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Straight Dope
The Research on Marijuana Safety
(Part 2 of 4) by Gary Stimeling
Copyright 2005 Psychotropics Cornucopia, Inc. All Rights Reserved.
Another Big Phat One
Because the active ingredient accumulates in fat cells, “even people using marijuana only once each month are continually exposing their brain, lungs, liver, and other vital tissues to the poisonous effects of THC,” wrote Robert I. DuPont,([1]) former head of the National Institute on Drug Abuse (NIDA), the federal agency charged with providing other agencies with accurate scientific information about illegal drugs. Although knowledge of THC’s pharmacodynamics has been refined since then, the salient features were already well known at the time of DuPont’s misstatement.([2])
After smoking, or processing by the liver if cannabis is eaten, THC is distributed by the blood throughout the body. About 1 percent of it reaches the brain and binds to the cannabinoid receptors.([3]) There are no known toxic effects to cells at any dose achievable in living humans, and there are no psychoactive effects when blood levels fall below about 15 nanograms per milliliter (` 10 ng), which generally happens about 2 to 4 hours after smoking moderately potent material. Most cells biotransform THC into water-soluble metabolites that are excreted in the urine within a few days.([4]) Like Valium, Thorazine, barbiturates, and other fat-soluble drugs, however, THC stays in fat cells longer and is slowly released back into the bloodstream in its original form. But even if people smoke heavily and constantly, the amount thus released is far too small to contribute to a high.([5]) Contrary to propaganda pamphlets, the brain doesn’t have many fat cells, THC does not accumulate significantly in the brain, fat cells have no cannabinoid receptors, and THC storage in fat cells has no known physiologic effect.([6]) Its only apparent consequence is that drug tests can detect marijuana use two weeks after the fact instead of two or three days—and perhaps as long as 4 to 6 weeks in some heavy users who have a slow metabolic rate and large amounts of adipose tissue.
Disruption of the Immune System
The idea that cannabis impairs the human immune system comes from Gabriel Nahas. In 1974, he compared the activation rate of T-cells extracted from marijuana users and nonusers. T-cells are the cells in blood and lymph that stimulate production of antibodies to kill invading bacteria and neutralize toxins. Nahas had expected enhanced activity in the pot smokers’ T-cells, which he thought would show that their bodies were fighting to get rid of the cannabinoids. Instead, he found reduced activity and claimed this meant that the drug had impaired the immune system.([7]) This study is routinely referenced as proof of immune-system damage, even though at least five research groups—including Nahas’s!—have disproved it, finding no difference between the T-cells of users and nonusers.([8])
Given the fact that one type of cannabinoid receptor (CB2) is abundant in several kinds of cells in the immune system, and that THC can either activate or deactivate CB2 receptors, depending on the chemical context,([9]) it is possible that large doses of THC may disturb the balance in a way that decreases resistance to certain diseases, especially in serious pre-existing conditions like HIV infection. Some researchers paint an alarmist picture, even while documenting the fact that there is no consistent evidence to date of immunosuppression in humans.([10]) Their fears are based almost exclusively on work with isolated cells and lab animals that is of dubious relevance to the intact human body.([11]) Like nearly all drugs, marijuana smoke and THC do diminish the activity of lymphocytes and other immune cells in Petri dishes. However, except for macrophages during smoking [see below], these cells do not encounter smoke or large amounts of THC in a living animal, so such research says little about the actual effect of ganja on immunity.([12])
Animal studies are potentially more relevant, and researchers have been able to generate some increased infection rates, e.g., with herpes simplex by dosing female rodents with THC and then applying concentrated virus to their vaginas—but only by blasting the victims with 40 to 1,000 times the tissue levels of THC attained in moderate human use.([13]) Decades ago, one doctor reported anecdotes that a few marijuana smokers had more herpes recurrences than nonsmokers.([14]) On the other hand, some patients have found that a tincture of strong cannabis in rubbing alcohol is an effective topical treatment for cold sores and genital herpes lesions.([15])
If cannabis interferes with the immune system, dopers should be getting sick more often than other people. With the possible exception of respiratory diseases among heavy smokers [see below], there is no evidence that they do. In 1992, the Food and Drug Administration, not noted for a favorable outlook on cannabinoids, approved Marinol (pure synthetic THC) as an appetite stimulant for people with the weakest immune systems of all—AIDS patients. Approval was based in part on two reports that showed no effect of marijuana smoking on immune function in AIDS.([16]) Those studies have been confirmed.([17]) Another study suggests that marijuana may help the immune system prevent non-Hodgkin’s lymphoma.([18])
Lung Damage and Cancer
Lung disease may be the only alleged major health risk from marijuana about which good-faith debate is still warranted. Like smoke from any burning plant material, marijuana smoke contains more or less the same kinds and amounts of particles, lung irritants, and poisonous gases as tobacco smoke, including vinyl chloride, ozone, nitrosamines, phenols, and polycyclic aromatic hydrocarbons (PAHs).([19]) UCLA pulmonologist Donald Tashkin, who probably knows more about smoking than anyone else on earth, recently summarized the evidence for and against various kinds of lung damage from smoking marijuana.([20])
Heat and irritation from tobacco smoke tend to cause chronic bronchitis by damaging the ciliated cells that remove particles from the lungs, replacing them with mucus-secreting “goblet” cells. Phlegm and persistent cough are the outward signs of this damage, which occurs years before precancerous changes. Several studies, including two by Tashkin’s group, have found a higher-than-average rate of bronchitis and ciliated-cell damage among heavy daily marijuana smokers, compared with the general population,([21]) and about as much as or slightly less of the phlegm and coughing symptoms as heavy tobacco smokers exhibited.([22]) However, a study of six years of records from the Kaiser Permanente Medical Care Program in California showed that daily marijuana-only smokers sought treatment for colds, flu, or bronchitis much less often than tobacco smokers and only slightly more often than nonsmokers.([23])
Chronic obstructive pulmonary disease (COPD) refers to a progressive decline in breathing capacity from bronchitis and/or emphysema (narrowing of the small airways), typically in response to tobacco smoking or industrial and workplace pollution. Three reports have indicated a decline in breath capacity among heavy marijuana smokers,([24]) but a study by Tashkin’s researchers using a more extensive sequence of tests on tokers who’d smoked three or four joints a day for an average of 15 years turned up no such effect.([25]) A project in which rats were forced to inhale progressively larger doses of cannabis smoke also found no evidence of COPD in them.([26]) To settle the issue, Tashkin and coworkers have continued to follow the same groups of nonsmokers and heavy tobacco and cannabis smokers they’ve been studying for decades. They have found the expected progressive decline in breath volume among smokers of tobacco only, but the lung capacity of marijuana smokers has not differed at all from that of the nonsmokers. Even the people who regularly smoke marijuana and tobacco continue to have near-normal lung function, suggesting a protective effect by cannabis. Tashkin has concluded, “Marijuana smokers probably will not develop emphysema.”([27]) In fact, Australian research on 268 people in the Nimbin area who had smoked cannabis weekly to daily for an average of 19 years found that they had less emphysema, and less asthma, than the population as a whole.([28])
The same may or may not hold true for lung cancer.
