Having trouble sleeping? Here’s the science on 3 traditional bedtime remedies



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Nenad Naumovski, University of Canberra; Amanda Bulman, University of Canberra; Nathan M D’Cunha, University of Canberra, and Wolfgang Marx, Deakin University

Sleep is essential for good health. Poor sleep quality, or not enough sleep, can negatively affect our mood, cognitive function, and immune system.

Stress can impact our sleep, and stress and anxiety associated with the COVID pandemic have meant many of us are not sleeping as well as we used to. A survey of 2,555 people across 63 countries found 47% of people were experiencing poorer sleep than usual during the pandemic, compared with 25% before COVID hit.

We also know stress is associated with poor dietary habits. People who are feeling stressed and tired may be more likely to reach for energy drinks and caffeinated beverages. But a high intake of caffeine as well as sugar-sweetened and energy drinks can keep us awake. So it’s something of a vicious cycle.

Similarly, people who are feeling stressed may be more likely to drink alcohol. Alcohol before bed, especially in excess, can also disrupt our sleep.

So what can you drink to improve your sleep?

Chamomile

Chamomile tea has been used in traditional medicine for centuries to treat a range of sleep ailments, such as insomnia.

The plant extract contains apigenin, a chemical compound that binds to the same receptors in the brain as benzodiazepines (drugs used to treat anxiety and insomnia), producing a sedative effect.




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Studies have shown chamomile (consumed in the form of an extract or a tea) leads to significant improvement in sleep quality.

However, although the evidence is positive, these studies were relatively small and we need larger, well-designed clinical trials to reinforce these observations.

A pot of chamomile tea.
If you’re having trouble sleeping, it might be worth trying a cup of chamomile tea before bed.
Irene Ivantsova/Unsplash

Milk

A warm cup of cow’s milk is a popular bedtime beverage in Western cultures, particularly for children.

Milk is a source of the essential amino acid tryptophan, which our bodies need to produce compounds including serotonin and melatonin in the brain. These compounds are involved in the sleep-wake cycle, which could explain why milk helps us sleep better — if indeed it does.

Scientists have studied the effects of milk and milk products (such as yogurt and cheese) on sleep quality for decades, but the evidence is still inconclusive.

It may simply be the ritual of drinking warm milk before bedtime that relaxes the brain and body, rather than the effects of compounds present in the milk itself. We’ll need more research evidence before we can be confident one way or the other.




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Cocoa

Hot cocoa (commonly dissolved in milk) is also regarded as a sleep-promoting drink. The cocoa bean is a rich source of many beneficial chemicals, including compounds called flavonoids.

Flavonoids have a range of potential health benefits, and may be used to treat some neurodegenerative disorders.

There’s limited research on the effects of cocoa on sleep quality. But a study in mice suggested natural cocoa may improve stress-induced insomnia.

In humans, consuming cocoa is associated with a reduction in blood pressure (in healthy people and those with high blood pressure). This lowering of blood pressure, which relaxes the smooth muscles that line our arteries, could produce a calming effect, making it easier to go to sleep.

A man sits on the couch reading a newspaper, with a mug in hand.
Some people like to drink a glass of milk or a cup of cocoa before bed.
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While these sleep remedies are unlikely to be harmful, the overall evidence on improvement in quality of sleep is weak. You may like to try them, but you shouldn’t see any of them as a quick fix.

At the end of the day, several lifestyle factors can influence our sleep quality, including screen time, physical activity, stress and diet.

If you are consistently struggling to sleep, it’s best to consult with your general practitioner.




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Why our brain needs sleep, and what happens if we don’t get enough of it


The Conversation


Nenad Naumovski, Associate Professor in Food Science and Human Nutrition, University of Canberra; Amanda Bulman, PhD Candidate, University of Canberra; Nathan M D’Cunha, PhD Candidate, University of Canberra, and Wolfgang Marx, Postdoctoral research fellow, Deakin University

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

Catching COVID from surfaces is very unlikely. So perhaps we can ease up on the disinfecting



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Hassan Vally, La Trobe University

A lot has happened over the past year, so you can be forgiven for not having a clear memory of what some of the major concerns were at the beginning of the pandemic.

However, if you think back to the beginning of the pandemic, one of the major concerns was the role that surfaces played in the transmission of the virus.

As an epidemiologist, I remember spending countless hours responding to media requests answering questions along the lines of whether we should be washing the outside of food cans or disinfecting our mail.

I also remember seeing teams of people walking the streets at all hours wiping down poles and cleaning public benches.

But what does the evidence actually say about surface transmission more than 12 months into this pandemic?

Before addressing this, we need to define the question we’re asking. The key question isn’t whether surface transmission is possible, or whether it can occur in the real world — it almost certainly can.

The real question is: what is the extent of the role of surface contact in the transmission of the virus? That is, what is the likelihood of catching COVID via a surface, as opposed to other methods of transmission?

The evidence is minimal

There’s little evidence that surface transmission is a common way in which the coronavirus is spread. The main way it’s spread is by the air, either by larger droplets via close contact, or by smaller droplets called aerosols. As a side note, the relative role these two routes play in transmission is probably a much more interesting and important question to clarify from a public health perspective.

One of the best commentaries on COVID surface transmission was published in the journal Lancet Infectious Diseases in July 2020 by Emanuel Goldman, a professor of microbiology from the United States.

As he described, one of the drivers for the exaggerated perception of the risk of surface transmission was the publication of a number of studies showing SARS-CoV-2 viral particles could be detected for long periods of time on various surfaces.

You probably saw these studies because they received enormous publicity worldwide and I remember doing numerous interviews in which I had to explain what these findings actually meant.

As I explained at the time, these studies could not be generalised to the real world, and in some instances the media releases accompanying them tended towards overstating the significance of these findings.

The key issue is that as a general principal the time required for a population of microoganisms to die is directly proportional to the size of that population. This means the greater the amount of virus deposited on a surface, the longer you will find viable viral particles on that surface.

