Antidote(s) for ED caused by antidepressants

January 12, 2011

Anyone who is taking an antidepressant, and also has ED (unless, perhaps, the

second came before the first), should be aware that their ED may be caused, at

least in part, by the antidepressant. Here's one link about the subject--

http://www.medscape.com/viewarticle/430614_5

I've often taken one of a couple of drugs (Amantadine or Bethanechol) during the

30-odd years I've been on my particular antidepressant, Nardil (an MAOI--and not

often prescribed today). They seem to have helped.

If it seems relevant, you may want to ask your doctor to prescribe an

appropriate anti- dote suited to the antidepressant you're on--and of course,

not likely to have adverse interactions or serious side-effects.

_________________________________________________________________________

From: < >

Subject: Digest Number 4652

Date: Wednesday, January 12, 2011, 7:08 PM

Men with Hypogonadism, Kleinfelters, etc

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F

January 13, 2011

I take Parnate, which is also an MAOI. If you can manage the dietary

restrictions, I have noticed also that the ED symptoms are lessened

considerably.

When I was on an SSRI or SSNRI like Effexor or Cymbalta, sometimes getting a

stable erection was next to impossible.

January 13, 2011

Clinically speaking once lifestyles, nutition imbalnace, sleep hygiene,

hormones, and underlying causes are identified and correct SSRI and other

psychiatric drugs are either reduce or stopped completely. There is only a small

percentage of people that need these drugs.

>

> I take Parnate, which is also an MAOI. If you can manage the dietary

restrictions, I have noticed also that the ED symptoms are lessened

considerably.

>

> When I was on an SSRI or SSNRI like Effexor or Cymbalta, sometimes getting a

stable erection was next to impossible.

>

January 13, 2011

You need to be a member to read this.

===============================================

Abstract & Introduction

Abstract

Sexual dysfunction is a common side effect of SSRIs, occurring in more than 30%

of patients.

Sexual side effects have emerged as a major clinical concern with many of the

newer antidepressants. Approximately 30% to 40% of patients on serotonergic

antidepressants experience sexual dysfunction. Clinical trials of techniques to

minimize or treat these side effects have been hampered by a lack of systematic

inquiry on sexual dysfunction in antidepressant-treated patients. General

strategies and specific drug antidotes to treat antidepressant-induced sexual

side effects are discussed. These include such drugs as cyproheptadine,

yohimbine, amantadine, buspirone, stimulants, and gingko biloba.

Introduction

Side effects associated with psychotropic medications are associated with

noncompliance that can potentially reduce clinical response to treatment.

Selective serotonin reuptake inhibitors (SSRIs) have emerged as the dominant

treatment for depression and other psychiatric disorders. However, sexual

dysfunction is a major side effect of this group of psychotropic medications.

Unfortunately, despite the astounding popularity of SSRIs in the US during the

past 10 years, information on the prevalence and treatment of SSRI-induced

sexual dysfunction is scant. This article reviews what is known about sexual

side effects of antidepressants and strategies to treat them, relying heavily on

the anecdotal data and case series that form the bulk of the published

literature.

Differential Diagnosis of Sexual Dysfunction

Depressed patients can manifest sexual dysfunction due to a variety of causes.

Clinicians should consider all possible causes before attributing sexual

dysfunction to a prescribed antidepressant (Table I).[1,2] Etiologies can be

grouped into 3 categories: (1) part of the presenting psychiatric disorder; (2)

comorbid physical or psychiatric disorders; and (3) drug-induced from medical

treatments.

Presenting Disorder

Psychiatric disorders themselves are associated with sexual dysfunction.

Depression is assumed to be linked with alterations in sexual functioning,

although the evidence for this assertion is less consistent than expected.[3]

Only a handful of experimental studies on sexuality in depressed individuals

have been published, and all these have evaluated only men.[3-9] These studies

show that diminished sexual satisfaction, as opposed to decreased sexual

interest or erectile dysfunction, is the most consistent finding in depressed

outpatient men.[3] This complaint of decreased satisfaction is probably related

to the diminished ability of many patients with depression to enjoy most

pleasurable activities.

