Substance abuse and addiction comprise a public health problem with wide-ranging social, economic, and physical consequences. Drug-related deaths have more than doubled since the early 1980s. Although substance abuse costs American society more than $135 billion a year, there is no real way to put a price on the overall costs to society. Increased crime, disease, devastation of families, and the cost to the community are all byproducts of substance abuse. According to the National Institute on Drug Abuse (NIDA), there are mores deaths, illness and disabilities from substance abuse than any other preventable health condition. NIDA officials say that one in four deaths is attributable to alcohol, tobacco, and used hallucinogens. While use of marijuana and cocaine declined slightly in this age group, use of pain relievers such as Vicodin®, Lortab®, OxyContin®, and oxycodone products increased. Rates of current illicit drug use also varied significantly among major racial/ethnic groups in 2004. The rate was highest among persons reporting two or more races (13.3%) and American Indians or Alaska Natives (12.3%). Rates were 8.1% for whites, 7.2% for Hispanics, and 8.7% for blacks. Asians had the lowest rates at 3.1%.
In 2004, males aged 12 years or older were twice more likely to be classified with substance abuse than females (12.7% vs. 6.2%, respectively). Among youths aged 12 to 17, however, the rate of substance dependence or abuse among males (8.7%) was similar to the rate among females (9.0%).
Alcohol, a legal substance, is still the number-one substance of abuse in the U.S.: 121 million Americans aged 12 or older drank alcoholic beverages in 2004 (50.3%). About 22.5%, or 55 million participated in binge drinking, defined as five or more drinks on at least one occasion in the 30 days prior to the survey. These numbers remained stable and were similar to statistics compiled in 2002 and 2003.The highest prevalence of binge and heavy drinking in 2004 was for young adult aged 18 to 25 (41.2% and 15.1%, respectively). The peak rate of both measures occurred at age 21. The rate of underage drinking was the same in 2004 as in 2002 and 2003: about 10.8 million persons aged 12 to 20 years reported drinking alcohol in the month before the survey interview in 2004.
In the second half of 2003, the Drug Abuse Warning Network (DAWN), a public health surveillance system that monitors drug-related visits to emergency departments (EDs) estimated that there were 627,923 drug-related visits nationwide. Overall, drug-related visits to the emergency department averaged 1.7 drugs (legal and illegal) per visit. The Substance Abuse and Mental Health Services Administration, of the U.S. Department of Health and Human Services estimates that 305,731 drug-related ED visits in 2003 involved alcohol or a major illicit drug; this is nearly half (49%) of all drug-related ED visits. The following drugs accounted for the rest: cocaine, 20%, marijuana, 13%, heroin, 8%, stimulants, including amphetamines and methamphetamine, nearly 7%.
According to the National Institute on Drug Abuse, the use of alcohol and recreational cocaine use has declined somewhat. And, efforts to educate Americans about the effects of drug abuse are having some impact. However, a disturbingly high number of younger persons are now experimenting with new combinations of drugs.
From earliest times: a history of altering mood and dulling pain
Since earliest recorded history, man has used herbs and medications to alter awareness or to dull pain. The Greeks used opium as early as 2000 BC, and opium was legal in the U.S. until 1909. People usually take drugs to alter mood, or to speed up or slow down, to tune out, or to tune in to new sights and sounds.
Athletes, people working in extremely demanding fields, and performers may take drugs in an effort to enhance performance or to overcome the stress of continuously performing at a high level. Teens may take drugs on a dare or to ‘see what happens.’ An alcoholic may realize that his problem really began with casual social drinking that quietly escalated over the years.
Researchers have isolated numerous causes for substance use and abuse, including genetic vulnerability, environmental factors, pain and self-medication, the ‘addictive personality,’ and sociocultural factors. Fifty percent of all alcoholics have a family member who is also alcoholic. This has been underscored by studies of twins and by adoption studies, where more alcoholic than nonalcoholic adoptees had biological parents who were alcoholic.
The alcoholism of foster parents did not correlate with the alcoholism of adoptees, suggesting that the environment had less influence than genetics.
Environmental stimuli and availability of drugs can predispose people to substance abuse. Sociocultural factors can also influence substance abuse. For example, young, single, unemployed, urban men have a high incidence of alcoholism. Some individuals, especially adolescents, try drugs due to peer pressure. Certain professional groups, especially physicians and nurses, are vulnerable to abuse because of availability of drugs and higher-than-normal stress levels. (A separate course, “The Impaired Healthcare Professional,” focuses on helping healthcare professionals deal with substance abuse among colleagues.)
What are Substance Abuse, Addiction, and Dependence?
The terms substance abuse, addiction, and dependence describe our current understanding of the body and the brain’s adaptive responses to repeated exposure to certain substances. Substances are chemicals, like alcohol, drugs, or food. Drugs belong to a more specific category, which includes substances with specific effects on the brain and the body in general.
Substance abuse has two distinct definitions. As a diagnostic term, substance abuse is intermittent impaired control of substance use, and represents a stage in the spectrum of substance use disorders. The more common definition of substance abuse is drug use that violates social standards or that causes self-harm. Addiction is compulsive use and impaired control of intake of a drug in spite of its adverse consequences. Some of the characteristics of addiction are: (1) preoccupation with acquisition of the drug, (2) compulsive use of a drug or substance, (3) a propensity to relapse, (4) loss of control, and (5) denial. Dependence is persistent drug intake to prevent or lessen the physical or psychological disturbances that come with withdrawal. Physical dependence is the combination of physical tolerance and withdrawal symptoms that occur when a drug is discontinued. Psychological dependence includes the nonphysical symptoms that emerge when a drug is discontinued, such as craving, agitation, anxiety, and depression. The Diagnostic and Statistical Manual of Mental Disorders (DSM-IV) criteria for substance abuse and dependence follow:
DSM-IV Criteria for Substance Abuse and Dependence Abuse:
- A maladaptive pattern of substance use, leading to clinically significant impairment or distress, as manifested by three or more of the following, occurring at any time in the same 12-month period: (Recurrent substance use resulting in a failure to fulfill major role obligations at work, school, or home (e.g., repeated absences or poor work performance related to substance use; substance-related absences, suspensions, or expulsions from school; neglect of children or household).
- Recurrent substance use in situations in which it is physically hazardous (e.g., driving an automobile or operating a machine when impaired by substance abuse). (Recurrent substance-related legal problems (e.g., driving an automobile or operating a machine when impaired by substance abuse).
- Continued substance use despite having persistent interpersonal problems caused or exacerbated by the effects of the substance (e.g., arguments with a spouse about the consequences of intoxication, or physical fights).
