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Self-Medication
C H A P T E R
24 Self-Medication Virginia Gil-Rivas, Linda McWhorter University of North Carolina, Charlotte, Charlotte, NC, USA
O U T L I N E Neurobiological Basis of Substance Use and Addiction The Brain Reward Circuit Stress and Substance Use
236 236 236
Substance Use and Psychiatric Disorders Mood Disorders Anxiety Disorders
237 237 237
Schizophrenia-Spectrum Disorders
Substance use, both licit (e.g. alcohol, nicotine) and illicit (e.g. marijuana, cocaine, and heroin), can have serious health, social, legal, and financial consequences for individuals and society. The estimated combined annual cost of the medical, economic, criminal, and social consequences of substance use in the United States is approximately half a trillion dollars. In 2008, approximately 8% of the US population aged 12 years or older reported using illicit substances during the past month. Further, 5% of adults reported heavy drinking (two or more drinks per day) and 15% reported binge drinking (five or more drinks in one occasion). Of those using drugs, it was estimated that 8.9% met diagnostic criteria for a substance use disorder (SUD) (i.e. substance use dependence or abuse) as defined by the Diagnostic and statistical manual of mental disorders, 4th edition (DSM-IV). SUDs are characterized by (1) a compulsion to seek and take a particular psychoactive substance; (2) lack of control over substance intake; (3) the presence of negative affective states (i.e. anxiety, dysphoria, and irritability) and somatic symptoms associated with discontinued use; and (4) a tendency to relapse after a period of abstinence. Researchers and clinicians remain puzzled by the fact that individuals continue to use substances despite Principles of Addiction, Volume 1 http://dx.doi.org/10.1016/B978-0-12-398336-7.00024-3
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Support for the SMH Substance Use to Manage Negative Affective States Substance Specificity
238 238 239
Summary
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negative consequences. Multiple explanations have been offered for substance use and addiction, and perhaps one of the most influential explanations is the self-medication hypothesis (SMH) proposed by Khantzian. The SMH views substance use as an effort to cope with stress and distressing emotions (e.g. depression, anxiety, anger) among individuals with deficits in emotion regulation, self-care, interpersonal skills, and self-esteem that may or may not be related to a psychiatric disorder. In other words, SUDs are disorders characterized by self-regulation deficits. Further, the theory also suggests that individuals select specific substances based on their expected ability to reduce or increase specific emotions. For example, opiate use is thought to be related to efforts to manage hostile and violent emotions, while alcohol is frequently used as a way of facilitating social interaction and the expression of emotions among individuals with deficits in these areas. In the short-term, the use of substances to manage distressing emotions can be adaptive as these substances provide individuals with a reprieve from intense emotional states. In the longer term, chronic use can contribute to the development of SUDs. Once individuals transition from occasional use to addiction, substance use withdrawal leads to distressing emotions
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Copyright Ó 2013 Elsevier Inc. All rights reserved.
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and somatic symptoms that contribute to relapse. Recent developments on the neurobiology of addiction provide some support for the idea that substance use has the potential of eliciting intensive positive affective states early in the process of addiction. Also, these findings suggest that in the longer term chronic substance use leads to neurobiological changes that are associated with psychiatric symptomatology.
NEUROBIOLOGICAL BASIS OF SUBSTANCE USE AND ADDICTION The Brain Reward Circuit The area of the brain known as the “reward circuit” or pleasure pathways that is located in the limbic regions including the ventral tegmental and nucleus accumbens has been shown to be activated at varying degrees by both licit and illicit substances. Although different drugs may affect these pathways somewhat differently, they all lead to the release of dopamine, a neurotransmitter that is associated with the experience of reward or pleasure. Importantly, the amount of dopamine released in the brain as a result of substance use is 2–10 times greater than the release associated with natural stimuli (e.g. food). The amount of dopamine released and the pattern of activation in the reward pathways explains the experience of euphoria or “high” associated with a particular substance. Thus congruent with the SMH, in the initial stages of addiction, substance use may be viewed by individuals as a way of achieving a reprieve from negative emotional states. After a period of experimentation, individuals may select a substance or family of substances (e.g. stimulants, opiates) that are the most effective in producing the desired affective state. It is important to consider that individuals’ initial motivation for substance use may or may not reflect a desire for ameliorating negative affective states. It is also possible that individuals’ motivation to use reflects a desire for the “high” associated with a substance, a need to regulate their overall emotional experiences, or an effort to obtain desired social rewards. Research on the neurobiological basis of addiction has shown that dopamine not only acts as a “reward” but also plays a role in the encoding reward expectancies and of memories of events or stimuli that are associated with its release. As a result, simply the expectation of the reward leads to dopamine release in the reward pathways. In addition, stimuli associated with substance use (e.g. specific settings, emotional states, and images) may elicit dopamine release and increase drug craving and substance seeking behaviors. In other words, learning processes may play a role in the maintenance of substance use.
Over time, chronic substance use leads to dysregulation or a state of hedonic allostasis in the reward pathways. Further, these changes persist long after discontinuing substance use. In particular, chronic use is associated with reductions in basal dopamine levels, the amount of stimulated dopamine released, and in the number of dopamine receptors in these areas of the brain. Downregulation of positive reward systems and the negative affective states (i.e. anxiety and dysphoria) that accompany substance use withdrawal seem to underlie continued use despite negative health and social consequences. Thus, these neurological changes seem to explain the transition from use that is motivated primarily by the desire to obtain the “high” or the desired affective states associated with a particular substance (positive reward), to use as a way of reducing negative affective states (negative reward) when the substance is not present. In other words, addicted individuals use substances with the goal of gaining a sense of “normalcy” rather than to simply achieve a high.
