Chapter 3.0: Key Definitions, Diagnostic Criteria, Classification of Substances, and Models
There is more involved in defining substance misuse and SUD than the clinical diagnostic protocols presented in the DSM-5 and ICD-11. As a start, consider the American Society of Addiction Medicine policy statement defining addiction (ASAM, 2011):
Addiction is a primary, chronic disease of brain reward, motivation, memory and related circuitry. Dysfunction in these circuits leads to characteristic biological, psychological, social and spiritual manifestations. This is reflected in an individual pathologically pursuing reward and/or relief by substance use and other behaviors. Addiction is characterized by inability to consistently abstain, impairment in behavioral control, craving, diminished recognition of significant problems with one’s behavior and interpersonal relationships, and a dysfunctional emotional response. Like other chronic diseases, addiction often involves cycles of relapse and remission. Without treatment or engagement in recovery activities, addiction is progressive and can result in disability or premature death (p. 1).
Important aspects of this definition are recognition of:
- the impact of addiction on biological, psychological/emotional, social, interpersonal, and spiritual aspects of life;
- the brain-behavior nexus in the development and maintenance of addictive behavior;
- the common experience of cyclical relapse and remission, and
- the potential for problem progression.
The ASAM definition reflects a “disease model” perspective—a model popular in the United States and many other areas, but not without controversy and critics, particularly in other parts of the world.
Original disease model of addiction.
The original disease model of addiction emerged during the 1950s and 1960s regarding alcoholism, viewing addiction as a primary disease, not secondary to other psychological conditions (Hartje, 2009). The original disease model of addiction was hailed as an important, less stigmatizing alternative than the prevailing moral model that placed blame on individuals for their addiction and deemed them deserving of its consequences and punishment (Thombs, 2009). Viewing addiction as a disease, instead, allowed the person to be seen as the “victim” of an illness, deserving of compassionate care and medically supervised treatment (Thombs, 2009). In the disease model, an individual’s choice to initially engage in substance may have been freely made; however, once initiated, the disease could take over: “intense cravings are triggered via physiological mechanisms, and these cravings lead to compulsive overuse. This mechanism is beyond the personal control of the addict” (Thombs, 2009, p. 561).
Research by E. Morton Jellinek was credited with providing early support for a disease model of addiction (Hartje, 2009). Based on a non-random sample of surveys completed by 98 men responding to an Alcoholics Anonymous newsletter, later expanded to include 2,000 histories, Jellinek (1952) identified four progressive phases of the disease: the prealcoholic symptomatic, prodromal, crucial, and chronic phases. The “Jellinek Curve” reflects how specific behaviors and experiences relate to the disease’s progression and recovery—its very design reflects the perception of a person “hitting bottom” before being able to recover from addiction (from ).
Despite methodological weaknesses in the evidence, the original disease model became popular with many practitioners and Alcoholics Anonymous programs, introducing significant implications:
- alcoholism was viewed as a chronic, progressive, incurable disease;
- professional treatment was specified as necessary to control this incurable disease;
- abstinence was viewed as the only defense against recurrence and the only reasonable goal for a person with this disease;
- substituting a different drug for alcohol was expected to manifest the same disease symptoms and progression (Hartje, 2009).
The original disease model and principles have greatly influenced assessment and treatment practices over the past 60 to 70 years. There exist several points around which the original disease model of addiction has been challenged.
Heterogeneity challenge to the original disease model.
Longitudinal studies documenting the natural course of alcoholism demonstrated significant inconsistencies with a disease progression premise: multiple patterns were observed among men still alive 60 years after beginning the study, including continued alcohol abuse, stable abstinence, and return to asymptomatic/controlled drinking (Vaillant, 2003). Tremendous individual variation exists in patterns of addictive behaviors, as well as the severity of problems experienced by individuals at different points in time. Jellinek (1952) admitted that his was an “average trend” model in which individuals do not necessarily exhibit all of the symptoms associated with a phase, may differ in the sequencing of symptoms, and may differ in the duration of each phase; furthermore, “nonaddictive alcoholic” individuals may experience the identified negative consequences of alcoholism without experiencing a loss of control over drinking, and women may experience the disease differently.
This high degree of variability (heterogeneity) in expression called into question the perspective that alcoholism (or any substance use disorder) represents a single disease. Emphasis on the addiction/dependence end of the continuum of substance misuse “has resulted in a myopic view of substance abuse problems that has characterized them as progressive, irreversible, and only resolved through treatment” (Sobell, 2007, p. 2). Observed heterogeneity has informed the diagnostic schedules’ differentiations: different substances (and addictive behaviors such as gambling disorder) have distinct diagnostic codes. If “addiction” were a single uniform event there would be no need for multiple diagnostic categories—or different intervention strategies.
