In terms of the model set out in the Introduction, the
expected rise in diagnoses of schizophrenia and psychoses did
not occur over a 10 year period. This study does not therefore
support the specific causal link between cannabis use and the
incidence of psychotic disorders based on the 3 assumptions
described in the Introduction. This concurs with other reports
indicating that increases in population cannabis use have not
been followed by increases in psychotic incidence (Macleod
et al., 2006; Arsenault et al., 2004; Rey and Tennant, 2002).
Assessing the impact of cannabis use on trends in diagnosed schizophrenia in the United Kingdom from 1996 to 2005
Martin Frisher a,
⁎, Ilana Crome b
, Orsolina Martino a
, Peter Croft c
The incidence and prevalence of patients showing schizophrenic syndromes are unchanged or have even fallen while the use of cannabis has increased enormously. We must conclude that either previous schizophrenic illnesses have become much less common or that cannabis schizophrenia is rare and perhaps it may not even exist.
21 December 2002, David H. Marjot, BMJ
In the largest study of its kind so far, we have shown that recreational cannabis users do not release significant amounts of dopamine from an oral THC dose equivalent to a standard cannabis cigarette. This result challenges current models of striatal dopamine release as the mechanism mediating cannabis as risk factor for schizophrenia.
The current data do not support low to moderate lifetime cannabis use to be a major contributor to psychosis or poor social and role functioning in high-risk youth.