TripSit Wiki - User contributions [en]

Buprenorphine

2017-06-10T01:55:06Z

Spacer: Added: * Dizziness and Vertigo + few spelling errors.

[[File:Suboxone.jpg|350px|right]]

'''Buprenorphine''' is a semi-synthetic opioid derived from thebaine which is typically used for treatment of opioid addiction. It is an analgesic, and has gained notoriety for its ability to successfully interrupt severe opiate addictions. Buprenorphine has a higher affinity for μ-opioid receptors compared to full opioid agonists. Because of this, buprenorphine can block the effects of other opioid agonists in a dose-dependent fashion. By its dual effects of reducing craving and attenuating the response to administered heroin, buprenorphine reduces the self-administration of heroin. Methadone, a full opioid agonist, also reduces the impact of additional heroin, but the effect of methadone is primarily due to the induction of cross-tolerance which is dose dependent. In contrast buprenorphine achieves its effect primarily by prolonged occupancy of a high proportion of opioid receptors, blocking the action of heroin and other opioid receptor agonists.

== History ==

Addiction therapeutics arose within the historical context of efforts to develop a non-addicting analgesic that began in the United States in the early 1920s. Early 20th century efforts to respond to the “opium problem,” through regulation and control at the source of supply and to address public health concerns through innovation in the research laboratory set the stage for the gradual shift in researchers’ interests toward developing a treatment for addiction therapeutics.

The solution to the “opium problem” was first sought at the laboratory bench at a time when the United States was becoming a major player within the evolving international drug control framework. For such a narrowly tailored goal to be understood as meeting a broad social problem of unclear etimology, it had to be translated into a feasible research program. Reliable methods to test compounds in animals and human beings had to be developed and validated. In the CDA’s first decade, some 150 compounds were produced and evaluated; all but one - Metopon (5-methylhydromorphone) - demonstrated the elusiveness of the goal.

Methadone was introduced into the United States in 1947 by Eli Lilly and Company, however, researchers opposed using methadone for maintenance given the results of studies on former morphine and/or heroin addicts in the late 1940s indicating that the subjects expressed increased satisfaction as dosage increased. They concluded that “narcotic drug addicts would abuse methadone and would become habituated to it if it were freely available and not controlled”. They also noted that methadone “completely alleviated the morphine abstinence syndrome in man,” yet itself exhibited a mild abstinence syndrome.

In 1974, Congress became concerned with methadone diversion and amended the Controlled Substances Act (CSA), in 1970 to give DEA considerable powers despite the inception of the National Institute on Drug Abuse (NIDA) and sunset of SAODAP in 1973. Many clinicians came to view the methadone regulations as government interference with the practice of medicine. The restrictive climate had led SAODAP to prioritize development of narcotic antagonists.

Buprenorphine was discovered in 1966, at the research labs of a home products company, Reckitt & Colman (hereafter Reckitts), in Hull, England.

The story of the development of buprenorphine as an "addict treatment" began in 1975, when Lexington Addiction Research Center (ARC) scientist Jasinski countered growing opposition to using prisoners as clinical research subjects by arguing that many prisoners were addicts and the pharmacology of buprenorphine made it such an “attractive candidate" as a treatment for opiate dependence that its human abuse potential was in urgent need of study.

Jasinski singled out buprenorphine as having an “especially unique pharmacology in man” because it produced “very little physical dependence”, even with chronic administration. Citing his 1978 study, he speculated that buprenorphine “would not only have a therapeutic application as an analgesic of low abuse potential but also as a new type of drug treatment of narcotic addiction."

Jasinski heralded buprenorphine’s unique potential because it alone produced long-lasting “changes in feelings that are acceptable to addicts,” and was “less toxic than methadone,” declaring that the committee’s 50-year project to “potentially utilize narcotics therapeutically to both relieve pain and treat addiction without the production of physical dependence” had yielded buprenorphine, which “appears to have the advantage of both methadone and naltrexone but without the major disadvantage of each”.

In 1979, following the ban on use of federal prisoners as research subjects, NIDA had moved the ARC’s Clinical Research Program, now under the direction of Jasinski, to the medical campus of The Johns Hopkins University (JHU) in Baltimore, Maryland; the preclinical program followed in 1981. The JHU site was chosen partly because Baltimore provided a suitable source of research subjects: inner-city heroin addicts. Addiction researchers considered it unethical and unwise to carry out research involving addictive substances on people who were not or had not been addicted.

By 1985, injectable buprenorphine had been marketed for analgesic applications in 29 countries and the sublingual tablet in 16 countries. In the United Kingdom, Reckitts had launched injectable buprenorphine for severe pain in 1978,with the sublingual analgesic following in 1982. It licensed Norwich–Eaton to distribute buprenorphine hydrochloride (Buprenex) in the United States, where the analgesic was launched in 1985, after FDA approval.

The difficulties of coordinating public and private interests, local and global effects, changes in domestic regulatory mechanisms, and perceptions of addiction and its treatment charted buprenorphine’s tortuous, 30-year path to FDA approval and market. Buprenorphine arose as a maintenance therapy at a time when addicts - like other citizens - were expected to take personal responsibility for health and healthcare, and where such decisions were seen as individual matters of choice and political entitlement.

== Uses ==

Buprenorphine is usually sold in the form of sublingual tablets (Suboxone), or trans dermal patches (Butrans). Patches can be attached to skin for long release as treatment for opioid withdrawal, or cut and chewed for recreational use. Usual (30 minutes) sub-lingual use of patches is not 100% effective, so patches can be re-used. Buprenorphine is water-soluble, and can be extracted with a [[Cold Water Extraction]] (takes more time, usually 24 hours, or around 4 hours with few drops of strong alcohol). Since buprenorphine is a long acting opioid antagonist, other opioids won't work for at least 36 hours after dosing buprenorphine (though some negative effects will be garnered).

Buprenorphine will cause withdrawal if you have an opioid tolerance and don't wait long enough (typically 48~ hours) before taking it.

Respiratory depression from buprenorphine (or buprenorphine/naloxone) overdose is less likely than from other opioids. There is no evidence of organ damage with chronic use of buprenorphine, although increases in liver enzymes are sometimes seen. Likewise, there is no evidence of significant disruption of cognitive or psycho motor performance with buprenorphine maintenance dosing.

== Dosage ==

Dosage is usually 2-3mg (assuming 100% effectiveness), and most users don't feel the need to take more. Ceiling effect is 16-32mg, and redosing is not effective.

600µg is considered equivalent to 10 mg morphine for pain relief.

{| class="wikitable"
|+ Sublingual
|-
| Light || 1-2mg
|-
| Common || 3-6mg
|-
| Strong || 6-8mg
|-
| Heavy || 8mg+
|-
| Ceiling || 16-32mg
|}

== Duration ==

{| class="wikitable"
|+ Sublingual
|-
| Onset || 30-60 minutes
|-
| Peak || 1-4 hours
|-
| Total (low dose) || 8-12 hours
|-
| Total (high dose) || 24-72 hours
|}

== Effects ==

Because of its ceiling effect and poor bio-availability, buprenorphine is safer in high doses compared to full opioid agonists. The maximal effects of buprenorphine appear to occur in the 16–32 mg dose range for sublingual tablets. Higher doses are unlikely to produce greater effects.

