emphasis on orgasm and ejaculation

Fertil Steril. Author manuscript; available in PMC 2016 Jun 7.

Published in final edited form as:

PMCID: PMC4896089

NIHMSID: NIHMS789951

, M.D., M.Sc.,^a,b, M.D., M.A.S.,^b and , M.D.^b

Amjad Alwaal

^aDepartment of Urology, King Abdulaziz University, Jeddah, Saudi Arabia

^bDepartment of Urology, University of California, San Francisco, California

Benjamin N. Breyer

^bDepartment of Urology, University of California, San Francisco, California

Tom F. Lue

^bDepartment of Urology, University of California, San Francisco, California

^aDepartment of Urology, King Abdulaziz University, Jeddah, Saudi Arabia

^bDepartment of Urology, University of California, San Francisco, California

Reprint requests: Amjad Alwaal, M.D., M.Sc., King Abdulaziz University, Department of Urology, P. O. Box 80215, Jeddah, Saudi Arabia 21589 (moc.oohay@lawdajma).The publisher’s final edited version of this article is available at Fertil SterilSee other articles in PMC that cite the published article.

Abstract

Orgasm and ejaculation are two separate physiological processes that are sometimes difficult to distinguish. Orgasm is an intense transient peak sensation of intense pleasure creating an altered state of consciousness associated with reported physical changes. Antegrade ejaculation is a complex physiological process that is composed of two phases (emission and expulsion), and is influenced by intricate neurological and hormonal pathways. Despite the many published research projects dealing with the physiology of orgasm and ejaculation, much about this topic is still unknown. Ejaculatory dysfunction is a common disorder, and currently has no definitive cure. Understanding the complex physiology of orgasm and ejaculation allows the development of therapeutic targets for ejaculatory dysfunction. In this article, we summarize the current literature on the physiology of orgasm and ejaculation, starting with a brief description of the anatomy of sex organs and the physiology of erection. Then, we describe the physiology of orgasm and ejaculation detailing the neuronal, neurochemical, and hormonal control of the ejaculation process.

Keywords: Erectile function, male sexual function, ejaculation, orgasm

Ejaculatory dysfunction is one of the most common male sexual dysfunctions that is often mis-diagnosed or disregarded. At present, there is no definitive cure for ejaculatory dysfunctions (1). New research on the physiology of ejaculation keeps emerging to identify targets of treatment. However, knowledge about this topic is still lacking. In the present article, we summarize the current literature on the physiology of ejaculation. We describe the anatomy of the organs involved and the erection physiology. We discuss the physiology of orgasm and ejaculation as two separate physiological processes. In addition, we describe the neurochemical and hormonal regulation of the ejaculation process.

FUNCTIONAL ANATOMY OF THE MALE GENITAL ORGANS

The male genital system consists of external and internal reproductive and sexual organs such as the penis, prostate, epididymis, and testes. shows the gross anatomy of the ejaculatory structures. provides a summary of the functional anatomy of these organs (2–5).

Gross anatomy of the ejaculation structures. (Reprinted with permission from Sheu G, Revenig LM, Hsiao W. Physiology of ejaculation. In: Mulhall JP, Hsiao W, eds. Men’s sexual health and fertility: a clinician’s guide. New York: Springer; 2014:15.)

TABLE 1

Summary of the functional anatomy of the male genital organs.

Organ	Characteristics
Penis	Composed of three chambers: paired corpora cavernosa (erectile bodies) and a midline ventral corpus spongiosum  (contains urethra)
	Main blood supply: internal pudendal artery
	Somatic sensation: pudendal nerve (S2-S4)
	Autonomic nerve fibers: cavernous nerves (pelvic plexus) contain both sympathetic (hypogastric plexus) and  parasympathetic nerve fibers (S2-S4)
Urethra	Four segments: prostatic urethra, membranous urethra (passes through the urogenital diaphragm), bulbar urethra,  and penile urethra (ends with a small dilatation at the fossa navicularis near the meatus)
	Cowper’s glands: located on both sides of the membranous urethra and open in the bulbar urethra
	Veromontanum: small elevation of the posterior wall of the membranous urethra, related to ejaculatory ducts, prostatic  utricle, and prostatic ducts
Testis	It is divided by fibrous septa into many lobules containing seminiferous tubules
	Leydig cells: main source of T production
	Seminiferous tubules: contain germ cells and sertoli cells. Forms the rete testis inside the testis mediastinum
	Rete testis: gives rise to 15–20 efferent ductules
Epididymis	Posterior and superior to the testicle
	Composed of head, body, and tail
	Efferent ductules unite to form the convoluted duct of the epididymis
	Becomes the vas deferens at the end of the tail
Vas deferens	Muscular tube; typically 45 cm long and has a 2.5 mm diameter
	It is a continuation of the epididymis
	Joins the seminal vesicle duct to form the ejaculatory duct, which then drains into the veromontanum
	Supplied by the vasal artery, a branch of the inferior vesical artery
Prostate	Surrounds the prostatic urethra
	Composed of 70% glandular component and 30% fibromuscular component
	Arterial supply: inferior vesical and middle rectal arteries
Seminal  vesicles	Paired structures; located lateral to the vas deferens
	Typically 5 cm long and 1 cm wide
	Joins the vas to form the ejaculatory duct
	Arterial supply: inferior vesical and middle rectal arteries

PHYSIOLOGY OF ERECTION

The penile erection results from complex neurovascular mechanisms. Several central and peripheral neurological factors in addition to molecular, vascular, psychological and endocrino-logical factors are involved, and the balance between these factors is what eventually determines the functionality of the penis. In this section, we summarize some of those mechanisms.

Cerebral Control

Cerebrally controlled penile erections are induced through erotic visual stimuli or thoughts. The main cerebral structures involved in erection are contained within the medial preoptic area (MPOA) and paraventricular nucleus (PVN) in the hypothalamus (6). Dopamine is the most important brain neurotransmitter for erection, likely through its stimulation of oxytocin release (7). Another important neurotransmitter is norepinephrine, which is demonstrated through the erectogenic effect of the α-2 agonist (Yohimbine) (8). Several other brain neurotransmitters are involved in the erection process to varying degrees such as nitric oxide (NO), α-melanocyte stimulating hormone (α-MSH), and opioid peptides (9).

Autonomic Control

Parasympathetic stimulation is the main mediator for penile tumescence, although central suppression of the sympathetic nervous system also plays a role. Parasympathetic supply to the penis is derived from the sacral segments S2-S4 (10). However, patients with sacral spinal cord injury still maintain erections through psychogenic stimulation, although of less rigidity than normal. These psychogenic erections do not occur in patients with lesions above T9 (11), suggesting that the main mechanism for these erections is central suppression of sympathetic stimulation (12). Patients with lesions above T9 still may maintain reflexogenic erections. This implies that the main mechanism for reflexogenic tumescence is the preservation of the sacral reflex arc, which mediates erection through tactile penile stimulation (13, 14).

Molecular Mechanisms

The penis at baseline is in a flaccid state maintained by the contraction of corporal smooth muscles and constriction of cavernous and helicine arteries leading to moderate state of hypoxia with partial pressure of oxygen of 30–40 mm Hg (15). During sexual arousal, NO is released from cavernous nerve terminals through the action of neuronal NO synthase (16). The NO activates guanylate cyclase, which in turn converts guanosine triphosphate to cyclic guanosine monophosphate (15, 17), leading eventually to smooth muscle relaxation and vasodilation (18). Although the initiation of tumescence is through neuronal NO synthase, the maintenance of erection is through endothelial NO synthase (19). The eventual smooth muscle relaxation and vasodilation results in blood flowing into the paired corpora and filling of the sinusoids, with increased intracorporal pressure (to >100 mm Hg during full erection) and compression of the subtunical venules, markedly reducing the venous outflow (13).

PHYSIOLOGY OF ORGASM

There is no standard definition of orgasm. Each specialty such as endocrinology or psychology examines this activity from each one’s perspective, making it difficult to reach a consensus on the definition. Orgasm is generally associated with ejaculation, although the two processes are physiologically different (20). Certain physiological features are associated with orgasm, including hyperventilation up to 40 breaths/min, tachycardia, and high blood pressure (21). In fact, faster heart rate was found to be an indicator of “real” male orgasm during intravaginal intercourse, differentiating it from “fake” orgasm (22). Orgasm is also associated with powerful and highly pleasurable pelvic muscle contractions (especially ischiocavernosus and bulbocavernosus) (23), along with rectal sphincter contractions and facial grimacing (21). There is also an associated release and elevation in PRL and oxytocin levels after orgasm; however, the significance of this elevation is not entirely clear (24).

Studies using positron emission tomography, which measures changes in regional cerebral blood flow, have identified areas of activation in the brain during orgasm. Primary intense activation areas are noted to be in the mesodiencephalic transition zones, which includes the midline, the zona incerta, ventroposterior and intralaminar thalamic nuclei, the lateral segmental central field, the suprafascicular nucleus, and the ventral tegmental area. Strong increases were seen in the cerebellum. Decreases were noted at the entorhinal cortex and the amygdale (25).

Quality and intensity of orgasms are variable. For instance, short fast buildup of sexual stimulation toward orgasm is associated with less intense orgasms than slow buildup. Early orgasms are less satisfying than later orgasms in life as the person learns to accept the pleasure associated with orgasms. Lower levels of androgen are associated with weaker orgasms, such as in hypogonadism or in older age (20). It has been suggested that pelvic muscle exercises, particularly the bulbocavernosus and ischiocavernosus muscles, through contracting those muscles 60 times, 3 times daily for 6 weeks will enhance the pleasure associated with orgasm (20). However, the effort and time associated with such exercises prevent their utilization. The orgasm induced through deep prostatic massage is thought to be different from the orgasm associated direct penile stimulation. Although penile stimulation orgasms are associated with 4–8 pelvic muscle contractions, prostatic massage orgasms are associated with 12 contractions. Prostatic massage orgasms are thought to be more intense and diffuse than penile stimulation orgasms, but they require time and practice and are not liked by many men (20, 26, 27).

Following orgasm in men is a temporary period of inhibition of erection or ejaculation called the refractory period. This is a poorly understood phenomenon, with some investigators suggesting a central rather than spinal mechanism causing it (28). Elevated levels of PRL and serotonin after orgasm have been suggested as a potential cause; however, there is much debate about their exact role (29). More research is still needed in the area of male orgasm (20).

PHYSIOLOGY OF EJACULATION

Ejaculation is a physiological process heavily controlled by the autonomic nervous system. It consists of two main phases: emission and expulsion. The main organs involved in ejaculation are the distal epididymis, the vas deferens, the seminal vesicle, the prostate, the prostatic urethra, and the bladder neck (30).

Emission

The first step in the emission phase is the closure of bladder neck to prevent retrograde spillage of the seminal fluid into the bladder. This is followed by the ejection of prostatic secretions (10% of the final semen volume) containing acid phosphatase, citric acid, and zinc, mixed with spermatozoa from the vas deferens (10% of the volume) into the prostatic urethra. Subsequently, the fructose-containing seminal vesicle fluid alkalinizes the final ejaculatory fluid. The seminal vesicle fluid constitutes 75%–80% of the final seminal fluid. Cowper’s glands and periurethral glands produce a minority of the seminal fluid (1, 31). The organs involved in the ejaculation process receive dense autonomic nerve supply, both sympathetic and parasympathetic, from the pelvic plexus. The pelvic plexus is located retroperitoneally on either side of the rectum, lateral and posterior to the seminal vesicle (32). It receives neuronal input from the hypogastric and pelvic nerves in addition to the caudal paravertebral sympathetic chain (33). The sympathetic neurons play the predominant role in the ejaculation process. Their nerve terminals secrete primarily norepinephrine, although other neurotransmitters such as acetylcholine and nonadrenergic/noncholinergic also play important roles (34). The role of the hypogastric plexus in emission is best demonstrated clinically by the loss of emission after non-nerve sparing para-aortic lymph node dissection for testicular cancer (35), and induction of emission in paraplegic men through electrical stimulation of superior hypogastric plexus (35). Input from genital stimulation is integrated at the neural sacral spinal level to produce emission (36). The emission phase of ejaculation is also under a considerable cerebral control, and can be induced through physical or visual erotic stimulation (37).

Expulsion

Expulsion follows emission as the process of ejaculation climaxes, and refers to the ejection of semen through the urethral meatus. The semen is propelled through the rhythmic contractions of the pelvic striated muscles in addition to the bulbospongiosus and ischiocavernosus muscles (23). To achieve antegrade semen expulsion, the bladder neck remains closed, whereas the external urethral sphincter is open. The external sphincter and the pelvic musculature are under somatic control; however, there is no evidence that voluntary control plays a role in the expulsion process (30). The exact trigger for expulsion is unknown. It has been suggested that a spinal center is triggered during emission of seminal fluid into the prostatic urethra (38). However, there is mounting evidence through clinical and experimental studies to suggest that this is not the case. For instance, men can still have rhythmic contractions during orgasm despite “dry ejaculation,” for example, due to prostatectomy (23, 39, 40). This, in addition to the identification of spinal generator for ejaculation (SGE) in rats, led to the postulation that the process of expulsion is a continuum of the process initiated through emission, after reaching a certain spinal activation threshold (30, 41).

NEURONAL CONTROL OF EJACULATION

Ejaculation is heavily controlled by the nervous system. summarizes the reflex circuit necessary to elicit ejaculation.

Reflex circuit needed to establish ejaculation. (Reprinted with permission from Sheu G, Revenig LM, Hsiao W. Physiology of ejaculation. In: Mulhall JP, Hsiao W, eds. Men’s sexual health and fertility: a clinician’s guide. New York: Springer; 2014:18.)

Peripheral Nervous System

Afferents

The main sensory input from the penis comes from the dorsal nerve of the penis, which transmits sensation from the glans, prepuce, and penile shaft. It transmits signals to the upper and lower segments of the sacral spinal cord (42). The glans contains encapsulated nerve endings, termed Krause-Finger corpuscles, whereas the remaining penile shaft contains free nerve endings. Stimulation of these corpuscles potentiated by stimulation from other genital areas, such the perineum, testes, and penile shaft, play an important role in the ejaculation process (43). A secondary afferent route is through the hypogastric nerve, which runs through the paravertebral sympathetic chain to enter the spinal cord through the thoracolumbar dorsal roots (44). The sensory afferents terminate in the medial dorsal horn and the dorsal gray commissure of the spinal cord (45).

