by Dale Gieringer, Ph.D., Director, California NORML – Rev. May 2011
Safety of Cannabis – Smoking and Lungs – Accidents – Drug Testing Potency – Brain – Sterility and Birth Defects – Heart – Immune System – Chromosomes – Gateway Effect – Schizophrenia & Psychosis

Myth: Marijuana is a Dangerous Drug
Any discussion of marijuana should begin with the fact that there have been numerous official reports and studies, every one of which has concluded that marijuana poses no great risk to society and should not be criminalized. These include: the National Academy of Sciences’ “Analysis of Marijuana Policy”(1982); the National Commission on Marihuana and Drug Abuse (the Shafer Report) (1973); the Canadian Government’s Commission of Inquiry (Le Dain Report) (1970); the British Advisory Committee on Drug Dependency (Wooton Report) (1968); the La Guardia Report (1944); the Panama Canal Zone Military Investigations (1916-29); and Britain’s monumental Indian Hemp Drugs Commission (1893-4).

It used to be claimed that there is “new evidence” showing marijuana is more harmful than was thought in the sixties. More recent studies have confirmed marijuana’s safety, refuting claims that it causes birth defects, brain damage, reduced testosterone, or increased drug abuse problems. Some studies even suggest that the active ingredients in the plant, know as cannabinoids, have anti-carcinogenic, anti-oxidant, and neuro-protective properties (see “Emerging Clincial Applications for Cannabis and Cannabinoids” by NORML Deputy Director Paul Armentano).

The current consensus is well stated in the 20th annual report of the California Research Advisory Panel (1990), which recommended that personal use and cultivation of marijuana be legalized: “An objective consideration of marijuana shows that it is responsible for less damage to society and the individual than are alcohol and cigarettes.”

References: For an excellent summary of the true health facts about marijuana, see Lynn Zimmer and Dr. John Morgan, Marijuana Myths, Marijuana Facts: A Review of the Scientific Evidence (Lindesmith Center, NY, 1997). The National Academy of Sciences report, Marijuana and Health (National Academy Press, 1982) remains a good overview, its major conclusions remaining largely unaffected by two decades of research. Lovinger and Jones, The Marihuana Question (Dodd, Mead & Co., NY 1985) is the most exhaustive and fair-handed summary of the evidence against marijuana. Good, positive perspectives may be found in Lester Grinspoon’s Marihuana, the Forbidden Medicine (Yale Press, 1993) and Marihuana Reconsidered (Harvard U. Press 1971), which debunks many of the older anti-pot myths.

Myth: Marijuana is Harmless
Just as most experts agree that occasional or moderate use of marijuana is innocuous, they also agree that excessive use can be harmful. Research shows that the two major risks of excessive marijuana use are: (1) respiratory disease due to smoking and (2) accidental injuries due to impairment. In addition, marijuana speeds the heartbeat, which can be dangerous for patients with serious heart disease.

Recent studies have also shown that marijuana can aggravate symptoms of mental illness in persons with schizophrenic tendencies. At least four studies – in Australia, Sweden, New Zealand and the Netherlands – have found that early, repeated use of cannabis is associated with exacerbation of schizophrenia in young patients so inclined (Source: British Medical Journal “Cannabis and Mental Health.” 23 Nov 2002). The risks appear greatest for those who start smoking in early youth. Marijuana is therefore generally disrecommended for young persons with a tendency to mental disorder, though it may also occasionally be medically useful for treatment of certain schizophrenic symptoms.

Marijuana and Smoking:

A survey by the Kaiser Permanente Center found that daily marijuana-only smokers have a 19% higher rate of respiratory complaints than non-smokers[01] These findings were not unexpected, since it has long been known that, aside from its psychoactive ingredients, marijuana smoke contains virtually the same toxic gases and carcinogenic tars as tobacco. Human studies have found that pot smokers suffer similar kinds of respiratory damage as tobacco smokers, putting them at greater risk of bronchitis, sore throat, respiratory inflammation and infections[02]

For many years, it was assumed that marijuana, like tobacco, could also cause lung cancer. Some researchers had reported apparently pre-cancerous cell changes in pot smokers[03] Others reported a higher-than-expected incidence of throat, neck and tongue cancer in younger, marijuana-only smokers [04]. although subsequent studies failed to confirm these results [04a].

Such concerns were dispelled by the first large-scale epidemiological study of marijuana smoking and lung cancer, conducted by a team of researchers led by Dr Donald Tashkin and Dr. Mia Hashibe at UCLA. After suveying 1,209 patients with lung, oral, and respiratory tract cancers, the team found no relation between marijuana smoking and cancer [05]. In one category – lung cancer among short-term users – the study even found reduced cancer risk. The results were a surprise to Dr. Tashkin, a leading expert on smoking-related disease, who had previously warned that marijuana smoking would likely cause lung cancer. Dr. Tashkin now believes that marijuana smoking does not cause lung cancer.

