查看“︁苯丙胺”︁的源代码

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{{expand English|Amphetamine|fa=yes}}
{{Rough translation|en:Amphetamine}}
{{Medical}}
<!--{{about|{{le|左旋苯丙胺|levoamphetamine|左旋苯丙胺}}和{{le|右旋苯丙胺|dextroamphetamine}}的混合物}}-->
{{redirect|安非他命}}
{{about|中文通称“苯丙胺”的管制药物1-苯基丙-2-胺|ACD软件索引名（ACD/Index Name）为“苯丙胺”（Benzenepropanamine）的化合物3-苯基丙-1-胺（{{script|Latn|C₆H₅CH₂CH₂CH₂NH₂}}）|3-苯丙胺}}
{{redirect|苯异丙胺}}
{{For2|中樞神經興奮劑|[[中樞神經刺激劑]]、[[哌甲酯]]以及[[注意力不足過動症#藥物]]}}
{{NoteTA|G1=Chemistry|G2=Medicine|1=zh-cn:安非他明;zh-hk:安非他明;zh-tw:安非他命;}}
{{Infobox drug
| drug_name = 安非他命（Amfetamine） ({{abbr|药名|国际非专利药品名称}})
| IUPAC_name = <center>(RS)-1-phenylpropan-2-amine <br/>(''RS'')-1-苯基丙-2-胺</center>
| image = Racemic amphetamine 2.svg
| alt = An image of the amphetamine compound
| image2 = D-Amphetamine-3D-balls.png
| alt2 = A 3d image of the D-amphetamine compound
<!-- Clinical data -->
| pronounce   = {{IPAc-en|audio=En-us-amphetamine.ogg|æ|m|ˈ|f|ɛ|t|ə|m|iː|n}}
| Drugs.com = {{Drugs.com|parent|amphetamine}}
| pregnancy_US = C
| legal_AU = Schedule 8
| legal_CA =Schedule I
| legal_CA_comment =第一級管制藥品 
| legal_DE = Anlage III
| legal_DE_comment =第三級管制藥品 
| legal_NZ =Class B
| legal_NZ_comment =第二級管制藥品 
| legal_UK =Class B
| legal_UK_comment =第二級管制藥品 
| legal_US =Schedule II
| legal_US_comment =第二級管制藥品 
| legal_UN = p ii
| legal_UN_comment =第二級管制藥品 
| legal_CN =第一类精神药品
| dependency_liability = [[生理依賴]]: 無<br>[[心理依賴]]: 中等
| addiction_liability = 中等
| routes_of_administration= 醫用：[[口服给药]]、[[鼻腔給藥]]、[[靜脈注射]]{{r|Amph Uses}}<br>非醫療用（Recreational）： [[口服给药]]、[[鼻腔給藥]], {{le|吹入劑|Insufflation (medicine)}}、[[栓剂]]、[[靜脈注射]]

<!--Pharmacokinetic data-->
| bioavailability = {{nowrap|口服 75–100%}}{{r|Drugbank-dexamph}}
| protein_bound = 15–40%{{r|Drugbank-amph}}
| metabolism = Amphetamine only:<br>[[CYP2D6]],{{r|FDA Pharmacokinetics}}[[多巴胺β羟化酶|Dopamine β-hydroxylase]],{{r|Substituted amphetamines, FMO, and DBH|DBH amph primary|DBH 4-HA primary}}{{le|含黃素的單加氧酶|Flavin-containing monooxygenas}}{{r|Substituted amphetamines, FMO, and DBH|FMO|FMO3-Primary}}
| metabolites = {{nowrap|{{le|4-hydroxyamphetamine}}}}, {{nowrap|{{le|4-hydroxynorephedrine}}}}, [[4-羟基苯基丙酮]], [[苯甲酸]], [[馬尿酸]], [[苯丙醇胺]], [[苯基丙酮]]{{r|FDA Pharmacokinetics|Pubchem Kinetics|Metabolites}}
| onset =短效型（{{abbr|IR|Immediate release}} 立即釋放藥物）<br> 使用後（dosing）：30–60&nbsp；分鐘內<ref name="Medscape Adderall Pharmacology">{{Cite encyclopedia|title=amphetamine/dextroamphetamine|section=Pharmacology|section-url=http://reference.medscape.com/drug/adderall-amphetamine-%20%20dextroamphetamine-342997#10|website=Medscape|publisher=WebMD|accessdate=2016-01-21|quote=Onset of action: 30–60 min|archive-date=2021-08-27|archive-url=https://web.archive.org/web/20210827214245/https://reference.medscape.com/drug/adderall-mydayis-amphetamine-dextroamphetamine-342997#10|dead-url=no}}</ref><br>長效型 （{{abbr|XR|Extended release}} 緩緩釋放藥物）<br> 使用後（dosing）：1.5–2&nbsp；小時內<ref name="Millichap: onset, peak, and duration">{{cite book|author=Millichap JG|editor=Millichap JG|title=Attention Deficit Hyperactivity Disorder Handbook: A Physician's Guide to ADHD|year=2010|publisher=Springer|location=New York, USA|isbn=9781441913968|pages=112|edition=2nd|chapter=Chapter 9: Medications for ADHD|quote=<br>Table 9.2 Dextroamphetamine formulations of stimulant medication<br>Dexedrine [Peak:2–3&nbsp;h] [Duration:5–6&nbsp;h]&nbsp;...<br>Adderall [Peak:2–3&nbsp;h] [Duration:5–7&nbsp;h]<br>Dexedrine spansules [Peak:7–8&nbsp;h] [Duration:12&nbsp;h]&nbsp;...<br>Adderall XR [Peak:7–8&nbsp;h] [Duration:12&nbsp;h]<br>Vyvanse [Peak:3–4&nbsp;h] [Duration:12&nbsp;h]}}</ref><ref name="XR onset-duration2">{{cite journal|title=Onset of efficacy of long-acting psychostimulants in pediatric attention-deficit/hyperactivity disorder|date=September 2008|journal=Postgrad. Med.|issue=3|doi=10.3810/pgm.2008.09.1909|volume=120|pages=69–88|pmid=18824827|vauthors=Brams M, Mao AR, Doyle RL}}</ref><ref name="XR onset-duration">{{cite journal|title=Onset of efficacy of long-acting psychostimulants in pediatric attention-deficit/hyperactivity disorder|date=September 2008|journal=Postgrad. Med.|issue=3|doi=10.3810/pgm.2008.09.1909|volume=120|pages=69–88|pmid=18824827|vauthors=Brams M, Mao AR, Doyle RL}}</ref>
| elimination_half-life = {{abbr|D-amph|Dextroamphetamine}}：9–11&nbsp；小時{{r|FDA Pharmacokinetics|Adderall IR}}<br>{{nowrap|{{abbr|L-amph|Levoamphetamine}}：11–14&nbsp；小時{{r|FDA Pharmacokinetics|Adderall IR}}}}<br>視[[PH值]]而定：8–31&nbsp；小時{{r|pH-dependent half-lives}}
| duration_of_action = 短效型（{{abbr|IR|Immediate release}} 立即釋放藥物）<br>使用後（dosing）：3–7&nbsp;小時內{{r|Millichap: onset, peak, and duration}}<ref name="Narcolepsy guide">{{cite journal|title=A practical guide to the therapy of narcolepsy and hypersomnia syndromes|date=October 2012|journal=Neurotherapeutics|issue=4|doi=10.1007/s13311-012-0150-9|volume=9|pages=739–752|pmc=3480574|pmid=23065655|vauthors=Mignot EJ}}</ref><br>長效型（{{abbr|XR|Extended release}} 緩緩釋放藥物）<br> 使用後(dosing): 12&nbsp；小時內{{r|Millichap: onset, peak, and duration|XR onset-duration|Narcolepsy guide}}
| excretion = 主要透過[[腎臟]];<br>視[[PH值]]而定 {{nowrap|範圍：1–75%}}{{r|FDA Pharmacokinetics}}

<!--Identifiers-->
| CAS_number_Ref = {{cascite|correct|CAS}}
| CAS_number = 300-62-9
| ATC_prefix = N06
| ATC_suffix = BA01
| ChEBI_Ref = {{ebicite|correct|EBI}}
| ChEBI = 2679
| PDB_ligand = FRD
| IUPHAR_ligand = 4804
| StdInChI_Ref = {{stdinchicite|correct|chemspider}}
| StdInChI = 1S/C9H13N/c1-8(10)7-9-5-3-2-4-6-9/h2-6,8H,7,10H2,1H3
| StdInChIKey_Ref = {{stdinchicite|correct|chemspider}}
| StdInChIKey = KWTSXDURSIMDCE-UHFFFAOYSA-N
| PubChem = 3007
| DrugBank_Ref = {{drugbankcite|correct|drugbank}}
| DrugBank = DB00182
| ChemSpiderID_Ref = {{chemspidercite|correct|chemspider}}
| ChemSpiderID = 13852819
| NIAID_ChemDB = 018564
| UNII_Ref = {{fdacite|correct|FDA}}
| UNII = CK833KGX7E
| KEGG_Ref = {{keggcite|correct|kegg}}
| KEGG = D07445
| ChEMBL_Ref = {{ebicite|correct|EBI}}
| ChEMBL = 405
| synonyms = α-甲基苯乙胺

<!--Chemical data-->
| C=9 | H=13 | N=1
| molecular_weight = 135.20622&nbsp;g/mol<ref name="PubChem Header">{{cite encyclopedia | title=Amphetamine | section-url=https://pubchem.ncbi.nlm.nih.gov/summary/summary.cgi?cid=3007 | work=PubChem Compound | publisher=United States National Library of Medicine&nbsp;– National Center for Biotechnology Information | accessdate=17 April 2015 | date=11 April 2015 | section=Compound Summary | archivedate=2013-10-13 | archiveurl=https://web.archive.org/web/20131013122604/http://pubchem.ncbi.nlm.nih.gov/summary/summary.cgi?cid=3007 | deadurl=no }}</ref>
| smiles = NC(CC1=CC=CC=C1)C
| density = 0.9±0.1
| density_notes    = at 25&nbsp;°C<ref name="PubChem - amphetamine density">{{cite encyclopedia | title=Amphetamine | section=Density | url=https://pubchem.ncbi.nlm.nih.gov/compound/amphetamine | section-url=https://pubchem.ncbi.nlm.nih.gov/compound/amphetamine#section=Density | work=PubChem Compound | publisher=United States National Library of Medicine&nbsp;– National Center for Biotechnology Information | accessdate=9 November 2016 | date=5 November 2016 | archivedate=2021-01-29 | archiveurl=https://web.archive.org/web/20210129215804/https://pubchem.ncbi.nlm.nih.gov/compound/amphetamine | deadurl=no }}</ref>
| boiling_point = 203
| boiling_notes = 為 760&nbsp;[[毫米汞柱]]<ref name="Properties">{{cite encyclopedia | title=Amphetamine | section-url=https://pubchem.ncbi.nlm.nih.gov/summary/summary.cgi?cid=3007#section=Chemical-and-Physical-Properties | work=PubChem Compound | publisher=United States National Library of Medicine&nbsp;– National Center for Biotechnology Information | accessdate=13 October 2013 | section=Chemical and Physical Properties | archivedate=2013-10-13 | archiveurl=https://web.archive.org/web/20131013122604/http://pubchem.ncbi.nlm.nih.gov/summary/summary.cgi?cid=3007#section=Chemical-and-Physical-Properties | deadurl=no }}</ref>
| melting_point = 11.3
| melting_notes = (預測)<ref name="Chemspider">{{cite encyclopedia | section-url=http://www.chemspider.com/Chemical-Structure.13852819.html | work=Chemspider | title=Amphetamine | accessdate=2013-11-06 | section=Properties: Predicted – EP{{pipe}}Suite | archivedate=2020-12-22 | archiveurl=https://web.archive.org/web/20201222010925/http://www.chemspider.com/Chemical-Structure.13852819.html | deadurl=no }}</ref>
}}
'''安非他命'''（英語：amphetamine, alpha-methylphenethylamine）（[[结构简式|化學式]]：{{script|Latn|C₆H₅CH₂CH(CH₃)NH₂}}，为[[中樞神經刺激劑]]，用來治療[[注意力不足過動症]]、[[嗜睡症]]、和[[肥胖症]]。英语源通称“安非他命”擷取自α-甲基苯乙胺的英文读法“{{lang|en|{{nowrap|[[Α-碳原子|<u>a</u>lpha]]‑[[甲基苯乙胺|<u>m</u>ethyl<u>ph</u>en<u>et</u>hyl<u>amine</u>]]}}}}”之缩读。安非他命是在1887年發現的，以兩種[[對映異構體]]的形式存在{{efn-ur|對映異構體指的是兩個形狀相同但方向相反的兩個分子，二個分子互為鏡像。<ref name="Enantiomers">{{cite web|title=Enantiomer|url=http://goldbook.iupac.org/E02069.html|accessdate=2014-03-14|work=IUPAC Goldbook|publisher=International Union of Pure and Applied Chemistry|doi=10.1351/goldbook.E02069|archiveurl=https://web.archive.org/web/20130317002318/http://goldbook.iupac.org/E02069.html|archivedate=2013-03-17|deadurl=no|quote=One of a pair of molecular entities which are mirror images of each other and non-superposable.}}</ref>Levoamphetamine 和 dextroamphetamine 分別被簡稱為 L-amph 或 levamfetamine ([[国际非专利药品名称|INN]]) 和 D-amph 或 dexamfetamine (INN)
{{r|PubChem Header}}}}，分別是[[左旋安非他命]]和[[右旋安非他命]]。准确来说，安非他命指的是特定的化學物質，是[[外消旋混合物|外消旋]]的{{le|純胺類型態|free base}}<ref name="WHO INN active moiety">{{cite web|title=Guidelines on the Use of International Nonproprietary Names (INNS) for Pharmaceutical Substances|url=http://apps.who.int/medicinedocs/en/d/Jh1806e/2.4.html|access-date=1 December 2014|date=1997|publisher=World Health Organization|archiveurl=https://web.archive.org/web/20150109232455/http://apps.who.int/medicinedocs/en/d/Jh1806e/2.4.html|archivedate=2015-01-09|deadurl=no|quote=In principle, INNs are selected only for the active part of the molecule which is usually the base, acid or alcohol. In some cases, however, the active molecules need to be expanded for various reasons, such as formulation purposes, bioavailability or absorption rate. In 1975 the experts designated for the selection of INN decided to adopt a new policy for naming such molecules. In future, names for different salts or esters of the same active substance should differ only with regard to the inactive moiety of the molecule.&nbsp;... The latter are called modified INNs (INNMs).}}</ref><ref name="Proper definition">{{cite book|author=Yoshida T|editor=Klee H|title=Amphetamine Misuse: International Perspectives on Current Trends|date=1997|publisher=Harwood Academic Publishers|location=Amsterdam, Netherlands|isbn=9789057020810|page=[https://archive.org/details/amphetaminemisus0000unse/page/2 2]|chapter-url=https://books.google.com/books?id=gVw_wzZU4x8C&pg=PA2|access-date=1 December 2014|chapter=Chapter 1: Use and Misuse of Amphetamines: An International Overview|quote=Amphetamine, in the singular form, properly applies to the racemate of 2-amino-1-phenylpropane.&nbsp;... In its broadest context, however, the term [''amphetamines''] can even embrace a large number of structurally and pharmacologically related substances.|url=https://archive.org/details/amphetaminemisus0000unse/page/2}}</ref>，這個物質等同於安非他命的兩個對映異構體：左旋安非他命和右旋安非他命等量之純胺類型態。不過，安非他命一詞已用來表示任何比例安非他命對映異構體的組合，或是任一種異構體{{r|DrugBank1|Proper definition}}<ref name="MeSHAmphetamine">{{cite web|title=Amphetamine|url=https://www.nlm.nih.gov/cgi/mesh/2009/MB_cgi?mode=&term=Amphetamine|access-date=16 December 2013|website=Medical Subject Headings|publisher=United States National Library of Medicine|archiveurl=https://web.archive.org/web/20150927095927/http://www.nlm.nih.gov/cgi/mesh/2009/MB_cgi?mode=&term=Amphetamine|archivedate=2015-09-27|deadurl=no}}</ref>。

以往曾用安非他命來治療[[鼻塞]]和[[抑鬱]]。在非醫療用途上，安非他命也有用作[[體能增強藥物]]、[[益智藥]]、[[春藥]]及[[欣快]]藥物。安非他命在許多國家為合法的[[處方藥]]。然而，私自散布和囤積安非他命被視為非法行為，因為安非他命被用於[[娛樂性藥物|非醫療用途的助興]]可能性極高，而且有明顯健康上的危害{{r|Proper definition|MeSHAmphetaminer|WHO INN active moiety}}。

首個藥用安非他命的藥品名稱為Benzedrine。當今[[#醫療|藥用安非他命]]{{RefTag|name=pharmaceutical amphetamine|1=英文名稱為：Pharmaceutical amphetamine}}以下列幾種形式存在：外消旋安非他命{{RefTag|name= racemic amphetamine|1=英文名稱為：racemic amphetamine}}、[[阿得拉尔]]
{{efn-ur|
"阿得拉尔"是一個[[品牌名稱]]而非[[公有領域]]的稱呼。但因為以下幾個安非他命的異構物的名稱及其英文名稱 ("''dextroamphetamine sulfate, dextroamphetamine saccharate, amphetamine sulfate, and amphetamine aspartate''") 太長了，因此本文將以此品牌名稱來表示此種安非他命的混合物。<ref name="NDCD">{{cite web | title = National Drug Code Amphetamine Search Results | url = http://www.accessdata.fda.gov/scripts/cder/ndc/results.cfm?beginrow=1&numberperpage=160&searchfield=amphetamine&searchtype=ActiveIngredient&OrderBy=ProprietaryName | work = National Drug Code Directory | publisher = United States Food and Drug Administration | accessdate = 2013-12-16 | archiveurl = https://web.archive.org/web/20131216080856/http://www.accessdata.fda.gov/scripts/cder/ndc/results.cfm?beginrow=1&numberperpage=160&searchfield=amphetamine&searchtype=ActiveIngredient&OrderBy=ProprietaryName | archivedate = 2013-12-16 | deadurl = no }}</ref>) }}、[[右旋安非他命]]，或[[前体药物|前驅藥物]][[甲磺酸赖氨酸安非他命]]。安非他命藉著自身作用於[[兒茶酚胺]]神經傳導元素：[[正腎上腺素]]及[[多巴胺]]的特點來活化{{le|trace amine receptor|TAAR1|痕量胺受体}}，進而增加[[单胺类神经递质]]和[[神经递质]]在腦內的活動。<ref name="Amph Uses">{{cite journal|title=Amphetamine, past and present – a pharmacological and clinical perspective|date=June 2013|journal=J. Psychopharmacol.|issue=6|doi=10.1177/0269881113482532|volume=27|pages=479–496|pmc=3666194|pmid=23539642|quote=The intravenous use of d-amphetamine and other stimulants still pose major safety risks to the individuals indulging in this practice. Some of this intravenous abuse is derived from the diversion of ampoules of d-amphetamine, which are still occasionally prescribed in the UK for the control of severe narcolepsy and other disorders of excessive sedation.&nbsp;... For these reasons, observations of dependence and abuse of prescription d-amphetamine are rare in clinical practice, and this stimulant can even be prescribed to people with a history of drug abuse provided certain controls, such as daily pick-ups of prescriptions, are put in place (Jasinski and Krishnan, 2009b).|vauthors=Heal DJ, Smith SL, Gosden J, Nutt DJ}}</ref><ref name="Adderall IR">{{cite web|title=Adderall IR Prescribing Information|url=http://www.accessdata.fda.gov/drugsatfda_docs/label/2015/011522s042lbl.pdf|accessdate=2016-05-18|date=October 2015|work=United States Food and Drug Administration|publisher=Teva Pharmaceuticals USA, Inc.|pages=1–6|archiveurl=https://web.archive.org/web/20180915111231/https://www.accessdata.fda.gov/drugsatfda_docs/label/2015/011522s042lbl.pdf|archivedate=2018-09-15|deadurl=no}}</ref><ref name="Miller">{{cite journal|title=The emerging role of trace amine-associated receptor 1 in the functional regulation of monoamine transporters and dopaminergic activity|author=Miller GM|date=January 2011|journal=J. Neurochem.|issue=2|doi=10.1111/j.1471-4159.2010.07109.x|volume=116|pages=164–176|pmc=3005101|pmid=21073468}}</ref>

在醫療用的劑量範圍內，安非他命能帶來情緒以及執行功能的變化，例如：[[欣快感]]的增强、[[性欲]]的改變、[[清醒|清醒度]]的提升、大腦[[執行功能]]的進化。安非他命所改變的生理反應包含：減少反應時間、降低疲勞、以及肌耐力的增強。若攝取劑量远超过醫療用的劑量範圍，將會導致大腦執行功能受損以及[[橫紋肌溶解症]]，攝取過份超越醫療用劑量範圍的安非他命可引发嚴重的[[成癮|藥物成癮]]，服用遠超醫療用劑量範圍的安非他命會引起精神疾病（例如：[[妄想]]、[[偏執]]）。然而長期攝取醫療劑量範圍的安非他命並不會引起上述疾病。那些为享乐而摄入的安非他命通常会遠超過醫療用劑量範圍，且伴隨著非常嚴重甚至致命的副作用。{{r|Adderall IR}}<ref name="Malenka_2009">
{{cite book|vauthors=Malenka RC, Nestler EJ, Hyman SE|veditors=Sydor A, Brown RY|title=Molecular Neuropharmacology: A Foundation for Clinical Neuroscience|year=2009|publisher=McGraw-Hill Medical|location=New York, USA|isbn=9780071481274|pages=318, 321|edition=2nd|chapter=Chapter 13: Higher Cognitive Function and Behavioral Control|quote=Therapeutic (relatively low) doses of psychostimulants, such as methylphenidate and amphetamine, improve performance on working memory tasks both in normal subjects and those with ADHD.&nbsp;... stimulants act not only on working memory function, but also on general levels of arousal and, within the nucleus accumbens, improve the saliency of tasks. Thus, stimulants improve performance on effortful but tedious tasks&nbsp;... through indirect stimulation of dopamine and norepinephrine receptors.&nbsp;...<br>Beyond these general permissive effects, dopamine (acting via D1 receptors) and norepinephrine (acting at several receptors) can, at optimal levels, enhance working memory and aspects of attention.}}</ref><ref name="Ergogenics">
{{cite journal|title=Nutritional supplements and ergogenic AIDS|date=June 2013|journal=Prim. Care|issue=2|doi=10.1016/j.pop.2013.02.009|volume=40|pages=487–505|pmid=23668655|quote=Amphetamines and caffeine are stimulants that increase alertness, improve focus, decrease reaction time, and delay fatigue, allowing for an increased intensity and duration of training&nbsp;...<br>Physiologic and performance effects<br>{{·}}Amphetamines increase dopamine/norepinephrine release and inhibit their reuptake, leading to central nervous system (CNS) stimulation<br>{{·}}Amphetamines seem to enhance athletic performance in anaerobic conditions 39 40<br>{{·}}Improved reaction time<br>{{·}}Increased muscle strength and delayed muscle fatigue<br>{{·}}Increased acceleration<br>{{·}}Increased alertness and attention to task|vauthors=Liddle DG, Connor DJ}}</ref>{{r|FDA Abuse & OD}}。

