Inter. J. of Phytotherapy / Vol 3 / Issue 1 / 2013 / 24-32.

e - ISSN - 2249-7722
Print ISSN - 2249-7730

International Journal of Phytotherapy

www.phytotherapyjournal.com

EFFECTS OF CANNABIS A REVIEW

G. Sangeetha, G. Balammal*, K. Umasankar
*Krishna Teja Pharmacy College, Chadalawada Nagar, Renigunta Road, Tirupati-517605, Andhra Pradesh, India.
ABSTRACT
The effects of cannabis are caused by chemical compounds in cannabis, including cannabinoids such
as tetrahydrocannabinol (THC). Cannabis has both psychologicaland physiological effects on the human body.
Acute effects while under the influence can include euphoria and anxiety. This review Concerns the potential effect
for long-term cannabis consumption to increase risk for schizophrenia, bipolar disorders, and major depression, but
the ultimate conclusions on these factors are disputed. The evidence of long-term effects on memory is preliminary
and hindered by confounding factors. For thousands of years people have believed that cannabis has religious and
spiritual effects.
Key words: Cannabis, Physiological effects, Long-term consumption.

INTRODUCTION
Cannabinoids and cannabinoid receptors
The most prevalent psychoactive substances
in cannabis are cannabinoids, most notably THC. Some
varieties, having undergone careful selection and growing
techniques, can yield as much as 29% THC. Another
psychoactive
cannabinoid
present
in Cannabis
sativa is tetrahydrocannabivarin (THCV), but it is only
found in small amounts and is a cannabinoid antagonist.
In addition, there are also similar compounds
contained in cannabis that do not exhibit any psychoactive
response but are obligatory for functionality cannabidiol
(CBD), an isomer of THC;
cannabinol
(CBN),
an oxidation product of THC; cannabivarin (CBV),
an analog of
CBN
with
a
different sidechain cannabidivarin (CBDV), an analog
of CBD with a different side chain, and cannabinolic acid.
How these other compounds interact with THC is not
fully understood. Some clinical studies have proposed that
CBD acts as a balancing force to regulate the strength of
the psychoactive agent THC. CBD is also believed to
regulate the bodys metabolism of THC by
inactivating cytochrome P450, an important class o f

enzymes that metabolize drugs. Experiments in which

mice were treated with CBD followed by THC showed
that CBD treatment was associated with a substantial
increase in brain concentrations of THC and its major
metabolites, most likely because it decreased the rate of
clearance of THC from the body. Cannabis cofactor
compounds have also been linked to lowering body
temperature, modulating immune functioning, and cell
protection. The essential oil of cannabis contains many
fragrant terpenoids which may synergize with the
cannabinoids to produce their unique effects. THC is
converted rapidly to 11-hydroxy-THC, which is also
pharmacologically active, so the drug effect outlasts
measurable THC levels in blood.
THC
and
cannabidiol
are
also neuroprotective antioxidants. Research in rats has
indicated
that
THC
prevented hydroperoxideinduced oxidative damage as well as or better than other
antioxidants in a chemical (Fenton reaction) system
and neuronal cultures. Cannabidiol was significantly more
protective
than
either vitamin
E or vitamin
C.

Corresponding Author:- G. Balammal Email: bala.hospira@gmail.com

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The cannabinoid receptor is a typical member of

