Alcohol
Structure of Ethanol
Alcohol may be the world's oldest known drug. Fermented
grain, fruit juice and honey have been used to make alcohol
(ethyl alcohol or ethanol) for thousands of years. The
production of products containing alcohol has become big
business in today's society and the consumption and abuse of
alcohol has become a major public health problem. On this
page, only the effects of alcohol on the brain and behavior will
be discussed.
Alcohol is a central nervous system depressant. Factors that influence how alcohol will
affect a person include:
1.
2.
3.
4.
5.
age
gender
physical condition
amount of food eaten
other drugs or medicines taken
The Path of Alcohol in the Body
1. Mouth: alcohol enters the body.
2. Stomach: some alcohol gets into the bloodstream in the stomach, but
most goes on to the small intestine.
3. Small Intestine: alcohol enters the bloodstream through the walls of
the small intestine.
4. Heart: pumps alcohol throughout the body.
5. Brain: alcohol reaches the brain.
6. Liver: alcohol is oxidized by the liver at a rate of about 0.5 oz per hour.
Alcohol is converted into water, carbon dioxide and energy.
In low doses,
alcohol produces:
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a relaxing
effect
reduces
tension
lowers
inhibitions
impairs
concentration
slows reflexes
impairs
reaction time
reduces
In medium doses,
alcohol produces:
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slur speech
cause
drowsiness
alter
emotions
In high doses,
alcohol produces:
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vomiting
breathing difficulties
unconsciousness
coma
coordination
Effects of Alcohol on the Nervous System
As mentioned above, alcohol is a central nervous system depressant. It
acts at many sites, including the reticular formation, spinal cord,
cerebellum and cerebral cortex, and on many neurotransmitter systems.
Alcohol is a very small molecule and is soluble in "lipid" and water
solutions. Because of these properties, alcohol gets into the bloodstream
very easily and also crosses the blood brain barrier. Some of the neurochemical effects of
alcohol are:
1.
2.
3.
4.
Increased turnover of norepinephrine and dopamine
Decreased transmission in acetylcholine systems
Increased transmission in GABA systems
Increased production of beta-endorphin in the hypothalamus
Chronic drinking can lead to dependence and addiction to alcohol and to additional neurological
problems. Typical symptoms of withholding alcohol from someone who is addicted to it are shaking
(tremors), sleep problems and nausea. More severe withdrawal symptoms include hallucinations and
even seizures.
Chronic alcohol use can:
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Damage the frontal lobes of the brain
Cause an overall reduction in brain size and increase in the size of the ventricles.
Lead to alcoholism (addiction to alcohol) and result in tolerance to the effects of alcohol and
variety of health problems.
Cause a vitamin deficiency. Because the digestion system of alcoholics is unable to absorb
vitamin B-1 (thiamine), a syndrome known as "Wernicke's Encephalopathy" may develop. This
syndrome is characterized by impaired memory, confusion and lack of coordination. Further
deficiencies of thiamine can lead to "Korsakoff's Syndrome". This disorder is characterized by
amnesia, apathy and disorientation. Widespread disease of the brain is a feature of both
Wernicke's and Korsakoff's Syndromes.
Barbiturates
What are Barbiturates?
The hustle and bustle of everyday life creates stress in many
people. To reduce stress, some people turn to drugs to bring back
a feeling of calm. Alcohol is one drug people use to deal with
stress; another class of drugs is called the "barbiturates." These
drugs act to depress the central nervous system and are often
called sleeping pills.
The first barbiturates were made in the 1860s by the Bayer laboratories in
Germany. In 1903, the first barbiturate ("barbital") was used in medical practices. In
1912, a common barbiturate, Phenobarbital, was introduced.
There are many different types of barbiturates. The names of some common ones
(and brand names) include Pentobarbital (Nembutal), Secobarbital (Seconal),
Amobarbital (Amytal) and Phenobarbital (Luminal); slang names for these
barbiturates include yellow jackets, reds, blues, Amy's, and rainbows.
Barbiturates
Image courtesy
of the
Indiana
Prevention
Resource Center
Barbiturates have been used extensively in the past as sedatives. However,
barbiturates are still used to treat some types of epilepsy.
Behavioral Effects of Barbiturates
Barbiturates have several effects on behavior depending on the
dose:
In low doses: barbiturates reduce anxiety; reduce respiration,
reduce blood pressure, reduce heart rate and reduce rapid eye movement (REM)
sleep. In higher doses: barbiturates can actually increase some types of behavior
and act like a stimulant. These effects may be caused by depression of inhibitory
brain circuits. In other words, barbiturates at these doses act to remove inhibitory
behavior.
Barbiturates can lead to excessive sedation and cause anesthesia, coma and even
death. Barbiturate overdoses may occur because the effective dose of the drug is not
too far away from the lethal dose.
Barbiturates
Image courtesy of
the
Indiana
Prevention
Resource Center
A major problem with barbiturates is that they may lead to tolerance and
dependence. Tolerance occurs when a greater and greater amount of the drug is
required to get the desired effect. For example, if barbiturates are used to help a
person sleep, over time, a greater dose of the drug will be needed to get the person
to sleep. Dependence occurs when a person feels like he or she must use the drug
and withdrawal symptoms occur when the person stops using the drug.
Withdrawal symptoms that occur when people try to "kick the habit" of using
barbiturates include:
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anxiety
insomnia
seizures
nausea, stomach problems
hallucinations
Effects of Barbiturates on the Brain
Barbiturates dissolve easily in fat. Therefore, barbiturates have ready access to
the brain because they can cross the blood brain barrier easily. Also, because
barbiturates dissolve into body fat, they can accumulate and re-enter the blood
stream later. Different barbiturates clear out of the blood stream at different rates.
Although the exact mechanisms by which barbiturates affect the brain are not
understood, it is thought that these drugs bind to sodium channels on neurons and
prevent the flow of sodium ions. Because sodium ions cannot flow across the
neuronal membrane, action potentials cannot be produced.
Barbiturates may also increase the flow of chloride ions across the neuronal membrane. This may occur
through binding to the receptor for the neurotransmitter called GABA. The increased chloride ion flow
reduces the chance that an action potential will be generated.
Did you
know?

The barbiturate called sodium pentothal is known as "truth serum." However, it really
does NOT cause people to tell the truth. Rather, it may lower a person's inhibitions
and make people more talkative.
Musician Jimi Hendrix died on September 18, 1970 of a barbiturate overdose.

