Medical Attributes of Cannabis sativa - Marijuana
by John Brady, Rachel Curtis, and Jared Nothstein
Wilkes University
Wilkes-Barre, PA
May, 2009
Commonly known as marijuana, hemp, pot, hashish, grass, or Mary Jane
(USDA 2009), Cannabis sativa
is a sprawling herb that is a member of the hemp family,
Cannabaceae. Thought to have evolved in China (Mikuriya 1969), it
was introduced to the United States as early as 1629 (Boyce 1900, cited
in Haney and Kutcheid 1975). It can now be found growing
throughout North America. As of 2009, five states listed the
plant as a noxious weed (USDA 2009).
Marijuana has been used as a medicinal plant throughout recorded
history. Chinese and Indian cultures used it since at least 1000
BCE (Mikuriya 1969), while Nicholas Culpeper included it in The English
Physician (Hosking and Zajicek 2008). It was used to treat
complaints such as whooping cough, asthma, pain, and as a sedative
(Fankhauser 2002 cited in Zuardi et al 2006).
In the US, the plant may have originally been cultivated for use as a
fiber and oilseed crop (Ranalli 1999). However, it was also known
for its ability to produce psychoactive effects. In the 1930s, it
was used throughout the Southern United States (Mikuriya 1969) and its
notorious reputation as a psychoactive was broadened in the 1960s, when
widespread use by young adults led to greater public and scientific
interest in the drug (Jones 1977). Since, 1970, marijuana has
been considered a Schedule I substance under the Controlled Substances
Act, defined as a drug “with no recognized medical use and great
potential harm to the user” (Courtwright 2004, Lundberg 2005). A
great deal of research has been conducted pertaining to the medicinal
benefits of Cannabis, particularly since the discovery of the active
compounds and their respective receptors (Kalant 2008).
Cannabis sativa contains cannabinoid compounds, a group of
terpenophenolic compounds that are secondary metabolites (Capasso et
al. 2008). Cannabinoids are structurally related, and include
cannabinol, cannabidiol, and Δ9-tetrahydrocannabinol (THC),
all of which bind cannabinoid receptors throughout the body (Capasso et
al. 2008). Cannabinoid receptors are divided into CB1 and CB2:
CB1 receptors are mainly found in the brain, but they can also be found
in the kidneys, lungs, and liver (Brown 2007). CB2 receptors are
found in the immune system and hematopoietic cells (Brown 2007).
CB1 and CB2 are G-protein receptors, and when activated by
cannabinoids, affect many intracellular structures such as calcium
channels and protein kinase A (Takahashi et al. 2006) (Brown 2007).
Benefits of cannabinoids include the suppression of inflammation and
various types of cell-mediated immunity (Weiss et al. 2006). A
study by Capasso et al (2008) found that cannabidiol selectively
reduced hypermotility and spasms caused by induced inflammation in the
small intestines of mice, making it a possible promising treatment for
the symptoms of inflammatory bowel disease.
Due to recent research suggesting a link between THC and Alzheimer’s, Cannabis sativa may be a new mode
of treatment for Alzheimer’s disease (Pacher et al 2006). The
mode of action for THC consists of competitive inhibition of the enzyme
acetylcholinesterase (AChE). Moreover, THC inhibits AChE-induced
amyloid β-peptide (Aβ) aggregation, the prime pathological marker of
Alzheimer’s disease (Eubanks et al 2006). Ultimately, marijuana
may be able to slow the progression of the disease and may serve as
another mode of treatment for Alzheimer’s disease.
The cannabinoid compounds are an effective treatment for glaucoma
(Tomida, et al 2004). Cannabinoids lower intraocular pressure
(IOP) by acting as vasodilators on blood vessels of the anterior uvea,
thus relieving the symptoms of glaucoma (Tomida, et al 2004).
However, THC produces side effects, which currently exclude it as the
preferred treatment for glaucoma because other drugs are as effective
without producing side effects. Side effects of Cannabis include reduction in
systemic blood pressure and psychotropic effects (Tomida et al 2004).
