Many of our buildings are poorly ventilated, and that adds to COVID risks



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Geoff Hanmer and Bruce Milthorpe, University of Technology Sydney

The virus that causes COVID-19 is much more likely to spread indoors rather than outdoors. Governments are right to encourage more outdoor dining and drinking, but it is important they also do everything they can to make indoor venues as safe as possible. Our recent monitoring of public buildings has shown many have poor ventilation.

Poor ventilation raises the risks of super-spreader events. The risk of catching COVID-19 indoors is 18.7 times higher than in the open air, according to the US Centers for Disease Control and Prevention.




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In the past month, we have measured air quality in a large number of public buildings. High carbon dioxide (CO₂) levels indicate poor ventilation. Multiple restaurants, two hotels, two major shopping centres, several university buildings, a pharmacy and a GP consulting suite had CO₂ levels well above best practice and also above the absolute maximum mandated in the National Construction Code.

Relative humidity readings of less than 40% associated with both heating and cooling air are also of concern. Evidence now suggests low humidity is associated with transmission.

If anyone had COVID-19 in these environments, particularly if people were in them for an extended period, as might happen at a restaurant or pub, there would be a risk of a super-spreader event. Less than 20% of individuals produce over 80% of infections.




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Many aged-care deaths were connected

It appears a relatively small number of super-spreader events, probably associated with airborne transmission of SARS-CoV-2, the virus that causes COVID-19, were responsible for most of the deaths in Victorian aged-care facilities.

Of the 907 people who have died of COVID-19 in Australia, 746, or 82% of COVID-19 deaths, were associated with aged care. In Victoria, there were 52 facilities with more than 20 infections. Three had over 200 infections. As a result, 639 of the 646 aged care residents who died in Victoria were located in just 52 facilities.

But official advice hasn’t changed

Aged-care operators and the states based their infection control on the advice of the Commonwealth Infection Control Expert Group (ICEG). As of September 6, the Coronavirus (COVID-19) Residential Aged Care Facilities Plan for Victoria stated:

Coronavirus (COVID-19) is transmitted via droplets, after exposure to contaminated surfaces or after close contact with an infected person (without using appropriate PPE). Airborne spread has not been reported [our emphasis] but could occur during certain aerosol-generating procedures (medical procedures which are not usually conducted in RACF). […] Respiratory hygiene and cough etiquette, hand hygiene and regular cleaning of surfaces are paramount to preventing transmission.

In early August, more than 3,000 health workers had signed a letter of no confidence in ICEG. The letter noted that aerosol transmission was causing infections in medical staff, many of whom worked in aged-care facilities.

On September 7, we wrote to the federal aged care minister, Richard Colbeck, drawing attention to our August 20 article in The Conversation, which referenced a July 8 article in Nature. The Nature article identified an emerging consensus that aerosol transmission of SARS-CoV-2 is probable in low-ventilation environments.




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The director of the Aged Care COVID-19 Measures Implementation Branch wrote back on Colbeck’s behalf on September 28 saying:

Current evidence suggests COVID-19 most commonly spreads from close contact with someone who is infectious. It can also spread from touching a surface that has recently been contaminated with the respiratory droplets (cough or sneeze) of an infected person and then touching your eyes, nose or mouth.

In other words, Commonwealth authorities were still playing down the significance of airborne transmission nearly two months after the letter of no confidence was sent to ICEG and three months after the article in Nature. By the end of September, Victorian aged-care facilities had reported over 4,000 cases of COVID-19, about half of them in staff.

On October 23, ICEG was still saying:

There is little clinical or epidemiological evidence of significant transmission of SARS-CoV-2 (the virus that causes COVID-19) by aerosols.

Focus on the ‘3 Vs’ to reduce risks

The key thing we need to do until a vaccine is rolled out is to try to prevent indoor super-spreader events. According to the University of Nebraska Medical Centre, we should remember the “three Vs” that super-spreader events have in common:

Venue: multiple people indoors, where social distancing is often harder

Ventilation: staying in one place with limited fresh air

Vocalization: lots of talking, yelling or singing, which can aerosolize the virus.

Measuring indoor ventilation is quick and easy using a carbon dioxide detector. Any CO₂ reading of over 800 parts per million is a cause for concern – the level for air outside is just over 400ppm.

There is no excuse for governments, health authorities and building owners not to monitor ventilation levels to help ensure members of the public are as safe as is reasonably practicable when indoors.

There is also no excuse for the Australian Building Control Board not to change the National Construction Code to require fall-back mechanical ventilation systems be fitted and CO₂ and humidity monitored in all buildings frequented by the public, particularly aged-care facilities.

With the knowledge we have now and a low rate of community infection, Australia should be able to make it through to vaccine roll-out with relatively few further infections and deaths. But that depends on being vigilant about the quality of ventilation indoors and the associated possibility of super-spreader events. This is especially important in aged-care facilities and quarantine hotels.

It’s probably a good idea for us all to open the windows and let the fresh air in.The Conversation

Geoff Hanmer, Adjunct Professor of Architecture and Bruce Milthorpe, Emeritus Professor, Faculty of Science, University of Technology Sydney

This article is republished from The Conversation under a Creative Commons license. Read the original article.

How to reduce COVID-19 risk at the beach or the pool


Brett Mitchell, University of Newcastle and Philip Russo, Monash University

Australians are emerging from winter and, where possible, enjoying trips to beaches and public pools. Beach-side picnics, barbecues and get-togethers are back on the cards for many of us.

While daily COVID-19 case numbers have been looking promising in most places lately, we are still very much in a pandemic; your spring and summertime social activities might look a little different this year.

