Why Rehab Doesn't Work for Celebrities
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For some people, the decision to go into rehab is one that could shape the rest of their lives. It is a decision packed with unknown questions and answers, and in many cases could mean the difference between life and death. Yet there is one section of society that flaunts rehab in the face of those who really need it, under the misconception that the word “rehab” stands for “hip and trendy” – they are celebrities.
So why are celebrities willing to jump on the rehab bandwagon in the popular belief that it is something not to be taken seriously? And why, when they get to a point in their lives when they actually need it, does it fail them?
Mass Publicity
It’s impossible to ignore the level of media coverage a celebrity receives when he or she enters rehab. The value to the media in terms of viewers or readers, as well as monetary gain, is enormous, and so the celebrity’s lifestyle will always be under the microscope.
Very often it is not just the rehab story that makes the newspapers, but rather the reason that got them there in the first place. Media outlets love nothing more than celebrities doing coke, or acting like they own the world – it sells.
In recent times, a string of celebrities have found their way through the doors of rehab centers while courting publicity. Lindsay Lohan was photographed leaving a Malibu rehab clinic last year, while showing off her alcohol-monitoring anklet to eager members of the paparazzi. Twenty-four hours later she was spotted partying with friends in a nightclub.
Britney Spears has been in the news constantly after her one-day session in an Antigua treatment center, which she then followed up with a double check-in to another clinic in a single month. Each time, she hit the headlines in newspapers, websites, and on television sets around the world.
In the UK, Amy Winehouse was questioned by police after The Sun newspaper published a video of her smoking crack cocaine in her London apartment. The news broke shortly after her much-publicized visit to an English rehab clinic, all of which coincided with her sellout UK tour.
For a celebrity in genuine need of rehab, the process is made much tougher under the constant glare of the media. However, it’s a glare they have charmed and manipulated for their own ends, and it's probably what contributed to them getting into these situations in the first place.
A Statement of Means
A celebrity checking into rehab is not just a hot story; it is also a statement of means. Where the average person on a normal income might struggle to meet the cost of ongoing drug rehabilitation treatment, it affords the celebrity the opportunity to flash some cash.
A popular clinic for celebrities in Malibu operates on a sliding scale, which increases depending on the perceived status of the celebrities involved, and the potential media coverage that can be gained from their admittance. Prices start from around $15,000 a month for the basic package, running up to $70,000 a month for the full works.
Who Cares?
Celebrities live privileged lives, surrounded by people who will do or get anything for them without asking questions. Many celebrities can, and do, get anything their hearts desire, which is part of the problem.
Being surrounded by “yes men” may sound wonderful to you and me, but it also means everything comes in excess. When the free availability of drugs is added to the equation, it provides for a potent mix that often ends in a trip to rehab.
A Serious Undertaking
For most people, it is not easy to make the decision to go into rehab. It is the realization that in order to survive, change must happen. It marks the beginning of a long and difficult battle.
When celebrities do it for the reasons mentioned above, in most cases they are doomed to fail. The decision to go into rehab is taken without proper advice and support (those yes men again), and celebrities go into it without committing themselves fully.
Rehab is often treated as a vacation by celebrities, because while inside that is exactly how they are treated. Celebrities can remove themselves from the spotlight very easily simply by walking into a rehab center; no more press, no more photographers, and no more hassle.
But it’s not all their fault; rehab centers are as much to blame. There is a tendency for the staff to treat celebrities like – well, celebrities, and not as people with serious addiction problems. Very often, the staff do not deal with the celebrity in a way conducive to his/her getting better, and are afraid that the celebrity will leave and this will be bad PR for the drug rehab
What Should Happen
If celebrities are to succeed in rehab they must be treated like normal people while undergoing treatment, and in the support they receive afterwards. Just like normal patients, they need to examine their habits, the circle of people around them, and their routines.
The treatment center must also play its part. When a celebrity is accepted into a program, only qualified staff should provide the best treatment that is relevant to the addiction. The center should provide ongoing support, and not wave them out the door expecting never to see them again – because they will be back.
Finally, the media must also accept its share of responsibility. Journalists and photographers must give celebrities in rehab the room to recover, and educate their audience that drug abuse harms millions of ordinary people. Rehab is not something to be taken lightly, and if this is the message the media and celebrities can get across, the battle against drug addiction will be closer to being won.
Rabu, 09 April 2008
Sabtu, 29 Maret 2008
Morphine Addiction
Morphine addiction is a very serious and sometimes life threatening dilemma. Not only is it difficult for the addict, it is extremely hard on those around them who care about them. For the addict, admitting they have an addiction problem can be difficult. However painful this may be, it must be acknowledged as the first gradient to overcoming the problem. The next hurdle is being willing to seek & accept help from an addiction professional. It can be hard for an addict to confront the fact that they can not do it alone. Once this fact is accepted, it is time to seek the appropriate professional treatment. Drug rehab programs based on the social education modality are highly successful. This means that individuals who are recovering from Morphine addiction are not made wrong for their past indiscretions, but are taught how to avoid future ones. They are provided with knowledge on how to change their lives and how to live comfortably without Morphine. Receiving treatment for addiction should be done in a safe & stable environment that is conducive to addiction recovery. Research studies show that residential treatment programs of at least 3 months in duration have the best success rates. 3 months may seem like a long time, but one day in the life of an individual addicted to Morphine can feel like an eternity. Addiction is a self imposed hellish slavery. The chains can be broken people do it everyday. You can be free!
Drug rehabilitation is a multi-phase, multi-faceted, long term process. Detoxification is only the first step on the road of addiction treatment. Physical detoxification alone is not sufficient to change the patterns of a drug addict. Recovery from addiction involves an extended process which usually requires the help of drug addiction professionals. To make a successful recovery, the addict needs new tools in order to deal with situations and problems which arise. Factors such as encountering someone from their days of using, returning to the same environment and places, or even small things such as smells and objects trigger memories which can create psychological stress. This can hinder the addict's goal of complete recovery, thus not allowing the addict to permanently regain control of his or her life.
Almost all addicts tell themselves in the beginning that they can conquer their addiction on their own without the help of outside resources. Unfortunately, this is not usually the case. When an addict makes an attempt at detoxification and to discontinue drug use without the aid of professional help, statistically the results do not last long. Research into the effects of long-term addiction has shown that substantial changes in the way the brain functions are present long after the addict has stopped using drugs. Realizing that a drug addict who wishes to recover from their addiction needs more than just strong will power is the key to a successful recovery. Battling not only cravings for their drug of choice, re-stimulation of their past and changes in the way their brain functions, it is no wonder that quitting drugs without professional help is an uphill battle.
Q) What is Morphine?
A) Morphine is a narcotic analgesic. Morphine was first isolated from opium in 1805 by a German pharmacist, Wilhelm Sertürner. Sertürner described it as the Principium Somniferum. He named it morphium - after Morpheus, the Greek god of dreams. Today morphine is isolated from opium in substantially larger quantities - over 1000 tons per year - although most commercial opium is converted into codeine by methylation. On the illicit market, opium gum is filtered into morphine base and then synthesized into heroin.
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Q) How is Morphine used?
A) Morphinecan be taken orally in tablet form, and can also injected subcutaneously, intramuscularly, or intravenously; the last is the route preferred by those who are dependent on morphine.
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Q) What are the side effects of Morphine?
A)
anxiety
involuntary movement of the eyeball blurred vision / double vision
constipation "pinpoint" pupils chills
depressed or irritable mood itching cramps
dizziness rash diarrhea
drowsiness rigid muscles inability to urinate
exaggerated sense of well-being seizure dreams
light - headedness swelling due to fluid retention dry mouth
nausea tingling or pins and needles facial flushing
sedation tremor fainting / faintness
sweating uncoordinated muscle movements floating feeling
vomiting weakness hallucinations
agitation abdominal pain headache
allergic reaction abnormal thinking high/low blood pressure
appetite loss accidental injury hives
apprehension memory loss insomnia
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Q) What is Morphine addiction?
A) Morphine is highly addictive. Tolerance (the need for higher and higher doses to maintain the same effect) and physical and psychological dependence develop quickly. Withdrawal from morphine causes nausea, tearing, yawning, chills, and sweating lasting up to three days. Morphine crosses the placental barrier, and babies born to morphine-using mothers go through withdrawal.
Addictive drugs activate the brain’s reward systems. The promise of reward is very intense, causing the individual to crave the drug and to focus his or her activities around taking the drug. The ability of addictive drugs to strongly activate brain reward mechanisms and their ability to chemically alter the normal functioning of these systems can produce an addiction. Drugs also reduce a person’s level of consciousness, harming the ability to think or be fully aware of present surroundings.
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Q) What are possible drug interactions when using Morphine?
A)
Alcohol
Certain analgesics such as Talwin, Nubain, Stadol, and Buprenex
Drugs that control vomiting, such as Compazine and Tigan
Drugs classified as MAO inhibitors, such as the antidepressants Nardil and Parnate
Major tranquilizers such as Thorazine and Haldol
Muscle relaxants such as Flexeril and Valium
Sedatives such as Dalmane and Halcion
Tranquilizers such as Librium and Xanax
Water pills such as Diuril and Lasix
morphineaddictiiondrugrehab
Drug rehabilitation is a multi-phase, multi-faceted, long term process. Detoxification is only the first step on the road of addiction treatment. Physical detoxification alone is not sufficient to change the patterns of a drug addict. Recovery from addiction involves an extended process which usually requires the help of drug addiction professionals. To make a successful recovery, the addict needs new tools in order to deal with situations and problems which arise. Factors such as encountering someone from their days of using, returning to the same environment and places, or even small things such as smells and objects trigger memories which can create psychological stress. This can hinder the addict's goal of complete recovery, thus not allowing the addict to permanently regain control of his or her life.
Almost all addicts tell themselves in the beginning that they can conquer their addiction on their own without the help of outside resources. Unfortunately, this is not usually the case. When an addict makes an attempt at detoxification and to discontinue drug use without the aid of professional help, statistically the results do not last long. Research into the effects of long-term addiction has shown that substantial changes in the way the brain functions are present long after the addict has stopped using drugs. Realizing that a drug addict who wishes to recover from their addiction needs more than just strong will power is the key to a successful recovery. Battling not only cravings for their drug of choice, re-stimulation of their past and changes in the way their brain functions, it is no wonder that quitting drugs without professional help is an uphill battle.
Q) What is Morphine?
A) Morphine is a narcotic analgesic. Morphine was first isolated from opium in 1805 by a German pharmacist, Wilhelm Sertürner. Sertürner described it as the Principium Somniferum. He named it morphium - after Morpheus, the Greek god of dreams. Today morphine is isolated from opium in substantially larger quantities - over 1000 tons per year - although most commercial opium is converted into codeine by methylation. On the illicit market, opium gum is filtered into morphine base and then synthesized into heroin.
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Q) How is Morphine used?
A) Morphinecan be taken orally in tablet form, and can also injected subcutaneously, intramuscularly, or intravenously; the last is the route preferred by those who are dependent on morphine.
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Q) What are the side effects of Morphine?
A)
anxiety
involuntary movement of the eyeball blurred vision / double vision
constipation "pinpoint" pupils chills
depressed or irritable mood itching cramps
dizziness rash diarrhea
drowsiness rigid muscles inability to urinate
exaggerated sense of well-being seizure dreams
light - headedness swelling due to fluid retention dry mouth
nausea tingling or pins and needles facial flushing
sedation tremor fainting / faintness
sweating uncoordinated muscle movements floating feeling
vomiting weakness hallucinations
agitation abdominal pain headache
allergic reaction abnormal thinking high/low blood pressure
appetite loss accidental injury hives
apprehension memory loss insomnia
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Q) What is Morphine addiction?
A) Morphine is highly addictive. Tolerance (the need for higher and higher doses to maintain the same effect) and physical and psychological dependence develop quickly. Withdrawal from morphine causes nausea, tearing, yawning, chills, and sweating lasting up to three days. Morphine crosses the placental barrier, and babies born to morphine-using mothers go through withdrawal.
Addictive drugs activate the brain’s reward systems. The promise of reward is very intense, causing the individual to crave the drug and to focus his or her activities around taking the drug. The ability of addictive drugs to strongly activate brain reward mechanisms and their ability to chemically alter the normal functioning of these systems can produce an addiction. Drugs also reduce a person’s level of consciousness, harming the ability to think or be fully aware of present surroundings.
--------------------------------------------------------------------------------
Q) What are possible drug interactions when using Morphine?
A)
Alcohol
Certain analgesics such as Talwin, Nubain, Stadol, and Buprenex
Drugs that control vomiting, such as Compazine and Tigan
Drugs classified as MAO inhibitors, such as the antidepressants Nardil and Parnate
Major tranquilizers such as Thorazine and Haldol
Muscle relaxants such as Flexeril and Valium
Sedatives such as Dalmane and Halcion
Tranquilizers such as Librium and Xanax
Water pills such as Diuril and Lasix
morphineaddictiiondrugrehab
What Is Alcohol Abuse?
Alcohol abuse differs from alcoholism in that it does not include an extremely strong craving for alcohol, loss of control over drinking, or physical dependence. Alcohol abuse is defined as a pattern of drinking that results in one or more of the following situations within a 12-month period:
Failure to fulfill major work, school, or home responsibilities
Drinking in situations that are physically dangerous, such as while driving a car or operating machinery
Having recurring alcohol-related legal problems, such as being arrested for driving under the influence of alcohol or for physically hurting someone while drunk
Continued drinking despite having ongoing relationship problems that are caused or worsened by the drinking
Although alcohol abuse is basically different from alcoholism, many effects of alcohol abuse are also experienced by alcoholics.
What Are the Signs of a Problem?
How can you tell whether you may have a drinking problem? Answering the following four questions can help you find out:
Have you ever felt you should cut down on your drinking?
Have people annoyed you by criticizing your drinking?
Have you ever felt bad or guilty about your drinking?
Have you ever had a drink first thing in the morning (as an "eye opener") to steady your nerves or get rid of a hangover?
One "yes" answer suggests a possible alcohol problem. If you answered "yes" to more than one question, it is highly likely that a problem exists. In either case, it is important that you see your doctor or other health care provider right away to discuss your answers to these questions. He or she can help you determine whether you have a drinking problem and, if so, recommend the best course of action.
Even if you answered "no" to all of the above questions, if you encounter drinking-related problems with your job, relationships, health, or the law, you should seek professional help. The effects of alcohol abuse can be extremely serious—even fatal—both to you and to others.
alcohol
Failure to fulfill major work, school, or home responsibilities
Drinking in situations that are physically dangerous, such as while driving a car or operating machinery
Having recurring alcohol-related legal problems, such as being arrested for driving under the influence of alcohol or for physically hurting someone while drunk
Continued drinking despite having ongoing relationship problems that are caused or worsened by the drinking
Although alcohol abuse is basically different from alcoholism, many effects of alcohol abuse are also experienced by alcoholics.
What Are the Signs of a Problem?
How can you tell whether you may have a drinking problem? Answering the following four questions can help you find out:
Have you ever felt you should cut down on your drinking?
Have people annoyed you by criticizing your drinking?
Have you ever felt bad or guilty about your drinking?
Have you ever had a drink first thing in the morning (as an "eye opener") to steady your nerves or get rid of a hangover?
One "yes" answer suggests a possible alcohol problem. If you answered "yes" to more than one question, it is highly likely that a problem exists. In either case, it is important that you see your doctor or other health care provider right away to discuss your answers to these questions. He or she can help you determine whether you have a drinking problem and, if so, recommend the best course of action.
Even if you answered "no" to all of the above questions, if you encounter drinking-related problems with your job, relationships, health, or the law, you should seek professional help. The effects of alcohol abuse can be extremely serious—even fatal—both to you and to others.
alcohol
Selasa, 18 Maret 2008
Hallucinogens
Hallucinogens are drugs that cause hallucinations - profound distortions in a person's perceptions of reality. Under the influence of hallucinogens, people see images, hear sounds, and feel sensations that seem real but do not exist. Some hallucinogens also produce rapid, intense emotional swings.
What are hallucinogens?
Hallucinogens cause their effects by disrupting the interaction of nerve cells and the neurotransmitter serotonin. Distributed throughout the brain and spinal cord, the serotonin system is involved in the control of behavioral, perceptual, and regulatory systems, including mood, hunger, body temperature, sexual behavior, muscle control, and sensory perception.
LSD (an abbreviation of the German words for "lysergic acid diethylamide") is the drug most commonly identified with the term "hallucinogen" and the most widely used in this class of drugs. It is considered the typical hallucinogen, and the characteristics of its action and effects described in this Research Report apply to the other hallucinogens, including mescaline, psilocybin, and ibogaine.
What are dissociative drugs?