安非他命屬於[[苯乙胺衍生物]]。安非他命的衍生物也歸在同一分類中{{RefTag|name=substituted amphetamine|1=英文名稱為：substituted amphetamine}}的分類中{{efn-ur|
「安非他命」一詞也意指一個化學分類，但與「安非他命衍生物」這個化學分類不同的是，「��非他命」類在學術上並無標準的定義。{{r|Substituted amphetamines, FMO, and DBH|Proper definition}}
有一個「安非他命」類的定義嚴格限定分類中僅有：安非他命的racemate and enantiomers和甲基安非他命methamphetamine的racemate and enantiomers。{{r|Proper definition}}
大多數「安非他命」類的定義為那些在藥理學上以及結構上與安非他命相關的化合物。{{r|Proper definition}}<br>
為避免讀者混淆，本條目中僅會使用amphetamine、amphetamines來表示racemic amphetamine, levoamphetamine, and dextroamphetamine；安非他命衍生物（substituted amphetamines）來表示安非他命的結構分類。}}，比如說：[[安非他酮]]{{RefTag|name=bupropion|1=英文名稱為：Bupropion}}、[[卡西酮]]、[[MDMA]]、和[[甲基苯丙胺]]{{RefTag|name=methamphetamine|英文名稱為：meth-amphetamine}}。安非他命也與人體內可自然生成的兩個屬於[[痕量胺]]的神經傳導物質——特別是[[苯乙胺]]和{{nowrap|[[N-甲基苯乙胺]]}}——有關。苯乙胺只比安非他命少了一个甲基，而{{nowrap|N-甲基苯乙胺}}則是安非他命的[[結構異構]]（差異只在於[[甲基]]位置的不同）。<ref name="Trace Amines">{{cite journal|title=The vascular effects of trace amines and amphetamines|author=Broadley KJ|date=March 2010|journal=Pharmacol. Ther.|issue=3|doi=10.1016/j.pharmthera.2009.11.005|volume=125|pages=363–375|pmid=19948186|quote=<!-- '''Fig. 2.''' Synthetic and metabolic pathways for endogenous and exogenously administered trace amines and sympathomimetic amines&nbsp;...<br> Trace amines are metabolized in the mammalian body via monoamine oxidase (MAO; EC 1.4.3.4) (Berry, 2004) (Fig. 2)&nbsp;... It deaminates primary and secondary amines that are free in the neuronal cytoplasm but not those bound in storage vesicles of the sympathetic neurone&nbsp;...<br>Thus, MAO inhibitors potentiate the peripheral effects of indirectly acting sympathomimetic amines&nbsp;... this potentiation occurs irrespective of whether the amine is a substrate for MAO. An α-methyl group on the side chain, as in amphetamine and ephedrine, renders the amine immune to deamination so that they are not metabolized in the gut. Similarly, β-PEA would not be deaminated in the gut as it is a selective substrate for MAO-B which is not found in the gut&nbsp;...<br> Brain levels of endogenous trace amines are several hundred-fold below those for the classical neurotransmitters noradrenaline, dopamine and serotonin but their rates of synthesis are equivalent to those of noradrenaline and dopamine and they have a very rapid turnover rate (Berry, 2004). Endogenous extracellular tissue levels of trace amines measured in the brain are in the low nanomolar range. These low concentrations arise because of their very short half-life&nbsp;... -->}}</ref><ref name="EMC">{{cite web|title=Amphetamine|url=http://www.emcdda.europa.eu/publications/drug-profiles/amphetamine|accessdate=2013-10-19|work=European Monitoring Centre for Drugs and Drug Addiction|archiveurl=https://web.archive.org/web/20200227184322/http://www.emcdda.europa.eu/publications/drug-profiles/amphetamine|archivedate=2020-02-27|deadurl=no}}</ref><ref name="Amphetamine - a substituted amphetamine">{{cite journal|title=Biosynthesis of amphetamine analogs in plants|date=2012|journal=Trends Plant Sci.|issue=7|doi=10.1016/j.tplants.2012.03.004|volume=17|pages=404–412|pmid=22502775|quote=Substituted amphetamines, which are also called phenylpropylamino alkaloids, are a diverse group of nitrogen-containing compounds that feature a phenethylamine backbone with a methyl group at the α-position relative to the nitrogen (Figure 1).&nbsp;... Beyond (1''R'',2''S'')-ephedrine and (1''S'',2''S'')-pseudoephedrine, myriad other substituted amphetamines have important pharmaceutical applications.&nbsp;... For example, (''S'')-amphetamine (Figure 4b), a key ingredient in Adderall<sup>®</sup> and Dexedrine<sup>®</sup>, is used to treat attention deficit hyperactivity disorder (ADHD) [79].&nbsp;... <br>[Figure 4](b) Examples of synthetic, pharmaceutically important substituted amphetamines.|vauthors=Hagel JM, Krizevski R, Marsolais F, Lewinsohn E, Facchini PJ}}</ref>

==用途==
===醫療===
{{see also|注意力不足過動症#藥物}}
安非他命可以治療[[注意力不足過動症]]（ADHD）、[[嗜睡症]]（一種睡眠疾病）、和[[肥胖症]]。有時候安非他命會以[[仿單標示外使用]]的方式處方來治療{{tsl|en|treatment-resistant depression|頑固性憂鬱症}}和頑固性強迫症{{r|Amph Uses|Adderall IR}}<ref name="Evekeo">{{cite web|title=Evekeo Prescribing Information|url=https://www.evekeo.com/assets/evekeo-pi.pdf|accessdate=2015-08-11|date=April 2014|publisher=Arbor Pharmaceuticals LLC|pages=1–2|archiveurl=https://web.archive.org/web/20160304042740/https://www.evekeo.com/assets/evekeo-pi.pdf|archivedate=2016-03-04|deadurl=no}}</ref><ref>{{cite web|title=Obsessive compulsive disorder (OCD)|url=http://www.nhs.uk/conditions/Obsessive-compulsive-disorder/Pages/Introduction.aspx|access-date=2017-04-04|date=2016-09-28|publisher=NHS Choice|archiveurl=https://web.archive.org/web/20171009014738/http://www.nhs.uk/conditions/obsessive-compulsive-disorder/pages/introduction.aspx|archivedate=2017-10-09|deadurl=no}}</ref>。在動物試驗中，已知非常高劑量的安非他命會造成某些動物的{{tsl|en|dopamine receptor|多巴胺系統}}和神經系統的受損。{{r|pmid22392347}}<ref name="AbuseAndAbnormalities">{{cite journal|title=Abuse of amphetamines and structural abnormalities in the brain|date=October 2008|journal=Ann. N. Y. Acad. Sci.|doi=10.1196/annals.1441.031|volume=1141|pages=195–220|pmc=2769923|pmid=18991959|vauthors=Berman S, O'Neill J, Fears S, Bartzokis G, London ED}}</ref>但是，在人體試驗中，注意力不足過動症患者在接受安非他命的治療後，則發現安非他命可促進大腦的發育及神經的成長。<ref name="Neuroplasticity 1">{{cite journal|title=Meta-analysis of functional magnetic resonance imaging studies of inhibition and attention in attention-deficit/hyperactivity disorder: exploring task-specific, stimulant medication, and age effects|url=https://archive.org/details/sim_jama-psychiatry_2013-02_70_2/page/185|date=February 2013|journal=JAMA Psychiatry|issue=2|doi=10.1001/jamapsychiatry.2013.277|volume=70|pages=185–198|pmid=23247506|vauthors=Hart H, Radua J, Nakao T, Mataix-Cols D, Rubia K}}</ref><ref name="Neuroplasticity 2">
{{cite journal|title=Effect of psychostimulants on brain structure and function in ADHD: a qualitative literature review of magnetic resonance imaging-based neuroimaging studies|url=https://archive.org/details/sim_journal-of-clinical-psychiatry_2013-09_74_9/page/902|date=September 2013|journal=J. Clin. Psychiatry|issue=9|doi=10.4088/JCP.12r08287|volume=74|pages=902–917|pmc=3801446|pmid=24107764|vauthors=Spencer TJ, Brown A, Seidman LJ, Valera EM, Makris N, Lomedico A, Faraone SV, Biederman J}}</ref><ref name="Neuroplasticity 3">
{{cite journal|title=Meta-analysis of structural MRI studies in children and adults with attention deficit hyperactivity disorder indicates treatment effects.|date=February 2012|journal=Acta psychiatrica Scand.|issue=2|doi=10.1111/j.1600-0447.2011.01786.x|volume=125|pages=114–126|pmid=22118249|quote=Basal ganglia regions like the right globus pallidus, the right putamen, and the nucleus caudatus are structurally affected in children with ADHD. These changes and alterations in limbic regions like ACC and amygdala are more pronounced in non-treated populations and seem to diminish over time from child to adulthood. Treatment seems to have positive effects on brain structure.|vauthors=Frodl T, Skokauskas N}}</ref>

回顧許多[[核磁共振成像|核磁共振照影]]（{{lang-en|Nuclear Magnetic Resonance Imaging}}）的研究後發現，長期以安非他命治療注意力不足過動症患者能顯著降低患者大腦結構及大腦執行功能上的異常。並且改善大腦中數個部位，例如：[[基底神經節]]的右[[尾狀核]]{{r|Neuroplasticity 1|Neuroplasticity 2|Neuroplasticity 3}}。

眾多臨床研究的系統性及統合性回顧已確立長期使用安非他命治療[[注意力不足過動症]]的療效及安全。<ref name="Millichap">
{{cite book|author=Millichap JG|editor=Millichap JG|title=Attention Deficit Hyperactivity Disorder Handbook: A Physician's Guide to ADHD|year=2010|publisher=Springer|location=New York, USA|isbn=9781441913968|pages=121–123, 125–127|edition=2nd|chapter=Chapter 9: Medications for ADHD|quote=Ongoing research has provided answers to many of the parents’ concerns, and has confirmed the effectiveness and safety of the long-term use of medication.}}</ref><ref name="Long-term 2015">{{cite journal|title=Effect of treatment modality on long-term outcomes in attention-deficit/hyperactivity disorder: a systematic review|date=February 2015|journal=PLoS ONE|issue=2|doi=10.1371/journal.pone.0116407|volume=10|pages=e0116407|pmc=4340791|pmid=25714373|quote=The highest proportion of improved outcomes was reported with combination treatment (83% of outcomes). Among significantly improved outcomes, the largest effect sizes were found for combination treatment. The greatest improvements were associated with academic, self-esteem, or social function outcomes.|vauthors=Arnold LE, Hodgkins P, Caci H, Kahle J, Young S}}
[https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4340791/figure/pone.0116407.g003/ Figure 3: Treatment benefit by treatment type and outcome group] {{Wayback|url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4340791/figure/pone.0116407.g003/ |date=20210827214244 }}</ref><ref name="Arnold Hodgkins Caci Kahle">{{cite journal|title=Effect of Treatment Modality on Long-Term Outcomes in Attention-Deficit/Hyperactivity Disorder: A Systematic Review|url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4340791/|last=Arnold|first=L. Eugene|last2=Hodgkins|first2=Paul|journal=PLoS ONE|accessdate=2017-05-15|issue=2|doi=10.1371/journal.pone.0116407|volume=10|pmid=25714373|archiveurl=https://web.archive.org/web/20201109023418/https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4340791/|archivedate=2020-11-09|last3=Caci|first3=Hervé|last4=Kahle|first4=Jennifer|last5=Young|first5=Susan|deadurl=no}}</ref><ref name="Long-Term Outcomes Medications">{{cite journal|title=Long-term outcomes with medications for attention-deficit hyperactivity disorder: current status of knowledge|date=July 2011|journal=CNS Drugs|issue=7|doi=10.2165/11589380-000000000-00000|volume=25|pages=539–554|pmid=21699268|quote=Recent studies have demonstrated that stimulants, along with the non-stimulants atomoxetine and extended-release guanfacine, are continuously effective for more than 2-year treatment periods with few and tolerable adverse effects. The effectiveness of long-term therapy includes not only the core symptoms of ADHD, but also improved quality of life and academic achievements. The most concerning short-term adverse effects of stimulants, such as elevated blood pressure and heart rate, waned in long-term follow-up studies.&nbsp;... In the longest follow-up study (of more than 10 years), lifetime stimulant treatment for ADHD was effective and protective against the development of adverse psychiatric disorders.|vauthors=Huang YS, Tsai MH}}</ref>

持續長達兩年的[[隨機對照試驗]]{{RefTag|name=randomized controlled trials |1=英文名稱為：Randomized controlled trials}}{{efn|又稱為「隨機分配且包含控制組的臨床試驗」，是臨床試驗的一種}}結果顯示：長期使用安非他命治療注意力不足過動症，是有效且安全的{{r|Millichap|Long-Term Outcomes Medications}}。

兩個系統性/統合性回顧的結果顯示長期且持續地使用中樞神經興奮劑治療注意力不足過動症能有效地減少注意力不足過動症的核心症狀（核心症狀即為：過動、衝動和分心/無法專心）、增進[[生活品質]]、提升學業成就、廣泛地強化大腦的執行功能。{{efn-ur|
研究證實，長期以中樞神經興奮劑治療ADHD能在下列這些方面產生大幅的進步：學業、駕駛、降低藥物濫用、降低肥胖、自尊、和社交功能等。{{r|Long-term 2015}}
<br><br>
在上述領域中，最為突出的領域為：
學業（例如：[[成绩|GPA]]分數、成果測驗分數、受教育的時間長度、和教育程度）、自尊（例如：自尊心測驗分數、嘗試自殺的次數、自殺率等）和社交功能（例如：peer nomination scores、社交技巧、家庭關係、同儕關係、和浪漫關係/情侶關係）{{r|Long-term 2015}}
<br><br>
長期以「藥物治療合併行為治療」的模式來治療ADHD，能夠比單獨以藥物治療，產生更全面且更長足的進步。
{{r|Long-term 2015}}}}這些執行功能分別與下列項目有關：學業、反社會行為、駕駛習慣、藥物濫用、肥胖、職業、日常活動、自尊心、服務使用（例如：學習、職業、健康、財金、和法律等）、社交功能{{r|Long-term 2015|Long-Term Outcomes Medications}}。

一篇系統性／統合性回顧標誌了一個重要發現：一個為期九個月的隨機雙盲試驗中，持續以安非他命治療的ADHD患者，其[[智力商數]]平均增加4.5單位{{NoteTag|1=智力測驗結果與專注力有關，詳見[[注意力不足過動症#智力]]}}，且在專注力、衝動、過動的改善皆呈現持續進步的態勢。{{r|Millichap}}另一篇系統性／統合性回顧則指出：根據迄今為止為時最長的數個[[臨床追蹤研究]]{{RefTag|name=prospective cohort study|1=英文名稱為：follow-up studies}}，可以得到一個結論：即便從兒童時期開始以中樞神經興奮劑治療直到老年，中樞神經興奮劑都能持續有效地控制ADHD的症狀並且減少[[物質濫用]]的風險。{{r|Long-Term Outcomes Medications}}
研究表明，ADHD與大腦的執行功能受損有關。而這些受損的執行功能分別與大腦中部分的{{tsl|en|neurostransmitter systems|神經傳導系統}}有關{{RefTag|name=neurotransmitter systems|1=英文名稱為：neurotransmitter systems}}<ref name="Malenka_2009_03">
{{cite book|vauthors=Malenka RC, Nestler EJ, Hyman SE|veditors=Sydor A, Brown RY|title=Molecular Neuropharmacology: A Foundation for Clinical Neuroscience|year=2009|publisher=McGraw-Hill Medical|location=New York, USA|isbn=9780071481274|pages=154–157|edition=2nd|chapter=Chapter 6: Widely Projecting Systems: Monoamines, Acetylcholine, and Orexin}}</ref>；又此部分受損的神經傳導系統和{{tsl|en|mesocorticolimbic projection|中腦皮質激素}}-[[多巴胺]]{{RefTag|name=dopamine|1=英文名稱為：dopamine}}的傳導及[[藍斑核]]{{RefTag|name=locus coeruleus|1=英文名稱為：locus coeruleus}}和[[前額葉]]{{RefTag|name=prefrontal coretex|1=英文名稱為：prefrontal cortex}}中的[[正腎上腺素]]{{RefTag|name=nor-adrenaline|英文名稱為：nor-epinephrine或nor-adrenaline}}的傳導相關。{{r|Malenka_2009_03}}

中樞神經興奮劑，例如：[[哌甲酯|methylphenidate]]和安非他命對於治療ADHD都是有效的，因為中樞神經興奮劑刺激了上述神經系統中的神經傳導物質活動。{{r|Malenka_2009|Malenka_2009_03}}<ref name="cognition enhancers">{{cite journal|title=Cognitive enhancers for the treatment of ADHD|date=August 2011|journal=Pharmacol. Biochem. Behav.|issue=2|doi=10.1016/j.pbb.2011.05.002|volume=99|pages=262–274|pmc=3353150|pmid=21596055|vauthors=Bidwell LC, McClernon FJ, Kollins SH}}</ref>

至少超過80%的ADHD患者在使用中樞神經興奮劑治療後，其ADHD的症狀可以獲得改善。<ref name="Long-term 36">
{{cite journal|title=The long-term outcomes of interventions for the management of attention-deficit hyperactivity disorder in children and adolescents: a systematic review of randomized controlled trials|date=September 2013|journal=Psychol. Res. Behav. Manag.|doi=10.2147/PRBM.S49114|volume=6|pages=87–99|type=systematic review (secondary source)|pmc=3785407|pmid=24082796|quote=Only one paper<sup>53</sup> examining outcomes beyond 36 months met the review criteria.&nbsp;... There is high level evidence suggesting that pharmacological treatment can have a major beneficial effect on the core symptoms of ADHD (hyperactivity, inattention, and impulsivity) in approximately 80% of cases compared with placebo controls, in the short term.|vauthors=Parker J, Wales G, Chalhoub N, Harpin V}}</ref>

使用中樞神經興奮劑治療的ADHD患者相較之下，普遍與同儕及家庭成員的關係較佳並且在學校擁有較好的表現。興奮劑能使ADHD患者較不易分心、衝動、且擁有較長的專注力時間和範圍。<ref name="Millichap_3">
{{cite book|author=Millichap JG|editor=Millichap JG|title=Attention Deficit Hyperactivity Disorder Handbook: A Physician's Guide to ADHD|year=2010|publisher=Springer|location=New York, USA|isbn=9781441913968|pages=111–113|edition=2nd|chapter=Chapter 9: Medications for ADHD}}</ref><ref name="ADHD">{{cite web|title=Stimulants for Attention Deficit Hyperactivity Disorder|url=http://www.webmd.com/add-adhd/childhood-adhd/stimulants-for-attention-deficit-hyperactivity-disorder|accessdate=2013-11-12|date=2010-04-12|work=WebMD|publisher=Healthwise|archiveurl=https://web.archive.org/web/20131113004717/http://www.webmd.com/add-adhd/childhood-adhd/stimulants-for-attention-deficit-hyperactivity-disorder|archivedate=2013-11-13|deadurl=no}}</ref>

根據[[考科藍|考科藍協作組織]]{{RefTag|name=Cochrane Collaboration|1=英文名稱為：Cochrane Collaboration}}所提供的文獻回顧結果{{efn-ur|考科藍協作組織對於歷年眾多的「隨機對照試驗」的[[系統綜述|系統性回顧]]、[[元分析|數據統整分析]]後所得出的總結，基本上都是非常有水準且深具參考價值的。
<ref name="pmid16052183">
{{cite journal 
|vauthors=Scholten RJ, Clarke M, Hetherington J 
|title=The Cochrane Collaboration 
|journal=Eur. J. Clin. Nutr. 
|volume=59 Suppl 1 
|pages=S147–S149; discussion S195–S196 
|date=August 2005 
|pmid=16052183 
|doi=10.1038/sj.ejcn.1602188}}</ref>}}指出：使用中樞神經興奮劑治療的ADHD患者即便其症狀改善，相較於使用非中樞神經興奮劑，仍因[[副作用]]而有較高的停藥率。<ref name="Cochrane Amphetamines ADHD">
{{cite journal|title=Amphetamines for Attention Deficit Hyperactivity Disorder (ADHD) in adults|date=June 2011|journal=Cochrane Database Syst. Rev.|issue=6|doi=10.1002/14651858.CD007813.pub2|pages=CD007813|pmid=21678370|vauthors=Castells X, Ramos-Quiroga JA, Bosch R, Nogueira M, Casas M|editor=Castells X}}</ref><ref name="pmid26844979">
{{cite journal|title=Amphetamines for attention deficit hyperactivity disorder (ADHD) in children and adolescents|date=February 2016|journal=Cochrane Database Syst. Rev.|doi=10.1002/14651858.CD009996.pub2|volume=2|pages=CD009996|pmid=26844979|vauthors=Punja S, Shamseer L, Hartling L, Urichuk L, Vandermeer B, Nikles J, Vohra S}}</ref>

回顧結果也發現，中樞神經興奮劑並不會惡化[[抽动综合症|抽動綜合症]]的症狀，例如：[[妥瑞氏症]]，除非服用[[dextroamphetamine]]{{efn|中樞神經興奮劑的一種}}的劑量過高才有可能在部分妥瑞氏症合併注意力不足過動症患者身上觀察到抽動綜合症的症狀惡化。<ref>{{cite journal|title=Pharmacological treatment for Attention Deficit Hyperactivity Disorder (ADHD) in children with comorbid tic disorders|url=https://archive.org/details/icememoirofgangs00icet|date=April 2011|journal=Cochrane Database Syst. Rev.|issue=4|doi=10.1002/14651858.CD007990.pub2|pages=CD007990|pmid=21491404|vauthors=Pringsheim T, Steeves T|editor=Pringsheim T}}</ref>

中樞神經興奮劑只要依照醫師指示用藥，都是相當安全的。<ref name="medlineplus1">{{cite web|title=Home of MedlinePlus→ Health Topics → Attention Deficit Hyperactivity Disorder Attention Deficit Hyperactivity Disorder Also called: ADHD|url=https://medlineplus.gov/attentiondeficithyperactivitydisorder.html|accessdate=2016-12-27|date=|publisher=Medlineplus.gov|archiveurl=https://web.archive.org/web/20161225115235/https://medlineplus.gov/attentiondeficithyperactivitydisorder.html|archivedate=2016-12-25|deadurl=no}}</ref><ref name="Taiwan_FDA_on_controlled_medications">{{cite web|title=衛生福利部-食品藥物管理署-管制藥品|url=http://www.fda.gov.tw/TC/site.aspx?sid=41|accessdate=2016-12-27|date=2013-12-30|publisher=Fda.gov.tw|archiveurl=https://web.archive.org/web/20170120033551/http://www.fda.gov.tw/TC/site.aspx?sid=41|archivedate=2017-01-20|deadurl=no}}</ref><ref name="NIDAAAS">{{cite web|title=Stimulant ADHD Medications: Methylphenidate and Amphetamines|url=https://www.drugabuse.gov/publications/drugfacts/stimulant-adhd-medications-methylphenidate-amphetamines|access-date=2017-04-05|date=|last=Abuse|first=National Institute on Drug|publisher=|archiveurl=https://web.archive.org/web/20200403001535/https://www.drugabuse.gov/publications/drugfacts/stimulant-adhd-medications-methylphenidate-amphetamines|archivedate=2020-04-03|deadurl=yes}}</ref>{{r|NIDAAAS}}<ref name="NHS">{{cite web|title=What is a controlled medicine (drug)? - Health questions - NHS Choices|url=http://www.nhs.uk/chq/Pages/1391.aspx?CategoryID=73|accessdate=2017-04-05|date=2016-12-12|last=Choices|first=N. H. S.|publisher=|archiveurl=https://web.archive.org/web/20170503060547/http://www.nhs.uk/chq/Pages/1391.aspx?CategoryID=73|archivedate=2017-05-03|deadurl=no}}</ref>中樞神經興奮劑，例如：利他能與專思達，可能導致：心悸、頭痛、胃痛、喪失食慾、失眠、因相對專注而變得冷淡（面無表情）等副作用，因此6歲以下的兒童不適宜服用。（副作用產生與否因人而異）<ref>{{cite web|title=Methylphenidate|url=https://medlineplus.gov/druginfo/meds/a682188.html|access-date=2017-02-27|date=2016-02-15|website=Home of MedlinePlus → Drugs, Herbs and Supplements → Methylphenidate Methylphenidate pronounced as (meth'' il fen'' i date)|archiveurl=https://web.archive.org/web/20170704210652/https://medlineplus.gov/druginfo/meds/a682188.html|archivedate=2017-07-04|deadurl=no}}</ref>

