Let’s imagine a day in the life of a legal drug user. It begins with a wake-up latte. By midday, several cigarettes have calmed frazzled nerves before an appointment at the plastic surgeon’s office for wrinkle-smoothing Botox injections. A diet pill before dinner helps stem the appetite, and its stimulating effects can later be partially offset with a glass of wine or two Advil PMs. And if performance needs enhancing, there are beta blockers for onstage performers, Viagra for middle-aged men, hormone-delivering “libido patches” for middle-aged women, and Adderall for students hoping to focus their concentration.

3-12 What are substance use disorders, and what roles do tolerance, withdrawal, and addiction play in these disorders?

Most of us manage to use some nonprescription drugs in moderation and without disrupting our lives. But some of us develop a self-harming substance use disorder (TABLE 3.3). Such substances are psychoactive drugs, chemicals that change perceptions and moods. A drug’s overall effect depends not only on its biological effects but also on the user’s expectations, which vary with social and cultural contexts (Ward, 1994). If one culture assumes that a particular drug produces euphoria (or aggression or sexual arousal) and another does not, each culture may find its expectations fulfilled. We’ll take a closer look at these interacting forces in the use and potential abuse of particular psychoactive drugs. But first, let’s consider how our bodies react to the ongoing use of psychoactive drugs.

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Why might a person who rarely drinks alcohol get buzzed on one can of beer while a long-term drinker shows few effects until the second six-pack? The answer is tolerance. With continued use of alcohol and some other drugs (not marijuana), the user’s brain chemistry adapts to offset the drug effect (a process called neuroadaptation). To experience the same effect, the user requires larger and larger doses (FIGURE 3.20). Ever-increasing doses of most psychoactive drugs may lead to addiction: The person craves and uses the substance despite its adverse consequences. (See Thinking Critically About: Addiction.) The World Health Organization (2008) has reported that, worldwide, 90 million people suffer from such problems related to alcohol and other drugs. Regular users often try to fight their addiction, but abruptly stopping the drug may lead to the undesirable side effects of withdrawal.

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The three major categories of psychoactive drugs are depressants, stimulants, and hallucinogens. All do their work at the brain’s synapses, stimulating, inhibiting, or mimicking the activity of the brain’s own chemical messengers, the neurotransmitters.

3-14 What are depressants, and what are their effects?

Depressants are drugs such as alcohol, barbiturates (tranquilizers), and opiates that calm neural activity and slow body functions.

Alcohol True or false? In small amounts, alcohol is a stimulant. False. Low doses of alcohol may, indeed, enliven a drinker, but they do so by acting as a disinhibitor—they slow brain activity that controls judgment and inhibitions. Alcohol is an equal-opportunity drug: It increases (disinhibits) helpful tendencies—as when tipsy restaurant patrons leave extravagant tips and social drinkers bond in groups (Hirsch et al., 2011; Lynn, 1988; Sayette et al., 2012). And it increases harmful tendencies, as when sexually aroused men become more disposed to sexual aggression. One University of Illinois campus survey showed that before sexual assaults, 80 percent of the male assailants and 70 percent of the female victims had been drinking (Camper, 1990). Another survey of 89,874 American collegians found alcohol or drugs involved in 79 percent of unwanted sexual intercourse experiences (Presley et al., 1997). When drinking, both men and women are more disposed to casual sex (Garcia et al., 2012; Rehm et al., 2012). “Beauty is in the eyes of the beer holder.” The bottom line: The urges you would feel if sober are the ones you will more likely act upon when intoxicated.