=== Positive ===

* Euphoria

* Sedation

* Pain relief

* Elevated mood

* Overall feeling of contentedness

=== Neutral ===

* Pupillary dilation

=== Negative ===

* Dysphoric mood

* Piloerection

* Nausea or vomiting

* Diarrhea

* Muscle aches/cramps

* Yawning

* Lacrimation

* Mild fever

* Rhinorrhea

* Insomnia

* Craving

* Sweating

* Distress/irritability

* Dizziness and Vertigo

== Harm Reduction ==

Unlike methadone, the effect of buprenorphine on respiratory depression reaches a ceiling, therefore higher doses do not increase risk of respiratory depression to a significant degree.

However, if buprenorphine is used in combination with other central nervous system depressants, such as benzodiazepines and other CNS [[Depressants]], the combined effect on respiration can be life threatening.

=== Interactions ===

[[Drug Combinations]]

Combination of buprenorphine and SSRIs [http://www.ncbi.nlm.nih.gov/pubmed/18774063 can cause] Serotonin Syndrome.

== Chemistry and Pharmacology ==

Buprenorphine is a derivative of the opioid alkaloid thebaine that is a more potent (25 – 40 times) and longer lasting analgesic than morphine. It appears to act as a partial agonist at the μ- and κ-opioid receptors and as an antagonist at δ-opioid-receptors. The lack of δ-opioid agonism has been suggested to account for the observation that buprenorphine tolerance may not develop with chronic use.

Buprenorphine is metabolised by the liver, via CYP3A4 (also CYP2C8 seems to be involved) isozymes of the cytochrome P450 enzyme system, into norbuprenorphine (by N-dealkylation).

== Links ==

[https://en.wikipedia.org/wiki/Buprenorphine Wikipedia]

[https://erowid.org/pharms/buprenorphine/buprenorphine.shtml Erowid]

http://buprenorphine.samhsa.gov/about.html

[http://www.ncbi.nlm.nih.gov/pubmed/22256949 The history of the development of buprenorphine as an addiction therapeutic.]

http://www.nationaldrugstrategy.gov.au/internet/drugstrategy/publishing.nsf/content/9011C92D2F6E1FC5CA2575B4001353B6/$File/bupren1.pdf

[http://www.reddit.com/r/opiates/comments/1f3ak7/suboxone_faq/ /r/opiates Suboxone FAQ]

[[Category:Drugs]]

[[Category:Depressant]]

[[Category:Opioid]]

Salvia

2017-06-10T01:38:21Z

Spacer:

[[File:salvia.jpg|350px|right]]

'''Salvia Divinorum''' is a plant of the genus Salvia, which is psychoactive and known to induce intense and dysphoric hallucinatory experiences. It can either be smoked or taken sublingually, though the former is preferred by most users. Many of the users do not consider the drug to have much 'recreational' potential, due to the intense and often scary experience it yields - however it has seen value as a tool for spiritual use.

== History ==

The plant was originally endemic to the Sierra Madre mountains in Mexico, and has a long history of having been used by the Mazatecs for shamanic healing rituals - entering a shamanic state of consciousness using the substance to divine a patient's illness in the spirit world by integrating the plant into a tea preparation called "yerba de Maria."

The drug was first discovered in the Western world by R Gordon Wasson, a widely renowned botanist brought the plant back from Mexico as an object of scientific research - witnessing the plant being used in a similar manner to mushrooms in shamanic religious practice. It remained in relative obscurity until the 90s, at which time Western psychedelic exploration of the plant began.

Now, due to the Internet, the drug is widely available on the Internet and many users partake in the drug recreational.

== Dosage ==

The doses for salvia vary wildly depending on the quality of the plant or extract. It is typically smoked in dried leaf form, while taken sublingually either as dried or fresh wet leaf. Salvia extracts are also commonly available, generally coming in 5x, 6x, 10x and even 20x concentrations - though the extraction process tends to lose a bit of the potency and therefore doses will not be accurately comparable with fresh product.

{| class="wikitable"
|+ Smoked
|-
| Threshold || 0.2g+
|-
| Common || 0.4g+
|-
| Heavy || 0.5g+
|}

{| class="wikitable"
|+ Sublingual (Wet Leaf)
|-
| Threshold || 10g+
|-
| Common || 30g+
|-
| Heavy || 50g+
|}

{| class="wikitable"
|+ Sublingual (Dried Leaf)
|-
| Threshold || 2g+
|-
| Common || 5g+
|-
| Heavy || 10g+
|}

== Duration ==

{| class="wikitable"
|+ All routes
|-
| Onset || 20-60 seconds
|-
| Total || 5-15 minutes
|-
| After-effects || 20-40 minutes
|}

== Effects ==

=== Postive ===

* Radical shift in perspective and perception

* Increase in sensual activity

* Introspective insight

* Powerful open/closed eye visuals

* Change in consciousness

=== Neutral ===

* Dissociation

* Perspiration

=== Negative ===

* Dysphoria

* Ataxia

* Dizziness

* Amnesia

* Nausea

== Harm Reduction ==

* Due to the ataxia and loss of body control, it is recommended to position yourself in a way that you will not aspirate during the experience (though vomiting from salvia is not a common occurrence).

* It is generally recommended to use a sitter while ingesting salvia, due to the mental intensity of the experience or potential for injury while in dysphoric state.

=== Potentiators ===

Users have reported an elongation and potentiation of the effects of the drug through using a [[MAOI]] such as Syrian Rue.

=== Interactions ===

== Chemistry and Pharmacology ==

The primary psychoactive constituent of salvia divinorum is a diterpenoid called salvinorin A, which is a potent k-opioid and d2 receptor agonist. Due to these properties, it has seen research indicating the drug may be of use as a treatment for opioid addiction - as well as providing research opportunities for the potential treatment of perception-altering diseases such as schizophrenia or Alzheimer's.

== Legal status ==

Salvia is legal in most countries, since its tendency to disable users and chemical safety mean that while users may not have a pleasant experience, it is very difficult to cause damage through physical or accidental means.

== Links ==

[https://en.wikipedia.org/wiki/Salvia_divinorum Wikipedia]

[https://www.erowid.org/plants/salvia/salvia.shtml Erowid]

[http://reddit.com/r/Drugs/comments/jkscw/rdrugs_ama_series_salvia_divinorum_salvia/?sort=top /r/Drugs FAQ]

[[Category:Drugs]]

[[Category:Dissociative]]

Salvia

2017-06-10T01:35:11Z

Spacer:

[[File:salvia.jpg|350px|right]]

'''Salvia Divinorum''' is a plant of the genus Salvia, which is psychoactive and known to induce intense and dysphoric hallucinatory experiences. It can either be smoked or taken sublingual, though the former is preferred by most users. Many of the users do not consider the drug to have much 'recreational' potential, due to the intense and often scary experience it yields - however it has seen value as a tool for spiritual use.

