Pausinystalia yohimbe

Common Names: Yohimbe, Johimbe

Clinical Names: Pausinystalia yohimbe, Corynanthe yohimbe

Summary

botanical name: Pausinystalia yohimbe, Corynanthe yohimbe

common name: Yohimbe, Johimbe.

overview of interactions:

• herb constituent affecting drug class toxicity: Monoamine Oxidase Inhibitors

• herbal constituent potentially affecting drug class performance and toxicity: SSRI's

• herb constituent affecting drug class toxicity: Tricyclic Antidepressants

• herb group synergy increasing activity: Neuroendocrine: Sympathomimetic Herbs

• herb group synergy increasing activity: Neuroendocrine: Antimuscarinic Herbs

AHPA Botanical Safety Rating: 2d




Clinical

botanical name: Pausinystalia yohimbe, Corynanthe yohimbe

common name: Yohimbe, Johimbe.

part used: Bark.

affinities: Eyes, genitals, sympathetic nervous system.

actions: Alpha-2 adrenergic antagonist, central nervous stimulant, vasodilator; yohimbine may inhibit monoamine oxidase (MAO).

dosage:
• Tincture: 5-10 drops three times per day.
• Standardized: Yohimbine component: 15-30 mg per day.

therapy:
• internal: Aphrodisiac (impotence), depression, posttraumatic stress disorder.

toxicity:
• LD50 (subcutaneous in mice for pure yohimbine hydrochloride) 40mg/Kg.
• May cause anxiety, psychic disturbances, tremor, tachycardia and hypertension with nausea and vomiting in excess.
• Patients with autonomic failure have increased sensitivity to Yohimbine.
• An early trial by Homberg and Gershon in 1961, claimed by Varro Tyler to show Yohimbe induced psychotic episodes in schizophrenic patients was based upon IV administration of high doses of pure yohimbine.
• Pausinystalia preparations are little used in modern herbal therapeutics, and availability is restricted in several countries. In the USA, despite FDA notices that the herb is unsafe and unproven as an "aphrodisiac", popular products containing Yohimbe and yohimbine are widely available.

contraindications:
• Excessive doses contraindicated in hypertension. Despite textbook claims of peripheral vasodilatation, yohimbine orally or intramuscularly causes sustained increases in blood pressure.
(DeSmet PAG, et al. 1997, 191-192.)
• Pregnancy and lactation. No data teratogenicity data is available; yohimbine has low mutagenicity and sedative effects on uterine muscle; however as with any powerful alkaloidal herb, it should be avoided during pregnancy and lactation.
(DeSmet PAG, et al. 1997, 199-200.)
• Commission E states without explanation that Yohimbe is contraindicated in pre-existing liver and kidney diseases. This is repeated by other sources, again without explanation.
(Blumenthal M, et al. 1998, 382: McGuffin M, et al.1997, 83.)

constituents:
• Alkaloid: Yohimbine and similar alkaloids.

clinical trials:
• Contraindications: Researchers in several double blind studies have found that yohimbine can be of benefit to men with impotence.
(Ernst E, Pittler MH. .J Urol 1998;159:433-436; Carey MP, Johnson BT. Arch Sex Behav 1996;25:341; Pittler MH, Ernst E. BMJ. 1998 Aug 15;317(7156):478.)

• Negative studies: Some researchers have been unable to confirm the therapeutic efficacy in the treatment of impotence.
(Kunelius P, et al. Urol 1997;49:441-444; Mann K, et al. Arch Sex Behav 1996;25:1-16.)



Interactions

herb constituent affecting drug class toxicity: Monoamine Oxidase Inhibitors

• research: According to animal screening studies, MAOI agents such as phenelzine increase the toxicity of yohimbine. Yohimbine has very weak MAOI activity.
(Quinton RM. B J Pharmacol 1963;21:51-66.)

• herbal concern: Despite lack of human data, individuals taking MAOI drugs would be prudent to avoid concurrent ingestion of yohimbine containing preparations.

herb constituent affecting drug class toxicity: Tricyclic Antidepressants

• mechanism: TCA's can interfere with uptake of norepinephrine, and yohimbine has been shown to interact with tricyclic antidepressants in human subjects. These studies were performed to examine whether yohimbine could ameliorate TCA adverse effects such as dry mouth; however the general finding is that a mutual increase in occurrence and intensity of adverse effects takes place when TCA's are combined with Yohimbine.

