Premature Ejaculation Can Be Treated! 

Find out how right now - treatment for premature ejaculation which actually enables you to make love for longer.

Premature Ejaculation Therapies - A History

Original article can be found here

1 Introduction 

There's an interesting article in the British Journal of Urology International, volume 93, issue two, pages 2 1:59 07, originally published January 2004.
It is entitled Lifelong Premature Ejaculation: From Authority Based To Evidence Based Medicine; it's by M D Waldinger, one of the foremost experts on premature ejaculation today.

He starts by making the observation that, historically, four periods can be distinguished in the approach to and treatment of lifelong premature ejaculation.

Waldinger claims that even though the treatment of choice for PE has been  psychotherapy at several times in the 20th and 21st centuries, there is little or no evidence-based scientific proof to support either behavioral treatment of PE or a psychological approach in general. Waldinger is an advocate of treating premature ejaculation with selective serotonin reuptake inhibitors, and he has made the observation that controlled trials of these compounds (and also of anesthetic ointments), have repeatedly shown a high level of evidence that they are efficient in delaying ejaculation. He draws the conclusion that an evidence-based approach is necessary to replace the authority-based attitude that premature ejaculation can be treated by psychological intervention.

Historically, psychological treatments and underlying theories have relied mostly on the opinions of leading psychotherapists, rather than properly controlled studies. Historically, the first period to which he refers was from 1887 to 1917, when premature ejaculation was viewed as an abnormal phenomenon rather than a psychological disturbance. This may be accounted for by the limited knowledge of the condition and the repressed attitudes to sexuality at the time.

The second period was between 1970 and 1950, when premature ejaculation was initially described as ejaculatio praecox, and treatment consisted of classic psychoanalysis. Even at this time there was an opinion among some doctors that premature ejaculation was the result of physical abnormalities such as a short frenulum or other variations in the form of the penis. It was 1943 before Shapiro argued that premature ejaculation is neither simply psychological nor somatic, but a condition which is truly psychosomatic in origin -- a combination of psychological issues such as anxiety plus some abnormality or deficiency of the ejaculatory system.
He also identified two types of premature ejaculation, Type A and Type B, which later became identified more clearly as the primary or lifelong, and secondary or acquired, respectively, variations of PE.

From 1950 to around 1990, the biological component of PE was ignored by most sexologists, who once again advocated psychotherapeutic intervention. After Masters and Johnson had pioneered a successful treatment for premature ejaculation in the form of the so-called squeeze technique, which was in fact in itself an adaptation of an earlier technique called the stop-start technique published by Dr J Semans in 1956, it was widely assumed that premature ejaculation was the result of men learning to ejaculate quickly because their initial attempts at masturbation or intercourse had to be hurried or lacked privacy.

The final period in the evolution of treatment is from 1990 to the present, at least in Waldinger's opinion, when neurobiology and genetics begin to assume a more prominent role in the investigation of both cause and treatment of rapid ejaculation. Waldinger has developed a neurobiological viewpoint which argues that premature ejaculation is related to disturbances of serotonin metabolism in the brain.

As far as evidence-based medicine is concerned, it's certainly true that psychotherapy is at a disadvantage. For one thing, psychotherapeutic intervention may be associated with an improvement in the time between intromission and ejaculation, but there is no clear evidence that the two are correlated. (Arguably, for a man suffering from premature ejaculation it wouldn't matter whether they were correlated or not provided that he sees an improvement in his sexual capacity, and some extent this does reflect a pragmatic approach on the part of the psychotherapists, many of whom would take the view that any improvement was worth having, even if you could not be sure of how it was achieved. Those who look for rigorous medical and scientific proof of cause and effect may, by contrast, require substantive evidence-based medicine. This may not be entirely appropriate in a condition which is so clearly associated with social and relationship issues.)

But, having said that, it's also true that the concept of unconscious conflicts as being responsible for premature ejaculation is not subject to rigorous scientific analysis. Masters and Johnson reflected this in a definition of premature ejaculation which spoke in terms of subjective satisfaction of the partners. Masters and Johnson claimed a 97% success rate for slowing down a man's ejaculation using the behavioral squeeze technique, but it is fair to say that this high percentage has not been replicated in subsequent studies or clinics -- a rate of around 80% is more usual. Perhaps because premature ejaculation is an area that scientists were (and remain) reluctant to investigate, very little critical analysis of Masters and Johnson's methodology or results has been presented. Without going into these objections in detail, it's certainly true that M & J did not follow the scientific method, but it's important to remember that this does not in itself invalidate their treatment, and subjecting their reports to critical scientific analysis does not diminish the influence they had on the field of premature ejaculation treatment.

