Cocaine
Also called Coke, Coca, Crack, Blow, Girl, White, Snow, Nose Candy, Yayo, Perico, Gear, Chari
Dosage
Insufflated bands as drawn from PsychonautWiki's ranges below. The table is the source of truth.
When sources disagree, both rows are shown as published. Nothing is averaged or merged.
Insufflated
| Source | Threshold | Light | Common | Strong | Heavy |
|---|---|---|---|---|---|
| PsychonautWiki | 5 mg PW | 10–30 mg PW | 30–60 mg PW | 60–90 mg PW | 90 mg+ PW |
| TripSit | – | 20–50 mg TS | 50–100 mg TS | 100–150 mg TS | 150 mg+ TS |
Bioavailability: 60–80%[65]
Intravenous
Bioavailability: 100% PW
Oral
| Source | Threshold | Light | Common | Strong | Heavy |
|---|---|---|---|---|---|
| PsychonautWiki | 13 mg PW | 13–75 mg PW | 75–150 mg PW | 150–225 mg PW | 225 mg+ PW |
Smoked
| Source | Threshold | Light | Common | Strong | Heavy |
|---|---|---|---|---|---|
| PsychonautWiki | 2.5 mg PW | 5–15 mg PW | 15–30 mg PW | 30–45 mg PW | 45 mg+ PW |
Rapid onset. Depending on purity, dosage will vary TS
TripSit dose text
TripSit's factsheet also states its doses as text.
Insufflated Light: 20-50mg Common: 50-100mg Strong: 100-150mg Heavy: 150mg+ | NOTE: Depending on purity, dosage will vary TS
What dose are you on? (self-reported, unverified)
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Duration
Insufflated, drawn at the midpoint of each PsychonautWiki range.
| Route · source | Onset | Come-up | Peak | Offset | Total | After-effects |
|---|---|---|---|---|---|---|
| Insufflated · PsychonautWiki | 3–10 minutes PW | 5–12 minutes PW | 7.5–16 minutes PW | 10–25 minutes PW | 10–90 minutes PW | Psychological craving and compulsive redosing PW |
| Intravenous · PsychonautWiki | 3–5 seconds PW | 1–2 minutes PW | 2–10 minutes PW | 1–5 minutes PW | 5–15 minutes PW | – |
| Oral · PsychonautWiki | 30–40 minutes PW | 40–50 minutes PW | 60–180 minutes PW | 10–25 minutes PW | 120–240 minutes PW | – |
| Smoked · PsychonautWiki | 3–5 seconds PW | 1–2 minutes PW | 2–10 minutes PW | 1–5 minutes PW | 5–15 minutes PW | – |
TripSit factsheet
Mixing
Acute combinations: what happens when these are taken close together. Entries backed by a medical journal or agency are listed first.
Backed by medical journals
Other documented combinations
- Dangerous ΑMT PW
- Dangerous 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. PW
- Dangerous Tramadol - Tramadol and stimulants both increase the risk of seizures. PW
- Dangerous MAOIs - This combination is poorly explored. PW
- Unsafe 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. PW
- Unsafe 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. PW
- Unsafe 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. PW
- Unsafe 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. PW
- Unsafe DXM - Both substances raise heart rate, in extreme cases, panic attacks caused by these drugs have led to more serious heart issues. PW
- Unsafe PCP - This combination can easily lead to hypermanic states. PW
- Unsafe 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. PW
- Uncertain Mushrooms - Stimulants increase anxiety levels and the risk of thought loops which can lead to negative experiences. PW
- Uncertain LSD - Stimulants increase anxiety levels and the risk of thought loops which can lead to negative experiences. PW
- Uncertain DMT - Stimulants increase anxiety levels and the risk of thought loops which can lead to negative experiences. PW
- Uncertain Mescaline - The focus and anxiety caused by stimulants is magnified by psychedelics and results in an increased risk of thought loops. PW
- Uncertain 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. PW
- Uncertain Cannabis - Stimulants increase anxiety levels and the risk of thought loops which can lead to negative experiences. PW
- Uncertain 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. PW
- Uncertain MXE - Stimulants taken with MXE can lead to hypermanic states much more easily, especially if sleep is avoided. PW
- Uncertain 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. PW
- Uncertain MDMA - Cocaine blocks some of the desirable effects of MDMA while increasing the risk of a heart attack. PW
- Uncertain Caffeine - Both stimulants, risk of tachycardia, hypertension, and in extreme cases heart failure. PW
- Uncertain 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. PW
- Uncertain 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. PW
TripSit combination chart
TripSit rates each pairing. Only pairings with a number carry a citation from TripSit. See the whole chart, with TripSit's note for every pairing.