Cocaine
Coca Leaf
From the plant called
Erythroxylon coca, cocaine is a
local anesthetic and central
nervous system stimulant. It
can be taken by chewing on
coca leaves, smoked, inhaled
("snorted") or injected.
Coca Plant
History of Cocaine
Early Spanish explorers noticed how the native people of South
America were able to fight off fatigue by chewing on coca leaves. A
medical account of the coca plant was published in 1569. In 1860,
Albert Neiman isolated cocaine from the coca leaf and described the
anesthetic action of the drug when it was put on his tongue. Angelo
Mariani, in the early 1880s produced a "medicinal" wine, called Vin
Mariani, that contained 11% alcohol and 6.5 mg of cocaine in every
ounce. The famous psychotherapist, Sigmund Freud, in 1884,
recommended cocaine for a variety of illnesses and for alcohol and
morphine addictions. Unfortunately, many of his patients went on to
become addicted to cocaine! In 1886, John Pemberton developed
Coca Cola, a drink that contained cocaine and caffeine. Cocaine
was REMOVED from Coca Cola in 1906 (but it still has the caffeine).
Coca Wine
In 1985, crack cocaine was introduced and rapidly became a major
drug problem.
Crack
Effects of Cocaine on the Nervous System
A dose of between 25 to 150 mg of cocaine is taken when it is inhaled. Within a few
seconds to a few minutes after it is taken, cocaine can cause:
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a feeling of euphoria
excitement
reduced hunger
a feeling of strength
After this "high" which lasts about one hour, users of cocaine may "crash" into a
period of depression. This crash causes cocaine users to seek more cocaine to get
out of this depression and results in addiction. Withdrawal from cocaine can cause the
addict to feel depressed, anxious, and paranoid. The addict may then go into a period
of exhaustion and they may sleep for a very long time.
Cocaine
Various doses of cocaine can also produce neurological and behavioral problems like:
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dizziness
headache
movement problems
anxiety
insomnia
depression
hallucinations
Emergency Room Visits due to Cocaine and Heroin
Death caused by too much cocaine (an overdose)
is not uncommon. Cocaine can cause large
increases in blood pressure that may result in
bleeding within the brain. Constriction of brain
blood vessels can also cause a stroke. An
overdose of cocaine can cause breathing and
heart problems that could result in death.
Comedian John Belushi also died from a
cocaine/heroin overdose in 1982.
Cocaine is highly "reinforcing": when it is given to
animals, they will give it to themselves. In fact, if
animals are given the choice, they will put up with
electrical shocks and give up food and water if
they can get cocaine.
Image courtesy of the Office of National Drug
Control Policy
Cocaine acts by blocking the reuptake of the
neurotransmitters dopamine, norepinephrine and
serotonin in the brain. Therefore, these
neurotransmitters stay in the synaptic cleft for a
longer time. Research has also shown that
cocaine can also cause the release of dopamine
from neurons in the brain.
Heroin
HORSE - CRANK - JIVE - SMACK -JUNK - SHAG – DOPE
You can even spell it by its chemical name: diacetylmorphine. It doesn't matter which way you spell it, it still
means HEROIN.
Heroin is an illegal opiate drug made from the opium poppy, Papaver somniferum.
The opium poppy is a plant found in the Middle East, Southeast Asia and parts of
Central and South America. To harvest opium, the seed pod of the poppy is cut
and a juice flows out. The main ingredient that is extracted from raw opium is
morphine. Morphine is easily converted to he
roin by a chemical process.
Opium Harvest
Papaver somniferum
Places where opium is produced (shown in red)
In 1973, scientists discovered that the brain had receptors for opiates. In other words, there are places on
neurons that recognize opiates. These receptors were located in parts of the brain important for breathing,
pain and emotions. The discovery of opiate receptors in the brain raised the question as to why neurons
would have such receptors. Two years later, scientists found the answer: the brain manufactures its own
opiates known as "endorphins." Endorphins are always in the brain, but they are released in greater
amounts when people and animals are in pain or under stress.
History of the Opiates
Records indicate that opium was used by the
ancient Egyptians, Greeks and Romans. The
poppy even appears on Egyptian art dating back
6,000 years. Opium was imported to China around
800 A.D. By the 1600s, opium smoking was
widespread throughout China. In 1680, a famous
English physician named Thomas Syndenham
introduced opium to the medical field.
In the 17th century, many people in Europe were
treated for a variety of health problems with opium.
In 1729, opium smoking was made illegal in China
and soon the importation of opium was banned.
This ban upset the British who were in charge of
trading this valuable product. Opium was still
smuggled into China and this caused the "Opium
Wars" (1839-1842 and 1856-1860) between the
British and the Chinese.
In the US, opium was used to treat soldiers during
the Civil War (1861-1865). During the late 1800s,
doctors prescribed "tonics" containing opiates for
many conditions. Rarely did these medicines list
opiates as one of the ingredients. In fact, heroin
was marketed as a cough medicine and a cure for
morphine addiction. However, many physicians
had concerns about possible addiction to these
medicines.
Important Dates in the History of Opiates
1803 - morphine was isolated from opium by Frederick Serturner.
1832 - codeine was extracted from opium.
1853 - the hypodermic needle was invented.
1874 - heroin was first produced from morphine.
1898 - The Bayer Company introduced heroin as a substitute for morphine.
1906 - Pure Food and Drugs Act - required medicines to be labeled with the materials
that they contained.
1914 - Harrison Narcotic Act - added a tax on opiate distribution.
1922 - Narcotic Import and Export Act - restricted the importation of crude opium except
for medical use.
1924 - Heroin Act - made manufacture and possession of heroin illegal.
1930 - Federal Bureau of Narcotics was created.
1970 - Controlled Substances Act was passed - divided drugs into categories, set
regulations and penalties for narcotics
How Heroin is Used
The purity of heroin can vary greatly. Heroin can be mixed with powdered milk,
sugar, baking soda, procaine and lidocaine (local anesthetics) or even laundry
detergent, talc, starch, curry powder, Ajax cleaner or strychinine. All of these
"additives" are dangerous if they are injected into the bloodstream. Heroin is
smoked or inhaled as a powder or it can be mixed with water, heated, then
injected. Heroin crosses through the blood brain barrier 100 times faster than
morphine because it is highly soluble in lipids.
Injecting heroin into a vein (intravenous use) produces effects in 7 to 8
seconds. Injecting heroin into a muscle (intramuscular use) or under the skin
(subcutaneous use) can produce effects in 5 to 8 minutes. Addicts sometimes
inject themselves up to 4 times in one day.
Effects of Heroin
The overall effect of heroin is a depression of the central nervous system.
Short Term Effects
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Analgesia (reduced pain)
Brief euphoria (the "rush" or feeling of well-being)
Nausea
Sedation, drowsiness
Reduced anxiety
Hypothermia
Reduced respiration; breathing difficulties
Reduced coughing
Death due to overdose - often the exact purity and content of the drug is not
known to the user. An overdose can cause respiration problems and coma
Morphine
Long Term Effects
