How quickly a potential drug addict does become addicted to a drug depends on many factors including the biology of their body. All drugs are potentially harmful and may have life-threatening consequences associated with their use. There are also vast differences among individuals in sensitivity to various drugs. While one person may use a drug one or many times and suffer no ill effects, another person may be particularly vulnerable and overdose with first use. There is no way of knowing in advance how someone may react.
Here are four questions to help determine if someone is at risk of becoming an addict.
- Have you ever felt you ought to cut down on your drug use?
- Have people ever annoyed you by criticizing your drug use?
- Have you ever felt bad or guilty about your drug use?
- Have you ever had a drink or taken a drug first thing in the morning to steady your nerves?
If a person is compulsively seeking and using a drug despite negative consequences, such as loss of job, debt, physical problems brought on by drug abuse, or family problems, then he or she is probably an addict. The physical signs of being an addict can vary depending on the person and the drug being abused. For example, someone who abuses marijuana may have a chronic cough or worsening of asthmatic conditions. THC, the chemical in marijuana responsible for producing its effects, is associated with weakening the immune system which makes the user more vulnerable to infections, such as pneumonia. Each drug has short-term and long-term physical effects; stimulants like cocaine increase heart rate and blood pressure, whereas opioids like heroin may slow the heart rate and reduce respiration.
Drug addiction is a complex brain disease. It is characterized by compulsive, at times uncontrollable, drug craving, seeking, and use that persist even in the face of extremely negative consequences. Drug seeking becomes compulsive, in large part as a result of the effects of prolonged drug use on brain functioning and, thus, on behavior. For most addicts, drug use becomes chronic, with relapses possible even after long periods of abstinence. There is no easy answer for the addict.
Cocaine is a powerfully addictive stimulant drug. The powdered, hydrochloride salt form of cocaine can be snorted or dissolved in water and injected. Crack is cocaine that has not been neutralized by an acid to make the hydrochloride salt. This form of cocaine comes in a rock crystal that can be heated and its vapors smoked. The term “crack” refers to the crackling sound heard when it is heated.*
Regardless of how cocaine is used or how frequently, a user can experience acute cardiovascular or cerebrovascular emergencies, such as a heart attack or stroke, which could result in sudden death. Cocaine-related deaths are often a result of cardiac arrest or seizure followed by respiratory arrest.
Cocaine is a strong central nervous system stimulant that interferes with the reabsorption process of dopamine, a chemical messenger associated with pleasure and movement. The buildup of dopamine causes continuous stimulation of “receiving” neurons, which is associated with the euphoria commonly reported by cocaine abusers.
Physical effects of cocaine use include constricted blood vessels, dilated pupils, and increased temperature, heart rate, and blood pressure. The duration of cocaine’s immediate euphoric effects, which include hyperstimulation, reduced fatigue, and mental clarity, depends on the route of administration. The faster the absorption, the more intense the high. On the other hand, the faster the absorption, the shorter the duration of action. The high from snorting may last 15 to 30 minutes, while that from smoking may last 5 to 10 minutes. Increased use can reduce the period of time a user feels high and increases the risk of addiction. Some users of cocaine report feelings of restlessness, irritability, and anxiety. A tolerance to the “high” may develop—many addicts report that they seek but fail to achieve as much pleasure as they did from their first exposure. Some users will increase their doses to intensify and prolong the euphoric effects. While tolerance to the high can occur, users can also become more sensitive to cocaine’s anesthetic and convulsant effects without increasing the dose taken. This increased sensitivity may explain some deaths occurring after apparently low doses of cocaine. Use of cocaine in a binge, during which the drug is taken repeatedly and at increasingly high doses, may lead to a state of increasing irritability, restlessness, and paranoia. This can result in a period of full-blown paranoid psychosis, in which the user loses touch with reality and experiences auditory hallucinations. Other complications associated with cocaine use include disturbances in hearth rhythm and heart attacks, chest pain and respiratory failure, strokes, seizures and headaches, and gastrointestinal complications such as abdominal pain and nausea. Because cocaine has a tendency to decrease appetite, many chronic users can become malnourished. Different means of taking cocaine can produce different adverse effects. Regularly snorting cocaine, for example, can lead to loss of sense of smell, nosebleeds, problems with swallowing, hoarseness, and a chronically runny nose. Ingesting cocaine can cause severe bowel gangrene due to reduced blood flow. People who inject cocaine can experience severe allergic reactions and, as with any injecting drug user, are at increased risk for contracting HIV and other blood-borne diseases. Added Danger: Cocaethylene
When people mix cocaine and alcohol consumption, they are compounding the danger each drug poses and unknowingly forming a complex chemical experiment within their bodies. NIDA-funded researchers have found that the human liver combines cocaine and alcohol and manufactures a third substance, cocaethylene, that intensifies cocaine’s euphoric effects, while potentially increasing the risk of sudden death.
