Antidepressant-InducedSexual Side Effects: Mechanisms,
Symptoms and Treatment
Eli Lilly's (manufacturer of Prozac) clinical trials state that Prozac has a 4 hance of decreasing libido compared to a 0% risk of the placebo. Pfizer Inc. admits that Zoloft causes ejaculation failure or delay in 14% and decreased libido in 50f its users compared to a 10lacebo risk for both. SmithKline Beecham's Paxil creates ejaculatory disturbance in 13% and decreased libido in 30f patients compared to a 00lacebo risk for both. Sexual side effects of Wyeth-Ayerst's Effexor include a 2% risk of libido decrease, 12% risk of abnormal ejaculation/orgasm, 6 hance of impotence and a 2% risk of orgasm disturbance compared to a 0% risk of the placebo for all sexual side effects. These selective serotonin reuptake inhibitor (SSRI) and heterocyclic drugs are just a few of the many antidepressants currently available on the market (by prescription only; see table 1). The data above was the result of these pharmaceutical companies' respective clinical trials for their drug which was presented to and approved by the Food and Drug Administration (FDA) for public use (These clinical trials are still the basis for these drugs' proven safety and efficacy). The approval was expected and justified, as the sexual side effects and many other side effects (which are not the focus of this paper) were not very severe.
However, after approximately ten years of market stature, clinical practice has shown that the above drugs have a much higher risk of sexual side effects than previously reported by the pharmaceutical companies. This increased risk is true of other antidepressants as well. Physicians are now reporting that the actual rate of secondary sexual dysfunction (sexual side effects caused by antidepressant medication) is between 40 to 75% (Balon 1997). The risk may even be higher as patients might feel too uncomfortable talking to their doctors about sexual dysfunction. This is a serious problem that the medical and scientific community needs to address because antidepressants
are causing depression in a lot of patients due to their sexual side effects.
The purpose of this paper is to show that sexual dysfunction associated with antidepressant medication is a serious problem which needs to be addressed and needs more scientific research. I will explain the general, molecular mechanisms of antidepressant induced sexual dysfunction, the symptoms of sexual dysfunction and various treatment strategies. I will also explain why I am interested in this topic; I will discuss my personal experience with antidepressants which supports the purpose of this paper.
Molecular Mechanisms
The molecular mechanisms of drug induced sexual side effects are tough to describe because very little is known about the mechanisms of normal sexual arousal. Because so little is known about the brain's functions in general, hardly any studies have been done to decipher the sexual pathway. However, there are a few molecular mechanism predictions and hypotheses of antidepressant induced sexual side effects.
Antidepressants normally act by blocking the reuptake transporters of serotonin (5-HT), dopamine and/or norepinepherine neurons, thereby increasing the duration/concentration of these monoamines in the synapse. Currently there are tricyclic, heterocyclic, SSRI and monoamine oxidase inhibitor (MAOI) antidepressants available on the market. SSRI's, the newest and most popular medication, only block serotonin reuptake transporters while the tricyclics and heterocyclics can block one or more of the above neurotransmitter reuptake transporters. The MAOI's are different in that they inhibit an enzyme in the presynaptic nerve terminal called monoamine oxidase which breaks down the monoamines. This inhibition produces a higher concentration of monoamines in the nerve terminal.
Four different mechanisms exist by which antidepressants can influence sexual functioning (Gitlin 1994): they can cause, (1) general central nervous system (CNS) effects such as sedation which will decrease sexual interest and function; (2) specific CNS effects by altering neurotransmitter concentration in certain parts of the brain; (3) specific peripheral effects by tinkering with neurotransmitter concentration at sexual end-organ sites; and (4) hormonal effects by altering hormonal levels which modulate sexual functioning. Antidepressants can have multiple mechanisms which may be contradictory. For example, "...an antidepressant may enhance sexual interest through CNS arousing mechanisms, while diminishing the expression of that interest by altering aspects of peripheral erectile function. For each medication and for each individual, the ultimate clinical result would express the multiple competing influences of central and peripheral effects (Gitlin 1995)." As far as neurotransmitters generally affecting sexual function, dopamine increases sexual behavior, serotonin inhibits sexual behavior, and norepinepherine does both due to the competing influences mentioned above (Gitlin 1994). I will refer to the above theory as the neurotransmitter hypothesis, which is the most common to date.
