2024-05-14

탐닉 - 위키백과, 嗜癖（しへき、英: addiction、アディクション）

탐닉 - 위키백과, 우리 모두의 백과사전


탐닉

위키백과, 우리 모두의 백과사전.

탐닉 및 의존증 관련 용어[1][2][3][4]
• 탐닉addiction보수자극과 관련되어 부정적 결과에도 불구하고 충동적 행동을 하는 것으로 특징지어지는 뇌기능 장애
• 탐닉성 행동addictive behavior보상과 보강 작용을 동시에 일으키는 행동
• 탐닉성 약물addictive drug보상과 보강 작용을 동시에 일으키는 약물
• 의존dependence자극에 대한 지속적 자극을 중단할 경우 금단증후군을 동반하는 적응 상태
• 내성tolerance약물을 정량 반복적으로 사용했을 때 효과가 감소하는 것
• 역내성reverse tolerance약물을 정량 반복적으로 사용했을 때 효과가 증가하는 것
• 약물 금단drug withdrawal약물의 반복적 사용을 중단했을 때 나타나는 증상
• 신체의존physical dependence지속적인 육체적 금단증상(피로감, 섬망 등)을 나타내는 의존
• 심리의존psychological dependence심리정신적 금단증상(불쾌감, 무쾌감 등)을 나타내는 의존
• 보강자극reinforcing stimuli자극을 받으면 행동을 반복할 가능성을 증가시키는 자극
• 보수자극rewarding stimuli뇌가 본질적으로 긍정적이고 욕망하고자 하는 것으로 받아들이는 자극
• 민감화sensitization자극에 반복적으로 노출됨으로써 자극에 대한 반응이 증폭되는 것
• 약물사용장애substance use disorder약물을 사용함으로써 임상적 기능적으로 심각한 해로움이나 고통을 유발하는 상태
(편집 | 역사)

탐닉(耽溺, addiction)[5]은 부정적 결과에도 불구하고 보수계 자극의 충동적 작용을 거듭하는 것으로 특징지어지는 뇌기능 장애다.[9] 여러 가지 심리적 요인이 작용하지만, 기본적으로 탐닉성 자극에 반복적으로 노출됨으로써 진행되는 생물학적 과정이 탐닉을 유발하고 또한 유지시키는 기본적 병리라고 할 수 있다.[2][10] 모든 탐닉성 자극은 양성 보강 작용(i.e. 자극에 노출된 사람이 반복적으로 노출될 가능성을 높인다)과 본질적 보수성(i.e. 그 자체로 긍정적이거나 욕망의 대상이거나 쾌락을 유발하는 것으로 인지된다)을 특성으로 갖는다.[2][3][8] 한자 문화권에서는 탐닉을 흔히 중독이라고 부르는 경우가 많으나, 중독과 탐닉은 서로 다른 별개의 개념으로 다루어질 필요성이 있다.[11]

탐닉성이 있는 약물,
헤로인 병.

탐닉은 높은 수준의 탐닉성 자극(e.g. 약물, 성행위, 도박 등)에 만성적으로 노출됨으로써 전사와 후생유전적 기작을 통하여 발생하게 되는 뇌의 보수계의 장애이다.[2][12][13] 모든 행동탐닉 및 약물탐닉의 형성에는 유전자 전사 인자 중 하나인 ΔFosB가 치명적이고 공통적인 요인으로 작용한다.[12][13][14][15] 탐닉에 있어서 ΔFosB의 역할을 20여년 간 연구한 결과 탐닉의 발생과 그에 수반하는 충동적 행동이 전뇌 측좌핵의 D₁ 중형 다극신경원에 ΔFosB가 과잉 표현되는 것과 함께 나타난다는 것이 밝혀졌다.[2][12][13][14] ΔFosB 표현은 탐닉과의 사이에 이러한 인과성 상관관계가 있기에 탐닉의 전임상적 생물지표로 사용된다.[2][12][14] 이 신경원들에 ΔFosB가 표현됨으로써 약물의 자가투여와 보상 민감화가 양성 보강을 통해 증가함과 동시에 혐오성 민감도는 감소한다.[2][12]

탐닉증은 개인 및 사회에 지극히 큰 재산피해 및 인명피해를 입힌다. 그 피해에는 탐닉성 약물 자체의 직접적 해악과, 거기에 수반하는 의료비용, 장기적 합병증(e.g. 흡연으로 인한 폐암, 음주로 인한 간경화 등), 뇌의 신경가소성의 기능적 변형, 생산성의 총체적 저하 등이 모두 포함된다.[16][17][18] 탐닉의 고전적 특징으로는 특정 물질이나 행동에 대한 자제력 감손, 그 물질 또는 행동에 대한 집착, 그리고 부정적 결과에도 불구하고 사용을 멈출 수 없음 등이 꼽힌다.[19] 탐닉과 유관한 습관 및 행동양식은 일반적으로 즉각적 만족감(단기간적 보상)과 그에 비해 오래 지속되는 해로운 효과(장기간적 비용)으로 특징지어진다.[20]

신경심리학[편집]

조작적 조건화와 고전적 조건화와 관련된 인지통제와 자극통제는 개인의 유도된 행동(elicited behavior)의 통제를 둘러싸고 경합하는 반대과정을 보여준다. (예 : 내적 대 외적, 혹은 내적 환경 대 외적 환경)[21] 인지통제, 특히 행동에 가해지는 억제통제(inhibitory control)는 중독이나 주의력결핍 과잉행동장애(attention deficit hyperactivity disorder) 환자에게서 이상이 보인다.[22][23] 자극통제와 같이 특정 보상자극과 연관된 자극추동 행동반응(stimulus-driven behavioral response)은 중독에 빠진 개인의 행동을 지배하는 경향이 있다.[23]

행동 중독[편집]

행동 중독이라는 용어는, 부정적인 결과에도 불구하고 바람직하거나 호소한다는 식으로 표현되는, 선천적으로 보상하게 하는 행동을 말하는 자연보상을 받으려는 강박을 말한다.[7][13][15] 자연보상에 반복적으로 과도하게 노출되는 것을 통한 ΔFosB의 발현이 증가하는 것은 약물중독에서 보이는 것과 같은 행동 효과와 신경가소성을 낳는다는 것을 임상전 증거들이 보여주었다.[13][24][25][26]

ΔFosB에 관한 임상연구와 임상전 연구에 대한 평가는 여느 유형의 성교든, 강박적 성행위는 성 의존증과 같은 중독이라고 규명하였다.[13][24] 게다가 암페타민과 성행위 간의 보상 교차민감화(reward cross-sensitization, 둘 중 어느 한 쪽에 노출되어도 양쪽 모두에 대한 욕구가 증가하는 것)는 전임상적으로 그리고 임상적으로 도파민 조절장애 증후군을 발생시켜왔다고 증명되어 왔다.[13][24][25][26] ΔFosB 발현은 교차민감화 영향에 대하여 필수적인데, 이는 ΔFosB 발현 수치를 강화한다.[13][25][26]

전임상 연구 리뷰는 고지방이나 설탕식품을 장기적으로 자주 과도하게 섭취하는 것은 음식중독을 일으킨다는 것을 보여준다.[13][15] 여기에는 초콜렛이 포함된다. 초콜렛의 달콤한 맛과 화학 재료는 강력한 갈망을 낳거나 중독된 느낌을 준다.[27] 초콜렛을 매우 좋아하는 사람은 스스로를 초코홀릭(chocoholic)이라 부른다. DSM-5에서는 아직 초콜렛을 진단가능한 중독으로 포함시키지 않는다.[28]

도박은 강박행동과 관련되어 있는 자연보상드로, 임상진단 메뉴얼인 DSM-5에서는 중독에 대한 진단 기준을 밝혔다.[13] 도박이 중독 기준을 충족시키는 데에는, 기분수정(mood modification), 강박(compulsivity), 철회(withdrawal) 등이 있다. 기능적 뇌영상을 통해 도박이 보상체계(reward ststem)과 중간변연경로(mesolimbic pathway)를 활성화한다는 증거가 있다.[13][29] 이와 비슷하게 쇼핑과 비디오게임은 강박행동과 연관되어 왔으며 중간변연경로와 보상체계 기타 부분을 활성화시킨다고 밝혀져 왔다.[13] 이 증거에 따라 도박중독, 비디오게임 중독, 쇼핑중독 등은 적절하게 분류된다.[13][29]

위험요인[편집]

중독으로 발전하는데 있어서는 전 인구를 통해 다양한 유전적 환경적 위험요인이 있다.[2][30] 유전적 위험요인과 환경적 위험요인은 각각 중독 발달 위험성의 절반 정도를 차지한다.[2] 후생적 위험요인에서부터 위험요인 전체에 끼치는 요인이 무엇인지에 대해서는 불명확하다.[30] 비교적 낮은 유전적 위험요인을 가지고 있거나, 몇 주 혹은 몇 달 동안 장기적으로 중독성 약물을 다량 복용하는 경우에도 중독을 일으킬 수 있다.[2]

유전적 요인[편집]

심리사회적 요인과 같은 환경적 요인과 더불어, 유전적 요인이 중독 취약성의 기여요인이라는 것은 오래전부터 알려져 왔다.[2][30] 역학연구들에서는 유전적 요인이 알코올중독 요인의 40-60%를 차지한다고 평가한다.[31] 다른 유형의 약물중독 유전가능성은 다른 연구들에서도 지적되어 왔다.[32] 1964년 네슬러(Knestler)는 여러 방식을 통하여 유전자 하나 혹은 여러 유전자 집단이 중독을 일으키는 소인에 원인이 될 수 있다고 가설을 제기하였다. 환경적 요인으로 정상 단백질이 치환된 수치를 가지고 있어도 발달 과정에서 특정 뇌의 뉴런의 구조나 기능을 바꿀 수 있다. 변환된 뉴런들은 최초 약물 사용에 대한 민감성을 변화시킬 수 있다. 이 가설을 지지하여, 동물 연구들에서는 스트레스와 같은 환경적 요인이 동물의 유전자형에 영향을 끼칠 수 있다고 제시하였다.[32]

결국 약물중독으로 발전하는데 있어서 특정 유전자가 관여한다는 것에 관한 데이터는 대부분의 유전자들과 연관되어 있다. 한 원인으로는 일반 변수에 관한 최신 연구의 한 초점때문인 것으로 보인다. 많은 중독 연구들에서는 일반 인구 중 5% 이상에서 보이는 대립유전자에 관한 일반 변수에 주목한다. 그러나 질병과 관련되는 경우 이는 1.1-1.3%의 오즈비 정도 수준에서 추가적인 위험을 수여할 뿐이다. 반대로 전체 인구 1% 미만에서 보이는 유전자는 질환으로의 발달에 더 큰 위험을 증가시킨다.[33]

전 유전자 연합 연구(Genome-wide association study, GWAS)는 의존, 중독, 약물 사용 등과 유전자 연관성을 검사하는데 사용된다. 이러한 연구는 특정 표현형(phenotype)에 관한 유전연관(genetic association)을 발견하는 편견 없는 접근법을 사용, 약물 대사나 반응에 외견상의 관계가 없는 것들을 포함한 DNA 영역 전체에 동일한 중요성을 부가한다. 이러한 연구들에서는 동물 넉아웃 모형(knockout model)과 후보 유전자 분석(candidate gene analysis)을 통하여 묘사되었돈 단백질들로부터 유전자를 확인하는 것은 거의 없다. 대신, 세포부착(cell adhesion)과 같은 과정에 관여하는 유전자 비율은 흔히 확인된다. 이는 이전의 발견이나 GWAS 발견이 오류가 있다는 것을 말하는 것은 아니다. 중요한 내적표현형(endophenotype) 효과는 이러한 방식으로 포착될 수 없다. 또한 약물중독을 위한 GWAS에서 확인된 유전자는 약물 복용 경험들보다 앞서거나 그것들의 뒤에 이어서 혹은 둘 다 두뇌 행동을 맞춰준다.[34]

중독에 있어서 유전학이 수행하는 중요한 역할을 강조하는 연구는 쌍둥이 연구이다. 쌍둥이는 유사하거나 동일한 유전자를 갖는다. 유전학에 관련하여 이러한 유전자를 분석하는 것은 유전학자가 역할 유전자가 중독에 얼마나 많은 일을 수행하는지를 알게 해준다. 쌍둥이에게 수행되는 연구는 쌍둥이 중 한 명만이 중독을 보이지는 않는다는 것이다. 대부분 사례에서, 최소한 쌍둥이 한 명만 중독이 있는 경우, 양쪽이 모두 다 그런 경우, 동일한 약물에 중독된다.[35] 교차 중독(cross addiction)은 소인중독(predisposed addiction)을 가진 경우이며, 다른 것에 중독되기 시작한다. 가족구성원 중 한 명만 중독 내력이 있으면, 친척이나 가까운 가족의 중독 가능성은 더 높다.[36] 2002-2017년 미국 약물중독연구소(National Institute on Drug Abuse)에서 시행한 연구에서, 약물 과다복용으로 인한 사망이 3배 가까이 증가하였다. 2017년 미국에서 72,306명이 약물 과다복용으로 사망하였다고 보고되었다.[37] 2020년 약물 과다복용 사망이 12개월 동안 보고되었다. 81,000명의 과다복용 사망자라 있었고, 2017년부터 기하급수적으로 늘었다.[38]

환경적 요인[편집]

중독의 환경적 요인은 개인의 중독 취약성이 증가하거나 감소하는 유전적 구성요소들과 상호작용하는 평생의 경험이다.[2] 많은 여러 환경적 요인들은 심리사회학적 스트레스 요인들을 포함한 중독의 위험요인으로서 내포되어 왔다. 미국국립약물남용연구소(National Institute on Drug Abuse, NIDA)는 부모의 지도감독이 없는 상태, 또래친구들의 일상적인 약물남용, 약물 이용 가능성, 빈곤을 유년기와 청소년기 약물 남용의 위험요인이라고 본다.[39] 중독의 두뇌 질병 모델(brain disease model)은 중독성 약물에의 노출이 가장 중대한 환경적 요인이라고 상정한다.[40] 그러나 신경과학자를 포함한 많은 연구자들은 두뇌 질병 모델은 진실을 오도하고 불완전하며 잘못된 설명이라고 지적한다.[41]

부정적 아동기 경험(adverse childhood experience, ACE)은 아동기에 경험한 아동학대이자 가정파괴이다. 미국 질병통제및방역센터(Centers for Disease Control and Prevention)가 수행한 부정적 아동기 경험 연구(Adverse Childhood Experiences Study)는 ACE와 약물 남용 등의 다양한 건강, 사회, 행동 관련 문제 간의 강력한 용량 반응 관계를 보여준다.[42] 신체적 학대, 정서적 학대, 성적 학대, 신체적 방임, 정서적 방임, 가정 내 폭력 목격, 부모 중 한 명이 수감중이거나 정신질환자인 경우 등 엄청난 스트레스 상황에 만성적으로 처하면서, 아이의 신경학적 발달은 지속적으로 뒤틀린다. 그 결과, 아이의 인지기능이나 부정적 혹은 왜곡된 정서 대응 능력에 지장이 발생할 수 있다. 시간이 흐르면서 아이는 주로 청소년기에 약물 남용을 일종의 대응 기제로 활용하게 된다.[42] 학대 및 남용 경험 아동에 관한 900건의 법원 판례 연구에서, 대다수 아동들은 청소년기나 성인기에 중독을 경험하게 된다는 것을 발견하였다.[43] 개인의 삶의 경험과 전문가 도움을 통하여 환경적 요인들을 변화시킴으로써, 유년기 스트레스 경험들을 겪으면서 발생하는 중독으로 빠지는 길을 피할 수 있다.[43] 친구가 약물 남용을 하게 되는 경우 중독으로 빠지는 가능성이 증가한다. 가족 내 갈등과 가정 관리 실패는 알코올이나 기타 약물 복용에 빠지는 요인이기도 하다.[44]

연령[편집]

청소년은 중독 발달 취약성이 두드러지는 시기이다.[45] 청소년기에는 인지조절센터 앞에서 두뇌에서의 장려-보상체계(incentive-rewards system)는 성숙한다. 그 결과 이는 행동 의사결정 과정에 있어서 장려-보상체계에 불균형한 힘을 부가한다. 따라서 청소년들은 결과를 헤아리기 전에 충동에 따라 행동하고 위험하거나 중독 가능성 있는 행동을 하게 된다.[46] 청소년들은 약물 사용을 실시하고 유지하려는 가능성이 높을 뿐 아니라, 한번 중독되면 이들은 치료에 저항을 갖게 되고 재반복 하기도 쉽다.[47][48]

어린 나이에 알코올을 복용하기 시작한 사람들은 나중에 더 의존하기 쉽다는 통계연구도 있다. 약 33%는 15-17세 사이, 18%는 이보다 앞선 나이에 알코올 복용을 경험한다. 알코올 남용이나 의존에 있어, 숫자는 12세 이전에 마시기 시작한 이들로 인하여 높아지기 시작하고 이후에 떨어진다. 예를 들어, 알코올 중독자 중 16%는 12세 이전에 마시기 시작하였지만, 9% 아동만이 15-17세 사이에 알코올에 손대기 시작한다. 21세 이후에 마시기 시작한 사람은 2.6%에 불과하다.[49]

대부분은 10대 때에 처음 중독성약물에 손을 댄다.[50] 미국에서 2013년 280만명 이상이 불법약물에 새로 손을 대어, 하루 평균 7,800명이 불법약물에 처음 접하였다.[50] 이들 중, 54.1%는 18세 미만이었다.[50] 2011년, 미국에서는 약 2,060만명의 12세 이상 인구가 중독에 처하였다.[51] 이들 중 90% 이상은 18세 이전에 음주, 흡연, 약물 복용을 시작하였다.[51]

동반질환[편집]

우울, 불안, 주의력결핍 과잉행동장애(ADHD), 외상후스트레스장애(PTSD) 등의 동반성 정신건강 장애(comorbid mental health disorder)를 앓고 있는 개인들은 약물 남용으로 발달할 가능성이 더 높다.[52][53][54] 미국국립약물남용연구소는 초기 공격성 행동을 약물남용의 위험요인으로 본다.[39] 전미경제조사회(National Bureau of Economic Research, NBER) 연구에 의하면, 정신질환과 중독성 약물 사용 간의 명백한 연관성이 있으며, 정신건강 문제 환자들 대다수는 약물 사용을 하고 있는데, 38%는 알코올, 44%는 코카인, 40%는 담배인 것으로 나타났다.[55]

후생적 요인[편집]

세대간 후성유전[편집]

후성유전자와 그 산물은 환경 영향이 유전자에 영향을 미치게 하는 요소들이다.[30] 환경적 영향이 부모 중 한 사람의 유전자에 끼치는 영향력이 관련 특성 및 자식의 행동 표현형(behavioral phenotype)(예 : 환경자극에의 행동 반응)에 영향을 줄 수 있다는 세대간 후성유전(transgenerational epigenetic inheritance) 담당 기전이기도 하다.[30] 후생적 기전은 병리학에서도 중요하다.[2] 중독성 자극에 만성적으로 노출되는 것을 통하여서 발생하는 후성유전체로의 변이 중 일부는 세대를 가로질러서 전송되고, 그 결과 어린 아이의 행동에 영향을 준다. 중독성 약물에 대한 아이의 행동 반응은 자연보상이 될 수 있다.[30][56]

세대간 후생유전에서 나타나는 후성유전적 변이(epigenetic alteration) 일반 등급은 DNA 메틸화, 히스톤단백질변형, microRNA의 상하향조절 등이 있다.[30] 중독으로부터 야기되는 특정 유전가능 후성유전적 변이와 자식 대에서 나타나는 후성유전적 변이로부터의 관련 행동 유전형이 무엇인지를 규명하는 연구가 필요하다.[30][56] 동물연구로부터 전임상적 증거에 근거하여, 쥐에게서 나타난 특정 중독성 후성유전적 변이가 부모에게서 자식에게 전달되며 자식의 중독 발달 위험성을 줄여주는 행동 유전형을 만든다는 것이 밝혀졌다.[note 1][30] 특히 중독에 관한 후성유전적 변이에서 유래하여 부모에게서 자식으로 전송되는 유전가능 행동 유전형은 자식의 중독 가능성을 늘리거나 줄여준다.[30][56]


남용 경향

남용 경향(Abuse Liability) 혹은 중독 경향(addiction liability)은 비의학적 상황에서의 약물사용 경향을 말한다. 행복감, 기분변화, 진정감을 위하여 나타난다.[57] 약물 사용자가 획득할 수 없는 무언가를 원할 때 남용 경향이 보인다. 무언가를 획득할 수 있는 유일한 방법은 약물 사용을 통해서일 뿐이다. 남용 경향을 살펴보면, 약물 남용 여부의 결정 요인이 다소 있다. 약물의 화학 구성, 두뇌로의 영향, 연령, 취약성, 연구 대상 신체적 정신적 건강이다.[57] 남용 경향을 높이는 화학구성의 약물로는 코카인, 헤로인, 흡입제, LSD, 마리화나, 엑스터시(MDMA), 메타암페타민, PCP, 합성 칸나비노이드, 합성 카티논(목욕소금), 담배, 알코올이 있다.[58]

기전[편집]

만성적인 중독성 약물 사용은 중피질변연계 투사(mesocorticolimbic projection)에서의 유전자 발현 변이를 야기한다.[15][59][60] 이러한 변이를 낳는 가장 중요한 전사인자는 (CREB) 단백질에 엮여있는 고리형 아데노신 일인산(cAMP) 반응 요소인 ΔFosB, 그리고 핵인자 카파비(NF-κB)이다.[15] 중독에 있어 ΔFosB는 가장 유의미한 생물분자기전인데, 이는 측좌핵 내 D1-type 중형돌기 신경세포(medium spiny neuron)에서의 ΔFosB의 과잉발현이 약물중독에서 보이는 신경적응과 행동효과(약물 자가 투여drug self-administration와 보상자각reward sensitization에서의 발현의존 증가expression-dependent increase)에 있어 필요충분조건이기 때문이다.[15] 이러한 ΔFosB 발현은 정적 강화를 통하여 약물 자가 투여와 보상자각을 직접적으로 정적으로 조절하면서 동시에 혐오감에 대한 민감도를 감소시킨다.[note 2][2][12] ΔFosB는 알코올, 암페타민. 치환암페타민, 카나비노이드, 코카인, 메틸페니데이트, 니코틴, 아편, 펜시클리딘, 프로포폴 등의 여러 약물류에 대한 중독을 매개하는 것으로 알려졌다.[12][15][59][61][62] 전사인자 ΔJunD와 히스톤 메틸기전사효소(histone methyltransferase) G9a는 ΔFosB 기능을 길항하고 ΔFosB 발현 증가를 억제한다.[2][15][63] 바이러스매개체가 매개하는 유전자 도입을 통한 측핵 ΔJunD 발현 증가, 혹은 약물적 수단을 통한 G9a 발현 감소, 혹은 폭증은, 중독성 약물의 만성적인 고용량 복용으로 인하여 발생한 신경변이와 행동변이, 즉 ΔFosB로 매개된 변이 대부분을 차단한다.[14][15]

ΔFosB는 음식, 성, 운동과 같은 자연보상에의 행동반응을 조절하는 데에도 중요한 역할을 한다.[15][64] 약물 남용, 측핵 내 ΔFosB 유도성 유전자 발현 등의 자연보상, 그리고 이러한 보상들의 만성적 획득은 ΔFosB 과잉발현을 통항 병적 중독과 유사한 상태를 야기한다.[13][15][64] 결국 ΔFosB는 자연보상에의 중독, 즉 행동 중독에 있어 핵심 전사인자이기도 하다.[15][13][64] 특히 측핵 내 ΔFosB는 성적 보상 효과 강화에 결정적이다.[64] 자연보상과 약물보상 간의 상호작용에 관한 연구는, 암페타민과 같은 도파민 작용 각성제와 성행위가 유사한 생물분자기전에 작용하여 측좌핵 내 ΔFosB를 유도하고, ΔFosB를 통해 매개되는 양방향성 교차감작 효과를 점한다.[13][25][26] 이 현상이 주목할 만한 것은, 성행위, 쇼핑, 도박 등 자연보상에서의 약물유도성 강박 행동을 특징으로 보이는 도파민 조절장애 증후군이 도파민 활성화 약제를 복용한 사람에게도 관찰되었기 때문이다.[13]

활동을 길항시키는 약물이나 치료법 등의 ΔFosB 억제제는 중독이나 중독성 장애에 효과적이다.[65]

측좌핵 내 도파민 분비는 음식이나 성 등의 자극을 자연적으로 강화하는 식의 여러 자극을 강화하는 역할을 수행한다.[66][67] 치환 도파민 신경전달(altered dopamine neurotransmission)은 중독성 상태 발달 이후에 자주 관찰된다.[13] 중독을 보이는 사람이나 실험실 동물에게 측좌핵이나 선조체의 다른 부위 내의 도파민 신경전달 혹은 아편 신경전달의 변이가 뚜렷하다.[13] 코카인 등의 약물 사용은 보상체계를 자극하는 콜린성 뉴런에 영향을 주고, 이로써 이 영역의 도파민 신호에도 영향을 준다.[68]

보상체계[편집]

중뇌피질변연경로[편집]

약물중독의 생물학적 기반을 검사할 때에 있어, 약물이 작용하는 경로와 약물이 이러한 경로를 변형시킬 수 있는 방식을 이해하는 것은 핵심이다. 중변연계경로라는 보상경로 혹은 그 확장인 중뇌피질변연경로는 뇌영역 일부의 상호작용을 특성으로 한다.

  • 배쪽 피개부(VTA)로부터의 투사는 함께 자리한 시냅스후 글루탐산 수용체(co-localized postsynaptic glutamate receptor)의 도파민 뉴런 네트워크이다.(AMPA 수용체(AMPAR)와 NMDA 수용체(NMDAR)). 이러한 세포들은 보상을 가리키는 자극이 나타날 때 반응한다. 배쪽 피개부는 특정 효과뿐 아니라 학습과 민감화 발달을 지지하고, DA를 전뇌에 방출한다.[69] 또한 이 신경 세포들은 중변연계경로를 통해 측좌핵으로 투사하여 DA를 방출하며,[70] 실제로 약물 중독을 일으키는 모든 약물은 중뇌변연경로를 통한 도파민 방출을 증가신다.[71]
  • 측좌핵(NAcc)은 배쪽 피개부 투사의 결과물 중 하나이다. 측핵 자체는 감마 아미노뷰티르산(GABA) 중형돌기 신경세포로 구성되어 있다.[72] 측핵은 조건화 행동(conditioned behavior)을 획득하고 유도하는 것과 연관되어 있으며, 중독 발전으로서 약물에 대한 민감도를 증가시킨다.[69] 측핵 내 ΔFosB 의 과잉발현은 모든 중독 유형에 있어 필수적인 공통인자이다.[2] ΔFosB는 정적 강화 행동의 강력한 정적 조절자이다.[2]
  • 전대상피질(anterior cingulate)과 안와전두피질(orbitofrontal cortex)[73] 등의 전전두피질은 중뇌피질변연경로에서 배쪽 피개부가 투사하는 또 다른 부위이다. 이는 어느 한 행동이 유도될지 여부를 결정하는데 도움을 주는 정보의 취합에 있어 중요하다.[74] 또한 이는 약물사용의 보상경험과 주변 환경에서 보내는 단서 간의 관련성을 형성하는 데에도 중요하다. 중요한 것은 이 단서들은 약물 탐색 행동을 유발하는 강력한 매개물이며, 수개월 혹은 수년 간의 약물 사용 중지 상황에서도 이를 촉발시킨다는 것이다.[75]

중독에 관여하는 다른 뇌구조로는 다음과 같다.

  • 기저측 편도(basolateral amygdala)는 측핵으로 투사하고 동기부여에 있어서도 중요하다고 여겨진다.[74]
  • 해마는 학습과 기억의 역할을 수행하기에 약물중독에 관여한다. 이는 해마 내 세포 조작이 측좌핵 내 도파민 수치와 배쪽 피개부 도파민세포의 폭발 빈도를 변화시킨다는 연구를 통하여 증명된다.[70]

도파민과 글루탐산의 역할[편집]

도파민은 두뇌 보상체계에 있어 주요 신경전달물질이다. 동작, 감정, 인지, 동기, 환희의 느낌을 조절하는 역할을 수행한다.[76] 음식물 섭취는 물론 오락용 약물 복용 등의 자연보상은 도파민 방출을 야기하고, 이러한 자극들이 가지고 있는 강화의 특성과도 연관되어 있다.[76][77] 거의 모든 중독성 약물들은 도파민 활동성을 고양하는 방식을 통하여 직간접적으로 두뇌 보상체계에 작용한다.[78]

많은 종류의 중독성 약물을 과도하게 복용하면 도파민 수치가 높게 방출되는 것이 반복되면서, 도파민 수용체 활성화 고양을 통하여 보상 경로에 직접적으로 영향을 준다. 시냅스틈 내 도파민 수치가 비정상적으로 높게 지속되는 것은 뉴런경로에서의 수용체 하향조절을 유도한다. 중변연계 도파민 수용체의 하향조절은 자연적 강화체에 대한 민감도 저하를 가져올 수 있다.[76]

약물탐색행동(drug seeking behavior)은 전전두피질에서 측핵으로의 글루탐산 투사(glutamatergic projection)를 통해 유도된다. 이는 측핵 내 AMPA 글루탐산 수용체와 글루탐산 방출의 억제를 통하여서 약물탐색행동이 차단될 수 있다는 실험결과를 통해 증명된다.[73]

보상민감화[편집]

보상민감화(reward sensitization)는 뇌가 보상자극에 부여하는 보상의 양을 늘리는 과정을 말한다. (특히 동기적 현저성(incentive salience)[note 3]) 간단히 말하면, 약물과 같은 특정 자극에 대한 보상민감화가 발동하면, 자극에 대한 결핍이나 욕망 및 이와 관련된 신호가 증가한다.[80][79][81] 보상민감화는 자극에 대한 노출이 만성적으로 높을 때 흔히 발생한다. 측좌핵 내 D1-type 중형돌기 신경세포에서의 ΔFosB 유전자 발현이 약물이나 자연보상에 관여한 보상민감화를 직접적으로 양성조절한다는 것이 밝혀졌다.[2][12][14]

중독에서 발생하는 갈망의 일종인 "단서 유도 결핍(cue-induced wanting)"이나 "단서 촉발 결핍(cue-triggered wanting)"은 중독자가 보이는 강박행동에 반응할 수 있다.[79][81] 중독의 발달 동안, 중립적 비보상적 자극과 약물 사용 간의 관련성은 이러한 중립적 자극을 중독성 약물 사용의 조건적 정적강화물(conditioned positive reinforcer)로서 작용하게 하는 연합학습과정(associative learning process)을 야기한다. 즉 이러한 자극들은 약물단서(drug cue)로 기능하는 것이다.[79][82][81] 중립적인 자극이었던 약물사용의 조건적 정적강화물은 갈망으로 모습을 드러내는 동기적 현저성에 부여된다. 동시적 현저성은 보상민감화로 인하여 병적 수준으로 높게 나타나기도 하는데, 원래 함께 병행되던 중독성 약물과 같은 일차적 강화물(primary reinforcer)로 변이될 수 있다.[79][82][81]

자연보상과 약물보상 간의 상호작용 연구는 암페타민과 같은 도파민 각성제와 성행위는 작용하여 측핵에서 ΔFosB를 유도하고, ΔFosB를 통한 양방향성 보상교차감작효과(bidirectional reward cross-sensitization effect)[note 4]를 보유하고 있는 생체분자기전(biomolecular mechanism)에 작용한다.[13][25][26] ΔFosB의 보상감작효과와 달리, CREB 전사활동은 약물의 보상효과에 대한 민감도를 낮춘다. 측핵 내 CREB 전사는 정신적 의존이나 금단 증상에서 보이는 쾌감상실과 같은 증상에도 보인다.[2][83][84]

G단백질 신호 조절자(regulators of G protein signaling, RGS)라는 단백질, 특히 RGS4와 RGS9-2는 보상감작을 포함한 아편감작을 조정하는데 있어서도 원인이 된다.[85]

신경후성유전 기전[편집]

두뇌 보상체계에서의 유전자 발현에 대한 후성유전적 조절의 변이는 약물 중독 발달에 있어 중대하고도 복잡한 역할을 수행한다.[63][86] 중독성 약물은 뉴런 내 후성유전적 변화의 세 유형과도 연관되어 있다.[63]

  1. 히스톤 변화
  2. 특정 유전자나 그 인근의 CpG site에서의 DNA의 후성유전적 메틸화
  3. 특정 타겟 유전자를 가지고 있는 microRNA의 후성유전적 하향조절 혹은 상향조절[63][15][86]

일례로 약물 복용 이후 측좌핵 세포에서의 유전자 수백 개가 히스톤 변화를 보이지만(특히 히스톤 잔기의 아세틸화 및 메틸화 상태로 치환된 상태에서) 대부분의 측좌핵 세포 내 유전자들은 이러한 변화를 보이지 않는다.[63]

진단[편집]

정신질환 진단 및 통계 편람(Diagnostic and Statistical Manual of Mental Disorders) 제5판(DSM-5)은 약물 사용 관련 장애의 스펙트럼을 의미하는 단어로 약물사용장애(substance use disorder)를 사용한다. DSM-5는 진단 범주에서 남용(abuse)이나 중독(dependence)라는 용어를 빼고 가벼운(mild), 보통의(moderate), 심각한(severe)이라는 세 등급으로 장애의 범위를 표현하고 있다. 이러한 등급은 주어진 사례에 보이는 진단기준의 수치로 결정된다. DSM-5에서 약물중독(drug addiction)은 심각한 약물사용장애(severe substance use disorder)와 동의어이다.[87][4]

DSM-5는 행동중독(behavioral addiction) 진단 범주를 새롭게 도입하였으나, 도박중독(problem gambling)만 들어가 있다.[88] 인터넷게임장애(Internet gaming disorder)는 DSM-5에서 '추가 연구가 필요한 증상(condition requiring further study)'으로 분류되어 있다.[89]

이전 판에서는 중독을 신체적 의존(physical dependence)과 관련 금단 증후군(withdrawal syndrome)이라는 용어를 사용하였다. 약물과 정상적 기능을 합성함으로써 신체가 적응될 때, 즉 항상성(homeostasis)을 획득할 때 신체적 의존은 발생하며, 약물 사용을 중지하면 신체적 금단 증후군(physical withdrawal symptom)이 발생한다.[90] 내성(tolerance)은 신체가 약물에 적응하여 약물의 본 효과를 보기 위하여 점점 더 많은 양을 복용해야 하는 과정을 의미한다. 금단(withdrawal)은 신체가 의존하는 약물을 줄이거나 끊을 때 겪는 신체적 심리적 증상을 말한다. 금단 증상은 가려움, 불안, 짜증, 약물에 대한 강한 갈망, 구역질, 환각, 두통, 오한, 진전(tremor), 발작 등을 보인다.

중독 연구자들은 DSM 분류가 결점이 있고 임의적이라고 지적한다.[91] 2013년 논문에러 미국국립정신건강연구소(United States National Institute of Mental Health)는 DSM-5의 정신질환 등급분류에 대한 비타당성을 논의하였다.[92]

DSM이 바이블로 여겨져 왔으나, 증상의 명명과 규정을 하는 사전집에 불과하다. DSM의 장점은 신뢰도(reliability)이다. 현장 임상 전문가들이 동일 용어를 동일한 방식으로 사용할 수 있게 한다. 약점은 타당성(validity)이 부족하다는 것이다. 허혈성 심장질환, 임파종, 에이즈 등의 정의와 달리, DSM 진단은 객관적인 실험 측정이 아닌 임상 증상들의 여러 사례에서 도출한 동의(consensus)에 기반한 것이다. 다른 병증에 있어서, 이는 흉통이나 열증에 기반한 진단 체계를 만드는 것과 동일하다고 하겠다.

중독으로 뇌구조 변화가 보인다는 점에서, MRI를 통한 비침투적 신경영상스캔(non-invasive neuroimaging scan)이 중독 진단에 유용할 것으로 보인다.[93] 진단의 바이오마커(biomarker)로서 ΔFosB 발현은 중독 진단에 사용될 수 있지만, 두뇌 생체검사(brain biopsy)가 필요하기에 임상 진단에선 사용되지 않는다.

약물중독의 예[편집]

의식주등의 활동으로 기본적이고 자연적인 평안함과 욕구충족을 인간 스스로 제공하는 것은 행동과 신경정신계통의 보상회로로 알려진 도파민의 상호반응적인 역할로 행복감을 느끼고 이러한 자연적이고 생리적인 보상시스템은 행동의 강화를 통해 적절하고 유연한 삶을 지속하도록 하고있다. 그러나 약물을 남용하게 되면 이전의 자연보상시스템에서 느끼던 즐거움의 정도보다 상대적으로 더 강력한 흥분을 경험하게 되고 이것은 상대적으로 자연보상에서 느끼게되는 행복감을 심각히 저하시키며 삶이 덜 생생해지고 우울감을 더 느끼게한다. 따라서 도파민 기능을 더 강화하기 위해 더 많은 약물을 더 자주 사용하게 됨으로써 뇌는 점점 더 많은 도파민을 필요로 하게 되고 결국 중독에 빠지고 이를 극복하기 어려워지는것으로 알려져있다.[94]

치료[편집]

한 보고에 의하면, 효과적인 중독 치료를 위해선, 약물기반치료나 생물학적치료로서만 하는 것을 인지행동치료(cognitive behavioral therapy, CBT), 개인심리치료 및 집단심리치료(individual and group psychotherapy), 행동수정치료(behavior-modification strategies), 12단계 프로그램(twelve-step programs), 거주형 요양시설(residential treatment facilities) 등과 같은 중독 재활 형태로 통합되어야 한다고 주장한다.

행동치료[편집]

약물 중독과 행동 중독에 관한 다양한 행동치료(behavioral therapy)의 효능에 관한 메타분석 보고서에서, 재발방지(relapse prevention)나 유관관리(contingency management)와 같은 인지행동치료, 동기부여면접(motivational interviewing), 커뮤니티 강화 접근(community reinforcement approach)이 적당한 효과 크기(effect size)를 보이는 효과적인 개입(intervention)임을 밝혔다. 꾸준한 에어로빅, 특히 마라톤과 같은 지구력운동이 약물중독으로 발전하는 것을 막아주며, 약물중독치료에 특히 정신자극제중독(psychostimulant addiction)에 효과적인 보조치료(adjunct treatment)가 되기도 한다. 꾸준한 에어로빅 운동은 약물중독의 위험을 자기강도의존적(magnitude-dependently)으로 다시 말해 지속적이고 강렬하게 감소시킨다. 이는 약물중독 관련 신경가소성(neuroplasticity)을 발생시키는 것으로 보인다. 한 리뷰는 선조체(striatum)나 보상체계(reward system)의 다른 부분에서 델타포스B(DeltaFosB)나 c-포스(c-Fos) 면역반응성(immunoreactivity)을 대체함으로써 약물중독으로의 발전을 막는다고 보았다. 에어로빅은 약물의 자가투여(self-administration)를 줄이고 재발 가능성을 감소시키며 선조체 도파민 수용체 D2(striatal dopamine receptor D2, DRD2) 신호(DRD2 밀도 증가)에 대한 역효과를 유도하여 몇몇 약물등급(DRD2 밀도 저하)의 증가를 통해 유도된 것으로 유도한다. 결국 꾸준한 에어로빅을 보조치료로 사용하면 치료 효과가 더 좋다.

