Marijuana
Jim Dimke
The intake of marijuana can have several different effects. 
The user may experience a feeling of euphoria, increased laughter 
or happiness, as well as a relaxed passive mood. The user may 
experience difficulties with short-term memory, attention span may 
be decreased, and senses may be distracted. Many users also report 
losing track of time, experiencing paranoia and anxiety, and 
having hallucinations. Their eyes may become bloodshot because of 
the dilation of blood vessels in the eye whites.  However, as 
opposed to popular belief, pupils do not become dilated.  Accurate 
measurements of pupil diameter after smoking marijuana have 
actually shown that there is a slight decrease in pupil size, but 
the change cannot be seen without precise instruments (McKim 
1991).  The more common identifier of one that has used marijuana 
is his/her eyelids frequently drooping.  This gives users a 
distinguishing look about them and one that many people can 
detect. In addition, marijuana sometimes causes a sensation of 
having a dry mouth accompanied by an increased appetite known as 
the "munchies". 
Depression, anxiety, and personality disturbances have also 
been associated with the use of marijuana.  Research supports that 
marijuana has the potential to either cause problems in every day 
life or make a person's existing problems worse.  Employment 
status also becomes an unfortunate side effect for many users.  
Workers who smoke marijuana are more likely than their coworkers 
to have problems on the job. Studies have linked workers' that 
smoke marijuana with increased absences, tardiness, accidents, 
workers' compensation claims, and job turnover.  One study of 
municipal workers found that those who used marijuana on or off 
the job reported more "withdrawal behaviors" such as leaving work 
without permission, daydreaming, spending work time on personal 
matters, and putting off tasks that adversely affect productivity 
and morale  (Lehman, Simpson, 1992). 
In another study, marijuana users reported that use of the 
drug impaired several important measures of life achievement 
including cognitive abilities, career status, social life, and 
physical and mental health (Gruber, Pope, 2003).  As marijuana 
compromises one's ability to learn and remember information, the 
more a person uses marijuana, the more that person is likely to 
fall behind in accumulating, intellectual, job, or social skills.  
This affect on memory has been known to last for days or weeks 
past the drug's initial effect.  
In a study of 129 college students, researchers found that 
heavy users of marijuana (people that had smoked at least 27 of 
the last 30 days) experienced critical attention, memory, and 
learning skill impairments (Pope, Yurgelun, 1996). All 
participants had not smoked for at least 24 hours prior to the 
study.  These same users had difficulties sustaining and shifting 
their attention, organizing, and using information than did the 
participants that had used marijuana no more than 3 of the 
previous 30 days.  This suggests that individuals who smoke 
marijuana every day may function at a reduced intellectual level 
all of the time.  
More recently, the same researchers showed that the ability 
of a group of long-term heavy marijuana users to recall words from 
a list remained impaired for a week after quitting, but returned 
to normal within 4 weeks. Thus, it is possible that some cognitive 
abilities may be restored in individuals who quit smoking 
marijuana, even after long-term heavy use.
A more detailed description of the short-term adverse effects 
is as follows. One of the most common is anxiety or feelings of 
panic. This is very common in elderly people, and occurs much less 
frequently in children. Psychosis has also been reported from 
marijuana usage.  A correlation has been made in incidences where 
patients have been admitted into psychiatric hospitals and test 
positive for marijuana use. However, a study of 10,000 psychiatric 
hospital admissions argues that little evidence shows that a 
psychotic disorder can arise in a previously non-psychotic 
(Gurley, 1998). Cannabinoids can cause damaging drug interactions 
that result in a decreased stomach acidity, and increase activity 
of the cytochrome P450 system (Gurley, 1998). Therefore, medical 
marijuana users should be very cautious of mixing it with other 
medications. Marijuana has also been known to be a source of 
infections and has been documented to be contaminated with many 
fungal species that may cause pulmonary and systemic infections 
(Gurley, 1998).  A Salmonella outbreak as well as a hepatitis B 
outbreak in U.S. military personnel in Europe was linked to 
marijuana use (Gurley, 1998). Because marijuana impairs 
perception, focus, coordination, reaction time and time 
perception, it has been acknowledged as a serious risk for 
automobile accidents as well. Adolescents who drove after smoking 
marijuana at least six times a month were 2.4 times more likely to 
be involved in an accident (Gurley, 1998). 
Long-term adverse effects include serious consequences, but 
many people are blissfully ignorant of them. The use of marijuana 
is linked to the impairment of fetal growth as well as a decreased 
length of gestation (Gurley, 1998).  Developmental delays of the 
fetus may also show up in pregnant women who use marijuana, but 
they have not been shown to be solely responsible.  Lung damage 
may occur as marijuana contains more tar than cigarettes and since 
most joints don't contain filters more of the particulates and 
carcinogens are inhaled. With that in mind it is easy to see that 
the potential for cancer and other lung diseases may be relatively 
high. Gynecomastia, the development of breast tissue in males, has 
also been linked as an adverse effect of marijuana use (Gurley, 
1998). One well-known concern among smokers is that marijuana may 
cause infertility, but this belief remains unconfirmed. Studies 
have shown that marijuana may inhibit the body's ability to 
respond to disease.  In turn, this leaves the body more vulnerable 
to infections. The long-term effects of marijuana certainly seem 
more menacing than the short-term effects, however they don't 
change the fact that marijuana is the most frequently used illicit 
drug in the United States.

