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Definitions
"Addictive" redirects here. For other uses, see Addiction (disambiguation) and Addictive (disambiguation).
Substance addiction
Not to be confused with Psychological dependence.
Behavioral addiction
Addiction is generally a neuropsychological disorder defining pervasive and intense urge to engage
Addiction
Signs and symptoms in maladaptive behaviors providing immediate sensory rewards (e.g. consuming drugs, excessively
Other Addictive behaviour (e.g. substance-use
Screening and assessment gambling), despite their harmful consequences. Dependence is generally an addiction that can names addiction, sexual addiction), dependence,
involve withdrawal issues. Addictive disorder is a category of mental disorders defining important addictive disorder, addiction disorder (e.g.
Causes
intensities of addictions or dependences, which induce functional disabilities. There are no agreed severe substance-use disorder, gambling
Risk factors definitions on these terms – see section on 'definitions'. disorder)

Mechanisms Repetitive drug use alters brain function in ways that perpetuate craving, and weakens (but does not
Diagnosis completely negate) self-control.[1][2] This phenomenon – drugs reshaping brain function – has led to

Prevention an understanding of addiction as a brain disorder with a complex variety of psychosocial as well as
neurobiological (and thus involuntary)[a] factors that are implicated in addiction's development.[3][4][5]
Treatment and management
Classic signs of addiction include compulsive engagement in rewarding stimuli, preoccupation with
Epidemiology
substances or behavior, and continued use despite negative consequences. Habits and patterns
Addiction and the humanities associated with addiction are typically characterized by immediate gratification (short-term
Social scientific models reward),[6][7] coupled with delayed deleterious effects (long-term costs).[4][8] Brain positron emission tomography images that
compare brain metabolism in a healthy individual and
See also Examples of drug (or more generally, substance) addictions include alcoholism, marijuana addiction, an individual with a cocaine addiction
amphetamine addiction, cocaine addiction, nicotine addiction, opioid addiction, and eating or food Specialty Psychiatry, clinical psychology, toxicology,
Endnotes
addiction. Alternatively, behavioral addictions may include gambling addiction, internet addiction, addiction medicine
Notes
social media addiction, video game addiction and sexual addiction. The DSM-5 and ICD-10 only
References recognise gambling addictions as behavioural addictions, but the ICD-11 also recognises gaming addictions.[9]
Further reading

External links
Definitions [ edit ]

Addictions or addictive behaviours, are polysemes defining both a category of mental disorders, neuropsychological symptoms, or merely
maladaptive/harmful habits and lifestyles.[10] A common use of addictions in medicine, is as neuropsychological symptoms defining pervasive/excessive
and intense urges to engage in a category of behavioural compulsions or impulses towards sensory rewards (e.g. alcohol, betel quid, drugs, sex, gambling,
video gaming).[11][12][13][14][15] Addictive disorders or addiction disorders, are mental disorders involving high intensities of addictions (as
neuropsychological symptoms) that induce functional disabilities (i.e. limit subjects' social/family and occupational activities), and whose the two addiction
categories are substance-use addictions and behavioural addictions.[16][10][14][15]

However, there is no agreement on the exact definition of addictions in medicine. Indeed, Volkow et al. (2016) report that the DSM-5 defines addictions as
the most severe degree of the addictive disorders due to pervasive/excessive substance-use or behavioural compulsions/impulses.[17] It is a definition that
many scientific papers and reports use.[18][19][20]

Dependences is also a polyseme defining either neuropsychological symptoms or mental disorders. In the DSM-5, dependences differ from addictions and
can even normally happen without addictions;[21] besides, substance-use dependences are severe stages of substance-use addictions (i.e. mental
disorders) involving withdrawal issues.[22] In the ICD-11, substance-use dependences is a synonym of substance-use addictions (i.e. neuropsychological
symptoms) that can but not necessarily involve withdrawal issues.[23]

Substance addiction [ edit ]

Main article: Substance use disorder

Further information: Substance abuse and Substance-related disorder

Drug addiction [ edit ] Addiction and dependence glossary[3][24][25]

Drug addiction, which belongs to the class of substance-related disorders, is a chronic addiction – a biopsychosocial disorder characterized by persistent
use of drugs (including alcohol) despite substantial harm and adverse
and relapsing brain disorder that features drug seeking and drug abuse, despite their
consequences
harmful effects.[26] This form of addiction changes brain circuitry such that the brain's
addictive drug – psychoactive substances that with repeated use
reward system is compromised,[2] causing functional consequences for stress are associated with significantly higher rates of substance use
management and self-control.[26] Damage to the functions of the organs involved can disorders, due in large part to the drug's effect on brain reward
persist throughout a lifetime and cause death if untreated.[26] Substances involved with systems
dependence – an adaptive state associated with a withdrawal
drug addiction include alcohol, nicotine, marijuana, opioids, cocaine, amphetamines,
syndrome upon cessation of repeated exposure to a stimulus (e.g.,
and even foods with high fat and sugar content.[27][28] Addictions can begin
drug intake)
experimentally in social contexts[29] and can arise from the use of prescribed drug sensitization or reverse tolerance – the escalating effect of a
medications or a variety of other measures.[30] drug resulting from repeated administration at a given dose
drug withdrawal – symptoms that occur upon cessation of repeated
Drug addiction has been shown to work in phenomenological, conditioning (operant and
drug use
classical), cognitive models, and the cue reactivity model. However, no one model physical dependence – dependence that involves persistent
completely illustrates substance abuse.[31] physical–somatic withdrawal symptoms (e.g., fatigue and delirium
tremens)
Risk factors for addiction include:
psychological dependence – dependence socially seen as being
Aggressive behavior (particularly in childhood) extremely mild compared to physical dependence (e.g., With enough
Availability of substance[29] willpower it could be overcome)
reinforcing stimuli – stimuli that increase the probability of repeating
Community economic status
behaviors paired with them
Experimentation[29] rewarding stimuli – stimuli that the brain interprets as intrinsically
Epigenetics positive and desirable or as something to approach
Impulsivity (attentional, motor, or non-planning)[32] sensitization – an amplified response to a stimulus resulting from
repeated exposure to it
Lack of parental supervision[29]
substance use disorder – a condition in which the use of
Lack of peer refusal skills[29] substances leads to clinically and functionally significant impairment
Mental disorders[29] or distress
Method substance is taken[26] tolerance – the diminishing effect of a drug resulting from repeated
administration at a given dose
Usage of substance in youth[29]
· ·

Food addiction [ edit ]

Main article: 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.[33][32] 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.[33] Long-term frequent and excessive consumption of foods high fat, salt, or sugar, such as chocolate, can produce an addiction[34][35] 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.[36][33][32] The
signals sent when consuming highly palatable foods have the ability to counteract the body's signals for fullness and persistent cravings will result.[36]
Those who show signs of food addiction may develop food tolerances, in which they eat more, despite the food becoming less satisfactory.[36]

Chocolate's sweet flavor and pharmacological ingredients are known to create a strong craving or feel 'addictive' by the consumer.[37] 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.[32]

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.[38][33][32] 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.[39][36] 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.[40][33] 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.[41]

The Barratt Impulsiveness Scale, specifically the BIS-11 scale, and the UPPS-P Impulsive Behavior subscales of Negative Urgency and Lack of
Perseverance have been shown to have relation to food addiction.[32]

Behavioral addiction [ edit ]

Main article: Behavioral addiction

The term behavioral addiction refers to a compulsion to engage in a natural reward – which is a behavior that is inherently rewarding (i.e., desirable or
appealing) – despite adverse consequences.[7][34][35] 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.[34][42][43][44]

Addiction can exist in the absence of psychotropic drugs, which was popularized by Peele.[45] These are termed behavioral addictions. Such addictions
may be passive or active, but they commonly contain reinforcing features, which are found in most addictions.[45] 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.[34] Based on this evidence, sexual addiction, gambling addiction, video game addiction, and shopping addiction are
classified accordingly.[34][46]

Sexual [ edit ]
Main article: 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.[47] Sexual addiction may be referred to as hypersexuality or compulsive sexual behavior
disorder.[47] The DSM-5 does recognize sexual addiction as a clinical diagnosis.[48] 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.[49] 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).[34][42] 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.[34][42][43][44] ΔFosB expression is required for this cross-sensitization effect, which intensifies with the level of ΔFosB expression.[34][43][44]

Gambling [ edit ]
Main articles: Gambling and Problem gambling

Gambling provides a natural reward that is associated with compulsive behavior.[34] Functional neuroimaging evidence shows that gambling activates the
reward system and the mesolimbic pathway in particular.[34][46] It is known that dopamine is involved in learning, motivation, as well as the reward
system.[50][2] The exact role of dopamine in gambling addiction has been debated.[50] Suggested roles for D2, D3, and D4 dopamine receptors, 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.[50] This in
turn was linked with greater dopamine release in the dorsal striatum.[50]

Gambling addictions are linked with comorbidities such as mental health disorders, substance abuse, alcohol use disorder, and personality disorders.[51]

Risk factors for gambling addictions include:

Antisocial behavior,
Impulsive personality,[32]
Male,
Sensation seeking,[52]
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.[52] Although some personality traits can be linked with gambling addiction, there is no
general description of individuals addicted to gambling.[52]