So in terms of designing experiments that are relevant to public health, one of the more important variables in these studies is the amount of virus deposited on a surface — and the extent to which this approximates what would happen in the real world.

If you understand this, it becomes apparent that a number of these virus survival studies stacked the odds of detecting viable virus by depositing large amounts of virus on surfaces far in excess of what would be reasonably expected to be found in the real world. What’s more, some of these studies customised conditions that would extend the life of viral particles, such as adjusting humidity and excluding natural light.

Although there was nothing wrong with the science here, it was the real world relevance and the interpretation that was amiss at times. It’s notable that other studies which more closely replicated real world scenarios found less impressive survival times for three other human coronaviruses (including SARS).

It’s important to note we’re relying on indirect evidence in assessing the role of surface transmission for the coronavirus. That is, you can’t actually do an ethical scientific experiment that confirms the role surface transmission plays because you’d have to deliberately infect people. Despite being such a seemingly straightforward question, it’s surprisingly difficult to determine the relative importance of the various transmission pathways for this virus.

What we have to do instead is look at all of the evidence we do have and see what it’s telling us, including case studies describing transmission events. And if we do this, there isn’t a lot out there to support surface transmission being of major importance in the spread of COVID.

We could save a lot of time and money

We need to put the risks of exposure to SARS-CoV-2 via the various modes of transmission into perspective, so we focus our limited energy and resources on the right things.

This isn’t to say surface transmission isn’t possible and that it doesn’t pose a risk in certain situations, or that we should disregard it completely. But, we should acknowledge the threat surface transmission poses is relatively small.

We can therefore mitigate this relatively small risk by continuing to focus on hand hygiene and ensuring cleaning protocols are more in keeping with the risk of surface transmission.

In doing this, we can potentially save millions of dollars being spent on obsessive cleaning practices. These are probably providing little or no benefit and being done solely because they’re easy to do and provide the reassurance of doing something, thereby relieving some of our anxieties.The Conversation

Hassan Vally, Associate Professor, La Trobe University

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

I was the Australian doctor on the WHO’s COVID-19 mission to China. Here’s what we found about the origins of the coronavirus


Dominic Dwyer, University of Sydney

As I write, I am in hotel quarantine in Sydney, after returning from Wuhan, China. There, I was the Australian representative on the international World Health Organization’s (WHO) investigation into the origins of the SARS-CoV-2 virus.

Much has been said of the politics surrounding the mission to investigate the viral origins of COVID-19. So it’s easy to forget that behind these investigations are real people.

As part of the mission, we met the man who, on December 8, 2019, was the first confirmed COVID-19 case; he’s since recovered. We met the husband of a doctor who died of COVID-19 and left behind a young child. We met the doctors who worked in the Wuhan hospitals treating those early COVID-19 cases, and learned what happened to them and their colleagues. We witnessed the impact of COVID-19 on many individuals and communities, affected so early in the pandemic, when we didn’t know much about the virus, how it spreads, how to treat COVID-19, or its impacts.

We talked to our Chinese counterparts — scientists, epidemiologists, doctors — over the four weeks the WHO mission was in China. We were in meetings with them for up to 15 hours a day, so we became colleagues, even friends. This allowed us to build respect and trust in a way you couldn’t necessarily do via Zoom or email.

This is what we learned about the origins of SARS-CoV-2.

Animal origins, but not necessarily at the Wuhan markets

It was in Wuhan, in central China, that the virus, now called SARS-CoV-2, emerged in December 2019, unleashing the greatest infectious disease outbreak since the 1918-19 influenza pandemic.

Our investigations concluded the virus was most likely of animal origin. It probably crossed over to humans from bats, via an as-yet-unknown intermediary animal, at an unknown location. Such “zoonotic” diseases have triggered pandemics before. But we are still working to confirm the exact chain of events that led to the current pandemic. Sampling of bats in Hubei province and wildlife across China has revealed no SARS-CoV-2 to date.

We visited the now-closed Wuhan wet market which, in the early days of the pandemic, was blamed as the source of the virus. Some stalls at the market sold “domesticated” wildlife products. These are animals raised for food, such as bamboo rats, civets and ferret badgers. There is also evidence some domesticated wildlife may be susceptible to SARS-CoV-2. However, none of the animal products sampled after the market’s closure tested positive for SARS-CoV-2.

We also know not all of those first 174 early COVID-19 cases visited the market, including the man who was diagnosed in December 2019 with the earliest onset date.

However, when we visited the closed market, it’s easy to see how an infection might have spread there. When it was open, there would have been around 10,000 people visiting a day, in close proximity, with poor ventilation and drainage.

There’s also genetic evidence generated during the mission for a transmission cluster there. Viral sequences from several of the market cases were identical, suggesting a transmission cluster. However, there was some diversity in other viral sequences, implying other unknown or unsampled chains of transmission.

A summary of modelling studies of the time to the most recent common ancestor of SARS-CoV-2 sequences estimated the start of the pandemic between mid-November and early December. There are also publications suggesting SARS-CoV-2 circulation in various countries earlier than the first case in Wuhan, although these require confirmation.

The market in Wuhan, in the end, was more of an amplifying event rather than necessarily a true ground zero. So we need to look elsewhere for the viral origins.




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Frozen or refrigerated food not ruled out in the spread

Then there was the “cold chain” hypothesis. This is the idea the virus might have originated from elsewhere via the farming, catching, processing, transporting, refrigeration or freezing of food. Was that food ice cream, fish, wildlife meat? We don’t know. It’s unproven that this triggered the origin of the virus itself. But to what extent did it contribute to its spread? Again, we don’t know.

Several “cold chain” products present in the Wuhan market were not tested for the virus. Environmental sampling in the market showed viral surface contamination. This may indicate the introduction of SARS-CoV-2 through infected people, or contaminated animal products and “cold chain” products. Investigation of “cold chain” products and virus survival at low temperatures is still underway.