隨著時間推進與各方的努力，中樞神經興奮劑的相關副作用已可藉由包括但不限於劑量調整、服藥時間、飯前飯後服用、服藥頻率等服藥模式之改變以及改變藥物組合等方式獲得相當程度的減少。{{r|NIDAAAS}}<ref name="Science_daily">{{cite web|title=Combining medications could offer better results for ADHD patients|url=https://www.sciencedaily.com/releases/2016/08/160801093232.htm|access-date=January 2017|date=2016-08-01|website=Science News|publisher=Elsevier|archiveurl=https://web.archive.org/web/20170102050323/https://www.sciencedaily.com/releases/2016/08/160801093232.htm|archivedate=2017-01-02|deadurl=no|quote="Three studies to be published in the August 2016 issue of the Journal of the American Academy of Child and Adolescent Psychiatry (JAACAP) report that combining two standard medications could lead to greater clinical improvements for children with attention-deficit/hyperactivity disorder (ADHD) than either ADHD therapy alone.", August, 2016}}</ref><ref>{{cite book|title=Adults with ADHD|publisher=NATIONAL LIBRARY OF MEDICINE at the NATIONAL INSTITUTES OF HEALTH|series=MedlinePlus the Magazine|volume=9|ISSN=1937-4712|date=Spring 2014|location=8600 Rockville Pike · Bethesda, MD 20894, United States of America|pages=19|language=en-us|url=https://medlineplus.gov/magazine/issues/spring14/articles/spring14pg19.html|access-date=2017-04-05|archivedate=2017-07-15|archiveurl=https://web.archive.org/web/20170715030133/https://medlineplus.gov/magazine/issues/spring14/articles/spring14pg19.html|deadurl=no}}</ref><ref>{{cite web|title=Attention deficit hyperactivity disorder|url=https://medlineplus.gov/ency/article/001551.htm|access-date=2017-02-27|date=2016-05-25|website=Home → Medical Encyclopedia → Attention deficit hyperactivity disorder|publisher=NATIONAL LIBRARY OF MEDICINE at the NATIONAL INSTITUTES OF HEALTH|archiveurl=https://web.archive.org/web/20170126193043/https://medlineplus.gov/ency/article/001551.htm|archivedate=2017-01-26|deadurl=no}}</ref><ref>{{cite web|title=All Disorders|url=http://www.ninds.nih.gov/disorders/adhd/adhd.htm|access-date=2017-02-27|website=National Institute of Neurological Disorders and Stroke|archiveurl=https://web.archive.org/web/20161202230225/http://www.ninds.nih.gov/disorders/adhd/adhd.htm|archivedate=2016-12-02|deadurl=no|quote=}}</ref>

===提昇表現===
;認知方面
2015年，一篇[[系統性回顧]]{{RefTag|name=systematic review|1=英文名稱為：systematic review}}和一篇[[元分析|元分析/整合分析]]{{RefTag|name=meta-analysis|1=英文名稱為：meta-analysis}}回顧了數篇優秀的[[臨床試驗]]{{RefTag|name=clinical trial|1=英文名稱為：clinical trial}}報告後發現，低劑量（醫療用劑量）的安非他命能適度但不強烈地促進一個人<!--（包含健康成人）-->的認知功能，包含[[工作記憶]]、長期的[[情節記憶]]、[[抑制控制]]以及在一些方面的[[注意力]]。<ref name="Unambiguous PFC D1 A2">{{cite journal|title=The Cognition-Enhancing Effects of Psychostimulants Involve Direct Action in the Prefrontal Cortex|journal=Biol. Psychiatry|issue=11|doi=10.1016/j.biopsych.2014.09.013|year=June 2015|volume=77|pages=940–950|pmid=25499957|quote=The procognitive actions of psychostimulants are only associated with low doses. Surprisingly, despite nearly 80 years of clinical use, the neurobiology of the procognitive actions of psychostimulants has only recently been systematically investigated. Findings from this research unambiguously demonstrate that the cognition-enhancing effects of psychostimulants involve the preferential elevation of catecholamines in the PFC and the subsequent activation of norepinephrine α2 and dopamine D1 receptors.&nbsp;... This differential modulation of PFC-dependent processes across dose appears to be associated with the differential involvement of noradrenergic α2 versus α1 receptors. Collectively, this evidence indicates that at low, clinically relevant doses, psychostimulants are devoid of the behavioral and neurochemical actions that define this class of drugs and instead act largely as cognitive enhancers (improving PFC-dependent function).&nbsp;... In particular, in both animals and humans, lower doses maximally improve performance in tests of working memory and response inhibition, whereas maximal suppression of overt behavior and facilitation of attentional processes occurs at higher doses.|vauthors=Spencer RC, Devilbiss DM, Berridge CW}}</ref>
<ref name="Cognitive and motivational effects">{{cite journal|title=Prescription Stimulants' Effects on Healthy Inhibitory Control, Working Memory, and Episodic Memory: A Meta-analysis|date=January 2015|journal=J. Cogn. Neurosci.|doi=10.1162/jocn_a_00776|pages=1–21|pmid=25591060|quote=Specifically, in a set of experiments limited to high-quality designs, we found significant enhancement of several cognitive abilities.&nbsp;... The results of this meta-analysis&nbsp;... do confirm the reality of cognitive enhancing effects for normal healthy adults in general, while also indicating that these effects are modest in size.|vauthors=Ilieva IP, Hook CJ, Farah MJ}}</ref>安非他命強化認知功能的效果已知是部分透過{{tsl|en|indirect agonist|indirect activation|間接活化}}在大腦[[前額葉]]的{{tsl|en|dopamine receptor D1|多巴胺受體D1|多巴胺受體D<sub>1</sub>}}和{{tsl|en|Alpha-2 adrenergic receptor|Alpha-2 adrenergic receptor|腎上腺素受體 α<sub>2</sub>}}。{{r|Malenka_2009}}
{{r|Unambiguous PFC D1 A2}}一篇2014年的系統性回顧發現，低劑量（醫療用劑量）的安非他命能促進和穩固[[记忆巩固]]的过程，進而提升一個人[[回忆]]的能力。<ref name="Cognition enhancement 2014 systematic review">
{{cite journal|title=Efficacy of stimulants for cognitive enhancement in non-attention deficit hyperactivity disorder youth: a systematic review|date=April 2014|journal=Addiction|issue=4|doi=10.1111/add.12460|volume=109|pages=547–557|pmc=4471173|pmid=24749160|quote=Amphetamine has been shown to improve consolidation of information (0.02&nbsp;≥&nbsp;P&nbsp;≤&nbsp;0.05), leading to improved recall.|vauthors=Bagot KS, Kaminer Y}}</ref>低劑量（醫療用劑量）的安非他命也可增加大腦皮層（質）區的效率，這能讓一個人的工作記憶獲得進步。{{r|Malenka_2009}}<ref name="pmid11337538">
{{cite journal|title=Regional cerebral blood flow response to oral amphetamine challenge in healthy volunteers|date=April 2001|journal=J. Nucl. Med.|issue=4|volume=42|pages=535–542|pmid=11337538|vauthors=Devous MD, Trivedi MH, Rush AJ}}</ref>安非他命和其他用於治療ADHD的中樞神經刺激劑能透過提升{{tsl|en|Incentive salience|task saliency}}來增加一個人去做事情的動機、並強化一個人的警覺心（清醒度），因而能刺激一個人開始做「以目標為導向」的行為。{{r|Malenka_2009}}<ref name="Malenka NAcc">
{{cite book|vauthors=Malenka RC, Nestler EJ, Hyman SE|veditors=Sydor A, Brown RY|title=Molecular Neuropharmacology: A Foundation for Clinical Neuroscience|year=2009|publisher=McGraw-Hill Medical|location=New York, USA|isbn=9780071481274|page=266|edition=2nd|chapter=Chapter 10: Neural and Neuroendocrine Control of the Internal Milieu|quote=Dopamine acts in the nucleus accumbens to attach motivational significance to stimuli associated with reward.}}</ref><ref name="Continuum">
{{cite journal|title=Psychostimulants and cognition: a continuum of behavioral and cognitive activation|date=January 2014|journal=Pharmacol. Rev.|issue=1|doi=10.1124/pr.112.007054|volume=66|pages=193–221|pmid=24344115|vauthors=Wood S, Sage JR, Shuman T, Anagnostaras SG}}</ref>中樞神經興奮劑（例如：安非他命）能提升一個人在困難且枯燥的任務中的表現。{{r|Malenka_2009|Continuum}}<ref name="Test taking aid">{{cite web|title=Pills become an addictive study aid|url=http://www.jsonline.com/story/index.aspx?id=410902|accessdate=2007-12-02|author=Twohey M|date=2006-03-26|work=JS Online|archiveurl=https://web.archive.org/web/20070815200239/http://www.jsonline.com/story/index.aspx?id=410902|archivedate=2007-08-15|deadurl=no}}</ref>超過醫療用劑量範圍（包含其誤差範圍及容許最大上限）的安非他命劑量將不利於[[工作記憶]]和其他的[[認知]]功能。{{r|Malenka_2009|Continuum}}

;生理
雖然安非他命可以提升速度、[[耐力]]（延遲[[疲勞]]的發生）、肌耐力、[[身體素質]]和警覺心並減少[[心理反應時間]]。{{r|Ergogenics|Westfall}}<ref name="Ergogenics2">
{{cite journal|title=Attention-deficit hyperactivity disorder and the athlete: new advances and understanding|url=https://archive.org/details/sim_clinics-in-sports-medicine_2011-07_30_3/page/591|author=Parr JW|date=July 2011|journal=Clin. Sports Med.|issue=3|doi=10.1016/j.csm.2011.03.007|volume=30|pages=591–610|pmid=21658550|quote=In 1980, Chandler and Blair<sup>47</sup> showed significant increases in knee extension strength, acceleration, anaerobic capacity, time to exhaustion during exercise, pre-exercise and maximum heart rates, and time to exhaustion during maximal oxygen consumption (VO2 max) testing after administration of 15 mg of dextroamphetamine versus placebo. Most of the information to answer this question has been obtained in the past decade through studies of fatigue rather than an attempt to systematically investigate the effect of ADHD drugs on exercise.}}</ref><ref name="Roelands_2013">
{{cite journal|title=Neurophysiological determinants of theoretical concepts and mechanisms involved in pacing|date=May 2013|journal=Sports Med.|issue=5|doi=10.1007/s40279-013-0030-4|volume=43|pages=301–311|pmid=23456493|quote=In high-ambient temperatures, dopaminergic manipulations clearly improve performance. The distribution of the power output reveals that after dopamine reuptake inhibition, subjects are able to maintain a higher power output compared with placebo.&nbsp;... Dopaminergic drugs appear to override a safety switch and allow athletes to use a reserve capacity that is ‘off-limits’ in a normal (placebo) situation.|vauthors=Roelands B, de Koning J, Foster C, Hettinga F, Meeusen R}}</ref>然而，「非因醫療需求使用安非他命」在各種運動場合都是被嚴格禁止的。<ref name="NCAA">{{cite web|title=National Study of Substance Use Trends Among NCAA College Student-Athletes|url=http://www.ncaapublications.com/productdownloads/SAHS09.pdf|accessdate=2013-10-08|author=Bracken NM|date=January 2012|work=NCAA Publications|publisher=National Collegiate Athletic Association|archiveurl=https://web.archive.org/web/20200820030018/http://www.ncaapublications.com/productdownloads/SAHS09.pdf|archivedate=2020-08-20|deadurl=no}}</ref><ref name="WADA & AD regulation">
{{cite journal|title=Pharmacology of stimulants prohibited by the World Anti-Doping Agency (WADA)|author=Docherty JR|date=June 2008|journal=Br. J. Pharmacol.|issue=3|doi=10.1038/bjp.2008.124|volume=154|pages=606–622|pmc=2439527|pmid=18500382}}</ref>

安非他命藉由抑制多巴胺在中樞神經系統中的回收及外流來促進耐力和反應時間的提升。{{r|Ergogenics2|Roelands_2013}}<ref name="Amph-DA reaction time">
{{cite journal|title=Executive dysfunction in Parkinson's disease and timing deficits|date=October 2013|journal=Front. Integr. Neurosci.|doi=10.3389/fnint.2013.00075|volume=7|page=75|pmc=3813949|pmid=24198770|quote=Manipulations of dopaminergic signaling profoundly influence interval timing, leading to the hypothesis that dopamine influences internal pacemaker, or “clock,” activity. For instance, amphetamine, which increases concentrations of dopamine at the synaptic cleft advances the start of responding during interval timing, whereas antagonists of D2 type dopamine receptors typically slow timing;... Depletion of dopamine in healthy volunteers impairs timing, while amphetamine releases synaptic dopamine and speeds up timing.|vauthors=Parker KL, Lamichhane D, Caetano MS, Narayanan NS}}</ref>安非他命和其他作用於多巴胺系統的藥物一樣，都能增加在固定施力（{{tsl|en|rating of perceived exertion|levels of perceived exertion}}）下的動力（能）輸出。這是因為安非他命能奪取（override）體溫的「安全開關」的控制權並將[[人體溫度|身體核心溫度]]的上限提高以取得在體溫安全上限提高前被身體保留的能量。{{r|Roelands_2013}}<ref name="Central mechanisms affecting exertion">
{{cite journal|title=Is it time to turn our attention toward central mechanisms for post-exertional recovery strategies and performance?|date=March 2015|journal=Front. Physiol.|doi=10.3389/fphys.2015.00079|volume=6|pages=79|pmc=4362407|pmid=25852568|quote=Aside from accounting for the reduced performance of mentally fatigued participants, this model rationalizes the reduced RPE and hence improved cycling time trial performance of athletes using a glucose mouthwash (Chambers et al., 2009) and the greater power output during a RPE matched cycling time trial following amphetamine ingestion (Swart, 2009).&nbsp;... Dopamine stimulating drugs are known to enhance aspects of exercise performance (Roelands et al., 2008)|vauthors=Rattray B, Argus C, Martin K, Northey J, Driller M}}</ref><ref name="Monoamine+drug effects on exercise - fatigue and heat">
{{cite journal|title=Neurophysiological effects of exercise in the heat|date=June 2015|journal=Scand. J. Med. Sci. Sports|doi=10.1111/sms.12350|volume=25 Suppl 1|pages=65–78|pmid=25943657|quote=This indicates that subjects did not feel they were producing more power and consequently more heat. The authors concluded that the “safety switch” or the mechanisms existing in the body to prevent harmful effects are overridden by the drug administration (Roelands et al., 2008b). Taken together, these data indicate strong ergogenic effects of an increased DA concentration in the brain, without any change in the perception of effort.|vauthors=Roelands B, De Pauw K, Meeusen R}}</ref>於醫療用劑量範圍（包含其誤差範圍），安非他命的副作用不至於影響運動員的運動表現；{{r|Ergogenics|Ergogenics2}}然而，當攝取的劑量過多時，安非他命可能會引起嚴重的後果，例如：[[橫紋肌溶解症]]和[[高熱]](體溫過高)。{{r|FDA Abuse & OD|FDA Effect|Ergogenics2}}

==醫療上的禁忌==
{{see also|苯丙胺#交互作用}}
根據[[國際化學品安全規劃署]]（IPCS, International Programme on Chemical Safety）和[[美國食品藥物管理局]](USFDA)，{{efn-ur|美國食品藥物管理局核准的藥品使用指引及醫療上的禁忌（放在藥盒中的仿單/說明書）並非為了限制醫師的決策而是為了避免藥商恣意宣稱藥物的作用。醫師可以此為參考，並依照每位病人的實際情況做出獨立的判斷。
<ref name="pmid8545689">
{{cite journal 
| vauthors = Kessler S 
| title = Drug therapy in attention-deficit hyperactivity disorder 
| url = https://archive.org/details/sim_southern-medical-journal_1996-01_89_1/page/33
| journal = South. Med. J. 
| volume = 89 
| issue = 1 
| pages = 33–38 
| date = January 1996 
| pmid = 8545689 
|quote = statements on package inserts are not intended to limit medical practice. Rather they are intended to limit claims by pharmaceutical companies.&nbsp;... the FDA asserts explicitly, and the courts have upheld that clinical decisions are to be made by physicians and patients in individual situations. | doi=10.1097/00007611-199601000-00005}}</ref>}}安非他命不建議處方給有[[物質濫用|藥物濫用]]、[[心血管疾病]]、對於各種刺激嚴重[[Agitation|反應過度]]、和嚴重[[焦慮]]歷史的人。{{efn-ur|然而根據一篇回顧性論文，安非他命可以處方給曾有藥物濫用歷史的人，不過需要有對患者適度的藥品控管，例如：每天由醫護人員配給處方劑量。{{r|Amph Uses}}}}{{r|FDA Contra Warnings}}<ref name="International">{{cite web|title=Amphetamine (PIM 934)|url=http://www.inchem.org/documents/pims/pharm/pim934.htm|accessdate=2014-06-24|website=INCHEM|publisher=International Programme on Chemical Safety|archiveurl=https://web.archive.org/web/20190418052642/http://www.inchem.org/documents/pims/pharm/pim934.htm|archivedate=2019-04-18|deadurl=no|vauthors=Heedes G, Ailakis J}}</ref>安非他命也不被建議處方給正經歷[[動脈血管硬化]]（血管硬化）、中度到重度[[高血壓]]、[[青光眼]]（眼壓過高）、或[[甲狀腺機能亢進]]（身體在體內製造出過量的甲狀腺[[賀爾蒙]]/[[激素]]）的人。{{r|FDA Contra Warnings|International|Dexedrine FDA}}曾對[[中樞神經刺激劑]]有[[超敏反應|藥物過敏]]的人以及正在服用[[单胺氧化酶抑制剂|單胺氧化酶抑制劑]](MAOI)或單胺氧化酶抑制劑類藥物(MAOIs)，可能不適合使用安非他命。即便曾有合併使用安非他命和單胺氧化酶抑制劑後仍一切平安的案例。{{r|FDA Contra Warnings|International}}<ref name="Review MAOI-amph">
{{cite journal|title=Combining stimulants with monoamine oxidase inhibitors: a review of uses and one possible additional indication|url=https://archive.org/details/sim_journal-of-clinical-psychiatry_2004-11_65_11/page/1520|date=November 2004|journal=J. Clin. Psychiatry|issue=11|doi=10.4088/jcp.v65n1113|volume=65|pages=1520–1524|pmid=15554766|vauthors=Feinberg SS}}</ref><ref name="Primary MAOI-amph">
{{cite journal|title=How treatable is refractory depression?|date=June 2014|journal=J. Affect. Disord.|doi=10.1016/j.jad.2014.05.047|volume=167|pages=148–152|pmid=24972362|vauthors=Stewart JW, Deliyannides DA, McGrath PJ}}</ref>
 
IPCS和美國食品藥物管理局也同意患有[[神經性厭食症]]、[[雙極性情感疾患]]、[[憂鬱]]、[[高血壓]]、[[狂躁]]、[[思覺失調症]]、[[雷諾氏症候群]]、[[癲癇發作]]、[[抽動綜合症]]、[[妥瑞氏症]]、和有[[甲狀腺]]問題、[[肝]][[腎]]問題的人在使用安非他命時應密切追蹤上述疾病的變化。{{r|FDA Contra Warnings|International}}

人體試驗證明，醫療用劑量下的安非他命並不會導致胎兒或新生兒畸形。然而超越醫療用劑量甚多的安非他命確實會增加胎兒或新生兒畸形的機會。{{r|International}}

研究觀察發現，安非他命會進入母親的母乳中，因此建議母親不要在使用安非他命藥物的期間內授乳。{{r|FDA Contra Warnings|International}}

由於安非他命可能影響食慾繼而導致可反轉的身高及體重的成長遲緩，{{efn-ur|曾受此副作用的用藥者，身高及體重在在短暫停藥後恢復至應有水準是可以被預期的。{{r|Millichap|Long-Term Outcomes Medications|pmid18295156}}
根據追蹤，持續三年過程不停歇的安非他命治療（沒有合併任何積極減少安非他命副作用的療法的情況下）平均會減少 2公分的最終身高。

{{r|pmid18295156}}|group="note"}}，因此建議兒童或青少年在用藥期間定期測量自己的身高及體重。{{r|FDA Contra Warnings}}

==副作用==
安非他命的[[副作用]]以及其發生率和嚴重度大致上與使用的劑量呈正相關。{{r|FDA Abuse & OD|FDA Effects|Westfall}}成分為安非他命的藥品，諸如：[[阿得拉尔]]、Dexedrine、和安非他命的<u>{{le|等價|equivalent}}物質（generic equivalents）</u>目前皆已獲得[[美國食品藥物管理署]]許可用於長期性的治療。{{r|FDA Effects|NDCD}}

攝取大幅超出醫療劑量的安非他命將大幅增加嚴重副作用出現的風險。{{r|Westfall}}

===生理===
在治療劑量下，生理副作用會因年齡或個人情況而有所不同{{r|FDA Effects}}。[[循环系统|心血管]]方面的副作用包含：{{le|迷走-血管反射|vasovagal response}}導致的[[高血壓]]或是[[低血壓]]、[[雷諾氏症]]（因小動脈收縮而導致流往手腳的血流減少）、以及[[心搏過速]]（tachycardia）。{{r|FDA Effects|Westfall}}<ref name="pmid18295156">{{cite journal |author=Vitiello B |title=Understanding the risk of using medications for attention deficit hyperactivity disorder with respect to physical growth and cardiovascular function |journal=Child Adolesc. Psychiatr. Clin. N. Am. |volume=17 |issue=2 |pages=459–474 |date=April 2008 |pmid=18295156 |pmc=2408826 |doi=10.1016/j.chc.2007.11.010 }}</ref>

男性性方面而言，副作用可能包含：[[勃起障礙]]、頻繁勃起、或是[[阴茎异常勃起|勃起时间过长]]。{{r|FDA Effects}}

消化方面的副作用可能包含：[[腹痛]]、[[喪失胃口]]、[[反胃]]以及[[體重降低]]。{{r|FDA Effects}}<ref name="Dyanavel">{{cite web |title=Dyanavel XR Prescribing Information |url=http://www.trispharma.com/DXRUSPI.pdf |publisher=Tris Pharmaceuticals |accessdate=2015-11-23 |pages=1–16 |date=October 2015 |quote=DYANAVEL XR contains d-amphetamine and l-amphetamine in a ratio of 3.2 to 1&nbsp;... The most common (≥2% in the DYANAVEL XR group and greater than placebo) adverse reactions reported in the Phase 3 controlled study conducted in 108 patients with ADHD (aged 6–12 years) were: epistaxis, allergic rhinitis and upper abdominal pain.&nbsp;... <br>DOSAGE FORMS AND STRENGTHS<br>Extended-release oral suspension contains 2.5 mg amphetamine base per mL. |deadurl=yes |archiveurl=https://web.archive.org/web/20161013103757/http://www.trispharma.com/DXRUSPI.pdf |archivedate=2016-10-13 }}</ref>其他潛在的副作用包含：[[視力模糊]]、[[口乾]]、[[磨牙]]、流鼻血、[[多汗症]]、{{le|藥物性鼻炎|rhinitis medicamentosa}}（藥物導致的[[鼻塞]]）、{{le|癲癇閾值|seizure threshold|癲癇閾值/觸發門檻}}降低，以及[[抽搐]]{{refn|group=來源組|{{r|FDA Effects|Westfall|pmid18295156|Dyanavel|rhinitis}}}}。在一般的治療劑量下鮮少發生危險副作用{{r|Westfall}}。

安非他命刺激{{le|呼吸中枢|Respiratory center|延腦的呼吸中樞}}，使得呼吸變得較快速且較深。<ref name="Westfall">{{cite book |veditors=Brunton LL, Chabner BA, Knollmann BC |title=Goodman & Gilman's Pharmacological Basis of Therapeutics |year=2010 |publisher=McGraw-Hill |location=New York, USA |isbn=9780071624428 |vauthors=Westfall DP, Westfall TC |section=Miscellaneous Sympathomimetic Agonists |edition=12th }}</ref>正常人在治療劑量下，此作用通常難以察覺；然而，此作用在呼吸已經受損的病人身上有可能變得明顯。{{r|Westfall}}

安非他命會使[[膀胱括約肌]][[肌肉收缩|收縮]]，而導致解尿困難{{r|Westfall}}。此效果可以應用在[[遺尿]]或是[[尿失禁|失去膀胱控制能力]]的病人身上。{{r|Westfall}}