== History ==

The plant was originally endemic to the Sierra Madre mountains in Mexico, and has a long history of having been used by the Mazatecs for shamanic healing rituals - entering a shamanic state of consciousness using the substance to divine a patient's illness in the spirit world by integrating the plant into a tea preparation called "yerba de Maria."

The drug was first discovered in the Western world by R Gordon Wasson, a widely renowned botanist brought the plant back from Mexico as an object of scientific research - witnessing the plant being used in a similar manner to mushrooms in shamanic religious practice. It remained in relative obscurity until the 90s, at which time Western psychedelic exploration of the plant began.

Now, due to the Internet, the drug is widely available on the Internet and many users partake in the drug recreational.

== Dosage ==

The doses for salvia vary wildly depending on the quality of the plant or extract. It is typically smoked in dried leaf form, while taken sublingual either as dried or fresh wet leaf. Salvia extracts are also commonly available, generally coming in 5x, 6x, 10x and even 20x concentrations - though the extraction process tends to lose a bit of the potency and therefore doses will not be accurately comparable with fresh product.

{| class="wikitable"
|+ Smoked
|-
| Threshold || 0.2g+
|-
| Common || 0.4g+
|-
| Heavy || 0.5g+
|}

{| class="wikitable"
|+ Sublingual (Wet Leaf)
|-
| Threshold || 10g+
|-
| Common || 30g+
|-
| Heavy || 50g+
|}

{| class="wikitable"
|+ Sublingual (Dried Leaf)
|-
| Threshold || 2g+
|-
| Common || 5g+
|-
| Heavy || 10g+
|}

== Duration ==

{| class="wikitable"
|+ All routes
|-
| Onset || 20-60 seconds
|-
| Total || 5-15 minutes
|-
| After-effects || 20-40 minutes
|}

== Effects ==

=== Postive ===

* Radical shift in perspective and perception

* Increase in sensual activity

* Introspective insight

* Powerful open/closed eye visuals

* Change in consciousness

=== Neutral ===

* Dissociation

* Perspiration

=== Negative ===

* Dysphoria

* Ataxia

* Dizziness

* Amnesia

* Nausea

== Harm Reduction ==

* Due to the ataxia and loss of body control, it is recommended to position yourself in a way that you will not aspirate during the experience (though vomiting from salvia is not a common occurrence).

* It is generally recommended to use a sitter while ingesting salvia, due to the mental intensity of the experience or potential for injury while in dysphoric state.

=== Potentiators ===

Users have reported an elongation and potentiation of the effects of the drug through using a [[MAOI]] such as Syrian Rue.

=== Interactions ===

== Chemistry and Pharmacology ==

The primary psychoactive constituent of salvia divinorum is a diterpenoid called salvinorin A, which is a potent k-opioid and d2 receptor agonist. Due to these properties, it has seen research indicating the drug may be of use as a treatment for opioid addiction - as well as providing research opportunities for the potential treatment of perception-altering diseases such as schizophrenia or Alzheimer's.

== Legal status ==

Salvia is legal in most countries, since its tendency to disable users and chemical safety mean that whiel users may not have a pleasant experience, it is very difficult to cause damage through physical or accidental means.

== Links ==

[https://en.wikipedia.org/wiki/Salvia_divinorum Wikipedia]

[https://www.erowid.org/plants/salvia/salvia.shtml Erowid]

[http://reddit.com/r/Drugs/comments/jkscw/rdrugs_ama_series_salvia_divinorum_salvia/?sort=top /r/Drugs FAQ]

[[Category:Drugs]]

[[Category:Dissociative]]

Cathinones

2017-06-09T07:13:04Z

Spacer: Created page with "Cathinone (also known as benzoylethanamine, or β-keto-amphetamine) is a monoamine alkaloid found in the shrub Catha edulis (khat) and is chemically similar to ephedrine, met..."

Cathinone (also known as benzoylethanamine, or β-keto-amphetamine) is a monoamine alkaloid found in the shrub Catha edulis (khat) and is chemically similar to ephedrine, methcathinone and other amphetamines. Cathinone differs from many other amphetamines in that it has a ketone functional group.

Other phenethylamines that share this structure include the stimulants methcathinone, MDPV, mephedrone and the antidepressant bupropion among others.

Cathinones has been found to stimulate the release of dopamine and inhibit the reuptake of epinephrine, norepinephrine and serotonin in the central nervous system (CNS).

The metabolites of cathinone, cathine and norephedrine also possess CNS stimulation, but create much weaker effects. The effects of cathinone on the body can be countered by a preceding administration of a dopamine-receptor antagonist.[12] The antagonist will keep the neuron at its resting state, so the cathinone cannot cause extraneous release of dopamine or other neurotransmitters.

It can also induce dry mouth, blurred vision and increased blood pressure and heart rate.

'''Experience'''

Cath's and syn cathinones are some of the dirtiest chemicals that do not have much positive effects. There form of action does not give much euphoria and can cause serious delusions.

Personally having done plenty in the past I can say that they should be avoided. Racing heart rate,, insomnia and delusions of police after you. Ultra focus is a side effect and as well as compulsive masturbation; paranoia. Avoid them at all costs... and if need be benzos can help bring you down. One of the better caths is Pentedrone; however, it is not so stimmy and has a nice euphoria.

User:Spacer

2017-06-07T19:01:28Z

Spacer: create user page

DXM

2017-06-07T18:41:30Z

Spacer: /* Extracted */

[[File:Romilarad.jpg|thumb|left|200px|Romilar 1968 Ad]]

'''Dextromethorphan''' (also known as 'DXM', 'DM' or 'robo') is an over-the-counter antitussive (cough medicine) which, when taken at doses exceeding the recommended therapeutic range, becomes a powerful [[Dissociatives|dissociative]] drug with psychedelic properties.

While DXM can be used safely it is not an inherently safe drug. Repeated use within a short period of time, combination with certain types of drugs, certain genetic factors and the prevalence of other active ingredients which become harmful at doses needed for disassociation make for a drug which must be used with caution.

The high is not for everyone; it is said to loosely follow the rule of thirds: one third hates it, one third doesn't care, and one third like it. It should not be underestimated as a hallucinogenic, at higher dosages it mimics high doses of ketamine but with more psychedelic properties.

DXM manifests its effects in a series of plateaus, with dose determining which plateau (and consequently which effects) one will experience. Lower dose plateaus can be well suited to relaxation, light social interaction and listening to music, while higher doses result in a more encompassing dissociative experience which does not lend itself to attentive social attention. At high doses it's common to have strong hallucinations, experiences of detachment, depersonalisation, and out-of-body experiences. These all-encompassing states can be startling and uncomfortable for some.

Its mechanisms of action are multiple, including action as a nonselective serotonin reuptake inhibitor and a sigma-1 receptor agonist. DXM and it's major metabolite, dextrorphan, also acts as an NMDA receptor antagonist at high doses, which produces effects similar to, yet distinct from, the dissociative states caused by other dissociative anaesthetics such as [[Ketamine]] and [[PCP]].

DXM does not typically show up in normal drug tests, however it can produce false positive results for PCP and/or opioids in extended or specialized drug tests. Occasional use should not produce these false-positive results after a couple days have passed.

