Cannabis
– suicide, schizophrenia and other ill-effects
A research paper on the consequences of acute and
chronic cannabis use
Drug Free
Edited by Herschel Baker
First Edition, March 2008
CONTENTS
ACKNOWLEDGEMENTS
EXECUTIVE SUMMARY
INTRODUCTION
CANNABIS USE
The
History of Cannabis Prohibition
A
description of the drug
Cannabis
increased potency
Cannabis
Gateway Drug
Cannabis
Dependence
CANNABIS HARMS
Adverse
health consequences
The
younger age, the worse the effects
Effects
on the immune system
Cannabis
and cardiovascular system
Cannabis
–chronic obstructive pulmonary disease
Cannabis
and cancer
Pregnancy
and newborns
Cannabis
– effects on the brain
Cannabis
and cognitive effects
Cannabis
and depression
Cannabis
and psychosis
Cannabis
and schizophrenia
Cannabis
and suicide
Cannabis effects on Australian Indigenous community
Cannabis
- Amotivational Syndrome
Cannabis
and impaired driving ability
QUITTING CANNABIS
RECOMMENDATIONS
REFERENCES
APPENDIX A & B Articles in Print –
ACKNOWLEDGEMENTS
This review of cannabis in -date
the National Cannabis Strategy in
The editor would like to thank the following people in
particular, for taking the time to provide assistance with the content of this
review.
Mr. Gary
Christian-National Director-Adventist Development & Relief Agency
Co-Author
Booklet The case for closure the kings cross injecting room http://www.drugfree.org.au/fileadmin/Media/Reference/DFA_Injecting_Room_Booklet.pdf
1986-1987 - Co-writer of the Quit Now Stop
Smoking Program.
1999 - Co-founder of the Cabramatta
ADRAcare Centre for drug dependent and homeless people of the area.
2000-2003 - President of Hassela Australia
Teen Drug Rehabilitation program.
Editor Mr. Herschel Mills Baker
Author review paper: Suicide/ Schizophrenia Consequences of Acute and Chronic Cannabis
Use 1988
http://www.drugfree.org.au/fileadmin/Media/Reference/CannabisSchizophrenia_APFDFY_1988.pdf
Author review paper: Suicide/ Schizophrenia
Consequences of Acute and Chronic Cannabis Use 1996
http://www.drugfree.org.au/fileadmin/Media/Reference/CannabisSchizophrenia_APFDFY_1996.pdf
Author “Drug Awareness” up-date booklet for Lions
International District 201.Q5 Zone 2
Author Manual “Drug Free Kids: A Parent’s Guide” Drug
Prevention Resource
Developer
of “Parent Drug Education Courses” successful used by: Queensland TAFE and many
organization in
President
and Founding Member of Australian Parents for Drug Free Youth, since 1986.
Mr. Craig Thompson Magistrate
Co-Author “Drug
Precipice”
Board
Member Ted Noffs Foundation 7 years.
Committee
member Australian National Council on Drugs (1998-2004).
Craig Thompson, Chair of Drug Free
Australia, who provided valuable background and structure for the document’s
evidence-base.
Retired Chair of the Ethics and Legislation Committee Pharmaceutical Society of
Australia (NSW branch). Community pharmacist.
Co-Author “Drug Precipice”
Author of papers “A Heroin trail is this the
answer?”, “Cannabis for Medicinal Purposes? A parmacist’s review 2003”,
“Australia’s Policy on Illicit Drugs”, “Legal Injecting Places- A Pharmacist’s
View”, “Australia’s Policy on Illicit Drugs”and
“Legal Injecting Places - A Pharmacist's View.
Mary Brett BSC (Hons), retired biology teacher and Board Member
of EURAD for her extensive international research in the areas of the impact of
cannabis use and its damaging effects. Her contribution to this publication
consists of substantial quotations especially in the sections on Pregnancy
and Newborns, Cardiovascular effects, Dependence and Cancer. These
excerpts were previously published by Eurad (Europe Against
Drugs) in 'Cannabis - A Cause for Concern? General Survey of its Harmful
Effects including a Discussion of its Use in Medicine and Drug Education in UK
Schools' (2006), available to view at www.eurad.net.
Josephine Baxter Executive Officer Drug Free Australia for
editorial research and publication.
Community Relations Manager – Odyssey House Victoria –
2004-2005
National Director – Programs and Training, Life
Education
Project Manager, Offshore Licensing (
Chief Executive – Life Education, SA – 2000-01
Dr
Ivan Van Damme’s (
I would like to give special thanks to Dr.
Ivan Van Damme’s contribution and the great effort he has put into the content
of this paper, the evidence he supplied was invaluable and gave weight to the
thrust and purpose of the information.
Thank you to the following
people who provided useful, and specific advice on issues covered in this
review paper that are related to their jurisdiction: Hon. Chris Foley, MP, Member for Maryborough,
Queensland and Member Travel Safe Committee, Nan Ott, Debbie Mason, Sharon Baker.
This
paper provides an overview of matters related to cannabis abuse in
In June 2007 the Department of
Parliamentary Services produced a Research Note which states “Cannabis is the
most commonly used illicit drug in
The Research Note also
underscores the important reality that the age of first experience has clearly declined with time, and the active
ingredient in cannabis Δ9-tetrahydrocannabinol (THC) is now present at greater
concentration in cannabis than previously, which increases the overall risk.
Added to this is the fact that cannabinoids are fat soluble, thus allowing THC
molecules to be absorbed by the lipids in cell membranes,
therefore leading to its accumulation in body tissues. The persistence of THC
in cell membranes exacerbates its interference with the neurotransmitters
affecting learning, concentration and memory all of which adversely influence
academic performance.
Cannabis has a plethora of other toxic substances (Hiller, 1984, Ranstrom,
2003, BMA, 1997) and 66 cannabinoids of which THC is the most psychoactive, the
other cannabinoids in cannabis are not eliminated quickly, but remain absorbed
for months at a time (Cabral 1989). Cannabis has 426 chemicals of which many
are unique to the cannabis plant. Some of them will interfere with the
transmission of sodium, potassium, calcium and chloride through membranes. These complex messenger are called
neurotransmitters. This disturbance in chemical transport and cellular
communication affects thought, behaviour, feelings, memory, motor co-ordination
and glandular activity. When smoked, cannabis creates over 2,000 chemicals
(Hoffmann 1975, 1984).
Moir
et al’s 2007 study of marijuana smoke
found:
“…ammonia was found in mainstream marijuana
smoke at levels up to 20-fold greater than that found in tobacco. Hydrogen
cyanide, NO, NOx, and some
aromatic amines were found in marijuana smoke at concentrations 3-5 times those
found in tobacco smoke. Mainstream marijuana smoke contained selected
polycyclic aromatic hydrocarbons (PAHs) at concentrations lower than those
found in mainstream tobacco smoke, while the reverse was the case for
sidestream smoke, with PAHs present at higher concentrations in marijuana
smoke. The confirmation of the presence, in both mainstream and sidestream
smoke of marijuana cigarettes, of known carcinogens and other chemicals
implicated in respiratory diseases is important information for public health
and communication of the risk related to exposure to such materials.”
Zammit and co-workers (Zammit,
S et al. 2002) report a re-analysis of Andreasson’s research (Andreasson S et
al. 1987) which found that heavy marijuana users were 6.7 times more likely
than non-users to be diagnosed with schizophrenia later in life. This was true for those who used marijuana
only, as opposed to other drugs. The
authors concluded that the findings are consistent with a causal relationship
between cannabis use and schizophrenia and that self-medication with cannabis
was an unlikely explanation for the association observed.
A separate review of five
studies from s of a variety of
factors that lead to onset of schizophrenia.
At the 5th
International Conference on Early Psychosis October 4-6, 2006 a symposium of particular interest to many
conference participants was on cannabis use and its relation to the symptoms
that signal early disease onset and early psychosis (Henquet, 2006). It is known that patients with schizophrenia,
including first-episode patients, have much higher rates of cannabis use
compared with their counterparts in the general population. Recent
epidemiologic research has discovered that cannabis is likely to be one element
in the development of psychosis, meaning that cannabis use in combination with
genetic and/or environmental factors exerts a causal influence on the onset of
psychosis in individuals at risk (Smit, 2004, DiForti, 2005 and Henquet 2005).
It has been argued that 27% of
the population carry a high risk genetic variant which produces the weak
VAL/VAL type of the COMT-gen. Catechol-O-Methyl Transferase (COMT) enzyme
(Henquet 2007). The COMT enzyme is
responsible for the break down of dopamine in the brain. Henquet states that
the excessive amounts of dopamine released by cannabis use places those with
the VAL/VAL type of the COMT enzyme at 10 times greater risk of developing
psychosis and, later in life, a higher risk of developing schizophrenia.
The conclusions reached in this
and many other review papers over the last ten years (Ramstrom, 2003, Moore,
2007, Solowij, 2007, Degenhardt, 2006, Zammit, 2002, Arsenault 2004, Drewe,
2004, Mattick, 2006, Rey, 2004, Semple, 2005 and Smit, 2004,) indicate that
there is enough evidence to inform people that using cannabis could increase
their risk of developing a psychotic illness later in life. It is incomprehensible that with all this
evidence which has built up over the last ten years some researchers, policy
makers and politicians in Australia still tend to dismiss the facts – that
cannabis is a complex, toxic substance and needs to be treated as such.
The following pages summarise
a large volume of research about the adverse effects of cannabis from different methodological perspectives
on a diverse range of systems.
SECTION 1 – CANNABIS USE
THE HISTORY OF CANNABIS
PROHIBITION
The worldwide prohibition of cannabis emerged as part of a
system of international controls first developed for other psychoactive drugs.
When the representatives of a dozen nations met in
In preparing for this Conference, which represented an
attempt to deal with the international opium traffic, the government of
Cannabis was discussed at The Hague Conference - but only briefly, and it was not included as a controlled substance. However, at the conference's closing, participants agreed that the "hemp question" should be studied, to allow later assessment of the need for international intervention (Lowes, 1966).
“The Conference considers it desirable to study the
question of Indian hemp from the statistical and scientific point of view, with
the object of regulating its abuses, should the necessity thereof be felt, by
internal legislation or by an international agreement” (Willoughby, 1912).
With reference to the proposal of the Government of the Union of South Africa that Indian hemp should be treated as one of the habit-forming drugs, the Advisory Committee recommended to the Council that, in the first instance, the “Governments should be invited to furnish to the League information as to the production and use of, and traffic in, this substance in their territories, together with their observations on the proposal of the Government of the Union of South Africa” (Willoughby, 1924).
At the urging of
At the meeting in
“The illicit use of hashish is the principal cause of most of the
cases of insanity occurring in
An
Egyptian report which is frequently quoted as incriminating cannabis as a cause
of insanity was written by (Warnoch, 1903) Medical Director of the Egyptian
Hospital for the Insane in Cairo at the turn of the century, and the first to
institute some record-keeping procedures in what was then the only, and
accordingly very crowded, psychiatric facility in Egypt. Some difficulties
common to most Eastern reports are especially evident in this one particularly
in relation to his development of categories.
In investigating the hypothesis that hashish is instrumental in causing
a large proportion of the insanity in
2.
Delirium from hashish, which is accompanied by hallucinations of sight,
hearing, taste, and smell, often of an unpleasant kind. Delusions of
persecution often occur. The idea that the subject is possessed by a devil or
spirit is common. Great exaltation and the belief that the individual is a
sultan or prophet may occur. Suicidal intentions are rare. Hashish delirium is a less grave state both
physically and mentally [than delirium tremens]. Some cases are stuporous in
type.
3.
Mania from hashish. - This varies in degree of acuteness from a mild short
attack of excitement to a prolonged attack of furious mania ending in
exhaustion or even death. Most cases are exalted, and have delusions of
grandeur or of religious importance; persecutory delusions occur frequently,
and provoke violence towards others, but not suicide. Restlessness, incoherent
talking, destructiveness, indecency, and loss of moral feelings and affections,
are all ordinary symptoms. A certain impudent daredevil demeanour is a
characteristic symptom. Hallucinations are not so marked as in alcoholic mania,
but those of hearing and taste are not uncommon; delusions of being poisoned
are often based on the latter variety. A few cases are more melancholic than
maniacal in demeanour, and exhibit extreme depression and terror with
hallucinations of hearing (threatening voices, etc.).
4.
Chronic mania from hashish, including a form of mania or persecution. Many of
these cases are not distinguishable from ordinary chronic mania.
5.
Chronic dementia from hashish describes the final stage of the preceding forms.
The Egyptian proposal was referred to a subcommittee for
study and later in the Conference this group reported that the use of Indian
hemp drugs should be limited to medical and scientific purposes. The
proceedings contain no record of what medical or scientific evidence might have
been brought forward to support the inclusion of the Indian hemp drugs in the
Convention (EL Guindy, 1924).
Nevertheless, they were the subject of Chapters IV and V of the
Convention (
The 1931 League of
Nations Convention, which sought to limit the production of opium, also banned
other drugs including cannabis and cocaine.
These steps formed the basis for later Australian laws.
CANNABIS
USE – A DESCRIPTION OF THE DRUG
Cannabis is a term that refers
to marijuana and other drugs made from the hemp plant Cannabis sativa. All forms of cannabis contain mind-altering
(psychoactive) drugs; they all contain THC
(Δ9-tetrahydrocannabinol) the main active chemical in
the plant. They also contain more than 400 other chemicals.
Table 1
|
Chemical Classes |
No. known |
|
Cannabinoids Cannabigerol (CBG) Cannabichromene (CBC) Cannabidiol (CBD) Delta-9-tetrahydrocannabinol Delta-8- tetrahydrocannabinol Cannabicyclol (CBL) Cannabielsoin
(CBE) Cannabinol (CBN) Cannabinodiol (CBND) Cannabitriol (CBT) Other cannabinoids Nitrogenous
Compounds Quarternary bases Amides Amines Spermidine alkaloids Amino acids Proteins, glycoproteins and enzymes Sugars and related compounds Monosaccharides Disaccharides Polysaccharides Cyclitois Aminosugares Hydrocarbons Simple alcohols Simple aldehydes Simple ketones Simple acids Fatty acids Simple esters and lactones Steroids Tepenes Monoterpenes Sesquiterpenes Diterpenese Tritepenese Miscellaneous compounds of terpenoid origin Noncannabinoid phenois Flavanoid glycosides Vitamins Pigments |
61 6 4 7 9 2 3 3 6 2 6 13 20 5 1 12 2 18 9 34 13 2 5 12 2 50 7 12 13 20 12 13 11 103 58 38 1 2 4 16 19 1 2 |
|
Total
|
421 |
Comparison of smoke from a marijuana cigarette and a tobacco cigarette:
Dr Dietrich Hoffmann of the
American Health Foundation compared smoke from a typical ‘street joint’ with
smoke from a typical tobacco cigarette. “Both smokes contained roughly equal
amounts of irritants and gaseous toxic agents such as
carbon monoxide, ammonia, benzene and others such as methylethylnitrosamine.
Both smokes had roughly the same compounds, including lung irritants and
potential carcinogens, but the carcinogens naphthalone, benzanthracene and
benzopyrene were present in marijuana smoke in amounts 50 to 100% greater than
in the smoke of an unfiltered high-tar cigarette as shown in the tables below”.
Table 1
|
Measurements |
Marijuana cigarette – 85 mm |
Tobacco cigarette – 85 mm |
|
Cigarettes
Average weight, mg Moisture Pressure drop cm Static burning rate mg/s Puff number Mainstream
smoke Gas Phase Carbon monoxide, vol % mg Carbon dioxide, vol % mg Ammonia HCN Cyanogen Isoprene Acetaldehyde Acetone Acrolein Acetonitrile Benzine Toluene Vinyl Chloride Dimethylnitrosamine Methylethylnitrosamine pH - third puff fifth seventh ninth tenth Particulate Phase Total particulate matter, dry mg Phenol o Cresol m and p Cresol Dimethylphenol Catechol Cannabidiol ▲Tetrahydrocannabinol Cannabinol Nicotine N-Nitrosonomicotine Napthalene 1. Methylnapthalene 2. Methylnapthaline Benz(a)anthracene Benzo(a)pyrene |
1.115 10.3 14.7 0.86 10.7 3.99 17.6 8.27 57.3 228 532 19 83 1200 443 92 132 76 112 5.4 75 27 6.56 6.57 6.58 6.56 6.58 22.7 76.8 17.9 54.5 6.8 188 190 820 400 --- --- 3.0 6.1 3.6 75 31 |
1.110 11.1 7.2 0.80 11.1 4.58 20.2 9.38 65.0 199 498 20 310 980 578 85 123 67 108 12.4 84 30 6.14 6.15 6.14 6.10 6.02 39.0 138.5 24 65 14.4 328 --- --- --- 2850 390 1.2 3.65 1.4 43 21.1 |
CANNABIS USE – INCREASED POTENCY
IN
At the outset it is necessary
to mention the position taken by the Australian National Council on Drugs on the
increase (potency) of cannabis in their paper called Evidence-based Answers to Cannabis Questions) titled 4.2 Evidence for change in strength (potency) of
cannabis.
“In fact, cannabis potency monitoring has
shown only small increases in THC over the
past few decades.”
In this section however
we will clearly show that the monitoring system that was used by the ANCD was
either biased or very selective in the samples used for testing.
