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Carl Olsen's Marijuana Archive
The Scientific And Legal Basis
for the End of Marijuana Prohibition

by Jon Gettman

        The Controlled Substances Act mandates that schedule I drugs have a
"high potential for abuse."  A judicious reading of both the statute and
the legislative history finds that this abuse potential is the key
criterion for its scheduling under the CSA.(NORML v. DEA, 559 F.2d 735
(1977))(21 USC  812 (b)(1))  However, it has long been recognized that
marijuana does not satisfy this essential criterion.  Therefore the
justification for marijuana's continued placement in schedule I is a
presumption rather than a finding.(See U.S. Cong. and Admin. News 1970 p.
4578, p. 4579, p. 4629. See also 51 FR 22947 (1986))

        As of April, 1995, the Drug Enforcement Administration was "unaware
of any new scientific studies of marijuana that would lead [them] to
re-evaluate its classification at this time."  According to a letter from
Thomas Constantine, Administrator of DEA, if this author "has access to
scientific data concerning marijuana which he wishes to bring to our
attention, we will be pleased to consider it, should he care to share the
documentation with us."  Extensive documentation was provided to
Constantine on July 10, 1995 as part of an administrative petition
subjecting DEA's consideration of these issues to judicial review.

        The CSA establishes an eight item list of scientific and medical
factors that are to be considered in scheduling decisions. (21 USC 822 (c))
These factors are defined further in the legislative history.(see U.S.
Cong. and Admin. News 1970 p 4601 - 4603)

        The first factor is the drug's relative or actual potential for
abuse.  The contemporary paradigm for evaluating the abuse potential of a
drug has been developed by the Committee on the Problems of Drug
Dependence.[7]  They have concluded that self-administration in animal
studies is the necessary characteristic of a drug with a significant,
severe potential for abuse.[3, 7, 21, 32]  However, animals will not self
administer marijuana.[1, 17, 32]

        The second factor is evidence of the drug's pharmacological
effects.  In 1989 Leo Hollister remarked that: "Our studies of cannabinoids
over the past 22 years have touched upon virtually every aspect of their
actions.  They constitute the largest series of studies of the human
pharmacology of marijuana on record."[15]  Since then further research by
the likes of Donald Tashkin, Mario Perez-Reyes, Julian Azorlosa, for
example, have supplemented the classic work on the chemistry and
pharmacology of marijuana by Agurell, Dewey, Hollister, Martin, Mechoulam,
and Razdan.

        The third factor considered in scheduling decisions is scientific
knowledge about the substance.  In 1988, it became obvious that scientists
had been wrong in their theories about how marijuana acted on the
brain.[17, 18, 27]  Recent Evidence affirms that marijuana activates a
unique receptor system in the brain.[16, 17, 18, 31]  In another
current finding, it has been discovered that tolerance to marijuana is the
result of receptor down-regulation, rather than receptor desensitization as
was previously believed.[25, 29]  In addition, the theory that marijuana's
lipophilic qualities produce a harmful effect has also been
contradicted.[22, 30]  The receptor has been cloned[23], an endogenous
ligand for the cannabinoid receptor has been discovered[9], and an orally
effective cannabinoid antagonist has been created.[28]

        The fourth factor is the history and current pattern of abuse,
including "social, economic, and ecological characteristics of the segments
of the population involved in such abuse."  Critical evaluations of the
National Household Survey, the Monitoring the Future Project, the Drug
Abuse Warning Network and other federally sponsored reports provide more
than adequate data to evaluate this factor.  Key observations are that
marijuana use and adolescent access persist despite increased enforcement.
Moreover, the National Household Survey indicates that risk perception
associated with marijuana use decreases as education and age increase.[34]

        The most interesting factor for advocates of harm reduction
policies, though, is the fifth factor: scope duration and significance of
abuse.  According to the legislative history, "in reaching [her] decision,
the Attorney General should consider the economics of regulation and
enforcement attendant to [a scheduling decision].  In addition, [she]
should be aware of the social significance and impact of such a decision
upon those people, especially the young, that would be affected by it."

        This fifth factor allows the introduction of several critical
issues, such as the impact of schedule I status and enforcement policies
have on the private therapeutic use of marijuana[12] as well as their
effects on the cultivation of marijuana for medicinal or personal use[11].
This factor also allows the introduction of cost/benefit analyses of
decriminalization laws in various states[2], as well as the evaluations of
various state legislatures on the significance of marijuana abuse as it is
reflected in the scheduling of the substance under state law.[24]

        The sixth factor concerns the risk, if any, to public health.  "If
a drug creates no danger to the public health, it would be inappropriate to
control the drug under this bill." A recent editorial in favor of harm
reduction policies in the American Journal of Public Health calls for
development of "a new system that is consistent with present scientific
knowledge and able to incorporate new scientific findings."[8]  The
Controlled Substances Act provides such a system, and reformers should try
and make the CSA work the way it was intended to before contemplating a new
system.  This factor alone allows for the introduction of harm reduction
policies into scheduling and national drug policy.

