Twosmallstudiespublished recently suggested most men hospitalised with COVID-19 are bald, generatingheadlinesaround the world.

While this may sound strange, science does offer a plausible explanation.

Male pattern baldness is associated with high levels of male sex hormones called androgens.

And androgens seem to play an important role in the entry of SARS-CoV-2, the coronavirus that causes COVID-19, into cells.

So it's possible high levels of androgens mightincrease the riskof severe infection and death from COVID-19.

This hypothesis is important to identify people at risk and raises the possibility of new treatment strategies for COVID-19.

It's been obvious from early in the pandemic. Men areat greater riskof severe infection and death from COVID-19 than women.

There are severalpossible factorsat play here. For one, men are more likely to suffer from chronic conditions known to pose ahigher riskof serious illness from COVID-19.

These includeheart diseaseanddiabetes.

Another is that men's immune systems are not as good aswomen'sat warding off the severe effects of viral infections.

These factors are indirectly influenced by sex hormones. Now it seems sex hormones might also have a direct effect on SARS-CoV-2's ability to enter our cells and establish infection.

In one study of 122 male COVID-19 patients admitted to hospitals in Madrid,79 per cent were bald about double the population frequency.

Anothersmall studyin Spain observed a similar overrepresentation of baldness among men in hospital with COVID-19.

Male pattern baldness isstrongly associatedwith a higher level of dihydrotestosterone (DHT), a more active derivative of testosterone, and one of the androgen family of male sex hormones.

Confirming this correlation between baldness and susceptibility to COVID-19 with larger samples, controlling for age and other conditions, would be significant.

It would suggest a higher DHT level could be a risk factor for severe COVID-19.

SARS-CoV-2 enters human lung cells when a protein on the virus' surface (thespike protein) latches onto protein receptors (ACE2 receptors) embedded in the cells' surfaces.

How does this work? Recently scientists discovered that an enzyme calledTMPRSS2cleaves the SARS-CoV-2's spike protein, enabling it to bind to the ACE2 receptor. This allows the virus to enter the cell.

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The gene that encodes TMPRSS2 is activated when male hormones, particularly DHT, bind to the androgen receptor (a protein on the surface of cells, including hair cells and lung cells).

So the more male hormone, the more androgen receptor binding, the more TMPRSS2 is present, and the easier it is for virus to get in.

Apreliminary, non-peer-reviewed studywhich correlated the androgen levels of hundreds of people in the UK with COVID-19 severity supports this theory.

Higher androgen level was associated with susceptibility to and severity of COVID-19 in men (but not women, who have much lower androgen levels in their blood).

The same researchers showed that inhibiting androgen receptors reduced the ability of SARS-CoV-2's spike protein to bind to ACE2 receptors on stem cells in culture.

Over or underproduction of androgens in the body causes a variety of conditions in both men and women.

For instance, men withbenign prostate enlargementoverproduce androgen, as do women withpolycystic ovary syndrome.

Many such conditions are treated with androgen deprivation therapy (ADT), which inhibits the production or effect of androgens.

For instance, prostate cancer, in which cancer cell growth is fuelled by androgens, is routinely treated with ADT.

Conversely, some people have low androgen production, or mutations that affect the binding and action of androgens such as women withandrogen insensitivity syndromecaused by mutations of the androgen receptor.

It will be important to find out whether, as the androgen hypothesis predicts, patients with over- or under-production of male hormones are at greater or lesser risk of COVID-19.

If the androgen link holds up, this would encourage exploration of anti-androgens as a way to prevent and treat COVID-19.

Many anti-androgens arealready approvedfor the treatment of other conditions. Some, like baldness treatments, have been used safely for years or decades.

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Some, like cancer treatments, can be tolerated for months.

A study which looked at men hospitalised with COVID-19 in Italy showed the rate of infection wasfour times lowerin prostate cancer patients on ADT than in untreated cancer patients.

Perhaps a single dose given to someone who tests positive to SARS-CoV-2, or has just been exposed, would suffice to lower the chance of the virus taking hold.

But we need research to confirm this. Several androgen-suppressing drugs are now undergoingclinical trialsto determine whether they reduce complications among men with COVID-19.

It will be important to verify that anti-androgen treatment works in the lungs as well as the prostate, and is effective in cancer-free patients.

We'd also need to find out what dose is effective, and when it should be administered.

Anti-androgen treatments have severalside effectsin men, including breast enlargement and sexual dysfunction, so medical oversight is a must.

The androgen link could go a long way to explaining why men are more susceptible to COVID-19 than women.

It also may explain why children younger than ten seem very resistant to COVID-19 because, until puberty, boys as well as girls makelittle androgen.

The more we know about who is at heightened risk from COVID-19, the better we can target information.

The androgen link also opens up an avenue for the discovery of drugs which might mitigate some of the impact of COVID-19 as it continues to sweep the globe.

Jenny Graves is a Distinguished Professor of Genetics and Vice Chancellor's Fellow at La Trobe University. This article originally appeared on The Conversation.

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