|Systematic (IUPAC) name|
|Pregnancy cat.||C (US)|
|Legal status||Controlled (S8) (AU) Schedule I (CA) Class B (UK) Schedule II (US) ℞ Prescription only|
|Routes||Oral, intravenous, vaporization, insufflation, rectal, sublingual|
|Bioavailability||nasal 75%; rectal 95–99%|
|Metabolism||Hepatic (CYP2D6), FMN|
|Half-life||10h average for d-isomer, 13h for l-isomer (in adults)|
|Excretion||Renal; significant portion unaltered|
|Synonyms||alpha-methylbenzeneethanamine, alpha-methylphenethylamine, beta-phenyl-isopropylamine|
|PDB ligand ID||FRD (, )|
|Solubility in water||50–100 mg/mL (16C°) mg/mL (20 °C)|
| (what is this?)
Amphetamine (USAN or amfetamine (INN) contracted from alphamethyl-phenethylamine or α-methylphenethylamine) is 1-phenylpropan-2-amine or C9H13N. It exists as two enantiomers: the levorotary form levamfetamine (INN) and dextrorotary form dexamfetamine (INN). It is a psychostimulant drug of the phenethylamine class that produces increased wakefulness and focus in association with decreased fatigue and appetite.
Amphetamine is used as a treatment for attention deficit hyperactivity disorder (ADHD) and narcolepsy, and is typically prescribed as amphetamine mixed salts or as dextroamphetamine. It has historically been used to treat obesity.
Amphetamine increases activity related to the neurotransmitters dopamine and norepinephrine in the brain. This causes resistance to fatigue, elevation of mood, heightened libido, euphoria, and loss of appetite. Repeated high-dose exposure can lead to a mental state characterized by delusions, psychosis, and paranoia. The effects of amphetamines on serotonin transmission may contribute to hallucinations, appetite suppression, and hyperthermia. Recreational doses are generally far larger than prescribed therapeutic doses, and recreational use therefore carries far greater risk and far more serious side effects.
Amphetamine is used recreationally, both in prescription form and in pure form synthesized by clandestine chemists. It is also used as a performance enhancer and a cognitive enhancer. It is closely chemically related to methamphetamine, but differs significantly in many areas.
While amphetamine is commonly prescribed to children, concerns have been raised over possible complications such as stunted growth, altered brain development, and rare episodes of psychosis. However, these concerns are still disputed and it appears that the associated brain alterations are actually due to the presence of ADHD itself rather than being from the stimulant use.
Psychological effects can include euphoria, anxiety, increased libido, alertness, concentration, energy, self-esteem, self-confidence, sociability, irritability, aggression, psychosomatic disorders, psychomotor agitation, grandiosity, repetitive and obsessive behaviors, and paranoia. With chronic and/or high doses, amphetamine psychosis can occur. Occasionally this psychosis can occur at therapeutic doses during chronic therapy as a treatment emergent side effect.
Side effects of amphetamine are many and varied. However, the amount of amphetamine consumed is the primary factor in determining the likelihood and severity of side effects. Therapeutic use in the form of amphetamine mixed salts and dextroamphetamine is approved by the United States Food and Drug Administration for long-term pharmaceutical use. recreational use of amphetamine generally involves far larger doses and is therefore significantly more dangerous, involving a greater risk of serious side effects
Physical side effects
Physical effects of amphetamine can include dilated pupils, vasoconstriction or vasodilation, tachycardia or bradycardia, hypertension or hypotension, blood shot eyes, flushing, erectile dysfunction, restlessness, dry mouth, bruxism, headache, tachypnea, fever, diaphoresis, diarrhea, constipation, blurred vision, dizziness, reduced seizure threshold, insomnia, numbness, palpitations, arrhythmias, tics, dry and/or itchy skin, acne, and pallor. Effects of extremely high doses can include coma, rhabdomyolysis, adrenergic storm, and stereotypy. Dangerous physical side effects are exceedingly rare in typical pharmaceutical doses.
Recent studies by the FDA indicate that, in children, young adults, and adults, there is no association between serious adverse cardiovascular events (sudden death, myocardial infarction, and stroke) and the use of amphetamines or other ADHD stimulants.
Amphetamine can elevate cardiac output and blood pressure, making it potentially dangerous for use by patients with a history of heart disease or hypertension. Amphetamine can cause potentially life-threatening complications in patients taking monoamine oxidase inhibitors (MAOIs), as both MAOIs and amphetamine increase the level of catecholamines in the body. The use of amphetamine and amphetamine-like drugs is contraindicated in patients with narrow-angle glaucoma or anatomically narrow angles. Like other sympathomimetic amines, amphetamine can induce transient mydriasis. In patients with narrow angles, pupillary dilation can provoke an attack of angle-closure glaucoma. These agents should also be avoided in patients with other forms of glaucoma, as mydriasis may occasionally increase interocular pressure.
Amphetamine has been shown to pass through into breast milk. Because of this, mothers taking amphetamine are advised to avoid breastfeeding during their course of treatment.
Abuse of amphetamines can result in a stimulant psychosis that can present as a number of psychotic disorders (e.g. paranoia, hallucinations, delusions). It has been suggested that about 5-15% of users fail to make a complete recovery from the psychosis in the long term.
Amphetamines have been shown to increase both systolic and diastolic blood pressure, and act as myocardial stimulants when administered orally. Some individuals may experience a reflexive slowing of heart rate, but at large doses arrhythmias have been noted.
Renal failure may occur secondarily to the dehydration and rhabdomyolysis that can result from acute amphetamine toxicity. Dehydration and compromised renal function can further cause fluctuations in fluid and electrolytes, particularly potassium. Increased bladder sphincter tone may lead to symptoms of dysuria, hesitancy and acute urinary retention. Dilation of renal vasculature, along with an increase in heart contractility, increases an individual’s risk of cardiogenic shock.
Amphetamines stimulate the medullary respiratory centers, which increases the rate of respiration and produces deeper breaths. In a normal individual, amphetamines do not noticeably increase the rate of respiration or produce deeper breaths, but when respiration is already compromised, amphetamines may stimulate respiration. Prior treatment with reserpine or guanethidine prevents the pulmonary effects of amphetamines. Chronic use of amphetamines can cause pulmonary hypertension.
Dependence and addiction
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Withdrawal symptoms of amphetamine consist primarily of mental fatigue, mental depression and increased appetite. Symptoms may last for days with occasional use and weeks or months with chronic use, with severity dependent on the length of time and the amount of amphetamine used. Withdrawal symptoms may also include anxiety, agitation, excessive sleep, vivid or lucid dreams, deep REM sleep and suicidal ideation.
Mechanism of action
Primary sites of action
Amphetamine exerts its behavioral effects by modulating several key neurotransmitters in the brain, including dopamine, serotonin, and norepinephrine. However, the activity of amphetamine throughout the brain appears to be site-specific; certain receptors that respond to amphetamine in some regions of the brain tend not to do so in other regions. For instance, dopamine D2 receptors in the hippocampus, a region of the brain associated with forming new memories, appear to be unaffected by the presence of amphetamine.
The major neural systems affected by amphetamine are largely implicated in the brain’s reward circuitry. Moreover, neurotransmitters involved in various reward pathways of the brain appear to be the primary targets of amphetamine. One such neurotransmitter is dopamine, a chemical messenger heavily active in the mesolimbic and mesocortical reward pathways. Therefore, the anatomical components of these pathways — including the striatum, the nucleus accumbens, and the ventral striatum — have been found to be primary sites of amphetamine action.
