Psychology: an introduction (Oxford Southern Africa) - Leslie Swartz 2011

Substance abuse and psycho-pharmacology
Psychology and health

Bronwyn Myers & Arvin Bhana; Elias Mpofu

CHAPTER OBJECTIVES

After studying this chapter you should be able to:

•define substance misuse, abuse and dependence

•discuss the continuum concept of problem severity

•understand the mechanisms underlying drug tolerance and dependency

•discuss a variety of theories explaining substance use disorders

•explain and discuss risk, vulnerability, resilience and protective factors with regard to substance abuse

•outline how risk, vulnerability, resilience and protective factors operate at multiple levels of influence

•describe the mechanisms of action of psychoactive drugs

•distinguish between drug potency, efficacy and dose

•explain the need to monitor drug consumption

•describe the classes, the uses and the effects of psychoactive drugs.

CASE STUDY

Xolani had grown up in a household where nobody drank alcohol but, like many South African teenagers, he had learned a great deal about drugs and alcohol while he was still at school. Many of the kids drank beer on the weekends, and Xolani had heard that it was really easy to buy drugs on the street or even inside the grounds of his high school. Xolani’s school teachers spoke to them quite a lot about the dangers of drugs, but he knew that most of the class didn’t take their warnings seriously. Some of the kids at school didn’t seem to be affected very much by their drinking, or even by taking drugs. But over time one could see that some kids were affected. There was one boy from his class who had been smoking white pipes, a mixture of dagga and mandrax. He dropped out of school before the end of Grade 10, even though he had been one of the bright kids in the class before he started smoking.

Since Xolani had come to university, he had also noticed how much drinking was regarded as a normal part of campus life. He would often overhear other students talking about how much they had had to drink the previous night and everyone would laugh as they held their heads complaining of a ’hangover’. Most social activities on campus seemed to involve drinking and sometimes he felt a bit left out.

Xolani had heard that some people were also addicted to prescription drugs or to medicines that didn’t need a prescription (over-the-counter medicines). Xolani had always believed that prescription drugs should only be taken as a last resort and that the body should be allowed to heal itself before a person started popping pills. But when his best friend, Clive, was diagnosed with panic disorder, Xolani advised him to try to deal with his irrational fears through talking to a psychotherapist and taking the medication his doctor had prescribed. Clive began to feel much better. He continued to see his psychotherapist and eventually was able to function as he had before the onset of his panic attacks. Today, almost a year later, Clive is no longer taking medication for his panic attacks and is only seeing his psychotherapist occasionally.

Introduction

Historically, the term ’substance use’ has been used to cover the broad spectrum of alcohol and drug use; these are known as psychoactive substances. These include any substance which when taken (swallowed, inhaled, injected, etc.) has the ability to alter a person’s consciousness, mood or cognitive processes. According to Morojele, Parry, Brook and Kekwaletswe (2012, p. 196), substance use refers to ’the use of any psychoactive substance, regardless of the frequency of use, or any problems associated with the use of the substance’. However, it is important to understand that substance use is often the first stage in a progression to ultimate disease. It often also leads to dependence on the substance. The next step is substance abuse or misuse. These terms are defined below:

•Substance misuse refers to substance use which results in some adverse consequences that are not recurrent (e.g. a single drunken-driving charge would be an example of alcohol misuse).

22.1THE CAUSES OF SUBSTANCE USE DISORDERS

Intrapersonal factors

Intrapersonal factors are those factors that are located within the individual, such as biological or psychological causes. According to the American Society of Addiction Medicine (2011), genetic inheritance accounts for about 50 per cent of the likelihood of an individual developing an addiction. The person may also be experiencing distortions in purpose, values and spiritual experience.

Interpersonal factors

Interpersonal factors are those factors that are located between individuals, such as peer influence and social learning experiences, as well as disruption in social support.

Environmental factors

Environmental factors are those factors that are located within a particular environment, such as a culture of drug use or a high availability of alcohol in a particular community.

•Substance abuse refers to a maladaptive pattern of substance use that manifests recurrently and has significant negative consequences (e.g. being late for work repeatedly due to a hangover from alcohol abuse use the previous night).

•Substance dependence refers to a cluster of cognitive, behavioural and physiological symptoms (including tolerance and withdrawal — see more on these later in the chapter) indicating that a person compulsively continues to use a substance despite significant substance-related problems. Alcoholism is a lay term for alcohol dependence.

Conceptual understandings of substance dependence

Historically, conceptual understandings of substance dependence have been dominated by categorical thinking that viewed substance dependence as either present or absent (Miller, 1996). Researchers have since argued that substance use behaviour occurs on a continuum of problem severity. That is, substance use behaviour ranges from non-problematic (recreational) use, through misuse, to substance abuse and, finally, substance dependence (Myers, Louw & Fakier, 2008). These categories suggest that substance abuse occurs as a sort of continuum from least serious (substance use) to most serious (substance dependence).

However, in terms of DSM-5, the former (DSM-IV-TR) categories of substance abuse and substance dependence have been combined to form the category substance use disorder. The notion of a continuum still exists in DSM-5, however, in the form of severity specifiers. For example, alcohol use disorder may be mild, moderate or severe, depending on the number of symptoms of the disorder shown by a person. In addition, each substance is addressed separately, such that a person may be diagnosed with alcohol use disorder and stimulant use disorder, for example.

Figure 22.1 Examples of common substances available today

Substance dependence can be understood as addiction. According to the American Society of Addiction Medicine (2011), addiction ’is a primary, chronic disease of brain reward, motivation, memory and related circuitry’. Addiction involves craving, an inability to abstain, reduced ability to recognise problems in behaviour and relationships and a problematic emotional response.

Different degrees of problem severity require different types of interventions (see Figure 22.2). The more severe the problem, the less likely it is that a person will be able to return to non-problematic use. For such individuals, the primary goal of treatment should be abstinence. In contrast, the less severe the problem, the more likely it is that the person will be able to maintain non-problematic use. For these individuals, a goal of treatment could be controlled use.

Figure 22.2 The continuum of substance-use behaviour

22.2THE EXTENT OF SUBSTANCE ABUSE AMONG PEOPLE ACCESSING SPECIALIST TREATMENT CENTRES AND PSYCHIATRIC HOSPITALS IN THREE AREAS IN SOUTH AFRICA

This data comes from the South African Community Epidemiology Network on Drug Use (SACENDU) & Medical Research Council. SACENDU is ’a network of researchers, practitioners and policy makers from six sentinel areas in South Africa’ surveying alcohol and other drug use trends (Johnson et al., 2014, p. 1). The data represents the primary substance of abuse among people accessing specialist treatment centres and psychiatric hospitals in three of the six sentinel areas.