Efferents

The efferent peripheral nervous system constitutes of sympathetic, parasympathetic, and motor nervous components (46). The soma of the preganglionic sympathetic cell bodies involved in ejaculation are located in the intermedio-lateral cell column and in the central autonomic region of the thoracolumbar segments (T12-L1) (47). The preganglionic sympathetic fibers emerge from the ventral roots of the spinal cord and travel through the paravertebral sympathetic chain to relay either directly through the splanchnic nerve, or through relaying first in the celiac superior mesenteric ganglia and then through the intermesenteric nerve, to the inferior mesenteric ganglia (48). The hypogastric nerve then emanates from the inferior mesenteric ganglia to join the parasympathetic pelvic nerve to form the pelvic plexus, which then sends fibers to the ejaculation structures (49). The preganglionic parasympathetic cell bodies are located in the sacral parasympathetic nucleus. The sacral parasympathetic nucleus neurons travel then in the pelvic nerve to the post-ganglionic parasympathetic cells located in the pelvic plexus. The motor neurons involved in ejaculation are located in Onuf’s nucleus in the sacral spinal cord, which projects fibers through the motor component of the pudendal nerve to reach the pelvic musculature, including the bulbospongiosus, ischiocavernosus, and external urethral sphincter (50).

Central Nervous System

Spinal network

The thoracolumbar sympathetic, sacral parasympathetic (mainly sacral parasympathetic nucleus), and somatic sacral Onuf’s nucleus ejaculatory spinal nuclei play an important role in the integration of peripheral and cerebral input and coordinating output to the pelviperineal structures involved in ejaculation (46). An additional spinal center is the SGE located in laminae X and VII of L3-L4 spinal segments (51). The SGE contains spinal interneurons called lumbar spinothalamic cells, which project fibers to the parvocellular subparafascicular nucleus of the thalamus in addition to preganglionic sympathetic and parasympathetic neurons innervating the pelvis (41). The SGE stimulation elicits a complete ejaculatory response resulting in collection of motile spermatozoa in anesthetized rats (52). Further research on the SGE spinal center is still needed, and it is unclear whether it contains other cells than lumbar spinothalamic cells.

Brain network

Sensory and motor areas in the brain play an important role in the ejaculation, which requires a highly coordinated and integrated central process. The study by Holstege et al. (25) using positron emission tomography showed that certain areas in the brain are activated in the orgasm and ejaculation process. Furthermore, specific areas in the brain have been involved in the ejaculation process, as demonstrated in animal immunohistochemical studies examining Fos protein pattern of expression (53–56), and confirmed using a serotonin 1A subtype receptor agonist proejaculatory pharmacologic agent in rats (57). These are discrete areas within the posteromedial bed nucleus of stria terminalis, the parvicellular part of the subparafascicular thalamus, the posterodorsal preoptic nucleus, and the posterodorsal medial amygdaloid nucleus. There are reciprocal connections that link those areas to the MPOA of the hypothalamus, a brain area with a well-established role in controlling sexual behavior as demonstrated by anatomical and functional studies (54, 55, 58). Electrical or chemical stimulation of the MPOA elicited ejaculation (59–62), whereas an MPOA lesion was shown to abolish both phases of ejaculation (63). No direct connections of MPOA to the spinal centers for ejaculation were found on neuroanatomical studies; however, there are projections of MPOA to other regions in the brain involved in ejaculation, such as PVN, the periaqueductal gray, and the paragigantocellular nucleus (nPGi) (64–66).

The PVN projects to pudendal motor neurons located in the L5-L6 spinal segment in addition to autonomic preganglionic neurons in the lumbosacral spinal cord in rats (45, 67, 68). It also projects to nPGI in the brainstem (69). Bilateral lesions of the PVN with N-methyl-D-aspartate (NMDA) results in a one-third reduction of the seminal ejaculate material weight (70). The parvicellular part of the subparafascicular thalamus was found to send projections to bed nucleus of stria terminalis, medial amygdala (MeA), and MPOA (71, 72) and receives input from lumbar spinothalamic cells (51). The precise role of these regions is still unclear but they are likely involved in relaying genital signals to MPOA (53, 55). The brainstem regions (nPGI and periaqueductal gray) have recently received increasing attention. The nPGI nucleus likely plays an inhibitory role in ejaculation as evidenced through the urethrogenital reflex experimental model, a rat model for the expulsion phase of ejaculation (73, 74). Using the same model, the periaqueductal gray was found to be important for the ejaculation process, likely by acting as a relay between MPOA and nPGI (75). Midbrain structures have a significant role in ejaculation; however, much is still unknown about their exact role and further research is needed. summarizes the putative brain structures involved in ejaculation.

Putative brain structures involved in ejaculation. BNSTpm = posteromedial bed nucleus of stria terminalis; MeApd = posterodorsal medial amygdaloid nucleus; MPOA = medial preoptic area; PAG = periaqueductal gray; nPGi = paragigantocellular nucleus; PNpd = posterodorsal preoptic nucleus; PVN = paraventricular thalamic nucleus; SPFp = parvicellular part of the subparafascicular thalamus. (Reprinted with permission from Clement P, Giuliano F. Physiology of ejaculation. In: Mulhall JP, Incrocci L, Goldstein I, Rosen RC, eds. Cancer and sexual health. New York: Springer; 2011:82.)

NEUROCHEMICAL REGULATION OF EJACULATION

Many neurotransmitters are involved in the ejaculation process. Defining the exact role of these neurotransmitters is difficult given the variety of sexual parameters affected, the different sites of action within the spinal and the supraspinal pathways, and the presence of multiple receptor types. Some of the molecules that received special attention for their role in ejaculation are mentioned later.

Dopaminergic Control

Dopamine is known to be important for normal male sexual response (76, 77). Two families of dopamine receptors exist, D1-like (D1 and D5 receptors) and D2-like (D2, D3, and D4 receptors) (46). In rats, D2-like receptors are known to stimulate ejaculation (78, 79), and trigger ejaculation even in anesthetized rats (80, 81). Systemic injection of the D3 receptor agonist 7-OH-DPAT has been shown to trigger ejaculation in rats without affecting arousal (82, 83). It also triggers ejaculation in anesthetized rats when injected directly into the cerebral ventricles or MPOA with the effect being specifically reversed by the D3, not the D2 antagonist (84, 85). The D3 receptor blockage has been shown to inhibit the expulsion phase of ejaculation and lengthen ejaculation latency in rats (86).

Serotonergic Control

Evidence suggests that serotonin (5HT) inhibits ejaculation (87). Selective serotonin reuptake inhibitors increase 5HT tone resulting in impairment of ejaculation, which led to their clinical use in premature ejaculation. This inhibitory effect is likely to occur in the brain (88), as 5HT effect on ejaculation in the spine is likely stimulatory (89). The amphetamine derivative p-chloroamphetamine leads to a sudden release of 5HT in synaptic clefts triggering ejaculation in anesthetized rats with complete spinal cord lesion (89). Intrathecal serotonin or selective serotonin reuptake inhibitor injection leads to enhancement of the expulsion phase of ejaculation (88). There are 14 receptor subtypes for 5HT, with 1A, 1B, and 2C being the ones involved in ejaculation (90). It is difficult to designate one influence for each receptor subtype, as each receptor could either activate or inhibit ejaculation depending on its location within the central nervous system (46).

Nitric Oxide

The role of NO in ejaculation has received special attention after the introduction of type-5 phosphodiesterase (PDE5) inhibitors and using them for premature ejaculation. Nitric oxide has an inhibitory role on the ejaculation process (1). Centrally, intrathecal sildenafil results in elevation of NO and cyclic guanosine monophosphate levels in MPOA causing a decreased peripheral sympathetic tone and inhibition of ejaculation (91). N-Nitro-l-arginine methyl-ester injection, an NO synthase inhibitor, was shown to increase the number of seminal emissions and reduce latency to first seminal emission in rats (92). Peripherally, nitronergic innervation and NO synthase were found in the seminal vesicle, vas deferens, prostate, and urethra (93–97). Therefore, drugs such as PDE5 inhibitors or NO donors are associated with reduced seminal vesicle contraction and inhibit seminal emission (92). The administration of NO inhibitors, such as l-nitroarginine-methylester, diminishes human seminal vesicle contraction (98), inhibits vasal contraction in guinea pigs (99), and decreases latency to ejaculation in rats (100). Furthermore, reduced latency to emission was found in knockout mice for the gene encoding endothelial NO synthase compared with their wild-type counterparts (101).

HORMONAL REGULATION OF EJACULATION

Although male sexual function is heavily regulated by the hormonal system, there are few clinical studies performed to evaluate hormonal regulation of ejaculation, and the knowledge about hormonal effect on ejaculation is still lacking. We discuss some of the studies examining the effect of different hormones on ejaculation.

Oxytocin

Oxytocin is an oligopeptide synthesized in the supraoptic and PVN of the hypothalamus and released from the posterior pituitary gland. Oxytocin serum level increases after male ejaculation to levels ranging from 20%–360% of normal levels before reaching baseline at 10 minutes after ejaculation (102). Pharmacologic oxytocin administration in humans and animals results in increased ejaculated spermatozoa (103), confirming that oxytocin has a role in male genital tract motility. It was specifically found to augment powerful epididymal contractions and sperm motility (104), an important effect blunted by pretreatment with the oxytocin antagonist (des Gly–Nh3d(Ch3)5–[d-Tyr2,Thr4] ornithine vasotocin) (105). Peripheral oxytocin receptors were found to be highly expressed in the epididymis and tunica albuginea (in smooth muscles more than epithelial cells), and to a lesser extent in the vas deferens and seminal vesicle (104). Oxytocin has a synergistic action on the epididymis with endothelin-1, where they augment epididymal contraction and propel spermatozoa forward (102, 106). Injection of oxytocin into the cerebral ventricles in male rats facilitated ejaculation by shortening the ejaculation latency and postejaculatory refractory periods (107), whereas these effects were curbed using the oxytocin receptor antagonist (d(Ch3)5–Tyr(Me)–[Orn8]vasotocin) injected into the cerebral ventricles (108). Despite these encouraging findings and some anecdotal evidence suggesting that intranasal oxytocin can facilitate orgasm in an anorgasmic male (109), a double-blind placebo-controlled clinical study (110) failed to demonstrate an effect of intranasal oxytocin on sexual behavior.

Prolactin

Hyperprolactinemia has a marked inhibitory effect on male sexual desire (111). A modest increase in serum PRL levels (15–20 ng/mL) has been detected in men after orgasm, and could be contributing to the after-orgasm refractory period (112). Some investigators have hypothesized that a low PRL level is a cause of premature ejaculation, where PRL levels were similarly low in those men with lifelong or acquired premature ejaculation (113). Further research is needed on this issue.

Thyroid Hormones

The relationship between thyroid hormonal abnormalities and ejaculatory dysfunction has been well documented (114–116). In rats, l-thyroxin administration has been shown to increase bulbospongiosus contractile activity and seminal vesicle contraction frequency (117). Clinically, the prevalence of suppressed TSH, which is a marker of hyperthyroidism, was found to be twofold higher in patients with premature ejaculation than in patients who reported normal ejaculatory timing (118). In the first prospective multicenter study (114) on the topic, half of hyperthyroidism patients had premature ejaculation, whereas only 15% reported this symptom after cure of their thyroid dysfunction. Another single-center prospective study by Cihan et al. (116) demonstrated a prevalence of 72% of premature ejaculation in hyperthyroidism, which was reduced after treatment. It also identified a positive correlation of TSH with intravaginal ejaculation latency time. Öztürk et al. (119) found similar results. However, Waldinger et al. (120) found no correlation between TSH and intravaginal ejaculation latency time in a cohort of Dutch men with lifelong premature ejaculation. A meta-analysis by Corona et al. (102) demonstrated a threefold increase of hyperthyroidism in patients with premature ejaculation compared with controls, a finding that was more pronounced in patients with acquired rather than lifelong premature ejaculation. They also showed an increase in intravaginal ejaculation latency time by 84.6 ± 34.2 seconds (P=.001) upon treatment of hyperthyroidism. These findings suggest that thyroid hormones do not only affect the ankle reflex, but also the ejaculatory reflex, and screening patients with ejaculatory dysfunction for thyroid hormone abnormalities is warranted (102).

Glucocorticoids

Cortisol (F) levels in several animal studies were found to be elevated during arousal and ejaculation (121–123). In horses and donkeys, F was elevated 30 minutes after ejaculation, with unknown significance of this finding (124, 125). In addition, F levels were sharply elevated after electroejaculation in several anesthetized animal studies (126, 127). In humans, however, there was no change in F levels whether during sexual stimulation or orgasm (128–131). Although hypercortisolism in men was associated with reduced libido, no effect was identified on orgasm or ejaculation (132). Replacement of F in Addison disease was associated with improvement in overall sexual function including orgasm (133). Data in humans are still too preliminary to draw final conclusions, and further research is needed.

Estrogens

Estradiol plays an important role in the regulation of the emission phase of ejaculation through the regulation of epididymal contractility, luminal fluid reabsorption, and sperm concentration (134, 135). This role in the epididymis is the reason for recommending Tamoxifen as a first-line treatment for idiopathic oligospermia by the World Health Organization (136). Finkelstein et al. (137) showed that E₂ deficiency, along with androgen deficiency, contributes to decreased libido and erectile function.

Androgens

Testosterone, through its central and peripheral androgen receptors, has a well-known role on male sexual function, particularly on libido (138). Low T levels are associated with delayed ejaculation, whereas high levels were associated with premature ejaculation (102). This is likely because the emission phase of the ejaculation relies on the NO-PDE5 system, which is influenced by T (138, 139). Testosterone facilitates the control of the ejaculatory reflex through its androgen receptors in the MPOA and other areas in the central nervous system (140). Furthermore, pelvic floor muscles involved in ejaculation are androgen dependent (141). There are likely multiple mechanisms involved in T action and further research is needed to identify specific targets for treatment in the ejaculatory reflex. summarizes the neurochemical and hormonal regulation of ejaculation.