== History ==

The racemic parent compound racemorphan was first described in a Swiss and US patent application from Hoffmann-La Roche in 1946 and 1947, respectively; a patent was granted in 1950. A resolution of the two isomers of racemorphan with tartaric acid was published in 1952, and DXM was successfully tested in 1954 as part of US Navy and CIA-funded research on nonaddictive substitutes for codeine.

The FDA approved DXM in 1958 after research supported its legitimacy and effectiveness as a cough suppressant. After its approval, it was introduced as an OTC medication under the name Romilar, which was introduced as a replacement for codeine containing cough remedies in an effort to cut down on abuse. In early 1960s Beat poets Allen Ginsberg and Peter Orlovsky, musicians such as Daevid Allen Soft Machine, and alternative authors such as Jack Kerouac known to have used DXM in the form of Romilar. In 1973, Romilar was taken off the shelves after a burst in sales because of frequent misuse, and was replaced by cough syrup in an attempt to cut down on abuse. In 1975, the popularity and extensive abuse of DXM was recognized, and Romilar was removed from the OTC market. However, DXM was specifically excluded from the Controlled Substances Act (CSA) of 1970, therefore, it was still legal to produce and use.

A few years after its removal from OTC, companies began introducing refined DXM products (e.g., Robitussin, Vicks-44, Dextrotussion) that were designed to limit recreational use by creating an unpleasant taste if consumed in large quantities. Within a short time those same manufactures began to produce forms of DXM with "some appealing flavoring," which led at least one researcher to suggest that the cycle of recreational abuse may be repeated. In 1996, DXM HBr powder could be purchased in bulk from online retailers, allowing users to avoid consuming DXM in syrup preparations.

== Different Forms ==

DXM is widely available in over-the-counter cough treatments which appear in different forms including gelcaps, lozenges and syrups. DXM is also less commonly found in a more pure powder form, either extracted or bought directly from a chemical manufacturer.

While there are some products available which contain only DXM as active medical ingredients it is common to find products which contain DXM but also contain enough of another active ingredient to pose a serious risk to the user's health.

=== Extracted ===

The ideal source of DXM would be pure powder or an extraction, but that requires time and a chemical procedure which most people are not equipped to do. It's not a complicated process, however it does carry some risks. There is a technique known as the 'Agent Lemon extraction'. [http://www.dextroverse.org/what-is-dxm/extraction/ Page with different extraction methods]

=== Pure DXM Hcl ===

Extracted forms of DXM Hbr still carry quite a few negative side effects that make the trip feel 'dirty'. There is another form of DXM Hcl (Hydrochloride) which is much cleaner than the Hbr that is in most syrups and gel caps. The Hcl form of DXM is the holy grail as it can be taken in a small capsule at doses around 500mg avoiding all the negative effects of the Hbr (Hydrobromide). Most woudl agree that it is far superior too Hbr and that it is quite close in effects to MDMA. Sadly is is very hard to find as it hasn't been synthesized in many years do to drug crack downs, even tho DXM is a OTC drug.

As a side note many MDMA pills in the early 2000's had DXM Hcl in them and many users would not feel the difference.

===Gel Caps===

DXM Gelcaps such as Robitussin Gelcaps or other no-name-brand products containing only DXM encased in a gelcap are often the preferred source for DXM users. For most users, gelcaps which contain only DXM produce a more clear headed high in lower doses. Most users experience fewer side effects from gelcaps than from syrup, however some users report an upset stomach, indicating that some users may have a sensitivity to the edible plastics used to make the gelcaps.

Some brands such as '''Cordicin Cough and Cold''' (also known as '''CCC''') have a variety of products, most of which contain other active ingredients such as antihistamines or CPM (Chlorpheniramine Maleate) and may have one or two products which contain only DXM.

'''WARNING''': Cordicin Cough & Cold is one of the most commonly used sources of DXM, and also one of the most dangerous. Nearly every single CCC product contains other active ingredients such as CPM, which can cause severe and life-threatening symptoms including seizures, shortness of breath or troubled breathing, weakness, loss of consciousness, severe dryness of the mouth, nose or throat, bleeding from the skin, mouth, eyes, rectum and vagina, and possibly death. CCC also is additionally harmful to your kidneys, liver and heart. Avoid it.

===Lozenges===

There are also sore-throat and cough medications containing DXM which exist in the form of a hard-candy like lozenge. These sometimes contain only DXM, however most brands of DXM lozenges also contain analgesics such as acetaminophen or benzocaine.

As always when using lozenges, choose a product which only has DXM in it.

=== Syrup ===

Cough syrup is the most common source for DXM users. While there are many brand name and no-name syrups which only contain DXM as an active ingredient there are many active and "inactive" ingredients commonly found in cough syrups which can cause negative effects ranging in severity. See [[DXM#Adulteration|Adulteration]] for more information.

Some have reported the high produced from syrup is mostly sedating. You may feel sluggish when using it to get high on DXM, possibly as a result of other ingredients found in syrup however because of the even dispersion of DXM throughout the syrup it is said to produce a more 'solid' trip.

===Delsym===

Delsym is brand with many formulations which contain Dextromethorphan Polistrex.

This is an extended release form of DXM which produces a longer lasting trip with weaker, more physical effects. It is somewhat more difficult to reach the third plateau using polistrex preparations, which may be preferable to beginners or users who would prefer these effects. Since it is an extended release dxm product, this means your enzyme is more able to keep up with the conversion of DXM to DXO, meaning more of a body high and less of the psychedelic DXM high. It is for this reason why it is difficult to reach 3rd plateau with polistrex. Generally, a 3rd plateau experience has a Higher percentage of DXM than DXO.

See Dosage information below

== Dosage ==

The dosage below refers to an "average" 180lbs / 80kg person taking DXM HBR. Before dosing it's important to note a few things:

* HBR and Polistirex doses vary significantly due to polistirex slow absorbsion rate.
**Dextromethorphan Polistrex, being extended release, means that your enzyme is more able to convert dxm into dxo. DXO being a more physical, less trippy drug, leads to this preparation of dxm feeling much less intense, and in many cases, very subtle. It is recommended to predose with grapefruit juice to fully enjoy polistrex because it slows down the conversion of dxm to dxo, effectively making polistrex "more trippy" because of a higher amount of dxm that didn't get converted.

* '''DXM doses are affected by weight'''. For more accurate dosage information, see the following resources:

* For a graphical chart of the dosage ranges [http://taimapedia.org/images/4/46/DXMDosingChart.png this chart] is helpful.

* For an easy calculator that does the math for you, [http://dxm.darkridge.com/calc.html this page] can be helpful.

'''Before dosing, be sure to read the Plateaus section to know which level you want to dose for.'''

