Treatment of Male Sexual Dysfunction

Cindy M. Meston and Amelia S. Stanton

Assessment of Male Hypoactive Sexual Desire Disorder

Assessment for MHSDD should include private meetings with each member of the couple, as well as a couples meeting. Individual meetings with the male partner may reveal a number of diagnostic factors, including atypical arousal patterns that are not being met by his current partner, decreased attraction to his current partner, or a sexual affair that is satisfying his sexual needs outside of his current relationship.

In addition to having individual and group? Do you mean couple meetings, clinicians should also assess for changes in health status, life stressors, and relationship factors around the time that the male partner started to experience a lack of sexual interest. These factors may become the target of the clinician’s treatment plan.

Clinicians should also consider the possibility that male patients presenting with complaints of low sexual desire may actually be suppressing their desires. This often occurs in men who are in long-standing heterosexual relationships who either have had sexual relations with men or who have fantasized about sexual relations with men during masturbation (Meana & Steiner, 2014b). The possibility that men who report low sexual desire may be asexual, meaning that they may not be sexually attracted to anyone or anything also needs to be explored.

Treatment of Male Hypoactive Sexual Desire Disorder

Treatment for low sexual desire in men should be etiologically oriented. If low testosterone level is determined to be the likely cause of MHSDD, biological treatment focuses primarily on increasing testosterone levels. As mentioned earlier, hypogonadism in males typically leads to low testosterone production, decreased sexual interest, and difficulties sustaining an erection. Testosterone replacement therapy can be delivered through the skin via an over the counter gel or patch, by injections, or by slow release pellets (Testopel) implanted under the skin. In a couple of studies, increasing testosterone levels has been shown to have beneficial effects on sexual motivations and sexual thoughts (Allan, Forbes, Strauss, & McLachlan, 2008; Wang et al., 2000).

There has been some concern about the overuse of testosterone gels, especially by men who have normal testosterone levels. According to Handelsman (2013), the prescribing of off-label testosterone, particularly transdermal testosterone, has increased in most countries between 2000 and 2011, and the rising trend accelerated over the last half decade of the survey period. One of the likely causes of this increase may be the permissive US and European guidelines for the prescription of testosterone, which promote the use of the drug for age-related functional androgen deficiency (Handelsman, 2013). In some countries, total testosterone prescribing exceeds the maximum amount that could be attributed to pathological androgen deficiency, which is known to occur in about 0.5% of men (Handelsman, 2010). In a study of older men randomly assigned to either daily application of testosterone gel or daily application of a placebo gel, men in the active condition had a greater frequency of cardiovascular, respiratory, and dermatologic events compared to men in the control condition (Basaria et al., 2010). The incidence of adverse cardiovascular events in the testosterone group was significant enough to stop the trial before the completion of enrollment.

If low sexual desire is determined to be caused by elevated prolactin, another endocrinologic disorder, or by depression, or anxiety, there are different biological treatment approaches to consider. Although organic hyperprolactinemia more frequently affects women than men, many psychotropic medications can cause increased prolactin in men (Rubio-Aurioles & Bivalacqua, 2013). Treatment of other endocrinolgic disorders, such as hypothyroidism and hyperthyroidism, can increase sexual desire, as it is often compromised by these conditions. Depression and anxiety may also lead to decreased sexual desire in men. Treatment for depression often entails the use of antidepressants, which have been shown to impact sexual function in both men and women. If a depressed patient is already experiencing decreases in sexual desire before starting an antidepressant regimen, then his doctor should consider prescribing an antidepressant that has more mild effects on sexual function, such as mirtazapine, buproprion, and SNRI’s like duloxetine (Clayton, Croft, et al., 2014).

It is also noteworthy that men with metabolic syndrome commonly report low sexual interest. If low sexual desire appears to be secondary to metabolic syndrome, then clinicians may recommend a combination of lifestyle changes, exercise, healthy diet, and testosterone replacement therapy (Glina, Sharlip, & Hellstrom, 2013).

Psychosocial treatment for MHSDD mirrors psychological treatment for FSIAD, as MHSDD and FSIAD share many causal psychological factors. Meana and Steiner (2014a) provide a thorough overview of efficacious psychosocial treatments for MHSDD. Cognitive-affective-behavioral therapy is a treatment approach that combines cognitive, emotion-centered, and behavioral strategies. The cognitive component of the treatment includes identifying and challenging maladaptive thoughts and sexual scripts that interfere with sexual desire (Meana & Steiner, 2014a). Therapists may encourage patients with low desire to refocus on sexual stimuli, either before or during sexual activity. The emotional regulation aspect may help men decrease or control emotional reactivity with acceptance techniques like mindfulness. Acceptance techniques come into play in situations when patients may not be able to achieve the sexual function or level of desire that they wish. In these cases, learning to accept certain realities may have as positive an impact as changing what can be modified (Meana & Steiner, 2014a). Effective psychosocial treatment for MHSDD also includes different behavioral activation strategies, such as sensate focus and optimizing the timing of sexual interactions, which help couples refocus on sensuality and encourage them to prioritize sexual activity.

Cognitive-affective-behavioral therapy for MHSDD also includes relationship skills-building and communication training, which are important for men who are having trouble talking about sexual preferences with their partners. Johnson and Zuccarini (2010) hypothesize that intimate connection between partners is the basis of sexual desire, so their treatment approach highlights the importance of communication. Conflict resolution is an important part of communication training, as therapists may help their male patients with desire concerns by teaching them strategies to minimize blaming and encourage self-soothing (Meana & Steiner, 2014a). Another relational approach to treating sexual desire is the adoption of the Good Enough Sex (GES) model, which embraces the acceptance of individual and couple differences in the meaning and importance of sexual desire within the context of the relationship (McCarthy & Metz, 2008; Metz & McCarthy, 2012).

Assessment of Erectile Disorder

The psychological assessment of ED includes identifying the situation(s) surrounding the onset of ED and the potential beliefs that were formed at that time. Beliefs may be specific to the relationship (i.e., a feeling of inadequacy with one specific partner) or generalize to all sexual encounters. Clinicians can determine if performance anxiety is present by assessing if the patient is able to obtain an erection during situations were performance is not required, such as during sleep or masturbation.

In cases where ED is the result of a vascular problem, laboratory assessments that measure genital blood inflow and outflow during sexual stimulation may be helpful. Blood outflow can be measured by injecting agents such as papaverine into the penile corpora cavernosa. The substance relaxes the smooth muscles at the base of the penis, which, in presence of normal blood outflow, produces penile erection even without sexual stimulation. When the drug fails to provide the expected erection, it is considered evidence for impairment in vascular mechanisms. Measurement of nocturnal penile erections which are expected to increase during the REM sleep cycle in sexually healthy men, is another commonly used technique for assessing potential vascular causes of ED. Assays of free and bioavailable serum testosterone are used to rule out abnormal hormone levels.

Treatment of Erectile Disorder

Biomedical treatments for ED include vacuum devices and constriction rings, intracavernosal injections, intraurethral pharmacotherapy, topical pharmacotherapy, oral pharmacotherapy, and penile implants. The first line of treatment is typically a form of PDE-5 inhibitor (Viagra, Levitra, Staxyn, Stendra, or Cialis). As described earlier, erection is a vascular phenomenon caused by increased blood pressure in the penis due to increased blood inflow and decreased blood outflow. The increment of blood inflow is regulated by the relaxation of the smooth muscles surrounding the arterioles, a phenomenon that allows the arteriole to dilate. Smooth muscle relaxation has been attributed to an increase in parasympathetic activity, which causes a release of the neurotransmitters acetylcholine, vasoactive intestinal polypeptide, and nitric oxide. Nitric oxide causes a greater amount of cyclic guanosine monophosphate (cGMP) to be available in the smooth muscles, and this causes the smooth muscles to relax. Normally, cGMP is broken down by enzymes known as phosphodiesterases (PDEs). However, this may be circumvented by inhibiting the activity of these enzymes. Viagra (sildenafil) and other drugs used to treat ED inhibit PDE Type 5. In doing so, these drugs enhance the concentration of cGMP, allowing for greater smooth muscle relaxation and therefore improved erection. Detumescence (i.e., loss of erection) occurs with the release of catecholamines during orgasm and ejaculation. Viagra and other PDE-5 inhibitors have a success rate of at least 65% (Shamloul & Ghanem, 2013). These drugs are typically well tolerated by a variety of patients, and their side effects are generally mild.

Despite these drugs’ success with facilitating erection, one study reported between 40% and 80% of men with ED who began treatment with Viagra stopped taking the medication . Similarly, in a more recent study, 50% of the sample discontinued PDE-5 treatment (Carvalheira, Pereira, Maroco, & Forjaz, 2012). Carvalheira and colleagues (2012) determined that the drop-out rate was highest in men with diabetes, and the majority of the men who discontinued treatment did so during the first three months. In the same study, a number of psychosocial factors, such as anxiety, negative emotions, and dysfunctional beliefs, were commonly cited reasons for discontinuation. It has been proposed that more comprehensive instruction at the beginning of pharmacological treatment as well as re-education throughout the course of treatment might improve the rates of medication compliance (Sato et al., 2007).

