うつ病、不安障害、注意欠陥・多動性障害（ADHD）、または心的外傷後ストレス障害などの併存する精神健康障害を持つ個人は、物質使用障害を発症する可能性が高い[93][94][95][23]。NIDA（国立薬物乱用研究所）は、幼少期の攻撃的行動を物質使用のリスク要因として挙げている[80]。National Bureau of Economic Researchは、「精神疾患と嗜癖性物質の使用の間には明確な関連がある」とし、精神健康患者の大多数がこれらの物質の使用に参加していることを発見した：38%がアルコール、44%がコカイン、40%がタバコを使用している[96]。
CRAFFT（Car-Relax-Alone-Forget-Family and Friends-Trouble）は医療センターで使用されるスクリーニングツールである。CRAFFTはバージョン2.1であり、ニコチンとタバコ使用のためのCRAFFT 2.1+Nと呼ばれるバージョンがある[141]。このツールは青少年の間で物質使用、物質関連運転リスク、および嗜癖を特定するために使用される。このツールは異なるシナリオのための一連の質問を使用する[142]。特定の回答の組み合わせの場合、より正確な回答を得るためにさまざまな質問セットを使用することができる。質問の後、DSM-5の基準を使用して、その人が物質使用障害を持つ可能性を特定する[142]。これらのテストが終了した後、臨床医は「5 RS」の簡潔なカウンセリングを与える。
^“Addiction, Compulsion, and Weakness of the Will: A Dual-Process Perspective.”. Addiction and Choice: Rethinking the Relationship. Oxford, UK: Oxford University Press. (2017). pp. 116–132
^ ab“Chapter 15: Reinforcement and Addictive Disorders”. Molecular Neuropharmacology: A Foundation for Clinical Neuroscience (second ed.). New York: McGraw-Hill Medical. (2009). pp. 364–65, 375.
ISBN978-0-07-148127-4. "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."
^“Chapter 15: Reinforcement and Addictive Disorders”. Molecular Neuropharmacology: A Foundation for Clinical Neuroscience (2nd ed.). New York: McGraw-Hill Medical. (2009). pp. 364–375.
ISBN9780071481274
^“Glossary of Terms”. Mount Sinai School of Medicine. Department of Neuroscience. 2015年2月9日閲覧。
^ ab“Neurobiologic Advances from the Brain Disease Model of Addiction”. N. Engl. J. Med.374 (4): 363–371. (January 2016). doi:10.1056/NEJMra1511480.
PMID26816013.
^ abcdefghijklmnopqr“Natural rewards, neuroplasticity, and non-drug addictions”. Neuropharmacology61 (7): 1109–22. (December 2011). doi:10.1016/j.neuropharm.2011.03.010. PMC3139704.
PMID21459101. https://pmc.ncbi.nlm.nih.gov/articles/PMC3139704/. "Functional neuroimaging studies in humans have shown that gambling (Breiter et al, 2001), shopping (Knutson et al, 2007), orgasm (コミサルク（英語版） et al, 2004), playing video games (Koepp et al, 1998; Hoeft et al, 2008) and the sight of appetizing food (Wang et al, 2004a) activate many of the same brain regions (i.e., the mesocorticolimbic system and extended amygdala) as drugs of abuse (Volkow et al, 2004). ... Cross-sensitization is also bidirectional, as a history of amphetamine administration facilitates sexual behavior and enhances the associated increase in NAc DA ... As described for food reward, sexual experience can also lead to activation of plasticity-related signaling cascades. The transcription factor delta FosB is increased in the NAc, PFC, dorsal striatum, and VTA following repeated sexual behavior (Wallace et al., 2008; Pitchers et al., 2010b). This natural increase in delta FosB or viral overexpression of delta FosB within the NAc modulates sexual performance, and NAc blockade of delta FosB attenuates this behavior (Hedges et al, 2009; Pitchers et al., 2010b). Further, viral overexpression of delta FosB enhances the conditioned place preference for an environment paired with sexual experience (Hedges et al., 2009). ... In some people, there is a transition from "normal" to compulsive engagement in natural rewards (such as food or sex), a condition that some have termed behavioral or non-drug addictions (Holden, 2001; Grant et al., 2006a). ... In humans, the role of dopamine signaling in incentive-sensitization processes has recently been highlighted by the observation of a dopamine dysregulation syndrome in some people taking dopaminergic drugs. This syndrome is characterized by a medication-induced increase in (or compulsive) engagement in non-drug rewards such as gambling, shopping, or sex (Evans et al, 2006; Aiken, 2007; Lader, 2008)."" Table 1: Summary of plasticity observed following exposure to drug or natural reinforcers"
^ abcdefghijklmn“Transcriptional and epigenetic mechanisms of addiction”. Nat. Rev. Neurosci.12 (11): 623–37. (November 2011). doi:10.1038/nrn3111. PMC3272277.
