Dear Dr G,

First of all, Gong Xi Fa Cai and Happy New Year to your family and all readers celebrating.

I have read with interest all the articles you wrote about “love pills”. I agree that the medication is unavoidable when ageing or unhealthy men are affected by erectile dysfunction.

Although you have provided reasonable scientific evidence that the blue pills are safe, I have several concerns.

You may think these concerns are myths, but I need to put you on the spot to debunk them before

“Chinese Valentine’s Day” or Chap Goh Meh.

First of all, is there evidence that taking too many of the pills at an early age can result in dependency?

Secondly, by taking the pills earlier in life, does it mean higher doses will be needed as we age?

Also, can too many blue pills cause renal failure?

Lastly, I often hear about sudden death associated with taking the pills. Has this happened?

Mythical Mike

Despite decades of clinical use and extensive research, phosphodiesterase type-5 inhibitors (PDE5 inhibitors) remain surrounded by persistent myths. These medications influence blood vessels and sexual function, so they often cause anxiety and attract misinformation.

Concerns about dependency, tolerance, kidney damage and sudden death continue to circulate, even though there is scientific evidence that clears the air. One of the most common fears is that people who use PDE5 inhibitors will become dependent on them. This belief likely arises from confusion with medications that affect the brain’s reward system, such as opioids or sedatives.

PDE5 inhibitors, however, do not act on addiction pathways in the brain. They do not produce cravings, withdrawal symptoms, or chemical dependence. Their action is purely physiological, as they enhance blood vessel relaxation.

When the medication is stopped, the body does not experience withdrawal. Instead, in some cases, individuals may develop psychological reliance because they feel more confident or comfortable when the medication works reliably.

This form of reliance is comparable to using glasses for vision correction rather than a sign of drug addiction. The underlying condition remains unchanged, and the medication simply helps manage its symptoms.

Another widespread misconception is that long-term use inevitably leads to tolerance, meaning the body becomes accustomed to the drug and requires increasing doses. This idea is common with substances such as alcohol or certain pain medications, and it is often incorrectly applied to PDE5 inhibitors.

Long-term clinical studies have shown that these medications maintain their effectiveness over many years without the need for progressively higher doses. When patients report that the medication seems less effective over time, the most likely explanation is progression of the underlying health condition rather than tolerance to the drug.

Erectile dysfunction is frequently linked to ageing, diabetes, high blood pressure and cardiovascular disease. As these conditions worsen, symptoms may become more severe, creating the impression that the medication is losing effectiveness. In reality, the disease may be progressing while the drug’s pharmacological action remains stable.

Concerns about kidney damage represent another enduring myth. Many people think that any medication processed by the body must place strain on the kidneys. PDE5 inhibitors are primarily metabolised by the liver and are then eliminated through both urine and stool.

In individuals with healthy kidney function, these medications are not known to cause kidney damage when used as prescribed. For patients with severe kidney disease, physicians may recommend lower doses because the drug can remain in the bloodstream for a longer period. This adjustment reflects careful medical practice rather than evidence of toxicity.

In fact, ongoing research is exploring whether or not PDE5 inhibitors might offer protective benefits in certain cardiovascular and kidney conditions because of their positive effects on blood vessel health and circulation. Perhaps the most alarming myth is the claim that PDE5 inhibitors can cause sudden death.

This fear gained attention shortly after the first medication in this class became widely available, when media reports highlighted isolated cases of heart attacks occurring during sexual activity. The crucial context often overlooked is that sexual activity itself is a form of physical exertion.

Many individuals who use PDE5 inhibitors are older and may already have cardiovascular disease, which increases the risk of heart events regardless of medication use. Large studies have demonstrated that PDE5 inhibitors do not independently cause sudden death when prescribed appropriately.

The primary safety concern involves combining these medications with nitrate drugs used to treat chest pain. This combination can cause a dangerous drop in blood pressure and is strictly avoided. Some research even suggests that they may improve cardiovascular health by enhancing blood vessel function and circulation.

These myths persist partly because the medications were highly publicised when introduced, and because they are associated with sensitive topics such as sexual health and heart disease. Public discussions often lack the nuance of scientific research, allowing fear to spread more easily than accurate information. Over time, repeated misconceptions can become accepted as fact despite the lack of supporting evidence.

In conclusion, the myths that PDE5 inhibitors cause dependency, tolerance, kidney damage, or sudden death are not supported by scientific research. These medications work by enhancing natural vascular processes and have been studied extensively for decades. When used under proper medical supervision and with attention to contraindications, they have an established safety profile.

Understanding the difference between myth and evidence allows patients to make informed decisions based on science rather than fear. American astronomer Carl Sagan once said: “Extraordinary claims require extraordinary evidence.”

When Dr G is put on the spot to debunk love pill myths before “Chinese Valentine’s Day”, his response is: after 28 years of overwhelming evidence, why are there still extraordinary claims?

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Dear Dr. G,

I am a sixty-year-old man who is reaching an age where it is becoming difficult to achieve a satisfactory erection for regular intimacy with my wife.

I accept that Erectile Dysfunction (ED) is a fact of life for an ageing man and is likely related to diabetes, hypertension and high cholesterol.

My wife agreed for me to try blue pills, and frankly, the pills have saved our marriage.

As our sex life is very regular, the frequent consumption of the pills has become cumbersome and quite expensive.

I recently went to the GP and discussed another ageing problem with my prostate.

He noticed that my frequent blue pills could be replaced by daily pills that can treat my prostate too.

The doctor also highlighted that daily pills can reduce the ups and downs of drug concentration, thereby reducing fluctuations in side effects.

I was curious, as he mentioned the daily dose is also good for other medical conditions.

I would like to put Dr G on the spot for some clarifications.

Firstly, can you please tell me how the daily dose of the hard pills works?

What are the pros and cons as compared to on-demand dosing?

Can the medications truly be used for other medical conditions?

Lastly, if I choose to take the pills on a daily basis, will I suddenly have Happy Valentines every night?