Amphetamine, specifically dextroamphetamine, at high therapeutic (1 mg/kg) and supratherapeutic (2 mg/kg) doses, also appears to enhance acetylcholine release, up to 110% and 210% in the hippocampus and up to 35% and 54% in the caudate nucleus respectively. It is believed that the mechanism by which amphetamine heightens acetylcholine release is through agonization of dopamine receptor D1. It's speculated that this release of acetylcholine is partly responsible for the nootropic effects that amphetamine has on memory and learning.
The fact that amphetamine influences neurotransmitter activity specifically in regions implicated in reward provides insight into the behavioral consequences of the drug, such as the stereotyped onset of euphoria. A better understanding of the specific mechanisms by which amphetamine operates may increase our ability to treat amphetamine addiction and possibly other addictions (because the brain’s reward circuitry has been widely implicated in addictions of many types).
Related endogenous compounds
Amphetamine has been found to have several endogenous analogues; that is, molecules of a similar structure found naturally in the brain. examples include β-Phenethylamine and the amino acid l-Phenylalanine. These molecules are thought to modulate levels of excitement and alertness, among other related affective states.
The most widely studied neurotransmitter with regard to amphetamine action in the central nervous system is dopamine. All of the addictive drugs appear to enhance synaptic dopamine, including amphetamine and methamphetamine. Studies have shown that, in certain brain regions, amphetamine increases the concentrations of dopamine in the synaptic cleft, thereby heightening the response of the post-synaptic neuron.
The specific mechanisms by which amphetamine affects dopamine concentrations have been studied extensively. Currently, two major hypotheses have been proposed, which are not mutually exclusive. One theory emphasizes amphetamine’s actions on the vesicular level, increasing concentrations of dopamine in the cytosol of the pre-synaptic neuron. The other focuses on the role of the dopamine transporter DAT, and proposes that amphetamine may interact with DAT to induce reverse transport of dopamine from the presynaptic neuron into the synaptic cleft.
The former hypothesis is backed by studies from David Sulzer's lab at Columbia University demonstrating that injections of amphetamine result in rapid increases of cytosolic dopamine concentrations, while the drug decreases the number of dopamine molecules inside the synaptic vesicle. Amphetamine is a substrate for a specific neuronal synaptic vesicle uptake transporter called VMAT2. When amphetamine is taken up by VMAT2, the vesicle releases dopamine molecules into the cytosol in exchange. The redistributed dopamine is then believed to interact with DAT to promote reverse transport. Amphetamine and amphetamine derivatives are also weak bases that accept protons, and can collapse acidic pH gradients in the vesicles that would otherwise provide free energy for neurotransmitter accumulation: the "weak base hypothesis" of amphetamine action suggests that collapse of this free energy contributes to redistribution of dopamine from very high (molar) concentrations in the vesicles to the cytosol. Calcium may be a key molecule involved in the interactions between amphetamine and VMATs.
The increase of cytosolic dopamine appears to trigger neurotoxicity, as dopamine readily auto-oxidizes, so that amphetamine or methamphetamine's increase in cytosolic dopamine can lead to oxidative stress in the cytosol that in turn promotes autophagy-related degradation of dopamine axons and dendrites.
The second hypothesis of amphetamine action on the plasma membrane dopamine transporter postulates a direct interaction between amphetamine and the DAT. The activity of DAT is believed to depend on specific phosphorylating kinases, such as protein kinase c, to be specific PKC-β. Upon phosphorylation, DAT undergoes a conformational change that results in the transport of DAT-bound dopamine from the extracellular to the intracellular environment. In the presence of amphetamine, however, DAT has been observed to function in reverse, spitting dopamine out of the presynaptic neuron and into the synaptic cleft. Thus, beyond inhibiting reuptake of dopamine, amphetamine also stimulates the release of dopamine molecules into the synapse.
In support of the above hypothesis, it has been found that PKC-β inhibitors eliminate the effects of amphetamine on extracellular dopamine concentrations in the striatum of rats. This data suggests that the PKC-β kinase may represent a key point of interaction between amphetamine and the DAT transporter.
Additional actions of amphetamine contribute to its ability to release dopamine from neurons; these include its being an inhibitor of monoamine oxidase (an enzyme responsible for dopamine breakdown in the cytosol), its ability to enhance dopamine synthesis due to actions on the enzyme tyrosine hydroxylase (the enzyme responsbile for synthesising the precursor of dopamine, L-DOPA) and some blockade of the DAT (an action that amphetamine shares with cocaine). Due to the combination of these actions and its long half-life, amphetamine can release far more dopamine than can cocaine or other addictive drugs.
Amphetamine has been found to exert similar effects on serotonin as on dopamine. Like DAT, the serotonin transporter SERT can be induced to operate in reverse upon stimulation by amphetamine. This mechanism is thought to rely on the actions of calcium ions, as well as on the proximity of certain transporter proteins.
The interaction between amphetamine and serotonin is apparent only in particular regions of the brain, such as the mesocorticolimbic projection. Recent studies suggest that amphetamine may indirectly alter the behavior of glutamatergic pathways extending from the ventral tegmental area to the prefrontal cortex by increasing inhibitory serotonin receptor activity on glutamatergic neurons. Glutamatergic pathways are strongly correlated with increased excitability at the level of the synapse. Increased extracellular concentrations of serotonin may thus modulate the excitatory activity of glutamatergic neurons.
The proposed ability of amphetamine to decrease excitability of glutamatergic pathways may be of significance when considering the role of serotonin in addiction, evidence of which has been quickly accumulating. An additional behavioral consequence of postulated serotonergic effects of amphetamine may be alterations in the stereotyped locomotor stimulation that occurs in response to amphetamine exposure. Despite this, at least one study suggests that serotonergic effects are not necessary for the development of stereotypy in rodents treated with stimulants.
Two studies on the brains of rats and cats have shown that, at extremely high doses (7.5–10 mg/kg), amphetamine reduces the activity of brain tryptophan hydroxylase, an enzyme involved in the biosynthesis of serotonin and melatonin. Interestingly, other studies have demonstrated that pretreatment with L-tryptophan (100 mg/kg) reduces the quantity of self-administered amphetamine (.125 mg/kg per administration, a low therapeutic dose in humans) in rats which have established stable self-administration patterns. Moreover, the magnitude and duration of the L-tryptophan pretreatment effect was observed to increase in a dose-dependent manner.
Other relevant neurotransmitters
Several other neurotransmitters have been linked to amphetamine activity. It is well-established that amphetamine causes increased brain and blood levels of norepinephrine, a neurotransmitter related to adrenaline. This is believed to occur via reuptake blockage as well as via interactions with the norepinephrine neuronal transport carrier. Many in vitro studies have demonstrated that amphetamine binds to and inhibits reuptake of norepinephrine(noradrenaline) via norepinephrine transporter expressed on the cell membranes of primary neurons and cell-lines. In addition, amphetamine acts as a substrate for the transporter, being moved from the outside to the inside of the cell via the transporter. Once inside the cell, amphetamine can bind to VMAT2 on neurotransmitter-containing vesicles and via actions that are not well-understood, amphetamine increases release of norepinephrine.
In addition, extracellular levels of glutamate, the primary excitatory neurotransmitter in the brain, have been shown to increase upon exposure to amphetamine. Consistent with other findings, this effect was found in the areas of the brain implicated in reward; namely, the nucleus accumbens, striatum, and prefrontal cortex.
