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{{Short description|Disorder resulting in compulsive behaviours}}
{{Redirect|Addictive|other uses|Addiction (disambiguation)|and|Addictive (disambiguation)}}
{{Distinguish|Psychological dependence}}
{{cs1 config|name-list-style=vanc|display-authors=6}}
{{Use American English|date=March 2023}}
{{Use dmy dates|date=February 2023}}
{{Infobox medical condition
| name = Addiction
| synonyms = Addictive behaviour (e.g., substance use disorder, sexual addiction), dependence, addictive disorder, addiction disorder
| image = Brain metabolism and drug addiction.jpg
| caption = [[Brain positron emission tomography]] images that compare [[Human brain#Metabolism|brain metabolism]] in a healthy individual and an individual with a cocaine addiction
| alt = PET images showing brain metabolism in drug addicts vs controls
| field = [[Psychiatry]], [[clinical psychology]], [[toxicology]], [[addiction medicine]]
| width = 
| pronounce = 
| specialty = 
| symptoms = Compulsive urge to engage in rewarding activity despite negative consequences
| complications = 
|  duration = 
| types = 
| causes = 
| risks = 
| diagnosis = 
| differential = 
| prevention = 
| treatment = 
| medication = 
| prognosis = 
| frequency = 
| deaths = 
}}
'''Addiction''' is a [[neuropsychological]] [[Mental disorder|disorder]] characterized by a persistent and intense urge to use a [[drug]] or engage in a behavior that produces natural reward, despite substantial harm and other negative consequences. Repetitive drug use often alters [[Brain#Function|brain function]] in ways that perpetuate [[Craving (withdrawal)|craving]], and weakens (but does not completely negate) [[self-control]].<ref name="Heilig-et-al-2021">{{cite journal | vauthors = Heilig M, MacKillop J, Martinez D, Rehm J, Leggio L, Vanderschuren LJ | title = Addiction as a brain disease revised: why it still matters, and the need for consilience | journal = Neuropsychopharmacology | volume = 46 | issue = 10 | pages = 1715–1723 | date = September 2021 | pmid = 33619327 | pmc = 8357831 | doi = 10.1038/s41386-020-00950-y | quote = pre-existing vulnerabilities and persistent drug use lead to a vicious circle of substantive disruptions in the brain that impair and undermine choice capacities for adaptive behavior, but do not annihilate them. |issn=0893-133X }}</ref> This phenomenon – drugs [[Neuroplasticity|reshaping]] [[Human brain|brain]] function – has led to an understanding of addiction as a [[brain disorder]] with a complex variety of [[Social psychology|psychosocial]] as well as [[Neuroscience|neurobiological]] (and thus involuntary){{efn|In other words, a person cannot control the neurobiological processes that occur in the body in response to using an addictive drug. A person can make a voluntary choice to, for example, start using a drug (or not), or to seek help after becoming addicted, although resisting the urge to use drug(s) becomes increasingly difficult as addiction worsens. See <ref name="Heilig-et-al-2021" /> for detailed discussion.}} factors that are implicated in the development of addiction.<ref name="Cellular basis" /><ref name="NIDA2020">{{cite web |author=<!--Staff writer(s); no by-line.--> |date=13 July 2020 |title=Drugs, Brains, and Behavior: The Science of Addiction – Drug Misuse and Addiction |url=https://www.drugabuse.gov/publications/drugs-brains-behavior-science-addiction/drug-misuse-addiction |website=www.drugabuse.gov |location=[[North Bethesda, Maryland]] |publisher=[[National Institute on Drug Abuse]] |access-date=23 December 2021}}</ref><ref>{{cite book | vauthors = Henden E | chapter = Addiction, Compulsion, and Weakness of the Will: A Dual-Process Perspective. | title = Addiction and Choice: Rethinking the Relationship | veditors = Heather N, Gabriel S | pages = 116–132 | location = Oxford, UK | publisher = Oxford University Press | date = 2017 }}</ref> 

Classic signs of addiction include [[Compulsive behavior|compulsive]] engagement in [[Reward system|rewarding]] stimuli, ''preoccupation'' with substances or behavior, and continued use despite negative consequences. [[Habit]]s and patterns associated with addiction are typically characterized by immediate [[gratification]] (short-term reward),<ref name="pmid18790142">{{cite journal | vauthors = Angres DH, Bettinardi-Angres K | title = The disease of addiction: origins, treatment, and recovery | journal = Disease-a-Month | volume = 54 | issue = 10 | pages = 696–721 | date = October 2008 | pmid = 18790142 | doi = 10.1016/j.disamonth.2008.07.002 }}</ref><ref name="NHM addiction-reward-reinforcement" /> coupled with delayed deleterious effects (long-term costs).<ref name="NIDA2020" /><ref name="pmid3278676">{{cite journal |vauthors=Marlatt GA, Baer JS, Donovan DM, Kivlahan DR | title = Addictive behaviors: etiology and treatment | journal = Annu Rev Psychol | volume = 39 | pages = 223–52 | year = 1988 | pmid = 3278676 | doi = 10.1146/annurev.ps.39.020188.001255 }}</ref>

<!-- addiction examples and classifications -->
Examples of substance addiction include [[alcoholism]], [[cannabis use disorder|cannabis addiction]], [[amphetamine addiction]], [[cocaine addiction]], [[nicotine#Reinforcement disorders|nicotine addiction]], [[opioid use disorder|opioid addiction]], and eating or [[food addiction]]. Behavioral addictions may include [[gambling addiction]], [[shopping addiction]], [[stalking]], [[Internet addiction disorder|internet addiction]], [[social media addiction]], [[video game addiction]], and [[sexual addiction]]. The [[DSM-5]] and [[ICD-10]] only recognize gambling addictions as behavioral addictions, but the [[ICD-11]] also recognizes gaming addictions.<ref>{{Cite journal|url=https://www.psychiatrictimes.com/article/gaming-addiction-icd-11-issues-and-implications|title=Gaming Addiction in ICD-11: Issues and Implications|vauthors=ME|date=12 September 2019|journal=Psychiatric Times|series=Psychiatric Times Vol 36, Issue 9|volume=36|issue=9|language=en|access-date=3 March 2020|archive-date=3 March 2020|archive-url=https://web.archive.org/web/20200303134538/https://www.psychiatrictimes.com/article/gaming-addiction-icd-11-issues-and-implications|url-status=dead}}</ref>
{{TOC limit|3}}

== Definitions ==
"'''Addiction'''" and "'''addictive behaviour'''"<!-- 'addictive behaviors' is even more polysemic; the literature uses this term both as a synonym of 'addictions', and as 'behaviors potentially triggering addictions' --> are [[polyseme]]s denoting a category of [[mental disorder]]s, of neuropsychological [[signs and symptoms|symptoms]], or of merely [[maladaptation|maladaptive]]/harmful [[habit]]s and [[lifestyle (social sciences)|lifestyle]]s.<ref name="Steverson (2020)">{{cite book |vauthors=Steverson |date=2020 |title=Addiction reimagined: challenging views of an enduring social problem |pages=206 |publisher=Vernon Press |isbn=978-1-62273-953-0}}</ref> A common use of "addiction" in medicine is for neuropsychological symptoms denoting pervasive/excessive and intense urges to engage in a category of behavioral [[Compulsive behavior|compulsions]] or [[Impulsivity#Impulse|impulses]] towards sensory [[Reward system|rewards]] (e.g., [[alcohol (drug)|alcohol]], [[betel quid]], drugs, sex, gambling, video gaming).<ref name="Gowing et al. (2015)">{{cite journal |vauthors= Gowing L, Ali R, Allsop S, Marsden J, Turf E, West E, Witton J |date=2015 |title=Global statistics on addictive behaviours: 2014 status report |journal=Addiction |volume=110 |issue=6 |pages=904–919 |doi=10.1111/add.12899|pmid=25963869 |url=https://discovery.ucl.ac.uk/id/eprint/1468912/5/West_global%2520addiction%2520report%2520final%2520mark%25202%2520clean_template.pdf }}</ref><ref name="Gilley (2018)">{{cite journal |vauthors=Gilley |date=2018 |title=The new science of attention deficit hyperactivity disorder: news from the cutting edge of research science |journal=Journal of Psychiatry and Psychiatric Disorders |volume=2 |issue=3 |doi=10.26502/jppd.2572-519X0043 |doi-broken-date=1 November 2024 |s2cid=150196703 |url=https://www.fortunejournals.com/articles/pthe-new-science-of-attention-deficit-hyperactivity-disorder-news-from-the-cutting-edge-of-research-sciencep.html|doi-access=free }}</ref><ref name="Lee et al. (2018)">{{cite journal |vauthors=Lee C, Ko A, Yang F |date=2018 |title=Association of DSM-5 betel-quid use disorder with oral potentially malignant disorder in 6 betel-quid endemic Asian populations |journal=JAMA Psychiatry |volume=75 |issue=3 |pages=261–269 |doi=10.1001/jamapsychiatry.2017.4307|pmid=29417149 |pmc=5885949 }}</ref><ref name="Sahithya et al. (2022)">{{cite journal |vauthors=Sahithya B, Kashyap R |date=2020 |title=Sexual Addiction Disorder&mdash;a review with recent updates |volume=4 |issue=2 |journal=Journal of Psychosexual Health |pages=95–101 |doi=10.1177/26318318221081080|s2cid=248835855 |doi-access=free }}</ref><ref name="ICD-11 (disorders due to substance use or addictive behaviours)">{{Cite web |title=International Classification of Diseases 11th revision &ndash; ICD-11. Disorders due to substance use or addictive behaviours |url=https://icd.who.int/browse11/l-m/en#/http://id.who.int/icd/entity/1602669465 |access-date=10 April 2023 |website=World Health Organization |location=Geneva |date=2023}}</ref> '''Addictive disorders''' or '''addiction disorders''' are mental disorders involving high intensities of addictions (as neuropsychological symptoms) that induce [[Disability|functional disabilities]] (i.e., limit subjects' social/family and occupational activities); the two categories of such disorders are ''substance-use addictions'' and ''behavioral addictions''.<ref name="Destoop et al. (2019)">{{cite journal |vauthors=Destoop M, Morrens M, Coppens V, Dom G |date=2019 |title=Addiction, anhedonia, and comorbid mood disorder. A narrative review |journal=Frontiers in Psychiatry |volume=10 |page=311 |doi=10.3389/fpsyt.2019.00311 |pmid=31178763 |pmc=6538808 |doi-access=free }}</ref><ref name="Steverson (2020)"/><ref name="Sahithya et al. (2022)"/><ref name="ICD-11 (disorders due to substance use or addictive behaviours)"/>

The [[DSM-5]] classifies addiction the most severe stage of substance use disorder, due to significant loss of control and the presence of compulsive behaviours despite the desire to stop.<ref name="Volkow et al. (2016)">{{cite journal |vauthors=Volkow N, Koob G, McLellan T |date=2016 |title=Neurobiologic advances from the brain disease model of addiction |journal=The New England Journal of Medicine |volume=374 |issue=4 |pages=363–371 |doi=10.1056/NEJMra1511480|pmid=26816013 |pmc=6135257 }}</ref> It is a definition that many scientific papers and reports use.<ref name="Koob et al. (2014)">{{cite journal |vauthors= Koob G, Buck G, Cohen A, Edwards S, Park P, Schlosburg J, Schmeichel B, Vendruscolo L, Wade C, Whitfield T, George O |date=2014 |title=Addiction as a stress surfeit disorder |journal=Neuropharmacology |volume=76 |pages=370–382 |doi=10.1016/j.neuropharm.2013.05.024|pmid=23747571 |pmc=3830720 }}</ref><ref name="Surgeon General severe SUD"/><ref name="Ko et al. (2020)">{{cite journal |vauthors=Ko C, Yen J, Yen C, Chen C, ChenC |date=2020 |title=The association between Internet addiction and psychiatric disorder: A review of the literature |journal=European Psychiatry |volume=27 |issue= 1|pages=1–8 |doi=10.1016/j.eurpsy.2010.04.011|pmid=22153731 |s2cid=3558840 }}</ref>

"'''Dependence'''" is also a polyseme denoting either neuropsychological symptoms or mental disorders. In the DSM-5, dependences differ from addictions and can even normally happen without addictions;<ref name="APA (2013)">{{cite web|author=American Psychiatric Association |title=Substance-Related and Addictive Disorders |date=2013 |url=http://www.dsm5.org/documents/substance%20use%20disorder%20fact%20sheet.pdf |publisher=American Psychiatric Publishing |access-date=8 April 2023 |pages=1–2 |quote=Additionally, the diagnosis of dependence caused much confusion. Most people link dependence with "addiction" when in fact dependence can be a normal body response to a substance. |url-status=dead |archive-url=https://web.archive.org/web/20150815050402/http://www.dsm5.org/Documents/Substance%20Use%20Disorder%20Fact%20Sheet.pdf |archive-date=15 August 2015 }}</ref> besides, substance-use dependences are severe stages of substance-use addictions (i.e. mental disorders) involving [[Drug withdrawal|withdrawal issues]].<ref>{{cite book |vauthors=Malenka R, Nestler E, Hyman S, Holtzman D |title=Molecular Neuropharmacology: A Foundation for Clinical Neuroscience |year=2015 |publisher=McGraw-Hill Medical |location=New York |isbn=978-0-07-182770-6 |edition=3rd |chapter=Chapter 16: Reinforcement and Addictive Disorders}}</ref> In the ICD-11, "substance-use dependence" is a synonym of "substance-use addiction" (i.e. neuropsychological symptoms) that can but do not necessarily involve withdrawal issues.<ref name=ICD-11>[[World Health Organization]] (2023). [[International Classification of Diseases]], eleventh  revision – ICD-11. Geneva – [https://icd.who.int icd.who.int].</ref>

== Substance addiction ==
{{Main|Substance use disorder}}
{{Further|Substance abuse|Substance-related disorder}}
{{addiction glossary|reverse citation order=yes}}

=== Drug addiction ===
[[Substance use disorder|Drug addiction]], which belongs to the class of [[substance-related disorder]]s, is a chronic and relapsing brain disorder that features drug seeking and drug abuse, despite their harmful effects.<ref name="NIDA_2020">{{Cite web |last=NIDA |date=13 July 2020 |title=Drug Misuse and Addiction |url=https://nida.nih.gov/publications/drugs-brains-behavior-science-addiction/drug-misuse-addiction |access-date=15 November 2022 | work = National Institute of Drug Abuse | publisher = U.S. Department of Health and Human Services }}</ref> This form of addiction changes brain circuitry such that the brain's reward system is compromised,<ref name="Levy2019" /> causing functional consequences for stress management and self-control.<ref name="NIDA_2020" /> Damage to the functions of the organs involved can persist throughout a lifetime and cause death if untreated.<ref name="NIDA_2020" /> Substances involved with drug addiction include alcohol, nicotine, marijuana, opioids, cocaine, amphetamines, and even foods with high fat and sugar content.<ref>{{Cite web |date=17 February 2020 |title=Food addiction: Symptoms and management |url=https://www.medicalnewstoday.com/articles/319670 |access-date=15 November 2022 |website=www.medicalnewstoday.com |language=en}}</ref> Addictions can begin experimentally in social contexts<ref name="Skylstad2022" /> and can arise from the use of prescribed medications or a variety of other measures.<ref>{{Cite web |title=Drug addiction (substance use disorder) – Symptoms and causes |url=https://www.mayoclinic.org/diseases-conditions/drug-addiction/symptoms-causes/syc-20365112 |access-date=15 November 2022 |website=Mayo Clinic |language=en}}</ref>

Drug addiction has been shown to work in [[Phenomenology (psychology)|phenomenological]], conditioning ([[Operant conditioning|operant]] and [[Classical conditioning|classical]]), cognitive models, and the [[cue reactivity]] model. However, no one model completely illustrates substance abuse.<ref>{{Cite journal |last=Drummond |first=D. Colin |date=May 3, 2002 |title=Theories of drug craving, ancient and modern |url=http://doi.wiley.com/10.1046/j.1360-0443.2001.961333.x |journal=Addiction |language=en |volume=96 |issue=1 |pages=33–46 |doi=10.1046/j.1360-0443.2001.961333.x|pmid=11177518 }}</ref>

Risk factors for addiction include:
* Aggressive behavior (particularly in childhood)
* Availability of substance<ref name="Skylstad2022" />
* Community economic status
* Experimentation<ref name="Skylstad2022" />
* [[Epigenetics]]
* [[Impulsivity]] (attentional, motor, or non-planning)<ref name="Maxwell2020" />
* Lack of parental supervision<ref name="Skylstad2022" />
* Lack of peer refusal skills<ref name="Skylstad2022" />
* Mental disorders<ref name="Skylstad2022" />
* Method substance is taken<ref name="NIDA_2020" />
* Usage of substance in youth<ref name="Skylstad2022" />

=== Food addiction ===
{{Main|Food addiction}}

The diagnostic criteria for food or eating addiction has not been categorized or defined in references such as the [[Diagnostic and Statistical Manual of Mental Disorders]] (DSM or DSM-5) and is based on subjective experiences similar to substance use disorders.<ref name="diGiacomo2022">{{cite journal | vauthors = di Giacomo E, Aliberti F, Pescatore F, Santorelli M, Pessina R, Placenti V, Colmegna F, Clerici M | title = Disentangling binge eating disorder and food addiction: a systematic review and meta-analysis | journal = Eating and Weight Disorders | volume = 27 | issue = 6 | pages = 1963–1970 | date = August 2022 | pmid = 35041154 | pmc = 9287203 | doi = 10.1007/s40519-021-01354-7 }}</ref><ref name="Maxwell2020">{{cite journal | vauthors =  Maxwell AL, Gardiner E, Loxton NJ | date = 9 February 2020 | title = Investigating the relationship between reward sensitivity, impulsivity, and food addiction: A systematic review | url = https://doi.org/10.1002/erv.2732 | journal = European Eating Disorders Review | issn = 1099-0968 | volume = 28 | issue = 4 | pages = 368–384 | doi = 10.1002/erv.2732 | pmid =  32142199 | s2cid = 212565361 | access-date = 9 March 2023 }}</ref> Food addiction may be found in those with eating disorders, though not all people with eating disorders have food addiction and not all of those with food addiction have a diagnosed eating disorder.<ref name="diGiacomo2022" /> Long-term frequent and excessive consumption of foods high in fat, salt, or sugar, such as chocolate, can produce an addiction<ref name="Natural and drug addictions" /><ref name="Nestler" /> similar to drugs since they trigger the brain's reward system, such that the individual may desire the same foods to an increasing degree over time.<ref name="Goodman_2022">{{Cite web | vauthors = Goodman B  | veditors = Casarella J | date = 3 September 2022 | title = Food Addiction Signs and Treatments | url = https://www.webmd.com/mental-health/eating-disorders/binge-eating-disorder/mental-health-food-addiction | access-date = 9 March 2023 | website = WebMD | language = en}}</ref><ref name="diGiacomo2022" /><ref name="Maxwell2020" /> The signals sent when consuming highly palatable foods have the ability to counteract the body's signals for fullness and persistent cravings will result.<ref name="Goodman_2022" /> Those who show signs of food addiction may develop food tolerances, in which they eat more, despite the food becoming less satisfactory.<ref name="Goodman_2022" />

Chocolate's sweet flavor and pharmacological ingredients are known to create a strong craving or feel 'addictive' by the consumer.<ref>{{cite book |title=Coffee, tea, chocolate, and the brain. |vauthors=Nehlig A |publisher=CRC Press |year=2004 |isbn=978-0-429-21192-8 |location=Boca Raton |pages=203–218}}</ref> A person who has a strong liking for chocolate may refer to themselves as a [[chocoholic]].

Risk factors for developing food addiction include excessive [[overeating]] and impulsivity.<ref name="Maxwell2020" />

The [[Yale Food Addiction Scale]] (YFAS), version 2.0, is the current standard measure for assessing whether an individual exhibits signs and symptoms of food addiction.<ref>{{Cite web |title=Yale Food Addiction Scale |url=https://sites.lsa.umich.edu/fastlab/yale-food-addiction-scale/ |access-date=1 November 2022 |work=Food and Addiction Science & Treatment Lab |publisher=Department of Psychology, University of Michigan}}</ref><ref name="diGiacomo2022" /><ref name="Maxwell2020" /> It was developed in 2009 at [[Yale University]] on the hypothesis that foods high in fat, sugar, and salt have addictive-like effects which contribute to problematic eating habits.<ref>{{cite journal |vauthors=Gearhardt AN, Corbin WR, Brownell KD |date=February 2016 |title=Development of the Yale Food Addiction Scale Version 2.0 |journal=Psychology of Addictive Behaviors |volume=30 |issue=1 |pages=113–121 |doi=10.1037/adb0000136 |pmid=26866783}}</ref><ref name="Goodman_2022" /> The YFAS is designed to address 11 substance-related and addictive disorders (SRADs) using a 25-item self-report questionnaire, based on the diagnostic criteria for SRADs as per DSM-5.<ref>{{cite journal |vauthors=Brunault P, Berthoz S, Gearhardt AN, Gierski F, Kaladjian A, Bertin E, Tchernof A, Biertho L, de Luca A, Hankard R, Courtois R, Ballon N, Benzerouk F, Bégin C |date=8 September 2020 |title=The Modified Yale Food Addiction Scale 2.0: Validation Among Non-Clinical and Clinical French-Speaking Samples and Comparison With the Full Yale Food Addiction Scale 2.0 |journal=Frontiers in Psychiatry |volume=11 |pages=480671 |doi=10.3389/fpsyt.2020.480671 |pmc=7509420 |pmid=33033480 |doi-access=free}}</ref><ref name="diGiacomo2022" /> A potential food addiction diagnosis is predicted by the presence of at least two out of 11 SRADs and a significant impairment to daily activities.<ref>{{cite journal |vauthors=Hauck C, Cook B, Ellrott T |date=February 2020 |title=Food addiction, eating addiction and eating disorders |journal=The Proceedings of the Nutrition Society |volume=79 |issue=1 |pages=103–112 |doi=10.1017/S0029665119001162 |pmid=31744566 |s2cid=208186539|doi-access=free }}</ref>

The [[Barratt Impulsiveness Scale]], specifically the BIS-11 scale, and the [[Impulsivity#UPPS Impulsive Behavior Scale|UPPS-P Impulsive Behavior]] subscales of Negative Urgency and Lack of Perseverance have been shown to have relation to food addiction.<ref name="Maxwell2020" />

==Behavioral addiction==
{{Main|Behavioral addiction}}

The term ''behavioral addiction'' refers to a [[compulsive behavior|compulsion]] to engage in a [[natural reward]] – which is a behavior that is inherently rewarding (i.e., desirable or appealing) – despite adverse consequences.<ref name="NHM addiction-reward-reinforcement">{{cite book |vauthors=Malenka RC, Nestler EJ, Hyman SE |veditors=Sydor A, Brown RY | title = Molecular Neuropharmacology: A Foundation for Clinical Neuroscience | year = 2009 | publisher = McGraw-Hill Medical | location = New York | isbn = 978-0-07-148127-4 | pages = 364–65, 375 | edition = second | chapter = Chapter 15: Reinforcement and Addictive Disorders | quote= The defining feature of addiction is compulsive, out-of-control drug use, despite negative consequences.&nbsp;...<br />compulsive eating, shopping, gambling, and sex&nbsp;– so-called "natural addictions"&nbsp;– Indeed, addiction to both drugs and behavioral rewards may arise from similar dysregulation of the mesolimbic dopamine system.}}</ref><ref name="Natural and drug addictions" /><ref name="Nestler" /> Preclinical evidence has demonstrated that marked increases in the expression of [[ΔFosB]] through repetitive and excessive exposure to a natural reward induces the same behavioral effects and [[neuroplasticity]] as occurs in a drug addiction.<ref name="Natural and drug addictions" /><ref name="Systematic review - yet another DSM fail" /><ref name="Amph-Sex X-sensitization through D1 signaling" /><ref name="Amph-Sex X-sensitization through NMDA signaling" />

Addiction can exist in the absence of psychotropic drugs, which was popularized by Peele.<ref name="Alavi_2012">{{cite journal | vauthors = Alavi SS, Ferdosi M, Jannatifard F, Eslami M, Alaghemandan H, Setare M | title = Behavioral Addiction versus Substance Addiction: Correspondence of Psychiatric and Psychological Views | journal = International Journal of Preventive Medicine | volume = 3 | issue = 4 | pages = 290–294 | date = April 2012 | pmid = 22624087 | pmc = 3354400 }}</ref> These are termed behavioral addictions. Such addictions may be passive or active, but they commonly contain reinforcing features, which are found in most addictions.<ref name="Alavi_2012" /> Sexual behavior, eating, gambling, playing video games, and shopping are all associated with compulsive behaviors in humans and have been shown to activate the mesolimbic pathway and other parts of the reward system.<ref name="Natural and drug addictions" /> Based on this evidence, [[sexual addiction]], [[gambling addiction]], [[video game addiction]], and [[shopping addiction]] are classified accordingly.<ref name="Natural and drug addictions" />

=== Sexual ===
{{Main|Sexual addiction}}

Sexual addiction involves an engagement in excessive, compulsive, or otherwise problematic sexual behavior that persists despite negative physiological, psychological, social, and occupational consequences.<ref name="Derbyshire_2015">{{cite journal | vauthors = Derbyshire KL, Grant JE | title = Compulsive sexual behavior: a review of the literature | journal = Journal of Behavioral Addictions | volume = 4 | issue = 2 | pages = 37–43 | date = June 2015 | pmid = 26014671 | pmc = 4500883 | doi = 10.1556/2006.4.2015.003 }}</ref> Sexual addiction may be referred to as [[hypersexuality]] or [[compulsive sexual behavior disorder]].<ref name="Derbyshire_2015" /> The [[DSM-5]] does not recognize sexual addiction as a clinical diagnosis. Hypersexuality disorder and internet addiction disorder were among proposed addictions to the DSM-5, but were later rejected due to the insufficient evidence available in support of the existence of these disorders as discrete mental health conditions.<ref>{{Cite book |url=https://www.worldcat.org/oclc/830807378 |title=Diagnostic and statistical manual of mental disorders : DSM-5. |date=2013 |publisher=American Psychiatric Association |last1=American Psychiatric Association |last2=American Psychiatric Association |last3=DSM-5 Task Force |isbn=978-0-89042-554-1 |edition=5th |location=Arlington, VA |oclc=830807378 |page=481}}</ref> Reviews of both clinical research in humans and preclinical studies involving ΔFosB have identified compulsive sexual activity – specifically, any form of [[sexual intercourse]] – as an addiction (i.e., sexual addiction).<ref name="Natural and drug addictions" /><ref name="Systematic review - yet another DSM fail" /> [[#Reward sensitization|Reward cross-sensitization]] between [[amphetamine]] and sexual activity, meaning that exposure to one increases the desire for both, has been shown to occur as a [[dopamine dysregulation syndrome]].<ref name="Natural and drug addictions" /><ref name="Systematic review - yet another DSM fail" /><ref name="Amph-Sex X-sensitization through D1 signaling" /><ref name="Amph-Sex X-sensitization through NMDA signaling" /> ΔFosB [[gene expression|expression]] is required for this cross-sensitization effect, which intensifies with the level of ΔFosB expression.<ref name="Natural and drug addictions" /><ref name="Amph-Sex X-sensitization through D1 signaling" /><ref name="Amph-Sex X-sensitization through NMDA signaling" />

=== Gambling ===
{{Main article|Gambling|Problem gambling}}

Gambling provides a natural reward that is associated with compulsive behavior.<ref name="Natural and drug addictions" /> Functional [[neuroimaging]] evidence shows that gambling activates the [[reward system]] and the [[mesolimbic pathway]] in particular.<ref name="Natural and drug addictions" /> It is known that [[dopamine]] is involved in learning, motivation, as well as the reward system.<ref name="Yau_2015">{{cite journal | vauthors = Yau YH, Potenza MN | title = Gambling disorder and other behavioral addictions: recognition and treatment | journal = Harvard Review of Psychiatry | volume = 23 | issue = 2 | pages = 134–146 | date = 2015 | pmid = 25747926 | pmc = 4458066 | doi = 10.1097/HRP.0000000000000051 }}</ref><ref name="Levy2019" /> The exact role of dopamine in gambling addiction has been debated.<ref name="Yau_2015" /> Suggested roles for [[Dopamine receptor D2|D2]], [[Dopamine receptor D3|D3]], and [[Dopamine receptor D4|D4]] [[dopamine receptor]]s, as well as D3 receptors in the [[substantia nigra]] have been found in rat and human models, showing a correlation with the severity of the gambling behavior.<ref name="Yau_2015" /> This in turn was linked with greater dopamine release in the [[Striatum|dorsal striatum]].<ref name="Yau_2015" />

[[Problem gambling|Gambling addictions]] are linked with [[Comorbidity|comorbidities]] such as [[Psychiatric disorder|mental health disorders]], [[substance abuse]], [[Alcoholism|alcohol use disorder]], and [[personality disorders]].<ref name="Ford_2020">{{cite journal | vauthors = Ford M, Håkansson A | title = Problem gambling, associations with comorbid health conditions, substance use, and behavioural addictions: Opportunities for pathways to treatment | journal = PLOS ONE | volume = 15 | issue = 1 | pages = e0227644 | date = 10 January 2020 | pmid = 31923269 | pmc = 6953879 | doi = 10.1371/journal.pone.0227644 | bibcode = 2020PLoSO..1527644F | doi-access = free }}</ref>

Risk factors for gambling addictions include antisocial behavior, impulsive personality,<ref name="Maxwell2020" /> male sex, sensation seeking,<ref name="Menchon_2018">{{cite journal | vauthors = Menchon JM, Mestre-Bach G, Steward T, Fernández-Aranda F, Jiménez-Murcia S | title = An overview of gambling disorder: from treatment approaches to risk factors | journal = F1000Research | volume = 7 | pages = 434 | date = 9 April 2018 | pmid = 30090625 | pmc = 5893944 | doi = 10.12688/f1000research.12784.1 | doi-access = free }}</ref> substance use, and young age.

