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成?

?基百科，自由的百科全?
   「 上? 」重定向至此。?于2016年中?大?同志?材???集，??「 上? (網路劇) 」。
?基百科 中的醫學?容 ?供?考 ，? 不能 視作專業意見。如需獲取醫療?助或意見，?咨???人士。詳見 醫學聲明 。
成?
Addiction
Brain positron emission tomography images that compare brain metabolism in a healthy individual and a cocaine addict
?型 行? 、 健康問題 [*] 、 ??
分?和外部?源
醫學專科 成?精神病學 （ 英? ： Addiction psychiatry ）
成?醫學 （ 英? ： Addiction medicine ）
[ ??此?目的?基?据 ]
「成?及生理、心理依賴」的相關術語詞彙表 [1] [2] [3] [4]
  • 成? ： 腦部失調 的情形，特徵是會?迫性的接觸?? 刺激 ，不去考慮其帶來的負面結果。
  • 成?行? ：具有??性及正向增?效應的行?
  • 成??物 ：具有??性及正向增?效應的藥物
  • 依?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
  • ?物敏化 或 逆耐?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?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? ：出現持續生理戒斷症狀（例如疲勞及 震顫性?妄 ）的依?性
  • 心理依? ：出現情?或是精神戒斷症狀（例如 煩躁 及 失? ）的依?性
  • 增强刺激 ：特定類型的刺激，接觸後會增加再接觸此刺激的可能性
  • ??刺激 ：特定類型的刺激，大腦會認?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?生的刺激增?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?生的藥物降低性反應

成? （英語： addiction ）是指一種重複性的 ?迫行? ，?使這些行?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?可能因中樞神經系統功能失調造成，重複這些行?也可以反過來造成神經功能受損 [6] 。 ? 可用于描述生理依賴或者?度的心理依?，例如 物質依賴 ， ?物?用 （?俗?的 ?? 、 毒 ?）、 酒? 、 烟 ?、 性成? 。或是持續出現特定行?（?、暴食）， 網路成?症 、 ?? 、 官 ?、?迷、 工作狂 、 暴食症 、 ??狂 、 ??狂 、 整形 迷?、 ?物狂 、 發表廢文 [來源請求] 甚至 ?物癖 等，是 生理 或者 心理 上，甚至是同時具?的一?依?症。

?有分?物質成?及 行?成? （ 英? ： Behavioral addiction ） ，行?成?是和物?无?的强迫症，如??和??。在???通常的用法中，?是描述一?某人高?率反??事可能?其身心健康和社交生活有害的活?的一? 强迫行? 。而 精神疾病診斷與統計手冊 的第五版 DSM-5 中有將 ?? （gambling disorder）列入 [7] 。有時成?（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?是?制性的攝取某種物質或從事特定行?，不一定有戒斷症狀。

物質成?會對個人和社會帶來顯著的影響，包括成?物質帶來的直接影響、伴隨的醫療費用、長期的?發症（例如吸煙可能造成的 肺癌 、酒?可能會有的 肝硬化 、靜脈注射甲基?丙?會出現的 ?毒嘴 （ 英? ： meth mouth ） 症狀）、 神?可塑性 （因?經驗原因引起大腦結構的改變）帶來的影響、以及後續生?力的下降 [9] [10] [11] 。成?的典型現象包括對於物質或是行?的無法控制及過度關注，雖然有不良結果，?仍然繼續攝取成?物質或從事特定行?的情形 [12] 。伴隨著成?的習慣或是行?模式通常是立?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?在口?上，?也用于指某些人的一些癖好，例如??、收集（集?）、看??、 玩游? 、?物、工作、上?、??及?食等。不過在本?目中，?主要是被用于 ?用?物 和物??用??，也就是有生理依賴或者?度心理依?的行?。

醫學觀點 [ ?? ]