 Tolerance: more and more drug is needed to produce the euphoria and other
effects on behavior.
 Addiction: psychological and physiological need for heroin. People are driven
to get more heroin and feel bad if they do not get it. People begin to crave heroin 4 to
6 hours after their last injection.
 Withdrawal: About 8-12 hours after their last heroin dose, addicts' eyes tear,
they yawn and feel anxious and irritable. Excessive sweating, fever, stomach and
muscle cramps, diarrhea and chills can follow several hours later. These withdrawal symptoms
can continue for 1 to 3 days after the last dose and can last 7 to 10 days. In some cases, full
recovery can take even longer.
Other Effects
In addition to the direct dangers of heroin, this powerful drug also carries the risk of:
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HIV/AIDS - due to sharing of needles
Poisoning - from the addition of toxin to the drug
Hepatitis - liver damage
Skin infections - from repeated intravenous injections
Other bacterial and viral infections
Increase risk of stroke
Collapsed veins
Lung infections
How Heroin Affects the Brain
Not all of the mechanisms by which heroin and other
opiates affect the brain are known. Likewise, the exact
brain mechanisms that cause tolerance and addiction are
not completely understood. Opiates stimulate a "pleasure
system" in the brain. This system involves neurons in the
midbrain that use the neurotransmitter called "dopamine."
These midbrain dopamine neurons project to another
structure called the nucleus accumbens which then projects to the cerebral
cortex. This system is responsible for the pleasurable effects of heroin and
for the addictive power of the drug. Other neurotransmitter systems, such as
those related to endorphins, are also likely to be involved with withdrawal
from and tolerance to heroin.
Treatment of Heroin Overdose and Addiction
Behavioral Methods
Heroin addiction is usually treated with both medical and behavioral
methods. Behavioral treatment might give rewards to people for
negative drug tests. Other treatments may attempt to change the drugseeking behavior of addicts.
Naloxone
People who overdose on heroin are given a drug called "naloxone."
Naloxone is an opiate receptor blocker that binds to neurons so opiates
cannot work.
Methadone
Methadone is a drug that blocks the effects of heroin and has been
used for several decades to treat heroin addiction. Methadone can be
swallowed (rather than injected) and it blocks heroin withdrawal
symptoms and does not have euphoric or sedative effects.
effects last longer. LAAM was approved by the US Food and Drug
Administration for treating heroin addiction in 1993.
Liquid
LSD
Lysergic acid diethylamide, better known as LSD, is a chemical that
alters a user's mood, thoughts or perceptions. For this reason, LSD is
grouped into a class of drugs known as hallucinogens or
psychedelics. These drugs can cause auditory, visual or
somatosensory hallucinations, paranoia or dream-like states.
LSD Pills
Image courtesy of the Indiana
Prevention Resource Center
LSD was first synthesized from a fungus that grows on rye and other grains. In 1938,
Albert Hofmann working in the Swiss pharmaceutical company called Sandoz,
produced LSD for the first time. He was hoping that this new drug could be used to
stimulate circulation and respiration. However, the tests he conducted were all failures
and he forgot about LSD for 5 years. In 1943, Hofmann accidentally ingested (or
somehow absorbed) a bit of LSD and experienced some of the psychedelic effects of
this chemical: dizziness, visual distortions and restlessness. A few days later he
prepared 0.25 mg of LSD in water and drank it. He again experienced the mood and
thought altering effects of LSD.
Effects of LSD on the Nervous System
LSD is water soluble, odorless, colorless and tasteless - it is a very powerful drug - a dose as small as a
single grain of salt (about 0.010 mg) can produce some effects. Psychedelic effects are produced at
higher doses of about 0.050-0.100 mg. The effects of LSD depend on a user's mood and expectations of
what the drug will do and last several hours. The behavioral effects that LSD can produce include:
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Feelings of "strangeness"
Vivid colors
Hallucinations
Confusion, panic, psychosis, anxiety
Emotional reactions like fear, happiness or sadness
Distortion of the senses and of time and space
"Flashback" reactions - these are the effects of LSD that occur
even after the user has not taken LSD for months or even
years.
Increases in heart rate and blood pressure
Chills
Muscle weakness
Tolerance to the effects of LSD develops quickly and users must increase their intake of LSD to get the
same effects. The exact neural pathways that are affected by LSD are not completely known. LSD has a
chemical structure that is very similar to the neurotransmitter called serotonin. It is thought that the
effects of LSD are caused by stimulation of serotonin receptors on neurons, perhaps in the brain area
called the raphe nuclei. However, it is still not clear what produces all the effects of LSD.
Nicotine (Tobacco)
A complete list of the reasons to avoid smoking and chewing
tobacco is not necessary here, but for starters, how about
lung cancer, lip cancer, throat cancer, respiratory problems,
heart disease and bad breath.
SURGEON GENERAL'S
WARNING: Quitting
Smoking Now Greatly
Reduces Serious Risks
to Your Health.GENE
Tobacco contains nicotine. Nicotine is a drug. Therefore, when people smoke
or chew tobacco, they are using a drug.
SURGEON GENERAL'S
WARNING: Smoking
Causes Lung Cancer,
Heart Disease,
Emphysema and May
Complicate Pregnancy..
Brief History of Tobacco
Christopher Columbus and his crewman on their voyage to the "New World" were the first
Europeans to see tobacco smoking. The tobacco plant is called Nicotiana tabacum and is
named after an early importer named Jean Nicot. A water/nicotine mixture has been used as
an insecticide since 1746. In 1828, nicotine was isolated from the leaves of the tobacco plant.
Effects of Nicotine on the Nervous System
In tobacco smoke, nicotine "rides" on small particles of tar. When the smoke with this
nicotine/tar mixture gets to the lungs, the nicotine is absorbed quickly - nicotine reaches
the brain about eight seconds after the smoke is inhaled. American cigarettes contain
about 9 mg of nicotine, but because much of the nicotine is burned off, a smoker gets
about 1 mg of nicotine in every cigarette. Nicotine reaches the central nervous system in
about 3-5 minutes when tobacco is chewed.
Smoking can be stimulating or relaxing - it depends on a person's mood and dosage of nicotine. Nicotine
acts on the central and peripheral nervous system. The rapid effects of nicotine include:
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Increases in blood pressure and heart rate
Faster respiration
Constriction of arteries
Stimulation of the central nervous system
Long term exposure to tobacco and nicotine increases the chances of
cancer and results in addiction and dependence. Exactly how nicotine
produces addiction and dependence is not clear, but there are some
theories. In the brain, limbic pathways that use the neurotransmitter
dopamine are affected by nicotine and may be responsible for some of
the addictive properties. It is clear though, that nicotine is one of the
most addicting substances known...just ask anyone who has tried to
quit smoking. Common withdrawal symptoms in people who are trying
to "kick the habit" of tobacco include:
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Anxiety
Fatigue
Headaches
Depression
Headaches
Fatigue
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Did you
know?