        The reputed threat to public health presented by marijuana is a
result of the drug's perceive relation to the use of other dangerous drugs.
The contemporary gateway theory, though, acknowledges that alcohol and
cigarette use precede marijuana use, and that marijuana use does not
predict in any way use of more serious drugs.[6, 20, 33, 35, 36]
Consequently, the policy ramification of the gateway theory is that the
public health would benefit from successful policies that delay the age of
first use of any drugs.[20]  Why is marijuana singled out?

        Norman Zinberg clarified the relationship of drug, set, and setting
to the understanding and treatment of drug use and abuse in 1984.[37]  An
emerging public health model that advocates harm reduction, the study of
use and abuse, and performance evaluation is evidence of gaining
recognition for the utility of Zinberg's ideas.[13, 34]  A meta-analysis of
correlations between school-aged use of alcohol, marijuana and tobacco
conducted by the Bowman Gray School of Medicine concluded that the primary
correlates of school aged drug use were prior use and access.[13]

        There is considerable social science data and theory to support the
rescheduling of marijuana under these last two factors representing the
epidemiology and the significance of a drug's actual use in the population.

        The animal models used to determine the abuse potential of a drug
represent synergy between pharmacology and root behavioralism.[4]  Despite
their excellent predictive validity, they do not present a biological
marker.  This lack of a biological clarification of marijuana's abuse
potential has been the excuse to keep marijuana in schedule I.  The
discovery of the cannabinoid receptor system annihilates that excuse.

        The seventh factor is the substances physic or physical dependence
liability.  It has been long recognized that marijuana is not physically
addictive.[1, 14, 17]

        Advances in neurobiology have provided a biological model for
explaining substance abuse.[19, 21, 33]  Drugs of abuse affect the
production of dopamine, a neurotransmitter associated with response and
reward and now held to explain the compulsive self-administration of
drugs.[10, 19, 21, 33]

        However, cannabinoid receptors are not located on dopamine
producing neurons.[17]  In vivo microdialysis has shown that unlike other
drugs[10] THC, the active chemical in marijuana, does not affect striatal
dopamine levels.[55]  (Earlier research that had indicated a cannabinoid
effect on dopamine was found to be strain-specific, and has not been
replicated in other animal studies.[1, 17, 33])

        Heroin (schedule I), cocaine (schedule II) and amphetamines
(schedule III) all affect dopamine production.  Marijuana, cannabinoids,
and THC do not.  Where shall we schedule marijuana under existing
provisions of controlled substances act?

        The eighth factor concerns the relation of the substance to other
scheduled chemicals.  The discovery of the receptor system provides the
scientific basis for considering cannabinoids as a family with a similar
mechanism of action.  This is especially accurate with regards to the
drug's dependence potential.  Scientists have long accepted the validity of
assertions about marijuana based on research on its constituent parts, such
as THC, cannabinol, marijuana smoke, and experimental cannabinoids.

        There is no basis for distinguishing between the marijuana and THC
in a consideration of dependence potential.

        As a result of this and other information, I believe that
marijuana, cannabinoids, and THC should be removed from schedules I and II,
and I have begun the administrative proceedings to consider this issue.

        By law, petitions for rulemaking changes are sent to the DEA.(21
CFR 1308.44)  The DEA then forwards the petition to the Department of
Health and Human Services for a scientific and medical evaluation that is
binding on DEA in regards to scheduling decisions.(21 USC  811 (b))  The
Court of Appeals has ruled that petitions must be judged on merit.(NORML v.
DEA, 559 F.2d 735 (1977))

        The United States has an international obligation under various
treaties to verify this information and take steps to change the
international scheduling of marijuana.  Meanwhile, the subject of where
marijuana should be scheduled pending treaty amendment is open for debate.

        Twenty five years ago the government acknowledged marijuana did not
deserve schedule I status. Unfortunately, however, it decided to wait for
more evidence before ending marijuana prohibition.  The scientific evidence
has been mounting ever since, and none of it legitimately supports
marijuana's schedule I status.

        Justice delayed is justice denied.  The time has come for an end to
marijuana prohibition, and to acknowledge that for the last 25 years
marijuana users have been denied equal protection under the laws of the
United States and its Constitution.

        (Jon Gettman is a former National Director of NORML, and is
currently enrolled in a doctoral program in the Institute of Public Policy
at George Mason University. His present research agenda concerns regional
development and the agricultural and industrial technologies required for
hemp-related development.  The petition for repeal was the result of a
research agenda concerning the policy implications of recent findings about
the cannabinoid receptor system.)