Drugs such as PCP (phencyclidine) and ketamine, which were initially developed as general anesthetics for surgery, distort perceptions of sight and sound and produce feelings of detachment - dissociation - from the environment and self. But these mind-altering effects are not hallucinations. PCP and ketamine are therefore more properly known as "dissociative anesthetics." Dextromethorphan, a widely available cough suppressant, when taken in high doses can produce effects similar to those of PCP and ketamine.
The dissociative drugs act by altering distribution of the neurotransmitter glutamate throughout the brain. Glutamate is involved in perception of pain, responses to the environment, and memory. PCP is considered the typical dissociative drug, and the description of PCP's actions and effects in this Research Report largely applies to ketamine and dextromethorphan as well.
Prevalence of Students Who Have Ever Used
Hallucinogens and PCP
Source: Monitoring the Future Survey, 2000
Note: Data not available for PCP Prevalence for 8th and 10th graders.
Why do people take hallucinogens?
Chemist Albert Hofmann, working at the Sandoz Corporation pharmaceutical laboratory in Switzerland, first synthesized LSD in 1938. He was conducting research on possible medical applications of various lysergic acid compounds derived from ergot, a fungus that develops on rye grass. Searching for compounds with therapeutic value, Hofmann created more than two dozen ergot-derived synthetic molecules. The 25th was called, in German, Lyserg-Säure-Diäthylamid 25, or LSD-25. Five years after he first created the drug, Hofmann accidentally ingested a small amount and experienced a series of frightening sensory effects:
"My surroundings . . . transformed themselves in more terrifying ways. Everything in the room spun around, and the familiar objects and pieces of furniture assumed grotesque, threatening forms. They were in continuous motion, animated, as if driven by an inner restlessness . . . . Even worse than these demonic transformations of the outer world were the alterations that I perceived in myself, in my inner being. Every exertion of my will, every attempt to put an end to the disintegration of the outer world and the dissolution of my ego, seemed to be wasted effort. A demon had invaded me, had taken possession of my body, mind, and soul."
Hallucinogenic drugs have played a role in human life for thousands of years. Cultures from the tropics to the arctic have used plants to induce states of detachment from reality and to precipitate "visions" thought to provide mystical insight. These plants contain chemical compounds, such as mescaline, psilocybin, and ibogaine, that are structurally similar to serotonin, and they produce their effects by disrupting normal functioning of the serotonin system. Historically, hallucinogenic plants were used largely for social and religious ritual, and their availability was limited by the climate and soil conditions they require. After the development of LSD, a synthetic compound that can be manufactured anywhere, abuse of hallucinogens became more widespread, and from the 1960s it increased dramatically. All LSD manufactured in this country is intended for illegal use, since LSD has no accepted medical use in the United States.
Physical characteristics of LSD
LSD is a clear or white, odorless, water-soluble material synthesized from lysergic acid, a compound derived from a rye fungus. LSD is the most potent mood- and perception-altering drug known: oral doses as small as 30 micrograms can produce effects that last 6 to 12 hours.
LSD is initially produced in crystalline form. The pure crystal can be crushed to powder and mixed with binding agents to produce tablets known as "microdots" or thin squares of gelatin called "window panes"; more commonly, it is dissolved, diluted, and applied to paper or other materials. The most common form of LSD is called "blotter acid" - sheets of paper soaked in LSD and perforated into 1/4-inch square, individual dosage units. Variations in manufacturing and the presence of contaminants can produce LSD in colors ranging from clear or white, in its purest form, to tan or even black. Even uncontaminated LSD begins to degrade and discolor soon after it is manufactured, and drug distributors often apply LSD to colored paper, making it difficult for a buyer to determine the drug's purity or age.
LSD's effects
The precise mechanism by which LSD alters perceptions is still unclear. Evidence from laboratory studies suggests that LSD, like hallucinogenic plants, acts on certain groups of serotonin receptors designated the 5-HT2 receptors, and that its effects are most prominent in two brain regions: One is the cerebral cortex, an area involved in mood, cognition, and perception; the other is the locus ceruleus, which receives sensory signals from all areas of the body and has been described as the brain's "novelty detector" for important external stimuli.
LSD's effects typically begin within 30 to 90 minutes of ingestion and may last as long as 12 hours. Users refer to LSD and other hallucinogenic experiences as "trips" and to the acute adverse experiences as "bad trips." Although most LSD trips include both pleasant and unpleasant aspects, the drug's effects are unpredictable and may vary with the amount ingested and the user's personality, mood, expectations, and surroundings.
Users of LSD may experience some physiological effects, such as increased blood pressure and heart rate, dizziness, loss of appetite, dry mouth, sweating, nausea, numbness, and tremors; but the drug's major effects are emotional and sensory. The user's emotions may shift rapidly through a range from fear to euphoria, with transitions so rapid that the user may seem to experience several emotions simultaneously.
LSD also has dramatic effects on the senses. Colors, smells, sounds, and other sensations seem highly intensified. In some cases, sensory perceptions may blend in a phenomenon known as synesthesia, in which a person seems to hear or feel colors and see sounds.
Hallucinations distort or transform shapes and movements, and they may give rise to a perception that time is moving very slowly or that the user's body is changing shape. On some trips, users experience sensations that are enjoyable and mentally stimulating and that produce a sense of heightened understanding. Bad trips, however, include terrifying thoughts and nightmarish feelings of anxiety and despair that include fears of insanity, death, or losing control.
LSD users quickly develop a high degree of tolerance for the drug's effects: After repeated use, they need increasingly larger doses to produce similar effects. LSD use also produces tolerance for other hallucinogenic drugs such as psilocybin and mescaline, but not to drugs such as marijuana, amphetamines, and PCP, which do not act directly on the serotonin receptors affected by LSD. Tolerance for LSD is short-lived it is lost if the user stops taking the drug for several days. There is no evidence that LSD produces physical withdrawal symptoms when chronic use is stopped.
Two long-term effects persistent psychosis and hallucinogen persisting perception disorder (HPPD), more commonly referred to as "flashbacks"-have been associated with use of LSD. The causes of these effects, which in some users occur after a single experience with the drug, are not known.
Psychosis. The effects of LSD can be described as drug-induced psychosis-distortion or disorganization of a person's capacity to recognize reality, think rationally, or communicate with others. Some LSD users experience devastating psychological effects that persist after the trip has ended, producing a long-lasting psychotic-like state. LSD-induced persistent psychosis may include dramatic mood swings from mania to profound depression, vivid visual disturbances, and hallucinations. These effects may last for years and can affect people who have no history or other symptoms of psychological disorder.
Hallucinogen Persisting Perception Disorder. Some former LSD users report experiences known colloquially as "flashbacks" and called "HPPD" by physicians. These episodes are spontaneous, repeated, sometimes continuous recurrences of some of the sensory distortions originally produced by LSD. The experience may include hallucinations, but it most commonly consists of visual disturbances such as seeing false motion on the edges of the field of vision, bright or colored flashes, and halos or trails attached to moving objects. This condition is typically persistent and in some cases remains unchanged for years after individuals have stopped using the drug.
Because HPPD symptoms may be mistaken for those of other neurological disorders such as stroke or brain tumors, sufferers may consult a variety of clinicians before the disorder is accurately diagnosed. There is no established treatment for HPPD, although some antidepressant drugs may reduce the symptoms. Psychotherapy may help patients adjust to the confusion associated with visual distraction and to minimize the fear, expressed by some, that they are suffering brain damage or psychiatric disorder.
What are the facts about dissociative drugs?
PCP's forms and effects
PCP, developed in the 1950s as an intravenous surgical anesthetic, is classified as a dissociative anesthetic: Its sedative and anesthetic effects are trance-like, and patients experience a feeling of being "out of body" and detached from their environment. PCP was used in veterinary medicine but was never approved for human use because of problems that arose during clinical studies, including delirium and extreme agitation experienced by patients emerging from anesthesia.
During the 1960s, PCP in pill form became widely abused, but the surge in illicit use receded rapidly as users became dissatisfied with the long delay between taking the drug and feeling its effects, and with the unpredictable and often violent behavior associated with its use. Powdered PCP - known as "ozone," "rocket fuel," "love boat," "hog," "embalming fluid," or "superweed" - appeared in the 1970s. In powdered form, the drug is sprinkled on marijuana, tobacco, or parsley, then smoked, and the onset of effects is rapid. Users sometimes ingest PCP by snorting the powder or by swallowing it in tablet form. Normally a white crystalline powder, PCP is sometimes colored with water-soluble or alcohol-soluble dyes.
When snorted or smoked, PCP rapidly passes to the brain to disrupt the functioning of sites known as NMDA (N-methyl-D-aspartate) receptor complexes, which are receptors for the neurotransmitter glutamate. Glutamate receptors play a major role in the perception of pain, in cognition - including learning and memory - and in emotion. In the brain, PCP also alters the actions of dopamine, a neurotransmitter responsible for the euphoria and "rush" associated with many abused drugs.
At low PCP doses (5 mg or less), physical effects include shallow, rapid breathing, increased blood pressure and heart rate, and elevated temperature. Doses of 10 mg or more cause dangerous changes in blood pressure, heart rate, and respiration, often accompanied by nausea, blurred vision, dizziness, and decreased awareness of pain. Muscle contractions may cause uncoordinated movements and bizarre postures. When severe, the muscle contractions can result in bone fracture or in kidney damage or failure as a consequence of muscle cells breaking down. Very high doses of PCP can cause convulsions, coma, hyperthermia, and death.
PCP's effects are unpredictable. Typically, they are felt within minutes of ingestion and last for several hours. Some users report feeling the drug's effects for days. One drug-taking episode may produce feelings of detachment from reality, including distortions of space, time, and body image; another may produce hallucinations, panic, and fear. Some users report feelings of invulnerability and exaggerated strength. PCP users may become severely disoriented, violent, or suicidal.
Repeated use of PCP can result in addiction, and recent research suggests that repeated or prolonged use of PCP can cause withdrawal syndrome when drug use is stopped. Symptoms such as memory loss and depression may persist for as long as a year after a chronic user stops taking PCP.
Nature and effects of ketamine
Ketamine ("K," "Special K," "cat Valium") is a dissociative anesthetic developed in 1963 to replace PCP and currently used in human anesthesia and veterinary medicine. Much of the ketamine sold on the street has been diverted from veterinarians' offices. Although it is manufactured as an injectable liquid, in illicit use ketamine is generally evaporated to form a powder that is snorted or compressed into pills.
Ketamine's chemical structure and mechanism of action are similar to those of PCP, and its effects are similar, but ketamine is much less potent than PCP with effects of much shorter duration. Users report sensations ranging from a pleasant feeling of floating to being separated from their bodies. Some ketamine experiences involve a terrifying feeling of almost complete sensory detachment that is likened to a near-death experience. These experiences, similar to a "bad trip" on LSD, are called the "K-hole."
Ketamine is odorless and tasteless, so it can be added to beverages without being detected, and it induces amnesia. Because of these properties, the drug is sometimes given to unsuspecting victims and used in the commission of sexual assaults referred to as "drug rape."
Extra-Strength cough syrup is the most common source of abused dextromethorphan
Nature and effects of dextromethorphan
Dextromethorphan (sometimes called "DXM" or "robo") is a cough-suppressing ingredient in a variety of over-the-counter cold and cough medications. Like PCP and ketamine, dextromethorphan acts as an NMDA receptor antagonist. The most common source of abused dextromethorphan is "extra-strength" cough syrup, which typically contains 3 milligrams of the drug per milliliter of syrup. At the doses recommended for treating coughs (1/6 to 1/3 ounce of medication, containing 15 mg to 30 mg dextromethorphan), the drug is safe and effective. At much higher doses (4 or more ounces), dextromethorphan produces dissociative effects similar to those of PCP and ketamine.
The effects vary with dose, and dextromethorphan users describe a set of distinct dose-dependent "plateaus" ranging from a mild stimulant effect with distorted visual perceptions at low (approximately 2-ounce) doses to a sense of complete dissociation from one's body at doses of 10 ounces or more. The effects typically last for 6 hours. Over-the-counter medications that contain dextromethorphan often contain antihistamine and decongestant ingredients as well, and high doses of these mixtures can seriously increase risks of dextromethorphan abuse.
Where can I get more scientific information on hallucinogens and dissociative drugs?
Fact sheets on LSD, PCP, other illicit drugs, and related topics are available free, in English and Spanish, with a call to NIDA Infofax at 1-888-NIH-NIDA (1-888-644-6432) or, for the deaf, 1-888-TTY-NIDA (1-888-889-6432).
Further information on hallucinogens and dissociative drugs can be obtained also through NIDA's home page (www.drugabuse.gov) and from the National Clearinghouse for Alcohol and Drug Information (NCADI) at 1-800-729-6686. NCADI's Web site is www.health.org.
Glossary
Acid: Common street name for LSD.
Angel dust: Common street name for PCP.
Cerebral cortex: Region of the brain responsible for cognitive functions including reasoning, mood, and perception of stimuli.
Dissociative anesthetic: Compound, such as phencyclidine or ketamine, that produces an anesthetic effect characterized by a feeling of being detached from the physical self.
DXM: Common street name for dextromethorphan.
Flashback: Slang term for HPPD (see below).
Glutamate: A neurotransmitter associated with pain, memory, and response to changes in the environment.
Hallucinogen: A drug that produces hallucinations - distortion in perception of sights and sounds - and disturbances in emotion, judgment, and memory.
HPPD: Hallucinogen persisting perception disorder; the spontaneous and sometimes continuous recurrence of perceptual effects of LSD long after an individual has ingested the drug.
Ketamine: Dissociative anesthetic abused for its mind-altering effects and sometimes used to facilitate sexual assault.
Locus ceruleus: Region of the brain that receives and processes sensory signals from all areas of the body.
Neurotransmitter: Chemical compound that acts as a messenger to carry signals or stimuli from one nerve cell to another.
NMDA: N-methyl-D-aspartate, a chemical compound that reacts with glutamate receptors on nerve cells.
PCP: Phencyclidine, a dissociative anesthetic abused for its mind-altering effects.
Persistent psychosis: Unpredictable and long-lasting visual disturbances, dramatic mood swings, and hallucinations experienced by some LSD users after they have discontinued use of the drug.
Robo: Common street name for dextromethorphan.
Serotonin: A neurotransmitter that causes a very broad range of effects on perception, movement, and the emotions by modulating the actions of other neurotransmitters in most parts of the brain
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What are hallucinogens?
Hallucinogens cause their effects by disrupting the interaction of nerve cells and the neurotransmitter serotonin. Distributed throughout the brain and spinal cord, the serotonin system is involved in the control of behavioral, perceptual, and regulatory systems, including mood, hunger, body temperature, sexual behavior, muscle control, and sensory perception.
LSD (an abbreviation of the German words for "lysergic acid diethylamide") is the drug most commonly identified with the term "hallucinogen" and the most widely used in this class of drugs. It is considered the typical hallucinogen, and the characteristics of its action and effects described in this Research Report apply to the other hallucinogens, including mescaline, psilocybin, and ibogaine.
What are dissociative drugs?
Drugs such as PCP (phencyclidine) and ketamine, which were initially developed as general anesthetics for surgery, distort perceptions of sight and sound and produce feelings of detachment - dissociation - from the environment and self. But these mind-altering effects are not hallucinations. PCP and ketamine are therefore more properly known as "dissociative anesthetics." Dextromethorphan, a widely available cough suppressant, when taken in high doses can produce effects similar to those of PCP and ketamine.
The dissociative drugs act by altering distribution of the neurotransmitter glutamate throughout the brain. Glutamate is involved in perception of pain, responses to the environment, and memory. PCP is considered the typical dissociative drug, and the description of PCP's actions and effects in this Research Report largely applies to ketamine and dextromethorphan as well.
Prevalence of Students Who Have Ever Used
Hallucinogens and PCP
Source: Monitoring the Future Survey, 2000
Note: Data not available for PCP Prevalence for 8th and 10th graders.
Why do people take hallucinogens?
Chemist Albert Hofmann, working at the Sandoz Corporation pharmaceutical laboratory in Switzerland, first synthesized LSD in 1938. He was conducting research on possible medical applications of various lysergic acid compounds derived from ergot, a fungus that develops on rye grass. Searching for compounds with therapeutic value, Hofmann created more than two dozen ergot-derived synthetic molecules. The 25th was called, in German, Lyserg-Säure-Diäthylamid 25, or LSD-25. Five years after he first created the drug, Hofmann accidentally ingested a small amount and experienced a series of frightening sensory effects:
"My surroundings . . . transformed themselves in more terrifying ways. Everything in the room spun around, and the familiar objects and pieces of furniture assumed grotesque, threatening forms. They were in continuous motion, animated, as if driven by an inner restlessness . . . . Even worse than these demonic transformations of the outer world were the alterations that I perceived in myself, in my inner being. Every exertion of my will, every attempt to put an end to the disintegration of the outer world and the dissolution of my ego, seemed to be wasted effort. A demon had invaded me, had taken possession of my body, mind, and soul."
