Heroin

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For other uses, see Heroin (disambiguation).
Heroin chemical structure
Heroin
Systematic (IUPAC) name
(5α,6α)-7,8-didehydro-4,5-epoxy-
17-methylmorphinan-3,6-diol diacetate (ester)
Identifiers
CAS number 561-27-3
ATC code N02AA09
PubChem 3592
Chemical data
Formula C21H23NO5 
Mol. weight 369.41
Pharmacokinetic data
Bioavailability <35%
Protein binding 0% (morphine metabolite 35%)
Metabolism hepatic
Half life 2-3 minutes
Excretion 90% renal as glucuronides, rest biliary
Therapeutic considerations
Pregnancy cat.

?

Legal status

 and  Substances Act">Schedule I(CA) Class A(UK) Schedule I(US)

Dependence Liability Extremely High
Routes Inhalation, Transmucosal, Intravenous, Oral, Intranasal, Rectal, Intramuscular

Heroin, also known as diamorphine (BAN) or  diacetylmorphine (INN), is  a semi-synthetic opioid. it  is the 3,6-diacetyl derivative of morphine (hence diacetylmorphine) and  is synthesised from it  by acetylation. The white crystalline form is  commonly the hydrochloride salt, diacetylmorphine hydrochloride. it  mimics endorphins and  thus causes a high sense of well-being when entered into the bloodstream (usually through injection). For this reason it  can be used both as a pain-killer and  a recreational drug. it  has a high addiction potential, and  frequent administration may cause a rapid development of tolerance by the user, especially when compared to other substances, though occasional use may not lead to symptoms of withdrawal.[1][2] Internationally, heroin is  controlled under Schedules I and  IV of the Single Convention on Narcotic Drugs.[3] it  is illegal to manufacture, possess, or  sell heroin in the United States; however, under the name diamorphine, heroin is  a legal prescription drug in the United Kingdom. Popular street names for heroin include gear, diesel, smack, B, skag, Bobby, black tar, horse, junk, jenny, brown, brown sugar, dark, Dope and  H.

Contents

[edit] History

Bayer Heroin (TM)
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Bayer Heroin (TM)
Bayer Heroin bottle.
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Bayer Heroin bottle.

The opium poppy was cultivated in lower Mesopotamia as long ago as 3400 BC.[4] Heroin was first synthesized in 1874 by C.R. Alder Wright, a British chemist working at St. Mary's Hospital Medical School, London. He had been experimenting with combining morphine with various acids. He boiled anhydrous morphine alkaloid with acetic anhydride over a stove for several hours and  produced a more  potent, acetylated form of morphine, now called diacetylmorphine. The compound was sent to F.M. Pierce of Owens College, Manchester, for analysis, who reported the following to Wright:

Doses … were subcutaneously injected into young dogs and  rabbits … with the following general results … great prostration, fear, and  sleepiness speedily following the administration, the eyes being sensitive, and  pupils dilated, considerable salivation being produced in dogs, and  slight tendency to vomiting in some cases, but no actual emesis. Respiration was at first quickened, but subsequently reduced, and  the heart's action was diminished, and  rendered irregular. Marked want of coordinating power over the muscular movements, and  loss of power in the pelvis and  hind limbs, together with a diminution of temperature in the rectum of about 4°(rectal failure).[5]

Felix Hoffmann, of Bayer in Elberfeld, Germany, created heroin as a medicine 11 days after inventing aspirin. Afraid of the possible side effects of aspirin, Bayer registered heroin (probably from heroisch, German for heroic, chosen because in field studies people using the medicine felt "heroic") as a trademark.

From 1898 through to 1910 it  was marketed as a non-addictive morphine substitute and  cough medicine for children. Bayer marketed heroin as a cure for morphine addiction before it  was discovered that heroin is  converted to morphine in the brain. The company felt somewhat embarrassed by this new finding and  it became a historical blunder for Bayer.[6] As with aspirin, Bayer lost some of its trademark rights to heroin following World War I.

In the United States in 1914 the Harrison Narcotics Tax Act was passed to control the sale and  distribution of heroin. The law still allowed heroin to be prescribed and  sold for medical purposes. In particular, addicts could often still be legally supplied with heroin. In 1924, the United States Congress passed additional legislation banning the sale, importation or  manufacture of heroin in the United States.

