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]

^ Smith, David E. (1 January 2012). "Editor's Note: The Process Addictions and the New ASAM Definition of Addiction". Journal of Psychoactive Drugs. 44 (1): 1–4. doi:10.1080/02791072.2012.662105. ISSN 0279-1072. PMID 22641960.
^ American Psychiatric Association (18 March 2022). Diagnostic and Statistical Manual of Mental Disorders (DSM-5-TR ed.). American Psychiatric Association Publishing. p. 661. doi:10.1176/appi.books.9780890425787. ISBN 978-0-89042-575-6. S2CID 249488050.
^ ^a ^b 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 substance-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.
^ ^a ^b 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.
^ 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.
^ 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.
^ 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.
^ Starcevic, Vladan (August 2016). "Behavioural addictions: A challenge for psychopathology and psychiatric nosology". The Australian and New Zealand Journal of Psychiatry. 50 (8): 721–725. doi:10.1177/0004867416654009. ISSN 1440-1614. PMID 27357713. S2CID 22843151.
^ Pinna, F.; Dell’Osso, B.; Di Nicola, M.; Janiri, L.; Altamura, A.C.; Carpiniello, B.; Hollander, E. (1 December 2015). "Behavioural addictions and the transition from DSM-IV-TR to DSM-5" (PDF). Journal of Psychopathology. 21 (4): 380–389.

[1] Smith, David E. (1 January 2012). "Editor's Note: The Process Addictions and the New ASAM Definition of Addiction". Journal of Psychoactive Drugs. 44 (1): 1–4. doi:10.1080/02791072.2012.662105. ISSN 0279-1072. PMID 22641960.

[2] American Psychiatric Association (18 March 2022). Diagnostic and Statistical Manual of Mental Disorders (DSM-5-TR ed.). American Psychiatric Association Publishing. p. 661. doi:10.1176/appi.books.9780890425787. ISBN 978-0-89042-575-6. S2CID 249488050.

[Nestler-3] 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 substance-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.

[Natural_and_drug_addictions-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.

[SteinHollander2009-5] 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.

[ΔFosB_reward-6] 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.

[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] Starcevic, Vladan (August 2016). "Behavioural addictions: A challenge for psychopathology and psychiatric nosology". The Australian and New Zealand Journal of Psychiatry. 50 (8): 721–725. doi:10.1177/0004867416654009. ISSN 1440-1614. PMID 27357713. S2CID 22843151.

[9] Pinna, F.; Dell’Osso, B.; Di Nicola, M.; Janiri, L.; Altamura, A.C.; Carpiniello, B.; Hollander, E. (1 December 2015). "Behavioural addictions and the transition from DSM-IV-TR to DSM-5" (PDF). Journal of Psychopathology. 21 (4): 380–389.

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