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CME

Sex, Sexuality, And Serotonin

  • Authors: Chair: Philip R. Muskin, MD; Co-Chair: Anita H. Clayton, MD; Faculty: Helen E. Fisher, PhD; Serena Yuan Volpp, MD, MPH
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Target Audience and Goal Statement

This program is intended for psychiatrists, primary care physicians, and other mental health professionals.

Upon completion of this activity, participants will be able to:

  1. Understand the separate brain circuitry/psychodynamics for love and sex; the impact of psychotropics on love, sex, and sexuality; and strategies to enhance adherence.
  2. Show how antidepressant-induced sexual dysfunction can inhibit a broad range of sociosexual behaviors that are often vital to patient well-being and recovery, and to encourage physicians to consider these hidden side effects when prescribing serotonin-enhancing antidepressants for extended periods.
  3. Demonstrate (1) knowledge of common sexual behaviors in gay men and lesbian individuals (2) familiarity with the trajectory of sexual relationships in gay and lesbian couples, and (3) recognition of sociocultural issues that affect the sexuality of gay patients.
  4. Recognize that individuals with psychiatric illness, treated or untreated, often experience impairment in one or more phases of the sexual response cycle, potentially resulting in medication noncompliance or reduction in quality of life.
  5. Review strategies to openly discuss sexual dysfunction to prevent patients from stopping medication prematurely.


Author(s)

  • Anita H. Clayton, MD

    David C. Wilson Professor & Vice Chair, Department of Psychiatric Medicine, University of Virginia Health System, Charlottesville, Virginia

    Disclosures

    Disclosure: Advisory Board/ Consultant: Bayer, Boehringer-Ingelheim, Eli Lilly & Co., GlaxoSmithKline, Organon, Inc., Pfizer, Inc., Somerset Pharmaceuticals, Wyeth; Research Grants: Bayer, Boehringer-Ingelheim, Eli Lilly & Co., GlaxoSmithKline, Organon, Inc., Pfizer, Inc., Pherin Pharmaceuticals, Merck & Co., Inc.; Speakers' Bureau: GlaxoSmithKline, Organon, Inc., Pfizer, Inc., Wyeth.

    Dr. Clayton has indicated that she will include off-label reference to investigational uses of in her presentation.

  • Helen E. Fisher, PhD

    Research Professor, Department of Anthropology, Rutgers University, New Brunswick, New Jersey

    Disclosures

    Disclosure: Speakers' Bureau: GlaxoSmithKline.

    Dr. Fisher has indicated that she will not include reference to off-label/unapproved uses of drugs or devices in her presentation.

  • Philip R. Muskin, MD

    Professor of Clinical Psychiatry, Columbia University College of Physicians & Surgeons, New York

    Disclosures

    Disclosure: Consultant: Bristol-Myers Squibb Co., Cephalon, Inc., Eli Lilly & Co., Forest Laboratories, GlaxoSmithKline, Janssen Pharmaceutica, Pfizer, Inc.; Research Grant: Bristol-Myers Squibb Co., Gay Men's Health Crisis; Speakers' Bureau: Bristol-Myers Squibb Co., Cephalon, Inc., Eli Lilly & Co., Forest Laboratories, GlaxoSmithKline, Janssen Pharmaceutica, Pfizer, Inc.

    Dr. Muskin has indicated that he will not include reference to off-label/unapproved uses of drugs or devices in his presentation.

  • Serena Yuan Volpp, MD, MPH

    Clinical Instructor in Psychiatry, New York University School of Medicine, New York.

    Disclosures

    Disclosure: Clinical Instructor in Psychiatry, New York University School of Medicine, New York.

    Dr. Volpp has indicated that she will not include reference to off-label/unapproved uses of drugs or devices in her presentation.


Accreditation Statements

    For Physicians

  • The College of Physicians and Surgeons of Columbia University is accredited by the Accreditation Council for Continuing Medical Education (ACCME) to provide continuing medical education for physicians.

