References

1. Heal DJ, Smith SL, Gosden J, Nutt DJ (June 2013). "Amphetamine,

past and present a pharmacological and clinical perspective". J.
Psychopharmacol. 27 (6): 479
496. doi:10.1177/0269881113482532.PMC 3666194. PMID 2353964
2. 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. ... 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).
2. "Pharmacology". Dextroamphetamine. DrugBank. University of
Alberta. 8 February 2013. Retrieved 5 November 2013.
3. "Pharmacology". Amphetamine. DrugBank. University of Alberta. 8
February 2013. Retrieved 5 November 2013.
4. "Adderall XR Prescribing Information" (PDF). United States Food and
Drug Administration. Shire US Inc. December 2013. pp. 1213.
Retrieved30 December 2013.
5. Glennon RA (2013). "Phenylisopropylamine stimulants:
amphetamine-related agents". In Lemke TL, Williams DA, Roche VF,
Zito W. Foye's principles of medicinal chemistry (7th ed.).
Philadelphia, USA: Wolters Kluwer Health/Lippincott Williams &
Wilkins. pp. 646648.ISBN 9781609133450. Retrieved 11
September 2015. The simplest unsubstituted phenylisopropylamine,
1-phenyl-2-aminopropane, or amphetamine, serves as a common
structural template for hallucinogens and psychostimulants.
Amphetamine produces central stimulant, anorectic, and
sympathomimetic actions, and it is the prototype member of this
class (39). ... The phase 1 metabolism of amphetamine analogs is
catalyzed by two systems: cytochrome P450 and flavin
monooxygenase. ... Amphetamine can also undergo aromatic
hydroxylation to p-hydroxyamphetamine. ... Subsequent oxidation
at the benzylic position by DA -hydroxylase affordsphydroxynorephedrine. Alternatively, direct oxidation of
amphetamine by DA -hydroxylase can afford norephedrine.
6. Taylor KB (January 1974). "Dopamine-beta-hydroxylase.
Stereochemical course of the reaction" (PDF). J. Biol. Chem. 249 (2):
454458.PMID 4809526. Retrieved 6 November 2014. Dopamine--

hydroxylase catalyzed the removal of the pro-R hydrogen atom and

the production of 1-norephedrine, (2S,1R)-2-amino-1-hydroxyl-1phenylpropane, from d-amphetamine.
7. Horwitz D, Alexander RW, Lovenberg W, Keiser HR (May 1973).
"Human serum dopamine--hydroxylase. Relationship to
hypertension and sympathetic activity". Circ. Res. 32 (5): 594
599.doi:10.1161/01.RES.32.5.594. PMID 4713201. Subjects with
exceptionally low levels of serum dopamine--hydroxylase activity
showed normal cardiovascular function and normal -hydroxylation
of an administered synthetic substrate, hydroxyamphetamine.
8. Krueger SK, Williams DE (June 2005). "Mammalian flavin-containing
monooxygenases: structure/function, genetic polymorphisms and
role in drug metabolism". Pharmacol. Ther. 106 (3): 357
387.doi:10.1016/j.pharmthera.2005.01.001. PMC 1828602. PMID 15
922018.
"Table 5: N-containing drugs and xenobiotics oxygenated by FMO"
9. Cashman JR, Xiong YN, Xu L, Janowsky A (March 1999). "Noxygenation of amphetamine and methamphetamine by the human
flavin-containing monooxygenase (form 3): role in bioactivation and
detoxication". J. Pharmacol. Exp. Ther. 288 (3): 1251
1260. PMID 10027866.
10."Pharmacology and Biochemistry". Amphetamine. Pubchem
Compound. National Center for Biotechnology Information.
Retrieved 12 October 2013.
11.Santagati NA, Ferrara G, Marrazzo A, Ronsisvalle G (September
2002). "Simultaneous determination of amphetamine and one of its
metabolites by HPLC with electrochemical detection". J. Pharm.
Biomed. Anal. 30 (2): 247255. doi:10.1016/S0731-7085(02)003308. PMID 12191709.
12."Pharmacology". amphetamine/dextroamphetamine. Medscape.
WebMD. Retrieved 21 January 2016. Onset of action: 3060 min
13.Millichap JG (2010). "Chapter 9: Medications for ADHD". In Millichap
JG. Attention Deficit Hyperactivity Disorder Handbook: A Physician's
Guide to ADHD (2nd ed.). New York, USA: Springer.
p. 112.ISBN 9781441913968.
Table 9.2 Dextroamphetamine formulations of stimulant medication
Dexedrine [Peak:23 h] [Duration:56 h] ...
Adderall [Peak:23 h] [Duration:57 h]
Dexedrine spansules [Peak:78 h] [Duration:12 h] ...
Adderall XR [Peak:78 h] [Duration:12 h]
Vyvanse [Peak:34 h] [Duration:12 h]

14.Brams M, Mao AR, Doyle RL (September 2008). "Onset of efficacy of

long-acting psychostimulants in pediatric attentiondeficit/hyperactivity disorder". Postgrad. Med. 120 (3): 69
88. doi:10.3810/pgm.2008.09.1909.PMID 18824827.
15."Adderall IR Prescribing Information" (PDF). United States Food and
Drug Administration. Barr Laboratories, Inc. March 2007. pp. 15.
Retrieved2 November 2013.
16."Biological Half-Life". AMPHETAMINE. United States National Library
of Medicine Toxnet. Hazardous Substances Data Bank. Retrieved 5
January2014. 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%.
17.Mignot EJ (October 2012). "A practical guide to the therapy of
narcolepsy and hypersomnia syndromes". Neurotherapeutics 9 (4):
739752.doi:10.1007/s13311-012-0150-9. PMC 3480574. PMID 2306
5655.
18."Compound Summary". Amphetamine. PubChem Compound.
National Center for Biotechnology Information. 11 April 2015.
Retrieved 17 April2015.
19.Yoshida T (1997). "Chapter 1: Use and Misuse of Amphetamines: An
International Overview". In Klee H. Amphetamine Misuse:
International Perspectives on Current Trends. Amsterdam,
Netherlands: Harwood Academic Publishers.
p. 2. ISBN 9789057020810. Retrieved 1
December2014. Amphetamine, in the singular form, properly
applies to the racemate of 2-amino-1-phenylpropane. ... In its
broadest context, however, the term [amphetamines] can even
embrace a large number of structurally and pharmacologically
related substances.
20."Properties: Predicted EP|Suite". Amphetamine. Chemspider.
Retrieved6 November 2013.
21."Chemical and Physical Properties". Amphetamine. PubChem
Compound. National Center for Biotechnology Information.
Retrieved 13 October 2013.
22."Identification". Amphetamine. DrugBank. University of Alberta. 8
February 2013. Retrieved 13 October 2013.
23.Greene SL, Kerr F, Braitberg G (October 2008). "Review article:
amphetamines and related drugs of abuse". Emerg. Med.

Australas 20 (5): 391402. doi:10.1111/j.17426723.2008.01114.x. PMID 18973636.

24."Enantiomer". IUPAC Goldbook. International Union of Pure and
Applied Chemistry. doi:10.1351/goldbook.E02069. Archived from the
original on 17 March 2013. Retrieved 14 March 2014. One of a pair
of molecular entities which are mirror images of each other and
non-superposable.
25.Malenka RC, Nestler EJ, Hyman SE (2009). "Chapter 13: Higher
Cognitive Function and Behavioral Control". In Sydor A, Brown
RY. Molecular Neuropharmacology: A Foundation for Clinical
Neuroscience (2nd ed.). New York, USA: McGraw-Hill Medical. p. 318,
321.ISBN 9780071481274. 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. ... 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 ...
through indirect stimulation of dopamine and norepinephrine
receptors. ...
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.
Drugs used for this purpose include, as stated above,
methylphenidate, amphetamines, atomoxetine, and desipramine.
26.Liddle DG, Connor DJ (June 2013). "Nutritional supplements and
ergogenic AIDS". Prim. Care 40 (2): 487
505. doi:10.1016/j.pop.2013.02.009.PMID 23668655. 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 ...
Physiologic and performance effects
Amphetamines increase dopamine/norepinephrine release and
inhibit their reuptake, leading to central nervous system (CNS)
stimulation
Amphetamines seem to enhance athletic performance in
anaerobic conditions 39 40
Improved reaction time
Increased muscle strength and delayed muscle fatigue
Increased acceleration
Increased alertness and attention to task
27."Adderall XR Prescribing Information" (PDF). United States Food and
Drug Administration. Shire US Inc. December 2013. p. 11.
Retrieved30 December 2013.

