Attention deficit hyperactive disorder is a neurologically based behavioral disorder that afflicts children and adults alike (1). Characterized by inability to pay attention, hyperactivity, and impulsive actions, attention deficit hyperactive disorder, or ADHD for short, this disorder has become a popular diagnosis for students who claim that they are unable to concentrate or focus on their studies (2). Much research has been done in recent years regarding ADHD, its neurological basis in the brain, and how to treat it effectively (1). Many prescription drugs have been released onto the market that effectively target the levels of certain hormones which in turn enable one to counteract the symptoms of ADHD (3).
However, drugs such as Adderall, which were developed solely for those properly diagnosed with the disorder, are beginning to be used recreationally by those whom admit to not having ADHD, but either find that they perform better with its aid or simply enjoy the high of the prescription drug (4). What does this mean for college students? Is recreational use of this drug dangerous physically? Mentally? Does the use of Adderall by those not diagnosed with pose the threat of an addiction? Is an addiction to a drug that seems to make you more efficient a bad thing?
To begin to answer these questions and more, one must understand a few of the basics of the neurobiology behind the disorder ADHD and the science behind drugs that treat it. Like many neurologically based disorders, scientists are not 100% sure of all of the complicated functions that play a role (1). However, by using state of the art brain imaging techniques, several studies have deduced that brains afflicted with ADHD malfunction in the frontal cortex (1). The frontal cortex is involved with primarily executive functions like reasoning, planning, focusing, and problem solving (1). It is in this part of the brain that dopamine, an important neurotransmitter, has been found to be deficient. Without proper concentrations of dopamine in the frontal cortex, these executive functions suffer (5).
To treat this disorder, prescription drugs like Adderall may be prescribed to patients. Adderall is a cocktail of several active ingredients that include amphetamine salts, an active ingredient in many ADHD medications. These amphetamines are thought to treat ADHD by blocking the reuptake of dopamine from the neural synapses and increasing the uptake into subsequent neurons. The increased dopamine flow in the frontal cortex then allows the brain to carry on its executive functions as a normal brain would, thus counteracting the effects of ADHD (6). But what happens when a brain whose executive functions work properly is treated with such a powerful stimulant?
The answer to this question lies in the 1 in 5 college students that admit to using this drug and not having ADHD (7). Why? Athletes have steroids, depressives have “happy-pills”, and those who wish to do it all, and do it fast, have Adderall. A person with a perfectly normal, functioning frontal cortex and dopamine levels will experience a heightened sense of motivation, focus, and concentration. Presumably this is the perfect mood to pull all-nighters, read hundreds of pages at a time, and write pages and pages of that final paper (8). “I didn't feel like I was becoming smarter or even like I was thinking more clearly. I just felt more directed, less distracted by rogue thoughts, less day-dreamy (7),” states Joshua Foer, a journalist who, after consulting many doctors, decided to try Adderall for himself. “I felt like I was clearing away underbrush that had been obscuring my true capabilities (7).” Before performing his experiment, Foer discussed his decision with psychiatrists who informed him, to his surprise, that when taken in small doses, irregularly, with or without a prescription, Adderall is most likely harmless (7). Other scientists beg to differ, and it is these accounts that are of particular interest.
The general consensus is that stimulant amphetamines like Adderall do indeed increase performance in those that do and do not have properly diagnosed ADHD. The promise of a better GPA with less effort is promise enough for college students across the board to obtain Adderall by any means necessary. Many students admit to actually seeing doctors and purposefully exaggerating symptoms of ADHD to acquire medication. Others simply pop a generously donated pill from their pals (8). The danger lies in the possibility of dependence and the rarely considered effect of the drug on those that have preexisting medical problems that can deteriorate with prolonged use (8).
Since many students assert that they use Adderall only for studying for large tests and completing important assignments, the risk of dependency is high. “I don’t think I’m addicted…..I just can’t imagine not taking it (8),” says student Susan. Says student Steve: “I attend a major university….I take two pills when I have a ton of work to do….Without Adderall I failed one class….I began to take Adderall again and saw a huge improvement (9).” The long term effects of using Adderall in this manner are relatively unknown, however it is well known that those that use amphetamines in larger doses by snorting or inhaling can very well be diagnosed with addiction. Just one example of an amphetamine of this nature is speed (10).