TABLE 2

Neurochemical and hormonal regulation of ejaculation.

In conclusion, ejaculation is a complex process involving several anatomical structures and under extensive neurochemical and hormonal regulation. Orgasm, although associated with ejaculation, is a distinct physiological process, different from ejaculation. Many aspects of these physiological processes are still unknown and further research is needed to identify treatments for ejaculatory dysfunction.

Footnotes

A.A. has nothing to disclose. B.N.B. has nothing to disclose. T.F.L. has nothing to disclose.

REFERENCES

1. Sheu G, Revenig LM, Hsiao W. Physiology of ejaculation. In: Mulhall JP, Hsiao W, editors. Men’s sexual health and fertility. Springer Science; New York: 2014. pp. 13–29. [Google Scholar]2. Bella AJ, Shamloul R. Functional anatomy of the male sex organs. In: Mulhall JP, Incocci L, Goldstein I, Rosen R, editors. Cancer and sexual health. Springer Science; New York: 2011. pp. 3–12. [Google Scholar]3. Meacham R, Lipshultz L, Howards S. Male infertility. In: Gillenwater JY, Grayhack JT, Howards S, Duckett JW, editors. Adult and pediatric urology. Mosby; St. Louis: 1996. pp. 1747–802. [Google Scholar]4. Hinman F. Normal surgical anatomy. In: Thomas Thomas AJ, Nagler HN, editors. Atlas of surgical management of male infertility. William & Wilkins; New York: 1995. pp. 9–20. [Google Scholar]5. Romanes G. The pelvis and perineum. In: Romanes G, Cunningham D, editors. Cunningham’s manual of practical anatomy. 13th ed Oxford University Press; London, UK: 1975. pp. 199–240. [Google Scholar]6. Tang Y, Rampin O, Calas A, Facchinetti P, Giuliano F. Oxytocinergic and serotonergic innervation of identified lumbosacral nuclei controlling penile erection in the male rat. Neuroscience. 1998;82:241–54. [PubMed] [Google Scholar]7. Danjou P, Lacomblez L, Warot D, Puech AJ. Assessment of erectogenic drugs by numeric plethysmography. J Pharmacol Methods. 1989;21:61–9. [PubMed] [Google Scholar]8. Clark JT, Smith ER, Davidson JM. Testosterone is not required for the enhancement of sexual motivation by yohimbine. Physiol Behav. 1985;35:517–21. [PubMed] [Google Scholar]9. Andersson KE. Mechanisms of penile erection and basis for pharmacological treatment of erectile dysfunction. Pharmacol Rev. 2011;63:811–59. [PubMed] [Google Scholar]10. Lue TF, Zeineh SJ, Schmidt RA, Tanagho EA. Neuroanatomy of penile erection: its relevance to iatrogenic impotence. J Urol. 1984;131:273–80. [PubMed] [Google Scholar]11. Paick JS, Lee SW. The neural mechanism of apomorphine-induced erection: an experimental study by comparison with electrostimulation-induced erection in the rat model. J Urol. 1994;152(6 Pt 1):2125–8. [PubMed] [Google Scholar]12. Chapelle PA, Durand J, Lacert P. Penile erection following complete spinal cord injury in man. Br J Urol. 1980;52:216–9. [PubMed] [Google Scholar]14. Courtois FJ, Charvier KF, Leriche A, Raymond DP. Sexual function in spinal cord injury men. I. Assessing sexual capability. Paraplegia. 1993;31:771–84. [PubMed] [Google Scholar]15. Sattar AA, Salpigidis G, Schulman CC, Wespes E. Relationship between intrapenile O2 lever and quantity of intracavernous smooth muscle fibers: current physiopathological concept. Acta Urol Belg. 1995;63:53–9. [PubMed] [Google Scholar]16. Prieto D. Physiological regulation of penile arteries and veins. Int J Impot Res. 2007;20:17–29. [PubMed] [Google Scholar]17. Andersson KE. Pharmacology of penile erection. Pharmacol Rev. 2001;53:417–50. [PubMed] [Google Scholar]18. Walsh MP. The Ayerst Award Lecture 1990. Calcium-dependent mechanisms of regulation of smooth muscle contraction. Biochem Cell Biol. 1991;69:771–800. [PubMed] [Google Scholar]19. Hurt KJ, Musicki B, Palese MA, Crone JK, Becker RE, Moriarity JL, et al. Akt-dependent phosphorylation of endothelial nitric-oxide synthase mediates penile erection. Proc Natl Acad Sci. 2002;99:4061–6. [PMC free article] [PubMed] [Google Scholar]20. Levin R. Physiology of orgasm. In: Mulhall JP, Incocci L, Goldstein I, Rosen R, editors. Cancer and sexual health. Springer Science; New York: 2011. pp. 35–48. [Google Scholar]21. Masters W, Johnson V. Human sexual response. Little Brown; Boston: 1966. [Google Scholar]22. Levin R, editor. Heart rate responses can be used to differentiate simulated from real orgasms in the human male: a pilot study. Proceedings of the first conference on orgasm. VRP Publishers; Bombay: 1991. [Google Scholar]23. Gerstenberg TC, Levin RJ, Wagner G. Erection and ejaculation in man—assessment of the electromyographic activity of the bulbocavernosus and ischiocavernosus muscles. Br J Urol. 1990;65:395–402. [PubMed] [Google Scholar]24. Levin R. Is prolactin the biological ‘off switch’ for human sexual arousal? Sex Relat Ther. 2003;18:289–343. [Google Scholar]25. Holstege G, Georgiadis JR, Paans AM, Meiners LC, van der Graaf FH, Reinders AS. Brain activation during human ejaculation. J Neurosci. 2003;23:9185–93. [PMC free article] [PubMed] [Google Scholar]26. Hite S. The Hite report on male sexuality. Ballantine Books; New York: 1981. [Google Scholar]27. Perry JF. Do men have a G-spot? Aust Forum. 1988;2:37–41. [Google Scholar]28. Levin R. Revisiting post-ejaculatory refractory time—what we know and what we do not know in males and females. J Sex Med. 2009;6:2376–89. [PubMed] [Google Scholar]29. Turley KR, Rowland DL. Evolving ideas about the male refractory period. BJU Int. 2013;112:442–52. [PubMed] [Google Scholar]30. Giuliano F, Clement P. Physiology of ejaculation: emphasis on serotonergic control. Eur Urol. 2005;48:408–17. [PubMed] [Google Scholar]31. Master VA, Turek PJ. Ejaculatory physiology and dysfunction. Urol Clin North Am. 2001;28:363–75. [PubMed] [Google Scholar]32. Schlegel PN, Walsh PC. Neuroanatomical approach to radical cystoprostatectomy with preservation of sexual function. J Urol. 1987;16:46–60. [PubMed] [Google Scholar]33. Keast JR. Pelvic ganglia. In: McLahlan EM, editor. Autonomic ganglia. Harwood Academic; Luxemberg: 1995. pp. 445–79. [Google Scholar]34. Dail WG, Moll MA. Localization of vasoactive intestinal polypeptide in penile erectile tissue and in the major pelvic ganglion of the rat. Neuroscience. 1983;10:1379–86. [PubMed] [Google Scholar]35. Brindley GS, Sauerwein D, Hendry WF. Hypogastric plexus stimulators for obtaining semen from paraplegic men. Br J Urol. 1989;64:72–7. [PubMed] [Google Scholar]36. Ver Voort SM. Ejaculatory stimulation in spinal-cord injured men. Urology. 1987;29:282–9. [PubMed] [Google Scholar]37. Comarr A. Sexual function among patients with spinal cord injury. Urol Int. 1970;25:134–68. [PubMed] [Google Scholar]38. McKenna KE, Chung SK, McVary KT. A model for the study of sexual function in anesthetized male and female rats. Am J Physiol. 1991;261:R1276–85. [PubMed] [Google Scholar]39. Bergman B, Nilsson S, Petersen I. The effect on erection and orgasm of cystectomy, prostatectomy and vesiculectomy for cancer of the bladder: a clinical and electromyographic study. Br J Urol. 1979;51:114–20. [PubMed] [Google Scholar]40. Holmes GM, Sachs BD. The ejaculatory reflex in copulating rats: normal bulbospongiosus activity without apparent urethral stimulation. Neurosci Lett. 1991;125:195–7. [PubMed] [Google Scholar]41. Truitt WA, Coolen LM. Identification of a potential ejaculation generator in the spinal cord. Science. 2002;297:1566–9. [PubMed] [Google Scholar]42. Nunez R, Gross GH, Sachs BD. Origin and central projections of rat dorsal penile nerve: possible direct projection to autonomic and somatic neurons by primary afferents of nonmuscle origin. J Comp Neurol. 1986;247:417–29. [PubMed] [Google Scholar]43. Halata Z, Munger BL. The neuroanatomical basis for the protopathic sensibility of the human glans penis. Brain Res. 1986;371:205–30. [PubMed] [Google Scholar]44. Baron R, Janig W. Afferent and sympathetic neurons projecting into lumbar visceral nerves of the male rat. J Comp Neurol. 1991;314:429–36. [PubMed] [Google Scholar]45. McKenna KE, Nadelhaft I. The organization of the pudendal nerve in the male and female rat. J Comp Neurol. 1986;248:532–49. [PubMed] [Google Scholar]46. Clement P, Giuliano F. Physiology of ejaculation. In: Mulhall JP, Incrocci L, Goldstein I, editors. Cancer and sexual health. Springer Science; New York: 2011. pp. 77–89. [Google Scholar]47. Morgan C, de Groat WC, Nadelhaft I. The spinal distribution of sympathetic preganglionic and visceral primary afferent neurons that send axons into the hypogastric nerves of the cat. J Comp Neurol. 1986;243:23–40. [PubMed] [Google Scholar]48. Owman C, Stjernquist M. The peripheral nervous system. In: Bjorklund A, Hokfelt T, Owman C, editors. Handbook of chemical neuroanatomy. Elsevier Science; Amsterdam, The Netherlands: 1988. pp. 445–544. [Google Scholar]49. Nadelhaft I, Booth AM. The location and morphology of preganglionic neurons and the distribution of visceral afferents from the rat pelvic nerve: a horseradish peroxidase study. J Comp Neurol. 1984;226:238–45. [PubMed] [Google Scholar]50. Schroder HD. Anatomical and pathoanatomical studies on the spinal efferent systems innervating pelvic structures. 1. Organization of spinal nuclei in animals. 2. The nucleus X-pelvic motor system in man. J Auton Nerv Syst. 1985;14:23–48. [PubMed] [Google Scholar]51. Coolen LM, Veening JG, Wells AB, Shipley MT. Afferent connections of the parvocellular subparafascicular thalamic nucleus in the rat: evidence for functional subdivisions. J Comp Neurol. 2003;463:132–56. [PubMed] [Google Scholar]52. Borgdorff AJ, Bernabé J, Denys P, Alexandre L, Giuliano F. Ejaculation elicited by microstimulation of lumbar spinothalamic neurons. Eur Urol. 2008;54:449–56. [PubMed] [Google Scholar]53. Hamson DK, Watson NV. Regional brainstem expression of Fos associated with sexual behavior in male rats. Brain Res. 2004;1006:233–40. [PubMed] [Google Scholar]54. Heeb MM, Yahr P. Anatomical and functional connections among cell groups in the gerbil brain that are activated with ejaculation. J Comp Neurol. 2001;439:248–58. [PubMed] [Google Scholar]55. Coolen LM, Peters HJ, Veening JG. Anatomical interrelationships of the medial preoptic area and other brain regions activated following male sexual behavior: a combined fos and tract-tracing study. J Comp Neurol. 1998;397:421–35. [PubMed] [Google Scholar]56. Kollack-Walker S, Newman SW. Mating-induced expression of c-fos in the male Syrian hamster brain: role of experience, pheromones, and ejaculations. J Neurobiol. 1997;32:481–501. [PubMed] [Google Scholar]57. Borgdorff AJ, Bernabé J, Denys P, Alexandre L, Giuliano F. Demonstration of ejaculation-induced neural activity in the male rat brain using 5-HT1A agonist 8-OH-DPAT. Physiol Behav. 1997;62:881–91. [PubMed] [Google Scholar]58. Meisel R, Sachs B. The physiology of male sexual behavior. In: Knobil E, Neill J, editors. The physiology of reproduction. Raven; New York: 1994. pp. 3–105. [Google Scholar]59. Pehek EA, Thompson JT, Hull EM. The effects of intracranial administration of the dopamine agonist apomorphine on penile reflexes and seminal emission in the rat. Brain Res. 1989;500:325–32. [PubMed] [Google Scholar]60. Hull EM, Eaton RC, Markowski VP, Moses J, Lumley LA, Loucks JA. Opposite influence of medial preoptic D1 and D2 receptors on genital reflexes: implications for copulation. Life Sci. 1992;51:1705–13. [PubMed] [Google Scholar]61. Marson L, McKenna KE. Stimulation of the hypothalamus initiates the urethrogenital reflex in male rats. Brain Res. 1994;638:103–8. [PubMed] [Google Scholar]62. Larsson K, van Dis H. Seminal discharge following intracranial electrical stimulation. Brain Res. 1970;23:381–6. [PubMed] [Google Scholar]63. Arendash GW, Gorski RA. Effects of discrete lesions of the sexually dimorphic nucleus of the preoptic area or other medial preoptic regions on the sexual behavior of male rats. Brain Res Bull. 1983;10:147–54. [PubMed] [Google Scholar]64. Simerly RB, Swanson LW. Projections of the medial preoptic nucleus: a Phaseolus vulgaris leucoagglutinin anterograde tract-tracing study in the rat. J Comp Neurol. 1988;270:209–42. [PubMed] [Google Scholar]65. Rizvi TA, Ennis M, Shipley MT. Reciprocal connections between the medial preoptic area and the midbrain periaqueductal gray in rat: A WGA-HRP and PHA-L study. J Comp Neurol. 1992;315:1–15. [PubMed] [Google Scholar]66. Murphy AZ, Rizvi TA, Ennis M, Shipley MT. The organization of preoptic medullary circuits in the male rat: evidence for interconnectivity of neural structures involved in reproductive behavior, antinociception and cardiovascular regulation. Neuroscience. 1999;91:1103–16. [PubMed] [Google Scholar]67. Saper CB, Loewy AD, Swanson LW, Cowan WM. Direct hypothalamo-autonomic connections. Brain Res. 1976;117:305–12. [PubMed] [Google Scholar]68. Luiten PG, Ter Horst GJ, Karst H, Steffens AB. The course of paraventricular hypothalamic efferents to autonomic structures in medulla and spinal cord. Brain Res. 1985;329:374–8. [PubMed] [Google Scholar]69. Bancila M, Verge D, Rampin O, Backstrom JR, Sanders-Bush E, McKenna KE, et al. 5-Hydroxytryptamine2C receptors on spinal neurons controlling penile erection in the rat. Neuroscience. 1999;92:1523–37. [PubMed] [Google Scholar]70. Ackerman AE, Lange GM, Clemens LG. Effects of paraventricular lesions on sex behavior and seminal emission in male rats. Physiol Behav. 1997;63:49–53. [PubMed] [Google Scholar]71. Yasui Y, Saper CB, Cechetto DF. Calcitonin gene-related peptide (CGRP) immunoreactive projections from the thalamus to the striatum and amygdala in the rat. J Comp Neurol. 1991;308:293–310. [PubMed] [Google Scholar]72. Canteras NS, Simerly RB, Swanson LW. Organization of projections from the medial nucleus of the amygdala: a PHAL study in the rat. J Comp Neurol. 