A maladaptive pattern of substance use, leading to clinically significant impairment or distress, as manifested by three or more of the following occurring in the same 12-month period:
1. Tolerance, as defined by either of the following:
a. A need for markedly increased amounts of the substance to achieve intoxication or a desired effect.Markedly diminished effect with continued use of the same amount of the substance.
2. Withdrawal, as manifested by either of the following:
a. The characteristic withdrawal syndrome for the substance.The same (or a closely related) substance is taken to relieve or avoid withdrawal symptoms.
3. The substance is often taken in larger amounts or over a longer period than was originally intended.
4. Any unsuccessful effort or unsuccessful efforts to cut down or control substance use.
5. A great deal of time is spent in activities necessary to obtain the substance (e.g., visiting multiple doctors or driving long distances), use of the substance (e.g., chain-smoking) or recovering from its effects.
6. Important social, occupational, or recreational activities are given up or reduced because of substance use.
7. Substance use continues despite knowledge of having a persistent or recurrent physical or psychological problem that is likely to have been caused or exacerbated by the substance.
- With physiological dependence: Evidence of tolerance or withdrawal (i.e., either item 1 or 2 is present).
- Without physiological dependence: No evidence of tolerance or withdrawal (i.e., neither item 1 nor 2 is present).
The Big Five: Alcohol, Cocaine, Marijuana, Heroin, and Methamphetamine
Any substance is subject to abuse. For example, we need look no further than our morning cups of coffee or tea to find caffeine, perhaps the world’s most widely abused substance. However, high doses of caffeine rarely disrupt a family, or lead to time in jail or loss of employment. In this course, we will concentrate on the five most widely abused drugs in the U.S., alcohol, cocaine, marijuana, heroin, and methamphetamine.
Beer, wine, and fermented beverages have been popular for at least 10,000 years. In ancient times, fermented beverages were usually safer to drink than water, which was often contaminated. Fermented liquids also helped maintain fluid balance and supplied calories. In the 12th century, Arabian civilizations introduced distillation to the West, and highly concentrated forms of alcohol were developed.
It’s been estimated that approximately 77% of full-time employees report using alcohol at least once in the past year; 60% of those who report drinking alcohol at least once a month, and 30% report consuming alcohol at least five or more times a month. More than 15 million Americans are estimated to suffer from alcoholism.
The consequences of alcohol use and abuse are staggering. In 2001, it was estimated that $186 billion was spent for alcohol treatment alone.
Most Americans drink alcoholic beverages in moderate amounts, and a third or more of young men drink to the point of getting into temporary difficulties. However, most do not go on to develop the persistent, serious problems typical of the chronic alcoholic. About 5% of adult Americans meet the criteria for alcohol dependency or alcoholism. However, another 20% (about 40 million persons) drink more than is recommended by federal guidelines at least some time during the year. Most adolescents report some exposure to alcohol, and use increases with age.10 Recent national student survey data show that 25% of eighth graders and 50% of twelfth graders report drinking alcohol within the last month. Fifteen percent of eighth graders and 28% of twelfth graders report having had more than 5 drinks in a row during the last 2 weeks, and just under 3% of the twelfth graders report drinking alcohol daily.
Chronic alcoholism is a pathologic condition resulting from habitual use of alcohol in excessive amounts. The criteria for diagnosing alcoholism listed in the DSM-IV focus on loss of control of the substance, a willingness to give up important events in order to take the substance, and consumption of the drug or alcohol in spite of the consequences. This is indicative of alcohol’s importance and central role in the alcoholic’s life.
For a diagnosis of alcoholism to be made, the individual must meet at least three of the DSM-IV criteria (see previous section). The problems must be repetitive and must cluster together so that three or more of them have occurred during the same 12-month period. Problems associated with alcohol must lead to clinically significant impairment or distress.
Alcohol is primarily absorbed in the small intestine and colon. The small intestine absorbs alcohol completely, with or without food. Maximum blood concentrations usually are reached within 30 to 90 minutes of the last sip. Ethanol is a small organic molecule that dissolves in both water and lipids, and thus can interact with neuronal membrane lipids. Its anesthetic effect results from an ethanol-induced disorganization of the membrane lipid layer, impairing normal neuronal function. Once absorbed, ethanol is almost uniformly distributed throughout all tissues and fluids of the body. Negative effects, such as slowed reaction time, diminished fine motor control, and impaired thinking appear when the blood alcohol concentration reaches 0.20 to 0.30 grams per deciliter (g/dl).
As the blood-alcohol concentration increases, euphoria sets in. However, as the blood-alcohol levels decrease, the euphoria begins to fade. Over time, greater amounts of alcohol are required to produce the same feelings of euphoria.
Most alcohol, 90% to 98%, is ultimately broken down into carbon dioxide and water. The remainder is excreted in sweat, urine, saliva, and tears. Regardless of the alcohol-blood concentration, ethanol is metabolized at a relatively constant rate. With normal liver function, alcohol is metabolized at a rate of about 120 mg/kg body weight/hour. Thus, drinking 44 g (4 oz) of whiskey on an empty stomach leads to a maximum blood concentration of 0.07 to 0.09 g/dl, compared to 0.03 to 0.05 g/dl after drinking the same amount with a meal.
Mouthwashes, aftershave lotion, cough syrups, cold remedies, and solid alcohol cooking fuels all contain alcohol and may be a hidden source of alcohol. It is estimated that as many as 20% of inpatient alcoholics at Veterans Administration hospitals and 50% of prisoners get their alcohol from nonalcoholic sources9
Some early warning signs of alcoholism include confusion and forgetfulness, a preoccupation with obtaining and drinking alcohol, self-deception, guilt, anxiety, and depression. Other signs that a person may be losing control due to alcoholism, include the following:
- Complaints of increased upheavals in personal relationships
- Driving violations, tickets, and accidents
- Absenteeism from work
- Missed appointments at work or with friends, to the point of losing friends, jobs, and even family support
- Injuries from trauma
- Aggressive, violent outbursts
Physical symptoms of alcoholism can include anorexia, diarrhea, weight loss, neurologic disorders, and fatty deterioration of the liver, which sometimes results in cirrhosis. Alcoholism often goes undetected in patients hospitalized after an accident, or for esophagitis, gastritis, peripheral neuropathy, anemia, or depression. If the underlying cause, unsuspected alcohol abuse, is not treated, the patient may not recover.
Alcoholics also have nutritional deficiencies, usually when alcohol takes the place of food in the diet or when the body’s demand for B vitamins (especially thiamin, or vitamin B1) increases in order to handle alcohol metabolism. A number of alcoholics also have a decreased ability to absorb thiamin and folic acid; altered pancreatic function also interferes with fat digestion.