SLOWED NEURAL PROCESSING Low doses of alcohol relax the drinker by slowing sympathetic nervous system activity. Larger doses cause reactions to slow, speech to slur, and skilled performance to deteriorate. Paired with sleep deprivation, alcohol is a potent sedative. Add these physical effects to lowered inhibitions, and the result can be deadly. Worldwide, several hundred thousand lives are lost each year in alcohol-related accidents and violent crime. As blood-alcohol levels rise and judgment falters, people’s qualms about drinking and driving lessen. In experiments, virtually all drinkers who had insisted when sober that they would not drive under the influence later decided to drive home from a bar, even if given a breathalyzer test and told they were intoxicated (Denton & Krebs, 1990; MacDonald et al., 1995). Alcohol can be life threatening when heavy drinking follows an earlier period of moderate drinking, which depresses the vomiting response. People may poison themselves with an overdose that their bodies would normally throw up.

MEMORY DISRUPTION Alcohol can disrupt memory formation, and heavy drinking can also have long-term effects on the brain and cognition. In rats, at a developmental period corresponding to human adolescence, binge drinking contributes to nerve cell death and reduces the birth of new nerve cells. It also impairs the growth of synaptic connections (Crews et al., 2006, 2007). In humans, heavy drinking may lead to blackouts, in which drinkers are unable to recall people they met the night before or what they said or did while intoxicated. These blackouts result partly from the way alcohol suppresses REM sleep, which helps fix the day’s experiences into permanent memories.

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The prolonged and excessive drinking that characterizes alcohol use disorder can shrink the brain (FIGURE 3.21). Women, who have less of a stomach enzyme that digests alcohol, are especially vulnerable (Wuethrich, 2001). Girls and young women can become addicted to alcohol more quickly than boys and young men do, and they are at risk for lung, brain, and liver damage at lower consumption levels (CASA, 2003).

REDUCED SELF-AWARENESS AND SELF-CONTROL In one experiment, those who consumed alcohol (rather than a placebo beverage) were doubly likely to be caught mind wandering during a reading task, yet were less likely to notice that they zoned out (Sayette et al., 2009). Alcohol not only reduces self-awareness, it also produces a sort of “myopia” by focusing attention on an arousing situation (say, provocation) and distracting it from normal inhibitions and future consequences (Giancola et al., 2010; Steele & Josephs, 1990).

Reduced self-awareness may help explain why people who want to suppress their awareness of failures or shortcomings are more likely to drink than are those who feel good about themselves. Losing a business deal, a game, or a romantic partner sometimes elicits a drinking binge.

EXPECTANCY EFFECTS As with other psychoactive drugs, expectations influence behavior. When people believe that alcohol affects social behavior in certain ways, and believe they have been drinking alcohol, they will behave accordingly (Moss & Albery, 2009). In a now-classic experiment, researchers gave Rutgers University men (who had volunteered for a study on “alcohol and sexual stimulation”) either an alcoholic or a nonalcoholic drink (Abrams & Wilson, 1983). (Both had strong tastes that masked any alcohol.) In each group, half the participants thought they were drinking alcohol and half thought they were not. After watching an erotic movie clip, the men who thought they had consumed alcohol were more likely to report having strong sexual fantasies and feeling guilt free. Being able to attribute their sexual responses to alcohol released their inhibitions—whether or not they had actually consumed any alcohol.

So, alcohol’s effect lies partly in that powerful sex organ, the mind. Fourteen “intervention studies” have educated college drinkers about that very point (Scott-Sheldon, et al., 2014). Most participants have come away with lower positive expectations of alcohol and have reduced their drinking the ensuing month.

Barbiturates Like alcohol, the barbiturate drugs, or tranquilizers, depress nervous system activity. Barbiturates such as Nembutal, Seconal, and Amytal are sometimes prescribed to induce sleep or reduce anxiety. In larger doses, they can impair memory and judgment. If combined with alcohol—as sometimes happens when people take a sleeping pill after an evening of heavy drinking—the total depressive effect on body functions can be lethal.