The widespread abuse of cocaine has stimulated extensive efforts to develop treatment programs for this type of drug abuse.
One of NIDA’s top research priorities is to find a medication to block or greatly reduce the effects of cocaine, to be used as one part of a comprehensive treatment program. NIDA-funded researchers are also looking at medications that help alleviate the severe craving that people in treatment for cocaine addiction often experience. Several medications are currently being investigated for their safety and efficacy in treating cocaine addiction.
In addition to treatment medications, behavioral interventions—particularly cognitive behavioral therapy—can be effective in decreasing drug use by patients in treatment for cocaine abuse. Providing the optimal combination of treatment and services for each individual is critical to successful outcomes.
Source: The National Institute on Drug Abuse (NIDA) website (http://www.nida.nih.gov/)
Methamphetamine is an addictive stimulant drug that strongly activates certain systems in the brain. Methamphetamine is chemically related to amphetamine, but the central nervous system effects of methamphetamine are greater. Both drugs have some limited therapeutic uses, primarily in the treatment of obesity.
Methamphetamine is made in illegal laboratories and has a high potential for abuse and addiction. Street methamphetamine is referred to by many names, such as “speed,” “meth,” and “chalk.” Methamphetamine hydrochloride, clear chunky crystals resembling ice, which can be inhaled by smoking, is referred to as “ice,” “crystal,” “glass,” and “tina.”
Methamphetamine releases high levels of the neurotransmitter dopamine, which stimulates brain cells, enhancing mood and body movement. It also appears to have a neurotoxic effect, damaging brain cells that contain dopamine as well as serotonin, another neurotransmitter. Over time, methamphetamine appears to cause reduced levels of dopamine, which can result in symptoms like those of Parkinson’s disease, a severe movement disorder.
Methamphetamine is taken orally or intranasally (snorting the powder), by intravenous injection, and by smoking. Immediately after smoking or intravenous injection, the methamphetamine user experiences an intense sensation, called a “rush” or “flash,” that lasts only a few minutes and is described as extremely pleasurable. Oral or intranasal use produces euphoria—a high, but not a rush. Users may become addicted quickly, and use it with increasing frequency and in increasing doses.
Animal research going back more than 20 years shows that high doses of methamphetamine damage neuron cell endings. Dopamine- and serotonin-containing neurons do not die after methamphetamine use, but their nerve endings (“terminals”) are cut back, and regrowth appears to be limited.
The central nervous system (CNS) actions that result from taking even small amounts of methamphetamine include increased wakefulness, increased physical activity, decreased appetite, increased respiration, hyperthermia, and euphoria. Other CNS effects include irritability, insomnia, confusion, tremors, convulsions, anxiety, paranoia, and aggressiveness. Hyperthermia and convulsions can result in death.