According to the World Health Organization, there are 1.1 billion smokers worldwide
and 6000 billion cigarettes are smoked every year.
According to the US Centers for Disease Control, there are about 46.2 million adult
cigarette smokers in the US. Moreover, tobacco use in the US results in more than
440,000 deaths each year (about 1 in 5 deaths.) The economic costs (medical
costs and lost productivity) of tobacco use are more than $150 billion.
The New Straits Times (August 11, 1997) reported on a "smoking contest" between
two young men (ages 19 and 21 years old). These two men wanted to see who
could smoke the most cigarettes at a single sitting. The result was tragic: the 19
year old died after smoking 100 cigarettes and the 21 year old was seriously
poisoned after smoking 80 cigarettes. It goes without saying, "Don't try this at
home!"
"Bidi" cigarettes are NOT safe alternatives to regular cigarettes. A bidi cigarette has
THREE times more nicotine and carbon monoxide and FIVE times more tar than a
regular American cigarette. (Statistic from Yen et al., Archives of Pediatric and
Adoles. Medicine, 154:1187-1189, 2000.)
The cost of a pack of cigarettes in New York is about $7.00. Therefore, a person
who smokes one pack of cigarettes each day will spend $2,555.00 each year on
tobacco. (Reference: Associated Press story, "With packs hitting $7, smokers try to
kick habit" reprinted in the Seattle Times, July 13, 2002.)
More than 100 chemicals are added to tobacco to make cigarettes. These
chemicals include benzaldehyde, butyric acid, decanoic acid, ethyl acetate,
hexanoic acid, 3-methylbutyraldehyde, methylcyclopentenolone, and
tolualdehydes. (Reference: Philip Morris USA.)
Gamma hydroxybutyrate (GHB)
Gamma hydroxybutyrate: An Overview
Have you heard of GHB? You may not have yet, but its use is increasing. Once limited to large
warehouse scenes such as "raves," GHB is showing up at parties, perhaps in neighborhoods like yours. It
gives the user a feeling of euphoria, that everything is fine. GHB, like alcohol, is a central nervous system
depressant that takes only minutes to make a user lose control, forget what is happening, or lose
consciousness. GHB is colorless, odorless, and has a slightly salty taste. The synthetic form of GHB
contains some of the same ingredients as floor stripper and industrial cleaners.
The same dose of GHB can have variable effects in different people. A dose that makes one person feel
euphoric can make another person sick. The US Drug Enforcement Agency has linked GHB to 58 deaths
since 1990 and there have been at least 5,700 overdoses recorded since then. Moreover, there are some
reports that GHB can cause dependence. Treatment of GHB overdoses is difficult because it is difficult for
emergency room doctors to detect the drug.
Possible symptoms of GHB use:
Dizziness | Vomiting | Seizures | Coma | Drowsiness
GHB was first developed as a general anesthetic, but because it did not work very well to prevent pain, its
use as an anesthetic declined. The observation that GHB may cause the release of growth hormone led
some people, especially athletes and body-builders, to take it because they thought it would increase
muscle development. At the time, GHB was available as a dietary supplement and as such was not
regulated by the US Food and Drug Administration. In 1990, after numerous reports that GHB caused
illness, the FDA began investigating the drug. It is now classified as an illegal substance. Research is
being conducted to investigate the use of GHB in the treatment of the sleep disorder called narcolepsy.
GHB has been grouped with other drugs in the "date-rape drug" category such as Rohypnol, because it
can be slipped easily into a drink and given to an unsuspecting victim, who often does not remember
being assaulted. GHB is especially dangerous when combined with alcohol.
GHB and the Brain
Although GHB can be made in the laboratory, it is also produced normally in the brain through the
synthesis of a neurotransmitter called GABA. Some of the greatest concentrations of GHB are found in
the substantia nigra, thalamus and hypothalamus. When GHB is ingested by a user, it affects several
different neurotransmitter systems in the brain:
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GHB can increase acetylcholine levels.
GHB can increase serotonin levels.
GHB can reduce dopamine activity, especially in the basal ganglia. This action is probably the
result of the inhibition of the release of dopamine from synaptic terminals. Some studies show
that GHB first inhibits the release of dopamine, then causes the release of dopamine. The effect
on the dopamine system may depend on the dose of GHB.
GHB can activate GHB receptors and GABA receptors on neurons in the brain.
Unfortunate Events Led to Tragedy
One case of GHB use ended in tragedy. On January 16th, 1999, three girls told their parents they were
going to a movie, but instead they ended up at a party at someone's house. Some kids were drinking
alcohol and some were smoking marijuana. One of the girls, ninth-grader Samantha, asked for a
Mountain Dew. A 19-year old boy got it for her. At one point, she told her friend the soda tasted "gross,"
but she drank it. A few minutes later she vomited and passed out. She was moved onto the bathroom
floor, beside another 14-year-old girl, Melanie, who also passed out after having a drink. Once the boys
became concerned that they could not wake the girls, they took them to the hospital. Both girls fell into
comas. Melanie recovered, but Samantha never regained consciousness and died in the hospital.
In February 2000 the four males involved (ages 18, 19, and 26) went on trial for the death of Samantha
and the poisoning of the other girls, one of whom ingested some GHB but had no symptoms. This was
the first trial of a GHB-related death. The younger males were found guilty of involuntary manslaughter
and lesser charges of poisoning. The 26-year-old was convicted of being an accessory to manslaughter,
poisoning, and possession of marijuana and GHB. The jail time for the manslaughter convictions is up to
15 years; the jail time for the poisoning convictions can be up to 5 years.
Amphetamines
Amphetamines are drugs such as dextroamphetamine, benzedrine, and Ritalin.
Amphetamines were originally developed to treat asthma, sleep disorders
(narcolepsy) and hyperactivity. In 1920, a drug called "ephedrine" was used to treat
asthma. In China, the ma huang plant (Ephedra vulgaris) had been used for
centuries to treat people with asthma. It is no wonder that the plant worked...the ma
huang plant contains ephedrine. In 1932, synthetic ephedrine was sold "over-thecounter" and was available without a prescription until 1954. During World War II,
amphetamines were given to soldiers and pilots to keep them alert and to fight off fatigue.
Amphetamine Effects on the Nervous System
Amphetamines are stimulants of the central nervous system and sympathetic
division of the peripheral nervous system. It appears that the main action of
amphetamines is to increase the synaptic activity of the dopamine and
norepinephrine neurotransmitter systems. Amphetamines can:
1.
2.
3.
4.
cause the release of dopamine from axon terminals.
block dopamine reuptake.
inhibit the storage of dopamine in vesicles.
inhibit the destruction of dopamine by enzymes.
All of these actions result in more dopamine in the synaptic cleft where it can act
on receptors.
Many of the effects of amphetamines are similar to cocaine. Addiction to and
withdrawal from amphetamines are both possible. Amphetamine use also causes
tolerance to its effects. This means that more and more amphetamine must be
used to get "high." Amphetamine withdrawal is characterized by severe depression
and fatigue. Users will go to extreme measures to avoid the "downer" that comes
when the effect of amphetamines wears off.
Short-term effects of amphetamine use include:






Increased heart rate
Increased blood pressure
Reduced appetite
Dilation of the pupils
Feelings of happiness and power
Reduced fatigue
Long term use of amphetamines can result in:






Insomnia, restlessness
"Paranoid psychosis"
Hallucinations
Violent and aggressive behavior
Weight loss
Tremors
Caffeine
You can call it 3,7-dihydro-1,3,7-trimethyl-1H-purine-2,6,-dione OR 1,3,7trimethylxanthine, but what we are really talking about is CAFFEINE. Caffeine may be
the most popular drug in the world. We consume caffeine in coffee, tea, cocoa,
chocolate, some soft drinks, and some drugs. The actual source of caffeine is the coffee
bean, tea leaf, kola nut and cacao pod. Pure caffeine is odorless and has a bitter taste.
Effects of Caffeine on the Nervous System
Caffeine is a central nervous system stimulant. In moderate
doses, caffeine can:

 increase alertness
 reduce fine motor coordination
 cause insomnia
cause headaches, nervousness and dizziness
In massive doses, caffeine is lethal. A fatal dose of caffeine has been calculated to be more than 10
grams (about 170 mg/kg body weight) - this is the same as drinking 80 to 100 cups of coffee in rapid
succession - not an easy thing to do.
Caffeine enters the bloodstream through the stomach and small intestine and can have its effects as soon
as 15 minutes after it is consumed. Once in the body, caffeine will stay around for hours: it takes about 6
hours for one half of the caffeine to be eliminated.
Caffeine belongs to the xanthine chemical group. Adenosine is a naturally occurring xanthine in the brain
that is used as a neurotransmitter at some synapses. One effect of caffeine is to interfere with adenosine
at multiple sites in the brain including the reticular formation. Caffeine also acts at other sites in the body
to increase heart rate, constrict blood vessels, relax air passages to improve breathing and allow some
muscles to contract more easily.
Some studies show that caffeine causes physical dependence. One way to tell if someone "needs" that
cup of coffee or bottle of Coke is to take it away from them and then see if they have any withdrawal
symptoms. Typical withdrawal symptoms associated with caffeine are headache, fatigue and muscle
pain. These symptoms can occur within 24 hours after the last dose of caffeine. One study has stated that
the minimum consumption of caffeine for physical dependence is 4 cups of coffee per day. Other studies
say that a few more cups of coffee are needed to develop dependence.
Did you
know?
The "Discovery" of Coffee
Legend has it that coffee was "discovered" around 850 AD in upper Egypt by a goat
herded named Khaldi. One night, Khaldi's goats did not return home. When he found his
goats, Khaldi saw them dancing around a shrub with red berries (coffee beans). After
Khaldi tried some of the berries, he started to dance too. Khaldi spoke with some monks
who used the berries to make a drink and....coffee was born!
Caffeine can be found in many drinks, food and drugs. The following items all contain various amounts of
caffeine:
Drinks
Item
Item Size
Caffeine Content (mg)
Coffee
150 ml (5 oz)
60-150
Coffee, decaf
150 ml (5 oz)
2-5
Tea
150 ml (5 oz)
40-80
Hot Cocoa
150 ml (5 oz)
1-8
Chocolate Milk
225 ml
2-7
Jolt Cola
12 oz
100
Mountain Dew
12 oz
55
Surge
12 oz
51
Diet Coca Cola
12 oz
45
Coca Cola
12 oz
64
Coca Cola Classic
12 oz
23
Tab
12 oz
46
RC Cola
12 oz
34
Dr. Pepper
12 oz
61
Mello Yellow
12 oz
35
Mr. Pibb
12 oz
27
Pepsi Cola
12 oz
43
Cherry Coca-Cola
8 oz
23
Surge
8 oz
35
7-Up
12 oz
0
Mug Root Beer
12 oz
0
Sprite
12 oz
0
Did you know?
An American tea and coffee merchant named Thomas Sullivan invented
the tea bag in 1904. He used the tea bag to send samples to his
customers.
Food
Item
Caffeine Content
(mg)
Item Size
Ben/Jerry No Fat Coffee
Fudge Froz. Yog.
1 cup
85
Starbucks Coffee Ice Cream
1 cup
40-60
Dannon Coffee Yogurt
8 oz.
45
Chocolate Bar
50 g
3-63
Chunky Bar
1 bar (40 g)
11.6
100 Grand Bar
1 bar (43 g)
11.2
Nestle Crunch Bar
1 bar (40 g)
10
Krackel Bar
1 bar (47 g)
8.5
Peanut Butter Cup
1 pk (51 g)
5.6
Kit Kat Bar
1 bar (46 g)
5
Mr. Goodbar
1 bar (50 g)
5
Raisinets
10 pieces (10 g)
2.5
Butterfinger Bar
1 bar (61 g)
2.4
Baby Ruth Bar
1 bar (60 g)
2.4
Special Dark Sweet Chocolate
Bar
1 bar (41 g)
31
Chocolate Brownie
1.25 oz
8
Chocolate Chip Cookie
30 g
3-5
Chocolate Ice Cream
50 g
2-5
Milk Chocolate
1 oz
1-15
Bittersweet Chocolate
1 oz
5-35
Butterfinger Bar
1 bar (2.16 oz)
2
After Eight Mint
2 pc (8 g)
1.6
Jell-O Pudding Pop
Chocolate
1 bar (77 g)
2
Non-prescription Drugs
Item (1 tablet or capsule) Caffeine Content(mg)
Dextrim
200
Vivarin
200
No Doz
100
Excedrin
65
Vanquish
33
Anacin
32
Midol
32
Triaminicin
30
Dristan
16
Sources: Pennington, J.A.T., Food Values of Portions Commonly Used (18th Edition), J.B. Lippincott, Philadelphia, 2005; Soft Drink
Manufacturers Association; United States Department of Agriculture, Human Nutrition Information Service, Handbook #8-14 (1986)
and Handbook #8-19 (1991); Starbuck Co. Information Pamphlet, American Beverage Association
Researchers have attempted to find out how much caffeine people consume every
day. Americans consume about 45 MILLION pounds of caffeine each year. In the
United States, coffee drinkers drink an average of 2.6 cups per day. Total caffeine
intake for coffee drinkers was 363.5 mg per day - this includes caffeine from coffee
AND other sources like soft drinks, food and drugs. Non-coffee drinkers even get
plenty of caffeine: former coffee drinkers get about 107 mg per day and people who
have never had coffee get about 91 mg per day.
(References for these numbers is Schreiber et al., Measurement of coffee and caffeine intake: Implications for epidemiolgic
research, Preventive Medicine, 17:280-294, 1988 and Chou, T., Wake up and smell the coffee. Caffeine, coffee and the medical
consequences, West. J. Med., 157:544-553, 1992)
One more thing to think about...Caffeine does NOT counteract the effects of alcohol. In other words,
coffee does NOT make a drunk person sober or fit to drive.
Ecstasy - MDMA
What is Ecstasy (MDMA)?
The American Heritage Dictionary defines ecstasy as "intense joy
or delight." Despite its peppy name, the illegal drug ecstasy can
damage nerve cells in the brain. Ecstasy, also known as 3,4
methylenedioxymethamphetamine or "MDMA" for short, is a
stimulant related to the drugs mescaline and amphetamine. Other
names for MDMA are "Adam," "XTC," "Doves" or just "E."
MDMA was first synthesized and patented in 1914 by the
German drug company called Merck. Scientists thought that this drug could be used as an appetite
suppressant. In the 1970s, MDMA was given to psychotherapy patients because it helped them open up
and talk about their feelings. This practice was stopped in 1986 when animal studies showed that ecstasy
caused brain damage.
Behavioral Effects of MDMA
Some users say they take ecstasy because it lowers
their inhibitions and relaxes them. MDMA is also
said to increase awareness and feelings of pleasure
and to give people energy. However, some people
report side effects after taking MDMA such as
headaches, chills, eye twitching, jaw clenching,
blurred vision and nausea. Some doses of MDMA
can cause dehydration, hyperthermia and seizures.
The effects of MDMA send some people to the
emergency room (see graph on right). Unlike the
drug LSD, MDMA in low doses does not cause
people to hallucinate. Ecstasy gained national
attention when it was the drug of choice at club
parties, called "raves." In a survey taken in 2004,
4.0% of 12th graders, 2.4% of 10th graders and
1.7% of 8th graders reported that they had used
MDMA at least once within the year.
Data from NIDA Notes, 2001
Effects of MDMA on the Brain
MDMA appears to have several effects on the brain. MDMA can:
1. cause the release of the neurotransmitter called serotonin.
2. block the reuptake of serotonin by the synaptic terminal that releases it.
3. deplete the amount of serotonin in the brain.
Data suggests that MDMA may be toxic to the brain. Dr. George Ricaurte, an
associate professor of neurology at Johns Hopkins University, analyzed brain scans of people who had
used ecstasy. The study included people who had used ecstasy an average of 200 times over five years.
Although the behavior of these people appeared normal, brain scans showed that the drug had damaged
their brains. In fact, those who used the drug more often had more brain damage than less frequent
users. Moreover, memory tests of people who have taken ecstasy as compared to non-drug users have
shown that the ecstasy users had lower scores.
Specifically, the drug damaged cells that release the neurotransmitter called serotonin. Using an imaging
technique called positron emission tomography (PET), Ricaurte noted a 20-60% reduction in healthy
serotonin cells in the drug users. Damage to these cells could affect a person's abilities to remember and
to learn.
At this point, scientists do not know if this damage is permanent, or if those damaged cells will replace
themselves. Also, it is not known if this loss of cells affects behavior or the ability to think. Ricaurte is
conducting other studies to gauge ecstasy's effect on mood, memory, cognition, and behaviors such as
eating and sleeping. In 2003, German researchers used PET scans to study the brains of current and
past users of ecstasy. This research demonstrated that ecstasy users had lower levels of serotonin
activity in several brain areas. However, ecstasy users who stopped using the drug 20 weeks before the
scan showed some recovery in serotonin function.
Information from brain scans of people is valuable, but it is difficult to control the different variables when
using human subjects. Perhaps some of the students didn't report their drug use accurately. Maybe they
didn't remember how many times they had used ecstasy. To be able to control the variables more
carefully in a study, Ricaurte looked for help from animal experiments. In an article published in The
Journal of Neuroscience (June 15, 1999), Ricaurte compared the data from monkeys who were given
ecstasy dissolved in a liquid twice a day for four days to other monkeys who received the same liquid
WITHOUT the ecstasy twice a day for four days. The study showed that the monkeys who were given
ecstasy had damage to the serotonin-containing nerve cells. This damage was still visible seven years
later!. Areas that were especially affected were the frontal lobe of the cerebral cortex, an area in the front
part of the brain that is used in thinking, and the hippocampus, an area deep in the brain that helps with
memory. Although damage was still observed seven years later, it was less severe than when it was
observed two weeks after drug use. This suggests that some regrowth could have occurred, but that it is
far from complete.
Effect of MDMA on serotonin neurons in the monkey brain.
Image courtesy of the National Institute on Drug Abuse
Now scientists must tease out what these results from monkeys mean to humans. Although the specifics
are lacking, at this point, the evidence points to loss of memory and cognitive ability among ecstasy
users.
Inhalants
QUESTION: What do nail polish,
paint and glue have in common?
ANSWER: They can:
 be found at home or school
 be inhaled by people looking
for a quick high
 cause damage to the body
including the brain
 STINK.
Inhaling (also called "huffing" or "sniffing") chemicals is a
problem for many people including teenagers. Inhalants are
cheap and can be found everywhere - in kitchens, garages
and schools. There are hundreds of different materials that
can be abused by people who inhale these dangerous
chemicals. Inhalants not only damage the nervous system,
DANGER
Extremely Flammable
Harmful of Fatal If Swallowed
Vapors May Cause Fire
DANGER: Keep away from heat and
flame. If swallowed or if excessive
inhalation occurs resulting in abnormal
reactions including dizziness or nausea,
contact a physician. Intentional misuse
by deliberately concentrating and
inhaling contents may be harmful or fatal.
(From a warning label on
waterproofing spray)
ER
or if excessive inhalation occurs resulting
in abnormal reactions including dizziness
but other organs such as the lungs, liver, heart and kidney
can be injured permanently.
or nausea, contact a physician.
Intentional se by)
Variety of Inhalants
Product
Chemical Content
Hair Spray
Fluorinated hydrocarbons; propane; isobutane
Nitrous Oxide
Nitrous Oxide
Cleaning Fluids
Chlorinated hydrocarbons; naphtha
Typewriter Correction Fluid
Trichloroethane; trichloroethylene
Nail Polish Remover
Acetone; aliphatic acetates; benzene
Gasoline
Hydrocarbons; tetraethyl lead
Glue; rubber cement
Toluene; acetone, benzene; xylene; ethanol; chloroform
Paint/Paint Thinner
Toluene; methylene chloride; benzene, ethanol
Lighter Fluid
Hydrocarbons
Room Deodorizers
Amyl, butyl and isobutyl nitrite
Marker pens
Toluene; xylene
Effects of Inhalants on the Nervous System
When vapors are inhaled (1), they are absorbed through the lungs (2) and
enter the bloodstream (3). Once in the bloodstream, the chemicals travel to the
brain (4) and other tissues throughout the body. Most inhalants that are
abused depress the functioning of the nervous system. However, the effects of
each inhalant are difficult to determine because each product in made up
many different chemicals and each person may breathe in different amounts of
each chemical. Nevertheless, these chemicals do have significant effects on
the nervous system.
Some of the effects of inhalants are simliar to those of alcohol. The immediate
effects of inhalants include:









