MORGAN, J.P. in chief 1

nil

(PROCEEDINGS RESUMED PURSUANT TO ADJOURNMENT)

JOHN PAUL MORGAN, recalled, testifies as follows:

that?

A I do.

THE COURT: There once was a manuscript right up here.

THE CLERK: Was it an exhibit, Your Honour?

THE COURT: I think so. Did it have a number?

A VOICE: I think it’s that one that right there.

All right? That’s it.

start—

very, very consistent statement and of course like many myths, it has some basis in truth. The dilemma regarding our interpretation of it is that it doesn’t seem to have any basis for toxicity. The fact that the drug persists so long in body fat is not associated with any evidence that that persistence causes harm.

Now let me try to approach it in a logical,

and I hope again, brief sequence.

Delta 9 T.H.C. is indeed highly lipid soluble,

a term used by many people not all of whom understand it. That is, most drugs that enter the brain are more lipid soluble than water soluble. Because if you put them in a beaker that’s half toluate and half water, most of it will go into the toluate, very little will go into the water when you shake it up. That’s a characteristic of basically all psychoactive drugs. It’s a characteristic of Valium, it’s a characteristic of methaqualone, it’s a characteristic of phenobarbital. Those drugs are more soluble in lipid, in non-polar solvents than in water.

more likely to enter the body’s cells, because the envelope of cells in mammals behaves as if it were a lipid envelope. So for drugs to enter the cell the drug behaves as if it’s going into solution in the outer membrane of the cell.

Okay, having said all of that, Delta 9 T.H.C.

has a half-life in human serum of five to six days. That means that once it starts its decline it takes five to six days for it to decline from one concentration to half of that concentration. If you begin measuring at one nanogram per ml. it will take five days for it to fall to a half nanogram per ml. This is important. In fact, the reason it’s most

important is that’s the reason why marihuana contributes almost all of the positives in urine testing programs in the workplace, because marihuana can be detected in the urine for up to a week or longer in a regular smoker. In fact, it can be detected for five to seven days in a one-time smoker, because the drug stays in the body fat for a lengthy period of time. It does not leave fat cells the way many other compounds do.

that one nanogram per ml. level which persists for five days there is no evidence that it’s having any effect. The analogy I like to use with my students is that we know that it takes three hundred milligrams of aspirin to relieve pain. Now if you take one milligram of aspirin, one-three hundredth, does that mean it relieves a little bit of pain or it will cause a little bit of stomach upset? Well, the answer is no. Drugs have to reach a critical concentration to bind to enough receptors to provoke an effect. And although the literature is a little unclear at what level marihuana’s effects go away, it is quite clear that below—I’ll take a conservative statement, below two nanograms per ml.—and it may be seven, it may be twenty—the drug has no effect. So, it persists in the fat for a lengthy period of time, comes out very slowly, is metabolized very slowly and appears in the urine, but it has no effect.

Now, I should be able to prove that,

that in the last twenty years many, many studies have looked to see if marihuana users have a persistent effect beyond the two to three hours that acute effects generally persist. People get high, they remain high for two to three to maybe four hours. You can detect some evidence. Either they say they feel high or you can detect some evidence in testing, that they’re—that they remain under the influence of marihuana.

studies showing that a subtle—a subtle effect was picked up eight hours or ten hours, or even in the one airplane simulator study a claim that effect persisted for twenty-four hours. Now we’ve dealt with all of those and I think the evidence is they were incorrect. For instance, the airplane simulator study, a group of papers which have been commented on in this case and others. Dr. Yesavage, Y-e-s-a-v-a-g-e, claimed that he could detect subtle effects in an airplane simulator in men twenty-four hours after they had smoked. But then a number of us criticized the study for methodology, and when he tried to repeat it the way we suggested he do it, he couldn’t find an effect. That publication achieved very little notoriety, that imposing some controls they could no longer find the twenty-four hour effect.

There’s a similar driving study by Dr. Moskowitz,

who’s referred to in previous testimony in this case, that he says he found a subtle effect for eight to ten hours. This is back in 1977, maybe 1981. No one has repeated that study.

studies are that marihuana has an effect in humans for two to four hours after smoking. The persistence of the drug in body fat, which is like the persistence of Valium and Thorazine, drugs which you can also detect for days after individuals stop using it, is not associated with effect in the sort of claim that we see here as in myth two or the myth statement two by a popular writer named Peggy Mann. "Cannabinoids accumulate in the fatty cells and the three-pound brain is one-third fat. Therefore, in the brain of the chronic pot smoker millions of axons are continually surrounded by T.H.C." Sounds pretty frightening. And then Robert Dupont, a former head of NIDA in the United States says, "Even people using marihuana only once each month are continually exposing their brains, lungs, liver and other vital tissues to the poisonous effects of T.H.C." Well—

from—

one-third by leaving out an important ingredient of the brain, the most important ingredient of the brain, which is water. The brain is probably about—brain is about sixty-five percent water, maybe a little bit more. Which is important of course, because that’s one of the reasons that water soluble chemicals don’t get into the brain very well. So the brain is only about one-third fat.

Marihuana does not preferentially go to the brain.

Take a smoked dose of marihuana and calculate how much enters the brain, it’s about one percent, maybe even a little bit less. And it doesn’t accumulate in the brain. It leaves the brain fairly quickly. It accumulates in fat cells where there are no receptors, where the drug is not changed, where it sits there for a while and then comes out at these low concentrations.

Maybe I’ve made all my points. What do you think?

It came to prominence initially in the early

1970’s and I’ll tell you how that occurred. But I’d like to start my comments here on the immune system by saying there has never been a single study of any sort in humans to show that marihuana has an anti-immune effect. There has never been a single study of any sort to show that marihuana has an anti-immune effect in humans. There are no studies, epidemiological, case survey, clinical, of any sort to show that marihuana users have an increased prevalence of infection of any kind.

alive since 1971. And in fact I see very little evidence of its final dissipation and disappearance, which should occur.

marihuana researcher named Gabriel Nauhaus talked about the anti-immune effect of—of marihuana. He’s written a couple of books in which he revealed his thinking about this and those have been very useful to us, because he thought when he studied the immune effect that he would find out that marihuana smokers had hyperactive immune systems. He knew that T.H.C. persisted in the body for a long time so he thought we would be making antigens against T.H.C. and we would be shown to be hyper-immune, and that was why he began his studies.

study he did that there appeared to be some immune suppression in marihuana users and he published that in 1971. Actually he published it four times between 1971 and 1974 and it established forevermore the idea, put it on the research agenda.

dental and medical students from Columbia College of Physicians and Surgeons in the upper west side in Manhattan and he asked them about their drug use. He divided them into marihuana users and non-marihuana users and he then took blood from them and harvested their white blood cells. Common research technique. And then you put the white blood cells in a culture medium, maintain them by giving them nutrients, and then you can study them in certain ways.

blood cells, which are part of our immune response, is to expose them to certain chemicals which are known to provoke an immune response, chemicals called mitogens. There’s a chemical derived from poke weed which works very well as a mitogen. There’s another chemical called phytohemagglutinin which always provokes white cells, human white cells to spark up. Now when I say "spark up", what do I mean? They get bigger, they take up more chemicals from the surrounding media, their appearance actually changes and they secrete immune modulators. This process is called lymphocyte transformation.

he said lymphocyte transformation in chronic marihuana smokers is impaired, their lymphocytes don’t take up as many chemicals from the surrounding medium and it is clear that in chronic marihuana smokers there is an anti-immune effect. Well, it in a certain sense was a revolutionary study because it’s changed the way everyone thinks about the drug. The only problem was that he was completely, utterly, absolutely, irrevocably incorrect. No one in five to six to seven attempts has ever been able to repeat that study. No one. Everyone has tried. I mean everyone interested in immune transformation has tried. What they—what they cannot find is that the cells of marihuana smokers are any different than the cells of non-marihuana smokers in their ability to transform. And in fact in 1979 Dr. Nauhaus published very quietly a little note that he couldn’t repeat the study, that he had tried to show it again in a group of chronic marihuana smokers whom he hospitalized and exposed to more marihuana and then did the transformation test again.

not carefully assess the tobacco use in his medical and dental students and workers. And the suppression of immune response in those marihuana smokers was almost certainly because they were—most of them were heavy tobacco smokers as well. There’s been some argument in the literature and he’s denied the contention I just made, but there’s plenty of evidence that that’s what was wrong, because—guess what? Tobacco smokers have impaired lymphocyte transformation. Always. I don’t—it’s not entirely clear what that means, but they do. Tobacco smoking impairs—tobacco smoking impairs lymphocyte transformation. Marihuana smoking does not.

Now one of the things that you can expose

them to is marihuana and tobacco smoke. And that very much impairs. In both instances the smoke will impair. Or condensates of smoke. Now if you expose normal human lymphocytes to high concentrations of T.H.C. you do see some change, some diminished transformation. And actually not always. In a couple of experiments people reported an increased transformation. But you do see with high concentrations—I’m talking about very high concentrations. I’m talking about ten to a thousand times the human psychoactive dose of T.H.C. placed in this dish, in this culture medium.

Now what you noted is what we’ve pointed out,

is that a variety of chemicals taken up by the lymphocyte will impair its transformation, including alcohol, Valium, aspirin, non-active cannabinoids such as cannabidiol or olivitol[phonetic], a

cannabinoid-like chemical that’s used to synthesize T.H.C. So a variety of chemicals dumped into this medium will interfere with this lymphocyte transformation, and it’s not clear what value the test has since so many things will interfere.

this problem, and in the 1983 Fehr and Kalant book from the W.H.O. Addiction Research Foundation text, which has been referred to here I know—

Now let me quickly switch to the fact that

finding a change in a cell dish, in a petri dish, in a culture in a laboratory has some meaning, often helps us understand the mechanisms by which drugs work. But it has almost no meaning in terms of human response to drugs. Because human response is a mixture of dose, a mixture of effect in one cell affecting another cell which affects a cascade of cells, inhibition of inhibition is stimulation in some cells but—in the intact organism. So isolated cells in a culture dish, the impact tells you almost nothing about human toxicity. Almost nothing.

there ever studies ever showing increased infections in smokers of marihuana? The answer is no. There are none. There are none.

T.H.C. there have been some reports of increased susceptibility to infection. Dr. Kabral, who works at the University of Virginia, has now published two papers, one in which he exposed rats and the other in which he exposed guinea pigs to very, very large doses of T.H.C. by injection. Not by smoking. And then he—in those animals he actually painted on herpes virus. He didn’t just expose them, he actually applied it. They were all female animals and so he applied the herpes virus to the vaginas of the female rodents and guinea pigs. And he saw a slight increased take; that is more of the guinea pigs and more of the rats exposed to T.H.C. got the herpes infection.

the human psychoactive dose. To do that in guinea pigs a little better, it only took forty times the human psychoactive dose applied many times over days.

some animal evidence of an impaired immune response. But it too is unclear what it means in terms of humans.

again, there is no evidence of any sort that marihuana causes impaired immune responses in humans.

No, I won’t close. I’ll say two minutes more.

the early demographic epidemiologic studies of men with H.I.V. positivity, those were—most of the people studied in the United States and Canada were men in the early days—it turned out that those men had an increased prevalence of drug use. They were prone to have taken inhalants, they were prone to have smoked marihuana, they were prone to have taken cocaine at a little bit higher rate than the people around them to whom they were compared. So there was some speculation, well the drugs may have contributed to their likelihood of getting AIDS.

meant was an evidence of a kind of lifestyle in which individuals had more sexual activity and therefore more—were more likely to be exposed to the virus. Since that time there have been two very important major studies to look and see if marihuana use in an AIDS population had anything to do with an increased likelihood of contracting AIDS and an increased likelihood of conversion from H.I.V. positivity to full-blown AIDS, and the answer is no. Marihuana makes no contribution to worsening of H.I.V. in AIDS patients. So that’s one of the reasons why the Food and Drug Administration in 1991 when a petition by the Unimed Corporation to add the label of H.I.V.-related wasting, the American Food and Drug Administration said yes and said not a word in the documentation about likelihood of immune dysfunction, even though the drug was to be given to people with serious immune dysfunction.