Hallucinogenic drugs have played a role in human life for thousands of years. Cultures from the tropics to the arctic have used plants to induce states of detachment from reality and to precipitate "visions" thought to provide mystical insight. These plants contain chemical compounds, such as mescaline, psilocybin, and ibogaine, that are structurally similar to serotonin, and they produce their effects by disrupting normal functioning of the serotonin system. Historically, hallucinogenic plants were used largely for social and religious ritual, and their availability was limited by the climate and soil conditions they require. After the development of LSD, a synthetic compound that can be manufactured anywhere, abuse of hallucinogens became more widespread, and from the 1960s it increased dramatically. All LSD manufactured in this country is intended for illegal use, since LSD has no accepted medical use in the United States.
Physical characteristics of LSD
LSD is a clear or white, odorless, water-soluble material synthesized from lysergic acid, a compound derived from a rye fungus. LSD is the most potent mood- and perception-altering drug known: oral doses as small as 30 micrograms can produce effects that last 6 to 12 hours.
LSD is initially produced in crystalline form. The pure crystal can be crushed to powder and mixed with binding agents to produce tablets known as "microdots" or thin squares of gelatin called "window panes"; more commonly, it is dissolved, diluted, and applied to paper or other materials. The most common form of LSD is called "blotter acid" - sheets of paper soaked in LSD and perforated into 1/4-inch square, individual dosage units. Variations in manufacturing and the presence of contaminants can produce LSD in colors ranging from clear or white, in its purest form, to tan or even black. Even uncontaminated LSD begins to degrade and discolor soon after it is manufactured, and drug distributors often apply LSD to colored paper, making it difficult for a buyer to determine the drug's purity or age.
LSD's effects
The precise mechanism by which LSD alters perceptions is still unclear. Evidence from laboratory studies suggests that LSD, like hallucinogenic plants, acts on certain groups of serotonin receptors designated the 5-HT2 receptors, and that its effects are most prominent in two brain regions: One is the cerebral cortex, an area involved in mood, cognition, and perception; the other is the locus ceruleus, which receives sensory signals from all areas of the body and has been described as the brain's "novelty detector" for important external stimuli.
LSD's effects typically begin within 30 to 90 minutes of ingestion and may last as long as 12 hours. Users refer to LSD and other hallucinogenic experiences as "trips" and to the acute adverse experiences as "bad trips." Although most LSD trips include both pleasant and unpleasant aspects, the drug's effects are unpredictable and may vary with the amount ingested and the user's personality, mood, expectations, and surroundings.
Users of LSD may experience some physiological effects, such as increased blood pressure and heart rate, dizziness, loss of appetite, dry mouth, sweating, nausea, numbness, and tremors; but the drug's major effects are emotional and sensory. The user's emotions may shift rapidly through a range from fear to euphoria, with transitions so rapid that the user may seem to experience several emotions simultaneously.
LSD also has dramatic effects on the senses. Colors, smells, sounds, and other sensations seem highly intensified. In some cases, sensory perceptions may blend in a phenomenon known as synesthesia, in which a person seems to hear or feel colors and see sounds.
Hallucinations distort or transform shapes and movements, and they may give rise to a perception that time is moving very slowly or that the user's body is changing shape. On some trips, users experience sensations that are enjoyable and mentally stimulating and that produce a sense of heightened understanding. Bad trips, however, include terrifying thoughts and nightmarish feelings of anxiety and despair that include fears of insanity, death, or losing control.
LSD users quickly develop a high degree of tolerance for the drug's effects: After repeated use, they need increasingly larger doses to produce similar effects. LSD use also produces tolerance for other hallucinogenic drugs such as psilocybin and mescaline, but not to drugs such as marijuana, amphetamines, and PCP, which do not act directly on the serotonin receptors affected by LSD. Tolerance for LSD is short-lived it is lost if the user stops taking the drug for several days. There is no evidence that LSD produces physical withdrawal symptoms when chronic use is stopped.
Two long-term effects persistent psychosis and hallucinogen persisting perception disorder (HPPD), more commonly referred to as "flashbacks"-have been associated with use of LSD. The causes of these effects, which in some users occur after a single experience with the drug, are not known.
Psychosis. The effects of LSD can be described as drug-induced psychosis-distortion or disorganization of a person's capacity to recognize reality, think rationally, or communicate with others. Some LSD users experience devastating psychological effects that persist after the trip has ended, producing a long-lasting psychotic-like state. LSD-induced persistent psychosis may include dramatic mood swings from mania to profound depression, vivid visual disturbances, and hallucinations. These effects may last for years and can affect people who have no history or other symptoms of psychological disorder.
Hallucinogen Persisting Perception Disorder. Some former LSD users report experiences known colloquially as "flashbacks" and called "HPPD" by physicians. These episodes are spontaneous, repeated, sometimes continuous recurrences of some of the sensory distortions originally produced by LSD. The experience may include hallucinations, but it most commonly consists of visual disturbances such as seeing false motion on the edges of the field of vision, bright or colored flashes, and halos or trails attached to moving objects. This condition is typically persistent and in some cases remains unchanged for years after individuals have stopped using the drug.
Because HPPD symptoms may be mistaken for those of other neurological disorders such as stroke or brain tumors, sufferers may consult a variety of clinicians before the disorder is accurately diagnosed. There is no established treatment for HPPD, although some antidepressant drugs may reduce the symptoms. Psychotherapy may help patients adjust to the confusion associated with visual distraction and to minimize the fear, expressed by some, that they are suffering brain damage or psychiatric disorder.
What are the facts about dissociative drugs?
PCP's forms and effects
PCP, developed in the 1950s as an intravenous surgical anesthetic, is classified as a dissociative anesthetic: Its sedative and anesthetic effects are trance-like, and patients experience a feeling of being "out of body" and detached from their environment. PCP was used in veterinary medicine but was never approved for human use because of problems that arose during clinical studies, including delirium and extreme agitation experienced by patients emerging from anesthesia.
During the 1960s, PCP in pill form became widely abused, but the surge in illicit use receded rapidly as users became dissatisfied with the long delay between taking the drug and feeling its effects, and with the unpredictable and often violent behavior associated with its use. Powdered PCP - known as "ozone," "rocket fuel," "love boat," "hog," "embalming fluid," or "superweed" - appeared in the 1970s. In powdered form, the drug is sprinkled on marijuana, tobacco, or parsley, then smoked, and the onset of effects is rapid. Users sometimes ingest PCP by snorting the powder or by swallowing it in tablet form. Normally a white crystalline powder, PCP is sometimes colored with water-soluble or alcohol-soluble dyes.
When snorted or smoked, PCP rapidly passes to the brain to disrupt the functioning of sites known as NMDA (N-methyl-D-aspartate) receptor complexes, which are receptors for the neurotransmitter glutamate. Glutamate receptors play a major role in the perception of pain, in cognition - including learning and memory - and in emotion. In the brain, PCP also alters the actions of dopamine, a neurotransmitter responsible for the euphoria and "rush" associated with many abused drugs.
At low PCP doses (5 mg or less), physical effects include shallow, rapid breathing, increased blood pressure and heart rate, and elevated temperature. Doses of 10 mg or more cause dangerous changes in blood pressure, heart rate, and respiration, often accompanied by nausea, blurred vision, dizziness, and decreased awareness of pain. Muscle contractions may cause uncoordinated movements and bizarre postures. When severe, the muscle contractions can result in bone fracture or in kidney damage or failure as a consequence of muscle cells breaking down. Very high doses of PCP can cause convulsions, coma, hyperthermia, and death.
PCP's effects are unpredictable. Typically, they are felt within minutes of ingestion and last for several hours. Some users report feeling the drug's effects for days. One drug-taking episode may produce feelings of detachment from reality, including distortions of space, time, and body image; another may produce hallucinations, panic, and fear. Some users report feelings of invulnerability and exaggerated strength. PCP users may become severely disoriented, violent, or suicidal.
Repeated use of PCP can result in addiction, and recent research suggests that repeated or prolonged use of PCP can cause withdrawal syndrome when drug use is stopped. Symptoms such as memory loss and depression may persist for as long as a year after a chronic user stops taking PCP.
Nature and effects of ketamine
Ketamine ("K," "Special K," "cat Valium") is a dissociative anesthetic developed in 1963 to replace PCP and currently used in human anesthesia and veterinary medicine. Much of the ketamine sold on the street has been diverted from veterinarians' offices. Although it is manufactured as an injectable liquid, in illicit use ketamine is generally evaporated to form a powder that is snorted or compressed into pills.
Ketamine's chemical structure and mechanism of action are similar to those of PCP, and its effects are similar, but ketamine is much less potent than PCP with effects of much shorter duration. Users report sensations ranging from a pleasant feeling of floating to being separated from their bodies. Some ketamine experiences involve a terrifying feeling of almost complete sensory detachment that is likened to a near-death experience. These experiences, similar to a "bad trip" on LSD, are called the "K-hole."
Ketamine is odorless and tasteless, so it can be added to beverages without being detected, and it induces amnesia. Because of these properties, the drug is sometimes given to unsuspecting victims and used in the commission of sexual assaults referred to as "drug rape."
Extra-Strength cough syrup is the most common source of abused dextromethorphan
Nature and effects of dextromethorphan
Dextromethorphan (sometimes called "DXM" or "robo") is a cough-suppressing ingredient in a variety of over-the-counter cold and cough medications. Like PCP and ketamine, dextromethorphan acts as an NMDA receptor antagonist. The most common source of abused dextromethorphan is "extra-strength" cough syrup, which typically contains 3 milligrams of the drug per milliliter of syrup. At the doses recommended for treating coughs (1/6 to 1/3 ounce of medication, containing 15 mg to 30 mg dextromethorphan), the drug is safe and effective. At much higher doses (4 or more ounces), dextromethorphan produces dissociative effects similar to those of PCP and ketamine.
The effects vary with dose, and dextromethorphan users describe a set of distinct dose-dependent "plateaus" ranging from a mild stimulant effect with distorted visual perceptions at low (approximately 2-ounce) doses to a sense of complete dissociation from one's body at doses of 10 ounces or more. The effects typically last for 6 hours. Over-the-counter medications that contain dextromethorphan often contain antihistamine and decongestant ingredients as well, and high doses of these mixtures can seriously increase risks of dextromethorphan abuse.
Where can I get more scientific information on hallucinogens and dissociative drugs?
Fact sheets on LSD, PCP, other illicit drugs, and related topics are available free, in English and Spanish, with a call to NIDA Infofax at 1-888-NIH-NIDA (1-888-644-6432) or, for the deaf, 1-888-TTY-NIDA (1-888-889-6432).
Further information on hallucinogens and dissociative drugs can be obtained also through NIDA's home page (www.drugabuse.gov) and from the National Clearinghouse for Alcohol and Drug Information (NCADI) at 1-800-729-6686. NCADI's Web site is www.health.org.
Glossary
Acid: Common street name for LSD.
Angel dust: Common street name for PCP.
Cerebral cortex: Region of the brain responsible for cognitive functions including reasoning, mood, and perception of stimuli.
Dissociative anesthetic: Compound, such as phencyclidine or ketamine, that produces an anesthetic effect characterized by a feeling of being detached from the physical self.
DXM: Common street name for dextromethorphan.
Flashback: Slang term for HPPD (see below).
Glutamate: A neurotransmitter associated with pain, memory, and response to changes in the environment.
Hallucinogen: A drug that produces hallucinations - distortion in perception of sights and sounds - and disturbances in emotion, judgment, and memory.
HPPD: Hallucinogen persisting perception disorder; the spontaneous and sometimes continuous recurrence of perceptual effects of LSD long after an individual has ingested the drug.
Ketamine: Dissociative anesthetic abused for its mind-altering effects and sometimes used to facilitate sexual assault.
Locus ceruleus: Region of the brain that receives and processes sensory signals from all areas of the body.
Neurotransmitter: Chemical compound that acts as a messenger to carry signals or stimuli from one nerve cell to another.
NMDA: N-methyl-D-aspartate, a chemical compound that reacts with glutamate receptors on nerve cells.
PCP: Phencyclidine, a dissociative anesthetic abused for its mind-altering effects.
Persistent psychosis: Unpredictable and long-lasting visual disturbances, dramatic mood swings, and hallucinations experienced by some LSD users after they have discontinued use of the drug.
Robo: Common street name for dextromethorphan.
Serotonin: A neurotransmitter that causes a very broad range of effects on perception, movement, and the emotions by modulating the actions of other neurotransmitters in most parts of the brain
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Prescription Drug Addiction
Prescription Drug Addiction
Prescription drugs are rapidly becoming primary drugs of abuse in the United States and throughout the world. There are many commonly held misconceptions of the abuse potential for powerful substances such as OxyContin®, because such substances can be obtained legally, and have legitimate use in the medical profession.
What are some of the commonly abused prescription drugs?
Although many prescription drugs can be abused or misused, there are three classes of prescription drugs that are most commonly abused:
Opioids, which are most often prescribed to treat pain;
CNS depressants, which are used to treat anxiety and sleep disorders;
Stimulants, which are prescribed to treat the sleep disorder narcolepsy, attention-deficit hyperactivity disorder (ADHD), and obesity.
Opioids
What are opioids?
Opioids are commonly prescribed because of their effective analgesic, or pain-relieving, properties. Medications that fall within this class - sometimes referred to as narcotics - include morphine, codeine, and related drugs. Morphine, for example, is often used before or after surgery to alleviate severe pain. Codeine, because it is less efficacious than morphine, is used for milder pain. Other examples of opioids that can be prescribed to alleviate pain include oxycodone (OxyContin®), propoxyphene (Darvon), hydrocodone (Vicodin), and hydromorphone (Dilaudid), as well as meperidine (Demerol), which is used less often because of its side effects. In addition to their pain-relieving properties, some of these drugs - for example, codeine and diphenoxylate (Lomotil) - can be used to relieve coughs and diarrhea.
Source: Office of Applied Studies, Substance Abuse and Mental Health Services Administration.
National Household Survey on Drug Abuse, 1999.
How do opioids affect the brain and body?
Opioids act by attaching to specific proteins called opioid receptors, which are found in the brain, spinal cord, and gastrointestinal tract. When these drugs attach to certain opioid receptors, they can block the transmission of pain messages to the brain. In addition, opioids can produce drowsiness, cause constipation, and, depending upon the amount of drug taken, depress respiration. Opioid drugs also can cause euphoria by affecting the brain regions that mediate what we perceive as pleasure.
What are the possible consequences of opioid use and abuse?
Chronic use of opioids can result in tolerance for the drugs, which means that users must take higher doses to achieve the same initial effects. Long-term use also can lead to physical dependence and addiction - the body adapts to the presence of the drug, and withdrawal symptoms occur if use is reduced or stopped. Symptoms of withdrawal include restlessness, muscle and bone pain, insomnia, diarrhea, vomiting, cold flashes with goose bumps ("cold turkey"), and involuntary leg movements. Finally, taking a large single dose of an opioid could cause severe respiratory depression that can lead to death. Many studies have shown, however, that properly managed medical use of opioid analgesic drugs is safe and rarely causes clinical addiction, defined as compulsive, often uncontrollable use of drugs. Taken exactly as prescribed, opioids can be used to manage pain effectively.
Is it safe to use opioid drugs with other medications?
Opioids are safe to use with other drugs only under a physician's supervision. Typically, they should not be used with other substances that depress the central nervous system, such as alcohol, antihistamines, barbiturates, benzodiazepines, or general anesthetics, as such a combination increases the risk of life-threatening respiratory depression.
CNS depressants
What are CNS depressants?
CNS depressants are substances that can slow normal brain function. Because of this property, some CNS depressants are useful in the treatment of anxiety and sleep disorders. Among the medications that are commonly prescribed for these purposes are the following:
Barbiturates, such as mephobarbital (Mebaral) and pentobarbital sodium (Nembutal), which are used to treat anxiety, tension, and sleep disorders.
Benzodiazepines, such as diazepam (Valium), chlordiazepoxide HCl (Librium), and alprazolam (Xanax), which can be prescribed to treat anxiety, acute stress reactions, and panic attacks; the more sedating benzodiazepines, such as triazolam (Halcion) and estazolam (ProSom) can be prescribed for short-term treatment of sleep disorders.
In higher doses, some CNS depressants can be used as general anesthetics.
How do CNS depressants affect the brain and body?
There are numerous CNS depressants; most act on the brain by affecting the neurotransmitter gamma-aminobutyric acid (GABA). Neurotransmitters are brain chemicals that facilitate communication between brain cells. GABA works by decreasing brain activity. Although the different classes of CNS depressants work in unique ways, ultimately it is through their ability to increase GABA activity that they produce a drowsy or calming effect that is beneficial to those suffering from anxiety or sleep disorders.