By contrast, of course, it's easy to prove that there is a relationship between drug treatment and changes in a man's ejaculatory capacity. Waldinger makes the observation that treatment with SSRI antidepressants is an effective therapy; that may be so, but it has still not been licensed by the FDA, who presumably have some reluctance to authorize the prescribing of compounds - SSRIs - originally developed for depression (and which have an impact on brain chemistry) for social conditions such as premature ejaculation. On the basis of the eight studies which fulfill all the correct and strict criteria of evidence-based medicine, Waldinger suggested that SSRIs should be the standard treatment for lifelong PE.

One of the things that evidence-based medicine requires is an operational definition of premature ejaculation. Because the definition of PE has been so conflicted, Waldinger makes an attempt to clarify it.

The conflicting characteristics of premature ejaculation had prevented general agreement on a working definition of the condition. The DSM IV manual defines PE as "persistent or recurrent ejaculation with minimal sexual stimulation before, upon, or shortly after penetration and before the person wishes it". However, there is little scientific basis for such a definition: you can understand this if you consider how vague the terms persistent, recurrent, and "shortly after" are. Each of these vague terms will need defining more clearly if they are to be incorporated in a working definition of premature ejaculation.

1a Experimentation

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.

3) Drug treatments

a) There may be value in daily treatment with SSRIs or "as-needed" treatment with SSRIs. As has now been well rehearsed in the literature, the SSRI Dapoxetine supposedly has the best characteristics for the treatment of rapid ejaculation: this will be discussed in greater detail on another page of this website.

b) The oldest treatment for rapid ejaculation is the use of an anesthetic ointment which is applied to the penis. Although there are many products available on the market which fulfill the requirements of an effective anesthetic to be applied topically to the penis, there has been very little scientific research about how effective they are. SS cream is a product manufactured (in Korea) from various herbs, and is reputed to have a significant delay effect on ejaculation.

Some men who use the alternative topical application of benzocaine or similar anesthetic report that whilst they lose feeling in the penis, they still ejaculate quite rapidly. Although these reports are pure anecdotal, mostly consisting of Emails to the authors of this site, this would seem to suggest that the problem for at least some men who are premature ejaculators is not excessive sensory input, but overactivity of the somatic motor output circuits of the brain.

Despite all of the above research, it's not correct to suggest that a critical appraisal of the scientific literature devalues or indeed discredits the work of Masters and Johnson. They suggested that premature ejaculation is a learned behavior. Nor is it correct to assume that the squeeze technique is ineffective and should be dismissed, simply because there is no evidence in its favor. Far from it; the effectiveness of this technique depends on the dedication of the man using it, and it neither proves nor disprove the theory that PE is a learned behavior. The first treatment of choice remains, in the opinion of the current authors, psychotherapy and sensate focus, combined in a program which is designed to awaken a man to the sensations in his body so that with greater awareness and skills of ejaculation control he can exert some kind of control over the speed with which he reaches the point of ejaculatory inevitability. It's a complete fallacy to suggest that the only reason why a man would find psychotherapy beneficial is that it would help him to come to terms with his rapid ejaculation.

REFERENCES

1 Eaton H. Clomipramine in the treatment of premature ejaculation. J Int Med Res 1973; 1: 432–4

2 Sackett DL, Rosenberg WMC, Muir Gray JA, Haynes RB, Richardson WS. Evidence based medicine. what it is and what it isn’t. BMJ 1996; 312: 71–2

3 Althof SE, Levine SB, Corty EW, Risen CB, Stern EB. A double-blind crossover trial of clomipramine for rapid ejaculation in 15 couples. J Clin Psychiatry 1995; 56: 402–7

4 Segraves RT, Saran A, Segraves K, Maguire E. Clomipramine vs placebo in the treatment of premature ejaculation: a pilot study. J Sex Marital Ther 1993; 19: 198–200

5 Waldinger MD, Hengeveld MW, Zwinderman AH. Paroxetine treatment of premature ejaculation: a double-blind, randomised, placebo-controlled study. Am J Psychiatry 1994; 151: 1377–9

6 Waldinger MD, Hengeveld MW, Zwinderman AH, Olivier B. Effect of SSRI antidepressants on ejaculation: a double-blind, randomized, placebo-controlled study with fluoxetine, fluvoxamine, paroxetine and sertraline. J Clin Psychopharmacol 1998; 18: 274–81

7 Mendels J, Camera A, Sikes C. Sertraline treatment for premature ejaculation. J Clin Psychopharmacol 1995; 15: 341–6

8 Kara H, Aydin S, Agargun Y, Odabas O, Yilmiz Y. The efficacy of fluoxetine in the treatment of premature ejaculation: a double-blind, placebo controlled study. J Urol 1996; 156: 1631–2

