How To Overcome Delayed Ejaculation

How Come You Can’t Ejaculate?

The Physical Causes Of Delayed Ejaculation

One of the problems with research in this field is that there are few well conducted studies on long term delayed ejaculation causes.

That is surprising considering that there are so many men with the condition – estimates range from around 6% to over 10% of men.

Long term delayed ejaculation is not a consciously determined condition – in fact it is completely involuntary, and produces many emotional and practical difficulties for both the man and his partner. You can read more about the treatment of delayed ejaculation in this book.

One of the most challenging consequences is the failure to conceive because of the lack of male climax, but frustration and low self-esteem are also very important.

Delayed ejaculation is also extremely challenging for a man’s partner, as she may consider herself to be unattractive, undesirable, and possibly even a sexual failure.

She may believe that another woman would be better at satisfying her man sexually, and even if she engages in intercourse with her partner, she may be very upset about the extended period of thrusting that may be necessary for him to achieve ejaculation (if he is able to reach orgasm at all).

Ejaculation and orgasm are two separate events in the male body: the first is an event that occurs in the genitals, mediated by nervous pathways through the spinal column.

Orgasm is a much more widespread event, with sensations of pleasure originating in the brain, and possibly spreading throughout the body. The  so-called “numb come”, more scientifically termed “anesthetic ejaculation”, is an illustration of how the two events may occur independently.

The idea of anesthetic ejaculation is rather strange; if you’ve never experienced it, you may find it hard to believe that one can ejaculate without any sensation of orgasm, but it’s not uncommon. It’s usually due to a lack of physical arousal, while the reflex of emission and release of seminal fluid continues normally.

This lack of understanding is reflected in the Diagnostic and Statistcal Manual DSM IV, which categorizes reatrded or delayed ejaculation as “male orgasmic disorder”. Having said that, DSM-IV does offer a reasonable definition of delayed ejaculation:

A persistent or recurrent delay in, or absence of, orgasm in a man who has experienced sexual excitement and arousal during sexual activity at a level which would normally produce an orgasm in a man of that age and circumstances.

Unfortunately the DSM-IV definition also includes the statement that the clinician is the judge of what would be “enough” sexual activity to normally produce an orgasm!

Taking this rather dubious proposition out of the definition allows us to define it in a different way: retarded ejaculation is a condition where a man finds it difficult or impossible to ejaculate despite receiving adequate sexual stimulation, becoming erect, and desiring to achieve orgasm and ejaculation. It is a condition that can occur in sexual intercourse, masturbation or oral sex.

There have been many terms used to refer to this particular problem: for example, lifelong or primary delayed ejaculation, and acquired or secondary delayed ejaculation.

These terms are probably self-explanatory.

The Scientific Bit 

What follows is my interpretation of a paper published electronically by Marcel D. Waldinger, Department of Psychiatry and Neurosexology, Leyenburg Haga Hospital, Leyweg and Dave H. Schweitzer, Department of Internal Medicine and Endocrinology, Reinier de Graaf Groep Hospital, Delft-Voorburg, The Netherlands.

Neurobiology and Neuropharmacology

In recent years, it has become clear that orgasm and ejaculation are mediated by different nerve pathways and involve different neurotransmitters. Clearly, the research into neurotransmitters raises the possibility of pharmacological intervention as an approach to curing retarded ejaculation.

Scientific research has investigated the neural pathways and cellular biochemistry of male sexual responses. We now know that orgasm and ejaculation are the product of the activity of different nerve circuits and different neurotransmitters.

Obviously, the possibility of pharmacological intervention to cure delayed ejaculation arises from ongoing research into neurotransmitters: however, rather more is known about the neurobiology of ejaculation than is known about the neurobiology of orgasm.

Neurobiological approach to lifelong problems

Certainly there must be a developmental aspect to delayed ejaculation because rats reared in isolation do not know how to copulate and achieve orgasm through mating when they reach adulthood.

