Cocaine is a crystalline tropane alkaloid (benzoylmethylecgonine, C17H21NO4) found in the leaves of the coca plant and best known in its concentrated form as an addictive, and generally illegal, psychoactive recreational drug.
Although the amount of cocaine in coca leaves is low, when this alkaloid is chemically extracted and concentrated it results in a powerful nervous system stimulant, which is generally used nasally, smoked, or injected. As such, cocaine can be highly addictive and have deleterious impacts on the brain, heart, respiratory system, kidneys, sexual system, and gastrointestinal tract. In most countries, the production, distribution, sale, and possession of cocaine products is restricted and/or illegal. However, cocaine also has some medical use and in some countries is available by prescription for such purposes as external application to the skin to numb pain, although derivatives such as lidocaine and novocaine have largely replaced it.
Use of concentrated cocaine yields pleasure through its interference with neurotransmitters of the sympathetic nervous system, such as blocking dopamine from being reabsorbed and thus resulting in continual stimulation. As such, cocaine subverts a natural system for experiencing pleasure and, ironically, the user can reach a state in which he or she has difficulty experiencing pleasure without the drug. In addition to medical problems from the drug, including sudden death, cocaine is one of the most addictive recreational drugs and intense cravings can be created even after one use. The use of cocaine can create a tolerance, requiring an increasing dose for stimulation.
There is a huge worldwide market for cocaine. The United Nations Office of Drugs and Crime estimated that in 2009 the US cocaine market was $37 billion and the West and Central European cocaine market was US$ 33 billion.
For the plant, cocaine seems to serve a valuable function as an effective insecticide, limiting damage from herbivorous insects.
OverviewThe chemical structure of tropane
Cocaine is a tropane alkaloid. Tropane alkaloids are a class of alkaloids (naturally occurring chemical compounds that contain mostly basic nitrogen atoms) and secondary metabolites in which the chemical structure includes a tropane ring (nitrogenous bicyclic organic structure). Well-known alkaloids include caffeine, nicotine, morphine, theobromine, mescaline, strychnine, quinine, and codeine. Well-known tropane alkaloids, in addition to cocaine, include atropine and ecgonine (a precursor and metabolite of cocaine). Cocaine has the chemical formula C17H21NO4 and is also known as benzoylmethylecgonine or methyl benzoyl ecgonine.
Cocaine is found in coca plants, which are indigenous to South America. There are four varieties of these tropical plants that are cultivated: Erythroxylum coca var. coca (Bolivian or Huánuco coca), E. coca var. ipadu (Amazonian coca), E. novogranatense var. novogranatense (Colombian coca), and E. novogranatense var. truxillense (Trujillo coca). The name cocaine comes from the name of the coca plant plus the alkaloid suffix -ine.Coca shrub in Colombia
Cocaine is the most concentrated of the dozen or more alkaloids that have been identified in the coca plant. Concentrations vary by variety and region, but leaves have been reported as having between 0.25% and 0.77% (Plowman and Rivier 1983), between 0.35% and 0.72% by dry weight (Nathanson et al. 1993), and between 0.3% and 1.5% and averaging 0.8% in fresh leaves (Casale and Klein 1993). In unprocessed form, coca leaves have been used for thousands of years in South America for various religious, social, medicinal, and nutritional purposes, including to control hunger and combat the impacts of high altitudes. However, since the alkaloid cocaine is present in only trace amounts in the leaves, it does not cause the euphoric and psychoactive effects associated with use of the drug.
When processed and concentrated by chemical extraction from large quantities of coca leaves, cocaine is a powerful stimulant. The extract from the leaves is hydrolysed and esterified with methanol and benzoic acid to produce the hydrochloride salt of cocaine.