The long-term effects of amphetamines use on neural development in children has not been well established. A study in rats suggests that high-dose amphetamine use during adolescence may impair adult working memory.
Amphetamine is a chiral compound. The racemic mixture can be divided into its optical isomers: levo- and dextro-amphetamine. Amphetamine is the parent compound of its own structural class, comprising a broad range of psychoactive derivatives, from empathogens, MDA (3,4-Methylenedioxyamphetamine) and MDMA (3,4-Methylenedioxy-N-methylamphetamine) known as ecstasy, to the N-methylated form, methamphetamine known as 'meth', and to decongestants such as ephedrine (EPH) . Amphetamine is a homologue of phenethylamine.
Amphetamine, both as d-amphetamine (dextroamphetamine) and l-amphetamine (or a racemic mixture of the two isomers), is believed to exert its effects by binding to the monoamine transporters and increasing extracellular levels of the biogenic amines dopamine, norepinephrine (noradrenaline) and serotonin. It is hypothesized that d-amphetamine acts primarily on the dopaminergic systems, while l-amphetamine is norepinephrinergic (noradrenergic). The primary reinforcing and behavioral-stimulant effects of amphetamine, however, are linked to enhanced dopaminergic activity, primarily in the mesolimbic dopamine system.
Amphetamine and other amphetamine-type stimulants act principally to release dopamine into the synaptic cleft. Amphetamine, unlike dopamine transporter inhibitor cocaine, acts as a substrate for DAT and slows reuptake by a secondary acting mechanism through the phosphorylation of dopamine transporters.
A primary action of amphetamine is mediated by vesicular monoamine transporters (VMATs); the transporters appear to provide a channel through which dopamine and other transmitters can exit the vesicle to the cytosol. According to the "weak base hypothesis" this is exacerbated by amphetamine acting to alkalinize the vesicle, which depletes the free energy favoring vesicle accumulation so that transmitter is redistributed to the cytosol. Together, these actions cause the release of dopamine, norepinephrine, and serotonin from monoamine vesicles, thereby increasing cytosolic concentrations of transmitter. This increase in concentration assists in the "reverse transport" of dopamine via the dopamine transporter (DAT) into the synapse. In addition, amphetamine binds reversibly to the DATs and blocks the transporter's ability to clear DA from the synaptic space. Amphetamine also acts in this way with norepinephrine (noradrenaline) and to a lesser extent serotonin.
Amphetamine has been identified as a potent agonist of trace amine-associated receptor 1 (TAAR1), a newly discovered GPCR important for regulation of monoaminergic systems in the brain. Activation of TAAR1 increases cAMP production via adenylyl cyclase activation and inhibits transporter function.
These effects increase monoamine efflux and prolong the amount of time monoamines remain in the synapse.
The half-life of amphetamines varies with age and stereochemistry. The dextrarotary amphetamine (D; also d and S) is processed faster than the levarotary amphetamine (L; also l and R) form. In adults, the half-life for the D-form is 10 hours and the L-form is 13 hours. For ages 13–17, the half-life is (D:L) 11:13-14hrs. For children 9–12 years of age the half-life of the drug is (D:L) 9:11.
Metabolism occurs mostly in the liver by the cytochrome P450 (CYP) detoxification system. The isoenzymes CYP2C9, CYP1A2, CYP2D6, CYP3A4 along with flavin monooxygenases are the primary metabolic enzymes. Deamination of amphetamine into phenylacetone (an inert metabolite) is performed by CYP2C. Other breakdown pathways in the liver include dealkylation and demethylation. These produce a variety excreted metabolic products, some of which are also biologically active, including parahydroxyamphetamine, hippuric acid, norephedrine and p-hydroxynorephedrine.
Amphetamine is eliminated renally with 70% of the drug being cleared in 24 hours, with a fraction of the drug being excreted unchanged (.21-.45). This process is dependent on urinary pH. Amphetamine is a weak base with a pKa of 9-10. Consequently, when the urinary pH is basic, more of the drug is in its free base form and less is excreted. Apparent half-life and duration of effect increase with repeated use and accumulation of drug.
Amphetamine was first synthesized in 1887 by the Romanian chemist Lazăr Edeleanu in Berlin, Germany. He named the compound phenylisopropylamine. It was one of a series of compounds related to the plant derivative ephedrine, which had been isolated from the plant Ma-Huang (Ephedra) that same year by Nagayoshi Nagai. No pharmacological use was found for amphetamine until 1927, when pioneer psychopharmacologist Gordon Alles resynthesized and tested it on himself, in search of an artificial replacement for ephedrine. From 1933 or 1934 Smith, Kline and French began selling the volatile base form of the drug as an inhaler under the trade name Benzedrine, useful as a decongestant but readily usable for other purposes. One of the first attempts at using amphetamine as a scientific study was done by M. H. Nathanson, a Los Angeles physician, in 1935. He studied the subjective effects of amphetamine in 55 hospital workers who were each given 20 mg of Benzedrine. The two most commonly reported drug effects were "a sense of well being and a feeling of exhilaration" and "lessened fatigue in reaction to work". During World War II amphetamine was extensively used to combat fatigue and increase alertness in soldiers. After decades of reported abuse, the FDA banned Benzedrine inhalers, and limited amphetamine to prescription use in 1965, but non-medical use remained common. Amphetamine became a schedule II drug in the USA under the Controlled Substances Act in 1971.
The related compound methamphetamine, in its crystallized form, was first synthesized from ephedrine in Japan in 1920 by chemist Akira Ogata, via reduction of ephedrine using red phosphorus and iodine. The pharmaceutical Pervitin was a tablet of 3 mg methamphetamine that was available in Germany from 1938 and widely used in the Wehrmacht, but by mid-1941 it became a controlled substance, despite this new classification, methamphetamine and the cocaine-derivative referred to as "Codename D-IX" were distributed by military doctors across both the Western and Eastern theatres of war. During the course of the war over 200 million Pervitin pills were prescribed to Wehrmacht combatants.
In 1997 and 1998, researchers at Texas A&M University claimed to have found amphetamine and methamphetamine in the foliage of two Acacia species native to Texas, A. berlandieri and A. rigidula. Previously, both of these compounds had been thought to be human inventions. These findings have never been duplicated, and the analyses are believed by many biochemists to be the result of experimental error, and as such the validity of the report has come into question. Alexander Shulgin, one of the most experienced biochemical investigators and the inventor of many novel psychotropic substances, has tried to contact the Texas A&M researchers and verify their findings. The authors of the paper have not responded; natural amphetamine remains an unconfirmed discovery.
Adderall, an amphetamine mixture, is used by some college and high-school students as a study and test-taking aid. Amphetamine works by increasing energy levels, concentration, and motivation, thus allowing students to study for an extended period of time. In individuals without ADHD, amphetamine has been shown to increase effortful behavior, improve the ability to detect errors, and reduce emotional reactions to frustration; however, an increased susceptibility to environmental distraction and the increased possibility of risky behavior may detract from the usefulness of amphetamine as a nootropic in the general population. Nonetheless, one study has shown that amphetamine (given at .2 mg/kg) does produce significant increases in performance on coding tests, although not on computational ones.