약물 치료[편집]

알코올 중독[편집]

알코올은 아편유사제(opioids)처럼 심각한 신체적 의존(physical dependence)을 유발하고 진전섬망(delirium tremens)과 같은 금단증상(withdrawal symptom)을 보인다. 이때문에 알코올 중독 치료는 의존과 중독을 동시에 다루는 복합적인 방법을 사용한다. 벤조디아제핀(benzodiazepin)은 금단증상과 해독(detoxification)에 가장 큰 효과를 발휘하고 있다. 약물치료에 사용되는 약으로는 아편유사제대항제(opiod antagonist)인 날트렉손(naltrexone), 디설피람(disulfiram), 아캄프로세이트(acamprosate), 토피라메이트(topiramate) 등이 있다. 이 약들은 알코올 대용제가 아니라 음주 욕구에 영향을 주는 것으로서, 직접적으로 알코올에 대한 갈망(craving)을 줄여주거나(아캄프로세이트, 토피라메이트) 음주시 불쾌한 느낌을 유발하는(디설피람) 작용을 한다. 러한 약물들은 치료가 꾸준히 진행되면 효과가 있지만, 과도한 부작용으로 환자가 사용을 중단하거나 복용을 잊는 경우 복약순응도(drug compliance)에 문제가 생길 수 있다. 의료 근거를 지공하는 영국의 비영리단체인 코크란(Cochrane Collaboration)의 보고에 의하면, 아편유사제대항제인 날트렉손이 치료 종결 후에도 3-12개월간 효과가 지속되어서 알코올 중독 치료에 효과가 있다는 것을 입증해 왔다고 전한다.

행동 중독[편집]

행동중독(behavioral addiction)은 치료 가능한 증상이다. 치료 옵션에는 심리치료(psychotherapy)와 정신질환약물치료(psychopharmacotherapy)가 있으며 양쪽을 혼용하기도 한다. 행동 중독에서 흔히 사용되어온 치료법은 인지행동치료이다. 이는 강박행동(compulsive behavior)을 촉발하는 행동패턴을 규명하고 건강한 행동을 증진하기 위하여 일상을 변화시키는 것에 초점을 맞춘다. 인지행동치료(cognitive behavioral therapy, CBT)는 단기치료에 해당하기에 치료 회기는 보통 5-20번 정도이다. 치료 회기동안 치료사는 문제가 무엇인지를 규명하고, 문제가 발생할 때 나타나는 사고를 알아차리고, 부정적이거나 잘못된 생각을 규명하고, 이러한 부정적이거나 잘못된 생각을 다른 생각으로 고치는 과정을 환자에게 유도한다. 인지행동치료가 행동 중독을 고치지 않더라도 건강한 장식으로 증상에 대처하는 것에 도움을 준다. 현재까지 행동 중독 치료를 위해 승인된 약은 없지만 일부 약물중독 치료약이 특정 행동 중독에 효과가 있음이 밝혀졌다. 행동 중독과는 무관한 정신장애라도 통제되어야 하고, 행동 중독을 유발하는 기여요인들과 구분되어야 한다.

카나비노이드중독[편집]

2010년까진 대마초의 화학성분인 카나비노이드(cannabinoid)의 중독에 대한 효과적인 약물치료는 없었다. 2013년 카나비노이드중독 관련 보고서에서는, 아레스틴 베타2(β-arrestin 2) 신호와의 상호작용을 감소시킨 CB1 수용체 작용제(CB1 receptor agonist)의 발달이 치료에 유용하다고 하였다.

니코틴중독[편집]

니코틴중독 치료에서도 약물중독치료가 널리 사용되어 왔다. 치료에는 니코틴 대체치료법(nicotine replacement therapy), 니코틴수용체대항제(nicotinic receptor antagonist), 니코틴 수용체 부분작용제(nicotinic receptor partial agonist)를 사용한다. 니코틴 수용체에 작용하여 니코틴중독 치료에 사용되어온 약물은 부프로피온(bupropion)과 같은 대항제나 바레니클린(varenicline)과 같은 부분작용제가 있다.

아편유사제중독[편집]

아편유사제(opioid)는 신체의존을 유발하기에 아편유사제중독 치료는 중독과 의존을 모두 다룬다. 신체의존은 부프레노르핀/날록손(Buprenorphine/naloxone, 제품명 서복손suboxone), 부프레노르핀(Buprenorphine, 제품명 수버텍스subutex), 메타돈(methadone) 등이 대체약물(replacement drug)로 사용된다. 비록 이러한 약물들은 신체의존을 계속 유지시키지만, 이러한 아편유지치료법(opiate maintenance)의 목적은 고통과 갈망(craving)을 모두 통제하는 수단을 제공하려는 것이다. 대체약물 사용은 중독자가 정상적으로 기능하는 능력을 증대시키고 규제약물(controlled substance)을 불법으로 입수하는 경로를 없앤다. 처방 복용량이 일정해지면 치료는 유지 혹은 감소 단계로 접어든다. 미국에서 아편대체약물치료는 메타돈클리닉(methadone clinic)에서 제한 사용되고 있고, DATA 2000 법률 제정 하에 엄격히 규제되고 있다. 일부 국가에서는, 디하이드로코데인(dihydrocodeine)이나 디하이드로에토핀(dihydroetorphine), 심지어 헤로인(heroin)과 같은 아편유도제(opioid derivative)들이 환자 개인의 필요에 따라 각각 알맞게 처방되는 형태로 불법 구매 아편을 대체하는 약물로 사용된다. 바클로펜(baclofen)은 정신자극제(stimulant), 알코올, 아편에 대한 갈망을 줄이고 알코올 금단증상을 경감시키는 데에도 효과를 보여왔다. 바클로펜 치료 이후, 많은 환자들이 아코올이나 코카인에 무관심해졌다고 진술한다. 아편해독과 과다투여로 인한 사망률 간의 상관관계를 연구한 경우도 있다.

정신자극제중독[편집]

2014년까지는 정신자극제중독(psychostimulant addiction)에 관한 효과적인 악물치료가 없었다. 2015년, 2016년, 2018년 보고서에서는 TAAR1-선택적 작용제(TAAR1-selective agonist)가 정신자극제중독 치료제로서 상당한 가능성이 있다는 것이 지적되었다. 그러나 2018년까지, TAAR1-선택적 작용제로서 기능하는 화합물은 승인되지 않은 시약(experimental drug) 단계에 머무르고 있다.

병인[편집]

문화적 다양성에 의하여, 특정 기간 내에 약물중독이나 행동중독으로 발전하는 사람들의 비중이 국가마다 연령별 사회경제적 지위에 따라 다양해지고 있다.[30]

아시아[편집]

알코올의존증(alcohol dependence)은 다른 지역만큼 높진 않다. 사회경제적 요인뿐 아니라 생물학적 요인이 음주 행위에 영향을 준다.[95]

스마트폰 보유 비중을 살펴보면 전체 62%인데, 중국 41%, 한국 82%에 해당한다. 온라인게임 참여 비중을 살펴보면 중국 11%, 일본 39%에 달한다. 홍콩은 청소년 인터넷 초과 사용 비중이 68%로 가장 높다. 인터넷중독장애(Internet addiction disorder)는 필리핀에서 가장 높아, IAT(Internet Addiction Test) 5%, CIAS-R(Revised Chen Internet Addiction Scale) 21%에 달하였다.[96]

호주[편집]

2009년 약물남용장애 비중이 5.1%에 이르렀다.[97]

유럽[편집]

2015년 성인인구 18.4%에서 심각한 과거 30일동안의 단편적 알코올사용(episodic alcohol use)을 보였다. 15.2%는 일상 흡연자였다. 2017년 대마초흡연자는 3.8%, 암페타민사용자는 0.77%, 아편사용자는 0.37% 코카인사용자는 0.35%였다. 알코올 및 불법약물 사용으로 인한 사망율은 동유럽에서 가장 높았다.[98]

미국[편집]

2011년 미국 청소년 대표표본(representative sample)에서, 알코올 및 불법약물 중독의 평생유병률(lifetime prevalence)[note 5]은 각각 8%와 2-3%로 추정되었다.[17] 2011년 미국 성인 인구 대표표본에서 알코올 및 불법약물중독의 12개월 유병률(12 month prevalence)은 각각 12%와 2–3%로 추정되었다.[17] 최근 처방약 평생유병률은 약 4.7%이다.[99]

2016년, 2,200만명 미국 국민은 알코올, 니코틴 등이 중독 치료가 필요한 실정이다.[18][100] 약 10% 혹은 200만 정도만이 약물 치료를 받고 있으며, 근거중심치료(evidence-based care)는 받지 않고 있다.[18][100] 미국 내 입원비용의 1/3과 사망자 중 20%는 치료를 받지 못하거나 위험한 약물 사용으로 인하여 발생한 것이다.[18][100] 당뇨나 항암 치료 비용보다도 더 큰 비용이 발생함에도 불구하고, 미국 내 의사 대부분은 약물중독 치료를 적절히 대응할 능력이 부족하다.[18][100]

행동중독으로 인한 평생유병률은, 강박적 도박 1–2%, 성중독 5%, 음식중독 2.8%, 강박적 쇼핑 5–6%에 해당한다.[13] 한 체계적 리뷰(systematic review)에 의하면, 성중독이나 강박적 성행위의 시불변 유병률(time-invariant prevalence rate)은 미국 전체 인구의 3–6%에 해당한다.[24]

Pew Research Center가 수행한 2017년 여론조사에 의하면, 미국 성인 절반 정도가 약물중독에 시달리고 있는 가족이나 친구를 알고 있다고 보고하였다.[101]

2019년 아편중독(opioid addiction)이 전 미국 내 위기로 인지되었다.[102]

남미[편집]

병인학적 발견에 국한시켰을 경우, 라틴아메리카의 아편 사용 및 남용 실태는 거짓일 수 있다. 유엔 마약 범죄 사무소(United Nations Office on Drugs and Crime) 보고서에,[103]세계 모르핀과 헤로인 생산량이 전세계 3%, 아편은 0.001%에 해당하지만, 사용량은 동등하지 않다. 전미대륙약물남용통제위원회(Inter-American Commission on Drug Abuse Control)에 의하면, 콜롬비아는 최대 아편 생산국이지만, 헤로인 사용은 라틴아메리카 국가 대부분에서 사용률이 낮다. 미국과 국경을 접한 멕시코는 사용률이 가장 높다.[104]

성격 이론[편집]

중독에 관항 성격 이론(Personality theories of addiction)은 성격특성(personality trait)이나 사고 방식 즉 정동 상태(affective state)와 중독을 일으키는 성향(proclivity)과의 연관을 시키는 심리학적 모델이다. 데이터분석(Data analysis)은 약물복용자와 일반인 간의 심리적 내력이 상당히 다르며, 각기 다른 약물을 사용하는 심리학적 소인도 각각 다르다는 것을 보여준다.[105] 심리학 문헌에서 제안된 중독 위험으로는, 정적 부적 심리학적 정서(positive and negative psychological affect)의 정동 조절장애 모델(affect dysregulation model), 충동성(impulsiveness)과 행동억제(behavioral inhibition)의 강화민감도이론모델(reinforcement sensitivity theory model), 보상민감화(reward sensitization)와 충동성의 충동모델(impulsivity model)이 있다.[106][107][108][109][110]

같이 보기[편집]

각주[편집]

  1. ↑ Malenka RC, Nestler EJ, Hyman SE (2009). 〈Chapter 15: Reinforcement and Addictive Disorders〉. Sydor A, Brown RY. 《Molecular Neuropharmacology: A Foundation for Clinical Neuroscience》 2판. New York: McGraw-Hill Medical. 364–375쪽. ISBN 9780071481274.
  2. ↑ 이동:가 나 다 라 마 바 사 아 자 차 카 타 파 하 거 너 더 러 머 버 Nestler EJ (December 2013). “Cellular basis of memory for addiction”. 《Dialogues Clin. Neurosci.》 15 (4): 431–443. PMC 3898681. PMID 24459410. Despite the importance of numerous psychosocial factors, at its core, drug addiction involves a biological process: the ability of repeated exposure to a drug of abuse to induce changes in a vulnerable brain that drive the compulsive seeking and taking of drugs, and loss of control over drug use, that define a state of addiction. ... A large body of literature has demonstrated that such ΔFosB induction in D1-type [nucleus accumbens] neurons increases an animal's sensitivity to drug as well as natural rewards and promotes drug self-administration, presumably through a process of positive reinforcement ... Another ΔFosB target is cFos: as ΔFosB accumulates with repeated drug exposure it represses c-Fos and contributes to the molecular switch whereby ΔFosB is selectively induced in the chronic drug-treated state.41. ... Moreover, there is increasing evidence that, despite a range of genetic risks for addiction across the population, exposure to sufficiently high doses of a drug for long periods of time can transform someone who has relatively lower genetic loading into an addict.
  3. ↑ 이동:가 나 다 “Glossary of Terms”. 《Mount Sinai School of Medicine》. Department of Neuroscience. 2015년 2월 9일에 확인함.
  4. ↑ 이동:가 나 다 Volkow ND, Koob GF, McLellan AT (January 2016). “Neurobiologic Advances from the Brain Disease Model of Addiction”. 《N. Engl. J. Med.》 374 (4): 363–371. doi:10.1056/NEJMra1511480. PMID 26816013. Substance-use disorder: A diagnostic term in the fifth edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-5) referring to recurrent use of alcohol or other drugs that causes clinically and functionally significant impairment, such as health problems, disability, and failure to meet major responsibilities at work, school, or home. Depending on the level of severity, this disorder is classified as mild, moderate, or severe.
    Addiction: A term used to indicate the most severe, chronic stage of substance-use disorder, in which there is a substantial loss of self-control, as indicated by compulsive drug taking despite the desire to stop taking the drug. In the DSM-5, the term addiction is synonymous with the classification of severe substance-use disorder.
  5. ↑ “질병분류목록 :: 정신활성물질의 사용에 의한 정신 및 행동 장애(F10-F19)”. 질병분류 정보센터. 313-315쪽. 2017년 9월 3일에 원본 문서에서 보존된 문서. 2017년 9월 3일에 확인함.
  6. ↑ Angres DH, Bettinardi-Angres K (October 2008). “The disease of addiction: origins, treatment, and recovery”. 《Dis Mon》 54 (10): 696–721. doi:10.1016/j.disamonth.2008.07.002. PMID 18790142.
  7. ↑ 이동:가 나 Malenka RC, Nestler EJ, Hyman SE (2009). 〈Chapter 15: Reinforcement and Addictive Disorders〉. Sydor A, Brown RY. 《Molecular Neuropharmacology: A Foundation for Clinical Neuroscience》 2판. New York: McGraw-Hill Medical. 364–65, 375쪽. ISBN 978-0-07-148127-4. 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.
  8. ↑ 이동:가 나 Taylor SB, Lewis CR, Olive MF (February 2013). “The neurocircuitry of illicit psychostimulant addiction: acute and chronic effects in humans”. 《Subst. Abuse Rehabil.》 4: 29–43. doi:10.2147/SAR.S39684. PMC 3931688. PMID 24648786.
  9. ↑ [2][3][4][6][7][8]
  10. ↑ American Society for Addiction Medicine (2012). “Definition of Addiction”. 2018년 6월 14일에 원본 문서에서 보존된 문서. 2017년 9월 3일에 확인함.
  11. ↑ (우리말샘) 중독,탐닉,중독성
  12. ↑ 이동:가 나 다 라 마 바 사 아 Ruffle JK (November 2014). “Molecular neurobiology of addiction: what's all the (Δ)FosB about?”. 《Am. J. Drug Alcohol Abuse》 40 (6): 428–437. doi:10.3109/00952990.2014.933840. PMID 25083822. 
    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.
  13. ↑ 이동:가 나 다 라 마 바 사 아 자 차 카 타 파 하 거 너 더 러 머 버 서 Olsen CM (December 2011). “Natural rewards, neuroplasticity, and non-drug addictions”. 《Neuropharmacology》 61 (7): 1109–22. doi:10.1016/j.neuropharm.2011.03.010. PMC 3139704. PMID 21459101. 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"
  14. ↑ 이동:가 나 다 라 마 Biliński P, Wojtyła A, Kapka-Skrzypczak L, Chwedorowicz R, Cyranka M, Studziński T (2012). “Epigenetic regulation in drug addiction”. 《Ann. Agric. Environ. Med.》 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
  15. ↑ 이동:가 나 다 라 마 바 사 아 자 차 카 타 파 Robison AJ, Nestler EJ (November 2011). “Transcriptional and epigenetic mechanisms of addiction”. 《Nat. Rev. Neurosci.》 12 (11): 623–37. doi:10.1038/nrn3111. PMC 3272277. PMID 21989194. 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.
  16. ↑ Malenka RC, Nestler EJ, Hyman SE (2009). 〈Chapter 1: Basic Principles of Neuropharmacology〉. Sydor A, Brown RY. 《Molecular Neuropharmacology: A Foundation for Clinical Neuroscience》 2판. New York: McGraw-Hill Medical. 4쪽. 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.
  17. ↑ 이동:가 나 다 KR Merikangas KR, McClair VL (June 2012). “Epidemiology of Substance Use Disorders”. 《Hum. Genet.》 131 (6): 779–789. doi:10.1007/s00439-012-1168-0. PMC 4408274. PMID 22543841.
  18. ↑ 이동:가 나 다 라 마 “American Board of Medical Specialties recognizes the new subspecialty of addiction medicine” (PDF). 《American Board of Addiction Medicine》. 2016년 3월 14일. 2021년 3월 21일에 원본 문서 (PDF)에서 보존된 문서. 2016년 4월 3일에 확인함. 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.
  19. ↑ Morse RM, Flavin DK (August 1992). “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》 268 (8): 1012–4. doi:10.1001/jama.1992.03490080086030. PMID 1501306.
  20. ↑ Marlatt GA, Baer JS, Donovan DM, Kivlahan DR (1988). “Addictive behaviors: etiology and treatment”. 《Annu Rev Psychol》 39: 223–52. doi:10.1146/annurev.ps.39.020188.001255. PMID 3278676.
  21. ↑ Washburn DA (2016). “The Stroop effect at 80: The competition between stimulus control and cognitive control”. 《J Exp Anal Behav》 105 (1): 3–13. doi:10.1002/jeab.194. PMID 26781048. 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.
  22. ↑ Diamond A (2013). “Executive functions”. 《Annu Rev Psychol》 64: 135–68. doi:10.1146/annurev-psych-113011-143750. PMC 4084861. PMID 23020641. 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).
  23. ↑ 이동:가 나 Malenka RC, Nestler EJ, Hyman SE (2009). 〈Chapter 13: Higher Cognitive Function and Behavioral Control〉. Sydor A, Brown RY. 《Molecular Neuropharmacology: A Foundation for Clinical Neuroscience》 2판. New York: McGraw-Hill Medical. 313–21쪽. ISBN 978-0-07-148127-4.  • 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 often 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.
  24. ↑ 이동:가 나 다 라 Karila L, Wéry A, Weinstein A, Cottencin O, Petit A, Reynaud M, Billieux J (2014). “Sexual addiction or hypersexual disorder: different terms for the same problem? A review of the literature”. 《Curr. Pharm. Des.》 20 (25): 4012–20. doi:10.2174/13816128113199990619. PMID 24001295. 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.
  25. ↑ 이동:가 나 다 라 마 Pitchers KK, Vialou V, Nestler EJ, Laviolette SR, Lehman MN, Coolen LM (February 2013). “Natural and drug rewards act on common neural plasticity mechanisms with ΔFosB as a key mediator”. 《The Journal of Neuroscience》 33 (8): 3434–42. doi:10.1523/JNEUROSCI.4881-12.2013. PMC 3865508. PMID 23426671. 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
  26. ↑ 이동:가 나 다 라 마 Beloate LN, Weems PW, Casey GR, Webb IC, Coolen LM (February 2016). “Nucleus accumbens NMDA receptor activation regulates amphetamine cross-sensitization and deltaFosB expression following sexual experience in male rats”. 《Neuropharmacology》 101: 154–64. doi:10.1016/j.neuropharm.2015.09.023. PMID 26391065. S2CID 25317397.
  27. ↑ Nehlig, Astrid (2004). 《Coffee, tea, chocolate, and the brain.》. Boca Raton: CRC Press. 203–218쪽. ISBN 9780429211928.
  28. ↑ Meule A, Gearhardt AN (September 2014). “Food addiction in the light of DSM-5”. 《Nutrients》 6 (9): 3653–71. doi:10.3390/nu6093653. PMC 4179181. PMID 25230209.
  29. ↑ 이동:가 나 Grant JE, Potenza MN, Weinstein A, Gorelick DA (September 2010). “Introduction to behavioral addictions”. 《Am. J. Drug Alcohol Abuse》 36 (5): 233–241. doi:10.3109/00952990.2010.491884. PMC 3164585. PMID 20560821. Naltrexone, a mu-opioid receptor antagonist approved by the US Food and Drug Administration for the treatment of alcoholism and opioid dependence, has shown efficacy in controlled clinical trials for the treatment of pathological gambling and kleptomania (76–79), and promise in uncontrolled studies of compulsive buying (80), compulsive sexual behavior (81), internet addiction (82), and pathologic skin picking (83). ... Topiramate, an anti-convulsant which blocks the AMPA subtype of glutamate receptor (among other actions), has shown promise in open-label studies of pathological gambling, compulsive buying, and compulsive skin picking (85), as well as efficacy in reducing alcohol (86), cigarette (87), and cocaine (88) use. N-acetyl cysteine, an amino acid that restores extracellular glutamate concentration in the nucleus accumbens, reduced gambling urges and behavior in one study of pathological gamblers (89), and reduces cocaine craving (90) and cocaine use (91) in cocaine addicts. These studies suggest that glutamatergic modulation of dopaminergic tone in the nucleus accumbens may be a mechanism common to behavioral addiction and substance use disorders (92).
  30. ↑ 이동:가 나 다 라 마 바 사 아 자 차 카 타 파 하 거 너 Vassoler FM, Sadri-Vakili G (2014). “Mechanisms of transgenerational inheritance of addictive-like behaviors”. 《Neuroscience》 264: 198–206. doi:10.1016/j.neuroscience.2013.07.064. PMC 3872494. PMID 23920159. 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 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. ...
    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.
  31. ↑ Mayfield RD, Harris RA,1, Schuckit MA (May 2008) "Genetic factors influencing alcohol dependence" PMID 18362899
  32. ↑ 이동:가 나 Kendler KS, Neale MC, Heath AC, Kessler RC, Eaves LJ (May 1994). “A twin-family study of alcoholism in women”. 《Am J Psychiatry》 151 (5): 707–15. doi:10.1176/ajp.151.5.707. PMID 8166312.
  33. ↑ Clarke TK, Crist RC, Kampman KM, Dackis CA, Pettinati HM, O'Brien CP, Oslin DW, Ferraro TN, Lohoff FW, Berrettini WH (2013). “Low frequency genetic variants in the μ-opioid receptor (OPRM1) affect risk for addiction to heroin and cocaine”. 《Neuroscience Letters》 542: 71–75. doi:10.1016/j.neulet.2013.02.018. PMC 3640707. PMID 23454283.
  34. ↑ Hall FS, Drgonova J, Jain S, Uhl GR (December 2013). “Implications of genome wide association studies for addiction: are our a priori assumptions all wrong?”. 《Pharmacology & Therapeutics》 140 (3): 267–79. doi:10.1016/j.pharmthera.2013.07.006. PMC 3797854. PMID 23872493.
  35. ↑ Crowe, J.R. “Genetics of alcoholism”. 《Alcohol Health and Research World》: 1–11. 2017년 12월 13일에 확인함.
  36. ↑ Melemis, Steven M. “The Genetics of Addiction – Is Addiction a Disease?”. 《I Want to Change My Life》. 2018년 9월 17일에 확인함.
  37. ↑ “Overdose Death Rates”. National Institute on Drug Abuse. 2018년 8월 9일. 2018년 9월 17일에 확인함.
  38. ↑ “Overdose Deaths Accelerating During Covid-19”. Centers For Disease Control Prevention. 2020년 12월 18일. 2021년 2월 10일에 확인함.
  39. ↑ 이동:가 나 “What are risk factors and protective factors?”. National Institute on Drug Abuse. 2020년 4월 30일에 원본 문서에서 보존된 문서. 2017년 12월 13일에 확인함.
  40. ↑ “Understanding Drug Use and Addiction”. 《www.drugabuse.gov》 (영어). National Institute on Drug Abuse. 2020년 5월 29일에 확인함.
  41. ↑ Lewis M (October 2018). Longo DL, 편집. “Brain Change in Addiction as Learning, Not Disease”. 《The New England Journal of Medicine》 379 (16): 1551–1560. doi:10.1056/NEJMra1602872. PMID 30332573. 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.
  42. ↑ 이동:가 나 “Adverse Childhood Experiences”. 《samhsa.gov》. Rockville, Maryland, United States: Substance Abuse and Mental Health Services Administration. 2016년 10월 9일에 원본 문서에서 보존된 문서. 2016년 9월 26일에 확인함.
  43. ↑ 이동:가 나 Enoch, Mary (2011). “The role of early life stress as a predictor for alcohol and drug dependence”. 《Psychopharmacology》 214 (1): 17–31. doi:10.1007/s00213-010-1916-6. PMC 3005022. PMID 20596857.
  44. ↑ “Environmental Risk Factors”. 《learn.genetics.utah.edu》. 2018년 9월 17일에 원본 문서에서 보존된 문서. 2018년 9월 17일에 확인함.
  45. ↑ Spear LP (June 2000). “The adolescent brain and age-related behavioral manifestations”. 《Neuroscience and Biobehavioral Reviews》 24 (4): 417–63. CiteSeerX 10.1.1.461.3295. doi:10.1016/s0149-7634(00)00014-2. PMID 10817843. S2CID 14686245.
  46. ↑ Hammond CJ, Mayes LC, Potenza MN (April 2014). “Neurobiology of adolescent substance use and addictive behaviors: treatment implications”. 《Adolescent Medicine》 25 (1): 15–32. PMC 4446977. PMID 25022184.
  47. ↑ Catalano RF, Hawkins JD, Wells EA, Miller J, Brewer D (1990). “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 Addictions》 25 (9A–10A): 1085–140. doi:10.3109/10826089109081039. PMID 2131328.
  48. ↑ Perepletchikova F, Krystal JH, Kaufman J (November 2008). “Practitioner review: adolescent alcohol use disorders: assessment and treatment issues”. 《Journal of Child Psychology and Psychiatry, and Allied Disciplines》 49 (11): 1131–54. doi:10.1111/j.1469-7610.2008.01934.x. PMC 4113213. PMID 19017028.
  49. ↑ “Age and Substance Abuse – Alcohol Rehab”.
  50. ↑ 이동:가 나 “Addiction Statistics – Facts on Drug and Alcohol Addiction”. 《AddictionCenter》. 2018년 9월 17일에 확인함.
  51. ↑ SAMHSA. “Risk and Protective Factors”. Substance Abuse and Mental Health Administration. 2016년 12월 8일에 원본 문서에서 보존된 문서. 2016년 12월 19일에 확인함.
  52. ↑ “Infographic – Risk Factors of Addiction | Recovery Research Institute”. 《www.recoveryanswers.org》. 2016년 12월 17일에 원본 문서에서 보존된 문서. 2016년 12월 19일에 확인함.
  53. ↑ “Drug addiction Risk factors – Mayo Clinic”. 《www.mayoclinic.org》. 2016년 12월 19일에 확인함.
  54. ↑ “The Connection Between Mental Illness and Substance Abuse | Dual Diagnosis”. 《Dual Diagnosis》. 2018년 9월 17일에 확인함.
  55. ↑ 이동:가 나 다 Yuan TF, Li A, Sun X, Ouyang H, Campos C, Rocha NB, Arias-Carrión O, Machado S, Hou G, So KF (2015). “Transgenerational Inheritance of Paternal Neurobehavioral Phenotypes: Stress, Addiction, Ageing and Metabolism”. 《Mol. Neurobiol.》 53 (9): 6367–76. doi:10.1007/s12035-015-9526-2. hdl:10400.22/7331. PMID 26572641. S2CID 25694221.
  56. ↑ 이동:가 나 “Drug abuse liability”. 《www.cambridgecognition.com》 (영어). 2021년 3월 9일에 확인함.
  57. ↑ Abuse, National Institute on Drug (2020년 8월 20일). “Commonly Used Drugs Charts”. 《National Institute on Drug Abuse》 (영어). 2021년 3월 9일에 확인함.
  58. ↑ 이동:가 나 Hyman SE, Malenka RC, Nestler EJ (2006). “Neural mechanisms of addiction: the role of reward-related learning and memory”. 《Annu. Rev. Neurosci.》 29: 565–98. doi:10.1146/annurev.neuro.29.051605.113009. PMID 16776597.
  59. ↑ Steiner H, Van Waes V (January 2013). “Addiction-related gene regulation: risks of exposure to cognitive enhancers vs. other psychostimulants”. 《Prog. Neurobiol.》 100: 60–80. doi:10.1016/j.pneurobio.2012.10.001. PMC 3525776. PMID 23085425.
  60. ↑ Kanehisa Laboratories (2013년 8월 2일). “Alcoholism – Homo sapiens (human)”. 《KEGG Pathway》. 2014년 4월 10일에 확인함.
  61. ↑ Kim Y, Teylan MA, Baron M, Sands A, Nairn AC, Greengard P (February 2009). “Methylphenidate-induced dendritic spine formation and DeltaFosB expression in nucleus accumbens”. 《Proc. Natl. Acad. Sci. USA》 106 (8): 2915–20. Bibcode:2009PNAS..106.2915K. doi:10.1073/pnas.0813179106. PMC 2650365. PMID 19202072.
  62. ↑ 이동:가 나 다 라 마 Nestler EJ (January 2014). “Epigenetic mechanisms of drug addiction”. 《Neuropharmacology》. 76 Pt B: 259–68. doi:10.1016/j.neuropharm.2013.04.004. PMC 3766384. PMID 23643695. 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.
  63. ↑ 이동:가 나 다 라 Blum K, Werner T, Carnes S, Carnes P, Bowirrat A, Giordano J, Oscar-Berman M, Gold M (2012). “Sex, drugs, and rock 'n' roll: hypothesizing common mesolimbic activation as a function of reward gene polymorphisms”. 《Journal of Psychoactive Drugs》 44 (1): 38–55. doi:10.1080/02791072.2012.662112. PMC 4040958. PMID 22641964. 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.
  64. ↑ Malenka RC, Nestler EJ, Hyman SE (2009). 〈Chapter 15: Reinforcement and addictive disorders〉. Sydor A, Brown RY. 《Molecular Neuropharmacology: A Foundation for Clinical Neuroscience》 2판. New York: McGraw-Hill Medical. 384–85쪽. ISBN 978-0-07-148127-4.
  65. ↑ Salamone JD (1992). “Complex motor and sensorimotor functions of striatal and accumbens dopamine: involvement in instrumental behavior processes”. 《Psychopharmacology》 107 (2–3): 160–74. doi:10.1007/bf02245133. PMID 1615120. S2CID 30545845.
  66. ↑ Kauer JA, Malenka RC (November 2007). “Synaptic plasticity and addiction”. 《Nature Reviews. Neuroscience》 8 (11): 844–58. doi:10.1038/nrn2234. PMID 17948030. S2CID 38811195.
  67. ↑ Witten IB, Lin SC, Brodsky M, Prakash R, Diester I, Anikeeva P, 외. (December 2010). “Cholinergic interneurons control local circuit activity and cocaine conditioning”. 《Science》 330 (6011): 1677–81. Bibcode:2010Sci...330.1677W. doi:10.1126/science.1193771. PMC 3142356. PMID 21164015.
  68. ↑ 이동:가 나 Jones S, Bonci A (2005). “Synaptic plasticity and drug addiction”. 《Current Opinion in Pharmacology》 5 (1): 20–25. doi:10.1016/j.coph.2004.08.011. PMID 15661621.
  69. ↑ 이동:가 나 Eisch AJ, Harburg GC (2006). “Opiates, psychostimulants, and adult hippocampal neurogenesis: Insights for addiction and stem cell biology”. 《Hippocampus》 16 (3): 271–86. doi:10.1002/hipo.20161. PMID 16411230. S2CID 23667629.
  70. ↑ Rang HP (2003). 《Pharmacology》. Edinburgh: Churchill Livingstone. 596쪽. ISBN 978-0-443-07145-4.
  71. ↑ Kourrich S, Rothwell PE, Klug JR, Thomas MJ (2007). “Cocaine experience controls bidirectional synaptic plasticity in the nucleus accumbens”. 《J. Neurosci.》 27 (30): 7921–28. doi:10.1523/JNEUROSCI.1859-07.2007. PMC 6672735. PMID 17652583.
  72. ↑ 이동:가 나 Kalivas PW, Volkow ND (August 2005). “The neural basis of addiction: a pathology of motivation and choice”. 《The American Journal of Psychiatry》 162 (8): 1403–13. doi:10.1176/appi.ajp.162.8.1403. PMID 16055761.
  73. ↑ 이동:가 나 Floresco SB, Ghods-Sharifi S (February 2007). “Amygdala-prefrontal cortical circuitry regulates effort-based decision making”. 《Cerebral Cortex》 17 (2): 251–60. CiteSeerX 10.1.1.335.4681. doi:10.1093/cercor/bhj143. PMID 16495432.
  74. ↑ Perry CJ, Zbukvic I, Kim JH, Lawrence AJ (October 2014). “Role of cues and contexts on drug-seeking behaviour”. 《British Journal of Pharmacology》 171 (20): 4636–72. doi:10.1111/bph.12735. PMC 4209936. PMID 24749941.
  75. ↑ 이동:가 나 다 Volkow ND, Fowler JS, Wang GJ, Swanson JM, Telang F (2007). “Dopamine in drug abuse and addiction: results of imaging studies and treatment implications”. 《Arch. Neurol.》 64 (11): 1575–79. doi:10.1001/archneur.64.11.1575. PMID 17998440.
  76. ↑ “Drugs, Brains, and Behavior: The Science of Addiction”. National Institute on Drug Abuse.
  77. ↑ “Understanding Drug Abuse and Addiction”. National Institute on Drug Abuse. November 2012. 2011년 8월 23일에 원본 문서에서 보존된 문서. 2015년 2월 12일에 확인함.
  78. ↑ 이동:가 나 다 라 마 바 Berridge KC (April 2012). “From prediction error to incentive salience: mesolimbic computation of reward motivation”. 《Eur. J. Neurosci.》 35 (7): 1124–43. doi:10.1111/j.1460-9568.2012.07990.x. PMC 3325516. PMID 22487042. 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 addicts.
    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.
  79. ↑ 이동:가 나 Malenka RC, Nestler EJ, Hyman SE (2009). Sydor A, Brown RY, 편집. 《Molecular Neuropharmacology: A Foundation for Clinical Neuroscience》 2판. New York: McGraw-Hill Medical. 147–48, 366–67, 375–76쪽. ISBN 978-0-07-148127-4. 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 human addicts, who state that their desire for drugs (wanting) increases with continued use even when pleasure (liking) decreases because of tolerance.
  80. ↑ 이동:가 나 다 라 Edwards S (2016). 〈Reinforcement principles for addiction medicine; from recreational drug use to psychiatric disorder〉. 《Neuroscience for Addiction Medicine: From Prevention to Rehabilitation - Constructs and Drugs》. 《Prog. Brain Res.》. Progress in Brain Research 223. 63–76쪽. doi:10.1016/bs.pbr.2015.07.005. ISBN 978-0-444-63545-7. PMID 26806771. 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 addition, cues and contexts that are intimately and repeatedly associated with drug use will often 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).
  81. ↑ 이동:가 나 Berridge KC, Kringelbach ML (May 2015). “Pleasure systems in the brain”. 《Neuron》 86 (3): 646–64. doi:10.1016/j.neuron.2015.02.018. PMC 4425246. PMID 25950633.
  82. ↑ Nestler EJ, Barrot M, Self DW (September 2001). “DeltaFosB: a sustained molecular switch for addiction”. 《Proc. Natl. Acad. Sci. U.S.A.》 98 (20): 11042–46. Bibcode:2001PNAS...9811042N. doi:10.1073/pnas.191352698. PMC 58680. PMID 11572966. Although the ΔFosB signal is relatively long-lived, it is not permanent. ΔFosB degrades gradually and can no longer be detected in brain after 1–2 months of drug withdrawal ... Indeed, ΔFosB is the longest-lived adaptation known to occur in adult brain, not only in response to drugs of abuse, but to any other perturbation (that doesn't involve lesions) as well.
  83. ↑ Nestler EJ (October 2008). “Review. Transcriptional mechanisms of addiction: role of DeltaFosB”. 《Philosophical Transactions of the Royal Society of London. Series B, Biological Sciences》 363 (1507): 3245–55. doi:10.1098/rstb.2008.0067. PMC 2607320. PMID 18640924. 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
  84. ↑ Traynor J (March 2012). “μ-Opioid receptors and regulators of G protein signaling (RGS) proteins: from a symposium on new concepts in mu-opioid pharmacology”. 《Drug Alcohol Depend》 121 (3): 173–80. doi:10.1016/j.drugalcdep.2011.10.027. PMC 3288798. PMID 22129844.
  85. ↑ 이동:가 나 Walker DM, Cates HM, Heller EA, Nestler EJ (February 2015). “Regulation of chromatin states by drugs of abuse”. 《Curr. Opin. Neurobiol.》 30: 112–21. doi:10.1016/j.conb.2014.11.002. PMC 4293340. PMID 25486626. Studies investigating general HDAC inhibition on behavioral outcomes have produced varying results but it seems that the effects are specific to the timing of exposure (either before, during or after exposure to drugs of abuse) as well as the length of exposure
  86. ↑ “Facing Addiction in America: The Surgeon General's Report on Alcohol, Drugs, and Health” (PDF). 《Office of the Surgeon General》. US Department of Health and Human Services. November 2016. 35–37, 45, 63, 155, 317, 338쪽. 2017년 1월 28일에 확인함.
  87. ↑ American Psychiatric Association (2013). “Substance-Related and Addictive Disorders” (PDF). American Psychiatric Publishing. 1–2쪽. 2015년 8월 15일에 원본 문서 (PDF)에서 보존된 문서. 2015년 7월 10일에 확인함. 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.
  88. ↑ Petry NM, Rehbein F, Gentile DA, Lemmens JS, Rumpf HJ, Mößle T, Bischof G, Tao R, Fung DS, Borges G, Auriacombe M, González Ibáñez A, Tam P, O'Brien CP (September 2014). “An international consensus for assessing internet gaming disorder using the new DSM-5 approach”. 《Addiction》 109 (9): 1399–406. doi:10.1111/add.12457. PMID 24456155.
  89. ↑ Torres G, Horowitz JM (1999). “Drugs of abuse and brain gene expression”. 《Psychosom Med》 61 (5): 630–50. CiteSeerX 10.1.1.326.4903. doi:10.1097/00006842-199909000-00007. PMID 10511013.
  90. ↑ Malenka RC, Nestler EJ, Hyman SE, Holtzman DM (2015). 〈Chapter 16: Reinforcement and Addictive Disorders〉. 《Molecular Neuropharmacology: A Foundation for Clinical Neuroscience》 3판. New York: McGraw-Hill Medical. ISBN 978-0-07-182770-6. 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.
  91. ↑ Insel, Thomas. “Transforming Diagnosis”. National Institute of Mental Health. 2013년 5월 29일에 원본 문서에서 보존된 문서. 2015년 6월 17일에 확인함.
  92. ↑ Hampton WH, Hanik I, Olson IR (2019). “Substance Abuse and White Matter: Findings, Limitations, and Future of Diffusion Tensor Imaging Research”. 《Drug and Alcohol Dependence》 (영어) 197 (4): 288–298. doi:10.1016/j.drugalcdep.2019.02.005. PMC 6440853. PMID 30875650. Despite this progress, our ability to predict, diagnose, and track addiction in humans based on brain images has been relatively limited. The difficulty elucidating such outcomes may be partly due to a relative dearth of research considering neural white matter, which constitutes over half of human brain volume and plays a vital role in governing communication between cortical areas (Fields, 2008). Diffusion mag- netic resonance imaging has emerged as a method to non-invasively examine white matter in the human brain and relate such connectivity to substance abuse and addictive behaviors (Suckling and Nestor, 2017)
  93. ↑ 보건복지부-약물중독
  94. ↑ Chen CC, Yin SJ. (Oct 2008) "Alcohol abuse and related factors in Asia". PMID: 19012127
  95. ↑ Mak KK, Lai CM, Watanabe H. (Nov 2014) "Epidemiology of internet behaviors and addiction among adolescents in six Asian countries". PMID: 25405785
  96. ↑ Slade T, Johnston A, Teesson M, Whiteford H, Burgess P, Pirkis J, Saw S (May 2009). “The Mental Health of Australians 2: Substance Use Disorders in Australia” (PDF). Department of Health and Ageing, Canberra. 2020년 8월 18일에 원본 문서 (PDF)에서 보존된 문서. 2021년 5월 6일에 확인함.
  97. ↑ Peacock A, Leung J, Larney S. (Oct 2018) "Global statistics on alcohol, tobacco and illicit drug use: 2017 status report." PMID: 29749059
  98. ↑ Manubay JM, Muchow C, Sullivan MA (March 2011). “Prescription drug abuse: epidemiology, regulatory issues, chronic pain management with narcotic analgesics”. 《Primary Care》 38 (1): 71–90. doi:10.1016/j.pop.2010.11.006. PMC 3328297. PMID 21356422.
  99. ↑ 이동:가 나 다 라 Volkow, Nora (2016년 3월 31일). “A Major Step Forward for Addiction Medicine”. 《National Institute on Drug Abuse》. National Institutes of Health. 2016년 4월 5일에 원본 문서에서 보존된 문서. 2016년 4월 3일에 확인함. 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.'
  100. ↑ Gramlich J (2017년 10월 26일). “Nearly half of Americans have a family member or close friend who's been addicted to drugs”. Pew Research Center. 2018년 1월 14일에 확인함.
  101. ↑ “We were addicted to their pill, but they were addicted to the money”. 《The Washington Post》 (영어). 2019년 7월 22일에 확인함.
  102. ↑ 《World Drug Report 2012》 (PDF). 《United Nations Office on Drugs and Crime》 (United Nations). June 2012. ISBN 978-92-1-148267-6.
  103. ↑ Pacurucu-Castillo SF, Ordóñez-Mancheno JM, Hernández-Cruz A, Alarcón RD (April 2019). “World opioid and substance use epidemic: a Latin American perspective.”. 《Psychiatric Research and Clinical Practice.》 1 (1): 32–8. doi:10.1176/appi.prcp.20180009.
  104. ↑ Fehrman E, Egan V, Gorban AN, Levesley J, Mirkes EM, Muhammad AK (2019). 《Personality Traits and Drug Consumption. A Story Told by Data》. Springer, Cham. arXiv:2001.06520. doi:10.1007/978-3-030-10442-9. ISBN 978-3-030-10441-2. S2CID 151160405.
  105. ↑ Cheetham A, Allen NB, Yücel M, Lubman DI (August 2010). “The role of affective dysregulation in drug addiction”. 《Clin Psychol Rev》 30 (6): 621–34. doi:10.1016/j.cpr.2010.04.005. PMID 20546986.
  106. ↑ Franken IH, Muris P (2006). “BIS/BAS personality characteristics and college students' substance use”. 《Personality and Individual Differences》 40 (7): 1497–503. doi:10.1016/j.paid.2005.12.005.
  107. ↑ Genovese JE, Wallace D (December 2007). “Reward sensitivity and substance abuse in middle school and high school students”. 《J Genet Psychol》 168 (4): 465–69. doi:10.3200/GNTP.168.4.465-469. PMID 18232522. S2CID 207640075.
  108. ↑ Kimbrel NA, Nelson-Gray RO, Mitchell JT (April 2007). “Reinforcement sensitivity and maternal style as predictors of psychopathology”. 《Personality and Individual Differences》 42 (6): 1139–49. doi:10.1016/j.paid.2006.06.028.
  109. ↑ Dawe S, Loxton NJ (May 2004). “The role of impulsivity in the development of substance use and eating disorders”. 《Neurosci Biobehav Rev》 28 (3): 343–51. doi:10.1016/j.neubiorev.2004.03.007. PMID 15225976. S2CID 24435589.
내용주
  1. ↑ According to a review of experimental animal models that examined the transgenerational epigenetic inheritance of epigenetic marks that occur in addiction, alterations in histone acetylation – specifically, di-acetylation of lysine residues 9 and 14 on histone 3 (i.e., H3K9ac2 and H3K14ac2) in association with BDNF gene promoters – have been shown to occur within the medial prefrontal cortex (mPFC), testes, and sperm of cocaine-addicted male rats.[30] These epigenetic alterations in the rat mPFC result in increased BDNF gene expression within the mPFC, which in turn blunts the rewarding properties of cocaine and reduces cocaine self-administration.[30] The male but not female offspring of these cocaine-exposed rats inherited both epigenetic marks (i.e., di-acetylation of lysine residues 9 and 14 on histone 3) within mPFC neurons, the corresponding increase in BDNF expression within mPFC neurons, and the behavioral phenotype associated with these effects (i.e., a reduction in cocaine reward, resulting in reduced cocaine-seeking by these male offspring).[30] Consequently, the transmission of these two cocaine-induced epigenetic alterations (i.e., H3K9ac2 and H3K14ac2) in rats from male fathers to male offspring served to reduce the offspring's risk of developing an addiction to cocaine.[30] 2018년 기준 neither the heritability of these epigenetic marks in humans nor the behavioral effects of the marks within human mPFC neurons has been established.[30]
  2. ↑ 혐오감에 대한 민감도가 감소한다는 것은 간단히 말해 행동이 바람직하지 않은 결과에 영향을 받을 가능성이 작아진다는 것이다.
  3. ↑ Incentive salience, the "motivational salience" for a reward, is a "desire" or "want" attribute, which includes a motivational component, that the brain assigns to a rewarding stimulus.[79][80] As a consequence, incentive salience acts as a motivational "magnet" for a rewarding stimulus that commands attention, induces approach, and causes the rewarding stimulus to be sought out.[79]
  4. ↑ In simplest terms, this means that when either amphetamine or sex is perceived as more alluring or desirable through reward sensitization, this effect occurs with the other as well.
  5. ↑ The lifetime prevalence of an addiction is the percentage of individuals in a population that developed an addiction at some point in their life.
====

