What some addictiveness to Heroin?

Answer 1

I dont quite understand, are you asking how someone becomes addicted to heroin? or asking how to tell if they are? the signs and symptoms? how to get them off of heroin?

Here is some information i hope it helps.....

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. 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.

HISTORY
The opium poppy was cultivated in lower Mesopotamia as long ago as 3400 BC. 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).
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. 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
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.

RISKS OF NON MEDICAL USAGE
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[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.

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.

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.

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. 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. 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. 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.

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.

Answer 2

If you're hooked on any drug, its 10 instances less complicated to get hooked on others adding alcohol. Alcohol has the one withdrawal signs that may kill you. If you must be on anything, stick with marijuana. At least it's not bodily addictive and has been verified to have a few wellness advantages. Even up to date stories are displaying that possibly even slight consuming is dangerous for you. A research I learn many years in the past mentioned that during phrases of harm to the individual financially and wellness clever, heroin and crack are practically identical. It sounds to me like you could have an addictive character. You are utilizing medications to change your moods, and desire it regardless. Think of alcohol, Adderall and weed as your alternative for crack and heroin. I.e. its well adequate to get you by means of, however you're nonetheless an addict. I know the way it's, I'm a improving alcoholic myself. I determined that I get hooked on matters like caffeine and nicotine, and Ive abused a few authorized medications earlier than like Kratom. My recommendation is to give up utilizing the whole lot. Its the one manner you're going to quite recuperate. (Keep in brain I nonetheless bite and drink espresso so I am no longer a primary instance of any one that did this, its simply an ultimate) My recommendation to you is not to get on Adderall. The talents for abuse is simply too excellent. Keep in brain plenty of men and women get identified with ADD whilst they do not quite have it.

Answer 3

it sure is!