Cocaine

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Summary sheet: Cocaine
Cocaine
Cocaine.svg
Chemical Nomenclature
Common names Cocaine, Coke, Coca, Crack, Blow, Girl, White, Snow, Nose Candy, Chari
Substitutive name Benzoylmethylecgonine
Systematic name Methyl (1R,2R,3S,5S)-3- (Benzoyloxy)-8-methyl-8-azabicyclo[3.2.1] octane-2-carboxylate
Class Membership
Psychoactive class Stimulant
Chemical class Tropane alkaloid
Routes of Administration

WARNING: Always start with lower doses due to differences between individual body weight, tolerance, metabolism, and personal sensitivity. See responsible use section.


Smoked
Dosage
Duration
Total 5 - 15 minutes
Onset 3 - 5 seconds
Come up 1 - 2 minutes
Peak 2 - 10 minutes
Offset 1 - 5 minutes




Insufflated
Dosage
Bioavailability 60[1]-80%[2]
Threshold 5 mg
Light 10 - 30 mg
Common 30 - 60 mg
Strong 60 - 90 mg
Heavy 90 mg +
Duration
Total 10 - 90 minutes
Onset 1 - 10 minutes
Come up 5 - 15 minutes
Peak 15 - 30 minutes
Offset 10 - 30 minutes






DISCLAIMER: PW's dosage information is gathered from users and resources for educational purposes only. It is not a recommendation and should be verified with other sources for accuracy.

Interactions
Mushrooms
LSD
DMT
Mescaline
2C-x
Cannabis
Ketamine
MXE
Amphetamines
MDMA
Caffeine
GHB
GBL
DOx
25x-NBOMe
2C-T-x
5-MeO-xxT
DXM
PCP
Alcohol
ΑMT
Opioids
Tramadol
MAOIs

Cocaine (also known as benzoylmethylecgonine, and informally as coke, cola, snow, blow, white, among others) is a classical stimulant substance of the tropane class. It is a naturally-occurring alkaloid extracted from the leaves of several coca plant species; namely Erythroxylum coca and Erythroxylum novogranatense.[3] The mechanism of action involves increasing levels of serotonin, dopamine, and norepinephrine in the brain.[citation needed]

Cocaine is one of the most widespread and highly controlled illicit substances in the world. According to a 2007 United Nations report, it was the second most widely used substance in the world, after cannabis.[4] It is considered a major so-called "street drug" and "drug of abuse", alongside heroin and methamphetamine.[citation needed]

Subjective effects include stimulation, increased blood pressure, appetite suppression, disinhibition, motivation enhancement, ego inflation, increased libido, and euphoria. Routes of administration include insufflation ("snorting" or "sniffing") and occasionally injection. Oral intake is rare but possible, and possesses a marketly longer duration; 60 minutes as opposed to 10 - 20 minutes when insufflated or 5 minutes smoked.[5][6]

The typical cocaine high is characterized by a rapid onset and a short duration, featuring a powerful euphoric "rush" that is followed by a marked comedown or "crash" — an experience that can promote compulsive redosing. Excessive use is reported to increase the risk of anxiety, paranoia, minor hallucinations, mania, and, in rare cases, psychosis.

It is known to have high abuse potential.[citation needed] Chronic use (i.e. high dose, repeat administration) is associated with escalating tolerance and physiological dependence, which can become severe if left untreated.

Additionally, some evidence suggests it poses unique cardiotoxic risks compared to other CNS stimulants, including the entire amphetamine class.[7] Even "regular" use has been linked to the development of permanent heart conditions and it also appears to cause sudden cardiac death in susceptible individuals (see this section for more).[8]

It is highly advised to use harm reduction practices if using this substance.

History and culture

History icon.svg

This History and culture section is a stub.

As a result, it may contain incomplete or wrong information. You can help by expanding it.