Figure 22.3 Alcohol and drug abuse in the Western Cape using specialist treatment data (Johnson et al., 2014)

Figure 22.4 Alcohol and drug abuse in KwaZulu-Natal using specialist treatment data (Johnson et al., 2014)

Figure 22.5 Alcohol and drug abuse in Gauteng using specialist treatment data (Johnson et al., 2014)

*Methamphetamine

SUMMARY

•The broad spectrum of alcohol and drug use includes misuse, abuse and dependence.

•Historically, substance dependence has been viewed as either present or absent. Other researchers have argued that substance use behaviour occurs on a continuum of problem severity.

•Most recently, DSM-5 has combined the abuse and dependence diagnoses into a single diagnosis of substance use disorder.

•Substance dependence can be understood as addiction.

•Different degrees of problem severity require different types of interventions.

Drug dependence and tolerance

One aspect of psychoactive substances is that people may develop dependence and/or tolerance of the substance. This section will briefly discuss the underlying mechanisms involved in drug dependence and tolerance.

Drug dependence may involve physical or psychological dependence (or both) (Parrott, Morinan, Moss & Scholey, 2004). In physical dependence, the person must maintain a certain level of drug in his/her bloodstream in order to function effectively. Not taking the drug and/or reduced blood levels of the drug result in withdrawal symptoms (or abstinence syndrome), and a compulsive need to find and use the drug to restore a drug-induced sense of well-being (Parrott et al., 2004). Some drugs produce psychological dependence more than physical dependence (Maisto, Galizio & Connors, 2004). For example, some cannabis users crave the positive feelings associated with using this drug, although the abstinence experience is not a strong as with nicotine, cocaine or amphetamines (Parrott et al., 2004). When people have drug dependence (or addiction), they seem to be driven by a bio-psychological need to maintain some equilibrium in the drug level present in the person’s blood circulation at any one moment, since re-taking the drug treats the withdrawal symptoms or restores a sense of well-being. Cross-dependence is a type of drug dependence where people develop a dependency on a drug that was initially used to relieve the withdrawal symptoms experienced when ceasing to use another drug.

Drug tolerance refers to the need to consume increasing amounts of a drug to experience the desired effect. Two processes have been linked to the development of drug tolerance: metabolic (pharmacokinetic) tolerance and pharmacodynamic tolerance (Julien, 1996; Parrott et al., 2004). Metabolic tolerance arises from the liver breaking down psychoactive drugs into usable derivatives or waste matter for eventual cleansing from the body. Psychoactive drugs typically increase the actions of enzymes of the liver cells. Repeated exposure to psychoactive drugs accelerates the rate at which these drugs are decomposed by the liver, leading to the need for higher dosages of a drug to achieve the same psychopharmacological effects as before.

Pharmacodynamic tolerance, by contrast, derives from cellular adaptation that occurs with repeated use of a psychoactive agent (Parrott et al., 2004). In this case, tolerance develops because the number of receptors for a particular psychoactive drug increases so that synaptic drug processing is rapid or has a ’washout’ effect. Pharmacodynamic tolerance is also possibly due to the fact that receptor sensitivity to a drug may be reduced by overexposure. In both cases, greater dosages of the drug will be required to achieve the desired effect. The fact that people who abuse alcohol develop a tolerance for it is due to both metabolic and cellular adaptation tolerance. Cross-tolerance is when a person has a reduced response to a drug because of previous exposure to another drug in the same family (Parrott et al., 2004).

SUMMARY

•Drug dependence may involve physical or psychological dependence.

•In physical dependence, the person must maintain a certain level of drug in his/her bloodstream in order to function effectively and to avoid withdrawal symptoms.

•In psychological dependence, users crave the positive feelings associated with using the drug.

•Cross-dependence occurs when people develop a dependency on a drug that was initially used to relieve the withdrawal symptoms experienced when stopping another drug.

•Drug tolerance refers to the need to consume increasing amounts of a drug to experience the desired effect.

•Metabolic tolerance arises from the liver breaking down psychoactive drugs into usable derivatives or waste matter for eventual cleansing from the body.

•Pharmacodynamic tolerance derives from cellular adaptation that occurs with repeated use of a psychoactive agent.

•Cross-tolerance is when a person has a reduced response to a drug because of previous exposure to another drug in the same family.

Understanding the causes of substance use disorders

Numerous theories have tried to identify the aetiology of substance use disorders. Aetiology is the term used for the study of the causes of disorders and diseases. Some theories have examined intrapersonal factors, such as inherited vulnerability. Other theories have identified interpersonal factors, such as family discord. The role of environmental factors in the aetiology of substance use disorders has also been explored. To date, no single cause has been able to explain fully the development of substance use disorders, and it is now widely recognised that substance use disorders have multiple causes.

The risk and resilience approach to substance use disorders among adolescents

Risk factors are those behaviours or environmental factors that increase susceptibility to a specific risk. The recognition that there are multiple factors that place an adolescent at risk for developing a substance use disorder led to the adoption of a risk-factor approach to understanding substance use among adolescents (De Wit & Silverman, 1995). Further research has shown that substance use disorders have a number of causes (Kilpatrick et al., 2000), and that as the number of risk factors increases, the risk of an individual developing a substance use disorder also increases (Cosden, 2001).

However, the risk of developing a substance use disorder is mediated by protective factors that provide adolescents with the resilience to withstand the pressures of living in a risky environment (Cosden, 2001; Fergus & Zimmerman, 2005). Risk factors and protective factors are thus seen as two conceptually distinct dimensions that together predict vulnerability to substance use (Cosden, 2001; Weinberg, 2001). Risk factors tend to predict the increased likelihood of vulnerability. In contrast, protective factors predict a decreased likelihood of vulnerability. But it should be noted that it is only in high-risk environments that protective factors act to buffer the probability of drug use occurring (Amaro, Blake, Schwarz & Flinchbaugh, 2001; Weinberg, 2001). A vulnerability model of substance use disorders is depicted in Figure 22.6.

Figure 22.6 A vulnerability model of substance use disorders

Individual, interpersonal and environmental aetiological factors

As mentioned, researchers have identified multiple sets of risk factors and protective factors that operate at the level of the individual, at the level of interpersonal functioning, and at the level of the environment (Amaro et al., 2001). The following subsections examine factors implicated in the development of substance use disorders for each level of functioning.

