“
上瘾”重定向至此。关于2016年中国大陆同志题材网络剧集，请见“
上瘾 (网络剧)”。
维基百科中的医学内容
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医学声明。
成瘾（英语：addiction）是指一种重复性的强迫行为，即使这些行为已知可能造成不良后果的情形下，仍然被持续重复[5]。这种行为可能因中枢神经系统功能失调造成，重复这些行为也可以反过来造成神经功能受损[6]。
More information 成瘾 Addiction, 类型 ...
成瘾
Addiction |
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 | | Brain positron emission tomography images that compare brain metabolism in a healthy individual and a cocaine addict | | 类型 | 行为、健康问题[*]、习惯 |
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| 医学专科 | 成瘾精神病学
成瘾医学 |
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| “成瘾及生理、心理依赖”的相关术语词汇表[1][2][3][4] |
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- 成瘾：脑部失调的情形，特征是会强迫性的接触犒赏刺激，不去考虑其带来的负面结果。
- 成瘾行为：具有犒赏性及正向增强效应的行为
- 成瘾药物：具有犒赏性及正向增强效应的药物
- 依赖性：之前曾频繁接触刺激源（例如药物摄取），中断接触后出现戒断症状的情形
- 药物敏化或逆耐药性：在固定药物剂量的情形下重复给药，而相同剂量的药物效果增强的情形
- 药物戒断：在重复药物使用后停药，出现的症状
- 生理依赖：出现持续生理戒断症状（例如疲劳及震颤性谵妄）的依赖性
- 心理依赖：出现情绪或是精神戒断症状（例如烦躁及失乐）的依赖性
- 增强刺激：特定类型的刺激，接触后会增加再接触此刺激的可能性
- 犒赏刺激：特定类型的刺激，大脑会认为此刺激是正向的，会想再进行的
- 敏化作用：重复接受某一刺激后产生的刺激增强性反应
- 物质使用疾患 ：使用特定物质，而且造成临床上或是功能上的损伤或是困境的情形
- 药物耐受性：重复接受某一药物后产生的药物降低性反应
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瘾可用于描述生理依赖或者过度的心理依赖，例如物质依赖，药物滥用（即俗称的滥药、毒瘾）、酒瘾、烟瘾、性成瘾。或是持续出现特定行为（赌、暴食），网络成瘾症、赌瘾、官瘾、财迷、工作狂、暴食症、跟踪狂、偷窃狂、整形迷恋、购物狂甚至恋物癖等，是生理或者心理上，甚至是同时具备的一种依赖症。
瘾有分为物质成瘾及行为成瘾，行为成瘾是和物质无关的强迫症，如赌瘾和网瘾。在这几种通常的用法中，瘾是描述一种某人高频率反复从事可能对其身心健康和社交生活有害的活动的一种强迫行为。而精神疾病诊断与统计手册的第五版DSM-5中有将赌瘾（gambling disorder）列入[7]。有时成瘾（addiction）会和物质依赖（substance dependence）混淆[8]。两者主要的不同是：物质依赖者在中断物质使用后，会出现戒断症状，甚至造成更多的使用该物质，而成瘾是强制性的摄取某种物质或从事特定行为，不一定有戒断症状。
物质成瘾会对个人和社会带来显著的影响，包括成瘾物质带来的直接影响、伴随的医疗费用、长期的并发症（例如吸烟可能造成的肺癌、酒瘾可能会有的肝硬化、静脉注射甲基苯丙胺会出现的冰毒嘴症状）、神经可塑性（因为经验原因引起大脑结构的改变）带来的影响、以及后续生产力的下降[9][10][11]。成瘾的典型现象包括对于物质或是行为的无法控制及过度关注，虽然有不良结果，却仍然继续摄取成瘾物质或从事特定行为的情形[12]。伴随着成瘾的习惯或是行为模式通常是立即性的满足（短期回报）及延迟出现的不良影响（长期不良结果）[13]。
有时在口语上，瘾也用于指某些人的一些癖好，例如读书、收集（集邮）、看电视、玩游戏、购物、工作、上网、运动及进食等。不过在本条目中，瘾主要是被用于滥用药物和物质滥用问题，也就是有生理依赖或者过度心理依赖的行为。
医学上，成瘾是脑中犒赏系统在基因转录及表观遗传机制上出现的失调，成瘾有许多心理上的原因，但依生理来说，是在长期暴露在高度的成瘾刺激原（addictive stimulus，例如吗啡、可卡因、性交、赌博等）后出现的情形[2][14][15]。重复暴露在成瘾刺激原是主要导致成瘾以及维持成瘾现象的主要病理因素[2][16]。成瘾刺激原有二个特性，一个是其正向增强（接触后会增加再去进行类似行为的可能性），另一个是内在犒赏（认为此物质或是行为有趣、会想要再去进行）[2][3][17]。
