Summary One page single spaced

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Please pick one article and write one page single spaced summary. Instruction and Example are below.

Thank you

Your summaries will include all the main ideas of the article that are worth remembering. Pls
write in full sentences (1 full page only just like you did the cases [no 1/2 or 3/4 pages pls]). Your
summary MUST be 2 equal-sized paragraphs (half-a-page each), and PLS USE New Times
Roman font type ONLY.
EXAMPLE:
Most sub-Saharan Africa countries like Tanzania prohibit abortion. It is an illegal practice unless
a woman’s life is in danger. This article discusses the study of abortion beliefs and practices
among adolescents and young adults in nine villages across four rural districts of Mwanza,
Tanzania. It examines the experiences of rural young women who attempt abortions who do not
have complications, minor complications, or severe complications for which they do not seek or
receive medical care. The study is drawn primarily on participant-observation (PO), which
focuses broadly on the social and cultural context of young people’s sexual behavior. In the
opening excerpt, the author states that the World Health Organization estimates that 3.1
percent of East African women aged 15-44 have had unsafe abortions, and 60 percent of unsafe
abortions involved women younger than 25. This estimate is based solely on hospital records for
women who suffer hemorrhage, sepsis, and other complications following an abortion. Those
who have had an induced abortion in Tanzania could face years of imprisonment; despite that,
abortion is still believed to be widely practiced in that part of sub-Saharan Africa. This study also
draws upon group discussions and interviews on reproductive beliefs and practices among
young women and men. Participants in the study may have underreported induced abortion
because they feared cultural rejection or disapproval, and others feared legal or religious
sanctions. Many young women also were afraid of potential health problems. The findings were
similar across the villages in Mwanza.
Most people reported that they are sexually active by age 15, and many wanted to prevent
pregnancy. The majority of young women and schoolgirls do not use protection because of
limited access; only a minority used birth control like Depo Provera injections or oral
contraceptives. Condoms are rarely used. Conception outside of an established relationship is
common along in tangent with early sexual activity and low use of contraceptives. Although
many women faced with these circumstances have carried their pregnancies to full term, a small
minority felt desperate to end them and attempted to induce abortion. Women induced
abortion by using wood ashes in solution, twigs, high doses of chloroquine, ‘blue’ solution (a
brand of laundry detergent in the form of a tablet), and local plants believed to cause the fetus
to abort. Not all women who attempted abortion succeeded; when the attempt failed, many of
them carried their pregnancies to full term without suffering any consequences. Those who
suffered negative consequences from attempting abortion received opposition from their sexual
partners, health problems, social ostracism, and sexual exploitation by practitioners. The
discussion indicates that many participants in this study had attempted an abortion at some
point, managing to keep it a secret whether or not the abortion was successful. The literature
also points out that some men aggressively prevent their partners from suspending pregnancy
because they feel entitled to potential offspring. In Tanzania, there are strong social norms and
highly restrictive laws that oppose abortion, yet there is no evidence that has been found
indicating if induced abortions have decreased or increased. Furthermore, the practice of
effective contraception will likely reduce the incidence of unsafe abortion, but may not
eliminate it.
___________________________________________________
#9697 Cannabis Use, Abuse, and Dependence
COURSE #9697 — 5 CONTACT HOURS/CREDITS Release Date: 08/01/12 Expiration Date: 07/31/15
Cannabis Use, Abuse,
and Dependence
HOW TO RECEIVE CREDIT
• Read the enclosed course.
• Complete the questions at the end of the course.
• Return your completed Evaluation to CME
Resource by mail or fax, or complete online
at www.NetCE.com. (If you are a physician,
behavioral health professional, or Florida nurse,
please return the included Answer Sheet.) Your
postmark or facsimile date will be used as your
completion date.
• Receive your Certificate(s) of Completion by mail,
fax, or email.
Faculty
Mark Rose, BS, MA, is a licensed psychologist and
researcher in the field of alcoholism and drug addiction
based in Minnesota. He has contributed to the authorship
of several papers on addiction, as well as other medical disorders, and serves as an Expert Advisor and Expert Witness
to various law firms on matters related to substance abuse.
He is on the Board of Directors of the Minneapolis-based
International Institute of Anti-Aging Medicine, and a
member of several professional organizations.
Faculty Disclosure
Contributing faculty, Mark Rose, BS, MA, has disclosed
no relevant financial relationship with any product manufacturer or service provider mentioned.
Division Planners
Accreditation
CME Resource is accredited by the Accreditation Council
for Continuing Medical Education to provide continuing
medical education for physicians.
CME Resource is accredited as a provider of continuing
nursing education by the American Nurses Cre­dentialing
Center’s Commission on Accreditation.
CME Resource, #1092, is approved as a provider for
continuing education by the Association of Social Work
Boards 400 South Ridge Parkway, Suite B, Culpeper, VA
22701. www.aswb.org. ASWB Approval Period: 3/13/2010
to 3/13/2013. Social workers should contact their regulatory board to determine course approval.
This program is approved by the National Association of
Social Workers (Approval #886531582-6972) for Substance Abuse Disorders continuing education contact
hours.
CME Resource is an NBCC-Approved Continuing Education Provider (ACEPâ„¢) and may offer NBCC-approved
clock hours for programs that meet NBCC requirements.
Programs for which NBCC-approved clock hours will be
awarded are identified on the course material and website.
CME Resource is solely responsible for all aspects of the
program. Provider number 6361.
CME Resource is approved as a provider of continuing
education by the Association for Addiction Professionals.
Provider Number 680.
CME Resource is approved as a provider of continuing
education by the California Association of Alcoholism and
Drug Abuse Counselors. Provider Number 5-08-151-0614.
Ronald Runciman, MD
Jane Norman, RN, MSN, CNE, PhD
Alice Yick Flanagan, PhD, MSW
CME Resource is approved as a provider of continuing
education by the California Association for Alcohol/Drug
Educators. Provider Number CP40 927 C 0614.
Division Planners Disclosure
Designation of Credit
The division planners have disclosed no relevant financial
relationship with any product manufacturer or service
provider mentioned.
Audience
This course is designed for health and mental health professionals who are involved in the evaluation or treatment of
persons who use cannabis, either illicitly or as an adjunct
to medical treatment.
CME Resource designates this enduring material for
a maximum of 5 AMA PRA Category 1 Credit(s)â„¢.
Physicians should claim only the credit commensurate with
the extent of their participation in the activity.
CME Resource designates this continuing education activity for 5 ANCC contact hours.
CME Resource designates this continuing education activity for 6 hours for Alabama nurses.
Copyright © 2012 CME Resource
A complete Works Cited list begins on page 25.
CME Resource • Sacramento, California
Mention of commercial products does not indicate endorsement.
Phone: 800 / 232-4238 • FAX: 916 / 783-6067
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#9697 Cannabis Use, Abuse, and Dependence ____________________________________________________
CME Resource designates this continuing education activity for 1 pharmacology contact hour.
AACN Synergy CERP Category A.
Social workers will receive 5 Clinical continuing education clock hours in participating in this intermediate to
advanced course.
CME Resource designates this continuing education activity for 2 NBCC clock hours.
This course meets the requirements for 5 Clinical hours
as required by the New Jersey Board of Social Work
Examiners.
CME Resource designates this continuing education
activity for 5 continuing education hours for addiction
professionals.
Individual State Nursing Approvals
In addition to states that accept ANCC, CME Resource
is approved as a provider of continuing education in nursing by: Alabama, Provider #ABNP0353 (valid through
December 12, 2013); California, BRN Provider #CEP9784;
California, LVN Provider #V10662; California, PT Provider #V10671; Florida, Provider #50-2405; Iowa, Provider
#295; Kentucky, Provider #7-0054 through 12/31/2017,
Kentucky Board of Nursing approval of an individual
nursing continuing education provider does not constitute
endorse­ment of program content.
Individual State Behavioral Health Approvals
In addition to states that accept ASWB, CME Resource
is approved as a provider of continuing education by the
following state boards: California Board of Behavioral
Sciences, Provider #PCE 1632; Florida Board of Clinical
Social Work, Marriage and Family Therapy and Mental
Health, Provider #50-2405; Illinois Division of Professional
Regulation for Social Workers, License #159.001094; Illinois Division of Professional Regulation for Licensed Professional and Clinical Counselors, License #197.000185;
Illinois Division of Professional Regulation for Marriage
and Family Therapists, License #168.000190; Texas State
Board of Social Work Examiners, Approval #3011; Texas
State Board of Examiners of Professional Counselors,
Approval #1121; Texas State Board of Examiners of Marriage and Family Therapists, Approval #425.
Special Approval
This activity is designed to comply with the requirements
of California Assembly Bill 1195, Cultural and Linguistic
Competency.
About the Sponsor
The purpose of CME Resource is to provide challenging
curricula to assist healthcare professionals to raise their levels of expertise while fulfilling their continuing education
requirements, thereby improving the quality of healthcare.
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CME Resource • October 5, 2012
Our contributing faculty members have taken care to
ensure that the information and recommendations are
accurate and compatible with the standards generally
accepted at the time of publication. The publisher disclaims any liability, loss or damage incurred as a consequence, directly or indirectly, of the use and application of
any of the contents. Participants are cautioned about the
potential risk of using limited knowledge when integrating
new techniques into practice.
Disclosure Statement
It is the policy of CME Resource not to accept commercial
support. Furthermore, commercial interests are prohibited
from distributing or providing access to this activity to
learners.
Course Objective
The purpose of this course is to allow healthcare professionals to effectively identify, diagnose, treat, and provide appropriate referrals for patients with cannabis use
disorders.
Learning Objectives
Upon completion of this course, you should be able to:
1. Review the history of cannabis use and define
the concepts of cannabis abuse and dependence.
2. Discuss the epidemiology of cannabis use in the
United States, including treatment utilization
and risk factors for cannabis use disorders.
3. Outline the pharmacology of cannabis.
4. Review the established and investigational
therapeutic uses of cannabis and delta-9-THC.
5. Identify acute effects of cannabis ingestion
on both physical and psychological systems.
6. Describe long-term effects of cannabis ingestion
and conditions associated with cannabis use,
including the associated withdrawal syndrome.
7. Discuss the prognosis and treatment approaches
for individuals who misuse cannabis, including
considerations for non-English proficient patients.
Sections marked with this symbol include
evidence-based practice recommen­dations.
