Addiction
| 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.[a][2][1] It is therefore understood as a brain disorder arising from a complex mix of psychosocial and neurobiological factors.[3][4][2] A number of researchers argue that this framing is incomplete, and that addiction is better understood as learned behavior shaped by choice and social context.[5][6]
Addiction takes both substance and non-substance forms. Substance addictions include alcoholism, cannabis addiction, amphetamine addiction, cocaine addiction, nicotine addiction and opioid 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,[7] while the ICD-11 additionally classifies gaming disorder as a disorder due to addictive behaviors.[8] Other candidate behavioral addictions, and the question of whether food can be addictive, are debated in the research literature but are not recognized in either manual.[9][10] Across these forms, addiction is defined less by any single symptom than by a pattern: impaired control over the substance or behavior, increasing priority given to it over other activities, and continued use despite harm, accompanied for many substances by tolerance and withdrawal.[7][2] It carries a substantial risk of further illness and early death, most immediately from overdose, and co-occurring psychiatric conditions are common.[2]
Genetic and environmental factors each account for roughly half of an individual's risk of developing an addiction.[3] Genetic vulnerability is polygenic, reflecting the small combined effects of many common variants rather than any single gene.[11][12] Environmental contributors include adverse childhood experiences, chronic stress, family and peer influences, socioeconomic constraint and the availability of substances, and adolescence is a period of heightened vulnerability.[2] At the level of mechanism, addiction is described as a recurring cycle in which dopaminergic signalling gives a drug and its associated cues a strong pull on attention and behavior, brain stress systems become overactive as ordinary pleasures are muted, and reduced prefrontal cortex control leaves craving poorly restrained.[2][13]
Addiction is diagnosed clinically. The DSM-5-TR grades substance use disorder as mild, moderate or severe and treats severe substance use disorder as synonymous with drug addiction.[14] The ICD-11 instead distinguishes a harmful episode of use, a harmful pattern of use, and dependence.[15] Prevention approaches with the strongest supporting evidence include family skills programs, school-based personal and social skills education, and policies that limit availability and raise price.[16] Addiction is managed as a chronic, relapsing condition, usually combining medication, where an effective one exists, with psychological and social support. Effective medications are available for opioid, alcohol and tobacco use disorders,[17][18][19] but none is approved for stimulant use disorder, for which psychosocial treatment remains the mainstay.[20] Harm reduction measures address the damage associated with continued use.[17] Outcomes vary widely: an estimated 35–54% of people with a substance use disorder reach remission, though typically only after many years.[21] The Global Burden of Disease Study estimated around 100 million cases of alcohol use disorder worldwide in 2016, followed by opioid and cannabis dependence,[22] and drug use was one of only three risk factors whose age-standardized attributable burden rose between 2010 and 2023.[23] Addiction carries substantial economic and social costs,[24][25] and anthropological and structural accounts situate heavy drug use within cultural norms and unequal distributions of power.[26]
Signs and symptoms
[edit source]Addiction is defined less by any single symptom and more by a pattern, including impaired control over the substance or behavior, increasing priority given to it over other activities, and continued use despite harm. Impaired control appears as using more or for longer than intended, persistent unsuccessful attempts to cut down, and a great deal of time spent obtaining, using or recovering. Social impairment follows, with failure to meet obligations at work, school or home, and the abandonment of former activities. Risky use (continuing despite knowledge of physical or psychological harm) and, for many substances, tolerance and withdrawal, complete the picture.[7][2] Specific physical and behavioral signs vary widely by substance and are covered in the articles on individual substance use disorders.
Complications
[edit source]
Addiction carries a substantial risk of further illness and of early death. The most immediate danger is overdose, which for opioids and other sedatives acts by suppressing breathing. Injecting drug use also carries a risk of blood-borne infection, including HIV and hepatitis C.[2] Long-term use damages particular organ systems depending on the substance, with liver cirrhosis and cognitive impairment following sustained heavy drinking and lung disease following tobacco smoking.[24]
Psychiatric conditions frequently co-occur with addiction, and each worsens the outlook for the other, so current guidance is that both be treated at the same time rather than one after the other.[2] Loss of pleasure in ordinary activities (anhedonia) is common and is associated with mood disorders.[27] Globally, alcohol use accounted for an estimated 99.2 million disability-adjusted life years in 2016 and drug use for 31.8 million.[22]
Types
[edit source]Substance use disorder
[edit source]| Addiction and dependence glossary[3][28][29] | |
|---|---|
| |
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.[30]
Substance use disorder is one of the substance-related disorders. It is a long-term, relapsing condition in which a person continues seeking and taking a substance despite the harm it causes.[2] Repeated use alters the brain circuits that handle reward, stress and self-control, which is why cutting down becomes harder over time.[2] The substances most often involved are alcohol, nicotine, cannabis, opioids, cocaine and amphetamines.[2] Use may begin socially,[31] or follow from a prescribed medication.[2] No single theory accounts for substance use disorder on its own. Phenomenological, operant and classical conditioning, cognitive, and cue reactivity models each explain part of it.[32]
Behavioral addiction
[edit source]The term behavioral addiction refers to a compulsion to engage in a natural reward despite adverse consequences.[33][34]
Addiction can exist without psychotropic drugs, an idea that was popularized by psychologist Stanton Peele.[35] These are termed behavioral addictions. Such addictions may be passive or active, but they commonly contain reinforcing features, which are found in most addictions.[35] Sexual behavior, eating, gambling, playing video games, and shopping are all associated with compulsive behaviors in humans and have been shown to activate the mesolimbic pathway and other parts of the reward system.[34] Diagnostic manuals recognize only some of these as disorders. Gambling disorder is the only behavioral addiction classified as a clinical disorder in the DSM-5-TR, which lists internet gaming disorder as a condition requiring further study; the ICD-11 classifies both gambling disorder and gaming disorder as disorders due to addictive behaviors.[9] Compulsive sexual behavior disorder, compulsive buying–shopping disorder and problematic use of social media are discussed in the research literature as candidate addictive disorders, but are not currently classified as addictions in either manual.[9]
Food addiction
[edit source]Whether food can be addictive is disputed. Neither the DSM-5-TR nor the ICD-11 recognises a food or eating addiction, and researchers disagree about whether the concept is best framed as an addiction to specific foods, a pattern of disordered eating, or neither.[10] Proponents argue that ultra-processed foods high in refined carbohydrate and fat meet the criteria conventionally used to identify an addictive substance, because processing delivers these nutrients faster and in higher concentrations than they occur in nature.[36] Critics respond that no single constituent has been isolated as the addictive agent, unlike the case for a drug.[10] Most research uses the Yale Food Addiction Scale, which applies the DSM-5 criteria for substance use disorder to eating.[36] Food addiction as measured this way overlaps with, but is not the same as, binge eating disorder: not everyone with an eating disorder screens positive, and not everyone screening positive has a diagnosed eating disorder.[37]
Causes
[edit source]Several genetic and environmental risk factors exist for developing an addiction.[3][38] Genetic and environmental risk factors each account for roughly half of an individual's risk for developing an addiction;[3] the contribution from epigenetic risk factors to the total risk is unknown.[38] Even in individuals with a relatively low genetic risk, exposure to sufficiently high doses of an addictive drug for a long period of time (e.g., weeks–months) can result in an addiction.[3] Adverse childhood events are associated with negative health outcomes, such as substance use disorder. Childhood abuse or exposure to violent crime is related to developing a mood or anxiety disorder, as well as a risk of substance dependence.[39]
While regarded biomedically as a neuropsychological disorder, addiction is multi-layered, with biological, psychological, social, cultural, and spiritual (biopsychosocial–cultural–spiritual) elements.[40] A biopsychosocial–cultural–spiritual approach fosters the crossing of disciplinary boundaries, and promotes holistic considerations of addiction.[41]
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.[42]
Genetic factors
[edit source]Genetic factors, along with socio-environmental (e.g., psychosocial) factors, have been established as significant contributors to addiction vulnerability.[3][38][43][37] Addiction is substantially heritable. Twin and adoption studies estimate the heritability of alcohol use disorder at approximately 50%,[44] with comparable estimates across other substances.[12] This risk is polygenic: it reflects the combined small effects of many common variants rather than any single gene.[11][12]
Genome-wide association studies (GWAS) are used to examine genetic associations with dependence, addiction, and drug use,[43] and have begun to map this architecture, and distinguish loci associated with a broad general liability to addiction across substances from loci conferring risk for a specific drug.[12][43] 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.[45] Individual common variants each contribute only a small increment of risk, so genetic vulnerability is best understood as an aggregate rather than as the effect of any identified gene.[12]
Environmental factors
[edit source]Environmental risk factors for addiction are the experiences of an individual during their lifetime that interact with the individual's genetic composition to increase or decrease his or her vulnerability to addiction.[3] For example, after the nationwide outbreak of COVID-19 in China, more people quit (vs. started) smoking. People who smoke, on average, reduced the quantity of cigarettes they consumed.[46] 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.[47][31] 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.[48] Many researchers, including neuroscientists, indicate that the brain disease model presents a misleading, incomplete, and potentially detrimental explanation of addiction.[6]
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.[49] 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.[50] 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.[50][31][49] Many children who experience abuse go on to develop an addiction in adolescence or adult life.[51] 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.[51]
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,[11] and adverse childhood experiences are recognised more generally as a social determinant of vulnerability to substance use disorders.[2] 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.[11] Because social risk factors are modifiable, prevention that targets them in childhood and adolescence can reduce the risk of later disorder.[2] Together, these levels of analysis present addiction as a dynamic condition emerging from the interaction of neurobiological processes, individual psychological traits and broader social environments.[2][11] Social factors act largely through chronic stress, peer modelling, socioeconomic constraint and the availability of substances, influencing both the likelihood of exposure and the risk of escalation or relapse.[2][11]
Stress and addiction
[edit source]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.[52] 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.[52]
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.[53][52] 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.[53][52]
