|• addiction – a state characterized by compulsive engagement in rewarding stimuli, despite adverse consequences|
|• reinforcing stimuli – stimuli that increase the probability of repeating behaviors paired with them|
|• rewarding stimuli – stimuli that the brain interprets as intrinsically positive or as something to be approached|
|• addictive drug – a drug that is both rewarding and reinforcing|
|• addictive behavior – a behavior that is both rewarding and reinforcing|
|• sensitization – an amplified response to a stimulus resulting from repeated exposure to it|
|• drug tolerance – the diminishing effect of a drug resulting from repeated administration at a given dose|
|• drug sensitization or reverse tolerance – the escalating effect of a drug resulting from repeated administration at a given dose|
|• drug dependence – an adaptive state associated with a withdrawal syndrome upon cessation of repeated drug intake|
|• physical dependence – dependence that involves persistent physical–somatic withdrawal symptoms (e.g., fatigue)|
|• psychological dependence – dependence that involves emotional–motivational withdrawal symptoms (e.g., dysphoria and anhedonia)|
|(edit | history)|
Behavioral addiction[note 1] is a form of addiction that involves a compulsion to repeatedly perform a rewarding non-drug-related behavior – sometimes called a natural reward – despite any negative consequences to the person's physical, mental, social, and/or financial well-being. Behavior persisting in spite of these consequences can be taken as a sign of addiction. The term "behavioral addiction" is not included in the new DSM-5 because, according to the authors, "there is insufficient peer-reviewed evidence to establish the diagnostic criteria and course descriptions needed to identify these behaviors as mental disorders." Nonetheless, research on the neuroscience of addiction has demonstrated ΔFosB is the critical progenitor of behavioral and drug addictions, and that behavioral addictions arise from the same neural adaptations that induce drug addictions.
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. Overexpression of ΔFosB in the nucleus accumbens is necessary and sufficient for many of the neural adaptations seen in drug addiction; it has been implicated in addictions to alcohol, cannabinoids, cocaine, nicotine, phenylcyclidine, and substituted amphetamines as well as addictions to natural rewards such as sex, exercise, and food. A recent study also demonstrated a cross-sensitization between drug reward (amphetamine) and a natural reward (sex) that was mediated by ΔFosB.
Besides increased ΔFosB expression in the nucleus accumbens, there are many other similarities in the neurobiology of behavior and 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 behavior addiction. One of the major areas of study includes the region, called the amygdala, 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. The cycle that is created is considered the dopamine reward system.
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. 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. 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 predict 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.
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.
Behavioral addiction, which is sometimes referred to as impulse control disorders, are increasingly recognized as treatable forms of addictions. The type of behaviors which some people have identified as being addictive include gambling, food, sex, viewing of pornography, use of computers, playing video games, use of the internet, work, exercise, spiritual obsession (as opposed to religious devotion), cutting, travel, and shopping.
When analyzing the addiction to food for example, a published study in 2009 from The Scripps Research Institute have shown for the first time that the same molecular mechanisms that drive people into drug addiction are behind the compulsion to overeat, pushing people into obesity. In this study, scientists focused on a particular receptor in the brain known to play an important role in vulnerability to drug addiction—the dopamine D2 receptor. The D2 receptor responds to dopamine, a neurotransmitter that is released in the brain by pleasurable experiences like food or sex or drugs like cocaine.
The term "soft addiction" was coined by Judith Sewell Wright to describe activities, moods or ways of being, avoidances, and things—edible and consumable but which do not pose a grave health disease risk—rather, they have the most effect on personal time and productivity. These behaviors were profiled in a 2007 ABC News story titled Bad Habits.
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."
The following excerpts are taken from the 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.
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. 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.
DSM or "Impulse control disorder"
There is disagreement as to the exact nature of behavioral addiction or dependency. However, the biopsychosocial model is generally accepted in scientific fields as the most comprehensive model for addiction. Historically, addiction has been defined with regard solely to psychoactive substances (for example alcohol, tobacco and other drugs) which cross the blood–brain barrier once ingested, temporarily altering the chemical milieu of the brain. However, "studies on phenomenology, family history, and response to treatment suggest that intermittent explosive disorder, kleptomania, problem gambling, pyromania, and trichotillomania may be related to mood disorders, alcohol and psychoactive substance abuse, and anxiety disorders (especially obsessive–compulsive disorder)."
In the case of pathological gambling, for example, the American Psychiatric Association has previously classified the condition as an impulse control disorder and not an addiction. However, the 5th edition includes it in the addictions section and not the impulse control group.
It is estimated that at least 90% of Americans have at least one form of soft addiction in their lives. Nadine Kaslow, professor of psychology and behavioral sciences at Emory University in Atlanta, has commented on the issue, saying that while it is healthy to relieve stress with behaviors like drinking coffee and watching television, when they become habitual they become problematic to one's health and happiness.