One of the most serious side effects chronic alcoholics face is Wernicke’s encephalopathy. These patients can have global confusion, apathy, ophthalmoplegia (paralysis of the eye muscles), and disturbances of gait. Most are disoriented, inattentive, unable to concentrate, and suffer with deranged perceptions and memory loss.
Alcoholic cardiomyopathy is another result of chronic alcohol abuse. The disease develops after 10 or more years of serious alcohol abuse, and is reported most often in African-American men. The most common outward sign is shortness of breath, often out of proportion to the normal signs of heart failure. Patients may also cough, especially at night, or have the so-called “holiday heart syndrome,” which can be a sign of early cardiomyopathy. These disturbances in heart rhythm occur after binge drinking.
Alcoholic cirrhosis is the leading cause of death due to alcohol abuse and the eighth leading cause of death in the U.S. Despite these statistics, surprisingly only 15% to 30% of heavy drinkers develop significant alcoholic liver disease. This may be due to the amazing resistance of the liver to the effects of ethanol. Before hepatitis or cirrhosis occurs, the average male alcoholic has drunk 10 to 13 drinks per day (150-200 g ethanol) for 10 to 20 years. Women seem a little more susceptible. The average woman with severe alcoholic liver disease has consumed 8 to 10 drinks per day (120-160 g of ethanol) for 12 to 15 years before cirrhosis or hepatitis occurs.
Treatment of alcohol abuse involves managing the effects of abuse, developing a treatment plan, monitoring recovery, and evaluating treatment outcome. Perhaps the most difficult part is the long-term management of a patient who may need repeated sessions of detoxification and rehabilitation before he or she can finally reach sobriety. And, a continuing challenge for healthcare professionals is the very high treatment failure rate-more than half of alcoholics who have been treated will return to alcohol within a year after treatment.
Alcohol intoxication is recent ingestion of alcohol, followed by changes in behavior, such as mood swings, impaired judgment, inability to function at work, and at least one of the following: lack of coordination, unsteady gait, nystagmus, or facial flushing.
In a few persons, usually those with no history of alcoholism or psychiatric/neurologic disorders, small amounts of alcohol trigger outbursts of blind fury, combativeness, and destructive behavior. Such outbursts usually end with the person falling into a deep sleep. He or she then awakens with no memory of the outburst. Some persons have blackouts, even when bystanders detect no change in consciousness-this is amnesia from intoxication so great that memory is affected.
Alcoholic coma is treated just like any other form of coma—the patient’s airway is protected, toxicologic screening of serum and urine are done, and supportive care is given. To prevent Wernicke’s encephalopathy, thiamin, 100 mg IV, and 50 mg of 50% dextrose are given. Individualized treatment with benzodiazepines, neuroleptics, anticonvulsants, and beta-blockers follows.
After a period of sustained, excessive alcohol consumption, discontinuing or decreasing alcohol intake (detoxification) may produce violent withdrawal symptoms. These can include tremors, hallucinations, seizures, and delirium.
Uncomplicated alcohol withdrawal begins with coarse tremors (a few very strong tremors) of the tongue, hands, or eyelids. Patients then may have symptoms such as nausea/vomiting, malaise/weakness, tachycardia, sweating, elevated blood pressure, anxiety, depressed mood/irritability, etc. Auditory hallucinations, the most common effect, feature either threatening or critical voices, or low-pitched humming, chants, buzzing, gunshots, or ringing in the ears. These hallucinations usually begin the first night after the patient stops drinking, and can last up to six days.
Delirium tremens (“the DTs”) is a serious reaction to withdrawal of alcohol that affects about 10% of patients. They are feverish and have tachycardia, profuse sweating, dilated pupils, nausea, confusion, disorientation, disorganized thinking, delusions, hallucinations, and sleeplessness. These symptoms usually peak two to three days after the patient abstains, and will resolve in three to five days. About 5% of patients will die, usually due to a combination of alcohol-related symptoms and high fever or peripheral circulatory collapse.
Acute and chronic intake of alcohol have distinct effects on the metabolism of other drugs. When drinking is acute, ethanol interferes with therapeutic actions of drugs by altering their metabolism or prolonging and enhancing drug effects.
Chronic alcohol ingestion speeds drug metabolism of certain products, such as warfarin, diphenylhydantoin, tolbutamide, and isoniazid, and usually produces cross-tolerance. Chronic alcoholic patients have increased susceptibility to the same drugs whether intoxicated or sober. A previous history of alcohol abuse influences the amount and types of drugs a person can take because the half-lives of these drugs tend to be 50% shorter in abstaining alcoholics than in nondrinkers.
Long-term therapy for recovering alcoholics involves helping the patient remain sober and healing the individual and family with the use of psychological and social interventions. To succeed, the patient must find ways to permanently avoid all forms of alcohol.
One of the most successful programs for recovering alcoholics is, of course, Alcoholics Anonymous (AA). AA is a program involving recovering and recovered alcoholics who attend discussion sessions and support groups. AA meetings have a good correlation with abstinence, perhaps because they undermine denial, which is a large part of the psychopathology of alcoholism. In many larger cities, AA meetings are held at virtually all hours of the day, seven days a week. AA also pairs a newly recovered alcoholic with a recovered one, and patients are encouraged to seek help 24 hours a day, to retain their newly won sobriety. Families of alcoholics can find support through organizations such as Al-Anon, Alateen, and Adult Children of Alcoholics.
For other patients, disulfiram (Antabuse®) can help maintain abstinence by acting as a deterrent to drinking alcohol. The drug inhibits the enzyme acetaldehyde dehydrogenase (ADH) if alcohol is consumed. Unpleasant symptoms, such as tachycardia, flushing, coughing, and nausea and vomiting follow. In order to avoid the symptoms, the patient must avoid alcohol. A few of the drawbacks are that the unpleasant reaction can occur even with the slightest amount of alcohol, such as that found in mouthwash or aftershave lotion, and, finally, the drug cannot be used by persons with liver disease.
Naltrexone helps curb cravings for alcohol and works as long as the person takes it. Both Antabuse and naltrexone are used to encourage abstinence; however, both cause a rebound effect when the user stops taking them.
Nutrition therapy is also warranted for many alcoholics. After years of abusing alcohol, serious physical problems and nutritional deficiencies can remain. One problem is the insulin resistance syndrome, a metabolic disorder where the body has difficulty processing sugars, leading to an unsteady supply of glucose to the bloodstream. A hypoglycemic diet can be prescribed, but this can affect behavior and emotions, and can undermine the success of treatment. All alcoholics should have a thorough nutritional evaluation by a registered dietitian.