Biologically, cocaine acts as a serotonin-norepinephrine-dopamine reuptake inhibitor, also known as a triple reuptake inhibitor (TRI). For example, Marieb and Hoehn (2010) note the impact of cocaine hooking up to the dopamine reuptake transporter protein, thus blocking reabsorption of dopamine. With this neurotransmitter remaining in the synapse, the post-synaptic receptor cells are stimulated again and again, allowing the body to experience over and over this reward system and associated high, along with increased heart rate, sexual appetite, and blood pressure. However, as a result, the system releases less and less dopamine and the reward system goes dry, and the cocaine user, in addition to becoming anxious, find himself or herself "in a very real sense, unable to experience pleasure without the drug." However, more cocaine just suppresses dopamine release even more.
Unlike most molecules, cocaine has pockets with both high hydrophilic and lipophilic efficiency, violating the rule of hydrophilic-lipophilic balance. This causes it to cross the blood-brain barrier far better than other psychoactive chemicals and may even induce blood-brain barrier breakdown (Sharma et al. 2009; Dietrich 2009). Marieb and Hoehn (2010) note that one way that might be developed to tackle addiction would be to prompt the immune system to bind cocaine molecules and prevent them from entering the brain.
Cocaine is best known worldwide for its illegal use as a recreational drug. This concentrated form of cocaine is used nasally (nasal insufflation is also known as "snorting," "sniffing," or "blowing" and involves absorption through the mucous membranes lining the sinuses), injected (the method that produces the highest blood levels in the shortest time), or smoked (notably the cheaper, more potent form called "crack"). It may also be administered orally (rubbed on gums). Among forms of cocaine use are cocaine hydrochloride, natural leaf, cocaine paste, or freebase.
Cocaine use can be highly addictive, causing intense cravings for the drug, and can have deleterious impacts on the brain, heart, respiratory system, kidneys, sexual system, and gastrointestinal tract (WebMD 2013a). For example, it can result in a heart attack or strokes, even in young people,and it can cause ulcers and sudden kidney failure, and it can impair sexual function (WebMD 2013a).
The possession, distribution, and sale of cocaine products is illegal for non-medicinal / non-government sanctioned purposes in virtually all parts of the world. Internationally, it is regulated by the Single Convention on Narcotic Drugs, and the United Nations Convention Against Illicit Traffic in Narcotic Drugs and Psychotropic Substances. In the United States, the manufacture, importation, possession, and distribution of cocaine is additionally regulated by the 1970 Controlled Substances Act. Cocaine is generally treated as a 'hard drug', with severe penalties for possession and trafficking.
The United Nations Office of Drugs and Crime estimated that in 2009, the US cocaine market was $37 billion (and shrinking over the past ten years) and the West and Central European Cocaine market was US$ 37 billion (and increasing over the past ten years) (USODC 2011).
The coca leaves have been used unprocessed for thousands of years in South America for various religious, social, medicinal, and nutritional purposes, including in the Andean countries to make a herbal tea with mild stimulant effects. However, since the alkaloid cocaine is present in only trace amounts in the leaves, it does not cause the euphoric and psychoactive effects associated with use of the drug. The Coca-Cola company uses a cocaine-free coca extract. In the early days of the manufacture of Coca-Cola beverage, the formulation did contain some cocaine, although within a few years of its introduction it already was only trace amounts. Cocaine is available as a prescription for such purposes as external application to the skin to numb pain.
For the plant, cocaine is believed to serve as a naturally occurring insecticide, with the alkaloid exerting such effects at concentrations normally found in the leaves (Nathanson et. al. 1993). It has been observed that compared to other tropical plants, coca seems to be relatively pest free, with little observed damage to the leaves and rare observations of herbivorous insects on plants in the field (Nathanson et al. 1993).