Here’s how to stay safe if you’re planning a trip to the beach or public pool.




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A person swims laps in a pool.
Your spring and summertime social activities might look a little different his year.
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The three golden rules

Outdoor activities are associated with reduced COVID-19 transmission risk compared to indoor activities. That said, whatever your plans, the three golden rules still apply: stay home if you are sick, keep up the hand hygiene and maintain physical distancing from others.

If you’re sick, you shouldn’t be socialising at all. You should be getting a COVID-19 test and self-isolating while you wait for results. Even outdoors, one sick person can spread COVID-19 to a large number of people.

Going to the beach

Firstly, pick a quieter beach. The extra time it takes to research and travel to a more secluded beach may be a hassle, but it’s less risky than going to a crowded beach (and often nicer, too).

Consider driving or cycling to the beach (if possible) rather than taking public transport. If you do use public transport, pick an off-peak time of day and wear a mask — avoid rush hour.

When you arrive, put your towels down in a spot on the sand at least 1.5m away from others — more is better, if you can. You should still swim between the flags, but you don’t need to be sitting close to other people.

An aerial shot of an ocean pool.
Pick a quieter swim spot or go at a less busy time.
Shutterstock

When swimming between the flags, it might feel crowded in the water during busy times or at busy beaches. If you are in that situation, think about reducing the time spent in the water — go in for five minutes, then come out for a bit, then go back in for another five, so you are not having prolonged contact next to another person.

If you see someone expelling mucus into a wave, try to avoid that wave and person if you can.

Remember to stay COVID-safe if you’re at a cafe for a post-swim snack or ice-block. Don’t bunch up in lines close to other people and maintain physical distance from others if you are sitting down for a meal.

In the past, it might have felt normal to share a plate of hot chips with mates or even offer a friend a sip of your drink — but we don’t do that anymore. If you’re having a beach-side picnic, make sure you’re not sharing utensils, double-dipping in the hummus or sticking your fingers into a shared bowl of olives.

Of course, all these general principles also apply to other outdoor swimming locations, such as rivers and dams.

Going to the pool

The ocean is probably less risky than going to the pool, because there’s more movement of water and a high level of dilution.

So you need to approach public pools with a degree of caution.

But if you have no choice, are living away from the coast and want a swim, it’s probably fine to go to an outdoor pool — especially if you are living in an area with a low level of community transmission. You can find out community transmission rates in your area from your state health department website.

Outdoor pools are less risky than indoor pools because of increased air flow. Confined spaces are associated with increased risk of COVID-19 transmission.

An outdoor pool in Sydney.
Outdoor pools are less risky than indoor pools,
Shutterstock

Choose the right time to go a pool. Transmission risk decreases with fewer people, so try to go at less busy times. In the morning, the pool water has likely had time to be well-filtered and well-chlorinated overnight and not many people have swum in it yet that day.

Chlorine kills coronavirus. The CDC says it is

not aware of any scientific reports of the virus that causes COVID-19 spreading to people through the water in pools, hot tubs, or water playgrounds […] including saltwater pools.

The risk of transmission, albeit potentially low, would also depend on how chlorinated the pool is and how long any coronavirus that may be in the water is exposed to chlorine before coming into contact with another person.

Theoretically, if someone is carrying the virus and some mucus goes out of their mouth and into the pool, there might be a certain period of time before any virus in that mucus is inactivated by the chlorine. If it gets to you before that inactivation happens, then it is possibly a bit more risky.

People swim at a pool in Sydney.
Whatever you have planned this summer, think about the local risks and what you can do to reduce them.
Shutterstock

Avoiding the change-rooms is another way to reduce risk, as these rooms are often in a confined space. Being careful to maintain physical distancing in the pool, poolside and at the cafe are also important measures.

In general, it should be fine to take the kids to the pool but, if there was a degree of community transmission in your area, perhaps reconsider. There is growing evidence kids are less susceptible to COVID-19 compared to adults but it doesn’t necessarily mean they are not transmitting it.

Whatever you have planned this summer, think about the local risks and what you can do to reduce them.




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The Conversation


Brett Mitchell, Professor of Nursing, University of Newcastle and Philip Russo, Associate Professor, Director Cabrini Monash University Department of Nursing Research, Monash University

This article is republished from The Conversation under a Creative Commons license. Read the original article.

Morrison government to invest $211 million in fuel security to protect against risk and price pressures


Michelle Grattan, University of Canberra

The Morrison government is acting to protect Australia’s fuel security as the international outlook becomes more uncertain and prices will be under increasing pressure.

Under the plan, operating through market and regulatory measures, the government will invest $211 million in new domestic diesel storage facilities, changes to create a minimum onshore stockholding, and support for local refineries.


Treasury

Announcing the program with Energy Minister Angus Taylor, Scott Morrison said the changes “will ensure Australian families and businesses can access the fuel they need, when they need it, for the lowest possible price”.

Australia’s fuel supplies are always potentially vulnerable to international instability, something that the pandemic – with its disruption to supply chains – has just reinforced. Local refineries are also under economic pressures, with potential consequences for prices.

The measures are:

  • a $200 million investment in a competitive grants program to build an extra 780 megalitres of onshore diesel storage with industry

  • creation of a minimum stockholding obligation for key transport fuels, and

  • working with refiners on a market design process for a refining production payment.

The government is seeking to have the $200 million grants for new storage matched by state governments or industry. Its focus will be on projects in strategic regional locations, connected to refineries and with connections to existing fuel infrastructure.

