Health Risks of Marijuana
Use
By James
Geiwitz, Ph.D.,September 19, 2001
- 1.0: INTRODUCTION
- 2.0: THE TOXICOLOGY OF THC
- 2.1: Genetic Effects
- 2.2: Pregnancy and Offspring
- 2.2.1: Pregnancy
- 2.2.2: Birth defects and brain
development
- 2.3: Hormonal Systems and Reproductive
Capabilities
- 2.4: Immune System
- 2.4.1: Suppression versus
enhancement
- 2.4.2: Humans and
disease
- 2.5: THC and Cancer
- 2.6: Miscellaneous Issues
- 2.6.1: Marijuana use in
children
- 2.6.2: Cannabinoids other than
THC
- 2.6.3: Health risks of smoking
marijuana
- 3.0: THE SCIENCE OF THC RISK ASSESSMENT
- 3.1: Extreme Dosing
- 3.2: Cannabinoid Receptors and
Tolerance
- 3.3: Extrapolation from Animal
Studies
- 3.6: The Fallibility and Abuse of
Science
- 4.0: CONCLUSIONS
- 5.0: REFERENCE
1.0: INTRODUCTION
The purpose of this report is to examine the research evidence
for and against the hypothesis that marijuana use involves risk to
the user’s health. It is prepared for Robert Moore Stewart (Attorney)
in two Constitutional Question Notices (Court File Numbers 112460
and 112476, Victoria Registry) on behalf of Leon Edward Smith
(Defendant).
My credentials for writing this report are as follow: I have a
Ph.D. in experimental design and analysis from the University of
Michigan. I have written 10 textbooks, all of which have had sections
on marijuana use and abuse in North America; therefore, I have
followed the research on marijuana for over 25 years. On January 15,
2001, the Committee on Hemp Risks prepared a report for Health Canada
on the health risks of THC (the psychoactive ingredient in marijuana)
in industrial hemp foods and cosmetics. I was the chair of
that committee and chief author of the report. Also on the committee
were the top marijuana researchers in the world, including
Franjo Grotenhermen, M.D., of the nova Institute in Germany; John P.
Morgan, M.D., Professor of Pharmacology, CUNY Medical School; Paul
Consroe, Ph.D., Professor of Pharmacology and Toxicology, University
of Arizona; and David Pate, Ph.D., Senior Technical Officer,
HortaPharm BV, Amsterdam. Dr. Grotenhermen is chair of the
International Association for Cannabis as Medicine. Dr. Morgan has
prepared the recreational drug section of the Merck Manual for many
editions. Dr. Consroe is a founding member of the International
Cannabinoid Research Society. Drs. Morgan, Consroe, and Pate presented
their research to the US Institute of Medicine’s task force on
medical marijuana and is included in their report, Marijuana and
Medicine: Assessing the Science Base (National Academy Press, 1999).
The Institute of Medicine prepared this report for the White House
Office of National Drug Control Policy as the “definitive” review
of research on medical marijuana in the US.
This report will focus on four areas of potential risk, the
four major areas in which toxic effects of THC have been suggested:
- acute neurological effects
- brain development
- reproductive system
- immune system
In addition, this report will discuss the scientific methods
of cannabis research, in an attempt to resolve conflicting claims
about health risks.
Much of the discussion in this report is based on two major
reviews of the health risks of THC, one by Dr. Grotenhermen et al.
(THC Limits for Food, nova Institute, 1998) and the other by Dr. Morgan
et al. (Marijuana Myths, Marijuana Facts: A Review of the
Scientific Evidence, Lindesmith Center, 1997), as well as the Institute
of Medicine’s report referenced above. (It is worthy of note that
the Grotenhermen and the Morgan reviews agree in every
significant conclusion; the Institute of Medicine report agrees in
substance, although it is more cautious, calling for further research.)
For critical issues, the primary research is cited.
2.0: THE TOXICOLOGY OF THC
The preponderance of evidence clearly indicates that THC is one
of the least toxic chemicals that humans ingest. At doses achieved
by heavy marijuana users, there is no evidence of genetic damage
or effects on fertility, pregnancy, or offspring. Similarly, there
is no evidence of damage to the hormonal or immune systems.