Factors located at the level of the individual

Biological factors

The possibility of a genetic predisposition to developing alcohol and other drug (AOD) problems has been widely investigated through the use of family, adoption and twin studies (Bevilaqua & Goldman, 2009). A review of controlled family studies reported that the risk for developing alcohol dependence was three times greater among first-degree relatives of alcoholics than controls, and the risk for developing drug dependence was two times greater among first-degree relatives of alcoholics than controls (Merikangas & Avenevdi, 2000), while the American Society of Addiction Prevention (2011) reports that 40 to 60 per cent of a person’s predisposition to addiction is the result of genetics.

Twin studies have compared monozygotic (identical) twins and dizygotic (fraternal) twins to establish the extent to which substance use disorders are hereditary. Heath, Bucholz, Madden et al. (1997) reported that two-thirds of the risk for developing alcohol-related problems was genetically mediated, with the remainder of the risk being determined by environmental factors not shared by the two members of the twin pair. Kendler and Prescott’s (in Weinberg, 2001) study of monozygotic and dizygotic twins found heritability for substance dependence of up to 80 per cent in some populations. There appears to be significantly greater heritability for substance dependence than for substance abuse, and significantly greater heritability for substance abuse than for non-problematic use (Merikangas & Avenevdi, 2000).

There seem to be two major neurological processes that contribute to the development of substance dependence (Miller, 2013):

•Reinforcement refers to the presence of a rewarding stimulus or the relief of an unpleasant sensation that increases the probability of a particular behavioural response (such as AOD use).

•Neuro-adaptation refers to the compensatory adjustment the brain makes in an attempt to continue normal functioning despite the presence of AODs.

Occurring together, reinforcement and neuro-adaptation seem to underlie both the acute response to AODs and the establishment of the long-term tolerance, craving and withdrawal characteristics of substance dependence.

Psychological factors

A number of personality traits have been identified as risk factors for substance use disorders. These include high levels of novelty seeking and sensation seeking (Ersche, Turton, Pradhan, Bullmore & Robbins, 2010). People with high levels of disinhibition (low levels of behaviour control and high levels of impulsivity) also appear to be at risk for substance use disorders (Amaro et al., 2001; Griffin, Botvin, Epstein, Doyle & Diaz, 2000; Weinberg, 2001). Ersche et al. (2010) found that impulsivity mediates the risk for AOD dependence, while ’abnormal sensation seeking’ may follow stimulant drug abuse.

The initiation of AOD use is also associated with an external locus of control and low self-esteem (Amaro et al., 2001). In addition, deficits in psychosocial skills such as poor coping and weak communication skills have been linked to drug use (Amaro et al., 2001). Similarly, unconventional attitudes including tolerance for deviance and delinquency are important predictors for adolescent drug use (Brook, Pahl, Morojele & Brook, 2006).

Psychiatric problems such as conduct disorder and antisocial behaviour also contribute to the development of substance use disorders (Amaro et al., 2001; Assanangkornchai, Geater, Saunders & McNeil, 2002). Depression and anxiety disorders have also been strongly linked to the initiation of AOD use (Amaro et al., 2001; Donovan, 2004; Merikangas & Avenevdi, 2000). For women, post-traumatic stress disorder (due to childhood abuse or intimate-partner violence) is a significant predictor of substance use disorders (Kilpatrick et al., 2000; Saloman, Bassuk & Huntington, 2002).

Various psychological characteristics that reduce the risk of AOD use in adolescents have been identified. These include autonomy, social competence, problem-solving ability, intelligence, and high levels of religiosity, self-esteem, affect regulation and conventionality (Fergus & Zimmerman, 2005; Wills, Sandy, Yaeger & Shinar, 2001).

Factors located at the level of interpersonal functioning

Family factors

Family dysfunction (drug use, criminal behaviour, negative life events, parent—child conflict or marital discord) has been associated with adolescent drug use (Brook et al., 2006). In contrast, positive family role models tend to buffer the risk of adolescent drug use (Fergus & Zimmerman, 2005; Wills et al., 2001).

The attachment and control aspects of the parent— adolescent relationship have also been associated with adolescent drug use. In terms of attachment, parental displays of affection and identification with the parent (Morojele & Brook, 2001) have been associated with reduced involvement with AODs as have a family environment with strong ties and high levels of social support (Amaro et al., 2001; Weinberg, 2001). In contrast, parental absences and poor parental monitoring have been associated with greater drug use (Donovan, 2004; Weinberg, 2001).

In terms of control, parental permissiveness and authoritarian disciplinary practices (Donovan, 2004; Morojele & Brook, 2001) as well as inadequate and inconsistent family management practices have been associated with greater drug use. In contrast, adolescents with high perceptions of family sanctions against drug use tend to be buffered against drug use (Weinberg, 2001). For example, a study of 826 adolescents revealed that family rules and parental monitoring provided a significant buffer against substance use (Stewart, 2002).

Peer factors

Peer-related variables, especially hanging out with friends after school, close involvement with drug-using peers and peer pressure, are powerful predictors of adolescent drug use (O’Connell, Boat & Warner, 2009; Weinberg, 2001). In general, the possibility of an adolescent engaging in AOD use increases the more they are embedded in a substance-using peer context (Hussang, 2002). Peer pressure is a common reason given by South African adolescents for AOD use and misuse (Brook et al., 2006).

Factors located at the level of the environment

Mainstream institutions

The degree of attachment to mainstream institutions (e.g. schools and religious organisations) is a significant predictor of AOD use among adolescents (Amaro et al., 2001; Donovan, 2004). Dropping out of school, poor school attendance (Amaro et al., 2001), school failure, low levels of educational achievement and/or educational aspirations (Morojele & Brook, 2001), and low investment in academic institutions (Hawkins, Catalano & Arthur, 2002) are significantly associated with increased involvement in AOD use. In contrast, where there is a high degree of attachment, these factors appear to operate as protective factors that buffer the risk of AOD use.

Social factors

Social factors include exposure to substance use/abuse in a person’s community, as well as the degree of acceptance or approval of such activities within the community (Morojele et al., 2012). The latter may be indicated by the way in which substance use is depicted in social media. This primarily relates to alcohol as it is a legal substance, although its use is restricted for vehicle drivers. In South Africa (and globally), there are frequent media campaigns against alcohol abuse, especially for drivers and pedestrians. In addition, the South African government has introduced draft legislation for a total ban on alcohol advertising. There is strong support for this from public health agencies. For example, Parry, Harker Burnhams and London (2012, p. 602) note that ’making alcohol less available and more expensive, and placing a ban on alcohol advertising, are the most cost-effective ways to reduce the harm caused by alcohol’. This move has been strongly opposed by the alcohol and advertising industries which cite the potential harm caused to the economy in terms of job losses and the anticipated increase in illicit sales of alcohol (Ramsoomar, 2015).

