Behavioral addiction

Addiction and dependence glossary[1][2][3][4]
• addiction – a brain disorder characterized by compulsive engagement in rewarding stimuli despite adverse consequences
• addictive behavior – a behavior that is both rewarding and reinforcing
• addictive drug – a drug that is both rewarding and reinforcing
• dependence – an adaptive state associated with a withdrawal syndrome upon cessation of repeated exposure to a stimulus (e.g., drug intake)
• drug sensitization or reverse tolerance – the escalating effect of a drug resulting from repeated administration at a given dose
• drug withdrawal – symptoms that occur upon cessation of repeated drug use
• physical dependence – dependence that involves persistent physical–somatic withdrawal symptoms (e.g., fatigue and delirium tremens)
• psychological dependence – dependence that involves emotional–motivational withdrawal symptoms (e.g., dysphoria and anhedonia)
• reinforcing stimuli – stimuli that increase the probability of repeating behaviors paired with them
• rewarding stimuli – stimuli that the brain interprets as intrinsically positive and desirable or as something to be approached
• sensitization – an amplified response to a stimulus resulting from repeated exposure to it
• substance use disorder - a condition in which the use of substances leads to clinically and functionally significant impairment or distress
• tolerance – the diminishing effect of a drug resulting from repeated administration at a given dose

Behavioral addiction[note 1] is a form of addiction that involves a compulsion to engage in a rewarding non-drug-related behavior – sometimes called a natural reward[8][9] – despite any negative consequences to the person's physical, mental, social or financial well-being.[10][11] 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.[8][9][12]

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.[8][9][12] Overexpression of ΔFosB in the nucleus accumbens is necessary and sufficient for many of the neural adaptations seen in drug addiction;[8] it has been implicated in addictions to alcohol, cannabinoids, cocaine, nicotine, phenylcyclidine, and substituted amphetamines[8][13][14][15] as well as addictions to natural rewards such as sex, exercise, and food.[9][12] A recent study also demonstrated a cross-sensitization between drug reward (amphetamine) and a natural reward (sex) that was mediated by ΔFosB.[16]

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.[17] 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.[18] 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.[19] Once the behavior is triggered, it is hard to work away from the dopamine reward system.

Behaviors like gambling have been linked to the new found 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.[19]

Summary of addiction-related plasticity
Form of neuroplasticity
or behavioral plasticity		 Type of reinforcer Sources
Opiates Psychostimulants High fat or sugar food Sexual intercourse Physical exercise
(aerobic)		 Environmental
enrichment
ΔFosB expression in
nucleus accumbens D1-type MSNs		 ↑ ↑ ↑ ↑ ↑ ↑ [9]
Behavioral plasticity
Escalation of intake Yes Yes Yes [9]
Psychostimulant
cross-sensitization		 Yes Not applicable Yes Yes Attenuated Attenuated [9]
Psychostimulant
self-administration		 ↑ ↑ ↓ ↓ ↓ [9]
Psychostimulant
conditioned place preference		 ↑ ↑ ↓ ↑ ↓ ↑ [9]
Reinstatement of drug-seeking behavior ↑ ↑ ↓ ↓ [9]
Neurochemical plasticity
CREB phosphorylation
in the nucleus accumbens		 ↓ ↓ ↓ ↓ ↓ [9]
Sensitized dopamine response
in the nucleus accumbens		 No Yes No Yes [9]
Altered striatal dopamine signaling ↓DRD2, ↑DRD3 ↑DRD1, ↓DRD2, ↑DRD3 ↑DRD1, ↓DRD2, ↑DRD3 ↑DRD2 ↑DRD2 [9]
Altered striatal opioid signaling No change or
↑μ-opioid receptors 		↑μ-opioid receptors
↑κ-opioid receptors 		↑μ-opioid receptors ↑μ-opioid receptors No change No change [9]
Changes in striatal opioid peptides ↑dynorphin
No change: enkephalin 		↑dynorphin ↓enkephalin ↑dynorphin ↑dynorphin [9]
Mesocorticolimbic synaptic plasticity
Number of dendrites in the nucleus accumbens ↓ ↑ ↑ [9]
Dendritic spine density in
the nucleus accumbens		 ↓ ↑ ↑ [9]

Psychiatric and medical classifications

Diagnostic models do not currently include the criteria necessary to identify behaviors as addictions in a clinical setting. Behavioral addictions has 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.[20][21]

Behavioral addictions, which are sometimes referred to as impulse control disorders, are increasingly recognized as treatable forms of addiction.[22] The type of excessive behaviors identified as being addictive include gambling, food, sexual intercourse, use of pornography, use of computers, playing video games, use of the internet, exercise, and shopping.

