The problem of documentation
Cannabis has been classified illegal for no specific scientific reason. We therefore started from a situation in which the harmfulness of this substance was, in some way, a postulate: it is considered harmful simply because it is illegal. It has been so that for some decades the institutions (political, judicial, but also medical and psychiatric) have attributed to cannabis a series of effects even more deadly than those of the most feared drugs, such as heroin, without feeling any need to disturb the scientific evidence: habituation, crime, madness, sexual perversion, drug addiction were the most sadly known effects of the “killer herb” (the “Killer Weed” was the title of a famous propaganda documentary filmed by the US Federal Narcotic Bureau over the 30’s on the effects of cannabis).
Subsequently, there has been a gradual re-examination of the problem, through which justice has been done to the grossest mystifications. At the same time, research techniques were progressing (THC was identified and synthesized, among other things) and a large amount of scientific documentation was developing around cannabis, which currently adds up to a few thousand works.
To assess the impact of this documentation on the mass media and public opinion, it is necessary to take into account the fact that the transmission of scientific information to the public is a complex and articulated operation, and therefore easily subject to manipulation. Manipulation takes concrete form in different ways and for different reasons.
First, the attitude of the media operators towards scientific research is often based on a series of confusing elements:
a) The tendency to consider scientific research as the custodian of an “absolute truth” detached from the “relativity” of the social context
b) Ignoring that scientific research is also subject to errors (of setting, procedure, interpretation) and above all to the influence of the dominant culture and its prejudices;
c) The image that the research proceeds along a linear and coherent “continuum” in which the latest data automatically delete the previous ones;
d) The tendency to underestimate the profound difference between pharmacological research (on laboratory animals) and clinical research (on human beings), and to ignore that the results of pharmacological research are difficult (and in any case not automatically) transferable to human beings: for example, morphine makes laboratory animals aggressive, but calms humans.
It was thus that, in the case of the use of cannabis, scientifically unreliable research had a disproportionate importance to their real validity.
Secondly, it is in the same nature of the mass media (newspapers in particular) to stress the elements of alarm rather than those of reassuring public opinion. As a result, the interview with a researcher who is not very authoritative who denounces the effects of cannabis on organ X or on the Y function is “more news” than a document by authoritative scientists gathered at the congress in which it is shown that this is not true.
Thirdly, it is probable, even if not demonstrable, that the mass media are influenced by the established authorities, which induce them to select the news among those that are more homogeneous to the institutions (and to the laws in force), and therefore to privilege negative news about the effects of cannabis.
For one or the other reason, public opinion has received incomplete, preconceived, confused information. In an attempt to give a correct picture of the situation, we will deal one by one with the individual problems that have been raised by scientific research regarding the harmful effects of cannabis, and in particular, given that the immediate effects are now well known and not controversial, long-term harmful effects, that is, after prolonged use of the substance.
Damage to chromosomes is reflected in the possibility of damaging the genetic heritage, that is, of having children with congenital physical or mental defects. The damage to the chromosomes can be permanent (in which case the risk of transmitting the damage to the offspring is permanent) or transitory (so the risk of transmission of the damage is limited at the moment of conception and, for women, during the period of pregnancy).
Transient damage to chromosomes is caused by many agents: virus diseases (from the most serious to the common herpes), X-ray exposure, many commonly used drugs such as aspirin, probably also nicotine and alcohol).The possibility that the use of cannabis damages the chromosomes has been excluded by the US commission and the Canadian commission, which also advise against the use of cannabis during pregnancy for obvious reasons of caution.
In 1973, M.A. Stenchever published an article showing that 20 men and 20 women, who had also used sporadic (once a week or less) marijuana, showed significantly greater chromosome modifications than a group of 20 non-consumers, and that this could cause the birth of deformed children. Although Stenchever admitted that chromosome damage could be transient (“We don’t know if the effect on the chromosomes will be permanent … we expect that within six months the alterations … will be repairable”, this meant for a country like the USA, which at the time had at least 8 million of fairly frequent consumers, a wave of births of deformed children of enormous social importance, and certainly higher than that which was caused in Europe by the use of thalidomide.
In fact, Stenchever himself did not seem very sure of this possibility, if he declared:
“There has not been a significant increase in deformed infants so far … but if there were an increase in the number of deformed infants, this would be significant”.
In reality, the meaning of chromosome alterations is not yet clear, in the sense that chromosome alterations do not necessarily correspond to defects in the offspring. On the other hand, the research in question did not bother to exclude that in the subjects there were other possible causes of damage to the chromosomes, indeed Stenchver himself admits that of the 47 subjects 22 had made use of LSD and amphetamines.
Nevertheless, in the search for Stenchever (which the same researcher presents as a hypothesis and not as a scientific proof of a cause-and-effect relationship) the world press has dedicated a huge space, assuming that “the children of those who take drugs with marijuana are born deformed “.
The possibility of chromosome damage from cannabis use was excluded from the 1973 NIDA report.