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.[53][52] 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.[53][52]
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.[52]
Social control theory
[edit source]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.[54]
Developmental stage
[edit source]Adolescence represents a period of increased vulnerability to developing an addiction.[55] 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.[56] 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.[57][58]
Most individuals are exposed to and use addictive drugs for the first time during their teenage years.[59] In the United States, there were just over 2.8 million new users of illicit drugs in 2013 (7,800 new users per day);[59] among them, 54.1% were under 18 years of age.[59]
Adolescence is a critical developmental period in which the prefrontal cortex (responsible for planning, inhibitory control, and evaluating long-term consequences) experiences significant maturation.[60][61] 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.[62]
Neuroimaging studies show that adolescents exhibit reduced prefrontal cortex activation during decision-making tasks, risk-taking behavior, and heightened dopamine reactivity compared with adults.[62] 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.[63]
Comorbid disorders
[edit source]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.[64][65][66][31] The NIDA cites early aggressive behavior as a risk factor for substance use.[47] 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.[2]
Psychological theories
[edit source]Psychological contributions include learning and conditioning processes, impulsivity, reward sensitivity, and the use of substances to cope with negative mood or trauma.[11] Conditioning models hold that environmental cues can acquire motivational significance of their own and trigger craving and relapse even after long periods of abstinence.[67][11] 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.[11] 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 biological and social vulnerabilities, each reinforcing the others.[11] 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.[67] 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.[67]
Personality theories
[edit source]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.[68] 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.[69][70][71][72][73]
Social learning theory
[edit source]Social learning theory, as originally proposed by Albert Bandura, holds that behavior is shaped by the reciprocal relationships between personal factors, the external environment, and the behavior itself (a principle known as reciprocal determinism).[74] Applied to addiction, this frames drug use as arising from the interaction between an individual's personal characteristics, their social environment, and drug-related behavior itself, and characterizes addiction as a chronically evolving biopsychosocial disorder.[74] On this account, effective treatment should target every node of the model and the relationships between them, rather than any single factor in isolation.[74]
Evolutionary perspectives
[edit source]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.[75] 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.[76][77] These perspectives do not replace proximate neurobiological models, but aim instead to situate contemporary patterns of vulnerability within a broader evolutionary framework.[78]
Mechanisms
[edit source]Addiction develops when repeated exposure to a rewarding stimulus produces lasting changes in the brain circuits that govern reward, stress and self-control. Current accounts describe this as a recurring three-stage cycle. During binge/intoxication, dopaminergic signalling in the basal ganglia gives the drug and the cues surrounding it a powerful pull on attention and behavior. During withdrawal/negative affect, brain stress systems in the extended amygdala become overactive and ordinary pleasures become muted, so that use is increasingly driven by relief rather than reward. During preoccupation/anticipation, reduced prefrontal cortex control over these systems leaves craving poorly restrained and makes relapse more likely.[2] Each stage is associated with persistent changes in gene expression and synaptic plasticity within the affected circuits.[2] Due to the causal relationship between ΔFosB expression and addictions, it is used preclinically as an addiction biomarker.[3] ΔFosB expression in these neurons directly and positively regulates drug self-administration and reward sensitization through positive reinforcement, while decreasing sensitivity to aversion.[note 1][3][79]
Reward circuitry
[edit source]The reinforcing effects of most addictive drugs depend on dopamine signalling in the nucleus accumbens, the same pathway that responds to natural rewards such as food and sex.[13] Altered dopamine neurotransmission is frequently observed following the development of an addictive state.[34] In people and in animals that have developed an addiction, altered dopamine or opioid neurotransmission is evident in the nucleus accumbens and elsewhere in the striatum.[34][13]
Cognitive and stimulus control
[edit source]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.[80] Cognitive control, and particularly inhibitory control over behavior, is impaired in both addiction and attention deficit hyperactivity disorder.[81][82] 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.[82]
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.[49]
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.[83][84] Cognitive functions such as learning, memory, and impulse control, are affected by drugs.[83] These effects promote drug use, as well as hinder the ability to abstain from it.[83] The increase in dopamine release is prominent in drug use, specifically in the ventral striatum and the nucleus accumbens.[83] 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.[83][84] This promotes the development of a maladaptive drug to stimulus relationship.[85] Early drug use leads to these maladaptive associations, later affecting cognitive processes used for coping, which are needed to abstain from them successfully.[83][49]
Mesocorticolimbic pathway
[edit source]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.[86] |
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,[84] or its extension, the mesocorticolimbic pathway, is characterized by the interaction of several areas of the brain.[2]
- Dopaminergic neurons in the ventral tegmental area (VTA) fire in response to cues that predict a reward, and project to the nucleus accumbens through the mesolimbic pathway. Nearly all addictive drugs increase dopamine release along this pathway, although they act on it by different routes.[13]
- The nucleus accumbens, made up largely of GABAergic medium spiny neurons, is a principal target of these projections. It is involved in learning conditioned responses to drug-associated cues, and in the growing sensitivity to those cues as addiction progresses.[13]
- The prefrontal cortex, including the anterior cingulate and orbitofrontal cortices, is a further target of the mesocorticolimbic pathway. It weighs competing information in determining whether a behavior is carried out, and forms the associations between drug reward and environmental cues that give those cues their power.[13] Importantly, these cues are strong mediators of drug-seeking behavior and can trigger relapse even after months or years of abstinence.[87][84]
Other brain structures that are involved in addiction include:
- The hippocampus contributes through its role in learning and memory, and influences activity in the same dopamine pathway.[13]
Role of dopamine and glutamate
[edit source]Dopamine is the primary neurotransmitter of the brain's reward system, and also has roles in movement, emotion, cognition and motivation. Natural rewards such as eating, and recreational drug use, both trigger dopamine release, which underlies their reinforcing quality.[13]
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.[13]
Drug seeking is driven by glutamatergic projections from the prefrontal cortex to the nucleus accumbens, and chronic drug exposure produces lasting glutamate-mediated changes along this route.[13]
Neuroadaptation and sensitization
[edit source]Reward sensitization is a process that causes an increase in the amount of reward (specifically, incentive salience[note 2]) 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.[89][88][90] Reward sensitization normally occurs following chronically high levels of exposure to the stimulus.[84]
"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.[88][90] 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).[88][91][90] 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.[88][91][90]
In contrast to ΔFosB's reward-sensitizing effect, CREB transcriptional activity decreases user's sensitivity to the rewarding effects of the substance. CREB transcription in the nucleus accumbens is implicated in psychological dependence and symptoms involving a lack of pleasure or motivation during drug withdrawal.[3][86][92]
Molecular and epigenetic mechanisms
[edit source]Epigenetics is the study of stable phenotypic changes that do not involve alterations in the DNA sequence.[93] Illicit drug use has been found to cause epigenetic changes in DNA methylation, as well as chromatin remodeling.[94] The epigenetic state of chromatin may pose a risk for the development of substance addictions.[94] 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.[94] This change may predispose one to experience a positive response to drug use.[94]
Altered epigenetic regulation of gene expression within the brain's reward system plays a significant and complex role in the development of drug addiction.[95][96] Addictive drugs are associated with three types of epigenetic modifications within neurons.[95] 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.[95][96] 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[96] – most other genes in the NAc cells do not show such changes.[95]
Transgenerational
[edit source]Epigenetic genes and their products (e.g., proteins) are the key components through which environmental influences can affect the genes of an individual:[38] 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).[38] In addiction, epigenetic mechanisms play a central role in the pathophysiology of the disease;[3] it has been noted that some of the alterations to the epigenome which arise through chronic exposure to addictive stimuli during an addiction can be transmitted across generations, in turn affecting the behavior of one's children (e.g., the child's behavioral responses to addictive drugs and natural rewards).[38][97]
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.[38] 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.[38][97] Based on preclinical evidence from animal research, certain addiction-induced epigenetic alterations in rats can be transmitted from parent to offspring and produce behavioral phenotypes that decrease the offspring's risk of developing an addiction.[note 3][38] 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.[38][97]
Diagnosis
[edit source]Diagnostic criteria
[edit source]DSM-5
[edit source]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.[14][29]
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.[98] Internet gaming disorder is listed as a "condition requiring further study" in the DSM-5.[99]
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.[100] Tolerance is the process of the body adapting to a substance so that larger amounts are needed for the same effect. Withdrawal describes the physical and psychological symptoms that appear when a substance the body has adapted to is reduced or stopped. Which symptoms occur, and how dangerous they are, depends heavily on the substance: withdrawal from alcohol or benzodiazepines can be life-threatening, whereas withdrawal from most other substances is distressing but not usually dangerous.[2]
Medical researchers who actively study addiction have criticized the DSM classification of addiction for being flawed and involving arbitrary diagnostic criteria.[101]
ICD-11
[edit source]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").[8] 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."[15] 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.[15]
Screening and assessment
[edit source]Screening instruments are used to identify people who may have a substance use problem and to gauge its severity, usually before a full diagnostic assessment. The World Health Organization's ASSIST covers lifetime and recent use, craving, and use-related problems across substance classes;[102] the TAPS tool combines screening and assessment in one instrument;[103] and the CRAFFT is designed for adolescents and includes items on substance-related driving risk.[104] The DAST is a self-report measure of problematic drug use.[105] Distinct from these, the Addictions Neuroclinical Assessment is a research framework that profiles people across three domains (executive function, incentive salience and negative emotionality) rather than a clinical screening questionnaire.[106]