Source: The National Institute on Drug Abuse (NIDA) website (http://www.nida.nih.gov/)
Prescription medications such as pain relievers, tranquilizers, stimulants, and sedatives are very useful treatment tools but sometimes people do not take them as directed and may become addicted. Pain relievers make surgery possible, and enable many individuals with chronic pain to lead productive lives. Most people who take prescription medications use them responsibly. However, the inappropriate or nonmedical use of prescription medications is a serious public health concern. Nonmedical use of prescription medications like opioids, central nervous system (CNS) depressants, and stimulants can lead to addiction, characterized by compulsive drug seeking and use.
Patients, healthcare professionals, and pharmacists all have roles in preventing misuse and addiction to prescription medications. For example, when a doctor prescribes a pain relief medication, CNS depressant, or stimulant, the patient should follow the directions for use carefully, learn what effects the medication could have, and determine any potential interactions with other medications. The patient should read all information provided by the pharmacist. Physicians and other healthcare providers should screen for any type of substance abuse during routine history-taking, with questions about which prescriptions and over-the-counter medicines the patient is taking and why. Providers should note any rapid increases in the amount of a medication needed or frequent requests for refills before the quantity prescribed should have been used, as these may be indicators of abuse.
Commonly Abused Prescription Medications
While many prescription medications can be abused or misused, these three classes are most commonly abused:
– Opioids – often prescribed to treat pain.
– CNS Depressants – used to treat anxiety and sleep disorders.
– Stimulants – prescribed to treat narcolepsy and attention deficit/hyperactivity disorder.
Opioids are commonly prescribed because of their effective analgesic, or pain relieving, properties. Studies have shown that properly managed medical use of opioid analgesic compounds is safe and rarely causes addiction. Taken exactly as prescribed, opioids can be used to manage pain effectively.
Among the compounds that fall within this class—sometimes referred to as narcotics—are morphine, codeine, and related medications. Morphine is often used before or after surgery to alleviate severe pain. Codeine is used for milder pain. Other examples of opioids that can be prescribed to alleviate pain include oxycodone (OxyContin—an oral, controlled release form of the drug); propoxyphene (Darvon); hydrocodone (Vicodin); hydromorphone (Dilaudid); and meperidine (Demerol), which is used less often because of side effects. In addition to their effective pain relieving properties, some of these medications can be used to relieve severe diarrhea (Lomotil, for example, which is diphenoxylate) or severe coughs (codeine).
Opioids act by attaching to specific proteins called opioid receptors, which are found in the brain, spinal cord, and gastrointestinal tract. When these compounds attach to certain opioid receptors in the brain and spinal cord, they can effectively change the way a person experiences pain.
In addition, opioid medications can affect regions of the brain that mediate what we perceive as pleasure, resulting in the initial euphoria that many opioids produce. They can also produce drowsiness, cause constipation, and, depending upon the amount taken, depress breathing. Taking a large single dose could cause severe respiratory depression or death.
Opioids may interact with other medications and are only safe to use with other medications under a physician’s supervision. Typically, they should not be used with substances such as alcohol, antihistamines, barbiturates, or benzodiazepines. Since these substances slow breathing, their combined effects could lead to life-threatening respiratory depression.
Long-term use also can lead to physical dependence—the body adapts to the presence of the substance and withdrawal symptoms occur if use is reduced abruptly. This can also include tolerance, which means that higher doses of a medication must be taken to obtain the same initial effects. Note that physical dependence is not the same as addiction—physical dependence can occur even with appropriate long-term use of opioid and other medications. Addiction, as noted earlier, is defined as compulsive, often uncontrollable drug use in spite of negative consequences.
Individuals taking prescribed opioid medications should not only be given these medications under appropriate medical supervision, but also should be medically supervised when stopping use in order to reduce or avoid withdrawal symptoms. Symptoms of withdrawal can include restlessness, muscle and bone pain, insomnia, diarrhea, vomiting, cold flashes with goose bumps (“cold turkey”), and involuntary leg movements.
Individuals who become addicted to prescription medications can be treated. Options for effectively treating addiction to prescription opioids are drawn from research on treating heroin addiction. Some pharmacological examples of available treatments follow:
– Methadone, a synthetic opioid that blocks the effects of heroin and other opioids, eliminates withdrawal symptoms and relieves craving. It has been used for over 30 years to successfully treat people addicted to opioids.