28.Rasmussen N (July 2006). "Making the first anti-depressant:

amphetamine in American medicine, 19291950". J . Hist. Med.
Allied Sci. 61 (3): 288
323. doi:10.1093/jhmas/jrj039. PMID 16492800.
29."Convention on psychotropic substances". United Nations Treaty
Collection. United Nations. Retrieved 11 November 2013.
30.Wilens TE, Adler LA, Adams J, Sgambati S, Rotrosen J, Sawtelle R,
Utzinger L, Fusillo S (January 2008). "Misuse and diversion of
stimulants prescribed for ADHD: a systematic review of the
literature". J. Am. Acad. Child Adolesc. Psychiatry 47 (1): 21
31.doi:10.1097/chi.0b013e31815a56f1. PMID 18174822. Stimulant
misuse appears to occur both for performance enhancement and
their euphorogenic effects, the latter being related to the intrinsic
properties of the stimulants (e.g., IR versus ER profile) ...
Although useful in the treatment of ADHD, stimulants are controlled
II substances with a history of preclinical and human studies
showing potential abuse liability.
31.Montgomery KA (June 2008). "Sexual desire disorders". Psychiatry
(Edgmont) 5 (6): 5055. PMC 2695750. PMID 19727285.
32."Amphetamine". Medical Subject Headings. National Institutes of
Health, National Library of Medicine. Retrieved 16 December 2013.
33."Guidelines on the Use of International Nonproprietary Names
(INNS) for Pharmaceutical Substances". World Health Organization.
1997. Retrieved1 December 2014. 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. ... The latter are called modified INNs
(INNMs).
34."Evekeo Prescribing Information" (PDF). Arbor Pharmaceuticals LLC.
April 2014. pp. 12. Retrieved 11 August 2015.
35."National Drug Code Amphetamine Search Results". National Drug
Code Directory. United States Food and Drug Administration.
Archived from the original on 7 February 2014. Retrieved 16
December 2013.

36."Adderall XR Prescribing Information" (PDF). United States Food and

Drug Administration. Shire US Inc. December 2013. pp. 48.
Retrieved30 December 2013.
37.Miller GM (January 2011). "The emerging role of trace amineassociated receptor 1 in the functional regulation of monoamine
transporters and dopaminergic activity". J. Neurochem. 116 (2):
164176.doi:10.1111/j.1471-4159.2010.07109.x. PMC 3005101. PMI
D 21073468.
38.Grandy DK, Miller GM, Li JX (February 2016). ""TAARgeting
Addiction"-The Alamo Bears Witness to Another Revolution: An
Overview of the Plenary Symposium of the 2015 Behavior, Biology
and Chemistry Conference". Drug Alcohol Depend. 159: 9
16.doi:10.1016/j.drugalcdep.2015.11.014. PMID 26644139. 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.
39.Westfall DP, Westfall TC (2010). "Miscellaneous Sympathomimetic
Agonists". In Brunton LL, Chabner BA, Knollmann BC. Goodman &
Gilman's Pharmacological Basis of Therapeutics (12th ed.). New
York, USA: McGraw-Hill. ISBN 9780071624428.
40.Shoptaw SJ, Kao U, Ling W (January 2009). Shoptaw SJ, Ali R, ed.
"Treatment for amphetamine psychosis". Cochrane Database Syst.
Rev. (1):
CD003026. doi:10.1002/14651858.CD003026.pub3. PMID 19160215
. 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 ...
About 515% of the users who develop an amphetamine psychosis
fail to recover completely (Hofmann 1983) ...
Findings from one trial indicate use of antipsychotic medications
effectively resolves symptoms of acute amphetamine psychosis.
41.Greydanus D. "Stimulant Misuse: Strategies to Manage a Growing
Problem" (PDF). American College Health Association (Review
Article). ACHA Professional Development Program. p. 20. Archived
from the original (PDF) on 3 November 2013. Retrieved 2
November 2013.

42.Kollins SH (May 2008). "A qualitative review of issues arising in the

use of psycho-stimulant medications in patients with ADHD and comorbid substance use disorders". Curr. Med. Res. Opin. 24 (5):
13451357.doi:10.1185/030079908X280707. PMID 18384709. 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.
43.Stolerman IP (2010). Stolerman IP, ed. Encyclopedia of
Psychopharmacology. Berlin, Germany; London, England: Springer.
p. 78.ISBN 9783540686989.
44.Broadley KJ (March 2010). "The vascular effects of trace amines and
amphetamines". Pharmacol. Ther. 125 (3): 363
375.doi:10.1016/j.pharmthera.2009.11.005. PMID 19948186.
45."Amphetamine". European Monitoring Centre for Drugs and Drug
Addiction. Retrieved 19 October 2013.
46.Carvalho M, Carmo H, Costa VM, Capela JP, Pontes H, Remio F,
Carvalho F, Bastos Mde L (August 2012). "Toxicity of amphetamines:
an update". Arch. Toxicol. 86 (8): 11671231. doi:10.1007/s00204012-0815-5.PMID 22392347.
47.Berman S, O'Neill J, Fears S, Bartzokis G, London ED (October
2008)."Abuse of amphetamines and structural abnormalities in the
brain". Ann. N. Y. Acad. Sci. 1141: 195
220. doi:10.1196/annals.1441.031. PMC 2769923.PMID 18991959.
48.Hart H, Radua J, Nakao T, Mataix-Cols D, Rubia K (February 2013).
"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". JAMA
Psychiatry 70(2): 185
198. doi:10.1001/jamapsychiatry.2013.277. PMID 23247506.
49.Spencer TJ, Brown A, Seidman LJ, Valera EM, Makris N, Lomedico A,
Faraone SV, Biederman J (September 2013). "Effect of
psychostimulants on brain structure and function in ADHD: a
qualitative literature review of magnetic resonance imaging-based
neuroimaging studies". J. Clin. Psychiatry 74 (9): 902
917. doi:10.4088/JCP.12r08287. PMC 3801446.PMID 24107764.
50.Frodl T, Skokauskas N (February 2012). "Meta-analysis of structural
MRI studies in children and adults with attention deficit hyperactivity
disorder indicates treatment effects.". Acta psychiatrica
Scand. 125 (2): 114126.doi:10.1111/j.16000447.2011.01786.x. PMID 22118249.