Other side effects of this drug include being irritable while under the influence (8) and feeling as though one’s creativity has been stifled in the name of creating order out of disorder and doing the one task at hand (7). “These medications allow you to be more structured and more rigid. That's the opposite of the impulsivity of creativity,” says Dr. Heiligenstein of the University of Wisconsin (7). Is this just a small price to pay for an “A?” Can one sacrifice their creativity for a few hours in the name of passing Chemistry?
There is even more to this issue than menacing side effects, however. What is it about academics today that have students popping pills to succeed? And is it fair? Athletes that use steroids are kicked off their sports teams because they are assumed to have an unfair advantage—so isn’t this the same general principle? Many students, especially those that actually suffer from ADHD reply “Yes.” “It’s the kind of medication that can help anyone,” says ADHD afflicted student Josie, “For people with ADD, it just makes them normal, and for people without ADD, it makes them above average. If both me and someone without ADD were both on Adderall, I could never outdo them (8).”
So, as a stressed out college student striving to succeed in school and boost my GPA, I sit here wondering how much faster and more efficiently I could have written this paper had I been taking Adderall. A nagging suspicion tells me that yes, maybe I would have finished before 2 am. Maybe I would have stopping pausing to check my e-mail and Facebook. But my gut tells me that this is the wrong thing to do. Not being afflicted with ADHD, I do not have a good reason to take a pill to succeed other than to counteract my own inability to “get down to business”, as they say. My motivation for writing this paper was to find out whether or not unprescribed use of Adderall was dangerous. It appears that though it is not. The risk of dependency, however, is real, and can be seen in those students that can no longer finish assignments without the help of this drug. My question now is whether or not it is morally correct for college students to continue taking this drug as a stimulant—a question that is up to the reader to decide for his or herself.
Works Cited List
Not to be confused with ephedrone.
|Pronunciation||( listen) or|
|Trade names||Bronkaid, Primatene|
|by mouth, IV, IM, SC|
|Onset of action||IV (seconds), IM (10 min to 20 min), by mouth (15 min to 60 min)|
|Biological half-life||3 h to 6 h|
|Duration of action||IV/IM (60 min), by mouth (2 h to 4 h)|
|Excretion||22% to 99% (urine)|
|Chemical and physical data|
|3D model (JSmol)|
|NY (what is this?) (verify)|
Ephedrine is a medication and stimulant. It is often used to prevent low blood pressure during spinal anesthesia. It has also been used for asthma, narcolepsy, and obesity but is not the preferred treatment. It is of unclear benefit in nasal congestion. It can be taken by mouth or by injection into a muscle, vein, or just under the skin. Onset with intravenous use is fast, while injection into a muscle can take 20 minutes, and by mouth can take an hour for effect. When given by injection it lasts about an hour and when taken by mouth it can last up to four hours.
Common side effects include trouble sleeping, anxiety, headache, hallucinations, high blood pressure, fast heart rate, loss of appetite, and inability to urinate. Serious side effects include stroke, heart attack, and abuse. While likely safe in pregnancy its use in this population is poorly studied. Use during breastfeeding is not recommended. Ephedrine works by turning on the α and β adrenergic receptors.
Ephedrine was first isolated in 1885. It is on the World Health Organization's List of Essential Medicines, the most effective and safe medicines needed in a health system. It is available as a generic medication. The wholesale cost in the developing world is about 0.69 to 1.35 USD per dose. In the United States it is not very expensive. It can normally be found in plants of the Ephedra type. Dietary supplements that contain ephedrine are illegal in the United States. An exception is when used in traditional Chinese medicine.
Both ephedrine and pseudoephedrine increase blood pressure and act as bronchodilators, with pseudoephedrine having considerably less effect.
Ephedrine promotes modest short-term weight loss, specifically fat loss, but its long-term effects are unknown. In mice ephedrine is known to stimulate thermogenesis in the brown adipose tissue, but because adult humans have only small amounts of brown fat, thermogenesis is assumed to take place mostly in the skeletal muscle. Ephedrine also decreases gastric emptying. Methylxanthines such as caffeine and theophylline have a synergistic effect with ephedrine with respect to weight loss. This led to creation and marketing of compound products. One of them, known as the ECA stack, contains caffeine and aspirin besides ephedrine. It is a popular supplement taken by bodybuilders seeking to cut body fat before a competition.