• research: Bagheri et al found that 10 mg of yohimbine increased both salivary outflow and plasma noradrenaline levels for four hours in patients treated with tricyclic antidepressants but also induced a relatively large number of side effects. However, they also determined that a lower dose of 4 mg of yohimbine increased salivary secretion for three hours without any side effects in patients treated with tricyclic antidepressants, though not in healthy volunteers, and could be useful in the treatment of dry mouth due to tricyclic antidepressants.
(Bagheri H, et al. Br J Clin Pharmacol 1994 Jan;37(1):93-96; Bagheri H, et al. Br J Clin Pharmacol 1992 Dec;34(6):555-558; Rispail Y, et al. Eur J Clin Pharmacol 1990;39(4):425-426.)

• herbal support: Individuals taking tricyclic antidepressants who are concerned about side effects such as dry mouth should not initiate use of Yohimbe or Yohimbine without first consulting their prescribing physician and/or a healthcare professional highly trained and experienced in herbal medicine.

herbal constituent potentially affecting drug class performance and toxicity: SSRI's

• herbal synergy: A potential synergy has been discussed between the alkaloid yohimbine from the African yohimbe tree and fluvoxamine based on the way they both affect the nervous system. While yohimbine itself is a prescription drug, standardized extracts of the herbal source yohimbe are commonly available. In one study individuals diagnosed with depression but unresponsive to fluvoxamine alone were given 5 mg of yohimbine three times each day in addition to the fluvoxamine. Apparently the combined effect was beneficial to a significant degree although some participants required higher doses of yohimbine in order to gain improvements in their depression.

• research: Sexual dysfunction, decreased sex drive, delayed ejaculation and difficulty achieving orgasm are common side effects associated with taking SSRI drugs. Various clinicians and researchers have suggested that yohimbine might act as a specific antidote to reverse these side effects in a limited number of cases.
(Gitlin MJ. J Clin Psychiatry. 1994 Sep;55(9):406-413. Schmauss M, Erfurth A. Fortschr Neurol Psychiatr 1996 Oct;64(10):390-402.)

• herbal support: Yohimbe is a powerful herb with significant potential for adverse side effects if improperly used. Individuals considering taking Yohimbe in relation to fluvoxamine or SSRI's are advised to consult with their prescribing physician and a healthcare provider trained in botanical medicine.

herb group synergy increasing activity: Neuroendocrine: Sympathomimetic Herbs

• mechanism: Yohimbine is known to have strong central alpha adrenergic antagonistic effects.
(DeSmet PAG, et al. 1997, 196.)

• herbal concern: Pausinystalia preparations containing yohimbine will additively synergize with the central stimulation actions of sympathomimetic herbs. Concurrent consumption should be avoided.

herb group synergy increasing activity: Neuroendocrine: Antimuscarinic Herbs

• mechanism: Pharmacological studies show a transient increase in toxicity of atropine when combined with yohimbine.
(DeSmet PAG, et al. 1997, 196.)

• herbal concern: Although these are not human studies, the potential for interaction between antimuscarinic herbs and Yohimbe theoretically exists. Recreational use, accidental toxicosis, or self-mediciation are more likely circumstances for this to occur.


Please read the disclaimer concerning the intent and limitations of the information provided here.
Do not rely solely on the information in this article.

The information presented in Interactions is for informational and educational purposes only. It is based on scientific studies (human, animal, or in vitro), clinical experience, case reports, and/or traditional usage with sources as cited in each topic. The results reported may not necessarily occur in all individuals and different individuals with the same medical conditions with the same symptoms will often require differing treatments. For many of the conditions discussed, treatment with conventional medical therapies, including prescription drugs or over-the-counter medications, is also available. Consult your physician, an appropriately trained healthcare practitioner, and/or pharmacist for any health concern or medical problem before using any herbal products or nutritional supplements or before making any changes in prescribed medications and/or before attempting to independently treat a medical condition using supplements, herbs, remedies, or other forms of self-care.