the largest known family of receptors called a G proteincoupled receptor. A signature of this type of receptor is
the distinct pattern of how the receptor molecule spans
the cell membrane seven times. The location of
cannabinoid receptors exists on the cell membrane, and
both outside (extracellularly) and inside (intracellularly)
the cell membrane. CB1 receptors, the bigger of the two,
are extraordinarily abundant in the brain: 10 times more
plentiful than -opioid receptors, the receptors responsible
for the effects of morphine. CB2 receptors are structurally
different (the sequence similarity between the two
subtypes of receptors is 44%), found only on cells of the
immune system, and seems to function similarly to its
CB1 counterpart. CB2 receptors are most commonly
prevalent on B-cells, natural killer cells, and monocytes,
but can also be found on polymorphonuclear neutrophil
cells, T8 cells, and T4 cells. In the tonsils the CB2
receptors appear to be restricted to B-lymphocyteenriched areas [1,2].
Biochemical mechanisms in the brain
In 1990 the discovery of cannabinoid
receptors located throughout the brain and body, along
with endogenous cannabinoid neurotransmitters like anan
damide (a lipidmaterial derived ligand from arachidonic
acid), suggested that the use of cannabis affects the brain
in the same manner as a naturally occurring brain
chemical.Cannabinoids usually contain a 1,1'-di-methylpyrane ring, a variedly derivatized aromatic ring and a
variedly unsaturated cyclohexyl ring and their immediate
chemical precursors, constituting a family of about 60 bicyclic and tri-cyclic compounds. Like most other
neurological processes, the effects of cannabis on the
brain follow the standard protocol of signal transduction,
the electrochemical system
of
sending
signals
through neurons for a biological response. It is now
understood that cannabinoid receptors appear in similar
forms in most vertebrates and invertebrates and have a
long evolutionary history of 500 million years. The
binding of cannabinoids to cannabinoid receptors
decrease adenylyl cyclase activity, inhibit calcium N
channels, and disinhibit K+A channels. There are two
types of cannabinoid receptors (CB1 and CB2) [3].
The CB1 receptor is found primarily in the brain
and mediates the psychological effects of THC. The CB2
receptor is most abundantly found on cells of the immune
system. Cannabinoids act as immunomodulators at CB2
receptors, meaning they increase some immune responses
and decrease others. For example, nonpsychotropic
cannabinoids can be used as a very effective antiinflammatory. The affinity of cannabinoids to bind to
either receptor is about the same, with only a slight
increase observed with the plant-derived compound CBD
binding to CB2 receptors more frequently. Cannabinoids

likely have a role in the brains control

of movement and memory, as well as natural pain
modulation. It is clear that cannabinoids can affect pain
transmission and, specifically, that cannabinoids interact
with the brain's endogenous opioid system and may affect
dopamine
transmission. This
is
an
important
physiological pathway for the medical treatment of pain.
Sustainability in the body
Most cannabinoids are lipophilic (fat
soluble)
compounds that are easily stored in fat, thus yielding a
long elimination half-life relative to other recreational
drugs. The THC molecule, and related compounds, are
usually detectable in drug tests from 3 days up to 10 days
according to Redwood Laboratories; heavy users can
produce positive tests for up to 3 months after ceasing
cannabis use.
Toxicity
THC, the principal psychoactive constituent of
the cannabis plant, has an extremely low toxicity and the
amount that can enter the body through the consumption
of cannabis plants poses no threat of death. In lab animal
tests, scientists have had much difficulty administering a
dosage of THC that is high enough to be lethal.
Accordingly, there is little reason to believe a human
would self-administer such doses. According to the Merck
Index, the LD50 of THC (the dose which causes the death
of 50% of individuals) is 1270 mg/kg for male rats and
730 mg/kg for female rats from oral consumption in
sesame oil, and 42 mg/kg for rats from inhalation.
The ratio of cannabis material required to
produce a fatal overdose to the amount required to
saturate cannabinoid receptors and cause intoxication is
approximately 40,000:1. A typical marijuana joint
contains less than 10 mg of THC, and one would have to
smoke thousands of those in a short period of time to
approach toxic levels. According to a 2006 United
Kingdom government report, using cannabis is much less
dangerous than tobacco, prescription drugs, and alcohol in
social harms, physical harm, and addiction. It was found
in 2007 that while tobacco and cannabis smoke are quite
similar, cannabis smoke contained higher amounts
ofammonia, hydrogen cyanide, and nitrogen oxides, but
lower levels of carcinogenic polycyclic aromatic
hydrocarbons (PAHs). This study found that directly
inhaled cannabis smoke contained as much as 20 times as
much ammonia and 5 times as much hydrogen cyanide as
tobacco smoke and compared the properties of both
mainstream and sidestream (smoke emitted from a
smouldering 'joint' or 'cone') smoke. Mainstream cannabis
smoke was found to contain higher concentrations of
selected polycyclic aromatic hydrocarbons (PAHs) than
sidestream tobacco smoke. However, other studies have
found much lower disparities in ammonia and hydrogen