In another study, Harvard researchers found that THC inhibited the growth of lung cancer tumors in laboratory animals, evidently by blocking a growth factor that is known to promote small-cell lung cancers [05a].

These results have not entirely dispelled concerns about respiratory toxins in marijuana smoke. Fortunately, these hazards can be reduced by various strategies: (1) use of higher-potency cannabis, which can be smoked in smaller quantities, (2) use of vaporizers and other smoke reduction technologies[06] and (3) ingesting pot orally instead of smoking it.

Myth: One Joint Equals One Pack (or 16, or maybe just 4) Cigarettes
Some critics exaggerate the dangers of marijuana smoking by fallaciously citing a study by Dr. Tashkin which found that daily pot smokers experienced a “mild but significant” increase in airflow resistance in the large airways greater than that seen in persons smoking 16 cigarettes per day[07] What they ignore is that the same study examined other, more important aspects of lung health, in which marijuana smokers did much better than tobacco smokers. Dr. Tashkin himself disavows the notion that one joint equals 16 cigarettes.

A more widely accepted estimate is that marijuana smokers consume four times as much carcinogenic tar as cigarettes smokers per weight smoked[08] This does not necessarily mean that one joint equals four cigarettes, since joints usually weigh less. In fact, the average joint has been estimated to contain 0.4 grams of pot, a bit less than one-half the weight of a cigarette, making one joint equal to two cigarettes (actually, joint sizes range from cigar-sized spliffs smoked by Rastas, to very fine sinsemilla joints weighing as little as 0.2 grams). It should be noted that there is no exact equivalency between tobacco and marijuana smoking, because they affect different parts of the respiratory tract differently: whereas tobacco tends to penetrate to the smaller, peripheral passageways of the lungs, pot tends to concentrate on the larger, central passageways[09] One consequence of this is that pot, unlike tobacco, does not appear to cause emphysema.

Myth: Prohibition Reduces the Harmfulness of Pot Smoking
Whatever the risks of pot smoking, the current laws make matters worse in many respects. Paraphernalia laws have impeded the development and marketing of vaporizers and other devices that could significantly reduce the harmfulness of marijuana smoke. Prohibition encourages the sale of pot that has been contaminated or adulterated by insecticides, Paraquat, etc., or mixed with other drugs such as PCP, crack and heroin. Finally, of course, criminal punishment is itself more harmful to personal welfare than smoking marijuana.

Unlike the government, NORML is interested in reducing the dangers of pot smoking. California NORML and MAPS (the Multidisciplinary Association for Psychedelic Studies) have sponsored research on alternative inhalation systems, in particular vaporizers, which are designed to deliver smoke-free cannabinoid vapors. The results indicate that it is possible to virtually eliminate the risk of smoking-related respiratory damage by using vaporizers instead.

Myth: No One Has Ever Died From Using Marijuana
The Kaiser study also found that daily pot users have a 30% higher risk of injuries, presumably from accidents. These figures are significant, though not as high as comparable risks for heavy drinkers or tobacco addicts. That pot can cause accidents is scarcely surprising, since marijuana has been shown to degrade short-term memory, concentration, judgment, and coordination at complex tasks including driving[10] There have been numerous reports of pot-related accidents – some of them fatal, belying the attractive myth that no one has ever died from marijuana. One survey of 1023 emergency room trauma patients in Baltimore found that fully 34.7% were under the influence of marijuana, more even than alcohol (33.5%); half of these (16.5% used both pot and alcohol in combination[11] This is perhaps the most troublesome research ever reported about marijuana; as we shall see, the overwhelming majority of accident studies have found pot to be less dangerous than alcohol.

Nonetheless, it is important to be informed on all sides of the issue. Pot smokers should be aware that accidents are the number one hazard of moderate pot use. In addition, of course, the psychoactive effects of cannabis can have many other adverse effects on performance, school work, and productivity.

Myth: Marijuana is a Major Road Safety Hazard
Numerous research studies have found that marijuana is on balance less of a public road hazard than alcohol. Various accident surveys have found that over half of fatal drivers have alcohol in their blood, as opposed to 7 – 20% with THC, the major psychoactive component of marijuana (a condition usually indicative of having smoked within the past 2-4 hours)[12] However, the great majority (70% – 90%) of THC-positive drivers also have alcohol in their blood. There is little accordingly little evidence that marijuana use by itself is a major public safety hazard [ 13].

Two major studies by the National Highway Transportation Safety Administration have confirmed marijuana’s relative safety compared to alcohol. The first, the most comprehensive U.S. drug accident study to date, surveyed blood samples from 1882 drivers killed in car, truck and motorchycle accidents in seven states during 1990-91[14] Alcohol was found in 51.5% of specimens, as against 17.8% for all other drugs combined. Marijuana, the second most common drug, appeared in just 6.7%. Two-thirds of the marijuana-using drivers also had alcohol. The report concluded that alcohol was by far the “dominant” drug-related problem in accidents. It went on to analyze the responsibility of drivers for the accidents they were involved in. It found that drivers who used alcohol were especially culpable in fatal accidents, and even more so when they combined it with marijuana or other drugs. However, those who used marijuana alone appeared to be if anything less culpable than non-drug users (though the date were insufficient to be statistically conclusive). The report concluded, “There was no indication that marijuana by itself was a cause of fatal accidents.” (It must be emphasized that this is not the case when marijuana is combined with alcohol or other drugs).