The
very important factor that must be considered is the increase in potency of
dimethylheptyl analogs of delta- 9-THC (Martin, 1995, p. 231
& 237; Järbe, et. al., 1989; Little, et. al., 1988), which is consistent
with previous studies.
"Incorporation
of a hydroxy at C11, along with this branched side chain resulted in an
extremely potent cannabinoid with ED50s of 0.01, 0.04, 0.16 and 0.04
mol/kg in depression of spontaneous activity.” (Martin 1995)
This is more than one
hundred-fold in several pharmacological measures (Martin, 1995, p.
231).
The side chain plays a
predominant role in the pharmacological potency of Δ9-tetrahydrocannabino (Martin, 1995). The addition of a dimethylheptyl side chain
enhanced potency as much as fifty-fold.
The brain registers the difference exponentially, so the
difference between one percent and ten percent THC was not nine percent, but
more like nine hundred percent (Garcia 1986), (Smith, 1987).
This potency is in addition to
the existing hybrid varieties of cannabis which are continuing to gain
popularity in
In
“Research shows that high potency
cannabis consistently impairs the executive function and motor control of the
brain. Use of higher doses of THC in
controlled studies may offer a reliable indication of THC induced impairments
as compared to lower doses of THC that have traditionally been used in
performance studies” (Ramaekers 2006).
It is important for Australians
to understand the harm caused to the whole community by so-called “skunk” or
“super skunk” or any other high potency cannabis, what ever its name.
See Appendix A & B for media articles supporting this
point.
“We must exercise caution in liberalising cannabis laws in ways that may
increase young individuals’ access to cannabis, decrease their age of first
use, or increase their frequency of cannabis use. We should consider the
feasibility of reducing the availability of high-potency cannabis products”
(Hall 2006).
CANNABIS USE – GATEWAY DRUG
The argument that cannabis is
a “gateway drug” the use of which encourages the use of other illicit drugs has
a long history and there have been many critics of the theory who have argued
that the linkages between cannabis use and other forms of illicit drug use do
not reflect a causal sequence in which the use of cannabis encourages use of,
and experimentation with, other forms of illicit drugs (Donnelly and Hall National Drug Strategy Monograph Series No. 27, Johnson, 1973, Hays et al.
1987). Essentially the critics of this
theory point to the presence of other confounding factors and processes that
encourage both cannabis use and other forms of illicit drug use. Despite these critics the research
does indeed support the hypothesis that cannabis
use may encourage other forms of illicit drug use. The following lines of evidence support this
conclusion:
.
(1) Temporal sequence. Following the general
predictions of stage theory there was clear evidence that the use of cannabis
almost invariably preceded the onset of other forms of illicit drug use.
(2) Dose/response. There was clear evidence of a
very strong and consistent dose/response relationship in which increasing
cannabis use was associated with increasing risks of the onset of illicit drug
use.
(3) Resilience to control for confounding. Even
following control for a range of prospectively measured social, family and
individual factors, strong and consistent associations remained between
cannabis use and the onset of other forms of illicit drug use.
(4) Specificity of association. The association could not be
explained as reflecting a more general process of transition to adolescent
deviant behaviour since even after control for contemporaneously assessed
measures of juvenile offending, alcohol use, cigarette smoking, unemployment
and other related measures a strong and consistent relationship between
cannabis use and the onset of other forms illicit drug use remained.
Results supported the concept
of gateway drugs in that subjects indicated they had progressed further through
the stages of heavier alcohol use then through the stages of heavier cigarettes
use, smokeless tobacco use, or marijuana use (Kelley 1999).
The results are consistent
with a version of ‘gateway hypothesis’ for the relationship between alcohol and
cannabis use (alcohol use leads to changes in cannabis expectancies and thereby
to cannabis use), but a proper test of the hypothesis requires a longitudinal
study (Willner, 2001).
Proneness to deviancy and drug
availability in the neighbourhood promote marijuana use.
These findings support the
common liability model of substance use behaviour and substance use disorder
(Tarter, 2006).
Two studies published in the
June 27, 1997 Science complete the
picture of marijuana as an addictive drug, demonstrating that marijuana affects
the neurochemistry of the brain in ways similar to heroin, cocaine, alcohol,
and tobacco. The strength of the
dopamine surge in the brain created by marijuana was shown to be similar to
that created by heroin. These studies
provide physiological evidence for marijuana acting as a gateway drug that
leads to other drug use. This “sends a powerful message that should raise
everyone’s awareness about the dangers of marijuana”(Wickelgren, 1997).
Very few try illicit drugs other than marijuana without prior use of
marijuana (Kandel 1992,1996). (Kandel
1984b p67) “persons who have not used marijuana have very small probabilities
of initiating other drugs ranging from 0.01 to 0.03 (men) or 0.02 (women)”
indicating that in their cohort, “marijuana appears to be necessary condition
for initiation of other drugs”. The gateway effects of marijuana along with
tobacco and alcohol are also well established in research (Clayton, 1992,
Bailey, 1992). In the journal Drugs and Alcohol Dependence (Poikolainen
et al. 2001) suggest that initiation to cannabis is often the first step in the
use of other illicit drugs.
Children who use gateway drugs (tobacco,
alcohol and cannabis) are up to 266 times more likely to use cocaine than those
who don’t use any gateway drugs.
Compared with people who used only one gateway drug tobacco, alcohol or
cannabis, children who used all three gateway drugs are 77 times more likely to
use cocaine (Centre on Addiction and Substance Abuse at Columbia University
[CASA] 1994). A study on 311 sets of
same-sex twins in which only one twin had smoked cannabis before age 17 found
that early cannabis smokers were to be up to five times more likely than their
twin to move on to harder drugs. Early use of cannabis independent of genetic
background and environment is associated with later drug use and abuse.
(Lynskey, 2003).
(Hurd, 2006) warns
that the human brain is not fully developed till around the age of 25. Chronic
periodic use of cannabis can interfere with the development of rat brains. She
says, “The developing brain is definitely more sensitive”. After training rats
to self-administer heroin by pushing a lever, rats exposed to THC took more
heroin than those not previously exposed to it. They were more sensitive to
lower concentrations of heroin and took more in response to stress. Her
conclusion reads: The current findings support the gateway hypothesis
demonstrating that adolescent cannabis exposure has an enduring impact on
hedonic processing resulting in increased opiate
intake, possibly as a consequence of alterations in limbic opioid neuronal
populations”.
‘Clinical
and Experimental Research’ carried an article about
smoking among adolescents and an increased risk of developing alcohol-use
disorders. Results indicate that smoking “primes” the brain for subsequent
addiction to alcohol and possibly other drugs.
Almost 75,000 adolescents and young adults were randomly selected for the study by (Grucza, 2006). Typically teenage smokers had a 50% higher risk of developing an alcohol-use disorder, “a range of problems including alcohol abuse and alcohol dependency”. (Grucza, 2006), “Addictive drugs all act on a part of the brain that is described as the central reward circuitry. Once this system is exposed to one drug, the brain may become more sensitive to the effects of other drugs, as demonstrated by a number of rodent studies. Our results are in line with an emerging literature that shows adolescence may be a unique window of vulnerability for addiction”.
(Ellgren 2007) set out “to determine whether cannabis exposure during periods of active brain development alters reward-related behaviour and neurobiology for psycho-stimulant and opioid drugs by the use of animal models”. Results did not support the cannabis gateway hypothesis in relation to subsequent psycho-stimulant use but did support it in relation to opioids. The typical pattern of intermittent use by adolescents was mimicked and discrete opioid-related alterations were revealed in brain regions highly implicated in reward and hedonic processing. This was coupled to increased heroin intake in a self-administration paradigm, and increased morphine conditioned place preference, indicating altered sensitivity to the reinforcing properties of opioids. In the limbic region, there were pronounced alterations in endocannabinoid levels in cognitive brain areas even though alterations were also apparent in reward-related regions. Pre-natal exposure induced discrete opioid-related alterations within brain regions highly implicated in reward and hedonic processing.
Regular or heavy cannabis use was associated with an increased risk of using other illicit drugs, abusing or becoming dependent upon other illicit drugs, and using a wider variety of other illicit drugs although the risks of use, abuse/dependence and use of a diversity of other drugs declined with increasing age. The finding may support a general causal model such as the cannabis gateway hypothesis, but the actual causal mechanisms underlying such a gateway, and the extent to which these causal mechanisms are direct or indirect, remain unclear (Fergusson, 2006). Fergusson & co-authors conclude, “Taken together, this thesis presents neurobiological support for the cannabis gateway hypothesis in terms of adult opiate, but not amphetamine abuse, with underlying long-term disturbances of discrete opioid-related systems within limbic brain regions”.
In the light of all the evidence, it is obvious that every effort must
be made to try to prevent vulnerable children from ever starting to use
cannabis.
CANNABIS
–DEPENDENCE
Cannabis use, due to continuing disagreement among researchers, was
included as a diagnostic unit in the DSM IV (Diagnostic and Statistical Manual
of Mental Disorders 1994) and ICD-10 (International Classification of Diseases) WHO 1992 categorising
protocols.
The European Description of The ICD-10
Classification of Mental and Behavioural Disorders, WHO,
A definite diagnosis of dependence should be
made only if three or more of the following have been experienced or exhibited
at some time during the previous year.
(a)
a strong desire or sense of compulsion to take
cannabinoid;
(b)
difficulties in controlling cannabinoid-taking
behaviour in terms of its onset, termination or levels of use;
(c)
a physiological withdrawal state when cannabinoid use
has ceased or been reduced, as evidenced by: the characteristic withdrawal
syndrome for cannabinoid; or use of the same(or a closely related) substance
with the intention of relieving or avoiding withdrawal symptoms;
(d)
evidence of tolerance, such that increased doses of
cannabinoid are required in order to achieve effects originally produced by
lower doses;
(e)
progressive neglect of alternative pleasures or
interests because of cannabinoid use, increased amount of time necessary to
obtain or take the substance or to recover from its effects;
(f)
persisting with cannabinoid use despite clear evidence
of overtly harmful consequences, such as depressive mood states consequent to
periods of heavy substance use, or drug-related impairment of cognitive
functioning; efforts should be made to determine that the user was actually, or
could be expected to be, aware of the nature and extent of the harm.
Narrowing of the personal repertoire of patterns of cannabinoid use has
also been described as a characteristic feature.
It is an essential characteristic of the dependence syndrome that either
cannabinoid taking or a desire to take cannabinoid should be present. The
subjective awareness of compulsion to use drugs is most commonly seen during
attempts to stop or control substance use.
(Morgenstern et al. 1994) found the DSM concept at least as valid as
those for dependence found in opiates, alcohol, stimulants and sedatives.
(Jan Ramstrom, 2003) who wrote “Adverse
Health Consequences of Cannabis Use - A Survey of Scientific Studies” said,
“…there is now general agreement on the issue of cannabis and dependence
including the importance of withdrawal symptoms”.
(Coffey et al 2003) reported that weekly use of
cannabis marks the threshold for an increased risk of later cannabis dependency
with selection of cannabis in preference to alcohol possibly indicating an
early addiction process. She found that 30% of teenagers smoking more than one
a week became addicted by their early twenties, those between 14 and 17 were 20
times more likely. Those starting between 14 and 15 progressed to the most
harmful use. Almost 66% of teenagers smoke cannabis and about 7% show signs of
dependence. The more they smoke, the higher the risk.
Interestingly, dependent cannabis users reported
compulsive and out-of-control use more frequently than dependent alcohol users,
withdrawal to a similar extent and tolerance considerably less often.
A study by (Chambers, 2003) on the development of the adolescent brain
warned of their increased vulnerability to addiction compared to adults. He
suggested that drug addiction should be thought of as a development disorder in
the brains of teenagers, in that the changing brain circuitry leaves them
especially vulnerable to the effects of drugs and alcohol. This brain circuitry is centred on the
chemical (neurotransmitter) dopamine. Addictive drugs stimulate parts of the
brain that change rapidly during adolescence. The circuitry that releases
chemicals that associate novel experiences with motivation to repeat them develops
far more quickly in adolescence than the mechanisms that inhibit urges and
impulses. Drugs tapping into this
neural imbalance may underlie a teenager’s affinity for impulsive and risky
behaviour. They are more likely to experiment with drugs but the experience
will have more profound effects, sometimes permanent, on the brain. “You have a situation where the motivational
brain areas are particularly active”, he said, “and the part of the brain that
is supposed to inhibit impulses is not working well, because it is sort of
under construction. The parts of the frontal cortex that are activated by
adults when they weigh risks and rewards lag developmentally”.
(Gardner 2003) reviewed 224 scientific papers, 75 of which were
published in the 1970s and 80s and the other 149 after 1989. He concluded
“cannabinoids act on the brain reward processes and reward-related behaviours
in strikingly similar fashion to other addictive drugs”.
(Budney and Hughes 2004)
concluded that “converging evidence from basic laboratory and clinical studies
indicates that a withdrawal syndrome reliably follows discontinuation of
chronic heavy use of cannabis or tetrahydrocannabinol. The onset and time
course of these symptoms appear similar to those of other substances withdrawal
symptoms. The magnitude and severity of these symptoms appear substantial, and
these findings suggest that the syndrome has clinical importance”.
(Budney and Hughes 2006) found evidence of a withdrawal syndrome in
cannabis. They noted that, “The demand for treatment for cannabis dependence
has grown dramatically. The majority of the people who enter treatment have
difficulty in achieving and maintaining abstinence from cannabis”. Among their
findings are, “The neurological basis for cannabis withdrawal has been
established via discovery of an endogenous cannabinoid system, identification
of cannabinoid receptors, and demonstrations of precipitated withdrawal with
cannabinoid receptor antagonists. Laboratory studies have established the
reliability, validity and time course of a cannabis withdrawal syndrome and
have begun to explore the effect of various medications on such withdrawal.
Reports from clinical samples indicate that the syndrome is common among
treatment seekers”. Another research report (Budney, 2006) found that
“…cannabis dependence is much more similar to, than different from, other types
of substance dependence, even with regard to withdrawal. The generic DSM-1V
dependence criteria can be applied fairly well to cannabis, and yield findings
similar to that observed with other substance dependence disorders….whether we
can do better by developing more sophisticated generic criteria or using
substance specific criteria”.
A substantial minority (9%) of this cohort met DSM-IV criteria for
cannabis dependence by age 21 years.
This is consistent with the findings of the
(Budney et al 2006) summarises, “The demonstration of a dose-dependent
suppression of cannabis withdrawal by oral THC provides additional support for
validity of the cannabis withdrawal syndrome and its inclusion in the DSM”.
Cambridge University Press has recently (2006) published a book “Cannabis Dependence: Its Nature,
Consequences and Treatment” in the series “International Research
Monographs in the Addictions”
which “breaks through the controversial politics of cannabis use
to give a clear, scientific synthesis of all the health-related issues relating
to cannabis use”.
It reviews and assesses all the interventions applied to both adult and
adolescent users, gives the criteria for diagnosis and scope of cannabis
dependence.
The abovementioned book report on over 2500 adult daily cannabis users
completing an Internet survey, fewer than half of daily cannabis users met the
DSM-IV-TR criteria for cannabis dependence. This study aimed to determine
whether the negative aspects associated with use of cannabis can be explained by
a proxy measure of dependence instead of by frequency of use. Comparing those
who were dependent (N=1111) with those who were not (N=1770), the former
consumed greater amounts of cannabis, various other drugs and alcohol. They
also exhibited higher levels of depression and lower levels of happiness,
motivation and satisfaction with life. The study concluded,
“ Although all of our subjects reported
daily use, only those meeting proxy criteria for cannabis dependence reported
significant associated problems. Our data suggests that dependence need not
arise from daily use, but consuming larger amounts of cannabis and other drugs
undoubtedly increases problems” (Looby, 2007).
(Vandrey 2008) and co-workers studying the effects of heavy marijuana use suggests that withdrawal from the use of marijuana is similar to what is experienced by people when they quit smoking cigarettes. Abstinence from each of these drugs appears to cause several common symptoms, such as irritability, anger and trouble sleeping - based on self reporting in this recent study of 12 heavy users of both marijuana and cigarettes.
“These results indicate that some marijuana users experience withdrawal effects when they try to quit, and that these effects should be considered by clinicians treating people with problems related to heavy marijuana use,”
Vandrey points out that a lack of data, until recently, has led to cannabis withdrawal symptoms not being characterised or included in medical reference literature such as the Diagnostic and Statistical Manual of Mental Disorders, 4th Edition, (DSM-IV) or the International Classification of Diseases, 10th edition (ICD-10).
Since the drafting of the DSM-IV in 1994, an increasing number of studies have surfaced suggesting that cannabis has significant withdrawal symptoms. What makes Vandrey’s recent study unique is that it is the first study that compares marijuana withdrawal symptoms to withdrawal symptoms that are clinically recognised by the medical community - specifically the tobacco withdrawal syndrome.
“Since tobacco withdrawal symptoms are well documented and included in the DSM-IV and the ICD-10, we can infer from the results of this comparison that marijuana withdrawal is also clinically significant and should be included in these reference materials and considered as a target for improving treatment outcomes,” says Vandrey.