Cultural and economic factors

Ethnic minorities often face a number of stressors, such as exposure to violence, lower educational attainment, lower income, the inability to secure employment and daily experiences of discrimination. These experiences appear to act as indirect risk factors that increase stress levels and therefore the likelihood of AOD use (Amaro et al., 2001; Brook et al., 2006). In South Africa, many families have been stressed by the economic and social changes associated with the end of apartheid and these environmental factors are associated with increased AOD use (Brook et al., 2006).

Poverty has also been a contributing factor to AOD use as micro-enterprises have developed around the production and distribution of AODs. These informal sales provide many with an income and play a significant role in the economy (Parry, Bhana, Plüddemann et al., 2002).

Occupational factors

In South Africa, certain occupational factors have also contributed to high levels of alcohol misuse. In the farming areas of the Western Cape, the dop system or tot system (where farm workers received alcohol as part payment of their wages) has been a significant contributing factor to high levels of alcohol dependence among these communities (London, 2000; Parry, Bhana, Myers et al., 2002) (for the effects of alcohol on unborn babies, see Chapter 3). The mining industry has also contributed to high levels of alcohol misuse. Lightfoot, Maree and Ananias (2009) report that various features of miners’ lifestyles encouraged alcohol misuse, especially the living conditions. Many migrant miners live in same-sex hostels where the only place to socialise is the local liquor outlet. Lightfoot et al. (2009) note that, apart from the direct consequences of the alcohol abuse, this situation creates a high-risk environment for the transmission of HIV.

SUMMARY

•It is now widely recognised that substance use disorders have multiple causes; it is thus helpful to take a risk and resilience approach to understanding the aetiology of these disorders.

•As the number of risk factors increases, the risk of an individual developing a substance use disorder also increases; however, the risk of developing a substance use disorder is also mediated by protective factors.

•Risk and protective factors may operate at individual, interpersonal and/or environmental levels.

•Biological factors include a genetic predisposition as well as the neurological processes of reinforcement and neuro-adaptation.

•Psychological factors include personality traits like novelty seeking and sensation seeking, impulsivity, external locus of control, low self-esteem, poor coping and weak communication skills.

•Conduct disorder and anti-social behaviour also contribute to the development of substance use disorders, as do depression and anxiety, and childhood abuse or intimate-partner violence.

•Family dysfunction in terms of weak or inappropriate role models, conflict, weak attachment and social support are significant factors. Parental permissiveness or authoritarian disciplinary practices are also important.

•Peer-related variables are powerful predictors of adolescent drug use.

•Degree of attachment to mainstream institutions like schools and religious organisations is a significant predictor of AOD use among adolescents.

•Social factors include community exposure to and/or approval for substance use; the social media have an important role to play in promoting or preventing substance use.

•Cultural (e.g. discrimination) and economic factors (e.g. poverty) also predict AOD use.

•In South Africa, the dop (tot) system has contributed to high levels of alcohol dependence among farm labourer communities. The mining industry has also contributed to high levels of alcohol misuse.

22.3THE AVAILABILITY OF AODS IN SOUTH AFRICA

According to the public health model, vulnerability to substance use disorders is linked to accessibility and availability of AODs (Gruenewald, 2011). Over the last few decades, AODs have been increasingly available and accessible in South Africa (Morojele et al., 2012). This is due in part to socio-political changes that have made South Africa an attractive new market for drug merchants. These changes include relaxed border controls, poorly resourced law enforcement agencies, increased international travel, good transport and banking facilities, and the country’s relative affluence in the region. South Africa’s geographic location also makes it a convenient transshipment point for drugs to Europe and the US (Parry, Bhana, Plüddemann et al., 2002).

Parry et al. (2012, p. 197) note that ’[r]ates of illicit drug use are particularly high among young people in South Africa’ and that there is an association between AOD use and involvement in crime, violence and injury. In 2013, News24 reported that a nine-year-old boy from Centurion was caught selling drugs to primary and high school learners for his parents. A Tshwane police inspector noted that the most popular drugs were dagga and nyaope. The inspector felt that teachers and parents or primary school children were often unaware of drug problems and called on them to be more alert to signs of AOD use among their children.

Implications of the risk factor approach for the prevention of substance use disorders

The public health model for the prevention of disease and disorders involves assessing the epidemiology of a disorder in the target population, identifying the risk factors associated with the problem, applying interventions known to reduce the risk factors and enhance the protective factors, and monitoring the impact of the intervention on the incidence and prevalence of the target disorder (Hawkins et al., 2002). This model recognises that there is no single, optimal strategy for reducing the health, social and economic burden associated with AOD misuse. Instead, the model emphasises the importance of designing and implementing interventions aimed at addressing the problem on multiple levels. In addition, Morojele et al. (2012) emphasise the need to investigate factors that are protective against initiating and continuing with AOD use.

Reviews of prevention research indicate that risk and protective factors should be the primary target for prevention interventions and that the risk reduction/protection enhancement model is the best available framework for preventing AOD problems in adolescence (Hawkins et al., 2002; Morojele et al., 2012). However, research has shown that interventions that reduce risk factors in both individuals and their environment hold promise for preventing AOD use among adolescents. For example, evaluations of prevention programmes in schools that taught social competence and established norms against substance abuse reported less favourable attitudes towards substance use and a reduction in substance use in the school population (Myers, Harker, Fakier, Kader & Mazok, 2008).

Many effective substance abuse prevention programmes have focused on preventing or delaying the start of AOD use in early adolescence because early use increases the risk of later substance abuse and dependence (Hawkins et al., 2002; Myers, Harker et al., 2008). Studies of these interventions have reported an almost immediate effect in preventing early initiation of use, and a more prolonged effect in preventing the use of substances in later adolescence (Hawkins et al., 2002). These results suggest that focusing on risk or protective factors in early adolescence is a useful approach for preventing later AOD abuse and dependence (Hawkins et al., 2002). However, Myers, Harker et al. (2008) caution that prevention programmes need to be carried out over the long term and that booster sessions can be helpful in this regard. Myers, Harker et al. (2008) also suggest that it is important to include peer leaders and adult facilitators in prevention programmes.

However, prevention programmes often fail when communities lack the resources to address all the potential risk factors; also, few programmes encourage communities to identify their most relevant risk and protective factors (Hawkins et al., 2002). Programmes are also more effective when they address broader issues, such as parenting skills training (Myers, Harker et al., 2008). There is clearly a need to select and implement effective evidence-based prevention strategies that match these priority factors (Myers, Harker et al., 2008). One effective programme that incorporates these prevention principles is the Communities That Care (CTC) programme (Hawkins et al., 2002). The social development model (SDM) (see Box 22.4) underpins the CTC programme.