References:

Lynskey M, Hall W: The effects of adolescent cannabis use on 
educational attainment: a review. Addiction 95(11):1621-1630, 
2000. 

Kandel DB, Davies M: High school students who use crack and other 
drugs. Arch Gen Psychiatry 53(1):71-80, 1996. 
 
Rob M, Reynolds I, Finlayson PF: Adolescent marijuana use: risk 
factors and implications. Aust NZ J Psychiatry 24(1):45-56, 1990.

Pope HG, Yurgelun-Todd D: The residual cognitive effects of heavy 
marijuana use in college students. JAMA 272(7):521-527, 1996.

Lehman WE, Simpson DD: Employee substance abuse and on-the-job 
behaviors. Journal of Applied Psychology 77(3):309-321, 1992.

Gurley, J., R. Aranow and M. Katz. Medicinal Marijuana: A 
Comprehensive Review. Journal of Psychoactive Drugs 30 (2): 137-
146, 1998.
Chemistry and Physics of Lipids, 121, 57-63


Autumn Spears

History of Marijuana

	Marijuana has been used both recreationally and medicinally for 
centuries. There are numerous accounts of its medicinal qualities in 
multiple historical artifacts. Its use dates back to 2737 B.C. when the 
Chinese emperor, Shen Nung, used it for medicinal purposes including 
malaria, gout, poor memory, rheumatism, and analgesia (Carter et. al., 
2003).  Eastern Indian documents, in the Atharvaveda, dating back to 
2000 B.C. also refer to its medicinal use.  The Jamestown settlers 
cultivated hemp produced by the marijuana plant.  They used these 
fibers to make clothing, rope, and canvas because of its quality and 
durability.   Physicians in the 19th century were prescribing cannabis 
as a pain reliever, an anticonvulsant, and for migraine headaches 
(Doweiko, 2002).  Following his work in India in the 1840's William 
O'Shaughnessy introduced medicinal marijuana to the United Kingdom. 
Queen Victoria used marijuana for dysmenorrhoea during the same time 
period (Carter et. al., 2003).  

	Smoking marijuana recreationally began to spread in the United 
States in the 1920's.  It began to spread from Mexico and New Orleans 
up the Mississippi river.  Jazz musicians, labor workers, and river 
boatmen were quickly taking to its euphoric effects (Gettman, 1995).  
Smoking marijuana also became more popular during Prohibition when more 
people began cultivation of the plant and importing it into the U.S. to 
replace alcohol (Doweiko, 2002).  In 1942, marijuana was removed from 
the United States Pharacopoeia and the Federal Government began to 
criminalize non-medicinal marijuana possession and use (Carter et al., 
2003).  Marijuana became extremely popular in the 1960's and, today, is 
considered the most widely used illicit drug in the world, Canada, and 
the United States (Gettman, 1995).