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Extremely unlikely the virus escaped from a lab

The most politically sensitive option we looked at was the virus escaping from a laboratory. We concluded this was extremely unlikely.

We visited the Wuhan Institute of Virology, which is an impressive research facility, and looks to be run well, with due regard to staff health.

We spoke to the scientists there. We heard that scientists’ blood samples, which are routinely taken and stored, were tested for signs they had been infected. No evidence of antibodies to the coronavirus was found. We looked at their biosecurity audits. No evidence.

We looked at the closest virus to SARS-CoV-2 they were working on — the virus RaTG13 — which had been detected in caves in southern China where some miners had died seven years previously.

But all the scientists had was a genetic sequence for this virus. They hadn’t managed to grow it in culture. While viruses certainly do escape from laboratories, this is rare. So, we concluded it was extremely unlikely this had happened in Wuhan.




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A team of investigators

When I say “we”, the mission was a joint exercise between the WHO and the Chinese health commission. In all, there were 17 Chinese and ten international experts, plus seven other experts and support staff from various agencies. We looked at the clinical epidemiology (how COVID-19 spread among people), the molecular epidemiology (the genetic makeup of the virus and its spread), and the role of animals and the environment.

The clinical epidemiology group alone looked at China’s records of 76,000 episodes from more than 200 institutions of anything that could have resembled COVID-19 — such as influenza-like illnesses, pneumonia and other respiratory illnesses. They found no clear evidence of substantial circulation of COVID-19 in Wuhan during the latter part of 2019 before the first case.

Where to now?

Our mission to China was only phase one. We are due to publish our official report in the coming weeks. Investigators will also look further afield for data, to investigate evidence the virus was circulating in Europe, for instance, earlier in 2019. Investigators will continue to test wildlife and other animals in the region for signs of the virus. And we’ll continue to learn from our experiences to improve how we investigate the next pandemic.

Irrespective of the origins of the virus, individual people with the disease are at the beginning of the epidemiology data points, sequences and numbers. The long-term physical and psychological effects — the tragedy and anxiety — will be felt in Wuhan, and elsewhere, for decades to come.




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The Conversation


Dominic Dwyer, Director of Public Health Pathology, NSW Health Pathology, Westmead Hospital and University of Sydney, University of Sydney

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

Can I choose what vaccine I get? What if I have allergies or side-effects? Key COVID vaccine rollout questions answered


Marc Pellegrini, Walter and Eliza Hall Institute

Australia’s keenly awaited COVID vaccine rollout begins today, with the ultimate goal of vaccinating all Australians by October.

Here are the answers to some key questions.

Can I choose which vaccine I get?

No, there won’t be a choice for the average person. The current initial rollout of the Pfizer vaccine isn’t enough doses to vaccinate all of Australia. So the first people vaccinated with the Pfizer vaccine will be frontline health-care workers, including aged care and hotel quarantine officers.

The AstraZeneca vaccine will be produced for the general public. It’s hoped that will be rolled out during March.

I can’t say how the logistics will run — that’s up to the government, presumably on a state-by-state basis. Most likely they will try to prioritise the highest-risk groups such as the elderly and people with chronic health conditions.

For most people it will be a case of waiting for further announcements as to when enough vaccine is available and it’s appropriate to make an appointment. Children are unlikely to be included in the vaccination program.

Infographic on COVID vaccine rollout

The Conversation, CC BY

How will I be monitored for side-effects?

As doctors, when we vaccinate people we generally like to look after them for about 15-30 minutes, just to check they haven’t had an adverse reaction. That should be the practice for the COVID jab, just the same as for any vaccine.

For those 15-30 minutes you will generally just be sitting in a waiting area at the clinic. You will be monitored to see if you develop any symptoms such as hives or a rash, or wheezing. In those cases you would be monitored even more carefully and staff would take your blood pressure and pulse rate.

If you experience any symptoms once you’ve gone home, it would be up to you to contact your local doctor. Obviously, when trying to vaccinate 25 million people, health authorities can’t follow up with every individual. It’s very much up to them to follow up with whoever gave them the vaccine — whether their GP clinic or other health service.




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Should I still have the vaccine if I have an allergy?

That needs to be a conversation between individuals and their doctor, who can advise on a case-by-case basis. But, generally speaking, there are no common allergies that should stop you having a COVID vaccine. If someone has a peanut allergy they can have the vaccine, and the same goes for shellfish, wheat, eggs or any other common allergies.

Some people are allergic to an ingredient called polyethylene glycol, or PEG, which is found in more than 1,000 different medications and is used in the Pfizer vaccine as a mechanism to help deliver the viral mRNA (genetic material) into your cells. In the US and UK vaccine rollouts, a very small proportion of people seemed to have an allergy to this compound: with a million doses you might see about ten people have this allergic reaction. It is rare, albeit less rare than allergic reactions to influenza vaccines.

But no one has yet died from being vaccinated against COVID, so these cases are being captured effectively and are generally detected within the initial observation period of 15-30 minutes. Severe reactions can be treated with an epipen; less severe cases are just monitored.

People might already know they’re allergic to PEG and they shouldn’t receive the Pfizer vaccine, but if they don’t know, there’s no way of knowing that in advance.




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The Oxford/AstraZeneca vaccine doesn’t contain PEG. It contains a related compound called polysorbate, which appears not to trigger the same allergy. If you have a known allergy to PEG you would probably be given the AstraZeneca vaccine.

It’s important to stress that these compounds are not preservatives — they are mechanisms to deliver the vaccines effectively.

Will I be fully protected? Do I still need to follow COVID restrictions?

The two vaccines have different efficacy rates — 95% for Pfizer, 62% for AstraZeneca — but these refer to their ability to prevent infection rather than disease. The fact is both are very good at preventing serious disease.