安非它命在胃腸道的作用是難以預測的{{r|Westfall}}。安非他命可能會減少{{le|胃腸活動力|gastrointestinal motility}}（內容物通過腸胃道的速率）{{r|Westfall}}；然而，安非他命亦可能在胃腸道的[[平滑肌]]處於鬆弛狀態時，增加其活動力。{{r|Westfall}}

安非他命有輕微的[[止痛]]作用且可以增強鴉片類物質的止痛作用。{{r|Westfall}}

美國食藥署2011年委任的研究發現：不論是小孩或是成人，「安非他命（於醫療情境下使用）」和「其他用於治療ADHD的中樞神經興奮劑」均和重大的心血管疾病（[[猝死]]、[[心臟病發]]、[[中風]]）無關{{refn|group=來源組|{{r|FDA - cardiovascular effects in young individuals|pmid22043968|FDA - cardiovascular effects in adults|pmid22161946}}}}；然而，當病患已有心血管方面的疾病時，禁用此藥。{{refn|group=來源組|{{r|FDA Contra Warnings|International|FDA - cardiovascular effects in young individuals|FDA - cardiovascular effects in adults}}}}

===心理===
在醫療用劑量範圍，最常見的[[副作用]]為：[[警覺心]]的增強、（對未來或即將發生的不愉快之事的）憂慮/擔心/恐懼、[[理解|理解力]]提升、[[專注力]]的提升、主動性/自主決斷行事的能力的提升、[[自信|自信心]]的提升、社交能力的提升；情緒陰晴不定、[[失眠]]或[[清醒]]、和[[疲勞|疲勞感]]的減退。{{r|FDA Effects|Westfall}}

比較少見的副作用包括[[焦慮]]、[[性慾]]改變、[[应激性]]、重複性的或強迫性的行為（repetitive or {{le|obsessive|Fixation (psychology)}} behaviors）、靜不下來;{{refn|group=來源組|{{r|Libido|FDA Effects|Westfall|Merck_Manual_Amphetamines}}}}。副作用出現與否因人而異，端視用藥者的[[個性]]及精神狀態（mental state）。

安非他命所引起的精神疾病，例如：[[妄想]]和[[偏執]]，可能出現在重度的使用者身上。<ref name="FDA Abuse & OD">{{cite web |title=Adderall XR Prescribing Information |url=http://www.accessdata.fda.gov/drugsatfda_docs/label/2013/021303s026lbl.pdf |page=11 |publisher=Shire US Inc |work=United States Food and Drug Administration |date=December 2013 |accessdate=2013-12-30 |archivedate=2018-07-18 |archiveurl=https://web.archive.org/web/20180718220437/https://www.accessdata.fda.gov/drugsatfda_docs/label/2013/021303s026lbl.pdf |deadurl=no }}</ref><ref name="FDA Effects">{{cite web |title=Adderall XR Prescribing Information |url=http://www.accessdata.fda.gov/drugsatfda_docs/label/2013/021303s026lbl.pdf |pages=4–8 |publisher=Shire US Inc |work=United States Food and Drug Administration |date=December 2013 |accessdate=2013-12-30 |archivedate=2018-07-18 |archiveurl=https://web.archive.org/web/20180718220437/https://www.accessdata.fda.gov/drugsatfda_docs/label/2013/021303s026lbl.pdf |deadurl=no }}</ref>{{r|Cochrane}}長期攝取醫療劑量的安非他命雖然有可能引起上一段文中所述的疾病，但這是[[副作用|非常罕見]]的。{{r|FDA Abuse & OD|FDA Effects}}<ref name="Stimulant Misuse">{{cite web |author=Greydanus D |title=Stimulant Misuse: Strategies to Manage a Growing Problem |type=Review Article |url=http://www.acha.org/prof_dev/ADHD_docs/ADHD_PDprogram_Article2.pdf |archiveurl=https://web.archive.org/web/20131103155156/http://www.acha.org/prof_dev/ADHD_docs/ADHD_PDprogram_Article2.pdf |work=American College Health Association |publisher=ACHA Professional Development Program |accessdate=2013-11-02 |archivedate=2013-11-03 |page=20 |deadurl=yes }}</ref>根據[[美國食品藥物管理局]]所提供的資訊，「目前沒有證據顯示『[[中樞神經刺激劑]]』會導致『攻擊性的行為（aggressive behavior）』或『敵意（hostility）』」。{{r|FDA Effects}}

使用醫療劑量的用藥者可能會培養出習慣在某個特定地方用藥的偏好。{{r|Cochrane Amphetamines ADHD}}<ref name="Human CPP">{{cite journal |vauthors=Childs E, de Wit H |title=Amphetamine-induced place preference in humans |journal=Biol. Psychiatry |volume=65 |issue=10 |pages=900–904 |date=May 2009 |pmid=19111278 |pmc=2693956 |doi=10.1016/j.biopsych.2008.11.016 |quote=This study demonstrates that humans, like nonhumans, prefer a place associated with amphetamine administration. These findings support the idea that subjective responses to a drug contribute to its ability to establish place conditioning.}}</ref>{{r|Human CPP|Addiction glossary}}
<!--{{see also|{{le|conditioned place preference}}}}-->

==法律==
安非他命在中華民國受毒品危害防制條例管制，若無處方箋，在司法上視為第二級[[管制藥品]]，持有、運輸、販賣皆為違法行為。<ref>{{Cite web |title=毒品危害防制條例 |url=https://law.moj.gov.tw/LawClass/LawAll.aspx?PCode=C0000008 |website=全國法規資料庫 |publisher=中華民國法務部 |access-date=2022-09-05 |archive-date=2019-06-11 |archive-url=https://web.archive.org/web/20190611153517/https://law.moj.gov.tw/LawClass/LawAll.aspx?pcode=C0000008 |dead-url=no }}</ref>

==嚴重過量==
安非他命過量使用會引起許多症狀，然而在適當的醫療照護下，不至於死亡。{{r|International}}<ref name="Amphetamine toxidrome">{{cite journal |vauthors=Spiller HA, Hays HL, Aleguas A |title=Overdose of drugs for attention-deficit hyperactivity disorder: clinical presentation, mechanisms of toxicity, and management |journal=CNS Drugs |volume=27| issue=7| pages=531–543|date=June 2013 |pmid=23757186 |doi=10.1007/s40263-013-0084-8 |quote=Amphetamine, dextroamphetamine, and methylphenidate act as substrates for the cellular monoamine transporter, especially the dopamine transporter (DAT) and less so the norepinephrine (NET) and serotonin transporter. The mechanism of toxicity is primarily related to excessive extracellular dopamine, norepinephrine, and serotonin.}}</ref>

藥物過量症狀的嚴重度與劑量成正比；與身體對安非他命的[[藥物耐受性]]成反比。{{r|Westfall|International}}已知每天攝取達到5公克的安非他命（每天最大攝取量的五十倍）會導致身體對安非他命產生藥物耐受性。{{r|International}}嚴重過量的安非他命攝取所致的症狀列於下方；安非他命中毒一旦到達出現全身[[抽搐]]和[[昏迷]]則必須立刻急救以避免死亡。{{r|FDA Abuse & OD|Westfall}}在2013年，安非他命、甲基安非他命和其他列於[[ICD-10 第五章：精神和行为障碍#.E4.BD.BF.E7.94.A8.E5.8C.96.E5.AD.B8.E8.97.A5.E7.89.A9.E3.80.81.E7.89.A9.E8.B3.AA.E6.88.96.E9.85.92.E7.B2.BE.E5.BC.95.E8.B5.B7.E7.9A.84.E7.B2.BE.E7.A5.9E.E5.92.8C.E8.A1.8C.E7.82.BA.E9.9A.9C.E7.A4.99|ICD-10 第五章：精神和行為障礙§使用化學藥物、物質或酒精引起的精神和行為障礙]]中的安非他命相關物質的過量使用在世界上共導致3788人死亡。(3,425–4,145人死亡、95%[[信賴區間]]）。{{efn-ur|「95% 信賴區間」指的是：有95%的機率，真實的死亡人數介於3,425 和 4,145 之間。}}<ref name=GDB2013>{{cite journal |vauthors=Collaborators |title=Global, regional, and national age-sex specific all-cause and cause-specific mortality for 240 causes of death, 1990–2013: a systematic analysis for the Global Burden of Disease Study 2013 |journal=Lancet |volume=385 |issue=9963 |pages=117–171 |year=2015 |pmid=25530442 |pmc=4340604 |doi=10.1016/S0140-6736(14)61682-2 |url=http://www.thelancet.com/cms/attachment/2023546115/2043770889/mmc1.pdf |accessdate=2015-03-03 |quote=Amphetamine use disorders&nbsp;... 3,788&nbsp;(3,425–4,145) }}</ref>

被過度活化達到病態程度的{{tsl|en|mesolimbic pathway|中腦邊緣迴路}}（一個連接[[腹側被蓋區]]和[[伏隔核]]的{{tsl|en|dopamine pathway|多巴胺通道}}），在安非他命的成癮中扮演著主要的角色。<ref name="Amphetamine KEGG – ΔFosB">{{cite web 
| title=Amphetamine – Homo sapiens (human) 
| url=http://www.genome.jp/kegg-bin/show_pathway?hsa05031 
| work=KEGG Pathway 
| accessdate=2014-10-31 
| author=Kanehisa Laboratories 
| date=2014-10-10 
| archivedate=2020-08-08 
| archiveurl=https://web.archive.org/web/20200808064501/https://www.genome.jp/kegg-bin/show_pathway?hsa05031 
| deadurl=no 
}}</ref>{{r|Magnesium}}

當一個人經常服用嚴重過量的安非他命，將伴隨安非他命成癮的高度風險，因為持續過量的安非他命會逐漸增加[[伏隔核]]的[[ΔFosB]]（「成癮」與否的分子開關和主控蛋白）的檔次。{{r|What the ΔFosB?|Cellular basis}}<ref name="Nestler_1">{{cite journal |vauthors=Robison AJ, Nestler EJ |title=Transcriptional and epigenetic mechanisms of addiction |journal=Nat. Rev. Neurosci. |volume=12 |issue=11 |pages=623–637 |date=November 2011 |pmid=21989194 |pmc=3272277 |doi=10.1038/nrn3111 |quote=ΔFosB serves as one of the master control proteins governing this structural plasticity.}}</ref>一旦伏隔核的ΔFosB過度表達，這個人的{{nowrap|「成癮性行為」}}{{NoteTag|1=因成癮所致的行為}}（例如：出現試圖取得安非他命的衝動行為）將開始隨之增加。<ref name="What the ΔFosB?">{{cite journal |author=Ruffle JK |title=Molecular neurobiology of addiction: what's all the (Δ)FosB about? |journal=Am. J. Drug Alcohol Abuse |volume=40 |issue=6 |pages=428–437 |date=November 2014 |pmid=25083822 |doi=10.3109/00952990.2014.933840 |quote=ΔFosB is an essential transcription factor implicated in the molecular and behavioral pathways of addiction following repeated drug exposure. }}</ref>{{r|Natural and drug addictions}}雖然目前沒有治療安非他命成癮的有效藥物，但規律的且每次都有持續一定時間的[[有氧運動]]能降低安非他命的成癮風險也是治療安非他命成癮的天然療法。{{r|Running vs addiction}}<ref name="Exercise, addiction prevention, and ΔFosB">{{cite journal |vauthors=Zhou Y, Zhao M, Zhou C, Li R |title=Sex differences in drug addiction and response to exercise intervention: From human to animal studies |journal=Front. Neuroendocrinol. |date=July 2015 |pmid=26182835 |doi=10.1016/j.yfrne.2015.07.001 |volume=40 |pages=24–41 |quote=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.&nbsp;... The postulate that exercise serves as an ideal intervention for drug addiction has been widely recognized and used in human and animal rehabilitation.}}</ref>{{refn|group=來源組|name="Exercise therapy"}}運動能提升{{tsl|en|clinical therapy|臨床治療}}的[[預後]]，且可能與[[認知行為治療]]（目前已知最有效的安非他命成癮的臨床治療法）相搭配為[[联合疗法]]。{{r|Running vs addiction|Exercise Rev 3|Nestler CBT}}
{| class="wikitable"
|+ 嚴重過量的安非他命劑量所致的症狀（依照體內生物系統分類）
! style="text-align:center"| 生物系統
!輕度、中度過量{{r|FDA Abuse & OD|Westfall|International}}
! 過量{{refn|group=來源組|{{r|Acute amph toxicity|FDA Abuse & OD|Westfall|Amphetamine toxidrome|Albertson_2011}}}}
|-
! [[心臟血管系統]]
|
* [[心律不整]]
* [[高血壓]]或[[低血壓]]
|
* [[心源性休克]]（心臟無法輸出足夠的血液）
* [[腦部大出血]]
* {{tsl|en|Circulatory collapse|循環系統衰竭}}（部分或全部的[[循環系統]]失去功能）
|-
! [[中樞神經系統]]
|
* 意识混浊
* {{tsl|en|Hyperreflexia|反射亢進}}（異常快速的反射）
* 嚴重的躁動
* [[顫抖]]（不自主的肌肉顫動）
|
* {{tsl|en|Stimulant psychosis#Substituted amphetamines|興奮劑精神病|急性安非他命中毒引起的嚴重精神病}}（例如[[妄想]]和[[偏執]]）
* {{tsl|en|Stereotypy|常同症|衝動的、突然的、重複的動作}}
* [[血清素#血清素綜合徵|血清素綜合症]]
* {{tsl|en|Sympathomimetic toxidrome|擬交感神經毒素}}
|-
! [[肌肉骨骼系统]]
|
* [[肌肉痠痛]]
|
* [[橫紋肌溶解症]]（快速的肌肉溶解）
|-
! [[呼吸系統]]
|
* 呼吸過速
|
* [[肺水腫]]（肺部積水）
* [[肺高壓]]（[[肺動脈]]的高血壓）
* [[呼吸性鹼中毒]]（血液中二氧化碳濃度異常減少）
|-
! [[生殖泌尿系統]]
|
* [[排尿疼痛]]
* [[尿液滯留]]（較不易排尿）
|
* [[無尿症]]
* [[腎功能衰竭|腎臟衰竭]]
|-
! 其他
|
* [[高熱|體溫升高]]
* [[瞳孔放大]]
|
* [[高鉀血症|高]]或[[钾#低血鉀（Hypokalemia）|低血鉀]]
* [[发热#分类（以口测法为准）|重度高燒]]
* {{tsl|en|Metabolic acidosis|代謝性酸中毒}}
|}

===成癮===
{{Addiction glossary}}
{{Psychostimulant addiction|align=right|header=
造成安非他命成癮的位於[[伏隔核]]中的[[signal casacade|訊息傳遞]]
}}
長期服用遠超醫療用劑量範圍的安非他命會導致安非他命[[成癮]]。然而長期攝取醫療劑量範圍的安非他命並不會引起上述問題。<ref name="NHM-Addiction doses">{{cite book |vauthors=Malenka RC, Nestler EJ, Hyman SE |editor=Sydor A, Brown RY |title=Molecular Neuropharmacology: A Foundation for Clinical Neuroscience |year=2009 |publisher=McGraw-Hill Medical |location=New York |isbn=9780071481274 |page=368 |edition=2nd |chapter=Chapter 15: Reinforcement and Addictive Disorders |quote= Such agents also have important therapeutic uses; cocaine, for example, is used as a local anesthetic (Chapter 2), and amphetamines and methylphenidate are used in low doses to treat attention deficit hyperactivity disorder and in higher doses to treat narcolepsy (Chapter 12). Despite their clinical uses, these drugs are strongly reinforcing, and their long-term use at high doses is linked with potential addiction, especially when they are rapidly administered or when high-potency forms are given.}}</ref><ref name="Addiction risk">{{cite journal |vauthors=Kollins SH |title=A qualitative review of issues arising in the use of psycho-stimulant medications in patients with ADHD and co-morbid substance use disorders |journal=Curr. Med. Res. Opin. |volume=24 |issue=5 |pages=1345–1357 |date=May 2008 |pmid=18384709 |doi=10.1185/030079908X280707 |quote=When oral formulations of psychostimulants are used at recommended doses and frequencies, they are unlikely to yield effects consistent with abuse potential in patients with ADHD.}}</ref><ref name="EncycOfPsychopharm">{{Cite book |author=Stolerman IP |editor=Stolerman IP |title=Encyclopedia of Psychopharmacology |year=2010 |publisher=Springer |location=Berlin, Germany; London, England |isbn=9783540686989 |page=78}}</ref>{{if pagename |Lisdexamfetamine= Compared to other amphetamine pharmaceuticals, lisdexamfetamine may have a lower liability for abuse as a recreational drug.<ref name="LDX abuse">{{cite journal |vauthors=Coghill DR, Caballero B, Sorooshian S, Civil R |title=A systematic review of the safety of lisdexamfetamine dimesylate |journal=CNS Drugs |volume=28 |issue=6 |pages=497–511 |date=June 2014 |pmid=24788672 |pmc=4057639 |doi=10.1007/s40263-014-0166-2 |quote=The prodrug formulation of LDX may also lead to reduced abuse potential of LDX compared with immediate-release d-AMP. }}</ref>| other=}}安非他命濫用（例如：長期攝取嚴重過量的安非他命）會導致大腦對於該劑量產生[[藥物耐受性]]。漸漸地，濫用者必須服用更大量的安非他命以換取同樣的效果。<ref>{{cite web |title=Amphetamines: Drug Use and Abuse |work=Merck Manual Home Edition |publisher=Merck |url=http://www.merckmanuals.com/home/special_subjects/drug_use_and_abuse/amphetamines.html |accessdate=2007-02-28 |archiveurl=https://web.archive.org/web/20070217053619/http://www.merck.com/mmhe/sec07/ch108/ch108g.html |date=February 2003 |archivedate=2007-02-17 |deadurl=no }}</ref><ref>{{cite journal |vauthors=Perez-Mana C, Castells X, Torrens M, Capella D, Farre M |title=Efficacy of psychostimulant drugs for amphetamine abuse or dependence |journal=Cochrane Database Syst. Rev. |volume=9 |pages=CD009695 |date=September 2013 |pmid=23996457 |doi=10.1002/14651858.CD009695.pub2 |editor=Pérez-Mañá C}}</ref>

====分子生物機轉====
當前關於「長期安非他命濫用所致的成癮」的[[模型]]中，已知會改變一些腦部的結構（特別是[[伏隔核]]）<ref name="Nestler, Hyman, and Malenka 2">{{cite journal |vauthors=Hyman SE, Malenka RC, Nestler EJ |title=Neural mechanisms of addiction: the role of reward-related learning and memory |journal=Annu. Rev. Neurosci. |volume=29 |pages=565–598 |date=July 2006 |pmid=16776597 |doi=10.1146/annurev.neuro.29.051605.113009}}</ref>{{r|Nestler|Addiction genetics}}。造成腦部結構改變的最重要的[[轉錄因子]]（transcription factor）為：[[ΔFosB]]、[[cAMP]]反应元件结合蛋白({{tsl|en|cAMP response element binding protein|CREB}})、和核因子κB([[NF-κB]])。{{efn-ur|
轉錄因子是一種可以增加或降低一個特定基因的[[基因表現]]的蛋白。<ref name="NHM-Transcription factor">{{cite book |vauthors=Malenka RC, Nestler EJ, Hyman SE |veditors=Sydor A, Brown RY |title=Molecular Neuropharmacology: A Foundation for Clinical Neuroscience |year=2009 |publisher=McGraw-Hill Medical |location=New York, USA |isbn=9780071481274 |page=94 |edition=2nd |chapter=Chapter 4: Signal Transduction in the Brain}}</ref>}}{{r|Nestler}}ΔFosB在藥物成癮的發展過程中扮演著至關重要的角色，主要的原因在於其在伏隔核中{{tsl|en|D1-type}}[[中型多棘神经元]]的过度表达，為「成癮」及「成癮衍生的行為」及「神經元為了適應新常態所做的調適」的[[充分且必要條件]]。{{efn-ur|簡單來說，這裡的「[[充分且必要]]（necessary and sufficient）」關係指的是「ΔFosB在伏隔核中的過度表達（over-expression）」與「成癮衍生的行為」及「神經元為了適應新常態所做的調適」永遠都是一起發生。}}{{r|What the ΔFosB?|Cellular basis|Nestler}}

一旦ΔFosB充分<u>过度表达（sufficiently overexpressed）</u>，將誘發越來越嚴重的成癮狀態並伴隨ΔFosB值的持續創新高。{{r|What the ΔFosB?|Cellular basis}}ΔFosB已被證明與[[酗酒|酒精成癮]]、[[大麻成癮]]、[[古柯鹼]]成癮、[[派醋甲酯]]成癮、[[尼古丁]]成癮、[[鴉片]]成癮、{{tsl|en|phencyclidine}}成癮、[[異丙酚]]、和{{tsl|en|substituted amphetamines|安非他命的替代性物質}}成癮、及其他成癮有關。{{refn|group=來源組|{{r|What the ΔFosB?|Natural and drug addictions|Nestler|Alcoholism ΔFosB|MPH ΔFosB}}}}{{tsl|en|ΔJunD}}為一個轉錄因子；而{{tsl|en|EHMT2|G9a}}為[[組織蛋白甲基轉移酶]]的一種。{{tsl|en|ΔJunD}}和{{tsl|en|EHMT2|G9a}}直接與伏隔核中的ΔFosB值的升高成反比。{{r|Cellular basis|Nestler}}<ref name="Nestler 2014 epigenetics">{{cite journal |vauthors=Nestler EJ |title=Epigenetic mechanisms of drug addiction |journal=Neuropharmacology |volume=76 Pt B |pages=259–268 |date=January 2014 |pmid=23643695 |pmc=3766384 |doi=10.1016/j.neuropharm.2013.04.004 }}</ref>

利用[[病毒載體|載體]]讓伏隔核中的ΔJunD充分過度表達，可以使由長期藥物濫用所致的漸進式神經元和行為改變完全停止。（比如說：ΔFosB所致的改變）。{{r|Nestler}}ΔFosB也在人們於{{tsl|en|natural reward|天然酬賞}}（natural rewards）中的行為反應調節上扮演重要的腳色。天然���賞包含：美味的食物、性愛、運動......。{{r|Natural and drug addictions|Nestler}}<ref name="ΔFosB reward">{{cite journal |vauthors=Blum K, Werner T, Carnes S, Carnes P, Bowirrat A, Giordano J, Oscar-Berman M, Gold M |title=Sex, drugs, and rock 'n' roll: hypothesizing common mesolimbic activation as a function of reward gene polymorphisms |journal=J. Psychoactive Drugs |volume=44 |issue=1 |pages=38–55 |date=March 2012 |pmid=22641964 |pmc=4040958 |doi=10.1080/02791072.2012.662112| quote=<!-- 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.&nbsp;... 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.&nbsp;... 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. -->}}</ref>因為天然酬賞以及成癮性藥物皆會{{tsl|en|inducible gene|激發}}ΔFosB（這些酬賞讓大腦刺激ΔFosB的增加），長期過度地從事上述行為將可能導致類似的成癮之病理生理（pathological）。{{r|Natural and drug addictions}}<ref name="Nestler">{{cite journal |vauthors=Robison AJ, Nestler EJ |title=Transcriptional and epigenetic mechanisms of addiction |journal=Nat. Rev. Neurosci. |volume=12 |issue=11 |pages=623–637 |date=November 2011 |pmid=21989194 |pmc=3272277 |doi=10.1038/nrn3111 |quote=<!-- ΔFosB has been linked directly to several addiction-related behaviors&nbsp;... Importantly, genetic or viral overexpression of ΔJunD, a dominant negative mutant of JunD which antagonizes ΔFosB- and other AP-1-mediated transcriptional activity, in the NAc or OFC blocks these key effects of drug exposure<sup>14,22–24</sup>. This indicates that ΔFosB is both necessary and sufficient for many of the changes wrought in the brain by chronic drug exposure. ΔFosB is also induced in D1-type NAc MSNs by chronic consumption of several natural rewards, including sucrose, high fat food, sex, wheel running, where it promotes that consumption<sup>14,26–30</sup>. This implicates ΔFosB in the regulation of natural rewards under normal conditions and perhaps during pathological addictive-like states. --> }}</ref>