PMID21989194. https://pmc.ncbi.nlm.nih.gov/articles/PMC3272277/. "ΔFosB has been linked directly to several addiction-related behaviors ... Importantly, genetic or viral overexpression of ΔJunD, a dominant negative mutant of JunD which antagonizes ΔFosB- and other AP-1-mediated transcriptional activity, in the NAc or OFC blocks these key effects of drug exposure14,22–24. This indicates that ΔFosB is both necessary and sufficient for many of the changes wrought in the brain by chronic drug exposure. ΔFosB is induced in D1-type NAc MSNs by chronic consumption of several natural rewards, including sucrose, high fat food, sex, wheel running, where it promotes that consumption14,26–30. This implicates ΔFosB in the regulation of natural rewards under normal conditions and perhaps during pathological addictive-like states."
^Coffee, tea, chocolate, and the brain.. Boca Raton: CRC Press. (2004). pp. 203–218.
ISBN978-0-429-21192-8
^“Yale Food Addiction Scale”. Food and Addiction Science & Treatment Lab. Department of Psychology, University of Michigan. 2022年11月1日閲覧。
^“Development of the Yale Food Addiction Scale Version 2.0”. Psychology of Addictive Behaviors30 (1): 113–121. (February 2016). doi:10.1037/adb0000136.
PMID26866783.
^“Food addiction, eating addiction and eating disorders”. The Proceedings of the Nutrition Society79 (1): 103–112. (February 2020). doi:10.1017/S0029665119001162.
PMID31744566.
^ ab“Sexual addiction or hypersexual disorder: different terms for the same problem? A review of the literature”. Curr. Pharm. Des.20 (25): 4012–20. (2014). doi:10.2174/13816128113199990619.
PMID24001295. "Sexual addiction, which is also known as hypersexual disorder, has largely been ignored by psychiatrists, even though the condition causes serious psychosocial problems for many people. A lack of empirical evidence on sexual addiction is the result of the disease's complete absence from versions of the Diagnostic and Statistical Manual of Mental Disorders. ... Existing prevalence rates of sexual addiction-related disorders range from 3% to 6%. Sexual addiction/hypersexual disorder is used as an umbrella construct to encompass various types of problematic behaviors, including excessive masturbation, cybersex, pornography use, sexual behavior with consenting adults, telephone sex, strip club visitation, and other behaviors. The adverse consequences of sexual addiction are similar to the consequences of other addictive disorders. Addictive, somatic and psychiatric disorders coexist with sexual addiction. In recent years, research on sexual addiction has proliferated, and screening instruments have increasingly been developed to diagnose or quantify sexual addiction disorders. In our systematic review of the existing measures, 22 questionnaires were identified. As with other behavioral addictions, the appropriate treatment of sexual addiction should combine pharmacological and psychological approaches."
^ abc“Natural and drug rewards act on common neural plasticity mechanisms with ΔFosB as a key mediator”. The Journal of Neuroscience（英語版）33 (8): 3434–42. (February 2013). doi:10.1523/JNEUROSCI.4881-12.2013. PMC3865508.