In addition, amphetamine is also used by some professional, collegiate and high school athletes for its strong stimulant effect; energy levels are perceived to be dramatically increased and sustained, which is believed to allow for more vigorous and longer play. At low to moderate therapeutic doses (10–40 mg), amphetamine has been shown to increase physical strength, stamina, and endurance in numerous studies; however, the presence and magnitude of associated increases appear to be sensitive to both the dosage and timing of administered amphetamine relative to the tests. While the mechanism of augmentation isn't examined in these studies, it is known that amphetamines affect some of the neurotransmitter systems that mediate physical processes during exercise, namely noradrenaline, adrenaline, and acetylcholine.
Amphetamine and amphetamine derivatives such as methamphetamine have been, and are still, used by militaries around the world. British troops used 72 million amphetamine tablets in the second world war and the RAF used so many that "Methedrine won the Battle of Britain" according to one report. American bomber pilots use amphetamine ("go pills") to stay awake during long missions. The Tarnak Farm incident, in which an American F-16 pilot killed several friendly Canadian soldiers on the ground, was blamed by the pilot on his use of amphetamine. A nonjudicial hearing rejected the pilot's claim.
Amphetamine use has historically been especially common among Major League Baseball players and is usually known by the slang term "greenies". In 2006, the MLB banned the use of amphetamine. The ban is enforced through periodic drug-testing. However, the MLB has received some criticism because the consequences for amphetamine use are dramatically less severe than for anabolic steroid use, with the first offense bringing only a warning and further testing.
Amphetamine was formerly in widespread use by truck drivers to combat symptoms of somnolence and to increase their concentration during driving, especially in the decades prior to the signing by former president Ronald Reagan of Executive Order 12564, which initiated mandatory random drug testing of all truck drivers and employees of other DOT-regulated industries. Although implementation of the order on the trucking industry was kept to a gradual rate in consideration of its projected effects on the national economy, in the decades following the order, amphetamine and other drug abuse by truck drivers has since dropped drastically. (See also Truck driver—Implementation of drug detection).
Detection in body fluids
Amphetamine is frequently measured in urine as part of a drug test, in plasma or serum to confirm a diagnosis of poisoning in hospitalized victims, or in whole blood to assist in the forensic investigation of a traffic or other criminal violation or a case of sudden death. Techniques such as immunoassay may cross-react with a number of sympathomimetic drugs, so chromatographic methods specific for amphetamine should be employed to prevent false positive results. Chiral techniques may be employed to help distinguish the source of the drug, whether obtained legally (via prescription) or illicitly, or possibly as a result of formation from a prodrug such as lisdexamfetamine or selegiline. Chiral separation is needed to assess the possible contribution of l-methamphetamine (Vicks Inhaler) toward a positive test result.
Society and culture
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The hippie counterculture was very critical of amphetamines due to the behaviors they cause; in an interview with the Los Angeles Free Press in 1965, beat writer Allen Ginsberg commented that "Speed is antisocial, paranoid making, it's a drag... all the nice gentle dope fiends are getting screwed up by the real horror monster Frankenstein speed freaks who are going round stealing and bad-mouthing everybody". However, he also acknowledged that he had used it to stay up all night writing.
The writers of the Beat Generation used amphetamine extensively, mainly under the Benzedrine brand name. Jack Kerouac was a particularly avid user of amphetamine, which was said to provide him with the stamina needed to work on his novels for extended periods of time.
Scottish author Irvine Welsh often portrays drug use in his novels, though in one of his journalism works he comments on how drugs (including amphetamine) have become part of consumerism and how his novels Trainspotting and Porno reflect the changes in drug use and culture during the years that elapse between the two texts.
Amphetamine is frequently mentioned in the work of American journalist Hunter S. Thompson. Speed not only appears among the inventory of drugs Thompson consumed for what could broadly be defined as recreational purposes but also receives frequent, explicit mention as an essential component of his writing toolkit, such as in his "Author's Note" in Fear and Loathing on the Campaign Trail '72.
"One afternoon about three days ago [the publishers] showed up at my door with no warning, and loaded about forty pounds of supplies into the room: two cases of Mexican beer, four quarts of gin, a dozen grapefruits, and enough speed to alter the outcome of six Super Bowls. ... Meanwhile, [...] with the final chapter still unwritten and the presses scheduled to start rolling in twenty-four hours . . . . unless somebody shows up pretty soon with extremely powerful speed, there might not be a final chapter. About four fingers of king-hell Crank would do the trick, but I am not optimistic."
The northern soul and mod subcultures in England were known for their characteristic amphetamine use. Their concerts generally involved people taking amphetamines to keep dancing all night. One DJ, Roger Eagle, got out of the northern soul scene saying: "All they wanted was fast-tempo black dance music... [but they were] too blocked on amphetamines to articulate exactly which Jackie Wilson record they wanted me to play."
Many songs have been written about amphetamine, for example in the track entitled "St. Ides Heaven" from singer/songwriter, Elliott Smith's self-titled album. Semi Charmed Life by Third Eye Blind also references amphetamine. Another blatant example would be the song simply labelled "Amphetamine" by Alternative rock band Everclear, the song "20 Dollar nose bleed" by the Pop-rock band Fall Out Boy, and the song "Headfirst For Halos" by My Chemical Romance. It has also influenced the aesthetics of many rock'n'roll bands (especially in the garage rock, mod R&B, death rock, punk/hardcore, gothic rock and extreme heavy metal genres). Hüsker Dü, Jesus and Mary Chain and The Who were keen amphetamine users early in their existence. Hollywood Undead references the drug as a negative effect in the song "City" off their breakout album Swan Songs. Land Speed Record is an allusion to Hüsker Dü's amphetamine use. Amphetamine was widely abused in the 1980s underground punk-rock scene. Punk-rock band NOFX have incorporated references to Amphetamines and other stimulants, the two most obvious being the song "Three on Speed" from the "Surfer" 8" LP (in reference to the three guys being on Amphetamine while recording the album), and earlier the album "The Longest Line" is in reference to a "line" of Amphetamine ready for insufflation. The Rolling Stones referenced the drug in their song "Can't You Hear Me Knocking" on the album Sticky Fingers ("Y'all got cocaine eyes / Yeah, ya got speed-freak jive now"). Lou Reed refers explicitly to the drug on his album Berlin, in the song "How Do You Think It Feels?". Reed's band The Velvet Underground, a creation of Andy Warhol's Factory Years, was fueled by amphetamines, as well as naming their second album White Light/White Heat after the drug and making reference to the song in "Sister Ray.". The Pulp song Sorted for E's & Wizz refers to British slang terms for ecstasy and amphetamines. English gothic rock band The Sisters of Mercy refers to the drug in their song "Amphetamine Logic" from their first album, First and Last and Always, and their singer Andrew Eldritch used amphetamines repeatedly. The Byrds referenced amphetamines in the 1968 song "Artificial Energy" on the album "The Notorious Byrd Brothers."
Many rock'n'roll bands have named themselves after amphetamine and drug slang surrounding it. For example Mod revivalists, The Purple Hearts named themselves after the amphetamine tablets popular with mods during the 1960s, as did the Australian band of the same name during the mid-1960s. The Amphetameanies, a ska-punk band, are also named after amphetamine, but also imitate its effects.[vague] Dexys Midnight Runners, of number one hit "Come On Eileen", are named after Dexedrine. Motörhead derived their name from the song of the same name, originally by Hawkwind where Ian "Lemmy" Kilmister was on bass before leaving to form Motörhead. Lemmy Kilmister is a long-term user of speed.
Producer David O. Selznick was an amphetamine user, and would often dictate long and rambling memos under the influence of amphetamine to his directors. The documentary Shadowing The Third Man relates that Selznick introduced The Third Man director Carol Reed to the use of amphetamine, which allowed Reed to bring the picture in below budget and on schedule by filming nearly 22 hours at a time.