Research that finds damaging effects of THC generally falls into
one of two categories: 1) studies that are not replicated by
later research using more appropriate experimental designs; and 2)
studies that use massive quantities of THC, far beyond the doses
employed by heavy marijuana users.
2.1: Genetic Effects
In doses typical for consumers of marijuana, THC is not
genotoxic, mutagenic, or carcinogenic, and it has no effect on cell
metabolism. THC does not result in chromosomal breaks.
At extremely high doses applied directly to cells, THC reduces
the synthesis of DNA, RNA, and proteins. These effects are
nonspecific, that is, unrelated to the typical receptor activation in
the human body.
In regard to genotoxic effects, marijuana consumption is
obviously safe for consumers.
2.2: Pregnancy and Offspring
Animal studies of the effects of THC on pregnancy are
inconsistent, even with doses of 10-20 mg/kg, a hundred times higher
than the Lowest Observed Effect Level (LOEL) for psychotropic effects.
A few studies purported to show impairment of cerebral development
in children of chronic cannabis consumers, but these studies were
never replicated and are now discredited. The No Observed Effect
Level (NOEL) for pregnancy variables (parturition, duration of
pregnancy, infantile abnormalities, birth weight) is above the range of
human consumption by chronic marijuana consumers.
There is no realistically demonstrated danger to pregnant women
or their offspring from consumption of marijuana.
2.2.1: Pregnancy
Greenland et al., 1982, found more meconium staining and
longer duration of labour in marijuana users, but this study has never
been replicated, even by Greenland’s lab. For centuries, cannabis
has been used for pain relief during birth. The general
conclusions permitted by the research are that no birth complications
can be observed in mothers who ingest marijuana levels of THC over a
long period of time.
Gibson et al., 1983, found more premature births in marijuana
users, but this study has never been replicated. Most studies find
no marijuana-induced change in the duration of gestation.
2.2.2: Birth defects and brain development
Birth defects associated with THC have been found only in
animal studies in which the THC was injected, in very high doses,
directly into the abdomen. In humans, there is no evidence whatsoever
for a link between marijuana use and fetal malformations or Minor
Physical Anomalies (MPAs).
Studies that show a decreased birth weight in rat pups after
THC ingestion have been clearly discredited. The decrease, when
it occurs (at high doses), is due to reduced food and water intake
of exposed dams; there is no difference between these animals
and pair-fed controls.
Evidence is accumulating that the cannabinoid-anandamide
receptor system might play a role in cerebral development in fetuses
and neonates. Daily administration of 5 mg/kg THC to pregnant
rats doubles the activity of the enzyme tyrosine hydroxilase (TH)
in specific brain cells of their fetuses (Hernandez et al., 1997).
TH is believed to be a key factor in the development of neurons.
In contrast, one animal study has established a disturbance
of mesolimbic dopaminergic neurons among perinatally THC-exposed
males which persists in adult animals (Garcia-Gil et al., 1997).
However, the significance of these data for humans smoking marijuana is
very probably nil.
Animal studies have generally found behavioural problems only at
high doses. For example, no behavioural effects in offspring
were observed after dosing the pregnant rats with 50 mg/kg/day.
Hutchings et al., 1987, found nipple attachment problems in rat
offspring exposed to 50 mg/kg/day, but the problems were clearly
related to decreased food and water intake in the dams; the offspring
of pair-fed controls were indistinguishable from the offspring
of experimental animals.
In humans, the offspring of chronic users show no differences
from normal in sleeping, eating, mental tests, and psychomotor tests.
One researcher (Dreher, 1994, 1997) found the offspring of chronic
users to be more lively and less irritable, with fewer tremors;
these babies were more easily quieted, yet more responsive to
novel stimuli. These results have not been replicated, but they show
the extreme inconsistency of marijuana studies. The more common
finding is, simply, no difference.
Studies that have attempted to find brain damage from THC have
been unsuccessful. Marijuana levels of THC do not kill brain cells.
In one study, monkeys were forced to inhale five marijuana cigarettes
a day for a year; there was no evidence of brain damage (Zimmer
& Morgan, 1997). In humans, with brain damage assessed by CAT
scans, no damage was observed in spite of the high dose: nine
marijuana cigarettes a day.
