IngredientesYohimbe (Pausinystalia yohimbe), formerly known as Corynanthe yohimbe, is an evergreen tree native to Africa. It is one of a number of Corynanthe evergreen species growing in West and Central Africa in lowland forests. The tree grows about 30 meters (98 ft) tall, with a straight bole rarely larger than 50–60 cm in diameter. The bark is grey to reddish-brown, with longitudinal fissures, easy to peel and bitter-tasting. The inner bark is pinkish and fibrous. It is native to southwestern Nigeria, Cameroon, Gabon, and the Congo.
Yohimbe is the common English name for the tree species P. johimbe and, by extension, the name of a medicinal preparation made from the bark of that tree. In contrast, yohimbine is a pure alkaloid that can be isolated from yohimbe bark. Yohimbine is just one of at least 55 indole alkaloids that have been isolated from the bark; and, while it has been described as the most active of these, it constitutes only 15% of the total alkaloid content. Others include rauwolscine, corynanthine, and ajmalicine; the bark also contains non-alkaloids about which virtually nothing is known. Yohimbe, thus a complex mixture, has been studied far less thoroughly than yohimbine, the pure compound.
Yohimbine also occurs in many other plants such as the quebracho blanco plant of South America. It can also be produced synthetically—made in a laboratory—as yohimbine hydrochloride. Pharmaceutical-grade yohimbine is usually presented as the hydrochloride, which is more soluble.
The supplement comes from the bark of Pausinystalia yohimbe, an evergreen tree found in western and central Africa. It is sold in capsule or tablet form and marketed as yohimbe bark extract or yohimbine, the active ingredient in yohimbe bark. Bark—the most commercially important product—is used in extractions to make tinctures for traditional medicine and dietary supplements. Yohimbine is clinically utilized as a prescription drug with its main dosage forms in powder and tablets, and is also available for purchase on the internet as an herbal supplement and oral liquid.
The tree is sought out primarily for its bark; in practice, harvesting the bark kills the tree. Tree density is relatively low (average approximately 4 harvestable trees per hectare). The high demand for medicines based on the bark has led to the tree's over-exploitation. The bark is traded in local markets and, because it is scarce, it is often adulterated with that of other species which contain little yohimbine. The species is becoming endangered. Around the year 2000, Cameroon was shipping P. johimbe to Europe at the rate of about 100 tonnes annually. Most bark is collected illegally by local people who are paid 150 CFA francs per kilo for delivery of pre-dried bark at the roadside.
Yohimbine has been used for centuries in traditional medicine, with a long history of use in West African traditional medicine to treat several health ailments. Historically, yohimbe bark was used in western Africa for fevers, leprosy, and coughs. It has also been used to dilate pupils, for heart disease, and as a local anesthetic. It has a more recent history of use as an aphrodisiac and a hallucinogen.
Extracts from yohimbe bark are used in West African traditional medicine in the belief that it is a herbal tonic and aphrodisiac. Both the crude drug and yohimbine have a long history of use as aphrodisiacs in Western medicine in both prescription and herbal markets.
Some important drugs like tubocurarine, camptothecin, and yohimbine were derived from African medicinal plants. As Western pharmacology advanced in the late nineteenth century, yohimbine was isolated and named: yohimbine was named as originally extracted from the bark of yohimbe in 1896. Yohimbine has been widely used for erectile dysfunction and was one of the most widely prescribed agents prior to the age of sildenafil (Viagra) and other phosphodiesterase inhibitors.
Chemical constituents from yohimbe bark include tannins and indole alkaloids. Yohimbe bark contains about 6% total alkaloid, in which yohimbine represents 10–15%. The main phytochemical in the extract is the indoloquinolizidine alkaloid yohimbine. It also contains other alkaloids, such as corynanthine and raubasine, with undefined properties, adding further to concerns about its safety. The bark contains up to 6% of a mixture of alkaloids, the principal one being yohimbine, which is also known as aphrodine, quebrachine, or corynine. The presence and amount of alkaloid activity in P. johimbe bark is highly variable.