Although overall use has declined slightly in recent years, cocaine abuse is still a major public health and social problem. In 1991,the Household Survey conducted by the National Institute on Drug Abuse reported that 23 million Americans had used cocaine at some point during their lives. Medical complications and deaths from cocaine abuse have continued to rise dramatically during the past decade. The cost of cocaine use to industry in lost productivity, job-related accidents, claims for health care benefits and poor employee morale is probably in the billions of dollars.
Data from the Drug Abuse Warning Network (DAWN) and Treatment Episode Data Set (TEDS) show opposing trends in the consequences of cocaine use since 1995. According to DAWN data, the estimated number of cocaine-related emergency department mentions increased sharply from 135,711 in 1995 to 199,198 in 2002.12 Similarly, DAWN data show a sharp increase in the rate of cocaine-related ED mentions from 58 per 100,000 population in 1995 to 78 per 100,000 population in 2002. However, TEDS data show that the number of treatment admissions for cocaine (smoked and nonsmoked) at publicly funded drug treatment facilities decreased during the same period from 272,386 in 1995 to 241,699 in 2002-this is the only drug type to show a decrease during that period.
Why do people use cocaine? The drug’s popularity can be traced to its powerful effects on the brain and consequently on behavior. Cocaine is highly valued for its ability to induce euphoria, enhance alertness, and alleviate fatigue.
Cocaine is derived from the South American coca plant, Erythroxylon coca. Its most important effects are upon the central nervous system, the brain and spinal cord, and it has the ability to produce local anesthesia. It is legally used as a topical anesthetic in eye, nose, and lacrimal duct surgery. The powdery white form of cocaine that is sniffed or taken intravenously is cocaine hydrochloride (HCL). Coca leaves are still chewed as an energy booster in many parts of Latin America.
In humans and animals, cocaine increases alertness and enhances mental acuity when first inhaled, injected, or smoked; this is accompanied by changes in brain electrical activity. Cocaine is the only drug for which laboratory animals will continually press a bar without stopping for food or rest. Animals persist in self-administration of cocaine even when it is accompanied by punishment, such as an electric shock. In fact, animals will choose a higher dose of cocaine given with an electric shock instead of a lower dose without a shock. Laboratory research also shows that cocaine is the most reinforcing of drugs, and that animals will self-administer it until they drop dead—this is not the case with heroin or alcohol.
The increased arousal and decreased need for sleep seen in cocaine use appears to be connected to the effects of the drug on certain central nervous system neurons that activate human behavior. Cocaine blocks the return, or reuptake, of neurotransmitters from the synaptic space into the presynaptic neurons, thus interfering with their metabolic breakdown. Normally, dopamine is released by a neuron into the synapse, where it can bind with dopamine receptors on neighboring neurons. Normally dopamine, a neurotransmitter linked to pleasure, is then recycled back in the transmitting neuron by a specialized protein, the dopamine transporter. If cocaine is present, it attaches to the dopamine transporter and blocks the normal recycling process, resulting in buildup of dopamine in the synapse. This contributes to the pleasurable effects of cocaine.
The drug may also increase the release of dopamine and norepinephrine into the synapse. These actions then increase the availability of norepinephrine and dopamine and increase nerve cell firing in areas of the brain that control wakefulness and arousal.
The brain-induced euphoria that cocaine produces delivers an immediate and powerful reward. Taking the drug repeatedly leads to a type of conditioning whereby euphoria leads to an increase in the behaviors that preceded or led to the euphoria. The frantic, obsessive pursuit of the drug-despite its effect on health, work, family, and finances-reflects how voluntary behavior becomes controlled by cocaine.
Cocaine magnifies the intensity of almost all pleasurable feelings without distorting them. Emotions and sexual feelings are enhanced; self-confidence and self-perception of mastery are increased, anxiety is decreased (at first), and social inhibitions are reduced. It is a tempting drug: The National Institute of Drug Abuse reports that about 10% to 15% of people who snort cocaine become regular users.
Susceptibility to addiction depends partly on the route of administration as well as the speed, degree, and duration of psychological and physical changes. Cocaine tends to be less addictive when taken in small doses. In small doses, the peak plasma levels of the drug are low, the onset of activity is slow, duration of action is long, and the unpleasant withdrawal symptoms are minimal. This pattern emerges when cocaine is taken orally or sniffed.
As cocaine abuse continues, tolerance often develops. This means that higher doses and more frequent doses of the drug are required for the brain to register the same level of pleasure experienced during the first use. Recent studies have shown that during periods of abstinence from cocaine, the memory of the euphoria associated with cocaine use, or mere exposure to cues associated with drug use can trigger tremendous craving and relapse to drug use, even after long periods of abstinence. Cocaine HCl is usually injected intravenously or snorted. Peak plasma levels occur about 30 minutes after it is sniffed. In contrast, when it is taken intravenously, cocaine produces an intense “rush” within two minutes. The elimination half-life of cocaine is approximately 40 to 60 minutes.
Smoking cocaine has the highest addictive potential. Although less of the drug is available by this route than by the intravenous route, smoked cocaine produces a potent, intense “high” that has an extremely quick onset. Euphoria is brief, followed by paranoia, depression, and anxiety. To get around these unpleasant and even painful feelings, the user craves the drug even more. Intravenous cocaine also has a high addictive potential and, given unlimited access to the drug, cocaine users who inject the drug intravenously escalate the amount of the drug until they have severe mental and physical deterioration or until death occurs.
When used over time, cocaine is powerfully addicting; in fact, it is our most addictive drug and unique among abused substances. Chronic cocaine use produces neurochemical changes, which may explain the withdrawal syndrome, which features lethargy, depression, oversleeping, and overeating in addition to the need for more cocaine.
Then comes a pattern of high-dose, extended binges. The pleasurable effects occur without the negative ones of anxiety, expense, or fear of loss of self-control-this is the classic pattern of addiction. Users may compulsively ingest the drug every 10 to 30 minutes, during which feelings of extreme euphoria contrast with the letdown of the post-binge period. Cocaine addicts average one to seven binges a week, each lasting four to 24 hours. During these binges, nearly all thoughts center on cocaine. With repeated doses the neurochemical mechanisms produce cravings that can interact with conditioning or learning mechanisms, producing severe addiction. Cocaine is extensively metabolized, mostly in the liver, and about 1% is excreted unchanged in the liver. When taken with alcohol, cocaine combines with the ethanol in the liver to form cocaethylene, which causes greater euphoria but also higher risk of cardiotoxicity than cocaine by itself.
