Understanding male ejaculation and preventing premature ejaculation (PE)

The most common sexual problem among men is premature ejaculation. Premature ejaculation was defined (only at 2014) as ejaculation within a minute of penetration (with no intent and with distress consequences) and it occurs routinely in 0.5% of men (1). There was a medical debate whether it is a pathology or just like there are tall and short people, there are those who ejaculate earlier and those who ejaculate later, and they are all healthy and it's not a pathology. In other words, it's natural that not everyone will ejaculate at exactly the same time. Therefore, some expert claimed that there was no pathology here and we deal with healthy men at the extreme end of the normal scale. In the end, due to the significant suffering of those who suffer from it, premature ejaculation was recognized as a medical problem. Whether it is a medical issue or not, many people want to prolong the time of penetration. (By the way, half of men 'cum' within 5:45 minutes (1)). This post is a rare summary of the solutions from a scientific perspective. In this post, I will try to translate for you the scientific understanding into practical steps that you can implement. Below, I will explain the mechanism of ejaculation and how psychology and behavior can change biology in the context of premature ejaculation. Not all men are the same. Therefore, I do not believe in a one-size-fits-all solution. In this post, you will receive the scientific explanation of "how the brain controls ejaculation" so that you can understand the logic behind the steps and apply them in a specific way that suits you or your patients. In my course, I give a two-hour lecture on the neurobiology of sexual function, and here I will do it briefly and only in the context of male ejaculation.

When there is a problem, many people want medication, to take a pill, close the issue, and move on. The medical debate I've mentioned above, has been preventing FDA-approval of a pill for this problem. However, in Europe, due to the significant suffering of those who suffer from premature ejaculation, the approval was given (it is marketed under the tradename Priligy, see latter). I suggest treating the psychological-behavioral aspect in parallel or even as a first step. From my perspective as a brain researcher, the psychological-behavioral aspect is entirely biological. From my perspective, non-pharmacological treatment - even just talking - can change things biologically in the brain.

So shall we begin? First, a brief introduction about our nervous system, which is important for what follows. You can think of the brain and the spinal cord as the management team of the body: the brain is the CEO (Chief Executive Officer) and the spinal cord is the COO (Chief Operating Officer). They communicate with the body through the rest of the nerve cells that compose the peripheral nervous system. The peripheral nervous system is divided into two parts: the somatic part, which is conscious, and the autonomic nervous system, which is unconscious and involuntary. The autonomic nervous system works all the time in the background without us being aware of it. For example, the control over heart rate or changes in blood pressure that we are not aware of. Erection, for example, is caused by the action of the autonomic nervous system, which causes relaxation of blood vessel muscles in the penis, and men cannot cause an erection or relaxation of the penis voluntarily, just as we cannot contract or dilate our pupils voluntarily.

The autonomous system has 2 branches that usually work in opposite ways, meaning that one activates while the other deactivates.

One branch is called the sympathetic system and it works in states of arousal (Fight, Flight, Freeze), and as we will see shortly also in sex (which, just think about it for a moment, is the fourth F...).

The second branch of the autonomous system works in states of relaxation (Rest and Digest) and is called the parasympathetic system.

This is a somewhat simplified description, in a following post (here) I explain this deeper.

Bottom line: we have a conscious somatic system and two unconscious systems: the sympathetic system for arousal states and the parasympathetic system for relaxation.

After this background, we can move on to discuss ejaculation.

Ejaculation has two stages. In the first stage, the sympathetic system is active; in the second stage, the voluntary (somatic) system is dominant, although the sympathetic system is also active. Confusing? I will try to clarify.

As mentioned, in the first stage of ejaculation the sympathetic system is activated. Adrenaline is released from the adrenal gland into the bloodstream and reaches the vas deferens and the various glands that produce seminal fluid. Adrenaline, together with neural signals from the spinal cord, activates the targets of the sympathetic system.

At this first stage of ejaculation, the sympathetic system causes the release of sperm from the epididymis, the secretion of seminal fluids from various glands, and contractions of the vas deferens that propel the sperm upward until it reaches the region where the urethra also passes. This region is surrounded by the prostate. The duct continues as a shared passage for urine and semen, but at the base of this region there is a circular muscle that, at the beginning of ejaculation, is closed and prevents the semen from continuing its movement. This muscle is called the external urethral sphincter. Thus, the semen accumulates in the prostatic urethra until the second stage of ejaculation; as a result, the duct expands to 2-3 times its normal diameter.