Additional evidence and theories surrounding this hypothesis exist. If elevated serotonin levels inhibit sexual function, than blocking postsynaptic serotonin receptor subtypes should increase sexual behavior. In fact, antagonists of the 5-HT type 2 postsynaptic receptor increase sexual function (Moore and Rothschild 1999). Also, central adrenergic (including alpha 2, which is a presynaptic receptor, antagonists) and central dopaminergic activation appears to increase sexual behavior and functioning.
An experimental study done by Nedergaard, Mellerup and Plenge in 1998 investigated a possible, common serotonergic mechanism in the mediation of the common sexual side effects of the antiandrogen cyproterone acetate (CPA) (which inhibits sexual behavior) and the SSRI, Paxil (paroxetine). Four groups of sexually active and experienced male rats were observed for four weeks. One group was administered CPA, another received Paxil, a third group was castrated and given saline, and the last group was the control which was given only saline. After four weeks, the male rats were introduced to sexually normal female rats. The number of mounts needed to reach ejaculation was significantly increased for the CPA and Paxil groups compared to the control group. Also, ejaculation latency time was significantly prolonged in the CPA and Paxil groups compared to the control. In addition, the 5-HT type 2A postsynaptic receptor density in the nucleus accumbens of the rat brain was examined using quantitative autoradiography (QAR) using a specific ligand. The Paxil, CPA, and castrate groups showed a significant reduction in 5-HT 2A density (as was expected for the SSRI due to down regulation) compared to the control group. The scientists concluded that decreasing 5-HT 2A receptors decreases sexual function (Nedergaard et al. 1998). This conclusion contradicts the above neurotransmitter hypothesis that 5-HT type 2 receptor antagonists increase sexual function.
These neurotransmitter hypotheses still do not fully describe the underlying mechanism(s) of mediating SSRI induced sexual dysfunction or why "...numerous drugs with disparate synaptic activities have been reported to reverse these side effects (WWW 1)." This underlying mechanism may be intracellular in nature. Based on human case reports of SSRI sexual side effects and experimental data from animals, the evidence points towards Nitric Oxide (NO) as being a key player in the sexual pathway. Penile erection, in general, is associated with smooth muscle relaxation in the penile cavernous tissue, allowing blood to flow into and erect the penis. NO is a central mediator of this smooth muscle/blood vessel relaxation. NO is synthesized through the conversion of L-arginine to L-citrulline by nitric oxide synthase (NOS) (WWW 1).
To inspect the NO hypothesis, consider rare, parodoxical SSRI sexual side effects like spontaneous sexual excitement and/or orgasms, the opposite of side effects discussed thus far. Just after it was marketed, a female patient taking Prozac (fluoxetine) complained of "spontaneous yawning in the absence of drowsiness and multiple orgasms associated with clitoral engorgement in the absence of voluntary sexual stimulation (Modell 1989)." When the patient quit the medication, the symptoms vanished. Upon re-administration, the symptoms reappeared which points to Prozac as being the culprit. Many other hypersexuality case reports have surfaced over the years, yet they remain relativeley rare compared to the amount of sexual dysfunction cases reported. This hypersexuality, or yawning-orgasm syndrome, has been reported in male and female patients taking Prozac, Anafranil (clomipramine), Paxil and Effexor (venlafaxine) (WWW 1).
Animal studies have been done which point to NO involvement in the yawning-orgasm syndrome. Injecting oxytocin, nitroglycerin, NMDA, 5-HT type 2C postsynaptic receptor agonists (like m-CPP), ACTH or dopamine agonists (like apomorphine), induce penile erections and yawning in rats (Melis and Argiolas 1997). All of these compounds increase the production of NO through different mechanisms. For example, oxytocin and NMDA increase NOS activity while nitroglycerin acts as a NO donor. Central and peripheral NOS is involved in the expression of male sexual activity. A correlation exists between male copulatory performance and NOS activity in the paraventricular nucleus of the hypothalamus. "NOS mRNA expression in this nucleus in sexually potent rats is about twice that in sexually impotent rats (WWW 1)." Peripherally, testosterone activates NOS in the corpora cavernosa of the penis to create erection (Zvara et al. 1995). NOS inhibitors prevent the above agents from inducing yawning and sexual behavior, and thus, have an anti-sexual effect in the rats. It has been demonstrated in vitro and in vivo, in both humans and animals, that the SSRI's act as potent NOS inhibitors and lower NO centrally and peripherally (Finkel et al. 1996). The NO hypothesis states that this lack of NO is responsible for the decreased sexual activity of most patients on antidepressants. It is the antidepressant molecule itself, and not the result of increased serotonin in the synapse or decreased 5-HT type 2 postsynaptic receptors, that causes sexual dysfunction. However, all of the above hypotheses are not very clear and require more scientific research.
