|Own your ow legal marijuana business||
Your guide to making money in the multi-billion dollar marijuana industry
|Major Studies of Drugs and Drug Policy|
|Canadian Senate Special Committee on Illegal Drugs|
|Volume I - General Orientation|
Chapter 5 - Cannabis: From Plant to Joint
Upon inhalation, and depending on the smoker's way of smoking and smoking experience, between 15% and 50% of the D9THC present in the smoke is absorbed into the bloodstream. The percentage also depends on the D9THC concentration in the smoked product. The substance is absorbed very quickly, and maximum blood concentrations are achieved in less than 15 minutes after the start of inhalation. The effects felt almost immediately after absorbing the smoke diminish gradually over the next 60 minutes and generally last a maximum of three hours after inhalation. In other words, THC levels in the blood plasma are highest immediately after absorption, whereas maximum effects are felt approximately 30 to 40 minutes later. The following table reproduced from the ISERM collective assessment, shows the time to appearance and duration of detection of cannabinoids in the blood.
Concentration, time to appearance1 and duration of detection2 of cannabinoids in the blood after smoking a marijuana cigarette containing 15.8 mg or 33.8 mg of D9THC
Bio‑availability of D9THC is
slower and weaker when the drug is ingested orally (cookies, cakes, herbal teas):
approximately 4% to 12%; although slower to be felt and different in quality,
its effects are longer lasting.
In all, we do not know how the
effects of THC (concentration) interact with personal factors (way of smoking,
health status, alcoholism or medication). However, it is likely that the same
THC concentration does not have the same effect on all smokers, which moreover
tend to be confirmed by the plasticity of cannabis in the hormonal stream (see
highly lipophilic and is quickly distributed to all fatty tissues, including
the brain. It is also characterized by an entero‑hepatic cycle and renal
reabsorption which results in persistent effects. In a driving simulator study,
a significant linear correlation was found up to seven hours following
absorption, particularly on the trajectory control.
undergoes oxydative metabolism resulting in the production of various elements,
in particular 11‑hydroxy‑tetrahydrocannabinol (11‑OH D9THC) a
psychoactive metabolite which, transported by albumin, whereas D9THC
attaches mainly to lipoproteins, penetrates the brain more deeply than D9THC;
potentially psychoactive but whose action would be negligible; and various
other components not known for their psychoactive effects. In addition to the
potentially psychoactive elements, cannabis contains approximately
200 derivatives of combustion and pyrolysis comparable to those found in
tobacco, though some of which are highly carcinogenic and are more concentrated
in cannabis smoke than tobacco smoke.
Cannabinoids are eliminated in
various ways: through digestion, the kidneys and perspiration. Approximately
15% to 30% of D9THC in the blood is eliminated in
urine, 30% to 65% through stools. Because it binds strongly to tissues, D9THC is
eliminated slowly in urine: the urine of regular heavy users contains traces of
D9THC‑COOH 27 days after
they have last used cannabis.
Regular users metabolize D9THC up to twice as fast as individuals who have never previously used the drug. One study showed, in particular, that the intravenous administration of one 5 mg dose of D9THC resulted in higher blood levels in regular users than occasional users.
Cannabinoids act on the body through
the endogenous cannabinoid system, consisting of neurochemical substances
(endogenous ligands) and specific receptors. The behavioural and central
effects of cannabis are due to the agonistic action of its main ingredients (in
particular D9THC, exogenous cannabinoid), on the
endogenous cannabinoid receptors (anandamide, 2‑arachidonoylglycerol)
present in the nervous tissues of the brain.
Although the chemical structure of D9THC was
identified by Mechoulam in 1964, it wasn't until very recently that
the characteristics and location of the endogenous cannabinoid system was
determined. Two types of cannabinoid receptors have been
isolated: CB1 in 1990 and CB2 in 1993. CB1 is mainly expressed in the central and
peripheral nervous system. CB2 is expressed essentially in the cells of the
immune system. It follows from this distribution that CB1 is essentially
involved in psychotropic effects and CB2 in immunomodulatory effects.
The main endocannabinoids are
arachidonoylethanolamide (also called anandamide - a word derived from
Sanskrit, literally meaning congratulated) and 2‑arachidonoylglycerol (2‑AG).
These are the only two endogenous molecules known to be capable of binding to
cannabinoids receptors CB1 and CB2 and replicating the pharmacological and
behavioural effects of D9THC.
Anandamide levels in the brain are comparable to those of other
neurotransmitters such as dopamine and serotonine. The highest levels
corresponding to high CB1 density areas, that is to say the hippocampus, striatum,
the cerebellum and the cortex. Like anandamide, 2‑AG reproduces all the
behavioural effects of D9THC or
anandamide, but its action is less powerful.