What are the possible consequences of CNS depressant use and abuse?
Despite their many beneficial effects, barbiturates and benzodiazepines have the potential for abuse and should be used only as prescribed. During the first few days of taking a prescribed CNS depressant, a person usually feels sleepy and uncoordinated, but as the body becomes accustomed to the effects of the drug, these feelings begin to disappear. If one uses these drugs long term, the body will develop tolerance for the drugs, and larger doses will be needed to achieve the same initial effects. In addition, continued use can lead to physical dependence and - when use is reduced or stopped - withdrawal. Because all CNS depressants work by slowing the brain's activity, when an individual stops taking them, the brain's activity can rebound and race out of control, possibly leading to seizures and other harmful consequences. Although withdrawal from benzodiazepines can be problematic, it is rarely life threatening, whereas withdrawal from prolonged use of other CNS depressants can have life-threatening complications. Therefore, someone who is thinking about discontinuing CNS depressant therapy or who is suffering withdrawal from a CNS depressant should speak with a physician or seek medical treatment.
Is it safe to use CNS depressants with other medications?
CNS depressants should be used with other medications only under a physician's supervision. Typically, they should not be combined with any other medication or substance that causes CNS depression, including prescription pain medicines, some over-the-counter cold and allergy medications, or alcohol. Using CNS depressants with these other substances - particularly alcohol - can slow breathing, or slow both the heart and respiration, and possibly lead to death.
Stimulants
What are stimulants?
As the name suggests, stimulants are a class of drugs that enhance brain activity - they cause an increase in alertness, attention, and energy that is accompanied by elevated blood pressure and increased heart rate and respiration. Stimulants were used historically to treat asthma and other respiratory problems, obesity, neurological disorders, and a variety of other ailments. But as their potential for abuse and addiction became apparent, the medical use of stimulants began to wane.
Now, stimulants are prescribed for the treatment of only a few health conditions, including narcolepsy, attention-deficit hyperactivity disorder, and depression that has not responded to other treatments. Stimulants may be used as appetite suppressants for short-term treatment of obesity, and they also may be used for patients with asthma.
How do stimulants affect the brain and body?
Stimulants, such as dextroamphetamine (Dexedrine) and methylphenidate (Ritalin), have chemical structures that are similar to a family of key brain neurotransmitters called monoamines, which include norepinephrine and dopamine. Stimulants increase the amount of these chemicals in the brain. This, in turn, increases blood pressure and heart rate, constricts blood vessels, increases blood glucose, and opens up the pathways of the respiratory system. In addition, the increase in dopamine is associated with a sense of euphoria that can accompany the use of these drugs.
What are the possible consequences of stimulant use and abuse?
The consequences of stimulant abuse can be dangerous. Although their use may not lead to physical dependence and risk of withdrawal, stimulants can be addictive in that individuals begin to use them compulsively. Taking high doses of some stimulants repeatedly over a short time can lead to feelings of hostility or paranoia. Additionally, taking high doses of a stimulant may result in dangerously high body temperatures and an irregular heartbeat. There is also the potential for cardiovascular failure or lethal seizures.
Is it safe to use stimulants with other medications?
Stimulants should be used with other medications only when the patient is under a physician's supervision. For example, a stimulant may be prescribed to a patient taking an antidepressant. However, health care providers and patients should be mindful that antidepressants enhance the effects of a stimulant. Patients also should be aware that stimulants should not be mixed with over-the-counter cold medicines that contain decongestants, as this combination may cause blood pressure to become dangerously high or lead to irregular heart rhythms.
Trends in prescription drug abuse
Several indicators suggest that prescription drug abuse is on the rise in the United States. According to the 1999 National Household Survey on Drug Abuse, in 1998, an estimated 1.6 million Americans used prescription pain relievers nonmedically for the first time. This represents a significant increase since the 1980s, when there were generally fewer than 500,000 first-time users per year. From 1990 to 1998, the number of new users of pain relievers increased by 181 percent; the number of individuals who initiated tranquilizer use increased by 132 percent; the number of new sedative users increased by 90 percent; and the number of people initiating stimulant use increased by 165 percent. In 1999, an estimated 4 million people - almost 2 percent of the population aged 12 and older - were currently (use in past month) using certain prescription drugs nonmedically: pain relievers (2.6 million users), sedatives and tranquilizers (1.3 million users), and stimulants (0.9 million users).
Although prescription drug abuse affects many Americans, some trends of concern can be seen among older adults, adolescents, and women. In addition, health care professionals - including physicians, nurses, pharmacists, dentists, anesthesiologists, and veterinarians - may be at increased risk of prescription drug abuse because of ease of access, as well as their ability to self-prescribe drugs. In spite of this increased risk, recent surveys and research in the early 1990s indicate that health care providers probably suffer from substance abuse, including alcohol and drugs, at a rate similar to rates in society as a whole, in the range of 8 to 12 percent.
Older adults
The misuse of prescription drugs may be the most common form of drug abuse among the elderly. Elderly persons use prescription medications approximately three times as frequently as the general population and have been found to have the poorest rates of compliance with directions for taking a medication. In addition, data from the Veterans Affairs Hospital System suggest that elderly patients may be prescribed inappropriately high doses of medications such as benzodiazepines and may be prescribed these medications for longer periods than are younger adults. In general, older people should be prescribed lower doses of medications, because the body's ability to metabolize many medications decreases with age.
An association between age-related morbidity and abuse of prescription medications likely exists. For example, elderly persons who take benzodiazepines are at increased risk for falls that cause hip and thigh fractures, as well as for vehicle accidents. Cognitive impairment also is associated with benzodiazepine use, although memory impairment may be reversible when the drug is discontinued. Finally, use of benzodiazepines for longer than 4 months is not recommended for elderly patients because of the possibility of physical dependence.
Source: Office of Applied Studies, Substance Abuse and Mental Health Services Administration.
National Household Survey on Drug Abuse, 1999.
Adolescents and young adults
Data from the National Household Survey on Drug Abuse indicate that the most dramatic increase in new users of prescription drugs for nonmedical purposes occurs in 12- to 17-year-olds and 18- to 25-year-olds. In addition, 12- to 14-year-olds reported psychotherapeutics (for example, painkillers or stimulants) as one of two primary drugs used. The 1999 Monitoring the Future survey showed that for barbiturates, tranquilizers, and narcotics other than heroin, the general, long-term declines in use among young adults in the 1980s leveled off in the early 1990s, with modest increases again in the mid- to late 1990s. For example, the use of methylphenidate (Ritalin) among high school seniors increased from an annual prevalence (use of the drug within the preceding year) of 0.1 percent in 1992 to an annual prevalence of 2.8 percent in 1997 before reaching a plateau.
It also appears that college students' nonmedical use of pain relievers such as oxycodone with aspirin (Percodan) and hydrocodone (Vicodin) is on the rise. The 1999 Drug Abuse Warning Network, which collects data on drug-related episodes in hospital emergency departments, reported that mentions of hydrocodone as a cause for visiting an emergency room increased by 37 percent among all age groups from 1997 to 1999. Mentions of the benzodiazepine clonazepam (Klonopin) increased by 102 percent since 1992.
Gender differences
Studies suggest that women are more likely than men to be prescribed an abusable prescription drug, particularly narcotics and anti-anxiety drugs - in some cases 48 percent more likely.
Overall, men and women have roughly similar rates of nonmedical use of prescription drugs. An exception is found among 12- to 17-year-olds: In this age group, young women are more likely than young men to use psychotherapeutic drugs nonmedically.
In addition, research has shown that women and men who use prescription opioids are equally likely to become addicted. However, among women and men who use either a sedative, anti-anxiety drug, or hypnotic, women are almost two times more likely to become addicted.
Assessing Prescription Drug Abuse:
Four Simple Questions for You and Your Physician
Have you ever felt the need to Cut down on your use of prescription drugs?
Have you ever felt Annoyed by remarks your friends or loved ones made about your use of prescription drugs?
Have you ever felt Guilty or remorseful about your use of prescription drugs?
Have you Ever used prescription drugs as a way to "get going" or to "calm down?"
Adapted from Ewing, J.A. "Detecting Alcoholism: The CAGE Questionnaire." Journal of the American Medical Association 252(14):1905-1907, 1984.
Preventing and detecting prescription drug abuse
Although most patients use medications as directed, abuse of and addiction to prescription drugs are public health problems for many Americans. However, addiction rarely occurs among those who use pain relievers, CNS depressants, or stimulants as prescribed; the risk for addiction exists when these medications are used in ways other than as prescribed. Health care providers such as primary care physicians, nurse practitioners, and pharmacists as well as patients can all play a role in preventing and detecting prescription drug abuse.
Role of health care providers
About 70 percent of Americans - approximately 191 million people - visit a health care provider, such as a primary care physician, at least once every 2 years. Thus, health care providers are in a unique position not only to prescribe needed medications appropriately, but also to identify prescription drug abuse when it exists and help the patient recognize the problem, set goals for recovery, and seek appropriate treatment when necessary. Screening for any type of substance abuse can be incorporated into routine history taking with questions about what prescriptions and over-the-counter medicines the patient is taking and why. Screening also can be performed if a patient presents with specific symptoms associated with problem use of a substance.
Over time, providers should note any rapid increases in the amount of a medication needed - which may indicate the development of tolerance - or frequent requests for refills before the quantity prescribed should have been used. They should also be alert to the fact that those addicted to prescription medications may engage in "doctor shopping," moving from provider to provider in an effort to get multiple prescriptions for the drug they abuse.
Preventing or stopping prescription drug abuse is an important part of patient care. However, health care providers should not avoid prescribing or administering strong CNS depressants and painkillers, if they are needed. (See box on pain and opiophobia.)
Role of pharmacists
Pharmacists can play a key role in preventing prescription drug misuse and abuse by providing clear information and advice about how to take a medication appropriately, about the effects the medication may have, and about any possible drug interactions. Pharmacists can help prevent prescription fraud or diversion by looking for false or altered prescription forms. Many pharmacies have developed "hotlines" to alert other pharmacies in the region when a fraud is detected.
Role of patients
There are several ways that patients can prevent prescription drug abuse. When visiting the doctor, provide a complete medical history and a description of the reason for the visit to ensure that the doctor understands the complaint and can prescribe appropriate medication. If a doctor prescribes a pain medication, stimulant, or CNS depressant, follow the directions for use carefully and learn about the effects that the drug could have, especially during the first few days during which the body is adapting to the medication. Also be aware of potential interactions with other drugs by reading all information provided by the pharmacist. Do not increase or decrease doses or abruptly stop taking a prescription without consulting a health care provider first. For example, if you are taking a pain reliever for chronic pain and the medication no longer seems to be effectively controlling the pain, speak with your physician; do not increase the dose on your own. Finally, never use another person's prescription.
Treating prescription drug addiction
Years of research have shown us that addiction to any drug, illicit or prescribed, is a brain disease that can, like other chronic diseases, be effectively treated. But no single type of treatment is appropriate for all individuals addicted to prescription drugs. Treatment must take into account the type of drug used and the needs of the individual. To be successful, treatment may need to incorporate several components, such as counseling in conjunction with a prescribed medication, and multiple courses of treatment may be needed for the patient to make a full recovery.
The two main categories of drug addiction treatment are behavioral and pharmacological. Behavioral treatments teach people how to function without drugs, how to handle cravings, how to avoid drugs and situations that could lead to drug use, how to prevent relapse, and how to handle relapse should it occur. When delivered effectively, behavioral treatments - such as individual counseling, group or family counseling, contingency management, and cognitive-behavioral therapies - also can help patients improve their personal relationships and ability to function at work and in the community.
Some addictions, such as opioid addiction, can also be treated with medications. These pharmacological treatments counter the effects of the drug on the brain and behavior. Medications also can be used to relieve the symptoms of withdrawal, to treat an overdose, or to help overcome drug cravings. Although a behavioral or pharmacological approach alone may be effective for treating drug addiction, research shows that a combination of both, when available, is most effective.
Treating addiction to prescription opioids
Several options are available for effectively treating addiction to prescription opioids. These options are drawn from experience and research regarding the treatment of heroin addiction. They include medications, such as methadone and LAAM (levo-alpha-acetyl-methadol), and behavioral counseling approaches.
A useful precursor to long-term treatment of opioid addiction is detoxification. Detoxification in itself is not a treatment for opioid addiction. Rather, its primary objective is to relieve withdrawal symptoms while the patient adjusts to being drug free. To be effective, detoxification must precede long-term treatment that either requires complete abstinence or incorporates a medication, such as methadone, into the treatment plan.
Methadone is a synthetic opioid that blocks the effects of heroin and other opioids, eliminates withdrawal symptoms, and relieves drug craving. It has been used successfully for more than 30 years to treat people addicted to opioids. Other medications include LAAM, an alternative to methadone that blocks the effects of opioids for up to 72 hours, and naltrexone, an opioid blocker that is often employed for highly motivated individuals in treatment programs promoting complete abstinence. Buprenorphine, another effective medication, is awaiting Food and Drug Administration (FDA) approval for treatment of opioid addiction. Finally, naloxone, which counteracts the effects of opioids, is used to treat overdoses.
National Center on Addiction and Substance Abuse at Columbia University (CASA). Missed Opportunity: National Survey of Primary Care Physicians and Patients on Substance Abuse, New York: CASA, 2000.
Treating addiction to CNS depressants
Patients addicted to barbiturates and benzodiazepines should not attempt to stop taking them on their own, as withdrawal from these drugs can be problematic, and in the case of certain CNS depressants, potentially life-threatening. Although no extensive body of research regarding the treatment of barbiturate and benzodiazepine addiction exists, patients addicted to these medications should undergo medically supervised detoxification because the dose must be gradually tapered off. Inpatient or outpatient counseling can help the individual during this process. Cognitive-behavioral therapy also has been used successfully to help individuals adapt to the removal from benzodiazepines.
Often the abuse of barbiturates and benzodiazepines occurs in conjunction with the abuse of another substance or drug, such as alcohol or cocaine. In these cases of polydrug abuse, the treatment approach must address the multiple addictions.
Treating addiction to prescription stimulants
Treatment of addiction to prescription stimulants, such as Ritalin, is often based on behavioral therapies proven effective for treating cocaine or methamphetamine addiction. At this time, there are no proven medications for the treatment of stimulant addiction. However, antidepressants may help manage the symptoms of depression that can accompany the early days of abstinence from stimulants.
Depending on the patient's situation, the first steps in treating prescription stimulant addiction may be tapering off the drug's dose and attempting to treat withdrawal symptoms. The detoxification process could then be followed by one of many behavioral therapies. Contingency management, for example, uses a system that enables patients to earn vouchers for drug-free urine tests. The vouchers can be exchanged for items that promote healthy living.
Prescription drugs are rapidly becoming primary drugs of abuse in the United States and throughout the world. There are many commonly held misconceptions of the abuse potential for powerful substances such as OxyContin®, because such substances can be obtained legally, and have legitimate use in the medical profession.
What are some of the commonly abused prescription drugs?
Although many prescription drugs can be abused or misused, there are three classes of prescription drugs that are most commonly abused:
Opioids, which are most often prescribed to treat pain;
CNS depressants, which are used to treat anxiety and sleep disorders;
Stimulants, which are prescribed to treat the sleep disorder narcolepsy, attention-deficit hyperactivity disorder (ADHD), and obesity.
Opioids
What are opioids?
Opioids are commonly prescribed because of their effective analgesic, or pain-relieving, properties. Medications that fall within this class - sometimes referred to as narcotics - include morphine, codeine, and related drugs. Morphine, for example, is often used before or after surgery to alleviate severe pain. Codeine, because it is less efficacious than morphine, is used for milder pain. Other examples of opioids that can be prescribed to alleviate pain include oxycodone (OxyContin®), propoxyphene (Darvon), hydrocodone (Vicodin), and hydromorphone (Dilaudid), as well as meperidine (Demerol), which is used less often because of its side effects. In addition to their pain-relieving properties, some of these drugs - for example, codeine and diphenoxylate (Lomotil) - can be used to relieve coughs and diarrhea.
Source: Office of Applied Studies, Substance Abuse and Mental Health Services Administration.
National Household Survey on Drug Abuse, 1999.
How do opioids affect the brain and body?
Opioids act by attaching to specific proteins called opioid receptors, which are found in the brain, spinal cord, and gastrointestinal tract. When these drugs attach to certain opioid receptors, they can block the transmission of pain messages to the brain. In addition, opioids can produce drowsiness, cause constipation, and, depending upon the amount of drug taken, depress respiration. Opioid drugs also can cause euphoria by affecting the brain regions that mediate what we perceive as pleasure.
What are the possible consequences of opioid use and abuse?