The title of the 2009 movie Amphetamine plays on the double meaning of the word in Chinese - besides the name for the drug it also means 'isn't this his fate?' which figuratively ties to the movie's plot. The word is transliterated as 安 非 他 命 - "ān fēi tā mìng" - and as commonly happens with transliteration of non-Chinese terms each character has independent meaning as an individual unrelated word.
Perhaps the most notable example of this is Paul Erdős, one of the most prolific and successful mathematicians in human history. He took amphetamine and methylphenidate from the age of 58, when a doctor prescribed them to him to allay the depression associated with his mother's death, until his death at the age of 83. He had previously sustained himself on copious amounts of coffee and caffeine pills. Erdős took amphetamine despite the concern of his friends, one of whom (Ron Graham) bet him $500 that he could not stop taking the drug for a month. Erdős won the bet, but complained: "You've showed me I'm not an addict. But I didn't get any work done. I'd get up in the morning and stare at a blank piece of paper. I'd have no ideas, just like an ordinary person. You've set mathematics back a month." He promptly resumed his amphetamine use.
- In the United Kingdom, amphetamines are regarded as Class B drugs. The maximum penalty for unauthorized possession is five years in prison and an unlimited fine. The maximum penalty for illegal supply is 14 years in prison and an unlimited fine.
- In the Netherlands, amphetamine and methamphetamine are List I drugs of the Opium Law, but the dextro isomer of amphetamine is indicated for ADD/ADHD and narcolepsy and available for prescription as 5 and 10 mg generic tablets, and 5 and 10 mg gel capsules.
- In the United States, amphetamine and methamphetamine are Schedule II drugs, classified as CNS (central nervous system) stimulants. A Schedule II drug is classified as one that has a high potential for abuse, has a currently accepted medical use and is used under severe restrictions, and has a high possibility of severe psychological and physiological dependence.
- In Canada, possession of amphetamines is a criminal offence under Schedule I of the Controlled Drugs and Substances Act, with a maximum penalty for repeat offenders of fines of up to $2,000, imprisonment for up to one year, or both.
- In Australia, the dextro isomer of amphetamine is sold under the name dexamphetamine, and is a Schedule 8 controlled drug (available for certain indications with authority, illegal to possess otherwise).
- In India, the drug is included in the psychotropic drugs listed by the Narcotics Bureau.
- In Japan, the use, production, and import of any medicine containing amphetamine are prohibited.
A number of substances have been shown to produce amphetamine and/or methamphetamine as metabolites, including amfecloral, amphetaminil, benzphetamine, clobenzorex, dimethylamphetamine, ethylamphetamine, famprofazone, fencamine, fenethylline, fenproporex, furfenorex, lisdexamfetamine, mefenorex, mesocarb, prenylamine, propylamphetamine, and selegiline, among others. These compounds may produce positive results for amphetamine on drug tests.
Amphetamine is most commonly prescribed as amphetamine mixed salts, but it is also prescribed as dextroamphetamine, benzphetamine and lisdexamfetamine. Benzphetamine and lisdexamfetamine are structurally different from amphetamine, but metabolize into it. Brand names of medications that contain, or metabolize into, amphetamine include:
- Adderall (amphetamine mixed salts)
- Dexedrine (dextroamphetamine)
- Dextroamphet (dextroamphetamine)
- Dextrostat (dextroamphetamine)
- Didrex (benzphetamine)
- ProCentra (dextroamphetamine)
- Vyvanse (lisdexamfetamine)
Benzedrine, Psychedrine, and Obestrol are examples of past pharmaceutical amphetamine formulations.
Amphetamine derivatives, often referred to as "amphetamines" or "substituted amphetamines", are chemicals that contain amphetamine as a "backbone". Some, such as methamphetamine, are also stimulants, while others like those in the DOx class have a serotonergic psychedelic effect. This class of chemicals is sometimes referred to collectively as the "amphetamine family".
|This section requires expansion. (May 2013)|
213 kg of amphetamine worth 40 million AED (Nearly $11 million) was seized by the United Arab Emirate Drug combat authorities on 30 November 2011 from an Iranian ship that was supposed to deliver the consignment in Malaysia and made a port stop in Sharjah.
The Gulf News published on 30 November 2011, saying "This is the biggest drug bust of its kind in 2011 and the second big one in the last three years worldwide," said Dr. Wadia Maalouf, International expert at the United Nation's Drug and Crime office.
Notes and references
- Miranda-G E, Sordo M, Salazar AM (2007). "Determination of amphetaminoe, methamphetamine, and hydroxyamphetamine derivatives in urine by gas chromatography-mass spectrometry and its relation to CYP2D6 phenotype of drug users". J Anal Toxicol 31 (1): 31–6. PMID 17389081.
- Trevor AJ, Katzung BG, Kruidering-Hall MM, Masters SB. Chapter 32. Drugs of Abuse. In: Trevor AJ, Katzung BG, Kruidering-Hall MM, Masters SB, eds. Katzung & Trevor's Pharmacology: Examination & Board Review. 10th ed. New York: McGraw-Hill; 2013. http://www.accesspharmacy.com/content.aspx?aID=56982610. Accessed March 23, 2013.
- Berman SM, Kuczenski R, McCracken JT, London ED (February 2009). "Potential adverse effects of amphetamine treatment on brain and behavior: a review". Mol. Psychiatry 14 (2): 123–42. doi:10.1038/mp.2008.90. PMC 2670101. PMID 18698321.
- "Brain Shrinkage in ADHD Not Caused by Medications". National Institute of Health. NIMH Press Office. Retrieved 10 June 2013.
- "Amphetamines | Merck Sharp & Dohme Corp". Merckmanuals.com. Retrieved 8 May 2012.
- "Adderall". FDA. Retrieved 11 June 2013.
- Vitiello B (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): 459–74, xi. doi:10.1016/j.chc.2007.11.010. PMC 2408826. PMID 18295156.
- "Amphetamine Poisoning". Emergency Central. Retrieved 11 June 2013.
- "ADHD Medications and Risk of Stroke In Young and Middle-Aged Adults". Retrieved 11 June 2013.
- "ADHD Medications and Risk of Serious Coronary Heart Disease in Young and Middle-Aged Adults". Retrieved 11 June 2013.
- "Attention Deficit Hyperactivity Disorder Medications and Risk of Serious Cardiovascular Disease in Children and Youth". Retrieved 11 June 2013.
- "Active ingredient: Amphetamine - Brands, Medical Use, Clinical Data". DrugLib.com. Retrieved 26 May 2013.
- Aklillu E, Karlsson S, Zachrisson OO, Ozdemir V, Agren H (April 2009). "Association of MAOA gene functional promoter polymorphism with CSF dopamine turnover and atypical depression". Pharmacogenet. Genomics 19 (4): 267–75. doi:10.1097/FPC.0b013e328328d4d3. PMID 19214141.
- "''Amphetamine Disease Interactions". Drugs.com. Retrieved 8 May 2012.
- Food and Drug Administration (2005). "ADDERALL XR capsule" (PDF). Retrieved 24 July 2009.
- Hofmann FG. A handbook on drug and alcohol abuse: the biomedical aspects. 2nd Edition. New York: Oxford University Press, 1983.
- Shoptaw SJ, Kao U, Ling W (2009). "Treatment for amphetamine psychosis (Review)". Cochrane Database of Systematic Reviews (1).