Prevention
[edit source]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.[2] Prevention is usually organized in three tiers: universal programs aimed at a whole population, selective programs aimed at groups at raised risk, and indicated programs aimed at individuals already showing early signs of problem use.[16] Interventions with the strongest evidence include family skills programs, personal and social skills education delivered in schools, and policies that limit availability and raise the price of alcohol and tobacco. Programs based on information provision alone, or on fear-based messaging, have not been found effective and may be counterproductive.[16]
Management
[edit source]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.[107] 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.[108][31]
Pharmacological
[edit source]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.[17] 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.[18] 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.[19] No medication has been approved for cocaine or amphetamine (stimulant) use disorder, for which psychosocial treatment remains the principal care.[20]
Psychological and behavioral
[edit source]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.[20][109] For stimulant use disorder, contingency management (particularly when combined with a community reinforcement approach) has the strongest supporting evidence among psychosocial treatments.[20] 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.[109] 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.[49][110]
Transtheoretical model (stages of change model)
[edit source]The transtheoretical model describes behavior 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.[49] 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.[49]
Harm reduction
[edit source]Harm reduction covers measures that reduce the damage associated with continued substance use rather than requiring abstinence. Approaches include needle and syringe programmes, naloxone distribution to reverse opioid overdose, drug checking, and supervised consumption facilities. Opioid agonist maintenance treatment also functions as harm reduction: independently of whether use stops, it is associated with reduced mortality and lower transmission of blood-borne infections.[17][medical citation needed]
Prognosis
[edit source]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.[2] 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.[21] 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.[21] Substance use disorders are treatable: there is evidence of clinically significant benefit for medications in opioid, nicotine and alcohol use disorders, for behavioral therapies across all substance use disorders, and for neuromodulation in nicotine use disorder.[2]
Epidemiology
[edit source]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.).[38] 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.[22] 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%.[22] Alcohol-attributable burden was heaviest in countries with a low Socio-demographic Index, whereas drug-attributable burden increased with higher socio-demographic development.[22] Between 2010 and 2023, drug use was one of only three risk factors worldwide whose age-standardised attributable DALY rate rose.[23]
Regional variation
[edit source]Patterns differ markedly by region. Alcohol-attributable burden falls most heavily on countries with a low Socio-demographic Index, whereas drug-attributable burden rises with higher socio-demographic development.[22] In Europe, mortality from alcohol and illicit drugs is highest in the east of the continent, and first alcohol use before age 13 was reported for 28% of European children in 2014.[31] Alcohol dependence is less prevalent across much of Asia than in Western countries, reflecting both socioeconomic and biological differences in drinking behavior.[111] In Latin America, heroin consumption is low in most countries despite regional opium production, with the highest incidence in Mexico.[112]
History
[edit source]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.[113] 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.[114] Today, addiction is understood both as a biopsychosocial and neurological disorder that negatively impacts those who are affected by it, most commonly associated with the use of drugs and excessive use of alcohol.[4]
Terminology
[edit source]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.[115]
Addiction and addictive behavior are polysemes denoting a category of mental disorders, of neuropsychological symptoms, or of merely maladaptive/harmful habits and lifestyles.[116] 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).[117][118][119][8] 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.[27][116][119][8]
The etymology of the term addiction throughout history has been misunderstood and has taken on various meanings associated with the word.[120] An example is the usage of the word in the religious landscape of early modern Europe.[121] "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".[122] The meaning of addiction during the early modern period was mostly associated with positivity and goodness;[121] during this early modern and highly religious era of Christian revivalism and Pietistic tendencies,[121] it was seen as a way of "devoting oneself to another".[122]
The suffixes "-holic" and "-holism"
[edit source]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 behavioral addictions recognised in current diagnostic manuals are gambling disorder and gaming disorder.[7][8]
Society and culture
[edit source]Economic and social cost
[edit source]Addiction causes an "astoundingly high financial and human toll" on individuals and society as a whole.[24][25][123] In the United States, the total economic cost to society is greater than that of all types of diabetes and all cancers combined.[123] 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.[24][25][123][124] 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.[125] 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.[126]
Structural and political accounts
[edit source]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'.[26] 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.[26]
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)[26]
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.[26] 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.[26] From the perspective of critical medical anthropology, heavy drug use and addiction are consequences of such larger-scale unequal distributions of power.[26]
Cultural and anthropological accounts
[edit source]Cultural model
[edit source]The cultural model, an anthropological understanding of the emergence of drug use and abuse, was developed by Dwight Heath.[26] Heath undertook ethnographic research and fieldwork with the Camba people of Bolivia from June 1956 to August 1957.[127] Heath observed that adult members of society drank 'large quantities of rum and became intoxicated for several contiguous days at least twice a month'.[26] This frequent, heavy drinking from which intoxication followed was typically undertaken socially, during festivals.[127] 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'.[128] 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.[127] 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.[26]
As noted by Merrill Singer, Heath's findings, when considered alongside subsequent cross-cultural experiences, challenged the perception that intoxication is socially 'inherently disruptive'.[26] 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'.[127][26]
The cultural model did face criticism by Sociologist Robin Room and others, who felt anthropologists could "downgrade the severity of the problem".[26] 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'.[26]
Subcultural model
[edit source]Historically, addiction has been viewed from the etic perspective, defining users through the pathology of their condition.[129] As reports of drug use rapidly increased, the cultural model found application in anthropological research exploring western drug subculture practices.[26]
The approach evolved from the ethnographic exploration into the lived experiences and subjectivities of 1960s and 70s drug subcultures.[26] 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.[130] These findings challenge popular narratives of immorality and deviance, conceptualizing substance use as a social phenomenon. The prevailing culture can influence drug-taking behaviors, along with the physical and psychological effects of the drug.[131] To marginalized individuals, drug subcultures can provide social connection, symbolic meaning, and socially constructed purpose that they may feel is unattainable through conventional means.[131] 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.[26]
Addiction in art
[edit source]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.[132][133] Proposed benefits include offering a non-verbal outlet for difficult emotions, containing shame, and strengthening self-awareness and engagement in treatment.[134] 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.[135]
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.[136]
Research directions
[edit source]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.[137] Candidates have been tested against nicotine, cocaine, opioids and fentanyl.[137][138]
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.[137] Anti-cocaine vaccine development has likewise not produced an approved product, and no pharmacological treatment for cocaine dependence is currently approved.[138]
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;[139] 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.[140]
See also
[edit source]Endnotes
[edit source]- ↑ In other words, a person cannot control the neurobiological processes that occur in the body in response to using an addictive drug. A person can make a voluntary choice to, for example, start using a drug (or not), or to seek help after becoming addicted. However, resisting the urge to use drug(s) becomes increasingly difficult as addiction worsens. See [1] for detailed discussion.
Notes
[edit source]- ↑ A decrease in aversion sensitivity, in simpler terms, means that an individual's behavior is less likely to be influenced by undesirable outcomes.
- ↑ Incentive salience, the "motivational salience" for a reward, is a "desire" or "want" attribute, which includes a motivational component, that the brain assigns to a rewarding stimulus.[88][89] As a consequence, incentive salience acts as a motivational "magnet" for a rewarding stimulus that commands attention, induces approach, and causes the rewarding stimulus to be sought out.[88]
- ↑ According to a review of experimental animal models that examined the transgenerational epigenetic inheritance of epigenetic marks that occur in addiction, alterations in histone acetylation – specifically, di-acetylation of lysine residues 9 and 14 on histone 3 (i.e., H3K9ac2 and H3K14ac2) in association with BDNF gene promoters – have been shown to occur within the medial prefrontal cortex (mPFC), testes, and sperm of cocaine-addicted male rats.[38] These epigenetic alterations in the rat mPFC result in increased BDNF gene expression within the mPFC, which in turn blunts the rewarding properties of cocaine and reduces cocaine self-administration.[38] The male but not female offspring of these cocaine-exposed rats inherited both epigenetic marks (i.e., di-acetylation of lysine residues 9 and 14 on histone 3) within mPFC neurons, the corresponding increase in BDNF expression within mPFC neurons, and the behavioral phenotype associated with these effects (i.e., a reduction in cocaine reward, resulting in reduced cocaine-seeking by these male offspring).[38] Consequently, the transmission of these two cocaine-induced epigenetic alterations (i.e., H3K9ac2 and H3K14ac2) in rats from male fathers to male offspring served to reduce the offspring's risk of developing an addiction to cocaine.[38] As of 2018,[update] neither the heritability of these epigenetic marks in humans nor the behavioral effects of the marks within human mPFC neurons has been established.[38]
- Image legend
References
[edit source]- 1 2 Heilig M, MacKillop J, Martinez D, Rehm J, Leggio L, Vanderschuren LJ (September 2021). "Addiction as a brain disease revised: why it still matters, and the need for consilience". Neuropsychopharmacology. 46 (10): 1715–1723. doi:10.1038/s41386-020-00950-y. ISSN 0893-133X. PMC 8357831. PMID 33619327.
pre-existing vulnerabilities and persistent drug use lead to a vicious circle of substantive disruptions in the brain that impair and undermine choice capacities for adaptive behavior, but do not annihilate them.