This means that, although you may still have a chance of being infected, you are much less likely to develop severe symptoms, and therefore less likely to infect others. Someone with severe COVID might be coughing and spluttering and spreading the virus more easily, while someone without symptoms might not.

Bear in mind there are two main reasons for the vaccine rollout. The first is to protect members of the public from getting very ill or dying.

The second aim is to provide a degree of immunity in the general population that will ultimately stop the virus circulating.

Of course, this second goal is much harder, which is why it’s still important that we follow any and all COVID precautions. But the hope is that over time we’ll see fewer and fewer people who are COVID-positive, and the risk of spread will fall.

Federal government information on the vaccine rollout.

Will the vaccine last forever or will I need to be revaccinated in future?

The current COVID vaccines require two doses, several weeks apart. It’s very tricky to say how long the resulting immunity will last, because globally we have only had these vaccines in use since December or so. It’s possible the immunity might last a year or longer, but at the moment it’s unclear. People might well have to be revaccinated at some stage.

We’ll start to get that data soon though. In fact we should have plenty more information by the time the AstraZeneca vaccine starts to be administered in high numbers in Australia around June or July.




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Will the vaccines work against mutant coronavirus strains?

In the fullness of time I expect we’ll start to see “escaped mutant” variants of the coronavirus that can evade the vaccine or make it less effective.

To an extent that’s happened already — the AstraZeneca vaccine looks to be less effective against the South African variant than against the other current variants. Having said that, although it’s not as effective at preventing infection, it still probably has a good chance of stopping you getting seriously sick.

Because we’re not vaccinating everyone in the world, there will always be a pool of people who can incubate new viral strains, potentially giving rise to new mutant variants.

There’s no doubt the vaccines will need to be updated from time to time to deal with this.

Thankfully this process will be relatively straightforward. mRNA vaccines such as Pfizer’s can be tweaked very quickly – virtually overnight – to accommodate new mutants. It’s a bit trickier with non-mRNA vaccines such as the AstraZeneca and Chinese vaccines, but it can still be done.

Will the vaccine rollout mean no more lockdowns?

The vaccine rollout should give us a much firmer handle on the spread of the virus. We can hope to stop seeing hotel quarantine workers being infected and spreading the virus outside, which is what has prompted the recent snap lockdowns in various Australian cities.

As for whether we’ll ever find ourselves in lockdown again, well, we’ll just have to wait and see. But if we’re still persisting with hotel quarantine and hosting arrivals from overseas, the vaccine program will hopefully mean we can afford to be much more liberal with opening our borders without fear that the virus will run rife.




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The Conversation


Marc Pellegrini, Researcher, Walter and Eliza Hall Institute

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

How do we know the COVID vaccine won’t have long-term side-effects?



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Samantha Carlson, Telethon Kids Institute; Christopher Blyth, University of Western Australia; Lucy Deng, University of Sydney; Margie Danchin, Murdoch Children’s Research Institute, and Nicholas Wood, University of Sydney

As Australia’s COVID-19 vaccine rollout begins this week, many people still have questions about the safety of COVID-19 vaccines, both in the short and long term.

As vaccine experts, we hear these concerns all the time, and it’s normal to have questions about a vaccine.

The good news is that scientists have already been testing COVID-19 vaccines for months. For starters, serious side-effects are very, very rare. And, together with what we know about previous vaccines, if side-effects are going to occur, they usually happen within a few months after getting a vaccine. This is why international medical regulators, including Australia’s Therapeutic Goods Administration (TGA), require the first few months of safety data before approving new vaccines. This, plus information coming from vaccine recipients in the northern hemisphere, gives us confidence that COVID-19 vaccines are safe.

In fact, most side-effects occur within the first one or two days. And most of these are minor, such as pain at the injection site, fatigue or fever — which are signs your immune system is building a response against the thing you’ve been vaccinated against.

What do we know about long-term side effects?

Since December, more than 200 million people have received at least one dose of a COVID-19 vaccine worldwide — more than the total number of people who have been infected with the virus (112 million).

Given the sheer number of vaccines administered to date, common, uncommon and rare side-effects would have been detected by now. What’s more, we’ve been testing these vaccines in clinical trials since mid-2020, and both the Pfizer and AstraZeneca vaccines have shown excellent safety results.

This gives us confidence the vaccines that’ll be used around Australia are safe.

We’ve also seen some people raise concerns online about mRNA vaccines, such as the Pfizer-BioNTech vaccine, being a “new” technology. mRNA (or “messenger” RNA) is found in all living cells. mRNA is a message that tells cells how to make proteins that trigger the immune response inside the body. That immune response is what protects against infection if an individual is exposed to the virus. mRNA is not the same as DNA (your genes), and it cannot combine with our DNA to change our genetic code. mRNA vaccines do not affect or interact with DNA in any way. So we can be assured there’ll be no long-term DNA-altering effects from these vaccines.

What’s more, checking the safety of the vaccines doesn’t just stop after they’ve been registered for use. Once a vaccine has been introduced, ongoing monitoring of its safety is a crucial part of the vaccine development process.

Australia has a robust system for this ongoing monitoring. The system was established to detect any unexpected side-effects from vaccines (if they occur) and ensure they’re investigated promptly. This type of monitoring is standard practise in Australia for vaccines. The data about COVID-19 vaccination collected in these surveillance systems will be published weekly on the TGA website. This should reassure Australians that if there’s a new serious side-effect, we will know about it, communicate it, and act on it quickly.




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Withdrawal of vaccines after introduction to the general population is a very rare event.
In the United States, a rotavirus vaccine called Rotashield led to a small increase in the number of small intestinal blockages. This prompted its withdrawal in the late 1990s. In Australia, an increased risk of febrile seizures in young children following a specific influenza vaccine was identified in 2010. It was subsequently withdrawn from use in that age group, and we now vaccinate with a different, safer flu vaccine. This vaccine is no longer available in Australia, and has been subsequently reformulated.

