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{{redirect|Addictive|other uses|Addiction (disambiguation)|and|Addictive (disambiguation)}}{{Redirect|Drug Addicts|the Lil Pump song|Drug Addicts (song)}}{{Use dmy dates|date=November 2018}}

| image = Brain metabolism and drug addiction.jpgBrain positron emission tomography images that compare Human brain#Metabolism>brain metabolism in a healthy individual and a cocaine addict| alt = PET images showing brain metabolism in drug addicts vs controls| field = Psychiatry| width = 390| pronounce = | specialty = | symptoms =| complications =| onset =| duration =| types = | causes =| risks = | diagnosis =| differential =| prevention =| treatment =| medication =| prognosis =| frequency =| deaths = }}{{addiction glossary|reverse citation order=yes|width=404px}}{{EngvarA|date=September 2016}}Addiction is a brain disorder characterized by compulsive engagement in rewarding stimuli despite adverse consequences.{{refn|JOURNAL, Angres DH, Bettinardi-Angres K, The disease of addiction: origins, treatment, and recovery, Disease-a-Month, 54, 10, 696–721, October 2008, 18790142, 10.1016/j.disamonth.2008.07.002, }} Despite the involvement of a number of psychosocial factors, a biological process â€“ one which is induced by repeated exposure to an addictive stimulus â€“ is the core pathology that drives the development and maintenance of an addiction.WEB, American Society for Addiction Medicine, Definition of Addiction, 2012,weblink The two properties that characterize all addictive stimuli are that they are reinforcing (i.e., they increase the likelihood that a person will seek repeated exposure to them) and intrinsically rewarding (i.e., they are perceived as being inherently positive, desirable, and pleasurable).Addiction is a disorder of the brain's reward system which arises through transcriptional and epigenetic mechanisms and develops over time from 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.). 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. 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. Due to the causal relationship between ΔFosB expression and addictions, it is used preclinically as an addiction biomarker.JOURNAL, Ruffle JK, Molecular neurobiology of addiction: what's all the (Δ)FosB about?, Am. J. Drug Alcohol Abuse, 40, 6, 428–37, November 2014, 25083822, 10.3109/00952990.2014.933840, The strong correlation between chronic drug exposure and ΔFosB provides novel opportunities for targeted therapies in addiction (118), and suggests methods to analyze their efficacy (119). Over the past two decades, research has progressed from identifying ΔFosB induction to investigating its subsequent action (38). It is likely that ΔFosB research will now progress into a new era – the use of ΔFosB as a biomarker. ...ConclusionsΔFosB is an essential transcription factor implicated in the molecular and behavioral pathways of addiction following repeated drug exposure. The formation of ΔFosB in multiple brain regions, and the molecular pathway leading to the formation of AP-1 complexes is well understood. The establishment of a functional purpose for ΔFosB has allowed further determination as to some of the key aspects of its molecular cascades, involving effectors such as GluR2 (87,88), Cdk5 (93) and NFkB (100). Moreover, many of these molecular changes identified are now directly linked to the structural, physiological and behavioral changes observed following chronic drug exposure (60,95,97,102). New frontiers of research investigating the molecular roles of ΔFosB have been opened by epigenetic studies, and recent advances have illustrated the role of ΔFosB acting on DNA and histones, truly as a molecular switch (34). As a consequence of our improved understanding of ΔFosB in addiction, it is possible to evaluate the addictive potential of current medications (119), as well as use it as a biomarker for assessing the efficacy of therapeutic interventions (121,122,124). Some of these proposed interventions have limitations (125) or are in their infancy (75). However, it is hoped that some of these preliminary findings may lead to innovative treatments, which are much needed in addiction., JOURNAL, BiliÅ„ski P, WojtyÅ‚a A, Kapka-Skrzypczak L, Chwedorowicz R, Cyranka M, StudziÅ„ski T, Epigenetic regulation in drug addiction, Ann. Agric. Environ. Med., 19, 3, 491–96, 2012, 23020045, For these reasons, ΔFosB is considered a primary and causative transcription factor in creating new neural connections in the reward centre, prefrontal cortex, and other regions of the limbic system. This is reflected in the increased, stable