ΔFosB是導致「安非他命成癮」、「安非他命引起的性成癮」中最關鍵的致癮因素。「安非他命引起的[[性成癮]]」為「安非他命使用」加上「過度的性活動」所引發的「衝動之下的性行為」。{{r|Natural and drug addictions}}<ref name="Amph-Sex X-sensitization through D1 signaling"><!--Supplemental primary source-->{{cite journal |vauthors=Pitchers KK, Vialou V, Nestler EJ, Laviolette SR, Lehman MN, Coolen LM |title=Natural and drug rewards act on common neural plasticity mechanisms with ΔFosB as a key mediator |journal=J. Neurosci. |volume=33 |issue=8 |pages=3434–3442 |date=February 2013 |pmid=23426671 |pmc=3865508 |doi=10.1523/JNEUROSCI.4881-12.2013}}</ref><ref name="Amph-Sex X-sensitization through NMDA signaling"><!--Supplemental primary source-->{{cite journal |vauthors=Beloate LN, Weems PW, Casey GR, Webb IC, Coolen LM |title=Nucleus accumbens NMDA receptor activation regulates amphetamine cross-sensitization and deltaFosB expression following sexual experience in male rats |journal=Neuropharmacology |volume=101 |pages=154–164 |date=February 2016 |pmid=26391065 |doi=10.1016/j.neuropharm.2015.09.023}}</ref>這類的性成癮與{{tsl|en|dopamine dysregulation syndrome|多巴胺失調症候群}}相關，有時此症會出現在正在服用{{tsl|en|dopaminergic#Supplements and drugs|dopaminergic drugs|作用於多巴胺的藥物}}的人身上。{{r|Natural and drug addictions|ΔFosB reward}}

安非他命基因调控（gene regulation）的效果端視劑量與通路（dose- and route-dependent）而定。<ref name="Addiction genetics">{{cite journal |vauthors=Steiner H, Van Waes V |title=Addiction-related gene regulation: risks of exposure to cognitive enhancers vs. other psychostimulants |journal=Prog. Neurobiol. |volume=100 |pages=60–80 |date=January 2013 |pmid=23085425 |pmc=3525776 |doi=10.1016/j.pneurobio.2012.10.001 }}</ref>絕大多數主題為「基因調節（gene regulation）」和「成癮」的研究都是透過動物試驗以及利用靜脈注射的方式對實驗動物注射超高劑量的安非他命來進行。{{r|Addiction genetics}}少數幾個透過人體試驗（依照體重來決定醫療用劑量）來進行的研究表明，<u>口服醫療用劑量</u>的安非他命並不會影響基因调控，即便有，也是極為輕微的。這表示安非他命用作醫療用途是十分安全的。{{r|Addiction genetics}}

====藥物治療====
{{Further information|成癮#研究}}
{{As of|2014|5}}並沒有能夠有效治療安非他命成癮的[[藥理療法]]<ref name="pmid24716825">{{cite journal |vauthors=Stoops WW, Rush CR |title=Combination pharmacotherapies for stimulant use disorder: a review of clinical findings and recommendations for future research |journal=Expert Rev Clin Pharmacol |volume=7 |issue=3 |pages=363–374 |date=May 2014 |pmid=24716825 |doi=10.1586/17512433.2014.909283 |quote=Despite concerted efforts to identify a pharmacotherapy for managing stimulant use disorders, no widely effective medications have been approved. |pmc=4017926 }}</ref><ref name="Cochrane 2013 treatments">{{cite journal |vauthors=Perez-Mana C, Castells X, Torrens M, Capella D, Farre M |title=Efficacy of psychostimulant drugs for amphetamine abuse or dependence |journal=Cochrane Database Syst. Rev. |volume=9 |pages=CD009695 |date=September 2013 |pmid=23996457 |doi=10.1002/14651858.CD009695.pub2 |quote=To date, no pharmacological treatment has been approved for [addiction], and psychotherapy remains the mainstay of treatment.&nbsp;... Results of this review do not support the use of psychostimulant medications at the tested doses as a replacement therapy}}</ref><ref name="pmid23039267">{{cite journal |vauthors=Forray A, Sofuoglu M |title=Future pharmacological treatments for substance use disorders |journal=Br. J. Clin. Pharmacol. |volume=77 |issue=2 |pages=382–400 |date=February 2014 |pmid=23039267 |pmc=4014020 |doi=10.1111/j.1365-2125.2012.04474.x }}</ref>。2015年到2016年間的論文回顧結果指出：選擇性{{tsl|en|TAAR1}}[[激动剂|促進劑]]有非常大的可能在將來被用來治療[[中樞神經興奮劑]]的成癮；{{r|Miller+Grandy 2016|TAAR1 addiction 2015}}然而，{{As of|2016|2|lc=y|post=,}}，已知可作為選擇性{{tsl|en|TAAR1}}[[激动剂|促進劑]]的物質都屬於{{tsl|en|experimental drug|試驗性藥物}}。<ref name="Miller+Grandy 2016">{{cite journal |vauthors=Grandy DK, Miller GM, Li JX |title="TAARgeting Addiction"-The Alamo Bears Witness to Another Revolution: An Overview of the Plenary Symposium of the 2015 Behavior, Biology and Chemistry Conference |journal=Drug Alcohol Depend. |volume=159 |pages=9–16 |date=February 2016 |pmid=26644139 |doi=10.1016/j.drugalcdep.2015.11.014 |quote=When considered together with the rapidly growing literature in the field a compelling case emerges in support of developing TAAR1-selective agonists as medications for preventing relapse to psychostimulant abuse.}}</ref><ref name="TAAR1 addiction 2015">{{cite journal |vauthors=Jing L, Li JX |title=Trace amine-associated receptor 1: A promising target for the treatment of psychostimulant addiction |journal=Eur. J. Pharmacol. |volume=761 |pages=345–352 |date=August 2015 |pmid=26092759 |doi=10.1016/j.ejphar.2015.06.019 |quote=Existing data provided robust preclinical evidence supporting the development of TAAR1 agonists as potential treatment for psychostimulant abuse and addiction. |pmc=4532615}}</ref>安非他命成癮與伏隔核中的{{tsl|en|dopamine receptor|多巴胺接收器}}們以及位置相同（co-localized）的[[NMDA 接受器]]們的活化高度相關；{{efn-ur|
NMDA接受器們為與電壓相關的{{tsl|en|ligand-gated ion channels}}。{{tsl|en|ligand-gated ion channels}}這個通道需要glutamate 以及一個共同[[促進劑]]（co-agonist ）：([[絲氨酸|{{smallcaps all|D}}-serine]] 或 [[大豆屬]]glycine)的同時連接才能被開啟。<br>
<ref name="NHM-NMDA">{{cite book |vauthors=Malenka RC, Nestler EJ, Hyman SE |veditors=Sydor A, Brown RY |title=Molecular Neuropharmacology: A Foundation for Clinical Neuroscience |year=2009 |publisher=McGraw-Hill Medical |location=New York, USA |isbn=9780071481274 |pages=124–125 |edition=2nd |chapter=Chapter 5: Excitatory and Inhibitory Amino Acids |quote=<!-- At membrane potentials more negative than approximately −50 mV, the Mg2+ in the extracellular fluid of the brain virtually abolishes ion flux through NMDA receptor channels, even in the presence of glutamate.&nbsp;... The NMDA receptor is unique among all neurotransmitter receptors in that its activation requires the simultaneous binding of two different agonists. In addition to the binding of glutamate at the conventional agonist-binding site, the binding of glycine appears to be required for receptor activation. Because neither of these agonists alone can open this ion channel, glutamate and glycine are referred to as coagonists of the NMDA receptor. The physiologic significance of the glycine binding site is unclear because the normal extracellular concentration of glycine is believed to be saturating. However, recent evidence suggests that D-serine may be the endogenous agonist for this site. -->}}</ref>}}{{r|Magnesium}}鎂離子藉由封鎖一個接受器-鈣離子通道，來阻斷 NMDA接受器們。{{r|Magnesium|NHM-NMDA}}一篇論文回顧做成結論：根據動物試驗，因成癮而使用中樞神經刺激劑的人，可以發現過量的中樞神經興奮劑顯著降低腦細胞內部的鎂離子活動。{{r|Magnesium}}利用[[鎂]]元素補充劑，能降低安非他命使用者{{tsl|en|self-administration|自我服用}}{{efn|（self-administration，i.e., doses given to oneself）}}的機會。然而這不被認為是有效治療安非他命成癮的[[單一療法]]（mono-therapy）。{{efn-ur|
該篇回顧表示{{tsl|en|magnesium aspartate|magnesium L-aspartate}} 及 [[氯化鎂]]能大幅改善成癮行為。}}<ref name="Magnesium">{{cite journal |author =Nechifor M |title=Magnesium in drug dependences |journal=Magnes. Res. |volume=21 |issue=1 |pages=5–15 |date=March 2008 |pmid=18557129}}</ref>

====行為治療====
[[認知行為治療]]是當前治療中樞神經刺激劑成癮的療法。<ref name="Nestler CBT">{{cite book |vauthors=Malenka RC, Nestler EJ, Hyman SE |veditors=Sydor A, Brown RY |title=Molecular Neuropharmacology: A Foundation for Clinical Neuroscience |year=2009 |publisher=McGraw-Hill Medical |location=New York, USA |isbn=9780071481274 |page=386 |edition=2nd |chapter=Chapter 15: Reinforcement and Addictive Disorders |quote= Currently, cognitive–behavioral therapies are the most successful treatment available for preventing the relapse of psychostimulant use.}}</ref>除此之外，{{tsl|en|neurobiological effects of physical exercise|運動在生物神經元產生的效果}}的研究中表明維持每天從事[[有氧運動]]（例如：跑步等）的習慣，能避免藥物成癮纏身；本身也是一個對於治療安非他命成癮的有效{{tsl|en|adjunct theraot|附加療法}}。{{refn|group=來源組|name="Exercise therapy"|{{r|Natural and drug addictions|Running vs addiction|Exercise, addiction prevention, and ΔFosB|Exercise Rev 3|Addiction review 2016}}}}運動能讓所有疾病的預後都更加樂觀，特別是對於中樞神經刺激劑成癮。<ref name="Running vs addiction">{{cite journal |vauthors=Lynch WJ, Peterson AB, Sanchez V, Abel J, Smith MA |title=Exercise as a novel treatment for drug addiction: a neurobiological and stage-dependent hypothesis |journal=Neurosci. Biobehav. Rev. |volume=37 |issue=8 |pages=1622–1644 |date=September 2013 |pmid=23806439 |pmc=3788047 |doi=10.1016/j.neubiorev.2013.06.011 |quote=These findings suggest that exercise may “magnitude”-dependently prevent the development of an addicted phenotype possibly by blocking/reversing behavioral and neuroadaptive changes that develop during and following extended access to the drug.&nbsp;... 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&nbsp;... 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.}}</ref><ref name="Exercise Rev 3">{{cite journal |vauthors=Linke SE, Ussher M |title=Exercise-based treatments for substance use disorders: evidence, theory, and practicality |journal=Am. J. Drug Alcohol Abuse |volume=41 |issue=1 |pages=7–15 |date=January 2015 |pmid=25397661 |doi=10.3109/00952990.2014.976708 |quote=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.&nbsp;... numerous theoretical and practical reasons support exercise-based treatments for SUDs, including psychological, behavioral, neurobiological, nearly universal safety profile, and overall positive health effects. |pmc=4831948}}</ref><ref name="Addiction review 2016">{{cite journal |vauthors=Carroll ME, Smethells JR |title=Sex Differences in Behavioral Dyscontrol: Role in Drug Addiction and Novel Treatments |journal=Front. Psychiatry |volume=6 |pages=175 |date=February 2016 |pmid=26903885 |pmc=4745113 |doi=10.3389/fpsyt.2015.00175 |quote=Physical Exercise<br>There is accelerating evidence that physical exercise is a useful treatment for preventing and reducing drug addiction&nbsp;... 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.&nbsp;... 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.&nbsp;... 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.}}</ref>值得一提的是，[[有氧運動]]能降低擅自服用中樞神經興奮劑的慾望，降低{{tsl|en|Relapse|復發|再次擅自服用中樞神經興奮劑的機率}}（reinstatment）(i.e., relapse)、降低「試圖取得藥物所做出的舉動（drug-seeking behavior）」、降低[[多巴胺受體D2]]在[[紋狀體]]中的密度。{{r|Natural and drug addictions|Addiction review 2016}}它在病生理學中的腳色是相對於「[[興奮劑]]的使用」和「興奮劑的效果」，它會引起紋狀體中[[DRD2]]密度的減少。<ref name="Natural and drug addictions">{{cite journal |author=Olsen CM |title=Natural rewards, neuroplasticity, and non-drug addictions |journal=Neuropharmacology |volume=61 |issue=7 |pages=1109–1122 |date=December 2011 |pmid=21459101 |pmc=3139704 |doi=10.1016/j.neuropharm.2011.03.010 |quote=Similar to environmental enrichment, studies have found that exercise reduces self-administration and relapse to drugs of abuse (Cosgrove et al., 2002; Zlebnik et al., 2010). There is also some evidence that these preclinical findings translate to human populations, as exercise reduces withdrawal symptoms and relapse in abstinent smokers (Daniel et al., 2006; Prochaska et al., 2008), and one drug recovery program has seen success in participants that train for and compete in a marathon as part of the program (Butler, 2005).&nbsp;... 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). }}</ref>一篇論文回顧提到，藉由改變紋狀體（striatum）中的ΔFosB、{{nowrap|{{tsl|en|c-Fos}} {{tsl|en|immunoreactivity}}}}或部份的[[腦內回饋系統]]來避免藥物成癮在一個人身上的發展。{{r|Exercise, addiction prevention, and ΔFosB}}

{{FOSB addiction table|Table title=成瘾相关的可塑性的总结}}

===依賴和戒斷症狀===
根據另一篇由考科藍協作組織所做的一篇論文回顧指出當一個長期嚴重攝取安非他命或[[甲基安非他命]]的藥物成癮者某天突然停止攝取安非他命或甲基安非他命，那麼根據許多成癮個案的報告顯示，具有時效性（time-limited）的[[藥物戒斷|戒斷症狀]]將在他們上一次攝取安非他命後的24小時內出現。
在成癮患者停用安非他命後，安非他命的[[藥物戒斷|戒斷症狀]]的出現率接近九成。這九成都出現至少六個定義在「《[[精神疾病診斷與統計手冊]]》安非他命戒斷症狀」中的症狀。年紀與劑量和戒斷症狀的嚴重度呈正相關。安非他命的戒斷症狀共有兩個階段且總共可能歷時三周或更多。第一階段（撞牆期marked "crush" phase）約持續一周。<ref name="Cochrane Withdrawal">{{cite journal |vauthors=Shoptaw SJ, Kao U, Heinzerling K, Ling W |title=Treatment for amphetamine withdrawal |journal=Cochrane Database Syst. Rev. |issue=2 |pages=CD003021 |date=April 2009 |pmid=19370579 |doi=10.1002/14651858.CD003021.pub2 |editor=Shoptaw SJ |quote=The prevalence of this withdrawal syndrome is extremely common (Cantwell 1998; Gossop 1982) with 87.6% of 647 individuals with amphetamine dependence reporting six or more signs of amphetamine withdrawal listed in the DSM when the drug is not available (Schuckit 1999)&nbsp;... The severity of withdrawal symptoms is greater in amphetamine dependent individuals who are older and who have more extensive amphetamine use disorders (McGregor 2005). Withdrawal symptoms typically present within 24 hours of the last use of amphetamine, with a withdrawal syndrome involving two general phases that can last 3 weeks or more. The first phase of this syndrome is the initial "crash" that resolves within about a week (Gossop 1982;McGregor 2005)&nbsp;... }}</ref>安非他命的戒斷症狀可能包含：[[irritability|對於各種刺激極度敏感、躁動不安（irritability）]]、[[焦慮]]、{{tsl|en|Craving (withdrawal)|drug craving|對於安非他命有難以抑制的渴求}}、[[煩躁]]、[[疲倦]]、[[多食症]]、過動或{{tsl|en|decreased movement|行動遲緩}}、缺乏動機、嗜睡、和[[清醒夢]]。{{r|Cochrane Withdrawal}}<ref name="Cantwell McBride 1998 pp. 157–163">{{cite journal |last=Cantwell |first=Bernadette |last2=McBride |first2=Andrew J |title=Self detoxication by amphetamine dependent patients: a pilot study |journal=Drug and Alcohol Dependence |publisher=Elsevier BV |volume=49 |issue=2 |year=1998 |pages=157–163 |url=https://doi.org/10.1016%2Fs0376-8716%2897%2900160-9 |doi=10.1016/s0376-8716(97)00160-9 |accessdate=2017-05-09}}</ref>

這些特徵及症狀必須非由其他疾病（包含心理疾病）引起，且無法歸因於其他物質的濫用。滿足上述條件，才符合「安非他命戒斷症狀」症候群的診斷標準。{{r|Cochrane Withdrawal}}<ref name="Medscape Reference 2015">{{cite web |title=Amphetamine-Related Psychiatric Disorders Clinical Presentation: History, Physical, Causes |website=Medscape Reference |date=2015-12-03 |url=http://emedicine.medscape.com/article/289973-clinical |accessdate=2017-05-09 |archivedate=2020-08-10 |archiveurl=https://web.archive.org/web/20200810055602/https://emedicine.medscape.com/article/289973-clinical |deadurl=no }}</ref>

通過美國食品藥物管理局嚴格審核的安非他命藥品說明書上並未提到任何安非他命在醫療用劑量下突然停用會導致任何安非他命戒斷症狀的出現。<ref name="Dexedrine FDA">{{cite web |title=Dexedrine Prescribing Information |url=http://www.accessdata.fda.gov/drugsatfda_docs/label/2013/017078s047lbl.pdf |publisher=Amedra Pharmaceuticals LLC |work=United States Food and Drug Administration |date=October 2013 |accessdate=2013-11-04 |archivedate=2016-03-04 |archiveurl=https://web.archive.org/web/20160304085041/http://www.accessdata.fda.gov/drugsatfda_docs/label/2013/017078s047lbl.pdf |deadurl=no }}</ref><ref>{{cite web |title=Adderall IR Prescribing Information |url=http://www.accessdata.fda.gov/drugsatfda_docs/label/2015/011522s042lbl.pdf |publisher=Teva Pharmaceuticals USA, Inc. |work=United States Food and Drug Administration |date=October 2015 |accessdate=2016-05-18 |archivedate=2018-09-15 |archiveurl=https://web.archive.org/web/20180915111231/https://www.accessdata.fda.gov/drugsatfda_docs/label/2015/011522s042lbl.pdf |deadurl=no }}</ref><ref>{{cite web |title=Adderall XR Prescribing Information |url=http://www.accessdata.fda.gov/drugsatfda_docs/label/2013/021303s026lbl.pdf |publisher=Shire US Inc |work=United States Food and Drug Administration |date=December 2013 |accessdate=2013-12-30 |archivedate=2018-07-18 |archiveurl=https://web.archive.org/web/20180718220437/https://www.accessdata.fda.gov/drugsatfda_docs/label/2013/021303s026lbl.pdf |deadurl=no }}</ref><ref name="Department of Health">{{cite web |title=The amphetamine withdrawal syndrome |website=Department of Health |url=http://www.health.gov.au/internet/publications/publishing.nsf/Content/drugtreat-pubs-modpsy-toc~drugtreat-pubs-modpsy-3~drugtreat-pubs-modpsy-3-7~drugtreat-pubs-modpsy-3-7-aws#amp |accessdate=2017-05-09 |archivedate=2017-02-08 |archiveurl=https://web.archive.org/web/20170208102025/http://health.gov.au/internet/publications/publishing.nsf/Content/drugtreat-pubs-modpsy-toc~drugtreat-pubs-modpsy-3~drugtreat-pubs-modpsy-3-7~drugtreat-pubs-modpsy-3-7-aws#amp |deadurl=no }}</ref>
====DSM中，安非他命中毒及戒斷症狀之標準====

[[精神疾病诊断与统计手册|DSM-5]]中关于兴奋剂中毒的标准如下：

A.最近曾经服用过安非他命类的物质、可卡因或其他兴奋剂

B.在服用兴奋剂时（或者服用后很快表现出）临床表现出显著问题行为或心理变化（如：欣快症或感情迟钝；群性、社交性的改变；过于警觉；人际交往敏感；焦虑、紧张或者恼怒；刻板行为；判断力受损）。

C.在服用兴奋剂时或服用后即刻表现出以下任意两种（或以上）症状：
* 心动过速或心动过缓
* 瞳孔扩散
* 血压升高或降低
* 出汗或发冷
* 感到恶心或呕吐
* 体重降低
* 精神运动性焦躁或精神运动性迟滞
* 肌肉无力、呼吸抑制、胸口疼痛或心律失常
* 精神错乱、癫痫、运动困难、肌张力障碍或昏迷

包括其他物质中毒的情况在内，其他身体情况不可能出现该发病迹象、症状，并且也无法理解为其他的精神问题。

DSM-5中关于兴奋剂戒断症状的标准如下：

A.停止服用（或减少服用）长期的安非他命类物质、可卡因或其他兴奋剂。

B.在A的情况发生后的几小时至几天内，出现烦躁的情绪并伴有以下任意两种（或以上）的心理变化：
* 疲劳
* 生动而不愉快的梦
* 失眠或嗜睡
* 食欲增大
* 精神运动性焦躁或精神运动性迟滞

B中的症状或迹象导致了临床显著的压力，或者在社会、工作等重要方面功能出现受损。

====安非他命戒断症状的频率列表====

{| class="wikitable"
|+停止服用硫酸安非他命后，个人报告的戒断症状的百分比
! 症状 !! 频率
|-
| 无症状 || 14%
|-
| 易怒 || 78%

|-
| 疼痛和痛苦 || 58%

|-
| 感到沮丧 || 50%

|-
| 社交能力受损 || 46%

|-
| 发抖、出冷汗 || 36%

|-
| 难以入睡 || 32%

|-
| 虚脱 || 22%

|-
| 恶心、呕吐 || 16%

|-
| 头痛 || 14%

|-
| 难以保持清醒 || 12%

|-
| 食欲增大 || 12%

|-
| 便秘 || 10%

|-
| 食欲缩小 || 8%

|-
| 腹泻 || 6%

|}
<ref name="ScienceDirect.com 2016">{{cite web |title=Self detoxication by amphetamine dependent patients: a pilot study |website=ScienceDirect.com |date=2016-01-01 |url=http://www.sciencedirect.com/science/article/pii/S0376871697001609 |accessdate=2017-05-09}}</ref>
{| class="wikitable"
|+ 个人尝试戒毒和接受医学指导戒毒的原因与百分比
! 原因 !! 个人尝试戒毒 !! 医学指导戒毒
|-
| 对生活整体现状（犯罪、无聊、金钱）不满 || 42（89%）|| 6（37%）
|-
| 对心理健康感到担忧（偏执、忧虑、依赖）||25（53%）|| 3（19%）
|-
| 家庭原因（父母或配偶的压力，子女出生） || 24（51%） || 5（31%）
|-
| 身体健康（动脉注射、血管萎陷、感染） || 17（36%）|| 4（25%）
|-
| 避免入狱 || 0 || 2（12%）
|-
| 其他原因 ||2（4%）|| 0
|}{{r|ScienceDirect.com 2016}}

{| class="wikitable"
|+用來協助戒毒的方法
! - !! 自我嘗試戒毒（Self detoxication） !! 被迫戒毒（Enforced detoxication）
|-
| 服用更多其他药物|| - || -
|-
| 大麻（Cannabis） || 22(27%) || 	10(59%)
|-
| 替马西泮（Temazepam） || 21(26%) || -
|-
| 酒精 || 17(21%) || 2(12%)
|-
| 鴉片類物質（Opiates） || 12(15%) || 1(6%)
|-
| 地西泮（Diazepam） || 4(5%) || -
|-
| 巴比妥類藥物（Barbiturates） || 3(4%) || 1(6%)
|-
| 心理學技巧 || - || -
|-
| 轉移注意力（例如：工作、看電視） || 35(21%) || 1(6%)
|-
| 不再與藥物成癮的朋友來往 || 31(19%) || -
|-
|獲得人們的支持（家庭、社會中的支持團體）|| 11(7%) || -
|-
| 把藥物及針頭丟掉|| 5(3%) || -
|}{{r|ScienceDirect.com 2016}}