relaxation
slurred speech
euphoria
hallucinations
drowsiness
dizziness
nausea
vomiting
DEATH - from heart failure or suffocating on plastic bags or vomit.
Long term use of inhalants can cause:



memory loss
concentration problems
visual disturbances; blindness


motor problems
peripheral nerve damage
Nervous System Targets of Inhalants
Inhalants may affect different parts the brain and nervous system and may cause a
variety of sensory, motor, psychological and emotional problems. One major effect of
inhalants is the destruction of the myelin sheath that surrounds neurons. This can result in
problems in the normal transmission of impulses through neurons and cell death.
Specific areas of the brain targeted by inhalants include:
1. Cerebral cortex: damage can cause changes in personality, memory loss, hallucinations and
learning problems.
2. Cerebellum: damage can cause problems in balance and movement.
3. Hippocampus: damage may result in the memory problems.
4. Visual System: damage to the peripheral nerves may cause visual disturbances.
Did you
know?
Nitrous oxide was discovered in 1776 by Sir Joseph Priestley. In 1799, Sir Humphrey
Davy suggested that nitrous oxide could be used during surgery to reduce pain.
Marijuana
Marijuana is one of the world's most commonly used illegal drugs. There are
approximately 300 million users worldwide and 28 million users in the United States
(Diaz, 1997). Marijuana comes from a plant called "Cannabis sativa." The chemical in
this plant that produces the altered states of consciousness is called "delta-9
tetrahydrocannabinol" or "THC." Marijuana is usually smoked like a cigarette, but it can
also be cooked into baked goods like brownies or cookies or brewed like a tea. THC is
also contained in "hashish" (hash) which is the resin from the marijuana plants. Hash is
usually smoked in a pipe. Other names for marijuana include: grass, pot, reefer and
weed.
Effects of Marijuana on the Nervous System
THC acts on "cannabinoid" receptors which are found on neurons in many places
in the brain. These brain areas are involved in memory (the hippocampus),
concentration (cerebral cortex), perception (sensory portions of the cerebral
cortex) and movement (the cerebellum, substantia nigra, globus pallidus). When
THC activates cannabinoid receptors, it interfers with the normal functioning of
these brain areas. In low to medium doses, marijuana causes:



relaxation
reduced coordination
reduced blood pressure
 sleepiness
 disruption in attention
 an altered sense of time and space...a good
reason not to drive or operate machinery while under the
influence.
In high doses, marijuana can cause:


 hallucinations
 delusions
impaired memory
disorientation.
Scientists have known for a long time that THC interacted with cannabinoid receptors in the brain, but did
not know why the brain would have such receptors. They thought that the brain must make some kind of
substance that naturally acted on these receptors. In 1992, they found the answer...anandamide.
Anandamide is the brain's own THC (just like "endorphin" is the brain's own morphine). Still, scientists are
not sure what the function of anandamide is in the normal brain.
The effects of marijuana start as soon as 1-10 minutes after it is taken and can last 3 to 4 hours or even
longer. Experiments have shown that THC can affect two neurotransmitters: norepinephrine and
dopamine. Serotonin and GABA levels may also be altered.
Whether marijuana can produce addiction is controversial. Also controversial is whether marijuana
causes long-term mental abnormalities. Only future research will give us the answers. It is interesting to
note that there are NO documented cases of a fatal overdose produced by marijuana. However, because
there is a high level of tar and other chemicals in marijuana, smoking it is similar to smoking cigarettes.
The lungs get a big dose of chemicals that increase the chances of lung problems and cancer later in life.
How long does THC stay in your body and for how long can it be detected
after you use marijuana?
The amount of time depends on several factors such as how much a person
has smoked, how long a person has smoked for, and the method used to detect
THC or its metabolites. Marijuana can be detected in urine, blood and saliva
using methods called thin layer chromatography, high pressure liquid
chromatography, gas chromatography, enzyme immunoassay and
radioimmunoassay. The most psychoactive ingredient in marijuana is delta-9tetrahydrocannabinol (THC). THC is broken down into several other compounds
that are also psychoactive. The half-life of THC is about 24 hours. However, the
metabolites of THC can be detected for 45 to 60 days after the last use.
According to Maistro et al., in the book Drug Use and Misuse (1991):
"Approximately half of the THC is excreted over several days, and the
remainder by the end of about a week. However, some metabolites of the THC, a number of which may
still be active in the system, can be detected in the body at least thirty days following ingestion of a single
dose and, following chronic use, in the urine for several weeks."