51.Millichap JG (2010). "Chapter 9: Medications for ADHD". In Millichap

JG. Attention Deficit Hyperactivity Disorder Handbook: A Physician's
Guide to ADHD (2nd ed.). New York, USA: Springer. pp. 121123,
125127. ISBN 9781441913968. 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.
52.Arnold LE, Hodgkins P, Caci H, Kahle J, Young S (February
2015). "Effect of treatment modality on long-term outcomes in
attention-deficit/hyperactivity disorder: a systematic review". PLoS
ONE 10 (2):
e0116407. doi:10.1371/journal.pone.0116407. PMC 4340791.PMID 2
5714373. 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.
53.Huang YS, Tsai MH (July 2011). "Long-term outcomes with
medications for attention-deficit hyperactivity disorder: current
status of knowledge".CNS Drugs 25 (7): 539
554. doi:10.2165/11589380-000000000-00000.PMID 21699268. Rec
ent studies have demonstrated that stimulants, along with the nonstimulants atomoxetine and extended-release guanfacine, are
continuously effective for more than 2-year treatment periods with
few and tolerable adverse effects.
54.Malenka RC, Nestler EJ, Hyman SE (2009). "Chapter 6: Widely
Projecting Systems: Monoamines, Acetylcholine, and Orexin". In
Sydor A, Brown RY.Molecular Neuropharmacology: A Foundation for
Clinical Neuroscience(2nd ed.). New York, USA: McGraw-Hill Medical.
pp. 154157.ISBN 9780071481274.
55.Bidwell LC, McClernon FJ, Kollins SH (August 2011). "Cognitive
enhancers for the treatment of ADHD". Pharmacol. Biochem.
Behav. 99 (2): 262
274. doi:10.1016/j.pbb.2011.05.002. PMC 3353150. PMID 21596055.
56.Parker J, Wales G, Chalhoub N, Harpin V (September 2013). "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". Psychol. Res.
Behav. Manag. 6: 87
99.doi:10.2147/PRBM.S49114. PMC 3785407. PMID 24082796. Only
one paper53 examining outcomes beyond 36 months met the review
criteria. ... 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.
57.Millichap JG (2010). "Chapter 9: Medications for ADHD". In Millichap
JG. Attention Deficit Hyperactivity Disorder Handbook: A Physician's
Guide to ADHD (2nd ed.). New York, USA: Springer. pp. 111
113.ISBN 9781441913968.
58."Stimulants for Attention Deficit Hyperactivity Disorder". WebMD.
Healthwise. 12 April 2010. Retrieved 12 November 2013.
59.Scholten RJ, Clarke M, Hetherington J (August 2005). "The Cochrane
Collaboration". Eur. J. Clin. Nutr. 59 Suppl 1: S147S149; discussion
S195S196. doi:10.1038/sj.ejcn.1602188. PMID 16052183.
60.Castells X, Ramos-Quiroga JA, Bosch R, Nogueira M, Casas M (June
2011). Castells X, ed. "Amphetamines for Attention Deficit
Hyperactivity Disorder (ADHD) in adults". Cochrane Database Syst.
Rev. (6):
CD007813. doi:10.1002/14651858.CD007813.pub2. PMID 21678370
.
61.Punja S, Shamseer L, Hartling L, Urichuk L, Vandermeer B, Nikles J,
Vohra S (February 2016). "Amphetamines for attention deficit
hyperactivity disorder (ADHD) in children and
adolescents". Cochrane Database Syst. Rev. 2:
CD009996. doi:10.1002/14651858.CD009996.pub2.PMID 26844979.
62.Pringsheim T, Steeves T (April 2011). Pringsheim T, ed.
"Pharmacological treatment for Attention Deficit Hyperactivity
Disorder (ADHD) in children with comorbid tic disorders". Cochrane
Database Syst. Rev. (4):
CD007990. doi:10.1002/14651858.CD007990.pub2. PMID 21491404
.
63.Spencer RC, Devilbiss DM, Berridge CW (June 2015). "The CognitionEnhancing Effects of Psychostimulants Involve Direct Action in the
Prefrontal Cortex". Biol. Psychiatry 77 (11): 940
950.doi:10.1016/j.biopsych.2014.09.013. PMID 25499957. 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 2 and dopamine D1 receptors. ... This differential
modulation of PFC-dependent processes across dose appears to be
associated with the differential involvement of noradrenergic 2
versus 1 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 PFCdependent function). This information has potentially important
clinical implications as well as relevance for public health policy
regarding the widespread clinical use of psychostimulants and for
the development of novel pharmacologic treatments for attentiondeficit/hyperactivity disorder and other conditions associated with
PFC dysregulation. ... 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.
64.Ilieva IP, Hook CJ, Farah MJ (January 2015). "Prescription Stimulants'
Effects on Healthy Inhibitory Control, Working Memory, and Episodic
Memory: A Meta-analysis". J. Cogn. Neurosci.: 1
21.doi:10.1162/jocn_a_00776. PMID 25591060.
65.Bagot KS, Kaminer Y (April 2014). "Efficacy of stimulants for
cognitive enhancement in non-attention deficit hyperactivity
disorder youth: a systematic review". Addiction 109 (4): 547
557. doi:10.1111/add.12460.PMC 4471173. PMID 24749160. Amphe
tamine has been shown to improve consolidation of information
(0.02 P 0.05), leading to improved recall.
66.Devous MD, Trivedi MH, Rush AJ (April 2001). "Regional cerebral
blood flow response to oral amphetamine challenge in healthy
volunteers". J. Nucl. Med. 42 (4): 535542. PMID 11337538.
67.Malenka RC, Nestler EJ, Hyman SE (2009). "Chapter 10: Neural and
Neuroendocrine Control of the Internal Milieu". In Sydor A, Brown
RY.Molecular Neuropharmacology: A Foundation for Clinical
Neuroscience(2nd ed.). New York, USA: McGraw-Hill Medical.
p. 266.ISBN 9780071481274. Dopamine acts in the nucleus
accumbens to attach motivational significance to stimuli associated
with reward.
68.Wood S, Sage JR, Shuman T, Anagnostaras SG (January 2014).
"Psychostimulants and cognition: a continuum of behavioral and
cognitive activation". Pharmacol. Rev. 66 (1): 193
221. doi:10.1124/pr.112.007054.PMID 24344115.
69.Twohey M (26 March 2006). "Pills become an addictive study aid". JS
Online. Archived from the original on 15 August 2007. Retrieved2
December 2007.
70.Teter CJ, McCabe SE, LaGrange K, Cranford JA, Boyd CJ (October
2006)."Illicit use of specific prescription stimulants among college
students: prevalence, motives, and routes of

administration". Pharmacotherapy 26(10): 1501

1510. doi:10.1592/phco.26.10.1501. PMC 1794223.PMID 16999660.
71.Weyandt LL, Oster DR, Marraccini ME, Gudmundsdottir BG, Munro
BA, Zavras BM, Kuhar B (September 2014). "Pharmacological
interventions for adolescents and adults with ADHD: stimulant and
nonstimulant medications and misuse of prescription
stimulants". Psychol. Res. Behav. Manag. 7: 223
249. doi:10.2147/PRBM.S47013. PMC 4164338. PMID 25228824.mis
use of prescription stimulants has become a serious problem on
college campuses across the US and has been recently documented
in other countries as well. ... Indeed, large numbers of students
claim to have engaged in the nonmedical use of prescription
stimulants, which is reflected in lifetime prevalence rates of
prescription stimulant misuse ranging from 5% to nearly 34% of
students.
72.Clemow DB, Walker DJ (September 2014). "The potential for misuse
and abuse of medications in ADHD: a review". Postgrad.
Med. 126 (5): 64
81.doi:10.3810/pgm.2014.09.2801. PMID 25295651. Overall, the
data suggest that ADHD medication misuse and diversion are
common health care problems for stimulant medications, with the
prevalence believed to be approximately 5% to 10% of high school
students and 5% to 35% of college students, depending on the
study.
73.Bracken NM (January 2012). "National Study of Substance Use
Trends Among NCAA College Student-Athletes" (PDF). NCAA
Publications. National Collegiate Athletic Association. Retrieved 8
October 2013.
74.Docherty JR (June 2008). "Pharmacology of stimulants prohibited by
the World Anti-Doping Agency (WADA)". Br. J. Pharmacol. 154 (3):
606622. doi:10.1038/bjp.2008.124. PMC 2439527. PMID 18500382.
75.Parr JW (July 2011). "Attention-deficit hyperactivity disorder and the
athlete: new advances and understanding". Clin. Sports Med. 30 (3):
591610. doi:10.1016/j.csm.2011.03.007. PMID 21658550. In 1980,
Chandler and Blair47 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. ... In 2008, Roelands and colleagues53 studied the effect
of reboxetine, a pure NE reuptake inhibitor, similar to atomoxetine,

in 9 healthy, well-trained cyclists. They too exercised in both

temperate and warm environments. They showed decreased power
output and exercise performance at both 18 and 30 degrees
centigrade. Their conclusion was that DA reuptake inhibition was the
cause of the increased exercise performance seen with drugs that
affect both DA and NE (MPH, amphetamine, and bupropion).
76.Roelands B, de Koning J, Foster C, Hettinga F, Meeusen R (May
2013). "Neurophysiological determinants of theoretical concepts
and mechanisms involved in pacing". Sports Med. 43 (5): 301
311. doi:10.1007/s40279-013-0030-4. PMID 23456493. In highambient 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. ... 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.
77.Parker KL, Lamichhane D, Caetano MS, Narayanan NS (October
2013)."Executive dysfunction in Parkinson's disease and timing
deficits". Front. Integr. Neurosci. 7:
75. doi:10.3389/fnint.2013.00075. PMC 3813949.PMID 24198770. M
anipulations 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.
78.Rattray B, Argus C, Martin K, Northey J, Driller M (March 2015). "Is it
time to turn our attention toward central mechanisms for postexertional recovery strategies and performance?". Front. Physiol. 6:
79.doi:10.3389/fphys.2015.00079. PMC 4362407. PMID 25852568. A
side 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). ... Dopamine stimulating
drugs are known to enhance aspects of exercise performance
(Roelands et al., 2008)
79.Roelands B, De Pauw K, Meeusen R (June 2015). "Neurophysiological
effects of exercise in the heat". Scand. J. Med. Sci. Sports. 25 Suppl
1: 6578. doi:10.1111/sms.12350. PMID 25943657. Retrieved 10
March 2016.Physical fatigue has classically been attributed to
peripheral factors within the muscle (Fitts, 1996), the depletion of

muscle glycogen (Bergstrom & Hultman, 1967) or increased

cardiovascular, metabolic, and thermoregulatory strain (Abbiss &
Laursen, 2005; Meeusen etal., 2006b). In recent decennia however,
it became clear that the central nervous system plays an important
role in the onset of fatigue during prolonged exercise (Klass etal.,
2008), certainly when ambient temperature is increased ... 5-HT,
DA, and NA have all been implicated in the control of
thermoregulation and are thought to mediate thermoregulatory
responses, certainly since their neurons innervate the hypothalamus
(Roelands & Meeusen, 2010). ... 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. ... The combined effects of DA and NA on performance in the
heat were studied by our research group on a number of
occasions. ... the administration of bupropion (DA/NA reuptake
inhibitor) significantly improved performance. Coinciding with this
ergogenic effect, the authors observed core temperatures that were
much higher compared with the placebo situation. Interestingly, this
occurred without any change in the subjective feelings of thermal
sensation or perceived exertion. Similar to the methylphenidate
study (Roelands et al., 2008b), bupropion may dampen or override
inhibitory signals arising from the central nervous system to cease
exercise because of hyperthermia, and enable an individual to
continue maintaining a high power output
80.Kessler S (January 1996). "Drug therapy in attention-deficit
hyperactivity disorder". South. Med. J. 89 (1): 33
38. doi:10.1097/00007611-199601000-00005. PMID 8545689. state
ments on package inserts are not intended to limit medical practice.
Rather they are intended to limit claims by pharmaceutical
companies. ... the FDA asserts explicitly, and the courts have upheld
that clinical decisions are to be made by physicians and patients in
individual situations.
81."Adderall XR Prescribing Information" (PDF). United States Food and
Drug Administration. Shire US Inc. December 2013. pp. 46.
Retrieved30 December 2013.
82.Heedes G, Ailakis J. "Amphetamine (PIM 934)". INCHEM.
International Programme on Chemical Safety. Retrieved 24
June 2014.
83."Dexedrine Prescribing Information" (PDF). United States Food and
Drug Administration. Amedra Pharmaceuticals LLC. October 2013.
Retrieved4 November 2013.

