to make assumptions (postulate theories) about how cannabis affects humans. Past and current human based studies show that the medicinal value of cannabis in controlled doses is a valuable and effective medicine for a wide range of conditions from neural pain to depression.

Cannabis needs to be validated as a medicine, rather than a 'stoner drug'.