Internet Addiction

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Theories and Models of Internet Addiction

Scholars have sought to explain the development and maintenance of Internet addiction using a wide range of conceptual and theoretical models, and several theories have been formulated to explain, predict, and further understand Internet addiction as an addictive behavior. It is important to note that all models of Internet addiction complement each other and help us understand the etiology, treatment, and prevention of Internet addiction.

2.1 The Cognitive-Behavioral Model

The cognitive-behavioral model (Davis, 2001) addresses the definition, conceptualization, and treatment of Internet addiction, which is referred to as pathological Internet use within this model. The cognitive-behavioral model of pathological Internet use distinguishes between specific pathological Internet use (SPIU) and generalized pathological Internet use (GPIU).

This distinction comes from the idea that Internet use can serve multiple purposes and goals. For instance, SPIU is broadly defined as a type of pathological Internet use whereby individuals become dependent on using a specific function or application of the Internet, whereas GPIU relates to a more general, multidimensional behavioral overuse pattern of pathological Internet use. According to this model, maladaptive cognitions play a key role in both development and maintenance of pathological Internet use.

The cognitive theory of pathological Internet use utilizes the concepts of distal and proximal contributory causes of pathological Internet use to better illustrate the nature of the cognitive theory of pathological Internet use. Accordingly, distal causes include preexisting psychopathology (depression, social anxiety, substance dependence, etc.) and behavioral reinforcement that is provided by the Internet itself throughout the experience of new functions and situational cues that contribute to conditioned responses. Proximal causes in turn involve maladaptive cognitions, which are regarded as a sufficient condition with the potential to lead to both GPIU and SPIU and also cause the set of symptoms associated with pathological Internet use (Davis, 2001).

The cognitive-behavioral model posits that GPIU involves spending abnormal amounts of time on the Internet, either wasting time with no direct purpose and/or spending excessive amounts of time in online chat rooms. For this reason, procrastination is also assumed to play an important contributory role toward the development and maintenance of GPIU. The cognitive-behavioral |27|model argues that symptoms of pathological Internet use derive primarily from individuals’ maladaptive cognitions (Davis, 2001). According to Davis (2001), these symptoms relate more to cognitive symptoms and include obsessive thoughts about the Internet, diminished impulse control, inability to cease Internet use, and a generalized feeling that the Internet is the only place where individuals feel good about themselves. Other symptoms may include thinking about the Internet while offline, anticipating future time online, decreasing interest in other activities or hobbies, and social isolation (Davis, 2001).

The cognitive-behavioral model remains a very influential way of understanding Internet addiction at both theoretical and measurement levels. In fact, the cognitive-behavioral model has also received extensive support from scholars in the field who have sought to operationalize the model within a psychometric framework (see Caplan, 2010). In addition, the model has been used in, and served as the basis of, treatment protocols for Internet addiction, such as the cognitive behavior therapy for Internet addiction (CBT-IA).

2.2 The Syndrome Model of Addiction

The syndrome model of addiction (Shaffer et al., 2004) is based on the idea that specific objects of addiction play a less central role in the development of all addictive disorders because there is evidence of multiple and interacting biopsychosocial antecedents, manifestation, and consequences (in both behavioral and substance-based addictions) that reflect an underlying addiction syndrome. Indeed, technological addictions such as Internet addiction can be defined within a syndrome model of addictions that is organized into three primary areas: (1) shared neurobiological antecedents, (2) shared psychosocial antecedents, and (3) shared experiences (manifestations and sequelae; Shaffer et al., 2004).

According to this model, syndromes and their respective signs and symptoms serve as identifying characteristics of the underlying condition (addiction). Moreover, given the potentially recursive nature of syndromes and their sequelae, the consequents of the addiction syndrome can influence existing antecedent factors (or become new antecedents) to change the existing risk matrix associated with developing different manifestations of the syndrome (Shaffer et al., 2004). This model suggests many commonalities occur across the different expressions of addiction, and these commonalities reflect a shared etiology.

The syndrome model of addiction developed by Shaffer et al. (2004) posits that all addictions develop via comparable distal antecedents (risk factors, including neurobiological and contextual factors), which render individuals more vulnerable to addictions. Given the presence of the identified distal antecedents, proximal antecedents precede the development of addictions, and may include negative events and stress experiences and the sustained use of a substance or persistent engagement in a particular behavior. The syndrome model of addiction also suggests that addictions only differ in their actual manifestation, and that given the distal and proximal risk factors, some individuals may develop an addiction to a substance, whereas others may develop an addiction to a specific behavior, such as Internet use.

|28|This model has important clinical implications. For example, it suggests the most effective addiction treatments are multimodal approaches, which include both object-specific and addiction-general treatments (Shaffer et al., 2004). Additionally, at the treatment level, patients develop new risk factors during treatment, which can hamper recovery efforts. Finally, because the model emphasizes the etiology of addictions, when adhering to this model, clinicians should use diagnostic gates, which require identification of central features of the syndrome (such as withdrawal symptoms accompanied by premorbid characteristics), without which a diagnosis should not be made (Shaffer et al., 2004).

2.3 The Components Model of Addiction

The components model of addiction (Griffiths, 2005) is a well-established and extensively investigated theoretical framework for conceptualizing behavioral and technological addictions as a whole. This model builds upon Griffiths’s early works (1995) and draws upon the (slightly modified) six core components (i.e., salience, mood modification, tolerance, withdrawal, conflict, and relapse). Accordingly, this model argues that all addictions share commonalities and are a part of a biopsychosocial process. Consequently, substance-related and behavioral addictions, such as Internet addiction, are thought to develop via similar biopsychosocial processes due to their shared characteristics (which have important implications for the treatment of addictions), most notably the following six addiction criteria as defined by Griffiths (2005):

• Salience refers to a particular activity becoming the most dominant and important activity in a person’s life. It dominates their thinking (through preoccupations and cognitive distortions), feelings (through cravings), and behavior (through deterioration of socialization).

• Mood modification refers to the subjective experience people report as a result of engaging in a particular activity in the form of an arousing buzz or a high or even a tranquilizing feeling of escape or numbing.

• Tolerance refers to the process whereby increasing amounts of a particular activity are needed to achieve initial positive effects (pleasure, satisfaction).

• Withdrawal symptoms refer to the unpleasant feeling states and/or physical effects that occur when an activity is discontinued or suddenly reduced. These symptoms may be psychological (moodiness and irritability) or more physiological (nausea, sweats, headaches, insomnia, ...