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.

10-3 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.

AlcoholTrue 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 10.2). 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.

BarbituratesLike 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.

OpiatesThe 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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10-4 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.

NicotineCigarettes 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.¹

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 10.3). 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 10.4). 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).

MethamphetamineMethamphetamine 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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EcstasyEcstasy, a street name for MDMA (methylenedioxymethamphetamine, 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.

10-5 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 10.5), 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).

LSDAlbert 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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MarijuanaMarijuana 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).

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Despite their differences, the psychoactive drugs summarized in TABLE 10.2 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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