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cyanide between cannabis and tobacco, and that some

other constituents (such as polonium-210, lead, arsenic,
nicotine, and tobacco-specific nitrosamines) are either
lower or non-existent in cannabis smoke [4,5].
Cannabis smoke contains thousands of organic
and inorganic chemical compounds. This tar is chemically
similar to that found in tobacco smoke or cigars. Over
fifty known carcinogens have been identified in cannabis
smoke. These include nitrosamines, reactive aldehydes,
and
polycylic
hydrocarbons,
including
benz[a]pyrene. Marijuana smoke was listed as a cancer
agent in California in 2009. A study by the British Lung
Foundation published in 2012 identifies cannabis smoke
as a carcinogen and also finds awareness of the danger is
low compared with the high awareness of the dangers of
smoking tobacco particularly among younger users. Other
observations include possible increased risk from each
cigarette; lack of research on the effect of cannabis smoke
alone; low rate of addiction compared to tobacco; and
episodic nature of cannabis use compared to steady
frequent smoking of tobacco.
Researches points out that the study cited by the
British Lung Foundation has been accused of both false
reasoning and incorrect methodology. Further, he notes
that other studies have failed to connect cannabis with
lung cancer, and accuses the BLF of scaremongering over
cannabis.
A study in the academic journal, Cancer
Epidemiology, Biomarkers & Prevention, demonstrated
that a marijuana cigarette deposits four times the amount
of tar in the human respiratory tract than a tobacco
cigarette.
According to Harvard's Lester Grinspoon, there
has never been a death associated directly to cannabis. In
defense of smoked Medical cannabis, Grinspoon noted,
there is very little evidence that smoking marijuana as a
means of taking it represents a significant health risk.
Although cannabis has been smoked widely in Western
countries for more than four decades, there have been no
reported cases of lung cancer or emphysema attributed to
marijuana. I suspect that a day's breathing in any city with
poor air quality poses more of a threat than inhaling a
day's dose -- which for many ailments is just a portion of
a joint of marijuana.
One study in 2005, the largest of its kind, found
no cannabis-cancer connection. Donald Tashkin,
a pulmonologist at UCLA's David Geffin School of
Medicine who studied marijuana for 30 years, noted: We
hypothesized that there would be a positive association
between marijuana use and lung cancer, and that the
association would be more positive with heavier use.
What we found instead was no association at all, and even
a suggestion of some protective effect.
Short-term effects

When smoked, the short-term effects of cannabis

manifest within seconds and are fully apparent within a
few minutes, typically lasting for 1-3 hours, varying by
the person and the strain of marijuana. The duration of
noticeable effects has been observed to diminish due to
prolonged, repeated use and the development of a
tolerance to cannabinoids.
Psychoactive effects
The psychoactive effects of cannabis, known as a
high, are subjective and can vary based on the person and
the method of use.
When THC enters the blood stream and reaches the
brain, it binds to cannabinoid receptors. The endogenous
ligand of these receptors is anandamide, the effects of
which THC emulates. This agonism of the cannabinoid
receptors results in changes in the levels of various
neurotransmitters,
especially dopamine and norepinephrine;
neurotransmitters which are closely associated with the
acute
effects
of
cannabis
ingestion,
such
as euphoria and anxiety. Some effects may include a
general alteration of conscious perception, euphoria,
feelings of well-being, relaxation or stress reduction,
increased appreciation of humor, music (especially
discerning its various components/instruments) or the
arts, joviality, metacognition and introspection, enhanced
recollection (episodic memory), increased sensuality,
increased awareness of sensation, increased libido, and
creativity. Abstract or philosophical thinking, disruption
of linear memory and paranoia or anxiety are also
typical. Anxiety is the most commonly reported side
effect of smoking marijuana. Between 20 and 30 percent
of recreational users experience intense anxiety
and/or panic attacks after smoking cannabis.
Cannabis also produces many subjective and
highly tangible effects, such as greater enjoyment of food
taste and aroma, an enhanced enjoyment of music and
comedy, and marked distortions in theperception of
time and space (where experiencing a rush of ideas from
the bank of long-term memory can create the subjective
impression of long elapsed time, while a clock reveals
that only a short time has passed). At higher doses, effects
can include altered body image, auditory and/or visual
illusions, pseudo-hallucinatory or (rarely, at very high
doses) fully hallucinatory experiences, and ataxia from
selective impairment of polysynaptic reflexes. In some
cases, cannabis can lead to dissociative states such
as depersonalization and derealization; such effects are
most often considered desirable, but have the potential to
induce panic attacks and paranoia in some unaccustomed
users [3].
Somatic effects
Some of the short-term physical effects of
cannabis use include increased heart rate, dry mouth,