Now you mention on page 4 again the

business of the smoke, the effect of the smoke. And you state there that, "While T.H.C. has no impact on immune function, the smoke is shown to alter what’s called alveolar macrophages."

Dr. Tashkin, whom I mentioned yesterday,

and other scientists have looked at the alveolar macrophages in smokers, and there are some abnormalities of the alveolar macrophages in smokers, tobacco smokers and marihuana smokers. Now if you expose the macrophage to high concentrations of T.H.C.—there’s a series of studies done by a man named Huber—you see no impact, even at quite high doses. So that the transformation or the disruption of the alveolar macrophage, if people worry may be an

anti-immune effect, occurs with smoke. It does not occur with T.H.C. It would occur probably with any smoke, but the only things that are smoked with much regularity in this culture are tobacco and marihuana.

many—

In the early seventies some people studied

marihuana smoke and published data claiming that marihuana smoke was dirtier than tobacco smoke. Dr. Kalant was among those who said there’s more tar, there’s more particulate matter.

probably incorrect, but I believe they were. Scientists make mistakes and come up with wrong answers often. Fortunately there is a corrective, and in the last ten years there have been many, many studies, Huber among others, indicating that—I think the truth of what I said yesterday, which is that marihuana smoke and tobacco smoke are essentially identical. There may be a few more—a little bit more particulate matter in very high T.H.C. marihuana smoke, there may be more carcinogens in tobacco smoke, but basically they’re about the same, with the exception of the two active chemicals, cannabinoids in marihuana smoke, nicotine in tobacco smoke. So that over the years it has I think become quite clear, particularly through Tashkin’s studies and some others, that the issue of lung damage is a matter of dose exposure to smoke. And I’ve made the point that heavy marihuana smokers have increased respiratory symptoms, they have more cough, more phlegm, more episodes of bronchitis. But that’s only in very heavy smokers. And most importantly, they do not develop the changes in airway function which we call chronic obstructive pulmonary disease, or emphysema. Something different about the two smoking experiences, and I think it almost certainly has to do with the exposure to smoke. It’s the dose that makes the poison. The same for smoke as for individual chemicals.

some evidence of pre-cancerous change in the bronchial cells of marihuana smokers. Those data were problematic in that almost all of the smokers from whom Dr. Tenant gathered those cells were also tobacco smokers. But—but Tashkin’s work again has helped us resolve the dilemma, and I believe the following to be true. That marihuana smokers have some pre-cancerous changes in the cells of the lining of the lung, in the bronchia-alveolar washings or lavage, as it’s often stated. So that people who smoke marihuana, particularly heavily, are at a risk of developing lung cancer. At this moment there are no convincing epidemiological linked case controlled studies showing that marihuana smokers develop lung cancer. And I’m actually becoming a little bit optimistic. I’m hopeful that marihuana smokers will not develop lung cancer, because again, they don’t inhale as much smoke. You know, tomorrow I could be proved wrong, but at the moment I—I have high hopes, I’m optimistic that they don’t inhale enough smoke to get lung cancer. But they do have the changes in their cells that tobacco smokers do that presage the development of cancer.

Now what I have to talk about now are

the level of carcinogens in marihuana smoke. Dr. Kalant and the A.R.F.W.H.O. document that I’ll refer to, both refer to a seventy percent greater concentration of benzopyrene in marihuana smoke than tobacco smoke. This has become one of the world’s—one of the mythmakers’ and claims makers’ favourite quotes. Our second quote here says, "Benzopyrene, a known cancer-causing chemical, produced in the burning process is seventy percent more abundant in marihuana smoke than in tobacco smoke."

in the 1970’s by a scientist who could analyze the chemical constituents of smoke. His name was Novotne[phonetic], and he published a paper which says there’s higher levels of benzopyrene in marihuana smoke than in tobacco smoke. And that was—if I recall, that was probably thirty-six parts per billion versus twenty-nine parts per billion. I think that was his first publication.

Now some other people published similar

data, but in later years we’ve referred to at least further analyses which indicate that the benzopyrene levels in tobacco and marihuana are essentially the same, as one would expect, both combusted vegetable materials. They could be different, but they appear to be about the same.

Now this argument has taken on very big

significance because there’s recent scientific evidence that benzopyrene is very important in the production of human lung cancer in tobacco smokers. It’s complicated evidence, but it looks as if benzopyrene may cause mutational changes in lung cell d.n.a. and benzopyrene may be very important in some lung cancers. So again this has heated up the claim that benzopyrene is higher in marihuana smoke and therefore it’s more dangerous.

about the same. And I also picked up what I cited in here, a very interesting study in Japan in which Japanese police gathered a lot of pipes, a lot of marihuana pipes and scraped out the residue and could find no benzopyrene. Now I don’t know what that means, I don’t know if that means that Japanese marihuana is different than western marihuana, but the issue of how much carcinogenic material is in marihuana smoke versus tobacco smoke is an unimportant statement because of the dose. The tobacco smoker inhales multiple times more carcinogens, more tar, more chemicals, more particulate matter, more hydrocarbon than the marihuana smoker, and that’s the critical issue. It has to be the critical issue.

to these, the marihuana smoker deposits more tar per cigarette than the cannabis smoker, and that’s because of this—I’m sorry. The marihuana smoker deposits more tar and particulate matter per cigarette than the tobacco smoker. And that’s because of the traditional way that marihuana is smoked, the deep inhalation and the lengthy breath-holding. Those cause the deposition of more tar and particulate matter per cigarette.

to that. The first is it’s still forty cigarettes a day versus one, in most people. And actually less than one in most people. And you can stop doing that. It’s out quite clear that that manoeuvre, which has become traditional for reasons that no one understands, doesn’t really increase the amount of T.H.C. very much. And so in a publication I recommended to marihuana smokers that they stop doing that, as a harm-reduction manoeuvre. Smoke it like a tobacco cigarette if you’re going to smoke it. There’s no reason to hold it into your lungs and increase the deposition of material. It might be more dangerous.

high-dose marihuana smoking produces some of the same changes as tobacco, more inflammation, more irritation, more changes in the alveolar macrophages. And smoking of marihuana and tobacco together may be additive. However, marihuana smokers will not get emphysema. Tashkin’s data indicate that very strongly. Marihuana smokers will not get emphysema. And that’s critical. Marihuana smokers may get cancer. It hasn’t happened yet and I’m optimistic that it won’t.

dose-related factor? If we take these populations who are consuming large amounts of tobacco and some who are consuming large amounts of marihuana we don’t seem to have the same consequences occurring as a result of the marihuana smokers. Is that—is that what you’re saying in terms of the dose thing—

is not under oath and I’m not going to be able to cross examine him on that statement. I would request that he ask the witness a question.

It’s important to put this in perspective,

that if you look at the overall range of tobacco smokers only one to two percent of them will get lung cancer. Now that’s an enormously high percentage, but of course it’s not the majority. Now very heavy smokers with a family history may get a higher prevalence, but overall in the smoking population it’s still a relatively rare event to get cancer. No one should take my remarks as approval of cigarette smoking. However, that means that if there were a

slight increase, even looking at the lower doses of marihuana smoke, it would be hard for us to find it.

the proper scientific demurring, there is no evidence that marihuana smoking is associated with significant pulmonary disease in this culture. And one might wonder, as some people speculated in the sixties, it would be emerging now, we would see it now. And we have not. And I hope it’s because of the low dose of smoke, and I think it may well be so.

studies with aerosol nebulizers of T.H.C. looking—looked at for therapeutic things, and they showed that at least at that concentration in alcohol T.H.C. was very irritating.

government laboratories to produce a heat vaporizer which will put the T.H.C. into pure—the T.H.C. into a vapour smoke that can be inhaled, and that might be useful.

to diminish the problem of smoking. At the moment those are not currently available. In fact, there’s even a patented enema preparation under examination in the United States, for medical purposes.

bronchia-dilator. Have those now been—

Then later on, almost as an extrapolation

of that, there was a claim that marihuana had adverse sexual hormone effects in females, that is by decreasing a particular brain hormone called luteinizing hormone it would interfere with female sexual maturation in adolescents and it would interfere with pregnancy.

whether marihuana has important effects on sex hormones, sexual maturation and fertility has led to the consistent answer it does not. That doesn’t mean that people have stopped worrying and people have stopped looking and people have stopped making claims such as smoking a single a marihuana cigarette suppresses production of the female hormone essential for the implantation of a fertilized egg in the uterus. If you give large doses of T.H.C. to monkeys and rodents you do see some immediate decrease in luteinizing hormones, some decrease in prolactin. Interestingly enough if you keep on dosing them with T.H.C. the effect goes away, they become tolerant to it. And that might be one of the things going on.

that marihuana has any impact on any pituitary hormones or sex hormones from the—from the ovaries or the testes. In most studies that have been carefully done, and I particularly refer to one here by a scientist named Bloch, in a group of chronic marihuana users saw no change in hormones. And when people tried to follow up Dr. Kaladni’s claim that testosterone was decreased, almost all laboratory studies showed either there was no decrease or if there was a decrease it was very evanescent, did not go below normal levels and had no obvious functional significance.

enormous number of animal studies looking at the adminstration of T.H.C. either by smoke or by injection to rodents and to primates. There are all the speculations about changes in males and female adolescents, interfering with their sexual development, masculinizing females, feminizing males. And I guess actually I should mention that one of the reasons this area became so approached was because of some early reports, I think in the early 1970’s, describing three cases of male breast enlargement in marihuana users. And this is commonly stated, smoking marihuana will cause males to develop breasts and will feminize them. It’s not true. In fact, the military, the United States military did a large study and looked at individuals who developed gynechromastia, something that occurs in males usually for unknown reasons, they develop some breast tissue, and there was no evidence of marihuana making any contribution to gynechromastia in young men. But that’s led us into this long, long dance about marihuana’s impact on sex hormones. And the bottom line is there appears most likely to be no effect. If there is an effect it’s evanescent, minor and of unknown functional significance. In fact, I recently told my students that I think the T.H.C. receptor in brain cells may down-modulate the secretion of some hormones very briefly. That may be one of its effects. So if we looked at cells in the pituitary and hypothalamus, the cannabinalant receptor in an endomyte may be one of the ways that that system is regulated. So it is possible that given large doses of T.H.C. one might see some slight changes in sex hormone secretion, although it’s been very difficult to do that. It could be true. However, there is no evidence that it has any functional significance in sexual maturation, sexual behaviour, fertility in human users of marihuana.

cultures where marihuana is used very, very extensively particularly by lower class, uneducated, illiterate people such as in India, such as in Egypt, to some degree in Jamaica—I want to be very careful because there are middle class users of marihuana in Jamaica, not so much in India and Egypt—there has been no evidence of diminished fertility. If anything, as you know, we are concerned about the high fertility among poor people in India and Egypt and the rest of the world, particularly in those cultures where cannabis is commonly used. There—there is no indirect evidence that marihuana interferes with fertility. Although again, the Partnership for a Drug-Free America ran a lot of ads in the United States showing a young couple sitting in their physician’s office and he’s saying, "I’m sorry, you’ll not be able to have a baby," and then the text goes rolling under that it was their marihuana use when they were young people. This is a means of frightening people in trying to promote a war on marihuana. But not a shred of evidence. Not a shred.

He just had a group of marihuana smokers

and he compared their testosterone levels to

non-marihuana smokers and said it was lower. Then he put people in a laboratory and had them smoke lots of marihuana and although they at the end of the laboratory time had the same testosterone levels, he said there was a slight decline and then it came back to normal. So he’s the genesis and put testosterone and other hormone measures on the research agenda by his publications in 1971 and ‘72, and they attracted enormous attention. Just they appear not to have been correct.

exposing the fetus to marihuana smoke, particularly if the pregnant—if the woman carrying the fetus is a marihuana smoker, that somehow that exposure to the marihuana smoke or T.H.C. is causing fetal harm. This is a very complicated issue because there are at least three kinds of—three or four kinds of fetal harm that have been proposed.

early studies—and again, Dr. Kalant in the 1983 document referred to the fact that there were some early studies indicating that children born to women who smoked marihuana had low birth weight, low head circumference, low gestational age, meant that they were small for the number of weeks they’d been in the uterus, and other minor abnormalities that might be attributable to marihuana. Well, after many, many years of study and after attempts to look at these issues very carefully it is our belief and we do cite one paper by Linn who studied twelve thousand newborns regarding their marihuana exposure, that there is no impact of marihuana use on the obvious physical integrity of the newborn or the fetus.