Chronic use of opioids can result in tolerance for the drugs, which means that users must take higher doses to achieve the same initial effects. Long-term use also can lead to physical dependence and addiction - the body adapts to the presence of the drug, and withdrawal symptoms occur if use is reduced or stopped. Symptoms of withdrawal include restlessness, muscle and bone pain, insomnia, diarrhea, vomiting, cold flashes with goose bumps ("cold turkey"), and involuntary leg movements. Finally, taking a large single dose of an opioid could cause severe respiratory depression that can lead to death. Many studies have shown, however, that properly managed medical use of opioid analgesic drugs is safe and rarely causes clinical addiction, defined as compulsive, often uncontrollable use of drugs. Taken exactly as prescribed, opioids can be used to manage pain effectively.
Is it safe to use opioid drugs with other medications?
Opioids are safe to use with other drugs only under a physician's supervision. Typically, they should not be used with other substances that depress the central nervous system, such as alcohol, antihistamines, barbiturates, benzodiazepines, or general anesthetics, as such a combination increases the risk of life-threatening respiratory depression.
CNS depressants
What are CNS depressants?
CNS depressants are substances that can slow normal brain function. Because of this property, some CNS depressants are useful in the treatment of anxiety and sleep disorders. Among the medications that are commonly prescribed for these purposes are the following:
Barbiturates, such as mephobarbital (Mebaral) and pentobarbital sodium (Nembutal), which are used to treat anxiety, tension, and sleep disorders.
Benzodiazepines, such as diazepam (Valium), chlordiazepoxide HCl (Librium), and alprazolam (Xanax), which can be prescribed to treat anxiety, acute stress reactions, and panic attacks; the more sedating benzodiazepines, such as triazolam (Halcion) and estazolam (ProSom) can be prescribed for short-term treatment of sleep disorders.
In higher doses, some CNS depressants can be used as general anesthetics.
How do CNS depressants affect the brain and body?
There are numerous CNS depressants; most act on the brain by affecting the neurotransmitter gamma-aminobutyric acid (GABA). Neurotransmitters are brain chemicals that facilitate communication between brain cells. GABA works by decreasing brain activity. Although the different classes of CNS depressants work in unique ways, ultimately it is through their ability to increase GABA activity that they produce a drowsy or calming effect that is beneficial to those suffering from anxiety or sleep disorders.
What are the possible consequences of CNS depressant use and abuse?
Despite their many beneficial effects, barbiturates and benzodiazepines have the potential for abuse and should be used only as prescribed. During the first few days of taking a prescribed CNS depressant, a person usually feels sleepy and uncoordinated, but as the body becomes accustomed to the effects of the drug, these feelings begin to disappear. If one uses these drugs long term, the body will develop tolerance for the drugs, and larger doses will be needed to achieve the same initial effects. In addition, continued use can lead to physical dependence and - when use is reduced or stopped - withdrawal. Because all CNS depressants work by slowing the brain's activity, when an individual stops taking them, the brain's activity can rebound and race out of control, possibly leading to seizures and other harmful consequences. Although withdrawal from benzodiazepines can be problematic, it is rarely life threatening, whereas withdrawal from prolonged use of other CNS depressants can have life-threatening complications. Therefore, someone who is thinking about discontinuing CNS depressant therapy or who is suffering withdrawal from a CNS depressant should speak with a physician or seek medical treatment.
Is it safe to use CNS depressants with other medications?
CNS depressants should be used with other medications only under a physician's supervision. Typically, they should not be combined with any other medication or substance that causes CNS depression, including prescription pain medicines, some over-the-counter cold and allergy medications, or alcohol. Using CNS depressants with these other substances - particularly alcohol - can slow breathing, or slow both the heart and respiration, and possibly lead to death.
Stimulants
What are stimulants?
As the name suggests, stimulants are a class of drugs that enhance brain activity - they cause an increase in alertness, attention, and energy that is accompanied by elevated blood pressure and increased heart rate and respiration. Stimulants were used historically to treat asthma and other respiratory problems, obesity, neurological disorders, and a variety of other ailments. But as their potential for abuse and addiction became apparent, the medical use of stimulants began to wane.
Now, stimulants are prescribed for the treatment of only a few health conditions, including narcolepsy, attention-deficit hyperactivity disorder, and depression that has not responded to other treatments. Stimulants may be used as appetite suppressants for short-term treatment of obesity, and they also may be used for patients with asthma.
How do stimulants affect the brain and body?
Stimulants, such as dextroamphetamine (Dexedrine) and methylphenidate (Ritalin), have chemical structures that are similar to a family of key brain neurotransmitters called monoamines, which include norepinephrine and dopamine. Stimulants increase the amount of these chemicals in the brain. This, in turn, increases blood pressure and heart rate, constricts blood vessels, increases blood glucose, and opens up the pathways of the respiratory system. In addition, the increase in dopamine is associated with a sense of euphoria that can accompany the use of these drugs.
What are the possible consequences of stimulant use and abuse?
The consequences of stimulant abuse can be dangerous. Although their use may not lead to physical dependence and risk of withdrawal, stimulants can be addictive in that individuals begin to use them compulsively. Taking high doses of some stimulants repeatedly over a short time can lead to feelings of hostility or paranoia. Additionally, taking high doses of a stimulant may result in dangerously high body temperatures and an irregular heartbeat. There is also the potential for cardiovascular failure or lethal seizures.
Is it safe to use stimulants with other medications?
Stimulants should be used with other medications only when the patient is under a physician's supervision. For example, a stimulant may be prescribed to a patient taking an antidepressant. However, health care providers and patients should be mindful that antidepressants enhance the effects of a stimulant. Patients also should be aware that stimulants should not be mixed with over-the-counter cold medicines that contain decongestants, as this combination may cause blood pressure to become dangerously high or lead to irregular heart rhythms.
Trends in prescription drug abuse
Several indicators suggest that prescription drug abuse is on the rise in the United States. According to the 1999 National Household Survey on Drug Abuse, in 1998, an estimated 1.6 million Americans used prescription pain relievers nonmedically for the first time. This represents a significant increase since the 1980s, when there were generally fewer than 500,000 first-time users per year. From 1990 to 1998, the number of new users of pain relievers increased by 181 percent; the number of individuals who initiated tranquilizer use increased by 132 percent; the number of new sedative users increased by 90 percent; and the number of people initiating stimulant use increased by 165 percent. In 1999, an estimated 4 million people - almost 2 percent of the population aged 12 and older - were currently (use in past month) using certain prescription drugs nonmedically: pain relievers (2.6 million users), sedatives and tranquilizers (1.3 million users), and stimulants (0.9 million users).
Although prescription drug abuse affects many Americans, some trends of concern can be seen among older adults, adolescents, and women. In addition, health care professionals - including physicians, nurses, pharmacists, dentists, anesthesiologists, and veterinarians - may be at increased risk of prescription drug abuse because of ease of access, as well as their ability to self-prescribe drugs. In spite of this increased risk, recent surveys and research in the early 1990s indicate that health care providers probably suffer from substance abuse, including alcohol and drugs, at a rate similar to rates in society as a whole, in the range of 8 to 12 percent.
Older adults
The misuse of prescription drugs may be the most common form of drug abuse among the elderly. Elderly persons use prescription medications approximately three times as frequently as the general population and have been found to have the poorest rates of compliance with directions for taking a medication. In addition, data from the Veterans Affairs Hospital System suggest that elderly patients may be prescribed inappropriately high doses of medications such as benzodiazepines and may be prescribed these medications for longer periods than are younger adults. In general, older people should be prescribed lower doses of medications, because the body's ability to metabolize many medications decreases with age.
An association between age-related morbidity and abuse of prescription medications likely exists. For example, elderly persons who take benzodiazepines are at increased risk for falls that cause hip and thigh fractures, as well as for vehicle accidents. Cognitive impairment also is associated with benzodiazepine use, although memory impairment may be reversible when the drug is discontinued. Finally, use of benzodiazepines for longer than 4 months is not recommended for elderly patients because of the possibility of physical dependence.
Source: Office of Applied Studies, Substance Abuse and Mental Health Services Administration.
National Household Survey on Drug Abuse, 1999.
Adolescents and young adults
Data from the National Household Survey on Drug Abuse indicate that the most dramatic increase in new users of prescription drugs for nonmedical purposes occurs in 12- to 17-year-olds and 18- to 25-year-olds. In addition, 12- to 14-year-olds reported psychotherapeutics (for example, painkillers or stimulants) as one of two primary drugs used. The 1999 Monitoring the Future survey showed that for barbiturates, tranquilizers, and narcotics other than heroin, the general, long-term declines in use among young adults in the 1980s leveled off in the early 1990s, with modest increases again in the mid- to late 1990s. For example, the use of methylphenidate (Ritalin) among high school seniors increased from an annual prevalence (use of the drug within the preceding year) of 0.1 percent in 1992 to an annual prevalence of 2.8 percent in 1997 before reaching a plateau.
It also appears that college students' nonmedical use of pain relievers such as oxycodone with aspirin (Percodan) and hydrocodone (Vicodin) is on the rise. The 1999 Drug Abuse Warning Network, which collects data on drug-related episodes in hospital emergency departments, reported that mentions of hydrocodone as a cause for visiting an emergency room increased by 37 percent among all age groups from 1997 to 1999. Mentions of the benzodiazepine clonazepam (Klonopin) increased by 102 percent since 1992.
Gender differences
Studies suggest that women are more likely than men to be prescribed an abusable prescription drug, particularly narcotics and anti-anxiety drugs - in some cases 48 percent more likely.
Overall, men and women have roughly similar rates of nonmedical use of prescription drugs. An exception is found among 12- to 17-year-olds: In this age group, young women are more likely than young men to use psychotherapeutic drugs nonmedically.
In addition, research has shown that women and men who use prescription opioids are equally likely to become addicted. However, among women and men who use either a sedative, anti-anxiety drug, or hypnotic, women are almost two times more likely to become addicted.
Assessing Prescription Drug Abuse:
Four Simple Questions for You and Your Physician
Have you ever felt the need to Cut down on your use of prescription drugs?
Have you ever felt Annoyed by remarks your friends or loved ones made about your use of prescription drugs?
Have you ever felt Guilty or remorseful about your use of prescription drugs?
Have you Ever used prescription drugs as a way to "get going" or to "calm down?"
Adapted from Ewing, J.A. "Detecting Alcoholism: The CAGE Questionnaire." Journal of the American Medical Association 252(14):1905-1907, 1984.
Preventing and detecting prescription drug abuse
Although most patients use medications as directed, abuse of and addiction to prescription drugs are public health problems for many Americans. However, addiction rarely occurs among those who use pain relievers, CNS depressants, or stimulants as prescribed; the risk for addiction exists when these medications are used in ways other than as prescribed. Health care providers such as primary care physicians, nurse practitioners, and pharmacists as well as patients can all play a role in preventing and detecting prescription drug abuse.
Role of health care providers
About 70 percent of Americans - approximately 191 million people - visit a health care provider, such as a primary care physician, at least once every 2 years. Thus, health care providers are in a unique position not only to prescribe needed medications appropriately, but also to identify prescription drug abuse when it exists and help the patient recognize the problem, set goals for recovery, and seek appropriate treatment when necessary. Screening for any type of substance abuse can be incorporated into routine history taking with questions about what prescriptions and over-the-counter medicines the patient is taking and why. Screening also can be performed if a patient presents with specific symptoms associated with problem use of a substance.
Over time, providers should note any rapid increases in the amount of a medication needed - which may indicate the development of tolerance - or frequent requests for refills before the quantity prescribed should have been used. They should also be alert to the fact that those addicted to prescription medications may engage in "doctor shopping," moving from provider to provider in an effort to get multiple prescriptions for the drug they abuse.
Preventing or stopping prescription drug abuse is an important part of patient care. However, health care providers should not avoid prescribing or administering strong CNS depressants and painkillers, if they are needed. (See box on pain and opiophobia.)
Role of pharmacists
Pharmacists can play a key role in preventing prescription drug misuse and abuse by providing clear information and advice about how to take a medication appropriately, about the effects the medication may have, and about any possible drug interactions. Pharmacists can help prevent prescription fraud or diversion by looking for false or altered prescription forms. Many pharmacies have developed "hotlines" to alert other pharmacies in the region when a fraud is detected.
Role of patients
There are several ways that patients can prevent prescription drug abuse. When visiting the doctor, provide a complete medical history and a description of the reason for the visit to ensure that the doctor understands the complaint and can prescribe appropriate medication. If a doctor prescribes a pain medication, stimulant, or CNS depressant, follow the directions for use carefully and learn about the effects that the drug could have, especially during the first few days during which the body is adapting to the medication. Also be aware of potential interactions with other drugs by reading all information provided by the pharmacist. Do not increase or decrease doses or abruptly stop taking a prescription without consulting a health care provider first. For example, if you are taking a pain reliever for chronic pain and the medication no longer seems to be effectively controlling the pain, speak with your physician; do not increase the dose on your own. Finally, never use another person's prescription.
Treating prescription drug addiction
Years of research have shown us that addiction to any drug, illicit or prescribed, is a brain disease that can, like other chronic diseases, be effectively treated. But no single type of treatment is appropriate for all individuals addicted to prescription drugs. Treatment must take into account the type of drug used and the needs of the individual. To be successful, treatment may need to incorporate several components, such as counseling in conjunction with a prescribed medication, and multiple courses of treatment may be needed for the patient to make a full recovery.
The two main categories of drug addiction treatment are behavioral and pharmacological. Behavioral treatments teach people how to function without drugs, how to handle cravings, how to avoid drugs and situations that could lead to drug use, how to prevent relapse, and how to handle relapse should it occur. When delivered effectively, behavioral treatments - such as individual counseling, group or family counseling, contingency management, and cognitive-behavioral therapies - also can help patients improve their personal relationships and ability to function at work and in the community.
Some addictions, such as opioid addiction, can also be treated with medications. These pharmacological treatments counter the effects of the drug on the brain and behavior. Medications also can be used to relieve the symptoms of withdrawal, to treat an overdose, or to help overcome drug cravings. Although a behavioral or pharmacological approach alone may be effective for treating drug addiction, research shows that a combination of both, when available, is most effective.
Treating addiction to prescription opioids
Several options are available for effectively treating addiction to prescription opioids. These options are drawn from experience and research regarding the treatment of heroin addiction. They include medications, such as methadone and LAAM (levo-alpha-acetyl-methadol), and behavioral counseling approaches.
A useful precursor to long-term treatment of opioid addiction is detoxification. Detoxification in itself is not a treatment for opioid addiction. Rather, its primary objective is to relieve withdrawal symptoms while the patient adjusts to being drug free. To be effective, detoxification must precede long-term treatment that either requires complete abstinence or incorporates a medication, such as methadone, into the treatment plan.
Methadone is a synthetic opioid that blocks the effects of heroin and other opioids, eliminates withdrawal symptoms, and relieves drug craving. It has been used successfully for more than 30 years to treat people addicted to opioids. Other medications include LAAM, an alternative to methadone that blocks the effects of opioids for up to 72 hours, and naltrexone, an opioid blocker that is often employed for highly motivated individuals in treatment programs promoting complete abstinence. Buprenorphine, another effective medication, is awaiting Food and Drug Administration (FDA) approval for treatment of opioid addiction. Finally, naloxone, which counteracts the effects of opioids, is used to treat overdoses.
National Center on Addiction and Substance Abuse at Columbia University (CASA). Missed Opportunity: National Survey of Primary Care Physicians and Patients on Substance Abuse, New York: CASA, 2000.
Treating addiction to CNS depressants
Patients addicted to barbiturates and benzodiazepines should not attempt to stop taking them on their own, as withdrawal from these drugs can be problematic, and in the case of certain CNS depressants, potentially life-threatening. Although no extensive body of research regarding the treatment of barbiturate and benzodiazepine addiction exists, patients addicted to these medications should undergo medically supervised detoxification because the dose must be gradually tapered off. Inpatient or outpatient counseling can help the individual during this process. Cognitive-behavioral therapy also has been used successfully to help individuals adapt to the removal from benzodiazepines.
Often the abuse of barbiturates and benzodiazepines occurs in conjunction with the abuse of another substance or drug, such as alcohol or cocaine. In these cases of polydrug abuse, the treatment approach must address the multiple addictions.
Treating addiction to prescription stimulants
Treatment of addiction to prescription stimulants, such as Ritalin, is often based on behavioral therapies proven effective for treating cocaine or methamphetamine addiction. At this time, there are no proven medications for the treatment of stimulant addiction. However, antidepressants may help manage the symptoms of depression that can accompany the early days of abstinence from stimulants.
Depending on the patient's situation, the first steps in treating prescription stimulant addiction may be tapering off the drug's dose and attempting to treat withdrawal symptoms. The detoxification process could then be followed by one of many behavioral therapies. Contingency management, for example, uses a system that enables patients to earn vouchers for drug-free urine tests. The vouchers can be exchanged for items that promote healthy living.
