^ by that logic we'd have opioid psychosis as well.
It's really not that simple. To get a better understanding of the endocannabinoid system's interaction with dopaminergic activity and psychosis, I recommend reading Leweke.
Here is a quasi-related excerpt-
We have previously shown that levels of the endocannabinoid anandamide in cerebrospinal fluid (CSF) in antipsychotic-naive patients with schizophrenia[1–3] are both markedly elevated and negatively correlated with psychotic symptoms. A model of dopamine/endocannabinoid interaction in acute schizophrenia was proposed where (over-)activation of dopamine D2 receptors is associated with an increased release of anandamide counter-balancing dopamine-mediated psychotic symptoms by strengthening an endogenous feedback loop. This model suggests an adaptation of endocannabinoidergic function over a long period to a slow, gradual increase in dopaminergic neurotransmission.[4] We investigated whether changes in the endocannabinoid system are already noticeable in initial prodromal states of psychosis and test the hypothesis that an elevation of anandamide in CSF is apparent in this early stage of the disease.
http://bjp.rcpsych.org/content/194/4/371.full
Leweke has also found that the phytocannabinoid cannabidiol (CBD), while it doesn't agonize CB receptors, does inhibit the degradation of anandamide leading to another finding that patients with higher CSF levels of anandamide have reduced psychotic symptoms showing potential utility of a drug that inhibits degradation of a natural cannabinoid in treating psychosis.
The 'dopamine hypothesis' for schizophrenia fails to comprehensively explain the condition and many in the field feel schizophrenia may be better understood via a 'endocannabinoid hypothesis' - either way, the two systems are complexly and inextricably linked, play a role in schizophrenia and excessive cannabinoid consumption has the potential to produce psychosis mimicking schizophrenia.