Symptoms
There are three phases of the normal sexual response cycle which antidepressants may commonly affect: sexual interest (libido), physiological arousal (including lubrication in women and erection in men), and orgasm (and ejaculation in men) (Gitlin 1995). Antidepressants usually cause decreased libido, decreased arousal, erectile dysfunction, delayed time to orgasm and/or anorgasmia, including ejaculatory dysfunction for men. Unusual sexual side effects include priapism (or constant erection), clitoral priapism, painful ejaculation, penile anesthesia, increased libido and/or spontaneous orgasm with yawning.
Sometimes it is difficult to diagnose someone with antidepressant induced sexual dysfunction because physicians and patients often feel uncomfortable in conversing about sexual behavior. One consequence is that antidepressant induced sexual side effects go unreported, and patients suffer. Or, a sexual behavior history was never discussed before starting antidepressant medication, and the physician is unable to blame the medication for causing the sexual side effects. Other factors can influence sexual functioning such as the depression effect, other psychiatric disorders (including substance abuse), medical disorders and/or other nonpsychiatric medications (Gitlin 1994). The physician/psychiatrist is usually to blame for this lack of communication as only "...11-370f primary care physicians routinely take a sexual history from new patients (Gitlin 1995)." When they do, they ask generic questions which the patient just dismisses. "Few clinical studies have systematically asked depressed patients about the various components of sexuality; fewer still have measured sexual functioning using experimental measures (Gitlin 1995)." One of these experiments questioned whether depression is associated with decreased sexuality, as the DSM-III (but not the DSM-IV) listed decreased libido as a diagnostic criterion for major depression. Using nocturnal penile tumescence (NPT) to directly measure erectile function, only 300f depressed men showed erectile dysfunction (Gitlin 1995). Another study showed that compared to a control population, outpatient depressed men were not less sexually active (Gitlin 1995). Also, erectile function in depressed men (as measured by NPT) did not change after successful treatment with psychotherapy (or cognitive behavior therapy (CBT)). Therefore, depression probably does not cause sexual dysfunction, and the pharmaceutical companies are wrong when they claim that depression, and not antidepressant medication, is the root of the problem.
The rates of sexual side effects of the antidepressants from highest to lowest are highest with the SSRI's and Anafranil, followed by MAOI's, tricyclics, and then Wellbutrin (bupropion) (Gitlin 1995). I will discuss specific examples of SSRI associated sexual side effects, although the other antidepressants have also been shown to have the same effects. For men, these side effects tend to be dysfunctional in nature, while sexual side effects in women can be either dysfunctional or hyperfunctional.
Piazza et al. treated 14 women and 11 men (all of whom had major depression) with either Zoloft (sertraline) or Paxil (Piazza et al. 1997). Sexual function was determined by the Arizona Sexual Experience Scale (ASex) (which is a questionaire regarding each phase of the sexual response cycle) before and after 6 weeks of treatment. Piazza et al. concluded that after SSRI treatment, "...difficulties with desire and psychological arousal in depressed women tend to remit, whereas in men orgasmic dysfunction appears to be a side effect of medication." Yet in another study, 18 out of 40 female patients (45%) experienced SSRI induced libido disturbances after 1 year of treatment (Aldrich et al. 1996).
In 1997, Labatte et al. used the visual analogue scale to treat 39 patients for 3 months with either Prozac, Paxil, or Zoloft. Both men and women experienced orgasm delay and decreased orgasm quality, while men also experienced a decrease in erectile function. However, lubrication, libido and sexual frequency did not change in either sex. 70f women also experienced anorgasmia after 3 months (Labatte et al. 1997).
A larger scale, multicenter study of 344 patients done by Montejo-Gonzalez found that drug related sexual dysfunction occurred in 540f patients taking Prozac, 560f patients taking Zoloft, and 650f patients taking Paxil (Montejo-Gonzalez et al. 1997). One third of these patients wanted to discontinue their medication because of the dysfunction. This study proves that the SSRI's induce a high rate of severe, sexual side effects.
