If I might suggest... The *attitude*(?) that would have one smoke a spliff-a-day as a tonic *could* keep the doctor away.
Too bad "tonics" aren't accepted as "legitimate" medicine
by the American medical establishment.
---- Original Message ---- From: Mike Ballard To: lbo lbo Sent: Monday, April 11, 2005 12:27 PM Subject: [lbo-talk] A joint a day keeps the doctor away....
> Nice to read some good news every once in awhile.
>
> Regards,
> Mike B)
> http://www.cnn.com/2005/HEALTH/conditions/04/06/marijuana.heart.disease.ap/index.html
>
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You might want to note that the analgesic properties of marijuana appear to be associated with CBCs & CBDs, not the THC.... it's the "tonic". =8>
>From Last week's mail:
Sponsored by: Johnson & Johnson Pharmaceutical Research & Development
http://www.the-scientist.com/2005/03/28/S34/1/printerfriendly
Pot For Pain
People have used marijuana and its derivatives to relieve pain as well as get high for thousands of years. Recently, researchers have been trying to divorce pot's pain-relieving properties from its psychoactive effects. Extricating the high could aid in generating novel pharmaceuticals free of the political opposition facing medical marijuana. It might also permit high doses, strong enough to boost the drug's intrinsically modest analgesic power without detrimental side effects to the central nervous system (CNS).
CB1, the first cannabinoid receptor discovered, acts in the CNS and is psychoactive. So, some researchers have focused on CB2, discovered in 1992. CB2 has been shown to inhibit acute, inflammatory, and neuropathic pain but is not expressed in the CNS, and selective agonists for CB2 do not cause CNS effects.
Researchers at the University of Arizona in Tucson recently reported how CB2 can relieve pain while present neither in the CNS nor on peripheral neurons. It does so indirectly: Activation in keratinocytes stimulates release of b-endorphins, which then work on opioid receptors at primary afferent neurons to inhibit pain.1 The work was done in rats. Senior author Philip Malan says it's not certain yet whether humans coexpress CB2 and b-endorphin in keratinocytes.
Activation of CB2 receptors is not the only approach to endocannabinoid pain relief without the high. An international research team has for some years investigated ajulemic acid (AJA, also known as CT-3), which was derived from d9-THC, the principal psychotropic molecule in marijuana. In preclinical studies and in short-term human studies, AJA has been shown to relieve neuropathic and inflammatory pain better than placebo without psychotropic actions.
How AJA reduces pain is unclear, but neither endorphins nor CB2 seem to be involved. AJA appears to be primarily working via CB1 receptors, because pretreatment with the selective CB1 antagonist SR141716A reverses antihyperalgesic effects from AJA in animal studies, according to team member Matthias Karst, of the Hannover Medical School in Germany. However, AJA displays weak binding affinity for CB1 and an even weaker one for CB2.
The researchers hypothesize a number of possible explanations. Karst speculates that perhaps in vivo AJA does not pass the brain barrier easily. Or perhaps AJA activates peroxisome proliferator-activated receptor-g (PPAR-g), which stimulates production of anti-inflammatory prosta-glandins. According to Sumner Burstein, of the University of Massachusetts Medical School in Worcester, who holds the patent on AJA, their data suggest this explanation could be correct.
Alternatively, AJA may bind mainly at peripheral CB1-like receptors outside the CNS, receptors that are somewhat different from central CB1 receptors, Karst says. In short, perhaps AJA's behavior is evidence for a third, thus far undiscovered, cannabinoid receptor. "There is tantalizing evidence for an additional CB receptor," according to Roger Nicoll of the University of California, San Francisco. "However, no one has succeeded in cloning the receptor."
--Tabitha M. Powledge
References
1. M.M. Ibrahim et al., "CB2 cannabinoid receptor activation produces antinociception by stimulating peripheral release of endogenous opioids," PNAS, 102:3093-8, February 22, 2005.
2. S.H. Burstein "Ajulemic acid: A novel cannabinoid
produces analgesia without a 'high,'" Life Sci, 75:1513-22, 2004. Sponsored by Johnson & Johnson Pharmaceutical Research & Development
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[Overposted allllrrrreeeaaddddy?]