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Cocaine abuse and addiction continues
to be a problem that plagues our nation. For instance, from 1965 to
1967, only 0.1
percent of youths had ever used cocaine, but rates rose throughout
the 1970s and 1980s, reaching 2.2 percent in 1987. After a
brief decline, lifetime prevalence rates peaked at 2.7 percent in
2002.
However, we now know more about where and how cocaine acts in the
brain, including how the drug produces its pleasurable
effects and why it is so addictive. Through the use of sophisticated
technology, scientists can actually see the dynamic
changes that occur in the brain as an individual takes the drug.
They can observe the different brain changes that occur as a
person experiences the "rush,” the "high,” and, finally, the craving
of cocaine. They can also identify parts of the brain
that become active when a cocaine addict sees or hears environmental
stimuli that trigger the craving for cocaine. Because
these types of studies pinpoint specific brain regions, they are
critical to identifying targets for developing medications
to treat cocaine addiction.
One of NIDA's most important goals is to translate what scientists
learn from research, in order to help the public better
understand drug abuse and addiction, and to develop more effective
strategies for their prevention and treatment. We hope
that this compilation of scientific information on cocaine will help
to inform readers about the harmful effects of cocaine
abuse, and that it will assist in prevention and treatment efforts.
Nora D. Volkow, M.D.
Director
National Institute on Drug Abuse
Cocaine is a powerfully addictive stimulant that directly affects
the brain. Cocaine was labeled the drug of the 1980s and
‘90s, because of its extensive popularity and use during this
period. However, cocaine is not a new drug. In fact, it is one
of the oldest known drugs. The pure chemical, cocaine hydrochloride,
has been an abused substance for more than 100 years,
and coca leaves, the source of cocaine, have been ingested for
thousands of years.
Pure cocaine was first extracted from the leaf of the Erythroxylon
coca bush, which grows primarily in Peru and Bolivia, in
the mid-19th century. In the early 1900s, it became the main
stimulant drug used in most of the tonics/elixirs that were
developed to treat a wide variety of illnesses. Today, cocaine is a
Schedule II drug, meaning that it has high potential for
abuse, but can be administered by a doctor for legitimate medical
uses, such as local anesthesia for some eye, ear, and
throat surgeries.
There are basically two chemical forms of cocaine: the hydrochloride
salt and the "freebase.” The hydrochloride salt, or
powdered form of cocaine, dissolves in water and, when abused, can
be taken intravenously (by vein) or intranasally (in the
nose). Freebase refers to a compound that has not been neutralized
by an acid to make the hydrochloride salt. The freebase
form of cocaine is smokable.
Cocaine is generally sold on the street as a fine, white,
crystalline powder, known as "coke,” "C,” "snow,” "flake,” or
"blow.” Street dealers generally dilute it with such inert
substances as cornstarch, talcum powder, and/or sugar, or with
such active drugs as procaine (a chemically related local
anesthetic) or with such other stimulants as amphetamines.
Crack is the street name given to a freebase form of cocaine that
has been processed from the powdered cocaine hydrochloride
form to a smokable substance. The term "crack” refers to the
crackling sound heard when the mixture is smoked. Crack cocaine
is processed with ammonia or sodium bicarbonate (baking soda) and
water, and heated to remove the hydrochloride.
Because crack is smoked, the user experiences a high in less than 10
seconds. This rather immediate and euphoric effect is
one of the reasons that crack became enormously popular in the mid
1980s. Another reason is that crack is inexpensive both to
produce and to buy. Crack cocaine remains a serious problem in the
United States. The National Survey on Drug Use and Health
(NSDUH) estimated the number of current crack users to be about
567,000 in 2002.
Trends in 30-day prevalence of cocaine abuse among eighth, tenth,
and twelfth graders, 1991-1998
Source: Monitoring the Future survey, University of Michigan
In 2002, an estimated 1.5 million Americans could be classified as
dependent on or abusing cocaine in the past 12 months,
according to the NSDUH. The same survey estimates that there are 2.0
million current (past-month) users. Cocaine initiation
steadily increased during the 1990s, reaching 1.2 million in 2001.
