Psychopathology: Substance Use & Impulse Control (eTextbook)

Book Title: eTextbook: Psychopathology: An Integrative Approach to Understanding, Assessing, and Treating Psychological Disorders, Seventh Canadian Edition Chapter 12. Substance Use and Impulse Control Chapter 12. Substance Use and Impulse Control 350 Medioimages/PhotoDisc/Getty Images Learning Objectives 351 LO12.1 Discuss the differences between substance intoxication and substance withdrawal in substance use disorders. LO12.2 List the categories of substances that can contribute to the development of substance use disorders. LO12.3 Compare the effectiveness of biological treatments, psychosocial treatments, and prevention efforts. LO12.4 Describe the similarities and differences of impulse-control disorders according to their symptoms as listed in the DSM-5-TR. Introduction According to the 2012 Canadian Community Health Survey—Mental Health (CCHS), 3.8 percent of Canadians had a substance use disorder in the previous year, with another 1.2 percent having both a substance use disorder and a mood or anxiety disorder (Khan, 2017). Some groups are more affected than others. For example, using census and hospital discharge data, Statistics Canada estimated that First Nations people living on and off reserve have, respectively, have acute care hospitalization rates for substance-related disorders that are seven and four times rates the for non-Indigenous Canadians (Carrière et al., 2018). In this chapter, we explore the substance-related and addictive disorders, the problematic use of drugs and other substances that people take to alter the way they think, feel, and behave. In addition, gambling disorder, which was added to this category in the DSM-5, will be discussed. These disorders have been around for millennia and continue to affect how we live, work, and play. Equally disruptive to the people affected, impulse-control disorders include several related problems that involve the inability to resist acting on a drive or temptation. Included in this group are those who cannot resist aggressive impulses or the impulse to steal, for example, or to set fires. Controversy surrounds substance-related, addictive, and impulse-control disorders because our society sometimes believes that these problems result simply from a lack of willpower. If you wanted to stop drinking, gambling, or stealing, you would just stop. It’s just not that simple. Book Title: eTextbook: Psychopathology: An Integrative Approach to Understanding, Assessing, and Treating Psychological Disorders, Seventh Canadian Edition Perspectives on Substance-Related and Addictive Disorders Perspectives on Substance-Related and Addictive Disorders The cost in lives, money, and emotional turmoil has made the issue of alcohol and drug misuse a major concern worldwide. In 1992, the Roman Catholic Church issued a new universal catechism, officially declaring that drug abuse and drunk driving are sins (Riding, 1992). Yet from the well-known heavy drug use of musician Neil Young in his early career and the death of two of his close friends from drug overdoses (McDonough, 2002) to the boozing and drug involvement of singer and songwriter Leonard Cohen (Walsh, 2001), illicit drug use and heavy drinking occupy the lives of many. At only 31 years of age, Canadian actor Cory Monteith died in a Vancouver hotel room of an accidental overdose of alcohol and heroin. Monteith was at the height of his fame, playing quarterback Finn Hudson on the hit television show Glee (“Cory Monteith’s Overdose,” 2013). Consider also the public controversies surrounding former Alberta premier Ralph Klein’s intoxicated behaviour while visiting a homeless shelter in 2001, former British Columbia premier Gordon Campbell’s embarrassing driving-while-intoxicated charge in Hawaii in 2003, and former Toronto mayor Rob Ford’s admission of using crack cocaine in 2013. Klein and Campbell eventually quit drinking (O’Malley & Missio, 2003), and Ford continued to struggle with substances (Church & Friesen, 2013). Stories such as these are not only about the rich and famous but are also retold in every corner of our society. Consider the case of Danny, who has the disturbing but common habit of polysubstance use (using multiple substances). Danny… Comorbid Substance Use Disorders At the age of 35, Danny was in jail, awaiting trial on charges that he broke into a gas station and stole money. Danny’s story illustrates the lifelong pattern that characterizes the behaviour of many people who are affected by substance-related disorders. Danny grew up in the suburbs. He was well liked in school and an average student. Like many of his friends, he smoked cigarettes in his early teens and drank beer with his friends at night behind his high school. Unlike most of his friends, however, Danny almost always drank until he was obviously drunk; he also experimented with many other drugs, including cocaine, heroin, speed (amphetamines), and downers (barbiturates). After high school, Danny attended a local community college for one semester, but he dropped out after failing most of his courses. His dismal performance seemed to be related to his missing many classes. He had difficulty getting up for classes after partying most nights. His moods were highly variable, and he was often unpleasant. Danny’s family knew he occasionally drank too much, but they didn’t know (or didn’t want to know) about his other drug use. He had forbidden anyone from going into his room, after his mother found little packets of white powder (probably cocaine) in his sock drawer. He said he was keeping them for a friend and that he would return them immediately. Money was sometimes missing from the house, and once some stereo equipment disappeared, but if anyone in his family suspected Danny, they never admitted it. 352 After he dropped out of college, Danny held a series of low-paying jobs, and when he was working, his family reassured themselves that he was back on track and things would be fine. Unfortunately, he rarely held a job for more than a few months. He was usually fired for poor job attendance and performance. Because he continued to live at home, Danny could survive despite frequent periods of unemployment. When he was in his late 20s, Danny announced that he needed help and planned to check into an alcohol rehabilitation centre; he still would not admit to using other drugs. His family’s joy and relief were overwhelming, and no one questioned his request for several thousand dollars to help pay for the private program he said he wanted to attend. Danny disappeared for several weeks, presumably because he was in the rehabilitation program. However, a call from the local police station put an end to this fantasy: Danny had been found quite high, living in an abandoned building. Danny had spent his family’s money on drugs and had had a three-week binge with some friends. Danny’s deceptiveness and financial irresponsibility greatly strained his relationship with his family. He was allowed to continue living at home, but his parents and siblings excluded him from their emotional lives. Danny seemed to straighten out, and he held a job at a gas station for almost two years. He became friendly with the station owner and his son. However, without any obvious warning, Danny resumed drinking and using drugs and was arrested for robbing the very place that had kept him employed for many months. Why did Danny’s drug use become so problematic when many of his friends’ and siblings’ use did not? Why did he steal from his family and friends? What ultimately became of him? We return to Danny’s frustrating story later when we look at the causes and treatment of substance-related disorders. Although each drug described in this chapter has unique effects, they have similarities in the ways they are used and how people who misuse them are treated. First, we present some concepts that apply to substance-related disorders in general, noting important terminology and addressing several diagnostic issues. Can you use drugs without meeting criteria for a disorder? Can you use drugs and not become addicted to or dependent on them? To answer these important questions, we first need to clarify what we mean by substance and then outline potential levels of involvement with substances: substance use, substance intoxication, and substance use disorder. The DSM-5-TR includes substance use disorders and substance-induced disorders under the umbrella term substance- related disorders. Substance use disorder refers to problematic use of a substance (e.g., the person continues to use despite experiencing severe consequences of use). Substance-induced disorders refer to specific conditions resulting from use (e.g., intoxication, withdrawal). In this chapter, we focus on substance use disorders, but we also touch on substance-induced disorders as well. The term substance refers to chemical compounds that are ingested to alter mood or behaviour. Psychoactive substances alter mood, behaviour, or both. Although you might first think of drugs such as cocaine and heroin, this definition also includes more commonplace legal drugs, such as alcohol, the nicotine found in tobacco, and the caffeine in coffee and tea. As we will see, these so-called safe drugs also affect mood and behaviour, they can be addictive, and they account for more health problems and mortality than all the illegal drugs combined. You could make a good argument for directing drug prevention efforts toward cigarette smoking (nicotine use) because of its addictive properties and negative health consequences. Book Title: eTextbook: Psychopathology: An Integrative Approach to Understanding, Assessing, and Treating Psychological Disorders, Seventh Canadian Edition Perspectives on Substance-Related and Addictive Disorders Levels of Involvement Levels of Involvement Use Substance use is the ingestion of psychoactive substances in moderate amounts that do not necessarily interfere with social, educational, or occupational functioning. Most of you reading this chapter probably use some sort of psychoactive substance on occasion. Drinking a cup of coffee in the morning to wake up or smoking a cigarette and having a drink with a friend to relax are 353 examples of substance use, as is the occasional ingestion of illegal drugs, such as amphetamines and cocaine. IVASHstudio/Shutterstock.com Substance use Intoxication Our physiological reaction to ingested substances—drunkenness or getting high—is substance intoxication. For a person to become intoxicated, many variables interact, including the type of drug taken, the amount ingested, and the person’s individual biological reaction. For many of the substances we discuss here, intoxication is experienced as impaired judgment, mood changes, and lowered motor ability (e.g., problems walking or talking). Monkey Business Images/Shutterstock.com Intoxication Substance Use Disorder Defining substance use disorder by how much of a substance is ingested is problematic. For example, is drinking two glasses of wine in an hour misuse? Three glasses? Six? Is taking one injection of heroin considered misuse? The DSM-5-TR (American Psychiatric Association, 2022) defines substance use disorder in terms of how significantly the use interferes with the user’s life. If substances disrupt your education, job, or relationships with others, and put you in physically dangerous situations (e.g., while driving), you would be considered to have a disorder. Danny seems to fit this definition of a disorder. His inability to complete a semester of community college was a direct result of drug use. Danny often drove while drunk or under the influence of other drugs, and he had already been arrested twice. In