Both of these side-effects were observed within weeks of vaccination.

We now have improved monitoring systems in Australia to detect such serious side-effects even sooner, in the general population after clinical trials, than we did a decade ago.

But what about short-term side-effects?

Pfizer-BioNTech COVID-19 vaccine

The expected side-effects of the Pfizer vaccine have been reported from trials involving roughly 43,000 participants aged 16 years and older from the US, Argentina, Brazil and South Africa. Half of the participants received the Pfizer vaccine and half received a placebo. And as part of COVID-19 vaccine rollouts around the world, millions of people have already been given this vaccine since December, meaning we have safety data now from both clinical trials and two months of “real world” vaccination.

For those receiving this vaccine in the large clinical trials which started in July 2020, about 80% have reported pain at the injection site. Other common side-effects included fatigue, headache, muscle pain, chills, joint pain and fever.

These were most often reported one or two days after the day of vaccination, and typically only lasted about one day. While some vaccine recipients may need a day off work due to some of these side-effects, this does not indicate the vaccine is unsafe.

In trials, no difference was seen in the rate of severe side-effects between the Pfizer vaccine and placebo. Early in the US program, 21 cases of anaphylaxis were reported. It’s estimated anaphylaxis occurs at a rate of 11 in every one million recipients (0.0011%) of the Pfizer COVID-19 vaccine. Most occurred within 15 minutes, and all patients recovered. This is why it’s a good idea though to remain at the vaccine clinic for up to 15 minutes after vaccination so that treatment and care can be provided if necessary.

A further concern was raised in January, after the death of 30 very frail elderly patients in Norway after receiving the Pfizer-BioNTech COVID-19 vaccine. But investigation by the European regulator concluded these weren’t related to the vaccine, but rather to underlying conditions present before vaccination.

Oxford-AstraZeneca COVID-19 vaccine

This vaccine has been tested in ongoing trials with around 55,000 participants from the United Kingdom, Brazil, South Africa and the US. About half received the Oxford-AstraZeneca vaccine and half a placebo. Millions of doses have been already been administered among the general population, particularly in the UK.

Data from four clinical trials which commenced in April 2020 in the UK, Brazil and South Africa, show the most common side-effects were pain at the injection site, fatigue, headache and muscle pain. Similar to the Pfizer vaccine, there was no difference in the rate of reported severe side-effects for the vaccine compared with the placebo.

Just 0.7% of participants (79 people) from the four clinical trials who received the Oxford-AstraZeneca vaccine reported a serious side-effect after receiving at least one dose, compared with 0.8% (89 people) of those in the placebo group. No additional safety concerns have been identified since the vaccination program began in the UK.




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If recommended a COVID-19 vaccine, take it

With countries continuing to monitor those who have received vaccines, we should be reassured there are no major safety concerns detected for serious side-effects so far. With millions of people vaccinated already, our confidence about the safety of COVID-19 vaccines is very high.

In Australia, and internationally, we have robust systems in place to continually monitor vaccine safety, ensuring Australians can be safely afforded the protection that COVID-19 vaccines are designed to provide.The Conversation

Samantha Carlson, Post Doctoral Research Officer, Telethon Kids Institute; Christopher Blyth, Paediatrician, Infectious Diseases Physician and Clinical Microbiologist, Telethon Kids Institute, University of Western Australia; Lucy Deng, Paediatrician, National Centre for Immunisation Research and Surveillance; Clinical Lecturer, Children’s Hospital Westmead Clinical School, University of Sydney; Margie Danchin, Associate Professor, University of Melbourne, Murdoch Children’s Research Institute, and Nicholas Wood, Associate Professor, Discipline of Childhood and Adolescent Health, University of Sydney

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

The $50 boost to JobSeeker will take Australia’s payment from the lowest in the OECD to the second-lowest after Greece



HARRYZH/Shutterstock

Peter Whiteford, Crawford School of Public Policy, Australian National University and Bruce Bradbury, UNSW

Fifty dollars sounds like a lot. But the increase in the JobSeeker unemployment benefit announced by Prime Minister Morrison on Tuesday is $50 per fortnight, which is just $25 per week. It will replace the temporary Coronavirus Supplement of $75 per week, which is itself well down on the $275 per week it began at in March last year.

It’s hard to see the increase as anything other than a cut, especially when coupled with another change which will allow recipients to earn other income of only $75 per week before JobSeeker gets cut. That’s down from the present $150 per week.

As the prime minister said, it’s better than it would have been if things returned to the level we had before special coronavirus provisions. At that time, recipients could earn only $53 per week before having their payment reduced.

But it’s not particularly generous. The Age and Sydney Morning Herald are quoting senior government sources as saying the $50 per fortnight increase in the rate was the lowest figure the party believed would be palatable to the public.

Morrison justified the increase of $50 per fortnight – rather than $150 (which would have kept what’s left of the coronavirus boost in place) or $100 or any other figure – by saying it will bring the payment to

41.2% of the national minimum wage, which puts us back in the realm of where we had been previously

Taking account of taxes paid and superannuation received by minimum wage workers gives a slightly higher replacement rate of 42.3%. That takes it back to roughly where it was at the end of the Howard government in 2007.

However, there’s no readily apparent reason why that should be a benchmark.

During the life of the Howard government the level of the single payment fell from around 50% of the minimum wage to 42%, meaning what’s proposed will return it to its lowest point relative to other benefits under Howard.


JobSeeker and age pension as a proportion of the minimum wage 1990-2021

Notes: Rates for single adult shown relative to net income when receiving a full-time minimum wage (deducting tax and Medicare levy, and adding employer superannuation contribution). Any casual loading not included. Rates shown at first of each month. Any rent assistance not included. Poverty line is half of median equivalised household income for non self-employed workers. Rates include coronavirus supplement and energy supplement, future rates are estimates.


Morrison also said the increase was the largest permanent increase in the unemployment benefit since 1986. It’s an increase of 9.7%.