- Westfall, David P., Westfall, Thomas, C. “Adrenergic Agonist and Antagonists”. Goodman and Gilman’s The Pharmacological bases of Therapeutics. 12th Edition, online via Access Medicine. Chapter 12. Retrieved March 12, 2013.
- Knoben, J.E. and P.O. Anderson (eds.) Handbook of Clinical Drug Data. 6th ed. Bethesda, MD: Drug Intelligence Publications, Inc. 1988., p. 90. http://toxnet.nlm.nih.gov/. Accessed March 23, 2013.
- Albertson, Timothy E. “Amphetamines”. Poisoning and Drug Overdose. 6th Edition, online via Access Medicine. Chapter 8. Retrieved March 12, 2013.
- "Amphetamines: Drug Use and Abuse: Merck Manual Home Edition". Merck. Archived from the original on 17 February 2007. Retrieved 28 February 2007.
- Nutt D, King LA, Saulsbury W, Blakemore C (March 2007). "Development of a rational scale to assess the harm of drugs of potential misuse". Lancet 369 (9566): 1047–53. doi:10.1016/S0140-6736(07)60464-4. PMID 17382831.
- "Symptoms of Amphetamine withdrawal". WrongDiagnosis.com. 1 February 2012. Retrieved 8 May 2012.
- "eMedTV | Dextroamphetamine Withdrawals". Sleep.emedtv.com. 5 March 2007. Retrieved 8 May 2012.
- "Dexedrine Information". Drug Abuse Help. Retrieved 8 May 2012.
- Jones S, Kornblum JL, Kauer JA (August 2000). "Amphetamine blocks long-term synaptic depression in the ventral tegmental area". J. Neurosci. 20 (15): 5575–80. PMID 10908593.
- Moore KE (June 1977). "The actions of amphetamine on neurotransmitters: a brief review". Biol. Psychiatry 12 (3): 451–62. PMID 17437.
- Del Arco A, González-Mora JL, Armas VR, Mora F (July 1999). "Amphetamine increases the extracellular concentration of glutamate in striatum of the awake rat: involvement of high affinity transporter mechanisms". Neuropharmacology 38 (7): 943–54. doi:10.1016/S0028-3908(99)00043-X. PMID 10428413.
- Drevets WC, Gautier C, Price JC (January 2001). "Amphetamine-induced dopamine release in human ventral striatum correlates with euphoria". Biol. Psychiatry 49 (2): 81–96. doi:10.1016/S0006-3223(00)01038-6. PMID 11164755.
- Brodie B. "Effects of cocaine and amphetamine on acetylcholine release in the hippocampus and caudate nucleus.". Publisher Medical. Department of Neuroscience, University of Cagliari, Italy. Retrieved 5 June 2013.
- Wise, RA. "Brain reward circuitry and addiction." Program and abstracts of the American Society of Addiction Medicine 2003 The State of the Art in Addiction Medicine; 30 October – 1 November 2003; Washington, DC. Session
- Sulzer D, Chen TK, Lau YY, Kristensen H, Rayport S, Ewing A (May 1995). "Amphetamine redistributes dopamine from synaptic vesicles to the cytosol and promotes reverse transport". J. Neurosci. 15 (5 Pt 2): 4102–8. PMID 7751968.
- Sulzer D (February 2011). "How addictive drugs disrupt presynaptic dopamine neurotransmission". Neuron 69 (4): 628–49. doi:10.1016/j.neuron.2011.02.010. PMC 3065181. PMID 21338876.
- Kuczenski R, Segal DS (May 1997). "Effects of methylphenidate on extracellular dopamine, serotonin, and norepinephrine: comparison with amphetamine". J. Neurochem. 68 (5): 2032–7. doi:10.1046/j.1471-4159.1997.68052032.x. PMID 9109529.
- Rothman RB, Baumann MH (August 2006). "Balance between dopamine and serotonin release modulates behavioral effects of amphetamine-type drugs". Ann. N. Y. Acad. Sci. 1074: 245–60. Bibcode:2006NYASA1074..245R. doi:10.1196/annals.1369.064. PMID 17105921.
- Johnson LA, Guptaroy B, Lund D, Shamban S, Gnegy ME (March 2005). "Regulation of amphetamine-stimulated dopamine efflux by protein kinase C beta". J. Biol. Chem. 280 (12): 10914–9. doi:10.1074/jbc.M413887200. PMID 15647254.
- Kahlig KM, Binda F, Khoshbouei H (March 2005). "Amphetamine induces dopamine efflux through a dopamine transporter channel". Proc. Natl. Acad. Sci. U.S.A. 102 (9): 3495–500. Bibcode:2005PNAS..102.3495K. doi:10.1073/pnas.0407737102. PMC 549289. PMID 15728379.
- "A mechanism for amphetamine-induced dopamine overload". PLoS Biology 2 (3): e87. 2004. doi:10.1371/journal.pbio.0020087. PMC 368179.
- Mosharov EV, Larsen KE, Kanter E, Phillips KA, Wilson K, Schmitz Y, Krantz DE, Kobayashi K, Edwards RH, Sulzer D (April 2009). "Interplay between cytosolic dopamine, calcium, and alpha-synuclein causes selective death of substantia nigra neurons". Neuron 62 (2): 218–29. doi:10.1016/j.neuron.2009.01.033. PMC 2677560. PMID 19409267.
- Sulzer D, Rayport S (December 1990). "Amphetamine and other psychostimulants reduce pH gradients in midbrain dopaminergic neurons and chromaffin granules: a mechanism of action". Neuron 5 (6): 797–808. doi:10.1016/0896-6273(90)90339-H. PMID 2268433.
- Larsen KE, Fon EA, Hastings TG, Edwards RH, Sulzer D (October 2002). "Methamphetamine-induced degeneration of dopaminergic neurons involves autophagy and upregulation of dopamine synthesis". J. Neurosci. 22 (20): 8951–60. PMID 12388602.
- Sulzer D, Sonders MS, Poulsen NW, Galli A (April 2005). "Mechanisms of neurotransmitter release by amphetamines: a review". Prog. Neurobiol. 75 (6): 406–33. doi:10.1016/j.pneurobio.2005.04.003. PMID 15955613.
- Schmitz Y, Lee CJ, Schmauss C, Gonon F, Sulzer D (August 2001). "Amphetamine distorts stimulation-dependent dopamine overflow: effects on D2 autoreceptors, transporters, and synaptic vesicle stores". J. Neurosci. 21 (16): 5916–24. PMID 11487614.
- Jones S, Kauer JA (November 1999). "Amphetamine depresses excitatory synaptic transmission via serotonin receptors in the ventral tegmental area". J. Neurosci. 19 (22): 9780–7. PMID 10559387.
- Hilber B, Scholze P, Dorostkar MM (November 2005). "Serotonin-transporter mediated efflux: a pharmacological analysis of amphetamines and non-amphetamines". Neuropharmacology 49 (6): 811–9. doi:10.1016/j.neuropharm.2005.08.008. PMID 16185723.
- Knapp S, Mandell AJ, Geyer MA (June 1974). "Effects of amphetamines on regional tryptophan hydroxylase activity and synaptosomal conversion of tryptophan to 5-hydroxytryptamine in rat brain". J. Pharmacol. Exp. Ther. 189 (3): 676–89. PMID 4843167.
- Trulson ME, Jacobs BL (February 1980). "Chronic amphetamine administration decreases brain tryptophan hydroxylase activity in cats". Life Sci. 26 (5): 329–35. PMID 6154217.