PMID23426671. https://pmc.ncbi.nlm.nih.gov/articles/PMC3865508/. "Drugs of abuse induce neuroplasticity in the natural reward pathway, specifically the nucleus accumbens (NAc), thereby causing development and expression of addictive behavior. ... Together, these findings demonstrate that drugs of abuse and natural reward behaviors act on common molecular and cellular mechanisms of plasticity that control vulnerability to drug addiction, and that this increased vulnerability is mediated by ΔFosB and its downstream transcriptional targets. ... Sexual behavior is highly rewarding (Tenk et al., 2009), and sexual experience causes sensitized drug-related behaviors, including cross-sensitization to amphetamine (Amph)-induced locomotor activity (Bradley and Meisel, 2001; Pitchers et al., 2010a) and enhanced Amph reward (Pitchers et al., 2010a). Moreover, sexual experience induces neural plasticity in the NAc similar to that induced by psychostimulant exposure, including increased dendritic spine density (Meisel and Mullins, 2006; Pitchers et al., 2010a), altered glutamate receptor trafficking, and decreased synaptic strength in prefrontal cortex-responding NAc shell neurons (Pitchers et al., 2012). Finally, periods of abstinence from sexual experience were found to be critical for enhanced Amph reward, NAc spinogenesis (Pitchers et al., 2010a), and glutamate receptor trafficking (Pitchers et al., 2012). These findings suggest that natural and drug reward experiences share common mechanisms of neural plasticity"
^ abc“Nucleus accumbens NMDA receptor activation regulates amphetamine cross-sensitization and deltaFosB expression following sexual experience in male rats”. Neuropharmacology101: 154–64. (February 2016). doi:10.1016/j.neuropharm.2015.09.023.
PMID26391065.
^“Prevalence of internet addiction and its association with stressful life events and psychological symptoms among adolescent internet users”. Addictive Behaviors39 (3): 744–747. (March 2014). doi:10.1016/j.addbeh.2013.12.010.
hdl:2436/622804.
PMID24388433.
^ ab“Internet addiction or excessive internet use”. The American Journal of Drug and Alcohol Abuse36 (5): 277–283. (September 2010). doi:10.3109/00952990.2010.491880.
PMID20545603.
^“Problematic usage among highly-engaged players of massively multiplayer online role playing games”. Cyberpsychology & Behavior11 (4): 481–484. (August 2008). doi:10.1089/cpb.2007.0140.
PMID18721098.
^“Risk factors associated with online game addiction: A hierarchical model” (英語). Computers in Human Behavior48: 706–713. (1 July 2015). doi:10.1016/j.chb.2015.02.008.
ISSN0747-5632.
^“BIS/BAS personality characteristics and college students' substance use”. Personality and Individual Differences40 (7): 1497–503. (2006). doi:10.1016/j.paid.2005.12.005.
^“Reward sensitivity and substance abuse in middle school and high school students”. J Genet Psychol168 (4): 465–69. (December 2007). doi:10.3200/GNTP.168.4.465-469.
PMID18232522.
^“Reinforcement sensitivity and maternal style as predictors of psychopathology”. Personality and Individual Differences42 (6): 1139–49. (April 2007). doi:10.1016/j.paid.2006.06.028.
^“The Stroop effect at 80: The competition between stimulus control and cognitive control”. J Exp Anal Behav105 (1): 3–13. (2016). doi:10.1002/jeab.194.
PMID26781048. "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."
^“Executive functions”. Annu Rev Psychol64: 135–68. (2013). doi:10.1146/annurev-psych-113011-143750. PMC4084861.