Gambling addiction has been associated with some personality traits, including: harm avoidance, low self direction, decision making and planning insufficiencies, impulsivity, as well as sensation seeking individuals.<ref name="Menchon_2018" /> Although some personality traits can be linked with gambling addiction, there is no general description of individuals addicted to gambling.<ref name="Menchon_2018" />

=== Internet ===
{{Main|Internet addiction disorder}}

[[Internet addiction disorder|Internet addiction]] does not have any standardized definition, yet there is widespread agreement that this problem exists.<ref name="Chou-2005">{{Cite journal | vauthors = Chou C, Condron L, Belland JC |date=2005 |title=A Review of the Research on Internet Addiction |journal=Educational Psychology Review |language=en |volume=17 |issue=4 |pages=363–388 |doi=10.1007/s10648-005-8138-1 |s2cid=7014879 |issn=1040-726X}}</ref> Debate over the classification of problematic internet use considers whether it should be thought of as a behavioral addiction, an impulse control disorder, or an obsessive-compulsive disorder.<ref>{{cite journal | vauthors = Musetti A, Cattivelli R, Giacobbi M, Zuglian P, Ceccarini M, Capelli F, Pietrabissa G, Castelnuovo G | title = Challenges in Internet Addiction Disorder: Is a Diagnosis Feasible or Not? | journal = Frontiers in Psychology | volume = 7 | pages = 842 | date = 2016 | pmid = 27375523 | pmc = 4894006 | doi = 10.3389/fpsyg.2016.00842 | doi-access = free }}</ref><ref>{{cite journal | vauthors = Bipeta R, Yerramilli SS, Karredla AR, Gopinath S | title = Diagnostic Stability of Internet Addiction in Obsessive-compulsive Disorder: Data from a Naturalistic One-year Treatment Study | journal = Innovations in Clinical Neuroscience | volume = 12 | issue = 3–4 | pages = 14–23 | date = 2015 | pmid = 26000201 | pmc = 4420165 }}</ref> Others argue that internet addiction should be considered a symptom of an underlying mental health condition and not a disorder in itself.<ref>{{cite journal | vauthors = Cash H, Rae CD, Steel AH, Winkler A | title = Internet Addiction: A Brief Summary of Research and Practice | journal = Current Psychiatry Reviews | volume = 8 | issue = 4 | pages = 292–298 | date = November 2012 | pmid = 23125561 | pmc = 3480687 | doi = 10.2174/157340012803520513 }}</ref> Internet addiction has been described as "a psychological dependence on the Internet, regardless of the type of activity once logged on."<ref name="Chou-2005" /> Problematic internet use may include a preoccupation with the internet and/or digital media, excessive time spent using the internet despite resultant distress in the individual, increase in the amount of internet use required to achieve the same desired emotional response, loss of control over one's internet use habits, withdrawal symptoms, and continued problematic internet use despite negative consequences to one's work, social, academic, or personal life.<ref>{{cite journal | vauthors = Block JJ | title = Issues for DSM-V: internet addiction | journal = The American Journal of Psychiatry | volume = 165 | issue = 3 | pages = 306–307 | date = March 2008 | pmid = 18316427 | doi = 10.1176/appi.ajp.2007.07101556 }}</ref>

Studies conducted in India, United States, Asia, and Europe have identified Internet addiction prevalence rates ranging in value from 1% to 19%, with the adolescent population having high rates compared to other age groups.<ref>{{cite journal | vauthors = Tang J, Yu Y, Du Y, Ma Y, Zhang D, Wang J | title = Prevalence of internet addiction and its association with stressful life events and psychological symptoms among adolescent internet users | journal = Addictive Behaviors | volume = 39 | issue = 3 | pages = 744–747 | date = March 2014 | pmid = 24388433 | doi = 10.1016/j.addbeh.2013.12.010 | hdl = 2436/622804 | hdl-access = free }}</ref><ref name="Joseph2021" /> Prevalence rates have been difficult to establish due to a lack of universally accepted diagnostic criteria, a lack of diagnostic instruments demonstrating cross-cultural validity and reliability, and existing controversy surrounding the validity of labeling problematic internet use as an addictive disorder.<ref name="Weinstein_2010">{{cite journal | vauthors = Weinstein A, Lejoyeux M | title = Internet addiction or excessive internet use | journal = The American Journal of Drug and Alcohol Abuse | volume = 36 | issue = 5 | pages = 277–283 | date = September 2010 | pmid = 20545603 | doi = 10.3109/00952990.2010.491880 | s2cid = 17713327 }}</ref><ref name="Joseph2021" /> The most common scale used to measure addiction is the Internet Addiction Test developed by [[Kimberly Young]].<ref name="Joseph2021">{{cite journal | vauthors = Joseph J, Varghese A, Vr V, Dhandapani M, Grover S, Sharma S, Khakha D, Mann S, Varkey BP | title = Prevalence of internet addiction among college students in the Indian setting: a systematic review and meta-analysis | journal = General Psychiatry | volume = 34 | issue = 4 | pages = e100496 | date = August 2021 | pmid = 34504996 | pmc = 8381302 | doi = 10.1136/gpsych-2021-100496 }}</ref>

People with internet addiction are likely to have a comorbid psychiatric disorder. Comorbid diagnoses identified alongside internet addiction include affective mood disorders, anxiety disorders, substance use disorders, and attention deficit hyperactivity disorder.<ref name="Weinstein_2010" />

=== Video games ===
{{Main|Video game addiction}}

Video game addiction is characterized by the [[World Health Organization]] (WHO) as excessive gaming behavior, potentially prioritized over other interests, despite the negative consequences that may arise, for a period of at least 12 months.<ref name="WHO_Gaming">{{Cite web |title=Addictive behaviours: Gaming disorder |url=https://www.who.int/news-room/questions-and-answers/item/addictive-behaviours-gaming-disorder |access-date=25 October 2022 |website=www.who.int |language=en}}</ref> In May 2019, the WHO introduced [[gaming disorder]] in the 11th edition of the International Classification of Diseases.<ref>{{Cite web |title=International Classification of Diseases 11th revision &ndash; ICD-11 |url=https://icd.who.int/en |access-date=25 October 2022 |website=icd.who.int |location=Geneva}}</ref> Video game addiction has been shown to be more prevalent in males than females, higher by 2.9 times.<ref name="Wittek_2016">{{cite journal | vauthors = Wittek CT, Finserås TR, Pallesen S, Mentzoni RA, Hanss D, Griffiths MD, Molde H | title = Prevalence and Predictors of Video Game Addiction: A Study Based on a National Representative Sample of Gamers | journal = International Journal of Mental Health and Addiction | volume = 14 | issue = 5 | pages = 672–686 | date = 2016 | pmid = 27688739 | pmc = 5023737 | doi = 10.1007/s11469-015-9592-8 }}</ref> It has been suggested that people of younger ages are more prone to become addicted to video games.<ref name="Wittek_2016" /> People with certain personalities may be more susceptible to gaming addictions.<ref name="Wittek_2016" /><ref>{{cite journal | vauthors = Peters CS, Malesky LA | title = Problematic usage among highly-engaged players of massively multiplayer online role playing games | journal = Cyberpsychology & Behavior | volume = 11 | issue = 4 | pages = 481–484 | date = August 2008 | pmid = 18721098 | doi = 10.1089/cpb.2007.0140 }}</ref>

Risk factors for video game addiction include:
* Male,
* Psychopathologies (e.g. ADHD or MDD), and
* Social anxiety.<ref>{{Cite journal | vauthors = Hyun GJ, Han DH, Lee YS, Kang KD, Yoo SK, Chung US, Renshaw PF |date=1 July 2015 |title=Risk factors associated with online game addiction: A hierarchical model |journal=Computers in Human Behavior |language=en |volume=48 |pages=706–713 |doi=10.1016/j.chb.2015.02.008 |issn=0747-5632}}</ref>

=== Shopping ===
{{Main|Shopping addiction|Compulsive buying disorder}}

Shopping addiction, or [[compulsive buying disorder]] (CBD), is the excessive urge to shop or spend, potentially resulting in unwanted consequences.<ref name="Hague_2016">{{cite journal | vauthors = Hague B, Hall J, Kellett S | title = Treatments for compulsive buying: A systematic review of the quality, effectiveness and progression of the outcome evidence | journal = Journal of Behavioral Addictions | volume = 5 | issue = 3 | pages = 379–394 | date = September 2016 | pmid = 27640529 | pmc = 5264404 | doi = 10.1556/2006.5.2016.064 }}</ref> These consequences can have serious impacts, such as increased [[consumer debt]], negatively affected relationships, increased risk of illegal behavior, and suicide attempts.<ref name="Hague_2016" /> Shopping addiction occurs worldwide and has shown a 5.8% prevalence in the United States.<ref name="Black_2007">{{cite journal | vauthors = Black DW | title = A review of compulsive buying disorder | journal = World Psychiatry | volume = 6 | issue = 1 | pages = 14–18 | date = February 2007 | pmid = 17342214 | pmc = 1805733 }}</ref> Similar to other behavioral addictions, CBD can be linked to mood disorders, substance use disorders, eating disorders, and other disorders involving a lack of control.<ref name="Black_2007" />

==Signs and symptoms==
Signs and symptoms of addiction can vary depending on the type of addiction. Symptoms of drug addictions may include:
* Continuation of drug use despite the knowledge of consequences<ref name="diGiacomo2022" />
* Disregarding financial status when it comes to drug purchases
* Ensuring a stable supply of the drug
* Experiencing withdrawal symptoms when stopping the drug<ref>{{Cite web |title=Drug addiction (substance use disorder) – Symptoms and causes |url=https://www.mayoclinic.org/diseases-conditions/drug-addiction/symptoms-causes/syc-20365112 |access-date=21 November 2022 |website=Mayo Clinic |language=en}}</ref><ref name="diGiacomo2022" />
* Needing more of the drug over time to achieve similar effects<ref name="diGiacomo2022" />
* Social and work life impacted due to drug use<ref name="diGiacomo2022" />
* Unsuccessful attempts to stop drug use<ref name="diGiacomo2022" />
* Urge to use drug regularly

Signs and symptoms of addiction may include:
{| class="wikitable"
!Behavioral Changes
!Physical Changes
!Social Changes
|-style="vertical-align:top;"
|
* Angry and irritable
* Changes to eating or sleeping habits
* Changes to personality and attitude
* Decreased attendance and performance in workplace or school setting<ref name="diGiacomo2022" />
* Fearful, paranoid and anxious without probable cause<ref name="mentalhealth.gov">{{Cite web |title=Mental Health and Substance Use Co-Occurring Disorders | work = MentalHealth.gov |url=https://www.mentalhealth.gov/what-to-look-for/mental-health-substance-use-disorders |access-date=29 November 2022 }}</ref>
* Frequently engaging in conflicts (fights, illegal activity)
* Frequent or sudden changes in mood and temperament
* Hiding or in denial of certain behaviors
* Lack of motivation
* Periodic hyperactivity
* Using substances in inappropriate settings
|
* Abnormal pupil size
* Bloodshot eyes
* Body odor
* Impaired motor coordination<ref name="mentalhealth.gov" />
* Periodic tremors
* Poor physical appearance
* Slurred speech
* Sudden changes in weight
|
* Changes in hobbies
* Changes to financial status (unexplained need for money)
* Legal problems related to substance abuse
* Sudden changes in friends and associates
* Use of substance despite consequences to personal relationships<ref name="mentalhealth.gov" />
|}

== Screening and assessment ==

=== Addictions Neuroclinical Assessment ===
The Addictions Neuroclinical Assessment is used to diagnose addiction disorders. This tool measures three different domains: [[Executive functions|executive function]], [[Motivational salience#Incentive salience|incentive salience]], and [[Emotionality#Negative|negative emotionality]].<ref name="Koob2020">{{cite journal |vauthors=Koob GF, Powell P, White A |title=Addiction as a Coping Response: Hyperkatifeia, Deaths of Despair, and COVID-19 |journal=Am J Psychiatry |volume=177 |issue=11 |pages=1031–1037 |date=November 2020 |pmid=33135468 |doi=10.1176/appi.ajp.2020.20091375 |s2cid=226233515 }}</ref><ref name="Kwako_2016">{{cite journal | vauthors = Kwako LE, Momenan R, Litten RZ, Koob GF, Goldman D | title = Addictions Neuroclinical Assessment: A Neuroscience-Based Framework for Addictive Disorders | journal = Biological Psychiatry | volume = 80 | issue = 3 | pages = 179–189 | date = August 2016 | pmid = 26772405 | pmc = 4870153 | doi = 10.1016/j.biopsych.2015.10.024 }}</ref> Executive functioning consists of processes that would be disrupted in addiction.<ref name="Kwako_2016" /> In the context of addiction, incentive salience determines how one perceives the addictive substance.<ref name="Kwako_2016" /> Increased negative emotional responses have been found with individuals with addictions.<ref name="Kwako_2016" />

=== Tobacco, Alcohol, Prescription Medication, and Other Substance Use (TAPS) ===
This is a screening and assessment tool in one, assessing commonly used substances. This tool allows for a simple diagnosis, eliminating the need for several screening and assessment tools, as it includes both TAPS-1 and TAPS-2, screening and assessment tools respectively. The screening component asks about the frequency of use of the specific substance (tobacco, alcohol, prescription medication, and other).<ref name="nida">{{Cite web |title=Tobacco, Alcohol, Prescription medication, and other Substance use (TAPS) Tool |url=https://nida.nih.gov/taps2/ |access-date=29 November 2022 |website=nida.nih.gov}}</ref> If an individual screens positive, the second component will begin. This dictates the risk level of the substance.<ref name="nida" />

=== CRAFFT ===
The CRAFFT (Car-Relax-Alone-Forget-Family and Friends-Trouble) is a screening tool that is used in medical centers. The CRAFFT is in version 2.1 and has a version for nicotine and tobacco use called the CRAFFT 2.1+N.<ref>{{Cite web |title=About the CRAFFT – CRAFFT |url=https://crafft.org/about-the-crafft/ |access-date=3 December 2022 |language=en-US}}</ref> This tool is used to identify substance use, substance related driving risk, and addictions among adolescents. This tool uses a set of questions for different scenarios.<ref name="crafft.org">{{Cite web |title=Use the CRAFFT – CRAFFT |url=https://crafft.org/use-the-crafft/ |access-date=3 December 2022 |language=en-US}}</ref> In the case of a specific combination of answers, different question sets can be used to yield a more accurate answer. After the questions, the DSM-5 criteria are used to identify the likelihood of the person having substance use disorder.<ref name="crafft.org" /> After these tests are done, the clinician is to give the "5 RS" of brief counseling.

The five Rs of brief counseling includes:
# REVIEW screening results
# RECOMMEND to not use
# RIDING/DRIVING risk counseling
# RESPONSE: elicit self-motivational statements
# REINFORCE self-efficacy<ref name="crafft.org" />

=== Drug Abuse Screening Test (DAST-10) ===
The Drug Abuse Screening Test (DAST) is a self-reporting tool that measures problematic substance use.<ref name="Yudko_2007">{{cite journal | vauthors = Yudko E, Lozhkina O, Fouts A | title = A comprehensive review of the psychometric properties of the Drug Abuse Screening Test | journal = Journal of Substance Abuse Treatment | volume = 32 | issue = 2 | pages = 189–198 | date = March 2007 | pmid = 17306727 | doi = 10.1016/j.jsat.2006.08.002 }}</ref> Responses to this test are recorded as yes or no answers, and scored as a number between zero and 28. Drug abuse or dependence, are indicated by a cut off score of 6.<ref name="Yudko_2007" /> Three versions of this screening tool are in use: DAST-28, DAST-20, and DAST-10. Each of these instruments are copyrighted by Dr. Harvey A. Skinner.<ref name="Yudko_2007" />

=== Alcohol, Smoking, and Substance Involvement Test (ASSIST) ===
The Alcohol, Smoking, and Substance Involvement Test (ASSIST) is an interview-based questionnaire consisting of eight questions developed by the WHO.<ref>{{cite journal | vauthors = Han BH, Moore AA | title = Prevention and Screening of Unhealthy Substance Use by Older Adults | journal = Clinics in Geriatric Medicine | volume = 34 | issue = 1 | pages = 117–129 | date = February 2018 | pmid = 29129212 | pmc = 5718360 | doi = 10.1016/j.cger.2017.08.005 }}</ref> The questions ask about lifetime use; frequency of use; urge to use; frequency of health, financial, social, or legal problems related to use; failure to perform duties; if anyone has raised concerns over use; attempts to limit or moderate use; and use by injection.<ref>{{cite journal | vauthors = Ali R, Meena S, Eastwood B, Richards I, Marsden J | title = Ultra-rapid screening for substance-use disorders: the Alcohol, Smoking and Substance Involvement Screening Test (ASSIST-Lite) | journal = Drug and Alcohol Dependence | volume = 132 | issue = 1–2 | pages = 352–361 | date = September 2013 | pmid = 23561823 | doi = 10.1016/j.drugalcdep.2013.03.001 }}</ref>

== Causes ==

===Personality theories===
{{Main|Personality theories of addiction}}

[[Personality theories of addiction]] are [[Psychology|psychological models]] that associate [[personality traits]] or modes of thinking (i.e., [[Affective science|affective states]]) with an individual's proclivity for developing an addiction. [[Data analysis]] demonstrates that psychological profiles of drug users and non-users have significant differences and the psychological predisposition to using different drugs may be different.<ref>{{cite book | vauthors = Fehrman E, Egan V, Gorban AN, Levesley J, Mirkes EM, Muhammad AK |title= Personality Traits and Drug Consumption. A Story Told by Data|doi = 10.1007/978-3-030-10442-9|publisher= Springer, Cham|isbn=978-3-030-10441-2 |arxiv= 2001.06520 |year= 2019|s2cid= 151160405}}</ref> Models of addiction risk that have been proposed in psychology literature include: an [[affect dysregulation]] model of positive and negative [[psychological affect]]s, the [[reinforcement sensitivity theory]] of [[impulsiveness]] and behavioral inhibition, and an impulsivity model of [[#Sensitization|reward sensitization]] and impulsiveness.<ref name="Cheetham_2010">{{cite journal |vauthors=Cheetham A, Allen NB, Yücel M, Lubman DI | title = The role of affective dysregulation in drug addiction | journal = Clin Psychol Rev | volume = 30 | issue = 6 | pages = 621–34 |date=August 2010| pmid = 20546986 | doi = 10.1016/j.cpr.2010.04.005 }}</ref><ref name=Franken_2006>{{cite journal |vauthors=Franken IH, Muris P | title = BIS/BAS personality characteristics and college students' substance use|journal=Personality and Individual Differences | year = 2006 | volume = 40 | issue = 7 | pages = 1497–503 | doi = 10.1016/j.paid.2005.12.005 }}</ref><ref name="pmid18232522">{{cite journal |vauthors=Genovese JE, Wallace D | title = Reward sensitivity and substance abuse in middle school and high school students | journal = J Genet Psychol | volume = 168 | issue = 4 | pages = 465–69 |date=December 2007| pmid = 18232522 | doi = 10.3200/GNTP.168.4.465-469 | s2cid = 207640075 }}</ref><ref name=Kimbrel_2007>{{cite journal |vauthors=Kimbrel NA, Nelson-Gray RO, Mitchell JT | title = Reinforcement sensitivity and maternal style as predictors of psychopathology | journal = Personality and Individual Differences |date=April 2007| volume = 42 | issue = 6 | pages = 1139–49 | doi = 10.1016/j.paid.2006.06.028 }}</ref><ref name="Dawe">{{cite journal |vauthors=Dawe S, Loxton NJ | title = The role of impulsivity in the development of substance use and eating disorders | journal = Neurosci Biobehav Rev | volume = 28 | issue = 3 | pages = 343–51 |date=May 2004| pmid = 15225976 | doi = 10.1016/j.neubiorev.2004.03.007 | s2cid = 24435589 }}</ref>

===Neuropsychology===

The [[transtheoretical model]] of change (TTM) can point to how someone may be conceptualizing their addiction and the thoughts around it, including not being aware of their addiction.<ref name="Hill2021" />

[[Cognitive control]] and [[stimulus control]], which is associated with [[operant conditioning|operant]] and [[classical conditioning]], represent opposite processes (i.e., internal vs external or environmental, respectively) that compete over the control of an individual's elicited behaviors.<ref name="Cognitive - stimulus">{{cite journal | vauthors = Washburn DA | title = The Stroop effect at 80: The competition between stimulus control and cognitive control | journal = J Exp Anal Behav | volume = 105 | issue = 1 | pages = 3–13 | year = 2016 | pmid = 26781048 | doi = 10.1002/jeab.194 | quote = Today, arguably more than at any time in history, the constructs of attention, executive functioning, and cognitive control seem to be pervasive and preeminent in research and theory. Even within the cognitive framework, however, there has long been an understanding that behavior is multiply determined, and that many responses are relatively automatic, unattended, contention-scheduled, and habitual. Indeed, the cognitive flexibility, response inhibition, and self-regulation that appear to be hallmarks of cognitive control are noteworthy only in contrast to responses that are relatively rigid, associative, and involuntary. }}</ref> Cognitive control, and particularly [[inhibitory control|inhibitory control over behavior]], is impaired in both addiction and [[attention deficit hyperactivity disorder]].<ref name="Executive functions">{{cite journal | vauthors = Diamond A | title = Executive functions | journal = Annu Rev Psychol | volume = 64 | pages = 135–68 | year = 2013 | pmid = 23020641 | pmc = 4084861 | doi = 10.1146/annurev-psych-113011-143750 | quote = Core EFs are inhibition [response inhibition (self-control&nbsp;– resisting temptations and resisting acting impulsively) and interference control (selective attention and cognitive inhibition)], working memory, and cognitive flexibility (including creatively thinking "outside the box," seeing anything from different perspectives, and quickly and flexibly adapting to changed circumstances).&nbsp;... EFs and prefrontal cortex are the first to suffer, and suffer disproportionately, if something is not right in your life. They suffer first, and most, if you are stressed (Arnsten 1998, Liston et al. 2009, Oaten & Cheng 2005), sad (Hirt et al. 2008, von Hecker & Meiser 2005), lonely (Baumeister et al. 2002, Cacioppo & Patrick 2008, Campbell et al. 2006, Tun et al. 2012), sleep deprived (Barnes et al. 2012, Huang et al. 2007), or not physically fit (Best 2010, Chaddock et al. 2011, Hillman et al. 2008). Any of these can cause you to appear to have a disorder of EFs, such as ADHD, when you do not. You can see the deleterious effects of stress, sadness, loneliness, and lack of physical health or fitness at the physiological and neuroanatomical level in prefrontal cortex and at the behavioral level in worse EFs (poorer reasoning and problem solving, forgetting things, and impaired ability to exercise discipline and self-control).&nbsp;...<br />EFs can be improved (Diamond & Lee 2011, Klingberg 2010).&nbsp;... At any age across the life cycle EFs can be improved, including in the elderly and in infants. There has been much work with excellent results on improving EFs in the elderly by improving physical fitness (Erickson & Kramer 2009, Voss et al. 2011)&nbsp;... Inhibitory control (one of the core EFs) involves being able to control one's attention, behavior, thoughts, and/or emotions to override a strong internal predisposition or external lure, and instead do what's more appropriate or needed. Without inhibitory control we would be at the mercy of impulses, old habits of thought or action (conditioned responses), and/or stimuli in the environment that pull us this way or that. Thus, inhibitory control makes it possible for us to change and for us to choose how we react and how we behave rather than being unthinking creatures of habit. It doesn't make it easy. Indeed, we usually are creatures of habit and our behavior is under the control of environmental stimuli far more than we usually realize, but having the ability to exercise inhibitory control creates the possibility of change and choice.&nbsp;... The subthalamic nucleus appears to play a critical role in preventing such impulsive or premature responding (Frank 2006).}}</ref><ref name="NHM-Cognitive Control">{{cite book |vauthors=Malenka RC, Nestler EJ, Hyman SE |veditors=Sydor A, Brown RY | title = Molecular Neuropharmacology: A Foundation for Clinical Neuroscience | year = 2009 | publisher = McGraw-Hill Medical | location = New York | isbn = 978-0-07-148127-4 | pages = 313–21 | edition = 2nd | chapter = Chapter 13: Higher Cognitive Function and Behavioral Control | quote ={{bull}} Executive function, the cognitive control of behavior, depends on the prefrontal cortex, which is highly developed in higher primates and especially humans.<br />{{bull}} Working memory is a short-term, capacity-limited cognitive buffer that stores information and permits its manipulation to guide decision-making and behavior.&nbsp;...<br />These diverse inputs and back projections to both cortical and subcortical structures put the prefrontal cortex in a position to exert what is called "top-down" control or cognitive control of behavior.&nbsp;... The prefrontal cortex receives inputs not only from other cortical regions, including association cortex, but also, via the thalamus, inputs from subcortical structures subserving emotion and motivation, such as the amygdala (Chapter 14) and ventral striatum (or nucleus accumbens; Chapter 15).&nbsp;...<br />In conditions in which prepotent responses tend to dominate behavior, such as in drug addiction, where drug cues can elicit drug seeking (Chapter 15), or in attention deficit hyperactivity disorder (ADHD; described below), significant negative consequences can result.&nbsp;... ADHD can be conceptualized as a disorder of executive function; specifically, ADHD is characterized by reduced ability to exert and maintain cognitive control of behavior. Compared with healthy individuals, those with ADHD have diminished ability to suppress inappropriate prepotent responses to stimuli (impaired response inhibition) and diminished ability to inhibit responses to irrelevant stimuli (impaired interference suppression).&nbsp;... <!--Inhibitory control brain structures-->Functional neuroimaging in humans demonstrates activation of the prefrontal cortex and caudate nucleus (part of the striatum) in tasks that demand inhibitory control of behavior. Subjects with ADHD exhibit less activation of the medial prefrontal cortex than healthy controls even when they succeed in such tasks and utilize different circuits.&nbsp;... Early results with structural MRI show thinning of the cerebral cortex in ADHD subjects compared with age-matched controls in prefrontal cortex and posterior parietal cortex, areas involved in working memory and attention.}}</ref> Stimulus-driven behavioral responses (i.e., stimulus control) that are associated with a particular [[rewarding stimulus]] tend to dominate one's behavior in an addiction.<ref name="NHM-Cognitive Control" />
{{Operant conditioning}}