Psychologist Kimberly Young, director of the Center for Online Addiction, has addressed Internet addiction as one of the most common types of soft addictions. Young has likened excessive Internet use to pathological gambling. Texting or similar repetitive behaviors may also be considered as soft addictions.
Research around addictions and social media sites has been growing. The Retrevo company recently came out with research suggesting that there is an obsessiveness to the way people are checking their pages.
- Addictive behavior
- Addictive personality
- Hypermobility (travel)
- Digital addict
- 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.
- Nestler EJ (December 2013). "Cellular basis of memory for addiction". Dialogues Clin Neurosci 15 (4): 431–443. PMC 3898681. 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 NAc 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
- Albrecht U, Kirschner NE, Grüsser SM; Kirschner; Grüsser (2007). "Diagnostic instruments for behavioural addiction: an overview". Psychosoc Med 4: Doc11. PMC 2736529. PMID 19742294.
- 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.
- 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.
- 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.
- Parashar A, Varma A; Varma (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.
- Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition. American Psychiatric Association. 2013.
- Robison AJ, Nestler EJ; Nestler (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 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.
- Blum K, Werner T, Carnes S, Carnes P, Bowirrat A, Giordano J, Oscar-Berman M, Gold M; Werner; Carnes; Carnes; Bowirrat; Giordano; Oscar-Berman; Gold (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. 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.
- 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.
- Hyman SE, Malenka RC, Nestler EJ; Malenka; Nestler (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.
- Steiner H, Van Waes V; Van Waes (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.
- Kanehisa Laboratories (2 August 2013). "Alcoholism – Homo sapiens (human)". KEGG Pathway. Retrieved 10 April 2014.
- Pitchers KK, Vialou V, Nestler EJ, Laviolette SR, Lehman MN, Coolen LM; Vialou; Nestler; Laviolette; Lehman; Coolen (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.
- 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.
- 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.
- 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.
- Grant, Jon: Impulse Control Disorders: A Clinician's Guide to Understanding and Treating Behavioral Addictions
- 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. doi:10.1038/nn.2519. PMC 2947358. PMID 20348917. Lay summary – ScienceDaily (March 29, 2010).
- Judith Wright (2006). The Soft Addiction Solution: Break Free of the Seemingly Harmless Habits that Keep You from the Life You Want (revised, reprint ed.). J.P. Tarcher/Penguin. ISBN 978-1-58542-532-7.
- "Judith Wright Appears on 20/20 Friday July 7" (Press release). Wright Institute. July 7, 2006. Archived from the original on March 1, 2009. Retrieved June 5, 2013.
- Levy, Joy (August 28, 2007). "Bad Habits". ABC News. Retrieved June 5, 2013.
- American Society of Addiction Medicine. (2011). Public Policy Statement: Definition of Addiction. http://www.asam.org/DefinitionofAddiction-LongVersion.html
- American Society of Addiction Medicine. (2011). DEFINITION OF ADDICTION: FREQUENTLY ASKED QUESTIONS. http://www.asam.org/pdf/Advocacy/20110816_DefofAddiction-FAQs.pdf
- 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. doi:10.1371/journal.pone.0030253. PMC 3256221. PMID 22253926.
- 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. doi:10.1016/j.jpsychires.2011.06.017. PMID 21764067.
- 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. doi:10.1016/j.neulet.2011.05.047. PMID 21645588.
- 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. doi:10.1371/journal.pone.0020708. PMC 3108989. PMID 21677775.
- 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. doi:10.1097/WNR.0b013e328346e16e. PMID 21499141.
- 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]. 中南大学学报 （医学版） [Journal of Central South University (Medical sciences)] (in Chinese) 36 (8): 744–9. doi:10.3969/j.issn.1672-7347.2011.08.008 (inactive 2015-01-10). PMID 21937800.
- 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. PMID 22091309.
- Goodman A (November 1990). "Addiction: definition and implications". Br J Addict 85 (11): 1403–8. doi:10.1111/j.1360-0443.1990.tb01620.x. PMID 2285834.
- McElroy, Susan L.; Hudson, James I.; Pope, Harrison G.; Keck, Paul E.; Aizley, Harlyn G. (1992). "The DSM-III-R impulse control disorders not elsewhere classified: clinical characteristics and relationship to other psychiatric disorders". American Journal of Psychiatry 149 (3): 318–27. PMID 1536268.
- Petry, Nancy M. (2006). "Should the scope of addictive behaviors be broadened to include pathological gambling?". Addiction 101: 152–60. doi:10.1111/j.1360-0443.2006.01593.x. PMID 16930172.
- Davis, Jeanie Lerche (January 31, 2005). "Let It Go: Taming Soft Addictions". WebMD. Retrieved June 5, 2013.
- Deardorff, Julie (March 17, 2007). "What's your soft addiction?". Chicago Tribune. Retrieved June 5, 2013.
- "Is Social Media a New Addiction?". Retrieved 2011-11-18.[dead link][unreliable source?]