Morrison said fuel security was essential for Australia’s national security and the country was fortunate there hadn’t been a significant supply shock in more than 40 years. Fuel security underpinned the entire economy, and the industry itself supported thousands of workers, he said. “This plan is also about helping keep them in work.”

Taylor acknowledged the pressure refineries are under.

The government says modelling indicates a domestic refining capability is worth some $4.9 billion over a decade to Australian consumers is terms of price suppression.

The construction of diesel storage will support up to 950 jobs, with 75 new ongoing jobs, many in the regions, the government says.

“A minimum stockholding obligation will act as a safety net for petrol and jet fuel stocks and increased diesel stockholdings by 40%,” Morrison and Taylor said in their statement.

They stressed the government’s commitment to onshore refining capacity. The industry’s viability is under threat.

The planned production payment scheme is to protect from an estimated 1 cent per litre rise that, according to modelling, would hit fuel if all refineries onshore were to close. Refineries receiving the support will have to commit to stay operating locally.

Under the minimum stockholding requirements, petrol and jet fuel stocks would be kept no lower than current commercial levels, which are about 24 consumption days.

Diesel stocks would increase by 40%, to be at 28 consumption cover days. This would add about 10 days to Australia’s International Energy Agency compliance total.

In July Australia had 84 IEA days including stocks on water. Implementing a minimum stock holding obligation would bring Australia into line with most IEA members which regulate their fuel industries to meet their security needs. Under the IEA treaty member countries are required to have 90 days of stocks.

(IEA days and consumption cover days are different.)

Refineries will be exempt from the obligations to hold additional stocks.

The production payments will ensure a minimum value of 1.15 cents per litre to refineries. A competitive process will determine the location of new storage facilities.

The government says it recognises “the future refining sector in Australia will not look like the past. However, this framework will ensure the market is viable for both our future needs and can support Australia during a severe fuel disruption.”The Conversation

Michelle Grattan, Professorial Fellow, University of Canberra

This article is republished from The Conversation under a Creative Commons license. Read the original article.

Type 2 diabetes: eating a diet rich in fruit and vegetables daily lowers risk, study shows



The more fruit and vegetables consumed, the lower the risk.
Anna Shkuratova/ Shutterstock

Nita Forouhi, University of Cambridge; Ju-Sheng Zheng, Westlake University, and Nick Wareham, University of Cambridge

Eating about five servings of fruit and vegetables a day is widely promoted as a key part of a healthy diet. This is because consuming fruit and vegetables is linked to lowering the risk of health problems such as coronary heart disease, stroke and some types of cancer.

But there’s still confusion about the role that fruit and vegetables have in preventing type 2 diabetes. Evidence from research has been inconsistent, partly because most studies have relied on participants remembering what they ate – which can be inaccurate. But our latest research found that people who regularly ate more fruit and vegetables in their diet had half the risk of developing type 2 diabetes compared to those who ate less.

Since research shows that type 2 diabetes can be prevented through a healthy diet, we wanted to know just how important eating fruit and vegetables is as part of that. We conducted the world’s largest study that measured blood levels of vitamins linked to fruit and vegetable consumption in a population. This method of using objective nutritional biomarkers – indicators of dietary intake, metabolism or nutritional status that are present in our blood – cuts out the errors and inaccuracies that affected previous studies. We also asked people to report what specific foods they ate to compare with the biomarker data.

We followed a group of 340,234 people from eight European countries. We specifically studied biomarkers in 10,000 people who developed type 2 diabetes during follow-up and compared them with 13,500 people who didn’t.

The biomarkers we measured were levels of vitamin C and six different carotenoids or plant pigments in the blood. These biomarkers tell us about the fruit and vegetables a person gets in their diet. We then calculated the total sum of these seven nutrient biomarkers as a composite score, then split scores into five categories ranging from lowest consumption to highest.

We found that the higher the biomarker score level, the lower the risk of future type 2 diabetes. People whose biomarker score was in the top 20% of the population had a 50% lower risk of developing type 2 diabetes compared to those with lower scores. We also found that eating around 66 grams of fruit and vegetables daily could potentially cut risk of type 2 diabetes by a quarter.

One to two portions daily cut risk by a quarter.
Rawpixel.com/ Shutterstock

Our findings build upon the results of a smaller study of 21,831 people living in England, 735 of whom developed type 2 diabetes. This study showed a strong link between higher blood vitamin C level and lower risk of diabetes. But the link was weaker when examining fruit and vegetable intake as reported by the participants. By repeating this work on a larger scale and in several countries, our results further strengthen evidence that these results are likely to be repeated in other populations, too.

Five a day

Since UK dietary guidelines consider each portion of fruit or vegetable to be 80 grams, our study shows eating even one portion per day could have health benefits. For instance, seven cherry tomatoes, two broccoli spears, or one banana would all roughly equal one portion.

Although “five a day” has been around for decades, fruit and vegetable consumption remains low. Only one in seven people over 15 eat at least five portions everyday – and one in three people don’t eat any daily. Encouragingly, our results show there are large potential benefits from making small changes to our diets.

Our research highlights that reduced risk isn’t just because of certain nutrients or vitamins. Rather, the benefits we observed are because of the combination of multiple beneficial components found in fruits and vegetables. Alongside vitamin C and carotenoids, other components including fibre, potassium and polyphenols, which have beneficial effects on weight, body inflammation, blood sugar levels, and keep gut bacteria healthy. And a diverse variety of fruit and vegetables has the greatest health benefits, as you consume more of these beneficial components.