and long-lasting level of sensitivity to cocaine and other drugs, and tendency to relapse even after long periods of abstinence. These newly constructed networks function very efficiently via new pathways as soon as drugs of abuse are further taken ... In this way, the induction of CDK5 gene expression occurs together with suppression of the G9A gene coding for dimethyltransferase acting on the histone H3. A feedback mechanism can be observed in the regulation of these 2 crucial factors that determine the adaptive epigenetic response to cocaine. This depends on ΔFosB inhibiting G9a gene expression, i.e. H3K9me2 synthesis which in turn inhibits transcription factors for ΔFosB. For this reason, the observed hyper-expression of G9a, which ensures high levels of the dimethylated form of histone H3, eliminates the neuronal structural and plasticity effects caused by cocaine by means of this feedback which blocks ΔFosB transcription, ΔFosB expression in these neurons directly and positively regulates drug self-administration and reward sensitization through positive reinforcement, while decreasing sensitivity to (wikt:aversion|aversion).{{#tag:ref|A decrease in aversion sensitivity, in simpler terms, means that an individual's behavior is less likely to be influenced by undesirable outcomes.|group="note"|name="ΔFosB behaviors"}}Addiction exacts an "astoundingly high financial and human toll" on individuals and society as a whole.BOOK, Malenka RC, Nestler EJ, Hyman SE, Sydor A, Brown RY, Molecular Neuropharmacology: A Foundation for Clinical Neuroscience, 2009, McGraw-Hill Medical, New York, 978-0-07-148127-4, 4, 2nd, Chapter 1: Basic Principles of Neuropharmacology, Drug abuse and addiction exact an astoundingly high financial and human toll on society through direct adverse effects, such as lung cancer and hepatic cirrhosis, and indirect adverse effects â€“for example, accidents and AIDS â€“ on health and productivity., JOURNAL, Merikangas KR, McClair VL, Epidemiology of Substance Use Disorders, June 2012, Hum. Genet., 779–89, 6, 131, 4408274, 10.1007/s00439-012-1168-0, 22543841, In the United States, the total economic cost to society is greater than that of all types of diabetes and all cancers combined. 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.BOOK, International Narcotics Control Board Report: 2013, 2013, United Nations â€“ International Narcotics Control Board, 978-92-1-148274-4,weblink 28 September 2018,weblink Economic consequences of drug abuse, Classic hallmarks of addiction include impaired control over substances or behavior, preoccupation with substance or behavior, and continued use despite consequences.JOURNAL, Morse RM, Flavin DK, The definition of alcoholism. The Joint Committee of the National Council on Alcoholism and Drug Dependence and the American Society of Addiction Medicine to Study the Definition and Criteria for the Diagnosis of Alcoholism, JAMA, 268, 8, 1012–14, August 1992, 1501306, 10.1001/jama.1992.03490080086030, Habits and patterns associated with addiction are typically characterized by immediate gratification (short-term reward), coupled with delayed deleterious effects (long-term costs).JOURNAL, Marlatt GA, Baer JS, Donovan DM, Kivlahan DR, Addictive behaviors: etiology and treatment, Annu Rev Psychol, 39, 223–52, 1988, 3278676, 10.1146/, Examples of drug and behavioral addictions include alcoholism, marijuana addiction, amphetamine addiction, cocaine addiction, nicotine addiction, opioid addiction, food addiction, gambling addiction, and sexual addiction. The only behavioral addiction recognized by the DSM-5 and the ICD-10 is gambling addiction. The term addiction is misused frequently to refer to other compulsive behaviors or disorders, particularly dependence, in news media.WEB, American Psychiatric Association, Substance-Related and Addictive Disorders,weblink American Psychiatric Publishing, 10 July 2015, 1–2, 2013, Additionally, the diagnosis of dependence caused much confusion. Most people link dependence with "addiction" when in fact dependence can be a normal body response to a substance., yes,weblink" title="">weblink 15 August 2015, An important distinction between drug addiction and dependence is that drug dependence is a disorder in which cessation of drug use results in an unpleasant state of withdrawal, which can lead to further drug use. Addiction is the compulsive use of a substance or performance of a behavior that is independent of withdrawal. Addiction can occur in the absence of dependence, and dependence can occur in the absence of addiction, although the two often occur together.{{TOC limit|3}}