Researching addiction to food, for example, a 2009 Scripps Research Institute study found evidence that the same molecular mechanisms correlated with human drug addiction also exist in compulsive overeating in obese rats. The dopamine D2 receptor studied is associated with vulnerability to drug addiction in humans. It was found downregulated in obese rats exposed to a high fat diet, and further reductions of the receptor increased compulsive eating. The D2 receptor responds to dopamine, a central neurotransmitter released in anticipation of rewarding, satiating experiences such as those involving food, sex or psychoactive drugs.[23]

On August 15, 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."[24]

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.[25]

Since ASAM released its statement, and shortly before its release, additional new studies have come out on Internet addiction. They reveal the same fundamental brain changes seen in other addicts of drugs.[26][27][28][29][30][31] Another 2011 study found that the risk of Internet addiction in men was about three times more than women. Researchers noted,

Internet addiction is a psychosocial disorder and its characteristics are as follows: tolerance, withdrawal symptoms, affective disorders, and problems in social relations. Internet usage creates psychological, social, school and/or work difficulties in a person's life. Eighteen percent of study participants were considered to be pathological Internet users, whose excessive use of the Internet was causing academic, social, and interpersonal problems. Excessive Internet use may create a heightened level of psychological arousal, resulting in little sleep, failure to eat for long periods, and limited physical activity, possibly leading to the user experiencing physical and mental health problems such as depression, OCD, low family relationships and anxiety.[32]

Treatment

{{#ifeq:Treatment|Treatment| tags in this section will be transcluded to that section in the addiction article.--> 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. 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.[33] }} Any unrelated psychiatric disorders should be kept under control, and differentiated from the contributing factors that cause the addiction.

Research

Another growing area is social media addiction. Psychology researchers surveyed 253 undergraduate students at the University of Albany and found that not only is social media (particularly Facebook) itself potentially addictive, those who use it may also be at greater risk for substance abuse.[34]

See also

Notes

  1. ↑ Synonyms of behavioral addiction include: process addiction and non-substance-related addiction.[5][6][7]