Caution
Low Risk & No Synergy
Risks and toxicity
Chronic cocaine use has been shown to lead to neurotoxicity, being associated with high morbidity and mortality rates. Its extended use or abuse does also cause short-term downregulation of neurotransmitters.[45]
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.
Moreover, long-term cocaine use may result in cocaine-related cardiomyopathy.[76]
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. PW
"Crack lung" is a term for various pulmonary diseases caused by smoking crack cocaine, and it can develop even after short-term or initial use. While crack lung is usually reversible with appropriate medical care and most people recover fully, in some cases—especially if complications arise—lasting lung damage may occur. PW
It is strongly recommended that one use harm reduction practices if using this substance. PW
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.[78] PW
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. PW
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). PW
Cocaine exhibits cross-tolerance with all dopaminergic stimulants, meaning that after the consumption of cocaine all stimulants will have a reduced effect. PW
Despite evidence of brain structure and function changes in chronic users, a 2018 systematic review found limited support for widespread cognitive impairment caused by long-term cocaine use, suggesting that common assumptions about pervasive cognitive deficits may be overstated.[79] PW
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. PW
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. PW⚠ PsychonautWiki itself has flagged this text: citation needed.
The misuse of cocaine has a high correlation with suicide. In those who use cocaine, the risk is greatest during the withdrawal phase.[80]
Psychosis
Cocaine has a similar potential to induce temporary psychosis with more than half of cocaine abusers reporting at least some psychotic symptoms at some point.[83]
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. Delusional parasitosis with formication ("cocaine bugs") is also a fairly common symptom.[85] PW
Cocaine-induced psychosis shows sensitization toward the psychotic effects of the drug. This means that psychosis becomes more severe with repeated intermittent use.[86] PW
Testing
Effects
Elevated moodIncrease in irritabilityhyper-inflated egoeuphoriastimulationraised heartratenumbing effects depending on ROAnausea (particularly at high doses) TS
Overview
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 two coca plant species; namely Erythroxylum coca and E. novogranatense that are native to South America. The mechanism of action involves increasing levels of serotonin, dopamine, and norepinephrine in the brain.[1] PW⚠ PsychonautWiki itself has flagged this text: citation needed.
A highly popular, short acting CNS stimulant that works by blocking the reuptake of dopamine, serotonin, and norepinephrine. It is known to increase euphoria, confidence, sex-drive, focus, body temperature, and heart rate. Cocaine can cause severe vasoconstriction and is known to be cardiotoxic and have a high potential for compulsive redosing and addiction.[2–22] TS
Cocaine is a central nervous system (CNS) stimulant and tropane alkaloid, derived primarily from the leaves of two coca species native to South America: Erythroxylum coca and E. novogranatense. The leaves are processed into cocaine paste, a crude mixture of coca alkaloids, from which cocaine base is isolated and then converted to cocaine hydrochloride. Although total synthesis is possible, it is complex and not used for production. Historically, cocaine was a standard topical medication used as a local anesthetic with intrinsic vasoconstrictor properties. However, its high abuse potential, adverse effects, and cost have limited its medical use and led to its replacement by alternative medicines.[23–31] WP
Street cocaine is commonly snorted, injected, or smoked as crack cocaine; its effects last up to 90 minutes depending on the route of administration. Pharmacologically, cocaine acts as a serotonin–norepinephrine–dopamine reuptake inhibitor (SNDRI), producing reinforcing effects such as euphoria, increased alertness, concentration, libido, and reduced fatigue and appetite.[26]
Cocaine has numerous adverse effects. Acute use can cause vasoconstriction, tachycardia, hypertension, hyperthermia, or seizures, while overdose may lead to stroke, heart attack, or sudden cardiac death. It also produces a spectrum of psychiatric symptoms, including agitation, paranoia, anxiety, irritability, psychosis, hallucinations, delusions, violence, and suicidal or homicidal thinking. Prenatal exposure poses risks to fetal development. Chronic use may result in cocaine dependence, withdrawal symptoms, neurotoxicity, and nasal damage, including cocaine-induced midline destructive lesions.[26]