??上，成?是腦中 ?賞系統 在基因 ?? 及 表觀遺傳 機制上出現的失調，成?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?刺激原（addictive stimulus，例如??、可?因、性交、賭博等）後出現的情形 [2] [14] [15] 。重複暴露在成?刺激原是主要導致成?以及維持成?現象的主要病理因素 [2] [16] 。成?刺激原有二個特性，一個是其 正向增? （接觸後會增加再去進行類似行?的可能性），?一個是 內在?賞 （認?此物質或是行?有趣、會想要再去進行） [2] [3] [17] 。

??因子 ΔFosB 是各種成?（行?成?或物質成?）發展中的關鍵成?及共同因素 [14] [15] [18] [19] 。二十多年針對ΔFosB在成?當中的?究，結果指出成?的出現以及伴隨的强迫行?加?或?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?ΔFosB基因表現與成?之間有因果關係，ΔFosB在 臨床前?究 （ 英? ： preclinical research ） 中常作?成?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 （ 英? ： Self-administration ） 及?賞敏感度，也會透過正增?達到這些效果，?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?與 神經生物學 理論中的 成? 現象有關。 [20] [21]

藥物成? [ ?? ]

主?目： 物質依賴

診斷藥物成?可診斷?生理成?、成?有增加或減退跡象、和沒有成?。 DSM-IV 中介紹的包括：

流行病學 [ ?? ]

因?文化的不同，特定時間內出現藥物成?或是行?成?的比例（? 患病率 ）會隨時代及國家而不同，也會因?年齡層、社會經濟地位等 人口? 資料而不同 [22] 。澳洲2009年的藥物濫用 患病率 ?5.1% [23] 。依照美國2011年在?少年中 抽樣 的結果來看，其酒?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] 。

?? [ ?? ]

?註 [ ?? ]

  1. ^ 降低對厭惡的敏感度，簡單來說，就是讓個人的行?比較不會被其不想要的負面結果而影，比較不因?有可能負面結果而不去做該行?

參考資料 [ ?? ]