- 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 Volkow ND, Blanco C (June 2023). "Substance use disorders: a comprehensive update of classification, epidemiology, neurobiology, clinical aspects, treatment and prevention". World Psychiatry. 22 (2): 203–229. doi:10.1002/wps.21073. PMC 10168177. PMID 37159360.
- 1 2 3 4 5 6 7 8 9 10 11 12 Nestler EJ (December 2013). "Cellular basis of memory for addiction". Dialogues in Clinical Neuroscience. 15 (4): 431–443. PMC 3898681. PMID 24459410.
Despite the importance of numerous psychosocial factors, at its core, drug addiction involves a biological process: the ability of repeated exposure to a drug of abuse to induce changes in a vulnerable brain that drive the compulsive seeking and taking of drugs, and loss of control over drug use, that define a state of addiction. ... A large body of literature has demonstrated that such ΔFosB induction in D1-type [nucleus accumbens] neurons increases an animal's sensitivity to drug as well as natural rewards and promotes drug self-administration, presumably through a process of positive reinforcement ... Another ΔFosB target is cFos: as ΔFosB accumulates with repeated drug exposure it represses c-Fos and contributes to the molecular switch whereby ΔFosB is selectively induced in the chronic drug-treated state.41 ... Moreover, there is increasing evidence that, despite a range of genetic risks for addiction across the population, exposure to sufficiently high doses of a drug for long periods of time can transform someone who has relatively lower genetic loading into an addict.
- 1 2 "Drugs, Brains, and Behavior: The Science of Addiction – Drug Misuse and Addiction". www.drugabuse.gov. North Bethesda, Maryland: National Institute on Drug Abuse. 13 July 2020. Retrieved 23 December 2021.
- ↑ Heather N, Best D, Kawalek A, Field M, Lewis M, Rotgers F, et al. (July 2018). "Challenging the brain disease model of addiction: European launch of the addiction theory network". Addiction Research & Theory. 26 (4): 249–255. doi:10.1080/16066359.2017.1399659.
- 1 2 Lewis M (October 2018). Longo DL (ed.). "Brain Change in Addiction as Learning, Not Disease". The New England Journal of Medicine. 379 (16): 1551–1560. doi:10.1056/NEJMra1602872. hdl:1807/97270. PMID 30332573. S2CID 205117578.
Addictive activities are determined neither solely by brain changes nor solely by social conditions ... the narrowing seen in addiction takes place within the behavioral repertoire, the social surround, and the brain — all at the same time.
- 1 2 3 4 American Psychiatric Association (2022). Diagnostic and Statistical Manual of Mental Disorders (5th, Text Revision ed.). Washington, DC: American Psychiatric Association Publishing.
- 1 2 3 4 5 "International Classification of Diseases 11th revision – ICD-11. Disorders due to substance use or addictive behaviours". World Health Organization. Geneva. 2023. Retrieved 10 April 2023.
- 1 2 3 Brand M, Antons S, Bőthe B, Demetrovics Z, Fineberg NA, Jimenez-Murcia S, et al. (February 2025). "Current Advances in Behavioral Addictions: From Fundamental Research to Clinical Practice". The American Journal of Psychiatry. 182 (2): 155–163. doi:10.1176/appi.ajp.20240092. PMID 39659159.
- 1 2 3 Gearhardt AN, Schulte EM (October 2021). "Is food addictive? A review of the science". Annual Review of Nutrition. 41: 387–410. doi:10.1146/annurev-nutr-110420-111710.
- 1 2 3 4 5 6 7 8 9 10 MacKillop J, Agabio R, Feldstein Ewing SW, Heilig M, Kelly JF, Leggio L, et al. (December 2022). "Hazardous drinking and alcohol use disorders". Nature Reviews. Disease Primers. 8 (1) 80. doi:10.1038/s41572-022-00406-1. PMC 10284465. PMID 36550121.
- 1 2 3 4 5 Bogdan R, Hatoum AS, Johnson EC, Agrawal A (January 2023). "The Genetically Informed Neurobiology of Addiction (GINA) model". Nature Reviews Neuroscience. 24 (1): 40–57. doi:10.1038/s41583-022-00656-8.
- 1 2 3 4 5 6 7 8 9 10 Volkow ND, Michaelides M, Baler R (October 2019). "The Neuroscience of Drug Reward and Addiction". Physiological Reviews. 99 (4): 2115–2140. doi:10.1152/physrev.00014.2018. PMID 31507244.
- 1 2 "Facing Addiction in America: The Surgeon General's Report on Alcohol, Drugs, and Health" (PDF). Office of the Surgeon General. US Department of Health and Human Services. November 2016. pp. 35–37, 45, 63, 155, 317, 338. Retrieved 28 January 2017.
- 1 2 3 "International Classification of Diseases 11th revision – ICD-11. Disorders due to substance use". World Health Organization. Geneva. 2023. Retrieved 24 March 2023.
- 1 2 3 United Nations Office on Drugs and Crime, World Health Organization (2018). International Standards on Drug Use Prevention (PDF) (Report) (Second updated ed.). Vienna: United Nations.
- 1 2 3 4 Mattick RP, Breen C, Kimber J, Davoli M (February 2014). "Buprenorphine maintenance versus placebo or methadone maintenance for opioid dependence". The Cochrane Database of Systematic Reviews. 2014 (2) CD002207. doi:10.1002/14651858.CD002207.pub4. PMID 24500948.
- 1 2 McPheeters M, O'Connor EA, Riley S, Kennedy SM, Voisin C, Kuznacic K, et al. (November 2023). "Pharmacotherapy for Alcohol Use Disorder: A Systematic Review and Meta-Analysis". JAMA. 330 (17): 1653–1665. doi:10.1001/jama.2023.19761. PMID 37934220.
- 1 2 Lindson N, Theodoulou A, Ordóñez-Mena JM, Fanshawe TR, Sutton AJ, Livingstone-Banks J, et al. (September 2023). "Pharmacological and electronic cigarette interventions for smoking cessation in adults: component network meta-analyses". The Cochrane Database of Systematic Reviews. 2023 (9) CD015226. doi:10.1002/14651858.CD015226.pub2. PMID 37696529.
- 1 2 3 4 De Crescenzo F, Ciabattini M, D'Alò GL, De Giorgi R, Del Giovane C, Cassar C, et al. (December 2018). "Comparative efficacy and acceptability of psychosocial interventions for individuals with cocaine and amphetamine addiction: A systematic review and network meta-analysis". PLOS Medicine. 15 (12) e1002715. doi:10.1371/journal.pmed.1002715. PMID 30586362.
- 1 2 3 Fleury MJ, Djouini A, Huynh C, Tremblay J, Ferland F, Ménard JM, et al. (November 2016). "Remission from substance use disorders: a systematic review and meta-analysis". Drug and Alcohol Dependence. 168: 293–306. doi:10.1016/j.drugalcdep.2016.08.625. PMID 27614380.
- 1 2 3 4 5 6 GBD 2016 Alcohol and Drug Use Collaborators (December 2018). "The global burden of disease attributable to alcohol and drug use in 195 countries and territories, 1990-2016: a systematic analysis for the Global Burden of Disease Study 2016". The Lancet. Psychiatry. 5 (12): 987–1012. doi:10.1016/S2215-0366(18)30337-7. PMC 6251968. PMID 30392731.
- 1 2 GBD 2023 Diseases and Injuries Collaborators (October 2025). "Burden of 375 diseases and injuries, risk-attributable burden of 88 risk factors, and healthy life expectancy in 204 countries and territories, including 660 subnational locations, 1990-2023: a systematic analysis for the Global Burden of Disease Study 2023". Lancet. 406 (10513): 1873–1922. doi:10.1016/S0140-6736(25)01637-X. PMC 12535840. PMID 41092926.
- 1 2 3 4 Malenka RC, Nestler EJ, Hyman SE (2009). "Chapter 1: Basic Principles of Neuropharmacology". In Sydor A, Brown RY (eds.). Molecular Neuropharmacology: A Foundation for Clinical Neuroscience (2nd ed.). New York: McGraw-Hill Medical. p. 4. ISBN 978-0-07-148127-4.
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 –for example, accidents and AIDS – on health and productivity.
- 1 2 3 Merikangas KR, McClair VL (June 2012). "Epidemiology of Substance Use Disorders". Hum. Genet. 131 (6): 779–89. doi:10.1007/s00439-012-1168-0. PMC 4408274. PMID 22543841.
- 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 Singer M (October 2012). "Anthropology and addiction: an historical review". Addiction. 107 (10): 1747–1755. doi:10.1111/j.1360-0443.2012.03879.x. PMID 22962955.
- 1 2 Destoop M, Morrens M, Coppens V, Dom G (2019). "Addiction, anhedonia, and comorbid mood disorder. A narrative review". Frontiers in Psychiatry. 10 311. doi:10.3389/fpsyt.2019.00311. PMC 6538808. PMID 31178763.
- ↑ Malenka RC, Nestler EJ, Hyman SE (2009). "Chapter 15: Reinforcement and Addictive Disorders". In Sydor A, Brown RY (eds.). Molecular Neuropharmacology: A Foundation for Clinical Neuroscience (2nd ed.). New York: McGraw-Hill Medical. pp. 364–375. ISBN 978-0-07-148127-4.