Cannabis may also play a role
in relieving nausea and vomiting of cancer patients undergoing
chemotherapy. This was proven through use of dronabinol, which is
a synthetic form of THC approved by the US Food and Drug Administration
(Galve-Roperh et al 2000, cited in Frazzetto 2003). Dronabinol has also
been administered to increase the appetite of AIDS patients, so as to
treat their anorexia and weight loss (Galve-Roperh et al 2000, cited in
Frazzetto 2003). THC may also be involved in treatment of
malignant brain tumors; when THC was injected into malignant brain
tumors in rats, the tumors were eliminated (Galve-Roperh et al 2000,
cited in Frazzetto 2003). Another area of therapeutic benefit may
involve the ability of Cannabis to treat symptoms of multiple
sclerosis, including muscle spasms and spasticity (Baker et al 2000,
cited in Frazzetto 2003).
Side effects of cannabinoids include mood changes, respiratory and
cardiovascular risks, and impairments of psychomotor performance
(Ashton 2001). Other side effects include anxiety and orthostatic
hypotension (Kalant 2008). The cannabinoids, however, vary in
their psychoactivity: cannabinol is much less active than THC, and
cannabidiol does not produce any psychoactivity (Hosking and Zajicek
2008). Moreover, clinical trials have suggested the use of
cannabidiol as a safe alternative treatment for schizophrenia. (Zuardi
et al. 2006) The addictiveness of marijuana is also of concern: some
report that withdrawal symptoms for marijuana resemble the symptoms of
abstinence from alcohols and opiates. They include nausea,
vomiting, confusion, tachycardia, and sweating (Hasking and Zajicek
2008).
While Cannabis
has been found to confer many beneficial qualities, the fact that it is
an illegal substance in the US, and has a variety of side effects must
also be taken into serious consideration. Since 1996, laws in
eight states allowed the medical use of marijuana. However, in
2001, the Supreme Court ruled that marijuana is an illegal drug despite
state laws (Horn et al 2001). As of 2009, the law prohibits the
use of marijuana, even in medical cases. Even if research does
suggests a benefit to health from using marijuana, the legalization of
the plant is hotly debated (Annas 1997, Watson et al. 2000, Robson
2001,
Taylor 2003). However, with advances in techniques of separation
of beneficial compounds from hallucinogenic compounds, and the ability
to test each compound found in the plant, it may be possible in the
future to selectively extract certain compounds from the plant for use
as medicinals.
LITERATURE CITED
Annas, G.J. 1997. Reefer Madness—The Federal response to
California’s medical-marijuana law. Legal Issues in Medicine.
337:435-439.
Ashton, C.H. 2001. Pharmacology and effects of cannabis: a
brief review. British Journal
of Psychiatry. 178:101-106.
Baker, D., G. Pryce, J.L. Croxford, P. Brown, R.G. Pertwee, J.W.
Huffman, & L. Layward. 2000. Cannabinoids control spasticity
and tremor in a multiple sclerosis model. Nature. 404:84-87.
Brown, A. 2007. Novel cannabinoid receptors. British Journal of Pharmacology.
152:5; 567-575.
Capasso, R, F. Borrelli, G. Aviello, B. Romano, C. Scalisi, F. Capasso,
& A.A. Izzo. 2008. Cannabidol, extracted from Cannabis sativa, selectively
inhibits inflammatory hypermotility in mice. British Journal of Pharmacology.
154:1001-1008.
Courtwright, D.T. 2004. The Controlled Substances Act: how
a “big tent” reform became a punitive drug law. Drug and Alcohol Dependence.
76:1; 9-15.
Eubanks, L.M., C.J. Roger, A.E.Beuscher, G.F. Koob, A.J. Olson, T.J.
Dickerson, & K.M. Janda. 2006. A molecular link between the
active component of marijuana and Alzheimer’s disease pathology. Mol. Pharm. 3:6; 773-777.
Fankhauser, M. History of cannabis in Western Medicine.
2002. In: Grotenhermen, F. & E. Russo. Cannabis and Cannabinoids.
The Haworth Integrative Healing Press, New York. 37-51.
Frazzetto, G. 2003. Does marijuana have a future in
pharmacopeia? European
Molecular Biology Organization. 4:7;651-653.
Galve-Roperh, I, C. Sanchez, M.L. Cortes, T. Gomez del Pulgar, M.
