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Brain blog showcase 2021: Occupational experiences may be associated with poorer memory and smaller memory structures within the brain

This week we’ve been showcasing the work of students who have been “researching the headlines” as part of their undergraduate studies. Their task was to describe an original research report exploring how lifestyle affects brain health in a manner accessible to non-experts, as well as evaluating the media coverage of the research. If you’re interested in using this approach in your own teaching, you can contact Alan Gow for more information and materials.

For our final “brain blog”, we have…

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Brain blog showcase 2021: Students “research the headlines”

At Research the Headlines we explore how research is discussed in the media. We try to add additional details to existing coverage, or help our readers get a clearer understanding of how new research might make its way from “lab to headline”. Through different activities, we also help others develop the skills needed to become more critical consumers of both research and media reporting; for example, via our How to “Research the Headlines” series and our “Rewrite the Headlines” workshops and competition for primary school children.

Many of our contributors also use the ideas behind Research the Headlines in their teaching. In one of his undergraduate courses, Alan Gow (Heriot-Watt University) has his students find a recent media article related to lifestyle factors and brain health. Their task is to describe the original research that report is based on in a manner accessible to non-experts, as well as evaluating the media coverage. A key aim of these “brain blogs” is to explain the important concepts and take home messages, and to highlight issues in interpretation either in the media report or the underlying research.

This week we’re showcasing the work of two students, all recent graduates in Psychology at Heriot-Watt. The blogs are presented as submitted by the students; they’ve not been edited. We hope you enjoy reading their work, and learning a bit more about the topics too! If you’re interested in using this approach in your own teaching, you can contact Alan Gow for more information and materials.

Starting the “brain blog” showcase, we have…

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Coronavirus: Cutting Through the Confusion

This post was written by Ed Roberts.

Over the last year we’ve all become amateur epidemiologists with newspapers feeding us a constant stream of news about the course of the pandemic, the promise and subsequent delivery of numerous vaccines, and the hopes for a release from lockdown. Amongst these numerous articles are a lot of scientific terms which are often unclear to a non-expert audience, and these are seldom explained (herd immunity anyone?). Adding to this confusion is that what we know about COVID-19 is rapidly changing and developing as we continue to study this new disease and start seeing the results from vaccines in the real world. To help with reading future articles in the field, here is a handy guide to some of the terms used and controversies covered in the news.

So what is COVID-19? COVID-19 is the disease caused by the virus SARS-CoV-2; while this may seem confusing this is similar to how AIDS is the disease caused by the HIV virus. However, in coverage of COVID-19 you may see references to “the virus that causes COVID-19” or to SARS-CoV-2, both of these refer to the same thing.

But I’ve heard about coronavirus, is SARS-CoV-2 just a name for coronavirus? While SARS-CoV-2 or the COVID-19 virus both refer to the same thing Coronavirus is not the same thing, although it is often used that way. There are a whole family of Coronaviruses which all share similar genetic and overall structure. These were identified as human pathogens in the 1960s. There are several human coronaviruses, many of which cause common colds or other relatively mild lung infections. There have been other coronaviruses which have caused more severe outbreaks in recent history. Notably, this includes SARS-CoV which caused the SARS outbreak in 2002 and MERS-CoV which caused an outbreak of MERS in 2012.

Ok, but where did this new virus come from? The origin of SARS-CoV-2 has been investigated extensively with the World Health Organisation (WHO) visiting Wuhan recently to look into various possibilities. The likeliest source of the virus causing COVID19 is that the virus jumped from bats to humans. This has been discussed widely and has been a source of conspiracy theories and racist rhetoric. But this kind of thing isn’t unique to our recent history, many other viruses jump from animals into humans and these are called zoonoses. Indeed, as humans invade the habitats of more and more species and keep various species of animals in close contact, this kind of event becomes more common. Bird flu, Ebola, HIV, Nipa and Zika are all zoonotic diseases. There are more than 1,400 species of bats around the world and these harbour at least 1,300 coronaviruses: MERS, SARS and SARS-CoV-2 – all examples of zoonoses from this family of viruses. Understanding the origin of zoonoses can inform future monitoring strategies but in recent times it has been discouraged to name viruses based on where they were reported as it is uninformative and encourages stigma.

Great, but now that it’s here we need to get the R-number down, but what does that mean? The R number represents how many people an infected person is likely to infect. It is a handy concept in epidemiology to characterise the transmissibility of a disease, for example measles is highly contagious and has an R number of 12-18 while influenza has an R number of 0.9-2.1. SARS-CoV-2 has an R number somewhere between 3.3 and 5.7 and so, in the absence of interventions, each infected person would infect roughly another 4 people meaning it would rapidly spread throughout a population. With interventions like social distancing, vaccinations, and mask wearing we can reduce the actual observed R number to below 1 and the number of infected people will gradually decrease. This is why seemingly small changes around 1 are very significant, with numbers greater than 1 leading to growth in the population, and numbers less than 1 leading to reduced infection rates.