Yohimbine is a nitrogenous organic compound with the chemical formula C21H26N2O3 and a molecular weight of 354.44 g/mol. It is a 17α-hydroxyyohimban-16α-carboxylic acid methyl ester. Tryptophan and the secoiridoid monoterpene secologanin are the sources of this pentacyclic monoterpenoid indole alkaloid.
Yohimbine has two stereoisomers (rauwolscine and corynanthine) that differ little in their physical properties or in their effects on serotonin and dopamine receptors. The three isomers, however, do differ significantly in their affinity for the alpha-1 and alpha-2 adrenoceptor subtypes. Several yohimbine stereoisomers have been identified based on their stoichiometric arrangement. The alkaloids are divided into four subfamilies based on the stereochemical arrangement around the D-ring: normal, allo, pseudo, and epiallo.
The pharmacological activity of yohimbine is mediated by the combined action of the central and peripheral nervous systems. It selectively blocks the pre- and postsynaptic α2-adrenergic receptors and has a moderate affinity for α1 and α2 subtypes. Yohimbine also binds to other behaviourally relevant monoaminergic receptors in the following order: α-2 NE > 5HT-1A > 5HT-1B > 1-D > D3 > D2 receptors.
Yohimbine works primarily by blocking alpha-2 adrenergic receptors. This action increases the release of norepinephrine, a neurotransmitter that raises heart rate, blood pressure, and circulation. The venous plasma concentration of noradrenaline increased 3-fold within 15 min after yohimbine injection, while plasma adrenaline and neuropeptide Y-like immunoreactivity remained unchanged. The plasma concentration-effect relationship of the changes in circulating noradrenaline followed counter-clockwise hysteresis. The results show that the hyperadrenergic state elicited by therapeutic doses of the alpha-2-adrenergic autoreceptor antagonist yohimbine is due to an interaction with noradrenaline but not to release of adrenaline or NPY in man.
Its proposed mechanism of action for fat metabolism involves antagonizing α2-adrenergic receptors, which are involved in regulating fat breakdown. By blocking these receptors, yohimbine may increase noradrenaline release, thereby stimulating lipolysis. Administered prior to exercise, it boosts lipolysis and serum free fatty acid levels both during and following exercise; blockade of adipocyte alpha-2 adrenoreceptors makes at least a modest contribution to this pro-lipolytic activity. These considerations suggest that pre-exercise administration of yohimbine will lower the respiratory quotient during and following exercise, thus promoting fat loss.
Yohimbine blocks alpha-2 adrenergic receptors, part of the sympathetic nervous system. It also dilates blood vessels. Blocking of α2-adrenoreceptors also results in increased blood supply to cavernous body tissue and increased plasma levels of noradrenaline by increasing its release from the sympathetic nervous system.
Yohimbine inhibits monoamine oxidase (MAO) and therefore may theoretically be of benefit in depressive disorders. However, it does not have the clinical research of other herbs used for depression, such as St. John's wort.
At higher doses (exceeding 1 mg/kg), yohimbine's mechanism shifts to that of a 5-HT1A agonist, activating serotonin receptors and potentially influencing physiological parameters such as heart rate and body temperature. These higher doses also trigger the release of stress-related hormones like ACTH and corticosterone.
The kinetic disposition of yohimbine was examined in eight young male subjects following a single oral dose of 10 mg yohimbine hydrochloride. The drug was rapidly absorbed (absorption half-time 0.17 ± 0.11 h) and rapidly eliminated from the plasma (elimination half-life 0.60 ± 0.26 h). This clearance of yohimbine from plasma was constant over approximately 10 elimination half-lives, suggesting that distribution into a second pharmacokinetically distinct compartment was not responsible for the rapid decline in plasma yohimbine levels.