The second NHTSA study, “Marijuana and Actual Driving Performance,” concluded that the adverse effects of cannabis on driving appear “relatively small” and are less than those of drunken driving[15] The study, conducted in the Netherlands, examined the performance of drivers in actual freeway and urban driving situations at various doses of marijuana. It found that marijuana produces a moderate, dose-related decrement in road tracking ability, but is “not profoundly impairing” and “in no way unusual compared to many medicinal drugs.” It found that marijuana’s effects at the higher doses preferred by smokers never exceed those of alcohol at blood concentrations of .08%, the minimum level for legal intoxication in stricter states such as California. The study found that unlike alcohol, which encourages risky diring, marijuana appears to produce greater caution, apparently because users are more aware of their state and able to compensate for it (similar results have been reported by other researchers[16]).

However, a recent Australian study by Drummer found that drivers with high blood levels of THC (> 5 ng/ml) had a significantly higher rate of accident culpability than drivers who were drug-free, comparable to drunken drivers [16A]. This was not true of drivers with only trace amounts of cannabinoids in their systems. High blood levels are indicative of recent use within the last couple of hours. This suggests that acute, current pot use is a driving hazard, though not residual after-effects of chronic use, which often show positive in drug tests.

Another survey of 2,500 drivers in South Australia failed to find evidence that marijuana is a significant road safety hazard[16B]. The researchers examined blood samples from drivers in non-fatal accidents for traces of alcohol, cannabinoids (marijuana), benzodiazepines (tranquilizers), and amphetamines. The researchers then assessed the drivers’ degree of culpability for the crashes. Overall, they found no increase in culpability for drivers showing cannabinoids alone compared to drug-free drivers. In contrast, there was a very strong relation between alcohol blood levels and accident culpability. The combination of marijuana with alcohol also showed strongly increased accident culpability. Benzodiazepines, but not amphetamines, also showed higher culpability. Another analysis of 1,052 fatal drivers in Australia suggested that marijuana is if anything associated with a decreased risk of accidents.

Similar results have been reported in other driving studies as well[16C]. It should be noted that these results may not apply to non-driving related situations, where forgetfulness or inattention can be more important than speed (this might explain the discrepancy in the Baltimore hospital study, which looked at accidents of all kinds). In addition, the second NHTSA study warned that marijuana could also be quite dangerous in emergency situations that put high demands on driving skills.

For a summary of the evidence on marijuana and driving safety, see Cal NORML’s “Marijuana and Driving” and “Drug Test Results and Accident Risks” . See also Dr. Franjo Grotenhermen’s IACM – DUIM Project site, and Cannabis and Driving: A Review of the Literature and Commentary (U.K. Department for Transport)

Myth: Marijuana Prohibition Improves Public Safety
There is no evidence that the prohibition of marijuana reduces the net social risk of accidents. U.S. highway and transportation safety improved steadily over the same period that marijuana was popularized in the 1960s through 1970s. Some studies suggest that marijuana may actually be beneficial in that it substitutes for alcohol and other, more dangerous drugs. Research by Karyn Model found that states with marijuana decrim had lower overall drug abuse rates than others; another study by Frank Chaloupka found decrim states have lower accident rates too[17] In Alaska, accident rates held constant or declined following the legalization of personal use of marijuana[18] In the Netherlands, authorities believe that cannabis has contributed to an overall decline in hard drug abuse.

Myth: Drug Urinalysis Improves Workplace Safety
There has never been a single, controlled scientific study showing drug urinalysis improves workplace safety. Claims that drug testing works are based on dubious anecdotal reports or the mere observation of a declining rate of drug positives in the working population, which has nothing to do with job performance. Such scientific studies as have been conducted have found little difference between the performance of drug-urine-positive workers and others. The largest survey to date, covering 4,396 postal workers nationwide, found no difference in accident records between workers who tested positive on pre-employment drug screens and those who did not[19] The study did find that drug-positive workers had a 50% higher rate of absenteeism and dismissals; put another way, however, drug users had a 93.4% attendance record (versus 95.8% for non-users) and fully 85% kept their jobs for a year (versus 89.5% for non-users)! An economic analysis of postal workers in Boston concluded that the net savings of drug testing were marginal, and that there could be many situations where it is not cost-effective[20] Another survey of health workers in Georgia found no difference in job performance between drug-positive and drug-negative workers[21]