84.Feinberg SS (November 2004). "Combining stimulants with

monoamine oxidase inhibitors: a review of uses and one possible
additional indication".J. Clin. Psychiatry 65 (11): 1520
1524. doi:10.4088/jcp.v65n1113.PMID 15554766.
85.Stewart JW, Deliyannides DA, McGrath PJ (June 2014). "How
treatable is refractory depression?". J. Affect. Disord. 167: 148
152.doi:10.1016/j.jad.2014.05.047. PMID 24972362.
86.Vitiello B (April 2008). "Understanding the risk of using medications
for attention deficit hyperactivity disorder with respect to physical
growth and cardiovascular function". Child Adolesc. Psychiatr. Clin.
N. Am. 17 (2): 459
474. doi:10.1016/j.chc.2007.11.010. PMC 2408826. PMID 18295156.
87."Dyanavel XR Prescribing Information" (PDF). Tris Pharmaceuticals.
October 2015. pp. 116. Retrieved 23 November 2015. DYANAVEL
XR contains d-amphetamine and l-amphetamine in a ratio of 3.2 to
1 ... 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 612
years) were: epistaxis, allergic rhinitis and upper abdominal pain. ...
DOSAGE FORMS AND STRENGTHS
Extended-release oral suspension contains 2.5 mg amphetamine
base per mL.
88.Ramey JT, Bailen E, Lockey RF (2006). "Rhinitis
medicamentosa" (PDF).J. Investig. Allergol. Clin. Immunol. 16 (3):
148155. PMID 16784007. Retrieved 29 April 2015. Table 2.
Decongestants Causing Rhinitis Medicamentosa
Nasal decongestants:
Sympathomimetic:
Amphetamine
89."FDA Drug Safety Communication: Safety Review Update of
Medications used to treat Attention-Deficit/Hyperactivity Disorder
(ADHD) in children and young adults". United States Food and Drug
Administration. 20 December 2011. Retrieved 4 November 2013.
90.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 (November 2011).
"ADHD drugs and serious cardiovascular events in children and
young adults". N. Engl. J. Med. 365 (20): 1896
1904. doi:10.1056/NEJMoa1110212.PMID 22043968.
91."FDA Drug Safety Communication: Safety Review Update of
Medications used to treat Attention-Deficit/Hyperactivity Disorder
(ADHD) in adults".United States Food and Drug Administration. 15
December 2011. Retrieved4 November 2013.

92.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 (December
2011). "ADHD medications and risk of serious cardiovascular events
in young and middle-aged adults". JAMA 306 (24): 2673
2683. doi:10.1001/jama.2011.1830.PMC 3350308. PMID 22161946.
93.O'Connor PG (February 2012). "Amphetamines". Merck Manual for
Health Care Professionals. Merck. Retrieved 8 May 2012.
94.Childs E, de Wit H (May 2009). "Amphetamine-induced place
preference in humans". Biol. Psychiatry 65 (10): 900
904.doi:10.1016/j.biopsych.2008.11.016. PMC 2693956. PMID 19111
278.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.
95.Malenka RC, Nestler EJ, Hyman SE (2009). "Chapter 15:
Reinforcement and Addictive Disorders". In Sydor A, Brown
RY. Molecular Neuropharmacology: A Foundation for Clinical
Neuroscience (2nd ed.). New York: McGraw-Hill Medical. pp. 364
375. ISBN 9780071481274.
96.Spiller HA, Hays HL, Aleguas A (June 2013). "Overdose of drugs for
attention-deficit hyperactivity disorder: clinical presentation,
mechanisms of toxicity, and management". CNS Drugs 27 (7): 531
543.doi:10.1007/s40263-013-0084-8. PMID 23757186. Amphetamin
e, 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.
97.Collaborators (2015). "Global, regional, and national age-sex
specific all-cause and cause-specific mortality for 240 causes of
death, 19902013: a systematic analysis for the Global Burden of
Disease Study 2013" (PDF).Lancet 385 (9963): 117
171. doi:10.1016/S0140-6736(14)61682-2.PMC 4340604. PMID 2553
0442. Retrieved 3 March 2015. Amphetamine use disorders ...
3,788 (3,4254,145)
98.Kanehisa Laboratories (10 October 2014). "Amphetamine Homo
sapiens (human)". KEGG Pathway. Retrieved 31 October 2014.
99.Nechifor M (March 2008). "Magnesium in drug
dependences". Magnes. Res. 21 (1): 515. PMID 18557129.

100.
Ruffle JK (November 2014). "Molecular neurobiology of
addiction: what's all the ()FosB about?". Am. J. Drug Alcohol
Abuse 40 (6): 428
437.doi:10.3109/00952990.2014.933840. PMID 25083822. FosB is
an essential transcription factor implicated in the molecular and
behavioral pathways of addiction following repeated drug exposure.
101.
Nestler EJ (December 2013). "Cellular basis of memory for
addiction".Dialogues Clin. Neurosci. 15 (4): 431
443. PMC 3898681.PMID 24459410.
102.
Robison AJ, Nestler EJ (November 2011). "Transcriptional and
epigenetic mechanisms of addiction". Nat. Rev. Neurosci. 12 (11):
623637.doi:10.1038/nrn3111. PMC 3272277. PMID 21989194. Fos
B serves as one of the master control proteins governing this
structural plasticity.
103.
Olsen CM (December 2011). "Natural rewards, neuroplasticity,
and non-drug addictions". Neuropharmacology 61 (7): 1109
1122.doi:10.1016/j.neuropharm.2011.03.010. PMC 3139704. PMID 2
1459101.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). ... 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).
104.
Lynch WJ, Peterson AB, Sanchez V, Abel J, Smith MA
(September 2013)."Exercise as a novel treatment for drug addiction:
a neurobiological and stage-dependent hypothesis". Neurosci.
Biobehav. Rev. 37 (8): 1622
1644.doi:10.1016/j.neubiorev.2013.06.011. PMC 3788047. PMID 238
06439.These findings suggest that exercise may magnitudedependently 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. ... 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 ... 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.
105.
Zhou Y, Zhao M, Zhou C, Li R (July 2015). "Sex differences in
drug addiction and response to exercise intervention: From human
to animal studies". Front.
Neuroendocrinol. doi:10.1016/j.yfrne.2015.07.001.PMID 26182835.
Collectively, these findings demonstrate that exercise may serve as
a substitute or competition for drug abuse by changing FosB or
cFos immunoreactivity in the reward system to protect against later
or previous drug use. ... As briefly reviewed above, a large number
of human and rodent studies clearly show that there are sex
differences in drug addiction and exercise. The sex differences are
also found in the effectiveness of exercise on drug addiction
prevention and treatment, as well as underlying neurobiological
mechanisms. The postulate that exercise serves as an ideal
intervention for drug addiction has been widely recognized and used
in human and animal rehabilitation. ... In particular, more studies on
the neurobiological mechanism of exercise and its roles in
preventing and treating drug addiction are needed.
106.
Linke SE, Ussher M (January 2015). "Exercise-based
treatments for substance use disorders: evidence, theory, and
practicality". Am. J. Drug Alcohol Abuse 41 (1): 7
15. doi:10.3109/00952990.2014.976708.PMID 25397661. The
limited research conducted suggests that exercise may be an
effective adjunctive treatment for SUDs. In contrast to the scarce
intervention trials to date, a relative abundance of literature on the
theoretical and practical reasons supporting the investigation of this
topic has been published. ... numerous theoretical and practical
reasons support exercise-based treatments for SUDs, including
psychological, behavioral, neurobiological, nearly universal safety
profile, and overall positive health effects.
107.
Malenka RC, Nestler EJ, Hyman SE (2009). "Chapter 15:
Reinforcement and Addictive Disorders". In Sydor A, Brown
RY. Molecular Neuropharmacology: A Foundation for Clinical
Neuroscience (2nd ed.). New York, USA: McGraw-Hill Medical.
p. 386. ISBN 9780071481274.Currently, cognitivebehavioral
therapies are the most successful treatment available for preventing
the relapse of psychostimulant use.
108.
Albertson TE (2011). "Amphetamines". In Olson KR, Anderson
IB, Benowitz NL, Blanc PD, Kearney TE, Kim-Katz SY, Wu
AHB. Poisoning & Drug Overdose (6th ed.). New York: McGraw-Hill
Medical. pp. 7779.ISBN 9780071668330.