Comorbid Disorder

Sexual dysfunction can occur as a primary condition from either a medical

disorder or from a poor relationship with the partner. Unfortunately, the rate

of primary sexual dysfunction in a normative population is still in doubt,

although the rate of DSM-IV hypoactive sexual desire is estimated at 20%.[10,11]

Rates of decreased libido in earlier studies of depressed patients have been

estimated as high as 77%.[12]

Given the number of possible causes of sexual dysfunction, clinicians should ask

about sexual function prior to prescribing antidepressants to any patient. A

minimal set of screening questions should include the 3 major areas of sexual

function: interest (or libido), arousal (erectile function in men, lubrication

and feelings of arousal in women), and orgasm.

Drug Effects

A number of medications besides psychotropics can cause sexual dysfunction,

including some antihypertensives and muscle relaxants. Antidepressants cause

sexual side effects in all 3 phases of the normal sexual response cycle,

including decreased libido, erectile dysfunction (in men), and delayed time to

orgasm or anorgasmia in men and women. In open case series of patients treated

with SSRIs, orgasmic dysfunction is the most common sexual dysfunction, followed

by decreased libido; arousal difficulties represent the least common form.[13]

Painful ejaculation was reported in as many as 20% of men in 2 case series of

men taking tricyclic antidepressants (TCAs).[14,15] As yet, this side effect has

not been reported to occur in association with the newer antidepressants such as

SSRIs, bupropion, nefazodone, and mirtazapine.

Paradoxically, antidepressants (especially those with serotonergic effects such

as SSRIs, monoamine oxidase inhibitors [MAOIs], and trazodone) have also been

reported, albeit infrequently, to cause occasional increased sexuality. Case

reports describe enhanced libido, spontaneous orgasm without sexual stimulation,

and spontaneous orgasm with yawning.[16-20]

Antidepressants and Sexual Dysfunction

All antidepressants are associated with potential sexual side effects. However,

it is difficult to estimate the percentage of patients experiencing these side

effects with any single antidepressant. This is because of the variability in

methodology between studies when ascertaining sexual side effects and because of

a paucity of studies specifically evaluating the rate of sexual side effects.

When patients in a recent study were asked about sexual dysfunction, the rate of

these complaints from SSRIs was 55%, compared with only 2% to 7% when sexual

side effects were voluntarily reported.[21]

Despite these methodological difficulties, patients taking the highly

serotonergic antidepressants -- SSRIs, clomipramine, and venlafaxine -- seem to

show the highest rates of sexual dysfunction, varying from 2% to 92%.[15,22] The

best estimate is that 30% to 40% of patients on serotonergic antidepressants

will have some sexual dysfunction. In descending order, MAOIs seem to be

associated with the next highest rate of sexual dysfunction, followed by TCAs.

Rates of sexual side effects seem to be consistently lowest with nefazodone,

bupropion, and mirtazapine. Rates of sexual dysfunction within a given drug

class are probably equal when equivalent dosages are compared.[13,23-25]

Treatment of Sexual Side Effects: General Strategies

Effective treatment of antidepressant-induced sexual dysfunction has advanced

little since it was first recognized as a significant problem within the last

decade.[26] No double-blind treatment study has yet been published, although one

with predominantly negative results has been presented.[27] The absence of a

systematic study precludes development of a clinically validated treatment

algorithm, since comparison of suggested treatments has not been researched.

Despite this limitation, treatment of antidepressant-induced sexual dysfunction

can be divided into general strategies and antidotes (Table II).[2]

General strategies for treating antidepressant-induced sexual side effects

include decreasing the dose, waiting, switching, and transient discontinuation.

Dosage Reduction

Clinical experience suggests that side effects are generally dose-related,

making dose reduction a reasonable first strategy to consider.[23,24] The

relative paucity of nonsexual side effects seen with SSRIs makes it likely that

at least some patients are on higher doses than necessary for antidepressant

efficacy. SSRIs typically show a flat dose-response curve in the treatment of

depression, meaning that increasing the doses above the typical doses

administered is not associated with greater efficacy.[28] The hope is that the

dose threshold for efficacy is lower than the dose threshold for sexual side

effects, thereby precipitating fewer side effects while preserving efficacy.[28]

