Cannabis Main Page


The hennep plant, Cannabis sativa, has been in use as a source of fibres for clothing and rope for 12,000 years. The first source for the use of the drug is the Pen Ts'ao, a Chinese standard work on medicinal herbs which dates from the 28th century B.C.
In Western Europe it was an important medicinal ingredient for a variety of disorders until the end of the last century. In the following decades, as we have seen, it was made a prohibited drug in the framework of prohibition. This was due in no small part to the actions of Anslinger, the head of the impoverished alcohol prohibition officials. His propaganda films like 'Reefer madness' created the image of a drug which could change angels into devils.

Cannabis achieved notoriety as an illegal drug in the Netherlands in the early 1960s. At first its use was mainly confined to a relatively small group of young people (students, artists), but it grew very rapidly in the second half of the 1960s. Around 1970 cannabis use had become the paramount symbol for the hippies. While in the late 1960s the cannabis market was mainly in the hands of a large number of small importers and there were few intermediate links between the importers and the consumers (in many cases the importer was also the retailer), this rapidly changed under the influence of prohibition.
With the growth in the number of consumers, the wholesale market was taken over more and more by the criminal sector. After the rapid growth in the early 1970s, its use has now stabilized, although there has been another upsurge in Europe and the US during the last couple of years.

The Netherlands has acquired an important position as a transit country. This is due less to the relatively low penalties for the international cannabis trade than to the fact that, as one of the major transshipment countries in Europe, the Netherlands exercises the same transit function for illegal as for legal goods.


The cannabis plant contains more than 60 different cannabinoids, the most active of which is tetrahydrocannabinol.


Cannabinol (CBN) has around onetenth of the strength of THC. THC is found in the plant in the form of THC acid, which has no effects, but it is totally transformed into THC when heated. Cannabis occurs in two forms: the dried tops of the female plant (marihuana) and the resin collected from the flowers and topmost leaves (hashish). The THC content in marihuana varies between 5 and 15%. Hashish is somewhat stronger.

The effective dose is between 2 and 22 mg when smoked, and between 20 and 90 mg when taken orally. Under normal smoking conditions, 16 to 19% of the THC in the joint is consumed, the rest is pyrolysed.
The lethal dose is not known. Tests with animals indicate that the relation between the lethal and the effective dose can be estimated at 4,000 - 40,000. For comparison, the corresponding relation for alcohol is 4 - 10.

When THC enters the blood stream, it is rapidly absorbed by the fatty tissue (halflife 30 mins.). It then returns gradually to the blood, is metabolized, and is eliminated in urine and faeces (halflife: a few days!). Repeated use leads to accumulation in fat and liver, but not in the brain. As a result, THC metabolites can still be found in the urine weeks after use.

When smoked, the acute effects begin to appear after a few minutes. The plasma concentration peaks after 7 to 10 minutes, but the peak effect is only felt after 20 to 30 minutes. It continues to take effect for 2 to 3 hours. When consumed orally (space cake), it only takes effect after 1 to 2 hours, and the effect lasts for 5 to 12 hours.

Operational mechanism

For a long time the operational mechanism of THC was a complete mystery. It was not until 1990 that the specific receptor for THC was found. Our body must therefore produce THClike substances as well.
These receptors were situated in the hippocampus (which explains the effects of THC on memory), in the amygdala (does this account for the low level of aggression in the contented smoker?), and in the cortex (responsible for freer associations?).

THC has a potentiating effect on the dopaminergic mesocortical reward system because presynaptic THC receptors are situated on the peptidergic axoaxonic synaptic link with the dopaminergic neurons (which in turn stimulate peptidergic neurons) in the nucleus accumbens. (note 84)

Dependence and tolerance

Physical dependence does not occur, psychic dependence is rare. Initially inverted tolerance occurs, later a mild tolerance can occur under chronic use. In some cases psychological dependence can occur.