Regards

Valentine Vincent

The history of phosphodiesterase type-5 (PDE5) inhibitors began in the late twentieth century, when research initially aimed at treating angina unexpectedly prompted a shift in focus toward sexual medicine and vascular physiology. In 1998, sildenafil became the first PDE5 inhibitor approved for erectile dysfunction, marking a turning point in both medical treatment and public awareness of sexual health. PDE5 inhibitors are widely associated with the treatment of erectile dysfunction, yet their medical significance extends far beyond this original purpose. Over time, their use has evolved from occasional, “as-needed” dosing to daily low-dose therapy designed to provide continuous physiological benefits.

Understanding the mechanism of PDE5 inhibitors helps explain why daily dosing can be effective. These medications inhibit the phosphodiesterase type 5 enzyme, which normally degrades cyclic guanosine monophosphate (cGMP). This molecule plays a crucial role in relaxing smooth muscle and widening blood vessels. By preventing the breakdown of cGMP, PDE5 inhibitors maintain blood vessel relaxation for longer periods, thereby improving circulation and tissue oxygenation. Although this effect is best known for improving erectile function, it also affects blood flow to the prostate, bladder, lungs, and other organs.

Daily dosing has demonstrated notable effectiveness in the treatment of erectile dysfunction, particularly for individuals with persistent symptoms or those who prefer spontaneity in sexual activity. Rather than planning medication use around specific occasions, patients taking daily therapy maintain a consistent level of medication in their system. This approach may improve baseline erectile function and reduce anxiety related to performance. Continuous treatment may also support long-term vascular health in penile tissue by improving oxygenation and reducing episodes of hypoperfusion. Hence, it is known to be effective for “penile rehabilitation” following the trauma of surgical intervention, such as radical prostatectomy for the treatment of prostate cancer.

Beyond sexual health, daily PDE5 inhibitor therapy has shown effectiveness in managing urinary symptoms caused by benign prostatic hyperplasia, a condition involving enlargement of the prostate gland. The medications relax smooth muscle in the bladder and prostate, thereby reducing urinary urgency, improving urine flow, and decreasing nocturnal urination. For patients experiencing both erectile dysfunction and urinary symptoms, daily dosing offers the advantage of treating multiple conditions with a single medication. Another important medical application is pulmonary arterial hypertension, a serious disorder characterised by narrowed blood vessels in the lungs. PDE5 inhibitors improve exercise tolerance and help reduce pulmonary blood pressure, illustrating the broader significance of their effects on the circulatory system.

The advantages of daily therapy include stable drug levels in the bloodstream and reduced fluctuations associated with higher, intermittent doses. Continuous dosing may produce more consistent therapeutic effects and may improve treatment adherence for individuals managing chronic conditions. However, these benefits must be weighed against potential side effects and the need for ongoing medical supervision.

The most common side effects of PDE5 inhibitors are generally mild and are associated with their vasodilatory effects. Headaches, facial flushing, nasal congestion, indigestion, and mild dizziness are among the most frequently reported symptoms. Some individuals experience muscle or back pain, particularly with longer-acting medications. These effects often diminish as the body adjusts to treatment. More serious risks are rare but important to consider. Because these drugs lower blood pressure, they must never be combined with nitrate medications used for heart disease, as this combination can cause a dangerous drop in blood pressure. In rare cases, individuals may experience changes in vision or hearing, and prolonged erections lasting several hours require immediate medical attention. Drug interactions with certain antibiotics, antifungals, and heart medications also require careful management by healthcare professionals.

Research into PDE5 inhibitors continues to expand, with scientists exploring their potential role in cardiovascular disease, circulation disorders such as Raynaud’s phenomenon, and other conditions related to vascular function. These ongoing investigations highlight the possibility that the medications may offer broader health benefits than initially recognised, potentially including the treatment of altitude sickness in both men and women.

In conclusion, daily-dose PDE5 inhibitors represent a significant evolution in pharmacology. What began as an accidental discovery during research on heart disease has evolved into a versatile therapeutic approach for several chronic conditions. Daily therapy offers consistent effectiveness and improved convenience, though it requires awareness of possible side effects and careful medical oversight. As scientific understanding of vascular health continues to develop, PDE5 inhibitors may play an increasingly important role in future medical treatments. American actress Mae West once said, “Sex is emotion in motion.” Men contemplating switching from “Valentine” pills to a daily dose for sexual benefits and beyond often put Dr G on the spot for his opinion. His view is: “Sexual health treatment is also evolution in motion!”

So, take advantage of this evolution and enjoy Happy Daily Valentines!

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Dear Dr G,

I am a 55-year-old man who is not in the best of health.

I was diagnosed with high cholesterol and high blood pressure during the pandemic.

Due to a sedentary lifestyle and family history, my most recent blood tests also revealed that I have diabetes.

Naturally, I was started on a range of medications to control these conditions.

Unfortunately, after starting these medications, I began to experience problems with my erections.

I explained to my doctors how the erectile issues were affecting my relationship with my wife and asked whether my medications could be reduced to improve rigidity.

The doctors assured me that the erectile weakness was caused by the underlying diseases and not necessarily by the medications they prescribed.

They explained that the way forward was to control my diet and exercise, and in the meantime to take medication to enhance erections.

I was somewhat surprised to discover that the blue pills have actually been around for nearly three decades.

I was even more surprised to learn that there are several options to choose from.

The doctors tried to explain how differences in drug mechanisms can result in varying effects and side effects.

I must admit that I do not fully understand all of them.

Can you explain the different types of medications for erectile dysfunction?

How are they taken? How quickly do they work?

And how long do they last?

Lastly, do they all have the same side effects?

Regards,

Choosing Choo

The phosphodiesterase-5 (PDE5) inhibitors sildenafil, vardenafil, udenafil, tadalafil and avanafil are closely related drugs used primarily to treat erectile dysfunction.

Although they share the same mechanism of action by enhancing nitric oxide–mediated increases in cyclic GMP to promote smooth muscle relaxation and penile blood flow, their pharmacokinetic differences strongly influence clinical efficacy, onset and duration of action, and side-effect profiles.

