Behavioral addiction

Behavioral addiction[note 1] is a form of addiction that involves a compulsion to engage in a rewarding non-substance-related behavior – sometimes called a natural reward[4][5] – despite any negative consequences to the person's physical, mental, social or financial well-being.[6] Addiction canonically refers to substance abuse; however, the term's connotation has been expanded to include behaviors that may lead to a reward (e.g., gambling, eating, or shopping)[7] since the 1990s. 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 in the reward system.[4][5][8]

Psychiatric and medical classifications

Diagnostic models do not currently include the criteria necessary to identify behaviors as addictions in a clinical setting. Behavioral addictions have been proposed as a new class in DSM-5, but the only category included is gambling addiction. Internet gaming addiction is included in the appendix as a condition for further study.[9][10]

Behavioral addictions, which are sometimes referred to as impulse control disorders, are increasingly recognized as treatable forms of addiction.[11] The type of excessive behaviors identified as being addictive include gambling, eating, having sexual intercourses, using pornography, computers, video games, internet and digital media, physical exercise, and shopping.

In August 2011, the American Society of Addiction Medicine (ASAM) issued a public statement defining all addiction in terms of brain changes. "Addiction is a primary, chronic disease of brain reward, motivation, memory and related circuitry."[12]

The following excerpts are taken from the organization's FAQs:

The new ASAM definition makes a departure from equating addiction with just substance dependence, by describing how addiction is also related to behaviors that are rewarding. This is the first time that ASAM has taken an official position that addiction is not solely "substance dependence." This definition says that addiction is about functioning and brain circuitry and how the structure and function of the brains of persons with addiction differ from the structure and function of the brains of persons who do not have addiction. It talks about reward circuitry in the brain and related circuitry, but the emphasis is not on the external rewards that act on the reward system. Food and sexual behaviors and gambling behaviors can be associated with the "pathological pursuit of rewards" described in this new definition of addiction.

We all have the brain reward circuitry that makes food and sex rewarding. In fact, this is a survival mechanism. In a healthy brain, these rewards have feedback mechanisms for satiety or 'enough.' In someone with addiction, the circuitry becomes dysfunctional such that the message to the individual becomes 'more', which leads to the pathological pursuit of rewards and/or relief through the use of substances and behaviors. So, anyone who has addiction is vulnerable to food and sex addiction.

Meanwhile, DSM-5 has deprecated the term "addiction".[13]

Treatment

Behavioral addiction is a treatable condition. 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. 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.[14][15] Any unrelated psychiatric disorders should be kept under control, and differentiated from the contributing factors that cause the addiction.

Research

A recent narrative review[16] in 2017 examined the existing literature for studies reporting associations between behavioural addictions (pathological gambling, problematic internet use, problematic online gaming, compulsive sexual behaviour disorder, compulsive buying and exercise addiction) and psychiatric disorders. Overall, there is solid evidence for associations between behavioural 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 behavioural 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 behavioural addictions are a cause or a consequence of psychiatric disorders.

Biomolecular mechanisms

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.[4][5][8] Overexpression of ΔFosB in the nucleus accumbens is necessary and sufficient for many of the neural adaptations seen in drug addiction;[4] it has been implicated in addictions to alcohol, cannabinoids, cocaine, nicotine, phenylcyclidine, and substituted amphetamines[4][17][18][19] as well as addictions to natural rewards such as sex, exercise, and food.[5][8] A recent study also demonstrated a cross-sensitization between drug reward (amphetamine) and a natural reward (sex) that was mediated by ΔFosB.[20]

Besides increased ΔFosB expression in the nucleus accumbens, there are many other correlations in the neurobiology of behavioral addictions with drug addictions.

One of the most important discoveries of addictions has been the drug based reinforcement and, even more important, reward based learning processes. Several structures of the brain are important in the conditioning process of behavioral addiction; these subcortical structures form the brain regions known as the reward system. 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.[21] 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.[22] 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.[23] 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.[23]

See also

  • Addictive behavior
  • Addictive personality
  • ANKK1 § Addictive behaviors
  • Habit

Notes

  1. ↑ Synonyms of behavioral addiction include: process addiction and non-substance-related addiction.[1][2][3]