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We also took into account how several factors – including age, gender, body mass index, education level, occupation, smoking, alcohol intake, physical activity and use of vitamin supplements – all affected the risk of type 2 diabetes. We found that the biomarker results linked to fruit and vegetables were independent of these other factors – so regardless of whether a person smoked or was physically active, eating a diet rich in more fruit and vegetables is relevant for lowering the risk of developing type 2 diabetes.

Our research doesn’t establish cause and effect, because we did not intervene with dietary change – rather we observed what happened over time to participants with different blood biomarker levels. But, by using these objective measures and a large sample size in different countries with varying diets, our confidence in these findings is increased. We still don’t yet know whether our findings would be different among different ethnic groups, which should be a focus of future research.

It’s well known that fruit and vegetables are an important part of maintaining good health throughout life, but we also know that in reality the majority of people do not eat enough of them. Our study shows that even just a small increase in the amount of fruits or vegetables you get in your diet can significantly reduce your risk of developing type 2 diabetes.The Conversation

Nita Forouhi, Programme Leader, MRC Epidemiology Unit, University of Cambridge; Ju-Sheng Zheng, Principal Investigator, Human Nutrition and Epidemiology, Westlake University, and Nick Wareham, Director of the MRC Epidemiology Unit, University of Cambridge

This article is republished from The Conversation under a Creative Commons license. Read the original article.

Victorians, and anyone else at risk, should now be wearing face masks. Here’s how to make one


C Raina MacIntyre, UNSW; Kerryn Phelps, Western Sydney University; Lisa Maher, UNSW, and Shovon Bhattacharjee, UNSW

After early success in suppressing COVID-19, we are facing a resurgence in Victoria, which is threatening disease control for the whole country.

Outbreaks in northwestern Melbourne, including in public housing tower blocks in inner Melbourne, and now in the twin border towns of Albury-Wodonga, signal a risk of losing our hard-won gains. These gains have already come at a heavy price to the economy and mental health, which is all the more reason to throw everything we can at this resurgence – including widespread use of face masks, as we have seen in other countries such as the United States and United Kingdom.

With 191 new cases announced on July 7, Victorian Premier Daniel Andrews has announced a return to stage 3 restrictions for six weeks from July 9 for metro Melbourne and Mitchell Shire. This means residents will be confined to their homes except for essential trips such as work, medical care, exercise or shopping for essentials. The evidence suggests both sick and healthy people wearing masks will help curb the spread of COVID-19 during this precarious time.




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Australia is one of the few countries that has suppressed COVID-19 after a peak in disease incidence in late March. The current resurgence, unlike the peak in March which was largely travel-related, has arisen mostly from community transmission, which is a more serious concern.

Health authorities have a range of measures at their disposal, including expanded testing to find all new cases, diligent contact tracing, travel bans, border closures and quarantine of returning travellers. As members of the public, there are five main things we can do to stop the spread: get tested if we have symptoms, download the COVIDSafe App, practise physical distancing, wash our hands often, and wear a face mask.

Why masks help

The most extreme form of physical distancing is a lockdown, already enforced in Melbourne. Keeping at least 1.5 metres away from others also dramatically reduces the risk of COVID-19, even in crowded households. Victorians should think about wearing a mask, especially in indoor spaces like shops or public transport or in outdoor crowds. There may be epidemics developing in other states, so people at risk in those states should think about masks too.

There’s no doubt masks help stop the spread. A recent study commissioned by the World Health Organisation showed that face masks reduce the risk of infection with viruses such as SARS-CoV-2, the coronavirus that causes COVID-19, by 67% if a disposable surgical mask is used, and up to 95% if specialist N95 masks are worn, although these are not widely available to the public.

This study prompted the WHO to change its position to recommending community mask use. It had long advised masks should be worn only by sick people to stop them infecting others, although this was perhaps motivated in part by concerns over supplies.

Many countries, perhaps most notably the United States, initially adopted this advice but then began to encourage community-wide mask use when the epidemic began to get out of hand.

Why not in Australia?

Australia has not yet adopted community masking as a tool in the fight against COVID-19. The WHO issued a long list of dangers of mask wearing, including that masks give “a false sense of security, leading to potentially lower adherence to other critical preventive measures such as physical distancing and hand hygiene”.

There is no scientific evidence to support this – in fact, the evidence suggests the opposite. In an illustrative exercise, Italian researcher Massimo Marchiori found people stayed more than twice as far away from him when he wore a mask.

Not all masks are the same, however. For community use, the options are surgical masks and cloth masks. Surgical masks are single-use only and should not be re-used. If they are unavailable or too expensive, you can make an effective cloth version yourself if you follow a few key principles.




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Cloth masks can vary widely depending on the material and design – a single or even double-layered mask or bandanna is likely not protective at all.

A cloth mask should have at least three or four layers, including a water-resistant outer layer, a fine weave and high thread count, and should be washed and worn fresh each day. It should fit snugly around your face, or air will flow through the gaps on the sides. A nylon stocking over the top can help.

Research shows a 12-layered cloth mask can be as good as a surgical mask, although you may not have the time or inclination to make a homemade version with 12 layers.

How to make an effective cloth mask.
Shovon Bhattacharjee, Author provided

Modelling shows that even a modestly effective mask that delivers just a 20% reduction in viral transmission can successfully flatten the COVID-19 curve. Masks have a double benefit, stopping infected people spreading the virus and protecting uninfected people from catching it.

Given the possibility this coronavirus can also be spread by people without symptoms or even people who have already left the room, handwashing and physical distancing may not be enough. We need every tool at our disposal, and that includes masks.




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Masks can be worn in public or indoors. Surgical masks worn at home can prevent the spread of the coronavirus to family members, which may be worth considering if you live with a health worker or someone else at high risk.