9 MacMahon CG. Treatment of premature ejaculation with sertraline hydrochloride: a single-blind placebo controlled crossover study. J Urol 1998; 159: 1935–8

10 Waldinger MD. The neurobiological approach to premature ejaculation. J Urol 2002; 168: 2359–67

11Gross S. Practical Treatise on Impotence and Sterility. Edinburgh: YJ Pentland 1887

12 Krafft-Ebing RF. Psychopathia Sexualis. 11th edn. Stuttgart: Publishing Hause Enke, 1901

13 Abraham K. Ueber Ejaculatio Praecox. Z Fur Aerztliche Psychoanalyse 1917; 4: 171

14 Schapiro B. Premature ejaculation. a review of 1130 cases. J Urol 1943; 50: 374–9

15 Godpodinoff ML. Premature ejaculation. clinical subgroups and etiology. J Sex Marital Ther 1989; 15: 130–4

16 Masters WH, Johnson VE. Premature ejaculation. MastersWH, JohnsonVE eds, Human Sexual Inadequacy. Boston MA: Little, Brown and Co 1970

17 Semans JH. Premature ejaculation: a new approach. South Med J 1956; 49: 353–7

18 Waldinger MD, Rietschel M, Nothen MM, Hengeveld MW, Olivier B. Familial occurrence of primary premature ejaculation. Psychiatric Genet 1998; 8: 37–40

19 DeAmicis LA, Goldberg DC, LoPiccolo J, Friedman J, Davies L. Clinical follow-up of couples treated for sexual dysfunction. Arch Sex Behav 1985; 14: 467–90

20 Hawton K, Catalan J, Martin P, Fagg J. Long-term outcome of sex therapy. Behav Res Ther 1986; 24: 665–75

21 Trudel G, Proulx S. Treatment of premature ejaculation by bibliotherapy: an experimental study. Sex Marital Ther 1987; 2: 163

22 Mosher DL. Awareness in Gestalt sex therapy. J Sex Marital Ther 1979; 5: 41–56

23 Zeiss RA, Christensen A, Levine AG. Treatment for premature ejaculation through male-only groups. J Sex Marital Ther 1978; 4: 139–43

24 Lowe CJ, Mikulas WL. Use of written material in learning self control of premature ejaculation. Psychol Reports 1975; 37: 295–8

25 Waldinger MD. Towards evidenced-based drug treatment research on premature ejaculation: a critical evaluation of methodology. J Impotence Res 2003; 15: 309–13

26 Waldinger MD, Zwinderman AH, Schweitzer DH, Olivier B. Relevance of methodological design for the interpretation of efficacy of drug treatment of premature ejaculation: a systematic review and meta-analysis. 2004; in press

27 Waldinger MD, Zwinderman AH, Olivier B. Antidepressants and ejaculation: a double-blind, randomized, placebo-controlled, fixed-dose study with paroxetine, sertraline, and nefazodone. J Clin Psychopharmacol 2001; 21: 293–7

28 Waldinger MD, Zwinderman AH, Olivier B. SSRIs and ejaculation: a double-blind, randomised, fixed-dose study with paroxetine and citralopram. J Clin Psychopharmacol 2001; 21: 556–60

29 Waldinger MD, Zwinderman AH, Olivier B. Antidepressants and ejaculation: a double-blind, randomised, fixed-dose study with mirtazapine and paroxetine. J Clin Psychopharmacol 2003; 23: 448–50

30 Novaretti JPT, Pompeo ACL, Arap S. Selective serotonin uptake inhibitor in the treatment of premature ejaculation. Brazilian J Urol 2002; 28: 116–22

31 Atmaca M, Kuloglu M, Tezcan E, Semercioz A. The efficacy of citalopram in the treatment of premature ejaculation: a placebo-controlled study. Int J Impotence Res 2002; 14: 502–5

32 American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders, 4th edn. Washington DC: American Psychiatric Association, 1994

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: 287–93

34 Waldinger MD, Olivier B. Selective serotonin reuptake inhibitors (SSRIs) and sexual side effects: differences in delaying ejaculation. In SacchettiE, SpanoEP eds, Advances in Preclinical and Clinical Psychiatry, Vol. I. Fluvoxamine: established and emerging roles in psychiatric disorders. Milan: Excerpta Medica, 2000: 117–30

35 Waldinger MD, Berendsen HHG, Blok BFM, Olivier B, Holstege G. Premature ejaculation and SSRI-induced delayed ejaculation: the involvement of the serotonergic system. Behav Brain Res 1998; 92: 111–8