Marijuana Addiction
Marijuana - often called "pot," "grass," "reefer," "weed," "herb," "mary jane," or "mj" - is a greenish-gray mixture of the dried, shredded buds, leaves, stems, seeds, and flowers of Cannabis sativa, the hemp plant. Most users smoke marijuana in hand-rolled cigarettes called joints, among other names; some use pipes or water pipes called bongs. Marijuana cigars called blunts have also become popular. To make blunts, users slice open cigars and replace the tobacco with marijuana, often combined with another drug, such as crack cocaine. Marijuana also is used to brew tea and is sometimes mixed into foods.
What is marijuana?
The major active chemical in marijuana is delta-9-tetrahydrocannabinol (THC), which causes the mind-altering effects of marijuana intoxication. The amount of THC (which is also the psychoactive ingredient in hashish) determines the potency and, therefore, the effects of marijuana. Between 1980 and 1997, the amount of THC in marijuana available in the United States rose dramatically.
What is the scope of marijuana use in the United States?
Marijuana is the Nation's most commonly used illicit drug. More than 83 million Americans (37 percent) age 12 and older have tried marijuana at least once, according to the 2001 National Household Survey on Drug Abuse (NHSDA).
Marijuana use is widespread among adolescents and young adults. The percentage of middle-school students who reported using marijuana increased throughout the early 1990s. In the past few years, according to the 2001 Monitoring the Future Study, an annual survey of drug use among the Nation's middle- and high-school students, illicit drug use by 8th-, 10th-, and 12th-graders has leveled off.> Still, in 2001, 20 percent of 8th-graders reported that they had tried marijuana, and 9 percent were current users (defined as having used the drug in the 30 days preceding the survey). Among 10th-graders, 40 percent had tried marijuana sometime in their lives, and almost 20 percent were current users. As would be expected, rates of use among 12th-graders were higher still: Nearly half had tried marijuana at some time, and 22 percent were current users.
The Drug Abuse Warning Network (DAWN), a system for monitoring the health impact of drugs, estimated that, in 2001, marijuana was a contributing factor in more than 110,000 emergency department (ED) visits in the United States, with about 15 percent of the patients between the ages of 12 and 17, and almost two-thirds male.
In 1999, the National Institute of Justice's Arrestee Drug Abuse Monitoring Program (ADAM), which collects data from 34 sites on the number of adult arrestees testing positive for various drugs, found that, on average, 39 percent of adult male arrestees and 26 percent of adult female arrestees tested positive for marijuana.ADAM collected data on juvenile arrestees in nine sites and found that marijuana was the most commonly used drug among these youths. On average, 53 percent of juvenile male and 38 percent of juvenile female arrestees tested positive for marijuana.
NIDA's Community Epidemiology Work Group (CEWG), a network of researchers that tracks trends in the nature and patterns of drug use in major U.S. cities, consistently reports that marijuana frequently is combined with other drugs, such as crack cocaine, PCP, formaldehyde, and codeine cough syrup, sometimes without the user being aware of it. Thus, the risks associated with marijuana use may be compounded by the risks of added drugs, as well.
How does marijuana affect the brain?
Scientists have learned a great deal about how THC acts in the brain to produce its many effects. When someone smokes marijuana, THC rapidly passes from the lungs into the bloodstream, which carries the chemical to organs throughout the body, including the brain. In the brain, THC connects to specific sites called cannabinoid receptors on nerve cells and thereby influences the activity of those cells. Some brain areas have many cannabinoid receptors; others have few or none. Many cannabinoid receptors are found in the parts of the brain that influence pleasure, memory, thought, concentration, sensory and time perception, and coordinated movement.
What are the acute effects of marijuana use?
Marijuana's effects begin immediately after the drug enters the brain and last from 1 to 3 hours. If marijuana is consumed in food or drink, the short-term effects begin more slowly, usually in 1/2 to 1 hour, and last longer, for as long as 4 hours. Smoking marijuana deposits several times more THC into the blood than does eating or drinking the drug.
Within a few minutes after inhaling marijuana smoke, an individual's heart begins beating more rapidly, the bronchial passages relax and become enlarged, and blood vessels in the eyes expand, making the eyes look red. The heart rate, normally 70 to 80 beats per minute, may increase by 20 to 50 beats per minute or, in some cases, even double. This effect can be greater if other drugs are taken with marijuana.
As THC enters the brain, it causes a user to feel euphoric - or "high" - by acting in the brain's reward system, areas of the brain that respond to stimuli such as food and drink as well as most drugs of abuse. THC activates the reward system in the same way that nearly all drugs of abuse do, by stimulating brain cells to release the chemical dopamine.
A marijuana user may experience pleasant sensations, colors and sounds may seem more intense, and time appears to pass very slowly. The user's mouth feels dry, and he or she may suddenly become very hungry and thirsty. His or her hands may tremble and grow cold. The euphoria passes after awhile, and then the user may feel sleepy or depressed. Occasionally, marijuana use produces anxiety, fear, distrust, or panic.
Marijuana use impairs a person's ability to form memories, recall events (see Marijuana, Memory, and the Hippocampus), and shift attention from one thing to another. THC also disrupts coordination and balance by binding to receptors in the cerebellum and basal ganglia, parts of the brain that regulate balance, posture, coordination of movement, and reaction time. Through its effects on the brain and body, marijuana intoxication can cause accidents. Studies show that approximately 6 to 11 percent of fatal accident victims test positive for THC. In many of these cases, alcohol is detected as well.
In a study conducted by the National Highway Traffic Safety Administration, a moderate dose of marijuana alone was shown to impair driving performance; however, the effects of even a low dose of marijuana combined with alcohol were markedly greater than for either drug alone. Driving indices measured included reaction time, visual search frequency (driver checking side streets), and the ability to perceive and/or respond to changes in the relative velocity of other vehicles.
Marijuana users who have taken high doses of the drug may experience acute toxic psychosis, which includes hallucinations, delusions, and depersonalization - a loss of the sense of personal identity, or self-recognition. Although the specific causes of these symptoms remain unknown, they appear to occur more frequently when a high dose of cannabis is consumed in food or drink rather than smoked.
Marijuana's Effects on the Brain
When marijuana is smoked, its active ingredient THC travels throughout the body, including the brain, to produce its many effects. THC attaches to sites called cannabinoid receptors on nerve cells in the brain, affecting the way those cells work. Cannabinoid receptors are abundant in parts of the brain that regulate movement, coordination, learning and memory, higher cognitive functions such as judgment, and pleasure.
Brain Region Functions by Region
Brain regions in which cannabinoid receptors are abundant:
Cerebellum Body movement coordination
Hippocampus Learning and memory
Cerebral cortex, especially cingulate, frontal, and parietal regions Higher cognitive functions
Nucleus accumbens Reward
Basal ganglia
Substantia nigra pars reticulata
Entopeduncular nucleus
Globus pallidus
Putamen
Movement control
Brain regions in which cannabinoid receptors are moderately concentrated:
Hypothalamus Body housekeeping functions (body temperature regulation, salt and water balance, reproductive function)
Amygdala Emotional response, fear
Spinal cord Peripheral sensation, including pain
Brain stem Sleep and arousal, temperature regulation, motor control
Central gray Analgesia
Nucleus of the solitary tract Visceral sensation, nausea and vomiting
How does marijuana use affect physical health?
Marijuana use has been shown to increase users' difficulty in trying to quit smoking tobacco. This was recently reported in a study comparing smoking cessation in adults who smoked both marijuana and tobacco with those who smoked only tobacco. The relationship between marijuana use and continued smoking was particularly strong in those who smoked marijuana daily at the time of the initial interview, 13 years prior to the followup interview.
A study of 450 individuals found that people who smoke marijuana frequently but do not smoke tobacco have more health problems and miss more days of work than nonsmokers do. Many of the extra sick days used by the marijuana smokers in the study were for respiratory illnesses.
Even infrequent marijuana use can cause burning and stinging of the mouth and throat, often accompanied by a heavy cough. Someone who smokes marijuana regularly may have many of the same respiratory problems that tobacco smokers do, such as daily cough and phlegm production, more frequent acute chest illnesses, a heightened risk of lung infections, and a greater tendency toward obstructed airways.
Cancer of the respiratory tract and lungs may also be promoted by marijuana smoke. A study comparing 173 cancer patients and 176 healthy individuals produced strong evidence that smoking marijuana increases the likelihood of developing cancer of the head or neck, and that the more marijuana smoked, the greater the increase. A statistical analysis of the data suggested that marijuana smoking doubled or tripled the risk of these cancers.
Marijuana has the potential to promote cancer of the lungs and other parts of the respiratory tract because it contains irritants and carcinogens. In fact, marijuana smoke contains 50 percent to 70 percent more carcinogenic hydrocarbons than does tobacco smoke. It also produces high levels of an enzyme that converts certain hydrocarbons into their carcinogenic form, levels that may accelerate the changes that ultimately produce malignant cells. Marijuana users usually inhale more deeply and hold their breath longer than tobacco smokers do, which increases the lungs' exposure to carcinogenic smoke. These facts suggest that, puff for puff, smoking marijuana may increase the risk of cancer more than smoking tobacco does.
Some adverse health effects caused by marijuana may occur because THC impairs the immune system's ability to fight off infectious diseases and cancer. In laboratory experiments that exposed animal and human cells to THC or other marijuana ingredients, the normal disease-preventing reactions of many of the key types of immune cells were inhibited. In other studies, mice exposed to THC or related substances were more likely than unexposed mice to develop bacterial infections and tumors.
One study has indicated that a person's risk of heart attack during the first hour after smoking marijuana is four times his or her usual risk. The researchers suggest that a heart attack might occur, in part, because marijuana raises blood pressure and heart rate and reduces the oxygen-carrying capacity of blood.
Marijuana, Memory, and the Hippocampus
Marijuana's damage to short-term memory seems to occur because THC alters the way in which information is processed by the hippocampus, a brain area responsible for memory formation. Laboratory rats treated with THC displayed the same reduced ability to perform tasks requiring short-term memory as other rats showed after nerve cells in their hippocampus were destroyed. In addition, the THC-treated rats had the greatest difficulty with the tasks precisely during the time when the drug was interfering most with the normal functioning of cells in the hippocampus.
As people age, they normally lose neurons in the hippocampus, which decreases their ability to remember events. Chronic THC exposure may hasten the age-related loss of hippocampal neurons. In one series of studies, rats exposed to THC every day for 8 months (approximately 30 percent of their lifespan), when examined at 11 to 12 months of age, showed nerve cell loss equivalent to that of unexposed animals twice their age.
The Body's Natural THC-Like Chemicals
THC owes many of its effects to its similarity to a family of chemicals called the endogenous cannabinoids, which are natural Cannabis-like chemicals. Because a THC molecule is shaped like these endogenous cannabinoids, it interacts with the same receptors on nerve cells, the cannabinoid receptors, that endogenous cannabinoids do, and it influences many of the same processes. Research has shown that the endogenous cannabinoids help control a wide array of mental and physical processes in the brain and throughout the body, including memory and perception, fine motor coordination, pain sensations, immunity to disease, and reproduction.
When someone smokes marijuana, THC overstimulates the cannabinoid receptors, leading to a disruption of the endogenous cannabinoids' normal control. This overstimulation produces the intoxication experienced by marijuana smokers. Over time, it may degrade some cannabinoid receptors, possibly producing permanent adverse effects and contributing to addiction and risk for a withdrawal syndrome.
The Science of Medical Marijuana
THC, the main active ingredient in marijuana, produces effects that potentially can be useful for treating a variety of medical conditions. It is the main ingredient in an oral medication that is currently used to treat nausea in cancer chemotherapy patients and to stimulate appetite in patients with wasting due to AIDS. Scientists are continuing to investigate other potential medical uses for cannabinoids. Research is underway to examine the effects of smoked marijuana and extracts of marijuana on appetite stimulation, certain types of pain, and spasticity due to multiple sclerosis.
Some clinical trials of smoked marijuana for therapy are underway, but the inconsistency of THC dosage in different marijuana samples poses a major hindrance to valid trials and to the safe and effective use of the drug. Moreover, the adverse effects of marijuana smoke on the respiratory system will offset the helpfulness of smoked marijuana for some patients. Finally, little is known about the many chemicals besides THC that are in marijuana, or their possible deleterious impact on patients with medical conditions.
How does marijuana use affect school, work, and social life?
Students who smoke marijuana get lower grades and are less likely to graduate from high school, compared with their nonsmoking peers. In one study, researchers compared marijuana smoking and nonsmoking 12th-graders' scores on standardized tests of verbal and mathematical skills. Although all of the students had scored equally well in 4th grade, the smokers' scores were significantly lower in 12th grade than the nonsmokers' scores were.
Workers who smoke marijuana are more likely than their co-workers to have problems on the job. Several studies have associated workers' marijuana smoking with increased absences, tardiness, accidents, workers' compensation claims, and job turnover. A study among municipal workers found that employees who smoked marijuana on or off the job reported more"withdrawal behaviors" - such as leaving work without permission, daydreaming, spending work time on personal matters, and shirking tasks - that adversely affect productivity and morale.
Depression, anxiety, and personality disturbances are all associated with marijuana use. Research clearly demonstrates that marijuana use has the potential to cause problems in daily life or make a person's existing problems worse. Because marijuana compromises the ability to learn and remember information, the more a person uses marijuana the more he or she is likely to fall behind in accumulating intellectual, job, or social skills. Moreover, research has shown that marijuana's adverse impact on memory and learning can last for days or weeks after the acute effects of the drug wear off.
For example, a study of 129 college students found that among heavy users of marijuana, those who smoked the drug at least 27 of the preceding 30 days, critical skills related to attention, memory, and learning were significantly impaired, even after they had not used the drug for at least 24 hours. The heavy marijuana users in the study had more trouble sustaining and shifting their attention and in registering, organizing, and using information than did the study participants who had used marijuana no more than 3 of the previous 30 days. As a result, someone who smokes marijuana once daily may be functioning at a reduced intellectual level all of the time. More recently, the same researchers showed that a group of long-term heavy marijuana users' ability to recall words from a list was impaired 1 week following cessation of marijuana use, but returned to normal by 4 weeks. An implication of this finding is that even after long-term heavy marijuana use, if an individual quits marijuana use, some cognitive abilities may be recovered.
Another study produced additional evidence that marijuana's effects on the brain can cause cumulative deterioration of critical life skills in the long run. Researchers gave students a battery of tests measuring problem-solving and emotional skills in 8th grade and again in 12th grade. The results showed that the students who were already drinking alcohol plus smoking marijuana in 8th grade started off slightly behind their peers but that the distance separating these two groups grew significantly by their senior year in high school. The analysis linked marijuana use, independently of alcohol use, to reduced capacity for self-reinforcement, a group of psychological skills that enable individuals to maintain confidence and persevere in the pursuit of goals.
Can marijuana use during pregnancy harm the baby?
Research has shown that babies born to women who used marijuana during their pregnancies display altered responses to visual stimuli, increased tremulousness, and a high-pitched cry, which may indicate problems with neurological development.< During infancy and preschool years, marijuana-exposed children have been observed to have more behavioral problems and to perform tasks of visual perception, language comprehension, sustained attention, and memory more poorly than nonexposed children do. In school, these children are more likely to exhibit deficits in decision-making skills, memory, and the ability to remain attentive.
Is marijuana use addictive?
Long-term marijuana use can lead to addiction for some people; that is, they use the drug compulsively even though it often interferes with family, school, work, and recreational activities. According to the 2001 National Household Survey on Drug Abuse, an estimated 5.6 million Americans age 12 or older reported problems with illicit drug use in the past year. Of these, 3.6 million met diagnostic criteria for dependence on an illicit drug. More than 2 million met diagnostic criteria for dependence on marijuana/hashish. In 1999, more than 220,000 people entering drug abuse treatment programs reported that marijuana was their primary drug of abuse.
Along with craving, withdrawal symptoms can make it hard for long-term marijuana smokers to stop using the drug. People trying to quit report irritability, difficulty sleeping, and anxiety. They also display increased aggression on psychological tests, peaking approximately 1 week after they last used the drug.
What treatments are available for marijuana abusers?
Treatment programs directed at marijuana abuse are rare, partly because many who use marijuana do so in combination with other drugs, such as cocaine and alcohol. However, with more people seeking help to control marijuana abuse, research has focused on ways to overcome problems with abuse of this drug.