Pharmacology and Chemistry of Marijuana

	Cannabis is known to contain over 400 chemicals in which about 70 
are classified as plant cannabinoids.  The human body produces 
naturally occurring cannabinoids.  The cannabinoids are lipophilic.  
Delta-8 and Delta-9 Tetrahydrocannabinol (THC) have been found to 
produce most of the psychoactive effects of marijuana (Carter et al., 
2003).  Delta-9 Tetrahydrocannabinol appears to be the most abundant 
cannabinoid and the main source of cannabis' impact.  Cannabidiol is 
the second most predominantly active ingredient.  It becomes 
Tetrahydrocannabinol as the 
cannabis plant matures and the Tetrahydrocannabinol then breaks down 
into cannabinol  Approximately 40 percent of the plant's resin in some 
strains of cannabis are cannabidiol.  Each cannabis strain differs in 
potency from the next.  Cannabidiol helps to reduce symptoms of 
anxiety, strains that lack this cannabinoid altogether or that have 
very little of it will increase feelings of anxiety in the user.  This 
cannabinoid slows down the liver's ability to metabolize 
Tetrahydrocannabinol (Carter et al., 2003).  In one study, mice were 
given cannabidiol and the result was increased brain concentration, 
increased pharmacological actions of other drugs, and increased brain 
levels of tetrahydrocannabinol by three times their normal effect.  
There is less research regarding the cannabinoid, cannabinol  What 
research does show about this cannabinoid is it has different 
pharmacological properties than cannabidiol and its properties include 
anticonvulsant effects, sedative-like effects, may protect against 
seizures, and may induce sleep (Carter et al., 2003).  
	
	Tetrahydrocannibinol (THC) has been found to bind to receptor 
sites in the cerebellum, hippocampus, cerebral cortex, and basal 
ganglia.  Research suggests that THC binding to these receptors may be 
responsible for the effects observed upon inhalation of marijuana 
(Doweiko, 2002).  Research has also found that marijuana inhibits the  
enzyme adenylate cyclase and may be the reason marijuana helps with 
pain relief. Marijuana effects the synthesis of the neurotransmitter 
acetylcholine (in the limbic region), which effects one's alertness and 
can possibly explain marijuana's sedative effect (Doweiko, 2002). 
	
	Anandamide (AEA) and 2-arachidonylglycerol (2-AG) are two 
naturally occurring lipids that have been identified as endogenous 
cannabinoids or endocannabinoids.  Research is limited on these 
endocannabinoids but what is suggested is that they function as short-
lived and diffusible intercellular messengers that modulate synaptic 
transmission (Carter et al., 2003).  Current research suggests that 
endogenous cannabinoids "mediate signals retrograde from depolarized 
postsynaptic neurons to presynaptic terminals to suppress subsequent 
neurotransmitter release, driving the synapse into an altered state" 
(Carter et al., 2003).  These signals by the endocannabinoids seem to 
act for a mechanism through which "neurons may communicate backwards 
across synapses to modulate their inputs" (Carter et al., 2003).  

	There are cannabinoid receptor subtypes.  There are two subtypes 
evident in cannabis research.  Subtype 1 is expressed mostly in the 
brain whereas subtype 2 is mainly expressed in the immune system. 
Cannabinoid receptors are similar to the receptors of other 
neurotransmitters including dopamine, serotonin, and norepinephrine.  

	The cannabis plant is very complex and is difficult to study its 
effects due to the variable potency of each plant.  The level of 
potency in each plant is dependent upon plant genetics, growing 
conditions, and how the plant is processed at harvest.  The highest 
potency is contained in the female flowers of the plant and can have 
THC levels from .3 percent to 25 percent depending on the strain and 
growing conditions (Carter et al., 2003).


References

Carter, G.T., Weydt, P., Kyashna-Tocha, M., & Abrams, D.I. (2003). 
Medical Cannabis: Rational Guidelines for Dosing. The University of 
Washington School of Medicine, Seattle, WA.

Doweiko, H.E. (2002). Marijuana abuse and addiction: Concepts of 
chemical dependency. Pacific Grove, CA: Brooks/Cole Publishers. 

Gettman, J. (1995). Marijuana and the Brain: High Times. Schaffer 
library of drug policy.