====Stimulus control of behavior====
{{See also|Stimulus control}}

In operant conditioning, behavior is influenced by outside stimulus, such as a drug. The operant conditioning theory of learning is useful in understanding why the mood-altering or stimulating consequences of drug use can reinforce continued use (an example of [[positive reinforcement]]) and why the addicted person seeks to avoid withdrawal through continued use (an example of [[negative reinforcement]]). Stimulus control is using the absence of the stimulus or presence of a reward to influence the resulting behavior.<ref name="Hill2021">{{cite book | vauthors = Hill R, Harris J | title = Seminars in addiction psychiatry | chapter = Psychological Approaches to Addiction | veditors = Day E | date = 2 November 2021 | publisher =  Cambridge University Press | location = Cambridge | isbn = 978-1-911623-19-9 | pages = 147–169 | edition = 2nd | doi = 10.1017/9781911623199.009 | s2cid = 242036830 }}</ref>

====Cognitive control of behavior====
{{See also|Cognitive control}}
Cognitive control is the intentional selection of thoughts, behaviors, and emotions, based on our environment. It has been shown that drugs alter the way our brains function, and its structure.<ref name="Gould_2010">{{cite journal | vauthors = Gould TJ | title = Addiction and cognition | journal = Addiction Science & Clinical Practice | volume = 5 | issue = 2 | pages = 4–14 | date = December 2010 | pmid = 22002448 | pmc = 3120118 }}</ref><ref name="Levy2019" /> Cognitive functions such as learning, memory, and impulse control, are affected by drugs.<ref name="Gould_2010" /> These effects promote drug use, as well as hinder the ability to abstain from it.<ref name="Gould_2010" /> The increase in dopamine release is prominent in drug use, specifically in the [[ventral striatum]] and the [[nucleus accumbens]].<ref name="Gould_2010" /> Dopamine is responsible for producing pleasurable feelings, as well driving us to perform important life activities. Addictive drugs cause a significant increase in this reward system, causing a large increase in dopamine signaling as well as increase in reward-seeking behavior, in turn motivating drug use.<ref name="Gould_2010" /><ref name="Levy2019" /> This promotes the development of a maladaptive drug to stimulus relationship.<ref>{{cite journal | vauthors = Feltenstein MW, See RE | title = The neurocircuitry of addiction: an overview | journal = British Journal of Pharmacology | volume = 154 | issue = 2 | pages = 261–274 | date = May 2008 | pmid = 18311189 | pmc = 2442446 | doi = 10.1038/bjp.2008.51 }}</ref> Early drug use leads to these maladaptive associations, later affecting cognitive processes used for coping, which are needed to successfully abstain from them.<ref name="Gould_2010" /><ref name="Hill2021" />

== Risk factors ==
{{Further|Addiction vulnerability}}

A number of genetic and environmental risk factors exist for developing an addiction.<ref name="Cellular basis" /><ref name="Transgenerational epigenetic inheritance in addiction" /> Genetic and environmental risk factors each account for roughly half of an individual's risk for developing an addiction;<ref name="Cellular basis" /> the contribution from epigenetic risk factors to the total risk is unknown.<ref name="Transgenerational epigenetic inheritance in addiction" /> Even in individuals with a relatively low genetic risk, exposure to sufficiently high doses of an addictive drug for a long period of time (e.g., weeks–months) can result in an addiction.<ref name="Cellular basis" /> Adverse childhood events are associated with negative health outcomes, such as substance use disorder. Childhood abuse or exposure to violent crime is related to developing a mood or anxiety disorder, as well as a substance dependence risk.<ref>{{cite journal | vauthors = Douglas KR, Chan G, Gelernter J, Arias AJ, Anton RF, Weiss RD, Brady K, Poling J, Farrer L, Kranzler HR | title = Adverse childhood events as risk factors for substance dependence: partial mediation by mood and anxiety disorders | journal = Addictive Behaviors | volume = 35 | issue = 1 | pages = 7–13 | date = January 2010 | pmid = 19720467 | pmc = 2763992 | doi = 10.1016/j.addbeh.2009.07.004 }}</ref>

=== Genetic factors ===
{{Main|Epigenetics of cocaine addiction|Molecular and epigenetic mechanisms of alcoholism}}
{{Further|Alcoholism#Genetic variation|History of drinking|History of smoking|Prevalence of tobacco use}}

Genetic factors, along with [[Social|socio]]-environmental (e.g., [[Biopsychosocial model|psychosocial]]) factors, have been established as significant contributors to addiction vulnerability.<ref name="Cellular basis" /><ref name="Transgenerational epigenetic inheritance in addiction" /><ref name="Nature 2022">{{cite journal | vauthors = Saunders GR, Wang X, Chen F, Jang SK, Liu M, Wang C, etal | title = Genetic diversity fuels gene discovery for tobacco and alcohol use | journal = Nature | volume = 612 | issue = 7941 | pages = 720–724 | date = December 2022 | pmid = 36477530 | pmc = 9771818 | doi = 10.1038/s41586-022-05477-4 | publisher = [[Nature Research]] | s2cid = 254434507 | doi-access = free | bibcode = 2022Natur.612..720S }}</ref><ref name="diGiacomo2022" /> Studies done on 350 hospitalized drug-dependent patients showed that over half met the criteria for alcohol abuse, with a role of familial factors being prevalent.<ref>{{cite journal | vauthors = Mirin SM, Weiss RD, Griffin ML, Michael JL | title = Psychopathology in drug abusers and their families | journal = Comprehensive Psychiatry | volume = 32 | issue = 1 | pages = 36–51 | date = 1 January 1991 | pmid = 2001619 | doi = 10.1016/0010-440X(91)90068-N }}</ref> Genetic factors account for 40–60% of the risk factors for alcoholism.<ref>{{cite journal | vauthors = Mayfield RD, Harris RA, Schuckit MA | title = Genetic factors influencing alcohol dependence | journal = British Journal of Pharmacology | volume = 154 | issue = 2 | pages = 275–287 | date = May 2008 | pmid = 18362899 | pmc = 2442454 | doi = 10.1038/bjp.2008.88 }}</ref> Similar rates of heritability for other types of drug addiction have been indicated, specifically in genes that encode the [[Alpha5 Nicotinic Acetylcholine Receptor]].<ref name=Kendler94/> Knestler hypothesized in 1964 that a gene or group of genes might contribute to predisposition to addiction in several ways. For example, altered levels of a normal protein due to environmental factors may change the structure or functioning of specific brain neurons during development. These altered brain neurons could affect the susceptibility of an individual to an initial drug use experience. In support of this hypothesis, animal studies have shown that environmental factors such as stress can affect an animal's genetic expression.<ref name=Kendler94>{{cite journal | vauthors = Kendler KS, Neale MC, Heath AC, Kessler RC, Eaves LJ | title = A twin-family study of alcoholism in women | journal = The American Journal of Psychiatry | volume = 151 | issue = 5 | pages = 707–715 | date = May 1994 | pmid = 8166312 | doi = 10.1176/ajp.151.5.707 }}</ref>

In humans, twin studies into addiction have provided some of the highest-quality evidence of this link, with results finding that if one twin is affected by addiction, the other twin is likely to be as well, and to the same substance.<ref name="Crowe1991">{{cite journal| vauthors = Crowe JR |title=Genetics of alcoholism|journal=Alcohol Health and Research World|pages=1–11|url=http://psycnet.apa.org/record/1993-22020-001|access-date=13 December 2017}}</ref> Further evidence of a genetic component is research findings from family studies which suggest that if one family member has a history of addiction, the chances of a relative or close family developing those same habits are much higher than one who has not been introduced to addiction at a young age.<ref>{{Cite news|url=https://www.addictionsandrecovery.org/is-addiction-a-disease.htm|title=The Genetics of Addiction – Is Addiction a Disease? | vauthors = Melemis SM | work = I Want to Change My Life|access-date=17 September 2018}}</ref>

The data implicating specific genes in the development of drug addiction is mixed for most genes. Many addiction studies that aim to identify specific genes focus on common variants with an allele frequency of greater than 5% in the general population. When associated with disease, these only confer a small amount of additional risk with an [[odds ratio]] of 1.1–1.3 percent; this has led to the development the rare variant hypothesis, which states that genes with low frequencies in the population (<1%) confer much greater additional risk in the development of the disease.<ref name="pmid23454283">{{cite journal | vauthors = Clarke TK, Crist RC, Kampman KM, Dackis CA, Pettinati HM, O'Brien CP, Oslin DW, Ferraro TN, Lohoff FW, Berrettini WH | title = Low frequency genetic variants in the μ-opioid receptor (OPRM1) affect risk for addiction to heroin and cocaine | journal = Neuroscience Letters | volume = 542 | pages = 71–75 | year = 2013 | pmid = 23454283 | doi = 10.1016/j.neulet.2013.02.018 | pmc=3640707}}</ref>

[[Genome-wide association study|Genome-wide association studies]] (GWAS) are used to examine genetic associations with dependence, addiction, and drug use.<ref name="Nature 2022" /> These studies rarely identify genes from proteins previously described via animal knockout models and candidate gene analysis. Instead, large percentages of genes involved in processes such as cell adhesion are commonly identified. The important effects of [[endophenotype]]s are typically not capable of being captured by these methods. Genes identified in GWAS for drug addiction may be involved either in adjusting brain behavior before drug experiences, subsequent to them, or both.<ref>{{cite journal | vauthors = Hall FS, Drgonova J, Jain S, Uhl GR | title = Implications of genome wide association studies for addiction: are our a priori assumptions all wrong? | journal = Pharmacology & Therapeutics | volume = 140 | issue = 3 | pages = 267–79 | date = December 2013 | pmid = 23872493 | pmc = 3797854 | doi = 10.1016/j.pharmthera.2013.07.006 }}</ref>

=== Environmental factors ===
Environmental risk factors for addiction are the experiences of an individual during their lifetime that interact with the individual's genetic composition to increase or decrease his or her vulnerability to addiction.<ref name="Cellular basis" /> For example, after the nationwide outbreak of COVID-19, more people quit (vs. started) smoking; and smokers, on average, reduced the quantity of cigarettes they consumed.<ref>{{cite journal | vauthors = Yang H, Ma J | title = How the COVID-19 pandemic impacts tobacco addiction: Changes in smoking behavior and associations with well-being | journal = Addictive Behaviors | volume = 119 | pages = 106917 | date = August 2021 | pmid = 33862579 | doi = 10.1016/j.addbeh.2021.106917 | pmc = 9186053 | s2cid = 233278782 | doi-access = free }}</ref> More generally, a number of different environmental factors have been implicated as risk factors for addiction, including various psycho[[social stress]]ors. The [[National Institute on Drug Abuse]] (NIDA) and studies cite lack of parental supervision, the prevalence of peer substance use, substance availability, and poverty as risk factors for substance use among children and adolescents.<ref name="Abuse">{{Cite news|url=https://www.drugabuse.gov/publications/preventing-drug-abuse-among-children-adolescents/chapter-1-risk-factors-protective-factors/what-are-risk-factors|title=What are risk factors and protective factors?|publisher=National Institute on Drug Abuse|access-date=13 December 2017|archive-date=30 April 2020|archive-url=https://web.archive.org/web/20200430061000/https://www.drugabuse.gov/publications/preventing-drug-abuse-among-children-adolescents/chapter-1-risk-factors-protective-factors/what-are-risk-factors|url-status=dead}}</ref><ref name="Skylstad2022" /> The brain disease model of addiction posits that an individual's exposure to an addictive drug is the most significant environmental risk factor for addiction.<ref>{{Cite web|title=Understanding Drug Use and Addiction|url=https://www.drugabuse.gov/publications/drugfacts/understanding-drug-use-addiction| publisher = National Institute on Drug Abuse|website=www.drugabuse.gov|date=6 June 2018|language=en|access-date=29 May 2020}}</ref> Many researchers, including neuroscientists, indicate that the brain disease model presents a misleading, incomplete, and potentially detrimental explanation of addiction.<ref>{{cite journal | vauthors = Lewis M | title = Brain Change in Addiction as Learning, Not Disease | journal = The New England Journal of Medicine | volume = 379 | issue = 16 | pages = 1551–1560 | date = October 2018 | pmid = 30332573 | doi = 10.1056/NEJMra1602872 | s2cid = 205117578 | veditors = Longo DL | quote = Addictive activities are determined neither solely by brain changes nor solely by social conditions ... the narrowing seen in addiction takes place within the behavioral repertoire, the social surround, and the brain — all at the same time. }}</ref>

The psychoanalytic theory model defines ''addiction'' as a form of defense against feelings of hopelessness and helplessness as well as a symptom of failure to regulate powerful emotions related to adverse childhood experiences (ACEs), various forms of maltreatment and dysfunction experienced in childhood. In this case, the addictive substance provides brief but total relief and positive feelings of control.<ref name="Hill2021" /> The [[Adverse Childhood Experiences Study]] by the [[Centers for Disease Control and Prevention]] has shown a strong [[dose–response relationship]] between ACEs and numerous health, social, and behavioral problems throughout a person's lifespan, including substance use disorder.<ref name=SAMHSA_ACE/> Children's neurological development can be permanently disrupted when they are chronically exposed to stressful events such as physical, emotional, or sexual abuse, physical or emotional neglect, witnessing violence in the household, or a parent being incarcerated or having a mental illness. As a result, the child's cognitive functioning or ability to cope with negative or disruptive emotions may be impaired. Over time, the child may adopt substance use as a coping mechanism or as a result of reduced impulse control, particularly during adolescence.<ref name=SAMHSA_ACE>{{cite web |title=Adverse Childhood Experiences |publisher=Substance Abuse and Mental Health Services Administration |location=Rockville, Maryland, United States |website=samhsa.gov |url=http://www.samhsa.gov/capt/practicing-effective-prevention/prevention-behavioral-health/adverse-childhood-experiences |access-date=26 September 2016 |archive-url=https://web.archive.org/web/20161009181048/http://www.samhsa.gov/capt/practicing-effective-prevention/prevention-behavioral-health/adverse-childhood-experiences |archive-date=9 October 2016 |url-status=dead }}</ref><ref name="Skylstad2022" /><ref name="Hill2021" /> Vast amounts of children who experienced abuse have gone on to have some form of addiction in their adolescence or adult life.<ref name="Enoch2011" /> This pathway towards addiction that is opened through stressful experiences during childhood can be avoided by a change in environmental factors throughout an individual's life and opportunities of professional help.<ref name="Enoch2011">{{cite journal | vauthors = Enoch MA | title = The role of early life stress as a predictor for alcohol and drug dependence | journal = Psychopharmacology | volume = 214 | issue = 1 | pages = 17–31 | date = March 2011 | pmid = 20596857 | pmc = 3005022 | doi = 10.1007/s00213-010-1916-6 }}</ref> If one has friends or peers who engage in drug use favorably, the chances of them developing an addiction increases. Family conflict and home management is a cause for one to become engaged in drug use.<ref>{{Cite web |url=https://learn.genetics.utah.edu/content/addiction/environment/ |title=Environmental Risk Factors |website=learn.genetics.utah.edu |access-date=17 September 2018 |archive-date=17 September 2018 |archive-url=https://web.archive.org/web/20180917105112/https://learn.genetics.utah.edu/content/addiction/environment/ |url-status=dead }}</ref>

==== Social control theory ====
{{Main|Social control theory}}

According to Travis Hirschi's social control theory, adolescents with stronger attachments to family, religious, academic, and other social institutions are less likely to engage in delinquent and maladaptive behavior such as drug use leading to addiction.<ref>{{Cite journal |last1=Marcos |first1=Anastasios C. |last2=Bahr |first2=Stephen J. |date=June 1988 |title=Control Theory and Adolescent Drug Use |url=http://journals.sagepub.com/doi/10.1177/0044118X88019004003 |journal=Youth & Society |language=en |volume=19 |issue=4 |pages=395–425 |doi=10.1177/0044118X88019004003 |s2cid=143860602 |issn=0044-118X}}</ref><!--[[Psychological trauma|Traumatic experiences]] have been linked to the development of [[Substance-related disorder|addictive and substance-related problems]].<ref name="pmid8711018">{{cite journal | vauthors = Stewart SH | title = Alcohol abuse in individuals exposed to trauma: a critical review | journal = Psychological Bulletin | volume = 120 | issue = 1 | pages = 83–112 | date = July 1996 | pmid = 8711018 | doi = 10.1037/0033-2909.120.1.83}}</ref><ref>{{cite book | vauthors = Bailey KM, Stewart SH | chapter = Relations among trauma, PTSD, and substance misuse: The scope of the problem. | title = Trauma and Substance Abuse: Causes, Consequences, and Treatment of Comorbid Disorders | edition = 2nd | veditors = Ouimette P, Read JP | publisher = American Psychological Association | location = Washington, DC| date = 2014 | pages = 11–34 }}</ref> Interpersonal traumas, such as [[child abuse]] and [[Assault|violent assaults]], are particularly predictive of substance-related problems.<ref>{{cite journal | vauthors = Guina J, Nahhas RW, Goldberg AJ, Farnsworth S | title = PTSD Symptom Severities, Interpersonal Traumas, and Benzodiazepines Are Associated with Substance-Related Problems in Trauma Patients | journal = Journal of Clinical Medicine | volume = 5 | issue = 8 | pages = 70 | date = August 2016 | pmid = 27517964 | pmc = 4999790 | doi = 10.3390/jcm5080070 }}</ref><ref name="pmid20472211">{{cite journal | vauthors = Ford JD, Elhai JD, Connor DF, Frueh BC | title = Poly-victimization and risk of posttraumatic, depressive, and substance use disorders and involvement in delinquency in a national sample of adolescents | journal = The Journal of Adolescent Health | volume = 46 | issue = 6 | pages = 545–52 | date = June 2010 | pmid = 20472211 | doi = 10.1016/j.jadohealth.2009.11.212 }}</ref><ref>{{cite journal = Sullivan TP, Cavanaugh CE, Buckner JD, Edmondson D | title = Intimate partner violence (IPV) and drug and alcohol use problems among community women: The roles of physical, sexual, and psychological IPV and PTSD. | journal = J. Trauma Stress | date = 2009 | volume = 22 | pages = 575–84 }}</ref>
-->

=== Age ===
Adolescence represents a period of increased vulnerability for developing an addiction.<ref>{{cite journal | vauthors = Spear LP | title = The adolescent brain and age-related behavioral manifestations | journal = Neuroscience and Biobehavioral Reviews | volume = 24 | issue = 4 | pages = 417–63 | date = June 2000 | pmid = 10817843 | doi = 10.1016/s0149-7634(00)00014-2 | citeseerx = 10.1.1.461.3295 | s2cid = 14686245 }}</ref> In adolescence, the incentive-rewards systems in the brain mature well before the cognitive control center. This consequentially grants the incentive-rewards systems a disproportionate amount of power in the behavioral decision-making process. Therefore, adolescents are increasingly likely to act on their impulses and engage in risky, potentially addicting behavior before considering the consequences.<ref>{{cite journal | vauthors = Hammond CJ, Mayes LC, Potenza MN | title = Neurobiology of adolescent substance use and addictive behaviors: treatment implications | journal = Adolescent Medicine | volume = 25 | issue = 1 | pages = 15–32 | date = April 2014 | pmid = 25022184 | pmc = 4446977 }}</ref> Not only are adolescents more likely to initiate and maintain drug use, but once addicted they are more resistant to treatment and more liable to relapse.<ref>{{cite journal | vauthors = Catalano RF, Hawkins JD, Wells EA, Miller J, Brewer D | title = Evaluation of the effectiveness of adolescent drug abuse treatment, assessment of risks for relapse, and promising approaches for relapse prevention | journal = The International Journal of the Addictions | volume = 25 | issue = 9A–10A | pages = 1085–140 | pmid = 2131328 | year=1990| doi = 10.3109/10826089109081039 }}</ref><ref>{{cite journal | vauthors = Perepletchikova F, Krystal JH, Kaufman J | title = Practitioner review: adolescent alcohol use disorders: assessment and treatment issues | journal = Journal of Child Psychology and Psychiatry, and Allied Disciplines | volume = 49 | issue = 11 | pages = 1131–54 | date = November 2008 | pmid = 19017028 | pmc = 4113213 | doi = 10.1111/j.1469-7610.2008.01934.x }}</ref>

Most individuals are exposed to and use addictive drugs for the first time during their teenage years.<ref name="Drug use trends" /> In the United States, there were just over 2.8&nbsp;million new users of illicit drugs in 2013 (7,800 new users per day);<ref name="Drug use trends" /> among them, 54.1% were under 18&nbsp;years of age.<ref name="Drug use trends">{{cite web|title=Nationwide Trends|url=http://www.drugabuse.gov/publications/drugfacts/nationwide-trends|publisher=National Institute on Drug Abuse|access-date=15 December 2017|date=June 2015}}</ref> In 2011, there were approximately 20.6&nbsp;million people in the United States over the age of 12 with an addiction.<ref name="AddictionCenter">{{Cite news|url=https://www.addictioncenter.com/addiction/addiction-statistics/|title=Addiction Statistics – Facts on Drug and Alcohol Addiction|work=AddictionCenter|access-date=17 September 2018}}</ref> Over 90% of those with an addiction began drinking, smoking or using illicit drugs before the age of 18.<ref name="AddictionCenter" />

=== Comorbid disorders ===
Individuals with [[comorbid]] (i.e., co-occurring) [[mental health]] disorders such as depression, anxiety, attention-deficit/hyperactivity disorder (ADHD) or post-traumatic stress disorder are more likely to develop substance use disorders.<ref>{{Cite web|url=https://www.samhsa.gov/capt/practicing-effective-prevention/prevention-behavioral-health/risk-protective-factors|title=Risk and Protective Factors|last=SAMHSA|publisher=Substance Abuse and Mental Health Administration|access-date=19 December 2016|archive-url=https://web.archive.org/web/20161208181514/http://www.samhsa.gov/capt/practicing-effective-prevention/prevention-behavioral-health/risk-protective-factors|archive-date=8 December 2016|url-status=dead}}</ref><ref>{{Cite web|url=http://www.recoveryanswers.org/pressrelease/infographic-risk-factors-addiction/|title=Infographic – Risk Factors of Addiction {{!}} Recovery Research Institute|website=www.recoveryanswers.org|access-date=19 December 2016|archive-url=https://web.archive.org/web/20161217014124/http://www.recoveryanswers.org/pressrelease/infographic-risk-factors-addiction/|archive-date=17 December 2016|url-status=dead}}</ref><ref>{{Cite web|url=http://www.mayoclinic.org/diseases-conditions/drug-addiction/basics/risk-factors/con-20020970|title=Drug addiction Risk factors – Mayo Clinic|website=www.mayoclinic.org|access-date=19 December 2016}}</ref><ref name="Skylstad2022" /> The {{Abbr|NIDA|National Institute on Drug Abuse}} cites early aggressive behavior as a risk factor for substance use.<ref name="Abuse" /> The [[National Bureau of Economic Research]] found that there is a "definite connection between mental illness and the use of addictive substances" and a majority of mental health patients participate in the use of these substances: 38% alcohol, 44% cocaine, and 40% cigarettes.<ref>{{Cite news|url=https://www.dualdiagnosis.org/mental-health-and-addiction/the-connection/|title=The Connection Between Mental Illness and Substance Abuse {{!}} Dual Diagnosis|work=Dual Diagnosis|access-date=17 September 2018}}</ref>

=== Epigenetic ===
[[Epigenetics]] is the study of stable [[Phenotype|phenotypic]] changes that do not involve alterations in the DNA sequence.<ref>{{cite journal | vauthors = Dupont C, Armant DR, Brenner CA | title = Epigenetics: definition, mechanisms and clinical perspective | journal = Seminars in Reproductive Medicine | volume = 27 | issue = 5 | pages = 351–357 | date = September 2009 | pmid = 19711245 | pmc = 2791696 | doi = 10.1055/s-0029-1237423 }}</ref> Illicit drug use has been found to cause epigenetic changes in [[DNA methylation]], as well as [[chromatin remodeling]].<ref name="Nielsen_2012">{{cite journal | vauthors = Nielsen DA, Utrankar A, Reyes JA, Simons DD, Kosten TR | title = Epigenetics of drug abuse: predisposition or response | journal = Pharmacogenomics | volume = 13 | issue = 10 | pages = 1149–1160 | date = July 2012 | pmid = 22909205 | pmc = 3463407 | doi = 10.2217/pgs.12.94 }}</ref> The epigenetic state of chromatin may pose as a risk for the development of substance addictions.<ref name="Nielsen_2012" /> It has been found that emotional stressors, as well as social adversities may lead to an initial epigenetic response, which causes an alteration to the reward-signalling pathways.<ref name="Nielsen_2012" /> This change may predispose one to experience a positive response to drug use.<ref name="Nielsen_2012" />

==== Transgenerational epigenetic inheritance ====
{{Main|Transgenerational epigenetic inheritance}}

[[Epigenetic]] genes and their products (e.g., proteins) are the key components through which environmental influences can affect the genes of an individual:<ref name="Transgenerational epigenetic inheritance in addiction" /> they serve as the mechanism responsible for [[transgenerational epigenetic inheritance]], a phenomenon in which environmental influences on the genes of a parent can affect the associated traits and [[behavioral phenotype]]s of their offspring (e.g., behavioral responses to environmental stimuli).<ref name="Transgenerational epigenetic inheritance in addiction" /> In addiction, epigenetic mechanisms play a central role in the [[pathophysiology]] of the disease;<ref name="Cellular basis" /> it has been noted that some of the alterations to the [[epigenome]] which arise through chronic exposure to addictive stimuli during an addiction can be transmitted across generations, in turn affecting the behavior of one's children (e.g., the child's behavioral responses to addictive drugs and natural rewards).<ref name="Transgenerational epigenetic inheritance in addiction">{{cite journal | vauthors = Vassoler FM, Sadri-Vakili G | title = Mechanisms of transgenerational inheritance of addictive-like behaviors | journal = Neuroscience | volume = 264 | pages = 198–206 | year = 2014 | pmid = 23920159 | pmc = 3872494 | doi = 10.1016/j.neuroscience.2013.07.064 | quote = However, the components that are responsible for the heritability of characteristics that make an individual more susceptible to drug addiction in humans remain largely unknown given that patterns of inheritance cannot be explained by simple genetic mechanisms (Cloninger et al., 1981; Schuckit et al., 1972). The environment plays a large role in the development of addiction as evidenced by great societal variability in drug use patterns between countries and across time (UNODC, 2012). Therefore, both genetics and the environment contribute to an individual's vulnerability to become addicted following an initial exposure to drugs of abuse.&nbsp;...<br />The evidence presented here demonstrates that rapid environmental adaptation occurs following exposure to a number of stimuli. Epigenetic mechanisms represent the key components by which the environment can influence genetics, and they provide the missing link between genetic heritability and environmental influences on the behavioral and physiological phenotypes of the offspring.}}</ref><ref name="pmid26572641">{{cite journal | vauthors = Yuan TF, Li A, Sun X, Ouyang H, Campos C, Rocha NB, Arias-Carrión O, Machado S, Hou G, So KF | title = Transgenerational Inheritance of Paternal Neurobehavioral Phenotypes: Stress, Addiction, Ageing and Metabolism | journal = Mol. Neurobiol. | volume = 53| issue = 9| pages = 6367–76| year = 2015 | pmid = 26572641 | doi = 10.1007/s12035-015-9526-2 | hdl = 10400.22/7331 | s2cid = 25694221 | hdl-access = free }}</ref>