Absorption is complete and peak plasma levels occur at 45 to 60 minutes after 10 mg orally. The bioavailability showed great variability, ranging from 7 to 87%. A separate study confirmed this variability: the oral bioavailability showed great variability, ranging from 7% to 87% (mean value was 33%). The incomplete oral bioavailability of yohimbine may reflect either incomplete absorption from the gastrointestinal tract or a hepatic first-pass effect.
The distribution of yohimbine hydrochloride indicates a high tissue binding capacity. Yohimbine has a plasma protein binding of approximately 82%. Only a small amount of yohimbine hydrochloride and the active metabolite 11-hydroxyyohimbine is detectable in cerebrospinal fluid.
Only 0.5 to 1% of unchanged yohimbine was found in the urine, indicating that the major part of the drug was eliminated by hepatic clearance. Total plasma clearance was 117 L/h, which exceeds the hepatic plasma flow. This means that yohimbine is a high extraction drug with considerable extra-hepatic metabolism. The half-life varies between 0.25 and 2.5 hours after a single dose. The active metabolite 11-hydroxyyohimbine has a higher elimination half-life of about 6 hours.
Maximum plasma concentrations and area under the curve of the active 11-OH-metabolite were significantly lower in elderly subjects compared with young volunteers, and in patients with Alzheimer's disease. There is great variability in the plasma distribution of yohimbine. Clinical relevance of use in the elderly is not assessable.
Erectile dysfunction (ED) is the most extensively studied clinical application of yohimbine. Randomised placebo-controlled, double-blind clinical trials (RCTs) examined yohimbine (5 to 10 mg, 3 times per day) or yohimbine hydrochloride (5, 5.4, or 6 mg, 3, 4, or 8 times per day) orally for a period of 2 to 10 weeks. A systematic review and meta-analysis of these RCTs, drawing on MEDLINE (1966–1997), EMBASE (1974–1997), and the Cochrane Library, concluded that yohimbine is clinically more effective than placebo. Furthermore, it is relatively safe, its oral administration has obvious advantages, and its costs are low. These characteristics render yohimbine an attractive therapeutic option in the treatment of erectile dysfunction that should be considered as initial pharmacological intervention.
In one double-blind, placebo-controlled trial: this trial included 86 patients with erectile dysfunction and without clearly detectable organic or psychologic causes. Yohimbine was administered orally in a dosage of 30 mg a day (two 5 mg tablets three times daily) for eight weeks. Patients were seen for follow-up after four weeks' treatment, and for a final visit after eight weeks. Efficacy evaluation was based on both subjective and objective criteria. Subjective criteria included improvement in sexual desire, sexual satisfaction, frequency of sexual contacts, and quality of erection during sexual contact/intercourse. Objective criteria of outcome were based on improvement in penile rigidity determined by use of polysomnography in the sleep laboratory. Overall, yohimbine was found significantly more effective than placebo in terms of response rate: 71 vs. 45%. Yohimbine was well-tolerated: only 7% of patients rated tolerability fair or poor, and most adverse experiences were mild. There was no serious adverse event.
An earlier double-blind, placebo-controlled, partial crossover trial enrolled 48 subjects meeting strict diagnostic criteria for psychogenic impotence in a 10-week placebo-controlled, double-blind, partial crossover trial of yohimbine (18 mg a day) for restoring erectile function. At the end of the first arm of the trial, 62% of the yohimbine group and 16% of the placebo group reported some improvement in sexual function.
Despite these positive findings from clinical trials of the pure compound, the NCCIH (U.S. National Center for Complementary and Integrative Health) maintains that it is illegal in the United States to market an over-the-counter product containing yohimbine as a treatment for erectile dysfunction without getting approval from the FDA. There is not enough research to say whether yohimbe as a dietary supplement is helpful for any condition, including erectile dysfunction, athletic performance, or obesity. Although widely used to treat erectile dysfunction before the approval of newer drugs, current guidelines do not recommend its use.