109.
"Glossary of Terms". Mount Sinai School of Medicine.
Department of Neuroscience. Retrieved 9 February 2015.
110.
Broussard JI (January 2012). "Co-transmission of dopamine
and glutamate". J. Gen. Physiol. 139 (1): 93
96. doi:10.1085/jgp.201110659.PMC 3250102. PMID 22200950.
111.
Descarries L, Berube-Carriere N, Riad M, Bo GD, Mendez JA,
Trudeau LE (August 2008). "Glutamate in dopamine neurons:
synaptic versus diffuse transmission". Brain Res. Rev. 58 (2): 290
302.doi:10.1016/j.brainresrev.2007.10.005. PMID 18042492.
112.
Kanehisa Laboratories (10 October 2014). "Amphetamine
Homo sapiens (human)". KEGG Pathway. Retrieved 31
October 2014.
113.
Renthal W, Nestler EJ (September 2009). "Chromatin
regulation in drug addiction and depression". Dialogues Clin.
Neurosci. 11 (3): 257268.PMC 2834246. PMID 19877494.
Retrieved 21 July 2014.
114.
Nestler EJ (October 2008). "Review. Transcriptional
mechanisms of addiction: role of DeltaFosB". Philos. Trans. R. Soc.
Lond., B, Biol. Sci.363 (1507): 3245
3255. doi:10.1098/rstb.2008.0067. PMC 2607320.PMID 18640924.
115.
Nestler EJ (December 2012). "Transcriptional mechanisms of
drug addiction". Clin. Psychopharmacol. Neurosci. 10 (3): 136
143.doi:10.9758/cpn.2012.10.3.136. PMC 3569166. PMID 23430970.
The 35-37 kD FosB isoforms accumulate with chronic drug
exposure due to their extraordinarily long half-lives. ... As a result of
its stability, the FosB protein persists in neurons for at least
several weeks after cessation of drug exposure. ... FosB
overexpression in nucleus accumbens induces NFB
116.
"Amphetamines: Drug Use and Abuse". Merck Manual Home
Edition. Merck. February 2003. Archived from the original on 17
February 2007. Retrieved 28 February 2007.
117.
Perez-Mana C, Castells X, Torrens M, Capella D, Farre M
(September 2013). Prez-Ma C, ed. "Efficacy of psychostimulant
drugs for amphetamine abuse or dependence". Cochrane Database
Syst. Rev. 9:
CD009695. doi:10.1002/14651858.CD009695.pub2. PMID 23996457
.
118.
Hyman SE, Malenka RC, Nestler EJ (July 2006). "Neural
mechanisms of addiction: the role of reward-related learning and
memory". Annu. Rev. Neurosci. 29: 565

598. doi:10.1146/annurev.neuro.29.051605.113009.PMID 16776597

.
119.
Robison AJ, Nestler EJ (November 2011). "Transcriptional and
epigenetic mechanisms of addiction". Nat. Rev. Neurosci. 12 (11):
623637.doi:10.1038/nrn3111. PMC 3272277. PMID 21989194.
120.
Steiner H, Van Waes V (January 2013). "Addiction-related gene
regulation: risks of exposure to cognitive enhancers vs. other
psychostimulants". Prog. Neurobiol. 100: 60
80. doi:10.1016/j.pneurobio.2012.10.001.PMC 3525776. PMID 23085
425.
121.
Malenka RC, Nestler EJ, Hyman SE (2009). "Chapter 4: Signal
Transduction in the Brain". In Sydor A, Brown RY. Molecular
Neuropharmacology: A Foundation for Clinical Neuroscience (2nd
ed.). New York, USA: McGraw-Hill Medical.
p. 94. ISBN 9780071481274.
122.
Kanehisa Laboratories (29 October 2014). "Alcoholism Homo
sapiens (human)". KEGG Pathway. Retrieved 31 October 2014.
123.
Kim Y, Teylan MA, Baron M, Sands A, Nairn AC, Greengard P
(February 2009). "Methylphenidate-induced dendritic spine
formation and DeltaFosB expression in nucleus accumbens". Proc.
Natl. Acad. Sci. U.S.A. 106 (8): 2915
2920. doi:10.1073/pnas.0813179106. PMC 2650365.PMID 19202072
.
124.
Nestler EJ (January 2014). "Epigenetic mechanisms of drug
addiction".Neuropharmacology. 76 Pt B: 259
268.doi:10.1016/j.neuropharm.2013.04.004. PMC 3766384. PMID 23
643695.
125.
Blum K, Werner T, Carnes S, Carnes P, Bowirrat A, Giordano J,
Oscar-Berman M, Gold M (March 2012). "Sex, drugs, and rock 'n' roll:
hypothesizing common mesolimbic activation as a function of
reward gene polymorphisms". J. Psychoactive Drugs 44 (1): 38
55.doi:10.1080/02791072.2012.662112. PMC 4040958. PMID 22641
964.
126.
Pitchers KK, Vialou V, Nestler EJ, Laviolette SR, Lehman MN,
Coolen LM (February 2013). "Natural and drug rewards act on
common neural plasticity mechanisms with FosB as a key
mediator". J. Neurosci. 33 (8): 3434
3442. doi:10.1523/JNEUROSCI.4881-12.2013. PMC 3865508.PMID 23
426671.
127.
Beloate LN, Weems PW, Casey GR, Webb IC, Coolen LM
(February 2016). "Nucleus accumbens NMDA receptor activation

regulates amphetamine cross-sensitization and deltaFosB

expression following sexual experience in male
rats". Neuropharmacology 101: 154
164.doi:10.1016/j.neuropharm.2015.09.023. PMID 26391065.
128.
Stoops WW, Rush CR (May 2014). "Combination
pharmacotherapies for stimulant use disorder: a review of clinical
findings and recommendations for future research". Expert Rev Clin
Pharmacol 7 (3): 363
374.doi:10.1586/17512433.2014.909283. PMID 24716825. Despite
concerted efforts to identify a pharmacotherapy for managing
stimulant use disorders, no widely effective medications have been
approved.
129.
Perez-Mana C, Castells X, Torrens M, Capella D, Farre M
(September 2013). "Efficacy of psychostimulant drugs for
amphetamine abuse or dependence". Cochrane Database Syst.
Rev. 9:
CD009695.doi:10.1002/14651858.CD009695.pub2. PMID 23996457.
To date, no pharmacological treatment has been approved for
[addiction], and psychotherapy remains the mainstay of
treatment. ... Results of this review do not support the use of
psychostimulant medications at the tested doses as a replacement
therapy
130.
Forray A, Sofuoglu M (February 2014). "Future
pharmacological treatments for substance use disorders". Br. J. Clin.
Pharmacol. 77 (2): 382400.doi:10.1111/j.13652125.2012.04474.x. PMC 4014020. PMID 23039267.
131.
Jing L, Li JX (August 2015). "Trace amine-associated receptor
1: A promising target for the treatment of psychostimulant
addiction". Eur. J. Pharmacol. 761: 345
352. doi:10.1016/j.ejphar.2015.06.019.PMID 26092759. Taken
together,the data reviewed here strongly support that TAAR1 is
implicated in the functional regulation of monoaminergic systems,
especially dopaminergic system, and that TAAR1 serves as a
homeostatic brake system that is involved in the modulation of
dopaminergic activity. Existing data provided robust preclinical
evidence supporting the development of TAAR1 agonists as
potential treatment for psychostimulant abuse and addiction. ...
Given that TAAR1 is primarily located in the intracellular
compartments and existing TAAR1 agonists are proposed to get
access to the receptors by translocation to the cell interior (Miller,
2011), future drug design and development efforts may need to
take strategies of drug delivery into consideration (Rajendran et al.,
2010).