Vandrey added that this is the first “controlled”
comparison of the two withdrawal syndromes in that data was obtained using
rigorous scientific methods - abstinence from drugs was confirmed objectively,
procedures were identical during each abstinence period, and abstinence periods
occurred in a random order. That tobacco and marijuana withdrawal symptoms were
reported by the same participants, thus eliminating the likelihood that results
reflect physiological differences between subjects, is also a strength of the
study.
A paper from STASH
(Science Threads of Addiction, Substance Use and Health), January 2007, looked
at the transition from drug use to dependence. Over 8000 participants were
involved in the study (a report of 3 papers). The probabilities of initiation
of drug use peaked at age 18 for alcohol and marijuana.
The
risk of developing dependence on these drugs also peaked in the teens.
Male marijuana users were approximately twice as
likely to become dependent in the 2 to 5 years after first use than female
users.
A plant extract that may block cannabis addiction has been discovered.
MLA (methyllycaconitine) from the seeds of Delphinium brownie, a plant in the
buttercup family was given to rats. They lost their craving for a synthetic
version of THC and a reward response to THC was blocked in the brain. By
analysing fluid from the nucleus acumbens in the reward signalling area of the
brain they found that release of dopamine was blocked by MLA. It is not known
exactly how MLA works but no side effects were reported. Dopamine levels were
not reduced below the normal (Goldberg
et al. 2007).
SECTION 2 – CANNABIS HARMS
CANNABIS HARMS - ADVERSE HEALTH CONSEQUENCES
Health consequences of
cannabis use. Their strategy then has
been to disseminate information regarding the hazards to health posed by the
drug cannabis to the entire community.
In 1984 a review called “Cannabis and Adverse Medical Effects on Health:
An Evaluation from Nordic Countries” and in 1997 the Sweden National Board of
Health Welfare asked psychiatrist (Jan Ramstrom, 1998) to do a review into the damage
to health caused by cannabis. It was
called “Adverse Health Consequences of Cannabis Use”. The major headings in
this review were cannabis and mental disorders, physical injury, psychological
and psychosocial injury.
In order to stay current with
research and to extend the review into areas, the National Institute of Public
Health Sweden requested (Jan Ramstrom, 2003) to do a survey of scientific
studies published up to and including the Autumn of 2003. The major headings in
this review were Cannabis and Mental Disorders, Some Psychological and
Psychosocial Harmful Effects, Physical Harm.
In the
It is important to note that not
one of the approximately 15,000 studies up to 2007 on cannabis has given it a
clean bill of health. Unfortunately, cannabis has
harmful effects on many organs
of the body.
CANNABIS HARMS
- THE YOUNGER THE AGE, THE WORSE THE EFFECTS
Modelling by (Gfroerer, 1999)
indicates that age of first marijuana use is an important predictor of
progression to heavier drug use and treatment need. The earlier cannabis is
first used the greater likelihood of treatment need (Kandel, Yamaguchi, 1985;
Robins, Przybeck, 1985, Adams, Gfroerer, 1988; Glantz, Pickens, 1992; Anthony;
Petronis, 1995). The risk of cannabis
abuse and dependence was found to increase with the frequency of smoking
occasions and slightly decreased with the age of the user. (Grant and Pickering, 1999).
In May 2003 NIDA issued a summary article titled
“Starting Marijuana Use in Mid-Teens or Younger May Result in Cognitive
Impairment Later in Life but Reasons are Unclear”. Researchers showed that
there is evidence that individuals who start to smoke marijuana at an early
age-while the brain is still developing –show deficits in cognition which are
not seen in individuals who begin use of drugs when they are older. (Pope et
al. 2003).
The
paper by (Giedd et al. 1999)
on development of the adolescent brain must be mentioned here. They conclude
that the brain does not finish its development till the mid twenties or beyond.
They warned that drug abuse could alter the normal course of the maturing of
the brain in the teenage years.
In (
Cannabis use in adolescence
appears to be less transient than many people would believe (Axel, 1999). Overall, ages 14-18 are peak hazard ages for
initiation to cannabinoid use and ages over 16 are the peak risk period for developing
abuse and dependence, with some indications that this latter risk increases
further with age (Anthony et al. 1994, Warner et al.1995, Kandel et al.
1997).
Age at which exposure to
marijuana begins is important. Early adolescence may be a critical period for
physiological and psychological effects that are not present when exposure
begins later. These results are
discussed in light of reported effects of marijuana on gonadal and pituitary
hormones (Wilson, 2000, Pope, 1995, Fletcher, 1996).
Of concern is that marijuana
use is related to later adolescent problems that limit the acquisition of
skills necessary for employment, heighten the risks of contracting HIV and
abusing legal and illegal substances (Brook, 1999 and Bailey, 1992).
The results also indicate a strong association between use of cannabis
and earlier age at first psychotic episode in male schizophrenia patients
(Veen, 2004).
The strongest relationship was
evident at age 15 reflecting a pattern of relatively “non-normative” early
cannabis use. Those with a mental health
disorder at that age were over four times more likely to report cannabis use
than those without. (Mc Gee, 2000). Studies of 2,000 Victorian high school
students over 10 years found those who were smoking cannabis at the age of 15
were as much as 15 times more likely to be using amphetamines in their early
20s. Teenagers using cannabis more heavily tend to continue selectively with
cannabis use.
Considering their poor young
adult outcomes, regular adolescent cannabis users appear to be on a problematic
trajectory (Patton, 2007).
An additional issue concerns
the extent to which age-related adverse effects of cannabis use (Fergusson,
2002), (Solowij, 2002) can potentially be interpreted as indicating that these
associations arise both because onset use serves as a marker for deviance (i.e.
the association may be non-causal) or because early-onset use sets in train a
range of events, described by (Kandel et al. 1986) as a cascade, including
potential disengagement from traditional roles such as involvement in education
(Lynskey, 2000) that may lead subsequently to increased risks for depression.
This is by no means the only interpretation of age-related differences in the
apparent adverse effects of cannabis use.
There is a growing preclinical literature suggesting that adolescent
versus adult exposure to cannabis may have differential varying effects
(Schramm-Sapyta, 2007, Schneider, 2003) such as reducing the potential
educational performance of the individual.
Cognitive deficits associated with the acute and
chronic use of cannabis have important
theoretical and clinical significance. Brain imaging
techniques do reveal neurotoxic effects of
cannabis. Thus, the deficits reflect changes to the
underlying cortical, sub-cortical and
neuromodulatory mechanisms that underpin cognition.
The main effect is on information
processing which implies a deficiency to utilise
cognitive capacity.
The epidemiological literature provides uneven
coverage of the possible health and
psychological effects of cannabis. However, the
research has helped to clarify the role that
cannabis plays in impairing educational performance,
mainly through the negative effect of
cannabis on prefrontal functions such as Executive
Functioning. Another negative effect is the loss of the individual’s ability to
perceive their reduced capacity to store adequate information in the episodic
memory (Lundqvist, 2003).
It is important
for the reader to understand the very young age that Australian children are
using cannabis, for example in The Sunday Mail October 26 2003 page 7 under the
headline “Children caught with pot” teachers
discovered the Year 5 boys aged 9 and 10 in the toilets of Shailer Park State
School in Brisbane’s South with cannabis and home made bongs. The then
Education Minister and now Queensland Premier Anna Bligh was horrified by the
news and
was reported to remark that “As a parent of a child in Year 5, I am outraged
that children so young have drugs”.
CANNABIS HARMS – EFFECTS ON THE IMMUNE SYSTEM
The immune system
is complex. Macrophages engulf and destroy foreign matter, natural killer cells
bind to target cells and destroy them. B-lymphocytes produce antibodies against
infective organisms and T-lymphocytes kill cells or activate macrophages or
their forerunners, monocytes.
Early
research on the effects of cannabis/THC on animals in the 70s and early 80s
produced consistent evidence of immunological defects. (1981/82 WHO Report into the adverse effects of
cannabis). Cannabis-tested mice showed decreased resistance to
Listeria monocytogenes and Herpes simplex.
Additionally Dormant genital herpes in humans was reactivated after
cannabis consumption (Zhu, 2000).
One of the earliest findings in marijuana research was the effect on various immune functions, which is evidenced by an inability in users to fight herpes infections and the discovery of a blunted response to therapy for genital warts during cannabis consumption (Cabral, 1993 and Gross, 1991). Evaluation of the effect of THC on NK-kB has suggested a possible effect on the HIV genome (Daaka,1997).
(Ishida 2008) “Daily cannabis use is strongly
associated with moderate to severe fibrosis” this study confirms an earlier
French study of 2004, in which daily cannabis use was also associated with an
increased risk for liver fibrosis. Authors conclude that "HCV-infected
individuals should be counseled to reduce or abstain from cannabis use."
Tashkin found that smokers of cannabis and tobacco have higher rates of respiratory symptoms than smokers of either alone. He suggests that cannabis and tobacco may have a synergistic effect, such that THC may suppress immune activity in the lung, thus reducing ability to counter bacterial infection or suppress tumour growth (Tashkin, 1987).
“Marijuana has been shown to decrease host resistance
to bacterial, protozoan and viral infections in experimental animal models and
in vitro systems” (Cabel, 1999).
In the late 90s it was discovered that THC induces apoptosis (programmed cell death) of lymphocytes. Alveolar macrophages protect the lungs from infection and kill tumour cells. Marijuana significantly impairs these macrophage cells. The proliferation of lymphocytes that also kill tumour cells is also suppressed. The National Academy of Sciences said, “…the risks of smoking marijuana should be seriously weighed before recommending its use in any patient with pre-existing immune deficits – including AIDS patients, cancer patients, and those receiving immunosuppressive therapies (for example, transplant or cancer patients.” (Sanchez, 1998, Zhu, 1998, Chan 1998).
Cells of the immune system play a part. Alveolar
macrophages help protect the lungs from infection and kill tumour cells;
significant impairment of these has been seen in marijuana and tobacco
smokers. Likewise the proliferation of
T-lymphocytes that destroy tumours is suppressed. Experiments on animals have provided
confirmation of the impact on the immune system and tar from marijuana smoke
painted on the skins of mice produced lesions correlated with malignancies
(Cabral and Pettit 1998).
In a review paper (Cabral 1988) on the subject of
cannabis and immunity, “This substance (THC) has
been shown to be immunosuppressive and to decrease host resistance to bacteria,
protozoan and viral infections. Macrophages, T-lymphocytes and natural killer
cells appear to be major targets of the immunosuppressive effects of THC.
Definitive data which directly links marijuana use to increased susceptibility
to infection in humans is currently unavailable, however, the fact that current
literature indicates that THC alters resistance to infection in vitro in a
variety of experiments on animals supports the hypothesis that a similar effect
occurs in humans.
Studies show that two cannabinoids, Δ9-tetrahydrocannabinol
(THC) and anandamide, induce dose-related immuno-suppression in both the
primary and secondary in vitro plaque-forming cell assays of antibody
formation. The immuno-suppression induced by both compounds could be blocked by
SR144528, an antagonist specific for the CB2 receptor, but not by SR141716, a
CB1 antagonist. These studies are novel in that they show that both anandamide
and THC are active in the nanomolar to picomolar (for anandamide) range in
these assays of immune function, and that both mediate
their effects directly on cells of the immune system through the CB2 receptor.
(Eisenstein, 2007).
The study does
suggest that cannabinoids may exert their immunosuppressive effects in part by
affecting the locomotion of T lymphocytes in response to chemokines. This could cause restricted transmigration
during injury and inflammation, and contribute to the increased susceptibility
to infections noted in cannabis abusers (Ghosh, 2007).
Cannabis use was
associated with a decrease in NK counts, lymphocyte proliferative
response by SI-PHA and SI-Con A, and levels of IL-2, and an increase
in levels of IL-10 and TGF
1.
No differences were found in counts of total lymphocytes or CD4,
CD8, and CD19 cells (TABLE).
The significant effect of cannabis consumption on immune measures
persisted after multivariate analysis controlling for the possible
confounding effects of sex and use of coffee, tobacco, and alcohol. A significant dose-response relationship was
found between cannabis exposure (total life consumption, as
the log-transformed number of cannabis "joints") and the decrease
in counts of total lymphocytes, CD4 or NK cells, and IL-2 levels, or
the increase in IL-10 levels. See link: http://jama.ama-assn.org/cgi/content/full/289/15/1929-a
note table page 1930 (Pacifici, 2003).
How cannabinoids influence immune function has been examined
extensively in the last 30 years. Studies on drug-abusing humans and
experimentation with animals and, in vitro models employing immune cell
cultures, have shown that marijuana, natural and manufactured cannabinoid
compounds are all immunomodulators. These substances modulate host resistance
to bacterial, protozoan and viral infections.
They also can profoundly affect the Th1/Th2 response. Recently, two types
of cannabinoid receptor, CB1 and CB2, have been discovered. While CB1 is
expressed primarily in the brain, CB2 is peculiar to the immune cells.
Cannabinoid receptors have been shown to be involved in some but not all of
immune effects. Nevertheless, their identification provides a specific
mechanism of action in the attempting to discover how exogenous cannabinoids
and endogenous cannabinoid system affect the immune apparatus, strengthen the
hypothesis of cannabinoids as immunomodulators.
As support to this theory, enough evidence exists to
suggest that the cannabinoid system significantly affects almost every
component of the immune response machinery and impacts the functioning also of
the cytokine network. The evaluation of the biological consequences of these
drug-induced cytokine changes has also become dramatically
important considering not only the impact of cytokines on immune system per se
but also envisaging their influence in cancer, inflammation, autoimmune
disease, brain injury, hematopoietic colony formation in which cannabinoids
have demonstrated a clear role as important modulators (Massi, 2006).
CANNABIS
AND THE CARDIOVASCULAR SYSTEM
Comparatively little research has been done in this area, but there are
sufficient published scientific papers to raise concern.
At first the intoxication produced by cannabis causes an increase in
heart rate of between 20% and 50% (Huber et al. 1988 and Jones, 1984). A rise
in blood pressure occurs if the person is sitting or lying, but on standing up
the pressure drops, in some cases causing the person to faint (Maykut, 1984). A
new and naive smoker may be concerned about these effects (Sidney 2002), but
someone with a healthy heart is not thought to be at risk.
Cannabis affects the cardiovascular system in other ways as well. THC
increases the production of chemicals called catecholamines which stimulate the
heart, it also has analgesic properties which may lessen any chest pain and
delay the seeking of treatment and the level of carboxyhaemoglobin is raised,
decreasing the supply of oxygen to the heart, placing it under greater strain
(Jones, 1982 and 1984).
It must be added, though, that tolerance quickly develops to the acute
cardiovascular effects of cannabis. (Benowitz, Jones 1975, Jones, Benowitz
1976, Nowlan, Cohen 1977, Jones 1984) showed that in people receiving daily
high doses by mouth, tolerance develops in 7 to 10 days. This could possibly
help to explain why toxic effects are sometimes not seen.
(Herning et al. 2001) using Transcranial Doppler Sonography (sound waves
to measure cerebral artery blood flow resistance) found that prolonged
marijuana use in 18 to 30 year olds increased the resistance in the arteries
and so restricted blood flow to the brain. 16 long-term male users were
compared with 19 non-users. The deficit persisted for 4 weeks after abstinence.
They compared the results to that of the brain of a 60 year old. Advancing age
increases the chance of a stroke. (Geller et al. 2004) records an incident in
which three teenagers, 15, 16 and 17, who “binge smoked” cannabis suffered
strokes, two died and one was left paralysed. In the two who died the stroke
appeared to have been triggered by a clot in the brain or a constriction of the
blood vessels over a wide area (Geller et al. 2004).
(Mittleman, 2001) interviewed 3882 patients with heart attacks. He
concluded that the risk of onset of myocardial infarction rose by almost 5
times in the hour following the smoking of a joint.
(Moussouttas, 2001) reviewed all reported cases of presumed cannabis
related cerebral ischemic events in the medical literature, as well as
pertinent human and animal experimental studies on the cardiovascular and
cerebro-vascular effects of cannabis. His conclusion was “Cannabis use seems to
have been causally related to several instances of cerebral ischemia and
infarction. Proposed etiologic mechanisms have included cerebral vasospasm,
cardio-embolisation and systematic hypotension with impaired cerebral
auto-regulation, but most of the available data points to a vaso-spastic
process. The exact relation to cerebro-vascular disease remains to be
determined”.
We still do not know the long term effects of exposure to cannabis smoke
on the cardiovascular system over extended periods of time but experience with
the problems of tobacco smoke should urge caution. (Jones, 1984) suggested
that, “after years of repeated exposure, there may be lasting, perhaps even
permanent alterations of the cardiovascular system function”. He says, “There
are enough similarities between THC and nicotine’s cardiovascular effects to
make the possibility plausible”.
A study by (Mach, 2004) study on genetically modified mice found that
THC helped prevent atherosclerosis, a “furring up” of the arteries caused by
plaques of protein and other material. Mach warned that smoking cannabis would
not be the answer as oxygen levels are reduced and THC increases the heart rate
and interferes with blood pressure as previously described. He called for THC (already available as a
medicine, Nabilone ) or other cannabinoid derivates to be
investigated for this role. This is in line with all licensed medicines that
are required to have a risk assessment to ensure the quality of the product and
also to be subjected to standard clinical testing. This request was repeated in another paper by
Mach in 2006.
Cannabis has
patho-physiological effects on the cardiovascular system, and previously an
association with an increased risk of myocardial infarction has been reported.