PMID23020641. https://pmc.ncbi.nlm.nih.gov/articles/PMC4084861/. "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 prefrontal cortex are the first to suffer, and suffer disproportionately, if something is not right in your life. They suffer first, and most, if you are stressed (Arnsten 1998, Liston et al. 2009, Oaten & Cheng 2005), sad (Hirt et al. 2008, von Hecker & Meiser 2005), lonely (Baumeister et al. 2002, Cacioppo & Patrick 2008, Campbell et al. 2006, Tun et al. 2012), sleep deprived (Barnes et al. 2012, Huang et al. 2007), or not physically fit (Best 2010, Chaddock et al. 2011, Hillman et al. 2008). Any of these can cause you to appear to have a disorder of EFs, such as ADHD, when you do not. You can see the deleterious effects of stress, sadness, loneliness, and lack of physical health or fitness at the physiological and neuroanatomical level in prefrontal cortex and at the behavioral level in worse EFs (poorer reasoning and problem solving, forgetting things, and impaired ability to exercise discipline and self-control). ... EFs can be improved (Diamond & Lee 2011, Klingberg 2010). ... At any age across the life cycle EFs can be improved, including in the elderly and in infants. There has been much work with excellent results on improving EFs in the elderly by improving physical fitness (Erickson & Kramer 2009, Voss et al. 2011) ... Inhibitory control (one of the core EFs) involves being able to control one's attention, behavior, thoughts, and/or emotions to override a strong internal predisposition or external lure, and instead do what's more appropriate or needed. Without inhibitory control we would be at the mercy of impulses, old habits of thought or action (conditioned responses), and/or stimuli in the environment that pull us this way or that. Thus, inhibitory control makes it possible for us to change and for us to choose how we react and how we behave rather than being unthinking creatures of habit. It doesn't make it easy. Indeed, we usually are creatures of habit and our behavior is under the control of environmental stimuli far more than we usually realize, but having the ability to exercise inhibitory control creates the possibility of change and choice. ... The subthalamic nucleus appears to play a critical role in preventing such impulsive or premature responding (Frank 2006)."
^ ab“Chapter 13: Higher Cognitive Function and Behavioral Control”. Molecular Neuropharmacology: A Foundation for Clinical Neuroscience (2nd ed.). New York: McGraw-Hill Medical. (2009). pp. 313–21.
ISBN978-0-07-148127-4. " • 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."
^ abcdefghijklmnop“Mechanisms of transgenerational inheritance of addictive-like behaviors”. Neuroscience264: 198–206. (2014). doi:10.1016/j.neuroscience.2013.07.064. PMC3872494.
PMID23920159. https://pmc.ncbi.nlm.nih.gov/articles/PMC3872494/. "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 a number of stimuli. Epigenetic mechanisms represent the key components by which the environment can influence genetics, and they provide the missing link between genetic heritability and environmental influences on the behavioral and physiological phenotypes of the offspring."
^ ab“A twin-family study of alcoholism in women”. The American Journal of Psychiatry151 (5): 707–715. (May 1994). doi:10.1176/ajp.151.5.707.
PMID8166312.
^“Brain Change in Addiction as Learning, Not Disease”. The New England Journal of Medicine379 (16): 1551–1560. (October 2018). doi:10.1056/NEJMra1602872.
PMID30332573. "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."
^ ab“Adverse Childhood Experiences”. samhsa.gov. Rockville, Maryland, United States: Substance Abuse and Mental Health Services Administration. 2016年10月9日時点のオリジナルよりアーカイブ。2016年9月26日閲覧。
^“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 Addictions25 (9A–10A): 1085–140. (1990). doi:10.3109/10826089109081039.
PMID2131328.
^ abcdefghij“Molecular neurobiology of addiction: what's all the (Δ)FosB about?”. Am. J. Drug Alcohol Abuse40 (6): 428–37. (November 2014). doi:10.3109/00952990.2014.933840.
PMID25083822. "ΔFosB is an essential transcription factor implicated in the molecular and behavioral pathways of addiction following repeated drug exposure. The formation of ΔFosB in multiple brain regions, and the molecular pathway leading to the formation of AP-1 complexes is well understood. The establishment of a functional purpose for ΔFosB has allowed further determination as to some of the key aspects of its molecular cascades[...]As a consequence of our improved understanding of ΔFosB in addiction, it is possible to evaluate the addictive potential of current medications (119), as well as use it as a biomarker for assessing the efficacy of therapeutic interventions (121,122,124). Some of these proposed interventions have limitations (125) or are in their infancy (75). However, it is hoped that some of these preliminary findings may lead to innovative treatments, which are much needed in addiction."
^ abcde“Epigenetic regulation in drug addiction”. Ann. Agric. Environ. Med.19 (3): 491–96. (2012).
