Behavioral addiction

Behavioral addiction, process addiction,[1] or non-substance-related disorder[2] is a form of addiction that involves a compulsion to engage in a rewarding non-substance-related behavior – sometimes called a natural reward[3][4] – despite any negative consequences to the person's physical, mental, social or financial well-being.[5] In the brain's reward system, a gene transcription factor known as ΔFosB has been identified as a necessary common factor involved in both behavioral and drug addictions, which are associated with the same set of neural adaptations.[3][4][6]

Addiction canonically refers to substance abuse; however, the term's connotation has been expanded to include behaviors that may lead to a reward (such as gambling, eating, or shopping)[7] since the 1990s. Still, the framework to diagnose and categorize behavioral addiction is a controversial topic in the psychopathology field.[8][9]

Psychiatric and medical classifications

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Diagnostic and Statistical Manual of Mental Disorders (DSM) recognized behavioral addictions for the first time in DSM-5 with gambling disorder, formerly pathological gambling, as the only non-substance-related disorder classified under the chapter of "Substance-Related and Addictive Disorders".[10] Internet gaming addiction was included in the appendix as a condition for further study.[11] Although "addiction" is commonly used to describe repetitive harmful behavior in nonmedical settings,[12] DSM-5 recommended the neutral term "disorder" instead of "addiction" under the clinical settings to avoid uncertain definition and potentially negative connotation.[13]

Similar to the changes in DSM-5, the eleventh revision of the International Classification of Diseases (ICD-11) introduced the category "Disorders due to substance use or addictive behaviours," based on the diagnostic framework of impaired control, repetitive harmful behavior, and continuation or escalation despite negative consequences.[14] The new sub-category "Disorders due to addictive behaviours" included gambling disorder (formerly under the habit and impulse disorders), gaming disorder (a new diagnosis), and two residual categories (other specified and unspecified) to raise attention among clinicians and the public and to facilitate further research.[14][15]

In 2019, the American Society of Addiction Medicine (ASAM) revised its definition of addiction including substance use and compulsive behaviors, stating: "addiction is a treatable, chronic medical disease involving complex interactions among brain circuits, genetics, the environment, and an individual’s life experiences."[16]

Other addictive behaviors which have received research attention but with insufficient or inconclusive evidence include pornography use disorder, compulsive buying disorder, social network use disorder, work addiction, exercise addiction, compulsive sexual behavior disorder, and food addiction.[13][17][18][19]

Treatment

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Behavioral addiction is a treatable condition.[20] Treatment options include psychotherapy and psychopharmacotherapy (i.e., medications) or a combination of both. Cognitive behavioral therapy (CBT) is the most common form of psychotherapy used in treating behavioral addictions; it focuses on identifying patterns that trigger compulsive behavior and making lifestyle changes to promote healthier behaviors. Because cognitive behavioral therapy is considered a short-term therapy, the number of sessions for treatment normally ranges from five to twenty.[21] During the session, therapists will lead patients through the topics of identifying the issue, becoming aware of one's thoughts surrounding the issue, identifying any negative or false thinking, and reshaping said negative and false thinking. While CBT does not cure behavioral addiction, it does help with coping with the condition in a healthy way. Currently, there are no medications approved for treatment of behavioral addictions in general, but some medications used for treatment of drug addiction may also be beneficial with specific behavioral addictions.[22][23]

Another form of treatment is recreational therapy. A Certified Therapeutic Recreation Specialist (CTRS) uses leisure and recreation to help individuals recover from their injuries, ailments, or addictions. Therapeutic recreation can help an individual struggling with addiction to improve their self-esteem, confidence, motivation, resiliency, autonomy, enjoyment, and overall emotional state.[24][25]

Research

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The classification and diagnostic framework of behavioral addictions under DSM-5 and ICD-11 has been a controversial subject among the clinical research field.[18] For example, this 2020 narrative review[17] considered ICD-11's guidelines to be adequate to include more behavioral addictions based on clinical relevance and empirical evidence, while this 2015 journal article questioned[26] the atheoretical and confirmatory research approaches on the accuracy of qualitative factors and criticized the lack of consideration of social elements and psychological processes.

A recent narrative review[27] in 2017 examined the existing literature for studies reporting associations between behavioral addictions (pathological gambling, problematic internet use, problematic online gaming, compulsive sexual behavior disorder, compulsive buying and exercise addiction) and psychiatric disorders. Overall, there is solid evidence for associations between behavioral addictions and mood disorder, anxiety disorder as well as substance use disorders. Associations between ADHD may be specific to problematic internet use and problematic online gaming. The authors also conclude that most of current research on the association between behavioral addictions and psychiatric disorders has several limitations: they are mostly cross-sectional, are not from representative samples, and are often based on small samples, among others. Especially more longitudinal studies are needed to establish the direction of causation, i.e. whether behavioral addictions are a cause or a consequence of psychiatric disorders.