탐닉

최근 수정 시각: 
44
편집토론역사
분류 
언어별 명칭
영어
프랑스어
addiction
Substance Use Disorder
스페인어
adicción
포르투갈어
vício, adicção
독일어
abhängigkeit
이탈리아어
dipendenza
스웨덴어
beroende
중국어
成瘾(chéng yǐn)
일본어
嗜癖しへき, 耽溺たんでき

1. 개요2. 설명
2.1. 단어의 특징2.2. 탐닉의 3대 요소2.3. 원인2.4. 해결책
3. 종류
3.1. 물질 탐닉3.2. 행위 탐닉
4. 관련 문서


1. 개요[편집]

탐닉(耽溺, Substance Use Disorder)은 신체적 혹은 정신적 원인으로 강화 효과가 생겨 특정 행동이나 물질 등에 집착하여 정상적 생활에 장애가 생긴 '정신적, 의존적 중독'이다. 신경증의 일종이며 '의존증(依存症)', 과몰입증, 또는 '의존증후군'이라고도 한다.

일시적 쾌락을 추구하는 행위를 장기적으로 하고 있으며 이로 인해 부정적인 결과가 발생해도 통제력을 상실하거나 개인이 스스로 노력해도 빠져나올 수 없는 상태를 의미한다.

2. 설명[편집]

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1953년 몬트리얼, Peter Milner와 James Olds는 수면과 각성주기를 조절한다는 중뇌망상계(망상체)를 표적으로 쥐의 뇌에 전극을 이식하는 수술 후 외부에서 전기 자극을 주는 실험을 했다. 그러나 이식된 전극이 표적을 벗어나 중격(septum)이란 영역에 닿았고, 예상치 못한 실험결과를 보여주었다. 이에 흥분한 올즈와 밀러는 "스키너의 방"을 개조해 지렛대를 쥐들이 누르면 이식된 전극을 통해 똑같은 위치의 뇌 부분을 직접 자극할 수 있는 방을 만들었다. 그리고 두 사람의 눈앞에서 행동 신경과학 역사상 가장 극적인 사건이 펼쳐졌다. 쥐들은 자신의 뇌를 자극하기 위해 시간당 무려 7천 번이나 지렛대를 눌렀다. 그들이 자극하고 있는 것은 '호기심의 중추'가 아니었다. 그것은 쾌감중추이자 보상회로였고, 그 활성화는 자연의 어떤 자극보다 훨씬 더 강했다. 쥐들은 물과 먹이보다 쾌감회로 자극을 더 좋아했다. 수컷들은 발정기의 암컷을 무시하고 지렛대를 눌러댔고, 암컷들은 갓 태어난 젖먹이 새끼를 내팽개치고 잇따라 지렛대를 눌러댔다. 어떤 쥐들은 다른 모든 활동을 제쳐두고 시간당 평균 2천번씩, 무려 24시간 동안 자기 자극을 가했다. 자발적 기아로 죽는걸 막기 위해선 쥐들을 다른 곳으로 옮기는 수 밖에 없었다. 그들에겐 이미 지렛대 누르기가 세상의 전부였다.
《고삐 풀린 뇌》, 데이비드 J. 린든
attachment/addic...
탐닉의 악순환. 원본은 일본의 약물의존증 포스터로, 많은 패러디가 존재한다.

2.1. 단어의 특징[편집]

한자문화권에서는 이것도 '중독'[1]으로 부르는 경우가 많은데 자세한 설명은 해당 문서를 참고할 것. 학계와 위키백과에서는 '중독'과 '탐닉'을 엄격히 구별한다.

사이비, 포탈과 같이 '닉'이라는 한자음이 익숙치 않아서인지 이것도 'Tomnick' 같은 영어일 것이라고 알고 있는 사람들이 가끔 있지만 탐닉은 한자어다.

2.2. 탐닉의 3대 요소[편집]

중독은 강박관념, 갈망, 부정적인 결과를 특징으로 합니다. 중독이 되기 위해 아래 사항을 모두 충족할 필요는 없습니다. 몇 개라도 충분하며 중독의 징후일 수 있습니다.
  • 의존성(Dependency): 한 번 해당 대상을 접하면 자신의 의지로 끊을 수 없게 되는 것. 탐닉을 의존증이라고도 하는 이유다.
  • 내성(Tolerance): 해당 대상을 반복해서 이용하면 몸이 익숙해져 지금까지의 양으로는 효과를 볼 수 없는 것.
  • 금단증세(Withdrawal): 무언가의 섭취를 끊었을 때 발생하는 신체의 이상적인 반응을 의미한다. 금단증상, 금단현상이라고도 한다. 일반적으로 의존성을 전제로 한다.
  • 갈망 (Cravings):물질의 긍정적인 효과를 경험하려는 마음
  • 제어 (Control): 사용을 줄이거나 통제하려고 노력함
  • 시간 (Time): 물질을 얻거나, 영향을 받거나 물질로부터 회복하는 데 많은 시간을 소비한다
  • 해로운 (Harmful): 해롭거나 좋지 않다는 것을 알면서도 사용하는 경우
  • 신체적 위험 (Physical danger):물질의 긍정적인 효과를 경험하려는 마음운전과 같은 신체적 위험 상황에서 물질을 사용한다.

2.3. 원인[편집]

태아기 때 임신 중인 엄마가 높은 스트레스를 받으면 그 아이들은 쉽게 과몰입 증세를 보일 수 있으며 이러한 사실은 환경적 요인이 얼마나 사람에게 큰 영향을 미치는지 보여준다.

개인의 감수성의 문제라고 하여 결국 탐닉은 개인의 문제라고 결론내리기 쉽지만 환경, 즉 타의에 의해 증세가 발생하는 경우도 많다. 전자의 경우 도피성 행동을, 후자의 경우 강박성 행동을 보인다. 예를 들자면 애들한테 공부를 시켰더니 하나는 잔소리 듣기 싫어서 더욱 게임에 매달렸고 다른 하나는 강박관념에 사로잡혀서 공부만 하고 놀거나 일상생활을 못 하게 되었다는 식이다.

누군가는 탐닉이 무서운 이유가 그러한 사람이 자신이 의존증이라는 사실을 전혀 인지하지 못하기 때문이라고 카더라. 실제로 "끊으려면 언제든지 끊을 수 있으니 의존 증세가 아니다. 다만 끊을 생각이 없을 뿐."이라는 식의 생각을 가진 사람들이 많기에 자기가 의존 상태임을 인정하지 않고 그 상태에 계속 머무르는 의존자들이 많다. 쉬운 예로 술에 취했는데 안 취했다고 말하는 사람이 있다. 물론 이 경우는 이해를 돕기 위한 극단적인 예시다.

가장 큰 원인은 역시 지속적인 강렬한 & 새로운 자극을 얻고 도파민이 과다분비되어 강화 효과로 인해 해당 자극을 계속 추구하면서 다른 일에 무기력해지는 것이 핵심이라고 볼 수 있다. 특히 초기에는 순수하게 쾌락을 얻기 위해 점차 횟수를 늘리다가 어느 순간부터는 쾌락은 별로 못 느끼고 도리어 강한 금단증상 때문에 그러한 금단증상을 없애기 위해 이러한 행동을 하는 경우가 많다.

이에 대한 자세한 설명으로 도구적 조건형성이란 게 있다. 이는 '강화'와 '처벌'을 통해서 "어떤 행동을 더 하게 만드는 작용"이라고 할 수 있다. 강화는 쾌감(도파민 분비)의 추구다. 전술한 대로 초기엔 그 행동, 약물을 하면서 도파민이 분비되기 때문에 그런 행동/약물을 하는 것이다. 두 번째로 처벌은 고통 회피다. 쉽게 말해 중증 흡연자나 습관성 약물 의존자들은 쾌감을 얻기 위해서가 아니라 금단증상이 불편하고 짜증나니까 담배와 약을 빠는 것이다.

의존증에 대한 생물학적인 작용기전은 동물실험이 용이한 약물중독을 중심으로 활발히 연구되어 왔으며 중뇌에 위치한 도파민 신경세포를 중심으로한 뇌 보상회로[2]에 대한 각종 작용기전이 보고되고 있다. 각종 약물의 작용기전을 비교적 쉽고(?) 재밌게 설명한 플래시

2000년대 중반에는 섬엽(insula)이라는 뇌 부위가 탐닉과 관련이 있으며 섬엽의 활동이 억제되는 경우 쉽게 탐닉에서 빠져나오는 걸로 보고되었다. 또한 안와전두피질도 관련이 있다고 보고되었다. 그리고 뇌에서 원함과 좋아함을 조절하는 부위가 서로 다르다는 사실도 보고되었다. 이 내용을 포함한 최근 연구결과나 관련 자료들은 아래와 같다.
[ 안와전두피질 설명 펼치기 · 접기 ]


[ 보상과 처벌의 작용원리 펼치기 · 접기 ]



[ 관련 신경전달물질 펼치기 · 접기 ]

2.4. 해결책[편집]

따라서 도구적 조건형성에 입각한 해결법은 대략 다음과 같다.
  • 정적 강화: 쾌자극 부여. 의존 상태를 줄이는데 성공하면 어떠한 보상(인센티브 현저성 Incentive salience 참고)을 준다. 다이어트할 때 일정기간마다 고칼로리 음식으로 욕구불만을 해소하는 걸 생각하면 된다.
  • 부적 강화: 혐오자극 제거. 어떤 제약이나 불이익을 가하고, 증상을 줄이는데 성공하면 그 불이익을 해제한다.
  • 약화: 만약 사소한 다른 자극(실제 자극, 상상 자극)에 보상심리, 쾌감을 느껴서 그로 인해 증상을 줄이거나, 자극에 점차 무뎌지는 과정, 심신단련이나 명상등을 통해 마인드 컨트롤을 하여 줄이는 방법 등이 있다.

여러 전략 중 자신에게 최적화된 전략을 사용하는 것이 핵심이라 볼 수 있다. 처벌에 상대적으로 더 민감한 사람인 경우, 강화 항목을 해당 목적을 이루지 못할 경우 부정적 강화와 긍정적 강화로 인한 잠재 미래 이익을 얻지 못하고 박탈당하는 처벌, 즉 부정적 처벌 등으로 조정하는 전략을 취할 수도 있다. 강화에 상대적으로 더 민감한 사람인 경우 처벌 항목을 해당 목적을 이룰 경우 긍정적 처벌과 부정적 처벌로 인한 잠재 미래 처벌과 위험을 면제 받는다는 이익, 즉 부정적 강화 등으로 조정하는 전략을 취할 수도 있다.

'미리 그 상황의 쾌감을 느끼는 상황'을 상상하여 역설적으로 욕구를 줄이는 방법도 가능한 것으로 보인다.
[ 관련 연구결과 펼치기 · 접기 ]

3. 종류[편집]

3.1. 물질 탐닉[편집]

3.2. 행위 탐닉[편집]

사실상 가능한 모든 행위가 탐닉의 대상이 될 수 있다. 특정 행위 자체가 문제는 아니다.

4. 관련 문서[편집]

[1] 단, 일본어에서는 구어 차원에서만 칭한다.[2] 중뇌 도파민 신경세포(특히 복측피개야 영역(ventral tegmental area)에 위치한 세포들)는 측좌핵(nucleus accumbens), 전전두피질(prefrontal cortex), 해마(hippocampus), 편도체(amygdala) 등 뇌의 각 부위로 연결되어 있으며, 이들 상호간에도 복잡한 연결망이 존재한다.[3] 돈이 좋다고 해도 이것에 빠지면 가장 큰 폐해를 불러 일으킬 가능성이 높다.[4] 주위 사람들의 칭찬, 아첨, 편 들어주기 등에 중독되면 매우 자기중심적인 사람으로 변하며 타인에 대한 공감능력이 많이 떨어지게 된다. 또 직접 사람들의 인정을 받지 않더라도 다른 사람이 여러 사람에게 칭찬 등을 받는 것을 보고 시기심, 열등감 등이 생겨서 사람들의 인정을 갈구하게 되는 경우도 매우 많다.[5] 현재 디지털 중독에 대해서는 실재 여부와 진단 가능 여부에 대해 논란이 있는데 진단 기준의 확립 등의 관련 연구가 진행되고 있는 상황이므로 일단 여기에 등재했다.[6] 2000년대 한정. 2010년대 이후부터는 드물다.[7] 믿음이 좋은 것과 종교 중독은 다른데 믿음이 좋은 사람은 자신과 뜻이 다른 사람들에 대해서도 마음으로부터 우러나오는 온유함이 있지만 종교에 중독된 사람은 특정 종교 기관, 특정 목사, 교리 등에 집착하면서 자신의 마음에 들지 않는 사람들에 대해 거친 태도를 보인다.
CC-white 이 문서의 내용 중 전체 또는 일부는  문서의 r254 판에서 가져왔습니다. 이전 역사 보러 가기
==

嗜癖

出典: フリー百科事典『ウィキペディア（Wikipedia）』
嗜癖と依存の用語集[1][2][3][4][5]
  • 嗜癖(アディクション) – 有害な結果にもかかわらず、報酬刺激に対しての強迫的関与を特徴とする脳障害。1950年代に世界保健機関WHOにより依存症のような意味で定義されたが、異なる意味である乱用の意味でも用いられるため、WHOの専門用語から除外した。2013年のDSM-5において大分類名に登場し、その下位にDSM-IVの依存症と乱用が統合された物質使用障害がある
  • 嗜癖性薬物 – 報酬と強化をもたらす薬物
  • 物質使用障害 - 物質使用が臨床的・機能的に重大な障害または苦痛をもたらす状態
  • 依存症(Dependence) – 反復暴露している刺激の中止時に、離脱を引き起こすような適応状態
  • 乱用(Abuse) – 依存の状態を満たさないが繰り返して薬物による問題を起こす状態
  • 習慣(Habit) - WHOは摂取量が増えず身体依存もない状態と定義し[6]、その後破棄した[7]。日本の薬事法において身体依存のある薬物も含めて分類している。
  • 中毒 - 日本で過去に依存症のような意味で使われたが、現行の医学的には大量摂取などで毒性が生じている状態
  • 離脱 –反復使用している薬物の中断時に起こる症状
  • 身体的依存 – 身体的・心身的症状が持続して発生する依存状態
  • 精神的依存 – 感情的・動機的な離脱症状が発生する依存状態
  • 強化刺激 – 対象行動を繰り返す確率を高める刺激
  • 報酬刺激 – 本質的に脳がポジティブまたは取り入れるべきと解釈する刺激
  • 耐性 – 与えられた用量での反復投与に起因する、薬物効果の減少
  • 逆耐性,感作 – 薬剤の反復投与によって、その効用が漸増していくこと

嗜癖（しへき、英: addiction、アディクション）とは、ある特定の物質や行動、人間関係を特に好む性向である。

薬物嗜癖（drug addiction）の用語は、異なる概念である薬物依存症と薬物乱用の定義との誤用があるため世界保健機関の専門用語から除外された[8]。薬物に対する嗜癖の用語は、一般的には広く用いられている[8]。日本の法律的な文脈では中毒という邦訳もあるが、医学的に薬物中毒とは、嗜癖ではなく過剰摂取などによって有害作用が生じている状態である[9]。さらなる詳細は、以下の定義節を参照のこと。

薬物関連のこの用語の定義と歴史[編集]

トランキライザーなどの乱用が問題となった1950年代には、世界保健機関のAddiction-Producing Drugsに関する専門委員会が、以下のように定義した[6]。

  • Addiction-producing：非常に強い渇望があり、用量は増える傾向にあり、精神依存と身体依存とがある。
  • Habit-formaing：用量は増えないか微増であり、身体依存が欠如しており、禁断症状がない。

当時の日本では、このAddiction-Producing Drugsが、耽溺性薬物などと翻訳されている[10]。薬物嗜癖（drug addiction）、薬物習慣性（drug habituation）としている重要語事典もある[11]。日本では睡眠薬の乱用が問題となったため、1961年に習慣性医薬品を指定し、処方箋を必要とする措置をとった[10]。

1960年代に嗜癖（Addiction）と習慣（Habit）の2つの用語は破棄され、依存（Dependence）の用語に変わった[12]。世界保健機関の専門委員会は、薬物依存に関する専門委員会（WHO Expert Committee on Drug Dependence）と変名される。

1975年時点で、日本の医薬品には「習慣性あり」の表示が残されているが、アメリカではそうした表示は過去のことであり、ここ10年で国内外で習慣性という語は見られなくなったとしている[13]。また、依存の語は広く普及し、嗜癖の語はいまだ散見されるとしている[13]。

アメリカ精神医学会（APA）による『精神障害の診断と統計マニュアル第4版』（DSM-IV）では、身体依存や使用量増加の診断基準は薬物依存症（Drug Dependence）の診断基準に含まれる。

しかし2011年の『グッドマン・ギルマン薬理書』第12版においては、1987年にアメリカ精神医学会が、使用を制御できない状態に対し依存（dependence）の語を使ったが、依存とは本来は離脱症状を呈する状態であり混乱が生じたとしている[14]。当時は嗜癖（addiction）の語が軽蔑語であったので避けるべきであったが、次のDSM-5ではこの混乱が正されるであろうと記している[14]。

DSM-5では、物質関連障害および嗜癖性障害群（Substance Related and Addictive Disorders）の分類名が登場した[15]。DSM-5においては薬物乱用と薬物依存症を統合したが、DSM-IVの編集委員長であるアレン・フランセスはこれを批判しており、嗜癖（addicion）の語による常用者のようなレッテルは、より単発的な乱用によって問題が生じた人々にとっては不利益を被りかねないスティグマ（烙印）であり、臨床においても乱用と依存の区別は対応の上で有益であるとして、これを区別している世界保健機関によるICDの診断コードを用いるべきだとしている[16]。

アメリカにおける薬物関連障害の報告などでは、薬物依存と薬物乱用の両方を含める形で、薬物嗜癖（Drug Addiction）の用語を使用すると定義している[17]。

どのような意図で用いられているか文脈によって判断することが必要である。

国際条約である1961年の麻薬に関する単一条約の邦訳文で、addctionを中毒と訳している[18]。日本の麻薬及び向精神薬取締法でも依存を生じた状態を中毒としているが、この日本の法律上の訳は「医学的な中毒の意味と異なり」、医学的に薬物中毒とは、過剰摂取などによって有害作用が生じている状態である[9]。1975年時点で、柳田知司は依存症の意味での中毒の語は破棄して、依存症の語の使用を提案している[13]。

分類[編集]

嗜癖は、その対象によって以下のように分類できる。

物質嗜癖[編集]

「薬物依存症」および「薬物乱用」も参照

特定の物質の摂取に関する嗜癖。酒、タバコ、乱用薬物に該当する種類の向精神薬が対象になりやすい。アルコールなら、ダメだとわかっていても朝から酒を飲まずにおれず、酒しか楽しみがなく、肝臓が悪くなっても酒をやめない、など。離脱症状が伴えば薬物依存症、伴わなければ薬物乱用の状態である。

行動嗜癖[編集]

詳細は「行動嗜癖」を参照

特定の行動過程に執着する嗜癖。その行動を抑えがたい欲求や衝動があり、他の娯楽を無視し、有害事象が起きてもその行動をやめない。パチンコなどのギャンブル、ショッピング、日常的暴力、性行為などが対象となる。「好きだから行う」という点において、強迫性障害において不快を避けるために行う強迫行為とは区別される。ギャンブル嗜癖では、ギャンブルをやめようと思った時点ではすでに借金を負っていることも多く、このため負けた金銭を取り返せるまでやめられず結果として更に借金が膨らむ強迫化が起こりえる。

クロス・アディクション[編集]

複数の対象を持つ嗜癖。嗜癖は対象が異っても、同じ空虚感から同じようなメカニズムで発症しているので、同時に2つ以上の嗜癖が合併することがある（酒とギャンブル、薬物と性行為など）。反社会性の強い対象へ移行しつつ（アルコール→ギャンブル→薬物）嗜癖が続くことも多い。

要因[編集]

環境要因[編集]

米国では8年でコカイン乱用者が8倍に増える時期があった。ベトナム戦争に行った米兵の約3割が麻薬嗜癖であったが、帰国後はその多くが乱用をやめている。これらの事実から、嗜癖には環境要因が大きくかかわっていると推測されている。

性格[編集]

性格は、薬物乱用の最も重要な成因とされる。意志薄弱、依存的、未熟性、逃避的、自信欠乏、情緒不安定、自己中心的、顕示的など。日本で治療を受けている大麻嗜癖者では、性格検査で気軽な衝動性、被支配性が高いプロフィールを持った者が多く、鎮痛薬嗜癖者は抑うつ、神経質、短気であるという報告がある[要出典]。

脚注[編集]

[脚注の使い方]
  1. ^ “Chapter 15: Reinforcement and Addictive Disorders”. Molecular Neuropharmacology: A Foundation for Clinical Neuroscience (2nd ed.). New York: McGraw-Hill Medical. (2009). pp. 364–375. ISBN 9780071481274
  2. ^ Nestler EJ (December 2013). “Cellular basis of memory for addiction”. Dialogues Clin. Neurosci. 15 (4): 431–443. PMC 3898681. PMID 24459410.
  3. ^ “Glossary of Terms”. Mount Sinai School of Medicine. Department of Neuroscience. 2015年2月9日閲覧。
  4. ^ “Neurobiologic Advances from the Brain Disease Model of Addiction”. N. Engl. J. Med. 374 (4): 363–371. (January 2016). doi:10.1056/NEJMra1511480. PMID 26816013.
  5. ^ 中村春香、成田健一「嗜癖とは何か-その現代的意義を歴史的経緯から探る」『人文論究』第60巻第4号、2011年2月、37-54頁、NAID 120003802584。
  6. ^ a b 世界保健機関 (1957). WHO Expert Committee on Addiction-Producing Drugs - Seventh Report / WHO Technical Report Series 116 (pdf) (Report). World Health Organization. pp. 9–10.
  7. ^ 世界保健機関 (1994) (pdf). Lexicon of alchol and drug term. World Health Organization. pp. 6. ISBN 92-4-154468-6 （HTML版 introductionが省略されている）
  8. ^ a b 世界保健機関 2003, p. 22.
  9. ^ a b (編集)日本緩和医療学会、緩和医療ガイドライン作成委員会「薬理学的知識」『がん疼痛の薬物療法に関するガイドライン』（第1版;2010年）金原出版、2010年6月20日。ISBN 978-4-307-10149-3。
  10. ^ a b 松枝亜希子「トランキライザーの流行―市販向精神薬の規制の論拠と経過」（pdf）『Core Ethics』第6巻、2010年、385-399頁。
  11. ^ 保崎秀夫（編集）、武正健一（編集）『医師国家試験のための精神科重要用語事典』金原出版、1982年。ISBN 4-307-15004-X。
  12. ^ 世界保健機関 (1994) (pdf). Lexicon of alchol and drug term. World Health Organization. pp. 6. ISBN 92-4-154468-6 （HTML版 introductionが省略されている）
  13. ^ a b c 柳田知司 1975.
  14. ^ a b Laurence Brunton(編集), Bjorn Knollman(編集), Bruce Chabner(編集)『グッドマン・ギルマン薬理書〈上〉薬物治療の基礎と臨床』廣川書店、2013年、840頁。ISBN 978-4567498005。、Goodman & Gilman's The Pharmacological Basis of Therapeutics, 12e, 2011
  15. ^ アメリカ精神医学会『DSM-5 精神疾患の診断・統計マニュアル』日本精神神経学会日本語版用語監修・高橋三郎・大野裕監訳・染矢俊幸・神庭重信・尾崎紀夫・三村將・村井俊哉訳、医学書院、2014年6月30日。ISBN 978-4260019071。
  16. ^ アレン・フランセス、大野裕（翻訳）、中川敦夫（翻訳）、柳沢圭子（翻訳）『精神疾患診断のエッセンス―DSM-5の上手な使い方』金剛出版、2014年3月、138-140頁。ISBN 978-4772413527。、Essentials of Psychiatric Diagnosis, Revised Edition: Responding to the Challenge of DSM-5®, The Guilford Press, 2013.
  17. ^ Addiction Medicine: Closing the Gap between Science and Practice. The National Center on Addiction and Substance Abuse at Columbia. (2012-06)
  18. ^ 麻薬に関する単一条約 英日対訳文 1 約2 約3）（日本語）（外務省）

参考文献[編集]

関連項目[編集]

ウィキメディア・コモンズには、嗜癖に関連するカテゴリがあります。

外部リンク[編集]


==

버릇

출처 : 무료 백과 사전 "Wikipedia (Wikipedia)"
습관과 의존 용어집 [1] [2] [3] [4] [5]
  • 습관 (적용) - 해로운 결과에도 불구하고 보상 자극에 대한 강박적인 참여를 특징으로하는 뇌 장애. 1950년대에 세계보건기구 WHO에 의해 중독과 같은 의미로 정의되었지만, 다른 의미인 남용의 의미에서도 사용되기 때문에 WHO의 전문 용어에서 제외했다. 2013년의 DSM-5에 있어서 대분류명에 등장해, 그 하위에 DSM-IV의 의존증과 남용이 통합된 물질 사용 장애가 있다
  • 습관성 약물 – 보상과 강화를 가져오는 약물
  • 물질 사용 장애 - 물질 사용이 임상 적 및 기능적으로 심각한 장애 또는 고통을 초래하는 상태
  • 중독 (Dependence) – 반복적으로 노출된 자극을 중단할 때 이탈을 일으키는 적응 상태
  • 남용 (Abuse) – 의존 상태를 충족시키지 않지만 반복하여 약물에 의한 문제를 일으키는 상태
  • 습관 (Habit) - WHO는 섭취량이 증가하지 않고 신체 의존도 없는 상태로 정의하고 [6] , 그 후 파기했다 [7] . 일본의 약사법에 있어서 신체 의존이 있는 약물도 포함하여 분류하고 있다.
  • 중독 - 일본에서 과거에 중독과 같은 의미로 사용되었지만, 현행 의학적으로는 대량 섭취 등으로 독성이 발생하고 있는 상태
  • 이탈 - 반복 사용중인 약물의 중단시 발생하는 증상
  • 신체적 의존 - 신체적 및 심신적 증상이 지속적으로 발생하는 의존 상태
  • 정신적 의존 – 감정적이고 동기적인 이탈 증상이 발생하는 의존 상태
  • 강화 자극 – 대상 행동을 반복할 확률을 높이는 자극
  • 보상 자극 – 본질적으로 뇌가 긍정적이거나 받아들여야 한다고 해석하는 자극
  • 내성 – 주어진 용량에서 반복 투여로 인한 약물 효과 감소
  • 역내성 , 감작 – 약물의 반복 투여에 의해 그 효용이 점증해 가는 것

嗜癖(시히키, 영 : addiction , 어딕션)이란 특정 물질이나 행동, 인간관계를 특히 선호하는 성향이다.

약물 습관 ( drug addiction )이라는 용어는 다른 개념인 약물 의존성 과 약물 남용 의 정의와의 오용이 있기 때문에 세계 보건 기관의 전문 용어에서 제외되었다 [8] . 약물에 대한 습관의 용어는 일반적으로 널리 사용됩니다 [8] . 일본의 법률적인 맥락에서는 중독 이라는 방역도 있지만, 의학적으로 약물 중독이란 습관 이 아닌 과잉섭취 등에 의해 유해작용이 발생하고 있는 상태이다 [9] . 자세한 내용은 다음 정의 섹션을 참조하십시오.

약물 관련 용어의 정의와 역사 [ 편집 ]

트렁크라이저 등의 남용이 문제가 된 1950년대에는 세계보건기구의 Addiction-Producing Drugs 에 관한 전문위원회가 다음과 같이 정의했다 [6] .

  • Addiction-producing : 매우 강한 갈망이 있으며, 복용량은 증가하는 경향이 있으며, 정신 의존과 신체 의존이 있습니다.
  • Habit-formaing : 복용량은 증가하지 않거나 미세 증가이며 신체 의존성이 부족하며 금단 증상이 없습니다.

당시의 일본에서는, 이 Addiction-Producing Drugs가 , 익사성 약물 등으로 번역되고 있다 [10] . 약물 습관(drug addiction), 약물 습관성(drug habituation)으로 하고 있는 중요어 사전도 있다 [11] . 일본에서는 수면제 남용이 문제가 되었기 때문에 1961년에 습관성 의약품을 지정하고 처방전을 필요로 하는 조치를 취했다 [10] .

1960년대에 습관(Addiction)과 습관(Habit)의 2개의 용어는 파기되어 의존(Dependence)의 용어로 바뀌었다 [12] . 세계보건기구의 전문위원회는 약물의존에 관한 전문위원회(WHO Expert Committee on Drug Dependence)로 변명된다.

1975년 시점에서, 일본의 의약품에는 「습관성 있음」의 표시가 남아있지만, 미국에서는 그러한 표시는 과거의 일이며, 지난 10년에 국내외에서 습관성이라는 단어는 볼 수 없게 되었다 하고 있다 [13] . 또 의존의 말은 널리 보급되고, 냄새의 말은 아직도 산견된다고 한다 [13] .

미국 정신의학회 (APA)에 의한 「정신장애의 진단과 통계 매뉴얼 제4판」(DSM-IV)에서는, 신체 의존 이나 사용량 증가의 진단 기준은 약물 의존증 (Drug Dependence)의 진단 기준에 포함된다 .

그러나 2011년의 「굿맨 길만 약리서」 제12판에 있어서는, 1987년에 미국 정신의학회가, 사용을 제어할 수 없는 상태에 대해 의존(dependence)의 말을 사용했지만, 의존과는 본래는 이탈 증상을 나타내는 상태이며 혼란이 발생했다고한다 [14] . 당시에는 습관(addiction)의 말이 경멸어이므로 피해야 했지만, 다음의 DSM-5에서는 이 혼란이 정정될 것이라고 기록하고 있다 [14] .

DSM-5에서는 물질 관련 장애 및 독성 장애군(Substance Related and Addictive Disorders)의 분류명이 등장했다 [15] . DSM-5에서는 약물 남용과 약물 의존증을 통합했지만, DSM-IV의 편집 위원장인 앨런 프란세스 는 이것을 비판하고 있으며, 습관(addicion)의 말에 의한 상용자와 같은 레텔은 , 보다 단발적인 남용에 의해 문제가 생긴 사람들에게는 불이익을 입을 수 있는 스티그마(낙인)이며, 임상에서도 남용과 의존의 구별은 대응상에서 유익하다고 하여, 이것을 구별하고 있다 세계 보건기구가 ICD 의 진단 코드를 사용해야한다고합니다 [16] .

