Do you rely on caffeine pick-me-ups, such as coffee or energy drinks, to keep you going? Caffeine is usually harmless, though it still qualifies as a psychoactive drug, a chemical substance that changes perceptions and mood. Most of us manage to use some of these substances—even alcohol and painkillers—in moderation, without disrupting our lives. But sometimes, drug use crosses the line between moderation and substance use disorder. This happens when we continue to crave and use a substance that is significantly disrupting our life or putting us at risk physically (TABLE 13.3). Substance use disorders can endanger relationships, job and school performance, caretaking abilities, and our own and others’ safety.

The three major categories of psychoactive drugs are depressants, stimulants, and hallucinogens. All do their work at the brain’s synapses. They stimulate, inhibit, or mimic the activity of the brain’s own chemical messengers, the neurotransmitters. But our reaction to psychoactive drugs depends on more than their biological effects. Psychological influences, including a user’s expectations, and cultural traditions also play a role (Scott-Sheldon et al., 2012; Ward, 1994). If one culture assumes that a particular drug produces good feelings (or aggression or sexual arousal), and another does not, each culture may find its expectations fulfilled. Later, in the discussions of particular drugs, we’ll take a closer look at the interaction of biopsychosocial forces. But first, let’s see 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 (but not marijuana), the user’s brain chemistry adapts to offset the drug’s effect. To experience the same effect, the user requires larger and larger doses (FIGURE 13.2).

Ever-increasing doses of most psychoactive drugs may lead a person to become addicted: The person comes to crave the drug and struggles when attempting to withdraw from it, continuing to use the substance despite harmful consequences. Heavy coffee drinkers who skip their usual caffeine intake know the feeling when a headache or grogginess strikes. For people who become addicted to heroin, prescription painkillers, or other depressants, withdrawal may mean much more than a headache. Worldwide, 90 million people are living with such problems related to alcohol and other drugs (WHO, 2008).

Sometimes even behaviors become compulsive and dysfunctional, much like abusive drug-taking. Estimates of problematic video game playing in Asia, Europe, and North America have ranged from 3 percent to 12 percent (Anderson & Warburton, 2012; Ferguson et al., 2011). One such “behavior addiction” listed in the DSM-5 is gambling disorder, and the DSM-5 proposes Internet gaming disorder “for further study” (American Psychiatric Association, 2013).

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

ALCOHOL True or false? Alcohol is a depressant in large amounts but is a stimulant in small amounts. False. In any amount, alcohol is a depressant—it reduces neural activity and slows body functions.

Slowed neural functions. Low doses of alcohol may, indeed, enliven a drinker, but they do so by acting as a disinhibitor. Alcohol slows activity in a part of the brain that controls judgment and inhibitions. As a result, the urges we would feel if sober are the ones we will more likely act upon when intoxicated. Alcohol is an equal-opportunity drug. It increases helpful tendencies, as when tipsy restaurant patrons leave big tips, or social drinkers bond as a group (Hirsh et al., 2011; Lynn, 1988; Sayette et al., 2012). And it increases harmful tendencies, as when sexually aroused men become more aggressive. When drinking, both men and women are more disposed to casual sex (Garcia et al., 2012).

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Even the belief that we have consumed alcohol can influence our judgment. In one classic experiment (supposedly a study on “alcohol and sexual stimulation”), researchers gave college male volunteers either an alcoholic or a nonalcoholic drink (Abrams & Wilson, 1983). (Both drinks had a strong taste that masked any alcohol.) 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—whether they had actually consumed it or not. When people believe that alcohol affects social behavior in certain ways, and believe that they have been drinking alcohol, they will behave accordingly (Scott-Sheldon et al., 2012). In 14 “intervention studies,” college drinkers who were educated about that point came away with lower positive expectations of alcohol, and they drank less in the following month (Scott-Sheldon et al., 2014).

Alcohol does more than lessen our normal inhibitions, however. It produces a sort of short-sightedness by focusing our attention on arousing situations (perhaps a sexually attractive person or some personal slight). This combination of lowered inhibitions and altered perceptions can reduce self-awareness and distract attention from future consequences (Giancola et al., 2010; Hull & Bond, 1986; Steele & Josephs, 1990).

The point to remember: Alcohol’s effect lies partly in that powerful sex organ, the mind. Expectations influence behavior.

Memory disruption. Sometimes, people drink to forget their troubles—a broken relationship, a lost game, a failed exam. And forget they do. Why? Because alcohol disrupts long-term memory processing. It does so in part by suppressing REM sleep, which helps fix the day’s experiences into permanent memories. Thus, people recovering from a night of heavy drinking may have blackouts—unable to recall who they met the night before, or what they said or did.