- 1 2 Volkow ND, Koob GF, McLellan AT (January 2016). "Neurobiologic Advances from the Brain Disease Model of Addiction". New England Journal of Medicine. 374 (4): 363–371. doi:10.1056/NEJMra1511480. PMC 6135257. PMID 26816013.
Substance-use disorder: A diagnostic term in the fifth edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-5) referring to recurrent use of alcohol or other drugs that causes clinically and functionally significant impairment, such as health problems, disability, and failure to meet major responsibilities at work, school, or home. Depending on the level of severity, this disorder is classified as mild, moderate, or severe.
Addiction: A term used to indicate the most severe, chronic stage of substance-use disorder, in which there is a substantial loss of self-control, as indicated by compulsive drug taking despite the desire to stop taking the drug. In the DSM-5, the term addiction is synonymous with the classification of severe substance-use disorder. - ↑ Diagnostic and Statistical Manual of Mental Disorders (DSM-5) (5th ed.). American Psychiatric Association. 2013. ISBN 978-0-89042-554-1.
- 1 2 3 4 5 6 Skylstad V, Babirye JN, Kiguli J, Solheim Skar AM, et al. (March 2022). "Are we overlooking alcohol use by younger children?". BMJ Paediatrics Open. 6 (1) e001242. doi:10.1136/bmjpo-2021-001242. PMC 8905875. PMID 36053657.
- ↑ Drummond DC (2001). "Theories of drug craving, ancient and modern". Addiction. 96 (1): 33–46. doi:10.1046/j.1360-0443.2001.961333.x. PMID 11177518.
- ↑ Malenka RC, Nestler EJ, Hyman SE (2009). "Chapter 15: Reinforcement and Addictive Disorders". In Sydor A, Brown RY (eds.). Molecular Neuropharmacology: A Foundation for Clinical Neuroscience (second ed.). New York: McGraw-Hill Medical. pp. 364–65, 375. ISBN 978-0-07-148127-4.
The defining feature of addiction is compulsive, out-of-control drug use, despite negative consequences. ...
compulsive eating, shopping, gambling, and sex – so-called "natural addictions" – Indeed, addiction to both drugs and behavioral rewards may arise from similar dysregulation of the mesolimbic dopamine system. - 1 2 3 4 Olsen CM (December 2011). "Natural rewards, neuroplasticity, and non-drug addictions". Neuropharmacology. 61 (7): 1109–22. doi:10.1016/j.neuropharm.2011.03.010. PMC 3139704. PMID 21459101.
- 1 2 Alavi SS, Ferdosi M, Jannatifard F, Eslami M, Alaghemandan H, Setare M (April 2012). "Behavioral Addiction versus Substance Addiction: Correspondence of Psychiatric and Psychological Views". International Journal of Preventive Medicine. 3 (4): 290–294. PMC 3354400. PMID 22624087.
- 1 2 Gearhardt AN, Bueno NB, DiFeliceantonio AG, Roberto CA, Jiménez-Murcia S, Fernandez-Aranda F (October 2023). "Social, clinical, and policy implications of ultra-processed food addiction". BMJ. 383 e075354. doi:10.1136/bmj-2023-075354.
- 1 2 di Giacomo E, Aliberti F, Pescatore F, Santorelli M, Pessina R, Placenti V, et al. (August 2022). "Disentangling binge eating disorder and food addiction: a systematic review and meta-analysis". Eating and Weight Disorders. 27 (6): 1963–1970. doi:10.1007/s40519-021-01354-7. PMC 9287203. PMID 35041154.
- 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 Vassoler FM, Sadri-Vakili G (2014). "Mechanisms of transgenerational inheritance of addictive-like behaviors". Neuroscience. 264: 198–206. doi:10.1016/j.neuroscience.2013.07.064. PMC 3872494. PMID 23920159.
However, the components that are responsible for the heritability of characteristics that make an individual more susceptible to drug addiction in humans remain largely unknown, given that patterns of inheritance cannot be explained by simple genetic mechanisms (Cloninger et al., 1981; Schuckit et al., 1972). The environment plays a large role in the development of addiction, as evidenced by great societal variability in drug use patterns between countries and across time (UNODC, 2012). Therefore, both genetics and the environment contribute to an individual's vulnerability to become addicted following an initial exposure to drugs of abuse. ...
The evidence presented here demonstrates that rapid environmental adaptation occurs following exposure to several stimuli. Epigenetic mechanisms are key components by which the environment can influence genetics, and they provide the missing link between genetic heritability and environmental influences on the behavioral and physiological phenotypes of the offspring. - ↑ Douglas KR, Chan G, Gelernter J, Arias AJ, Anton RF, Weiss RD, et al. (January 2010). "Adverse childhood events as risk factors for substance dependence: partial mediation by mood and anxiety disorders". Addictive Behaviors. 35 (1): 7–13. doi:10.1016/j.addbeh.2009.07.004. PMC 2763992. PMID 19720467.
- ↑ Daley DC (December 2013). "Family and social aspects of substance use disorders and treatment". Journal of Food and Drug Analysis. 21 (4): S73–S76. doi:10.1016/j.jfda.2013.09.038. PMC 4158844. PMID 25214748.
- ↑ Saad M, de Medeiros R, Mosini AC (October 2017). "Are We Ready for a True Biopsychosocial-Spiritual Model? The Many Meanings of "Spiritual"". Medicines. 4 (4): 79. doi:10.3390/medicines4040079. PMC 5750603. PMID 29088101.
- ↑ Bourgois P (23 December 2002). In Search of Respect: Selling Crack in El Barrio. Structural Analysis in the Social Sciences (2 ed.). Cambridge University Press. doi:10.1017/cbo9780511808562. ISBN 978-0-521-01711-4.
- 1 2 3 Saunders GR, Wang X, Chen F, Jang SK, Liu M, Wang C, et al. (December 2022). "Genetic diversity fuels gene discovery for tobacco and alcohol use". Nature. 612 (7941). Nature Research: 720–724. Bibcode:2022Natur.612..720S. doi:10.1038/s41586-022-05477-4. PMC 9771818. PMID 36477530. S2CID 254434507.
- ↑ Verhulst B, Neale MC, Kendler KS (April 2015). "The heritability of alcohol use disorders: a meta-analysis of twin and adoption studies". Psychological Medicine. 45 (5): 1061–1072. doi:10.1017/S0033291714002165. PMID 25171596.
- ↑ Hall FS, Drgonova J, Jain S, Uhl GR (December 2013). "Implications of genome wide association studies for addiction: are our a priori assumptions all wrong?". Pharmacology & Therapeutics. 140 (3): 267–79. doi:10.1016/j.pharmthera.2013.07.006. PMC 3797854. PMID 23872493.
- ↑ Yang H, Ma J (August 2021). "How the COVID-19 pandemic impacts tobacco addiction: Changes in smoking behavior and associations with well-being". Addictive Behaviors. 119 106917. doi:10.1016/j.addbeh.2021.106917. PMC 9186053. PMID 33862579. S2CID 233278782.
- 1 2 "What are risk factors and protective factors?". National Institute on Drug Abuse. Archived from the original on 30 April 2020. Retrieved 13 December 2017.
- ↑ "Understanding Drug Use and Addiction". www.drugabuse.gov. National Institute on Drug Abuse. 6 June 2018. Retrieved 29 May 2020.
- 1 2 3 4 5 6 7 Hill R, Harris J (2 November 2021). "Psychological Approaches to Addiction". In Day E (ed.). Seminars in addiction psychiatry (2nd ed.). Cambridge: Cambridge University Press. pp. 147–169. doi:10.1017/9781911623199.009. ISBN 978-1-911623-19-9. S2CID 242036830.
- 1 2 "Adverse Childhood Experiences". samhsa.gov. Rockville, Maryland, United States: Substance Abuse and Mental Health Services Administration. Archived from the original on 9 October 2016. Retrieved 26 September 2016.
- 1 2 Enoch MA (March 2011). "The role of early life stress as a predictor for alcohol and drug dependence". Psychopharmacology. 214 (1): 17–31. doi:10.1007/s00213-010-1916-6. PMC 3005022. PMID 20596857.
- 1 2 3 4 5 6 7 Sinha R (October 2008). "Chronic stress, drug use, and vulnerability to addiction". Annals of the New York Academy of Sciences. 1141: 105–130. doi:10.1196/annals.1441.030. PMC 2732004. PMID 18991954.
- 1 2 3 4 Piazza PV (1998). "The role of stress in drug self-administration". Trends in Pharmacological Sciences. 19 (2): 67–74. doi:10.1016/s0165-6147(97)01115-2. PMID 9550944.
- ↑ Marcos AC, Bahr SJ (June 1988). "Control Theory and Adolescent Drug Use". Youth & Society. 19 (4): 395–425. doi:10.1177/0044118X88019004003. ISSN 0044-118X. S2CID 143860602.
- ↑ Spear LP (June 2000). "The adolescent brain and age-related behavioral manifestations". Neuroscience and Biobehavioral Reviews. 24 (4): 417–63. Bibcode:2000NBRev..24..417S. CiteSeerX 10.1.1.461.3295. doi:10.1016/s0149-7634(00)00014-2. PMID 10817843. S2CID 14686245.