미국에서의 약물 관련 장애의 보고 등에서는, 약물 의존 및 약물 남용을 모두 포함하는 형태로, 약물 습관( Drug Addiction )의 용어를 사용하는 것으로 정의하고 있다 [17] .

어떠한 의도로 사용되고 있는지 문맥에 의해 판단하는 것이 필요하다.

국제조약인 1961년의 마약에 관한 단일조약 의 방역문으로, addction을 중독 이라고 번역하고 있다 [18] . 일본의 마약 및 향정신약 단속법에서도 의존을 일으킨 상태를 중독으로 하고 있지만, 이 일본의 법률상의 번역은 「의학적 중독의 의미와 다르다」, 의학적으로 약물 중독 이란, 과잉섭취 등에 의해 유해 작용이 발생하고 있는 상태이다 [9] . 1975년 시점에서, 야나기타 지사는 중독의 의미에서 중독의 말은 파기하고, 중독의 말의 사용을 제안하고 있다 [13] .

분류 [ 편집 ]

습관은 그 대상에 따라 다음과 같이 분류할 수 있다.

물질 습관 [ 편집 ]

" 약물 중독 " 및 " 약물 남용 " 참조

특정 물질의 섭취에 관한 습관. 술 , 담배 , 남용 약물에 해당하는 종류의 향정 신약이 대상이 되기 쉽다. 알코올이라면 안된다고 알고 있어도 아침부터 술을 마시지 않고 술밖에 즐거움이 없고 간이 나빠져도 술을 그만두지 않는 등. 이탈 증상이 동반되면 약물 의존증 , 동반하지 않으면 약물 남용 상태이다.

행동 습관 [ 편집 ]

자세한 것은 「행동 버릇」을 참조

특정 행동 과정에 집착하는 습관. 그 행동을 억제하기 어려운 욕구나 충동이 있어, 다른 오락을 무시하고, 유해 사건이 일어나도 그 행동을 그만두지 않는다. 파칭코 등의 도박, 쇼핑, 일상적 폭력, 성행위 등이 대상이 된다. 「좋아하기 때문에 한다」라는 점에 있어서, 강박성 장애 에 있어서 불쾌를 피하기 위해 실시하는 강박 행위 와는 구별된다. 도박 버릇에서는 도박을 그만두려고 했던 시점에서는 이미 빚을 지고 있는 경우도 많아, 이 때문에 잃은 돈을 되찾을 수 있을 때까지 그만둘 수 없어 결과적으로 더욱 부채가 부풀어 오르는 강박화가 일어날 수 있다.

크로스 어딕션 [ 편집 ]

여러 대상을 가진 습관. 습관은 대상이 다르더라도 같은 공허감에서 유사한 메커니즘으로 발병하고 있기 때문에 동시에 2개 이상의 습관이 합병될 수 있다(술과 도박, 약물과 성행위 등). 반사회성이 강한 대상으로 이행하면서(알코올→도박→약물) 냄새가 계속되는 경우도 많다.

요인 [ 편집 ]

환경 요인 [ 편집 ]

미국에서는 8년 만에 코카인 남용자가 8배로 늘어나는 시기가 있었다. 베트남 전쟁 에 간 미병의 약 30%가 마약 습관이었지만, 귀국 후에는 그 대부분이 남용을 그만두고 있다. 이러한 사실로부터, 습관에는 환경 요인이 크게 관련되어 있다고 추측되고 있다.

성격 [ 편집 ]

성격은 약물 남용의 가장 중요한 성인으로 여겨진다. 의지 박약, 의존적, 미숙성, 도피적, 자신감 결핍, 정서 불안정, 자기 중심적, 현시적 등. 일본에서 치료를 받고 있는 대마초 버릇자는 성격검사 로 부담스러운 충동성, 피지배성이 높은 프로필을 가진 사람이 많고, 진통약 치사자는 우울증, 신경질, 단기라는 보고가 있다 요출전 ] .

각주 [ 편집 ]

[ 각주 사용법 ]
  1. ↑ “Chapter 15: Reinforcement and Addictive Disorders”. Molecular Neuropharmacology: A Foundation for Clinical Neuroscience (2nd ed.). New York: McGraw-Hill Medical. (2009). pp. 364–375  .
  2. ↑ Nestler EJ (December 2013). “Cellular basis of memory for addiction” . Dialogues Clin. Neurosci. 15 (4): 431–443. PMC  3898681 . PMID 24459410 . 
  3. ↑ “ Glossary of Terms ”. Mount Sinai School of Medicine . Department of Neuroscience. 2015년 2월 9일에 확인함.
  4. ↑ “Neurobiologic Advances from the Brain Disease Model of Addiction”. N. Engl. J. Med. 374 (4 ) : 363–371. (January 2016) . doi : 10.1056 / NEJMra1511480 
  5. ^ 나카무라 하루카, 나리타 켄이치 「냄새란 무엇인가-그 현대적 의의를 역사적 경위로부터 찾는다」 「인문논구」 제60권 제4호, 2011년 2월, 37-54페이지, NAID 120003802584 . 
  6. ↑ a b 세계 보건기구 (1957). WHO Expert Committee on Addiction-Producing Drugs - Seventh Report / WHO Technical Report Series 116 (pdf) (Report). World Health Organization. pp. 9–10.
  7. ↑ 세계보건기구 (1994) (pdf). Lexicon of alchol and drug term . World Health Organization. pp. 6. ISBN 92-4-154468-6  (HTML판 introduction 생략 )
  8. ^ a b 세계 보건기구 2003 , p. 22.
  9. ^ a b (편집) 일본 완화 의료 학회, 완화 의료 가이드 라인 작성 위원회 「약리학적 지식」 「암 통증의 약물 치료에 관한 가이드 라인」(제1판; 2010년) 김원 출판, 2010년 6월 20일 . ISBN 978-4-307-10149-3 . 
  10. ^ a b 마츠에다 아키코 「트랑키라이저의 유행-시판향 정신약의 규제의 논거와 경과」(pdf) 「Core Ethics」 제6권, 2010년, 385-399쪽.
  11. ↑ 호사키 히데오(편집), 타케마사 켄이치(편집) 『의사 국가 시험을 위한 정신과 중요 용어 사전』 김원 출판, 1982년. ISBN 4-307-15004-X . 
  12. ↑ 세계보건기구 (1994) (pdf). Lexicon of alchol and drug term . World Health Organization. pp. 6. ISBN 92-4-154468-6  (HTML판 introduction 생략 )
  13. ^ a b c 야나기 타치지 1975 .
  14. ^ a b Laurence Brunton(편집), Bjorn Knollman(편집), Bruce Chabner(편집) 『굿맨 길만 약리서 <상> 약물 치료의 기초와 임상』 히로카와 서점, 2013년, 840페이지. ISBN 978-4567498005 .  , Goodman & Gilman's The Pharmacological Basis of Therapeutics, 12e, 2011
  15. ↑ 미국 정신의학회 “DSM-5 정신 질환의 진단·통계 매뉴얼” 일본 정신 신경 학회 일본어판 용어 감수·타카하시 사부로· 오노 유감역 ·스미야 토시유키·진정 시게노부·오자키 기오·미무라 다카시· 무라이 토시야 번역, 의학 서원 , 2014년 6월 30일. ISBN 978-4260019071 . 
  16. ^ 알렌 프란세스 , 오노 유우(번역), 나카가와 아츠오(번역), 야나기사와 케이코(번역) 「정신 질환 진단의 에센스-DSM-5의 능숙한 사용법」금강 출판, 2014년 3월, 138-140페이지. ISBN 978-4772413527 .  , Essentials of Psychiatric Diagnosis, Revised Edition: Responding to the Challenge of DSM-5® , The Guilford Press, 2013.
  17. ^ Addiction Medicine: Closing the Gap between Science and Practice . The National Center on Addiction and Substance Abuse at Columbia. (2012-06)
  18. ^ 마약에 관한 단일 조약 영일 대역문 1 약 2 약 3 ) (일본어) (외무성)

참고 문헌 [ 편집 ]

관련 항목 [ 편집 ]

위키미디어 커먼즈에는 습관 과 관련된 카테고리가 있습니다.

외부 링크 [ 편집 ]

스텁 아이콘

이 항목은 사회과학과 관련된 쓰기 항목 입니다. 이 항목을 가필·정정 등 해 주시는 협력자를 요구하고 있습니다 ( PJ:사회과학 ).


==

Addiction

From Wikipedia, the free encyclopedia
"Addictive" redirects here. For other uses, see Addiction (disambiguation) and Addictive (disambiguation).
Not to be confused with Psychological dependence.
Addiction
Other namesAddictive behaviour (e.g. substance-use addiction, sexual addiction), dependence, addictive disorder, addiction disorder (e.g. severe substance-use disorder, gambling disorder)
PET images showing brain metabolism in drug addicts vs controls
Brain positron emission tomography images that compare brain metabolism in a healthy individual and an individual with a cocaine addiction
SpecialtyPsychiatry, clinical psychology, toxicology, addiction medicine

Addiction is a neuropsychological disorder characterized by a persistent and intense urge to use a drug or engage in a behaviour that produces natural reward, despite substantial harm and other negative consequences. Repetitive drug use often alters brain function in ways that perpetuate craving, and weakens (but does not completely negate) self-control.[1] This phenomenon – drugs reshaping brain function – has led to an understanding of addiction as a brain disorder with a complex variety of psychosocial as well as neurobiological (and thus involuntary)[a] factors that are implicated in addiction's development.[2][3][4] Classic signs of addiction include compulsive engagement in rewarding stimuli, preoccupation with substances or behavior, and continued use despite negative consequences. Habits and patterns associated with addiction are typically characterized by immediate gratification (short-term reward),[5][6] coupled with delayed deleterious effects (long-term costs).[3][7]

Examples of drug (or more generally, substance) addictions include alcoholism, cannabis addiction, amphetamine addiction, cocaine addiction, nicotine addiction, opioid addiction, and eating or food addiction. Behavioral addictions may include gambling addiction, shopping addiction, stalking, internet addiction, social media addiction, obsessive–compulsive disorder, video game addiction and sexual addiction. The DSM-5 and ICD-10 only recognize gambling addictions as behavioral addictions, but the ICD-11 also recognizes gaming addictions.[8]

Definitions[edit]

"Addiction" and "addictive behaviour" are polysemes denoting a category of mental disorders, of neuropsychological symptoms, or of merely maladaptive/harmful habits and lifestyles.[9] A common use of "addiction" in medicine is for neuropsychological symptoms denoting pervasive/excessive and intense urges to engage in a category of behavioral compulsions or impulses towards sensory rewards (e.g. alcohol, betel quid, drugs, sex, gambling, video gaming).[10][11][12][13][14] Addictive disorders or addiction disorders are mental disorders involving high intensities of addictions (as neuropsychological symptoms) that induce functional disabilities (i.e. limit subjects' social/family and occupational activities); the two categories of such disorders are substance-use addictions and behavioral addictions.[15][9][13][14]

However, there is no agreement on the exact definition of addiction in medicine. Indeed, Volkow et al. (2016) report that the DSM-5 defines addictions as the most severe degree of the addictive disorders, due to pervasive/excessive substance-use or behavioural compulsions/impulses.[16] It is a definition that many scientific papers and reports use.[17][18][19]

"Dependence" is also a polyseme denoting either neuropsychological symptoms or mental disorders. In the DSM-5, dependences differ from addictions and can even normally happen without addictions;[20] besides, substance-use dependences are severe stages of substance-use addictions (i.e. mental disorders) involving withdrawal issues.[21] In the ICD-11, "substance-use dependence" is a synonym of "substance-use addiction" (i.e. neuropsychological symptoms) that can but do not necessarily involve withdrawal issues.[22]

Substance addiction[edit]

Main article: Substance use disorder
Further information: Substance abuse and Substance-related disorder
Addiction and dependence glossary[2][23][24]
  • addiction – a biopsychosocial disorder characterized by persistent use of drugs (including alcohol) despite substantial harm and adverse consequences
  • addictive drug – psychoactive substances that with repeated use are associated with significantly higher rates of substance use disorders, due in large part to the drug's effect on brain reward systems
  • dependence – an adaptive state associated with a withdrawal syndrome upon cessation of repeated exposure to a stimulus (e.g., drug intake)
  • drug sensitization or reverse tolerance – the escalating effect of a drug resulting from repeated administration at a given dose
  • drug withdrawal – symptoms that occur upon cessation of repeated drug use
  • physical dependence – dependence that involves persistent physical–somatic withdrawal symptoms (e.g., fatigue and delirium tremens)
  • psychological dependence – dependence socially seen as being extremely mild compared to physical dependence (e.g., with enough willpower it could be overcome)
  • reinforcing stimuli – stimuli that increase the probability of repeating behaviors paired with them
  • rewarding stimuli – stimuli that the brain interprets as intrinsically positive and desirable or as something to approach
  • sensitization – an amplified response to a stimulus resulting from repeated exposure to it
  • substance use disorder – a condition in which the use of substances leads to clinically and functionally significant impairment or distress
  • tolerance – the diminishing effect of a drug resulting from repeated administration at a given dose

Drug addiction[edit]

Drug addiction, which belongs to the class of substance-related disorders, is a chronic and relapsing brain disorder that features drug seeking and drug abuse, despite their harmful effects.[25] This form of addiction changes brain circuitry such that the brain's reward system is compromised,[26] causing functional consequences for stress management and self-control.[25] Damage to the functions of the organs involved can persist throughout a lifetime and cause death if untreated.[25] Substances involved with drug addiction include alcohol, nicotine, marijuana, opioids, cocaine, amphetamines, and even foods with high fat and sugar content.[27] Addictions can begin experimentally in social contexts[28] and can arise from the use of prescribed medications or a variety of other measures.[29]

Drug addiction has been shown to work in phenomenological, conditioning (operant and classical), cognitive models, and the cue reactivity model. However, no one model completely illustrates substance abuse.[30]

Risk factors for addiction include:

  • Aggressive behavior (particularly in childhood)
  • Availability of substance[28]
  • Community economic status
  • Experimentation[28]
  • Epigenetics
  • Impulsivity (attentional, motor, or non-planning)[31]
  • Lack of parental supervision[28]
  • Lack of peer refusal skills[28]
  • Mental disorders[28]
  • Method substance is taken[25]
  • Usage of substance in youth[28]

Food addiction[edit]

Main article: Food addiction

The diagnostic criteria for food or eating addiction has not been categorized or defined in references such as the Diagnostic and Statistical Manual of Mental Disorders (DSM or DSM-5) and is based on subjective experiences similar to substance use disorders.[32][31] Food addiction may be found in those with eating disorders, though not all people with eating disorders have food addiction and not all of those with food addiction have a diagnosed eating disorder.[32] Long-term frequent and excessive consumption of foods high in fat, salt, or sugar, such as chocolate, can produce an addiction[33][34] similar to drugs since they trigger the brain's reward system, such that the individual may desire the same foods to an increasing degree over time.[35][32][31] The signals sent when consuming highly palatable foods have the ability to counteract the body's signals for fullness and persistent cravings will result.[35] Those who show signs of food addiction may develop food tolerances, in which they eat more, despite the food becoming less satisfactory.[35]

Chocolate's sweet flavor and pharmacological ingredients are known to create a strong craving or feel 'addictive' by the consumer.[36] A person who has a strong liking for chocolate may refer to themselves as a chocoholic.

Risk factors for developing food addiction include excessive overeating and impulsivity.[31]

The Yale Food Addiction Scale (YFAS), version 2.0, is the current standard measure for assessing whether an individual exhibits signs and symptoms of food addiction.[37][32][31] It was developed in 2009 at Yale University on the hypothesis that foods high in fat, sugar, and salt have addictive-like effects which contribute to problematic eating habits.[38][35] The YFAS is designed to address 11 substance-related and addictive disorders (SRADs) using a 25-item self-report questionnaire, based on the diagnostic criteria for SRADs as per DSM-5.[39][32] A potential food addiction diagnosis is predicted by the presence of at least two out of 11 SRADs and a significant impairment to daily activities.[40]

The Barratt Impulsiveness Scale, specifically the BIS-11 scale, and the UPPS-P Impulsive Behavior subscales of Negative Urgency and Lack of Perseverance have been shown to have relation to food addiction.[31]

Behavioral addiction[edit]

Main article: Behavioral addiction

The term behavioral addiction refers to a compulsion to engage in a natural reward – which is a behavior that is inherently rewarding (i.e., desirable or appealing) – despite adverse consequences.[6][33][34] Preclinical evidence has demonstrated that marked increases in the expression of ΔFosB through repetitive and excessive exposure to a natural reward induces the same behavioral effects and neuroplasticity as occurs in a drug addiction.[33][41][42][43]

Addiction can exist in the absence of psychotropic drugs, which was popularized by Peele.[44] These are termed behavioral addictions. Such addictions may be passive or active, but they commonly contain reinforcing features, which are found in most addictions.[44] Sexual behavior, eating, gambling, playing video games, and shopping are all associated with compulsive behaviors in humans and have been shown to activate the mesolimbic pathway and other parts of the reward system.[33] Based on this evidence, sexual addiction, gambling addiction, video game addiction, and shopping addiction are classified accordingly.[33][45]

Sexual[edit]

Main article: Sexual addiction

Sexual addiction involves an engagement in excessive, compulsive, or otherwise problematic sexual behavior that persists despite negative physiological, psychological, social, and occupational consequences.[46] Sexual addiction may be referred to as hypersexuality or compulsive sexual behavior disorder.[46] The DSM-5 does not recognize sexual addiction as a clinical diagnosis. Hypersexuality disorder and internet addiction disorder were among proposed addictions to the DSM-5, but were later rejected due to the insufficient evidence available in support of the existence of these disorders as discrete mental health conditions.[47] Reviews of both clinical research in humans and preclinical studies involving ΔFosB have identified compulsive sexual activity – specifically, any form of sexual intercourse – as an addiction (i.e., sexual addiction).[33][41] Reward cross-sensitization between amphetamine and sexual activity, meaning that exposure to one increases the desire for both, has been shown to occur as a dopamine dysregulation syndrome.[33][41][42][43] ΔFosB expression is required for this cross-sensitization effect, which intensifies with the level of ΔFosB expression.[33][42][43]

Gambling[edit]

Main articles: Gambling and Problem gambling

Gambling provides a natural reward that is associated with compulsive behavior.[33] Functional neuroimaging evidence shows that gambling activates the reward system and the mesolimbic pathway in particular.[33][45] It is known that dopamine is involved in learning, motivation, as well as the reward system.[48][26] The exact role of dopamine in gambling addiction has been debated.[48] Suggested roles for D2, D3, and D4 dopamine receptors, as well as D3 receptors in the substantia nigra have been found in rat and human models, showing a correlation with the severity of the gambling behavior.[48] This in turn was linked with greater dopamine release in the dorsal striatum.[48]

Gambling addictions are linked with comorbidities such as mental health disorders, substance abuse, alcohol use disorder, and personality disorders.[49]

Risk factors for gambling addictions include antisocial behavior, impulsive personality,[31] male sex, sensation seeking,[50] substance use, and young age.

Gambling addiction has been associated with some personality traits, including: harm avoidance, low self direction, decision making and planning insufficiencies, impulsivity, as well as sensation seeking individuals.[50] Although some personality traits can be linked with gambling addiction, there is no general description of individuals addicted to gambling.[50]

Internet[edit]

Main article: Internet addiction disorder

Internet addiction does not have any standardized definition, yet there is widespread agreement that this problem exists.[51] Debate over the classification of problematic internet use considers whether it should be thought of as a behavioral addiction, an impulse control disorder, or an obsessive-compulsive disorder.[52][53] Others argue that internet addiction should be considered a symptom of an underlying mental health condition and not a disorder in itself.[54] Internet addiction has been described as "a psychological dependence on the Internet, regardless of the type of activity once logged on."[51] Problematic internet use may include a preoccupation with the internet and/or digital media, excessive time spent using the internet despite resultant distress in the individual, increase in the amount of internet use required to achieve the same desired emotional response, loss of control over one's internet use habits, withdrawal symptoms, and continued problematic internet use despite negative consequences to one's work, social, academic, or personal life.[55]

Studies conducted in India, United States, Asia, and Europe have identified Internet addiction prevalence rates ranging in value from 1% to 19%, with the adolescent population having high rates compared to other age groups.[56][57] Prevalence rates have been difficult to establish due to a lack of universally accepted diagnostic criteria, a lack of diagnostic instruments demonstrating cross-cultural validity and reliability, and existing controversy surrounding the validity of labeling problematic internet use as an addictive disorder.[58][57] The most common scale used to measure addiction is the Internet Addiction Test developed by Kimberly Young.[57]

People with internet addiction are likely to have a comorbid psychiatric disorder. Comorbid diagnoses identified alongside internet addiction include affective mood disorders, anxiety disorders, substance use disorders, and attention deficit hyperactivity disorder.[58]

Video games[edit]

Main article: Video game addiction

Video game addiction is characterized by the World Health Organization (WHO) as excessive gaming behavior, potentially prioritized over other interests, despite the negative consequences that may arise, for a period of at least 12 months.[59] In May 2019, the WHO introduced gaming disorder in the 11th edition of the International Classification of Diseases.[60] Video game addiction has been shown to be more prevalent in males than females, higher by 2.9 times.[61] It has been suggested that people of younger ages are more prone to become addicted to video games.[61] People with certain personalities may be more susceptible to gaming addictions.[61][62]

Risk factors for video game addiction include:

  • Male,
  • Psychopathologies (e.g. ADHD or MDD), and
  • Social anxiety.[63]

Shopping[edit]

Main articles: Shopping addiction and Compulsive buying disorder

Shopping addiction, or compulsive buying disorder (CBD), is the excessive urge to shop or spend, potentially resulting in unwanted consequences.[64] These consequences can have serious impacts, such as increased consumer debt, negatively affected relationships, increased risk of illegal behavior, and suicide attempts.[64] Shopping addiction occurs worldwide and has shown a 5.8% prevalence in the United States.[65] Similar to other behavioral addictions, CBD can be linked to mood disorders, substance use disorders, eating disorders, and other disorders involving a lack of control.[65]

Signs and symptoms[edit]

Signs and symptoms of addiction can vary depending on the type of addiction. Symptoms of drug addictions may include:

  • Continuation of drug use despite the knowledge of consequences[32]
  • Disregarding financial status when it comes to drug purchases
  • Ensuring a stable supply of the drug
  • Experiencing withdrawal symptoms when stopping the drug[66][32]
  • Needing more of the drug over time to achieve similar effects[32]
  • Social and work life impacted due to drug use[32]
  • Unsuccessful attempts to stop drug use[32]
  • Urge to use drug regularly

Signs and symptoms of addiction may include:

Behavioral ChangesPhysical ChangesSocial Changes
  • Angry and irritable
  • Changes to eating or sleeping habits
  • Changes to personality and attitude
  • Decreased attendance and performance in workplace or school setting[32]
  • Fearful, paranoid and anxious without probable cause[67]
  • Frequently engaging in conflicts (fights, illegal activity)
  • Frequent or sudden changes in mood and temperament
  • Hiding or in denial of certain behaviors
  • Lack of motivation
  • Periodic hyperactivity
  • Using substances in inappropriate settings
  • Abnormal pupil size
  • Bloodshot eyes
  • Body odor
  • Impaired motor coordination[67]
  • Periodic tremors
  • Poor physical appearance
  • Slurred speech
  • Sudden changes in weight
  • Changes in hobbies
  • Changes to financial status (unexplained need for money)
  • Legal problems related to substance abuse
  • Sudden changes in friends and associates
  • Use of substance despite consequences to personal relationships[67]

Screening and assessment[edit]

Addictions Neuroclinical Assessment[edit]

The Addictions Neuroclinical Assessment is used to diagnose addiction disorders. This tool measures three different domains: executive function, incentive salience, and negative emotionality.[68][69] Executive functioning consists of processes that would be disrupted in addiction.[69] In the context of addiction, incentive salience determines how one perceives the addictive substance.[69] Increased negative emotional responses have been found with individuals with addictions.[69]

Tobacco, Alcohol, Prescription Medication, and Other Substance Use (TAPS)[edit]

This is a screening and assessment tool in one, assessing commonly used substances. This tool allows for a simple diagnosis, eliminating the need for several screening and assessment tools, as it includes both TAPS-1 and TAPS-2, screening and assessment tools respectively. The screening component asks about the frequency of use of the specific substance (tobacco, alcohol, prescription medication, and other).[70] If an individual screens positive, the second component will begin. This dictates the risk level of the substance.[70]

CRAFFT[edit]

The CRAFFT (Car-Relax-Alone-Forget-Family and Friends-Trouble) is a screening tool that is used in medical centers. The CRAFFT is in version 2.1 and has a version for nicotine and tobacco use called the CRAFFT 2.1+N.[71] This tool is used to identify substance use, substance related driving risk, and addictions among adolescents. This tool uses a set of questions for different scenarios.[72] In the case of a specific combination of answers, different question sets can be used to yield a more accurate answer. After the questions, the DSM-5 criteria are used to identify the likelihood of the person having substance use disorder.[72] After these tests are done, the clinician is to give the "5 RS" of brief counseling.

The five Rs of brief counseling includes:

  1. REVIEW screening results
  2. RECOMMEND to not use
  3. RIDING/DRIVING risk counseling
  4. RESPONSE: elicit self-motivational statements
  5. REINFORCE self-efficacy[72]

Drug Abuse Screening Test (DAST-10)[edit]

The Drug Abuse Screening Test (DAST) is a self-reporting tool that measures problematic substance use.[73] Responses to this test are recorded as yes or no answers, and scored as a number between zero and 28. Drug abuse or dependence, are indicated by a cut off score of 6.[73] Three versions of this screening tool are in use: DAST-28, DAST-20, and DAST-10. Each of these instruments are copyrighted by Dr. Harvey A. Skinner.[73]

Alcohol, Smoking, and Substance Involvement Test (ASSIST)[edit]

The Alcohol, Smoking, and Substance Involvement Test (ASSIST) is an interview-based questionnaire consisting of eight questions developed by the WHO.[74] The questions ask about lifetime use; frequency of use; urge to use; frequency of health, financial, social, or legal problems related to use; failure to perform duties; if anyone has raised concerns over use; attempts to limit or moderate use; and use by injection.[75]

Causes[edit]

Personality theories[edit]

Main article: Personality theories of addiction

Personality theories of addiction are psychological models that associate personality traits or modes of thinking (i.e., affective states) with an individual's proclivity for developing an addiction. Data analysis demonstrates that psychological profiles of drug users and non-users have significant differences and the psychological predisposition to using different drugs may be different.[76] Models of addiction risk that have been proposed in psychology literature include: an affect dysregulation model of positive and negative psychological affects, the reinforcement sensitivity theory of impulsiveness and behavioral inhibition, and an impulsivity model of reward sensitization and impulsiveness.[77][78][79][80][81]

Neuropsychology[edit]

The transtheoretical model of change (TTM) can point to how someone may be conceptualizing their addiction and the thoughts around it, including not being aware of their addiction.[82]

Cognitive control and stimulus control, which is associated with operant and classical conditioning, represent opposite processes (i.e., internal vs external or environmental, respectively) that compete over the control of an individual's elicited behaviors.[83] Cognitive control, and particularly inhibitory control over behavior, is impaired in both addiction and attention deficit hyperactivity disorder.[84][85] Stimulus-driven behavioral responses (i.e., stimulus control) that are associated with a particular rewarding stimulus tend to dominate one's behavior in an addiction.[85]

Operant conditioningExtinction
Reinforcement
Increase behavior		Punishment
Decrease behavior
Positive reinforcement
Add appetitive stimulus
following correct behavior		Negative reinforcementPositive punishment
Add noxious stimulus
following behavior		Negative punishment
Remove appetitive stimulus
following behavior
Escape
Remove noxious stimulus
following correct behavior		Active avoidance
Behavior avoids noxious stimulus

See also: Stimulus control

In operant conditioning, behavior is influenced by outside stimulus, such as a drug. The operant conditioning theory of learning is useful in understanding why the mood-altering or stimulating consequences of drug use can reinforce continued use (an example of positive reinforcement) and why the addicted person seeks to avoid withdrawal through continued use (an example of negative reinforcement). Stimulus control is using the absence of the stimulus or presence of a reward to influence the resulting behavior.[82]

Cognitive control of behavior[edit]

See also: Cognitive control

Cognitive control is the intentional selection of thoughts, behaviors, and emotions, based on our environment. It has been shown that drugs alter the way our brains function, and its structure.[86][26] Cognitive functions such as learning, memory, and impulse control, are affected by drugs.[86] These effects promote drug use, as well as hinder the ability to abstain from it.[86] The increase in dopamine release is prominent in drug use, specifically in the ventral striatum and the nucleus accumbens.[86] Dopamine is responsible for producing pleasurable feelings, as well driving us to perform important life activities. Addictive drugs cause a significant increase in this reward system, causing a large increase in dopamine signaling as well as increase in reward-seeking behavior, in turn motivating drug use.[86][26] This promotes the development of a maladaptive drug to stimulus relationship.[87] Early drug use leads to these maladaptive associations, later affecting cognitive processes used for coping, which are needed to successfully abstain from them.[86][82]

Risk factors[edit]

Further information: Addiction vulnerability

A number of genetic and environmental risk factors exist for developing an addiction.[2][88] Genetic and environmental risk factors each account for roughly half of an individual's risk for developing an addiction;[2] the contribution from epigenetic risk factors to the total risk is unknown.[88] Even in individuals with a relatively low genetic risk, exposure to sufficiently high doses of an addictive drug for a long period of time (e.g., weeks–months) can result in an addiction.[2] Adverse childhood events are associated with negative health outcomes, such as substance use disorder. Childhood abuse or exposure to violent crime is related to developing a mood or anxiety disorder, as well as a substance dependence risk.[89]

Genetic factors[edit]

Main articles: Epigenetics of cocaine addiction and Molecular and epigenetic mechanisms of alcoholism
Further information: Alcoholism § Genetic variation, History of drinking, History of smoking, and Prevalence of tobacco use

Genetic factors, along with socio-environmental (e.g., psychosocial) factors, have been established as significant contributors to addiction vulnerability.[2][88][90][32] Studies done on 350 hospitalized drug-dependent patients showed that over half met the criteria for alcohol abuse, with a role of familial factors being prevalent.[91] Genetic factors account for 40–60% of the risk factors for alcoholism.[92] Similar rates of heritability for other types of drug addiction have been indicated, specifically in genes that encode the Alpha5 Nicotinic Acetylcholine Receptor.[93] Knestler hypothesized in 1964 that a gene or group of genes might contribute to predisposition to addiction in several ways. For example, altered levels of a normal protein due to environmental factors may change the structure or functioning of specific brain neurons during development. These altered brain neurons could affect the susceptibility of an individual to an initial drug use experience. In support of this hypothesis, animal studies have shown that environmental factors such as stress can affect an animal's genetic expression.[93]

In humans, twin studies into addiction have provided some of the highest-quality evidence of this link, with results finding that if one twin is affected by addiction, the other twin is likely to be as well, and to the same substance.[94] Further evidence of a genetic component is research findings from family studies which suggest that if one family member has a history of addiction, the chances of a relative or close family developing those same habits are much higher than one who has not been introduced to addiction at a young age.[95]

The data implicating specific genes in the development of drug addiction is mixed for most genes. Many addiction studies that aim to identify specific genes focus on common variants with an allele frequency of greater than 5% in the general population. When associated with disease, these only confer a small amount of additional risk with an odds ratio of 1.1–1.3 percent; this has led to the development the rare variant hypothesis, which states that genes with low frequencies in the population (<1%) confer much greater additional risk in the development of the disease.[96]

Genome-wide association studies (GWAS) are used to examine genetic associations with dependence, addiction, and drug use.[90] These studies rarely identify genes from proteins previously described via animal knockout models and candidate gene analysis. Instead, large percentages of genes involved in processes such as cell adhesion are commonly identified. The important effects of endophenotypes are typically not capable of being captured by these methods. Genes identified in GWAS for drug addiction may be involved either in adjusting brain behavior before drug experiences, subsequent to them, or both.[97]

Environmental factors[edit]

Environmental risk factors for addiction are the experiences of an individual during their lifetime that interact with the individual's genetic composition to increase or decrease his or her vulnerability to addiction.[2] For example, after the nationwide outbreak of COVID-19, more people quit (vs. started) smoking; and smokers, on average, reduced the quantity of cigarettes they consumed.[98] More generally, a number of different environmental factors have been implicated as risk factors for addiction, including various psychosocial stressors. The National Institute on Drug Abuse (NIDA) and studies cite lack of parental supervision, the prevalence of peer substance use, substance availability, and poverty as risk factors for substance use among children and adolescents.[99][28] The brain disease model of addiction posits that an individual's exposure to an addictive drug is the most significant environmental risk factor for addiction.[100] Many researchers, including neuroscientists, indicate that the brain disease model presents a misleading, incomplete, and potentially detrimental explanation of addiction.[101]

The psychoanalytic theory model defines addiction as a form of defense against feelings of hopelessness and helplessness as well as a symptom of failure to regulate powerful emotions related to adverse childhood experiences (ACEs), various forms of maltreatment and dysfunction experienced in childhood. In this case, the addictive substance provides brief but total relief and positive feelings of control.[82] The Adverse Childhood Experiences Study by the Centers for Disease Control and Prevention has shown a strong dose–response relationship between ACEs and numerous health, social, and behavioral problems throughout a person's lifespan, including substance use disorder.[102] Children's neurological development can be permanently disrupted when they are chronically exposed to stressful events such as physical, emotional, or sexual abuse, physical or emotional neglect, witnessing violence in the household, or a parent being incarcerated or having a mental illness. As a result, the child's cognitive functioning or ability to cope with negative or disruptive emotions may be impaired. Over time, the child may adopt substance use as a coping mechanism or as a result of reduced impulse control, particularly during adolescence.[102][28][82] Vast amounts of children who experienced abuse have gone on to have some form of addiction in their adolescence or adult life.[103] This pathway towards addiction that is opened through stressful experiences during childhood can be avoided by a change in environmental factors throughout an individual's life and opportunities of professional help.[103] If one has friends or peers who engage in drug use favorably, the chances of them developing an addiction increases. Family conflict and home management is a cause for one to become engaged in alcohol or other drug use.[104]

Social control theory[edit]

Main article: Social control theory

According to Travis Hirschi's social control theory, adolescents with stronger attachments to family, religious, academic, and other social institutions are less likely to engage in delinquent and maladaptive behavior such as drug and alcohol use leading to addiction.[105]

Age[edit]

Adolescence represents a period of increased vulnerability for developing an addiction.[106] In adolescence, the incentive-rewards systems in the brain mature well before the cognitive control center. This consequentially grants the incentive-rewards systems a disproportionate amount of power in the behavioral decision-making process. Therefore, adolescents are increasingly likely to act on their impulses and engage in risky, potentially addicting behavior before considering the consequences.[107] Not only are adolescents more likely to initiate and maintain drug use, but once addicted they are more resistant to treatment and more liable to relapse.[108][109]

Most individuals are exposed to and use addictive drugs for the first time during their teenage years.[110] In the United States, there were just over 2.8 million new users of illicit drugs in 2013 (7,800 new users per day);[110] among them, 54.1% were under 18 years of age.[110] In 2011, there were approximately 20.6 million people in the United States over the age of 12 with an addiction.[111] Over 90% of those with an addiction began drinking, smoking or using illicit drugs before the age of 18.[111]

Comorbid disorders[edit]

Individuals with comorbid (i.e., co-occurring) mental health disorders such as depression, anxiety, attention-deficit/hyperactivity disorder (ADHD) or post-traumatic stress disorder are more likely to develop substance use disorders.[112][113][114][28] The NIDA cites early aggressive behavior as a risk factor for substance use.[99] The National Bureau of Economic Research found that there is a "definite connection between mental illness and the use of addictive substances" and a majority of mental health patients participate in the use of these substances: 38% alcohol, 44% cocaine, and 40% cigarettes.[115]

Epigenetic[edit]

Epigenetics is the study of stable phenotypic changes that do not involve alterations in the DNA sequence.[116] Illicit drug use has been found to cause epigenetic changes in DNA methylation, as well as chromatin remodeling.[117] The epigenetic state of chromatin may pose as a risk for the development of substance addictions.[117] It has been found that emotional stressors, as well as social adversities may lead to an initial epigenetic response, which causes an alteration to the reward-signalling pathways.[117] This change may predispose one to experience a positive response to drug use.[117]

Transgenerational epigenetic inheritance[edit]

Main article: Transgenerational epigenetic inheritance

Epigenetic genes and their products (e.g., proteins) are the key components through which environmental influences can affect the genes of an individual:[88] they serve as the mechanism responsible for transgenerational epigenetic inheritance, a phenomenon in which environmental influences on the genes of a parent can affect the associated traits and behavioral phenotypes of their offspring (e.g., behavioral responses to environmental stimuli).[88] In addiction, epigenetic mechanisms play a central role in the pathophysiology of the disease;[2] it has been noted that some of the alterations to the epigenome which arise through chronic exposure to addictive stimuli during an addiction can be transmitted across generations, in turn affecting the behavior of one's children (e.g., the child's behavioral responses to addictive drugs and natural rewards).[88][118]

The general classes of epigenetic alterations that have been implicated in transgenerational epigenetic inheritance include DNA methylation, histone modifications, and downregulation or upregulation of microRNAs.[88] With respect to addiction, more research is needed to determine the specific heritable epigenetic alterations that arise from various forms of addiction in humans and the corresponding behavioral phenotypes from these epigenetic alterations that occur in human offspring.[88][118] Based on preclinical evidence from animal research, certain addiction-induced epigenetic alterations in rats can be transmitted from parent to offspring and produce behavioral phenotypes that decrease the offspring's risk of developing an addiction.[note 1][88] More generally, the heritable behavioral phenotypes that are derived from addiction-induced epigenetic alterations and transmitted from parent to offspring may serve to either increase or decrease the offspring's risk of developing an addiction.[88][118]

Mechanisms[edit]

Addiction is a disorder of the brain's reward system developing through transcriptional and epigenetic mechanisms as a result of chronically high levels of exposure to an addictive stimulus (e.g., eating food, the use of cocaine, engagement in sexual activity, participation in high-thrill cultural activities such as gambling, etc.) over extended time.[2][119][33] DeltaFosB (ΔFosB), a gene transcription factor, is a critical component and common factor in the development of virtually all forms of behavioral and drug addictions.[119][33][120][34] Two decades of research into ΔFosB's role in addiction have demonstrated that addiction arises, and the associated compulsive behavior intensifies or attenuates, along with the overexpression of ΔFosB in the D1-type medium spiny neurons of the nucleus accumbens.[2][119][33][120] Due to the causal relationship between ΔFosB expression and addictions, it is used preclinically as an addiction biomarker.[2][119][120] ΔFosB expression in these neurons directly and positively regulates drug self-administration and reward sensitization through positive reinforcement, while decreasing sensitivity to aversion.[note 2][2][119]

