The Green’s Bill was voted down but we should still use the opportunity to challenge the myths surrounding cannabis without the debate being dominated by the hysteria of the corporate media and the lobbyists for big pharma. Our target should be the pseudo scientific and bureaucratic devotion to the myths underlying prohibition that has stymied all genuine cannabis reform in NZ. The biggest lie is that cannabis causes psychosis.
Progress with cannabis law reform is cripplingly slow. Why? A century of stigmatisation and prohibition has embedded a reactionary ‘harm’ mythology from the days of ‘reefer madness’ to today’s ‘cannabis psychosis’ in the popular culture, health science and medical practice. The mythology claims that cannabis is addictive, leads to ‘harder’ drugs, makes you anti-social, dumbs you down, makes you fail in education, perform poorly at work, and in the end, it makes you mad. These are myths that conveniently blame individuals as ‘dope fiends’ rather than the victims of the alienating capitalist society into which they are born.
We won’t make any headway towards the liberalisation of cannabis and other drugs until we debunk these ‘harm’ myths, and understand the nature of capitalism and its effects, inequality, poverty, social breakdown etc, as the real cause of drug use, and that drug abuse is a consequence of a policy of prohibition. But let’s skip the historical lecture and go straight to the misuse of science to bolster a hysterical prohibition culture.
NZ Misuse of Drugs Act and the myth of ‘harm’
The NZ Misuse of Drugs Act makes cannabis use a crime (unless waived by Ministerial approval) rather than a health need, on the grounds that it causes harm to health. Even if Cannabis were ‘decriminalised’ the assumption of ‘harm’ requires a ‘least harm’ approach to law reform by the Ministry of Health (MOH) which considers that cannabis ‘contributes’ to 32 deaths per year in NZ.
The NZ Drug Foundation (NZDF) rejects the MOH method of arriving at 32 deaths. It adopts a more moderate approach; that harm does not arise from “toxic overdoses”, but the “long-term effects” of use.
Cannabis does cause harm, but the harm comes from heavy long-term use and is mostly linked to mental health – lasting physical harm is unlikely, while poisoning or death is unheard of.
So, the NZDF proposes ‘decriminalisation’ of cannabis use by 2020 combined with heavy state regulation and licensing to minimise ‘harm’. It seems that the Drug Foundation is trying to steer the public debate for law reform down the path of least resistance. Yet that resistance seems to be coming mainly from the Government and Health bureaucracy rather than in the general population.
This conflict between ‘harm’ and ‘health’ is evident in the Drug Foundation itself. On the one hand, the NZDF Executive Director Ross Bell argues that the District of Columbia (US) legalisation of use, but not trade, might be best for NZ:
Mr Bell looks to the District of Columbia which changed its approach towards marijuana as recently as last year. It legalised its use, but not the trade in it, so under a new law, people can grow it, use it and give it away, but they can’t sell it. This is most closely in line with how Kiwis use it, Mr Bell said, suggesting it could be a starting point for discussion here. “If you think of the way Kiwis use cannabis, often they’re not getting it from the tinny house. It might be the first thing we allow is for people to grow and give.”
However, the Drug Foundation’s official new reform proposal repeats the ‘cannabis causes harm’ mantra.
We know that the majority of people use cannabis without serious harm.
However, a small proportion experience negative impacts such as anxiety, depression, memory loss and mood swings. Those who use cannabis long term may face health risks such as respiratory disease (if smoked) and mental illnesses such as schizophrenia, at least for those who may be predisposed.
Cannabis impairs driving, especially when combined with alcohol. It also carries the risk of dependency in around one in 10 users. Heavy use by young people has been linked to poorer outcomes in education and employment as well as a reduction in IQ points, though the research on this is mixed.
Our verdict? Cannabis can be harmful, so our law should focus on minimising harm, especially to young people. The best way to minimise harm is to tightly regulate use.
The evidence for and against ‘harm’
The evidence contests the ‘harm’ myth. It shows that the “negative effects” attributed to cannabis such as anxiety and depression, mood swings and even memory loss are are widely experienced in society by many who don’t use cannabis, and when they occur among the few users who ‘overdose’, this like any drug overdose, is largely the result of prohibition which works against safe and controlled conditions for drug use.
Dependency is another word for addiction and this claim is widely disputed, notably by Carl Hart, not only for cannabis, but for other ‘hard’ drugs as well (to his own surprise). He finds that when offered choices between drugs and money his experimental subjects will often reject drugs and take the money proving that drug addiction is learned behaviour in situations where you don’t get to choose money.
And the familiar story that cannabis ‘abuse’ by youth harms their schooling, college prospects and can lead to suicide, and so on, is probably the effect of prohibition. When kids who are expelled from school, denied financial support and criminalised explains much of the risk of suicide.