– Buprenorphine, another synthetic opioid, is a recent addition to the arsenal of medications for treating addiction to heroin and other opiates.
– Naltrexone is a long-acting opioid blocker often used with highly motivated individuals in treatment programs promoting complete abstinence. Naltrexone also is used to prevent relapse.
– Naloxone counteracts the effects of opioids and is used to treat overdoses.
Central Nervous System (CNS) Depressants
CNS depressants slow normal brain function. In higher doses, some CNS depressants can become general anesthetics. Tranquilizers and sedatives are examples of CNS depressants.
CNS depressants can be divided into two groups, based on their chemistry and pharmacology:
– Barbiturates, such as mephobarbital (Mebaral) and pentobarbitalsodium (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. Benzodiazepines that have a more sedating effect, such as estazolam (ProSom), can be prescribed for short-term treatment of sleep disorders.
There are many CNS depressants, and most act on the brain similarly—they affect the neurotransmitter gamma-aminobutyric acid (GABA). Neurotransmitters are brain chemicals that facilitate communication between brain cells. GABA works by decreasing brain activity. Although different classes of CNS depressants work in unique ways, ultimately it is their ability to increase GABA activity that produces a drowsy or calming effect. Despite these beneficial effects for people suffering from anxiety or sleep disorders, barbiturates and benzodiazepines can be addictive and should be used only as prescribed.
CNS depressants should not be combined with any medication or substance that causes sleepiness, including prescription pain medicines, certain over-the-counter cold and allergy medications, or alcohol. If combined, they can slow breathing, or slow both the heart and respiration, which can be fatal.
Discontinuing prolonged use of high doses of CNS depressants can lead to withdrawal. Because they work by slowing the brain’s activity, a potential consequence of abuse is that when one stops taking a CNS depressant, the brain’s activity can rebound to the point that seizures can occur. Someone thinking about ending their use of a CNS depressant, or who has stopped and is suffering withdrawal, should speak with a physician and seek medical treatment.
In addition to medical supervision, counseling in an in-patient or out-patient setting can help people who are overcoming addiction to CNS depressants. For example, cognitive-behavioral therapy has been used successfully to help individuals in treatment for abuse of benzodiazepines. This type of therapy focuses on modifying a patient’s thinking, expectations, and behaviors while simultaneously increasing their skills for coping with various life stressors.
Often the abuse of CNS depressants 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 should address the multiple addictions.
Stimulants increase alertness, attention, and energy, which are accompanied by increases in blood pressure, heart rate, and respiration.
Historically, stimulants were used to treat asthma and other respiratory problems, obesity, neurological disorders, and a variety of other ailments. As their potential for abuse and addiction became apparent, the use of stimulants began to wane. Now, stimulants are prescribed for treating only a few health conditions, including narcolepsy, attention-deficit hyperactivity disorder (ADHD), and depression that has not responded to other treatments. Stimulants may also be used for short-term treatment of obesity and for patients with asthma.
Stimulants such as dextroamphetamine (Dexedrine) and methylphenidate (Ritalin) have chemical structures that are similar to key brain neurotransmitters called monoamines, which include norepinephrine and dopamine. Stimulants increase the levels of these chemicals in the brain and body. 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 stimulants.
Research indicates that people with ADHD do not become addicted to stimulant medications, such as Ritalin, when taken in the form and dosage prescribed. However, when misused, stimulants can be addictive.
The consequences of stimulant abuse can be extremely dangerous. Taking high doses of a stimulant can result in an irregular heartbeat, dangerously high body temperatures, and/or the potential for cardiovascular failure or seizures. Taking high doses of some stimulants repeatedly over a short period of time can lead to hostility or feelings of paranoia in some individuals.