===中毒與致病===
<!-- {{see also|Stimulant psychosis}} -->
====中毒====
在囓齒動物（rodents）和靈長類動物（primates）的藥物試驗發現到，夠高的安非他命劑量會導致多巴胺{{tsl|en|neurotoxicity|神經中毒}}甚或致使多巴胺{{tsl|en|axon terminal|末梢神經}}[[神经退行性疾病|受損退化]]並降低[[多巴胺轉運體|轉運體]]和{{tsl|en|dopaminergic receptor|多巴胺接收器|接收器}}的功能。<ref name="Humans&Animals">{{cite journal| author=Advokat C| title=Update on amphetamine neurotoxicity and its relevance to the treatment of ADHD |journal=J. Atten. Disord. |date=July 2007 |volume= 11 |issue= 1 |pages= 8–16 |pmid=17606768 |doi=10.1177/1087054706295605}}</ref>{{r|Amph-induced hyperthermia and neurotoxicity review}}目前並無證據顯示安非他命會直接荼毒人類的神經。<ref>{{cite web |title=Amphetamine |url=http://toxnet.nlm.nih.gov/cgi-bin/sis/search/r?dbs+hsdb:@term+@rn+@rel+300-62-9 |work=Hazardous Substances Data Bank |publisher=United States National Library of Medicine&nbsp;– Toxicology Data Network |accessdate=2014-02-26 |quote=Direct toxic damage to vessels seems unlikely because of the dilution that occurs before the drug reaches the cerebral circulation. |archivedate=2017-10-02 |archiveurl=https://web.archive.org/web/20171002194327/https://toxnet.nlm.nih.gov/cgi-bin/sis/search2/cgi-bin/sis/search2/f?.%2Ftemp%2F~mdjW95%3A1%3AFULL |deadurl=no }}</ref><ref name="Malenka_2009_02">{{cite book |vauthors=Malenka RC, Nestler EJ, Hyman SE |veditors=Sydor A, Brown RY |title=Molecular Neuropharmacology: A Foundation for Clinical Neuroscience |year=2009 |publisher=McGraw-Hill Medical |location=New York, USA |isbn=9780071481274 |page=370 |edition=2nd |chapter=Chapter 15: Reinforcement and addictive disorders |quote=Unlike cocaine and amphetamine, methamphetamine is directly toxic to midbrain dopamine neurons.}}</ref>然而，超高劑量（large doses）的安非他命攝取量可能會產生[[hyperpyrexia|高熱]]（體溫過高）的現象並間接導致：多巴胺的神經性中毒（dopaminergic neurotoxicity）、過多的[[活性氧类]]（reactive oxygen species）生成、[[自然氧化]]（autoxidation）增加。{{refn|group=來源組|{{r|Amph-induced hyperthermia and neurotoxicity review|Autoxidation1|Autoxidation2}}}}從高劑量的安非他命攝取量引起的神經中毒的[[模式生物|生物模式]]中發現，[[人體溫度|人體核心體溫]]高於40°C是「高劑量的安非他命攝取量」<u>是否</u>引起神經中毒的「[[必要條件]]」。<ref name="Amph-induced hyperthermia and neurotoxicity review">{{cite journal |vauthors=Bowyer JF, Hanig JP |title=Amphetamine- and methamphetamine-induced hyperthermia: Implications of the effects produced in brain vasculature and peripheral organs to forebrain neurotoxicity |journal=Temperature (Austin) |volume=1 |issue=3 |pages=172–182 |date=November 2014 |pmid=27626044 |pmc=5008711 |doi=10.4161/23328940.2014.982049 |quote=Hyperthermia alone does not produce amphetamine-like neurotoxicity but AMPH and METH exposures that do not produce hyperthermia (≥40°C) are minimally neurotoxic. Hyperthermia likely enhances AMPH and METH neurotoxicity directly through disruption of protein function, ion channels and enhanced ROS production.&nbsp;... The hyperthermia and the hypertension produced by high doses amphetamines are a primary cause of transient breakdowns in the blood-brain barrier (BBB) resulting in concomitant regional neurodegeneration and neuroinflammation in laboratory animals.&nbsp;... In animal models that evaluate the neurotoxicity of AMPH and METH, it is quite clear that hyperthermia is one of the essential components necessary for the production of histological signs of dopamine terminal damage and neurodegeneration in cortex, striatum, thalamus and hippocampus.}}</ref>在動物試驗中，若動物的腦溫長期超過40°C，容易因過多的[[活性氧类]]生成、受干擾的細胞蛋白功能和短暫的[[血腦屏障]]標準放寬而促使安非他命性的神經中毒發生。{{r|Amph-induced hyperthermia and neurotoxicity review}}

====致病====
嚴重的安非他命過量可能造成「中樞神經刺激劑過量所引發的精神異常（stimulant psychosis）」，症狀包含但不限於幻覺（delusion）和被害妄想、疑神疑鬼、[[delusion|妄想]]、[[paranoia|偏執]]等。{{r|Cochrane}}此機制用於[[思覺失調症]]研究時誘發精神病發作的藥物。<ref name=Neal_R._Swerdlow>{{Cite journal|title=Lessons learned by giving amphetamine to antipsychotic-medicated schizophrenia patients|author=Neal R. Swerdlow|journal=Neurophsychopharmacology|others=Savita G. Bhakta , Jo Talledo, Lindsay Benster, Juliana Kotz, Maria Lavadia and Gregory A. Light|year=2019}}</ref>一篇由考科藍協作組織所做的論文回顧及統整發現在所有因攝取嚴重過量的「安非他命、dextro-安非他命、及甲基安非他命」而導致精神異常的患者中，有5%-15%的患者即便經過治療，仍無法完全康復。<ref name="Cochrane">{{cite journal |editor =Shoptaw SJ, Ali R |vauthors=Shoptaw SJ, Kao U, Ling W |title=Treatment for amphetamine psychosis |journal=Cochrane Database Syst. Rev. |issue=1 |pages=CD003026 |date=January 2009 |pmid=19160215 |doi=10.1002/14651858.CD003026.pub3 |quote=A minority of individuals who use amphetamines develop full-blown psychosis requiring care at emergency departments or psychiatric hospitals. In such cases, symptoms of amphetamine psychosis commonly include paranoid and persecutory delusions as well as auditory and visual hallucinations in the presence of extreme agitation. More common (about 18%) is for frequent amphetamine users to report psychotic symptoms that are sub-clinical and that do not require high-intensity intervention&nbsp;...<br>About 5–15% of the users who develop an amphetamine psychosis fail to recover completely (Hofmann 1983)&nbsp;...<br>Findings from one trial indicate use of antipsychotic medications effectively resolves symptoms of acute amphetamine psychosis.}}</ref><ref name="Hofmann">{{cite book |author=Hofmann FG |title=A Handbook on Drug and Alcohol Abuse: The Biomedical Aspects |publisher=Oxford University Press |isbn=9780195030570 |location=New York, USA |year=1983 |page=329 |edition=2nd }}</ref>

根據同一篇由考科藍協作組織所做的論文回顧及統整，至少一個實驗（trial）顯示[[抗精神病藥物]]（antipsychotic）能有效解決因嚴重過量的安非他命所致的急性精神異常症狀。
{{r|Cochrane}}另外，穩定在服用[[抗精神病藥物]]的人使用安非他命後心跳血壓等生理變化也較一般人來的少。{{r|Neal_R._Swerdlow}}

「攝取醫療劑量的安非他命所致的急性精神異常」是[[副作用|非常罕見的（very rare）]]。<br>（非常罕見 very rare： < 1/10000 ；罕見 rare：>= 1/10000 & <1/1000）{{r|Stimulant Misuse}}<ref name="FDA Contra Warnings">{{cite web |title=Adderall XR Prescribing Information |url=http://www.accessdata.fda.gov/drugsatfda_docs/label/2013/021303s026lbl.pdf |pages=4–6 |publisher=Shire US Inc |work=United States Food and Drug Administration |date=December 2013 |accessdate=2013-12-30 |archivedate=2018-07-18 |archiveurl=https://web.archive.org/web/20180718220437/https://www.accessdata.fda.gov/drugsatfda_docs/label/2013/021303s026lbl.pdf |deadurl=no }}</ref>

==交互作用==
{{See also|苯丙胺#醫療上的禁忌}}

目前已知许多种物质都会和安非他命发生[[药物相互作用]]，导致安非他命或参与作用的另一物质的{{tsl|en|drug action|药效}}或[[药物代谢|代谢过程]]发生改变。{{r|FDA Pharmacokinetics|FDA Interactions}}用于分解安非他命的酶的抑制剂（如[[CYP2D6]]、{{tsl|en|Flavin-containing monooxygenase 3#Ligands||FMO3}}）都会延长其[[生物半衰期|半衰期]]，这意味着药效会更持久。{{r|FMO}}<ref name="FDA Interactions">{{cite web | title = Adderall XR Prescribing Information | url = http://www.accessdata.fda.gov/drugsatfda_docs/label/2013/021303s026lbl.pdf | pages = 8–10 | publisher = Shire US Inc | work = United States Food and Drug Administration | date = December 2013 | accessdate = 2013-12-30 | archivedate = 2018-07-18 | archiveurl = https://web.archive.org/web/20180718220437/https://www.accessdata.fda.gov/drugsatfda_docs/label/2013/021303s026lbl.pdf | deadurl = no }}</ref>安非他命也會和{{abbr|MAOIs|monoamine oxidase inhibitors}}產生交互作用，特別是[[MAOI]]類中的{{tsl|en|monoamine oxidase A||monoamine oxidase A}}[[抑制劑]]（monoamine oxidase A<font color="#777777"> </font>inhibitors）。

因為[[MAOIs]]和安非他命兩者都會增加[[兒茶酚胺]]（i.e.,正腎上腺素和多巴胺）在[[血漿]]中的濃度{{r|FDA Interactions}}；因此MAOIs與安非他命合併使用是危險的{{r|FDA Interactions}}。

安非他命會調節幾乎所有作用於中樞神經的藥物的活動。特別需要注意的是，安非他命可能會降低[[鎮靜劑]]和[[中樞神經抑制劑]]）的效果，並增加其他[[中樞神經刺激劑]]和[[抗憂鬱藥]]的效果。{{r|FDA Interactions}}

安非他命也可能降低[[抗高血壓藥]]和[[抗精神病藥]]（anti-psychotics）的藥效，這是因為安非他命本身對於血壓及多巴胺系統的作用。{{r|FDA Interactions}}

[[鋅|鋅的補充劑]]可能會降低安非他命用於治療注意力不足過動症時的最小[[有效劑量]]（minimum effective dose）。{{efn-ur|The human [[多巴胺轉運體|dopamine transporter]] contains a [[配體 (生物化學)|high affinity]] extracellular zinc {{tsl|en|binding site||binding site}} which, upon zinc binding, inhibits dopamine {{tsl|en|reuptake||reuptake}} and amplifies amphetamine-induced {{tsl|en|neurotransmitter efflux||dopamine efflux}} ''[[in vitro]]''.<ref name="Zinc binding sites + ADHD review">{{cite journal | vauthors = Krause J | title = SPECT and PET of the dopamine transporter in attention-deficit/hyperactivity disorder | journal = Expert Rev. Neurother. | volume = 8 | issue = 4 | pages = 611–625 | date = April 2008 | pmid = 18416663 | doi = 10.1586/14737175.8.4.611 | quote = Zinc binds at&nbsp;... extracellular sites of the DAT [103], serving as a DAT inhibitor. In this context, controlled double-blind studies in children are of interest, which showed positive effects of zinc [supplementation] on symptoms of ADHD [105,106]. It should be stated that at this time [supplementation] with zinc is not integrated in any ADHD treatment algorithm.}}</ref><ref name="Review - cites 2002 amph-zinc primary study">{{cite journal | vauthors = Sulzer D | title = How addictive drugs disrupt presynaptic dopamine neurotransmission | journal = Neuron | volume = 69 | issue = 4 | pages = 628–649 | date = February 2011 | pmid = 21338876 | pmc = 3065181 | doi = 10.1016/j.neuron.2011.02.010 | quote = They did not confirm the predicted straightforward relationship between uptake and release, but rather that some compounds including AMPH were better releasers than substrates for uptake. Zinc, moreover, stimulates efflux of intracellular [3H]DA despite its concomitant inhibition of uptake (Scholze et al., 2002).}}</ref><ref name="Primary 2002 amph-zinc study">{{cite journal | vauthors = Scholze P, Nørregaard L, Singer EA, Freissmuth M, Gether U, Sitte HH | title = The role of zinc ions in reverse transport mediated by monoamine transporters | journal = J. Biol. Chem. | volume = 277 | issue = 24 | pages = 21505–21513 | date = June 2002 | pmid = 11940571 | doi = 10.1074/jbc.M112265200 | quote = The human dopamine transporter (hDAT) contains an endogenous high affinity Zn<sup>2+</sup> binding site with three coordinating residues on its extracellular face (His193, His375, and Glu396).&nbsp;... Although Zn<sup>2+</sup> inhibited uptake, Zn<sup>2+</sup> facilitated [3H]MPP+ release induced by amphetamine, MPP+, or K+-induced depolarization specifically at hDAT but not at the human serotonin and the norepinephrine transporter (hNET).}}</ref>The human [[血清素轉運體|serotonin transporter]] and [[去甲腎上腺素轉運體|norepinephrine transporter]] do not contain zinc binding sites.{{r|Primary 2002 amph-zinc study}}}}<ref name="Zinc and PEA">{{cite journal |vauthors=Scassellati C, Bonvicini C, Faraone SV, Gennarelli M | title = Biomarkers and attention-deficit/hyperactivity disorder: a systematic review and meta-analyses | journal = J. Am. Acad. Child Adolesc. Psychiatry | volume = 51 | issue = 10 | pages = 1003–1019.e20 | date = October 2012 | pmid = 23021477 | doi = 10.1016/j.jaac.2012.08.015 | quote = With regard to zinc supplementation, a placebo controlled trial reported that doses up to 30&nbsp;mg/day of zinc were safe for at least 8&nbsp;weeks, but the clinical effect was equivocal except for the finding of a 37%&nbsp;reduction in amphetamine optimal dose with 30&nbsp;mg per day of zinc.<sup>110</sup>}}</ref>

整體來說，安非他命並不會與日常生活中常見的食物起任何重大的交互作用，但安非他命的吸收和排泄會分別受到腸胃內容物（gastrointestinal content）的[[pH值]]和尿液的[[酸鹼值]]影響。{{r|FDA Interactions}}
酸性物質會減少安非他命的吸收並增加尿液的排泄；鹼性物質則相反。

由於pH值在安非他命的吸收這件事上具有影響力，所以安非他命也會和 [[氫離子幫浦阻斷劑]]（PPI, proton pump inhibitors）和[[H2受体阻抗剂|H<sub>2</sub>受体阻抗剂]]（H<sub>2</sub> antihistamines）等中和胃酸的[[制酸劑]]產生交互作用。{{r|FDA Interactions}}

==藥學==
===藥物代謝動力學===
安非他命的口服[[生物利用度|生物體可利用率]]{{RefTag|name=bioavailability|1=英文名稱為：bioavailability}}與腸胃的[[pH值]]連動；{{r|FDA Interactions}}安非他命非常容易在腸道被吸收，右旋苯丙胺的生體可利用率在多數的情況下高於75%。<ref name="Drugbank-dexamph">{{cite encyclopedia 
| title=Dextroamphetamine 
| section-url=http://www.drugbank.ca/drugs/DB01576#pharmacology 
| work=DrugBank 
| publisher=University of Alberta 
| accessdate=2013-11-05 
| date=2013-02-08 
| section=Pharmacology 
| archivedate=2019-08-06 
| archiveurl=https://web.archive.org/web/20190806163223/https://www.drugbank.ca/drugs/DB01576#pharmacology 
| deadurl=no 
}}</ref>安非他命呈弱鹼性，其[[酸度系数|pKa值]]介於{{nowrap|9–10}}之間;<ref name="FDA Pharmacokinetics">{{cite web 
| title=Adderall XR Prescribing Information 
| url=http://www.accessdata.fda.gov/drugsatfda_docs/label/2013/021303s026lbl.pdf 
| pages=12–13 
| publisher=Shire US Inc 
| work=United States Food and Drug Administration 
| date=December 2013 
| accessdate=2013-12-30 
| archivedate=2018-07-18 
| archiveurl=https://web.archive.org/web/20180718220437/https://www.accessdata.fda.gov/drugsatfda_docs/label/2013/021303s026lbl.pdf 
| deadurl=no 
}}</ref>因此，當pH值呈鹼性時，多數的安非他命會以其易溶於[[脂類]]的{{tsl|en|free base|純胺類型態}}形式存在。在此情況下，身體會通過腸道[[上皮組織]]富含脂類的[[細胞膜]]{{RefTag|name=cell membrane|英文名稱為：cell membrane}}來吸收安非他命。{{r|FDA Pharmacokinetics|FDA Interactions}}相反地，酸性的pH值表示安非他命主要以易溶於水的[[离子#.E9.98.B3.E7.A6.BB.E5.AD.90.28.2B.29|離子]]（鹽）形式存在，因此較少能被吸收。{{r|FDA Pharmacokinetics}}大約{{nowrap|15–40%}}循環於血管中的安非他命與[[血漿蛋白]]{{RefTag|name=plasma protein|1=英文名稱為：plasma protein}}相連接。<ref name="Drugbank-amph">{{cite encyclopedia 
| title=Amphetamine 
| section-url=http://www.drugbank.ca/drugs/DB00182#pharmacology 
| work=DrugBank 
| publisher=University of Alberta 
| accessdate=2013-11-05 
| date=2013-02-08 
| section=Pharmacology 
| archivedate=2013-10-12 
| archiveurl=https://web.archive.org/web/20131012061802/http://www.drugbank.ca/drugs/DB00182#pharmacology 
| deadurl=no 
}}</ref>安非他命的對映異構物的[[生物半衰期|半衰期]]會隨著尿液的pH值而有所不同。{{r|FDA Pharmacokinetics}}當尿液的[[酸鹼值]]落在正常範圍中，右旋苯丙胺和左旋苯丙胺的[[生物半衰期|半衰期]]分別為{{nowrap|9–11}}小時及{{nowrap|11–14}}小時。{{r|FDA Pharmacokinetics}}酸性飲食會導致安非他命的對映異構物的半衰期降低至{{nowrap|8–11}}小時；鹼性飲食則會使安非他命的對映異構物的半衰期增加到{{nowrap|16–31}}小時。{{r|Pubchem Kinetics}}<ref name="pH-dependent half-lives">{{cite encyclopedia
| title=AMPHETAMINE
| section=Biological Half-Life
| section-url=http://toxnet.nlm.nih.gov/cgi-bin/sis/search/r?dbs+hsdb:@term+@rn+@rel+300-62-9
| work=United States National Library of Medicine – Toxnet
| publisher=Hazardous Substances Data Bank
| accessdate=2014-01-05
| quote=Concentrations of (14)C-amphetamine declined less rapidly in the plasma of human subjects maintained on an alkaline diet (urinary pH > 7.5) than those on an acid diet (urinary pH < 6). Plasma half-lives of amphetamine ranged between 16-31 hr & 8-11 hr, respectively, & the excretion of (14)C in 24 hr urine was 45 & 70%.
| archivedate=2017-10-02
| archiveurl=https://web.archive.org/web/20171002194327/https://toxnet.nlm.nih.gov/cgi-bin/sis/search2/cgi-bin/sis/search2/f?.%2Ftemp%2F~mdjW95%3A1%3AFULL
| deadurl=no
}}</ref>

成分為安非他命或其衍生物的<u>短效</u>藥品大約在口服後三小時在體內達到最高{{tsl|en|plasma concentration|血漿濃度}}；而成分為安非他命或其衍生物的<u>長效</u>藥品則在口服後大約七小時在體內達到最高血漿濃度。{{r|FDA Pharmacokinetics}}

安非他命主要透過[[腎臟]]來代謝，大約{{nowrap|30–40%}}的藥物以藥物本身原始的型態從酸鹼度正常的尿液中排出。{{r|FDA Pharmacokinetics}}
尿液是鹼性時，安非他命傾向以其純胺類型態存在，因此較少被排泄。{{r|FDA Pharmacokinetics}}

當尿液的pH值失常時，各種安非他命的分解物在尿液中重新結合的程度將從最低1%到最高75%。該程度的高低大多取決於於尿液的酸鹼值，尿液越酸，結合率越高；尿液愈鹼，結合率越低。{{r|FDA Pharmacokinetics}}安非他命通常於口服後兩天內自體內完全代謝完畢。{{r|Pubchem Kinetics}}安非他命確切的半衰期及藥效作用期隨著（小於兩天的）重複服用導致的血漿內安非他命濃度（plasma concentration of amphetamine）的增加而延長。<ref name="Flomenbaum_2006">{{cite encyclopedia |author=Richard RA |title=Chapter 5—Medical Aspects of Stimulant Use Disorders |series=Treatment Improvement Protocol 33 |year=1999 |work=National Center for Biotechnology Information Bookshelf |publisher=Substance Abuse and Mental Health Services Administration |section-url=http://www.ncbi.nlm.nih.gov/books/NBK64323/ |section=Route of Administration |access-date=2017-04-06 |archivedate=2020-11-11 |archiveurl=https://web.archive.org/web/20201111231142/https://www.ncbi.nlm.nih.gov/books/NBK64323/ |deadurl=no }}</ref>

對人體無藥效的前藥（prodrug）：赖氨酸安非他命並不若安非他命一樣容易受腸胃道環境的pH值影響；<ref name="FDA Vyvanse">{{cite web 
| title=Vyvanse Prescribing Information 
| url=http://www.accessdata.fda.gov/drugsatfda_docs/label/2015/021977s036s037lbledt.pdf 
| pages=12–16 
| publisher=Shire US Inc 
| work=United States Food and Drug Administration 
| date=January 2015 
| accessdate=2015-02-24 
| archivedate=2015-02-25 
| archiveurl=https://web.archive.org/web/20150225015712/http://www.accessdata.fda.gov/drugsatfda_docs/label/2015/021977s036s037lbledt.pdf 
| deadurl=no 
}}</ref>赖氨酸安非他命在腸道被吸收進入血管的血液後很快就會透過[[水解]]的方式轉化為右旋安非他命。而參與這水解反應的酶與紅血球有關。{{r|FDA Vyvanse}}

Lisdexamfetamine的[[生物半衰期|半衰期]]通常小於一個小時。{{r|FDA Vyvanse}}

[[CYP2D6|細胞色素 P450 2D6]]（Cytochrome P450 2D6、或CYP2D6）、[[多巴胺β羟化酶|多巴胺β羥化酶]]（Dopamine β-hydroxylase、或DBH）、{{tsl|en|flavin-containing monooxygenase 3}}、{{tsl|en|butyrate-CoA ligase}}、和{{tsl|en|glycine N-acyltransferase}}為已知在人體中參與{{NoteTag|1=酶做為反應的催化劑catalyst，並不實際參與反應。}}「安非他命」及「安非他命代謝後之產物」的代謝反應的[[酶]]。{{refn|group=來源組|{{r|FDA Pharmacokinetics|Substituted amphetamines, FMO, and DBH|DBH amph primary"|DBH 4-HA primary|FMO|FMO3-Primary|Benzoic1|Benzoic2}}}} 