As a phenethylamine, ephedrine has a similar chemical structure to amphetamines and is a methamphetamineanalogue having the methamphetamine structure with a hydroxyl group at the β position. Because of ephedrine's structural similarity to methamphetamine, it can be used to create methamphetamine using chemical reduction in which ephedrine's hydroxyl group is removed; this has made ephedrine a highly sought-after chemical precursor in the illicit manufacture of methamphetamine. The most popular method for reducing ephedrine to methamphetamine is similar to the Birch reduction, in that it uses anhydrous ammonia and lithium metal in the reaction. The second-most popular method uses red phosphorus, iodine, and ephedrine in the reaction.
Through oxidation, ephedrine can be easily synthesized into methcathinone. Ephedrine is listed as a table-I precursor under the United Nations Convention Against Illicit Traffic in Narcotic Drugs and Psychotropic Substances.
Detection of use
Ephedrine may be quantified in blood, plasma, or urine to monitor possible abuse by athletes, confirm a diagnosis of poisoning, or assist in a medicolegal death investigation. Many commercial immunoassay screening tests directed at the amphetamines cross-react appreciably with ephedrine, but chromatographic techniques can easily distinguish ephedrine from other phenethylamine derivatives. Blood or plasma ephedrine concentrations are typically in the 20-200 µg/l range in persons taking the drug therapeutically, 300-3000 µg/l in abusers or poisoned patients and 3–20 mg/l in cases of acute fatal overdosage. The current WADA limit for ephedrine in an athlete's urine is 10 µg/ml.
Ephedrine should not be used in conjunction with certain antidepressants, namely norepinephrine-dopamine reuptake inhibitors (NDRIs), as this increases the risk of symptoms due to excessive serum levels of norepinephrine.
Bupropion is an example of an antidepressant with an amphetamine-like structure similar to ephedrine, and it is an NDRI. Its action bears more resemblance to amphetamine than to fluoxetine in that its primary mode of therapeutic action involves norepinephrine and to a lesser degree dopamine, but it also releases some serotonin from presynaptic clefts. It should not be used with ephedrine, as it may increase the likelihood of side effects.
Ephedrine should be used with caution in patients with inadequate fluid replacement, impaired adrenal function, hypoxia, hypercapnia, acidosis, hypertension, hyperthyroidism, prostatic hypertrophy, diabetes mellitus, cardiovascular disease, during delivery if maternal blood pressure is >130/80 mmHg, and lactation.
Contraindications for the use of ephedrine include: closed-angle glaucoma, phaeochromocytoma, asymmetric septal hypertrophy (idiopathic hypertrophic subaortic stenosis), concomitant or recent (previous 14 days) monoamine oxidase inhibitor (MAOI) therapy, general anaesthesia with halogenated hydrocarbons (particularly halothane), tachyarrhythmias or ventricular fibrillation, or hypersensitivity to ephedrine or other stimulants.
Ephedrine should not be used at any time during pregnancy unless specifically indicated by a qualified physician and only when other options are unavailable.
Ephedrine is a potentially dangerous natural compound; as of 2004[update] the US Food and Drug Administration had received over 18,000 reports of adverse effects in people using it.
Adverse drug reactions (ADRs) are more common with systemic administration (e.g. injection or oral administration) compared to topical administration (e.g. nasal instillations). ADRs associated with ephedrine therapy include:
- Cardiovascular: tachycardia, cardiac arrhythmias, angina pectoris, vasoconstriction with hypertension
- Dermatological: flushing, sweating, acne vulgaris
- Gastrointestinal: nausea
- Genitourinary: decreased urination due to vasoconstriction of renal arteries, difficulty urinating is not uncommon, as alpha-agonists such as ephedrine constrict the internal urethral sphincter, mimicking the effects of sympathetic nervous system stimulation
- Nervous system: restlessness, confusion, insomnia, mild euphoria, mania/hallucinations (rare except in previously existing psychiatric conditions), delusions, formication (may be possible, but lacks documented evidence) paranoia, hostility, panic, agitation
- Respiratory: dyspnea, pulmonary edema
- Miscellaneous: dizziness, headache, tremor, hyperglycemic reactions, dry mouth
The neurotoxicity of l-ephedrine is disputed. 