{| class="wikitable"

|+ Plateau range dosage for a 80kg (180lb) person.

|-

| First || 122-200mg

|-

| Second || 200-600mg

|-

| Third || 600-1200mg

|-

| Fourth || 1200-1600mg

|-

| Risk of death || 2.2g+

|}

== Duration ==

{| class="wikitable"

|+ Oral HBR

|-

| High of 6-8 hours || Afterglow effect of 8-16 hours after dose, depending on dose

|}

{| class="wikitable"

|+ Oral Polistirex

|-

| High of 8-12 hours || Afterglow effect of 16-36 hours after dose, depending on dose

|}

=== Redosing ===

Redosing is not advised because of potential risk of risk of sigma. For more information, see [[DXM#Plateau Sigma|Plateau Sigma]]

It's better to know how much you've taken at the start of the trip, rather than guesstimate how much you're on as you keep dosing. The effects will start to come in waves and may not be pleasant. If you feel the need, it's recommended to take a high initial dose and a lower dose 1-2 hours in. As the duration of the trip is extended with dose boosting or redosing, the dysphoric aspects of the experience increase, until eventually most people report feeling like the walking dead. Not to mention by extending the duration of the trip you are increasing the chance for adverse effects and brain damage.

=== Predosing ===

Grapefruit juice effects dxm due to interactions with cytochrome P450-2D6. Essentially, it inhibits the enzyme that converts dxm to dxo, making a higher DXM:DXO ratio, meaning a higher, more psychedelic high, and less of a body high. With 1st and 2nd plateau, it can make it much more "trippy" and less of a physical high.<ref>http://medicine.iupui.edu/clinpharm/ddis/2d6references/#dextromethorphanSub</ref> <ref>https://en.wikipedia.org/wiki/CYP2D6</ref>

In order to properly predose, drink around 16oz (500mL) of grapefruit juice 1-2 hours prior to the point where you dose the dxm itself.

== Effects ==

As previously stated, the effects of this drug vary wildly from plateau to plateau, this list is in general from ALL plateaus.

=== Positive ===

* Euphoria, mood lift

* Increased giggling and laughing

* Dissociation of mind from body (positive when sought)

* Creative dream-like experiences

* Increased tactile sensation

* Some users report empathy and forgiveness towards other people

=== Neutral ===

* Pupil dilation

* Visual stop motion effect (flanging or strobing)

* Visual and aural (auditory) hallucinations

* Decreased sexual functioning (difficulty achieving orgasm)

* Confusion, disorientation

* Skin sensitivity, alters tactile (touch) and skin sensations

* Robotic, zombie-like walking, "robo-walk"

* Dis-coordination, reduced agility

* Loss of appetite

* Involuntary flexing of muscles

* Feelings of merging with adjacent objects like a couch or bed (with higher doses)

* Some users report feeling disconnected, isolated from others, (positive when sought)

=== Negative ===

* Vomiting

* Dizziness

* Body itching

* Rash, red blotchy skin (similar to a niacin rush)

* Diarrhea

* Fever

* Tachycardia (racing, pounding heart)

=== After-Effects ===

The after-effects of DXM are referred to as the afterglow.

The afterglow is almost non-existent on the First Plateau.

For a Second Plateau dose, the afterglow can be quite pleasurable, although some feel depressed/hungover afterwards for up to 14-16 hours after the initial dose. Expect to feel lazy and fairly tired the next day, easily remediable with caffeine and/or nootropics.

For a Third Plateau dose, the afterglow may additionally add a headache, feel more like an alcohol hangover, and almost like a 1st plateau trip for most of the day after. The effects of this may last for up to 16-20 hours, with some people feeling the "brain-dead", tired and lazy effects up to 72 hours! The tired and "brain-dead" effects can be remedied with caffeine and/or nootropics.

For a Fourth Plateau dose, don't plan anything for the day after, because you will be very "out of it" for a good 24-32 hours after dosing, with some people feeling the sedation/"brain-dead"/lazy effects up to 72 hours!. Definitely plan a Fourth Plateau dose at least a good 2 days away from social events, work, school, ect. (IE, do it Friday night/Saturday Morning if you have to work Monday). Eating becomes a difficult task during a Fourth Plateau afterglow. The best things to eat during this period are soft foods like yogurt, mashed potatoes, soups, and nutritional milkshakes like SlimFast or ENU Total Nutrition Meal Replacement Shakes. This afterglow may be fairly painful like an alcohol hangover, but can be slightly remedied with Ibuprofen/Acetaminophen, a multivitamin and the aforementioned supplements/food, caffeine and/or nootropics. . You will also appear to be extremely high from an outward appearance. Expect to feel very tired, lethargic and "brain-dead" for up to 72 hours.

=== Robo-Walk ===

The robo-walk feels like all of the muscles in your body are activated at once and while strange to the observer is not painful to the user. You can still walk but detailed coordination such as running, jumping, or maneuvering around furniture becomes much harder if not impossible. However, when you you start getting the effects of robo-walk, you really wouldn't want to be moving around anyway. The best thing to do is get a good pair of headphones, turn off the lights, close your eyes and let your mind wander.

It's similar to being overly aware that you are walking incorrectly and overcompensating because of it. Not much you can do about it except to minimize your walking by having everything ready before you start (food, water, triptoys, grapefruit juice, dxm in whatever preparation, ect).

== Plateaus ==

There are various 'stages' to DXM trips called ''plateaus''. Traditionally, there are only four plateaus that someone should try to aim for. All of them share general feelings of dissociation, but the strength and effects of these feelings are more pronounced in the later two plateaus.

The first two plateaus are commonly associated with a mix of being high on THC and drunk on alcohol. If you take a First Plateau dose, it's totally possible to socialize. At second, it becomes harder, but not impossible. Lower plateau doses are relatively easy to hide compared to higher plateau doses and talking with others becomes a lot easier while under the influence of DXM. It would also be fun to chill in your room alone and do whatever you normally do for fun, but it's suggested to try something that will take up most of your attention but allow your mind to wander at the same time. Something like playing a casual video game, or drawing whatever comes to mind.

If you take a Third or Fourth plateau dose, it is recommend to trip alone or with a close friend, as it is not a social drug at this dose. The best way to enjoy it is to lay back and listen to music with your eyes closed.

Choosing your destination plateau will depend a lot on what other drugs you've done and how comfortable you are with your own mind. People who have never tried any hallucinogen other than marijuana and/or alcohol should start with a First Plateau dose, while people with mushrooms or [[LSD]] experience could start at a Second Plateau dose. '''It is not advised to start at the Third or Fourth plateau''' unless you have extensive experience with other dissociatives.

=== First Plateau ===

The First Plateau is the lightest in effect. It feels a bit 'off', and is often likened to something of a cross between the effects of [[MDA]] and Alcohol. First plateau is usually slightly stimulating. The First plateau has also been described as "basically like a hit or two of good weed and 2-3 beers with 10 minutes of a 'trip' about 2 hours in."

Effects commonly experienced at the first plateau level

* A shift in thinking perspective; things look and feel 'different'

* Increased tactile sensation

* Increased appreciation of music

* Feeling heavy, sensation of increased body weight

* Enhanced emotional response & sensitivity

* Some dizziness or vertigo

'''First Plateau dose: 1.5-2.5mg/kg.'''