Medical effectsData from The Lancet suggests cocaine is ranked both the 2nd most addictive and the 2nd most harmful of 20 popular recreational drugs.5
Cocaine acts in the brain on areas that acts to reward people with pleasure for behaviors important to survival individually and as a species, such as food, sex, and healthy pleasure (Marieb and Hoehn 2010; WebMD 2013a; Spanage and Weiss 1999). Involving the brain neurotransmitters in this area, it is a powerful nervous system stimulant (WHO 2004). Its effects can last from 15-30 minutes to an hour or two, depending on dosage and the route of administration (WHO 2007; WebMD 2013a). However, it can have serious negative effects on the heart, brain, lungs, and emotions, including the danger of sudden death (WebMD). It was ranked the second most addictive and harmful recreational drug (of 20 studied) by Nutt et al. (2007), exceeded only by heroin.
On the one hand, users of cocaine report a euphoria (feeling "high"), with an increased sense of alertness, feelings of well-being, competence, and "supremacy," enhanced energy and motor activity, and sexuality (WebMD 2013a).
On the other hand, some users report the high as also being accompanied with anxiety, irritability, paranoia, and restlessness, particularly during the comedown (WebMd 2013a). With excessive dosage or prolonged use, itching, tachycardia, tremors, convulsions, hallucinations, and paranoid delusions can result (WHO 2004; Zhao 2008). Overdoses cause hyperthermia (elevated body temperature) and a marked elevation of blood pressure. Cocaine constricts blood vessels, dilates the pupils, and increases heart rate and blood pressure.
In terms of the circulatory system, the increase of heart rate and blood pressure, while restricting arteries supplying blood, can result in a heart attack, even in youth without heart disease (WebMD 2013a). An abnormal heart rhythm called arrhythmia can be triggered. In terms of the brain, the constriction of blood vessels in the brain can cause strokes, even in young people without other stroke risk factors (WebMD 2013a). Cocaine can double both the risks of hemorrhagic and ischemic strokes (Jeffrey and Vega 2008) and increase the risk of other infarctions, such as myocardial infarction (Vasica and Tennant 2002). Cocaine can cause seizures. Sudden death has been known to occur, such as the case of Len Bias, considered by some as one of the greatest American college basketball athletes, who died two days after being drafted by the Boston Celtics because of a cardiac arrhythmia induced by use of cocaine.
The constriction of blood vessels supplying the gastrointestinal tract can lead to oxygen starvation and the development of ulcers or perforation of the stomach and intestines (WebMD 2013a). Cocaine use can also cause a wide array of kidney diseases and renal failure (Jaffe and Kimmel 2006; van der Woude 2000). Kidney failure can suddenly occur through a process known as rhabdomyolysis (WebMD 2013a).Side effects of chronic cocaine use
While sexual appetite may be increased, cocaine use can impair sexual function in men and women, including impaired ejaculation in men (WebMd 2013a).
In terms of the lungs and respiratory system, physical side effects from chronic smoking of cocaine include hemoptysis, bronchospasm, pruritus, fever, diffuse alveolar infiltrates without effusions, pulmonary and systemic eosinophilia, chest pain, lung trauma, sore throat, asthma, hoarse voice, dyspnea (shortness of breath), and an aching, flu-like syndrome. Permanent lung damage can result in some users.
The experience of insatiable hunger, aches, insomnia/oversleeping, lethargy, and persistent runny nose are often described as very unpleasant. Depression with suicidal ideation may develop in very heavy users.
Chronic intranasal usage can degrade the cartilage separating the nostrils (the septum nasi), leading eventually to its complete disappearance. Due to the absorption of the cocaine from cocaine hydrochloride, the remaining hydrochloride forms a dilute hydrochloric acid (Pagliaro and Pagliaro 2004).
Cocaine may also greatly increase this risk of developing rare autoimmune or connective tissue diseases such as lupus, Goodpasture's disease, vasculitis, glomerulonephritis, Stevens-Johnson syndrome and other diseases (Trozak and Gould 1984; Peces et al. 1999; Moore and Richardson 1998).