Author's note:  The complete text of the petition for repeal will soon be
available at the web site of the National Organization for the Reform of
Marijuana Laws, http://norml.myhouse.com/.


[1] Abood, M., Martin, B. (1992), "Neurobiology of Marijuana Abuse," Trends
in Pharmacological Sciences 13:201-206,.

[2] Aldrich, M., Mikuriya, T. (1988),  Savings in California Marijuana Law
Enforcement Costs Attributable to the Moscone Act of 1976 -- A Summary.
Journal of Psychoactive Drugs.  Jan-Mar 1988 20(1):75-81.

[3] Brady, J. (1988) "The Reinforcing Functions of Drugs and Assessment of
Abuse Liability."  In: Problems of Drug Dependence, 1987.  Proceedings of
the 49th Annual Scientific Meeting, The Committee on Problems of Drug
Dependence, Inc.  Harris, L. (ed), National Institute on Drug Abuse
Research Monograph 81.  Washington, D.C.: U.S. Govt. Print. Off., 1988.
pp. 440 - 456.

[4] Brady, J.  What's a Radical Behaviorist Like You Doing in a nice
Pharmacology Club like CPDD?  In: Problems of Drug Dependence, 1992.
Proceedings of the 54th Annual Scientific Meeting, The Committee on
Problems of Drug Dependence, Inc.  Harris, L. (ed), National Institute on
Drug Abuse Research Monograph 132.  Washington, D.C.: U.S. Govt. Print.
Off., 1993.  pg. 19 -28.

[5] Castaneda, E., Moss, D.E., et al. (1991) "THC Does Not Affect Striatal
Dopamine Release:  Microdialysis in Freely Moving Rats"  Pharmacology,
Biochemistry & Behavior, Vol. 40, pp. 587-591.

[6] Chen, K., Kandel, D. (1995) "The Natural History of Drug Use from
Adolescence to the Mid Thirties in a General Population Sample.  American
Journal of Public Health, January 1995. 85:41-47.

[7] Cicero, T. (1992) Assessment of Dependence Liability of Psychotropic
Substances:  Nature of the Problem and the Role of the College on Problems
on Drug Dependence.  Contractor Document for the Office of Technology
Assessment. (Springfield, VA: National Technical Information Service.
1992.) (NTIS Doc. #PB94-175643)

[8] Des Jarlais, D. (1995)  "Editorial: Harm Reduction--A Framework for
Incorporating Science into Drug Policy."  American Journal of Public
Health.  January 1995, 85:1 pg. 10-12.

[9] Devane, W., Dysarz, F., et al (1992)  Isolation and structure of a
brain constituent that binds to the cannabinoid receptor.  Science 258:

[10] Di Chiara, G. and Imperato, A. (1988), "Drugs abused by humans
preferentially increase synaptic dopamine concentrations in the mesolimbic
system of freely moving rats."  Proc. Natl. Acad. Sci., 85:5274.

[11] Gettman, J. (1993) Cannabis Suppression and Marijuana Crop Value.
Washington, D.C.:NORML.

[12] Grinspoon, L. (1993) Marihuana, The Forbidden Medicine.  New Haven:
Yale University Press.

[13] Hansen, W. (1994), Drug abuse in Schools: Contributing Factors and
Preventive Interventions. Springfield, VA: National Technical Information
Service. (PB#94-175635)  1994.

[14] Hollister, L.E. (1986), "Health Aspects of Cannabis", Pharmacological
Reviews, 38:1, 1-20.

[15] Hollister, L. (1989)  "Peregrinations Among Drugs of Dependence:
Nathan B. Eddy Memorial Award Lecture."  In: Problems of Drug Dependence,
1989.  Proceedings of the 49th Annual Scientific Meeting, The Committee on
Problems of Drug Dependence, Inc.  Harris, L. (ed), National Institute on
Drug Abuse Research Monograph 95.  Washington, D.C.: U.S. Govt. Print.
Off., 1990.  pgs. 36-43.

[16] Herkenham, M., Lynn, A.B. et al.(1990), "Cannabinoid Receptor
Localization in Brain,"  Proceedings of the National Academy of Sciences,

[17] Herkenham, M. (1992), "Cannabinoid Receptor Localization in Brain:
Relationship to Motor and Reward Systems,"  P.W. Kalivas and H.H.Samson
(eds), The Neurobiology of Drug and Alcohol Addiction, Annals of the
American Academy of Sciences.  654:19-32.

[18] Howlett, A.C., Bidaut-Russell, et al (1990),  "The Cannabinoid
Receptor:  Biochemical, anatomical, and behavioral characterization."
Trends in Neuroscience  13:10, 420-423.

