Can Covid–19 Cause Erectile Dysfunction?

Covid–19 and Erectile Dysfunction

Science continues to unravel the widespread effects of COVID‐19 on different organs. Initially thought to affect only lung tissue, COVID-19 has now been shown to damage the cardiovascular, digestive, nervous, and urinary systems. One point that often goes unspoken, however, is the link between COVID-19 and the most common male sexual dysfunction, erectile dysfunction (ED), defined as the inability to maintain an erection for satisfactory sexual intercourse.

The Prevalence of Erectile Dysfunction Related to COVID-19 

Since the pandemic started, numerous studies began to reveal a strong association between ED and the onset of COVID-19. Although the percentage of males with COVID-19 reporting ED stayed in a similar range to that of the general population (20-32%), the number of patients diagnosed with ED during the pandemic rose considerably since the societal introduction of the virus.^1–3 It was also noted that sales for ED medication steadily increased after only several months of the pandemic, despite a reported decline in sexual activity.^4,5

A couple of years on and there is now a pool of evidence from both small and large-scale observational studies which have found that male adults are 1.2-5.7 more likely to have ED if previously diagnosed with COVID-19.^6,7 These associations appear to remain even when other factors that causally relate to sexual health have been accounted for, such as age, cardiovascular disease, body mass index, and psychological health.

Some researchers have even tracked the same group of individuals over time to analyse changes in erectile function score; for instance, one study found that there was a significant reduction in the average erectile function scores of 156 males after hospitalisation for COVID-19 compared to before, which was paired with anxiety and depression in most cases.⁸ Genetic studies have also been instructive in showing those who are biologically most vulnerable to COVID-19 have slightly elevated rates of ED—although calls for more comprehensive types of genetic research have been proposed to confirm such findings.⁹

What Might Explain ED From COVID-19?

While evidence is mounting, questions still remain about the type of relationship that COVID-19 and ED share. As common risk factors underpin both conditions, such as cardiovascular disease, endothelial dysfunction, inflammation, diabetes, and obesity, it is challenging to tease out whether the consistently reported associations are causal or spurious. Some experts hypothesise that COVID-19-related ED may simply be a byproduct of partners spending more time away from each other, a reduction in sexual desire, or increased stress and anxiety, as opposed to any direct effect of the virus itself.

Despite the need for more evidence, however, especially from more robust clinical trials, it is certainly plausible that ED is a direct consequence of the virus’s effects in the body. A couple of studies have now discovered that, in many patients with mild to severe forms of COVID-19, their penile tissue still tests positive for the virus after seven months of a negative test.¹⁰ By obtaining high resolution images, researchers have captured clear images of viral particles in the penis. These viral particles also happen to be found near the endothelial cells (cells lining the blood vessels) in the penis, which is an interesting consideration given that endothelial dysfunction is the most well-documented cause of ED.¹¹

What may also be exacerbating the issue is the effect of COVID-19 in the testes. Similar to studies which have found the virus within penile tissue, COVID-19 has also been visually detected in the testes. ¹¹ In fact, beyond just identifying the viral particles, morphologic evaluation of male patients who have died from COVID-19 has shown that, in more than half of cases, an injury pattern suggestive of testicular oxidative damage is apparent.^12,13 Details are still relatively unknown, but since the immune cells characterising COVID-19 infections tend to be those associated with worsening male sexual dysfunction, the oxidative damage may be a result of a viral inflammatory cascade within the penile region.¹⁴

Other mechanisms such as psychological distress, immunological disorders, and blood clotting, have been speculated by experts as potential causative factors. In any case, these types of explanations would align with numerous studies which find that COVID-19 can impair the synthesis of steroid hormones, also known as steroidogenesis, and reduce serum testosterone levels, which are both conditions known to exacerbate ED outside the context of COVID-19.^15,16

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Can ED From COVID-19 Be Treated?

It’s important to know that several treatments exist for improving ED. These include a variety of medical therapies and invasive methods, some of which are clinically beneficial.¹⁷ How common treatments for ED apply to cases related to COVID-19 is largely unknown, although early evidence in COVID-19 outpatients reporting erectile dysfunction has already shown that ED treatment leads to significantly greater improvement in sexual function compared to placebo.¹⁸ It’s recommended for anyone noticing poor erectile function to visit a healthcare professional, regardless of whether symptoms were noted before or after contracting COVID-19.

Interested in learning more about ED treatments?

Take-home Points and Remaining Questions

Converging lines of research support the claim that COVID-19 is a potential cause of ED. At the very least, based on an analysis of the risks versus the benefits, it’s wise to use the principle of precaution to avoid contracting COVID-19 in an attempt to minimise the risk of ED. Future research will help to provide more clarity on the matter, as well as answer related questions such as:

• Does COVID-19 worsen symptoms in patients who already report ED?

• Can vaccines or other treatments mitigate the risk of COVID-related ED?
• Is COVID-related ED more or less self-limiting than generalised ED?

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Continue the conversation on the TRTed Community!

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References

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14. Ma X, et al. Cellular & Molecular Immunology 2021;18:487–489.  

15. Pedersen SF, et al. J Clin Invest 2020;130(5):2202–2205.

16. Flaifel A, et al. Arch Pathol Lab Med 2021;145(1):8–9.

17. Yuan J, et al. Eur Urol 2013;63(5):902–12.  

18. Pyrgidis N, et al. Sex Med Rev 2022;10(4):782–790.