Addiction

"Addictive" redirects here. For other uses, see Addiction (disambiguation) and Addictive (disambiguation).

Not to be confused with Addition.

Addiction
Brain positron emission tomography images that compare brain metabolism in a healthy individual and an individual with a cocaine addiction
Specialty	Psychiatry, clinical psychology, toxicology, addiction medicine
Symptoms	Recurrent compulsion to engage in a rewarding activity despite negative consequences
Complications	Suicide, overdose (if drugs), depression, coma
Risk factors	Family history, adverse childhood experiences, attention deficit hyperactivity disorder
Treatment	Cognitive behavioral therapy, behavior modification, medication

Addiction is a neuropsychological disorder characterized by a persistent and intense urge to use a drug or engage in a behavior that produces an immediate psychological reward, despite substantial harm and other negative consequences. Repeated substance use produces long-lasting changes in brain networks involved in reward, executive function, stress reactivity and mood; these changes underlie both the intense drive to use a substance and the reduced capacity to control that urge. It is therefore understood as a brain disorder arising from a complex mix of psychosocial and neurobiological factors. A number of researchers argue that this framing is incomplete, and that addiction is better understood as learned behaviour shaped by choice and social context.

Classic signs of addiction include compulsive engagement in rewarding stimuli, preoccupation with substances or behavior, and continued use despite negative consequences. Habits and patterns associated with addiction are typically characterized by immediate gratification (short-term reward), coupled with delayed deleterious effects (long-term costs).

Examples of substance addiction include alcoholism, cannabis addiction, amphetamine addiction, cocaine addiction, nicotine addiction, and opioid addiction. Behavioral addictions may include gambling addiction, shopping addiction, pornography addiction, internet addiction, video game addiction, and sexual addiction. The DSM-5-TR recognizes only gambling disorder as a behavioral (non-substance) addiction and lists internet gaming disorder as a condition for further study, while the ICD-11 additionally classifies gaming disorder as a disorder due to addictive behaviors.

Signs and symptoms

Signs and symptoms of drug addiction can vary depending on the type of addiction. Symptoms may include:

• Continuation of drug use despite the knowledge of consequences
• Disregarding financial status when it comes to drug purchases
• Ensuring a stable supply of the drug
• Needing more of the drug over time to achieve similar effects
• Social and work life impacted due to drug use
• Unsuccessful attempts to stop drug use
• Urge to use the drug regularly

Other signs and symptoms can be categorized across relevant dimensions:

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

Substance use disorder

Main article: Substance use disorder

Further information: Substance abuse and Substance-related disorder

Addiction and dependence glossary
addiction – a neuropsychological disorder characterized by a persistent and intense urge to use a drug or engage in a behavior that produces natural reward addictive drug – psychoactive substances that with repeated use are associated with significantly higher rates of substance use disorders, due in large part to the drug's effect on brain reward systems dependence – an adaptive state associated with a withdrawal syndrome upon cessation of repeated exposure to a stimulus (e.g., drug intake) drug sensitization or reverse tolerance – the escalating effect of a drug resulting from repeated administration at a given dose drug withdrawal – symptoms that occur upon cessation of repeated drug use physical dependence – dependence that involves persistent physical–somatic withdrawal symptoms (e.g., delirium tremens and nausea) psychological dependence – dependence that is characterized by emotional-motivational withdrawal symptoms (e.g., anhedonia and anxiety) that affect cognitive functioning. reinforcing stimuli – stimuli that increase the probability of repeating behaviors paired with them rewarding stimuli – stimuli that the brain interprets as intrinsically positive and desirable or as something to approach sensitization – an amplified response to a stimulus resulting from repeated exposure to it substance use disorder – a condition in which the use of substances leads to clinically and functionally significant impairment or distress drug tolerance – the diminishing effect of a drug resulting from repeated administration at a given dose

The DSM-5 discourages using the term "drug addiction" because of its "uncertain definition and its potentially negative connotation" and prefers the term "substance use disorder" to describe the wide range of the disorder, from a mild form to a severe state of chronically relapsing, compulsive pattern of drug taking.

SUD belongs to the class of substance-related disorders, is a chronic and relapsing brain disorder that features drug seeking and drug abuse, despite their harmful effects. This form of addiction changes brain circuitry such that the brain's reward system is compromised, causing functional consequences for stress management and self-control. Damage to the functions of the organs involved can persist throughout a lifetime and cause death if untreated. Substances involved with drug addiction include alcohol, nicotine, marijuana, opioids, cocaine, amphetamines, and even foods with high fat and sugar content. Addictions can begin experimentally in social contexts and can arise from the use of prescribed medications or a variety of other measures.

It has been shown to work in phenomenological, conditioning (operant and classical), cognitive models, and the cue reactivity model. However, no one model completely illustrates substance abuse.

Risk factors for addiction include:

• Aggressive behavior (particularly in childhood)
• Availability of substance
• Experimentation
• Epigenetics
• Impulsivity (attentional, motor, or non-planning)
• Lack of parental supervision
• Lack of peer refusal skills
• Mental disorders
• Method substance is taken
• Usage of substance in youth

Food addiction

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) and is based on subjective experiences similar to substance use disorders. 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. Long-term frequent and excessive consumption of foods high in fat, salt, or sugar, such as chocolate, can produce an addiction 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. The signals sent when consuming highly palatable foods have the ability to counteract the body's signals for fullness and persistent cravings will result. Those who show signs of food addiction may develop food tolerances, in which they eat more, despite the food becoming less satisfactory.