- Lyness WH (1983). "Effect of L-tryptophan pretreatment on d-amphetamine self administration". Subst Alcohol Actions Misuse 4 (4): 305–12. PMID 6670054.
- Leccese AP, Lyness WH (June 1984). "The effects of putative 5-hydroxytryptamine receptor active agents on D-amphetamine self-administration in controls and rats with 5,7-dihydroxytryptamine median forebrain bundle lesions". Brain Res. 303 (1): 153–62. PMID 6610461.
- Florin SM, Kuczenski R, Segal DS (August 1994). "Regional extracellular norepinephrine responses to amphetamine and cocaine and effects of clonidine pretreatment". Brain Res. 654 (1): 53–62. doi:10.1016/0006-8993(94)91570-9. PMID 7982098.
- "Adderall". RxList. 4 October 2010. Retrieved 8 May 2012.
- "Amphetamine use in adolescence may impair adult working memory". Archived from the original on 10 November 2009. Retrieved 22 October 2009.
- Brussee, J.; Jansen A. C. A. (1983). "A highly stereoselective synthesis of s(-)-[1,1′-binaphthalene]-2,2′-diol". Tetrahedron Letters 24 (31): 3261–3262. doi:10.1016/S0040-4039(00)88151-4.
- WikiAnswers google cached page: 'Does Namenda memantine work in preventing tolerance to adderall ADD amphetamine type drugs?'
- Sulzer D, Sonders MS, Poulsen NW, Galli A (April 2005). "Mechanisms of neurotransmitter release by amphetamines: a review". Prog. Neurobiol. 75 (6): 406–33. doi:10.1016/j.pneurobio.2005.04.003. PMID 15955613.
- Bunzow JR, Sonders MS, Arttamangkul S, Harrison LM, Zhang G, Quigley DI, Darland T, Suchland KL, Pasumamula S, Kennedy JL, Olson SB, Magenis RE, Amara SG, Grandy DK (December 2001). "Amphetamine, 3,4-methylenedioxymethamphetamine, lysergic acid diethylamide, and metabolites of the catecholamine neurotransmitters are agonists of a rat trace amine receptor". Mol. Pharmacol. 60 (6): 1181–8. PMID 11723224.
- Xie Z, Miller GM (July 2009). "A receptor mechanism for methamphetamine action in dopamine transporter regulation in brain". J. Pharmacol. Exp. Ther. 330 (1): 316–25. doi:10.1124/jpet.109.153775. PMC 2700171. PMID 19364908.
- 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): 8966–71. doi:10.1073/pnas.151105198. PMC 55357. PMID 11459929.
- Xie Z, Westmoreland SV, Miller GM (May 2008). "Modulation of monoamine transporters by common biogenic amines via trace amine-associated receptor 1 and monoamine autoreceptors in human embryonic kidney 293 cells and brain synaptosomes". J. Pharmacol. Exp. Ther. 325 (2): 629–40. doi:10.1124/jpet.107.135079. PMID 18310473.
- Xie Z, Westmoreland SV, Bahn ME, Chen GL, Yang H, Vallender EJ, Yao WD, Madras BK, Miller GM (April 2007). "Rhesus monkey trace amine-associated receptor 1 signaling: enhancement by monoamine transporters and attenuation by the D2 autoreceptor in vitro". J. Pharmacol. Exp. Ther. 321 (1): 116–27. doi:10.1124/jpet.106.116863. PMID 17234900.
- Shargel, Leon; Wu-Pong, Susanna; Yu, Andrew B.C. (2012) Applied Biopharmaceutics & Pharmacokinetics (6th Edition).. McGraw-Hill.
- Flomenbaum, Neal E.; Goldfrank, Lewis R.; Hoffman, Robert S.; Howland, Mary Ann; Lewin, Neal A.; Nelson, Lewis S. (2006). Goldfrank's Toxicologic Emergencies (8th Edition).. McGraw-Hill.
- Edeleano L (1887). "Ueber einige Derivate der Phenylmethacrylsäure und der Phenylisobuttersäure". Berichte der deutschen chemischen Gesellschaft 20 (1): 616–622. doi:10.1002/cber.188702001142.
- Shulgin, Alexander; Shulgin, Ann (1992). "6 – MMDA". PiHKAL. Berkeley, California: Transform Press. p. 39. ISBN 0-9630096-0-5.
- Rasmussen N (July 2006). "Making the first anti-depressant: amphetamine in American medicine, 1929–1950". J Hist Med Allied Sci 61 (3): 288–323. doi:10.1093/jhmas/jrj039. PMID 16492800.
- Iverson, Leslie. Speed, Ecstasy, Ritalin: the science of amphetamines. Oxford, New York. Oxford University Press, 2006.
- Rasmussen, Nicolas (2008). "Ch. 4". On Speed: The Many Lives of Amphetamine. New York, New York: New York University Press. ISBN 0-8147-7601-9.
- "Nazis Secret Weapon: They were all high". http://www.news.com.au. 2 April 2011. Retrieved 9 July 2012.
- Clement B.A., Goff C.M., Forbes T.D.A. (1998). "Toxic amines and alkaloids from Acacia rigidula". Phytochemistry 49 (5): 1377–1380. doi:10.1016/S0031-9422(97)01022-4.
- Clement B.A., Goff C.M., Forbes T.D.A. (1997). "Toxic amines and alkaloids from Acacia berlandieri". Phytochemistry 46 (2): 249–254. doi:10.1016/S0031-9422(97)00240-9.
- "Ask Dr. Shulgin Online: Acacias and Natural Amphetamine". Cognitiveliberty.org. 26 September 2001. Retrieved 8 May 2012.
- Twohey M (25 March 2006). "Pills become an addictive study aid". JS Online. Archived from the original on 15 August 2007. Retrieved 2 December 2007.
- Advokat C, Scheithauer M (2013). "Attention-deficit hyperactivity disorder (ADHD) stimulant medications as cognitive enhancers". Front Neurosci 7: 82. doi:10.3389/fnins.2013.00082. PMID 23754970.
- Smith GM, Weitzner M, Levenson SR, Beecher HK (July 1963). "Effects of amphetamine and secobarbital on coding and mathematical performance". J. Pharmacol. Exp. Ther. 141: 100–4. PMID 13989424.
- Yesalis CE, Bahrke M (2005-12). "Anabolic Steroid and Stimulant Use in North American Sport between 1850 and 1980". Sport in History 25 (3): 434–451. doi:10.1080/17460260500396251. Retrieved 2 December 2007.
- National Collegiate Athletic Association (2006-01), NCAA Study of Substance Use Habits of College Student-Athletes (PDF), National Collegiate Athletic Association, pp. 2–4, 11–13, retrieved 2 December 2007
- Chandler JV, Blair SN (1980). "The effect of amphetamines on selected physiological components related to athletic success". Med Sci Sports Exerc 12 (1): 65–9. PMID 7392905.
- Borg G, Edström CG, Linderholm H, Marklund G (1972). "Changes in physical performance induced by amphetamine and amobarbital". Psychopharmacologia 26 (1): 10–8. PMID 5051458.
- Smith GM, Beecher HK (May 1959). "Amphetamine sulfate and athletic performance. I. Objective effects". J Am Med Assoc 170 (5): 542–57. PMID 13653995.