Evidence assessment: Moderate-quality RCT and meta-analytic evidence supports the efficacy of pure yohimbine hydrochloride (the pharmaceutical compound) over placebo for psychogenic or mild-to-moderate ED. Evidence for yohimbe bark extract supplements specifically is insufficient, due to variable alkaloid content. Yohimbine for ED is not endorsed by contemporary clinical guidelines, which prioritize PDE5 inhibitors.
Yohimbine has been investigated as a potential adjunct in weight management strategies due to its purported effects on metabolism and lipolysis. Its proposed mechanism of action involves antagonizing α2-adrenergic receptors, which are involved in regulating fat breakdown. By blocking these receptors, yohimbine may increase noradrenaline release, thereby stimulating lipolysis and potentially promoting fat loss. Some studies have demonstrated modest weight reduction outcomes with yohimbine supplementation, particularly when combined with exercise and dietary modifications.
One frequently cited human trial is the Ostojic (2006) randomized, double-blind, placebo-controlled study: the study in 20 elite soccer players gave yohimbine 20 mg daily (split twice) for 21 days alongside their normal training. The yohimbine group lost 2.2% body fat versus the placebo group, with no significant change in lean mass, sprint performance, or vertical jump.
There is not enough evidence for the use of yohimbe- and yohimbine-containing dietary supplements for athletic performance or weight loss. Research studies on the effects of yohimbe and yohimbine on athletic performance are limited, involve a small number of participants, and provide inconsistent results.
Evidence assessment: Clinical evidence for fat loss is preliminary and limited. The available trials are small in sample size and short in duration. Mechanistically, the alpha-2 blockade rationale is plausible, but real-world effects in overweight populations are not well-established. The OPSS and NCCIH consider the evidence insufficient to support its use for weight loss.
Severely affected patients with autonomic failure may have residual sympathetic tone that can be engaged to increase blood pressure with the alpha-2 adrenergic antagonist yohimbine. This medication activates sympathetic outflow centrally and unrestrains norepinephrine release from noradrenergic neurons. In a clinical study at Vanderbilt University comparing yohimbine to pyridostigmine in patients with severe autonomic failure, yohimbine significantly improved standing diastolic blood pressure as compared to placebo (11 ± 3 mm Hg, 95% CI: 6 to 16, P <0.001). By contrast, pyridostigmine did not increase the standing diastolic blood pressure.
An earlier double-blind, crossover, placebo-controlled study tested the effect of low doses (4 mg three times daily) of yohimbine in 12 patients with depression and clomipramine-induced orthostatic hypotension. Yohimbine, a selective alpha-2-adrenoceptor antagonist, had a favorable effect in orthostatic hypotension and induced a significant increase in blood pressure.
Evidence assessment: Small but controlled clinical studies support a role for yohimbine in treating orthostatic hypotension secondary to autonomic failure and to tricyclic antidepressant use. Data are limited and this remains a specialized, clinically supervised use of the pharmaceutical-grade compound.
Yohimbine inhibits monoamine oxidase (MAO) and therefore may theoretically be of benefit in depressive disorders. The alkaloid yohimbine from the African yohimbe tree affects the nervous system in a way that may complement fluvoxamine. One report studied depressed people who had not responded to fluvoxamine. When 5 mg of yohimbine was added three times each day, there was significant improvement. Some people required higher amounts of yohimbine before their depression improved.
A 50-year-old woman who was unresponsive to traditional antidepressant therapy was reported to have a marked and persistent improvement in mood when yohimbine was added to her bupropion therapy. Further research is necessary to determine the significance of this finding.
Evidence assessment: Evidence for an antidepressant effect of yohimbine consists primarily of case reports and small uncontrolled clinical observations. No robust RCTs support its use for depression as a standalone therapy. The evidence is too weak to draw conclusions.
