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Heroin

Drugs & Medication

Heroin

From Wikipedia the free encyclopedia, by MultiMedia

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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
Legal status 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 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

History

Bayer Heroin (TM)
Bayer Heroin (TM)
Bayer Heroin bottle.
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 liver. All opiates are converted by the human liver into the identical molecule with varying degrees of concentration in the blood stream. 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.

Usage and effects

Indicated for:

Relief of extreme pain

Recreational uses:

Euphoria
Relaxation

Other uses:

Pain relief
Cough suppressant
anti-diarrheal

Contraindications:

Alcohol

Barbiturates and Benzodiazepines

Stimulants

Other opioids (depends heavily on tolerance)

Side effects:
Severe:

Respiratory arrest, seizure, coma, death
Spontaneous abortion

Cardiovascular & Respiratory:

Lowered heart rate
Slowed, shallow or ineffective respiration

Eyes, Ears, nose, and mouth:

Dry mouth
Pupil constriction

Gastrointestinal:

Nausea
Vomiting (protracted)
Constipation

Urinary System:

Urinary retention

Musculoskeletal:

Analgesia

Ataxia

Neurological:

Analgesia

Physical dependence

Psychological:

Anxiolytic

Confusion
Euphoria
Somnolence
Addiction

Skin:

Itching

Flushing/Rash

Diamorphine ampoules for medicinal use
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 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.

Production and trafficking

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

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 it (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.

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.

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.

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.

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.

Trafficking

See also: Opium production
Asian heroin
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.
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.

Heroin is one of the most profitable illicit drugs since it is compact and easily concealed. 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. 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. 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.

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.

Risks of non-medical use

  • Overdose, possibly causing death
    For intravenous users of heroin, the use of non-sterile needles and syringes and other related equipment leads to the risk of contracting blood-borne pathogens such as HIV and hepatitis, as well as the risk of contracting bacterial or fungal endocarditis and possibly Venous sclerosis
    Poisoning from contaminants added to "cut" or dilute heroin
    Chronic constipation
    Heroin-induced leukoencephalopathy (very rare, smokers only)

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, 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.

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. Contrary to popular rumor, aluminum foil probably has nothing to do with the development of leukoencephalopathy in heroin users.

Withdrawal

Black tar heroin
Black tar heroin

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 benzodiazepines and sometimes even the obsolete 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.  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.

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. 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. 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.

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]

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]

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.

See also

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.
  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.
  13. ^ Thomas, Josephine (May 2001). Buprenorphine Proves Effective, Expands Options For Treatment of Heroin Addiction (PDF). NIDA Notes: Articles that address research on Heroin pp. 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.

Literature

  • Heroin (1998) ISBN 1-568-38153-0
  • Heroin Century (2002) ISBN 0-415-27899-6
  • This is Heroin (2002) ISBN 1-860-74424-9
  • The Heroin User's Handbook by Francis Moraes (paperback 2004) ISBN 1-559-50216-9
  • The Little Book of Heroin by Francis Moraes (paperback 2000) ISBN 0-914-17198-4
  • Heroin: A True Story of Addiction, Hope and Triumph by Julie O'Toole (paperback 2005) ISBN 1-905-37901-3

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