The semen cannot flow upward through the urethra into the bladder because another circular muscle - the internal urethral sphincter - closes involuntarily in response to sexual stimulation and prevents this. The closure of this muscle is also mediated by the sympathetic system.

Usually, when the bladder is full, the internal urethral sphincter opens involuntarily under parasympathetic control, and all that remains for us to do is to voluntarily open the second circular muscle, the external urethral sphincter.

Does the external urethral sphincter also open voluntarily during ejaculation? I will address that in a moment.

In the second stage of ejaculation, the external urethral sphincter receives a neural command to relax, thereby removing the blockage of the duct. At the same time, the sympathetic system instructs involuntary muscles in the prostate to contract, adding pressure to the now-open duct. As a result, the pressure is released and the semen is expelled, assisted by contractions of additional voluntary muscles that propel it through the urethra.

In fact, the external urethral sphincter does not simply relax and remain relaxed; rather, it undergoes a series of rhythmic contractions and relaxations, as do the pelvic floor muscles. This is what creates the “pulses” of ejaculation.

Meanwhile, the sympathetic system keeps the internal urethral sphincter closed, ensuring that the semen moves forward rather than flowing backward into the bladder.

As noted, to urinate we voluntarily open the external urethral sphincter, whereas during ejaculation the same muscle first closes and then opens in an involuntary manner. The pelvic floor muscles (more precisely, the bulbospongiosus muscle) also undergo a series of involuntary contractions, although these are normally voluntary muscles. How is it possible that the same muscles are controlled both voluntarily and involuntarily? Neural Control of the Second Stage of Ejaculation

Both voluntary and involuntary control over the same muscle occurs in other systems in the body. For example, breathing can be controlled voluntarily, even though it normally occurs involuntarily. If we hold our breath for a prolonged period, the involuntary system will eventually take over, override the voluntary control, and force us to breathe. Another example is blinking: we can blink voluntarily, but blinking usually occurs involuntarily.

How does this happen—and specifically in ejaculation?

The activity of voluntary muscles (the external urethral sphincter and the pelvic floor muscles) is regulated by motor neurons of the voluntary, or somatic, nervous system. These neurons are called lower motor neurons (LMNs). They reside in the spinal cord and send axons directly to the muscles they control. But what controls the controllers? In other words, what regulates the lower motor neurons?

This is the core of the matter. In general, voluntary lower motor neurons are controlled by higher, voluntary motor neurons located in the brain, called upper motor neurons (UMNs). Since upper motor neurons are located in the brain and lower motor neurons in the spinal cord, the upper motor neurons send long descending processes called axons through the spinal cord to the lower motor neurons, thereby transmitting neural commands to them.

The relay point between these two neurons in the spinal cord also allows additional neurons to intervene and send their own signals to the lower motor neurons.

Spinal Ejaculation Generator (SEG)

In the case of ejaculation, there is a neural center in the spinal cord responsible for synchronizing the entire ejaculatory process. This center is called the Spinal Ejaculation Generator (SEG).

The SEG also sends neural commands to the relay point with the lower motor neurons, and these commands are unconscious and involuntary. In other words, the lower motor neurons are regulated both by voluntary signals from the upper motor neurons and by involuntary signals from the Spinal Ejaculation Generator.

The SEG is not part of the voluntary (somatic) system, nor is it part of the autonomic system, even though its function is involuntary. It can be thought of as a “small brain” within the spinal cord that synchronizes the autonomic and somatic neural activity required for ejaculation.

If the brain is the CEO, the SEG is the COO. The COO can function entirely independently. This is observed in individuals with spinal cord injury: even when the spinal cord is cut and communication between the brain and the SEG is gone, activation of the SEG (for example, through sensory stimulation of the penis—which the person does not consciously feel due to the injury—or through direct electrical stimulation of the SEG) can often still produce ejaculation, as long as the SEG itself is intact.

Ejaculation will occur almost inevitably about two seconds after activation of the SEG crosses a certain threshold of activity. In other words, the “point of no return” refers to the moment when activation of the SEG surpasses a critical threshold, after which the SEG coordinates the activity of all the nerves involved in ejaculation.