The level of evidence and/or strength
of recommendation, as provided by the
evidence-based source, are also included
so you may determine the validity or relevance of the
information. These sections may be used in conjunction with the course material for better application to
your daily practice.
www.NetCE.com
___________________________________________________ #9697 Cannabis Use, Abuse, and Dependence
INTRODUCTION
Cannabis products such as marijuana and hashish
comprise the most widely used recreational drugs
both in the United States and worldwide [55].
Although, with a few exceptions, these drugs lack
the liability of abuse and dependence seen with
other illicit drugs, such as cocaine, methamphetamine, and heroin, physical and psychological
withdrawal symptoms can occur with cannabis
products, posing an additional consideration in
the management of these patients. This course will
provide the most pertinent, up-to-date information
regarding the demographics and characteristics
of cannabis users, the history of therapeutic and
recreational use of the drug, the pharmacology
and clinical effects, adverse effects and conditions,
and the management and treatment of overdose,
toxicity, and abuse and dependence.
HISTORY OF CANNABIS USE
Although the later part of the 20th century saw
a rise in the use of cannabis for recreational, religious/spiritual, and medicinal purposes, humans
have been consuming cannabis since prehistory.
Cannabis, native to Central Asia, is one of the
oldest known psychotropic drugs. Cultivated and
consumed long before recorded history, archeological discovery indicates that it was used in China
since around 4000 B.C.E. There are several species
of cannabis, including Cannabis sativa, Cannabis
indica, and Cannabis ruderalis. Cannabis sativa is the
most widely used variety and can be cultivated in
a variety of climates [1; 13].
The two main derivatives of cannabis are marijuana and hashish. The term marijuana originated
in Mexico to describe cheap tobacco; today, it refers
to the dried leaves and flowers of the Cannabis
plant. Hashish, an Arabic term, is the viscous resin
of the plant [1; 13].
CME Resource • Sacramento, California
The Chinese emperor Shen Nung is believed to be
the first to describe the properties and therapeutic
uses of cannabis, which appeared in his compendium of Chinese medicinal herbs written in 2737
B.C.E. Following this, cannabis was cultivated
for its fiber, seeds, medicinal use, and recreational
consumption, which then spread to India from
China [1].
In 1839, William O’Shaughnessy, a British physician and surgeon working in India, was the first
individual in Western medicine to discover the
use of cannabis as an analgesic, appetite stimulant, antiemetic, muscle relaxant, or anticonvulsant. In 1854, cannabis was listed in the United
States Dispensatory; however, after prohibition
was repealed, American authorities condemned
the use of cannabis, claiming it responsible for
insanity, intellectual deterioration, violence, and
various crimes. In 1937, the U.S. Government
introduced the Marihuana Tax Act. According to
this legislation, a tax of $1 per ounce was collected
when cannabis was used for medical purposes and
$100 per ounce when it was used for unapproved
purposes [13]. Cannabis was removed from the
United States Pharmacopoeia in 1942 [1].
DEFINITION OF CANNABIS
ABUSE AND DEPENDENCE
Although severe problems associated with abuse
and dependence are less common among cannabis
users than among other drug users, they do occur.
Furthermore, cannabis had the highest rate of
past year dependence or abuse in 2010 of all illicit
drugs [5].
Cannabis dependence is best described as a chronic
relapsing disease characterized by compulsive
seeking and use of cannabis, accompanied by
functional and molecular changes to the brain
[2]. The single most defining aspect of cannabis
dependence is the salience of the relationship
with the drug. The stronger the relationship, the
more likely the patient will continue problematic
use despite internal and external consequences.
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#9697 Cannabis Use, Abuse, and Dependence ____________________________________________________
Psychological dependence, whereby the patient
believes cannabis is necessary to get through daily
activities, alleviate stress, and cope with problems,
is a symptom of cannabis dependence. Physiological adaptation, evidenced by tolerance and withdrawal, is often present but is not sufficient for a
diagnosis of dependence. Cannabis dependence is
diagnosed behaviorally and is evidenced by cravings for cannabis, preoccupation with use of the
drug, sneaking and concealing ingestion, loss of the
ability to control cannabis use, and continued use
despite significant physical, psychological, social,
occupational, or legal consequences [3].
Cannabis abuse is a condition of frequent or
binge-type use and continued use despite legal
consequences or failure to meet work, school, or
domestic obligations. However, abuse is characterized by less severity and fewer behavioral symptoms
than with the dependence syndrome [3].
Identifying patients with a cannabis-related
disorder can be difficult, as abuse and associated
problems are typically slow to develop. Patients
frequently do not recognize they have a problem
or do not want to give up their drug use. They may
also be attempting to conceal their drug use from
parents, physicians, and other authority figures.
Unexplained deterioration in academic or work
performance, problems with or changes in social
relationships, and changes in recreational activities
are signs of a possible problem [4].
EPIDEMIOLOGY
OF CANNABIS USE
The 2010 National Household Survey on Drug
Abuse found that more than 125 million (41.9%)
Americans 12 years of age and older had tried cannabis at least once in their lifetimes, and 17.4 million (6.9%) had used cannabis in the past month
[5]. Twelfth grade boys in all ethnic groups are more
likely than girls to have used cannabis in the last
30 days [57]. Among ethnic groups, Native Hawaiian/Other Pacific Islander (1.8%) adolescents are
the least likely to have used cannabis within the
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CME Resource • October 5, 2012
last month, followed by Asian (2.6%) and white,
black, or African American (7.5%) adolescents.
Hispanic or Latino (8.0%), non-Hispanic/Latino
mixed race (8.2%), and Native American/Alaska
Native (9.1%) teens are the most likely to have
used cannabis in the past month [57].
Of the 22.6 million illicit drug users in the United
States, 76.8% were current (past month) users
of cannabis, with the majority (60.1%) using
cannabis exclusively [5]. In 2010, the National
Household Survey on Drug Abuse found that 4.5
million Americans met the criteria for cannabis
dependence [5]. Approximately 6% of those who
have used cannabis in the past year meet the
Diagnostic and Statistical Manual of Mental Disorders 4th edition (DSM-IV) criteria for cannabis
dependence [7]. Analysis of data from 1992 to
2002 by researchers at the National Institutes
of Health revealed that while dependence/abuse
rates (using DSM-IV criteria) grew only slightly
overall during that decade, a sharp increase was
noted among particular subgroups (e.g., black men/
women and Hispanic men 18 to 29 years of age;
white men and black women 45 to 64 years of age)
[61]. The researchers noted that the increase in
use disorders was unrelated to a substantial overall
increase in frequency or quantity of use and was
possibly associated with higher cannabis potency,
decreased cost, and various societal factors [5; 57].
It is estimated that there are 6,600 cannabis initiates (12 years of age and older) every day [5].
Approximately 10% of persons who have ever tried
cannabis become daily users, and cannabis dependence affects 1.8% of the population, a higher
rate than any other illicit drug [5; 9]. This rate is
mainly attributable to the greater numbers of cannabis users relative to users of other substances [8].
When examining the risk of dependence among
those who have ever used a particular substance
(referred to as conditional dependence), the rates
for alcohol (15%), cocaine (17%), heroin (23%),
and tobacco (32%) are significantly higher than
for cannabis (9%); however, this study used DSMIII-R criteria and data from 1990 through 1992 [8].
www.NetCE.com
___________________________________________________ #9697 Cannabis Use, Abuse, and Dependence
The rate of cannabis use by children and adolescents doubled during the 1990s [9]. After a
steady decline from 2000 to 2006, use leveled off
and, as of 2008, cannabis use is again on the rise
[5]. Occasional cannabis experimentation, while
illegal, is often considered normative behavior for
adolescents and is not strongly correlated with
behavioral or emotional disorders in the general
population [9]. Although the exact number is
unclear, approximately one-half of “very young”
individuals who use cannabis more than monthly
exhibit behavioral or emotional difficulties. It is
unclear if these difficulties exist before or are an
effect of cannabis use. Genetic behavior disorders,
parents who use cannabis, family disintegration,
and “loss of trusting attachments to key adults”
have been implicated as both causes of adversity
leading to cannabis use and of anxiety, depression, and risk taking behaviors in pre-adolescents
[9]. The perceived impact that cannabis has on
physical and psychological health, along with other
negative factors, strongly predicts use patterns; use
rates were 1.3% among adolescents who saw “great
risk” versus 10.2% among those who perceived
lesser or no risks [5].
TREATMENT UTILIZATION
Increases in both the prevalence of cannabis use
and the potency of cannabis have contributed to
the 732% increase in cannabis-related emergency
department episodes reported from 1995 to 2009
[10; 62; 63]. When population growth was taken
into account, the increase was still 545% (19
episodes per 100,000 population in 1995 compared to 122.6 episodes per 100,000 in 2009).
Cannabis-related conditions that may be seen in
an emergency department include chronic addiction to cannabis, acute cannabis psychosis, and
cannabis-related schizophrenia [10].
Utilization of treatment services for cannabis
dependence has also increased. Patients entering
substance abuse treatment programs with cannabisrelated problems doubled in the 1990s, and primary
admissions for cannabis rose from 13% in 1999 to
18% in 2009 [64]. The 2010 percentage of can-
CME Resource • Sacramento, California
nabis treatment admissions (24.7%) has surpassed
those for cocaine and heroin and is second only
to admissions for alcohol treatment (67.7%) [5].
However, these statistics are dramatically higher
among adolescents. Cannabis was either the primary or secondary reason for 86% of U.S. adolescent treatment admissions in 2009, and in 2010,
cannabis accounted for 53.6% of all adolescent
primary treatment admissions (155,000 patients)
[5; 64]. As was witnessed with adults in the 1990s,
the number of adolescents receiving treatment
at public treatment centers for cannabis abuse or
dependence also doubled during this period [12].
Overall, the proportion of those seeking treatment
for cannabis dependence is relatively low in the
United States. This may be partially due to the
perception of cannabis as a relatively innocuous
drug [13]. A sample of 243 long-term cannabis users
who reported smoking 3 to 4 times a week found
a lifetime prevalence of cannabis dependence of
57%. However, only one-quarter of the sample
believed that they had a cannabis problem [14].
The leading reasons for failure to seek treatment
are not having health coverage/not being able
to afford the cost, not being ready to stop using,
perception that it might cause a negative opinion
among acquaintances, and belief it would negatively affect a job [5].
RISK FACTORS FOR
CANNABIS USE DISORDERS
Cannabis use typically begins in early to middle
adolescence, and use tends to peak during late
adolescence and young adulthood [13]. Many
people first use cannabis out of curiosity, peer
pressure, or both, and continue to use it for the
desired effects of euphoria, relaxation, heightened
sensations and perceptions, and socialization with
other users. Factors that contribute to chronic use
include easy access, the expectation of few or no
legal consequences for use, and attempts to selfmedicate physical and emotional problems. For
some, chronic use develops into cannabis dependence [4].
