Presentation on theme: "Quintin T. Chipley, M.A., M.D.. This presenter has no funding from any institution, corporation, or agency regarding the content of this presentation."— Presentation transcript:
This presenter has no funding from any institution, corporation, or agency regarding the content of this presentation. Although he loves his work at the University of Louisville as the Counseling Coordinator for the Health Sciences Center students, that institution should in no way be held responsible for the content of this presentation.
Then JAMA Psychiatry (Formerly The Archives of General Psychiatry) published an article in February, 2011that corroborated the material. http://archpsyc.jamanetwork.com/article.aspx? articleid=211301 Of course, their article had been written, reviewed, and approved long before it saw print, but we have some bragging rights here:
Increase Psychotic Disorders, even among people without a genetic predisposition: One study indicates an extra 1 in 1400 people will develop chronic psychosis. The intereaction effect with a genetic predisposition becomes much larger Depressive and anxiety disorders are probably even more prevalent and with greater social and financial burden
Dose dependent Age dependent: the younger the abuser, the greater the risk
THC is the active agent in the “mind expanding” hallucinatory-type experiences. These include distortions in perception of time an space. (A metabolite produce in the liver may also be responsible for increased heart rate, anxiety. a.k.a sympathomemetic.) Cannabidiol produces sedation and even reduces distortions
D9-THC dose-response curve keeps on rising: The greater the dose, the greater the response Cannabidiol has a dose-response curve that tends to “flatten” out: after a certain plasma level is reach, an increase in plasma level does not create more effect
In Cannabis sativa the ratio of D9-THC: Cannabidiol is high even before horticultural selection In Cannabis indica the ratio of D9–THC : Cannabidiol is not nearly as high
By the time we consider individual differences in human physiology (liver function: acytelation and cytochrome p450 actions), differences in genetic predispositions for psychotic, mood, and anxiety disorders, and differences in relative concentrations of the major psychoactive components of Cannabis as acquired on the streets and in “pharmacies” we are looking at a crap-shoot regarding the outcome.
If you remember, it did not take long for major tobacco companies to learn how to use post-harvest chemistry (essentially free- basing tobacco) to make the nicotine more bioavailable, rendering the product more popular. How long do you think it will be before research shows a way to close the ring in Cannabidiol so that it becomes D9-THC?
Obviously, substance use abstinence is first Should an anti-psychotic medication be used in the presentation of psychosis secondary to Cannabis use? Frankly, there is not enough evidence –based material in the literature to say. If you follow the theory-based notion that the longer a person stays in a psychotic state, the more permanent is the neuronal architecture change, then aggressive treatment is warranted. But anti-psychotic meds have considerable risks.
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