1995;360:213–45. [PubMed] [Google Scholar]73. Marson L, McKenna KE. A role for 5-hydroxytryptamine in descending inhibition of spinal sexual reflexes. Exp Brain Res. 1990;88:313–20. [PubMed] [Google Scholar]74. Marson L, McKenna KE. The identification of a brainstem site controlling spinal sexual reflexes in male rats. Brain Res. 1990;515:303–8. [PubMed] [Google Scholar]75. Marson L. Lesions of the periaqueductal gray block the medial preoptic area-induced activation of the urethrogenital reflex in male rats. Neurosci Lett. 2004;367:278–82. [PubMed] [Google Scholar]76. Hull EM, Muschamp JW, Sato S. Dopamine and serotonin: influences on male sexual behavior. Physiol Behav. 2004;83:291–307. [PubMed] [Google Scholar]77. Peeters M, Giuliano F. Central neurophysiology and dopaminergic control of ejaculation. Neurosci Biobehav Rev. 2007;32:438–53. [PubMed] [Google Scholar]78. Ferrari F, Giuliani D. The selective D2 dopamine receptor antagonist eticlopride counteracts the ejaculatio praecox induced by the selective D2 dopamine agonist SND 919 in the rat. Life Sci. 1994;55:1155–62. [PubMed] [Google Scholar]79. Ferrari F, Giuliani D. Sexual attraction and copulation in male rats: effects of the dopamine agonist SND 919. Pharmacol Biochem Behav. 1995;50:29–34. [PubMed] [Google Scholar]80. Clément P, Bernabé J, Kia HK, Alexandre L, Giuliano F. D2-like receptors mediate the expulsion phase of ejaculation elicited by 8-hydroxy-2-(di-N-propylamino) tetralin in rats. J Pharmacol Exp Ther. 2006;316:830–4. [PubMed] [Google Scholar]81. Stafford SA, Coote JH. Activation of D2-like receptors induces sympathetic climactic-like responses in male and female anaesthetised rats. Br J Pharmacol. 2006;148:510–6. [PMC free article] [PubMed] [Google Scholar]82. Ferrari F, Giuliani D. Behavioral effects induced by the dopamine D3 agonist 7-OH-DPAT in sexually-active and -inactive male rats. Neuropharmacology. 1996;35:279–84. [PubMed] [Google Scholar]83. Ahlenius S, Larsson K. Effects of the dopamine D3 receptor ligand 7-OH-DPAT on male rat ejaculatory behavior. Pharmacol Biochem Behav. 1995;51:545–7. [PubMed] [Google Scholar]84. Clement P, Bernabe J, Denys P, Alexandre L, Giuliano F. Ejaculation induced by i.c.v. injection of the preferential dopamine D(3) receptor agonist 7-hydroxy-2-(di-N-propylamino)tetralin in anesthetized rats. Neuroscience. 2007;145:605–10. [PubMed] [Google Scholar]85. Kitrey ND, Clément P, Bernabé J, Alexandre L, Giuliano F. Microinjection of the preferential dopamine receptor D3 agonist 7-OH-DPAT into the hypothalamic medial preoptic area induced ejaculation in anesthetized rats. Neuroscience. 2007;149:636–41. [PubMed] [Google Scholar]86. Clément P, Pozzato C, Heidbreder C, Alexandre L, Giuliano F, Melotto S. Delay of ejaculation induced by SB-277011, a selective dopamine D3 receptor antagonist, in the rat. J Sex Med. 2009;6:98–108. [PubMed] [Google Scholar]87. Giuliano F. 5-hydroxytryptamine in premature ejaculation: opportunities for therapeutic intervention. Trends Neurosci. 2007;30:79–84. [PubMed] [Google Scholar]88. Clément P, Bernabé J, Gengo P, Denys P, Laurin M, Alexandre L, et al. Supraspinal site of action for the inhibition of ejaculatory reflex by dapoxetine. Eur Urol. 2007;51:825–32. [PubMed] [Google Scholar]89. Stafford SA, Bowery NG, Tang K, Coote JH. Activation by p-chloroamphetamine of the spinal ejaculatory pattern generator in anaesthetized male rats. Neuroscience. 2006;140:1031–40. [PubMed] [Google Scholar]90. Giuliano F, Clement P. Serotonin and premature ejaculation: from physiology to patient management. Eur Urol. 2006;50:454–66. [PubMed] [Google Scholar]91. Sato Y, Zhao W, Christ GJ. Central modulation of the NO/cGMP pathway affects the MPOAinduced intracavernous pressure response. Am J Physiol Regul Integr Com Physiol. 2001;281:R269–78. [PubMed] [Google Scholar]92. Hull EM, Lumley LA, Matuszewich L, Dominguez J, Moses J, Lorrain DS. The roles of nitric oxide in sexual function of male rats. Neuropharmacology. 1994;33:1499–504. [PubMed] [Google Scholar]93. Dixon JS, Jen PY. Development of nerves containing nitric oxide synthase in the human male urogenital organs. Br J Urol. 1995;76:719–25. [PubMed] [Google Scholar]94. Hedlund P, Ekström P, Larsson B, Alm P, Andersson KE. Heme oxygen-ase and NO-synthase in the human prostate—relation to adrenergic, cholinergic and peptide-containing nerves. J Auton Nerv Syst. 1997;63:115–26. [PubMed] [Google Scholar]95. Jen PY, Dixon JS, Gosling JA. Co-localization of nitric oxide synthase, neuropeptides and tyrosine hydroxylase in nerves supplying the human postnatal vas deferens and seminal vesicle. Br J Urol. 1997;80:291–9. [PubMed] [Google Scholar]96. Kaminski HJ, Andrade FH. Nitric oxide: biologic effects on muscle and role in muscle diseases. Neuromuscul Disord. 2001;11:517–24. [PubMed] [Google Scholar]97. Ückert S, Bazrafshan S, Scheller F, Mayer ME, Jonas U, Stief CG. Functional responses of isolated human seminal vesicle tissue to selective phosphodiesterase inhibitors. Urology. 2007;70:185–9. [PubMed] [Google Scholar]98. Bultmann R, Klebroff W, Starke K. Nucleotide-evoked relaxation of rat vas deferens: possible mechanisms. Eur J Pharmacol. 2002;436:135–43. [PubMed] [Google Scholar]99. Kato K, Furuya K, Tsutsui I, Ozaki T, Yamagishi S. Cyclic AMP-mediated inhibition of noradrenaline-induced contraction and Ca2+ in flux in guinea-pig vas deferens. Exp Physiol. 2000;85:387–98. [PubMed] [Google Scholar]100. Bialy M, Beck J, Abramczyk P, Trzebskj A, Przybylski J. Sexual behavior in male rats after nitric oxide synthesis inhibition. Physiol Behav. 1996;60:139–43. [PubMed] [Google Scholar]101. Kriegsfeld LJ, Demas GE, Huang PL, Burnett AL, Nelson RJ. Ejaculatory abnormalities in mice lacking the gene for endothelial nitric oxide synthase (eNOS) Physiol Behav. 1999;67:561–6. [PubMed] [Google Scholar]102. Corona G, Jannini EA, Vignozzi L, Rastrelli G, Maggi M. The hormonal control of ejaculation. Nat Rev Urol. 2012;9:508–19. [PubMed] [Google Scholar]103. Maggi M, Kassis S, Malozowski S. Identification and characterization of a vasopressin isoreceptor in porcine seminal vesicles. Proc Natl Acad Sci. 1986;83:8824–8. [PMC free article] [PubMed] [Google Scholar]104. Filippi S, Vannelli GB, Granchi S. Identification, localization and functional activity of oxytocin receptors in epididymis. Mol Cell Endocrinol. 2002;193:89–100. [PubMed] [Google Scholar]105. Nicholson HD, Parkinson TJ, Lapwood KR. Effects of oxytocin and vasopressin on sperm transport from the cauda epididymis in sheep. J Reprod Fertil. 1999;117:299–305. [PubMed] [Google Scholar]106. Einspanier A, Ivell R. Oxytocin and oxytocin receptor expression in reproductive tissues of the male marmoset monkey. Biol Reprod. 1997;56:416–22. [PubMed] [Google Scholar]107. Arletti R, Bazzani C, Castelli M. Oxytocin improves male copulatory performance in rats. Horm Bev. 1985;19:14–20. [PubMed] [Google Scholar]108. Argiolas A, Collu M, d’Aquila P, Gessa GL, Melis MR, Serra G. Apomorphine stimulation of male copulatory behavior is prevented by the oxytocin antagonist d(Ch3)5Tyr(Me)-Orn8-vasotocin in rats. Pharmacol Biochem Behav. 1988;33:81–3. [PubMed] [Google Scholar]109. Ishak WW, Berman DS, Peters A. Male anorgasmia treated with oxytocin. J Sex Med. 2008;5:1022–4. [PubMed] [Google Scholar]110. Burri A, Heinrichs M, Schedlowski M, Kruger TH. The acute effects of intra-nasal oxytocin administration on endocrine and sexual function in males. Psychoneuroendocrinology. 2008;33:591–600. [PubMed] [Google Scholar]111. Buvat J. Hyperprolactinemia and sexual function in men: a short review. Int J Impot Res. 2003;15:373–7. [PubMed] [Google Scholar]112. Exton MS, Krüger TH, Koch M, Paulson E, Knapp W, Hartmann U, et al. Coitus-induced orgasm stimulates prolactin secretion in healthy subjects. Psychoneuroendocrinology. 2001;26:31–44. [PubMed] [Google Scholar]113. Corona G, Mannucci E, Jannini EA, Lotti F, Ricca V, Monami M, et al. Hypoprolactinemia: a new clinical syndrome in patients with sexual dysfunction. J Sex Med. 2009;6:1457–66. [PubMed] [Google Scholar]114. Carani C, Isidori AM, Granata A, Carosa E, Maggi M, Lenzi A, et al. Multicenter study on the prevalence of sexual symptoms in male hypo- and hyperthyroid patients. J Clin Endocrinol Metab. 2005;90:6472–9. [PubMed] [Google Scholar]115. Corona G, Mannucci E, Petrone L, Fisher AD, Balercia G, Scisciolo G, et al. Psychobiological correlates of delayed ejaculation in male patients with sexual dysfunctions. J Androl. 2006;27:453–8. [PubMed] [Google Scholar]116. Cihan A, Demir O, Demir T, Aslan G, Comlekci A, Esen A. The relationship between premature ejaculation and hyperthyroidism. J Urol. 2009;181:1273–80. [PubMed] [Google Scholar]117. Cihan A, Demir O, Demir T, Aslan G, Comlekci A, Esen A. Investigation of the neural target level of hyperthyroidism in premature ejaculation in a rat model of pharmacologically induced ejaculation. J Sex Med. 2011;8:90–6. [PubMed] [Google Scholar]118. Corona G, Ricca V, Bandini E, Rastrelli G, Casale H, Jannini E, et al. SIEDY Scale 3, a new instrument to detect psychological component in subjects with erectile dysfunction. J Sex Med. 2012;9:2017–26. [PubMed] [Google Scholar]119. Öztürk MI, Koca O, Tüken M, Keleş MO, Ilktac A, Karaman MI. Hormonal evaluation in premature ejaculation. Urol Int. 2011;88:454–8. [PubMed] [Google Scholar]120. Waldinger MD, Zwinderman AH, Olivier B, Schweitzer DH. Thyroid-stimulating hormone assessments in a Dutch cohort of 620 men with lifelong premature ejaculation without erectile dysfunction. J Sex Med. 2005;2:865–70. [PubMed] [Google Scholar]121. Rabb MH, Thompson DL, Barry BE, Colborn DR, Garza F, Hehnke KE. Effects of sexual stimulation, with and without ejaculation, on serum concentrations of, LH, FSH, testosterone, cortisol and prolactin in stallions. J Anim Sci. 1989;67:2724–9. [PubMed] [Google Scholar]122. Borg KE, Esbenshade KL, Johnson BH. Cortisol, growth hormone, and testosterone concentrations during mating behavior in the bull and boar. J Anim Sci. 1991;69:3230–40. [PubMed] [Google Scholar]123. Bishop JD, Malven PV, Singleton WL, Weesner GD. Hormonal and behavioural correlates of emotional states in sexually trained boars. J Anim Sci. 1999;77:3339–45. [PubMed] [Google Scholar]124. Veronesi MC, Tosi U, Villani M, Govoni N, Faustini M, Kindahl H, et al. Oxytocin, vasopressin, prostaglandin F(2α), luteinizing hormone, testosterone, estrone sulfate, and cortisol plasma concentrations after sexual stimulation in stallions. Theriogenology. 2010;73:460–7. [PubMed] [Google Scholar]125. Veronesi MC, de Amicis I, Panzani S, Kindahl H, Govoni N, Probo M, et al. PGF(2α), LH, testosterone, oestrone sulphate, and cortisol plasma concentrations around sexual stimulation in jackass. Theriogenology. 2011;75:1489–98. [PubMed] [Google Scholar]126. Wildt DE, Phillips LG, Simmons LG, Chakraborty PK, Brown JL, Howard JG, et al. A comparative analysis of ejaculate and hormonal characteristics of the captive male cheetah, tiger, leopard, and puma. Biol Reprod. 1988;38:245–55. [PubMed] [Google Scholar]127. Brown JL, Wildt DE, Phillips LG, Seidensticker J, Fernando SB, Miththapala S, et al. Adrenal–pituitary–gonadal relationships and ejaculate characteristics in captive leopards (Panthera pardus kotiya) isolated on the island of Sri Lanka. J Reprod Fertil. 1989;85:605–13. [PubMed] [Google Scholar]128. Carani C, Bancroft J, Del Rio G, Granata ARM, Facchinetti F, Marrama P. The endocrine effects of visual erotic stimuli in normal men. Psychoneuroendocrinology. 1990;15:207–16. [PubMed] [Google Scholar]129. Krüger T, Exton MS, Pawlak C, von zur Mühlen A, Hartmann U, Schedlowski M. Neuroendocrine and cardiovascular response to sexual arousal and orgasm in men. Psychoneuroendocrinology. 1998;23:401–11. [PubMed] [Google Scholar]130. Exton NG, Truong TC, Exton MS, Wingenfeld SA, Leygraf N, Saller B, et al. Neuroendocrine response to film-induced sexual arousal in men and women. Psychoneuroendocrinology. 2000;25:187–99. [PubMed] [Google Scholar]131. Ismail AA, Davidson DW, Loraine JA. Relationship between plasma cortisol and human sexual activity. Nature. 1972;237:288–9. [PubMed] [Google Scholar]132. Valassi E, Santos A, Yaneva M, Tóth M, Strasburger CJ, Chanson P, et al. The European Registry on Cushing’s syndrome: 2-year experience. Baseline demographic and clinical characteristics. J Endocrinol. 2011;165:383–92. [PubMed] [Google Scholar]133. Granata A, Tirabassi G, Pugni V, Arnaldi G, Boscaro M, Carani C, et al. Sexual dysfunctions in men affected by autoimmune addison’s disease before and after short-term gluco- and mineralocorticoid replacement therapy. J Sex Med. 2013;10:2036–43. [PubMed] [Google Scholar]134. Vignozzi L, Filippi S, Morelli A, Luconi M, Jannini E, Forti G, et al. Regulation of epididymal contractility during semen emission, the first part of the ejaculatory process: a role for estrogen. J Sex Med. 2008;5:2480. [PubMed] [Google Scholar]136. Rowe P, Comhaire F. WHO manual for the standardized investigation, diagnosis and management of the infertile male. Cambridge University Press; Cambridge: 2000. [Google Scholar]137. Finkelstein JS, Lee H, Burnett-Bowie SAM, Pallais JC, Yu EW, Borges LF, et al. Gonadal steroids and body composition, strength, and sexual function in men. N Engl J Med. 2013;369:1011–22. [PMC free article] [PubMed] [Google Scholar]138. Corona G, Maggi M. The role of testosterone in erectile dysfunction. Nat Rev Urol. 2010;7:46–56. [PubMed] [Google Scholar]139. Morelli A, Filippi S, Mancina R, Luconi M, Vignozzi L, Marini M, et al. Androgens regulate phosphodiesterase type 5 expression and functional activity in corpora cavernosa. Endocrinology. 2004;145:2253–63. [PubMed] [Google Scholar]140. Swaab DF. Sexual differentiation of the brain and behavior. Best Pract Res Clin Endocrinol Metab. 2007;21:431–44. [PubMed] [Google Scholar]