In chemical synthesis, ephedrine is used in bulk quantities as a chiral auxiliary group. 
In saquinavir synthesis, the half-acid is resolved as its salt with l-ephedrine.
Chemistry and nomenclature
Ephedrine is a sympathomimeticamine and substituted amphetamine. It is similar in molecular structure to phenylpropanolamine, methamphetamine, and epinephrine (adrenaline). Chemically, it is an alkaloid with a phenethylamine skeleton found in various plants in the genus Ephedra (family Ephedraceae). It works mainly by increasing the activity of norepinephrine (noradrenaline) on adrenergic receptors. It is most usually marketed as the hydrochloride or sulfate salt.
Ephedrine exhibits optical isomerism and has two chiral centres, giving rise to four stereoisomers. By convention, the pair of enantiomers with the stereochemistry (1R,2S) and (1S,2R) is designated ephedrine, while the pair of enantiomers with the stereochemistry (1R,2R) and (1S,2S) is called pseudoephedrine. Ephedrine is a substituted amphetamine and a structural methamphetamine analogue. It differs from methamphetamine only by the presence of a hydroxyl group (—OH).
The isomer which is marketed is (1R,2S)-(–)-ephedrine.
Ephedrine hydrochloride has a melting point of 187−188 °C.
In the outdated D/L system (+)-ephedrine is also referred to as L-ephedrine and (−)-ephedrine as D-ephedrine (in the Fisher projection, then the phenyl ring is drawn at bottom).
Often, the D/L system (with small caps) and the d/l system (with lower-case) are confused. The result is that the levorotary l-ephedrine is wrongly named L-ephedrine and the dextrorotary d-pseudoephedrine (the diastereomer) wrongly D-pseudoephedrine.
The IUPAC names of the two enantiomers are (1R,2S)- respectively (1S,2R)-2-methylamino-1-phenylpropan-1-ol. A synonym is erythro-ephedrine.
Ephedrine is obtained from the plant Ephedra sinica and other members of the Ephedra genus. Raw materials for the manufacture of ephedrine and traditional Chinese medicines are produced in China on a large scale. As of 2007, companies produced for export US$13 million worth of ephedrine from 30,000 tons of ephedra annually, 10 times the amount used in traditional Chinese medicine.
Most of the l-ephedrine produced today for official medical use is made synthetically as the extraction and isolation process from E. sinica is tedious and no longer cost effective.[unreliable source?]
Ephedrine was long thought to come from modifying the amino acid L-phenylalanine.L-Phenylalanine would be decarboxylated and subsequently attacked with ω-aminoacetophenone. Methylation of this product would then produce ephedrine. This pathway has since been disproven. A new pathway proposed suggests that phenylalanine first forms cinnamoyl-CoA via the enzymes phenylalanine ammonia-lyase and acyl CoA ligase. The cinnamoyl-CoA is then reacted with a hydratase to attach the alcohol functional group. The product is then reacted with a retro-aldolase, forming benzaldehyde. Benzaldehyde reacts with pyruvic acid to attach a 2 carbon unit. This product then undergoes transamination and methylation to form ephedrine and its stereoisomer, pseudoephedrine.
Mechanism of action
Ephedrine, a sympathomimetic amine, acts on part of the sympathetic nervous system (SNS). The principal mechanism of action relies on its indirect stimulation of the adrenergic receptor system by increasing the activity of norepinephrine at the postsynaptic α and β receptors. The presence of direct interactions with α receptors is unlikely, but still controversial.L-ephedrine, and particularly its stereoisomer norpseudoephedrine (which is also present in Catha edulis) has indirect sympathomimetic effects and due to its ability to cross the blood-brain barrier, it is a CNSstimulant similar to amphetamines, but less pronounced, as it releases noradrenaline and dopamine in the substantia nigra.
The presence of an N-methyl group decreases binding affinities at α receptors, compared with norephedrine. Ephedrine, though, binds better than N-methylephedrine, which has an additional methyl group at the nitrogen atom. Also the steric orientation of the hydroxyl group is important for receptor binding and functional activity.