转录因子ΔFosB是各种成瘾（行为成瘾或物质成瘾）发展中的关键成分及共同因素[14][15][18][19]。二十多年针对ΔFosB在成瘾当中的研究，结果指出成瘾的出现以及伴随的强迫行为加剧或减弱，都和伏隔核中D1型中度多刺神经元中ΔFosB的基因过度表现（genetic overexpression）有关[2][14][15][18]。因为ΔFosB基因表现与成瘾之间有因果关系，ΔFosB在临床前研究中常作为成瘾的生物标记[2][14][18]。ΔFosB在这些神经元的表现一方面会直接调高药物Self-administration及犒赏敏感度，也会透过正增强达到这些效果，另一方面也会降低对厌恶（aversion）的敏感度[note 1][2][14]。
腹侧被盖区被认为与神经生物学理论中的成瘾现象有关。[20][21]
诊断药物成瘾可诊断为生理成瘾、成瘾有增加或减退迹象、和没有成瘾。DSM-IV中介绍的包括：
因为文化的不同，特定时间内出现药物成瘾或是行为成瘾的比例（即患病率）会随时代及国家而不同，也会因为年龄层、社会经济地位等人口学资料而不同[22]。澳洲2009年的药物滥用患病率为5.1%[23]。依照美国2011年在青少年中抽样的结果来看，其酒瘾及非法药物滥用的lifetime prevalence（个体从出生后，一直到接受抽样之前，曾出现过的比例）分别是8%及2-3%[10]。
降低对厌恶的敏感度，简单来说，就是让个人的行为比较不会被其不想要的负面结果而影，比较不因为有可能负面结果而不去做该行为
Glossary. Icahn School of Medicine. [2021-04-29]. American Psychiatric Association. Substance-Related and Addictive Disorders (PDF). American Psychiatric Publishing: 1–2. 2013 [10 July 2015]. （原始内容存档 (PDF)于2015-08-15）. 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.
Malenka RC, Nestler EJ, Hyman SE. Chapter 1: Basic Principles of Neuropharmacology. Sydor A, Brown RY (编). Molecular Neuropharmacology: A Foundation for Clinical Neuroscience 2nd. New York: McGraw-Hill Medical. 2009: 4. ISBN 9780071481274. 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.
Morse RM, Flavin DK. The definition of alcoholism. The Joint Committee of the National Council on Alcoholism and Drug Dependence and the American Society of Addiction Medicine to Study the Definition and Criteria for the Diagnosis of Alcoholism. JAMA. August 1992, 268 (8): 1012–4. PMID 1501306. doi:10.1001/jama.1992.03490080086030. Ruffle JK. Molecular neurobiology of addiction: what's all the (Δ)FosB about?. Am. J. Drug Alcohol Abuse. November 2014, 40 (6): 428–437. PMID 25083822. doi:10.3109/00952990.2014.933840.
The strong correlation between chronic drug exposure and ΔFosB provides novel opportunities for targeted therapies in addiction (118), and suggests methods to analyze their efficacy (119). Over the past two decades, research has progressed from identifying ΔFosB induction to investigating its subsequent action (38). It is likely that ΔFosB research will now progress into a new era – the use of ΔFosB as a biomarker. ...