Will this all be solved though when we have all been infected and achieve Herd Immunity? Herd immunity is a situation where a high enough proportion of the population are immune to an infection, which ensures protection for the population as a whole. Remember that the R-number refers to how many an infected individual is likely to spread the disease to in a population. The more people who are immune, the fewer contacts an infected individual makes with people who could be infected. By reducing this number you ensure that, as a whole, people infect less than 1 other person. In this sense, you may get some infections, but you can’t get an outbreak. The level of protection needed for herd immunity depends on a few things including how infectious the virus is and how effective anti-viral immunity is. So although the level of immunity in the population will reduce the R number, it’s unlikely that we will totally eliminate SARS-CoV-2 through herd immunity, just as we haven’t eliminated the common cold.

Now that we have the vaccine this will help us bring down the R number, but how do the vaccines work; are they changing our DNA? The first vaccine which reported its effectiveness as protecting against SARS-CoV-2 was produced by Pfizer and is an RNA vaccine. RNA stands for ribonucleic acid – an acid that can be found in all living cells. The vaccine also produced by Moderna is similarly an RNA vaccine. These are a new vaccine technology and work by injecting RNA into a patient which sounds like science fiction or genetic engineering. In reality, RNA serves as a blueprint for a protein; in this case the RNA vaccines contain the blueprints for the SARS-CoV-2 spike protein. Once inside the patient, this RNA is picked up and read by immune cells which then make the spike protein before using that to train an immune response to recognise that protein in future. This means that when exposed to the virus in future the immune system is already primed and ready to go – leading to the infection either not establishing at all, or being cleared more rapidly. The RNA itself is not particularly stable and is cleared, it also doesn’t interact with the DNA inside host cells so there is no worry about any genetic changes occurring.

So what are the other vaccines that are available?  Other major vaccines, AstraZeneca/Oxford, Janssen, and Sputnik V are all more conventional. For these vaccines a different virus has been modified so that it expresses the spike protein. This new virus doesn’t cause disease but does stimulate an immune response. The follow up from this is very similar to the RNA vaccine where if in future you encounter the actual SARS-CoV-2 virus, your immune system is primed to eliminate it before it can make you sick.

But what about second doses? Most of the vaccines have been trialled where people are given 2 doses of the vaccine with a short period of time between those 2 doses. The idea is that you challenge the immune system and get an initial response, and thereafter you rechallenge them with the vaccine again to get an even more robust response in future. This led to some concerns being raised after the UK government decided to prioritise getting as many people their first dose and left the second doses for longer than were tested in the clinical trials. As vaccinations moved forward, the efficacy of the first dose has now been established and it looks like even that first dose provides quite a lot of protection. But you still do need that second dose at some point!

What exactly is vaccine efficacy though? Is there an obvious “best” vaccine? Many newspaper articles have been written about the efficacy of different vaccines but it can be unclear what these mean and so it is important to read carefully! The most common efficacy number refers to the reduction in moderate to severe disease and hospitalisations. This means that numerous people received either the vaccine or a placebo (dummy substance) and then were monitored. The number of people in each group who became moderately or severely ill were compared. In this way you can use the placebo group to determine roughly the percentage of people expected to become ill, and can see what reduction there is in the vaccinated group.

However, it is possible to also measure reductions in mild disease, transmissions, and deaths. These are all being calculated now that larger populations are being vaccinated and all of these give different and complementary information. For example, reduced transmission will lower the R number while reductions in deaths will not; as such it is important to check what the statistics being presented actually refer to.

The vaccines target the spike protein, but what does that mean? The spike protein is a protein which sticks out from the surface of the virus and is made of 2 subunits. One of these subunits recognizes and binds to the protein ACE2 which is found on cells in the lungs. This binds the virus to the cell, and then another protein on the cell surface activates the spike protein and then the other subunit drives cell invasion. This allows the virus to get inside the host cell where it can take over the cellular machinery to produce more virus particles. As such, this spike protein is important for function but also covers the surface of the virus meaning it’s the main thing exposed to the immune system while outside of infected cells. Antibodies against this spike protein can block the virus associating with the cell surface thereby preventing it from continuing to infect.

