His452Tyr 5-HT2A polymorphism and intravaginal ejaculation latency time in Dutch men with lifelong premature ejaculation

Abstract

published version features the final layout of the paper including the volume, issue and page numbers. Link to publication General rightsCopyright and moral rights for the publications made accessible in the public portal are retained by the authors and/or other copyright owners and it is a condition of accessing publications that users recognise and abide by the legal requirements associated with these rights.• Users may download and print one copy of any publication from the public portal for the purpose of private study or research. • You may not further distribute the material or use it for any profit-making activity or commercial gain • You may freely distribute the URL identifying the publication in the public portal.If the publication is distributed under the terms of Article 25fa of the Dutch Copyright Act, indicated by the "Taverne" license above, please follow below link for the End User

Selective serotonin reuptake inhibitors combined with traditional Chinese medicine for premature ejaculation: A systematic review and meta‐analysis

“…The neural centers involved in ejaculation include the spinal cord ejaculatory center, the brain regions associated with the ascending fibers of the spinal cord ejaculatory center, and the descending fibers of some brain regions, which are involved by a variety of neurotransmitters. 42,43 At present, there are three hypotheses about the pathological mechanism of PE: central 5-hydroxytryptamine (5-HT) neurotransmitter disorder; the sensitivity of penis head is higher, and the representative area of genital cerebral cortex is wider; genetic variation of primary premature ejaculation. Among them, the influence of central 5-HT neurotransmitter disorder on ejaculation is a research hotspot in recent years.…”

“…Based on the new International Society for Sexual Medicine 41 guidelines, PE is defined as “ejaculation that always occurs after less than 1 min of vaginal penetration from the first sexual experience (lifelong PE), or a clinically significant and bothersome reduction in latency time, often ≤3 min (acquired PE), and the inability to delay ejaculation on all or nearly all vaginal penetrations,and negative personal consequences, such as distress, frustration and/or the avoidance of sexual intimacy.” Hence, we adopted IELT as the main index to assess the endpoint of PE. The neural centers involved in ejaculation include the spinal cord ejaculatory center, the brain regions associated with the ascending fibers of the spinal cord ejaculatory center, and the descending fibers of some brain regions, which are involved by a variety of neurotransmitters 42,43 . At present, there are three hypotheses about the pathological mechanism of PE: central 5‐hydroxytryptamine (5‐HT) neurotransmitter disorder; the sensitivity of penis head is higher, and the representative area of genital cerebral cortex is wider; genetic variation of primary premature ejaculation.…”

Possible Pathophysiological Roles of Neurotransmitter Systems in Men With Lifelong Premature Ejaculation: Protocol for a Scoping Review

“…Additionally, neurobiological causes for LPE are supported by the findings that demonstrate that single-psychotherapeutic treatments or sex therapy is not effective for a significant remission of symptoms [ 5 , 33 - 36 ]. It has been pointed out that neurotransmitter pathways have multiple complex mechanisms, multiple families, and subtypes of receptors, all of which affect one another, making one polymorphism unlikely to be the sole cause of LPE [ 10 , 12 , 37 , 38 ]. It is therefore likely that a subset of polymorphisms in one or more neurotransmitter systems may lead to LPE.…”

Possible Pathophysiological Roles of Neurotransmitter Systems in Men With Lifelong Premature Ejaculation: Protocol for a Scoping Review (Preprint)

“…Additionally, neurobiological causes for LPE are supported by the findings that demonstrate that single-psychotherapeutic treatments or sex therapy is not effective for a significant remission of symptoms [5,[33][34][35][36]. It has been pointed out that neurotransmitter pathways have multiple complex mechanisms, multiple families, and subtypes of receptors, all of which affect one another, making one polymorphism unlikely to be the sole cause of LPE [10,12,37,38]. It is therefore likely that a subset of polymorphisms in one or more neurotransmitter systems may lead to LPE.…”