References

Bagheri H, Schmitt L, Berlan M, Montastruc JL. Effect of 3 weeks treatment with yohimbine on salivary secretion in healthy volunteers and in depressed patients treated with tricyclic antidepressants. Br J Clin Pharmacol 1992 Dec;34(6):555-558.
Abstract: The effect of yohimbine treatment (4 mg three times daily) for 3 weeks on salivary secretion was investigated. In healthy volunteers, acute administration of yohimbine increased salivary volume within 1 h to a similar extent before and at the end of the treatment period. In depressed patients treated with tricyclic antidepressants (and exhibiting a reduced salivary flow), yohimbine also acutely increased salivary volume. In contrast, the alpha 2-adrenoceptor antagonist failed to modify resting values measured in the morning (i.e. 10 and 14 h after the last administration in healthy volunteers and depressed patients respectively). This result indicates that alpha 2-adrenoceptor antagonists may have a potential therapeutic use in the treatment of dry mouth caused by tricyclic antidepressant drugs.

Bagheri H, Picault P, Schmitt L, Houin G, Berlan M, Montastruc JL. Pharmacokinetic study of yohimbine and its pharmacodynamic effects on salivary secretion in patients treated with tricyclic antidepressants. Br J Clin Pharmacol 1994 Jan;37(1):93-96.
Abstract: The pharmacokinetic parameters and the time course of the effect after acute oral administration of yohimbine on salivary secretion in patients treated with tricyclic antidepressants were investigated. Yohimbine (10 mg) increased both salivary outflow and plasma noradrenaline levels for 4 h. Pharmacokinetic parameters (t1/2, tmax, Cmax and AUCexp) and plasma concentrations of noradrenaline were higher in patients treated with tricyclic antidepressants than in controls. At this dose, yohimbine induced a relatively large number of side effects. A lower dose (4 mg) increased salivary secretion for 3 h without any side effects in patients treated with tricyclic antidepressants but not in healthy volunteers. These data describe an interaction between yohimbine and tricyclic antidepressants and thus show that a relatively low dose (4 mg) of yohimbine could be useful in the treatment of dry mouth due to tricyclic antidepressants.

Blumenthal M, Busse WR, Goldberg A, et al, eds. The Complete Commission E Monographs: Therapeutic Guide to Herbal Medicines. Boston, MA: Integrative Medicine Communications, 1998.

Bremner JD, Innis RB, Ng CK, et al. Positron emission tomography measurement of cerebral metabolic correlates of yohimbine administration in combat-related posttraumatic stress disorder. Arch Gen Psychiatry 1997;54:246-254.

Brinker F. Herb Contraindications and Drug Interactions. Second edition., Sandy, OR. Eclectic Institute Inc, 1998.

Cappiello A, McDougle CJ, Malison RT, Heninger GR, Price LH. Yohimbine augmentation of fluvoxamine in refractory depression: A single-blind study. Biol Psychol 1995 Dec 1;38(11):765-767.

Carey MP, Johnson BT. Effectiveness of yohimbine in the treatment of erectile disorder: Four meta-analytic integrations. Arch Sex Behav 1996;25:341.

Charney DS, Woods SW, Goodman Wk, Heninger GR. Neurobiological mechanisms of panic anxiety: Biochemical and behavioral correlates of yohimbine-induced panic attacks. Am J Psychiatry 1987;144:1030-1036.

DeSmet PAG, et al .(eds) Adverse Effects of Herbal Drugs 3. NY Springer Verlag, 1997.

Duke JA. CRC Handbook of Medicinal Herbs Boca Raton, FL. CRC Press, 1985, 351.

Ernst E, Pittler MH. Yohimbine for erectile dysfunction: A systematic review and meta-analysis of randomized clinical trials. J Urol 1998;159:433-436.
Abstract: PURPOSE: Erectile dysfunction is a common problem, particularly in diabetics. It is associated with a considerable burden of suffering. No generally accepted drug treatment exists. We systematically reviewed and meta-analyzed all randomized, placebo controlled trials of yohimbine monotherapy for erectile dysfunction to determine its therapeutic efficacy. Our secondary aim was to evaluate the safety of yohimbine. MATERIALS AND METHODS: We used computerized literature searches and standardized data extraction to rate methodological quality in a meta-analysis using computer statistical software. RESULTS: Seven trials fit the predefined inclusion criteria. Overall methodological quality of these studies was satisfactory. The meta-analysis demonstrated that yohimbine is superior to placebo in the treatment of erectile dysfunction (odds ratio 3.85, 95% confidence interval 6.67 to 2.22). Serious adverse reactions were infrequent and reversible. CONCLUSIONS: The benefit of yohimbine medication for erectile dysfunction seems to outweigh its risks. Therefore, yohimbine is believed to be a reasonable therapeutic option for erectile dysfunction that should be considered as initial pharmacological intervention.