The length of time needed for side effects to diminish after dose reduction

depends on the half-life of the antidepressant. With fluoxetine's long

half-life, a few weeks at the lower dose may be needed to evaluate the

regression of side effects. One study demonstrated that 14 days after

discontinuing fluoxetine, only 13% of patients with sexual side effects had

recovered orgasmic function.[29] For the other serotonergic agents, a period of

a few days (for venlafaxine and paroxetine) to a week (for sertraline and

fluvoxamine) is probably sufficient to evaluate the success of dose reduction in

diminishing sexual side effects.[30]

Drug Accommodation

This strategy of waiting for the patient to adjust to the medication is based on

the observation that other drug-induced side effects, such as nausea and

excessive stimulation, diminish after several days to weeks of treatment.[31] A

few case reports and case series have noted resolution of sexual dysfunction

secondary to administration of TCAs or SSRIs.[23,24,32,33] Although

accommodation to these side effects may occur, clinical experience demonstrates

that the patient usually experiences partial rather than absolute improvement,

and it can take many months of treatment, not days to weeks, before improvements

are noted.[20] For example, anorgasmia may diminish to delayed orgasm but rarely

to full baseline orgasmic function.

Drug Switching

Switching to a different antidepressant is a logical and effective strategy when

the first prescribed medication produces a higher rate of sexual dysfunction

than the alternative. This has been clearly demonstrated in studies in which

patients have switched from an SSRI to bupropion or nefazodone.[23,24,29,34]

In the few studies examining this strategy,[31,35] there is no evidence of a

depressive relapse when patients are switched across antidepressant classes.

However, reemergence of depressive symptoms is always a risk with this strategy.

Switching within a medication class is theoretically less risky for inducing

relapse, but its efficacy as a strategy for reversing sexual side effects is

less clear. Case reports have demonstrated successful switches from one TCA to

another.[35,36] Within the SSRI class, no systematic data exist, but anecdotes

about successful switches have been reported.[23,24] A study by Ashton and

colleagues[13] noted that sexual dysfunction with one SSRI did not necessarily

predict dysfunction with another; however, no data were provided.

Drug Discontinuation

The most controversial general strategy involves temporary discontinuation of

medication. This technique requires either discontinuing the antidepressant for

1 or 2 days or dramatically lowering the dose for several days.[24,37,38] In the

largest study examining this strategy, half the patients taking a short

half-life SSRI showed clear improvement in sexual functioning after a 2-day

discontinuation, whereas patients taking fluoxetine (with its long half-life)

showed no improvement.[37] Other cases have been described in which even a 1-day

discontinuation of fluoxetine resulted in diminished sexual side effects.[23]

One case report described the successful use of a partial drug holiday with

fluvoxamine to treat anorgasmia: Fluvoxamine was lowered from 300mg daily to

100mg daily for 2 days, and the patient had complete resolution of

anorgasmia.[38] However, then increasing the daily dose to 200mg rather than

restoring it to 300mg resulted in the

re-emergence of depression.

The strategy of transient medication discontinuation to treat side effects is

controversial because of the potential effects on mood, compliance issues, and

withdrawal symptoms. In a study by Rothschild,[37] discontinuation of medication

was associated with a mild increase in the scores for 2 of 20 patients on the

Hamilton Rating Scale for Depression. Some patients may view this strategy as an

indication that compliance with antidepressants is not to be attended to

seriously. Lastly, transient discontinuation of a short half-life serotonergic

medication (especially paroxetine or venlafaxine) confers the risk of inducing

an unpleasant withdrawal syndrome characterized by dizziness, light-headedness,

insomnia, fatigue, anxiety, nausea, and sensory disturbances.[39-41]

Treatment of Sexual Side Effects: Antidotes

A variety of antidotes have been reported to treat SSRI-induced sexual

dysfunction effectively; however, virtually all the data on these agents are

derived from open case reports and case series. Insofar as sexual function

improvement may be responsive to placebo effects, it is impossible to estimate

the true efficacy of these antidotes.[27]

Most of these antidotes either have serotonin-blocking properties (especially

5HT-2 antagonistic effects) or augment catecholamine activity, especially that

of dopamine. The antiserotonergic antidotes are cyproheptadine, buspirone,

nefazodone, and mianserin. Medications enhancing dopaminergic tone include

amantadine, bupropion, and stimulants, with yohimbine showing noradrenergic

effects. Among the reported antidotes, the only 2 without antiserotonergic

effects or catecholaminergic activity are gingko biloba and urecholine.