One study of adult marijuana users found comparable benefits from a 14-session cognitive-behavioral group treatment and a 2-session individual treatment that included motivational interviewing and advice on ways to reduce marijuana use. Participants were mostly men in their early thirties who had smoked marijuana daily for over 10 years. By increasing patients' awareness of what triggers their marijuana use, both treatments sought to help them devise avoidance strategies. Use, dependence symptoms, and psychosocial problems decreased for at least 1 year after both treatments. About 30 percent of users were abstinent during the last 3-month followup period. Another study suggests that giving patients vouchers for abstaining from marijuana can improve outcomes. Vouchers can be redeemed for such goods as movie passes, sports equipment, or vocational training.
No medications are now available to treat marijuana abuse. However, recent discoveries about the workings of THC receptors have raised the possibility that scientists may eventually develop a medication that will block THC's intoxicating effects. Such a medication might be used to prevent relapse to marijuana abuse by reducing or eliminating its appeal.
What is marijuana?
The major active chemical in marijuana is delta-9-tetrahydrocannabinol (THC), which causes the mind-altering effects of marijuana intoxication. The amount of THC (which is also the psychoactive ingredient in hashish) determines the potency and, therefore, the effects of marijuana. Between 1980 and 1997, the amount of THC in marijuana available in the United States rose dramatically.
What is the scope of marijuana use in the United States?
Marijuana is the Nation's most commonly used illicit drug. More than 83 million Americans (37 percent) age 12 and older have tried marijuana at least once, according to the 2001 National Household Survey on Drug Abuse (NHSDA).
Marijuana use is widespread among adolescents and young adults. The percentage of middle-school students who reported using marijuana increased throughout the early 1990s. In the past few years, according to the 2001 Monitoring the Future Study, an annual survey of drug use among the Nation's middle- and high-school students, illicit drug use by 8th-, 10th-, and 12th-graders has leveled off.> Still, in 2001, 20 percent of 8th-graders reported that they had tried marijuana, and 9 percent were current users (defined as having used the drug in the 30 days preceding the survey). Among 10th-graders, 40 percent had tried marijuana sometime in their lives, and almost 20 percent were current users. As would be expected, rates of use among 12th-graders were higher still: Nearly half had tried marijuana at some time, and 22 percent were current users.
The Drug Abuse Warning Network (DAWN), a system for monitoring the health impact of drugs, estimated that, in 2001, marijuana was a contributing factor in more than 110,000 emergency department (ED) visits in the United States, with about 15 percent of the patients between the ages of 12 and 17, and almost two-thirds male.
In 1999, the National Institute of Justice's Arrestee Drug Abuse Monitoring Program (ADAM), which collects data from 34 sites on the number of adult arrestees testing positive for various drugs, found that, on average, 39 percent of adult male arrestees and 26 percent of adult female arrestees tested positive for marijuana.ADAM collected data on juvenile arrestees in nine sites and found that marijuana was the most commonly used drug among these youths. On average, 53 percent of juvenile male and 38 percent of juvenile female arrestees tested positive for marijuana.
NIDA's Community Epidemiology Work Group (CEWG), a network of researchers that tracks trends in the nature and patterns of drug use in major U.S. cities, consistently reports that marijuana frequently is combined with other drugs, such as crack cocaine, PCP, formaldehyde, and codeine cough syrup, sometimes without the user being aware of it. Thus, the risks associated with marijuana use may be compounded by the risks of added drugs, as well.
How does marijuana affect the brain?
Scientists have learned a great deal about how THC acts in the brain to produce its many effects. When someone smokes marijuana, THC rapidly passes from the lungs into the bloodstream, which carries the chemical to organs throughout the body, including the brain. In the brain, THC connects to specific sites called cannabinoid receptors on nerve cells and thereby influences the activity of those cells. Some brain areas have many cannabinoid receptors; others have few or none. Many cannabinoid receptors are found in the parts of the brain that influence pleasure, memory, thought, concentration, sensory and time perception, and coordinated movement.
What are the acute effects of marijuana use?
Marijuana's effects begin immediately after the drug enters the brain and last from 1 to 3 hours. If marijuana is consumed in food or drink, the short-term effects begin more slowly, usually in 1/2 to 1 hour, and last longer, for as long as 4 hours. Smoking marijuana deposits several times more THC into the blood than does eating or drinking the drug.
Within a few minutes after inhaling marijuana smoke, an individual's heart begins beating more rapidly, the bronchial passages relax and become enlarged, and blood vessels in the eyes expand, making the eyes look red. The heart rate, normally 70 to 80 beats per minute, may increase by 20 to 50 beats per minute or, in some cases, even double. This effect can be greater if other drugs are taken with marijuana.
As THC enters the brain, it causes a user to feel euphoric - or "high" - by acting in the brain's reward system, areas of the brain that respond to stimuli such as food and drink as well as most drugs of abuse. THC activates the reward system in the same way that nearly all drugs of abuse do, by stimulating brain cells to release the chemical dopamine.
A marijuana user may experience pleasant sensations, colors and sounds may seem more intense, and time appears to pass very slowly. The user's mouth feels dry, and he or she may suddenly become very hungry and thirsty. His or her hands may tremble and grow cold. The euphoria passes after awhile, and then the user may feel sleepy or depressed. Occasionally, marijuana use produces anxiety, fear, distrust, or panic.
Marijuana use impairs a person's ability to form memories, recall events (see Marijuana, Memory, and the Hippocampus), and shift attention from one thing to another. THC also disrupts coordination and balance by binding to receptors in the cerebellum and basal ganglia, parts of the brain that regulate balance, posture, coordination of movement, and reaction time. Through its effects on the brain and body, marijuana intoxication can cause accidents. Studies show that approximately 6 to 11 percent of fatal accident victims test positive for THC. In many of these cases, alcohol is detected as well.
In a study conducted by the National Highway Traffic Safety Administration, a moderate dose of marijuana alone was shown to impair driving performance; however, the effects of even a low dose of marijuana combined with alcohol were markedly greater than for either drug alone. Driving indices measured included reaction time, visual search frequency (driver checking side streets), and the ability to perceive and/or respond to changes in the relative velocity of other vehicles.
Marijuana users who have taken high doses of the drug may experience acute toxic psychosis, which includes hallucinations, delusions, and depersonalization - a loss of the sense of personal identity, or self-recognition. Although the specific causes of these symptoms remain unknown, they appear to occur more frequently when a high dose of cannabis is consumed in food or drink rather than smoked.
Marijuana's Effects on the Brain
When marijuana is smoked, its active ingredient THC travels throughout the body, including the brain, to produce its many effects. THC attaches to sites called cannabinoid receptors on nerve cells in the brain, affecting the way those cells work. Cannabinoid receptors are abundant in parts of the brain that regulate movement, coordination, learning and memory, higher cognitive functions such as judgment, and pleasure.
Brain Region Functions by Region
Brain regions in which cannabinoid receptors are abundant:
Cerebellum Body movement coordination
Hippocampus Learning and memory
Cerebral cortex, especially cingulate, frontal, and parietal regions Higher cognitive functions
Nucleus accumbens Reward
Basal ganglia
Substantia nigra pars reticulata
Entopeduncular nucleus
Globus pallidus
Putamen
Movement control
Brain regions in which cannabinoid receptors are moderately concentrated:
Hypothalamus Body housekeeping functions (body temperature regulation, salt and water balance, reproductive function)
Amygdala Emotional response, fear
Spinal cord Peripheral sensation, including pain
Brain stem Sleep and arousal, temperature regulation, motor control
Central gray Analgesia
Nucleus of the solitary tract Visceral sensation, nausea and vomiting
How does marijuana use affect physical health?
Marijuana use has been shown to increase users' difficulty in trying to quit smoking tobacco. This was recently reported in a study comparing smoking cessation in adults who smoked both marijuana and tobacco with those who smoked only tobacco. The relationship between marijuana use and continued smoking was particularly strong in those who smoked marijuana daily at the time of the initial interview, 13 years prior to the followup interview.
A study of 450 individuals found that people who smoke marijuana frequently but do not smoke tobacco have more health problems and miss more days of work than nonsmokers do. Many of the extra sick days used by the marijuana smokers in the study were for respiratory illnesses.
Even infrequent marijuana use can cause burning and stinging of the mouth and throat, often accompanied by a heavy cough. Someone who smokes marijuana regularly may have many of the same respiratory problems that tobacco smokers do, such as daily cough and phlegm production, more frequent acute chest illnesses, a heightened risk of lung infections, and a greater tendency toward obstructed airways.
Cancer of the respiratory tract and lungs may also be promoted by marijuana smoke. A study comparing 173 cancer patients and 176 healthy individuals produced strong evidence that smoking marijuana increases the likelihood of developing cancer of the head or neck, and that the more marijuana smoked, the greater the increase. A statistical analysis of the data suggested that marijuana smoking doubled or tripled the risk of these cancers.
Marijuana has the potential to promote cancer of the lungs and other parts of the respiratory tract because it contains irritants and carcinogens. In fact, marijuana smoke contains 50 percent to 70 percent more carcinogenic hydrocarbons than does tobacco smoke. It also produces high levels of an enzyme that converts certain hydrocarbons into their carcinogenic form, levels that may accelerate the changes that ultimately produce malignant cells. Marijuana users usually inhale more deeply and hold their breath longer than tobacco smokers do, which increases the lungs' exposure to carcinogenic smoke. These facts suggest that, puff for puff, smoking marijuana may increase the risk of cancer more than smoking tobacco does.
Some adverse health effects caused by marijuana may occur because THC impairs the immune system's ability to fight off infectious diseases and cancer. In laboratory experiments that exposed animal and human cells to THC or other marijuana ingredients, the normal disease-preventing reactions of many of the key types of immune cells were inhibited. In other studies, mice exposed to THC or related substances were more likely than unexposed mice to develop bacterial infections and tumors.
One study has indicated that a person's risk of heart attack during the first hour after smoking marijuana is four times his or her usual risk. The researchers suggest that a heart attack might occur, in part, because marijuana raises blood pressure and heart rate and reduces the oxygen-carrying capacity of blood.
Marijuana, Memory, and the Hippocampus
Marijuana's damage to short-term memory seems to occur because THC alters the way in which information is processed by the hippocampus, a brain area responsible for memory formation. Laboratory rats treated with THC displayed the same reduced ability to perform tasks requiring short-term memory as other rats showed after nerve cells in their hippocampus were destroyed. In addition, the THC-treated rats had the greatest difficulty with the tasks precisely during the time when the drug was interfering most with the normal functioning of cells in the hippocampus.
As people age, they normally lose neurons in the hippocampus, which decreases their ability to remember events. Chronic THC exposure may hasten the age-related loss of hippocampal neurons. In one series of studies, rats exposed to THC every day for 8 months (approximately 30 percent of their lifespan), when examined at 11 to 12 months of age, showed nerve cell loss equivalent to that of unexposed animals twice their age.
The Body's Natural THC-Like Chemicals
THC owes many of its effects to its similarity to a family of chemicals called the endogenous cannabinoids, which are natural Cannabis-like chemicals. Because a THC molecule is shaped like these endogenous cannabinoids, it interacts with the same receptors on nerve cells, the cannabinoid receptors, that endogenous cannabinoids do, and it influences many of the same processes. Research has shown that the endogenous cannabinoids help control a wide array of mental and physical processes in the brain and throughout the body, including memory and perception, fine motor coordination, pain sensations, immunity to disease, and reproduction.
When someone smokes marijuana, THC overstimulates the cannabinoid receptors, leading to a disruption of the endogenous cannabinoids' normal control. This overstimulation produces the intoxication experienced by marijuana smokers. Over time, it may degrade some cannabinoid receptors, possibly producing permanent adverse effects and contributing to addiction and risk for a withdrawal syndrome.
The Science of Medical Marijuana
THC, the main active ingredient in marijuana, produces effects that potentially can be useful for treating a variety of medical conditions. It is the main ingredient in an oral medication that is currently used to treat nausea in cancer chemotherapy patients and to stimulate appetite in patients with wasting due to AIDS. Scientists are continuing to investigate other potential medical uses for cannabinoids. Research is underway to examine the effects of smoked marijuana and extracts of marijuana on appetite stimulation, certain types of pain, and spasticity due to multiple sclerosis.
Some clinical trials of smoked marijuana for therapy are underway, but the inconsistency of THC dosage in different marijuana samples poses a major hindrance to valid trials and to the safe and effective use of the drug. Moreover, the adverse effects of marijuana smoke on the respiratory system will offset the helpfulness of smoked marijuana for some patients. Finally, little is known about the many chemicals besides THC that are in marijuana, or their possible deleterious impact on patients with medical conditions.
How does marijuana use affect school, work, and social life?
Students who smoke marijuana get lower grades and are less likely to graduate from high school, compared with their nonsmoking peers. In one study, researchers compared marijuana smoking and nonsmoking 12th-graders' scores on standardized tests of verbal and mathematical skills. Although all of the students had scored equally well in 4th grade, the smokers' scores were significantly lower in 12th grade than the nonsmokers' scores were.
Workers who smoke marijuana are more likely than their co-workers to have problems on the job. Several studies have associated workers' marijuana smoking with increased absences, tardiness, accidents, workers' compensation claims, and job turnover. A study among municipal workers found that employees who smoked marijuana on or off the job reported more"withdrawal behaviors" - such as leaving work without permission, daydreaming, spending work time on personal matters, and shirking tasks - that adversely affect productivity and morale.
Depression, anxiety, and personality disturbances are all associated with marijuana use. Research clearly demonstrates that marijuana use has the potential to cause problems in daily life or make a person's existing problems worse. Because marijuana compromises the ability to learn and remember information, the more a person uses marijuana the more he or she is likely to fall behind in accumulating intellectual, job, or social skills. Moreover, research has shown that marijuana's adverse impact on memory and learning can last for days or weeks after the acute effects of the drug wear off.
For example, a study of 129 college students found that among heavy users of marijuana, those who smoked the drug at least 27 of the preceding 30 days, critical skills related to attention, memory, and learning were significantly impaired, even after they had not used the drug for at least 24 hours. The heavy marijuana users in the study had more trouble sustaining and shifting their attention and in registering, organizing, and using information than did the study participants who had used marijuana no more than 3 of the previous 30 days. As a result, someone who smokes marijuana once daily may be functioning at a reduced intellectual level all of the time. More recently, the same researchers showed that a group of long-term heavy marijuana users' ability to recall words from a list was impaired 1 week following cessation of marijuana use, but returned to normal by 4 weeks. An implication of this finding is that even after long-term heavy marijuana use, if an individual quits marijuana use, some cognitive abilities may be recovered.
Another study produced additional evidence that marijuana's effects on the brain can cause cumulative deterioration of critical life skills in the long run. Researchers gave students a battery of tests measuring problem-solving and emotional skills in 8th grade and again in 12th grade. The results showed that the students who were already drinking alcohol plus smoking marijuana in 8th grade started off slightly behind their peers but that the distance separating these two groups grew significantly by their senior year in high school. The analysis linked marijuana use, independently of alcohol use, to reduced capacity for self-reinforcement, a group of psychological skills that enable individuals to maintain confidence and persevere in the pursuit of goals.
Can marijuana use during pregnancy harm the baby?
Research has shown that babies born to women who used marijuana during their pregnancies display altered responses to visual stimuli, increased tremulousness, and a high-pitched cry, which may indicate problems with neurological development.< During infancy and preschool years, marijuana-exposed children have been observed to have more behavioral problems and to perform tasks of visual perception, language comprehension, sustained attention, and memory more poorly than nonexposed children do. In school, these children are more likely to exhibit deficits in decision-making skills, memory, and the ability to remain attentive.
Is marijuana use addictive?
Long-term marijuana use can lead to addiction for some people; that is, they use the drug compulsively even though it often interferes with family, school, work, and recreational activities. According to the 2001 National Household Survey on Drug Abuse, an estimated 5.6 million Americans age 12 or older reported problems with illicit drug use in the past year. Of these, 3.6 million met diagnostic criteria for dependence on an illicit drug. More than 2 million met diagnostic criteria for dependence on marijuana/hashish. In 1999, more than 220,000 people entering drug abuse treatment programs reported that marijuana was their primary drug of abuse.
Along with craving, withdrawal symptoms can make it hard for long-term marijuana smokers to stop using the drug. People trying to quit report irritability, difficulty sleeping, and anxiety. They also display increased aggression on psychological tests, peaking approximately 1 week after they last used the drug.
What treatments are available for marijuana abusers?
Treatment programs directed at marijuana abuse are rare, partly because many who use marijuana do so in combination with other drugs, such as cocaine and alcohol. However, with more people seeking help to control marijuana abuse, research has focused on ways to overcome problems with abuse of this drug.