The general classes of epigenetic alterations that have been implicated in transgenerational epigenetic inheritance include DNA methylation, [[histone modification]]s, and [[Downregulation and upregulation|downregulation or upregulation]] of [[microRNA]]s.<ref name="Transgenerational epigenetic inheritance in addiction" /> With respect to addiction, more research is needed to determine the specific [[Heredity|heritable]] epigenetic alterations that arise from various forms of addiction in humans and the corresponding behavioral phenotypes from these epigenetic alterations that occur in human offspring.<ref name="Transgenerational epigenetic inheritance in addiction" /><ref name="pmid26572641" /> Based on preclinical evidence from [[animal research]], certain addiction-induced epigenetic alterations in rats can be transmitted from parent to offspring and produce behavioral phenotypes that decrease the offspring's risk of developing an addiction.{{#tag:ref|According to a review of experimental animal models that examined the transgenerational epigenetic inheritance of [[epigenetic mark]]s that occur in addiction, alterations in [[histone acetylation]] – specifically, di-acetylation of [[lysine]] [[residue (amino acid)|residues]] 9 and 14 on [[histone 3]] (i.e., [[H3K9ac2]] and [[H3K14ac2]]) in association with [[BDNF]] [[gene promoter]]s – have been shown to occur within the [[medial prefrontal cortex]] (mPFC), [[testes]], and [[sperm]] of cocaine-addicted male rats.<ref name="Transgenerational epigenetic inheritance in addiction" /> These epigenetic alterations in the rat mPFC result in increased BDNF [[gene expression]] within the mPFC, which in turn blunts the [[Reward system|rewarding properties]] of cocaine and reduces cocaine [[self-administration]].<ref name="Transgenerational epigenetic inheritance in addiction" /> The male but not female offspring of these cocaine-exposed rats inherited both epigenetic marks (i.e., di-acetylation of lysine residues 9 and 14 on histone 3) within mPFC neurons, the corresponding increase in BDNF expression within mPFC neurons, and the behavioral phenotype associated with these effects (i.e., a reduction in cocaine reward, resulting in reduced cocaine-seeking by these male offspring).<ref name="Transgenerational epigenetic inheritance in addiction" /> Consequently, the transmission of these two cocaine-induced epigenetic alterations (i.e., H3K9ac2 and H3K14ac2) in rats from male fathers to male offspring served to reduce the offspring's risk of developing an addiction to cocaine.<ref name="Transgenerational epigenetic inheritance in addiction" /> {{As of|2018|post=,}} neither the heritability of these epigenetic marks in humans nor the behavioral effects of the marks within human mPFC neurons has been established.<ref name="Transgenerational epigenetic inheritance in addiction" />|group="note"}}<ref name="Transgenerational epigenetic inheritance in addiction" /> More generally, the heritable behavioral phenotypes that are derived from addiction-induced epigenetic alterations and transmitted from parent to offspring may serve to either increase or decrease the offspring's risk of developing an addiction.<ref name="Transgenerational epigenetic inheritance in addiction" /><ref name="pmid26572641" />

==Mechanisms{{anchor|Biomolecular mechanisms}}==
Addiction is a disorder of the brain's reward system developing through [[transcriptional]] and epigenetic mechanisms as a result of chronically high levels of exposure to an addictive stimulus (e.g., eating food, the use of cocaine, engagement in sexual activity, participation in high-thrill cultural activities such as gambling, etc.) over extended time.<ref name="Cellular basis" /><ref name="What the ΔFosB?" /><ref name="Natural and drug addictions" /> [[FOSB#DeltaFosB|DeltaFosB]] (ΔFosB), a gene [[transcription factor]], is a critical component and common factor in the development of virtually all forms of behavioral and drug addictions.<ref name="What the ΔFosB?" /><ref name="Natural and drug addictions" /><ref name="G9a reverses ΔFosB plasticity" /><ref name="Nestler" /> Two decades of research into ΔFosB's role in addiction have demonstrated that addiction arises, and the associated compulsive behavior intensifies or attenuates, along with the [[overexpression]] of ΔFosB in the [[D1-type]] [[medium spiny neuron]]s of the nucleus accumbens.<ref name="Cellular basis" /><ref name="What the ΔFosB?" /><ref name="Natural and drug addictions" /><ref name="G9a reverses ΔFosB plasticity" /> Due to the causal relationship between ΔFosB expression and addictions, it is used [[preclinical research|preclinically]] as an addiction [[biomarker (medicine)|biomarker]].<ref name="Cellular basis" /><ref name="What the ΔFosB?">{{cite journal | vauthors = Ruffle JK | title = Molecular neurobiology of addiction: what's all the (Δ)FosB about? | journal = Am. J. Drug Alcohol Abuse | volume = 40 | issue = 6 | pages = 428–37 | date = November 2014 | pmid = 25083822 | doi = 10.3109/00952990.2014.933840 | s2cid = 19157711 | quote = ΔFosB is an essential transcription factor implicated in the molecular and behavioral pathways of addiction following repeated drug exposure. The formation of ΔFosB in multiple brain regions, and the molecular pathway leading to the formation of AP-1 complexes is well understood. The establishment of a functional purpose for ΔFosB has allowed further determination as to some of the key aspects of its molecular cascades[...]As a consequence of our improved understanding of ΔFosB in addiction, it is possible to evaluate the addictive potential of current medications (119), as well as use it as a biomarker for assessing the efficacy of therapeutic interventions (121,122,124). Some of these proposed interventions have limitations (125) or are in their infancy (75). However, it is hoped that some of these preliminary findings may lead to innovative treatments, which are much needed in addiction.}}</ref><ref name="G9a reverses ΔFosB plasticity">{{cite journal | vauthors = Biliński P, Wojtyła A, Kapka-Skrzypczak L, Chwedorowicz R, Cyranka M, Studziński T | title = Epigenetic regulation in drug addiction | journal = Ann. Agric. Environ. Med. | volume = 19 | issue = 3 | pages = 491–96 | year = 2012 | pmid = 23020045 |url=http://www.aaem.pl/fulltext.php?ICID=1010966 | quote = [...]ΔFosB is considered a primary and causative transcription factor in creating new neural connections in the reward centre, prefrontal cortex, and other regions of the limbic system. This is reflected in the increased, stable and long-lasting level of sensitivity to cocaine and other drugs, and tendency to relapse even after long periods of abstinence.}}</ref> ΔFosB expression in these neurons directly and positively regulates drug self-administration and [[#Sensitization|reward sensitization]] through positive reinforcement, while decreasing sensitivity to aversion.{{#tag:ref|A decrease in aversion sensitivity, in simpler terms, means that an individual's behavior is less likely to be influenced by undesirable outcomes.|group="note"|name="ΔFosB behaviors"}}<ref name="Cellular basis" /><ref name="What the ΔFosB?" />

{{Transcription factor glossary|width=610px}}
{{Psychostimulant addiction|Colorcode=yes|align=right}}
Chronic addictive drug use causes alterations in gene expression in the [[mesocorticolimbic projection]].<ref name="Nestler" /><ref name="Nestler, Hyman, and Malenka 2">{{cite journal |vauthors=Hyman SE, Malenka RC, Nestler EJ |title=Neural mechanisms of addiction: the role of reward-related learning and memory |journal=Annu. Rev. Neurosci. |volume=29 |pages=565–98 |year=2006 |pmid=16776597 |doi=10.1146/annurev.neuro.29.051605.113009 }}</ref><ref name="Addiction genetics">{{cite journal |vauthors=Steiner H, Van Waes V |title=Addiction-related gene regulation: risks of exposure to cognitive enhancers vs. other psychostimulants |journal=Prog. Neurobiol. |volume=100 |pages=60–80 |date=January 2013 |pmid=23085425 |pmc=3525776 |doi=10.1016/j.pneurobio.2012.10.001 }}</ref> The most important transcription factors that produce these alterations are ΔFosB, [[cyclic adenosine monophosphate|cAMP]] response element binding protein ([[cAMP response element binding protein|CREB]]), and nuclear factor kappa B ([[nuclear factor kappa B|NF-κB]]).<ref name="Nestler" /> ΔFosB is the most significant biomolecular mechanism in addiction because the overexpression of ΔFosB in the D1-type medium spiny neurons in the nucleus accumbens is [[necessary and sufficient]] for many of the neural adaptations and behavioral effects (e.g., expression-dependent increases in drug self-administration and [[#Sensitization|reward sensitization]]) seen in drug addiction.<ref name="Nestler" /> ΔFosB expression in nucleus accumbens D1-type medium spiny neurons directly and positively regulates drug [[self-administration]] and [[#Sensitization|reward sensitization]] through positive reinforcement while decreasing sensitivity to [[wikt:aversion|aversion]].<ref name="ΔFosB behaviors" group="note" /><ref name="Cellular basis" /><ref name="What the ΔFosB?" /> ΔFosB has been implicated in mediating addictions to many different drugs and drug classes, including alcohol, amphetamine and other [[substituted amphetamines]], [[cannabinoid]]s, [[cocaine]], [[methylphenidate]], [[nicotine]], [[opiates]], [[phenylcyclidine]], and [[propofol]], among others.<ref name="What the ΔFosB?" /><!--Preceding review covers ΔFosB in propofol addiction--><ref name="Nestler" /><ref name="Nestler, Hyman, and Malenka 2" /><ref name="Alcoholism ΔFosB">{{cite web | title=Alcoholism – Homo sapiens (human) | url=http://www.genome.jp/kegg-bin/show_pathway?hsa05034+2354 | work=KEGG Pathway | access-date=10 April 2014 | author=Kanehisa Laboratories | date=2 August 2013}}</ref><ref name="MPH ΔFosB">{{cite journal | vauthors = Kim Y, Teylan MA, Baron M, Sands A, Nairn AC, Greengard P | title = Methylphenidate-induced dendritic spine formation and DeltaFosB expression in nucleus accumbens | journal = Proc. Natl. Acad. Sci. USA | volume = 106 | issue = 8 | pages = 2915–20 | date = February 2009 | pmid = 19202072 | pmc = 2650365 | doi = 10.1073/pnas.0813179106 | quote = <!--Despite decades of clinical use of methylphenidate for ADHD, concerns have been raised that long-term treatment of children with this medication may result in subsequent drug abuse and addiction.&nbsp;... Thus, although oral administration of clinical doses of methylphenidate is not associated with euphoria or with abuse problems, nontherapeutic use of high doses or i.v. administration may lead to addiction (39, 40).--> | bibcode = 2009PNAS..106.2915K| doi-access = free }}</ref> [[ΔJunD]], a transcription factor, and [[EHMT2|G9a]], a [[histone methyltransferase]], both oppose the function of ΔFosB and inhibit increases in its expression.<ref name="Cellular basis" /><ref name="Nestler" /><ref name="Nestler 2014 epigenetics">{{cite journal | vauthors = Nestler EJ | title = Epigenetic mechanisms of drug addiction | journal = Neuropharmacology | volume = 76 | issue = Pt B | pages = 259–68 | date = January 2014 | pmid = 23643695 | pmc = 3766384 | doi = 10.1016/j.neuropharm.2013.04.004 | quote = Short-term increases in histone acetylation generally promote behavioral responses to the drugs, while sustained increases oppose cocaine's effects, based on the actions of systemic or intra-NAc administration of HDAC inhibitors.&nbsp;... Genetic or pharmacological blockade of G9a in the NAc potentiates behavioral responses to cocaine and opiates, whereas increasing G9a function exerts the opposite effect (Maze et al., 2010; Sun et al., 2012a). Such drug-induced downregulation of G9a and H3K9me2 also sensitizes animals to the deleterious effects of subsequent chronic stress (Covington et al., 2011). Downregulation of G9a increases the dendritic arborization of NAc neurons, and is associated with increased expression of numerous proteins implicated in synaptic function, which directly connects altered G9a/H3K9me2 in the synaptic plasticity associated with addiction (Maze et al., 2010).<br />G9a appears to be a critical control point for epigenetic regulation in NAc, as we know it functions in two negative feedback loops. It opposes the induction of ΔFosB, a long-lasting transcription factor important for drug addiction (Robison and Nestler, 2011), while ΔFosB in turn suppresses G9a expression (Maze et al., 2010; Sun et al., 2012a).&nbsp;... Also, G9a is induced in NAc upon prolonged HDAC inhibition, which explains the paradoxical attenuation of cocaine's behavioral effects seen under these conditions, as noted above (Kennedy et al., 2013). GABAA receptor subunit genes are among those that are controlled by this feedback loop. Thus, chronic cocaine, or prolonged HDAC inhibition, induces several GABAA receptor subunits in NAc, which is associated with increased frequency of inhibitory postsynaptic currents (IPSCs). In striking contrast, combined exposure to cocaine and HDAC inhibition, which triggers the induction of G9a and increased global levels of H3K9me2, leads to blockade of GABAA receptor and IPSC regulation. }}</ref> Increases in nucleus accumbens ΔJunD expression (via [[viral vector]]-mediated gene transfer) or G9a expression (via pharmacological means) reduces, or with a large increase can even block, many of the neural and behavioral alterations that result from chronic high-dose use of addictive drugs (i.e., the alterations mediated by ΔFosB).<ref name="G9a reverses ΔFosB plasticity" /><ref name="Nestler" />

ΔFosB plays an important role in regulating behavioral responses to natural rewards, such as palatable food, sex, and exercise.<ref name="Nestler" /><ref name="ΔFosB reward">{{cite journal |vauthors=Blum K, Werner T, Carnes S, Carnes P, Bowirrat A, Giordano J, Oscar-Berman M, Gold M | title = Sex, drugs, and rock 'n' roll: hypothesizing common mesolimbic activation as a function of reward gene polymorphisms | journal = Journal of Psychoactive Drugs | volume = 44 | issue = 1 | pages = 38–55 | year = 2012 | pmid = 22641964 | pmc = 4040958 | doi = 10.1080/02791072.2012.662112| quote = 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.&nbsp;... 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. }}</ref> Natural rewards, like drugs of abuse, [[inducible gene|induce gene expression]] of ΔFosB in the nucleus accumbens, and chronic acquisition of these rewards can result in a similar pathological addictive state through ΔFosB overexpression.<ref name="Natural and drug addictions">{{cite journal | vauthors = Olsen CM | title = Natural rewards, neuroplasticity, and non-drug addictions | journal = Neuropharmacology | volume = 61 | issue = 7 | pages = 1109–22 |date=December 2011 | pmid = 21459101 | pmc = 3139704 | doi = 10.1016/j.neuropharm.2011.03.010 | quote = Functional neuroimaging studies in humans have shown that gambling (Breiter et al, 2001), shopping (Knutson et al, 2007), orgasm ([[Barry Komisaruk|Komisaruk]] et al, 2004), playing video games (Koepp et al, 1998; Hoeft et al, 2008) and the sight of appetizing food (Wang et al, 2004a) activate many of the same brain regions (i.e., the mesocorticolimbic system and extended amygdala) as drugs of abuse (Volkow et al, 2004).&nbsp;... Cross-sensitization is also bidirectional, as a history of amphetamine administration facilitates sexual behavior and enhances the associated increase in NAc DA&nbsp;... As described for food reward, sexual experience can also lead to activation of plasticity-related signaling cascades. The transcription factor delta FosB is increased in the NAc, PFC, dorsal striatum, and VTA following repeated sexual behavior (Wallace et al., 2008; Pitchers et al., 2010b). This natural increase in delta FosB or viral overexpression of delta FosB within the NAc modulates sexual performance, and NAc blockade of delta FosB attenuates this behavior (Hedges et al, 2009; Pitchers et al., 2010b). Further, viral overexpression of delta FosB enhances the conditioned place preference for an environment paired with sexual experience (Hedges et al., 2009).&nbsp;... In some people, there is a transition from "normal" to compulsive engagement in natural rewards (such as food or sex), a condition that some have termed behavioral or non-drug addictions (Holden, 2001; Grant et al., 2006a).&nbsp;... In humans, the role of dopamine signaling in incentive-sensitization processes has recently been highlighted by the observation of a dopamine dysregulation syndrome in some people taking dopaminergic drugs. This syndrome is characterized by a medication-induced increase in (or compulsive) engagement in non-drug rewards such as gambling, shopping, or sex (Evans et al, 2006; Aiken, 2007; Lader, 2008)."}}<br /><!--The following link is outside the template to make it hyperlinked while appearing to be part of the quote.-->[https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3139704/table/T1/ Table 1: Summary of plasticity observed following exposure to drug or natural reinforcers]"</ref><ref name="Nestler" /><ref name="ΔFosB reward" /> Consequently, ΔFosB is the key transcription factor involved in addictions to natural rewards (i.e., behavioral addictions) as well;<ref name="Nestler">{{cite journal |vauthors=Robison AJ, Nestler EJ | title = Transcriptional and epigenetic mechanisms of addiction | journal = Nat. Rev. Neurosci. | volume = 12 | issue = 11 | pages = 623–37 |date=November 2011 | pmid = 21989194 | pmc = 3272277 | doi = 10.1038/nrn3111 | quote = ΔFosB has been linked directly to several addiction-related behaviors&nbsp;... 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 exposure<sup>14,22–24</sup>. This indicates that ΔFosB is both necessary and sufficient for many of the changes wrought in the brain by chronic drug exposure. ΔFosB is 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 consumption<sup>14,26–30</sup>. This implicates ΔFosB in the regulation of natural rewards under normal conditions and perhaps during pathological addictive-like states. }}</ref><ref name="Natural and drug addictions" /><ref name="ΔFosB reward" /> in particular, ΔFosB in the nucleus accumbens is critical for the [[reinforcing]] effects of sexual reward.<ref name="ΔFosB reward" /> Research on the interaction between natural and drug rewards suggests that dopaminergic psychostimulants (e.g., amphetamine) and sexual behavior act on similar biomolecular mechanisms to induce ΔFosB in the nucleus accumbens and possess bidirectional cross-[[sensitization]] effects that are mediated through ΔFosB.<ref name="Natural and drug addictions" /><ref name="Amph-Sex X-sensitization through D1 signaling"><!--Supplemental primary source-->{{cite journal |vauthors=Pitchers KK, Vialou V, Nestler EJ, Laviolette SR, Lehman MN, Coolen LM | title = Natural and drug rewards act on common neural plasticity mechanisms with ΔFosB as a key mediator |journal=[[The Journal of Neuroscience]] |volume=33 | issue = 8 | pages = 3434–42 |date=February 2013 | pmid = 23426671 | pmc = 3865508 | doi = 10.1523/JNEUROSCI.4881-12.2013 | quote = Drugs of abuse induce neuroplasticity in the natural reward pathway, specifically the nucleus accumbens (NAc), thereby causing development and expression of addictive behavior.&nbsp;... 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.&nbsp;... Sexual behavior is highly rewarding (Tenk et al., 2009), and sexual experience causes sensitized drug-related behaviors, including cross-sensitization to amphetamine (Amph)-induced locomotor activity (Bradley and Meisel, 2001; Pitchers et al., 2010a) and enhanced Amph reward (Pitchers et al., 2010a). Moreover, sexual experience induces neural plasticity in the NAc similar to that induced by psychostimulant exposure, including increased dendritic spine density (Meisel and Mullins, 2006; Pitchers et al., 2010a), altered glutamate receptor trafficking, and decreased synaptic strength in prefrontal cortex-responding NAc shell neurons (Pitchers et al., 2012). Finally, periods of abstinence from sexual experience were found to be critical for enhanced Amph reward, NAc spinogenesis (Pitchers et al., 2010a), and glutamate receptor trafficking (Pitchers et al., 2012). These findings suggest that natural and drug reward experiences share common mechanisms of neural plasticity}}</ref><ref name="Amph-Sex X-sensitization through NMDA signaling"><!--Supplemental primary source-->{{cite journal | vauthors = Beloate LN, Weems PW, Casey GR, Webb IC, Coolen LM | title = Nucleus accumbens NMDA receptor activation regulates amphetamine cross-sensitization and deltaFosB expression following sexual experience in male rats | journal = Neuropharmacology | volume = 101 | pages = 154–64 | date = February 2016 | pmid = 26391065 | doi = 10.1016/j.neuropharm.2015.09.023 | s2cid = 25317397 }}</ref> This phenomenon is notable since, in humans, a dopamine dysregulation syndrome, characterized by drug-induced compulsive engagement in natural rewards (specifically, sexual activity, shopping, and gambling), has been observed in some individuals taking [[dopaminergic]] medications.<ref name="Natural and drug addictions" />

ΔFosB inhibitors (drugs or treatments that oppose its action) may be an effective treatment for addiction and addictive disorders.<ref name="Malenka_2009_04">{{cite book |vauthors=Malenka RC, Nestler EJ, Hyman SE |veditors=Sydor A, Brown RY | title = Molecular Neuropharmacology: A Foundation for Clinical Neuroscience | year = 2009 | publisher = McGraw-Hill Medical | location = New York | isbn = 978-0-07-148127-4 | pages = 384–85 | edition = 2nd | chapter = Chapter 15: Reinforcement and addictive disorders }}</ref>

The release of dopamine in the nucleus accumbens plays a role in the reinforcing qualities of many forms of stimuli, including naturally reinforcing stimuli like palatable food and sex.<ref name=Salamone>{{cite journal | vauthors = Salamone JD | title = Complex motor and sensorimotor functions of striatal and accumbens dopamine: involvement in instrumental behavior processes | journal = Psychopharmacology | volume = 107 | issue = 2–3 | pages = 160–74 | year = 1992 | pmid = 1615120 | doi = 10.1007/bf02245133 | s2cid = 30545845 }}</ref><ref name=Kauer>{{cite journal | vauthors = Kauer JA, Malenka RC | title = Synaptic plasticity and addiction | journal = Nature Reviews. Neuroscience | volume = 8 | issue = 11 | pages = 844–58 | date = November 2007 | pmid = 17948030 | doi = 10.1038/nrn2234 | s2cid = 38811195 | doi-access = free }}</ref><ref name="diGiacomo2022" /> Altered dopamine [[neurotransmission]] is frequently observed following the development of an addictive state.<ref name="Natural and drug addictions" /><ref name="Levy2019" /> In humans and lab animals that have developed an addiction, alterations in dopamine or [[opioid]] neurotransmission in the nucleus accumbens and other parts of the striatum are evident.<ref name="Natural and drug addictions" /> Use of certain drugs (e.g., cocaine) affect [[cholinergic neuron]]s that innervate the reward system, in turn affecting dopamine signaling in this region.<ref name=Witten>{{cite journal | vauthors = Witten IB, Lin SC, Brodsky M, Prakash R, Diester I, Anikeeva P, Gradinaru V, Ramakrishnan C, Deisseroth K | title = Cholinergic interneurons control local circuit activity and cocaine conditioning | journal = Science | volume = 330 | issue = 6011 | pages = 1677–81 | date = December 2010 | pmid = 21164015 | pmc = 3142356 | doi = 10.1126/science.1193771 | bibcode = 2010Sci...330.1677W }}</ref>

A recent study in [[Addiction (journal)|Addiction]] reports that [[GLP-1 receptor agonist|GLP-1 agonist]] medications, such as [[semaglutide]], which are commonly used for [[diabetes]] and weight management, may also reduce the risk of overdose and alcohol intoxication in people with substance use disorders.<ref>{{Cite journal |last1=Qeadan |first1=Fares |last2=McCunn |first2=Ashlie |last3=Tingey |first3=Benjamin |date=2024-10-16 |title=The association between glucose-dependent insulinotropic polypeptide and/or glucagon-like peptide-1 receptor agonist prescriptions and substance-related outcomes in patients with opioid and alcohol use disorders: A real-world data analysis |url=https://onlinelibrary.wiley.com/doi/10.1111/add.16679 |journal=Addiction |language=en |doi=10.1111/add.16679 |issn=0965-2140|doi-access=free }}</ref> The study analyzed nearly nine years of health records from 1.3 million individuals across 136 U.S. hospitals, including 500,000 with opioid use disorder and over 800,000 with alcohol use disorder.<ref>{{Cite web |last=Shareef |first=Faizah |title=Weight loss drugs like Ozempic may help reduce overdose risks: Study |url=https://abcnews.go.com/Health/weight-loss-drugs-ozempic-reduce-overdose-risks-study/story?id=114875203 |access-date=2024-10-18 |website=ABC News |language=en}}</ref> Researchers found that those who used Ozempic or similar medications had a 40% lower risk of opioid overdose and a 50% lower risk of alcohol intoxication compared to those not using these drugs. 