[19] Izenwasser, S., Kornetsky, C. (1992) "Brain-Stimulation Reward: A
Method For Assessing the Neurochemical Bases Of Drug-Induced Euphoria." In
Watson, R.A.  (1992) Drugs of Abuse and Neurobiology.  Boca Raton: CRC

[20] Kandel, D.B., Yamaguchi, K., Chen, K. (1992), "Stages of Progression
in Drug Involvement from Adolescence to Adulthood:  Further Evidence for
the Gateway Theory."  J. Stud. Alcohol 53: 447-457, 1992.

[21] Koob, G. (1995)  Animal Models of Drug Addiction.  In Bloom, F.,
Kupler, D. (eds.) Psychopharmacology: The Fourth Generation of Progress.
New York: Raven Press.  pgs. 759 - 772.

[22] Lynn, A.B., and Herkenham, M. (1993), "Localization of Cannabinoid
Receptors and Nonsaturable High-Density Cannabinoid Binding Sites in
Peripheral Tissues of the Rat:  Implications for Receptor-Mediated Immune
Modulation by Cannabinoids"  Journal of Pharmacology and Experimental
Therapeutics, 268:3  1612-1623.

[23] Matsuda, L., Lolait, S., et al (1990) Structure of a cannabinoid
receptor and functional expression of the cloned cDNA.  Nature 346:561-564.

[24] National Criminal Justice Association (1991) A Guide to State
Controlled Substances Acts.  Washington, D.C.: National Institute of
Justice.  NIJ Ref No. 132321.

[25] Oviedo, A., Glowa, J, and Herkenham, M.(1993), "Chronic cannabinoid
administration alters cannabinoid receptor binding in rat brain: a
quantitative autoradiographic study." Brain Research, 616:293-302.

[26] Pertwee, R. (1993)  The Evidence for the Existence of Cannabinoid
Receptors.  General Pharmacology. 29:4 pg 811-824.

[27] Richardson, S., Mirasedeghi, S., et al (1990).  "Synthetic and
Biological Studies of Potential Affinity Ligands for the Cannabinoid
Receptor Based on CP-55,244."  In: Problems of Drug Dependence, 1990.
Proceedings of the 52th Annual Scientific Meeting, The Committee on
Problems of Drug Dependence, Inc.  Harris, L. (ed), National Institute on
Drug Abuse Research Monograph 105.  Washington, D.C.: U.S. Govt. Print.
Off., 1990. pgs. 140 - 146.

[28] Rinaldi-Carmona, M., Barth, F., et al (1994). "SR141716A, a potent and
selective antagonist of the brain cannabinoid receptor.  FEBS Letters 350
(1994) pg 240 - 244.

[29] Rodriguez De Foncesa, F., Gorriti, M., et al (1994) Downregulation of
Rat Brain Cannabinoid Binding Sites After Chronic D9-Tetrahydrocannabinol
Treatment.  Pharmacology, Biochemistry, and Behavior.  47:33-40.

[30] Thomas, B., Compton, D., Martin, N. (1990)  Characterization of the
Lipophilicity of Natural and Synthetic Analogs of D9-Tetrahydrocannabinol
and Its Relationships to Pharmacological Potency. Journal of Pharmacology
and Experimental Therapeutics .  255:2 pgs. 624 - 630.

[31] Thomas, B., Wie, X., Martin, B. (1992)  Characterization and
Autoradiographic Localization of the Cannabinoid Binding Site in Rat Brain
Using [3H]11-OH-D9-THC-DMH.  Journal of Pharmacology and Experimental
Therapeutics .  263:3 pgs. 1383 - 1390.

[32] U.S. Congress, Office of Technology Assessment (1993), Biological
Components of Substance Abuse and Addiction, OTA-BP-BBS-117 (Washington,
DC: US Government Printing Office, September 1993).

[33] U.S. Congress, Office of Technology Assessment (1994) Technologies for
Understanding and Preventing Substance Abuse and Addiction, OTA-EHR-597
(Washington, DC: U.S. Government Printing Office, September 1994).

[34] U.S. Department of Health and Human Services, Public Health Service,
Substance Abuse and Mental Health Services Administration, Office of
Applied Studies. (1994)  Advance Report Number 5. Preliminary Estimates
From the Drug Abuse Warning Network.  Rockville, MD: SAMSHA.  March, 1994.

[35] Yamaguchi, K., Kandel, D. (1984) "Patterns of Drug Use From Adolesence
to Young Adulthood: II. Sequences of Progression."  American Journal of
Public Health 74:7, July, 1984.

[36] Yamaguchi, K., Kandel, D. (1984) "Patterns of Drug Use From
Adolescence to Young Adulthood: III. Predictors of Progression."  American
Journal of Public Health 74:7, July, 1984.

[37] Zinberg, N. (1984) Drug, Set, and Setting.  New Haven: Yale University

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