Cocaine’s rapid entrance into the workplace beginning in the 1980s is related both to social factors and to the nature of the drug itself. In spite of widespread education about the dangers of using cocaine, the drug still holds a glamorous allure for some. Within some peer groups, cocaine use is socially sanctioned, very much like drinking alcohol is in other parts of society. In addition, amounts of cocaine that are strong enough to produce multiple episodes of intoxication can be easily transported in a small vial or aspirin bottle, and the drug is easy to conceal. It can be consumed in seconds, and intoxication occurs almost immediately. Many people who use cocaine believe that they are capable of “normal” function, and that no one will suspect they are using the drug. In the beginning, even small doses of cocaine deliver euphoria, increased alertness, and a sense of well-being.
“Crack” cocaine is a form of the drug that gives an intense “high” when smoked. Crack is produced by mixing cocaine HCl with water and sodium bicarbonate (baking soda). This mixture is then heated until all the water has evaporated, leaving small chips that resemble white pebbles. The term “crack” comes from the popping sounds the crystals make as they are heated. These rocks can be smoked, usually in a pipe. Smoking the “rocks” in a small pipe (“freebasing”) provides a more potent rush, more intense euphoria, and a much more powerful high than does inhaling cocaine powder. After a few moments, however, the euphoria is gone, leaving an irritable craving for more.
Crack cocaine is much cheaper per dose than the powder form: A rock of cocaine can be purchased for as little as $5 to $10 per packet, compared to $80 to $100 per gram for the powder form. A kilogram of 90% pure cocaine HCL now sells for from $18,000 (New Orleans) to $29,000 (Atlanta).
Crack possesses a high addiction potential, and it is possible for recreational use to escalate to addiction within days to weeks. Crack is so potent that it is believed that it quickly depletes brain neurotransmitters and produces super-sensitivity of their receptors. The neurochemical changes produced explain the rapid leap from experimentation to addiction. Personality changes and psychiatric disorders produce symptoms such as depression, irritability, social withdrawal, and paranoia. The withdrawal syndrome is also much more marked with crack abuse than with intranasal or intravenous use. Crack users are often much more difficult to treat because their addiction is usually severe by the time they enter treatment.
The former Director of Federal Drug Policy, William Bennett, called crack addition “our biggest and most immediate problem.” Crack cocaine is no longer an inner-city problem that only affects minority groups. In fact, many middle-class communities are unaware of the easy local availability of crack cocaine. Some estimate that as many as 70% of New York City drug users may be affluent; thus, doctors, nurses, professors, and Wall Street executives have fallen victim to the crack epidemic,14 and drug distribution networks have also spread into rural areas in the Midwest and South.
Freebase cocaine, smoked with marijuana or tobacco cigarettes or in freebase pipes, produces a rush in about 8 to 10 seconds. This usually lasts no more than 20 minutes (compared to the effects of snorting, which may last an hour or an hour and a half). When the drug is taken orally, a common practice of frequent users, about 30% to 40% of the drug is available, and the remainder is eliminated by first-pass metabolism in the liver.
Many cocaine users turn to other drugs to reduce the anxiety that can come with a cocaine high and to buffer the post-use “crash.” Alcohol, benzodiazepines, and opiates are popular choices. “Speedballing,” a practice that led to the death of the comedian John Belushi, refers to a practice of injecting cocaine and heroin together, to “mellow out” the stimulant effects of the cocaine with the more sedating, relaxing effects of heroin, and to guard against the depression that often follows cocaine use. The combination of these drugs is much more dangerous than each alone because the cocaine increases heroin’s tendency to depress respiration.
Certain physical signs appear after intense, repeated use of cocaine. In acute cocaine overdose, patients have tachycardia, hypertension, sweating, and dilated pupils. With long-term use, other physical signs appear. One of the best known signs is a perforated nasal septum, which was first described in the early 1900s when snorting cocaine became popular. Cocaine is not actually inhaled by sniffing; instead, the drug coats and is absorbed through the mucous membranes lining the sinuses. With this method, about 80% of the powder is absorbed.
Another sign is cocaine “tracks,” which are sites of recent injection of the drug. These can appear as salmon-colored bruises, sometimes with a clear central zone around the needle puncture site. With time, the lesions turn yellow and blue and eventually heal without scarring. Cocaine abusers can also have slowly healing cutaneous ulcers with reddish to grayish bases and blanched or whitened borders.
“Crack thumb” and “crack hand” may also be giveaway clues to cocaine abuse. A callus on the outer edge of the thumb results from repeated contact of the thumb with a cigarette lighter wheel. “Crack hand” features blackened, scarred burn lesions on the palms resulting from repeatedly handling hot crack pipes. Oral or nasal use of cocaine bathes the teeth in acid, which erodes tooth enamel. The gums are also ulcerated at the site of application. These are but a few of the outward effects. One of cocaine’s most serious targets is the heart. Chest pain and other cardiac problems are widespread but underreported, according to a recent study from the University of Michigan, Ann Arbor.15 Dr. Jim Edward Weber and colleagues, who conducted the study among 344 patients, reports that the risk of heart attack in the first hour after using cocaine is 24 times the normal risk, and cocaine users have a seven-fold lifetime risk of having a heart attack. The researchers also note that the new study should help doctors decide who needs the most intensive cardiac care, says Dr. Weber. Care for these patients runs at about $83 million in hospital costs only. The new protocol divides patients into high-risk and low-risk categories. High-risk patients had signs of acute heart attack or ischemia on their electrocardiograms. The researchers also standardly performed urine tests because previous studies had shown that nearly a third of cocaine users lie bout cocaine use in the emergency department, even when they are told that the answer would help their care. None of the 344 patients treated prospectively under the new protocol died of a heart-related cause during the month-long follow-up period after their visit to the emergency room.
Just like alcohol, cocaine abuse affects nearly every major system in the body. Cocaine is a potent central nervous system stimulant; its effects can last from 20 minutes to several hours, depending on dosage and the method of administration. The most serious result of acute cocaine abuse is sudden death, which can occur after administration of cocaine by any route. With excessive doses, hallucinations, paranoid delusions, tachycardia, itching, and formication (a feeling that bugs are crawling on the skin).
Warning signs include convulsions or mental confusion, and death can occur with doses approaching 1 gm.15 Persons born with a deficiency of the enzymepseudocholinesterase, necessary for metabolizing the drug, are at great risk if they use cocaine. They can die even if they have 10 or 20 mg of cocaine administered with a local anesthetic because the drug is never broken down or destroyed. Warning signs include agitation, tachycardia, hypertension, fever, and acidosis. It is possible to overdose on cocaine, and cocaine-related deaths have been increasing. In 1991, for example, 3,000 people died from cocaine overdose- six times as many as were in 1985. Cocaine users are also at greatly increased risk of hepatitis and AIDS, from shared needles and unprotected sex.