In another important study, twenty healthy, non-depressed volunteers monitored sexual function with an adverse-effect, self-report questionnaire while being treated with Luvox (fluvoxamine) for four weeks (Nafziger et al. 1997). "None of the subjects reported sexual dysfunction prior to Luvox, while 200f subjects (2 men, 2 women) and 350f subjects (3 men, 4 women) reported sexual dysfunction at 2 weeks and 4 weeks of Luvox therapy, respectively." Sexual dysfunction included decreased ability to achieve orgasm, decreased libido and impaired erection. This study is direct proof that the SSRI's cause sexual side effects, and that depression is irrelevant to these effects.
Treatment
Various treatment strategies exist for antidepressant induced sexual dysfunction. One can try waiting (which does not really work) for a spontaneous remission of symptoms as tolerance to the drug may develop, decreasing the dose of the current antidepressant, or switching to a different antidepressant (Gitlin 1995). Decreasing the dose is very logical as the SSRI's have a flat dose-response curve with the threshold for the loss of sexual side effects occurring at a much higher dose than the loss of the therapeutic effect (Beasley et al. 1990). When switching antidepressants, Wellbutrin is the best alternative with minimal side effects, and it may even increase sexual behavior. St. John's Wort is also an effective antidepressant with minimal side effects.
Although sometimes effective, these strategies scare patients as switching from an antidepressant that works to one which may not work as well, decreasing the dose of the current drug, and/or taking a drug holiday (purposely skipping medication for a period of time when sexual activity is anticipated) may cause a relapse of depression. Preventing a relapse or worsening of depression is of utmost importance to the patient, even more so than a healthy sex life. Therefore, the most promising treatment is to stick with the current, effective antidepressant, and add another medication (or antidote) by a trial and error method to suppress sexual side effects. However, no perfect solution exists to date as these antidotes have their own adverse effects.
Cyproheptadine, an antihistamine with antiserotonergic properties, is often prescribed for anorgasmia. The antiserotonergic properties probably make this an effective antidote. A dose between 2-16 mg should be taken 1-2 hours before sexual activity as needed, and if not cured, it should then be taken daily (Gitlin 1995). Side effects of cyproheptadine include severe sedation and a possible relapse of depression.
BuSpar (Buspirone) is a non-benzodiazepine anxiolytic which is a 5-HT type 1A partial agonist. At 15-60 mg/day, BuSpar reversed SSRI induced, decreased libido and anorgasmia in 11 of 16 patients (Gitlin 1995). Increased irritability was the main side effect.
Bethanechol, a cholinergic agonist, was reported to reverse tricyclic and MAOI induced sexual dysfunction (Gross 1982). Doses, from 10 to 40 mg taken as needed, have reversed erectile and ejaculatory disturbances. "Side effects from bethanechol include diarrhea, cramps and excessive sweating (Gitlin 1995)."
The dopamine agonists are a newer, alternative treatment of antidepressant induced sexual side effects. These agents include amantadine (anti-viral, anti Parkinsons), pemoline (stimulant), d-amphetamine (stimulant), and Wellbutrin (a dopamine/norepinepherine reuptake inhibitor, antidepressant). A proposed mechanism of action of these dopaminergic agents, is that they promote nitric oxide synthesis (WWW 1). 100 mg/day of amantadine reversed Prozac induced anorgasmia in 5 of 7 cases with no side effects (Balogh et al. 1992). 5 mg of d-amphetamine (sublingually) or 18.75 mg/day of pemoline reportedly reversed decreased libido, erectile dysfunction and anorgasmia in three men (two treated with SSRI's, and one with a MAOI) with no side effects (Gitlin 1995; WWW 3). Wellbutrin is a very effective antidote to SSRI induced sexual dysfunction and may even compliment the SSRI's in reducing depression. 75 mg/day of Wellbutrin, for ten days, was effective in treating decreased libido, erectile impotence and delayed orgasm (Gitlin 1995). However, Wellbutrin commonly has its own side effects such as anxiety, tremor and agitation (WWW 3). Other usefull antidotes, that increase NO, include apomorphine (a NOS activator), M-CPP (a 5-HT 2C receptor agonist), Serzone (nefazodone), L-arginine (a NO precursor) and nitroglycerin (a NO donor, transdermal application) (WWW 1).