    The College of Physicians & Surgeons of Columbia University designates this educational activity for a maximum of 3.0 category 1 credits toward the AMA Physician's Recognition Award. Each physician should claim only those credits that he/she actually spent in the activity.

For questions regarding the content of this activity, contact the accredited provider for this CME/CE activity noted above. For technical assistance, contact [email protected]


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This activity is designed to be completed within the time designated on the title page; physicians should claim only those credits that reflect the time actually spent in the activity. To successfully earn credit, participants must complete the activity online during the valid credit period that is noted on the title page.

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CME

Sex, Sexuality, And Serotonin: Effects of Psychiatric Illness and Medication on Sexual Function

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Effects of Psychiatric Illness and Medication on Sexual Function, Presented by Anita H. Clayton, MD

Dysfunctions and Disorders and Etiology

  • I'm going to discuss very specifically physiologic function and the types of things we can look at in terms of biology of sexual functioning and how that may impact on our patients.

  • Slide 1.

    Slide 1.

    Effects of Psychiatric Illness and Medication on Sexual Function

    (Enlarge Slide)
  • I think it's really important when we're talking about sexual function and dysfunction, particularly as it relates to psychiatric illness and treatment, that we define our terms upfront. Sexual complaint is really just an expression of discontent or an expression of sexual pain. Sexual dysfunction, on the other hand, is an actual disturbance in one or more phases of the sexual response cycle or sexual pain that impacts on one of those phases. And a sexual disorder is where you have a sexual dysfunction plus significant distress or interpersonal conflict. These are the criteria required to meet the definition of a sexual disorder in the Diagnostic and Statistical Manual of Mental Disorders (DSM)-IV and the more recent American Foundation for Urologic Disease criteria.

  • Slide 2.

    Slide 2.

    Defining Dysfunctions and Disorders

    (Enlarge Slide)
  • When we talk about the sexual problems that people may have, there really are a myriad of these types of problems. Interestingly enough, we don't often hear people complain of enhanced desire, even when people are hypersexual perhaps with bipolar and lesser mania. They don't come in and say: I'm way oversexed and my judgment is poor; can you stop it? They really don't recognize this and people generally do not view a high level of desire as a problem, but we do view a low level of desire as a problem, especially if we've had a higher level before and our level has decreased or we have a new partner whose level of interest is higher than our own. In terms of arousal, this phase can be very complicated physiologically. I'm going to show you some of the physiology in a few minutes, but I want you to keep in mind that there are really 2 aspects to arousal: one is central, going on in the brain; and one is peripheral, going on in the genitalia. Sometimes these are disconnected. Thistends to happen particularly in women; men are much more likely to be able to sustain focus through the arousal phase, but women actually may have inhibited sexual excitement -- that is, they don't feel as interested, or they get distracted by a noise in the next room or some other concern that pops into their head while they still may have adequate vaginal lubrication. On the flip side, some of the medications we use to treat psychiatric conditions actually can affect sensation in the genitalia and if you have diminished genital sensation, that requires a lot more stimulation or a longer period of stimulation to reach the same level of arousal. Then we can have erectile dysfunction, which in the past, was called impotence, and in women, failure to achieve or maintain vaginal lubrication.

    With regard to orgasm, many of the drugs that we use cause the individual to take longer or more stimulation to achieve an orgasm. This issue of delayed orgasm really has to do with the fact that it's requiring more stimulation for a longer period. Some people will tell you that they have anorgasmia (the inability to achieve an orgasm sometimes when they have sex, but not all the time). And they can often tell you right at the beginning of the sexual activity: I knew this time I wasn't going to have an orgasm. So there's some awareness of what's going on in this level of delay in many individuals. I'm not going to talk about premature ejaculation because there's something different about this phenomenon; it's now being defined as rapid ejaculation, which frankly I think is a misnomer. It's currently being defined on the part of the man feeling that he has ejaculated or come to orgasm sooner than he would like. Very often, this is in comparison with the time he would like to spendpleasuring his partner. There's something different physiologically about this phenomenon because we can actually find differences among various drugs in the effect on premature ejaculation. We don't understand it; I'm not going to talk about it further.