Internet [ edit ]
Main article: Internet addiction disorder

Internet addiction does not have any standardized definition, yet there is widespread agreement that this problem exists.[53] 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.[54][55] Others argue that internet addiction should be considered a symptom of an underlying mental health condition and not a disorder in
itself.[56] Internet addiction has been described as "a psychological dependence on the Internet, regardless of the type of activity once logged on."[53]
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.[57]

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.[58][59] 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.[60][59] The most common scale used to measure addiction is the Internet Addiction Test
developed by Kimberly Young.[59]

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.[60]

Video games [ edit ]

Main article: 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.[61] In May 2019, the WHO introduced gaming disorder in the 11th
edition of the International Classification of Diseases.[62] Video game addiction has been shown to be more prevalent in males than females, higher by 2.9
times.[63] It has been suggested that people of younger ages are more prone to become addicted to video games.[63] This may be due to video games
being relatively new, hence the higher prevalence in younger groups.[64] People with certain personalities may be more susceptible to gaming
addictions.[63][65]

Risk factors for video game addiction include:

Male,
Psychopathologies (e.g. ADHD or MDD), and
Social anxiety.[66]

Shopping [ edit ]
Main articles: Shopping addiction and Compulsive buying disorder

Shopping addiction, or compulsive buying disorder (CBD), is the excessive urge to shop or spend, potentially resulting in unwanted consequences.[67]
These consequences can have serious impacts, such as increased consumer debt, negatively affected relationships, increased risk of illegal behavior, and
suicide attempts.[67] Shopping addiction occurs worldwide and has shown a 5.8% prevalence in the United States.[68] 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.[68]

Signs and symptoms [ edit ]

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[33]

Disregarding financial status when it comes to drug purchases
Ensuring a stable supply of the drug
Experiencing withdrawal symptoms when stopping the drug[69][33]
Needing more of the drug over time to achieve similar effects[33]
Social and work life impacted due to drug use[33]
Unsuccessful attempts to stop drug use[33]
Urge to use drug regularly

Signs and symptoms of addiction may include:

Behavioral Changes Physical Changes Social Changes

Angry and irritable Abnormal pupil size Changes in hobbies

Changes to eating or sleeping habits Bloodshot eyes Changes to financial status (unexplained need for
Changes to personality and attitude Body odor money)
Decreased attendance and performance in workplace or Impaired motor Legal problems related to substance abuse
school setting[33] coordination[70] Sudden changes in friends and associates
Fearful, paranoid and anxious without probable cause[70] Periodic tremors Use of substance despite consequences to personal
Frequently engaging in conflicts (fights, illegal activity) Poor physical appearance relationships[70]
Frequent or sudden changes in mood and temperament Slurred speech
Hiding or in denial of certain behaviors Sudden changes in weight
Lack of motivation
Periodic hyperactivity
Using substances in inappropriate settings

Screening and assessment [ edit ]

Addictions Neuroclinical Assessment [ edit ]

The Addictions Neuroclinical Assessment is used to diagnose addiction disorders. This tool measures three different domains: executive function, incentive
salience, and negative emotionality.[71][72] Executive functioning consists of processes that would be disrupted in addiction.[72] In the context of addiction,
incentive salience determines how one perceives the addictive substance.[72] Increased negative emotional responses have been found with individuals
with addictions.[72]

Tobacco, Alcohol, Prescription Medication, and Other Substance Use (TAPS) [ edit ]

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).[73] If an individual screens positive, the
second component will begin. This dictates the risk level of the substance.[73]

CRAFFT [ edit ]

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.[74] 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.[75] 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.[75] After these tests are done, the clinician is to give the "5 RS" of brief counseling.

The five Rs of brief counseling includes:

1. REVIEW screening results

2. RECOMMEND to not use
3. RIDING/DRIVING risk counseling
4. RESPONSE: elicit self-motivational statements
5. REINFORCE self-efficacy[75]

Drug Abuse Screening Test (DAST-10) [ edit ]

The Drug Abuse Screening Test (DAST) is a self-reporting tool that measures problematic substance use.[76] 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.[76] 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.[76]

Alcohol, Smoking, and Substance Involvement Test (ASSIST) [ edit ]

The Alcohol, Smoking, and Substance Involvement Test (ASSIST) is an interview-based questionnaire consisting of eight questions developed by the
WHO.[77] 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.[78]

Causes [ edit ]

Personality theories [ edit ]

Main article: Personality theories of addiction

Personality theories of addiction are psychological models that associate personality traits or modes of thinking (i.e., 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.[79] Models of addiction risk that have been proposed in psychology literature
include: an affect dysregulation model of positive and negative psychological affects, the reinforcement sensitivity theory of impulsiveness and behavioral
inhibition, and an impulsivity model of reward sensitization and impulsiveness.[80][81][82][83][84]

Neuropsychology [ edit ]

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.[85]

Cognitive control and stimulus control, which is associated with 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.[86] Cognitive control, and particularly inhibitory control
over behavior, is impaired in both addiction and attention deficit hyperactivity disorder.[87][88] 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.[88]

Stimulus control of behavior [ edit ] Operant conditioning Extinction

See also: Stimulus control

In operant conditioning, behavior is Reinforcement Punishment

Increase behavior Decrease behavior
influenced by outside stimulus, such
as a drug. The operant conditioning
theory of learning is useful in Positive reinforcement Positive punishment Negative punishment
understanding why the mood-altering Add appetitive stimulus Negative reinforcement Add noxious stimulus Remove appetitive stimulus
following correct behavior following behavior following behavior
or stimulating consequences of drug
use can reinforce continued use (an
example of positive reinforcement) Escape
Active avoidance
and why the addicted person seeks to Remove noxious stimulus
Behavior avoids noxious stimulus
following correct behavior
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.[85]

Cognitive control of behavior [ edit ]

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.[89][2] Cognitive functions such as learning, memory, and impulse control, are affected by drugs.[89] These effects
promote drug use, as well as hinder the ability to abstain from it.[89] The increase in dopamine release is prominent in drug use, specifically in the ventral
striatum and the nucleus accumbens.[89] 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.[89][2] This promotes the development of a maladaptive drug to stimulus relationship.[90] Early drug use leads to these
maladaptive associations, later affecting cognitive processes used for coping, which are needed to successfully abstain from them.[89][85]

Risk factors [ edit ]

Further information: Addiction vulnerability

A number of genetic and environmental risk factors exist for developing an addiction.[3][91] Genetic and environmental risk factors each account for roughly
half of an individual's risk for developing an addiction;[3] the contribution from epigenetic risk factors to the total risk is unknown.[91] 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.[3] 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.[92]

Genetic factors [ edit ]

Main articles: Epigenetics of cocaine addiction and Molecular and epigenetic mechanisms of alcoholism
Further information: Alcoholism § Genetic variation, History of drinking, History of smoking, and Prevalence of tobacco use

Genetic factors, along with socio-environmental (e.g., psychosocial) factors, have been established as significant contributors to addiction
vulnerability.[3][91][93][33] 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.[94] Genetic factors account for 40–60% of the risk factors for alcoholism.[95] Similar rates of heritability for other types of
drug addiction have been indicated, specifically in genes that encode the Alpha5 Nicotinic Acetylcholine Receptor.[96] 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.[96]

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.[97] 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.[98]

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.[99]

Genome-wide association studies (GWAS) are used to examine genetic associations with dependence, addiction, and drug use.[93] 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 endophenotypes 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.[100]

Environmental factors [ edit ]

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.[3] 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.[101] More generally, a number of different environmental factors
have been implicated as risk factors for addiction, including various psychosocial stressors. 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.[102][29] 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.[103] Many researchers, including neuroscientists, indicate that the brain disease model presents a misleading, incomplete, and
potentially detrimental explanation of addiction.[104]

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.[85] 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.[105] 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.[105][29][85] Vast amounts of children who experienced abuse have gone on to have some form of addiction in their
adolescence or adult life.[106] 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.[106] 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 alcohol
or other drug use.[107]

Age [ edit ]

Adolescence represents a period of increased vulnerability for developing an addiction.[108] 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.[109] 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.[110][111]

Most individuals are exposed to and use addictive drugs for the first time during their teenage years.[112] In the United States, there were just over
2.8 million new users of illicit drugs in 2013 (7,800 new users per day);[112] among them, 54.1% were under 18 years of age.[112] In 2011, there were
approximately 20.6 million people in the United States over the age of 12 with an addiction.[113] Over 90% of those with an addiction began drinking,
smoking or using illicit drugs before the age of 18.[113]

Comorbid disorders [ edit ]

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.[114][115][116][29] The NIDA cites early aggressive behavior as a risk factor for
substance use.[102] 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.[117]

Epigenetic [ edit ]

Epigenetics is the study of stable phenotypic changes that do not involve alterations in the DNA sequence.[118] Illicit drug use has been found to cause
epigenetic changes in DNA methylation, as well as chromatin remodeling.[119] The epigenetic state of chromatin may pose as a risk for the development of
substance addictions.[119] 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.[119] This change may predispose one to experience a positive response to drug use.[119]

Transgenerational epigenetic inheritance [ edit ]

Main article: 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:[91] 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 phenotypes of their offspring (e.g., behavioral responses to environmental stimuli).[91]
In addiction, epigenetic mechanisms play a central role in the pathophysiology of the disease;[3] 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).[91][120]

The general classes of epigenetic alterations that have been implicated in transgenerational epigenetic inheritance include DNA methylation, histone
modifications, and downregulation or upregulation of microRNAs.[91] With respect to addiction, more research is needed to determine the specific 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.[91][120] 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.[note 1][91] 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.[91][120]