Adults 18 to 25 years old have a higher rate of current cocaine use
than those in any other age group. Overall, men have a
higher rate of current cocaine use than do women. Also, according to
the 2002 NSDUH, estimated rates of current cocaine users
were 2.0 percent for American Indians or Alaskan Natives, 1.6
percent for African-Americans, 0.8 percent for both Whites and
Hispanics, 0.6 percent for Native Hawaiian or other Pacific
Islanders, and
0.2 percent for Asians.
The 2003 Monitoring the Future Survey, which annually surveys teen
attitudes and recent drug use, reports that crack cocaine
use decreased among 10th-graders in 30-day, annual, and lifetime use
prevalence periods. This was the only statistically
significant change affecting cocaine in any form. Past-year use of
crack declined from 2.3 percent in 2002 to 1.6 percent in
2003. Last year, the rate increased from 1.8 percent to 2.3 percent,
and this year's decline brings it to approximately its
2001 level.
Data from the Drug Abuse Warning Network (DAWN) showed that
cocaine-related emergency department visits increased 33 percent
between 1995 and 2002, rising from 58 to 78 mentions per 100,000
population.
The principal routes of cocaine administration are oral, intranasal,
intravenous, and inhalation. The slang terms for these
routes are, respectively, "chewing,” "snorting,” "mainlining” or
"injecting,” and "smoking” (including freebase and crack
cocaine). Snorting is the process of inhaling cocaine powder through
the nostrils, where it is absorbed into the bloodstream
through the nasal tissues. Injecting releases the drug directly into
the bloodstream, and heightens the intensity of its
effects. Smoking involves the inhalation of cocaine vapor or smoke
into the lungs, where absorption into the bloodstream is
as rapid as by injection. The drug also can be rubbed onto mucous
tissues. Some users combine cocaine powder or crack with
heroin in a "speedball.”
Cocaine use ranges from occasional use to repeated or compulsive
use, with a variety of patterns between these extremes.
Other than medical uses, there is no safe way to use cocaine. Any
route of administration can lead to absorption of toxic
amounts of cocaine, leading to acute cardiovascular or
cerebrovascular emergencies that could result in sudden death.
Repeated cocaine use by any route of administration can produce
addiction and other adverse health consequences.
A great amount of research has been devoted to understanding the way
cocaine produces its pleasurable effects, and the
reasons it is so addictive. One mechanism is through its effects on
structures deep in the brain. Scientists have discovered
regions within the brain that are stimulated by rewards. One neural
system that appears to be most affected by cocaine
originates in a region located deep within the brain called the
ventral tegmental area (VTA). Nerve cells originating in the
VTA extend to the region of the brain known as the nucleus accumbens,
one of the brain's key areas involved in reward. In
studies using animals, for example, all types of rewarding stimuli,
such as food, water, sex, and many drugs of abuse, cause
increased activity in the nucleus accumbens.
Cocaine in the brain — In the normal communication process, dopamine
is released by a neuron into the synapse, where it can
bind with dopamine receptors on neighboring neurons. Normally,
dopamine is then recycled back into the transmitting neuron by
a specialized protein called the dopamine transporter. If cocaine is
present, it attaches to the dopamine transporter and
blocks the normal recycling process, resulting in a buildup of
dopamine in the synapse, which
contributes to the pleasurable effects of cocaine.