Several lines of reasoning and research suggest that continual heavy marijuana smoking may eventually cause lung cancer.([29])
· Holding the breath deposits 40 percent more tar in the lungs from a joint than from smoking a tobacco cigarette in the usual way. Some chemists have found more of one especially carcinogenic PAH, benzo-alpha-pyrene, in marijuana smoke,([30]) but more recent work found more in tobacco smoke.([31]) However, THC apparently stimulates production of an enzyme that enhances the carcinogenicity of PAHs in the lung, although it may simultaneously reduce the enzyme’s effectiveness somewhat.([32])
· In a standard lab-culture test for cancerous cellular mutations, cannabis tar (but not THC) induces the same number and type of mutations as tobacco tar.([33]) Hamster lung cells kept alive in culture for two years and bombarded with equal amounts of cannabis and tobacco smoke showed more cancerous changes from the pot smoke.([34]) Marijuana tar painted on the skin of mice induces skin cancer.([35])
· Several studies suggest that direct contact with THC may inhibit the immune system cells that eradicate bacteria and tumor cells.([36]) Macrophages (“big eater”) cells extracted from the lungs of regular marijuana smokers have a diminished ability to kill bacteria and tumor cells.([37]) This suggests that smoking marijuana could be life-threatening to AIDS patients who are fighting pneumonia, although in practice this detriment has not been observed, perhaps because the appetite-stimulating and weight-gaining effect of marijuana counteracts it. At least three studies have found that marijuana smoke’s effect on macrophages is much weaker than tobacco’s,([38]) so it may not be significant for persons with intact immune systems.
· Bronchial-cell biopsies by Tashkin’s research group showed numerous precancerous changes in 40 regular heavy marijuana smokers.([39])
· There have been three reports of lung and head or neck cancers at an unusually early age among small groups of regular marijuana smokers.([40]) A larger group (173 patients) with head and neck cancer, matched with an equal number of cancer-free controls, also indicated an association with marijuana smoking, which was strongest among the heaviest smokers.([41])
On the other hand, there are several reasons to believe that even heavy cannabis smoking may not cause lung cancer:
· It’s the total lifetime volume of inhaled smoke that counts most as a risk factor in lung cancer,([42]) and all but the most extreme marijuana smokers are unlikely to approach the volume inhaled by even moderately heavy tobacco smokers. Very few cannabis users in the West smoke even the 3 to 4 joints per day consumed on average by the group that has been studied long-term by Dr. Tashkin.
· As medical marijuana researcher Franjo Grotenherman has noted, “No relationship between heavy cannabis use and human mortality has been discovered.”([43]) Studies that included physical exams of heavy ganja smokers in Jamaica, Greece, and Costa Rica found no lung cancers. A epidemiological review of the medical records of 64,000 patients showed no link between marijuana smoking and lung cancer.([44]) Bear in mind, however, that it took forty years and even larger studies to prove the connection with tobacco smoking.
· THC itself exerts a strong anticancer effect against at least nine kinds of tumors commonly used in the laboratory to assess drugs for human use([45]) [see the Medical page under Anticancer Agent]. Mice pre-dosed with THC get fewer tumors than do controls, those they do get grow more slowly or shrink when THC is given, and THC-treated animals live about twice as long as untreated ones. These results increase with higher doses and longer regimens, indicating a genuine direct effect.([46])
· Intensive exams of four patients legally using federal pot showed great improvement in their conditions, much-reduced use of pharmaceuticals, no side effects—and no precancerous changes in their lungs. This is a very small sample because the feds have never been very compassionate in their “compassionate use” program. Still, it’s significant that these people showed no lung damage despite having smoked very large quantities of very low-quality government marijuana (standardized at 2 percent THC) almost every day for 10 to 19 years.([47])
In any event, while waiting for the final scientific word, there are several ways to drastically reduce or eliminate any risks from smoking ganja:
· Don’t hold your breath. The fat-soluble THC is absorbed by the lungs almost instantly. Exhaling immediately after the inhalation expels most of the carcinogenic compounds, which are solid particles or water-soluble gases, before they can be absorbed, without sacrificing any of the high.([48]) The fact that this has been known since 1971 but never publicized qualifies as a war crime. Clamping down to “pressurize” the smoke into the lungs is even worse. It can tear a hole in a lung and force air into the chest cavity, which can be fatal.([49])
· Don’t use a standard bong or water pipe. They cool the smoke and reduce toxic gases, but they actually increase the ratio of tars to THC by as much as a third. Multiphase hot and cold water pipes are better, keeping the tar-THC ratio comparable to that from joints or nonliquid pipes.([50]) Joints burn a little cooler than all pipes, destroying less THC in combustion.
