Cindy M. Meston & Amelia M. Stanton
Definition, Diagnosis, and Prevalence
Erectile disorder (ED) is defined in the DSM-5 as the recurrent inability to achieve an erection, the inability to maintain an adequate erection, and/or a noticeable decrease in erectile rigidity during partnered sexual activity. In order to meet the diagnostic criteria, these symptoms must have persisted for at least six months and must have occurred on at least 75% of occasions. The disorder can be specified by severity and subtyped as either generalized or situational.
Men of all ages occasionally have difficulty obtaining or maintaining an erection, but true erectile disorder is more common after age 50. Laumann, Paik, and Rosen (1999) reported approximately 7% of men ages 18 to 29 years have erectile problems compared to 18% of men ages 50 to 59 years. Feldman and colleagues (1994) found that 10% of men under the age of 35 experience ED, while more than 50% of men over the age of 60 report erectile problems. The Global Study of Sexual Attitudes and Behaviors revealed that 18.8% of men over the age of 40 indicated that they sometimes experience erectile problems, but only 3.5% of them reported consistent erectile problems (Edward O Laumann et al., 2005; Nicolosi et al., 2004).
There are a number of factors beyond age that are associated with the prevalence of ED. Married men are less likely to report erectile problems compared to never married or divorced men (Laumann et al., 1999). Men with cardiovascular disease, diabetes, and metabolic syndrome are more likely to have ED than men without these diseases (Grover et al., 2006). Health factors such as smoking, obesity, and lack of exercise have been linked to higher prevalence of ED (Rosen, Miner, & Wincze, 2014).
Factors Associated With Erection and Erectile Disorder
There has been a great deal of research on erectile disorder, identifying a number of key biological and psychological causes. Biological factors are related to changes in blood flow to the penis, and psychological factors involve anxiety and negative expectations for performance.
Biological Factors
Erection is caused by increased blood pressure in the corpora cavernosa via increased blood inflow and decreased blood outflow. A large body of evidence indicates that the likelihood of ED increases with different types of vascular disease, such as hyperlipidemia, coronary heart disease, and diabetes (e.g. Kirby et al., 2005; Roumeguère, Wespes, Carpentier, Hoffmann, & Schulman, 2003; Seftel, Sun, & Swindle, 2004). The link between vascular problems and ED is so strong that ED is considered an early warning sign of vascular disease, especially in men under the age of 40 (Chew et al., 2010; Miner, 2009). Some researchers are in favor of viewing ED as a vascular disorder (Schouten et al., 2008; Thompson et al., 2005).
Surgery, diabetes, alcoholism, infectious diseases such as HIV and other viral infections, and pelvic pathologies such as systemic lupus are all potential causes of ED. Drugs that decrease dopamine or reduce testosterone production are also implicated in ED. These include antihypertensive medications, antipsychotic drugs, anxiolitics, antiandrogens, anti-cholesterol agents, and drugs used to regulate heart rate. Antiparkinsonian medications increase dopamine and facilitate erection.
Psychological Factors
With respect to the different psychological factors that play a role in male sexual function, Perelman (2009) proposed the sexual tipping point model, defined as any one individual’s characteristic threshold for the expression of a sexual response. Perelman suggested that one’s sexual tipping point is determined by a variety of multidimensional factors that fall into two general categories, physiological or organic issues and psychosocial, cultural, and behavioral issues. For men, psychosocial issues may include performance anxiety, spectatoring, strong religious backgrounds that lead to guilt or strong avoidance behaviors, and a history of sexual trauma (Perelman & Rowland, 2006; Waldinger & Schweitzer, 2005).
The major psychological contributors to ED as identified by Barlow’s (1986) feedback model of sexual dysfunction are anxiety, negative expectations, and spectatoring. Men who are anxious about not being able to have an erection tend to focus on themselves and how they are performing more than on what gives them pleasure. This spectatoring increases anxiety, which, physiologically, inhibits the relaxation of the smooth muscles necessary for erection and, psychologically, leads to a negative mood state and a focus on negative expectancies. Since the result is impaired erectile responding, the man’s fears of not being able to perform are confirmed, and they are likely to repeat the process in subsequent sexual situations. Performance anxiety is inherent in most cases of ED. As a man’s penis is visible to both the man and his partner, the occurrence—or absence—of an erection is a known event, which increases focus on performance. According to Rosen and colleagues (2014), men experiencing performance anxiety will not only worry about erections during sexual activity, but they also engage in visual or tactile checking of the penis.
By contrast, men with normal erectile response approach sexual situations with positive expectancies and a focus on erotic cues. Consequently, they become aroused and are able to obtain and sustain an erection, which creates a positive feedback loop for future sexual encounters. Although spectatoring can be detrimental for men of any age, it appears to be particularly problematic in young men when they are first becoming sexually active. In the absence of sexual experience and a variety of sexual events in which to view evidence of their ability to attain an erection, these young men are particularly vulnerable to the influence of negative expectations about erectile performance.
Other psychosocial factors can contribute to the development and maintenance of ED. According to Nobre and Pinto-Gouveia (2006, 2009), men are likely to meet for ED if they (1) endorse myths about male sexuality (e.g. “men always want to have sex”), (2) view themselves as incompetent, and (3) view their sexual problem as internal and stable over time. Mental health conditions, such as depression, generalized anxiety disorder, obsessive-compulsive disorder, and paraphilic disorders, have been linked to ED. In a survey of college-aged men, Harte and Meston (2011) found a high incidence of off-label Viagra use that was correlated with erectile disorder. They suggested that recreational Viagra use could lead to subsequent cause erectile problems by making users psychologically dependent on the drug for performance.
Assessment and Treatment of Erectile Disorder
The assessment of erectile disorder can be conducted via interview and may also include a physiological test. It is important for the assessor to determine the primary cause of the disorder, be it organic or psychogenic. Treatment approach will depend on the etiology of the erectile disorder, and the most common treatments include medication, individual psychotherapy, and lifestyle modifications.
Assessment
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
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 (Leiblum, 2002). 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).