If PDE-5 inhibitors fail to treat the erectile problem, clinicians typically recommend vacuum constriction devices, vasoactive gels, and intracavernosal injections. Vacuum devices typically consist of a tube that is placed over the penis, and a vacuum pump that draws blood into the penile arteries. A constriction ring is placed at the base of the penis to prevent blood outflow so that the erection is maintained until completion of the sexual act. Vasoactive gels can be produced in different dosage levels and with different mixtures of vasodilators, such as alprostadil, prostaglandin EL, phentolamine, and papavarine. These gels are inserted into the urethra and are typically effective within 15 minutes of insertion.  Intracavernosal injections are the next line of treatment. Much like the gels, they are injected into the corpus cavernosum of the penis to induce erection. Although intracavernosal injections are effective in approximately 70% to 90% of patients, a large percentage of users discontinue treatment due to the inconvenience, cost, and/or invasiveness of treatment.

Penile implants are generally considered a last resort treatment technique when tissue damage or deterioration is severe or when all other treatments have failed. This may be the case in men with severe diabetes mellitus or who have had radical prostatectomy. Implants can be hydraulic, semi-rigid or soft silicone and consist of two or three cylinders placed in the space normally occupied by the spongy tissue in the penis. The patient’s ability to ejaculate after the implant surgery remains intact, however, the implant does not restore sensitivity or sexual desire that may have been present prior to the onset of ED. Implant surgeries usually result in decreased penis size which may dissuade some men from undergoing surgery.

Researchers are investigating the application of gene therapy principles to the treatment of ED. According to Burchardt and colleagues (2005), the penis provides an ideal location for gene therapy. Gene therapy offers hope for a potentially successful long-term treatment of ED, possibly even a cure for the disorder (Shamloul & Ghanem, 2013). Other new areas of ED treatment research include angiogenesis (Xie, Annex, & Donatucci, 2008), the growth of new blood cells from preexisting vasculature, and stem cell therapy (Bivalacqua et al., 2007).

Psychosocial treatments for ED include sensate focus, increasing the level of erotic stimulation during sexual activity, sex education, and interpersonal therapy (Shamloul & Ghanem, 2013). Sensate focus is considered to be the cornerstone of sex therapy. Developed by Masters and Johnson (1970), sensate focus centers on heightening awareness of the sensations associated with sexual activity rather than on the performance of the sexual act. In certain cases of ED, the patient may not experiencing sufficient erotic stimulation to achieve an erection. This may be due to the environment or to a lack of variety or skill on the part of the male and/or his partner. Couples in long-standing relationships may have a routine, predictable approach to sexual activity and thus may be more vulnerable to erectile problems as well as decreased sexual interest. Sex education involves therapist guidance on the different aspects of sexual intercourse, and interpersonal therapy focuses on the relationship problems that may be driving psychogenic erectile disorder.

Lifestyle modifications can significantly improve erectile function. Studies have shown that targeting factors associated with erectile problems, such as smoking, obesity, alcohol consumption, and physical activity reduces the rate of sexual dysfunction. In a meta-analysis of over 700 men, Gupta and colleagues (2011) assessed the effects of lifestyle modification on the severity of erectile problems. They found that, regardless of PDE-5 use, the adoption of lifestyle modifications provide incremental benefits on erectile function. However, the combination of lifestyle modifications and PDE-5 inhibitors may more effectively improve erectile function than either method alone. In a randomized controlled trial that compared the use of a PDE-5 inhibitor alone with a PDE-5 inhibitor plus at least three hours of aerobic exercise per week, the combined approach was more effective in the treatment of ED (Maio, Saraeb, & Marchiori, 2010).

Assessment of Delayed Ejaculation

Both physical and psychological assessment are necessary in order to gain a thorough understanding of the factors contributing to DE. To provide a thorough assessment, clinicians should conduct a genitourinary examination, check androgen levels, identify any physical anomalies, and assess any contributing neurological factors. Specific attention should be paid to the identification of urethral, prostatic, epididymal, and testicular infections (Corona, Jannini, Vignozzi, Rastrelli, & Maggi, 2012). Assessment of variables that improve or worsen performance in a given context may be informative, especially psychosocial factors like the use of fantasy during sex, anxiety during sexual activity, masturbatory patterns, and perceived partner attractiveness (Perelman, 2014).

Treatment of Delayed Ejaculation

There has been limited success in the development and testing of pharmacological agents aimed at treating DE. Drugs that have been shown to be somewhat effective may only indirectly affect ejaculatory latency by altering other components of the sexual response cycle or by countering the effects of the drugs that led to the ejaculatory problem in the first place (Rowland et al., 2010). In the future, alpha-1 adrenergic receptor agonists, such as imipramine, ephedrine, and midocrine, may play a role in the pharmacological treatment of DE. One study indicated that midocrine facilitated ejaculation in men who were previously unable to ejaculate (Safarinejad, 2009), but further research is necessary. According to Rowland (2010) other pharmacological agents, including yohimbine, buspirone, and oxytocin have been anecdotally associated with decreased ejaculation latency in men with DE. However, well-controlled studies with large sample sizes are needed to conclusively determine the effects of these drugs on ejaculation.

If the disorder is determined to be primarily psychological in origin, there are a number of psychosocial interventions that have been shown to effectively reduce ejaculation latency. Most sex therapists who treat DE rely on masturbatory retraining (Masters & Johnson, 1970) as a way to induce higher levels of arousal and help men rehearse for partnered sexual activity (Apfelbaum, 2000; Perelman, 2003; Perelman & Rowland, 2006). This intervention may be particularly helpful for men who have grown accustomed to masturbating in idiosyncratic ways, such as with specific objects or under certain conditions. Masturbatory retraining typically entails introducing the patient to an alternative style of masturbation that mimics the sensations of partnered sexual activity. According to Apfelbaum (2000), masturbation exercises that progress from neutral to pleasurable sensations remove the “demand aspects” of performance. If the disorder is derives from insufficient stimulation, therapists typically recommend vibrator stimulation, enhanced mental stimulation, and vigorous pelvic thrusting (Althof, 2012). For those who are experiencing DE due to heightened concern for the sexual pleasure of their partners, therapists encourage less focus on pleasing the partner and more attention to the self and the sensations experienced during sexual activity.

Assessment of Premature (Early) Ejaculation

A thorough assessment of PE includes measuring three factors; length of time from penetration to ejaculation (ejaculation latency), subjective feelings of control over ejaculation, and personal and relational distress caused by the condition. Usually these dimensions of PE are assessed with retrospective self-reports provided by the patient. Sometimes the patient is asked to measure the time from insertion to ejaculation or to have their partner provide an estimate of the man’s ejaculatory latency in order to help increase measurement reliability.

Treatment of Premature (Early) Ejaculation

The most commonly used psychotherapy for increasing ejaculatory latency is an integration of psychodynamic, behavioral, and cognitive approaches in a short-term model (Althof et al., 2005; Metz & McCarthy, 2003). According to Althof (2014), the focus of psychotherapy for men with PE is to learn to control ejaculation while understanding the meaning of the symptom and the context in which the symptom occurs. Psychodynamically-oriented therapists consider PE to be a metaphor for conflict in the relationship, while behavior-oriented therapists view the disorder as a conditioned response to certain interpersonal or environmental contexts (Althof, 2014). Common behavioral techniques for increasing ejaculatory latency are the squeeze technique developed by Masters and Johnson (1970) and the pause technique (Kaplan, 1989). The squeeze technique consists of engaging in sexual stimulation alone or with a partner for as long as possible before ejaculation. Before reaching the “point of inevitable ejaculation” the man is instructed to stop the activity and apply tactile pressure to the penile glans to decrease the urge to ejaculate but not to the point that he completely loses his erection. When the urge has subsided, the man resumes masturbation or intercourse stopping as many times as needed to delay ejaculation. The pause technique is similar to the squeeze technique with the exception that no pressure is applied to the penis. At times, clinicians may suggest using a PDE5 inhibitor (e.g., Viagra) along with these techniques so that the man can practice delaying ejaculation without worrying about maintaining an erection. Recent treatments combine these techniques and experimentation with new sexual positions that may reduce the propensity towards premature ejaculation. In one of the few well-controlled premature (early) ejaculation treatment studies, there was significant increase in ejaculation latency time among men treated with the squeeze technique compared to men in a wait-list control condition (Carufel & Trudel, 2006).

Medical treatments include the use of topical anesthetics, such as prilocaine/lidocaine, to diminish sensitivity used in combination with condoms (to prevent to the partner’s genitals from being anesthetized). In men with lifelong PE, treatment with pharmacological antidepressants have been shown to increase the ejaculation latency and increase sexual pleasure and satisfaction. Selective serotonin reuptake inhibitors, such as sertraline, fluoxetine, and paroxetine, have most often been used to treat PE because of their known side effects of delaying or inhibiting orgasm. These medications can be taken either daily or on demand 4 to 6 hours before sexual activity. Clinicians who treat men with PE have come to view the disorder as a “couple’s problem” and recommend including the partner in treatment as much as possible to enhance both treatment compliance and treatment efficacy (Rowland & Cooper, 2011).

Daproxetine has been approved for treatment of premature (early) ejaculation in over 30 countries, but not in the United States. It is considered to be a rapid-acting SSRI with a short half-life (Buvat, Tesfaye, Rothman, Rivas, & Giuliano, 2009; McMahon, Althof, & Kaufman, 2009) (Buvat et al., 2009). In clinical trials, daproxetine taken before sexual activity was shown to significantly increase ejaculation latency compared to a pill placebo (Levine, 2006).