  1. ^ Nestler, Eric J.; Malenka, Robert C. Chapter 15: Reinforcement and Addictive Disorders. Molecular neuropharmacology : a foundation for clinical neuroscience 2nd. New York: McGraw-Hill Medical. 2009: 364?375. ISBN  978-0-07-164119-7 . OCLC 273018757 .  
  2. ^ 2.0 2.1 2.2 2.3 2.4 2.5 2.6 Nestler, Eric J. Cellular basis of memory for addiction . Dialogues in Clinical Neuroscience. 2013-12, 15 (4): 431?443. ISSN 1294-8322 . PMC 3898681   可免费查阅. PMID 24459410 . doi:10.31887/DCNS.2013.15.4/enestler .  
  3. ^ 3.0 3.1 Glossary . Icahn School of Medicine. [ 2021-04-29 ] .  
  4. ^ Volkow, Nora D.; Koob, George F.; McLellan, A. Thomas. Longo, Dan L. , ?. Neurobiologic Advances from the Brain Disease Model of Addiction . New England Journal of Medicine. 2016-01-28, 374 (4): 363?371. ISSN 0028-4793 . PMC 6135257   可免费查阅. PMID 26816013 . doi:10.1056/NEJMra1511480 （英?） .  
  5. ^ Angres DH, Bettinardi-Angres K. The disease of addiction: origins, treatment, and recovery. Dis Mon. October 2008, 54 (10): 696?721. PMID 18790142 . doi:10.1016/j.disamonth.2008.07.002 .  
  6. ^ American Society for Addiction Medicine. Definition of Addiction . 2012 [ 2013-06-25 ] . （原始?容 存? 于2018-06-14）.  
  7. ^ Clinical and Research Implications of Gambling Disorder in DSM-5 . [ 2017-05-04 ] . （原始?容 存? 于2021-08-09）.  
  8. ^ American Psychiatric Association. Substance-Related and Addictive Disorders (PDF) . American Psychiatric Publishing: 1?2. 2013 [ 10 July 2015] . （原始?容 存? (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.  
  9. ^ Malenka RC, Nestler EJ, Hyman SE. Chapter 1: Basic Principles of Neuropharmacology. Sydor A, Brown RY (?). 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.  
  10. ^ 10.0 10.1 KR Merikangas KR, McClair VL. Epidemiology of Substance Use Disorders . Hum. Genet. June 2012, 131 (6): 779?789. PMC 4408274   可免费查阅. PMID 22543841 . doi:10.1007/s00439-012-1168-0 .  
  11. ^ AMERICAN BOARD OF MEDICAL SPECIALTIES RECOGNIZES THE NEW SUBSPECIALTY OF ADDICTION MEDICINE (PDF) . American Board of Addiction Medicine. 14 March 2016 [ 3 April 2016] . （原始?容 存? (PDF) 于2021-03-21）.  
  12. ^ 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 .  
  13. ^ Marlatt GA, Baer JS, Donovan DM, Kivlahan DR. Addictive behaviors: etiology and treatment . Annu Rev Psychol. 1988, 39 : 223?52. PMID 3278676 . doi:10.1146/annurev.ps.39.020188.001255 .  
  14. ^ 14.0 14.1 14.2 14.3 14.4 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.      
  15. ^ 15.0 15.1 15.2 Olsen CM. Natural rewards, neuroplasticity, and non-drug addictions . Neuropharmacology. December 2011, 61 (7): 1109?1122. PMC 3139704   可免费查阅. 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 （ ?面存??? ，存于 互???案? ）"
  16. ^ American Society for Addiction Medicine. Definition of Addiction . 2012 [ 2013-06-25 ] . （原始?容 存? 于2018-06-14）.  
  17. ^ 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   可免费查阅. 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.  
  18. ^ 18.0 18.1 18.2 Bili?ski P, Wojtyła A, Kapka-Skrzypczak L, Chwedorowicz R, Cyranka M, Studzi?ski 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  
  19. ^ Robison AJ, Nestler EJ. Transcriptional and epigenetic mechanisms of addiction . Nat. Rev. Neurosci. November 2011, 12 (11): 623?637. PMC 3272277   可免费查阅. 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 exposure 14,22?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 consumption 14,26?30 . This implicates ΔFosB in the regulation of natural rewards under normal conditions and perhaps during pathological addictive-like states.  
  20. ^ 2050科幻大成?：超能力、心智控制、人造記憶、遺忘藥丸、奈米機器人，?將改變我們的世界 . 博客來: 187. [ 2018-12-23 ] . （原始?容 存? 于2021-01-25）.  
  21. ^ 國外的一些?究機構來告訴?，毒品是??樣?掉?一生的 . 9900 新聞頻道 - 9900 台灣網站導航. [ 2018-12-23 ] . （原始?容 存? 于2021-08-09）.  
  22. ^ Vassoler FM, Sadri-Vakili G. Mechanisms of transgenerational inheritance of addictive-like behaviors . Neuroscience. 2014, 264 : 198?206. PMC 3872494   可免费查阅. PMID 23920159 . doi:10.1016/j.neuroscience.2013.07.064 . The environment also 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.  
  23. ^ Slade, T.; Johnston, A.; Teesson, M.; Whiteford, H.; Burgess, P.; Pirkis, J.; Saw, S. The Mental Health of Australians 2: Substance Use Disorders in Australia (PDF) . Department of Health and Ageing, Canberra. May 2009 [ 2017-05-02 ] . （原始?容 存? (PDF) 于2020-08-18）.  

外部連結 [ ?? ]

增? 症候群： 成? 和 物質依賴
成?
藥物
細胞的機制(機轉)
（ 粗體 表示?關鍵致?因子）
物質依賴
?念
症候群
參見
基?科?
臨床神經科學 （ 英? ： Clinical neuroscience ）
認知神經科學
跨領域
?念
取自“ https://zh.wikipedia.org/w/index.php?title=成?&oldid=81870411 ”