Cocaine is among one of the oldest recreational drugs with a 1000-year-old collection of drug paraphernalia being found in a rock shelter in Bolivia featuring traces of five psychoactive chemicals, including cocaine and components of ayahuasca.[9]

However, it's highly likely that it was consumed as powder cocaine and instead as coca leaves which can be chewed to create a less intense stimulant effect, subjectively comparable to that of caffeine. Coca leaves do not One of the earliest documentations of cocaine alkaloid isolation are 1855 [10] where German chemist Friedrich Gaedcke published a description in the journal "Archiv der Pharmazie", naming the alkaloid "erythoxyline." 5 years later, 1860, Albert Niemann describes the isolation of an alkaloid from coca and calls it cocaine. With this, the history of cocaine begins, splitting from coca leaf use. Western medicine was quick to exploit the many perceivable surface level benefits of the drug, and research publications within pharmaceutical communities began.

One such highlight of the papers published would be Sigmund Freud's collection of publications referred to as the "Cocaine Papers"[11] which can be considered partly responsible for the surge in popularity both when published and upon the rediscovery of the papers, around 1974. In these papers he correctly speculates the medical use of cocaine as an anaesthesia due to its numbing effects: "The capacity of cocaine [...], to anesthetize cutaneous and mucous membranes suggests a possible future use, especially in cases of local infections .... Some additional uses of cocaine based on this anesthetic property are likely to be developed in the near future." Furthermore to cocaine's numbing effects on the lips and mouth being observed by Freud.

Freud notes his studied effects on hunger, sleep, and fatigue. describing; "...exhilaration and lasting euphoria, which in no way differs from the normal euphoria of the healthy person .... You perceive an increase of selfcontrol and possess more vitality and capacity for work .... In other words, you are simply normal, and it is soon hard to believe that you are under the influence of any drug .... Long intensive mental or physical work is performed without any fatigue .... This result is enjoyed without any of the unpleasant after-effects that follow exhilaration brought about by alcohol. ... Absolutely no craving for the further use of cocaine appears after the first, or even repeated, taking of the drug; one feels rather a certain curious aversion to it." The final statement contradicting much of the modern reputation surrounding the cravings cocaine induces following use (compulsive redosing).

Freud also suggests that cocaine be used for morphine withdrawal treatment.

The first major article on the drug and part of the collection of "Cocaine Papers" would be Sigmund Freud's 1884 "Uber Coca." that outlines many major observed effects and offers a scientific breakdown of the potential uses of the drug. Freud observes:

"A few minutes after taking cocaine, one experiences a sudden exhilaration and feeling of lightness. One feels a certain furriness on the lips and palate, followed by a feeling of warmth in the same areas; if one now drinks cold water, it feels warm on the lips and cold in the throat. On other occasions the predominant feeling is a rather pleasant coolness in the mouth and throat" The euphoria or physical euphoria felt from the drug is referenced. The trademark mouth numbing can be read from the experience narration too.

According to a 2007 United Nations report, cocaine is the second most widely used illicit substance in the world, after cannabis.[4]

In terms of user rates (as of 2007), Spain is the country with the highest rate of cocaine usage (3.0% of adults in the previous year). Other countries where the usage rate meets or exceeds 1.5% are the United States (2.8%), England and Wales (2.4%), Canada (2.3%), Italy (2.1%), Bolivia (1.9%), Chile (1.8%), and Scotland (1.5%).[12]

Etymology

The name cocaine is derived from "coca" and the alkaloid suffix "-ine".[citation needed]

Common names

Cocaine has numerous common or street names, including coke, coca, cola, snow, ski, blow, nose candy, white, and girl. Spanish-influenced names include lello, yayo, yeyo, or yay. More regional to the UK are biff, charlie, lemos, flake among others.

Chemistry

Cocaine is a tropane alkaloid found in the leaves of the coca plant, Erythroxylum coca. It is most commonly consumed as the hydrochloride salt which is typically produced in clandestine laboratories in nations like Colombia. Cocaine decomposes when heated strongly so the freebase and hydrogen carbonate salts of cocaine, which have much lower boiling points compared to the hydrochloride salt, are typically used when the substance is to be vaporized and are known as cocaine base and "crack" respectively.

The chemical structure of cocaine consists of three parts; the hydrophilic methyl ester moiety and the lipophilic benzoyl ester moiety, which are located in place of the carboxylic acid and hydroxyl groups of ecgonine respectively. This structure allows for its rapid absorption through nasal membranes and blood-brain barrier.

The presence of the two ester groups makes cocaine relatively unstable in warm, humid environments and cocaine stored in an open container or with a high moisture content will lose apparent potency over time due to hydrolysis to methyl ecgonine or benzoylecgonine.