This stage occurs between the two phases of ejaculation.

The key question, then, is how the SEG makes its decision. It appears that the SEG integrates a variety of sensory inputs: conscious sensory stimuli (that is, what we experience as pleasurable), unconscious sensory stimuli (for example, the sensation of pressure from seminal fluid trapped in the duct), as well as unconscious commands from the brain that may be inhibitory (via the neurotransmitter serotonin) or facilitatory (via oxytocin, vasopressin, and noradrenaline). In addition, through the upper motor neurons, we can voluntarily intervene and attempt to prevent the opening of the external urethral sphincter despite commands from the SEG to open it.

Exactly how the integration of these multiple inputs within the SEG is performed remains unknown. However, if you thought that the sensation of pressure from the accumulating semen in the duct is the decisive factor that pushes the SEG past its activation threshold, you would be mistaken. It turns out that even when the sensation of pressure from the trapped seminal fluid is prevented, ejaculation can still occur, demonstrating that this is not the determining factor (Coolen LM, Allard J, Truitt WA, McKenna KE. Central regulation of ejaculation, 2004).

In simple terms, the SEG in the spinal cord (the “COO”) receives instructions from the brain and also receives bodily sensations via sensory nerves. The SEG synchronizes ejaculation through nerves of the three systems described earlier: the sympathetic, the parasympathetic, and the somatic (voluntary) systems.

The SEG was first identified in rats in 2002 (2), and in humans only in 2013 (3).

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So far I explained that ejaculation is caused by the involuntary sympathetic system, which also has a voluntary component - the somatic. The spinal cord (the deputy director) manages the operation and receives instructions from the brain, the CEO.

Now, in short about the CEO: the mechanisms within the brain that control male sexual activity. In the past decades, neural networks were found in a part of the brain called the hypothalamus that control male sexual behavior. In a previous post (here), I showed how their discovery made it possible to activate them artificially and to cause male sexual behavior including ejaculation. The substance dopamine activates these neural networks, so that an increase in dopamine raises sexual desire and enhance erection and ejaculation. (This explains the action of plant-based dietary supplements that increase dopamine and speed up erection and ejaculation, and increase sexual desire, such as Mucuna pruriens, Magic Velvet Bean). Activation of the center enhances male sexual activity, and therefore increasing dopamine may be a solution for men who suffer from delayed ejaculation. In contrast, the substance serotonin inhibits this center in the brain and thus slows down the progression of sexual activity. In other words, increasing serotonin will delay ejaculation. At the end, after all brain calculations, the electrical signal from the brain (the CEO) reaches the spinal cord, (the COO), where it is translated into a chemical signal. The chemical signal can either increase the SEG’s readiness to act (the brain issues such facilitative signals through the neurochemicals oxytocin, vasopressin, and noradrenaline) or decrease the SEG’s readiness to act (via serotonin—this is in addition to serotonin’s activity in the brain that inhibits sexual function, as described earlier).

Thus, when a sensory stimulus reaches the SEG, it may encounter the “COO” in a state where even a mild stimulus is sufficient to push it past the activation threshold and initiate ejaculation, or in a state where only a very strong stimulus will produce that effect.

In addition, the “CEO”—that is, the brain—can issue a voluntary command to the motor neurons controlling the external urethral sphincter so that it remains closed, and can also inhibit the contractions of the pelvic floor muscles.

This is the background information you need to understand the following: How can ejaculation be controlled with pharmaceutical and non-pharmaceutical treatments?

So now, let's get down to it. After we understand how it works, let's see what we can do to delay ejaculation. I'll start with pharmacological intervention, and then I'll write about non-pharmacological treatments.

In fact, there is only one drug approved for use for premature ejaculation and only in Europe: Priligy (Dapoxetine). This drug increases the amount of serotonin in the synapses, which delays sexual activity. This is similar to how antidepressants of the SSRIs family work, so people who take SSRIs often experience suppression of sexual drive and delay in ejaculation. However, unlike SSRIs, Priligy is not taken every day. It increases serotonin strongly and quickly, but for a relatively short time.

In summary, Priligy increases the amount of serotonin - both in the brain itself and from the brain to the spinal cord - and thereby it delays premature ejaculation.