Stimulants should not be mixed with antidepressants or over-the-counter cold medicines containing decongestants. Antidepressants may enhance the effects of a stimulant, and stimulants in combination with decongestants may cause blood pressure to become dangerously high or lead to irregular heart rhythms.
Treatment of addiction to prescription stimulants, such as methylphenidate and amphetamines, is 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. Antidepressants, however, may be used to manage the symptoms of depression that can accompany early abstinence from stimulants.
Depending on the patient’s situation, the first step in treating prescription stimulant addiction may be to slowly decrease the drug’s dose and attempt to treat withdrawal symptoms. This process of detoxification could then be followed with one of many behavioral therapies. Contingency management, for example, improves treatment outcomes by enabling patients to earn vouchers for drug-free urine tests; the vouchers can be exchanged for items that promote healthy living. Cognitive-behavioral therapies, which teach patients skills to recognize risky situations, avoid drug use, and cope more effectively with problems, are proving beneficial. Recovery support groups may also be effective in conjunction with a behavioral therapy.
MDMA (3-4 methylenedioxymethamphetamine) is a synthetic, psychoactive drug chemically similar to the stimulant methamphetamine and the hallucinogen mescaline. Street names for MDMA include Ecstasy, Adam, XTC, hug, beans, and love drug. In 2003, an estimated 470,000 people in the U.S. age 12 and older used MDMA in the past 30 days, a significant decrease from 2002*
Research in animals indicates that MDMA is neurotoxic; whether or not this is also true in humans is currently an area of intense investigation. MDMA can also be dangerous to health and, on rare occasions, lethal.
MDMA exerts its primary effects in the brain on neurons that use the chemical serotonin to communicate with other neurons. The serotonin system plays an important role in regulating mood, aggression, sexual activity, sleep, and sensitivity to pain.
Chronic users of MDMA perform more poorly than nonusers on certain types of cognitive or memory tasks. Some of these effects may be due to the use of other drugs in combination with MDMA, among other factors.
In high doses, MDMA can interfere with the body’s ability to regulate temperature. This can lead to a sharp increase in body temperature (hyperthermia), resulting in liver, kidney, and cardiovascular system failure.Because MDMA can interfere with its own metabolism (breakdown within the body), potentially harmful levels can be reached by repeated drug use within short intervals.
Users of MDMA face many of the same risks as users of other stimulants such as cocaine and amphetamines. These include increases in heart rate and blood pressure, a special risk for people with circulatory problems or heart disease, and other symptoms such as muscle tension, involuntary teeth clenching, nausea, blurred vision, faintness, and chills or sweating.
These can include confusion, depression, sleep problems, drug craving, and severe anxiety. These problems can occur during and sometimes days or weeks after taking MDMA.
Research in animals links MDMA exposure to long-term damage to neurons that are involved in mood, thinking, and judgment. A study in nonhuman primates showed that exposure to MDMA for only 4 days caused damage to serotonin nerve terminals that was evident 6 to 7 years later. While similar neurotoxicity has not been definitively shown in humans, the wealth of animal research indicating MDMA’s damaging properties suggests that MDMA is not a safe drug for human consumption.
Hidden Risk: Drug Purity
Other drugs chemically similar to MDMA, such as MDA (methylenedioxyamphetamine, the parent drug of MDMA) and PMA (paramethoxyamphetamine, associated with fatalities in the U.S. and Australia) are sometimes sold as ecstasy. These drugs can be neurotoxic or create additional health risks to the user. Also, ecstasy tablets may contain other substances in addition to MDMA, such as ephedrine (a stimulant); dextromethorphan (DXM, a cough suppressant that has PCP-like effects at high doses); ketamine (an anesthetic used mostly by veterinarians that also has PCP-like effects); caffeine; cocaine; and methamphetamine. While the combination of MDMA with one or more of these drugs may be inherently dangerous, users might also combine them with substances such as marijuana and alcohol, putting themselves at further physical risk.
Source: The National Institute on Drug Abuse (NIDA) website (http://www.nida.nih.gov/)