Cannabis smokers who have cardiovascular disease should be warned that it is
likely to aggravate coronary ischaemia, and may even trigger myocardial
infarction (Lindsay, 2005).
Fisher et al (2005) warns of cardiovascular complications of cannabis,
presenting a case for a constant reviewing of the literature because it is argued
that it is likely that the incidence of arrhythmias associated with cannabis is
grossly underestimated.
Paroxysmal atrial fibrillation (AF) is a common arrhythmia that may
occur after various triggers. Cannabis
is an unusual trigger for AF that might be underestimated in young
healthy
adults. Once the standard work-up has
ruled out common causes for AF, the physician should look for cannabis
ingestion, Δ9-tetrahydrocannabinol
(THC)
could precipitate arrhythmia (Charbonney, 2005).
CANNABIS HARMS – CHRONIC OBSTRUCTIVE PULMONARY DISEASE
A systematic review of 34 studies on pulmonary
function and respiratory complications was carried out by (Tetrault et al.
2007). The summarised findings are as
follows. Short-term marijuana smoking
was associated with improved airway response in 10 of 11 challenge studies
(effects assessed immediately or shortly afterwards, 15 minutes to one hour).
However the results of the other one suggested a reversal of this effect after
1.5 to 2 months of marijuana smoking.
Longer-term marijuana smoking was inconsistently
associated with airflow obstruction. Results from pulmonary function tests were
worse in marijuana smokers than in controls in 8 of 14 studies. Longer-term
marijuana smoking was associated with an increased risk of various respiratory
complications (cough, sputum production, wheezing, dyspnea, pharyngitis,
worsening of asthma symptoms) in 14 of 14 studies. The overall quality of
studies varied, many failed to control for tobacco smoking and none defined a
standardised measure of marijuana dose (Tetrault et al. 2007).
Smoking cannabis was associated with a dose-related
impairment of large airways function resulting in airflow obstruction and
hyperinflation. In contrast, cannabis
smoking was seldom associated with macroscopic emphysema. The 1:2.5 to 6 dose
equivalence between cannabis joints and tobacco cigarettes for adverse effects
on lung function is of major public health significance (Aldington, 2007).
In cases of emphysema in young individuals, marijuana
abuse has to be considered in the differential diagnosis. The period of marijuana smoking seems to play
an important role in the development of lung emphysema. This obviously quite frequent condition in
young and so far asymptomatic patients will have medical, financial, and
ethical impact, as some patients may be severely handicapped or even become
lung transplant candidates in the future (Beshay, 2007).
The following study
found that among people 40 and older, smokers were two-and-a-half times as
likely as non-smokers to develop chronic obstructive pulmonary disease (COPD)
while smoking cigarettes and marijuana together boosted the odds of developing
COPD to three-and-a-half times the risk of someone who did not smoke either
cigarettes or marijuana. In other words, adding
marijuana smoking to cigarette smoking increased the risk by one-third. The odds of cigarette smokers having any
respiratory symptoms was 2.36 times that of non-smokers, while the odds of
someone who smoked both cigarettes and marijuana having respiratory symptoms
was 18 times that of someone who smoked neither-an eightfold jump in risk (Tan,
2007).
Marijuana smoking leads to
Asymmetrical Bullous disease, often in the setting of normal CXR and lung
function. In subjects who smoke
marijuana, these pathological changes occur at a younger age (approximately 20
years earlier) than tobacco smokers. (HII, 2008).
Daily cannabis use is strongly
associated with moderate to severe fibrosis, and HCV-infected individuals
should be counselled to reduce or abstain from cannabis use (Ishida, 2008).
CANNABIS HARMS - CANCER
Cannabis smoke is usually inhaled more deeply, held in
the lungs for longer and smoked right down to the butt to get full money value.
Cannabis cigarettes generally lack filters (Wu et al. 1988). More tar is
inhaled from the cannabis butt than from its tip (Tashkin et al. 1999).
Cannabis smoke contains 4 to 5 times as much tar as tobacco smoke so the amount
of tar deposited in the lungs daily in a user smoking 4-5 joints per day is
comparable to that of a tobacco smoker with a 20 a day habit (Benson et al.
1995).
Also the tar from cannabis contains 50% more of some
of the carcinogens found in tobacco, notably benzopyrene, a potent carcinogen
and a key factor in the promotion of lung cancer (Hoffman et al. 1997, Tashkin
et al. 1997, Novotny et al. 1976, Leuchtenberger et al. 1983). For lung cells to become cancerous, a
particular combination of cell-growth regulating genes (oncogenes) must become
activated or undergo mutation (suppressor genes of tumours). Marijuana smoke
has been reported to produce chromosome aberrations in bacteria as demonstrated
by the Ames test (Busch et al. 1979 and Wehner et al. 1980).
Cannabis contains about 50% more benzopyrene, a potent
carcinogen, than tobacco. For cancers to occur, the DNA of some genes needs to
be affected. Cell abnormality has been
detected in many papers on cannabis, akin to the numbers observed in tobacco
smokers, with a combination of the two resulting in an additive effect and
producing a higher total (Tashkin 1993).
(Zhang et al. in 1999) studied 173 patients with
carcinoma of the head and neck and compared them with 176 cancer-free controls.
Age, sex, race, education, alcohol consumption and exposure to cigarette smoke
either actively or passively, were all controlled for. Marijuana smoking
increased the risk of squamous cell carcinoma of the head or neck, and a
further increased risk was suggested with rising doses. Among people who smoked
once a day the risk factor was 2.1 times compared with non-smokers, with those
using it more than once a day the risk factor rose to 4.9. With patients who
smoked cannabis and tobacco the risk was 36 times that for non-smokers.
Long-term cannabis use
increases the risk of lung cancer in young adults, particularly in those who
start smoking at a young age, (Aldington, 2007). Human data concerning the carcinogenicity of
cannabis shows that a number of neoplasms may be attributed to smoking of
marijuana and, moreover these neoplasms are presented in younger ages than
usual (Marios Marselos & Petros Karamanakos 1999).
The strongest reason for concern is that cannabis
smoke contains many of the same carcinogens as tobacco smoke and it is
mutagenic in microbial assays and carcinogenic in some animal tests. It is
therefore a potential cause of cancer in body cells that are regularly and
chronically exposed to smoke such as those of the aero-digestive and
respiratory tracts (Hall, 2002).
In light of the evidence that one joint of cannabis
equals up to five tobacco cigarettes (Aldington et al. 2007) the following is
significant the “Long-term cannabis use increases the risk of lung cancer in
young adults, particularly in those who start smoking cannabis at a young age.”
(Aldington et al. 2007). A study by
(Groopman, 2007) indicated that marijuana smoking was associated with Kaposi’s
Sarcoma. This is the first to demonstrate that THC itself can assist the virus
in entering endothelial cells, which comprise skin and related tissue.
Heavy cannabis use is associated with cancer of the
larynx (Zang, 1999) and lung (Sridar, 1994) (British Lung Foundation “A Smoking
Gun?” 2002). Marijuana exposure either recreationally or medicinally may
increase the susceptibility to and/or incidence of breast cancer as well as
other cancers that do not express cannabinoid receptors and are resistant to
Delta9-THC-induced apoptosis (McKallip, 2005).
In June 2005 Roth
and Tashkin of UCLA, the two leading authors of many papers linking cannabis
and cancer for over 10 years, described an epidemiological study at the meeting
of the International Cannabinoid Research Society in
Tashkin reviewed the literature on lung injury caused by smoking marijuana. He concluded, “Regular marijuana smoking produces a number of long-term pulmonary consequences including chronic cough and sputum, histopathologic evidence of widespread airway inflammation and injury and immunohistochemical evidence of dysregulated growth of respiratory epithelial cells that may be pre-cursors of cancer…….Habitual use of marijuana is also associated with abnormalities in structure and function of alveolar macrophages including impairment in microbial phagocytosis and killing that is associated with defective production of immuno-stimulatory cytokines and nitric oxide thereby potentially predisposing to pulmonary infection” (Tashkin, 2005).
A study reported
that, of 52 men between 44 and 60 with transitional cell bladder cancer, 88.5%
had a history of marijuana smoking. Almost 31% were still using the drug. 104
controls were seekers of urological care other than bladder cancer. Tobacco
smoking is the major risk for bladder cancer but is only common in the over
60s. Since marijuana metabolites have a half-life in urine about 5 times
greater than tobacco metabolites, they warned “Marijuana smoking may be an even
more potent stimulant of malignant transformation in transitional epithelium
than tobacco smoking.” (Terris et al. 2006).
A systematic
review of 34 studies on pulmonary function and respiratory complications was
carried out by (Tetrault et al. 2007).
The summarised findings are as follows.
Short-term marijuana smoking was associated with improved airway
response in 10 of 11 challenge studies (the effects were assessed immediately
or shortly afterwards, then at 15 minutes to one hour). However the results of
the other one suggested a reversal of this effect after 1.5 to 2 months of
marijuana smoking.
Smoking a joint is
equivalent to 20 cigarettes in terms of lung cancer risk. Studies in the past have
demonstrated that cannabis can cause cancer, but few have established a strong
link between cannabis use and the actual incidence of lung cancer. Cannabis
could be expected to harm the airways more than tobacco as its smoke contained
twice the level of carcinogens, such as polyaromatic hydrocarbons, compared
with tobacco cigarettes.
The method of
smoking also increases the risk, since joints are typically smoked without a
proper filter and almost to the very tip, which increases the amount of smoke
inhaled. The cannabis smoker inhales more deeply and for longer, facilitating
the deposition of carcinogens in the airways.
"Cannabis smokers end up with five times more carbon
monoxide in their bloodstream (than tobacco smokers).” The researchers
interviewed 79 lung cancer patients and sought to identify the main risk factors
for the disease, such as smoking, family history and occupation. The patients
were questioned about alcohol and cannabis consumption.
In this high-exposure group, lung cancer
risk rose by 5.7 times for patients who smoked more than a joint a day for 10
years, or two joints a day for 5 years, after adjusting for other variables,
including cigarette smoking. Additionally long term cannabis use
increases the risk of lung cancer in young adults particularly in those who
start smoking at a young age (Aldington, 2008).
THC contributes to
DNA damage, inflammation and alterations in apoptosis (programmed
cell death) in tracheo-bronchial epithelium and (Sarafian et al. 2005)
concluded that, “THC delivered as a component of marijuana smoke, may induce a
profile of gene expression that contributes to the pulmonary pathology
associated with marijuana use”.
A systematic
review by (Mehra et al. 2006) was carried out of
19 studies into the impact of marijuana smoking on the development of
pre-malignant lung changes and lung cancer.
Deficiences in the methodology of some of the studies were noted. The
conclusion was as follows: “ Given the prevalence of marijuana smoking and
studies predominantly supporting biological plausibility of an association of
marijuana smoking with lung cancer on the basis of molecular, cellular, and
histo-pathologic findings, physicians should advise patients regarding
potential adverse health outcomes until further rigorous studies are performed
that permit definitive conclusions”.
Chronic marijuana smoking is associated with increased
toxicity and the risk of cancer of the respiratory tract. There is evidence of disturbance of the
immune system and teratogenic effects of chronic cannabis use (Drewe,
2003). Cannabis increases
the risk of head and neck cancer in a dose-response manner for frequency and
duration of use (Carriot, 2000).
The conclusion of our editorial is that
yes, cannabis is dangerous. We have to alert our authorities and, more
practically, to ask in our every day practice ‘‘do you smoke
tobacco and/or cannabis?’’ in order to
systematically provide minimal council to our patients, friends and children.
(Brambilla 2008).
CANNABIS HARMS – PREGNANCY AND NEWBORNS
THC readily crosses the
placenta early in pregnancy. First trimester use of marijuana also increased
the odds of minor physical abnormalities in newborns. An important measure of success is the
health and well-being of the next generation. (Bada 2006, Cornelius, 1995 and
Bailey, 1987).
Marijuana exposure during pregnancy
alters the neurobehavioral performance of term newborn infants of adolescent
mothers (Jobe, 2006) (Barros,
2006). Marijuana use during pregnancy
was associated with increased risk of neuroblastoma in offspring (Bluhm, 2006).
Babies born to mothers who use
marijuana during pregnancy have an eleven-fold increase in nonlymphoblastic
leukaemia (Robinson et.al. 1989).
Exposure to marijuana during
pregnancy is associated with changes in size, weight and neurologic
abnormalities in the newborn (Fried 1980, 1984, Zimmerman 1991, Zuckerman
1989). Additionally, hormonal function
in both males and females is disrupted (Barnett 1983, Mendelson 1985, 1986).
A paper by
(Klonoff-Cohen et al. 2006) studying the effects of marijuana use on the
outcomes of IVF (In Vitro Fertilisation) and GIFT (Gamete Intra-Fallopian
Transfer) fertility treatments found that the prospect of a good outcome is
reduced if either partners use marijuana. Females produced fewer eggs and the
child had a significantly lower birth weight. The more recent the use, the
worse the effects. Male marijuana use
was also associated with lower birth weight. Both timing and amount of the drug
used negatively affected IVF and GIFT.
(Hollister, 1986)
has argued that the reductions in testosterone and spermatogenesis observed in
the positive studies are probably of "little consequence in adults",
although he conceded that they could be of "major importance in the
pre-pubertal male who may use cannabis.” He cited a case of growth arrest in a
16-year-old male who began heavy cannabis use at the age of 11, and who
experienced a retardation of growth and the development of secondary sexual
characteristics which partially remitted after three months abstinence from
cannabis (Copeland, Underwood, Van Wyck, 1980). The possible effects of
cannabis use on testosterone and spermatogenesis may therefore be most relevant
to males whose fertility is already impaired for other reasons, e.g. a low
sperm count.
The risk of
miscarriage or ectopic pregnancy of women smoking cannabis in the early stages
of pregnancy was highlighted in recent research by (Day, 2006). Anandamide
controls the development of the embryo so the level of the neurotransmitter is
crucial. THC, by mimicking anandamide,
disrupts the correct signaling process. The embryos of mice treated with THC
had more cell abnormalities than the controls and the embryos failed to travel
to the uterus.
A review by (Huizink and Mulder, 2006) came to the
conclusion that pre-natal exposure to either maternal smoking, alcohol or
cannabis use is related to some common neuro-behavioural and cognitive
outcomes, including symptoms of ADHD (inattention, impulsivity), increased
externalising behaviour, decreased general cognitive functioning, and deficits
in learning and memory tasks.
Barros and
colleagues, writing in The Journal of Paediatrics in January 2007 found that
marijuana-exposed infants born to adolescent mothers scored differently on
measures of arousal, regulation and excitability compared to non-exposed infants,
where they displayed subtle behavior changes in the first few days of life,
they cried more, startled more easily and were more jittery. The authors said
this may interfere with mother-child bonding.
Harkany et al. in
a paper in January 2007 found that endocannabinoid signaling modulates CNS
(Central Nervous System) patterning so that “pharmacological interference with
endocannabinoid signals during foetal development leads to long-lasting
modifications of synaptic structure and functioning. Marijuana abuse during pregnancy can impair
social behaviours, cognition and motor functions in the offspring with the
impact lasting into adulthood”.
Another paper in
May 2007 had similar findings. Endocannabinoids in the human body play a vital
role in the development of a baby’s brain. They are responsible for controlling
how the complex system of nerves develop in the embryonic brain. Dr Ann
Rajnicek said “Smoking cannabis could interfere with the signals that are being
used in the brain to wire it up correctly in the first place. As the brain
develops further, there will be functional problems – potential brain damage”
(Berghuis et al. 2007).
The most recent
study on the effects of pre-natal marijuana exposure (Day et al September 2006)
has concluded that, “Prenatal exposure to marijuana, in addition to other
factors, is a significant predictor of marijuana use at age 14”. Other
variables controlled for were the child’s current alcohol and tobacco abuse,
pubertal stage, sexual activity, peer drug use, delinquency, family history of
drug abuse and parental depression, current drug use, strictness and levels of
supervision.
The reason for the late
appearance of this damage is assumed to be that the functions involved are
“executive” cognitive functions that are not taken into use until the child is
four to six years old. Another long-term study shows similar associations
between exposure during the foetal stage and relatively late (at age 6 and 10
respectively) behavioural disturbances (Ramstrom, 2003).
CANNABIS HARMS – EFFECTS ON THE BRAIN
It is undeniable that cannabis
affects brain function adversely. The
evidence is conclusive that heavy marijuana use for five years or more may
impair memory and slow cognitive function.
Moreover, while the impairment
was greater among long term users, (those who regularly used marijuana for at
least 10 years), it was also evident among those who used for only five years.
These findings support other studies that have linked long term marijuana use
to “subtle deficits in specific neuropsychological domains” (Lambros, 2006).
Short-term effects of cannabis
can include problems with memory and learning, distorted perception, difficulty
in thinking and problem solving, loss of coordination, and increased heart
rate. Long-term marijuana abuse indicates some changes in the brain similar to
those seen after long-term abuse of other major drugs (Rodriguez de Fonseca,
1997).
Cannabinoid receptors are found
in the parts of the brain that influence pleasure, memory, thought, concentration,
sensory and time perception, and coordinated movement (Herkenham, 1990).