Stress and Substance Use In addition to the pleasure pathways, changes in the area of the brain associated with stress regulation play a role in substance use initiation, maintenance, and relapse. The stress response involves the activation of the hypothalamic-pituitary-adrenal (HPA) axis and the sympathetic adrenomedullary (SAM) system in response to stressful stimuli. The HPA activation begins with the release of corticotropin-releasing factor (CRF) from the paraventricular neurons of the hypothalamus. In turn, CRF stimulates the synthesis and release of adrenocorticotropin hormone (ACTH) by the anterior pituitary. ACTH stimulates the adrenal cortex to synthesize and release glucocorticoids (cortisol in humans). Activation of the SAM results in the release of catecholamines (adrenaline and noradrenaline). The activation of both the SAM and HPA results in the physiological changes (i.e. increase heart rate, blood pressure, respiration, and circulating glucose) associated with the physiological stress response. Importantly, the stress response also involves an increase of CRF in the amygdala, an area of the brain that plays an important role in anxiety-related affective states. Available research suggests that early in the addiction process the activation of the HPA by both stress and substance use contributes to the sensitization of the reward pathways by glucocorticoids. In fact, animal studies have shown that glucocorticoids will trigger the release of dopamine in these pathways. Further, glucocorticoids augment the positive reinforcing effects of substances by altering the dopamine signaling in these areas. As individuals continue to use substances,
I. THE NATURE OF ADDICTION
SUBSTANCE USE AND PSYCHIATRIC DISORDERS
stress and glucocorticoids contribute to dysregulation of the brain reward pathways leading to increased substance use. Once individuals become addicted, high levels of glucocorticoids and other substances associated with the stress response lead to internally generated negative affective states. Additionally, substance use withdrawal is associated with increases in anxietylike affective states. These negative affective states seem to contribute to craving and substance-seeking behaviors and in turn to continued substance use. In sum, the combined effects of chronic stress and substance use can result in neuroendocrine changes that can lead to dysfunction in the brain reward pathways and contribute to the development of addiction. Substance use, however, does not always lead to the development of SUDs; rather it seems that genetic, individual, social, and environmental factors make some individuals more vulnerable to transition from occasional use to addiction. At the individual level, neurobiological studies suggest that differences in HPA axis activity may help explain why some individuals are more vulnerable to the development of SUDs compared to others. For example, adults who secrete high levels of cortisol are also high dopamine releasers and report greater effects from psychostimulants (e.g. cocaine, methamphetamines) compared to individuals with low cortisol and low dopamine levels. In addition, exposure to traumatic events (e.g. combat, physical assault, major disasters) and chronic stress have been shown to be associated with increases in substance use. The clinical and developmental literatures also suggest that exposure to unresponsive and insensitive caregiving environments and trauma (e.g. physical and sexual abuse) early in life affects the developing brain and the physiological systems associated with the stress response. Further, individuals with histories of exposure to adverse childhood environments seem to have diminished capacity to regulate their negative emotions and behavior, and to cope effectively with stress. As suggested by the SMH, these deficits in regulatory capacity could explain the increased risk for the development of SUDs later on in life among these individuals. Chronic stress and traumatic experiences in both childhood and adulthood seem to contribute not only to the development of SUDs, but also to the emergence of some psychiatric disorders. In fact, some researchers have characterized psychiatric disorders as chronic stress states.
SUBSTANCE USE AND PSYCHIATRIC DISORDERS Current estimates among community samples indicate that 45–72% of adults with SUDs also have at least
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one co-occurring psychiatric disorder. Among individuals diagnosed with a psychiatric disorder (e.g. schizophrenia, major depression, posttraumatic stress disorder (PTSD), attention deficit disorder) approximately 30% also meet criteria for a concurrent SUD. Importantly, the presence of co-occurring disorders has been found to compromise both mental health and substance abuse treatment outcomes. Neurobiological studies have identified some abnormalities in the stress pathways that are involved in both psychiatric disorders and SUDs. In particular, researchers have focused on a potential common neurobiological basis for SUDs, depression/mood disorders, anxiety disorders, and schizophrenia.
Mood Disorders Substantial symptom overlap between mood disorders (e.g. major depression, dysthamia, bipolar disorder) and SUDs exists. For example, irritability, sleep difficulties, anxiety, and concentration difficulties are frequently reported among individuals with major depression and those undergoing substance use withdrawal. Large population studies have found that about 32% of individuals with any mood disorder also met DSM-IV criteria for an SUD. At the neuroendocrine level, individuals diagnosed with major depression present abnormalities in the reward and stress pathways that are also seen among individuals with SUDs. For example, in response to CRF stimulation, depressed individuals have been found to have lower levels of ACTH and cortisol responses compared to healthy individuals, suggesting increased HPA axis activity. Longitudinal studies examining the temporal association between SUDs and mood disorders generally indicate that mood disorders emerge after the onset of SUDs. These findings suggest that neurobiological changes associated with addiction may contribute to the emergence of mood disorders, and thus contrary to the SMH, depressed mood seems to be a consequence of substance use.
Anxiety Disorders Epidemiological studies have found that individuals with an anxiety disorder are more likely to also have SUD compared to those without such histories. Mixed empirical findings have emerged regarding the temporal association between SUDs and anxiety disorders. Some studies have found that the presence of a lifetime anxiety disorder (e.g. general anxiety, social phobia) is associated with an increased risk for the development of SUDs later on in life. In contrast, a recent study found that alcohol dependence preceded the onset
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of several anxiety disorders (i.e. general anxiety, panic) but followed the onset of other disorders (i.e. specific phobia and social phobia). Congruent with the SMH, these findings suggest that some individuals may have started using substances as a way of managing anxiety-related symptoms. In support of this idea, some studies have found that individuals with lower tolerance for internally generated negative affective states and who rely on emotional avoidance are more likely to have co-occurring anxiety and SUDs. Contrary to the SMH, however, it seems that in some cases substance use may have contributed to the development of some anxiety disorders. PTSD is an anxiety disorder that seems to be strongly related to SUDs. Specifically, current estimates indicate that among individuals seeking substance abuse treatment, 19–62% also meet diagnostic criteria for PTSD. Rates of co-occurring PTSD in community samples of adults range from 52 to 35% for men and 28 to 27% for women. Investigators have identified potential pathways that may link these disorders. Specifically, the following pathways have been suggested: (1) SUDs can increase the likelihood of exposure to trauma and thus contribute to the development of PTSD; (2) chronic substance use and the anxiety-like symptoms associated with withdrawal from use may make individuals with SUDs more vulnerable to the development of PTSD after trauma exposure; (3) consistent with the SMH, individuals may use substances in an attempt to alleviate memories and painful symptoms associated with PTSD; and (4) contrary to the SMH, substance use may interfere with the processing of traumatic memories and thus contribute to the exacerbation of PTSD symptoms. Epidemiological studies have shown that typically PTSD precedes the development of SUDs providing support for the component of the SMH suggesting that individuals use substances with the goal of alleviating negative affective states. Neurobiological and neuroimaging studies suggest some common pathways that may help explain their co-occurrence. Specifically, the HPA axis and SAM are involved in stress, PTSD, and SUDs. Recent studies have identified high levels of CRF in the amygdala and chronically increased levels of catecholamines among individuals with PTSD which are suggestive of chronically increased stress responses and are believed to contribute to an increased risk of developing SUDs.
Schizophrenia-Spectrum Disorders Schizophrenia-spectrum (i.e. schizophrenia, schizophreniform, or schizoaffective) disorders show high levels of co-occurrence with SUDs. Epidemiological estimates indicate that approximately 50% of individuals
with these disorders have a lifetime history of substance use and 27% meet criteria for an SUD. These rates are significantly higher than those among the general population. In particular, alcohol and marijuana use are common among individuals diagnosed with schizophrenia. Researchers have suggested that SUD and schizophrenia may share some common biological, individual, and social risk factors that may explain their high rates of co-occurrence. Of particular relevance, are changes in the reward pathways involving dopamine and glutamate that are associated with schizophrenia. These changes may render individuals more vulnerable to SUDs. In addition, the SMH has been a dominant framework for understanding their cooccurrence as individuals report using substances as a way of reducing symptoms such as social withdrawal, apathy, cognitive impairment, and as a way of managing the side effects of antipsychotic medications.