2.3: Hormonal Systems and Reproductive
Capabilities
Some high-dosage animal studies suggest that THC may act on
the hypothalamus pituitary-adrenal axis and adversely affect the
sex steroid hormones. However, there is no reliable finding of
adverse effects in animals (male or female) within the range of
human consumption of marijuana. The slight effects that sometimes
appear, disappear with repeated doses (tolerance). In humans, no
effects were discovered regarding the function or concentration of
sexual hormones or other parameters relevant for reproduction such as
sperm quantity and quality.
In one representative study, men were dosed with up to 20
marijuana cigarettes a day (!) for a month (Hembree et al., 1979).
The researchers found some decrease in sperm concentrations and
motility. The decreased factors were not outside of “normal” range, and
by the end of the month, the sperm factors had returned to normal,
despite continued dosing.
In men, a few studies found effects of chronic marijuana use
on luteinizing hormone (LH), which is related to
testosterone production, although the effect disappears with time, even
if THC doses remain constant. Other studies found no such LH effect.
There is no effect of THC on testosterone, follicle stimulating
hormone (FSH), or prolactin. There are no effects on puberty.
A representative study (Mendelson et al., 1978) found no effect
of marijuana smoking on testosterone level, in spite of the high
doses: 120 marijuana cigarettes in 21 days.
In women, the conclusions are the same: There are no
reliable effects of THC on the menstrual cycle, estrogen levels,
progesterone, prolactin, LH, or FSH. The few studies of positive
effects involved high-dosage inhalation, effects that quickly
disappeared as tolerance developed.
In some animal studies, THC reduced the level of
adrenocorticotropin (ACTH), which is secreted by the adenohypophysis
and stimulates the production of glucocorticoids (cortisol) in the
suprarenal cortex. This result could not be replicated in human chronic
consumers of marijuana. THC has no effect in humans on the thyroid
hormones or on glucose metabolism.
2.4: Immune System
“Cell experiments and animal studies demonstrate that THC
has suppressive effects on the humoral and cell-mediated
immunity. However, the majority of those can be attributed to toxic
unspecific effects. Many analysed parameters required extremely high
doses to exhibit any significant effect and the effects were
dose-dependent with the threshold concentration being precisely
determinable. When applying lower doses, one often observed
differentially immunostimulating effects or no effects at all. For many
immune parameters the NOEL is … irrelevant to the human
consumption situation. In studies of man or of cells of marijuana users
the effects observed were often contradictory. If such effects
were found at all, they were weak even in case of heavy cannabis use
and of questionable relevance to health. The World Health
Organisation summarised in its most recent cannabis report: ‘Many of
their effects appear to be relatively small, totally reversible after
removal of the cannabinoids, and produced only at concentrations or
doses higher than those required for psychoactivity (WHO, 1997, p.
27)’” (Grotenhermen et al, 1998, p. 53).
2.4.1: Suppression versus enhancement
THC and the immune system is the most thoroughly researched topic
in the area of subliminal biological effects. Much of the
early research, which demonstrated immune system suppression, has
been discredited. For example, Nahas et al. (1974) found that
THC decreases the number of T-lymphocytes - which control
cell-mediated, acquired immunity. Later studies found no such decrease.
Dax et al. (1989), for example, found no change in T- or B-lymphocytes
(humoural immunity) or in T-cell subtypes before, during, or subsequent
to administration of THC to chronic users. Wallace et al.
(1988) reported similar findings, with a twist: an increase in
helper T-cells (CD4). These findings should be interpreted
as immunoenhancement, because helper T-cells stimulate the
proliferation and activation of other immune cells.
Nahas et al. (1977) found in vitro suppression of
T-cell proliferation in response to mitogens, which stimulate cell
division. Other researchers criticized Nahas’s method - applying THC in
massive doses to human cells in a petri dish - and called the
results “meaningless.” Better studies failed to replicate Nahas’s work
and, instead, found immune system stimulation at lower doses (Pross
et al., 1993; Luo et al., 1992).