Pharmacology

The most extensively studied effect of cocaine on the central nervous system is the blockade of the dopamine transporter. This substance acts as a reuptake inhibitor and prevents dopamine from being recycled, causing excessive amounts to build up in the synapse, or junction between neurons. The result is an enhanced and prolonged post-synaptic effect of dopaminergic signaling. To a lesser extent, cocaine also exhibits functionally similar effects of reuptake inhibition upon the neurotransmitters of serotonin and noradrenaline.[13] It is this sudden flood of neurotransmitters that causes cocaine’s characteristic high.

The pharmacodynamics of cocaine involve the complex relationships of neurotransmitters (inhibiting monoamine uptake in rats with ratios of about: serotonin:dopamine = 2:3, serotonin:norepinephrine = 2:5). The most extensively studied effect of cocaine on the central nervous system is the blockade of the dopamine transporter protein. Dopamine transmitter released during neural signaling is normally recycled via the transporter; i.e., 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.

Cocaine binds tightly at the dopamine transporter forming 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. The increased concentration of dopamine in the synapse activates post-synaptic dopamine receptors, which makes the drug rewarding and promotes the compulsive use of cocaine.[14]

Subjective effects

Disclaimer: The effects listed below cite the Subjective Effect Index (SEI), an open research literature based on anecdotal user reports and the personal analyses of PsychonautWiki contributors. As a result, they should be viewed with a healthy degree of skepticism.

It is also worth noting that these effects will not necessarily occur in a predictable or reliable manner, although higher doses are more liable to induce the full spectrum of effects. Likewise, adverse effects become increasingly likely with higher doses and may include addiction, severe injury, or death ☠.

The cognitive effects of cocaine can be broken down into several components which progressively intensify proportional to dosage. The general headspace of cocaine is described as one of extreme mental stimulation, increased motivation, increased sex drive, and overwhelming euphoria and/or satisfaction. Subjective experience of the drug can heavily depend quality and purity however which can vary drastically.


Physical effects
Child.svg

Cognitive effects
User.svg

After effects
Aftereffects (3).svg

Experience reports

There are currently no anecdotal reports which describe the effects of this compound within our experience index. Additional experience reports can be found here:

Common usage

Cocaine is often adulterated when sold on black markets and this can significantly alter its effects on the body. Even when adulterants are pharmacologically inactive, their combination with the long-term perishability of cocaine due to moisture can lead to vastly differing apparent potencies between dosages of cocaine, and as such, it can be challenging to determine a "typical" recreational dose.

Pure cocaine is very potent and generates perceptible local anesthetic (numbing) effects from 1 mg and perceptible CNS stimulation from 5-7 mg; however, much higher doses tend to be used in recreational settings.

Forms

In order for cocaine (in plastic bag at bottom) to be converted to crack, several supplies are needed. Pictured here are baking soda (a commonly used base in making crack) a metal spoon, a tea light, and a cigarette lighter. The spoon is held over the heat source in order to "cook" the cocaine into crack.
  • Cocaine paste: A crude extract of the coca leaf, which contains 40% to 91% cocaine sulfate along with companion coca alkaloids and varying quantities of benzoic acid, methanol, and kerosene.
  • 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 quite soluble in water.
  • Freebase: “Freebase” is the base form of cocaine, as opposed to the salt form. It is practically insoluble in water whereas hydrochloride salt is water soluble. This prevents cocaine in its basic form from being usable for sublingual usage and insufflation. Freebase cocaine can be treated with ethers, isopropyl alcohol, and hydrochloric acid to turn it into the salt form. [18]
  • "Crack": "Crack" refers to a lower purity form of freebase 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.

    Smoking or vaporizing cocaine and inhaling it into the lungs produces an almost immediate "high" that can be very powerful and addictive. This initial buildup of stimulation is known as a "rush". While the stimulating effects may last for hours, the euphoric sensation is very brief, prompting the user to smoke more immediately.

  • Coca leaf infusions: Coca herbal infusion (also referred to as coca tea) is used in coca-leaf producing countries as much as any herbal medicinal infusion would be elsewhere in the world. The free and legal commercialization of dried coca leaves under the form of filtration bags to be used as "coca tea" has been actively promoted by the governments of Peru and Bolivia for many years as a drink having medicinal properties. The leaves are also very widely used by native populations for a variety of purposes including the treatment of altitude sickness.
  • Coca leaf chewing: Chewing the leaves (with lime) is also common in producing regions, which numbs the mouth and causes mild stimulation.