SUPPORT FOR THE SMH Substance Use to Manage Negative Affective States The SMH has garnered a great deal of interest among clinicians and researchers attempting to find potential explanations for SUDs. Despite the intuitive appeal of this hypothesis, the empirical literature provides mixed support for each of its components. The first component of the SMH, that is, the assumption that substance use represents a way of managing negative affective states or symptoms among individuals with self-regulation deficits, has received the most attention in the literature. Studies with nonclinical samples of adolescents and young adults suggest that self-medication may not be the only or the most important factor predicting the initiation of substance use in this group. In particular, it seems that individual differences in sensation seeking and the social meaning given to substance use play an important role in the initiation of substance use. Compelling evidence for the limited role of management of negative mood in explaining substance use among adolescents and young adults has been provided by studies using momentary assessment methodology. This methodology allows for the examination of the temporal association between negative mood states and substance use. For example, adolescents high in novelty seeking have been found to be more likely to use alcohol and marijuana when they are experiencing high levels of positive mood, rather than when experiencing distressing emotions. In contrast, a study of adults that also made use of momentary assessment methodology showed that both anxious mood and pleasant mood states were associated with increases in later alcohol consumption.
I. THE NATURE OF ADDICTION
SUPPORT FOR THE SMH
Further, among those reporting anxious mood, alcohol consumption contributed to reductions in anxiety. Studies using more traditional methodologies suggest that compared to emotional states, personality characteristics are stronger predictors of substance use among youths. Specifically, trait anxiety, trait aggression, and attention and behavioral difficulties in school have been found to be associated with an increased risk for developing SUDs later in life accounting for risk factors such as parental education and mental health. Overall, these findings suggest that individuals may have a variety of reasons for using substances and that the management of negative affective states may be the primary reason for only a subset of individuals. The evidence supporting the SMH among individuals with SUDs and those with co-occurring psychiatric conditions is also mixed. Substance use motivated by the need to alleviate negative affective states seems to be common among individuals with SUDs and those with psychiatric disorders; however, this is not the only reported reason for use. A review of the literature of self-reported reasons for substance use among individuals with schizophrenia-spectrum disorders indicated that while 2–86% of respondents endorsed substance use as a way of relieving negative affective states, 62–95% of these individuals reported using to increase pleasure and 35–98% reported using to achieve the “high” or intoxicating effects. It is important to consider that although individuals may use substances in an attempt to relieve negative or distressing emotions, substance use may also elicit feelings of shame, guilt, and powerlessness leading to an exacerbation of these negative states. In light of these findings, some addiction models suggest that negative affective states and substance use form a feedback loop in which changes in one of these factors influence changes in the other. Support for this feedback loop was reported in a recent longitudinal study that found that changes in negative affect (i.e. anger and depression) were associated with alcohol use and that changes in drinking were associated with changes in negative affect after alcohol treatment. The SMH has also been used to understand substance use relapse after a period of abstinence. The literature suggests that both intrapersonal and interpersonal factors are common precursors to substance use relapse. Intrapersonal factors are those generated by the individual and include negative emotions (i.e. depressed and anxious mood), negative physiological states (e.g. pain), positive emotional states, testing personal control, and urges and temptations. In contrast, interpersonal factors involve external or environmental influences such as social pressure, and interpersonal conflict. Consistent with the SMH, anger, frustration, interpersonal conflict, and depressed mood have been shown to be the most
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commonly reported antecedents of substance use relapse. Similarly, among individuals with co-occurring SUDs and psychiatric disorders, depression, boredom, insecurity, anxiety, loneliness, and sleep difficulties frequently precede relapse to substance use after treatment. Among individuals with psychiatric disorders, substance use early in the addiction process may serve to reduce psychiatric symptoms; however, over time substance use may lead to an exacerbation of symptoms. In fact, some investigators have proposed that substance use among addicted individuals may have a rebound effect, leading to the exacerbation of psychiatric symptoms rather than symptom improvement. From this perspective, the neurobiological changes associated with chronic substance use and the ability of these substances to occasionally elicit symptoms improvement may help explain the maintenance of this behavior. Further, some substances may help alleviate some symptoms and contribute to an increase of other symptoms on termination of their psychoactive effects. Congruent with the proposed rebound effects, recent empirical findings suggest that although increases in mental health symptoms (i.e. anxiety, depression, and sleep disturbances) may be reported before substance use relapse, substance use does not seem to ameliorate these symptoms. For example, a recent study tested the SMH and the “rebound hypothesis” among adults with SUDs and those with co-occurring disorders. Congruent with the SMH, individuals reported increases in symptoms before substance use relapse. In contrast, a majority (about 60%) of participants demonstrated an exacerbation of symptoms immediately after use and 2 weeks later, and only 25% of the sample reported any symptom improvement after use. Further, substance use resulted in an exacerbation of symptoms that were related to individuals’ lifetime mental health diagnosis. Specifically, individuals with bipolar disorders experienced an exacerbation of depressive symptoms and those diagnosed with schizophrenia reported increases in psychotic symptoms. Similarly, a study with adolescents with SUDs found that psychiatric and depressive symptoms preceded substance use relapse; however, substance use contributed to increased symptom severity for over half of these individuals, while only 20% reported symptom improvement. Overall, these findings provide support for the rebound effects of substance use among individuals with SUDs and cooccurring disorders and mixed support for the SMH.
Substance Specificity By and large, support for the “specificity” component of the SMH suggesting that individuals select specific substances based on their expected pharmacological effects is based on case studies and anecdotes from
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substance-abusing patients receiving psychotherapy. The empirical literature, however, provides mixed support for this assertion. Importantly, the available literature testing this component of the SHM has focused on individuals who were receiving substance abuse treatment, and thus it is unclear to what extent early in the addiction process specific substances were selected by individuals based on their ability to induce the desired effects. Studies among individuals with psychiatric disorders have not found strong evidence for a match between the symptoms that characterize the disorder and the type of substance used by individuals. Partial support for the “specificity” component of the SMH emerged in a study of individuals receiving inpatient mental health treatment. Specifically, participants with depressive disorders were more likely to meet criteria for opiate abuse compared to those diagnosed with a bipolar disorder or schizophrenia. Further, individuals with schizophrenia were more likely to abuse alcohol compared to the other two groups, while individuals with bipolar disorder were more likely to meet criteria for marijuana abuse. However, it is important to note that in this study a majority of participants reported using more than one substance. Other studies have not found support for the specificity component of the SMH among individuals with SUDs and those with co-occurring disorders.