Viagra (sildenafil) is a novel medication for the treatment of SSRI related erectile dysfunction. In normal erectile mechanics, NO stimulates guanalyl cyclase to convert GTP into cGMP which is then active, and can relax smooth muscle in the corpus cavernosum of the penis to produce erection. Phosphodiesterase 5 (PDE 5) inactivates cGMP by converting it to GMP which allows erection to cease. Viagra inhibits PDE 5, which allows cGMP to accumulate and cause erection. Viagra has been shown to restore normal sexual function to a patient suffering from Effexor induced erectile dysfunction (WWW 4). The patient tried using yohimbine and Wellbutrin before Viagra, but these two antidotes did not work.
Herbal remedies comprise another group of antidotes which are used for the treatment of antidepressant induced sexual dysfunction. Yohimbine hydrochloride is an alkaloid isolated from the bark of the yohimbe tree (Pausinystalia yohimbe) native to tropical West Africa (WWW 2). It is a sympathomimetic, acting as a presynaptic alpha-2 blocker, and probably functions centrally (by increasing libido). Peripherally, yohimbine constricts blood vessels and probably creates erection by preventing venous outflow from the corpora cavernosa of the penis in men (Gitlin 1995). Yohimbine should be prescribed as 2.7-16.2 mg/dose, taken on an as-needed basis, 2-4 hours before sex. Maximum effect takes 2-3 weeks to manifest itself. In contrast to cyproheptadine (which just reverses anorgasmia), yohimbine has been reported to reverse decreased libido, erectile dysfunction and anorgasmia (Gitlin 1995). Common side effects of yohimbine include nausea, anxiety, insomnia, urinary urgency and sweating. In rare cases, it can cause hallucinations, increased blood pressure/heart rate, dizziness, headache and skin flushing. Also, foods containing tyramine should be avoided while taking this medication. One study compared yohimbine, cyproheptadine and amantadine as antidotes for SSRI induced sexual dysfunction. 17 (81%) of the 21 patients taking yohimbine improved in sexual functioning, while only 480f those taking cyproheptadine and 420f those taking amantadine improved (Ashton et al. 1997). Agitation was reported as a side effect to the yohimbine antidote, whereas sedation and weight gain occured with use of the other two antidotes.
Ginkgo biloba generally has a positive effect on desire, erection/lubrication and orgasm (WWW 5). This antidote, taken for 4 weeks at 209 mg/day, alleviated antidepressant induced sexual dysfunction in 910f women and 760f men (WWW 5). The common side effects were gastrointestinal (GI) disturbances, headache and general CNS activation.
Oriental ginseng has a long history of being a sexual energizer for men. Its root contains ginsenosides "...which are known to increase resistance to stress, improve hormonal balance, benefit metabolism, and aid skin and muscle tone (WWW 6)." Ginseng is a stimulant and can cause insomnia, nausea and/or anxiety. Ashwaganda (Withania somnifera) is popular in India for boosting the male sex drive and might be of use as an antidote (WWW 6). Ho Shou Wu, the Chinese tonic from the root of Polygonum multiflorum, is also a powerful aphrodesiac that increases sexual energy, improves male sperm production, and promotes fertility in women (WWW 6). The Mexican shrub, damiana (Turnera diffusa), has a reputation of being a female aphrodesiac (WWW 6). Muira puama, a Brazilian shrub, has been shown to improve libido and sexual function in patients (WWW 2). Dr. Jacques Waynberg supervised a clinical study of 262 patients with sexual dysfunction, and patients were treated with 1 to 1.5 g/day of muira puama for two weeks. This antidote increased libido in 620f patients, while it improved erection in 510f patients. Muira puama appears to be free of side effects which would make it more marketable than yohimbine.
Antidepressants do not always have negative effects on sexual functioning. SSRI's are now being used to treat premature ejaculation because of their orgasm-delaying effects. They are also useful in treating nymphomaniacs because of their libido shrinking qualities.
The antidote prescribing era described above is still in its infancy as more scientific research needs to be done. For now, physicians should work with the patients on a "knowledgeable" trial and error basis to find an appropriate mix of antidepressant and antidote.
