Dear Dr G,

I can see that you are discussing various preventable viral infections in May.

I am a bit surprised that the elephant in the room, Covid-19, is not being highlighted, as it should still be fresh in our minds.

I am in my early twenties and, unfortunately, like many other people, my wife and I contracted Covid-19 during the pandemic. My wife was very lucky, as her symptoms were relatively mild, but I unfortunately ended up in the ICU due to severe respiratory distress.

Our biggest worry at the time was that my wife was also pregnant with our first child. We were very concerned about how the virus or the vaccine could adversely affect our baby.

Thankfully, our daughter is now three years old. She has achieved all her normal developmental milestones and is flourishing.

Despite life returning to normal, I cannot help but wonder what impact the virus and the Covid vaccine may have had on my family and me.

I would like to take this opportunity to put Dr G on the spot for his wisdom!

Five years down the line, what data are there on children born during the Covid pandemic?

What are the adverse reproductive consequences of Covid and the vaccine on both men and women?

Lastly, I have also read about men suffering from Covid-induced sexual dysfunction. Should I be worried that this might come back to haunt me?

Regards,

Covid-Christopher

Five years after the Covid-19 pandemic changed the world, its impact on sexual and reproductive health is still being felt. What began as a respiratory illness quickly affected many other areas of life, including fertility, pregnancy, mental health, relationships, and access to healthcare. Both the virus and the vaccines became major topics of concern, especially when questions about infertility and pregnancy safety began spreading online. Many researchers are still analysing the physical and psychological effects associated with both the virus and the vaccine.

Research over the years has shown that Covid-19 infection itself can affect reproductive health in several ways. In men, severe infection has been linked to temporary reductions in sperm quality and hormonal changes caused by fever, inflammation, and overall stress on the body. Women have also reported menstrual irregularities after infection, including delayed or heavier periods. Most of these effects appear to be temporary, but they clearly demonstrate that the virus can influence the reproductive system. Although most men and women recover completely without long-term reproductive impairment, a small proportion of individuals may experience irreversible infertility following more severe Covid-19 infection.

Pregnancy was another major concern during the pandemic. Studies found that pregnant individuals who contracted Covid-19 faced higher risks of severe illness, hospitalisation, and complications such as preterm birth. Hospitals and healthcare systems were also overwhelmed, making access to prenatal care and reproductive services more difficult in many countries. Fertility treatments, contraception services, and sexual health clinics were often delayed or interrupted during lockdowns. Encouringly, data collected during the peak of the pandemic did not show an increase in stillbirths or major birth abnormalities. The vaccines have been shown to be safe for both mother and fetus during pregnancy and after birth.

Covid-19 vaccines soon became surrounded by controversy and misinformation. Many people feared that the vaccines could cause infertility, but years of scientific studies have found no evidence to support these claims. Research involving millions of vaccinated individuals has shown that the vaccines do not reduce fertility in men or women. Some women experienced temporary changes in their menstrual cycles after vaccination, but these effects were generally mild and short-lived. Health experts have consistently concluded that vaccination is far safer than the risks associated with Covid-19 infection, especially for pregnant individuals. There is no evidence that the vaccines reduce sperm quality, and no association has been found between Covid-19 vaccination and sexual dysfunction.

The pandemic also affected sexual health emotionally and socially. Lockdowns, stress, anxiety, loneliness, and financial difficulties placed considerable pressure on relationships and mental well-being. Many people experienced depression, isolation, or reduced intimacy during this period. At the same time, telemedicine became more common, allowing people to access reproductive and sexual healthcare online when in-person visits were difficult. Although mental health issues were highlighted during the pandemic, most individuals who experienced stress and depression have demonstrated resilience and largely returned to their usual level of mental well-being. Post-infection depression and sexual dysfunction are well-documented, but they are also highly treatable with counselling and appropriate medical care.

Five years later, the evidence suggests that Covid-19 infection posed far greater risks to sexual and reproductive health than the vaccines developed to prevent severe illness. The pandemic also revealed the importance of resilient healthcare systems, robust scientific research, and clear public communication. Although scientists continue to study the long-term effects of Covid-19, the pandemic has permanently changed how society views reproductive health, public health, and medical trust. The Lebanese-American poet Khalil Gibran once said, “Out of suffering have emerged the strongest souls.” Five years after the beginning of the Covid-19 pandemic, Dr George is still being challenged by doubtful patients about the aftermath of the virus on their sexual, reproductive, and overall health. His view is: “Despite emerging as stronger souls with minimal lasting harm, our sufferings should serve as a reminder to live more mindfully and pursue a healthier life.”

The post Covid, babies and the bedroom: five years on appeared first on George Lee.my.

Dear Dr G,

I understand that you are outlining various viral infections that can be prevented by vaccination during the month of May.

Personally, as a Hepatitis B carrier, I am somewhat confused about the ABC of viral hepatitis and their impact on my sexual health.

I contracted hepatitis as a child from my mother.

All my life, I have been told to be cautious about my liver function and to take precautions when engaging in sexual activity.

After I got married, I became paranoid about transmitting the virus sexually to my wife.

I often tried to read up more about other forms of hepatitis and the role I play in preventing transmission of the virus to my wife and children.

Apart from vaccination and the use of barrier protection during intercourse, I often worry about other ways I can prevent transmission of my disease.

I wish to put Dr G on the spot to outline the ABC of hepatitis and how they impact sexual health.

What exactly are hepatitis viruses, and how are they transmitted?

Are hepatitis A, B, and C all different, or are they just different strains of the same virus?

How do these viruses affect sexual and reproductive health?

Looking forward to your answers.

Yours truly,

Hepatitis Howard

Viral hepatitis is a major public health problem worldwide and is responsible for significant illness, liver failure, and death. The three most important forms are hepatitis A, hepatitis B, and hepatitis C. These viral infections primarily target the liver, causing inflammation. Although they share similar effects on the liver, they differ in their modes of transmission, disease progression, and long-term complications. Viral hepatitis is also closely linked to sexual and reproductive health because some forms are transmitted through sexual contact, can affect fertility and pregnancy, and may be passed from mother to child.

Hepatitis A is caused by an RNA virus that spreads mainly via the faecal–oral route, often through contaminated food or water or poor sanitation. After entering the body through the digestive tract, the virus travels through the bloodstream to the liver. The pathogenesis of hepatitis A is mainly immune-mediated, meaning that liver damage occurs when the immune system attacks infected liver cells. This inflammatory response leads to symptoms such as fever, fatigue, nausea, abdominal pain, loss of appetite, dark urine, and jaundice. Unlike hepatitis B and C, hepatitis A does not usually become chronic because the immune system can generally clear the infection completely. Although hepatitis A is not commonly considered a sexually transmitted infection, it can spread through sexual practices involving oral–anal contact. Poor hygiene and close physical contact during sexual activity may increase the risk of transmission.

Hepatitis B is caused by a DNA virus that is transmitted through blood and body fluids, including semen and vaginal secretions. It spreads through unprotected sexual intercourse, contaminated needles, blood transfusions, and from mother to child during childbirth. After entering the body, the virus infects liver cells and replicates within them. The virus itself causes little direct damage, but the immune system attacks infected hepatocytes, resulting in inflammation and liver injury. In some individuals, especially infants infected at birth, the immune response fails to eliminate the virus completely, leading to chronic infection. Chronic hepatitis B can progress to fibrosis, cirrhosis, liver failure, and hepatocellular carcinoma.

Hepatitis B has major implications for sexual and reproductive health because it is highly infectious through sexual contact. Individuals with multiple sexual partners or those who do not use protection are at greater risk of acquiring the infection. The virus may also coexist with other sexually transmitted infections, increasing transmission rates. One of the most serious reproductive health concerns is vertical transmission from mother to baby during delivery. Infants infected at birth are much more likely to develop chronic hepatitis B, which can later lead to severe liver disease. Chronic HBV infection may also interfere with reproductive hormones and contribute to infertility and sexual dysfunction.

Hepatitis C is caused by an RNA virus that spreads mainly through blood exposure, particularly through shared needles, unsafe injections, and contaminated blood products. Sexual transmission is less common than with hepatitis B, but it can occur, especially among individuals with multiple sexual partners, HIV coinfection, or traumatic sexual practices. After infecting hepatocytes, the virus mutates rapidly, allowing it to escape immune detection and persist in the body. The continuous immune response against infected cells causes chronic inflammation and progressive liver damage. Over time, this can result in fibrosis, cirrhosis, and liver cancer.

The reproductive and sexual health effects of hepatitis C are also important. Pregnant individuals with HCV can transmit the virus to their infants, especially if they have high viral loads or coinfection with HIV. Chronic liver disease associated with HCV may affect hormone production and lead to menstrual disturbances, infertility, reduced libido, and complications during pregnancy. In the past, some antiviral treatments for hepatitis C were unsafe during pregnancy, although newer therapies are more effective and safer when given before conception.

In conclusion, hepatitis A, B, and C are serious viral infections that affect the liver through immune-mediated inflammation and hepatocyte injury. Hepatitis A usually causes an acute, self-limiting illness, while hepatitis B and C can become chronic and lead to cirrhosis and liver cancer. These infections are strongly connected to sexual and reproductive health because they may spread through sexual contact, affect fertility and pregnancy outcomes, and be transmitted from mother to child. Effective prevention through vaccination, safe sexual practices, antenatal screening, and early treatment remains essential in reducing the burden of viral hepatitis and protecting reproductive health. WHO Director-General Tedros Ghebreyesus once said, “Viruses know no borders.” When Dr G is put on the spot to outline the sexual health implications of hepatitis A, B, and C, his response is always: “Knowledge creates borders for these viruses!”

The post ABC of hepatitis and implications on sexual health appeared first on George Lee.my.

Dear Dr G,

I read with interest your explanation of how German measles affects women and how the disease itself has minimal effect in men.

I am somewhat surprised you did not outline the risks associated with another dangerous virus, mumps, which can have a more detrimental impact on young adult males.

As a child, I contracted mumps after missing vaccination at school.

I was horrified when I learned mumps may sometimes lead to infertility, and this information has caused me concern.

Many people tend to think of mumps as only a childhood illness, but I understand complications can occur when adults are infected.

As I am venturing into adulthood, I worry the aftermath of mumps may cause havoc to both my sexual and reproductive health.

I would like to put you on the spot so you can address how mumps may affect sexual and reproductive health in young men.

What exactly is mumps and how is the infection transmitted?

How common are complications such as inflammation of the testicles, reduced fertility, or other long-term effects?

Are these risks rare, or should young adults be more cautious?

I also hope you can explain whether vaccination still provides good protection in adulthood and what steps people can take to reduce their risk of infection.

I believe this is an important public health topic that many readers, especially young adults and parents, would benefit from understanding better.

Yours sincerely,

Mumps Matthew

For many people, mumps is remembered as a common childhood illness marked by swollen cheeks, fever and a few days away from school. However, beneath this seemingly harmless infection lies a virus that can sometimes lead to serious complications, especially among adolescents and young adults.

Although vaccination has dramatically reduced the number of cases worldwide, mumps remains an important public health concern because outbreaks still occur and complications can affect long-term health and fertility. Mumps is a contagious disease caused by the mumps virus, which belongs to the Paramyxovirus family.

The illness mainly affects the salivary glands, particularly the parotid glands near the ears, producing the characteristic swelling of the face and jaw. The disease has been recognised since ancient times. The Greek physician Hippocrates described symptoms resembling mumps as early as the fifth century BCE.

However, it was not until 1934 that scientists Claude Johnson and Ernest Goodpasture proved mumps was caused by a virus spread through saliva and respiratory droplets. Before the development of vaccines, large epidemics occurred every few years, especially among schoolchildren.

Most people contracted the infection during childhood, and outbreaks spread rapidly in crowded communities. The introduction of the measles-mumps-rubella (MMR) vaccine changed the situation dramatically. In countries with strong immunisation programmes, the incidence of mumps dropped by more than 90%.

Nevertheless, the disease has not disappeared. Thousands of cases continue to be reported globally every year, particularly in places where vaccination rates have declined, or where young adults live in close-contact environments such as universities, dormitories and military camps.

The virus spreads easily through coughing, sneezing, talking, or sharing utensils and drinks. Once it enters the body through the nose or mouth, it multiplies in the respiratory tract before spreading through the bloodstream to other organs. Children infected with mumps often develop fever, headache, tiredness, muscle aches and swelling of the salivary glands.

In many cases, the illness resolves within 1–2 weeks without lasting problems. However, complications become more common and more severe in adolescents and adults. One of the most worrying complications among post-pubertal males is orchitis, which is inflammation of the testicles.

This condition can develop several days after the onset of facial swelling and may cause severe pain, swelling, tenderness and fever. Although most men recover fully, some may experience shrinkage of the affected testicle. In rare cases, particularly when both testicles are involved, fertility may be reduced. Complete infertility is uncommon, but the possibility has caused understandable concern among many young men.

Mumps may also affect other organs, including the pancreas, brain and inner ear, sometimes leading to meningitis, encephalitis or hearing loss. Vaccination has proven to be one of the greatest achievements in modern medicine.

The MMR vaccine provides strong protection against mumps and significantly reduces the risk of serious complications. High vaccination coverage also contributes to herd immunity, protecting vulnerable members of society who cannot be vaccinated.

Unfortunately, misinformation and vaccine hesitancy in some communities have allowed outbreaks to re-emerge in recent years. Public education therefore remains essential in reminding people that diseases once considered “mild childhood illnesses” can still produce serious consequences. Scientists believe mumps can potentially be controlled to very low levels through widespread vaccination, strong public health systems and rapid outbreak response.

Although complete global elimination remains difficult because immunity may decrease over time and vaccination coverage differs between countries, the dramatic decline in cases over recent decades demonstrates prevention works.

The story of mumps reminds us medical progress should never be taken for granted. Infectious diseases that once caused widespread suffering can return if societies become complacent. Continued scientific research, vaccination programmes and public awareness are necessary to protect future generations from preventable illnesses.

American astronomer Carl Sagan once said: “The consequence of today is determined by actions of the past”

Dr G is often put on the spot by infertile men questioning whether the aftermath of mumps results in irreversible damage to fertility.

His view is: “We will definitely prevent the consequence of today, when we are determined in the actions of vaccination tomorrow!”

The post Sexual and reproductive aftermath of mumps appeared first on George Lee.my.

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?

The post Debunking the ‘love pill’ myths appeared first on George Lee.my.

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!

The post Turning Valentine pills into everyday thrills appeared first on George Lee.my.

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.

The post Choosing the right pill for erectile dysfunction appeared first on George Lee.my.

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!”

The post Hard pills, good times appeared first on George Lee.my.

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”. 

The post Understanding hypospermia and dry orgasm in men appeared first on George Lee.my.

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!”

The post How not to get shortchanged in the bedroom appeared first on George Lee.my.

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!”

The post Rooting out the causes of early release appeared first on George Lee.my.