1. WASUA Western Australian Substance Users Association

2. “Two of my favorite things are sitting on my front porch SMOKING a pipe of sweet HEMP, and playing my Hohner harmonica” President Abraham Lincoln. “Make the most you can of the Indian HEMP seeds and sow it everywhere” “Make the most you can of the Indian HEMP seeds and sow it everywhere” President George Washington. “I now have absolute proof that smoking even one Marijuana cigarette is equal in brain damage to being on Bikini Island during an H-bomb blast” “I now have absolute proof that smoking even one Marijuana cigarette is equal in brain damage to being on Bikini Island during an H-bomb blast” President Ronald Reagan.

3. Reefer Madness Uncomfortable truths about Cannabis use

4. Do Drug Laws influence per-capita use of Cannabis?

5. 1998-2004 Household Survey 19981998 2001 2004 DrugEver Recent RecentRecent Ever % % % % % Alcohol90 81 8384 91 Tobacco65 26 2321 47 Cannabis39 18 1311 34 Hallucinogens10 3 10.7 8 Amphetamines9 4 43 9 Benzodiazepines6 3 11 3 MDMA5 2 33.5 8 Inhalants4 1 0.40.4 3 Cocaine4 1 11 5 Heroin 2 1 0.20.2 1.4

6. Does banning smoking implements reduce cannabis consumption?

7. How physically harmful is Cannabis? Cannabis is the least toxic psychoactive drug known. However, acute toxicity is not the only measure of drug-related harm.

10. Reported increases in potency are an artifact of changing practices in growing technique. Is Cannabis getting “stronger”?

11. Cannabinoids as Drug Treatment. Injections of THC eliminate dependence on opiates in stressed rats, according to a research team at the Laboratory for Physiopathology of Diseases of the Central Nervous System (France) in the journal Neuropsychopharmacology.

12. Cannabinoids as Drug Treatment. Deprived of their mothers at birth, rats become hypersensitive to the rewarding effect of morphine and heroin (substances belonging to the opiate family), and rapidly become dependent. When these rats were administered THC, they no longer developed typical morphine-dependent behavior. In the striatum, a region of the brain involved in drug dependence, the production of endogenous enkephalins was restored under THC, whereas it diminished in rats stressed from birth which had not received THC. Researchers believe the findings could lead to therapeutic alternatives to existing substitution treatments.

13. Cannabinoids as Drug Treatment. In humans, drug treatment subjects who use cannabis intermittently are found to be more likely to adhere to treatment for opioid dependence, according to clinical trial data published in the July/August 2009 issue of American Journal on Addictions. Historically, similar findings were reported by Dr. Clendinning, who in 1843 utilized cannabis substitution for the treatment of alcoholism and opium addiction and Dr. Birch, in 1889, who reported success in treating opiate and chloral addiction with cannabis.

14. Does Cannabis use “cause” Psychosis?

15. The psychosocial sequelae of use of cannabis and other illicit drugs by young people: systematic review of longitudinal, general population studies. Macleod et al. Lancet 2004 http://www.thelancet.com/journals/lancet/article/PIIS014067360761135 0/fulltext “Available evidence does not strongly support an important causal relation between cannabis use by young people and psychosocial harm, but cannot exclude the possibility that such a relation exists”. Cannabis use and risk of psychotic or affective mental health outcomes: a systematic review. Moore et al. Lancet 2007 http://www.thelancet.com/journals/lancet/article/PIIS014067360761162 3/abstract “There was an increased risk of any psychotic outcome in individuals who had ever used cannabis (pooled adjusted odds ratio=1·41, 95% CI 1·20–1·65). Findings were consistent with a dose-response effect, with greater risk in people who used cannabis most frequently (2·09, 1·54–2·84)”.

16. Causal Association Between Cannabis and Psychosis: Examination of the Evidence. Louise Arseneault, et al British Journal of Psychiatry 2004 http://www.focus.psychiatryonline.org/cgi/content/abstract/5/2/270 (Cannabis use is described as a “component cause”, neither necessary nor sufficient in itself… it is suggested that the epidemiology can be explained if vulnerability is largely confined to those with a genetic predisposition). CNR1, central cannabinoid receptor gene, associated with susceptibility to hebephrenic schizophrenia. H Ujike et al. Molecular Psychiatry 2002. http://www.nature.com/mp/journal/v7/n5/abs/4001029a.html http://www.nature.com/mp/journal/v7/n5/abs/4001029a.html Action of Cannabidiol on the Anxiety and Other Effects Produced by Δ9-THC in Normal Subjects. Zuardi et al Psychopharmacology 1982 http://www.springerlink.com/content/qx40446564488706/fulltext.pdf?page=1 (THCΔ9 in isolation can provoke anxiety and panic attacks or transient psychosis in healthy individuals. CBD is an antipsychotic).