Cocaine often is a cause of involuntary tooth grinding, known as bruxism, which can deteriorate tooth enamel and lead to gingivitis (Baigent 2003). Additionally, stimulants like cocaine, methamphetamine, and even caffeine cause dehydration and dry mouth. Since saliva is an important mechanism in maintaining one's oral pH level, chronic stimulant abusers who do not hydrate sufficiently may experience demineralization of their teeth due to the pH of the tooth surface dropping too low (below 5.5).Cocaine hydrochloride
Chronic cocaine intake causes brain cells to adapt functionally to strong imbalances of transmitter levels in order to compensate extremes. Thus, receptors disappear from the cell surface or reappear on it, resulting more or less in an "off" or "working mode" respectively, or they change their susceptibility for binding partners (ligands)Template:Spaced ndashmechanisms called down-/upregulation. Marieb and Hoehn (2010) state that the blocking of dopamine uptake by repeated use of cocaine causes the reward system to effectively go dry, as the system releases less and less dopamine, and "the cocaine user becomes anxious and, in a very real sense, unable to experience pleasure without the drug." As the postsynaptic cells sprout new receptors to pick up the dopamine signals, a vicious cycle begins where cocaine "is needed to experience pleasure, but using it suppresses dopamine release even more" (Marieb and Hoehn 2010). A loss of vesicular monoamine transporters, neurofilament proteins, and other morphological changes appear to indicate a long term damage of dopamine neurons. All these effects contribute a rise in tolerance thus requiring a larger dosage to achieve the same effect (Lowinson et al. 2004). On the other hand, a study by D'Haenen et al. (2002) suggests cocaine abusers do not show normal age-related loss of striatal dopamine transporter (DAT) sites, suggesting cocaine has neuroprotective properties for dopamine neurons.
Cocaine can often cause reduced food intake, many chronic users lose their appetite and can experience severe malnutrition and significant weight loss.
The lack of normal amounts of serotonin and dopamine in the brain is the cause of the dysphoria and depression felt after the initial high.
Cocaine is extensively metabolized, primarily in the liver, with only about 1% excreted unchanged in the urine. The metabolism is dominated by hydrolytic ester cleavage, so the eliminated metabolites consist mostly of benzoylecgonine (BE), the major metabolite, and other significant metabolites in lesser amounts such as ecgonine methyl ester (EME) and ecgonine. Further minor metabolites of cocaine include norcocaine, p-hydroxycocaine, m-hydroxycocaine, p-hydroxybenzoylecgonine (pOHBE), and m-hydroxybenzoylecgonine (Kolbrich et al. 2006).
Cocaine has been held responsible for more visits to US emergency rooms than any other illegal drug (WebMD 2013a). The amount of sudden-deaths from cocaine also is not a rare phenomenon and in one study the cause of cocaine-related sudden death was found to cardiovascular in 62% of the cases, cerebrovascular in 14%, excited delirium in 14%, respiratory in 5%, and and metabolic in 5% (Nainggolan 2010). Drs. Richard Lange and L David Hillis of the University of Texas Health Science Center note "The notion that recreational cocaine use is 'safe' should be dispelled, since even small amounts may have catastrophic consequences" (Nainggolan 2010).
Cocaine dependence (or addiction) is psychological dependency on the regular use of cocaine. Cocaine dependency may result in physiological damage, lethargy, psychosis, depression, akathisia, and fatal overdose.
Physical withdrawal is not dangerous. Physiological changes caused by cocaine withdrawal include vivid and unpleasant dreams, insomnia or hypersomnia, increased appetite and psychomotor retardation or agitation (Lowinson et al. 2004).
Celebrities who died from cocaine-related causes
Among the notable cocaine-related deaths from cocaine have been basketball player Len Bias, baseball player Ken Caminiti, Quiet Riot singer Kevin DuBrow, The Who musician John Entwistle, actor Chris Farley (along with morphine), model Katy French, The Righteous Brothers musician Bobby Hatfield, the Pretenders musician James Honeyman-Scott, Blind Melon singer Shannon Hoon, actress/singer Whitney Houston (drowning under the influence), Grateful Dead musician Brent Mydland, actor River Phoenix (along with heroin), the Temptations musician David Ruffin, baseball player Rod Scurry, and musician Ike Turner.