Researchers have discovered that, when a rewarding event is
occurring, it is accompanied by a large increase in the amounts
of dopamine released in the nucleus accumbens by neurons originating
in the VTA. In the normal communication process,
dopamine is released by a neuron into the synapse (the small gap
between two neurons), where it binds with specialized
proteins (called dopamine receptors) on the neighboring neuron,
thereby sending a signal to that neuron. Drugs of abuse are
able to interfere with this normal communication process. For
example, scientists have discovered that cocaine blocks the
removal of dopamine from the synapse, resulting in an accumulation
of dopamine. This buildup of dopamine causes continuous
stimulation of receiving neurons, which is associated with the
euphoria commonly reported by cocaine abusers.
As cocaine abuse continues, tolerance often develops. This means
that higher doses and more frequent use of cocaine are
required for the brain to register the same level of pleasure
experienced during initial use. Recent studies have shown that,
during periods of abstinence from cocaine use, the memory of the
euphoria associated with cocaine use, or mere exposure to
cues associated with drug use, can trigger tremendous craving and
relapse to drug use, even after long periods of abstinence.
Cocaine's effects appear almost immediately after a single dose, and
disappear within a few minutes or hours. Taken in small
amounts (up to 100 mg), cocaine usually makes the user feel
euphoric, energetic, talkative, and mentally alert, especially to
the sensations of sight, sound, and touch. It can also temporarily
decrease the need for food and sleep. Some users find that
the drug helps them perform simple physical and intellectual tasks
more quickly, while others experience the opposite effect.
The duration of cocaine's immediate euphoric effects depends upon
the route of administration. The faster the absorption, the
more intense the high. Also, the faster the absorption, the shorter
the duration of action. The high from snorting is
relatively slow in onset, and may last 15 to 30 minutes, while that
from smoking may last 5 to 10 minutes.
The short-term physiological effects of cocaine include constricted
blood vessels; dilated pupils; and increased temperature,
heart rate, and blood pressure. Large amounts (several hundred
milligrams or more) intensify the user's high, but may also
lead to bizarre, erratic, and violent behavior. These users may
experience tremors, vertigo, muscle twitches, paranoia, or,
with repeated doses, a toxic reaction closely resembling amphetamine
poisoning. Some users of cocaine report feelings of
restlessness, irritability, and anxiety. In rare instances, sudden
death can occur on the first use of cocaine or
unexpectedly thereafter. Cocaine-related deaths are often a result
of cardiac arrest or seizures followed by respiratory
arrest.
Long-term effects of cocaine
Addiction
Irritability and mood disturbances
Restlessness
Paranoia
Auditory hallucinations
Cocaine is a powerfully addictive drug. Thus, an individual may have
difficulty predicting or controlling the extent to which
he or she will continue to want or use the drug. Cocaine's stimulant
and addictive effects are thought to be primarily a
result of its ability to inhibit the reabsorption of dopamine by
nerve cells. Dopamine is released as part of the brain's
reward system, and is either directly or indirectly involved in the
addictive properties of every major drug of abuse.
An appreciable tolerance to cocaine's high may develop, with many
addicts reporting that they seek but fail to achieve as
much pleasure as they did from their first experience. Some users
will frequently increase their doses to intensify and
prolong the euphoric effects. While tolerance to the high can occur,
users can also become more sensitive (sensitization) to
cocaine's anesthetic and convulsant effects, without increasing the
dose taken. This increased sensitivity may explain some
deaths occurring after apparently low doses of cocaine.
Use of cocaine in a binge, during which the drug is taken repeatedly
and at increasingly high doses, leads to a state of
increasing irritability, restlessness, and paranoia. This may result
in a full-blown paranoid psychosis, in which the
individual loses touch with reality and experiences auditory
hallucinations.
Medical consequences of cocaine abuse
Cardiovascular effects
disturbances in heart rhythm
heart attacks
Respiratory effects
chest pain
respiratory failure
Neurological effects
strokes
seizures and headaches
Gastrointestinal complications
abdominal pain
nausea
There can be severe medical complications associated with cocaine
use. Some of the most frequent complications are
cardiovascular effects, including disturbances in heart rhythm and
heart attacks; respiratory effects such as chest pain and
respiratory failure; neurological effects, including strokes,
seizures, and headaches; and gastrointestinal complications,
including abdominal pain and nausea.