Coca cultivation and initial processing occur primarily in Latin America, especially in the Andes regions of Bolivia, Peru, and Colombia. Cultivation is expanding into Central America, including Honduras, Guatemala, and Belize. Violence linked to the cocaine trade continues to affect Latin America and the Caribbean and is expanding into Western Europe, Asia, and Africa as transnational organized crime groups compete globally. Cocaine remains the world's fastest-growing illicit drug market.[27]
Coca chewing dates back at least 8,000 years in South America. Large-scale cultivation occurred in Taiwan and Java prior to World War II. The cocaine boom—a sharp rise in illegal production and trade—began in the late 1970s and peaked in the 1980s. Cocaine is regulated under international drug control conventions, though its legal status varies nationally: several countries have decriminalized possession of small quantities.[57–64] WP
History
History
Coca leaves have been used by indigenous South Americans for thousands of years, both as a stimulant and for medicinal purposes.[87] WP
When the Spanish arrived in South America, they initially banned coca but soon legalized and taxed it after seeing its importance to local labor. The active ingredient was first isolated in 1855 by Friedrich Gaedcke and later refined by Albert Niemann, who named it "cocaine". In the late 1800s, cocaine became popular in Western medicine as a local anesthetic and was widely used in various products, including drinks and remedies. and James Leonard Corning demonstrated peridural anesthesia. However, due to its toxic effects and potential for abuse, safer alternatives eventually replaced it in medical practice.[29]
Large-scale coca cultivation and cocaine production occurred in Asia, on Taiwan (then known as Formosa) and Java (today part of Indonesia) before World War II.[58]
Since the 1980s, the cocaine trade was dominated by centralized, hierarchical drug cartels such as Medellín and Cali, along with their successors and early FARC factions. By the early 2000s, this model fragmented into a diverse network of global trafficking links, allowing South American cocaine production to easily supply markets in Europe, Africa, Asia, and Oceania through various routes.[94] WP
Legal status
- Australia: Cocaine is a Schedule 8 (controlled) drug permitting some medical use, but is otherwise outlawed. Personal quantities under 1.5 grams are decriminalized in the Australian Capital Territory (ACT) as of 28 October 2023.[95]
[96] PW - Austria: Cocaine is illegal to possess, produce and sell under the SMG (Suchtmittelgesetz Österreich).[97] PW
- 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. PW⚠ PsychonautWiki itself has flagged this text: citation needed.
- Brazil: Personal use of cocaine is decriminalized although public consumption is considered a crime. It is illegal to cultivate, transport and sell.[98] PW
- Canada: Cocaine is a Schedule I drug under the Controlled Drugs and Substances Act of Canada.[99] PW
- Colombia: Even though possession of less than 1 gram of cocaine was legalized for personal use in 1994 by the supreme court, sale and possession are now illegal under the new nationwide police code.[61]
[62] PW⚠ PsychonautWiki itself has flagged this text: citation needed. - Germany: Cocaine was listed in the initial version of the Opiumgesetz (Opium Act) of December 10, 1929. In accordance to the Narcotics Act reform of 1981, it is controlled under Anlage III BtMG (Narcotics Act, Schedule III). 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. In these cases, the prosecution can cease the proceeding.[100]
[101] [102] PW - Hong Kong: Use and possession of cocaine is illegal unless a license was issued by the Department of Health. PW⚠ PsychonautWiki itself has flagged this text: citation needed.
- India: Use and possession of cocaine is illegal with a mandatory 10-year sentence. PW⚠ PsychonautWiki itself has flagged this text: citation needed.
- Lithuania: Cocaine is a schedule I substance. Possession, production, and trade are not allowed.[103] PW
- 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.[104–108] PW
- 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.[109]
[110] PW - 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. PW⚠ PsychonautWiki itself has flagged this text: citation needed.
- Nigeria: It is a crime to be seen with cocaine. PW⚠ PsychonautWiki itself has flagged this text: citation needed.