So how do we have variants with changes in the spike protein if it’s that important? When a virus reproduces within a host cell there is a low chance that a mutation will be introduced. These mutations are likely to make the resulting virus less effective because they will disrupt normal function. However, rare mutations might make the virus more able to spread or to evade our immune defences. These rare events lead to new variants which can spread more effectively. Since the spike protein plays such an important role in infection many of these variants have changes in their spike proteins. The spike proteins are also the target of the vaccines which currently exist against SARS-CoV-2 and so these changes may allow variants to escape from the protection current vaccines provide. This is why new studies of vaccine efficiency are looking at their ability to protect from new variants and why vaccine studies carried out before the emergence of these variants are hard to compare to the studies being carried out now. 

If we don’t eliminate the virus, what does that mean for the future? Recently, discussion has moved from the idea of elimination to the idea that COVID-19 may become an endemic disease in the population. This means that the disease may be regularly found in the population at a fairly stable level from year to year. That would mean that COVID-19 became a disease we will have to live with in the long term. There is speculation as to what this might mean, however, observations from previous diseases suggests that over time the disease might become less severe.

So what does it all mean? Well before COVID-19 there were estimates of how much disruption to the world an influenza pandemic with a higher death rate than we have seen with COVID19 would cause. The estimates were much lower than we have seen with this pandemic, suggesting consequences were grossly underestimated. Moving forward we can take the lessons from this pandemic, be they personal lessons about how small behaviours like hand washing can prevent the spread of disease; public health lessons about the importance of surveillance or even lessons about how we interact with the natural world and the risks that brings for human health, all of which will hopefully make us better equipped for future challenges. While the COVID-19 pandemic has been a once in a lifetime experience we must remember that it’s not an aberration  but, rather reflects some of the challenges associated with a global community living closely with animals and encroaching on new environments.

Smartphone “addiction” and sleep

This blog was written by Rita Kanevski & Sinead Rhodes.

Excessive phone use is probably something we’ve all had to reflect upon at some point in our lives. Let’s set the scene.

You jump in the car to go to the supermarket. As you stop at the traffic lights, you remember that earlier you left your mum on ‘read’. The itch for your phone begins to build.  By the time you get to your favourite parking spot, a big queue of people awaits outside the store (since it’s COVID after all), all with their heads dug deep down into their screens. You are suddenly inspired to seize this opportunity to reply to your mum and, while you’re at it, scroll through Twitter, Facebook, Instagram, Reddit, your emails, the news, and the list goes on.  Alas, as your reach into your (unusually light) pocket, you realise your phone isn’t there. The panic sets in.

Is the phone in the car? Did I leave it at home? Where should I look? I better remember to text my mum back when I get home… That is if I even have a phone anymore. Will I need to fork out on a new phone now? Waiting in queues is so boring.

Okay maybe that’s a slight exaggeration, but you get the drift.  Why is it that some of us are so attached to our phones? Researchers at Institute of Psychiatry at King’s College London wanted to answer just that.

What did the study do?

The study investigated the relationship between smartphone “addiction” and sleep quality in 1,043 young adults from the UK aged 18-30 years. To explore smartphone use habits, researchers asked participants to answer some questions about how much time they spent on their phones on an average weeknight and what they typically used their phones for (e.g. texting, social media, music).  Participants (adults) also completed the short version of the Smartphone Addiction Scale – a 10-item questionnaire originally developed to measure smart phone “addiction” in adolescents. This scale asked participants to rate whether they agreed with statements indicative of smartphone “addiction”, such as for example “Using smartphone longer than intended”. Participants were also asked to rate their quality of sleep by asking questions on things like what time they go to bed, how many hours of sleep they get, and how they rate their ability to fall asleep.

The results showed that 39% of the young adults surveyed scored as higher risk for problematic smartphone use. Longer daily phone use (~ 5hrs or more) and use at later times in the day (e.g.  after midnight) was associated with higher self-rated smartphone “addiction” scores.  Additionally, participants scoring higher on the Smartphone Addiction Scale were 41% more likely to experience poor sleep quality. Lower screen time (i.e., 2 or less hrs) reduced risk for poor sleep by 38%. The relationship between phone “addiction” and poor sleep outcomes remained even after taking into account (or, statistically controlling for) duration of screen time. This was interpreted to suggest that the relationship between smartphone “addiction” and sleep quality can’t simply be due to how long a person spends on their phone, and other risk factors are likely involved.

How well did the media cover the findings?