Myth: Random Urinalysis is Needed in Safety-Sensitive Transportation Jobs
Government rules mandating random drug testing were promulgated without any prior statistical evidence that illicit drugs constituted an inordinate safety hazard. Not a single commercial passenger airline accident has ever been attributed to marijuana (or, for that matter, alcohol) abuse[22] Drug tests on rail workers found no elevated incidence of drug use among workers involved in accidents[23]

Random drug testing of transportation workers was enacted as a hysterical reaction to a single 1987 train collision, in which 16 Amtrak passengers were killed by a Conrail train that failed to stop. The engineer and brakeman of the Conrail train at fault were found to have recently smoked marijuana, though it was never firmly proven that marijuana caused the accident. The Conrail engineer had an extensive record of speeding and drunken driving offenses and was known by management to have drinking problems. Critical safety equipment that would have averted the accident was missing or disabled. A subsequent investigation by the National Transportation Safety Board recommended that Conrail improve both its management and equipment, but did not recommend random testing. Nonetheless, Congress responded by mandating random drug testing on the entire transportation industry, from airline flight attendants to gas pipeline workers.

Myth: A Single Joint Has Effects That Linger for Days and Weeks
While it is true that THC and other cannabinoids are fat-soluble and linger in the body for prolonged periods, they do not normally affect behavior beyond a few hours except in chronic users. Most impairment studies have found that the adverse effects of acute marijuana use wear off in 2-6 hours, commonly faster than alcohol[24] The one notable exception was a pair of flight simulator studies by Leirer, Yesavage, and Morrow, which reported effects on flight simulator performance up to 24 hours later[25] The differences, described by Leirer as “very subtle” and “very marginal,” were less than those due to pilot age. Another flight simulator study by the same group failed to find any effects beyond 4 hours[26] Similar “hangover” effects have been noted for alcohol[27]

Chronic users may experience more prolonged effects due to a build-up of cannabinoids in the tissues. Some heavy users have reported feeling effects weeks or even months after stopping. However, there is no evidence that these are detrimental to safety.

References on Accidents and Drug Testing: Alcohol, Drugs and Driving: Abstracts and Reviews Vol. 2 #3-4 (Brain Information Service, UCLA 1986); Dale Gieringer, “Marijuana, Driving, and Accident Safety,” Journal of Psychoactive Drugs 20 (1): 93-101 (Jan.-Mar 1988); Dr. John Morgan, “Impaired Statistics and the Unimpaired Worker,” Drug Policy Letter 1(2): May/June 1989, and “The ‘scientific’ justification for drug urine testing,” The University of Kansas Law Review 36: 683-97 (1988); John Horgan, “Test Negative: A look at the evidence justifying illicit-drug tests,” Scientific American, March 1990 pp. 18-22, and “Postal Mortem,” Scientific American, Feb. 1991 pp. 22-3; Dale Gieringer, “Urinalysis or Uromancy?” in Strategies for Change: New Directions in Drug Policy (Drug Policy Foundation, 1992).

Myth: Pot is Ten Times More Potent and Dangerous Now Than in the Sixties
The notion that pot has increased dramatically in potency is a DEA myth based on biased government data, as shown in a recent NORML report by Dr. John Morgan[28] Samples of pot from the early ’70s came from stale, low-potency Mexican “kilobricks” left in police lockers, whose potency had deteriorated to sub-smokable levels of less than 0.5%. These were compared to later samples of decent-quality domestic marijuana, making it appear that potency had skyrocketed. A careful examination of the government’s data show that average marijuana potency increased modestly by a factor of two or so during the seventies, and has been more or less constant ever since.

In fact, there is nothing new about high-potency pot. During the sixties, it was available in premium varieties such as Acapulco Gold, Panama Red, etc. , as well as in the form of hashish and hash oil, which were every bit as strong as today’s sinsemilla, but were ignored in government potency statistics. While the average potency of domestic pot did increase with the development of sinsemilla in the seventies, the range of potencies available has remained virtually unchanged since the last century, when extremely potent tonics were sold over the counter in pharmacies. In Holland, high-powered hashish and sinsemilla are currently sold in coffee shops with no evident problems.

Contrary to popular myth, greater potency is not necessarily more dangerous, due to the fact that users tend to adjust (or “self-titrate”) their dose according to potency. Thus, good quality sinsemilla is actually healthier for the lungs because it reduces the amount of smoke one needs to inhale to get high.

Myth: Pot Kills Brain Cells
Government experts now admit that pot doesn’t kill brain cells[29] This myth came from a handful of animal experiments in which structural changes (not actual cell death, as is often alleged) were observed in brain cells of animals exposed to high doses of pot. Many critics still cite the notorious monkey studies of Dr. Robert G. Heath, which purported to find brain damage in three monkeys that had been heavily dosed with cannabis[30] This work was never replicated and has since been discredited by a pair of better controlled, much larger monkey studies, one by Dr. William Slikker of the National Center for Toxicological Researc[31] and the other by Charles Rebert and Gordon Pryor of SRI International[32] Neither found any evidence of physical alteration in the brains of monkeys exposed to daily doses of pot for up to a year. Human studies of heavy users in Jamaica and Costa Rica found no evidence of abnormalities in brain physiology[33] A 15-year study of 1,318 chronic marijuana users by Johns Hopkins University found no evidence of long-term decline in mental function[34] Even though pot does not appear to cause permanent brain damage, users should be aware that persistent deficits in short-term memory have been noted in chronic, heavy marijuana smokers after 6 to 12 weeks of abstinence[35] It is worth noting that other drugs, including alcohol, are known to cause brain damage.