Conclusions
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, involving effectors such as GluR2 (87,88), Cdk5 (93) and NFkB (100). Moreover, many of these molecular changes identified are now directly linked to the structural, physiological and behavioral changes observed following chronic drug exposure (60,95,97,102). New frontiers of research investigating the molecular roles of ΔFosB have been opened by epigenetic studies, and recent advances have illustrated the role of ΔFosB acting on DNA and histones, truly as a ‘‘molecular switch’’ (34). As a consequence of our improved understanding of ΔFosB in addiction, it is possible to evaluate the addictive potential of current medications (119), as well as use it as a biomarker for assessing the efficacy of therapeutic interventions (121,122,124). Some of these proposed interventions have limitations (125) or are in their infancy (75). However, it is hoped that some of these preliminary findings may lead to innovative treatments, which are much needed in addiction.
Olsen CM. Natural rewards, neuroplasticity, and non-drug addictions. Neuropharmacology. December 2011, 61 (7): 1109–1122. PMC 3139704 
. PMID 21459101. doi:10.1016/j.neuropharm.2011.03.010. Functional neuroimaging studies in humans have shown that gambling (Breiter et al, 2001), shopping (Knutson et al, 2007), orgasm (Komisaruk et al, 2004), playing video games (Koepp et al, 1998; Hoeft et al, 2008) and the sight of appetizing food (Wang et al, 2004a) activate many of the same brain regions (i.e., the mesocorticolimbic system and extended amygdala) as drugs of abuse (Volkow et al, 2004). ... Cross-sensitization is also bidirectional, as a history of amphetamine administration facilitates sexual behavior and enhances the associated increase in NAc DA ... As described for food reward, sexual experience can also lead to activation of plasticity-related signaling cascades. The transcription factor delta FosB is increased in the NAc, PFC, dorsal striatum, and VTA following repeated sexual behavior (Wallace et al., 2008; Pitchers et al., 2010b). This natural increase in delta FosB or viral overexpression of delta FosB within the NAc modulates sexual performance, and NAc blockade of delta FosB attenuates this behavior (Hedges et al, 2009; Pitchers et al., 2010b). Further, viral overexpression of delta FosB enhances the conditioned place preference for an environment paired with sexual experience (Hedges et al., 2009). ... In some people, there is a transition from "normal" to compulsive engagement in natural rewards (such as food or sex), a condition that some have termed behavioral or non-drug addictions (Holden, 2001; Grant et al., 2006a). ... In humans, the role of dopamine signaling in incentive-sensitization processes has recently been highlighted by the observation of a dopamine dysregulation syndrome in some patients 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 （页面存档备份，存于互联网档案馆）" Taylor SB, Lewis CR, Olive MF. The neurocircuitry of illicit psychostimulant addiction: acute and chronic effects in humans. Subst. Abuse Rehabil. February 2013, 4: 29–43. PMC 3931688 . PMID 24648786. doi:10.2147/SAR.S39684. 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 (ie, 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 cognitive behavioral therapy, individual and group psychotherapy, behavior-modification strategies, twelve-step programs, and residential treatment facilities.
Biliński P, Wojtyła A, Kapka-Skrzypczak L, Chwedorowicz R, Cyranka M, Studziński T. Epigenetic regulation in drug addiction. Ann. Agric. Environ. Med. 2012, 19 (3): 491–496. PMID 23020045. For these reasons, ΔFosB is considered a primary and causative transcription factor in creating new neural connections in the reward centre, prefrontal cortex, and other regions of the limbic system. This is reflected in the increased, stable and long-lasting level of sensitivity to cocaine and other drugs, and tendency to relapse even after long periods of abstinence. These newly constructed networks function very efficiently via new pathways as soon as drugs of abuse are further taken ... In this way, the induction of CDK5 gene expression occurs together with suppression of the G9A gene coding for dimethyltransferase acting on the histone H3. A feedback mechanism can be observed in the regulation of these 2 crucial factors that determine the adaptive epigenetic response to cocaine. This depends on ΔFosB inhibiting G9a gene expression, i.e. H3K9me2 synthesis which in turn inhibits transcription factors for ΔFosB. For this reason, the observed hyper-expression of G9a, which ensures high levels of the dimethylated form of histone H3, eliminates the neuronal structural and plasticity effects caused by cocaine by means of this feedback which blocks ΔFosB transcription
Robison AJ, Nestler EJ. Transcriptional and epigenetic mechanisms of addiction. Nat. Rev. Neurosci. November 2011, 12 (11): 623–637. PMC 3272277 . PMID 21989194. doi:10.1038/nrn3111. 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 also 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.