· Vaporizers solve the carcinogen problem, but some of them deliver more cannabinol than THC.([51]) Cannabinol is the oxidized form of THC and is less than one-tenth as psychoactive. For up-to-date information on vaporizer types, go to Dr. Tod Mikuriya’s Vaporizer Page, the California NORML Vaporizer Survey, or Kevin’s Vaporizer Picks.
· Use the best available material—high-grade ganja, kif, hash, bubble hash, or hash oil. The lower the potency, the more toxins in the smoke and the more you have to inhale to get high.([52]) In the United States, research can only be done legally with standard lousy government pot, thus preventing scientific study of how different cannabis products vary in their effect on the lungs.
· Risks of smoking can be avoided completely by ingesting cannabinoids in a tincture, in bhang, or in food, but it’s harder to titrate the dose for the desired effect this way. Under the inquisition, it’s also far too expensive for most people, although using cut-rate low-grade weed can make it more cost-effective.
Prohibitionists often claim their efforts are about public health, but when presented with a challenge to actually foster public health, such as by allowing distribution of sterile syringes to slow the spread of AIDS, they always fail the test. To make safer cannabis use possible (as well as end the social harm of mass incarceration), legalization is a crucial public health measure.
Motivation, School, and Work
Some Westernizers from the Third World have blamed poverty and cultural stagnation on hashish, saying it makes the fellahin lazy.([53]) It’s certainly easier than examining the role of neocolonial economics. In the late Sixties, a few American scientists made a big media splash by claiming that a generation of dope-smoking students would sabotage industrial productivity with an amotivational syndrome.([54]) Despite extensive disproof, their work is still widely quoted as evidence that cannabis turns people into shiftless zombies.
Let’s leave aside the question whether unrelenting output in competitive mode is the way to real achievement and happiness. Even under their own assumptions, these writers often confused cause and effect. For example, the voluminous research that resulted from the amotivation scare has shown that, in high school, heavy use of marijuana (and alcohol and other drugs) is but one symptom of pre-existing problems that lead to failure to graduate or to depression in adulthood.([55])
It’s hard to be sane in a crazy world. True sanity requires knowing one’s inmost desires and figuring out how to fulfill them despite forces that try to thwart both the knowledge and the fulfillment at every turn.([56]) Few try, and most of them fail. Young people who begin to reject materialist norms of success—and who, perhaps in consequence, become depressed—sometimes retreat into apathy and constant marijuana smoking.([57]) In northern Africa, those who fall into this trap are called nchaioui. But most people, including pot smokers, find a better way out. College students who use cannabis are more apt than nonusers to delay choosing a major or to take a leave of absence and rechart their course in life, but they are also more likely to go to graduate school.([58]) Other than this occasional delay, science shows that cannabis either has no significant effect on academic performance([59]) or actually improves it.([60])
Interviews of 268 long-term heavy Australian marijuana smokers found that 21 percent said it made them tired and lazy, but many of these also used alcohol and other drugs that have that effect.([61]) A small study that excluded users of other drugs found that 3 of 37 chronic smokers said weed decreased their initiative, while 8 said the drug increased it.([62]) Clinical psychologists find a lack of motivation in about 5 percent of people whether they use cannabis or not.([63])
Several scientists have investigated marijuana’s effect on work by setting up artificial mini-economies in live-in laboratories. In one, male volunteers stayed in a hospital ward for three months. They had to smoke one joint per day and do office-style make-work. They were paid in tokens, which they could use to buy extra weed during the project or redeem for cash at its end. The men’s average consumption of 5 joints a day had no effect on their work time, efficiency, or scores on psychological tests.([64])
In a similar one-month residential study, heavy cannabis smokers worked harder, produced more, and earned more tokens than moderate smokers or abstainers, even though they took time off now and then to kick back and get thoroughly stoned. Because they worked harder when they were working, they were able to use many tokens to buy extra pot yet still turn in the same number for cash as the other two groups.([65]) Apparently the privilege of smoking ganja is itself a powerful motivation.
A Canadian study had 6 live-in workers do moderately satisfying manual labor for 70 days—making chairs. It began with a period of abstinence to establish a baseline production rate. Once the subjects were given cannabis to smoke, their productivity declined for a few days, then soon exceeded the baseline level. Again, the heaviest smokers spent the least time working but achieved the same output as the others by working more efficiently when they did work. And during the period of greatest allowed intake, the smokers organized two strikes and got higher pay for everyone! Maybe that’s the real reason the herb is illegal. Following a short production decline after the strikes, output again surpassed the baseline.([66])
At Johns Hopkins University School of Medicine, Richard Foltin had found that, when high, people would rather relax than do something boring.([67]) To confirm this alleged evidence that marijuana saps ambition, he put new testees through two weeks of “low-probability activities”—insanely dull assignments designed to mimic the worst jobs, like sorting bins of plastic chips by color and size, or alphabetizing lists of 500 nonsense words. After finding out which tasks each person considered the most and least onerous, he made subjects work many hours at their worst job for the right to do their least detested one. Foltin predicted that marijuana would make them less willing to get through the bad crap for the slightly better crap, but actually the reverse was true.([68]) He refused to accept his own results and called for more research to find amotivational syndrome.