fact, Danny’s use of multiple substances was so relentless and pervasive that he would probably be diagnosed with a severe form of the disorder. Substance use disorder is usually described as addiction. Although we use the term addiction routinely when we describe people who seem to be under the control of drugs, there is some disagreement about how to define addiction (Rehm et al., 2013; G. Edwards, 2012). To meet the criteria for a disorder, a person must have at least two symptoms in the last year that interfered with their life or bothered the person a great deal. When a person has four or five symptoms, they are considered to fall in the moderate range. A severe substance use disorder would be someone like Danny who has six or more symptoms. Symptoms for substance use disorders can include a physiological dependence on the drug or drugs, meaning the use of increasingly greater amounts of the drug to experience the same effect ( tolerance), and a negative physical response when the substance is no longer ingested (withdrawal) (Higgins et al., 2014). Chris Schmidt/Getty Images Substance dependence Tolerance and withdrawal are physiological reactions to the chemicals being ingested. Have you ever experienced a headache when you didn’t have your morning coffee? You were probably going through caffeine withdrawal. In a more extreme example, withdrawal from alcohol can cause alcohol withdrawal delirium (or delirium tremens—the DTs), in which a person can experience frightening hallucinations and body tremors. Withdrawal from many substances can bring on chills, fever, diarrhea, nausea and vomiting, and aches and pains. Not all substances are physiologically addicting, however. For example, you do not go through severe physical withdrawal when you stop taking LSD. Cocaine withdrawal has a pattern that includes anxiety, sleep changes, lack of motivation, and boredom, and withdrawal from cannabis includes such symptoms as irritability, nervousness, appetite change, and sleep disturbance. We return to the ways drugs act on our bodies when we examine the causes of problematic drug use. Other symptoms that make up a substance use disorder include drug-seeking behaviours. The repeated use of a drug, a desperate need to ingest more of the substance (stealing money to buy drugs, standing outside in the cold to smoke), and the likelihood that use will resume after a period of abstinence are behaviours that define the extent of substance use disorders. Such behavioural reactions are different from the physiological responses to drugs we described before and are sometimes referred to in terms of psychological dependence. The previous version of the DSM considered substance abuse and substance dependence as separate diagnoses. The DSM-5 combined the two into the general definition of substance use disorders based on research that suggests the two co-occur (Dawson, Goldstein, & Grant, 2012; O’Brien, 2011). Let’s return to the questions we started with: Can you use drugs and not misuse them? Can you use drugs and not become addicted to them? The answer to the first question is yes. Obviously, some people drink wine or beer regularly without drinking to excess. And contrary to popular belief, some people use drugs, such as heroin, cocaine, or crack (a form of cocaine), on an occasional basis (for instance, several times a year) without problems (Ray, 2012). What is 354 disturbing is that we do not know ahead of time who is likely to become dependent with even a passing use of a substance. It may seem counterintuitive, but dependence can be present without misuse. For example, cancer patients who take morphine for pain may become dependent on the drug—build up a tolerance and go through withdrawal if it is stopped (Flemming, 2010; Portenoy & Mathur, 2009). Later in this chapter, we discuss biological and psychosocial theories of the causes of substance use disorders and why we have individualized reactions to these substances. Book Title: eTextbook: Psychopathology: An Integrative Approach to Understanding, Assessing, and Treating Psychological Disorders, Seventh Canadian Edition Perspectives on Substance-Related and Addictive Disorders Diagnostic Issues Diagnostic Issues In early editions of the DSM, alcoholism and drug misuse were not treated as disorders in and of themselves. Instead, they were categorized as sociopathic personality disturbances (a forerunner of the current antisocial personality disorder, which we discuss in Chapter 13), because substance use was seen as a symptom of other problems. It was considered a sign of moral weakness, and the influence of genetics and biology was hardly acknowledged. A separate category was created in the DSM-III in 1980, and since then we have acknowledged the complex biological and psychological nature of the problem. In the DSM-5, the term substance use disorders included 11 symptoms that range from relatively mild (e.g., substance use results in a failure to fulfill major role obligations) to more severe (e.g., occupational or recreational activities are given up or reduced because of substance use). The DSM-5 removed the previous symptom that related to substance-related legal problems and added a symptom that indicates the presence of craving or a strong desire to use the substance. No further changes were made to substance use disorder in the DSM-5-TR. These distinctions help clarify the problem and focus treatment on the appropriate aspect of the disorder. Danny would be considered to have a cocaine use disorder in the severe range because of the tolerance he showed for the drug, his use of larger amounts than he intended, his unsuccessful attempts to stop using it, and the activities he gave up to buy it. Symptoms of other disorders can complicate the picture significantly. For example, do some people drink to excess because they are depressed, or do drinking and its consequences (e.g., loss of friends, job) create depression? Some researchers have estimated that more than half the people with alcohol disorders have an additional psychiatric disorder, such as major depression, antisocial personality disorder, or bipolar disorder (Compton et al., 2003; Conrod & Stewart, 2005; Lieb, 2015; McGovern et al., 2006). For example, in an epidemiological study of six countries, including Canada, alcohol disorders were found to be highly comorbid with mood and anxiety disorders (Merikangas et al., 1998). As another example, in reviews of the literature by Canadian researchers (Crockford & el-Guebaly, 1998; Stewart & Kushner, 2003), alcohol disorders were shown to be highly comorbid with pathological gambling. Substance use disorder might occur concurrently with other disorders for several reasons (Strain, 2009). First, substance use disorders and anxiety and mood disorders are highly prevalent in our society and may occur together frequently just by chance. Second, drug intoxication and withdrawal can cause symptoms of anxiety, depression, and psychosis, and can increase risk taking. A laboratory-based study by Ellery and colleagues (2005) showed that ingestion of alcohol led to increased risk taking among regular gamblers when they were using a video lottery terminal relative to gamblers ingesting a nonalcoholic control beverage. This finding suggests that alcohol’s effects in increasing risk taking may contribute to the high co-occurrence of alcohol and gambling disorders. A third explanation for the high comorbidity of substance use disorders with other mental health problems is that the mental health disorders cause the substance use disorder. For example, people with anxiety disorders like post-traumatic stress disorder or social phobia may self-medicate with substances for their anxiety symptoms (Stewart, Morris, et al., 2006). The DSM-5-TR tries to define when a symptom is a result of substance use and when it is not. For example, if symptoms seen in schizophrenia or in extreme states of anxiety appear during intoxication or within six weeks after withdrawal from drugs, they are not considered signs of a separate psychiatric disorder. And individuals who show signs of severe depression just after they have stopped taking heavy doses of stimulants would not be diagnosed with a major mood disorder. However, individuals who were severely depressed before they used stimulants and those whose symptoms persist for more than six weeks after they stop might have a separate disorder (Sheperis et al., 2015). 355 We now turn to the individual substances themselves, their effects on our brains and bodies, and how they are used in our society. We have grouped the substances into five general categories: 1. Depressants : These substances result in behavioural sedation and can induce relaxation. They include alcohol (ethyl alcohol) and the sedative and hypnotic drugs in the families of barbiturates (e.g., Seconal) and benzodiazepines (e.g., Valium, Halcion, Xanax). 2. Stimulants : These substances cause us to be more active and alert and can elevate mood. Included in this group are amphetamines, cocaine, nicotine, and caffeine. 3. Opioids : The major effect of these substances is to produce analgesia temporarily (reduce pain) and euphoria. Heroin, opium, kratom, codeine, morphine, and oxycodone are included in this group. 4. Hallucinogens : These substances alter sensory perception and can produce delusions, paranoia, and hallucinations. Cannabis and LSD are included in this category. 5. Other drugs: Other substances that are misused but do not fit neatly into one of the categories here include inhalants (e.g., airplane glue), anabolic steroids, and other over-the-counter and prescription medications (e.g., nitrous oxide). These substances produce a variety of psychoactive effects that are characteristic of the substances described in the previous categories. Concept Check 12.1 To check your understanding of substance-related definitions, read the following case summaries and then state whether they describe (a) use, (b) intoxication, or (c) dependence. 1. Jonas is a member of the high school football team and is out celebrating a big win. Jonas doesn’t drink alcohol but doesn’t mind taking a puff of cannabis every now and then. Because Jonas had such a good game, he decides to smoke cannabis to celebrate. Despite his great performance in the game, Jonas is easily irritated, laughing one minute, and yelling the next. During a game of darts, at which he usually excels, Jonas barely hits the target. And the more Jonas boasts about his stats, the more difficult it is to understand him. ANSWER 2. Jill routinely drinks diet cola. Instead of having coffee in the morning, she heads straight for the fridge. Another habit of Jill’s is having a cigarette immediately after dinner. If Jill is unable to have her diet cola in the morning or her cigarette in the evening, she is not dependent on them and can still function normally. Jill also smokes cannabis with her friends every few weeks to escape the real world. ANSWER 3. Steve is a 23-year-old university student who started drinking heavily when he was 16. Instead of getting drunk at weekend parties, Steve drinks a moderate amount every night. In high school, Steve would become drunk after about six beers; now his tolerance has more than doubled. Steve claims alcohol relieves the pressures of university life. He once attempted to quit drinking, but he had chills, fever, diarrhea, nausea and vomiting, and body aches and pains. At one point, he even experienced scary hallucinations and tremors. ANSWER Book Title: eTextbook: Psychopathology: An Integrative Approach to Understanding, Assessing, and Treating Psychological Disorders, Seventh Canadian Edition Depressants Depressants Depressants primarily decrease central nervous system activity. Their principal effect is to reduce our levels of physiological arousal and help us relax. Included in this group are alcohol and the sedative, hypnotic, and anxiolytic drugs, such as those prescribed for insomnia. These substances are among those most likely to produce symptoms of tolerance and withdrawal. We first look at the most used of these substances—alcohol—and the alcohol-related disorders that can result; see DSM Table 12.1. DSM-5-TR Table 12.1 Diagnostic Criteria for Alcohol Use Disorder A. A problematic pattern of alcohol use leading to clinically significant impairment or distress, as manifested by at least two of the following, occurring within a 12-month period: 1. Alcohol is often taken in larger amounts or over a longer period than was intended. 