22.4THE SOCIAL DEVELOPMENT MODEL

The social development model (SDM) was developed by Catalano and Hawkins (1996) and is based on social learning theory. The SDM argues that bonding to prosocial groups and clear norms against antisocial behaviour act as protective factors that inhibit the development of substance use behaviour.

Bonding consists of attachment and commitment to the family, school, community and positive peers as well as a belief in the shared values of these social units. As prosocial bonding increases, adolescents are less likely to violate the norms for the behaviour of the group. Clear norms thus provide behavioural guidelines for people bonded to the group.

The SDM argues that bonding is created when people are given opportunities to become involved or make a contribution to the social unit, when they have the skills to take advantage of these opportunities, and when they are recognised for their contribution. The SDM thus assumes that interventions that involve opportunity, skill and recognition are likely to improve bonding to prosocial groups, the adoption of healthy beliefs, and clear standards of behaviour.

SUMMARY

•According to the public health model, the epidemiology of a disorder must be addressed.

•This involves identifying the risk factors associated with the problem, applying interventions known to reduce the risk factors and enhance the protective factors, and monitoring the impact of the intervention on the incidence and prevalence of the target disorder.

•The Communities That Care (CTC) programme (based on the social development model) is an example of an effective intervention programme.

Psychopharmacology

The previous sections discussed alcohol and other drugs as substances of misuse, abuse or dependence. This section will focus on a particular class of drug, namely prescription psychoactive drugs. It must be noted that these drugs are also open to misuse, abuse and dependence. Their use in the management of mental health is referred to as psychopharmacology. As psychopharmacological interventions, prescription psychoactive drugs are typically used to treat the symptoms of psychiatric illness. They can also serve a prophylactic function when they are used to prevent the onset or recurrence of symptoms (Pompili et al., 2010), for example, or when used to counteract the side effects (unintended effects) of another drug that a person may be taking at the same time. The treatment of psychiatric illness with prescription psychoactive drugs is based on the fact that all behaviour (including certain maladaptive behaviours) has a neuropsychological basis (Mpofu, 2002; Mpofu & Conyers, 2003).

The mechanisms of action of psychoactive drugs

Mechanism of action refers to the particular process by which a psychoactive drug achieves its effects. To understand these mechanisms of action it is useful to summarise how the transmission of nerve impulses occurs (see Chapter 7 for a fuller explanation). To recap briefly: neurons are structures of the nervous system that are involved in the transmission of messages throughout the nervous system. The messages are in the form of electrical impulses or signals. Each neuron comprises a cell body, dendrites and an axon. An axon carries nerve impulses to an adjacent cell where dendrites receive the impulses. Between each axon and a dendrite is a space called a synaptic cleft. In transmitting nerve impulses, axons release chemicals called neurotransmitters that help conduct the nerve impulse across the synapse to the next neuron.

For the purposes of this chapter, it is important to note that a psychoactive drug may achieve its effects by:

•facilitating or inhibiting the actions of a neurotransmitter receptor site, and/or

•regulating neurotransmitter availability in the synaptic cleft (Oslon, 2001).

When a drug molecule occupies a receptor site, it facilitates or blocks the actions of a neurotransmitter, leading to the expected treatment effect and associated side effects. Drug molecules can also indirectly enhance or inhibit the signal transmission of a receptor site by impacting on other cellular events that are associated with signal transmission or reception.

Drug potency, efficacy and dose

Apart from the chemical basis of the actions of drugs on particular receptor sites, the effect of a psychoactive agent also depends on:

•drug potency (the absolute amount of a drug that is required to achieve a desired effect)

•drug efficacy (the ability of a drug to produce the desired therapeutic effect)

•drug dose (the quantity or volume of the drug that is administered)

•the method of administration.

The term ’effective dose’ (ED) refers to the dose of the drug that has been determined to produce the desired effect in the majority of people with the fewest possible side effects (Maisto et al., 2004). The ED for individuals may vary within certain limits due to differences in their genetic make-up, their previous experience with the same (or a different) class of drugs, and their age. For example, people who use a certain type of drug repeatedly develop tolerance for the drug and might need to take higher doses of the drug to achieve the same effect (Parrott et al., 2004). There is also significant variability in drug absorption and metabolism among younger and older people compared to the general population (Maisto et al., 2004).

Highly potent drugs tend to achieve the desired effects at lower dosages than less potent drugs (Parrott et al., 2004). At higher dosages, the more potent drugs are toxic and can lead to significant organ damage or death. With highly potent drugs, the absolute increase in dosage necessary to reach toxicity is very small. For that reason, highly potent drugs need to be used with a high degree of medical care or supervision. Part of this supervision includes ongoing monitoring of drug levels in a patient’s blood. This would be done for a number of reasons, including checking that the person is taking the correct dosage, avoiding reaching levels that are toxic, matching levels of the drug in the person’s blood with any changes in symptoms, and checking the levels of various types of blood cells.

SUMMARY

•Psychoactive drugs are substances that achieve their effect by altering mood, thoughts and behaviour; they are also open to misuse, abuse and dependence.

•Psychoactive drugs are usually used to treat or prevent psychiatric illness.

•The treatment of psychiatric illness with psychoactive drugs is based on the fact that all behaviour has a neuropsychological basis.

•The mechanisms of psychoactive drugs involve the transmission of nerve impulses between neurons.

•In transmitting nerve impulses, axons release chemicals called neurotransmitters that help conduct the nerve impulse across the synapse to the next neuron.

•A psychoactive drug may achieve its effects by facilitating or inhibiting the actions of a neurotransmitter receptor site and/or regulating neurotransmitter availability in the synaptic space.

•The effect of a psychoactive agent also depends on:

”drug potency (the absolute amount of a drug that is required to achieve a desired effect)

”drug efficacy (the ability of a drug to produce the desired therapeutic effect)

”drug dose (the quantity or volume of the drug that is administered)

”method of administration.

•The effective dose (ED) of a drug is the amount that produces the desired effect in most people with the fewest side effects. This varies between individuals, depending on metabolism, age, etc.

•Highly potent drugs tend to achieve the desired effects at lower dosages than less potent drugs.

Classes, uses and effects of psychoactive drugs

In this section, the uses and effects of four main classes of psychoactive drugs are briefly discussed: central nervous system depressants, psychostimulants, anti-depressants and mood stabilisers, and anti-psychotics.