SUMMARY The SMH suggests that (1) individuals with selfregulation deficits use substances in an attempt to manage negative or distressing affective states and (2) individuals select specific substances based on their ability to elicit desired affective states. Congruent with the SMH, substance use early in the addiction process can successfully lead to reductions in negative affect among individuals who lack more adaptive emotion and self-regulation skills. In the longer term, chronic substance use contributes to neurobiological changes in the reward and stress pathways, which play an important role in motivation, learning, and behavior. These changes may underlie the transition from substance use motivated by achieving the “high” or relief associated with substance use to use that is motivated by the need to regain a sense of normalcy. The empirical literature supporting the SMH is mixed. Among nonclinical samples of adolescents and young adults, the primary motivation for substance use does not seem to be the management of negative affective states. Rather, sensation seeking and the social meaning given to the use of these substances seem to be the primary motivating force for substance use.
Importantly, positive rather than negative affective states seem to increase the likelihood of substance use among adolescents. Among adults, a majority of studies aiming to test the SMH have been conducted with clinical samples of individuals diagnosed with SUDs and/or psychiatric disorders. Available research indicates that these individuals report using to relieve negative affective states as well as to obtain the “high” or pleasurable effects associated with a particular substance. Further, the evidence suggests that substance use increases rather than alleviates negative affective states. It is possible that during the intoxication period substance use provides relief but leads to increases in symptomatology once the effects have worn off. In fact, these findings provide support for the “rebound” hypothesis and addiction models that propose a feedback loop between substance use and negative affective states. Support for the second component of the SMH, that is, the idea that individuals select “specific” substances based on their effects on relieving distress or negative affective states, is rather limited. Specifically, the available studies have not examined whether individuals experiment with different substances early in the addiction process until they identify the substance that most effectively elicits the desired effects. Studies among individuals diagnosed with SUDs and a psychiatric disorder also provide mixed support for the “specificity” assumption. These individuals typically report using multiple substances. Further, a pattern of substance selectivity based on symptoms or psychiatric diagnosis has not been consistently identified. In conclusion, empirical support for the SMH is mixed. Reliance on cross-sectional studies and methodologies that do not allow for an adequate assessment of the temporal relationship between negative affective states and substance use has not allowed for an adequate test of the SMH at all stages of the addiction process. Future research is needed to clarify the role of negative affective states in the initiation, progression, and maintenance of substance use.
SEE ALSO Behavioral Economic Factors in Addictive Processes, The Biopsychosocial Model of Addiction, Cognitive Factors in Addictive Processes, Emotions and Addictive Processes, Contextual Factors in Addiction, Relapse and Lapse, Stress and Addiction, Neural Correlates of Craving for Psychoactive Drugs, Models of Relationships between Substance Use and Mental Disorders, Substance Use and Mood Disorders, Substance Use in Response to Anxiety Disorders
I. THE NATURE OF ADDICTION
FURTHER READING
Glossary ACTH adrenocorticotropin hormone – A hormone produced by the pituitary in response to stimulation by CRF. This hormone stimulates the cortex of the adrenal glands to release glucocorticoids as part of the physiological response to stress. CRF corticotropin-releasing factor – a hormone released by the hypothalamus as part of the stress response. This hormone stimulates the pituitary to produce ACTH. DSM-IV Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition – a manual published by the American Psychiatric Association that provides standard criteria for the classification of mental disorders. HPA hypothalamic-pituitary-adrenal axis – a component of the neuroendocrine system that plays an important role in the body’s physiological response to stress. Activation of this system leads to the release of glucocorticoids by the adrenal glands. PTSD posttraumatic stress disorder – an anxiety disorder that can develop after exposure to traumatic events. This disorder is characterized by persistent thoughts or memories about the traumatic event, sleep difficulties, emotional numbness, and high levels of emotional arousal. SAM sympathetic adrenomedullary system – a neuroendocrine system involved in the body’s physiological response to stress. Activation of this system during stress leads to the release of catecholamines (epinephrine and norepinephrine). SMH self-medication hypothesis – a hypothesis that suggests that addiction is the result of self-regulation deficits. Specifically it proposes that (1) individuals use substances as a way of coping or managing with negative emotional states and (2) individuals select specific substances for their expected ability to reduce or increase specific emotions. SUD substance use disorder – a disorder that involves the repeated use or abuse of psychoactive substances despite negative consequences.
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Brady, K.T., Sinha, R., 2005. Co-occurring mental and substance use disorders: the neurobiological effects of chronic stress. American Journal of Psychiatry 162, 1483–1493. Cicchetti, D., Curtis, W.J., 2006. The developing brain and neural plasticity: implications for normality, psychopathology, and resilience. In: Cicchetti, D., Cohen, D. (Eds.), Developmental Psychopathology 2: Developmental Neuroscience, second ed.). Wiley, New York, pp. 1–64. Gregg, L., Barrowclough, C., Haddock, G., 2007. Reasons for increased substance use in psychosis. Clinical Psychology Review 27, 494–510. Khantzian, E.J., 1997. The self-medication hypothesis of substance use disorders: a consideration and recent applications. Harvard Review of Psychiatry 4, 231–244. Khantzian, E.J., 2003. Understanding addictive vulnerability: an evolving psychodynamic perspective. Neuro-Psychoanalysis 5, 5–21. Koob, G.F., Le Moal, M., 2008. Addiction and the brain antireward system. Annual Review of Psychology 58, 29–53. McCarthy, D.M., Tomlinson, K.L., Anderson, K.G., Marlatt, G.A., Brown, S.A., 2005. Relapse in alcohol- and drug-disordered adolescents with comorbid psychopathology: changes in psychiatric symptoms. Psychology of Addictive Behaviors 19, 28–34. Tomlinson, K.L., Tate, S.R., Anderson, K.G., McCarthy, D.M., Brown, S.A., 2006. An examination of self-medication before and after alcohol or drug relapse. Addictive Behaviors 31, 461–474. Uhart, M., Wand, G.S., 2008. Stress, alcohol and drug interaction: an update of human research. Addiction Biology 14, 43–64. Volkow, N.D., Fowler, J.S., Wang, G.J., Baler, R., Telang, F., 2009. Imaging dopamine’s role in drug abuse and addiction. Neuropharmacology 56, 3–8. Witkiewitz, K., Villarroel, N.A., 2009. Dynamic association between negative affect and alcohol lapses following alcohol treatment. Journal of Consulting and Clinical Psychology 77, 633–644.
Relevant Websites
Further Reading Blume, A.W., Schmaling, K.B., Marlatt, G.A., 2000. Revisiting the selfmedication hypothesis from a behavioral perspective. Cognitive and Behavioral Practice 7, 379–384.
http://drugabuse.gov/nidahome.html – National Institute on Drug Abuse. http://www.samhsa.gov/ – Substance Abuse and Mental Health Services Administration.