=== Second Plateau ===

This plateau is a bit more intense. You may feel like you are stoned and movement may become difficult. The second plateau can be fun yet disorienting. Music sounds much deeper, clearer, almost like you are there at the concert. Walking/Moving your body becomes slightly difficult at this point. Some may experience some closed eye visuals at this point. You can socialize with ''close'' friends and you could say you're slightly drunk. A slight warning, DXM is almost like a truth serum and you may share embarrassing or "secret" things you wouldn't normally share. You may start to get a bit of disassociation, and the high starts to get somewhat intense in the second plateau.

'''Second Plateau dose: 2.5-7.5mg/kg.'''

'''Transitional'''

Most people stop their DXM journey here, as the higher two plateaus are not really '''fun''' but ''introspective'' and ''enlightening''. We don't recommend crossing this threshold until you're ready to move on from a lighter, happier experience to a sometimes darker and definitely more introspective full blown trip. Enjoy the 2nd plateau as long as you can because it's more of a fun experience and one tends to enjoy second plateau less after visiting the third plateau. "Once you see what's behind the curtain, you can't enjoy the show" so they say.

Additionally, exactly at 7.5mg/kg there is an elusive "Eiffel Tower" dose where you may experience the effects of both the Second and Third plateaus simultaneously.

=== Third Plateau ===

Third Plateau is a full on dissociative experience. You cannot ignore the feeling inside of you and at this point its no longer a social drug and should be done by yourself or with a sitter. The third plateau isn't 'party-mode' or even 'socialize-mode'. Its more like 'alone-and-tripping-mode'. Closed eye visuals are more prominent at this level. You will lose track of time quit easily as it becomes meaningless quite quickly. Large amounts of dissociation happens at this level, and the internal thoughts can be quite interesting. To explain further, you may start to feel like you don't belong in your own body, or that your mind and body are two separate beings. Additionally, thoughts may be similar to "My body is only what everyone else sees but not really me, because I am just my mind, not my body."

'''Third Plateau dose: 7.5-15 mg/kg.'''

=== Fourth Plateau ===

This is the deep meditative state. This is most akin to a "k-hole" that people experience after taking large amounts of ketamine. Few people enjoy going this far, as all one can really do (or really wants to do) is sit, listen to music, close your eyes, and experience a full blown dissociative trip. You can create universes in your mind just by thinking of them. DXM users have been known to have extremely vivid, controllable hallucinations and out of body experiences at this level. Full blown disassociation from everything and full on ego death is very common at this level. Other very common hallucinations at this level are people visiting aliens, meeting god (sometimes the two being the same entity) and becoming god.
One explanation of the fourth plateau "It's kind of like the top of your skull pops off and all the knowledge of the universe is poured into your head, but by the end of the trip it's all seeped out again and you are left with the realization that you really don't much of anything at all."
Another explanation is : "A total detachment from the body. The ego is pulled inside. Everything is very distant. Walking, talking, moving is not possible. Thinking is however. Left free to observe the self from a dark quiet immobility. A strange taste in the mouth. Like the numb of the dentist in every tissue. Loss of emotion, loss of anything earthly. "

It is quite difficult to recall these very powerful hallucinations as post-trip amnesia is very common.

'''Fourth Plateau dose: 15mg/kg-20mg/kg. Higher is possible, but not advised, because risk of death around 25mg/kg, but varies slightly from person to person'''

=== Plateau Sigma ===

There is another level that DXM can take you to, but it is not higher in dosage than 4th plateau, it is more of an extension of 2nd and 3rd plateaus. In order to get to this state, you must binge. For this reason '''WE HIGHLY RECOMMEND AGAINST IT!''' For example, a user has said "I took a 3rd plateau dose, then when it was starting to wear off, I took a 2nd plateau dose, when that was finally coming down, I took a 3rd plateau dose again, and when that came down, I did ANOTHER 2nd plateau dose. When that final dose hit, I was stuck in Plateau Sigma."

Many people refer to this level as "plateau sigma" because when you get to this state, your sigma receptors are hit on, and HARD. This completely changes the trip. This mind state is generally referred to as dysphoric, dark, confusing and "a hellish introspective nightmare". As one user put it "it's a dark and confusing dream-like state where everything you think you know is insanely hard to grasp while all of your wildest, most bizarre fantasies are merely common, boring every day events that feel as normal as waking up and drinking coffee."

As with 4th plateau, it's hard to describe as amnesia is quite common and information about this state is quite rare as it is. That being said, this state has VERY RARELY been reported as being pleasurable '''AT ALL'''. Most people describe it as dark and confusing, like a living nightmare.

For more information, the William White FAQ has a section on Plateau Sigma at [https://www.erowid.org/chemicals/dxm/faq/dxm_experience.shtml#toc.5.9 This Page]

== Harm Reduction ==

There is only three '''MAJOR''' rules about dxm use, and they are as follows :

*'''NEVER''' use any preparation of DXM that has '''ANY''' other active ingredients, as they can make you sick and/or dead. See [[DXM#Adulteration|Adulteration]]
*Keep in mind this general rule of thumb for DXM : 1 plateau/week.
**In other words, If you take a Third Plateau Dose, wait 3 weeks before using again. If you use a Second Plateau dose, wait 2 weeks before using again.
*Watch out what you are mixing DXM with, as mixing with certain drugs can cause serotonin syndrome, or Ataxia, see [[DXM#Interactions|Interactions]]

See [[Dissociatives#Harm_Reduction|Dissociative Harm Reduction]] for general information.

=== Adulteration ===

Many products which contain DXM also contain other medication or otherwise non-medically-active ingredients that can cause serious harm in the doses found in DXM containing products. If a user intends to use an OTC cough medication in order to get high on DXM they almost always will have to consume a dangerous quantity of other dangerous ingredients if they are present in the medication. For this reason it is strongly recommended to find a source which contains '''''DXM''''' as the '''ONLY''' ''active'' ingredient

The following is a summary of other ingredients commonly found in DXM products.