PMID23020045. http://www.aaem.pl/fulltext.php?ICID=1010966. "[...]ΔFosB is considered a primary and causative transcription factor in creating new neural connections in the reward centre, prefrontal cortex, and other regions of the limbic system. This is reflected in the increased, stable and long-lasting level of sensitivity to cocaine and other drugs, and tendency to relapse even after long periods of abstinence."
^ abcde“Epigenetic mechanisms of drug addiction”. Neuropharmacology76 (Pt B): 259–68. (January 2014). doi:10.1016/j.neuropharm.2013.04.004. PMC3766384.
PMID23643695. https://pmc.ncbi.nlm.nih.gov/articles/PMC3766384/. "Short-term increases in histone acetylation generally promote behavioral responses to the drugs, while sustained increases oppose cocaine's effects, based on the actions of systemic or intra-NAc administration of HDAC inhibitors. ... Genetic or pharmacological blockade of G9a in the NAc potentiates behavioral responses to cocaine and opiates, whereas increasing G9a function exerts the opposite effect (Maze et al., 2010; Sun et al., 2012a). Such drug-induced downregulation of G9a and H3K9me2 also sensitizes animals to the deleterious effects of subsequent chronic stress (Covington et al., 2011). Downregulation of G9a increases the dendritic arborization of NAc neurons, and is associated with increased expression of numerous proteins implicated in synaptic function, which directly connects altered G9a/H3K9me2 in the synaptic plasticity associated with addiction (Maze et al., 2010). G9a appears to be a critical control point for epigenetic regulation in NAc, as we know it functions in two negative feedback loops. It opposes the induction of ΔFosB, a long-lasting transcription factor important for drug addiction (Robison and Nestler, 2011), while ΔFosB in turn suppresses G9a expression (Maze et al., 2010; Sun et al., 2012a). ... Also, G9a is induced in NAc upon prolonged HDAC inhibition, which explains the paradoxical attenuation of cocaine's behavioral effects seen under these conditions, as noted above (Kennedy et al., 2013). GABAA receptor subunit genes are among those that are controlled by this feedback loop. Thus, chronic cocaine, or prolonged HDAC inhibition, induces several GABAA receptor subunits in NAc, which is associated with increased frequency of inhibitory postsynaptic currents (IPSCs). In striking contrast, combined exposure to cocaine and HDAC inhibition, which triggers the induction of G9a and increased global levels of H3K9me2, leads to blockade of GABAA receptor and IPSC regulation."
^ abcd“Sex, drugs, and rock 'n' roll: hypothesizing common mesolimbic activation as a function of reward gene polymorphisms”. Journal of Psychoactive Drugs44 (1): 38–55. (2012). doi:10.1080/02791072.2012.662112. PMC4040958.
PMID22641964. https://pmc.ncbi.nlm.nih.gov/articles/PMC4040958/. "It has been found that deltaFosB gene in the NAc is critical for reinforcing effects of sexual reward. Pitchers and colleagues (2010) reported that sexual experience was shown to cause DeltaFosB accumulation in several limbic brain regions including the NAc, medial pre-frontal cortex, VTA, caudate, and putamen, but not the medial preoptic nucleus. Next, the induction of c-Fos, a downstream (repressed) target of DeltaFosB, was measured in sexually experienced and naive animals. The number of mating-induced c-Fos-IR cells was significantly decreased in sexually experienced animals compared to sexually naive controls. Finally, DeltaFosB levels and its activity in the NAc were manipulated using viral-mediated gene transfer to study its potential role in mediating sexual experience and experience-induced facilitation of sexual performance. Animals with DeltaFosB overexpression displayed enhanced facilitation of sexual performance with sexual experience relative to controls. In contrast, the expression of DeltaJunD, a dominant-negative binding partner of DeltaFosB, attenuated sexual experience-induced facilitation of sexual performance, and stunted long-term maintenance of facilitation compared to DeltaFosB overexpressing group. Together, these findings support a critical role for DeltaFosB expression in the NAc in the reinforcing effects of sexual behavior and sexual experience-induced facilitation of sexual performance. ... both drug addiction and sexual addiction represent pathological forms of neuroplasticity along with the emergence of aberrant behaviors involving a cascade of neurochemical changes mainly in the brain's rewarding circuitry."