Transcription factor glossary
  • gene expression – the process by which information from a gene is used in the synthesis of a functional gene product such as a protein
  • transcription – the process of making messenger RNA (mRNA) from a DNA template by RNA polymerase
  • transcription factor – a protein that binds to DNA and regulates gene expression by promoting or suppressing transcription
  • transcriptional regulation – controlling the rate of gene transcription for example by helping or hindering RNA polymerase binding to DNA
  • upregulation, activation, or promotion – increase the rate of gene transcription
  • downregulation, repression, or suppression – decrease the rate of gene transcription
  • coactivator – a protein (or a small molecule) that works with transcription factors to increase the rate of gene transcription
  • corepressor – a protein (or a small molecule) that works with transcription factors to decrease the rate of gene transcription
  • response element – a specific sequence of DNA that a transcription factor binds to
Signaling cascade in the nucleus accumbens that results in psychostimulant addiction
The image above contains clickable links
This diagram depicts the signaling events in the brain's reward center that are induced by chronic high-dose exposure to psychostimulants that increase the concentration of synaptic dopamine, like amphetamine, methamphetamine, and phenethylamine. Following presynaptic dopamine and glutamate co-release by such psychostimulants,[121][122] postsynaptic receptors for these neurotransmitters trigger internal signaling events through a cAMP-dependent pathway and a calcium-dependent pathway that ultimately result in increased CREB phosphorylation.[121][123][124] Phosphorylated CREB increases levels of ΔFosB, which in turn represses the c-Fos gene with the help of corepressors;[121][125][126] c-Fos repression acts as a molecular switch that enables the accumulation of ΔFosB in the neuron.[127] A highly stable (phosphorylated) form of ΔFosB, one that persists in neurons for 1–2 months, slowly accumulates following repeated high-dose exposure to stimulants through this process.[125][126] ΔFosB functions as "one of the master control proteins" that produces addiction-related structural changes in the brain, and upon sufficient accumulation, with the help of its downstream targets (e.g., nuclear factor kappa B), it induces an addictive state.[125][126]

Chronic addictive drug use causes alterations in gene expression in the mesocorticolimbic projection.[34][128][129] The most important transcription factors that produce these alterations are ΔFosB, cAMP response element binding protein (CREB), and nuclear factor kappa B (NF-κB).[34] ΔFosB is the most significant biomolecular mechanism in addiction because the overexpression of ΔFosB in the D1-type medium spiny neurons in the nucleus accumbens is necessary and sufficient for many of the neural adaptations and behavioral effects (e.g., expression-dependent increases in drug self-administration and reward sensitization) seen in drug addiction.[34] ΔFosB expression in nucleus accumbens D1-type medium spiny neurons directly and positively regulates drug self-administration and reward sensitization through positive reinforcement while decreasing sensitivity to aversion.[note 2][2][119] ΔFosB has been implicated in mediating addictions to many different drugs and drug classes, including alcohol, amphetamine and other substituted amphetamines, cannabinoids, cocaine, methylphenidate, nicotine, opiates, phenylcyclidine, and propofol, among others.[119][34][128][130][131] ΔJunD, a transcription factor, and G9a, a histone methyltransferase, both oppose the function of ΔFosB and inhibit increases in its expression.[2][34][132] Increases in nucleus accumbens ΔJunD expression (via viral vector-mediated gene transfer) or G9a expression (via pharmacological means) reduces, or with a large increase can even block, many of the neural and behavioral alterations that result from chronic high-dose use of addictive drugs (i.e., the alterations mediated by ΔFosB).[120][34]

ΔFosB plays an important role in regulating behavioral responses to natural rewards, such as palatable food, sex, and exercise.[34][133] Natural rewards, like drugs of abuse, induce gene expression of ΔFosB in the nucleus accumbens, and chronic acquisition of these rewards can result in a similar pathological addictive state through ΔFosB overexpression.[33][34][133] Consequently, ΔFosB is the key transcription factor involved in addictions to natural rewards (i.e., behavioral addictions) as well;[34][33][133] in particular, ΔFosB in the nucleus accumbens is critical for the reinforcing effects of sexual reward.[133] Research on the interaction between natural and drug rewards suggests that dopaminergic psychostimulants (e.g., amphetamine) and sexual behavior act on similar biomolecular mechanisms to induce ΔFosB in the nucleus accumbens and possess bidirectional cross-sensitization effects that are mediated through ΔFosB.[33][42][43] This phenomenon is notable since, in humans, a dopamine dysregulation syndrome, characterized by drug-induced compulsive engagement in natural rewards (specifically, sexual activity, shopping, and gambling), has been observed in some individuals taking dopaminergic medications.[33]

ΔFosB inhibitors (drugs or treatments that oppose its action) may be an effective treatment for addiction and addictive disorders.[134]

The release of dopamine in the nucleus accumbens plays a role in the reinforcing qualities of many forms of stimuli, including naturally reinforcing stimuli like palatable food and sex.[135][136][32] Altered dopamine neurotransmission is frequently observed following the development of an addictive state.[33][26] In humans and lab animals that have developed an addiction, alterations in dopamine or opioid neurotransmission in the nucleus accumbens and other parts of the striatum are evident.[33] Use of certain drugs (e.g., cocaine) affect cholinergic neurons that innervate the reward system, in turn affecting dopamine signaling in this region.[137]

Reward system[edit]

Main article: Reward system

Mesocorticolimbic pathway[edit]

ΔFosB accumulation from excessive drug use
ΔFosB accumulation graph
Top: this depicts the initial effects of high dose exposure to an addictive drug on gene expression in the nucleus accumbens for various Fos family proteins (i.e., c-Fos, FosB, ΔFosB, Fra1, and Fra2).
Bottom: this illustrates the progressive increase in ΔFosB expression in the nucleus accumbens following repeated twice daily drug binges, where these phosphorylated (35–37 kilodalton) ΔFosB isoforms persist in the D1-type medium spiny neurons of the nucleus accumbens for up to 2 months.[126][138]

Understanding the pathways in which drugs act and how drugs can alter those pathways is key when examining the biological basis of drug addiction. The reward pathway, known as the mesolimbic pathway,[26] or its extension, the mesocorticolimbic pathway, is characterized by the interaction of several areas of the brain.

  • The projections from the ventral tegmental area (VTA) are a network of dopaminergic neurons with co-localized postsynaptic glutamate receptors (AMPAR and NMDAR). These cells respond when stimuli indicative of a reward are present.[32] The VTA supports learning and sensitization development and releases dopamine (DA) into the forebrain.[139] These neurons project and release DA into the nucleus accumbens,[140] through the mesolimbic pathway. Virtually all drugs causing drug addiction increase the DA release in the mesolimbic pathway.[141][26]
  • The nucleus accumbens (NAcc) is one output of the VTA projections. The nucleus accumbens itself consists mainly of GABAergic medium spiny neurons (MSNs).[142] The NAcc is associated with acquiring and eliciting conditioned behaviors, and is involved in the increased sensitivity to drugs as addiction progresses.[139][31] Overexpression of ΔFosB in the nucleus accumbens is a necessary common factor in essentially all known forms of addiction;[2] ΔFosB is a strong positive modulator of positively reinforced behaviors.[2]
  • The prefrontal cortex, including the anterior cingulate and orbitofrontal cortices,[143][31] is another VTA output in the mesocorticolimbic pathway; it is important for the integration of information which helps determine whether a behavior will be elicited.[144] It is critical for forming associations between the rewarding experience of drug use and cues in the environment. Importantly, these cues are strong mediators of drug-seeking behavior and can trigger relapse even after months or years of abstinence.[145][26]

Other brain structures that are involved in addiction include:

  • The basolateral amygdala projects into the NAcc and is thought to be important for motivation.[144]
  • The hippocampus is involved in drug addiction, because of its role in learning and memory. Much of this evidence stems from investigations showing that manipulating cells in the hippocampus alters DA levels in NAcc and firing rates of VTA dopaminergic cells.[140]

Role of dopamine and glutamate[edit]

Dopamine is the primary neurotransmitter of the reward system in the brain. It plays a role in regulating movement, emotion, cognition, motivation, and feelings of pleasure.[146] Natural rewards, like eating, as well as recreational drug use cause a release of dopamine, and are associated with the reinforcing nature of these stimuli.[146][147][32] Nearly all addictive drugs, directly or indirectly, act on the brain's reward system by heightening dopaminergic activity.[148][26]

Excessive intake of many types of addictive drugs results in repeated release of high amounts of dopamine, which in turn affects the reward pathway directly through heightened dopamine receptor activation. Prolonged and abnormally high levels of dopamine in the synaptic cleft can induce receptor downregulation in the neural pathway. Downregulation of mesolimbic dopamine receptors can result in a decrease in the sensitivity to natural reinforcers.[146]

Drug seeking behavior is induced by glutamatergic projections from the prefrontal cortex to the nucleus accumbens. This idea is supported with data from experiments showing that drug seeking behavior can be prevented following the inhibition of AMPA glutamate receptors and glutamate release in the nucleus accumbens.[143]

Reward sensitization[edit]

Neural and behavioral effects of validated ΔFosB transcriptional targets in the striatum[119][149]
Target
gene		Target
expression		Neural effectsBehavioral effects
c-Fos↓Molecular switch enabling the chronic
induction of ΔFosB[note 3]		–
dynorphin↓
[note 4]		 • Downregulation of κ-opioid feedback loop • Increased drug reward
NF-κB↑ • Expansion of NAcc dendritic processes
 • NF-κB inflammatory response in the NAcc
 • NF-κB inflammatory response in the CPTooltip caudate putamen		 • Increased drug reward
 • Locomotor sensitization
GluR2↑ • Decreased sensitivity to glutamate • Increased drug reward
Cdk5↑ • GluR1 synaptic protein phosphorylation
 • Expansion of NAcc dendritic processes		Decreased drug reward
(net effect)

Reward sensitization is a process that causes an increase in the amount of reward (specifically, incentive salience[note 5]) that is assigned by the brain to a rewarding stimulus (e.g., a drug). In simple terms, when reward sensitization to a specific stimulus (e.g., a drug) occurs, an individual's "wanting" or desire for the stimulus itself and its associated cues increases.[151][150][152] Reward sensitization normally occurs following chronically high levels of exposure to the stimulus.[26] ΔFosB expression in D1-type medium spiny neurons in the nucleus accumbens has been shown to directly and positively regulate reward sensitization involving drugs and natural rewards.[2][119][120]

"Cue-induced wanting" or "cue-triggered wanting", a form of craving that occurs in addiction, is responsible for most of the compulsive behavior that people with addictions exhibit.[150][152] During the development of an addiction, the repeated association of otherwise neutral and even non-rewarding stimuli with drug consumption triggers an associative learning process that causes these previously neutral stimuli to act as conditioned positive reinforcers of addictive drug use (i.e., these stimuli start to function as drug cues).[150][153][152] As conditioned positive reinforcers of drug use, these previously neutral stimuli are assigned incentive salience (which manifests as a craving) – sometimes at pathologically high levels due to reward sensitization – which can transfer to the primary reinforcer (e.g., the use of an addictive drug) with which it was originally paired.[150][153][152]

Research on the interaction between natural and drug rewards suggests that dopaminergic psychostimulants (e.g., amphetamine) and sexual behavior act on similar biomolecular mechanisms to induce ΔFosB in the nucleus accumbens and possess a bidirectional reward cross-sensitization effect[note 6] that is mediated through ΔFosB.[33][42][43] In contrast to ΔFosB's reward-sensitizing effect, CREB transcriptional activity decreases user's sensitivity to the rewarding effects of the substance. CREB transcription in the nucleus accumbens is implicated in psychological dependence and symptoms involving a lack of pleasure or motivation during drug withdrawal.[2][138][149]

Summary of addiction-related plasticity
Form of neuroplasticity
or behavioral plasticity		Type of reinforcerSources
OpiatesPsychostimulantsHigh fat or sugar foodSexual intercoursePhysical exercise
(aerobic)		Environmental
enrichment
ΔFosB expression in
nucleus accumbens D1-type MSNsTooltip medium spiny neurons		↑↑↑↑↑↑[33]
Behavioral plasticity
Escalation of intakeYesYesYes[33]
Psychostimulant
cross-sensitization		YesNot applicableYesYesAttenuatedAttenuated[33]
Psychostimulant
self-administration		↑↑↓↓↓[33]
Psychostimulant
conditioned place preference		↑↑↓↑↓↑[33]
Reinstatement of drug-seeking behavior↑↑↓↓[33]
Neurochemical plasticity
CREBTooltip cAMP response element-binding protein phosphorylation
in the nucleus accumbens		↓↓↓↓↓[33]
Sensitized dopamine response
in the nucleus accumbens		NoYesNoYes[33]
Altered striatal dopamine signaling↓DRD2, ↑DRD3↑DRD1, ↓DRD2, ↑DRD3↑DRD1, ↓DRD2, ↑DRD3↑DRD2↑DRD2[33]
Altered striatal opioid signalingNo change or
↑μ-opioid receptors		↑μ-opioid receptors
↑κ-opioid receptors		↑μ-opioid receptors↑μ-opioid receptorsNo changeNo change[33]
Changes in striatal opioid peptides↑dynorphin
No change: enkephalin		↑dynorphin↓enkephalin↑dynorphin↑dynorphin[33]
Mesocorticolimbic synaptic plasticity
Number of dendrites in the nucleus accumbens↓↑↑[33]
Dendritic spine density in
the nucleus accumbens		↓↑↑[33]

Neuroepigenetic mechanisms[edit]

Further information: Neuroepigenetics and Chromatin remodeling

Altered epigenetic regulation of gene expression within the brain's reward system plays a significant and complex role in the development of drug addiction.[132][154] Addictive drugs are associated with three types of epigenetic modifications within neurons.[132] These are (1) histone modifications, (2) epigenetic methylation of DNA at CpG sites at (or adjacent to) particular genes, and (3) epigenetic downregulation or upregulation of microRNAs which have particular target genes.[132][34][154] As an example, while hundreds of genes in the cells of the nucleus accumbens (NAc) exhibit histone modifications following drug exposure – particularly, altered acetylation and methylation states of histone residues[154] – most other genes in the NAc cells do not show such changes.[132]

Diagnosis[edit]

Further information: Substance use disorder § Diagnosis, and Problem gambling § Diagnosis

Classification[edit]

DSM-5[edit]

The fifth edition of the DSM uses the term substance use disorder to refer to a spectrum of drug use-related disorders. The DSM-5 eliminates the terms abuse and dependence from diagnostic categories, instead using the specifiers of mild, moderate and severe to indicate the extent of disordered use. These specifiers are determined by the number of diagnostic criteria present in a given case. In the DSM-5, the term drug addiction is synonymous with severe substance use disorder.[18][24]

The DSM-5 introduced a new diagnostic category for behavioral addictions. Problem gambling is the only condition included in this category in the fifth edition.[20] Internet gaming disorder is listed as a "condition requiring further study" in the DSM-5.[155]

Past editions have used physical dependence and the associated withdrawal syndrome to identify an addictive state. Physical dependence occurs when the body has adjusted by incorporating the substance into its "normal" functioning – i.e., attains homeostasis – and therefore physical withdrawal symptoms occur on cessation of use.[156] Tolerance is the process by which the body continually adapts to the substance and requires increasingly larger amounts to achieve the original effects. Withdrawal refers to physical and psychological symptoms experienced when reducing or discontinuing a substance that the body has become dependent on. Symptoms of withdrawal generally include but are not limited to body aches, anxiety, irritability, intense cravings for the substance, dysphoria, nausea, hallucinations, headaches, cold sweats, tremors, and seizures. During acute physical opioid withdrawal, symptoms of restless legs syndrome are common and may be profound. This phenomenon originated the idiom "kicking the habit".

Medical researchers who actively study addiction have criticized the DSM classification of addiction for being flawed and involving arbitrary diagnostic criteria.[157]

ICD-11[edit]

The eleventh revision of the International Classification of Diseases, commonly referred to as ICD-11, conceptualizes diagnosis somewhat differently. ICD-11 first distinguishes between problems with psychoactive substance use ("Disorders due to substance use") and behavioral addictions ("Disorders due to addictive behaviours").[14] With regard to psychoactive substances, ICD-11 explains that the included substances initially produce "pleasant or appealing psychoactive effects that are rewarding and reinforcing with repeated use, [but] with continued use, many of the included substances have the capacity to produce dependence. They have the potential to cause numerous forms of harm, both to mental and physical health."[158] Instead of the DSM-5 approach of one diagnosis ("Substance Use Disorder") covering all types of problematic substance use, ICD-11 offers three diagnostic possibilities: 1) Episode of Harmful Psychoactive Substance Use, 2) Harmful Pattern of Psychoactive Substance Use, and 3) Substance Dependence.[158]

Prevention[edit]

Main articles: Harm reduction and Preventive healthcare

Abuse liability[edit]

Abuse or addiction liability is the tendency to use drugs in a non-medical situation. This is typically for euphoria, mood changing, or sedation.[159] Abuse liability is used when the person using the drugs wants something that they otherwise can not obtain. The only way to obtain this is through the use of drugs. When looking at abuse liability there are a number of determining factors in whether the drug is abused. These factors are: the chemical makeup of the drug, the effects on the brain, and the age, vulnerability, and the health (mental and physical) of the population being studied.[159] There are a few drugs with a specific chemical makeup that leads to a high abuse liability. These are: cocaine, heroin, inhalants, marijuana, MDMA (ecstasy), methamphetamine, PCP, synthetic cannabinoids, synthetic cathinones (bath salts), nicotine (e.g. tobacco), and alcohol.[160]

Potential vaccines for addiction to substances[edit]

Vaccines for addiction have been investigated as a possibility since the early 2000s.[161] The general theory of a vaccine intended to "immunize" against drug addiction or other substance abuse is that it would condition the immune system to attack and consume or otherwise disable the molecules of such substances that cause a reaction in the brain, thus preventing the addict from being able to realize the effect of the drug. Addictions that have been floated as targets for such treatment include nicotine, opioids, and fentanyl.[162][163][164][165] Vaccines have been identified as potentially being more effective than other anti-addiction treatments, due to "the long duration of action, the certainty of administration and a potential reduction of toxicity to important organs".[166]

Specific addiction vaccines in development include:

As of September 2023, it was further reported that a vaccine "has been tested against heroin and fentanyl and is on its way to being tested against oxycontin".[173]

Treatment and management[edit]

See also: Addiction recovery groups, Cognitive behavioral therapy, and Drug rehabilitation

To be effective, treatment for addiction that is pharmacological or biologically based need to be accompanied by other interventions such as cognitive behavioral therapy (CBT), individual and group psychotherapy, behavior modification strategies, twelve-step programs, and residential treatment facilities.[174][28] The TTM can be used to determine when treatment can begin and which method will be most effective. If treatment begins too early, it can cause a person to become defensive and resistant to change.[82][175]

A biosocial approach to the treatment of addiction brings to the fore the social determinants of illness and wellbeing and considers the dynamic and reciprocal relationships that exist for, and influence, the individual's experience.[176]

The work of A.V. Schlosser (2018) aims to pronounce the individual lived experiences of women receiving medication-assisted treatment (e.g., methadone, naltrexone, burprenorphine) in a long-term rehabilitation setting, through a twenty month long ethnographic fieldwork investigation. This person-centered research shows how the experiences of these women "emerge from stable systems of inequality based in intersectional gender, race, and class marginalization entangled with processes of intra-action."[177] Viewing addiction treatment through this lens highlights the importance of framing clients' own bodies as "social flesh". As Schlosser (2018) points out, "client bodies" as well as the "embodied experiences of self and social belonging emerge in and through the structures, temporalities, and expectations of the treatment centre."[177]

Biotechnologies make up a large portion of the future treatments for addiction[178] including deep-brain stimulation, agonist and antagonist implants and hapten conjugate vaccines. Vaccinations against addiction specifically overlaps with the belief that memory plays a large role in the damaging effects of addiction and relapses.[medical citation needed] Hapten conjugate vaccines are designed to block opioid receptors in one area, while allowing other receptors to behave normally. Essentially, once a high can no longer be achieved in relation to a traumatic event, the relation of drugs to a traumatic memory can be disconnected and therapy can play a role in treatment.[179]

Behavioral therapy[edit]

CBT proposes four assumptions essential to the approach to treatment: addiction is a learned behavior, it emerges in an environmental context, it is developed and maintained by particular thought patterns and processes, and CBT can be integrated well with other treatment and management approaches as they all have similar goals.[82] CBT, (e.g., relapse prevention), motivational interviewing, and a community reinforcement approach are effective interventions with moderate effect sizes.[180]

Interventions focusing on impulsivity and sensation seeking are successful in decreasing substance use.[31] Cue exposure uses ideas from classical conditioning theory to change the learned behavioral response of someone addicted to a cue or trigger. Contingency management uses ideas from operant conditioning to use meaningful positive reinforcements to influence addiction behaviors towards sobriety.[82]

Addiction recovery groups draw on different methods and models and rely on the success of vicarious learning, where people imitate behavior they observe as rewarding among their own social group or status as well as those perceived as being of a higher status.[82]

Substance addiction in children is complex and requires multifacted behavioral therapy. Family therapy and school-based interventions have had minor but lasting results. Innovative treatments are still needed for areas where relevant therapies are unavailable.[28]

Consistent aerobic exercise, especially endurance exercise (e.g., marathon running), prevents the development of certain drug addictions and is an effective adjunct treatment for drug addiction, and for psychostimulant addiction in particular.[33][181][182][183][184] Consistent aerobic exercise magnitude-dependently (i.e., by duration and intensity) reduces drug addiction risk, which appears to occur through the reversal of drug induced addiction-related neuroplasticity.[33][182] Exercise may prevent the development of drug addiction by altering ΔFosB or c-Fos immunoreactivity in the striatum or other parts of the reward system.[184] Aerobic exercise decreases drug self-administration, reduces the likelihood of relapse, and induces opposite effects on striatal dopamine receptor D2 (DRD2) signaling (increased DRD2 density) to those induced by addictions to several drug classes (decreased DRD2 density).[33][182] Consequently, consistent aerobic exercise may lead to better treatment outcomes when used as an adjunct treatment for drug addiction.[33][182][183]

With a combination of tools such as behavioral therapy, a balanced lifestyle, and individualized relapse plans, relapse is can be more successfully avoided.[82]

Medication[edit]

Alcohol addiction[edit]

Main article: Alcoholism
Further information: Alcohol and health and Long-term effects of alcohol

Alcohol, like opioids, can induce a severe state of physical dependence and produce withdrawal symptoms such as delirium tremens. Because of this, treatment for alcohol addiction usually involves a combined approach dealing with dependence and addiction simultaneously. Benzodiazepines have the largest and the best evidence base in the treatment of alcohol withdrawal and are considered the gold standard of alcohol detoxification.[185]

Pharmacological treatments for alcohol addiction include drugs like naltrexone (opioid antagonist), disulfiram, acamprosate, and topiramate.[186][187] Rather than substituting for alcohol, these drugs are intended to affect the desire to drink, either by directly reducing cravings as with acamprosate and topiramate, or by producing unpleasant effects when alcohol is consumed, as with disulfiram. These drugs can be effective if treatment is maintained, but compliance can be an issue as patients with disordered alcohol use may forget to take their medication, or discontinue use because of excessive side effects.[188][189] The opioid antagonist naltrexone has been shown to be an effective treatment for alcoholism, with the effects lasting three to twelve months after the end of treatment.[190]

Behavioral addictions[edit]

This section is transcluded from Behavioral addiction. (edit | history)

Behavioral addiction is a treatable condition.[191] Treatment options include psychotherapy and psychopharmacotherapy (i.e., medications) or a combination of both. Cognitive behavioral therapy (CBT) is the most common form of psychotherapy used in treating behavioral addictions; it focuses on identifying patterns that trigger compulsive behavior and making lifestyle changes to promote healthier behaviors. Because cognitive behavioral therapy is considered a short-term therapy, the number of sessions for treatment normally ranges from five to twenty.[192] During the session, therapists will lead patients through the topics of identifying the issue, becoming aware of one's thoughts surrounding the issue, identifying any negative or false thinking, and reshaping said negative and false thinking. While CBT does not cure behavioral addiction, it does help with coping with the condition in a healthy way. Currently, there are no medications approved for treatment of behavioral addictions in general, but some medications used for treatment of drug addiction may also be beneficial with specific behavioral addictions.[45]

Cannabinoid addiction[edit]

Main article: Cannabis addiction

The development of CB1 receptor agonists that have reduced interaction with β-arrestin 2 signaling might be therapeutically useful.[193] As of 2019, there has been some evidence of effective pharmacological interventions for cannabinoid addiction, but none have been approved.[194]

Nicotine addiction[edit]

Transdermal patch used in nicotine replacement therapy
Main article: Nicotine addiction
Further information: Smoking cessation and Tobacco harm reduction

Another area in which drug treatment has been widely used is in the treatment of nicotine addiction, which usually involves the use of nicotine replacement therapy, nicotinic receptor antagonists, and/or nicotinic receptor partial agonists.[195][196] Examples of drugs that act on nicotinic receptors and have been used for treating nicotine addiction include antagonists like bupropion and the partial agonist varenicline.[195][196] Cytisine, a partial agonist, is an effective, and affordable cessation treatment for smokers.[197] When access to varenicline and nicotine replacement therapy is limited (due to availability or cost), cytisine is considered the first line of treatment for smoking cessation.[197]

Opioid addiction[edit]

Main article: Opioid use disorder
Further information: Opioid epidemic

Opioids cause physical dependence and treatment typically addresses both dependence and addiction. Physical dependence is treated using replacement drugs such as buprenorphine (the active ingredient in products such as Suboxone and Subutex) and methadone.[198][199] Although these drugs perpetuate physical dependence, the goal of opiate maintenance is to provide a measure of control over both pain and cravings. Use of replacement drugs increases the addicted individual's ability to function normally and eliminates the negative consequences of obtaining controlled substances illicitly. Once a prescribed dosage is stabilized, treatment enters maintenance or tapering phases. In the United States, opiate replacement therapy is tightly regulated in methadone clinics and under the DATA 2000 legislation. In some countries, other opioid derivatives such as dihydrocodeine,[200] dihydroetorphine[201] and even heroin[202][203] are used as substitute drugs for illegal street opiates, with different prescriptions being given depending on the needs of the individual patient. Baclofen has led to successful reductions of cravings for stimulants, alcohol, and opioids and alleviates alcohol withdrawal syndrome. Many patients have stated they "became indifferent to alcohol" or "indifferent to cocaine" overnight after starting baclofen therapy.[204] Some studies show the interconnection between opioid drug detoxification and overdose mortality.[205]

Psychostimulant addiction[edit]

There is no effective and FDA- or EMA-approved pharmacotherapy for any form of psychostimulant addiction.[206] Experimental TAAR1-selective agonists have significant therapeutic potential as a treatment for psychostimulant addictions.[207]

Research[edit]

Anti-drug vaccines (active immunizations) for treatment of cocaine and nicotine addictions were successful in animal studies. Vaccines tested on humans have been shown as safe with mild to moderate side effects, though did not have firm results confirming efficacy despite producing expected antibodies.[208] Vaccines which use anti-drug monoclonal antibodies (passive immunization) can mitigate drug-induced positive reinforcement by preventing the drug from moving across the blood–brain barrier.[209] Current[as of?] vaccine-based therapies are only effective in a relatively small subset of individuals.[209][210] As of November 2015, vaccine-based therapies are being tested in human clinical trials as a treatment for addiction and preventive measure against drug overdoses involving nicotine, cocaine, and methamphetamine.[209] The study shows that the vaccine may save lives during a drug overdose. In this instance, the idea is that the body will respond to the vaccine by quickly producing antibodies to prevent the opioids from accessing the brain.[211]

Since addiction involves abnormalities in glutamate and GABAergic neurotransmission,[212][213] receptors associated with these neurotransmitters (e.g., AMPA receptors, NMDA receptors, and GABAB receptors) are potential therapeutic targets for addictions.[212][213][214][215] N-acetylcysteine, which affects metabotropic glutamate receptors and NMDA receptors, has shown some benefit involving addictions to cocaine, heroin, and cannabinoids.[212] It may be useful as an adjunct therapy for addictions to amphetamine-type stimulants, but more clinical research is required.[212]

Current medical reviews of research involving lab animals have identified a drug class – class I histone deacetylase inhibitors[note 7] – that indirectly inhibits the function and further increases in the expression of accumbal ΔFosB by inducing G9a expression in the nucleus accumbens after prolonged use.[120][132][216][154] These reviews and subsequent preliminary evidence which used oral administration or intraperitoneal administration of the sodium salt of butyric acid or other class I HDAC inhibitors for an extended period indicate that these drugs have efficacy in reducing addictive behavior in lab animals[note 8] that have developed addictions to ethanol, psychostimulants (i.e., amphetamine and cocaine), nicotine, and opiates.[132][154][217][218] Few clinical trials involving humans with addictions and any HDAC class I inhibitors have been conducted to test for treatment efficacy in humans or identify an optimal dosing regimen.[note 9]

Gene therapy for addiction is an active area of research. One line of gene therapy research involves the use of viral vectors to increase the expression of dopamine D2 receptor proteins in the brain.[220][221][222][223][224]

Epidemiology[edit]

Further information: Countries by alcohol consumption, Opioid epidemic, and Prevalence of tobacco use

Due to cultural variations, the proportion of individuals who develop a drug or behavioral addiction within a specified time period (i.e., the prevalence) varies over time, by country, and across national population demographics (e.g., by age group, socioeconomic status, etc.).[88] Where addiction is viewed as unacceptable, there will be fewer people addicted.

Asia[edit]

The prevalence of alcohol dependence is not as high as is seen in other regions. In Asia, not only socioeconomic factors but biological factors influence drinking behavior.[225]

Internet addiction disorder is highest in the Philippines, according to both the IAT (Internet Addiction Test) – 5% and the CIAS-R (Revised Chen Internet Addiction Scale) – 21%.[226]

Australia[edit]

Further information: Alcoholism in rural Australia

The prevalence of substance use disorder among Australians was reported at 5.1% in 2009.[227] In 2019 the Australian Institute of Health and Welfare conducted a national drug survey that quantified drug use for various types of drugs and demographics.[228] The national[specify] found that in 2019, 11% of people over 14 years old smoke daily; that 9.9% of those who drink alcohol, which equates to 7.5% of the total population age 14 or older, may qualify as alcohol dependent; that 17.5% of the 2.4 million people who used cannabis in the last year may have hazardous use or a dependence problem; and that 63.5% of about 300000 recent users of meth and amphetamines were at risk for developing problem use.[228]

Europe[edit]

Further information: Alcoholism in Ireland and Alcoholism in Russia

In 2015, the estimated prevalence among the adult population was 18.4% for heavy episodic alcohol use (in the past 30 days); 15.2% for daily tobacco smoking; and 3.8% for cannabis use, 0.77% for amphetamine use, 0.37% for opioid use, and 0.35% for cocaine use in 2017. The mortality rates for alcohol and illicit drugs were highest in Eastern Europe.[229] Data shows a downward trend of alcohol use among children 15 years old in most European countries between 2002 and 2014. First-time alcohol use before the age of 13 was recorded for 28% of European children in 2014.[28]

United States[edit]

Further information: Cocaine in the United States, Crack epidemic in the United States, and Opioid epidemic in the United States

Based on representative samples of the US youth population in 2011, the lifetime prevalence[note 10] of addictions to alcohol and illicit drugs has been estimated to be approximately 8% and 2–3% respectively.[230] Based on representative samples of the US adult population in 2011, the 12-month prevalence of alcohol and illicit drug addictions were estimated at 12% and 2–3% respectively.[230] The lifetime prevalence of prescription drug addictions is around 4.7%.[231]

As of 2021, 43.7 million people aged 12 or older surveyed by the National Survey on Drug Use and Health in the United States needed treatment for an addiction to alcohol, nicotine, or other drugs. The groups with the highest number of people were 18–25 years (25.1%) and "American Indian or Alaska Native" (28.7%).[232] Only about 10%, or a little over 2 million, receive any form of treatments, and those that do generally do not receive evidence-based care.[233][234] One-third of inpatient hospital costs and 20% of all deaths in the US every year are the result of untreated addictions and risky substance use.[233][234] In spite of the massive overall economic cost to society, which is greater than the cost of diabetes and all forms of cancer combined, most doctors in the US lack the training to effectively address a drug addiction.[233][234]

Estimates of lifetime prevalence rates in the US are 1–2% for compulsive gambling, 5% for sexual addiction, 2.8% for food addiction, and 5–6% for compulsive shopping.[33] The time-invariant prevalence rate for sexual addiction and related compulsive sexual behavior (e.g., compulsive masturbation with or without pornography, compulsive cybersex, etc.) within the US ranges from 3–6% of the population.[41]

According to a 2017 poll conducted by the Pew Research Center, almost half of US adults know a family member or close friend who has struggled with a drug addiction at some point in their life.[235]

In 2019, opioid addiction was acknowledged as a national crisis in the United States.[236] An article in The Washington Post stated that "America's largest drug companies flooded the country with pain pills from 2006 through 2012, even when it became apparent that they were fueling addiction and overdoses."

The National Epidemiologic Survey on Alcohol and Related Conditions found that from 2012 to 2013 the prevalence of Cannabis use disorder in U.S. adults was 2.9%.[237]

Canada[edit]

A Statistics Canada Survey in 2012 found the lifetime prevalence and 12-month prevalence of substance use disorders were 21.6%, and 4.4% in those 15 and older.[238] Alcohol abuse or dependence reported a lifetime prevalence of 18.1% and a 12-month prevalence of 3.2%.[238] Cannabis abuse or dependence reported a lifetime prevalence of 6.8% and a 12-month prevalence of 3.2%.[238] Other drug abuse or dependence has a lifetime prevalence of 4.0% and a 12-month prevalence of 0.7%.[238] Substance use disorder is a term used interchangeably with a drug addiction.[239]

In Ontario, Canada between 2009 and 2017, outpatient visits for mental health and addiction increased from 52.6 to 57.2 per 100 people, emergency department visits increased from 13.5 to 19.7 per 1000 people and the number of hospitalizations increased from 4.5 to 5.5 per 1000 people.[240] Prevalence of care needed increased the most among the 14–17 age group overall.[240]

South America[edit]

The realities of opioid use and opioid use disorder in Latin America may be deceptive if observations are limited to epidemiological findings. In the United Nations Office on Drugs and Crime report,[241] although South America produced 3% of the world's morphine and heroin and 0.01% of its opium, prevalence of use is uneven. According to the Inter-American Commission on Drug Abuse Control, consumption of heroin is low in most Latin American countries, although Colombia is the area's largest opium producer. Mexico, because of its border with the United States, has the highest incidence of use.[242]

Addiction and the humanities[edit]

History and etymology[edit]

Main article: Recreational drug use
Further information: Evolutionary models of human drug use, History of drinking, History of smoking, and Substance abuse in Ancient Rome

The etymology of the term addiction throughout history has been misunderstood and has taken on various meanings associated with the word.[243] An example is the usage of the word in the religious landscape of early modern Europe.[244] "Addiction" at the time meant "to attach" to something, giving it both positive and negative connotations. The object of this attachment could be characterized as "good or bad".[245] The meaning of addiction during the early modern period was mostly associated with positivity and goodness;[244] during this early modern and highly religious era of Christian revivalism and Pietistic tendencies,[244] it was seen as a way of "devoting oneself to another".[245]

Modern research on addiction has led to a better understanding of the disease with research on the topic dating back to 1875, specifically on morphine addiction.[246] This furthered the understanding of addiction being a medical condition. It was not until the 19th century that addiction was seen and acknowledged in the Western world as a disease, being both a physical condition and mental illness.[247] Today, addiction is understood both as a biopsychosocial and neurological disorder that negatively impacts those who are affected by it, most commonly associated with the use of drugs and excessive use of alcohol.[3] The understanding of addiction has changed throughout history, which has impacted and continues to impact the ways it is medically treated and diagnosed.

The suffixes "-holic" and "-holism"[edit]

In contemporary modern English "-holic" is a suffix that can be added to a subject to denote an addiction to it. It was extracted from the word alcoholism (one of the first addictions to be widely identified both medically and socially) (correctly the root "alcohol" plus the suffix "-ism") by misdividing or rebracketing it into "alco" and "-holism". There are correct medico-legal terms for such addictions: dipsomania is the medico-legal term for alcoholism;[248] other examples are in this table:

Colloquial termAddiction toMedico-legal term
chocoholicchocolate
danceaholicdancechoreomania
rageaholicrage
sexaholicsexerotomania, satyriasis, nymphomania
sugarholicsugarsaccharomania
workaholicworkergomania

Arts[edit]

The arts can be used in a variety of ways to address issues related to addiction. Art can be used as a form of therapy in the treatment of substance use disorders. Creative activities like painting, sculpting, music, and writing can help people express their feelings and experiences in safe and healthy ways. The arts can be used as an assessment tool to identify underlying issues that may be contributing to a person's substance use disorder. Through art, individuals can gain insights into their own motivations and behaviors that can be helpful in determining a course of treatment. Finally, the arts can be used to advocate for those suffering from a substance use disorder by raising awareness of the issue and promoting understanding and compassion. Through art, individuals can share their stories, increase awareness, and offer support and hope to those struggling with substance use disorders.

As therapy[edit]

Addiction treatment is complex and not always effective due to engagement and service availability concerns, so researchers prioritize efforts to improve treatment retention and decrease relapse rates.[249][250] Characteristics of substance abuse may include feelings of isolation, a lack of confidence, communication difficulties, and a perceived lack of control.[251] In a similar vein, people suffering from substance use disorders tend to be highly sensitive, creative, and as such, are likely able to express themselves meaningfully in creative arts such as dancing, painting, writing, music, and acting.[252] Further evidenced by Waller and Mahony (2002)[253] and Kaufman (1981),[254] the creative arts therapies can be a suitable treatment option for this population especially when verbal communication is ineffective.