===Reward system===
{{main|Reward system}}

====Mesocorticolimbic pathway====
{{Annotated image 4
| caption = Top: this depicts the initial effects of high dose exposure to an addictive drug on [[gene expression]] in the [[nucleus accumbens]] for various Fos family proteins (i.e., [[c-Fos]], [[FosB]], [[ΔFosB]], [[Fra1]], and [[Fra2]]).<br />Bottom: this illustrates the progressive increase in ΔFosB expression in the nucleus accumbens following repeated twice daily drug binges, where these [[phosphorylated]] (35–37&nbsp;[[kilodalton]]) ΔFosB [[isoform]]s persist in the [[D1-type]] [[medium spiny neurons]] of the nucleus accumbens for up to 2&nbsp;months.<!--The following named ref is transcluded in from "Template:Psychostimulant addiction"--><ref name="Nestler2" /><ref name="pmid11572966">{{cite journal |vauthors=Nestler EJ, Barrot M, Self DW | title = DeltaFosB: a sustained molecular switch for addiction | journal = Proc. Natl. Acad. Sci. U.S.A. | volume = 98 | issue = 20 | pages = 11042–46 |date=September 2001 | pmid = 11572966 | pmc = 58680 | doi = 10.1073/pnas.191352698 | quote = Although the ΔFosB signal is relatively long-lived, it is not permanent. ΔFosB degrades gradually and can no longer be detected in [the] brain after 1–2 months of drug withdrawal&nbsp;... Indeed, ΔFosB is the longest-lived adaptation known to occur in [the] adult brain, not only in response to drugs of abuse, but to any other perturbation (that doesn't involve lesions) as well. | bibcode = 2001PNAS...9811042N | doi-access = free }}</ref>
| header = ΔFosB accumulation from excessive drug use
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| alt = ΔFosB accumulation graph
| image = ΔFosB accumulation.svg
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Understanding the pathways in which drugs act and how drugs can alter those pathways is key when examining the biological basis of drug addiction. The reward pathway, known as the [[mesolimbic system|mesolimbic pathway]],<ref name="Levy2019" /> or its extension, the [[mesocorticolimbic pathway]], is characterized by the interaction of several areas of the brain.
* The projections from the [[ventral tegmentum|ventral tegmental area]] (VTA) are a network of [[dopaminergic]] [[neurons]] with [[wikt:colocalize|co-localized]] postsynaptic [[glutamate]] receptors ([[AMPAR]] and [[NMDAR]]). These cells respond when stimuli indicative of a reward are present.<ref name="diGiacomo2022" /> The VTA supports learning and sensitization development and releases dopamine (DA) into the [[forebrain]].<ref name="Jones and Bonci">{{cite journal |vauthors=Jones S, Bonci A |title=Synaptic plasticity and drug addiction |journal=Current Opinion in Pharmacology |volume=5 |issue=1 |pages=20–25 |year=2005 |pmid=15661621 |doi=10.1016/j.coph.2004.08.011}}</ref> These neurons project and release DA into the nucleus accumbens,<ref name="Eisch and Harburg">{{cite journal |vauthors=Eisch AJ, Harburg GC |title=Opiates, psychostimulants, and adult hippocampal neurogenesis: Insights for addiction and stem cell biology |journal=Hippocampus |volume=16 |issue=3 |pages=271–86 |year=2006 |pmid=16411230 |doi=10.1002/hipo.20161|s2cid=23667629 }}</ref> through the [[mesolimbic pathway]]. Virtually all drugs causing drug addiction increase the DA release in the mesolimbic pathway.<ref name=Rang>{{cite book | vauthors = Rang HP |title=Pharmacology |publisher=Churchill Livingstone |location=Edinburgh |year=2003 |page=596 |isbn=978-0-443-07145-4}}</ref><ref name="Levy2019" />
* The [[nucleus accumbens]] (NAcc) is one output of the VTA projections. The nucleus accumbens itself consists mainly of [[GABA]]ergic [[medium spiny neuron]]s (MSNs).<ref name="Kourrich">{{cite journal |vauthors=Kourrich S, Rothwell PE, Klug JR, Thomas MJ |title=Cocaine experience controls bidirectional synaptic plasticity in the nucleus accumbens |journal=J. Neurosci. |volume=27 |issue=30 |pages=7921–28 |year=2007 |pmid=17652583 |pmc=6672735 |doi=10.1523/JNEUROSCI.1859-07.2007}}</ref> The NAcc is associated with acquiring and eliciting conditioned behaviors, and is involved in the increased sensitivity to drugs as addiction progresses.<ref name="Jones and Bonci" /><ref name="Maxwell2020" /> Overexpression of [[ΔFosB]] in the nucleus accumbens is a necessary common factor in essentially all known forms of addiction;<ref name="Cellular basis" /> ΔFosB is a strong positive modulator of [[positively reinforced]] behaviors.<ref name="Cellular basis" />
* The [[prefrontal cortex]], including the [[anterior cingulate]] and [[orbitofrontal cortex|orbitofrontal]] cortices,<ref name="Kalivas and Volkow">{{cite journal | vauthors = Kalivas PW, Volkow ND | title = The neural basis of addiction: a pathology of motivation and choice | journal = The American Journal of Psychiatry | volume = 162 | issue = 8 | pages = 1403–13 | date = August 2005 | pmid = 16055761 | doi = 10.1176/appi.ajp.162.8.1403 }}</ref><ref name="Maxwell2020" /> is another VTA output in the mesocorticolimbic pathway; it is important for the integration of information which helps determine whether a behavior will be elicited.<ref name="Floresco">{{cite journal | vauthors = Floresco SB, Ghods-Sharifi S | title = Amygdala-prefrontal cortical circuitry regulates effort-based decision making | journal = Cerebral Cortex | volume = 17 | issue = 2 | pages = 251–60 | date = February 2007 | pmid = 16495432 | doi = 10.1093/cercor/bhj143 | citeseerx = 10.1.1.335.4681 }}</ref> It is critical for forming associations between the rewarding experience of drug use and cues in the environment. Importantly, these cues are strong mediators of drug-seeking behavior and can trigger relapse even after months or years of abstinence.<ref>{{cite journal | vauthors = Perry CJ, Zbukvic I, Kim JH, Lawrence AJ | title = Role of cues and contexts on drug-seeking behaviour | journal = British Journal of Pharmacology | volume = 171 | issue = 20 | pages = 4636–72 | date = October 2014 | pmid = 24749941 | pmc = 4209936 | doi = 10.1111/bph.12735 }}</ref><ref name="Levy2019" />
Other brain structures that are involved in addiction include:
* The [[basolateral amygdala]] projects into the NAcc and is thought to be important for motivation.<ref name="Floresco" />
* The [[hippocampus]] is involved in drug addiction, because of its role in learning and memory. Much of this evidence stems from investigations showing that manipulating cells in the hippocampus alters DA levels in NAcc and firing rates of VTA dopaminergic cells.<ref name="Eisch and Harburg" />

====Role of dopamine and glutamate====
Dopamine is the primary neurotransmitter of the reward system in the brain. It plays a role in regulating movement, emotion, cognition, motivation, and feelings of pleasure.<ref name=arch>{{cite journal | vauthors = Volkow ND, Fowler JS, Wang GJ, Swanson JM, Telang F | title = Dopamine in drug abuse and addiction: results of imaging studies and treatment implications | journal = Arch. Neurol. | volume = 64 | issue = 11 | pages = 1575–79 | year = 2007 | pmid = 17998440 | doi = 10.1001/archneur.64.11.1575 | doi-access = free }}</ref> Natural rewards, like eating, as well as recreational drug use cause a release of dopamine, and are associated with the reinforcing nature of these stimuli.<ref name=arch/><ref name=drugs-brain>{{cite web|url=http://www.drugabuse.gov/publications/science-addiction/drugs-brain|title=Drugs, Brains, and Behavior: The Science of Addiction|publisher=National Institute on Drug Abuse}}</ref><ref name="diGiacomo2022" /> Nearly all addictive drugs, directly or indirectly, act on the brain's reward system by heightening dopaminergic activity.<ref name=addict>{{cite web|url=http://www.drugabuse.gov/infofacts/understand.html|title=Understanding Drug Abuse and Addiction|publisher=National Institute on Drug Abuse|date=November 2012|access-date=12 February 2015|archive-date=16 August 2011|archive-url=https://web.archive.org/web/20110816044828/http://www.drugabuse.gov/infofacts/understand.html|url-status=dead}}</ref><ref name="Levy2019" />

Excessive intake of many types of addictive drugs results in repeated release of high amounts of dopamine, which in turn affects the reward pathway directly through heightened dopamine receptor activation. Prolonged and abnormally high levels of dopamine in the [[synaptic cleft]] can induce receptor downregulation in the neural pathway. Downregulation of [[mesolimbic]] dopamine receptors can result in a decrease in the sensitivity to natural reinforcers.<ref name=arch/>

Drug seeking behavior is induced by glutamatergic projections from the prefrontal cortex to the nucleus accumbens. This idea is supported with data from experiments showing that drug seeking behavior can be prevented following the inhibition of [[AMPA]] glutamate receptors and glutamate release in the nucleus accumbens.<ref name="Kalivas and Volkow" />

===Reward sensitization{{anchor|Sensitization|Drug sensitization}}===<!--"Drug sensitization" redirects here, do not change without correcting the redirect-->
{| class="wikitable" style="text-align:center; float:right; margin-left:1em;"
|+ Neural and behavioral effects of validated ΔFosB transcriptional targets in the [[striatum]]<ref name="What the ΔFosB?" /><ref name="pmid18640924">{{cite journal | vauthors = Nestler EJ |title=Review. Transcriptional mechanisms of addiction: role of DeltaFosB |journal=Philosophical Transactions of the Royal Society of London. Series B, Biological Sciences |volume=363 |issue=1507 |pages=3245–55 |date=October 2008 |pmid=18640924 |doi=10.1098/rstb.2008.0067 |pmc=2607320|quote=Recent evidence has shown that ΔFosB also represses the c-fos gene that helps create the molecular switch – from the induction of several short-lived Fos family proteins after acute drug exposure to the predominant accumulation of ΔFosB after chronic drug exposure&nbsp;– cited earlier (Renthal et al. in press). The mechanism responsible for ΔFosB repression of c-fos expression is complex and is covered below.&nbsp;...<br />Examples of validated targets for ΔFosB in nucleus accumbens&nbsp;... GluR2&nbsp;... dynorphin&nbsp;... Cdk5&nbsp;... NFκB&nbsp;... c-Fos}}<br />[https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2607320/table/tbl3/ Table 3]</ref>
! scope="col" | Target<br />gene
! scope="col" | Target<br />[[gene expression|expression]]
! scope="col" | Neural effects
! scope="col" | Behavioral effects
|-
| scope="row" style="height: 40px"| [[c-Fos]] || ↓ || Molecular switch enabling the chronic<br />induction of ΔFosB{{#tag:ref|In other words, c-Fos [[gene repression|repression]] allows ΔFosB to more rapidly accumulate within the D1-type medium spiny neurons of the nucleus accumbens because it is selectively induced in this state.<ref name="Cellular basis" /> Before c-Fos repression, all Fos family proteins (e.g., c-Fos, [[Fra1]], [[Fra2]], [[FosB]], and ΔFosB) are induced together, with ΔFosB expression increasing to a lesser extent.<ref name="Cellular basis" />|group="note"}} || –
|-
| scope="row" style="height: 40px"| [[dynorphin]] || ↓<br />{{#tag:ref|According to two medical reviews, ΔFosB has been implicated in causing both increases and decreases in dynorphin expression in different studies;<ref name="What the ΔFosB?" /><ref name="pmid18640924" /> this table entry reflects only a decrease. |group="note"}} || style="text-align:left" | {{bull}}Downregulation of [[κ-opioid receptor|κ-opioid]] feedback loop || style="text-align:left" | {{bull}}Increased drug reward
|-
| scope="row" style="height: 40px"| [[NF-κB]] || ↑ || style="text-align:left" | {{bull}}Expansion of [[Nucleus accumbens|NAcc]] dendritic processes<br />{{bull}}NF-κB inflammatory response in the {{abbr|NAcc|nucleus accumbens}}<br />{{bull}}NF-κB inflammatory response in the {{abbrlink|CP|caudate putamen}}|| style="text-align:left" | {{bull}}Increased drug reward<br />{{bull}}[[Stereotypy|Locomotor sensitization]]
|-
| scope="row" style="height: 40px"| [[GluR2]] || ↑ || style="text-align:left" | {{bull}}Decreased [[sensitization|sensitivity]] to [[glutamate]] || style="text-align:left" | {{bull}}Increased drug reward
|-
| scope="row" style="height: 40px"| [[Cdk5]] || ↑ || style="text-align:left" | {{bull}}[[GluR1]] synaptic protein phosphorylation<br />{{bull}}Expansion of {{abbr|NAcc|nucleus accumbens}} dendritic processes || Decreased drug reward<br /><small>(net effect)</small>
|}
'''Reward sensitization''' is a process that causes an increase in the amount of reward (specifically, [[incentive salience]]{{#tag:ref|Incentive salience, the "[[motivational salience]]" for a reward, is a "desire" or "want" attribute, which includes a motivational component, that the brain assigns to a rewarding stimulus.<ref name="Incentive salience and motivation review" /><ref name="NAcc function" /> As a consequence, incentive salience acts as a motivational "magnet" for a rewarding stimulus that commands attention, induces approach, and causes the rewarding stimulus to be sought out.<ref name="Incentive salience and motivation review">{{cite journal | vauthors = Berridge KC | title = From prediction error to incentive salience: mesolimbic computation of reward motivation | journal = Eur. J. Neurosci. | volume = 35 | issue = 7 | pages = 1124–43 | date = April 2012 | pmid = 22487042 | pmc = 3325516 | doi = 10.1111/j.1460-9568.2012.07990.x | quote = Here I discuss how mesocorticolimbic mechanisms generate the motivation component of incentive salience. Incentive salience takes Pavlovian learning and memory as one input and as an equally important input takes neurobiological state factors (e.g. drug states, appetite states, satiety states) that can vary independently of learning. Neurobiological state changes can produce unlearned fluctuations or even reversals in the ability of a previously learned reward cue to trigger motivation. Such fluctuations in cue-triggered motivation can dramatically depart from all previously learned values about the associated reward outcome.&nbsp;... Associative learning and prediction are important contributors to motivation for rewards. Learning gives incentive value to arbitrary cues such as a Pavlovian conditioned stimulus (CS) that is associated with a reward (unconditioned stimulus or UCS). Learned cues for reward are often potent triggers of desires. For example, learned cues can trigger normal appetites in everyone, and can sometimes trigger compulsive urges and relapse in individuals with addictions.<br />Cue-triggered 'wanting' for the UCS<br />A brief CS encounter (or brief UCS encounter) often primes a pulse of elevated motivation to obtain and consume more reward UCS. This is a signature feature of incentive salience.<br />Cue as attractive motivational magnets<br />When a Pavlovian CS+ is attributed with incentive salience it not only triggers 'wanting' for its UCS, but often the cue itself becomes highly attractive – even to an irrational degree. This cue attraction is another signature feature of incentive salience&nbsp;... Two recognizable features of incentive salience are often visible that can be used in neuroscience experiments: (i) UCS-directed 'wanting' – CS-triggered pulses of intensified 'wanting' for the UCS reward; and (ii) CS-directed 'wanting' – motivated attraction to the Pavlovian cue, which makes the arbitrary CS stimulus into a motivational magnet.}}</ref>|group="note"}}) that is assigned by the brain to a rewarding stimulus (e.g., a drug). In simple terms, when reward sensitization to a specific stimulus (e.g., a drug) occurs, an individual's "wanting" or desire for the stimulus itself and its associated [[cue reactivity|cues]] increases.<ref name="NAcc function">{{cite book |vauthors=Malenka RC, Nestler EJ, Hyman SE |veditors=Sydor A, Brown RY | title = Molecular Neuropharmacology: A Foundation for Clinical Neuroscience | year = 2009 | publisher = McGraw-Hill Medical | location = New York | isbn = 978-0-07-148127-4 | pages = 147–48, 366–67, 375–76 | edition = second | quote= VTA DA neurons play a critical role in motivation, reward-related behavior (Chapter 15), attention, and multiple forms of memory. This organization of the DA system, wide projection from a limited number of cell bodies, permits coordinated responses to potent new rewards. Thus, acting in diverse terminal fields, dopamine confers motivational salience ("wanting") on the reward itself or associated cues (nucleus accumbens shell region), updates the value placed on different goals in light of this new experience (orbital prefrontal cortex), helps consolidate multiple forms of memory (amygdala and hippocampus), and encodes new motor programs that will facilitate obtaining this reward in the future (nucleus accumbens core region and dorsal striatum). In this example, dopamine modulates the processing of sensorimotor information in diverse neural circuits to maximize the ability of the organism to obtain future rewards.&nbsp;...<br />The brain reward circuitry that is targeted by addictive drugs normally mediates the pleasure and strengthening of behaviors associated with natural reinforcers, such as food, water, and sexual contact. Dopamine neurons in the VTA are activated by food and water, and dopamine release in the NAc is stimulated by the presence of natural reinforcers, such as food, water, or a sexual partner.&nbsp;...<br />The NAc and VTA are central components of the circuitry underlying reward and memory of reward. As previously mentioned, the activity of dopaminergic neurons in the VTA appears to be linked to reward prediction. The NAc is involved in learning associated with reinforcement and the modulation of motoric responses to stimuli that satisfy internal homeostatic needs. The shell of the NAc appears to be particularly important to initial drug actions within reward circuitry; addictive drugs appear to have a greater effect on dopamine release in the shell than in the core of the NAc.&nbsp;... If motivational drive is described in terms of wanting, and hedonic evaluation in terms of liking, it appears that wanting can be dissociated from liking and that dopamine may influence these phenomena differently. Differences between wanting and liking are confirmed in reports by humans with addictions, who state that their desire for drugs (wanting) increases with continued use even when pleasure (liking) decreases because of tolerance.}}</ref><ref name="Incentive salience and motivation review" /><ref name="Reinforcement in addiction" /> Reward sensitization normally occurs following chronically high levels of exposure to the stimulus.<ref name="Levy2019" /> ΔFosB expression in D1-type medium spiny neurons in the nucleus accumbens has been shown to directly and positively regulate reward sensitization involving drugs and natural rewards.<ref name="Cellular basis" /><ref name="What the ΔFosB?" /><ref name="G9a reverses ΔFosB plasticity" />

"Cue-induced wanting" or "cue-triggered wanting", a form of craving that occurs in addiction, is responsible for most of the compulsive behavior that people with addictions exhibit.<ref name="Incentive salience and motivation review" /><ref name="Reinforcement in addiction">{{cite book |doi=10.1016/bs.pbr.2015.07.005 |chapter=Reinforcement principles for addiction medicine; from recreational drug use to psychiatric disorder |title=Neuroscience for Addiction Medicine: From Prevention to Rehabilitation - Constructs and Drugs |series=Progress in Brain Research |year=2016 | vauthors = Edwards S |volume=223 |pages=63–76 |pmid=26806771 |isbn=978-0-444-63545-7 |quote=An important dimension of reinforcement highly relevant to the addiction process (and particularly relapse) is secondary reinforcement (Stewart, 1992). Secondary reinforcers (in many cases also considered conditioned reinforcers) likely drive the majority of reinforcement processes in humans. In the specific case of drug addiction, cues and contexts that are intimately and repeatedly associated with drug use will themselves become reinforcing&nbsp;... A fundamental piece of Robinson and Berridge's incentive-sensitization theory of addiction posits that the incentive value or attractive nature of such secondary reinforcement processes, in addition to the primary reinforcers themselves, may persist and even become sensitized over time in league with the development of drug addiction (Robinson and Berridge, 1993).}}</ref> During the development of an addiction, the repeated association of otherwise neutral and even non-rewarding [[stimulation|stimuli]] with drug consumption triggers an [[associative learning]] process that causes these previously neutral stimuli to act as [[Reinforcement#Secondary reinforcers|conditioned positive reinforcers]] of addictive drug use (i.e., these stimuli start to function as [[drug cues]]).<ref name="Incentive salience and motivation review" /><ref name="Pleasure system - incentive sensitization">{{cite journal | vauthors = Berridge KC, Kringelbach ML | title = Pleasure systems in the brain | journal = Neuron | volume = 86 | issue = 3 | pages = 646–664 | date = May 2015 | pmid = 25950633 | pmc = 4425246 | doi = 10.1016/j.neuron.2015.02.018 }}</ref><ref name="Reinforcement in addiction" /> As conditioned positive reinforcers of drug use, these previously neutral stimuli are assigned incentive salience (which manifests as a craving)&nbsp;– sometimes at pathologically high levels due to reward sensitization&nbsp;– which can [[Pavlovian-instrumental transfer|transfer to the primary reinforcer]] (e.g., the use of an addictive drug) with which it was originally paired.<ref name="Incentive salience and motivation review" /><ref name="Pleasure system - incentive sensitization" /><ref name="Reinforcement in addiction" />

Research on the interaction between natural and drug rewards suggests that dopaminergic psychostimulants (e.g., amphetamine) and sexual behavior act on similar biomolecular mechanisms to induce ΔFosB in the nucleus accumbens and possess a bidirectional '''reward cross-sensitization''' effect{{#tag:ref|In simplest terms, this means that when either amphetamine or sex is perceived as more alluring or desirable through reward sensitization, this effect occurs with the other as well.|group="note"}} that is mediated through ΔFosB.<ref name="Natural and drug addictions" /><ref name="Amph-Sex X-sensitization through D1 signaling" /><ref name="Amph-Sex X-sensitization through NMDA signaling" /> In contrast to ΔFosB's reward-sensitizing effect, [[CREB]] transcriptional activity decreases user's sensitivity to the rewarding effects of the substance. CREB transcription in the nucleus accumbens is implicated in [[psychological dependence]] and symptoms involving a [[anhedonia|lack of pleasure or motivation]] during [[drug withdrawal]].<ref name="Cellular basis" /><ref name="pmid11572966" /><ref name="pmid18640924" />

{{Clear}}
{{Addiction-related plasticity|title=Summary of addiction-related plasticity}}
{{Clear}}

===Neuroepigenetic mechanisms===
{{Further|Neuroepigenetics|Chromatin remodeling}}

<!--{{Expand section|the table of drug-induced chromatin modifications from figure 2 of this<ref name="Chromatin states" /> review; an explanation of the relationship between class I [[HDAC]]s—[[H3K9ac]]/[[H3K9ac2]], [[G9a]]—[[H3K9me2]], and transcriptional mechanisms (i.e., phospho-CREB and FosB–ΔFosB)|date=June 2018|small=no}}

--><!--
-Should probably mention the following since it's related to both the mechanisms and research sections:
1) Prolonged inhibition of class I HDACs results in histone hyper-acetylation, which in turn increases G9a expression and H3K9me2 synthesis
2) G9a catalyzes H3K9 dimethylation (H3K9me2 synthesis)
3) H3K9me2 is a repressive epigenetic mark that inhibits the induction of DeltaFosB in the NAcc by preventing transcription of the FosB gene
i.e., +HDACi → ↑ H3 acetylation & ↑H4 acetylation → ↑G9a → ↑H3K9me2 synthesis
4) The feedback loop involving: +drug → ↑ΔFosB → ↓G9a → ↓H3K9me2 → ↑ΔFosB
-->
Altered epigenetic regulation of gene expression within the brain's reward system plays a significant and complex role in the development of drug addiction.<ref name="Nestler 2014 epigenetics" /><ref name="Chromatin states">{{cite journal | vauthors = Walker DM, Cates HM, Heller EA, Nestler EJ | title = Regulation of chromatin states by drugs of abuse | journal = Curr. Opin. Neurobiol. | volume = 30 | pages = 112–21 | date = February 2015 | pmid = 25486626 | doi = 10.1016/j.conb.2014.11.002 | quote = Studies investigating general HDAC inhibition on behavioral outcomes have produced varying results but it seems that the effects are specific to the timing of exposure (either before, during or after exposure to drugs of abuse) as well as the length of exposure | pmc=4293340}}</ref> Addictive drugs are associated with three types of epigenetic modifications within neurons.<ref name="Nestler 2014 epigenetics" /> These are (1) histone modifications, (2) [[epigenetic methylation]] of DNA at [[CpG site]]s at (or adjacent to) particular genes, and (3) epigenetic downregulation or upregulation of microRNAs which have particular target genes.<ref name="Nestler 2014 epigenetics" /><ref name="Nestler" /><ref name="Chromatin states" /> As an example, while hundreds of genes in the cells of the nucleus accumbens (NAc) exhibit histone modifications following drug exposure – particularly, altered acetylation and methylation states of [[histone]] [[Residue (chemistry)#Biochemistry|residues]]<ref name="Chromatin states" /> – most other genes in the NAc cells do not show such changes.<ref name="Nestler 2014 epigenetics" />

==Diagnosis==
{{Further|Substance use disorder#Diagnosis|Problem gambling#Diagnosis}}

===Classification===

====DSM-5====
The fifth edition of the DSM uses the term ''substance use disorder'' to refer to a spectrum of drug use-related disorders. The DSM-5 eliminates the terms ''[[drug abuse|abuse]]'' and ''dependence'' from diagnostic categories, instead using the specifiers of ''mild'', ''moderate'' and ''severe'' to indicate the extent of disordered use. These specifiers are determined by the number of diagnostic criteria present in a given case. In the DSM-5, the term ''drug addiction'' is synonymous with ''severe substance use disorder''.<ref name="Surgeon General severe SUD">{{cite web | title=Facing Addiction in America: The Surgeon General's Report on Alcohol, Drugs, and Health | url=https://addiction.surgeongeneral.gov/sites/default/files/surgeon-generals-report.pdf | website = Office of the Surgeon General | publisher=US Department of Health and Human Services | date=November 2016 | access-date=28 January 2017 | pages = 35–37, 45, 63, 155, 317, 338 }}</ref><ref name="Brain disease" />

The DSM-5 introduced a new diagnostic category for behavioral addictions. Problem gambling is the only condition included in this category in the fifth edition.<ref name="APA (2013)" /> [[Internet gaming disorder]] is listed as a "condition requiring further study" in the DSM-5.<ref>{{cite journal | vauthors = Petry NM, Rehbein F, Gentile DA, Lemmens JS, Rumpf HJ, Mößle T, Bischof G, Tao R, Fung DS, Borges G, Auriacombe M, González Ibáñez A, Tam P, O'Brien CP | title = An international consensus for assessing internet gaming disorder using the new DSM-5 approach | journal = Addiction | volume = 109 | issue = 9 | pages = 1399–406 | date = September 2014 | pmid = 24456155 | doi = 10.1111/add.12457 }}</ref>

Past editions have used [[physical dependence]] and the associated withdrawal syndrome to identify an addictive state. Physical dependence occurs when the body has adjusted by incorporating the substance into its "normal" functioning – i.e., attains [[homeostasis]] – and therefore physical withdrawal symptoms occur on cessation of use.<ref name="pmid10511013">{{cite journal |vauthors=Torres G, Horowitz JM | title = Drugs of abuse and brain gene expression | journal = Psychosom Med | volume = 61 | issue = 5 | pages = 630–50 | year = 1999 | pmid = 10511013 | doi = 10.1097/00006842-199909000-00007| citeseerx = 10.1.1.326.4903 }}</ref> Tolerance is the process by which the body continually adapts to the substance and requires increasingly larger amounts to achieve the original effects. Withdrawal refers to physical and psychological symptoms experienced when reducing or discontinuing a substance that the body has become dependent on. Symptoms of withdrawal generally include but are not limited to body aches, [[anxiety]], [[irritability]], intense [[craving (withdrawal)|cravings]] for the substance, [[dysphoria]], [[nausea]], [[hallucinations]], [[headaches]], cold sweats, [[tremor]]s, and seizures. During acute physical opioid withdrawal, symptoms of [[restless legs syndrome]] are common and may be profound. This phenomenon originated the idiom "kicking the habit".