Chocolate's sweet flavor and pharmacological ingredients are known to create a strong craving or feel 'addictive' to consumers. 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.

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. 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. 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 the DSM-5. 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.

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 a relation to food addiction.

Behavioral addiction

Main article: Behavioral addiction

The term behavioral addiction refers to a compulsion to engage in a natural reward – which is an inherently rewarding behavior (i.e., desirable or appealing) – despite adverse consequences. 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.

Addiction can exist without psychotropic drugs, an idea that was popularized by psychologist Stanton Peele. These are termed behavioral addictions. Such addictions may be passive or active, but they commonly contain reinforcing features, which are found in most addictions. 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. Based on this evidence, sexual addiction, gambling addiction, video game addiction, and shopping addiction are classified accordingly.

Causes

Personality theories

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. 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.

Neuropsychology

The transtheoretical model of change (TTM) can point to how someone may be conceptualizing their addiction and the thoughts around it, including not being aware of their addiction.

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. Cognitive control, and particularly inhibitory control over behavior, is impaired in both addiction and attention deficit hyperactivity disorder. 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

Operant conditioning

Extinction

Reinforcement Increase behavior

Punishment Decrease behavior

Positive reinforcement Add appetitive stimulus following correct behavior

Negative reinforcement

Positive punishment Add noxious stimulus following behavior

Negative punishment Remove appetitive stimulus following behavior

Escape Remove noxious stimulus following correct behavior

Active avoidance Behavior avoids noxious stimulus

See also: Stimulus control

In operant conditioning, behavior is influenced by outside stimuli, such as a drug. The operant conditioning theory of learning is useful in understanding why the mood-altering or stimulating consequences of drug use can reinforce continued use (an example of positive reinforcement) and why the addicted person seeks to avoid withdrawal through continued use (an example of negative reinforcement). Stimulus control is using the absence of the stimulus or the presence of a reward to influence the resulting behavior.

Cognitive control of behavior

See also: Cognitive control

Cognitive control is the intentional selection of thoughts, behaviors, and emotions based on our environment. It has been shown that drugs alter the way our brains function and their structure. Cognitive functions such as learning, memory, and impulse control, are affected by drugs. These effects promote drug use, as well as hinder the ability to abstain from it. The increase in dopamine release is prominent in drug use, specifically in the ventral striatum and the nucleus accumbens. Dopamine is responsible for producing pleasurable feelings, as well as 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. This promotes the development of a maladaptive drug to stimulus relationship. Early drug use leads to these maladaptive associations, later affecting cognitive processes used for coping, which are needed to abstain from them successfully.

Evolutionary perspectives

Some scholars have proposed evolutionary explanations for addiction, suggesting that vulnerabilities to substance or behavioral dependence reflect by-products or dysregulated expressions of reward and learning systems that were adaptive in ancestral environments. Classic accounts argue that purified drugs and rapid delivery methods exploit ancient motivational circuitry by providing "false fitness signals" that mimic cues once linked to survival or reproduction. Other reviews emphasise how psychoactive substances and behavioral reinforcers act on conserved mechanisms for reward, reinforcement, and emotion, which in modern settings can be overstimulated or maladapted. These perspectives do not replace proximate neurobiological models, but aim instead to situate contemporary patterns of vulnerability within a broader evolutionary framework.

Risk factors

Further information: Addiction vulnerability

Several genetic and environmental risk factors exist for developing an addiction. 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. 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 risk of substance dependence.

Genetic factors

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. Genetic factors account for 40–60% of the risk factors for alcoholism. Similar rates of heritability for other types of drug addiction have been indicated, specifically in genes that encode the alpha-5 nicotinic acetylcholine receptor. 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.

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.

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 allele frequencies 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 of 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.

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

Stress and addiction

Stress can play a central and key role in the development and persistence of addiction. It can influence neurophysiological pathways, decision-making processes, and relapse risk. Acute and chronic stress can activate the hypothalamic pituitary adrenal gland, which can result in elevated cortisol and corticotropin-releasing factor. These hormonal changes alter reward processing and increase the motivational value of substances, mainly those that temporarily reduce negative affect.

In preclinical models, repeated stress exposure aids dopamine release in the nucleus accumbens and sensitizes the mesolimbic reward system, increasing the reinforcing aspects of drugs. Chronic stress also disturbs glutamatergic signaling in the prefrontal cortex, which impairs executive functions including inhibitory control and self-regulation. These changes increase the susceptibility to compulsive drug seeking and decrease the ability to ignore conditioned cues that are associated with substance use.

Stress can also be one of the most reliable predictors of a potential relapse. Human neuroimaging studies show that stress-induced activation of the amygdala and reduced prefrontal cortex regulation correlate with self-reported craving and subsequent return to use. Individuals that have a history of trauma or chronic social stress (things like discrimination, poverty, or unstable housing) show an increased risk for substance use disorders due to both neurobiological sensitization and behavioral coping responses.