Cyproheptadine is an antihistamine with antiserotonergic properties that has

been reported for over a decade to reverse antidepressant-induced sexual

dysfunction. Only case reports and case series attest to its efficacy.[13,42-44]

Effective doses range from 2mg to 16mg. In the most recent and largest case

series, 12 of 25 patients described improvement in sexual function when treated

with cyproheptadine (mean dose, 8.6mg).[13] Anorgasmia is the sexual side effect

most often reported to be alleviated by cyproheptadine. Cyproheptadine is

effective when taken either on an as-needed basis (typically, 1 to 2 hours

before intercourse) or on a regular basis.

However, cyproheptadine's utility is often limited by its potential side

effects. Excessive sedation and the reversal of the therapeutic effect of the

antidepressant are major problems that limit its usefulness. Effectively treated

depression and bulimic symptoms have been reported to reemerge soon after

cyproheptadine was started.[42,45-48] This reversal of therapeutic effects is

itself reversible upon discontinuation.

Buspirone is a serotonin-IA partial agonist typically prescribed to treat

persistent anxiety. One case series reported that buspirone reversed both

decreased sexual interest and orgasmic dysfunction caused by SSRIs.[49] Most

patients using buspirone to treat sexual dysfunction take it daily. The dosage

is the same as that used for anxiety (15mg to 60mg daily). The mechanism of

action of buspirone in treating sexual dysfunction may be reduction of

serotonergic tone via stimulation of presynaptic autoreceptors or the alpha-2

antagonist effects of one of buspirone's major metabolites,

1-pyrimidinylpiperazine.

Nefazodone and mianserin are antidepressants with strong postsynaptic blocking

properties. In one case report, nefazodone 150mg taken 1 hour prior to sexual

activity completely reversed sertraline-induced anorgasmia.[50] Mianserin, an

antidepressant with 5HT-2 and alpha-2 adrenergic antagonist properties, is

available in many countries but not in the US. It has been reported to reverse

serotonin reuptake inhibitor-induced sexual dysfunction in 9 of 15 patients.[51]

Mirtazapine is similar in its biological activity to mianserin and might also be

effective in reversing sexual side effects. No case reports or case series have

yet been published attesting to this, although clinicians have described such an

effect. The putative capacity of mianserin and mirtazapine to reverse sexual

side effects can be attributed either to their serotonergic activity or

presynaptic alpha-2 activity.

Amantadine, a dopamine agonist, is used both as an antiviral agent and as a

treatment for Parkinson's disease. It has been shown in a number of small case

series to reverse anorgasmia.[13,52-54] Reported effective doses have ranged

between 100mg to 400mg taken either on a daily or as-needed basis. In the most

recent case series, 8 (42%) out of 19 patients with SSRI-induced sexual

dysfunction improved with amantadine 200mg daily.[13] Given dopamine's

consistent effect as a neurotransmitter involved in sexual arousal, a number of

other dopamine agonists have been explored as treatments for sexual side

effects.[2,55,56]

Bupropion is another commonly touted antidote for SSRI-induced sexual

dysfunction.[57,58] It is assumed that the mechanism of action by which

bupropion reverses sexual side effects is its weak dopamine agonism. The

evidence for bupropion's efficacy is scant, except for unpublished, anecdotal

reports, one case report,[57] and a case series[58] in which 31 (66%) of 47

patients showed improvement when bupropion was added to the regimen along with

the serotonergic antidepressant. Most patients (18/31) with a successful outcome

responded to as-needed use of bupropion 75mg to 150mg. Libido, arousal, and

orgasmic difficulties were all effectively reversed. Fifteen percent of treated

patients stopped taking bupropion because of its stimulation side effects. It is

unclear whether bupropion doses need to be somewhat lower than usual when added

to fluoxetine or paroxetine, to compensate for pharmacokinetic interactions

resulting in increased bupropion levels.[59]

Stimulants, such as methylphenidate, D-amphetamine, and pemoline, are reported

to reverse a variety of sexual side effects caused by SSRIs or MAOIs.[60-62] Low

doses of 10mg-25mg of methylphenidate or D-amphetamine have been effective. One

should add stimulants to an MAOI with extreme caution because of the risk of a

hypertensive episode. However, use of an MAOI/stimulant combination has been

shown to be safe in a case series.[63] SSRI/stimulant combinations show no

similar risks.