Medical researchers who actively study addiction have criticized the DSM classification of addiction for being flawed and involving arbitrary diagnostic criteria.<ref>{{cite book | vauthors = Malenka RC, Nestler EJ, Hyman SE, Holtzman DM | title = Molecular Neuropharmacology: A Foundation for Clinical Neuroscience | year = 2015 | publisher = McGraw-Hill Medical | location = New York | isbn = 978-0-07-182770-6 | edition = 3rd | chapter = Chapter 16: Reinforcement and Addictive Disorders | quote = The official diagnosis of drug addiction by the Diagnostic and Statistic Manual of Mental Disorders (2013), which uses the term substance use disorder, is flawed. Criteria used to make the diagnosis of substance use disorders include tolerance and somatic dependence/withdrawal, even though these processes are not integral to addiction as noted. It is ironic and unfortunate that the manual still avoids use of the term addiction as an official diagnosis, even though addiction provides the best description of the clinical syndrome.}}</ref>

====ICD-11====
The eleventh revision of the [[International Classification of Diseases]], commonly referred to as [[ICD-11]], conceptualizes diagnosis somewhat differently. ICD-11 first distinguishes between problems with psychoactive substance use ("Disorders due to substance use") and behavioral addictions ("Disorders due to addictive behaviours").<ref name="ICD-11 (disorders due to substance use or addictive behaviours)"/> With regard to psychoactive substances, ICD-11 explains that the included substances initially produce "pleasant or appealing psychoactive effects that are rewarding and reinforcing with repeated use, [but] with continued use, many of the included substances have the capacity to produce dependence. They have the potential to cause numerous forms of harm, both to mental and physical health."<ref name="substance-disorder">{{Cite web |title=International Classification of Diseases 11th revision &ndash; ICD-11. Disorders due to substance use |url=https://icd.who.int/browse11/l-m/en#/http://id.who.int/icd/entity/590211325 |access-date=24 March 2023 |website=World Health Organization |location=Geneva |date=2023}}</ref> Instead of the DSM-5 approach of one diagnosis ("Substance Use Disorder") covering all types of problematic substance use, ICD-11 offers three diagnostic possibilities: 1) Episode of Harmful Psychoactive Substance Use, 2) Harmful Pattern of Psychoactive Substance Use, and 3) Substance Dependence.<ref name="substance-disorder" />

== Prevention ==
{{Main|Harm reduction|Preventive healthcare}}

=== Abuse liability ===
Abuse or addiction liability is the tendency to use drugs in a non-medical situation. This is typically for euphoria, mood changing, or sedation.<ref name="cambridgecognition">{{Cite web|title=Drug abuse liability|url=https://www.cambridgecognition.com/research-areas/drug-abuse-liability-research/|access-date=9 March 2021| work = Cambridge Cognition |language=en}}</ref> Abuse liability is used when the person using the drugs wants something that they otherwise can not obtain. The only way to obtain this is through the use of drugs. When looking at abuse liability there are a number of determining factors in whether the drug is abused. These factors are: the chemical makeup of the drug, the effects on the brain, and the age, vulnerability, and the health (mental and physical) of the population being studied.<ref name="cambridgecognition" /> There are a few drugs with a specific chemical makeup that leads to a high abuse liability. These are: cocaine, heroin, inhalants, marijuana, MDMA (ecstasy), methamphetamine, PCP, synthetic cannabinoids, synthetic cathinones (bath salts), nicotine (e.g. tobacco), and alcohol.<ref>{{Cite web | author = National Institute on Drug Abuse |date=20 August 2020|title=Commonly Used Drugs Charts|url=https://www.drugabuse.gov/drug-topics/commonly-used-drugs-charts|access-date=9 March 2021|website=National Institute on Drug Abuse|language=en}}</ref>

=== Potential vaccines for addiction to substances ===
[[Vaccine]]s for addiction have been investigated as a possibility since the early 2000s.<ref>{{Cite book|url=https://www.ncbi.nlm.nih.gov/sites/books/NBK24623/|title=Vaccines and Immunotherapies to Control Addiction in Minors: The Legal Framework|first1=Henrick J.|last1=Harwood|first2=Tracy G.|last2=Myers|first3=National Research Council (US) and Institute of Medicine (US) Committee on Immunotherapies and Sustained-Release Formulations for Treating Drug|last3=Addiction|date=July 23, 2004|publisher=National Academies Press (US)|via=National Center for Biotechnology Information }}</ref> The general theory of a vaccine intended to "immunize" against drug addiction or other [[substance abuse]] is that it would condition the [[immune system]] to attack and consume or otherwise disable the molecules of such substances that cause a reaction in the brain, thus preventing the addict from being able to realize the effect of the drug. Addictions that have been floated as targets for such treatment include [[nicotine]], [[opioid]]s, and [[fentanyl]].<ref>{{cite web|url=https://www.scripps.edu/news-and-events/press-room/2020/20200730-janda-heroinvaccine.html |title='Heavy' heroin vaccine provides hope for addiction treatment|publisher=[[Scripps Research]]|date=July 30, 2020}}</ref><ref>{{Cite web|url=https://www.cuimc.columbia.edu/news/experimental-opioid-vaccine-being-tested-columbia|title=Experimental Opioid Vaccine Being Tested at Columbia|date=July 1, 2021|website=Columbia University Irving Medical Center}}</ref><ref>{{Cite web|url=https://www.seattletimes.com/seattle-news/mental-health/to-fight-opioid-crisis-uw-researchers-take-new-shot-at-developing-vaccine-against-addictive-drugs/|title=To fight opioid crisis, UW researchers take new shot at developing vaccine against addictive drugs|first1=Hannah|last1=Furfaro|date=January 5, 2022|website=The Seattle Times}}</ref><ref>{{Cite web|url=https://www.addictioncenter.com/news/2022/01/vaccine-against-addiction/|title=A Vaccine Against Addiction|website=Addiction Center|date=12 January 2022 }}</ref> Vaccines have been identified as potentially being more effective than other anti-addiction treatments, due to "the long duration of action, the certainty of administration and a potential reduction of [[toxicity]] to important organs".<ref name="AAC">{{Cite web|url=https://drugabuse.com/blog/why-dont-we-have-addiction-vaccines/|title=Why Don't We Have Addiction Vaccines?|author=American Addiction Centers Editorial Staff|orig-date=December 29, 2016|date=January 4, 2022|website=DrugAbuse.com}}</ref>

Specific addiction vaccines in development include:

*[[NicVAX]], a [[conjugate vaccine]] intended to reduce or eliminate physical dependence on nicotine.<ref name="drugabusegov">{{cite web|url=http://www.drugabuse.gov/NIDA_Notes/NNVol15N5/Vaccine.html |title=Nicotine Vaccine Moves Toward Clinical Trials |author=Barbara Shine |publisher=National Institute on Drug Abuse |date=October 2000 |access-date=2006-09-19 |archive-url=https://web.archive.org/web/20060810101935/http://www.drugabuse.gov/NIDA_Notes/NNVol15N5/Vaccine.html |archive-date=2006-08-10 |url-status=dead }}</ref> This proprietary vaccine is being developed by Nabi Biopharmaceuticals<ref name="Nabiwebsite">{{cite web | url=http://www.nabi.com | title = Nabi Biopharmaceuticals Website}}</ref> of Rockville, MD. with the support from the [[U.S. National Institute on Drug Abuse]]. NicVAX consists of the [[hapten]] 3'-aminomethylnicotine which has been conjugated (attached) to ''[[Pseudomonas aeruginosa]]'' [[exotoxin A]].<ref name="cpt-p459">{{cite journal | last = Hatsukami | first = Dorothy K. | author-link = Dorothy Hatsukami|author2=Rennard S |author3=Jorenby D |author4=Fiore M |author5=Koopmeiners J |author6=de Vos A |author7=Horwith G |author8=Pentel PR  | title = Safety and immunogenicity of a nicotine conjugate vaccine in current smokers | journal = Clinical Pharmacology & Therapeutics | volume = 78 | issue = 5 | pages = 456–467 |year= 2005 | doi = 10.1016/j.clpt.2005.08.007 | pmid = 16321612 | s2cid = 1218556 }}</ref>
* [[TA-CD]], an active [[vaccine]]<ref name="pmid16038686">{{cite journal |vauthors=Martell BA, Mitchell E, Poling J, Gonsai K, Kosten TR |title=Vaccine pharmacotherapy for the treatment of cocaine dependence |journal=Biol. Psychiatry |volume=58 |issue=2 |pages=158–64 |date=July 2005 |pmid=16038686 |doi=10.1016/j.biopsych.2005.04.032 |s2cid=22415520 }}</ref> developed by the Xenova Group which is used to negate the effects of [[cocaine]]. It is created by combining [[norcocaine]] with inactivated [[cholera]] toxin. It works in much the same way as a regular vaccine.  A large [[protein]] molecule attaches to cocaine, which stimulates response from [[antibodies]], which destroy the molecule.  This also prevents the cocaine from crossing the [[blood–brain barrier]], negating the euphoric high and [[Reward system|rewarding]] effect of cocaine caused from stimulation of [[dopamine]] release in the [[mesolimbic reward pathway]].  The vaccine does not affect the user's "desire" for cocaine—only the physical effects of the drug.<ref>{{cite web |url=http://news.bbc.co.uk/2/hi/health/3804741.stm |title=Cocaine vaccine 'stops addiction' |access-date=2009-10-07|work=[[BBC News]] |date=14 June 2004 }}</ref>
*[[TA-NIC]], used to create human antibodies to destroy [[nicotine]] in the human body so that it is no longer effective.<ref>{{Cite web |url=http://www.celticpharma.com/theportfolio/ta-nic.html |title=CelticPharma: TA-NIC Nicotine Dependence. |access-date=2009-10-27 |archive-url=https://web.archive.org/web/20091206100218/http://www.celticpharma.com/theportfolio/ta-nic.html |archive-date=2009-12-06 |url-status=dead }}</ref>

As of September 2023, it was further reported that a vaccine "has been tested against [[heroin]] and [[fentanyl]] and is on its way to being tested against [[oxycontin]]".<ref>{{cite news|url=https://www.kiro7.com/news/local/uw-researcher-explains-new-vaccine-being-made-prevent-opioid-overdoses/HXFQ3AZ2YBAGDIELRDIGKCWN6M/ |title=UW researcher explains new vaccine in the works to prevent opioid overdoses|author=KIRO 7 News Staff|work=[[KIRO 7]]|date=September 19, 2023}}</ref>

==Treatment and management==
{{Main|Treatment and management of addiction}}
To be effective, treatment for addiction that is pharmacological or biologically based need to be accompanied by other interventions such as [[cognitive behavioral therapy]] (CBT), individual and group psychotherapy, [[behavior modification]] strategies, [[twelve-step program]]s, and residential treatment facilities.<ref name="Reward system and psychostimulants">{{cite journal | vauthors = Taylor SB, Lewis CR, Olive MF | title = The neurocircuitry of illicit psychostimulant addiction: acute and chronic effects in humans | journal = Subst. Abuse Rehabil. | volume = 4 | pages = 29–43 | date = February 2013 | pmid = 24648786 | pmc = 3931688 | doi = 10.2147/SAR.S39684 | quote = Initial drug use can be attributed to the ability of the drug to act as a reward (ie, a pleasurable emotional state or positive reinforcer), which can lead to repeated drug use and dependence.<sup>8,9</sup> A great deal of research has focused on the molecular and neuroanatomical mechanisms of the initial rewarding or reinforcing effect of drugs of abuse.&nbsp;... At present, no pharmacological therapy has been approved by the FDA to treat psychostimulant addiction. Many drugs have been tested, but none have shown conclusive efficacy with tolerable side effects in humans.<sup>172</sup>&nbsp;...<!--These drugs have included DA-receptor ligands, such as DA receptor agonists, partial agonists, and antagonists, as well as DA-reuptake inhibitors.<sup>173,174</sup> One newer dopaminergic drug that has shown some promise is the antipsychotic medication aripiprazole, a partial agonist at D2-like receptors, which is currently approved for the treatment of schizophrenia, depression, and bipolar disorder.<sup>175</sup> Clinical trials have thus far been mixed, with one study finding reduced cocaine craving and use, and another study showing increased cocaine use.<sup>176,177</sup>&nbsp;...
Recent evidence for dysregulation of glutamatergic signaling in addiction has led to the testing of N-acetylcysteine, a derivative of the amino acid cysteine that normalizes extracellular levels of Glu following cocaine administration.<sup>178,179</sup> Clinical trials found that N-acetylcysteine treatment attenuates cocaine craving and use and normalizes brain glutamate levels.<sup>180–182</sup> Other recent studies found trends toward significant reductions in METH use and craving produced by the antidepressant buproprion and the anticonvulsant topiramate, which has glutamate release-inhibiting properties.<sup>183,184</sup> While these compounds have not demonstrated overwhelming efficacy in reducing psychostimulant use or craving in all subjects tested, trends toward effects were observed and thus merit further investigation.
Other compounds that have been tested, with disappointing results, include β-adrenergic antagonists, opioid-receptor antagonists, 5-HT3-receptor antagonists, antidepressants, and anticonvulsants.<sup>172,185–190</sup> Despite the lack of past successes, several newer medications are currently being investigated and have shown some initial success, such as the smoking-cessation aid varenicline, the α2 adrenergic agonist clonidine, and the antidepressant mirtazapine.<sup>191–194</sup> In addition, preclinical evidence strongly suggests potential therapeutic effects of compounds targeting receptors for endocannabinoids, the neuropeptide orexin, and CRF for the prevention of relapse to psychostimulant use.<sup>195–197</sup>
Future approaches for the treatment of psychostimulant-induced cognitive deficits and dependence include the use of cognitive enhancers.<sup>198–200</sup> Two promising examples include prescription stimulants, such as modafinil and methylphenidate, which have shown modest but potential treatment effects in METH users and cocaine users with comorbid attention deficit/hyperactivity disorder, respectively.<sup>201–205</sup> In addition, galantamine, a cholinergic modulator and cognitive enhancer, has been reported to both decrease cocaine use and improve sustained attention in dependent subjects.<sup>206,207</sup> Together, these studies indicate that clinical trials of cognitive enhancers in the treatment of psychostimulant addiction are warranted. In addition to the pharmacological trials reviewed above, less conventional strategies that are gaining scientific momentum include vaccine therapies to immunoneutralize drug molecules and impede penetrance across the blood–brain barrier, enzyme conjugates that dramatically increase the metabolic breakdown of abused drugs, pharmacogenetic approaches based on individual genetic polymorphisms in addiction-related genes, and epigenetic modulators of drug-induced changes in gene expression.<sup>208–211</sup> While still in their relative infancy, these exciting new avenues of research offer a significant expansion of possible biologically based targets for the treatment of psychostimulant addiction.&nbsp;...
The tremendous need for more effective pharmacological treatments for psychostimulant addiction is a mainstay of contemporary addiction research. However, the recent downsizing of many major pharmaceutical companies away from psychiatric indications (including addiction) due to the lack of efficacy of experimental compounds in humans may require a sea change in the translational research approach.<sup>212,213</sup> --> A new emphasis on larger-scale biomarker, genetic, and epigenetic research focused on the molecular targets of mental disorders has been recently advocated.<sup>212</sup> In addition, the integration of cognitive and behavioral modification of circuit-wide neuroplasticity (i.e., computer-based training to enhance executive function) may prove to be an effective adjunct-treatment approach for addiction, particularly when combined with cognitive enhancers.<sup>198,213–216</sup> Furthermore, in order to be effective, all pharmacological or biologically based treatments for addiction need to be integrated into other established forms of addiction rehabilitation, such as CBT, individual and group psychotherapy, behavior-modification strategies, twelve-step programs, and residential treatment facilities. | doi-access = free }}</ref><ref name="Skylstad2022" /> The {{Abbr|TTM|transtheoretical model of change}} can be used to determine when treatment can begin and which method will be most effective. If treatment begins too early, it can cause a person to become defensive and resistant to change.<ref name="Hill2021" /><ref>{{Cite journal |last=Scott |first=Cynthia G. |date=July 2000 |title=Ethical Issues in Addiction Counseling |url=http://journals.sagepub.com/doi/10.1177/003435520004300405 |journal=Rehabilitation Counseling Bulletin |language=en |volume=43 |issue=4 |pages=209–214 |doi=10.1177/003435520004300405 |pmid=15714702 |s2cid=28556555 |issn=0034-3552}}</ref>

==Epidemiology==
{{Further|Countries by alcohol consumption|Opioid epidemic|Prevalence of tobacco use}}

Due to cultural variations, the proportion of individuals who develop a drug or behavioral addiction within a specified time period (i.e., the [[prevalence]]) varies over time, by country, and across national [[demographics|population demographics]] (e.g., by age group, socioeconomic status, etc.).<ref name="Transgenerational epigenetic inheritance in addiction" /> Where addiction is viewed as unacceptable, there will be fewer people addicted.

===Asia===
The prevalence of alcohol dependence is not as high as is seen in other regions. In Asia, not only socioeconomic factors but biological factors influence drinking behavior.<ref>{{cite journal | vauthors = Chen CC, Yin SJ | title = Alcohol abuse and related factors in Asia | journal = International Review of Psychiatry | volume = 20 | issue = 5 | pages = 425–433 | date = October 2008 | pmid = 19012127 | doi = 10.1080/09540260802344075 | s2cid = 24571763 }}</ref>

Internet addiction disorder is highest in the Philippines, according to both the IAT (Internet Addiction Test) – 5% and the CIAS-R (Revised Chen Internet Addiction Scale) – 21%.<ref>{{cite journal | vauthors = Mak KK, Lai CM, Watanabe H, Kim DI, Bahar N, Ramos M, Young KS, Ho RC, Aum NR, Cheng C | title = Epidemiology of internet behaviors and addiction among adolescents in six Asian countries | journal = Cyberpsychology, Behavior and Social Networking | volume = 17 | issue = 11 | pages = 720–728 | date = November 2014 | pmid = 25405785 | doi = 10.1089/cyber.2014.0139 }}</ref>

===Australia===
{{Further|Alcoholism in rural Australia}}

The prevalence of substance use disorder among Australians was reported at 5.1% in 2009.<ref>{{Cite web | vauthors = Slade T, Johnston A, Teesson M, Whiteford H, Burgess P, Pirkis J, Saw S | author-link3= Maree Teesson | title = The Mental Health of Australians 2: Substance Use Disorders in Australia | publisher = Department of Health and Ageing, Canberra | date = May 2009 | url = https://www.health.gov.au/internet/main/publishing.nsf/Content/A24556C814804A99CA257BF0001CAC45/$File/mha26.pdf }}</ref>  In 2019 the [[Australian Institute of Health and Welfare]] conducted a national drug survey that quantified drug use for various types of drugs and demographics.<ref name="AIHW_2019">{{Cite report |url=https://www.aihw.gov.au/reports/illicit-use-of-drugs/national-drug-strategy-household-survey-2019/contents/table-of-contents |title=National Drug Strategy Household Survey 2019 |last=Australian Institute of Health and Welfare (AIHW) |date=2020 |doi=10.25816/E42P-A447 |language=en}}</ref> The survey found that in 2019, 11% of people over 14 years old smoke daily; that 9.9% of those who drink alcohol, which equates to 7.5% of the total population age 14 or older, may qualify as alcohol dependent; that 17.5% of the 2.4&nbsp;million people who used cannabis in the last year may have hazardous use or a dependence problem; and that 63.5% of about 300000 recent users of meth and amphetamines were at risk for developing problem use.<ref name="AIHW_2019" />

===Europe===
{{Further|Alcoholism in Ireland|Alcoholism in Russia}}

In 2015, the estimated prevalence among the adult population was 18.4% for heavy episodic alcohol use (in the past 30 days); 15.2% for daily tobacco smoking; and 3.8% for cannabis use, 0.77% for amphetamine use, 0.37% for opioid use, and 0.35% for cocaine use in 2017. The mortality rates for alcohol and illicit drugs were highest in Eastern Europe.<ref>{{cite journal | vauthors = Peacock A, Leung J, Larney S, Colledge S, Hickman M, Rehm J, Giovino GA, West R, Hall W, Griffiths P, Ali R, Gowing L, Marsden J, Ferrari AJ, Grebely J, Farrell M, Degenhardt L | title = Global statistics on alcohol, tobacco and illicit drug use: 2017 status report | journal = Addiction | volume = 113 | issue = 10 | pages = 1905–1926 | date = October 2018 | pmid = 29749059 | doi = 10.1111/add.14234 | hdl = 11343/283940 | s2cid = 13674349 | url = https://discovery.ucl.ac.uk/id/eprint/10049286/ | doi-access = free | hdl-access = free }}</ref> Data shows a downward trend of alcohol use among children 15 years old in most European countries between 2002 and 2014. First-time alcohol use before the age of 13 was recorded for 28% of European children in 2014.<ref name="Skylstad2022">{{cite journal | vauthors = Skylstad V, Babirye JN, Kiguli J, Solheim Skar AM, et al. | title = Are we overlooking alcohol use by younger children? | journal = BMJ Paediatrics Open | date = March 2022 | volume = 6 | issue = 1 | page = e001242 | doi = 10.1136/bmjpo-2021-001242 | pmid = 36053657 | pmc = 8905875 }}</ref>

===United States===
{{Further|Cocaine in the United States|Crack epidemic in the United States|Opioid epidemic in the United States}}

Based on [[representative sample]]s of the US youth population in {{As of|2011|bare=y}}, the [[lifetime prevalence]]{{#tag:ref|The lifetime prevalence of an addiction is the percentage of individuals in a population that developed an addiction at some point in their life.|group="note"}} of addictions to alcohol and illicit drugs has been estimated to be approximately 8% and 2–3% respectively.<ref name="Epidem">{{cite journal |vauthors=Merikangas KR, McClair VL |date=June 2012 |title=Epidemiology of Substance Use Disorders |journal=Hum. Genet. |volume=131 |issue=6 |pages=779–89 |doi=10.1007/s00439-012-1168-0 |pmc=4408274 |pmid=22543841}}</ref> Based on representative samples of the US adult population in {{As of|2011|bare=y}}, the [[period prevalence|12-month prevalence]] of alcohol and illicit drug addictions were estimated at 12% and 2–3% respectively.<ref name="Epidem" /> The lifetime prevalence of [[prescription drug]] addictions is around 4.7%.<ref>{{cite journal | vauthors = Manubay JM, Muchow C, Sullivan MA | title = Prescription drug abuse: epidemiology, regulatory issues, chronic pain management with narcotic analgesics | journal = Primary Care | volume = 38 | issue = 1 | pages = 71–90 | date = March 2011 | pmid = 21356422 | pmc = 3328297 | doi = 10.1016/j.pop.2010.11.006 }}</ref>

{{As of|2021|post=,}} 43.7&nbsp;million people aged 12 or older surveyed by the National Survey on Drug Use and Health in the United States needed treatment for an addiction to alcohol, nicotine, or other drugs. The groups with the highest number of people were 18–25 years (25.1%) and "American Indian or Alaska Native" (28.7%).<ref name="2021 NSDUH Report">{{cite report |vauthors=((Substance Abuse and Mental Health Services Administration)) |date=2022 |title=Key substance use and mental health indicators in the United States: Results from the 2021 National Survey on Drug Use and Health |url=https://www.samhsa.gov/data/report/2021-nsduh-annual-national-report |publisher=Center for Behavioral Health Statistics and Quality, Substance Abuse and Mental Health Services Administration |access-date = 24 March 2023 }}</ref> Only about 10%, or a little over 2&nbsp;million, receive any form of treatments, and those that do generally do not receive [[evidence-based medicine|evidence-based care]].<ref name="ABAM">{{cite web|title=American Board of Medical Specialties recognizes the new subspecialty of addiction medicine|url=http://www.abam.net/wp-content/uploads/2016/03/1.-News-Release-ADM.pdf|website=American Board of Addiction Medicine|access-date=3 April 2016|date=14 March 2016|quote=Sixteen percent of the non-institutionalized U.S. population age 12 and over – more than 40 million Americans – meets medical criteria for addiction involving nicotine, alcohol or other drugs. This is more than the number of Americans with cancer, diabetes or heart conditions. In 2014, 22.5 million people in the United States needed treatment for addiction involving alcohol or drugs other than nicotine, but only 11.6 percent received any form of inpatient, residential, or outpatient treatment. Of those who do receive treatment, few receive evidence-based care. (There is no information available on how many individuals receive treatment for addiction involving nicotine.)<br />Risky substance use and untreated addiction account for one-third of inpatient hospital costs and 20 percent of all deaths in the United States each year, and cause or contribute to more than 100 other conditions requiring medical care, as well as vehicular crashes, other fatal and non-fatal injuries, overdose deaths, suicides, homicides, domestic discord, the highest incarceration rate in the world and many other costly social consequences. The economic cost to society is greater than the cost of diabetes and all cancers combined. Despite these startling statistics on the prevalence and costs of addiction, few physicians have been trained to prevent or treat it.|archive-date=21 March 2021|archive-url=https://web.archive.org/web/20210321082744/http://www.abam.net/wp-content/uploads/2016/03/1.-News-Release-ADM.pdf|url-status=dead}}</ref><ref name="NIDA Addiction Medicine">{{cite web|vauthors=Volkow N|title=A Major Step Forward for Addiction Medicine|url=https://www.drugabuse.gov/about-nida/noras-blog/2016/03/major-step-forward-addiction-medicine|website=National Institute on Drug Abuse|publisher=National Institutes of Health|access-date=3 April 2016|date=31 March 2016|quote=Only about 10 percent of the 21 million Americans who meet the need for care for an alcohol or drug use disorder receive any form of treatment, and much of the treatment available does not meet standards for evidence-based care. There are many attitudinal and systemic reasons for this treatment gap, including stigma against treating people with addictions and institutional barriers to providing or funding addiction treatment.&nbsp;... A major milestone was reached on March 14, 2016, when the American Board of Medical Specialties (ABMS) formally announced recognition of the field of Addiction Medicine as a medical subspecialty.&nbsp;... In a statement issued to mark this milestone, ABAM President Robert J. Sokol summed up its significance: 'This landmark event, more than any other, recognizes addiction as a preventable and treatable disease, helping to shed the stigma that has long plagued it. It sends a strong message to the public that American medicine is committed to providing expert care for this disease and services designed to prevent the risky substance use that precedes it.'|archive-date=5 April 2016|archive-url=https://web.archive.org/web/20160405133536/https://www.drugabuse.gov/about-nida/noras-blog/2016/03/major-step-forward-addiction-medicine|url-status=dead}}</ref> One-third of [[inpatient care|inpatient]] hospital costs and 20% of all deaths in the US every year are the result of untreated addictions and risky substance use.<ref name="ABAM" /><ref name="NIDA Addiction Medicine" /> In spite of the massive overall economic cost to society, which is greater than the cost of [[diabetes]] and all forms of cancer combined, most doctors in the US lack the training to effectively address a drug addiction.<ref name="ABAM" /><ref name="NIDA Addiction Medicine" />

Estimates of lifetime prevalence rates in the US are 1–2% for compulsive gambling, 5% for sexual addiction, 2.8% for food addiction, and 5–6% for compulsive shopping.<ref name="Natural and drug addictions" /> The time-invariant prevalence rate for sexual addiction and related compulsive sexual behavior (e.g., compulsive masturbation with or without pornography, compulsive cybersex, etc.) within the US ranges from 3–6% of the population.<ref name="Systematic review - yet another DSM fail">{{cite journal | vauthors = Karila L, Wéry A, Weinstein A, Cottencin O, Petit A, Reynaud M, Billieux J | title = Sexual addiction or hypersexual disorder: different terms for the same problem? A review of the literature | journal = Curr. Pharm. Des. | volume = 20 | issue = 25 | pages = 4012–20 | year = 2014 | pmid = 24001295 | doi = 10.2174/13816128113199990619| s2cid = 19042860 | quote = Sexual addiction, which is also known as hypersexual disorder, has largely been ignored by psychiatrists, even though the condition causes serious psychosocial problems for many people. A lack of empirical evidence on sexual addiction is the result of the disease's complete absence from versions of the Diagnostic and Statistical Manual of Mental Disorders.&nbsp;... Existing prevalence rates of sexual addiction-related disorders range from 3% to 6%. Sexual addiction/hypersexual disorder is used as an umbrella construct to encompass various types of problematic behaviors, including excessive masturbation, cybersex, pornography use, sexual behavior with consenting adults, telephone sex, strip club visitation, and other behaviors. The adverse consequences of sexual addiction are similar to the consequences of other addictive disorders. Addictive, somatic and psychiatric disorders coexist with sexual addiction. In recent years, research on sexual addiction has proliferated, and screening instruments have increasingly been developed to diagnose or quantify sexual addiction disorders. In our systematic review of the existing measures, 22 questionnaires were identified. As with other behavioral addictions, the appropriate treatment of sexual addiction should combine pharmacological and psychological approaches.}}</ref>

According to a 2017 poll conducted by the [[Pew Research Center]], almost half of US adults know a family member or close friend who has struggled with a drug addiction at some point in their life.<ref>{{cite web|title=Nearly half of Americans have a family member or close friend who's been addicted to drugs|url=http://www.pewresearch.org/fact-tank/2017/10/26/nearly-half-of-americans-have-a-family-member-or-close-friend-whos-been-addicted-to-drugs/|publisher=Pew Research Center| vauthors = Gramlich J|date=26 October 2017|access-date=14 January 2018}}</ref>

In 2019, opioid addiction was acknowledged as a national crisis in the United States.<ref>{{cite news |title=We were addicted to their pill, but they were addicted to the money |url=https://www.washingtonpost.com/video/national/we-were-addicted-to-their-pill-but-they-were-addicted-to-the-money/2019/07/21/7c006bc0-4e9b-46a5-bc80-c7e95e46d513_video.html?wpisrc=nl_headlines&wpmm=1 |access-date=22 July 2019 |newspaper=[[The Washington Post]] |language=en}}</ref> An article in ''[[The Washington Post]]'' stated that "America's largest drug companies flooded the country with pain pills from 2006 through 2012, even when it became apparent that they were fueling addiction and overdoses."