Mechanism of actionComparison of the mechanism of cocaine versus that of amphetamines. Cocaine binds directly to the DAT1 transporter, inhibiting reuptake with more efficacy than amphetamines, which phosphorylate it causing internalization. Amphetamines, primarily releasing DAT (which cocaine does not do), only inhibite reuptake as a secondary, and much more minor, mode of action than cocaine.
The human brain appears to be hardwired with a reward system that provides pleasure when humans engage in various behaviors that are important to individual or species survival, such as romantic love, sex, and food. Humans ability to feel good involves brain neurotransmitters in this reward system, including dopamine released by neurons in areas known as the ventral tegmental area (VTA), the amygdala, and the nucleus accumbens (Marieb and Hoehn 2010; Spanage and Weiss 1999).
Various drugs of abuse can subvert this reward system, one of which is cocaine. These drugs can cause an addictive pleasure flush by flooding the brain with neurotransmitter-like chemicals or causing a build-up of neurotransmitters such as dopamine. However, this short-lived pleasure also comes with some serious side-effects, including the brain making and releasing less neurotransmitters on its own.
A major effect of cocaine on the central nervous system is the blockade of the dopamine reuptake transporter protein and thus blocking the reabsorption of dopamine. Dopamine transmitter released during neural signaling is normally recycled via the transporter protein; in other words, the transporter binds the transmitter and pumps it out of the synaptic cleft back into the presynaptic neuron, where it is taken up into storage vesicles. By binding tightly with the dopamine transporter, cocaine forms a complex that blocks the transporter's function. The dopamine transporter can no longer perform its reuptake function, and thus dopamine accumulates in the synaptic cleft. This results in an enhanced and prolonged postsynaptic effect of dopaminergic signaling at dopamine receptors on the receiving neuron. In other words, by the dopamine remaining in the synapse, the post-synaptic receptor cells are triggered again and again, allowing a prolonged pleasure flush.
When the dopamine uptake is blocked by repeated use of cocaine, the system reacts by releasing less and less dopamine and "the reward system effectively goes dry" (Marieb and Hoehn 2010). In other words, prolonged exposure to cocaine leads to homeostatic dysregulation of normal dopaminergic signaling via down-regulation of dopamine receptors and enhanced signal transduction. The decreased dopaminergic signaling after chronic cocaine use may contribute to depressive mood disorders and sensitize this important brain reward circuit to the reinforcing effects of cocaine (for example, enhanced dopaminergic signaling only when cocaine is self-administered). This sensitization contributes to the intractable nature of addiction and relapse.
Dopamine-rich brain regions such as the ventral tegmental area, nucleus accumbens, and prefrontal cortex are frequent targets of cocaine addiction research. Of particular interest is the pathway consisting of dopaminergic neurons originating in the ventral tegmental area that terminate in the nucleus accumbens. This projection may function as a "reward center," in that it seems to show activation in response to drugs of abuse like cocaine in addition to natural rewards like food or sex (Spanage and Weiss 1999). While the precise role of dopamine in the subjective experience of reward is highly controversial among neuroscientists, the release of dopamine in the nucleus accumbens is widely considered to be at least partially responsible for cocaine's rewarding effects. This hypothesis is largely based on laboratory data involving rats that are trained to self-administer cocaine. If dopamine antagonists are infused directly into the nucleus accumbens, well-trained rats self-administering cocaine will initially increase responding only to stop completely, thereby indicating that cocaine is no longer reinforcing (i.e. rewarding) the drug-seeking behavior.
Cocaine also effects seratonin (5-hydroxytryptamine, 5-HT), a monoamine neurotransmitter widely thought to be a contributor to feelings of well-being and happiness. Cocaine has been shown to inhibit the re-uptake of 5-HT3. The overabundance of 5-HT3 receptors in cocaine conditioned rats display this trait; however, the exact effect of 5-HT3 in this process is unclear (Carta et al. 2003). The 5-HT2 receptor (particularly the subtypes 5-HT2AR, 5-HT2BR and 5-HT2CR) show influence in the evocation of hyperactivity displayed in cocaine use (Filip et al. 2004).
