成癮

成癮（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。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。
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Behavioral addiction，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。有時成癮（addiction）會和物質依賴（substance dependence）混淆。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meth mouth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。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。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）。
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。

**醫學觀點**
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. ...ConclusionsΔFosB 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. Table 1: Summary of plasticity observed following exposure to drug or natural reinforcers date=20210809043020 "。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。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）。
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。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。因為ΔFosB基因表現與成癮之間有因果關係，ΔFosB在preclinical research中常作為成癮的生物標記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. ...ConclusionsΔFosB 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.。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name="ΔFosB behaviors"。
腹側被蓋區被認為與神經生物學理論中的成癮現象有關。

**藥物成癮**
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：
*303.90 酒精依賴
*304.00 鴉片依賴
*304.10 鎮靜劑依賴、催眠藥依賴、或抗焦慮藥依賴（包括苯二氮平類藥物成癮和巴比妥依賴）
*304.20 可卡因依賴
*304.30 大麻依賴
*304.40 安非他命依賴（或似安非他命類）
*304.50 致幻劑依賴
*304.60 Inhalant依賴
*304.80 多種物質依賴
*304.90 苯環利定（或似苯環利定類）依賴
*304.90 其他（或未知）物質依賴
*305.10 尼古丁依賴

**流行病學**
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。澳洲2009年的藥物濫用患病率為5.1%。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%。

**參見**
 毒品- 吸菸- 酗酒- 檳榔- 賭博- 性成癮- 網絡成癮症- 精神鴉片- 匿名戒酒會- 理性成癮- 固著

**腳註**

**參考資料**

**外部連結**
 臺灣成癮科學學會 date=20201104051416