If Netflix’s controversial documentary, The Social Dilemma wasn’t enough to prompt you to re-evaluate your phone habits, these headlines could certainly do the trick:

Are you addicted to your smartphone? More than a THIRD of young adults report symptoms including poor sleep and anxiety when away from their phone – regardless of how long they spend on it each day Daily Mail

One in three young Brits unable to sleep because they are ‘addicted to their smartphonesThe Sun

But before you consider writing your phone off, let’s examine the credibility of these headlines. Indeed, as suggested by the Daily Mail, more than a third of the participants scored high on the Smartphone Addition Scale and reported poor sleep outcomes. But levels of anxiety were never measured in these participants so there is no basis for asserting that these young adults reported anxiety when away from their phones. The Sun also appears to misconceive this issue by implying that the participants surveyed “became upset when they couldn’t get to their phone and lost control over how long they spent scrolling”. Looking at the study, this is simply not the case. The authors do mention that previous research had shown that participants who experience smartphone “addiction” struggle with impaired control over their devices and anxiety when their phones are not easily accessible. These phenomena, however, were not addressed as part of the study. This implies an exaggeration on the media’s part to make the findings sound a bit more dramatic than they actually are. At Research the Headlines we have frequently spoken about the need to try and look at what the research actually involved and what has been exaggerated

Nonetheless, the use of quotation marks to refer to ‘“addiction”’ in both articles is somewhat reassuring. Indeed, it would be crude to suggest that a 10-item smartphone “addiction” questionnaire, originally developed to assess problematic phone use in teenagers, would be indicative of a clinical diagnosis of “addiction”. Addiction is quite a strong word, and in medical terms it can be defined as a “chronic, relapsing disorder characterized by compulsive seeking, continued use despite harmful consequence, and long-lasting changes in the brain.” It would be a bit of stretch to suggest that 10 questions, used to assess problematic phone use in a sample of adolescents, would indicate clinical addiction in adults as we know it.

Both news articles stated that participants experienced problematic phone use “regardless of how much time they spent on them daily”. Again, this isn’t quite accurate. The study explicitly reported that longer duration of screen use was substantially related to smartphone “addiction”. In fact, 20% of those using their phone for 2hrs or less were classified as “addicted”, and this figure more than doubled to 54% for participants who reported using their phone for more than 5hrs a day. This suggests the less time people spent on their smartphone, the less likely they were to be “addicted”.

Key conclusions/other things to keep in mind

The study was cross-sectional, meaning that observations were collected from participants at a specific point in time. As the authors acknowledge, we cannot definitively say that smartphone “addiction” causes poor sleep, and reverse causality can’t be ruled out. For example, it is equally compelling to suggest that people who can’t get to sleep for other reasons (e.g. stress or poor mental health, not assessed as part of the study) tend to use their phones for longer periods of time, and so be generally more dependent on their phones. We have spoken about the importance of working out what is an association or can be considered a causal relationship in another blog.

The second issue the authors raise is the possibility that phones merely provide easy access to addictive material such as social media. This raises the question whether we are addicted to the material, rather than the smartphone itself? They point out that future research would benefit from exploring specifically the types of use associated with “addiction”. Although it’s important to note that as part of the data collected for this study participants were asked to indicate what they use their phones for (e.g. music, games, social media) and so it’s unclear why this wasn’t explored in more detail.

Lastly, the study relied on self-report questionnaires. Another study cautions against relying on self-reported estimates of phone use as these only moderately reflect participants’ actual behaviour. They suggest that objective measures of smartphone use data should be used in addition to self-reports to collect more accurate data.

To conclude, it sounds like there’s still much work to be done before we can say that young Brits are phone addicts. It’s equally important to consider some of the benefits smartphones have carried over the years, allowing us to interact with each other particularly during times where face to face interactions have been out of the question. 

Looking back at Research the Headlines in 2020

2020 definitely goes down on record as the most challenging year for evidence-based media reporting of research. Daily exposure to health related research has impacted everyone this year. Research the Headlines was set up in 2013 to examine how research is portrayed in the media, and to give the public helpful advice and tools when trying to get to the heart of a news story. Through different activities, we also help others develop the skills needed to become more critical consumers of both research and media reporting; for example, via our How to “Research the Headlines” series and our “Rewrite the Headlines” workshops and competition for primary school children.

During 2020 we posted about media coverage of both COVID-19 and non-pandemic topics. Of course many of our posts did focus on media coverage of COVID-19 research. Fairly early in the pandemic, back in March, we highlighted the research efforts already up and running to decipher the genetic code of the virus, to produce and test vaccines and to develop appropriate treatments. Nine months on and the impact of that research can now be seen. Just yesterday we had the exciting news of the approval of the vaccine developed at the University of Oxford. We highlighted the mixed media coverage of COVID-19 evidence with most reporting accurately but some sensationalist headlines evident.

Media coverage of COVID-19 research has pretty much followed that pattern throughout the last 9 months with most journalists reporting accurately and appropriately but other reporting has unfortunately fuelled myths. We wrote early on about research that reported on the impact of school closures. Since then we have continued to see reporting that is misleading such as media reports at the start of the pandemic that children are ‘super-spreaders’.   More recently we highlighted media reports of immunity being short-lasting and media discussion of products that may protect against COVID-19.     