Yohimbine is available with or without a prescription (and with unclear purity)

in health food stores. It is an alkaloid from the bark of Corynanthe yohimbi

(family, Rubiaceae) and has been used for decades to reverse erectile

dysfunction.[64-66] Its efficacy in treating sexual dysfunction may be

associated with its ability to block presynaptic alpha-2 adrenergic sites,

leading to enhanced adrenergic tone.[65] A variety of sexual side effects have

been reported to be alleviated by yohimbine in doses ranging from 2.7mg to

16.2mg daily, prescribed either on a regular 5.4mg 3 times daily basis or on an

as-needed basis with single doses up to 16.2mg.[13,67-69] In the largest case

series, 17 (81%) of 21 patients showed improvement of sexual side effects when

treated with yohimbine (mean dose, 16.2mg).[12]

Typical side effects associated with yohimbine include anxiety, nausea,

flushing, urinary urgency, and sweating. Yohimbine has been the subject of the

only double-blind, placebo-controlled study to evaluate treatment of sexual

dysfunction occurring as a drug side effect.[27] Unfortunately, the placebo

effect was marked, showing a minimal drug-placebo difference with yohimbine

given at a dose of 5.4mg 3 times daily. Yohimbine is also available in lower

potency without a prescription. The purity, potency, and safety of these

preparations, however, are unknown.

Bethanechol is a cholinergic agonist that has occasionally been useful in

reversing sexual dysfunction associated with TCAs and MAOIs.[70-73] Typical

doses are 10mg to 20mg as needed or 30mg to 100mg daily in a divided dose.

Potential side effects with bethanechol include diarrhea, cramps, and

diaphoresis. No reports have evaluated or suggested the efficacy of bethanechol

for treating SSRI-induced sexual side effects.

Gingko biloba is an herbal extract reported to reverse a variety of sexual

dysfunctions associated with antidepressants. Information about gingko's ability

in this regard is derived from the experience of 1 clinician presenting a large

case series.[74] The response rate was greater than 80%, with doses ranging from

60mg twice daily to 120mg twice daily (mean daily dose, 207mg). Reported side

effects include gastrointestinal upset, lightheadedness, and stimulation

effects. Because gingko may inhibit platelet-activating factor, caution should

be used in considering its use by any patient with a bleeding diathesis. The

mechanism by which gingko might alleviate sexual dysfunction is unknown.

Summary

Treating sexual dysfunction associated with antidepressant medication is an

important but relatively unexplored issue in psychopharmacology. A thoughtful

diagnostic evaluation, including examination of the possibility that some sexual

difficulties attributed to the antidepressant may have another etiology, is

mandatory. Should the sexual dysfunction be reasonably attributed to the

antidepressant, both general and antidote treatments should be considered using

an individualized approach.

[ CLOSE WINDOW ]

References

Gitlin MJ: Psychotropic medications and their effects on sexual dysfunction:

Diagnosis, biology and treatment approaches. J Clin Psychiatry 55:406-413, 1994.

Gitlin MJ: Sexual side effects of psychotropic medications, in Dunner DL,

Rosenbaum JF (eds): Psychiatric Clin North Am Annual Drug Ther 4:61-90, 1997.

Nofzinger EA, Thase ME, Reynolds CF, et al: Sexual function in depressed men:

Assessment by self-report, behavioral and nocturnal penile tumescence measures

before and after treatment with cognitive behavior therapy. Arch Gen Psychiatry

40:24-30, 1993.

Howell JR, Reynolds CF, Thase ME, et al: Assessment of sexual function, interest

and activity in depressed men. J Affect Disord 13:61-66, 1987.

Roose SP, Glassman AH, Walsh BT, et al: Reversible loss of nocturnal penile

tumescence during depression: A preliminary report. Neuropsychobiology

8:284-288, 1982.