Treatment for a cocaine-dependent person usually involves two stages: (1) initiation of abstinence and (2) relapse prevention. Cocaine abusers rarely seek help because their use of the drug is out of control. The immediate craving to use more cocaine is strong and very common because of the euphoria that comes with use. Good feelings become associated with the drug and a frequent user takes it to counter bad news or mild depression. Successful treatment greatly depends upon the individual. Some persons can stop using cocaine on their own, some go to self-help groups, some seek individual psychotherapy, and some must be hospitalized. They all have one thing in common: they must avoid cocaine and all people associated with it. Cocaine use must stop all at once, not gradually. Cocaine must be removed from the environment or the person has to be removed from a setting where cocaine is readily available. This may involve a move to a new town, changing telephone numbers, and having spouses and other family members undergo counseling about the patient’s cocaine use.
Choice of treatment also has to take into consideration the family’s responses to the cocaine user. Most families suffer greatly because of the patient’s addiction. By the time the patient is in treatment, the family has been hurt by lies, extramarital affairs, and depletion of the family’s finances. The cocaine abuser may have turned to dealing the drug or burglary, or even to pawning family heirlooms to support his or her habit. Thus, part of treatment must include family counseling to help family members deal with their anger and guilt.
Outpatient therapy involves individual and group counseling, family or marital therapy, regular attendance at self-help groups such as Cocaine Anonymous, or CA (modeled on AA, the Alcoholics Anonymous program), and random urine tests to monitor the presence of cocaine (see later section on urine testing). CA uses a 12-Step model for establishing abstinence and recovery from all drugs. Like AA, social support is available around the clock. A New York study found that more than 80% of persons receiving outpatient treatment once a week relapsed and started using cocaine again within one year.
Certain patients are candidates for hospitalization or enrollment in a long-term residential drug treatment center. These patients, who are at higher risk of relapse, include:
- crack cocaine users;
- those dependent on cocaine and other drugs or alcohol;
- those who have medical or psychiatric problems or who cannot function socially or psychologically;
- those who show destructive behavior from cocaine use, such as stealing;
- those who don’t have adequate family or social support;
- those who have failed at treatment before;
- those with ready access to large amounts of cocaine; and
- those who strongly resist treatment.
Crack cocaine addicts are the most difficult of all cocaine abusers to treat. Since they progress so quickly from user to addict, often within days to weeks, or after one exposure to the drug, rather than one to three years, as is the case with nasal cocaine, neurochemical changes, personality changes, and psychiatric disorders are seen much sooner. Crack abusers are also more difficult to treat because their addiction is usually very severe by the time they enter treatment.
Methadone clients also are a problem group. Long-term methadone maintenance is designed to support and stabilize opiate-dependent patients for months or even years. Methadone markedly reduces narcotic cravings, induces enough tolerance to block the euphoric effects of cocaine, and causes few side effects. Some methadone patients find the combination of cocaine with methadone acts like a “speedball,” and that cocaine takes over their lives. Dopamine agonists have been somewhat helpful.
Others have reported that clients who cross over to take buprenorphine dramatically reduced and often stopped using cocaine, perhaps because of the opiate antagonist effects.
Three drugs are currently showing promise in early studies. Gamma vinyl-aminobutyric acid (GVC), a drug normally used to treat epilepsy, blocks cocaine’s action in the brains of primates. The drug increases the amount of the neurotransmitter GABA in the brain and reduces the level of dopamine in the region of the brain that is thought to be involved in addiction. In January 2005, the FDA granted permission for a Phase 1 clinical trial of GVC for the treatment of addiction. Another drug currently being tested for anti-addictive properties is the cannabinoid antagonist rimonabant. GBR 12909 (Vanoxerine®) is a selective dopamine uptake inhibitor. Because of this, it reduces cocaine’s effect on the brain and may help to treat cocaine addiction. Venlafaxine (Effexor®) is a potent serotonin-norepinephrine reuptake inhibitor that has been used to combat the depression caused by cocaine and to some extent, the addiction associated with the drug itself-a drawback is that it has significant withdrawal symptoms itself.
One very successful treatment approach for cocaine abuse has been the neurobehavioral model, such as the one used at the Matrix Institute on Addictions, located near Los Angeles. This approach divides cocaine problem areas into four areas: behavioral, cognitive, emotional, and relationship-related. The treatment then focuses on particular issues in each of these areas that emerge during the stages of recovery. Characteristic periods and the stages of recovery include the following:
- 0-15 days after cocaine is discontinued—Withdrawal
- 15-45 days post-cocaine—-Honeymoon
- 46-120 days post-cocaine—The Wall
- 121-180 days post-cocaine—Adjustment
- 181+ days post-cocaine—Resolution
During the first one to three days of abstinence, the long-term cocaine user will have a “crash,” with depression, irritability, and other symptoms. During withdrawal, patients are disoriented, depressed, tired, and feel they have lost control. They have an increased need for sleep, are impulsive and erratic, depressed, anxious, and feel shame and self-doubt. Many have difficulty concentrating, loss of short-term memory, and are hostile, confused, and fearful, even with close family members.
After the initial crash, the patient has one to five days of good sleep, little craving for cocaine, and generally feels much better. During the “honeymoon” stage, cravings for cocaine are reduced, overall mood improves, energy returns, and confidence and optimism return. They may return to use of alcohol and drop out of treatment believing they are cured. However, their overall activity is scattered and inefficient.
During the time called “The Wall,” former cocaine abusers hit a major hurdle in their recovery. Insomnia, loss of sex drive, inability to concentrate, and loss of a sense of pleasure all return. They begin to remember the euphoria that came with cocaine use, and begin to think about and crave cocaine once more. They are irritable, and feel they have made no progress. At home, they either threaten to leave or are asked to leave.
Once the former cocaine user gets past the “Wall” stage, there is a sense of accomplishment, and a feeling that finally everything will be “normal” again. However, there is a tendency to return to use of alcohol and high-risk situations, even though depression, anxiety, and irritability are reduced.
The final stage, Resolution, comes as the patient shifts from learning new skills to monitoring for signs of relapse, trying to maintain a balanced lifestyle, and developing new interests. Other excessive behaviors, such as gambling, overeating, overworking, and use of alcohol, can also emerge. Patients also begin to challenge the need for long-term monitoring and support.