    The last phase of the sexual response cycle is the resolution phase and this is a passive phase that once an orgasm is achieved, occurs spontaneously. So I'm not going to talk about this anymore, either. Instead, I think we should consider satisfaction because many patients will report what I would consider a minor sexual disturbance, which they think is really significant and they will say: "I can't put up with this." Other people will report really what I would consider significant global sexual dysfunction and they will say: "Well, we can work around this; we're using a device or something along those lines." Their satisfaction level is higher than I might have expected. So we need to know what that individual thinks, not what I project on to them.

    In addition, more data are being looked at with regard to sexual pain. What we mean by that is pain associated with sexual activity, which tends to occur in women or pain associated with orgasm, which has been mostly reported in men, and associated with certain antidepressant medications. I think it is important for us to start to look at pain because this tends to then have reverberations on other phases of the sexual response cycle. If you have pain with orgasm, you may then want to avoid sex because of the pain. Or if you have pain with penetration, you may not be very interested in sex because, again, of anticipatory fear of the pain.

  • Slide 3.

    Slide 3.

    Types of Sexual Problems

    (Enlarge Slide)
  • I also want to point out some of the aspects of physiology because some of this carries over from things we've already heard, and it will also help you understand how it is that various medications may have a negative or positive impact on sexual functioning. You can see there's a lot of overlap between the phases of the sexual response cycle and that's one of the reasons it's hard to necessarily diagnose one specific disorder; many people will have more than one diagnosis of a sexual disorder when they meet these criteria. But there's a lot of overlap here and various hormones influence sexual functioning. Testosterone really is the hormone driving sexual interest and behavior in men. It also is important in women, primarily related to things like cognition, spontaneous thoughts about sex, and sexual fantasies. Testosterone also is permissive in terms of estrogen stimulating desire. In addition, progesterone function appears to be important in a woman's interest in sex in terms ofresponsiveness to her partner's approach. So if her partner says: "I'd like to participate in sex tonight" -- however that is said -- if her progesterone function is adequate, she might go along with that and say: "Okay, yeah, that's a good idea even though I hadn't thought of it." We also know that prolactin increases, even small ones above the normal range, significantly contribute to sexual dysfunction, usually beginning in the arousal phase but progressing to other phases. We've already heard that oxytocin levels rise at the time of orgasm and so are related to this phenomenon. In addition, oxytocin levels fluctuate across the menstrual cycle in women and also may relate to interest in participating in sex. In addition, some of these hormones affect neurotransmitters, which are very specific in their effects on sexual functioning in the brain.

    We've already heard about dopamine, which really does appear to drive motivated sexual behavior. It's the thing that gets us doing something to get into a position to have sex or to give the signals that we're interested in sex. In addition, it also helps us focus and maintain attention, and that's very important in the arousal phase, particularly for women because they can be so easily distracted. Norepinephrine is also very important in generalized arousal, so it's very important specifically in sexual arousal as well. Unfortunately, serotonergic enhancements have negative effects on both dopamine and norepinephrine function.

  • Slide 4.

    Slide 4.

    Central Effects on Sexual Function

    (Enlarge Slide)
  • In terms of looking at the periphery or the genitalia, the sex steroids also are important in maintaining structure and function in the genitalia. When we're talking about sexual stimulation and arousal, what really is going on down there is vasocongestion. In men, it results in an erection and in women, it results in engorgement and subsequent exudate that is vaginal lubrication. Lots of things can contribute to vasocongestion and in men in particular, as we've seen with the phosphodiesterase 5 inhibitors, nitric oxide is driving this phenomenon. Unfortunately, low levels of testosterone may contribute to this not being as important a mechanism in women and serotonin enhancement also can negatively affect nitric oxide function. In addition, norepinephrine is active in the genitalia, stimulating arousal in the form of vasocongestion, and it seems to be one of the things that turns on this system. But it also turns on a feedback loop through 5-hydroxytryptamine-2A receptors thatturns this off. You don't want to have vasocongestion and sexual arousal all the time; it needs something to shut it down. This appears to be mediated through serotonin systems.

