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 hydrochloride (also known as quebrachine) is a naturally-occurring stimulant substance of the indole alkaloid class derived from the bark of the African tree Pausinystalia johimbe. It is the major active constituent of the bark, with the active ingredient being yohimbine hydrochloride. 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.

Chemistry

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

Pharmacology

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Yohimbine antagonize alpha-2 adrenergic receptors, leading to increased blood flow to the genital area, where blocking the presynaptic alpha-2 receptors will lead to an increase in both nitric oxide and noradrenaline release. Blocking alpha-2 adrenoceptors increases blood pressure, releases insulin, and decreases blood sugar levels. Yohimbine also, however, interacts with alpha-1 adrenergic receptors, albeit with lower affinity, therefore, at higher doses an α1 blockade can occur and overwhelm the effects of the α2 blockade, making it difficult to predict the response (alpha-1 antagonism reduces blood pressure and overall CNS stimulation). 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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The effects listed below are based upon the subjective effects index and personal experiences of PsychonautWiki contributors. These effects should be taken with a grain of salt and will rarely (if ever) occur all at once, but heavier 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.

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 has a low toxicity relative to dose. Side effects associated with the use of yohimbine include anxiety, an increased urinary frequency, and increases in blood pressure at higher doses.[4] 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.[10]

Dependence and abuse potential

Yohimbine may potentially be mildly habit forming and the desire to use it may actually increase with use. However, in comparison to other more traditional stimulants such as amphetamine or methylphenidate, it is not nearly as addictive or compulsive.

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.[11] 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.[12]

Legal status

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 4.2 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. Yohimbine enhancement of exposure therapy for social anxiety disorder: a randomized controlled trial. (PubMed.gov / NCBI) | https://www.ncbi.nlm.nih.gov/pubmed/24237691
  7. Cognitive Enhancers for Anxiety Disorders (PubMed.gov / NCBI) | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3114287/
  8. 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
  9. Stimulation of the noradrenergic system enhances and blockade reduces memory for emotional material in man. (PubMed.gov / NCBI) | https://www.ncbi.nlm.nih.gov/pubmed/10576300
  10. Case study: two fatal case reports of acute yohimbine intoxication. (PubMed.gov / NCBI) | https://www.ncbi.nlm.nih.gov/pubmed/23846025
  11. 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
  12. 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