In July 1974 W.W. Nichols published a study showing that in 24 subjects analyzed, they did not suffer any damage to the chromosomes. Nichols checked the conditions of the subjects’ chromosomes before administering the drug, and strictly excluded, for the research period only, the use of any substance that could damage the chromosomes.
From a scientific methodological point of view, Nichols’ work is flawless. It has also been confirmed by studies carried out in Jamaica (on 30 subjects who have been smoking cannabis for at least a decade in large quantities), by the S. Cohen study in Los Angeles on 30 subjects at 65 days of heavy marijuana use and by research carried out in Colombia.
The only denial to this massive documentation is that brought to the Eastland Committee by A. Morishima, which reported in the observed subjects an incidence of chromosomal damage similar to that observed by Stenchever. This research was also widely publicized in the USA; but the fact that it concerned only three subjects was not mentioned.
The idea that cannabis harms the brain arose out of prejudice during the 30’s. It is hypothesized on a scientific level by an experiment on rats carried out in 1971. It gains maximum evidence in December 1971, when A.M.G. Campbell reports in the Lancet that radiographic tests on the brains of 10 heavy marijuana users have found evidence of brain atrophy.
Campbell study was immediately commented by other scholars in a series of letters that appeared in subsequent issues of the magazine, in which both the choice of subjects (who were all hospitalized in the psychiatric hospital), and the technical procedure and the choice of the controls carried out.
A Grinspoon article highlighted the fact that all Campbell’s subjects had used LSD, 8 had used amphetamines, 4 had suffered from major head injuries, and some had used sedatives, barbiturates, heroin or morphine; to make matters worse, everyone had used alcohol, a substance that has been proven to damage the brain. The same researchers, in a letter to the magazine, specified that the relationship between the use of cannabis and brain injury was to be considered a hypothesis and not a scientific certainty.
Again, all the press gave enormous emphasis to Campbell’s study, drew the arbitrary conclusion that “marijuana atrophies the brain”, and did not care or publish the critical articles and the corrections of the same researchers, nor to specify that brain atrophy is however an ascertained effect of alcohol. Meanwhile, the hypothesis of cerebral atrophy was refuted by the report of the US commission and by the report of the Canadian commission, which devotes no more than five highly critical lines to Campbell’s research.
In April 1973 a research was published by A.J. Stunkard, in which a group of 29 students who regularly used marijuana for a three-year period was compared to a group of controls; no sign of cerebral atrophy resulted from neurological and neuropsychological findings. The Eastland committee counterattacked with R.G. Health, who reported that he had administered heavy doses of marijuana to 6 rhesus monkeys, and that he had noticed persistent brain wave variations;
another participant in the investigation, Nobel laureate J. Axelrod (famous for his studies on the effects of drugs on the brain) could not help noticing that Heath had violated one of the fundamental principles of drug research, by administering to the unfortunate animals a toxic dose, corresponding to 50-100 marijuana cigarettes per day. The existence of brain atrophy in heavy cannabis smokers was then disproved by all the studies in the NYAS report (especially those carried out in Jamaica and Costa Rica).
At this point the brain atrophy hypothesis should be definitively buried, but is not so. Many still believe that marijuana damages the brain. And it’s not just about the uninitiated V. Milliman, director of the MDART (Maryland Drug Abuse Research & Treatment Foundation of Baltimore), who claimed not only the existence of a “cannabis syndrome” caused by “an organic brain disorder “and manifesting itself as” mental activity disorders “, but he also said that some scholars who suffer from the need to change marijuana laws are affected by this disorder.
The hypothesis that the use of cannabis causes psychosis was launched in 1957 by the Moroccan psychiatrist Benabud, who identified a specific “cannabis psychosis”. Upon careful inspection, it was then found that these were not permanent psychoses, but intoxications due to enormous dosages (20-30 pipes of Kif), in some cases determined or aggravated by undernutrition or infections.
However, in 1971 a research by H. Kolansky and W. Moore was published on 38 psychiatric patients who had used marijuana; it turned out that 8 had become psychotic, 4 had attempted suicide, and the others had shown varying degrees of sexual promiscuity and disordered life. The same researchers testified before the U.S. National Commission that marijuana use was the primary cause of all these problems.
Finally, the relationship between the use of cannabis and psychosis was definitely denied by the studies carried out in Jamaica, Costa Rica, USA and Greece, all included in the NYAS report. On the other hand, if this hypothesis was credible it would have had a clinical confirmation among the tens of millions of regular consumers between Europe and North America; however, it does not appear that even a minimally significant number of cannabis users have been hospitalized with a diagnosis of psychosis. On the contrary, it has been hypothesized by several researchers (Fort, Grinspoon, Murphy) cited by the Canadian commission report a relationship between cannabis use and psychosis which proceeds in the opposite direction to that described so far:
“It is possible that the use of cannabis could mask and compensate for certain situations of mental pathology, and mitigate the most evident symptoms in certain individuals. This would result in a lower incidence of mental pathology in certain groups of cannabis users than in comparable subjects taken from the mass of the population. This interesting hypothesis has not been adequately tested, even though cannabis has been used as a tranquilizer in many cultures “