{| class="wikitable"
|+ Adulterant Table
|-
| Name
| Description
| Common Brands
| Danger
|-
| Acetaminophen/Paracetamol/APAP
| a painkiller found in headache/flu medicine
| Tylenol, Vicks (NyQuil), TheraFlu, Triaminic
| is hepatoxic in high doses. This means it will damage your liver if taken in high doses. Your body can only process a certain amount of APAP at once before it the normal pathways become saturated Once the regular pathways used for metabolizing APAP have been saturated the remaining APAP gets broken down in the liver by an enzyme called ''cytochrome P450'' '''When forced to break down APAP this enzyme produces toxic metabolites!'''
|-
| Guaifenesin
| Guaifenesin is an expectorant.
| Robitussin DM, Mucinex, Robefen
| Guaifenesin overdoses cause severe nausea and vomiting in most users.
|-
| Antihistamines
| Found in Allergy/Sleep/Nighttime medications
| Coricidin Cough and Cold, Zicam, Dimetapp, Chloraseptic
| When taken in high doses antihistamines can cause dizzyness, nausea, a strong dysphoria, paranoia, delirium and hallucinations. Many antihistamines can also have a dangerous synergy with DXM
|-
| PPA, pseudoephedrine, and phenyleprine
| Decongestant agents
| Sudafed, Vescadril, Curedex, Watkins, Hardex
| Vasoconstriction (constriction of blood vessels) and decreased nasal secretions , and ''with larger doses'' insomnia, hypertension, heart rhythm abnormalities, hemorrhaging, stroke, or death. Note that these are extreme reactions, and that individual tolerance to sympathomimetics tends to vary considerably. Tolerance can build quickly, and a fatal dose for one person may have only a mild effect on another person.
|}
{| class="wikitable"
|+ Inactive Ingredients Adulterant Table
|-
| Name
| Description
| Common Brands
| Danger
|-
| Food Coloring/Dyes
| Dyes added for color
| Almost ALL brands except Zarbee's Naturals and Chestal Naturals
| Usually these dyes are not harmful in low doses however in doses which may be required for DXM's effects they can become problematic. '''Tartrazine (FD&C Yellow #5)''' is one of the most notable coloring ingredients to cause reactions. Not necessarily dangerous unless you are allergic to certain dyes. Check out the ingredients list if you are.
|-
| Glucose, sucrose, fructose, invert sugar
| Cough syrups usually contain one or more chemicals used to make them taste sweet.
| Pretty much all brands except Prospan, Diabetic Tussin and Scot-Tussin
| These sweeteners pose an obvious risk to people with blood sugar conditions such as diabetes or hypoglycemia. If you have diabetes or hypoglycemia, make sure you get a diabetic brand, gel-caps, or even an extraction instead of syrup. In rare cases, excessive, chronic use of cough syrup '''HAS''' led to people getting diabetes.
|-
| Propylene glycol or Polyethylene glycol
| Thickening agents
| Pretty much all brands of syrup
| These are not toxic nor inherently dangerous but may cause an upset stomach when consumed in large doses.
|}

=== Interactions ===

DXM has several potentially dangerous interactions with pharmaceutical and recreational drugs including analgesics (painkillers), antihistamines, antidepressants and stimulants.

DXM has the potential to cause [[Wikipedia:Serotonin Syndrome|Serotonin Syndrome]] if mixed with other serotonergic drugs such as [[Antidepressants|antidepressants]] that act as SSRIs, MAOIs, empathogens which affect serotonin release such as [[MDMA]], [[MDA]], [[Mephedrone]], [[Tramadol]], 2-c-t-x drugs, [[MXE]], aMT, 5-HTP, ect.
Serotonin Syndrome causes discomfort, excitability, irritability, diarrhea, moodswings, seizures, coma and can be deadly <ref>http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2464814/</ref> if not treated.

* See [[Drug_Combinations|Drug combinations]] and [[Dissociatives#Interactions|Dissociative Interactions]] for more information.

== Chemistry and Pharmacology ==

IUPAC:(4bS,8aR,9S)-3-Methoxy-11-methyl-6,7,8,8a,9,10-hexahydro-5H-9,4b-(epiminoethano)phenanthrene.

Dextromethorphan is the dextrorotartory enantiomer of levomethophan, which is the methyl ether of levophanol, both opioid analgesics.

=== Pharmacodynamics ===

{| class="wikitable"

|+ Binding receptors

|-

| NMDA - 7253

|-

| SERT - 2015

|-

| NET - 110606

|-

| Sigma-1 - 23

|-

| Sigma-2 - 240

|}

=== Pharmacokinectics ===

Following oral dosing, DXM is rapidly absorbed from the GI tract. Where it enters the bloodstream, and crosses the blood-brain barrier.

At therapeutic doses, DXM acts centrally (brain) as opposed to locally (Respiratory tract). It's rapidly absorbed from the GI tract into the active metabolite Dextrophan (DXO) in the liver by the cytochrome P450 enzyme CYP2D6.

Around 10 percent of the Caucasian population has little or no CYP2D6 enzyme activity, leading to long-lived high drug levels. ALL Caucasians should take a small test dose (1st plateau or medical levels) to feel for this ahead of time.

== Images ==

<gallery mode="packed-hover">

Image:Dxm1.jpg|''Robitussin brand DXM Gel Caps''

Image:Dxm_gelcap.jpg

</gallery>

== Links ==
* [http://tripsit.me/the-dexterous-world-of-dxm/ The Dexterous World of DXM from TripSit]
* [http://www.erowid.org/chemicals/dxm/faq/dxm_faq.shtml DXM FAQ]
* [https://www.erowid.org/chemicals/dxm/dxm_timeline.php DXM timeline on Erowid]
* [http://en.wikipedia.org/wiki/Dextromethorphan Wikipedia]
* [http://www.dextroverse.org Dextroverse]
== References ==

<references />

[[Category:Dissociative]]

[[Category:Drugs]]

Buprenorphine

2017-06-07T18:26:49Z

Spacer: /* Negative */

[[File:Suboxone.jpg|350px|right]]

'''Buprenorphine''' is a semi-synthetic opioid derived from thebaine which is typically used for treatment of opioid addiction. It is an analgesic, and has gained notoriety for its ability to successfully interrupt severe opiate addictions. Buprenorphine has a higher affinity for μ-opioid receptors compared to full opioid agonists. Because of this, buprenorphine can block the effects of other opioid agonists in a dose-dependent fashion. By its dual effects of reducing craving and attenuating the response to administered heroin, buprenorphine reduces the self-administration of heroin. Methadone, a full opioid agonist, also reduces the impact of additional heroin, but the effect of methadone is primarily due to the induction of cross-tolerance which is dose dependent. In contrast buprenorphine achieves its effect primarily by prolonged occupancy of a high proportion of opioid receptors, blocking the action of heroin and other opioid receptor agonists.

== History ==

Addiction therapeutics arose within the historical context of efforts to develop a non-addicting analgesic that began in the United States in the early 1920s. Early 20th century efforts to respond to the “opium problem,” through regulation and control at the source of supply and to address public health concerns through innovation in the research laboratory set the stage for the gradual shift in researchers’ interests toward developing a treatment for addiction therapeutics.

The solution to the “opium problem” was first sought at the laboratory bench at a time when the United States was becoming a major player within the evolving international drug control framework. For such a narrowly tailored goal to be understood as meeting a broad social problem of unclear etimology, it had to be translated into a feasible research program. Reliable methods to test compounds in animals and human beings had to be developed and validated. In the CDA’s first decade, some 150 compounds were produced and evaluated; all but one - Metopon (5-methylhydromorphone) - demonstrated the elusiveness of the goal.

Methadone was introduced into the United States in 1947 by Eli Lilly and Company, however, researchers opposed using methadone for maintenance given the results of studies on former morphine and/or heroin addicts in the late 1940s indicating that the subjects expressed increased satisfaction as dosage increased. They concluded that “narcotic drug addicts would abuse methadone and would become habituated to it if it were freely available and not controlled”. They also noted that methadone “completely alleviated the morphine abstinence syndrome in man,” yet itself exhibited a mild abstinence syndrome.

In 1974, Congress became concerned with methadone diversion and amended the Controlled Substances Act (CSA), in 1970 to give DEA considerable powers despite the inception of the National Institute on Drug Abuse (NIDA) and sunset of SAODAP in 1973. Many clinicians came to view the methadone regulations as government interference with the practice of medicine. The restrictive climate had led SAODAP to prioritize development of narcotic antagonists.