Sigma receptors are affected by cocaine, as cocaine functions as a sigma ligand agonist (NIH/NIDA 2003). Sigma receptors are proteins found in the brain (and other parts of the body). The impact of cocaine on these sigma receptions may be part of the reason for cocaine's suppression of the immune system (NIH/NIDA 2003). Another specific receptor cocaine has been demonstrated to function on is NMDA (Lluch et al. 2005).
Cocaine also blocks sodium channels, thereby interfering with the propagation of action potentials; thus, like lignocaine and novocaine, it acts as a local anesthetic. It also functions on the binding sites to the dopamine and serotonin sodium dependent transport area as targets as separate mechanisms from its reuptake of those transporters; unique to its local anesthetic value, which makes it in a class of functionality different from both its own derived phenyltropanes analogues (which have that removed) and the amphetamine class of stimulants (which as well altogether lack that). In addition to this cocaine has some target binding to the site of the Kappa-opioid receptor as well. Cocaine also causes vasoconstriction, thus reducing bleeding during minor surgical procedures. The locomotor enhancing properties of cocaine may be attributable to its enhancement of dopaminergic transmission from the substantia nigra.
The impact of the neurotransmitter glutamate is also believed to be important to maintaining addiction, as glutamate signaling seems to cause permanent brain changes that lead to "compulsive drug-seeking behavior elicited by external cues" (Marieb and Hoehn 2010). Mice lacking a particular glutamate receptor are willing to try cocaine but do not become addicted (Marieb and Hoehn 2010). These combined dopamine and glutamate systems are so strong that years later, certain setting can create intense cravings for cocaine (Marieb and Hoehn 2010).
Because nicotine increases the levels of dopamine in the brain, many cocaine users find that consumption of tobacco products during cocaine use enhances the euphoria. This, however, may have undesirable consequences, such as uncontrollable chain smoking during cocaine use (even users who do not normally smoke cigarettes have been known to chain smoke when using cocaine), in addition to the detrimental health effects and the additional strain on the cardiovascular system caused by tobacco.
FormsA pile of cocaine hydrochlorideA piece of compressed cocaine powder
Cocaine in its purest form is a white, pearly product. Cocaine appearing in powder form is a salt, typically cocaine hydrochloride. Street market cocaine is frequently adulterated or “cut” with various powdery fillers to increase its weight; the substances most commonly used in this process are baking soda; sugars, such as lactose, dextrose, inositol, and mannitol; and local anesthetics, such as lidocaine or benzocaine, which mimic or add to cocaine's numbing effect on mucous membranes. Cocaine may also be "cut" with other stimulants such as methamphetamine. Adulterated cocaine is often a white, off-white or pinkish powder.
Salts. Cocaine is a weakly alkaline compound (an "alkaloid") and can therefore combine with acidic compounds to form various salts. The hydrochloride (HCl) salt of cocaine is by far the most commonly encountered, although the sulfate (-SO4) and the nitrate (-NO3) are occasionally seen. Different salts dissolve to a greater or lesser extent in various solvents. The hydrochloride salt is polar in character and is quite soluble in water. Powdered cocaine is commonly known as "coke" or "blow" and users can snort the powder (inhale through the nose) and into the bloodstream, or dissolve in water and inject directly into the bloodstream.
Basic. As the name implies, “freebase” or "free base" is the base form of cocaine, as opposed to the salt form. It is practically insoluble in water whereas hydrochloride salt is water soluble. (Most alkaloids are unstable in their pure form and exist in ionic salt form. The salts usually exhibit greater water solubility. Common counterions include chloride, bromide, acetate and oxalate. Because of the ubiquity of chloride salts, formed from the reaction of the amine with hydrochloric acid, these amine derivatives are known as the hydrochlorides.) Pure cocaine is prepared by neutralizing its compounding salt with an alkaline solution, which will precipitate to non-polar basic cocaine. It is further refined through aqueous-solvent Liquid-liquid extraction.