Thase ME, Nofzinger E, Reynolds CF, et al: Effect of antidepressant treatment on

sexual function in depressed men. Psychopharmacol Bull 30:83, 1994.

Thase M, Reynolds CF, Glanz LM, et al: Nocturnal penile tumescence in depressed

men. Am J Psychiatry 144:89-92, 1987.

Thase ME, Reynolds CF, Jennings JR, et al: Nocturnal penile tumescence is

diminished in depressed men. Biol Psychiatry 24:33-46, 1988.

Thase ME, Reynolds CF, Jennings R, et al: Diminished nocturnal tumescence in

depression: A replication study. Biol Psychiatry 31:1136-1142, 1992.

S: The epidemiology of the DSM-III psychosexual dysfunctions. J Sex

Marital Ther 12:267-281, 1986.

Sadock VA: Normal human sexuality and sexual dysfunctions, in Kaplan HI, Sadock

BJ (eds): Comprehensive Textbook of Psychiatry, ed 6. Baltimore, &

Wilkins, 1995, pp 1295-1321.

Casper RC, Redmond DZ, Katz MM, et al: Somatic symptoms in primary affective

disorder. Arch Gen Psych 42:1098-1104, 1985.

Ashton AK, Hamer R, Rosen R: Serotonin reuptake inhibitor-induced sexual

dysfunction and its treatment: A large-scale retrospective study of 596

psychiatric outpatients. J Sex Marital Ther 23(3):165-175, 1997.

Balon R, Yeragani VK, Pohl R, et al: Sexual dysfunction during antidepressant

treatment. J Clin Psychiatry 54:209-212, 1993.

Monteiro WO, Noshirvani HF, Marks IM, et al: Anorgasmia from clomipramine in

obsessive-compulsive disorder: A controlled trial. Br J Psychiatry 151:107-112,

1987.

Gartrell N: Increased libido in women receiving trazodone. Am J Psychiatry

143:781-782, 1986.

Modell JG: Repeated observations of yawning, clitoral engorgement, and orgasm

associated with fluoxetine administration. J Clin Psychopharmacol 9:63-65, 1989.

Letter.

DM, Levitte SS: Association of fluoxetine and return of sexual potency in

three elderly men. J Clin Psychiatry 54:317-319, 1993.

Sullivan G: Increased libido in three men treated with trazodone. J Clin

Psychiatry 49:202-203, 1988.

Ellison JM: Exercise-induced orgasms associated with fluoxetine treatment of

depression. J Clin Psychiatry 57:12 596-597, 1996.

Montejo AL, Llorca G, Izquierdo JA, et al: Sexual dysfunction with SSRIs: A

comparative analysis. New Research Programs and Abstracts of the Annual Meeting

of the American Psychiatric Association, New York, 1996, p 266. Abstract NR717.

Physician's Desk Reference. Montvale, NJ, Medical Economics Co., 1995.

Hsu JH, Shen WW: Male sexual side effects associated with antidepressants: A

descriptive clinical study of 32 patients. Int J Psychiatry Med 25:191-201,

1995.

Shen WW, Hsu JH: Female sexual side effects associated with selective serotonin

reuptake inhibitors: A descriptive clinical study of 33 patients. Int J

Psychiatry Med 25:239-248, 1995.

Modell JG, Katholi CR, Modell JD, et al: Comparative sexual side effects of

bupropion, fluoxetine, paroxetine and sertraline. Clin Pharmacol Ther

61:476-487, 1997.

Herman JB, Brotman AW, Pollack MH, et al: Fluoxetine-induced sexual dysfunction.

J Clin Psychiatry 51:25-27, 1990.

sen FM: A double-blind placebo-controlled trial of yohimbine for treatment

of SRI-induced sexual dysfunction. New Research Program and Abstracts of the

Annual Meeting of the American Psychiatric Association, New York, 1996, p 266.

Abstract NR716.

Beasley CM, Bosomworth JC, Wernicke JK: Fluoxetine: Relationships among dose,

response, adverse events, and plasma concentrations in the treatment of

depression. Psychopharmacol Bull 26:18-24, 1990.

PW, Cole JO, Gardner EA, et al: Improvement in fluoxetine-associated

sexual dysfunction in patients switched to bupropion. J Clin Psychiatry

54:459-465, 1993.