「安非他命代謝後之產物」包含：{{nowrap|{{tsl|en|4-hydroxyamphetamine}}}}、{{nowrap|{{tsl|en|4-hydroxynorephedrine}}}}、[[4-羟基苯基丙酮]]、[[苯甲酸]]、[[馬尿酸]]、[[苯丙醇胺]]、[[苯基丙酮]]{{NoteTag|1=不是[[苯丙酮]]}}{{r|FDA Pharmacokinetics}}<ref name="Pubchem Kinetics">{{cite encyclopedia 
| title=Amphetamine 
| section-url=http://pubchem.ncbi.nlm.nih.gov/summary/summary.cgi?cid=3007#section=Pharmacology-and-Biochemistry 
| work=Pubchem Compound 
| publisher=National Center for Biotechnology Information 
| accessdate=2013-10-12 
| section=Pharmacology and Biochemistry 
| archivedate=2014-10-09 
| archiveurl=https://web.archive.org/web/20141009013756/http://pubchem.ncbi.nlm.nih.gov/summary/summary.cgi?cid=3007#section=Pharmacology-and-Biochemistry 
| deadurl=no 
}}</ref><ref name="Metabolites">
{{cite journal 
| author=Santagati NA, Ferrara G, Marrazzo A, Ronsisvalle G 
| title=Simultaneous determination of amphetamine and one of its metabolites by HPLC with electrochemical detection 
| journal=J. Pharm. Biomed. Anal. 
| volume=30 
| issue=2 
| pages=247–255 
|date=September 2002 
| pmid=12191709 
| doi =10.1016/S0731-7085(02)00330-8 }}</ref>。

在這些「安非他命代謝後之產物」之中，有實際藥效的產物（[[拟交感神经药|sympathomimetics]]）為：{{nowrap|4‑hydroxyamphetamine}}{{r|sympathomimetics}}、{{nowrap|4‑hydroxynorephedrine}}{{r|Metabolites}}、和norephedrine{{r|norephedrine}}。
<ref name="sympathomimetics">{{cite encyclopedia 
| title=p-Hydroxyamphetamine 
| section-url=http://pubchem.ncbi.nlm.nih.gov/summary/summary.cgi?cid=3651 
| work=PubChem Compound 
| publisher=National Center for Biotechnology Information 
| accessdate=2013-10-15 
| section=Compound Summary 
| archivedate=2013-06-07 
| archiveurl=https://web.archive.org/web/20130607202440/http://pubchem.ncbi.nlm.nih.gov/summary/summary.cgi?cid=3651 
| deadurl=no 
}}</ref>{{nowrap|4‑hydroxynorephedrine}},<ref name="metabolites">{{cite encyclopedia |title=p-Hydroxynorephedrine |section-url=http://pubchem.ncbi.nlm.nih.gov/summary/summary.cgi?cid=11099 |work=PubChem Compound |publisher=National Center for Biotechnology Information |accessdate=2013-10-15 |section=Compound Summary |archivedate=2013-10-15 |archiveurl=https://web.archive.org/web/20131015073126/http://pubchem.ncbi.nlm.nih.gov/summary/summary.cgi?cid=11099 |deadurl=no }}</ref>and norephedrine.<ref name="norephedrine">{{cite encyclopedia |title=Phenylpropanolamine |section-url=http://pubchem.ncbi.nlm.nih.gov/summary/summary.cgi?cid=26934 |work=PubChem Compound |publisher=National Center for Biotechnology Information |accessdate=2013-10-15 |section=Compound Summary |archivedate=2014-10-18 |archiveurl=https://web.archive.org/web/20141018170912/http://pubchem.ncbi.nlm.nih.gov/summary/summary.cgi?cid=26934 |deadurl=no }}</ref>

安非他命的主要代謝途徑包含：芳香对羟基化、脂肪族α-、β-羟基化、N-氧化、N-脱烷基、和脱氨基。{{r|FDA Pharmacokinetics|Pubchem Kinetics}}

下圖為已知的「安非他命」代謝途徑和「安非他命代謝後之產物」：{{r|FDA Pharmacokinetics|FMO|Metabolites}}
{{Amphetamine Pharmacokinetics
|caption=
在這些「安非他命代謝後之產物」之中，主要的且有實際藥效的產物為：{{nowrap|4-hydroxyamphetamine}} 和{{nowrap|去甲麻黃鹼（norephedrine）}}。{{r|Metabolites}}
從酸鹼度正常的尿液中可發現，大約30–40%的「安非他命」以本身原始的型態排出；大約50%的安非他命以不具藥效的「安非他命代謝後之產物」（即為圖片中最下列的產物）的型態排出。
{{r|FDA Pharmacokinetics}}

剩下的{{nowrap|10–20%}}則為「安非他命代謝後之產物」之中，有實際藥效的產物。
{{r|FDA Pharmacokinetics}}

苯甲酸（Benzoic acid）被butyrate-CoA連接酶（butyrate-CoA ligase）代謝後成為一個中介物質/中間產物（intermediate product）：{{tsl|en|benzoyl-CoA}}
<ref name="Benzoic1">{{cite encyclopedia
| title=butyrate-CoA ligase
| section-url=http://www.brenda-enzymes.info/enzyme.php?ecno=6.2.1.2&Suchword=&organism%5B%5D=Homo+sapiens&show_tm=0
| work=BRENDA
| publisher=Technische Universität Braunschweig.
| accessdate=2014-05-07
| section=Substrate/Product
| archivedate=2017-06-22
| archiveurl=https://web.archive.org/web/20170622234353/http://www.brenda-enzymes.info/enzyme.php?ecno=6.2.1.2&Suchword=&organism%5B%5D=Homo+sapiens&show_tm=0
| deadurl=no
}}</ref>
隨後透過glycine N-acyltransferase代謝並轉化為馬尿酸（hippuric acid）。<ref name="Benzoic2">{{cite encyclopedia
| title=glycine N-acyltransferase
| section-url=http://www.brenda-enzymes.info/enzyme.php?ecno=2.3.1.13&Suchword=&organism%5B%5D=Homo+sapiens&show_tm=0
| work=BRENDA
| publisher=Technische Universität Braunschweig.
| accessdate=2014-05-07
| section=Substrate/Product
| archivedate=2017-06-23
| archiveurl=https://web.archive.org/web/20170623000309/http://www.brenda-enzymes.info/enzyme.php?ecno=2.3.1.13&Suchword=&organism%5B%5D=Homo+sapiens&show_tm=0
| deadurl=no
}}</ref>}}

===藥物效應動力學===
{{For|安非他明作用机制的一个更简单且比较非技术性的解释|阿得拉尔#Mechanism of action}}
{{amphetamine pharmacodynamics}}

安非他命藉由將[[单胺类神经递质]]在腦中（主要於腦中那酬賞與執行功能路徑上的[[儿茶酚胺]]的神經元）的用途改變為神經訊號來產生療效。{{r|Miller|cognition enhancers}}

安非他命作用於{{tsl|en|monoamine transporter||monoamine transporter}}上的效應使得[[犒赏系统]]和[[管控功能]]中的主要神經傳導物質（多巴胺、正腎上腺素）依安非他命的劑量，成比例的迅速上升。{{r|Miller|cognition enhancers}}<ref name="E Weihe">{{cite journal |vauthors=Eiden LE, Weihe E |title=VMAT2: a dynamic regulator of brain monoaminergic neuronal function interacting with drugs of abuse |journal=Ann. N. Y. Acad. Sci. |volume=1216 |pages=86–98 |date=January 2011 |pmid=21272013 |pmc=4183197 |doi=10.1111/j.1749-6632.2010.05906.x |quote=VMAT2 is the CNS vesicular transporter for not only the biogenic amines DA, NE, EPI, 5-HT, and HIS, but likely also for the trace amines TYR, PEA, and thyronamine (THYR)&nbsp;... [Trace aminergic] neurons in mammalian CNS would be identifiable as neurons expressing VMAT2 for storage, and the biosynthetic enzyme aromatic amino acid decarboxylase (AADC).&nbsp;... AMPH release of DA from synapses requires both an action at VMAT2 to release DA to the cytoplasm and a concerted release of DA from the cytoplasm via "reverse transport" through DAT.}}</ref>

服用安非他命所帶來的[[增强]]和促進{{tsl|en|motivational salience||motivational salience}}的效果起因於[[中脑边缘通路]]中的多巴胺活動變得更加活躍之故。{{r|Malenka_2009}}

安非他命帶給使用者的[[欣快感]]和{{tsl|en|locomotor stimulation|locomotor stimulation|運動協調激勵}}之效果和安非他命刺激{{tsl|en|striatum||紋狀體}}的神經突觸之多巴胺和正腎上腺素濃度增加的速度和規模成正比{{r|Amph Uses}}。

安非他命已經被確認為{{tsl|en|TAAR1||trace amine-associated receptor 1}}(TAAR1){{noteTag|1=a {{nowrap|{{tsl|en|Gs alpha subunit||G<sub>s</sub>-coupled}}}} and {{nowrap|{{tsl|en|Gq alpha subunit||G<sub>q</sub>-coupled}}}} [[G蛋白偶联受体|G protein-coupled receptor]] (GPCR) discovered in 2001, which is important for regulation of brain monoamines.}}的強[[激动剂|刺激劑]]（potent full agonist）。{{r|Miller}}<ref name="TAAR1 IUPHAR">{{cite web|title=TA<sub>1</sub> receptor|url=http://www.iuphar-db.org/DATABASE/ObjectDisplayForward?objectId=364|work=IUPHAR database|publisher=International Union of Basic and Clinical Pharmacology|accessdate=8 December 2014|vauthors=Maguire JJ, Davenport AP|date=2 December 2014|quote=<!-- Comments: Tyramine causes an increase in intracellular cAMP in HEK293 or COS-7 cells expressing the TA1 receptor in vitro [4,6,18]. In addition, coupling to a promiscuous Gαq has been observed, resulting in increased intracellular calcium concentration [24]. -->|archivedate=2015-06-29|archiveurl=https://web.archive.org/web/20150629065449/http://www.iuphar-db.org/DATABASE/ObjectDisplayForward?objectId=364|deadurl=no}}</ref>

{{abbr|TAAR1|trace amine-associated receptor 1}}受額外刺激後會藉由活化[[腺苷酸环化酶]]和抑制{{tsl|en|monoamine transporter|單胺轉運蛋白}}的功能而增加{{abbrlink|cAMP|环腺苷酸}}的生成。{{r|Miller}}<ref name="pmid11459929">{{cite journal |vauthors=Borowsky B, Adham N, Jones KA, Raddatz R, Artymyshyn R, Ogozalek KL, Durkin MM, Lakhlani PP, Bonini JA, Pathirana S, Boyle N, Pu X, Kouranova E, Lichtblau H, Ochoa FY, Branchek TA, Gerald C |title=Trace amines: identification of a family of mammalian G protein-coupled receptors |journal=Proc. Natl. Acad. Sci. U.S.A. |volume=98 |issue=16 |pages=8966–8971 |date=July 2001 |pmid=11459929 |pmc=55357 |doi=10.1073/pnas.151105198}}</ref>

單胺的{{tsl|en|autoreceptors||自身受體}}（例如：[[多巴胺受體D2|D<sub>2</sub> short]]、{{tsl|en|Alpha-2 adrenergic receptor||presynaptic α<sub>2</sub>}}、和{{tsl|en|5-HT1A||presynaptic 5-HT<sub>1A</sub>}})）具有與TAAR1相反的效果，而這些受體形成了一個對於單胺的管理系統。{{r|Miller|Miller+Grandy 2016}}

值得注意的是，安非他命和[[痕量胺]]擁有對TAAR1相當高的[[配體 (生物化學)|連結親緣性（連結吸引力）]]，但對於單胺之{{tsl|en|autoreceptors||autoreceptors}}則不然。{{r|Miller|Miller+Grandy 2016}}

神經造影研究表示，安非他命和痕量胺對单胺类神经递质的再回收抑制作用具有位置上的針對性，進一步來說，就是針對那些相關且有TAAR1同時存在的单胺类神经递质神經元。{{r|Miller}}

{{As of|2010|post=,}}，TAAR1和[[多巴胺轉運體]]的「共同位置化」{{nowrap|co-localization}}現象已可在恒河猴身上透過視覺化的方式觀察到，但【帶有[[去甲腎上腺素轉運體]](NET)的TAAR1】和【[[血清素轉運體]](SERT)】的共同位置化現象迄今只能透過[[信使核糖核酸]](mRNA)的表現（expression）來證明。{{r|Miller}}

{{trans H}}

In addition to the neuronal monoamine [[Membrane transport protein|transporters]], amphetamine also inhibits both [[vesicular monoamine transporter]]s, [[VMAT1]] and [[VMAT2]], as well as [[SLC1A1]], [[SLC22A3]], and [[SLC22A5]].{{refn|group=來源組|name="Reuptake inhibition"|{{r|E Weihe|EAAT3|IUPHAR VMATs|SLC1A1|SLC22A3|SLC22A5|pmid13677912}}}} SLC1A1 is [[excitatory amino acid transporter 3]] (EAAT3), a glutamate transporter located in neurons, SLC22A3 is an extraneuronal monoamine transporter that is present in [[astrocyte]]s, and SLC22A5 is a high-affinity [[carnitine]] transporter.{{refn|name="Reuptake inhibition"|group=來源組}}Amphetamine is known to strongly induce [[cocaine- and amphetamine-regulated transcript]] (CART) [[gene expression]],{{r|Drugbank-amph}}<ref name="CART NAcc">{{cite journal |vauthors=Vicentic A, Jones DC |title=The CART (cocaine- and amphetamine-regulated transcript) system in appetite and drug addiction |url=https://archive.org/details/sim_journal-of-pharmacology-and-experimental-therapeutics_2007-02_320_2/page/499 |journal=J. Pharmacol. Exp. Ther. |volume=320 |issue=2 |pages=499–506 |date=February 2007 |pmid=16840648 |doi=10.1124/jpet.105.091512 |quote=The physiological importance of CART was further substantiated in numerous human studies demonstrating a role of CART in both feeding and psychostimulant addiction.&nbsp;... Colocalization studies also support a role for CART in the actions of psychostimulants.&nbsp;... CART and DA receptor transcripts colocalize (Beaudry et al., 2004). Second, dopaminergic nerve terminals in the NAc synapse on CART-containing neurons (Koylu et al., 1999), hence providing the proximity required for neurotransmitter signaling. These studies suggest that DA plays a role in regulating CART gene expression possibly via the activation of CREB.}}</ref>a [[neuropeptide]] involved in feeding behavior, stress, and reward, which induces observable increases in neuronal development and survival ''[[in vitro]]''.{{r|Drugbank-amph}}<ref name="CART functions">{{cite journal |vauthors=Zhang M, Han L, Xu Y |title=Roles of cocaine- and amphetamine-regulated transcript in the central nervous system |journal=Clin. Exp. Pharmacol. Physiol. |volume=39 |issue=6 |pages=586–592 |date=June 2012 |pmid=22077697 |doi=10.1111/j.1440-1681.2011.05642.x |quote=Recently, it was demonstrated that CART, as a neurotrophic peptide, had a cerebroprotective against focal ischaemic stroke and inhibited the neurotoxicity of β-amyloid protein, which focused attention on the role of CART in the central nervous system (CNS) and neurological diseases.&nbsp;... The literature indicates that there are many factors, such as regulation of the immunological system and protection against energy failure, that may be involved in the cerebroprotection afforded by CART}}</ref><ref name="CART">{{cite journal |vauthors=Rogge G, Jones D, Hubert GW, Lin Y, Kuhar MJ |title=CART peptides: regulators of body weight, reward and other functions |journal=Nat. Rev. Neurosci. |volume=9 |issue=10 |pages=747–758 |date=October 2008 |pmid=18802445 |pmc=4418456 |doi=10.1038/nrn2493 |quote=Several studies on CART (cocaine- and amphetamine-regulated transcript)-peptide-induced cell signalling have demonstrated that CART peptides activate at least three signalling mechanisms. First, CART 55–102 inhibited voltage-gated L-type Ca2+ channels&nbsp;...}}</ref>The CART receptor has yet to be identified, but there is significant evidence that CART binds to a unique {{nowrap|[[Gi alpha subunit|G<sub>i</sub>/G<sub>o</sub>-coupled]]}} {{abbr|GPCR|G protein-coupled receptor}}.{{r|CART}}<ref name="pmid21855138">{{cite journal |vauthors=Lin Y, Hall RA, Kuhar MJ |title=CART peptide stimulation of G protein-mediated signaling in differentiated PC12 cells: identification of PACAP 6–38 as a CART receptor antagonist |journal=Neuropeptides |volume=45 |issue=5 |pages=351–358 |date=October 2011 |pmid=21855138 |pmc=3170513 |doi=10.1016/j.npep.2011.07.006 }}</ref>Amphetamine also inhibits [[monoamine oxidase]]s at very high doses, resulting in less monoamine and trace amine metabolism and consequently higher concentrations of synaptic monoamines.<ref name="PubChem Header">{{cite encyclopedia |title=Amphetamine |section-url=https://pubchem.ncbi.nlm.nih.gov/summary/summary.cgi?cid=3007 |work=PubChem Compound |publisher=United States National Library of Medicine&nbsp;– National Center for Biotechnology Information |accessdate=17 April 2015 |date=11 April 2015 |section=Compound Summary }}</ref><ref name="BRENDA MAO Homo sapiens">{{cite encyclopedia |title=Monoamine oxidase (Homo sapiens) |url=http://www.brenda-enzymes.info/enzyme.php?ecno=1.4.3.4&Suchword=&organism%5B%5D=Homo+sapiens&show_tm=0 |work=BRENDA |publisher=Technische Universität Braunschweig |accessdate=4 May 2014 |date=1 January 2014 |archivedate=2020-07-27 |archiveurl=https://web.archive.org/web/20200727221409/https://www.brenda-enzymes.info/enzyme.php?ecno=1.4.3.4&Suchword=&organism%5B%5D=Homo+sapiens&show_tm=0 |deadurl=no }}</ref>In humans, the only post-synaptic receptor at which amphetamine is known to bind is the [[5-HT1A receptor|{{nowrap|5-HT1A}} receptor]], where it acts as an agonist with [[micromolar]] affinity.{{r|5HT1A secondary|5HT1A Primary}}

The full profile of amphetamine's short-term drug effects in humans is mostly derived through increased cellular communication or [[neurotransmission]] of [[dopamine]],<ref name="Miller"/>[[serotonin]],{{r|Miller}}[[norepinephrine]],{{r|Miller}}[[epinephrine]],<ref name="E Weihe"/>[[histamine]],{{r|E Weihe}}[[cocaine and amphetamine regulated transcript|CART peptides]],{{r|Drugbank-amph|CART NAcc}}[[endogenous opioid]]s,<ref name="Amphetamine-induced endogenous opioid release review">{{cite journal |vauthors=Finnema SJ, Scheinin M, Shahid M, Lehto J, Borroni E, Bang-Andersen B, Sallinen J, Wong E, Farde L, Halldin C, Grimwood S |title=Application of cross-species PET imaging to assess neurotransmitter release in brain |journal=Psychopharmacology |volume=232 |issue=21–22 |pages=4129–4157 |date=November 2015 |pmid=25921033 |pmc=4600473 |doi=10.1007/s00213-015-3938-6 |quote=More recently, Colasanti and colleagues reported that a pharmacologically induced elevation in endogenous opioid release reduced [<sup>11</sup>C]carfentanil binding in several regions of the human brain, including the basal ganglia, frontal cortex, and thalamus (Colasanti et al. 2012). Oral administration of d-amphetamine, 0.5&nbsp;mg/kg, 3&nbsp;h before [<sup>11</sup>C]carfentanil injection, reduced BPND values by 2–10&nbsp;%. The results were confirmed in another group of subjects (Mick et al. 2014). However, Guterstam and colleagues observed no change in [<sup>11</sup>C]carfentanil binding when d-amphetamine, 0.3&nbsp;mg/kg, was administered intravenously directly before injection of [<sup>11</sup>C]carfentanil (Guterstam et al. 2013). It has been hypothesized that this discrepancy may be related to delayed increases in extracellular opioid peptide concentrations following amphetamine-evoked monoamine release (Colasanti et al. 2012; Mick et al. 2014).}}</ref><ref name="Opioids">{{cite journal |vauthors=Loseth GE, Ellingsen DM, Leknes S |title=State-dependent μ-opioid modulation of social motivation |journal=Front. Behav. Neurosci. |volume=8 |pages=1–15 |date=December 2014 |pmid=25565999 |pmc=4264475 |doi=10.3389/fnbeh.2014.00430 |quote=Similar MOR activation patterns were reported during positive mood induced by an amusing video clip (Koepp et al., 2009) and following amphetamine administration in humans (Colasanti et al., 2012). }}</ref><ref name="Opioids cited primary source">{{cite journal |vauthors=Colasanti A, Searle GE, Long CJ, Hill SP, Reiley RR, Quelch D, Erritzoe D, Tziortzi AC, Reed LJ, Lingford-Hughes AR, Waldman AD, Schruers KR, Matthews PM, Gunn RN, Nutt DJ, Rabiner EA |title=Endogenous opioid release in the human brain reward system induced by acute amphetamine administration |journal=Biol. Psychiatry |volume=72 |issue=5 |pages=371–377 |date=September 2012 |pmid=22386378 |doi=10.1016/j.biopsych.2012.01.027}}</ref>[[adrenocorticotropic hormone]],{{r|Human amph effects|Primary: Human HPA axis}}[[corticosteroid]]s,{{r|Human amph effects|Primary: Human HPA axis}}and [[glutamate]],{{r|EAAT3|SLC1A1}}which it effects through interactions with {{abbr|CART|cocaine- and amphetamine-regulated transcript}}, {{nowrap|{{abbr|5-HT1A|serotonin receptor 1A}}}}, {{abbr|EAAT3|excitatory amino acid transporter 3}}, {{abbr|TAAR1|trace amine-associated receptor 1}}, {{abbr|VMAT1|vesicular monoamine transporter 1}}, {{abbr|VMAT2|vesicular monoamine transporter 2}}, and possibly other [[biological target]]s.{{refn|group=來源組|{{r|Miller|E Weihe|IUPHAR VMATs|SLC1A1|CART NAcc|5HT1A secondary}}}}

Dextroamphetamine is a more potent agonist of {{abbr|TAAR1|trace amine-associated receptor 1}} than levoamphetamine.{{r|TAAR1 stereoselective}}Consequently, dextroamphetamine produces greater {{abbr|CNS|central nervous system}} stimulation than levoamphetamine, roughly three to four times more, but levoamphetamine has slightly stronger cardiovascular and peripheral effects.{{r|Westfall}}<ref name="TAAR1 stereoselective">{{cite journal |vauthors=Lewin AH, Miller GM, Gilmour B |title=Trace amine-associated receptor 1 is a stereoselective binding site for compounds in the amphetamine class |journal=Bioorg. Med. Chem. |date=December 2011 |volume=19 |issue=23 |pages=7044–7048 |pmid=22037049 |doi= 10.1016/j.bmc.2011.10.007 |pmc= 3236098}}</ref>

{{trans F}}

==歷史、社會與文化==
===成药===
目前几种安非他命的处方药配方含有两种对映异构体，包括阿得拉尔，Dyanavel XR和Evekeo，其中最后一种是外消旋的安非他命硫酸盐。{{r|Amph Uses|Evekeo|Dyanavel}}目前的一些品牌及其通用等同物如下。