Primary advantages of art therapy in the treatment of addiction have been identified as:[255][256]

  • Assess and characterize a client's substance use issues
  • Bypassing a client's resistances, defenses, and denial
  • Containing shame or anger
  • Facilitating the expression of suppressed and/or complicated emotions
  • Highlighting a client's strengths
  • Providing an alternative to verbal communication (via use of symbols) and conventional forms of therapy
  • Providing clients with a sense of control
  • Tackling feelings of isolation

Art therapy is an effective method of dealing with substance abuse in comprehensive treatment models. When included in psychoeducational programs, art therapy in a group setting can help clients internalize taught concepts in a more personalized manner.[257] During the course of treatment, by examining and comparing artwork created at different times, art therapists can be helpful in identifying and diagnosing issues, as well as charting the extent or direction of improvement as a person detoxifies.[257] Where increasing adherence to treatment regimes and maintaining abstinence is the target; art therapists can aid by customizing treatment directives (encourage the client to create collages that compare pros and cons, pictures that compare past and present and future, and drawings that depict what happened when a client went off medication).[257]

Art therapy can function as a complementary therapy used in conjunction with more conventional therapies and can can integrate with harm reduction protocols to minimize the negative effects of drug use.[258][256] An evaluation of art therapy incorporation within a pre-existing Addiction Treatment Programme based on the 12 step Minnesota Model endorsed by the Alcoholics Anonymous found that 66% of participants expressed the usefulness of art therapy as a part of treatment.[259][256] Within the weekly art therapy session, clients were able to reflect and process the intense emotions and cognitions evoked by the programme. In turn, the art therapy component of the programme fostered stronger self-awareness, exploration, and externalization of repressed and unconscious emotions of clients, promoting the development of a more integrated 'authentic self'.[260][256]

Despite the large number of randomized control trials, clinical control trials, and anecdotal evidence supporting the effectiveness of art therapies for use in addiction treatment, a systematic review conducted in 2018 could not find enough evidence on visual art, drama, dance and movement therapy, or 'arts in health' methodologies to confirm their effectiveness as interventions for reducing substance misuse.[261] Music therapy was identified to have potentially strong beneficial effects in aiding contemplation and preparing those diagnosed with substance use for treatment.[261]

As an assessment tool[edit]

The Formal Elements Art Therapy Scale (FEATS) is an assessment tool used to evaluate drawings created by people suffering from substance use disorders by comparing them to drawings of a control group (consisting of individuals without SUDs).[262][256] FEATS consists of twelve elements, three of which were found to be particularly effective at distinguishing the drawings of those with SUDs from those without: Person, Realism, and Developmental. The Person element assesses the degree to which a human features are depicted realistically, the Realism element assesses the overall complexity of the artwork, and the Developmental element assesses "developmental age" of the artwork in relation to standardized drawings from children and adolescents.[262] By using the FEATS assessment tool, clinicians can gain valuable insight into the drawings of individuals with SUDs, and can compare them to those of the control group. Formal assessments such as FEATS provide healthcare providers with a means to quantify, standardize, and communicate abstract and visceral characteristics of SUDs to provide more accurate diagnoses and informed treatment decisions.[262]

Other artistic assessment methods include the Bird's Nest Drawing: a useful tool for visualizing a client's attachment security.[263][256] This assessment method looks at the amount of color used in the drawing, with a lack of color indicating an 'insecure attachment', a factor that the client's therapist or recovery framework must take into account.[264]

Art therapists working with children of parents suffering from alcoholism can use the Kinetic Family Drawings assessment tool to shed light on family dynamics and help children express and understand their family experiences.[265][256] The KFD can be used in family sessions to allow children to share their experiences and needs with parents who may be in recovery from alcohol use disorder. Depiction of isolation of self and isolation of other family members may be an indicator of parental alcoholism.[265]

Advocacy[edit]

Stigma can lead to feelings of shame that can prevent people with substance use disorders from seeking help and interfere with provision of harm reduction services.[266][267][268] It can influence healthcare policy, making it difficult for these individuals to access treatment.[269]

Artists attempt to change the societal perception of addiction from a punishable moral offense to instead a chronic illness necessitating treatment. This form of advocacy can help to relocate the fight of addiction from a judicial perspective to the public health system.[270]

Artists who have personally lived with addiction and/or undergone recovery may use art to depict their experiences in a manner that uncovers the "human face of addiction". By bringing experiences of addiction and recovery to a personal level and breaking down the "us and them", the viewer may be more inclined to show compassion, forego stereotypes and stigma of addiction, and label addiction as a social rather than individual problem.[270]

According to Santora[270] the main purposes in using art as a form of advocacy in the education and prevention of substance use disorders include:

  • Addiction art exhibitions can come from a variety of sources, but the underlying message of these works is the same: to communicate through emotions without relying on intellectually demanding/gatekept facts and figures. These exhibitions can either stand alone, reinforce, or challenge facts.
  • A powerful educational tool for increasing awareness and understanding of addiction as a medical illness. Exhibitions featuring personal stories and images can help to create lasting impressions on diverse audiences (including addiction scientists/researchers, family/friends of those affected by addiction etc.), highlighting the humanity of the problem and in turn encouraging compassion and understanding.
  • A way to destigmatize substance use disorders and shift public perception from viewing them as a moral failing to understanding them as a chronic medical condition which requires treatment.
  • Provide those who are struggling with addiction assurance and encouragement of healing, and let them know that they are not alone in their struggle.
  • The use of visual arts can help bring attention to the lack of adequate substance use treatment, prevention, and education programs and services in a healthcare system. Messages can encourage policymakers to allocate more resources to addiction treatment and prevention from federal, state, and local levels.

The Temple University College of Public Health department conducted a project to promote awareness around opioid use and reduce associated stigma by asking students to create art pieces that were displayed on a website they created and promoted via social media.[271] Quantitative and qualitative data was recorded to measure engagement, and the student artists were interviewed, which revealed a change in perspective and understanding, as well as greater appreciation of diverse experiences. Ultimately, the project found that art was an effective medium for empowering both the artist creating the work and the person interacting with it.[271]

Another author critically examined works by contemporary Canadian artists that deal with addiction via the metaphor of a cultural landscape to "unmap" and "remap" ideologies related to Indigenous communities and addiction to demonstrate how colonial violence in Canada has drastically impacted the relationship between Indigenous peoples, their land, and substance abuse.[272]

A project known as "Voice" was a collection of art, poetry and narratives created by women living with a history of addiction to explore women's understanding of harm reduction, challenge the effects of stigma and give voice to those who have historically been silenced or devalued.[273] In the project, nurses with knowledge of mainstream systems, aesthetic knowing, feminism and substance use organized weekly gatherings, wherein women with histories of substance use and addiction worked alongside a nurse to create artistic expressions. Creations were presented at several venues, including an International Conference on Drug Related Harm, a Nursing Conference and a local gallery to positive community response.[273]

Narrative Approach and Addiction[edit]

The narrative medicine to addiction focuses on recognizing, absorbing, and interpreting the stories of those suffering from addiction, allowing for better understanding of their experiences[274] with narrative analysis being used to study the discourse of those with addiction. This knowledge can be used to develop better care plans with the potential to increase patient compliance and make treatment more effective.

A narrative study demonstrated and studied cognitive and emotional tendencies among substance abusers during treatment periods to learn more about motivation and ambivalence inherent in recovery over the course of a residential treatment program.[275] Seven narrative types emerged from the overall analysis: optimistic, overly optimistic, pessimistic, overly pessimistic, "tough life," troubled/confused, and balanced. Narratives tended to express a basic level of emotionality in early stages of treatment ("optimistic", "pessimistic" narrative). Over time, as clients progressed through the program, their stories became more complex and detailed, including their drug abuse and recovery efforts, more skeptical positions towards treatment began to emerge. Clients began to distinguish between the positive and negative aspects of treatment, creating more "balanced" narratives in the process.[275]

Due to higher medication consumption, social isolation, financial worries, and other factors, older adults are particularly vulnerable to substance use problems.[276] Incidence of addiction among this population is inaccurately reported. Narrative therapy can provide an avenue to unearth stories of addiction in an empowering manner, and thus serves as a viable therapeutic tool in applied gerontology.[276] When treating substance abuse in older adults, it is essential to ensure that the client is respected and comfortable disclosing information. This should be done at the outset of treatment when the therapist and older adult are developing the therapeutic relationship.[277] The social breakdown model is an important tool that can consider the compounded effects of ageism, physical changes, social changes, and substance abuse. The narrative approach integrates the social breakdown model with substance abuse challenges and can be an effective way to address addiction in this population.[277]

A study conducted in 2009 in the Republic of Moldova looked into the social dynamics of initiating injection drug usage by examining 42 audio-recorded, semi-structured interviews with present and former injectors.[278] A thematic analysis suggested that self-injection was viewed as a symbolic transition of identity, enabled by interpersonal interactions and collective influences. Personal narratives of self-transition were connected to larger narratives of social transitions. The personal narratives of self-initiation and transition are contextualized and understood in terms of political (social) narratives within the core concept of the 'transitional society'.[278] Another study examined the narratives of 'initiators': people who help people who inject drugs (PWID) with their first injection.[279] Through their accounts, respondents described initiation events as meaningful transitions to a life characterized by predictable downfalls of homelessness, infections, and social stigma. Initiators used examples from their own personal experience to explain the process of initiation and assistance, attributing personal agency and predicting specific injection-related harms for initiates. They distinguished between two forms of harm: potentially avoidable proximal harm caused by risky injection practices (e.g. overdose, HIV) and perceived inevitable distal harm caused by long-term injection (e.g. socioeconomic decline).[279] In this way, these narratives reflect a balance of individual agency, harm reduction intentions, and accepted notions of 'life after initiation' interact with the narrative experiences and intentions of PWIDs.[278][279]

Philosophy[edit]

From a philosophy perspective, the behavior of many with addiction that is not explained by executive dysfunction or biological reasons can be explained by folk psychology – specifically the belief–desire model.[26] According to this model, a person acquires and uses a substance or does an addictive activity in belief that it will help them achieve a goal.

Social scientific models[edit]

Acute confusional state caused by alcohol withdrawal, otherwise known as delirium tremens

Biopsychosocial–cultural–spiritual[edit]

While regarded biomedically as a neuropsychological disorder, addiction is multi-layered, with biological, psychological, social, cultural, and spiritual (biopsychosocial–cultural–spiritual) elements.[280][281] A biopsychosocial–cultural–spiritual approach fosters the crossing of disciplinary boundaries, and promotes holistic considerations of addiction.[282][283][284] A biopsychosocial–cultural–spiritual approach considers, for example, how physical environments influence experiences, habits, and patterns of addiction.

Ethnographic engagements and developments in fields of knowledge have contributed to biopsychosocial–cultural–spiritual understandings of addiction, including the work of Philippe Bourgois, whose fieldwork with street-level drug dealers in East Harlem highlights correlations between drug use and structural oppression in the United States.[285] Prior models that have informed the prevailing biopsychosocial–cultural–spiritual consideration of addiction include:

Cultural model[edit]

The cultural model, an anthropological understanding of the emergence of drug use and abuse, was developed by Dwight Heath.[286] Heath undertook ethnographic research and fieldwork with the Camba people of Bolivia from June 1956 to August 1957.[287] Heath observed that adult members of society drank 'large quantities of rum and became intoxicated for several contiguous days at least twice a month'.[286] This frequent, heavy drinking from which intoxication followed was typically undertaken socially, during festivals.[287] Having returned in 1989, Heath observed that while much had changed, 'drinking parties' remained, as per his initial observations, and 'there appear to be no harmful consequences to anyone'.[288] Heath's observations and interactions reflected that this form of social behavior, the habitual heavy consumption of alcohol, was encouraged and valued, enforcing social bonds in the Camba community.[287] Despite frequent intoxication, "even to the point of unconsciousness", the Camba held no concept of alcoholism (a form of addiction), and no visible social problems associated with drunkenness, or addiction, were apparent.[286]

As noted by Merrill Singer, Heath's findings, when considered alongside subsequent cross-cultural experiences, challenged the perception that intoxication is socially 'inherently disruptive'.[286] Following this fieldwork, Heath proposed the 'cultural model', suggesting that 'problems' associated with heavy drinking, such as alcoholism – a recognised form addiction – were cultural: that is, that alcoholism is determined by cultural beliefs, and therefore varies among cultures. Heath's findings challenged the notion that 'continued use [of alcohol] is inexorably addictive and damaging to the consumer's health'.[287][286]

The cultural model did face criticism by Sociologist Robin Room and others, who felt anthropologists could "downgrade the severity of the problem".[286] Merrill Singer found it notable that the ethnographers working within the prominence of the cultural model were part of the 'wet generation': while not blind to the 'disruptive, dysfunctional and debilitating effects of alcohol consumption', they were products 'socialized to view alcohol consumption as normal'.[286]

Subcultural model[edit]

Historically, addiction has been viewed from the etic perspective, defining users through the pathology of their condition.[289] As reports of drug use rapidly increased, the cultural model found application in anthropological research exploring western drug subculture practices.[286]

The approach evolved from the ethnographic exploration into the lived experiences and subjectivities of 1960s and 1970s drug subcultures.[286] The seminal publication "Taking care of business", by Edward Preble and John J. Casey, documented the daily lives of New York street-based intravenous heroin users in rich detail, providing unique insight into the dynamic social worlds and activities that surrounded their drug use.[290] These findings challenge popular narratives of immorality and deviance, conceptualizing substance abuse as a social phenomenon. The prevailing culture can have a greater influence on drug taking behaviors than the physical and psychological effects of the drug itself.[291][better source needed] To marginalized individuals, drug subcultures can provide social connection, symbolic meaning, and socially constructed purpose that they may feel is unattainable through conventional means.[291] The subcultural model demonstrates the complexities of addiction, highlighting the need for an integrated approach. It contends that a biosocial approach is required to achieve a holistic understanding of addiction.[286]

Critical medical anthropology model[edit]

Emerging in the early 1980s, the critical medical anthropology model was introduced, and as Merrill Singer offers 'was applied quickly to the analysis of drug use'.[286] Where the cultural model of the 1950s looked at the social body, the critical medical anthropology model revealed the body politic, considering drug use and addiction within the context of macro level structures including larger political systems, economic inequalities, and the institutional power held over social processes.[286]

Highly relevant to addiction, the three issues emphasized in the model are:

These three key points highlight how drugs may come to be used to self-medicate the psychological trauma of socio-political disparity and injustice, intertwining with licit and illicit drug market politics.[286] Social suffering, "the misery among those on the weaker end of power relations in terms of physical health, mental health and lived experience", is used by anthropologists to analyze how individuals may have personal problems caused by political and economic power.[286] From the perspective of critical medical anthropology heavy drug use and addiction is a consequence of such larger scale unequal distributions of power.[286]

The three models developed here – the cultural model, the subcultural model, and the Critical Medical Anthropology Model – display how addiction is not an experience to be considered only biomedically. Through consideration of addiction alongside the biological, psychological, social, cultural and spiritual (biopsychosocial–spiritual) elements which influence its experience, a holistic and comprehensive understanding can be built.

Social learning models[edit]

Social learning theory[edit]

Main article: Social learning theory

Albert Bandura's 1977 social learning theory posits that individuals acquire addictive behaviors by observing and imitating models in their social environment.[292][293] The likelihood of engaging in and sustaining similar addictive behaviors is influenced by the reinforcement and punishment observed in others. The principle of reciprocal determinism suggests that the functional relationships between personal, environmental, and behavioral factors act as determinants of addictive behavior.[294] Thus, effective treatment targets each dynamic facet of the biopsychosocial disorder.

Transtheoretical model (stages of change model)[edit]

Main article: Transtheoretical model

The transtheoretical model of change suggests that overcoming an addiction is a stepwise process that occurs through several stages.[295]

Precontemplation: This initial stage precedes individuals considering a change in their behavior. They might be oblivious to or in denial of their addiction, failing to recognize the need for change.

Contemplation is the stage in which individuals become aware of the problems caused by their addiction and are considering change. Although they may not fully commit, they weigh the costs and benefits of making a shift.

Preparation: Individuals in this stage are getting ready to change. They might have taken preliminary steps, like gathering information or making small commitments, in preparation for behavioral change.

Action involves actively modifying behavior by making specific, observable changes to address the addictive behavior. The action stage requires significant effort and commitment.

Maintenance: After successfully implementing a change, individuals enter the maintenance stage, where they work to sustain the new behavior and prevent relapse. This stage is characterized by ongoing effort and consolidation of gains.

Termination/relapse prevention: Recognizing that relapse is a common part of the change process, this stage focuses on identifying and addressing factors that may lead to a return to old behaviors. Relapse is viewed as an opportunity for learning and strategy adjustment, with the ultimate goal of eliminating or terminating the targeted behavior.

The transtheoretical model can be helpful in guiding development of tailored behavioral interventions that can promote lasting change. Progression through these stages may not always follow a linear path, as individuals may move back and forth between stages. Resistance to change is recognized as an expected part of the process.

Addiction causes an "astoundingly high financial and human toll" on individuals and society as a whole.[296][230][233] In the United States, the total economic cost to society is greater than that of all types of diabetes and all cancers combined.[233] These costs arise from the direct adverse effects of drugs and associated healthcare costs (e.g., emergency medical services and outpatient and inpatient care), long-term complications (e.g., lung cancer from smoking tobacco products, liver cirrhosis and dementia from chronic alcohol consumption, and meth mouth from methamphetamine use), the loss of productivity and associated welfare costs, fatal and non-fatal accidents (e.g., traffic collisions), suicides, homicides, and incarceration, among others.[296][230][233][297] The US National Institute on Drug Abuse has found that overdose deaths in the US have almost tripled among male and females from 2002 to 2017, with 72,306 overdose deaths reported in 2017 in the US.[298] 2020 marked the year with highest number of overdose deaths over a 12-month period, with 81,000 overdose deaths, exceeding the records set in 2017.[299]

See also[edit]

Endnotes[edit]

  1. ^ In other words, a person cannot control the neurobiological processes that occur in the body in response to using an addictive drug. A person can make a voluntary choice to, for example, start using a drug (or not), or to seek help after becoming addicted, although resisting the urge to use drug(s) becomes increasingly difficult as addiction worsens. See [1] for detailed discussion.

Notes[edit]

  1. ^ According to a review of experimental animal models that examined the transgenerational epigenetic inheritance of epigenetic marks that occur in addiction, alterations in histone acetylation – specifically, di-acetylation of lysine residues 9 and 14 on histone 3 (i.e., H3K9ac2 and H3K14ac2) in association with BDNF gene promoters – have been shown to occur within the medial prefrontal cortex (mPFC), testes, and sperm of cocaine-addicted male rats.[88] These epigenetic alterations in the rat mPFC result in increased BDNF gene expression within the mPFC, which in turn blunts the rewarding properties of cocaine and reduces cocaine self-administration.[88] The male but not female offspring of these cocaine-exposed rats inherited both epigenetic marks (i.e., di-acetylation of lysine residues 9 and 14 on histone 3) within mPFC neurons, the corresponding increase in BDNF expression within mPFC neurons, and the behavioral phenotype associated with these effects (i.e., a reduction in cocaine reward, resulting in reduced cocaine-seeking by these male offspring).[88] Consequently, the transmission of these two cocaine-induced epigenetic alterations (i.e., H3K9ac2 and H3K14ac2) in rats from male fathers to male offspring served to reduce the offspring's risk of developing an addiction to cocaine.[88] As of 2018, neither the heritability of these epigenetic marks in humans nor the behavioral effects of the marks within human mPFC neurons has been established.[88]
  2. ^ Jump up to:a b A decrease in aversion sensitivity, in simpler terms, means that an individual's behavior is less likely to be influenced by undesirable outcomes.
  3. ^ In other words, c-Fos repression allows ΔFosB to more rapidly accumulate within the D1-type medium spiny neurons of the nucleus accumbens because it is selectively induced in this state.[2] Before c-Fos repression, all Fos family proteins (e.g., c-Fos, Fra1, Fra2, FosB, and ΔFosB) are induced together, with ΔFosB expression increasing to a lesser extent.[2]
  4. ^ According to two medical reviews, ΔFosB has been implicated in causing both increases and decreases in dynorphin expression in different studies;[119][149] this table entry reflects only a decrease.
  5. ^ Incentive salience, the "motivational salience" for a reward, is a "desire" or "want" attribute, which includes a motivational component, that the brain assigns to a rewarding stimulus.[150][151] As a consequence, incentive salience acts as a motivational "magnet" for a rewarding stimulus that commands attention, induces approach, and causes the rewarding stimulus to be sought out.[150]
  6. ^ In simplest terms, this means that when either amphetamine or sex is perceived as more alluring or desirable through reward sensitization, this effect occurs with the other as well.
  7. ^ Inhibitors of class I histone deacetylase (HDAC) enzymes are drugs that inhibit four specific histone-modifying enzymes: HDAC1, HDAC2, HDAC3, and HDAC8. Most of the animal research with HDAC inhibitors has been conducted with four drugs: butyrate salts (mainly sodium butyrate), trichostatin A, valproic acid, and SAHA;[216][154] butyric acid is a naturally occurring short-chain fatty acid in humans, while the latter two compounds are FDA-approved drugs with medical indications unrelated to addiction.
  8. ^ Specifically, prolonged administration of a class I HDAC inhibitor appears to reduce an animal's motivation to acquire and use an addictive drug without affecting an animals motivation to attain other rewards (i.e., it does not appear to cause motivational anhedonia) and reduce the amount of the drug that is self-administered when it is readily available.[132][154][217]
  9. ^ Among the few clinical trials that employed a class I HDAC inhibitor, one used valproate for methamphetamine addiction.[219]
  10. ^ The lifetime prevalence of an addiction is the percentage of individuals in a population that developed an addiction at some point in their life.
Image legend
  1. ^
      Ion channel
      G proteins & linked receptors
      (Text color) Transcription factors

References[edit]

