Can Covid-19 Cause Erectile Dysfunction?
COVID-19 has been the most dangerous and life-threatening disease for almost two years. It is known as a great simulator, affecting so many organs and systems that it can mimic any disease.
Fortunately, its mechanism of onset and all the damages it produces are already well known. However, many long-term consequences, including erectile dysfunction (ED), are still under study. Let's take a closer look at what we know to date.
It was not thought that COVID-19 could impair sexual function until just a few months ago. But considering that part of the disease is based on blood vessels damage, it is now quite likely that it does.
What Is Erectile Dysfunction, And How Does It Occur?
Erectile dysfunction is the inability to achieve or maintain a good erection for sexual intercourse. Most cases are related to vascular, neurological, psychological, or hormonal disorders.
Male sexual function and the role of blood vessels in erection
There are 4 main components of male sexual function:
- Libido
- Erection
- Ejaculation
- Orgasm
Sexual dysfunction results as a problem in one of the above components that interferes with the interest or ability to have sex.
Erection is a response that depends on nerve impulses and blood flow to certain psychological or tactile stimuli, such as the stimulus before sexual intercourse involving touching.
The impulse travels through the cavernous nerves, which pass through the side of the prostate. Upon reaching the blood vessels of the penis, these nerve fibers release nitric oxide (NO), a gas. This is a very important signaling substance in the blood vessels, a vital regulator of blood pressure.
Nitric oxide is produced in the endothelium, the layer of cells that forms the inside of blood vessels. It acts as a dilator in the larger muscular arteries and prevents neighboring cells from relaxing or widening to control blood pressure.
During the erection, nitric oxide diffuses into the penile arterial smooth muscle cells, relaxing the arteries and allowing more blood to flow through them to the corpora cavernosa.
As the corpora fill with blood, intracavernosal pressure increases, which compresses the surrounding small veins causing venous occlusion and decreased venous flow. The increased blood inflow and decreased outflow further increase intracavernous pressure, contributing to the erection.
In erectile dysfunction, the vascular cause is the most common with atherosclerosis of the cavernous arteries of the penis, often caused by smoking, endothelial dysfunction, and diabetes. Generally, there is a decreased production and release of nitric oxide in these chronic conditions, interfering with the key to the erection.
Understanding the COVID-19
COVID-19 disease caused by the SARS-CoV-2 virus consists of three main phases: Early infection with increased viral load, pulmonary where pneumonia becomes evident, and finally hyperinflammation. Although not all patients with COVID go through these three phases, the few who do experience serious and even life-threatening symptoms.
The last phase is the most dangerous and the one that leaves the greatest after-effects. In this phase, there is a storm of proteins called cytokines, which are among the main tools the immune system uses to regulate cell communication.
Although the lungs are the primary target of SARS-CoV-2 and the cytokine storm, the entire cardiovascular system is affected, including small blood vessels.
Vascular damage comes as a consequence of uncontrolled inflammation and cytokine storm. Evidence in this regard supports the notion that overproduction of cytokines such as tumor necrosis factor (TNF), interleukin-1β, -6 and -10, increases the artery's permeability, possibly progressing to multiorgan failure. The vascular dysfunction at multiple levels, including pulmonary embolisms, bleeding into the alveoli, small thrombi, and vasculitis, may implicate damage to small vessels in the penis.
The hypothesis of male sexual impairment by COVID-19
Two hypotheses seek to explain the subsequent sexual dysfunction in men who suffered from COVID-19.
Testosterone
In males, adult Leydig cells express an enzyme called ACE2, which is the entry point for SARS-CoV-2. Testicular damage in COVID-19 could therefore induce a state of hypogonadism as evidenced by a decreased testosterone/LH ratio in COVID-19 patients, suggesting impaired steroidogenesis resulting in a non-evident testicular dysfunction.
Endothelial damage
The artery's integrity is more than necessary to achieve an erection. The vascular damage linked with COVID-19 is likely to affect the fragile arteries and veins of the penis, resulting in weakened erectile function.
A recent study evaluated the penile microscopic characteristics of two individuals who had COVID-19 and subsequently developed ED.
Samples were obtained from both penises to evaluate the characteristics and compare them with normal penises.
In the COVID-19 samples, viral particles were found near the endothelial cells in the blood vessels. Also, these cells had low nitric oxide production, probably due to the viral damage, compared to the control samples.
Importantly, one of these patients did not have hypertension, coronary artery disease, or diabetes mellitus. In contrast, the other did, and both patients had a normal erectile function before the disease.
According to our analysis, it is very likely that COVID-19 produces long-term erectile dysfunction. However, it still needs to be studied because two patients are not significant enough to reach a strong conclusion.
Although erectile dysfunction is a frequent and often serious sexual problem that destroys male self-esteem, it is also a condition that can be treated and solved. Currently, many pharmacological options can improve sexual performance, such as Sildenafil, Tadalafil, Vardenafil, and their derivatives.
More than 3.5 million people have recovered from COVID-19; however, the long-term consequences of the disease are still largely unknown. Because of this, some are already being elucidated; erectile dysfunction could be one of them. Let's wait for more research.
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