[ and  effects">edit] Usage and  effects

Indicated for:
  • Relief of extreme pain

Recreational uses:

Other uses:

Contraindications:
Side effects:

Cardiovascular & Respiratory:

Eyes, Ears, nose, and  mouth:

Gastrointestinal:

Urinary System:

Musculoskeletal:

Neurological:

Psychological:

Skin:

  • Itching
  • Flushing/Rash
Diamorphine ampoules for medicinal use
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Diamorphine ampoules for medicinal use

In the United Kingdom, heroin is  available on prescription, though it  is a restricted Class A drug. According to the British National Formulary (BNF) edition 50, diamorphine hydrochloride may be used in the treatment of acute pain, myocardial infarction, acute pulmonary edema, and  chronic pain. The treatment of chronic non-malignant pain must be supervised by a specialist. The BNF notes that all opioid analgesics cause dependence and  tolerance but that this is  "no deterrent in the control of pain in terminal illness". When used in the palliative care of cancer patients, heroin is  often injected using a syringe driver. In comparison to morphine, it  may cause less  nausea, hypotension, but more  sedation and  euphoria and  can be dissolved in a smaller quantity of liquid.

Heroin is  also widely (and usually illegally) used as a powerful and  addictive drug that produces intense euphoria, which often disappears with increasing tolerance. it  is thought that heroin's popularity with recreational users, compared to morphine or  other opiates, comes from its somewhat different perceived effects.[7] This in turn comes from its high lipid solubility provided by the two acetyl groups, resulting in a very rapid penetration of the blood-brain barrier after use. Heroin can be taken or  administered in a number of ways, including snorting and  injection. it  may also be smoked by inhaling the vapors produced when heated from below (known as "chasing the dragon").

Many users in the United Kingdom dissolve the drug together with crack cocaine in a so-called "speedball" or  "snowball", which is  injected intravenously. This causes an  even more  intense rush but is  more dangerous than heroin alone because the mixture of short-acting stimulant with longer-acting depressant increases the risk of overdosing on one or  both drugs. Cocaine is  an irritant to all bodily tissues causing eventual necrosis at any site with which it  is in frequent contact. Because crack must be acidified with extra citric acid or  vitamin C to allow it  to dissolve in water, worse vein damage may result than from injecting heroin alone.

Once in the brain, heroin is  rapidly metabolized into morphine by removal of the acetyl groups. it  is the morphine molecule that then binds with opioid receptors and  produces the subjective effects of the heroin high. Heroin is  therefore a prodrug.

The onset of heroin's effects is  dependent on the method of administration. Orally, the heroin is  totally metabolized in vivo into morphine before crossing the blood-brain barrier, so the effects are  the same as morphine when taken by mouth. Snorting heroin results in onset within 10 to 15 minutes. Smoking heroin results in an  almost immediate, though mild effect which strengthens the longer it  is used in that particular session. Intravenous injection results in rush and  euphoria within 7 to 8 seconds, while intramuscular injection takes longer, having an  effect within 5 to 8 minutes.

Heroin is  a μ-opioid (mu-opioid) agonist. it  acts on endogenous μ-opioid receptors that are  spread in discrete packets throughout the brain, spinal cord and  gut in almost all mammals. Heroin, along with other opioids, are  agonists to four endogenous neurotransmitters. They are  β-endorphin, dynorphin, leu-enkephalin, and  met-enkephalin. The body responds to heroin in the brain by reducing (and sometimes stopping) production of the endogenous opioids when heroin is  present. Endorphins are  regularly released in the brain and  nerves and  attenuate pain. Their other functions are  still obscure, but are  probably related to the effects produced by heroin besides analgesia (antitussin, anti-diarrheal). The reduced endorphin production in heroin users creates a dependence on the heroin, and  the cessation of heroin results in extremely uncomfortable symptoms including pain (even in the absence of physical trauma). This set of symptoms is  called withdrawal syndrome. it  has an  onset 6 to 8 hours after the last dose of heroin.

[ and  trafficking">edit] Production and  trafficking

Primary worldwide producers of heroin.
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Primary worldwide producers of heroin.