I. THE NATURE OF ADDICTION
24 Self-Medication Virginia Gil-Rivas, Linda McWhorter University of North Carolina, Charlotte, Charlotte, NC, USA
O U T L I N E Neurobiological Basis of Substance Use and Addiction The Brain Reward Circuit Stress and Substance Use
236 236 236
Substance Use and Psychiatric Disorders Mood Disorders Anxiety Disorders
237 237 237
Schizophrenia-Spectrum Disorders
Substance use, both licit (e.g. alcohol, nicotine) and illicit (e.g. marijuana, cocaine, and heroin), can have serious health, social, legal, and financial consequences for individuals and society. The estimated combined annual cost of the medical, economic, criminal, and social consequences of substance use in the United States is approximately half a trillion dollars. In 2008, approximately 8% of the US population aged 12 years or older reported using illicit substances during the past month. Further, 5% of adults reported heavy drinking (two or more drinks per day) and 15% reported binge drinking (five or more drinks in one occasion). Of those using drugs, it was estimated that 8.9% met diagnostic criteria for a substance use disorder (SUD) (i.e. substance use dependence or abuse) as defined by the Diagnostic and statistical manual of mental disorders, 4th edition (DSM-IV). SUDs are characterized by (1) a compulsion to seek and take a particular psychoactive substance; (2) lack of control over substance intake; (3) the presence of negative affective states (i.e. anxiety, dysphoria, and irritability) and somatic symptoms associated with discontinued use; and (4) a tendency to relapse after a period of abstinence. Researchers and clinicians remain puzzled by the fact that individuals continue to use substances despite Principles of Addiction, Volume 1 http://dx.doi.org/10.1016/B978-0-12-398336-7.00024-3
238
Support for the SMH Substance Use to Manage Negative Affective States Substance Specificity
238 238 239
Summary
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negative consequences. Multiple explanations have been offered for substance use and addiction, and perhaps one of the most influential explanations is the self-medication hypothesis (SMH) proposed by Khantzian. The SMH views substance use as an effort to cope with stress and distressing emotions (e.g. depression, anxiety, anger) among individuals with deficits in emotion regulation, self-care, interpersonal skills, and self-esteem that may or may not be related to a psychiatric disorder. In other words, SUDs are disorders characterized by self-regulation deficits. Further, the theory also suggests that individuals select specific substances based on their expected ability to reduce or increase specific emotions. For example, opiate use is thought to be related to efforts to manage hostile and violent emotions, while alcohol is frequently used as a way of facilitating social interaction and the expression of emotions among individuals with deficits in these areas. In the short-term, the use of substances to manage distressing emotions can be adaptive as these substances provide individuals with a reprieve from intense emotional states. In the longer term, chronic use can contribute to the development of SUDs. Once individuals transition from occasional use to addiction, substance use withdrawal leads to distressing emotions
235
Copyright Ó 2013 Elsevier Inc. All rights reserved.
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and somatic symptoms that contribute to relapse. Recent developments on the neurobiology of addiction provide some support for the idea that substance use has the potential of eliciting intensive positive affective states early in the process of addiction. Also, these findings suggest that in the longer term chronic substance use leads to neurobiological changes that are associated with psychiatric symptomatology.
NEUROBIOLOGICAL BASIS OF SUBSTANCE USE AND ADDICTION The Brain Reward Circuit The area of the brain known as the “reward circuit” or pleasure pathways that is located in the limbic regions including the ventral tegmental and nucleus accumbens has been shown to be activated at varying degrees by both licit and illicit substances. Although different drugs may affect these pathways somewhat differently, they all lead to the release of dopamine, a neurotransmitter that is associated with the experience of reward or pleasure. Importantly, the amount of dopamine released in the brain as a result of substance use is 2–10 times greater than the release associated with natural stimuli (e.g. food). The amount of dopamine released and the pattern of activation in the reward pathways explains the experience of euphoria or “high” associated with a particular substance. Thus congruent with the SMH, in the initial stages of addiction, substance use may be viewed by individuals as a way of achieving a reprieve from negative emotional states. After a period of experimentation, individuals may select a substance or family of substances (e.g. stimulants, opiates) that are the most effective in producing the desired affective state. It is important to consider that individuals’ initial motivation for substance use may or may not reflect a desire for ameliorating negative affective states. It is also possible that individuals’ motivation to use reflects a desire for the “high” associated with a substance, a need to regulate their overall emotional experiences, or an effort to obtain desired social rewards. Research on the neurobiological basis of addiction has shown that dopamine not only acts as a “reward” but also plays a role in the encoding reward expectancies and of memories of events or stimuli that are associated with its release. As a result, simply the expectation of the reward leads to dopamine release in the reward pathways. In addition, stimuli associated with substance use (e.g. specific settings, emotional states, and images) may elicit dopamine release and increase drug craving and substance seeking behaviors. In other words, learning processes may play a role in the maintenance of substance use.
Over time, chronic substance use leads to dysregulation or a state of hedonic allostasis in the reward pathways. Further, these changes persist long after discontinuing substance use. In particular, chronic use is associated with reductions in basal dopamine levels, the amount of stimulated dopamine released, and in the number of dopamine receptors in these areas of the brain. Downregulation of positive reward systems and the negative affective states (i.e. anxiety and dysphoria) that accompany substance use withdrawal seem to underlie continued use despite negative health and social consequences. Thus, these neurological changes seem to explain the transition from use that is motivated primarily by the desire to obtain the “high” or the desired affective states associated with a particular substance (positive reward), to use as a way of reducing negative affective states (negative reward) when the substance is not present. In other words, addicted individuals use substances with the goal of gaining a sense of “normalcy” rather than to simply achieve a high.