Mechanisms [ edit ]

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.[3][121][34] 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.[121][34][122][35] 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 neurons of the nucleus accumbens.[3][121][34][122] Due to the causal relationship between ΔFosB expression and addictions, it is used
preclinically as an addiction biomarker.[3][121][122] ΔFosB expression in these neurons directly and positively regulates drug self-administration and reward
sensitization through positive reinforcement, while decreasing sensitivity to aversion.[note 2][3][121]

Chronic addictive drug use causes alterations in gene

expression in the mesocorticolimbic
projection.[35][130][131] The most important transcription
factors that produce these alterations are ΔFosB,
cAMP response element binding protein (CREB), and
nuclear factor kappa B (NF-κB).[35]
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
reward sensitization) seen in drug addiction.[35]
ΔFosB expression in nucleus accumbens D1-type
Transcription factor glossary
gene expression – the process by which information from a gene is used in the synthesis of a functional
gene product such as a protein
transcription – the process of making messenger RNA (mRNA) from a DNA template by RNA polymerase
transcription factor – a protein that binds to DNA and regulates gene expression by promoting or
ΔFosB is the most suppressing transcription
transcriptional regulation – controlling the rate of gene transcription for example by helping or hindering
RNA polymerase binding to DNA
upregulation, activation, or promotion – increase the rate of gene transcription
downregulation, repression, or suppression – decrease the rate of gene transcription
coactivator – a protein (or a small molecule) that works with transcription factors to increase the rate of
gene transcription
corepressor – a protein (or a small molecule) that works with transcription factors to decrease the rate of
gene transcription
response element – a specific sequence of DNA that a transcription factor binds to

medium spiny neurons directly and positively · ·

regulates drug self-administration and reward

Signaling cascade in the nucleus accumbens that results in psychostimulant addiction
sensitization through positive reinforcement while
· ·
decreasing sensitivity to aversion.[note 2][3][121] ΔFosB
Note: colored text
has been implicated in mediating addictions to many
contains article links.
different drugs and drug classes, including alcohol, [Color legend 1]
Cav1.2
amphetamine and other substituted amphetamines,
cannabinoids, cocaine, methylphenidate, nicotine,
opiates, phenylcyclidine, and propofol, among NMDAR CaMKII
CaM
others.[121][35][130][132][133] ΔJunD, a transcription
factor, and G9a, a histone methyltransferase, both
PP2B PP1 CREB
oppose the function of ΔFosB and inhibit increases in
its expression.[3][35][134] Increases in nucleus AMPAR
accumbens ΔJunD expression (via viral vector- DARPP-32
ΔFosB
mediated gene transfer) or G9a expression (via DRD1 c-Fos
JunD
pharmacological means) reduces, or with a large Gs
increase can even block, many of the neural and SIRT1
DRD5 AC PKA
behavioral alterations that result from chronic high- HDAC1
dose use of addictive drugs (i.e., the alterations DRD2 Gi/o Nuclear pore
cAMP
mediated by ΔFosB).[122][35]
DRD3 Nuclear membrane
ΔFosB plays an important role in regulating
DRD4
behavioral responses to natural rewards, such as
palatable food, sex, and exercise.[35][135] Natural Plasma membrane
rewards, like drugs of abuse, 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.[34][35][135] Consequently, ΔFosB is
the key transcription factor involved in addictions to
natural rewards (i.e., behavioral addictions) as
cAMP
well;[35][34][135] in particular, ΔFosB in the nucleus
accumbens is critical for the reinforcing effects of This diagram depicts the signaling events in the brain's reward center that are induced by chronic high-
sexual reward.[135] Research on the interaction dose exposure to psychostimulants that increase the concentration of synaptic dopamine, like
amphetamine, methamphetamine, and phenethylamine. Following presynaptic dopamine and glutamate co-
between natural and drug rewards suggests that
release by such psychostimulants,[123][124] postsynaptic receptors for these neurotransmitters trigger internal
dopaminergic psychostimulants (e.g., amphetamine) signaling events through a cAMP-dependent pathway and a calcium-dependent pathway that ultimately
and sexual behavior act on similar biomolecular result in increased CREB phosphorylation.[123][125][126] Phosphorylated CREB increases levels of ΔFosB,
mechanisms to induce ΔFosB in the nucleus which in turn represses the c-Fos gene with the help of corepressors;[123][127][128] c-Fos repression acts as a
molecular switch that enables the accumulation of ΔFosB in the neuron.[129] A highly stable (phosphorylated)
accumbens and possess bidirectional cross- form of ΔFosB, one that persists in neurons for 1–2 months, slowly accumulates following repeated high-
sensitization effects that are mediated through dose exposure to stimulants through this process.[127][128] ΔFosB functions as "one of the master control
ΔFosB.[34][43][44] This phenomenon is notable since, proteins" that produces addiction-related structural changes in the brain, and upon sufficient accumulation,
with the help of its downstream targets (e.g., nuclear factor kappa B), it induces an addictive state.[127][128]
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.[34]

ΔFosB inhibitors (drugs or treatments that oppose its action) may be an effective treatment for addiction and addictive disorders.[136]

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.[137][138][33] Altered dopamine neurotransmission is frequently observed following the development of an addictive state.[34][2] 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.[34] Use of certain drugs (e.g., cocaine) affect cholinergic neurons that innervate the reward system, in turn affecting dopamine
signaling in this region.[139]

Reward system [ edit ]

Main article: Reward system

Mesocorticolimbic pathway [ edit ]

Understanding the pathways in which drugs act and how drugs can alter those ΔFosB accumulation from excessive drug use
pathways is key when examining the biological basis of drug addiction. The reward
pathway, known as the mesolimbic pathway,[2] or its extension, the mesocorticolimbic
pathway, is characterized by the interaction of several areas of the brain.

The projections from the ventral tegmental area (VTA) are a network of
dopaminergic neurons with co-localized postsynaptic glutamate receptors
(AMPAR and NMDAR). These cells respond when stimuli indicative of a reward
are present.[33] The VTA supports learning and sensitization development and
releases dopamine (DA) into the forebrain.[141] These neurons project and
release DA into the nucleus accumbens,[142] through the mesolimbic pathway.
Virtually all drugs causing drug addiction increase the DA release in the
mesolimbic pathway.[143][2]
The nucleus accumbens (NAcc) is one output of the VTA projections. The nucleus
accumbens itself consists mainly of GABAergic medium spiny neurons
(MSNs).[144] The NAcc is associated with acquiring and eliciting conditioned
behaviors, and is involved in the increased sensitivity to drugs as addiction
progresses.[141][32] Overexpression of ΔFosB in the nucleus accumbens is a
necessary common factor in essentially all known forms of addiction;[3] ΔFosB is
a strong positive modulator of positively reinforced behaviors.[3]
The prefrontal cortex, including the anterior cingulate and orbitofrontal
cortices,[145][32] is another VTA output in the mesocorticolimbic pathway; it is
Top: this depicts the initial effects of high dose exposure to an addictive
important for the integration of information which helps determine whether a
drug on gene expression in the nucleus accumbens for various Fos
behavior will be elicited.[146] It is critical for forming associations between the family proteins (i.e., c-Fos, FosB, ΔFosB, Fra1, and Fra2).
rewarding experience of drug use and cues in the environment. Importantly, these Bottom: this illustrates the progressive increase in ΔFosB expression in
the nucleus accumbens following repeated twice daily drug binges,
cues are strong mediators of drug-seeking behavior and can trigger relapse even
where these phosphorylated (35–37 kilodalton) ΔFosB isoforms persist
after months or years of abstinence.[147][2] in the D1-type medium spiny neurons of the nucleus accumbens for up
to 2 months.[128][140]
Other brain structures that are involved in addiction include:

The basolateral amygdala projects into the NAcc and is thought to be important
for motivation.[146]
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.[142]

Role of dopamine and glutamate [ edit ]

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.[148] 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.[148][149][33] Nearly all addictive drugs, directly or indirectly, act on the brain's reward system by heightening dopaminergic
activity.[150][2]

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.[148]

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.[145]

Reward sensitization [ edit ]

Reward sensitization is a process that causes an Neural and behavioral effects of validated ΔFosB transcriptional targets in the
increase in the amount of reward (specifically, striatum[121][151]
incentive salience[note 5]) that is assigned by the
Target Target
brain to a rewarding stimulus (e.g., a drug). In simple Neural effects Behavioral effects
gene expression
terms, when reward sensitization to a specific
stimulus (e.g., a drug) occurs, an individual's Molecular switch enabling the chronic
c-Fos ↓ –
"wanting" or desire for the stimulus itself and its induction of ΔFosB[note 3]

associated cues increases.[153][152][154] Reward ↓

dynorphin [note 4]
• Downregulation of κ-opioid feedback loop • Increased drug reward
sensitization normally occurs following chronically
high levels of exposure to the stimulus.[2] ΔFosB
• Expansion of NAcc dendritic processes
expression in D1-type medium spiny neurons in the • Increased drug reward
NF-κB ↑ • NF-κB inflammatory response in the NAcc
nucleus accumbens has been shown to directly and • Locomotor sensitization
• NF-κB inflammatory response in the CP
positively regulate reward sensitization involving
drugs and natural rewards.[3][121][122] GluR2 ↑ • Decreased sensitivity to glutamate • Increased drug reward

