Quintin T. Chipley, M.A., M.D.
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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
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Of course, their article had been written,
reviewed, and approved long before it saw
print, but we have some bragging rights here:
CAPTASA
scooped
JAMA!
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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
 Age
dependent
dependent: the younger
the abuser, the greater the risk
D9-THC
here
Cannabidiol
here

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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

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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
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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.
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
If you remember, it did not take long for
major tobacco companies to learn how to use
post-harvest chemistry (essentially freebasing 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?
D9-THC
here
Cannabidiol
here
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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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Bhattacharyya S, Fusar-Poli P, Borgwardt S, Martin-Santos R, Nosarti C, O'Carroll
C, Allen P, Seal ML, Fletcher PC, Crippa JA, Giampietro V, Mechelli A, Atakan Z,
McGuire P. Modulation of mediotemporal and ventrostriatal function in humans by
Delta9-tetrahydrocannabinol: a neural basis for the effects of Cannabis sativa on
learning and psychosis. Arch Gen Psychiatry. 2009 Apr;66(4):442-51. PMID:
19349314
Bhattacharyya S, Morrison PD, Fusar-Poli P, Martin-Santos R, Borgwardt S,
Winton-Brown T, Nosarti C, O' Carroll CM, Seal M, Allen P, Mehta MA, Stone JM,
Tunstall N, Giampietro V, Kapur S, Murray RM, Zuardi AW, Crippa JA, Atakan Z,
McGuire PK. Opposite effects of delta-9-tetrahydrocannabinol and cannabidiol on
human brain
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Bossong MG, Niesink RJ. Adolescent brain maturation, the endogenous
cannabinoid system and the neurobiology of cannabis-induced schizophrenia.
Prog Neurobiol. 2010 Jul 15. PMID: 20624444
Di Forti M, Morgan C, Dazzan P, Pariante C, Mondelli V, Marques TR, Handley R,
Luzi S, Russo M, Paparelli A, Butt A, Stilo SA, Wiffen B, Powell J, Murray RM. Highpotency cannabis and the risk of psychosis. Br J Psychiatry. 2009 Dec;195(6):48891. PMID: 19949195
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Hickman M, Vickerman P, Macleod J, Lewis G, Zammit S, Kirkbride J, Jones P. If cannabis
caused schizophrenia--how many cannabis users may need to be prevented in order to
prevent one case of schizophrenia? England and Wales calculations. Addiction. 2009
Nov;104(11):1856-61. PMID: 19832786
Large, Matthew, Swapnil Sharma, Michael T. Compton,Tim Slade, Olav Nielssen, M Crim,
Archives of Geneneral Psychiatry (now JAMA Psychiatry). 2011;68(6):555-561.
doi:10.1001/archgenpsychiatry.2011.5
Mahajan SD, Aalinkeel R, Sykes DE, Reynolds JL, Bindukumar B, Adal A, Qi M, TohJ, Xu G,
Prasad PN, Schwartz SA. Methamphetamine alters blood brain barrier permeability via
the modulation of tight junction expression: Implication for HIV-1 neuropathogenesis
in the context of drug abuse. Brain Res. 2008 Apr 8;1203:133-48. PMID: 18329007
Malone DT, Jongejan D, Taylor DA. Cannabidiol reverses the reduction in social
interaction produced by low dose Delta(9)-tetrahydrocannabinol in rats. PMID:
19393686
Morgan CJ, Freeman TP, Schafer GL, Curran HV. Cannabidiol attenuates the appetitive
effects of Delta 9-tetrahydrocannabinol in humans smoking their chosen cannabis.
Neuropsychopharmacology. 2010 Aug;35(9):1879-85. PMID: 20428110
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Müller H, Sperling W, Köhrmann M, Huttner HB, Kornhuber J, Maler JM. The
synthetic cannabinoid Spice as a trigger for an acute exacerbation of
cannabis induced recurrent psychotic episodes. Schizophr Res. 2010
May;118(1-3):309-10. PMID: 20056392
Pierre JM. Psychosis associated with medical marijuana: risk vs. benefits of
medicinal cannabis use. Am J Psychiatry. 2010 May;167(5):598-9. PMID:
20439399