At 40 I felt my life was just starting. I married an incredible and virtuous wife 15 years younger and settled in Perth where I bought a house and had 3 kids. All was good in my life until I started to have trouble getting and maintaining an erection. For the first two years it was intermittent and would be a problem and not be a problem with no rhyme or reason. But then it started to become more frequent. I knew I had Erectile Dysfunction, although I didn’t know the name for it back then.
This was in 1997 before Viagra was introduced to the Australian public. The internet and everyone having a computer was pretty new in Australia at this time and there just wasn’t the resources available like there is today.
At the urging of my wife I visited a urologist who essentially told me there were no options for consistent treatment of Erectile Dysfunction. Penis pumps and vasodilator pills were the only choices which I found to be subpar. I didn’t give a single second of thought to penis pumps. I gave Vasodilators a try. They have a systemic effect so it is not targeted treatment and the results were hit or miss. They helped getting an erection sometimes but it wasn’t a big improvement.
What is Erectile dysfunction?
Erectile Dysfunction is usually caused by a physical problem with the nerves or blood vessels leading to the penis that allow the sacral nerves to trigger an erection from touch or from the brain when thinking stimulating thoughts. Some risk factors for ED are high blood pressure, high cholesterol, diabetes, obesity, and heart disease. Recent studies in the U.S and Europe have found ED as a good predictor of atherosclerotic heart disease and clogged arteries. But I didn’t have any of these conditions. I was healthy, active, had good lab numbers and in 2019 the same is true.
In 1999 I had heard about a drug from a friend at work that was exploding in America
It had just been approved for prescription in Australia. It was called Viagra. A phosphodiesterase 5 inhibitor, it works by blocking an enzyme that breaks down cGMP, which is what causes blood vessels to dilate in the penis and fill with blood to form an erection. Taking a PDE5 blocker makes it easier for an erection to be formed. I knew I had to give it a try. My wife was extremely supportive throughout the time I suffered from Erectile Dysfunction but I felt I owed her a fully functioning sexual life.
At first I was nervous as I’m sure most are when starting not just a new drug for me but a new drug that was just introduced on the market. My biggest concern was after hearing about its efficacy from people at work and my doctor, getting an erection when I was out and about and not with my wife. It’s a thing all boys face when becoming teenagers but we outgrow. To my relief, Viagra only allows for an erection when one is sexually stimulated as one normally is in life. The cGMP is only activated when the brain or sacral nerves controlling an erection are stimulated.
When I was ready on a weekend trip to Sydney
with my wife while my kids were at home with their grandparents, I took my first Viagra, 100mg
. An hour later I felt like I did at 30 with no problems obtaining or maintaining an erection. I had found the answer I had been searching for the preceding few years. I thought to myself what a miracle it is to get Erectile Dysfunction a few years before Viagra came out instead of wallowing in defeat that I’m sure prior generations of men experienced.
I have been a loyal user of Viagra ever since
About 10 years ago I decided to experiment with the dosages to see what worked and didn’t work. I found 50mg had the same effect on me as 100mg and then tried 25mg. 25mg worked fairly well but I had more difficulty maintaining an erection with it. 50mgs is what I ended up with and take it to this day. In recent years Cialis and other drugs have hit the market but I am happy to stick with the original as it has worked tried and true for 20 years.
Viagra is the most common commercial name of a drug used for erectile dysfunction or impotentia erigendi treatment; it was originally synthesized in 1989 by a group of Pfizer chemists who researched substances suitable for the treatment of arterial hypertension and angina pectoris. The drug showed immediately to have little effect on these pathologies but to be very effective in the treatment of erectile dysfunction. The first marketing took place in fact in 1998 exclusively with this clinical indication.
The sildenafil over time has been the subject of disease mongering phenomena, as well as its peers, since it is often used outside the precise and rigid medical criteria of treatment of erectile dysfunction, but rather for recreational use as by now a relevant scientific literature on phosphodiesterase-5 inhibitors documents. Indeed, it was launched in 1998 with an unprecedented global public relations campaign, as Joel Lexchin describes in an issue of PLos Medicine, according to refined disease mongering techniques.
The phenomenon of the erection is due to a relaxation of the smooth muscles of the cavernous bodies of the penis followed by arterial vasodilation. The parallel constriction of the venous vessels causes stagnation of blood which is followed by an erection. The relaxation of the smooth muscles of the corpora cavernosa is a phenomenon mediated by nitric oxide (NO). It activates the enzyme guanylate cyclase which catalyzes the transformation of guanosine triphosphate (GTP) into cyclic guanosine monophosphate (cGMP) which stimulates muscle relaxation. The cGMP is degraded by a phosphodiesterase of which at least six isoenzymes are known. In the corpus cavernosum the phosphodiesterase involved is type 5 phosphodiesterase (5PDE). The sildenafil acts by inhibiting 5PDE, which causes an increase in the blood supply due to the increased concentration of cGMR followed by an improvement in erection. At therapeutic doses sildenafil does not produce erection in the absence of sexual stimulation.
There are other drugs on the market that can inhibit 5PDE: tadalafil (Cialis), vardenafil (Levitra) and avanafil (Spedra)
The sildenafil is taken by mouth and is rapidly absorbed from the intestine. The blood concentration of the drug, in fact, reaches its maximum values within an hour of intake. Its bioavailability is around 40% due to the strong first pass liver effect. The sildenafil travels in blood over 95% bound to plasma proteins. The drug is metabolized in the liver by two cytochromes: cytochrome 3A4 and cytochrome 2C9. The main metabolite obtained is N-demethyl sildenafil which is still pharmacologically active (it is able to inhibit 5PDE with a power, compared to sildenafil, of 50%). Both the drug and its metabolites are eliminated, mainly through bile, in faeces. A small part, however, is eliminated through the urine.
The sildenafil half-life is about 3.5 hours
In the elderly or in people with renal or hepatic insufficiency the metabolism of the drug is reduced. For severe pulmonary arterial hypertension or class three, since 2005 the use of the drug has been confirmed in patients severely limited in normal daily activities and with dyspnea at rest. The use of vasodilators in the case of pulmonary hypertension associated with veno-occlusive pulmonary disease can induce pulmonary edema, even fatal. In the event of pulmonary edema with sildenafil, assess the possibility of associated veno-occlusive pulmonary disease. The sildenafil is used for the treatment of erectile dysfunction due to organic or psychogenic causes. The medicine should be taken about an hour before sexual intercourse on an empty stomach although its effects may occur up to four hours later.
Generally, doses of drug varying between 25 and 100 mg are used, starting from the lowest quantities and then increasing according to the response. Before starting to use sildenafil it is necessary to carry out a complete clinical evaluation of the person. In reality, sildenafil is not necessarily used in erectile dysfunction but also in idiopathic or secondary pulmonary hypertension, a dangerous pathology due to the appearance of heart failure in the long run. It has been shown that this drug at low doses, by inhibiting phosphodiesterase 5, is able to dilate the pulmonary arteries and block the progression of symptoms without activating any erection process. Recent studies have shown that sildenafil has a certain influence in the conversion of white adipose tissue to brown adipose tissue.