Nancy Day, who publishes many papers out of Pittsburgh, recently published a study in which she looked very carefully at marihuana use during the three trimesters in a large group of—of poor urban women. And she looked at all the things that are supposed to have been affected by marihuana and she found no impact on head circumference, no impact on birth weight, no impact on age of gestation, no impact on usual abnormalities and the Apgar score, the score of infant robustness when it’s born, how well does it cry, how well does it move. However, she published that depending upon exposure in I believe the second trimester, that the marihuana exposed infants were shorter than the non-marihuana exposed infants. Shorter. I don’t know what that means. It also turned out it was two-tenths of an inch shorter. Other people have not found that. However, it was published with great fanfare. It was not published with quite so much fanfare that women who use marihuana in the third trimester had heavier infants, which is generally thought to be a good thing.

surveys of children born to marihuana users. If you’re not careful with your controls you can claim that there’s low birth weight. But it turns out if you control for nutrition, the birth of that woman’s—the weight of that woman’s previous pregnancy, etcetera, etcetera, that there is no evidence of an impact on birth weight, head circumference, birth length, etcetera. In fact, there are a few studies in Jamaica which show improved statistics in marihuana smokers. The marihuana-smoking women seemed to be a little healthier and their children seemed to be a little healthier in terms of size, etcetera.

as Nancy Day’s finding of two-tenths of an inch shorter in the infants, and then that will be published as evidence of marihuana harm. Well, those—those findings are inconsistent, they’re not repeated from study to study, they do not seem to correlate with the amount of marihuana used so it’s unclear how they can be a pharmacological or toxicological effect of marihuana. And they tend to be quite minor and of no functional significance. So that’s why we’ve arrived at our conclusion that there is no evidence of physical harm to the developing infant, to the developing fetus because of mother’s exposure to marihuana.

important to say, pregnant women should not smoke marihuana. Of course they should not smoke marihuana. Just as they should not do many things. On the other hand, we don’t live with them and control what they do. And in fact, even imposing laws on them does not control what they do. The prevalence of marihuana exposure during pregnancy in surveys in the United States is probably up to thirty percent, which becomes important in another discussion we’re going to have.

marihuana. I don’t think they should live with people who blow marihuana smoke into their faces. On the other hand, there is no evidence that marihuana harms the developing fetus in terms of birth weight, head circumference, etcetera, etcetera, etcetera. Okay?

But I don’t believe there is any impact

of marihuana, even at fairly high doses of use, on the developing fetus. But I don’t believe that women should smoke marihuana while they’re pregnant and I counsel all who ask me, not to do so.

non-lymphoblastic lymphoma or non-lymphoblastic leukemia—hold on a second—non-lymphoblastic leukemia occurs at a higher rate in marihuana smokers. This—it’s astonishing how much publicity this report gave—how much publicity this report provoked. Hundreds of newspapers in the United States as well as government spokesmen and anti-marihuana spokesmen and supporters of prohibition said, "Look, here is this unusual, rare cancer that occurs at a higher rate in marihuana-smoking women. This is of obvious critical importance. It may indicate the impact of marihuana smoking and/or T.H.C. on the developing infant’s cells. It’s obviously of critical importance." I actually have a publication about to appear in a journal called the Forensic Drug Abuse Advisor, in which I analyze the study, the Robison study which claimed to show the increased prevalence of acute non-lymphoblastic leukemia.

case control method that I described before in which you look at the illness, in this case the acute

non-lymphoblastic leukemia, a rare tumour in children, an important tumour although interestingly enough they’re most often cured of nowadays. So you look at those children and then you look back into the mother’s history and see what she was exposed to. Was her—was she a worker in a factory where there were chemicals? Did she use marihuana or cocaine? What was her nutrition like? Did she live in a particular place? All the things, all the demographic and dietary and health things that might have had an impact. And then you take a group of women who again, as I said before, resemble the pregnant woman—and they were pregnant women. They were women who gave birth at about the same time. They resembled the—the experimental women, the women with—whose babies had leukemia in every way except they did not have leukemia. So then you add up, you know, were they too big? Were they too small? Were they all black? Were they all from a small indigenous people sect? Did they all smoke marihuana? Etcetera, etcetera. So you add those up and look for differences.

that there was a difference in the prevalence of marihuana use. That is, he published a paper which said the risk of marihuana exposure was tenfold in women who had infants who developed acute

non-lymphoblastic leukemia. Tenfold. And what that means is that the prevalence of marihuana use in the mothers of leukemic children was five percent. The prevalence of marihuana use in the mothers who did not have children with leukemia was one-half of five percent, .5 percent.

THE COURT: All right.

A Okay? Did I have that right?

Now I bet everybody here knows where I’m

going. How did we find out the prevalence of marihuana use in those women? We called on the telephone and asked them. We called on the telephone and asked them.

leukemia had been affiliated with this hospital program. They then received a phone call and said, "We’d like to interview you about a variety of things during your pregnancy," and included in that list of questions would be, "Did you ever use illegal drugs during pregnancy, such as marihuana or cocaine?" Five percent of those women told what was almost certainly the truth, that they had used marihuana. Now those women of course had been actively involved in the care of their children. They, despite the guilt that might come down on them, would tell the truth to some degree, about their drug use. So we got a five percent prevalence. Five of them said, "Yes, I used marihuana."

Now we called a control group by telephone,

women we didn’t know, women who’d never been to the hospital, said, "We’re going to ask you some questions about your recent pregnancy. Did you use marihuana?" One out of two hundred women said yes. So immediately the question is raised, was this incorrect reporting.

Now, the next question, as a student of

pharmacology, is what is the prevalence of marihuana use during pregnancy? It’s fifteen to thirty percent in most surveys in the United States. So both groups of women under-reported because of the embarrassment of telling somebody over the telephone, "I smoked marihuana and maybe harmed my child." But the mothers whose children were leukemic were much more honest than the women contacted randomly by phone. The study is useless. That’s my most charitable comment. It is useless. It has been harmful because of all the publicity it’s generated.

me, so let me take a moment—if you look at the bottom of 10-5 you’ll see what we think Dr. Freed’s published by reading his papers. He found that age one—incidentally, at birth there was—he maybe had one test that said that the marihuana exposed children were different than non-marihuana exposed children, but it was inconsequential. He’s not said very much about that. But then at age one he found that marihuana exposed infants scored higher on one set of cognitive tests, that is the marihuana exposed kids were smarter. But at age three the children of moderate marihuana users again had higher scores on a test of psychomotor ability. So in Dr. Freed’s first two findings, at age one and at age three, marihuana exposed children were not harmed but actually seemed to be a little bit better, a little bit healthier.

were very heavy marihuana smokers, nineteen joints a week during pregnancy, scored lower on one sub-scale of one cognitive test. Imagine that, you know, you have a cognitive test that can be given to a four-year old. It may have—and I’m not a child psychologist, but it may have twenty scales. In fact some I.Q. tests have twenty-five, thirty scales. So they found one abnormal scale, one abnormal sub-scale score in the marihuana exposed infants. And by and large such a finding—you know, one out of twenty-five tests is abnormal on the basis of chance alone. Actually one out of twenty if you use a .05 level of significance. So you find one test out of twenty-five, it’s generally dismissable.

apparently of marihuana use on these children. But at age five and six this difference was no longer present. He said maybe it’s because they went to school and the effect went away. Maybe so.

Then measures of attentional behaviour added

at age six years old and a lower score on one

computer-based test of vigilance among the children of heavy marihuana users. Then eleven new psychological and cognitive tests given to six to nine year olds revealed no statistically significant difference between the children of marihuana users and non-users. So we’re now to these group of children who are approximately nine years old, we’ve had these occasionally abnormal tests as they’ve developed, but now at age nine we find absolutely nothing.

were asked about behaviour. And the mothers of the marihuana using kids said that their children were a little bit more often behavioural problems than the non-marihuana exposed children, but once—there were a number of compounding variables having to do with educational levels of the mother and family income, etcetera, etcetera, this difference in behaviour disappeared.

a hundred million dollars of American taxpayers’ money following these children—and I’m envious because he got all that money to do research, quite envious—and basically though what he’s given us, up to age nine was no real difference in these children due to marihuana exposure.

recent paper. "Instruments that provide a general description of cognitive abilities may not be capable of identifying nuances in neuro-behaviour that may discriminate between the marihuana exposed and

non-marihuana exposed children. Tests that examine specific characteristics that may underlie cognitive performance may be more appropriate and more successful."

give me more money because I have some other tests that I’m going to conduct."

I’m not—I’m being a little flippant here,

and I hope you’ll forgive me if it’s too much so. But I’m not being insulting to Dr. Freed. This is what researchers do. "I’ve got some new ideas, I’ve got some new tests, maybe I can try those."

tests. If five years after you started the testing you come up with a new test and a new index and a new batch of post-designed studies, there are some research psychologists who will say, "No, no, no, you can’t do that. You can’t change the playing field five years after you started examining the children, particularly if you haven’t found anything heretofore, because then it looks to us like maybe you’re trying to find a way to find something." That’s what he did. He’s now generated something called executive function. Now this is a new series of tests—it’s been proposed by other psychologists that it’s a way to look at development in children, helping them—helping you see their development of flexibility, their ability to assess input that’s going on, their ability to make decisions. I’m being vague about this because I—I don’t understand it in any more than a vague way. But it’s a test of executive function.

1995 at a Washington conference with his funders, Dr. Freed stood up and said, "I think there’s a possibility that tests of executive function may identify differences in the marihuana exposed children." Although he’s down now to fewer than thirty marihuana exposed children because they’ve dropped out, mothers have moved away, he can’t follow them so regularly. But I knew what was about to happen, that sure enough he’s found some differences in tests of executive function. And this has now been jumped on by American media saying marihuana damages the cognitive ability of the fetus twelve years later.

This is very interesting because of course

drug exposure, if it has an impact, seems to have an impact early. And with passage of time drug-caused impact disappeared. I learned that from Peter Freed who has shown quite clearly that the adverse tobacco effects, which are pretty high, at least easily measurable, have dissipated over the years. But however, we now have a new test out, executive function in marihuana exposed infants, which supposedly shows some harm.

I think he has manipulated the research process to such a degree that I find him untrustworthy now. I’ve not said that about anybody else we’ve talked about, I don’t think, in terms of the production of studies regarding marihuana effect. I don’t think Dr. Freed is to be trusted any longer. Excuse me, the fact that he’s a Canadian had nothing to do with my comments.

(WITNESS ASIDE)

JOHN PAUL MORGAN, recalled, testifies as follows:

Dr. Bloom published a paper regarding

pulmonary symptoms and pulmonary function in a group of people around Tuscon, Arizona who were surveyed as part of a measure of pulmonary health and the impact of smoking. And Bloom had a question on his survey about non-tobacco cigarettes. Now I’m in agreement with Bloom that those cigarettes were almost certainly marihuana cigarettes, and there was some argument about why he chose to ask the question "non-tobacco cigarettes". That’s not important. In fact, in my chapter I refer to a paper by Sherrill et al—that’s my reference number eleven—and that’s Sherrill, Bloom and other authors. So there are two publications then of this survey of pulmonary health of volunteers around Tuscon, Arizona. And basically what the Department of Medicine and Pulmonary Function did was to interview large numbers of people at intervals over time and to ask them about questions and to measure pulmonary function. Now Sherrill—then the two papers, one by Bloom and one by Sherrill, they said that the non-tobacco cigarette smokers had some evidence, at least on one test, of airway malfunction of the sort that I’ve said did not occur in any of Tashkin’s prospective patients.

showing that the smoking of non-tobacco cigarettes, almost certainly marihuana cigarettes, does cause some pulmonary damage. Now we have discussed the paper briefly, not solely to dismiss it but to point out that there is a very, very small number of non-tobacco cigarette smokers. It is unclear from Sherrill’s publication how much tobacco they smoked.

is that the diminished pulmonary function in one test of four given was abnormal only in people with a history of non-tobacco cigarette smoking and not current non-tobacco cigarette smokers. So it’s a little unclear how an abnormality of pulmonary function could occur more in past marihuana smokers rather than in current marihuana smokers.

finding not reliable, and Dr. Tashkin agrees with us. Recently had a long discussion with him about the Bloom and Sherrill papers.