As Melbourne and Australia struggle to regain control of COVID-19, positive promotion of face masks, and simple how-to guides for making, as well as wearing and removing them could be a powerful addition to our armoury. A clear, consistent public health directive in relation to masks is needed now to help avoid longer lockdowns and more draconian measures, and enable safer community activities.The Conversation

C Raina MacIntyre, Professor of Global Biosecurity, NHMRC Principal Research Fellow, Head, Biosecurity Program, Kirby Institute, UNSW; Kerryn Phelps, Adjunct Professor, NICM Health Research Institute, Western Sydney University; Lisa Maher, Professor, Faculty of Medicine, UNSW, and Shovon Bhattacharjee, PhD Candidate, The Kirby Institute, UNSW

This article is republished from The Conversation under a Creative Commons license. Read the original article.

Coronavirus and sex hormones — baldness may be a risk factor and anti-androgens a treatment


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Jenny Graves, La Trobe University

Two small studies published recently suggested most men hospitalised with COVID-19 are bald, generating headlines around 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 might increase the risk of 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.

Sign up to The Conversation

Men suffer more than women from COVID-19

It’s been obvious from early in the pandemic. Men are at greater risk of severe infection and death from COVID-19 than women.

There are several possible factors at play here. For one, men are more likely to suffer from chronic conditions known to pose a higher risk of serious illness from COVID-19. These include heart disease and diabetes.

Another is that men’s immune systems are not as good as women’s at 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.

Baldness and COVID-19

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

Another small study in Spain observed a similar overrepresentaton of baldness among men hospitalised with COVID-19.




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Male pattern baldness is strongly associated with 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.

How does this link make biological sense?

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

How does this work? Recently scientists discovered that an enzyme called TMPRSS2 cleaves the SARS-CoV-2’s spike protein, enabling it to bind to the ACE2 receptor. This allows the virus to enter the cell.

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.

SARS-CoV-2 gets into our cells by latching onto ACE2 receptors.
Shutterstock

A preliminary, non-peer-reviewed study which 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.

Androgen disruptions are linked to different diseases

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

For instance, men with benign prostate enlargement overproduce androgen, as do women with polycystic 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 with androgen insensitivity syndrome caused 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.




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A potential treatment option?

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 are already approved for the treatment of other conditions. Some, like baldness treatments, have been used safely for years or decades. 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 was four times lower in 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 undergoing clinical trials to 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 several side effects in men, including breast enlargement and sexual dysfunction, so medical oversight is a must.

Men who are bald have higher levels of the hormone dihydrotestosterone.
Shutterstock

A promising new direction in COVID-19 research

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 make little 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.




Read more:
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The Conversation


Jenny Graves, Distinguished Professor of Genetics and Vice Chancellor’s Fellow, La Trobe University

This article is republished from The Conversation under a Creative Commons license. Read the original article.

A disease that breeds disease: why is type 2 diabetes linked to increased risk of cancer and dementia?



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Rachel Climie, Baker Heart and Diabetes Institute and Jonathan Shaw, Baker Heart and Diabetes Institute

In Australia, more than 1.1 million people currently have type 2 diabetes.

A host of potential complications associated with the disease mean a 45-year-old diagnosed with type 2 diabetes will live on average six years less than someone without type 2 diabetes.

This week we published a report bringing together the latest evidence on the health consequences of type 2 diabetes.

Aside from demonstrating the complications we know well – like the link between diabetes and heart disease risk – our report highlights some newer evidence that suggests type 2 diabetes is associated with an increased risk of cancer and dementia.




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Common complications of type 2 diabetes

Type 2 diabetes, which typically develops after the age of 40, is usually due to a combination of the pancreas failing to produce enough of the hormone insulin, and the cells in the body failing to adequately respond to insulin.

Since insulin is the key regulator of blood glucose (sugar), this causes a rise in the blood sugar levels.

Risk factors for developing type 2 diabetes include being overweight, being physically inactive, having a poor diet, high blood pressure and family history of type 2 diabetes.

Being overweight is a risk factor for type 2 diabetes – but not all people with type 2 diabetes are overweight.
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People with type 2 diabetes are about twice as likely to develop heart disease than people without type 2 diabetes.

While heart attacks, due to blockages in the coronary arteries, are perhaps the better recognised form of heart disease, heart failure, where the heart muscle is unable to pump enough blood around the body, is becoming more common, especially in people with type 2 diabetes.

This is due to a number of factors, including better treatment and prevention of heart attacks, which has allowed more people to survive long enough to develop heart failure.

People with type 2 diabetes are up to eight times more likely to develop heart failure compared to those without diabetes.




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Meanwhile, diabetes is the most common cause of kidney failure and vision loss in working age adults, and accounts for more than 50% of foot and leg amputations.

But beyond these common and familiar complications of diabetes, there’s mounting evidence to suggest type 2 diabetes increases the risk of other diseases.

Emerging complications of type 2 diabetes

People with type 2 diabetes are approximately two times more likely to develop pancreatic, endometrial and liver cancer, have a 30% higher chance of getting bowel cancer and a 20% increased risk of breast cancer.

Increased cancer risk is of particular concern for the growing number of people under 40 living with type 2 diabetes. In Australia, this group saw a significant increase in deaths from cancer between 2000 and 2011.

Dementia, too, is a recently recognised complication of type 2 diabetes. A meta-analysis involving data from two million people showed people with type 2 diabetes have a 60% greater risk of developing dementia compared to those without diabetes.




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Why the increased risk?

It’s important to acknowledge the studies we looked at are observational and can’t tell us diabetes necessarily caused these conditions. But they do suggest having diabetes is associated with an increased risk.