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reddening
of
the eyes (congestion
of
the conjunctival blood vessels), a reduction in intra-ocular
pressure, muscle relaxation and a sensation of cold or hot
hands and feet.
Electroencephalography or
EEG
shows
somewhat more persistent alpha waves of slightly
lower frequency than usual. Cannabinoids produce a
marked depression of motor activity via activation of
neuronal cannabinoid receptors belonging to the CB1
subtype.
Duration
Effects of cannabis generally range from 10
minutes to 8 hours, depending on the potency of the dose,
other drugs consumed, route of administration, set,
setting, and personal tolerance to the drug's various
effects.

related increase of physical effects (such as increase of

heart rate, and decrease of blood pressure) and
psychomotor effects (such as reacting more slowly,
decreased ability to focus and concentrate, making more
mistakes during performance testing, having less motor
control, and experiencing drowsiness). It was also
observed during the study that the effects from a
single joint lasted for more than eight hours. Reaction
times remained impaired five hours after smoking, when
the THC serum concentrations were significantly reduced,
but still present. However, it is important to note that the
subjects (without knowing the potency) were told to finish
their (unshared) joints rather than titrate their doses,
leading in many cases to significantly higher doses than
they would normally take. Also, when subjects smoke on
several occasions per day, accumulation of THC in bloodserum may occur [5].

Smoked

Oral

The total short-term duration of cannabis use

when smoked is based on the potency and how much is
smoked. Effects can typically last two to three hours.
A study of ten healthy, robust, male volunteers
who resided in a residential research facility sought to
examine both acute and residual subjective, physiologic,
and performance effects of smoking marijuana cigarettes.
On
three
separate
days,
subjects
smoked
one NIDA marijuana cigarette containing either 0%,
1.8%, or 3.6% THC, documenting subjective,
physiologic, and performance measures prior to smoking,
five times following smoking on that day, and three times
on the following morning. Subjects reported robust
subjective effects following both active doses of
marijuana, which returned to baseline levels within 3.5
hours. Heart rate increased and the pupillary light
reflex decreased following active dose administration
with return to baseline on that day. Additionally,
marijuana smoking acutely produced decrements
in smooth pursuit eye tracking. Although robust acute
effects of marijuana were found on subjective and
physiological measures, no effects were evident the day
following administration, indicating that the residual
effects of smoking a single marijuana cigarette are
minimal [4].
A Dutch double blind, randomized, placebocontrolled, cross-over study examining male volunteers
aged 1845 years with a self-reported history of regular
cannabis use concluded that smoking of cannabis with
very high THC levels (marijuana with 923% THC), as
currently sold in coffee shops in the Netherlands, may
lead to higher THC blood-serum concentrations. This is
reflected by an increase of the occurrence of impaired
psychomotor skills, particularly among younger or
inexperienced cannabis smokers, who do not always adapt
their smoking-style to the higher THC content. High THC
concentrations in cannabis were associated with a dose-