Diffusion tensor imaging
(DTI), studied the brains of groups of adolescents comparing, healthy, non-drug
users, heavy marijuana smokers (daily use for at least one year), and
schizophrenic patients. Unlike magnetic resonance imaging (MRI), which provides
a static picture of brain structures, DTI detects and measures the motion of
water molecules in the brain, which can reveal microscopic abnormalities. DTI is used to examine the arcuate
fasciculus, a bundle of fibres’ connecting the Broca’s area in the left frontal
lobe and the Wernicke’s area in the left temporal lobe of the brain. Researchers found that repeated exposure to
marijuana was related to abnormalities in the development of this fibre
pathway, which is associated with the higher aspects of language auditory
functions (Manzar, 2005).
Because the language/auditory
pathway continues to develop during adolescence, it is most susceptible to the
neurotoxins introduced into the body through marijuana use. (Manzar,
2005). Smoking marijuana often causes
temporary problems with memory and learning. Tetrahydrocannabinoid (THC)
disrupts the way nerves fire in the brain’s memory centre. This helps explain
why users high on marijuana sometimes
lose their train of thought in mid-sentence (Robbe, 2006).
This study demonstrates
abnormal brain chemistry in otherwise healthy chronic marijuana
users and some additive and
interactive effects on brain chemistry in HIV patients who used
marijuana chronically (Chang,
2006). The brain is not fully developed
until after the early
20’s (Giedd, 1999). The brain system that regulates logic and
reasoning develops before the
area that regulates impulse
and emotions. The immature brains are
not capable of avoiding
risky behaviours the mere
physical presence of peers increased the likelihood of teens taking
risks (Giedd, 2007).
Evidence on brain development
clearly demonstrates that the adolescent brain, which is still developing, is
particularly vulnerable to the ill effects of substance abuse, including
cannabis (Chambers 2003, Pistis, 2004).
Adolescents seem to be at particular risk for numerous negative
psychosocial consequences from marijuana use (Fergusson, 2002, Stefanis, 2004). In addition, several large longitudinal
studies have demonstrated a link between cannabis use during adolescence and
later development of mood disorders and schizophrenia (Arseneault 2002, Zammit
2002, Patton 2002).
The dorsal lateral prefrontal
cortex, important for controlling impulses, is among the brain regions to
mature without reaching adult dimensions until the early 20s. It is therefore
vital that cannabis not be used until the brain matures. (Giedd, 2004).
Drug abusers may experience
similar changes in the patterns of global gene expression in their brains,
irrespective of their drug of choice.
Whether long-time drug abusers favour cocaine, marijuana, or PCP, their autopsied brains
showed a number of common gene changes consistent with diminished brain
plasticity i.e. the ability to learn from new experiences and adapt to new
situations. Therefore, brain functions
may be similarly impaired as the result of chronically abusing different drugs
(Lehrmann, 2006).
Futher evidence suggest a neural
mechanism by which disinhibition of angry aggression may occur in those
individuals who, by virtue of affective impulsivity or mental disorder, are
predisposed to respond to cannabis with acts of violence while in a confused or
psychotic state (Niveau and Dang 2003, Howard and Menkes 2007).
CANNABIS HARMS – COGNITIVE EFFECTS
Cannabis induces loss of
internal control and cognitive impairments, especially of attention and memory,
for the duration of intoxication. Heavy
cannabis use is associated with reduced function of the attention/executive
system, as exhibited by decreased mental flexibility, increased perseveration,
and reduced learning, to shift and/or sustain attention (Lundqvist, 2005). Two very important parameters of driving
ability, namely perceptual motor speed and accuracy, seem to be impaired
immediately after cannabis consumption (Kurathaler, 1999).
A controlled clinical study
demonstrated the negative influence on fitness to drive after medium or high
dose oral THC or the synthetic cannabinoid Dronabinol (Menetrey, 2005). There is no dispute that cannabis
causes cognitive impairment during acute intoxication. The effects can be shown using driving or flight
simulators. It is very clear that
regular cannabis use (several times a week) is associated with impaired
functioning-both by objective measurements and by the admission of users
themselves (Pope Jr, 2004).
Regular cannabis users are
significantly more prone to cognitive and perceptual distortions as well as
disorganisation, but not interpersonal deficits, than non-regular users and
those who have never used (Schiffman, 2005). There may be a developmental
relationship between cannabis use and schizotypal symptoms (Bailey, 2004).
The most recent evidence on cannabis and cognitive functioning comes
from
(Ranganathan, 2006) reviewed the literature on the acute effects of
cannabinoids on memory tasks in humans.
Their conclusion suggested that cannabinoids impair all stages of memory
including encoding, consolidation and retrieval.
The measures on which the heavy abusers had comparative deficits
included verbal and visual memory, executive functioning, visual perception
psychomotor speed, and manual dexterity.
On some tests, quantity of marijuana use accounted for more than half
the variance in test scores. “We found a
dose-response relationship the more marijuana people used, the worse they
performed on the tests, especially those for memory.” Cognitive performance in individuals with
lower IQ scores decreased as the number of joints smoked per week increased,
while those with higher IQ scores had fewer decrements even as marijuana use
increased. “This finding demonstrates
the concept of cognitive reserve, people with higher IQs do better than those
with lower IQs; the fewer cognitive reserves you have, the more impact you will
see from a slight change in brain function” (Bolla, 2002).
Solowij et al. examined the effects of the duration of cannabis use on
specified areas of cognitive functioning among users seeking treatment for
cannabis dependence. Their results confirmed that long-term heavy cannabis
users show impairments in memory and attention that endure beyond the period of
intoxication and worsen with increasing years of regular cannabis use. Bolla
and colleagues also found heavy cannabis use to be associated with persistent
decrements in neurocognitive performance even after 28 days of abstention. They
said it was unclear if these decrements would resolve with continued abstinence
or grow progressively worse with continued heavy marijuana use. (Solowij,
2002).
CANNABIS AND DEPRESSION
Longitudinal research has
provided evidence of a connection between marijuana use, depression and suicide. One 16-year study showed that individuals who were
not depressed and then used marijuana were four times more likely to be
depressed at follow up.
(Bovasso, 2001).
Another study investigated
changes over a 14-year period and found that marijuana use was a predictor of
later major depressive disorder (Brook, 2002).
This study of 1,265
A study of 3,239 Australian
young adults from birth to age 21 found a relationship between early
initiation, and frequent use of cannabis and symptoms of anxiety and
depression, regardless of a personal or family history of mental illness.
(Hayatbakhsh, 2007).
CANNABIS HARMS – PSYCHOSIS
Cannabis,
particularly hydroponically grown cannabis, contributes to
drug induced psychosis.
In 2002 there were close to
40,000 hospitalisations across
Mental
health admissions in England due to cannabis were up 946 in 2005-6, a rise of
65 per cent over the last five years Professor Robin Murray, Professor of
Psychiatry at the London Institute of Psychiatry and member of the Royal
College of Psychiatrists said: “ There is
no doubt that cannabis-related psychiatric problems have increased
substantially. This might be down to
better recognition, but I would say these figures are just the tip of the
iceberg. It’s only more recently
that psychiatrists have understood the importance of cannabis use”.
Epidemiological evidence
suggests a persistent association between cannabis use and psychosis that is
robust in the face of methodological challenges. Neuroscientific studies show that cannabis
may lead to psychosis through effects on the processing of dopamine in the
brain. Taken together, this evidence
suggests a causal relation in which frequent use of cannabis leads to a greater
risk of psychotic symptoms (Fergusson, 2006).
A three year follow-up of a Dutch group of
4,045 people free of psychosis and 59 with a baseline diagnosis of psychotic
disorders showed a strong association between use of cannabis and psychosis
(Van Os, 2002).
Exposure to cannabis during
adolescence and young adulthood increases the risk of psychotic symptoms later
in life. The findings confirm earlier suggestions that this association is
stronger for individuals with predisposition for psychosis (Van Os, 2002 and
Verdoux, 2003) and stronger for the more severe psychotic outcomes. Frequent use of cannabis was associated with
higher levels of risk in a dose-response fashion. Associations were independent of other
variables known to increase the risk for psychosis. Also, the effect of cannabis remained
significant after correction for baseline use of other drugs, tobacco, and
alcohol (Henquet, 2004).
An appreciable proportion of cannabis users report short-lived adverse
effects, including psychotic states following heavy consumption, and regular
users are at risk of dependence. People
with major mental illnesses such as schizophrenia are especially vulnerable in
that cannabis generally provokes relapse and aggravates existing symptoms
(Andrews, 2001).
Cannabis-induced psychotic
symptoms are important risk factors for subsequent development of severe
psychopathological disorder. This is in
contrast to previous studies describing the condition as harmless (Arendt,
2005).
A 15-year study conducted in
An extensive analysis of 35
longitudinal studies found that marijuana use increases the risk of developing
schizophrenia by 40 percent. The authors
conclude that “there is now sufficient evidence to warn young people that using
cannabis could increase their risk of developing a psychotic illness later in
life.” (
Cécile Henquet, PhD (Department of Psychiatry
and Neuropsychology, South Limburg Mental Health Research and Teaching Network,
European Graduate School of Neuroscience, Maastricht University, Maastricht,
The Netherlands), discussed her research on a recently discovered gene-environment
interaction in the context of psychosis a multifactorial disease with both
genetic and environmental factors (Henquet, 2006). Several risk factors, such as prenatal
exposure to the influenza virus and urban place of birth and upbringing, although
controversial, have been associated with odds ratios (OR) in the range of 1.2
to 2.4. (Selten 1999, Takei 1994, Van Os 2003, Pedersen 2006 and Selten 2005).
On the other hand, the relative risk for a first-degree relative of someone
with schizophrenia is approximately 10.0, suggesting a prominent role for
genetics in the etiology of schizophrenia. Nonetheless, only weak evidence
exists for specific susceptibility genes for schizophrenia despite numerous
studies evaluating the potential association of candidate genes.
Recent years have witnessed a clear association
between cannabis and psychosis, though the causal nature of this association is
still somewhat controversial. In a recent meta-analysis, the pooled estimate
for the development of psychosis associated with prior cannabis use was an OR
of 2.1 (95% confidence interval [CI], 1.7 to 2.5) (Henquet, 2005). The risk is
higher for those using cannabis in adolescence and in those with greater
vulnerability toward the disease (Arseneault, 2004). Many people who use cannabis do not develop
schizophrenia, and many individuals with schizophrenia have never used the
drug. These converging lines of evidence suggest that a gene-environment
interaction may underlie the association between cannabis use and schizophrenia.
A gene-environment interaction occurs when specific genes moderate the
individual's sensitivity to an environmental risk factor. Dr. Henquet reviewed
the criteria for identifying a gene-environment interaction described by
Moffitt and colleagues (Moffitt, 2005).
One gene of substantial interest to
schizophrenia researchers is the Ceatechol-O-Methyl Transferase (COMT)
gene, and specifically the Val158Met functional polymorphism. Though only
weakly associated with risk for psychotic illness, this polymorphism is
associated with working memory and executive functioning, both of which are
part of the cognitive phenotype of the illness. The Val/Val genotype is
associated with higher enzymatic activity and lower dopamine levels in the
prefrontal cortex, compared with the Met/Met genotype (with the Val/Met
genotype being in between). In a recent sentinel study, Caspi and co-workers
(Caspi, 2005) confirmed the hypothesis that those with the Val/Val genotype are
more vulnerable to psychosis when exposed to cannabis during adolescence versus
those with the Met/Met genotype (Caspi, 2005).
Thus, the COMT Val158Met polymorphism genotype appears to moderate the
effects of adolescent-onset cannabis use on the later development of
psychosis. Cannabis use increases the
risk of psychotic symptoms in young people, particularly those with an
underlying predisposition for psychosis (Henquet, 2005).
Cannabis
is the most widely used illegal drug in -O-Methyl
Tranferase (COMT) is an enzyme in the brain that breaks down the dopamine.
Drugs, such as cannabis, release an excessive amount of dopamine. The enzyme
COMT is responsible for the metabolisation of dopamine. But 27% of the
population possesses the weak VAL/VAL type of the COMT enzyme, and as a
consequence, cannabis users with the VAL/VAL type of the COMT enzyme have a 10
times greater risk of developing psychosis. These people are also more at risk
to develop schizophrenia later in life.
Dr.
Robin Murray explained during an interview on the BBC, psychosis is due to an
excess of dopamine in the middle of the brain and it is known that an excess of
dopamine for any reason can make a person psychotic. The other function of
dopamine is that it is a reward or pleasure chemical. Similarly all the drugs
that used to treat psychosis decrease dopamine in the mid-section of the brain.
When cannabis is consumed it stimulates the dopamine system and for most it
simply gives pleasure, while for those vulnerable the stimulation of the
dopamine system can induce psychosis.
It is known that in adolescence there are many changes in dopamine
receptors, and if cannabis is first used while the brain is still developing,
it is possible that while they are sculpted into a final sort adult
pattern, that cannabis can alter these receptors permanently. (
A number of studies add to the
growing body of evidence suggesting that regular cannabis use may increase
risks of psychosis. (Fergusson, 2005) suggests that: (a) the association between use and
psychotic symptoms is unlikely to be due to confounding factors; and (b) the
direction of causality is from cannabis use to psychotic symptoms. It is crucial that emerging evidence about
the links between cannabis use and mental-health problems is communicated
clearly (particularly to those most at risk) and in a way that acknowledges the
complexity of the issues involved without obscuring the level; and gravity of
the risks posed by cannabis use to vulnerable groups (Degenhardt, 2007). People
who used cannabis had a greater risk of developing psychotic outcome than
people who didn’t use cannabis. There is
a need to warn the public of these dangers, as well as to establish treatment
to help young, frequent cannabis users (Zammit, 2007)
While there have been scientific
questions asked of this study which interviewed 50,087 members of the Swedish
Army, the British Medical Journal (BMJ)
in 2002 reported on a longer follow up study and re-analysis of the data. Those who were heavy consumers of cannabis at
age 18 were over 600% more likely to be diagnosed with schizophrenia over the
next 15 years than those did not use cannabis.
It confirmed that the Swedish findings were correct. It clarified that cannabis use and not other
drugs, was associated with later schizophrenia (Zammit 2002).
In a study using new
brain-scanning techniques (Kumra, 2007) identified abnormalities in
schizophrenics which the author concludes are the same abnormalities in
adolescents who frequently use cannabis. These defects are in that part of the
brain still developing during adolescence and associated with emotion and other
higher cognitive functions such as language, perception, creativity, and
problem solving.
Frontal and Limbic regions may
not be equally vulnerable to gray matter attrition, which is consistent with
cognitive, metabolic, and functional vulnerability of frontal cortices in
schizophrenia.
(Vidal, 2006). Cannabis use in
the year prior to presentation with schizophrenia increased markedly between
1965 and 1999, disproportionately so compared to increase in cannabis use in
other psychiatric disorders. (Boydell, 2006).
A review paper found that the same areas of the
brain that show cognitive dysfunction or problems in thinking and reasoning,
are similar among heavy or long-term marijuana users and schizophrenics
(Solowij, 2007). A study from
A review of 35 longitudinal studies found that
cannabis use increased the risk of developing a psychotic illness, such as
schizophrenia, by 40 percent compared to non-users. The risk is doubled for frequent or heavy
marijuana users, compared to non-users.
The authors concluded “there is now sufficient evidence to warn young
people that using cannabis could increase their risk of developing a psychotic
illness later in life” (Moore et al. 2007).
This review found growing evidence that
cannabis use can cause acute psychosis, as well as increasing the likelihood of
an early, first schizophrenic episode.
It also concludes that cannabis use would worsen the prognosis with
psychotic disorders (Rey, 2007).
Another review also tried to
determine whether cannabis is a cause of schizophrenia. All the available population-based studies on
the issue have found that cannabis use is associated with later schizophrenia
outcomes. All studies support the
concept of temporal priority by showing that cannabis use most probably
preceded schizophrenia. They also
provide evidence for directional by showing that the association between
adolescent cannabis use and adult psychosis persists after controlling for many
potential confounding variables such as disturbed behaviour, low IQ, place of
upbringing, cigarette smoking, poor social integration, gender, age, ethnic
group, level of education, unemployment, single marital status and previous
psychotic symptoms (Ramstrom, 2003).
(D’ Souza, 2005) found that
Delta-9-tetrahydrocannabinol is associated with transient exacerbation in core
psychotic and cognitive deficits in schizophrenia.
Evidence suggests that
cannabis is a component cause in its development and prognosis, in which
mechanisms of gene-environment interaction are most likely to explain this
association (Henquet, 2005).
The available evidence
supports the hypothesis that cannabis is an independent risk factor, both for
psychosis and development of psychosis symptoms. Addressing cannabis use, particularly in
vulnerable populations, is likely to have beneficial effects on psychiatric
morbidity (Semple, 2005).
Prior cannabis use was
recorded at index admission for 112 participants in the
Further evidence for a causal
relationship is provided by the presence of a dose-response relationship
between cannabis use and schizophrenia (Andreasson et al. 1988; van Os et al.
2002; Zammit et al. 2002) specificity of exposure (Arseneault et al. 2002; Van
Os et al. 2002; Zammit et al. 2002; Fergusson et al. 2003) and specificity of
the outcome (Arseneault et al. 2002).
Overall, cannabis use appears to confer a twofold risk of later schizophreniform
disorder (Arseneault, 2004).