Heavy drinking can have long-term effects on the brain. In rats, at a development period corresponding to human adolescence, binge drinking contributes to the death of nerve cells and reduces the birth rates of new nerve cells. It also impairs the growth of synaptic connections (Crews et al., 2006, 2007).

Slowed body functions. Alcohol slows sympathetic nervous system activity. In low doses, it relaxes the drinker. In larger doses, it causes reactions to slow, speech to slur, and skilled performance to decline.

Paired with lack of sleep, 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. When sober, most drinkers believe that driving under the influence of alcohol is wrong, and they insist they would not do so. That belief disappears as blood-alcohol level rises and judgments become fuzzy. Most will drive home from a bar, even if given a Breathalyzer test and told they are intoxicated (Denton & Krebs, 1990; MacDonald et al., 1995).

Alcohol can be life threatening when heavy drinking follows an earlier period of moderate drinking, which suppresses the vomiting response. People may poison themselves with an overdose their body would normally throw up.

Alcohol use disorder. Alcoholism is the popular name for alcohol use disorder. Its symptoms are tolerance, withdrawal, and a drive to continue using alcohol despite significant problems associated with that use. Girls and young women are especially vulnerable because they have less of a stomach enzyme that digests alcohol (Wuethrich, 2001). They can become addicted to alcohol more quickly than boys and young men. They also suffer lung, brain, and liver damage at lower consumption levels (CASA, 2003) (FIGURE 13.3).

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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, the total depressive effect on body functions can lead to death. This sometimes happens when people take a sleeping pill after an evening of heavy drinking.

OPIATESThe opiates—opium and its offshoots—also depress nervous system activity. Opiates include heroin and also medically prescribed pain-relief narcotics, such as codeine, morphine, and methadone (a synthetic opiate sometimes prescribed as a heroin substitute). As pleasure replaces pain and anxiety, the user’s pupils constrict, breathing slows, and lethargy (a feeling of extreme relaxation and a lack of energy) sets in. Those who become addicted to this short-term pleasure 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 feel-good opiates. If the artificial opiate is then withdrawn, the brain will lack the normal level of these natural painkillers. Those who cannot or choose not to endure this state may pay an ultimate price—death by overdose.

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

Stimulants include caffeine, nicotine, and the more powerful cocaine, amphetamines, methamphetamine, 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 enough to impair sleep.

NICOTINEOne of the most addictive stimulants is nicotine, found in cigarettes, e-cigarettes, and other tobacco products. Are tobacco products at least as addictive as heroin and cocaine? Yes (see TABLE 13.4). Attempts to quit even within the first weeks of smoking often fail (DiFranza, 2008). And, as with other addictions, smokers develop tolerance. Those who attempt to quit will experience nicotine-withdrawal symptoms—craving, insomnia, anxiety, irritability, and distractibility. When trying to focus on a task, their mind wanders at three times the normal rate (Sayette et al., 2010). And to make all this go away, all it takes is a single puff on a cigarette—a portable nicotine dispenser.

Source: National Academy of Science, Institute of Medicine (Brody, 2003).

Within 7 seconds (twice as fast as intravenous heroin), a rush of nicotine will signal the central nervous system to release a flood of neurotransmitters (FIGURE 13.4). Epinephrine and norepinephrine will diminish appetite and boost alertness and mental efficiency. Dopamine and opioids will calm anxiety and reduce sensitivity to pain (Ditre et al., 2011; Gavin, 2004). No wonder some ex-smokers, under stress, return to smoking. Some 1 million Americans did so 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, 2013b). Each year, fewer than 1 in 7 who want to quit will be able to resist. Smokers die, on average, at least a decade before nonsmokers, but even those who know they are committing slow-motion suicide may be unable to stop (Saad, 2002). By 2030, the number of tobacco-related deaths worldwide is expected to reach 8 million people each year. That means that 1 billion twenty-first century people may be killed by tobacco (WHO, 2012). Eliminating smoking would increase life expectancy more than any other preventive measure.

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The good news is that repeated attempts to quit smoking seem to pay off. Half of all Americans who have ever smoked have quit, some with the aid of a nicotine replacement drug and a support group. Success is equally likely whether smokers quit abruptly or gradually (Fiore et al., 2008; Lichtenstein et al., 2010; Lindson et al., 2010). The acute craving and withdrawal symptoms do go away gradually over six months (Ward et al., 1997). After a year’s abstinence, only 10 percent return to smoking in the next year (Hughes et al., 2008).

COCAINE Cocaine is a powerful and addictive stimulant derived from the coca plant. The recipe for Coca-Cola originally included an extract of that 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 as the street drug crack cocaine. It enters the bloodstream quickly, producing a rush of euphoria—feelings of great happiness and well-being. Those feelings continue until the brain’s supply of the neurotransmitters dopamine, serotonin, and norepinephrine drops off (FIGURE 13.5). Then, within the hour, a crash of agitated depression follows. Many regular cocaine users chasing this high become addicted.

