Pubdate:  1 Oct 2000
Source: Australian and New Zealand Journal of Public Health (Australia)
Copyright: 2000 Public Health Association of Australia Inc.
Page:  503-508
Mail:  PO Box 319, Curtin ACT 2605
Fax: (06) 282 5438
Authors: Wayne Hall and Wendy Swift, National Drug and Alcohol Research 
Centre, University of New South Wales
Note: Footnote references have been placed in [brackets] to allow easier 


A number of commentators in the alcohol and other drugs field have recently 
claimed that the THC (tetrahydrocannabinol) content of cannabis products 
used in Australia has increased up to 30 times over the past two decades. 
[1-3] The increased THC content has been attributed to the cultivation of 
particular cannabis strains, including hybrids of the Cannabis sativa plant 
such as 'skunk', and the use of hydroponic growing methods.

Since THC is the psychoactive substance in cannabis that is responsible for 
most of its effects, [4] these claims have been used to explain an apparent 
increase in the adverse health and psychological effects of cannabis use 
among young people who are regular users of the drug.

These claims have been widely and uncritically reported in the popular 
media and have played a prominent role in recent debates about proposed 
changes to legal penalties for cannabis use. They accordingly require 
critical analysis. In this report, we examine evidence on three linked claims:

1. That the THC content of Australian cannabis plants has increased up to 
30 times.

2. That problems related to cannabis use have increased among young adults 
in Australia in recent years.

3. That increased THC content is the most plausible explanation of any rise 
in the rate of cannabis-related problems.


To address the first question, we investigated the availability of 
published data on the THC content of cannabis collected by government 
analytical laboratories, police and health departments in New South Wales 
(NSW), Queensland, South Australia (SA), Victoria and Western Australia 
(WA). We also examined data reported in the National Illicit Drug Reports 
compiled by the Australian Bureau of Criminal Intelligence. We also 
obtained data on the THC content of cannabis in the United States (US) and 
New Zealand (NZ).

The second question was addressed by examining available morbidity data on: 
the number of hospitalisations for cannabis-- related diagnoses (e.g. abuse 
and dependence); rates of addiction treatment for cannabis-related problems 
reported in national censuses of treatment agencies; and surveys of the 
prevalence of cannabis use among high-risk populations, such as young 
people in juvenile justice settings, young people with first episode 
psychoses, and young people who are being treated for alcohol and other 
drug problems.

We explored alternative explanations for any increase, real or apparent, in 
cannabis-- related problems by undertaking secondary analyses of 
self-report data on cannabis use, type of cannabis consumed and method of 
use from the 1998 National Drug Strategy (NDS) Household Surveys (a 
household survey of 10,030 Australians aged 14 years and older). The unit 
record file of the NDS survey was purchased from the Social Science Data 
Archive. All data are weighted to the Australian population using weights 
provided with the NDS unit record file.


Has The Average THC Content Of Australian Cannabis Plants Increased?

The THC content of Australian cannabis products has not been systematically 
tested over the two decades in which average THC content is claimed to have 
increased up to 30 times. Penalties under law for cannabis offences in 
Australian States do not distinguish between cannabis products of differing 
potency, so there is no reason for police services to test THC content.

Samples of seized cannabis are occasionally tested. In NSW, for example, 
the Division of Analytical Laboratories analysed a sample of compressed, 
hydroponically grown 'heads' from SA, which had a THC content of 15%. [6] 
Media publicity about the THC content of single samples such as this can 
create a false impression that these levels are typical of the cannabis 
products consumed in Australia.