Stress and Substance Use In addition to the pleasure pathways, changes in the area of the brain associated with stress regulation play a role in substance use initiation, maintenance, and relapse. The stress response involves the activation of the hypothalamic-pituitary-adrenal (HPA) axis and the sympathetic adrenomedullary (SAM) system in response to stressful stimuli. The HPA activation begins with the release of corticotropin-releasing factor (CRF) from the paraventricular neurons of the hypothalamus. In turn, CRF stimulates the synthesis and release of adrenocorticotropin hormone (ACTH) by the anterior pituitary. ACTH stimulates the adrenal cortex to synthesize and release glucocorticoids (cortisol in humans). Activation of the SAM results in the release of catecholamines (adrenaline and noradrenaline). The activation of both the SAM and HPA results in the physiological changes (i.e. increase heart rate, blood pressure, respiration, and circulating glucose) associated with the physiological stress response. Importantly, the stress response also involves an increase of CRF in the amygdala, an area of the brain that plays an important role in anxiety-related affective states. Available research suggests that early in the addiction process the activation of the HPA by both stress and substance use contributes to the sensitization of the reward pathways by glucocorticoids. In fact, animal studies have shown that glucocorticoids will trigger the release of dopamine in these pathways. Further, glucocorticoids augment the positive reinforcing effects of substances by altering the dopamine signaling in these areas. As individuals continue to use substances,
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stress and glucocorticoids contribute to dysregulation of the brain reward pathways leading to increased substance use. Once individuals become addicted, high levels of glucocorticoids and other substances associated with the stress response lead to internally generated negative affective states. Additionally, substance use withdrawal is associated with increases in anxietylike affective states. These negative affective states seem to contribute to craving and substance-seeking behaviors and in turn to continued substance use. In sum, the combined effects of chronic stress and substance use can result in neuroendocrine changes that can lead to dysfunction in the brain reward pathways and contribute to the development of addiction. Substance use, however, does not always lead to the development of SUDs; rather it seems that genetic, individual, social, and environmental factors make some individuals more vulnerable to transition from occasional use to addiction. At the individual level, neurobiological studies suggest that differences in HPA axis activity may help explain why some individuals are more vulnerable to the development of SUDs compared to others. For example, adults who secrete high levels of cortisol are also high dopamine releasers and report greater effects from psychostimulants (e.g. cocaine, methamphetamines) compared to individuals with low cortisol and low dopamine levels. In addition, exposure to traumatic events (e.g. combat, physical assault, major disasters) and chronic stress have been shown to be associated with increases in substance use. The clinical and developmental literatures also suggest that exposure to unresponsive and insensitive caregiving environments and trauma (e.g. physical and sexual abuse) early in life affects the developing brain and the physiological systems associated with the stress response. Further, individuals with histories of exposure to adverse childhood environments seem to have diminished capacity to regulate their negative emotions and behavior, and to cope effectively with stress. As suggested by the SMH, these deficits in regulatory capacity could explain the increased risk for the development of SUDs later on in life among these individuals. Chronic stress and traumatic experiences in both childhood and adulthood seem to contribute not only to the development of SUDs, but also to the emergence of some psychiatric disorders. In fact, some researchers have characterized psychiatric disorders as chronic stress states.
SUBSTANCE USE AND PSYCHIATRIC DISORDERS Current estimates among community samples indicate that 45–72% of adults with SUDs also have at least
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one co-occurring psychiatric disorder. Among individuals diagnosed with a psychiatric disorder (e.g. schizophrenia, major depression, posttraumatic stress disorder (PTSD), attention deficit disorder) approximately 30% also meet criteria for a concurrent SUD. Importantly, the presence of co-occurring disorders has been found to compromise both mental health and substance abuse treatment outcomes. Neurobiological studies have identified some abnormalities in the stress pathways that are involved in both psychiatric disorders and SUDs. In particular, researchers have focused on a potential common neurobiological basis for SUDs, depression/mood disorders, anxiety disorders, and schizophrenia.
Mood Disorders Substantial symptom overlap between mood disorders (e.g. major depression, dysthamia, bipolar disorder) and SUDs exists. For example, irritability, sleep difficulties, anxiety, and concentration difficulties are frequently reported among individuals with major depression and those undergoing substance use withdrawal. Large population studies have found that about 32% of individuals with any mood disorder also met DSM-IV criteria for an SUD. At the neuroendocrine level, individuals diagnosed with major depression present abnormalities in the reward and stress pathways that are also seen among individuals with SUDs. For example, in response to CRF stimulation, depressed individuals have been found to have lower levels of ACTH and cortisol responses compared to healthy individuals, suggesting increased HPA axis activity. Longitudinal studies examining the temporal association between SUDs and mood disorders generally indicate that mood disorders emerge after the onset of SUDs. These findings suggest that neurobiological changes associated with addiction may contribute to the emergence of mood disorders, and thus contrary to the SMH, depressed mood seems to be a consequence of substance use.
Anxiety Disorders Epidemiological studies have found that individuals with an anxiety disorder are more likely to also have SUD compared to those without such histories. Mixed empirical findings have emerged regarding the temporal association between SUDs and anxiety disorders. Some studies have found that the presence of a lifetime anxiety disorder (e.g. general anxiety, social phobia) is associated with an increased risk for the development of SUDs later on in life. In contrast, a recent study found that alcohol dependence preceded the onset
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of several anxiety disorders (i.e. general anxiety, panic) but followed the onset of other disorders (i.e. specific phobia and social phobia). Congruent with the SMH, these findings suggest that some individuals may have started using substances as a way of managing anxiety-related symptoms. In support of this idea, some studies have found that individuals with lower tolerance for internally generated negative affective states and who rely on emotional avoidance are more likely to have co-occurring anxiety and SUDs. Contrary to the SMH, however, it seems that in some cases substance use may have contributed to the development of some anxiety disorders. PTSD is an anxiety disorder that seems to be strongly related to SUDs. Specifically, current estimates indicate that among individuals seeking substance abuse treatment, 19–62% also meet diagnostic criteria for PTSD. Rates of co-occurring PTSD in community samples of adults range from 52 to 35% for men and 28 to 27% for women. Investigators have identified potential pathways that may link these disorders. Specifically, the following pathways have been suggested: (1) SUDs can increase the likelihood of exposure to trauma and thus contribute to the development of PTSD; (2) chronic substance use and the anxiety-like symptoms associated with withdrawal from use may make individuals with SUDs more vulnerable to the development of PTSD after trauma exposure; (3) consistent with the SMH, individuals may use substances in an attempt to alleviate memories and painful symptoms associated with PTSD; and (4) contrary to the SMH, substance use may interfere with the processing of traumatic memories and thus contribute to the exacerbation of PTSD symptoms. Epidemiological studies have shown that typically PTSD precedes the development of SUDs providing support for the component of the SMH suggesting that individuals use substances with the goal of alleviating negative affective states. Neurobiological and neuroimaging studies suggest some common pathways that may help explain their co-occurrence. Specifically, the HPA axis and SAM are involved in stress, PTSD, and SUDs. Recent studies have identified high levels of CRF in the amygdala and chronically increased levels of catecholamines among individuals with PTSD which are suggestive of chronically increased stress responses and are believed to contribute to an increased risk of developing SUDs.
Schizophrenia-Spectrum Disorders Schizophrenia-spectrum (i.e. schizophrenia, schizophreniform, or schizoaffective) disorders show high levels of co-occurrence with SUDs. Epidemiological estimates indicate that approximately 50% of individuals
with these disorders have a lifetime history of substance use and 27% meet criteria for an SUD. These rates are significantly higher than those among the general population. In particular, alcohol and marijuana use are common among individuals diagnosed with schizophrenia. Researchers have suggested that SUD and schizophrenia may share some common biological, individual, and social risk factors that may explain their high rates of co-occurrence. Of particular relevance, are changes in the reward pathways involving dopamine and glutamate that are associated with schizophrenia. These changes may render individuals more vulnerable to SUDs. In addition, the SMH has been a dominant framework for understanding their cooccurrence as individuals report using substances as a way of reducing symptoms such as social withdrawal, apathy, cognitive impairment, and as a way of managing the side effects of antipsychotic medications.