Cannabis-induced psychotic disorders are of great clinical and
prognostic importance (Arendt 2005).
A paper,
“Cannabinoids Influence Lipid-Arachidonic Acid Pathways in Schizophrenia”
(Smesny et al. 2007) concluded, “Results demonstrate an impact of long-term
cannabis use on lipid-arachidonic acid pathways. Considering pre-existing
vulnerability of lipid metabolism in schizophrenia, observed effects of
cannabis use support the notion of a gene x environment interaction”.
CANNABIS HARMS
- SUICIDE
A study by (Beautrais et al.
1999) examined the relationship between cannabis abuse/dependence and risk of
medically serious suicide attempts among 302 individuals attempting suicide and
1,028 random controls and found that marijuana use may be connected to the risk
of a serious suicide attempt. Another
study (Fergusson, 2002) of 1,265
Young people aged 12 to 17 who
smoke marijuana weekly are three times more likely than non-users to have
thoughts about committing suicide. (Greenblatt, 1998). A study of 600 same-sex twins, one of whom
was dependent upon marijuana and one of whom was not found that the twin who was
dependent on marijuana was almost three times more likely to think about
suicide and attempt suicide than his/her non-marijuana dependent co-twin
(Lynskey et al. 2004).
Cannabis using schizophrenic patients
were more likely to be younger and male than non users. The duration of
hospitalisation was significantly longer for the group with cannabis abuse and
the prevalence of suicide attempts in schizophrenia is closely correlated to
cannabis abuse (Dervaux, 2003).
It was found that there is a
convincing relationship between suicidal behaviour and cannabis use, the latter
awakening depressive experiences (Maharajh, 2005). Nevertheless, the possibility remains that
cannabis abuse/dependence may make an independent contribution to risk of
serious suicide attempt, both directly and through the possible effects of
cannabis abuse on risk of other mental disorders (Beautrais, 1999).
See Appendix B for media articles supporting this section
CANNABIS
EFFECTS ON THE AUSTRALIAN INDIGENOUS
COMMUNITY
Among those interviewed in
Aboriginal communities in
Substance misuse is both the cause and result
considerable pain and suffering in Aboriginal communities and is linked to
other issues such as dispossession, physical and mental ill-health, poverty,
unemployment, loss of cultural identity, family violence and imprisonment.
It is clear from literature available that the range
of illicit drugs commonly available has an impact on the Aboriginal community.
Alcohol, heroin, prescription drugs, cannabis, amphetamines and volatile
substances all form part of the recurring theme of increased poly drug use by
Aboriginal people. The Australian Bureau of Statistics reports that illicit
drug experimentation and use is more widespread among the Aboriginal urban
community than the general community with some 50% (compared with 38% of the
general population) having tried at least one illicit drug and 24% having used an
illicit drug in the past 12 months (compared with 15% of the general
population). (South Australia Department of State Aboriginal Affairs 2002).
After tobacco and alcohol, cannabis—known as “ganja”
to the children—was the most frequently used drug. The kids who had used
cannabis eight or more times in the previous month, and twice or more in the
previous week, were arbitrarily classified as frequent users; and those who had
used it less frequently as occasional users. The mean age at which cannabis was
first used was 12.4 years. (Gray, 1996)
Increasing anecdotal and other documented evidence
have now become available to suggest that the use of cannabis, particularly
amongst young ATSI people, is becoming more prevalent. Obviously the use of any
drugs by young people can have a negative impact on their development. The
advice received by the Australian National Council on Drugs (ANCD), that there
is a general belief amongst young people that cannabis is harmless, is a
further cause for concern (ANCD, 2002).
Recent literature and anecdote suggest high rates of
cannabis use among Indigenous people in remote communities in Australia’s
Northern Territory (NT) with rapid and widespread uptake occurring from the
late 1990s (Clough, Cairney, 2002). A
survey in the mid-1980s did not detect cannabis use in the NT’s ‘Top End’
communities (Watson 1987). But by the late 1990s, unpublished data collected by
one of (ANCD).
Unpublished data collected by a co-worker suggested
that 31% of males and 8% of females (aged over 15 years) were using cannabis in
eastern
Of current concern is the possibility that cannabis
use combined with alcohol use, perhaps in association with co-morbid mental
disorders (Beautrais, 1999) lowers the threshold of suicide risk in those
already disinhibited by alcohol use
(Hillman, 2000) even though average consumption levels appear moderate.
Further study is required to more clearly describe harzardous alcohol use and
cannabis use in combination in this population. In the meantime, data reported
here should alert policy makers in the NT to unusually high rates of cannabis
use in Indigenous communities especially among males. The close association
between cannabis use, alcohol use, petrol sniffing and the use of other illicit
drugs needs to be closely monitored. The data also suggest that the impact of
the cannabis trade on community economies is substantial. Urgent action in
close consultation with communities is warranted in order to reduce cannabis
use and to reduce the combined use of cannabis with other substances,
especially alcohol (Clough, Abbs 2002).
One of the most important Government Report in 2007 in
the view of Drug Free Australia (DFA) was by The Northern Territory Board of
Inquiry called Ampe Akelyernemane Meke
Mekarle “Little Children are Sacred” which found that cannabis which found that cannabis use was identified
as a significant issue at nearly every community meeting it held. Participants
in these meetings related that cannabis is present in their community and they
believe it was having negative effects on community and family life and in
particular, with consequential negative effect on the care and protection of
children. The Inquiry formed a view that the use of cannabis in Indigenous
communities is widespread, particularly among young people, with age of
initiation to first use decreasing. This is of great concern because of the
harms associated with its use. Regarding cannabis in particular, the Inquiry
acknowledges the need for action in three areas - prevention, intervention and
enforcement.
The Inquiry also noted the comments of Dr Alan Clough,
who has clearly shown the harm cause by cannabis by his research over a number
of years and long before the (NDARC)
2007 report on cannabis it should be noted that Jan Copeland of NDARC report “Illicit drug use in Australia:Epidemiology, use patterns and
associated harm 2nd Edition” cites Dr. Clough’s research a
number of times but still says “Rates of cannabis use among indigenous
Australia, however, appear to have increased over this time but data is of poor quality” Chapter 4:
page 4 Jan Copeland conclusion regarding
cannabis use by Indigenous communities in the Northern Territory. “it’s important to remember that this is
the most remote and under funded research battlefield in Australia and more
weight should be given by NDARC and ANCD to Dr. Alan Clough and others research
it is DFA view that the use of this type of wording is without merit and has
been used by some scientist hire by the tobacco industry for over forty years
for the late 1950’s. It appears that only the few indigenous communities in
Rates of cannabis use among indigenous Australian,
however, appear to have increased over this time but the data is of poor
quality. It must be noted that at the
date of this publication both the ANCD and NDARC in its leadership role for the National Cannabis strategy,
have not publicly come out with any strong support or programs to support the
Inquiry Ampe Akelyernemane Meke Mekarle
“Little Children are Sacred” Recommendation
number 70.
Recommendation 70
That government develop and implement a multi-faceted
approach to address the abuse
of illicit substances in Aboriginal communities, in
particular cannabis abuse, including
prevention, intervention and enforcement strategies which
recognise:
a.
the geographic context of substance abuse, that is, urban and remote locations
and the implications this has for effective
prevention, intervention and enforcement.
b. population-based, youth-focused
prevention and intervention strategies that integrate substance abuse, mental health,
and other health and welfare concerns into youth programs.
There is little national data available on drug use
amongst Aboriginal and Torres Straight Islander (ATSI) people. Based on the
1998 National Drug Strategy Household survey, illicit drug use is more
widespread among the ATSI urban community than in the general population,
though the low number of ATSI people interviewed needs to be acknowledged.
Nonetheless it is reported that 50% have tried an
illicit drug compared with 38% in the general community. 24% are current users
compared with 15% in the general population with marijuana being the most
popular illicit drug.
CANNABIS HARMS –
AMOTIVATIONAL SYNDROME (BURN OUT)
(Smith 1968) introduced the term “amotivational
syndrome”, and in the same year (McGlothin, West 1968) described the particular
personality traits of cannabis smokers under the heading of “amotivational
personality characteristics”. These two notions referred to the same condition,
which the researchers had observed mainly in North American young people
(Cohen, 1982). Although it has been difficult to find scientific evidence for
the existence of such a cannabis-induced syndrome, the ubiquity of the term
“amotivational syndrome” is remarkable. It is clear that it has struck a chord
as an apt description of the particular personality traits frequently observed
in chronic cannabis smokers.
At the scientific level, it has been difficult to pin
down this condition, which refers to a cannabis-induced mental state
characterised by “apathy, loss of effectiveness, and reduced ability to carry
out complex, long-term plans, deal with frustration, concentrate for any length
of time, follow routines, or deal successfully with new situations” (Cohen,
1982). Yet remarkably, the descriptions
of the condition tally with historical observations of large-scale consumers of
cannabis preparations in certain developing countries.
The clinical reports that support the existence of
amotivational syndrome appear primarily to build on observations of young
individuals in Western industrialised countries (Cohen in Marijuana and Youth, 1982; Tunving, 1987). (Newcomb, Bentler 1988)
also claimed to have found some evidence supporting the existence of
amotivational syndrome in their longitudinal study of a large group of young
people.
(Cohen 1982), drawing support from a study by (Soueif
1976), claims that chronic cannabis abuse does not produce these
motivation-inhibiting effects in illiterate abusers who are manual labourers
and live in a rural, intellectually less demanding culture. Instead, those
affected by the condition are mostly young people living in the complex, urban
environments of the modern Western world, where considerable demands are made
on people with regard to intellectual performance, a readiness to adapt rapidly
to change and a willingness to re-learn quickly.
What (Soueif 1976) discovered was that the differences
(in terms of scores on tests of cognitive and psychomotor functions) observed
in a large study between a group of chronic cannabis smokers and a group of
non-smokers more or less disappeared when the subgroup of “illiterate rural
people” within the broader group of cannabis smokers was compared with the
non-smokers. On the other hand, the differences were amplified when the
subgroup of “literate urban people” was compared with the non-smokers.
Musty and Kaback (1995) maintain that amotivational
syndrome does exist, but that it is a manifestation of depression. However, the
study is unclear on a number of points relating to the delimitation of the
definition of depression; and moreover, the methodology used to measure the
study group’s poor level of motivation is open to question.
Amongst the cognitive
functions considered, memory-related, attention-related, psychomotor and
motivation-related functions were proven deteriorated by acute and chronic
cannabis use. This is very important in
that, especially among teenagers, as negative alteration at the social and
academic level could be the outcome. (Karila, 2005).
One circumstance worth drawing attention to is the
fact that in many studies, including the two just mentioned, poor levels of
motivation are equated with lower scores on tests that primarily measure
cognitive and psychomotor ability. While the effect exerted by chronic cannabis
smoking on cognitive functions undoubtedly affects mental processes that may
contribute to “amotivation”, the processes we are dealing with here are
probably not exclusively cognitive in nature.
In conclusion, then, it can be said that the term
“amotivational syndrome” seems to be a strikingly apt description of the
particular psychosocial personality traits of a not insignificant proportion of
chronic cannabis abusers, especially among young cannabis smokers in Western
industrialised countries. These traits, which seem to be elusive to scientific
documentation, can be confused with or reinforce other states or conditions,
including periods of regression during the teenage years which are appropriate
to that phase from the perspective of developmental psychology, as well as
depression, chronic tranquil schizophrenic psychosis and certain personality
disorders.
These psychosocial
personality traits are in all probability nothing other than a manifestation of
certain effects of chronic cannabis intoxication. This would be consistent with the varying frequency
of occurrence and with the way in which the syndrome is dependent on the
psychosocial circumstances of the individual.
The markedness of these personality traits would seem
to be dependent on the “cerebral reserve” at the individual’s disposal as well
as on the social demands placed upon him or her. It seems reasonable to say
that our modern high-tech society, with the many demands it places on
individuals and its rapid pace of change, is a social environment that is more
or less incompatible with chronic cannabis intoxication.
CANNABIS HARMS –
IMPAIRED DRIVING ABILITY
Road fatalities related to marijuana
intoxication have steadily increased over the last 10 years (Drummer, 1994;
Drummer, 1998; Drummer & Gerostamoulos, 1999). This has led to the
introduction of sobriety testing in
These findings indicate that marijuana impairs driving
ability and since the prevalence of marijuana use is high among young
Australians this poses a significant risk on our roads. While cannabis
manifests differently to alcohol, it can be equally as dangerous. The study also found that driver errors
occurred more frequently when the driver was under the influence of cannabis and alcohol
(Papafotiou, 2001, 2005).
Drugs are detected commonly among those involved in
motor vehicle accidents, with studies reporting up to 25% of accident-involved
drivers positive for drugs. Cannabis is
generally the most common drug detected in accident-involved drivers (Kelly,
2004). Furthermore, the use of cannabis
is associated with an increased incidence of trauma, increased number of
injuries, increased trauma severity and longer hospital stays (Griggs, 2007).
One paper found the risk of accident when cannabis was
combined with alcohol was 16 times higher than use of either drug alone. Since the two are frequently taken together,
this is an important warning for young people.
A positive test for cannabis alone was associated with a three times
greater risk of being responsible for a fatal road crash (Laumon et al. 2005).
The acute effects of cannabis can adversely affect
driving ability and increase the risk
of an accident. Laboratory studies have shown that
even low doses of THC compromise
reaction time, attention, decision making, time and
distance perception, short term
memory, hand-eye coordination and concentration. Overall, most (but not all) driving simulator
studies, field studies of accidents, and self-report studies have shown that
cannabis has an adverse effect on driving.(McLaren & Mattick, Monograph No. 57
Cannabis in Australia)
In an appalling example of drug driving on a Victorian
country road, a 38-year-old driver, high on marijuana sailed right through an
intersection. The driver was so stoned he didn’t realize he had to give
way. The result was catastrophic. Seven people were instantly wiped out,
incinerated by the explosive impact (Sixty-Minutes
“Out of Control” 20.9.07). Random roadside drug testing of motorists for
cannabis has been initiated and will be continued by Victoria Police. Drug-drivers are seen as a threat to others
on the road and testing is considered to enhance road safety by removing such
drivers (Victoria Police 2006).
SECTION 3 – QUITTING CANNABIS
QUITTING CANNABIS
While it is acknowledged that it is far easier and
less expensive to adopt preventative measures than treatment, for those who are
addicted to cannabis, it is important to provide the means to be able to stop
smoking – just as it is with tobacco smoking.
Professionals working with cannabis dependent people
often see them relapse repeatedly.
Relapse may involve the length of detoxification; ease of access to the
substance; social pressure `to use marijuana in many school, work,
entertainment, social and family settings; persistent denial; or the high level
of functioning many addicts have when they entre recovery. Marijuana addicts who
have not shown extensive drinking histories often believe they can consume
alcohol and this can lead to marijuana relapse as well. (Chacin, 1996).
Clients in treatment require a sense of hope and
positive expectations are especially critical when facing a protracted period
of withdrawal. (Zweben, O’Connell,1992).
Programs designed to aid cessation should focus on the
negative effects of marijuana and should offer alternative ways to relieve
negative physical and psychological conditions such as stress (Weiner, 1999).
There is a need for effective treatment of cannabis
misuse. Psychological therapies have
been developed based on principles of motivational interviewing,
cognitive-behavioural therapy and relapse prevention. The evidence base for these therapies is
explored in this review, and studies targeting both adult users and young
people are considered. Possible new
pharmacological treatments are also discussed. (Maddock, Babbs,
2006).
Contributors (Roffman, Stephens, Marlatt 2006) to
“Cannabis Dependence, Its Nature, Consequences and Treatment” say the symptoms
of cannabis withdrawal are: “irritability, anger, nervousness, sleep
difficulty, change in appetite, physical discomfort”.
The Editor of the same publication states that
research shows that staying clean is just as hard for cannabis addicts as for
heroin addicts “Our findings confirm previous reports of an abstinence syndrome
associated with chronic marijuana use and suggest that aggressive behavior should
be an additional component of this syndrome” (Kouri, 1999).
Cannabis dependence is a relatively common phenomenon
associated with significant psychosocial impairment. Basic research has identified a
neurobiological system specific to the actions of cannabinoids. Human and nonhuman studies have demonstrated
a valid withdrawal syndrome that is relatively common among heavy marijuana
users. Last, clinical trails evaluating
treatment for cannabis dependence suggest that this disorder, like other substance
dependence disorders, is responsive to intervention, yet the majority of
patients have difficulty achieving and maintaining abstinence (Budney, Brent
and Moore, 2002).
Recent research shows that a significant number of
adults are dependent on marijuana and experience negative consequences
secondary to their use of marijuana. This is found in a treatment manual by
Substance Abuse and Mental Health Services Administration SAMHSA called “Brief Counseling for Marijuana Dependence a
Manual for Treating Adults”. Increasing
evidence suggests that counseling for marijuana dependence is effective. The
abovementioned manual outlines procedures for individuals who use marijuana
chronically as their primary drug. They tend not to seek treatment in
traditional drug treatment settings, but it appears from the Marijuana
Treatment Project (MTP) and other studies that when given the opportunity, they
respond to treatment.