References

  1. ↑ Albrecht U, Kirschner NE, Grüsser SM (2007). "Diagnostic instruments for behavioural addiction: an overview". Psychosom Med. 4: Doc11. PMC 2736529. PMID 19742294.
  2. ↑ Potenza MN (September 2006). "Should addictive disorders include non-substance-related conditions?". Addiction. 101 Suppl 1: 142–51. doi:10.1111/j.1360-0443.2006.01591.x. PMID 16930171. S2CID 18535096.
  3. ↑ Shaffer, Howard J. (1996). "Understanding the means and objects of addiction: Technology, the internet, and gambling". Journal of Gambling Studies. 12 (4): 461–9. doi:10.1007/BF01539189. PMID 24234163. S2CID 20470452.
  4. 1 2 3 4 5 Robison AJ, Nestler EJ (November 2011). "Transcriptional and epigenetic mechanisms of addiction". Nat. Rev. Neurosci. 12 (11): 623–637. doi:10.1038/nrn3111. PMC 3272277. PMID 21989194. ΔFosB has been linked directly to several subtstance-related behaviors ... Importantly, genetic or viral overexpression of ΔJunD, a dominant negative mutant of JunD which antagonizes ΔFosB- and other AP-1-mediated transcriptional activity, in the NAc or OFC blocks these key effects of drug exposure14,22–24. This indicates that ΔFosB is both necessary and sufficient for many of the changes wrought in the brain by chronic drug exposure. ΔFosB is also induced in D1-type NAc MSNs by chronic consumption of several natural rewards, including sucrose, high fat food, sex, wheel running, where it promotes that consumption14,26–30. This implicates ΔFosB in the regulation of natural rewards under normal conditions and perhaps during pathological addictive-like states.
  5. 1 2 3 4 Olsen CM (December 2011). "Natural rewards, neuroplasticity, and non-drug addictions". Neuropharmacology. 61 (7): 1109–22. doi:10.1016/j.neuropharm.2011.03.010. PMC 3139704. PMID 21459101.
  6. ↑ Stein, Dan J.; Hollander, Eric; Rothbaum, Barbara Olasov (31 August 2009). Textbook of Anxiety Disorders. American Psychiatric Pub. pp. 359–. ISBN 978-1-58562-254-2. Retrieved 24 April 2010.
  7. ↑ Holden, Constance (2 November 2001). "'Behavioral' Addictions: Do They Exist?". Science. 294 (5544): 980–982. doi:10.1126/science.294.5544.980. ISSN 0036-8075. PMID 11691967. S2CID 27235598.
  8. 1 2 3 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.
  9. ↑ Kuss, Daria (2013). "Internet gaming addiction: current perspectives". Psychology Research and Behavior Management. 6 (6): 125–137. doi:10.2147/PRBM.S39476. PMC 3832462. PMID 24255603.
  10. ↑ Shenfield, Tali (21 February 2015). "Is your child a gaming addict?". Advanced Psychology.
  11. ↑ Grant, Jon: Impulse Control Disorders: A Clinician's Guide to Understanding and Treating Behavioral Addictions
  12. ↑ American Society of Addiction Medicine. Public Policy Statement: Definition of Addiction. https://www.asam.org/resources/definition-of-addiction
  13. ↑ American Psychiatric Association (2013). Diagnostic and Statistical Manual of Mental Disorders (Fifth ed.). Arlington, VA: American Psychiatric Publishing. p. 485. ISBN 978-0-89042-555-8. Note that the word addiction is not applied as a diagnostic term in this classification, although it is in common usage in many countries to describe severe problems related to compulsive and habitual use of substances.
  14. ↑ Grant JE, Potenza MN, Weinstein A, Gorelick DA (September 2010). "Introduction to behavioral addictions". Am. J. Drug Alcohol Abuse. 36 (5): 233–241. doi:10.3109/00952990.2010.491884. PMC 3164585. PMID 20560821. Naltrexone, a mu-opioid receptor antagonist approved by the US Food and Drug Administration for the treatment of alcoholism and opioid dependence, has shown efficacy in controlled clinical trials for the treatment of pathological gambling and kleptomania (76–79), and promise in uncontrolled studies of compulsive buying (80), compulsive sexual behavior (81), internet addiction (82), and pathologic skin picking (83). ... Topiramate, an anti-convulsant which blocks the AMPA subtype of glutamate receptor (among other actions), has shown promise in open-label studies of pathological gambling, compulsive buying, and compulsive skin picking (85), as well as efficacy in reducing alcohol (86), cigarette (87), and cocaine (88) use. N-acetyl cysteine, an amino acid that restores extracellular glutamate concentration in the nucleus accumbens, reduced gambling urges and behavior in one study of pathological gamblers (89), and reduces cocaine craving (90) and cocaine use (91) in cocaine addicts. These studies suggest that glutamatergic modulation of dopaminergic tone in the nucleus accumbens may be a mechanism common to behavioral addiction and substance use disorders (92).
  15. ↑ "Drug Addiction Treatment & Admissions Overview". River Oaks. Retrieved 18 November 2020.
  16. ↑ Starcevic, Vladan; Khazaal, Yasser (7 April 2017). "Relationships between Behavioural Addictions and Psychiatric Disorders: What Is Known and What Is Yet to Be Learned?". Frontiers in Psychiatry. 8: 53. doi:10.3389/fpsyt.2017.00053. ISSN 1664-0640. PMC 5383701. PMID 28439243.
  17. ↑ Hyman SE, Malenka RC, Nestler EJ (2006). "Neural mechanisms of addiction: the role of reward-related learning and memory". Annu. Rev. Neurosci. 29: 565–598. doi:10.1146/annurev.neuro.29.051605.113009. PMID 16776597. S2CID 15139406.
  18. ↑ 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.
  19. ↑ Kanehisa Laboratories (2 August 2013). "Alcoholism – Homo sapiens (human)". KEGG Pathway. Retrieved 10 April 2014.
  20. ↑ 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.
  21. ↑ 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.
  22. ↑ 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.
  23. 1 2 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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