Orgasms

What’s an orgasm?

An orgasm is what usually happens when you reach the height of sexual arousal. It usually feels really good. When you have an orgasm — aka cum or climax — sexual tension increases until it reaches a peak, and pressure in your body and genitals is released.  

What happens when you have an orgasm?

Every person’s body is different, but there are a few physical signs of an orgasm. The most noticeable sign is a very intense, pleasurable feeling in your genitals and throughout your body. The muscles in your vagina or penis, as well as your anus, contract (squeeze) about once per second, 5-8 times. Your heart rate and breathing levels also go up. 

During an orgasm, your penis usually squirts a small amount (1-2 tablespoons) of semen (cum) — this is called ejaculation. It’s possible to have an orgasm without ejaculating or to ejaculate without having an orgasm, but they usually happen together.

It’s common for your vagina to get really wet before and during an orgasm. It’s also possible for a different fluid to squirt or dribble out of your vulva before or during an orgasm (this is sometimes called female ejaculation, or squirting). This fluid isn’t pee. Ejaculation from a vulva is less common than ejaculation from a penis  — some people do it and some people don’t — either is totally normal. 

Right after an orgasm, your clitoris or the glans (head) of your penis can feel very sensitive or uncomfortable to touch. You may have “sex flush” — your chest, neck, and face change color for a short amount of time. Orgasms release endorphins (feel-good hormones), so you might feel sleepy, relaxed, and happy afterwards — this is why some people orgasm to relieve pain, stress, or help them go to sleep.

Orgasms don’t feel the same for every person, or every time you have one — some are very intense, some are very mild, and some are in-between. They vary for a number of reasons, including how comfortable you are, how sexually excited you are, and how much sexual tension you built up before you had your orgasm. 

Having an Orgasm

How do you know how to orgasm? 

Most orgasms happen during masturbation or sex (like oral, anal, or vaginal sex), when you or a partner stimulates (touches or rubs) your genitals. People with vulvas usually have orgasms through stimulation of their clitoris, vagina, and/or anus. People with penises usually have orgasms through stimulation of their penis, testicles, and/or anus. A few people can have orgasms from other things, like nipple stimulation or even just thinking sexy thoughts.

Many things can impact your ability to have an orgasm, like your hormones, emotions, past experiences, beliefs, lifestyle, relationships, physical or mental health, taking certain medicines, and using alcohol or drugs.

Some people can have orgasms quickly and easily, others need more time and effort. You might be able to have an orgasm in some circumstances but not others, depending on who you’re with or what you’re doing. Everyone’s body is different and there’s not one “right” way to have an orgasm. 

Some people need to have certain parts of their body stimulated in a very specific way or with certain objects (like vibrators) to have an orgasm. A lot of people with vulvas have orgasms by stimulating their clitorises, but not by penetrating their vaginas — some can’t have an orgasm through their vagina at all. All of these differences are normal. It may take time and practice to learn how to have an orgasm. Experimenting with what feels good can help you understand your body and what feels good for you.

Try not to put any pressure on yourself or your partner to have an orgasm. Not everybody can have orgasms during sex or with other people around. Or sometimes the circumstances just aren’t right (you’re nervous, tired, or distracted for example). Some people never have orgasms at all. If you and/or your partner don’t have an orgasm, it doesn’t mean you’re not into each other or you’re bad at sex. Sex and masturbation can be intimate, enjoyable, and fun with or without orgasms. If you’re struggling to have orgasms and it bothers you, you may have orgasm disorder. It’s really common, and there are treatments to help.

Was this page helpful?

Help us improve. How could this information be more helpful? (optional)

How did this information help you? (optional)

You’re the best! Thanks for your feedback.

Thanks for your feedback.

What It Is and How It Happens

Squirting refers to fluid expelled from the vagina during orgasm. Not all people with vaginas squirt during orgasm, and those who do may only squirt some of the time. This type of orgasm includes a rapid ejection of urine from the bladder.

Squirting sometimes also involves secretions from the skene’s gland. The skene’s glands are sometimes called the female prostate because they function similarly to the male prostate.

Other Names for a Squirting Orgasm

A squirting orgasm is sometimes called female ejaculation. But this term excludes non-binary and trans people who are not female but have vaginas. 

A recent study has shown that there is a difference between squirting, female ejaculation, and incontinence during sex. However, the term squirting is used to describe all three in everyday language.

What is the Difference Between a Squirting Orgasm, Female Ejaculation, and Sexual Incontinence?

All three of these phenomena involve fluid coming from the bladder during sex. Squirting is the expulsion of urine during an orgasm. Female ejaculation is a release of both urine and a substance from the skene’s glands. Sexual incontinence — also called coital incontinence —  is when someone loses control of their bladder during sex.

Ejaculation in people with vaginas may include a small release of a milky white liquid that does not gush out. Squirting, on the other hand, is usually a higher volume. It is possible to squirt and ejaculate at the same time. 

Myths and Misconceptions About Squirting Orgasms

Myth: Squirting is Fake

Squirting is real. In fact, scientists have documented the phenomenon. However, more research is needed to determine the exact causes of squirting and female ejaculation. 

Part of the ambiguity about squirting is that the skene’s glands vary from person to person. Some people with vaginas don’t have any, while others have very small ones.

Myth: Everyone Can Squirt If They Try the Same Method

Each person’s experience with squirting is different. While some methods can make people squirt more than others, there is no one proven method that makes every person with a vagina squirt. This is because each vagina is different. As mentioned, some vaginas lack the skene’s glands which are thought to create the fluid released during ejaculation in people who have vulvas. 

Myth: Squirting Orgasms are Always High Volume

Squirting isn’t always a high volume event that soaks the sheets. Sometimes it is a small trickle or a stream of fluid. 

The depiction of squirting in porn movies often shows large gushes of squirting liquid. Porn producers fake some of these depictions for dramatic effect. All volumes and forms of squirting are valid. Squirting at different volumes is a normal occurrence during sex for many people.

Myth: Squirting or Ejaculation Only Happens During Orgasm

Some people can squirt or ejaculate before or after an orgasm. Squirting can also occur at the same time as an orgasm. Some people also have multiple spurts of squirting spread over a few minutes.

How to Explore Squirting

Explore squirting by yourself or with a partner to find out what works for you.

Some sex experts recommend stimulating the g-spot to achieve a squirting orgasm. Either by yourself or with a partner, take some time to find the g-spot with your fingers and/or sex toys. Pressure on the g-spot may make you feel the need to urinate.

Experiment with different methods of bringing yourself or your partner to a squirting orgasm with g-spot stimulation. Some ideas include:

• Using sex toys specifically designed to stimulate the g-spot
• Combining clitoral stimulation with g-spot stimulation
• Using lots of lubrication
• Bearing down on your pubococcygeal (pelvic) muscles when nearing orgasm
• Strengthen your vaginal muscles with kegel exercises
• Urinate before trying to have a squirting orgasm

Safety Advice and Special Considerations

For some people, putting too much pressure on the g-spot can feel uncomfortable. Listen to your body and do what feels good. If you are too tense it may be harder to orgasm or squirt. 

Female ejaculation comes in two forms, scientists find

By Helen Thomson

Use your imagination

Rolf Hicker/Getty

What do you think of when you hear the words “female ejaculation”? Come to think of it, the answer may be best kept to yourself. You may have heard that it was banned from being shown in British porn films last year. But what exactly is it?

Researchers have now come a step closer to defining this controversial phenomenon, by performing the first ultrasound scans on women who express large amounts of liquid at orgasm.

Some women express liquid from their urethra when they climax. For some, this consists of a small amount of milky white fluid – this, technically, is the female ejaculate. Other women report “squirting” a much larger amount of fluid – enough to make it look like they’ve wet the bed.

A few small studies have suggested the milky white fluid comes from Skene glands – tiny structures that drain into the urethra. Some in the medical community believe these glands are akin to the male prostate, although their size and shape differ greatly between women and their exact function is unknown.

Climax in the lab

To investigate the nature and origins of the fluid, Samuel Salama, a gynaecologist at the Parly II private hospital in Le Chesnay, France, and his colleagues recruited seven women who report producing large amounts of liquid – comparable to a glass of water – at orgasm.

First, these women were asked to provide a urine sample. An ultrasound scan of their pelvis confirmed that their bladder was completely empty. The women then stimulated themselves through masturbation or with a partner until they were close to having an orgasm – which took between 25 and 60 minutes.

“Some women express liquid from their urethra when they climax”

A second pelvic ultrasound was then performed just before the women climaxed. At the point of orgasm, the squirted fluid was collected in a bag and a final pelvic scan performed.

Even though the women had urinated just before stimulation began, the second scan – performed just before they climaxed – showed that their bladder had completely refilled. Each woman’s final scan showed an empty bladder, meaning the liquid squirted at orgasm almost certainly originated from the bladder.

A chemical analysis was performed on all of the fluid samples. Two women showed no difference between the chemicals present in their urine and the fluid squirted at orgasm.

The other five women had a small amount of prostatic-specific antigen (PSA) present in their squirted fluid – an enzyme not detected in their initial urine sample, but which is part of the “true” female ejaculate

PSA, produced in men by the prostate gland, is more commonly associated with male ejaculate, where its presence helps sperm to swim. In females, says Salama, PSA is produced mainly by the Skene glands.

Two kinds of fluid

Beverly Whipple, a neurophysiologist from Rutgers University in Newark, New Jersey, says that the term female ejaculation should only really refer to the production of the small amount of milky white liquid at orgasm and not the “squirting” investigated in this paper. “This study shows the other two kinds of fluids that can be expelled from the female urethra – urine alone, and urine diluted with substances from the female prostate,” she says.

“This study presents convincing evidence that squirting in women is chemically similar to urine, and also contains small amounts of PSA that is present in men’s and women’s true ejaculate,” says Barry Komisaruk, also at Rutgers.

“This study helps to reconcile the controversy over the fluids that many women report being released at orgasm,” he adds. “There are evidently two different fluids, with two different sources. Whether either of these fluids plays a physiological role – that is, whether they serve any adaptive function, is not known.”