Stress interacts very strongly with reward circuitry and decision-making systems; this means many treatment approaches integrate stress-reduction strategies. These include cognitive behavioral therapy, mindfulness-based interventions, and medications targeting stress-related neurochemistry.

Environmental factors

Environmental risk factors for addiction are the experiences of an individual during their lifetime that interact with the individual's genetic composition to increase or decrease his or her vulnerability to addiction. For example, after the nationwide outbreak of COVID-19 in China, more people quit (vs. started) smoking. People who smoke, on average, reduced the quantity of cigarettes they consumed. More generally, several 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. 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. Many researchers, including neuroscientists, indicate that the brain disease model presents a misleading, incomplete, and potentially detrimental explanation of addiction.

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. 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. 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. Many children who experience abuse go on to develop an addiction in adolescence or adult life. 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.

Social control theory

Main article: Social control theory

According to Travis Hirschi's social control theory, adolescents with stronger attachments to family, religious, academic, and other social institutions are less likely to engage in delinquent and maladaptive behavior, such as drug use leading to addiction.

Age

Adolescence represents a period of increased vulnerability to developing an addiction. In adolescence, the incentive-rewards systems in the brain mature well before the cognitive control center. This consequently grants the incentive-rewards systems disproportionate power in the behavioral decision-making process. Therefore, adolescents are increasingly likely to act on their impulses and engage in risky, potentially addictive behavior before considering the consequences. 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.

Most individuals are exposed to and use addictive drugs for the first time during their teenage years. In the United States, there were just over 2.8 million new users of illicit drugs in 2013 (7,800 new users per day); among them, 54.1% were under 18 years of age.

Prefrontal cortex maturation and addiction risk

Adolescence is a critical developmental period in which the prefrontal cortex (responsible for planning, inhibitory control, and evaluating long-term consequences) experiences significant maturation. During this period, limbic reward circuits mature earlier than prefrontal cortex regulatory networks, creating a developmental imbalance in which reward sensitivity is high, but cognitive control is not fully developed yet. This mismatch contributes to higher experimentation with substances and vulnerability to addiction.

Neuroimaging studies show that adolescents exhibit reduced prefrontal cortex activation during decision-making tasks, risk-taking behavior, and heightened dopamine reactivity compared with adults. Exposure to substances during this early period of their life can disrupt synaptic pruning and myelination. This can produce long-term alterations in executive functioning and reward processing that increase the chance of developing a substance use disorder.

Comorbid disorders

Individuals with comorbid mental health disorders such as depression, anxiety, attention deficit hyperactivity disorder, or post-traumatic stress disorder are more likely to develop substance use disorders. The NIDA cites early aggressive behavior as a risk factor for substance use. Substance use disorders frequently co-occur with other psychiatric conditions, and current guidance recommends that comorbid psychiatric and physical conditions be treated concurrently rather than sequentially.

Epigenetic

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

Transgenerational epigenetic inheritance

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: 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). In addiction, epigenetic mechanisms play a central role in the pathophysiology of the disease; 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).

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. 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. 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. 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.

Mechanisms

Addiction is a disorder of the brain's reward system developing through transcriptional and epigenetic mechanisms as a result of chronically high levels of exposure to an addictive stimulus (e.g., eating food, the use of cocaine, engagement in sexual activity, participation in high-thrill cultural activities such as gambling, etc.) over an extended time. 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. ΔFosB expression in these neurons directly and positively regulates drug self-administration and reward sensitization through positive reinforcement, while decreasing sensitivity to aversion.

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 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

Signaling cascade in the nucleus accumbens that results in psychostimulant addiction

Note: colored text contains article links.

Nuclear pore

Nuclear membrane

Plasma membrane

Ca_v1.2

NMDAR

AMPAR

DRD1

DRD5

DRD2

DRD3

DRD4

G_s

G_i/o

AC

cAMP

cAMP

PKA

CaM

CaMKII

DARPP-32

PP1

PP2B

CREB

ΔFosB

JunD

c-Fos

SIRT1

HDAC1

This diagram depicts the signaling events in the brain's reward center that are induced by chronic high-dose exposure to psychostimulants that increase the concentration of synaptic dopamine, like amphetamine, methamphetamine, and phenethylamine. Following presynaptic dopamine and glutamate co-release by such psychostimulants, postsynaptic receptors for these neurotransmitters trigger internal signaling events through a cAMP-dependent pathway and a calcium-dependent pathway that ultimately result in increased CREB phosphorylation. Phosphorylated CREB increases levels of ΔFosB, which in turn represses the c-Fos gene with the help of corepressors; c-Fos repression acts as a molecular switch that enables the accumulation of ΔFosB in the neuron. A highly stable (phosphorylated) form of ΔFosB, one that persists in neurons for 1–2 months, slowly accumulates following repeated high-dose exposure to stimulants through this process. ΔFosB functions as "one of the master control 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.