Other Australian data on cannabis samples tested for other purposes 
suggests that the above sample had an unusually high THC level. In 1997, a 
small number of cannabis seizures (leaf and head) from a number of 
Australian States were tested for THC content. [7] Their THC content was 
between 0.6-13% of plant material, with the majority of samples having a 
THC content of 0.6-2.5%. The mean THC content of 168 samples tested by 
Western Australian police between March and May 1996 was 3.8% for all 
samples, and 6.4% in 59 samples of 'heads'. [8]

Better data have been collected on the THC potency of cannabis in the US, 
where a similar claim of a 30-fold increase in cannabis potency has been 
made. [9] The Research Institute of Pharmaceutical Sciences at the 
University of Mississippi has tested the THC content of cannabis seizures 
for the National Institute on Drug Abuse since the middle 1970s (The 
Potency Monitoring Project). [10,11] These data suggest that THC content in 
US cannabis increased between 1975 and 1998. Mikuriya and Aldrich, however, 
have argued that samples from the middle 1970s were not representative of 
cannabis consumed at that time and that the samples from the 1970s 
under-estimated THC potency because they were not properly stored, allowing 
their THC content to degrade. [12] Data from the Marijuana Potency 
Monitoring Project have shown an increase in the THC content of 31,000 
samples from 1.2% in 1980 to 4.2% in 1997. [10]

The NZ Government has tested the THC content of cannabis samples over the 
past two decades. These have not shown any sizeable increase in average THC 
content which has remained within the range of 2.0% to 4%. [13]

Why Is It Believed That The THC Content Of Cannabis Has Increased?

A number of factors probably explain the persistence of the belief that the 
THC content of cannabis plants in Australia has increased 30-fold in the 
absence of any supporting data.

First, defenders of the claim often point to reports of single samples with 
unusually high THC content tested by the police. At best, such samples 
indicate the maximum THC content that has been achieved (assuming that 
there were no errors in the test results) but they do not tell us what the 
THC content is in the cannabis that is typically used by consumers.

Second, biases in the sampling of tested cannabis are amplified by the 
attention that the print and electronic media give to unusually potent 
samples, creating a false impression that cannabis with exceptionally high 
THC is the norm.

Third, uncontested repetition of these assertions in the media has 
established them as 'facts'; those who contest these claims are asked to 
prove that they are false rather than the (usually nameless) proponents 
being asked to provide evidence that they are true.

Fourth, an increase in average THC content seems to explain an apparent 
increase in the number of cannabis users who experience problems as a 
consequence of their use. [14]

Has The Prevalence Of Cannabis-Related Problems Increased In Australia?

Data from household and school-based surveys show that cannabis use has 
substantially increased among young Australians over the past 20 years. 
[15-17] If the experience with alcohol is applicable to cannabis, then a 
rising prevalence of use would predict increased rates of problems. [18] 
There are, however, no indicators of cannabis-related mortality and 
morbidity that are as directly related to cannabis use as alcoholic liver 
cirrhosis and alcoholic psychosis are to alcohol and overdose deaths are to 
heroin use. Cannabis-related problems, such as cannabis-induced psychosis 
and cannabis dependence are contested entities that are not well recognised 
clinically. [19,20]

A number of indicators suggest that cannabis-related problems have probably 
increased. National censuses of Australian addiction treatment services 
indicate that the proportion of persons presenting for a primary 
cannabis-related problem has steadily increased from 4% in 1990 to 7% in 
1995. [21] A recent study of drug and alcohol services for the National 
Minimum Data Set Project found that 10.8% of 1395 clients sought help for a 
cannabis problem in 1997. [22] The number of first-time hospital admissions 
for cannabis abuse and dependence among young non-- Aboriginal adults in 
Western Australia substantially increased from 185 in 1980-1985 to 1617 in 
1990-1995. [23]

There are also high rates of cannabis use among subgroups of young 
Australians. For example, 25% of a nationally representative sample of 
persons with psychotic disorders in contact with services had a lifetime 
history of cannabis abuse and 24% were daily or near-daily cannabis users 
[24] compared with 2% in the general population. [25] High rates of daily 
cannabis use are also reported among persons with first episode psychoses, 
juvenile offenders before the courts and adolescents in treatment programs 
for alcohol and drug problems. [26-28] While we do not have good data on 
the prevalence ofthese disorders over time, the high prevalence of heavy 
cannabis use in these populations has contributed to a perception that 
cannabis-related problems have increased among young Australians.