But the biggest driver of the ‘minimal harm’ orthodoxy in the NZDF model reform relies on the
Canterbury Study led by David Fergusson. Take the link between smoking cannabis and the risk of lung cancer. A US study using a large sample, led by Tashkin, showed that the ‘normal, moderate’ level of cannabis smoking had no measurable link to lung cancer. Not only that, cannabis smoking was better than non-smoking for some people! This study, however, was contradicted by the NZ study which did find a ‘correlation’ between heavy smoking and lung damage.
The largest epidemiologic (case-control) study of the association between marijuana use and lung cancer failed to demonstrate that marijuana increases the risk of developing lung (or, for that matter, upper airway) cancer.” He notes that a much smaller, recent study from New Zealand did claim to find a link, but only in very heavy users. He says, “The authors’ interpretation of their data can be faulted because of the small numbers of their subjects exhibiting such heavy use, which rendered their estimates of risk imprecise. [My emphasis]
The Scientific American, however, is more precise:
… looking at residents of Los Angeles County, the scientists found that even those who smoked more than 20,000 joints in their life did not have an increased risk of lung cancer. [my emphasis]
Tashkin is saying that the Canterbury study cannot claim to have found that heavy smoking of cannabis causes lung damage. His Los Angeles sample of heavy users found no significant correlation. The NZ sample of heavy smokers was too small to exclude all other factors that may explain the correlation between cannabis and lung damage. Therefore, the positive correlation in the NZ study between cannabis use and lung damage may be a consequence of lung damage caused by some other unmeasured cause.
While very heavy smoking of cannabis causing lung damage may be ‘common sense’, Tashkin’s large study was able to control for confounding factors and did not find any correlation, or causal link. If there are doubts about the Canterbury project’s results on lung damage, perhaps the NZDF concern about a studies ‘suggesting’ a causal link between cannabis use and ‘psychosis’ in adolescents should be also be re-examined.
Cannabis and Psychosis: Search for a causal link…
One of the reviews of studies (7, one of which was the Christchurch study) into this link by Le Bec PY et. al. (2009) found that “cannabis may be an independent risk factor” for psychosis:
Together, the seven studies were all prospective cohorts and represented 50,275 human subjects. There were three European studies (from Sweden, Holland and Germany), one from New Zealand and one from Australia. Only one study of the seven did not show a significant association between cannabis consumption and increase of the risk of developing a psychosis. However, this study had some bias, such as low level of cannabis use and the lack of evaluation of cannabis use after inclusion. For the six other studies, data show the existence of a significant association between cannabis use and psychotic disorders (with an increased risk between 1.2 and 2.8 in Zammit et al.’s study), particularly among vulnerable individuals (that is with a pre-psychotic state at the time of inclusion). Therefore, all the studies that assessed a dose-effect relationship showed this link between cannabis use and the emergence of psychosis or psychotic symptoms. The fact that all causal criteria were present in the studies suggests that cannabis use may be an independent risk factor for the development of psychosis. Results seem to be more consistent for vulnerable individuals with the hypothesis that cannabis use may precipitate psychosis, notably among vulnerable subjects. In particular, early onset of cannabis use during adolescence should be an environmental stressor that interacts with a genetic predisposition to induce a psychotic disorder. [my emphasis]
Note that the closest that this review comes to finding that cannabis may be a cause of psychosis, is that, “…cannabis use may be an independent risk factor for the development of psychosis.” The strength of that suggestion comes down to what are referred to as “all causal criteria” being controlled as potential confounders, that is, alternative causes. So, what is the strength of this claim in the Christchurch study? In their 2004 paper Fergusson et. al. addressed the problem of testing ‘causal linkages’ to eliminate other explanations. I will summarise their paper.
Fergusson et. al. (2004) describe how their statistical method allowed them to control for ‘confounders” (i.e. other possible causes) both, “fixed” influences, such as age, gender etc that did not change over the time-frame of the data, and “time-dynamic” influences, such as education, employment etc., that did change over the time-frame and could ‘confound’ the association between cannabis use and psychosis. By testing the association among all confounders, against cannabis use, and against psychiatric symptoms, the study concludes that there is still a residual association between cannabis use and psychosis, ‘independent’ (with its own causal effect) of the influence of all confounders, that justifies treating cannabis as a contributory cause.
The second important conclusion was that the study was able to compare the subjects scores on all the relevant variables over a time frame between 18, 21 and 25 years of age, and data collected at those three points showed that the “direction of cause” was from cannabis to psychosis, rather than the reverse.
How does one include all possible alternative causes in a longitudinal cohort study with a relatively small sample size, so that cannabis stands out as the ‘independent’ cause? Note that for the sake of the argument about ’cause’ I am not challenging the validity and reliability of the data such as ‘psychiatric symptoms’ at this point. Nor am I competent to assess the statistical methods used to perform these ‘tests’ in the Christchurch study. However, an assessment of such statistical methods was included in the review of the field by Ksir and Hart in 2016. They reviewed the evidence in support of two competing theories (hypotheses) between cannabis and psychosis; the “contributing cause” view held by the Christchurch study, and the “shared vulnerability” view held by the review authors.