"Cue-induced wanting" or "cue-triggered wanting", a

• GluR1 synaptic protein phosphorylation Decreased drug reward
form of craving that occurs in addiction, is Cdk5 ↑
• Expansion of NAcc dendritic processes (net effect)
responsible for most of the compulsive behavior that
people with addictions exhibit.[152][154] During the
development of an addiction, the repeated association of otherwise neutral and even non-rewarding stimuli with drug consumption triggers an associative
learning process that causes these previously neutral stimuli to act as conditioned positive reinforcers of addictive drug use (i.e., these stimuli start to
function as drug cues).[152][155][154] As conditioned positive reinforcers of drug use, these previously neutral stimuli are assigned incentive salience (which
manifests as a craving) – sometimes at pathologically high levels due to reward sensitization – which can transfer to the primary reinforcer (e.g., the use of
an addictive drug) with which it was originally paired.[152][155][154]

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[note 6] that
is mediated through ΔFosB.[34][43][44] 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
lack of pleasure or motivation during drug withdrawal.[3][140][151]

Summary of addiction-related plasticity

Type of reinforcer
Form of neuroplasticity Physical
High fat or Sexual Environmental Sources
or behavioral plasticity Opiates Psychostimulants exercise
sugar food intercourse enrichment
(aerobic)

ΔFosB expression in
nucleus accumbens D1-type ↑ ↑ ↑ ↑ ↑ ↑ [34]

MSNs

Behavioral plasticity

Escalation of intake Yes Yes Yes [34]

Psychostimulant [34]
Yes Not applicable Yes Yes Attenuated Attenuated
cross-sensitization

Psychostimulant [34]
↑ ↑ ↓ ↓ ↓
self-administration

Psychostimulant
conditioned place ↑ ↑ ↓ ↑ ↓ ↑ [34]

preference

Reinstatement of drug- [34]

↑ ↑ ↓ ↓
seeking behavior

Neurochemical plasticity

CREB phosphorylation [34]

↓ ↓ ↓ ↓ ↓
in the nucleus accumbens

Sensitized dopamine
response No Yes No Yes [34]

in the nucleus accumbens

Altered striatal dopamine ↑DRD1, ↓DRD2, ↑DRD1, ↓DRD2, [34]

↓DRD2, ↑DRD3 ↑DRD2 ↑DRD2
signaling ↑DRD3 ↑DRD3

No change or
Altered striatal opioid ↑μ-opioid receptors ↑μ-opioid ↑μ-opioid [34]
↑μ-opioid No change No change
signaling ↑κ-opioid receptors receptors receptors
receptors

↑dynorphin
Changes in striatal opioid [34]
No change: ↑dynorphin ↓enkephalin ↑dynorphin ↑dynorphin
peptides
enkephalin

Mesocorticolimbic synaptic plasticity

Number of dendrites in the [34]

↓ ↑ ↑
nucleus accumbens

Dendritic spine density in [34]

↓ ↑ ↑
the nucleus accumbens

Neuroepigenetic mechanisms [ edit ]

Further information: Neuroepigenetics and Chromatin remodeling

Altered epigenetic regulation of gene expression within the brain's reward system plays a significant and complex role in the development of drug
addiction.[134][156] Addictive drugs are associated with three types of epigenetic modifications within neurons.[134] These are (1) histone modifications, (2)
epigenetic methylation of DNA at CpG sites at (or adjacent to) particular genes, and (3) epigenetic downregulation or upregulation of microRNAs which
have particular target genes.[134][35][156] 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 residues[156] – most other genes in the NAc cells do not show
such changes.[134]

Diagnosis [ edit ]

Further information: Substance use disorder § Diagnosis, and Problem gambling § Diagnosis

Classification [ edit ]

DSM-5 [ edit ]

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
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.[19][25]

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.[21] Internet gaming disorder is listed as a "condition requiring further study" in the DSM-5.[157]

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.[158] 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
cravings for the substance, dysphoria, nausea, hallucinations, headaches, cold sweats, tremors, 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.[159]

ICD-11 [ edit ]

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").[15] 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."[160] 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.[160]

Prevention [ edit ]

Main articles: Harm reduction and Preventive healthcare

Abuse liability [ edit ]

Abuse or addiction liability is the tendency to use drugs in a non-medical situation. This is typically for euphoria, mood changing, or sedation.[161] 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.[161] 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.[162]

Treatment and management [ edit ]

See also: Addiction recovery groups, Cognitive behavioral therapy, and Drug rehabilitation

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 programs, and residential treatment
facilities.[163][29] The TTM 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.[85]

A biosocial approach to the treatment of addiction brings to the fore the social determinants of illness and wellbeing and considers the dynamic and
reciprocal relationships that exist for, and influence, the individual's experience.[164]

The work of A.V. Schlosser (2018) aims to pronounce the individual lived experiences of women receiving medication-assisted treatment (e.g., methadone,
naltrexone, burprenorphine) in a long-term rehabilitation setting, through a twenty month long ethnographic fieldwork investigation. This person-centered
research shows how the experiences of these women "emerge from stable systems of inequality based in intersectional gender, race, and class
marginalization entangled with processes of intra-action."[165] Viewing addiction treatment through this lens highlights the importance of framing clients'
own bodies as "social flesh". As Schlosser (2018) points out, "client bodies" as well as the "embodied experiences of self and social belonging emerge in
and through the structures, temporalities, and expectations of the treatment centre."[165]

Biotechnologies make up a large portion of the future treatments for addiction[citation needed] including deep-brain stimulation, agonist and antagonist
implants and hapten conjugate vaccines. Vaccinations against addiction specifically overlaps with the belief that memory plays a large role in the damaging
effects of addiction and relapses.[medical citation needed] Hapten conjugate vaccines are designed to block opioid receptors in one area, while allowing other
receptors to behave normally. Essentially, once a high can no longer be achieved in relation to a traumatic event, the relation of drugs to a traumatic
memory can be disconnected and therapy can play a role in treatment.[166]

Behavioral therapy [ edit ]

CBT proposes four assumptions essential to the approach to treatment: addiction is a learned behavior, it emerges in an environmental context, it is
developed and maintained by particular thought patterns and processes, and CBT can be integrated well with other treatment and management
approaches as they all have similar goals.[85] CBT, (e.g., relapse prevention), motivational interviewing, and a community reinforcement approach are
effective interventions with moderate effect sizes.[167]

Interventions focusing on impulsivity and sensation seeking are successful in decreasing substance use.[32] Cue exposure uses ideas from classical
conditioning theory to change the learned behavioral response of someone addicted to a cue or trigger. Contingency management uses ideas from operant
conditioning to use meaningful positive reinforcements to influence addiction behaviors towards sobriety.[85]

Addiction recovery groups draw on different methods and models and rely on the success of vicarious learning, where people imitate behavior they
observe as rewarding among their own social group or status as well as those perceived as being of a higher status.[85]

Substance addiction in children is complex and requires multifacted behavioral therapy. Family therapy and school-based interventions have had minor but
lasting results. Innovative treatments are still needed for areas where relevant therapies are unavailable.[29]

Consistent aerobic exercise, especially endurance exercise (e.g., marathon running), prevents the development of certain drug addictions and is an
effective adjunct treatment for drug addiction, and for psychostimulant addiction in particular.[34][168][169][170][171] Consistent aerobic exercise magnitude-
dependently (i.e., by duration and intensity) reduces drug addiction risk, which appears to occur through the reversal of drug induced addiction-related
neuroplasticity.[34][169] Exercise may prevent the development of drug addiction by altering ΔFosB or c-Fos immunoreactivity in the striatum or other parts
of the reward system.[171] Aerobic exercise decreases drug self-administration, reduces the likelihood of relapse, and induces opposite effects on striatal
dopamine receptor D2 (DRD2) signaling (increased DRD2 density) to those induced by addictions to several drug classes (decreased DRD2
density).[34][169] Consequently, consistent aerobic exercise may lead to better treatment outcomes when used as an adjunct treatment for drug
addiction.[34][169][170]

With a combination of tools such as behavioral therapy, a balanced lifestyle, and individualized relapse plans, relapse is can be more successfully
avoided.[85]

Medication [ edit ]

Alcohol addiction [ edit ]

Main article: Alcoholism
Further information: Alcohol and health and Long-term effects of alcohol

Alcohol, like opioids, can induce a severe state of physical dependence and produce withdrawal symptoms such as delirium tremens. Because of this,
treatment for alcohol addiction usually involves a combined approach dealing with dependence and addiction simultaneously. Benzodiazepines have the
largest and the best evidence base in the treatment of alcohol withdrawal and are considered the gold standard of alcohol detoxification.[172]

Pharmacological treatments for alcohol addiction include drugs like naltrexone (opioid antagonist), disulfiram, acamprosate, and topiramate.[173][174] Rather
than substituting for alcohol, these drugs are intended to affect the desire to drink, either by directly reducing cravings as with acamprosate and topiramate,
or by producing unpleasant effects when alcohol is consumed, as with disulfiram. These drugs can be effective if treatment is maintained, but compliance
can be an issue as patients with disordered alcohol use may forget to take their medication, or discontinue use because of excessive side effects.[175][176]
The opioid antagonist naltrexone has been shown to be an effective treatment for alcoholism, with the effects lasting three to twelve months after the end
of treatment.[177]

Behavioral addictions [ edit ]

This section is transcluded from Behavioral addiction. (edit | history)

Behavioral addiction is a treatable condition. Treatment options include psychotherapy and psychopharmacotherapy (i.e., medications) or a combination of
both. Cognitive behavioral therapy (CBT) is the most common form of psychotherapy used in treating behavioral addictions; it focuses on identifying
patterns that trigger compulsive behavior and making lifestyle changes to promote healthier behaviors. Because cognitive behavioral therapy is considered
a short term therapy, the number of sessions for treatment normally ranges from five to twenty. During the session, therapists will lead patients through the
topics of identifying the issue, becoming aware of one's thoughts surrounding the issue, identifying any negative or false thinking, and reshaping said
negative and false thinking. While CBT does not cure behavioral addiction, it does help with coping with the condition in a healthy way. Currently, there are
no medications approved for treatment of behavioral addictions in general, but some medications used for treatment of drug addiction may also be
beneficial with specific behavioral addictions.[46] Any unrelated psychiatric disorders should be kept under control, and differentiated from the contributing
factors that cause the addiction.