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#9697 Cannabis Use, Abuse, and Dependence ____________________________________________________
A major risk factor for adolescent substance abuse,
including cannabis use, is the presence of conduct
problems in childhood. This may be because family conflict, poor parental monitoring, parental
substance use, academic problems, and association with deviant peers are all risk factors for both
substance abuse and conduct problems. More
than one-half of adolescents with substance abuse
problems also exhibit conduct problems [12]. Cooccurrence of these problems is a strong predictor
of poor outcome following substance abuse treatment [12]. Factors associated with cannabis dependence include male gender, ethnic minority status,
and evidence of adolescent risk-taking behaviors,
such as cigarette smoking, conduct problems, and
involvement in a delinquent peer group [14].
Early subjective response to cannabis is associated
with later risk of dependence [16]. Participants in
a survey reporting 5 positive reactions to the drug
had 20 times greater risk of later dependence than
those who did not experience positive reactions,
even after controlling for confounding factors.
These findings suggest that early subjective and
physiological reactions to cannabis are predictive
of later dependence and possibly reflect underlying
genetic differences in vulnerability to dependence.
These possible genetic predispositions are likely
mediated by individual differences in the responsiveness of the mesolimbic dopamine system to
substance use [16].
Several factors associated with successful cessation
of cannabis use have been identified. These factors
include older age, female gender, married marital
status, infrequent cannabis use, absence of delinquent behavior, and high school completion [17].
Genetic Vulnerability Theory
A review of several adoption, family, and twin
studies that examined the relationship between
cannabis use and heritable factors determined that
the use of cannabis (and other licit and illicit substances) is due in part to genetic vulnerability and
an overlap of environmental influences [18]. The
authors explain that there are substantial genetic
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CME Resource • October 5, 2012
influences on measures of cannabis involvement
that correlate with progression to greater levels
of addiction, and an individual’s vulnerability to
cannabis abuse/dependence is shaped by a common
susceptibility to multiple substance abuse and also
by risk factors unique to cannabis. Researchers in
one twin study clarified the basics of this theory in
their conclusion, stating that genetic factors predispose individuals to substance use/abuse whereas
environmental experiences determine which class
of psychoactive substances a predisposed individual
will prefer over another [65].
ESCALATION OF CANNABIS
USE TO OTHER ILLICIT DRUGS
Early onset and frequency of cannabis use are
strong predictors of escalation in other illicit drug
use across sexes, populations, ethnicities, and
socioeconomic strata. Frequent cannabis use during young adulthood significantly increases the risk
of polysubstance abuse, earlier onset of substance
dependence, poorer educational and occupational
outcomes, multiple health and psychiatric problems, and criminal justice system involvement [15].
Cannabis and other illicit drug use may be correlated. Studies have shown that cannabis is a potential “gateway drug,” leading to the use and abuse of
more dangerous drugs, such as cocaine and heroin
[18]. However, it should be noted that evidence
of a causal relationship between cannabis use and
progression to other drug use has been speculative
at best [18]. A report from the National Center on
Addiction and Substance Abuse at Columbia University found that cannabis’s “gateway” effect (if
any) is far less important than that of cigarettes and
alcohol, and teens who use alcohol and nicotine
are 30 times more likely to try cannabis [66]. The
authors refer to cannabis instead as a “bridge” substance. However, teens who use alcohol, nicotine,
and cannabis are 16 times more likely to try other
drugs [66]. One theory is that dopaminergic effects
of alcohol, cannabis, and nicotine lead users to
seek similar effects from other, more potent drugs.
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___________________________________________________ #9697 Cannabis Use, Abuse, and Dependence
PHARMACOLOGY
Cannabis contains more than 460 known chemicals, more than 60 of which are grouped under
the category of cannabinoids [1]. The primary
psychoactive ingredient is delta 9-tetrahydrocannabinol (delta-9-THC), which accounts for up to
25% of the total dry weight of high-potency strains
[69]. Other cannabinoids, including delta-8-THC,
cannabinol, cannabicyclol, cannabichromene,
and cannabigerol, are present in small quantities
(typically less than 5% dry weight) and have no
significant psychotropic effects compared to THC.
It is unknown whether these compounds may have
an impact on the overall effect of cannabis [1].
One notable exception is cannabidiol (CBD),
which in some cannabis strains can account for up
to 5% dry weight and has demonstrated therapeutic
efficacy for psychosis, anxiety, and other disorders
in small-scale studies [69; 70; 71]. The psychotomimetic and anxiogenic effects of THC itself are
thought to be attenuated by CBD [72]. In a 2008
study, cannabis users who had ingested higher
CBD to THC ratios (as tested in hair samples)
were less likely to have paranoid delusions and
schizophrenic-type symptoms than users with hair
samples containing only THC [70]. At present, it
is unclear if CBD’s effects are primarily mediated
by facilitation of the endocannabinoid system or
if other channels are affected; for example, CBD
is a known 5-HT1A (serotonin) receptor agonist
and may also bind at other sites [72; 73]. CBD
also exhibits significant anti-inflammatory and
analgesic effects [74].
Cannabis is ingested in many forms, but it is most
often smoked in the form of a cigarette (“joint”)
or out of a pipe, water pipe (e.g., “bong”), or
improvised vessel (e.g., sawn-off plastic bottle).
It may also be added as an ingredient in baked
goods, eaten, or drunk as an extract. Because of
its relative water insolubility, it is unsuitable for
intravenous use [21]. Vaporizing cannabis (heating
CME Resource • Sacramento, California
below its flash point), either with a purpose-built
vaporizer unit or with a heating wand and a conventional pipe or water pipe, is becoming increasingly popular, especially among medicinal and/or
“health conscious” users. This method of use offers
slightly elevated THC availability (allowing the
user to “smoke” less) and greatly reduced combustion byproduct toxicity compared to smoking [67].
Cannabinoids are present in the stalks, leaves, flowers, and seeds of the plant, but they are particularly
abundant in the resin secreted by the female plant.
THC content varies among the available sources
and preparations of cannabis. Advances in cultivation (such as hydroponic farming) and plantbreeding techniques have increased the potency
of cannabis products [21].
During the 1960s and 1970s, an average joint
contained about 10 mg of THC. Today, a similarsize joint made of a potent subspecies of Cannabis
sativa may contain 60–150 mg of THC. This can
increase to 300 mg if the joint is laced with hashish
oil or resin. The substantial increase in potency in
cannabis products today exposes cannabis smokers
to many times the THC dose compared to their
counterparts in the 1960s and 1970s. This is an
important fact, as the effects of THC are doserelated and most research on cannabis was conducted in the 1970s using doses of 5–25 mg THC.
Some researchers consider the research published
on cannabis use during the 1960s and 1970s to be
obsolete [21; 22].
PHARMACOKINETICS
OF CANNABINOIDS
Approximately 50% of the THC and other cannabinoids present in a cannabis cigarette enter the
mainstream smoke and are inhaled [22]. Smoking
style affects the amount absorbed through the
lungs, with experienced smokers who inhale deeply
and hold the smoke in the lungs for some seconds
before exhaling, ingesting virtually all of the cannabinoids present in the mainstream smoke [22].
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#9697 Cannabis Use, Abuse, and Dependence ____________________________________________________
The onset of action of inhaled cannabis is within
seconds, and full effect is achieved within minutes.
The bioavailability after oral ingestion is lower
than that seen with inhalation; blood concentrations are as low as 25% to 30% of those obtained
by smoking the same dose, partly due to hepatic
first-pass metabolism [21]. The onset of effect is
delayed (0.5 to 2 hours) after oral ingestion, but
the duration is prolonged because of continued
slow absorption from the gut [21].
As little as 2.5 mg THC is enough to produce
measurable psychological and physical effects in
the occasional cannabis user. Upon transferring
to the bloodstream, cannabinoids are distributed
rapidly systemically, first reaching the tissues with
the highest blood flow, such as the brain, lungs,
and liver [22]. Within the brain, cannabinoids are
differentially distributed, reaching high concentrations in the neocortical areas, especially the frontal
cortex; the limbic areas, including the hippocampus and amygdala; sensory areas, such as the visual
and auditory cortex; motor areas, including the
basal ganglia and cerebellum; and the pons [22].
Cannabinoids are highly fat soluble and accumulate in fatty tissues. From these tissues, the compounds are very slowly released into other parts of
the body. In occasional users, the plasma elimination half-life of THC is approximately 56 hours; in
chronic users it is shortened to 28 hours. However,
due to its sequestration in fat, the tissue half-life is
approximately 7 days and complete elimination of
one dose may take as long as 30 days [22].
Cannabinoids are metabolized in the liver, where
they produce more than 20 metabolites, some of
which are psychoactive and many of which have
plasma elimination half-lives of the order of 50
hours. A major metabolite is 11-hydroxy-THC.
This metabolite may be more potent than the
parent compound and may be responsible for some
of the effects of cannabis. Further metabolism
produces inactive metabolites, of which 15% to
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30% are excreted in urine. Active and inactive
metabolites are also excreted into the intestine and
bile. Approximately 15% are reabsorbed back into
the body, prolonging the action of cannabis, while
35% to 65% are finally eliminated in the feces [22].
PHARMACODYNAMICS
Cannabinoids act primarily by binding to cannabinoid receptors type 1 and 2 (CB1 and CB2). Both
of these receptors are part of the G-protein coupled
class, and their activation results in inhibition of
adenylate cyclase activity. Identification of agonists
and antagonists of these receptors has stimulated
interest in medical uses of cannabis [1; 13].
Cannabinoids exert many of their effects by combining with specific receptors in the central nervous system (CNS) and peripheral nervous system.
The discovery of cannabinoid receptors led to a
search for the endogenous ligand with which the
receptors naturally interact. The first substance,
discovered in 1992, was eventually isolated and
named anandamide after the Sanskrit word for
bliss, ananda; 2-arachidonoylglycerol was discovered soon after. Anandamides are derivatives of
arachidonic acid, a polyunsaturated omega-6 fatty
acid, and are related to prostaglandins [22; 68].