Subtypes versus stages of disease.
There exist marked differences in how substance misuse/SUDs are expressed even within a single substance type. Challenging Jellinek’s stage model of alcoholism, for example, is evidence of heterogeneity in “types” of alcoholism derived from a national sample (U.S.). The investigators based their typology on clinical characteristics of individuals meeting criteria for an alcohol dependence per the DSM-IV-R criteria that preceded the DSM-5 (Moss, Chen, & Yi, 2007). This analysis of U.S. National Epidemiological Survey on Alcohol and Related Conditions (NESARC) data led the authors to identify five “subtypes” of alcohol dependence, demonstrating clinical heterogeneity within the single diagnostic classification. The subtypes they identified were based on how participants clustered on diagnostic criteria, age of onset, family history, and presence of other co-occurring disorders. The five statistically determined clusters they identified were labelled: young adult, young antisocial, functional, intermediate familial, and chronic severe subtypes (see Figure 1). The groups demonstrated differences in their patterns of drinking, help-seeking, and response to intervention, as well. This study, based on a large, nationally representative sample reflected heterogeneity among persons engaged in a specific addictive behavior, and the wisdom of avoiding stereotypes about them—for instance, while the chronic severe subtype was the least common, it reflects a common stereotype of alcohol dependence.
Figure 1. Subtypes of alcoholism (based on data from Moss, Chen, & Yi, 2007).
Treatment and the disease model.
Additional important challenges to the disease model of addiction appear in the literature. Asserting that formal treatment for addiction is necessary has been challenged by evidence that many individuals experience significant, long-lasting improvement without engaging in formal treatment—sometimes referred to as “natural recovery” or “self-change”—typically, persons whose alcohol misuse is not of the most severe dependant nature (Sobell, 2007). Little is known about natural recovery in other substance misuse, though some evidence for its existence appears in the literature (e.g., Chen, 2006; Erickson & Alexander, 1989; Price, Risk, & Spitznagel, 2001). Possibly, the necessity for engaging in formal treatment varies by individual, severity of the problem, and characteristics of the substances or addictive behaviors involved.
Abstinence only based on disease model.
There are two parts of an abstinence only perspective that need to be unpacked. The first pertains to controlled drinking, and the second pertains to medication used to treat substance use disorders.
Viewing abstinence from substance use as the only defense against “disease” recurrence and the only reasonable goal for a person experiencing a substance use disorder has been challenged. Complete abstinence from all psychoactive substances is at one end of a continuum in treatment strategies, commonly applied in U.S. medical practice (Glenn & Wu, 2009). A debated position is that the continuum of recovery includes controlled substance use, including the type of substance which a person previously used problematically. For some individuals, their goal is safer, more controlled use, and harm reduction.
Controlled drinking. The word “sobriety” originally, historically implied temperate, moderated indulgence, not necessarily complete abstinence—an abstinence interpretation emerged during the 1900s (Glenn & Wu, 2009). Evidence since the 1970s indicates that some individuals achieve controlled drinking despite having previously engaged in an “out-of-control” drinking pattern, contrary to “the prevailing belief that any alcohol consumption causes an inevitable loss of control over one’s alcohol use” (Klingemann, 2016, p. 436). The debate about “controlled drinking,” “reduced-risk drinking,” and “moderation management” continues, and it is unclear how the evidence for and against it might apply to other substances and addictive behaviors. Reduced-risk drinking (RRD) is seen in many Western European countries as one pathway out of addiction, and a legitimate treatment goal (Klingemann, 2016). Importantly, the ability to engage in controlled use following a substance use disorder may vary by individual, severity of the problem, and characteristics of the substances or addictive behaviors involved. Unsuccessful attempts at controlled use suggest the need for abstinence as a treatment goal. Conversely, if an individual is able to resolve the negative consequences of use, and sustain this change over a long period of time through controlled use, is this an acceptable resolution?
Medication used to treat substance use disorders.
Closely associated with the abstinence issue lies an additional point of contention with the disease model of addiction–the belief that substituting medication for the primary addictive substance simply continues manifestation of the same disease of “addiction.”
This stance contributes to the hesitancy expressed by some practitioners to promote the use of medically assisted treatment (MAT) and pharmacotherapies to treat substance use disorders because they believe some medications maintain the disease rather than treating it. Of concern, this viewpoint sometimes serves as a barrier for those who would benefit from medication.