Herran A, Palacios-Araus L, Vazquez-Barquero JL, et al: Sexual dysfunction

associated with serotonin specific reuptake inhibitors. J Clin Psychopharmacol

17(1):67-68, 1997.

Gitlin MJ, Suri R: Management of side-effects of SSRIs and newer

antidepressants, in Balon R (ed): Practical Management of Psychotropic Drug

Side-Effects. New York, Marcel Dekker. In press.

Reimherr FW, Chouinard G, Cohn CK, et al: Antidepressant efficacy of sertraline:

A double-blind, placebo- and amitriptyline-controlled multicenter comparison

study in outpatients with major depression. J Clin Psychiatry 51(suppl

:S18-S27, 1990.

Labbate LA, Grimes JB, Hines AH, et al: Sexual dysfunction induced by SRIs.

Abstracts of the Annual Meeting of the American Psychiatric Association, San

Diego, 1997, pp 15-16. Paper Session # 12.

Ferguson JM, Shrivastava RK, Stahl SM, et al: Effect of double-blind treatment

with nefazodone or sertraline on reemergence of sexual dysfunction in depressed

patients. New Program and Abstracts of the Annual Meeting of the American

Psychiatric Association, New York, 1996, p 164. Abstract NR358.

Sovner R: Anorgasmia associated with imipramine but not desipramine: Case

report. J Clin Psychiatry 44:346-346, 1983.

Shen WW: Female orgasmic inhibition by amoxapine. Am J Psychiatry 139:1220-1221,

1982. Letter.

Rothschild AJ: Selective serotonin reuptake inhibitor-induced sexual

dysfunction: Efficacy of a drug holiday. Am J Psychiatry 152:1514-1516, 1995.

Nemeth A, Arato M, Treuer T, et al: Treatment of fluvoxamine-induced anorgasmia

with a partial drug holiday. Am J Psychiatry 153:1365, 1996.

Balon R: Drug holidays to counter sexual dysfunction. Am J Psychiatry

153:1370-1371, 1996.

Schatzberg AF, Haddad P, Kaplan EM, et al: Serotonin reuptake inhibitor

discontinuation syndrome: A hypothetical definition. J Clinical Psychiatry

58(suppl 7):S5-S10, 1997.

Coupland NJ, Bell CJ, Potokar JP: Serotonin reuptake inhibitor withdrawal. J

Clin Psychopharmacol 16:356-362, 1996.

Goldbloom DS, Kennedy SH: Adverse interaction of fluoxetine and cyproheptadine

in two patients with bulimia nervosa. J Clin Psychiatry 52:261-262, 1991.

McCormick S, Olin J, Brotman AW: Reversal of fluoxetine-induced anorgasmia by

cyproheptadine in two patients. J Clin Psychiatry 51:383-384, 1990.

Zajecka J, Fawcett J, Schaff M, et al: The role of serotonin in sexual

dysfunction: Fluoxetine-associated orgasm dysfunction. J Clin Psychiatry

52:66-68, 1991.

Feder R: Reversal of antidepressant activity of fluoxetine by cyproheptadine in

three patients. J Clin Psychiatry 52:163-164, 1991.

Katz RJ, Rosenthal M: Adverse interaction of cyproheptadine with serotonergic

antidepressants. J Clin Psychiatry 55:314-315, 1994.

Price J, Grunhaus LJ: Treatment of clomipramine-induced anorgasmia with

yohimbine: A case report. J Clin Psychiatry 51:32-33, 1990.

Zubieta JK, Demitrack MA: Depression after cyproheptadine: MAO treatment. Biol

Psychiatry 31:1172-1178, 1992. Letter.

Norden MJ: Buspirone treatment of sexual dysfunction associated with selective

serotonin reuptake inhibitors. Depression 2:109-112, 1994.

Reynolds RD: Sertraline-induced anorgasmia treated with intermittent nefazodone.

J Clin Psychiatry 58:89, 1997.

Aizenberg D, Gur S, Zemishlany Z, et al: Mianserin, a 5-HT2a/2c and alpha 2

antagonist, in the treatment of sexual dysfunction induced by serotonin reuptake

inhibitors. Clin Neuropharmacol 20(3):210-214, 1997.