2. There is a persistent desire or unsuccessful efforts to cut down or control alcohol use. 3. A great deal of time is spent in activities necessary to obtain alcohol, use alcohol, or recover from its effects. 4. Craving, or a strong desire or urge to use alcohol. 5. Recurrent alcohol use resulting in a failure to fulfill major role obligations at work, school, or home. 6. Continued alcohol use despite having persistent or recurrent social or interpersonal problems caused or exacerbated by the effects of alcohol. 7. Important social, occupational, or recreational activities are given up or reduced because of alcohol use. 8. Recurrent alcohol use in situations in which it is physically hazardous. 9. Alcohol use is continued despite knowledge of having a persistent or recurrent physical or psychological problem that is likely to have been caused or exacerbated by alcohol. 10. Tolerance, as defined by either or both of the following: a. A need for markedly increased amounts of alcohol to achieve intoxication or desired effect. b. A markedly diminished effect with continued use of the same amount of alcohol. 11. Withdrawal, as manifested by either of the following: a. The characteristic withdrawal syndrome for alcohol. b. Alcohol (or a closely related substance such as benzodiazepine) is taken to relieve or avoid withdrawal symptoms. Specify current severity: Mild: Presence of 2–3 symptoms. Moderate: Presence of 4–5 symptoms. Severe: Presence of 6 or more symptoms. American Psychiatric Association. (2022). Diagnostic and statistical manual of mental disorders (5th ed., Text Revision). Book Title: eTextbook: Psychopathology: An Integrative Approach to Understanding, Assessing, and Treating Psychological Disorders, Seventh Canadian Edition Depressants Alcohol-Related Disorders Alcohol-Related Disorders 356 Danny’s substance use problems began when he drank beer with friends, a rite of passage for many teenagers. Alcohol has been widely used throughout history. For example, scientists have found evidence of wine and beer in pottery jars at the site of a Sumerian trading post in western Iran and in the country of Georgia that date back 7000 years (McGovern, 2007). For hundreds of years, Europeans drank beer, wine, and hard liquor. When they came to North America in the early 1600s, they brought their considerable thirst for alcohol with them. Alcohol was not a problem for Indigenous peoples until the French introduced brandy and the British introduced rum (Stewart, 2002). Reports of the early missionaries contain many descriptions of intoxication among early settlers and Indigenous peoples (e.g., Dailey, 1968); government controlled activities and antidrinking movements quickly followed. For example, the Temperance Movement allowed for the benefits of moderate drinking while morally condemning the heavy use of spirits. The Women’s Christian Temperance Union tried to have alcohol education courses introduced into schools and was successful in several Canadian provinces. The work of Temperance Movement proponents paved the way for the American Prohibition (1919–1933). Although prohibition did reduce overall levels of use in the United States, it had some unintended side effects, such as increases in organized crime and bootlegging, some of which originated in Canada. These problems led to the repeal of prohibition near the beginning of the Depression era. Clinical Description Apparent stimulation is the initial effect of alcohol, although it is a depressant. We generally experience a feeling of well-being, our inhibitions are reduced, and we become more outgoing. These reactions occur partly because the inhibitory centres in the brain are initially depressed (in the sense of slowed). With continued drinking, however, alcohol depresses more areas of the brain, which impedes the ability to function properly. Motor coordination is impaired (staggering, slurred speech), reaction time is slowed, we become confused, our ability to make judgments is reduced, and even vision and hearing can be negatively affected, all of which help to explain why driving while intoxicated is very dangerous. Effects Alcohol affects many parts of the body (see Figure 12.1). After it is ingested, it passes through the esophagus (1) and into the stomach (2), where small amounts are absorbed. From there, most of it travels to the small intestine (3), where it is easily absorbed into the bloodstream. The circulatory system distributes the alcohol throughout the body, where it contacts every major organ, including the heart (4). Some of the alcohol goes to the lungs, where it vaporizes and is exhaled, a phenomenon that is the basis for the breath analyzer test that measures levels of intoxication. As alcohol passes through the liver (5), it is broken down or metabolized into carbon dioxide and water by enzymes (Maher, 1997). An average-size person can metabolize about 7 to 10 grams of alcohol per hour, an amount comparable to about one glass of beer or 30 millilitres (one ounce) of 90-proof spirits (Moak & Anton, 1999). Figure 12.1 The path travelled by alcohol throughout the body (see text for complete description). Most of the substances we describe in this chapter, including cannabis, the opioids, and tranquilizers, interact with specific receptors in the brain cells. Alcohol influences several neuroreceptor systems, which makes it difficult to study (Lees et al., 2020; Ray, 2012). For example, the gamma-aminobutyric acid (GABA) system, which we discussed in Chapters 2 357 and 5, seem to be particularly sensitive to alcohol. GABA, as you will recall, is an inhibitory neurotransmitter. Its major role is to interfere with the firing of the neuron it attaches to. Because the GABA system seems to affect anxiety, alcohol’s antianxiety properties may result from its interaction with the GABA system. Also, when GABA attaches to its receptor, chloride ions enter the cell and make it less sensitive to the effects of other neurotransmitters. Alcohol seems to reinforce the movement of these chloride ions; as a result, the neurons have difficulty firing. In other words, although alcohol seems to loosen our tongues and makes us more sociable, it makes it difficult for neurons to communicate with each other (Joslyn et al., 2010). There is some evidence from genetic research (further discussed below) that the genes responsible for communication between neurons may also be responsible for individual differences in response to alcohol. Blackouts, the loss of memory for what happens during intoxication, may result from the interaction of alcohol with the glutamate system. The serotonin system also appears to be sensitive to alcohol. This neurotransmitter system affects mood, sleep, and eating behaviour and is thought to be responsible for alcohol cravings (Müller et al., 2020). Alcohol also exerts effects on the dopamine reward system, and these effects may be responsible for the pleasurable feelings people experience when drinking alcohol (Conrod et al., 1997). Finally, as noted by Christina Gianoulakis of McGill University, at certain doses, alcohol also results in release of endogenous opioids—our bodies’ naturally occurring analgesics—which may explain why alcohol has pain- numbing effects (Gianoulakis, 2001). Because alcohol affects so many neurotransmitter systems, we should not be surprised that it has such widespread and complex effects. The long-term effects of heavy drinking are often severe. Withdrawal from chronic alcohol use typically includes hand tremors and, within several hours, nausea or vomiting, anxiety, transient hallucinations, agitation, insomnia, and, at its most extreme, withdrawal delirium (or delirium tremens (DTs)), a condition that can produce frightening hallucinations and body tremors. The devastating experience of DTs can be reduced with adequate medical treatment (Schuckit, 2014). Whether alcohol causes organic damage depends on genetic vulnerability, frequency of use, the length of drinking binges, the blood alcohol levels attained during the drinking periods, and whether the body is given time to recover between binges (Mack et al., 2003). Consequences of long-term excessive drinking include liver disease, pancreatitis, cardiovascular disorders, and brain damage (see Figures 12.2 and 12.3). 358 Figure 12.2 Southern Illinois University/Science Source; Martin M Rotker/Getty Images A healthy liver (left) and a cirrhotic liver scarred by years of alcohol misuse (right). Figure 12.3 Source : Dr. Adolf Pfefferbaum,Stanford University The dark areas in the top brain images show the extensive loss of brain tissue that result from heavy alcohol use. Part of the folklore concerning alcohol is that it permanently kills brain cells (neurons). As you will see later, this may not be true. Some evidence for brain damage comes from the experiences of people who are heavy alcohol users and experience blackouts, seizures, and hallucinations. Memory and the ability to perform certain tasks may also be impaired. Two types of organic brain syndromes may result from long-term heavy alcohol use: dementia and Wernicke-Korsakoff syndrome. Dementia, which we discuss more fully in Chapter 16, involves the general loss of intellectual abilities and can be a direct result of neurotoxicity or poisoning of the brain by excessive amounts of alcohol (Ridley et al., 2013). Wernicke-Korsakoff syndrome results in confusion, loss of muscle coordination, and unintelligible speech (Isenberg-Grzeda et al., 2012); it is believed to be caused by a deficiency of thiamine, a vitamin metabolized poorly by heavy drinkers. The dementia caused by this disease does not go away once the brain is damaged. Although it was previously thought that mild to moderate intake of alcohol (especially wine) could actually serve a protective role in cognitive decline as we age, further research shows that this is not the case (Immonen et al., 2020; Topiwala et al., 2017). The effects of problematic alcohol use extend beyond the health and well-being of the drinker. Although alcohol was suspected for years to negatively affect prenatal development, this connection has been studied in earnest only since the 1960s (Jones & Smith, 1973; Lemoine et al., 1968). Fetal alcohol spectrum syndrome (FASS) is now generally recognized as a combination of problems that can occur in children whose mothers drank while they were pregnant. These problems include fetal growth retardation, cognitive deficits, behaviour problems, and learning difficulties (Douzgou et al., 2012; Hamilton et al., 2003). In addition, children with FAS often have characteristic facial features (Caprara et al., 2007). Science History Images/Alamy Stock Photo Physical characteristics of FASS include skin folds at the corners of the eyes, a low nasal bridge, a short nose, a flattened groove between nose and upper lip, small head circumference, small eye openings, a small midface, and a thin upper lip. Statistics on Use and Misuse Because alcohol