Cannabinoid addiction [ edit ]

Main article: Cannabis addiction

The development of CB1 receptor agonists that have reduced interaction with β-arrestin 2 signaling might be therapeutically useful.[178] As of 2019, there
has been some evidence of effective pharmacological interventions for cannabinoid addiction, but none have been approved.[179]

Nicotine addiction [ edit ]

Main article: Nicotine addiction
Further information: Smoking cessation and Tobacco harm reduction

Another area in which drug treatment has been widely used is in the treatment of nicotine addiction, which usually
involves the use of nicotine replacement therapy, nicotinic receptor antagonists, and/or nicotinic receptor partial
agonists.[180][181] Examples of drugs that act on nicotinic receptors and have been used for treating nicotine
addiction include antagonists like bupropion and the partial agonist varenicline.[180][181] Cytisine, a partial agonist,
is an effective, and affordable cessation treatment for smokers.[182] When access to varenicline and nicotine
replacement therapy is limited (due to availability or cost), cytisine is considered the first line of treatment for Transdermal patch used in nicotine
replacement therapy
smoking cessation.[182]

Opioid addiction [ edit ]

Main article: Opioid use disorder
Further information: Opioid epidemic

Opioids cause physical dependence and treatment typically addresses both dependence and addiction. Physical dependence is treated using replacement
drugs such as buprenorphine (the active ingredient in products such as Suboxone and Subutex) and methadone.[183][184] Although these drugs perpetuate
physical dependence, the goal of opiate maintenance is to provide a measure of control over both pain and cravings. Use of replacement drugs increases
the addicted individual's ability to function normally and eliminates the negative consequences of obtaining controlled substances illicitly. Once a prescribed
dosage is stabilized, treatment enters maintenance or tapering phases. In the United States, opiate replacement therapy is tightly regulated in methadone
clinics and under the DATA 2000 legislation. In some countries, other opioid derivatives such as dihydrocodeine,[185] dihydroetorphine[186] and even
heroin[187][188] are used as substitute drugs for illegal street opiates, with different prescriptions being given depending on the needs of the individual
patient. Baclofen has led to successful reductions of cravings for stimulants, alcohol, and opioids and alleviates alcohol withdrawal syndrome. Many
patients have stated they "became indifferent to alcohol" or "indifferent to cocaine" overnight after starting baclofen therapy.[189] Some studies show the
interconnection between opioid drug detoxification and overdose mortality.[190]

Psychostimulant addiction [ edit ]

There is no effective and FDA- or EMA-approved pharmacotherapy for any form of psychostimulant addiction.[191] Experimental TAAR1-selective agonists
have significant therapeutic potential as a treatment for psychostimulant addictions.[192]

Research [ edit ]

Anti-drug vaccines (active immunizations) for treatment of cocaine and nicotine addictions were successful in animal studies. Vaccines tested on humans
have been shown as safe with mild to moderate side effects, though did not have firm results confirming efficacy despite producing expected
antibodies.[193] Vaccines which use anti-drug monoclonal antibodies (passive immunization) can mitigate drug-induced positive reinforcement by
preventing the drug from moving across the blood–brain barrier.[194] Current[as of?] vaccine-based therapies are only effective in a relatively small subset of
individuals.[194][195] As of November 2015, vaccine-based therapies are being tested in human clinical trials as a treatment for addiction and preventive
measure against drug overdoses involving nicotine, cocaine, and methamphetamine.[194] The study shows that the vaccine may save lives during a drug
overdose. In this instance, the idea is that the body will respond to the vaccine by quickly producing antibodies to prevent the opioids from accessing the
brain.[196]

Since addiction involves abnormalities in glutamate and GABAergic neurotransmission,[197][198] receptors associated with these neurotransmitters (e.g.,
AMPA receptors, NMDA receptors, and GABAB receptors) are potential therapeutic targets for addictions.[197][198][199][200] N-acetylcysteine, which affects
metabotropic glutamate receptors and NMDA receptors, has shown some benefit involving addictions to cocaine, heroin, and cannabinoids.[197] It may be
useful as an adjunct therapy for addictions to amphetamine-type stimulants, but more clinical research is required.[197]

Current medical reviews of research involving lab animals have identified a drug class – class I histone deacetylase inhibitors[note 7] – that indirectly inhibits
the function and further increases in the expression of accumbal ΔFosB by inducing G9a expression in the nucleus accumbens after prolonged
use.[122][134][201][156] These reviews and subsequent preliminary evidence which used oral administration or intraperitoneal administration of the sodium
salt of butyric acid or other class I HDAC inhibitors for an extended period indicate that these drugs have efficacy in reducing addictive behavior in lab
animals[note 8] that have developed addictions to ethanol, psychostimulants (i.e., amphetamine and cocaine), nicotine, and opiates.[134][156][202][203] Few
clinical trials involving humans with addictions and any HDAC class I inhibitors have been conducted to test for treatment efficacy in humans or identify an
optimal dosing regimen.[note 9]

Gene therapy for addiction is an active area of research. One line of gene therapy research involves the use of viral vectors to increase the expression of
dopamine D2 receptor proteins in the brain.[205][206][207][208][209]

Epidemiology [ edit ]

Further information: Countries by alcohol consumption, Opioid epidemic, and 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 population demographics (e.g., by age group, socioeconomic status, etc.).[91] Where addiction is viewed
as unacceptable, there will be fewer people addicted.

Asia [ edit ]

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.[210]

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%.[211]

Australia [ edit ]
Further information: Alcoholism in rural Australia

The prevalence of substance use disorder among Australians was reported at 5.1% in 2009.[212] 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.[213] The national[specify] 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 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.[213]

Europe [ edit ]
Further information: Alcoholism in Ireland and 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.[214] 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.[29]

United States [ edit ]

Further information: Cocaine in the United States, Crack epidemic in the United States, and Opioid epidemic in the United States

Based on representative samples of the US youth population in 2011, the lifetime prevalence[note 10] of addictions to alcohol and illicit drugs has been
estimated to be approximately 8% and 2–3% respectively.[215] Based on representative samples of the US adult population in 2011, the 12-month
prevalence of alcohol and illicit drug addictions were estimated at 12% and 2–3% respectively.[215] The lifetime prevalence of prescription drug addictions
is around 4.7%.[216]

As of 2021, 43.7 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%).[217] Only about 10%, or a little over 2 million, receive any form of treatments, and those that do generally do not receive evidence-based
care.[218][219] One-third of inpatient hospital costs and 20% of all deaths in the US every year are the result of untreated addictions and risky substance
use.[218][219] 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.[218][219]

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.[34] 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.[42]

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.[220]

In 2019, opioid addiction was acknowledged as a national crisis in the United States.[221] 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%.[222]

Canada [ edit ]

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.[223] Alcohol abuse or dependence reported a lifetime prevalence of 18.1% and a 12-month prevalence of 3.2%.[223] Cannabis abuse or
dependence reported a lifetime prevalence of 6.8% and a 12-month prevalence of 3.2%.[223] Other drug abuse or dependence has a lifetime prevalence of
4.0% and a 12-month prevalence of 0.7%.[223] Substance use disorder is a term used interchangeably with a drug addiction.[224]

In 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.[225]
Prevalence of care needed increased the most among the 14–17 age group overall.[225]

South America [ edit ]

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,[226] 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.[227]

Addiction and the humanities [ edit ]

History and etymology [ edit ]

Main article: Recreational drug use
Further information: Evolutionary models of human drug use, History of drinking, History of smoking, and 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.[228] An
example is the usage of the word in the religious landscape of early modern Europe.[229] "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".[230] The meaning of addiction during the
early modern period was mostly associated with positivity and goodness;[229] during this early modern and highly religious era of Christian revivalism and
Pietistic tendencies,[229] it was seen as a way of "devoting oneself to another".[230]

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
addiction.[231] 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.[232] Today, addiction is understood both as a
biopsychosocial and neurological disorder that negatively impacts those who are affected by it, most commonly associated with the use of drugs and
excessive use of alcohol.[4] 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" [ edit ]

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" 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;[233]
other examples are in this table:

Colloquial term Addiction to Medico-legal term

chocoholic chocolate

danceaholic dance choreomania

rageaholic rage

sexaholic sex erotomania, satyriasis, nymphomania

sugarholic sugar saccharomania

workaholic work ergomania

Arts [ edit ]

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 [ edit ]

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.[234][235] Characteristics of substance abuse may include feelings of isolation, a lack of confidence,
communication difficulties, and a perceived lack of control.[236] 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.[237] Further
evidenced by Waller and Mahony (2002)[238] and Kaufman (1981),[239] 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:[240][241]