Because their mechanism is identical, variations in absorption rate, half-life, selectivity and metabolism largely determine how each drug performs in real-world treatment.

Sildenafil, the first drug in this class, has a relatively rapid onset of action.

Peak plasma concentration is typically reached in about one hour.

Its half-life of up to five hours produces a therapeutic window of roughly four to six hours.

Clinical trials consistently show that sildenafil improves erectile function in a majority of patients, with response rates commonly around 60–80% in the general population.

Response rates are lower in individuals with diabetes or post-prostatectomy erectile dysfunction.

Because sildenafil also inhibits PDE6 in the retina, visual disturbances such as blue-tinted vision and increased light sensitivity are common side effects.

Systemic vasodilation can also cause headache, flushing, nasal congestion, dizziness and heartburn.

Due to its short half-life, these side effects are usually transient and resolve within several hours.

Vardenafil has pharmacokinetic properties similar to sildenafil but is slightly more potent and more selective for PDE5. Peak levels occur within about one hour, and the half-life is approximately four to five hours, providing a slightly longer duration of action than sildenafil. Efficacy studies show that vardenafil performs particularly well in more challenging patient populations, including men with diabetes and those who did not respond adequately to sildenafil.

Because of its improved selectivity, visual disturbances occur less frequently.

Adverse effects are similar to others in the class and include headache, flushing, rhinitis and dyspepsia.

Tadalafil differs significantly due to its long half-life of approximately 17.5 hours. This allows efficacy for up to 36 hours after a single dose. The extended duration supports both on-demand dosing and daily low-dose therapy. Clinical trials show high efficacy comparable to other PDE5 inhibitors. The prolonged effect improves spontaneity and satisfaction, as sexual activity does not need to be precisely timed.

However, tadalafil’s pharmacokinetics also explain its distinctive side effects. Because it inhibits PDE11 in skeletal muscle, muscle aches and lower back pain occur more frequently than with other drugs.

Headache, flushing and nasal congestion may also occur and can last longer due to the extended half-life.

Udenafil occupies an intermediate position between shorter-acting agents and tadalafil. It has a half-life of about 11 to 13 hours, with peak levels reached in one to two hours. Clinical studies indicate that udenafil has efficacy comparable to sildenafil and tadalafil. It is often preferred by patients who want longer action without effects lasting more than a day.

The side-effect profile is similar to the class overall, with headache and flushing being most common.

Visual disturbances are relatively uncommon due to improved selectivity. The intermediate half-life means that side effects usually resolve within half a day.

Avanafil represents the newest generation of PDE5 inhibitors. It is characterised by rapid absorption and high selectivity for PDE5. Peak plasma levels occur within 30 to 45 minutes. Some patients experience effects as early as 15 minutes.

Its half-life of about five hours produces a duration similar to sildenafil and vardenafil.

High selectivity reduces off-target effects.

Clinical trials show efficacy comparable to earlier drugs, with faster onset and improved tolerability.

Visual disturbances and muscle pain are less common. Headache and flushing remain the most frequently reported side effects.

Because of its rapid onset and favourable side-effect profile, avanafil is often considered a convenient option for on-demand use.

The pharmacokinetic differences among PDE5 inhibitors strongly influence their clinical performance.

Shorter half-life drugs such as sildenafil and vardenafil provide reliable short-term efficacy with transient side effects.

Tadalafil offers prolonged efficacy along with longer-lasting adverse effects. Udenafil provides an intermediate duration of action. Avanafil prioritises rapid onset and improved selectivity.

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Dear Dr G,

I am a sixty-year-old man who is reaching an age where it is harder to “stand up and be counted for”, especially when I have had a bit too much to drink.

I understand that Erectile Dysfunction (ED) is also likely to be related to my diabetes, hypertension and high cholesterol.

As issues around erectile dysfunction become less taboo, I am tempted to welcome the “blue pills” to the rescue.

My wife knows I am a careful chap and will not take any medication without considering the risks.

Therefore, she really wants to weigh out the pros and cons before treatment.

Because of the embarrassment of seeing a doctor about my condition and worries about cost, I would like to put Dr G on the spot for some clarification.

Firstly, can you please tell me what the track record of the “blue pills” is?

How exactly do these pills work?

How common is the use of the pills globally, and how effective are they?

I also hear horror stories about side effects such as heartburn and headaches. Will these lead to heart attack, stroke or sudden death?

Are there any individuals who are unsuitable to take the medications?

Lastly, do you think I should surrender to a sexless life with Erectile Dysfunction, or embrace these Hard Pills to swallow?

These are difficult decisions to make.

Regards

Hard Henry

The discovery of “blue pills” is one of the most famous examples of accidental success in modern pharmaceutical history. The drug’s active compound, sildenafil citrate, was developed in the early 1990s by researchers at Pfizer in the United Kingdom. At the time, the company was investigating new treatments for hypertension. Sildenafil is a phosphodiesterase type 5 (PDE5) inhibitor initially intended as a cardiovascular medication.

However, during these trials, researchers observed improved erectile function, which prompted Pfizer to redirect development toward the treatment of erectile dysfunction. Sildenafil was approved for erectile dysfunction in 1998, becoming the first widely available oral medication for this condition and transforming both clinical practice and public discussion of sexual health.

Erectile dysfunction is common, particularly with increasing age and in people with conditions such as diabetes, hypertension, and cardiovascular disease. As awareness increased and stigma gradually decreased, use of sildenafil expanded rapidly. Sildenafil has become widely used worldwide. Over time, tens of millions of men globally have used the medication, and its availability increased further once patent protection expired and lower-cost generic versions entered the market. Usage varies significantly by region, influenced by cultural attitudes and healthcare access.

Sildenafil has been shown in numerous randomised controlled trials to be effective for many causes of erectile dysfunction. By inhibiting PDE5, the drug enhances the effects of nitric oxide in penile tissue, leading to relaxation of smooth muscle and increased blood flow during sexual stimulation. Clinical studies consistently demonstrate that sildenafil improves the ability to achieve and maintain erections up to 80%. The medication does not cause spontaneous erections or increase sexual desire; sexual stimulation is still required for it to be effective.