The term "freebasing" means converting an ionic form into free base. It can refer to deprotonating the hydrochloride salt form of cocaine to free base form. The free base is preferred for smoking. Smoking freebase cocaine has the additional effect of releasing methylecgonidine into the user's system due to the pyrolysis of the substance (a side effect which insufflating or injecting powder cocaine does not create). Some research suggests that smoking freebase cocaine can be even more cardiotoxic than other routes of administration (Scheidweiler et al. 2003; Yang et al. 2001; Fandiño et al. 2002).A woman smoking crack cocaine
Crack cocaine. Crack is a lower purity form of free-base cocaine that is usually produced by neutralization of cocaine hydrochloride with a solution of baking soda (sodium bicarbonate, NaHCO3) and water, producing a very hard/brittle, off-white-to-brown colored, amorphous material that contains sodium carbonate, entrapped water, and other by-products as the main impurities. The color of “crack” cocaine depends upon several factors including the origin of the cocaine used, the method of preparation-with ammonia or baking soda-and the presence of impurities, but will generally range from white to a yellowish cream to a light brown. Its texture will also depend on the adulterants, origin and processing of the powdered cocaine, and the method of converting the base. It ranges from a crumbly texture, sometimes extremely oily, to a hard, almost crystalline nature.
The "freebase" and "crack" forms of cocaine are usually administered by vaporization of the powdered substance into smoke, which is then inhaled. The origin of the name "crack" comes from the "crackling" sound (and hence the onomatopoeic moniker “crack”) that is produced when the cocaine and its impurities (i.e. water, sodium bicarbonate) are heated past the point of vaporization (Nelson 1998). Pure cocaine base/crack can be smoked because it vaporizes smoothly, with little or no decomposition at 98 °C (208 °F) (Miller et al. 2009), which is below the boiling point of water. In contrast, cocaine hydrochloride does not vaporize until heated to a much higher temperature (about 197°C), and considerable decomposition/burning occurs at these high temperatures. This effectively destroys some of the cocaine, and yields a sharp, acrid, and foul-tasting smoke.
Unprocessed coca leaf. Coca leaves have been used unprocessed for thousands of years in South America for various religious, social, medicinal, and nutritional purposes, including to control hunger and combat the impacts of high altitudes. Chewing of unadulterated coca leaves has been a tradition in the Andes for thousands of years and remains practiced by millions in South America today (Cortes 2013). Individuals may suck on wads of the leaves and keep them in their cheeks for hours at a time, often combining with chalk or ask to help dissolve the alkaloids into the saliva (Boucher 1991). Unprocessed coca leaves are also commonly used in the Andean countries to make a herbal tea with mild stimulant effects. However, since the alkaloid cocaine is present in only trace amounts in the leaves, it does not cause the euphoric and psychoactive effects associated with use of the drug. (See the article coca.)
Routes of administration
Cocaine powder can be inhaled through the nose or dissolved in water and injected into the bloodstream, as well as rubbed along the gum line. The freebase form can be smoked. Cocaine can also be applied to the skin as an topical anesthetic. Coca leaf can be chewed and brewed into a tea. Injecting and smoking leads to faster absorption into the bloodstream than snorting and a quicker, stronger high, but faster absorption also tends to mean a shorter duration of the high (5-10 minutes for smoking versus 15-30 minutes for snorting)(Botany Central 2013).A man sniffing cocaine
Insufflation ("snorting," "sniffing," or "blowing") involves breathing in the powder through the nose and in that manner absorption into the bloodstream. Prior to insufflation, cocaine powder is divided into very fine particles. Rolled up banknotes, hollowed-out pens, cut straws, and other such items are often used to insufflate cocaine. Upon snorti