- ↑ Hammond CJ, Mayes LC, Potenza MN (April 2014). "Neurobiology of adolescent substance use and addictive behaviors: treatment implications". Adolescent Medicine. 25 (1): 15–32. PMC 4446977. PMID 25022184.
- ↑ Catalano RF, Hawkins JD, Wells EA, Miller J, Brewer D (1990). "Evaluation of the effectiveness of adolescent drug abuse treatment, assessment of risks for relapse, and promising approaches for relapse prevention". The International Journal of the Addictions. 25 (9A–10A): 1085–140. doi:10.3109/10826089109081039. PMID 2131328.
- ↑ Perepletchikova F, Krystal JH, Kaufman J (November 2008). "Practitioner review: adolescent alcohol use disorders: assessment and treatment issues". Journal of Child Psychology and Psychiatry, and Allied Disciplines. 49 (11): 1131–54. doi:10.1111/j.1469-7610.2008.01934.x. PMC 4113213. PMID 19017028.
- 1 2 3 "Nationwide Trends". National Institute on Drug Abuse. June 2015. Retrieved 15 December 2017.
- ↑ Spear LP (February 2013). "Adolescent neurodevelopment". The Journal of Adolescent Health. 52 (2 Suppl 2): S7–S13. doi:10.1016/j.jadohealth.2012.05.006. PMC 3982854. PMID 23332574.
- ↑ Casey BJ (2008). "The adolescent brain". Annals of the New York Academy of Sciences. 1141: 270–283. doi:10.1196/annals.1441.011. PMC 2757631. PMID 18991963.
- 1 2 Somerville LH, Jones RM, Casey BJ (February 2010). "A time of change: behavioral and neural correlates of adolescent sensitivity to appetitive and aversive environmental cues". Brain and Cognition. 72 (1): 124–133. doi:10.1016/j.bandc.2009.07.003. PMC 2814936. PMID 19695759.
- ↑ Squeglia LM, Jacobus J, Tapert SF (January 2009). "The influence of substance use on adolescent brain development". Clinical EEG and Neuroscience. 40 (1): 31–38. doi:10.1177/155005940904000110. PMC 2827693. PMID 19278130.
- ↑ SAMHSA. "Risk and Protective Factors". Substance Abuse and Mental Health Administration. Archived from the original on 8 December 2016. Retrieved 19 December 2016.
- ↑ "Infographic – Risk Factors of Addiction". www.recoveryanswers.org. Archived from the original on 17 December 2016. Retrieved 19 December 2016.
- ↑ "Drug addiction Risk factors – Mayo Clinic". www.mayoclinic.org. Retrieved 19 December 2016.
- 1 2 3 Tiffany ST (1990). "A cognitive model of drug urges and drug-use behavior: Role of automatic and nonautomatic processes". Psychological Review. 97 (2): 147–168. doi:10.1037/0033-295X.97.2.147. ISSN 1939-1471. PMID 2186423.
- ↑ Fehrman E, Egan V, Gorban AN, Levesley J, Mirkes EM, Muhammad AK (2019). Personality Traits and Drug Consumption. A Story Told by Data. Springer, Cham. arXiv:2001.06520. doi:10.1007/978-3-030-10442-9. ISBN 978-3-030-10441-2. S2CID 151160405.
- ↑ Cheetham A, Allen NB, Yücel M, Lubman DI (August 2010). "The role of affective dysregulation in drug addiction". Clin Psychol Rev. 30 (6): 621–34. doi:10.1016/j.cpr.2010.04.005. PMID 20546986.
- ↑ Franken IH, Muris P (2006). "BIS/BAS personality characteristics and college students' substance use". Personality and Individual Differences. 40 (7): 1497–503. doi:10.1016/j.paid.2005.12.005.
- ↑ Genovese JE, Wallace D (December 2007). "Reward sensitivity and substance abuse in middle school and high school students". J Genet Psychol. 168 (4): 465–69. doi:10.3200/GNTP.168.4.465-469. PMID 18232522. S2CID 207640075.
- ↑ Kimbrel NA, Nelson-Gray RO, Mitchell JT (April 2007). "Reinforcement sensitivity and maternal style as predictors of psychopathology". Personality and Individual Differences. 42 (6): 1139–49. doi:10.1016/j.paid.2006.06.028.
- ↑ Dawe S, Loxton NJ (May 2004). "The role of impulsivity in the development of substance use and eating disorders". Neurosci Biobehav Rev. 28 (3): 343–51. doi:10.1016/j.neubiorev.2004.03.007. PMID 15225976. S2CID 24435589.
- 1 2 3 Smith MA (February 2021). "Social learning and addiction". Behavioural Brain Research. 398 112954. doi:10.1016/j.bbr.2020.112954. PMC 7719575. PMID 33053384.
- ↑ Nesse R (1998). "Emotional disorders in evolutionary perspective". British Journal of Medical Psychology. 71 (4): 397–415. doi:10.1111/j.2044-8341.1998.tb01000.x. ISSN 2044-8341. PMID 9875953.
- ↑ Durrant R, Adamson S, Todd F, Sellman D (13 November 2009). "Drug use and addiction: evolutionary perspective". Australian and New Zealand Journal of Psychiatry. 43 (11): 1049–1056. doi:10.3109/00048670903270449. ISSN 0004-8674. PMID 20001400.
- ↑ Saah T (29 June 2005). "The evolutionary origins and significance of drug addiction". Harm Reduction Journal. 2 (1) 8. doi:10.1186/1477-7517-2-8. ISSN 1477-7517. PMC 1174878. PMID 15987511.
- ↑ Sullivan RJ, Hagen EH, Hammerstein P (March 2008). "Revealing the paradox of drug reward in human evolution". Proceedings of the Royal Society B: Biological Sciences. 275 (1640): 1231–1241. doi:10.1098/rspb.2007.1673. PMC 2367444. PMID 18353749.
- ↑ Ruffle JK (November 2014). "Molecular neurobiology of addiction: what's all the (Δ)FosB about?". Am. J. Drug Alcohol Abuse. 40 (6): 428–37. doi:10.3109/00952990.2014.933840. PMID 25083822. S2CID 19157711.
- ↑ Washburn DA (2016). "The Stroop effect at 80: The competition between stimulus control and cognitive control". J Exp Anal Behav. 105 (1): 3–13. doi:10.1002/jeab.194. PMID 26781048.
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.
- ↑ Diamond A (2013). "Executive functions". Annu Rev Psychol. 64: 135–68. doi:10.1146/annurev-psych-113011-143750. PMC 4084861. PMID 23020641.
Core EFs are inhibition [response inhibition (self-control – 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 the 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 the 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, or emotions to override a strong internal predisposition or external lure, and instead do what is more appropriate or needed. Without inhibitory control, we would be at the mercy of impulses, old habits of thought or action (conditioned responses), 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). - 1 2 Malenka RC, Nestler EJ, Hyman SE (2009). "Chapter 13: Higher Cognitive Function and Behavioral Control". In Sydor A, Brown RY (eds.). Molecular Neuropharmacology: A Foundation for Clinical Neuroscience (2nd ed.). New York: McGraw-Hill Medical. pp. 313–21. ISBN 978-0-07-148127-4.
• Executive function, the cognitive control of behavior, depends on the prefrontal cortex, which is highly developed in higher primates and especially humans.
• 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 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. - 1 2 3 4 5 6 Gould TJ (December 2010). "Addiction and cognition". Addiction Science & Clinical Practice. 5 (2): 4–14. PMC 3120118. PMID 22002448.
- 1 2 3 4 5 Levy N (2019). "Chapter 5 Addiction: The belief oscillation hypothesis". In Pickard H, Ahmed SH (eds.). The Routledge handbook of philosophy and science of addiction. Wellcome Trust–Funded Monographs and Book Chapters. Oxon (UK): Routledge. doi:10.4324/9781315689197-6. ISBN 978-1-138-90928-1. OCLC 1042341025. PMID 31017751. S2CID 242067468.
- ↑ Feltenstein MW, See RE (May 2008). "The neurocircuitry of addiction: an overview". British Journal of Pharmacology. 154 (2): 261–274. doi:10.1038/bjp.2008.51. PMC 2442446. PMID 18311189.
- 1 2 Nestler EJ, Barrot M, Self DW (September 2001). "DeltaFosB: a sustained molecular switch for addiction". Proc. Natl. Acad. Sci. U.S.A. 98 (20): 11042–46. Bibcode:2001PNAS...9811042N. doi:10.1073/pnas.191352698. PMC 58680. PMID 11572966.
Although the ΔFosB signal is relatively long-lived, it is not permanent. ΔFosB degrades gradually and can no longer be detected in [the] brain after 1–2 months of drug withdrawal ... Indeed, ΔFosB is the longest-lived adaptation known to occur in [the] adult brain, not only in response to drugs of abuse, but to any other perturbation (that doesn't involve lesions) as well.
- ↑ Perry CJ, Zbukvic I, Kim JH, Lawrence AJ (October 2014). "Role of cues and contexts on drug-seeking behaviour". British Journal of Pharmacology. 171 (20): 4636–72. doi:10.1111/bph.12735. PMC 4209936. PMID 24749941.
- 1 2 3 4 5 6 Berridge KC (April 2012). "From prediction error to incentive salience: mesolimbic computation of reward motivation". Eur. J. Neurosci. 35 (7): 1124–43. doi:10.1111/j.1460-9568.2012.07990.x. PMC 3325516. PMID 22487042.