Addiction and the reward system

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Main articles: ΔFosB and Reward system

ΔFosB, a gene transcription factor, has been identified as playing a critical role in the development of addictive states in both behavioral addictions and drug addictions.[3][4][6] Overexpression of ΔFosB in the nucleus accumbens is necessary and sufficient for many of the neural adaptations seen in drug addiction;[3] it has been implicated in addictions to alcohol, cannabinoids, cocaine, nicotine, phenylcyclidine, and substituted amphetamines[3][28][29][30] as well as addictions to natural rewards such as sex, exercise, and food.[4][6] A recent study also demonstrated a cross-sensitization between drug reward (amphetamine) and a natural reward (sex) that was mediated by ΔFosB.[31]

One of the major areas of study is the amygdala, a brain structure which involves emotional significance and associated learning. Research shows that dopaminergic projections from the ventral tegmental area facilitate a motivational or learned association to a specific behavior.[32] Dopamine neurons take a role in the learning and sustaining of many acquired behaviors. Research specific to Parkinson's disease has led to identifying the intracellular signaling pathways that underlie the immediate actions of dopamine. The most common mechanism of dopamine is to create addictive properties along with certain behaviors.[33] There are three stages to the dopamine reward system: bursts of dopamine, triggering of behavior, and further impact to the behavior. Once electronically signaled, possibly through the behavior, dopamine neurons let out a 'burst-fire' of elements to stimulate areas along fast transmitting pathways. The behavior response then perpetuates the striated neurons to further send stimuli. The fast firing of dopamine neurons can be monitored over time by evaluating the amount of extracellular concentrations of dopamine through micro dialysis and brain imaging. This monitoring can lead to a model in which one can see the multiplicity of triggering over a period of time.[34] Once the behavior is triggered, it is hard to work away from the dopamine reward system.

Behaviors like gambling have been linked to the newfound idea of the brain's capacity to anticipate rewards. The reward system can be triggered by early detectors of the behavior, and trigger dopamine neurons to begin stimulating behaviors. But in some cases, it can lead to many issues due to error, or reward-prediction errors. These errors can act as teaching signals to create a complex behavior task over time.[34]

See also

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References

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  6. ^ a b c Blum K, Werner T, Carnes S, Carnes P, Bowirrat A, Giordano J, Oscar-Berman M, Gold M (2012). "Sex, drugs, and rock 'n' roll: hypothesizing common mesolimbic activation as a function of reward gene polymorphisms". Journal of Psychoactive Drugs. 44 (1): 38–55. doi:10.1080/02791072.2012.662112. PMC 4040958. PMID 22641964. It has been found that deltaFosB gene in the NAc is critical for reinforcing effects of sexual reward. Pitchers and colleagues (2010) reported that sexual experience was shown to cause DeltaFosB accumulation in several limbic brain regions including the NAc, medial pre-frontal cortex, VTA, caudate, and putamen, but not the medial preoptic nucleus. Next, the induction of c-Fos, a downstream (repressed) target of DeltaFosB, was measured in sexually experienced and naive animals. The number of mating-induced c-Fos-IR cells was significantly decreased in sexually experienced animals compared to sexually naive controls. Finally, DeltaFosB levels and its activity in the NAc were manipulated using viral-mediated gene transfer to study its potential role in mediating sexual experience and experience-induced facilitation of sexual performance. Animals with DeltaFosB overexpression displayed enhanced facilitation of sexual performance with sexual experience relative to controls. In contrast, the expression of DeltaJunD, a dominant-negative binding partner of DeltaFosB, attenuated sexual experience-induced facilitation of sexual performance, and stunted long-term maintenance of facilitation compared to DeltaFosB overexpressing group. Together, these findings support a critical role for DeltaFosB expression in the NAc in the reinforcing effects of sexual behavior and sexual experience-induced facilitation of sexual performance. ... both drug addiction and sexual addiction represent pathological forms of neuroplasticity along with the emergence of aberrant behaviors involving a cascade of neurochemical changes mainly in the brain's rewarding circuitry.
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  29. ^ Steiner H, Van Waes V (January 2013). "Addiction-related gene regulation: risks of exposure to cognitive enhancers vs. other psychostimulants". Prog. Neurobiol. 100: 60–80. doi:10.1016/j.pneurobio.2012.10.001. PMC 3525776. PMID 23085425.
  30. ^ Kanehisa Laboratories (2 August 2013). "Alcoholism – Homo sapiens (human)". KEGG Pathway. Retrieved 10 April 2014.
  31. ^ Pitchers KK, Vialou V, Nestler EJ, Laviolette SR, Lehman MN, Coolen LM (February 2013). "Natural and drug rewards act on common neural plasticity mechanisms with ΔFosB as a key mediator". J. Neurosci. 33 (8): 3434–42. doi:10.1523/JNEUROSCI.4881-12.2013. PMC 3865508. PMID 23426671. Together, these findings demonstrate that drugs of abuse and natural reward behaviors act on common molecular and cellular mechanisms of plasticity that control vulnerability to drug addiction, and that this increased vulnerability is mediated by ΔFosB and its downstream transcriptional targets.
  32. ^ Brewer, Judson A.; Potenza, Marc N. (2008). "The neurobiology and genetics of impulse control disorders: Relationships to drug addictions". Biochemical Pharmacology. 75 (1): 63–75. doi:10.1016/j.bcp.2007.06.043. PMC 2222549. PMID 17719013.
  33. ^ Girault, Jean-Antoine; Greengard, P (2004). "The Neurobiology of Dopamine Signaling". Archives of Neurology. 61 (5): 641–4. doi:10.1001/archneur.61.5.641. PMID 15148138.
  34. ^ a b Dichiara, G; Bassareo, V (2007). "Reward system and addiction: What dopamine does and doesn't do". Current Opinion in Pharmacology. 7 (1): 69–76. doi:10.1016/j.coph.2006.11.003. PMID 17174602.
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