Myth: Marijuana Causes Sterility and Lowers Testosterone
Government experts also concede that pot has no permanent effect on the male or female reproductive systems[36] A few studies have suggested that heavy marijuana use may have a reversible, suppressive effect on male testicular function[37] A recent study by Dr. Robert Block has refuted earlier research suggesting that pot lowers testosterone or other sex hormones in men or women[38] In contrast, heavy alcohol drinking is known to lower testosterone levels and cause impotence. A couple of lab studies indicated that very heavy marijuana smoking might lower sperm counts. However, surveys of chronic smokers have turned up no indication of infertility or other abnormalities.

Less is known about the effects of cannabis on human females. Some animal studies suggest that pot might temporarily lower fertility or increase the risk of fetal loss, but this evidence is of dubious relevance to humans[39] One human study suggested that pot may mildly disrupt ovulation. It is possible that adolescents are peculiarly vulnerable to hormonal disruptions from pot. However, not a single case of impaired fertility has ever been observed in humans of either sex.

Myth: Marijuana Causes Birth Defects
While experts generally recommend against any drug use during pregnancy, marijuana has little evidence implicating it in fetal harm, unlike alcohol, cocaine or tobacco. Epidemiological studies have found no evident link between prenatal use of marijuana and birth defects in humans[40] A recent study by Dr. Susan Astley at the University of Washington refuted an earlier work suggesting that cannabis might cause fetal alcohol syndrome[41]

Although some research has found that prenatal cannabis use is associated with slightly reduced average birth weight and length[42] these studies have been open to methodological criticism. More recently, a well-controlled study found that cannabis use had a positive impact on birthweight during the third trimester of pregnancy with no adverse behavioral consequences[43] The same study found a slight reduction in birth length with pot use in the first two months of pregnancy. Another study of Jamaican women who had smoked pot throughout pregnancy found that their babies registered higher on developmental scores at the age of 30 days, while experiencing no significant effects on birthweight or length[44]

While cannabis use is not recommended in pregnancy, it may be of medical value to some women in treating morning sickness or easing childbirth.

Myth: Pot Causes High Blood Pressure
According to the NAS, the effects of marijuana on blood pressure are complex, depending on dose, administration, and posture[45] Marijuana often produces a temporary, “moderate” increase in blood pressure immediately after ingestion; however, heavy chronic doses may depress blood pressure instead. Many medical users report that marijuana helps lower their blood pressure. One common reaction is to cause decreased blood pressure while standing and increased blood pressure while lying down, causing people to faint if they stand up too quickly. There is no evidence that pot use causes persisting hypertension or heart disease; some users even claim that it helps them control hypertension by reducing stress.

One thing THC does do is to increase pulse rates for about an hour, a condition known as tachycardia. This is not generally harmful and may even be beneficial since exercise does the same thing. However, just like hard exercise, pot use may precipitate heart attacks in patients with pre-existing heart disease. A study by Dr. Murray Mittleman found that users face an elevated risk of heart attack within an hour of pot smoking, similar to the risk from physical exercise or having sex [46]. Chronic users may develop a tolerance to tachycardia and other cardiovascular reactions.

Myth: Marijuana Damages the Immune System
A variety of studies indicate that THC and other cannabinoids exercise mild, reversible immuno-suppressive effects by inhibiting the activity of immune system cells know as lymphocytes (T- and B-cells) and macrophages. Immune suppression was first raised as an issue by the stridently anti-pot researcher Dr. Gabriel Nahas in the 1970s, but a flurry of subsequent research failed to find anything alarming. Not a single case of marijuana-induced immune deficiency has been clinically detected in humans.

More recent research indicates that cannabis acts as an “immunomodulator,” meaning that it tends to restore balance to the immune system [47]. This can have beneficial effects for patients suffering auto-immune diseases such as MS or rheumatoid arthritis, in which the immune system is overactive.

One exception may be the lungs, where chronic pots smokers have been shown to suffer damage to the immune cells known as alveolar macrophages and other defense mechanisms[48]. This may help explain the propensity of chronic pot smokers to respiratory infections. It is unclear how much of this damage is due to THC, as opposed to all of the other toxins that occur in smoke, exposure to which can be avoided by oral ingestion or use of vaporizers.