    Vasoactive intestinal peptide, prostaglandin E, and cholinergic stimulation also have effects on vasocongestion. We're not sure what neuropeptide Y (NPY) and substance P do, but we know those receptors are in the genitalia. We also know that serotonin can have negative effects on sensation, both diminishing sensation and heightening painful sensations in the genitalia.

  • Slide 5.

    Slide 5.

    Peripheral Effects on Sexual Function

    (Enlarge Slide)
  • So you can see how some of the medications that we use may have an impact on sexual functioning.

  • Slide 6.

    Slide 6.

    Presumed Etiology of Sexual Dysfunction (SD)

    (Enlarge Slide)

Prevalence

  • These are the Laumann data and what happened in this study was that randomly selected people in the general population were asked questions. If people reported that they had had some sexual activity in the previous year, they were then asked if they had had any problems. Complaints were reported from 43% of women and about 30% of men. This was just a complaint; it doesn't mean that they had a disturbance, a dysfunction, or a disorder, and these were not evaluated for in these data. In patients with depression, they asked them: "Is your libido diminished as a result of your depression or associated with onset of your other symptoms?" Approximately 70% to 80% of them will report diminished sexual interest. A number of these patients also will report problems with arousal, but you usually don't hear complaints that they're having orgasmic dysfunction as a symptom of depression.

  • Slide 7.

    Slide 7.

    Prevalence of Sexual Complaint

    (Enlarge Slide)
  • One of the problems with looking at this issue is that it's grossly underreported; there's reluctance on the part of patients and their providers to bring up this topic. In a study done by psychiatrists in Spain, 344 patients taking selective serotonin reuptake inhibitors (SSRIs) who came in for an office visit were asked the very question we ask in clinical trials in this country: "Have you noticed anything since your last visit?" It's very general and it's made that way in order to elicit whatever is going on with that patient and not what we expect to see. Fourteen percent of these patients reported sexual dysfunction; in the very same office visit, researchers then asked direct questions about side effects including sexual side effects. Almost 60% of these patients reported a sexual problem. This suggests that the rate is 3 times the spontaneous report or greater, and we really need to keep this in mind when talking to our patients.

  • Slide 8.

    Slide 8.

    Antidepressant-Induced SD Is Often Underestimated

    (Enlarge Slide)
  • I don't know how many of you are Trivial Pursuit players; have you seen the 20th anniversary silver edition? Well, if you've gone through all the cards, you might have seen this one (on the green marker): "What percent of men taking antidepressants experienced sexual dysfunction in Dr. Anita Clayton's 2001 study?" Is the answer 17%, 37%, or 57%?

  • Slide 9.

    Slide 9.

    Trivial Pursuit 20th Anniversary Edition Question

    (Enlarge Slide)
  • The answer is 37% and the reason is because of how we defined sexual dysfunction in planning our study. If we defined it differently, this rate would be different.

  • Slide 10.

    Slide 10.

    Trivial Pursuit 20th Anniversary Edition Answer

    (Enlarge Slide)

2001 Study

  • I'm going to show you those data now. This was a study done in 1100 primary care doctors' offices around the country. If patients were taking just one antidepressant -- they couldn't be taking multiple antidepressants -- and if they came into their doctor's office for any reason, they were invited to participate in a study looking at sexual functioning. Seventy percent of these people who had not expected to be invited to do this agreed to talk about their sexual functioning right then and there. Of the 30% who declined, only 6% said it's too intimate or personal a topic. The rest said they were too busy or too sick and they couldn't do it at that point. The 70% who agreed signed informed consent forms and then filled out our changes in sexual functioning questionnaire; nearly 6300 people completed it. We defined sexual dysfunction, in this study; as a total score in which all 14 items added up to less than the threshold that we found separates patients with sexual dysfunction fromindividuals who report normal or adequate or satisfactory sexual functioning.