Common adverse effects include headache, facial flushing, nasal congestion, and indigestion, all of which result from vasodilation in different parts of the body. Some users experience visual disturbances, such as increased light sensitivity or a bluish tinge to vision, because sildenafil has a mild effect on the enzyme PDE6, which is involved in retinal photoreceptor signalling. These visual symptoms are usually temporary and reversible. Less commonly, sildenafil can cause dizziness, low blood pressure, or muscle aches. Reports of heart attacks and sudden cardiac death occurring after sildenafil use prompted regulatory warnings and further investigation. Extensive clinical trials and pooled safety analyses, however, have not shown an

increased rate of myocardial infarction or cardiovascular death in patients taking sildenafil.

Contraindications to sildenafil are therefore essential to its safe use. The most important absolute contraindication is concurrent use of nitrates or nitric oxide donors, commonly prescribed for angina, because the combination can cause a severe and potentially life-threatening drop in blood pressure. Sildenafil is also contraindicated in patients taking certain medications that strongly interact with its metabolic pathway, as well as in those with the rare eye condition Retinitis Pigmentosa. Caution or avoidance is recommended in individuals with a recent heart attack or stroke, unstable angina, severe heart failure, very low blood pressure, or conditions in which sexual activity itself is medically inadvisable.

The “blue pills” journey from an unsuccessful heart drug to a revolutionary treatment for erectile dysfunction highlights the role of observation and adaptability in medical discovery. Its widespread global use reflects both its effectiveness and the prevalence of erectile dysfunction. When used appropriately, sildenafil is highly efficacious and generally safe, with side effects that are usually mild and predictable based on its mechanism of action. Serious risks, including cardiovascular events, are uncommon and largely related to improper use or underlying disease rather than the medication itself. Careful attention to contraindications and patient selection remains crucial to ensuring its benefits outweigh its risks. Famous American novelist G. Michael Hopf once said, “Hard times create strong men, strong men create good times.” Men coming to terms with the weakening erection and contemplating swallowing the hard pills often put Dr G on the spot for some advice. His view is: “After careful assessment by the doctors, hard pills create strong men, strong men definitely will enjoy good times!”

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Dear Dr G,

I read with interest your articles in the last few weeks on premature ejaculation.

Truthfully, I do not experience any issues of early ejaculation, however my sex life has taken a curious turn lately with some ejaculatory disorder.

I was recently diagnosed with hypertension and diabetes, and was started on blood pressure and diabetic medications.

Since the diagnosis and treatment of my conditions, I have noticed the amount I ejaculate is diminishing significantly over the last few months. 

Don’t get me wrong, the erection, libido and even the climax is satisfactory, however I don’t seem to be able to produce any semen.

My wife commented on the reduction in semen and thought I don’t get so aroused anymore during sex. In fact, I was accused of faking my orgasm.

Although I already have two wonderful children, and having ejaculation is definitely not for having more children.

However, I am just curious why I am no longer producing any semen?

I went to the doctor and was diagnosed with retrograde or dry ejaculation.

Therefore, I would like to put Dr G on the spot for the mystery of my missing sperms.

First of all, can you tell me how much an average man ejaculates?

Is it normal to have less sperm as men age? 

How common is retrograde ejaculation and how is the diagnosis made?

Once diagnosed, what treatment is available for my condition.

Regards,

Faking Frederick

The World Health Organisation (WHO) outlines the average volume of ejaculate for men at 3.7ml, roughly equivalent to three-quarter of a teaspoon. The normal ejaculation volume in a man after a few days of abstinence actually ranges from 2-6 ml. However, this varies greatly with mood, state of arousal, physical health and the interval of prior ejaculation. The low volume of ejaculation in a man is called hypospermia. This is generally defined as a total ejaculation volume of less than 1.5ml. 

It is common to assume that ejaculation volume declines with age as do the rest of the sexual parameters, including libido and erectile rigidity. The age related decline starts in any decade of the men’s life and gradually over a five to 10 years interval. On the other hand, the sudden decline in the emission semen volume is more likely to be associated with certain medical conditions.

The complete absence of the emission of semen can be caused by retrograde ejaculation or “dry orgasm”. This occurs when the semen that is supposed to be propelling forward is directed backwards to the urinary bladder. The normal reproductive physiology requires the bladder sphincter to contract prior to ejaculation, prohibiting the mixture of urine and semen. The semen is then forced to exit the urethra through the penile opening. When the bladder sphincter does not function properly, retrograde ejaculation can occur.

The malfunction of bladder sphincter is generally caused by the derangement of the nerve supply to the bladder neck. The most common cause of pelvic nerve destruction is diabetes, causing retrograde ejaculation.

Other neurological causes of retrograde ejaculation can be multiple sclerosis and spinal cord injuries, resulting in the backflow of semen in addition to erectile dysfunction. Other non-neurological factors causing derangement of sphincter include prostate operations such as TURP, which destroy the bladder neck to overcome obstructions.

The other common aetiology of low ejaculate is the side effects of certain medications. The use of prostate and blood pressure medications, such as alpha-blockers are well recognised to relax the bladder neck resulting in retrograde ejaculation. Other groups of medications such as antidepressants and antipsychotics are also known to cause dry orgasm. The incidence of drug induced retrograde ejaculation is a common manifestation of men with low semen volume, which is completely reversible. 

The diagnosis of retrograde ejaculation requires a simple urinalysis obtained shortly after sexual climax. In the cases of retrograde ejaculation, the urine will contain copious amounts of sperms, which can be identified by microscopic examinations. In fact, for men facing the challenges of male-factor infertility related to ejaculatory dysfunction, the retrieval of the live sperms from the urine can often be used for IVF fertilisation.