When taken orally (in the form of capsules, food

or drink), the psychoactive effects take longer to manifest
and generally last longer, typically lasting for 410 hours
after consumption. Very high doses may last even longer.
Also, oral ingestion use eliminates the need to inhale toxic
combustion products created by smoking and therefore
reduces the risk of respiratory harm associated with
cannabis smoking [6].
Neurological effects
The areas of the brain where cannabinoid
receptors are most prevalently located are consistent with
the behavioral effects produced by cannabinoids. Brain
regions in which cannabinoid receptors are very abundant
are the basal ganglia, associated with movement control;
the cerebellum, associated with body movement
coordination; the hippocampus, associated with learning,
memory, and stress control; thecerebral cortex, associated
with higher cognitive functions; and the nucleus
accumbens, regarded as the reward center of the brain.
Other regions where cannabinoid receptors are
moderately concentrated are the hypothalamus, which
regulates homeostatic functions; the amygdala, associated
with emotional responses and fears; the spinal cord,
associated with peripheral sensations like pain; the brain
stem, associated with sleep, arousal, and motor control;
and the nucleus of the solitary tract, associated with
visceral sensations like nausea and vomiting.
Most notably, the two areas of motor control and
memory are where the effects of cannabis are directly and
irrefutably evident. Cannabinoids, depending on the dose,
inhibit the transmission of neural signals through the basal
ganglia and cerebellum. At lower doses, cannabinoids
seem to stimulate locomotion while greater doses inhibit
it, most commonly manifested by lack of steadiness (body
sway and hand steadiness) in motor tasks that require a lot
of attention. Other brain regions, like the cortex, the

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cerebellum, and the neural pathway from cortex

to striatum, are also involved in the control of movement
and contain abundant cannabinoid receptors, indicating
their possible involvement as well.
Experiments on animal and human tissue have
demonstrated
a
disruption
of short-term
memory formation, which is consistent with the
abundance of CB1 receptors on the hippocampus, the
region of the brain most closely associated with memory.
Cannabinoids
inhibit
the
release
of
several
neurotransmitters
in
the
hippocampus
such
as acetylcholine, norepinephrine, and glutamate, resulting
in a major decrease in neuronal activity in that region.
This decrease in activity resembles a temporary
hippocampal lesion.
In in-vitro experiments THC at extremely high
concentrations, which could not be reached with
commonly
consumed
doses,
caused competitive
inhibition of the AChE enzyme and inhibition of amyloidpeptide
aggregation,
implicated
in the
development of Alzheimer's disease. Compared to
currently approved drugs prescribed for the treatment of
Alzheimer's disease, THC is a considerably superior
inhibitor of aggregation, and this study provides a
previously unrecognized molecular mechanism through
which cannabinoid molecules may impact the progression
of this debilitating disease [6].
Effects on driving
Cannabis usage has been shown to have a
negative effect on driving ability.[54] The British Medical
Journal indicated that drivers who consume cannabis
within three hours of driving are nearly twice as likely to
cause a vehicle collision as those who are not under the
influence of drugs or alcohol [7].
In Cannabis and driving: a review of the
literature
and
commentary,
the
United
Kingdom's Department for Transport reviewed data on
cannabis and driving, finding Cannabis impairs driving
behaviour. However, this impairment is mediated in that
subjects under cannabis treatment appear to perceive that
they are indeed impaired. Where they can compensate,
they do, for example ... effects of driving behaviour are
present up to an hour after smoking but do not continue
for extended periods. The report summarizes current
knowledge about the effects of cannabis on driving and
accident risk based on a review of available literature
published since 1994 and the effects of cannabis on
laboratory based tasks. The study identified young males,
amongst whom cannabis consumption is frequent and
increasing, and in whom alcohol consumption is also
common, as a risk group for traffic accidents. The cause,
according to the report, is driving inexperience and
factors associated with youth relating to risk taking,
delinquency and motivation. These demographic and
psychosocial variables may relate to both drug use and

