Many psychotropics can cause erectile dysfunction (ED) and other sexual problems (Tables 1 and 2). This side effect can discourage treatment compliance and jeopardize outcomes.
This article offers evidence-based strategies for preventing and treating psychotropic-induced ED. We also review information psychiatrists need to share with primary care physicians when treating a patient with ED.
Case report: A good relationship
Mr. A, age 52, has experienced diminishing erectile function for 6 months and now cannot achieve an erection. His relationship with his wife is good; he attributes loss of libido to his erection problem.
A pack-a-day smoker since age 18, Mr. A has type 2 diabetes and has been taking metformin, 850 mg bid, for 2 years. For about 2 months he has been taking sertraline, 50 mg, for depression and reports significantly improved mood, sleep, concentration, and appetite. He also has been taking lisinopril, 20 mg/d, for hypertension, and simvastatin, 40 mg nightly, for hyperlipidemia.
Table 1
Antidepressants associated with sexual dysfunction
| Drug class/agent | Proposed mechanism | Dysfunction |
|---|---|---|
| Monoamine oxidase inhibitors | Unknown | ED (rare), retarded ejaculation(rare) |
| Selective serotonin reuptake inhibitors | Increased serum prolactin (possible) Increased relative dopamine-to-serotonin reuptake inhibition Increased central serotonin | Decreased libido ED Anorgasmia Delayed/retarded ejaculation |
| Tricyclic antidepressants | CNS depression Anticholinergic activity | Decreased libido ED |
| Venlafaxine | Increased relative dopamine-to-serotonin reuptake inhibition Increased central serotonin | ED Anorgasmia Delayed/retarded ejaculation |
| ED: Erectile dysfunction | ||
Mr. A’s hemoglobin A1C is 9.8%, indicating poor diabetes control. His blood pressure is 168/94 mm Hg, well above his goal of <135/80. He has no chest pain or history of myocardial infarction; a recent exercise stress test indicated no coronary disease.
Discussion. Several medical causes—diabetes, hypertension, hyperlipidemia, and 34 years of heavy smoking—could explain Mr. A’s ED. Vascular disease is suspected, although the stress test was negative.
Identifying a specific cause is crucial to treating ED but may be difficult. Up to 80% of cases can be traced to one or more organic causes.1 Mr. A’s depression could be a factor, although psychogenic ED is not common. Adding the selective serotonin reuptake inhibitor (SSRI) sertraline may also have worsened his ED.
Other possible causes of ED include:
- nonpsychotropic drugs (to view a list of agents, see this article at currentpsychiatry.com)
- decreased libido, delayed orgasm, and anorgasmia. Decreased libido and anorgasmia are often misdiagnosed as primary ED because the presenting symptoms are similar.
ED treatment begins with managing underlying medical problems, although optimal control alone may not alleviate ED. Encourage the patient to stop smoking and offer smoking cessation strategies.
Alert the primary care physician and patient when prescribing a psychotropic associated with sexual side effects, and explain the drug’s potential benefits. Assess baseline sexual function before starting the psychotropic so that changes in sexual function can be detected. Report your findings to the referring physician after each visit.
If ED is believed to be psychotropic-induced:
- maintain the psychotropic regimen for 6 to 8 weeksto see if the patient builds a tolerance to its sexual side effects.
- lower the psychotropic dosage. In one study,2 nearly 75% of patients whose SSRI dosages were reduced by one-half reported improved sexual function with sustained antidepressant effectiveness. This SSRIeffect has been replicated and has also been demonstrated with imipramine.3-5
- schedule 1- to 2-day drug “holidays” (on weekends, for example) for medications with a short halflife (such as sertraline or paroxetine) if the underlying condition permits.7
Table 2
Other psychotropics associated with sexual dysfunction
| Drug class/agent | Proposed mechanism | Dysfunction |
|---|---|---|
| Amphetamines | Increased relative sympathetic nervous syndrome/parasympathetic nervous system activity | ED |
| Anticholinergics | Anticholinergic activity | ED |
| Antipsychotics (typical and atypical) | CNS depression, increased serum prolactin Anticholinergic activity Alpha1-receptor blockade Decreased internal urethral sphincter closure | Decreased libido ED Retarded ejaculation Retrograde ejaculation |
| Barbiturates, benzodiazepines, CNS depressants | CNS depression | Decreased libido |
| Carbamazepine, gabapentin | Decreased androgenic activity | Decreased libido, ED, retarded ejaculation |
| Disulfiram | Unknown | ED |
| Dopamine-receptor agonists | Unknown | ED |
| Dopamine-receptor antagonists | Increased serum prolactin | Decreased libido |
| ED: Erectile dysfunction | ||
If these measures do not work, individualized treatment of the sexual dysfunction becomes necessary. For some patients, switching psychotropics may be necessary to ensure compliance and preserve response. In cases such as Mr. A’s, however, the physician and patient may not want to stop a psychotropic that is working. For these patients, consider adding a drug to restore sexual function.
If ED persists after treatment, the primary care physician may refer the patient to a urologist.
Case report:Continued
Mr. A was advised to quit smoking and control his blood pressure and diabetes. His primary care doctor restarted lisinopril, 20 mg/d, increased his metformin to 1,000 mg bid, and added sildenafil, 50 mg before anticipated sexual activity. Mr. A says sildenafil has worked well.
Psychotropics and sexual dysfunction
Several physiologic processes contribute to psychotropics’ sexual side effects.
Libido is primarily a function of hormonal and CNS control. By contrast, erectile functions are mediated through local parasympathetic stimulation and ejaculation, which are controlled by norepinephrine. Orgasm is a cerebral cortical event distinct from ejaculation; either process can be disturbed independently. Elevated central serotonin levels inhibit orgasm and, to a lesser extent, ejaculation. Dopamine elevation over time leads to hyperprolactinemia and resultant hypotestosteronemia, decreasing libido.