We also covered a range of other topical issues discussed in the media. One of our most popular posts discussed the benefits of playing video-games for well-being. In a time where we are all staying at home this is of course a highly topical issue! We posted several articles on children’s development and trauma and stress. Neither of these posts were specifically related to the pandemic but the stressful nature of life experiences for many in the last year means these are highly topical.  As usual there were many news stories this year about positive and negative effects of alcohol. In this case we analysed media claims that beer can improve concentration and reduce dementia which were unpicked by the blog authors.

In most cases there was accurate reporting of research. We saw examples of excellent reporting in our post about the link between irregular periods and premature death. Most journalists explained the difference between association and causality in relation to the research covered and also included the view of independent experts. Both of these are key priorities we have covered in our Top Tips series. Frequently we saw good examples of sound reporting such as use of references to NHS website information to learn more about a health issue – dementia in this case.  Often media reports focused solely on reporting the one study without providing the wider context or relevance of the finding in relation to the broader science known on the topic. Examples of this often related to important health issues such as heart disease and the danger of parasites.  In our Top Tips series we focused on this issue of ‘no study stands alone’.

We will continue with our range of activities in 2021 and look forward to continue working with early career researchers and offering them opportunities to develop their blogging skills!

Benefits of playing video games for your well-being

This blog was written by Iain Donald, Senior Lecturer at the Abertay University’s School of Design and Informatics.

In November 2020, it was widely reported in The Guardian, The Times, Sky News, Daily Mail and elsewhere that time spent playing video games can be good for players wellbeing. A study undertaken by academics (Niklas Johannes, Matti Vuorre, and Andrew K. Przybylski), at the Oxford Internet Institute, gained significant attention largely because the results focus on the positive aspects of game playing. Historically, when the mainstream press has featured videogames it has often focused on long-standing debates about whether violence in video games leads to real-world aggression, or whether video game ‘addiction’ is a health concern (in May 2019 the World Health Organization officially voted to include an entry on “gaming disorder” as a behavioural addiction to its International Classification of Diseases), or more recently whether ‘loot boxes’ are a form of gambling and require regulation.

What did the study do?

The study included adult players of two popular video games, Plants vs Zombies: Battle for Neighborville and Animal Crossing: New Horizons. The researchers conducted an online survey on players’ well-being by asking questions about frequency of negative and positive feelings over a two-week period. Participants were also assessed on self-reported play time, as well as using objective telemetry data obtained on time spent playing from the Electronic Arts and Nintendo of America, for their respective game titles. Results showed that players with higher objective playtime reported experiencing higher well-being across both games. Notably, participants tended to overestimate time spent playing by two hours, and self-reported play time was only significantly related to well-being of those playing Animal Crossing. The authors concluded that self-reports of play time (on which much previous research in this area relies) might not be accurate indicators of actual play time.  The study concluded that time spent playing video games can be good for players wellbeing. This research may seem to some as common sense or less than ground-breaking largely because we know that billions of people worldwide play games because they enjoy them. What is novel about the research was that it was based on data from two of the leading publishers of games.

Notably, the study is limited in scope. It only looks at two games and a tiny portion of the respective player bases with the datasets of some 471 players Plants vs Zombies: Battle for Neighborville and 2,756 of Animal Crossing: New Horizons. Nevertheless, represents a significant academic-industry engagement, although one that has garnered more attention because of the games, and arguably the University, rather than the output. Participants were from a limited geographical spread (Canada, UK and the US) and, as such,  may only be generalisable to these populations. The study was also correlational which doesn’t always imply causation, as discussed in our previous blog entry.

How well did the media cover the findings?

Reading or hearing about games or gaming in the news is often focused on the more negative aspects. This study was widely reported on, as having found a positive correlation between time spent gaming and people’s wellbeing. Depending on the publication and the intended audience, the same study was headlined in a variety of different ways. The Guardian’s succinctly put this as “Video gaming can benefit mental health, find Oxford academics” whereas The Daily Mail preferred to shout “Good news for gamers: Playing video games BENEFITS mental health, Oxford University scientist claims”.  Others brought a wry smile to my face (emphasis mine), I liked Business Insider’s “Video games might actually be good for you, Oxford study finds” and Time 24 News’ accurate yet underwhelming “There are two games that can be positive for mental health, according to Oxford study”. Just two everybody, all the others can’t be any good!

Understandably the media have represented the findings as somehow going against established but undefined norms. That somehow, somewhere, it had previously been decided or decreed that videogames are bad for our health. I’ve grown up with video games and consider myself fortunate to have worked in the industry, and now to teach and research them. I think most people that play video games probably think that it’s great that Oxford are catching up. Keza MacDonald reflecting on the study in The Guardian succinctly sums this up as “For anyone who actually plays video games, this is hardly news. Video games are fun and interesting, and doing fun, interesting things makes you happy.”