SUPPORT FOR THE SMH Substance Use to Manage Negative Affective States The SMH has garnered a great deal of interest among clinicians and researchers attempting to find potential explanations for SUDs. Despite the intuitive appeal of this hypothesis, the empirical literature provides mixed support for each of its components. The first component of the SMH, that is, the assumption that substance use represents a way of managing negative affective states or symptoms among individuals with self-regulation deficits, has received the most attention in the literature. Studies with nonclinical samples of adolescents and young adults suggest that self-medication may not be the only or the most important factor predicting the initiation of substance use in this group. In particular, it seems that individual differences in sensation seeking and the social meaning given to substance use play an important role in the initiation of substance use. Compelling evidence for the limited role of management of negative mood in explaining substance use among adolescents and young adults has been provided by studies using momentary assessment methodology. This methodology allows for the examination of the temporal association between negative mood states and substance use. For example, adolescents high in novelty seeking have been found to be more likely to use alcohol and marijuana when they are experiencing high levels of positive mood, rather than when experiencing distressing emotions. In contrast, a study of adults that also made use of momentary assessment methodology showed that both anxious mood and pleasant mood states were associated with increases in later alcohol consumption.
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Further, among those reporting anxious mood, alcohol consumption contributed to reductions in anxiety. Studies using more traditional methodologies suggest that compared to emotional states, personality characteristics are stronger predictors of substance use among youths. Specifically, trait anxiety, trait aggression, and attention and behavioral difficulties in school have been found to be associated with an increased risk for developing SUDs later in life accounting for risk factors such as parental education and mental health. Overall, these findings suggest that individuals may have a variety of reasons for using substances and that the management of negative affective states may be the primary reason for only a subset of individuals. The evidence supporting the SMH among individuals with SUDs and those with co-occurring psychiatric conditions is also mixed. Substance use motivated by the need to alleviate negative affective states seems to be common among individuals with SUDs and those with psychiatric disorders; however, this is not the only reported reason for use. A review of the literature of self-reported reasons for substance use among individuals with schizophrenia-spectrum disorders indicated that while 2–86% of respondents endorsed substance use as a way of relieving negative affective states, 62–95% of these individuals reported using to increase pleasure and 35–98% reported using to achieve the “high” or intoxicating effects. It is important to consider that although individuals may use substances in an attempt to relieve negative or distressing emotions, substance use may also elicit feelings of shame, guilt, and powerlessness leading to an exacerbation of these negative states. In light of these findings, some addiction models suggest that negative affective states and substance use form a feedback loop in which changes in one of these factors influence changes in the other. Support for this feedback loop was reported in a recent longitudinal study that found that changes in negative affect (i.e. anger and depression) were associated with alcohol use and that changes in drinking were associated with changes in negative affect after alcohol treatment. The SMH has also been used to understand substance use relapse after a period of abstinence. The literature suggests that both intrapersonal and interpersonal factors are common precursors to substance use relapse. Intrapersonal factors are those generated by the individual and include negative emotions (i.e. depressed and anxious mood), negative physiological states (e.g. pain), positive emotional states, testing personal control, and urges and temptations. In contrast, interpersonal factors involve external or environmental influences such as social pressure, and interpersonal conflict. Consistent with the SMH, anger, frustration, interpersonal conflict, and depressed mood have been shown to be the most
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commonly reported antecedents of substance use relapse. Similarly, among individuals with co-occurring SUDs and psychiatric disorders, depression, boredom, insecurity, anxiety, loneliness, and sleep difficulties frequently precede relapse to substance use after treatment. Among individuals with psychiatric disorders, substance use early in the addiction process may serve to reduce psychiatric symptoms; however, over time substance use may lead to an exacerbation of symptoms. In fact, some investigators have proposed that substance use among addicted individuals may have a rebound effect, leading to the exacerbation of psychiatric symptoms rather than symptom improvement. From this perspective, the neurobiological changes associated with chronic substance use and the ability of these substances to occasionally elicit symptoms improvement may help explain the maintenance of this behavior. Further, some substances may help alleviate some symptoms and contribute to an increase of other symptoms on termination of their psychoactive effects. Congruent with the proposed rebound effects, recent empirical findings suggest that although increases in mental health symptoms (i.e. anxiety, depression, and sleep disturbances) may be reported before substance use relapse, substance use does not seem to ameliorate these symptoms. For example, a recent study tested the SMH and the “rebound hypothesis” among adults with SUDs and those with co-occurring disorders. Congruent with the SMH, individuals reported increases in symptoms before substance use relapse. In contrast, a majority (about 60%) of participants demonstrated an exacerbation of symptoms immediately after use and 2 weeks later, and only 25% of the sample reported any symptom improvement after use. Further, substance use resulted in an exacerbation of symptoms that were related to individuals’ lifetime mental health diagnosis. Specifically, individuals with bipolar disorders experienced an exacerbation of depressive symptoms and those diagnosed with schizophrenia reported increases in psychotic symptoms. Similarly, a study with adolescents with SUDs found that psychiatric and depressive symptoms preceded substance use relapse; however, substance use contributed to increased symptom severity for over half of these individuals, while only 20% reported symptom improvement. Overall, these findings provide support for the rebound effects of substance use among individuals with SUDs and cooccurring disorders and mixed support for the SMH.
Substance Specificity By and large, support for the “specificity” component of the SMH suggesting that individuals select specific substances based on their expected pharmacological effects is based on case studies and anecdotes from
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substance-abusing patients receiving psychotherapy. The empirical literature, however, provides mixed support for this assertion. Importantly, the available literature testing this component of the SHM has focused on individuals who were receiving substance abuse treatment, and thus it is unclear to what extent early in the addiction process specific substances were selected by individuals based on their ability to induce the desired effects. Studies among individuals with psychiatric disorders have not found strong evidence for a match between the symptoms that characterize the disorder and the type of substance used by individuals. Partial support for the “specificity” component of the SMH emerged in a study of individuals receiving inpatient mental health treatment. Specifically, participants with depressive disorders were more likely to meet criteria for opiate abuse compared to those diagnosed with a bipolar disorder or schizophrenia. Further, individuals with schizophrenia were more likely to abuse alcohol compared to the other two groups, while individuals with bipolar disorder were more likely to meet criteria for marijuana abuse. However, it is important to note that in this study a majority of participants reported using more than one substance. Other studies have not found support for the specificity component of the SMH among individuals with SUDs and those with co-occurring disorders.