Cocaine use has been linked to many types of heart disease. Cocaine
has been found to trigger chaotic heart rhythms, called
ventricular fibrillation; accelerate heartbeat and breathing; and
increase blood pressure and body temperature. Physical
symptoms may include chest pain, nausea, blurred vision, fever,
muscle spasms, convulsions, coma, and death.
Different routes of cocaine administration can produce different
adverse effects. Regularly snorting cocaine, for example,
can lead to loss of sense of smell, nosebleeds, problems with
swallowing, hoarseness, and an overall irritation of the nasal
septum, which can lead to a chronically inflamed, runny nose.
Ingested cocaine can cause severe bowel gangrene, due
to reduced blood flow. And, persons who inject cocaine have puncture
marks and "tracks,” most commonly in their forearms.
Intravenous cocaine users may also experience an allergic reaction,
either to the drug, or to some additive in street
cocaine, which can result, in severe cases, in death. Because
cocaine has a tendency to decrease food intake, many chronic
cocaine users lose their appetites and can experience significant
weight loss and malnourishment.
Research has revealed a potentially dangerous interaction between
cocaine and alcohol. Taken in combination, the two drugs
are converted by the body to cocaethylene. Cocaethylene has a longer
duration of action in the brain and is more toxic than
either drug alone. While more research needs to be done, it is
noteworthy that the mixture of cocaine and alcohol is the most
common two-drug combination that results in drug-related death.
Yes. Cocaine abusers, especially those who inject, are at increased
risk for contracting such infectious diseases as human
immunodeficiency virus (HIV/AIDS) and viral hepatitis. In fact, use
and abuse of illicit drugs, including crack cocaine, are
major risk factors for new cases of HIV. Drug abuse-related spread
of HIV can result from direct transmission of the virus
through the sharing of contaminated needles and paraphernalia
between injecting drug users. It can also result from indirect
transmission, such as an HIV-infected mother transmitting the virus
perinatally to her child. This is particularly alarming
given that 30 percent of all new AIDS cases are among women.
Research has also shown that drug use can interfere with judge-
ment about risk-taking behavior, and can potentially lead to reduced
precautions regarding sexual behaviors, the sharing of
needles and injection paraphernalia, and the trading of sex for
drugs, by both men and women.
Additionally, hepatitis C (HCV) has spread rapidly among injection
drug users; Centers for Disease Control and Prevention
(CDC) estimates indicate infection rates of 50 to 80 percent in this
population. While currently available treatment is not
effective for everyone and can have significant side effects,
medical followup is essential for all those who are infected.
At present, there is no vaccine for the hepatitis C virus. The virus
is highly transmissible via injection, and HCV testing
is recommended for any individual who has ever injected drugs.
The full extent of the effects of prenatal drug exposure on a child
is not completely known, but many scientific studies have
documented that babies born to mothers who abuse cocaine during
pregnancy are often prematurely delivered, have low birth
weights and smaller head circumferences, and are often shorter in
length.
Estimating the full extent of the consequences of maternal drug
abuse is difficult, and determining the specific hazard of a
particular drug to the unborn child is problematic for many reasons.
Multiple factors—such as the amount and number of all
drugs abused; extent of prenatal care; possible neglect or abuse of
the child; exposure to violence in the environment;
socioeconomic conditions; maternal nutrition; other health
conditions; and exposure to sexually-transmitted diseases—can
contribute to the difficulty in determining direct impact of
prenatal cocaine use on maternal, fetal, and child outcomes.