Serotonin is produced in the body from a substance abbreviated as 5-HTP, which itself is derived from a substance called tryptophan. The step that is difficult for the body to perform is the conversion from tryptophan to 5-HTP. Once 5-HTP is already present in the cell, it is converted almost immediately into serotonin.

People who take the drug MDMA experience low levels of serotonin in the days afterward (as well as reduced levels of the enzyme that produces 5-HTP). To restore serotonin levels back to normal, some take 5-HTP, which can be purchased at pharmacies. As mentioned, 5-HTP that reaches the brain is converted almost immediately into serotonin.

So instead of taking Priligy (dapoxetine), could one take 5-HTP to prevent premature ejaculation? In rats, this does indeed work - but at a high dose: 25 mg/kg, which would amount to about 2 grams for a man weighing 80 kg (for my Americans readers: 0.07055 ounces for 76 pounds). No clinical trial has been conducted in humans using 5-HTP for this purpose, so I cannot say whether it works or does not work in humans, or at what dose - because humans are not simply large rats. In addition, 5-HTP is broken down quickly; about half of it disappears within roughly two hours. 5-HTP also has side effects, and in short, it seems to me that the preferred approach is to use a medication that has been properly tested and proven effective. Moreover, these are substances that affect the brain, and taking such compounds without consulting a physician is risky. For example, you may be taking another medication that, when combined with high-dose 5-HTP, could cause serious problems.

Another drug, Silodosin, inhibits the activation of the sympathetic system in the pathway from the spinal cord to the reproductive organ. It does so by inhibiting norepinephrine activity in a relatively specific manner in the Epididymis and sperm duct, thereby preventing the semen from exiting. It also prevents the prostate contractions that propel the semen out afterwards.

In many older men, the prostate enlarges and interferes with bladder emptying. As a result, they wake up multiple times during the night to urinate, which negatively affects their quality of life. This medication is used to treat prostate enlargement because it relaxes the prostate.

This drug has shown good efficacy in treating premature ejaculation in humans and extends the time to ejaculation in 3-8 folds depending on the particular research (4). It has few side effects, but has not yet received (as of now?) approval for preventing premature ejaculation. Researchers noted that it is used off-label for delaying premature ejaculation, meaning that it does not have an approved indication for this purpose.

Since unlike Priligy, Silodosin does not act on the brain at all but only on the level of the spinal cord-reproductive organ, the question arises of what happens in the brain when it gives the signal for ejaculation but no semen comes out. Is the brain aware of this or is it considered an ejaculation from its perspective? I believe that from the brain perspective there was ejaculation because once the SEG passes the point of no return it sends a message to the brain. It would make sense that if there was ejaculation, From the brain's perspective, serotonin and prolactin would be released within the brain to suppress sexual drive. I haven't seen an answer to this in the literature. If you have used Silodosin, I would be interested in hearing about your experience so that I can share the information with others.

In general, this field does not receive enough scientific attention, and in my opinion, it is because of shame, guilt, and fear on the part of scientists to deal with it. Another example of this is that my course is unique and does not exist, to the best of my knowledge, anywhere else. In contrast to this scientific neglect, erectile dysfunction drugs are best sellers, which shows that there is definitely a demand from consumers for improving sexual function.

Important note: serotonin and norepinephrine serve many other important functions in the body, and therefore, a drug that changes their levels in the body can have a negative impact on other things in the body. Using them together with other drugs/substances can be very problematic (for example, the combination of ecstasy, MDMA, with serotonin-raising drugs is very dangerous). Therefore, these drugs require a doctor's prescription. There is no shame in consulting with a doctor. What about Viagra? Viagra (and similar medications, all of which contain the active ingredient known as PDE5i), primarily works on the smooth muscle cells in the walls of blood vessels in the penis (and clitoris), causing them to relax and dilate, which leads to an erection. This effect has no connection to ejaculation what so ever. However, beyond its effects on blood vessels in the penis, PDE5i has other effects in the body (side effects) that could explain findings from several studies showing that Viagra prolongs ejaculation time in men with premature ejaculation (3).