   
Kiersten Kotaka
Chemistry Part Two
     Delta 9 Tetrahydrocannabinol is the primary psychoactive 
constituent of Cannibis sativa, and is bound to two cannabinoid 
receptors: CB1 receptors, located primarily in the brain, and CB2 
receptors, located primarily in the periphery (Wiley & Martin 
2002). A cannabinoid is defined as a substance that has 
pharmacological properties that resemble those of delta 9 THC i.e. 
" a drug that binds to CB1 and /or CB2 receptors in vitro and 
produces a profile of in vivo effects in the tetrad model" (Wiley 
2002). THC inhibits the function of the enzyme adenylate cyclase 
which is involved in the transmission of pain messages. While 
there are over 60 cannibinoids identified in the plant Cannabis 
sativa, Delta 9 tetrahydrocannabinol is the primary mood altering 
psychoactive agent in marijuana. Marijuana effects acetylcholine 
synthesis and turnover in the limbic region of the brain and in 
the cerebellum. (Harwood 2005) 
	Eldreth, Matochik Cadet, and Bolla (2004) used PET 15 and a 
modified version of the Stroop task to determine if 25 day 
abstinent heavy marijuana users experienced persistent deficits in 
executive cognitive functioning and brain activity. The 
performance on a modified version of the Stroop task and brain 
activity was compared between 25 day abstinent, heavy users, and a 
matched comparison group. The 25 day abstinent users showed no 
deficits in performance on the modified version of the Stroop task 
when compared to the comparison group. They also found that 
despite the lack of performance differences, the anterior 
cingulated cortex and the left lateral prefrontal cortex had 
hyperactivity in the hippocampus bilaterally, when compared to the 
comparison group.  The results suggested that users display 
persistent metabolic alterations in brain regions responsible for 
executive cognitive functioning. (Eldreth, Matochik, Cadet, & 
Bolla 2004). 
	When performing the Stoop task, marijuana users were found to 
have greater activation compared to the comparison group in the 
left and right hippocampus. Marijuana users also failed to 
activate to the same extent as the comparison group in the left 
lateral prefrontal cortex and the left perigenual anterior 
cingulated cortex.   
	According to Gardner (2002) drugs that are addictive to 
humans are similar to animal model systems in five ways. First, 
drugs enhance electrical brain stimulation reward in the core 
meso-accumbens reward circuitry of the brain, a circuit 
encompassing that portion of the medial forebrain bundle which 
links the ventral tegmental area of the mesencephalic midbrain 
with the nucleus accumbens of the ventreal limbic forebrain. The 
next similarity is that they enhance neural firing of a core 
dopamine component of this meso accumbens reward circuit. They 
also enhance dopamine tone in this reward relevant meso accumbens 
dopamine circuit with resultant enhancement of extracellular Ach 
DA. They produce conditioned place preference, a behavioral model 
of incentive motivation. And finally they are self administered 
and they trigger reinstatement of drug seeking behavior and 
pharmacologically detoxified from their self administered drug. 
(Gardner 2002). 
Addictive drugs enhance brain reward processes by acting at 
different anatomic sites within the brain's reward circuitry, 
different addictive drugs enhance brain reward processes by acting 
through different mechanisms within the brain's reward circuitry. 
(Gardner 2002). THC's site of action is in the vicinity of the 
reward relevant ACH Dopamine axon terminals. (Gardner 2002)
	Cannabinoids enhance AcH Dopamine by acting at various brain 
loci: 1. within the AcH acting on mechanisms closely linked to 
axon terminal Dopamine releas; 2. within the VTA acting on 
endogenous opiod mechanisms not linked to activation of neuronal 
firing but rather linked to mechanisms of Dopamine synthesis, 
transport and release and 3. within the VTA acting on 
nonendogenous opiod mechanisms linked to activation of neuronal 
firing. (Gardner 2002).
	In a study by Oleary et al 2002, researchers found that 
smoking marijuana significantly increased heart rate and blood 
pressure and resulted in extensive changes in regional cerebral 
blood flow in comparison to presmoking conditions and to the 
conditions following smoking placebo. The regional cerebral blood 
flow changes observed reflected the direct changes caused by 
smoking marijuana upon brain metabolism and blood flow as well as 
less direct effects resulting from its intoxicating and mood 
enhancing effects.(Oleary et al. 2002). 
	The molecular structure is unlike that of any known 
transmitter but it does not seem related to steroids(similar to 
testosterone and estradiol that seem to be involved in depression. 
(Palfai & Jankiewicz 1991). Cannabinoids are increased by the 
synthesis of catecholamines in the brain through a direct action 
on neurons. There is also a decrease in Ach synthesis. The 
greatest density of cannabinoids are found in the basal ganglia, 
hippocampus, and cerebellum (Palfai & Jankiewicz 1991). 