Izquierdo, & M. Guzman. 2000. Anti-tumoral action of
cannabinoids: involvement of sustained ceramide accumulation and
extracellular signal-regulated kinase activation. Nature Med. 6:313-319.
Haney, A. & B.B. Kutscheid. 1975. An ecological study
of naturalized hemp (Cannabis sativa
L.) in East-Central Illinois. The
American Midland Naturalist. 93: 1-24.
Horn, C.H., S. Althoff, & M. Nachatelo. 2001. Medical
marijuana’s legal battle: eight states okay the medical use of
marijuana. The Supreme Court thinks it’s a bad idea. Here’s
where the issue stands. Natural Health. Accessed 5 May
2009. http://findarticles.com/p/articles/mi_m0NAH/is_6_31/ai_80088274/.
Hosking, R.D. & J.P. Zajicek. 2008. Therapeutic
potential of cannabis in pain medicine. British Journal of Anaesthesia.
101:1; 59-68.
Jones, H.C. 1977. Sensual Drugs: deprivation and
rehabilitation of the mind. CUP
Archive. 373 pp.
Kalant, H. 2008. Smoked Marijuana as Medicine: Not Much
Future. Clinical Pharmacology
& Therapeutics. 83:4; 517-519.
Lundberg, G.D. 2005. It is time for marijuana to be
reclassified as something other than a Schedule I Drug. MedGenMed. 7:3; 47.
Mikuriya, T.H. 1969. Marijuana in medicine: past, present
and future. Calif. Med.
110:1; 34-40.
Pacher, P, S. Batkai, & G. Kunos. 2006. The
endocannabinoid system as an emerging target of pharmacotherapy. Pharmacol Rev. 58:3; 389-462.
Ranalli, P. 1999. Advances
in hemp research. Haworth Press. New Jersey.
272 pp.
Robson, P. 2001. Therapeutic aspects of cannabis and
cannabinoids. The British
Journal of Psychiatry. 178:107-115.
Takahashi, K. & P. Castillo. 2006. The CB1 cannabinoid
receptor mediates glutamatergic synaptic suppression in the
hippocampus. Neuroscience.
139: 795-802.
Taylor, D.R. 2003. Respiratory health effects of cannabis:
Position statement of the Thoracic Society of Australia and New
Zealand. Internal Medicine
Journal. 33: 310-313.
Tomida, I., R.G. Pertwee, & A. Azuara-Blanco. 2004.
Cannabinoids and glaucoma. Br
J Ophthalmol. 88:708-713.
USDA, NRCS. The PLANTS Database (http://plants.usda.gov/java/profile?symbol=CASA3,
12 April 2009). National Plant Data Center, Baton Rouge, LA
70874-4490 USA.
Watson, S.J., J.A. Benson, & J.E. Joy. 2000. Marijuana
and medicine: Assessing the science base: A summary of the 1999
Institute of Medicine report. Arch
Gen Psychiatry. 57:547-552.
Weiss, L., M. Zeira, S. Reich, M. Har-Noy, R. Mechoulam, S. Slavin, and
R. Gallily. 2006. Cannabidiol lowers incidence of diabetes in non-obese
diabetic mice. Autoimmunity.
39: 143-151.
Zuardi, A.W., J.A.S. Crippa, J.E.C. Hallak, F.A. Moreira, & F.S.
Guimaraes. 2006. Cannabidiol, a Cannabis
sativa constituent, as an antipsychotic drug. 2006. Braz J Med Biol Res. 39:4;
421-429.
This paper was developed as part of the BIO 368 - Medical Botany
course offered at Wilkes University during the spring of 2009. Course
instructor was Kenneth M. Klemow, Ph.D.
(kenneth.klemow@wilkes.edu).
The information contained herein is based on published sources, and
is made available for academic purposes only. No warrantees,
expressed or implied, are made about the medical usefulness or
dangers associated with the plant species in question.
Return to Plant Summaries page
This page posted and maintained by Kenneth M.
Klemow, Ph.D., Biology Department,
Wilkes University, Wilkes-Barre,
PA 18766. (570) 408-4758,
kenneth.klemow@wilkes.edu.