I did want to mention it because it was referred

to by Dr. Kalant in that testimony you provided me.

Now—so Campbell having been set aside and

dismissed by most people—although it’s occasionally discussed—comes Dr. Heath. Now Dr. Heath had reviewed the literature showing by and large one could not find changes in the electroencephalogram of marihuana smokers, either acutely or chronically. The electroencephalogram is the technique in which electrodes are applied to the scalp and these monitor brain electrical activity and produce a wave form printout. Most people are familiar with the electroencephalogram. And a number of people had looked at the electroencephalogram, the surface electroencephalogram in marihuana smokers both acutely and chronic users, and could find no changes at all.

Now Dr. Heath conducted a study in which

he first in a single human patient—and I’ll not comment very much about that individual—but then in a group of monkeys he planted deep electrodes, deep in the brain and exposed those animals to—these were mostly Rhesus monkeys. And he exposed them to marihuana smoke and he said he saw important changes in some important areas of the brain where marihuana might work. It showed changes in the septal area, the area which is the division of the brain from right and left. And then in a particular area of the cortex called the hypocampus[phonetic]. The hypocampus is frequently referred to in fact because of Heath’s work. So Heath’s first publication was, "Yes, I can see brainwave abnormalities." And then Heath, before he had any data, said, "I think with repeated exposure these brainwave abnormalities will become permanent." He said that before he had any data to support it. But then he published some data saying that in the early exposure these changes in the brainwaves, which had reverted to normal an hour after exposure, persisted even during times the animals were no longer being exposed to T.H.C. or marihuana smoke.

second or two. That it’s impossible to make a monkey smoke cigarettes. Monkeys will not smoke cigarettes. They will not smoke tobacco. They’ll not smoke T.H.C. They actually will inject tobacco intravenously if you—I’m sorry, nicotine, if you provide them with a pack and an apparatus in which they can get a reward by pushing a lever. They’ll do that for nicotine, but they won’t do it for T.H.C.

have to engage in some difficult, problematic techniques. And what Dr. Heath did was to actually blow the smoke through a tube which was inserted down into the—into the monkey’s airway. Well, he admitted he had a lot of trouble doing that. Monkeys didn’t like it very much, fought against the tube. It was unclear how much smoke they got, how much smoke they managed to get rid of. So his dosage levels were never very, very well understood. But still, along with the animals given T.H.C. intravenously he said the animals exposed to smoke one, had these abnormal brainwave forms which persisted. And then, although he ended up with very few monkeys, he sacrificed those monkeys, he killed the monkeys and looked at their brain tissue. He actually ended up with only one or two monkeys who had been chronically exposed to marihuana smoke. But he published in the early 1970’s the claim that exposure to marihuana smoke produced irreversible brain damage in this particular area of the cortex, the hypocampus, in Rhesus monkeys. And this claim persisted for twenty years. And every time you turned around someone was saying, "Well yes, but marihuana kills brain cells, at least in monkeys."

Heath study had many, many problems. It’s unclear how much smoke they got in. The monkeys fought against the smoke. It’s unclear how much oxygen deprivation they had because of the administration of large amounts of smoke through a catheter. But the studies were talked about over and over again as evidence of brain damage.

National Centre for Toxicological Studies at Jefferson City, Arkansas. It’s a large federally funded unit which looks at toxicity, which looks at harm in humans, animals and other preparations by exposure to chemicals. The researchers at the National Centre for Toxicology conducted in the early 1990’s a series of studies which showed that Dr. Heath was completely wrong. They repudiated everything that Dr. Heath and others had been saying for twenty years. What they did was to take a group—four groups of monkeys, sixteen each, and the monkeys this time were exposed by face mask. That is, a face mask was placed on them and the marihuana smoke was delivered to the face mask and they had to breathe it in but it wasn’t being injected down to their throat. So it’s a little closer to the smoking experience. And the amount of oxygen they were given was controlled. They were given adequate oxygen, just that marihuana smoke was puffed in. So you had one group of monkeys who were exposed to the human equivalent of five joints a day and exposed—they exposed them for a year to five joints per day. You had a second group of monkeys who were weekend smokers, they were exposed to the smoke of four to five joints a day only on Saturdays and Sundays and then the rest of the week they—they didn’t get smoke. Then he had a group of animals who were exposed to smoke without T.H.C. in it. And then they had a group of monkeys on whom the masks were placed but no smoke was blown in whatsoever. So these animals were followed for this year period of time in which they were delivered either large doses of marihuana or small doses of marihuana or smoke or nothing.

And a large number of studies were done,

neuroendocrine studies, hormone level studies, adaptational studies, learning studies, etcetera, etcetera. Then the smoke experiment was stopped and the monkeys for seven months were allowed to go about monkey life. And their behaviour was measured during those seven months off the drug. And then all of the animals were killed and their brains were examined.

papers Drs. Slicker and Paul and Ali and Scallett, all from Arkansas, published the fact that there was no cellular changes in the marihuana smoking monkeys. None. No changes in the cellular architecture in the hypocampus, no changes in the neurotransmitter concentration, no changes in the synaptic space. No changes whatsoever after a year of smoking.

take a quote from the Arkansas people, although we have in the past which basically says year-long exposure to marihuana smoke produced some acute changes, we found some increased levels in blood cortisone, they found some changes in pulmonary macrophages, they found that during the height of marihuana exposure the monkeys wouldn’t work as hard for food as they had before. You know, when they were stoned they wouldn’t work so hard for food as they had before. But then at the end of a seven-month non-exposure time there were no abnormalities at all. These were adolescent monkeys, interestingly enough. That was done on purpose because of the fears that adolescent exposure in humans is—is the issue we’re most concerned about.

for a year in a Rhesus monkey produces no permanent effects of any measurable sort.

some attention, although not as much attention as you would like. It’s—it’s among the category of studies funded by the federal government in which the federal government doesn’t talk about the study very much in the United States.

anti-drug statement and we’ll place it for you." So the largest advertising agencies in New York and elsewhere have made anti-drug ads for the Partnership and then the Partnership places it in the New York Times or the Wall Street Journal or N.B.C. local and national affiliates. Partnership is—well, the Partnership places a million dollars of ad space per day in the United States.

to the concept of a drug, any drug killing brain cells or altering brain cell structures or functions permanently.

in relation to alcohol consumption and the effect on brain cells?

in human marihuana smokers to indicate brain damage of any sort. Doesn’t mean of course it’s absolutely impossible that it occurs, but there have been many studies in alcohol consumption indicating that brain damage actually occurs.

studies of course, showing tobacco damage to pulmonary and other tissues. There have—I mentioned to you before that Dr. Freed’s study shows development problems in tobacco-exposed infants but I’m not aware of any studies showing that tobacco smoke harms brain cells. I don’t know of any.

Now I think it’s very important to note

that two drinks of alcohol a day in humans is associated with positive health outcomes. Although there is some argument about that, by and large it appears to be true.

Q This is the wine and the beer—

preferred consciousness-alteration agent is weak and requires large doses and is therefore particularly dangerous.

is a particularly interesting one because of course no one doubts that marihuana, like all psychoactive agents, produces acute changes, immediate changes on intellectual function. At high enough doses marihuana stops almost all intellectual function because it puts you to sleep, just the same as high enough doses of alcohol and phenobarbital would. You can’t measure much intellectual function when people are asleep.

seventies and actually the first important studies in the late 1960’s, people have given marihuana acutely, that is immediately to individuals and then assessed their intellectual function in a number of spheres, sometimes their psychomotor function, their ability to perform tasks. But the biggest set of studies were those that looked at acute dosage producing acute alteration in thoughts, ideas and perceptions. Now we can’t really measure thoughts, ideas and perceptions but we can give tests to see what marihuana or other drugs does acutely.

me to the fact that the test which is almost always found abnormal is a test of acute recall. So marihuana, in the language that everyone knows, has an important impact on short-term memory.

memory, causes a high, causes the heart to beat fast, causes the eyes to get red, it doesn’t do much else. I think that’s important. At fifty to a hundred micrograms per kilogram, the low dose of marihuana that’s effective, you see red eyes, fast heart rate, "I’m high", people tell you, "I’m high," and you see this change, quite predictable change in memory.

for you because it’s important. Under the influence of marihuana individuals can recall what they’ve learned before. You know, if an hour before you got them high you asked them to learn a series of words or you asked them to learn a series of concepts or you said, "I want you to tell me an hour from now when you’re high the story of Uncle Remus or something that Stephen Leacock has written," they can do it quite well. However, if they’re high and you give them something to learn they have a fairly specific defect. And again I’ll tell you what it is, I’ll tell you what it is.

high, let’s say you give them paired list of words, you give them words that are related, black-white,

coat-sweater, hair-beard, give that to them while they’re high and then give them the cues later on, they do quite well. You say "beard", they’ll say "hair". "Coat", "sweater". They’ll do that. However, if you show them a list of words and then take the list away and later ask them to recall those words, a process that the psychologists call free recall, people can’t do it when they’re high on marihuana. Their free recall is impaired.

is not impaired only because they can’t remember exactly the list of words, but they keep remembering things that they weren’t taught. The marihuana high, as everyone who’s been high a few times knows, is associated with the intrusion of memories from someplace else. The intrusion of words that were not part of what I’m supposed to recall at this moment, the intrusion of ideas that are not what I’m discussing with my friend at this moment. That’s what marihuana does. It loosens associations, it promotes what people, if they’re not being critical, refer to as lateral thinking. It causes intrusions of things which the—which the user then thinks, "Well, that’s on the list I’m supposed to recall. You gave me a list—" You actually gave him a list that said "beard" and then he recalls Morgan the pirate. You can actually find those keys, those things that have provoked a memory that intrudes on him.

impaired recall of a variety of things, words, concepts, pictures, sounds. They’re all affected.

Now most of the other things we’ve looked at,

such as simple reflex time, questions of calculation, questions of perception in which he doesn’t have to recall things, he’ll do pretty well. In fact, there’s no regular defect that you can identify consistently much beyond the memory recall. There are some other things, some changes in perception, some changes in ability to calculate, but particularly those tend to be related to memory, the ability to recall. So by and large that’s the most important impact on marihuana.

Now what individuals note, of course, is

that they’ll be having a conversation under marihuana and then they’ll—suddenly the conversation will cease because nobody can remember what exactly was being talked about. And everybody who’s had a marihuana experience has had that experience.

short-lived effect. It occurs two to three hours of smoking, occurs during the high, which is almost always over by four hours. And I’ve actually seen a number of studies that show that it’s pretty well over by two hours. So marihuana has an impact of distractibility. People are turned away from what they’re supposed to recall and intrusions occur.

chronic effect. Does it persist when individuals don’t use marihuana? And we spent twenty-five years trying to find out if there is a problem of memory in

long-term users. And that’s a long story. Shall I begin it?

Should we break now and then carry on—

THE COURT: We may as well break now before we—

MR. CONROY: All right.

THE COURT: -- commence this story. For lunch, back

at one thirty.

THE WITNESS: Thank you.

MR. CONROY: Thank you.