Balogh S, Hendricks SE, Kang J: Treatment of fluoxetine-induced anorgasmia with

amantadine. J Clin Psychiatry 53:212-213, 1992. Letter.

Shrivastava RK, Shrivastava S, Overweg N, et al: Amantadine in the treatment of

sexual dysfunction associated with selective serotonin reuptake inhibitors. J

Clin Psychopharmacol 15:83-84, 1993.

Balon R: Intermittent amantadine for fluoxetine-induced anorgasmia. J Sex

Marital Ther 22: 290-292, 1996.

Bitran D, Hull EM: Pharmacological analysis of male rat sexual behavior.

Neurosci Biobehav Rev 11:365-389, 1987.

Segraves RT: Effects of psychotropic drugs on human erection and ejaculation.

Arch Gen Psychiatry 46:275-284, 1989.

Labbate LA, Pollack MH: Treatment of fluoxetine-induced sexual dysfunction with

bupropion: A case report. Ann Clin Psychiatry 6:13-15, 1994.

Ashton AK, Rosen RC: Bupropion as an antidote for serotonin reuptake

inhibitor-induced sexual dysfunction: A retrospective study. J Clin Psychiatry

59:112-115, 1998.

Kraupl TF: Loss of libido in depression. BMJ 1:305, 1972.

Bartlik BD, Kaplan PM, Kocsis JH, et al: Stimulants for SSRIs-induced sexual

dysfunction. New Research Program and Abstracts of the Annual Meeting of the

American Psychiatric Association, New York, 1996, p 246. Abstract NR644.

Gitlin MJ: Treatment of sexual side effects with dopaminergic agents. J Clin

Psychiatry 56:24, 1995.

Bartlik BD, Kaplan PM, Kaplan HS: Psychostimulants apparently reverse sexual

dysfunction secondary to selective serotonin reuptake inhibitors. J Sex Marital

Ther 21:264-271, 1995.

hner JP, Herbstein J, Damlouji NF: Combined MAOI, TCA, and direct stimulant

therapy of treatment-resistant depression. J Clin Psychiatry 46:206-209, 1985.

Morales A, Condra M, Owen JA, et al: Is yohimbine effective in the treatment of

organic impotence? Results of a controlled trial. J Urol 137:1168-1172, 1987.

RP: Nonoperative management of impotence. J Urol 139:2-3, 1988.

Reid K, Morales A, C, et al: Double-blind trial of yohimbine in treatment

of psychogenic impotence. Lancet 2:421-423, 1987.

Hollander E, McCarley A: Yohimbine treatment of sexual side effects induced by

serotonin reuptake blockers. J Clin Psychiatry 53(6):207-209, 1992.

sen FM: Fluoxetine-induced sexual dysfunction and an open trial of

yohimbine. J Clin Psychiatry 53:119-122, 1992.

Price J, Grunhaus LJ: Treatment of clomipramine-induced anorgasmia with

yohimbine: A case report. J Clin Psychiatry 51:32-33, 1990.

Gross MD: Reversal by bethanechol of sexual dysfunction caused by

anticholinergic antidepressants. Am J Psychiatry 139:1193-1194, 1982.

Sorscher SM, Dilsaver SC: Antidepressant-induced sexual dysfunction in men: Due

to cholinergic blockade? J Clin Psychopharmacol 6:53-55, 1986.

Wandzel L, Falicki Z: Reversal by bethanechol of imipramine-induced ejaculatory

dysfunction. Am J Psychiatry 144:1243-1244, 1987. Letter.

Yager J: Bethanechol chloride can reverse erectile and ejaculatory dysfunction

induced by tricyclic antidepressants and mazindol: Case report. J Clin

Psychiatry 47:210-211, 1986.

Cohen AJ: Gingko biloba for drug-induced sexual dysfunction. Abstracts of the

Annual Meeting of the American Psychiatric Association, San Diego, Calif., 1997,

p 15.

[CLOSE WINDOW]

Authors and Disclosures

Dr. Gitlin is Clinical Professor of Psychiatry, UCLA School of Medicine, Los

Angeles, Calif.

Co-Moderator

Phil

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