Both anandamides and their receptors lie in neuronal lipid membranes and modulate neuronal activity through intracellular G-proteins that control
cyclic adenosine monophosphate formation and
calcium and potassium ion transport [21]. The
physiological function of the cannabinoid system
is not fully understood, but it is thought to have
important interactions with opioid, GABAergic, dopaminergic, noradrenergic, serotonergic,
cholinergic, glucocorticoid, and prostaglandin
systems [22]. A number of the cannabinoids’ pharmacological effects can be explained on the basis
of these interactions, examples being tachycardia
and xerostomia, which are caused by the effects of
THC on acetylcholine [23].
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CB2 receptors are primarily found in immune cells,
suggesting that cannabinoids may play a role in the
immune response [68]. CB1 receptors are found
throughout the body but are concentrated in the
brain, with the highest density in the basal ganglia.
Other brain regions with high CB1 receptor density
include the cerebellum, hippocampus, cerebral
cortex, and nucleus accumbens. The distribution
of CB receptors suggests that the endocannabinoid
system may have effects on a broad range of behaviors [13]. A growing body of research shows that
this system modulates the hypothalamic-pituitaryadrenal axis and reduces the negative effects of
stress hormones among other functions [68].
TOXICITY
The median lethal dose of oral THC in rats is
80–1900 mg/kg, depending on the sex of the rat
and the strain of cannabis [21]. There are no cases
of death due to toxicity following the maximum
oral THC dose in animal studies. No deaths
directly attributable to acute cannabis use have
ever been reported [21].
TOLERANCE
Tolerance to most of the THC effects eventually
develops in regular users. In a 30-day study, volunteers developed tolerance both to the associated
cognitive and psychomotor impairment and to
the subjective high by the end of the study. The
increased heart rate present upon acute ingestion of
the drug at the beginning of the study was replaced
by a normal or a slowed heart rate after several days.
Tolerance to cannabis is attributable to pharmacodynamic changes, presumably based on receptor
down-regulation and/or receptor desensitization,
although the rate and duration of tolerance varies
with different effects [23].
DRUG-DRUG INTERACTIONS
As with many drugs, THC can enhance or attenuate the effects of other medications. A combination
of dronabinol (a cannabinoid) and prochlorperazine is more effective in reducing chemotherapyassociated nausea and vomiting than prochlorperazine alone [33]. Cannabis can also augment the
CME Resource • Sacramento, California
sedating effects of other psychotropic substances,
such as alcohol and benzodiazepines. A number of
synergistic effects may be therapeutically desirable,
such as the enhancement of:
• Muscle relaxants, bronchodilators,
and antiglaucoma medication
• Opiate analgesia
• Phenothiazines’ antiemetic effect
• Benzodiazepines’ antiepileptic action
The cyclooxygenase inhibitors, indomethacin,
acetylsalicylic acid, and other nonsteroidal antiinflammatory drugs antagonize THC effects,
reflecting the involvement of cyclooxygenase
activity in several THC effects [23].
THERAPEUTIC
USE OF CANNABIS
Use of cannabis for medical purposes was first documented in China thousands of years ago, where it
was reportedly used to treat malaria, constipation,
rheumatism, and childbirth pain [33]. There are
also reports of cannabis mixed with wine being
used as an analgesic. Throughout history, the
medical use of cannabis has been found in records
from Asia, the Middle East, Southern Africa, and
South America [33].
Despite being categorized as illegal, cannabis
has continued to be an attractive option for
self-medication among some patients. In 1978, a
compassionate program for medicinal cannabis was
established by the U.S. government; this program
stopped accepting new candidates in 1991 [1].
Since then, 16 states and the District of Columbia
have enacted laws to ensure that patients may use
cannabis for medical purposes without criminal
penalties [60]. It is important to note that many
of the effects discussed in this section result from
cannabinoids in pharmacological preparations,
not smoked cannabis. These effects are generally
categorized according to the strength of available
evidence.
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ESTABLISHED EFFECTS
Dronabinol, a synthetic THC derivative, is
approved for the treatment of refractory nausea
and vomiting caused by antineoplastic drugs used
for the treatment of cancer and for appetite loss
in anorexia and cachexia of patients with human
immunodeficiency virus/acquired immunodeficiency syndrome (HIV/AIDS) [23]. Dronabinol
and nabilone, another synthetic derivative, are
generally considered safe, effective antiemetics and
are recommended by the National Comprehensive Cancer Network for this use [74]. However,
comparisons with 5-hydroxytryptamine3 (5-HT3)
antagonists are lacking, and their role in modern
antiemetic regimens remains to be determined [33].
Cannabinoid therapy for chronic cancer pain
has been shown to work both independently and
synergistically with other classes of medications,
such as NSAIDs and opioids [74]. In one study,
10 mg and 20 mg doses of THC were found to be
roughly equivalent to 60 mg and 120 mg codeine
doses, respectively, and a strong sedative effect
was observed [75]. A 2010 British study found that
improved analgesia was realized with a THC/CBD
extract oromucosal spray in patients whose pain
was not alleviated with strong opioids [76]. Twice
as many patients given the THC/CBD extract had
a 30% reduction in pain (the measure of success)
than those administered placebo or a pure THC
extract.
RELATIVELY WELLCONFIRMED EFFECTS
Patients with multiple sclerosis have reported
an improvement in symptoms associated with
cannabis use, and small controlled trials support
this use, although the effect upon posture and
balance requires clarification [33]. There is also
mounting support for the use of THC and cannabinoid extracts (e.g., CBD) in the treatment
of spasticity due to spinal cord injury, chronic
pain, and Tourette’s syndrome. Clinical effects in
the treatment of asthma and glaucoma are also
relatively well-confirmed [23]. The mechanism for
cannabis bronchodilation likely differs from that
of beta-2-stimulants, indicating that synergistic
combinations may be possible. Additionally, the
effectiveness of cannabis and THC derivatives as
appetite stimulants, coupled with their antiemetic,
analgesic, anxiolytic, hypnotic, and antipyretic
properties, suggests a unique role in alleviating
symptoms in selected patients with cancer or AIDS
[33]. Several clinical trials in the 1980s and 1990s
found that dronabinol and inhaled cannabis significantly improved appetite in HIV/AIDS patients,
causing weight stabilization in treatment groups
while weight loss continued in placebo groups
[74]. Studies of patients with advanced cancer who
were administered THC have shown mixed results
regarding use as an appetite stimulant; however,
perception of taste was improved, allowing ingestion of more nutritious foods.
POSSIBLE EFFECTS
Several indications suggest benefits in patients with
epilepsy, intractable hiccups, depression, bipolar
disorder, anxiety disorder, post-traumatic stress
disorder, opiate or alcohol dependence, and disturbed behavior in Alzheimer’s disease [23]. These
possible uses have been mainly supported through
case reports and animal experiments.
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BASIC RESEARCH STAGE
Several promising areas of possible future therapeutic uses of cannabis are in the basic research stage.
Neuroprotection is an important physiological role
of endocannabinoids, and a clinical study investigating the therapeutic potential of a nonpsychotropic derivative of THC in hypoxia and ischemia
resulting from traumatic injury has yielded positive
preliminary results [23]. Other areas of promising
investigation related to neuroprotection include
nerve gas damage and stroke.
Possible antineoplastic activity of THC was discovered in an animal study designed to investigate
the potential carcinogenicity of THC; long-term
treatment of rats with THC resulted in improved
survival due to the lower incidence of several types
of cancer compared to control rats. Subsequent
studies have found that cannabinoids have antineoplastic activity on malignant gliomas and skin
tumors, inhibit angiogenesis of malignant gliomas,
and induce apoptosis of breast cancer cells [77; 78].
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The immunological mechanisms of THC indicate
that the compound may be helpful in treating
autoimmune diseases. Other conditions of possible
cannabis utility include cardiovascular disease
and hypertension [23]. Because cannabis has an
extensive history of use for a variety of purposes,
it is very unlikely that unknown adverse events
will develop, as occasionally occurs with newly
designed synthetic drugs [23].
ACUTE CANNABIS EFFECTS
Similar to other drugs with an abuse liability, such
as heroin, cocaine, amphetamines, and nicotine,
the pleasurable effects of cannabis are the result
of the release of dopamine in the reward circuitry,
comprised of the subcortical ventral tegmentum,
nucleus accumbens, striatum, and medial prefrontal cortex [9; 24]. Transmission of dopamine
is increased in the nucleus accumbens following
acute administration of cannabinoid agonists. This
effect may be blocked by the CB1 receptor antagonist rimonabant, a drug that had been available in
Europe until 2008 [13; 58].
BEHAVIORAL AND
PSYCHOLOGICAL EFFECTS
The pharmacological actions of cannabinoids are
very complex. The resulting effects are a unique
combination of those found with the use of depressants and hallucinogens. Because cannabinoid
receptors are widely distributed through the body,
numerous body systems are affected [22]. The
experience of intoxication is highly variable and
is influenced by the dose, the environment, and
the experience and expectations of the user [24].
Effects on Mood
The euphoriant potential of cannabis is probably
the single most important characteristic in sustaining its widespread and often chronic recreational
use. This effect varies greatly with dose, route of
administration, expectation, environment, and
personality of the user. However, dysphoric reactions to cannabis are not uncommon. In some
cases, use may result in severe anxiety and panic,
CME Resource • Sacramento, California
unpleasant somatic sensations, and paranoia. Anxiety-panic reactions are the most common adverse
psychological effects of cannabis use. Flashbacks,
whereby the original drug experience (usually dysphoria) is re-experienced weeks or months later, are
possible and may represent a psychological reaction
similar to that of post-traumatic stress disorder [22].
Sedative and Anxiolytic Effects
Following an initial period of excitement after
acute ingestion of cannabis, a generalized CNS
depressant effect is observed. This may lead to
drowsiness and sleep toward the end of a period of
intoxication [22].
Effects on Perception
The changes in perception that result from cannabis and THC affect all sensory modalities. Color
and sound perception may be heightened, and
musical appreciation may be increased. Temporal
and spatial perception is distorted, impairing judgment of distance and time. Even after small doses,
persons under the influence of cannabis consistently overestimate the passage of time. Persistent
visual changes, some lasting for months, have been
documented [22].
Effects on Motor Function
As noted, the initial period of excitement and
increased motor activity after cannabis ingestion is
followed by a state of physical inertia, with ataxia,
dysarthria, and general incoordination possibly
lasting for several hours. Motor performance,
including measurements of body sway, tracking
ability, pursuit motor performance, hand-eye coordination, reaction time, and physical strength, is
demonstrably impaired [22].