The 12-month program also includes psychotherapy sessions. Families and patients also have educational sessions during which they learn about the biology of addiction, including brain structure and function, drug tolerance, and the relationship between exercise and endorphins, for example.
Marijuana has been around for at least 8,000 years. At first the hemp plant Cannabis sativa was a crop harvested for rope and textiles. Then, about 3,000 years ago, the Chinese began experimenting with its medicinal effects; in 500 BC, the Greek historian Herodotus documented its psychoactive properties. In the 1960s and 1970s, the drug became a symbol of self-exploration and experimentation among American youth.
Today marijuana use is increasing, particularly among the 18-to-25-year age group. In most areas, primary marijuana users are generally younger than cocaine or heroin users. Results of a survey in six metropolitan areas (Chicago, Denver, Los Angeles, Minneapolis/St. Paul, Philadelphia, and Seattle) showed that the under-17 group account for the highest percentages of admissions for problems related to marijuana. Males outnumber females by more than two to one.
To track changes in the prevalence of marijuana use, abuse and dependence in the U.S. between 1991-1992 and 2001-2002, face-to-face interviews were conducted in two large national surveys done 10 years apart. The first was the 1991-1992 National Longitudinal Epidemiologic Survey and the second was the 2001-2002 National Epidemiologic Survey on Alcohol and Related Conditions.
Among the adult population, the prevalence of marijuana use remained stable, at about 4%. In contrast, the prevalence of DSM-IV marijuana abuse or dependence significantly increased between 1991 and 1992. The greatest increases were reported among young Black men and women and young Hispanic men. Further, marijuana use disorders increased significantly in the absence of increased frequency and quantity of marijuana use, suggesting that the increase in potency of its addictive component, delta-9-tetrahydrocannabinol, or THC.
THC may have contributed to the rising rates. Despite the stability of the overall prevalence of use of marijuana, more adults had a marijuana use disorder in 2001-2002 than in 1991-1992. Increases in use disorders were highest among young Black men and women and young Hispanic men. Minority youth thus seem to be at highest risk.
Marijuana can be eaten or smoked. One popular use is mixing marijuana with cigar tobacco, as a “blunt” or “vega,” taking its name from the original cigar brand name. The strong cigar smell also serves to hide the telltale odor of marijuana.
Few substances have raised more debate than marijuana. Proponents feel that the drug is harmless, and perhaps even beneficial, particularly for several medical conditions. Some of its medical benefits have included relieving nausea among cancer chemotherapy patients, reducing intraocular pressure in persons with glaucoma, and aiding bronchodilation in asthmatic patients.
People who treat patients with substance abuse usually have a very different view of marijuana. To them, it is a “gateway drug.” That is, casual social use of marijuana may eventually lead to use of ever-stronger drugs, in search of an ever-greater “high.” In 1992, the National Institutes of Health switched marijuana from a Schedule II controlled substance (available for treatment of some conditions) to a Schedule I (prohibited) substance.
Marijuana, hashish, and hashish oil are all derived from C. sativa. Marijuana is the dried, crushed flowers and leaves of some varieties of the cannabis plant. Cannabis, which grows well in nearly all parts of the world, is a complex powerhouse of multiple chemicals. For example, the typical marijuana “joint” contains 60 separate chemical components, or cannabinoids. The most important is THC.
THC, first isolated by Israeli scientists in 1964, is the most psychoactive cannabinoid and, the chemical that contains the drug’s mind-altering properties. THC has an extremely long half-life, at least 30 days. When radioactive tracking methods are used to trace the course of cannabinoids in the body, cannabis has been detected as long as four weeks after the last marijuana cigarette was smoked.
Inhalation from smoking is the most common route of administration, but cannabinoids may also be chewed, brewed in tea, or baked in foods such as brownies. Smoking delivers about 50% of absorbable THC to the bloodstream, and peak plasma levels are reached within 70 minutes. The level then declines in an hour, and subjective effects disappear after six hours. When marijuana is eaten, about one-third less THC is delivered to the blood than with smoking, and the effects disappear 30 to 120 minutes after ingestion. From the bloodstream, THC either enters cells, remains bound to plasma proteins, or is deposited in fat, where it can be detected two to three weeks later. The half-life of THC in plasma is about two days.
Marijuana acts as a stimulant, sedative, and, at high dosages, a hallucinogenic. The most notable effects are reported in the central nervous system and cardiovascular system. Marijuana is a relaxant that causes a feeling of well-being or euphoria that is dose-related. Users have a sense of pleasure, a dreamy and carefree state of relaxation, and changes in sensory perception. This pleasant state can then give way to periods of anxiety and confusion, with hallucination-like “flashbacks,” loss of insight, and marked cognitive impairment.
Hallucinations and fantasies associated with high-THC doses can cause distorted body image, loss of personal identity, and sensory and mental illusions. Getting “high” impairs the psychomotor skills needed for complex motor and cognitive functions such as driving and processing information. The usual post-intoxication period is marked by calmness, clarity of mind, a ravenous appetite, and restful sleep.
Most casual users wouldn’t suspect that, along with altering their sense of reality, marijuana can change the structure of brain cells. A New Orleans researcher, Dr. Robert Mann of Tulane University, uncovered a striking pattern among persons who smoked marijuana and who did not take other drugs. These persons had what was termed an “amotivational syndrome,” or a dropout mentality with abnormally long periods of irritability and hostility, abrupt mood swings, and impaired short-term memory. Some of Dr. Mann’s patients had panic attacks and were diagnosed as paranoid.
Studies in laboratory monkeys subsequently showed brain cell atrophy, and cellular damage, particularly in areas that govern memory; such as the hippocampus and the amygdala, areas that also correlate with negative emotions such as irritability and hostility. Another researcher, Dr. John P. McGahan at the University of California at Los Angeles, used computed tomography to investigate results in laboratory studies with monkeys given THC doses equivalent to that of a human smoking one joint a day for three to five years. The atropic changes he found were in the frontal portion of the brain, in the caudate nucleus, a center that helps regulate the neurotransmitter content of the cerebral cortex. This area is rich in dopamine, a neurotransmitter that is involved in brain arousal and muscle coordination and movement.
It is a rare patient who comes in for treatment of acute marijuana use. Instead, routine drug screening (see later section) is the most common way that marijuana use and abuse is detected. Even then, false-positive results can be problematic; for example, passive inhalation of marijuana smoke at a party may produce a positive result on urine screening.