[edit] Manufacturing

Heroin is  produced for the black market through opium refinement processes. Unlike drugs such as LSD, the production of which requires considerable expertise in chemistry and  access to constituents which are  now tightly controlled, the refinement of the first three grades of heroin from opium is  a relatively simple process requiring only moderate technical expertise and  common chemicals. The final grade of heroin favored in the west is  more difficult to produce and  involves a potentially dangerous chemical procedure.

First, morphine is  isolated from crude opium by being dissolved in water, reacted with lime fertilizer such that the morphine precipitates out, and  then reacted again  with ammonia. What remains is  then mechanically filtered to yield a final product of morphine weighing about 90% less  than the original quantity of opium. The morphine is  reacted with acetic anhydride — a chemical also used in the production of aspirin — in the complicated five-step process used by most refineries in the Golden Triangle. The first step is  to cook the morphine at 85°C (185°F) for six hours with an  equivalent weight of acetic anhydride. In the second, a treatment of water and  hydrochloric acid then purifies the product moderately. When the chemists add sodium carbonate, the particulates settle. Step four involves heating the heroin in a mixture of alcohol and  activated charcoal until the alcohol evaporates. The fifth step is  optional, as it  only changes the heroin into a finer white powder, more  easily injectable; this so-called "no. 4 heroin" is  principally exported to the Western markets. In this last, most dangerous step, the heroin (after being dissolved in alcohol), precipitates out in tiny white flakes when a mixture of ether and  hydrochloric acid is  injected; this step is  dangerous due to the fact that the ether may explode, leveling or  severely damaging the refinery (as has happened to a number of such facilities).

The purity of the extracted morphine determines in large part the quality of the resulting heroin. Most black market heroin is  highly impure due to contaminants left after refinement of opium into morphine which then remain in the final product; even if the final product is  in the upper range of purity (80–99% pure), once it  reaches the consumer, it  typically has been cut multiple times.

[edit] History of heroin traffic

The origins of the present international illegal heroin trade can be traced back to laws passed in many countries in the early 1900s that closely regulated the production and  sale of opium and  its derivatives including heroin. At first, heroin flowed from countries where it  was still legal into countries where it  was no longer legal. By the mid-1920s, heroin production had been made illegal in many parts of the world. an  illegal trade developed at that time between heroin labs in China (mostly in Shanghai and  Tientsin) and  other nations. The weakness of government in China and  conditions of civil war enabled heroin production to take root there. Chinese triad gangs eventually came to play a major role in the heroin trade.

Heroin trafficking was virtually eliminated in the U.S. during World War II due to temporary trade disruptions caused by the war. Japan's war with China had cut the normal distribution routes for heroin and  the war had generally disrupted the movement of opium. After the second world war, the Mafia took advantage of the weakness of the postwar Italian government and  set up heroin labs in Sicily. The Mafia took advantage of Sicily's location along the historic route opium took from Iran westward into Europe and  the United States. Large scale international heroin production effectively ended in China with the victory of the communists in the civil war in the late 1940s. The elimination of Chinese production happened at the same time that Sicily's role in the trade developed.

Although it  remained legal in some countries until after World War II, health risks, addiction, and  widespread abuse led most western countries to declare heroin a controlled substance by the latter half of the 20th century.

Between the end of World War II and  the 1970s, much of the opium consumed in the west was grown in Iran, but in the late 1960s, under pressure from the U.S. and  the United Nations, Iran engaged in anti-opium policies. While opium production never ended in Iran, the decline in production in those countries led to the development of a major new cultivation base in the so-called "Golden Triangle" region in South East Asia. In 1970-71, high-grade heroin laboratories opened in the Golden Triangle. This changed the dynamics of the heroin trade by expanding and  decentralizing the trade. Opium production also increased in Afghanistan due to the efforts of Turkey and  Iran to reduce production in their respective countries. Lebanon, a traditional opium supplier, also increased its role in the trade during years of civil war.

After the overthrow of the Shah of Iran, the new Iranian regime was much more  tolerant of opium production. At the same time, the Soviet-Afghan war led to increased production in the Pakistani-Afghani border regions. Both events led to increased international production of heroin at lower prices in the 1980s. The trade shifted away from Sicily in the late 1970s as various criminal organizations violently fought with each other over the trade. The fighting also led to a stepped up government law enforcement presence in Sicily. All of this combined to greatly diminish the role of the country in the international heroin trade.