The two leading theories for why cancer risk is increased in people with type 2 diabetes relate to glucose and insulin.

Many types of cancer cells use glucose as a key fuel, so the more glucose in the blood, potentially, the more rapidly cancer will grow.

Alternatively, insulin can promote the growth of cells. And since in the early stages of type 2 diabetes insulin levels are elevated, this might also promote the development of cancer.

It’s especially important people with diabetes take up cancer screening programs.
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There are several possible explanations for the link between diabetes and dementia. First, strokes are more common in people with type 2 diabetes, and both major and repeated mini-strokes can lead to dementia.

Second, diabetes affects the structure and function of the smallest blood vessels throughout the body (the capillaries), including in the brain. This may impair the delivery of nutrients to a person’s brain cells.

Third, high glucose levels and other metabolic disturbances associated with diabetes may, over time, directly affect the way certain types of brain cells function.

Room for improvement

Despite well-established recommendations for the management of type 2 diabetes, such as guidelines for medication use, healthy diet and regular physical activity, there remains a significant gap between the evidence and what happens in practice.

A study from the US showed only one in four patients with type 2 diabetes met all the recommended targets for healthy levels of glucose, cholesterol and blood pressure.

Australian data has shown having diabetes is associated with 14% increased likelihood of discontinuing cholesterol medication after one year.

In our report, we showed increasing the use of a range of effective medications would prevent many hundreds of people with diabetes developing heart disease, strokes and kidney failure each year.




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With the burden of diabetes complications in our community casting such a large shadow in terms of death rates, disability and impact on the health system, we need greater education and support for people with living diabetes, as well as health professionals treating the condition.

For people with type 2 diabetes, close monitoring for other diseases such as cancer through screening programs is particularly important.

And alongside managing their blood sugar levels, it’s essential Australians with type 2 diabetes are supported to keep risk factors for complications, such as blood pressure and cholesterol, at healthy levels.

A healthy diet and regular physical activity is a good place to start.The Conversation

Rachel Climie, Exercise Physiologist and Research Fellow, Baker Heart and Diabetes Institute and Jonathan Shaw, Deputy Director, Baker Heart and Diabetes Institute

This article is republished from The Conversation under a Creative Commons license. Read the original article.

Donald Trump is taking hydroxychloroquine to ward off COVID-19. Is that wise?


Teresa G. Carvalho, La Trobe University

The White House’s confirmation that US President Donald Trump has been taking hydroxychloroquine every day for the past two weeks, with his doctor’s blessing, has reignited the controversy over the drug. It has long been used against malaria but has not been approved for COVID-19.

Trump said he has “heard a lot of good stories” about hydroxychloroquine, and incorrectly claimed there is no evidence of harmful side-effects from taking it. His previous claims in March that the drug could be a “game changer” in the pandemic prompted many people, including Australian businessman and politician Clive Palmer, to suggest stockpiling and distribution of the drug to the public.

But the dangers of acting on false or incomplete health information were underlined by the death of an Arizona man in March after inappropriate consumption of the related drug chloroquine. It’s important to know the real science behind the touted health benefits.

How do these medicines work?

Hydroxychloroquine is an analogue of chloroquine, meaning both compounds have similar chemical structures and a similar mode of action against malaria. Both medications are administered orally and have common side-effects such as nausea, diarrhoea and muscle weakness. However, hydroxychloroquine is less toxic, probably because it is easier for the body to metabolise.

Chloroquine and hydroxychloroquine are listed by the World Health Organisation as an essential medicine. Both drugs have been used to treat malaria for more than 70 years, and hydroxychloroquine has also proved effective against auto-immune diseases such as systemic lupus erythematosus and rheumatoid arthritis. The US Food and Drug Administration has approved both chloroquine and hydroxychloroquine for treating malaria, but not for COVID-19.




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We don’t know exactly how these drugs work to combat the malaria parasite. But we know chloroquine disrupts the parasite’s digestive enzymes by altering the pH inside the parasite cell, presumably effectively starving it to death.

Malaria parasites and coronaviruses are very different organisms. So how can the same drugs work against both? In lab studies, chloroquine hinders replication of the SARS coronavirus, apparently by changing the pH inside particular parts of human cells where the virus replicates.

This offers a glimmer of hope that these pH changes inside cells could hold the key to thwarting such different types of pathogens.

Is it OK to repurpose drugs like this?

Existing drugs can be extremely valuable in an emergency like a pandemic, because we already know the maximum dose and any potential toxic side-effects. This gives us a useful basis on which to consider using them for a new purpose. Chloroquine is also cheap to manufacture, and has already been widely used in humans.

But we shouldn’t be complacent. There are significant gaps in our understanding of the biology of SARS-CoV-2, which causes COVID-19, because it is a brand new virus. There is a 20% genetic difference between SARS-CoV-2 and the previous SARS coronavirus, meaning we should not assume a drug shown to act against SARS will automatically work for SARS-CoV-2.

Widely used, but with common side effects.
Gary L. Hider/Shutterstock

Even in its primary use against malaria, long-term chloroquine exposure can lead to increased risks such as vision impairment and cardiac arrest. Hydroxychloroquine offers a safer treatment plan with reduced tablet dosages and lessened side-effects. But considering their potentially lethal cardiovascular side-effects, these drugs are especially detrimental to those who are overweight or have pre-existing heart conditions. Despite the urgent need to confront COVID-19, we need to tread carefully when using existing medicines in new ways.