Effects on Cognition and Memory
The effects of cannabis on cognitive processes are
characterized initially by subjective feelings of
accelerated speed of thought, flight of ideas that
may seem unusually profound, and a crowding of
perceptions. Higher doses can result in out-ofcontrol thoughts, fragmented thinking, and mental
confusion. Cannabis is associated with short-term
memory deficits; it is believed that these deficits
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#9697 Cannabis Use, Abuse, and Dependence ____________________________________________________
may be caused by an attention deficit combined
with an inability to filter out irrelevant information and the intrusion of extraneous thoughts.
Memory lapses may contribute to the distortion
in the perception of time and poor psychomotor
performance in complex tasks [22].
Psychomotor Performance
Even low doses of THC (5–15 mg) can significantly
impair an individual’s ability to perform complex or
demanding tasks, including those involved in fine
hand-eye coordination, complex tracking, divided
attention tasks, visual information processing, digit
code tests, and alternate addition-subtraction tasks
[22]. Psychomotor performance further deteriorates
at higher doses, and impairment can persist several
hours following a single dose [22].
Aggression and Violence
Cannabis typically decreases aggression and
increases sociability. However, in rare cases, individuals, particularly those under stress and predisposed to violence, become aggressive after taking
cannabis. It has also been suggested that violent
behavior may be more common among those with
acute paranoid or manic psychosis induced by cannabis and polydrug use [22].
Psychiatric Symptoms
Cannabis use can lead to a range of short-lived
psychiatric symptoms, including depersonalization,
derealization, a feeling of loss of control, fear of
dying, irrational panic, and paranoid ideas [14].
After taking a large dose of THC, vulnerable users
may temporarily experience a form of drug-induced
psychosis. These are classified in the DSM-IV-TR
as cannabis-induced psychotic disorders with delusions or hallucinations or as a substance-induced
anxiety disorder and are diagnosed if the “disturbance is not better accounted for by a psychotic
disorder that is not substance induced” and if the
symptoms appear during or within one month of
substance use or withdrawal [84].
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Cannabis-induced psychosis has the potential
to require hospital admission. During the initial
diagnosis, this psychosis may be misidentified as
schizophrenia, as patients may display characteristic schizophrenic symptoms, such as delusions of
control, grandiose identity, persecution, thought
insertion, auditory hallucinations, altered perception, and blunted affect [24].
PHYSICAL EFFECTS
Cardiovascular Effects
Acute doses of cannabis may induce tachycardia
with peripheral vasodilatation, which can result in
postural hypotension and a slight decrease in body
temperature. Cardiac output may be increased by
as much as 30%, accompanied by increased cardiac
work and oxygen demand. Because of this, cannabis can aggravate pre-existing heart disease. The
absorption of relatively large amounts of carbon
monoxide from smoking cannabis also contributes
to the long-term cardiovascular risk of chronic cannabis use [22]. Reddening of the conjunctivae, a
characteristic sign of cannabis use, is the result of
widespread vasodilation [21].
Respiratory Effects
Cannabis smoke contains many of the same constituents as tobacco smoke (minus the nicotine),
including bronchial irritants, tumor initiators
(mutagens), tumor promoters, and carcinogens.
The tar from cannabis smoke also contains higher
concentrations of the carcinogens benzanthracenes and benzopyrenes than tobacco smoke tar.
Smoking a cannabis cigarette results in inhalation of three times the amount of tar of a tobacco
cigarette, and respiratory tract retention is greater
than smoking a tobacco cigarette [21; 22]. As a
result, cannabis use may result in impairment of
lung function, leading to airflow obstruction and
hyperinflation [59].
A University of California San Francisco study
found that vaporizing cannabis eliminates many of
the harmful combustion byproducts (e.g., benzene,
naphthalene, toluene, other aromatic hydrocarbon
toxins) and greatly reduces tar and carbon monoxide from the inhaled charge [67]. Therapeutic
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___________________________________________________ #9697 Cannabis Use, Abuse, and Dependence
plasma THC levels are slightly increased with this
administration, and it was determined that vaporizing cannabis is much safer than smoking and significantly more cost-effective than administering
THC in pill form.
Endocrine/Reproductive System Effects
Cannabinoids, including THC, bind to androgen
receptors, and cannabis is considered antiandrogenic. However, the drug’s effects, if any, on fertility
are unclear. In women, regular cannabis smoking
may be associated with suppression of ovulation.
Chronic use may cause galactorrhea in women and
gynecomastia in men. Endocrine changes resulting
from cannabis use may be inconsequential in adults
but significant in prepubertal users, in whom cannabis use may suppress sexual maturation as well
as social and personal development and learning
of coping skills. There is no evidence of teratogenicity during pregnancy, but some studies suggest
low neonatal birth weight from chronic maternal
cannabis smoking, possibly related to fetal hypoxia
[21; 22].
Developmental Effects
Adolescents who regularly use cannabis may have
impairments of learning and personal development. However, the possible effects of cannabis
consumption on educational performance are
difficult to demonstrate [14]. As noted, social
development and the acquisition of coping skills
may also be stunted.
LONG-TERM CANNABIS EFFECTS
RESPIRATORY EFFECTS
Chronic cannabis smoking is associated with
bronchitis, emphysema, and squamous metaplasia
(a pre-cancerous change), which all occur more
frequently in those who have only smoked cannabis than in those who have only smoked tobacco.
Chronic cannabis and tobacco smokers are at an
increased risk for respiratory symptoms and histopathological changes than those who only smoke
tobacco or cannabis [21; 22].
CME Resource • Sacramento, California
IMMUNOSUPPRESSANT EFFECTS
There is not sufficient evidence of significant
immunological damage in humans from cannabis
[22]. However, it is important to note that cannabis may be contaminated with micro-organisms,
such as Aspergillus and Salmonella, as well as fecal
matter. Therefore, a potentially serious adverse
effect of cannabis is the risk of infection. In addition, chronic cannabis use may lead to impaired
pulmonary defense against infection. The risk of
infection is of particular concern in patients with
HIV/AIDS due to their increased susceptibility to
infection from fungal and bacterial contaminants
and epithelial damage from the smoke [4].
NEUROPSYCHOLOGICAL IMPAIRMENT
Chronic cannabis use has been reported to
adversely affect cognitive functioning, demonstrated by impaired cognitive performance on a
wide range of tasks, including memory and executive functioning [13]. Impairment of short-term
visual and verbal memory persisting for 6 weeks
after cessation of cannabis use has been reported,
and there is a potential for persisting memory
deficits in academic performance in school-aged
children and college students. Adolescents and
those with borderline or low intelligence quotient
(IQ) may be particularly susceptible to these effects
[22]. A small drop in overall IQ among current but
not previous heavy users has also been shown [9].
Computed tomography (CT) studies in cannabis
users have failed to identify gross structural brain
changes, such as cerebral atrophy. In one study,
older long-term cannabis users (mean age: 36 years)
and control subjects with no history of cannabis
abuse or dependence were compared, with cannabis
users displaying no significant adjusted differences
in volumes of gray matter, white matter, cerebrospinal fluid, or left and right hippocampus. Moreover,
hippocampal volume in the cannabis users was not
associated with age of onset or total lifetime use.
This supports studies suggesting that cannabis use is
not associated with structural changes in the brain
as a whole or the hippocampus in particular [25].
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In another study of possible neurotoxic effects of
chronic cannabis use, neuropsychological tests
were administered to 77 current heavy cannabis
users who had smoked cannabis at least 5000
times in their lives and to 87 control subjects who
had smoked no more than 50 times in their lives.
During a supervised abstinence period, the heavy
smokers showed memory deficits on days 0, 1, and
7. However, few significant differences were found
between the two groups by day 28, and significant
associations between total lifetime cannabis consumption and test performance were scarce. The
authors conclude from these results that cannabisassociated cognitive deficits are reversible and
related to recent cannabis exposure rather than
cumulative lifetime use [26].
Overall, claims that chronic cannabis use is permanently neurotoxic have produced little scientific
validation. Modestly impaired attention and ability to filter out irrelevant information in former
cannabis users has been found in some studies,
but other studies have not revealed impairment
in cognitive function [24].
Although a degree of controversy exists surrounding whether heavy long-term consumption results
in cognitive impairment, irreversible impairment
seems to be minimal, if it exists at all. Medical use
of cannabis for more than 15 years is generally
considered to be well-tolerated without significant
physical or cognitive impairment [23].
PSYCHIATRIC COMORBIDITY
AND CANNABIS USE
Cannabis use disorders are associated with high
rates of other psychiatric diagnoses. The most
frequent psychiatric comorbidities are depressed
mood, major depression, and dysthymia [14]. It is
also possible that cannabis use is a risk factor for
serious mental illness, such as schizophrenia [14].
Patients with a history of cannabis dependence are
at an increased lifetime risk for a variety of other
psychiatric disorders, and current cannabis depen-
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dence is strongly associated with alcohol misuse,
affective and anxiety disorders, and tobacco use in
the past year [17]. However, the pathogenesis of
most psychoses is not well understood. Based on
postmortem and other studies, abnormalities and
dysfunction of the endocannabinoid system may
play a significant role in psychological disorders
(e.g., depression, suicide, schizophrenia), making
the use/misuse of exogenous cannabinoids an ongoing area of research for both therapeutic potential
and causation [83].
Depression
Although there is little evidence to support a correlation between depression and infrequent cannabis use, a modest association between early-onset
habitual cannabis use and later depression has been
reported. Because there is little evidence of an
increased risk of later cannabis use among patients
diagnosed with depression, the self-medication
hypothesis is not supported. However, research has
shown that depression and chronic use of cannabis
are associated, and evidence indicates that heavy
cannabis use may increase depressive symptoms in
some users. It is important to note that this correlation may be the result of common social, family,
and contextual factors that increase the risk of
both heavy cannabis use and depression. Overall,
heavy cannabis use appears to play a minor role
in explaining population rates of depression [27].
The National Institute for Health
and Clinical Excellence recommends
evidence-based psychological treatments
(in particular, cognitive behavioral
therapy) be considered for the treatment
of comorbid depression and anxiety for
people who misuse cannabis.
(http://www.guidelines.gov/content.aspx?id=11087.
Last accessed June 26, 2012.)
Level of Evidence: Expert Opinion/Consensus
Statement
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Psychoses
Healthcare professionals have observed a possible
association between habitual cannabis use and psychosis for many years. However, there is considerable disagreement regarding the degree of causation
attributable to cannabis use in the development of
psychosis among users without an obvious vulnerability to this effect (e.g., genetic factors).
There is biological evidence of a possible causal
relationship between cannabis use and psychosis
[19; 20]. When administered intravenously, delta9-THC has been found to induce dose-dependent
positive and negative psychotic symptoms in
individuals with schizophrenia; an interaction
between cannabis use and a polymorphism of the
catechol-o-methyltransferase gene that codes for
dopamine has also been reported [19].