Cannabis and Psychosis: Critical Overview of the Relationship.
According to Ksir and Hart (2016)
Interest in the relationship between cannabis use and psychosis has increased dramatically in recent years, in part because of concerns related to the growing availability of cannabis and potential risks to health and human functioning. There now exists a plethora of scientific articles addressing this issue, but few provide a clear verdict about the causal nature of the cannabis-psychosis association. Here, we review recent research reports on cannabis and psychosis, giving particular attention to how each report provides evidence relating to two hypotheses: (1) cannabis as a contributing cause and (2) shared vulnerability. Two primary kinds of data are brought to bear on this issue: studies done with schizophrenic patients and studies of first-episode psychosis. Evidence reviewed here suggests that cannabis does not in itself cause a psychosis disorder. Rather, the evidence leads us to conclude that both early use and heavy use of cannabis are more likely in individuals with a vulnerability to psychosis. The role of early and heavy cannabis use as a prodromal [symptomatic of an attack or disease] sign merits further examination, along with a variety of other problem behaviors (e.g., early or heavy use of cigarettes or alcohol and poor school performance). Future research studies that focus exclusively on the cannabis-psychosis association will therefore be of little value in our quest to better understand psychosis and how and why it occurs. [my emphasis]
In other words, the authors conclude that cannabis cannot be shown to be a cause of psychosis, and the best interpretation of the limited evidence is that it suggests that cannabis may be part of a “shared vulnerability” where those ‘vulnerable’ to psychosis may use cannabis along with other substances as a means of self-medication.
The policy conclusions that flow from this conclusion are to reject cannabis as a cause of psychosis on the basis of a weak claim of “contributory causation”, and to address the common social and genetic factors that cause this ‘shared vulnerability’ associated with cannabis use. This shifts the focus away from the prevailing model of “harm” towards a model of “preventative health”.
That this is a highly politicized area is attested to by the debate between Ksir and Hart and the authors of one of the studies they reviewed, over why a correlation cannot as a rule be a cause, and whether the the appropriate policy response is the legalization of cannabis and other drugs or continued prohibition.
The significance of these policy options is clear if the most obvious cause of ‘harm’ is prohibition itself rather than the ‘harm’ attributed to cannabis. For example, the US study referred to above claiming that cannabis use led to school dropouts, failure to attend college, and more suicide attempts, could easily be explained as the effects of prohibition. The author advocates that prohibition should be replaced by prevention.
Conclusion: Prohibition causes the harm attributed to cannabis
The reform debate therefore comes down to one of two approaches. First the ‘harm’ model. Modest and incremental change via decriminalisation leaves the growth, sale and consumption, regulated and licensed, redirecting drug policy from prohibition towards state control and regulation. This is the moderate road which makes the assumption of ‘harm’ an excuse to protect individuals from harming themselves. The question of what constitutes ‘harm’ is reviewed, and the myths that cannabis is a ‘gateway drug’, that overdoses are ‘toxic’ and can even cause death, are rejected. Nevertheless, cannabis is still held to cause ‘harm’ among youth, long-term heavy users and those genetically or socially at risk of mental illness. For that reason law reform must be gradual, based on ‘best science’ and guided by the medical model of ‘least harm’.
The second approach is that cannabis is a harmless natural plant, used as a preventative and palliative medicine over millennia. Cannabis and our endocannabinoid system have co-adapted over our history of evolution. It is not only ‘harmless’ it is ‘harm-killing’ with many (including as yet undiscovered) health benefits. These include pain relief replacing opioids, stopping spasms in MS, and seizures in epileptics and pain in advanced cancer etc. And coming over the horizon is the prevention and elimination of diseases including cancer, Alzheimer’s, schizophrenia, etc. In assessing these health benefits, we should combine all sources of evidence: anecdotal, medical, laboratory research, epidemiological, as well as the ‘gold standard’ clinical trials, to understand fully the important role of cannabis in our lives.
I conclude that the ‘harm’ associated with cannabis is mainly caused by the policy of prohibition that reflects the objectives of powerful groups and class interests in society, and is reproduced in research assumptions and media sensationalism. It is not an attribute of cannabis itself but of politically loaded economic and social policies. We can see this clearly in the benefits that have accrued in many nations such as Portugal and Paraguay, and in those US states where decriminalisation or legalisation has occurred. Medical Cannabis has now been approved by WHO. But we still have to overcome the fear of THC as the cause of ‘reefer madness’ and prove that in a safe, legal environment, CDB cannot be separated from THC and the other components of cannabis without losing the full health benefits of the herb.
We can make a start as capitalism goes into its terminal decline and fall, but only fully reap the benefits of cannabis as part of the socialisation of production for need and not profit in a socialist society that has returned to nature in time to avoid human extinction.
Dave Brownz is TDBs Marxist blogger because every Left wing blog needs a Marxist