There is evidence from many studies that yohimbine, the active ingredient of yohimbe, can improve sexual problems associated with medications used for depression. Yohimbe contains a chemical called yohimbine which can increase blood flow and nerve impulses to the penis or vagina. It also helps counteract the sexual side effects of certain medications used for depression.
Evidence assessment: Preliminary evidence from controlled studies suggests yohimbine may partially reverse SSRI-associated sexual dysfunction. Study quality and sample sizes remain limited; this is not a standard clinical recommendation.
There is mixed evidence about the effectiveness of yohimbine for treating anxiety related to phobias. Some research suggests that it does not improve anxiety when combined with exposure-based therapy used to reduce fear of flying. However, other research suggests that taking yohimbine along with exposure-based therapy helps treat claustrophobia better than exposure-based therapy alone. The effect of yohimbe bark on anxiety is not clear.
Yohimbine, an alpha-adrenergic antagonist, is a noradrenaline probe that increases norepinephrine, autonomic activity, and awareness, thereby producing a panic-like state resembling a classic panic attack. Yohimbine induces mild anxiety and increases impulsivity in healthy volunteers, but has more detrimental effects in some psychiatric populations, triggering mania in bipolar patients and drug-craving in substance-dependent individuals.
Evidence assessment: The evidence on yohimbine and anxiety is mixed and context-dependent. As a pharmacological challenge agent (used in research to provoke noradrenergic activity and model stress responses), it is well-established. Its therapeutic role in anxiety disorders—including as an adjunct to exposure therapy—is limited and inconsistent.
Yohimbine is used clinically for the management of orthostatic hypotension secondary to autonomic failure, tricyclic antidepressant therapy, and dry mouth. Data are limited on the use of yohimbine for PTSD, orthostatic hypotension, athletic performance, and xerostomia.
Evidence assessment: Case series and limited studies have evaluated yohimbine for drug-induced dry mouth (xerostomia). Evidence is insufficient to support therapeutic use.
The following dosages reflect those reported in published clinical trials or referenced in authoritative sources; they are not recommendations.
Most yohimbe products do not say how much yohimbine they contain. The amount may vary a lot among products, according to a 2015 analysis of 49 brands of supplements labeled as containing yohimbe or yohimbine for sale in the United States. Some of the yohimbine was either synthetic or from highly processed plant extracts. Most of the supplements did not provide information about known side effects.
The quantity of the most active alkaloid, yohimbine, per recommended serving ranged from none detected to 12.1 mg. Only 11 supplement brands (22% of 49) listed a specific quantity of yohimbine on the label. Most of these were inaccurately labeled (actual content ranged from 23% to 147% of the content on the label). Eighteen percent (9 of 49) of the supplements' labels did not provide any information about yohimbine's adverse effects. Of the 49 yohimbine supplement brands sold at seven major retail chains in the USA, only 4.1% (2 of 49) provided consumers with both accurate information about the quantity of yohimbine as well as information about yohimbine's known adverse effects.
A total of 238 cases were identified in a retrospective review of the California Poison Control System (CPCS) over seven years (2000–2006). The majority (98.7%) of cases involved herbal (versus prescription) yohimbine products. Common reasons for use included sexual enhancement (27.7%), weight loss (9.2%), and stimulant effects (7.6%). Common adverse drug reactions reported included: gastrointestinal distress (46%), tachycardia (43%), anxiety/agitation (33%), and hypertension (25%). Yohimbine exposures were associated with a significantly greater proportion of severe outcomes and were more likely to require management at a health-care facility than the average substance exposure reported to the CPCS.
The adverse effects of yohimbine include gastrointestinal distress, hypertension, tachycardia, manic reactions, bronchospasm, palpitations, insomnia/anxiety, chills/cold/shivering, sweating, flushing, and headaches, which can be attributed to its central adrenergic activity.
Severe adverse drug reactions have constituted myocardial infarctions, atrial fibrillation, QTc prolongation, seizures, acute renal failure, and priapism. In 2007, the AAPCC's National Poison Data System disclosed that 60 yohimbine exposures out of the 277 reported had mounted to causing moderate to severe harm.
