Pathophysiology of Premature Ejaculation

Abstract

Introduction Although the characteristics of premature ejaculation (PE) are established, the exact aetiology is largely unknown. Genetic, neurobiological, pharmacological, psychological, urological and endocrine factors have all been proposed. In addition PE and erectile dysfunction are often co-morbid. Aim This article provides an overview of the proposed biological and psychological aetiologies of PE. Methods Review of the literature. Main Outcome Measures Current data on the pathophysiology of PE. Results This review shows that most of the proposed biological and psychological aetiologies of PE are not evidence-based and/or that attempts to confirm them have given conflicting results. There are good data to support roles for genetic and psychological factors, either causal, or secondary to PE for the latter, in lifelong PE. Conversely, more evidence-based data support the responsibility of opioid substance withdrawal, prostatic inflammation or hyperthyroidism in some cases of acquired PE, in addition to a probable role of psychological factors. Conclusions The determinants of PE are certainly complex and multifactorial, while each partner's reaction to the frustration caused by the sexual dysfunction may exacerbate or perpetuate it. It is important to understand, as far as possible, the aetiology in the individual patient to ensure appropriate assessment and treatment. It should be noted that identification of an aetiological factor does not necessarily mean the cause of the PE has been completely explained, and the patient may require a combination of treatment approaches.

Pharmacology for the Treatment of Premature Ejaculation

“…The existence of a genetic component for lifelong PE could support the fact there are inherited differences in ejaculatory threshold. The allele of the polymorphic 5-HT transporter promoter region gene has been studied in a few genetic studies, different methods providing conflicting results (for review, see Buvat, 2011). It has recently been proposed that serotonergic genetic polymorphisms may be found only in men with PE who respond to SSRI treatment with an ejaculation delay (Waldinger, 2011).…”

“…It has recently been proposed that serotonergic genetic polymorphisms may be found only in men with PE who respond to SSRI treatment with an ejaculation delay (Waldinger, 2011). Overall genetic predisposition, which probably influences central 5-HT neurotransmission, should be considered as a hereditary susceptibility to a short IELT that needs, in most cases, to be maintained and heightened by psychological/environmental factors to lead to PE, because genetic effects represent only approximately 30% of the condition variance (Buvat, 2011). Serotonin dysregulation as an etiological hypothesis for PE explains only a small percentage (2-5%) of complaints of PE in the general population (Waldinger and Schweitzer, 2008).…”

Evolving therapeutic strategies for premature ejaculation: The search for on-demand treatment – topical versus systemic

“…Lifelong PE may be genetically determined, [8][9][10] due to specific genetic polymorphisms in the dopamine transporter gene. 11,12 Acquired PE is often attributed to endocrine, urological and neurological factors, or may be precipitated by psychological issues.…”

Diagnosis and Treatment of Premature Ejaculation by Urologists in South Korea

“…It has been suspected that PE may occur due to genetic, neurological, psychological, urological, and/or endocrine causes, but it is not yet certain which causes are the most relevant [7]. Since the etiology of PE has not yet been clarified, a range of treatment methods such as behavioral management; pharmacological treatment, including oral medications and topical anesthetics; and surgical treatment, which remains controversial, have been developed.…”