The treatment of retrograde ejaculation usually depends on the cause. The cessation of medications such as antidepressants and alpha-blockers are usually effective in reversing the bladder neck dysfunctions. Other neurological and surgical causes of retrograde ejaculation may also be treated with medications such as tricyclic antidepressants and antihistamines like chlorphenamine. However, the success rates of such intervention are not so favourable.

Apart from the issues of infertility, the diminished or absence of ejaculation in men pose no threat to health whatsoever. Although retrograde ejaculation may just be a bit of a nuisance for some men, others may have significant frustration when facing such sexual dysfunction. Understanding the pathophysiology of retrograde ejaculation is crucial to avoid certain medications and nerve destructions that interfere with the intricate control of the forward propulsion of semen. Apart from disease awareness, open communication with a partner is also important to avoid misunderstanding of “faking an orgasm”. 

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Dear Dr G,

I read with interest your article about the causes of premature ejaculation.

I have often assumed that premature ejaculation in men occurs because of anxiety and, as it is usually perceived as psychological, that there is no real medicine for a cure.

My wife and I have had an “acceptable” sexual relationship since we were married in our mid-twenties. Although the timing of my ejaculation is not ideal, we have accepted this shortcoming.

Although my wife has never complained about this condition, I cannot help thinking that I have shortchanged her in this relationship.

We have now been married for twelve years, and there is no better way to start the new year than by exploring ways to enhance the timing of our intimacy.

When I read about the causes of premature ejaculation, I could not help but check what medications are available for its treatment.

I also know my wife might be against medications, so I wonder whether any non-medical treatments are also available for premature ejaculation.

I am putting Dr G on the spot for clarification on how to overcome these sexual shortcomings!

First of all, what has been tried to enhance the timing of sex?

What medications are approved and effective in treating premature ejaculation?

Lastly, what are the shortcomings of these treatment modalities?

Yours truly,

Shortchanged Stephen

Premature ejaculation (PE) is one of the most common male sexual dysfunctions and has been reported across cultures and throughout history. Clinically, it is defined as ejaculation that occurs sooner than desired, accompanied by a lack of control and personal or interpersonal distress. PE may be lifelong, present from a man’s first sexual experiences, or acquired, developing later in life, often in association with other medical or psychological factors. Understanding its treatment requires an appreciation of how concepts of causation, therapy, and patient adherence have evolved.

Early and effective treatment of premature ejaculation is essential not only for sexual satisfaction but also for psychological well-being and relationship health. Untreated PE is associated with reduced self-esteem, performance anxiety, avoidance of intimacy, and partner distress. Modern management begins by determining whether PE is lifelong or acquired and by addressing contributing factors such as erectile dysfunction, anxiety disorders, thyroid disease or chronic pelvic symptoms.

Historically, premature ejaculation was mainly viewed through a psychological or moral lens. Before the mid-20th century, medical literature attributed PE to anxiety, excessive sexual desire, relationship conflict, or poor self-control. During the 1960s and 1970s, behavioural therapies such as the “stop–start” and “squeeze” techniques were introduced. These methods aimed to train men to recognise pre-ejaculatory sensations and delay climax through repeated practice. Their success depended heavily on sustained effort and partner cooperation, which limited long-term adherence.

A significant shift in treatment occurred in the late 20th century with the observation that certain antidepressants delayed ejaculation as an unintended side effect. Selective serotonin reuptake inhibitors (SSRIs) were found to significantly prolong intravaginal ejaculatory latency time, leading to their off-label use for PE. Daily SSRIs such as paroxetine, sertraline, fluoxetine, and escitalopram became widely used in clinical practice, although daily SSRI therapy is associated with systemic side effects.

In response to the need for a more targeted therapy, dapoxetine was developed as a short-acting SSRI specifically for PE. Unlike conventional SSRIs, dapoxetine is taken on demand, typically one to three hours before sexual activity, and is approved for the treatment of PE in many countries. Clinical trials have shown that dapoxetine produces modest to significant improvements in ejaculatory control and patient satisfaction. Common side effects include nausea, dizziness, headache and diarrhoea, with rare episodes of fainting related to vasovagal responses.

Topical anaesthetic therapies represent another long-standing and effective treatment strategy. Creams, sprays, or wipes containing agents such as lidocaine or a lidocaine–prilocaine combination reduce penile sensitivity and delay ejaculation. SS cream with similar anaesthetic qualities has also been used. These treatments act locally, avoid systemic side effects, and provide rapid benefit, often from the first use. Their main drawbacks include penile numbness, reduced sexual pleasure, local irritation, and the risk of transferring anaesthetic to a partner, potentially causing vaginal numbness unless precautions are taken.

Other pharmacological options have been explored off-label. Tramadol, an analgesic with serotonergic activity, has demonstrated efficacy in delaying ejaculation when taken on demand. However, its use is limited by side effects such as nausea, dizziness, sedation, constipation, and, importantly, the risk of dependence and drug interactions, particularly with antidepressants. For these reasons, tramadol is generally reserved for carefully selected cases and is not considered a first-line therapy.

Combination therapy has become increasingly common in clinical practice. Using behavioural techniques alongside pharmacological treatment, or combining topical anaesthetics with systemic medication, often yields better outcomes than any single modality alone. However, combination therapy also increases the likelihood of side effects and may further challenge patient adherence.

The treatment of premature ejaculation has evolved from purely psychological approaches to evidence-based behavioural and pharmacological strategies. Officially approved therapies, such as topical anaesthetics and dapoxetine in certain regions, coexist with widely used off-label treatments, including daily SSRIs and selected adjunctive medications. The most successful long-term outcomes are achieved through individualised treatment, realistic expectations, and a balanced approach that combines medical therapy with education and behavioural support. George Bernard Shaw famously said: “The greatest tragedy is not being opposed, but being shortchanged by low expectation!” Shortchanged men often put Dr G on the spot for treatment options. His view is: “The greatest tragedy is continuing to be shortchanged without any expectation of overcoming the shortcoming!”

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Dear Dr G,

I read with interest your article about the diagnosis of Premature Ejaculation.

I am a man in my early fifties and I am rather curious about having such a problem in my old age.