Given the promising initial research on treatment for
cannabis dependence and the potential benefits of brief motivational and
cognitive behavioral relapse prevention therapies, there is now sufficient
evidence to support the development of focused treatment programs for this
population. The manual-guided therapies developed for these projects, particularly
Marijuana Treatment Project MTP,
should be transferable to specialised outpatient clinics and to behavioral
health care practitioners. Evidence
suggests that counseling for marijuana dependence is effective and accompanied
by other positive changes in client’s lives (Steinberg et al. 2002, SAMHSA
2005).
Increased recognition that marijuana can
cause addiction and significant negative consequences in a subset of users has
prompted the development of marijuana-specific interventions and treatment materials
paralleling those for other substance use disorders. These advances have
increased users’ and caregivers’ perceptions that it is acceptable to seek and
provide treatment for marijuana use and have contributed to an increase in the
number of individuals requesting help. Optimistic expectations for enhancements
to current treatment approaches appear warranted, as our growing understanding
of the principles underlying behavioral treatments continues to produce
innovative applications that demonstrate incremental gains in efficacy. Rapid
advances in the neurobiology associated with marijuana and the cannabinoid
system provide further hope for increasingly effective treatment options. As well, check-up interventions hold promise
both for preventing more severe cases of marijuana dependence and for
increasing therapeutic contacts with marijuana abusers who might benefit from
treatment (Budney 2007).
Not one, of the approximately 15,000 studies up to the
end of 2007 on cannabis has given it a clean bill of health. Cannabis has a harmful effect on many organs
of the body.
Research literature has long
shown a link between marijuana use and a wide variety of adverse effects on an
individual’s and community health. It is
also linked to illnesses such as depression, schizophrenia, and suicidal
ideation. Beyond comorbidity, however,
more recent research makes a stronger case that cannabis smoking itself is a causal agent in psychiatric symptoms,
particularly schizophrenia. During the
past five years a number of prominent studies have strengthened our
understanding of that association and found that the age when marijuana is
first smoked and the frequency of use are crucial risk factors in later
development of mental health problems.
SECTION 4 – RECOMMENDATIONS
RECOMMENDATIONS
The
evidence is clear that the younger the age of initiation to cannabis use, the
greater the risk of harmful effects to the individual. The following
recommendations aim to provide advice and strategies to politicians,
decision-makers and researchers to ensure that the level of cannabis use in
:
Drug Free Australia’s research recommends:
- That all Australian Governments
urgently implement effective preventative drug education in all States and
Territories, focusing on cannabis in both primary and secondary schools
and further, that this education includes the latest scientific research
on the harmful effects of cannabis on the developing brain, together with
information on issues related to the risk of suicide, schizophrenia and
depression.
- That the
Federal Government urgently implements a national media campaign, similar
to the “Bloody Idiot” alcohol campaign, in order to inform the community
of the harmful effects of cannabis use for all community members (parents,
teachers, police, sports people etc). This would be an appropriate respond
to the concerns of the Australian community, as measured in the
Pfizer/NDARC report of 2007, in where 77% of Australian expected the
government to run a public health campaign alerting the public to the
harms of cannabis.
- That clear cannabis prevention policies should be
issued by the Commonwealth Department of Health and Ageing, to be
implemented state-side in all schools and further, that these be regularly
updated and reinforced.
- That
Federal and State police are resourced to implement ‘NOAH’ blitzes every
three months for a two-year period. This should focus equally on
plantation and hydroponically grown cannabis, trafficking, financing,
and/or selling drugs. Further, that the Proceeds of Crime funds be used to
continue a NOAH cannabis campaign after the two-year period.
- That all
professionals in the Drug and Alcohol
field be required by law to strongly discourage any cannabis use by those
whom they counsel or to whom they provide treatment for drug related
problems.
- That the
Federal and all States Governments resource a long-term Cannabis QUIT
Campaign, to be organised and implemented along similar lines as the
successful “QUIT Tobacco” campaign. Further, that the Anti-Cancer Councils
be required and resourced to combine messages about cannabis (as well as
tobacco) and the fact that cannabis has carcinogenic properties that cause
the same adverse health consequences as tobacco.
- That preventive education programs be developed
to target all members of society-especially parents, educators and
police.
- That stronger methods should be introduced to
prosecute users far more effectively, directing them into compulsory
treatment rather than jail.
- That clear messages should be issued by the
Commonwealth Health Dept to be used in all schools and constantly
reinforced.
10. That Recommendation number 70 of the report to the Inquiry called Ampe Akelyernemane Meke Mekarle “Little Children are Sacred”
be fully implemented. This recommends that government develop and implement a
multi-faceted approach to address the abuse of illicit substances in Aboriginal
communities, in particular cannabis abuse, including prevention, intervention
and enforcement strategies which recognise:
a. the geographic context of substance abuse, that is,
urban and remote locations,
and the implications this has for effective
prevention, intervention and enforcement.
b. population-based, youth-focused prevention and
intervention strategies that integrate
substance abuse, mental health, and other health and welfare concerns into youth programs.
11. That drug testing be implemented in schools,
giving a clear message that drug use is not permitted. Many youngsters do not see
cannabis as a drug and think that smoking cannabis will not harm them.
Implementing drug testing in schools gives a clear signal that drug use is not
permitted. Drug testing is an anti-dote for the denial of the harms of
cannabis. By drug testing, early cannabis use may be detected, (long before a
dependence treatment is necessary and the process then becomes more
complicated) and the youngster can be saved more easily from the use of
cannabis (and other drugs). Parents must also be informed about the possibility
of performing a drug test on their children. It is the task of the government
to provide parents with comprehensive information regarding the performance of
drug tests at home. In fact, it is only when a parent knows their child has a
problem, long before a dependence has become entrenched. In this way, after an appropriate assessment
by a drug test, something can be done about the drug using behaviour of the
child.
12. To implement roadside tests to facilitate a first step, i.e.
identification of road-users who
are impaired. The best of these is the Drug Evaluation and Classification Program developed for the Los Angeles
Police Department. While this program is
expensive, it is extremely
effective. An evaluation has shown that
officers correctly identified drug
impairment in 98.7% of cases. The Standardised Field Sobriety Test, also developed in the
REFERENCES
AND ADDITIONAL
Adams
IB, Martin BR: “Cannabis: pharmacology
and toxicology in animals and humans”. Addiction 91 (11):1585-1614, 1996.
Alan
H. Jobe. MD. PhD “Marijuana effects on
neurobehavior of newborns” The Journal of Pediatrics 149: 6: 781 2006.
Almadori G, Paludetti G,
Cerullo M, Ottaviani F, D’Alatri L. “Marijuana
smoking as a possible cause of tongue carcinoma
in young patients”. Laryngol Otol 1990;104:896-9.
Aldington,
S. 2007. “Cannabis linked to lung cancer risk” Thoracic Society conference
Auckland Medical Research Institute in
Aldington,
S., Harwood M., Cox B., Weatherall M., Beckert L., Robinson G., Beasley R. “Cannabis use and risk of lung cancer: A
case-control study” European Respiratory Journal issue:31(2)
2008.
Aldington S, Williams M, Nowitz M, Weatherall M,
Pritchard A, Mc Naughton A, Robinson G, Beasley R,
“The effects of cannabis on pulmonary structure, function and symptoms.”
Thorax doi:10.1136/thx.2006.077081 2007.
Alex Perkonigg, Roselind Lied, Michael Hofler, Peter Schuster, Holger Sonntag & Hans-Ulrich Wittchen “Patterns of cannabis use, abuse and dependence over time: incidence, progression and stability in a sample of 1228 adolescents “ Addiction (1999) 94(11), 1663-1678.
ANCD
Andréasson,
S., Allebeck, P., Engstrom, A., Rydberg, U., "Cannabis and Schizophrenia: a longitudinal study of
Swedish conscripts", The Lancet, December 26,
1987, pp. 1483‑1485.
Andréasson,
S., Allebeck, P., Rydberg, U., "Schizophrenia
in users and nonusers of cannabis", Acta Psychiatrica Scandinavica, 79, 1989, pp. 505-510.
Andreasson.
S et al. “Cannabis and schizophrenia: A
longitudinal study of Swedish conscripts”. Lancet, 26:1483-1486, 1987.
Anthony,
J.C. Petronis, K.R., 1995.”Early-onset
drug use and risk of later drug problems”. Drug Alcohol Depend. 40, 9-15.
Anthony,
J.C. Warner, L.A. & Kessler, R.C. (1994)
“Comparative epidemiology of dependence on tobacco, alcohol, controlled
substances, and inhalants:” basic findings from the National Comorbidity Survey, Experimental and Clinical
Psychopharmacology, 2, 244-268.
Andrew
J. “Psychiatric effects of cannabis”. British Journal of Psychiatry 178, 116-122 2001.
Arendt
M,
Arseneault
L Cannon M, Poulton R,
Arseneault,
L., Cannon, M., Witton, J Murray Robin M.., et al “Causal association between cannabis and psychosis: examination of the
evidence” British Journal of Psychiatry. 184, 110-117 2004.
Ashton,
C.H. (7) “Adverse effects of cannabis and
cannabinoids”, British Journal of Anaesthesia 83 (4) 1999. pp 637-649. 1999.
Australian
Bureau of Criminal Intelligence, 1993 Australian Drug Intelligence Assessment,
p. 22.
Australian
Crime Commission, (Illicit Drug Data Report 2005/6).
Australian
Federal Police: http://www.afp.gov.au/site_search?
Cannabis.
Bailey JR,, Cunny HC, Paule MG,
Slikker W Jr. “Fetal disposition of delta
9-tetrahydrocannabinol (THC) during
late pregnancy in the rhesus monkey”. Toxicol Appl Pharmacol 1987; 90: 315-21.
Bailey S L, Flewelling R L, and Rachal J V. “Predicting
continued use of marijuana among adolescents: the relative influence of drug-specific and social context factors.” Journal of Health and
Social Behavior. 1992; 33:51-66.
Bailey
EL, Swallow BL. “The relationship between
cannabis and schizotypal syptoms” Eur Psychiatry. (2):113-4 2004.
Barnett G, Chiang C N. “Effects of
marijuana on testosterone in male subjects.” J. Theor Biol. 1983;104:685-692.
BBC
News: “Under 10s treated for drug abuse”.
Mike Linnell Oldham Lifeline Project
and Jamelia Rashid Alcohol Substance Intervention Service
(Oasis) 2007.
Beshay
M., Kaiser H., Niedhart D., Reymond M., Schmid R., “Emphysema and secondary pneumothorax in young adults smoking cannabis”
European Journal of Cardio-thoracic Surgery xxx( 2007) xxx-xxx
Beautrais
A.L., Joyce P. R. and Mulder R. T. “Cannabis abuse and serious suicide
attempts” Addiction 94(8), 1155-1164, 1999.
Bem DJ. Self-perception theory.
In: Berkowitz L, ed. “Cognitive Theories
in Social Psychology”.
Benowitz NL and Jones RT, 1975 Cardiovascular
effects of prolonged delta-9-tetrahydrocannabinol ingestion. Clinical
Pharmacology and Therapeutics; 18:
287-297.
Benson M Bentley AM Lung disease induced
by drug addiction Thorax 50:1125-1127
1995.
Bensusan Ad (1971).”Marijuana withdrawal symptoms”,
British Medical Journal, 3, 112.
Berghuis P,
Rajnicek AM, Morozov YM, Ross R, Mulder J, Urban GM et al Hardwiring the Brain:
Endocannabinoids Shape Neuronal Connectivity. Science 2007 May 25; 316(5828):1212-6.
Bluhm EC; Daniels J; Pollock
BH; Olshan AF; “Maternal use of
recreational drugs and neuroblastoma in offspring: a report from the Children’s
Oncology Group (
BMA “Therapeutic Uses of Cannabis” Harwood
Academic Publisher 1997.
BMA (British Medical Association) “Therapeutis Uses
of Cannabis”
Academic Publishers, 1998.
Bolla, K.I., et al. “Dose-related neurocognitive effects of marijuana use” Neurology 59
(9) 1337-1343 2002.
Bovasso,
GB. “Cannabis abuse as a risk factor for
depressive symptoms”. The American Journal of Psychiatry, 158:2033-2037, 2001.
Boydell
J, Van Os J, Caspi A, Kennendy N, Giouroukou E, Fearon P, Farrell M, Murray RM “Trends
in cannabis use prior to first presentation with schizophrenia, in
South-East London between 1965 and 1999” Psychol Med. 36(10):1441-6.
2006.
Brambilla C.
Colonna M. “Cannabis: the next villain on
the lung cancer battlefield?” European
Respiratory Journal Editorial 31:
227-228 2008.
Brett “CANNABIS” A general survey of its Harmful Effects Including a
Discussion of its use in Medicine and Drug Education in UK Schools 2006.
Bridget
F. Grant, Roger Pickering “The
relationship between cannabis use and DSM-IV cannabis abuse and dependence:
Results from the National Longitudinal Alcohol Epidemiologic Survey” Journal
of Substance Abuse, 10, 3, 255-264
1999.
British
Lung Foundation “A Smoking Gun?” 2002.
Brook,
DW et al. “Drug use and the risk of major
depressive disorder, alcohol dependence, and substance use disorders”. Archives
of General Psychiatry, 59:1039-1044,
2002.
BudneyAJ Are specific dependence criteria necessary for different
substances: how can research on cannabis inform this issue?
Addiction 101 (suppl. 1): 125-133 2006.
Budney AJ, Brent A, Moore. “Development
and Consequences of Cannabis Dependence” J Clin Pharmacol 42:28S-33S.
Budney AJ, Hughes JR, Moore BA, Vandrey R Review of the validity and significance of
cannabis withdrawal syndrome American J of Psychiatry Nov. 2004; 161(11);1967-77.
Budney AJ, Hughes JR “The
Cannabis Withdrawal Syndrome” Curr.
Opin. Psychiatry 19: 233-238 2006.
Budney A. J., Rooffman R., Stephens R.S., Walker D “Marijuana Dependence and its Treatment” Addiction Science &
Clinical Practice December 2007 pp 4-16. e-mail: ajbudney@uams.edu
Budney AJ, Vandrey RG, Hughes JR, Moore BA, Bahrenburg B “Oral
delta-9-tetrahydrocannabinol suppresses cannabis withdrawal symptoms” Drug
and Alcohol Dependence; in press
Available online at www.sciencedirect.com 2006.
Busch FW Seid DA Wei EJ “Mutagenic activity of
marijuana smoke condensates Cancer” lett. 6: 319-324
1979.
Cabral
G.A. Dove Pettit DA “Drugs and immunity:
cannabinoids and their role in decreased resistance to infectious disease.” J
Neuroimmunol 83: 116-113 1998.
Cabral G A, Vasquez R. “Delta-9-Tetrahydrocannabinol
suppresses macrophage extrinsic anti-herpesvirus activity.” Cannabis: Physiopathology, Epidemiology, Detection. CRC
Press1993:137-153.
Cantwell R, Brwein J,
Glazebrook C, et al. “Prevalence of
substance misuse in first-episode psychosis”. British Journal of
Psychiatry.;174:150-153 1999.
Carriiot F; Sasco AJ “Cannabis and Cancer” Rev Epidemiol
Sante Publique 2000; 48(5):473-83
ISSN: 0398-7620.
Caspi A, Moffitt TE, Cannon M,
McClay J, Murray R, Harrington H, and others. “Moderation of the effect of adolescent-onset cannabis use on adult
psychosis by a functional polymorphism in the catechol-O-methyltransferase
gene: Longitudinal evidence of a gene x environment interaction”. Biol Psychiatry 2005;57:1117-27.
Centre
on Addiction and Substance Abuse at
Chacin
S., “Women’s Marijuana Problems: An
Overview with Implications for Outreach, Intervention, Treatment, and Research”
Journal of Chemical Dependency Treatment Vol. 6, No. ½, pp, 129-167 1996.
Chacko JA, Heiner
JG, Siu W, Macy M, Terris MK (2006). “Association
between marijuana use and transitional cell carcinoma.” Urology 67:100-104.
Chambers RA, Taylor JR,
Chang
L., C. Clock, Yakupov R., Ernst T.“Combined
and Independent Effects of Chronic Marijuana Use and HIV on Brain
Metabolites” Neuroimmune Phrmacol 1:
65-76 2006.
Charbonney
E., Sztajzel J., Polletti P., Rutschmann O. Paroxysmal
atrial fibrillation after recreational marijuana smoking:another “holiday
heart”? Swiss Med Wkly 135:
412-414 2005.
Christine
N Vidal, PhD; Judith L. Rapoport, MD; Kiralee M. Hayashi, BS; Jennifer A.
Geaga, BS; Yihong Sui, BS; Lauren E. Mclemore, BS; and others: “Dynamically Spreading Frontal and Cingulate
Deficits Mapped in Adolescents with
Schizophrenia” Arch Gen Psychiatry. 2006; 63: 25-34.
Clayton R R, Leukefeld C G. “The
prevention of drug use among youth: implications of “legalization.” Journal of Primary
Prevention. 1992;12:289-302.
Clough AR, D’Abbs
P, Cairney S, Gray D, Maruff P, Parker R, O’Reilly B “Emerging patterns of cannabis and other substance use in Aboriginal
communities in Arnhem Land, Northern territory: a study of two communities” Drug
Alcohol Rev 23(4):381-90 2004.
Coffey C, Lynskey M, Wolfe R, Patton GC Initiation and Progression of
cannabis use in a population-based Australian adolescent longitudinal
study Addiction 2000; 95:1679-1690.
(A large cohort study of 2032 students from 44 secondary schools
following the outcome and predictors of escalation to harmful daily cannabis
use).
Coffey C, Carlin J, Lynskey M, Ning Li, Patton GC
Adolescent
Precursors of Cannabis Dependence: Findings from the Victorian Adolescent
Health Cohort Study Br. J. Psychiatry 2003; 182: 330-336.
Cohen
S. “Cannabis: Effects upon Adolescent
Motivation. In: Marijuana and Youth: Clinical Observations on Motivation and Learning.” Report.
Cornelius MD, Taylor PM, Geva
D, Day NL. “Prenatal tobacco and
marijuana use among adolescents: effects on offspring gestational age, growth, and morphology”. Pediatrics
1995; 95: 738-43.
Copeland, Underwood and
Van Wyck “The health and psychological
consequences of cannabis use – chapter.6.5” http://www.healthconnect.gov.au/internet/wcms/publishing.nsf/Content/health-pubs-drug-cannab2-ch65.htm
(1980).
Daaka
Y, Zhu W, Friedman H, Klein T W. “Induction
of Interleukin-2 alpha gene by delta-9-THC is mediated by
nuclear factor kB and CBa cannabinoid receptor.” DNA and Cell Biology
1997;16:301-309.
Day NL et al Effect
of Prenatal Marijuana Exposure on the Cognitive Development of Offspring at Age
Three Neurotoxicology and Teratology 1994; 16(2): 169-75.
Day NL,
Goldschmidt, Lidush, Thomas, Carrie Prenatal marijuana exposure contributes
to the prediction of marijuana use at age 14. Addiction Sept 2006;
101(9): 1313-22.
Dean, B et al. “Studies on [3H]CP-55940 binding in the
human central nervous system: regional specific changes in density of
cannabinoid-1 receptors associated with schizophrenia and cannabis use”.
Neuroscience, 103:9-15, 2001.
Degenhardt LD, Hall W. “Is
cannabis a contributory cause of psychosis:examination of the evidence”. Br
J Pschiatry 2004;184:110-7.
Degenhardt LD, Jureidini J,
Wells B, Rosenman S, “Does cannabis use
lead to mental-health problems?: findings from the research Parliamentary
Library no.21, 2006-2007 ISSN
1449-8456 7 June 2007.
Department of Parliamentary
Services Research Note. ‘Does cannabis
use lead to mental-health problems?: findings from the research’. June
2007, no. 21.
Dervaux A, Laqueille X, Bourdel
MC, Leborgne MH, Olie JP, Loo H, Krebs MO.
“Cannabis and schizophrenia: demographic and clinical
correlates” Encephale 2003 29(1):11-7.
Deykin EY, Levy JC, Wells V.
(1986). “Adolescent depression, alcohol
and drug abuse.” American Journal of Public Health, 76, 178-182.
Diana M, Melis M,
Muntoni AL et al. “Mesolimbic kipaminergic
decline after cannabinoid withdrawal”. Proc Natl Acad Sci
95(17):10269-10273, 1998.
Di Forti M, Murray RM. Cannabis
consumption and risk of developing schizophrenia: myth or reality? Epidemiol
Psichiatr Soc. 2005;14:184-187.
Donald PJ. “Marijuana smoking – possible cause of head and neck carcinoma in
young patients”. Otolaryngol Head
Neck Surg 1986;94:517-21.
Drewe J “Desired effects and adverse effects of cannabis use” Ther Umsch.
2003; 60(6):313-6.
Drummer, O.H. “Drugs in drivers killed in Victorian road
traffic accidents. The use of responsibility analysis to investigate the
contribution of drugs to fatal accidents”.
Drummer, O.H. “Drugs in drivers killed in Victorian road
traffic accidents”.
Drummer, O.H. &
Gerostamoulos, J. “The involvement of
drugs in car drivers killed in Victorian road traffic accidents.”
D’Souza
DC, Abi-Saab W, Madonick S, Forselius-Bielen K, Doersch A, Braley G, et al. “Delta-9-tetrahydrocannabinol effects in
schizophrenia: implications for cognition, psychosis, and addicition”. BMJ
Psychiatry 57: 594-608 2005.
D’Souza DC, Abi-Saab W,
Madonick S, Forselius-Bielen K, Doersch A, Braley G, Gueorguieva R, Cooper T,
Krystal J “Delta-9-tetrahydrocannabinol effects in schizophrenia: implications
for cognition, psychosis, and addiction” Biol Psychiatry 15;57(6):594-608 2005.
Duffy A, Milin R (1996). “Case study: withdrawal syndrome in
adolescent chronic cannabis users”, Journal of the American Acadeny of Child and Adelescent Psychiatry, 35, 1618-1621.
Dupont
R.L. “Testimony before Congressional Committee” 1984.
Dupont, R. L. 1984 “Getting
tough on gateway drugs,”
Eisenstein K Toby, Joseph J
Meissler, Qiana Wilson, John P Gaughan, Martin W. Adler “Anandamide
and Delta9-tetrahydrocannabinol directly inhibit cells of the immune
system via CB2 receptors” Journal of
Neuroimmunology xx(2007)1-6.
Eldreth DA, Matochink JA,
Cadet JL, Bolla KI. “Abnormal brain activity in
prefrontal brain regions in
abstinent marijuana
users”. Neuroimage 2004;23(3):914-20.
EL Gunindy. “Generally speaking, the proportion of cases
of insanity caused by the use of hashish varies from 3 to 60 percent of total
number of cases occurring in
Ellgren M,
(Karolinska Institutet) “Neurobiological
effects of early life cannabis exposure in relation to the gateway hypothesis”. http://diss.kib.ki.se/2007/978-91-7357-064-0/ ISBN:978-91-7357-064-0. 2007.
Endicott JN, Skipper P,
Hernandez L. “ Marijuana and head and
neck cancer”. Adv Exp Med Biol 1993;335:107-13.
Ernst
T, Chang L, Arnold S (2003) “Increased
glial markers predict increased working memory network activation in HIV
patients”. Neuroimage 19:
1686-1693.
Ferdinand.
RF et al. “Cannabis—psychosis pathway
independent of other types of psychopathology”. Schizophrenia Research, 79(2-3):289-95, 2005.
Fergusson,
DM et al. “Cannabis use and psychosocial
adjustment in adolescence and young adulthood”. Addiction 97:1123-1135,
2002.
Fergusson,
DM et al. “Cannabis dependence and
psychotic symptoms in young people”. Psychological Medicine, 33:15-21, 2003.
Fergusson,
DM et al. “Tests of causal linkages
between cannabis use and psychotic symptoms”. Addiction, 100, 3:
354-366, 2005.
Fergusson
DM, Boden JM, Horwood LJ Cannabis use and
other illicit drug use: testing the cannabis gateway hypothesis Addiction
101(4):556-69 2006.
Addiction
92; 279-296. 1997.
Fergusson
DM Horwood LJ “Does cannabis use
encourage other forms of illicit drug use?” Addiction 95(4), 505-520 2000.
Fergusson
DM, Horwood LJ “Cannabis use and
dependence in a
Fergusson DM, Horwood LJ,
Swian-Campbell NR. “Cannabis dependence
and psychotic symptoms in young people”
Psychol Med ;33:5-21 2003.
Fergusson
D.H., Horwood L.J., Swain-Campbell N. “Cannabis
use and psychosocial adjustment in adolescence and young adulthood”.
Addiction 97; 1123-35 2002.
Fergusson
D.M., Richie Poulton., Paul F Smith., Joseph M Boden. “Cannabis and Psychosis” BMJVolume
332; 172-175 2006.
Fisher
et al “Dangers of Cannabis” Emergency
Medicine Journal 22:612a 2005.
Fletcher
JM, Page JB, Francis DJ, Copeland K,
Naus MJ, Davis CM, Morris R, Krauskopf D, Satz P. “Cognitive correlates
of long-term cannabis use in Costa Rican men”.
Arch Gen Psychiatry. 1996; 53:1051-1057.
Fraser JD (1949). “Withdrawal symptoms in cannabis-indica
addicts”, Lancet, 2, 747-748.
Fried P A,. “ Adolescents Prenatally Exposed to Marijuana:
Examination of Facts of Comples Behaviors and Comparisons with the Influence of
In Utero Cigarettes” J Clin Pharmacol
42:97S-102S 2002.
Fried P A,. “Marijuana use
by pregnant women: Neurobehavioral
effects in neonates” Drug and Alcohol Dependence. 1980 6:415-424.
Fried P A,. Watkinson B, and Willan. “Marijuana
use during pregnancy and decreased length of Gestation. “American Journal of Obstet. Gynecol.
1984;150:23-27.
Friedman
H,
Garavan
H. “Cannabis far more toxic to the
adolescent brain”
Gardner EL, Addictive
Potential of Cannabinoids: The underlying neurobiology
CPL
Chemistry and Physics of Lipids 2002 121;
267-297.
Geller T, Loftis L, Brink D, 2004 Cerebellar Infarction in Adolescent
Males Associated with Acute Marijuana Use Pediatrics; 113: 365-70.
Geneva Convention of 1925
Ghosg S, Preet A, Groopman J, Ganju R “Cannabiniod receptor CB2 modulates the CXCL12/CXCR4-mediated
chemotaxis of T lymphocytes” Molecular Immunology xxx(2006)xxx-xxx.
Giedd
Jay Current Direction in Psychological
Science 2007.
Glantz,
M., Pickens, R., 1992.“Vulnerability to
Drug Abuse”. American Psychological Association,
Golub A, Johnson BD,”The Shifting Importance of Alcohol and
Marijuana as Gateway Substances among Serious Drug
Abusers” J.
Stud Alcohol 1994;55:607-614.
Goncharov
I, Weiner L, Vogel Z (2005) “Delta
9-tetrahydrocannabinol increases C6 glioma cell death produced by oxidative
stress”. Neuroscience 134:
567-574.
Gray
D, Morfitt B, Williams S, Ryan K, Coyne L. “Drug
Use and Related Issues among young aboriginal people in Albany” National
Centre for Research into the Prevention of Drug Abuse Curtin University of
Technology 1996.
Greenblatt,
J. “Adolescent self-reported behaviours
and their association with marijuana use”. Based on data from the National
Household Survey on Drug Abuse, 1994-1996, SAMSHA, 1998.
Griggs
W, Caldicott, Pfeiffer J, Edwards N, Pearce A, Davey M “The impact of drugs on road crashes, assaults and other trauma-a
prospective trauma toxicology study” National
Drug Law Enforcement Fund an initiative of the National Drug Strategy Trauma
Service, Royal Adelaide Hospital and Emergency Department, Royal Adelaide
Hospital 2007.
Groopman
Jerome E. M.D. “Marijuana component opens
the door for virus that causes kaposi’s sarcoma” American Associarion for
Cancer Research 2007.
Gross G, Roussaki A, Ikenberg, Drees N. “Genital
warts do not respond to systemic recombinant interferon alfa-2 treatment
during cannabis consumption.” Dermatologica 1991; 183:203-207.
Handbook
for medical practitioners
Grucza RA, Chen
KW, Bierut LJ Cigarette Smoking and the Risk for Alcohol Use Disorders Among
Adolescent Drinkers Alcoholism: Clinical and Experimental Research 2006
(December).
Hall
W. ‘Cannabis policy challenges’ in Matters
of Substance Nov/Dec 2007 produced by the New Zealand Drug Foundation. www.drugfoundation.org.nz.
Hall,
W., Degenhardt L. “Cannabis and
psychosis” Aust N Z J Psychiatry 34:26-34
2000.
Hall, W., Degenhardt L. “What are the policy Implications of the evidence on cannabis and Psychosis? Can J
Psychiatry, Vol 51, No 9, 2006.
Hall W,. Macphee D. “Cannabis use and cancer” Addiction 97,243-247 2002.
`
Hansteen, R. W., Miller, R. D.,
Lonero, L., Reid, L.D. & Jones, B. “Effects
of cannabis and alcohol on automobile driving and psychomotor tracking.” Annals of
HarkanyT, Guzman M,
Galve-Roperh I, Berghuis P, Devi LA, Mackie K
The emerging functions of endocannabinoid signaling during CNS
development
Trends in
Pharmacological Sciences 2007; 28(2):
88-92.
Harrison
G. Pope Jr., M.D. “Cognitive Effects of
Long-Term Cannabis Use: The Devil is in the confounding variables” McaLean Hospital/Harvard Medical School
2004.
Hashibe
M; Straif K; Tashkin DP; Morgenstem H; Greenland S; Zhang ZF “Epidemiologic review of marijuana and
cancer risk” Alcohol 35(3):265-75 2005.
Hayatbakhsh,
MR et al. “Cannabis and anxiety and
depression in young adults: a large prospective study.”. Journal of the
Hays
RD, Widaman KF, Dimatteo MR , Stacy AW (1987).
“Structural equation models of current drug use: are appropriate models so
simple(x)?” Journal of Personality and
Social Psychology, 57, 134-144.
Hennetta
S. Bada, MD, MPH, Eric W. Reynolds, MD, Wendy F Hansen, MD “Marijuana use, adolescent pregnancy, and alteration in newborn
behaviour: complex can it get?” The
Journal of Pediatrics 149:742-5
2006.
Henquet
C. COMT “Val158Met moderation of
cannabis-induced effects on psychosis and cognition.” Presented at the 13th
Association of European Psychiatrists (AEP) Symposium by the Section on
Epidemiology and Social Psychiatry; June 15-17, 2006;
Henquet
C. ‘The Effects of COMT VAL158Met
Egnotype and Cannabis Use on Psychosis and Cognition’. Presented at the 13th
Association of European Psychiatrists (AEP) Symposium by the Section on
Epidemiology and Social Psychiatry held June 14-17, 2006.
Henquet
C, Corcoran C. “Cannabis and psychosis:
from genetics and biology to functional outcome and treatment:” Program of the
5th International Conference on Early Psychosis; October 4-6, 2006;
Henquet
C, Krabbendam L, Spauwen J, et al.
“Prospective cohort study of cannabis use, predisposition for psychosis, and
psychotic symptoms in young people.” BMJ. 2005;330:11-15. Epub 2004 Dec 1.
Henquet
C, Murray R, Linszen D, van Os J. “The
environment and schizophrenia: the role of cannabis use”. Schizophr Bull.
2005;31:608-612. Epub 2005 Jun 23.
Henquet
C, Rosa A, van Os J, Myin-Germeys I. COMT VAL158MET moderation of
cannabis induced psychosis: an experience sampling study (ESM). Program and
abstracts of the 5th International Conference on Early Psychosis; October 4-6,
2006;
Herkenham
M, Little L.A., Johnson M.R. et al. “Cannabinoid
receptor localization in the brain.” Proc Natl Acad Sci,
Hill
S.W., Tan JDC, Thompson B.R. Naughton M.T. “Bullous
lung disease due to marijuana” Respirology 13: 122-127 2008.
Hiller
C.F., Wilson F.J., Mazumder M.K., Wilson
J.D., Bone R.C. Concentration and
Particle Size Distribution in smoke from Marijuana Cigarettes with Different
Delta9-Tetrahydrocannabinol Content Oxford University Press Vol 4 Number 3
page 451-454 1984.
Hoffmann D Brunnemann KD Gori GB Wynder EL “On the
carcinogenicity of marijuana smoke.”Recent Advances Phytochem. 9:63-8
1975.
Hollister L,“HealthAspectsof Cannabis” http://www.druglibrary.org/schaffer/hemp/medical/hollisterhealth.htm
Howard Richard C, Menkes David B, “Changes in brain function during acute cannabis intoxication:
preliminary findings suggest a mechanism for cannabis-induced violence” Criminal
Behaviour and Mental Health 17:113-117
2007.
Huber GL, Griffith DL,
Langsjoen PM,“The effects of marijuana on the respiratory and
cardio-vascular systems.” In G Chesher, P Consroe, R Musty editors, Marijuana:
An International Research Report. National Campaign Against Drug
Abuse Monograph Number 7,
Huizink AC, Mulder
EJ Maternal smoking, drinking or cannabis use during pregnancy and
neurobehavioural and cognitive functioning in human offspring Neurosci Biobehav
Rev 2006 30(1) 24-41.
Hurd Y,
Professor of Psychiatry, Pharmacology and Biological Chemistry.
Ongoing research
into neurotransmitter levels in animals to mimic adolescent drug exposure,
especially cannabis, seen in humans. Paper now available:
Neuropsychopharmacology advance online publication 5th July 2006
doi:10.1038/sj.nnp.1301127 Correspondence to yasmin.hurd@mssm.edu.
Ilse
Kurzthaler, Martina Hummer, Carl Miller, Barbara Sperner-Unterweger, Verena
Gunther, Heinrich Wechdorn, M.S.; Hans-Jurgen Battista, Wolfgang Fleischhacker, “Effects of Cannabis Use on Cognitive
Functions and Driving Ability” J Clin Psychiatry 1999;60:395-399.
Ishida
J, Peters M, Jin C, Louie K, Tan V, Bacchetti P and Terraut N “Influence of Cannabis Use on Deverity of
Hepatitis C Disease” Clinical Gastroenterology and Hepatology” 6 69-75 2008.