(WITNESS ASIDE)

JOHN PAUL MORGAN, recalled, testifies as follows:

you—

Now in addition to that—and she has—she

has I think a big impact on the chapters on cognitive influences of marihuana. Dr. Solowij has done two or three studies now in which she believes that she’s identified a brain abnormality in chronic users of marihuana. I’ll introduce it by saying that her study is done the way most of the studies in the latter days have been done, in which one identifies usually by advertisement a group of individuals who admit to being chronic, heavy marihuana users. And you recruit them and ask them if they will take part in your studies. And then of course you have to construct a control group. You have to identify a group of people whom you will subject to the same kind of testing. And these are people who are matched again as best one can to the chronic use group in every way except they’re not chronic users of marihuana.

probably hundreds of them done in the last decade, are beset with the difficulty is that it’s unclear what should be a control group for chronic marihuana users. That is, chronic marihuana users are—first of all, they make up a very small proportion of marihuana users, since most marihuana users are not chronic, heavy users, very small percentage. So then you try to match people for intelligence and education and other drug use, which is often a very big problem because chronic marihuana users, high dose marihuana users are often users of other psychoactive drugs.

Dr. Solowij has published. And I suspect that it will come up again. We’ve talked already about the electroencephalogram in which you attach electrodes to the scalp and measure electrical brain activity. And this is a technique that’s been utilized a long time and people look for diseases of the brain using electroencephalogram, look for epilepsy, look for evidence of brain tumour, look for evidence of vascular disease. But there is a very specialized electroencephalographic technique that I must explain to you. I think we can do it quickly.

electroencephalogram and then you give him a stimulus, a tone, have him open his eyes, have him even think of a particular thing—although it’s most often done with a tone—you will get a response which has for years been called an evoked potential. In recent literature and in Dr. Solowij’s papers it is always called an event-related potential. So that this is not just a routine electroencephalogram, although the individual has all the routine electrodes attached. But you give a particular stimulus and you tell him to pay attention to that stimulus. You often give him directions to anticipate the stimulus. So then the event-related potential not only measures something about the brain’s intactness, but it also tells you something about the individual’s ability to pay attention.

following way. People sit in a room with headphones on. They are told that there’s going to be a series of tones that come through the headphones. And then they’re told to look for, to anticipate a particular tone. The tone is described to the individual before it occurs. "It will be high-pitched, it will be louder than the other tones and it will occur only in the left ear." So the individual’s listening to this random set of tones and then the tone comes and he’s to push a button. I hope all—I’ll hope that’s clear.

potential is a particular curve, particular wave form. And the most important one, although there is more than one, is called a P-300. If you look through the brain literature you’ll see many references to the P-300. And that means that it occurs three hundred milliseconds, .3 seconds after the event. So electroencephalographers have in recent years spent enormous amounts of time looking at the P-300 wave. Measures brain intactness, it measures brain pathways, but it also measures the ability of your subject to pay attention to his directions and to focus his attention. Because actually if he’s not focused you’ll see a blip but it won’t be the normal P-300 blip.

in individuals under the influence of drugs, said to be abnormal in patients with schizophrenia, said to be abnormal in a group of people. So Dr. Solowij has now published two papers in which she says, with all this introduction, that the P-300 wave is abnormal in chronic marihuana users. It’s abnormal. It has less amplitude, it has a slightly unusual wave form, and so she’s now published this as evidence—although she has only a few subjects—that there is a chronic brain damage in marihuana users.

are often people who have used for more than fifteen years and often at you know, more than one—one—once a day, for fifteen hundred years—sorry, for fifteen years, more than once a day, hundreds of ingestions of marihuana. There’s a small percentage of marihuana users who are chronic heavy users.

everybody does and as she does, about the adequacy of the control group. I mean, are these people really the same as the chronic marihuana users? And they have these different tone responses and therefore is there something that was different about them even before, or different about the marihuana users before they became chronic users, etcetera, etcetera.

way I have not treated her with disrespect as a scientist, but I pointed out that there is a similar study by an electrophysiologist named Gloria Patrick who works at Tulane University in Louisiana. Gloria Patrick has now published two studies, the first one in which she agreed with Solowij and said chronic marihuana users have abnormal P-300 e.r.p.’s,

event-related potentials.

she controlled for age and she made sure that her chronic marihuana users were psychiatrically and medically normal. She excluded from the group anybody who had a psychiatric diagnosis, anybody who had any kind of medical disease. And having done that, she published a paper in a very important journal called Life Sciences, in which she said there is no difference between chronic marihuana users who are medically and psychiatrically normal and age-matched to a control group in terms of the P-300 e.r.p.

So I believe at this moment, although Dr.

Solowij’s publications have gotten lots of attention and identification of a brain abnormality in chronic marihuana users, I believe that her work has been called into question, quite seriously into question. And again, I believe that that little bit of evidence of chronic brain damage in marihuana users recently raised by Solowij and discussed widely in the Hall book which I know has been part of the Court’s consideration, that she’s wrong. I believe she’s wrong.

Event-Related Potentials are Not Altered in Medically and Psychiatrically Normal Chronic Marihuana Users" was published in 1995.

article by Nadia Solowij which I didn’t refer to here although I refer to it elsewhere in the document.

important comment/observation, which I think everyone here knows, that when only one investigator has made a finding it really has to be confirmed by other investigators. If it’s in the hands of one scientist or one group of scientists, although it’s evidence, it’s not acceptable evidence to the scientific community as a reflection of truth at a certain level. So the first group of people to try to confirm

Solowij’s findings have said, "No, we can’t find it." And no one else has confirmed it yet. So it hangs in abeyance. Okay?

placed on the research agenda—no, let me not do that yet. Let me say again as I said about Solowij, that studies of cognitive function rely upon this case control phenomenon that I’ve described to you before. I described it to you with the study of the mothers and the babies with leukemia. I’ve described it to you with Dr. Solowij’s work. Which means that the way studies are done in this area is to take a group of people who are chronic marihuana users—they say, "I’m a chronic marihuana user." In some cultures, saying you’re a chronic marihuana user brings about trouble, in others it doesn’t. But, "I am a chronic marihuana user. Yes, I volunteer to be in your studies."

control group. And I realize I’ve done this about ten times now, hold my hands up: the experimental group, the control group. And we assume they are alike in every way except their chronic marihuana use. And that’s a big problem. It’s unclear if such control groups are alike. There always is a problem in constructing the control group.

are in Egypt and in India where there is a large group of chronic marihuana users largely confined to the lower classes in terms of educational status,

socio-economic status, education and literacy. That’s not what happened in the western world but that’s what happened in Egypt, where a psychologist named Sawif published a large number of studies in which he said marihuana users have chronic brain deficits, they have intellectual impairment, they have lower i.q.’s, they have many, many things wrong with them.

in prison. Most of them were there because of cannabis-related offences and he constructed a cannabis-using group and compared them to a control group and said they have cognitive abnormalities, memory abnormalities, calculating abnormalities; they are significantly harmed by their marihuana use. Published these papers in the late sixties and early seventies. Almost every commentator in the western world said these studies are seriously flawed. I can easily express to you why. That the marihuana cohort were less educated, more—more often illiterate, more often rural, and there was very reason to believe they might have scored low on tests whether they’d used cannabis or not.

commonly still cited, have not been acceptable by western psychologists. But again, Sawif accomplished the function of putting the psychological damage, the brain damage issue on the map and on the research agenda.

There actually were a number of studies in India which are the same sort, that they were done in a cohort of lower class, uneducated, economically depressed individuals. And it’s unclear if those findings, which are not so consistent as Sawif’s, relate to marihuana or relate to something else.

people in the western world decided we had to find out about the likely intellectual and other harms of chronic marihuana use. The United States government funded three important studies, commonly referred to as field studies. They are studies which all in general looked at a cohort of heavy users of marihuana and tried to construct a control group to see what the differences of heavy use were. The three sites of study were Jamaica, Costa Rica and in Greece.

scientists who were not part of the initial group also went to Costa Rica—I think Costa—I’m sorry, no, they went to Jamaica. So there’s a separate report by some Canadian scientists very much the same as the studies done by the Americans, it just happens they were not funded by the American research apparatus.

studies resulted in no findings. There was no evidence of cognitive harm, brain dysfunction, memory loss in any of the three field studies in the 1970’s. Although again, small groups of people, the difficulty of constructing a control group, but using standard tests of psychological function, memory, intellect, none of these field sites identified cognitive harms related to marihuana use.

stopped there. But we didn’t, of course. Everybody always wants to do more research.

even though they didn’t have history of chronic use, they only had a few years’ use. And in the paper—I’ll come back to the follow-up of the Costa Rican users—on page 12-5 in the middle paragraph I’ve gone through quickly a large group of studies mostly focused on memory, to see if chronic marihuana users had altered memory functions. And these were done by recruiting young people, most of them college age or thereafter who had already developed heavy marihuana use habits in the late sixties and early seventies. Almost all of these studies gave a negative result. There were a couple that showed some evidence of impaired memory and I’ve mentioned that. "Two studies in the 1970’s found memory deficits related to chronic high dose marihuana use, but three others found no related marihuana differences. On a variety of other tests no differences." And then I cited the fairly well known study of American Rastafarians who are very, very heavy users of cannabis and who had no obvious abnormality on any psychological test and compared to standard scores. They had normal i.q.’s. They had been smoking enormous amounts of marihuana daily for years. Okay.

of the 1980’s I think western scientists had lost some of their zeal for studying the possibility of chronic brain damage or brain damage in chronic marihuana users. There were very few studies conducted in the 1980’s, very few.

important studies which have gotten lots of attention. The one by Harrison Pope I’ll discuss first because it was done in college students in the Boston area. They were heavy users but actually only of about three years’ duration. And most people would not have figured this kind of use, even heavy use to have caused cognitive impairment. Pope brought them into the laboratory, had them do a number of studies, and found some abnormalities compared to a control group.

difficulty constructing a control group because his controls had less use of other psychoactive drugs, they had lower S.A.T. scores—I’m sorry, they had higher S.A.T. scores than the control—than the marihuana use group. They also had slightly higher i.q.’s. So there’s a reason that they might do a little bit better on tests. But he tried to adjust for all of this, pointing out that it’s hard to control a control group.

of the American Medical Association showing some abnormalities of a few tests, particularly something called the Wisconsin Card-Sorting Task, which is designed to measure mental flexibility. Basically people are just given a deck of cards and told to sort them. Jacks here, clubs there, rules change sometimes but—in fact I’m not even sure if they’re always standard cards of jacks, kings and queens. But they’re card-sorting and you look and you—you—we measure how—how many cards you can sort and how many abnormalities. And his chronic marihuana users were able to do less card sorting. For example, in the first but not the second trial of the card-sorting task heavy marihuana users sorted fewer items correctly, 51.3 compared to 53.3 for light users.

group were not people who abstained completely, but who were in a light use group. That raised some questions, but he was able to justify what he did.

given five chances to recall words from a list of twenty words. At the test completion the average number of words recalled by light users was 15.3 and the average for heavy users was 14.9.

everyone knows these are not very dramatic differences in people who have been heavy marihuana users for three years. And I again cite the fact that he had a great deal of difficulty in constructing a control group and that his marihuana users were—had lower i.q.’s, lower S.A.T. scores and heavier drug use of other sorts. But the paper’s now there in the medical literature and says that there is a cognitive impact of chronic marihuana use, and it’s received a lot of attention. People will wait to see if he can reproduce those results.

Bloch’s studies received a lot of attention

because he had their fourth grade test scores. These are all Iowa residents and they were all willing to give him their names and so he was able to try to balance his groups as to their fourth grade intellectual capacity. So then when they were adults, the non-users and the chronic users, or the light users versus the chronic users, he thought he had matched them beforehand for their intellectual abilities. And the study again raises some—some interesting questions. Bloch for instance said that heavy marihuana users who reported seven or more uses per week for an average of 6.5 years scored lower on two sub-scales of the i.q. test—that’s the standard twelfth grade test—and one computerized test of memory.

people and a very slight effect, it’s raised again the possibility that we’re discussing here, does chronic marihuana use cause cognitive defect and apparent brain damage.