The foregoing evidence for motivational syndrome is corroborated by research on actual workers. Anthropologists have studied farm laborers in Jamaica, Costa Rica, and Greece, and confirmed what their subjects told them, that ganja breaks help them work harder.([69]) In Costa Rica, the heaviest users had the best jobs, even though cannabis users on the whole were more often unemployed, due to being arrested under the drug laws.
In the United States, several groups of scientists have used data from a long-term study of 400 men in New York State and another of 12,000 adults throughout the country. Two of them found more unemployment and fewer work hours among marijuana users, but also found they averaged higher wages.([70]) Another, using a larger sample of workers who’d held several jobs, found no difference in work hours between users and nonusers. Again, higher wages and greater cannabis use were linked.([71]) Either the more grass people smoke, the more money they make, or the more money they make, the more grass they buy. A flurry of studies in the 1990s confirmed that cannabis smokers get paid as much as or more than their abstaining peers.([72]) Nor do pot smokers get fired more often than abstainers,([73]) unless they get snagged by a piss test. In fact, two unpublished in-house reviews in the electric utility industry suggest that workers who test positive for only marijuana get promoted more often, are absent 30 percent less often, and use fewer health insurance benefits than workers who never failed a drug test.([74]) Since cannabis is by far the most popular illicit drug, and since its metabolites remain in the body much longer than those of other illegal drugs, the vast majority of workplace urine-test positives are for marijuana use off the job. Firing these workers is beating a live horse—to death.
Driving
Scientists have studied marijuana’s effect on driving by using the same tests that established the hazards of driving under the influence of alcohol and numerous prescription drugs. They have not found equal dangers.
Tests in driving simulators have shown slight impairment from cannabis, especially in visual perception of multiple simultaneous stimuli, but even at high doses the effect is much less than that produced by low, legal blood levels of alcohol.([75]) Tests on closed laboratory courses and in actual traffic have confirmed these results.([76]) A comprehensive Dutch study of driving at low, medium, and high doses of THC found a bit more weaving from side to side within the lane, but otherwise no decrease in driving ability or safety.([77]) Drivers tend to take more risks if they are even a little bit tipsy, but stoned persons tend to drive more cautiously than those who are sober. They drive more slowly, follow further behind the car in front of them, and take fewer chances.([78]) Scientists reviewing the evidence for the Department of Transportation concluded that of all legal or illegal drugs people use before driving, “marijuana may well be among the least harmful.”([79])
The legal limit for blood alcohol concentration is 0.1 percent, which makes a crash 7 times more likely than when sober.([80]) More than half of all drivers killed in accidents have blood alcohol levels over the legal limit.([81]) In contrast, only 3 to 11 percent of dead drivers have THC in their blood, and 70 to 90 percent of those have alcohol, too.([82]) So only about 0.6–2.2 percent of the deceased operators tested positive for marijuana alone, far less than its rate of use among the population.
Of course, the real question is not whether driving stoned is safer than driving drunk, but whether it is more dangerous than driving sober. To find the answer, at least nine research teams have studied assessments of culpability in a large number of fatal and nonfatal accidents, and compared the rate of causation for sober, alcohol-positive, and cannabis-positive drivers. As expected, all found booze to be by far the greatest contributor to highway wreckage. Five found a slightly lower percentage of culpability among pot smokers than among sober drivers,([83]) and none found any statistically significant difference one way or the other.([84])
However, cannabis may still decrease driving ability in some people at some times, especially inexperienced or tired drivers or novice users. The National Association for Reform of Marijuana Laws (NORML) strongly urges people not to drive while high as a basic principle of responsible use.([85]) Personally, I believe I drive less competently if stoned, especially in a situation requiring quick, accurate reflexes, and I stopped doing it long ago. I feel that it’s a waste of an expensive drug, and that if the herb doesn’t impair my driving at least a little, I got burned. More important, I believe that, even if voluminous research were to prove beyond a shadow of a doubt that marijuana has no effect whatsoever or even improves driving, refraining is an act of goodwill toward fearful nonusers, which eventually might accrue toward the trust needed for legalization.
[1]. Robert I. DuPont, Getting Tough on Gateway Drugs, American Psychiatric Press, Washington DC, 1984, p. 68.
[2]. The Pharmacology of Marijuana, ed. M. C. Braude and S. Szara, Raven Press, New York, 1976.
E. R. Garrett, “Pharmacokinetics and Disposition of Delta-9-Tetrahydrocannabinol and Its Metabolites,” Advances in Bioscience, vol. 22–23, pp. 105–121, 1978.
At least seven other papers precede and contradict DuPont’s statement. See bibliographic notes in Zimmer and Morgan, p. 215.
[3]. B. R. Martin, “Cellular Effects of Cannabinoids,” Pharmacological Reviews, vol. 38, pp. 45–74, 1986.
[4]. R. Swatek, “Marijuana Use: Persistence and Urinary Elimination,” Journal of Substance Abuse Treatment, vol. 1, pp. 265–270, 1984.
[5]. R. R. Garrett, ibid.
Leo E. Hollister, “Health Aspects of Cannabis,” Pharmacological Reviews, vol. 38, pp. 1–20, 1986.
Rudolf Brenneisen, “Pharmacokinetics,” Grotenherman and Russo, chapter 6.
[6]. D. S. Kreuz and J. Axelrod, “Delta-9-Tetrahydrocannabinol: Localization in Body Fat,” Science, vol. 179, pp. 391–392, 1973.