    We found that 37% had a significant and global sexual dysfunction impacting on all phases of the sexual response cycle. That means that almost two thirds did not meet those criteria. We also planned, in advance, to look at those patients who didn't have any other reason for their sexual dysfunction other than their depression and their antidepressant therapy. This brings us down to only about 800 patients, and most of our patients are going to have more than one reason for their sexual dysfunction.

  • Slide 11.

    Slide 11.

    Prevalence of SD Study Flow Chart

    (Enlarge Slide)
  • These are the data. This is a point prevalence study. The dot under overall is the mean for each of these, so this is the overall mean at 37% and these are each of the drugs. Regarding the vertical lines, if they're very large, it means there's a question as to where that dot really falls on that line; that's a confidence interval. If there's overlap of a confidence overall -- if you draw a line across, for example, and it overlaps with others -- that means that those are not statistically different from each other. So the overall rate of patients who had significant and global sexual dysfunction was 37%. All the SSRIs, including the serotonin/norepinephrine reuptake inhibitor (SNRI), were grouped together as a class because the serotonergic effects predominate in terms of effects on sexual functioning. The only 2 drugs that differed statistically significantly were nefazodone at about 28% and bupropion sustained release (SR) at about 24%. These rates still seem high in terms ofsome of the drugs that we've been thinking are less likely to cause sexual dysfunction.

  • Slide 12.

    Slide 12.

    Prevalence of SD: All Patients

    (Enlarge Slide)
  • We looked at some of the risk factors people had. People over age 50 were at greater risk because their sex steroids are changing at that point and may potentially contribute to problems in this area. Married people, though, were at greater risk, contrary to a lot of data. We went back and looked and actually age and marital status sorted together in this study so more of the older people were married and more of the younger people were single. The better educated people were, the less likely they were to have sexual dysfunction, and if people were employed full time, they had the best sexual functioning. This surprised us, too, but we think that this may be related to the fact that they're more functional in the occupational aspects of their life and may be more functional in other areas as well. Smokers were at greater risk for sexual dysfunction. Patients taking higher daily doses of the antidepressant, that is in the upper half of the normal range of dosing, were at greaterrisk for sexual dysfunction than those taking a dose in the lower half of the normal range. The exceptions to this were mirtazapine and bupropion where higher doses were associated with better sexual functioning. Any concomitant medication was associated with sexual dysfunction, and the following factors are not very likely to be changed: illnesses known to contribute to sexual dysfunction, prior history of antidepressant-induced sexual dysfunction, and if patients never enjoyed sex or didn't think it was important, they had problems.

  • Slide 13.

    Slide 13.

    Risk Factors for SD Identified in Study

    (Enlarge Slide)
  • These are the data for the group that didn't have any other risk factors for their sexual dysfunction except residual symptoms of depression and the antidepressant. The rate drops to about 25%, so a quarter of the patients still have sexual dysfunction when they don't have any other known reason. All the SSRIs, including the SNRI, were again grouped together as a class. The only drug that differed statistically significantly was bupropion SR with a rate of less than 7%, compared with 27% for the SSRIs and SNRI. This is a class effect of serotonergic drugs; they do not differ from each other. It doesn't even make any sense that they would because their mechanism of action is the same.

  • Slide 14.

    Slide 14.

    Prevalence of SD: Sub-Population of Patients Without Other Probable Causes of SD

    (Enlarge Slide)
  • We went back and looked at those patients who didn't meet the total changes in sexual function questionnaire score for sexual dysfunction in order to look at which phases might have been impacted upon. What we found was that about 70% of people had at least one phase in which they had a complaint. What we also found was that men were statistically significantly more likely to complain of problems with desire and orgasmic function and women were more likely than men to complain of arousal phase problems. So these can also help guide us in our evaluation of patients in terms of the effects of medications on their sexual functioning.