- Pakistan: Use and possession of cocaine is illegal. PW⚠ PsychonautWiki itself has flagged this text: 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. However, the reality of how police treats it might be very different. 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.[111]
[112] PW - Poland: Cocaine is listed in "Wykaz środków odurzających i substancji psychotropowych" group "I-N". Use and possession of cocaine is illegal.[113] PW
- Portugal: Personal use of cocaine is decriminalized. Drug abuse is dealt with by administrative and medical intervention. Trafficking is illegal.[114] PW
- Saudi Arabia: Use and possession of cocaine is punishable by death. PW⚠ PsychonautWiki itself has flagged this text: 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. PW⚠ PsychonautWiki itself has flagged this text: citation needed.
- South Africa: Cocaine is a controlled substance. PW⚠ PsychonautWiki itself has flagged this text: citation needed.
- Switzerland: Cocaine is a controlled substance specifically named under Verzeichnis A.[115] PW
- 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. PW⚠ PsychonautWiki itself has flagged this text: citation needed.
- United States: Cocaine is classified as a Schedule II Narcotic under the Controlled Substances Act of the United States.[116] PW
Society and culture
Both the pharmaceutical supply chain and the illicit supply chain obtain cocaine from coca cultivated in Latin America, but they operate under very different controls and oversight. In Peru, for example, legal coca cultivation is monopolized by the state company National Coca Company (ENACO), yet approximately 90% of coca leaves produced in the country are diverted to illegal actors for cocaine manufacturing. As a result, these illicit coca crops are a primary target of ongoing government-led coca eradication efforts.[117]
Cocaine is prohibited in competition for athletes by the World Anti-Doping Agency (WADA), which lists it as a stimulant on its International Standard for the Prohibited List.[119] WP
Slang names
Cocaine is sometimes referred to on the street as blow, coca, coke, crank, flake, snow, or soda cot. Slang terms for free base cocaine include crack or rock.[120] WP
Levamisole syndromes
Levamisole is one of the most common cutting agents used to lace illicit cocaine, with studies showing that between 2009 and 2016, 50–70% of all cocaine specimens worldwide contained levamisole, reflecting similar high rates of contamination across North America and Europe. Before trafficking to the United States, the cocaine is frequently adulterated with levamisole. By October 2017, this figure had risen further, with the US Drug Enforcement Administration (DEA) reporting that 87% of seized and analyzed cocaine bricks in the United States contained levamisole, making it the most common adulterant in cocaine at that time.[121]
In the body, levamisole is converted into aminorex, a substance with amphetamine-like stimulant effects and a long duration of action. Levamisole-adulterated cocaine is associated with cocaine/levamisole-associated autoimmune syndrome (CLAAS) and cocaine- and levamisole-induced vasculitis (CLIV). Reagent testing kits can be used to detect the presence of cocaine and levamisole.[124]
Legal status
The production, distribution, and sale of cocaine products is restricted (and illegal in most contexts) in most countries as 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 are additionally regulated by the 1970 Controlled Substances Act. WP
Some countries, such as Bolivia, Colombia, and Peru, permit the cultivation of coca leaf for traditional consumption by the local indigenous population, but nevertheless, prohibit the production, sale, and consumption of cocaine. The provisions as to how much a coca farmer can yield annually is protected by laws such as the Bolivian Cato accord. In addition, some parts of Europe, the United States, and Australia allow processed cocaine for medicinal uses only.[127]
Australia
Cocaine is a Schedule 8 controlled drug in Australia under the Poisons Standard. It is the second most popular illicit recreational drug in Australia behind cannabis.[129]
In Western Australia under the Misuse of Drugs Act 1981, 4.0g of cocaine is the amount of prohibited drugs determining a court of trial, 2.0g is the amount of cocaine required for the presumption of intention to sell or supply, and 28.0g is the amount of cocaine required for purposes of drug trafficking.[131] WP
United states
