Premature ejaculation

There is no uniform cut-off defining "premature", but a consensus of experts at the International Society for Sexual Medicine endorsed a definition of around one minute after penetration.

[3] Several physiological mechanisms have been hypothesized to contribute to causing premature ejaculation, including serotonin receptors, a genetic predisposition, elevated penile sensitivity and nerve conduction atypicalities.

The pathophysiology of lifelong PE is mediated by a complex interplay of central and peripheral serotonergic, dopaminergic, oxytocinergic, endocrinological, genetic and epigenetic factors.

It involves deposition of fluid from the ampullary vas deferens, seminal vesicles and prostate gland into the posterior urethra.

It involves closure of bladder neck, followed by the rhythmic contractions of the urethra by pelvic-perineal and bulbospongiosus muscle and intermittent relaxation of the external male urethral sphincter.

These motor neurons are located in the thoracolumbar and lumbosacral spinal cord and are activated in a coordinated manner when sufficient sensory input to reach the ejaculatory threshold has entered the central nervous system.

[15][16] The 1948 Kinsey Report suggested that three-quarters of men ejaculate within two minutes of penetration in over half of their sexual encounters.

[17] Current evidence supports an average intravaginal ejaculation latency time (IELT) of six and a half minutes in 18- to 30-year-olds.

[22] The Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5) defines premature ejaculation as "A persistent or recurrent pattern of ejaculation occurring during partnered sexual activity within approximately 1 minute following vaginal penetration and before the person wishes it," with the additional requirements that the condition occurs for a duration longer than 6 months, causes clinically significant distress, and cannot be better explained by relationship distress, another mental disorder, or the use of medications.

[2] The DSM-5 allows for specifiers whether the condition is lifelong or acquired, applying in general or only to certain situations, and severity based on the time under one minute, however these subtypes have been criticised as lacking validity due to insufficient evidence.

Other self-treatments include thrusting more slowly, withdrawing the penis altogether, purposefully ejaculating before sexual intercourse, and using more than one condom.

Sensing it, they were to signal their partner, who squeezed the head of the penis between thumb and index finger, suppressing the ejaculatory reflex and allowing the male to last longer.

[35] Dapoxetine, a selective serotonin reuptake inhibitor (SSRI), has been approved for the treatment of premature ejaculation in several countries.

[36] Premature ejaculation can return upon discontinuation,[36] and the side effects of these SSRIs can also include anorgasmia, erectile dysfunction, and diminished libido.

[42] Two different surgeries, both developed in South Korea, are available to permanently treat premature ejaculation: selective dorsal neurectomy (SDN)[43] and glans penis augmentation using a hyaluronan gel.

[62] Sex researcher Alfred Kinsey did not consider rapid ejaculation a problem, but viewed it as a sign of "masculine vigor" that could not always be cured.

[64] In the 19th century, a symptom called spermatorrhoea invented by William Acton in 1857, meaning excessive or involuntary semen discharge, was developed and at the time used as a medical justification of celibacy.

[66] The origin of the modern version of ejaculatio praecox, called premature ejaculation, is thought to have begun with Alfred Adler before major developments of psycohanalytic theory.