References

Eldreth,D. Matochik,J. Cadet,J. & Bolla,K.(2004) Abnormal brain 
activity in prefrontal brain regions in abstinent users. 
NeuroImage, 23, 914-920.
Gardner, E. (2002). Addictive potential of cannabinoids: the 
underlying neurobiology. Intramural Research Program, National 
Institute of Health and Human services. Baltimore Maryland. 
Harwood,T.(2005). Lecture Notes handout. Personal Communication.  
Oleary et al. (2002). Effects of smoking on brain perfusion and 
cognition. Neuropsychopharmacology, 26, 802-816.
Palfai, T. & Jankiewicz (1991) Drugs and human behavior. Iowa: WM 
C Brown.
Wiley,J. Martin, B. (2002). Cannabinoid pharmacology: implications 
for additional cannabinoid receptor subtypes.  


Socorro Valdez
The physiological effects of marijuana
March 30, 2004 

	Marijuana derives from the dried leaves and flower of the 
hemp plant Cannabis sativa; for thousands of years, physicians 
regarded marijuana as a useful pharmaceutical agent that could be 
used to treat a number of different disorders. In the 19th 
century, 
physicians in the United States and Europe used marijuana as an 
analgesic, as a treatment for migraine headaches, and as an 
anticonvulsant (Grinspoon & Bakalar, 1993, 1995).  In 1938, a 
physician used marijuana (hashish) to completely control the 
terror and excitement of a patient who had contracted rabies 
(Elliot, 1992, p. 600). Results from a research conducted in the 
1880s indicated that smoking marijuana might help manage certain 
forms of glaucoma; regrettably, other studies disproved such 
claims. (Watson, Benson, & Joy, 2000).  Even though smoking 
marijuana temporarily reduces the pressure within the eye, 60 to 
65 of the patients who smoked marijuana, experienced the desired 
medicating effects (Green, 1998). New findings indicated that in 
order for an individual to obtain and maintain    satisfactory 
results in the reduction of eye pressure levels, the patient would 
have to smoke between 2 to 3 cigarettes every hour.  Marijuana is 
believed to be an effective treatment of multiple sclerosis and 
rheumatoid arthritis; furthermore, it seems to yield positive 
results in the treatment of chronic pain conditions (Watson, 
Benson, & Joy, 2000). However, although marijuana has served as a 
medicinal agent, marijuana can also produce some adverse 
physiological effects; especially with patients with pre-existing 
medical conditions who use marijuana may be at particular risk.  
For instance, although THC acutely increases the respiratory rate 
and the diameter of bronchial airways, chronic use of marijuana 
results in epithelial damage to the trachea and major bronchi, and 
decreased diameter of the bronchial airways (Schackit, 1989). 
However, when it comes to immediate lethality, marijuana is 
reasonably safe; nevertheless, its content can produce long term 
physical effects caused by Delta-9-tetrahydrocannabinol (THC), the 
active chemical ingredient in marijuana that inhibits the immune 
system's ability to fight of infectious diseases and cancer 
(Adams, & Martin 1996). Even occasional marijuana smokers may 
experience unpleasant effects; such as burning and stinging of the 
mouth and throat, often followed by a heavy cough. Regular 
marijuana users may have similar respiratory problems than tobacco 
users: daily cough, frequent chest illness, and an increased risk 
of lung infections (Tashkin, 1990). Because marijuana contains 50 
to 70 percent more carcinogenogenic hydrocarbons than tobacco 
smoke, and it also produces high levels of the enzyme that 
converts certain hydrocarbons into their carcinogenic form-levels 
that may speed-up the changes that ultimately produce malignant 
cells; and thereby, increasing  the likelihood of promoting cancer 
of the lungs, and other parts of the respiratory system. 
Furthermore, smoking marijuana increases the risk of developing 
cancer of the head or neck (Hoffman, D. Brunnemann, K.D. & Gori, 
G. B, et al., 1975).  The greater the amount of marijuana use, the 
greater the risk.  The primary common effect of marijuana is 
evident within a few hours of it use; it produces cardiovascular 
effect known as Tachycardia a rapid increase in heart rate, blood 
pressure, bronchitis, and asthma. Marijuana use has been 
implicated as the cause of a number of reproductive system 
dysfunctions, such as a decline in sexual desire in the user. For 
male users, it may contribute to erectile and delayed ejaculation, 
a reduction of sperm count and a reduction of testicular size; 
furthermore, male chronic marijuana users have been found to have 
50 percent lower blood testosterone levels than men who do not use 
marijuana (Bloodworth, 1987). Research has shown women who used 
marijuana during their pregnancy give birth to innocent babies who 
will have long term physiological, psychological, neurological, 
and behavioral effects; these children who were directly exposed 
to marijuana, have been observed to exhibit more behavioral 
problems, deficits in decision making, difficulties paying 
attention, and low levels of performance on task that require 
visual perception (Fried, 1995) Also, women who are chronic 
marijuana users have been found to experience menstrual 
abnormalities and or/failure to ovulate. (Hubbard, Franco, & 
Onaivi, 1999).   Contrary to popular belief, there is evidence 
that chronic use of marijuana causes physical changes in the 
brain, and the smoke from marijuana cigarettes has been found to 
be even more harmful than tobacco smoke (Smith, 1997).  THC 
(Delta-9- tetrahydrocannabinol); is the he active chemical 
ingredient in marijuana, which produces psychoactive reactions on 
the user (Schuckit. 1989). The delta-9-tetrahydrocannabinol (THC) 
substance of marijuana is currently higher than that of the 
marijuana used in past decades, although its potency depends on 
the method used for preparation; for example, Ganja is close to 
three times more powerful, and at the same time, hashish is five 
to eight times pore potent.  Ever since the 1950's, marijuana 
abusers have sought ways to enhance the effects of the chemical(s) 
in the plant by adding other substances to the marijuana before 
smoking it, or by using strains with highest possible 
concentration of the compounds thought to cause marijuana's 
effects.(Lewis & Guttman, 1997). Marijuana is known to be the most 
frequently used illicit substance in the world; because the 
content of its compounds when introduced to the body produces 
effects that the individual user deems desirable. There is other 
possible reason for people to become addicted to marijuana.  Many 
people first use marijuana because of curiosity, peer pressure or 
both; after the initial exposure to the effects of euphoria, 
relaxation, heightened sensations and socialization with other 
users places the user at risk for becoming addicted.. Other 
encouragers for its use, is the easy access, expectations of few 
or no legal consequences, self medication (for physical and 
emotional problems), and eventual dependence contribute to chronic 
use.  People, who are addicted to different type of chemicals, 
have the tendency to deny or accept that they are chemically 
dependent.  However two of the fundamental symptoms of addiction 
to any chemicals are the development of tolerance to a particular 
chemical substance, and the experiencing of a withdrawal syndrome 
which creates physical discomfort for the individual when he/she 
discontinues the use of marijuana (Bloodworth, 1987). Although it 
is not clear what percentage of heavy users are actually addicted, 
it is suggested that one out of eleven people who smoke marijuana, 
will become a heavy user for at least a period of time.  

