Talk:Yohimbine

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Summary sheet: Yohimbine
Yohimbine
Yohimbine.png
Chemical Nomenclature
Common names Yohimbine, Yocon, Yocoral or quebrachine
Systematic name methyl (1S,15R,18S,19R,20S)-18-hydroxy-1,3,11,12,14,15,16,17,18,19,20,21-dodecahydroyohimban-19-carboxylate
Class Membership
Psychoactive class Stimulant
Chemical class Indole alkaloid
Routes of Administration

WARNING: Always start with lower doses due to differences between individual body weight, tolerance, metabolism, and personal sensitivity. See responsible use section.



Oral
Dosage
Threshold 0.5 - 2 mg
Light 2 - 5 mg
Common 5 - 12 mg
Strong 12 - 25 mg
Heavy 25 mg +
Duration
Total 3 - 5 hours
Onset 15 - 30 minutes
Peak 1 - 2 hours









DISCLAIMER: PW's dosage information is gathered from users and resources for educational purposes only. It is not a recommendation and should be verified with other sources for accuracy.


Yohimbine (also known as quebrachine) is a naturally-occurring stimulant substance of the indoloquinolizidine class derived from the bark of the African tree Pausinystalia johimbe. It has various uses including as an aphrodisiac and a weight loss agent. Yohimbine is also used as a mydriatic and sympatholytic and has been suggested as an antidote to clonidine and xylazine overdose.

According to many users, yohimbine, in comparison with other psychoactive stimulants, is not a recreational substance and does not cause euphoria.

Chemistry

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Yohimbine is an indole alkaloid molecule of the indoloquinolizidine chemical class. It is structurally related to mitragynine but shows a totally different pharmacology.

Pharmacology

The primary and most researched mechanism of yohimbine is antagonism of a class of receptors known as alpha-2 adrenergic receptors, thus it increases noradrenaline levels by preventing their uptake into subsequent neurons. Blocking alpha-2 adrenoceptors increases blood pressure, releases insulin, and decreases blood sugar levels. Yohimbine also, however, blocking alpha-1 adrenergic receptors, albeit with lower affinity. It also has been shown to weak inhibit monoamine oxidase.[1]

In high concentrations yohimbine behaves as an antagonist at dopamine D2 and D3 receptors, serotonin 5-HT1B, 5-HT1D, and 5-HT2B receptors, and as a partial agonist at 5-HT1A.[2]

Subjective effects

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This subjective effects section is a stub.

As such, it is still in progress and may contain incomplete or wrong information.

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Compared to other stimulants, yohimbine can be described as less recreational. For many users, it is unpleasant, and often even with a small dosage causes anxiety and irritability.

Disclaimer: The effects listed below are taken from the subjective effect index, which is based on anecdotal reports and the personal experiences of PsychonautWiki contributors. As a result, they should be treated with a healthy degree of skepticism. It is worth noting that these effects will rarely (if ever) occur all at once, although higher doses will increase the chances of inducing a full range of effects. Likewise, adverse effects become much more likely on higher doses and may include serious injury or death.

Physical effects
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Cognitive effects
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Experience reports

There are currently no anecdotal reports which describe the effects of this compound within our experience index. Additional experience reports can be found here:

Toxicity and harm potential

Yohimbine is not known to cause harm in reasonable doses, and has an low toxicity relative to dose. Various studies have shown that in reasonable doses in a careful context, it presents few negative cognitive, psychiatric or toxic physical consequences, though some exist. Higher doses (200 – 5,000 mg) result in stronger side effects and can be toxic to the brain. Extremely high doses (above 5,000 mg) can be lethal.[7]

It is strongly recommended that one be familiar with harm reduction practices when using this drug.

Dependence and abuse potential

Yohimbine is not known to be not habit-forming and the desire to use it can actually decrease with use. It is most often self-regulating.

Tolerance to the effects of yohimbine are quickly built after repeated and frequent usage. After that, it takes about 7 days for the tolerance to be reduced to half and 14 days to be back at baseline (in the absence of further consumption). Yohimbine does not produce cross-tolerance with most other stimulants.