For those seeking a deeper understanding, these additional effects occur at the level of smooth muscle cells and even in the brain: At the level of muscle cells, just as Viagra relaxes smooth muscle in the walls of blood vessels, it also relaxes smooth muscle cells in the sperm duct (the vas deferens) which reduces sperm movement, it also relaxes smooth muscle in the seminal vesicles meaning less addition of fluids to semen and lastly it relaxes smooth muscles cells in the prostate which inhibits expulsion of the semen (6). It is intriguing to consider whether these effects on muscle cells might also delay the brain’s experience of orgasm.

Additionally, the active ingredient in the drug, PDE5i, crosses from the blood into the brain and has various effects on the brain 10), potentially even directly influencing nerve cells and by that prolonging the brain command to ejaculate but the mechanism is unclear (7).

Furthermore, for some men, there might be a psychological connection where achieving an erection translates into increased confidence. This confidence can reduce the activity of the sympathetic nervous system, meaning it delays the first stage of ejaculation. That is, if the man feels performance anxiety and lack of confidence, Viagra may help by increasing confidence. As far as I know, a study on the effect of PDE5i on the subset of men with PE due to anxiety has not been done (as appose to studying all men with PE as an homogenic group) a If you are trying this direction, I would be happy to hear feedback from you!

The course

In conclusion of the medical part, there are creams designed to reduce sensation in the penis by locally anesthetizing its sensory nerves. At least some of them are based on the substance Lidocaine, which prevents nerve cell activation. This can help men who have increased sensitivity in their penis skin. A reduced sensation would lead to less activation of the SEG. However, it will not help when the trigger for ejaculation is not over-sensitivity in the penis but psychological factors, as we will see shortly. Now I will refer to non-pharmacological treatments. Since the sympathetic system is responsible for the first stage of ejaculation, before the SEG crosses the point-of-no-return, slowing it down delays reaching the second stage of ejaculation and by that would delay ejaculation. What increases the activity of the sympathetic system?

Fear, stress, anxiety - all of these intensify the sympathetic system and therefore accelerate the arrival of ejaculation. Why might someone feel fear, anxiety, or tension during sex? There could be many reasons, and each man is a unique case. For example: the man feels in a test, he is afraid of commitment, he is afraid of the overwhelming feminine sensuality, he is afraid of losing control over himself or of his partner losing control, etc. Any intense emotion can activate the sympathetic system. Even a pleasant emotion, for example, when we fall in love.

In-depth psychological work allows the man to identify the psychological factors that activate his sympathetic system. Identifying these factors may allow him to remove the sting from them so that in future sexual situations, he will not enter an such emotional excitement that activates the sympathetic system, or he will learn to reduce the emotional response.

A popular theory of emotion states that emotions, such as fear and anxiety, are the brain's interpretation of a situation, and another different interpretation will lead to a different emotion (see a previous post on this model). That is, the first solution is not to reach the emotional state that triggers the sympathetic system. This is not something that can be decided easily but rather requires therapeutic work. We will move on to the second solution based on the following fact: when the sympathetic system is active, breathing becomes shorter. There are findings that also show the opposite: slow and deep breathing weakens the function of the sympathetic system (probably through oxygen receptors in the brain steam). Tantric techniques indeed emphasize the importance of breathing in sexuality. That is, the solution is deep breathing and inhaling a lot of air to reduce the activity of the sympathetic system. This is a way to consciously slow down the approach to ejaculation through behavior (breathing).

The third solution is behavioral-physical, using the pelvic floor muscles. As mentioned, a ring-muscle (the external urethral sphincter) opens in the second stage of ejaculation, causing the semen to burst out with the help of other muscles. It is possible to learn to strengthen the muscle and its voluntary control to delay ejaculation. The idea is to contract and relax the muscle repeatedly, slowly gaining more specific and increased control over it.

The fourth solution is called "Stop and Start," initially proposed in 1956 by the urologist Dr. James Semans and I believe it's still the most popular approach.

The idea is to sense the moment of approaching ejaculation, the “point of no return,” and then stop.

This pause reduces arousal and the activity of the sympathetic nervous system. Once the excitement subsides, stimulation can resume. Over time, an association forms between rising arousal and the act of reducing excitement, making this process increasingly automatic. According to Dr. Semans, the stimulation is provided by the partner, initially with a dry penis, and once successful, transitioning to a lubricated penis.