17. Henquet et al; doi.wiley.com/10.1111/j.1600-0447.2008.01265.x http://www3.interscience.wiley.com/journal/121414232/abstract?CRET RY=1&SRETRY=0http://www3.interscience.wiley.com/journal/121414232/abstract?CRET RY=1&SRETRY=0 The finding that in Val ⁄ Val subjects cannabis use was associated with increased levels of hallucinations rather than delusions is in line with the tonic-phasic dopamine theory and previous work on abnormal reactivity of the dopamine system to environmental stimuli. Neither cannabis nor COMT Val/Met genotype alone may be sufficient to substantially influence these phenomena, but their combination may produce functional increases in phasic dopamine, independent of, or hyper-reactive to, external stimulation. In the flow of daily life, hallucinations may thus arise after cannabis exposure, but only so in individuals with pre-existing subcortical hyperdopaminergia, and ⁄ or a sensitized dopaminergic system.

18. Cerebrospinal Anandamide Levels are Elevated in Acute Schizophrenia and are Inversely Correlated with Psychotic Symptoms Andrea Giuffrida et al Neuropsychopharmacology 2004 http://www.cmcr.ucsd.edu/geninfo/Giuffrida.pdf http://www.cmcr.ucsd.edu/geninfo/Giuffrida.pdf What, if any, are the functional consequences of elevated anandamidergic activity in the schizophrenic brain? Pharmacological experiments in the rat have suggested that anandamide release may serve as an inhibitory feedback signal countering dopamine activation of motor behavior (Giuffrida et al, 1999; Beltramo et al, 2000). The negative correlation of CSF anandamide with psychopathological symptoms in acute, antipsychotic- naı¨ve paranoid schizophrenics suggests that anandamide might play a similar adaptive role in acute schizophrenia.

19. Cerebrospinal Anandamide Levels are Elevated in Acute Schizophrenia and are Inversely Correlated with Psychotic Symptoms Giuffrida et al Neuropsychopharmacology 2004 http://www.cmcr.ucsd.edu/geninfo/Giuffrida.pdf http://www.cmcr.ucsd.edu/geninfo/Giuffrida.pdf Heavy cannabis use is considered a risk factor for the clinical manifestation of schizophrenia and might promote psychotic episodes in vulnerable individuals (Andre´asson et al, 1987; Arseneault et al, 2002; Linszen et al, 1994). How do these clinical observations relate to the present findings? One possibility is that heavy cannabis abuse may lead to desensitization of brain CB1 receptors, which may in turn facilitate psychoses. This hypothesis needs to be tested in humans, but is supported by animal studies showing that CB1 receptors undergo rapid desensitization in vivo (Sim-Selley and Martin, 2002) and that D9- THC antagonizes Damphetamine-induced stereotypies in naı¨ve rats, but not in animals made cannabinoid tolerant by repeated D9- THC injections (Gorriti et al, 1999).

20. Neurocognitive performance of methamphetamine users discordant for history of marijuana exposure. Gonzalez et al. http://dx.doi.org/10.1016/j.drugalcdep.2004.04.014 Revisiting the self-medication hypothesis from a behavioral perspective. Blume et al. Cognitive and Behavioral Practice 2000, http://linkinghub.elsevier.com/retrieve/pii/S1077722900800486 The neuropsychological correlates of cannabis use in schizophrenia: Lifetime abuse/dependence, frequency of use, and recency of use. Carissa et al. Schizophrenia Research 2007 doi:10.1016/j.schres.2007.08.006

21. The Arendt study reviewed records of all individuals born in Denmark between January 1,1955, and July 1, 1990 (n=2,276,309), with 21.9 million person-years of follow- up between 1994 and 2005. It examined familial histories for those Danes who were diagnosed with “cannabis-induced-psychosis” and those who were diagnosed with schizophrenia. Arendt et al; http://archpsyc.highwire.org/cgi/content/abstract/65/11/1269 Discussion at Reuters Health; http://www.reuters.com/article/healthNews/idUSTRE4A26JV20081103 In a previous study, Arendt and colleagues found that nearly half of people who had an episode of cannabis- induced psychosis went on to develop schizophrenia within the next six years…

22. …In the current study, the researchers looked at the genetic roots of both conditions by comparing the family histories of 609 people treated for cannabis-induced psychosis and 6,476 who had been treated for schizophrenia or a related psychiatric condition. They found that individuals treated for cannabis-related psychotic episodes had the same likelihood of having a mother, sister or other "first-degree" relative with schizophrenia as did the individuals who had actually been treated for schizophrenia themselves. This suggests that cannabis-induced psychosis and schizophrenia are one and the same, the researchers note. Based on the findings, the researcher says, "cannabis- induced psychosis is probably not a valid diagnosis. It should be considered schizophrenia."

23. WASUA “Because sometimes, what you don’t know CAN hurt you…” Paul Dessauer, Outreach Coordinator. outreach@wasua.com.au