- Compounds with decreasing α-receptor affinity
Norephedrine Ephedrine N-Methylephedrine
Ephedrine in its natural form, known as má huáng (麻黄) in traditional Chinese medicine, has been documented in China since the Han dynasty (206 BC – 220 AD) as an antiasthmatic and stimulant. In 1885, the chemical synthesis of ephedrine was first accomplished by Japanese organic chemistNagai Nagayoshi based on his research on traditional Japanese and Chinese herbal medicines. The industrial manufacture of ephedrine in China began in the 1920s, when Merck began marketing and selling the drug as ephetonin. Ephedrine exports between China and the West grew from 4 to 216 tonnes between 1926 and 1928.
In traditional Chinese medicine, má huáng has been used as a treatment for asthma and bronchitis for centuries.
In January 2002, Health Canada issued a voluntary recall of all ephedrine products containing more than 8 mg per dose, all combinations of ephedrine with other stimulants such as caffeine, and all ephedrine products marketed for weight-loss or bodybuilding indications, citing a serious risk to health. Ephedrine is still sold as an oral nasal decongestant in 8 mg pills, OTC.
In 1997, the FDA proposed a regulation on ephedra (the herb from which ephedrine is obtained), which limited an ephedra dose to 8 mg (of active ephedrine) with no more than 24 mg per day. This proposed rule was withdrawn, in part, in 2000 because of "concerns regarding the agency's basis for proposing a certain dietary ingredient level and a duration of use limit for these products." In 2004, the FDA created a ban on ephedrine alkaloids marketed for reasons other than asthma, colds, allergies, other disease, or traditional Asian use. On April 14, 2005, the U.S. District Court for the District of Utah ruled the FDA did not have proper evidence that low dosages of ephedrine alkaloids are actually unsafe, but on August 17, 2006, the U.S. Court of Appeals for the Tenth Circuit in Denver upheld the FDA's final rule declaring all dietary supplements containing ephedrine alkaloids adulterated, and therefore illegal for marketing in the United States. Furthermore, ephedrine is banned by the NCAA, MLB, NFL, and PGA. Ephedrine is, however, still legal in many applications outside of dietary supplements. Purchasing is currently limited and monitored, with specifics varying from state to state.
The House passed the Combat Methamphetamine Epidemic Act of 2005 as an amendment to the renewal of the USA PATRIOT Act. Signed into law by President George W. Bush on March 6, 2006, the act amended the US Code (21 USC 830) concerning the sale of ephedrine-containing products. The federal statute included these requirements for merchants who sell these products:
- A retrievable record of all purchases identifying the name and address of each party to be kept for two years
- Required verification of proof of identity of all purchasers
- Required protection and disclosure methods in the collection of personal information
- Reports to the Attorney General of any suspicious payments or disappearances of the regulated products
- Non-liquid dose form of regulated product may only be sold in unit-dose blister packs
- Regulated products are to be sold behind the counter or in a locked cabinet in such a way as to restrict access
- Daily sales of regulated products not to exceed 3.6 g without regard to the number of transactions
- Monthly sales not to exceed 9 g of pseudoephedrine base in regulated products
The law gives similar regulations to mail-order purchases, except the monthly sales limit is only 7.5 g.
As a pure herb or tea, má huáng, containing ephedrine, is still sold legally in the USA. The law restricts/prohibits its being sold as a dietary supplement (pill) or as an ingredient/additive to other products, like diet pills.
All Ephedra spp and ephedrine itself are considered schedule 4 substances under the Poisons Standard (October 2015). A schedule 4 drug is considered a Prescription Only Medicine, or Prescription Animal Remedy – Substances, the use or supply of which should be by or on the order of persons permitted by State or Territory legislation to prescribe and should be available from a pharmacist on prescription under the Poisons Standard (October 2015).
In South Africa, ephedrine was moved to schedule 6 on 27 May 2008, which makes it illegal to have ephedrine in higher doses than 8 mg per pill. Lower than 8 mg pills are still available Otc for sinus, head colds and flu, but is completely illegal in over the counter weight loss products.
Ephedrine was freely available in pharmacies in Germany until 2001. Afterwards, access was restricted since it was mostly bought for unindicated uses. Similarly, ephedra can only be bought with a prescription. Since April 2006, all products, including plant parts, that contain ephedrine are only available with a prescription.
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