36 Waldinger MD, Olivier B. Selective serotonin reuptake inhibitor-induced sexual dysfunction. clinical and research considerations. Int Clin Psychopharmacol 1998; 13 (Suppl. 6): S27–S33

37 Marson L, McKenna KE. The identification of a brainstem site controlling spinal sexual reflexes in male rats. Brain Res 1990; 515: 303–8

38 Yells DP, Prendergast MA, Hendricks SE, Nakamura M. Fluoxetine-induced inhibition of male rat copulatory behavior: modification by lesions of the nucleus paragigantocellularis. Pharmacol Biochem Behav 1994; 49: 121–7

39 MacLean PD. Brain mechanisms of primal sexual functions and related behavior. In SandlerM, GessaGL eds, Sexual Behavior: Pharmacology and Biochemistry. New York: Raven Press, 1975

40 Veening JG, Coolen LM. Neural activation following sexual behavior in the male and female rat brain. Behav Brain Res 1998; 92: 181–93

41 Coolen LM, Peters HJ, Veening JG. Fos immunoreactivity in the rat brain following consumatory elements of sexual behavior. Brain Res 1996; 738: 67–82

42 Coolen LM, Olivier B, Peters HJ, Veening JG. Demonstration of ejaculation- induced neural activity in the male rat brain using 5-HT1A agonist 8-OH-DPAT. Physiol Behav 1997; 62: 881–91

43 Coolen LM, Peters HJ, Veening JG. Anatomical interrelationships of the medial preoptic area and other brain regions activated following male sexual behavior: a combined fos and tract-tracing study. J Comp Neurol 1998; 397: 421–35ces

44 Truitt WA, Coolen LM. Identification of a potential ejaculation generator in the spinal cord. Science 2002; 297: 1566–9

45 Xin ZC, Choi YD, Rha KH, Choi HK. Somatosensory evoked potentials in patients with primary premature ejaculation. J Urol 1997; 158: 451–5

46 Opsomer RJ, Guerit JM, Wese FX, Van Cangh PJ. Pudendal cortical somatosensory evoked potentials. J Urol 1986; 135: 1216–8

47 Colpi GM, Fanciullaci F, Beretta G, Negri L, Zanollo A. Evoked sacral potentials in subjects with true premature ejaculation. Andrologia 1986; 18: 583–6

48 Fanciullaci F, Colpi GM, Beretta G, Zanollo A. Cortical evoked potentials in subjects with true premature ejaculation. Andrologia 1988; 20: 326–30

49 Haensel SM, Rowland DL, Kallan KTHK, Slob AK. Clomipramine and sexual function in men with premature ejaculation and controls. J Urol 1996; 156: 1310–5

50Strassberg DS, De Gouveia Brazao CA, Rowland DL, Tan P, Slob AK. Clomipramine in the treatment of rapid (premature) ejaculation. J Sex Marital Ther 1999; 25: 89–101

51 Kim SW, Paick JS. Short-term analysis of the effects of as needed use of sertraline at 5 pm for the treatment of premature ejaculation. Urology 1999; 54: 544–7

52 McMahon CG, Touma K. Treatment of premature ejaculation with paroxetine hydrochloride as needed: 2 single-blind, placebo-controlled, crossover studies. J Urol 1999; 161: 1826–30

53 Abdel-Hamid IA, El Naggar EA, El Gilany AH. Assessment of as needed use of pharmacotherapy and the pause-squeeze technique in premature ejaculation. Int J Impotence Res 2001; 13: 41–5

54 Chia SJ. Management of premature ejaculation – a comparison of treatment outcome in patients with and without erectile dysfunction. Int J Androl 2002; 25: 301–5
 

Other helpful sources of information on the subject of rapid ejaculation

Premature ejaculation is said to occur when a man reaches orgasm during sexual intercourse before he or his partner wishes to achieve climax.

Round one third of men experience the frustration of premature or rapid ejaculation. Happily it can be successfully treated. Therapist Paula Hall explains how.

Premature ejaculation (PE) means reaching orgasm too quickly, and it's probably the most common sexual problem. In a survey of thousands of British men, around one in ten often or sometimes had this trouble.

People ask what is the most common question received by this column. By a long way, it is: "How do I solve my rapid ejaculation problem?" So we look at ways to cure an issue that plagues many men.

As you may expect, PE is much more common in younger men - there's a marked tendency for IELT to improve with age. Men generally get better ejaculation control as they grow older.

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Anxiety and premature ejaculation

Psychoanalysis and premature ejaculation - understanding premature-like ejaculatory dysfunction