  • Slide 15.

    Slide 15.

    Burden of SD by Gender

    (Enlarge Slide)

Management Strategies

  • What can we do if patients have antidepressant-induced sexual dysfunction? We can wait for tolerance to develop, but this only happens in 5%-10% of patients and it takes 4-6 months -- not a very effective strategy. We can lower the dose, but you risk re-emergence of depressive symptoms. A drug holiday can be tried, but unfortunately you can often see SSRI discontinuation symptoms after a couple of days of not taking a short-acting SSRI. In addition, patients in whom this is effective in improving their sexual functioning may not adhere to their treatment regimen on other days of the week. You can substitute a different antidepressant; you've all had the experience where you switched someone with SSRI-induced sexual dysfunction to another SSRI and their sexual function appeared to improve. I personally think this is probably related to better treatment of the depression by a particular agent, so you have less residual symptoms of depression. In general, I switch to one of theantidepressants less likely to cause sexual dysfunction when an antidepressant has already contributed to this problem.

    For some people, though, who have been tried on multiple medications in which they've not had a good response and finally found one that works but it causes sexual dysfunction, this is probably not the best option because of their fear of therapeutic failure. Instead, using an antidote may be of benefit in those individuals. I will tell you there are no medications approved by the United States Food and Drug Administration for use for this purpose; however, there are just a few placebo-controlled trials that also can help us in terms of improving quality of life in our patients.

  • Slide 16.

    Slide 16.

    Strategies for Managing SD

    (Enlarge Slide)
  • Bupropion at doses between 300 and 400 mg/day added to the antidepressant -- the SSRI in the case of these studies -- has been found to be effective in men and women in improving sexual functioning compared with placebo. Buspirone, also at higher doses, 30-60 mg/day, has been found to be helpful for sexual dysfunction induced by SSRIs in women. Sildenafil has been found to be effective in SSRI-induced sexual dysfunction in men. There are no data to support using each of these latter 2 agents in the other gender. There also are open-label trials and case studies that suggest that using these other agents also may benefit patients in whom these other treatments have failed.

  • Slide 17.

    Slide 17.

    Antidotes in Antidepressant-Induced SD

    (Enlarge Slide)

Anxiety Disorders

  • When we talk about the other disorders that we might see in psychiatric practice, anxiety disorders are very common. As much as we lump them together as a group, anxiety disorders differ from each other quite dramatically, as do the sexual dysfunctions associated with these disorders. Social phobia has been the most systematically studied in terms of effects on sexual functioning. People with social phobia have far fewer sexual relationships than other individuals. Their primary dysfunction is in the arousal phase, suggesting hyperadrenergic effects or again norepinephrine being involved. Sexual dysfunction is more pervasive in women. Men are more likely to pay for sex and objectify their sexual object so they don't have to have an intimate relationship, even though they're having an intimate encounter. Also there may be significant performance anxiety in men and again, having sex that is objectified may limit or reduce that performance anxiety. So we think maybe with social phobiathat behavioral and pharmacologic hyperadrenergic stimulation is important.

  • Slide 18.

    Slide 18.

    SD With Anxiety Disorders

    (Enlarge Slide)
  • In terms of other anxiety disorders, women with obsessive-compulsive disorder (OCD) are more likely to be both avoidant and anorgasmic than women with generalized anxiety disorder (GAD), even though women with GAD have far more somatic symptoms than women with OCD. Men with posttraumatic stress disorder have very generalized sexual dysfunction and it's made worse by the SSRIs used to treat this disorder. Also, if a patient has a sexual disorder, they're more likely to have a current comorbid anxiety disorder than someone without a sexual disorder.

  • Slide 19.

    Slide 19.