The sex researchers Masters and Johnson added to this technique by including a "squeeze" on the head of the penis during the pause. The squeeze is maintained until arousal decreases (8). The basis for their addition, however, is unclear to me, it is assumed to send an inhibitory command to the SEG. At the end of this post you will find a detailed behavioral protocol.

The next solution, the 5th on this list, is to use biofeedback to learn to control the unconscious system. But wait, didn't I write earlier that it's impossible to control the autonomous system? so what's happening here? The (amazing) answer is that sometimes, it is possible to voluntary control the involuntary muscles. In biofeedback, the ability to control things that are not normally under conscious control is acquired. People learn with biofeedback to control their heart rate, reduce the activity of the sympathetic system to reduce migraines and urinary incontinence (9). People can even learn to control their brain waves!

In biofeedback, the disabled can, by changing their brain waves, give instructions to a mechanical arm to hand them a cup of coffee! In another application, by consciously controlling the brain waves of disabled people who have lost the ability to speak, they can communicate with the world for the first time by moving the computer cursor. This is actually done by focusing the mind in a certain way (!). Electrodes on the head detect brain waves and different types of waves move the computer mouse differently. Even mice can learn to activate certain cells in their brains and silence other specific nerve cells in order to receive a reward (11)!

All of this is amazing to me and sounds like science fiction, but it is already happening. Not everything is possible with biofeedback, and the biological mechanism of biofeedback is still not clear. However, the treatment for premature ejaculation with biofeedback is much more conventional than controlling brain waves or heart rate. The treatment takes several months and is quite effective (50% effectiveness and prolongation of penetration time from 2 minutes to over 10). In patients under the age of 35, the effectiveness was higher - 65% (11). I believe this is a promising direction that has not been sufficiently investigated.

The current treatment for premature ejaculation using biofeedback aims to activate the voluntary ring-muscle just before ejaculation in men  thereby keeping the urethra closed (ref. ref ). In other words, this is an addition to the start-stop strategy. Initially, men cannot activate the muscle, but over time they learn to contract it at the appropriate moment. In addition, they learn to better recognize and avoid passing the point of no return by increasing awareness of their physical and emotional state (8). Through biofeedback, men also learn to relax their voluntary pelvic floor muscles (specifically the bulbocavernosus and ischiocavernosus muscles) (ref). These muscles normally undergo rhythmic contraction-relaxation cycles to propel semen outward during the second phase of ejaculation.

A less conventional biofeedback treatment for premature ejaculation might provide voluntary access to the neural pathway that controls the autonomic system in order to reduce the activity of the sympathetic system.

For example: when I’m walking down the street and see a snake on the sidewalk a meter in front of me, I immediately tense up and my sympathetic system becomes highly active. A second look shows me that it’s just a black rubber hose, and I gradually relax. This example illustrates how information from the environment reaches the brain, is interpreted, and -according to that interpretation - is translated into a change in sympathetic nervous system activity. In other words, the “CEO” (the brain) manages the autonomic nervous system.

A less conventional treatment for premature ejaculation using biofeedback would aim to gain voluntary access to the brain pathway that regulates the autonomic nervous system, in order to reduce sympathetic activity.

This type of learning is like learning a language. People often find it difficult to describe in words exactly what they are doing mentally in order to change their brain waves or, for example, their heart rate.

In any case, as far as I have seen, such a treatment has not yet been implemented.

If you're still counting, I'm moving on to solution number 7. :) In certain cases, early ejaculation may occur because the man learned to ejaculate quickly. For example, if a man had no privacy during childhood and hurried to 'cum' before being caught. Learning is a possible reason for premature ejaculation based on research in lab animals: when a female is repeatedly placed in a cage with a male for a short time, the male learns to ejaculate quickly, and this habit remains with him afterwards (8). Therefore, the idea is to create a new habit. That is, a new learning process that will compete with the previous learning. So, the man learns that there is time! Again, the experience of "not having time" is an experience of pressure that may increase the activity of the sympathetic nervous system (through adrenalin release from the adrenal). Apparently, the previous learning never disappears, but the new learning competes with it in influencing behavior. This is generally what happens with learning. You can think of it as complementary mind-set to the stop-start approach.