  1. ^ Jump up to:a b Heilig M, MacKillop J, Martinez D, Rehm J, Leggio L, Vanderschuren LJ (September 2021). "Addiction as a brain disease revised: why it still matters, and the need for consilience". Neuropsychopharmacology. 46 (10): 1715–1723. doi:10.1038/s41386-020-00950-y. PMC 8357831. PMID 33619327. pre-existing vulnerabilities and persistent drug use lead to a vicious circle of substantive disruptions in the brain that impair and undermine choice capacities for adaptive behavior, but do not annihilate them.
  2. ^ Jump up to:a b c d e f g h i j k l m n o p q r s t Nestler EJ (December 2013). "Cellular basis of memory for addiction". Dialogues in Clinical Neuroscience. 15 (4): 431–443. PMC 3898681. PMID 24459410. Despite the importance of numerous psychosocial factors, at its core, drug addiction involves a biological process: the ability of repeated exposure to a drug of abuse to induce changes in a vulnerable brain that drive the compulsive seeking and taking of drugs, and loss of control over drug use, that define a state of addiction. ... A large body of literature has demonstrated that such ΔFosB induction in D1-type [nucleus accumbens] neurons increases an animal's sensitivity to drug as well as natural rewards and promotes drug self-administration, presumably through a process of positive reinforcement ... Another ΔFosB target is cFos: as ΔFosB accumulates with repeated drug exposure it represses c-Fos and contributes to the molecular switch whereby ΔFosB is selectively induced in the chronic drug-treated state.41 ... Moreover, there is increasing evidence that, despite a range of genetic risks for addiction across the population, exposure to sufficiently high doses of a drug for long periods of time can transform someone who has relatively lower genetic loading into an addict.
  3. ^ Jump up to:a b c "Drugs, Brains, and Behavior: The Science of Addiction – Drug Misuse and Addiction". www.drugabuse.gov. North Bethesda, Maryland: National Institute on Drug Abuse. 13 July 2020. Retrieved 23 December 2021.
  4. ^ Henden E (2017). "Addiction, Compulsion, and Weakness of the Will: A Dual-Process Perspective.". In Heather N, Gabriel S (eds.). Addiction and Choice: Rethinking the Relationship. Oxford, UK: Oxford University Press. pp. 116–132.
  5. ^ Angres DH, Bettinardi-Angres K (October 2008). "The disease of addiction: origins, treatment, and recovery". Disease-a-Month. 54 (10): 696–721. doi:10.1016/j.disamonth.2008.07.002. PMID 18790142.
  6. ^ Jump up to:a b Malenka RC, Nestler EJ, Hyman SE (2009). "Chapter 15: Reinforcement and Addictive Disorders". In Sydor A, Brown RY (eds.). Molecular Neuropharmacology: A Foundation for Clinical Neuroscience (second ed.). New York: McGraw-Hill Medical. pp. 364–65, 375. ISBN 978-0-07-148127-4. 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.
  7. ^ Marlatt GA, Baer JS, Donovan DM, Kivlahan DR (1988). "Addictive behaviors: etiology and treatment". Annu Rev Psychol. 39: 223–52. doi:10.1146/annurev.ps.39.020188.001255. PMID 3278676.
  8. ^ ME (12 September 2019). "Gaming Addiction in ICD-11: Issues and Implications". Psychiatric Times. Psychiatric Times Vol 36, Issue 9. 36 (9). Archived from the original on 3 March 2020. Retrieved 3 March 2020.
  9. ^ Jump up to:a b Steverson (2020). Addiction reimagined: challenging views of an enduring social problem. Vernon Press. p. 206. ISBN 978-1-62273-953-0.
  10. ^ Gowing L, Ali R, Allsop S, Marsden J, Turf E, West E, et al. (2015). "Global statistics on addictive behaviours: 2014 status report" (PDF). Addiction. 110 (6): 904–919. doi:10.1111/add.12899. PMID 25963869.
  11. ^ Gilley (2018). "The new science of attention deficit hyperactivity disorder: news from the cutting edge of research science". Journal of Psychiatry and Psychiatric Disorders. 2 (3). doi:10.26502/jppd.2572-519X0043 (inactive 31 January 2024). S2CID 150196703.
  12. ^ Lee C, Ko A, Yang F (2018). "Association of DSM-5 betel-quid use disorder with oral potentially malignant disorder in 6 betel-quid endemic Asian populations". JAMA Psychiatry. 75 (3): 261–269. doi:10.1001/jamapsychiatry.2017.4307. PMC 5885949. PMID 29417149.
  13. ^ Jump up to:a b Sahithya B, Kashyap R (2020). "Sexual Addiction Disorder—a review with recent updates". Journal of Psychosexual Health. 4 (2): 95–101. doi:10.1177/26318318221081080. S2CID 248835855.
  14. ^ Jump up to:a b c "International Classification of Diseases 11th revision – ICD-11. Disorders due to substance use or addictive behaviours". World Health Organization. Geneva. 2023. Retrieved 10 April 2023.
  15. ^ Destoop M, Morrens M, Coppens V, Dom G (2019). "Addiction, anhedonia, and comorbid mood disorder. A narrative review". Frontiers in Psychiatry. 10: 311. doi:10.3389/fpsyt.2019.00311. PMC 6538808. PMID 31178763.
  16. ^ Volkow N, Koob G, McLellan T (2016). "Neurobiologic advances from the brain disease model of addiction". The New England Journal of Medicine. 374 (4): 363–371. doi:10.1056/NEJMra1511480. PMC 6135257. PMID 26816013.
  17. ^ Koob G, Buck G, Cohen A, Edwards S, Park P, Schlosburg J, et al. (2014). "Addiction as a stress surfeit disorder". Neuropharmacology. 76: 370–382. doi:10.1016/j.neuropharm.2013.05.024. PMC 3830720. PMID 23747571.
  18. ^ Jump up to:a b "Facing Addiction in America: The Surgeon General's Report on Alcohol, Drugs, and Health" (PDF). Office of the Surgeon General. US Department of Health and Human Services. November 2016. pp. 35–37, 45, 63, 155, 317, 338. Retrieved 28 January 2017.
  19. ^ Ko C, Yen J, Yen C, Chen C, ChenC (2020). "The association between Internet addiction and psychiatric disorder: A review of the literature". European Psychiatry. 27 (1): 1–8. doi:10.1016/j.eurpsy.2010.04.011. PMID 22153731. S2CID 3558840.
  20. ^ Jump up to:a b American Psychiatric Association (2013). "Substance-Related and Addictive Disorders" (PDF). American Psychiatric Publishing. pp. 1–2. Archived from the original (PDF) on 15 August 2015. Retrieved 8 April 2023. 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.
  21. ^ Malenka R, Nestler E, Hyman S, Holtzman D (2015). "Chapter 16: Reinforcement and Addictive Disorders". Molecular Neuropharmacology: A Foundation for Clinical Neuroscience (3rd ed.). New York: McGraw-Hill Medical. ISBN 978-0-07-182770-6.
  22. ^ World Health Organization (2023). International Classification of Diseases, eleventh revision – ICD-11. Geneva – icd.who.int.
  23. ^ Malenka RC, Nestler EJ, Hyman SE (2009). "Chapter 15: Reinforcement and Addictive Disorders". In Sydor A, Brown RY (eds.). Molecular Neuropharmacology: A Foundation for Clinical Neuroscience (2nd ed.). New York: McGraw-Hill Medical. pp. 364–375. ISBN 978-0-07-148127-4.
  24. ^ Jump up to:a b Volkow ND, Koob GF, McLellan AT (January 2016). "Neurobiologic Advances from the Brain Disease Model of Addiction". New England Journal of Medicine. 374 (4): 363–371. doi:10.1056/NEJMra1511480. PMC 6135257. PMID 26816013. Substance-use disorder: A diagnostic term in the fifth edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-5) referring to recurrent use of alcohol or other drugs that causes clinically and functionally significant impairment, such as health problems, disability, and failure to meet major responsibilities at work, school, or home. Depending on the level of severity, this disorder is classified as mild, moderate, or severe.
    Addiction: A term used to indicate the most severe, chronic stage of substance-use disorder, in which there is a substantial loss of self-control, as indicated by compulsive drug taking despite the desire to stop taking the drug. In the DSM-5, the term addiction is synonymous with the classification of severe substance-use disorder.
  25. ^ Jump up to:a b c d NIDA (13 July 2020). "Drug Misuse and Addiction". National Institute of Drug Abuse. U.S. Department of Health and Human Services. Retrieved 15 November 2022.
  26. ^ Jump up to:a b c d e f g h i j k Levy N (2019). "Chapter 5 Addiction: The belief oscillation hypothesis". In Pickard H, Ahmed SH (eds.). The Routledge handbook of philosophy and science of addiction. Wellcome Trust–Funded Monographs and Book Chapters. Oxon (UK): Routledge. doi:10.4324/9781315689197-6. ISBN 978-1-138-90928-1. OCLC 1042341025. PMID 31017751. S2CID 242067468.
  27. ^ "Food addiction: Symptoms and management". www.medicalnewstoday.com. 17 February 2020. Retrieved 15 November 2022.
  28. ^ Jump up to:a b c d e f g h i j k l m Skylstad V, Babirye JN, Kiguli J, Solheim Skar AM, et al. (March 2022). "Are we overlooking alcohol use by younger children?". BMJ Paediatrics Open. 6 (1): e001242. doi:10.1136/bmjpo-2021-001242. PMC 8905875. PMID 36053657.
  29. ^ "Drug addiction (substance use disorder) – Symptoms and causes". Mayo Clinic. Retrieved 15 November 2022.
  30. ^ Drummond DC (3 May 2002). "Theories of drug craving, ancient and modern". Addiction. 96 (1): 33–46. doi:10.1046/j.1360-0443.2001.961333.x. PMID 11177518.
  31. ^ Jump up to:a b c d e f g h i j Maxwell AL, Gardiner E, Loxton NJ (9 February 2020). "Investigating the relationship between reward sensitivity, impulsivity, and food addiction: A systematic review". European Eating Disorders Review. 28 (4): 368–384. doi:10.1002/erv.2732. ISSN 1099-0968. PMID 32142199. S2CID 212565361. Retrieved 9 March 2023.
  32. ^ Jump up to:a b c d e f g h i j k l m n o di Giacomo E, Aliberti F, Pescatore F, Santorelli M, Pessina R, Placenti V, et al. (August 2022). "Disentangling binge eating disorder and food addiction: a systematic review and meta-analysis". Eating and Weight Disorders. 27 (6): 1963–1970. doi:10.1007/s40519-021-01354-7. PMC 9287203. PMID 35041154.
  33. ^ Jump up to:a b c d e f g h i j k l m n o p q r s t u v w x y z aa ab ac ad ae af ag ah ai aj ak al Olsen CM (December 2011). "Natural rewards, neuroplasticity, and non-drug addictions". Neuropharmacology. 61 (7): 1109–22. doi:10.1016/j.neuropharm.2011.03.010. PMC 3139704. PMID 21459101. 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 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"
  34. ^ Jump up to:a b c d e f g h i j k l m Robison AJ, Nestler EJ (November 2011). "Transcriptional and epigenetic mechanisms of addiction". Nat. Rev. Neurosci. 12 (11): 623–37. doi:10.1038/nrn3111. PMC 3272277. PMID 21989194. 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.
  35. ^ Jump up to:a b c d Goodman B (3 September 2022). Casarella J (ed.). "Food Addiction Signs and Treatments". WebMD. Retrieved 9 March 2023.
  36. ^ Nehlig A (2004). Coffee, tea, chocolate, and the brain. Boca Raton: CRC Press. pp. 203–218. ISBN 978-0-429-21192-8.
  37. ^ "Yale Food Addiction Scale". Food and Addiction Science & Treatment Lab. Department of Psychology, University of Michigan. Retrieved 1 November 2022.
  38. ^ Gearhardt AN, Corbin WR, Brownell KD (February 2016). "Development of the Yale Food Addiction Scale Version 2.0". Psychology of Addictive Behaviors. 30 (1): 113–121. doi:10.1037/adb0000136. PMID 26866783.
  39. ^ Brunault P, Berthoz S, Gearhardt AN, Gierski F, Kaladjian A, Bertin E, et al. (8 September 2020). "The Modified Yale Food Addiction Scale 2.0: Validation Among Non-Clinical and Clinical French-Speaking Samples and Comparison With the Full Yale Food Addiction Scale 2.0". Frontiers in Psychiatry. 11: 480671. doi:10.3389/fpsyt.2020.480671. PMC 7509420. PMID 33033480.
  40. ^ Hauck C, Cook B, Ellrott T (February 2020). "Food addiction, eating addiction and eating disorders". The Proceedings of the Nutrition Society. 79 (1): 103–112. doi:10.1017/S0029665119001162. PMID 31744566. S2CID 208186539.
  41. ^ Jump up to:a b c d Karila L, Wéry A, Weinstein A, Cottencin O, Petit A, Reynaud M, et al. (2014). "Sexual addiction or hypersexual disorder: different terms for the same problem? A review of the literature". Curr. Pharm. Des. 20 (25): 4012–20. doi:10.2174/13816128113199990619. PMID 24001295. S2CID 19042860. 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.
  42. ^ Jump up to:a b c d e Pitchers KK, Vialou V, Nestler EJ, Laviolette SR, Lehman MN, Coolen LM (February 2013). "Natural and drug rewards act on common neural plasticity mechanisms with ΔFosB as a key mediator". The Journal of Neuroscience. 33 (8): 3434–42. doi:10.1523/JNEUROSCI.4881-12.2013. PMC 3865508. PMID 23426671. 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
  43. ^ Jump up to:a b c d e Beloate LN, Weems PW, Casey GR, Webb IC, Coolen LM (February 2016). "Nucleus accumbens NMDA receptor activation regulates amphetamine cross-sensitization and deltaFosB expression following sexual experience in male rats". Neuropharmacology. 101: 154–64. doi:10.1016/j.neuropharm.2015.09.023. PMID 26391065. S2CID 25317397.
  44. ^ Jump up to:a b Alavi SS, Ferdosi M, Jannatifard F, Eslami M, Alaghemandan H, Setare M (April 2012). "Behavioral Addiction versus Substance Addiction: Correspondence of Psychiatric and Psychological Views". International Journal of Preventive Medicine. 3 (4): 290–294. PMC 3354400. PMID 22624087.
  45. ^ Jump up to:a b c Grant JE, Potenza MN, Weinstein A, Gorelick DA (September 2010). "Introduction to behavioral addictions". Am. J. Drug Alcohol Abuse. 36 (5): 233–241. doi:10.3109/00952990.2010.491884. PMC 3164585. PMID 20560821. Naltrexone, a mu-opioid receptor antagonist approved by the US Food and Drug Administration for the treatment of alcoholism and opioid dependence, has shown efficacy in controlled clinical trials for the treatment of pathological gambling and kleptomania (76–79), and promise in uncontrolled studies of compulsive buying (80), compulsive sexual behavior (81), internet addiction (82), and pathologic skin picking (83). ... Topiramate, an anti-convulsant which blocks the AMPA subtype of glutamate receptor (among other actions), has shown promise in open-label studies of pathological gambling, compulsive buying, and compulsive skin picking (85), as well as efficacy in reducing alcohol (86), cigarette (87), and cocaine (88) use. N-acetyl cysteine, an amino acid that restores extracellular glutamate concentration in the nucleus accumbens, reduced gambling urges and behavior in one study of pathological gamblers (89), and reduces cocaine craving (90) and cocaine use (91) in cocaine addicts. These studies suggest that glutamatergic modulation of dopaminergic tone in the nucleus accumbens may be a mechanism common to behavioral addiction and substance use disorders (92).
  46. ^ Jump up to:a b Derbyshire KL, Grant JE (June 2015). "Compulsive sexual behavior: a review of the literature". Journal of Behavioral Addictions. 4 (2): 37–43. doi:10.1556/2006.4.2015.003. PMC 4500883. PMID 26014671.
  47. ^ American Psychiatric Association, American Psychiatric Association, DSM-5 Task Force (2013). Diagnostic and statistical manual of mental disorders : DSM-5 (5th ed.). Arlington, VA: American Psychiatric Association. p. 481. ISBN 978-0-89042-554-1. OCLC 830807378.
  48. ^ Jump up to:a b c d Yau YH, Potenza MN (2015). "Gambling disorder and other behavioral addictions: recognition and treatment". Harvard Review of Psychiatry. 23 (2): 134–146. doi:10.1097/HRP.0000000000000051. PMC 4458066. PMID 25747926.
  49. ^ Ford M, Håkansson A (10 January 2020). "Problem gambling, associations with comorbid health conditions, substance use, and behavioural addictions: Opportunities for pathways to treatment". PLOS ONE. 15 (1): e0227644. Bibcode:2020PLoSO..1527644F. doi:10.1371/journal.pone.0227644. PMC 6953879. PMID 31923269.
  50. ^ Jump up to:a b c Menchon JM, Mestre-Bach G, Steward T, Fernández-Aranda F, Jiménez-Murcia S (9 April 2018). "An overview of gambling disorder: from treatment approaches to risk factors". F1000Research. 7: 434. doi:10.12688/f1000research.12784.1. PMC 5893944. PMID 30090625.
  51. ^ Jump up to:a b Chou C, Condron L, Belland JC (2005). "A Review of the Research on Internet Addiction". Educational Psychology Review. 17 (4): 363–388. doi:10.1007/s10648-005-8138-1. ISSN 1040-726X. S2CID 7014879.
  52. ^ Musetti A, Cattivelli R, Giacobbi M, Zuglian P, Ceccarini M, Capelli F, et al. (2016). "Challenges in Internet Addiction Disorder: Is a Diagnosis Feasible or Not?". Frontiers in Psychology. 7: 842. doi:10.3389/fpsyg.2016.00842. PMC 4894006. PMID 27375523.
  53. ^ Bipeta R, Yerramilli SS, Karredla AR, Gopinath S (2015). "Diagnostic Stability of Internet Addiction in Obsessive-compulsive Disorder: Data from a Naturalistic One-year Treatment Study". Innovations in Clinical Neuroscience. 12 (3–4): 14–23. PMC 4420165. PMID 26000201.
  54. ^ Cash H, Rae CD, Steel AH, Winkler A (November 2012). "Internet Addiction: A Brief Summary of Research and Practice". Current Psychiatry Reviews. 8 (4): 292–298. doi:10.2174/157340012803520513. PMC 3480687. PMID 23125561.
  55. ^ Block JJ (March 2008). "Issues for DSM-V: internet addiction". The American Journal of Psychiatry. 165 (3): 306–307. doi:10.1176/appi.ajp.2007.07101556. PMID 18316427.
  56. ^ Tang J, Yu Y, Du Y, Ma Y, Zhang D, Wang J (March 2014). "Prevalence of internet addiction and its association with stressful life events and psychological symptoms among adolescent internet users". Addictive Behaviors. 39 (3): 744–747. doi:10.1016/j.addbeh.2013.12.010. hdl:2436/622804. PMID 24388433.
  57. ^ Jump up to:a b c Joseph J, Varghese A, Vr V, Dhandapani M, Grover S, Sharma S, et al. (August 2021). "Prevalence of internet addiction among college students in the Indian setting: a systematic review and meta-analysis". General Psychiatry. 34 (4): e100496. doi:10.1136/gpsych-2021-100496. PMC 8381302. PMID 34504996.
  58. ^ Jump up to:a b Weinstein A, Lejoyeux M (September 2010). "Internet addiction or excessive internet use". The American Journal of Drug and Alcohol Abuse. 36 (5): 277–283. doi:10.3109/00952990.2010.491880. PMID 20545603. S2CID 17713327.
  59. ^ "Addictive behaviours: Gaming disorder". www.who.int. Retrieved 25 October 2022.
  60. ^ "International Classification of Diseases 11th revision – ICD-11". icd.who.int. Geneva. Retrieved 25 October 2022.
  61. ^ Jump up to:a b c Wittek CT, Finserås TR, Pallesen S, Mentzoni RA, Hanss D, Griffiths MD, et al. (2016). "Prevalence and Predictors of Video Game Addiction: A Study Based on a National Representative Sample of Gamers". International Journal of Mental Health and Addiction. 14 (5): 672–686. doi:10.1007/s11469-015-9592-8. PMC 5023737. PMID 27688739.
  62. ^ Peters CS, Malesky LA (August 2008). "Problematic usage among highly-engaged players of massively multiplayer online role playing games". Cyberpsychology & Behavior. 11 (4): 481–484. doi:10.1089/cpb.2007.0140. PMID 18721098.
  63. ^ Hyun GJ, Han DH, Lee YS, Kang KD, Yoo SK, Chung US, et al. (1 July 2015). "Risk factors associated with online game addiction: A hierarchical model". Computers in Human Behavior. 48: 706–713. doi:10.1016/j.chb.2015.02.008. ISSN 0747-5632.
  64. ^ Jump up to:a b Hague B, Hall J, Kellett S (September 2016). "Treatments for compulsive buying: A systematic review of the quality, effectiveness and progression of the outcome evidence". Journal of Behavioral Addictions. 5 (3): 379–394. doi:10.1556/2006.5.2016.064. PMC 5264404. PMID 27640529.
  65. ^ Jump up to:a b Black DW (February 2007). "A review of compulsive buying disorder". World Psychiatry. 6 (1): 14–18. PMC 1805733. PMID 17342214.
  66. ^ "Drug addiction (substance use disorder) – Symptoms and causes". Mayo Clinic. Retrieved 21 November 2022.
  67. ^ Jump up to:a b c "Mental Health and Substance Use Co-Occurring Disorders". MentalHealth.gov. Retrieved 29 November 2022.
  68. ^ Koob GF, Powell P, White A (November 2020). "Addiction as a Coping Response: Hyperkatifeia, Deaths of Despair, and COVID-19". Am J Psychiatry. 177 (11): 1031–1037. doi:10.1176/appi.ajp.2020.20091375. PMID 33135468. S2CID 226233515.
  69. ^ Jump up to:a b c d Kwako LE, Momenan R, Litten RZ, Koob GF, Goldman D (August 2016). "Addictions Neuroclinical Assessment: A Neuroscience-Based Framework for Addictive Disorders". Biological Psychiatry. 80 (3): 179–189. doi:10.1016/j.biopsych.2015.10.024. PMC 4870153. PMID 26772405.
  70. ^ Jump up to:a b "Tobacco, Alcohol, Prescription medication, and other Substance use (TAPS) Tool". nida.nih.gov. Retrieved 29 November 2022.
  71. ^ "About the CRAFFT – CRAFFT". Retrieved 3 December 2022.
  72. ^ Jump up to:a b c "Use the CRAFFT – CRAFFT". Retrieved 3 December 2022.
  73. ^ Jump up to:a b c Yudko E, Lozhkina O, Fouts A (March 2007). "A comprehensive review of the psychometric properties of the Drug Abuse Screening Test". Journal of Substance Abuse Treatment. 32 (2): 189–198. doi:10.1016/j.jsat.2006.08.002. PMID 17306727.
  74. ^ Han BH, Moore AA (February 2018). "Prevention and Screening of Unhealthy Substance Use by Older Adults". Clinics in Geriatric Medicine. 34 (1): 117–129. doi:10.1016/j.cger.2017.08.005. PMC 5718360. PMID 29129212.
  75. ^ Ali R, Meena S, Eastwood B, Richards I, Marsden J (September 2013). "Ultra-rapid screening for substance-use disorders: the Alcohol, Smoking and Substance Involvement Screening Test (ASSIST-Lite)". Drug and Alcohol Dependence. 132 (1–2): 352–361. doi:10.1016/j.drugalcdep.2013.03.001. PMID 23561823.
  76. ^ Fehrman E, Egan V, Gorban AN, Levesley J, Mirkes EM, Muhammad AK (2019). Personality Traits and Drug Consumption. A Story Told by Data. Springer, Cham. arXiv:2001.06520. doi:10.1007/978-3-030-10442-9. ISBN 978-3-030-10441-2. S2CID 151160405.
  77. ^ Cheetham A, Allen NB, Yücel M, Lubman DI (August 2010). "The role of affective dysregulation in drug addiction". Clin Psychol Rev. 30 (6): 621–34. doi:10.1016/j.cpr.2010.04.005. PMID 20546986.
  78. ^ Franken IH, Muris P (2006). "BIS/BAS personality characteristics and college students' substance use". Personality and Individual Differences. 40 (7): 1497–503. doi:10.1016/j.paid.2005.12.005.
  79. ^ Genovese JE, Wallace D (December 2007). "Reward sensitivity and substance abuse in middle school and high school students". J Genet Psychol. 168 (4): 465–69. doi:10.3200/GNTP.168.4.465-469. PMID 18232522. S2CID 207640075.
  80. ^ Kimbrel NA, Nelson-Gray RO, Mitchell JT (April 2007). "Reinforcement sensitivity and maternal style as predictors of psychopathology". Personality and Individual Differences. 42 (6): 1139–49. doi:10.1016/j.paid.2006.06.028.
  81. ^ Dawe S, Loxton NJ (May 2004). "The role of impulsivity in the development of substance use and eating disorders". Neurosci Biobehav Rev. 28 (3): 343–51. doi:10.1016/j.neubiorev.2004.03.007. PMID 15225976. S2CID 24435589.
  82. ^ Jump up to:a b c d e f g h i j Hill R, Harris J (2 November 2021). "Psychological Approaches to Addiction". In Day E (ed.). Seminars in addiction psychiatry (2nd ed.). Cambridge: Cambridge University Press. pp. 147–169. doi:10.1017/9781911623199.009. ISBN 978-1-911623-19-9. S2CID 242036830.
  83. ^ Washburn DA (2016). "The Stroop effect at 80: The competition between stimulus control and cognitive control". J Exp Anal Behav. 105 (1): 3–13. doi:10.1002/jeab.194. PMID 26781048. 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.
  84. ^ Diamond A (2013). "Executive functions". Annu Rev Psychol. 64: 135–68. doi:10.1146/annurev-psych-113011-143750. PMC 4084861. PMID 23020641. 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).
  85. ^ Jump up to:a b Malenka RC, Nestler EJ, Hyman SE (2009). "Chapter 13: Higher Cognitive Function and Behavioral Control". In Sydor A, Brown RY (eds.). Molecular Neuropharmacology: A Foundation for Clinical Neuroscience (2nd ed.). New York: McGraw-Hill Medical. pp. 313–21. ISBN 978-0-07-148127-4.  • 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.
  86. ^ Jump up to:a b c d e f Gould TJ (December 2010). "Addiction and cognition". Addiction Science & Clinical Practice. 5 (2): 4–14. PMC 3120118. PMID 22002448.
  87. ^ Feltenstein MW, See RE (May 2008). "The neurocircuitry of addiction: an overview". British Journal of Pharmacology. 154 (2): 261–274. doi:10.1038/bjp.2008.51. PMC 2442446. PMID 18311189.
  88. ^ Jump up to:a b c d e f g h i j k l m n o p Vassoler FM, Sadri-Vakili G (2014). "Mechanisms of transgenerational inheritance of addictive-like behaviors". Neuroscience. 264: 198–206. doi:10.1016/j.neuroscience.2013.07.064. PMC 3872494. PMID 23920159. 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.
  89. ^ Douglas KR, Chan G, Gelernter J, Arias AJ, Anton RF, Weiss RD, et al. (January 2010). "Adverse childhood events as risk factors for substance dependence: partial mediation by mood and anxiety disorders". Addictive Behaviors. 35 (1): 7–13. doi:10.1016/j.addbeh.2009.07.004. PMC 2763992. PMID 19720467.
  90. ^ Jump up to:a b Saunders GR, Wang X, Chen F, Jang SK, Liu M, Wang C, et al. (December 2022). "Genetic diversity fuels gene discovery for tobacco and alcohol use". Nature. 612 (7941). Nature Research: 720–724. Bibcode:2022Natur.612..720S. doi:10.1038/s41586-022-05477-4. PMC 9771818. PMID 36477530. S2CID 254434507.
  91. ^ Mirin SM, Weiss RD, Griffin ML, Michael JL (1 January 1991). "Psychopathology in drug abusers and their families". Comprehensive Psychiatry. 32 (1): 36–51. doi:10.1016/0010-440X(91)90068-N. PMID 2001619.
  92. ^ Mayfield RD, Harris RA, Schuckit MA (May 2008). "Genetic factors influencing alcohol dependence". British Journal of Pharmacology. 154 (2): 275–287. doi:10.1038/bjp.2008.88. PMC 2442454. PMID 18362899.
  93. ^ Jump up to:a b Kendler KS, Neale MC, Heath AC, Kessler RC, Eaves LJ (May 1994). "A twin-family study of alcoholism in women". The American Journal of Psychiatry. 151 (5): 707–715. doi:10.1176/ajp.151.5.707. PMID 8166312.
  94. ^ Crowe JR. "Genetics of alcoholism". Alcohol Health and Research World: 1–11. Retrieved 13 December 2017.
  95. ^ Melemis SM. "The Genetics of Addiction – Is Addiction a Disease?". I Want to Change My Life. Retrieved 17 September 2018.
  96. ^ Clarke TK, Crist RC, Kampman KM, Dackis CA, Pettinati HM, O'Brien CP, et al. (2013). "Low frequency genetic variants in the μ-opioid receptor (OPRM1) affect risk for addiction to heroin and cocaine". Neuroscience Letters. 542: 71–75. doi:10.1016/j.neulet.2013.02.018. PMC 3640707. PMID 23454283.
  97. ^ Hall FS, Drgonova J, Jain S, Uhl GR (December 2013). "Implications of genome wide association studies for addiction: are our a priori assumptions all wrong?". Pharmacology & Therapeutics. 140 (3): 267–79. doi:10.1016/j.pharmthera.2013.07.006. PMC 3797854. PMID 23872493.
  98. ^ Yang H, Ma J (August 2021). "How the COVID-19 pandemic impacts tobacco addiction: Changes in smoking behavior and associations with well-being". Addictive Behaviors. 119: 106917. doi:10.1016/j.addbeh.2021.106917. PMC 9186053. PMID 33862579. S2CID 233278782.
  99. ^ Jump up to:a b "What are risk factors and protective factors?". National Institute on Drug Abuse. Archived from the original on 30 April 2020. Retrieved 13 December 2017.
  100. ^ "Understanding Drug Use and Addiction". www.drugabuse.gov. National Institute on Drug Abuse. 6 June 2018. Retrieved 29 May 2020.
  101. ^ Lewis M (October 2018). Longo DL (ed.). "Brain Change in Addiction as Learning, Not Disease". The New England Journal of Medicine. 379 (16): 1551–1560. doi:10.1056/NEJMra1602872. PMID 30332573. S2CID 205117578. 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.
  102. ^ Jump up to:a b "Adverse Childhood Experiences". samhsa.gov. Rockville, Maryland, United States: Substance Abuse and Mental Health Services Administration. Archived from the original on 9 October 2016. Retrieved 26 September 2016.
  103. ^ Jump up to:a b Enoch MA (March 2011). "The role of early life stress as a predictor for alcohol and drug dependence". Psychopharmacology. 214 (1): 17–31. doi:10.1007/s00213-010-1916-6. PMC 3005022. PMID 20596857.
  104. ^ "Environmental Risk Factors". learn.genetics.utah.edu. Archived from the original on 17 September 2018. Retrieved 17 September 2018.
  105. ^ Marcos AC, Bahr SJ (June 1988). "Control Theory and Adolescent Drug Use". Youth & Society. 19 (4): 395–425. doi:10.1177/0044118X88019004003. ISSN 0044-118X. S2CID 143860602.
  106. ^ Spear LP (June 2000). "The adolescent brain and age-related behavioral manifestations". Neuroscience and Biobehavioral Reviews. 24 (4): 417–63. CiteSeerX 10.1.1.461.3295. doi:10.1016/s0149-7634(00)00014-2. PMID 10817843. S2CID 14686245.
  107. ^ Hammond CJ, Mayes LC, Potenza MN (April 2014). "Neurobiology of adolescent substance use and addictive behaviors: treatment implications". Adolescent Medicine. 25 (1): 15–32. PMC 4446977. PMID 25022184.
  108. ^ Catalano RF, Hawkins JD, Wells EA, Miller J, Brewer D (1990). "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 Addictions. 25 (9A–10A): 1085–140. doi:10.3109/10826089109081039. PMID 2131328.
  109. ^ Perepletchikova F, Krystal JH, Kaufman J (November 2008). "Practitioner review: adolescent alcohol use disorders: assessment and treatment issues". Journal of Child Psychology and Psychiatry, and Allied Disciplines. 49 (11): 1131–54. doi:10.1111/j.1469-7610.2008.01934.x. PMC 4113213. PMID 19017028.
  110. ^ Jump up to:a b "Addiction Statistics – Facts on Drug and Alcohol Addiction". AddictionCenter. Retrieved 17 September 2018.
  111. ^ SAMHSA. "Risk and Protective Factors". Substance Abuse and Mental Health Administration. Archived from the original on 8 December 2016. Retrieved 19 December 2016.
  112. ^ "Infographic – Risk Factors of Addiction | Recovery Research Institute". www.recoveryanswers.org. Archived from the original on 17 December 2016. Retrieved 19 December 2016.
  113. ^ "Drug addiction Risk factors – Mayo Clinic". www.mayoclinic.org. Retrieved 19 December 2016.
  114. ^ "The Connection Between Mental Illness and Substance Abuse | Dual Diagnosis". Dual Diagnosis. Retrieved 17 September 2018.
  115. ^ Dupont C, Armant DR, Brenner CA (September 2009). "Epigenetics: definition, mechanisms and clinical perspective". Seminars in Reproductive Medicine. 27 (5): 351–357. doi:10.1055/s-0029-1237423. PMC 2791696. PMID 19711245.
  116. ^ Jump up to:a b c d Nielsen DA, Utrankar A, Reyes JA, Simons DD, Kosten TR (July 2012). "Epigenetics of drug abuse: predisposition or response". Pharmacogenomics. 13 (10): 1149–1160. doi:10.2217/pgs.12.94. PMC 3463407. PMID 22909205.
  117. ^ Jump up to:a b c Yuan TF, Li A, Sun X, Ouyang H, Campos C, Rocha NB, et al. (2015). "Transgenerational Inheritance of Paternal Neurobehavioral Phenotypes: Stress, Addiction, Ageing and Metabolism". Mol. Neurobiol. 53 (9): 6367–76. doi:10.1007/s12035-015-9526-2. hdl:10400.22/7331. PMID 26572641. S2CID 25694221.
  118. ^ Jump up to:a b c d e f g h i j Ruffle JK (November 2014). "Molecular neurobiology of addiction: what's all the (Δ)FosB about?". Am. J. Drug Alcohol Abuse. 40 (6): 428–37. doi:10.3109/00952990.2014.933840. PMID 25083822. S2CID 19157711. 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.
  119. ^ Jump up to:a b c d e f Biliński P, Wojtyła A, Kapka-Skrzypczak L, Chwedorowicz R, Cyranka M, Studziński T (2012). "Epigenetic regulation in drug addiction". Ann. Agric. Environ. Med. 19 (3): 491–96. PMID 23020045. [...]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.
  120. ^ Jump up to:a b c Renthal W, Nestler EJ (September 2009). "Chromatin regulation in drug addiction and depression". Dialogues in Clinical Neuroscience. 11 (3): 257–268. doi:10.31887/DCNS.2009.11.3/wrenthal. PMC 2834246. PMID 19877494. [Psychostimulants] increase cAMP levels in striatum, which activates protein kinase A (PKA) and leads to phosphorylation of its targets. This includes the cAMP response element binding protein (CREB), the phosphorylation of which induces its association with the histone acetyltransferase, CREB binding protein (CBP) to acetylate histones and facilitate gene activation. This is known to occur on many genes including fosB and c-fos in response to psychostimulant exposure. ΔFosB is also upregulated by chronic psychostimulant treatments, and is known to activate certain genes (eg, cdk5) and repress others (eg, c-fos) where it recruits HDAC1 as a corepressor. ... Chronic exposure to psychostimulants increases glutamatergic [signaling] from the prefrontal cortex to the NAc. Glutamatergic signaling elevates Ca2+ levels in NAc postsynaptic elements where it activates CaMK (calcium/calmodulin protein kinases) signaling, which, in addition to phosphorylating CREB, also phosphorylates HDAC5.
    Figure 2: Psychostimulant-induced signaling events
  121. ^ Broussard JI (January 2012). "Co-transmission of dopamine and glutamate". The Journal of General Physiology. 139 (1): 93–96. doi:10.1085/jgp.201110659. PMC 3250102. PMID 22200950. Coincident and convergent input often induces plasticity on a postsynaptic neuron. The NAc integrates processed information about the environment from basolateral amygdala, hippocampus, and prefrontal cortex (PFC), as well as projections from midbrain dopamine neurons. Previous studies have demonstrated how dopamine modulates this integrative process. For example, high frequency stimulation potentiates hippocampal inputs to the NAc while simultaneously depressing PFC synapses (Goto and Grace, 2005). The converse was also shown to be true; stimulation at PFC potentiates PFC–NAc synapses but depresses hippocampal–NAc synapses. In light of the new functional evidence of midbrain dopamine/glutamate co-transmission (references above), new experiments of NAc function will have to test whether midbrain glutamatergic inputs bias or filter either limbic or cortical inputs to guide goal-directed behavior.
  122. ^ Kanehisa Laboratories (10 October 2014). "Amphetamine – Homo sapiens (human)". KEGG Pathway. Retrieved 31 October 2014. Most addictive drugs increase extracellular concentrations of dopamine (DA) in nucleus accumbens (NAc) and medial prefrontal cortex (mPFC), projection areas of mesocorticolimbic DA neurons and key components of the "brain reward circuit". Amphetamine achieves this elevation in extracellular levels of DA by promoting efflux from synaptic terminals. ... Chronic exposure to amphetamine induces a unique transcription factor delta FosB, which plays an essential role in long-term adaptive changes in the brain.
  123. ^ Cadet JL, Brannock C, Jayanthi S, Krasnova IN (2015). "Transcriptional and epigenetic substrates of methamphetamine addiction and withdrawal: evidence from a long-access self-administration model in the rat". Molecular Neurobiology. 51 (2): 696–717 (Figure 1). doi:10.1007/s12035-014-8776-8. PMC 4359351. PMID 24939695.
  124. ^ Jump up to:a b c Robison AJ, Nestler EJ (November 2011). "Transcriptional and epigenetic mechanisms of addiction". Nature Reviews Neuroscience. 12 (11): 623–637. doi:10.1038/nrn3111. PMC 3272277. PMID 21989194. ΔFosB serves as one of the master control proteins governing this structural plasticity. ... ΔFosB also represses G9a expression, leading to reduced repressive histone methylation at the cdk5 gene. The net result is gene activation and increased CDK5 expression. ... In contrast, ΔFosB binds to the c-fos gene and recruits several co-repressors, including HDAC1 (histone deacetylase 1) and SIRT 1 (sirtuin 1). ... The net result is c-fos gene repression.
    Figure 4: Epigenetic basis of drug regulation of gene expression
  125. ^ Jump up to:a b c d Nestler EJ (December 2012). "Transcriptional mechanisms of drug addiction". Clinical Psychopharmacology and Neuroscience. 10 (3): 136–143. doi:10.9758/cpn.2012.10.3.136. PMC 3569166. PMID 23430970. The 35-37 kD ΔFosB isoforms accumulate with chronic drug exposure due to their extraordinarily long half-lives. ... As a result of its stability, the ΔFosB protein persists in neurons for at least several weeks after cessation of drug exposure. ... ΔFosB overexpression in nucleus accumbens induces NFκB ... In contrast, the ability of ΔFosB to repress the c-Fos gene occurs in concert with the recruitment of a histone deacetylase and presumably several other repressive proteins such as a repressive histone methyltransferase
  126. ^ Nestler EJ (October 2008). "Transcriptional mechanisms of addiction: Role of ΔFosB". Philosophical Transactions of the Royal Society B: Biological Sciences. 363 (1507): 3245–3255. doi:10.1098/rstb.2008.0067. PMC 2607320. PMID 18640924. 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
  127. ^ Jump up to:a b Hyman SE, Malenka RC, Nestler EJ (2006). "Neural mechanisms of addiction: the role of reward-related learning and memory". Annu. Rev. Neurosci. 29: 565–98. doi:10.1146/annurev.neuro.29.051605.113009. PMID 16776597.
  128. ^ Steiner H, Van Waes V (January 2013). "Addiction-related gene regulation: risks of exposure to cognitive enhancers vs. other psychostimulants". Prog. Neurobiol. 100: 60–80. doi:10.1016/j.pneurobio.2012.10.001. PMC 3525776. PMID 23085425.
  129. ^ Kanehisa Laboratories (2 August 2013). "Alcoholism – Homo sapiens (human)". KEGG Pathway. Retrieved 10 April 2014.
  130. ^ Kim Y, Teylan MA, Baron M, Sands A, Nairn AC, Greengard P (February 2009). "Methylphenidate-induced dendritic spine formation and DeltaFosB expression in nucleus accumbens". Proc. Natl. Acad. Sci. USA. 106 (8): 2915–20. Bibcode:2009PNAS..106.2915K. doi:10.1073/pnas.0813179106. PMC 2650365. PMID 19202072.
  131. ^ Jump up to:a b c d e f g h Nestler EJ (January 2014). "Epigenetic mechanisms of drug addiction". Neuropharmacology. 76 (Pt B): 259–68. doi:10.1016/j.neuropharm.2013.04.004. PMC 3766384. PMID 23643695. 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.
  132. ^ Jump up to:a b c d Blum K, Werner T, Carnes S, Carnes P, Bowirrat A, Giordano J, et al. (2012). "Sex, drugs, and rock 'n' roll: hypothesizing common mesolimbic activation as a function of reward gene polymorphisms". Journal of Psychoactive Drugs. 44 (1): 38–55. doi:10.1080/02791072.2012.662112. PMC 4040958. PMID 22641964. 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.
  133. ^ Malenka RC, Nestler EJ, Hyman SE (2009). "Chapter 15: Reinforcement and addictive disorders". In Sydor A, Brown RY (eds.). Molecular Neuropharmacology: A Foundation for Clinical Neuroscience (2nd ed.). New York: McGraw-Hill Medical. pp. 384–85. ISBN 978-0-07-148127-4.
  134. ^ Salamone JD (1992). "Complex motor and sensorimotor functions of striatal and accumbens dopamine: involvement in instrumental behavior processes". Psychopharmacology. 107 (2–3): 160–74. doi:10.1007/bf02245133. PMID 1615120. S2CID 30545845.
  135. ^ Kauer JA, Malenka RC (November 2007). "Synaptic plasticity and addiction". Nature Reviews. Neuroscience. 8 (11): 844–58. doi:10.1038/nrn2234. PMID 17948030. S2CID 38811195.
  136. ^ Witten IB, Lin SC, Brodsky M, Prakash R, Diester I, Anikeeva P, et al. (December 2010). "Cholinergic interneurons control local circuit activity and cocaine conditioning". Science. 330 (6011): 1677–81. Bibcode:2010Sci...330.1677W. doi:10.1126/science.1193771. PMC 3142356. PMID 21164015.
  137. ^ Jump up to:a b Nestler EJ, Barrot M, Self DW (September 2001). "DeltaFosB: a sustained molecular switch for addiction". Proc. Natl. Acad. Sci. U.S.A. 98 (20): 11042–46. Bibcode:2001PNAS...9811042N. doi:10.1073/pnas.191352698. PMC 58680. PMID 11572966. Although the ΔFosB signal is relatively long-lived, it is not permanent. ΔFosB degrades gradually and can no longer be detected in [the] brain after 1–2 months of drug withdrawal ... Indeed, ΔFosB is the longest-lived adaptation known to occur in [the] adult brain, not only in response to drugs of abuse, but to any other perturbation (that doesn't involve lesions) as well.
  138. ^ Jump up to:a b Jones S, Bonci A (2005). "Synaptic plasticity and drug addiction". Current Opinion in Pharmacology. 5 (1): 20–25. doi:10.1016/j.coph.2004.08.011. PMID 15661621.
  139. ^ Jump up to:a b Eisch AJ, Harburg GC (2006). "Opiates, psychostimulants, and adult hippocampal neurogenesis: Insights for addiction and stem cell biology". Hippocampus. 16 (3): 271–86. doi:10.1002/hipo.20161. PMID 16411230. S2CID 23667629.
  140. ^ Rang HP (2003). Pharmacology. Edinburgh: Churchill Livingstone. p. 596. ISBN 978-0-443-07145-4.
  141. ^ Kourrich S, Rothwell PE, Klug JR, Thomas MJ (2007). "Cocaine experience controls bidirectional synaptic plasticity in the nucleus accumbens". J. Neurosci. 27 (30): 7921–28. doi:10.1523/JNEUROSCI.1859-07.2007. PMC 6672735. PMID 17652583.
  142. ^ Jump up to:a b Kalivas PW, Volkow ND (August 2005). "The neural basis of addiction: a pathology of motivation and choice". The American Journal of Psychiatry. 162 (8): 1403–13. doi:10.1176/appi.ajp.162.8.1403. PMID 16055761.
  143. ^ Jump up to:a b Floresco SB, Ghods-Sharifi S (February 2007). "Amygdala-prefrontal cortical circuitry regulates effort-based decision making". Cerebral Cortex. 17 (2): 251–60. CiteSeerX 10.1.1.335.4681. doi:10.1093/cercor/bhj143. PMID 16495432.
  144. ^ Perry CJ, Zbukvic I, Kim JH, Lawrence AJ (October 2014). "Role of cues and contexts on drug-seeking behaviour". British Journal of Pharmacology. 171 (20): 4636–72. doi:10.1111/bph.12735. PMC 4209936. PMID 24749941.
  145. ^ Jump up to:a b c Volkow ND, Fowler JS, Wang GJ, Swanson JM, Telang F (2007). "Dopamine in drug abuse and addiction: results of imaging studies and treatment implications". Arch. Neurol. 64 (11): 1575–79. doi:10.1001/archneur.64.11.1575. PMID 17998440.
  146. ^ "Drugs, Brains, and Behavior: The Science of Addiction". National Institute on Drug Abuse.
  147. ^ "Understanding Drug Abuse and Addiction". National Institute on Drug Abuse. November 2012. Archived from the original on 16 August 2011. Retrieved 12 February 2015.
  148. ^ Jump up to:a b c Nestler EJ (October 2008). "Review. Transcriptional mechanisms of addiction: role of DeltaFosB". Philosophical Transactions of the Royal Society of London. Series B, Biological Sciences. 363 (1507): 3245–55. doi:10.1098/rstb.2008.0067. PMC 2607320. PMID 18640924. 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
  149. ^ Jump up to:a b c d e f Berridge KC (April 2012). "From prediction error to incentive salience: mesolimbic computation of reward motivation". Eur. J. Neurosci. 35 (7): 1124–43. doi:10.1111/j.1460-9568.2012.07990.x. PMC 3325516. PMID 22487042. 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.
  150. ^ Jump up to:a b Malenka RC, Nestler EJ, Hyman SE (2009). Sydor A, Brown RY (eds.). Molecular Neuropharmacology: A Foundation for Clinical Neuroscience (second ed.). New York: McGraw-Hill Medical. pp. 147–48, 366–67, 375–76. ISBN 978-0-07-148127-4. 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.
  151. ^ Jump up to:a b c d Edwards S (2016). "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. Vol. 223. pp. 63–76. doi:10.1016/bs.pbr.2015.07.005. ISBN 978-0-444-63545-7. PMID 26806771. 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).
  152. ^ Jump up to:a b Berridge KC, Kringelbach ML (May 2015). "Pleasure systems in the brain". Neuron. 86 (3): 646–664. doi:10.1016/j.neuron.2015.02.018. PMC 4425246. PMID 25950633.
  153. ^ Jump up to:a b c d e f g Walker DM, Cates HM, Heller EA, Nestler EJ (February 2015). "Regulation of chromatin states by drugs of abuse". Curr. Opin. Neurobiol. 30: 112–21. doi:10.1016/j.conb.2014.11.002. PMC 4293340. PMID 25486626. Studies investigating general HDAC inhibition on behavioral outcomes have produced varying results but it seems that the effects are specific to the timing of exposure (either before, during or after exposure to drugs of abuse) as well as the length of exposure
  154. ^ Petry NM, Rehbein F, Gentile DA, Lemmens JS, Rumpf HJ, Mößle T, et al. (September 2014). "An international consensus for assessing internet gaming disorder using the new DSM-5 approach". Addiction. 109 (9): 1399–406. doi:10.1111/add.12457. PMID 24456155.