The National Epidemiologic Survey on Alcohol and Related Conditions found that from 2012 to 2013 the prevalence of [[Cannabis use disorder]] in U.S. adults was 2.9%.<ref>{{cite journal | vauthors = Hasin DS, Saha TD, Kerridge BT, Goldstein RB, Chou SP, Zhang H, Jung J, Pickering RP, Ruan WJ, Smith SM, Huang B, Grant BF | title = Prevalence of Marijuana Use Disorders in the United States Between 2001–2002 and 2012–2013 | journal = JAMA Psychiatry | volume = 72 | issue = 12 | pages = 1235–1242 | date = December 2015 | pmid = 26502112 | pmc = 5037576 | doi = 10.1001/jamapsychiatry.2015.1858 }}</ref>

===Canada===
A [[Statistics Canada]] Survey in 2012 found the lifetime prevalence and 12-month prevalence of substance use disorders were 21.6%, and 4.4% in those 15 and older.<ref name= "StatisticsCanada">{{Cite web | publisher = Government of Canada | work = Statistics Canada |date=18 September 2013 |title=Mental and substance use disorders in Canada |url=https://www150.statcan.gc.ca/n1/pub/82-624-x/2013001/article/tbl/tbl1-eng.htm |access-date=8 November 2022 }}</ref> Alcohol abuse or dependence reported a lifetime prevalence of 18.1% and a 12-month prevalence of 3.2%.<ref name="StatisticsCanada" /> Cannabis abuse or dependence reported a lifetime prevalence of 6.8% and a 12-month prevalence of 3.2%.<ref name="StatisticsCanada" /> Other drug abuse or dependence has a lifetime prevalence of 4.0% and a 12-month prevalence of 0.7%.<ref name="StatisticsCanada" /> ''Substance use disorder'' is a term used interchangeably with ''a drug addiction''.<ref>{{Cite news |title=Drug addiction (substance use disorder) – Symptoms and causes |url=https://www.mayoclinic.org/diseases-conditions/drug-addiction/symptoms-causes/syc-20365112 |access-date=8 November 2022 |website=Mayo Clinic |language=en}}</ref>

In [[Ontario|Ontario, Canada]] between 2009 and 2017, outpatient visits for mental health and addiction increased from 52.6 to 57.2 per 100 people, emergency department visits increased from 13.5 to 19.7 per 1000 people and the number of hospitalizations increased from 4.5 to 5.5 per 1000 people.<ref name="Ontario_Scorecard">{{Cite web |title=Mental Health and Addictions System Performance in Ontario: 2021 Scorecard |url=https://www.ices.on.ca/Publications/Atlases-and-Reports/2021/Mental-Health-and-Addictions-System-Performance-in-Ontario-2021-Scorecard |access-date=8 November 2022 |website=www.ices.on.ca}}</ref> Prevalence of care needed increased the most among the 14–17 age group overall.<ref name="Ontario_Scorecard" />

===South America===
The realities of opioid use and [[opioid use disorder]] in Latin America may be deceptive if observations are limited to epidemiological findings. In the [[United Nations Office on Drugs and Crime]] report,<ref>{{cite book |url=https://www.unodc.org/documents/data-and-analysis/WDR2012/WDR_2012_web_small.pdf |title=World Drug Report 2012 |date=June 2012 |publisher=United Nations Office on Drugs and Crime |isbn=978-92-1-148267-6}}</ref> although South America produced 3% of the world's morphine and heroin and 0.01% of its opium, prevalence of use is uneven. According to the Inter-American Commission on Drug Abuse Control, consumption of heroin is low in most Latin American countries, although Colombia is the area's largest opium producer. Mexico, because of its border with the United States, has the highest incidence of use.<ref>{{cite journal | vauthors = Pacurucu-Castillo SF, Ordóñez-Mancheno JM, Hernández-Cruz A, Alarcón RD | title = World opioid and substance use epidemic: a Latin American perspective. | journal = Psychiatric Research and Clinical Practice | date = April 2019 | volume = 1 | issue = 1 | pages = 32–8 | doi = 10.1176/appi.prcp.20180009 | pmid = 36101564 | pmc = 9175731 | doi-access = free }}</ref>

== Addiction and the humanities ==

=== History and etymology ===
{{Main|Recreational drug use}}
{{Further|Evolutionary models of human drug use|History of drinking|History of smoking|Substance abuse in Ancient Rome}}
 
The [[etymology]] of the term ''addiction'' throughout history has been misunderstood and has taken on various meanings associated with the word.<ref name="Crocq 2007">{{cite journal | vauthors = Crocq MA | title = Historical and cultural aspects of man's relationship with addictive drugs | journal = Dialogues in Clinical Neuroscience | volume = 9 | issue = 4 | pages = 355–361 | date = December 2007 | pmid = 18286796 | pmc = 3202501 | doi = 10.31887/DCNS.2007.9.4/macrocq | publisher = [[Laboratoires Servier]] | s2cid = 12682928 | doi-access = free | oclc = 62869913 | veditors = Thibaut F }}</ref> An example is the usage of the word in the religious landscape of [[early modern Europe]].<ref name="Lemon 2018">{{cite book | vauthors = Lemon R |year=2018 |chapter=Introduction: Addiction in (Early) Modernity |chapter-url=https://books.google.com/books?id=mwVKDwAAQBAJ&pg=PA1 |title=Addiction and Devotion in Early Modern England |location=[[Philadelphia]] |publisher=[[University of Pennsylvania Press]] |series=Haney Foundation Series |pages=1–23 |isbn=978-0-8122-4996-5}}</ref> "Addiction" at the time meant "to attach" to something, giving it both positive and negative connotations. The object of this attachment could be characterized as "good or bad".<ref name="Rosenthal_2019">{{cite journal | vauthors = Rosenthal R, Faris S |date=February 2019 |title=The etymology and early history of 'addiction' |journal=Addiction Research & Theory |publisher=[[Taylor & Francis]] |volume=27 |issue=5 |pages=437–449 |doi=10.1080/16066359.2018.1543412 |doi-access=free |issn=1476-7392 |s2cid=150418396}}</ref> The meaning of addiction during the [[early modern period]] was mostly associated with positivity and goodness;<ref name="Lemon 2018" /> during this early modern and highly religious era of [[Christian revivalism]] and [[Pietism|Pietistic tendencies]],<ref name="Lemon 2018" /> it was seen as a way of "devoting oneself to another".<ref name="Rosenthal_2019" />

[[Addiction medicine|Modern research on addiction]] has led to a better understanding of the disease with research on the topic dating back to 1875, specifically on [[Morphine|morphine addiction]].<ref>{{cite book |last1=Institute of Medicine |title=Pathways of Addiction: Opportunities in Drug Abuse Research |date=1996 |publisher=National Academies Press |location=Washington}}</ref> This furthered the understanding of addiction being a medical condition. It was not until the 19th century that addiction was seen and acknowledged in the Western world as a disease, being both a physical condition and [[mental illness]].<ref>{{cite journal | vauthors = Bettinardi-Angres K, Angres DH |date=July 2010 |title=Understanding the Disease of Addiction | veditors = Alexander M |journal=Journal of Nursing Regulation |publisher=[[Elsevier]] on behalf of the [[National Council of State Boards of Nursing]] |volume=1 |issue=2 |pages=31–37 |doi=10.1016/S2155-8256(15)30348-3 |issn=2155-8256 |s2cid=143289528}}</ref> Today, addiction is understood both as a biopsychosocial and [[Brain disorder|neurological disorder]] that negatively impacts those who are affected by it, most commonly associated with the use of drugs and [[Alcohol use disorder|excessive use of alcohol]].<ref name="NIDA2020" /> The understanding of addiction has changed throughout history, which has impacted and continues to impact the ways it is medically treated and diagnosed.

=== The suffixes "-holic" and "-holism" ===
In contemporary modern English "-holic" is a [[suffix]] that can be added to a subject to denote an addiction to it. It was extracted from the word alcoholism (one of the first addictions to be widely identified both medically and socially) (correctly the root "[[wikt:alcohol|alcohol]]" plus the suffix "-ism") by misdividing or [[rebracketing]] it into "alco" and "-holism". There are correct [[medico-legal]] terms for such addictions: [[dipsomania]] is the medico-legal term for ''alcoholism'';<ref>{{cite web | url = http://www.etymonline.com/index.php?search=alcohol&searchmode=none | work = Online Etymology Dictionary | title = Alcohol }}</ref> other examples are in this table:

{| class="wikitable"
|-
! Colloquial term
! Addiction to
! Medico-legal term
|-
| [[chocoholic]]
| chocolate
|
|-
| danceaholic
| dance
| choreomania
|-
| [[rageaholic]]
| [[Rage (emotion)|rage]]
|
|-
| sexaholic
| sex
| [[erotomania]], [[satyriasis]], [[nymphomania]]
|-
| sugarholic
| sugar
| saccharomania
|-
| [[workaholic]]
| work
| ergomania
|}

=== Arts ===

The arts can be used in a variety of ways to address issues related to addiction. Art can be used as a form of therapy in the treatment of substance use disorders. Creative activities like painting, sculpting, music, and writing can help people express their feelings and experiences in safe and healthy ways. The arts can be used as an assessment tool to identify underlying issues that may be contributing to a person's substance use disorder. Through art, individuals can gain insights into their own motivations and behaviors that can be helpful in determining a course of treatment. Finally, the arts can be used to advocate for those suffering from a substance use disorder by raising awareness of the issue and promoting understanding and compassion. Through art, individuals can share their stories, increase awareness, and offer support and hope to those struggling with substance use disorders.

==== As therapy ====
Addiction treatment is complex and not always effective due to engagement and service availability concerns, so researchers prioritize efforts to improve treatment retention and decrease relapse rates.<ref>{{cite journal | vauthors = Appel PW, Ellison AA, Jansky HK, Oldak R | title = Barriers to enrollment in drug abuse treatment and suggestions for reducing them: opinions of drug injecting street outreach clients and other system stakeholders | journal = The American Journal of Drug and Alcohol Abuse | volume = 30 | issue = 1 | pages = 129–153 | date = 2004 | pmid = 15083558 | doi = 10.1081/ada-120029870 | s2cid = 20193011 }}</ref><ref>{{cite journal | vauthors = Megranahan K, Lynskey MT | journal=The Arts in Psychotherapy | title=Do creative arts therapies reduce substance misuse? A systematic review | volume=57 | pages=50–58 | date= February 2018 | issn=0197-4556 | doi=10.1016/j.aip.2017.10.005}}</ref> Characteristics of substance abuse may include feelings of isolation, a lack of confidence, communication difficulties, and a perceived lack of control.<ref>{{cite journal | vauthors= Moore RW, W | journal=The Arts in Psychotherapy | title=Art therapy with substance abusers: A review of the literature | volume=10 | issue=4 | pages=251–260 | date=1 December 1983 | issn=0197-4556 | doi=10.1016/0197-4556(83)90026-6}}</ref> In a similar vein, people suffering from substance use disorders tend to be highly sensitive, creative, and as such, are likely able to express themselves meaningfully in creative arts such as dancing, painting, writing, music, and acting.<ref>{{Citation | vauthors=((North American Drama Therapy Association)) | year=2016 | title=Drama therapy with addictions populations}}</ref> Further evidenced by Waller and Mahony (2002)<ref>{{cite book | veditors= Waller D, Mahony J | date=9 December 1998 | title=Treatment of Addiction: Current Issues for Arts Therapists | publisher=Routledge | doi=10.4324/9780203132395 | isbn=978-0-203-13239-5}}</ref> and Kaufman (1981),<ref>{{cite journal | vauthors = Kaufman GH | title = Art therapy with the addicted | journal = Journal of Psychoactive Drugs | volume = 13 | issue = 4 | pages = 353–360 | date = 1 July 1981 | pmid = 7040619 | doi = 10.1080/02791072.1981.10471892 | publisher = Taylor & Francis }}</ref> the creative arts therapies can be a suitable treatment option for this population especially when verbal communication is ineffective.

Primary advantages of art therapy in the treatment of addiction have been identified as:<ref>{{cite book |title=Treatment of Addiction: Current Issues for Arts Therapists |date=9 December 1998 |publisher=Routledge |isbn=978-0-203-13239-5 |veditors= Waller D, Mahony J |doi=10.4324/9780203132395}}</ref><ref name="Schmanke_2015">{{cite book |chapter-url=https://onlinelibrary.wiley.com/doi/abs/10.1002/9781118306543.ch35 |chapter=Art Therapy and Substance Abuse |vauthors= Schmanke L |title=The Wiley Handbook of Art Therapy |date=2015 |publisher=John Wiley & Sons, Ltd |isbn=978-1-118-30654-3 |pages=361–374 |doi=10.1002/9781118306543.ch35}}</ref>
* Assess and characterize a client's substance use issues
* Bypassing a client's resistances, defenses, and denial
* Containing shame or anger
* Facilitating the expression of suppressed and/or complicated emotions
* Highlighting a client's strengths
* Providing an alternative to verbal communication (via use of symbols) and conventional forms of therapy
* Providing clients with a sense of control
* Tackling feelings of isolation

Art therapy is an effective method of dealing with substance abuse in comprehensive treatment models. When included in psychoeducational programs, art therapy in a group setting can help clients internalize taught concepts in a more personalized manner.<ref name="Schmanke_2019">{{cite book | vauthors= Schmanke L | title= Art and Expressive Therapies within the Medical Model | date= 2019 | chapter=Art Therapy Applications and Substance Abuse | publisher=Routledge | edition=1st | pages=177–187 | doi=10.4324/9780429400087-16 | isbn=978-0-367-02340-9| s2cid= 208386296 }}</ref> During the course of treatment, by examining and comparing artwork created at different times, art therapists can be helpful in identifying and diagnosing issues, as well as charting the extent or direction of improvement as a person detoxifies.<ref name="Schmanke_2019" /> Where increasing adherence to treatment regimes and maintaining abstinence is the target; art therapists can aid by customizing treatment directives (encourage the client to create collages that compare pros and cons, pictures that compare past and present and future, and drawings that depict what happened when a client went off medication).<ref name="Schmanke_2019" />

Art therapy can function as a complementary therapy used in conjunction with more conventional therapies and can can integrate with harm reduction protocols to minimize the negative effects of drug use.<ref>{{cite journal | vauthors = Chiang M, Reid-Varley WB, Fan X | title = Creative art therapy for mental illness | journal = Psychiatry Research | volume = 275 | pages = 129–136 | date = May 2019 | pmid = 30901671 | doi = 10.1016/j.psychres.2019.03.025 | s2cid = 78090920 }}</ref><ref name="Schmanke_2015" /> An evaluation of art therapy incorporation within a pre-existing Addiction Treatment Programme based on the 12 step Minnesota Model endorsed by the Alcoholics Anonymous found that 66% of participants expressed the usefulness of art therapy as a part of treatment.<ref>{{cite journal |vauthors= Dickson C |date=June 2007 |title=An evaluation study of art therapy provision in a residential Addiction Treatment Programme (ATP) |journal=International Journal of Art Therapy |volume=12 |issue=1 |pages=17–27 |doi=10.1080/17454830701265220 |s2cid=72987664 |issn=1745-4832}}</ref><ref name="Schmanke_2015" /> Within the weekly art therapy session, clients were able to reflect and process the intense emotions and cognitions evoked by the programme. In turn, the art therapy component of the programme fostered stronger self-awareness, exploration, and externalization of repressed and unconscious emotions of clients, promoting the development of a more integrated 'authentic self'.<ref>{{cite journal |vauthors= Matto H, Corcoran J, Fassler, A |date=January 2003 |title=Integrating solution-focused and art therapies for substance abuse treatment: guidelines for practice |journal=The Arts in Psychotherapy |volume=30 |issue=5 |pages=265–272 |doi=10.1016/j.aip.2003.08.003 |issn=0197-4556}}</ref><ref name="Schmanke_2015" />

Despite the large number of randomized control trials, clinical control trials, and anecdotal evidence supporting the effectiveness of art therapies for use in addiction treatment, a systematic review conducted in 2018 could not find enough evidence on visual art, drama, dance and movement therapy, or 'arts in health' methodologies to confirm their effectiveness as interventions for reducing substance misuse.<ref name="Megranahan_2018">{{cite journal |vauthors= Megranahan K, Lynskey MT |date=February 2018 |title=Do creative arts therapies reduce substance misuse? A systematic review |journal=The Arts in Psychotherapy |volume=57 |pages=50–58 |doi=10.1016/j.aip.2017.10.005 |issn=0197-4556}}</ref> Music therapy was identified to have potentially strong beneficial effects in aiding contemplation and preparing those diagnosed with substance use for treatment.<ref name="Megranahan_2018" />

==== As an assessment tool ====
The Formal Elements Art Therapy Scale (FEATS) is an assessment tool used to evaluate drawings created by people suffering from substance use disorders by comparing them to drawings of a control group (consisting of individuals without SUDs).<ref name="Rockwell_2006">{{cite journal |vauthors= Rockwell P, Dunham M |date=January 2006 |title=The Utility of the Formal Elements Art Therapy Scale in Assessment for Substance Use Disorder |journal=Art Therapy |volume=23 |issue=3 |pages=104–111 |doi=10.1080/07421656.2006.10129625 |s2cid=5541133 |issn=0742-1656}}</ref><ref name="Schmanke_2015" /> FEATS consists of twelve elements, three of which were found to be particularly effective at distinguishing the drawings of those with SUDs from those without: Person, Realism, and Developmental. The Person element assesses the degree to which a human features are depicted realistically, the Realism element assesses the overall complexity of the artwork, and the Developmental element assesses "developmental age" of the artwork in relation to standardized drawings from children and adolescents.<ref name="Rockwell_2006" /> By using the FEATS assessment tool, clinicians can gain valuable insight into the drawings of individuals with SUDs, and can compare them to those of the control group. Formal assessments such as FEATS provide healthcare providers with a means to quantify, standardize, and communicate abstract and visceral characteristics of SUDs to provide more accurate diagnoses and informed treatment decisions.<ref name="Rockwell_2006" />

Other artistic assessment methods include the Bird's Nest Drawing: a useful tool for visualizing a client's attachment security.<ref>{{cite journal |vauthors= Francis D, Kaiser D, Deaver SP |date=22 April 2011 |title=Representations of Attachment Security in the Bird's Nest Drawings of Clients with Substance Abuse Disorders |url=https://www.tandfonline.com/doi/abs/10.1080/07421656.2003.10129571 |journal=Art Therapy |volume=20 |issue=3 |pages=125–137 |publisher=Routledge |doi=10.1080/07421656.2003.10129571 |s2cid=142341708 |issn=0742-1656 |access-date=4 December 2022}}</ref><ref name="Schmanke_2015" /> This assessment method looks at the amount of color used in the drawing, with a lack of color indicating an 'insecure attachment', a factor that the client's therapist or recovery framework must take into account.<ref>{{cite journal | vauthors = Ball SA, Legow NE | title = Attachment theory as a working model for the therapist transitioning from early to later recovery substance abuse treatment | journal = The American Journal of Drug and Alcohol Abuse | volume = 22 | issue = 4 | pages = 533–547 | date = November 1996 | pmid = 8911591 | doi = 10.3109/00952999609001679 | publisher = Taylor & Francis }}</ref>

Art therapists working with children of parents suffering from alcoholism can use the Kinetic Family Drawings assessment tool to shed light on family dynamics and help children express and understand their family experiences.<ref name="Indicators of Familial Alcoholism i">{{cite journal |vauthors= Holt ES, Kaiser DH |date=January 2001 |title=Indicators of Familial Alcoholism in Children's Kinetic Family Drawings |journal=Art Therapy |volume=18 |issue=2 |pages=89–95 |doi=10.1080/07421656.2001.10129751 |s2cid=141669979 |issn=0742-1656 }}</ref><ref name="Schmanke_2015" /> The KFD can be used in family sessions to allow children to share their experiences and needs with parents who may be in recovery from alcohol use disorder. Depiction of isolation of self and isolation of other family members may be an indicator of parental alcoholism.<ref name="Indicators of Familial Alcoholism i" />

==== Advocacy ====
Stigma can lead to feelings of shame that can prevent people with substance use disorders from seeking help and interfere with provision of harm reduction services.<ref>{{cite journal | vauthors = Ashford RD, Brown AM, Curtis B | title = Systemic barriers in substance use disorder treatment: A prospective qualitative study of professionals in the field | journal = Drug and Alcohol Dependence | volume = 189 | pages = 62–69 | date = August 2018 | pmid = 29883870 | doi = 10.1016/j.drugalcdep.2018.04.033 | s2cid = 47011510 }}</ref><ref>{{cite journal | vauthors = Barry CL, McGinty EE, Pescosolido BA, Goldman HH | title = Stigma, discrimination, treatment effectiveness, and policy: public views about drug addiction and mental illness | journal = Psychiatric Services | volume = 65 | issue = 10 | pages = 1269–1272 | date = October 2014 | pmid = 25270497 | doi = 10.1176/appi.ps.201400140 | pmc = 4285770 }}</ref><ref>{{Citation |title=Philly Council bill to block supervised injection sites advances - WHYY |url=https://whyy.org/articles/bill-to-prevent-supervised-injection-sites-from-opening-in-philly-advances/ |year=2020 |access-date=14 December 2022 |vauthors= Feldman N}}</ref> It can influence healthcare policy, making it difficult for these individuals to access treatment.<ref>{{Citation |title=Implementation of the Provision of the Comprehensive Addiction and Recovery Act of 2016 Relating to the Dispensing of Narcotic Drugs for Opioid Use Disorder |url=https://www.federalregister.gov/documents/2018/01/23/2018-01173/implementation-of-the-provision-of-the-comprehensive-addiction-and-recovery-act-of-2016-relating-to |year=2018 |access-date=14 December 2022 |vauthors=((Drug Enforcement Administration))}}</ref>

Artists attempt to change the societal perception of addiction from a punishable moral offense to instead a chronic illness necessitating treatment. This form of advocacy can help to relocate the fight of addiction from a judicial perspective to the public health system.<ref name="Henningfield_2010">{{Cite book |url=https://www.worldcat.org/oclc/794700340 |title=Addiction and art |date=2010 |publisher=Johns Hopkins University Press | vauthors = Henningfield JE, Dowell ML, Santora PB |isbn=978-1-4214-0023-5 |location=Baltimore |oclc=794700340}}</ref>

Artists who have personally lived with addiction and/or undergone recovery may use art to depict their experiences in a manner that uncovers the "human face of addiction". By bringing experiences of addiction and recovery to a personal level and breaking down the "us and them", the viewer may be more inclined to show compassion, forego stereotypes and stigma of addiction, and label addiction as a social rather than individual problem.<ref name="Henningfield_2010" />

According to Santora<ref name="Henningfield_2010" /> the main purposes in using art as a form of advocacy in the education and prevention of substance use disorders include:
* Addiction art exhibitions can come from a variety of sources, but the underlying message of these works is the same: to communicate through emotions without relying on intellectually demanding/gatekept facts and figures. These exhibitions can either stand alone, reinforce, or challenge facts.
* A powerful educational tool for increasing awareness and understanding of addiction as a medical illness. Exhibitions featuring personal stories and images can help to create lasting impressions on diverse audiences (including addiction scientists/researchers, family/friends of those affected by addiction etc.), highlighting the humanity of the problem and in turn encouraging compassion and understanding.
* A way to destigmatize substance use disorders and shift public perception from viewing them as a moral failing to understanding them as a chronic medical condition which requires treatment.
* Provide those who are struggling with addiction assurance and encouragement of healing, and let them know that they are not alone in their struggle.
* The use of visual arts can help bring attention to the lack of adequate substance use treatment, prevention, and education programs and services in a healthcare system. Messages can encourage policymakers to allocate more resources to addiction treatment and prevention from federal, state, and local levels.

The Temple University College of Public Health department conducted a project to promote awareness around opioid use and reduce associated stigma by asking students to create art pieces that were displayed on a website they created and promoted via social media.<ref name="Dingman_2021" /> Quantitative and qualitative data was recorded to measure engagement, and the student artists were interviewed, which revealed a change in perspective and understanding, as well as greater appreciation of diverse experiences. Ultimately, the project found that art was an effective medium for empowering both the artist creating the work and the person interacting with it.<ref name="Dingman_2021">{{cite journal | vauthors= Dingman DA, Zibalese-Crawford, M | journal=Journal of Alcohol & Drug Education | title=Reducing Substance Use Related Stigma through Expressions of Artwork | volume=65 | issue=1 | pages=29–39 | publisher=American Alcohol & Drug Information Foundation | date= April 2021 | issn=0090-1482}}</ref>

Another author critically examined works by contemporary Canadian artists that deal with addiction via the metaphor of a cultural landscape to "unmap" and "remap" ideologies related to Indigenous communities and addiction to demonstrate how colonial violence in Canada has drastically impacted the relationship between Indigenous peoples, their land, and substance abuse.<ref>{{cite journal | vauthors= Skelly J | journal=Journal of Canadian Studies | title=Alternative Paths: Mapping Addiction in Contemporary Art by Landon Mackenzie, Rebecca Belmore, Manasie Akpaliapik, and Ron Noganosh | volume=49 | issue=2 | pages=268–295, 356 | publisher=University of Toronto Press | date= 2015 | issn=0021-9495 | doi=10.3138/jcs.49.2.268| s2cid=148421461 }}</ref>

A project known as "Voice" was a collection of art, poetry and narratives created by women living with a history of addiction to explore women's understanding of harm reduction, challenge the effects of stigma and give voice to those who have historically been silenced or devalued.<ref name="Paivinen_2008" /> In the project, nurses with knowledge of mainstream systems, aesthetic knowing, feminism and substance use organized weekly gatherings, wherein women with histories of substance use and addiction worked alongside a nurse to create artistic expressions. Creations were presented at several venues, including an International Conference on Drug Related Harm, a Nursing Conference and a local gallery to positive community response.<ref name="Paivinen_2008">{{cite journal | vauthors = Paivinen H, Bade S | title = Voice: challenging the stigma of addiction; a nursing perspective | journal = The International Journal on Drug Policy | volume = 19 | issue = 3 | pages = 214–219 | date = June 2008 | pmid = 18439812 | doi = 10.1016/j.drugpo.2008.02.011 }}</ref>

=== Narrative Approach and Addiction ===
The narrative medicine to addiction focuses on recognizing, absorbing, and interpreting the stories of those suffering from addiction, allowing for better understanding of their experiences<ref>{{Cite book | vauthors = Marini MM  |url= https://www.worldcat.org/oclc/922640395 |title=Narrative medicine : bridging the gap between evidence-based care and medical humanities |date=2016 |isbn=978-3-319-22090-1 |location=Cham |oclc=922640395}}</ref> with narrative analysis being used to study the discourse of those with addiction. This knowledge can be used to develop better care plans with the potential to increase patient compliance and make treatment more effective.

