ABSTRACT

Animal and human sexual psychopharmacological studies have attributed a serotonergic basis and possible genetic etiology to PE. 6-9 Male rat studies demonstrate that serotonin (5-hydroxytryptamine, 5-HT) and 5-HT receptors are involved in the ejaculatory process. The speed of ejaculation appears to be determined by 5-HT-2C and 5-HT-1A receptors. Stimulation of 5-HT-2C receptors with non-selective 5-HT-2C agonists delays ejaculation in male rats whereas stimulation of postsynaptic 5-HT-1A receptors results in shorter ejaculation latency.10 Administration of selective serotonin reuptake inhibitors (SSRIs) results in active blockade of presynaptic membrane 5-HT transporters, and the resultant higher synaptic cleft levels of 5-HT activate postsynaptic 5-HT-2C and 5-HT-1A receptors and delay ejaculation. 7,11

Premature ejaculation The American Psychiatric Association’s Diagnostic and Statistical Manual, 4th edition, text revision (DSM-IV-TR) defines PE as ‘… persistent or recurrent ejaculation with minimal stimulation before, on, or shortly after penetration, and before the person wishes it’. DSM-IV-TR goes on: ‘The clinician must take into account factors that affect duration of the excitement phase (such as age, novelty of the sexual partner or situation, and recent frequency of sexual activity); whether the disturbance causes marked distress or interpersonal difficulty; and whether the PE is not due exclusively to the direct effects of a substance (e.g., withdrawal from opioids).’ 12

This multivariate definition is manifestly inadequate, with a low predictive value for PE, 13 but it does encompass the

253 men (25.6%). 23 Men with PE appear younger than those without, and after adjusting for concomitant erectile dysfunction (ED) the risk of PE significantly decreased with aging. 24 Higher levels of education, divorce, and the presence of social phobia appear to increase the risk of PE. 24,25 A decreased risk of PE has been reported in men with treated diabetes, and no association was found with hypertension, cardiac disease, hypercholesterolemia, and peripheral or central neuropathy. Men with self-reported PE have a lower frequency of sexual intercourse and higher levels of intercourse-related anxiety, and they note greater impairment in intercourse satisfaction and sexual relationship satisfaction compared with men without PE. 26 However, they do not report a reduced quality of life, reduced sexual desire, or a reduced ability to become sexually aroused. 26,27

There are few published data on impact of birth country, religion, or culture on the prevalence of PE. An increased susceptibility to PE in men from the Indian subcontinent has been reported. 28,29 Kinsey’s observation that Asian men have shorter times to ejaculation than Caucasian men, who in turn have shorter times to ejaculation than Afro-Caribbean men, has been interpreted to suggest that some races are more ‘sexually restrained’ than others. 30,31 A recent study reported a preponderance of men from Middle Eastern and Asian backgrounds presenting for treatment of PE which exceeded the representation of these ethnic groups in the local population. 32,33

Classification of premature ejaculation

The premise that PE is a psychosomatic disturbance and due to

main dimensions of PE – ejaculatory latency, control, sexual satisfaction, and distress.