In theory, cannabis use may precipitate a psychosis
in several ways [14]:
• Acute induction of a toxic or organic
psychosis, with symptoms of confusion and
hallucination, that remits on abstinence
• Induction of an acute functional psychosis,
similar to an acute schizophreniform state,
that lacks the organic features of a toxic
psychosis
• Induction of a chronic psychosis that
persists after abstinence
• An organic psychosis induced by longterm use that only partially remits after
abstinence, leaving a residual deficit
state (an amotivational syndrome)
Based on the literature, it is likely that cannabis use
induces psychotic disorders in vulnerable individuals, defined as those with a history of unusual experiences that may be in part genetically mediated
[19]. The relationship between cannabis use and
vulnerability may explain the small (2 to 3 times)
increase in risk for psychosis among cannabis users.
This interaction has also been used to elucidate
the lack of large increases in the incidence rates
of psychoses to correspond with the increase in
cannabis use rates among young adults and the
CME Resource • Sacramento, California
earlier age of onset of schizophrenia-form disorders
in cannabis users [19].
There appears to be at least some evidence linking cannabis use to the development of psychotic
disorders, but some argue that the studies have
been flawed. Criticisms of studies linking cannabis
and psychosis include failure to separate organic
and functional psychotic reactions to cannabis;
insufficient discrimination between psychoses;
and lack of weighing the evidence for and against
the category of cannabis psychosis [14]. Although
there is evidence to support the belief that cannabis use may contribute to psychosis in certain
circumstances, the possible causal mechanisms are
complex [14].
Robust evidence associating regular cannabis use
with the development of psychoses comes from
a 2007 meta-analysis by Moore et al. [20]. The
researchers found consistent increased risk for psychosis in individuals with any history of cannabis
use, with a correlation between frequency of use
and heightened risk that suggests a dose-dependent
effect. Pooled analysis showed a 40% increase in
the risk of any psychotic outcome in individuals
who had ever used cannabis, with the most frequent users showing a 50% to 200% increase in
risk for psychosis [20]. The elevated risk of the late
development of psychotic symptoms remained consistent even after adjusting for confounding factors,
including polysubstance use, personality disorders,
family relationships, criminality, socioeconomic
factors, intellectual functioning, and mental health
problems. The results of this analysis indicated that
cannabis use was associated with increased lifetime
risk of developing psychosis [20].
Researchers have linked new high-potency cannabis strains with increased emergency admissions
for psychosis, implicating not only higher levels
of THC but also the absence of CBD, which
ordinarily tempers the psychotomimetic effects
of THC [79; 80]. A British study noted that the
typical cannabis product available in the United
Kingdom before 2000 was hashish resin, containing
essentially equal parts THC and CBD (each up to
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#9697 Cannabis Use, Abuse, and Dependence ____________________________________________________
4% by weight), and that the typical high-potency
herbal cannabis that now dominates the market
contains 12% to 18% THC and less than 1.5%
CBD. (This is also typical of cannabis available
in the United States, particularly strains grown
in California [82].) Researchers suspect that the
rise in admissions for psychosis is related to this
shift. The study concluded that individuals with
a longer duration of use and with a preference for
high-potency cannabis are at a much greater risk
for enduring psychosis than individuals who occasionally smoke hashish [79]. This is supported by
research showing that cannabis psychosis is THC
dose dependent and that CBD can reverse indicators of THC-induced psychosis in test subjects
[80; 81].
There has also been criticism of the belief that
chronic heavy cannabis use leads to an amotivational syndrome, described as personality deterioration with loss of energy and drive to work [14].
Some have argued that the supporting evidence
for this theory largely originates from uncontrolled
studies of long-term cannabis users in various
cultures and may be a reflection of ongoing intoxication in frequent users of the drug [14]. More
research in this area is required.
Panic Disorder
Cannabis use has also been linked to the development of panic disorder. A study involving 1000
people 18 to 25 years of age found that 22%
reported panic attacks or anxiety symptoms during
cannabis intoxication, with women twice as likely
as men to report these symptoms [14].
An individual’s experience of cannabis intoxication may be variable; the same person given the
same dose at different times may report different
subjective effects. Although many users report a
calming, tranquilizing effect, cannabis use may
provoke feelings of anxiety or panic in some cases.
For patients for whom cannabis use induces panic,
a history of previous panic attacks (while sober)
may not be present. A study of 66 panic disorder
patients found that 24 experienced their first panic
attack within 48 hours of cannabis use [54]. Inges-
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tion of high doses of delta-9-THC produces intense
anxiety in nearly all users predisposed to anxiety,
and the high THC:CBD ratio of cannabis available
today may lead to a rise in anxiety/panic disorders
among cannabis users in general [82]. It has been
suggested that cannabis may provoke anxiety
reactions via gamma-aminobutyric acid (GABA)
antagonism, which may provoke CNS excitatory
neurotransmission and brain hyperexcitability [54].
Psychosocial Impairment
Antisocial behavior commonly occurs among cannabis users, and this is particularly evident among
adolescent users. Adolescents who use cannabis
regularly are at risk of experiencing delinquency,
school failure, physical and psychological problems, and selling illegal drugs [12].
CANNABIS
WITHDRAWAL SYNDROME
A cannabis withdrawal syndrome has been clearly
demonstrated and is characterized by a variety of
symptoms, including restlessness, nervousness,
anxiety, dysphoria, irritability, insomnia, anorexia,
muscle tremor, increased reflexes, autonomic
effects (e.g., changes in heart rate and blood
pressure), sweating, diarrhea, and in some cases
aggressive behavior [14; 28; 29]. The most frequent
symptoms of cannabis withdrawal are emotional
and behavioral in nature and do not typically cause
significant physical, medical, or psychiatric disorders [30]. Regular daily use of cannabis can lead to
withdrawal symptoms or a full-blown withdrawal
syndrome upon cessation of use. The DSM-IVTR contains no reference to cannabis withdrawal
syndrome; however, the syndrome is proposed for
the DSM-5 revision [85]. Three of the following 7
symptom clusters must be identified for a diagnosis
according to the DSM-5 proposed definition [85]:
• Irritability, anger, or aggression
• Nervousness or anxiety
• Sleep difficulty (e.g., insomnia,
disturbing dreams)
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•
•
•
•
Decreased appetite or weight loss
Restlessness
Depressed mood
At least one of the following physical
symptoms causing significant discomfort
– Stomach pain
– Shakiness/tremors
– Sweating
– Fever
– Chills
– Headache
Using the proposed DSM-5 criteria, researchers
asked 384 lifetime, non-treatment-seeking cannabis addicts about their worst abstinence experience and found that 40% would be diagnosed with
cannabis withdrawal syndrome [56]. The study
identified additional symptom clusters not included
in the proposal. A 1976 research project in India
found that 98% of chronic cannabis users felt
uncomfortable if they were unable to obtain their
daily supply, with 86% experiencing strong drug
cravings and 74% experiencing mental irritability
and anxiety upon cessation [31].
Cannabis withdrawal syndrome typically requires
heavy, prolonged use to develop and may significantly impact social, educational, and occupational
functioning [85]. In a sample of adolescent cannabis
users, the majority reported cannabis withdrawal,
with an associated inability to perform school work
and increased arguing, that began within 24 hours
and worsened during the first several days of the
abstinence period, especially in heavy users [32].
The majority of adults seeking treatment for a
cannabis use disorder report a history of cannabis
withdrawal, with most reporting a co-occurrence
of 4 or more symptoms of substantial severity [30].
Neurochemical causes of cannabinoid withdrawal
include reduced dopaminergic activity along the
ventral tegmental area-nucleus accumbens pathway, and upregulated expression and release of
corticotropin-releasing hormone (CRH) in the
central nucleus of the amygdala [13].
CME Resource • Sacramento, California
COURSE
The onset of abstinence symptoms consistently
occurs during the first 1 to 2 days following cessation of cannabis or oral THC administration. Most
symptoms return to baseline or to comparisongroup levels within 1 to 2 weeks, although irritability, muscle tension, and sleep problems, particularly
unusual dreams, may not return to baseline for an
extended period. Because most transient symptoms return to baseline and because persons with
psychiatric disorders are excluded from studies
examining cannabis withdrawal, it is believed that
the withdrawal symptoms are not rebound effects
indicative of the participants’ condition before
initiation of cannabis smoking [30].
The administration of cannabis during the first 24
to 96 hours of abstinence results in an abrupt reduction and return to baseline of multiple abstinence
symptoms, suggesting that cannabis withdrawal
syndrome is specific to THC in humans [30].
CLINICAL SIGNIFICANCE
Cannabis withdrawal has important treatment
implications. Multiple symptoms of cannabis
withdrawal syndrome are experienced among
non-treatment-seeking daily cannabis users as
well as inpatients and outpatients with cannabis
dependence. In most cases, withdrawal symptoms
are clearly observable to persons living with the
user, who are able to document the disruption to
daily living caused by the symptoms. The majority of persons enrolled in treatment for cannabis
dependence acknowledge cannabis withdrawal
symptoms, label at least some as moderate-tosevere, and complain that they make cessation of
cannabis use more difficult [13; 30]. The significance of cannabis withdrawal and its potentially
negative impact on treatment retention and relapse
to cannabis use has not escaped the attention of
researchers; several pharmacotherapy trials investigating medications of possible utility in cannabis
withdrawal have been undertaken.
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#9697 Cannabis Use, Abuse, and Dependence ____________________________________________________
TREATMENT OF CANNABIS
ABUSE AND DEPENDENCE
Until fairly recently, cannabis was not considered a
drug with a liability of dependence and addiction.
Withdrawal did not lead to any obvious physical
symptoms, and animals failed to self-administer
the drug, a behavior usually associated with drugs
of addiction [24]. Few studies had focused on the
treatment of cannabis abuse or dependence. However, research suggests that individuals can develop
a chronic use pattern associated with dependence
symptoms and recurrent psychosocial problems
[6]. Two factors have contributed to the lack of
research: the common beliefs that cannabis abuse
rarely occurred as a primary problem and that
cannabis use did not produce a true dependence
syndrome. Data contrary to these assumptions first
appeared in the late 1980s, and treatment development and efficacy studies specific to cannabis
dependence first began to appear in the scientific
literature during the 1990s [11].