During the Hawke and Keating administrations, the payment increased 23% in real terms. During the Whitlam administration it increased 50%. This means that while what’s offered is substantial by the standards of recent decades, it’s less so in the longer run.

But what about the supplements?

Morrison also argued in his press conference JobSeeker is more adequate than the base rate would suggest because

on top of that, if they’re receiving Commonwealth Rent Assistance, that payment would increase to $760.40; and on top of that, the average value of stand-alone supplements, the energy supplement and so on, is an additional $13.03. So the suggestion that anyone who was on JobSeeker is simply on that payment alone and there aren’t additional supports that are provided is not correct.

It’s true all people on income support receive the energy supplement (included in the figure above). But for a single person on JobSeeker, the supplement is only $8.80 per fortnight or less than 65 cents a day.

Many people do indeed get rent assistance, but after paying rent they become worse off rather than better off.

That’s because to get the maximum rate of rent assistance for a single person of $140 per fortnight (9% of the minimum wage), that person has to be paying around $310 per fortnight in rent. If that person is paying more, they get no extra help. The maximum is also lower for people in shared accommodation.

Private sector renters are amongst the worst off recipients of income support.




Read more:
Top economists want JobSeeker boosted $100+ per week, tied to wages


Other supplements such as the remote area allowance are indeed available, but are of no help to people who do not live in remote areas and may be inadequate to cover the higher costs involved. Supplements for help with language and literacy are only paid to people in special educational programmes.

Producing an average that includes supplementary payments most people don’t receive is inherently misleading.

How Australia compares

Net replacement rates measure the proportion of previous in-work income that is maintained after several months of unemployment. They are the benchmark used by the the prime minister to compare benefits to the minimum wage.

Using two months in unemployment as the measuring point (and using the most recently published 2019 rankings) before the pandemic, Australia’s replacement rate was the lowest in the OECD — even after rental assistance was added in.


Unemployment benefit, share of previous income after two months

Net replacement rates in unemployment including rent assistance, 2019 or latest available data.
OECD.Stat

When the maximum rate of Coronavirus Supplement was briefly in force in 2020, Australia moved to around the OECD average.

The new rate from April 2021 will move Australia from the lowest to the second lowest, ahead of Greece only.


Unemployment benefit, share of previous income, after Australian increase

Net replacement rates in unemployment including rent assistance after two months, 2019 or latest available data.
OECD.Stat

It should be acknowledged Australia’s system is based on different principles to many other OECD countries in which workers and their employers make contributions to and withdrawals from unemployment insurance.




Read more:
$50 a fortnight rise in JobSeeker comes with tougher job search requirements


But the difference in philosophy does not change the brutal reality that when Australian workers lose their job, their incomes fall more than in almost any other high income country.

Even after what the government has trumpeted as a historic increase, there will be few developed countries where people will be as worse off after losing work. Any permanent increase is welcome, but there is a long way to go.The Conversation

Peter Whiteford, Professor, Crawford School of Public Policy, Australian National University and Bruce Bradbury, Associate Professor, Social Policy Research Centre, UNSW

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

COVID’s mental health fallout will last a long time. Here’s how we’re targeting pandemic depression and anxiety



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Richard Bryant, UNSW

Although Australia is now largely COVID-free, the repercussions of the pandemic are ongoing.

As the pandemic enters its second year, many people will be continuing to suffer with poor mental health, or facing new mental health challenges.

The effects of recurrent lockdowns, fears about the effectiveness of the vaccines, restricted movement within and beyond Australia, and the bleak economic outlook are taking their toll on psychological well-being.

Now is the time to think about sustainable, evidence-based mental health programs that will serve Australians as we confront the mental fallout of the pandemic in 2021 and beyond.

The evidence is in

We now have incontrovertible evidence mental health has deteriorated during the pandemic. Large studies that assessed people’s mental health before and during COVID-19 have reported marked increases in anxiety, depression and post-traumatic stress since the pandemic began.

Although many experts predicted people with pre-existing mental disorders would be most vulnerable, we’ve seen even greater increases in psychological distress among those without a history of mental illness.

Unemployment and financial stress have exacerbated psychological problems during the pandemic. The major concern is that the increase in mental health problems will persist for years because of the economic downturn facing most nations.

Importantly, suicide rates increase during economic downturns. One study showed each 1% increase in unemployment was associated with a 1% increase in suicides.

The impact of unemployment and financial hardship on mental health is relevant for many Australians, as fears of reduced support from the JobSeeker and JobKeeper schemes loom. Although the government this week announced the JobSeeker payment will go up, welfare groups have warned it’s still not enough.




Read more:
Greater needs, but poorer access to services: why COVID mental health measures must target disadvantaged areas


So what can we do?

The question now facing many nations is how to manage the unprecedented number of people who may need mental health assistance. There are several challenges.

First, lockdowns, social isolation, and fear of infection impede the traditional form of receiving mental health care in clinics. These obstacles might now be greater in other countries with higher infection rates, but we’ve certainly seen these challenges in Australia over the past year.

Second, many people who have developed mental health conditions during the pandemic would never have had reason to seek help before, which can impede their motivation and ability to access care.

Third, many people experiencing distress will not have a clinical mental disorder, and in this sense, don’t require therapy. Instead, they need new skills to help them cope.




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Stressed out, dropping out: COVID has taken its toll on uni students


Since the pandemic began, there’s been widespread promotion of smartphone mental health apps as a remedy for our growing mental health problems.

While these programs often work well in controlled trials, in reality most people don’t download health apps, and even fewer continue using them. Further, most people who do use health apps are richer, younger, and often in very good health.

Evidence does suggest apps can play a role in delivering mental health programs, but they don’t represent the panacea to the current mental health crisis. We need to develop more effective programs that can be scaled up and delivered in an affordable manner.

One approach

A few years ago, the World Health Organization and the University of New South Wales (UNSW) jointly developed a mental health treatment program.