Here I discuss how mesocorticolimbic mechanisms generate the motivation component of incentive salience. Incentive salience takes Pavlovian learning and memory as one input and as an equally important input takes neurobiological state factors (e.g., drug states, appetite states, satiety states) that can vary independently of learning. Neurobiological state changes can produce unlearned fluctuations or even reversals in the ability of a previously learned reward cue to trigger motivation. Such fluctuations in cue-triggered motivation can dramatically depart from all previously learned values about the associated reward outcome. ... Associative learning and prediction are important contributors to motivation for rewards. Learning gives incentive value to arbitrary cues such as a Pavlovian conditioned stimulus (CS) that is associated with a reward (unconditioned stimulus or UCS). Learned cues for reward are often potent triggers of desires. For example, learned cues can trigger normal appetites in everyone, and can sometimes trigger compulsive urges and relapse in individuals with addictions.
Cue-triggered 'wanting' for the UCS
A brief CS encounter (or brief UCS encounter) often primes a pulse of elevated motivation to obtain and consume more reward UCS. This is a signature feature of incentive salience.
Cue as attractive motivational magnets
When a Pavlovian CS+ is attributed with incentive salience, it not only triggers 'wanting' for its UCS, but often the cue itself becomes highly attractive – even to an irrational degree. This cue attraction is another signature feature of incentive salience ... Two recognizable features of incentive salience are often visible that can be used in neuroscience experiments: (i) UCS-directed 'wanting' – CS-triggered pulses of intensified 'wanting' for the UCS reward; and (ii) CS-directed 'wanting' – motivated attraction to the Pavlovian cue, which makes the arbitrary CS stimulus into a motivational magnet. - 1 2 Malenka RC, Nestler EJ, Hyman SE (2009). Sydor A, Brown RY (eds.). Molecular Neuropharmacology: A Foundation for Clinical Neuroscience (second ed.). New York: McGraw-Hill Medical. pp. 147–48, 366–67, 375–76. ISBN 978-0-07-148127-4.
VTA DA neurons play a critical role in motivation, reward-related behavior (Chapter 15), attention, and multiple forms of memory. This organization of the DA system, with wide projection from a limited number of cell bodies, permits coordinated responses to potent new rewards. Thus, acting in diverse terminal fields, dopamine confers motivational salience ("wanting") on the reward itself or associated cues (nucleus accumbens shell region), updates the value placed on different goals in light of this new experience (orbital prefrontal cortex), helps consolidate multiple forms of memory (amygdala and hippocampus), and encodes new motor programs that will facilitate obtaining this reward in the future (nucleus accumbens core region and dorsal striatum). In this example, dopamine modulates the processing of sensorimotor information in diverse neural circuits to maximize the ability of the organism to obtain future rewards. ...
The brain reward circuitry that is targeted by addictive drugs normally mediates the pleasure and strengthening of behaviors associated with natural reinforcers, such as food, water, and sexual contact. Dopamine neurons in the VTA are activated by food and water, and dopamine release in the NAc is stimulated by the presence of natural reinforcers, such as food, water, or a sexual partner. ...
The NAc and VTA are central components of the circuitry underlying reward and memory of reward. As previously mentioned, the activity of dopaminergic neurons in the VTA appears to be linked to reward prediction. The NAc is involved in learning associated with reinforcement and the modulation of motoric responses to stimuli that satisfy internal homeostatic needs. The shell of the NAc appears to be particularly important to initial drug actions within reward circuitry; addictive drugs appear to have a greater effect on dopamine release in the shell than in the core of the NAc. ... If motivational drive is described in terms of wanting, and hedonic evaluation in terms of liking, it appears that wanting can be dissociated from liking and that dopamine may influence these phenomena differently. Differences between wanting and liking are confirmed in reports by humans with addictions, who state that their desire for drugs (wanting) increases with continued use even when pleasure (liking) decreases because of tolerance. - 1 2 3 4 Edwards S (2016). "Reinforcement principles for addiction medicine; from recreational drug use to psychiatric disorder". Neuroscience for Addiction Medicine: From Prevention to Rehabilitation - Constructs and Drugs. Progress in Brain Research. Vol. 223. pp. 63–76. doi:10.1016/bs.pbr.2015.07.005. ISBN 978-0-444-63545-7. PMID 26806771.
An important dimension of reinforcement highly relevant to the addiction process (and particularly relapse) is secondary reinforcement (Stewart, 1992). Secondary reinforcers (in many cases also considered conditioned reinforcers) likely drive the majority of reinforcement processes in humans. In the specific case of drug addiction, cues and contexts that are intimately and repeatedly associated with drug use will themselves become reinforcing ... A fundamental piece of Robinson and Berridge's incentive-sensitization theory of addiction posits that the incentive value or attractive nature of such secondary reinforcement processes, in addition to the primary reinforcers themselves, may persist and even become sensitized over time in league with the development of drug addiction (Robinson and Berridge, 1993).
- 1 2 Berridge KC, Kringelbach ML (May 2015). "Pleasure systems in the brain". Neuron. 86 (3): 646–664. doi:10.1016/j.neuron.2015.02.018. PMC 4425246. PMID 25950633.
- ↑ Nestler EJ (October 2008). "Review. Transcriptional mechanisms of addiction: role of DeltaFosB". Philosophical Transactions of the Royal Society of London. Series B, Biological Sciences. 363 (1507): 3245–55. doi:10.1098/rstb.2008.0067. PMC 2607320. PMID 18640924.
- ↑ Dupont C, Armant DR, Brenner CA (September 2009). "Epigenetics: definition, mechanisms and clinical perspective". Seminars in Reproductive Medicine. 27 (5): 351–357. doi:10.1055/s-0029-1237423. PMC 2791696. PMID 19711245.
- 1 2 3 4 Nielsen DA, Utrankar A, Reyes JA, Simons DD, Kosten TR (July 2012). "Epigenetics of drug abuse: predisposition or response". Pharmacogenomics. 13 (10): 1149–1160. doi:10.2217/pgs.12.94. PMC 3463407. PMID 22909205.
- 1 2 3 4 Nestler EJ (January 2014). "Epigenetic mechanisms of drug addiction". Neuropharmacology. 76 (Pt B): 259–68. doi:10.1016/j.neuropharm.2013.04.004. PMC 3766384. PMID 23643695.
- 1 2 3 Walker DM, Cates HM, Heller EA, Nestler EJ (February 2015). "Regulation of chromatin states by drugs of abuse". Curr. Opin. Neurobiol. 30: 112–21. doi:10.1016/j.conb.2014.11.002. PMC 4293340. PMID 25486626.
Studies investigating general HDAC inhibition on behavioral outcomes have produced varying results but it seems that the effects are specific to the timing of exposure (either before, during or after exposure to drugs of abuse) as well as the length of exposure
- 1 2 3 Yuan TF, Li A, Sun X, Ouyang H, Campos C, Rocha NB, et al. (2015). "Transgenerational Inheritance of Paternal Neurobehavioral Phenotypes: Stress, Addiction, Ageing and Metabolism". Mol. Neurobiol. 53 (9): 6367–76. doi:10.1007/s12035-015-9526-2. hdl:10400.22/7331. PMID 26572641. S2CID 25694221.
- ↑ American Psychiatric Association (2013). "Substance-Related and Addictive Disorders" (PDF). American Psychiatric Publishing. pp. 1–2. Archived from the original (PDF) on 15 August 2015. Retrieved 8 April 2023.
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.
- ↑ Petry NM, Rehbein F, Gentile DA, Lemmens JS, Rumpf HJ, Mößle T, et al. (September 2014). "An international consensus for assessing internet gaming disorder using the new DSM-5 approach". Addiction. 109 (9): 1399–406. doi:10.1111/add.12457. PMID 24456155.
- ↑ Torres G, Horowitz JM (1999). "Drugs of abuse and brain gene expression". Psychosom Med. 61 (5): 630–50. CiteSeerX 10.1.1.326.4903. doi:10.1097/00006842-199909000-00007. PMID 10511013.
- ↑ Malenka RC, Nestler EJ, Hyman SE, Holtzman DM (2015). "Chapter 16: Reinforcement and Addictive Disorders". Molecular Neuropharmacology: A Foundation for Clinical Neuroscience (3rd ed.). New York: McGraw-Hill Medical. ISBN 978-0-07-182770-6.
The official diagnosis of drug addiction by the Diagnostic and Statistic Manual of Mental Disorders (2013), which uses the term substance use disorder, is flawed. Criteria used to make the diagnosis of substance use disorders include tolerance and somatic dependence/withdrawal, even though these processes are not integral to addiction as noted. It is ironic and unfortunate that the manual still avoids use of the term addiction as an official diagnosis, even though addiction provides the best description of the clinical syndrome.
- ↑ Han BH, Moore AA (February 2018). "Prevention and Screening of Unhealthy Substance Use by Older Adults". Clinics in Geriatric Medicine. 34 (1): 117–129. doi:10.1016/j.cger.2017.08.005. PMC 5718360. PMID 29129212.
- ↑ "Tobacco, Alcohol, Prescription medication, and other Substance use (TAPS) Tool". nida.nih.gov. Archived from the original on 14 August 2022. Retrieved 29 November 2022.
- ↑ "Use the CRAFFT – CRAFFT". Retrieved 3 December 2022.
- ↑ Yudko E, Lozhkina O, Fouts A (March 2007). "A comprehensive review of the psychometric properties of the Drug Abuse Screening Test". Journal of Substance Abuse Treatment. 32 (2): 189–198. doi:10.1016/j.jsat.2006.08.002. PMID 17306727.