[edit] Dr Alfred W. McCoy's account of the history of the heroin trade

Although it  was beginning to become more  prevalent by the 1930s, Asian historian and  drug traffic expert Dr Alfred W. McCoy reports that heroin trafficking was virtually eliminated in the U.S. during World War II due to temporary trade disruptions caused by the war. McCoy contends the Mafia was able to gain control of the heroin trade thanks in large measure due to the unintended consequences of a covert deal between top Mafia leader Lucky Luciano and  American military intelligence. The deal resulted in a large increase in Mafia influence in Sicily after the 1943 American invasion. [citation needed]

In southeast Asia, the governments of most countries and  many colonial officials had been involved in the opium trade for a very long time. Thanks to Corsican Mafia connections in the former French colony of Vietnam, Luciano was able to begin to develop Southeast Asia as a new source of Opium even as Iranian production declined. The Vietnam War and  CIA operations in Laos had the unintended consequence of first opening up many areas of Southeast Asia to modern transportation and  then presenting a ready-made market for the drug among the U.S. military personnel stationed in the region. [citation needed]

The turning point came in 1970-71 when the first high-grade heroin laboratories opened in the Golden Triangle. Prior to this, the chemical skills for refinement had existed only in Europe. This gave the opium producers control over the creation of the final product. The hundreds of thousands of American servicemen in Vietnam provided a perfect market for the heroin producers, and  heroin use among soldiers rapidly increased. In 1971 the first large consignments of South East Asian heroin were intercepted in Europe and  America, and  by the mid-1970s heroin addiction fulfilled its promise as a serious social problem in the United States, Australia, the United Kingdom, and  many other nations.[citation needed]

[edit] Trafficking

See also: Opium production
Asian heroin
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Asian heroin

Traffic is  heavy worldwide, with the biggest producer being Afghanistan.[8] According to U.N. sponsored survey,[9] as of 2004, Afghanistan accounted for production of 87 percent of the world's heroin.[10] Opium production in that country has increased rapidly since, reaching an  all-time high in 2006. War once again  appeared as a facilitator of the trade.[11]

Heroin concealed under the clothes of a drug smuggler.
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Heroin concealed under the clothes of a drug smuggler.

Dr. Alfred W. McCoy has claimed that the C.I.A. secretly collaborated with Asian drug syndicates and  was complicit in the expansion of the global heroin trade from 1970 to 1973 in order to prosecute the Cold War. While the Vietnam War brought modern transportation to remote opium areas, McCoy himself does not claim that the CIA set up the drug labs in Southeast Asia or  created the trade. [citation needed]

At present, opium poppies are  mostly grown in the Middle East, Pakistan, and  Afghanistan, and  in Asia, especially in the region known as the Golden Triangle straddling Myanmar, Thailand, Vietnam, Laos and  Yunnan province in the People's Republic of China. There is  also cultivation of opium poppies in the Sinaloa region of Mexico and  in Colombia. The majority of the heroin consumed in the United States comes from Mexico and  Colombia[citation needed]. Up until 2004, Pakistan was considered one of the biggest opium-growing countries. However, the efforts of Pakistan's Anti-Narcotics Force have  since reduced the opium growing area by 59% as of 2001[citation needed]. Some suggest that the decline in Pakistani production is  inversely proportional to the rise of Afghani production, and  that rather than anti-narcotics activity, the decline in Pakistan is  due more  to changed market forces.[citation needed]

Conviction for trafficking in heroin carries the death penalty in most Southeast Asia and  some East Asia, southern Asia and  Middle East countries (see Use of death penalty worldwide for details), among which Malaysia, Singapore and  Thailand are  the most strict. The penalty applies even to citizens of countries where the penalty is  not in place, sometimes causing controversy when foreign visitors are  arrested for trafficking, for example the arrest of nine Australians in Bali or  the hanging of Australian citizen Van Tuong Nguyen in Singapore, both in 2005.

[edit] Risks of non-medical use

Many countries and  local governments have  begun funding programs that supply sterile needles to people who inject illegal drugs in an  attempt to reduce these contingent risks and  especially the contraction and  spread of blood-borne diseases. The Drug Policy Alliance reports that up to 75% of new AIDS cases among women and  children are  directly or  indirectly a consequence of drug use by injection. But despite the immediate public health benefit of needle exchanges, some see such programs as tacit acceptance of illicit drug use. The United States does not support needle exchanges federally by law, and  although some state and  local governments do support needle exchange programs, they continue to face harassment by police in most areas. Needle exchanges have  been instrumental in arresting the spread of HIV/AIDS in many communities with a significant heroin using population[citation needed], Australia being a leader due to its early inception of needle exchanges. Needle exchange programs have  also been attributed to saving the public significant amounts of tax dollars by preventing medical costs which would have  been required otherwise for the treatment of diseases spread through the practice of sharing and  reusing needles.