Buprenorphine was discovered in 1966, at the research labs of a home products company, Reckitt & Colman (hereafter Reckitts), in Hull, England.

The story of the development of buprenorphine as an "addict treatment" began in 1975, when Lexington Addiction Research Center (ARC) scientist Jasinski countered growing opposition to using prisoners as clinical research subjects by arguing that many prisoners were addicts and the pharmacology of buprenorphine made it such an “attractive candidate" as a treatment for opiate dependence that its human abuse potential was in urgent need of study.

Jasinski singled out buprenorphine as having an “especially unique pharmacology in man” because it produced “very little physical dependence”, even with chronic administration. Citing his 1978 study, he speculated that buprenorphine “would not only have a therapeutic application as an analgesic of low abuse potential but also as a new type of drug treatment of narcotic addiction."

Jasinski heralded buprenorphine’s unique potential because it alone produced long-lasting “changes in feelings that are acceptable to addicts,” and was “less toxic than methadone,” declaring that the committee’s 50-year project to “potentially utilize narcotics therapeutically to both relieve pain and treat addiction without the production of physical dependence” had yielded buprenorphine, which “appears to have the advantage of both methadone and naltrexone but without the major disadvantage of each”.

In 1979, following the ban on use of federal prisoners as research subjects, NIDA had moved the ARC’s Clinical Research Program, now under the direction of Jasinski, to the medical campus of The Johns Hopkins University (JHU) in Baltimore, Maryland; the preclinical program followed in 1981. The JHU site was chosen partly because Baltimore provided a suitable source of research subjects: inner-city heroin addicts. Addiction researchers considered it unethical and unwise to carry out research involving addictive substances on people who were not or had not been addicted.

By 1985, injectable buprenorphine had been marketed for analgesic applications in 29 countries and the sublingual tablet in 16 countries. In the United Kingdom, Reckitts had launched injectable buprenorphine for severe pain in 1978,with the sublingual analgesic following in 1982. It licensed Norwich–Eaton to distribute buprenorphine hydrochloride (Buprenex) in the United States, where the analgesic was launched in 1985, after FDA approval.

The difficulties of coordinating public and private interests, local and global effects, changes in domestic regulatory mechanisms, and perceptions of addiction and its treatment charted buprenorphine’s tortuous, 30-year path to FDA approval and market. Buprenorphine arose as a maintenance therapy at a time when addicts - like other citizens - were expected to take personal responsibility for health and healthcare, and where such decisions were seen as individual matters of choice and political entitlement.

== Uses ==

Buprenorphine is usually sold in the form of sublingual tablets (Suboxone), or transdermal patches (Butrans). Patches can be attached to skin for long release as treatment for opioid withdrawal, or cut and chewed for recreational use. Usual (30 minutes) sub-lingual use of patches is not 100% effective, so patches can be re-used. Buprenorphine is water-soluble, and can be extracted with a [[Cold Water Extraction]] (takes more time, usually 24 hours, or around 4 hours with few drops of strong alcohol). Since buprenorphine is a long acting opioid antagonist, other opioids won't work for at least 36 hours after dosing buprenorphine (though some negative effects will be garnered).

Buprenorphine will cause withdrawal if you have an opioid tolerance and don't wait long enough (typically 48~ hours) before taking it.

Respiratory depression from buprenorphine (or buprenorphine/naloxone) overdose is less likely than from other opioids. There is no evidence of organ damage with chronic use of buprenorphine, although increases in liver enzymes are sometimes seen. Likewise, there is no evidence of significant disruption of cognitive or psychomotor performance with buprenorphine maintenance dosing.

== Dosage ==

Dosage is usually 2-3mg (assuming 100% effectiveness), and most users don't feel the need to take more. Ceiling effect is 16-32mg, and redosing is not effective.

600µg is considered equivalent to 10 mg morphine for pain relief.

{| class="wikitable"
|+ Sublingual
|-
| Light || 1-2mg
|-
| Common || 3-6mg
|-
| Strong || 6-8mg
|-
| Heavy || 8mg+
|-
| Ceiling || 16-32mg
|}

== Duration ==

{| class="wikitable"
|+ Sublingual
|-
| Onset || 30-60 minutes
|-
| Peak || 1-4 hours
|-
| Total (low dose) || 8-12 hours
|-
| Total (high dose) || 24-72 hours
|}

== Effects ==

Because of its ceiling effect and poor bio-availability, buprenorphine is safer in high doses compared to full opioid agonists. The maximal effects of buprenorphine appear to occur in the 16–32 mg dose range for sublingual tablets. Higher doses are unlikely to produce greater effects.

=== Positive ===

* Euphoria

* Sedation

* Pain relief

* Elevated mood

* Overall feeling of contentedness

=== Neutral ===

* Pupillary dilation

=== Negative ===

* Dysphoric mood

* Piloerection

* Nausea or vomiting

* Diarrhea

* Muscle aches/cramps

* Yawning

* Lacrimation

* Mild fever

* Rhinorrhea

* Insomnia

* Craving

* Sweating

* Distress/irritability

* Dizziness and Vertigo

== Harm Reduction ==

Unlike methadone, the effect of buprenorphine on respiratory depression reaches a ceiling, therefore higher doses do not increase risk of respiratory depression to a significant degree.

However, if buprenorphine is used in combination with other central nervous system depressants, such as benzodiazepines and other CNS [[Depressants]], the combined effect on respiration can be life threatening.

=== Interactions ===

[[Drug Combinations]]

Combination of buprenorphine and SSRIs [http://www.ncbi.nlm.nih.gov/pubmed/18774063 can cause] Serotonin Syndrome.

== Chemistry and Pharmacology ==

Buprenorphine is a derivative of the opioid alkaloid thebaine that is a more potent (25 – 40 times) and longer lasting analgesic than morphine. It appears to act as a partial agonist at the μ- and κ-opioid receptors and as an antagonist at δ-opioid-receptors. The lack of δ-opioid agonism has been suggested to account for the observation that buprenorphine tolerance may not develop with chronic use.

Buprenorphine is metabolised by the liver, via CYP3A4 (also CYP2C8 seems to be involved) isozymes of the cytochrome P450 enzyme system, into norbuprenorphine (by N-dealkylation).

== Links ==

[https://en.wikipedia.org/wiki/Buprenorphine Wikipedia]

[https://erowid.org/pharms/buprenorphine/buprenorphine.shtml Erowid]

http://buprenorphine.samhsa.gov/about.html

[http://www.ncbi.nlm.nih.gov/pubmed/22256949 The history of the development of buprenorphine as an addiction therapeutic.]

http://www.nationaldrugstrategy.gov.au/internet/drugstrategy/publishing.nsf/content/9011C92D2F6E1FC5CA2575B4001353B6/$File/bupren1.pdf

[http://www.reddit.com/r/opiates/comments/1f3ak7/suboxone_faq/ /r/opiates Suboxone FAQ]

[[Category:Drugs]]

[[Category:Depressant]]

[[Category:Opioid]]