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

Stimulus control of behavior

{{see also|Stimulus control}}

Cognitive control of behavior

{{see also|Cognitive control}}

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.BOOK, Malenka RC, Nestler EJ, Hyman SE, Sydor A, Brown RY, Molecular Neuropharmacology: A Foundation for Clinical Neuroscience, 2009, McGraw-Hill Medical, New York, 978-0-07-148127-4, 364–65, 375, 2nd, Chapter 15: Reinforcement and Addictive Disorders, The defining feature of addiction is compulsive, out-of-control drug use, despite negative consequences. ...compulsive eating, shopping, gambling, and sex â€“ so-called "natural addictions" â€“ Indeed, addiction to both drugs and behavioral rewards may arise from similar dysregulation of the mesolimbic dopamine system., 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.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). Moreover, reward cross-sensitization between amphetamine and sexual activity, meaning that exposure to one increases the desire for both, has been shown to occur preclinically and clinically as a dopamine dysregulation syndrome; ΔFosB expression is required for this cross-sensitization effect, which intensifies with the level of ΔFosB expression.Reviews of preclinical studies indicate that long-term frequent and excessive consumption of high fat or sugar foods can produce an addiction (food addiction).Gambling is a natural reward which is associated with compulsive behavior and for which clinical diagnostic manuals, namely the DSM-5, have identified diagnostic criteria for an "addiction". In order for a person's gambling behavior to meet criteria of an addiction, it shows certain characteristics, such as mood modification, compulsivity, and withdrawal. There is evidence from functional neuroimaging that gambling activates the reward system and the mesolimbic pathway in particular. Similarly, shopping and playing video games are associated with compulsive behaviors in humans and have also been shown to activate the mesolimbic pathway and other parts of the reward system. Based upon this evidence, gambling addiction, video game addiction, and shopping addiction are classified accordingly.

Risk factors

{{See|Addiction vulnerability}}There are a number of genetic and environmental risk factors for developing an addiction, that vary across the population. Genetic and environmental risk factors each account for roughly half of an individual's risk for developing an addiction; the contribution from epigenetic risk factors to the total risk is unknown. 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.

Genetic factors

{{See also|Alcoholism#Genetic variation}}It has long been established that genetic factors along with environmental (e.g., psychosocial) factors are significant contributors to addiction vulnerability. Epidemiological studies estimate that genetic factors account for 40–60% of the risk factors for alcoholism.{{Citation needed|date=June 2018}} Similar rates of heritability for other types of drug addiction have been indicated by other studies. 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 could then change the structure or functioning of specific brain neurons during development. These altered brain neurons could change 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 genotype.JOURNAL, Kendler KS, Neale MC, Heath AC, Kessler RC, Eaves LJ, A twin-family study of alcoholism in women, Am J Psychiatry, 151, 5, 707–15, May 1994, 8166312, 10.1176/ajp.151.5.707, Overall, the data implicating specific genes in the development of drug addiction is mixed for most genes. One reason for this may be that the case is due to a focus of current research on common variants. Many addiction studies focus on common variants with an allele frequency of greater than 5% in the general population; however, when associated with disease, these only confer a small amount of additional risk with an odds ratio of 1.1–1.3 percent. On the other hand, the rare variant hypothesis states that genes with low frequencies in the population (

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