Marijuana is not dangerous to HIV patients despite their compromised immune systems. On the contrary, research by Dr. Donald Abrams has shown that marijuana may actually boost subjects’ immune system T-cell counts, as well as reduce appetite loss and nausea due to HIV [49]. Other studies by the California Center for Medicinal Cannabis have found that marijuana may be helpful in treating HIV-related neuropathic pain [50]. Studies have failed to find any evidence that marijuana increases the risk of AIDS or the intensity of HIV infections [51].

Myth: Marijuana Causes Chromosome and Cell Damage
According to the NAS[52] “Studies suggesting that marijuana probably does not break chromosomes are fairly conclusive.” Cannabinoids in themselves are neither mutagenic nor carcinogenic, though the tars produced by marijuana combustion are. Some laboratory studies have suggested that high dosages of THC might interfere with cell replication and produce abnormal numbers of chromosomes; however, there is no evidence of such damage in realistic situations.

Myth: Marijuana Leads to Harder Drugs
There is no scientific evidence for the theory that marijuana is a “gateway” drug. The cannabis-using cultures in Asia, the Middle East, Africa and Latin America show no propensity for other drugs. The gateway theory took hold in the sixties, when marijuana became the leading new recreational drug. It was refuted by events in the eighties, when cocaine abuse exploded at the same time marijuana use declined.

As shown above, there is evidence that cannabis may substitute for alcohol and other “hard” drugs. A survey by Dr. Patricia Morgan of the University of California at Berekeley found that a significant number of pot smokers and dealers switched to methamphetamine “ice” when Hawaii’s marijuana eradication program created a shortage of pot[53]. Dr. Morgan noted a similar phenomenon in California, where cocaine use soared in the wake of the CAMP helicopter eradication campaign. In its report “Marijuana and Medicine,” the National Institute of Medicine found no scientific evidence for the gateway theory[54].

The one way in which marijuana does lead to other drugs is through its illegality: persons who deal in marijuana are likely to deal in other illicit drugs as well.

MYTH: Marijuana Is a Major Cause of Schizophrenia & Psychosis
Some studies have indicated that marijuana may be a risk factor in schizophrenia, psychosis, or other mental illnesses. For example, a study of Swedish military personnel found that chronic marijuana users were twice as likely to be schizophrenic [55]. However, no increase in the rate of schizophrenia or psychosis has been detected in those parts of the world where cannabis use has increased greatly in recent decades. It therefore appears that cannabis does not increase the incidence of such problems in the general population, as concluded by the New Zealand Parliamentary Committee [56].

On the other hand, several studies have found that marijuana use may precipitate earlier onset of schizophrenia or aggravate its symptoms in those already so predisposed. [57] However, the effects of cannabis on schizophrenics are not necessarily detrimental. Cannabis has also been observed to mitigate symptoms in many patients. [58] It may therefore be that the purported link between marijuana use and schizophrenia is due to self-medication.

In general, the evidence regarding cannabis and schizophrenia / psychosis is conflicting, so caution is advisable. Persons with psychotic tendencies should consult their physicians before using cannabis.

[01] Michael R. Polen et al. “Health Care Use by Frequent Marijuana Smokers Who Do Not Smoke Tobacco,” Western Journal of Medicine 158 #6: 596-601 (June 1993).

[02] Donald Tashkin, “Is Frequent Marijuana Smoking Hazardous To Health?” Western Journal of Medicine 158 #6: 635-7 (June 1993).

[03] D. Tashkin et al, “Effects of Habitual Use of Marijuana and/or Cocaine on the Lung,” in Research Findings on Smoking of Abused Substances, NIDA Research Monograph 99 (1990).

[04] Paul Donald, “Advanced malignancy in the young marijuana smoker,” Adv Exp Med Biol 288:33-56 (1991); FM Taylor, “Marijuana as a potential respiratory tract carcinogen,” South Med Journal 81:1213-6 (1988).

[04a] K Rosenblatt et al., “Marijuana Use and Risk of Oral Squamous Cell Carcinoma,” Cancer Research 64: 4049-54 (2004).

[05] M. Hashibe et al, “Marijuana Use and the Risk of Lung and Upper Aerodigestive Tract Cancers: Results of a Population-Based Case-Control Study ” Cancer Epidemiol. Biomarkers Prev 15.10: 1829-34 (2006).

[05a] A Preet et al., “Delta-9 THC inhibits epithelial growth factor-induced lung cancer cell migration in vitro as well as its growth and metastasis in vivo” Oncogene 27: 339-46 (2008).

[06] Contrary to what might be expected, waterpipes do not reduce the proportion of tars in marijuana smoke; the most promising alternative may be to “vaporize” the THC with devices that heat marijuana below the point of combustion. D. Gieringer, “Marijuana Waterpipe/Vaporizer Study,” MAPS (Multidisciplinary Association for Psychedelic Studies) Newsletter, VI#3, 1996, pp. 59-66)

[07] D. Tashkin, “Respiratory Status of 74 Habitual Marijuana Smokers,” Chest 78 #5: 699-706 (Nov. 1980).