References:

Adams I. B., Martin, B. R. (1996). Cannabis: Pharmacology and 
toxicology in 	animas and humans. Addiction 91: 1585-1614. 
Bloodworth, R. C. (1987). Major problems associated with marijuana 
abuse.  	Psychiatric Medicine, 3 (3), 173-184 
Elliot & Bakalar, J.B. (1993).  Marijuana: The forgotten medicine. 
New 
	Haven, CT: Yale University Press	
Fried, P.A. (1995). Prenatal exposure to marihuana and tobacco 
during infancy, 	early and middle childhood and an attempt at 
synthesis. Arch Toxicol Srpp 	17: 233-60. 
Green, K. (1998).Marijuana smoking vs cannabinoids for glaucoma 
therapy.  	Archive of Opthalmology, 116, 1433-1437. 
	Lewis, D. C (1997); Guttman (1996). The role of the 
generalist in the care 	of the substance-abusing client.   
Medical Clinics of North America, 81, 	831-843.
Hoffman, D. Brunnemann, K.D. & Gori, G. B, et al., (1975).The 
carcinogenicity of 	marijuana smoke. Resent Advances in 
Phytochemistry. New York, 
Kouri, E. M., Pope, H.G., & Lukas, S.E (1999). Changes in 
aggressive behavior  	during withdrawal from long-term 
marijuana use.  Psychopharmacology, 	143, 302-305 
Schuckit Ma. (1998). Cannabinols. In: drug and alcool abuse: a 
Clinical Guide to 	Diagnosis and Treatment. 3rd Ed. New York; 
Plenum Medical, 143-57 
Watson, S. J.,  Benson, J. A. & Joy, J. E. (2000). Marijuana and 
medicine: 	Assessing the science base. Archives of General 
Psychiatry, 57, 547-552.
Tashkin, D. P. (1990). Pulmonary complications of smoked substance 
	 	abuse. West Med 152: 524-530. 
                               