Toxicity and harm potential

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This toxicity and harm potential section is a stub.

As a result, it may contain incomplete or even dangerously wrong information! You can help by expanding upon or correcting it.
Note: Always conduct independent research and use harm reduction practices if using this substance.

Nasal septum perforation caused from cocaine abuse.
Radar plot showing relative physical harm, social harm, and dependence of cocaine[19]

Chronic cocaine use has been shown to lead to neurotoxicity in rodents and humans, being associated with high morbidity and mortality rates.[20] Its extended use or abuse does also cause short-term downregulation of neurotransmitters.

The most potentially harmful physical effects of cocaine appear to be not neurological but cardiovascular. Severe cardiac adverse events, particularly sudden cardiac death, become a serious risk at high doses due to cocaine's blocking effect on cardiac sodium channels.[8] Moreover, long-term cocaine use may result in cocaine-related cardiomyopathy.[21]

Regular cocaine insufflation, the most popular method of ingestion, can have extremely adverse effects on one's nostrils, nose, and nasal cavities. These include a loss of the sense of smell, nosebleeds, difficulty swallowing, hoarseness, or a chronically runny nose.

It is strongly recommended that one use harm reduction practices if using this substance.

Lethal dosage

Susceptible individuals have died from as little as 30 mg applied to mucous membranes, whereas addicts may tolerate up to 5 grams daily.[22]

Dependence and abuse potential

As with other stimulants, the chronic use of cocaine can be considered highly addictive with a high potential for abuse and is capable of causing psychological dependence among certain users. When addiction has developed, cravings and withdrawal effects may occur if a person suddenly stops their usage. Addiction is a serious risk with heavy recreational cocaine use but is unlikely to arise from typical medical use.

Tolerance to many of the effects of cocaine develops with prolonged and repeated use. This results in users having to administer increasingly large doses to achieve the same effects. After that, it takes about 3 - 7 days for the tolerance to be reduced to half and 1 - 2 weeks to be back at baseline (in the absence of further consumption).

Cocaine exhibits cross-tolerance with all dopaminergic stimulants, meaning that after the consumption of cocaine all stimulants will have a reduced effect.

Withdrawal symptoms

After taking cocaine on a regular basis, some users will become addicted. When the substance is discontinued immediately, the user will experience what has come to be known as a "crash" along with a number of other cocaine withdrawal symptoms including paranoia, depression, Decreased libido, anxiety, itching, mood swings, irritability, fatigue, insomnia, an intense craving for more cocaine, and, in some cases, nausea and vomiting.

These symptoms can last for weeks or, in some cases, months. Even after most withdrawal symptoms dissipate most users feel the need to continue using the drug; this feeling can last for years and may peak during times of stress. About 30-40% of cocaine addicts will turn to other substances such as medication and alcohol after giving up cocaine.[citation needed]

Psychosis

Main article: Stimulant psychosis

Cocaine has a similar potential to induce temporary psychosis[23] with more than half of cocaine abusers reporting at least some psychotic symptoms at some point.[24]

Typical symptoms of sufferers include paranoid delusions that they are being followed and that their drug use is being watched accompanied by hallucinations that support the delusional beliefs.[25] Delusional parasitosis with formication ("cocaine bugs") is also a fairly common symptom.[25]

Cocaine-induced psychosis shows sensitization toward the psychotic effects of the drug. This means that psychosis becomes more severe with repeated intermittent use.[26]

Dangerous interactions

Warning: Many psychoactive substances that are reasonably safe to use on their own can suddenly become dangerous and even life-threatening when combined with certain other substances. The following list provides some known dangerous interactions (although it is not guaranteed to include all of them).

Always conduct independent research (e.g. Google, DuckDuckGo, PubMed) to ensure that a combination of two or more substances is safe to consume. Some of the listed interactions have been sourced from TripSit.