Let us be clear about these findings: What the research shows
is immune system suppression at very high doses, but immune
system stimulation (enhancement) at low doses. These effects have
been demonstrated for both the T- and B-lymphocytes. This means that
the amounts of THC in marijuana probably strengthen the immune system
of humans. High doses have nonspecific toxic effects, likely the
cause of any damage, whereas low doses act through specific
receptor-based effects. It’s a basic principle of pharmacology: low
doses may be curative whereas high doses are poisonous.
One last point: With an oral dose of THC of 0.1-0.2 mg/kg
(the psychotropic threshold), the blood plasma reaches a
maximum concentration of 3-5 ng/ml. In the cell studies, the
concentration is 10 ug/ml, or 10,000 ng/ml - 2000 to 3000 times the
dose that produces the marijuana “high.”
2.4.2: Humans and disease
Marijuana smokers show an enhanced response to antigens
(which trigger antibodies) compared to cigarette smokers and cancer
patients (Hollister, 1992), which supports the conclusion of THC
strengthening the immune system and casts additional doubt on the high
dosage cell studies. On a more general level. absolutely no
epidemiological evidence exists relating marijuana use and infectious
diseases (Hall et al., 1994). In cancer and AIDS patients, THC is used
to reduce pain and depression, stimulate appetite, and prevent nausea
and vomiting. AIDS patients, who suffer from a damaged immune
system, are not harmed by THC (Di Franco et al., 1996).
2.5: THC and Cancer
Immune-system stimulation by THC at low doses should be apparent
in macro-level health benefits. The stunning (but rarely
reported) success of THC treatments of cancer may be representative.
One of the first studies had rats ingest a large dose (50 mg/kg) of
THC daily for two years. At the completion of the experiment, 70
percent of the dosed animals were still alive, but only 45 percent of
the control (undosed) animals survived. This sizeable difference was
due almost entirely to a reduced incidence of cancer in the animals
given THC (Chan et al., 1996).
A more direct test of THC’s cancer-fighting properties was
performed on rats with brain tumours (Galve-Roperh et al., 2000). The
tumours, called gliomas, are fatal in humans. The researchers infused
THC directly into the rats’ brains. The control rats (no THC) died
in two to three weeks. In a third of the THC-dosed rats, the tumour
was eliminated. Another third lived eight to nine weeks, instead of
the two to three weeks of the control (no THC) rats. A third of
the THC-dosed rats gained no benefit. The researchers claim that the
THC works by stimulating the cancer cells to “commit suicide” in
a natural process called “apoptosis.” Normal cells were unharmed.
The THC in this experiment was very low dosage, and the cancers were at
a late stage, when untreated rats were already starting to die.
The researchers suggest that THC would work even better if given
earlier.
2.6: Miscellaneous Issues
2.6.1: Marijuana use in children
It is true that children generally respond more severely to
chemical toxins; alcohol consumption, for example, is riskier for
children than for adults. But in the case of THC, which operates on
specific receptors, children’s use of marijuana is actually safer
than adult’s use because children have fewer receptors. Children
with cancer, for example, tolerate considerably higher doses of THC
than adults, with no symptoms of psychoactivity (Abrahamov et al.,
1995; Fride & Mechoulam, 1996). A similar study of children with
cancer taking nabilone, a THC analog, found that high doses were
well tolerated: “Particularly for some adolescent patients, it can turn
a five day course of chemotherapy from a dreaded ordeal into
something accepted with a shrug of the shoulders” (Dalzell et al.,
1986).
2.6.2: Cannabinoids other than THC
Anti-marijuana scientists often make the point that there are
66 cannabinoids in marijuana, that THC is only the best known and
most frequently studied. Therefore, even if THC were found safe, one
of the other 65 might be unsafe. This number is misleading.
It represents the sum total of cannabinoids found in detectable
quantity in at least one cannabis variety in at least one study in the
history of cannabis research. The only cannabinoids proven to
be manufactured by the marijuana plant are THC, CBD, CBC,
and (presumably) their common biogenetic precursor, CBG (Pate,
2000). CBD predominates, with an accompanying fraction of THC. CBC is
found in significant quantities only in tropical marijuana. CBG is
found only in very small amounts. To this short list can be added
minor quantities of the THC degradation products, CBN and delta-8 THC.
The remaining 60 cannabinoids exist in almost undetectable amounts -
in fact, usually none at all - in any given sample.
