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CANNABIS USE IN TEENS: BENIGN HIGH OR PATHWAY TO PSYCHOSIS?
Jeffrey Hunt MD
Professor and Director of Training CAP Fellowship and TB Residency Alpert Medical School at Brown University Director of Inpatient and Intensive Services Bradley Hospital
Bradley Hospital
Hassan Minhas, MD Chief Fellow, CAP Fellowship Alpert Medical School at Brown University
Disclosures:
J Hunt
• NIMH grant support
• Wiley Publishers
• Bradley Hospital
• No industry support
• H Minhas
• RIH
Outline
1. Case study
2. Review of scope of cannabis use in teens
3. Neurobiology of cannabis use and its effect on developing brain
4. Impact of cannabis use on the course of psychiatric disorders including the development of psychosis
5. What about synthetic cannabis?
6. Summary and discussion of next steps
Case: Part 1
• 17 year old male admitted for sudden onset severe paranoid ideation and disturbance in thought processes • No prior psychiatric treatment
• Star athlete and good student
• Infrequent use of cannabis but after a long week of final exams he had 5-6 bong hits over a 2-3 hour period
• Became progressively more paranoid later that night • Couldn’t sleep, became hypervigilant, restless, fearful, perplexed
• This worsened through weekend. Went to school Monday AM but abruptly tried to leave
• Brought to ED. Admitted to medical floor. Tried to jump out of window at hospital during period of agitation
Case: Part 2
• Admitted to inpatient unit • MSE: agitated, sleep disturbance, perplexed, paranoid
• Started on antipsychotic medication
• 1 To 1 supervision
• Improved within one week
• Discharged soon after
• Informed team that he had smoked “sour diesel” • Multiple “hits” in short amount of time
• Had multiple relapses of thought disorder over the next 8-9 months in absence of using cannabis • Multiple negative tox screens
• Missed significant number of school days
• Finally stabilized after 10 months
Outline
1. Case study
2. Review of scope of cannabis use in teens
3. Neurobiology of cannabis use and its effect on developing brain
4. Impact of cannabis use on the course of psychiatric disorders including the development of psychosis
5. What about synthetic cannabis?
6. Summary and discussion
• Shift in the US in favor of relaxing marijuana laws
• 1969-12% favored
legalization • 2013- 60% favored
legalization
• RI is 1 of 20 states that
allows the sale of medical marijuana
• IN RI Legislation was introduced recently calling for the legalization of marijuana for recreational purposes, establishment of a system to tax the drug like liquor sales
Slide courtesy L Whiteley
"As has been well documented, I smoked pot as a kid and I view it as a bad habit and a vice, not very different from the cigarettes that I smoked as a young person up through a big chunk of my adult life, I don't think it is more dangerous than alcohol.''
• Dr. Sonjay Gupta for CNN endorses the decriminalization of marijuana and its use for medicinal purposes
• His only caveat- “ research hints at a possible heightened risk of developing
psychosis.”
Medical Marijuana and Legalization Efforts • Are associated with increased use • Are associated with decreased perceptions of both risk and
social disapproval of marijuana But, what’s the problem if its safe enough to be a medicine…. There is compelling scientific evidence that marijuana is not be as benign as perceived by teens and young adults
Outline
1. Case study
2. Review of scope of cannabis use in teens
3. Neurobiology of cannabis use and its effect on developing brain
4. Impact of cannabis use on the course of psychiatric disorders including the development of psychosis
5. What about synthetic cannabis?
6. Summary and discussion
Cannabinoid Receptors in the Brain We are all born with “cannabinoid” receptors on our brain cells to which THC binds These receptors are widespread: prefrontal cortex, cerebellum, hippocampus hypothalamus & thalamus These areas regulate: Brain development Memory and cognition Motivation and reward Appetite Immunological function Reproduction Movement Pain
Endocannabinoid System is Important in Brain Development
• Present in the fetal brain
• Guides neuron growth
• Helps to control how brain cells “learn” whether to grow new synapses and connections to other neurons
• Plays a role in the myelination of brain cells
Our brain produces endogenous endocannabinoids that bind to the cannabinoid receptors- One of these is called anandamide. Essentially, THC and anandamide have some similarities in chemical structure which is why THC can “fool” the brain by binding to the same receptors that anandamide does
Early onset of regular use of cannabis decreases axonal fiber connectivity
Hazardous to developing brain – disturbed brain connectivity underlies cognitive impairment and vulnerability to psychosis, depression, and anxiety
• Results of this study indicate that in young, recreational marijuana users, structural abnormalities in gray matter density, volume, and shape of the nucleus accumbens and amygdala can be observed. Relate to reward processing and euphoria
• 1,000 participants (13 -38yrs) completed neuropsychological assessments (IQ test, executive functioning, memory, processing speed) at 5 time points beginning at age 13 before cannabis use
• Significant relationship between years of marijuana dependence and change in IQ scores. • Impairment worse for weekly use before age 18 • After age 18 = no significant difference