Opiates The opiates—opium and its derivatives—also depress neural functioning. When using the opiates, which include heroin, pupils constrict, breathing slows, and lethargy sets in as blissful pleasure replaces pain and anxiety. For this short-term pleasure, opiate users may pay a long-term price: a gnawing craving for another fix, a need for progressively larger doses (as tolerance develops), and the extreme discomfort of withdrawal. When repeatedly flooded with an artificial opiate, the brain eventually stops producing endorphins, its own opiates. If the artificial opiate is then withdrawn, the brain lacks the normal level of these painkilling neurotransmitters. Those who cannot or choose not to tolerate this state may pay an ultimate price—death by overdose. Opiates include the narcotics, such as codeine and morphine (and the synthetic methadone, a heroin substitute), which physicians may prescribe for pain relief and which can also lead to addiction.

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3-15 What are stimulants, and what are their effects?

A stimulant excites neural activity and speeds up body functions. Pupils dilate, heart and breathing rates increase, and blood sugar levels rise, causing a drop in appetite. Energy and self-confidence also rise.

Stimulants include caffeine, nicotine, the amphetamines, cocaine, methamphetamine (“speed”), and Ecstasy. People use stimulants to feel alert, lose weight, or boost mood or athletic performance. Unfortunately, stimulants can be addictive, as you may know if you are one of the many who use caffeine daily in your coffee, tea, soda, or energy drinks. Cut off from your usual dose, you may crash into fatigue, headaches, irritability, and depression (Silverman et al., 1992). A mild dose of caffeine typically lasts three or four hours, which—if taken in the evening—may be long enough to impair sleep.

Nicotine Cigarettes and other tobacco products deliver highly addictive nicotine. Imagine that cigarettes were harmless—except, once in every 25,000 packs, an occasional innocent-looking one is filled with dynamite instead of tobacco. Not such a bad risk of having your head blown off. But with 250 million packs a day consumed worldwide, we could expect more than 10,000 gruesome daily deaths (more than three times the 9/11 fatalities each and every day)—surely enough to have cigarettes banned everywhere.²

The lost lives from these dynamite-loaded cigarettes approximate those from today’s actual cigarettes. A teen-to-the-grave smoker has a 50 percent chance of dying from the habit, and each year, tobacco kills nearly 5.4 million of its 1.3 billion customers worldwide. (Imagine the outrage if terrorists took down an equivalent of 25 loaded jumbo jets today, let alone tomorrow and every day thereafter.) By 2030, annual deaths are expected to increase to 8 million. That means that 1 billion twenty-first-century people may be killed by tobacco (WHO, 2012).

Smoke a cigarette and nature will charge you 12 minutes—ironically, just about the length of time you spend smoking it (Discover, 1996). Compared with nonsmokers, smokers’ life expectancy is “at least 10 years shorter” (CDC, 2013). Eliminating smoking would increase life expectancy more than any other preventive measure. Why, then, do so many people smoke?

Those drawn to nicotine find it very hard to quit, because tobacco products are powerfully and quickly addictive. Attempts to quit even within the first weeks of smoking often fail (DiFranza, 2008). As with other addictions, smokers develop tolerance, and quitting causes withdrawal symptoms, including craving, insomnia, anxiety, irritability, and distractibility. Nicotine-deprived smokers trying to focus on a task experience a tripled rate of mind wandering (Sayette et al., 2010). When not craving a cigarette, they tend to underestimate the power of such cravings (Sayette et al., 2008).

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All it takes to relieve this aversive state is a single puff on a cigarette. Within 7 seconds, a rush of nicotine signals the central nervous system to release a flood of neurotransmitters (FIGURE 3.22). Epinephrine and norepinephrine diminish appetite and boost alertness and mental efficiency. Dopamine and opioids temporarily calm anxiety and reduce sensitivity to pain (Ditre et al., 2011; Scott et al., 2004). Thus, ex-smokers will sometimes, under stress, return to smoking—as did some 1 million Americans after the 9/11 terrorist attacks (Pesko, 2014).

These rewards keep people smoking, even among the 3 in 4 smokers who wish they could stop (Newport, 2013). Each year, fewer than 1 in 7 smokers who want to quit will be able to resist. Even those who know they are committing slow-motion suicide may be unable to stop (Saad, 2002).

