What Are The Causes of Premature Ejaculation?The causes of premature ejaculation
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From here - the causes of premature ejaculation Discussion about the causes and origins of premature ejaculation 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, and 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 identified premature ejaculation with what could be called "learned behavior", so that an initial rapid ejaculation when the man first has sex, is credited with the establishment of a rapid ejaculation response as a man's habitual sexual pattern, and this is swiftly followed by the development of performance anxiety. The most recent phase in the explanation of the origins
of PE started with studies which revealed how premature ejaculation
could be treated with clomipramine and
various other selective serotonin reuptake inhibitors (SSRIs), published
in the 1990s. This has been taken to mean that there's a neurological basis for
premature ejaculation
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. Of course, premature ejaculation may have a psychological cause, which 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. Support for a physiological etiology behind premature ejaculation largely comes from the surprising, not to say unlikely, theory that premature ejaculation has a genetic component. Schapiro reported a genetic link in cases of premature ejaculation 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. 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 premature ejaculation may be either cause or effect. Admittedly, a genetic predisposition might underpin other theories about the etiology of premature ejaculation: 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 premature ejaculation. 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 premature ejaculation. Another theory has been proposed that premature ejaculation is the result of 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. Colpi et al. found that men who show a tendency to premature ejaculation seem to have a hyperexcitable bulbocavernosus reflex, while Godpodinoff et al. demonstrated that men with primary (non-acquired) premature ejaculation had a shorter bulbocavernosus reflex latency time when compared with men who had secondary (acquired) premature ejaculation and men who had "normal" ejaculation times (whatever "normal" means in this context). However, perhaps not surprisingly, there is evidence that men with acquired premature ejaculation have a longer BCR latency than men with normal ejaculatory latency, all of which probably means that a hyperexcitable bulbocavernosus reflex has a (not very surprising) role in the etiology of premature ejaculation. 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 with PE are indeed difficult to treat and do not in fact 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 premature ejaculation 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 premature ejaculation among men is difficult. This is not helped by the absence of a clear definition of "normal" and a clear definition of "premature". Neither is there a widely accepted definition of premature ejaculation, and confirmed measures of I E L T and partners' sexual satisfaction are lacking. 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 of premature ejaculation 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 strategies for prevention of 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. |
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