A Little Bit Of History….
Discussion about the causes and origins of premature ejaculation (PE for short) have been going on for decades. First of all, between 1887 and 1917, it was called rapid ejaculation in the medical literature; next, between 1917 and 1950, it was termed ejaculatio praecox. Typical of this time, Abraham came up with a psychodynamic theory for the origin of premature ejaculation, suggesting that PE was the adult expression of unresolved narcissism during infancy, a narcissism which caused exaggerated importance to be assigned to the penis.
Between 1950 and 1990, the psychological aspects of the condition were emphasized, as was a behavioral approach to treatment, largely because of the pioneering work by Masters and Johnson. This suggested premature ejaculation might be a “learned behavior”. In other words, an initial experience of rapid ejaculation when a man first has sex, or is very sexually excited, establishes a pattern of rapid ejaculation as the man’s normal sexual pattern. Then he develops anxiety about this, which doesn’t help matters at all. In fact, it makes him come even faster. The most recent phase in the explanation of the origins started with 1990s studies which revealed how premature ejaculation could be treated with clomipramine and various other selective serotonin reuptake inhibitors (SSRIs).
How exciting! A drug to cure premature ejaculation…. or not? This has been taken to mean that there’s a neurological basis for PE which involves a dysfunction of the central serotonergic neurotransmission process. But what is cause and what is effect remains unproven.
Physical Or Emotional?
It has been claimed that there’s a general move towards the acceptance of premature ejaculation as a condition based on an underlying organic component which is exacerbated by emotional issues like performance anxiety. Psychological causes could include the development of a habit of ejaculating prematurely, caused perhaps by anxiety, although this has not been proved.
Some authors believe that anxiety is more probably a result of premature ejaculation, and not the cause. See this book for more information. Support for a physiological etiology behind premature ejaculation largely comes from the surprising, not to say unlikely, theory that the condition has a genetic component.
Schapiro reported a genetic link in cases of PE in 1943, and more recently, Waldinger et al. demonstrated that around 70% first-degree relatives of men with “non-acquired” life-long premature ejaculation had the condition. But they were probably brought up in the same environment, where sex was, most likely, taboo, shameful, anxiety provoking… or worse. Waldinger found PE to be associated with anomalies in the central serotonin (5-HT) signaling system, and hypothesized that premature ejaculation represented a single point on a normal distribution of ejaculatory latency through the male population.
This suggests the etiology of premature ejaculation might involve a genetic predisposition. Of course, others think that emotional, cognitive and psychological influences are the primary cause of PE, and that the psychological disturbances associated with PE may be either cause or effect. Admittedly, a genetic predisposition might underpin other theories about the etiology. These include the idea of penile hypersensitivity, and the suggestion of a hyperexcitable ejaculatory reflex, as well as central 5-HT receptor sensitivity.
Penile hypersensitivity has been suggested by many authors as an important factor in the organic etiology of PE. The idea is that men with penile hypersensitivity may reach their ejaculatory threshold more quickly, or even have a lower threshold, when compared with men who have more “normal” ejaculatory latency. However, this theory cannot account for secondary premature ejaculation, and evidence has been lacking to support the idea in men with lifelong non-acquired PE. Another theory has been proposed that PE is caused by an inadequate or over-excitable ejaculatory reflex, which causes the emission and/or expulsion phases of ejaculation to occur more quickly.
The bulbocavernosus muscle, which surrounds the urethral bulb, is one of several important muscles associated with the expulsion phase of ejaculation.
A Little Bit Of Science
Studies on animals have demonstrated that serotonin receptors are essentially involved in the central nervous system control of the ejaculatory sequence.
The 5-HT2c and 5-HT1A receptor subtypes are especially important: stimulation of 5-HT2c receptors in rats slows down ejaculation, while stimulation of 5-HT1A receptors speeds it up.
Waldinger and Olivier’s hypothesis is therefore predicated on the viewpoint that premature ejaculation is the result of hypersensitivity of 5HT1A and/or hyposensitivity of the 5-HT2c receptors.
In other words, premature ejaculation is associated with a threshold I E L T that is genetically predetermined at a lower point, and is determined by the ex tent of imbalance between the 5-HTIA/5-HT2C systems. As yet this remains unproven. What may be more important is the experience of men who have PE. This suggests that premature ejaculation is probably multifactorial with a combination of physiological and psychological causes.
Supporting evidence behind this theory is circumstantial, but it does seem sensible, and many men’s PE is indeed difficult to treat and does not respond to any current therapies or behavioral treatment strategies. There are various psychological factors linked to premature ejaculation, including sexual inexperience, lack of sexual intercourse, fear and anxiety, and relationship problems.
This means that a strategy for treatment of this issue must really involve a man’s sexual partner. Education is sometimes necessary, as is treatment of all comorbidities, which include poor sexual education, urinary tract infections, diabetes, prescription drug regimes, non-prescription drugs, and erectile dysfunction. However, men in whom erectile dysfunction and premature ejaculation occur together are a separate population from men with premature ejaculation who have a firm erection, and they require different treatments.
Understanding the real frequency of PE among men is difficult. This is not helped by the absence of a clear definition of “normal” and a clear definition of “premature”. Having said that, we do know that PE is widespread, affecting about one man in three in all age groups, and we know it can have a major effect on the quality of life of a man and his partner.
While the exact origin and cause still has to be defined, it’s likely PE is, at least in part, a neurophysiological issue which is associated with dysfunctional serotonergic neurotransmission in the brain and central nervous system. This means the best treatment for premature ejaculation might be drugs that act on the brain combined with other treatment strategies which reduce the impact of the psychological causes and consequences. But in truth, there is very little hard and fast medical evidence about the causes of rapid ejaculation.