132.
Malenka RC, Nestler EJ, Hyman SE (2009). "Chapter 5:
Excitatory and Inhibitory Amino Acids". In Sydor A, Brown
RY. Molecular Neuropharmacology: A Foundation for Clinical
Neuroscience (2nd ed.). New York, USA: McGraw-Hill Medical.
pp. 124125.ISBN 9780071481274.
133.
Shoptaw SJ, Kao U, Heinzerling K, Ling W (April 2009).
Shoptaw SJ, ed. "Treatment for amphetamine withdrawal". Cochrane
Database Syst. Rev.(2):
CD003021. doi:10.1002/14651858.CD003021.pub2. PMID 19370579
.
134.
"Adderall IR Prescribing Information" (PDF). United States
Food and Drug Administration. Barr Laboratories, Inc. March 2007.
Retrieved 4 November2013.
135.
"Adderall XR Prescribing Information" (PDF). United States
Food and Drug Administration. Shire US Inc. December 2013.
Retrieved 30 December2013.
136.
Advokat C (July 2007). "Update on amphetamine neurotoxicity
and its relevance to the treatment of ADHD". J. Atten. Disord. 11 (1):
816.doi:10.1177/1087054706295605. PMID 17606768.
137.
"Amphetamine". Hazardous Substances Data Bank. National
Library of Medicine. Retrieved 26 February 2014. Direct toxic
damage to vessels seems unlikely because of the dilution that
occurs before the drug reaches the cerebral circulation.
138.
Malenka RC, Nestler EJ, Hyman SE (2009). "Chapter 15:
Reinforcement and addictive disorders". In Sydor A, Brown
RY. Molecular Neuropharmacology: A Foundation for Clinical
Neuroscience (2nd ed.). New York, USA: McGraw-Hill Medical.
p. 370. ISBN 9780071481274.Unlike cocaine and amphetamine,
methamphetamine is directly toxic to midbrain dopamine neurons.
139.
Sulzer D, Zecca L (February 2000). "Intraneuronal dopaminequinone synthesis: a review". Neurotox. Res. 1 (3): 181
195.doi:10.1007/BF03033289. PMID 12835101.
140.
Miyazaki I, Asanuma M (June 2008). "Dopaminergic neuronspecific oxidative stress caused by dopamine itself". Acta Med.
Okayama 62 (3): 141150. PMID 18596830.
141.
Hofmann FG (1983). A Handbook on Drug and Alcohol Abuse:
The Biomedical Aspects (2nd ed.). New York, USA: Oxford University
Press. p. 329. ISBN 9780195030570.

142.
"Adderall XR Prescribing Information" (PDF). United States
Food and Drug Administration. Shire US Inc. December 2013. pp. 8
10. Retrieved30 December 2013.
143.
Eiden LE, Weihe E (January 2011). "VMAT2: a dynamic
regulator of brain monoaminergic neuronal function interacting with
drugs of abuse". Ann. N. Y. Acad. Sci. 1216: 86
98. doi:10.1111/j.1749-6632.2010.05906.x.PMC 4183197. PMID 212
72013.
144.
Ledonne A, Berretta N, Davoli A, Rizzo GR, Bernardi G, Mercuri
NB (July 2011). "Electrophysiological effects of trace amines on
mesencephalic dopaminergic neurons". Front. Syst. Neurosci. 5:
56.doi:10.3389/fnsys.2011.00056. PMC 3131148. PMID 21772817.
145.
mct (28 January 2012). "TAAR1". GenAtlas. University of Paris.
Retrieved29 May 2014.
tonically activates inwardly rectifying K(+) channels, which
reduces the basal firing frequency of dopamine (DA) neurons of the
ventral tegmental area (VTA)
146.
Maguire JJ, Davenport AP (2 December
2014). "TA1 receptor". IUPHAR database. International Union of Basic
and Clinical Pharmacology. Retrieved 8 December 2014.
147.
Underhill SM, Wheeler DS, Li M, Watts SD, Ingram SL, Amara
SG (July 2014). "Amphetamine modulates excitatory
neurotransmission through endocytosis of the glutamate transporter
EAAT3 in dopamine neurons".Neuron 83 (2): 404
416. doi:10.1016/j.neuron.2014.05.043. PMC 4159050.PMID 250331
83. 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).
148.
Vaughan RA, Foster JD (September 2013). "Mechanisms of
dopamine transporter regulation in normal and disease
states". Trends Pharmacol. Sci.34 (9): 489
496. doi:10.1016/j.tips.2013.07.005. PMC 3831354.PMID 23968642.
149.
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
(July 2001)."Trace amines: identification of a family of mammalian G
protein-coupled receptors". Proc. Natl. Acad. Sci. U.S.A. 98 (16):
89668971.doi:10.1073/pnas.151105198. PMC 55357. PMID 114599
29.

150.
"SLC18 family of vesicular amine transporters". IUPHAR
database. International Union of Basic and Clinical Pharmacology.
Retrieved13 November 2015.
151.
"SLC1A1 solute carrier family 1 (neuronal/epithelial high
affinity glutamate transporter, system Xag), member 1 [ Homo
sapiens (human) ]". NCBI Gene. National Center for Biotechnology
Information. Retrieved11 November 2014. Amphetamine modulates
excitatory neurotransmission through endocytosis of the glutamate
transporter EAAT3 in dopamine neurons. ... internalization of EAAT3
triggered by amphetamine increases glutamatergic signaling and
thus contributes to the effects of amphetamine on
neurotransmission.
152.
Zhu HJ, Appel DI, Grndemann D, Markowitz JS (July
2010). "Interaction of organic cation transporter 3 (SLC22A3) and
amphetamine". J. Neurochem. 114 (1): 142
149. doi:10.1111/j.1471-4159.2010.06738.x.PMC 3775896. PMID 20
402963.
153.
Rytting E, Audus KL (January 2005). "Novel organic cation
transporter 2-mediated carnitine uptake in placental
choriocarcinoma (BeWo) cells". J. Pharmacol. Exp. Ther. 312 (1):
192198. doi:10.1124/jpet.104.072363.PMID 15316089.
154.
Inazu M, Takeda H, Matsumiya T (August 2003). "[The role of
glial monoamine transporters in the central nervous system]". Nihon
Shinkei Seishin Yakurigaku Zasshi (in Japanese) 23 (4): 171
178. PMID 13677912.
155.
Vicentic A, Jones DC (February 2007). "The CART (cocaineand amphetamine-regulated transcript) system in appetite and drug
addiction". J. Pharmacol. Exp. Ther. 320 (2): 499
506. doi:10.1124/jpet.105.091512.PMID 16840648. The
physiological importance of CART was further substantiated in
numerous human studies demonstrating a role of CART in both
feeding and psychostimulant addiction. ... Colocalization studies
also support a role for CART in the actions of psychostimulants. ...
CART and DA receptor transcripts colocalize (Beaudry et al., 2004).
Second, dopaminergic nerve terminals in the NAc synapse on CARTcontaining 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.
156.
"Biomolecular Interactions and
Pathways". Amphetamine. PubChem Compound. National Center for
Biotechnology Information. Retrieved13 October 2013.

157.
Zhang M, Han L, Xu Y (June 2012). "Roles of cocaine- and
amphetamine-regulated transcript in the central nervous
system". Clin. Exp. Pharmacol. Physiol. 39 (6): 586
592. doi:10.1111/j.1440-1681.2011.05642.x.PMID 22077697. Recen
tly, it was demonstrated that CART, as a neurotrophic peptide, had a
cerebroprotective against focal ischaemic stroke and inhibited the
neurotoxicity of -amyloid protein, which focused attention on the
role of CART in the central nervous system (CNS) and neurological
diseases. 3. In fact, little is known about the way in which CART
peptide interacts with its receptors, initiates downstream cascades
and finally exerts its neuroprotective effect under normal or
pathological conditions. 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
158.
Rogge G, Jones D, Hubert GW, Lin Y, Kuhar MJ (October
2008). "CART peptides: regulators of body weight, reward and other
functions". Nat. Rev. Neurosci. 9 (10): 747
758. doi:10.1038/nrn2493. PMC 4418456.PMID 18802445. 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
55102 inhibited voltage-gated L-type Ca2+ channels ...
159.
Lin Y, Hall RA, Kuhar MJ (October 2011). "CART peptide
stimulation of G protein-mediated signaling in differentiated PC12
cells: identification of PACAP 638 as a CART receptor
antagonist". Neuropeptides 45 (5): 351
358. doi:10.1016/j.npep.2011.07.006. PMC 3170513. PMID 2185513
8.
160.
"Monoamine oxidase (Homo sapiens)". BRENDA. Technische
Universitt Braunschweig. 1 January 2014. Retrieved 4 May 2014.
161.
"Targets". Amphetamine. T3DB. University of Alberta.
Retrieved24 February 2015.
162.
Toll L, Berzetei-Gurske IP, Polgar WE, Brandt SR, Adapa ID,
Rodriguez L, Schwartz RW, Haggart D, O'Brien A, White A, Kennedy
JM, Craymer K, Farrington L, Auh JS (March 1998). "Standard binding
and functional assays related to medications development division
testing for potential cocaine and opiate narcotic treatment
medications". NIDA Res. Monogr.178: 440466. PMID 9686407.
163.
Hutson PH, Tarazi FI, Madhoo M, Slawecki C, Patkar AA
(September 2014). "Preclinical pharmacology of amphetamine:
implications for the treatment of neuropsychiatric