{| class="wikitable sortable" style="text-align:center; width:500px;"
|+ 成分為安非他命的藥品<br>Amphetamine pharmaceuticals
!scope="col"|藥物商品名稱 
!scope="col"| [[United States Adopted Name|United States<br>Adopted Name]]
!scope="col" class="unsortable" style="text-align:center"| [[wikt:enantiomeric ratio|(D:L) ratio]]
!scope="col"|藥劑型<br>Dosage<br>form
!scope="col" class="unsortable"| 上市日期Marketing<br>start date
!scope="col" class="unsortable"| {{small|來源}}
|-
| Adderall || – || 3:1 {{small|(salts)}}<!--DO NOT CHANGE THIS RATIO: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3666194/table/table1-0269881113482532/ -->|| [[錠劑]]<br>tablet || 1996 || {{r|Amph Uses|NDCD}}
|-
| Adderall XR || – || 3:1 {{small|(salts)}} || [[膠囊]]<br>capsule || 2001 || {{r|Amph Uses|NDCD}}
|-
| Adzenys XR || amphetamine || 3:1 {{small|(base)}} || {{tsl|en|Orally disintegrating tablet||ODT}} || 2016 || <ref name="Adzenys">{{cite web|title=Adzenys XR Prescribing Information|url=http://www.accessdata.fda.gov/drugsatfda_docs/label/2016/204326s000lbl.pdf|accessdate=2016-03-07|date=January 2016|website=United States Food and Drug Administration|publisher=Neos Therapeutics, Inc.|archiveurl=https://web.archive.org/web/20201030024233/https://www.accessdata.fda.gov/drugsatfda_docs/label/2016/204326s000lbl.pdf|archivedate=2020-10-30|deadurl=no|quote=ADZENYS XR-ODT (amphetamine extended-release orally disintegrating tablet) contains a 3 to 1 ratio of d- to l-amphetamine, a central nervous system stimulant.|page=15}}</ref><ref name="FDA Adzenys approval date">{{cite web|title=Adzenys XR|url=http://www.accessdata.fda.gov/scripts/cder/drugsatfda/index.cfm?fuseaction=Search.SearchAction&SearchTerm=Adzenys&SearchType=BasicSearch|accessdate=2016-03-07|website=United States Food and Drug Administration}}</ref>
|-
| Dyanavel XR || amphetamine || 3.2:1 {{small|(base)}} || suspension || 2015 || {{r|Dyanavel}}<ref name="FDA Dyanavel approval date">{{cite web|title=Dyanavel XR|url=http://www.accessdata.fda.gov/scripts/cder/drugsatfda/index.cfm?fuseaction=Search.SearchAction&SearchTerm=Dyanavel&SearchType=BasicSearch|accessdate=2016-01-01|website=United States Food and Drug Administration}}</ref>
|-
| Evekeo || amphetamine sulfate || 1:1 {{small|(salts)}} || tablet || 2012 || {{r|Evekeo}}<ref name="Racemic amph - FDA Evekeo status">{{cite web|title=Evekeo|url=http://www.accessdata.fda.gov/scripts/cder/drugsatfda/index.cfm?fuseaction=Search.SearchAction&SearchTerm=Evekeo&SearchType=BasicSearch|accessdate=2015-08-11|website=United States Food and Drug Administration}}</ref>
|-
| Dexedrine || dextroamphetamine sulfate || 1:0 {{small|(salts)}} || capsule || 1976 || {{r|Amph Uses|NDCD}}
|-
| ProCentra || dextroamphetamine sulfate || 1:0 {{small|(salts)}} || liquid || 2010 || {{r|NDCD}}
|-
| Zenzedi || dextroamphetamine sulfate || 1:0 {{small|(salts)}} || tablet || 2013 || {{r|NDCD}}
|-
|rowspan=2| Vyvanse ||rowspan=2| lisdexamfetamine dimesylate ||rowspan=2| 1:0 {{small|(prodrug)}} || capsule ||rowspan=2| 2007 ||rowspan=2| {{r|Amph Uses|FDA Vyvanse}}
|-
| tablet
|}[[File:Lisdexamfetamine-Structural Formula V.1.svg|thumb|left|The skeletal structure of lisdexamfetamine|alt=An image of the lisdexamfetamine compound]]{{已上市安非他命藥物中的安非他命物質組成}}

==備註A==
<!--Notes list-->
{{reflist|group=note}}
{{notelist-ur}}

==備註B==
{{noteFoot}}

==備註C==
<!--Notes list-->
{{reflist|group=Color legend}}

==註釋==
{{notelist}}

<!-- {{reflist|group=Color legend}} -->
==英文名稱對照==
{{div col|cols=2}}
{{refFoot}}
{{div col end}}

==引用==
{{reflist|group=來源組|33em}}

===來源===
{{Reflist|3|refs=
<ref name="rhinitis">{{cite journal |vauthors=Ramey JT, Bailen E, Lockey RF |title=Rhinitis medicamentosa |journal=J. Investig. Allergol. Clin. Immunol. |volume=16 |issue=3 |pages=148–155 |year=2006 |pmid=16784007 |accessdate=2015-04-29 |url=http://www.jiaci.org/issues/vol16issue03/1.pdf |quote=Table 2. Decongestants Causing Rhinitis Medicamentosa<br> – Nasal decongestants:<br>&nbsp; – Sympathomimetic:<br>&nbsp;&nbsp; · Amphetamine |archivedate=2020-05-10 |archiveurl=https://web.archive.org/web/20200510160743/http://www.jiaci.org/issues/vol16issue03/1.pdf |deadurl=no }}</ref>

<ref name="FDA - cardiovascular effects in young individuals">{{cite web |title=FDA Drug Safety Communication: Safety Review Update of Medications used to treat Attention-Deficit/Hyperactivity Disorder (ADHD) in children and young adults |date=2011-12-20 |url=http://www.fda.gov/Drugs/DrugSafety/ucm277770.htm |work=United States Food and Drug Administration |accessdate=2013-11-04 |archivedate=2013-10-30 |archiveurl=https://web.archive.org/web/20131030042927/http://www.fda.gov/Drugs/DrugSafety/ucm277770.htm |deadurl=no }}</ref>

<ref name="pmid22043968">{{cite journal |vauthors=Cooper WO, Habel LA, Sox CM, Chan KA, Arbogast PG, Cheetham TC, Murray KT, Quinn VP, Stein CM, Callahan ST, Fireman BH, Fish FA, Kirshner HS, O'Duffy A, Connell FA, Ray WA |title=ADHD drugs and serious cardiovascular events in children and young adults |journal=N. Engl. J. Med. |volume=365 |issue=20 |pages=1896–1904 |date=2011-11 |pmid=22043968 |doi=10.1056/NEJMoa1110212 |pmc=4943074}}</ref>

<ref name="FDA - cardiovascular effects in adults">{{cite web |title=FDA Drug Safety Communication: Safety Review Update of Medications used to treat Attention-Deficit/Hyperactivity Disorder (ADHD) in adults |date=2011-12-15 |url=http://www.fda.gov/Drugs/DrugSafety/ucm279858.htm |work=United States Food and Drug Administration |accessdate=2013-11-04 |archivedate=2013-10-30 |archiveurl=https://web.archive.org/web/20131030064843/http://www.fda.gov/Drugs/DrugSafety/ucm279858.htm |deadurl=no }}</ref>

<ref name="pmid22161946">{{cite journal |vauthors=Habel LA, Cooper WO, Sox CM, Chan KA, Fireman BH, Arbogast PG, Cheetham TC, Quinn VP, Dublin S, Boudreau DM, Andrade SE, Pawloski PA, Raebel MA, Smith DH, Achacoso N, Uratsu C, Go AS, Sidney S, Nguyen-Huynh MN, Ray WA, Selby JV |title=ADHD medications and risk of serious cardiovascular events in young and middle-aged adults |date=2011-12 |journal=JAMA |volume=306 |issue=24 |pages=2673–2683 |pmid=22161946 |pmc=3350308 |doi=10.1001/jama.2011.1830 }}</ref>

<ref name="Libido">{{cite journal |author=Montgomery KA |title=Sexual desire disorders |journal=Psychiatry (Edgmont) |volume=5 |issue=6 |pages=50–55 |date=2008-06 |pmid=19727285 |pmc=2695750}}</ref>

<ref name="Merck_Manual_Amphetamines">{{cite web |url=http://www.merckmanuals.com/professional/special_subjects/drug_use_and_dependence/amphetamines.html |author=O'Connor PG |title=Amphetamines |work=Merck Manual for Health Care Professionals |publisher=Merck |date=2012-02 |accessdate=2012-05-08 |archivedate=2012-05-06 |archiveurl=https://web.archive.org/web/20120506232123/http://www.merckmanuals.com/professional/special_subjects/drug_use_and_dependence/amphetamines.html |deadurl=no }}</ref>

<ref name="Acute amph toxicity">{{cite journal |vauthors=Greene SL, Kerr F, Braitberg G |title=Review article: amphetamines and related drugs of abuse |journal=Emerg. Med. Australas |volume=20 |issue=5 |pages=391–402 |date=2008-10 |pmid=18973636 |doi=10.1111/j.1742-6723.2008.01114.x }}</ref>

<ref name="Albertson_2011">{{cite book|veditors=Olson KR, Anderson IB, Benowitz NL, Blanc PD, Kearney TE, Kim-Katz SY, Wu AH |title=Poisoning & Drug Overdose |author=Albertson TE |year=2011 |publisher=McGraw-Hill Medical |location=New York |isbn=9780071668330 |chapter=Amphetamines |pages=77–79 |edition=6th }}</ref>

<ref name="Alcoholism ΔFosB">{{cite web |title=Alcoholism – Homo sapiens (human) |url=http://www.genome.jp/kegg-bin/show_pathway?hsa05034+2354 |work=KEGG Pathway |accessdate=2014-10-31 |author=Kanehisa Laboratories |date=2014-10-29 |archivedate=2019-11-12 |archiveurl=https://web.archive.org/web/20191112211634/https://www.genome.jp/kegg-bin/show_pathway?hsa05034+2354 |deadurl=no }}</ref>

<ref name="MPH ΔFosB">{{cite journal |vauthors=Kim Y, Teylan MA, Baron M, Sands A, Nairn AC, Greengard P |title=Methylphenidate-induced dendritic spine formation and DeltaFosB expression in nucleus accumbens |journal=Proc. Natl. Acad. Sci. U.S.A. |volume=106 |issue=8 |pages=2915–2920 |date=2009-02 |pmid=19202072 |pmc=2650365 |doi=10.1073/pnas.0813179106 }}</ref>

<ref name="pmid22392347">{{cite journal |vauthors=Carvalho M, Carmo H, Costa VM, Capela JP, Pontes H, Remião F, Carvalho F, Bastos Mde L |title=Toxicity of amphetamines: an update |journal=Arch. Toxicol. |volume=86 |issue=8 |pages=1167–1231 |date=August 2012 |pmid=22392347 |doi=10.1007/s00204-012-0815-5}}</ref>

<ref name="Autoxidation1">{{cite journal |vauthors=Sulzer D, Zecca L |title=Intraneuronal dopamine-quinone synthesis: a review |journal=Neurotox. Res. |volume=1 |issue=3 |pages=181–195 |date=February 2000 |pmid=12835101 |doi=10.1007/BF03033289 }}</ref>

<ref name="Autoxidation2">{{cite journal |vauthors=Miyazaki I, Asanuma M |title=Dopaminergic neuron-specific oxidative stress caused by dopamine itself |journal=Acta Med. Okayama |volume=62 |issue=3 |pages=141–150 |date=2008-06 |pmid=18596830 |url=http://ousar.lib.okayama-u.ac.jp/files/public/3/30980/20160528022138672578/fulltext.pdf |access-date=2017-04-30 |archivedate=2020-12-22 |archiveurl=https://web.archive.org/web/20201222011254/http://ousar.lib.okayama-u.ac.jp/files/public/3/30980/20160528022138672578/fulltext.pdf |deadurl=no }}</ref>

<ref name="Substituted amphetamines, FMO, and DBH">{{cite book |author=Glennon RA |editor=Lemke TL, Williams DA, Roche VF, Zito W |section-url=https://books.google.com/books?id=Sd6ot9ul-bUC&pg=PA646&q=substituted%20derivatives%20substituents%20hydroxyamphetamine%20flavin%20monooxygenase#v=onepage |title=Foye's principles of medicinal chemistry |section=Phenylisopropylamine stimulants: amphetamine-related agents |year=2013 |publisher=Wolters Kluwer Health/Lippincott Williams & Wilkins |location=Philadelphia, USA |accessdate  =2015-09-11 |archivedate=2019-06-09 |archiveurl=https://web.archive.org/web/20190609143420/https://books.google.com/books?id=Sd6ot9ul-bUC&pg=PA646&q=substituted%20derivatives%20substituents%20hydroxyamphetamine%20flavin%20monooxygenase#v=onepage |deadurl=no |isbn=9781609133450 |pages=646–648 |edition=7th |quote=The phase 1 metabolism of amphetamine analogs is catalyzed by two systems: cytochrome P450 and flavin monooxygenase.&nbsp;... Amphetamine can also undergo aromatic hydroxylation to ''p''-hydroxyamphetamine. &nbsp;... Subsequent oxidation at the benzylic position by DA β-hydroxylase affords ''p''-hydroxynorephedrine. Alternatively, direct oxidation of amphetamine by DA β-hydroxylase can afford norephedrine. }}</ref>

<ref name="DBH amph primary">{{cite journal |author=Taylor KB |url=http://www.jbc.org/content/249/2/454.full.pdf |title=Dopamine-beta-hydroxylase. Stereochemical course of the reaction |date=1974-01 |accessdate=2014-11-06 |archivedate=2019-04-04 |archiveurl=https://web.archive.org/web/20190404164303/http://www.jbc.org/content/249/2/454.full.pdf |journal=J. Biol. Chem. |volume=249 |issue=2 |pages=454–458 |pmid=4809526 |deadurl=no |quote=Dopamine-β-hydroxylase catalyzed the removal of the pro-R hydrogen atom and the production of 1-norephedrine, (2S,1R)-2-amino-1-hydroxyl-1-phenylpropane, from d-amphetamine.}}</ref>

<ref name="DBH 4-HA primary">{{cite journal |author=Horwitz D, Alexander RW, Lovenberg W, Keiser HR |title=Human serum dopamine-β-hydroxylase. Relationship to hypertension and sympathetic activity |url=https://archive.org/details/sim_circulation-research_1973-05_32_5/page/n59 |journal=Circ. Res. |volume=32 |issue=5 |pages=594–599 |date=May 1973 |pmid=4713201 |doi=10.1161/01.RES.32.5.594 |quote=Subjects with exceptionally low levels of serum dopamine-β-hydroxylase activity showed normal cardiovascular function and normal β-hydroxylation of an administered synthetic substrate, hydroxyamphetamine. }}</ref>

<ref name="FMO">{{cite journal |author=Krueger SK, Williams DE |title=Mammalian flavin-containing monooxygenases: structure/function, genetic polymorphisms and role in drug metabolism |journal=Pharmacol. Ther. |volume=106 |issue=3 |pages=357–387 |date=2005-06 |pmid=15922018 |pmc=1828602 |doi=10.1016/j.pharmthera.2005.01.001}}<br>"[https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1828602/table/T5/ Table 5: N-containing drugs and xenobiotics oxygenated by FMO] {{Wayback|url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1828602/table/T5/ |date=20180916144516 }}"</ref>

<ref name="FMO3-Primary">{{cite journal |author=Cashman JR, Xiong YN, Xu L, Janowsky A |title=N-oxygenation of amphetamine and methamphetamine by the human flavin-containing monooxygenase (form 3): role in bioactivation and detoxication |journal=J. Pharmacol. Exp. Ther. |volume=288 |issue=3 |pages=1251–1260 |date=March 1999 |pmid=10027866 }}</ref>

<ref name="EAAT3">{{cite journal |vauthors=Underhill SM, Wheeler DS, Li M, Watts SD, Ingram SL, Amara SG |title=Amphetamine modulates excitatory neurotransmission through endocytosis of the glutamate transporter EAAT3 in dopamine neurons |journal=Neuron |volume=83 |issue=2 |pages=404–416 |date=2014-07 |pmid=25033183 |pmc=4159050 |doi=10.1016/j.neuron.2014.05.043 |quote=AMPH also increases intracellular calcium (Gnegy et al., 2004) that is associated with calmodulin/CamKII activation (Wei et al., 2007) and modulation and trafficking of the DAT (Fog et al., 2006; Sakrikar et al., 2012).&nbsp;... For example, AMPH increases extracellular glutamate in various brain regions including the striatum, VTA and NAc (Del Arco et al., 1999; Kim et al., 1981; Mora and Porras, 1993; Xue et al., 1996), but it has not been established whether this change can be explained by increased synaptic release or by reduced clearance of glutamate.&nbsp;... DHK-sensitive, EAAT2 uptake was not altered by AMPH (Figure 1A). The remaining glutamate transport in these midbrain cultures is likely mediated by EAAT3 and this component was significantly decreased by AMPH}}</ref>

<ref name="IUPHAR VMATs">{{cite web|title=SLC18 family of vesicular amine transporters|url=http://www.guidetopharmacology.org/GRAC/FamilyDisplayForward?familyId=193|website=IUPHAR database|publisher=International Union of Basic and Clinical Pharmacology|accessdate=2015-11-13 |archivedate=2020-10-28|archiveurl=https://web.archive.org/web/20201028082500/https://www.guidetopharmacology.org/GRAC/FamilyDisplayForward?familyId=193|deadurl=no}}</ref>

<ref name="SLC1A1">{{cite web |title=SLC1A1 solute carrier family 1 (neuronal/epithelial high affinity glutamate transporter, system Xag), member 1 [ Homo sapiens (human) ] |url=https://www.ncbi.nlm.nih.gov/gene/6505 |website=NCBI Gene |publisher=United States National Library of Medicine&nbsp;– National Center for Biotechnology Information |accessdate=2014-11-11 |quote=Amphetamine modulates excitatory neurotransmission through endocytosis of the glutamate transporter EAAT3 in dopamine neurons.&nbsp;... internalization of EAAT3 triggered by amphetamine increases glutamatergic signaling and thus contributes to the effects of amphetamine on neurotransmission. |archivedate=2020-10-21 |archiveurl=https://web.archive.org/web/20201021172834/https://www.ncbi.nlm.nih.gov/gene/6505 |deadurl=no }}</ref>

<ref name="SLC22A3">{{cite journal |vauthors=Zhu HJ, Appel DI, Gründemann D, Markowitz JS |title=Interaction of organic cation transporter 3 (SLC22A3) and amphetamine |journal=J. Neurochem. |volume=114 |issue=1 |pages=142–149 |date=2010-07 |pmid=20402963 |pmc=3775896 |doi=10.1111/j.1471-4159.2010.06738.x}}</ref>

<ref name="SLC22A5">{{cite journal |vauthors=Rytting E, Audus KL |title=Novel organic cation transporter 2-mediated carnitine uptake in placental choriocarcinoma (BeWo) cells |url=https://archive.org/details/sim_journal-of-pharmacology-and-experimental-therapeutics_2005-01_312_1/page/192 |journal=J. Pharmacol. Exp. Ther. |volume=312 |issue=1 |pages=192–198 |date=January 2005 |pmid=15316089 |doi=10.1124/jpet.104.072363}}</ref>

<ref name="pmid13677912">{{cite journal |vauthors=Inazu M, Takeda H, Matsumiya T |title=[The role of glial monoamine transporters in the central nervous system] |language=ja |journal=Nihon Shinkei Seishin Yakurigaku Zasshi |volume=23 |issue=4 |pages=171–178 |date=August 2003 |pmid=13677912}}</ref>
}}

==參見==
* [[配體 (生物化學)#受體與配體間的結合親和性|結合親和性]]
* [[體能鍛煉]]
* [[血管收縮]]

==外部連結==
<!--Sidebar templates-->
{{Commons|Amphetamine}}
{{Commons category|Amphetamine|Category:Amphetamine}}
<!--List of external links-->
* {{PubChem|3007}}&nbsp;– Amphetamine
* {{PubChem|5826}}&nbsp;– Dextroamphetamine
* {{PubChem|32893}}&nbsp;– Levoamphetamine
* [http://ctdbase.org/query.go?type=ixn&chemqt=equals&chem=name%3AAmphetamine&actionDegreeTypes=increases&actionDegreeTypes=decreases&actionDegreeTypes=affects&actionTypes=ANY&geneqt=equals&gene=&pathwayqt=equals&pathway=&taxonqt=equals&taxon=TAXON%3A9606&goqt=equals&go=&sort=chemNmSort&perPage=500&action=Search Comparative Toxicogenomics Database entry: Amphetamine] {{Wayback|url=http://ctdbase.org/query.go?type=ixn&chemqt=equals&chem=name%3AAmphetamine&actionDegreeTypes=increases&actionDegreeTypes=decreases&actionDegreeTypes=affects&actionTypes=ANY&geneqt=equals&gene=&pathwayqt=equals&pathway=&taxonqt=equals&taxon=TAXON%3A9606&goqt=equals&go=&sort=chemNmSort&perPage=500&action=Search |date=20200710184244 }}
* [http://ctdbase.org/detail.go?type=gene&acc=9607&qid=2119242 Comparative Toxicogenomics Database entry: CARTPT]{{Wayback|url=http://ctdbase.org/detail.go?type=gene&acc=9607&qid=2119242 |date=20140302115529 }}
* {{youtube|PLbKSbFnKYVY07Rmg3OOd8OpHMCu1dDaUq| Drug abuse and drug addictions}}
* {{youtube|NxHNxmJv2bQ| Mechanism of Drug Addiction in the Brain, Animation.}}
* {{youtube|PLbKSbFnKYVY052TitB2-YHF2mGJp3_QJH| Drug dependence}}
[https://law.moj.gov.tw/LawClass/LawAll.aspx?PCode=C0000008 毒品危害防制條例-全國法規資料庫] {{Wayback|url=https://law.moj.gov.tw/LawClass/LawAll.aspx?PCode=C0000008 |date=20190611153517 }}

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Module:Hatnote（查看源代码）（全保护）
Module:Hatnote/styles.css（查看源代码）（全保护）
Module:Hatnote list（查看源代码）（模板保护）
Module:IPAc-en（查看源代码）（半保护）
Module:IPAc-en/data（查看源代码）（半保护）
Module:IPAc-en/phonemes（查看源代码）（半保护）
Module:IPAc-en/pronunciation（查看源代码）（半保护）
Module:If empty（查看源代码）（全保护）
Module:If preview（查看源代码）（全保护）
Module:If preview/configuration（查看源代码）（全保护）
Module:If preview/styles.css（查看源代码）（全保护）
Module:Ilh（查看源代码）（全保护）
Module:Ilh/data（查看源代码）（全保护）
Module:Infobox（查看源代码）（全保护）
Module:Infobox/styles.css（查看源代码）（全保护）
Module:InfoboxImage（查看源代码）（全保护）
Module:Labelled list hatnote（查看源代码）（模板保护）
Module:Lan（查看源代码）（全保护）
Module:Lan2（查看源代码）（全保护）
Module:Lang（查看源代码）（全保护）
Module:Lang/ISO 639 synonyms（查看源代码）（全保护）
Module:Lang/data（查看源代码）（全保护）
Module:Language/data/iana languages（查看源代码）（全保护）
Module:Language/data/iana regions（查看源代码）（全保护）
Module:Language/data/iana scripts（查看源代码）（全保护）
Module:Language/data/iana suppressed scripts（查看源代码）（全保护）
Module:Language/data/iana variants（查看源代码）（全保护）
Module:List（查看源代码）（全保护）
Module:Message box（查看源代码）（全保护）
Module:Message box/configuration（查看源代码）（全保护）
Module:Namespace（查看源代码）（全保护）
Module:Namespace/data（查看源代码）（全保护）
Module:Namespace detect（查看源代码）（全保护）
Module:Namespace detect/config（查看源代码）（全保护）
Module:Namespace detect/data（查看源代码）（全保护）
Module:Navbar（查看源代码）（全保护）
Module:Navbar/configuration（查看源代码）（全保护）
Module:Navbar/styles.css（查看源代码）（全保护）
Module:Navbox（查看源代码）（全保护）
Module:Navbox/styles.css（查看源代码）（全保护）
Module:No globals（查看源代码）（全保护）
Module:NoteTA（查看源代码）（全保护）
Module:Pagetype（查看源代码）（全保护）
Module:Pagetype/config（查看源代码）（全保护）
Module:Redirect（查看源代码）（模板保护）
Module:Redirect hatnote（查看源代码）（半保护）
Module:Separated entries（查看源代码）（全保护）
Module:Side box（查看源代码）（全保护）
Module:Side box/styles.css（查看源代码）（全保护）
Module:String（查看源代码）（全保护）
Module:TableTools（查看源代码）（全保护）
Module:TemplatePar（查看源代码）（半保护）
Module:Template invocation（查看源代码）（模板保护）
Module:Unicode data（查看源代码）（全保护）
Module:Unstrip（编辑）
Module:Unsubst（查看源代码）（全保护）
Module:WikidataCheck（查看源代码）（模板保护）
Module:WikitextLC（查看源代码）（全保护）
Module:Yesno（查看源代码）（全保护）
返回苯丙胺。
检索自“https://zh.wikipedia.org/wiki/苯丙胺”
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