^“Chapter 15: Reinforcement and addictive disorders”. Molecular Neuropharmacology: A Foundation for Clinical Neuroscience (2nd ed.). New York: McGraw-Hill Medical. (2009). pp. 384–85.
ISBN978-0-07-148127-4
^“Complex motor and sensorimotor functions of striatal and accumbens dopamine: involvement in instrumental behavior processes”. Psychopharmacology107 (2–3): 160–74. (1992). doi:10.1007/bf02245133.
PMID1615120.
^ ab“The neural basis of addiction: a pathology of motivation and choice”. The American Journal of Psychiatry162 (8): 1403–13. (August 2005). doi:10.1176/appi.ajp.162.8.1403.
PMID16055761.
^ abc“Dopamine in drug abuse and addiction: results of imaging studies and treatment implications”. Arch. Neurol.64 (11): 1575–79. (2007). doi:10.1001/archneur.64.11.1575.
PMID17998440.
^ abc“Review. Transcriptional mechanisms of addiction: role of DeltaFosB”. Philosophical Transactions of the Royal Society of London. Series B, Biological Sciences363 (1507): 3245–55. (October 2008). doi:10.1098/rstb.2008.0067. PMC2607320.
PMID18640924. https://pmc.ncbi.nlm.nih.gov/articles/PMC2607320/. "Recent evidence has shown that ΔFosB also represses the c-fos gene that helps create the molecular switch – from the induction of several short-lived Fos family proteins after acute drug exposure to the predominant accumulation of ΔFosB after chronic drug exposure – cited earlier (Renthal et al. in press). The mechanism responsible for ΔFosB repression of c-fos expression is complex and is covered below. ... Examples of validated targets for ΔFosB in nucleus accumbens ... GluR2 ... dynorphin ... Cdk5 ... NFκB ... c-Fos" Table 3
^ abcdef“From prediction error to incentive salience: mesolimbic computation of reward motivation”. Eur. J. Neurosci.35 (7): 1124–43. (April 2012). doi:10.1111/j.1460-9568.2012.07990.x. PMC3325516.
PMID22487042. https://pmc.ncbi.nlm.nih.gov/articles/PMC3325516/. "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."
^ abMolecular Neuropharmacology: A Foundation for Clinical Neuroscience (second ed.). New York: McGraw-Hill Medical. (2009). pp. 147–48, 366–67, 375–76.
ISBN978-0-07-148127-4. "VTA DA neurons play a critical role in motivation, reward-related behavior (Chapter 15), attention, and multiple forms of memory. This organization of the DA system, wide projection from a limited number of cell bodies, permits coordinated responses to potent new rewards. Thus, acting in diverse terminal fields, dopamine confers motivational salience ("wanting") on the reward itself or associated cues (nucleus accumbens shell region), updates the value placed on different goals in light of this new experience (orbital prefrontal cortex), helps consolidate multiple forms of memory (amygdala and hippocampus), and encodes new motor programs that will facilitate obtaining this reward in the future (nucleus accumbens core region and dorsal striatum). In this example, dopamine modulates the processing of sensorimotor information in diverse neural circuits to maximize the ability of the organism to obtain future rewards. ... The brain reward circuitry that is targeted by addictive drugs normally mediates the pleasure and strengthening of behaviors associated with natural reinforcers, such as food, water, and sexual contact. Dopamine neurons in the VTA are activated by food and water, and dopamine release in the NAc is stimulated by the presence of natural reinforcers, such as food, water, or a sexual partner. ... The NAc and VTA are central components of the circuitry underlying reward and memory of reward. As previously mentioned, the activity of dopaminergic neurons in the VTA appears to be linked to reward prediction. The NAc is involved in learning associated with reinforcement and the modulation of motoric responses to stimuli that satisfy internal homeostatic needs. The shell of the NAc appears to be particularly important to initial drug actions within reward circuitry; addictive drugs appear to have a greater effect on dopamine 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."