Anti-marijuana researchers admit that CBD poses few risks. CBN is
considered to be “as dangerous as THC,” but the research that “proves”
this is the same research that “proves” that THC is risky. We believe
this research to be problematic, if not invalid.
Since heavy, chronic consumption of whole marijuana has been shown
to be safe, it is highly unlikely that any ingredient of marijuana
would be found to pose health risks.
2.6.3: Health risks of smoking marijuana
Like tobacco smoke, marijuana smoke contains a number of
irritants and carcinogens. Early research showing that lung damage by a
single marijuana cigarette was greater than by a single tobacco
cigarette have been superseded by better research concluding the two
types of smoking are equally harmful. A tobacco smoker, however, may
consume 40 or more cigarettes a day, whereas marijuana smokers are
considered “heavy users” if they consume 5 joints in 24 hours. There
have been zero cases of lung cancer or emphysema attributable to
marijuana smoking.
Because of prohibition, marijuana growers have developed
new varieties with higher levels of THC. Police reports of 30%
abound, but the highest recorded in the research literature is 14%;
the marijuana of the sixties was about 3%. In any case, high levels
of THC actually make marijuana safer, because less smoke need
be inhaled to achieve the “high.”
AIDS patients who use marijuana face an increased risk
of aspergillosis, a pulmonary disease. Aspergillosis is caused
by fungal spores that sometimes develop in improperly stored
marijuana. Careful screening of marijuana supplies for AIDS patients is
a good idea.
It is clear that most of the health risks of marijuana are due to
the method of ingestion: smoking. Other, safer methods, such as
baked goods, are available and should be used by people with lung
disorders.
3.0: THE SCIENCE OF THC RISK ASSESSMENT
There are research reviews that claim no health risks from
marijuana use and there are other reviews that claim just the opposite.
The science of THC is not unlike other areas of science: Science
does not prove anything. It deals in probabilities, and its methods
are designed to estimate the degree of error in an estimate or in
a probabilistic relationship. Most scientists view their procedures
as a search for error, whereas the general public perceives it as
a search for truth. In reality, it is a search for truth by way
of estimating error.
The nature of science is such that one can always argue the
opposite to a suggested proposition, with some evidence in support.
Global warming, for example, is supported by the bulk of the evidence,
but there are enough data leaning toward the opposite conclusion that
the National Post can claim that global warming is a hoax.
Similarly, scientists paid by the tobacco industry can mount a claim,
with data support, that smoking does not cause lung cancer.
When a scientific question has political ramifications (such
as global warming or smoking), the goals of science are often
perverted, as different camps seek to generate evidence for their
position. The US War on Drugs is such a camp. Beginning in the 1960s,
the US government offered scientists millions of dollars to “prove
that marijuana is harmful.” The research cited by opponents of
marijuana decriminalization includes much of this “advocacy science,”
which produced highly misleading conclusions about the effects of
THC.
The following section is, in effect, a manual on how to do advocacy
science.
3.1: Extreme Dosing
The major deficiency with most reports of harm from THC is
the massive doses required to demonstrate such effects. In one
study, monkeys were given the human equivalent of 15 kg of marijuana in
a single dose. Similarly, the petri-dish studies of the effects of
THC on body cells used concentrations 2000 to 3000 times the
threshold level for psychotropic effects.
In a review of the effects of THC on the human immune system
(which found none), the reviewers note that some animals given large
doses do show effects; doses are forty to one thousand times
the psychoactive doses for humans (Zimmer & Morgan, 1997).
Similarly, an attempt to find brain damage in monkeys failed to do so,
in spite of the dose: five marijuana cigarettes a day for a year.
These are extreme examples, but far from rare. Almost all of
the studies that show damage from THC use high to very high doses,
even compared to marijuana levels. When compared to the low doses
from hemp foods and cosmetics, the high-dose studies are
irrelevant.
THC at marijuana levels acts on compound-specific binding
sites (cannabinoid receptors). Only at high concentrations (far
beyond that encountered in marijuana use) do nonspecific, toxic
effects occur. Most if not all chemicals will damage body cells and
systems at high concentrations - for example, numerous deaths have
been recorded in people who for psychiatric reasons drink
excessive amounts of water. And pharmaceuticals that are toxic at
high concentrations are often beneficial at low doses, as seems to be
the case with THC and the immune system.