Personal Case Report
As an otherwise healthy, sexually active 18 year old male with perfect sexual function, I was diagnosed with having obsessive compulsive disorder (OCD) and minor depression by a psychiatrist. I was prescribed 50 mg/day of Zoloft (aside from depression, the antidepressants are also used to treat OCD and panic disorder), which has gradually increased over three years to the maximum 200 mg/day (current dose at age 21), for my disorder. I gradually noticed, over the course of the first year, that the SSRI was working, and my disorder and depression were going away. The only adverse side effects were nausea/diarreah at first, and anxiety. An additional side effect was delayed orgasm/ejaculation which improved my sexual performance and was a thrilling bonus. This came as a surprise as my psychiatrist never told me about this pleasant, sexual side effect. The Zoloft was dramatically improving the quality of my life.
However, after a year of treatment, I began to notice (off and on) erectile dysfunction and anorgasmia when engaged in sexual activity. I was worried, upset, and self conscious about my erratic sexual problem which could occur at any time. Yet, due to embarassment, I did not tell my psychiatrist.
After two years of treatment, the Zoloft induced sexual side effects worsened, and I experienced a decreased libido. I completely lost my interest in having or thinking about sex. This was a serious side effect which by itself, started to cause a relapse of depression. This time, I told my psychiatrist. Since the current dose of Zoloft was maximally effective in treating my depression and OCD, we decided not to decrease the dose, take a drug holiday, or switch to a different antidepressant. Instead, my psychiatrist prescribed the antidote, Wellbutrin, at 75 mg/day. After two weeks, the depression and OCD were still contained as before, but there was no improvement in sexual function. Also, the Wellbutrin had its own, adverse side effects such as increased irritability, agitation, anxiety and tremor.
However, after another two weeks, this time taking 150 mg/day of Wellbutrin, I felt a gain in sexual desire and function. My depression and OCD were at an all time low, and the other, adverse side effects were minimal. This is my current status, as I have never been happier. The combination of Zoloft and Wellbutrin is working for me.
Conclusion
From my experience, I can guarantee that the sexual side effects of the SSRI's exist and are a serious problem for its users. The above evidence, although not absolute, definitely points to the antidepressants causing sexual dysfunction. Although confusing, as the molecular mechanisms of normal sexual function, sexual dysfunction, and antidote treatment of this dysfunction are not clear, the currently available antidotes provide a start for managing sexual dysfunction.
The SSRI's are usually effective, but the patients are not adhering to their dosage regimen due to the sexual dysfunction, thus rendering the SSRI's ineffective. The scientific community needs more concrete, accurate research in order to prove to the medical community that the antidepressants unequivocally cause adverse sexual side effects. Once this happens, the pharmaceutical companies will then make the statistics, in the antidepressants' product information, accurate. This process will then enable the physicians and their patients to work together in making accurate, educated decisions about antidepressant treatment. To facilitate this process, a universal, checklist-like questionnaire, like the ASex, needs to be developed so that physicians can accurately monitor their patients sexual function before and throughout treatment. Also, a coherent treatment algorithm eventually needs to be established to help physicians decide what doses of which drug treatment to prescribe and in what order forwhich patient in what combination should these drugs be prescribed. Until then, the antidepressants will continue to cause adverse, sexual side effects in most patients.
References
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WWW 2. http://rain-tree.com/article3.nim. Yohimbine vs. Muira puama in the treatment of erectile dysfunction.
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Table 1
Type of Antidepressant
Trade Name
Generic Name
Tricyclic
Elavil
Amitriptyline
Tricyclic
Anafranil
Clomipramine
Tricyclic
Norpramin
Desipramine
Tricyclic
Sinequan
Doxepin
Tricyclic
Tofranil
Imipramine
Tricyclic
Aventyl
Nortriptyline
Tricyclic
Vivactil
Protriptyline
Tricyclic
Surmontil
Trimipramine
Heterocyclic
Asendin
Amoxapine
Heterocyclic
Wellbutrin
Bupropion
Heterocyclic
Ludiomil
Maprotiline
Heterocyclic
Remeron
Mirtazapine
Heterocyclic
Serzone
Nefazodone
Heterocyclic
Desyrel
Trazodone
Heterocyclic
Effexor
Venlafaxine
SSRI
Prozac
Fluoxetine
SSRI
Luvox
Fluvoxamine
SSRI
Paxil
Paroxetine
SSRI
Zoloft
Sertraline
MAOI
Nardil
Phenelzine
MAOI
Parnate
Tranylcypromine
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