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This entire section, under pharmacology, is nonsensical and has no scientific grounding

"If taken in combination with a powerful cannabinoid receptor agonist such as JWH-018, CP 55,940 or the super-potent HU-210, it could greatly increase the aforementioned effects. It is possible that this kind of combination could allow a human to experience a rare and never-before experienced overdose of cannabinoids. Although this could be a potentially dangerous experiment, the use of less potent, natural cannabinoids (like the ones found in cannabis) in combination with eCBRIs could turn out to have some recreational value as cannabis enhancers."

Cannabinoid receptor agonists do not enhance the production or release of eCBs, and therefore will have no interaction whatsoever with eCBRIs. The above advice is not only misleading, but also contains some false information, including the notion that cannabinoid overdose has never before been experienced- when in actuality, cannabinoid overdoses are well reported upon. —Preceding unsigned comment added by 64.108.197.81 (talk) 03:32, 29 March 2011 (UTC)[reply]

The second statement,

"As one might expect, combining a cannabinoid receptor antagonist with an eCBRI reverses the effects of the reuptake inhibitor, and therefore could hinder treatment. Cannabinoid receptor antagonists aren't something common, so normally this isn't something to worry about. But if smoked cannabis or cannabis extract is to be used as a treatment, it would be necessary to cultivate varieties with little to no amounts of these compounds, as they are found in low concentrations in most varieties. One example of these antagonist compounds which is found in the cannabis plant is THCV (tetrahydrocannabivarin)."

requires citation, and clarification. For instance, a silent antagonist will simply abolish any effect of a eCBRI. Alternatively, an inverse agonist (the CBRs are constitutively active GPCRs) will actually work against the effects of an eCBRI, but this is dependent upon the comparative affinities of the eCB in question and the CBR-inverse agonist in question.

Additionally, there is no recorded history of recreational eCBRI use, so that needs to be taken out of the first statement.

Finally, the last statement in the first paragraph ("which only adds to the controversy around cannabinoids and the cannabis plant as medicine") is a non-encyclopedic opinion, and actually has no bearing on the current state of the pharmacological research, in which the use of cannabinoids as medication is not controversial, but actually widely accepted as a possibility (there are hundreds of current patents for potential medications and routes of administration for synthetic cannabinoids) and in reference to the use of cannabis plant, this article has no relation to that (it would be like talking about opium in an article about o-desmethyltramadol or oxycodone, just because the two function in the same biological system).