3.2: Cannabinoid Receptors and Tolerance
The fact that THC at marijuana doses acts not nonspecifically
but, rather, specifically at receptor sites on neurons provides a
further margin of safety for users. For one reason, neurochemical
receptors generally show tolerance - that is, decreasing effect with
repeated or sustained exposure. For most harmful chemicals, the
toxicity increases (and the NOEL decreases) with duration of exposure.
But, with THC, the opposite occurs, because of tolerance. For
example, high doses of THC in female monkeys resulted in hormonal
changes and a disruption of their menstrual cycle. After six months of
high doses, the hormone levels and the menstrual cycles returned to
normal (Smith et al., 1983). Tolerance can be observed in the cases of
most THC effects.
Chronic exposure to THC does not irreversibly alter the
cannabinoid receptors (Westlake et al, 1991).
At marijuana doses, THC’s effects are almost entirely receptor
based, with little or no nonspecific toxicity. This means that even if
a troubling effect of THC were to be established, the risk would
be shortlived.
3.3: Extrapolation from Animal Studies
A major disagreement exists between the camps finding no health
risks of marijuana and those claiming the opposite regarding the value
of animal studies. Many of the risks reported by
anti-marijuana researchers come from studies in which high doses were
given to rats or mice. That’s OK, they say, because of “similarities”
between humans and rodents in the pharmacokinetics and metabolism of
THC and in the brain distribution of cannabinoid receptors.
However, the application of rat data to human risk assessments is
an uncertain and often misleading extrapolation, with numerous
pitfalls. For example, the extrapolation of doses is problematic.
Typically, a dose given to rats is reported in milligrams of THC per
kilogram of body weight. The dose for humans to produce the same
effects is then calculated using the body weight of humans. The average
human weighs about 70 kg. So an effect caused by a 2 mg dose to a rat
weighing 0.2 kg translates to a 700 mg dose to humans (about 50 times
the dose for a human “high”).
This kind of extrapolation may be meaningless, because
many biological processes (e.g., metabolic rate) are unrelated to
body weight. For this reason, some researchers use comparisons of
body surface (mg/m2) instead of body weight. It has been found
that body-surface comparisons predict more accurately human tolerance
for anti-cancer drugs from animal data than do body-weight
comparisons. But body surface is also a poor basis for extrapolation
for many drugs. Other bases include pharmacokinetics (absorption,
metabolism, excretion, etc.) and toxicological estimates such as the
“lethal dose” studies.
The lethal-dose studies are a lesson: In rats, the lethal dose
is around 1300 mg/kg. Extrapolated on the basis of body surface,
the lethal dose in dogs should be about 350 mg/kg and in monkeys,
about 650 mg/kg. But dogs lived after a dose of 3000 mg/kg, and monkeys
survived 9000 mg/kg. The lethal dose in these animals could not be
established. The primates should have been 50 percent more sensitive to
THC than rats, but were at least five to ten times less sensitive. The
extrapolation from rats to higher mammals was wildly inaccurate.
There are significant differences between the reproductive
and hormonal systems of rats and mice and those of humans (Mendelson
and Mello, 1984). Mice, for example, are especially disposed to
fetal malformations. In general, data on smaller animals leads to
highly inaccurate estimates of THC toxicity in larger animals.
Reliable data on the toxicity of marijuana in humans must be based
on studies with human subjects.
3.6: The Fallibility and Abuse of Science
Studies of the effects of THC on humans are inconsistent, for
a number of reasons: Many studies use small samples (that is,
few subjects), and small-sample studies are notoriously unreliable
(that is, inconsistent). For scientific purposes, small-sample studies
are practically worthless. A young man who smokes pot fails to
go through puberty; the child of a pot smoker develops cancer:
These are meaningless anecdotes, although such studies are widely
touted as proof of THC’s dangers.
Most of the marijuana studies on humans compare chronic users
with “matched” control subjects. This experimental design produces
data that are often misleading, because the researchers are comparing
two groups that differ in many ways. True matching is impossible,
since one can never know all the factors that influence the life of a
test subject. For example, many chronic marijuana smokers use other
drugs as well, including cigarettes and alcohol. In addition,
human subjects often lie about their drug use, making assignment to
groups difficult. Results from such studies are often unreliable
or difficult to interpret.