The program consisted of face-to-face group sessions teaching people affected by adversity new skills to manage stress more effectively. It has been shown to reduce anxiety and mood problems in multiple trials.

A young woman is on her laptop at home.
We’ve tailored a program to address the mental health challenges of the COVID pandemic.
Brooke Cagle/Unsplash

My team at UNSW has adapted this program during COVID-19 to specifically address the mental health needs of people affected by the pandemic. A clinical psychologist leads weekly sessions via video-conferencing over six weeks, with four participants in each group. The sessions cover skills to manage low mood, stress and worries resulting from the pandemic.

Typically, mental health programs have attempted to reduce negative mood and stress by using strategies that target problem areas. A newer approach, which we use in this program, focuses on boosting positive mood, and giving people strategies to optimally experience positive events and pleasure when faced with difficulties.

In controlled trials this strategy has effectively improved mental health outcomes, even more than a traditional program.

Trialling this tailored program around Australia in recent months, we’ve found it effectively improves mood and reduces stress. Although we haven’t yet published our results in a peer-reviewed journal, our preliminary data suggest the program results in a 20% greater reduction in depression than a control treatment (where we give participants resources with strategies to manage stress and mood).

This raises the possibility agencies could provide simple but effective programs like these to people anywhere in Australia. Delivering a program by video-conferencing means it can reach people in remote areas, and those not wishing to attend clinics.




Read more:
Is your mental health deteriorating during the coronavirus pandemic? Here’s what to look out for


One of the common patterns we’ve seen in previous disasters and pandemics is that once the immediate threat has passed, governments and agencies often neglect the longer-term mental health toll.

Now is the time to plan for the delivery of sustainable, evidence-based mental health programs.


Australians experiencing distress related to the pandemic can express interest in participating in the trial program here.

If this article has raised issues for you, or if you’re concerned about someone you know, call Lifeline on 13 11 14.The Conversation

Richard Bryant, Professor & Director of Traumatic Stress Clinic, UNSW

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

The AstraZeneca vaccine and over-65s: we may not have all the data yet, but limiting access could be counterproductive


Kylie Quinn, RMIT University

Last week, a German vaccine advisory committee recommended the AstraZeneca vaccine only be used in 18-64-year-olds, citing a lack of data on the efficacy of the vaccine in people over 65.

Subsequently, the European regulator, the European Medicines Agency, conditionally approved the vaccine for anyone over 18.

What can we make of this? Should we be giving this vaccine to older people or not?

While we don’t yet have all the data we’d like, we don’t have reason to believe this vaccine won’t be at least somewhat effective in older adults. To exclude them from receiving it wouldn’t necessarily be the right approach.

The recommendation

STIKO, a German vaccine advisory committee that reports to the country’s government, was responsible for the draft recommendation which caused the stir. It released a similar final recommendation at the weekend.

While the German government may elect to follow STIKO’s advice or the European Medicines Agency’s guidelines, the latter’s approval carries significant weight. Equivalent to the Therapeutic Goods Administration (TGA) in Australia, this body decides which vaccines may legally be supplied in Europe.

The AstraZeneca vaccine has already received approvals, not singling out older age groups, from multiple international regulators, including those in the United Kingdom, India and Mexico.




Read more:
Germany may not give the Oxford-AstraZeneca vaccine to over-65s, but that doesn’t mean it won’t work


Why did STIKO make this recommendation?

STIKO’s advice is based on the fact it didn’t have enough data to definitively say whether the vaccine will work in older people — not because it won’t.

According to the data we have so far from AstraZeneca’s phase 3 trials, only two out of 660 people in the trial aged over 65 got sick with COVID-19. Two sick people isn’t enough for a strong statistical analysis.

AstraZeneca initially enrolled younger people in its trials, with older people enrolled only later. So data on older people in the original trials and another trial in the United States are still on the way.

A doctor prepares to vaccinate a grey-haired woman.
AstraZeneca’s early trials didn’t include as many older people as younger people.
Shutterstock

What do we know about the vaccine?

We have very good safety data for the AstraZeneca vaccine in older people. Older people actually have significantly lower levels of early side effects after vaccination. This makes sense, as older people’s immune systems don’t tend to react as strongly to vaccines, which would reduce many of these early side effects.

But the vaccine has been shown to induce strong immune responses in older people, which are likely to provide a degree of protection. The European Medicine Agency’s press release on their decision refers to a reasonable likelihood of protection based on this data.

So, just looking at immune responses, it’s reasonable to anticipate the AstraZeneca vaccine will be of some benefit, at least, to older people.




Read more:
Why we should prioritise older people when we get a COVID vaccine


What do we know from other vaccines?

Often, vaccines aren’t as effective in older people as compared to younger people, because their immune responses can be less robust. For example, in 2010-2011 in the US, the flu vaccine was 60% effective in the general population, but only 38% effective in people over 65.

There’s more information on efficacy in older people for other COVID-19 vaccines. Notably, the Pfizer vaccine maintained efficacy of 93.7% for people over 55, compared to 95% overall. Accordingly, it would be reasonable to prioritise the Pfizer vaccine for older people.

But we’re beginning to see that vaccine supply and distribution can be unpredictable, with supply issues for Pfizer and AstraZeneca starting to affect vaccine rollout.

Importantly, all COVID-19 vaccines assessed so far, including the AstraZeneca vaccine, provide a high level of protection against severe disease and death across variants of the SARS-CoV-2 virus.

A health-care worker administers a vaccine to a senior man.
Older people are more susceptible to the coronavirus.
Shutterstock

Limiting access limits options for older people

The question that advisory committees and regulators are weighing up is, should the AstraZeneca vaccine, or any vaccine, be recommended for older people if we know:

  • the vaccine has low risk of side effects

  • the vaccine has a fair but unconfirmed likelihood of providing some benefit

  • COVID-19 has a higher likelihood of severe disease and death in the demographic.

