Premature Ejaculation

Premature ejaculation (PE) is a common condition, and it can have a very significant effect on a man and his partner's sexual pleasure, and indeed on the quality of their relationship. However, it isn't difficult to increase dramatically the time between penetration and ejaculation, and this can be done both with behavioral training techniques and various drugs.

Premature ejaculation (PE) is probably the most common sexual dysfunction presented by men or couples. It's also been called rapid or early ejaculation; it can affect men of all ages, both from the beginning of their sexual career, or it may develop unexpectedly later in life.

Definition of premature ejaculation

The very nature of this condition means that there is no clear definition of PE.  Indeed, some authors have speculated that in fact far from being a dysfunction, it is actually the normal state of the male reproductive system! Authors have tended to come up with their own definitions based on their interest in the field, influenced by their research bias and individual judgments. So, for example, the two most common definitions are completely different: the first, due mainly to Waldinger, suggests that a man has PE if he ejaculates within a minute of vaginal penetration; while the second, which originated with Masters and Johnson, states that a man has PE if he ejaculates before his partner has obtained sexual satisfaction. This implies, of course, that a woman will indeed reach orgasm during intercourse, which is a challenging assumption. Many surveys have demonstrated that, at the most, 15% of women regularly reach orgasm during intercourse.

Implicit in the Masters and Johnson definition of PE, then, is the presumption that were a man able to continue making love for longer, his partner would be able to reach orgasm during intercourse. This is highly questionable since most women achieve orgasm by stimulation of the clitoris, which tends not to happen during regular intercourse. In practical terms, therefore, this definition has to be seen as unworkable, and much better is the definition proposed by the American neurological Association. They suggest PE is defined as "ejaculation that occurs sooner than desired either before or shortly after penetration, causing distress to one or both partners".

Anatomy and Physiology

Before we discuss the nature of PE, we need to briefly review the anatomy and physiology of the male reproductive system. Ejaculatory fluid is formed by an amalgam of secretions from the seminal vesicles, the prostate, and the glands that open into the urethra. The bladder neck is located proximal to the paired ejaculatory ducts, and during ejaculation it acts as a sphincter to prevent flow of semen into the bladder. During ejaculation, the smooth muscle around the urethra is subject to the control of the autonomic nervous system, and contracts to activate the sphincter.

On the distal side of the ejaculatory ducts there is an external urethral sphincter, which consists of two layers of muscle: the central layer is under the control of the autonomic nervous system, and the outer layer is under somatic control. This muscle contracts before the emission of semen into the base of the urethra so that in effect there is an enclosed pressure chamber created in the prostatic area of the urethra. The ejaculation process involves relaxation of the sphincter so that the semen can flow down the urethra and out of the penis.

In neurological terms, ejaculation is a process which is controlled by both the central and peripheral nervous system. To start with, the cutaneous nerves of the penis are fundamental to the mechanism of the ejaculatory process. When stimulated, these nerves send impulses through the pudendal nerve to the spinal-cord: the specific area in the brain which acts as the control centre of ejaculation has not been fully determined, although the hypothalamus seems to play a major role in the process.

The nerves which are responsible for ejaculation travel down from the cerebral  cortex to the thoracolumbar and sympathetic nervous system chains at the area of T10 to T3. Postsynaptic adrenergic fibers then take a route through the superior hypo-gastric plexus located at the aortic bifurcation, before they disburse laterally near the area of the bladder and rectum to the end organs (which include the epididymis, the seminal vesicles, the vas deferens, prostate gland and the neck of the bladder. The actual expulsion of semen from the pressure chamber in the posterior urethra is stimulated by activation of the nervous system fibers within the pudendal nerves originating from S2 to S4.

The physiology of ejaculation

As we've seen, ejaculation is basically a co-ordinated activity of different systems of the body so that the seminal fluid, once deposited into the posterior urethra, is then subsequently expelled through the urethra and urethral meatus. There are actually three phases of the ejaculatory process: the first is bladder neck contraction, the second is emission (the moment when semen is released into the base of the urethra), and the third is ejaculation. Naturally enough, these three events occur in a very ordered and systematic physiological sequence. To start with, during emission, smooth muscles located inside the prostate gland, seminal vesicles, and vas deferens contract in a rhythmic fashion that causes the semen to be deposited into the posterior urethra. At the same time, the neck of the bladder, which contains smooth muscle fibres, is contracting so as to prevent the retrograde flow of semen into the bladder. After the semen has been successfully deposited into the posterior urethra,
the external urethral sphincter relaxes and the urethral skeletal muscles contract in a rhythmic fashion to ejaculate semen in pulses through the urethra.

This latter sequence of the ejaculatory process is the result of stimulation from branches of the pudendal nerves originating from S2-S4. These are muscles which are normally under voluntary control; however, during the process of ejaculation all of the events are in voluntary once the reflex has been initiated.