^ abcd“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. 223. (2016). pp. 63–76. doi:10.1016/bs.pbr.2015.07.005.
ISBN978-0-444-63545-7.
PMID26806771. "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)."
^American Psychiatric Association (2013年). “Substance-Related and Addictive Disorders”. American Psychiatric Publishing. pp. 1–2. 2015年8月15日時点のオリジナルよりアーカイブ。2023年4月8日閲覧。 “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.”
^“An international consensus for assessing internet gaming disorder using the new DSM-5 approach”. Addiction109 (9): 1399–406. (September 2014). doi:10.1111/add.12457.
PMID24456155.
^“Chapter 16: Reinforcement and Addictive Disorders”. Molecular Neuropharmacology: A Foundation for Clinical Neuroscience (3rd ed.). New York: McGraw-Hill Medical. (2015).
ISBN978-0-07-182770-6. "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."
^“Addiction as a Coping Response: Hyperkatifeia, Deaths of Despair, and COVID-19”. Am J Psychiatry177 (11): 1031–1037. (November 2020). doi:10.1176/appi.ajp.2020.20091375.
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^ abc“A comprehensive review of the psychometric properties of the Drug Abuse Screening Test”. Journal of Substance Abuse Treatment32 (2): 189–198. (March 2007). doi:10.1016/j.jsat.2006.08.002.
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^“Ultra-rapid screening for substance-use disorders: the Alcohol, Smoking and Substance Involvement Screening Test (ASSIST-Lite)”. Drug and Alcohol Dependence132 (1–2): 352–361. (September 2013). doi:10.1016/j.drugalcdep.2013.03.001.
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^Hatsukami, Dorothy K.; Rennard S; Jorenby D; Fiore M; Koopmeiners J; de Vos A; Horwith G; Pentel PR (2005). “Safety and immunogenicity of a nicotine conjugate vaccine in current smokers”. Clinical Pharmacology & Therapeutics78 (5): 456–467. doi:10.1016/j.clpt.2005.08.007.
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^“The neurocircuitry of illicit psychostimulant addiction: acute and chronic effects in humans”. Subst. Abuse Rehabil.4: 29–43. (February 2013). doi:10.2147/SAR.S39684. PMC3931688.
PMID24648786. https://pmc.ncbi.nlm.nih.gov/articles/PMC3931688/. "Initial drug use can be attributed to the ability of the drug to act as a reward (ie, a pleasurable emotional state or positive reinforcer), which can lead to repeated drug use and dependence.8,9 A great deal of research has focused on the molecular and neuroanatomical mechanisms of the initial rewarding or reinforcing effect of drugs of abuse. ... At present, no pharmacological therapy has been approved by the FDA to treat psychostimulant addiction. Many drugs have been tested, but none have shown conclusive efficacy with tolerable side effects in humans.172 ... A new emphasis on larger-scale biomarker, genetic, and epigenetic research focused on the molecular targets of mental disorders has been recently advocated.212 In addition, the integration of cognitive and behavioral modification of circuit-wide neuroplasticity (i.e., computer-based training to enhance executive function) may prove to be an effective adjunct-treatment approach for addiction, particularly when combined with cognitive enhancers.198,213–216 Furthermore, in order to be effective, all pharmacological or biologically based treatments for addiction need to be integrated into other established forms of addiction rehabilitation, such as CBT, individual and group psychotherapy, behavior-modification strategies, twelve-step programs, and residential treatment facilities."
^“Epidemiology of internet behaviors and addiction among adolescents in six Asian countries”. Cyberpsychology, Behavior and Social Networking17 (11): 720–728. (November 2014). doi:10.1089/cyber.2014.0139.