Central nervous system depressants

Central nervous system (CNS) depressants are also commonly called sedatives, tranquilisers, anxiolytics and hypnotics. The drugs in this class share the common characteristic of depressing psychomotor behaviour; that is, they diminish environmental awareness and responsiveness. They are useful for relieving anxiety and inducing sleep, unconsciousness and coma (e.g. when a patient with brain injuries needs to be placed in a coma). They are also used as anti-convulsants. The effects of CNS depressants are additive in that the use of one CNS depressant (e.g. alcohol) together with another (e.g. barbiturates) results in more severe behavioural depression. Use of a CNS depressant may also have an additive effect on a person’s pre-existing mental state. For example, a person with mental fatigue is likely to experience a higher level of psychomotor retardation with the ingestion of a CNS depressant, such as alcohol.

Benzodiazepines (e.g. Valium) are CNS depressants with a long history in the treatment of anxiety, panic attacks and phobias (Katzung, 2001). Most anxiolytics used today are in this class (Spiegel, 2003). Benzodiazepines are widely used for neurotic and vegetative conditions due to their limited side effects.

However, benzodiazepines (also referred to as minor tranquilisers) are not effective in treating major psychosis (Lido, 2000). Unfortunately, their use has been associated with higher suicide rates, respiratory problems and ataxia (staggering) (Spiegel, 2003).

Barbiturates are primarily used to treat convulsions. However, they have a high risk for inducing drug dependence or abuse; in addition, they cause respiratory depression and may lead to accidental deaths (Parrott et al., 2004).

Buspirone is a newer type of CNS depressant with a lower risk profile and is the drug of choice in the longer term treatment of anxiety and panic disorders (Spiegel, 2003).

Psychostimulants

Psychostimulants are used to increase mental alertness, increase motor activity, reduce fatigue, relieve boredom and enhance task performance (Parrott et al., 2004). At lower doses, they raise the heart rate and blood pressure, cause the pupils to dilate and increase the flow of blood to the muscles. They also suppress the appetite through their action on serotonin neurons. Caffeine and nicotine are among the most widely used non-prescription psy-chostimulant drugs. Amphetamines and amphetamine derivatives such as methylphenidate (Ritalin) and pemoline (Cylert) are prescription psychostimulants that are widely used for attention deficit/hyperactivity disorder, while other stimulants are used for obesity (through appetite suppression) (Maisto et al., 2004; Parrott et al., 2004). Cocaine is a psychostimulant that is currently an illegal drug in most countries, although it was an ingredient in early versions of Coca-Cola (Maisto et al., 2004).

Table 22.1 Commonly used psychoactive drugs and their effects

Psychostimulants carry the risk of compulsive abuse because of dopamine-induced reinforcement (Maisto et al., 2004). For example, repeated use of amphetamines appears to have the effect of suppressing the dopamine-releasing neurons, leading to the experience of a high energy level. The memory of having achieved a high with the drug reinforces dependency on the drug. A vicious circle of drug use and withdrawal symptoms ensues. At higher doses, psychostimulants may cause anxiety, insomnia, irritability, hypertension, sexual dysfunction and a variety of psychotic behaviours (e.g. paranoia and persecutory fears). In addition, tolerance develops rapidly, leading to a need for increased doses and worse withdrawal symptoms (Spiegel, 2003).

Anti-depressants and mood stabilisers

Anti-depressants (see Box 22.6) are used to elevate mood, to increase physical activity, and to improve appetite and sleep patterns in people with mood disorders, particularly major depression (Spiegel, 2003). People with major depression experience symptoms that cannot be explained by their objective circumstances. These symptoms include profound sadness, pessimism, diminished energy, mental fatigue, hopelessness and lack of sleep. (People experiencing sadness resulting from loss or bereavement, for example, tend not to show some of these symptoms, including psychosis, and are not candidates for treatment with anti-depressants.)

People with major depression can be treated with a variety of anti-depressants. They also respond to electrocon-vulsive shock and psychotherapy in combination with psychopharmacological treatment.

With few exceptions, anti-depressants have a side-effect profile that includes impaired memory, attention deficits, poor dexterity and sedation (Spiegel, 2003). For that reason, most anti-depressants are best taken at bedtime so as to minimise the disruption of personal effectiveness during normal daytime hours.

Major depression is a unipolar affective disorder; however, some people suffer from bipolar disorders which are characterised by some degree of mania interspersed with depression (Parrott et al., 2004). The most common (and longest standing) treatment for bipolar disorders is lithium, a mood stabiliser. This increases the period between manic episodes (Spiegel, 2003). However, some people are not responsive to lithium and others cannot tolerate the side effects. More recently, drugs first developed to treat epilepsy have been used as mood stabilisers. These include carbamazapine (Tegretol) and valproate (Maisto et al., 2004; Parrott et al., 2004).

Anti-psychotics

Drugs used to treat major psychoses, such as schizophrenia, are referred to as anti-psychotics, major tranquillisers, neuroleptics or anti-schizophrenics (Lido, 2000). The side effects of anti-psychotic medications are often incapacitating, which may incline people with psychosis towards noncompliance with the medication.

As discussed in Chapter 24, people with schizophrenia, for whom these drugs are primarily intended, often present with disturbances in thought, emotional regulation and behaviour, with a loss of contact with reality (American Psychiatric Association, 2013; Parrott et al., 2004). Behavioural excesses (e.g. hallucinations and delusions) in people with schizophrenia are referred to as positive symptoms, whereas the symptoms of behavioural inhibition (e.g. lack of affect) are called negative symptoms (American Psychiatric Association, 2013). Anti-psychotic medications are intended to reduce both positive and negative symptoms. However, the majority of anti-psychotic medications are more effective with positive symptoms than negative symptoms (Spiegel, 2003).

22.5THE ACTIVITIES OF NEUROTRANSMITTERS AND PSYCHOACTIVE AGENTS ARE COMPLEX

Neurotransmitter activity is complex, and the factors influencing such activity are not completely understood. For instance, one kind of neurotransmitter will be involved in multiple activities (e.g. behavioural arousal and temperature regulation). Therefore this neurotransmitter’s response to a psychoactive agent will include both the intended effects of the psychoactive agent and interactions involving other activities in which that neurotransmitter is involved.

Similarly, a specific psychoactive agent (e.g. aspirin) may achieve a variety of actions (e.g. pain control, temperature control and inflammation control) through its inhibitory actions on a receptor site that interacts with an enzyme (or enzymes) involved in tissue inflammation.