Did you
know?
In 1969, the Journal of the American Medical Association (JAMA, vol. 207, pages
1349-1350, 1969) published a paper that described the psychoactive effects of
catnip in people. People who smoked catnip were said to become happy and
relaxed. Catnip (from the plant Nepeta cataria) DOES cause most cats to act
strangely: they roll around, shake their heads, rub against things, and try to get
the plant all over their bodies. Interestingly, cats are only affected when they
smell it - it has NO EFFECT if they eat it. It appears that catnip has little or no
psychoactive effects in people. Actually, in the 1969 JAMA paper, the authors

mislabeled the pictures of marijuana and catnip. They labeled the pictures of
marijuana as catnip and that of catnip as marijuana.
THC was identified as the major psychoactive chemical in marijuana in 1964.
Rohypnol
What is Rohypnol?
"Roofies." Sounds like a cartoon character or a piece of candy. However,
nothing could be further from the truth about Roofies, also known as the drug
Rohypnol.
Rohypnol (Flunitrazepam) is a type of benzodiazepine, a class of drugs that
depresses the central nervous system. You may have heard of Valium and
Xanax. These are also benzodiazepines used as sedatives and antianxiety
agents. Rohypnol was developed as a sleeping aid. It is also used in therapy
settings to relax patients and to get them talking. Rohypnol is manufactured in
Europe and Latin American and is sold in many countries around the world.
However, it is illegal in the United States and Canada. The pills are round,
white and smaller than aspirin.
Rohypnol Tablets
Image courtesy of the
U.S. Department of
Justice
Because Rohypnol is inexpensive, it is becoming popular with high school and
college students. In the US, Rohypnol is used mostly at parties, and usually
taken with alcohol. It has a synergistic effect with other drugs such as alcohol.
This means that one drug increases the effect of the other.
Behavioral Effects of Rohypnol
Rohypnol can produce amnesia (memory loss) and muscle relaxation and make people
lower their inhibitions. An inhibition is when you feel like you can't do something. When
inhibitions are lowered, people feel as if an obstacle has been removed. Therefore, they
can talk more freely and feel less shy.
Because Rohypnol is colorless, odorless and flavorless, it can be slipped into drinks
unnoticed. This is one reason this drug is so dangerous. People may consume it without
knowing it. It dissolves quickly and takes effect in 20-30 minutes. Its effects can last 8-12 hours. Within
the past few years, Rohypnol has become known as the "date rape" drug. People will come home from a
party and have no idea what happened to them because they unknowingly ingested Rohypnol, passed
out, and woke up several hours later with no memory of the evening.
Continued, repeated use of Rohypnol may result in addiction and although Rohypnol is a sedative, it can
cause aggressive behavior in some people. Withdrawal symptoms may occur and include headaches,
sore muscles, hallucinations, convulsions, and possibly seizures 1-2 weeks after quitting the drug.
Although overdoses are rarely fatal, emergency services are sometimes required because Rohypnol can
cause a person to vomit, hallucinate, have trouble breathing and fall into a coma. When Rohypnol is
combined with alcohol the outcome is usually worse.
Street names for Rohypnol include rophies, ruffies, R2, roofenol, Roche, la rocha, rope, roopies, ropies,
and rib.
Effects of Rohypnol on the Brain
The benzodiazepines influence behavior by interacting with receptors on neurons in the brain that use the
neurotransmitter called GABA. When GABA binds to receptors, it usually inhibits a neuron and acts to
reduce neuronal activity. When benzodiazepines attach to GABA receptors, they increase GABA binding
to other receptors. In this way, benzodiazepines enhance the effects of GABA and reduce brain activity.
PCP - Phencyclidine
What is PCP?
"Angel Dust," "Hog," "Rocket Fuel," "DOA," "Peace Pill" - these are other
names for the illegal drug phencyclidine (PCP). PCP was developed in the
1950s as an anesthetic. However, the use of PCP as an anesthetic was
stopped after some people experienced psychotic reactions after using the
drug. PCP is now made illegally and has found its way onto the street, often
contaminating other street drugs. In fact, PCP is often sold in place of drugs
such as LSD and mescaline.
PCP is classified as a dissociative anesthetic because users appear to be
"disconnected" from their environment: they know where they are, but they do
not feel as if they are part of it. The drug has different effects on different
people. It can act as a stimulant, a depressant, an analgesic (decreasing pain)
or a hallucinogen depending on the dose and route of administration. The
effects produced by PCP are different from those caused by hallucinogens
such as LSD. Rather than producing visual hallucinations, PCP causes
changes in body image. In addition to these distortions of reality, PCP can
cause frightening side effects such as feelings of terror and confusion.
PCP (Image courtesy
of the Indiana
Prevention Resource
Center)
Behavioral Effects of PCP
PCP can be eaten, snorted, injected or smoked.
Depending on how a person takes the drug, the
effects are felt within a few minutes (2-5 minutes
when smoked) to an hour. PCP can stay in a
person's body for a long time; the half-life of PCP
ranges from 11 to 51 hours. Furthermore, because
PCP is made illegally under uncontrolled conditions,
users have no way of knowing how much PCP they
are taking. This makes PCP especially dangerous.
PCP users are often characterized as violent or
suicidal. However, this portrait of a PCP user may
not be accurate. Dr. Jaime Diaz, a professor in the
Department of Psychology at the University of
Washington, reviewed many of the published
reports of PCP use in his book, How Drugs
Influence Behavior. A Neuro-Behavioral Approach
(Upper Saddle River (NJ): Prentice Hall, 1997). He
states that PCP use rarely results in violence and
concludes that: "Phencyclidine does not cause
% of 12th Graders Who Have Used PCP
Sometime During Their Lifetime
(Source: Monitoring The Future Survey)
aggression or criminal behavior."
Dr. Diaz believes that the reported violent behavior
is not due to the pharmacological effect of PCP, but
rather is the result of the way people under the
influence of PCP perceive things and are
subsequently treated by law enforcement personnel.
People under the influence of PCP may not feel pain
and their perception of sensory stimuli may be
altered, possibly causing police officers to use
stronger methods to control such individuals.
Dose
Low
Effect
Feelings of euphoria (well-being), relaxation, numbness, sensory distortions, feelings of
detachment from one's own body, anxiety, confusion, amnesia, illogical speech, blurred vision,
blank stare
Medium Confusion, agitation, analgesia, fever, excessive salivation, "schizophrenic-type" behavior
High
Seizures, respiratory failure, coma, fever, stroke, DEATH
Tolerance and dependence on PCP are possible. Withdrawal symptoms include diarrhea, chills, tremors.
PCP affects multiple neurotransmitter
systems
Effects of PCP on the Brain
PCP affects multiple neurotransmitter systems in the brain. For
example, PCP inhibits the reuptake of dopamine,
norepinephrine and serotonin and also inhibits the action of
glutamate by blocking NMDA receptors. Some types of opioid
receptors in the brain are also affected by PCP. These
complex effects on multiple chemical systems in the brain most
likely underlie the behavioral effects of PCP.
Hallucinogenic Mushrooms
What are Hallucinogenic Mushrooms?
Mushrooms, a kind of fungus, come in many varieties. From those on a pizza to those
in spaghetti sauce, mushrooms enhance our cuisine and flavor our lives. But not all
mushrooms are so harmless. Some contain toxic and/or hallucinogenic compounds.
Hallucinogens are substances that alter or produce false perceptions of sight, sound,
taste, smell or touch. Some toxic substances in mushrooms can cause severe illness
and even death. Most hallucinogenic substances, including synthetic ones such as
LSD, are illegal.
Historical Background
The hallucinogenic properties of certain mushrooms have been known for centuries.
The discovery of mushroom sculptures in ancient Central and South American ruins
suggests that hallucinogenic mushrooms were used by native people during religious
ceremonies. The Aztecs used the term "teonanacatl" meaning "flesh of the gods" to
describe hallucinogenic mushrooms. Historians have proposed that Aztec spiritual
leaders used these hallucinogens to induce an altered state of consciousness that
they believed would allow them to communicate with their gods and other spirits.
Types of Hallucinogenic Mushrooms
1. Psilocybin/Psilocin Mushrooms
Mushrooms that contain the hallucinogens psilocybin and/or
psilocin belong mainly to the genera: Psilocybe, Stropharia,
Conocybe, and Panaeolus. The word "psilocybin" comes from
the Greek words "psilo" meaning "bald" and "cybe" meaning
"head."
Psilocybe
Mushroom
2. Amanita muscaria
The Amanita muscaria mushroom is also known as "fly agaric" because of its
ability to attract and kill flies. The Amanita muscaria does not contain psilocybin
or psilocin. Rather, the hallucinogenic chemicals this mushroom contain are
muscimol and ibotenic acid.
The fly agaric is related to other deadly mushrooms: the Amanita virosa (the
"Destroying Angel"); Amanita verna and Amanita phalloides (the "Death Cap").
These deadly mushrooms contain toxins that destroy cells in the liver and
kidneys. Five to 24 hours after eating one of these toxic mushrooms people may
become sick with nausea and stomach problems. Later, severe liver and kidney
damage may occur.
Psilocybe cubensis
Photographs courtesy of
the
Indiana Prevention
Center
Effects on Behavior
Psilocybin/Psilocin Mushrooms
Both psilocybin and psyilocin produce yawning, inability to concentrate, restlessness,
increased heart rate, and hallucinations (visual and auditory). These symptoms may
appear 30 to 60 minutes after the mushroom is eaten and can last about four hours.
Amanita muscaria
Amanita muscaria contains muscimol that produces feelings of euphoria, hallucinations, muscle jerks,
drowsiness, sweating, pupil dilation, and increased body temperature. Symptoms appear 30 to 90
minutes after eating this mushroom and are most intense after two or three hours. People who eat these
mushrooms usually fall into a deep sleep. Some people describe the effects of eating Amanita muscaria
as similar to being intoxicated by alcohol.
Effects on the Nervous System
The chemical structure of psilocybin and psilocin is similar to the
neurotransmitter called serotonin. In fact, the primary effect of psilocin is
on the receptors for serotonin. There is also evidence that psilocybin
reduces the reuptake of serotonin by neurons in the brain allowing this
neurotransmitter more time to act in the synapse.
Muscimol and ibotenic acid from the Amanita muscaria appear to act on
the GABA neurotransmitter system. Muscimol activates GABA receptors
on neurons. The GABA neurotransmitter system is one of the brain's major
inhibitory systems. Therefore, muscimol acts to inhibit the activity of
neurons in the brain.
CAUTION
Picking and consuming mushrooms can be a dangerous activity! Identification of
hallucinogenic mushrooms can be difficult because they look similar to toxic, deadly
mushrooms. It is also possible that mushrooms bought from "street dealers" may be
contaminated with drugs such as LSD or PCP. The images used on this web page are
NOT meant to be used for mushroom identification purposes.
Steroids
Anabolic-androgenic steroids are man-made substances related to male sex hormones. “Anabolic” refers
to muscle-building, and “androgenic” refers to increased masculine characteristics. “Steroids” refers to the
class of drugs.
These drugs are available legally only by prescription, to treat conditions that occur when the body
produces abnormally low amounts of testosterone, such as delayed puberty and some types of
impotence. They are also prescribed to treat body wasting in patients with AIDS and other diseases that
result in loss of lean muscle mass.
Abuse of anabolic steroids, however, can lead to serious health problems, some irreversible.
Today, athletes and others abuse anabolic steroids to enhance performance and also to improve physical
appearance. Anabolic steroids are taken orally or injected, typically in cycles of weeks or months (referred
to as “cycling”), rather than continuously. Cycling involves taking multiple doses of steroids over a specific
period of time, stopping for a period, and starting again. In addition, users often combine several different
types of steroids to maximize their effectiveness
while minimizing negative effects (referred to as “stacking”).
Health Hazards
The major side effects from abusing anabolic steroids can include:
 liver tumors and cancer
 jaundice (yellowish pigmentation of skin, tissues, and body fluids),
 fluid retention, high blood pressure, increases in LDL (bad cholesterol)
 decreases in HDL (good cholesterol)
Other side effects include:
 kidney tumors
 severe acne
 trembling
 aggression and other psychiatric side effects (ROID RAGE)
In addition, there are some gender-specific side effects:

For men — shrinking of the testicles, reduced sperm count, infertility, baldness,
development of breasts, increased risk for prostate cancer.

For women — growth of facial hair, male-pattern baldness, changes in or cessation of the
menstrual cycle, enlargement of the clitoris, deepened voice.

For adolescents — growth halted prematurely through premature skeletal
maturation and accelerated puberty changes. This means that adolescents risk
remaining short for the remainder of their lives if they take anabolic steroids before
the typical adolescent growth spurt.
In addition, people who inject anabolic steroids run the added risk of contracting or transmitting HIV/AIDS
or hepatitis, which causes serious damage to the liver.
Scientific research also shows that aggression and other psychiatric side effects may result from abuse of
anabolic steroids. Many users report feeling good about themselves while on anabolic steroids, but
researchers report that extreme mood swings also can occur, including manic-like symptoms
leading to violence. Depression often is seen when the drugs are stopped and may contribute
to dependence on anabolic steroids. Researchers report also that users may suffer from
paranoid jealousy, extreme irritability, delusions, and impaired judgment stemming from feelings
of invincibility.
Research also indicates that some users might turn to other drugs to alleviate some of the negative
effects of anabolic steroids. For example, a study of 227 men admitted in 1999 to a private treatment
center for dependence on heroin or other opioids found that 9.3 percent had abused anabolic steroids
before trying any other illicit drug. Of these 9.3 percent, 86 percent first used opioids to counteract
insomnia and irritability resulting from the anabolic steroids.2
Extent of Use
Monitoring the Future (MTF) Survey *
MTF annually assesses drug use among the Nation’s 8th, 10th, and 12th grade students.

Annual** use of anabolic steroids remained stable at under 1.5 percent for students in 8th, 10th, and
12th grades in the early 1990s, then started to rise.

Peak rates of annual use occurred in 2002 for 12th-graders (2.5 percent), in 2000 and 2002 for 10thgraders (2.2 percent), and in 1999 and 2000 for 8th-graders (1.7 percent).

Eight-graders reported significant decreases in lifetime and annual steroid use in 2004, as well as a
decrease in perceived availability of these drugs. A significant decrease in lifetime use was also
measured among 10th-graders for 2004.

Most anabolic steroids users are male, and among male students, past year use of these substances
was reported by 1.3 percent of 8th-graders, 2.3 percent of 10th-graders, and 3.3 percent of 12thgraders in 2004.
Anabolic Steroid Use by Students
Year 2004 Monitoring the Future Survey
8th-Graders
10th-Graders
12th-Graders
Lifetime
1.9%
2.4%
3.4%
Annual
1.1
1.5
2.5
30-day
0.5
0.8
1.6
1
Pope, H.G., and Katz, D. L. Affective and psychotic symptoms associated with anabolic steroid use. American Journal of
Psychiatry 145(4):487-490, 1988.
2
The New England Journal of Medicine 320:1532, 2000.
* These data are from the 2004 Monitoring the Future Survey, funded by the National Institute on Drug Abuse, National Institutes of
Health, DHHS, and conducted by the University of Michigan’s Institute for Social Research. The survey has tracked 12th-graders’
illicit drug use and related attitudes since 1975; in 1991, 8th- and 10th-graders were added to the survey. The latest data are online
at http://www.drugabuse.gov.
** "Lifetime" refers to use at least once during a respondent's lifetime. "Annual" refers to an individual's drug use at least once during
the year preceding their response to the survey. "30-day" refers to an individual's drug use at least once during the month preceding
their response to the survey.