If subsequently exposed to other rats, some of these rats will learn how to achieve orgasm and ejaculate; others will not.

Animal studies of delayed ejaculation

Research by Marcel Waldinger used rats in which hyposexual behavior was created by raising the rats with different levels of sexual experience. Of 278 sexually naive rats, 23 showed no sexual activity, 211 displayed sexual activity but failed to ejaculate, and 44 were able to copulate and ejaculate.

The rats’ sexual performance improved when they were treated with 5-HT1A receptor agonists. In particular, 8-OH-DPAT and flesinoxan increased sexual behavior almost to the level of the sexually experienced rats.

Sexual performance was also improved after administration of partial 5-HT1A receptor agonists buspirone and ipsapirone. Furthermore, 2-adrenoceptor antagonists such as yohimbine and idazoxan also have a degree of efficacy in reducing the ejaculation time of these sexually naive rats

Mos et al. also demonstrated that male rats which received 5-HT1A receptor agonists (flesinoxan, gepirone) were in fact more attractive to sexually receptive females than a control groups of rats. These results contrast with the finding that 2-adrenoceptor antagonist treated male rats showed no increase in sexual attractiveness to estrus females.

Hyposexual behavior can be reversed by the opioid receptor antagonist naloxone. And other research studies have demonstrated that certain pharmacological compounds and various neuropeptides may also increase and improve copulatory behavior in sexually inactive rats.

For example, the 5-HT1A receptor agonist 8-OH-DPAT clearly increased sexual activity in rats that demonstrated hyposexual behavior.  Similarly, the erection promoting drug Viagra (sildenafil) when administered with low doses of the hormone melatonin also demonstrated the capacity to reverse hyposexual behavior in these sexually inactive rats.

All in all, such pharmacological studies indicate with a fair degree of certainty that specific neurobiological mechanisms are responsible for hyposexual behavior. And it is a fact that neurobiological differences have actually been demonstrated in rats that are not sexually active when compared to those which show normal sexual behavior.

A compound implicated in facilitating ejaculation is the neurotransmitter oxytocin. The neurons which produce oxytocin are mostly located in the paraventricular nucleus situated in the hypothalamus; it may be no coincidence that projections from these areas of the hypothalamus reach into the lumbosacral area of the spinal cord.

Arletti and colleagues demonstrated that the expression of oxytocin mRNA is reduced in the paraventricular nucleus of sexually inactive rats; one conclusion which may be drawn from this is that oxytocin is intimately involved in the copulatory behavior of male rats. However, the exact role of oxytocin is as yet uncertain.

As implied above, more brain neuropeptides, the opioids, may well be associated with the neurobiology of copulatory behavior. Thus, for example, mRNA expression of pro-enkephalin and pro-dynorphin, in addition to endogenous opioid octapeptide levels, actually increase in the hypothalami of rats showing sexually inactive behavior. It is not clear yet if hypothalamic endogenous opioid expression lies behind changes in copulatory behavior, though it is worth remarking that this seems to support the idea that brain opioids inhibit sexual behavior.

Clearly, transferring this research to the human male is rather problematic, for all kinds of ethical and practical reasons.

Since the administration of compounds which function as 5-HT1A receptor agonists (8-OH-DPAT or flesinoxan) to male rats showing deficient sexual behavior produces a large increase in ejaculation latency times, it’s not unreasonable to draw the conclusion that lifelong delayed ejaculation is associated with hypofunction (low functioning) of 5-HT1A receptors and/or  hyperfunction (high functioning) of 5-HT2C receptors.

In contrast, treatment with 5-HT2C receptor antagonists in men (more specifically, nefazodone and mirtazapine), did not have any noticeable effect on ejaculation time [32, 33]. The evidence for hyperfunction of the 5-HT2C receptor as a cause for delayed ejaculation is therefore not sustainable. But, in practice, Waldinger suggests that safe 5-HT1A receptor agonists should be researched on the basis that they may form a class of drugs which acts to alleviate this particular ejaculatory disorder in men.