CHARACTERISTICS OF PATIENTS
SEEKING TREATMENT FOR
CANNABIS USE DISORDERS
Although an increasing number of individuals
are seeking treatment specifically for a primary
problem of cannabis dependence, most do not do
so until they are older than 30 years of age. Young
adults and adolescents generally seek treatment
only when it is mandated by school officials, parents, or the criminal justice system [15].
The constellation of concerns that bring cannabis
users to treatment may not be major socioeconomic
or psychosocial problems. Rather, patients tend to
express more subtle dissatisfaction with multiple
areas of functioning and concerns about future
health problems, which motivate the desire to quit
or reduce use [6]. Individuals seeking treatment
for cannabis use tend to exhibit social impairment
and psychiatric distress, report multiple adverse
consequences associated with cannabis use, and
have a history of repeated unsuccessful attempts
to stop using. Most patients perceive themselves
as unable to quit [10].
Contrary to the popular belief that dependent
individuals have to want treatment before it can
be effective, most enter treatment in a relatively
involuntary state, often to avoid or to undo the
consequences of the drug use [34]. A significant
opportunity to intervene is often the point at
which drug abusers confront the legal consequences of their substance, especially taking into
consideration the fact that more drug users are
involved with the legal system than with the drug
abuse treatment system [15].
PHARMACOTHERAPY
The majority of treatment studies to date involving
cannabis use disorders have investigated behavioral
and psychosocial therapies. However, given the
high rate of relapse and overwhelming numbers of
cannabis-dependent individuals, the importance of
pharmacotherapy for the treatment of cannabisdependent individuals, particularly those who have
been unresponsive to other treatment modalities,
is important [13].
Treatment of Cannabis Withdrawal Symptoms
As cannabis withdrawal symptoms may be a factor
contributing to continuing cannabis use, medications alleviating these symptoms could be useful.
Unfortunately, there is little research completed
that evaluates the effectiveness of potential
treatment medications on cannabis withdrawal
in humans. According to completed studies, no
medication has been shown to definitively decrease
cannabis use by humans [13].
According to the American Psychiatric
Association, studies of treatment for
cannabis use disorders are limited and no
specific pharmacotherapies for withdrawal
or dependence can be recommended.
(http://www.guidelines.gov/content.
aspx?id=9316. Last accessed June 26, 2012.)
Level of Evidence: I (Recommended with
substantial clinical confidence)
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CME Resource • October 5, 2012
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___________________________________________________ #9697 Cannabis Use, Abuse, and Dependence
A study evaluating bupropion for cannabis withdrawal was performed by Haney et al. [35]. This
study was based on the observation that bupropion
facilitates abstinence from cigarette smoking, in
part through its ability to decrease negative mood
symptoms. Because similar mood symptoms have
also been associated with cannabis withdrawal,
it was suggested that this medication may have
a place in the treatment of cannabis withdrawal.
However, the authors found that bupropion worsened several ratings of mood, possibly caused by
bupropion-associated enhanced norepinephrine
activity [13; 35].
The efficacy of nefazodone (450 mg/day) was used
in another study by the same research group [13;
36]. Nefazodone was chosen because of its demonstrated effectiveness in clinical populations
with conditions also associated with cannabis
withdrawal, including depression, agitation, and
anxiety. Nefazodone decreased some symptoms
associated with cannabis withdrawal (i.e., ratings
of anxiety and myalgia) but in general had no effect
on most symptoms (e.g., ratings of irritability and
disordered sleep).
A third study evaluated the effectiveness of divalproex, which was chosen for testing based on evidence of successful treatment of some symptoms
associated with cannabis withdrawal, such as irritability and mood lability [13; 37]. Divalproex was
not found to positively affect cannabis withdrawal
symptoms; in fact, many withdrawal symptoms
(e.g., anxiety and irritability) increased compared
to placebo. Divalproex also resulted in psychomotor performance disruptions.
Another agent evaluated for its effect on attenuating cannabis withdrawal was oral delta-9-THC
[37]. Use of oral THC in the treatment of withdrawal symptoms was based on the concept of
substituting a longer-acting, pharmacologically
equivalent drug for the abused substance to stabilize
the patient, with the intent to gradually withdraw
the substituted drug. Oral delta-9-THC markedly
reduced withdrawal symptoms, including self
reports of drug craving, anxiety, misery, and sleep
disturbance. Withdrawal-associated psychomotor
CME Resource • Sacramento, California
performance deficits, anorexia, and weight loss
were also ameliorated. The authors conclude that
moderate doses of oral delta-9-THC might be
beneficial in the treatment of cannabis dependence
[13; 37].
An issue of potential concern related to treating
cannabis-dependent patients with delta-9-THC is
the abuse potential. Abuse liability is influenced
by the neurochemical effects as determined by
the route of administration, drug concentrations,
and the maximum drug concentrations. Thus, oral
administration of delta-9-THC would be expected
to produce much less reinforcement than smoked
cannabis. Another advantage is that, unlike
smoked cannabis, oral delta-9-THC is not associated with adverse pulmonary effects. Considering
all of these factors, the benefits of oral delta-9-THC
in the treatment of cannabis withdrawal appear to
outweigh potential risks [13].
One study compared the treatment efficacy of
oral dronabinol and the synthetic THC analogue
nabilone [86]. The results showed that nabilone
has a longer time to peak effect, is more sustained,
has fewer negative cognitive effects, and results
in greater mood enhancement characteristics
compared to dronabinol. Also, the effects are
more dose-related, perhaps making it the better
option for cannabinoid-replacement withdrawal
treatment. Although dronabinol also decreases
symptoms of cannabis withdrawal, the drug is ineffective in preventing relapse [86]. Researchers hope
nabilone can prove effective for both purposes in
clinical trials.
Pharmacotherapy for Relapse Prevention
A 12-week, open-label trial investigated the
usefulness of a flexible dose of buspirone (mean
daily dose: 39.1 mg) with 11 cannabis-dependent
patients. Reductions in frequency and duration of
craving and degree of irritability were produced,
and participants had a 76.9% reduction in cannabis use during the study. Participants reported
using cannabis on nearly 75% of the days in the 3
months prior to study entry and on 38.9% of the
days during the study. A significant reduction was
also seen on an anxiety rating scale during the
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19
#9697 Cannabis Use, Abuse, and Dependence ____________________________________________________
study. Although 44% of urine drug screens collected during treatment were cannabis-negative,
only 2 subjects completed treatment [38].
In another study, 25 adult outpatients were randomized to either 6 weeks of placebo or divalproex,
then switched to the alternate treatment for an
additional 6 weeks. No significant between-groups
differences were found in regards to treatment
retention, with 38% of divalproex subjects and
33% of control subjects completing the entire
study. Persons started on divalproex did not display better outcomes in terms of improvement
in cannabis use or psychological symptoms than
those started on placebo. All 25 patients had low
blood levels of the study medications, suggesting
poor compliance. However, retention during the
first 8 study weeks was high (>75%), suggesting
the medication was discontinued because it was
poorly tolerated in this population [31]. Other
medications studied for alcohol relapse prevention,
including baclofen and mirtazapine, have proven
ineffective for cannabis relapse prevention [87].
Pharmacotherapy of Cannabis Dependence
in Patients with Comorbid Mental Illness
In a pilot study, Potvin treated 8 cannabis-dependent patients with schizophrenia or affective bipolar disorder with quetiapine 100–1200 mg daily for
a mean of 5.8 months [39]. Cannabis use declined
from a mean of 35.6 g/week at baseline to 1.1 g/
week, a 97.3% reduction. The mean daily dose of
quetiapine during the study period was 388 mg.
PSYCHOSOCIAL THERAPY
Several psychosocial therapy modalities have been
evaluated in the treatment of patients with cannabis use disorders.
Individual Drug Counseling
Cannabis users seeking therapy to quit may participate in standard counseling that is typically offered
in community-based substance abuse clinics. Individual drug counseling emphasizes abstinence from
cannabis and other drugs through use of self-help
groups and a 12-step approach [15].
20
CME Resource • October 5, 2012
Contingency Management (CM)
Contingency management approaches to adult
substance abuse are effective behavioral interventions to increase drug abstinence and other
treatment goals when integrated with other effective psychosocial treatments [40]. Essentially, CM
interventions use reinforcement or punishment
contingencies to increase or decrease the frequency
of predetermined therapeutic and behavioral
objectives [12].
Relapse Prevention
Relapse prevention assists patients with decreasing
their vulnerability to relapse by addressing topics
such as lifestyle balance and managing high-risk
situations [11].
Social Support
Social support is based on the necessity of group
support for change. Topics discussed in the group
setting include getting and giving support, dealing
with denial and mood swings, and interacting with
peers who continue to use cannabis [11].
Brief Motivational Interviewing
In brief motivational interviewing, a therapist
provides feedback from a comprehensive assessment using motivational interviewing techniques.
The therapist also instructs subjects on cognitivebehavioral therapy (CBT) techniques that could
be used to abstain from cannabis use [11; 41].
In terms of psychosocial therapies, the
American Psychiatric Association notes
that an intensive relapse prevention
approach that combines motivational
interventions with the development of
coping skills may be effective for the
treatment of cannabis dependence, but further study
of these approaches is necessary.
(http://www.guidelines.gov/content.aspx?id=9316.
Last accessed June 26, 2012.)
Level of Evidence: III (May be recommended
on the basis of individual circumstances)
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___________________________________________________ #9697 Cannabis Use, Abuse, and Dependence
Psychosocial Treatment of Adults
In the first study published in which interventions
specifically targeting cannabis dependence were
evaluated, a 10-week social support group treatment was compared with a 10-week cognitivebehavioral relapse prevention group treatment
using a sample of 212 adults [11; 42]. Results of the
study indicated no significant differences between
treatment conditions; both groups experienced a
reduction in cannabis use throughout the followup period. After 1 year, about 17% of participants
reported abstinence from cannabis use and an
additional 19% of participants were considered
“improved,” defined as cannabis use 50% or less
of pretreatment levels.
The authors conducted a follow-up study comparing a cognitive-behavioral relapse-prevention
treatment; a brief, 2-session motivational intervention; and a delayed-treatment control group
[41]. The active treatment interventions resulted
in greater reductions in cannabis use than delayed
treatment. Four months post-intake, participants
in the two active groups reported reduced cannabis use compared to the delayed treatment group,
reductions in frequency of use per day, lower number of dependence symptoms, and fewer problems
related to cannabis use. At 16-month assessment,
cannabis use increased in both active treatment
groups but was lower than pretreatment levels.
Urine drug screens were not obtained, and all drug
use data was based on self-report and collateral
verification.