The fact that a single psychoactive drug or receptor action is involved in multiple effects is central to an appreciation of the use of psychopharmacology in the treatment of mental health conditions. Differences in dosage levels, even by the same psychoactive agent, can alter how a person behaves.

Anti-psychotic medications carry significant risk for akathisia, dystonia and neuroleptic-induced Parkinsonism (Parrott et al., 2004):

•Akathisia refers to subjective feelings of anxiety and restlessness, as well as repetitive, purposeless actions (e.g. pacing and rocking).

•Dystonia refers to involuntary muscle spasms and bizarre posturing of the limbs, trunk, face and tongue.

•Neuroleptic-induced Parkinsonism is evidenced by tremors of the limbs while at rest, with rigidity, slowness of movement and a lack of spontaneity.

The use of anti-psychotic medications is also associated with the experience of tardive dyskinesia, which is characterised by involuntary twitching movements of the face, tongue, limbs and trunk, and also sucking or smacking of the lips, darting, pushing or twisting of the tongue, and lateral movements of the jaws (Maisto et al., 2004).

SUMMARY

•Central nervous system (CNS) depressants are also commonly called sedatives, tranquilisers, anxiolytics and hypnotics. The drugs in this class depress psychomotor behaviour and are useful for relieving anxiety and inducing sleep.

•The effects of CNS depressants are additive.

•CNS depressants include benzodiazepines, barbiturates and buspirone.

•Psychostimulants are used to increase mental alertness, increase motor activity, reduce fatigue, relieve boredom and enhance task performance. They also suppress appetite.

•Psychostimulants include cocaine, caffeine, nicotine, amphetamines and amphetamine derivatives.

•The use of psychostimulants may result in tolerance and compulsive abuse. They may also cause anxiety, insomnia, irritability, hypertension, sexual dysfunction and psychotic behaviours.

•Anti-depressants are used to elevate mood, to increase physical activity, and to improve appetite and sleep patterns in people with mood disorders, particularly major depression.

•People with ’normal’ sadness or depression should not need anti-depressants.

•Most anti-depressants have varied side effects, including impaired memory, attention deficits, poor dexterity and sedation.

•People with bipolar disorders are treated with mood stabilisers; the most common of these is lithium. Certain drugs developed for epilepsy are also used as mood stabilisers.

•Anti-psychotics are used to treat major psychoses, such as schizophrenia.

•The side effects of these medications are often incapacitating, which may lead to non-compliance.

•Anti-psychotic medications aim to reduce both positive and negative symptoms in schizophrenia although they tend to be more effective with positive symptoms.

•Serious side effects include akathisia, dystonia, neuroleptic-induced Parkinsonism and tardive dyskinesia.

22.6BIOCHEMISTRY AND DEPRESSION

The biochemical causes of major depression are not completely understood (Burke, 2014). For many years, it has been widely accepted that depression is caused by abnormally low levels of the neurotransmitters norepinephrine, serotonin and dopamine (Thase & Howland, 1995, in Burke, 2012). However, many other neurotransmitters systems may be affected in depressive disorders. The depletion of these neurotransmitters may be due to an enzyme that metabolises them. It may also be due to high conductivity of the neurotransmitters across the synapse (Julien, 1996). A third possibility is that the re-uptake of the neurotransmitters back into the pre-synaptic vesicles is overly rapid (Parrott et al., 2004).

However, one observation has cast doubt on this explanation for major depression. A change in mood would be expected as soon as the levels of the neurotransmitters are elevated; however, there is a significant time lag between this and an elevation of mood (Spiegel, 2003).

There have been various explanations as to why elevated levels and availability of these neurotransmitters in the synaptic cleft do not lead to an immediate elevation of mood (Julien 1996). First, it takes time for post-synaptic neuronal activity to normalise. Alternatively, mood elevation occurs with an adaptive change in the serotonin receptors rather than the norepinephrine and dopamine receptors and this may take time to achieve (Parrott et al., 2004).

22.7RESEARCH INTO SCHIZOPHRENIA

Source: Andrade, Radhakrishnan and Fernandes (2012)

Goal

The study aimed to examine the pharmacological treatment of schizophrenia in a context of the ongoing poor prognosis for schizophrenia patients despite effective medications having been available for 50 years.

Method

Andrade et al. (2012) argue that the main problem with treating schizophrenia is a poor understanding of the underlying pathophysiology. In addition, they point out that schizophrenia is not a single disorder; rather, it consists of a group of conditions with diverse characteristics and outcomes. Current anti-psychotics may be useful and effective for treating the symptoms of schizophrenia, but if the cause of the disorder is not identified and treated, the patient may relapse. Unfortunately, the various possible causes are as diverse as the variations of the disorder.

Discussion

Treatment at a primary level (preventative) is impossible because it is very difficult to identify people at risk or to modify genetic inheritance. At a secondary level (early diagnosis and treatment), high-risk individuals could be treated; however, the patient may be exposed to stigma and to unnecessary and unpleasant side effects. In practice, drug therapy is only used at the tertiary level (once the disease has taken hold), but can do nothing about brain changes that have been developing. Thus, the most that can be done is to limit symptoms to facilitate possible rehabilitation.

Conclusion

The future of pharmacotherapy in the treatment of schizophrenia appears bleak.

Conclusion

Psychoactive drugs are substances that alter thoughts, moods and behaviour. They are used to treat mental health conditions because of the way they are thought to interact with neurons, which utilise biochemicals called neurotransmitters. Mental health problems are associated with abnormalities in the quality of neurotransmitter activity, therefore psychoactive agents are used to regulate and normalise dysfunctional neuro-transmission, and thereby restore a level of mental health.

However, the use of psychoactive agents to manage mental health is not without cost. For instance, psychoactive agents have side effects in addition to their intended effects, and sometimes the side effects can outweigh the advantages of taking the psychoactive agent.

Psychoactive agents, other drugs and alcohol can all lead to misuse, abuse, tolerance and dependence. No single factor completely accounts for AOD-use problems. The vulnerability model that examines both risk and protective factors, and which includes psychosocial, environmental and genetic factors, allows intervention to occur at multiple levels. Prevention efforts need to match the available resources and the relevance of risk and protective factors in community settings.