The CB1 receptors are among the most
abundant neuronal receptors in the central nervous system, and their
distribution correlates remarkably with the behavioural effects of cannabinoids
on memory, sensory perception and control of movements, as shown in the table
Location of CB1 receptors in the CNS and correlated pharmacological effects 
++: abundant marking; +: intermediate marking; ‑: little or no
This concentration of CB1 receptors
largely explains the effects of D9THC.
Intense expression of CB1 receptors in the basal nucleus and molecular layer of
the cerebellum is thus consistent with the inhibiting effects of cannabinoids
on psychomotor performance and motor coordination. Their expression in the
cortex and hippocampus is consistent with the modulation of elementary forms of
learning, explaining in particular the reversible deleterious effects on
short-term memory and cognitive function. Their lack of marking in the
brainstem explains the absence of acute toxicity or lethal doses of cannabis
derivatives. The CB1 receptors in the thalamocortical system participate in the
sensory disturbances and analgesic properties of cannabis. Similarly, the
presence of receptors in the periaqueductal area and the dorsal horn of the
spinal cord contribute to its antinociceptive power.
We also note that the CB1 receptors
do not merely inhibit brain function. As a result of circuit effects,
cannabinoids can stimulate certain neuron populations, in particular
dopaminergic cells in the mesolimbic pathway. Together with the observation
that prolonged treatment with cannabis (at doses corresponding to the
equivalent of 575 cannabis cigarettes a day!) appears to induce lasting
adaptive changes to the central nervous system and to the positive relationship
between cannabinoids and stress hormones (corticotrophine), this explains the
difficulties (irritability, sleep disorders and so on) observed in regular
users when they have stopped using cannabis. We return to this issue in the
Chapter 7 in the discussion on cannabis tolerance and dependence.
Lastly, recent works suggest there
are significant interindividual variations in the effects of cannabinoids
depending on sex steroid hormones in men and women: it appears that the effects
of exogenous and endogenous cannabinoids can be modulated by the hormonal state
of each individual and that, in exchange, the CB1 receptors and
endocannabinoids are able to regulate hormonal activity.
As was observed in the WHO report in
1997, various research questions remain unanswered, in particular how and to
what extent cannabis use alters the endogenous cannabinoid and what the
relationship is between blood plasma cannabinoid levels and induced behavioural
This section is based to a large extent on the INSERM 2001 report as well
as the European scientific report 2002 and the survey work done by Wheelock
2002 for the Committee.
INSERM (2001) Cannabis. Quels
effets sur le comportement et la santé? Paris: author, page 340.
Cited in INSERM (2001) op. cit.,
Guoli and Mechoulam (1964) op. cit.
Devane, W.A. et al.
(1992) "Isolation and structure of a brain constituent that binds to the
cannabinoid receptor", Science,
258 (5090): 1946‑1949.
Matsuda, L.A. et al. (1990) "Structure of a cannabinoid
receptor and functional expression of the cloned DNA", Nature, 346(6284) 5561‑564.
Munro, S. et al. (1993) "Molecular
characterization of a peripheral receptor for cannabinoids", Nature, 365: 61‑65. Note that a
recent scientific conference of the National Institute on Drug Abuse in the
United States reported on the work of researchers on the hypothesis that there
are additional receptors and other ligands. To our knowledge, the latter have
not yet been formally identified in the research setting.
Table reproduced from INSERM (2001), op.
cit., page 298.
Schaffer Library of Drug Policy
Major Studies of Drug and Drug Policy
Marihuana, A Signal of Misunderstanding - The Report of the US National Commission on Marihuana and Drug Abuse
Licit and Illicit Drugs
Short History of the Marijuana Laws
The Drug Hang-Up
Congressional Transcripts of the Hearings for the Marihuana Tax Act of 1937
Frequently Asked Questions About Drugs
Basic Facts About the Drug War
Charts and Graphs about Drugs
Information on Alcohol
Guide to Heroin - Frequently Asked Questions About Heroin
LSD, Mescaline, and Psychedelics
Drugs and Driving
Children and Drugs
Drug Abuse Treatment Resource List
American Society for Action on Pain
Let Us Pay Taxes
Marijuana Business News
Reefer Madness Collection
Medical Marijuana Throughout History
Drug Legalization Debate
Legal History of American Marijuana Prohibition
Marijuana, the First 12,000 Years
DEA Ruling on Medical Marijuana
Legal References on Drugs
GAO Documents on Drugs
Response to the Drug Enforcement Agency
|Drug Information Articles|
Taking a drug test:
How To Pass A Drug Test
Beat Drug Test
Pass Drug Test
Drug Screening Tests
Drug Addiction Treatment