  • Mushrooms - Stimulants increase anxiety levels and the risk of thought loops which can lead to negative experiences.
  • LSD - Stimulants increase anxiety levels and the risk of thought loops which can lead to negative experiences.
  • DMT - Stimulants increase anxiety levels and the risk of thought loops which can lead to negative experiences.
  • Mescaline - The focus and anxiety caused by stimulants is magnified by psychedelics and results in an increased risk of thought loops.
  • 2C-x - The anxiogenic and focusing effects of stimulants increase the chance of unpleasant thought loops. The combination is generally unnecessary because of the stimulating effects of psychedelics. A combination of the stimulating effects may be uncomfortable.
  • Cannabis - Stimulants increase anxiety levels and the risk of thought loops which can lead to negative experiences.
  • Ketamine - No unexpected interactions, though likely to increase blood pressure but not an issue with sensible doses. Moving around on high doses of this combination may be ill-advised due to the risk of physical injury.
  • MXE - Stimulants taken with MXE can lead to hypermanic states much more easily, especially if sleep is avoided.
  • Amphetamines - This combination of stimulants will increase strain on the heart. It is not generally worth it as cocaine has a mild blocking effect on dopamine releasers like amphetamine.
  • MDMA - Cocaine blocks some of the desirable effects of MDMA while increasing the risk of a heart attack.
  • Caffeine - Both stimulants, risk of tachycardia, hypertension, and in extreme cases heart failure.
  • GHB - Stimulants increase respiration rate allowing a higher dose of sedatives. If the stimulant wears off first then the sedative may overcome the patient and cause respiratory arrest. Likewise the G can wear off and leave a dangerous concentration of cocaine behind.
  • GBL - Stimulants increase respiration rate allowing a higher dose of sedatives. If the stimulant wears off first then the sedative may overcome the patient and cause respiratory arrest. Likewise the G can wear off and leave a dangerous concentration of cocaine behind.
  • DOx - The combined stimulating effects of the two can lead to an uncomfortable body-load, while the focusing effects of cocaine can easily lead to thought loops. Coming down from cocaine while the DOx is still active can be quite anxiogenic.
  • 25x-NBOMe - Cocaine and NBOMes both provide considerable stimulation. When combined they can result in severe vasoconstriction, tachycardia, hypertension, and in extreme cases heart failure.
  • 2C-T-x - Cocaine and 2C-T-x both provide considerable stimulation. When combined they can result in severe vasoconstriction, tachycardia, hypertension, and in extreme cases heart failure.
  • 5-MeO-xxT - The anxiogenic and focusing effects of stimulants increase the chance of unpleasant thought loops. The combination is generally unnecessary because of the stimulating effects of psychedelics.
  • DXM - Both substances raise heart rate, in extreme cases, panic attacks caused by these drugs have led to more serious heart issues.
  • PCP - This combination can easily lead to hypermanic states.
  • Alcohol - Drinking while using stimulants is risky because the sedative effects of alcohol are reduced. These are what the body uses to gauge “drunkenness”. This typically leads to excessive drinking with greatly reduced inhibitions, high risk of liver damage and increased dehydration. They will also allow you to drink past a point where you might normally pass out, increasing the risk. If you do decide to do this then you should set a limit of how much you will drink each hour and stick to it, bearing in mind that you will feel alcohol less. Cocaine is potentiated somewhat by alcohol because of the formation of cocaethylene.
  • ΑMT
  • Opioids - Stimulants increase respiration rate allowing a higher dose of opiates. If the stimulant wears off first then the opiate may overcome the patient and cause respiratory arrest.
  • Tramadol - Tramadol and stimulants both increase the risk of seizures.
  • MAOIs - This combination is poorly explored.