The US federal government instituted a national drug labelling requirement for cocaine and cocaine-containing products through the Pure Food and Drug Act of 1906. The next important federal regulation was the Harrison Narcotics Tax Act of 1914. While this act is often seen as the start of prohibition, the act itself was not actually a prohibition on cocaine, but instead it set up a regulatory and licensing regime. The Harrison Act did not recognize addiction as a treatable condition and therefore the therapeutic use of cocaine, heroin, or morphine to such individuals was outlawed – leading a 1915 editorial in the journal American Medicine to remark that the addict "is denied the medical care he urgently needs, open, above-board sources from which he formerly obtained his drug supply are closed to him, and he is driven to the underworld where he can get his drug, but of course, surreptitiously and in violation of the law." The Harrison Act left manufacturers of cocaine untouched so long as they met certain purity and labeling standards. Despite that cocaine was typically illegal to sell and legal outlets were rarer, the quantities of legal cocaine produced declined very little. Legal cocaine quantities did not decrease until the Jones–Miller Act of 1922 put serious restrictions on cocaine manufactures.[132]
Before the early 1900s, newspapers primarily portrayed addiction (rather than violence or crime) as the main problem caused by cocaine use, and depicted cocaine users as upper or middle class White people. In 1914, The New York Times published an article titled "Negro Cocaine 'Fiends' Are a New Southern Menace," portraying Black people who used cocaine as dangerous and able to withstand wounds that would normally be fatal. The Anti-Drug Abuse Act of 1986 mandated the same prison sentences for distributing 500 grams of powdered cocaine and just 5 grams of crack cocaine. In the National Survey on Drug Use and Health, white respondents reported a higher rate of powdered cocaine use, and Black respondents reported a higher rate of crack cocaine use.[135]
Prevalence and trends
Cocaine production, seizures, and use all reached record levels in 2023, making it the world's fastest-growing illicit drug market. Seizures rose by 68% from 2019 to 2023, while the number of users increased from 17 million in 2013 to 25 million in 2023, according to the UNODC World Drug Report 2025. Concurrently, record levels of cocaine production have enabled traffickers to enter new markets across Asia and Africa, reflecting the expanding global reach of cocaine trafficking.[53]
The U.S. is disproportionately the world's largest consumer of cocaine, while South America, collectively as a continent, ranks third in terms of consumer market size. Europe ranks cocaine as the second most commonly used illicit drug.[27]
Cocaine is among the most widely consumed recreational stimulants worldwide.[36] WP
Impact on impoverished communities
In countries where cocaine is illicitly produced, an intermediate product known as cocaine paste—often referred to as "poor man's cocaine"—is frequently smoked in impoverished communities. This substance is favored in these areas primarily because it is inexpensive and more accessible than refined cocaine. However, the use of cocaine paste poses severe health risks. During its production, various toxic chemicals are used to extract coca alkaloids from the coca leaves. Many of these hazardous substances, such as solvents and acids, remain in the paste after processing. When the paste is smoked, individuals are exposed not only to the addictive effects of the drug itself but also to the dangerous residual chemicals, which can cause significant harm to the lungs, nervous system, and overall health. This combination of affordability, accessibility, and toxicity makes cocaine paste particularly damaging to vulnerable populations in cocaine-producing regions.[33]
Environmental impact
Most of the world's cocaine is produced in South America, particularly in the Andean region. The environmental destruction caused by the production of cocaine has been well documented, with reports made the UN and other government bodies. Due to the illegal nature of coca production, farmers make little effort in soil conservation and sustainability practices as seen in the high mobility and short life of coca plots in Colombia.[143]
One of the major implications of cocaine production is deforestation as large areas of forest are cleared for coca cultivation. The UNODC approximated that 97,622 hectares of primary forest were cleared for coca cultivation during 2001–2004 in the Andean region. This further causes habitat destruction, especially in biodiversity hotspots, areas rich in a variety of species. Such areas are chosen for coca cultivation due to their remote locations, minimising chances of detection. Deforestation impacts soil erosion which further inhibits the survival of native species.[143]
The use of pesticides can also severely affect the environment. Farmers are able to use unregulated and highly toxic pesticides due to the clandestine nature of drug production. The use of such pesticides can have both direct and indirect effects on the ecosystem. Where lethal levels of exposure directly cause the death of fauna, which is further carried up the food chain where secondary feeders who consume the poisoned animals are also impacted. Furthermore, non-lethal levels of exposure can also cause weaker immune system development and neurological issues, further increasing mortality rates.[145] WP
Impact of illicit cocaine trade
Cocaine is extremely expensive on the black market, with prices rising sharply at each distribution level—often more than its weight in gold.[146] WP