A narrative study demonstrated and studied cognitive and emotional tendencies among substance abusers during treatment periods to learn more about motivation and ambivalence inherent in recovery over the course of a residential treatment program.<ref name="Taylor & Francis Ltd">{{cite journal | vauthors=((Flora, K.)) | journal=Journal of Social Work Practice in the Addictions | title=Recovery From Substance Abuse: A Narrative Approach to Understanding the Motivation and Ambivalence About Change | volume=12 | issue=3 | pages=302–315 | publisher=Taylor & Francis Ltd | date= July 2012 | issn=1533-256X | doi=10.1080/1533256X.2012.702630| s2cid=143901063 }}</ref> Seven narrative types emerged from the overall analysis: optimistic, overly optimistic, pessimistic, overly pessimistic, "tough life," troubled/confused, and balanced. Narratives tended to express a basic level of emotionality in early stages of treatment ("optimistic", "pessimistic" narrative). Over time, as clients progressed through the program, their stories became more complex and detailed, including their drug abuse and recovery efforts, more skeptical positions towards treatment began to emerge.  Clients began to distinguish between the positive and negative aspects of treatment, creating more "balanced" narratives in the process.<ref name="Taylor & Francis Ltd" />

Due to higher medication consumption, social isolation, financial worries, and other factors, older adults are particularly vulnerable to substance use problems.<ref name="Gardner_2009" /> Incidence of addiction among this population is inaccurately reported. Narrative therapy can provide an avenue to unearth stories of addiction in an empowering manner, and thus serves as a viable therapeutic tool in applied gerontology.<ref name="Gardner_2009">{{cite journal | vauthors= Gardner PJ, Poole JM | journal=Journal of Applied Gerontology | title=One Story at a Time: Narrative Therapy, Older Adults, and Addictions | volume=28 | issue=5 | pages=600–620 | date= October 2009 | issn=0733-4648 | doi=10.1177/0733464808330822| s2cid=71341761 }}</ref> When treating substance abuse in older adults, it is essential to ensure that the client is respected and comfortable disclosing information. This should be done at the outset of treatment when the therapist and older adult are developing the therapeutic relationship.<ref name = "Morgan_2011" /> The social breakdown model is an important tool that can consider the compounded effects of ageism, physical changes, social changes, and substance abuse. The narrative approach integrates the social breakdown model with substance abuse challenges and can be an effective way to address addiction in this population.<ref name = "Morgan_2011">{{cite journal | vauthors= Morgan ML, Brosi WA, Brosi MW | journal=American Journal of Family Therapy | title=Restorying Older Adults' Narratives About Self and Substance Abuse | volume=39 | issue=5 | pages=444–455 | date=10 December 2011 | issn=0192-6187 | doi=10.1080/01926187.2011.560784| s2cid=145136521 }}</ref>

A study conducted in 2009 in the Republic of Moldova looked into the social dynamics of initiating injection drug usage by examining 42 audio-recorded, semi-structured interviews with present and former injectors.<ref name="Rhodes_2011" /> A thematic analysis suggested that self-injection was viewed as a symbolic transition of identity, enabled by interpersonal interactions and collective influences. Personal narratives of self-transition were connected to larger narratives of social transitions. The personal narratives of self-initiation and transition are contextualized and understood in terms of political (social) narratives within the core concept of the 'transitional society'.<ref name="Rhodes_2011">{{cite journal | vauthors=Rhodes T, Bivol S, Scutelniciuc O, Hunt N, Bernays S, Busza J | journal=International Journal of Drug Policy | title=Narrating the social relations of initiating injecting drug use: Transitions in self and society | volume=22 | issue=6 | pages=445–454 | publisher=Elsevier B.V. | date= November 2011 | issn=0955-3959 | doi=10.1016/j.drugpo.2011.07.012| pmid=21903372 }}</ref> Another study examined the narratives of 'initiators': people who help people who inject drugs (PWID) with their first injection.<ref name="Weicker_2021">{{cite journal | vauthors= Weicker NP, Whaley S, Urquhart G, Park JN, Sherman SG, Owczarzak J | journal=Substance Use & Misuse | title="I Know It Is Going to Ruin Their Life:" Fortune-Telling, Agency, and Harm Reduction in Narratives Concerning Injection Initiation Assistance | volume=56 | issue=12 | pages=1860–1868 | date= October 2021 | doi=10.1080/10826084.2021.1958854 | pmid=34348070 | s2cid=236928168 | issn=1082-6084}}</ref> Through their accounts, respondents described initiation events as meaningful transitions to a life characterized by predictable downfalls of homelessness, infections, and [[social stigma]]. Initiators used examples from their own personal experience to explain the process of initiation and assistance, attributing personal agency and predicting specific injection-related harms for initiates. They distinguished between two forms of harm: potentially avoidable proximal harm caused by risky injection practices (e.g. overdose, HIV) and perceived inevitable distal harm caused by long-term injection (e.g. socioeconomic decline).<ref name="Weicker_2021" /> In this way, these narratives reflect a balance of individual agency, harm reduction intentions, and accepted notions of 'life after initiation' interact with the narrative experiences and intentions of PWIDs.<ref name="Rhodes_2011" /><ref name="Weicker_2021" />

=== Philosophy ===

From a philosophy perspective, the behavior of many with addiction that is not explained by executive dysfunction or biological reasons can be explained by folk psychology{{spaced ndash}}specifically the [[Folk psychology#Belief–desire model|belief–desire model]].<ref name="Levy2019">{{Cite book | vauthors = Levy N | veditors = Pickard H, Ahmed SH |chapter-url=http://www.ncbi.nlm.nih.gov/books/NBK540394/ |title=The Routledge handbook of philosophy and science of addiction |chapter=Chapter 5 Addiction: The belief oscillation hypothesis |series=Wellcome Trust–Funded Monographs and Book Chapters |isbn=978-1-138-90928-1 |oclc=1042341025 |pmid=31017751 |doi=10.4324/9781315689197-6 |date=2019 |place=Oxon (UK) |publisher=Routledge| s2cid = 242067468 }}</ref> According to this model, a person acquires and uses a substance or does an addictive activity in belief that it will help them achieve a goal.

== Social scientific models ==
[[File:An alcoholic man with delirium Wellcome L0060780 (level correction).jpg|thumb|right|Acute confusional state caused by [[Alcohol withdrawal syndrome|alcohol withdrawal]], otherwise known as ''[[delirium tremens]]'']]

=== Biopsychosocial–cultural–spiritual ===
While regarded [[Biomedicine|biomedically]] as a [[Neuropsychology|neuropsychological]] disorder, addiction is multi-layered, with [[Biology|biological]], psychological, social, [[Culture|cultural]], and [[Spirituality|spiritual]] (biopsychosocial–cultural–spiritual) elements.<ref>{{Cite journal | vauthors = Rau BL |date=September 2014 |title=The Oxford Handbook of Evidence-Based Management, Rousseau DM 2012. 432 pages, hardcover. New York, NY: Oxford University Press. |journal=Academy of Management Learning & Education |volume=13 |issue=3 |pages=485–487 |doi=10.5465/amle.2013.0309 |issn=1537-260X}}</ref><ref>{{cite journal | vauthors = Daley DC | title = Family and social aspects of substance use disorders and treatment | journal = Journal of Food and Drug Analysis | volume = 21 | issue = 4 | pages = S73–S76 | date = December 2013 | pmid = 25214748 | pmc = 4158844 | doi = 10.1016/j.jfda.2013.09.038 }}</ref> A biopsychosocial–cultural–spiritual approach fosters the crossing of [[Academic discipline|disciplinary]] boundaries, and promotes [[Holism|holistic]] considerations of addiction.<ref>{{cite journal | vauthors = Saad M, de Medeiros R, Mosini AC | title = Are We Ready for a True Biopsychosocial-Spiritual Model? The Many Meanings of "Spiritual" | journal = Medicines | volume = 4 | issue = 4 | pages = 79 | date = October 2017 | pmid = 29088101 | pmc = 5750603 | doi = 10.3390/medicines4040079 | doi-access = free }}</ref><ref>{{Cite book | veditors = Farmer P, Kleinman A, Kim J, Basilico M |title=Reimagining Global Health: An Introduction |date=31 December 2019 |publisher=University of California Press |doi=10.1525/9780520954632 |s2cid=168489288 |isbn=978-0-520-95463-2 }}</ref><ref>{{Cite journal | vauthors = Weakland JH |date=October 1961 |title=The Essence of Anthropological Education  |journal=American Anthropologist |volume=63 |issue=5 |pages=1094–1097 |doi=10.1525/aa.1961.63.5.02a00130 |issn=0002-7294}}</ref> A biopsychosocial–cultural–spiritual approach considers, for example, how physical environments influence experiences, habits, and patterns of addiction.

[[Ethnography|Ethnographic]] engagements and developments in fields of knowledge have contributed to biopsychosocial–cultural–spiritual understandings of addiction, including the work of [[Philippe Bourgois]], whose [[Field research#In anthropology|fieldwork]] with street-level drug dealers in [[East Harlem]] highlights correlations between drug use and structural [[oppression]] in the United States.<ref>{{Cite book | vauthors = Bourgois P |url=https://www.cambridge.org/core/product/identifier/9780511808562/type/book |title=In Search of Respect: Selling Crack in El Barrio |series=Structural Analysis in the Social Sciences |date=23 December 2002 |publisher=Cambridge University Press |isbn=978-0-521-01711-4 |edition=2 |doi=10.1017/cbo9780511808562}}</ref> Prior models that have informed the prevailing biopsychosocial–cultural–spiritual consideration of addiction include:

=== Cultural model ===
The cultural model, an [[Anthropology|anthropological]] understanding of the emergence of drug use and abuse, was developed by [[Dwight B. Heath|Dwight Heath]].<ref name="Singer_2012">{{cite journal | vauthors = Singer M | title = Anthropology and addiction: an historical review | journal = Addiction | volume = 107 | issue = 10 | pages = 1747–1755 | date = October 2012 | pmid = 22962955 | doi = 10.1111/j.1360-0443.2012.03879.x }}</ref> Heath undertook ethnographic research and [[Field research|fieldwork]] with the [[Camba]] people of [[Bolivia]] from June 1956 to August 1957.<ref name="Heath_1958">{{cite journal | vauthors = Heath DB | title = Drinking patterns of the Bolivian Camba | journal = Quarterly Journal of Studies on Alcohol | volume = 19 | issue = 3 | pages = 491–508 | date = September 1958 | pmid = 13579177 | doi = 10.15288/qjsa.1958.19.491 }}</ref> Heath observed that adult members of society drank 'large quantities of [[rum]] and became intoxicated for several contiguous days at least twice a month'.<ref name="Singer_2012" /> This frequent, heavy drinking from which [[Alcohol intoxication|intoxication]] followed was typically undertaken socially, during festivals.<ref name="Heath_1958" /> Having returned in 1989, Heath observed that while much had changed, 'drinking parties' remained, as per his initial observations, and 'there appear to be no harmful consequences to anyone'.<ref>{{Cite journal | vauthors = Heath DB |date=January 1995 |title=Changes in Drinking Patterns in Bolivian Cultures: A Cautionary Tale About Historical Approaches |journal=Addiction Research |language=en |volume=2 |issue=3 |pages=307–318 |doi=10.3109/16066359509005215 |issn=1058-6989}}</ref> Heath's observations and [[Social interaction|interactions]] reflected that this form of [[social behavior]], the habitual heavy consumption of alcohol, was encouraged and valued, enforcing social bonds in the Camba community.<ref name="Heath_1958" /> Despite frequent intoxication, "even to the point of unconsciousness", the Camba held no concept of alcoholism (a form of addiction), and no visible social problems associated with drunkenness, or addiction, were apparent.<ref name="Singer_2012" />

As noted by [[Merrill Singer]], Heath's findings, when considered alongside subsequent cross-cultural experiences, challenged the perception that [[Substance intoxication|intoxication]] is socially 'inherently disruptive'.<ref name="Singer_2012" /> Following this [[fieldwork]], Heath proposed the 'cultural model', suggesting that 'problems' associated with heavy drinking, such as alcoholism – a recognised form addiction – were cultural: that is, that alcoholism is determined by cultural beliefs, and therefore varies among cultures. Heath's findings challenged the notion that 'continued use [of alcohol] is inexorably addictive and damaging to the consumer's health'.<ref name="Heath_1958" /><ref name="Singer_2012" />

The cultural model did face criticism by [[Sociology|Sociologist]] [[Robin Room]] and others, who felt anthropologists could "downgrade the severity of the problem".<ref name="Singer_2012" /> Merrill Singer found it notable that the ethnographers working within the prominence of the cultural model were part of the 'wet generation': while not blind to the 'disruptive, dysfunctional and debilitating effects of alcohol consumption', they were products 'socialized to view alcohol consumption as normal'.<ref name="Singer_2012" />

=== Subcultural model ===
Historically, addiction has been viewed from the [[Emic and etic|etic]] perspective, defining users through the [[pathology]] of their condition.<ref>{{Cite encyclopedia | vauthors = Burraway J |date=October 2020 | veditors = Stein F, Diemberger H, Stasch R, Robbins J, Sanchez A, Lazar S, Candea M |title=Addiction |url=https://www.anthroencyclopedia.com/entry/addiction |encyclopedia=[[Open Encyclopedia of Anthropology]]|doi=10.29164/20addiction|s2cid=241689890 |doi-access=free }}</ref> As reports of drug use rapidly increased, the cultural model found application in anthropological research exploring western drug [[subculture]] practices.<ref name="Singer_2012" />

The approach evolved from the ethnographic exploration into the lived experiences and [[Subjectivity|subjectivities]] of 1960s and 1970s drug subcultures.<ref name="Singer_2012" /> The seminal publication "Taking care of business", by Edward Preble and John J. Casey, documented the daily lives of New York street-based intravenous heroin users in rich detail, providing unique insight into the dynamic social worlds and activities that surrounded their drug use.<ref>{{Cite journal | vauthors = Preble E, Casey JJ |date=January 1969 |title=Taking Care of Business—The Heroin User's Life on the Street |url=http://dx.doi.org/10.3109/10826086909061998 |journal=International Journal of the Addictions |volume=4 |issue=1 |pages=1–24 |doi=10.3109/10826086909061998 |issn=0020-773X}}</ref> These findings challenge popular narratives of [[immorality]] and [[Deviance (sociology)|deviance]], conceptualizing substance abuse as a social [[phenomenon]]. The prevailing culture can have a greater influence on drug taking behaviors than the physical and psychological effects of the drug itself.<ref name="Golub_2005">{{cite journal | vauthors = Golub A, Johnson BD, Dunlap E | title = Subcultural evolution and illicit drug use | journal = Addiction Research & Theory | volume = 13 | issue = 3 | pages = 217–229 | date = May 2005 | pmid = 23805068 | pmc = 3690817 | doi = 10.1080/16066350500053497 }}</ref>{{Better source needed|reason=The source doesn't really say the prevailing culture has a "greater influence" in addition to being old per MEDRS.|date=March 2023}} To [[Social exclusion|marginalized]] individuals, drug subcultures can provide social connection, [[symbol]]ic meaning, and socially constructed purpose that they may feel is unattainable through conventional means.<ref name="Golub_2005" /> The subcultural model demonstrates the complexities of addiction, highlighting the need for an integrated approach. It contends that a [[Biosocial theory|biosocial]] approach is required to achieve a holistic understanding of addiction.<ref name="Singer_2012" />

=== Critical medical anthropology model ===
Emerging in the early 1980s, the critical medical anthropology model was introduced, and as Merrill Singer offers 'was applied quickly to the analysis of drug use'.<ref name="Singer_2012" /> Where the cultural model of the 1950s looked at the social body, the critical medical anthropology model revealed the [[body politic]], considering drug use and addiction within the context of macro level structures including larger political systems, [[Economic inequality|economic inequalities]], and the institutional power held over social processes.<ref name="Singer_2012" />

Highly relevant to addiction, the three issues emphasized in the model are:
* [[Self-medication]]
* The social production of suffering
* The political economy ([[Licit and Illicit Drugs]])<ref name="Singer_2012" />

These three key points highlight how drugs may come to be used to self-medicate the [[psychological trauma]] of socio-political disparity and [[injustice]], intertwining with [[Licit and Illicit Drugs|licit and illicit drug]] market politics.<ref name="Singer_2012" /> Social suffering, "the misery among those on the weaker end of power relations in terms of physical health, mental health and lived experience", is used by anthropologists to analyze how individuals may have personal problems caused by political and economic power.<ref name="Singer_2012" /> From the perspective of critical medical anthropology heavy drug use and addiction is a consequence of such larger scale unequal distributions of power.<ref name="Singer_2012" />

The three models developed here – the cultural model, the subcultural model, and the Critical Medical Anthropology Model – display how addiction is not an experience to be considered only biomedically. Through consideration of addiction alongside the biological, psychological, social, cultural and spiritual (biopsychosocial–spiritual) elements which influence its experience, a holistic and comprehensive understanding can be built.

== Social learning models ==

=== Social learning theory ===
{{Main|Social learning theory}}

Albert Bandura's 1977 social learning theory posits that individuals acquire addictive behaviors by observing and imitating models in their social environment.<ref>Falk, Richard; Kim, Samuel S. (2019-08-15). ''The War System: An Interdisciplinary Approach''. Routledge. {{ISBN|978-1-000-23507-4}}</ref><ref>"Bandura, Albert: Social Learning Theory", ''Encyclopedia of Criminological Theory'', 2455 Teller Road, Thousand Oaks California 91320 United States: SAGE Publications, Inc., 2010, retrieved 2023-11-09</ref> The likelihood of engaging in and sustaining similar addictive behaviors is influenced by the reinforcement and punishment observed in others. The principle of reciprocal determinism suggests that the functional relationships between personal, environmental, and behavioral factors act as determinants of addictive behavior.<ref>Smith, Mark A. (2021-02-01). "Social Learning and Addiction". ''Behavioural Brain Research''. '''398''': 112954. {{doi|10.1016/j.bbr.2020.112954}} {{ISSN|0166-4328}}</ref> Thus, effective treatment targets each dynamic facet of the biopsychosocial disorder.

=== Transtheoretical model (stages of change model) ===
{{Main|Transtheoretical model}}

The transtheoretical model of change suggests that overcoming an addiction is a stepwise process that occurs through several stages.<ref>Brinthaupt, Thomas M.; Lipka, Richard P. (1994-10-11). ''Changing the Self: Philosophies, Techniques, and Experiences''. State University of New York Press. {{ISBN|978-0-7914-9754-8}}</ref>

'''Precontemplation:''' This initial stage precedes individuals considering a change in their behavior. They might be oblivious to or in denial of their addiction, failing to recognize the need for change.

'''Contemplation''' is the stage in which individuals become aware of the problems caused by their addiction and are considering change. Although they may not fully commit, they weigh the costs and benefits of making a shift.

'''Preparation:''' Individuals in this stage are getting ready to change. They might have taken preliminary steps, like gathering information or making small commitments, in preparation for behavioral change.

'''Action''' involves actively modifying behavior by making specific, observable changes to address the addictive behavior. The action stage requires significant effort and commitment.

'''Maintenance:''' After successfully implementing a change, individuals enter the maintenance stage, where they work to sustain the new behavior and prevent relapse. This stage is characterized by ongoing effort and consolidation of gains.

'''Termination/relapse prevention:''' Recognizing that relapse is a common part of the change process, this stage focuses on identifying and addressing factors that may lead to a return to old behaviors. Relapse is viewed as an opportunity for learning and strategy adjustment, with the ultimate goal of eliminating or terminating the targeted behavior.

The transtheoretical model can be helpful in guiding development of tailored behavioral interventions that can promote lasting change. Progression through these stages may not always follow a linear path, as individuals may move back and forth between stages. Resistance to change is recognized as an expected part of the process.

Addiction causes an "astoundingly high financial and human toll" on individuals and society as a whole.<ref name="Societal toll">{{cite book |title=Molecular Neuropharmacology: A Foundation for Clinical Neuroscience |vauthors=Malenka RC, Nestler EJ, Hyman SE |publisher=McGraw-Hill Medical |year=2009 |isbn=978-0-07-148127-4 |veditors=Sydor A, Brown RY |edition=2nd |location=New York |page=4 |chapter=Chapter 1: Basic Principles of Neuropharmacology |quote=Drug abuse and addiction exact an astoundingly high financial and human toll on society through direct adverse effects, such as lung cancer and hepatic cirrhosis, and indirect adverse effects&nbsp;–for example, accidents and AIDS&nbsp;– on health and productivity.}}</ref><ref name="Epidem" /><ref name="ABAM" /> In the United States, the total economic cost to society is greater than that of all types of diabetes and all cancers combined.<ref name="ABAM" /> These costs arise from the direct adverse effects of drugs and associated healthcare costs (e.g., emergency medical services and outpatient and inpatient care), long-term complications (e.g., lung cancer from smoking tobacco products, [[liver cirrhosis]] and [[Alcohol-related dementia|dementia]] from chronic alcohol consumption, and [[meth mouth]] from methamphetamine use), the loss of productivity and associated welfare costs, fatal and non-fatal accidents (e.g., traffic collisions), suicides, homicides, and incarceration, among others.<ref name="Societal toll" /><ref name="Epidem" /><ref name="ABAM" /><ref name="INCB 2013">{{cite book |url=https://www.incb.org/documents/Publications/AnnualReports/AR2013/English/AR_2013_E.pdf |title=International Narcotics Control Board Report: 2013 |date=2013 |publisher=United Nations&nbsp;– [[International Narcotics Control Board]] |isbn=978-92-1-148274-4 |chapter=Economic consequences of drug abuse |access-date=28 September 2018 |chapter-url=https://www.incb.org/documents/Publications/AnnualReports/Thematic_chapters/English/AR_2013_E_Chapter_I.pdf}}</ref> The US National Institute on Drug Abuse has found that overdose deaths in the US have almost tripled among male and females from 2002 to 2017, with 72,306 overdose deaths reported in 2017 in the US.<ref>{{Cite news |date=9 August 2018 |title=Overdose Death Rates |publisher=National Institute on Drug Abuse |url=https://www.drugabuse.gov/related-topics/trends-statistics/overdose-death-rates |access-date=17 September 2018}}</ref> 2020 marked the year with highest number of overdose deaths over a 12-month period, with 81,000 overdose deaths, exceeding the records set in 2017.<ref>{{Cite news |date=18 December 2020 |title=Overdose Deaths Accelerating During Covid-19 |publisher=Centers For Disease Control Prevention |url=https://www.cdc.gov/media/releases/2020/p1218-overdose-deaths-covid-19.html |access-date=10 February 2021}}</ref>

== See also ==
{{Columns-list|colwidth=30em
|
* [[Autonomic nervous system]]
* [[Binge drinking]]
* [[Binge eating disorder]]
* [[Cognitive liberty]]
* [[Discrimination against drug addicts]]
* [[Dopaminergic pathways]]
* [[Pavlovian-instrumental transfer]]
* [[Philosophy of medicine]]
* [[Substance dependence]]
}}

==Endnotes==
{{Notelist}}

==Notes==
{{Reflist|group=note}}

; Image legend
{{Reflist|group=Color legend}}

==References==
{{Reflist}}

==Further reading==
{{Refbegin}}
* {{Cite journal | vauthors = Pelchat ML |date=March 2009 |title=Food Addiction in Humans |journal=The Journal of Nutrition |language=en |volume=139 |issue=3 |pages=620–622 |doi=10.3945/jn.108.097816|pmid=19176747 |doi-access=free }}
* {{cite journal | vauthors = Gordon HW | title = Laterality of Brain Activation for Risk Factors of Addiction | journal = Current Drug Abuse Reviews | volume = 9 | issue = 1 | pages = 1–18 | date = April 2016 | pmid = 26674074 | pmc = 4811731 | doi = 10.2174/1874473709666151217121309 }}
* {{cite book | vauthors = Szalavitz M |title=Unbroken Brain |year=2016 |isbn=978-1-250-05582-8 |publisher=St. Martin's Press |url-access=registration |url=https://archive.org/details/unbrokenbrainrev0000szal }}
{{Refend}}

==External links==
{{wiktionary|-ism}}
{{wiktionary|-holic}}
{{Commons category}}
* {{cite web |url=http://learn.genetics.utah.edu/content/addiction/ |title=The Science of Addiction: Genetics and the Brain |author=<!--Staff writer(s); no by-line.--> |website=learn.genetics.utah.edu |publisher=Learn.Genetics – [[University of Utah]] }}
* [http://www.tedmed.com/talks/show?id=309096 Why do our brains get addicted?]&nbsp;– a [[TEDMED]] 2014 talk by [[Nora Volkow]], the director of the [[National Institute on Drug Abuse]] at [[National Institutes of Health|NIH]].
[[Kyoto Encyclopedia of Genes and Genomes]] (KEGG) signal transduction pathways:
* [http://www.genome.jp/kegg-bin/show_pathway?hsa05034+2354 KEGG – human alcohol addiction]
* [http://www.genome.jp/kegg-bin/show_pathway?hsa05031+2354 KEGG – human amphetamine addiction]
* [http://www.genome.jp/kegg-bin/show_pathway?hsa05030+2354 KEGG – human cocaine addiction]
{{Medical resources
| ICD10 = {{ICD10|F10-F19}} subdivision .2
}}

{{Addiction|state=collapsed}}
{{Drug use|state=collapsed}}
{{Portal bar|Psychology|Medicine|Biology}}
{{Authority control}}

[[Category:Addiction| ]]
[[Category:Behavioral addiction|*]]
[[Category:Brain disorders]]
[[Category:Substance-related disorders]]
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Module:Disambiguation/templates (view source) (protected)
Module:Distinguish (view source) (template editor protected)
Module:EditAtWikidata (view source) (protected)
Module:Error (view source) (template editor protected)
Module:Format link (view source) (template editor protected)
Module:GetParameters (view source) (template editor protected)
Module:Hatnote (view source) (template editor protected)
Module:Hatnote/styles.css (view source) (template editor protected)
Module:Hatnote list (view source) (template editor protected)
Module:Icon (view source) (template editor protected)
Module:Icon/data (view source) (template editor protected)
Module:Infobox (view source) (template editor protected)
Module:Infobox/styles.css (view source) (template editor protected)
Module:InfoboxImage (view source) (template editor protected)
Module:Labelled list hatnote (view source) (template editor protected)
Module:List (view source) (protected)
Module:Namespace detect/config (view source) (protected)
Module:Namespace detect/data (view source) (protected)
Module:Navbar (view source) (protected)
Module:Navbar/configuration (view source) (protected)
Module:Navbar/styles.css (view source) (protected)
Module:Navbox (view source) (template editor protected)
Module:Navbox/configuration (view source) (template editor protected)
Module:Navbox/styles.css (view source) (template editor protected)
Module:Navbox with collapsible groups (view source) (template editor protected)
Module:Navbox with collapsible groups/configuration (view source) (template editor protected)
Module:Ns has subpages (view source) (protected)
Module:Pagetype (view source) (protected)
Module:Pagetype/config (view source) (protected)
Module:Pagetype/disambiguation (view source) (protected)
Module:Pagetype/rfd (view source) (protected)
Module:Pagetype/setindex (view source) (protected)
Module:Pagetype/softredirect (view source) (protected)
Module:Portal (view source) (template editor protected)
Module:Portal/images/b (view source) (template editor protected)
Module:Portal/images/m (view source) (template editor protected)
Module:Portal/images/p (view source) (template editor protected)
Module:Portal bar (view source) (template editor protected)
Module:Portal bar/styles.css (view source) (template editor protected)
Module:Redirect (view source) (protected)
Module:Redirect hatnote (view source) (template editor protected)
Module:SDcat (view source) (protected)
Module:Side box (view source) (template editor protected)
Module:Side box/styles.css (view source) (template editor protected)
Module:String (view source) (protected)
Module:String2 (view source) (template editor protected)
Module:TableTools (view source) (protected)
Module:Template wrapper (view source) (template editor protected)
Module:Tree chart (view source) (template editor protected)
Module:Tree chart/data (view source) (template editor protected)
Module:Unsubst (view source) (protected)
Module:WikidataIB (view source) (template editor protected)
Module:WikidataIB/nolinks (view source) (template editor protected)
Module:WikidataIB/titleformats (view source) (template editor protected)
Module:Wikitext Parsing (view source) (protected)
Module:Yesno (view source) (protected)
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Retrieved from "https://en.wikipedia.org/wiki/Addiction"