Any medication that has not been thoroughly tested for the disease in question can have seriously toxic side-effects. What’s more, different diseases may require different doses of the same drug. So we would need to ensure any dose that can protect against SARS-CoV-2 would actually be safe to take.

The evidence so far

Although many clinical trials are under way, there is still not enough evidence chloroquine and hydroxychloroquine will be useful against COVID-19. The few trials completed and published so far, despite claiming positive outcomes, have been either small and poorly controlled or lacking in detail.

A recent hydroxychloroquine trial in China showed no significant benefits for COVID-19 patients’ recovery rate. A French hydroxychloroquine trial was similarly discouraging, with eight patients prematurely discontinuing the treatment after heart complications.

The fascination with chloroquine and hydroxychloroquine has also adversely affected other drug trials. Clinical trials of other possible COVID-19 treatments, including HIV drugs and antidepressants, have seen reduced enrolments. Needless to say, in a pandemic we should not be putting all our eggs in one basket.

Then there is the issue of chloroquine hoarding, which not only encourages dangerous self-medication, but also puts malaria patients at greater risk. With malaria transmission season looming in some countries, the anticipated shortage of chloroquine and hydroxychloroquine will severely impact current malaria control efforts.




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Overall, despite their tantalising promise as antiviral drugs, there isn’t enough evidence chloroquine and hydroxychloroquine are safe and suitable to use against COVID-19. The current preliminary data need to be backed up by multiple properly designed clinical trials that monitor patients for prolonged periods.

During a pandemic there is immense pressure to find drugs that will work. But despite Trump’s desperation for a miracle cure, the risks of undue haste are severe.


This article was coauthored by Liana Theodoridis, an Honours student in Microbiology at La Trobe University.The Conversation

Teresa G. Carvalho, Senior Lecturer in Microbiology, La Trobe University

This article is republished from The Conversation under a Creative Commons license. Read the original article.

Aged care visitor guidelines balance residents’ rights and coronavirus risk – but may be hard to implement



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Yun-Hee Jeon, University of Sydney

One in four Australians who have died from COVID-19 is from an aged care facility.

These deaths show how fatal and fast the spread of the infection can be, and the extreme challenge of containing the virus once a positive case appears in aged care homes.

But there is also community pressure to ease social distancing rules for aged care residents and, for facilities that banned visits, to start allowing family members and friends to see their loved ones again.




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To address these concerns, on Friday the aged care sector and consumer advocacy organisations released a draft visitor access code. The code aims to meet the needs of residents to see their families and friends while minimising any risk of spreading COVID-19.

But putting the code into practice will require more staff time to implement them. And while additional funding is on its way, existing workforce shortages may mean a delay to boosting the front-line workforce.

Rights and responsibilities of residents and visitors

According to the code, visitors should be provided with regular updates and information about what’s happening in the facility.

They should also have the option to talk to their loved one via video conference or telephone calls to supplement in-person visits.

But they can’t visit while they have cold or flu symptoms. They must also have had their flu vaccination, wash their hands, remain in the resident’s room or designated area, and to call ahead before visiting. They may also have their temperature taken on arrival.

The code says residents should have access to video conferencing or phone calls.
Georg Arthur Pflueger /Unsplash

Each facility will create its own guidelines about where residents can have guests visit – whether it’s in a dedicated room, the resident’s room, a visiting window or something else.

Most visits should be brief. But residents in their final weeks of life and those with an established pattern of care from a family member or friend, for example to help them eat, should be allowed longer and/or more frequent visits.

The code states residents can continue to use public spaces in the facility, including outdoor spaces. But if there is an outbreak, they will need to be confined to their rooms.

Rights and responsibilities of providers

Facilities have the right to refuse entry to someone for a justifiable reason, and to move to lockdown if there is an outbreak.

They have a responsibility to ensure all staff have their flu shots, to facilitate video conferencing or phone calls with family and friends, and enable in-person visits.

These changes require more staff

All of these changes require additional staff to facilitate better communication, video conferencing and increased visits during the pandemic.

Use of new technologies requires a significant amount of staff time. Many residents would need help holding the phone or dialling the number, or using Zoom or Facetime and maintaining a video conversation online. For some residents, such technologies may be a whole new world of experience.




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Taking bookings for visit times and screening visitors for temperature, flu vaccination status and hand sanitising takes considerable staff time. As does escorting visitors to the room and back out of the facility while ensuring they’re keeping physical distance throughout.

Staff increases will take time to implement

Residential aged care has long experienced workforce problems, including high staff turnover, failure to attract staff with sufficient qualification and training, and leadership issues, to name a few.

A timely and effective response to the COVID-19 outbreak is likely to be hampered by the sector’s existing challenges.

Implementing the guidelines will take up more staff time.
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The Australian government, as the primary funder and regulator of the aged care system, has promised to inject more than A$850 million into the aged care sector in response to the COVID-19 pandemic to:

  • address workforce issues, through staff up-skilling, boosting numbers and helping to retain staff
  • support new services such as telehealth and the use of technologies to help residents and their families and friends communicate
  • continue to improve quality and safety.

However, it’s likely to take some time to see the real effect of this funding on the ground and across the whole sector.




Read more:
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The draft code is a positive step in addressing some confusion around social distancing measures in aged care homes. Many providers have already been implementing the principles in the code, and beyond. But some haven’t.

Hopefully the code will be more broadly and consistently practised by all aged care providers.

Public consultations about the code are underway and close 3pm Thursday May 7. If you are a family member or friend of someone living in aged care, or you’re an aged care provider or staff member, you can raise concerns or views about the code here. The code is due to be finalised on May 11.The Conversation

Yun-Hee Jeon, Susan and Isaac Wakil Professor of Healthy Ageing, University of Sydney

This article is republished from The Conversation under a Creative Commons license. Read the original article.