A heroin overdose is  usually treated with an  opioid antagonist, such as naloxone (Narcan) or  naltrexone, which have  a high affinity for opioid receptors but do not activate them. This blocks heroin and  other opioid agonists and  causes an  immediate return of consciousness and  the beginning of withdrawal symptoms when administered intravenously. The half-life of these antagonists is  usually much shorter than that of the opiate drugs they are  used to block, so the antagonist usually has to be re-administered multiple times until the opiate has been metabolized by the body.

Depending on drug interactions and  numerous other factors, death from overdose can take anywhere from several seconds to several hours. an  overdose is  immediately reversible with an  opioid antagonist injection. Heroin overdoses can occur due to an  unexpected increase in the dose or  purity or  due to diminished opiate tolerance. However, many fatalities reported as overdoses are  probably caused by interactions with other depressant drugs like alcohol or  benzodiazepines.[12]

The LD50 for a person already addicted is  prohibitively high, to the point that there is  no general medical consensus on where to place it. Several studies done in the 1920s gave addicts doses of 1,600–1,800 mg of heroin in one sitting, and  no adverse effects were reported. This is  approximately 160–180 times a normal recreational dose. Even for a non-addict, the LD50 can be credibly placed above 350 mg.

Street heroin is  of widely varying and  unpredictable purity. This means that an  addict may prepare what they consider to be a moderate dose while actually taking far more  than intended. Also, relapsing addicts after a period of abstinence have  tolerances below what they were during active addiction. If a dose comparable to their previous use is  taken an  overdose often results.[citation needed]

A final source of overdose in addicts comes from place conditioning. Heroin use, like other drug abuse behaviors, is  highly ritualized. While the mechanism has yet to be clearly elucidated, it  has been shown that longtime heroin users, immediately before injecting in a common area for heroin use, show an  acute increase in metabolism and  a surge in the concentration of opiate-metabolizing enzymes. This acute increase, a reaction to a location where the addict has repeatedly injected heroin, imbues the addict with a strong (but temporary) tolerance to the toxic effects of the drug. When the addict injects in a different location, this place-conditioned tolerance does not occur, giving the addict a much lower-than-expected ability to metabolize the drug. The user's typical dose of the drug, in the face of decreased tolerance, becomes far too high and  can be toxic, leading to overdose.[1]

A small percentage of heroin smokers may develop symptoms of leukoencephalopathy. This is  believed to be caused by an  uncommon adulterant that is  only active when heated. Symptoms include slurred speech and  difficulty walking.

[edit] Withdrawal

The withdrawal syndrome from heroin may begin starting from within 6 to 24 hours of discontinuation of sustained use of the drug; however, this time frame can fluctuate with the degree of tolerance as well as the amount of the last consumed dose. Symptoms may include: sweating, malaise, anxiety, depression, persistent and  intense penile erection in males (priapism), extra sensitivity of the genitals in females, general feeling of heaviness, cramp-like pains in the limbs, yawning and  lacrimation, sleep difficulties, cold sweats, chills, severe muscle and  bone aches not precipitated by any physical trauma, nausea and  vomiting, diarrhea, goose bumps, cramps, and  fever. Many addicts also complain of a painful condition, the so-called "itchy blood", which often results in compulsive scratching that causes bruises and  sometimes ruptures the skin leaving scabs. Abrupt termination of heroin use causes muscle spasms in the legs of the user (restless leg syndrome). Users taking the "cold turkey" approach (withdrawal without using symptom-reducing or  counteractive drugs) are  more likely to experience the negative effects of withdrawal in a more  pronounced manner.

Two general approaches are  available to facilitate the physical part of opioid withdrawal. The first is  to substitute a longer-acting opioid such as methadone or  buprenorphine for heroin or  another short-acting opioid and  then slowly taper the dose.

In the second approach, benzodiazepines such as diazepam (Valium) may temporarily ease the often extreme anxiety of opioid withdrawal. The most common benzodiazepine employed as part of the detox protocol in these situations is  oxazepam (Serax). Benzodiazepine use must be prescribed with care because benzodiazepines have  a great addiction potential, and  many opioid addicts also use other central nervous system depressants including barbiturates. Also, though unpleasant, opioid withdrawal seldom has the potential to be fatal, whereas complications related to withdrawal from benzodiazepines, barbiturates and  alcohol (such as epileptic seizures, cardiac arrest, and  delirium tremens) can prove hazardous and  potentially fatal. Many symptoms of opioid withdrawal are  due to rebound hyperactivity of the sympathetic nervous system, which can be suppressed with clonidine (Catapres), a centrally-acting alpha-2 agonist primarily used to treat hypertension.

Buprenorphine is  one of the substances most recently licensed for the substitution of illegal opioids. Being a partial opioid agonist/antagonist, it  develops a lower grade of tolerance than heroin or  methadone due to the so-called ceiling effect. it  also has less  severe withdrawal symptoms than heroin when discontinued abruptly, which should never be done without proper medical supervision. it  is usually administered every 24-48 hrs. Buprenorphine is  a kappa-opioid receptor antagonist. This gives the drug an  anti-depressant effect, increasing physical and  intellectual activity. [citation needed] Buprenorphine also acts as a partial agonist at the same μ-receptor where illicit opioids like heroin exhibit their action. Due to its effects on this receptor, all patients whose tolerance is  above a certain level are  unable to obtain any "high" from other opioids during buprenorphine treatment except for very high doses.

Researchers at Johns Hopkins University have  been testing a sustained-release "depot" form of buprenorphine that can relieve cravings and  withdrawal symptoms for up to six weeks.[13] A sustained-release formulation would allow for easier administration and  adherence to treatment, and  reduce the risk of diversion or  misuse.

Methadone is  another μ-opioid agonist most often used to substitute for heroin in treatment for heroin addiction. Compared to heroin, methadone is  well (but slowly) absorbed by the gastrointestinal tract and  has a much longer duration of action of approximately 24 hours. Thus methadone maintenance avoids the rapid cycling between intoxication and  withdrawal associated with heroin addiction. In this way, methadone has shown some success as a "less harmful substitute"; despite bearing about the same addiction potential as heroin, it  is recommended for those who have  repeatedly failed to complete withdrawal or  have recently relapsed. As of 2005, the μ-opioid agonist buprenorphine is  also being used to manage heroin addiction, being a superior, though still imperfect and  not yet widely known alternative to methadone. Methadone, since it  is longer-acting, produces withdrawal symptoms that appear later than with heroin, but usually last considerably longer and  can in some cases be more  intense. Methadone withdrawal symptoms can potentially persist for over a month, compared to heroin where significant physical symptoms would subside by 4 days.

Two opioid antagonists are  known: naloxone and  the longer-acting naltrexone. These two medications block the effects of heroin, as well as the other opioids at the receptor site. Recent studies have  suggested that the addition of naloxone and  naltrexone may improve the success rate in treatment programs when combined with the traditional therapy. [citation needed]

The University of Chicago undertook preliminary development of a heroin vaccine in monkeys during the 1970s, but it  was abandoned. There were two main reasons for this. Firstly, when immunised monkeys had an  increase in dose of x16, their antibodies became saturated and  the monkey had the same effect from heroin as non-immunised monkeys. Secondly, until they reached the x16 point immunised monkeys would substitute other drugs to get a heroin-like effect. These factors suggested that immunised human addicts would simply either take massive quantities of heroin, or  switch to other hard drugs, which is  known as cross-tolerance.

There is  also a controversial treatment for heroin addiction based on a plant-derived African psychedelic drug, ibogaine. Many people travel abroad for ibogaine treatments that generally interrupt the addiction for 3 - 6 months or  more in up to 80% of patients.[citation needed] Relapse often occurs when the person returns home to their normal environment however, where drug seeking behaviour may return in response to social and  environmental cues.[citation needed] Ibogaine treatments are  carried out in several countries in South America and  in Europe but can be dangerous. Some addicts find the ibogaine therapy most effective when it  is given several times over the course of a few months or  years, but this can be very expensive. A synthetic derivative of ibogaine, 18-methoxycoronaridine is  in phase 2 trials in humans as an  anti-addictive drug.