KEY CONCEPTS

addiction: a physiological disease involving craving, an inability to abstain, reduced ability to recognise problems in behaviour and relationships, and a problematic emotional response

aetiology: the study of the causes of disorders and diseases

akathisia: a side effect of anti-psychotic drugs that leads to subjective feelings of anxiety and restlessness, and repetitive, purposeless actions

anti-depressants: a class of drugs used to elevate mood, increase physical activity, and improve appetite and sleep patterns in people with mood disorders

anti-psychotics: a class of drugs used to treat major psychoses, such as schizophrenia

axon: a component of a neuron that carries nerve impulses to adjacent cells

central nervous system (CNS) depressants: a class of drugs that diminish environmental awareness and responsiveness, and which are useful for relieving anxiety, inducing sleep, unconsciousness and coma, and controlling convulsions

cross-dependence: a type of drug dependence, where people develop a dependency on a drug that was initially used to relieve the withdrawal symptoms experienced when ceasing to use some other drug

cross-tolerance: a type of drug tolerance whereby a person has a lessened response to a drug because of previous exposure to another drug

dendrites: the components of a neuron that receives nerve impulses from adjacent cells

dopamine: a neurotransmitter located in the brain that is involved in mood, learning and memory, movement disorders and muscle disorders, and Parkinson’s disease

drug dependence: person needs to maintain a certain level of drug in his/her bloodstream in order to function effectively

drug dose: the quantity or volume of a drug that is administered

drug efficacy: the ability of a drug to produce the desired therapeutic effect

drug potency: the absolute amount of a drug that is required to achieve a desired effect

drug tolerance: the need to consume increasing amounts of a drug

dystonia: a side effect of anti-psychotic drugs that leads to involuntary muscle spasms and bizarre posturing of the limbs, trunk, face and tongue

effective dose (ED): the dose of a drug that has been determined to produce the desired effect in the majority of people with the fewest possible side effects

environmental factors: factors that are located within a particular environment, such as a culture of drug use and high availability of alcohol in a particular community, which can cause substance abuse disorders

epidemiology: the study of factors that affect the health and illness of entire populations

interpersonal factors: as causes of substance use disorders, those factors that are located between individuals, such as peer influence and social learning experiences

intrapersonal factors: factors that are located within the individual, such as biological or psychological causes, which can cause substance abuse disorders

metabolic tolerance: drug tolerance that arises from the actions of the liver in breaking down psychoactive drugs

neuro-adaptation: the compensatory adjustment that the brain makes in an attempt to continue normal functioning despite the presence of alcohol or other drug use

neuroleptic-induced Parkinsonism: a side effect of anti-psychotic drugs that leads to the experience of tremors of the limbs while at rest, as well as rigidity, slowness of movement and a lack of spontaneity

neuron: a cell in the nervous system that is involved in the transmission of nerve impulses

neurotransmitters: chemicals released by axons that help conduct nerve impulses across the synapse to the next neuron

norepinephrine: a neurotransmitter located in the brain that is involved with eating, sleep, arousal, emotion and expression

pharmacodynamic tolerance: drug tolerance that derives from cellular adaptation that occurs with repeated or compulsive use of a psychoactive agent

psychopharmacology: the use of psychoactive drugs in the management of mental health

psychostimulants: a class of drugs that increase mental alertness, increase motor activity or reduce fatigue, relieve boredom and enhance task performance, while also suppressing appetite

reinforcement: the presence of rewarding stimuli or the relief of an unpleasant sensation that increases the probability of alcohol or other drug use

risk factor approach to understanding substance use: an approach that assumes that as the number of risk factors increases, the risk of an individual developing a substance use disorder also increases

serotonin: a neurotransmitter located in the brain that is involved in sleep, arousal and depression

social development model (SDM): a theoretical model that argues that bonding to prosocial groups and clear norms against anti-social behaviour act as protective factors that inhibit the development of substance use behaviour

substance abuse: a maladaptive pattern of substance use that manifests recurrently and has significant negative consequences

substance dependence: a cluster of cognitive, behavioural and physiological symptoms indicating that a person continues to use a substance despite significant substance-related problems

substance misuse: a pattern of substance use that results in some adverse consequences that are not recurrent

synaptic cleft: the space between each axon and dendrite

tardive dyskinesia: a side effect of anti-psychotic drugs that leads to involuntary twitching movements of the face, tongue, limbs and trunk

EXERCISES

Multiple choice questions

1.Substance abuse refers to:

a)adverse consequences following binge drinking

b)recurrent maladaptive substance use that has significant negative consequences

c)compulsive drug taking

d)being in an intoxicated state.

2.Substance dependence refers to:

a)non-recurrent substance use that has significant negative consequences

b)being in an intoxicated state

c)a pattern of repeated use resulting in tolerance, withdrawal symptoms and compulsive drug taking

d)a cluster of cognitive and behavioural symptoms.

3.The best approach to intervention for substance use is:

a)specialised substance abuse treatment

b)brief intervention

c)prevention

d)all of the above are correct.

4.Family studies indicate that the risk for developing alcohol dependence is:

a)three times greater among first-degree relatives

b)two times greater among fraternal twins

c)five times greater among identical twins

d)all of the above are correct.

5.The following psychological factor has been identified as a risk factor for substance use:

a)an external locus of control

b)low self-esteem

c)sensation seeking

d)all of the above are correct.

6.Psychoactive drugs are typically used to:

a)treat symptoms of mental illness

b)prevent the onset of symptoms of mental illness

c)avoid the development of symptoms of mental illness

d)all of the above are correct.

7.Dopamine is found in the __________, and is involved in __________.

a)spinal cord; eating, sleeping, arousal and emotion

b)brain; mood disorders and Parkinson’s disease

c)brain; depression and schizophrenia

d)spinal cord; mental disorders and Parkinson’s disease.

8.Two of the side effects of anti-psychotic drugs are:

a)akathisia and Parkinson’s disease

b)dystonia and Parkinson’s disease

c)dystonia and akathisia

d)none of the above is correct.

9.Drug tolerance refers to:

a)the need to consume increasing amounts of a drug

b)the need to treat a mental illness with drugs rather than therapy

c)the ability to absorb and utilise drugs optimally in the body

d)the compulsive use of a drug for physical and psychological reinforcement.

10.Anti-depressants are also known as:

a)CNS depressants

b)psychostimulants

c)mood stabilisers

d)anti-psychotics.

Short-answer questions

1.What is meant by a risk factor approach to understanding substance use?

2.Explain vulnerability, protective factors and resilience in substance use.

3.How do twin studies help explain genetic influences in substance use disorders?

4.What parent—adolescent relationship factors are involved in risk for substance abuse?

5.How does the social development model explain risk factors in substance abuse?

6.Describe the uses and effects of anti-psychotic drugs.

7.Distinguish between drug potency, efficacy and dose.

8.Why is drug monitoring important to psychopharmacological treatment?

9.Define each of the following terms:

a)drug dependence

b)drug tolerance

c)cross-dependence

d)cross-tolerance.