People with coronavirus are at risk of blood clots and strokes. Here’s what we know so far



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Karlheinz Peter, Baker Heart and Diabetes Institute; Hannah Stevens, Baker Heart and Diabetes Institute, and James McFadyen, Baker Heart and Diabetes Institute

As well as causing severe respiratory problems, there is mounting evidence COVID-19 causes abnormalities in blood clotting. Patients with severe COVID-19 infection appear to be at greater risk of developing blood clots in the veins and arteries.

Blood clots can occur deep in the veins of the leg (deep vein thrombosis) and can move to the lungs, causing a pulmonary embolism, which restricts blood flow and oxygen, and can be fatal.




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Blood clots in arteries can cause heart attacks when they block blood supply to the heart, or strokes when they block oxygen supply to the brain.

So what is going on in the bodies of people with coronavirus? And what are clinicians doing to treat or prevent this complication?

What do these clots do?

Recent data from the Netherlands and France suggest that of the patients with coronavirus who are admitted to intensive care units (ICU), 30-70% develop blood clots in the deep veins of the legs, or in the lungs.

Around one in four coronavirus patients admitted to ICU will develop a pulmonary embolism.

These rates are much higher than we would usually see in patients requiring admission to ICU for reasons other than COVID-19.

Greater risk of stroke

Patients who present to hospital with COVID-19 are also more likely to have a stroke when compared with the general population.

Typically, the chance of having a stroke is associated with increasing age, as well as other risk factors such as high blood pressure, elevated cholesterol levels, or smoking.

Usually it’s older people who have strokes.
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However, higher rates of strokes in patients with COVID-19 is somewhat unusual because it also seems to be happening in people under 50 years of age, with no other risk factors for stroke.

Low levels of oxygen

COVID-19 also appears to be associated with blood clots in the tiny blood vessels that are important for the transfer of oxygen in organs. Autopsy reports have shown elements of SARS-CoV-2, the virus causing COVID-19, in cells lining these small blood vessels in the lungs, kidney, and gut.

This may result in tiny blood clots in these small blood vessels that disturb normal blood flow and the ability of the blood to deliver oxygen to these organs.




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Importantly, these small blood clots could reduce normal lung function. If these small blood clots reach the lungs it may prevent oxygen getting into the blood as efficiently as normal. This may explain why patients with severe COVID-19 can have very low oxygen levels.

Treating and diagnosing clots is difficult

When patients are admitted to hospital, for coronavirus or any other condition that leaves them bed-bound, it is common practice to administer low-dose blood thinners to prevent the development of blood clots.

However, given that patients with COVID-19 seem to be at a higher risk of developing blood clots, it’s currently being debated whether higher doses of blood thinners are required to prevent these clotting complications.

Trials are underway to attempt to answer this important question.

Higher doses of blood thinners might one day play a role in treating COVID-19.
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Diagnosing these blood clots in patients with COVID-19 can also be particularly challenging.

Firstly, the symptoms of a worsening lung infection associated with the virus can be indistinguishable from the symptoms of a pulmonary embolism.

Another challenge in COVID-19 is that the virus can impact laboratory tests which may also be used to diagnose venous blood clots.

A good example of this is a test called D-dimer, which is a measure of clotting in the body. Normally, this test would be higher in almost everyone with new venous blood clots. However, people with severe COVID-19 infection can also have an elevated D-dimer simply due to the severe infection.

In some patients, this means that the test is no longer helpful to diagnose blood clots.

Why does COVID-19 cause blood clotting?

One theory is that the increased rate of blood clots in COVID-19 is simply a reflection of being particularly unwell and immobile.

However, the current data suggest the risk of blood clots is significantly greater in patients with COVID-19 than what is usually see in patients admitted to hospital and ICUs.

We still don’t know why clotting occurs.
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Another potential explanation is that the virus is directly impacting on the cells lining our blood vessels. When the body fights an infection, the immune system becomes activated to try and kill the invader, and research shows an activated immune system can cause blood clots.

In severe COVID-19, the immune system appears to go into overdrive. This could lead to the unchecked activation of cells that typically stop blood clotting.




Read more:
Coronavirus ‘cytokine storm’: this over-active immune response could be behind some fatal cases of COVID-19


Another possibility is that the virus triggers blood clotting to provide it with a survival advantage.

The SARS virus, another member of the coronavirus family, can be further “activated” by a blood clotting protein, enabling the virus to more efficiently invade cells.

However, whether this is the case with COVID-19 remains to be investigated.

Intriguingly, preliminary research suggests that a commonly used blood thinner, heparin, may have antiviral effects by binding to SARS-CoV-2 and inhibiting a key protein the virus uses to latch onto cells.

What we know for sure is that blood-clotting complications are rapidly emerging as a significant threat from COVID-19. In this area, we still have much to learn about the virus, how it affects blood clotting, and the best options for prevention and treatment of these blood clots.The Conversation

Karlheinz Peter, Lab Head, Atherothrombosis and Vascular Biology and Deputy Director, Baker Heart and Diabetes Institute; Interventional Cardiologist, Alfred Hospital; Professor of Medicine and Immunology, Monash University, Baker Heart and Diabetes Institute; Hannah Stevens, Haematologist and PhD student, Baker Heart and Diabetes Institute, and James McFadyen, Research Fellow, Baker Heart and Diabetes Institute, Haematologist, Alfred Hospital, Baker Heart and Diabetes Institute

This article is republished from The Conversation under a Creative Commons license. Read the original article.