Latin america
Drug war policies in Latin America and the Caribbean have led to more violence, higher incarceration rates, health crises, and deeper poverty, while undermining trust in institutions and worsening inequality. There is increasing support for shifting toward drug policies that focus on sustainable development and human rights instead of punitive measures.[54] WP
West africa
Cocaine trafficking in West Africa has become closely linked with the activities of several terrorist organizations.[147]
Impact of coca eradication
In December 2000, Dutch journalist Marjon van Royen found that "because the chemical is sprayed in Colombia from planes on inhabited areas, there have been consistent health complaints [in humans]. Burning eyes, dizziness and respiratory problems being most frequently reported." In some areas, 80 percent of the children of the indigenous community fell sick with skin rashes, fever, diarrhoea and eye infections. Because the glyphosate is sprayed from the air, there is a much higher chance of human error when spraying suspected illegal coca plantations. In many cases the wrong fields are sprayed, resulting in not only a total loss of the farmer's crop- but the loss of that field altogether as nothing will grow where the herbicide has been sprayed. Though official documentation of the health effects of glyphosate spraying in Colombia are virtually non-existent, neighbouring Ecuador has conducted studies to determine the cause of mysterious illnesses amongst people living along the border of Colombia and has since demanded that no aerial sprayings occur within 10 km of the border because of the damages caused to the people, animals and environment in that area. In 2015, Colombia announced a ban on using glyphosate in these programs due to concerns about human toxicity of the chemical.[150]
Impact of interdiction
The Consolidated Counterdrug Database (CCDB) is a U.S. government dataset created in the 1990s that compiles vetted data on cocaine trafficking and seizures in the Western Hemisphere "transit zone," involving 26 U.S. agencies and 20 foreign partners. It provides a highly reliable, conservative record of cocaine movements and interdiction efforts, revealing that despite large seizures, interdiction captures only a small fraction of trafficking events and has minimal impact on U.S. cocaine prices. The CCDB challenges optimistic views of drug interdiction effectiveness and underscores the need for new policy approaches, yet remains underutilized in research despite being unclassified.[153] WP
Etymology
The word cocaine derives from French Cocaïne, from Spanish coca, ultimately from Quechua kúka.[154] WP
Pharmacology
Pharmacokinetics
The extent of absorption of cocaine into the circulatory system after nasal insufflation is similar to that after oral ingestion. The rate of absorption after nasal insufflation is limited by cocaine-induced vasoconstriction of capillaries in the nasal mucosa. Onset of absorption after oral ingestion is delayed because cocaine is a weak base with a pKa of 8.6, and is thus in an ionized form that is poorly absorbed from the gastric acid and easily absorbed from the alkaline duodenum. The rate and extent of absorption from inhalation of cocaine is similar or greater than with intravenous injection, as inhalation provides access directly to the capillary bed. The delay in absorption after oral ingestion may account for the popular belief that cocaine bioavailability from the stomach is lower than after insufflation. Compared with ingestion, the faster absorption of insufflated cocaine results in quicker attainment of maximum drug effects. Snorting cocaine produces maximum physiological effects within 40 minutes and maximum psychotropic effects within 20 minutes. Physiological and psychotropic effects from nasally insufflated cocaine are sustained for approximately 40–60 minutes after the peak effects are attained.[65]
Cocaine crosses the blood–brain barrier via both a proton-coupled organic cation antiporter and (to a lesser extent) via passive diffusion across cell membranes. As of September 2022, the gene or genes encoding the human proton-organic cation antiporter had not been identified.[156–159] WP
Cocaine has a short elimination half-life of 0.7–1.5 hours and is extensively metabolized by plasma esterases and also by liver cholinesterases, 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 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.[32]
Depending on liver and kidney functions, cocaine metabolites are detectable in urine between three and eight days. Generally speaking benzoylecgonine is eliminated from someone's urine between three and five days. In urine from heavy cocaine users, benzoylecgonine can be detected within four hours after intake and in concentrations greater than 150 ng/mL for up to eight days later.[162] WP
Body fluids