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.[242] 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.[242] 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).[242]

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.[243][241] 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.[244][241] 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'.[245][241]

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.[246] Music therapy was identified to have potentially
strong beneficial effects in aiding contemplation and preparing those diagnosed with substance use for treatment.[246]

As an assessment tool [ edit ]

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).[247][241] 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.[247] 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.[247]

Other artistic assessment methods include the Bird's Nest Drawing: a useful tool for visualizing a client's attachment security.[248][241] 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.[249]

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.[250][241] 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.[250]

Advocacy [ edit ]

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.[251][252][253] It can influence healthcare policy, making it difficult for these individuals to access treatment.[254]

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.[255]

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.[255]

According to Santora[255] 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.[256] 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.[256]

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.[257]

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.[258] 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.[258]

Narrative Approach and Addiction [ edit ]

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[259] 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.[260] 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.[260]

Due to higher medication consumption, social isolation, financial worries, and other factors, older adults are particularly vulnerable to substance use
problems.[261] 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.[261] 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.[262] 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.[262]

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.[263] 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'.[263] Another study examined the narratives of 'initiators': people who help people who inject drugs (PWID) with their first
injection.[264] 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).[264] 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.[263][264]

Philosophy [ edit ]

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 – specifically the belief–desire model.[2] 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 [ edit ]

Biopsychosocial–cultural–spiritual [ edit ]

While regarded biomedically as a neuropsychological disorder, addiction is multi-layered, with biological,

psychological, social, cultural, and spiritual (biopsychosocial–cultural–spiritual) elements.[265][266] A
biopsychosocial–cultural–spiritual approach fosters the crossing of disciplinary boundaries, and promotes holistic
considerations of addiction.[267][268][269] A biopsychosocial–cultural–spiritual approach considers, for example, how
physical environments influence experiences, habits, and patterns of addiction.

Ethnographic engagements and developments in fields of knowledge have contributed to biopsychosocial–

cultural–spiritual understandings of addiction, including the work of Philippe Bourgois, whose fieldwork with street-
level drug dealers in East Harlem highlights correlations between drug use and structural oppression in the United
States.[270][3] Prior models that have informed the prevailing biopsychosocial–cultural–spiritual consideration of
addiction include:

Cultural model [ edit ]

The cultural model, an anthropological understanding of the emergence of drug use and abuse, was developed by Acute confusional state caused by
Dwight Heath.[271] Heath undertook ethnographic research and fieldwork with the Camba people of Bolivia from alcohol withdrawal, otherwise known
June 1956 to August 1957.[272] Heath observed that adult members of society drank 'large quantities of rum and as delirium tremens

became intoxicated for several contiguous days at least twice a month'.[271] This frequent, heavy drinking from
which intoxication followed was typically undertaken socially, during festivals.[272] 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'.[273] Heath's observations and
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.[272] 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.[271]

As noted by Merrill Singer, Heath's findings, when considered alongside subsequent cross-cultural experiences, challenged the perception that intoxication
is socially 'inherently disruptive'.[271] 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'.[272][271]

The cultural model did face criticism by Sociologist Robin Room and others, who felt anthropologists could "downgrade the severity of the problem".[271]
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'.[271]

Subcultural model [ edit ]

Historically, addiction has been viewed from the etic perspective, defining users through the pathology of their condition.[274] As reports of drug use rapidly
increased, the cultural model found application in anthropological research exploring western drug subculture practices.[271]

The approach evolved from the ethnographic exploration into the lived experiences and subjectivities of 1960s and 1970s drug subcultures.[271] 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.[275] These findings
challenge popular narratives of immorality and 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.[276][better source needed] To marginalized individuals,
drug subcultures can provide social connection, symbolic meaning, and socially constructed purpose that they may feel is unattainable through
conventional means.[276] The subcultural model demonstrates the complexities of addiction, highlighting the need for an integrated approach. It contends
that a biosocial approach is required to achieve a holistic understanding of addiction.[271]

Critical medical anthropology model [ edit ]

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'.[271] 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 inequalities, and the
institutional power held over social processes.[271]

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)[271]

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 drug market politics.[271] 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.[271] From the perspective of critical medical anthropology heavy drug use and addiction is a consequence of such larger scale unequal
distributions of power.[271]

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.

Addiction causes an "astoundingly high financial and human toll" on individuals and society as a whole.[277][215][218] In the United States, the total
economic cost to society is greater than that of all types of diabetes and all cancers combined.[218] 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 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.[277][215][218][278] 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.[279] 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.[280]

See also [ edit ]

Autonomic nervous system Dopaminergic pathways

Binge drinking Pavlovian-instrumental transfer
Binge eating disorder Philosophy of medicine
Discrimination against drug addicts Substance dependence

Endnotes [ edit ]

a. ^ 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 to seek help after becoming addicted, although resisting the urge to use becomes increasingly difficult as addiction
worsens. See[1] for detailed discussion.

Notes [ edit ]

1. ^ According to a review of experimental animal models that examined the transgenerational epigenetic inheritance of epigenetic marks that occur in addiction,
alterations in histone acetylation – specifically, di-acetylation of lysine residues 9 and 14 on histone 3 (i.e., H3K9ac2 and H3K14ac2) in association with BDNF gene
promoters – have been shown to occur within the medial prefrontal cortex (mPFC), testes, and sperm of cocaine-addicted male rats.[91] These epigenetic alterations
in the rat mPFC result in increased BDNF gene expression within the mPFC, which in turn blunts the rewarding properties of cocaine and reduces cocaine self-
administration.[91] 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).[91] 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.[91] As of 2018, neither the heritability of these epigenetic marks in humans nor the behavioral effects of the marks within human mPFC neurons has been
established.[91]
2. ^ a b A decrease in aversion sensitivity, in simpler terms, means that an individual's behavior is less likely to be influenced by undesirable outcomes.
3. ^ In other words, c-Fos 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.[3] 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.[3]
4. ^ According to two medical reviews, ΔFosB has been implicated in causing both increases and decreases in dynorphin expression in different studies;[121][151] this
table entry reflects only a decrease.
5. ^ 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.[152][153] 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.[152]
6. ^ 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.
7. ^ Inhibitors of class I histone deacetylase (HDAC) enzymes are drugs that inhibit four specific histone-modifying enzymes: HDAC1, HDAC2, HDAC3, and HDAC8.
Most of the animal research with HDAC inhibitors has been conducted with four drugs: butyrate salts (mainly sodium butyrate), trichostatin A, valproic acid, and
SAHA;[201][156] butyric acid is a naturally occurring short-chain fatty acid in humans, while the latter two compounds are FDA-approved drugs with medical indications
unrelated to addiction.
8. ^ Specifically, prolonged administration of a class I HDAC inhibitor appears to reduce an animal's motivation to acquire and use an addictive drug without affecting
an animals motivation to attain other rewards (i.e., it does not appear to cause motivational anhedonia) and reduce the amount of the drug that is self-administered
when it is readily available.[134][156][202]
9. ^ Among the few clinical trials that employed a class I HDAC inhibitor, one used valproate for methamphetamine addiction.[204]
10. ^ The lifetime prevalence of an addiction is the percentage of individuals in a population that developed an addiction at some point in their life.

Image legend
1. ^
Ion channel
G proteins & linked receptors
(Text color) Transcription factors

References [ edit ]