disorders". Pharmacol. Ther. 143 (3): 253

264. doi:10.1016/j.pharmthera.2014.03.005. PMID 24657455.
164.
Dickson SL, Egecioglu E, Landgren S, Skibicka KP, Engel JA,
Jerlhag E (June 2011). "The role of the central ghrelin system in
reward from food and chemical drugs". Mol. Cell.
Endocrinol. 340 (1): 80
87.doi:10.1016/j.mce.2011.02.017. PMID 21354264.
165.
Loseth GE, Ellingsen DM, Leknes S (December 2014). "Statedependent -opioid modulation of social motivation". Front. Behav.
Neurosci. 8: 1
15.doi:10.3389/fnbeh.2014.00430. PMC 4264475. PMID 25565999. S
imilar 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).
166.
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
(September 2012). "Endogenous opioid release in the human brain
reward system induced by acute amphetamine administration". Biol.
Psychiatry 72 (5): 371
377.doi:10.1016/j.biopsych.2012.01.027. PMID 22386378.
167.
Gunne LM (2013). "Effects of Amphetamines in
Humans". Drug Addiction II: Amphetamine, Psychotogen, and
Marihuana Dependence. Berlin, Germany; Heidelberg, Germany:
Springer. pp. 247260.ISBN 9783642667091. Retrieved 4
December 2015.
168.
Oswald LM, Wong DF, McCaul M, Zhou Y, Kuwabara H, Choi L,
Brasic J, Wand GS (April 2005). "Relationships among ventral striatal
dopamine release, cortisol secretion, and subjective responses to
amphetamine".Neuropsychopharmacology 30 (4): 821
832. doi:10.1038/sj.npp.1300667.PMID 15702139. Findings from
several prior investigations have shown that plasma levels of
glucocorticoids and ACTH are increased by acute administration of
AMPH in both rodents and humans
169.
Stuber GD, Hnasko TS, Britt JP, Edwards RH, Bonci A (June
2010)."Dopaminergic terminals in the nucleus accumbens but not
the dorsal striatum corelease glutamate". J. Neurosci. 30 (24):
82298233.doi:10.1523/JNEUROSCI.1754-10.2010. PMC 2918390. P
MID 20554874.
170.
Lewin AH, Miller GM, Gilmour B (December 2011). "Trace
amine-associated receptor 1 is a stereoselective binding site for
compounds in the amphetamine class". Bioorg. Med. Chem. 19 (23):

70447048.doi:10.1016/j.bmc.2011.10.007. PMC 3236098. PMID 22

037049.
171.
Maguire JJ, Parker WA, Foord SM, Bonner TI, Neubig RR,
Davenport AP (March 2009). "International Union of Pharmacology.
LXXII. Recommendations for trace amine receptor
nomenclature". Pharmacol. Rev.61 (1): 1
8. doi:10.1124/pr.109.001107. PMC 2830119. PMID 19325074.
172.
Revel FG, Moreau JL, Gainetdinov RR, Bradaia A, Sotnikova
TD, Mory R, Durkin S, Zbinden KG, Norcross R, Meyer CA, Metzler V,
Chaboz S, Ozmen L, Trube G, Pouzet B, Bettler B, Caron MG,
Wettstein JG, Hoener MC (May 2011). "TAAR1 activation modulates
monoaminergic neurotransmission, preventing hyperdopaminergic
and hypoglutamatergic activity". Proc. Natl. Acad. Sci.
U.S.A. 108 (20): 8485
8490.doi:10.1073/pnas.1103029108. PMC 3101002. PMID 21525407
.
173.
Richard RA (1999). "Route of Administration". Chapter 5
Medical Aspects of Stimulant Use Disorders. National Center for
Biotechnology Information Bookshelf. Treatment Improvement
Protocol 33. Substance Abuse and Mental Health Services
Administration.
174.
"Vyvanse Prescribing Information" (PDF). United States Food
and Drug Administration. Shire US Inc. January 2015. pp. 1216.
Retrieved24 February 2015.
175.
"Substrate/Product". butyrate-CoA ligase. BRENDA.
Technische Universitt Braunschweig. Retrieved 7 May 2014.
176.
"Substrate/Product". glycine N-acyltransferase. BRENDA.
Technische Universitt Braunschweig. Retrieved 7 May 2014.
177.
"Compound Summary". p-Hydroxyamphetamine. PubChem
Compound. National Center for Biotechnology Information.
Retrieved 15 October 2013.
178.
"Compound Summary". p-Hydroxynorephedrine. PubChem
Compound. National Center for Biotechnology Information.
Retrieved 15 October 2013.
179.
"Compound Summary". Phenylpropanolamine. PubChem
Compound. National Center for Biotechnology Information.
Retrieved 15 October 2013.
180.
Lindemann L, Hoener MC (May 2005). "A renaissance in trace
amines inspired by a novel GPCR family". Trends Pharmacol.

Sci. 26 (5): 274

281. doi:10.1016/j.tips.2005.03.007. PMID 15860375.
181.
"Amphetamine Hydrochloride". Pubchem Compound. National
Center for Biotechnology Information. Retrieved 8 November 2013.
182.
"Amphetamine Phosphate". Pubchem Compound. National
Center for Biotechnology Information. Retrieved 8 November 2013.
183.
Brussee J, Jansen ACA (May 1983). "A highly stereoselective
synthesis of s()-[1,1'-binaphthalene]-2,2'-diol". Tetrahedron
Lett. 24 (31): 32613262.doi:10.1016/S0040-4039(00)88151-4.
184.
Schep LJ, Slaughter RJ, Beasley DM (August 2010). "The
clinical toxicology of metamfetamine". Clin. Toxicol. (Phila.) 48 (7):
675694.doi:10.3109/15563650.2010.516752. ISSN 1556-3650. PMI
D 20849327.
185.
Lillsunde P, Korte T (March 1991). "Determination of ring- and
N-substituted amphetamines as heptafluorobutyryl
derivatives". Forensic Sci. Int. 49 (2): 205213. doi:10.1016/03790738(91)90081-s. PMID 1855720.
186.
"Historical overview of methamphetamine". Vermont
Department of Health. Government of Vermont. Retrieved 29
January 2012.
187.
Allen A, Ely R (April 2009). "Review: Synthetic Methods for
Amphetamine" (PDF). Crime Scene (Northwest Association of
Forensic Scientists) 37 (2): 1525. Retrieved 6 December 2014.
188.
Allen A, Cantrell TS (August 1989). "Synthetic reductions in
clandestine amphetamine and methamphetamine laboratories: A
review". Forensic Science International 42 (3): 183
199. doi:10.1016/0379-0738(89)90086-8.
189.
"Recommended methods of the identification and analysis of
amphetamine, methamphetamine, and their ring-substituted
analogues in seized materials"(PDF). United Nations Office on Drugs
and Crime. United Nations. 2006. pp. 912. Retrieved 14
October 2013.
190.
Pollard CB, Young DC (May 1951). "The Mechanism of the
Leuckart Reaction". J. Org. Chem. 16 (5): 661
672. doi:10.1021/jo01145a001.
191.
US patent 2276508, Nabenhauer FP, "Method for the
separation of optically active alpha-methylphenethylamine",
published 17 March 1942, assigned to Smith Kline French

192.
Gray DL (2007). "Approved Treatments for Attention Deficit
Hyperactivity Disorder: Amphetamine (Adderall), Methylphenidate
(Ritalin), and Atomoxetine (Straterra)". In Johnson DS, Li JJ. The Art
of Drug Synthesis. New York, USA: Wiley-Interscience.
p. 247. ISBN 9780471752158.
193.
Patrick TM, McBee ET, Hass HB (June 1946). "Synthesis of
arylpropylamines; from allyl chloride". J. Am. Chem. Soc. 68: 1009
1011.doi:10.1021/ja01210a032. PMID 20985610.
194.
Ritter JJ, Kalish J (December 1948). "A new reaction of nitriles;
synthesis of t-carbinamines". J. Am. Chem. Soc. 70 (12): 4048
4050.doi:10.1021/ja01192a023. PMID 18105933.
195.
Krimen LI, Cota DJ (March 2011). "The Ritter
Reaction". Organic Reactions 17:
216. doi:10.1002/0471264180.or017.03.
196.
US patent 2413493, Bitler WP, Flisik AC, Leonard N, "Synthesis
of isomer-free benzyl methyl acetoacetic methyl ester", published
31 December 1946, assigned to Kay Fries Chemicals Inc
197.
Collins M, Salouros H, Cawley AT, Robertson J, Heagney AC,
Arenas-Queralt A (June 2010). "13C and 2H isotope ratios in
amphetamine synthesized from benzaldehyde and
nitroethane". Rapid Commun. Mass Spectrom. 24 (11): 1653
1658. doi:10.1002/rcm.4563. PMID 20486262.
198.
Kraemer T, Maurer HH (August 1998). "Determination of
amphetamine, methamphetamine and amphetamine-derived
designer drugs or medicaments in blood and urine". J. Chromatogr.
B Biomed. Sci. Appl. 713 (1): 163187.doi:10.1016/S03784347(97)00515-X. PMID 9700558.
199.
Kraemer T, Paul LD (August 2007). "Bioanalytical procedures
for determination of drugs of abuse in blood". Anal. Bioanal.
Chem. 388 (7): 14151435. doi:10.1007/s00216-007-12716. PMID 17468860.
200.
Goldberger BA, Cone EJ (July 1994). "Confirmatory tests for
drugs in the workplace by gas chromatography-mass
spectrometry". J. Chromatogr. A674 (12): 7386. doi:10.1016/00219673(94)85218-9. PMID 8075776.
201.
"Clinical Drug Testing in Primary Care" (PDF). Substance
Abuse and Mental Health Services Administration. Technical
Assistance Publication Series 32. United States Department of
Health and Human Services. 2012. Retrieved 31 October 2013.