    SD with Anxiety Disorders (cont'd)

    (Enlarge Slide)
  • Unfortunately, studies specifically looking at medications in the treatment of anxiety disorders have not been done, but we can extrapolate somewhat in terms of the antidepressants because they're used with these disorders. Benzodiazepines also are used and can contribute to sexual dysfunction. We also don't know how to manage sexual dysfunction with anxiety disorders, but again, we can try to use some of the information we found with depression.

  • Slide 20.

    Slide 20.

    SD and Medications for Anxiety Disorders

    (Enlarge Slide)

Psychotic Illness

  • In terms of psychotic illnesses, unfortunately, patients who have these disorders have significant sexual dysfunction associated with the conditions with which they suffer. Fifty percent of men and 30% of women with psychotic illnesses report sexual dysfunction, but women are twice as likely as men to be involved in a sexual relationship. Unfortunately, however, 40% of both genders have never had a sexual relationship but this really does suggest that men with psychotic illnesses have far more solitary sexual behaviors than women. Compared with controls, again, men with schizophrenia have more pervasive sexual dysfunctions affecting all phases of the sexual response cycle.

  • Slide 21.

    Slide 21.

    Psychotic Illness and SD

    (Enlarge Slide)
  • In addition, when we look at what's going on in terms of the medication effects, sexual dysfunction is seen in 40%-70% of patients on conventional antipsychotics and that is a higher rate than is seen with the atypical antipsychotic medications. Also, sexual dysfunction in men who have normal prolactin levels appears to be associated again with autonomic side effects, whereas hyperprolactinemia tends to be the primary cause of both sexual dysfunction and reproductive dysfunction in women.

  • Slide 22.

    Slide 22.

    Antipsychotic Medications and Effect on SD

    (Enlarge Slide)
  • We think that this is related to hyperprolactinemia due to dopaminergic antagonism in the tuberoinfundibular system. We know that prolactin is increased with conventional antipsychotics and risperidone. We also know that it's decreased with clozapine and aripiprazole and we're not sure whether it's a steady state or no effect on prolactin or a decrease with olanzapine, quetiapine, and ziprasidone because of some conflicting studies. But it's worth taking this into account, particularly in women with psychotic illness.

  • Slide 23.

    Slide 23.

    Antipsychotic Agents and Effect on Sexual Function

    (Enlarge Slide)
  • If we look at the effects of antipsychotics in men, again, 40%-71% of them report decreased sexual function and all phases are affected. Priapism also is a problem seen in men receiving antipsychotic medications and this is related to alpha-1 adrenergic antagonism. It's important to keep that in mind in patients who are on the agents that affect this system, particularly if they're on more than one agent affecting the alpha adrenergic system.

  • Slide 24.

    Slide 24.

    Sexual Side Effects of Antipsychotics in Men

    (Enlarge Slide)
  • We know that medication side effects are related to non-adherence to treatment in patients with psychotic illnesses, and sexual dysfunction is among the group of problems that contribute to noncompliance. We can do a few things in patients with psychotic illnesses; we can improve comorbid conditions or other risk factors. Many patients with psychotic illnesses have diabetes, which puts them at risk for sexual dysfunction through effects on the vasculature and neurologic systems. If we can improve their state in terms of their diabetes management, we may improve their sexual functioning. You can reduce their dose but you may result in the same risk factor we see associated with antidepressant dose reduction, that is, reemergence of symptoms. You can switch from conventional antipsychotic agents to atypical agents. Two open label studies suggest that the use of amantidine and sildenafil in men with erectile dysfunction related to antipsychotic treatment may be of benefit.

  • Slide 25.

    Slide 25.

    Psychotic Illness and SD

    (Enlarge Slide)

Conclusions

  • I hope I've been able to show you that psychiatric illness can be associated with sexual dysfunction, as can the treatment of these disorders. It is important for us to be discussing these issues with patients, both before and throughout treatment because we can always use some of those strategies that I mentioned to potentially continue remission of their symptoms while enhancing their quality of sexual life.

  • Slide 26.

    Slide 26.

    Conclusions

    (Enlarge Slide)