1. ^ a b Heilig M, MacKillop J, Martinez D, Rehm J, Leggio L, Vanderschuren LJ 140. ^ a b Nestler EJ, Barrot M, Self DW (September 2001). "DeltaFosB: a
(September 2021). "Addiction as a brain disease revised: why it still matters, sustained molecular switch for addiction" . Proc. Natl. Acad. Sci. U.S.A. 98
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addictions" – Indeed, addiction to both drugs and behavioral rewards may
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34. ^ a b c d e f g h i j k l m n o p q r s t u v w x y z aa ab ac ad ae af ag ah ai aj ak al
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addictions" . Neuropharmacology. 61 (7): 1109–22.
doi:10.1016/j.neuropharm.2011.03.010 . PMC 3139704
PMID 21459101 . "Functional neuroimaging studies in humans have shown
that gambling (Breiter et al, 2001), shopping (Knutson et al, 2007), orgasm
(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). ... Cross-sensitization is
also bidirectional, as a history of amphetamine administration facilitates
sexual behavior and enhances the associated increase in NAc DA ... 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). ... 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). ... 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)." "
Table 1: Summary of plasticity observed following exposure to drug or natural
reinforcers "
35. ^ a b c d e f g h i j k l m Robison AJ, Nestler EJ (November 2011).
"Transcriptional and epigenetic mechanisms of addiction"
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PMID 21989194 . "ΔFosB has been linked directly to several addiction-
related behaviors ... Importantly, genetic or viral overexpression of ΔJunD, a
dominant negative mutant of JunD which antagonizes ΔFosB- and other AP-
1-mediated transcriptional activity, in the NAc or OFC blocks these key effects
of drug exposure14,22–24. This indicates that ΔFosB is both necessary and
sufficient for many of the changes wrought in the brain by chronic drug
exposure. ΔFosB is induced in D1-type NAc MSNs by chronic consumption of
several natural rewards, including sucrose, high fat food, sex, wheel running,
where it promotes that consumption14,26–30. This implicates ΔFosB in the
regulation of natural rewards under normal conditions and perhaps during
pathological addictive-like states."
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Lab. Department of Psychology, University of Michigan. Retrieved
1 November 2022.
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42. ^ abcd Karila L, Wéry A, Weinstein A, Cottencin O, Petit A, Reynaud M,
Billieux J (2014). "Sexual addiction or hypersexual disorder: different terms
for the same problem? A review of the literature". Curr. Pharm. Des. 20 (25):
4012–20. doi:10.2174/13816128113199990619 . PMID 24001295
S2CID 19042860 . "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. ...
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."
43. ^ a b c d e Pitchers KK, Vialou V, Nestler EJ, Laviolette SR, Lehman MN,
Coolen LM (February 2013). "Natural and drug rewards act on common
neural plasticity mechanisms with ΔFosB as a key mediator"
of Neuroscience. 33 (8): 3434–42. doi:10.1523/JNEUROSCI.4881-
12.2013 . PMC 3865508 . PMID 23426671 . "Drugs of abuse induce
neuroplasticity in the natural reward pathway, specifically the nucleus
accumbens (NAc), thereby causing development and expression of addictive
behavior. ... 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. ... 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"
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the US Food and Drug Administration for the treatment of alcoholism and
opioid dependence, has shown efficacy in controlled clinical trials for the
treatment of pathological gambling and kleptomania (76–79), and promise in
uncontrolled studies of compulsive buying (80), compulsive sexual behavior
(81), internet addiction (82), and pathologic skin picking (83). ... Topiramate,
an anti-convulsant which blocks the AMPA subtype of glutamate receptor
(among other actions), has shown promise in open-label studies of
pathological gambling, compulsive buying, and compulsive skin picking (85),
as well as efficacy in reducing alcohol (86), cigarette (87), and cocaine (88)
use. N-acetyl cysteine, an amino acid that restores extracellular glutamate
concentration in the nucleus accumbens, reduced gambling urges and
behavior in one study of pathological gamblers (89), and reduces cocaine
craving (90) and cocaine use (91) in cocaine addicts. These studies suggest
that glutamatergic modulation of dopaminergic tone in the nucleus
accumbens may be a mechanism common to behavioral addiction and
substance use disorders (92)."
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and (ii) CS-directed 'wanting' – motivated attraction to the Pavlovian cue,
which makes the arbitrary CS stimulus into a motivational magnet."
153. ^ a b Malenka RC, Nestler EJ, Hyman SE (2009). Sydor A, Brown RY (eds.).
. Molecular Neuropharmacology: A Foundation for Clinical Neuroscience
ISBN 978-0-07-148127-4. "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. ...
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. ...
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
. New England
release in the shell than in the core of the NAc. ... 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."
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PMID 26806771 . "An important dimension of reinforcement highly relevant
to the addiction process (and particularly relapse) is secondary reinforcement
. National
(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
reinforcing ... 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)."
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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"
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Medical. ISBN 978-0-07-182770-6. "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."
160. ^ a b "International Classification of Diseases 11th revision – ICD-11.
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to act as a reward (ie, a pleasurable emotional state or positive reinforcer),
which can lead to repeated drug use and dependence.8,9 A great deal of
research has focused on the molecular and neuroanatomical mechanisms of
the initial rewarding or reinforcing effect of drugs of abuse. ... 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.172 ... A new
emphasis on larger-scale biomarker, genetic, and epigenetic research
focused on the molecular targets of mental disorders has been recently
advocated.212 In addition, the integration of cognitive and behavioral
modification of circuit-wide neuroplasticity (i.e., computer-based training to
. Nat. Rev.
enhance executive function) may prove to be an effective adjunct-treatment
.
approach for addiction, particularly when combined with cognitive
enhancers.198,213–216 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,
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PMID 26903885 . "Environmental Enrichment ...
In humans, non-drug rewards delivered in a contingency management (CM)
format successfully reduced drug dependence ... In general, CM programs
promote drug abstinence through a combination of positive reinforcement for
. drug-free urine samples. For instance, voucher-based reinforcement therapy
drug screenings reinforced with vouchers to local business (e.g., movie
theater, restaurants, etc.) directly reinforces drug abstinence, provides
competing reinforcers, enriches the environment, and it is a robust treatment
. across a broad range of abused drugs (189). ...
Physical Exercise
There is accelerating evidence that physical exercise is a useful treatment for
preventing and reducing drug addiction ... In some individuals, exercise has
its own rewarding effects, and a behavioral economic interaction may occur,
such that physical and social rewards of exercise can substitute for the
rewarding effects of drug abuse. ... The value of this form of treatment for
drug addiction in laboratory animals and humans is that exercise, if it can
substitute for the rewarding effects of drugs, could be self-maintained over an
extended period of time. Work to date in [laboratory animals and humans]
regarding exercise as a treatment for drug addiction supports this
hypothesis. ... However, a RTC study was recently reported by Rawson et al.
(226), whereby they used 8 weeks of exercise as a post-residential treatment
for METH addiction, showed a significant reduction in use (confirmed by urine
screens) in participants who had been using meth 18 days or less a month. ...
Animal and human research on physical exercise as a treatment for stimulant
addiction indicates that this is one of the most promising treatments on the
horizon. [(emphasis added)]"
169. ^ a b c d Lynch WJ, Peterson AB, Sanchez V, Abel J, Smith MA (September
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. The Journal PMID 23806439 . "[exercise] efficacy may be related to its ability to
normalize glutamatergic and dopaminergic signaling and reverse drug-
induced changes in chromatin via epigenetic interactions with brain-derived
neurotrophic factor (BDNF) in the reward pathway. ... these data show that
exercise can affect dopaminergic signaling at many different levels, which
may underlie its ability to modify vulnerability during drug use initiation.
Exercise also produces neuroadaptations that may influence an individual's
vulnerability to initiate drug use. Consistent with this idea, chronic moderate
levels of forced treadmill running blocks not only subsequent
methamphetamine-induced conditioned place preference, but also stimulant-
induced increases in dopamine release in the NAc (Chen et al., 2008) and
striatum (Marques et al., 2008). ... [These] findings indicate the efficacy of
exercise at reducing drug intake in drug-dependent individuals ... wheel
running [reduces] methamphetamine self-administration under extended
access conditions (Engelmann et al., 2013) ... These findings suggest that
exercise may "magnitude"-dependently prevent the development of an
addicted phenotype possibly by blocking/reversing behavioral and neuro-
adaptive changes that develop during and following extended access to the
drug. ... Exercise has been proposed as a treatment for drug addiction that
may reduce drug craving and risk of relapse. Although few clinical studies
have investigated the efficacy of exercise for preventing relapse, the few
studies that have been conducted generally report a reduction in drug craving
and better treatment outcomes (see Table 4). ... Taken together, these data
suggest that the potential benefits of exercise during relapse, particularly for
relapse to psychostimulants, may be mediated via chromatin remodeling and
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PMC 4831948 . PMID 25397661 . "The limited research conducted
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. International contrast to the scarce intervention trials to date, a relative abundance of
. literature on the theoretical and practical reasons supporting the investigation
reasons support exercise-based treatments for SUDs, including
psychological, behavioral, neurobiological, nearly universal safety profile, and
. overall positive health effects."
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substitute or competition for drug abuse by changing ΔFosB or cFos
immunoreactivity in the reward system to protect against later or previous
drug use. ... As briefly reviewed above, a large number of human and rodent
studies clearly show that there are sex differences in drug addiction and
exercise. The sex differences are also found in the effectiveness of exercise
on drug addiction prevention and treatment, as well as underlying
neurobiological mechanisms. The postulate that exercise serves as an ideal
intervention for drug addiction has been widely recognized and used in
human and animal rehabilitation. ... In particular, more studies on the
neurobiological mechanism of exercise and its roles in preventing and
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addictive drugs play an important role in neuronal plasticity and in drug-
doi:10.1002/jeab.194 . PMID 26781048 . "Today, arguably more than at
induced behavioral responses. Although few studies have investigated the
any time in history, the constructs of attention, executive functioning, and
effects of AMPH on gene regulation (Table 1), current data suggest that
cognitive control seem to be pervasive and preeminent in research and
AMPH acts at multiple levels to alter histone/DNA interaction and to recruit
theory. Even within the cognitive framework, however, there has long been an
transcription factors which ultimately cause repression of some genes and
understanding that behavior is multiply determined, and that many responses
activation of other genes. Importantly, some studies have also correlated the
are relatively automatic, unattended, contention-scheduled, and habitual.
epigenetic regulation induced by AMPH with the behavioral outcomes caused
Indeed, the cognitive flexibility, response inhibition, and self-regulation that
by this drug, suggesting therefore that epigenetics remodeling underlies the
appear to be hallmarks of cognitive control are noteworthy only in contrast to
behavioral changes induced by AMPH. If this proves to be true, the use of
responses that are relatively rigid, associative, and involuntary."
specific drugs that inhibit histone acetylation, methylation or DNA methylation
87. ^ Diamond A (2013). "Executive functions" . Annu Rev Psychol. 64: 135–68.
might be an important therapeutic alternative to prevent and/or reverse AMPH
doi:10.1146/annurev-psych-113011-143750 . PMC 4084861 .
addiction and mitigate the side effects generate by AMPH when used to treat
PMID 23020641 . "Core EFs are inhibition [response inhibition (self-
ADHD."
control – resisting temptations and resisting acting impulsively) and
202. ^ a b Primary references involving sodium butyrate:
interference control (selective attention and cognitive inhibition)], working
• Kennedy PJ, Feng J, Robison AJ, Maze I, Badimon A, Mouzon E,
memory, and cognitive flexibility (including creatively thinking "outside the
Chaudhury D, Damez-Werno DM, Haggarty SJ, Han MH, Bassel-Duby R,
box," seeing anything from different perspectives, and quickly and flexibly
Olson EN, Nestler EJ (April 2013). "Class I HDAC inhibition blocks cocaine-
adapting to changed circumstances). ... EFs and prefrontal cortex are the first
induced plasticity by targeted changes in histone methylation" . Nat.
to suffer, and suffer disproportionately, if something is not right in your life.
Neurosci. 16 (4): 434–40. doi:10.1038/nn.3354 . PMC 3609040 .
They suffer first, and most, if you are stressed (Arnsten 1998, Liston et al.
PMID 23475113 . "While acute HDAC inhibition enhances the behavioral
2009, Oaten & Cheng 2005), sad (Hirt et al. 2008, von Hecker & Meiser
effects of cocaine or amphetamine1,3,4,13,14, studies suggest that more
2005), lonely (Baumeister et al. 2002, Cacioppo & Patrick 2008, Campbell et
chronic regimens block psychostimulant-induced plasticity3,5,11,12. ... The
al. 2006, Tun et al. 2012), sleep deprived (Barnes et al. 2012, Huang et al.
effects of pharmacological inhibition of HDACs on psychostimulant-induced
2007), or not physically fit (Best 2010, Chaddock et al. 2011, Hillman et al.
plasticity appear to depend on the timecourse of HDAC inhibition. Studies
2008). Any of these can cause you to appear to have a disorder of EFs, such
employing co-administration procedures in which inhibitors are given acutely,
as ADHD, when you do not. You can see the deleterious effects of stress,
just prior to psychostimulant administration, report heightened behavioral
sadness, loneliness, and lack of physical health or fitness at the physiological
responses to the drug1,3,4,13,14. In contrast, experimental paradigms like the
and neuroanatomical level in prefrontal cortex and at the behavioral level in
one employed here, in which HDAC inhibitors are administered more
worse EFs (poorer reasoning and problem solving, forgetting things, and
chronically, for several days prior to psychostimulant exposure, show inhibited
impaired ability to exercise discipline and self-control). ...
expression3 or decreased acquisition of behavioral adaptations to drug5,11,12.
EFs can be improved (Diamond & Lee 2011, Klingberg 2010). ... At any age
The clustering of seemingly discrepant results based on experimental
across the life cycle EFs can be improved, including in the elderly and in
methodologies is interesting in light of our present findings. Both HDAC
infants. There has been much work with excellent results on improving EFs in
inhibitors and psychostimulants increase global levels of histone acetylation
the elderly by improving physical fitness (Erickson & Kramer 2009, Voss et al.
in NAc. Thus, when co-administered acutely, these drugs may have
2011) ... Inhibitory control (one of the core EFs) involves being able to control
synergistic effects, leading to heightened transcriptional activation of
one's attention, behavior, thoughts, and/or emotions to override a strong
psychostimulant-regulated target genes. In contrast, when a psychostimulant
internal predisposition or external lure, and instead do what's more
is given in the context of prolonged, HDAC inhibitor-induced hyperacetylation,
appropriate or needed. Without inhibitory control we would be at the mercy of
homeostatic processes may direct AcH3 binding to the promoters of genes
impulses, old habits of thought or action (conditioned responses), and/or
(e.g., G9a) responsible for inducing chromatin condensation and gene
stimuli in the environment that pull us this way or that. Thus, inhibitory control
repression (e.g., via H3K9me2) to dampen already heightened transcriptional
makes it possible for us to change and for us to choose how we react and
activation. Our present findings thus demonstrate clear cross talk among
how we behave rather than being unthinking creatures of habit. It doesn't
histone PTMs and suggest that decreased behavioral sensitivity to
make it easy. Indeed, we usually are creatures of habit and our behavior is
psychostimulants following prolonged HDAC inhibition might be mediated
under the control of environmental stimuli far more than we usually realize,
through decreased activity of HDAC1 at H3K9 KMT promoters and
but having the ability to exercise inhibitory control creates the possibility of
subsequent increases in H3K9me2 and gene repression."
change and choice. ... The subthalamic nucleus appears to play a critical role
• Simon-O'Brien E, Alaux-Cantin S, Warnault V, Buttolo R, Naassila M,
in preventing such impulsive or premature responding (Frank 2006)."
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148127-4. " • Executive function, the cognitive control of behavior, depends
hypothesis that HDACi may have a potential use in alcohol addiction
on the prefrontal cortex, which is highly developed in higher primates and
treatment."
especially humans.
• Castino MR, Cornish JL, Clemens KJ (April 2015). "Inhibition of histone
• Working memory is a short-term, capacity-limited cognitive buffer that
deacetylases facilitates extinction and attenuates reinstatement of nicotine
stores information and permits its manipulation to guide decision-making and
self-administration in rats" . PLOS ONE. 10 (4): e0124796.
behavior. ...
Bibcode:2015PLoSO..1024796C . doi:10.1371/journal.pone.0124796 .
These diverse inputs and back projections to both cortical and subcortical
PMC 4399837 . PMID 25880762 . "treatment with NaB significantly
structures put the prefrontal cortex in a position to exert what is called "top-
attenuated nicotine and nicotine + cue reinstatement when administered
down" control or cognitive control of behavior. ... The prefrontal cortex
immediately ... These results provide the first demonstration that HDAC
receives inputs not only from other cortical regions, including association
inhibition facilitates the extinction of responding for an intravenously self-
cortex, but also, via the thalamus, inputs from subcortical structures
administered drug of abuse and further highlight the potential of HDAC
subserving emotion and motivation, such as the amygdala (Chapter 14) and
inhibitors in the treatment of drug addiction."
ventral striatum (or nucleus accumbens; Chapter 15). ...
203. ^ Kyzar EJ, Pandey SC (August 2015). "Molecular mechanisms of synaptic
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"Increased HDAC2 expression decreases the expression of genes important
negative consequences can result. ... ADHD can be conceptualized as a
for the maintenance of dendritic spine density such as BDNF, Arc, and NPY,
disorder of executive function; specifically, ADHD is characterized by reduced
leading to increased anxiety and alcohol-seeking behavior. Decreasing
ability to exert and maintain cognitive control of behavior. Compared with
HDAC2 reverses both the molecular and behavioral consequences of alcohol
healthy individuals, those with ADHD have diminished ability to suppress
addiction, thus implicating this enzyme as a potential treatment target (Fig. 3).
inappropriate prepotent responses to stimuli (impaired response inhibition)
HDAC2 is also crucial for the induction and maintenance of structural
and diminished ability to inhibit responses to irrelevant stimuli (impaired
synaptic plasticity in other neurological domains such as memory formation
interference suppression). ... Functional neuroimaging in humans
[115]. Taken together, these findings underscore the potential usefulness of
demonstrates activation of the prefrontal cortex and caudate nucleus (part of
HDAC inhibition in treating alcohol use disorders ... Given the ability of HDAC
the striatum) in tasks that demand inhibitory control of behavior. Subjects with
inhibitors to potently modulate the synaptic plasticity of learning and memory
ADHD exhibit less activation of the medial prefrontal cortex than healthy
[118], these drugs hold potential as treatment for substance abuse-related
controls even when they succeed in such tasks and utilize different circuits. ...
disorders. ... Our lab and others have published extensively on the ability of
Early results with structural MRI show thinning of the cerebral cortex in ADHD
HDAC inhibitors to reverse the gene expression deficits caused by multiple
subjects compared with age-matched controls in prefrontal cortex and
models of alcoholism and alcohol abuse, the results of which were discussed
posterior parietal cortex, areas involved in working memory and attention."
above [25,112,113]. This data supports further examination of histone
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Further reading [ edit ]