Gabriel G. Nahas, et al., “The Kinetics of Cannabinoid Distribution and Storage with Special Reference to the Brain and Testes,” Journal of Clinical Pharmacology, vol. 21, pp. 208–214S, 1981.
M. Bronson, et al., “Distribution and Disposition of Delta-9-Tetrahydrocannabinol (THC) in Different Tissues of the Rat,” in The Cannabinoids: Chemical, Pharmacological, and Therapeutic Aspects, ed. S. Agurell, W. Dewy, and R. Willette, Academic Press, New York and Orlando FL, 1984, pp. 309–317.
Leo E. Hollister, ibid.
G. J. Siegel, et al., Basic Neurochemistry, Raven Press, New York, 1989.
[7]. Gabriel G. Nahas, “Inhibition of Cellular Mediated Immunity in Marihuana Smokers,” Science, vol. 183, pp. 419–420, 1974.
[8]. S. C. White, et al., “Mitogen-Induced Blastogenetic Responses to Lymphocytes from Marihuana Smokers,” Science, vol. 188, pp. 71–72, 1975.
R. J. Lau, et al., “Phytohemagglutinin-Induced Lymphocyte Transformation in Humans Receiving Delta-9-Tetrahydrocannabinol,” Science, vol. 192, pp. 805–807, 1976.
E. Kaklamani, et al., “Hashish Smoking and T-Lymphocytes,” Archives of Toxicology, vol. 40, pp. 97–101, 1978.
E. M. Dax, et al., “The Effects of 9-ene-Tetrahydrocannabinol on Hormone Release and Immune Function,” Journal of Steroid Biochemistry, vol. 34, pp. 263–270, 1989.
Leo E. Hollister, “Marijuana and Immunity,” Journal of Psychoactive Drugs, vol. 24, pp. 159–164, 1992.
Nahas admits failing to reproduce his initial finding in the 5th edition of Keep Off the Grass, Paul S. Eriksson, Middlebury VT, 1990.
[9]. Roger G. Pertwee, “Sites and Mechanisms of Action,” chapter 7 of Grotenherman and Russo, p. 80.
[10]. H. Friedman and T. W. Klein, “Marijuana and Immunity,” Science and Medicine, vol. 6, no. 2, pp. 12–21, 1999.
Guy A. Cabral, “Immune System,” Grotenherman and Russo, chapter 25.
[11]. Zimmer and Morgan, chapter 14.
[12]. Hollister, ibid.
B. Watzl, et al., “Influence of Marijuana Components (THC and CBD) on Human Mononuclear Cell Cytokine Secretion in Vitro,” in Drugs of Abuse, Immunity, and Immunodeficiency, ed. H. Friedman, et al., Plenum Press, New York, 1991.
Guy A. Cabral, ibid.
[13]. E. M. Mishkin and Guy A. Cabral, “Delta-9-Tetrahydrocannabinol Decreases Host Resistance to Herpes Simplex Virus Type 2 Vaginal Infection in the BGC3F1 Mouse,”Journal of General Virology, vol. 66, pp. 2539–2549, 1985.
Guy A. Cabral, et al., “Effect of Delta-9-Tetrahydrocannabinol on Herpes Simplex Virus Type 2 Vaginal Infection in the Guinea Pig,” Proceedings of the Society for Experimental Biology and Medicine, vol. 182, pp. 181–186, 1986.
[14]. B. E. Juel-Jensen, “Cannabis and Recurrent Herpes Simplex,” British Medical Journal, 1972, no. iv, p. 296.
[15]. Anecdotal reports are found on many Web sites. See, for example, “THC and the Herpes Virus,” by Darrell Heiner, at http://www.onlinepot.org/medical/herpesthc.htm.
[16]. R. A. Kaslow, et al., “No Evidence for a Role of Alcohol or Other Psychoactive Drugs in Accelerating Immunodeficiency in HIV-1-Positive Individuals,” Journal of the American Medical Association, vol. 261, pp. 3424–3429, 1989.
R. A. Coates, et al., “Cofactors of Progression to Acquired Immunodeficiency Syndrome in a Cohort of Male Sexual Contacts of Men with Immunodeficiency Virus Disease,” American Journal of Epidemiology, vol. 132, pp. 717–722, 1990.
[17]. M. J. DiFranco, et al., “The Lack of Association of Marijuana and Other Recreational Drugs with Progression to AIDS in the San Francisco Men’s Health Study,” Annals of Epidemiology, vol. 6, no. 4, pp. 283–289, 1996.
[18]. E. A. Holly, et al., “Case-Control Study of Non-Hodgkin’s Lymphoma Among Women and Heterosexual Men in the San Francisco Bay Area,” American Journal of Epidemiology, vol. 150, pp. 375–389, 1999.
[19]. G. L. Huber, et al., “Marijuana and Tobacco Smoke: Gas-Phase Cytotoxins,” Pharmacology, Biochemistry and Behavior, vol. 40, pp. 629–636, 1991.
[20]. Donald P. Tashkin, “Respiratory Risks from Marijuana Smoking,” Grotenherman and Russo, chapter 29.
[21]. J. W. Bloom, et al., “Respiratory Effects of Nontobacco Cigarettes,” British Medical Journal, vol. 295, no. 6612, pp. 1516–1518, 1987.
Donald P. Tashkin, et al., “Respiratory Symptoms and Lung Function in Habitual, Heavy Smokers of Marijuana Alone, Smokers of Marijuana and Tobacco, Smokers of Tobacco Alone, and Nonsmokers,” American Review of Respiratory Disease, vol. 135, no. 1, pp. 209–216, 1987.