I am now attaching the behavioral protocol developed by Helen Kaplan for treatment, as sent to me by Miriam Brener, a certified sex therapist and one of the pioneers of the sex therapy field in Israel. Miriam studied under Helen Kaplan and even attended a workshop with the rock stars of the field: Masters and Johnson!

Guidelines for home practice for premature ejaculation, regardless of the cause of the phenomenon. The guidelines are suitable for primary premature ejaculation, which has been consistent in all situations. They can be used and adapted for secondary or situational premature ejaculation as well.

General guidelines: Avoid penetration and ejaculation until the penetration stage in the treatment process. It is however important that there is touch, foreplay, and pleasure for the woman during the treatment process. It is essential to practice in private and in a relaxed environment (both during masturbation and partnered practice), focusing on sensations. It is preferable that the male practice masturbation in bed rather than in the shower, as the water may increase stimulation. For the male: Avoid fantasies or pornography during the treatment period, until there is internalization and integration of the skill to control ejaculation timing.

First Exercise: Stop-Start Masturbate while focusing on the sensations in the penis. Pay attention to when you feel you are getting close to the point of no return. Retract your hand for a few seconds, repeat this 3 times, and on the fourth time, ejaculate. If you miss the moment and do not recognize it, treat it as a learning process, and with practice, you will learn to identify when the point of no return is approaching. Practice Stop-Start about 3 times a week until you can identify the point of no return without effort. This usually takes several weeks if the man has not previously identified the point of no return; sometimes it takes less. Optional - continue this exercise with the partner's hand, where you guide her verbally or with signals when to give you stimulation and when to stop.

Second Exercise: Sensation Range Imagine a range of arousal levels from 0 to 10, where at 0 there is no arousal, at 10 it’s ejaculation and orgasm, and at 9 is the point of no return. Masturbate while focusing on the sensations in the penis, adjusting the intensity of touch, speed of touch, and the area of touch on the penis. Initially, guide the arousal to a low level, 0-3, even when there is no erection or the erection is weak, rising and falling deliberately within this stage, e.g., 1.5, 2, 2.5, 2, 3. The increases and decreases in each level of arousal are through different combinations of intensity, speed, and area of stimulation on the penis. Later in practice, rise and fall in arousal levels similarly in the 3-6 range of arousal, e.g., 3.5, 4, 3.5, 4.5, 5, 4.5, 5, 6. In this range, the erection is moderate, and it’s important to pay attention to the various arousal levels in this stage. Continue to the 6-8 range — still not approaching the point of no return, in order to experience and recognize the higher arousal levels, e.g., 6.5, 7, 7.5, 7, 6.5, 7.5, 8.

Next, at level 8 or 8.5, decide when to continue to ejaculation, which is effectively a decision about the timing of ejaculation.

This whole process, practiced about 3 times a week, usually takes several weeks or more. Optional - continue this exercise with the partner’s hand, where you guide her when to change the intensity, speed, and area of touch.

Application to penetration: General guideline: Engage in penetration when you are not highly aroused, around arousal level 7. If it is suitable for both, it is preferable for the partner to be on top at first. Be passive and do not make penetration movements at this stage, focus on the sensations in the penis. Penetrate when you signal that it is suitable, and stay still. Signal to your partner (verbally or with signals) when you feel she can make a slow movement, and another slow movement. In this exercise, it’s important to completely follow his rhythm, make very slow movements, and be attentive to the signals he gives. It’s preferable not to stop or interrupt the penetration. If you ejaculate before you wanted to, try to accept it as part of the learning process and continue practicing next time.

Gradually, as it becomes possible, make faster movements, signal to her if you want her to slow down. When you decide it is suitable, guide her to faster movements until ejaculation. Over time, there will be internalization and integration of the skill, so that it happens more automatically.

The next step in this exercise — with the man on top, a gradual start similar to the previous stage.

It should be noted that this exercise requires special cooperation between the partners, and most couples need couples therapy during the sexual therapy process, while also supporting and strengthening the partner, who temporarily sets aside her own sexual desires during the practice. Therefore, it is important that the man also provides pleasure and invests in his partner separately. Once the issue is resolved, it is important to follow up to check if this skill is maintained. It’s important to prepare the couple for regressions, not to panic, and to use the tools they learned even when there is regression. Over time, fantasies and pornography can be reintroduced gradually.