Florian Wimpissinger at Rudolfstiftung Hospital in Vienna, Austria, suggests that the presence of PSA in some women’s squirted fluid and not others might be because the emissions from the Skene glands could travel into the bladder at orgasm. It may also have something to do with the known variation in size and shape of the glands, or be that some women don’t produce PSA in the first place.

Every woman capable

Why some women experience these different types of ejaculation and others don’t is not yet clear, says Salama, but he believes every woman is capable of squirting “if their partner knows what they are doing”.

For now, Salama is not investigating that particular avenue, but instead working on a protocol to test whether the kidneys work faster to produce urine during sexual stimulation than at other times, and if so, why.

The ban on female ejaculation in UK porn is based on the fact that the British Board of Film Classification (BBFC) considers films which include material featuring “urolagnia” – sexual pleasure associated with urination – as obscene under the UK Obscene Publications Act.

However, the wording of the law actually appears to be referring to squirting – not female ejaculation. So this new paper may support the current legal position, since it shows it is essentially involuntary urination. Presumably, under current UK law, if a woman were to have what is considered a true female ejaculation – the expulsion of a small amount of milky white fluid – and the BBFC were satisfied that this did not contain urea – this act would not be subject to the ban.

Journal reference: The Journal of Sexual Medicine, DOI: 10.1111/jsm.12799

More on these topics:

Orgasm and ejaculation | Prostate cancer

Some prostate cancer treatments can have an effect on orgasms and ejaculation. Find out more about why this happens.

How treatments can affect orgasms and ejaculation

Hormone therapy or radiotherapy

Hormone therapy can change the intensity of orgasms. Men who have had hormone therapy or radiotherapy might produce less semen or no semen. This is called a dry orgasm or retrograde ejaculation. 

Surgery to remove the prostate

You no longer ejaculate semen if you have had a radical prostatectomy. This is because the prostate gland and 2 glands called the seminal vesicles are removed. The seminal vesicles make the liquid part of the sperm. Your testicles will still make sperm cells but they will be reabsorbed back into your body.

You are still able to have an orgasm, but it will be a dry orgasm. Some men say that a dry orgasm without semen feels normal. But other men find that their orgasm is less intense and pleasurable.  The loss of a visible ejaculation can be significant for some men and their partners. Some men say that it feels different but they have managed to find ways to adjust to this.

If you are used to having anal sex and you are the receiving partner, surgery to remove the prostate gland can change this experience. Some men can find the penis rubbing against the prostate gland pleasurable. So if the prostate gland is no longer there, anal sex might feel different. You could look at different ways of enjoying sex and being intimate. Counselling and sex therapy might help.

Pain during erection or ejaculation

Some men find that erections and ejaculating is painful after surgery, or during and after their course of radiotherapy.

Painful erections following surgery could be due to internal bruising caused by the operation. The tube which carries urine from the bladder to the outside of the body (urethra) gets inflamed by the radiotherapy treatment.

This side effect should disappear a few weeks after you finish radiotherapy or as you recover from surgery. Talk to your specialist nurse for specific advice. If masturbation and sex is important to you, it’s important to keep stimulating the penis to keep it healthy. On the other hand, if erections are very painful, you might need to avoid ejaculation for a while and try again later.

The penile injections to stimulate an erection can cause painful erections in some men. This pain might lessen with continued treatment.

SMSNA – Delayed Ejaculation

There are several treatments for delayed orgasm/ejaculation. Treatment is mainly determined by the suspected cause of the problem.

If a prescribed medication is suspected to be the cause of the man’s delayed orgasm/ejaculation, finding an alternative prescription with a doctor’s guidance can usually solve the problem. For example, replacing an SSRI antidepressant with bupropion might reduce the risk of delayed orgasm/ejaculation. However, certain essential prescriptions can neither be removed nor replaced, so never discontinue a prescribed medication without consulting the prescribing physician.

Since delayed orgasm/ejaculation and erection problems are very common among excessive drinkers, the solution to this is simple: limit drinking. The same is true of individuals whose use of illicit drugs is the suspected cause of their delayed orgasm.

Since many experts think that the majority of delayed orgasm/ejaculation problems are due to behavioral or psychological causes, counseling and sex therapy with a licensed professional specializing in this area is a common treatment for restoring sexual function.

Generally, the objective of psychological therapy is to gradually diffuse the man’s sexual anxieties and shed any “baggage” he may be bringing into his sexual encounters so that he can more readily reach climax and have a pleasurable experience.

Men with low testosterone may find improvement with testosterone replacement. Several other prescriptions medications have been used for delayed orgasm/ejaculation, but no single medication has been reliably effective or universally accepted. Some medications which have been proposed include cabergoline, oxytocin, bupropion and amphetamine/dextroamphetamine salts (Adderall).

Penile vibratory stimulation (using a vibrator) may also be useful for some men.

For heterosexual couples desiring pregnancy in which the man is unable to ejaculate inside the vagina, couples can achieve pregnancy through several measures. These men can produce an ejaculate by masturbation, or by the use of electrical stimulation of the prostate area, called electroejaculation. These samples can be used for intrauterine insemination (IUI) or in vitro fertilization (IVF) in order to conceive. If this is not successful and fertility is still a concern, it is also possible for a trained physician to extract sperm from the testicles and use artificial insemination in order to initiate pregnancy. If artificial insemination fails, IVF (egg-sperm fertilization in a test tube and then inserted into uterus of mother) or single sperm injection can be attempted.

How Cancer Can Affect Ejaculation

This information is for adult males with cancer. If you are a transgender person, please talk to your cancer care team about any needs that are not addressed here.

Cancer treatment can interfere with ejaculation by damaging the nerves that control the prostate, seminal vesicles, and the opening to the bladder. It can also stop semen from being made in the prostate and seminal vesicles, or it can cut off the path that semen normally takes out of the body. Despite this, a man can still feel the sensation of pleasure that makes an orgasm. The difference is that, at the moment of orgasm, little or no semen comes out. This is referred to as a “dry orgasm.”

Over time, many men adjust to having an orgasm without semen. Some others say the orgasm does not feel as strong, while others report that the orgasm is stronger and feels more pleasurable. Men might worry that their partners may notice a change since there is no actual fluid release during sex.

Some men are most concerned that their orgasms are less satisfying than before. Others are upset by dry orgasms because they want to father a child. If a man knows before treatment that he may want to have a child after treatment, he may be able to bank (save and preserve) sperm for future use. (See Fertility and Male Adults with Cancer for more on this.)

A mild decrease in the intensity of orgasm is normal with aging, but it can be more severe in men whose cancer treatments interfere with ejaculation. See Treating Sexual Problems for Men With Cancer.

Surgery effect on ejaculation

Surgery can affect ejaculation in different ways. For example, if surgery removes the prostate and seminal vesicles, a man can no longer make semen. Surgery might also damage the nerves that come from the spine and control emission (when sperm and fluid mix to make semen). Note that these are not the same nerve bundles that pass next to the prostate and control erections (which are discussed in How Cancer Can Affect Erections). The surgeries that cause ejaculation problems are discussed in more detail here.

Dry orgasm

After radical prostatectomy (removal of the prostate) or cystectomy (removal of the bladder), a man will no longer produce any semen because the prostate and seminal vesicles have been removed. The testicles still make sperm cells, but then the body simply reabsorbs them. This is not harmful. After these cancer surgeries, a man will have a dry orgasm.

Sometimes the semen is there, but it doesn’t leave the body

Other operations can cause the ejaculate (semen) to go back inside the body rather than come out. This is called retrograde ejaculation. At the moment of orgasm, the semen shoots backward into the bladder rather than out through the penis. This is because the valve between the bladder and urethra stays open after some surgical procedures. This valve normally shuts tightly during ejaculation. When it’s open, the path of least resistance for the semen becomes the backward path into the bladder. This is not painful or harmful, although when a man urinates after this type of dry orgasm, his urine might look cloudy because the semen mixes in with it during the orgasm.

A transurethral resection of the prostate (TURP) is an example of an operation that usually causes retrograde ejaculation because it damages the bladder valve. This surgery cores out the prostate by passing a special scope into it through the urethra.

Nerve damage

We have already discussed the nerve bundles that sit on both sides of the prostate and help cause erections. Here, we will talk about the nerves that come from the spine and control ejaculation. Cancer operations that can cause dry orgasm by damaging the nerves that control emission (the mixing of the sperm and fluid to make semen) include:

• Abdominoperineal (AP) resection, which removes the rectum and lower colon
• Total mesorectal excision (TME), which removes the rectum as well as the mesorectum for treatment for rectal cancer
• Retroperitoneal lymph node dissection (RPLND), which removes lymph nodes in the back of the abdomen (belly), usually in men who have testicular cancer

Some of the nerves that control emission run close to the lower colon and are damaged by AP resection or a TME. Lymph node dissection can damage the nerves higher up, where they surround the aorta (the large main artery in the abdomen).

The effects of these operations are probably very much alike, but more is known about sexual function after RPLND. Sometimes this surgery only causes retrograde ejaculation. But it usually stops emission as well. When this happens, the prostate and seminal vesicles cannot contract to mix the semen with the sperm cells. In either case the result is a dry orgasm. The difference between no emission at all and retrograde ejaculation is important if a man wants to father a child. Retrograde ejaculation is better for would-be fathers because sperm cells may be collected from a man’s urine and purified in a lab to be used make a woman pregnant.

Sometimes the nerves that control emission recover from the damage caused by RPLND. But, if ejaculation of semen does resume, it can take up to several years for it to happen. Because men with testicular cancer are often young and have not finished having children, surgeons use nerve-sparing methods that often allow normal ejaculation after RPLND. In experienced hands, these techniques have a very high rate of preserving the nerves and normal ejaculation. (See Testicular Cancer for more information.)

Some medicines can also restore ejaculation of semen just long enough to collect sperm for conception.

If sperm cells cannot be recovered from a man’s semen or urine, infertility specialists may be able to retrieve them directly from the testicle by minor surgery, then use them to fertilize a woman’s egg to produce a pregnancy.

RPLND does not stop a man’s erections or ability to reach orgasm. But it may mean that his pleasure at orgasm will be less intense.

Urine leakage during ejaculation

Climacturia is the term used to describe the leakage of urine during orgasm. This is fairly common after prostate surgery, but it might not even be noticed. The amount of urine varies widely – anywhere from a few drops to more than an ounce. It may be more common in men who also have stress incontinence. (Men with stress incontinence leak urine when they cough, laugh, sneeze, or exercise. It’s caused by weakness in the muscles that control urine flow.)

Urine is not dangerous to the sexual partner, though it may be a bother during sex. The leakage tends to get better over time, and condoms and constriction bands can help. (Constriction bands are tightened at the base of the erect penis and squeeze the urethra to keep urine from leaking out.) If you or your partner is bothered by climacturia, talk to your doctor to learn what you can do about it.

Other cancer treatment effects on ejaculation

Some cancer treatments reduce the amount of semen that’s produced. After radiation to the prostate, some men ejaculate less semen. Toward the end of radiation treatments, men often feel a sharp pain as they ejaculate. The pain is caused by irritation in the urethra (the tube that carries urine and semen through the penis). It should go away over time after treatment ends.

In most cases, men who have hormone therapy for prostate cancer also make less semen than before.

Chemotherapy and other drugs used to treat cancer very rarely affects ejaculation. But there are some drugs that may cause retrograde ejaculation by damaging the nerves that control emission.

To learn more about ejaculation see Cancer, Sex, and the Male Body.

90,000 Female ejaculation – myth or reality ?. Treatment in Moscow, prices, appointment and consultation

Ejaculation is a specific release of sperm from the male genital tract, accompanied by orgasm. This does not require much explanation. But now they talk about female ejaculation – and what kind of animal is this?
If a woman secretes a large amount of fluid from somewhere in the genital tract during orgasm, it is almost always considered involuntary urination. The attitude to this fact is different, but, as a rule, both the woman herself and her partner do not really like the moment when the liquid soaks the bed.
Women undergo treatment, take physiotherapy, undergo psychotherapeutic treatment, sometimes undergo surgery – but for what? The head of the Institute for Therapy of Psychogenic Sexual Disorders (Vienna, Austria), Dr. Karl F. Stifter, on the basis of historical records of famous doctors of antiquity and the Middle Ages, as well as his own research, believes that in many cases a process occurs in women that can be equated with male ejaculation. The fluid that is thrown out of the woman’s urethra is not urine at all, but the juice of specific glands that open partly into the urethra, and partly near its external opening.
In his book “The Third Aspect of Pleasure” Stifter refers to the Kamasutra, Hippocrates, Aristotle, Chinese doctors and many authorities closer to us in time. Finally, since 1980, he has more than 20 publications in the serious medical literature that support his point of view.
According to Stifter, female ejaculation is a level of pleasure higher than the normal female orgasm. Unfortunately, although, according to various authors, almost half of women are capable of ejaculation, only a few consider it a normal and even desirable phenomenon, and the rest suppress such manifestations over time out of embarrassment.
Female ejaculation consists in the fact that when orgasm approaches or during it, a stream of liquid, not like urine, is involuntarily released from the urethra. These are not drops, but a jet, although the total volume of liquid may be small (on average, up to 50 ml – this amount is enough to leave a wet spot the size of two palms on the sheet). The liquid is whitish, more viscous than urine, does not smell, and according to the stories of women who have ejaculation, it smells “like a cat, but more pleasant”, “like new wine”, “slightly bitter”, “the smell and taste change 4 times per month: first spicy, then sour-tart, then very sweet – about 3 days before menstruation.The taste is exquisite, the liquid is similar to honey, but not so viscous. ”
Contrary to the established opinion of anatomists, Stifter suggests that the glands surrounding the female urethra be considered as the female prostate – with all its functions, including the production of prostatic juice.
Research conducted by the author has shown dramatic differences in the composition of urine and female ejaculation. Some indicators differ thousands of times, so there is no doubt that the examined fluid is really not urine.
An even more interesting test was suggested to the doctor by one woman who had ejaculation and participated in a study.She took a pill that stains urine, and after intercourse with ejaculation, examined the wet bed. There was no hint of a color change anywhere. Then, for control, she slightly urinated on the sheet – and it was colored urine.
In Austria itself, Stifter was bullied by feminists: they want to teach us women to ejaculate like men – but do we need that? But the researcher very correctly notes that, on the one hand, female ejaculation, like orgasm in general, is not at all the only and unchanging variant of female pleasure. And on the other hand, how many women can be saved from psychological trauma if they know that their sharp hydration is not a pathology at all, but a manifestation of a phenomenon unknown to many.
The experience of a sexologist allows us to assert that the described phenomenon really exists and is not so rare. Another thing is that many women, not understanding what is happening to them, suppress their reaction in every possible way – and thereby achieve its complete disappearance. It’s a pity …

Prokopenko Yu.P., Candidate of Medical Sciences

Retrograde ejaculation | Memorial Sloan Kettering Cancer Center

This information will help you understand what retrograde ejaculation is and how it might affect you.

to come back to the beginning

About retrograde ejaculation

Ejaculation refers to the release of sperm from the penis after orgasm (intense pleasure). With retrograde ejaculation, sperm travels in the opposite direction, entering the bladder rather than exiting through the penis.