[edit] Heroin prescription

In 1994 Switzerland began a trial program featuring a heroin prescription for addicts not well suited for withdrawal programs—e.g. those that had failed multiple withdrawal programs. The aim is  maintaining the health of the addict in order to avoid medical problems stemming from low-quality street heroin. Reducing drug-related crime was another goal. Addicts can more  easily get or  maintain a paid job through the program as well. The first trial in 1994 began with 340 addicts and  it was later expanded to 1000 after medical and  social studies suggested its continuation. Participants are  prescribed to inject heroin in specially designed pharmacies for about US $13 per dose.[14]

The success of the Swiss trials led German, Dutch,[15] and  Canadian[16] cities to trial their own heroin prescription programs.[17] Some Australian cities (such as Sydney) have  trialed legal heroin injecting rooms, in line with other wider harm minimisation programs. Heroin is  unavailable on prescription however, and  remains illegal outside the injecting room, and  effectively decriminilised inside of the injecting room. [citation needed]

[edit] Drug interactions

Opioids are  strong central nervous system depressants, but regular users develop physiological tolerance allowing gradually increased dosages. In combination with other central nervous system depressants, heroin may still kill even experienced users, particularly if their tolerance to the drug has reduced or  the strength of their usual dose has increased.

Toxicology studies of heroin-related deaths reveal frequent involvement of other central nervous system depressants, including alcohol, benzodiazepines such as diazepam (valium), and, to a rising degree, methadone. Ironically, benzodiazepines are  often used in the treatment of heroin addiction while they cause much more  severe withdrawal symptomes.

Cocaine also proves to be often fatal when used in combination with heroin. Though "speedballs" (when injected) or  "moonrocks" (when smoked) are  a popular mix of the two drugs among users, combinations of stimulants and  depressants can have  unpredictable and  sometimes fatal results. In the United States in early 2006, a rash of deaths was attributed to either a combination of fentanyl and  heroin, or  pure fentanyl masquerading as heroin particularly in the Detroit Metro Area; one news report refers to the combination as 'laced heroin', though this is  likely a generic rather than a specific term.[18]

[edit] Culture

Heroin has inspired countless writers, musicians and  other artists over the past century of use. However, its influence is  often misunderstood or  unfairly assumed; many creative people have  used or  been addicted to heroin, but the extent to which the drug affected their creativity is  debatable. Relatively few artists with great talent have  credited heroin use with major epiphanies. A notable song by Lou Reed is  titled "Heroin".

[edit] See also


[edit] References

  1. ^ David Shewan, Phil Dalgarno (2005). "Evidence for controlled heroin use? Low levels of negative health and  social outcomes among non-treatment heroin users in Glasgow". British Journal of Health Psychology 10: 33-48. DOI:10.1348/135910704X14582.
  2. ^ Hamish Warburton, Paul J Turnbull, Mike Hough. "Occasional and  controlled heroin use: Not a problem?", 2005.
  3. ^ Yellow List: List of Narcotic Drugs Under International Control (PDF). International Narcotics Control Board (December 2004). Retrieved on May 5, 2006. Referring URL = http://www.incb.org/incb/yellow_list.html
  4. ^ Opium Throughout History. PBS Frontline. Retrieved on 2006-10-22.
  5. ^ Wright, C.R.A. (2003-08-12). On the Action of Organic Acids and  their Anhydrides on the Natural Alkaloids. Archived from the original on 2004-06-06. Note: this is  an annotated excerpt of Wright, C.R.A. (1874). "On the Action of Organic Acids and  their Anhydrides on the Natural Alkaloids". Journal of the Chemical Society 27: 1031–1043.
  6. ^ How aspirin turned hero. Sunday Times (September 13 1998). Retrieved on 2006-10-22.
  7. ^ Tschacher W, Haemmig R, Jacobshagen N. (2003). "Time series modeling of heroin and  morphine drug action.". Psychopharmacology.
  8. ^ Nazemroaya, Mahdi Darius (October 17 2006). The War in Afghanistan: Drugs, Money Laundering and  the Banking System. GlobalResearch.ca. Retrieved on 2006-10-22.
  9. ^ Afghanistan opium survey - 2004. Retrieved on 2006-10-22.
  10. ^ McGirk, Tim (August 2 2004). Terrorism's Harvest: How al-Qaeda is  tapping into the opium trade to finance its operations and  destabilize Afghanistan. Time Magazine Asia. Retrieved on 2006-10-22.
  11. ^ Gall, Carolotta (September 3 2006). Opium Harvest at Record Level in Afghanistan. New York Times - Asia Pacific. Retrieved on 2006-10-22.
  12. ^ Shane Darke, Deborah Zador (1996). "Fatal Heroin 'Overdose': a Review". Addiction 91 (12): 1765-1772.
  13. ^ Thomas, Josephine (May 2001). Buprenorphine Proves Effective, Expands Options For Treatment of Heroin Addiction (PDF). NIDA Notes: Articles that address research on Heroin 23. National Institute on Drug Abuse. Retrieved on May 5, 2006.
  14. ^ Nadelmann, Ethan (July 10 1995). Switzerland's Heroin Experiment. Drug Policy Alliance. Retrieved on 2006-10-22.
  15. ^ Heroin prescription 'cuts costs'. BBC News (June 5 2005). Retrieved on 2006-10-22.
  16. ^ About the study. North American Opiate Medication Initiative. Retrieved on 2006-10-22.
  17. ^ Incidence of heroin use in Zurich, Switzerland: a treatment case register analysis (PDF). The Lancet (367, 1830-4, 2006). Retrieved on 2006-10-22.
  18. ^ Brown, Robin. "Heroin's Hell", The News Journal, 2006-05-04, pp. A1,A12.