Pelchat ML (March 2009). "Food Addiction in Humans" . The Journal of Nutrition. 139 (3): 620–622. doi:10.3945/jn.108.097816 . PMID 19176747 .
Gordon HW (April 2016). "Laterality of Brain Activation for Risk Factors of Addiction" . Current Drug Abuse Reviews. 9 (1): 1–18.
doi:10.2174/1874473709666151217121309 . PMC 4811731 . PMID 26674074 .
Szalavitz M (2016). Unbroken Brain . St. Martin's Press. ISBN 978-1-250-05582-8.

External links [ edit ]

"The Science of Addiction: Genetics and the Brain" . learn.genetics.utah.edu. Learn.Genetics – University of
Look up -ism in Wiktionary,
Utah. the free dictionary.
Why do our brains get addicted? – a TEDMED 2014 talk by Nora Volkow, the director of the National
Look up -holic in Wiktionary,
Institute on Drug Abuse at NIH.
the free dictionary.
Kyoto Encyclopedia of Genes and Genomes (KEGG) signal transduction pathways:
Wikimedia Commons has
KEGG – human alcohol addiction media related to Addictions.
KEGG – human amphetamine addiction
KEGG – human cocaine addiction

Classification ICD-10: F10-F19 subdivision .2 D

· · Reinforcement disorders: Addiction and Dependence [show]

· · Recreational drug use [show]

Portals: Psychology Medicine Biology

Authority control [show]

Categories: Addiction Behavioral addiction Brain disorders Substance-related disorders

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