As we’ve mentioned, the US War on Drugs has distorted the
scientific infrastructure and produced a plethora of biased findings. A
study that purports to have found deleterious THC effects is
quickly published, whereas a study that finds THC safe is not. In the
latter case, researchers may suppress the data or peer review
might disparage the experiments (Levy and Koren, 1990). Finally,
if well-designed experiments demonstrating the safety of THC
are published, government publications often ignore them,
focusing instead on the studies that support the official view.
This pseudo-science we have termed “advocacy science.”
True science consists of a search for conclusions to
explain previously established facts, theories to explain observed
data. Advocacy science consists of a search for facts to support
a previously established opinion.
4.0: CONCLUSIONS
Reviews that do show health risks of marijuana are typically based
on poorly-designed research, e.g., using massive doses of THC, far
more than even those levels consumed by the heaviest marijuana
smokers. Every study showing health risks has been discredited or
refuted; cannot be replicated; or has been shown to be in error by a
majority of studies on a given topic.
Apart from potential dangers from nonTHC factors in marijuana
smoke, the best research shows clearly that there are no
substantiated health risks associated with marijuana use. Indeed, there
may well be health benefits (in addition to the proven benefits of
medical marijuana), as marijuana levels of THC seem to strengthen the
immune system.
Laws prohibiting marijuana on the basis of health risks cannot
be justified by the research literature.
5.0: REFERENCES
Abrahamov, A., Abrahamov, A. & Mechoulam. R. (1995). An
efficient new cannabinoid antiemetic in pediatric oncology. Life Sci.,
56, 2097-2102.
Chan, P.C., Sills, R.C., Braun, A.G., Haseman, J.K., & Bucher,
J.R. (1996). Toxicity and carcinogenicity of delta
9-tetrahydrocannabinol in Fischer rats and B6C3F1 mice. Fundam. Appl.
Toxicol., 30, 109-117.
Dalzell et al. (1986). Cited by Grotenhermen, Cannabinoid
receptors in children and adults. Personal communication, 2000.
Dax, E.M., Pilotte, N.S., Adler, W.H., Nagel, J.E., & Lange,
W.R. (1989). The effects of 9 ene-tetrahydrocannabinol on hormone
release and immune function. J. Steroid Biochem., 34, 263-270.
Di Franco, M.J., Shepard, H.W., & Hunter, D.J. (1996). The lack
of association of marijuana and other recreational drugs
with progression to AIDS in the San Francisco mens’s health study.
Ann. Epidemiol., 6, 3283-3289.
Dreher, M.C., Nugent, K., Hudgins, R. (1994). Prenatal
marijuana exposure and neonatal outcomes in Jamaica: an ethnographic
study. Pediatrics, 93, 254-260.
Dreher, M.C. (1997). Cannabis and pregnancy. In M.L. Mathre
(Ed.), Cannabis in medical practice. McFarland.
Fride, E., & Mechoulam, R. (1996). Ontogenetic development of
the response to anandamide and delta 9–tetrahydrocannabinol in
mice. Brain Res. Dev. Brain Res., 95((1), 131-134.
Galve-Roperh, I., et al. (2000). The effect of THC on
gliomas. Nature Medicine, March.
Garcia-Gil, L., De Miguel, R., Munoz, R.M., Cebeira, M.
Villanua, M.A., Ramos, J.A., & Fernandez-Ruiz, J.J.
Perinatal delta(9)-tetrahydrocannabinol exposure alters the
responsiveness of hypothalamic dopaminergic neurons to dopamine-acting
drugs in adult rats. Neurotoxicol. Teratol., 19, 477-487.
Gibson, G.T., Baghurst, P.A., & Colley, D.P. (1983).
Maternal alcohol, tobacco and cannabis consumption and the outcome
of pregnancy. Aust. N.Z. J. Obstet. Gynaecol., 23, 15-19.
Greenland, S., Staisch, K.J., Brown, N., & Gross, S.J. (1982).