S. E. G. Fligiel, et al. (Tashkin’s group), “Tracheobronchial Histopathology in Habitual Smokers of Cocaine, Marijuana and/or Tobacco,” Chest, vol. 112, no. 2, pp. 319–326, 1997.
D. R. Taylor, et al., “The Respiratory Effects of Cannabis Dependence in Young Adults,” Addiction, vol. 95, no. 11, pp. 1669–1677, 2000.
[22]. Donald P. Tashkin, et al., “Effects of Habitual Use of Marijuana and/or Cocaine on the Lung,” in Research Findings on Smoking of Abused Substances, ed. N. Chiang and R. L. Hawkins, NIDA, Rockville MD, 1990.
D. L. Sherrill, et al., “Respiratory Effects of Nontobacco Cigarettes: A Longitudinal Study in General Population,” International Journal of Epidemiology, vol. 20, no. 1, pp. 132–137, 1991. This was a follow-up by the same group on the work in which Bloom [see previous note] was lead investigator.
[23]. M. R. Polen, “Health Care Use by Frequent Marijuana Smokers Who Do Not Smoke Tobacco,” Western Journal of Medicine, vol. 158, pp. 596–601, 1993.
[24]. J. W. Bloom, ibid.
D. L. Sherrill, ibid. Oddly, this study found a link between lowered breath capacity and past heavy marijuana smoking but not present smoking.
D. R. Taylor, ibid.
[25]. Donald P. Tashkin, ibid.
[26]. G. L. Huber and V. K. Mahajan, “The Comparative Response of the Lung to Marihuana or Tobacco Smoke Inhalation,” in Marijuana: An International Research Report, ed. Gregory B. Chesher, Paul Consroe, and Richard E. Musty, Proceedings of the Melbourne Symposium on Cannabis, National Campaign Against Drug Abuse Monograph Series, No. 7, Australian Government Publishing Service, Canberra, 1987, pp. 19–24.
[27]. L. Gagnon, “Marijuana Less Harmful to Lungs Than Cigarettes,” Quebec Medical Post, September 6, 1994.
[28]. P. Didcott, et al., Long-Term Cannabis Users on the New South Wales North Coast, Australian Government Publishing Service, Canberra, 1997.
[29]. Donald P. Tashkin, “Respiratory Risks from Marijuana Smoking,” Grotenherman and Russo, chapter 29.
[30]. D. Hoffman, et al., “On the Carcinogenicity of Marijuana Smoke,” Recent Advances in Phytochemistry, vol. 9, pp. 63–81, 1975.
M. L. Lee, et al., “Gas Chromatography/Mass Spectrometric and Nuclear Magnetic Resonance Spectrometric Studies of Carcinogenic Polynuclear Aromatic Hydrocarbons in Tobacco and Marijuana Smoke Condensates,” Analytical Chemistry, vol. 48, no. 2, pp. 405–416, 1976.
[31]. R. G. Harvey, Polycyclic Aromatic Hydrocarbons: Chemistry and Carcinogenicity, Oxford University Press, New York, 1991.
[32]. M. D. Roth, et al. (Tashkin’s group), “Delta-9-Tetrahydrocannabinol Acts as Both an Inducer of the CYP1A1 Gene and an Inhibitor of Cytochrome P4501A1 Enzyme Activity,” in 1998 Symposium on the Cannabinoids, International Cannabinoid Research Society, Burlington VT, 1998, p. 69.
[33]. F. C. Wehner, et al., “Mutagenicity of Marijuana and Transkei Tobacco Smoke Condensates in the Salmonella/Microsome Assay,” Mutation Research, vol. 77, no. 2, pp. 135–142, 1980.
[34]. C. and R. Leuchtenberger, “Cytological and Cytochemical Studies of the Effects of Fresh Marihuana Cigarette Smoke on Growth and DNA Metabolism of Animal and Human Lung Cultures,” in The Pharmacology of Marijuana, ed. M. C. Braude and S. Szara, Raven Press, New York, 1976, pp. 595–612.
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L. X. Zhu, et al. (Tashkin’s group), “Delta-9-Tetrahydrocannabinol Inhibits Antitumor Immunity by a CB2 Receptor-Mediated, Cytokine-Dependent Pathway,” Journal of Immunology, vol. 165, no. 1, pp. 373–380, 2000.
Guy A. Cabral, “Immune System,” Grotenherman and Russo, chapter 25.
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M. P. Sherman, et al., “Effects of Smoking Marijuana, Tobacco or Cocaine Alone or in Combination on DNA Damage in Human Alveolar Macrophages, Life Sciences, vol. 56, pp. 2201–2207, 1995.
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S. H. Barsky, et al., “Similar Molecular Alterations in Bronchial Epithelium Are Observed in Habitual Smokers of Marijuana, Cocaine, and/or Tobacco,” Journal of the National Cancer Institute, vol. 90, pp. 1198–1204, 1998.
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K. S. Sridhar, et al., “Possible Role of Marijuana Smoking as a Carcinogen in the Development of Lung Cancer at a Young Age,” Journal of Psychoactive Drugs, vol. 26, no. 3, pp. 285–288, 1994. Note that 12 of the 13 cancer patients in this group also smoked tobacco.
P. J. Donald, “Advanced Malignancy in the Young Marijuana Smoker,” Advances in Experimental Medicine and Biology, vol. 288, pp. 33–56, 1991.
[41]. Z.-F. Zhang, et al. (Tashkin’s group), “Marijuana Use and Increased Risk of Squamous Cell Carcinoma of the Head and Neck,” Cancer Epidemiology, Biomarkers and Prevention, vol. 8, no. 12, pp. 1071–1078, 1999.