Legal status

  • Australia: Cocaine is a Schedule 8 (controlled) drug permitting some medical use, but is otherwise outlawed.[27] Personal quantities under 1.5 grams are decriminalized in the Australian Capital Territory (ACT) as of 28 October 2023.[28]
  • Austria: Cocaine is illegal to possess, produce and sell under the SMG (Suchtmittelgesetz Österreich).[29]
  • Bolivia: Limited cultivation of coca is legal in Bolivia, where chewing the leaves and drinking coca tea are considered cultural practices, in particular, in the mountainous regions. Processed cocaine is illegal.[citation needed]
  • Brazil: Personal use of cocaine is decriminalized although public consumption is considered a crime. It is illegal to cultivate, transport and sell.[30]
  • Canada: Cocaine is a Schedule I drug under the Controlled Drugs and Substances Act of Canada.[31]
  • Colombia: Even though possession of less than 1 gram of cocaine was legalized for personal use in 1994 by the supreme court,[32][33] sale and possession are now illegal under the new nationwide police code.[citation needed]
  • Germany: Cocaine was listed in the initial version of the Opiumgesetz (Opium Act) of December 10, 1929.[34] In accordance to the Narcotics Act reform of 1981, it is controlled under Anlage III BtMG (Narcotics Act, Schedule III).[35] It can only be prescribed on a narcotic prescription form. If owned illegaly, a quantity of up to 5 grams is regarded as a small amount.[36] In these cases, the prosecution can cease the proceeding.
  • Hong Kong: Use and possession of cocaine is illegal unless a license was issued by the Department of Health.[citation needed]
  • India: Use and possession of cocaine is illegal with a mandatory 10-year sentence.[citation needed]
  • Lithuania: Cocaine is a schedule I substance. Possession, production, and trade are not allowed.[37]
  • Mexico: As of August 25, 2009, the Mexican legislature officially legalized small doses of cocaine, heroin, marijuana, crystal meth, and ecstasy for personal use. No action will be taken for those carrying up to half a gram of cocaine.[38][39][40][41][42]
  • The Netherlands: Cocaine is considered an illegal hard drug. Possession, production, and trade are not allowed as stated in the Opium Law of 1928. Although technically illegal, possession of less than half a gram usually goes unpunished.[43][44]
  • New Zealand: Cocaine is a Class A drug. The coca leaf and preparations of cocaine containing no more than 0.1% cocaine base, in such a way that the cocaine cannot be recovered, are both classified as Class C.[citation needed]
  • Nigeria: It is a crime to be seen with cocaine.[citation needed]
  • Pakistan: Use and possession of cocaine is illegal.[citation needed]
  • Peru: Cultivation of coca plants is legal and coca leaves are sold openly on markets. Similarly to Bolivia, chewing leaves and drinking coca tea belong to cultural practices. Possession of up to 2 grams of cocaine or up to 5 grams of cocaine basic paste is legal for personal use in Peru per Article 299 of Peruvian Penal Code.[45] However, the reality of how police treats it might be very different.[46] An important part of Article 299 is that person may not possess two or more kinds of drugs at the same time -- this would make it a criminal offense.
  • Portugal: Personal use of cocaine is decriminalized. Drug abuse is dealt with by administrative and medical intervention. Trafficking is illegal.[47]
  • Saudi Arabia: Use and possession of cocaine is punishable by death.[citation needed]
  • Singapore: Possession of more than 30 grams of cocaine results in a mandatory death sentence, but can be issued by the Department of Health.[citation needed]
  • South Africa: Cocaine is a controlled substance.[citation needed]
  • Switzerland: Cocaine is a controlled substance specifically named under Verzeichnis A.[48]
  • United Kingdom: Cocaine is a Class A drug, controlled by the Misuse of Drugs Act 1971. However, medical use by doctors for controlling pain is permitted.[citation needed]
  • United States: Cocaine is classified as a Schedule II Narcotic under the Controlled Substances Act of the United States.[49]