accident risk, thereby presenting an artificial relationship

between use of drugs and accident involvement [8].
Kelly, Darke and Ross show similar results, with
laboratory studies examining the effects of cannabis on
skills utilised while driving showing impairments in
tracking, attention, reaction time, short-term memory,
hand-eye coordination, vigilance, time and distance
perception, and decision making and concentration. An
EMCDDA review concluded that the acute effect of
moderate or higher doses of cannabis impairs the skills
related to safe driving and injury risk, specifically
attention, tracking and psychomotor skills. In their review
of driving simulator studies, Kelly et al. conclude that
there is evidence of dose-dependent impairments in
cannabis-affected drivers' ability to control a vehicle in
the areas of steering, headway control, speed variability,
car following, reaction time and lane positioning. The
researchers note that even in those who learn to
compensate for a drug's impairing effects, substantial
impairment in performance can still be observed under
conditions of general task performance (i.e. when no
contingencies are present to maintain compensated
performance).
A
report
from
the University
of
Colorado, Montana State University, and the University
of Oregon found that on average, states that have
legalized Medical cannabis had a decrease in trafficrelated fatalities by 8-11%. Drunk drivers take more risk,
they tend to go faster. They dont realize how impaired
they are. People who are under the influence of marijuana
drive slower, they dont take as many risks. Another
consideration, they added, was the fact that users of
marijuana tend not to go out as much [9].
Cardiovascular effects
Cannabis arteritis is a very rare peripheral
vascular disease similar to Buerger's disease. There were
about 50 confirmed cases from 1960 to 2008, all of which
occurred in Europe. However, all of the cases also
involved tobacco (a known cause of Buerger's disease) in
one way or another, and nearly all of the cannabis use was
quite heavy. In Europe, cannabis is typically mixed with
tobacco, in contrast to North America.
A 2008 study by the National Institutes of
Health Biomedical Research Centre in Baltimore found
that heavy, chronic smoking of marijuana (138 joints per
week) changed blood proteins associated with heart
disease and stroke. This may be a result of raised
carboxyhemoglobin levels from carbon monoxide. A
similar increase in heart disease and ischemic strokes is
observed in tobacco smokers, which suggests that the
harmful effects come from a variety of combustion
products, not just marijuana.
A 2005 article in the Journal of Neurology,
Neurosurgery and Psychiatry reported on a 36-year-old
man who suffered a stroke on three separate occasions

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after smoking a large amount of marijuana, despite having

no known risk factors for the disorder, suggesting that a
rare side effect of marijuana use may be an increase in the
incidence of strokes among young smokers. A 2000 study
by researchers at Boston's Beth Israel Deaconess Medical
Center, Massachusetts General Hospital and Harvard
School of Public Health also found that a middle-age
person's risk of heart attack rises nearly fivefold in the
first hour after smoking marijuana, about twice the risk as
vigorous exercise or sexual intercourse [10].
Adulterated cannabis
Contaminants may be found in hashish obtained
from soap bar-type sources. The dried flowers of the plant
may be contaminated by the plant taking up heavy metals
and other toxins from its growing environment, or by the
addition of lead or glass beads, used to increase the
weight or to make the cannabis appear as if it has more
crystal-looking trichomes indicating a higher THC
content. Users who burn hot or mix cannabis with tobacco
are at risk of failing to detect deviations from appropriate
cannabis taste.
Despite cannabis being generally perceived as a
natural or chemical-free product, in a recent Australian
survey one in four Australians consider cannabis grown
indoors under hydroponic conditions to be a greater health
risk due to increased contamination, added to the plant
during cultivation to enhance the plant growth and quality
[11].
Combination with other drugs
The most obvious confounding factor in
cannabis research is the prevalent usage of other
recreational drugs, especially alcohol and nicotine. Such
complications demonstrate the need for studies on
cannabis that have stronger controls, and investigations
into alleged symptoms of cannabis use that may also be
caused by tobacco. Some critics question whether
agencies doing the research make an honest effort to
present an accurate, unbiased summary of the evidence, or
whether they cherry-pick their data to please funding
sources which may include the tobacco industry or
governments dependent on cigarette tax revenue; others
caution that the raw data, and not the final conclusions,
are what should be examined.
Cannabis also has been shown to have a
synergistic cytotoxic effect on lung cancer cell cultures in
vitro
with
the
food
additive butylated
hydroxyanisole (BHA) and possibly the related
compound butylated hydroxytoluene (BHT). The study
concluded, Exposure to marijuana smoke in conjunction
with BHA, a common food additive, may promote
deleterious health effects in the lung. BHA & BHT are
human-made fat preservatives, and are found in many
packaged foods including: plastics in boxed cereal, Jello,
Slim Jims, and more.