Cocaine and its major metabolites may be quantified in blood, plasma, or urine to monitor for use, confirm a diagnosis of poisoning, or assist in the forensic investigation of a traffic or other criminal violation or sudden death. Most commercial cocaine immunoassay screening tests cross-react appreciably with the major cocaine metabolites, but chromatographic techniques can easily distinguish and separately measure each of these substances. When interpreting the results of a test, it is important to consider the cocaine usage history of the individual, since a chronic user can develop tolerance to doses that would incapacitate a cocaine-naive individual, and the chronic user often has high baseline values of the metabolites in his system. Cautious interpretation of testing results may allow a distinction between passive or active usage, and between smoking versus other routes of administration.[163] WP
Hair
Hair analysis can detect cocaine metabolites in regular users until after the sections of hair grown during the period of cocaine use are cut or fall out.[164] WP
Pharmacodynamics
Cocaine acts as a serotonin–norepinephrine–dopamine reuptake inhibitor (SNDRI). Cocaine increases levels of serotonin, norepinephrine, and dopamine in the synaptic cleft, leading to heightened post-synaptic activation, with dopamine contributing to euphoria and arousal, and the other monoamines enhancing additional effects.[34]
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 neurotransmitter 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.[26]
Cocaine affects certain serotonin (5-HT) receptors; in particular, it has been shown to antagonize the 5-HT₃ receptor, which is a ligand-gated ion channel. An overabundance of 5-HT₃ receptors is reported in cocaine-conditioned rats, though 5-HT₃'s role is unclear. The 5-HT₂ receptor (particularly the subtypes 5-HT2A, 5-HT2B and 5-HT2C) are involved in the locomotor-activating effects of cocaine.[170]
Cocaine has been demonstrated to bind as to directly stabilize the DAT transporter on the open outward-facing conformation. Further, cocaine binds in such a way as to inhibit a hydrogen bond innate to DAT. Cocaine's binding properties are such that it attaches so this hydrogen bond will not form and is blocked from formation due to the tightly locked orientation of the cocaine molecule. Research studies have suggested that the affinity for the transporter is not what is involved in the habituation of the substance so much as the conformation and binding properties to where and how on the transporter the molecule binds.[172] WP
Conflicting findings have challenged the widely accepted view that cocaine functions solely as a reuptake inhibitor. To induce euphoria an intravenous dose of 0.3-0.6 mg/kg of cocaine is required, which blocks 66-70% of DAT in the brain. Re-administering cocaine beyond this threshold does not significantly increase DAT occupancy but still results in an increase of euphoria which cannot be explained by reuptake inhibition alone. This discrepancy is not shared with other dopamine reuptake inhibitors like bupropion, sibutramine, mazindol or tesofensine, which have similar or higher potencies than cocaine as dopamine reuptake inhibitors. Furthermore, a similar response-occupancy discrepancy has been observed with methylphenidate, which also stabilizes the dopamine transporter in an open outward-facing conformation. These findings have evoked a hypothesis that cocaine may also function as a so-called "DAT inverse agonist" or "negative allosteric modifier of DAT" resulting in dopamine transporter reversal, and subsequent dopamine release into the synaptic cleft from the axon terminal in a manner similar to but distinct from amphetamines.[173–176] WP
Sigma receptors are affected by cocaine, as cocaine functions as a sigma ligand agonist. Further specific receptors it has been demonstrated to function on are NMDA and the D₁ dopamine receptor.[177]
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. In addition to this, cocaine has some target binding to the site of the κ-opioid receptor. Cocaine also causes vasoconstriction, thus reducing bleeding during minor surgical procedures. Recent research points to an important role of circadian mechanisms and clock genes in behavioral actions of cocaine.[76]
Cocaine is known to suppress hunger and appetite by increasing co-localization of sigma σ₁R receptors and ghrelin GHS-R1a cell surface receptors, thereby increasing ghrelin-mediated signaling of satiety and possibly via other effects on appetitive hormones.[183]
Cocaine effects, further, are shown to be potentiated for the user when used in conjunction with new surroundings and stimuli, and otherwise novel environs.[185] WP
Chemistry
- Formula
- C17H21NO4 PC
- CAS number
- 50-36-2 PC
- Molar mass (g/mol)
- 303.35 PC
- IUPAC name (computed by PubChem)
- methyl (1R,
2R, PC3S, 5S) - 3- benzoyloxy- 8- methyl- 8- azabicyclo[3.2.1] octane- 2- carboxylate - SMILES
- CN1[C@H]
2CC[C@@H] PC1[C@H] ([C@H] (C2) OC(=O) C3=CC=CC=C3) C(=O) OC - InChIKey
- ZPUCINDJVBIVPJ-
LJISPDSOSA- PCN - PubChem CID
- 446220
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References
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