Ejaculation is normally caused by a combination of sexual activity which results in sensory stimulation from the genitals coordinated with erotic imagery and thoughts in the cerebral cortex. This input from the cortex actually enhances the sensory stimulation of the penis, but nonetheless, the ejaculation reflex is something which can be activated by cerebral input alone -- as demonstrated by the phenomenon of nocturnal emission.

Premature ejaculation

It's remarkable that despite the fact that PE is a problem for so many men (estimates ranging from 50 to 75% of the male population), its etiology is not understood fully. In the era when psychodynamic explanations held sway, premature ejaculation was thought to be the result of an unconscious conflict (such as between sexual desire and hostility towards one sexual partner). However, in the later era where behavioral theory tended to hold precedence, PE was regarded as a learned behavior and/or the product of performance anxiety.

In recent times a neurobiological explanation has been favored, and rapid ejaculation has tended to be regarded as a condition that results from anomalies within the nervous system such as oversensitive penile nerves or an imbalance of dopamine and serotonin in the brain (within the central nervous system, dopamine seems to act as an excitatory agent, while serotonin appears to be excitatory). There has even been a suggestion that PE is caused by a delay in processing sensory nerve stimulation in the central nervous system.

One has to keep in mind that since almost all men are rapid ejaculators at the start of their sexual career, and only a small percentage manage to achieve greater control of their ejaculation, particularly to the point where it becomes a voluntary decision to ejaculate, it may well be that we are biologically programmed to ejaculate quickly:
it actually makes good sense for a mammal in a hostile environment to mount, penetrate, and ejaculate inside its partner as quickly as possible. It could well be that in seeking an explanation and cure for premature ejaculation, categorizing it as a disease or a problem, or at the very least as a sexual dysfunction, we have the wrong orientation in our enquiry. It may be more appropriate to ask how it is that men learn to last for as long as they desire when they make love, and then to explore and analyze the methods that they have used, either consciously or unconsciously, to become longer lasting lovers.

Despite this, of course, scientists continue to search for an explanation and treatment. One of the basic criteria for describing sexual dysfunction is to classify it, and PE is no exception: it has been divided into two types - primary and secondary, where primary PE refers to the presence of rapid ejaculation since puberty; men who have secondary PE will experience the onset of rapid ejaculation later in life. If premature ejaculation is acquired, i.e. it develops later in life after previously successful attempts to control ejaculation, it is vital that the doctor or therapist addresses the issue of when the PE started, or what events were happening when it began.

Other factors to establish is whether the PE is situational and whether it occurs with only certain partners. It is also relevant to establish the length of time between the beginning of sexual sensory stimulation and ejaculation during masturbation, oral sex, and intercourse: in assessing a man's sexual function, the degree of voluntary control that he believes he has over his ejaculation is also important. Lastly, for those who are seeking to treat the disease in a face-to-face interaction, it's important to establish how much the man and his partner experience distress because of his rapid ejaculation. (Some couples are not disturbed by the phenomenon because they have incorporated it into their lovemaking in a way that allows both of them to reach satisfaction. A common model for this would be the man bringing the woman to orgasm before he penetrates her; many couples report that under these conditions the woman is much less bothered by his failure to maintain long lasting thrusting.)

Treatment of premature ejaculation

Because there isn't any clear agreement about the origin of premature ejaculation, it's not surprising that a variety of treatment strategies have evolved, including psychological, behavioral, and pharmacological (the latter uses medication in an attempt to alter sensory input or affect the operation of the ejaculatory reflex).

Sex therapy

If PE is a learned behavior caused by performance anxiety, then sexual therapy part would be the treatment of choice. Indeed, acquired or situational PE does seem likely to have a psychological basis, most likely caused by over-arousal of the nervous system due to a high level of stress, worry, or performance anxiety. Sex therapy for premature ejaculation takes the form of counseling or therapy to investigate the deeper issues such as underlying anxiety, together with behavioral techniques which enable a man to gain greater control over his ejaculation. Many men with PE report that they arrive at the moment of ejaculation without sensing it is coming upon them; any form of sensitivity training which raises a man's awareness of the level of arousal and his body will allow him to have more awareness of the moment of ejaculation, and enable him to slow down or stop thrusting altogether as it approaches.

The method described on this website is neither the squeeze technique nor the stop-start technique (see below), but a system of behavioral training with a partner in which a man is exposed to gradually more stimulating situations as he learns to accommodate the level of arousal that he feels without ejaculating.

The squeeze technique was formulated by Masters and Johnson in the late 1960s and early 70s. It's a technique during which the man or his female partner squeeze the head of the penis just underneath the frenulum where it joins the shaft when the man is aware that he is nearing the point of ejaculation. He may lose a degree of erection, but the squeeze reduces his arousal so that he is in no danger to ejaculating. Timing is crucial, of course; if the squeeze is left to late then he may well ejaculate anyway. This technique is disruptive to intercourse, and a man must have the co-operation of a willing partner. Intercourse is resumed after the man's arousal has dropped. The squeeze technique produces reasonable results in the short term, but does not appear to produce long lasting change.