Looking past the headlines, some reports were lighter on the details than others. The researchers admit the study only provides a snapshot. They also acknowledge that a player’s subjective experiences during play might be a bigger factor for wellbeing than mere play time. Andrew Przybylski, one of the authors of the study noted that “Previous research has relied mainly on self-report surveys to study the relationship between play and wellbeing,” and that “Without objective data from games companies, those proposing advice to parents or policymakers have done so without the benefit of a robust evidence base.” Working with games publishers is a significant advance. Most major games companies have, for a variety of commercial and competitive reasons, been reluctant to share sales, never mind player data. This was summed up in The British Psychological Society’s Research Digest where it stated that the most interesting and exciting part of the study was not necessarily the findings, but the fact that the “researchers have collaborated with industry and obtained real data on people’s playing habits. The lack of access to data from media companies has long been a major obstacle to this kind of work”.

There were other revelations which could have profound impacts. Andrew Przybylski noted that “Players tend to overestimate the amount of time they play, a pattern which is similar to what we see in smartphone/social media/news research.” This finding was undersold, and one that I think most game players, would be surprised at. As Keza MacDonald stated “There are so many more interesting conversations to be had than “are video games somehow bad for you?” and “gosh, look how much money this industry makes”. Try talking to people who actually play them, which these days is 85% of people under 35 and plenty of older folks too, and you’ll find the real stories.”

Key conclusions and other things to keep in mind

Games are more than entertainment now. The use of video games in health and care settings is an established yet growing area of research. Various types of video games have been used in these settings to support players’ physical, cognitive, and emotional health, aligning with desirable clinical outcomes, such as enhanced motivation, empowerment, and improved cognitive functions. Bespoke experiences – termed “serious games” or “applied games” – have been developed based on the identification of, and focus on, a specific purpose in an individual’s personal wellbeing. One such example is SuperBetter (2015), a mobile game in which the player self-reports on the completion of real-world challenges in order to earn points. SuperBetter utilises techniques such as self-determination and cognitive behavioural therapy to build the player’s mental and emotional resilience. Studies suggest that the use of SuperBetter improved symptoms of depression, anxiety, and motivation after a thirty-day period, as well as rating among the most-effective mobile applications for pain management. Equally, there are also examples of ‘traditional’, commercial games that have evidenced many health benefits: from encouraging players to walk in order to locate and catch virtual monsters in Pokemon GO! to performing dance routines in Just Dance 2020.I’ve seen the power that games have on my own children from inviting them to build and explore vast new virtual worlds in Minecraft, through to the unrestrained laughter and unbridled chaos of the massively multiplayer party game, Fall Guys: Ultimate Knockout, where up to 60 players online battle it out in a free-for-all struggle. When the pandemic stopped all football, FIFA20 became a substitute. Not quite the same, but enough to keep football-obsessed children engaged and has somehow led to a certain Edson Arantes do Nascimento (Pelé) establishing himself as my 8-year olds favourite footballer. The fact that Pelé last played 43 years ago is no longer an obstacle due to the virtual football world.

Will the planned water releases from the Fukushima Dai’ichi nuclear plant be harmful to people?

This blog was written by Leslie Mabon, a Senior Lecturer in Social Science at the Scottish Association for Marine Science-University of the Highlands and Islands and a Future Earth Coasts Fellow.

In October 2020, it was reported in The Guardian, Japan Times, New Scientist and elsewhere that the government of Japan intends to approve plans to release treated water stored at the site of the Fukushima Dai’ichi nuclear plant into the north-west Pacific Ocean. The Great East Japan Earthquake and Tsunami of 11 March 2011 disabled cooling systems at the power station, triggering hydrogen explosions and causing three of the plant’s reactors to suffer meltdowns. Since then, water used to keep the damaged reactors cool, plus recovered groundwater, has been treated to remove the most harmful radioactive substances and then retained on-site in storage tanks. However, plant operator Tokyo Electric Power Company claims they will run out of space by 2022. An expert panel has concluded that releasing the treated water into the sea is the most effective response. Yet a breadth of news sources report that local fishers and environmental NGOs object to the releases on the grounds of potential health effects and/or stigmatization of Fukushima seafood. In one Guardian article, Greenpeace even claimed that the water could damage human DNA if released.

The Fukushima Dai’ichi nuclear power plant (source: Leslie Mabon)

What does the underpinning science say?