Outline
1. Case study
2. Review of scope of cannabis use in teens
3. Neurobiology of cannabis use and its effect on developing brain
4. Impact of cannabis use on the course of psychiatric disorders including the development of psychosis
5. What about synthetic cannabis?
6. Summary and discussion
Frequency of a cannabis diagnosis at Bradley Hospital
631 Total admissions to adolescent inpatient program over last year
209 of those had a cannabis diagnosis (comorbidity) at discharge
Cannabisdiagnosis
No cannabisdiagnosis
33%
67%
Sour Diesel
• THC > 20%
“East Coast Sour Diesel is crossed with Mexican/Afghani Diesel to produce the Sour Diesel marijuana strain. It emits strong scents of vanilla, lemon and cream and displays heavily potent characteristics of stoniness. Its 90% Sativa concentration yields excellent high-end cerebral buzzes that are sure to expand your consciousness every time you toke up. Excellent in the early morning, Sour Diesel gives you a bright, energetic, and quite possibly talkative wake-n-bake experience; mixed with just enough Indica calming to make you chill and thoughtful.”
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Odds ratio
Resin (hash) andtraditional importedherbal cannabis (D9-THCand CBD both 1%)
Sinsemilla (skunk) (D9-THC 12–18%; CBD 0%)
British Journal of Psychiatry (2009)
The finding that people with a first episode of psychosis had smoked higher-potency cannabis, for longer and with greater frequency, than a healthy control group is consistent with the hypothesis
that D9-THC is the active ingredient increasing risk of psychosis.
Cannabis and schizophrenia
Andreasson, Lancet 1987
Six fold increase in risk of of developing schizophrenia for high consumers of cannabis (>50 occasions)
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Odds ratio
Cannabis use by age 15
Cannabis use by age 18
BMJ, 2002
Those who used cannabis by age 15 were four times as likely to have a diagnosis of schizophreniform disorder at age 26 than controls.
Prospective Dunedin Study (N=1037)
• 35 large longitudinal studies, data from 7 cohort studies • Increased risk of any psychotic outcome in individuals who had ever used cannabis
• Dose response effect/ greater risk with more frequent use
• “We conclude that there is sufficient evidence to warn young people that cannabis
use could increase their risk for psychotic illness in later life”
• Meta analysis (8 longitudinal studies) revealed that the age of onset of psychosis
was 2.70 years earlier among samples of cannabis users • Supports hypothesis that cannabis use plays causal role in the development of
psychosis in some patients
• “The results suggest need for renewed warning about potentially harmful effects of cannabis”
Cunha et al Schizophrenia Research 2012
FEP C+ have less structural brain abnormalities and less cognitive impairments when compared with the group of FEPs without a history of Cannabis use.
Cannabis use is a crucial factor for the development or for the precipitation of psychosis in an otherwise not so compromised brain.
Schizophrenia Research 121 (2010) 107–117
Repeated exposure to THC may sensitize an individual to the psychotic effects of THC, in interaction with other environmental risk factors such as stress.
• Genetic variations can affect the likelihood of developing psychosis following exposure to cannabis in adolescence
• COMT involved in metabolism of dopamine and
disturbances are implicated in pathogenesis of schizophrenia
• A functional polymorphism in the catechol-O-methyltransferase (COMT) gene moderated the influence of adolescent cannabis use on developing adult psychosis.
• Individuals with two copies of the Val variant of
COMT gene have a higher risk of developing schizophrenic-type disorders if they used cannabis during adolescence.
Biol Psychiatry. 2005 May 15;57(10):1117-27.
Functional polymorphism in the catechol-O-methyltransferase gene: longitudinal evidence of a gene X environment interaction. Caspi A1, Moffitt TE, Cannon M, McClay J, Murray R, Harrington H, Taylor A, Arseneault L, Williams B, Braithwaite A, Poulton R, Craig IW.
Regular cannabis use increases risk of schizophrenia in those with AKTI gene
BIOL PSYCHIATRY 2012;72:811–816
AKT1 gene codes for a protein kinase that forms an integral part of the dopamine receptor signaling cascade in the striatum .
Summary of risk factors for psychosis
• Highest risk for
• Those with a family history of the disorders- genetics
• Those who start using in earlier adolescence
• Risks increase with higher frequency of use
40
Outline
1. Case study
2. Review of scope of cannabis use in teens
3. Neurobiology of cannabis use and its effect on developing brain
4. Impact of cannabis use on the course of psychiatric disorders including the development of psychosis
5. What about synthetic cannabis?
6. Summary and discussion
What are synthetic cannibanoids?