Bloch’s study for the following reason. We found out that Bloch published a preliminary version of the study and that preliminary version was published in a United States government publication. And in that version he did not have a division between the heavy use group, people who use seven or more times, and the division of people that use five to six times. And that’s actually a bit of a strange division. They all seem to be pretty heavy users, that is, people using five to six times a week versus seven times or more per week for 6.5 years. But he in his first publication, his preliminary results, he collapsed these two groups together and the differences were nowhere near as dramatic. In fact, they had a difference from the control group on only one scale, i.q. scale, and they also were different on their fourth grade scores.

published his final paper, and made the division between the seven times more who had abnormalities on the two i.q. tests and one computerized test of memory. And it is striking to us that the individuals who used five to six times a week had no abnormalities. But he broke out a group of seven or more times a week who had abnormalities. And it raises the question, since he had not brought out that group before when he presented his data the first time, why did he bring it out this time. And one of the reasons he may have done so is to get more dramatic differences. That doesn’t mean the differences are not there, but it looks a little bit like post-analysis manipulation.

has been criticized because he brought these users into the laboratory, many of whom who had used seven times per week or more for 6.5 years, and he told them not to use marihuana the night before, the day before, and to come into the laboratory clean. But he did no urine testing to insure that was true. So people have raised the possibility that Bloch’s findings had to do with requesting daily marihuana users of 6.5 years to abstain and then not doing any testing to see that they had abstained, so that his findings may indeed in fact relate to use on the day of the test.

that I’m—I might you know, sound as if I’m looking for reasons to criticize the studies. And at a certain level of course, I am. I’m a critical reader. It’s my job to not just report what these people have said, but since there are these—only—only these two studies to show some slight cognitive harm with chronic marihuana use, then I—it’s my responsibility to be very critical of the studies. So I have looked very carefully for reasons to worry about these findings, which have not been found by other people and were not found generally in multiple studies in the 1970’s.

I have concluded our chapter—we’ve actually talked about a few other studies which have shown some memory deficit supposedly in chronic users. We’ve not felt them to be very strong studies. So we’ve concluded our chapter by saying that we think there’s no convincing evidence that chronic marihuana use is associated with cognitive deficit. Now if we’re wrong, the cognitive deficit appears to be pretty minimal, maybe of no functional importance, and it occurs only in an extremely small group of marihuana users who are very high dose users. In fact, Dr. Bloch’s data could be interpreted that individuals who use marihuana daily for 6.5 years have no cognitive deficits five to six times per week, while those who are using seven or more have this slight finding, which may be lost in the analysis—or found in the analysis. Okay?

Now what Pope did was to try very hard

to balance and he had a group of chronic female users. In other words, in his high use group there were a group of females. He then did the analysis by gender, and all of the deficits melted away. That means that this evidence of chronic harm occurs only in male users. Well, what does that make one think of? It makes me think that this is not a pharmacological issue. This is not necessarily an effect of marihuana at all. I’m not automatically saying that chronic using women are smarter than chronic using men. They may be. But that males are heavier users than other drugs, play more football and soccer, a variety of other things that might diminish their cognitive abilities in this kind of testing. And—but more important than that, merely dividing the subjects by gender and suddenly having all of your intellectual deficits disappear, raises questions about the probity of your publication, the probity of your scientific analysis. Because I can’t think of any reason why all differences should disappear in women who’ve also been users at this high level for three years.

Thanks for reminding me of that. I’d forgotten.

anti-marihuana front. He’s a hard fighter. He’s a colleague of Dr. Nauhaus, colleague of Dr. Tenant. Works together with them to fight the marihuana reformers and to identify immoral actions on the part of the marihuana reformers.

has attracted a lot of attention. In fact, both Bloch and Pope refer to Dr. Richard Schwartz’s study. Now I’ve been aware of Dr. Schwartz’s study almost since the day it came out. I know him well. He published this paper in 1989. And I looked at the paper and I have previously criticized it. Let me tell you quickly what he found.

treatment program based in the United States called Straight Incorporated. Straight Incorporated had come under lots and lots of criticism and in fact—although it may be a little unfair—its licence has been removed in the United States. It no longer exists. And the reason the licence was removed, because of multiple lawsuits and complaints by young people who were forced to go to Straight by their parents because they were marihuana users and users of other drugs and in trouble, but once they were in Straight they discovered that they were subject to corporal punishment by graduates of the program, they were subject to physical restraint and were not permitted to leave when they wanted to even though they had not been committed legally. But this treatment program looked like a jail.

Now many of the graduates of Straight say,

"It saved my life. It’s wonderful." Many of the parents think it was the greatest thing in the world, etcetera. But its licence has been removed in four states in the United States, it no longer exists.

Now—so Dr. Schwartz published this

study which said the following. He studied ten heavy users of marihuana, adolescents whom he said were marihuana dependent, that is they were using so much marihuana that it was their main medical problem. And they were admitted by their parents to this program. At the time of their admission he measured a number of tests of their memory. And in fact he measured it two to three days afterward and they had abnormalities in two tests of memory of the seven he administered. That’s in itself an interesting finding.

they’d been in the program, and although they’d improved somewhat, one of the tests was still abnormal, that is comparing inside the heavy use group, still abnormal.

Now of course what am I going to talk about now?

I’m going to talk about the control group. Dr. Schwartz generated two control groups for comparison of memory testing to these adolescent marihuana dependent people. And in two papers he’s published about this study since, in conferences held in Paris by Dr. Nauhaus, he’s taken on a pretty self-congratulatory tone about, "We had two control groups and they showed that this memory deficit persisted for six weeks, therefore if all of this previous research to say that the memory defect doesn’t persist is wrong, all of you people are wrong."

five or six years until Professor Zimmer and I began preparing this book and this chapter. And then we looked at it very carefully and discovered some pretty amazing problems. The abnormality in the memory two to three days after admission was abnormal compared to the control groups when the control groups were combined, nine people from one control group and ten people from another. So then if you compared the memory function in his marihuana using young people to the two control groups combined, seventeen people, they were abnormal, two to three days after admission.

when he compared them to his control group at the end of six weeks they were abnormal from the combined control group.

groups were. One, like the adolescent marihuana users, were admitted to the program. They were committed to Straight Incorporated. They didn’t have marihuana problems. In fact, it’s a little difficult to tell what their problems were; they may have been alcohol, but it’s not clear. And in fact at the time of admission he said they didn’t have too many drug problems, but they were admitted.

and sisters of the marihuana patients who had no drug use problems as far as anyone knows. And he tried to match them as to age and intellect, etcetera, etcetera.

the two control groups, the abnormality in memory at both ends disappeared when he compared it to the committed patients. That means that the control group for the adolescent marihuana use which consisted of people who were also in the treatment program, there was no difference. There was no memory deficit between those two. So if there was a memory deficit from the community controls, the brothers and sisters, then the memory deficit didn’t have to do with marihuana, it had to do with being admitted to this program. And having interviewed a number of people from this program, the most likely explanation for Dr. Schwartz’s studies is how angry and furious those kids were at him as the medical director of this program and at their parents for forcing them to stay in this program where they were physically restrained, not permitted to leave, had to follow a series of rules, told they were marihuana addicted and that they were no good.

defects in this testing, because they didn’t cooperate with the testing. And I have very strong evidence for that, since there was no difference in memory scores between the two admitted patient groups, and the only difference occurred when he added in the outpatient controls, who were not good controls. After all, they were not drug users. They were not in trouble. They were community samples.

floating around, Professor Zimmer and I have read it carefully and think it adds very little to this argument.

important to this argument. It shows that if the control group is constructed properly you may see no difference in chronic marihuana users. If you construct a control group of individuals who are admitted to a program, that looks like a good control group and you don’t see any impact of the drug. If you compare them to outpatient, smart kids who are not in trouble, then you see differences. Outpatient, cooperative, smart kids, then you see differences. That shows that by constructing your control group properly you learn something, which is that marihuana had no impact on the memory of these children.

And then in 1971 or ‘72 two people

in the group of scientists who were collected together to question what we believed about marihuana, two psychiatrists named Kalanski and Moore, published findings in which they showed that a group of adolescent marihuana users had a very distinct amotivational syndrome, that is they didn’t—would not work, they had dropped out of their previous life, they were apathetic, listless, withdrawn, lethargic, had no taste for life, had anomie, and that this was caused by marihuana.

1971 or 1972 that marihuana causes an amotivational syndrome is perhaps the most important and frequently stated claim of those who are concerned about adolescent marihuana use, and it’s stated over and over and over again. Our quotes are fairly contemporary. "The marihuana issue is about the costs to society of drug-related lost productivity." Donna Shelalagh said that in July of 1995, the Secretary of Health Human—Health and Human Services in the United States. "An amotivational syndrome has been reported in heavy chronic marihuana users. It is characterized by decreased drive and ambition." That’s a NIDA publication. Although it’s undated I know it came out in 1995.

at full potential. It makes an above average student average and an average student below average." That’s the Attorney General of the state of Pennsylvania. Again, I don’t know exactly the date but it was the 1990’s.

recognized," etcetera, etcetera.

subject to review because there’s so many ways to look at it. We found for instance a series of laboratory studies in which individuals who were willing to be admitted to a hospital site were given work tasks or ability to earn money or a variety of tasks and then they were given marihuana and their productivity on the task was compared to their non-marihuana use or a group of controls. In fact, the most interesting and most—in many ways most important one of these was done in Canada. That would probably be—

So, a series of laboratory studies in which

we give the drug to individuals and see if it decreases their commitment to work in a variety of settings. We have those kinds of studies.

you about, Jamaica and Costa Rica in particular, the economic capacity of those men who were cannabis users was compared to controls, and in fact in one instance there was actually a study done using a quantitative assessment of the amount of work that a Jamaican farm labourer performed after smoking marihuana. It was done a number of times to see if his commitment, his ability to work decreased because he smoked marihuana.

United States of grade—school grade performance of marihuana users versus non-marihuana users in high school and in college.

in the arguments about workplace-based urine testing, there are now four publications coming out of the same database about wage-earnings in marihuana users versus non-marihuana users. In the United States there is something called the National Longitudinal Survey of Youth in which twelve thousand young people have been interviewed quite extensively over the years, then in two years, four years apart they were asked a series of questions about their drug use. And then there’s a New York State sample of young people who’ve been interviewed extensively by a group of epidemiologists at Columbia University, learning lots about their work, their life, their performance, their drug use, etcetera, etcetera.

is no support for an amotivational effect of marihuana. None. Zero.

Let me—

There have been four studies of that

data set, the National Longitudinal Survey for Youth, and somewhat to the embarrassment of the investigators, in one study the wages of marihuana users and

non-marihuana users was the same. In the other three the marihuana users all earned significantly more money. So the ability to generate wages, which is at least one measure of motivation, would seem to not be impacted by marihuana.

1984 sample said that marihuana users actually were—even though they earned as much money or more, were absent more often, they were not so good workers. But then that scientist did a longitudinal study in which he looked at ‘94 and 1988, and found that there was no difference in the number of hours worked per year. That is, they didn’t have more absences if they were marihuana users, and they earned significantly more wages. And in fact in one of the four studies I think the differential was twenty percent higher wages by marihuana users. Now that’s a pretty strong blow against the idea that marihuana use causes amotivation.

Canadian study because it is—it in fact is really very impressive. I then will go back to the—the field studies.

token economy study,"—that is, individuals had to work. I can’t remember whether they were putting together stools or—they had some task they had to do. And if you worked hard you got more tokens which you could cash in for money at the end of the study. Other studies have been done in which you could use your tokens to buy marihuana, but in this one that was not done.

token economy study to evaluate marihuana’s impact on motivation. They found some reduction in work efficiency at the beginning of the marihuana use period. However, efficiency quickly increased and surpassed abstinence levels. And although subjects consuming the most marihuana spent the least amount of time working, they were no less productive because when they worked they worked harder. In addition, during the period of highest marihuana use subjects at the Addiction Research Foundation, organized a unified collective action and successfully demanded and negotiated for increased wages. At the end of that time they worked even harder."