Alternative Explanations Of The Apparent Increase In Cannabis-Related Problems

If we assume for the purposes of argument that cannabis-- related problems 
have increased in prevalence, it does not follow that an increase in the 
THC content produced by cannabis plants is the most plausible explanation. 
Two more plausible alternative explanations of this apparent increase in 
cannabis-related problems are: cannabis users more often use more potent 
forms of cannabis that dominate the cannabis market in Australia; and an 
earlier age of initiation and heavier patterns of cannabis use among young 
Australians have increased the prevalence of harmful patterns of cannabis use.

Changing Cannabis Markets

The THC content of cannabis varies between different cannabis products. 
Cannabis leaf contains the least THC and the flowering 'heads' contain the 
highest amount of THC. [29] Cannabis resin harvested from the flowering 
heads and compressed into hash is one of the most potent forms of cannabis. 
[30] Leaf, heads and hash have been available in Australia for several 
decades. [31] So too have more potent strains of marijuana. The Mullumbimby 
and the Byron Bay districts of northern NSW, for example, had a reputation 
for producing high-potency cannabis known as 'Mullumbimby madness' in 1981. 

We need to distinguish between two ways in which THC content may have 
increased: more potent THC-producing strains of cannabis plant (e.g. 
'skunk'), and more potent cannabis products derived from existing plants. 
The popular media give greatest attention to the first possibility; the 
data suggest that the latter is more plausible.

Over the past two decades, a large-scale illicit cannabis industry has 
developed in Australia [33] to meet the demand for cannabis among a growing 
number of regular cannabis users. In the 1998 NDS Survey, persons who 
smoked cannabis weekly, or more frequently, comprised 31% of those who had 
used cannabis in the past year but they accounted for an estimated 96% of 
the cannabis consumed making conservative assumptions about their frequency 
of use by daily users.

Regular users generally prefer the more potent forms - heads of the plant 
[34,35] - probably because they develop tolerance to the effects of THC. 
[29,36] In the 1998 NDS Survey, 94% of daily and 88% of weekly cannabis 
users reported that they typically smoked 'heads', 'skunk' or other potent 
forms of cannabis. This means that 91% of the cannabis consumed in 
Australia is 'heads' and other potent forms of cannabis.

Changing Patterns Of Cannabis Use

A major change in patterns of cannabis use among Australian adolescents and 
young adults is that larger numbers of younger users use more potent forms 
of cannabis at an earlier age. The 1998 NDS data show a strong trend 
towards an earlier age of initiation among younger cannabis users. One in 
five cannabis users (21%) born between 1940 and 1949 had initiated cannabis 
use by age 18, compared to 43% of those born in 1950-59, 66% of those born 
1960-69 and 78% of those born in 1970-79.

Earlier initiation of cannabis use increases the chances that these users 
will become daily or nearly daily cannabis users. [37,38] This, in turn, 
increases the risks of becoming dependent on cannabis and experiencing 
problems as a result of their use. [29,37] Levels of consumption among some 
adolescent cannabis users can be very high. For example, 40% of a sample of 
NSW juvenile offenders reported smoking [40] or more 'cones' of cannabis a 
week. [39]

The greater expense of cannabis heads also encourages regular users to 
smoke them in waterpipes or 'bongs' in the belief that this maximises the 
delivery of THC. In the 1998 NDS Survey just over half of all persons who 
had used cannabis in the past year smoked 'heads' (57%) using bongs (56%). 
Younger users were more likely than older users to prefer bongs or pipes to 
joints and heads to leaf, with the trend reversed in older users.

All these changes in patterns of use - earlier initiation of cannabis use, 
greater use of more potent cannabis products such as heads and the use of 
waterpipes - have probably increased the amount of THC consumed by regular 
cannabis users more than any speculative increase in the THC content of 
cannabis plants.

What Are The Health Implications Of Any Increase In THC Content?

Proponents of the claim that THC content has increased regard it as 
self-evident that it will increase the adverse health effects of cannabis 
use. [1,3] Critics of the claim have countered that increased THC potency 
may have little or no adverse effect because users are able to adjust or 
'titrate' their dose of THC to achieve the desired state of intoxication. 
[9,12] If users were able to titrate their dose of THC, as tobacco smokers 
do with nicotine, [40] then the use of more potent cannabis products would 
reduce the amount of cannabis material that was smoked. This would 
marginally reduce the risks of developing respiratory diseases, the most 
likely adverse health effect of regular cannabis smoking.

There is very little research on whether cannabis users are able to titrate 
their dose of THC by modifying the amount of smoke that they inhale. Some 
earlier studies suggested that they could [41] but more recent studies 
report that cannabis users have limited ability to titrate their dose of 
THC [42,43] so the issue has not yet been resolved.

If users do not titrate their dose of THC, the health effects of using more 
potent cannabis products may depend upon the user's experience. Higher 
average doses of THC will probably increase the risk of adverse 
psychological effects of cannabis use (such as anxiety and panic attacks) 
in first-time cannabis users [29] which might discourage further use of the 
drug. [29] Among regular cannabis users, an increased dose of THC may 
increase the risks of accidents among those who drive while intoxicated, 
especially if cannabis use is combined with alcohol. [29,44] Research to 
date has not confirmed that the use of cannabis alone impairs on-road 
driving or increases the risks of motor vehicle accidents [44] but the use 
of higher doses of THC may change this risk. The use of more potent 
cannabis products may also increase the risk of regular cannabis users 
developing dependence. [30] Regular use of higher potency cannabis by 
persons with schizophrenia may exacerbate their illness. [19]

Implications For Policy

1. We need better evidence on the THC content of cannabis. Unsubstantiated 
media assertions are a poor basis for public policy in any areas of public 

2. We need analyses of the THC content of samples of cannabis consumed by 
regular users. A systematic method of sampling should be used to ensure 
that it is not only the exceptionally potent samples of cannabis that are 
tested. Annual sampling of 100 to 200 samples of cannabis products would 
provide indications of THC content of cannabis.

3. We also need studies of the extent to which regular cannabis users are 
able to titrate their dose of THC. The assumed capacity of users to do so 
is used by some to discount concerns about any increase in the use of more 
potent forms of cannabis.

4. We need better assessments of the nature and extent of cannabis-related 
problems among adolescents and young adults.

5. More attention needs to be paid to the problems that may arise from 
cannabis use in health promotion efforts directed at young Australians. 
This could be done as part of programs that aim to prevent tobacco use and 
hazardous alcohol use among adolescents, [45] and as part of harm 
minimisation efforts to encourage less risky patterns of cannabis use among 
current users. [46]


The limited Australian data and data from the US and New Zealand suggest 
that there has been a modest increase in the THC content of cannabis 
plants. There probably has been an increase in the amount of THC consumed 
by Australian cannabis users as a result of an increased use of more potent 
cannabis products at an earlier age. Policies towards cannabis would be 
better informed if data were collected on the THC content of Australian 
cannabis products.


We would like to thank the following persons for their assistance: Keith 
Bedford, Greg Chesher, Paul Christie, Louisa Degenhardt, Paul Dillon, Paul 
Donkin, Linda Gowing, John Hannifin, Bill Lee, Simon Lenton, Michael 
Lynskey, Paddy Mahony, Jane Maxwell, Vince Murtagh, Helen Poulsen, James 
Robertson, Hari Singh, Greg Swensen and Paul Williams.



1. Malouf I Speech to New South Wales Drug Summit, 18 May 1999, Sydney. 
Proceedings of the New South Wales Drug Summit, 1999, Sydney. Retrieved 
November 4, 1999 available from:

2. Moffit A. Drug alert.- A guide to illicit drugs for parents. teachers, 
everyone. Sydney: Pan MacMillan; 1998.

3. Walters E. Marijuana: An Australian crisis. Malvern (Vic): Elaine 
Walters; 1993.

4. Adams IB, Martin BR. Cannabis: pharmacology and toxicology in animals 
and humans. Addiction 1996;91:1585-614.

5. Australian Institute of Health and Welfare. 1998 National Drug Strategy 
Household Survey: First results. Canberra: Australian Institute of Health 
and Welfare; 1999.

6. Australian Bureau of Criminal Intelligence. Australian Illicit Drug 
Report 1997-98. Canberra: Australian Bureau of Criminal Intelligence; 1999.

7. Gowing LR, Ali RL, White JM. Respiratory harms of smoked cannabis. 
Adelaide: Drug and Alcohol Services Council; 2000. DASC Monograph Research 
Series No.:8.

8. Western Australian Drug Abuse Strategy Office. Tends in drug purity 
levels in Western Australia. Perth: Western Australian Drug Abuse Strategy 
Office, 1999. Retrieved November 4, 1999. Available from: drugwestaus/html/cast/frames/statdata.html

9. Zimmer L, Morgan J. Marijuana myths, marijuana facts: a review of the 
scientific evidence. New York: The Lindesmith Center; 1997.

10. ElSohly MA, Ross SA, Mehmedic Z, Arafat R, et al. Potency trends of 
D9THC and other cannabinoids in confiscated marijuana from 1980-1997. J 
Forensic Sci 2000;45:24-30.

11. ElSohly MA, Ross SA. Quarterly report: Potency monitoring project. 
Report 69: January 1, 1999-March 31, 1999. University (MS): National Center 
for Development of Natural Products, University of Mississippi; 1999. NIDA 
Contract No.:NOIDA-4-7404.

12. Mikuriya T, Aldrich MR. Cannabis 1988, old drug, new dangers: the 
potency question J Psychoactive Drugs 1988;20:47-55.

13. Poulsen HA, Sutherland GJ. The potency of cannabis in New Zealand from 
1976 to 1996. Sci Justice. 2000;40:171-6.

14. More potent drug in use. Sutherland and St George Shire Leader 1995 
August 17: 5.

15. McAllister I, Moore R, Makkai T. Drugs in Australian society: Patterns, 
attitudes and policies. Melbourne: Longman Cheshire; 1991.

16. Makkai T, McAllister I. Marijuana in Australia: Patterns and attitudes. 
Canberra: Commonwealth Department of Health and Family Services; 1997. 
National Drug Strategy Monograph No.: 31.

17. Lynskey M, White V, Hill D, Letcher T, et al. Prevalence of illicit 
drug use among youth: Results from the Australian School Students' Alcohol 
and Drugs Survey. Aust N Z J Public Health 1999;23:519-24.

18. Edwards G, Anderson P, Babor TF, Casswell S, et al. Alcohol policy and 
the public good. Oxford: Oxford University Press; 1994.

19. Hall W. Cannabis and psychosis. Drug Alcohol Rev 1998, 17: 433-44.

20. Swift W, Hall W, Teesson M. Characteristics of DSM-IV and ICD-1 0 
cannabis dependence among Australian adults: results from the National 
Survey of Mental Health and Wellbeing. Drug Alcohol Depend. In press.

21. Torres ML, Mattick RP, Chen R, Baillie A. Clients of treatment service 
agencies: March 1995 Census findings. Canberra: Commonwealth Department of 
Human Services and Health; 1995.

22. Conroy A, Copeland J. The National Minimum Data Set Project for Alcohol 
and Other Drug Treatment Services: Report of the pilot study and 
recommended data items. Sydney: National Drug and Alcohol Research Centre; 
1998. Technical Report No.: 65.

23. Patterson KM, Holman DJ, English DR, Hulse GK, et al. First-time 
hospital admissions with illicit drug problems in Indigenous and 
non-Indigenous Western Australians: an application of record linkage to 
public health surveillance. Aust N Z J Public Health 1999;23:460-3.

24. Jablensky A, McGrath J, Herrman H, Castle C, et al. People living with 
psychotic illness: An Australian study 1997-98. Canberra: Mental Health 
Branch, Australian Commonwealth Department of Health and Aged Care; 1999. 
National Survey of Mental Health and Wellbeing - Report 4.

25. Hall W, Teesson M, Lynskey M, Degenhardt L. The prevalence in the past 
year of substance use and ICD-10 substance use disorders in Australian 
adults: Findings from the National Survey of Mental Health and Well-being. 
Addiction 1999;94:1541-50.