References

  1. ↑ Malenka RC, Nestler EJ, Hyman SE (2009). "Chapter 15: Reinforcement and Addictive Disorders". In Sydor A, Brown RY. Molecular Neuropharmacology: A Foundation for Clinical Neuroscience (2nd ed.). New York: McGraw-Hill Medical. pp. 364–375. ISBN 9780071481274.
  2. ↑ Nestler EJ (December 2013). "Cellular basis of memory for addiction". Dialogues Clin. Neurosci. 15 (4): 431–443. PMC 3898681 Freely accessible. PMID 24459410. Despite the importance of numerous psychosocial factors, at its core, drug addiction involves a biological process: the ability of repeated exposure to a drug of abuse to induce changes in a vulnerable brain that drive the compulsive seeking and taking of drugs, and loss of control over drug use, that define a state of addiction. ... A large body of literature has demonstrated that such ΔFosB induction in D1-type [nucleus accumbens] neurons increases an animal's sensitivity to drug as well as natural rewards and promotes drug self-administration, presumably through a process of positive reinforcement ... Another ΔFosB target is cFos: as ΔFosB accumulates with repeated drug exposure it represses c-Fos and contributes to the molecular switch whereby ΔFosB is selectively induced in the chronic drug-treated state.41. ... Moreover, there is increasing evidence that, despite a range of genetic risks for addiction across the population, exposure to sufficiently high doses of a drug for long periods of time can transform someone who has relatively lower genetic loading into an addict.
  3. ↑ "Glossary of Terms". Mount Sinai School of Medicine. Department of Neuroscience. Retrieved 9 February 2015.
  4. ↑ Volkow ND, Koob GF, McLellan AT (January 2016). "Neurobiologic Advances from the Brain Disease Model of Addiction". N. Engl. J. Med. 374 (4): 363–371. PMID 26816013. doi:10.1056/NEJMra1511480. Substance-use disorder: A diagnostic term in the fifth edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-5) referring to recurrent use of alcohol or other drugs that causes clinically and functionally significant impairment, such as health problems, disability, and failure to meet major responsibilities at work, school, or home. Depending on the level of severity, this disorder is classified as mild, moderate, or severe.
    Addiction: A term used to indicate the most severe, chronic stage of substance-use disorder, in which there is a substantial loss of self-control, as indicated by compulsive drug taking despite the desire to stop taking the drug. In the DSM-5, the term addiction is synonymous with the classification of severe substance-use disorder.
  5. ↑ Albrecht U, Kirschner NE, Grüsser SM (2007). "Diagnostic instruments for behavioural addiction: an overview". Psychosoc Med. 4: Doc11. PMC 2736529 Freely accessible. PMID 19742294.
  6. ↑ Potenza MN (September 2006). "Should addictive disorders include non-substance-related conditions?". Addiction. 101 Suppl 1: 142–51. PMID 16930171. doi:10.1111/j.1360-0443.2006.01591.x.
  7. ↑ Shaffer, Howard J. (1996). "Understanding the means and objects of addiction: Technology, the internet, and gambling". Journal of Gambling Studies. 12 (4): 461–9. PMID 24234163. doi:10.1007/BF01539189.
  8. 1 2 3 4 5 Robison AJ, Nestler EJ (November 2011). "Transcriptional and epigenetic mechanisms of addiction". Nat. Rev. Neurosci. 12 (11): 623–637. PMC 3272277 Freely accessible. PMID 21989194. doi:10.1038/nrn3111. ΔFosB has been linked directly to several addiction-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.
  9. 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 Olsen CM (December 2011). "Natural rewards, neuroplasticity, and non-drug addictions". Neuropharmacology. 61 (7): 1109–22. PMC 3139704 Freely accessible. PMID 21459101. doi:10.1016/j.neuropharm.2011.03.010.
  10. ↑ 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.
  11. ↑ Parashar A, Varma A (April 2007). "Behavior and substance addictions: is the world ready for a new category in the DSM-V?". CNS Spectr. 12 (4): 257; author reply 258–9. PMID 17503551.
  12. 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". J. Psychoactive Drugs. 44 (1): 38–55. PMC 4040958 Freely accessible. PMID 22641964. doi:10.1080/02791072.2012.662112. 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.
  13. ↑ 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. PMID 16776597. doi:10.1146/annurev.neuro.29.051605.113009.
  14. ↑ 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. PMC 3525776 Freely accessible. PMID 23085425. doi:10.1016/j.pneurobio.2012.10.001.
