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, as always with such issues in brain chemistry, 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.
I do not accept this, but even if I did, I’d see the issue as thrown immediately into confusion because of the need that some experts feel to distinguish between lifelong (primary) and acquired (secondary) premature ejaculation. These two forms of the condition are supposed to have separate causes.
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 www.delayingyourejaculation.com 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 that proves nothing…. 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, there are those who think this might be a spurious theory, instead believing 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 (It’s Not Compulsory!)
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 dysfunction 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.”
And for those who support drug treatments, as we shall see, it is reasoning after the event to identify a particular characteristic of men with PE and then infer that this causes PE.
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. This idea has not been proved by any research whatsoever as far as I am aware.