The Australian National Household Survey of

2001 showed that cannabis use in Australia is rarely used
without other drugs. 95% of cannabis users also drank
alcohol; 26% took amphetamines; 19% took ecstasy and
only 2.7% reported not having used any other drug with
cannabis. While research has been undertaken on the
combined effects of alcohol and cannabis on performing
certain tasks, little research has been conducted on the
reasons why this combination is so popular. Evidence
from a controlled experimental study undertaken by
Lukas and Orozco suggests that alcohol causes THC to be
absorbed more rapidly into the blood plasma of the user.
Data from the Australian National Survey of Mental
Health and Wellbeing found that three-quarters of recent
cannabis users reported using alcohol when cannabis was
not available [12].
Memory and learning
Studies on cannabis and memory are hindered by
small sample sizes, confounding drug use, and other
factors. The strongest evidence regarding cannabis and
memory focuses on its temporary negative effects on
short-term and working memory.
In a 2001 study looking at neuropsychological
performance in long-term cannabis users, researchers
found some cognitive deficits appear detectable at least 7
days after heavy cannabis use but appear reversible and
related to recent cannabis exposure rather than
irreversible and related to cumulative lifetime use. On his
studies regarding cannabis use, lead researcher and
Harvard professor Harrison Pope said he found marijuana
is not dangerous over the long term, but there are shortterm effects. From neuropsychological tests, Pope found
that chronic cannabis users showed difficulties, with
verbal memory in particular, for at least a week or two
after they stopped smoking. Within 28 days, memory
problems vanished and the subjects were no longer
distinguishable from the comparison group.
Researchers from the University of California,
San Diego School of Medicine failed to show substantial,
systemic neurological effects from long-term recreational
use of cannabis. Their findings were published in the July
2003 issue of the Journal of the International
Neuropsychological Society. The research team, headed
by Dr Igor Grant, found that cannabis use did affect
perception, but did not cause permanent brain damage.
Researchers looked at data from 15 previously published
controlled studies involving 704 long-term cannabis users
and 484 nonusers. The results showed long-term cannabis
use was only marginally harmful on the memory and
learning. Other functions such as reaction time, attention,
language, reasoning ability, perceptual and motor skills
were unaffected. The observed effects on memory and
learning, they said, showed long-term cannabis use
caused selective memory defects, but that the impact was
of a very small magnitude.

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Appetite
The feeling of increased appetite following the
use of cannabis has been documented for hundreds of
years, and is known as the munchies in popular culture.
Clinical studies and survey data have found that cannabis
increases food enjoyment and interest in food. Scientists
have claimed to be able to explain what causes the
increase in appetite, concluding that endocannabinoids in
the hypothalamus activate cannabinoid receptors that are
responsible for maintaining food intake. Rarely, chronic
users experience a severe vomiting disorder, cannabinoid
hyperemesis syndrome, after smoking and find relief by
taking hot baths.
Endogenous cannabinoids (endocannabinoids)
were
discovered
in
cow's
milk
and
soft
cheeses. Endocannabinoids were also found in human
breast milk. It is widely accepted that the neonatal
survival of many species is largely dependent upon their
suckling behavior, or appetite for breast milk and recent
research has identified the endogenous cannabinoid
system to be the first neural system to display complete
control over milk ingestion and neonatal survival. It is
possible that cannabinoid receptors in our body interact
with the cannabinoids in milk to stimulate a suckling
response in newborns so as to prevent growth failure [13].
Long-Term Effects
Though the long-term effects of cannabis have
been studied, there remains much to be concluded;
debated topics include the drug's addictiveness, its
potential as a gateway drug, its effects on intelligence and
memory, and its contributions to mental disorders such as
schizophrenia and depression. On some such topics, such
as the drug's effects on the lungs, relatively little research
has been conducted, leading to division as to the severity
of its impact. However, a study funded by the US
government on the long term lung-related effects of
marijuana has concluded that moderate marijuana use
does not impair pulmonary function.
More research is no guarantee of greater
consensus in the field of cannabis studies, however; both
advocates and opponents of the drug are able to call upon
multiple scientific studies supporting their respective
positions. Cannabis has been correlated with the
development of various mental disorders in multiple
studies, for example a recent 10 year study on 1,923
individuals from the general population inGermany, aged
1424, concluded that cannabis use is a risk factor for the
development of incident psychotic symptoms. Continued
cannabis use might increase the risk for psychotic
disorder.
Efforts to prove the gateway drug hypothesis that
cannabis and alcohol makes users more inclined to
become addicted to harder drugs like cocaine and heroin
have produced mixed results, with different studies
finding varying degrees of correlation between the use of

cannabis and other drugs, and some finding none.