My wife and I had a normal sexual relationship since we were married in our mid-twenties.

Sadly, she passed away a few years ago and I did not engage in any intimate relationships until I recently met a co-worker.

To my surprise, I began to notice I ejaculate a lot faster than how it used to be.

Admittedly my partner is a lot younger than me and I am somewhat out of practice.

However, I still cannot work out how my sexual timing was normal before.

What better way to start the new year than by putting Dr G on the spot for clarification over the timing matters of sex!

First of all, can you tell me what causes Premature Ejaculation?

Is Premature Ejaculation purely a psychological dysfunction?

Can this sexual dysfunction be associated with any illnesses?

And lastly, why was I normal and now so fast in bed?

Yours truly,

Fast Fabien

Premature ejaculation is a complex male sexual disorder whose pathogenesis reflects an interplay between biological vulnerability and acquired modifying factors. Contemporary understanding no longer frames it as a purely psychological condition but rather as a disorder of ejaculatory threshold regulation, in which central neurobiological control, peripheral sensory input, autonomic balance, and contextual psychological influences converge.

Appreciating this multifactorial pathogenesis is essential, because correct identification of the underlying etiology directly determines effective treatment.

At the core of premature ejaculation lies dysregulation of central serotonergic neurotransmission. Serotonin exerts an inhibitory influence on ejaculation through specific receptor subtypes within the brain and spinal cord.

Reduced serotonergic tone, increased sensitivity of excitatory serotonin receptors, or diminished activity of inhibitory receptors lowers the ejaculatory threshold, resulting in rapid ejaculation with minimal stimulation.

This neurobiological vulnerability explains why many men with lifelong premature ejaculation experience symptoms from their first sexual encounters and why pharmacologic agents that enhance serotonergic signaling reliably prolong ejaculatory latency.

Genetic polymorphisms affecting serotonin transporters and receptors further support the concept that, in a substantial proportion of men, premature ejaculation represents a constitutional neurophysiological trait rather than a learned behavior.

Peripheral mechanisms may amplify this central vulnerability. Increased penile sensory input, particularly from the glans penis, can accelerate afferent signaling to spinal ejaculatory centers, triggering ejaculation before higher cortical inhibition can intervene.

Evidence for this mechanism includes heightened penile sensitivity on sensory testing and partial therapeutic responses to topical anesthetics. In some men, hyperexcitability of the spinal ejaculatory reflex itself appears contributory, leading to reflexive ejaculation that is poorly modulated by voluntary control.

Hormonal and systemic factors play a particularly important role in acquired premature ejaculation. Hyperthyroidism, for example, increases adrenergic tone and sensitises the ejaculatory reflex, and normalisation of thyroid function often restores normal ejaculatory latency.

Urogenital inflammatory conditions such as chronic prostatitis or urethritis can also shorten ejaculation time through local irritation and heightened reflex sensitivity. Erectile dysfunction frequently coexists with premature ejaculation, not as a primary cause but as a reinforcing factor, where fear of losing erection promotes hurried sexual activity and rapid climax.

Psychological factors, while historically overemphasised, are best understood as modulators rather than primary drivers in most cases. Performance anxiety, relationship conflict, early conditioning to rapid ejaculation, and hypervigilant monitoring of sexual performance can all increase sympathetic nervous system activity and further lower ejaculatory control.

These factors are particularly prominent in acquired premature ejaculation and may perpetuate symptoms even after an initial biological trigger has resolved.

Etiological clarification requires targeted clinical evaluation. Assessment of thyroid function, screening for prostatitis or other urogenital pathology, and evaluation for erectile dysfunction help identify reversible medical contributors.

Focused questions regarding penile sensitivity, response to condoms or topical agents, and changes in sexual arousal patterns can suggest a significant peripheral sensory component.

Psychological assessment should explore anxiety, depressive symptoms, relational dynamics, and maladaptive sexual beliefs, not as presumptive causes but as factors that may sustain or exacerbate the condition.

Premature ejaculation arises from a lowered ejaculatory threshold driven primarily by central serotonergic dysregulation, with genetic predisposition, peripheral hypersensitivity, spinal reflex hyperexcitability, hormonal influences, and psychological modulation contributing to varying degrees.

Accurate identification of etiology depends on careful differentiation between lifelong and acquired forms, comprehensive sexual and medical history-taking, and selective investigation of biological and psychosocial factors.

This etiological clarity is essential, as it transforms premature ejaculation from a vague complaint into a treatable condition with rational, targeted therapeutic strategies.

Comedian Groucho Marx, one of the famous Marx Brothers, once said: “Early to bed and early to rise makes a man healthy, wealthy but grumpy.”

Men who face late onset of early ejaculation often put Dr G on the spot for some explanation.

His view is: “Despite being healthy and having a wealth of experience, unexplained early climax can still make men very grumpy!”

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Dear Dr. G,

I am in my early twenties and started having sexual relationships about a year ago. I have no previous experience, but my girlfriend believes that I might be suffering from premature ejaculation (PE).

I often wonder why I can control the timing during masturbation, but when it comes to sexual intercourse, I seem to get excited and climax too quickly. Honestly, I’m not sure if I actually have PE, as I don’t know what is considered normal.

As we begin the new year, I want to put Dr G on the spot for clarification regarding the timing matters of sex.

First, can you tell me how long the average man lasts in bed?

If I do suffer from PE, what qualifies as “too fast” for ejaculation?

Additionally, what tests are performed to diagnose this condition?

What is considered an ideal duration for sex?

What timing is deemed too long or too short?

Should we even stress about the timing of sexual intercourse?

Incidentally, Happy New Year!

Yours truly,

Timing Timothy

Premature ejaculation is one of the most frequently discussed male sexual concerns. According to the International Society of Sexual Medicine, premature ejaculation is a male sexual dysfunction characterised by ejaculation that always or nearly always occurs very soon after vaginal penetration, an inability to delay ejaculation on almost all penetrations, and negative personal consequences such as distress, frustration, or avoidance of sexual intimacy. The society further distinguishes between lifelong premature ejaculation, in which ejaculation occurs from the very first sexual experiences and typically within about one minute of penetration, and acquired premature ejaculation, in which there is a reduction in ejaculation time after a period of previously normal function, often to around three minutes or less. These criteria underline the importance of consistency and impact on quality of life, rather than relying solely on an arbitrary time cut-off.