[08] T-C. Wu, D. Tashkin, B. Djahed and J.E. Rose, “Pulmonary hazards of smoking marijuana as compared with tobacco,” New England Journal of Medicine 318: 347-51 (1988).

[09] D. Tashkin et al, “Effects of Habitual Use of Marijuana and/or Cocaine on the Lung,” loc.cit.

[10] Herbert Moskowitz, “Marihuana and Driving,” Accident Analysis and Prevention 17#4: 323-45 (1985).

[11] Carl Soderstrom et al., “Marijuana and Alcohol Use Among 1023 Trauma Patients,” Archives of Surgery, 123: 733-7 (1988).

[12] Dale Gieringer, “Marijuana, Driving, and Accident Safety,” Journal of Psychoactive Drugs 20 (1): 93-101 (Jan-Mar 1988).

[13] H. Klonoff, “Marijuana and driving in real-life situations,” Science 186: 317-24 (1974).

[14] K.W. Terhune et al., “The Incidence and Role of Drugs in Fatally Injured Drivers,” NHTSA Report # DOT-HS-808-065 (1994).

[15] Hendrik Robbe and James O’Hanlon, “Marijuana and Actual Driving Performance,” NHTSA Report #DOT-HS-808-078 (1994).

[16] Klonoff, loc. cit.; A. Smiley, “Marijuana: On-road and driving simulator studies,” Alcohol, Drugs and Driving: Abstracts and Reviews 2#3-4: 15-30 (1986).

[16A] Olaf Drummer et al, ‘The involvement of drugs in drivers of motor vehicles killed in Australian road traffic crashes,” Accident Analysis and Prevention c (2004) 36(2):239-48.

[16B]C.E. Hunter, R.J. Lokan, M.C. Longo, J.M White and M.A. White, “The Prevalence and Role of Alcohol, Cannabinoids, Benzodiazepines and Stimulants in Non-Fatal Crashes.” Forensic Science, Department for Administrative and Information Services, 21 Divett Place, Adelaide, South Australia 5000, May 1998.

[16C] A good summary is given in Michael Bates and Tony Blakely, “Role of Cannabis in Motor Vehicle Crashes,” Epidemiological Reviews 21#2: 222-32 (1999).

[17] Frank Chaloupka and Adit Laixuthal, “Do Youths Substitute Alcohol and Marijuana? Some Empirical Evidence,” Working Paper No. 4662, National Bureau of Economic Research, Cambridge Mass. (1994); K.E. Model, “The Effect of Marijuana Decriminalization on Hospital Emergency Room Episodes: 1975-8,” Journal of the American Statistical Association, 88:423, 737-47; cited in Peter Passell, “Less Marijuana, More Alcohol?” New York Times June 17, 1992.

[18] Michael Dunham, “When the Smoke Clears,” Reason March 1983 pp.33-6.

[19] Norman, Salyard and Mahoney, “An Evaluation of Preemployment Drug Testing,” Journal of Applied Psychology 75(6) 629-39 (1990).

[20] Zwerling, Ryan and Orav, “Costs and Benefits of Preemployment Drug Screening,” JAMA 267(1): 91-3 (1992).

[21] David Charles Parish, “Relation of the Pre-employment Drug Testing Result to Employment Status: A One-year Follow-up,” Journal of General Internal Medicine 4:44-7 (1989).

[22] Dale Gieringer, “Urinalysis or Uromancy?” in Strategies for Change: New Directions in Drug Policy (Drug Policy Foundation, 1992); testimony of R.B. Stone in Hearings on the Airline and Rail Service Protection Act of 1987, Senate Committee on Commerce, Science and Transportation, Feb. 20, 1987.

[23] Gieringer, op. cit.; statistics reported in Federal Register Vol. 53 #224, Nov. 21, 1988 p. 47104.

[24] Alison Smiley, “Marijuana: On-Road and Driving Simulator Studies,” Alcohol, Drugs, and Driving 2 #3-4: 121-34 (1986).

[25] V.O. Leirer, J.A. Yesavage and D.G. Morrow, “Marijuana Carry-Over Effects on Aircraft Pilot Performance,” Aviation Space and Environmental Medicine 62: 221-7 (March 1991); Yesavage, Leirer, et al., “Carry-Over effects of marijuana intoxication on aircraft pilot performance: a preliminary report,” American Journal of Psychiatry 142: 1325-9 (1985).

[26] Leirer, Yesavage and Morrow, “Marijuana, Aging and Task Difficulty Effects on Pilot Performance,” Aviation Space and Environmental Medicine 60: 1145-52 (Dec. 1989).

[27] Yesavage and Leirer, “Hangover Effects on Aircraft Pilots 14 Hours After Alcohol Ingestion: A Preliminary Report,” American Journal of Psychiatry 143: 1546-50 (Dec. 1986).