Dangerous interactions

Although many psychoactive substances are reasonably safe to use on their own, they can quickly become dangerous or even life-threatening when taken with other substances. The following lists some known dangerous combinations, but cannot be guaranteed to include all of them. Independent research should always be conducted to ensure that a combination of two or more substances is safe to consume. Some interactions listed have been sourced from TripSit.

  • MDMA - The neurotoxic effects of MDMA may be increased when combined with other amphetamines.
  • Cocaine - This combination may increase strain on the heart.
  • Stimulants - Yohimbine can be potentially dangerous in combination with other stimulants as it can increase one's heart rate and blood pressure to dangerous levels.
  • 25x-NBOMe & 25x-NBOH - Members of the 25x family are highly stimulating and physically straining. Combinations with stimulants should be avoided due to the risk of excessive stimulation. This can result in panic attacks, thought loops, seizures, increased blood pressure, vasoconstriction, and heart failure in extreme cases.
  • Alcohol - Alcohol can be dangerous to combine with stimulants due to the risk of accidental over-intoxication. Stimulants mask the sedative effects of alcohol, which is the main factor people use to assess their degree of intoxication. Once the stimulant wears off, the depressant effects of alcohol are left unopposed, which can result in blackouts and respiratory depression. If combined, one should strictly limit themselves to only drinking a certain amount of alcohol per hour.
  • DXM - Combinations with DXM should be strictly avoided due to DXM's effects on serotonin and dopamine reuptake. This can lead to panic attacks, hypertensive crisis, or serotonin syndrome.
  • MXE - Combinations with MXE may dangerously elevate blood pressure and increase the risk of psychosis.
  • Tramadol - Tramadol lowers the seizure threshold.[8] Combinations with stimulants may further increase this risk.
  • MAOIs - This combination may increase the amount of neurotransmitters such as dopamine to dangerous or even fatal levels. Examples include syrian rue, banisteriopsis caapi, 2C-T-2, 2C-T-7, αMT, and some antidepressants.[9]

Legal status

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This legality section is a stub.

As such, it may contain incomplete or wrong information. You can help by expanding it.

Yohimbine is legal in nearly all parts of the world.

See also

External links

References

  1. 1.0 1.1 1.2 1.3 1.4 1.5 1.6 1.7 1.8 Encyclopedia of Toxicology | https://www.sciencedirect.com/science/article/pii/B9780123864543007995
  2. Agonist and antagonist actions of yohimbine as compared to fluparoxan at alpha(2)-adrenergic receptors (AR)s, serotonin (5-HT)(1A), 5-HT(1B), 5-HT(1D) and dopamine D(2) and D(3) receptors. Significance for the modulation of frontocortical monoaminergic transmission and depressive states. (PubMed.gov / NCBI) | https://www.ncbi.nlm.nih.gov/pubmed/10611634
  3. Yohimbine and rauwolscine reduce food intake of genetically obese (obob) and lean mice. (PubMed.gov / NCBI) | https://www.ncbi.nlm.nih.gov/pubmed/6145164
  4. 4.0 4.1 Reference Module in Biomedical Sciences | https://www.sciencedirect.com/science/article/pii/B9780128012383988627
  5. Evidence for activation of both adrenergic and cholinergic nervous pathways by yohimbine, an alpha 2-adrenoceptor antagonist. (PubMed.gov / NCBI) | https://www.ncbi.nlm.nih.gov/pubmed/7557820
  6. Differential effects of noradrenergic drugs on anxiety and arousal in healthy volunteers with high and low anxiety. (PubMed.gov / NCBI) | https://www.ncbi.nlm.nih.gov/pubmed/9004342
  7. Case study: two fatal case reports of acute yohimbine intoxication. (PubMed.gov / NCBI) | https://www.ncbi.nlm.nih.gov/pubmed/23846025
  8. Talaie, H., Panahandeh, R., Fayaznouri, M. R., Asadi, Z., & Abdollahi, M. (2009). Dose-independent occurrence of seizure with tramadol. Journal of Medical Toxicology, 5(2), 63-67. https://doi.org/10.1007/BF03161089
  9. Gillman, P. K. (2005). Monoamine oxidase inhibitors, opioid analgesics and serotonin toxicity. British Journal of Anaesthesia, 95(4), 434-441. https://doi.org/10.1093/bja/aei210