Chapter 7 - Cannabis: Effects and Consequences

Acute effects of cannabis

 

In toxicology, acute effects are those that are produced immediately after use and while the psychoactive effects are being experienced. These effects also correspond to what has been called cannabis intoxication ever since Moreau de Tours in 1845.[1][17] The “real” effects – on biological systems – and the effects experienced by users can vary based on a set of factors, such as the user’s experience with cannabis and other drugs (including tobacco), the user’s expectations and the context of use. In fact, [translation] “the psychoactive effects of cannabis, more than any other substance, vary from one subject to another and, for the same subject, from one experience to another.”[2][18] Additionally, with no reliable method to measure THC content in plasma, it is difficult to link the duration and strength of effects to the various cannabis preparations, in particular because of variations in the composition of the substance and in the bioavailability of THC. It is even more difficult to attribute relatively rare effects (for example, the appearance of psychotic symptoms) insofar as it is hard to decide if the co-occurrence is coincidental, if these effects stem from other substances often associated with cannabis use or from very high doses of cannabis, or from interactions between these various factors.[3][19]

The acute effects of cannabis are relatively well documented. Research sometimes distinguishes between central and peripheral effects[4][20], sometimes between somatic effects and psychological or psychomotor effects[5][21], and sometimes is simply content to list the effects of one type or another.[6][22]

Cannabis intoxication is generally considered to consist of two main phases:

 

·v    The first phase, the “high”, includes the following effects:

··               A change in general mood, accompanied by gaiety or even hilarity, talkativeness, and a carefree feeling

··               A change in physical experience, including a feeling of well-being and satisfaction, a feeling of calm and relaxation, sociability

··               Alteration of intellectual functions, including increased self-confidence, magical thinking (feeling of being able to perform tasks more easily), distorted perception of time, space and self-image

··               Sensory changes, marked by increased sensory perceptions (colours, sounds sometimes seem more intense), stronger tactile impressions.

· 

·v    The second phase, “coming down”, is characterized by a feeling of sluggishness or drowsiness that appears gradually a little while after use.

 

More specifically, depending on their type of action, a distinction is made between truly somatic effects and more psychological ones.

 

·v    Somatic Effects:

··               Cardiovascular effects: approximately 10 minutes after use, heart rate, cardiac output and cerebral blood flow increase. Tachycardia (accelerated heart rate) can achieve increases of 20% to 50% compared to normal rhythm and could help trigger anxiety and panic attacks in some subjects. It can be responsible for palpitations, reduced exercise tolerance in subjects with heart conditions, and can even facilitate the development of heart problems in subjects who are at risk or are predisposed. A recent study suggests that the risk of myocardial infarction increases by 4.8 times in the first hour after using marijuana and is 1.7 times higher in the second hour, thus suggesting that cannabis may represent a risk in the 60 minutes following its use. Hypotension while the subject is lying down is also mentioned. These effects vary based on the dose and concentration of THC.

··               Bronchopulmonary effects: the effects are similar to those of tobacco. Bronchodilator activity in the 60 minutes following use is mentioned. However this does not prevent the inflammatory consequences of smoking cannabis nor the secondary bronchial hyperreactivity that is translated in particular by a cough that results from the action of the THC and the irritating potential of the products of combustion;

··               Ocular effects: redness of the eyes due to vasodilation and conjunctival irritation is mentioned;

··               Other somatic effects: dry mouth due to decreased saliva secretion, increased appetite due to hypoglycemia (drop in blood sugar level), and more rarely nausea and vomiting, diarrhea and urine retention.

 

·v    Psychological and Psychomotor Effects:

··               Diminished short term memory (so-called “working” memory): remembering words, pictures, stories and sounds;

··               Disturbances in psychomotor performance, including diminished ability to pay attention and concentrate, diminished reflexes, slowed reaction time, problems with coordination of movements, and impaired and diminished ability to perform complex tasks. Thus, a study by Fant et al. describes diminished visual tracking in the central and peripheral fields of vision after 15 minutes, capable of lasting for more than 5 hours.[7][23] Moreover, we note that according to professor Roques, studies on the effects of cannabis on learning abilities, in particular short term memory and working memory, are open to criticism from the standpoint of methodology and their contradictory results, “the heaviest users were the least affected”.[8][24] [translation]

 

Somatic, cognitive and psychomotor effects are related to the amount of cannabis inhaled and the concentration of THC. Thus, according to INSERM:

 

A quantity that corresponds to 25 puffs impairs psychomotor skills and cognitive performance, and more markedly than consumption of 10 puffs or 4 puffs. Maximum plasma levels then rise from 57 ng/ml (for 4 puffs from a cigarette containing 1.75% D⁹THC) to 268 ng/ml (for 25 puffs from a cigarette containing 3.55% D⁹THC). Heishman et al. (1997) established an approximate equivalence between 16 puffs at 3.55 % D⁹THC and approximately 70g of alcohol. At these levels, memory, cognitive and psychomotor performance and mood are impaired. [9][25] [translation]

 

The cognitive and psychomotor effects may continue for more than five hours, and some cognitive impairment may extend for 24 hours.

At high doses, or with inexperienced users, cannabis may cause a certain number of negative reactions that can even include a genuine paranoid, hallucinatory, manic or hypomanic psychotic experience. However these experiences are brief. Some disorders documented with high doses include:

 

··               Anxiety, even panic attacks

··               Confusion or disorientation

··               Vertigo, nausea or vomiting

··               Convulsions

··               Depersonalization

··               Hallucinations

··               Paranoia

··               Acute psychosis

 

These phenomena are relatively rare (less than 1 in a thousand psychiatric admissions). Primarily, it is difficult to establish that cannabis was the cause. In fact, in most cases, the most likely hypothesis is that these subjects were already predisposed, or had even already had psychotic or schizophrenic experiences. Use of other substances, alcohol, other illicit drugs, or medications, could also play an important role.

 

The link between cannabis use and psychosis is a very controversial issue. At the moment, we lack a corpus of comparable, methodologically sound studies repeatedly yielding similar conclusions. The results of existing studies are often complex or ambiguous and the personal opinions of the researchers often interfere with the interpretations. Further deepening our scientific knowledge is still necessary. However, there is extensive, albeit incomplete, consensus on the ability of heavy cannabis consumption or intoxication to induce an acute transitory psychotic state in healthy subjects. The frequency of this condition is unknown and the mechanisms are hypothetical. [10][26]

 

In accordance with the collective expertise of INSERM, we can establish the following:

 

The psychotic disorders caused by cannabis use are brief psychotic episodes that last less than two months, even four months[sic], sometimes a week. The premorbid personality does not present a pathological aspect. Regular users are at greater risk than occasional users. Onset is abrupt, in two or three days, with or without a recent increase in the use of toxic agents, sometimes with a psychological or somatic precipitating factor. Some symptoms appear more specific: behavioural problems, aggression, visual hallucinations, polymorphic nature of the delirium along various themes, psychomotor disinhibition. (…) Compared to a schizophrenic disorder, subjects are younger, 20 to 30 years of age rather than 25 to 30, with a greater proportion of poorly socialized males. [11][27] [translation]

 

However, here too, the data are relatively contradictory and, according to professor Roques, there is support for the belief that usage is more widespread among people with previous mental disorders.[12][28]