Nevertheless, repeated attempts seem to pay off. Half of all Americans who have ever smoked have quit, sometimes aided by a nicotine replacement drug and with encouragement from a counselor or support group. Success is equally likely whether smokers quit abruptly or gradually (Fiore et al., 2008; Lichtenstein et al., 2010; Lindson et al., 2010). For those who endure, the acute craving and withdrawal symptoms gradually dissipate over the ensuing six months (Ward et al., 1997). After a year’s abstinence, only 10 percent will relapse in the next year (Hughes, 2010). These nonsmokers may live not only healthier but also happier lives. Smoking correlates with higher rates of depression, chronic disabilities, and divorce (Doherty & Doherty, 1998; Edwards & Kendler, 2012; Vita et al., 1998). Healthy living seems to add both years to life and life to years.

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CocaineCocaine use offers a fast track from euphoria to crash. The recipe for Coca-Cola originally included an extract of the coca plant, creating a cocaine tonic for tired elderly people. Between 1896 and 1905, Coke was indeed “the real thing.” But no longer. Cocaine is now snorted, injected, or smoked. It enters the bloodstream quickly, producing a rush of euphoria that depletes the brain’s supply of the neurotransmitters dopamine, serotonin, and norepinephrine (FIGURE 3.23). Within the hour, a crash of agitated depression follows as the drug’s effect wears off.

In situations that trigger aggression, ingesting cocaine may heighten reactions. Caged rats fight when given foot shocks, and they fight even more when given cocaine and foot shocks. Likewise, humans who voluntarily ingest high doses of cocaine in laboratory experiments impose higher shock levels on a presumed opponent than do those receiving a placebo (Licata et al., 1993). Cocaine use may also lead to emotional disturbances, suspiciousness, convulsions, cardiac arrest, or respiratory failure.

In national surveys, 3 percent of U.S. high school seniors and 6 percent of British 18- to 24-year-olds reported having tried cocaine during the past year (ACMD, 2009; Johnston et al., 2014). Nearly half had smoked crack, a faster-working crystallized form of cocaine that produces a briefer but more intense high, followed by a more intense crash. After several hours, the craving for more wanes, only to return several days later (Gawin, 1991).

Cocaine’s psychological effects depend in part on the dosage and form consumed, but the situation and the user’s expectations and personality also play a role. Given a placebo, cocaine users who thought they were taking cocaine often had a cocaine-like experience (Van Dyke & Byck, 1982).

Methamphetamine Methamphetamine is chemically related to its parent drug, amphetamine (NIDA, 2002, 2005) but has greater effects. Methamphetamine triggers the release of the neurotransmitter dopamine, which stimulates brain cells that enhance energy and mood, leading to eight hours or so of heightened energy and euphoria. Its aftereffects may include irritability, insomnia, hypertension, seizures, social isolation, depression, and occasional violent outbursts (Homer et al., 2008). Over time, methamphetamine may reduce baseline dopamine levels, leaving the user with continuing depressed functioning.

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Ecstasy Ecstasy, a street name for MDMA (methylenedioxymetham-phetamine, also known in its powder form as “Molly”), is both a stimulant and a mild hallucinogen. As an amphetamine derivative, Ecstasy triggers dopamine release, but its major effect is releasing stored serotonin and blocking its reuptake, thus prolonging serotonin’s feel-good flood (Braun, 2001). Users feel the effect about a half-hour after taking an Ecstasy pill. For three or four hours, they experience high energy, emotional elevation, and (given a social context) connectedness with those around them (“I love everyone”).

During the 1990s, Ecstasy’s popularity soared as a “club drug” taken at nightclubs and all-night dance parties (Landry, 2002). The drug’s popularity crosses national borders, with an estimated 60 million tablets consumed annually in Britain (ACMD, 2009). There are, however, reasons not to be ecstatic about Ecstasy. One is its dehydrating effect, which—when combined with prolonged dancing—can lead to severe overheating, increased blood pressure, and death. Another is that long-term, repeated leaching of brain serotonin can damage serotonin-producing neurons, leading to decreased output and increased risk of permanently depressed mood (Croft et al., 2001; McCann et al., 2001; Roiser et al., 2005). Ecstasy also suppresses the disease-fighting immune system, impairs memory, slows thought, and disrupts sleep by interfering with serotonin’s control of the circadian clock (Laws & Kokkalis, 2007; Schilt et al., 2007; Wagner et al., 2012). Ecstasy delights for the night but dispirits the morrow.