Many users develop tolerance to many of the effects of the cannabinoids. To obtain the euphoria they seek, they must increase the doses and frequency of smoking or eating marijuana. Marijuana can cause mild physical dependence and a withdrawal syndrome of irritability, restlessness, nervousness, loss of appetite, weight loss, insomnia, rebound increase in rapid-eye-movement (REM) sleep, fever, chills, and tremors. These symptoms can appear as soon as a few hours after smoking the drug and can last up to four or five days. Chronic and periodic marijuana users often crave the euphoria of the drug, probably due to the effect of THC-induced neuroadaptations in the brain.
Marijuana is also used in combination with other substances, particularly alcohol and crack cocaine (“oolies,” “diablitos,” or “primos”), and sometimes with phencyclidine (PCP), a strongly hallucinogenic drug (“dream team” or “love boat”). Alcohol is the most common companion drug to marijuana.
Just as with other types of drug use and abuse, denial can interfere with treatment. Teenage and young adult populations, particularly, may feel that marijuana helps them cope with life stresses, improves their self-image, and gives them individuality. It seems helpful, not harmful. For acute reactions, such as panic attacks, drug toxicity, flashbacks, and hysterical reactions, clinicians often use a quiet room with a “talk-down” approach without physical restraints. Low doses of an anxiolytic drug, such as 10-50 mg of chlordiazepoxide, may be used in severe cases. Marijuana can also trigger LSD-like flashbacks, which usually last only a few minutes. Reassurance and anxiolytics will usually suffice in such cases. If, however, these severe reactions occur six months or more after the patient has abstained from smoking or ingesting marijuana, further psychiatric and neurologic evaluations are indicated.
The greatest barrier to successful treatment is the craving for the drug. Because withdrawal symptoms may not occur for a week after marijuana use, many people may find it hard to associate them with marijuana. The addiction cycle often occurs at this time because the person craves marijuana but doesn’t associate this with stopping smoking. Educating the person about symptoms and the time course of withdrawal helps somewhat.
HEROIN: Rapid & Highly Addictive
Heroin is an illegal, highly addictive drug. It is both the most widely abused and the most rapid-acting of the opiates. Heroin is processed from morphine, a naturally occurring substance extracted for the seed pod of specific varieties of poppy plants. It is typically sold as a white or brownish power or as the black sticky substance known on the streets as “black tar heroin.” According to the 2003 National Survey on Drug use and Health (which may actually underestimate illicit opiate use), an estimated 3.7 million people had used heroin at some time in their lives and more than 119,000 of them reported using it in the month before the survey was taken. The group with the highest number of users had a mean age of 26 years or older.
Dr. Nora D. Voldrow, Director of the National Institute on Drug Abuse, has written, “Although heroin abuse has tended downward during the past several years, its prevalence is still higher than in the early 1990s. The relatively high rate of abuse, especially among school age youth and the glamorization of heroin in music and films makes it imperative that the public has the latest scientific information on this topic. Heroin is also increasing in purity and decreasing in price, which makes it an attractive option for young people.”
A scientist at Bayer Pharmaceuticals in Elberfeld, Germany, created heroin as a medicine 11 days after he invented aspirin. From 1898 through 1910, heroin was marketed as a non-addictive morphine substitute and cough medicine for children. Bayer marketed heroin as a “cure” for morphine addiction before it was discovered that heroin is converted to morphine in the liver—this became a landmark historical blunder for the drug company. In 1924, the U.S. Congress passed legislation banning the sale, importation, or manufacture of heroin in the U.S. Internationally, heroin is controlled under Schedules I and IV of the Single Convention on Narcotic Drugs and it is illegal to manufacture, sell, or possess heroin in the U.S. Under the name diamorphine, heroin can be legally prescribed in the United Kingdom.
Heroin produces an intense euphoria, which often disappears with increasing tolerance. Heroin very rapidly penetrates the blood-brain barrier after use. It can be taken in a number of ways, including snorting, injecting, smoking it by inhaling the vapors produced when it is heated from below (“chasing the dragon”), and inserting it anally.
Typically, a heroin abuser may inject the drug up to four times a day. Intravenous injection produces the greatest intensity and most rapid onset of euphoria-from 7 to 8 seconds, while intramuscular injection produces a relatively slow onset of euphoria—5 to 8 minutes. When heroin is sniffed or smoked, peak effects are usually felt within 10 to 15 minutes.
Once in the brain, heroin is rapidly metabolized into morphine by removal of the acetyl groups. The morphine molecule then binds with opioid receptors and produces the subjective effects of the heroin high. Abusers report feeling a surge or pleasurable sensation, or the “rush.” The intensity of the rush is a function of how much drug is taken and how rapidly the drug enters the brain and binds to the natural opiate receptors. The drug is particularly addictive because it enters the brain so quickly. The rush is usually accompanied by warm flushing to the skin, dry mouth, and a heavy feeling in the arms and legs, which may be accompanied by nausea, vomiting, and severe itching. Then drowsiness sets in for several hours. Heroin’s effects on the central nervous system cloud mental function; breathing is also severely slowed, which sometimes leads to death. The body responds to heroin in the brain by reducing and sometimes stopping production of the endogenous opioids when heroin is present. Normally endorphins are regularly released in the brain and nerves and ease pain. This reduced production of endorphins in heroin users creates a dependence on the drug. When use of the drug is stopped, users have extreme symptoms, including pain even in the absence of any injury. This set of symptoms is called the withdrawal syndrome.
The withdrawal syndrome from heroin (or any other short-acting opioid) can begin within 6 hours after the last dose, and is characterized by sweating, malaise, depression, persistent and intense erections in men (priapism), a general feeling of heaviness, cramp-like pains in the limbs, yawning and tearing, sleep difficulties, cold sweats, chills, and severe muscle aches. Many addicts also complain of a painful condition, the so-called “itchy blood,” which results in compulsive scratching, bruising, and sometimes tearing of the skin, leaving scabs. Abrupt termination of heroin use causes muscle spasms in the legs (restless leg syndrome), which may explain the origin of the term “kicking the habit.” A heroin overdose is not fast-acting; stories about people who “OD with the needle still in their arm” are not attributable to heroin overdoses. Instead, these rapid deaths result from a fatal reaction with materials used as filler with the heroin. One of the hazards of street heroin is that it can contain unsuspected filler materials, which can be cornstarch, sugar, flour, or quinine, for example.
Heroin users are also at increased risk of contracting HIV/AIDS, hepatitis C (HVC), and other infectious diseases through sharing and reuse of syringes and injection paraphernalia that have been used by infected persons, or though unprotected sex with an infected person. Injection drug users represent the group at the highest risk of acquiring HVC infection: an estimated 70 to 80% of the 35,000 new HCV cases that occur in the U.S. each year are among intravenous drug users.