One of the most up-to-date overviews of the situation at the Fukushima Dai’ichi plant was published by Ken Buesseler of Woods Hole Oceanographic Institution in Sciencein summer 2020. Buesseler explains that tritium – the radioactive substance most commonly cited as a cause for concern when the releases are discussed – is relatively harmless and does not exist at the Fukushima Dai’ichi site at a volume higher than what would normally be released by a nuclear power station. However, Buesseler also points out that the storage tanks may also contain other radioactive substances such as ruthenium-106, cobalt-60, and strontium-90. These materials may behave differently to tritium in the ocean, and may be more readily incorporated into marine species or the seabed. Buesseler concludes that to fully understand the consequences of releasing treated water into the sea, a full assessment of what is contained in the tanks needs to be undertaken.

Although the science addressing the material contained in the tanks at Fukushima Dai’ichi is still emerging, there is a wider body of research addressing the effects of radioactivity on the marine environment since the 2011 accident. For example, in a 2016 commentary, Jordi Vives i Batlle summarises that whilst the risks to humans and marine species are low, the contamination of the marine environment in Fukushima is significant. A team of researchers led by Fukushima University and Fukushima Prefecture’s fisheries experimental station similarly concluded in 2016 that with the procedures and regulations that are in place for monitoring and screening of Fukushima produce, the risk of consumption of Fukushima seafood is low or negligible, with no additional radiological effects for consumers.

In sum, whilst it is true that radioactivity from the plant exists in the Fukushima environment and that uncertainties over the treated water remain, the peer-reviewed science suggests it is very unlikely that humans will be exposed to harmful radiation. Nonetheless, a team led by the Scottish Association for Marine Science and Tokyo University of Marine Science and Technology interviewed local fishers in Fukushima to understand their views towards the releases, publishing their results in autumn 2020 in the International Journal of Disaster Risk Reduction. They found that fishers in Fukushima were worried about the future of the plant, and about the effects of treated water releases on public perceptions of Fukushima seafood given their pride in the fish they caught. Crucially, this paper found that more than concerns over the safety of treated water or of marine produce, fishers very much valued the opportunities that trial-scale fishing had given them to rebuild their livelihoods post-disaster. Accordingly, anything that jeopardised this fragile recovery was viewed as having the potential to undo the gains made since 2011 in helping Fukushima fishers to rebuild their lives.

How well does the media describe the science?

New Scientist carries the views of a breadth of marine scientists on the releases. It reports a general consensus that the releases are unlikely to pose risks to humans or marine species, but also acknowledges Buesseler’s concern over remaining uncertainties around what is contained in the tanks and also the need for close monitoring once treated water is released. The Guardian’s reporting around the subject touches on the views of fisheries officials from Fukushima Prefecture, but otherwise engages to only a limited extent with the peer-reviewed literature whilst reporting the assessments of a Greenpeace investigation. Deutsche Welle similarly reports the scientific assessment of Greenpeace and also a study carried out by a local newspaper, but does not carry the views of scientists working at academic research organisations or refer to peer-reviewed studies.

Abalone caught in Fukushima waters post-disaster for sale in Iwaki City, Fukushima Prefecture (source: Leslie Mabon)

Other points to bear in mind

The concerns expressed by fishers and citizens of Fukushima Prefecture are not only about the safety of treated water or of local seafood. Fisheries are a significant component of local identity on the Fukushima coast. Efforts to rehabilitate local fisheries following the 2011 nuclear accident have gone a long way to re-establish a sense of pride and purpose among fishers and coastal communities. Catching and selling high-quality seafood is not only an economic activity, but rather a whole way of life for those involved, and an important part of a sense of belonging for those that live on the Fukushima coast. Consequently, anything such as a release of treated water that may jeopardise this recovery or lead to Fukushima fish being viewed as ‘tainted’ is likely to be met with concern.

Similarly, there is a strong body of social science research which tells us that people’s perceptions of radioactivity are complex, and thus that it is a mistake to dismiss concerns as ‘irrational’ or ‘wrong’. Different groups of people may interpret uncertainties and unknowns differently, depending on what they consider an acceptable level of risk. Our interpretation of risks can be informed by a breadth of factors, including whether we trust the individual or organisation taking the risk on our behalf, what our political views are, and whether we consider the distribution of risks and benefits (or the decision-making process) to be fair. Providing ‘more’ or ‘better’ science alone is unlikely to be effective when it is issues of value that are at stake.

Useful links

An explainer about the Fukushima Dai’ichi treated water situation on Leslie Mabon’s research blog

A virtual tour of the Fukushima coast on Leslie Mabon’s research blog

Fukushima InFORM – monitoring the effects of the Fukushima nuclear accident on Canada’s oceans

Woods Hole Oceanographic Institution – Center for Marine and Environmental Radioactivity

‘The Sea of Fukushima Will Not Give In’ – short film about Fukushima fisheries produced by Fukushima Prefecture

Leslie Mabon’s current work on the coasts and seas of Fukushima Prefecture is supported by Economic and Social Research Council-Arts and Humanities Research Council UK-Japan Social Sciences and Humanities Connections Grant ES/S013296/1, ‘Building social resilience to environmental change in marginalised coastal communities.