Elevated yohimbine levels, such as 8,000 µg/L (the highest ever reported in cases of yohimbine intoxication), have been associated with severe cardiovascular complications, including type II myocardial injury and acute, potentially fatal intoxication.
Yohimbine use has been associated with occasional severe adverse events, but has not been linked to serum enzyme elevations or clinically apparent acute liver injury. In small clinical trials and case series, yohimbine therapy has not been linked to serum enzyme elevations or clinical liver disease. Although yohimbine is often found in weight loss and muscle building herbal combinations, it has not been associated with cases of clinically apparent acute liver injury. Likelihood score: E (unlikely cause of clinically apparent liver injury).
Yohimbe should not be used if a person is taking types of antidepressant medications called monoamine oxidase inhibitors or tricyclic antidepressants. Yohimbe can interact with these medications.
Yohimbe products are among supplements with the largest number of documented contraindications, toxic effects, and severe events requiring hospitalization.
Yohimbine, a component of yohimbe, has been associated with cardiac arrhythmia (irregular heartbeat), blood pressure problems, heart attacks, and seizures. Because of inaccurate labeling and potential for serious side effects, yohimbe supplements have been restricted or banned in many countries.
Some of the chemicals in yohimbe bark, including yohimbine and rauwolscine, are stimulants that can increase mental alertness and energy levels. But the actual amount of each stimulant in yohimbe bark naturally varies. Some products may contain very high amounts of yohimbine and rauwolscine, which can cause serious side effects. Other products may contain low amounts that have no effects in the body.
It might be unsafe to use yohimbe orally (taken by mouth) during pregnancy or while breastfeeding.
Yohimbine induces mild anxiety and increases impulsivity in healthy volunteers, but has more detrimental effects in some psychiatric populations, triggering mania in bipolar patients and drug-craving in substance-dependent individuals.
Yohimbine hydrochloride was previously available as an FDA-approved prescription medication to treat certain types of erectile dysfunction with moderate results. Supplements containing yohimbe bark and its preparations (such as bark extract or yohimbine as a substance) are banned in Canada, Australia, the Netherlands, and the United Kingdom because of the potential harmful health effects.
Substances purported to be extracts from the yohimbe tree have been marketed as dietary supplements for various purposes, especially for erectile dysfunction, but they contain highly variable amounts of yohimbine, if any. In the United States, it is illegal to market an over-the-counter supplement product containing yohimbine as a treatment for any supposed health effect without having approval from the FDA.
Condiciones de salud que Yohimbe puede ayudar a apoyar.
Yohimbe bark contains yohimbine, an alpha-2 adrenergic receptor antagonist documented in peer-reviewed clinical trials to improve erectile dysfunction—one of the defining symptoms of andropause. Multiple controlled trials and meta-analyses support its efficacy for organic and psychogenic erectile dysfunction. It is one of the few plant-derived compounds with a well-characterized pharmacological mechanism for andropause-related sexual dysfunction.
Yohimbine has been investigated as an adjunct to exposure-based therapy for anxiety disorders and phobias, with mixed clinical results. Some randomized controlled trials show it can accelerate fear extinction and reduce self-reported anxiety when given prior to exposure sessions. Other trials, notably in virtual-reality treatment of flight phobia, found no benefit over placebo. At the same time, yohimbine itself can provoke anxiety as a side effect via noradrenergic stimulation.
Limited clinical evidence suggests yohimbine may modestly improve body composition in trained athletes, primarily via alpha-2 adrenergic blockade that enhances fat mobilization during exercise. A small RCT in elite soccer players found a significant reduction in body fat percentage over 21 days. Effects on direct performance metrics such as sprint speed or strength are inconsistent or absent. Evidence overall is limited and results are not uniform across studies.