Chronic addictive drug use causes alterations in gene expression in the mesocorticolimbic projection. The most important transcription factors that produce these alterations are ΔFosB, cAMP response element binding protein (CREB), and nuclear factor kappa B (NF-κB). ΔFosB is the most significant biomolecular mechanism in addiction because the overexpression of ΔFosB in the D1-type medium spiny neurons in the nucleus accumbens is necessary and sufficient for many of the neural adaptations and behavioral effects (e.g., expression-dependent increases in drug self-administration and reward sensitization) seen in drug addiction. ΔFosB expression in nucleus accumbens D1-type medium spiny neurons directly and positively regulates drug self-administration and reward sensitization through positive reinforcement while decreasing sensitivity to aversion. ΔFosB has been implicated in mediating addictions to many different drugs and drug classes, including alcohol, amphetamine and other substituted amphetamines, cannabinoids, cocaine, methylphenidate, nicotine, opiates, phenylcyclidine, and propofol, among others. ΔJunD, a transcription factor, and G9a, a histone methyltransferase, both oppose the function of ΔFosB and inhibit increases in its expression. Increases in nucleus accumbens ΔJunD expression (via viral vector-mediated gene transfer) or G9a expression (via pharmacological means) reduces, or with a large increase can even block, many of the neural and behavioral alterations that result from chronic high-dose use of addictive drugs (i.e., the alterations mediated by ΔFosB).

ΔFosB plays an important role in regulating behavioral responses to natural rewards, such as palatable food, sex, and exercise. Natural 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. Consequently, ΔFosB is the key transcription factor involved in addictions to natural rewards (i.e., behavioral addictions) as well; in particular, ΔFosB in the nucleus accumbens is critical for the reinforcing effects of sexual reward. Research on the interaction between natural and drug rewards suggests that dopaminergic psychostimulants (e.g., amphetamine) and sexual behavior act on similar biomolecular mechanisms to induce ΔFosB in the nucleus accumbens and possess bidirectional cross-sensitization effects that are mediated through ΔFosB. This phenomenon is notable since, in humans, a dopamine dysregulation syndrome, characterized by drug-induced compulsive engagement in natural rewards (specifically, sexual activity, shopping, and gambling), has been observed in some individuals taking dopaminergic medications.

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

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

GLP-1 receptor agonist medications such as semaglutide, developed for type 2 diabetes and obesity, have attracted interest as possible treatments for substance use disorders because they act on the brain's reward system and reduce reward-driven behavior. Large observational studies have associated their use with lower rates of alcohol- and opioid-related harm; however, the small number of completed randomized controlled trials has not yet confirmed a consistent benefit, and specialists currently describe these medications as promising but unproven for this indication.

Reward system

Main article: Reward system

Mesocorticolimbic pathway

ΔFosB accumulation from excessive drug use

Top: this depicts the initial effects of high dose exposure to an addictive drug on gene expression in the nucleus accumbens for various Fos family proteins (i.e., c-Fos, FosB, ΔFosB, Fra1, and Fra2).
Bottom: this illustrates the progressive increase in ΔFosB expression in the nucleus accumbens following repeated twice daily drug binges, where these phosphorylated (35–37 kilodalton) ΔFosB isoforms persist in the D1-type medium spiny neurons of the nucleus accumbens for up to 2 months.

Understanding the pathways in which drugs act and how drugs can alter those pathways is key when examining the biological basis of drug addiction. The reward pathway, known as the mesolimbic pathway, 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. The VTA supports learning and sensitization development and releases dopamine (DA) into the forebrain. These neurons project and release DA into the nucleus accumbens, through the mesolimbic pathway. Virtually all drugs causing drug addiction increase the DA release in the mesolimbic pathway.
• The nucleus accumbens (NAcc) is one output of the VTA projections. The nucleus accumbens itself consists mainly of GABAergic medium spiny neurons (MSNs). The NAcc is associated with acquiring and eliciting conditioned behaviors, and is involved in the increased sensitivity to drugs as addiction progresses. Overexpression of ΔFosB in the nucleus accumbens is a necessary common factor in essentially all known forms of addiction; ΔFosB is a strong positive modulator of positively reinforced behaviors.
• The prefrontal cortex, including the anterior cingulate and orbitofrontal cortices, is another VTA output in the mesocorticolimbic pathway; it is important for the integration of information, which helps determine whether a behavior will be elicited. It is critical for forming associations between the rewarding experience of drug use and cues in the environment. Importantly, these cues are strong mediators of drug-seeking behavior and can trigger relapse even after months or years of abstinence.

Other brain structures that are involved in addiction include:

• The basolateral amygdala projects into the NAcc and is thought to be important for motivation.
• The hippocampus is involved in drug addiction because of its role in learning and memory. Much of this evidence stems from research showing that manipulating cells in the hippocampus alters DA levels in NAcc and firing rates of VTA dopaminergic cells.

Role of dopamine and glutamate

Dopamine is the primary neurotransmitter of the reward system in the brain. It plays a role in regulating movement, emotion, cognition, motivation, and feelings of pleasure. 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. Nearly all addictive drugs, directly or indirectly, act on the brain's reward system by heightening dopaminergic activity.

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.

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.