[edit] Literature

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Analgesics (N02A, N02B) edit
Opioids:

6-methylene-dihydromorphine, Acedicon, Acetorphine, Acetyldihydrocodeine, Acetyldihydrocodeinone, Acetylmorphone, Alfentanil, Allylprodine, Alphaprodine, Anileridine, Bemidone, Benzylmorphine, Betmeprodine, Betaprodine, Bezitramide, Buprenorphine, Butorphanol, Carfentanil, Clonitazene, Codeine-N-Oxide, Codeine, Codeineone, Cyclazocine, Cyclorphan, Desomorphine, Dextromethorphan, Dextropropoxyphene, Dextromoramide, Dezocine, Diacetyldihydromorphine, Diethylthiambutene, Difenoxin, Dihydromorphine, Dihydrocodeine, Dihydrocodeine enol acetate, Dihydroetorphine, Dihydroisocodeine, Dimethylthiambutene, Diphenoxylate, Dipipanone, Ethylketocyclazocine, Ethylmorphine, Etonitazene, Etorphine, Fentanyl, Diamorphine (Heroin), Hydromorphone, Hydrocodone, Isomethadone, Ketobemidone, Laudanum, Lefetamine, Levallorphan, Levo-alphacetylmethadol, Levomethadone, Levomethorphan, Levorphanol, Loperamide, Meptazinol, Metazocine, MPPP, Methadone, Methyldihydromorphine, Metopon, Morphine, Morphineone, Morphine-N-Oxide, Myorphine, Nalbuphine, Nicocodeine, Nicodicodeine, Nicomorphine, Norcodeine, Ohmefentanyl, Omnopon, Opium, Oxycodone, Oxymorphone, PEPAP, Pantopon, Papaveretum, Paregoric, Pentazocine, Pethidine(Meperidine), Phenadoxone, Phenazocine, Phenoperidine, Pholcodeine, Piminodine, Piritramide, Prodine, Proheptazine, Propiram, Propoxyphene, Racemethorphan, Racemorphan, Remifentanil, Sufentanil, Tetrapon, Thebacon, Tilidine, Tramadol, Trimeperidine

Salicylic acid and  derivatives: Aspirin (Acetylsalicylic Acid), Diflunisal, Ethenzamide -- See also: NSAIDs
Pyrazolones:

Aminophenazone, Metamizole, Phenazone

Anilides:

Paracetamol (acetaminophen), Phenacetin

Others:

Ziconotide, Tetrahydrocannabinol, Ibuprofen, Ketoprofen, Mefenamic Acid, Naproxen, Diclofenac, Flurbiprofen, Diflunisal, Fenoprofen, Indomethacin, Ketorolac; Meclofenamate, Meloxicam, Piroxicam, Tolmetin,


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