This is one of the reasons why it has proved so difficult to treat medically – with drugs or other medical treatments – there is nothing that you can pin down as a cause and say, “Oh, yes, we can deal with this medically.”
One example is the suggestion that the pelvic muscles, and in particular the muscles around the erectile bodies in the penis, are hyperactive in men who experience premature ejaculation. Ejaculation involves increased activity of these muscle groups; ergo, it seems men who come too soon may have hyperactive muscles already aroused and approaching the threshold of ejaculation.
One of the experts at The Male Health Center observes that he has been evaluating and treating men with sexual problems including impotence and premature ejaculation for several years. He has observed that men with premature ejaculation show increased sensitivity to vibration in the penis, at least when set alongside men who do not have the problem. He infers that PE may be caused by hypersensitivity of the penis and pelvic muscle hyperspasticity.
Mostly due to difficulties in researching sexual issues, and in defining premature ejaculation, the frequency of premature ejaculation in the male population is not actually know with any degree of certainty.
For one thing, there are different degrees of the condition: it may occur in all situations, with all partners (generalized premature ejaculation), or it may occur only at certain times with certain partners (situational). It may be present for man’s entire life (lifelong premature ejaculation), or it may be acquired later in life. Furthermore, anyone who is working in the field of sex therapy will know only too clearly that when a man is stimulating himself during masturbation, he subjectively experiences himself as having a much greater degree of control over ejaculatory latency than when he’s enjoying sexual relationships with a partner.
Could this mean there are interpersonal dynamics at work in the etiology of premature ejaculation? Of course! It’s also worth recording at this point that the female partners of men who regard themselves as having rapid ejaculation report lower levels of sexual satisfaction, and higher levels of interpersonal difficulty, than partners of men who do not see themselves as having premature ejaculation.
Hartmann and his colleagues have reported that men with PE tend to think about ejaculatory control (or lack of it) and tend to experience anxiety during sex, while men who do not have this problem seem to think about sexual arousal and sexual satisfaction.
Michael Perelman works at Cornell University and has developed ideas for sexual therapy around the diagnosis and treatment of premature ejaculation. In an article published in the Journal of Sexual Medicine in 2006, he proposed that the best therapy for premature ejaculation would be a combination of sex therapy and pharmaceuticals.
Etiology of Ejaculation Problems
Just to recap briefly about the mechanism of ejaculation: as you may be aware, ejaculation is the end product of the sexual response cycle which begins with arousal, moves through the so-called plateau phase, and ends with ejaculation and orgasm, followed by resolution or recovery.
Of course, ejaculation is a physical event caused by a reflex in the body, while orgasm is a mental phenomenon which is subjectively experienced as feelings of great pleasure.
Ejaculation itself is composed of two events: emission and expulsion. The emission phase involves the deposition of seminal fluid into the posterior urethra, an event which is experienced as the point of ejaculatory inevitability, commonly known as the point of no return. This terms describes a physiological reality, because once emission has occurred, ejaculation is but seconds away.
Ejaculation is the muscular expulsion of seminal fluid from the penis, a sophisticated series of events involving co-ordinated contraction of a number of muscles around the pelvic area, in particular the bulbospongiosus muscle. In the approach to ejaculation a man will experience a number of bodily sensations and changes associated with the peak of arousal, including the movement of the testicles upwards, myotonia, raised blood pressure, rapid heart rate and muscular tension.
These are the signals which can be used to enable a man to recognize that he’s on the verge of ejaculation, and which, if he’s sufficiently motivated, can be used as an indicator that prompts him to change his behaviour and enables him to delay his ejaculation during sexual intercourse.
In essence, what a man with premature ejaculation must do to find a complete remedy for the condition is to reduce the level of his mental and physical arousal so that it remains below the point of no return as he receives sexual stimulation.
The Role of the Nervous System
The central nervous system obviously plays a major role in the ejaculatory reflex, involving both serotonergic and dopaminergic neurons. The exact neurological pathways that control the ejaculatory reflex are the subject of continuing research; what is known for certain is that the serotonergic system is involved in ejaculation, and there are close associations between the level of serotonin in certain male mammals and the speed with which they ejaculate.
Waldinger and his colleagues have been the most active proponents of the brain chemistry explanation for rapid ejaculation, but it does seem clear that in most cases of the etiology of premature ejaculation is the product of a combination of emotional, psychosocial, and physical factors. If you regard the point of ejaculation as the product of a number of factors, it is clear that for any individual, there may be considerable differences in the particular combination of factors that leads them to ejaculate quickly.
The causes of premature ejaculation are a reflection of both man’s genetic disposition to short ejaculatory latency time, interacting with social, relationship, emotional and psychodynamic issues. This is not a particularly helpful explanation of the condition: after all Genes + Behavior = Outcome. In many trials of treatments for PE, it is the intravaginal ejaculatory latency time (IELT) which is used as a kind of diagnostic measure, as well as a measure of the success of any treatment method. However, many clinicians actually ignore the IELT and use their own subjective impression of whether a man is a premature ejaculator or not.
A fact that Perelman emphasizes is that while some men naturally last longer than others, it’s a man’s ability to actually identify the signals that his body gives him in advance of his approach to the point of no return that allows him to exercise some kind of control over premature ejaculation by changing his behaviour. In other words, for a man to voluntarily delay ejaculation, he must choose to respond to the sensations that he receives before he ejaculates in such a way that he delays his orgasm. Many men report that they try and avoid ejaculation by focusing on distracting thoughts, although as you may already know, this rarely works!