3-16 What are hallucinogens, and what are their effects?

Hallucinogens distort perceptions and evoke sensory images in the absence of sensory input (which is why these drugs are also called psychedelics, meaning “mind-manifesting”). Some, such as LSD and MDMA (Ecstasy), are synthetic. Others, including the mild hallucinogen marijuana, are natural substances.

Whether provoked to hallucinate by drugs, loss of oxygen, or extreme sensory deprivation, the brain hallucinates in basically the same way (Siegel, 1982). The experience typically begins with simple geometric forms, such as a lattice, cobweb, or spiral. The next phase consists of more meaningful images; some may be superimposed on a tunnel or funnel, others may be replays of past emotional experiences. As the hallucination peaks, people frequently feel separated from their body and experience dreamlike scenes so real that they may become panic-stricken or harm themselves.

These sensations are strikingly similar to the near-death experience, an altered state of consciousness reported by about 10 to 15 percent of patients revived from cardiac arrest (Agrillo, 2011; Greyson, 2010; Parnia et al., 2013). Many describe visions of tunnels (FIGURE 3.24), bright lights or beings of light, a replay of old memories, and out-of-body sensations (Siegel, 1980). Given that oxygen deprivation and other insults to the brain are known to produce hallucinations, it is difficult to resist wondering whether a brain under stress manufactures the near-death experience. During epilepsy seizures and migraines, patients may experience similar hallucinations of geometric patterns (Billock & Tsou, 2012). So have solitary sailors and polar explorers while enduring monotony, isolation, and cold (Suedfeld & Mocellin, 1987). Such experiences represent “neural funny business,” surmises philosopher-neuroscientist Patricia Churchland (2013, p. 70; Zuger, 2013).

LSD Albert Hofmann, a chemist, created—and on one Friday afternoon in April 1943 accidentally ingested—LSD (lysergic acid diethylamide). The result—“an uninterrupted stream of fantastic pictures, extraordinary shapes with intense, kaleidoscopic play of colors”—reminded him of a childhood mystical experience that had left him longing for another glimpse of “a miraculous, powerful, unfathomable reality” (Siegel, 1984; Smith, 2006). The user’s current mood and expectations color the emotional experience, which may vary from euphoria to detachment to panic.

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Marijuana Marijuana leaves and flowers contain THC (delta-9-tetrahydrocannabinol). Whether smoked (getting to the brain in about 7 seconds) or eaten (causing its peak concentration to be reached at a slower, unpredictable rate), THC produces a mix of effects. Synthetic marijuana (“K2,” also called “Spice”) mimics THC. Its harmful side effects, which can include agitation and hallucinations, led to its ingredient becoming illegal under the U.S. Synthetic Drug Abuse Prevention Act of 2012.

Marijuana is a mild hallucinogen, amplifying sensitivity to colors, sounds, tastes, and smells. But like alcohol, marijuana relaxes, disinhibits, and may produce a euphoric high. Both alcohol and marijuana impair the motor coordination, perceptual skills, and reaction time necessary for safely operating an automobile or other machine. “THC causes animals to misjudge events,” reported Ronald Siegel (1990, p. 163). “Pigeons wait too long to respond to buzzers or lights that tell them food is available for brief periods; and rats turn the wrong way in mazes.”

Marijuana and alcohol also differ. The body eliminates alcohol within hours. THC and its by-products linger in the body for more than a week, which means that regular users experience less abrupt withdrawal and may achieve a high with smaller than usual drug amounts. This is unlike typical tolerance, in which repeat users need to take larger doses to feel the same effect.