Indeed, some 12 step meeting attendees suggest that MAT is inconsistent with sobriety (https://www.statnews.com/2017/10/04/medication-assisted-therapy-12-step/). The American Society of Addiction Medicine (ASAM) has weighed in, saying, “this so- called “advice” from well-intended but misinformed members is not founded in scientific or 12-step philosophy and violates a long held 12- step policy of ‘AA members should not give medical advice to each other'” (see here for detailed explanation https://www.asam.org/Quality-Science/publications/magazine/read/article/2014/06/12/twelve-step-recovery-and-medication-assisted-therapies). ASAM posits, since substance use disorder is a brain disease, some people appropriately require medication in order to attain sobriety. Evidence supports this contention. For example, on the issue of the use of pharmacotherapy to assist in controlled drinking, recent meta-analysis concluded that three medications showed controlled drinking outcomes superior to a placebo (Palpcuer et al., 2018).
Loss of Control Concept.
The original disease model of addiction expresses another point with which scholars and practitioners have taken issue: applying “loss of control” as a defining criterion. The prior moral model attributed individuals’ use/misuse of alcohol, tobacco, or other drugs to moral failure or personality weakness, holding them “personally responsible for creating suffering for themselves and others” (Thombs, 2009, p. 561). The original disease model, as previously discussed, did not take a position on a person’s initial decision to use a substance, but argued that the “disease” may take over, eventually rendering an individual helpless to control the behavior. Heather (2017) has argued against the “compulsion” aspect of the disease model where addictive behavior “is said to be carried out against the will,” and “marks the turning point from normal, recreational drug use to addictive drug use” (p. 15). His counter-argument does not support a moral failure/blame stance toward addiction; instead, he emphasized the power of environmental, contextual, and reinforcement paradigms operating to influence behavioral choices related to continued engagement in substance misuse (or other addictive behaviors). One problem with the loss of control concept is that individuals may reframe it in terms of, “I can’t help myself,” excusing themselves from taking responsibility for the behavior or taking steps toward recovery. Reinforcing the notion of each individual’s personal responsibility to manage their health, despite disease is an important counterpoint.
Contemporary brain disease model and bio-psycho-social-spiritual perspective.
As previously noted, recognition of the brain-behavior nexus in the development and maintenance of addictive behavior is important and necessary to understanding, intervening around, and recovery involving addictive behavior and related problems. Evidence concerning the neurobiology of substance use and mechanisms involved in the transition to substance use disorders has expanded in many directions over the past two decades, contributing to a widening variety of treatment and prevention intervention strategies (Volkow & Koob, 2015; Volkow, Koob, & McLellan, 2016).
Proponents of a contemporary brain disease model of addiction argue that: “After centuries of efforts to reduce addiction and its related costs by punishing addictive behaviors failed to produce adequate results, recent basic and clinical research has provided clear evidence that addiction might be better considered and treated as an acquired disease of the brain” (Volkow, Koob, & McLellan, 2016, p. 364). The U.S. National Institute on Drug Abuse applies the following definition of addiction:
“Addiction is defined as a chronic, relapsing disorder characterized by compulsive drug seeking and use despite adverse consequences. It is considered a brain disorder, because it involves functional changes to brain circuits involved in reward, stress, and self-control, and those changes may last a long time after a person has stopped taking drugs. Addiction is a lot like other diseases, such as heart disease. Both disrupt the normal, healthy functioning of an organ in the body, both have serious harmful effects, and both are, in many cases, preventable and treatable. If left untreated, they can last a lifetime and may lead to death” (NIDA, 2018).
Chronic, relapsing diseases like diabetes or high blood pressure often have a strong behavioral health component—just as substance use disorders. While these disease conditions may worsen over time, the outcome is not immutable—outcomes can be affected by behavioral health interventions, as well as self-directed changes in behavior and/or environment.
Biology and psychology intersect where substances altering the brain’s reward and emotional circuits influence individuals’ experiences, learning, memory, affect, executive function, decision-making, expectancies, withdrawal symptoms, and cravings, with profound implications for continued engagement in addictive behavior, as well as strategies for changing addictive behavior patterns. Understanding brain-behavior processes is necessary; however, this alone does not impart sufficient knowledge. Biological and psychological processes do not occur in a vacuum, but within complex, impactful social and spiritual contexts and physical environments. For example, evidence that early exposure to alcohol and other substance misuse increases the odds of developing a substance use disorder later in life (Odgers et al., 2008) invokes mechanisms of multiple types: changes to the brain (biology); learning, social learning, and expectancies (psychology); social norms and access (social context/environment). Not only does recovery occur within social contexts (Heather et al., 2018), biological, psychological, and social interventions all may play a role. Furthermore, social, psychological, and spiritual interventions can influence neurobiological processes (Volkow, Koob, & McLellan, 2016); biology does not confer destiny but has a powerful iterative relationship with the other domains. Viewing addictive behaviors from an integrated biopsychosocial framework is required and reflected throughout this book.
*Note that some contents presented in this chapter are both adapted from and informed the writing of an introductory chapter by Begun and Murray (in press), to the Handbook of Social Work and Addictive Behavior from Routledge.