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[43]. Grotenherman and Russo, p. 234.
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National Toxicology Program, Toxicology and Carcinogenesis: Studies of 1-Trans-Delta-9-Tetrahydrocannabinol in F344/N Rats and B6c3F1 Mice, Department of Health and Human Services, Rockville MD, 1996. Publication of this study was delayed, allegedly due to a shortage of personnel: AIDS Treatment News, January 17, 1997; Boston Globe, January 30, 1997.
Manuel Guzmán, “Cannabinoids: Potential Anticancer Agents,” Nature Reviews: Cancer, vol. 3, October 2003.
[47]. Ethan Russo, Mary Lynn Mathre, et al., “Chronic Cannabis Use in the Compassionate Investigational New Drug Program: An Examination of Benefits and Adverse Effects of Legal Clinical Cannabis,” Journal of Cannabis Therapeutics, vol. 2, no. 1, pp. 3–58, 2002.
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J. P. Zacny and L. D. Chait, “Breathhold Duration and Response to Marijuana Smoke,” Pharmacology, Biochemistry and Behavior, vol. 33, pp. 481–484, 1989.
J. P. Zacny and L. D. Chait, “Response to Marijuana as a Function of Potency and Breathhold Duration,” Psychopharmacology, vol. 103, pp. 223–226, 1991.
J. Zorilosa, et al., “Marijuana Smoking: Effects of Varying Puff Volumes and Breathholding Duration,” Journal of Pharmacology and Experimental Therapeutics, vol. 272, pp. 560–569, 1995.
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K. L. Mattox, “Pneumomediastinum in Heroin and Marijuana Users,” Journal of the American College of Emergency Physicians, vol. 5, no. 1, pp. 26–28, 1976.
A. L. Feldman, et al., “Pneumothorax in Polysubstance-Abusing Marijuana and Tobacco Smokers: Three Cases,” Journal of Substance Abuse, vol. 5, no. 2, pp. 183–186, 1993.
[50]. R. Doblin, “The MAPS/California NORML Marijuana Waterpipe/Vaporizer Study,” Newsletter of the Multidisciplinary Association for Psychedelic Studies, vol. 5, no. 1, pp. 19–22, 1994. This study continues despite federal refusal to release standardized government research marijuana for it, thus preventing publication in mainstream journals. Check for updates at http://www.maps.org/mmj/vaporizer.html.
[51]. Dale Gieringer, “Marijuana Water Pipe and Vaporizer Study.” Newsletter of the Multidisciplinary Association for Psychedelic Studies, vol. 6, no. 1, pp. 5–9.
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[53]. The Bulletin on Narcotics, inspired by Harry Anslinger and put out by the United Nations Office on Drugs and Crime, often featured the lazy hash smoker. A typical issue was vol. 9, which included “Psychopathological Aspects of the Cannabis Situation in Morocco,” by A. Benabud, pp. 1–16, and “The Use of Cannabis Drugs in India,” by I. C. Chopra and R. N. Chopra, pp. 17–29. Gabriel Nahas continued the tradition, culminating in his “Hashish and Drug Abuse in Egypt During the 19th and 20th Centuries,” Bulletin of the New York Academy of Medicine, vol. 61, pp. 428–444, 1985.
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David E. Smith, “The Acute and Chronic Toxicity of Marijuana,” Journal of Psychedelic Drugs, vol. 2, pp. 37–48, 1968.
H. Kolansky and W. T. Moore, “Effects of Marihuana on Adolescents and Young Adults,” Journal of the American Medical Association, vol. 216, pp. 486–492, 1971; and “Toxic Effects of Chronic Marihuana Use,” Journal of the American Medical Association, vol. 222, pp. 35–41, 1972.
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Jack Block, et al., “Longitudinally Foretelling Drug Usage in Adolescence: Early Childhood Personality and Environmental Precursors,” Child Development, vol. 59, pp. 336–355, 1988.
J. Shedler and Jack Block, “Adolescent Drug Use and Psychosocial Health,” American Psychologist, vol. 45, pp. 612–630, 1990.
R. Dembo, et al., “A Longitudinal Study of the Relationships Among Alcohol Use, Marijuana/Hashish Use, Cocaine Use, and Emotional/Psychological Functioning Problems in a Cohort of High-Risk Youth,” International Journal of the Addictions, vol. 25, pp. 1341–1382, 1990.
J. D. Hawkins, et al., “Risk and Protective Factors for Alcohol and Other Drug Problems in Adolescence and Early Adulthood: Implications for Substance Abuse Prevention,” Psychological Bulletin, vol. 112, pp. 65–105, 1992.
A. D. Farrell, et al., “Relationship Between Drug Use and Other Problem Behaviors in Urban Adolescents,” Journal of Consulting and Clinical Psychology, vol. 60, pp. 705–712, 1992.
Denise P. Kandel and K. Yamaguchi, “From Beer to Crack: Developmental Patterns of Drug Involvement,” American Journal of Public Health, vol. 83, pp. 851–855, 1993.
Denise B. Kandel and M. Davies, “High School Students Who Use Crack and Other Drugs,” General Archives of Psychiatry, vol. 53, pp. 71–80, 1996.
J. E. Donovan, “Problem Behavior Theory and the Explanation of Adolescent Marijuana Use,” Journal of Drug Issues, vol. 26, pp. 379–404, 1996.
B. E. Green and C. Ritter, “Marijuana Use and Depression,” Journal of Health and Social Behavior, vol. 41, pp. 40–49, 2000.