  155. ^ Torres G, Horowitz JM (1999). "Drugs of abuse and brain gene expression". Psychosom Med. 61 (5): 630–50. CiteSeerX 10.1.1.326.4903. doi:10.1097/00006842-199909000-00007. PMID 10511013.
  156. ^ Malenka RC, Nestler EJ, Hyman SE, Holtzman DM (2015). "Chapter 16: Reinforcement and Addictive Disorders". Molecular Neuropharmacology: A Foundation for Clinical Neuroscience (3rd ed.). New York: McGraw-Hill Medical. ISBN 978-0-07-182770-6. 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.
  157. ^ Jump up to:a b "International Classification of Diseases 11th revision – ICD-11. Disorders due to substance use". World Health Organization. Geneva. 2023. Retrieved 24 March 2023.
  158. ^ Jump up to:a b "Drug abuse liability". Cambridge Cognition. Retrieved 9 March 2021.
  159. ^ National Institute on Drug Abuse (20 August 2020). "Commonly Used Drugs Charts". National Institute on Drug Abuse. Retrieved 9 March 2021.
  160. ^ Harwood HJ, Myers TG, Addiction NR (23 July 2004). Vaccines and Immunotherapies to Control Addiction in Minors: The Legal Framework. National Academies Press (US) – via National Center for Biotechnology Information.
  161. ^ "'Heavy' heroin vaccine provides hope for addiction treatment". Scripps Research. 30 July 2020.
  162. ^ "Experimental Opioid Vaccine Being Tested at Columbia". Columbia University Irving Medical Center. 1 July 2021.
  163. ^ Furfaro H (5 January 2022). "To fight opioid crisis, UW researchers take new shot at developing vaccine against addictive drugs". The Seattle Times.
  164. ^ "A Vaccine Against Addiction". Addiction Center. 12 January 2022.
  165. ^ American Addiction Centers Editorial Staff (4 January 2022) [December 29, 2016]. "Why Don't We Have Addiction Vaccines?". DrugAbuse.com.
  166. ^ Barbara Shine (October 2000). "Nicotine Vaccine Moves Toward Clinical Trials". National Institute on Drug Abuse. Archived from the original on 10 August 2006. Retrieved 19 September 2006.
  167. ^ "Nabi Biopharmaceuticals Website".
  168. ^ Hatsukami DK, Rennard S, Jorenby D, Fiore M, Koopmeiners J, de Vos A, et al. (2005). "Safety and immunogenicity of a nicotine conjugate vaccine in current smokers". Clinical Pharmacology & Therapeutics. 78 (5): 456–467. doi:10.1016/j.clpt.2005.08.007. PMID 16321612. S2CID 1218556.
  169. ^ Martell BA, Mitchell E, Poling J, Gonsai K, Kosten TR (July 2005). "Vaccine pharmacotherapy for the treatment of cocaine dependence". Biol. Psychiatry. 58 (2): 158–64. doi:10.1016/j.biopsych.2005.04.032. PMID 16038686. S2CID 22415520.
  170. ^ "Cocaine vaccine 'stops addiction'". BBC News. 14 June 2004. Retrieved 7 October 2009.
  171. ^ "CelticPharma: TA-NIC Nicotine Dependence". Archived from the original on 6 December 2009. Retrieved 27 October 2009.
  172. ^ KIRO 7 News Staff (19 September 2023). "UW researcher explains new vaccine in the works to prevent opioid overdoses". KIRO 7.
  173. ^ Taylor SB, Lewis CR, Olive MF (February 2013). "The neurocircuitry of illicit psychostimulant addiction: acute and chronic effects in humans". Subst. Abuse Rehabil. 4: 29–43. doi:10.2147/SAR.S39684. PMC 3931688. PMID 24648786. 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.
  174. ^ Scott CG (July 2000). "Ethical Issues in Addiction Counseling". Rehabilitation Counseling Bulletin. 43 (4): 209–214. doi:10.1177/003435520004300405. ISSN 0034-3552. PMID 15714702. S2CID 28556555.
  175. ^ Magnusson D (1998). Theoretical Models of Human development. New York: John Wiley & sons. pp. 685–759.
  176. ^ Jump up to:a b Schlosser AV (September 2018). "'They Medicated Me Out': Social Flesh and Embodied Citizenship in Addiction Treatment". Contemporary Drug Problems. 45 (3): 188–207. doi:10.1177/0091450918781590. S2CID 149842084.
  177. ^ Wolfe D, Saucier R (1 August 2021). "Reprint of: Biotechnologies and the future of opioid addiction treatments". International Journal of Drug Policy. 94: 103273. doi:10.1016/j.drugpo.2021.103273. ISSN 0955-3959. PMID 34391533. S2CID 237093884.
  178. ^ Wolfe D, Saucier R (February 2021). "Biotechnologies and the future of opioid addiction treatments". The International Journal on Drug Policy. 88: 103041. doi:10.1016/j.drugpo.2020.103041. PMID 33246267. S2CID 227191111.
  179. ^ Walter M, Dürsteler KM, Petitjean SA, Wiesbeck GA, Euler S, Sollberger D, et al. (April 2015). "[Psychosocial Treatment of Addictive Disorders—An Overview of Psychotherapeutic Options and their Efficacy]" [Psychosocial Treatment of Addictive Disorders – An Overview of Psychotherapeutic Options and their Efficacy]. Fortschritte der Neurologie-Psychiatrie (in German). 83 (4): 201–210. doi:10.1055/s-0034-1399338. PMID 25893493.
  180. ^ Carroll ME, Smethells JR (February 2016). "Sex Differences in Behavioral Dyscontrol: Role in Drug Addiction and Novel Treatments". Front. Psychiatry. 6: 175. doi:10.3389/fpsyt.2015.00175. PMC 4745113. PMID 26903885. Environmental Enrichment ...
    In humans, non-drug rewards delivered in a contingency management (CM) format successfully reduced drug dependence ... In general, CM programs promote drug abstinence through a combination of positive reinforcement for drug-free urine samples. For instance, voucher-based reinforcement therapy in which medication compliance, therapy session attendance, and negative drug screenings reinforced with vouchers to local business (e.g., movie theater, restaurants, etc.) directly reinforces drug abstinence, provides competing reinforcers, enriches the environment, and it is a robust treatment across a broad range of abused drugs (189). ...
    Physical Exercise
    There is accelerating evidence that physical exercise is a useful treatment for preventing and reducing drug addiction ... In some individuals, exercise has its own rewarding effects, and a behavioral economic interaction may occur, such that physical and social rewards of exercise can substitute for the rewarding effects of drug abuse. ... The value of this form of treatment for drug addiction in laboratory animals and humans is that exercise, if it can substitute for the rewarding effects of drugs, could be self-maintained over an extended period of time. Work to date in [laboratory animals and humans] regarding exercise as a treatment for drug addiction supports this hypothesis. ... However, a RTC study was recently reported by Rawson et al. (226), whereby they used 8 weeks of exercise as a post-residential treatment for METH addiction, showed a significant reduction in use (confirmed by urine screens) in participants who had been using meth 18 days or less a month. ... Animal and human research on physical exercise as a treatment for stimulant addiction indicates that this is one of the most promising treatments on the horizon. [(emphasis added)]
  181. ^ Jump up to:a b c d Lynch WJ, Peterson AB, Sanchez V, Abel J, Smith MA (September 2013). "Exercise as a novel treatment for drug addiction: a neurobiological and stage-dependent hypothesis". Neurosci Biobehav Rev. 37 (8): 1622–44. doi:10.1016/j.neubiorev.2013.06.011. PMC 3788047. PMID 23806439. [exercise] efficacy may be related to its ability to normalize glutamatergic and dopaminergic signaling and reverse drug-induced changes in chromatin via epigenetic interactions with brain-derived neurotrophic factor (BDNF) in the reward pathway. ... these data show that exercise can affect dopaminergic signaling at many different levels, which may underlie its ability to modify vulnerability during drug use initiation. Exercise also produces neuroadaptations that may influence an individual's vulnerability to initiate drug use. Consistent with this idea, chronic moderate levels of forced treadmill running blocks not only subsequent methamphetamine-induced conditioned place preference, but also stimulant-induced increases in dopamine release in the NAc (Chen et al., 2008) and striatum (Marques et al., 2008). ... [These] findings indicate the efficacy of exercise at reducing drug intake in drug-dependent individuals ... wheel running [reduces] methamphetamine self-administration under extended access conditions (Engelmann et al., 2013) ... These findings suggest that exercise may "magnitude"-dependently prevent the development of an addicted phenotype possibly by blocking/reversing behavioral and neuro-adaptive changes that develop during and following extended access to the drug. ... Exercise has been proposed as a treatment for drug addiction that may reduce drug craving and risk of relapse. Although few clinical studies have investigated the efficacy of exercise for preventing relapse, the few studies that have been conducted generally report a reduction in drug craving and better treatment outcomes (see Table 4). ... Taken together, these data suggest that the potential benefits of exercise during relapse, particularly for relapse to psychostimulants, may be mediated via chromatin remodeling and possibly lead to greater treatment outcomes.
  182. ^ Jump up to:a b Linke SE, Ussher M (2015). "Exercise-based treatments for substance use disorders: evidence, theory, and practicality". Am J Drug Alcohol Abuse. 41 (1): 7–15. doi:10.3109/00952990.2014.976708. PMC 4831948. PMID 25397661. The limited research conducted suggests that exercise may be an effective adjunctive treatment for SUDs. In contrast to the scarce intervention trials to date, a relative abundance of literature on the theoretical and practical reasons supporting the investigation of this topic has been published. ... numerous theoretical and practical reasons support exercise-based treatments for SUDs, including psychological, behavioral, neurobiological, nearly universal safety profile, and overall positive health effects.
  183. ^ Jump up to:a b Zhou Y, Zhao M, Zhou C, Li R (July 2015). "Sex differences in drug addiction and response to exercise intervention: From human to animal studies". Front. Neuroendocrinol. 40: 24–41. doi:10.1016/j.yfrne.2015.07.001. PMC 4712120. PMID 26182835. Collectively, these findings demonstrate that exercise may serve as a substitute or competition for drug abuse by changing ΔFosB or cFos immunoreactivity in the reward system to protect against later or previous drug use. ... As briefly reviewed above, a large number of human and rodent studies clearly show that there are sex differences in drug addiction and exercise. The sex differences are also found in the effectiveness of exercise on drug addiction prevention and treatment, as well as underlying neurobiological mechanisms. The postulate that exercise serves as an ideal intervention for drug addiction has been widely recognized and used in human and animal rehabilitation. ... In particular, more studies on the neurobiological mechanism of exercise and its roles in preventing and treating drug addiction are needed.
  184. ^ Sachdeva A, Choudhary M, Chandra M (September 2015). "Alcohol Withdrawal Syndrome: Benzodiazepines and Beyond". Journal of Clinical and Diagnostic Research. 9 (9): VE01–VE07. doi:10.7860/JCDR/2015/13407.6538. PMC 4606320. PMID 26500991.
  185. ^ Soyka M, Roesner S (December 2006). "New pharmacological approaches for the treatment of alcoholism". Expert Opinion on Pharmacotherapy. 7 (17): 2341–53. doi:10.1517/14656566.7.17.2341. PMID 17109610. S2CID 2587029.
  186. ^ Pettinati HM, Rabinowitz AR (October 2006). "Choosing the right medication for the treatment of alcoholism". Current Psychiatry Reports. 8 (5): 383–88. doi:10.1007/s11920-006-0040-0. PMID 16968619. S2CID 39826013.
  187. ^ Bouza C, Angeles M, Magro A, Muñoz A, Amate JM (July 2004). "Efficacy and safety of naltrexone and acamprosate in the treatment of alcohol dependence: a systematic review". Addiction. 99 (7): 811–28. doi:10.1111/j.1360-0443.2004.00763.x. PMID 15200577.
  188. ^ Williams SH (November 2005). "Medications for treating alcohol dependence". American Family Physician. 72 (9): 1775–80. PMID 16300039.
  189. ^ Rösner S, Hackl-Herrwerth A, Leucht S, Vecchi S, Srisurapanont M, Soyka M (December 2010). Srisurapanont M (ed.). "Opioid antagonists for alcohol dependence". The Cochrane Database of Systematic Reviews (12): CD001867. doi:10.1002/14651858.CD001867.pub2. PMID 21154349.
  190. ^ Rosenberg KP, Feder LC (2014), "An Introduction to Behavioral Addictions", Behavioral Addictions, Elsevier, pp. 1–17, doi:10.1016/b978-0-12-407724-9.00001-x, ISBN 9780124077249, retrieved 3 November 2023
  191. ^ Bannink FP (26 June 2013). "Positive CBT: From Reducing Distress to Building Success". Journal of Contemporary Psychotherapy. 44 (1): 1–8. doi:10.1007/s10879-013-9239-7. ISSN 0022-0116. S2CID 24029889.
  192. ^ Fratta W, Fattore L (August 2013). "Molecular mechanisms of cannabinoid addiction". Curr. Opin. Neurobiol. 23 (4): 487–92. doi:10.1016/j.conb.2013.02.002. PMID 23490548. S2CID 40849553. 14. Nguyen PT, Schmid CL, Raehal KM, Selley DE, Bohn LM, Sim-Selley LJ: b-Arrestin2 regulates cannabinoid CB1 receptor signaling and adaptation in a central nervous system region dependent manner. Biol Psychiatry 2012, 71:714–24.
    A pioneering study revealing both positive and negative modulatory effects of beta-arrestin2 on THC tolerance. By demonstrating that tolerance to antinociception is reduced whereas tolerance to catalepsy is enhanced in beta-arrestin2 knockout mice, authors suggest that development of cannabinoid agonists that minimize interactions between CB1Rs and beta-arrestin2 might produce improved cannabinoid analgesics with reduced motor suppression, and be therapeutically beneficial.
  193. ^ Sabioni P, Le Foll B (April 2019). "Psychosocial and Pharmacological Interventions for the Treatment of Cannabis Use Disorder". Focus. 17 (2): 163–168. doi:10.1176/appi.focus.17202. PMC 6527000. PMID 32021586.
  194. ^ Jump up to:a b Garwood CL, Potts LA (August 2007). "Emerging pharmacotherapies for smoking cessation". American Journal of Health-System Pharmacy. 64 (16): 1693–1698. doi:10.2146/ajhp060427. PMID 17687057.
  195. ^ Jump up to:a b Crooks PA, Bardo MT, Dwoskin LP (2014). "Nicotinic Receptor Antagonists as Treatments for Nicotine Abuse". Emerging Targets & Therapeutics in the Treatment of Psychostimulant Abuse. Advances in Pharmacology. Vol. 69. pp. 513–551. doi:10.1016/B978-0-12-420118-7.00013-5. ISBN 978-0-12-420118-7. PMC 4110698. PMID 24484986.
  196. ^ Jump up to:a b Tutka P, Vinnikov D, Courtney RJ, Benowitz NL (November 2019). "Cytisine for nicotine addiction treatment: a review of pharmacology, therapeutics and an update of clinical trial evidence for smoking cessation". Addiction. 114 (11): 1951–1969. doi:10.1111/add.14721. PMID 31240783. S2CID 195660208.
  197. ^ Johnson RE, Chutuape MA, Strain EC, Walsh SL, Stitzer ML, Bigelow GE (November 2000). "A comparison of levomethadyl acetate, buprenorphine, and methadone for opioid dependence". The New England Journal of Medicine. 343 (18): 1290–7. doi:10.1056/NEJM200011023431802. PMID 11058673.
  198. ^ Connock M, Juarez-Garcia A, Jowett S, Frew E, Liu Z, Taylor RJ, et al. (March 2007). "Methadone and buprenorphine for the management of opioid dependence: a systematic review and economic evaluation". Health Technology Assessment. 11 (9): 1–171, iii–iv. doi:10.3310/hta11090. PMID 17313907.
  199. ^ Robertson JR, Raab GM, Bruce M, McKenzie JS, Storkey HR, Salter A (December 2006). "Addressing the efficacy of dihydrocodeine versus methadone as an alternative maintenance treatment for opiate dependence: A randomized controlled trial". Addiction. 101 (12): 1752–9. doi:10.1111/j.1360-0443.2006.01603.x. PMID 17156174.
  200. ^ Qin BY (1998). "Advances in dihydroetorphine: From analgesia to detoxification". Drug Development Research. 39 (2): 131–34. doi:10.1002/(SICI)1098-2299(199610)39:2<131::AID-DDR3>3.0.CO;2-Q. S2CID 201878290.
  201. ^ Metrebian N, Shanahan W, Wells B, Stimson GV (June 1998). "Feasibility of prescribing injectable heroin and methadone to opiate-dependent drug users: associated health gains and harm reductions". The Medical Journal of Australia. 168 (12): 596–600. doi:10.5694/j.1326-5377.1998.tb141444.x. PMID 9673620. S2CID 43302721.
  202. ^ Metrebian N, Mott J, Carnwath Z, Carnwath T, Stimson GV, Sell L (2007). "Pathways into receiving a prescription for diamorphine (heroin) for the treatment of opiate dependence in the United kingdom". European Addiction Research. 13 (3): 144–7. doi:10.1159/000101550. PMID 17570910. S2CID 7397513.
  203. ^ Kenna GA, Nielsen DM, Mello P, Schiesl A, Swift RM (2007). "Pharmacotherapy of dual substance abuse and dependence". CNS Drugs. 21 (3): 213–37. doi:10.2165/00023210-200721030-00003. PMID 17338593. S2CID 25979050.
  204. ^ Strang J, McCambridge J, Best D, Beswick T, Bearn J, Rees S, et al. (May 2003). "Loss of tolerance and overdose mortality after inpatient opiate detoxification: follow up study". BMJ (Clinical Research Ed.). 326 (7396): 959–60. doi:10.1136/bmj.326.7396.959. PMC 153851. PMID 12727768.
  205. ^ Chan B, Freeman M, Kondo K, Ayers C, Montgomery J, Paynter R, et al. (December 2019). "Pharmacotherapy for methamphetamine/amphetamine use disorder-a systematic review and meta-analysis". Addiction. 114 (12): 2122–2136. doi:10.1111/add.14755. PMID 31328345. S2CID 198136436.
  206. ^ Liu JF, Li JX (December 2018). "Drug addiction: a curable mental disorder?". Acta Pharmacologica Sinica. 39 (12): 1823–1829. doi:10.1038/s41401-018-0180-x. PMC 6289334. PMID 30382181.
  207. ^ Scendoni R, Bury E, Ribeiro IA, Cameriere R, Cingolani M (November 2022). "Vaccines as a preventive tool for substance use disorder: A systematic review including a meta-analysis on nicotine vaccines' immunogenicity". Human Vaccines & Immunotherapeutics. 18 (6). doi:10.1080/21645515.2022.2140552. PMC 9746524. PMID 36351881.
  208. ^ Jump up to:a b c Zalewska-Kaszubska J (November 2015). "Is immunotherapy an opportunity for effective treatment of drug addiction?". Vaccine. 33 (48): 6545–51. doi:10.1016/j.vaccine.2015.09.079. PMID 26432911.
  209. ^ Laudenbach M, Baruffaldi F, Vervacke JS, Distefano MD, Titcombe PJ, Mueller DL, et al. (June 2015). "The frequency of naive and early-activated hapten-specific B cell subsets dictates the efficacy of a therapeutic vaccine against prescription opioid abuse". J. Immunol. 194 (12): 5926–36. doi:10.4049/jimmunol.1500385. PMC 4458396. PMID 25972483. Translation of therapeutic vaccines for addiction, cancer, or other chronic noncommunicable diseases has been slow because only a small subset of immunized subjects achieved effective Ab levels.
  210. ^ Painter A. (2019) "Researchers working to develop vaccines to fight opioid addiction" Vtnews.vt.edu
  211. ^ Jump up to:a b c d Cao DN, Shi JJ, Hao W, Wu N, Li J (March 2016). "Advances and challenges in pharmacotherapeutics for amphetamine-type stimulants addiction". Eur. J. Pharmacol. 780: 129–35. doi:10.1016/j.ejphar.2016.03.040. PMID 27018393.
  212. ^ Jump up to:a b Moeller SJ, London ED, Northoff G (February 2016). "Neuroimaging markers of glutamatergic and GABAergic systems in drug addiction: Relationships to resting-state functional connectivity". Neurosci Biobehav Rev. 61: 35–52. doi:10.1016/j.neubiorev.2015.11.010. PMC 4731270. PMID 26657968.
  213. ^ Agabio R, Colombo G (April 2015). "[GABAB receptor as therapeutic target for drug addiction: from baclofen to positive allosteric modulators]". Psychiatr. Pol. (in Polish). 49 (2): 215–23. doi:10.12740/PP/33911. hdl:11584/102912. PMID 26093587.
  214. ^ Filip M, Frankowska M, Sadakierska-Chudy A, Suder A, Szumiec L, Mierzejewski P, et al. (January 2015). "GABAB receptors as a therapeutic strategy in substance use disorders: focus on positive allosteric modulators". Neuropharmacology. 88: 36–47. doi:10.1016/j.neuropharm.2014.06.016. PMID 24971600. S2CID 207229988.
  215. ^ Jump up to:a b McCowan TJ, Dhasarathy A, Carvelli L (February 2015). "The Epigenetic Mechanisms of Amphetamine". J. Addict. Prev. 2015 (Suppl 1). PMC 4955852. PMID 27453897. Epigenetic modifications caused by addictive drugs play an important role in neuronal plasticity and in drug-induced behavioral responses. Although few studies have investigated the effects of AMPH on gene regulation (Table 1), current data suggest that AMPH acts at multiple levels to alter histone/DNA interaction and to recruit transcription factors which ultimately cause repression of some genes and activation of other genes. Importantly, some studies have also correlated the epigenetic regulation induced by AMPH with the behavioral outcomes caused by this drug, suggesting therefore that epigenetics remodeling underlies the behavioral changes induced by AMPH. If this proves to be true, the use of specific drugs that inhibit histone acetylation, methylation or DNA methylation might be an important therapeutic alternative to prevent and/or reverse AMPH addiction and mitigate the side effects generate by AMPH when used to treat ADHD.
  216. ^ Jump up to:a b Primary references involving sodium butyrate:
     • Kennedy PJ, Feng J, Robison AJ, Maze I, Badimon A, Mouzon E, et al. (April 2013). "Class I HDAC inhibition blocks cocaine-induced plasticity by targeted changes in histone methylation". Nat. Neurosci. 16 (4): 434–40. doi:10.1038/nn.3354. PMC 3609040. PMID 23475113. While acute HDAC inhibition enhances the behavioral effects of cocaine or amphetamine1,3,4,13,14, studies suggest that more chronic regimens block psychostimulant-induced plasticity3,5,11,12. ... The effects of pharmacological inhibition of HDACs on psychostimulant-induced plasticity appear to depend on the timecourse of HDAC inhibition. Studies employing co-administration procedures in which inhibitors are given acutely, just prior to psychostimulant administration, report heightened behavioral responses to the drug1,3,4,13,14. In contrast, experimental paradigms like the one employed here, in which HDAC inhibitors are administered more chronically, for several days prior to psychostimulant exposure, show inhibited expression3 or decreased acquisition of behavioral adaptations to drug5,11,12. The clustering of seemingly discrepant results based on experimental methodologies is interesting in light of our present findings. Both HDAC inhibitors and psychostimulants increase global levels of histone acetylation in NAc. Thus, when co-administered acutely, these drugs may have synergistic effects, leading to heightened transcriptional activation of psychostimulant-regulated target genes. In contrast, when a psychostimulant is given in the context of prolonged, HDAC inhibitor-induced hyperacetylation, homeostatic processes may direct AcH3 binding to the promoters of genes (e.g., G9a) responsible for inducing chromatin condensation and gene repression (e.g., via H3K9me2) to dampen already heightened transcriptional activation. Our present findings thus demonstrate clear cross talk among histone PTMs and suggest that decreased behavioral sensitivity to psychostimulants following prolonged HDAC inhibition might be mediated through decreased activity of HDAC1 at H3K9 KMT promoters and subsequent increases in H3K9me2 and gene repression.
     • Simon-O'Brien E, Alaux-Cantin S, Warnault V, Buttolo R, Naassila M, Vilpoux C (July 2015). "The histone deacetylase inhibitor sodium butyrate decreases excessive ethanol intake in dependent animals". Addict Biol. 20 (4): 676–89. doi:10.1111/adb.12161. PMID 25041570. S2CID 28667144. Altogether, our results clearly demonstrated the efficacy of NaB in preventing excessive ethanol intake and relapse and support the hypothesis that HDACi may have a potential use in alcohol addiction treatment.
     • Castino MR, Cornish JL, Clemens KJ (April 2015). "Inhibition of histone deacetylases facilitates extinction and attenuates reinstatement of nicotine self-administration in rats". PLOS ONE. 10 (4): e0124796. Bibcode:2015PLoSO..1024796C. doi:10.1371/journal.pone.0124796. PMC 4399837. PMID 25880762. treatment with NaB significantly attenuated nicotine and nicotine + cue reinstatement when administered immediately ... These results provide the first demonstration that HDAC inhibition facilitates the extinction of responding for an intravenously self-administered drug of abuse and further highlight the potential of HDAC inhibitors in the treatment of drug addiction.
  217. ^ Kyzar EJ, Pandey SC (August 2015). "Molecular mechanisms of synaptic remodeling in alcoholism". Neurosci. Lett. 601: 11–19. doi:10.1016/j.neulet.2015.01.051. PMC 4506731. PMID 25623036. Increased HDAC2 expression decreases the expression of genes important for the maintenance of dendritic spine density such as BDNF, Arc, and NPY, leading to increased anxiety and alcohol-seeking behavior. Decreasing HDAC2 reverses both the molecular and behavioral consequences of alcohol addiction, thus implicating this enzyme as a potential treatment target (Fig. 3). HDAC2 is also crucial for the induction and maintenance of structural synaptic plasticity in other neurological domains such as memory formation [115]. Taken together, these findings underscore the potential usefulness of HDAC inhibition in treating alcohol use disorders ... Given the ability of HDAC inhibitors to potently modulate the synaptic plasticity of learning and memory [118], these drugs hold potential as treatment for substance abuse-related disorders. ... Our lab and others have published extensively on the ability of HDAC inhibitors to reverse the gene expression deficits caused by multiple models of alcoholism and alcohol abuse, the results of which were discussed above [25,112,113]. This data supports further examination of histone modifying agents as potential therapeutic drugs in the treatment of alcohol addiction ... Future studies should continue to elucidate the specific epigenetic mechanisms underlying compulsive alcohol use and alcoholism, as this is likely to provide new molecular targets for clinical intervention.
  218. ^ Kheirabadi GR, Ghavami M, Maracy MR, Salehi M, Sharbafchi MR (2016). "Effect of add-on valproate on craving in methamphetamine depended patients: A randomized trial". Advanced Biomedical Research. 5: 149. doi:10.4103/2277-9175.187404. PMC 5025910. PMID 27656618.
  219. ^ "Gene Therapy For Addiction: Flooding Brain With 'Pleasure Chemical' Receptors Works On Cocaine, As On Alcohol". Sciencedaily.
  220. ^ "Gene Transfer Therapy for Cocaine Addiction Passes Tests in Animals". National Institute on Drug Abuse. 14 January 2016. Archived from the original on 27 November 2020. Retrieved 25 June 2017.
  221. ^ Murthy V, Gao Y, Geng L, LeBrasseur NK, White TA, Parks RJ, et al. (2014). "Physiologic and metabolic safety of butyrylcholinesterase gene therapy in mice". Vaccine. 32 (33): 4155–62. doi:10.1016/j.vaccine.2014.05.067. PMC 4077905. PMID 24892251.
  222. ^ "Using Adeno-Associated Virus (AAV) Mediated Sustained Expression of an Anti-methamphetamine Antibody Fragment to Alter Methamphetamine Disposition in Mice" (PDF). Archived from the original (PDF) on 3 March 2018. Retrieved 25 June 2017.
  223. ^ "ATTC – Addiction Science Made Easy". www.attcnetwork.org. Archived from the original on 27 September 2018. Retrieved 25 June 2017.
  224. ^ Chen CC, Yin SJ (October 2008). "Alcohol abuse and related factors in Asia". International Review of Psychiatry. 20 (5): 425–433. doi:10.1080/09540260802344075. PMID 19012127. S2CID 24571763.
  225. ^ Mak KK, Lai CM, Watanabe H, Kim DI, Bahar N, Ramos M, et al. (November 2014). "Epidemiology of internet behaviors and addiction among adolescents in six Asian countries". Cyberpsychology, Behavior and Social Networking. 17 (11): 720–728. doi:10.1089/cyber.2014.0139. PMID 25405785.
  226. ^ Slade T, Johnston A, Teesson M, Whiteford H, Burgess P, Pirkis J, et al. (May 2009). "The Mental Health of Australians 2: Substance Use Disorders in Australia" (PDF). Department of Health and Ageing, Canberra.
  227. ^ Jump up to:a b Australian Institute of Health and Welfare (AIHW) (2020). National Drug Strategy Household Survey 2019 (Report). doi:10.25816/E42P-A447.
  228. ^ Peacock A, Leung J, Larney S, Colledge S, Hickman M, Rehm J, et al. (October 2018). "Global statistics on alcohol, tobacco and illicit drug use: 2017 status report". Addiction. 113 (10): 1905–1926. doi:10.1111/add.14234. hdl:11343/283940. PMID 29749059. S2CID 13674349.
  229. ^ Jump up to:a b c d Merikangas KR, McClair VL (June 2012). "Epidemiology of Substance Use Disorders". Hum. Genet. 131 (6): 779–89. doi:10.1007/s00439-012-1168-0. PMC 4408274. PMID 22543841.
  230. ^ Manubay JM, Muchow C, Sullivan MA (March 2011). "Prescription drug abuse: epidemiology, regulatory issues, chronic pain management with narcotic analgesics". Primary Care. 38 (1): 71–90. doi:10.1016/j.pop.2010.11.006. PMC 3328297. PMID 21356422.
  231. ^ Substance Abuse and Mental Health Services Administration (2022). Key substance use and mental health indicators in the United States: Results from the 2021 National Survey on Drug Use and Health (Report). Center for Behavioral Health Statistics and Quality, Substance Abuse and Mental Health Services Administration. Retrieved 24 March 2023.
  232. ^ Jump up to:a b c d e f "American Board of Medical Specialties recognizes the new subspecialty of addiction medicine" (PDF). American Board of Addiction Medicine. 14 March 2016. Archived from the original (PDF) on 21 March 2021. Retrieved 3 April 2016. 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.
  233. ^ Jump up to:a b c Volkow N (31 March 2016). "A Major Step Forward for Addiction Medicine". National Institute on Drug Abuse. National Institutes of Health. Archived from the original on 5 April 2016. Retrieved 3 April 2016. 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.'
  234. ^ Gramlich J (26 October 2017). "Nearly half of Americans have a family member or close friend who's been addicted to drugs". Pew Research Center. Retrieved 14 January 2018.
  235. ^ "We were addicted to their pill, but they were addicted to the money". The Washington Post. Retrieved 22 July 2019.
  236. ^ Hasin DS, Saha TD, Kerridge BT, Goldstein RB, Chou SP, Zhang H, et al. (December 2015). "Prevalence of Marijuana Use Disorders in the United States Between 2001–2002 and 2012–2013". JAMA Psychiatry. 72 (12): 1235–1242. doi:10.1001/jamapsychiatry.2015.1858. PMC 5037576. PMID 26502112.
  237. ^ Jump up to:a b c d "Mental and substance use disorders in Canada". Statistics Canada. Government of Canada. 18 September 2013. Retrieved 8 November 2022.
  238. ^ "Drug addiction (substance use disorder) – Symptoms and causes". Mayo Clinic. Retrieved 8 November 2022.
  239. ^ Jump up to:a b "Mental Health and Addictions System Performance in Ontario: 2021 Scorecard". www.ices.on.ca. Retrieved 8 November 2022.
  240. ^ World Drug Report 2012 (PDF). United Nations Office on Drugs and Crime. June 2012. ISBN 978-92-1-148267-6.
  241. ^ Pacurucu-Castillo SF, Ordóñez-Mancheno JM, Hernández-Cruz A, Alarcón RD (April 2019). "World opioid and substance use epidemic: a Latin American perspective". Psychiatric Research and Clinical Practice. 1 (1): 32–8. doi:10.1176/appi.prcp.20180009. PMC 9175731. PMID 36101564.
  242. ^ Crocq MA (December 2007). Thibaut F (ed.). "Historical and cultural aspects of man's relationship with addictive drugs". Dialogues in Clinical Neuroscience. 9 (4). Laboratoires Servier: 355–361. doi:10.31887/DCNS.2007.9.4/macrocq. OCLC 62869913. PMC 3202501. PMID 18286796. S2CID 12682928.
  243. ^ Jump up to:a b c Lemon R (2018). "Introduction: Addiction in (Early) Modernity". Addiction and Devotion in Early Modern England. Haney Foundation Series. Philadelphia: University of Pennsylvania Press. pp. 1–23. ISBN 978-0-8122-4996-5.
  244. ^ Jump up to:a b Rosenthal R, Faris S (February 2019). "The etymology and early history of 'addiction'". Addiction Research & Theory. 27 (5). Taylor & Francis: 437–449. doi:10.1080/16066359.2018.1543412. ISSN 1476-7392. S2CID 150418396.
  245. ^ Institute of Medicine (1996). Pathways of Addiction: Opportunities in Drug Abuse Research. Washington: National Academies Press.
  246. ^ Bettinardi-Angres K, Angres DH (July 2010). Alexander M (ed.). "Understanding the Disease of Addiction". Journal of Nursing Regulation. 1 (2). Elsevier on behalf of the National Council of State Boards of Nursing: 31–37. doi:10.1016/S2155-8256(15)30348-3. ISSN 2155-8256. S2CID 143289528.
  247. ^ "Alcohol". Online Etymology Dictionary.
  248. ^ Appel PW, Ellison AA, Jansky HK, Oldak R (2004). "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 Abuse. 30 (1): 129–153. doi:10.1081/ada-120029870. PMID 15083558. S2CID 20193011.
  249. ^ Megranahan K, Lynskey MT (February 2018). "Do creative arts therapies reduce substance misuse? A systematic review". The Arts in Psychotherapy. 57: 50–58. doi:10.1016/j.aip.2017.10.005. ISSN 0197-4556.
  250. ^ Moore RW, W (1 December 1983). "Art therapy with substance abusers: A review of the literature". The Arts in Psychotherapy. 10 (4): 251–260. doi:10.1016/0197-4556(83)90026-6. ISSN 0197-4556.
  251. ^ North American Drama Therapy Association (2016), Drama therapy with addictions populations
  252. ^ Waller D, Mahony J, eds. (9 December 1998). Treatment of Addiction: Current Issues for Arts Therapists. Routledge. doi:10.4324/9780203132395. ISBN 978-0-203-13239-5.
  253. ^ Kaufman GH (1 July 1981). "Art therapy with the addicted". Journal of Psychoactive Drugs. 13 (4). Taylor & Francis: 353–360. doi:10.1080/02791072.1981.10471892. PMID 7040619.
  254. ^ Waller D, Mahony J, eds. (9 December 1998). Treatment of Addiction: Current Issues for Arts Therapists. Routledge. doi:10.4324/9780203132395. ISBN 978-0-203-13239-5.
  255. ^ Jump up to:a b c d e f g Schmanke L (2015). "Art Therapy and Substance Abuse". The Wiley Handbook of Art Therapy. John Wiley & Sons, Ltd. pp. 361–374. doi:10.1002/9781118306543.ch35. ISBN 978-1-118-30654-3.
  256. ^ Jump up to:a b c Schmanke L (2019). "Art Therapy Applications and Substance Abuse". Art and Expressive Therapies within the Medical Model (1st ed.). Routledge. pp. 177–187. doi:10.4324/9780429400087-16. ISBN 978-0-367-02340-9. S2CID 208386296.
  257. ^ Chiang M, Reid-Varley WB, Fan X (May 2019). "Creative art therapy for mental illness". Psychiatry Research. 275: 129–136. doi:10.1016/j.psychres.2019.03.025. PMID 30901671. S2CID 78090920.
  258. ^ Dickson C (June 2007). "An evaluation study of art therapy provision in a residential Addiction Treatment Programme (ATP)". International Journal of Art Therapy. 12 (1): 17–27. doi:10.1080/17454830701265220. ISSN 1745-4832. S2CID 72987664.
  259. ^ Matto H, Corcoran J, Fassler, A (January 2003). "Integrating solution-focused and art therapies for substance abuse treatment: guidelines for practice". The Arts in Psychotherapy. 30 (5): 265–272. doi:10.1016/j.aip.2003.08.003. ISSN 0197-4556.
  260. ^ Jump up to:a b Megranahan K, Lynskey MT (February 2018). "Do creative arts therapies reduce substance misuse? A systematic review". The Arts in Psychotherapy. 57: 50–58. doi:10.1016/j.aip.2017.10.005. ISSN 0197-4556.
  261. ^ Jump up to:a b c Rockwell P, Dunham M (January 2006). "The Utility of the Formal Elements Art Therapy Scale in Assessment for Substance Use Disorder". Art Therapy. 23 (3): 104–111. doi:10.1080/07421656.2006.10129625. ISSN 0742-1656. S2CID 5541133.
  262. ^ Francis D, Kaiser D, Deaver SP (22 April 2011). "Representations of Attachment Security in the Bird's Nest Drawings of Clients with Substance Abuse Disorders". Art Therapy. 20 (3). Routledge: 125–137. doi:10.1080/07421656.2003.10129571. ISSN 0742-1656. S2CID 142341708. Retrieved 4 December 2022.
  263. ^ Ball SA, Legow NE (November 1996). "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. 22 (4). Taylor & Francis: 533–547. doi:10.3109/00952999609001679. PMID 8911591.
  264. ^ Jump up to:a b Holt ES, Kaiser DH (January 2001). "Indicators of Familial Alcoholism in Children's Kinetic Family Drawings". Art Therapy. 18 (2): 89–95. doi:10.1080/07421656.2001.10129751. ISSN 0742-1656. S2CID 141669979.
  265. ^ Ashford RD, Brown AM, Curtis B (August 2018). "Systemic barriers in substance use disorder treatment: A prospective qualitative study of professionals in the field". Drug and Alcohol Dependence. 189: 62–69. doi:10.1016/j.drugalcdep.2018.04.033. PMID 29883870. S2CID 47011510.
  266. ^ Barry CL, McGinty EE, Pescosolido BA, Goldman HH (October 2014). "Stigma, discrimination, treatment effectiveness, and policy: public views about drug addiction and mental illness". Psychiatric Services. 65 (10): 1269–1272. doi:10.1176/appi.ps.201400140. PMC 4285770. PMID 25270497.
  267. ^ Feldman N (2020), Philly Council bill to block supervised injection sites advances - WHYY, retrieved 14 December 2022
  268. ^ Drug Enforcement Administration (2018), Implementation of the Provision of the Comprehensive Addiction and Recovery Act of 2016 Relating to the Dispensing of Narcotic Drugs for Opioid Use Disorder, retrieved 14 December 2022
  269. ^ Jump up to:a b c Henningfield JE, Dowell ML, Santora PB (2010). Addiction and art. Baltimore: Johns Hopkins University Press. ISBN 978-1-4214-0023-5. OCLC 794700340.
  270. ^ Jump up to:a b Dingman DA, Zibalese-Crawford, M (April 2021). "Reducing Substance Use Related Stigma through Expressions of Artwork". Journal of Alcohol & Drug Education. 65 (1). American Alcohol & Drug Information Foundation: 29–39. ISSN 0090-1482.
  271. ^ Skelly J (2015). "Alternative Paths: Mapping Addiction in Contemporary Art by Landon Mackenzie, Rebecca Belmore, Manasie Akpaliapik, and Ron Noganosh". Journal of Canadian Studies. 49 (2). University of Toronto Press: 268–295, 356. doi:10.3138/jcs.49.2.268. ISSN 0021-9495. S2CID 148421461.
  272. ^ Jump up to:a b Paivinen H, Bade S (June 2008). "Voice: challenging the stigma of addiction; a nursing perspective". The International Journal on Drug Policy. 19 (3): 214–219. doi:10.1016/j.drugpo.2008.02.011. PMID 18439812.
  273. ^ Marini MM (2016). Narrative medicine : bridging the gap between evidence-based care and medical humanities. Cham. ISBN 978-3-319-22090-1. OCLC 922640395.
  274. ^ Jump up to:a b Flora, K. (July 2012). "Recovery From Substance Abuse: A Narrative Approach to Understanding the Motivation and Ambivalence About Change". Journal of Social Work Practice in the Addictions. 12 (3). Taylor & Francis Ltd: 302–315. doi:10.1080/1533256X.2012.702630. ISSN 1533-256X. S2CID 143901063.
  275. ^ Jump up to:a b Gardner PJ, Poole JM (October 2009). "One Story at a Time: Narrative Therapy, Older Adults, and Addictions". Journal of Applied Gerontology. 28 (5): 600–620. doi:10.1177/0733464808330822. ISSN 0733-4648. S2CID 71341761.
  276. ^ Jump up to:a b Morgan ML, Brosi WA, Brosi MW (10 December 2011). "Restorying Older Adults' Narratives About Self and Substance Abuse". American Journal of Family Therapy. 39 (5): 444–455. doi:10.1080/01926187.2011.560784. ISSN 0192-6187. S2CID 145136521.
  277. ^ Jump up to:a b c Rhodes T, Bivol S, Scutelniciuc O, Hunt N, Bernays S, Busza J (November 2011). "Narrating the social relations of initiating injecting drug use: Transitions in self and society". International Journal of Drug Policy. 22 (6). Elsevier B.V.: 445–454. doi:10.1016/j.drugpo.2011.07.012. ISSN 0955-3959. PMID 21903372.
  278. ^ Jump up to:a b c Weicker NP, Whaley S, Urquhart G, Park JN, Sherman SG, Owczarzak J (October 2021). ""I Know It Is Going to Ruin Their Life:" Fortune-Telling, Agency, and Harm Reduction in Narratives Concerning Injection Initiation Assistance". Substance Use & Misuse. 56 (12): 1860–1868. doi:10.1080/10826084.2021.1958854. ISSN 1082-6084. PMID 34348070. S2CID 236928168.
  279. ^ Rau BL (September 2014). "The Oxford Handbook of Evidence-Based Management, Rousseau DM 2012. 432 pages, hardcover. New York, NY: Oxford University Press". Academy of Management Learning & Education. 13 (3): 485–487. doi:10.5465/amle.2013.0309. ISSN 1537-260X.
  280. ^ Daley DC (December 2013). "Family and social aspects of substance use disorders and treatment". Journal of Food and Drug Analysis. 21 (4): S73–S76. doi:10.1016/j.jfda.2013.09.038. PMC 4158844. PMID 25214748.
  281. ^ Saad M, de Medeiros R, Mosini AC (October 2017). "Are We Ready for a True Biopsychosocial-Spiritual Model? The Many Meanings of "Spiritual"". Medicines. 4 (4): 79. doi:10.3390/medicines4040079. PMC 5750603. PMID 29088101.
  282. ^ Farmer P, Kleinman A, Kim J, Basilico M, eds. (31 December 2019). Reimagining Global Health: An Introduction. University of California Press. doi:10.1525/9780520954632. ISBN 978-0-520-95463-2. S2CID 168489288.
  283. ^ Weakland JH (October 1961). "The Essence of Anthropological Education". American Anthropologist. 63 (5): 1094–1097. doi:10.1525/aa.1961.63.5.02a00130. ISSN 0002-7294.
  284. ^ Bourgois P (23 December 2002). In Search of Respect: Selling Crack in El Barrio. Structural Analysis in the Social Sciences (2 ed.). Cambridge University Press. doi:10.1017/cbo9780511808562. ISBN 978-0-521-01711-4.
  285. ^ Jump up to:a b c d e f g h i j k l m n o p Singer M (October 2012). "Anthropology and addiction: an historical review". Addiction. 107 (10): 1747–1755. doi:10.1111/j.1360-0443.2012.03879.x. PMID 22962955.
  286. ^ Jump up to:a b c d Heath DB (September 1958). "Drinking patterns of the Bolivian Camba". Quarterly Journal of Studies on Alcohol. 19 (3): 491–508. doi:10.15288/qjsa.1958.19.491. PMID 13579177.
  287. ^ Heath DB (January 1995). "Changes in Drinking Patterns in Bolivian Cultures: A Cautionary Tale About Historical Approaches". Addiction Research. 2 (3): 307–318. doi:10.3109/16066359509005215. ISSN 1058-6989.
  288. ^ Burraway J (October 2020). "Addiction". In Stein F, Diemberger H, Stasch R, Robbins J, Sanchez A, Lazar S, Candea M (eds.). Open Encyclopedia of Anthropology. doi:10.29164/20addiction. S2CID 241689890.
  289. ^ Preble E, Casey JJ (January 1969). "Taking Care of Business—The Heroin User's Life on the Street". International Journal of the Addictions. 4 (1): 1–24. doi:10.3109/10826086909061998. ISSN 0020-773X.
  290. ^ Jump up to:a b Golub A, Johnson BD, Dunlap E (May 2005). "Subcultural evolution and illicit drug use". Addiction Research & Theory. 13 (3): 217–229. doi:10.1080/16066350500053497. PMC 3690817. PMID 23805068.
  291. ^ Falk, Richard; Kim, Samuel S. (2019-08-15). The War System: An Interdisciplinary Approach. Routledge. ISBN 978-1-000-23507-4
  292. ^ "Bandura, Albert: Social Learning Theory", Encyclopedia of Criminological Theory, 2455 Teller Road, Thousand Oaks California 91320 United States: SAGE Publications, Inc., 2010, retrieved 2023-11-09
  293. ^ Smith, Mark A. (2021-02-01). "Social Learning and Addiction". Behavioural Brain Research. 398: 112954. doi:10.1016/j.bbr.2020.112954 ISSN 0166-4328
  294. ^ Brinthaupt, Thomas M.; Lipka, Richard P. (1994-10-11). Changing the Self: Philosophies, Techniques, and Experiences. State University of New York Press. ISBN 978-0-7914-9754-8
  295. ^ Jump up to:a b Malenka RC, Nestler EJ, Hyman SE (2009). "Chapter 1: Basic Principles of Neuropharmacology". In Sydor A, Brown RY (eds.). Molecular Neuropharmacology: A Foundation for Clinical Neuroscience (2nd ed.). New York: McGraw-Hill Medical. p. 4. ISBN 978-0-07-148127-4. 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.
  296. ^ "Economic consequences of drug abuse" (PDF). International Narcotics Control Board Report: 2013 (PDF). United Nations – International Narcotics Control Board. 2013. ISBN 978-92-1-148274-4. Retrieved 28 September 2018.
  297. ^ "Overdose Death Rates". National Institute on Drug Abuse. 9 August 2018. Retrieved 17 September 2018.
  298. ^ "Overdose Deaths Accelerating During Covid-19". Centers For Disease Control Prevention. 18 December 2020. Retrieved 10 February 2021.

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