At the time of sexual arousal, sperm leave the testicles and travel through the vas deferens (the duct that carries sperm from the testicles to the urethra) into the ejaculatory canal (see picture).picture 1). Upon reaching the ejaculatory duct, the sperm are mixed with the seminal fluid produced by the seminal glands and the prostate gland.

Figure 1. Male reproductive system

During orgasm, the bladder neck closes and semen is excreted through the penis. By closing, the bladder neck prevents sperm from going backwards and into the bladder.With retrograde ejaculation, the bladder neck does not close during orgasm. This causes sperm to flow in the opposite direction, entering the bladder instead of exiting through the penis.

to come back to the beginning

Causes of retrograde ejaculation

Retrograde ejaculation may be due to retroperitoneal lymph node dissection (RPLND) surgery. RPLND is surgery to remove multiple lymph nodes in the abdomen (belly).It is used to treat testicular cancer. During surgery, the nerves that control the bladder neck can be damaged. In some cases, these nerves can be preserved, but their function can take from a month to several years to resume. Whether a treatment such as surgery is right for you, your doctor can tell you.

Retrograde ejaculation may also occur after transurethral resection of the prostate. This is an operation performed to correct urinary problems caused by an enlarged prostate.Nerves can be damaged during surgery, leaving the neck of the bladder open during orgasm.

Retrograde ejaculation can also be caused by diabetes, multiple sclerosis, certain medications, and spinal cord injury.

to come back to the beginning

Sex life

Retrograde ejaculation is not harmful or painful, but it can change the sensation of sex because semen will not be released from the penis.This is called dry ejaculation. Dry ejaculation does not affect erection (hardening of the penis before intercourse) or orgasm. You will still be able to enjoy sexual activity. After having sex, your urine may be cloudy as it contains semen.

to come back to the beginning

Fertility

If you are planning to start a family after surgery, please tell your doctor before surgery that you want to donate sperm for storage. If you have not deposited sperm prior to surgery and still want to have children, your doctor can tell you about your options and refer you to a specialist.Read the resource Guidelines for Preparing for Retrograde Spermogram for more information.

to come back to the beginning

90,000 Delayed ejaculation: a modern perspective on the problem (abstract review according to the International Society for Sexual Medicine, ISSM)

Delayed ejaculation (EE) or retarded ejaculation is the least studied type of male sexual dysfunction.Problems with “difficulty” ejaculation can range from various delays in ejaculation to complete inability to ejaculate (anejaculation). Decreases in volume, strength and sensation during ejaculation may also occur. Anejaculation and retrograde ejaculation can be extreme values, but GE is more common.

According to the 2nd WHO Sexual Disorders Consultation, GE is defined as persistent or repetitive difficulty, delay or lack of orgasm, accompanied by sufficient sexual stimulation, which causes personal stress.

There are currently no clear criteria for GE. It is known that the majority of sexually active men ejaculate within 4-10 minutes from the start of intercourse. The clinician should assume that men with ejaculatory latency of about 25 or 30 minutes (21-23 minutes on average) who notice the development of stress, or men who stop having sex due to exhaustion, devastation, and irritation, qualify for this diagnosis. These symptoms, as well as a man’s and / or his partner’s visit to a doctor with a similar problem, are usually sufficient to establish a diagnosis of GE.

The inability to ejaculate can be a lifelong primordial phenomenon (congenital anorgasmia) or acquired. This can be repeated with every sexual encounter, or it can appear from time to time. There are still no normative descriptive data from large studies conducted on a large number of patients with GE, but a recent analysis found the percentage of congenital delayed ejaculation to acquired GE as 1: 3. Although coital anejaculation is often the main focus of therapy (especially with regard to fertility problems for highly religious men), men also seek treatment when they are stressed by the inability to orgasm in response to oral or manual stimulation from their partners.Some men with acquired ZE can achieve orgasm by masturbating, others cannot or will not for various reasons.

Psychodynamic interpretation emphasizes the psychosexual cause of development and connects congenital GE with various conditions: fear, anxiety, hostility, relationship difficulties, etc.

Masters and Johnson first discovered that GE in some men may be associated with orthodoxy in religious belief. Faith in God to such an extent can limit the sexual experience necessary to develop the necessary knowledge about the process of ejaculation, and can also lead to inhibition of the normal function of ejaculation.Many godly male believers masturbated very little or never, and for some, feelings of guilt and anxiety about “losing semen” often led to GE. These men often had little sexual experience before marriage. These very religious men could, but less often than ordinary secular people, have an orgasm during vaginal sex.

Many men with ZE use stimulation because it is appropriate for the speed, pressure, direction and intensity required to achieve orgasm, and different from the sensations they experience during sex with a partner.Thus, they may subsequently have difficulty having sex with a partner, and secondary GE may also develop.

Table. Causes of GE, anejaculation and anorgasmia

Treatment should be etiologically justified and should be aimed at treating infertility in men of reproductive age.Initially, you need to establish whether the problem is congenital or acquired, as well as whether organic factors are involved. The assessment begins with an analysis of the conditions in which a man can ejaculate. It is also determined: whether it was previously possible to achieve orgasm, life events / circumstances that temporarily coincide with orgasm disorders. The events in the survey can include the following aspects: medications, diseases, different types of stressors in life and other psychological reasons.For example, after a wife’s mastectomy, a man is afraid to harm her and therefore achieves only partial arousal. It also takes into account social / religious attitudes, which reduce emotional arousal. Last but not least, questions are asked about the quality of non-sexual relationships, problems are analyzed. In addition to the general examination, according to the indications, more detailed specific diagnostics can be carried out. It may include procedures such as: imaging the obstruction of the vas deferens; electrophysiological assessment of nerve fibers that control ejaculation; somatosensory and motor induced potentials from the external genital organs; test diagnostics of the sacral reflex arc; sympathetic skin reaction.

A variety of psychotherapeutic treatments have been described for the treatment of retarded or GE, but none has been tested in a large cohort of patients. Among them are the following: sexual training; reducing anxiety to achieve the ultimate goal; increased stimulation, more focused on the genitals; role behavior of the patient with a presumed strongly pronounced ejaculation from the position of a man and from the position of a partner; retraining masturbation; restructuring of sexual fantasies and arousal strategies.Men with congenital anorgasmia (complete lack of ejaculatory response), like their partners, usually need help in establishing their preferences for sexual arousal.

As with other counseling situations, men with GE may resist a doctor’s advice. For example, a doctor’s suggestion to temporarily stop masturbating may be met with resistance by the patient. In the treatment process, cooperation from the partner is also necessary, not only to increase a man’s arousal, but also to realize the need to use erotic films, books and other various sexual fantasies, which can also be attracted by a couple during lovemaking.Now it is necessary to note the issues of reproduction, since the issue of conception is often the initiating factor in the treatment of the patient. If there is an inconsistency in the goals of having children in the couple, then the doctor’s task is to at least temporarily focus the treatment on the fundamental points of these goals, so that the treatment of GE is successful.

The success of GE treatment is difficult to assess from the literature. Masters and Johnson reported a low efficacy of treatment (17.6%), consisting of a combination of focusing sensations, intense stimulation of the penis without coitus, and modifications to the technique of intercourse.Other studies have reported 70-80% efficacy with a variety of treatments.

Drug treatment ZE

Treatment of GE with medication has had limited success. None of the drugs have been approved as a permanent drug for this purpose. Most potentially useful drugs have limited efficacy, significant side effects, or are still in clinical trials. Some drugs affect ejaculatory latency indirectly by acting on other components of the sexual response, other drugs were originally used to remove the inhibitory effect on ejaculation of other drugs.The following drugs can be used:

1. Alpha-1-adrenergic agonists and monoamine reuptake inhibitors such as imipramine may play a role in the pharmacological treatment of GE.
2. According to scattered information, antagonists of 5-HT-serotonin receptors, which increase the level of serotonin in the brain, reverse the development of anorgasmia induced by the action of antidepressants of the group of selective serotonin reuptake inhibitors. However, no controlled studies have been published.Reception can be carried out systematically or on demand. Sedative effects can reduce overall effectiveness.
3. 1-adamantylamine hydrochloride is an indirect stimulant of dopaminergic nerve fibers by the central and peripheral pathways. It has been reported to stimulate sexual behavior, ejaculation, and other sexual reflexes in experimental animals. Several authors reported on their positive experience with its use in the reversal of anorgasmia induced by the intake of antidepressants of the group of selective serotonin reuptake inhibitors.The drug was prescribed 5-6 hours before intercourse at a dosage of 100 mg
4. Buspirone hydrochloride is used in patients with severe anxiety disorders at a dose of 15-60 mg per day.
5. A variety of other drugs, including natural biostimulants, alkaloids, and posterior pituitary hormones, are thought to increase the likelihood of ejaculation in men with GE. There have been no large, multi-patient studies using these drugs, and their use has been experimental, limited, and sporadic.Therefore, the data obtained are not reliable enough to recommend these drugs for use in the treatment of GE.

Treatment should be etiologically justified and focused on the problems of infertility in men of reproductive age. Men who have never had an orgasm or achieved orgasm may need a more detailed medical examination. They complain of insufficient ejaculate or psychogenic GE. Men, who sometimes experience orgasm and ejaculation, usually complain of psychogenic ZE or decreased sensitivity of the penis due to age-related degeneration of its afferent nerve fibers.They may respond well to a variety of cognitive-behavioral therapies, including learning, heightened stimulation, and other sexual techniques designed to maximize arousal. They should be examined to rule out retrograde ejaculation. The presence of sperm and fructose in centrifuged post-ejaculatory urine confirms the diagnosis. Treatment includes patient education, pharmacotherapy, or, in rare cases, bladder neck reconstruction. Absence of sperm suggests absence or agenesis of the testicles or vas deferens, or obstruction.The tactics include ultrasound and radiological examination to determine the side of the obstruction and appropriate treatment.

Undoubtedly, more research is needed on the effectiveness of drug and combination therapy for GE. The development of new pharmacological drugs will only improve existing treatment algorithms and improve the ability of patients to achieve satisfactory ejaculation.

Average rating:

Your rating: None Average rating: 4.3 (3 votes)

Page not found |

Page not found |

404.Page not found

Monthly archive

MonTueWedThuFrSaSun

15161718192021

22232425262728

2930

12

12

1

3031

12

15161718192021

25262728293031

123

45678910

12

17181920212223

31

2728293031

1

1234

567891011

12

891011121314

11121314151617

28293031

1234

12

12345

6789101112

567891011

12131415161718

19202122232425

3456789

17181920212223

24252627282930

12345

13141516171819

20212223242526

2728293031

15161718192021

22232425262728

2930

Archives

Tags

Settings
for visually impaired

90,000 Causes of the problem of premature ejaculation in men | Treatment of premature ejaculation (ejaculation) in the urology clinic MGMSU

Ejaculation is a complex physiological process that combines two processes – emission and ejaculation itself. The emission phase is the result of a reflex response from the nervous system (and reflexes, if you remember, depend on our will to a very limited extent).

This occurs after erotic stimulation (visual or direct contact). In the emission phase, sperm is released into the urethral lumen due to the contraction of the vas deferens, seminal vesicles and prostate. While the sensation of approaching ejaculation increases, the capacity for volitional control progressively decreases, reaching a certain point where ejaculation cannot be stopped.

Immediately after the emission is , the expulsion phase is also the result of the unconditional, i.e. not amenable to volitional control , reflex. In this phase, the internal sphincter of the urinary bladder is closed in order to prevent the reverse flow of semen. After that, the external sphincter opens and sperm is thrown out due to the contraction of the pelvic floor muscles.

If you dig even deeper, then at the biochemical level, ejaculation is an even more complex process.I do not urge you to memorize these complex names, I will designate them only so that you can imagine how difficult it is even for a very competent doctor to understand why this or that man has this problem.

So, the participants in the process: norepinephrine, serotonin, gamma-amino-butyric acid, nitric oxide. Increased levels of estrogen hormones (they are also called “female”, although a certain amount of estrogen should be in men) or decreased levels of testosterone – the main male hormone – can cause ejaculation disorders.If a man is out of order with the thyroid gland, then this, as a rule, leads to problems in the sexual sphere. If the amount of thyroid hormones is elevated, there may be premature ejaculation (PE). If it is reduced, then, as a rule, the process of erection is disrupted.

Now judge for yourself – is it simple, difficult to treat premature ejaculation …

Is it premature when?

Indeed, what is considered premature ejaculation? After all, even an hour is not enough for someone, but for many, three minutes is enough.in the medical literature, you can find several different definitions of what is “premature ejaculation”.

For example, in 1943 Schapiro B. proposed to divide PE into primary and secondary (acquired).

Primary is when PE occurs within the first 30 seconds – 2 minutes with every or almost every sexual intercourse, and from the very beginning of sexual activity. Secondary PE occurs after several years of normal sexual activity, and, as a rule, can be associated with the following reasons:

• Psychological problems (in this case, one partner is normal, on the other – nothing works)
• Erectile dysfunction
• Prostatitis
• Diseases of the thyroid gland, accompanied by an increase in its function (according to “scientific” – hyperthyroidism)
• Testosterone deficiency
• Taking drugs or psychoactive substances that interfere with the ejaculation process (such as marijuana).

