In 1964 THC was obtained in its pure form and the structure elucidated (Gaoni and Mechoulam, 1964). Lilly Research Laboratories, in 1968 initiated a cannabinoid research program. Early clinical studies investigated the pharmacological actions of THC and synthetic analogues. The objective was to derive a compound with the benefits of cannabis but without the adverse effects. As a result nabilone came to the forefront and was marketed as an anti emetic in Canada in 1982 and the UK in 1983.
On May 13, 1986, the Drug Enforcement Administration (DEA) in America transferred a synthetic form of THC from Schedule 1 to Schedule 2 for use as an antiemetic for cancer patients undergoing chemotherapy. In effect, this action by the DEA resulted in a dual scheduling of an identical molecule. A molecule of THC derived from the cannabis plant is a schedule 1 molecule, since the definition of "cannabis" includes all derivatives of the plant; but an identical molecule when synthetically derived and encapsulated in a gelatin capsule, is a Schedule 2 molecule.
In 1988 in America, an Administrative Law Judge stated cannabis to be "...one of the safest drugs known to man." The DEA overruled this and in 1992 gave its final rejection to the medicinal use of cannabis. In the same year, Hewlett in St Louis USA discovered the first cannabinoid receptor in neuronal tissue (Devane et al., 1988) which led to the discovery of the first endogenous ligand anandamide, the body's own natural cannabinoid in 1992 (Devane et al., 1992).
Pain protects the body from external harm and prevents activity after damage due to trauma and surgery, while it heals. It is also the result of many pathological processes.
To most people the mechanism is similar to an electrical alarm system but this is much too simplistic.
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