Friesen K, Palatnick W, Tenenbein M. Benign course after massive ingestion of yohimbine. J Emerg Med 1993;11:287-288.

Gitlin MJ. Psychotropic medications and their effects on sexual function: diagnosis, biology, and treatment approaches. J Clin Psychiatry. 1994 Sep;55(9):406-413. (Review)
Abstract: BACKGROUND: The recognition and treatment of sexual side effects caused by psychotropic agents have become topics of increasing clinical concern. Gaps in our understanding of the biology of sex and in our knowledge of the effect of Axis I disorders on sexual functioning have made both recognition of sexual side effects and a coherent treatment approach to these side effects difficult. METHOD: The author reviews case reports, case series, and animal studies derived from a MEDLINE search for English language articles on the topics of the effects of psychiatric disorders on sexual functioning, the biology of sex, rates of sexual dysfunction associated with each medication class, and treatment approaches when these side effects occur. RESULTS: In evaluating sexual function in patients taking psychotropic medications, clinicians should first consider other potential causes of sexual dysfunction. In general, dopamine increases sexual behavior, serotonin inhibits it, while norepinephrine has conflicting effects. Sexual side effects have been described in association with all the major classes of psychotropic medications. Neuroleptics are often associated with sexual side effects. Priapism, seen with neuroleptics and trazodone, should be treated as a urological emergency. Anxiolytics cause mild, nonspecific sexual side effects as do the mood stabilizers. Among the antidepressants, the more powerful serotonergic medications--e.g., the serotonin selective reuptake inhibitors (SSRIs), clomipramine, and MAO inhibitors--may cause more sexual side effects than the tricyclics. Potential strategies to treat antidepressant-induced sexual side effects include lowering the dose, waiting, and switching to another agent. A number of specific antidotes, such as cyproheptadine and yohimbine, have been reported to reverse these side effects in a limited number of cases. CONCLUSION: Clinicians must be aware of and specifically ask about medication-induced sexual side effects. More effective treatments of these side effects must await much needed double-blind studies of various approaches, especially those to treat SSRI-induced sexual dysfunction.

Glasby JS. Encyclopedia of Alkaloids. New York: Plenum Press, 1975.

Goldberg KA. Yohimbine in the treatment of male erectile sexual dysfunction—a clinical review. Today’s Ther Trends J New Dev Clin Med 1996;14:25-33.

Holmberg G, Gershow S. Autonomic and Psychic Effects of Yohimbine Hydrochloride. Psychopharm. 1961;2:93-106.

Ingram CG. Some pharmacologic actions of yohimbine and chlorpromazine in man. Clin Pharmacol Therap. 1962;3:345-352.

Krystal JH, Webb E, Grillon C, Cooney N, Casal L, Morgan CA 3rd, Southwick SM, Davis M, Charney DS. Evidence of acoustic startle hyperreflexia in recently detoxified early onset male alcoholics: modulation by yohimbine and m-chlorophenylpiperazine (mCPP). Psychopharmacology (Berl). 1997 Jun;131(3):207-215.
Abstract: Preclinical studies suggest that acoustic startle amplitude is increased during ethanol withdrawal. The current study evaluated the effects of intravenous infusion of the alpha 2-adrenergic antagonist, yohimbine (0.4 mg/kg), the serotonin partial agonist m-chlorophenylpiperazine (mCPP, 0.1 mg/kg), and placebo administered to 22 male patients meeting DSM-III-R criteria for alcohol dependence and 13 male healthy subjects. Patients and healthy subjects completed 3 test days under double-blind conditions in a randomized order. Patients were sober for 12-26 days prior to testing. On each test day, participants completed startle testing 80 min following drug infusion. Stimuli with varying intensities (90, 96, 102, 108, 114 dB) were presented in a randomized order balanced across four blocks. Stimuli consisted of 40-ms bursts of white noise administered every 45-60 s for 15-20 min through headphones. Analyses indicated that patients exhibited elevated acoustic startle magnitudes on the placebo day relative to healthy subjects. In patients, the magnitude of startle amplitudes elicited at 90 dB, but not 114 dB, correlated significantly with the number of previous alcohol detoxifications. Yohimbine increased startle magnitudes and reduced startle latencies relative to placebo and mCPP in both patients and healthy subjects. mCPP did not alter startle magnitude in either group. Yohimbine also increased the probability that a 90-dB stimulus produced a startle response in healthy subjects, but not in patients. Blunting of yohimbine effects on startle probability may reflect the baseline elevations in startle probability levels in patients, but may also be consistent with other evidence of reduced postsynaptic, but not presynaptic, noradrenergic function in these same patients. These data replicate and extend previous reports indicating that yohimbine facilitates the acoustic startle response in humans. They also further implicate the number of episodes of ethanol withdrawal as a factor influencing subsequent neurobiological responsivity in chronic alcoholic patients. Based on the current data, future research should explore whether measurement of the acoustic startle response provides an objective quantitative severity measure of ethanol withdrawal.