However, believe the gateway effect, currently being
pinned on the use of marijuana, should not be attributed to
the drug itself but rather the illegality of the drug in most
countries. Supporters of this theory believe that the
grouping of marijuana and harder drugs in law is, in fact,
the cause of users of marijuana to move on to those harder
drugs.
There have been debates as to whether cannabis
can lead to heavy addiction. According to one of the
studies on the issue, the La Guardia Committee of 1944,
smoking marijuana could help to get out of the addiction
from substances like cocaine or morphine.
Cannabis withdrawal is included in the proposed
revision of DSM-5. Several drugs have been investigated
in an attempt to ameliorate the symptoms of cannabis
withdrawal.
Such
drugs
include
bupropion
, divalproex, nefazodone, lofexidine,and dronabinol. Of
these, dronabinol has proven the most effective.
Effects In Pregnancy
A study of 600 mothers that reported smoking
cannabis during pregnancy suggested that it was not
associated
with
increased
risk
of perinatal
mortality. However, frequent and regular use of cannabis
throughout pregnancy may be associated with a small but
statistically detectable decrease in birth weight.
Melanie Dreher, dean of nursing at Rush
Medical Center in Chicago, conducted a study of
Jamaican women who used cannabis throughout their
pregnancies, as well as their babies' first year. The study
was published in the American Journal of Pediatrics in
1994. Dreher expected to see a decrease in birth weight,
but saw none. Instead, the exposed babies socialized and
made eye contact more quickly, had better organization
and modulation of sleeping and waking, and were less
prone to anxiety. On difference between the Jamaican and
other
studies'
results,
Medicine
hunter Chris
Kilham noted, In U.S. studies where we've seen a similar
investigation, women have concurrently been abusing
alcohol and other drugs as well [14].
Pathogens and microtoxins
Most microorganisms found in cannabis only
affect plants and not humans, but some microorganisms,
especially those that proliferate when the herb is not
correctly dried and stored, can be harmful to humans.
Some users may store marijuana in an airtight bag or jar
in a refrigerator to prevent fungal and bacterial growth
[15].
Fungi
The
fumigatus,
parasiticus,
sulphureus,

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fungi Aspergillus
flavus, Aspergillus
Aspergillus
niger,
Aspergillus
Aspergillus
tamarii, Aspergillus
Aspergillus
repens,
Mucor

Inter. J. of Phytotherapy / Vol 3 / Issue 1 / 2013 / 24-32.

hiemalis,
Penicillium
chrysogenum, Penicillium
italicum and Rhizopus nigrans have been found in moldy
cannabis. Aspergillus mold species can infect the lungs
via smoking or handling of infected cannabis and cause
opportunistic and sometimes deadlyaspergillosis. Some of
the microorganisms found create aflatoxins, which
are toxic and carcinogenic. Researchers suggest that
moldy cannabis thus be discarded.
Mold is also found in smoke from mold infected
cannabis, and the lungs and nasal passages are a major
means of contracting fungal infections. Levitz and
Diamond (1991) suggested baking marijuana in home

ovens at 150 C [302 F], for five minutes before

smoking.
Oven
treatment
killed conidia of A.
fumigatus, A. flavus and A. niger, and did not degrade the
active component of marijuana, tetrahydrocannabinol
(THC) [16].
Bacteria
Cannabis
contaminated
with Salmonella
muenchen was positively correlated with dozens of cases
of salmonellosis in
1981. Thermophilic actinomycetes
were also found in cannabis [17].

Fig 1. The structural formula of tetrahydrocannabinol

Fig 2. Tetrahydrocannabivarin

Fig 3. Cannabidiol

Fig 4. Cannabinol

Fig 5. Cannabivarin

Fig 6. Cannabidivarin

Fig 7. Aspergillus fumigatus

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Inter. J. of Phytotherapy / Vol 3 / Issue 1 / 2013 / 24-32.

CONCLUSION
In many countries, experimental science regarding
cannabis is restricted due to its illegality. Thus, cannabis
as a drug is often hard to fit into the structural confines of

medical research because appropriate, research-grade

samples are difficult to obtain for research purposes,
unless granted under authority of national governments.

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