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^ abcdef“American Board of Medical Specialties recognizes the new subspecialty of addiction medicine”. American Board of Addiction Medicine (2016年3月14日). 2021年3月21日時点のオリジナルよりアーカイブ。2016年4月3日閲覧。 “Sixteen percent of the non-institutionalized U.S. population age 12 and over – more than 40 million Americans – meets medical criteria for addiction involving nicotine, alcohol or other drugs. This is more than the number of Americans with cancer, diabetes or heart conditions. In 2014, 22.5 million people in the United States needed treatment for addiction involving alcohol or drugs other than nicotine, but only 11.6 percent received any form of inpatient, residential, or outpatient treatment. Of those who do receive treatment, few receive evidence-based care. (There is no information available on how many individuals receive treatment for addiction involving nicotine.) Risky substance use and untreated addiction account for one-third of inpatient hospital costs and 20 percent of all deaths in the United States each year, and cause or contribute to more than 100 other conditions requiring medical care, as well as vehicular crashes, other fatal and non-fatal injuries, overdose deaths, suicides, homicides, domestic discord, the highest incarceration rate in the world and many other costly social consequences. The economic cost to society is greater than the cost of diabetes and all cancers combined. Despite these startling statistics on the prevalence and costs of addiction, few physicians have been trained to prevent or treat it.”
^ abc“A Major Step Forward for Addiction Medicine”. National Institute on Drug Abuse. National Institutes of Health (2016年3月31日). 2016年4月5日時点のオリジナルよりアーカイブ。2016年4月3日閲覧。 “Only about 10 percent of the 21 million Americans who meet the need for care for an alcohol or drug use disorder receive any form of treatment, and much of the treatment available does not meet standards for evidence-based care. There are many attitudinal and systemic reasons for this treatment gap, including stigma against treating people with addictions and institutional barriers to providing or funding addiction treatment. ... A major milestone was reached on March 14, 2016, when the American Board of Medical Specialties (ABMS) formally announced recognition of the field of Addiction Medicine as a medical subspecialty. ... In a statement issued to mark this milestone, ABAM President Robert J. Sokol summed up its significance: 'This landmark event, more than any other, recognizes addiction as a preventable and treatable disease, helping to shed the stigma that has long plagued it. It sends a strong message to the public that American medicine is committed to providing expert care for this disease and services designed to prevent the risky substance use that precedes it.'”
^“Barriers to enrollment in drug abuse treatment and suggestions for reducing them: opinions of drug injecting street outreach clients and other system stakeholders”. The American Journal of Drug and Alcohol Abuse30 (1): 129–153. (2004). doi:10.1081/ada-120029870.
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^“Do creative arts therapies reduce substance misuse? A systematic review”. The Arts in Psychotherapy57: 50–58. (February 2018). doi:10.1016/j.aip.2017.10.005.
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^“An evaluation study of art therapy provision in a residential Addiction Treatment Programme (ATP)”. International Journal of Art Therapy12 (1): 17–27. (June 2007). doi:10.1080/17454830701265220.
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^ abc“The Utility of the Formal Elements Art Therapy Scale in Assessment for Substance Use Disorder”. Art Therapy23 (3): 104–111. (January 2006). doi:10.1080/07421656.2006.10129625.
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^“Attachment theory as a working model for the therapist transitioning from early to later recovery substance abuse treatment”. The American Journal of Drug and Alcohol Abuse (Taylor & Francis) 22 (4): 533–547. (November 1996). doi:10.3109/00952999609001679.
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^ ab“Reducing Substance Use Related Stigma through Expressions of Artwork”. Journal of Alcohol & Drug Education (American Alcohol & Drug Information Foundation) 65 (1): 29–39. (April 2021).
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^“Alternative Paths: Mapping Addiction in Contemporary Art by Landon Mackenzie, Rebecca Belmore, Manasie Akpaliapik, and Ron Noganosh”. Journal of Canadian Studies (University of Toronto Press) 49 (2): 268–295, 356. (2015). doi:10.3138/jcs.49.2.268.
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^ ab“Voice: challenging the stigma of addiction; a nursing perspective”. The International Journal on Drug Policy19 (3): 214–219. (June 2008). doi:10.1016/j.drugpo.2008.02.011.
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^“Changes in Drinking Patterns in Bolivian Cultures: A Cautionary Tale About Historical Approaches” (英語). Addiction Research2 (3): 307–318. (January 1995). doi:10.3109/16066359509005215.
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ISBN978-0-07-148127-4. "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."
Category:依存症