consumption is legal in North America, we know more about it than most of the other psychoactive substances that we discuss in this chapter (with the possible exceptions of nicotine and caffeine). The World Health Organization (2018) has examined alcohol consumption around the world. Alcohol use in Canada was similar to that in other countries, as shown in Figure 12.4. Figure 12.4 (Source: World Health Organization, Global Health Observatory Data Repository, 2018.) Prevalence of self-reported past-year alcohol use among the general population, age 15+, by country. Canada has established low-risk drinking guidelines to help avoid long-term health problems associated with alcohol use (Butt et al. 2011). Women are advised to consume no more than two drinks per day and have only ten drinks per week. Men should consume no more than 3 drinks per day and 15 drinks per week. At the time of printing, the Canadian Centre on Substance Use and Addiction drastically revised its recommendation for low-risk drinking: 0–2 drinks per week for everyone (https://ccsa.ca/canadas-guidance-alcohol-and- health). The 2017 Canadian Tobacco Alcohol and Drugs Survey (CTADS) asked 359 Canadians about the amount they drank in the previous week. Similar to other national surveys, the CTADS covers Canadians 15 years of age or older and excludes residents in the three territories, as well as those living in institutions. Twenty-one percent of Canadians who consumed alcohol in the previous 7 days exceeded these low-risk guidelines. A slightly larger proportion of men exceeded the suggested limits than women (22 percent versus 19 percent; Canadian Centre on Substance Use and Addiction [CCSA], 2019). The low-risk guidelines also encourage Canadians to have non-drinking days every week and, to avoid acute injury or harm, on any single occasion, women should have no more than three drinks and men four drinks. Heavy drinking is considered four or more drinks on one occasion for women, five or more for men, at least once a month in the past year. According to data from the 2019 Canadian Community Health Survey, 18 percent of Canadians over the age of 12 years engaged in heavy drinking (Statistics Canada, 2021d). A greater proportion of men engaged in heavy drinking than women (23 percent versus 14 percent). Alcohol binge consumption (episodic heavy drinking) is frequent among students: in a 2019 survey of over 50,000 students attending 58 postsecondary institutions in Canada, 33 percent of male students and 28 percent of female students reported consuming five or more drinks in one sitting in the last two weeks (American College Health Association, 2019). One quarter of students indicated that they did not drink alcohol and almost half, 46 percent, said they had not engaged in this type of heavy drinking. LightField Studios/Shutterstock.com Males ages 18 to 29 are most vulnerable to drinking problems. A study of health inequalities in Canada revealed that, compared to non- Indigenous peoples, heavy drinking was more prevalent among Inuit, Métis, and First Nations people living both on and off reserve (Public Health Agency of Canada [PHAC], 2018b). These results are discussed in light of the challenges faced by many Indigenous communities (e.g., unemployment, inadequate health services, language barriers), the legacy of colonization, and the evidence suggesting that abstaining from drinking alcohol is more prevalent among First Nations people living on and off reserve and among Inuit than in the Canadian general population. Progression Remember that Danny went through periods of heavy alcohol and drug use but also had times when he was relatively sober and did not use drugs. Similarly, many people with an alcohol use disorder fluctuate between drinking heavily, drinking socially without negative effects, and being abstinent, not drinking at all (McCrady, 2014). It seems that about 20 percent of people with severe alcohol dependence have a spontaneous remission and do not re-experience 360 problems with drinking (Ludwig, 1985; Vaillant, 1983). It appears instead that the course of a severe alcohol use disorder may be progressive for most people, however. For example, early use of alcohol predicts later misuse. A study of almost 6000 lifetime drinkers by David DeWit and his colleagues at the Centre for Addiction and Mental Health found that drinking at an early age—from age 11 to 14—was predictive of later alcohol- related disorders (DeWit et al., 2000). Similarly, a study tracking alcohol use onset and later use found that those who started drinking at age 11 or earlier were at higher risk for chronic and severe alcohol use disorders (Guttmannova et al., 2011). A third study followed 636 male inpatients in an alcohol rehabilitation centre (Schuckit et al., 1993). Among these chronically alcohol- dependent men, a general progression of alcohol-related life problems unfolded. Three-quarters of the men reported moderate consequences of their drinking in their 20s, such as demotions at work. During their 30s, the men had more serious problems, such as regular blackouts and signs of alcohol withdrawal. By their late 30s and early 40s, these men demonstrated long-term serious consequences of their drinking, which included hallucinations, withdrawal convulsions, and hepatitis or pancreatitis. This study suggests a common pattern among people with chronic alcohol misuse and dependence, one with increasingly severe consequences. This progressive pattern is not inevitable for everyone who misuses alcohol, although we do not yet understand what distinguishes those who are and those who are not susceptible (Krenek & Maisto, 2013). Research on the mechanism responsible for the differences in early alcohol use suggests that a person’s response to the sedative effects of the substance affects later use. In other words, those individuals who tend not to develop the slurred speech, staggering, and other sedative effects of alcohol use are more likely to use it in the future (Chung & Martin, 2009; Schuckit, 2014). This is of particular concern, given the trend to mix highly caffeinated energy drinks with alcohol (Nadeem et al., 2020) because this combination of drinks can reduce the sedative effect of alcohol. Finally, statistics frequently link alcohol with violent behaviour (Boden et al., 2012; Bye, 2007). A review of numerous studies conducted by Robert Pihl and his colleagues established that many people who commit such violent acts as murder, rape, and assault are often intoxicated at the time of the crime (Rossow & Bye, 2012). We hope you are skeptical of this type of correlation. Just because drunkenness and violence overlap does not mean that alcohol will necessarily make you violent. Laboratory studies show that alcohol may increase participants’ aggression (Bushman, 1993; see also review by Hoaken & Stewart, 2003). Whether people behave aggressively outside the laboratory, however, probably involves several interrelated factors, such as the quantity and timing of alcohol consumed, their history of violence, their expectations about drinking, and what happens to the individuals while intoxicated. Alcohol may reduce the fear associated with being punished, and it may impair the ability to consider the consequences of acting impulsively (Kuypers et al., 2020). sdecoret/Shutterstock.com Intoxication is often involved in cases of intimate partner violence. Robert Pihl suggested that people with poorer executive cognitive function (planning, organizing abilities) are more likely than others to behave aggressively when intoxicated (Hoaken et al., 2003; Pihl et al., 2003). Toronto- based researchers Christine Wekerle and Anne-Marie Wall (2002) have further noted that alcohol intoxication can also increase the risk of being the victim of violence. In an impressive longitudinal study of couples who soon were going to be parents, Victoria researchers found that harmful alcohol use in men was predictive of intimate partner violence (Woodin et al., 2014). Photo by Owen Egan/McGill University Robert Pihl, a clinical psychologist at McGill University, has made many notable contributions to the understanding and treatment of problematic alcohol use and dependence. In particular, his work has focused on understanding the relation between alcohol and aggression, and on identifying factors that mediate familial-genetic risk for alcohol use disorder. Book Title: eTextbook: Psychopathology: An Integrative Approach to Understanding, Assessing, and Treating Psychological Disorders, Seventh Canadian Edition Depressants Sedative-, Hypnotic-, and Anxiolytic-Related Disorders Sedative-, Hypnotic-, and Anxiolytic-Related Disorders The general group of depressants also includes sedative (calming), hypnotic (sleep-inducing), and anxiolytic (anxiety-reducing) drugs (Black & Andreasen, 2021d). These drugs include the barbiturates and the benzodiazepines. Barbiturates (which include Amytal, Seconal, and Nembutal) are a family of sedative drugs first synthesized in Germany in 1882 (McKim, 1991). They were prescribed to help people sleep and replaced such drugs as alcohol and opium. Barbiturates were widely prescribed by physicians during the 1930s and 1940s, before their addictive properties were fully understood. By the 1950s, they 361 were among the drugs most misused by adults in North America (Franklin & Frances, 1999). The benzodiazepines (which today include Valium, Xanax, and Ativan) have been used since the 1960s, primarily to reduce anxiety. These drugs were originally touted as a miracle cure for the anxieties of living in our highly pressured technological society. Although it has been known since the 1980s that they are not appropriate for reducing the tension and anxiety resulting from everyday stresses and strains (Cooperstock & Hill, 1982), billions of doses of benzodiazepines are consumed by North Americans each year (Olfson et al., 2015). Sixteen million prescriptions of benzodiazepines were made to Canadians in 2000 alone (Gadsby, 2001). According to the Canadian Institute for Health Information (CIHI, 2018), 12 248 daily doses per 1000 people were prescribed in Canada in 2017 (the highest rate was in New Brunswick, and the lowest, in Ontario; the territories were not included in the study). In general, benzodiazepines are considered safer than barbiturates, with less risk of dependence (Warneke, 1991). Nonetheless, as noted by clinical psychologist Henny Westra of York University, the potential for developing dependence on benzodiazepines for those using them in the treatment of anxiety or sleep disorders should not be minimized (Westra & Stewart, 1998). The potential for benzodiazepine dependence was recognized as early as the 1970s, as is illustrated in the case study of Susan, published in the Canadian Psychiatric Association Journal in 1978. Susan… Taking a Harmless Muscle Relaxant or an Addictive Drug? Susan was a 30-year-old Caucasian woman with a small child. She had recently separated from her husband. Susan had originally been prescribed a low dose of Diazepam by her general practitioner as a muscle relaxant for a backache. Over three months, Susan increased her dose until she reached a level 12 times greater than the dose prescribed by her physician. On her initial psychiatric evaluation, Susan stated that Diazepam helped her to be “fully awake,” “to get energy,” and “to get motivated.” She would take a dose immediately upon awakening, and thereafter every two to three hours. Susan reported that when she failed to take the drug, she would experience dizziness, vomiting, headaches, and drowsiness. Following her visit to a psychiatrist, she was admitted to hospital, where she displayed extreme restlessness, anxiety, trembling, irritability, and suspiciousness. She was put on a gradual dose reduction to withdraw her from the medication. During this process, Susan was administered other (nonaddictive) medications to minimize her experience of anxiety and agitation, and to prevent seizures, which can occur during benzodiazepine withdrawal. Susan cooperated fully with the gradual tapering of her Diazepam for five days. Despite her intense craving for the medication, she was willing to remain at the lower dose. However, on the fifth day, Susan refused to go through gradual withdrawal any longer and demanded abrupt cessation of the medication. At this point her withdrawal symptoms became quite severe: insomnia, trembling, agitation, emotional lability, photophobia (aversion to light), blurred vision, pain behind the eyes, headaches, nausea, and muscle and stomach cramps. She became very paranoid, hostile, irritable, and tearful. Susan developed visual hallucinations (e.g., seeing insects) and illusions (e.g., seeing the sink faucet moving). These symptoms subsided over two weeks. On a follow-up visit to her psychiatrist a week after her discharge, Susan reported that she had been free of all the withdrawal symptoms she experienced while in hospital. Her sleep had also returned to normal. Source: Adapted from Agrawal (1978). Susan’s case illustrates the features of benzodiazepine dependence. High tolerance developed in that Susan escalated her dose over time to achieve the original effect, to the point that she was able to take very large doses without drowsiness. She experienced a severe set of benzodiazepine withdrawal symptoms during her hospitalization—some of which she had experienced previously in milder form when she missed a dose of her medication at home. The author of this case study published this report to warn other doctors about the potential for addiction to this type of medication and to argue against its indiscriminate prescription by physicians (Agrawal, 1978). In addition to the potential for dependence with anxiolytics, reports on the misuse of Rohypnol show how dangerous some benzodiazepine drugs can be. Rohypnol (otherwise known as “roofies”) gained a following among teenagers in the 1990s because it has the same effect as alcohol without the telltale odour. 362 There have been numerous incidents of victims being drugged without their knowledge (Sandal, 2020). Clinical Description At low doses, barbiturates relax the muscles and can produce a mild feeling of well-being. Larger doses can have results similar to those of heavy drinking: slurred speech and problems walking, concentrating, and working. At extremely high doses the diaphragm muscles can relax so much as to cause death by suffocation. In fact, overdosing on barbiturates is a common means of suicide. Like the barbiturates, benzodiazepines are used to calm an individual and induce sleep. In addition, drugs in this class are prescribed as muscle relaxants and anticonvulsants (anti-seizure medications; Black & Andreasen, 2021d). People who use them for nonmedical reasons report first feeling a pleasant high and a reduction of inhibition, similar to the effects of drinking alcohol. With continued use, however, tolerance and dependence can develop. Users who try to stop taking the drug experience symptoms like those of alcohol withdrawal (anxiety, insomnia, tremors, and delirium; Westra & Stewart, 1998). The DSM-5-TR criteria for sedative-, hypnotic-, and anxiolytic-related drug use disorders do not differ substantially from those for alcohol disorders (see DSM Table 12.2). Both include maladaptive behavioural changes, such as inappropriate sexual or aggressive behaviour, variable moods, impaired judgment, impaired social or occupational functioning, slurred speech, motor coordination problems, and unsteady gait. DSM-5-TR Table 12.2 Diagnostic Criteria for Sedative-, Hypnotic-, or Anxiolytic-Related Disorders A. A problematic pattern of sedative, hypnotic, or anxiolytic use leading to clinically significant impairment or distress, as manifested by at least two of the following, occurring within a 12- month period: 1. Sedatives, hypnotics, or anxiolytics are often taken in larger amounts or over a longer period than was intended. 2. There is a persistent desire or unsuccessful efforts to cut down or control sedative, hypnotic, or anxiolytic use. 3. A great deal of time is spent in activities necessary to obtain the sedative, hypnotic, or anxiolytic; use the sedative, hypnotic, or anxiolytic; or recover from its effects. 4. Craving, or a strong desire to use the sedative, hypnotic, or anxiolytic. 5. Recurrent sedative, hypnotic, or anxiolytic use resulting in a failure to fulfill major role obligations at work, school, or home (e.g., repeated absences from work or poor work performance related to sedative, hypnotic, or anxiolytic use; sedative-, hypnotic-, or anxiolytic-related absences, suspensions, or expulsions from school; neglect of children or household). 6. Continued sedative, hypnotic, or anxiolytic use despite having persistent or recurrent social or interpersonal problems caused or exacerbated by the effects of sedatives, hypnotics, or anxiolytics (e.g., arguments with a spouse about consequences of intoxication; physical fights). 7. Important social, occupational, or recreational activities are given up or reduced because of sedative, hypnotic, or anxiolytic use. 8. Recurrent sedative, hypnotic, or anxiolytic use in situations in which it is physically hazardous (e.g., driving an automobile or operating a machine when impaired by sedative, hypnotic, or anxiolytic use). 9. Sedative, hypnotic, or anxiolytic use is continued despite knowledge of having a persistent or recurrent physical or psychological problem that is likely to have been caused or exacerbated by the sedative, hypnotic, or anxiolytic. 10. Tolerance, as defined by either of the following: a. A need for markedly increased amounts of sedative, hypnotic, or anxiolytic to achieve intoxication or desired effect. b. A markedly diminished effect with continued use of the same amount of sedative, hypnotic, or anxiolytic. Note: This criterion is not considered to be met for individuals taking sedatives, hypnotics, or anxiolytics under medical supervision. 11. Withdrawal, as manifested by either of the following: a. The characteristic withdrawal syndrome for sedatives, hypnotics, or anxiolytics. b. Sedatives, hypnotics, or anxiolytics (or closely related substance, such as alcohol) are taken to relieve or avoid withdrawal symptoms. Note: This criterion is not considered to be met for individuals taking sedatives, hypnotics, or anxiolytics under medical supervision. Specify current severity: Mild: Presence of 2–3 symptoms. Moderate: Presence of 4–5 symptoms. Severe: Presence of 6 or more symptoms. American Psychiatric Association. (2022). Diagnostic and statistical manual of mental disorders (5th ed., Text Revision). Sedative, hypnotic, and anxiolytic drugs affect the brain by acting on the GABA neurotransmitter system (Jufer-Phipps & Levine, 2020), although by mechanisms slightly different from those involving alcohol. As a result, when people combine alcohol with any of these drugs, there can be synergistic effects (Fils-Aime, 1993). In other words, if you drink alcohol after taking a benzodiazepine or barbiturate, the total effects can reach dangerous levels. 363 One theory about actor Marilyn Monroe’s death in 1962 is that she combined alcohol with too many barbiturates and unintentionally killed herself. Actor Heath Ledger’s death in 2008 was attributed to the combined effects of oxycodone and a variety of barbiturates and benzodiazepines. Statistics Data from the CIHI (2018) suggest that the amount of benzodiazepines (and related drugs) dispensed in Canada dropped by almost 6 percent between 2016 and 2017. In the 2017 CTADS (Health Canada, 2019), 12 percent of Canadians reported using sedatives in the past year, 9 percent of men and 14 percent of women. Book Title: eTextbook: Psychopathology: An Integrative Approach to Understanding, Assessing, and Treating Psychological Disorders, Seventh Canadian Edition Stimulants Stimulants Of all the psychoactive drugs used in Canada, the most consumed are the stimulants. Included in this group are caffeine (in coffee, chocolate, and many soft drinks and energy drinks), nicotine (in tobacco products such as cigarettes), amphetamines, and cocaine. You probably used caffeine when you got up this morning. In contrast to the depressant drugs, stimulants—as their name suggests—make you more alert and energetic. They have a long history of use. Chinese physicians, for example, have used an amphetamine compound called Ma-huang for more than 5000 years (Iqbal et al., 2020). Ma-huang (or ephedra) was marketed in North America in health food stores as a dietary supplement and weight-loss aid. Ma-huang made the news when its manufacture and sale was banned, given its links to serious health problems (e.g., it can cause a dangerous rise in blood pressure) and even deaths (Canadian Press, 2003). The case of Ma-huang provides an important illustration of how natural compounds can be just as dangerous as manufactured drugs. We describe several stimulants and their effects on behaviour, mood, and cognition. DSM Table 12.3 displays the diagnostic criteria for stimulant use disorder. DSM-5-TR Table 12.3 Diagnostic Criteria for Stimulant Use Disorder A. A pattern of amphetamine-type substance, cocaine, or other stimulant use leading to clinically significant impairment or distress, as manifested by at least two of the following, occurring within a 12-month period: 1. The stimulant is often taken in larger amounts or over a longer period than was intended. 2. There is a persistent desire or unsuccessful efforts to cut down or control stimulant use. 3. A great deal of time is spent in activities necessary to obtain the stimulant, use the stimulant, or recover from its effects. 4. Craving, or a strong desire or urge to use the stimulant. 5. Recurrent stimulant use resulting in a failure to fulfill major role obligations at work, school, or home. 6. Continued stimulant use despite having persistent or recurrent social or interpersonal problems caused or exacerbated by the effects of the stimulant. 7. Important social, occupational, or recreational activities are given up or reduced because of stimulant use. 8. Recurrent stimulant use in situations in which it is physically hazardous. 9. Stimulant use is continued despite knowledge of having a persistent or recurrent physical or psychological problem that is likely to have been caused or exacerbated by the stimulant. 10. Tolerance, as defined by either of the following: a. A need for markedly increased amounts of the stimulant to achieve intoxication or desired effect. b. A markedly diminished effect with continued use of the same amount of the stimulant. Note: This criterion is not considered to be met for those taking stimulant medications solely under appropriate medical supervision, such as medications for attention- deficit/hyperactivity disorder or narcolepsy. 11. Withdrawal, as manifested by either of the following: a. The characteristic withdrawal syndrome for the stimulant (refer to Criteria A and B of the criteria for stimulant withdrawal). b. The stimulant (or a closely related substance) is taken to relieve or avoid withdrawal symptoms. Note: This criterion is not considered to be met for those taking stimulant medications solely under appropriate medical supervision, such as medications for attention- deficit/hyperactivity disorder or narcolepsy. Specify current severity: Mild: Presence of 2–3 symptoms. Moderate: Presence of 4–5 symptoms. Severe: Presence of 6 or more symptoms. American Psychiatric Association. (2022). Diagnostic and statistical manual of mental disorders (5th ed., Text Revision). Book Title: eTextbook: Psychopathology: An Integrative Approach to Understanding, Assessing, and Treating Psychological Disorders, Seventh Canadian Edition Stimulants Stimulant-Related Disorders Stimulant-Related Disorders 364 Amphetamines At low doses, amphetamines can induce feelings of elation and vigour, and can reduce fatigue. You feel “up.” After a period of elevation, however, you come back down and crash, feeling depressed or tired. Amphetamines are manufactured in laboratories; they were first synthesized in 1887 and later used as a treatment for asthma and as a nasal decongestant (Carvalho et al., 2012). Because amphetamines also reduce appetite, some people take them to lose weight. Long-haul truck drivers, pilots, and some university students trying to pull all-nighters use amphetamines to get an extra energy boost and stay awake. The use of amphetamines by two U.S. pilots to stay awake was implicated in the friendly fire death of four Canadian soldiers in Afghanistan in 2002. The case increased awareness of how common amphetamine use is among pilots and has raised consciousness of possible negative consequences of this practice such as impaired judgment (Campbell, 2003). Amphetamines are prescribed for people with narcolepsy, a sleep disorder characterized by excessive sleepiness (see Chapter 10). Some of these drugs (Ritalin) are even given to children with attention-deficit/hyperactivity disorder (discussed in Chapter 15). Amphetamines too are being misused for their psychostimulant effects (Barrett et al., 2006). The DSM-5-TR diagnostic criteria for intoxication in amphetamine use disorders include significant behavioural symptoms, such as euphoria or affective blunting, changes in sociability, interpersonal sensitivity, anxiety, tension, anger, stereotyped behaviours, impaired judgment, and impaired social or occupational functioning. In addition, physiological symptoms occur during or shortly after amphetamine or related substances are ingested, including heart rate or blood pressure changes, perspiration or chills, nausea or vomiting, weight loss, muscular weakness, respiratory depression, chest pain, seizures, or coma. The danger in using amphetamines and the other stimulants is their negative effects, like those experienced by the pilots involved in the friendly fire incident in Afghanistan. Severe intoxication or overdose can cause hallucinations, panic, agitation, and paranoid delusions (Black & Andreasen, 2021d). Amphetamine tolerance builds quickly, making it doubly dangerous. Withdrawal often results in apathy, prolonged periods of sleep, irritability, and depression. Periodically, certain designer drugs appear in local epidemics. An amphetamine called methylenedioxymethamphetamine (MDMA), first synthesized in 1912 in Germany, was used as an appetite suppressant (McCann & Ricaurte, 2009). Recreational use of this drug, now commonly called ecstasy, rose sharply in the late 1980s. In the 2017 CTADS, 1 percent reported using ecstasy (Health Canada, 2019). Rates may be much higher in some groups. For example, a study by Dalhousie clinical psychologist Sean Barrett and his colleagues examined drug use among rave attendees in Montréal. They found that 65 percent of rave- goers had used ecstasy (Gross et al., 2002). The effects of this drug are best described by a user: “just like speed but without the comedown, and you feel warm and trippy like acid, but without the possibility of a major freak-out” (O’Hagan, 1992, p. 10). A purified crystallized form of amphetamine, called ice, is ingested through smoking. This drug causes aggressive tendencies and stays in the system longer than cocaine, making it particularly dangerous (Stein & Ellinwood, 1993). However enjoyable these new amphetamines may be in the short term, the potential for users to become dependent on them is extremely high, with great risk for long-term difficulties. Repeated use of MDMA can cause lasting memory problems (Wagner, Becker, et al., 2013) and even death. In August 2019, in British Columbia, a 14-year-old died after taking ecstasy for the first time; he was trying to fit in. Tragically, his so-called friends posted videos of his intoxication on social media two hours before he died (McDonald, 2019). The Canadian Centre on Substance Use and Addiction (2017) has also highlighted that while people may expect ecstasy to contain only MDMA, substitutions are often made, some of which have deadly consequences. One study documented 27 deaths in Alberta and British Columbia between June 2011 and April 2012 that were due to paramethoxymethamphetamine or PMMA (Nicol et al., 2015). Peter Dazeley/The Image Bank/Getty Images Designer drugs, especially ecstasy, are popular among young people. Amphetamines stimulate the central nervous system by enhancing the activity of norepinephrine and dopamine. Specifically, amphetamines help the release of these neurotransmitters and block their reuptake, thereby making more of them available throughout the system (Black & Andreasen, 2021d). Too much amphetamine—and therefore too much dopamine and norepinephrine—can lead to hallucinations and delusions. As we see in Chapter 14, this effect has stimulated theories on the causes of schizophrenia, which can also include hallucinations and delusions. 365 Cocaine The use and misuse of drugs wax and wane according to societal fashion, moods, and sanctions (Uddo et al., 1993). Cocaine replaced amphetamines as the stimulant of choice in the 1970s (Jaffe et al., 2005). Cocaine is derived from the leaves of the coca plant, a flowering bush indigenous to South America. Latin Americans have chewed coca leaves for centuries to get relief from hunger and fatigue (Mendoza-Azpur et al., 2021). Cocaine was introduced into North America in the late 19th century and was widely used from then until the 1920s. In 1885, Parke, Davis & Co. manufactured coca and cocaine in 15 different forms, including coca-leaf cigarettes and cigars, inhalants, and crystals. For people who couldn’t afford these products, a cheaper alternative was in Coca-Cola, which up until 1903 contained 60 milligrams of cocaine per 240 millilitre serving (Daamen et al., 2012). Shanti Hesse/Shutterstock.com For centuries, Latin Americans have chewed coca leaves to get relief from hunger and fatigue. Clinical Description Like amphetamines, in small amounts cocaine increases alertness, produces euphoria, increases blood pressure and pulse, and causes insomnia and loss of appetite. Remember that Danny snorted (inhaled) cocaine when he partied through the night with his friends. He later said the drug made him feel powerful and invincible—the only way he really felt self-confident. The effects of cocaine are short-lived; for Danny they lasted less than an hour, and he had to snort repeatedly to keep himself up. During these binges he often became paranoid, experiencing exaggerated fears that he would be caught or that someone would steal his cocaine. Such paranoia is common among cocaine users, occurring in two-thirds or more (Karsinti et al., 2020). Cocaine also makes the heartbeat more rapidly and irregularly, and it can have fatal consequences, depending on a person’s physical condition and the amount of the drug ingested. We saw that alcohol can damage the developing fetus. It has also been suspected that the use of cocaine by pregnant women may adversely affect their babies. Susan Potter of Acadia University, Philip Zelazo of McGill University, and their colleagues (Potter et al., 2000) conducted a study of the cognitive effects of cocaine exposure on the developing fetus. They found subtle deficits in auditory information processing in the cocaine-exposed infants that may help explain the growing evidence that fetal cocaine exposure is associated with subsequent language deficits among children exposed to this drug while still developing in the mother’s uterus. Statistics Surveys indicate low levels of past-year cocaine use in the general population in Canada. For example, a 1998–1999 Toronto survey found that about 1 percent of adults and about 6 percent of students used cocaine in the past year (Bernstein et al., 2002). The 2017 CTADS reported that 2 percent of Canadians used cocaine, an increase from the 1 percent reported in the 2015 and 2013 cycles of the survey (Health Canada, 2019). Cocaine is most often snorted through the nose, but it may also be injected. Crack cocaine is a crystallized form of cocaine that is smoked rather than snorted or injected (Closser, 1992). In Toronto, use of crack cocaine is reported in surveys by less than 1 percent of adults and by about 2 percent of students (Bernstein et al., 2002). Cocaine is in the same group of stimulants as amphetamines because it has similar effects on the brain. The “up” seems to come primarily from the effect of cocaine on the dopamine system. Cocaine enters the bloodstream and is carried to the brain. There, the cocaine molecules block the reuptake of dopamine. As you know, neurotransmitters released at the synapse stimulate the next neuron and then are recycled back to the original neuron. Cocaine seems to bind to places where dopamine neurotransmitters re-enter their home neuron, blocking their reuptake by the neuron. The dopamine that cannot be taken in by the neuron remains in the synapse, causing repeated stimulation of the next neuron. This stimulation of the dopamine neurons in the “pleasure pathway” (the site in the brain that seems to be involved in the experience of pleasure) causes the high associated with cocaine use. In the 1980s many felt cocaine was a wonder drug that produced feelings of euphoria without being addictive (Weiss & Iannucci, 2009). Even the Comprehensive Textbook of Psychiatry in 1980 indicated that “taken no more than two or three times per week, cocaine creates no serious problems” (Grinspoon & Bakalar, 1980). Just imagine—a drug that gives you extra energy, helps you think clearly and more creatively, and lets you accomplish more 366 throughout the day, all without any negative side effects! In our highly competitive and complex technological society, this would be a dream come true. But, as you probably realize, such temporary benefits have a high cost. Cocaine fooled us. Addiction does not resemble that of many other drugs early on, and typically people only find that they have a growing inability to resist taking more (Black & Andreasen, 2021d). Few negative effects are noted at first; however, with continued use, sleep is disrupted, increased tolerance causes a need for higher doses, paranoia and other negative symptoms set in, and the cocaine user gradually becomes socially isolated. Chronic use may result in premature aging of the brain (Vicario et al., 2020). Again, Danny’s case illustrates this pattern. He was a social user for a number of years, using cocaine only with friends and only occasionally. Eventually, he had more frequent episodes of excessive use or binges, and he found himself increasingly craving the drug between binges. After the binges, Danny would crash and sleep. Cocaine withdrawal isn’t like that of alcohol. Instead of rapid heartbeat, tremors, or nausea, withdrawal from cocaine produces pronounced feelings of apathy and boredom. Think for a minute about how dangerous this type of withdrawal is. First, you’re bored with everything and find little pleasure in the everyday activities of work or relationships. The one thing that can bring you back to life is cocaine. As you can imagine, a particularly vicious cycle develops: cocaine is used, withdrawal causes apathy, and cocaine use resumes. The atypical withdrawal pattern misled people into believing that cocaine was not addictive. We now know that cocaine users go through patterns of tolerance and withdrawal comparable to those experienced by users of other psychoactive drugs (Denomme & Shane, 2020). John Greim/LightRocket/Getty Images This little girl’s mother used cocaine during her pregnancy. Research continues into the effects of the drug on children of dependent mothers. Book Title: eTextbook: Psychopathology: An Integrative Approach to Understanding, Assessing, and Treating Psychological Disorders, Seventh Canadian Edition Stimulants Tobacco-Related Disorders Tobacco-Related Disorders When you think of people addicted to drugs, what image comes to mind? Do you see dirty and dishevelled people huddled on an old mattress in an abandoned building, waiting for the next fix? Do you picture businesspeople huddled outside a city building on a rainy afternoon furtively smoking cigarettes? Both these images are accurate because the nicotine in tobacco is a psychoactive substance that produces patterns of dependence, tolerance, and withdrawal—tobacco-related disorders—comparable to the other drugs we have discussed so far (Kong & Krishnan-Sarin, 2020). In 1942, Scottish physician Lennox Johnson shot up nicotine extract and found after 80 injections that he liked it more than cigarettes and felt deprived without it (Kanigel, 1988). This colourless, oily liquid is what gives smoking its pleasurable qualities. The tobacco plant is native to North America. Various Indigenous peoples cultivated and used the leaves starting centuries ago and continuing today as part of ceremony, prayer, and medicinal practice. Little evidence suggests that Indigenous peoples used tobacco recreationally before contact with Europeans. In traditional usage, tobacco can be inhaled through a pipe but also placed on a fire, in water, or on the ground, and is often given as a gift (Rafferty & Mann, 2014). According to the 2017 CTADS, only 15 percent of Canadians 15 years of age and older smoke, down from the 50 percent who smoked in 1965 (Health Canada, 2019; Physicians for a Smoke-Free Canada, 2012). This downward trend continued throughout 2019 and 2020. Data collected as part of the new Canadian Tobacco and Nicotine Survey (CTNS) has only 1 in 10 Canadians reporting that they regularly smoke cigarettes (Statistics Canada, 2021f). More men than women reported smoking cigarettes (12 percent vs. 9 percent). The CTNS also looked at the prevalence of vaping (e.g., e-cigarettes, vaporizer) among Canadians. More young Canadians reported vaping than older Canadians. Only 3 percent of Canadians over 25 years of age reported vaping in the last 30 days whereas 14 percent of Canadian youth (ages 15–19) and 13 percent of Canadians between the ages of 20 and 24 reported vaping in the past 30 days. The reverse trend is seen for smoking regular cigarettes: Older Canadians are more likely to report smoking cigarettes. Similar to other national surveys, the CTNS covers only Canadians 15 years of age or older and excludes residents in the territories, as well as those living in institutions. A study of health inequalities in Canada determined that smoking prevalence increases as socioeconomic status decreases and that prevalence is higher among Indigenous than non-Indigenous people (PHAC, 2018b). The DSM-5-TR does not describe an intoxication pattern for tobacco-related disorders. Rather, it lists withdrawal symptoms, which include depressed mood, insomnia, irritability, anxiety, difficulty concentrating, restlessness, and increased appetite and weight gain. Once smokers are dependent on nicotine, going without it causes these withdrawal symptoms (Slade, 1999). Nicotine is inhaled into the lungs, where it enters the bloodstream. Only 7 to 19 seconds after a person inhales the smoke, the nicotine reaches the brain (Benowitz, 1996). Nicotine in small doses stimulates the central nervous system; it can also relieve stress and improve mood. However, it can also cause high blood pressure and increase the risk of heart disease and cancer and is the leading 367 cause of preventable disease and death worldwide (Kong & Krishnan-Sarin, 2020). High doses can blur vision, cause confusion, lead to convulsions, and sometimes even cause death. Nicotine appears to stimulate specific receptors— nicotinic acetylcholine receptors (nAChRs)—in the midbrain reticular formation and the limbic system, the site of the brain’s pleasure pathway (the dopamine system responsible for feelings of euphoria) (Kong & Krishnan-Sarin, 2020). Smokers dose themselves throughout the day in an effort to keep nicotine at a steady level in the bloodstream (10 to 50 nanograms per millilitre; Dalack et al., 1993). Some evidence also points to how maternal smoking can predict later substance-related disorders in children, but this appears to be an environmental (e.g., home environment) rather than a biological influence (D’Onofrio et al., 2012). Severe depression occurs significantly more often among people with nicotine dependence. Does this mean that smoking causes depression or depression causes smoking? There is a complex and bi-directional relationship between cigarette smoking and negative affect (N. H. Liu et al., 2021). In other words, being depressed increases your risk of becoming dependent on nicotine, and at the same time, being dependent on nicotine will increase your risk of becoming depressed. Genetic studies suggest that a genetic vulnerability and certain life stresses may combine to make you vulnerable to both a nicotine use disorder and depression (e.g., A. C. Edwards & Kendler, 2012). Book Title: eTextbook: Psychopathology: An Integrative Approach to Understanding, Assessing, and Treating Psychological Disorders, Seventh Canadian Edition Stimulants Caffeine-Related Disorders Caffeine-Related Disorders Caffeine is the most common of the psychoactive substances, used regularly by about 90 percent of all North Americans (Mitchell et al., 2014). Called the gentle stimulant because it is thought to be the least harmful of all the addictive drugs, caffeine can still lead to problems like those caused by other drugs (e.g., interfering with social and work obligations; Meredith et al., 2013). This drug is found in tea, coffee, many soft drinks, and cocoa products. High levels of caffeine are added to the energy drinks that are widely consumed in North America today but are banned in some European countries (including France, Denmark, and Norway) because of health concerns (Thorlton et al., 2014). As most of you have experienced firsthand, caffeine in small doses can elevate your mood and decrease fatigue. In larger doses, it can make you feel jittery and can cause insomnia. Because caffeine takes a relatively long time to leave our bodies (it has a blood half-life of about six hours), sleep can be disturbed if the caffeine is ingested close to bedtime. This effect is especially pronounced among those already suffering from insomnia (Byrne et al., 2012). As with the other psychoactive drugs, people react differently to caffeine; some are very sensitive to it and others can consume relatively large amounts with little effect. Previously it was though that moderate use of caffeine (a cup of coffee per day) by pregnant women did not harm the developing fetus (Loomans et al., 2012). More recent research suggests that developing a fetus may be negatively impacted by maternal caffeine use (Christensen et al., 2021). The DSM-5-TR includes caffeine use disorder, defined as problematic caffeine use that causes significant impairment and distress, as a condition for further study, not as a formal disorder (American Psychiatric Association, 2022). As with other stimulants, regular caffeine use can result in tolerance and dependence on the drug, and also intoxication and withdrawal (part of the substance-induced disorders). Those of you who have experienced headaches, drowsiness, and a generally unpleasant mood when denied your morning coffee have had the withdrawal symptoms characteristic of this drug (Favrod- Coune & Broers, 2021). Caffeine’s effect on the brain seems to involve the neuromodulator adenosine and, to a lesser extent, the neurotransmitter dopamine (Juliano et al., 2015). Adenosine plays an important role in the release of dopamine and glutamate in the striatum, which may explain the elation and increased energy that come with caffeine use (Juliano et al., 2015). Book Title: eTextbook: Psychopathology: An Integrative Approach to Understanding, Assessing, and Treating Psychological Disorders, Seventh Canadian Edition Chapter 12. Substance Use and Impulse Control Opioids Opioids The word opiate refers to the natural chemicals in the opium poppy that have a narcotic effect (they relieve pain and induce sleep; see DSM Table 12.4). In some circumstances, they can cause opioid-related disorders. The broader term opioids refers to the family of substances that includes natural opiates, synthetic variations (e.g., heroin, fentanyl, methadone, hydrocodone, oxycodone), and the comparable substances that occur naturally in the brain (enkephalins, beta-endorphins, and dynorphins; Arias et al., 2020). In The Wizard of Oz, the Wicked Witch of the West puts Dorothy, Toto, and the Cowardly Lion to sleep by poisoning poppies in a field that is on the way to Oz, an allusion to the opium poppies used to produce morphine, codeine, and heroin. DSM-5-TR Table 12.4 Diagnostic Criteria for Opioid Use Disorder A. A problematic pattern of opioid use leading to clinically significant impairment or distress, as manifested by at least two of the following, occurring within a 12-month period: 1. Opioids are often taken in larger amounts or over a longer period than was intended. 2. There is a persistent desire or unsuccessful efforts to cut down or control opioid use. 3. A great deal of time is spent in activities necessary to obtain the opioid, use the opioid, or recover from its effects. 4. Craving, or a strong desire or urge to use opioids. 5. Recurrent opioid use resulting in a failure to fulfill major role obligations at work, school, or home. 6. Continued opioid use despite having persistent or recurrent social or interpersonal problems caused or exacerbated by the effects of opioids. 7. Important social, occupational, or recreational activities are given up or reduced because of opioid use. 8. Recurrent opioid use in situations in which it is physically hazardous. 9. Continued opioid use despite knowledge of having a persistent or recurrent physical or psychological problem that is likely to have been caused or exacerbated by the substance. 10. Tolerance, as defined by either of the following: a. A need for markedly increased amounts of opioids to achieve intoxication or desired effect. b. A markedly diminished effect with continued use of the same amount of an opioid. Note: This criterion is not considered to be met for those taking opioids solely under appropriate medical supervision. 11. Withdrawal, as manifested by either of the following: a. The characteristic opioid withdrawal syndrome. b. Opioids (or a closely related substance) are taken to relieve or avoid withdrawal symptoms. Note: This criterion is not considered to be met for those taking opioids solely under appropriate medical supervision. Specify current severity: Mild: Presence of 2–3 symptoms. Moderate: Presence of 4–5 symptoms. Severe: Presence of 6 or more symptoms. American Psychiatric Association. (2022). Diagnostic and statistical manual of mental disorders (5th ed., Text Revision). Just as the poppies lull Dorothy, the Cowardly Lion, and Toto, opioids induce euphoria, drowsiness, and slowed breathing. High doses can lead to death if respiration is completely depressed. Opioids are also analgesics, substances that help relieve pain (Hammond et al., 2020). People are sometimes given morphine before and after surgery to calm them and help block pain. In the early 2000s, a newer prescription opioid drug used in the treatment of pain, oxycodone (OxyContin), raised concerns because of its potential for misuse and for lethal overdose. Oxycodone was featured prominently in the news on the Canadian east coast, particularly in Cape Breton, Nova Scotia, where it had become a popular street drug. Along with other prescription narcotics, oxycodone was linked to the death of 12 residents in 2003–2004. The Nova Scotia College of Physicians and Surgeons sent out a letter to its members, providing practice guidelines to minimize inappropriate prescribing of oxycodone and thus minimize its misuse potential (Moulton, 2004). The manufacturers of oxycodone were fined $635 million for misleading the public about the addictive properties of the drug (Lindsey, 2007). Today, Canada is in the grip of an opioid crisis, one powered by the use of both prescription and illegal opioids (Belzak & Halverson, 2018). It has been 368 estimated that between the years 2000 and 2017 the opioid mortality rate in Canada increased almost six hundred percent. The rates rose gradually between 2000 and 2015 and more dramatically afterwards (Alsabbagh et al., 2021). According to a national report on opioid-related deaths, 11 500 Canadians died from overdose between January 2016 and December 2018 (Special Advisory Committee on the Epidemic of Opioid Overdoses, 2019). Most of the deaths in 2018, 94 percent, were deemed accidental. Fentanyl and related substances were a major focus of analysis, with almost three-quarters of the accidental opioid-related deaths in 2018 attributed to them. The rate of hospitalizations for opioid poisoning increased between 2007 and 2017, with the highest rates occurring among some of our most vulnerable citizens: Canadians over the age of 65 (O’Connor et al., 2018). Concerns are also being raised about high rates of opioid-related hospitalizations and deaths among First Nations people (as cited in Belzak & Halverson, 2018, pp. 228–229). 369 The CIHI (2018) reported that 21.3 million prescriptions for opioids were dispensed in 2017 in Canada, a small drop from 21.7 million in 2016. The 2015/2016 First Nations Regional Health Survey reported that one-quarter of First Nations adults living on-reserve, and 10 percent of youth (12 to 17 years of age), had used prescription opioids in the past year (First Nations Information Governance Centre, 2018). In 2017, the CTADS estimated 3.5 million Canadians (12 percent) used opioid pain relievers (Health Canada, 2019). The COVID-19 pandemic has added fuel to the opioid crisis. Over 5000 Canadians died from opioid toxicity between April and December 2020 alone (Special Advisory Committee on the Epidemic of Opioid Overdoses, 2021). The majority of these deaths were deemed accidental or unintentional and involved fentanyl. This represented an 88 percent increase in such deaths compared to the same time period in 2019 (pre-COVID-19). Hospitalizations for opioid poisonings also increased sharply during 2020. Eighty-five percent of these deaths and almost 90 percent of hospitalizations occurred in British Columbia, Alberta, and Ontario. In addition to a more toxic drug supply, these increases were attributed to the pandemic intensifying feelings of isolation, stress, and anxiety, while at the same time reducing access to mental health services for those who use drugs (e.g., Slavova et al., 2020). Withdrawal from opioids can be so unpleasant that people continue to use these drugs despite a sincere desire to stop (Sneyers et al., 2020). People who cease or reduce their opioid intake begin to experience symptoms within 6 to 12 hours; these include excessive yawning, nausea and vomiting, chills, muscle aches, diarrhea, and insomnia—temporarily disrupting work, school, and social relationships. The symptoms can persist for one to three days, and the process is completed in about a week. People who use opioids face risks beyond addiction and the threat of overdose. Because some of these drugs are usually injected intravenously, users are at increased risk for HIV infection and therefore AIDS. In fact, a survey conducted in the late 1990s (Strathdee et al., 1997) showed that HIV incidence among injection drug users in Vancouver, British Columbia, was the highest ever documented among injection drug users in the developed world (Wood & Kerr, 2006). An estimated 171 900 Canadians between the ages of 16 and 64 (0.70 percent of the population) injected drugs in 2016 (Jacka et al., 2020). Prevalence varied by province with British Columbia having the highest prevalence rate (1.5 percent). This number will likely have increased in recent years, and we know that 21.5 percent of new HIV infections in 2019 were likely related to injection drug use (Haddad et al., 2021). The life of someone addicted to an opioid is bleak. Mortality rates in this population range from 6 to 20 times that of the general population. Those individuals who live face much hardship when recovering from addiction, with stable abstinence rates as low as 30 percent and most individuals undergoing many relapses. Even those who discontinue opioids often use alcohol and other drugs in their place (Hser et al., 2015). Results from a 33-year follow-up study of more than 80 opioid users in an English town highlight this pessimistic view (Rathod et al., 2005). At the follow-up, 22 percent of opioid users had died, about twice the national rate of about 12 percent for the general population. More than half the deaths were the result of drug overdose, and several people took their own lives. The good news from this study was that of those who survived, 80 percent were no longer using opioids and the remaining 20 percent were being treated with methadone. Persistent opioid use may be related to comorbid mental disorders and sexual or physical abuse. Long-term recovery has been shown to be associated with family and social support, employment, and opioid abstinence of at least five years (Hser et al., 2015) HLPhoto/Shutterstock.com Opium poppies The high or rush experienced by users comes from activation of the body’s natural opioid system. In other words, the brain already has its own opioids— called enkephalins and endorphins—that provide narcotic effects (Blum et al., 2020). Heroin, opium, morphine, and other opioids activate this system (just as does alcohol at certain doses; Gianoulakis, 2001; Peterson et al., 1996). The discovery of the natural opioid system has allowed us to study the effects of addictive drugs on the brain and has led to important discoveries that may help us treat people dependent on these drugs. Book Title: eTextbook: Psychopathology: An Integrative Approach to Understanding, Assessing, and Treating Psychological Disorders, Seventh Canadian Edition Hallucinogens Hallucinogens On a Monday afternoon in April 1943, Albert Hoffmann, a scientist at a large Swiss chemical company, prepared to test a newly synthesized compound. He had been studying derivatives of ergot, a fungus that grows on diseased kernels 370 of grain, and sensed that he had missed something important in the 25th compound of the lysergic acid series. Ingesting what he thought was an infinitesimally small amount of this drug, which he referred to in his notes as LSD-25, he waited to see what subtle changes might come over him as a result. Thirty minutes later he reported no change; but some 40 minutes after taking the drug he began to feel dizzy and had a noticeable desire to laugh. Riding his bicycle home, he hallucinated that the buildings he passed were moving and melting. By the time he arrived home, he was terrified that he was losing his mind. Albert Hoffmann was experiencing the first recorded “trip” on LSD (Stevens, 1987). LSD (d-lysergic acid diethylamide), sometimes referred to as acid, is a common hallucinogenic drug. It is produced synthetically in laboratories, although naturally occurring derivatives of this grain fungus (ergot) have been found historically. In Europe during the Middle Ages, an outbreak of illnesses occurred after people ate grain that was infected with the fungus. One version of this illness—later called ergotism—constricted the flow of blood to the arms or legs and eventually resulted in gangrene and the loss of limbs. Another type of illness resulted in convulsions, delirium, and hallucinations. Years later, scientists connected ergot with the illnesses and began studying versions of this fungus for possible benefits. This is the type of work Albert Hoffmann was engaged in when he discovered LSD’s hallucinogenic properties. LSD largely remained in the laboratory until the 1960s, when it was first produced illegally for recreational use. The U.S. Central Intelligence Agency did, however, test LSD as a “truth serum” during interrogations though the agency abandoned their efforts after several serious incidents and no evidence of truth (Lee & Shlain, 1992). The mind-altering effects of the drug suited the social effort to reject established culture and enhanced the search for enlightenment that characterized the mood and behaviour of many people during that decade (Parrott, 2012). The late Timothy Leary, at the time a Harvard research professor, first used LSD in 1961 and immediately began a movement to have every child and adult try the drug and “turn on, tune in, and drop out.” During this time, LSD was also being experimented with in the context of therapy. For example, based on the spirituality theory of sobriety (i.e., that spirituality can induce sobriety from alcohol among those with alcohol disorders), some reasoned that therapists could exploit the spiritual aspect of the LSD trip to assist in recovery from alcohol use disorder (then usually called alcoholism). In the 1950s, Dr. Humphrey Osmond performed an experiment to test this theory on a sample of 1000 patients with a history of severe alcoholism receiving treatment at the Weyburn Hospital in Saskatchewan. Participants were administered a single high dose of LSD. Osmond reported that 50 percent did not drink alcohol again, leading him to argue strongly for the efficacy of this approach (Lee & Shlain, 1985). In fact, William (Bill) Wilson, co-founder of Alcoholics Anonymous (AA), is known to have experimented with and advocated this controversial approach to the treatment of alcoholism (Roberts & Hruby, 1984). There has been a resurgence, in recent years, in research examining the potential therapeutic impact of hallucinogens for people struggling with psychological disorders (e.g., Begola & Schillerstrom, 2019). Several other hallucinogens exist, some occurring naturally in a variety of plants: psilocybin (found in certain species of mushrooms), lysergic acid amide (found in the seeds of the morning glory plant), dimethyltryptamine (DMT; found in the bark of the Virola tree, which grows in South and Central America), and mescaline (found in the peyote cactus plant); and some produced synthetically phencyclidine (PCP). The DSM-5-TR diagnostic criteria include perceptual changes, such as the subjective intensification of perceptions, depersonalization, and hallucinations. Physical symptoms include pupillary dilation, rapid heartbeat, sweating, and blurred vision (American Psychiatric Association, 2022). Many users have written about hallucinogens, and they describe a variety of experiences. The kinds of sensory distortions reported by Hoffmann are characteristic reactions. People tell of watching intently as a friend’s ear grows a

Psychopathology: Substance Use & Impulse Control (eTextbook)

Document Details

Tags

Related

Summary

Full Transcript

Upgrade to continue