The stop-start method was introduced by Doctor James Seaman several years before Masters and Johnson developed their squeeze technique: the technique involves masturbatory stimulation of the penis to the point where a man feels highly aroused, but he stops before he reaches the point of ejaculatory inevitability. When the man's level of arousal has dropped, stimulation recommences. Eventually, it will be possible for man to take considerable stimulation to the head and shaft of his penis without reaching the point of ejaculatory inevitability.

A less satisfactory treatment involves applying anesthetic to the head of the penis.
2.5 g of prilocaine-lidocaine cream can be applied to the glans of the penis 30 minutes before intercourse. To keep this in place, a condom maybe worn, although the cream has to be wiped off before intercourse to prevent it being transferred to the partner's vagina. Many couples find condom is unacceptable, particularly if they're in long-term relationships which are monogamous. Men have reported to me that these creams do not work: they come just as quickly, but they now feel no physical sensations in their penis.

A high percentage of men reported an improvement in their PE with a product called SS cream. This is manufactured in the Far East and apparently has considerable impact on premature ejaculation when applied to the head of the penis. Details remain scare at the moment, though it has been evaluated in some controlled trials.

Pharmacological therapy for premature ejaculation

The treatment of PE appears to be possible using several medications designed for other purposes. However, the FDA has not approved any of these drugs for this purpose. This does not appear to have prevented doctors routinely prescribing them, and studies, where they have been done, indicate some success in the treatment of PE with these medications.

The first medical treatment discovered to have an effect on PE was the use of medications to inhibit alpha receptors. The alpha adrenergic blocker phenoxybenzamine was used in a study reported in 1984 to treat PE in nine men. Possibly due to side effects, which include aspermia, this medication has not been reported in the literature to any significant degree.

The tricyclic antidepressant clomipramine does have an effect on PE in double-blind studies where the trial doses range between 10 and 50 mg per day. Clomipramine may work by inhibiting the autonomic processes involved in the ejaculatory reflex or by diminishing psychological arousal. Once again this does not appear to be a treatment which has received widespread acceptance.

It's mostly the selective serotonin reuptake inhibitors (SSRIs) which have received attention as possible medical treatments for PE. These drugs work because they have a powerful effect on the level of serotonin in the central nervous system: you may recall that serotonin inhibits the central ejaculatory reflex. In many studies these inhibitors have indeed been demonstrated as effective in delaying ejaculation, so that they have become the most common class of medications used to treat PE.

Recommended doses of the various SSRIs include fluoxetine (20 to 40 mg a day), sertraline (5200 mg a day), paroxetine (20 to 40 mg a day), and fluvoxamine (hundred milligrams a day). Side-effects include gastrointestinal upsets and anxiety. Balding has established that paroxetine seems to have the strongest delaying effect on a man's ejaculation.

Of course, one of the problems in prescribing SSRI is as medication for PE is that they need to be taken continuously. Various studies have investigated whether or not they may be taken "as needed": various studies have demonstrated that there is some effectiveness in treatment when clomipramine is administered 20 to 24 hours before intercourse, sertraline is administered 4 to 8 hours before intercourse, and paroxetine is administered 3 to 4 hours before intercourse.

There have been suggestions that sell Sildenafil citrate (Viagra) can be used as part of a combined therapy with paroxetine to treat rapid ejaculation. The results cane from a study without a control group, and the results are therefore somewhat in doubt: it seems intuitively unlikely that a drug which is designed to enhance erection would have an impact on ejaculatory latency, so it remains unclear if phosphodiesterase inhibitors do indeed have any role to play in pharmacological treatment for men with PE.

Dapoxetine is a new compound which has been the subject of much investigation because of the promise that it holds for the drug treatment of PE. In one study by Pryor and Althhof, over 2600 men with PE underwent a 12 week treatment period, during which their IELT (intra vaginal ejaculatory latency time) was measured by using a stop watch -- being held by the sexual partner! You may think that this investigation methodology leaves a considerable amount be desired, nonetheless since all men were using the same method it is indicative of the success or failure of the treatment.

After a two-week baseline period, men were divided into groups with either placebo or Dapoxetine prescribed in 30 or 60 mg doses on an "as needed" basis for three months. The investigators questioned the men about the feelings they had of control over ejaculation and the level of satisfaction they experienced with sexual intercourse.

There was a significant difference between the treatment groups, in that the IELT improved from 0.9 to 1.75 minutes in the placebo group, 0.92 to 2.78 minutes in the 30 mg Dapoxetine group, and 0.91 to 3.32 minutes in the 60 mg Dapoxetine group.

Men receiving both 30 and 60 mg Dapoxetine were significantly better in increasing IELT after the first dose. Unfortunately, side-effects included nausea (almost 10% of men taking the 30 mg dose, and 20% of the men taking the 60 mg dose), headaches, diarrhea and dizziness. It seems unlikely that the medication is going to be licensed for use in this context in the near future.

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