26. Fowler IL, Carr VJ, Carter NT, Lewin TJ. Patterns of current and 
lifetime substance use in schizophrenia. Schizophr Bull 1998;24:443-55.

27. Trimboli L, Coumerlos C. Cannabis and crime: treatment programs for 
adolescent cannabis use. Crime Justice Bull 1998;41:1-16.

28. Spooner C, Mattick R, Noffs W The nature and treatment of adolescent 
substance abuse: Supplement to Monograph 26. Sydney: National Drug and 
Alcohol Research Centre; 1998. Monograph No.: 40.

29. Hall W, Solowij N, Lemon J. The Health and Psychological Consequences 
of Cannabis Use.. Canberra: AGPS; 1994. National Drug Strategy Monograph 
Series No.: 25.

30. Hall W, Solowij N. The adverse effects of cannabis use. Lancet 

31. Senate Select Committee on Drug Trafficking and Drug Abuse. Report from 
the Senate Select Committee on Drug Trafficking and Drug Abuse. Part 1: 
Report. Canberra: Commonwealth Government Printing Office; 1971. 
Parliamentary Paper No.: 204.

32. Brouwer S. Mullumbimby madness. Australian Playboy 1981 August.

33. Queensland Advisory Committee on Illicit Drugs. Cannabis and the law in 
Queensland: A discussion paper. Toowong (Qld): Queensland Criminal Justice 
Commission; 1993.

34. Reilly D, Didcott P, Swift W, Hall W Long-term cannabis use: 
Characteristics of users in an Australian rural area. Addiction 1998;93:837-46.

35. Swift W, Hall W, Copeland J. Characteristics of long-term cannabis 
users in Sydney Australia. Eur Addict Res 1998;4:190-7.

36. Compton D, Dewey W, Martin B. Cannabis dependence and tolerance 
production. Adv Alcohol Subst Abuse 1990;9:129-47.

37. Fergusson DM, Horwood LJ. Early onset cannabis use and psychosocial 
adjustments in young adults. Addiction 1997;92:279-96.

38. Kandel DB, Davies M. Progression to regular marijuana involvement: 
phenomenology and risk factors for near daily use. In: Glantz M, Pickens R. 
editors. Vulnerability to drug abuse. Washington (DC): American 
Psychological Association; 1992:211-53.

39. Salmelainen P The correlates of offending frequency: A study of 
juvenile theft offenders in detention. Sydney: New South Wales Bureau of 
Crime Statistics and Research; 1995.

40. Herring RI, Jones RT, Bachman J, Mines AH. Puff volume increases when 
low-nicotine cigarettes are smoked. Br MedJ 1981;283:187-9.

41. Perez-Reyes M, DiGuiseppi S, Davis KH, Scnidler VH, et al. Comparison 
of marijuana cigarettes of three different potencies. Clin Pharmacol Ther 

42. Matthias P, Tashkin DP, Marques-Magallanes JA, Wilkins IN, et al. 
Effects of varying marijuana potency on deposition of tar and D-THC in the 
lung during smoking. Pharmacol Biochem Behav 1997;58:1145-50.

43. Wu TC, Tashkin DP, Rose JE, Djahed B. Influence of marijuana potency 
and amount of cigarette consumed on marijuana smoking pattern J 
Psychoactive Drugs 1988;20:43-6.

44. Smiley A. Marijuana: on road and driving simulator studies. In: Kalant 
H, Corrigal W, Hall W, Smart R,editors. The Health Effects of Cannabis. 
Toronto: Addiction Research Foundation; 1999:172-94.

45. Hall W, Nelson J. Public Perceptions ofthe Health and Psychological 
Consequences of Cannabis Use. Canberra: AGPS; 1995. National Drug Strategy 
Monograph No.: 29.

46. Swift W, Copeland J, Lemon S. Cannabis and harm reduction (Harm 
Reduction Digest 8). Drug Alcohol Rev 2000;19:101-12.
- ---
MAP posted-by: Richard Lake