See also

External links

References

  1. Barnett, G., Hawks, R., Resnick, R. (March 1981). "Cocaine pharmacokinetics in humans". Journal of Ethnopharmacology. 3 (2–3): 353–366. doi:10.1016/0378-8741(81)90063-5. ISSN 0378-8741. 
  2. Jeffcoat, A. R., Perez-Reyes, M., Hill, J. M., Sadler, B. M., Cook, C. E. (April 1989). "Cocaine disposition in humans after intravenous injection, nasal insufflation (snorting), or smoking". Drug Metabolism and Disposition: The Biological Fate of Chemicals. 17 (2): 153–159. ISSN 0090-9556. 
  3. Aggrawal, A. (1995). Narcotic Drugs. National Book Trust. ISBN 9788123713830. 
  4. 4.0 4.1 http://www.unodc.org/pdf/research/wdr07/WDR_2007.pdf
  5. Wilkinson, P., Van Dyke, C., Jatlow, P., Barash, P., Byck, R. (March 1980). "Intranasal and oral cocaine kinetics". Clinical Pharmacology and Therapeutics. 27 (3): 386–394. doi:10.1038/clpt.1980.52. ISSN 0009-9236. 
  6. Coe, M. A., Jufer Phipps, R. A., Cone, E. J., Walsh, S. L. (1 June 2018). "Bioavailability and Pharmacokinetics of Oral Cocaine in Humans". Journal of Analytical Toxicology. 42 (5): 285–292. doi:10.1093/jat/bky007. ISSN 0146-4760. 
  7. Nutt, D., King, L. A., Saulsbury, W., Blakemore, C. (24 March 2007). "Development of a rational scale to assess the harm of drugs of potential misuse". The Lancet. 369 (9566): 1047–1053. doi:10.1016/S0140-6736(07)60464-4. ISSN 0140-6736. 
  8. 8.0 8.1 O’Leary, M. E., Hancox, J. C. (28 January 2010). "Role of voltage-gated sodium, potassium and calcium channels in the development of cocaine-associated cardiac arrhythmias: Voltage-gated ion channels and cocaine-induced arrhythmia". British Journal of Clinical Pharmacology. 69 (5): 427–442. doi:10.1111/j.1365-2125.2010.03629.x. ISSN 0306-5251. 
  9. Miller, M. J., Albarracin-Jordan, J., Moore, C., Capriles, J. M. (4 June 2019). "Chemical evidence for the use of multiple psychotropic plants in a 1,000-year-old ritual bundle from South America". Proceedings of the National Academy of Sciences. 116 (23): 11207–11212. doi:10.1073/pnas.1902174116. ISSN 0027-8424. 
  10. Gaedcke, F. (1855). Ueber das Erythroxylin, dargestellt aus den Blättern des in Südamerika cultivirten Strauches Erythroxylon Coca Lam. https://doi.org/10.1002/ardp.18551320208
  11. https://libgen.top/ads3b7a7a253eb54644e9ca79039ca3e0f105V1622B
  12. http://www.unodc.org/pdf/research/wdr07/WDR_2007.pdf
  13. Rothman, R. B., Baumann, M. H., Dersch, C. M., Romero, D. V., Rice, K. C., Carroll, F. I., Partilla, J. S. (1 January 2001). <32::AID-SYN5>3.0.CO;2-3 "Amphetamine-type central nervous system stimulants release norepinephrine more potently than they release dopamine and serotonin". Synapse. 39 (1): 32–41. doi:10.1002/1098-2396(20010101)39:1<32::AID-SYN5>3.0.CO;2-3. ISSN 0887-4476. 
  14. Hummel, M., Unterwald, E. M. (April 2002). "D1 dopamine receptor: A putative neurochemical and behavioral link to cocaine action". Journal of Cellular Physiology. 191 (1): 17–27. doi:10.1002/jcp.10078. ISSN 0021-9541. 
  15. Morani, A. S., Panwar, V., Grasing, K. (March 2013). "Tactile Hallucinations with Repetitive Movements Following Low-Dose Cocaine: Implications for Cocaine Reinforcement and Sensitization: Case Report". The American Journal on Addictions. 22 (2): 181–182. doi:10.1111/j.1521-0391.2013.00336.x. ISSN 1055-0496. 
  16. Urban Dictionary: Coke Rage 
  17. https://one.nhtsa.gov/people/injury/research/job185drugs/cocain.htm
  18. Ask Erowid : ID 3151 : Can freebase cocaine be converted back to powder? 
  19. Nutt, D., King, L. A., Saulsbury, W., Blakemore, C. (24 March 2007). "Development of a rational scale to assess the harm of drugs of potential misuse". The Lancet. 369 (9566): 1047–1053. doi:10.1016/S0140-6736(07)60464-4. ISSN 0140-6736. 
  20. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7874143/
  21. "Cocaine-Related Cardiomyopathy: Overview, Cardiac Effects of Cocaine, Epidemiology". 16 October 2021. 
  22. Cocaine and crack drug profile 
  23. Brady, K. T., Lydiard, R. B., Malcolm, R., Ballenger, J. C. (December 1991). "Cocaine-induced psychosis". The Journal of Clinical Psychiatry. 52 (12): 509–512. ISSN 0160-6689. 
  24. Psychosis Among Substance Users 
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