Tons more ink has been spilled on adolescent marijuana use and motivation, but this selection will guide the interested reader to other papers. A review of the literature concluded that, absent other factors, marijuana use has no significant effect on performance in high school: Wayne Hall, et al., The Health and Psychological Consequences of Cannabis Use, Australian Government Publishing Service, Canberra, 1994.
[56]. Do not think then that by Non-Action thou doest follow the Way of the Tao, for thy Nature is Action, and by hindering the Discharge of thy Potential thou doest perpetuate and aggravate the Stress. If thou ease not Nature, she will bring thee to Dis-Ease. Free therefore every Function of thy Body and of every other Part of thee according to its true Will. This also is most necessary, that thou discover that true Will in every Case, for thou art born into Dis-Ease; where are many false and perverted Wills, monstrous Growths, Parasites, Vermin are they, adherent to thee by Vice of Heredity, or of Environment or of evil Training. And of all these Things the subtlest and most terrible, Enemies without Pity, destructive to thy Will, and a Menace and Tyranny even to thy Self, are the Ideals and Standards of the Slave-gods, false Religion, false Ethics, even false Science. —Aleister Crowley, Liber Aleph: The Book of Wisdom and Folly, AD. De Via Libertatis (29. The Way of Freedom)
[57]. H. Hendin, et al., Adolescent Marijuana Users and Their Families, NIDA, Rockville MD, 1981.
Richard E. Musty and L. Kaback, “Relationships Between Motivation and Depression in Chronic Marijuana Users,” Life Sciences, vol. 56, pp. 2151–2158, 1995.
[58]. J. S. Hochman and N. Q. Brill, “Chronic Marijuana Use and Psychosocial Adaptation,” American Journal of Psychiatry, vol. 130, pp. 132–139, 1973.
N. O. Brill and R. L. Christie, “Marihuana Use and Psychosocial Adaptation,” Archives of General Psychiatry, vol. 31, pp. 713–719, 1974.
G. D. Mellinger, et al., “Drug Use, Academic Performance, and Career Indecision: Longitudinal Data in Search of a Model,” in Longitudinal Research on Drug Use: Empirical Findings and Methodological Issues, American Psychological Association, Washington DC, 1978, pp. 157–177.
[59]. J. L. Anker, et al., “Drug Usage and Related Patterns of Behavior in University Students: I. General Survey and Marihuana Use,” Journal of the American College Health Association, vol. 19, pp. 178–186, 1971.
P. A. Walters, “Drug Use and Life-Style Among 500 College Undergraduates,” Archives of General Psychiatry, vol. 26, pp. 92–96, 1972; Harrison G. Pope, et al., “Drug Use and Life-Style Among College Undergraduates: Nine Years Later, “ Archives of General Psychiatry, vol. 38, pp. 588–591, 1981; Harrison G. Pope, et al., “Drug Use and Life Style Among College Undergraduates in 1989: A Comparison with 1969 and 1978,” American Journal of Psychiatry, vol. 147, pp. 998–1001, 1990.
D. J. Kupfer, et al., “A Comment on the Amotivational Syndrome in Marihuana Smokers,” American Journal of Psychiatry, vol. 130, pp. 1319–1322, 1973.
N. O. Brill and R. L. Christie, ibid.
A. C. Miranne, “Marijuana Use and Achievement Orientations of College Students,” Journal of Health and Social Behavior, vol. 20, pp. 194–199, 1979.
[60]. R. Blum, Students and Drugs, Jossey-Bass, San Francisco, 1969.
Erich Goode, “Drug Use and Grades in College,” Nature, vol. 234, pp. 225–227, 1971.
M. K. Gergen, et al., “Correlates of Marijuana Use Among College Students,” Journal of Applied Social Psychology, vol. 2, pp. 1–16, 1972.
G. D. Mellinger, et al., ibid.
[61]. D. Reilly, et al., “Long-Term Cannabis Use: Characteristics of Users in an Australian Rural Area,” Addiction, vol. 93, pp. 837–846, 1998.
[62]. A. J. Gruber, et al., “Very Long-Term Users of Marijuana in the United States: A Pilot Study,” Substance Use and Misuse, vol. 32, pp. 249–264, 1997.
[63]. D. F. Duncan, “Lifetime Prevalence of ‘Amotivational Syndrome’ Among Users and Non-Users of Hashish,” Psychology of Addictive Behaviors, vol. 1, pp. 114–119, 1987.
[64]. P. J. Lessin and S. A. Thomas, “Assessment of the Chronic Effects of Marihuana on Motivation and Achievement: A Preliminary Report,” in The Pharmacology of Marihuana, ed. M. C. Braude, and S. Szara, Raven Press, New York, 1976, vol. 2, pp. 681–697.
Sidney Cohen, “The 94-Day Cannabis Study,” Annals of the New York Academy of Sciences, vol. 282, pp. 211–220, 1976.
[65]. J. H. Mendelson, et al., “The Effects of Marihuana Use on Human Operant Behavior: Individual Data,” in The Pharmacology of Marihuana, ed. M. C. Braude, and S. Szara, Raven Press, New York, 1976, vol. 2, pp. 643–653; “Operant Acquisition of Marihuana in Man,” Journal of Pharmacology and Experimental Therapeutics, vol. 198, pp. 42–53, 1976.
[66]. C. G. Miles, et al., An Experimental Study of the Effects of Daily Cannabis Smoking on Behavioural Patterns, Addiction Research Foundation, Toronto, 1974.
I. Campbell, “The Amotivational Syndrome and Cannabis Use with Emphasis on the Canadian Scene,” Annals of the New York Academy of Sciences, vol. 282, pp. 33–36, 1976.
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