202.
Paul BD, Jemionek J, Lesser D, Jacobs A, Searles DA
(September 2004). "Enantiomeric separation and quantitation of
()-amphetamine, ()-methamphetamine, ()-MDA, ()-MDMA, and
()-MDEA in urine specimens by GC-EI-MS after derivatization with
(R)-()- or (S)-(+)--methoxy--(trifluoromethyl)phenylacetyl
chloride (MTPA)". J. Anal. Toxicol. 28 (6): 449
455. doi:10.1093/jat/28.6.449. PMID 15516295.
203.
"Part 341 cold, cough, allergy, bronchodilator, and
antiasthmatic drug products for over-the-counter human use". Code
of Federal Regulations Title 21: Subchapter D Drugs for human
use. United States Food and Drug Administration. April 2015.
Retrieved 7 March 2016. Topical nasal decongestants --(i) For
products containing levmetamfetamine identified in 341.20(b)(1)
when used in an inhalant dosage form. The product delivers in each
800 milliliters of air 0.04 to 0.150 milligrams of levmetamfetamine.
204.
"Identification". Levomethamphetamine. Pubchem Compound.
National Center for Biotechnology Information. Retrieved 2
January 2014.
205.
Verstraete AG, Heyden FV (August 2005). "Comparison of the
sensitivity and specificity of six immunoassays for the detection of
amphetamines in urine". J. Anal. Toxicol. 29 (5): 359
364. doi:10.1093/jat/29.5.359.PMID 16105261.
206.
Baselt RC (2011). Disposition of Toxic Drugs and Chemicals in
Man (9th ed.). Seal Beach, USA: Biomedical Publications. pp. 85
88.ISBN 9780962652387.
207.
Musshoff F (February 2000). "Illegal or legitimate use?
Precursor compounds to amphetamine and
methamphetamine". Drug Metab. Rev. 32(1): 15
44. doi:10.1081/DMR-100100562. PMID 10711406.
208.
Cody JT (May 2002). "Precursor medications as a source of
methamphetamine and/or amphetamine positive drug testing
results". J. Occup. Environ. Med. 44 (5): 435
450. doi:10.1097/00043764-200205000-00012. PMID 12024689.
209.
"Annual prevalence of drug use by regions and globally by
drug types". United Nations Office on Drugs and Crime. June 2015.
Retrieved 27 August2015.
210.
Rassool GH (2009). Alcohol and Drug Misuse: A Handbook for
Students and Health Professionals. London, England: Routledge.
p. 113.ISBN 9780203871171.
211.
Sulzer D, Sonders MS, Poulsen NW, Galli A (April 2005).
"Mechanisms of neurotransmitter release by amphetamines: a

review". Prog. Neurobiol. 75(6): 406

433. doi:10.1016/j.pneurobio.2005.04.003. PMID 15955613.
212.
Bett WR (August 1946). "Benzedrine sulphate in clinical
medicine; a survey of the literature". Postgrad. Med. J. 22: 205
218. PMC 2478360.PMID 20997404.
213.
Rasmussen N (August 2011). "Medical science and the
military: the Allies' use of amphetamine during World War II". J.
Interdiscip. Hist. 42 (2): 205
233. doi:10.1162/JINH_a_00212. PMID 22073434.
214.
Defalque RJ, Wright AJ (April 2011). "Methamphetamine for
Hitler's Germany: 1937 to 1945". Bull. Anesth. Hist. 29 (2): 2124,
32.doi:10.1016/s1522-8649(11)50016-2. PMID 22849208.
215.
"Controlled Substances Act". United States Food and Drug
Administration. 11 June 2009. Retrieved 4 November 2013.
216.
Gyenis A. "Forty Years of On the Road 1957
1997".wordsareimportant.com. DHARMA beat. Archived from the
original on 14 February 2008. Retrieved 18 March 2008.
217.
Wilson A (2008). "Mixing the Medicine: The unintended
consequence of amphetamine control on the Northern Soul
Scene" (PDF). Internet Journal of Criminology. Retrieved 25
May 2013.
218.
Hill J (4 June 2004). "Paul Erdos, Mathematical Genius, Human
(In That Order)" (PDF). Retrieved 2 November 2013.
219.
Mohan J, ed. (June 2014). "World Drug Report
2014" (PDF). United Nations Office on Drugs and Crime. p. 3.
Retrieved 18 August 2014.
220.
"European drug report 2014: Trends and
developments" (PDF). Lisbon, Portugal: European Monitoring Centre
for Drugs and Drug Addiction. May 2014: 13,
24. doi:10.2810/32306. ISSN 2314-9086. Retrieved 18
August2014. 1.2 million or 0.9% of young adults (1534) used
amphetamines in the last year
221.
United Nations Office on Drugs and Crime (2007). Preventing
Amphetamine-type Stimulant Use Among Young People: A Policy
and Programming Guide (PDF). New York, USA: United
Nations.ISBN 9789211482232. Retrieved 11 November 2013.
222.
"List of psychotropic substances under international
control" (PDF).International Narcotics Control Board. United Nations.
August 2003. Archived from the original (PDF) on 5 December 2005.
Retrieved19 November 2005.

223.
Park Jin-seng (25 May 2012). "Moving to Korea brings medical,
social changes". The Korean Times. Retrieved 14 November 2013.
224.
"Importing or Bringing Medication into Japan for Personal
Use". Japanese Ministry of Health, Labour and Welfare. 1 April 2004.
Retrieved3 November 2013.
225.
"Controlled Drugs and Substances Act". Canadian Justice Laws
Website. Government of Canada. Retrieved 11 November 2013.
226.
"Opiumwet". Government of the Netherlands. Retrieved 3
April 2015.
227.
"Schedule 8". Poisons Standard. Australian Government
Department of Health. October 2015. Retrieved 15 December 2015.
228.
"Table of controlled Narcotic Drugs under the Thai Narcotics
Act" (PDF).Thailand Food and Drug Administration. 22 May 2013.
Archived from the original (PDF) on 8 March 2014. Retrieved 11
November 2013.
229.
"Class A, B and C drugs". Home Office, Government of the
United Kingdom. Archived from the original on 4 August 2007.
Retrieved 23 July2007.
230.
"Identification". Lisdexamfetamine. Drugbank. University of
Alberta. 8 February 2013. Retrieved 13 October 2013.
231.
"Adzenys XR". United States Food and Drug Administration.
Retrieved7 March 2016.
232.
"Adzenys XR Prescribing Information" (PDF). United States
Food and Drug Administration. Neos Therapeutics, Inc. January
2016. p. 15. Retrieved7 March 2016. 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.
233.
"Dyanavel XR". United States Food and Drug Administration.
Retrieved1 January 2016.
234.
"Evekeo". United States Food and Drug Administration.
Retrieved11 August 2015.
235.
"Molecular Weight Calculator". Lenntech. Retrieved 19
August 2015.
236.
"Dextroamphetamine Sulfate USP". Mallinckrodt
Pharmaceuticals. March 2014. Retrieved 19 August 2015.
237.
"D-amphetamine sulfate". Tocris. 2015. Retrieved 19
August 2015.

238.
"Amphetamine Sulfate USP". Mallinckrodt Pharmaceuticals.
March 2014. Retrieved 19 August 2015.
239.
"Dextroamphetamine Saccharate". Mallinckrodt
Pharmaceuticals. March 2014. Retrieved 19 August 2015.
240.
"Amphetamine Aspartate". Mallinckrodt Pharmaceuticals.
March 2014. Retrieved 19 August 2015.
External links