[28] John Morgan, “American Marijuana Potency: Data Versus Conventional Wisdom,” NORML report (1994). See also T. Mikuriya and M. Aldrich, “Cannabis 1988: Old drug, new dangers, the potency question,” Journal of Psychoactive Drugs 20:47-55.

[29] Dr. Christine Hartel, Acting Director of Research, National Institute of Drug Abuse, cited by the State of Hawaii Dept of Health, Alcohol and Drug Abuse Division in memo of Feb. 4, 1994.

[30] For an overview, see NAS Report, op. cit., pp. 81-2. R.G. Heath et al, “Cannabis sativa: effects on brain function and ultrastructure in Rhesus monkeys,” Biol. Psychiatry 15: 657-90 (1980).

[31] William Slikker et al., “Chronic Marijuana Smoke Exposure in the Rhesus Monkey,” Fundamental and Applied Toxicology 17: 321-32 (1991).

[32] Charles Rebert & Gordon Pryor – “Chronic Inhalation of Marijuana Smoke and Brain Electrophysiology of Rhesus Monkeys,” International Journal of Psychophysiology V 14, p.144, 1993.

[33] NAS Report, pp. 82-7.

[34] American Journal of Epidemiology, May 1, 1999.

[35] “Cannabis and Memory Loss,” (editorial) British Journal of Addiction 86: 249-52 (1991)

[36] Dr. Christine Hartel, loc. cit.

[37] NAS Report, pp. 94-9.

[38] Dr. Robert Block in Drug and Alcohol Dependence 28: 121-8 (1991).

[39]NAS Report, p. 97-8.

[40] NAS Report, p. 99.

[41] Dr. Susan Astley, “Analysis of Facial Shape in Children Gestationally Exposed to Marijuana, Alcohol, and/or Cocaine,” Pediatrics 89#1: 67-77 ( June 1992).

[42] Dr. Barry Zuckerman et al. “Effects of Maternal Marijuana and Cocaine Use on Fetal Growth,” New England Journal of Medicine 320 #12: 762-8 (March 23, 1989); Dr. Ralph Hingson et al., “Effects of maternal drinking and marijuana use on fetal growth and development,” Pediatrics 70: 439-46 (1982).

[43] Nancy Day et al., “Prenatal Marijuana Use and Neonatal Outcome,” Neurotoxicology and Teratology 13: 329-34 (1992).

[44] Janice Hayes, Melanie Dreher and J. Kevin Nugent, “Newborn Outcomes With Maternal Marihuana Use in Jamaican Women,” Pediatric Nursing 14 #2: 107-10 (Mar-Apr. 1988).

[45] NAS Report, pp. 66-67.

[46] Murray Mittelman, article inCirculation June 12, 2001; cited in Science News 160:31, Jul. 14, 2001.

[47] D. Gieringer, E. Rosenthal and G. Carter, Marijuana Medical Handbook (Quick American, Oakland CA 2008), p. 48, 75, 80.

[48] D. Tashkin, “Is Frequent Marijuana Smoking Hazardous To Health,?” Western Journal of Medicine 158 #6: 635-7 (June 1993).

[49] D. Abrams et al., “Short -Term Effects of Cannabinoids in Patients with HIV-1 Infection: A Randomized, Placebo-Controlled Clinical Trial,” Annals of Internal Medicine 139.4: 258-266 (2003).

[50] D. Abrams et al, “Cannabis in painful HIV-associated sensory neuropathy: a randomized, placebo-controlled trial,”Neurology 68:515-21 (2007); R. Ellis et al, “Smoked Medicinal Cannabis for Neuropathic Pain in HIV: A Randomized Crossover Trial,” Neuropsychopharmacology, Aug. 6, 2008.

[51] Richard A Kaslow et al, “No Evidence for a Role of Alcohol or Other Psychoactive Drugs in Accelerating Immunodeficiency in HIV-1-Positive Individuals,” JAMA 261:3424-9 (June 16, 1989).

[52] NAS Report, p. 101.

[53] “Survey: Hawaii war on pot pushed users to ‘ice,'” Honolulu Advertiser, April 1, 1994 p. 1.

[54] “Marijuana and Medicine: Assessing the Science Base,” Institute of Medicine, National Academy Press (1999) pp 3.22-23

[55] S. Andreasson et al, “Cannabis and Schizophrenia: A Longitudinal Study of Swedish Conscripts,” Lancet 2: 1483-6 (1986).

[56]”An inquiry into the public health strategies related to cannabis use and the most appropriate legal status,” New Zealand Parliament, August 2003, p. 17

[57] Three articles with such findings were published in British Medical Journal, 325 (23 Nov. 2002)

[58] K.T. Mueser et al, “Prevalence of Substance Abuse in Schizophrenic Demographis and Clinical Correlates,” Schizophrenia Bulletin 16: 31-56 (1990); R. Warner et al., “Substance Use Among the Mentally Ill: Prevalence, Reasons for Use, and Effects on Illness,” American Journal of Orthopsychiatry 64: 30-39 (1994).

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