A marijuana user’s experience can vary with the situation. If the person feels anxious or depressed, marijuana may intensify the feelings. The more often the person uses marijuana, especially during adolescence, the greater the risk of anxiety, depression, or addiction (Bambico et al., 2010; Hurd et al., 2013; Murray et al., 2007).

Marijuana also disrupts memory formation and interferes with immediate recall of information learned only a few minutes before (Bossong et al., 2012). Such cognitive effects outlast the period of smoking (Messinis et al., 2006). Heavy adult use for over 20 years is associated with a shrinkage of brain areas that process memories and emotions (Yücel et al., 2008). One study, which has tracked more than 1000 New Zealanders from birth, found that the IQ scores of persistent teen marijuana users dropped eight points from age 13 to 38 (Meier et al., 2012). (This mental decline was seen only in those who started regular use before age 18, while their brains were still rapidly developing.) Prenatal exposure through maternal marijuana use impairs brain development (Berghuis et al., 2007; Huizink & Mulder, 2006).

To free up resources to fight crime, some states and countries have passed laws legalizing the possession of small quantities of marijuana. In some cases, legal medical marijuana use has been granted to relieve the pain and nausea associated with diseases such as AIDS and cancer (Munsey, 2010; Watson et al., 2000). In such cases, the Institute of Medicine recommends delivering the THC with medical inhalers. Marijuana smoke, like cigarette smoke, is toxic and can cause cancer, lung damage, and pregnancy complications (BLF, 2012).

***

Despite their differences, the psychoactive drugs summarized in TABLE 3.4 below share a common feature: They trigger negative aftereffects that offset their immediate positive effects and grow stronger with repetition. And that helps explain both tolerance and withdrawal. As the opposing, negative aftereffects grow stronger, it takes larger and larger doses to produce the desired high (tolerance), causing the after-effects to worsen in the drug’s absence (withdrawal). This in turn creates a need to switch off the withdrawal symptoms by taking yet more of the drug.

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3-17 Why do some people become regular users of consciousness-altering drugs?

Drug use by North American youth increased during the 1970s. Then, with increased drug education and a more realistic and deglamorized media depiction of taking drugs, drug use declined sharply (except for a small rise in the mid-1980s). After the early 1990s, the cultural antidrug voice softened, and some drugs for a time were again glamorized in music and films. Consider, for example, historical trends in the use of marijuana:

For some adolescents, occasional drug use represents thrill seeking. Why, though, do others become regular drug users? In search of answers, researchers have engaged biological, psychological, and social-cultural levels of analysis.

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Some people may be biologically vulnerable to particular drugs. For example, evidence accumulates that heredity influences some aspects of substance use problems, especially those appearing by early adulthood (Crabbe, 2002):

Biological influences on drug use extend to other drugs as well. One study tracked 18,115 Swedish adoptees. Those with drug-abusing biological parents were at doubled risk of drug abuse, indicating a genetic influence. But then those with drug-abusing adoptive siblings also had a doubled risk of drug abuse, indicating an environmental influence (Kendler et al., 2012). Let’s next see what those environmental influences might be.

Throughout this text, you will see that biological, psychological, and social-cultural factors interact to produce behavior. So, too, with disordered drug use (FIGURE 3.26 below). One psychological factor that has appeared in studies of youth and young adults is the feeling that life is meaningless and directionless (Newcomb & Harlow, 1986). This feeling is common among school dropouts who subsist without job skills, without privilege, and with little hope.

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Sometimes the psychological influence is obvious. Many heavy users of alcohol, marijuana, and cocaine have experienced significant stress or failure and are depressed. Girls with a history of depression, eating disorders, or sexual or physical abuse are at risk for substance addiction. So are youth undergoing school or neighborhood transitions (CASA, 2003; Logan et al., 2002). Collegians who have not yet achieved a clear identity are also at greater risk (Bishop et al., 2005). By temporarily dulling the pain of self-awareness, psychoactive drugs may offer a way to avoid coping with depression, anger, anxiety, or insomnia. (As Chapter 7 explains, behavior is often controlled more by its immediate consequences than by its later ones.)