Kunelius P, Häkkinen J, Lukkarinen O. Is high-dose yohimbine hydrochloride effective in the treatment of mixed-type impotence? A prospective, randomized, controlled double-blind crossover study. Urol 1997 Mar;49(3):441-444.
Abstract: OBJECTIVES: To determine the effectiveness and safety of high-dose yohimbine for the treatment of mixed-type impotence. METHODS: Twenty-nine patients who had mixed-type impotence diagnosed on the basis of a sexual history, results of a physical examination, laboratory analysis, assessment of the sensory pain threshold of the dorsal nerve of the penis, and dynamic color Doppler sonography of the cavernosal arteries were entered into a randomized, double-blind, placebo-controlled, crossover comparison of a placebo with high-dose yohimbine hydrochloride (36 mg per day orally). The treatment consisted of two 25-day courses; after a 14-day washout period, the patients who initially received the placebo for 25 days were switched to yohimbine hydrochloride for 25 days. Erectile function, ejaculation, interest in sex, physical examination findings, blood pressure, pulse rate, weight, and audiovisual sexual stimulation test were investigated before treatment and at the end of each drug period. The Mann-Whitney test was used for the statistical analysis. RESULTS: Twenty-seven patients (93%) completed the whole treatment schedule. Positive clinical results (complete and partial responses) were obtained in 12 cases (44%) at the end of the yohimbine phase and in 13 (48%) after the placebo period. No statistical difference was indicated. Drug-related adverse effects occurred in 2 patients in the yohimbine group (7%). CONCLUSIONS: Yohimbine is no better than placebo as a first-line treatment for mixed-type impotence.

Mann K, Klingler T, Noe S, Roschke J, Muller S, Benkert O. Effect of yohimbine on sexual experiences and nocturnal tumescence and rigidity in erectile dysfunction. Arch Sex Behav 1996 Feb;25(1):1-16.
Abstract: The therapeutic effect of the alpha 2-antagonist yohimbine in erectile dysfunction was studied in a double-blind placebo-controlled design. Thirty-one male patients underwent extensive clinical, urological, and psychiatric diagnosis and were dichotomically classified into an organic and a nonorganic subgroup. Following a 1-week placebo run-in period, patients were randomly assigned to a placebo or a verum group (yohimbine 15 mg daily) for a treatment period of 7 weeks. The Clinical Global Impression (CGI) scale was used as the primary efficacy parameter. Additionally, nocturnal penile tumescence and rigidity (NPTR) were measured. Global assessment of erectile function applying the CGI scale revealed, beyond a placebo effect in both organic and nonorganic patients, a therapeutic effect in the subgroup of nonorganic patients, with a significantly greater improvement in the yohimbine group compared to the placebo group. No superiority of yohimbine compared to placebo was found in the organic patients. These findings on the subjective level had no correlate in the NPTR recordings. The NPTR parameters were unchanged under yohimbine treatment in both the nonorganic and organic subgroup. No interrelation was found between subjective improvement and NPTR alterations. Polysomnographic control of the NPTR registrations ensured that the duration of REM sleep under treatment was not influenced.

McGuffin M, et al.(eds.) AHPA Botanical Safety Handbook . CRC Press, 1997.

Pittler MH, Ernst E. Trials have shown yohimbine is effective for erectile dysfunction. BMJ. 1998 Aug 15;317(7156):478. (Letter)

Quinton RM. The increase in the toxicity of yohimbine induced by imipramine and other drugs in mice. B J Pharmacol 1963;21:51-66.