  15. ↑ Kanehisa Laboratories (2 August 2013). "Alcoholism – Homo sapiens (human)". KEGG Pathway. Retrieved 10 April 2014.
  16. ↑ 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. PMC 3865508 Freely accessible. PMID 23426671. doi:10.1523/JNEUROSCI.4881-12.2013. 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.
  17. ↑ 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. PMC 2222549 Freely accessible. PMID 17719013. doi:10.1016/j.bcp.2007.06.043.
  18. ↑ Girault, Jean-Antoine; Greengard, P (2004). "The Neurobiology of Dopamine Signaling". Archives of Neurology. 61 (5): 641–4. PMID 15148138. doi:10.1001/archneur.61.5.641.
  19. 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. PMID 17174602. doi:10.1016/j.coph.2006.11.003.
  20. ↑ Kuss, Daria (2013). "Internet gaming addiction: current perspectives". Psychological Research and Behavior Management. 6 (6): 125–137. PMC 3832462 Freely accessible. PMID 24255603. doi:10.2147/PRBM.S39476.
  21. ↑ Shenfield, Tali. "Is your child a gaming addict?". Advanced Psychology.
  22. ↑ Grant, Jon: Impulse Control Disorders: A Clinician's Guide to Understanding and Treating Behavioral Addictions
  23. ↑ Johnson, Paul M; Kenny, Paul J (2010). "Dopamine D2 receptors in addiction-like reward dysfunction and compulsive eating in obese rats". Nature Neuroscience. 13 (5): 635–41. PMC 2947358 Freely accessible. PMID 20348917. doi:10.1038/nn.2519. Lay summary – ScienceDaily (March 29, 2010).
  24. ↑ American Society of Addiction Medicine. (2011). Public Policy Statement: Definition of Addiction. http://www.asam.org/DefinitionofAddiction-LongVersion.html
  25. ↑ American Society of Addiction Medicine. (2011). DEFINITION OF ADDICTION: FREQUENTLY ASKED QUESTIONS. http://www.asam.org/pdf/Advocacy/20110816_DefofAddiction-FAQs.pdf
  26. ↑ Lin, Fuchun; Zhou, Yan; Du, Yasong; Qin, Lindi; Zhao, Zhimin; Xu, Jianrong; Lei, Hao (2012). Frasch, Martin Gerbert, ed. "Abnormal White Matter Integrity in Adolescents with Internet Addiction Disorder: A Tract-Based Spatial Statistics Study". PLoS ONE. 7 (1): e30253. Bibcode:2012PLoSO...730253L. PMC 3256221 Freely accessible. PMID 22253926. doi:10.1371/journal.pone.0030253.
  27. ↑ Dong, Guangheng; Huang, Jie; Du, Xiaoxia (2011). "Enhanced reward sensitivity and decreased loss sensitivity in Internet addicts: An fMRI study during a guessing task". Journal of Psychiatric Research. 45 (11): 1525–9. PMID 21764067. doi:10.1016/j.jpsychires.2011.06.017.
  28. ↑ Dong, Guangheng; Zhou, Hui; Zhao, Xuan (2011). "Male Internet addicts show impaired executive control ability: Evidence from a color-word Stroop task". Neuroscience Letters. 499 (2): 114–8. PMID 21645588. doi:10.1016/j.neulet.2011.05.047.
  29. ↑ Yuan, Kai; Qin, Wei; Wang, Guihong; Zeng, Fang; Zhao, Liyan; Yang, Xuejuan; Liu, Peng; Liu, Jixin; et al. (2011). Yang, Shaolin, ed. "Microstructure Abnormalities in Adolescents with Internet Addiction Disorder". PLoS ONE. 6 (6): e20708. Bibcode:2011PLoSO...620708Y. PMC 3108989 Freely accessible. PMID 21677775. doi:10.1371/journal.pone.0020708.
  30. ↑ Kim, Sang Hee; Baik, Sang-Hyun; Park, Chang Soo; Kim, Su Jin; Choi, Sung Won; Kim, Sang Eun (2011). "Reduced striatal dopamine D2 receptors in people with Internet addiction". NeuroReport. 22 (8): 407–11. PMID 21499141. doi:10.1097/WNR.0b013e328346e16e.
  31. ↑ Du, W; Liu, J; Gao, X; Li, L; Li, W; Li, X; Zhang, Y; Zhou, S (2011). "Functional magnetic resonance imaging of brain of college students with internet addiction" 网络成瘾大学生脑功能性磁共振成像特点 [Functional magnetic resonance imaging of brain of college students with internet addiction] (PDF). 中南大学学报 （医学版） [Journal of Central South University (Medical sciences)] (in Chinese). 36 (8): 744–9. PMID 21937800. doi:10.3969/j.issn.1672-7347.2011.08.008 (inactive 2017-01-15).
  32. ↑ Alavi, SS; Maracy, MR; Jannatifard, F; Eslami, M (2011). "The effect of psychiatric symptoms on the internet addiction disorder in Isfahan's University students". Journal of Research in Medical Sciences. 16 (6): 793–800. PMC 3214398 Freely accessible. PMID 22091309.
  33. ↑ Grant JE, Potenza MN, Weinstein A, Gorelick DA (September 2010). "Introduction to behavioral addictions". Am. J. Drug Alcohol Abuse. 36 (5): 233–241. PMC 3164585 Freely accessible. PMID 20560821. doi:10.3109/00952990.2010.491884. 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).
  34. ↑ "Craving Facebook? UAlbany Study Finds Social Media to be Potentially Addictive, Associated with Substance Abuse".
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