Understanding what constitutes “normal” ejaculation timing is equally important. There is no single normal duration that applies to all men or all sexual encounters. Large population studies measuring intravaginal ejaculatory latency time, which is the time from vaginal penetration to ejaculation, have demonstrated a broad range of expected values. In a well-known multinational study, the median intravaginal ejaculatory latency time was approximately 5.5 minutes, with considerable variation across individuals and countries. Some men naturally ejaculate in two or three minutes and experience no distress, while others may last much longer. Therefore, normality is best understood as a spectrum rather than a fixed target, and premature ejaculation represents a point at which short latency is combined with lack of control and negative consequences.

In research and clinical trials, ejaculation timing is most commonly assessed using intravaginal ejaculatory latency time. This is often measured with a stopwatch, typically started at the moment of vaginal penetration and stopped at ejaculation, sometimes by the sexual partner. Stopwatch measurement is considered the most objective method and has been widely used to establish diagnostic thresholds and treatment outcomes. In routine clinical practice, however, many clinicians rely on patient-estimated latency times rather than strict stopwatch measurements. This is partly because stopwatch timing can feel intrusive or anxiety-provoking. Regardless of the method used, timing is interpreted alongside perceived control and distress rather than in isolation.

One of the most widely used tools is the Premature Ejaculation Diagnostic Tool, a short questionnaire that assesses perceived control over ejaculation, frequency of rapid ejaculation, ejaculation with minimal stimulation, personal distress, and interpersonal difficulty. Scores above established thresholds suggest probable or definite premature ejaculation and can help clinicians identify men who may benefit from further evaluation or treatment. Another commonly used instrument is the Premature Ejaculation Profile, which focuses on control, distress, interpersonal difficulty, and satisfaction with sexual intercourse. These questionnaires do not replace a clinical interview, but they provide standardised ways to quantify symptoms and monitor response to therapy.

Estimates of the worldwide prevalence of premature ejaculation vary widely, largely because different studies use different definitions and methods. Surveys that ask men whether they feel they ejaculate too quickly often report prevalence rates in the range of 20-30%, reflecting the common experience of dissatisfaction with ejaculation timing at some point in life. In contrast, studies that apply stricter diagnostic criteria, incorporating specific latency thresholds, lack of control, and distress, generally report lower prevalence figures, often between 5-15%. When lifelong premature ejaculation is defined narrowly as ejaculation consistently within about one minute from first sexual experience, prevalence estimates are even lower, commonly cited at around 2-4% of men. These differences highlight the importance of distinguishing between subjective concern and clinically defined premature ejaculation.

Normal ejaculation timing varies widely, and a short duration alone does not necessarily indicate a disorder. Clinically significant premature ejaculation is defined by consistently short latency, impaired control, and meaningful distress or interpersonal difficulty, assessed through a combination of sexual history, timing estimates, and validated questionnaires. Worldwide prevalence figures depend heavily on how the condition is defined, ranging from a minority of men when strict criteria are applied to a much larger proportion when subjective dissatisfaction is included. Appreciating these distinctions is essential for accurate diagnosis, appropriate counselling, and effective treatment. When Dr G is put on the spot regarding Premature Ejaculation, his view is: “Timing matters in sex, no matter if you let it be your everything!” On that timely note, have an Amazing 2026!

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Dear Dr G,

I read with interest the recent articles you published on penile enlargement and piercing. I was somewhat surprised that you didn’t mention the insertion of beads or pearls, which are well recognised for enhancing the sexual experience for couples.

I’m a thirty-year-old man who is sexually active, and I have an open relationship with my twenty-eight-year-old girlfriend. We communicate openly about our sexual needs and are willing to explore various possibilities in bed.

My girlfriend recently came across some articles discussing the insertion of beads or pearls in the upper part of the penis, which apparently heightens stimulation of the G-spot. I began researching this practice and found that it is common in Southeast Asia and Japan. I found that the use of pearls is popular because their inert properties may help prevent immune rejection.

I would like to take this opportunity to ask Dr G about his views on the use of pearls for sexual pleasure enhancement.

Firstly, how long has the practice of penile beading been around?

Who typically performs the bead insertions?

What are the risks associated with penile pearl insertions?

Lastly, what scientific evidence exists to support the idea that this practice enhances sexual pleasure?

Yours truly,

Pearly Pete

The insertion of beads or other foreign objects beneath the skin of the penis is often referred to as penile implants, subcutaneous nodules, or pearling. This practice has existed for centuries across cultures and social groups. While sometimes such practice is portrayed as a modern body modification trend, its roots extend into traditional rituals, incarceration subcultures, and contemporary sexual experimentation. Despite its persistence, penile bead insertion remains medically controversial due to the significant risks involved.

Historically, penile bead insertion has been documented in parts of Southeast Asia, Japan, and among seafaring communities. Such cultures have beliefs that are associated with rites of passage, masculinity, or sexual prowess. In modern times, for unknown reasons, the practice of penile bead insertion has also been observed more frequently in prison populations. These improvised materials, such as plastic, metal, or glass, are inserted without sterile technique. Only until more recently, elective insertion procedures under sterile techniques, using silicone beads or medical-grade implants, have emerged in some underground or informal cosmetic and medical settings.

Accurately determining the prevalence of penile bead insertion is challenging, as many men do not disclose the practice to healthcare providers unless complications arise. Studies suggest a higher prevalence among incarcerated men and in some areas of East and Southeast Asia, though isolated cases are reported worldwide. In clinical settings, urologists typically encounter the practice incidentally during examinations or when treating complications such as infection or pain. Under such circumstances, patients have no choice but to disclose their thought process regarding the insertion. In other words, the true prevalence of penile beadings will never be known.

Men who undergo penile bead insertion often report perceived sexual benefits, including increased stimulation for a partner, heightened self-confidence, or a sense of uniqueness or control over their body. The perceived benefits are often associated with the location of the beads having the ability to stimulate the G spot in the vagina. Some also describe psychological benefits rather than consistent physical effects, and reported sexual enhancement varies widely between individuals. Importantly, there is no scientific evidence demonstrating consistent improvement in sexual function or satisfaction attributable to penile beads.

From a medical standpoint, the risks associated with penile bead insertion are significant, particularly when the procedure is performed outside of a sterile medical environment. Immediate risks include bleeding, tissue trauma, nerve injury, and severe pain. Infections are common, ranging from localised abscesses to more severe soft-tissue infections that may require surgical drainage or implant removal. Long-term complications can include scarring, chronic inflammation, erectile discomfort, altered sensation, and migration or extrusion of the bead through the skin. In rare but severe cases, complications may interfere with urination or lead to deformity of the penis. Removal of beads is sometimes necessary and can be surgically challenging, especially when scar tissue has formed or when multiple objects are present. The psychological impact should also be considered, as regret, anxiety, or body image concerns may arise following complications.

Penile bead insertion is a practice rooted in cultural tradition and personal choice, but it carries notable medical risks with no established health or sexual benefit. Awareness, accurate information, and access to medical care are critical in reducing harm and ensuring men can make informed decisions about their bodies. Medical organisations and urologists generally advise against penile bead insertion due to the lack of proven benefit and the substantial risk profile. Men considering any form of genital modification are strongly encouraged to seek professional medical advice and to avoid non-medical or improvised procedures. Education and open discussion with healthcare providers are essential, as early intervention can prevent more serious outcomes.

Men contemplating the precious pearly penis as a form for sexual enhancement often put Dr G on the spot for his opinion. His view is “Risking penis with a pearl can potentially turn precious to grey and ulcerous!” On that note, wishing all readers a precious, pearly Christmas!

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Dear Dr G,

It’s the season to be jolly and we’re all enjoying the festivities. Of course, it is also a time to think about getting special gifts for spouses.

My wife and I are newly married, and I’m blessed that we thoroughly enjoy our sex life. We have open communications about our likes and dislikes in bed.

We’ve recently experimented with adding spice to our sex lives and are getting more adventurous, considering genital piercing. I understand this idea originated in the Victorian Era, named after Prince Albert.

I hope to surprise my wife with a Prince Albert for Christmas. With the piercing intended to enhance our sexual pleasure, I hope to put Dr. G on the spot for some penile piercing enquiries.

Can you tell me why people get their genitals pierced? What is the origin of this practice and how is it performed? Is it purely for accessory purposes or are there sexual benefits?

Are the piercings for men only? What are the possible options for the piercing? Are they uncomfortable? Any risks involved?

The excitement and anxiety are equally piercing in my head. I hope you can help clear my mind.

Regards,

Piercing Peter

The practice of genital piercing is believed to date back as far as 2,000 years, as depicted in the writings of the Kama Sutra.

During the Roman era, genital piercings were also used to prohibit sexual intimacy.

Modern documentation of genital piercing has largely been found among tribal communities in Southeast Asia, especially in our own country.

Dutch explorers were the first to describe traditional genital piercing among various tribes in Borneo.

The Ampallang ring, which is passed horizontally through the glans penis, is common among different tribes throughout Sabah and Sarawak.

Apparently, Dayak women have the right to insist upon the Ampallang and, if the man does not consent, it can be grounds for separation.

Such practices were introduced to Western societies in the 19th century.

Historians believe that, in Victorian times, the primary purpose of genital piercing was to secure the penis in a certain manner, rather than for sexual or cultural reasons.

There were even suggestions that the ring was used to keep the foreskin retracted, ensuring no foul smell in uncircumcised men.

The association of genital piercing with the Prince Consort of Queen Victoria has no historical documentation; some suggest that such rumours were fabricated by Hollywood piercing artists in the 1960s.

In modern times, genital piercing involves passing a device through part of the genitalia as a form of ornament or jewellery.

Technically, genital piercing also includes other sexually related organs, including nipples, the pubis, anus, and perineum.

Such piercings are carried out in both men and women, mainly for beautification and individuality, although some argue that piercings can enhance sexual experience.

A Prince Albert piercing specifically refers to “a ring-style piercing that extends along the underside of the glans penis, from the urethral opening to where the glans meets the shaft”, while the reverse Prince Albert piercing “passes through the urethra and exits through a hole in the top of the glans”.

Piercings in circumcised men are usually performed through the frenulum in the midline.

An off-centre approach is common for uncircumcised men, as the surrounding skin repositions itself.

The initial piercing is generally performed with a small diameter (2.5mm), followed by gradual stretching for jewellery insertion up to 9mm.

Some piercers may opt for immediate stretching to accommodate wider rings during the initial procedure, but this may risk delayed wound healing or even a “cheese-cutter” effect.

Generally, healing time for genital piercings ranges from one to six months, with mild complications such as bleeding, swelling, and local inflammation to be expected.

Jewellery suitable for piercing may include circular barbells, curved barbells, captive beads, or a Prince’s wand.

Of course, the choice of jewellery ranges from stainless steel to implant-grade titanium or solid 18kt gold, depending on personal preference.

Most wearers find genital jewellery comfortable at all times and rarely remove it; this obviously depends on the weight and size of the jewellery, and the manhood to begin with!

There is no robust medical evidence to support claims of enhanced sexual performance in men with genital piercings.

Some anecdotal reports suggest that certain piercings, such as apadravya and ampallang (both passing through the head of the penis vertically or horizontally), may heighten sensation for female partners.

Conversely, many reports also highlight discomfort for female partners when the piercing encounters the cervix.

Genital piercings are predominantly decorative and an expression of non-conformist individuality.

Whether these decorative pieces are purely for aesthetic enhancement or for enriching sexual pleasure is open to debate.

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