In August 2007, experts of the International Society for Sexual Medicine, based on the generalization of numerous observations, came to an agreement that premature ejaculation should be called “sexual dysfunction in men, in which ejaculation occurs within the first minute after vaginal penetration, as well as the inability to delay ejaculation during time in all or almost all cases, accompanied by such negative emotional reactions as stress, anxiety, frustration and avoidance of sexual relations. “

How often do men have problems with ejaculation?

Some time ago in the USA, Germany and Italy, more than twelve thousand men from 18 to 70 years old were interviewed, and it turned out that premature ejaculation is a problem of almost every fourth! (more precisely, it occurs in 22.7% of men).

As it turned out, men who experience problems with ejaculation more often than others complain of erectile dysfunction, decreased sex drive, depression, anxiety, orgasm disorders.At the same time, only every tenth went to the doctor, and of those who tried to be treated, more than 90% are not satisfied with the results.

What is the most common age for having problems with ejaculation?

According to a survey of a large number (more precisely – 12 thousand. 133) men – in any. From young to old. Only in the age group from 18 to 24 years of age there are slightly fewer men with PE (scientifically speaking, statistically significantly less).

Does it matter: married or single?

It turns out that it does.In married men (or living in couples), PE is more common, but only by 7%. But married people live longer …

Does lifestyle affect PE?

If you play sports (meaning regular physical education, not exhausting professional sports) only a few times a month or less, then the chances of “quick sex” increase.
This implies the following pattern: the less physical activity, the more adipose tissue, and the more you weigh (meaning overweight), the worse for sexual function.

Smokers are also much more likely to condemn themselves to PE.

Some time ago I had a chance to communicate with a colleague from the Netherlands. He informed me that there is just an epidemic of premature ejaculation in his country. As you know, smoking is prohibited in Holland, but “soft” drugs are allowed there. Marijuana is one of the worst enemies of manhood.

Draw conclusions: you need to start with yourself, with a change in lifestyle.
Just in case, I remind you of the ideal weight formula: height in cm minus 100.

Is there a relationship between BPH and PE?

Statistics tell us no. So do not look for a black cat in a dark room where she is not.

Erectile dysfunction and premature ejaculation: different problems or one whole?

Again, let’s turn to statistics: men with PE have 3 times more erectile dysfunction than those who have long-term sex …
Accordingly, if you have risk factors for erectile dysfunction, namely: high cholesterol, overweight, high blood pressure, diabetes mellitus, you are more likely to develop PE.

Hence the next lesson: do not allow the development of erectile dysfunction, and if this happens, then first you need to treat ED, not PE …

Where to start treatment for PE?

I think we have already partially answered this question (see previous answers). To summarize the above, here are some simple tips:

• Answer yourself to the question: at what point in your life have you noticed that the process has become shorter? If right away, then most likely you need a sex therapist (or a psychologist who knows sexual problems).But still, this does not exclude everything that relates to secondary or acquired PE.
• If PE is secondary, i.e. did not appear immediately, but after some experience of normal sex, then ask yourself this question: what went wrong in my life? Maybe it’s a relationship with a partner? Or maybe you have gained weight and are sedentary? How many cigarettes do you smoke? In case of positive answers, do not rush to look for miracle cures – change your lifestyle.
• If all of the above does not apply to you, or you have eliminated all risk factors, then proceed to the next stage – examination and examination by a doctor.Here, unfortunately, it is very important what kind of doctor will be. If literate – the chances of prolonging the same sexual intercourse increase. If he promises to save you from PE, but at the same time will fool your head with expensive and unnecessary examinations and treatment regimens – think about it, maybe you need another doctor …
• In addition to a general examination and a special one (examination of the genitals, prostate), a number of laboratory tests are required, primarily hormonal ones (which hormones you need to take, you can read in paragraph 2 of our article).Advice: better let the doctor prescribe tests. In my experience, patients themselves go to different laboratories, and either they pass the wrong tests, or in the wrong laboratories.
• The last step – the actual treatment or pills …

Are there drugs for the treatment of PE?

If it’s not difficult for you, go back to point # 1 and pay attention to the “participants” in the ejaculation process. The main actor is serotonin, its lack is the main cause of PE.

Therefore, the most effective treatment for PE is considered to be the use of drugs from the group of antidepressants, namely the group of “selective serotonin reuptake inhibitors” – SSRIs, which increase the concentration of this hormone.As a result, the moment of onset of ejaculation is delayed. These are drugs such as paroxetine, dapoxetine, sertraline, but they are sold strictly according to the doctor’s prescription, I strongly advise against using them on your own.

Once again I draw your attention, if there are any problems with erection, then you need to start with this. It is only very important to remember: there are medications for the treatment of ED, and there are biologically active additives (dietary supplements). The dietary supplements are not worth your attention!

It is necessary to be treated with normal, proven drugs.The first line of treatment for ED today is type 5 phosphodiesterase inhibitors. They increase blood flow to the penis, causing a full erection.

If you come back to point # 1, you will notice that another important “participant” in the ejaculation process is nitric oxide. This substance with a simple formula (NO) is perhaps the most necessary for “masculine strength”. It is thanks to him, in the end, that the penis is filled with blood and an erection occurs.

Levitra increases the concentration of nitric oxide in the vessels, which causes them to expand.
There are a number of contraindications to the drug, it is better to consult a doctor first.

Is it necessary and possible to take phosphodiesterase inhibirotes if everything is in order with an erection, and ejaculation is premature?

PE is not an indication for type 5 phosphodiesterase inhibitors, but it’s worth a try anyway. Why? It has been noticed that hypererection contributes to the delay of ejaculation.

What if the test reveals that testosterone is low?

It is very simple: it is necessary to replenish its supply in the body (BUT ONLY AFTER THE DOCTOR’S CONSULTATION – THERE ARE CONTRAINDICATIONS!).A testosterone preparation has now become available and only needs to be done 4 times a year.

Agree, it’s very convenient. The restoration of testosterone levels is sometimes enough to increase the time to ejaculation.

For details of the appointment, indications and contraindications for testosterone treatment, consult your doctor.

Why are doctors reluctant to prescribe SSRIs?

The fact is that prescribing antidepressants of the group of “selective serotonin reuptake inhibitors – SSRIs” for the treatment of premature ejaculation, doctors use, in fact, their side effect – to delay ejaculation.Premature ejaculation does not appear in the indications for these drugs.

And it is not entirely correct to use the side effect of the drug as the main one (to be honest, it is generally incorrect!). But despite this, the drugs of this group in all Recommendations (for example, the Recommendations of the American Association of Urologists, the European Association of Urologists) are the first line of therapy. This is the case when science and practice go forward, and the paperwork stands still … I am always faced with a dilemma – to break the law or help a patient? Of course, it is possible to justify the appointment of the same paroxetine by the presence of depression in a man, but we mean premature ejaculation.

In addition, I always warn about the possible side effects of antidepressants, including not only nausea and headache, but also such as insomnia (or, conversely, drowsiness), tremors, fatigue, confusion, convulsions, etc. …

But most importantly, these drugs can significantly worsen erection and reduce libido, i.e. cause completely opposite effects! So decide – are you ready to take risks? I hope you understand the seriousness with which you need to approach the decision to take these drugs? Of course, they can and should be prescribed ONLY by a DOCTOR!

What if you still have to take SSRIs?

If your doctor prescribes paroxetine or sertraline, you need to take them regularly, starting with the lowest dose, gradually increasing (how to do this, the doctor will tell you!).As a rule, the course lasts at least 3 months.

Why? The fact is that 3 months is the period after which you will receive a certain effect that will not grow further. For example, the time to ejaculation before starting treatment was 1.5 minutes, and after three months it increased to 3 minutes. This means that there will be only 3 minutes further … i.e. the time for which the drug is maximally “capable”. In the future, if there is an effect (and there are no side effects), SSRIs can be taken once, approximately 6 hours before intercourse.

The undesirable side effects listed in clause 13 may become an obstacle to the continuation of SSRIs. Agree, if you want to sleep, or feel sick, before sex?
But the problem of deterioration of potency against the background of antidepressants will help to solve the same vardenafil. It must be taken with paroxetine or sertraline.

Delayed ejaculation. Etiology, diagnosis, treatment. Reproductive aspects of the problem

Abstract

Abstract Delayed or suppressed ejaculation (GE) is one of the least studied forms of sexual dysfunction in men.GE has a relatively low prevalence (<3%). ZE is a type of ejaculation disorder and is a subtype of orgasmic disorder in men. Pathology causes depression, anxiety, loss of sexual confidence. Ejaculation disorder can be a lifelong (primary) and acquired (secondary) problem. In some cases, somatic problems can cause ejaculation disorders. Disruption of sympathetic or somatic innervation is a potential factor influencing the processes of ejaculation and orgasm.Normally, ejaculation and orgasm occur simultaneously. However, in accordance with modern ideas about the neurophysiological mechanisms of these processes, the terms "ejaculation" and "orgasm" are not identical. The ejaculatory reflex includes sensory receptors and regions, afferent pathways, cerebral sensory and motor centers, spinal motor centers, and efferent pathways. The neurochemical reflex involves a complex interaction between central serotonergic and dopaminergic neurons.The cholinergic, adrenergic and oxytocinergic systems play a secondary role. Dopamine and serotonin are the dominant neurotransmitters, and there are currently no effective and safe drugs to speed up ejaculation time. The most effective methods of correcting lifelong GE are psycho - and sex therapy. The best way to treat men with primary GE is by informing about the factors that can slow down ejaculation and by counseling. The beneficial effect of therapy depends on the severity of the GE and the patient's responsiveness to therapy.Psychotherapy can be effective in some groups of patients, especially when drug therapy is ineffective and unsafe. However, the psychological approach to solving this problem is often frustrating. Further investigation of the neurophysiological aspects of ejaculation is important for understanding the pathological mechanisms of GE and the creation of new ways to solve this problem. Key words: delayed ejaculation, orgasm, serotonin, dopamine, infertility, DNA fragmentation of spermatozoa.

90,000 How to prolong intercourse up to 1 hour

Premature ejaculation is one of the most common problems men turn to a sex therapist ¹ . It can cause self-doubt, psychological depression, and also contributes to the deterioration of relations between partners.

Among the causes of this problem, experts call congenital features. This is a reduced content of serotonin in brain cells, as well as an increased sensitivity of receptors in the skin of the penis ⁶ .

There are also acquired reasons. These are stress, unbalanced diet, lack of regular physical activity and other factors that can worsen overall health and negatively affect “male strength”.

Also, various diseases can lead to premature ejaculation: neuroses, prostatitis, infectious diseases, etc.

In the event of a problem of premature ejaculation, it is recommended not to dwell on the question “what to do to prolong sexual intercourse?” but first of all consult a doctor.An independent search for causes and attempts to self-medicate may end in failure. Lost time can make diagnosis and treatment more difficult.

Therefore, the best solution in the event of a delicate problem is to consult a doctor.

Psychological and physiological methods of prolonging sex up to an hour

• Balanced nutrition . Unhealthy diet is one of the main health risk factors ² . A complete diet will help you feel much better.Doctors recommend consuming at least 5 servings of fruits and vegetables a day, reducing the amount of sugary foods, replacing fats from animals with vegetable oils (olive, flaxseed, mustard and other oils, avocados).
• Adequate sleep . The optimal amount of sleep varies from person to person. It depends on age, activity and other factors. Presumably, at least 8 hours of sleep a day will add to your strength and endurance.
• Regular physical activity .You don’t have to go in for professional sports to feel good. Enough regular walks in the fresh air, cycling, active games with children ³ .
• Repeated intercourse . Some men note that after a short first intercourse, they are quite quickly ready to continue. This can be a suitable way to prolong the pleasure of having sex with a girlfriend or wife .
• Use of desensitizing agents .A man can be helped by using lubricants or condoms with substances that desensitize the penis. It is believed that alcohol acts in a similar way and allows you to prolong sexual intercourse, but it cannot be called an effective help for solving the problem of premature ejaculation. Experts recommend avoiding its frequent use due to health risks ⁷ .
• Taking care of your health . Certain chronic illnesses can cause premature ejaculation.Therefore, it is so important to see a doctor and undergo the necessary examinations in order to find out the possible causes of failures in bed and effectively influence them.

Medicines to prolong intercourse

Premature ejaculation is sometimes accompanied by insufficient erection. In this case, the man may feel an involuntary desire to end sexual intercourse as soon as possible, which seems to him inferior ⁴ . Your doctor may recommend medications to help improve your erection.

✓ These drugs work when a man is sexually aroused. They allow you to make an erection more stable and allow you to perform repeated intercourse, which is important for the problem of premature ejaculation.

Tablets for men can be used in cases of concomitant diseases. For example, it is possible to take these drugs in men with arterial hypertension, Parkinson’s disease, depression, diabetes mellitus, after surgery to remove the prostate, etc.In each case, the doctor determines the possibility of taking medications for a particular disease.

✓ Studies show that long-term use of PDE5 inhibitor drugs in some men showed improvement in the lower urinary tract (discomfort during urination disappeared), as well as improved erectile function and overall quality of life. ⁸

Prolonged intercourse in sex is achieved through an integrated approach.

The solution to the problem of premature ejaculation is individual in each case. Mutual support and understanding of partners are very important. A doctor’s consultation is necessary to rule out diseases that can cause problems in bed, and to select the optimal treatment program.

List of used literature

1. Laumann E.O., Paik A., Rosen R.C. Sexual dysfunction in the United States: prevalence and predictors. JAMA. 1999 Feb 10; 281 (6): 537–44.
2. WHO official website.Healthy eating. Newsletter # 394. September 2015
3. WHO official website. 10 facts about physical activity.
4. Shcherbakov D.V. “Diagnosis and treatment of premature ejaculation associated with erectile dysfunction.” 2011
5. A.G. Martov, D.V. Ergakov, “Sildenafil in modern urological practice” // EFFECTIVE PHARMACOTHERAPY. Urology and Nephrology. No. 2 (15) / 2014.
6. Alyaev Yu.G., Akhvlediani N.D. “Premature ejaculation – Terra incognita in andrology // Doctor 2007, no.