Acute effects

These are: euphoria, altered perception of time, a disturbance of the shortterm memory (imprint disturbance), reduced aggression. Increased sensitivity to sound (music) and a freer power of association are subjectively experienced. There is sometimes a sharp rise in appetite. Somatic: tachycardia, an increased blood pressure when horizontal, but a drop when vertical; increased blood supply to the conjunctivae, increased cerebral blood supply, especially in the frontal regions. (note 85) An increase in waves is perceptible on the EEG. There is a reduction in REM sleep.

High doses can lead to hallucinations, delusions and paranoid feelings, resulting in the symptoms of a toxic psychosis.

The ability to drive is negatively affected, but since the negative effects are overrated, this is partly compensated by more cautious behavior, in contrast to the effect of alcohol, the effects of which are underrated. (note 86)

There is an increasing demand for the medical application of herbal marihuana. Pure THC is already applied under the brand name Marinol for glaucoma, to counteract nausea for cytostatics to increase appetite.

A combination of cannabis and alcohol can result in temporary collapse and vomiting.

Chronic effects

A large number of claims on the harmful effects of the use of cannabis have been made over the years.

The use of cannabis has been supposed to lead to psychopathology, antisocial and criminal behavior, psychoses, the use of harder drugs on pharmacological grounds (the steppingstone theory), and the 'amotivational syndrome'.

These claims cannot be verified by epidemiological research because, even if a connection is found, this need not necessarily be a causal one. A connection can also be the result of common underlying factors. This is best illustrated by an investigation in which 101 children were followed from the age of 3 to the age of 18. When they were eighteen, it proved possible to divide these children up on the basis of their drug use into the following categories: abstainers, experimenters and frequent users. These distinctions could be traced back to differences during their early years and were related to the parent/child relationship. Incidentally, the experimenters were shown to be the most balanced, which thus does not mean that experimenting with drugs promotes equilibrium! This study also showed that the amotivational syndrome is related, not to the use of cannabis, but to the early years of childhood. (note 87) The general consensus is that cannabis acts as an inhibitor on violent and aggressive behavior, except perhaps in the case of a few unstable individuals.
Similarly, there is no indication that the use of cannabis leads to chronic psychoses. The steppingstone theory should also be rejected.
While it is true that many heroin users started with cannabis, only very few cannabis users move on to the harder drug. If there is a precondition for cannabis use, it is the use of tobacco! Nonsmokers will only use cannabis very rarely. (for an extensive survey of the literature see 88, 89, 90)

The imprinting disturbance as an acute result of cannabis use leads to the question of whether chronic use leads to similar persistent effects, but the literature does not provide a clearcut answer to this question. Moreover, no prospective studies have been carried out.

At the physical level, there are no indications for neurotoxicity, disturbed cerebral circulation, cerebral atrophy or reduced cerebral function. (notes 91, 92, 93)

Although the presence of THC receptors on leucocytes suggests an immunosuppressive effect, a synthetic THC derivative dronabinol has been approved as a medicine against AIDS anorexia and there is no clinical confirmation.

The chronic effects on the lungs are probably the most striking.
Chronic cannabis smoking causes potential bronchitis, emphysema and lung cancer. Cannabis contains larger quantities of carcinogenic substances than tobacco, but this is compensated by the fact that cannabis is smoked in much smaller quantities than tobacco.

Although a drop in the testosterone, FSH, LH and prolactin content has been perceived in some studies (note 94), these findings proved to be unsubstantiated.(note 95) There have been repeated reports of negative effects on sperm, supported by the presence of (only a few) THC receptors in the testicles. It is possible that THC inhibits the growth of the fetus, (note 96) but this hypothesis has not been confirmed in a prospective study.(note 97, 98) Tests on children aged 1, 2 and 3 who had been prenatally exposed to THC did not reveal any deviations, although they displayed more tremors as neonates. It was not until the age of 4 that very subtle differences were detected, but the authors claim that these could also be the result of the poor diet during pregnancy or the postnatal mother/child relationship. (note 99)

Tips for visitors of coffeeshops

The Marijuana Myths

The Case for Regulated Production
Paper for 1995 International Harm Reduction Conference by Mario Lap on Cannabis in Europe and particularly The Netherlands

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