Smoking usually begins during early adolescence. (If you are in college or university, and the cigarette manufacturers haven’t yet made you their devoted customer, they almost surely never will.) Adolescents, self-conscious and often thinking the world is watching their every move, are vulnerable to smoking’s allure. They may first light up to imitate glamorous celebrities, to project a mature image, to handle stress, or to get the social reward of being accepted by other smokers (Cin et al., 2007; Tickle et al., 2006). Mindful of these tendencies, cigarette companies have effectively modeled smoking with themes that appeal to youths: attractiveness, independence, adventurousness, social approval (Surgeon General, 2012). Typically, teens who start smoking also have friends who smoke, who suggest its pleasures and offer them cigarettes (Rose et al., 1999). Among teens whose parents and best friends are nonsmokers, the smoking rate is close to zero (Moss et al., 1992; also see FIGURE 3.27). Most teen drinking is also done for social reasons, not as a way to cope with problems (Kuntsche et al., 2005).

Rates of drug use also vary across cultural and ethnic groups. One survey of 100,000 teens in 35 European countries found that marijuana use in the prior 30 days ranged from zero to 1 percent in Romania and Sweden to 20 to 22 percent in Britain, Switzerland, and France (ESPAD, 2003). Independent U.S. government studies of drug use in households nationwide and among high schoolers in all regions reveal that African-American teens have sharply lower rates of drinking, smoking, and cocaine use (Johnston et al., 2007). Alcohol and other drug addiction rates have also been low among actively religious people, with extremely low rates among Orthodox Jews, Mormons, Mennonites, and the Amish (Salas-Wright et al., 2012; Vaughn et al., 2011; Yeung et al., 2009).

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Whether in cities or rural areas, peers influence attitudes about drugs. They also throw the parties and provide (or don’t provide) the drugs. If an adolescent’s friends use drugs, the odds are that he or she will, too. If the friends do not, the opportunity may not even arise. Teens who come from happy families, who do not begin drinking before age 15, and who do well in school tend not to use drugs, largely because they rarely associate with those who do (Bachman et al., 2007; Hingson et al., 2006; Odgers et al., 2008).

Peer influence is more than what friends do or say. Adolescents’ expectations—what they believe friends are doing and favoring—influence their behavior (Vitória et al., 2009). One study surveyed sixth graders in 22 U.S. states. How many believed their friends had smoked marijuana? About 14 percent. How many of those friends acknowledged doing so? Only 4 percent (Wren, 1999). University students are not immune to such misperceptions: Drinking dominates social occasions partly because students overestimate their fellow students’ enthusiasm for alcohol and underestimate their views of its risks (Prentice & Miller, 1993; Self, 1994) (TABLE 3.5). When students’ overestimates of peer drinking are corrected, alcohol use often subsides (Moreira et al., 2009).

People whose beginning use of drugs was influenced by their peers are more likely to stop using when friends stop or their social network changes (Kandel & Raveis, 1989). One study that followed 12,000 adults over 32 years found that smokers tend to quit in clusters (Christakis & Fowler, 2008). Within a social network, the odds of a person quitting increased when a spouse, friend, or co-worker stopped smoking. Similarly, most soldiers who became drug addicted while in Vietnam ceased their drug use after returning home (Robins et al., 1974).

As always with correlations, the traffic between friends’ drug use and our own may be two-way: Our friends influence us. Social networks matter. But we also select as friends those who share our likes and dislikes.

What do the findings on drug use suggest for drug prevention and treatment programs? Three channels of influence seem possible:

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People rarely abuse drugs if they understand the physical and psychological costs, feel good about themselves and the direction their lives are taking, and are in a peer group that disapproves of using drugs. These educational, psychological, and social-cultural factors may help explain why 26 percent of U.S. high school dropouts, but only 6 percent of those with a postgraduate education, report smoking (CDC, 2011).