I absolutely love that.

way to control for the influence that might be present by virtue of the fact that the subjects are actually participating in this study? In other—in other words, in their normal life they may behave one way but when they participate in this study they would—might behave another.

point averages in which college students by and large where marihuana users have had either equal or better grades than non-marihuana users. High school it’s a little different, a little more disparate and there are some evidences of heavy marihuana users being quite dysfunctional in high school, although almost all the studies we’ve found have indicated that their dysfunction preceded their heavy use of marihuana. They were already having grade trouble before—they cleaved to marihuana perhaps as an answer.

question, all laboratory studies are artificial. Almost all studies in which drugs are evaluated in humans under controlled circumstances are artificial. They give us important information but they form only some part of the picture. And real world studies, surveys, questionnaires, observations all make up part of the package of information, usually inadequate, with which we have to determine policies, decisions and regulation.

quickly mention to you that after all of these years, twenty years of amotivational studies, no one had ever found anything to support the amotivational syndrome. And then a NIDA-funded scientist in the late—in the early 1990’s named Fulton did an astonishing experiment in which people were allowed to work—people were—under the influence of marihuana were assessed on four tasks. They were all terrible tasks. They were all extremely boring. One of them was to sort pieces of metal by colour and size into different bins. One of them was to alphabetize a series of

seven-letter nonsense words generated by a computer. Just had to alphabetize it as a-b versus c-d, even though the word made no sense. So there were four terribly boring tasks.

motivation was how hard would someone work on his most boring task, the one he hated the most, so he could then spend some time on his least boring task. Strange set of ideas to begin with. However—and I believe it was designed to show that marihuana would have an amotivational effect, that is people wouldn’t work very hard to escape their most boring task. They all did. On marihuana they worked the hardest to get rid of the boring task.

study, Fulton and his associates conclude that the complicated effects of smoked marihuana on the motivational aspects of human performance need to be studied more rigorously, under a wider range of clinical epidemiological and experimental conditions. Remember I told you that’s the language that people use in grant applications.

There is no evidence for an amotivational

effect of marihuana.

Now there has been a claim that there’s

a specific cannabis or cannabinoid psychosis. It’s very rarely been reported in the western world. It may have—it may occur occasionally in individuals who consume large doses of cannabis orally, which I’ve already discussed with you as being a different issue. But I do—I must focus on one thing because I’m pretty sure it’s going to come up, and this is the Swedish conscripts study in which Swedish scientists have looked at a group of schizophrenic patients and discovered that they had lots of data on them because they were once in the military. And as they came into the military they answered very extensive questionnaires and demographic and other data in hopes that one would learn something from this kind of study. And what—I—Dr. Andreasson found was he described cannabis use as a risk factor in the occurrence of schizophrenia. That is, in the conscripts who became schizophrenics a few of them had significant consumption of marihuana before they became schizophrenic. So Dr. Andreasson and some critics of marihuana reform have decided that marihuana can cause schizophrenia in some people.

There are many, many other interpretations.

The most common one is that if you look at schizophrenic patients who are using marihuana, versus those who are not, that in general you find a pattern of less severe schizophrenia, less florid hallucinations, less life problems, less withdrawal. So the assumption is either that marihauna’s helping them and they’re using marihuana to treat some of their own symptoms, or that they are a little bit better than the other schizophrenics and were social enough, involved enough in social lives that they could get marihuana. And so there’s all these interpretations to detract from Andreasson’s idea that in a few young men marihuana use was related to the later occurrence of schizophrenia.

about six percent of the schizophrenics who had been marihuana users beforehand. If marihuana has an impact on schizophrenia it may be more likely to be used by people to diminish the symptoms, although in some schizophrenic patients marihuana use might precipitate the schizophrenia or might cause it to emerge, might interfere with other medication. So I’m not saying that marihuana can be used without risk by individuals with serious mental illness, but I don’t think there’s any evidence that marihuana causes crying mental illness.

But despite that advice and despite the fact

that it occurred, most of these young people were naive users and given a little reassurance and a little time, little talk, they were fine.

non-marihuana users and there’s no real association of marihuana with criminal behaviour, except for the crime of the possession of marihuana. And that marihuana users are not over-represented in any kind of criminal statistic.

all marihuana myths none of them ever die. And this one has come back again. The strong use(sic) between marihuana use and violence which was stated by the last American drug czar, "Chronic effects of frequent marihuana use may include pervasive anger with easy provocation to hostile aggression even against loved ones." And so we now hear these things being stated once again.

scholar and government commission examining the relationship between marihuana and crime reached the same conclusion, including prominently the—the Ledain Commission. The vast majority of marihuana users do not commit crimes. Among marihuana users who do commit crimes, marihuana does not play a causal role. Almost all human and animal studies show that marihuana decreases rather than increases aggression. So the idea of the crazed marihuana user painted by Harry Anslinger, which we thought had gone away, has not entirely gone away and is being described again. But there is not any evidence, any evidence that such a thing is true.

Q The Reefer Madness movie.

I’ll make one quick comment. Reference

number thirteen was recently cited in the debate about the impact of marihuana on homicide. A prominent and respected investigator in New York interviewed a number of men who had been admitted—admitted, had been incarcerated for homicide in New York State. And fifteen percent of those men said that they had been on marihuana at the time of the homicide. And I think of those maybe half of them said they’d been only on marihuana at the time of the homicide, which cut it then down I guess to about six percent. And in the investigator—and in questioning the individual felt that there was no evidence that marihuana had contributed to the homicide, although this is well after the fact.

it was recently cited in the debate as proof that marihuana caused homicidal behaviour in humans. The fact that some people who had committed a homicide said that they had been on marihuana was accepted by him as evidence that marihuana caused the homicide. There is no evidence that’s acceptable to say such a thing.

non-users, not because they use marihuana, because they happen to be the kinds of people who would be expected to have a higher crime rate wholly apart from the use of marihuana. In most cases, the difference in crime rates between users and non-users are dependent not on marihuana use per se but on these other factors." And we quoted that because it was stated by President Nixon’s conservative commission in 1972, and it seems to us to still be true.

required to pay attention to two things at once. They are not driving a car, but they’re sitting there monitoring a set of lights which when it comes up red they have to push a button. But at the same time they’re monitoring those set of lights they have to monitor something else a little bit out to their periphery. So they have to keep looking back and forth.

marihuana diminishes people’s ability to perform this kind of psychological function well, a divided attention task. Okay?

this kind of skill is related to automobile driving, I fear that marihuana may cause people to drive badly."

there are many such laboratory studies to show a diminution in psychomotor skills, reflex time, etcetera, etcetera, that might relate to driving. So let’s set those on one side, large numbers of studies that say that in laboratory assessment that marihuana may diminish some of the skills that might relate to driving. An important issue.

studies, which are driving simulator studies and you know, almost like the car tracking things in penny arcades. Investigators have done many studies with the driving simulators in which you may be even given a panoramic t.v. screen and the road moves in front of you, and you may be given noises and you’re asked to brake or pass or do various things. You’re actually not driving a car but you’re in a simulator.

because by and large marihuana, even at relatively high doses, has relatively little impact on people in driving simulators. There’s no—not much of an increase in braking errors. People can put on their brakes just fine. They’ll swerve the wheels when you send something into them. They’ll do pretty well. In driving simulator studies marihuana’s been shown to have an effect on some performance measures, particularly those involving divided attention. However, overall impairment from marihuana is much less severe than that produced by alcohol at doses below intoxicating levels. That is, that two drinks which gives you a blood alcohol level of .04 percent or .05, you see a much greater impact on simulator studies than people given larger doses of marihuana. I’ll explain larger dose of marihuana later. It becomes real important.

the fears that Dr. Moskowitz and other students of driving skills had.

you give people actual on the road tests of their driving ability. There are many, many of these and they’ve been done in many ways, sometimes with an observer sitting next to the driver, sometimes with an observer with a dual set of controls in case somebody gets into trouble. Sometimes the observer is in the back seat giving a global assessment of driving. And of course certain other things can be measured such as distance behind a car that’s being tracked, does the marihuana user get too close, a driving task in which the individual is told to pass as soon as the road is clear ahead, measurement of braking time, how often the individual makes braking or steering errors. And again the general finding is that low doses of marihuana caused little or no impairment on on-road studies. Even high doses of marihuana caused less impairment than low doses of alcohol. And the study which causes marihuana critics to laugh derisively but which has been shown over and over again, that people under the influence of marihuana become more cautious. When they perceive themselves to be high they drive more cautiously. They slow down, they increase their distance behind a car they’re following, and they are very hesitant to pass in any sort of situation even though they’ve been directed to pass. If there’s a hill way up ahead, they still have a dotted line but they can see the white line up in front, they’re hesitant to pull out. And if you interview them, the reason is quite clear. "I felt high. I was afraid I couldn’t do it so I slowed down."

Now the reason I mention this is because

there is then a significant literature that says

risk-taking while driving a car on marihuana is reduced. And that’s compared to a literature regarding alcohol which says risk-taking while individuals taking alcohol is markedly increased. Individuals who are under a psychomotor deleterious effect of alcohol seem not to realize it. They drive faster and more aggressively and take more risks and their judgment is more impaired.

So a little bit high on alcohol appears to be

much dangerous than a little bit high on marihuana.

I quickly say, should people drive while high

on marihuana? No, no, no, no. But giving those two things, giving those three things I’ve mentioned, psychomotor tests, driving simulators and on the road driving, there is relatively little evidence that marihuana is an important contributor to vehicular mishaps.

And then I have two other things I want to say.

You wanted to ask me something.

So Dr. Klanoff, who’s also a Canadian

investigator, has published a number of studies in which he’s talked about the fact it’s very hard to know what’s going on. You say it’s reflex time, but it may be perception. It may be motor—muscle relaxation. It may be impaired memory. All of those things can influence what looks like a simple outcome of psychomotor impairment.

You cannot do it with blood levels of T.H.C.

You cannot do it. And I don’t think we’ll ever be able to do it. We’re not going to be able to have a blood T.H.C. measurement that will tell us whether the influence was under—whether the individual was under the influence of marihuana because the range is so high. There are people with a hundred nanograms of T.H.C. per millilitre who are not at all high. There are people with ten nanograms who cannot walk. So we—and that’s because of the compartmentalization. It’s not the amount that’s in the blood, it’s the amount that’s in the brain. And the amount that goes into the brain is delayed and then it comes out quickly and looking at the blood levels we don’t know where we are.

if the blood level is below four or three or two, the assumption is the individual is not likely to be under the influence. And that’s germane in something else I’m going to talk about.

don’t believe we shall ever have a per se blood level, as we do for alcohol. It’s going to have to be something else.

So to try to draw this quickly to a

Now in terms of dosage, which is a critical

issue, Dr. Robe gave three doses of marihuana. And he determined them in part by allowing people to smoke and telling him what they liked as their high dose. And it wasn’t much difference than had been done in other studies. It was, in the way pharmacologists like to calculate the dose, by weight, it was either one hundred, two hundred or three hundred micrograms of Delta 9 T.H.C. per kilogram of body weight. That’s the equivalent of two to three milligrams in most people and four to five in big people. Six to seven in real big people.

doses—incidentally, Dr. Moskowitz, whom I mentioned to you before, has found this impact on selective and divided attention at doses one half Robe’s lowest, at fifty micrograms per kilogram. So Robe’s doses were clearly enough to affect the kind of measures that Moskowitz and others have worried about as important in driving behaviours.

of studies. He gave people the hundred or two hundred or three hundred and compared it to placebo smoke, and then he did a number of studies, such as the memory, the ability to estimate the passage of time, measured their heart rate, looked at their red eyes, a variety of other things that are generally accepted as evidence of a marihuana high, including the individual’s rating was, "Am I high on marihuana?" So he did those to see that these were effective doses.

in two separate trials, the first on a highway closed to traffic. And I actually saw a videotape of Robe’s operation in which the Maastricht police have cooperated with them to give them a real section of road, but it’s easily closed to traffic with a bypass for the regular traffic. And people drove on that road which was controlled access, and the vehicle ahead of them was instructed on how to track and how to slow and how to speed ahead.

a hundred micrograms per kilogram in busy city driving in Maastricht, which is a small to medium Dutch town.

closed highway and on the occupied highway, marihuana’s effect on driving performance is found to be insignificant on nearly every measure. Marihuana did impair the driver’s ability to maintain a steady lateral position and higher doses produced greater impairment. That is, they would weave more. However, even with the highest dose marihuana’s effect was relatively minor, similar to that observed in drivers using legal medications in therapeutic doses and similar to that of drivers with blood alcohol concentrations well below intoxicated levels. In fact, in the urban driving trial, which compared marihuana’s influence on driving to alcohol at a .04 percent blood level, which is two beers in an average weight person, alcohol produced significant reductions in driving ability while marihuana produced none.