Many recall that "crack babies,” or babies born to mothers who used
crack cocaine while pregnant, were at one time written
off by many as a lost generation. They were predicted to suffer from
severe, irreversible damage, including reduced
intelligence and social skills. It was later found that this was a
gross exaggeration. However, the fact that most of these
children appear normal should not be overinterpreted as indicating
that there is no cause for concern. Using sophisticated
technologies, scientists are now finding that exposure to cocaine
during fetal development may lead to subtle, yet
significant, later deficits in some children, including deficits in
some aspects of cognitive performance, information-
processing, and attention to tasks—abilities that are important for
success in school.
There was an enormous increase in the number of people seeking
treatment for cocaine addiction during the 1980s and 1990s.
Treatment providers in most areas of the country, except in the West
and Southwest, report that cocaine is the most commonly
cited drug of abuse among their clients. The majority of individuals
seeking treatment smoke crack, and are likely to be
polydrug users, or users of more than one substance. The widespread
abuse of cocaine has stimulated extensive efforts to
develop treatment programs for this type of drug abuse. Cocaine
abuse and addiction is a complex problem involving biological
changes in the brain as well as a myriad of social, familial, and
environmental factors. Therefore, treatment of cocaine
addiction is complex, and must address a variety of problems. Like
any good treatment plan, cocaine treatment strategies need
to assess the psychobiological, social, and pharmacological aspects
of the patient's drug abuse.
Pharmacological Approaches
There are no medications currently available to treat cocaine
addiction specifically. Consequently, NIDA is aggressively
pursuing the identification and testing of new cocaine treatment
medications. Several newly emerging compounds are being
investigated to assess their safety and efficacy in treating cocaine
addiction. Topiramate and modafanil, two marketed
medications, have shown promising signals as potential cocaine
treatment agents. Additionally, baclofen, a GABA-B agonist,
showed promise in a subgroup of cocaine addicts with heavy use
patterns. Because of mood changes experienced during the early
stages of cocaine abstinence, antidepressant drugs have been shown
to be of some benefit. In addition to the problems of
treating addiction, cocaine overdose results in many deaths every
year, and medical treatments are being developed to deal
with the acute emergencies resulting from excessive cocaine abuse.
Behavioral Interventions
Many behavioral treatments have been found to be effective for
cocaine addiction, including both residential and outpatient
approaches. Indeed, behavioral therapies are often the only
available, effective treatment approaches to many drug problems,
including cocaine addiction, for which there is, as yet, no viable
medication. However, integration of both types of
treatments may ultimately prove to be the most effective approach
for treating addiction. Disulfiram (a medication that has
been used to treat alcoholism), in combination with behavioral
treatment, has been shown, in clinical studies, to be
effective in reducing cocaine abuse. It is important that patients
receive services that match all of their treatment needs.
For example, if a patient is un-employed, it may be helpful to
provide vocational rehabilitation or career counseling.
Similarly, if a patient has marital problems, it may be important to
offer couples counseling. A behavioral therapy component
that is showing positive results in many cocaine-addicted
populations is contingency management. Contingency management may
be particularly useful for helping patients achieve initial
abstinence from cocaine. Some contingency management programs use
a voucher-based system to give positive rewards for staying in
treatment and remaining cocaine free. Based on drug-free urine
tests, the patients earn points, which can be exchanged for items
that encourage healthy living, such as joining a gym, or
going to a movie and dinner.
Cognitive-behavioral therapy, or "Relapse Prevention,” is another
approach. Cognitive-behavioral treatment, for example, is a
focused approach to helping cocaine-addicted individuals abstain—and
remain abstinent—from cocaine and other substances. The
underlying assumption is that learning processes play an important
role in the development and continuation of cocaine abuse
and dependence. The same learning processes can be employed to help
individuals reduce drug use and successfully cope with
relapse. This approach attempts to help patients recognize, avoid,
and cope; i.e., recognize the situations in which they are
most likely to use cocaine, avoid these situations when appropriate,
and cope more effectively with a range of problems and
problematic behaviors associated with drug abuse. This therapy is
also noteworthy because of its compatibility with a range
of other treatments patients may receive, such as pharmacotherapy.
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