- Smith, Gene M. (30 May 1959). "AMPHETAMINE SULFATE AND ATHLETIC PERFORMANCE<subtitle>I. OBJECTIVE EFFECTS</subtitle>". JAMA: The Journal of the American Medical Association 170 (5): 542. doi:10.1001/jama.1959.63010050001008.
- Pullinen T, Huttunen P, Komi PV (May 2000). "Plasma catecholamine responses and neural adaptation during short-term resistance training". Eur. J. Appl. Physiol. 82 (1-2): 68–75. doi:10.1007/s004210050653. PMID 10879445.
- Suleman, Amer. "Exercise Physiology". Medscape. Retrieved 13 June 2013.
- De Mondenard, Dr Jean-Pierre: Dopage, l'imposture des performances, Chiron, France, 2000
- Grant, D.N.W.; Air Force, UK, 1944
- "Air force rushes to defend amphetamine use". The Age. 18 January 2003. Archived from the original on 13 January 2009. Retrieved 26 January 2009.
- Frias, Carlos (2 April 2006). "Baseball and amphetamines". Palm Beach Post. Archived from the original on 17 December 2007. Retrieved 2 December 2007.
- Kreidler, Mark (15 November 2005). "Baseball finally brings amphetamines into light of day". ESPN.com. Retrieved 2 December 2007.
- Klobuchar, Jim (31 March 2006). "Can baseball make a clean sweep?". Christian Science Monitor. Archived from the original on 16 December 2007. Retrieved 2 December 2007.
- Associated Press (18 January 2007). "MLB owners won't crack down on 'greenies'". MSNBC.com. Archived from the original on 25 December 2007. Retrieved 2 December 2007.
- Lund, Adrian K; David F. Preusser, Richard D. Blomberg, Allan F. Williams, J. Michael Walsh (1989). "Drug Use by Tractor-Trailer Drivers". In Steven W. Gust (ed.). Drugs in the Workplace: Research and Evaluation Data. National Institute on Drug Abuse Research. Rockville, MD: National Institute on Drug Abuse. pp. 47–67. Retrieved 2 December 2007. "This study has provided the first objective data regarding the use of potentially abusive drugs by tractor-trailer drivers... Prescription stimulants, such as amphetamine, methamphetamine, and phentermine were found in 5 percent of the  drivers [who participated in the study], often in combination with similar but less potent stimulants, such as phenylpropanolamine. Nonprescription stimulants were detected in 12 percent of the drivers, about half of whom gave no medical explanation for their presence... One limitation of these findings is that 12 percent of the randomly selected drivers refused to participate in the study or provided insufficient urine and blood for testing; the distribution of drugs among these 42 drivers is unknown... Finally, the results apply to tractor-trailer drivers operating on a major east-west interstate route in Tennessee. Drug incidence among other truck-driver populations are unknown and may be higher or lower than reported here. (64)"
- Verstraete AG, Heyden FV (2005). "Comparison of the sensitivity and specificity of six immunoassays for the detection of amphetamines in urine". J Anal Toxicol 29 (5): 359–64. PMID 16105261.
- 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)-(+)-alpha-methoxy-alpha-(trifluoromethy)phenylacetyl chloride (MTPA)". J Anal Toxicol 28 (6): 449–55. doi:10.1093/jat/28.6.449. PMID 15516295.
- R. Baselt, Disposition of Toxic Drugs and Chemicals in Man, 9th edition, Biomedical Publications, Foster City, CA, 2011, pp. 85-88.
- Brecher, Edward M.; the editors of Consumer Reports Magazine (1972). "How speed was popularized". The Consumers Union Report on Licit and Illicit Drugs. Schaffer Drug Library. Retrieved 1 June 2010.
- Gyenis, Attila (1997). "Forty Years of On the Road 1957–1997". Archived from the original on 14 February 2008. Retrieved 18 March 2008.
- Welsh, Irvine (10 August 2006). "Drug Cultures in Trainspotting and Porno". irvinewelsh.net. Retrieved 13 October 2008.
- Carr, David (29 June 2008). "Fear and Loathing on a Documentary Screen" (in en-US). New York Times. pp. AR7. Archived from the original on 8 February 2009. Retrieved 18 March 2009.
- Thompson, Hunter S. (1973). Fear and Loathing on the Campaign Trail '72. New York: Warner Books. pp. 15–16, 21. ISBN 0-446-31364-5.
- Dr. Andrew Wilson (2008). "Mixing the Medicine: The unintended consequence of amphetamine control on the Northern Soul Scene" (PDF). Internet Journal of Criminology. Retrieved 2013-05-25.
- Keith Rylatt and Phil Scott, Central 1179: The Story of Manchester's Twisted Wheel Club, BeeCool Publishing. 2001
- Memo From David O. Selznick, http://www.amazon.com/Memo-David-Selznick-Memorandums-Autobiographical/dp/0375755314
- Shadowing the Third Man, http://www.imdb.com/title/tt0429086/
- Hill, J. Paul Erdos, Mathematical Genius, Human (In That Order)
- Hoffman, Paul (1998). "The Man Who Loved Only Numbers". The New York Times. Retrieved 23 May 2013.
- "Class A, B and C drugs". Archived from the original on 4 August 2007. Retrieved 23 July 2007.
- "Trends in Methamphetamine/Amphetamine Admissions to Treatment: 1993–2003". Substance Abuse and Mental Health Services Administration. Retrieved 28 February 2007.
- "Straight Facts About Drugs & Drug Abuse". Health Canada. Retrieved 23 April 2011.
- "List of psychotropic substances under international control" (PDF). International Narcotics Control Board. Archived from the original on 5 December 2005. Retrieved 19 November 2005.
- Musshoff F (February 2000). "Illegal or legitimate use? Precursor compounds to amphetamine and methamphetamine". Drug Metabolism Reviews 32 (1): 15–44. doi:10.1081/DMR-100100562. PMID 10711406.
- Cody JT (May 2002). "Precursor medications as a source of methamphetamine and/or amphetamine positive drug testing results". Journal of Occupational and Environmental Medicine / American College of Occupational and Environmental Medicine 44 (5): 435–50. PMID 12024689.
- Craig Medical Distribution. "Drug Test FAQ | Craig Medical Distribution, Inc". Craigmedical.com. Retrieved 8 May 2012.
- Drevets WC, Gautier C, Price JC, Kupfer DJ, Kinahan PE, Grace AA, Price JL, Mathis CA (January 2001). "Amphetamine-induced dopamine release in human ventral striatum correlates with euphoria". Biol. Psychiatry 49 (2): 81–96. PMID 11164755. Retrieved 23 May 2009.
- Rang and Dale, Pharmacology
- Schep LJ, Slaughter RJ, Beasley DM (August 2010). "The clinical toxicology of metamfetamine". Clinical Toxicology (Philadelphia, Pa.) 48 (7): 675–94. doi:10.3109/15563650.2010.516752. ISSN 1556-3650. PMID 20849327.
- "Nine arrested in biggest drug haul of the year". gulfnews.com. 30 November 2011. Retrieved 30 November 2011.
- CID 5826 from PubChem (D-form—dextroamphetamine)
- CID 3007 from PubChem (L-form and D, L-forms)
- CID 32893 from PubChem (L-form—Levamphetamine or L-amphetamine)
- List of 504 Compounds Similar to Amphetamine (PubChem)
- EMCDDA drugs profile: Amphetamine (2007)
- Drugs.com - Amphetamine
- Asia & Pacific Amphetamine-Type Stimulants Information Centre
- U.S. National Library of Medicine: Drug Information Portal - Amphetamine