So Robe did everything that could have

been expected of him. He gave the marihuana, assessed that it had an impact, did a series of physiological and other studies. He then put people on the road in three different settings, a highway with controlled access, and it always included following behind a car at a certain distance and then responding to that car as the driver took his foot off the accelerator and let the car slow and to see how the marihuana driver would behave. That was a standard part of the test.

driving the drivers were evaluated by two means, one in which someone sitting in the car was given a checklist and was supposed to every few seconds check and see if he was maintaining distance where he was, was his speed okay, etcetera, etcetera. And then another assessor in the same car did a global evaluation, was this skilled driving at this level or skilled driving at a different level. And basically, marihuana produced no

impact on these global driving evaluative scores. Produced an impact on lateral deviation. And the marihuana drivers tended to stay further behind the car they were to track than they were supposed to. In other words they slowed down because of the apparent cautionary influence. The marihuana drivers told in the city driving test that they were worried, they were scared because they felt high on marihuana and a few of them said, "I don’t want to drive." But they were convinced to do so. And they tended to be very careful because of this. While the alcohol drivers at .04 percent, although they had significant impairment, felt just fine.

So Robe’s studies are I think critically

important.

urban driving trial was at a low dose and some people have said it was too low a dose to have an impact. It was a dose sufficient to produce marihuana effect in almost every sphere. A hundred micrograms per kilogram is a standard social dose of marihuana. Everybody gets high on it. So I don’t believe the criticisms are apt, but you will hear those criticisms, that the Robe study should be discounted because the lowest dose was too low.

of those of us who care about marihuana and its impact on the culture and its impact on human performance, the Robe study is almost revolutionary. It has to me answered every question that people have asked about marihuana and driving. Maybe not every, but an awful lot of them.

the—the final piece of information. So we’ve got psychological, psychomotor tests, we’ve got driving simulators, we’ve got on-road performance, we’ve got Robe’s study which in a certain sense combines almost everything. And all of those say, "Well gee, I don’t see much evidence that marihuana is an important contributor to highway problems." Then in our last—almost—not our last, but on 16-4, "More compelling evidence of marihuana’s minimal effect on driving comes from epidemiologic surveys of drivers involved in fatal highway accidents." And I want to particularly comment on that, because in Dr. Kalant’s commentary in Haman[phonetic], he discussed the fact that there were some studies which seemed to indicate that marihuana positives were over-represented in serious accidents, and some early studies may indeed have said that. But there’s been significant information generated in the past few years. "Compelling evidence of marihuana’s minimal effect on driving comes from epidemiologic surveys of drivers involved in fatal highway accidents." That is in the United States, Canada and Australia. "And found T.H.C. in the blood of from three to eleven percent of fatally injured drivers. However, in the majority, seventy to ninety percent of these cases, alcohol was detected as well and probably contributed to the outcome. To evaluate marihuana’s specific contribution to accidents some researchers have rated the culpability of drivers who test positive for marihuana only." That is, someone using the road report, the police report, the characteristics of the accident have said, "Now was this driver responsible for this accident? Did he bear responsibility to a large degree or to a small degree? Is there any evidence that maybe he was not guilty of anything at all, just had the bad fortune to be ploughed into by another driver?"

to an important Canadian study of T.H.C. in the blood of fatally injured drivers. That’s the study by Sinbora[phonetic] which is referred to here.

who test positive for marihuana only one study found a higher culpability for marihuana positive drivers than drug-free drivers. That means that marihuana appeared to be at fault. But it relied on a very small sample. Three other studies found not only that marihuana positive drivers were less culpable than alcohol positive drivers, but were also less culpable than drug-free drivers. That is, fewer drivers in the marihuana positive group than in the drug-free group were judged to be responsible for the accidents. The author of one of these studies suggests that either the cannabis actually increases driving ability or that drivers taking cannabis overcompensate for loss of driving skills." And obviously I quoted that because I believe that’s what happens. The cannabis drivers overcompensate, they slow down, they won’t pass, they won’t speed, they’re very careful.

ability and I think no one should drive having smoked marihuana in the last few hours. No one should drive. However, there is no acceptable evidence, no convincing evidence to me that marihuana is an important contributor to vehicular accidents or vehicular fatalities on the roads of North America.

be going ‘til four or later today? There’s the ceremonies for the judges that are being called. I don’t—

THE COURT: I’ll leave that to counsel. I’m quite

prepared to sit through the regular court day, knowing that we have an out-of-town witness.

MR. CONROY: Thursday night, so.

A Thursday—I can’t remember.

MR. CONROY: Thursday evening.

THE COURT: I’m not sure you should have told us that.

A Well—

MR. CONROY: Thursday evening.

A -- I felt I had to.

let’s take the break, get as much as we can—

ceremony or not, I’ll leave that up to you. It appears that Dr. Morgan will be here tomorrow anyway. I don’t know if you want the extra half hour today or if you wish to attend—

bit more maybe until four and then—

THE COURT: We’ll come back at least until—

MR. CONROY: Four.

THE COURT: -- five to four.

MR. CONROY: I’ll speak with my friend at the break and

(WITNESS ASIDE)

JOHN PAUL MORGAN, recalled, testifies as follows:

that my learned friend is cross examining his witness. He asked him a question identical in substance to that before the break and the witness said he wasn’t aware of a device that would measure the person’s level of intoxication, and he went further and said that he didn’t think that one would ever be created.

that people look at?

I think counsel’s entitled to ask about—if he

have published two papers now in which they’ve given marihuana of a known amount to individuals with no T.H.C. in their bloodstream and then measured these two factors. And by a ratio of the metabolite to the parent compound they have been able to do pretty well at saying this was consumed within an hour, this was consumed within five hours. So the newspaper article is incorrect. It doesn’t tell you whether the individual is intoxicated or not, and my answer is that I don’t know that we’ll ever be able to do that (indiscernible). However, this may be an important estimate of when the material was consumed. And so for all I know a state legislature might then say, "Well, if it was consumed within the last hour we’re going to presume the individual was." But that’s all speculative. That’s what’s going on with that test.

medi-toxicity, and this is of course a very important one, that after you’ve argued with people about the harms of marihuana and whether you’ve convinced them of the minimal harms of the substance, then the idea of the gateway is trotted out, that somehow the use of marihuana is associated with a cause, some kind of factor that will lead to the use of other drugs. We’re fond of pointing out that in the sixties all discussions of gateway had to do with progression from marihuana to heroin use. No one has those discussions any longer because we now have plenty of evidence that almost no marihuana smokers progress to heroin use and the level of heroin use has remained quite low and fairly steady in this culture, with some ups and downs.

then became if you use marihuana you’ll use L.S.D. Well, that has not worked out. And in the States now

that we think the evidence merits. There is no pharmacological basis for the gateway theory. There is no impact of marihuana on the brain which leads individuals to need, want, search for, suck up cocaine or any other drugs. The gateway is a description of a very logical statistical observation which goes as follows. In a culture there are a group of drugs, intoxicants available. If an individual has used an intoxicant of very low prevalence, such as cocaine or heroin, then he is very likely to have used an intoxicant of high prevalence. Therefore, if you examine users of heroin, users of cocaine, you will almost always find that they have heretofore used marihuana, tobacco and alcohol. Those are the intoxicants of high prevalence and their use almost always precedes the use of a low prevalence intoxicant such as cocaine.

Now—but to describe marihuana as a

gateway to cocaine is not supportable by any evidence. In other words, true, most users of cocaine have used marihuana. But only a minority of marihuana users ever use cocaine. The last number, the high school senior survey in the United States was that of all of the high school seniors who had experimented with marihuana only fourteen percent had tried cocaine. So, for eighty-six percent of high school seniors marihuana is not a gateway drug, it’s a terminus drug.

life, although they drop somewhat, logically enough. And I believe of individuals who are twenty-nine or thirty who have used marihuana about two-thirds of them have never used another illegal drug, in other words, sixty-seven percent. And that tends to hold fairly well throughout the culture.

drug if only a minority of individuals who use it go on to other drugs.

In the United States we have been presented with a sound byte which goes as follows, "Users of marihuana are eighty-five times more likely to use cocaine than non-users of marihuana." This number has come from something called the Centre for Addiction and Substance Abuse affiliated with Columbia and headed by a man who was once in the drug czar’s office and headed by another man who was once Secretary of Health, Education and Welfare in the United States in the Carter administration, a man named Joseph Calofono[phonetic]. So let me state it for you again. "Users of

marihuana are eighty-five times more likely to have used cocaine than those who have not used marihuana." Now this is not at all a statement of the gateway. What it is is the statement of how unusual it is for someone to have used cocaine to have never used marihuana before.

done a year before the fourteen percent so it was sixteen percent. So you put it in your numerator sixteen, that is the percentage of marihuana users who have used cocaine, and then your denominator you put the percentage of cocaine users who have never used marihuana, which happens to be .02. And then you divide sixteen by .02 and you get eighty-five. Clear? It’s—maybe I can make it clearer with one

other thing that Professor Zimmer and I have used in this chapter. Anytime there are two associated events of high prevalence and low prevalence you’ll see this association. For instance, only a few Americans ride motorcycles. Of those Americans who ride motorcycles, almost all of them have ridden bicycles before. Yet, of those individuals who ride bicycles only a small percentage of them go on to use—to ride motorcycles. Is therefore bicycling a gateway to motorcycling, or does bicycling cause motorcycling? There is no gateway theory at all and there is no evidence that the use of marihuana leads in any causal, pharmacological factor to the use of other drugs.

a lot about the shifting prevalence of drugs over time. Well, marihuana use declined in the United States from 1979 ‘til 1991. For the first part of that cocaine use went up. And while marihuana use declined for a long period of time L.S.D. stayed about the same.

able to generate was that—you heard me say before that the prevalence of cocaine experimentation in individuals who had used marihuana who were high school seniors, was fourteen percent. That’s the lowest it has been in a decade. In 1986 the percentage of marihuana users who had experimented with cocaine was thirty-three percent. That’s when cocaine was on its upsurge in the United States. So it’s fallen every year since that time. This gateway factor has fallen every year since 1986. 1986, thirty-three percent of marihuana smokers who were high school seniors had tried cocaine. In 1995 fourteen percent of high school seniors who had used marihuana had used cocaine. There is no gateway. There is no gateway. There is no stepping stone. There is no theory here at all.

1986 --

Q All right.

Well, our experience has told us that this

is not true, that marihuana enforcement is very important in the United States. And so we simply engaged in gathering data to see what marihuana law enforcement in the United States is like. I have no idea what it’s like in Canada, but I can tell you that the number of people arrested for marihuana offences in the United States reached an all-time high in 1995. That year there were more than a half million marihuana arrests, eighty-six percent of which were—were for marihuana possession. Tens of thousands of people are now in prison for marihuana offences and an even greater number are punished with probations, fines and civil sanctions such as having their property seized, their drivers’ licences revoked and their employment terminated.

Conroy asks another question, I’m trying to figure out whether this is anywhere near the Doctor’s qualifications either as a medical doctor or as a psychopharmacologist.

We did a number of things to try to gather

this information and to portray the fact that nothing has changed from the opinion of the Schaeffer Committee, which is that the greatest hazard facing a user of marihuana is not toxic, but the likelihood that he’ll be arrested and prosecuted.

over the evening. It’s a few minutes to four. And if it’s not within the expertise we’ll leave it and go on to the next.

morning at nine thirty.

(WITNESS ASIDE)

(PROCEEDINGS ADJOURNED TO 29 JANUARY 1997 AT 9:30 A.M.)