The effects of marijuana use during pregnancy. I. A
preliminary epidemiologic study. Am. J. Obstet. Gynecol., 143,
408-413.
Grotenhermen, F., Karus, M., & Lohmeyer, D. (1998). THC limits
for food. nova Institute, Hurth, Germany.
Hall, W., Solowij, N., & Lemon, J. (1994). The health
and psychological consequences of cannabis use. Commonwealth
Department of Human Services and Health, Monograph Series No. 25,
Canberra.
Hembree, W.C., et al. (1979). Changes in human
spermatozoa associated with high dose marihuana smoking. In G. Nahas
& W. Paton (Eds.), Marihuana: Biological effects. Pergamon
Press.
Hernandez, M.L., Garcia-Gil, L., Berrendero, F., Ramos, J.A.,
& Fernandez-Ruiz, J.J. (1997). Delta 9-tetrahydrocannabinol
increases activity of tyrosine hydroxylase in cultured fetal
mesencephalic neurons. J. Mol. Nerosci., 8, 83-91.
Hollister, L.E. (1992). Marijuana and immunity. J.
Psychoactive Drugs, 24, 159-164.
Hutchings, D.E., Brake, S., Morgan, B., Lasalle, E., & Shi,
T.M. (1987). Developmental toxicity of
prenatal delta-9-tetrahydrocannabinol: Effects of maternal
nutrition, offspring growth, and behavior. NIDA Res. Monogr., 76,
363-369.
Institute of Medicine. (1999). Marijuana and medicine: Assessing
the science base. National Academy Press.
Levy, M., & Koren, G. (1990). Obstetric and neonatal effects of
drugs of abuse. Emerg. Asp. Drug Abuse, 8, 633-652.
Luo, Y.D., Patel, M.K., Wiederhold, M.D., & Ou, D.W. (1992).
Effects of cannabinoids and cocaine on the mitogen-induced
transformations of lymphocytes of human and mouse origins. Int. J.
Immunopharmacol., 14, 49-56.
Mendelson, J.H., Ellingboe, J., Kuehnle, J.C., & Mello, N.K.
(1978). Effects of chronic marihuana use on integrated plasma
testosterone and luteinizing hormone levels. J. Pharmacol. Exp. Ther.,
207, 611-617.
Mendelson, J.H., & Mello, N.K. (1984). Effects of marijuana
on neuroendocrine hormones in human males and females. NIDA
Res. Monogr., 44, 97-114.
Nahas, G.G., Morishima, A., & Desoize, B. (1977). Effects
of cannabinoids on macromolecular synthesis and replication of
cultured lymphocytes. Fed. Proc., 36, 1748-1752.
Nahas, G.G., Suciu-Foca, N., Armand, J.P., & Morishima, A.
(1974). Inhibition of cellular mediated immunity in marihuana
smokers. Science, 183, 419-420.
Pate, D. (2000). The number of cannabinoids in hemp foods
and cosmetics. Personal Communication.
Pross, S.H., Nakano, Y., McHugh, S., Widen, R., Klein, T.W.,
& Friedman, H. (1992). Contrasting effects of THC on adult murine
lymph node and spleen cell populations stimulated with mitogen or
anti-CD3 antibody. Immunopharmacol. Immunotoxicol., 14, 675-687.
Smith, C.G., Almirez, R.G., Berenberg, J., & Asch, R.H.
(1983). Tolerance develops to the disruptive effects of
delta 9-tetrahydrocannabinol on primate menstrual cycle. Science,
219, 1453-1455.
Wallace, J.M., Tashkin, D.P., & Oishi, J.S. (1988). Peripheral
blood lymphocytes subpopulations and mitogen responsiveness in tobacco
and marijuana smokers. J. Psychoactive Drugs, 20, 9-14.
Westlake, T.M., Howlett, A.C., Ali, S.F., Paule, M.G., Scallet,
A.C., & Slikker, W. (1991). Brain Research, 544(1), 145-149.
WHO. (1997). Cannabis: A health perspective and research
agenda. World Health Organization.
Zimmer, L., & Morgan, J. P. (1997). Marijuana myths, marijuana
facts: A review of the scientific evidence. The Lindesmith
Center. Return to Medical Research Index
|
|