SUMMARY The SMH suggests that (1) individuals with selfregulation deficits use substances in an attempt to manage negative or distressing affective states and (2) individuals select specific substances based on their ability to elicit desired affective states. Congruent with the SMH, substance use early in the addiction process can successfully lead to reductions in negative affect among individuals who lack more adaptive emotion and self-regulation skills. In the longer term, chronic substance use contributes to neurobiological changes in the reward and stress pathways, which play an important role in motivation, learning, and behavior. These changes may underlie the transition from substance use motivated by achieving the “high” or relief associated with substance use to use that is motivated by the need to regain a sense of normalcy. The empirical literature supporting the SMH is mixed. Among nonclinical samples of adolescents and young adults, the primary motivation for substance use does not seem to be the management of negative affective states. Rather, sensation seeking and the social meaning given to the use of these substances seem to be the primary motivating force for substance use.
Importantly, positive rather than negative affective states seem to increase the likelihood of substance use among adolescents. Among adults, a majority of studies aiming to test the SMH have been conducted with clinical samples of individuals diagnosed with SUDs and/or psychiatric disorders. Available research indicates that these individuals report using to relieve negative affective states as well as to obtain the “high” or pleasurable effects associated with a particular substance. Further, the evidence suggests that substance use increases rather than alleviates negative affective states. It is possible that during the intoxication period substance use provides relief but leads to increases in symptomatology once the effects have worn off. In fact, these findings provide support for the “rebound” hypothesis and addiction models that propose a feedback loop between substance use and negative affective states. Support for the second component of the SMH, that is, the idea that individuals select “specific” substances based on their effects on relieving distress or negative affective states, is rather limited. Specifically, the available studies have not examined whether individuals experiment with different substances early in the addiction process until they identify the substance that most effectively elicits the desired effects. Studies among individuals diagnosed with SUDs and a psychiatric disorder also provide mixed support for the “specificity” assumption. These individuals typically report using multiple substances. Further, a pattern of substance selectivity based on symptoms or psychiatric diagnosis has not been consistently identified. In conclusion, empirical support for the SMH is mixed. Reliance on cross-sectional studies and methodologies that do not allow for an adequate assessment of the temporal relationship between negative affective states and substance use has not allowed for an adequate test of the SMH at all stages of the addiction process. Future research is needed to clarify the role of negative affective states in the initiation, progression, and maintenance of substance use.
SEE ALSO Behavioral Economic Factors in Addictive Processes, The Biopsychosocial Model of Addiction, Cognitive Factors in Addictive Processes, Emotions and Addictive Processes, Contextual Factors in Addiction, Relapse and Lapse, Stress and Addiction, Neural Correlates of Craving for Psychoactive Drugs, Models of Relationships between Substance Use and Mental Disorders, Substance Use and Mood Disorders, Substance Use in Response to Anxiety Disorders
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FURTHER READING
Glossary ACTH adrenocorticotropin hormone – A hormone produced by the pituitary in response to stimulation by CRF. This hormone stimulates the cortex of the adrenal glands to release glucocorticoids as part of the physiological response to stress. CRF corticotropin-releasing factor – a hormone released by the hypothalamus as part of the stress response. This hormone stimulates the pituitary to produce ACTH. DSM-IV Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition – a manual published by the American Psychiatric Association that provides standard criteria for the classification of mental disorders. HPA hypothalamic-pituitary-adrenal axis – a component of the neuroendocrine system that plays an important role in the body’s physiological response to stress. Activation of this system leads to the release of glucocorticoids by the adrenal glands. PTSD posttraumatic stress disorder – an anxiety disorder that can develop after exposure to traumatic events. This disorder is characterized by persistent thoughts or memories about the traumatic event, sleep difficulties, emotional numbness, and high levels of emotional arousal. SAM sympathetic adrenomedullary system – a neuroendocrine system involved in the body’s physiological response to stress. Activation of this system during stress leads to the release of catecholamines (epinephrine and norepinephrine). SMH self-medication hypothesis – a hypothesis that suggests that addiction is the result of self-regulation deficits. Specifically it proposes that (1) individuals use substances as a way of coping or managing with negative emotional states and (2) individuals select specific substances for their expected ability to reduce or increase specific emotions. SUD substance use disorder – a disorder that involves the repeated use or abuse of psychoactive substances despite negative consequences.
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Brady, K.T., Sinha, R., 2005. Co-occurring mental and substance use disorders: the neurobiological effects of chronic stress. American Journal of Psychiatry 162, 1483–1493. Cicchetti, D., Curtis, W.J., 2006. The developing brain and neural plasticity: implications for normality, psychopathology, and resilience. In: Cicchetti, D., Cohen, D. (Eds.), Developmental Psychopathology 2: Developmental Neuroscience, second ed.). Wiley, New York, pp. 1–64. Gregg, L., Barrowclough, C., Haddock, G., 2007. Reasons for increased substance use in psychosis. Clinical Psychology Review 27, 494–510. Khantzian, E.J., 1997. The self-medication hypothesis of substance use disorders: a consideration and recent applications. Harvard Review of Psychiatry 4, 231–244. Khantzian, E.J., 2003. Understanding addictive vulnerability: an evolving psychodynamic perspective. Neuro-Psychoanalysis 5, 5–21. Koob, G.F., Le Moal, M., 2008. Addiction and the brain antireward system. Annual Review of Psychology 58, 29–53. McCarthy, D.M., Tomlinson, K.L., Anderson, K.G., Marlatt, G.A., Brown, S.A., 2005. Relapse in alcohol- and drug-disordered adolescents with comorbid psychopathology: changes in psychiatric symptoms. Psychology of Addictive Behaviors 19, 28–34. Tomlinson, K.L., Tate, S.R., Anderson, K.G., McCarthy, D.M., Brown, S.A., 2006. An examination of self-medication before and after alcohol or drug relapse. Addictive Behaviors 31, 461–474. Uhart, M., Wand, G.S., 2008. Stress, alcohol and drug interaction: an update of human research. Addiction Biology 14, 43–64. Volkow, N.D., Fowler, J.S., Wang, G.J., Baler, R., Telang, F., 2009. Imaging dopamine’s role in drug abuse and addiction. Neuropharmacology 56, 3–8. Witkiewitz, K., Villarroel, N.A., 2009. Dynamic association between negative affect and alcohol lapses following alcohol treatment. Journal of Consulting and Clinical Psychology 77, 633–644.
Relevant Websites
Further Reading Blume, A.W., Schmaling, K.B., Marlatt, G.A., 2000. Revisiting the selfmedication hypothesis from a behavioral perspective. Cognitive and Behavioral Practice 7, 379–384.
http://drugabuse.gov/nidahome.html – National Institute on Drug Abuse. http://www.samhsa.gov/ – Substance Abuse and Mental Health Services Administration.
I. THE NATURE OF ADDICTION