• Synthetic chemicals synthesized in a lab, and sprayed on herbs
• “Not for human consumption” in order to circumvent the Controlled Substances Analogues Enforcement Act of the United States of America
47
Stronger than regular weed!
• Whereas THC is only a partial agonist at cannibanoid receptors, synthetic cannabis can be a full agonist
• Affinity can be 800 times that of regular cannabis
• Often contaminated with other substances like Clenbuterol(beta agonist)
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More likely to cause psychosis
• Several theories
• higher affinity
• dose-potency variations
• natural cannabis contains cannabidiol (compound with antipsychotic properties)
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Clinical challenges
• Not detected in routine urine drug screens
• Requires special lab tests (not offered in RI)
• Liquid gas chromatography tandem mass spectrometry
• Matrix assisted laser desorption/ionization time of flight mass spectrometry
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Outline
1. Case study
2. Review of scope of cannabis use in teens
3. Neurobiology of cannabis use and its effect on developing brain
4. Impact of cannabis use on the course of psychiatric disorders including the development of psychosis
5. What about synthetic cannabis?
6. Summary and discussion of next steps
Discussion
• What is best way to reach adolescents relating to risks of cannabis use ?
• Specifically how should we educate adolescents about the risk of psychosis?
Clinical Prevention Strategies
oMotivational Interviewing
oFamily Involvement – Monitoring and rewards
MI examples
I: Your parents are worried that pot is a problem. But what have you noticed? [Reflection; open question]
I: It must be confusing. On one hand you see some problems like poor grades. But you like hanging with your friends. [Reflection of feeling and ambivalence]
I: Going to college is very important to you. [Reflection reinforcing important value]
MI examples I: It seems to you that this handout must be wrong. [Reflection on information]
I: Most people compare themselves to friends who are also using drugs frequently, “more than average.” [Giving information after getting permission]
I: I have given you a lot of information. What are you thinking at this point? [Goal setting]
MI for Substance Use Disorders
Does it work?
Cochrane review (2011) 15 RCTs (n=2,327) -Small short term effect from ~1 session
compared to no treatment Meta-analysis of MI for adolescents 21 studies (N = 5, 471) - Small effect d = 0.17
Jensen et al, J Cons Clin Psych 2011
MI for Adolescent SUDs
What’s the impact and should I use it?
oSmall but consistent effects
• 6 Joints/day (SD = 6) 5 Joints/day
oMI useful for:
- Prevention
- Engagement for those unmotivated
oEasily integrated Rx– it’s brief!
oRepeated over time
How can families help?
• Discuss substance use
• Reinforce prosocial behavior
• Monitor behavior
• Provide rewards
Monitoring Worksheet
Situation (What behavior? Where? When?)
Reasons I am concerned (Put in teen language)
Things that CAN be negotiated:
Things that CANNOT be negotiated (What are the limits?)
Decision/Plan (Plan should be observable)
Ways of staying consistent with this plan (Consequences and Rewards)
Early Intervention
oAdolescents often unmotivated for change
- Parents & others more motivated
oEngagement is first step
o MI to listen / assess / feedback
oParental involvement
oImprove discussions and monitoring
Information and Assessment
oNIDA for teens
oPartnership at Drugfree.org
oHealthTeamWorks.org (guidance on marijuana)
oCRAFFT - Adolescent self-report screener Knight et al, 2002
oCustomary Drinking and Drug Use Record
Straight Facts About Marijuana Marijuana is the most widely used illicit drug in the United States and tends to be the first
illegal drug teens use. The physical effects of marijuana use, particularly on developing adolescents, can be acute. (SAMSHA website: www.health.org/govpubs/rpo884)
Short-term effects of using marijuana:
sleepiness difficulty keeping track of time, impaired or reduced short-term memory
reduced ability to perform tasks requiring concentration and coordination, such as driving a car
increased heart rate potential cardiac dangers for those with preexisting heart disease
bloodshot eyes dry mouth and throat
decreased social inhibitions paranoia, hallucinations
Long-term effects of using marijuana: enhanced risk for cancer and psychosis
decrease in testosterone levels for men; also lower sperm counts and difficulty having children
increase in testosterone levels for women; also increased risk of infertility diminished or extinguished sexual pleasure
psychological dependence requiring more of the drug to get the same effect
Marijuana blocks the messages going to your brain and alters your perceptions and emotions, vision, hearing, and coordination. A recent study of 1,023 trauma patients admitted to a shock trauma unit found that one-third had marijuana in their blood.
Treatment of Cannabis Use Disorders (CUDs)
oMotivational Interviewing / CBT
oFamily treatment
oContingency management
oNovel treatment - N-Acetylcysteine