In another study, 136 cannabis-dependent adults,
18 to 25 years of age, referred by the criminal
justice system, were randomized to one of four
treatment conditions. CM consistently produced
positive effects in terms of treatment retention
and cannabis use, both of which were specifically
targeted. There were few significant main effects
for motivational enhancement therapy/cognitivebehavioral therapy (MET/CBT) over drug counseling. However, additional analysis suggested that
a combination of CM and MET/CBT resulted in
better outcomes than MET/CBT without CM and
drug counseling plus CM. All three treatments
CME Resource • Sacramento, California
were found to be significantly more effective than
drug counseling without CM. Participants assigned
to MET/CBT continued to reduce the frequency
of their cannabis use through a 6-month followup. The study population was noteworthy in that
the participants were primarily young African
American men with an average of five arrests by 21
years of age, 43% of whom met diagnostic criteria
for antisocial personality disorder. Most had not
completed high school and were unemployed [15].
In another study, efficacy of two brief interventions for cannabis-dependent adults across three
study conditions was compared: two sessions of
MET; nine sessions of multicomponent therapy
(MET, CBT, and case management); and a delayed
treatment control. The study followed 450 adult
cannabis smokers with a diagnosis of cannabis
dependence at baseline who were evaluated at 4,
9, and 15 months following treatment assignment.
The nine-session intervention produced superior
outcomes compared with the two-session treatment in terms of reductions in cannabis use and its
consequences up to 12 months following treatment
termination. The two-session treatment was more
effective in use reduction than the control. Overall,
the findings suggest that treatment for cannabis
dependence could have a significant impact on
chronic cannabis use, and both substance abuse
treatment programs and behavioral healthcare
providers should consider making cannabisspecific treatment more available and accessible.
The authors also conclude that cannabis-focused
treatments may be necessary for this population
to achieve abstinence or to significantly reduce
cannabis use; complete abstinence is not the only
clinically meaningful outcome of treatment, and
when given the opportunity, many cannabis abusers respond to treatment primarily by cutting back
rather than quitting entirely [6].
A study of 90 cannabis-dependent adults seeking treatment randomly assigned participants to
receive CBT, abstinence-based voucher incentives,
or a combination of CBT and vouchers for 14
weeks. The authors found that, during treatment,
abstinence-based vouchers were effective for facilitating prolonged periods of cannabis abstinence.
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#9697 Cannabis Use, Abuse, and Dependence ____________________________________________________
CBT did not contribute to during-treatment
abstinence, but it did enhance the post-treatment
maintenance of the initial positive effect of vouchers. These results indicate that abstinence-based
vouchers are a valuable treatment option, the use of
which leads to greater rates of cannabis abstinence
during treatment in comparison with a commonly
used with CBT for cannabis dependence [43].
Psychosocial Treatment of Adolescents
Approximately one-third of high school seniors
(34.8%) used cannabis at least once in 2010 [5].
Less than 10% of adolescents who report substance
use disorder symptoms in the past year have ever
received treatment, and when adolescents do enter
treatment for cannabis use, only 20% believe their
use is problematic [44]. These findings suggest the
need for interventions to increase motivation for
change and encourage treatment entry for this
population.
One study of the efficacy of psychosocial treatments
in this patient population included 97 adolescents
who had used cannabis at least 9 times in the
previous month. Participants were randomized
to either an immediate 2-session motivational
enhancement intervention or a 3-month delayed
treatment control. The majority (two-thirds) of
the sample described themselves as in the precontemplation or contemplation stages of change
regarding cannabis use. Cannabis use and negative
consequences were assessed at baseline and at
3-month follow-up, and the assessment battery was
carefully constructed to not appear biased toward
demanding change. Both groups significantly
reduced cannabis use at the 3-month follow-up,
with an overall reduction in cannabis use by 16%
(6 less days) over a 60-day period. Although reductions were modest and no differences between
treatments were observed, the study succeeded
in recruiting non-treatment-seeking adolescent
cannabis smokers who were predominantly in the
early stages of readiness for change, overcoming
barriers in reaching adolescents who were frequent
cannabis users [44].
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CME Resource • October 5, 2012
Kamon et al. reported the results of a 14-week
feasibility study of family-based CM with 19 adolescents 15 to 18 years of age [12]. The intervention
consisted of a clinic-administered, abstinencebased incentive program; parent-directed CM
targeting substance use and conduct problems; a
clinic-administered incentive program targeting
parental participation; and individual CBT for
the adolescent patients. Twice-weekly urine and
breath testing was conducted to monitor substance use. The adolescents attended an average
of 10.3 of 14 weekly sessions; parents attended an
average of 10.6 sessions. By the end of treatment,
substance use, externalizing behaviors, and negative parenting behaviors had decreased. Based on
results of the urine testing, abstinence increased
from 37% at intake to 74% by the end of the study
period; 53% of adolescents were abstinent 30 days
post-treatment. The efficacy of a family-based CM
model to treat adolescent substance use and conduct problems was demonstrated [12].
Psychosocial Treatment of Patients
with Comorbid Mental Illness
Cannabis is the most commonly used illicit drug
among persons with mental illness and is associated with increased rates of recurrent psychiatric
symptomatology and relapse [45]. To study the
impact of voucher-based contingent reinforcement in cannabis-dependent patients with serious
mental illness, Sigmon and Higgins assigned 7
adults with schizophrenia and other serious mental illness to three conditions: a 4-week baseline,
then a 12-week voucher intervention followed by
another 4-week baseline [45]. Subjects received
$10 vouchers per urine specimen regardless of the
results during baseline, but during the intervention period, vouchers were only given for THCnegative urine tests. The participants were not
required to seek treatment for cannabis abuse or
be interested in quitting but to simply be willing to
participate in a study in which they could receive
incentives for cannabis abstinence. There was a
significantly greater percentage of THC-negative
specimens during the intervention than during
either baseline. The authors state that this study
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___________________________________________________ #9697 Cannabis Use, Abuse, and Dependence
supports the use of voucher-based incentives to
decrease problem cannabis use among individuals
with serious mental illness. More research with this
population is necessary in order to draw definitive
conclusions.
12-STEP/SELF-HELP THERAPY
Many persons addicted to cannabis lack the
resources for inpatient or outpatient treatment
for their substance abuse problem or may be in
need of ongoing support following treatment. To
meet these needs, self-help groups provide a vital
resource for those seeking support for abstinence.
Self-help groups are non-professional organizations
operated by peers who share the same addictive
disorder. Self-help group attendance is free [46].
The most successful self-help groups employ the
12-step program and are modeled after Alcoholics
Anonymous (AA). These groups include Narcotics Anonymous (NA) and Marijuana Anonymous
(MA). The 12-step model emphasizes acceptance
of addiction as a chronic progressive disease that
can be arrested through abstinence but not cured.
Additional elements of the 12-step model include
spiritual growth, personal responsibility, and helping other addicted persons. By inducing a shift in
the consciousness of the addict, 12-step programs
offer a holistic solution. Groups such as NA and
MA are also a resource for emotional support and
are perhaps more accurately classified as “mutual
help” organizations [46; 47].
Spiritual beliefs and endorsement of the disease
concept are not prerequisites for NA or MA attendance, and spiritual beliefs have not been found to
cause external attribution for previous drug use or
possible future lapse events [48].
Narcotics Anonymous (NA)
Relative to the more established AA, there are few
studies published on NA. However, the studies that
have been conducted reveal important information
about how NA functions to help the new member
abstain from drug use.
CME Resource • Sacramento, California
Improvement in psychological functioning as a
result of NA involvement has been observed [49].
Studies have shown that individuals who have
been off drugs and involved with NA for longer
periods tend to have lower trait anxiety and higher
self-esteem scores. Those who are abstinent for
more than 3 years exhibit levels of anxiety and
self-esteem similar to the general population [49].
Being active as an NA sponsor over a 1-year period
has been found to be strongly associated with
substantial improvements in sustained abstinence
rates, which suggests that providing direction and
support to other newer addicts is a way to enhance
the likelihood of one’s own abstinence [50].
Marijuana Anonymous (MA)
Marijuana Anonymous (MA), a self-help program
specific to persons with a desire to stop using cannabis, was formed in California in 1989 by cannabis addicts who felt their addiction to cannabis
was not taken seriously in other 12-step meetings.
MA is modeled after AA and NA, and members
use the same 12-step model. MA meetings can
be found in 36 states in the United States and in
many countries [51].
As of 2012, there are no reports in the published
research on outcome related to MA participation.
However, participation in 12-step groups during and after treatment has been associated with
positive outcomes among substance users, including cannabis-dependent patients [52]. Clinicians
should encourage 12-step group participation as
an aspect of treatment. A study conducted by
Laudet identified two major obstacles to 12-step
program participation: motivation and readiness
for change and the perceived need for help [52].
Other obstacles to participation include perceived
convenience and scheduling issues. This underscores the importance of promoting motivation
for change and the need to assess patient beliefs
regarding experiences with 12-step programs on a
case-by-case basis in order to find a good fit between
patient needs and 12-step resources [52].
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#9697 Cannabis Use, Abuse, and Dependence ____________________________________________________
INTERVENTIONS FOR NONENGLISH PROFICIENT PATIENTS
For those who are not proficient in English, it
is important that information regarding the use
and potential abuse of cannabis and available
resources be provided in their native language,
if possible. When there is an obvious disconnect
in the communication process between the practitioner and patient due to the patient’s lack of
proficiency in the English language, an interpreter
is required. Interpreters can be a valuable resource
to help bridge the communication and cultural
gap between clients/patients and practitioners.
Interpreters are more than passive agents who
translate and transmit information from party to
party. When they are enlisted and treated as part
of the interdisciplinary clinical team, they serve
as cultural brokers who ultimately enhance the
clinical encounter. In any case in which information regarding diagnostic procedures, treatment
options, and medication/treatment measures are
being provided, the use of an interpreter should
be considered. Print materials are also available
in many languages, and these should be offered
whenever necessary.
Studies of treatment efficacy show that cannabisdependent adults tend to respond well to a variety
of interventions. Although continuous abstinence
is a less common outcome, all psychosocial therapies tested demonstrate utility in reducing cannabis
use when delivered in both individual and group
sessions [6]. Furthermore, CM combined with
CBT or motivational enhancement may enhance
outcomes [10]. However, low abstinence rates are
an indicator of the difficulty in treating cannabis
dependence by psychotherapies in outpatient settings. These suboptimal drug use outcomes suggest
that continued development and testing of more
effective treatments for cannabis dependence
should remain a priority [43].
PROGNOSIS
Ca…
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