Advanced Psychopharmacology

Joseph Waters
Effects reported by users of marijuana:

The following are interviews conducted by myself. I obtained 
verbal consent from the individuals and informed them that their 
confidentiality would be completely protected. To insure their 
confidentiality is protected I am using pseudonyms for the 
individuals interviewed. They were also informed that they could 
stop the interview at any time with no questions asked and there 
would be no penalty of any kind if they chose to do so. 

Interview number 1; female, 47 years old, Africa Board
Question (Q): Why do you use?
Answer (A): (There is a long pause) …it's hard to put into words. 
I like it obviously, it seems to keep me centered and focused. 
(Q): What do you get out of it?
(A): It is a solitary thing more than a group thing so it is not 
social, it's not a party thing. I like the quiet, and the 
focusing. 
(Q): How long have you used?
(A): On and off since I was a teenager.
 (Q): What are the positives of using?
(A): The focusing, it seems like my creativity is increased, and I 
like getting in touch with nature.
(Q): What are the negatives of using?
(A): Society's attitude, it seems like there is a lot of judgment 
placed on marijuana that is not necessarily fair or accurate. 
(Q): Why do you think society has a particular attitude towards 
marijuana? 
(A):I think because of the 1960s when people were experimenting 
with lots of drugs, people were dropping out of school. The 
establishment did not like people thinking for themselves so they 
medicated people with television and propaganda that inaccurately 
portrays marijuana. 
(Q): Do you feel addicted?
(A)	No because there have been times where I haven't smoked. When 
I went to Mexico I didn't use, it's not worth the risk, not 
worth jail time. I quit when I was pregnant and sometimes I just 
don't feel like using.

Interview Number 2; female, 29 years old, Jasmine Grant
(Q): Why do you use?
(A): I don't anymore. It was a social thing. All of my friends 
were doing it so I thought "why not".
(Q): What do you get out of it?
(A): It made me feel accepted, not just because of peer pressure 
but also because my words seemed to flow better and I felt less 
self-conscious. I liked the way it took the edge off reality. It 
numbed a small piece of me and allowed me to relax.
(Q): How long have you used?
(A): I used from my early teenage years until my early twenties.
(Q): What are the positives of using?
(A): I felt accepted and it got me through a rough point in my 
life. 
(Q): What are the negatives of using?
(A): It affected my short term memory in small ways. It distracted 
me, almost unmotivated me. It is easier to sit around doing 
nothing than face the work that needed to be done. It also started 
causing anxiety. 
(Q): Do you feel addicted? 
(A): No, I chose to stop on my own and I have not chosen to go 
back. Every time I was pregnant I quit. 

Interview Number 3; male, 52 years old, Kevin Ivers
(Q): Why do you use? 
(A): I like the high. It is the only thing that takes the pain 
away. I have arthritis and I have tried many different 
medications. Marijuana works the best.
(Q): What do you get out of it?
(A): Pain relief. The high, I feel less pain and I feel relaxed. 
(Q): How long have you used?
(A): I started smoking herb when I was around 19 or 20 years old.
(Q): What are the positives of using?
(A): Well obviously I like the pain relief. I feel worry free, and 
it seems to help me clear my mind.
(Q): What are the negatives of using?
(A): I feel like it should not be so taboo. I feel like I need to 
hide and sneak around and do it because it is illegal, even though 
I have a 215. There are so many things out there much worse. For 
example, alcohol is known to cause more fights, deaths, aggressive 
behaviors than marijuana but it is not banned.  
(Q): Do you feel addicted?
(A): No, not at all. 

References
All face to face interviews. 

Copyright © 2005, Dr. John M. Morgan, All rights reserved - This page last edited 04-23, 2004
If you have any feedback for the author, E-mail me