Yohimbine has well-documented, pharmacologically verified effects on blood pressure. At standard oral doses it raises blood pressure in normal volunteers via increased sympathetic outflow and norepinephrine spillover; this effect is significantly greater in hypertensive patients. Conversely, it has been used therapeutically to raise blood pressure in conditions of pathologically low pressure such as neurogenic orthostatic hypotension.
Yohimbine has documented effects on peripheral circulation, primarily increasing norepinephrine spillover and raising blood pressure by blocking α2-adrenergic receptors. It has been studied for neurogenic orthostatic hypotension, where it can delay the blood pressure fall on standing by increasing sympathetic tone. Increased forearm blood flow at rest has been observed in controlled human studies.
Yohimbine has been investigated for depression primarily as an augmenter of antidepressant therapy rather than as a monotherapy. Early research suggests it does not reliably improve depression symptoms when used alone. Some clinical trial evidence indicates it may reduce self-reported depressive symptoms when given as an adjunct to exposure-based psychotherapy, though findings are not consistent. It is also studied for reversing SSRI-induced sexual dysfunction.
Yohimbine has clinical evidence supporting its use as a sialogogue (saliva stimulant), particularly for drug-induced xerostomia. Placebo-controlled trials demonstrate it significantly increases salivary secretion in healthy volunteers and in patients on psychotropic drugs. It works by blocking α2-adrenoceptors on salivary gland nerve pathways and by activating cholinergic mechanisms.
Yohimbe is the bark of Pausinystalia yohimbe, the primary natural source of the alkaloid yohimbine, which has established alpha-2 adrenergic blocking activity relevant to erectile function. It has long traditional use in West Africa as an aphrodisiac. Multiple RCTs of yohimbine (the purified alkaloid) support the mechanism; the bark extract is the traditional delivery form.
Yohimbine has been tested in clinical trials for fat loss, with mixed results. A well-cited RCT in elite soccer players showed a significant reduction in body fat percentage versus placebo over 21 days. However, other trials using higher doses in overweight men found no significant fat loss advantage. Overall, evidence suggests modest effects at low doses in conjunction with exercise and caloric restriction, particularly in a fasted state.
Yohimbine has documented effects on metabolic processes, primarily through increasing norepinephrine and stimulating lipolysis via α2-adrenergic receptor blockade. It raises circulating free fatty acids, potentiates postprandial insulin secretion, and has been shown to increase plasma norepinephrine but not adrenaline under chronic dosing in healthy volunteers. These are pharmacologically verified metabolic actions, though clinical endpoints such as sustained metabolic rate elevation remain less well-established.
Yohimbine has been studied in the context of diabetic neuropathy, specifically diabetic autonomic neuropathy and associated neurogenic orthostatic hypotension. It is listed as a pharmacological option for neurogenic orthostatic hypotension, including that arising from diabetic autonomic neuropathy, though with very low quality of evidence. It has also historically been noted as a use for diabetic nerve pain.
Yohimbine is pharmacologically classified as a thermogenic agent. It increases heat production in thermoneutral conditions by amplifying adrenergic and metabolic responses. Its thermogenic effect occurs through α2-adrenergic blockade leading to enhanced sympathetic activation, increased lipolysis, and facilitation of shivering thermogenesis, distinguishing it mechanistically from norepinephrine-driven non-shivering thermogenesis.
Traditionally, yohimbe bark was used in West African medicine as a tonic to reduce fatigue and enhance physical stamina, analogous in cultural context to ginseng. Modern use as an energy supplement is largely driven by its known stimulant properties via noradrenergic activation, but no dedicated clinical trials on energy or fatigue endpoints specifically have been identified in the literature.
Yohimbe (Pausinystalia johimbe) is the bark source of yohimbine alkaloid, used for generations in West Africa as an aphrodisiac and sexual stimulant. Traditional use predates pharmaceutical extraction and remains the basis for modern yohimbine supplements targeting male erectile function and libido.
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