Rasmusson AM, Southwick SM, Hauger RL, Charney DS. Plasma neuropeptide Y (NPY) increases in humans in response to the alpha 2 antagonist yohimbine. Neuropsychopharmacology. 1998 Jul;19(1):95-98.
Abstract: Previous studies have shown that the intravenous administration of yohimbine, an alpha 2 antagonist, increases norepinephrine turnover and has related anxiogenic effects in humans. We herein report that yohimbine also increases plasma neuropeptide Y (NPY) in healthy human subjects. This finding is consistent with previous reports in animals, but contrasts with a previously reported study in humans. NPY is a 36 amino acid peptide neurotransmitter located in sympathetic and nonsympathetic nerve fibers, as well as in brain structures such as the locus coeruleus, where it is colocalized with norepinephrine. NPY has been shown to inhibit locus coeruleus neuronal firing, decrease norepinephrine release, and increase postsynaptic noradrenergic signal transduction. When administered centrally, NPY also has anxiolytic properties. This study therefore suggests that yohimbine challenge may be useful in assessing NPY and noradrenergic system interactions in neuropsychiatric disorders such as panic disorder or post traumatic stress disorder in which noradrenergic system dysfunction has been observed.

Riley AJ. Yohimbine in the treatment of erectile disorder. Br J Clin Pract 1994;48:133-36.

Rispail Y, Schmitt L, Berlan M, Montastruc JL, Montastruc P. Yohimbine increases salivary secretion in depressed patients treated with tricyclic antidepressants. Eur J Clin Pharmacol 1990;39(4):425-426.

Sandler B, Aronson P. Yohimbine-induced cutaneous drug eruption, progressive renal failure, and lupus-like syndrome. Urology. 1993;41:343-345.

Schmauss M, Erfurth A. [Combination therapies in antidepressive drug refractory depression--an overview]. Fortschr Neurol Psychiatr 1996 Oct;64(10):390-402. [Article in German]
Abstract: Despite the availability of a wide range of effective antidepressant drugs, nearly 30% of depressed patients fail to respond to antidepressant treatment. Various pharmacological strategies have been developed to treat such refractory depression, of which augmentation therapies are one of the most important. This article reviews both benefits and risks of all known augmentation therapies. Among these treatment strategies the efficacy of lithium augmentation is very well documented by a large number of controlled studies - lithium augmentation can therefore be recommended in depression refractory to antidepressant treatment. The efficacy of triiodothyronine (T3) augmentation and the combination of different antidepressants - like a TCA-MAOI combination - is described in a large number of case reports and uncontrolled studies; the number of placebo controlled double blind studies, confirming the efficacy of these treatment strategies, is however relatively small. T3 augmentation and combined antidepressant treatment may therefore be considered in the treatment of refractory depression; in contrast to lithium augmentation these combination therapies are however only second-line strategies. Other augmentation therapies (TCA + stimulants, TCA + reserpine, TCA + yohimbine, TCA + fenfluramine, SSRI + buspirone) are very interesting clinical research strategies, but don't have too much importance in clinical practice at the moment.

Southwick SM, Morgan CA 3rd, Charney DS, High JR. Yohimbine use in a natural setting: effects on posttraumatic stress disorder. Biol Psychiatry. 1999 Aug 1;46(3):442-444.
Abstract: BACKGROUND: Numerous laboratory-based studies have shown that chronic posttraumatic stress disorder (PTSD) is associated with alterations in catecholamines. In a recent neuroendocrine challenge study, IV yohimbine caused exaggerated subjective, behavioral, cardiovascular and catecholamine responses among combat veterans with PTSD compared to healthy controls. Yohimbine is an alpha-2-adrenergic receptor antagonist that activates noradrenergic neurons. METHODS: This report describes the experience of 4 individuals with PTSD who took over-the-counter oral yohimbine that they had purchased from a health food store or pharmacy. RESULTS: All 4 subjects experienced a marked exacerbation of anxiety/panic and PTSD-specific symptoms immediately after ingesting yohimbine in a natural setting. CONCLUSIONS: The response in these individuals closely resembled the response observed after IV yohimbine in combat veterans with PTSD. The present cases occurred in a natural setting and thus complement laboratory-based findings. The authors caution against the recreational or medical use of yohimbine in individuals who have PTSD.

Spoerke DG, Jr. Herbal Medications. Santa Barbara, CA: Woodbridge Press Publishing Company, 1980.

Tyler VE, Brady LR, Robbers JE. Pharmacognosy. Ninth ed. Philadelphia: Lea and Febiger, 1988.