One study of adult marijuana users found comparable benefits from a 14-session cognitive-behavioral group treatment and a 2-session individual treatment that included motivational interviewing and advice on ways to reduce marijuana use. Participants were mostly men in their early thirties who had smoked marijuana daily for over 10 years. By increasing patients' awareness of what triggers their marijuana use, both treatments sought to help them devise avoidance strategies. Use, dependence symptoms, and psychosocial problems decreased for at least 1 year after both treatments. About 30 percent of users were abstinent during the last 3-month followup period. Another study suggests that giving patients vouchers for abstaining from marijuana can improve outcomes. Vouchers can be redeemed for such goods as movie passes, sports equipment, or vocational training.
No medications are now available to treat marijuana abuse. However, recent discoveries about the workings of THC receptors have raised the possibility that scientists may eventually develop a medication that will block THC's intoxicating effects. Such a medication might be used to prevent relapse to marijuana abuse by reducing or eliminating its appeal.
Cocaine
Cocaine is a powerfully addictive stimulant that directly affects the brain. Cocaine has been 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.
What is Cocaine?
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 a local anesthetic 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.
What is crack?
Crack is the street name given to the 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.
What is the scope of cocaine use in the United States?
Trends in 30-day prevalence of cocaine abuse among eighth, tenth, and twelfth graders, 1991-1998
In 1997, an estimated 1.5 million Americans (0.7 percent of those age 12 and older) were current cocaine users, according to the 1997 National Household Survey on Drug Abuse (NHSDA). This number has not changed significantly since 1992, although it is a dramatic decrease from the 1985 peak of 5.7 million cocaine users(3 percent of the population). Based upon additional data sources that take into account users underrepresented in the NHSDA, the Office of National Drug Control Policy estimates the number of chronic cocaine users at 3.6 million.
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 1997 NHSDA, rates of current cocaine use were 1.4 percent for African Americans, 0.8 percent for Hispanics, and 0.6 percent for Caucasians.
Crack cocaine remains a serious problem in the United States. The NHSDA estimated the number of current crack users to be about 604,000 in 1997, which does not reflect any significant change since 1988.
The 1998 Monitoring the Future Survey, which annually surveys teen attitudes and recent drug use, reports that lifetime and past-year use of crack increased among eighth graders to its highest levels since 1991, the first year data were available for this grade. The percentage of eighth graders reporting crack use at least once in their lives increased from 2.7 percent in 1997 to 3.2 percent in 1998. Past-year use of crack also rose slightly among this group, although no changes were found for other grades.
Data from the Drug Abuse Warning Network (DAWN) showed that cocaine-related emergency room visits, after increasing 78 percent between 1990 and 1994, remained level between 1994 and 1996, with 152,433 cocaine-related episodes reported in 1996.
How is cocaine used?
The principal routes of cocaine administration are oral, intranasal, intravenous, and inhalation. The slang terms for these routes are, respectively, "chewing," "snorting," "mainlining," "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 can also 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. 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.
How does cocaine produce its effects?
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, when stimulated, produce feelings of pleasure. 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 pleasure centers. In studies using animals, for example, all types of pleasurable 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 build-up of dopamine in the synapse which contributes to the pleasurable effects of cocaine.
Researchers have discovered that, when a pleasurable 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, probably resulting in 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.
Short-term effects of cocaine
Increased energy
Decreased appetite
Mental alertness
Increased heart rate and blood pressure
Constricted blood vessels
Increased temperature
Dilated pupils
What are the short-term effects of cocaine use?
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 to perform simple physical and intellectual tasks more quickly, while others can 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.
What are the long-term effects of cocaine use?
Long-term effects of cocaine
Addiction
Irritability and mood disturbances
Restlessness
Paranoia
Auditory hallucinations
Cocaine is a powerfully addictive drug. Once having tried cocaine, an individual may have difficulty predicting or controlling the extent to which he or she will continue to 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 incre?g 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.
What are the medical complications of cocaine abuse?
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 are enormous medical complications associated with cocaine use. Some of the most frequent complications are cardiovascular effects, including disturbances in heart rhythm and heart attacks; such respiratory effects as chest pain and respiratory failure; neurological effects, including strokes, seizure, 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 and coma.
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.
Are cocaine abusers at risk for contracting HIV/AIDS and hepatitis B and C?
Yes. Cocaine abusers, especially those who inject, are at increased risk for contracting such infectious diseases as human immunodeficiency virus (HIV/AIDS) and hepatitis. In fact, use and abuse of illicit drugs, including crack cocaine, have become the leading 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 more than 60 percent of new AIDS cases are women. Research has also shown that drug use can interfere with judgement about risk-taking behavior, and can potentially lead to reduced precautions about having sex, the sharing of needles and injection paraphernalia, and the trading of sex for drugs, by both men and women.
Additionally, hepatitis C is spreading rapidly among injection drug users; current estimates indicate infection rates of 65 to 90 percent in this population. At present, there is no vaccine for the hepatitis C virus, and the only treatment is expensive, often unsuccessful, and may have serious side effects.
What is the effect of maternal cocaine use?
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 even more problematic, given that, typically, more than one substance is abused. Such factors as the amount and number of all drugs abused; inadequate prenatal care; abuse and neglect of the children, due to the mother's lifestyle; socio-economic status; poor maternal nutrition; other health problems; and exposure to sexually transmitted diseases, are just some examples of the difficulty in determining the direct impact of perinatal cocaine use, for example, on maternal and fetal outcome.
Many may recall that "crack babies," or babies born to mothers who used cocaine while pregnant, were written off by many a decade ago 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. Most crack-exposed babies appear to recover quite well. However, the fact that most of these children appear normal should not be over-interpreted as a positive sign. Using sophisticated technologies, scientists are now finding that exposure to cocaine during fetal development may lead to subtle, but significant, deficits later, especially with behaviors that are crucial to success in the classroom, such as blocking out distractions and concentrating for long periods of time.
What treatments are effective for cocaine abusers?
There has been 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 poly-drug 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. For example, one of the most promising anti-cocaine drug medications to date, selegeline, is being taken into multi-site phase III clinical trials in 1999. These trials will evaluate two innovative routes of selegeline administration: a transdermal patch and a time-released pill, to determine which is most beneficial. Disulfiram, a medication that has been used to treat alcoholism, has also been shown, in clinical studies, to be effective in reducing cocaine abuse. 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 is ultimately the most effective approach for treating addiction. It is important to match the best treatment regimen to the needs of the patient. This may include adding to or removing from an individual's treatment regimen a number of different components or elements. For example, if an individual is prone to relapses, a relapse component should be added to the program. A behavioral therapy component that is showing positive results in many cocaine-addicted populations, is contingency management. Contingency management uses 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 is another approach. Cognitive-behavioral coping skills treatment, for example, is a short-term, focused approach to helping cocaine-addicted individuals become 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. This approach attempts to help patients to 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.
Therapeutic communities, or residential programs with planned lengths of stay of 6 to 12 months, offer another alternative to those in need of treatment for cocaine addiction. Therapeutic communities are often comprehensive, in that they focus on the resocialization of the individual to society, and can include on-site vocational rehabilitation and other supportive services. Therapeutic communities typically are used to treat patients with more severe problems, such as co-occurring mental health problems and criminal involvement.
Where can I get further scientific information about cocaine addiction?
To learn more about cocaine and other drugs of abuse, contact the National Clearinghouse for Alcohol and Drug Information (NCADI) at 1-800-729-6686. Information specialists are available to assist you in locating needed information and resources.
Fact sheets on the health effects of drug abuse and other topics can be ordered free of charge, in English and Spanish, by calling NIDA INFOFAX at 1-888-NIH-NIDA (1-888-644-6432), or for hearing impaired persons, 1-888-TTY-NIDA (1-888-889-6432).
Information can also be accessed through the NIDA World Wide Web site (http://www.nida.nih.gov/) or the NCADI Web site (http://www.health.org/).
Glossary
Addiction: A chronic, relapsing disease, characterized by compulsive drug-seeking and use and by neurochemical and molecular changes in the brain.
Anesthetic: An agent that causes insensitivity to pain.
Antidepressants: A group of drugs used in treating depressive disorders.
Cocaethylene: Potent stimulant created when cocaine and alcohol are used together.
Coca: The plant, Erythroxylon, from which cocaine is derived. Also refers to the leaves of this plant.
Crack: Short term for a smokable form of cocaine.
Craving: A powerful, often uncontrollable desire for drugs.
Dopamine: A neurotransmitter present in regions of the brain that regulate movement, emotion, motivation, and the feeling of pleasure.
Neuron: A nerve cell in the brain.
Physical dependence: An adaptive physiological state that occurs with regular drug use and results in a withdrawal syndrome when drug use is stopped; usually occurs with tolerance.
Poly-drug user: An individual who uses more than one drug.
Rush: A surge of pleasure that rapidly follows administration of some drugs.
Tolerance: A condition in which higher doses of a drug are required to produce the same effect as during initial use; often is associated with physical dependence.
Vertigo: The sensation of dizziness.
Withdrawal: A variety of symptoms that occur after use of an addictive drug is reduced or stopped.
cocainehref="http://www.technorati.com/tag/drugrehab"rel="tag">drugrehab
What is Cocaine?
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 a local anesthetic 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.
What is crack?
Crack is the street name given to the 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.
What is the scope of cocaine use in the United States?
Trends in 30-day prevalence of cocaine abuse among eighth, tenth, and twelfth graders, 1991-1998
In 1997, an estimated 1.5 million Americans (0.7 percent of those age 12 and older) were current cocaine users, according to the 1997 National Household Survey on Drug Abuse (NHSDA). This number has not changed significantly since 1992, although it is a dramatic decrease from the 1985 peak of 5.7 million cocaine users(3 percent of the population). Based upon additional data sources that take into account users underrepresented in the NHSDA, the Office of National Drug Control Policy estimates the number of chronic cocaine users at 3.6 million.
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 1997 NHSDA, rates of current cocaine use were 1.4 percent for African Americans, 0.8 percent for Hispanics, and 0.6 percent for Caucasians.
Crack cocaine remains a serious problem in the United States. The NHSDA estimated the number of current crack users to be about 604,000 in 1997, which does not reflect any significant change since 1988.
The 1998 Monitoring the Future Survey, which annually surveys teen attitudes and recent drug use, reports that lifetime and past-year use of crack increased among eighth graders to its highest levels since 1991, the first year data were available for this grade. The percentage of eighth graders reporting crack use at least once in their lives increased from 2.7 percent in 1997 to 3.2 percent in 1998. Past-year use of crack also rose slightly among this group, although no changes were found for other grades.
Data from the Drug Abuse Warning Network (DAWN) showed that cocaine-related emergency room visits, after increasing 78 percent between 1990 and 1994, remained level between 1994 and 1996, with 152,433 cocaine-related episodes reported in 1996.
How is cocaine used?
The principal routes of cocaine administration are oral, intranasal, intravenous, and inhalation. The slang terms for these routes are, respectively, "chewing," "snorting," "mainlining," "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 can also 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. 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.
How does cocaine produce its effects?
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, when stimulated, produce feelings of pleasure. 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 pleasure centers. In studies using animals, for example, all types of pleasurable 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 build-up of dopamine in the synapse which contributes to the pleasurable effects of cocaine.
Researchers have discovered that, when a pleasurable 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, probably resulting in 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.
Short-term effects of cocaine
Increased energy
Decreased appetite
Mental alertness
Increased heart rate and blood pressure
Constricted blood vessels
Increased temperature
Dilated pupils
What are the short-term effects of cocaine use?
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 to perform simple physical and intellectual tasks more quickly, while others can 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.
What are the long-term effects of cocaine use?
Long-term effects of cocaine
Addiction
Irritability and mood disturbances
Restlessness
Paranoia
Auditory hallucinations
Cocaine is a powerfully addictive drug. Once having tried cocaine, an individual may have difficulty predicting or controlling the extent to which he or she will continue to 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 incre?g 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.
What are the medical complications of cocaine abuse?
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 are enormous medical complications associated with cocaine use. Some of the most frequent complications are cardiovascular effects, including disturbances in heart rhythm and heart attacks; such respiratory effects as chest pain and respiratory failure; neurological effects, including strokes, seizure, 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 and coma.
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.
Are cocaine abusers at risk for contracting HIV/AIDS and hepatitis B and C?
Yes. Cocaine abusers, especially those who inject, are at increased risk for contracting such infectious diseases as human immunodeficiency virus (HIV/AIDS) and hepatitis. In fact, use and abuse of illicit drugs, including crack cocaine, have become the leading 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 more than 60 percent of new AIDS cases are women. Research has also shown that drug use can interfere with judgement about risk-taking behavior, and can potentially lead to reduced precautions about having sex, the sharing of needles and injection paraphernalia, and the trading of sex for drugs, by both men and women.
Additionally, hepatitis C is spreading rapidly among injection drug users; current estimates indicate infection rates of 65 to 90 percent in this population. At present, there is no vaccine for the hepatitis C virus, and the only treatment is expensive, often unsuccessful, and may have serious side effects.
What is the effect of maternal cocaine use?
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 even more problematic, given that, typically, more than one substance is abused. Such factors as the amount and number of all drugs abused; inadequate prenatal care; abuse and neglect of the children, due to the mother's lifestyle; socio-economic status; poor maternal nutrition; other health problems; and exposure to sexually transmitted diseases, are just some examples of the difficulty in determining the direct impact of perinatal cocaine use, for example, on maternal and fetal outcome.
Many may recall that "crack babies," or babies born to mothers who used cocaine while pregnant, were written off by many a decade ago 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. Most crack-exposed babies appear to recover quite well. However, the fact that most of these children appear normal should not be over-interpreted as a positive sign. Using sophisticated technologies, scientists are now finding that exposure to cocaine during fetal development may lead to subtle, but significant, deficits later, especially with behaviors that are crucial to success in the classroom, such as blocking out distractions and concentrating for long periods of time.
What treatments are effective for cocaine abusers?
There has been 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 poly-drug 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. For example, one of the most promising anti-cocaine drug medications to date, selegeline, is being taken into multi-site phase III clinical trials in 1999. These trials will evaluate two innovative routes of selegeline administration: a transdermal patch and a time-released pill, to determine which is most beneficial. Disulfiram, a medication that has been used to treat alcoholism, has also been shown, in clinical studies, to be effective in reducing cocaine abuse. 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 is ultimately the most effective approach for treating addiction. It is important to match the best treatment regimen to the needs of the patient. This may include adding to or removing from an individual's treatment regimen a number of different components or elements. For example, if an individual is prone to relapses, a relapse component should be added to the program. A behavioral therapy component that is showing positive results in many cocaine-addicted populations, is contingency management. Contingency management uses 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 is another approach. Cognitive-behavioral coping skills treatment, for example, is a short-term, focused approach to helping cocaine-addicted individuals become 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. This approach attempts to help patients to 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.
Therapeutic communities, or residential programs with planned lengths of stay of 6 to 12 months, offer another alternative to those in need of treatment for cocaine addiction. Therapeutic communities are often comprehensive, in that they focus on the resocialization of the individual to society, and can include on-site vocational rehabilitation and other supportive services. Therapeutic communities typically are used to treat patients with more severe problems, such as co-occurring mental health problems and criminal involvement.
Where can I get further scientific information about cocaine addiction?
To learn more about cocaine and other drugs of abuse, contact the National Clearinghouse for Alcohol and Drug Information (NCADI) at 1-800-729-6686. Information specialists are available to assist you in locating needed information and resources.
Fact sheets on the health effects of drug abuse and other topics can be ordered free of charge, in English and Spanish, by calling NIDA INFOFAX at 1-888-NIH-NIDA (1-888-644-6432), or for hearing impaired persons, 1-888-TTY-NIDA (1-888-889-6432).
Information can also be accessed through the NIDA World Wide Web site (http://www.nida.nih.gov/) or the NCADI Web site (http://www.health.org/).
Glossary
Addiction: A chronic, relapsing disease, characterized by compulsive drug-seeking and use and by neurochemical and molecular changes in the brain.
Anesthetic: An agent that causes insensitivity to pain.
Antidepressants: A group of drugs used in treating depressive disorders.
Cocaethylene: Potent stimulant created when cocaine and alcohol are used together.
Coca: The plant, Erythroxylon, from which cocaine is derived. Also refers to the leaves of this plant.
Crack: Short term for a smokable form of cocaine.
Craving: A powerful, often uncontrollable desire for drugs.
Dopamine: A neurotransmitter present in regions of the brain that regulate movement, emotion, motivation, and the feeling of pleasure.
Neuron: A nerve cell in the brain.
Physical dependence: An adaptive physiological state that occurs with regular drug use and results in a withdrawal syndrome when drug use is stopped; usually occurs with tolerance.
Poly-drug user: An individual who uses more than one drug.
Rush: A surge of pleasure that rapidly follows administration of some drugs.
Tolerance: A condition in which higher doses of a drug are required to produce the same effect as during initial use; often is associated with physical dependence.
Vertigo: The sensation of dizziness.
Withdrawal: A variety of symptoms that occur after use of an addictive drug is reduced or stopped.
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