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成癮（英語：addiction）是指一種重複性的強迫行為，即使這些行為已知可能造成不良後果的情形下，仍然被持續重複[5]。這種行為可能因中樞神經系統功能失調造成，重複這些行為也可以反過來造成神經功能受損[6]。
More information 成癮 Addiction, 類型 ...
成癮
Addiction |
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 | | Brain positron emission tomography images that compare brain metabolism in a healthy individual and a cocaine addict | | 類型 | 行為、健康問題[*]、習慣 |
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| 醫學專科 | 成癮精神病學
成癮醫學 |
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| [編輯此條目的維基數據] |
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| 「成癮及生理、心理依賴」的相關術語詞彙表[1][2][3][4] |
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- 成癮：腦部失調的情形，特徵是會強迫性的接觸犒賞刺激，不去考慮其帶來的負面結果。
- 成癮行為：具有犒賞性及正向增強效應的行為
- 成癮藥物：具有犒賞性及正向增強效應的藥物
- 依賴性：之前曾頻繁接觸刺激源（例如藥物攝取），中斷接觸後出現戒斷症狀的情形
- 藥物敏化或逆耐藥性：在固定藥物劑量的情形下重複給藥，而相同劑量的藥物效果增強的情形
- 藥物戒斷：在重複藥物使用後停藥，出現的症狀
- 生理依賴：出現持續生理戒斷症狀（例如疲勞及震顫性譫妄）的依賴性
- 心理依賴：出現情緒或是精神戒斷症狀（例如煩躁及失樂）的依賴性
- 增強刺激：特定類型的刺激，接觸後會增加再接觸此刺激的可能性
- 犒賞刺激：特定類型的刺激，大腦會認為此刺激是正向的，會想再進行的
- 敏化作用：重複接受某一刺激後產生的刺激增強性反應
- 物質使用疾患 ：使用特定物質，而且造成臨床上或是功能上的損傷或是困境的情形
- 藥物耐受性：重複接受某一藥物後產生的藥物降低性反應
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癮可用於描述生理依賴或者過度的心理依賴，例如物質依賴，藥物濫用（即俗稱的濫藥、毒癮）、酒癮、煙癮、性成癮。或是持續出現特定行為（賭、暴食），網路成癮症、賭癮、官癮、財迷、工作狂、暴食症、跟蹤狂、偷竊狂、整形迷戀、購物狂甚至戀物癖等，是生理或者心理上，甚至是同時具備的一種依賴症。
癮有分為物質成癮及行為成癮，行為成癮是和物質無關的強迫症，如賭癮和網癮。在這幾種通常的用法中，癮是描述一種某人高頻率反覆從事可能對其身心健康和社交生活有害的活動的一種強迫行為。而精神疾病診斷與統計手冊的第五版DSM-5中有將賭癮（gambling disorder）列入[7]。有時成癮（addiction）會和物質依賴（substance dependence）混淆[8]。兩者主要的不同是：物質依賴者在中斷物質使用後，會出現戒斷症狀，甚至造成更多的使用該物質，而成癮是強制性的攝取某種物質或從事特定行為，不一定有戒斷症狀。
物質成癮會對個人和社會帶來顯著的影響，包括成癮物質帶來的直接影響、伴隨的醫療費用、長期的併發症（例如吸煙可能造成的肺癌、酒癮可能會有的肝硬化、靜脈注射甲基苯丙胺會出現的冰毒嘴症狀）、神經可塑性（因為經驗原因引起大腦結構的改變）帶來的影響、以及後續生產力的下降[9][10][11]。成癮的典型現象包括對於物質或是行為的無法控制及過度關注，雖然有不良結果，卻仍然繼續攝取成癮物質或從事特定行為的情形[12]。伴隨著成癮的習慣或是行為模式通常是立即性的滿足（短期回報）及延遲出現的不良影響（長期不良結果）[13]。
有時在口語上，癮也用於指某些人的一些癖好，例如讀書、收集（集郵）、看電視、玩遊戲、購物、工作、上網、運動及進食等。不過在本條目中，癮主要是被用於濫用藥物和物質濫用問題，也就是有生理依賴或者過度心理依賴的行為。
醫學上，成癮是腦中犒賞系統在基因轉錄及表觀遺傳機制上出現的失調，成癮有許多心理上的原因，但依生理來說，是在長期暴露在高度的成癮刺激原（addictive stimulus，例如嗎啡、可卡因、性交、賭博等）後出現的情形[2][14][15]。重複暴露在成癮刺激原是主要導致成癮以及維持成癮現象的主要病理因素[2][16]。成癮刺激原有二個特性，一個是其正向增強（接觸後會增加再去進行類似行為的可能性），另一個是內在犒賞（認為此物質或是行為有趣、會想要再去進行）[2][3][17]。
轉錄因子ΔFosB是各種成癮（行為成癮或物質成癮）發展中的關鍵成份及共同因素[14][15][18][19]。二十多年針對ΔFosB在成癮當中的研究，結果指出成癮的出現以及伴隨的強迫行為加劇或減弱，都和伏隔核中D1型中度多刺神經元中ΔFosB的基因過度表現（genetic overexpression）有關[2][14][15][18]。因為ΔFosB基因表現與成癮之間有因果關係，ΔFosB在臨床前研究中常作為成癮的生物標記[2][14][18]。ΔFosB在這些神經元的表現一方面會直接調高藥物Self-administration及犒賞敏感度，也會透過正增強達到這些效果，另一方面也會降低對厭惡（aversion）的敏感度[note 1][2][14]。
腹側被蓋區被認為與神經生物學理論中的成癮現象有關。[20][21]
診斷藥物成癮可診斷為生理成癮、成癮有增加或減退跡象、和沒有成癮。DSM-IV中介紹的包括：
因為文化的不同，特定時間內出現藥物成癮或是行為成癮的比例（即患病率）會隨時代及國家而不同，也會因為年齡層、社會經濟地位等人口學資料而不同[22]。澳洲2009年的藥物濫用患病率為5.1%[23]。依照美國2011年在青少年中抽樣的結果來看，其酒癮及非法藥物濫用的lifetime prevalence（個體從出生後，一直到接受抽樣之前，曾出現過的比例）分別是8%及2-3%[10]。
降低對厭惡的敏感度，簡單來說，就是讓個人的行為比較不會被其不想要的負面結果而影，比較不因為有可能負面結果而不去做該行為
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]. （原始內容存檔 (PDF)於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 (編). 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 （頁面存檔備份，存於網際網路檔案館）" 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.