This is tricky to navigate and advice may differ across different vaccines and countries. For example, China is delaying vaccine rollout to older people while it waits for more data.

But conditional approval is a reasonable path to take. It allows for some uncertainty and maintains contact with the manufacturer. It also recognises that the likely benefit of giving older people any available vaccine could outweigh the hypothetical risk that it might not work in the midst of a crushing pandemic.




Read more:
The Oxford vaccine has unique advantages, as does Pfizer’s. Using both is Australia’s best strategy


In any case, approvals from regulators, such as the European Medicines Agency and the TGA, have the most impact — defining who the vaccine can be supplied to in a country.

If regulatory guidelines are kept open to all age groups above 18, it will facilitate access to vaccines for many people who could benefit from them. The next steps are distributing these vaccines, and educating and updating the public with the latest information as it comes to hand.

Crucially, we should support older people in vaccine decisions with two things; good information and easy access to an array of safe, protective vaccines.The Conversation

Kylie Quinn, Vice-Chancellor’s Research Fellow, School of Health and Biomedical Sciences, RMIT University

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

Doctors must now prescribe drugs using their chemical name, not brand names. That’s good news for patients



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Matthew Grant, Monash University

From today (February 1), when you receive a prescription in Australia, it will list the name of the medication’s active ingredient rather than the brand name. So, for example, instead of receiving a prescription for Ventolin, your script will say “salbutamol”.

This national legislation change, called active ingredient prescribing, is long overdue for Australian health care.

Using the name of the drug — instead of the brand name, of which there are often many — will simplify how we talk about and use medications.

This could have a range of benefits, including fewer medication errors by both doctors and patients.

What is an active ingredient?

The active ingredient describes the main chemical compound in the medicine that affects your body. It’s the ingredient that helps control your asthma or headache, for example.

Drugs are tested to ensure they contain exactly the same active ingredients regardless of which brand you buy.

There’s only one active ingredient name for each type of medical compound, although they may come in different strengths. Some types of medications may contain multiple active ingredients, such as Panadeine Forte, which contains both paracetamol and codeine.




Read more:
Prescribing generic drugs will reduce patient confusion and medication errors


There can be several brand names

Until now, doctors and other prescribers have used a mixture of brand and active ingredient names when prescribing medicines. An Australian study found doctors used brand names for 80.5% of prescriptions.

Different brands are available for most medications — up to 12 for some. Combined with active ingredient names, this equates to thousands of different names — too many for any patient, doctor, nurse or pharmacist to remember.

A senior man taking a tablet. There are a variety of medications on the table.
Older people are at higher risk of making medication errors, as they tend to take more medications.
Shutterstock

Here’s an example of the problem.

I ask John, a patient whom I’ve just met, whether he takes cholesterol medications, commonly called statins. The active ingredient names for this group of medications all end in “statin” (for example, pravastatin, simvastatin).

“Ummm, I’m not sure, is it a blue pill?” John asks.

“It could come in many colours. It might be called atorvastatin, or Lipitor,” I reply. “Perhaps rosuvastatin, or Crestor, or Zocor?”

“Ah yes, Crestor, I am taking that,” John exclaims, after deliberating for some time.

This is a common and important conversation, but could be simpler for both of us if John was familiar with the active ingredient name.

And while we did eventually come to the answer, this medication could have easily been overlooked, by both John and myself. This may have significant implications and interact with other medicines I might prescribe.




Read more:
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Cause for confusion

The main problem with using brand names for medications is the potential for confusion, as we see with John.

A prescription written using a brand name doesn’t mean you can’t buy other brands. And your pharmacist may offer to substitute the brand specified for an equivalent generic drug. So, people often leave the pharmacy with a medication name or package that bears no resemblance to the prescription.

When the terms we use to describe medicines in conversation, on prescriptions and what’s written on the medication packet can all be different, patients might not understand which medications they’re taking, or why.

This often leads to doubling up (taking two brands of the same medication), or forgetting to take a certain medication because the name on the package doesn’t match what’s written on your medication list or prescription.

Confusion resulting from using brand names has been associated with serious medication errors, including overdoses. Elderly people are the most susceptible, as they’re most likely to take multiple medications.

Even when the confusion doesn’t cause harm, it can be problematic in other ways. If patients don’t understand their medicines, they may be less likely to be proactive in making decisions with their doctor or pharmacist about their health care.

Health professionals can also get confused, potentially leading to prescribing errors.

What are the benefits of active ingredient prescribing?

The main benefit of the switch is to simplify the language around medications.

Once we become accustomed to using one standardised name for each medicine, it will be easier to talk about medicines, whether with a family member, pharmacist or doctor.

The better we understand the medications we’re using, the fewer errors we make, and the more control we can take over our medication use and decisions.

A pharmacist studies a woman's prescription.
A pharmacist can let you know which brands of your medication are are available.
Shutterstock

This change will also serve to promote choice.

When you’re prescribed a medicine with a certain name, you’re more likely to buy that brand. In some cases there may be generic medicines that are cheaper and just as effective. Or there may be other forms of the medication that better suit your needs, such as a capsule only available in another brand.

Not too much will change

This new rule is not expected to lead to extra work for doctors, pharmacists or other health professionals who prescribe medicines, as most clinical software will make the transition automatically.

Doctors can elect to still include the brand name on the prescription, if they feel it’s important for the patient. But aside from some limited exceptions, the active ingredient name will need to be listed, and will be listed first.

Some active ingredient names may be a bit longer and more complex than certain brand names, so there might be a period of adjustment for consumers.

But in the long term, this change will streamline terminology around medicines and make things easier, and hopefully safer, for everyone.

Next time you receive your prescription, have a look at the name of the active ingredient. Remember it, and use that name when you talk to your family, doctor and pharmacist.




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The Conversation


Matthew Grant, Palliative Medicine Physician, Research Fellow, Monash University

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