Cocaine use may heighten reactions, such as aggression (Licata et al., 1993). It may also lead to emotional disturbances, suspiciousness, convulsions, cardiac arrest, or respiratory failure. The drug’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).

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METHAMPHETAMINE Amphetamines stimulate neural activity. As body functions speed up, the user’s energy rises and mood soars. Amphetamines are the parent drug for the highly addictive methamphetamine, which is chemically similar but has greater effects (NIDA, 2002, 2005). Methamphetamine triggers the release of the neurotransmitter dopamine, which stimulates brain cells that enhance energy and mood. Eight or so hours of heightened energy and mood then follow. Aftereffects may include irritability, insomnia, high blood pressure, seizures, social isolation, depression, and occasional violent outbursts (Homer et al., 2008). Over time, methamphetamine may reduce the brain’s normal output of dopamine.

ECSTASY Ecstasy is the street name for MDMA (methylenedioxymethamphetamine, also known in its powdered form as “Molly”). This powerful drug is both a stimulant and a mild hallucinogen. (Hallucinogens distort perceptions and lead to false sensory images. More on that later.) Ecstasy is an amphetamine derivative that triggers the brain’s release of dopamine. 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 and emotional elevation. In a social setting, they will feel intimately connected to the people around them. (“I love everyone!”)

During the late 1990s, Ecstasy’s popularity soared as a “club drug” taken at nightclubs and all-night dance parties (Landry, 2002). There are, however, reasons not to be ecstatic about Ecstasy. One is its ability to cause dehydration. With prolonged dancing, this effect can lead to severe overheating, increased blood pressure, and death. Long-term, repeated use can also damage serotonin-producing neurons. Serotonin does more than just make us feel happy. It helps regulate our body rhythms (including sleep), our disease-fighting immune system, and our memory and other cognitive functions (Laws & Kokkalis, 2007; Pacifici et al., 2001; Schilt et al., 2007; Wagner et al., 2012b). Ecstasy interferes with all these functions. The decreased serotonin output can be permanent and can lead to a permanently depressed mood (Croft et al., 2001; McCann et al., 2001; Roiser et al., 2005). Ecstasy delights for the night but darkens our tomorrows.

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Hallucinogens distort perceptions and call up sensory images (such as sounds or sights) without any input from the senses. This helps explain why these drugs are also called psychedelics, meaning “mind-manifesting.” Some are synthetic. The best known synthetic hallucinogens are MDMA (Ecstasy), discussed earlier, and LSD. Others, such as 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 criss-cross, a cobweb, or a spiral. The next phase consists of more meaningful images. Some images may be seen in front of a tunnel; others may be replays of past emotional experiences. As the hallucination peaks, people frequently feel separated from their body. Dreamlike scenes feel so real that people may become panic-stricken or harm themselves.

These sensations are strikingly similar to the near-death experience. This altered state of consciousness is reported by about 10 to 15 percent of those revived from cardiac arrest (Agrillo, 2011; Greyson, 2010; Parnia et al., 2014). Many describe visions of tunnels (FIGURE 13.6), bright lights or beings of light, a replay of old memories, and out-of-body sensations (Siegel, 1980). Oxygen deprivation and other insults to the brain can produce what one philosopher-neuroscientist calls “neural funny business” (Churchland, 2013, p. 70). During epileptic seizures and migraines, for example, people sometimes experience hallucinations of geometric patterns (Billock & Tsou, 2012). Solitary sailors and polar explorers have reported profound mystical experiences while enduring monotony, isolation, and cold (Suedfeld & Mocellin, 1987).

LSD In 1943, Albert Hofmann reported perceiving “an uninterrupted stream of fantastic pictures, extraordinary shapes with an intense, kaleidoscopic play of colors” (Siegel, 1984). Hofmann, a chemist, had created and accidentally ingested LSD (lysergic acid diethylamide). LSD, like Ecstasy, interferes with the serotonin neurotransmitter system. An LSD “trip” can take users to unexpected places. Emotions may vary from euphoria to detachment to panic, depending in part on the person’s mood and expectations.

MARIJUANA For 5000 years, hemp has been cultivated for its fiber. The leaves and flowers of this plant, which are sold as marijuana, contain THC (delta-9-tetrahydrocannabinol). Whether smoked (getting to the brain in a mere 7 seconds) or eaten (traveling at a slower, less predictable pace), THC produces a mix of effects. Synthetic marijuana (“K-2,” also called “Spice”) mimics THC but can have harmful side effects—such as agitation, seizures, hallucinations, and suicidal or aggressive thoughts and actions. Lawmakers have passed legislation, such as the U.S. Synthetic Drug Abuse Prevention Act of 2012, to make K-2 illegal.

