Cannabis – suicide, schizophrenia and other ill-effects

 

A research paper on the consequences of acute and chronic cannabis use

 

 

 

 

Drug Free Australia

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 – United Kingdom and Australia

 

 

 


ACKNOWLEDGEMENTS

 

This review of cannabis in Australia was written to provide up-to-date evidence to key researchers including the National Drug and Alcohol Research Centre (NDARC) and those who compiled the National Cannabis Strategy 2006-2009. It is intended that this research paper will provide useful information for the preparation of the necessary evidence to up-date the National Cannabis Strategy in Australia.

 

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 Queensland Australia.

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 Wide Bay Queensland e.g. Lions Clubs Seminar; Quota Club; Church’s in the Wide Bay Queensland.

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.

 

John Malouf  Pharmacist’s
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 Australia, NSW – 2002-2004

Project Manager, Offshore Licensing (India & Bangladesh), Centre for International Education and Training, 2001-2002

Chief Executive – Life Education, SA – 2000-01

 

Dr Ivan Van Damme’s (Belgium) Member International Task Force on Strategic Drug Policy  peer- review and input to this publication consists of substantial quotations especially in the sections on The History of Cannabis Prohibition, Cannabis effects on Australian Indigenous communities, Cannabis, Cannabis-Chronic Obstructive Pulmonary Disease, Cardiovascular System and Cannabis – Effects on the Brain.

 

 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.

EXECUTIVE SUMMARY

 

This paper provides an overview of matters related to cannabis abuse in Australia at the present time. Unfortunately, as (Hall, 2007) stated in his article for the New Zealand Drug Foundation’s latest edition of Matters of Substance, “public debate often presents highly polarised evaluations of the health effects of cannabis, with any rational discussion of its health risks the first casualty”. The evidence presented here is intended to help correct the insufficiencies and inaccuracies of the present National Cannabis Strategy 2006-2009. The latest scientific evidence has been cited on the major adverse effects of acute and chronic cannabis use on the physical and psychological health of all Australians, with special attention given to our indigenous communities. The evidence has been grouped according to the effect of cannabis abuse on specific adverse health outcomes. The paper concludes with a list of recommendations that it is hoped will be taken up by Federal and State Governments.

 

INTRODUCTION

 

In June 2007 the Department of Parliamentary Services produced a Research Note which states “Cannabis is the most commonly used illicit drug in Australia. According to the 2004 National Drug Strategy Household Survey, one in three (33.6 per cent, 5.5 million) Australians aged 14 years and older have used cannabis in their lifetime.”

 

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 United States, Europe and Australia (Arsenault L et al. 2004) found that all available population-based studies have concluded that cannabis use is associated with the later development of schizophrenia and that cannabis use is a component causes 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 Shanghai in 1909 to discuss the possibility of a drug-control treaty, the focus was entirely on limiting opium's importation into China.  During a second meeting held in The Hague in 1912 cocaine was added to the discussion and, thereafter was included in all international agreements (Zimmer, 1997).

In preparing for this Conference, which represented an attempt to deal with the international opium traffic, the government of Italy proposed that the production and traffic in Indian hemp drugs be included as part of the agenda of the Conference (Wright, 1912).

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 Egypt, South-Africa and Turkey, whose indigenous populations had been decimate by the devastating effects of cannabis, discussion centred on cannabis, and in order to turn the tide, Egypt asked for the illegality of cannabis, to decrease the availability of the drug (Lowes, 1996).  We can learn a lot from history. Cannabis became illegal because of its devastating effects to the indigenous communities.

At the meeting in Geneva in 1924, an Egyptian delegate presented a paper on the effects and use of hashish in Egypt, taking an international lead and by proposing that hashish be included within the Convention (Willoughby, 1924). Mr. El Guindy's study is so typical of the so-called scientific, empirical evidence that has been presented to justify the drug's prohibition that the following excerpt must be included. In stating that the real danger of hashish is that it will produce insanity, the Egyptian delegate presented the following:

“The illicit use of hashish is the principal cause of most of the cases of insanity occurring in Egypt. In support of this contention, it may be observed that there are three times as many cases of mental alienation among men as among women, and it is an established fact that men are much more addicted to hashish than women” (EL Guindy, 1924).

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 Egypt, (Warnoch, 1903) developed five categories of "hashish insanity." Aside from those cases of temporary intoxication (type 1) or pleasant, dreamlike states, which do not require hospitalisation, he reported observing numerous instances of the following hashish-induced conditions:

 

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 (Geneva, 1925)

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.  Australia prohibited cannabis in 1961 when it signed the United Nations Convention on Narcotic Drugs. The great harm done to the Australian Indigenous community was clearly identified in 2007 by The Northern Territory Board of Inquiry report called Ampe Akelyernemane Meke Mekarle “Little Children are Sacred” This report identified that cannabis is present in Indigenous communities and proposed it is having negative effects on community and family life and in particular, consequential effects 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 first age of use apparently decreasing. This is of great concern because of the harms associated with its use. Noting cannabis in particular, the Inquiry acknowledged the need for action in three areas - prevention, intervention and enforcement.

 

 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