For religious couples: If they have no issue with masturbation and ejaculation at the vaginal opening or near the vaginal opening, this protocol is suitable for them. If, due to the prohibition of "spilling seed in vain," this protocol is not suitable, they can start with penetration and further adjust it, focusing heavily on cooperative effort between the couple.

For a man without a partner: He can practice the exercises through masturbation and return to therapy once he has a partner, or receive guidance on how to apply the exercises to penetration. He may also consider taking medication to delay erection for a new relationship, then continue sexual therapy and gradually reduce the medication. (It is not recommended to use local anesthetics that reduce pleasure or think about something unexciting).

You won't believe it but this is the end... By the way, it's fascinating (in my opinion) that in lab animals, males who chronically ejaculate quickly do not enjoy sex, but they continue to want it! This is another example that the two systems of wanting and enjoying are separate systems in the brain, and I'll write on it in a separate post.  Here, I have examined the existing treatments from a practical perspective and their scientific basis. I make a great effort to bring the most up-to-date and accurate scientific knowledge and make it accessible in simple language. If I missed something, I would be happy to hear and add/correct it. You can contact me at doctoramosg@gmail.com .

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I delved into the subject because premature ejaculation is the most common sexual problem among young men. In my opinion, this post is a rare summary of the biological perspective and I hope it was interesting and helpful. I would appreciate if you could spread it further.

In my course, I talk about everything sex, both broadly and in-depth. I bring the most up-to-date science in an interesting and accessible way to everyone. It's worth reading more posts on the blog, and of course, signing up for the upcoming course!

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Sources (this is a limited list, this post is based on dozens more)

1. Proposal for a definition of lifelong premature ejaculation based on epidemiologic.al stopwatch data. Waldinger et al. (2005). Journal of Sexual Medicine.

2. Identification of a potential ejaculation generator in the spinal cord, (2002), Science. William A. Truitt, Lique M.Coolen,

3. The spinal control of ejaculation revisited: a systematic review and meta-analysis of anejaculation in spinal cord injured patients. (2013), Human reproduction update, Clément Chéhensse, Stéphane Bahrami, Pierre Denys, Pierre Clément, Jacques Bernabé, François Giuliano.

4. Effectiveness of 'on demand' silodosin in the treatment of premature ejaculation in patients dissatisfied with dapoxetine: a randomized control study. Bhat et al. (2016). Central European Journal of Urology free reading here https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5057054/

5. The role of phosphodiesterase type 5 inhibitors in the management of premature ejaculation: a critical analysis of basic science and clinical data, (2007), Juza Chen, Gal Keren-Paz, Yuval Bar-Yosef, Haim Matzkin, European Urology. Review.

6. Current and emerging treatment options for premature ejaculation, (2022), Murat Gul,

   Kadir Bocu, Ege Can Serefoglu, Nature Reviews Urology

7. PDE5 Exists in Human Neurons and is a Viable Therapeutic Target for Neurologic Disease, (2016), Andrew F Teich, Mikako Sakurai, Mitesh Patel, Cameron Holman, Faisal Saeed, Jole Fiorito, Ottavio Arancio, Journal of Alzheimer's Disease.

8. Biofeedback for treating pre-mature ejaculation - Awareness and timing of pelvic floor muscle contraction, pelvic exercises and rehabilitation of pelvic floor in lifelong premature ejaculation: 5 years experience (2014). Archivio Italiano di Urologia e Andrologiahttps://pubmed.ncbi.nlm.nih.gov/25017593/

9. Efficacy of Biofeedback for Medical Conditions: an Evidence Map, (2019), Journal of General Internal Medicine. Here 

10. Context-Dependent Acquisition of Copulatory Behavior in the Male Rat: Role of Female Availability, Pfaus, (2008), Behavioral Neuroscience Here 

11. Biofeedback in lab-animals:

https://pubmed.ncbi.nlm.nih.gov/24728268/

https://www.nature.com/articles/ncomms6551

12 Closed-loop brain training: the science of neurofeedback, (2016) Nature Reviews      Neuroscience Here 

13. A comprehensive review of EEG-brain–computer interface paradigms, (2019), Journal of Neural Engineering And Brain Computer Interfaces, a Review (2012) Sensors. link:

link