Reward sensitization

Neural and behavioral effects of validated ΔFosB transcriptional targets in the striatum

Target gene	Target expression	Neural effects	Behavioral effects
c-Fos	↓	Molecular switch enabling the chronic induction of ΔFosB	–
dynorphin	↓	• Downregulation of κ-opioid feedback loop	• Increased drug reward
NF-κB	↑	• Expansion of NAcc dendritic processes  • NF-κB inflammatory response in the NAcc  • NF-κB inflammatory response in the CPTooltip caudate putamen	• Increased drug reward  • Locomotor sensitization
GluR2	↑	• Decreased sensitivity to glutamate	• Increased drug reward
Cdk5	↑	• GluR1 synaptic protein phosphorylation  • Expansion of NAcc dendritic processes	Decreased drug reward (net effect)

Reward sensitization is a process that causes an increase in the amount of reward (specifically, incentive salience) that is assigned by the brain to a rewarding stimulus (e.g., a drug). In simple terms, when reward sensitization to a specific stimulus (e.g., a drug) occurs, an individual's "wanting" or desire for the stimulus itself and its associated cues increases. Reward sensitization normally occurs following chronically high levels of exposure to the stimulus. ΔFosB expression in D1-type medium spiny neurons in the nucleus accumbens has been shown to directly and positively regulate reward sensitization involving drugs and natural rewards.

"Cue-induced wanting" or "cue-triggered wanting", a form of craving that occurs in addiction, is responsible for most of the compulsive behavior that people with addictions exhibit. 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). 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.

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 that is mediated through ΔFosB. 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.

Summary of addiction-related plasticity

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

Neuroepigenetic mechanisms

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. Addictive drugs are associated with three types of epigenetic modifications within neurons. 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. 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 – most other genes in the NAc cells do not show such changes.

Diagnosis

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

Classification

DSM-5

The fifth edition of the DSM uses the term substance use disorder to refer to a spectrum of drug use-related disorders. The DSM-5 eliminates the terms abuse and dependence from diagnostic categories, instead using the specifiers of mild, moderate, and severe to indicate the extent of disordered use. The number of diagnostic criteria present in a given case determines these specifiers. In the DSM-5, the term drug addiction is synonymous with severe substance use disorder.

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

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. 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.

ICD-11

The eleventh revision of the International Classification of Diseases, commonly referred to as ICD-11, conceptualizes diagnosis somewhat differently. ICD-11 first distinguishes between problems with psychoactive substance use ("Disorders due to substance use") and behavioral addictions ("Disorders due to addictive behaviours"). 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." 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.

Screening and assessment

Addictions Neuroclinical Assessment

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

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

This is a screening and assessment tool in one, assessing commonly used substances. This tool allows for a simple diagnosis, eliminating the need for several screening and assessment tools, as it includes both TAPS-1 and TAPS-2, screening and assessment tools, respectively. The screening component asks about the frequency of use of the specific substance (tobacco, alcohol, prescription medication, and other). If an individual screens positive, the second component will begin. This dictates the risk level of the substance.

CRAFFT

The CRAFFT (Car-Relax-Alone-Forget-Family and Friends-Trouble) is a screening tool that is used in medical centers. The CRAFFT is in version 2.1 and has a version for nicotine and tobacco use called the CRAFFT 2.1+N. 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. 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. After these tests are done, the clinician is to give the "5 RS" of brief counseling.

The five Rs of brief counseling include:

1. REVIEW screening results
2. RECOMMEND to not use
3. RIDING/DRIVING risk counseling
4. RESPONSE: elicit self-motivational statements
5. REINFORCE self-efficacy

Drug Abuse Screening Test (DAST-10)

The Drug Abuse Screening Test (DAST) is a self-reporting tool that measures problematic substance use. Responses to this test are recorded as yes or no answers, and scored as a number between zero and 28. Drug abuse or dependence is indicated by a cut off score of 6. Three versions of this screening tool are in use: DAST-28, DAST-20, and DAST-10. Each of these instruments is copyrighted by Dr. Harvey A. Skinner.

Alcohol, Smoking, and Substance Involvement Test (ASSIST)

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

Prevention

Main articles: Harm reduction and Preventive healthcare

Because many risk factors for addiction are social and modifiable, prevention strategies that target them can improve outcomes; when delivered during childhood and adolescence, such strategies reduce the risk of later substance use disorder.

Abuse liability

Abuse or addiction liability is the tendency to use drugs in a non-medical situation. This is typically for euphoria, mood changing, or sedation. 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 several 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 health (mental and physical) of the population being studied. There are a few drugs with a specific chemical makeup that lead 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.

Treatment

Main article: Treatment and management of addiction

Addiction is generally managed as a chronic, relapsing condition rather than something resolved in a single episode of care. The most effective treatment combines medication (where an effective one is available) with psychological and social support, emphasising long-term management and relapse prevention. To be effective, pharmacological or biologically based treatment needs to be accompanied by other interventions such as cognitive behavioral therapy (CBT) and dialectical behavioral therapy (DBT), individual and group psychotherapy, behavior modification strategies, twelve-step programs, and residential treatment facilities.

The medications available differ between substances. For opioid use disorder, opioid agonist maintenance treatment with methadone or buprenorphine is common. It retains people in treatment and suppresses illicit opioid use more effectively than no opioid replacement, and is associated with reduced mortality and lower transmission of blood-borne infections such as HIV and hepatitis C. The opioid antagonist naltrexone is an alternative for some patients. For alcohol use disorder, oral naltrexone and acamprosate are recommended as first-line medications alongside psychosocial support, whereas trial evidence that disulfiram reduces drinking is weaker. For tobacco (nicotine) dependence, varenicline, cytisine and nicotine e-cigarettes are among the most effective aids for quitting long-term, followed closely by using two forms of nicotine replacement therapy at once (for example a patch together with gum or a lozenge), bupropion is also used. No medication has been approved for cocaine or amphetamine (stimulant) use disorder, for which psychosocial treatment remains the principal care.

Psychological and behavioral therapies are used across all forms of addiction, both alone and together with medication; commonly used approaches include CBT, motivational interviewing, contingency management (which provides tangible rewards for verified abstinence), and twelve-step facilitation. For stimulant use disorder, contingency management (particularly when combined with a community reinforcement approach) has the strongest supporting evidence among psychosocial treatments. For alcohol use disorder, structured twelve-step facilitation programmes that encourage participation in Alcoholics Anonymous are at least as effective as other established therapies such as CBT for sustaining abstinence and may lower health-care costs. The transtheoretical model (TTM) can help determine when treatment should begin and which method is likely to be most effective, as beginning too early may make a person defensive and resistant to change.

Prognosis

Addiction is generally understood as a chronic, relapsing condition rather than one resolved in a single episode of care, and long-term outcomes vary widely. A systematic review and meta-analysis of long-term follow-up studies estimated that between 35% and 54% of people with a substance use disorder achieved remission (defined as no longer meeting diagnostic criteria for at least six months) but that this typically occurred only after a mean follow-up of around 17 years, with roughly 7–9% of cases remitting in any given year. Its authors concluded that for a substantial proportion of people the condition behaves more like a long-term than an acute disorder, and argued for treatment models designed around chronicity. Substance use disorders are treatable: there is evidence of clinically significant benefit for medications in opioid, nicotine and alcohol use disorders, for behavioural therapies across all substance use disorders, and for neuromodulation in nicotine use disorder.

Epidemiology

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.). The Global Burden of Disease Study estimated that in 2016 alcohol use disorders were the most prevalent substance use disorder worldwide, with about 100 million cases, followed by opioid dependence at about 27 million and cannabis dependence at about 22 million. In the same year, alcohol use as a risk factor accounted for an estimated 99.2 million disability-adjusted life years (DALYs), or 4.2% of the global total, and drug use for 31.8 million DALYs, or 1.3%. Alcohol-attributable burden was heaviest in countries with a low Socio-demographic Index, whereas drug-attributable burden increased with higher socio-demographic development. Between 2010 and 2023, drug use was one of only three risk factors worldwide whose age-standardised attributable DALY rate rose.

Asia

The prevalence of alcohol dependence is not as high as it is in other regions. In Asia, not only socioeconomic factors but also biological factors influence drinking behavior.

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%.

Australia

Further information: Alcoholism in rural Australia

The prevalence of substance use disorder among Australians was reported at 5.1% in 2009. 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. The survey found that in 2019, 11% of people over 14 years old smoke daily; that 9.9% of those who drink alcohol, which equates to 7.5% of the total population age 14 or older, may qualify as alcohol dependent; that 17.5% of the 2.4 million people who used cannabis in the last year may have hazardous use or a dependence problem; and that 63.5% of about 300,000 recent users of meth and amphetamines were at risk for developing problem use.

Europe

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. 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.

United States

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 of addictions to alcohol and illicit drugs has been estimated to be approximately 8% and 2–3%, respectively. 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. The lifetime prevalence of prescription drug addictions is around 4.7%.

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%). 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. 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. Despite 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 address a drug addiction effectively.

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. 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.

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.

The National Epidemiologic Survey on Alcohol and Related Conditions found that from 2012 to 2013, the prevalence of Cannabis use disorder in US adults was 2.9%.

Canada

A Statistics Canada Survey in 2012 found the lifetime prevalence and 12-month prevalence of substance use disorders were 21.6% and 4.4% in those 15 and older. Alcohol abuse or dependence reported a lifetime prevalence of 18.1% and a 12-month prevalence of 3.2%. Cannabis abuse or dependence reported a lifetime prevalence of 6.8% and a 12-month prevalence of 3.2%. Other drug abuse or dependence has a lifetime prevalence of 4.0% and a 12-month prevalence of 0.7%. Substance use disorder is a term used interchangeably with a drug addiction.

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. Prevalence of care needed increased the most among the 14–17 age group overall.

South America

The realities of opioid use and opioid use disorder in Latin America may be deceptive if observations are limited to epidemiological findings. In the United Nations Office on Drugs and Crime report, 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.

Etymology

The word addiction derives from the Latin "addico", meaning "giving over" with both positive connotations (devotion, dedication) and negative ones (being enslaved to a creditor in Roman law). This dual meaning persisted in traditional English dictionaries, encompassing both legal surrender and personal devotion to habits. Later, the 19th century temperance movements narrowed the definition of addiction to just drug-related disease, ignoring behavioral addictions and the possibility of positive or neutral addictions. This restrictive view opposes the current understanding of addiction.

Addiction and addictive behavior are polysemes denoting a category of mental disorders, of neuropsychological symptoms, or of merely maladaptive/harmful habits and lifestyles. A common use of the term addiction in medicine is for neuropsychological symptoms denoting pervasive/excessive and intense urges to engage in a category of behavioral compulsions or impulses towards sensory rewards (e.g., alcohol, betel quid, drugs, sex, gambling, video gaming). 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); the two categories of such disorders are substance-use addictions and behavioral addictions.

The etymology of the term addiction throughout history has been misunderstood and has taken on various meanings associated with the word. An example is the usage of the word in the religious landscape of early modern Europe. "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". The meaning of addiction during the early modern period was mostly associated with positivity and goodness; during this early modern and highly religious era of Christian revivalism and Pietistic tendencies, it was seen as a way of "devoting oneself to another".

The suffixes "-holic" and "-holism"

In contemporary 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 "alcohol" plus the suffix "-ism") by misdividing or rebracketing it into "alco" and "-holism". Terms formed this way, such as chocoholic and workaholic, are colloquial rather than diagnostic; the only behavioural addictions recognised in current diagnostic manuals are gambling disorder and gaming disorder.

History

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. 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. 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.

Addiction and art

The creative arts therapies (including art therapy, music therapy, drama and dance) are sometimes used as complementary treatments for substance use disorders, generally alongside conventional therapy. Artwork produced during treatment has also been used as an informal aid to assessment and to tracking progress. Proposed benefits include offering a non-verbal outlet for difficult emotions, containing shame, and strengthening self-awareness and engagement in treatment. However, a 2018 systematic review found insufficient evidence to confirm that visual art, drama, or dance and movement therapies reduce substance misuse, although music therapy showed some promise in preparing people for treatment.

The arts are used in advocacy and public education about addiction. Artists (particularly those with lived experience of addiction and recovery) use their work to reduce stigma and to reframe addiction as a treatable health condition rather than a moral failing, an approach intended to promote public compassion and shift responses from the criminal-justice system toward the public-health system.

Social scientific models

Acute confusional state caused by alcohol withdrawal, otherwise known as delirium tremens

Biopsychosocial model

While regarded biomedically as a neuropsychological disorder, addiction is multi-layered, with biological, psychological, social, cultural, and spiritual (biopsychosocial–cultural–spiritual) elements. A biopsychosocial–cultural–spiritual approach fosters the crossing of disciplinary boundaries, and promotes holistic considerations of addiction. 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.

Biological factors

Biological contributions include inherited risk and drug-induced neuroadaptation in the brain's reward, stress and executive-control circuits. Twin and adoption studies estimate the heritability of alcohol use disorder at approximately 50%, with modest shared-environmental effects also contributing to familial aggregation. This genetic risk is polygenic rather than attributable to any single gene. Persistent substance exposure produces long-term changes in the mesolimbic dopamine system. This includes altered activity in the ventral tegmental area and nucleus accumbens, which contribute to things like incentive salience, craving, and compulsive drug-seeking behavior. These biological factors contribute to things like the initial vulnerability and the development of drug-seeking behaviors. It does this by altering factors like reward sensitivity, stress reactivity, and executive control systems. These adaptations, specifically those impacting the dopaminergic responsivity and prefrontal regulation, interact with psychological traits and social experiences. Examples are interacting with impulsivity, coping style, or chronic stress exposure. Together, these interactions increase the motivational value of drug cues. It also increases the chance that dopaminergic activity will drive compulsive use. This makes biology just one component of a broader system that shapes addiction.

Psychological factors

Psychological contributions include learning and conditioning processes, impulsivity, reward sensitivity, and the use of substances to cope with negative mood or trauma. Conditioning models hold that environmental cues can acquire motivational significance of their own and trigger craving and relapse even after long periods of abstinence. Reviews of alcohol use disorder identify overvaluation of the drug's reinforcing effects, elevated impulsivity across several dimensions, the acute effects of stress and environmental triggers, and a lack of alternative rewarding activities as well-established psychological determinants. Psychological factors primarily shape how people perceive, react to, and regulate internal states. This shows how these factors influence the use of substances as coping strategies or sources of reinforcement. These processes interact with vulnerabilities in both biological and social contexts by making each one strengthen the other. Biological sensitivities make a person more strongly react to social challenges. These social challenges repeatedly activate and increase biological sensitivity. A cycle is created where both types of vulnerabilities keep reinforcing each other. These include: impaired inhibitory control, heightened reward drive, stress, and trauma. These interactions determine whether substance use will evolve into damaging patterns (compulsive drug seeking behaviors, loss of control of drug use, reliance on substance for coping) that are characteristic of addiction.

Social and environmental factors

Social and environmental influences include family dynamics, early and adverse experiences, socioeconomic status, peer networks, and cultural norms. Adverse childhood exposures and maladaptive developmental trajectories are robust environmental influences on the development of alcohol use disorder, and adverse childhood experiences are recognised more generally as a social determinant of vulnerability to substance use disorders. Social networks exert a bidirectional influence, while wider sociocultural factors — including public-health control policies and the social determinants of health — shape both exposure and outcome. Because social risk factors are modifiable, prevention that targets them in childhood and adolescence can reduce the risk of later disorder. Together, these levels of analysis highlight addiction as a complex and dynamic condition emerging from the interaction of several aspects including: neurobiological processes, individual psychological traits, and broader social environments. This model is widely used in contemporary clinical practice and public health because it accounts for a lot of variability in addiction trajectories, relapse patterns, and treatment outcomes across several individuals. Social factors exhibit their greatest influence on things like exposure to substances, motivation, and the probability of a potential escalation or relapse. Social factors act through mechanisms like chronic stress, peer modeling, socioeconomic constraints, and the availability of substances. Social factors act through mediums like chronic stress, which dysregulates the HPA axis and sensitizes neural circuits involved in threat detection. Substance availability can increase the chance of repeated exposure and reinforcement. This will strengthen habit circuits and lower the threshold for dependence on the substance. Environmental pressures interact with biological predispositions and psychological coping mechanisms to show that addictive behavior will emerge from the combined effects of social context, brain function, and individual psychological processes.

Cultural model

The cultural model, an anthropological understanding of the emergence of drug use and abuse, was developed by Dwight Heath. Heath undertook ethnographic research and fieldwork with the Camba people of Bolivia from June 1956 to August 1957. Heath observed that adult members of society drank 'large quantities of rum and became intoxicated for several contiguous days at least twice a month'. This frequent, heavy drinking from which intoxication followed was typically undertaken socially, during festivals. 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'. 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. 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.

As noted by Merrill Singer, Heath's findings, when considered alongside subsequent cross-cultural experiences, challenged the perception that intoxication is socially 'inherently disruptive'. Following this fieldwork, Heath proposed the 'cultural model', suggesting that 'problems' associated with heavy drinking, such as alcoholism – a recognised form of 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'.

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

Subcultural model

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

The approach evolved from the ethnographic exploration into the lived experiences and subjectivities of 1960s and 70s drug subcultures. 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 detail, providing insight into the dynamic social worlds and activities that surrounded their drug use. These findings challenge popular narratives of immorality and deviance, conceptualizing substance abuse as a social phenomenon. The prevailing culture can influence drug-taking behaviors, along with the physical and psychological effects of the drug. To marginalized individuals, drug subcultures can provide social connection, symbolic meaning, and socially constructed purpose that they may feel is unattainable through conventional means. 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.

Critical medical anthropology model

Emerging in the early 1980s, the critical medical anthropology model was introduced, and as Merrill Singer offers 'was applied quickly to the analysis of drug use'. 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.

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)

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. 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. From the perspective of critical medical anthropology, heavy drug use and addiction are consequences of such larger-scale unequal distributions of power.

Social learning models

Social learning theory

Main article: Social learning theory

Social learning theory, as originally proposed by Albert Bandura, holds that behaviour is shaped by the reciprocal relationships between personal factors, the external environment, and the behaviour itself (a principle known as reciprocal determinism). Applied to addiction, this frames drug use as arising from the interaction between an individual's personal characteristics, their social environment, and drug-related behaviour itself, and characterises addiction as a chronically evolving biopsychosocial disorder. On this account, effective treatment should target every node of the model and the relationships between them, rather than any single factor in isolation.

Transtheoretical model (stages of change model)

Main article: Transtheoretical model

he transtheoretical model describes behaviour change as a stepwise progression through a series of stages (precontemplation, contemplation, preparation, action and maintenance) through which people commonly move back and forth rather than in a single linear sequence, with relapse treated as an expected part of the process rather than a failure. In addiction treatment the model is used to gauge a person's readiness to change and to time intervention accordingly, since beginning too early may make a person defensive and resistant to change.

Addiction causes an "astoundingly high financial and human toll" on individuals and society as a whole. 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. The US National Institute on Drug Abuse has found that overdose deaths in the US have almost tripled among males and females from 2002 to 2017, with 72,306 overdose deaths reported in 2017 in the US. 2020 marked the year with the highest number of overdose deaths over a 12-month period, with 81,000 overdose deaths, exceeding the records set in 2017.

Research directions

Vaccines intended to reduce the effects of addictive drugs have been investigated since the early 2000s. The approach conjugates the drug molecule to a carrier protein so that the immune system produces antibodies that bind the drug in the bloodstream, reducing the amount that reaches the brain. Candidates have been tested against nicotine, cocaine, opioids and fentanyl.

No such vaccine is licensed for use in any country. A Cochrane review found no evidence that nicotine vaccines improve long-term smoking cessation, and two phase III trials of NicVAX reported quit rates of approximately 11% in both the vaccine and the placebo groups. Anti-cocaine vaccine development has likewise not produced an approved product, and no pharmacological treatment for cocaine dependence is currently approved.

See also

• Autonomic nervous system
• Binge drinking
• Binge eating disorder
• Cognitive liberty
• Darwinian hedonism
• Discrimination against drug addicts
• Dopaminergic pathways
• Pavlovian-instrumental transfer
• Philosophy of medicine
• Substance dependence

Notes

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Further reading

• 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.
• Courtwright DT (2019). The Age of Addiction: How Bad Habits Became Big Business. Cambridge, Massachusetts: Harvard University Press. ISBN 978-0-674-24822-9.

External links

• "The Science of Addiction: Genetics and the Brain". learn.genetics.utah.edu. Learn.Genetics – University of Utah.
• Why do our brains get addicted? – a TEDMED 2014 talk by Nora Volkow, the director of the National Institute on Drug Abuse at NIH.

Kyoto Encyclopedia of Genes and Genomes (KEGG) signal transduction pathways:

• KEGG – human alcohol addiction
• KEGG – human amphetamine addiction
• KEGG – human cocaine addiction