- ↑ Kwako LE, Momenan R, Litten RZ, Koob GF, Goldman D (August 2016). "Addictions Neuroclinical Assessment: A Neuroscience-Based Framework for Addictive Disorders". Biological Psychiatry. 80 (3): 179–189. doi:10.1016/j.biopsych.2015.10.024. PMC 4870153. PMID 26772405.
- ↑ Volkow ND, Koob GF, McLellan AT (28 January 2016). "Neurobiologic Advances from the Brain Disease Model of Addiction". New England Journal of Medicine. 374 (4): 363–371. doi:10.1056/NEJMra1511480. ISSN 0028-4793. PMC 6135257. PMID 26816013.
- ↑ Taylor SB, Lewis CR, Olive MF (February 2013). "The neurocircuitry of illicit psychostimulant addiction: acute and chronic effects in humans". Substance Abuse and Rehabilitation. 4: 29–43. doi:10.2147/SAR.S39684. PMC 3931688. PMID 24648786.
- 1 2 Kelly JF, Humphreys K, Ferri M (March 2020). "Alcoholics Anonymous and other 12-step programs for alcohol use disorder". The Cochrane Database of Systematic Reviews. 2020 (3) CD012880. doi:10.1002/14651858.CD012880.pub2. PMID 32159228.
- ↑ Scott CG (July 2000). "Ethical Issues in Addiction Counseling". Rehabilitation Counseling Bulletin. 43 (4): 209–214. doi:10.1177/003435520004300405. ISSN 0034-3552. PMID 15714702.
- ↑ Chen CC, Yin SJ (October 2008). "Alcohol abuse and related factors in Asia". International Review of Psychiatry. 20 (5): 425–433. doi:10.1080/09540260802344075. PMID 19012127. S2CID 24571763.
- ↑ Pacurucu-Castillo SF, Ordóñez-Mancheno JM, Hernández-Cruz A, Alarcón RD (April 2019). "World opioid and substance use epidemic: a Latin American perspective". Psychiatric Research and Clinical Practice. 1 (1): 32–8. doi:10.1176/appi.prcp.20180009. PMC 9175731. PMID 36101564.
- ↑ Institute of Medicine (1996). Pathways of Addiction: Opportunities in Drug Abuse Research. Washington: National Academies Press.
- ↑ Bettinardi-Angres K, Angres DH (July 2010). Alexander M (ed.). "Understanding the Disease of Addiction". Journal of Nursing Regulation. 1 (2). Elsevier on behalf of the National Council of State Boards of Nursing: 31–37. doi:10.1016/S2155-8256(15)30348-3. ISSN 2155-8256. S2CID 143289528.
- ↑ Alexander BK, Schweighofer AR (1988). "Defining "addiction"". Canadian Psychology. 29 (2): 151–162. doi:10.1037/h0079767.
- 1 2 Steverson (2020). Addiction reimagined: challenging views of an enduring social problem. Vernon Press. p. 206. ISBN 978-1-62273-953-0.
- ↑ Gowing L, Ali R, Allsop S, Marsden J, Turf E, West E, et al. (2015). "Global statistics on addictive behaviours: 2014 status report" (PDF). Addiction. 110 (6): 904–919. doi:10.1111/add.12899. PMID 25963869.
- ↑ Lee C, Ko A, Yang F (2018). "Association of DSM-5 betel-quid use disorder with oral potentially malignant disorder in 6 betel-quid endemic Asian populations". JAMA Psychiatry. 75 (3): 261–269. doi:10.1001/jamapsychiatry.2017.4307. PMC 5885949. PMID 29417149.
- 1 2 Sahithya B, Kashyap R (2020). "Sexual Addiction Disorder—a review with recent updates". Journal of Psychosexual Health. 4 (2): 95–101. doi:10.1177/26318318221081080. S2CID 248835855.
- ↑ Crocq MA (December 2007). Thibaut F (ed.). "Historical and cultural aspects of man's relationship with addictive drugs". Dialogues in Clinical Neuroscience. 9 (4). Laboratoires Servier: 355–361. doi:10.31887/DCNS.2007.9.4/macrocq. OCLC 62869913. PMC 3202501. PMID 18286796. S2CID 12682928.
- 1 2 3 Lemon R (2018). "Introduction: Addiction in (Early) Modernity". Addiction and Devotion in Early Modern England. Haney Foundation Series. Philadelphia: University of Pennsylvania Press. pp. 1–23. ISBN 978-0-8122-4996-5.
- 1 2 Rosenthal R, Faris S (February 2019). "The etymology and early history of 'addiction'". Addiction Research & Theory. 27 (5). Taylor & Francis: 437–449. doi:10.1080/16066359.2018.1543412. ISSN 1476-7392. S2CID 150418396.
- 1 2 3 "American Board of Medical Specialties recognizes the new subspecialty of addiction medicine" (PDF). American Board of Addiction Medicine. 14 March 2016. Archived from the original (PDF) on 21 March 2021. Retrieved 3 April 2016.
- ↑ "Economic consequences of drug abuse" (PDF). International Narcotics Control Board Report: 2013 (PDF). United Nations – International Narcotics Control Board. 2013. ISBN 978-92-1-148274-4. Retrieved 28 September 2018.
- ↑ "Overdose Death Rates". National Institute on Drug Abuse. 9 August 2018. Retrieved 17 September 2018.
- ↑ "Overdose Deaths Accelerating During Covid-19". Centers For Disease Control Prevention. 18 December 2020. Retrieved 10 February 2021.
- 1 2 3 4 Heath DB (September 1958). "Drinking patterns of the Bolivian Camba". Quarterly Journal of Studies on Alcohol. 19 (3): 491–508. doi:10.15288/qjsa.1958.19.491. PMID 13579177.
- ↑ Heath DB (January 1995). "Changes in Drinking Patterns in Bolivian Cultures: A Cautionary Tale About Historical Approaches". Addiction Research. 2 (3): 307–318. doi:10.3109/16066359509005215. ISSN 1058-6989.
- ↑ Burraway J (October 2020). "Addiction". In Stein F, Diemberger H, Stasch R, Robbins J, Sanchez A, Lazar S, Candea M (eds.). Open Encyclopedia of Anthropology. doi:10.29164/20addiction. S2CID 241689890.
- ↑ Preble E, Casey JJ (January 1969). "Taking Care of Business—The Heroin User's Life on the Street". International Journal of the Addictions. 4 (1): 1–24. doi:10.3109/10826086909061998. ISSN 0020-773X.
- 1 2 Golub A, Johnson BD, Dunlap E (May 2005). "Subcultural evolution and illicit drug use". Addiction Research & Theory. 13 (3): 217–229. doi:10.1080/16066350500053497. PMC 3690817. PMID 23805068.
- ↑ Schmanke L (2019). "Art Therapy Applications and Substance Abuse". Art and Expressive Therapies within the Medical Model (1st ed.). Routledge. pp. 177–187. doi:10.4324/9780429400087-16. ISBN 978-0-367-02340-9.
- ↑ Rockwell P, Dunham M (January 2006). "The Utility of the Formal Elements Art Therapy Scale in Assessment for Substance Use Disorder". Art Therapy. 23 (3): 104–111. doi:10.1080/07421656.2006.10129625. ISSN 0742-1656.
- ↑ Schmanke L (2015). "Art Therapy and Substance Abuse". The Wiley Handbook of Art Therapy. John Wiley & Sons. pp. 361–374. doi:10.1002/9781118306543.ch35. ISBN 978-1-118-30654-3.
- ↑ Megranahan K, Lynskey MT (February 2018). "Do creative arts therapies reduce substance misuse? A systematic review". The Arts in Psychotherapy. 57: 50–58. doi:10.1016/j.aip.2017.10.005. ISSN 0197-4556.
- ↑ Henningfield JE, Dowell ML, Santora PB (2010). Addiction and Art. Baltimore: Johns Hopkins University Press. ISBN 978-1-4214-0023-5. OCLC 794700340.
- 1 2 3 Hartmann-Boyce J, Cahill K, Hatsukami D, Cornuz J (August 2012). "Nicotine vaccines for smoking cessation". The Cochrane Database of Systematic Reviews. 2012 (8) CD007072. doi:10.1002/14651858.CD007072.pub2. PMC 6486305. PMID 22895958.
- 1 2 Stephenson RJ, Toth I (May 2023). "Anti-cocaine vaccine development: where are we now and where are we going?". Journal of Medicinal Chemistry. 66 (11): 7086–7100. doi:10.1021/acs.jmedchem.3c00366. PMID 37227096.
- ↑ Qeadan F, McCunn A, Tingey B (2024). "The association between glucose-dependent insulinotropic polypeptide and/or glucagon-like peptide-1 receptor agonist prescriptions and substance-related outcomes in patients with opioid and alcohol use disorders: A real-world data analysis". Addiction. 120 (2): 236–250. doi:10.1111/add.16679. PMC 11707322. PMID 39415416.
- ↑ Leggio L, Hendershot CS, Farokhnia M, et al. (December 2023). "GLP-1 receptor agonists are promising but unproven treatments for alcohol and substance use disorders". Nature Medicine. 29 (12): 2993–2995. doi:10.1038/s41591-023-02634-8. PMID 38001271.
Further reading
[edit source]- 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
[edit source]- "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: