Canvassing for Opinion - aka "Blairs Brain on Cannabis"

IMHO prohibition sentiment requires inherent addiction to status quo, an incapacity to visualise beyond the here and now and a desperate desire to know others might feel the same... Reform is not revolutionary, rather it is evolutionary. Having survived banging your head against a brick wall the evolutionist relishes having stopped. / Blair

Thursday, September 08, 2011

Naughty Science, Hush Yourself!

Every now and then the science turns up the irrefutable evidence that we, as a nation and as participants in a international convention, actively and purposefully constrain both debate and research into cannabis and all that that means.

We wax lyrical about being kinder and gentler about medicinal cannabis use (but not supply) and periodically say 'no objection to that' meanwhile the political shills say no change on our watch despite massive support across many jurisdictions for a change in the law.

So as a member of the biomedical  expert community I should rightly be frustrated  that mainstream media fail to pick up on the implications of this given cannabis's multi-purpose utility, prevelence of use and the continuum of 'emerging science' that validates how wrong we have current policy and how we have improperly impugned cannabis these past 40-50 years.

Here is an abstract from the latest British Journal of Pharmacology by several of my cultural hero's of the science of pot. It makes for depressing reading given the scale and magnitude of the problem we face as our population ages.

Cannabinoids are promising medicines to slow down disease progression in neurodegenerative disorders including Parkinson's disease (PD) and Huntington's disease (HD), two of the most important disorders affecting the basal ganglia. Two pharmacological profiles have been proposed for cannabinoids being effective in these disorders. On the one hand, cannabinoids like Δ(9) -tetrahydrocannabinol or cannabidiol protect nigral or striatal neurons in experimental models of both disorders, in which oxidative injury is a prominent cytotoxic mechanism. This effect could be exerted, at least in part, through mechanisms independent of CB(1) and CB(2) receptors and involving the control of endogenous antioxidant defences. On the other hand, the activation of CB(2) receptors leads to a slower progression of neurodegeneration in both disorders. This effect would be exerted by limiting the toxicity of microglial cells for neurons and, in particular, by reducing the generation of proinflammatory factors. It is important to mention that CB(2) receptors have been identified in the healthy brain, mainly in glial elements and, to a lesser extent, in certain subpopulations of neurons, and that they are dramatically up-regulated in response to damaging stimuli, which supports the idea that the cannabinoid system behaves as an endogenous neuroprotective system. This CB(2) receptor up-regulation has been found in many neurodegenerative disorders including HD and PD, which supports the beneficial effects found for CB(2) receptor agonists in both disorders. In conclusion, the evidence reported so far supports that those cannabinoids having antioxidant properties and/or capability to activate CB(2) receptors may represent promising therapeutic agents in HD and PD, thus deserving a prompt clinical evaluation.

Fernández-Ruiz, J; Moreno-Martet, M; Rodríguez-Cueto, C; Palomo-Garo, C; Gómez-Cañas, M; Valdeolivas, S; Guaza, C; Romero, J; Guzmán, M; Mechoulam, R; Ramos, JA
Br. J. Pharmacol. 163, 13650 (2011) /  Departamento de Bioquímica y Biología Molecular III, Instituto Universitario de Investigación en Neuroquímica, Facultad de Medicina, Universidad Complutense, Madrid, Spain.

Blair Anderson
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