The straight dope on marijuana: It is usually classified as a mild hallucinogen, because it increases sensitivity to colors, sounds, tastes, and smells. But in other ways, marijuana is like alcohol. It relaxes, disinhibits, and may produce a euphoric high. And, like alcohol, it impairs motor coordination, perceptual skills, and reaction time, so it interferes with safe operation of 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 may experience a less abrupt withdrawal. They may also achieve a high with smaller-than-usual amounts. This is the opposite of typical tolerance, in which repeat users need to take larger doses to feel the same effect.

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

Does marijuana harm the brain and impair cognition? Some evidence indicates that it disrupts memory formation (Bossong et al., 2012). Such effects on thinking outlast the period of smoking (Messinis et al., 2006). Heavy adult use for over 20 years has been associated with shrinkage of brain areas that process memories and emotions (Filbey et al., 2014; Yücel et al., 2008). And one long-term study tracking 1000 people from birth found a link between persistent marijuana use before age 18 and lower intelligence test scores in adulthood (Meier et al., 2012b). Other researchers are unconvinced that smoking marijuana harms the brain (Rogeberg, 2013; Weiland et al., 2015).

In some cases, medical marijuana use has been legalized as treatment for the pain and nausea associated with diseases such as AIDS and cancer (Munsey, 2010; Watson et al., 2000). In such treatments, 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).

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TABLE 13.5 summarizes the psychoactive drugs discussed in this section. They share some features. All trigger negative aftereffects that offset their immediate positive effects and grow stronger with repetition. This helps explain both tolerance and withdrawal. As the negative aftereffects grow stronger, larger and larger doses are typically needed to produce the desired high (tolerance). These increasingly larger doses produce even worse aftereffects in the drug’s absence (withdrawal). The worsening aftereffects, in turn, create a need to switch off the withdrawal symptoms by taking yet more of the drug.

Substance use by North American youth increased during the 1970s. Then, with increased drug education and a shift toward more realism and less glamorous media portrayals of the effects of drugs, substance use declined sharply, except for a small, brief rebound in the mid-1980s. After the early 1990s, the cultural antidrug voice softened, and drugs for a time were again glamorized in music and films. Even so, drug use among high school students has been holding fairly steady (FIGURE 13.7).

For many adolescents, occasional drug use represents thrill seeking. Yet why do some adolescents, but not others, become regular drug users? In search of answers, researchers have tried to sort out biological, psychological, and social-cultural influences.

Biological Influences

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Are some of us biologically vulnerable to particular drugs? Evidence indicates we are (Crabbe, 2002):

Psychological and Social-Cultural Influences

Throughout this text, you have seen a recurring theme: Biological, psychological, and social-cultural influences interact to influence behavior. So, too, with problematic drug use. We have considered some biological influences on substance use and abuse. 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 try to make their way in life without job skills, without privilege, and with little hope.

Sometimes, a 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). By temporarily dulling the pain of self-awareness, psychoactive drugs may offer a way to avoid coping with depression, anger, anxiety, or insomnia. The relief may be temporary, but as Chapter 6 explains, behavior is often controlled more by its immediate consequences than by its later ones.

Rates of substance use also vary across cultural and ethnic groups. Among actively religious people, alcohol and other substance addiction rates have been low, 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). African-American teens’ rates of drinking, smoking, and cocaine use are sharply lower than among other U.S. teens (Johnston et al., 2007).

Substance use can also have social roots. Adolescents, self-conscious and often thinking the world is watching them, are especially vulnerable. Smoking, for example, usually begins in the early teen years. Teens may first light up to imitate glamorous celebrities, to project a mature image, to handle stress, or to get the social reward of acceptance by other smokers (Cin et al., 2007; DeWall & Pond, 2011; Tickle et al., 2006).

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Whether in cities or in rural areas, peers influence attitudes about substance use. They throw the parties and provide (or don’t provide) the drugs. If an adolescent’s friends abuse drugs, the odds are that he or she will, too. If the friends do not, the opportunity may not even arise.

Peer influence is more than what friends do and say. Adolescents’ expectations—what they believe their friends are doing and favoring—matter too. 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 said they had smoked it? Only 4 percent (Wren, 1999). College students are not immune to such misperceptions, either. Drinking dominates social occasions partly because students overestimate their fellow students’ enthusiasm for alcohol and underestimate their view of its risks (Moreira et al., 2009; Prentice & Miller, 1993; Self, 1994). As always with correlations, the traffic between friends’ drug use and our own may be two-way. Our friends influence us, but we also select as friends those who share our likes and dislikes.

Teens rarely abuse drugs if they understand the physical and psychological costs, do well in school, feel good about themselves, and are in a peer group that disapproves of early drinking and using drugs (Bachman et al., 2007; Hingson et al., 2006). These findings suggest three tactics for preventing and treating substance use and addiction among young people: