Physical Causes Of Premature Ejaculation

Physical factors in premature ejaculation

This question was investigated by Donald Strassberg and his colleagues at the University of Utah. Since the days of Helen Kaplan's pioneering sex therapy it's been believed that men with premature ejaculation are less aware of how sexually aroused they are than men who do not experience premature ejaculation. However, Donald Strassberg's work suggested that all men are equally able to make an assessment of their level of sexual arousal. This has been confirmed by other researchers as well.

What's interesting about this is that Strassberg's research revealed that men with premature ejaculation and men who do not have premature ejaculation differ very significantly in their estimates of how long it takes them to reach orgasm during both masturbation and intercourse. For example, men who define themselves as having premature ejaculation say that they reached orgasm during masturbation on average in 3.4 minutes, compared with 8.8 minutes for those men who do not define themselves as having premature ejaculation.

This has led to the hypothesis that one of the causes of premature ejaculation is physiological hypersensitivity to sexual stimulation. Bear in mind however that this hypothesis is based on self-reported latency times whose accuracy is uncertain. The purpose of the research reported here was to establish whether or not the hypothesis of hypersensitivity was actually true. In essence, hypersensitivity would mean that men with a tendency to reach orgasm and ejaculate quickly have a lower threshold for genital stimulation of all kinds.

As part of this research Strassberg and his colleagues also investigated the experience of anxiety in sexual functioning of men with rapid ejaculation.

There were only 32 men in this study, of whom 15 defined themselves as premature ejaculators. They all fulfilled the criteria which has often been put forward as characterizing a man as having PE: that they reached the point of ejaculation within two minutes or less on at least 50% of the times that they had sexual intercourse, while experiencing little personal control over the onset of their orgasm and ejaculation. (Men without premature ejaculation estimated their ejaculatory latency time as being three minutes or more on at least 50% of occasions when they had sex.) None of the men had taken part in sex therapy and none of them were taking any drugs which might have affected their ejaculatory capacity.

All the men in the study answered two questionnaires, one under laboratory conditions and one at home. The first questionnaire was designed to establish what each man thought his ejaculatory latency period had been in the laboratory test conditions, and also established his level of anxiety during both the experiment and during intercourse at home. The second questionnaire was designed to establish the men's estimate of their ejaculatory latency when they were masturbating at home.

The study was conducted in a small private office where men were shown explicit sexual  activity on video while their heart rate was ostensibly being monitored during masturbation. In reality the subject was being monitored to establish the time between starting self-stimulation and ejaculation. The men were left alone in complete privacy with facilities for masturbation and instructed to operate a switch on the supposed "heart rate monitor" just before they started masturbating (on) and when they had ejaculated (off). This switched a timer on and off and established the period between start of self stimulation and orgasm/ejaculation.

After each laboratory session the men were requested to repeat the procedure at home next day, and for this purpose they were given another so-called "heart monitor", a device which was in fact simply the same timer as used in the lab. They were also given a questionnaire which contained questions around anxiety and orgasmic latency period.

The orgasmic latency periods of men with premature ejaculation and those men without premature ejaculation were compared in three dimensions: the objective latency measured in the laboratory, the objective latency measured at home, and the report by the men of the latency period in the laboratory conditions which the men estimated as part of the questionnaire.

In all cases the men with premature ejaculation did indeed have shorter ejaculatory latency periods than the other men, in fact between 75% and 100% longer. Answers from the questionnaires were examined so as to explore the men's level of anxiety during their sexual experience, and to establish what role that might have played in causing their premature ejaculation. The men were asked to assess the degree of anxiety they felt during various sexual experiences, including during masturbation in the laboratory and during sexual intercourse in normal conditions.

Strassberg and his colleagues discovered in this experiment that men who had premature ejaculation reached orgasm in about half the time that men without premature ejaculation did whether they were masturbating in the laboratory or at home. Psychological issues like  performance anxiety, anger and the need to be in control are often put forward as explanations for premature ejaculation. But if, as Strassberg assumed, anxiety would be absent when a man masturbated at home, the finding that men with PE still came more quickly suggested another factor was at work. And in addition, the men's responses to the questionnaire suggested that there was no difference in anxiety during sexual intercourse between the men who had PE and those who did not.

From this self-reporting Strassberg concluded that hypersensitivity to sexual stimulation, rather than anxiety, may be partly responsible for rapid ejaculation.

He acknowledges that generalized sexual guilt or conflict about sex could play a role in causing anxiety and hence promoting premature ejaculation, even during masturbation, but he returns to the finding that the responses from the questionnaire indicated that all the men alike reported very low levels of anxiety during self-stimulation in the laboratory. (What he doesn't seem to have considered is that this may be because the men with PE were simply unaware of how anxious they were.)

It's not a rigorous experiment and it goes against a whole body of circumstantial evidence presented in the course of sexual therapy which suggests that men who have premature ejaculation do in fact have an anxious personality type. Nonetheless, Strassberg proposed in his discussion that an alternative model which could explain premature ejaculation would be one in which an individual has somatic or bodily "vulnerability" which interacts with the  experience of stress to produce rapid ejaculation.

In other words, some men who have a particularly strong somatic vulnerability might find very little anxiety causes them to reach their orgasmic threshold. For others who have less somatic vulnerability, greater degrees of anxiety may be necessary before they manifest premature ejaculation.

It's not a new idea, in fact it was first proposed by Shapiro in 1943. Circumstantial evidence to support this view does exist: certain men with premature ejaculation do indeed seem to be much more susceptible to the effects of anxiety - it appears to play a much stronger role in their tendency to ejaculate rapidly than it does in other men. The idea that somatic factors play a role in inducing a quick ejaculation may also be supported by the fact that drug treatment is capable of increasing the orgasmic latency time in some men who come quickly.

Read more about this work here.

Waldinger's Work On The Biology Of Premature Ejaculation

Waldinger and his colleagues conducted an investigation on 110 men who had experienced lifelong premature ejaculation. (The study is reported in reference 33 below.) In this study, both the men and their heterosexual partners used a stop watch during sexual activity for a period of a month to establish the duration of intercourse.

The results were as follows: about one man in 10 ejaculated after 1 to 2 minutes of intercourse, while around 90% of them reached a climax within one minute of the moment of penetration. Indeed, almost 8 out of every 10 of the men were ejaculating within 30 seconds of penetration. Waldinger found that the age of the men and the length of time for which the couple had been in relationship had no correlation with the duration of time that elapsed before ejaculation. It was on this basis that the Waldinger defined lifelong premature ejaculation as a condition where a man was able to delay ejaculation for less than one minute on more than 90% of the occasions on which he had sexual intercourse, regardless of how long the relationship had been established, and regardless of the man's age.

By implication, this definition regards premature ejaculation as a condition that is independent of any sort of stress caused by psychological or stressful relationship issues (although it is by no means certain that the men in the study were not in fact experiencing such difficulties). Nonetheless, what is surprising about this result is that the use of the stop watch reveals that premature ejaculation can indeed be considered as a matter of seconds rather than minutes.

In the light of this, Waldinger has come up with a new theory about the etiology of lifelong PE. His theory is that lifelong rapid ejaculation is not in fact an acquired disorder caused by hurried intercourse or other conditioning processes from adolescence onwards such as rapid masturbation, but is in fact a normal part of the genetic variability of the human male condition. The quality which is variable is the IELT, or intravaginal ejaculatory latency time.

This is the time between penetration and ejaculation. In this model, a man who reaches his climax rapidly, and has consistently done so throughout his sexual career, may be experiencing the consequence of a neurobiological phenomenon, one which may be the cause of psychological or relationship stress. Not every man with rapid ejaculation regards himself as having premature ejaculation: a man's psychological interpretation of his physical performance during sex may or may not lead to him perceiving himself that he has premature ejaculation. It's likely, but unproven, but there is a normal distribution of IELT in the human male population, although studies remain to be conducted on this question.

Waldinger has conducted studies on both animals and humans, and has come to the conclusion that lifelong PE is the product of decreased levels of serotonergic neurotransmitters, 5-hydroxytryptamine2C receptor hyposensitivity, or 5-HT1A receptor hypersensivity. He advises treatment which is designed to stimulate the 5HT2C receptors (or, conversely, inhibit 5-HT1A receptors if these are hypersensitive). The evidence for this thesis comes from stop watch studies where 5HT2C receptor stimulating and five HT2C blocking antidepressants were found, respectively, to prolong the IELT and leave it unchanged respectively.

Waldinger proposed a model to explain these variations in the serotonergic system: he proposed the existence of a threshold IELT. In cases where a man has a low threshold, he can only take a little sexual stimulation before he is so aroused that he ejaculates. Whatever men with a low threshold do in a sexual situation, and regardless of what they think or fantasize about during sexual activity, they ejaculate easily, even if they have not reached a level of full or complete sexual arousal. Waldinger assumes that the low threshold these men experience is associated with low 5-HT  neurotransmission and most likely also reduced functioning of the 5-HT2C receptor (or, as we mentioned above, over activity of the 5-HT1A receptor.

When a man's threshold is higher, he will have more control over his ejaculation and will be able to take more sexual stimulation and reach a higher level of arousal before he ejaculates. You'd expect men who fall into this category to have 5-HT levels around normal or average, with normal functioning of their receptors. What this means in practice is that these men have the ability to choose whether to come quickly or to wait and ejaculate after longer period of intercourse.

When the threshold is very high indeed, men may actually have difficulty in ejaculating, possibly not being able to do so, even if they are fully aroused sexually. In this model, 5-HT neurotransmission is increased, while the 5-HT2C receptor activity and sensitivities and/or the 5-HT1A receptor sensitivity is decreased.

SSRI antidepressants are found to activate the 5-HT2C receptor, which therefore means that the threshold level goes up, producing a corresponding delay in the man's ejaculation.

As you may know, there is a general belief that ageing delays ejaculation, but this idea has never been tested scientifically. And certainly among men with lifelong PE, it appears that this assumption is untrue: Waldinger investigated 110 men with lifelong PE, and 76% said that there had never been any change in the speed with which they ejaculated, even when they aged. Interestingly, almost a quarter of these men said that their ejaculation had become even faster as they had aged, and only 1% claimed that the time between penetration and ejaculation had actually increased. While rapid ejaculation is clearly a normal part of normal biological variation among men, it's still a real problem, and the discovery that IELT appears to be fixed throughout such a man's life may add to the distress caused. What makes this worse is that any drug treatment that is offered is only effective for as long as the drugs continue to be taken.

Waldinger concluded that the biological studies which have been conducted on treating PE with pharmaceuticals suggests that ejaculation is regulated by a number of areas within the central nervous system, and that the speed with which a man ejaculates is determined by the level of activity of neurotransmitters such as serotonin and dopamine in rather specific areas of his central nervous system. Unfortunately, most of the knowledge around functional neuroanatomy and ejaculation has been derived from studying a species not particularly closely related to man: the male rat. In these animals, the medial pre-optic area in the hypothalamus and the nucleus paragigantocellularis (nPGi) in the ventral medulla are both implicated in the series of events that leads to the point of ejaculation. Electrical stimulation to the medial preoptic area certainly seems to promote ejaculation. One hypothesis that has emerged from this research is that ejaculation is tonically inhibited by serotonergic pathways between the nucleus paragigantocellularis and the lumbosacral motor nuclei. Specifically, the nucleus paragigantocellularis itself is supposed to be inhibited by stimulation from the medial preoptic area. Disinhibition of the nucleus paragigantocellularis  is the triggering factor for ejaculation. There is a high frequency of serotonergic neurons in the nucleus paragigantocellularis, a fact which, combined with the effect of SSRIs in delaying ejaculation, suggests an action of SSRIs on the nucleus paragigantocellularis .

Other work conducted on other mammal species has shown that there are several ejaculation-related areas, including the posteromedial part of the nucleus of the stria terminalis, a lateral subarea in the posterodorsal part of the medial amygdala, and various other areas. All of these areas are extensively interconnected, and also connected to the medial preoptic area, which forms an ejaculation circuit of neurones within the larger circuit of those neurones which control male sexual behavior. The function of these circuits is as yet poorly understood, and the value and importance of this knowledge in the search for a cure of premature ejaculation is debatable.

In addition, a study (number 44 on the list of references below) has highlighted the role of the lumbar spinal cord in the ejaculatory function. Certain cells within the lumbar region of the spinal column are activated after ejaculation and provide input directly into the ejaculation sub-circuit in the brain. It seems that these cells naturally contribute to the triggering of the ejaculatory reflex and to the sensations that accompany ejaculation, which we would conventionally describe as orgasm. All of this work, and other studies reported below -- specifically numbers 45 to 48 -- suggest that one of the most important issues in current research around ejaculation is the issue of whether rapid ejaculation is the result of a higher level of excitability in the general part of the somatosensory cortex, or an inability to delay ejaculation -- something which presumably would be associated with the motor output side of the brain rather than sensory input side. Brain imaging studies may produce more evidence about the neural networks that underlie the ejaculatory process in men.

33Waldinger MD, Hengeveld MW, Zwinderman AH, Olivier B. An empirical operationalization study of DSM-IV diagnostic criteria for premature ejaculation. Int J Psychiatry Clin Practice 1998; 2: 28793