How long does immunity last after having COVID-19?

This blog was co-authored by Allison Jackson & Fiona Henriquez

The coronavirus pandemic has affected the lives of everyone in 2020. People are, quite rightly, wanting to know if they catch the virus, and are they then protected from further infections? Recently, a team of researchers at Imperial College London and their collaborators published a pre-print showing a survey they conducted looking at the prevalence of antibodies against the virus that causes COVID-19, the novel coronavirus SARS-CoV2, decreases over time. In many media outlets, including the Guardian, the Herald Scotland and the BBC Science Focus Magazine the headlines screamed that immunity to coronavirus could be lost in months. But is this really true?

What did the study do?

The Real-time Assessment of Community Transmission (REACT) Study surveyed 365,000 adults in England using a home testing kit to see whether they had antibodies to SARS-CoV2. They sampled three random groups of adults in England using a self-administered home antibody testing kit. Each sample was a different group of adults that had volunteered for the study.

What is an antibody?

An antibody (also known as immunoglobulin –Ig) is a molecule produced by our immune system in response to infection. Antibodies are created to be highly specific to a part of an invading microbe, such as SARS-CoV2. There are five different classes of antibodies in the human body and they are produced for distinct purposes and in specific locations. When you get infected by a microbe for the first time, for example with the novel coronavirus, the first antibody that is produced is IgM. It is highly efficient during new and early infections. Upon secondary exposure to the same microbe, the body’s immune system has acquired a memory from the first exposure and now the most abundant antibody that is produced is IgG. IgG will be present at low levels after an initial infection. SARS-CoV2 predominantly affects the respiratory system and as a result IgA is also produced. Like any other molecule secreted from cells, antibodies degrade after a period of time. IgG has the longest half-life of 20-24 days.

What were the results?

The first survey of 105,000 individuals in June 2020 found that 6% of the adult population had detectable IgG antibodies. The third and final survey, conducted in September 2020, showed the levels had decreased to 4.4%.

What did the researchers conclude?

The researchers conclude the prevalence of antibodies decreased between rounds 1 and 3 – but not in healthcare workers, presumably due to repeated exposure. They suggest this is consistent with evidence that immunity to seasonal coronavirus declines after infection, but that the relevance of this decrease has not been determined for SARS-CoV2. They also suggest their first sample may have underestimated the total of those infected in the first UK wave. The limitations of their study are described – namely the possibility that people exposed to the virus were less likely to take part over time, which may explain the decrease in antibody prevalence.

What does this mean for people’s immunity to the virus that causes COVID-19?

Viruses must replicate inside a host cell. They hijack host cell machinery so that the virus can replicate, produce its own components and be packaged up into about a thousand (in the case of SARS-CoV2) new virus particles in order to be released from the host cell before going on to infect other cells. Damaged host cells release signals that flag to the immune system that a viral infection is present and needs to be eliminated. Antibodies are only part of this process.

The main cells that are effective in eliminating viral infections are actually T cells, which develop in the thymus, hence the “T”. A subset of T cells, cytotoxic T cells, target infected host cells to kill them. Cytotoxic T cells are activated through a cascade of events that is initiated by ingestion of the virus by a dendritic cell. The dendritic cell proceeds to present the virus through specialised cellular pathways to a T helper cell, that in turn activates the cytotoxic T cell. T helper cells also provide a signal to make more of the antibody-producing cells. All these check points are necessary and highly regulated because, if not, there is a surge of immune over-activity that can lead to the so-called ‘cytokine storm’. There is evidence that suggests that a subgroup of COVID-19 patients do experience the ‘cytokine storm’ and, it is in these cases that the anti-inflammatory drug dexamethasone works well to reduce the over-active immune response.

Once the infection is resolved, the immune system returns to a resting state with only specific antibodies (for a brief period) and memory cells that recognise the virus, in circulation. Memory cells are those cells that vaccination seeks to create, so that the next time a person becomes infected, the immune system responds efficiently and rapidly to the virus infection. At this point, antibodies are generated swiftly and act to block entry of the virus to the host cell (Figure 1) or surround the virus so it is easily identified by the other cells of the immune system.

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Figure 1: Antibodies that bind to surface proteins can block virus entry into host cells. Created with

What did the media say?

Given that we have only known about SARS-CoV for less than a year, and the huge disruption it is having on our lives, one of the main questions researchers are searching for answer to is ‘will someone who has been infected, be protected from further infections?’. This study is in important step on the way to answering this question, however it is only a small part of the answer. The media headlines however have misrepresented the story and said that immunity wanes in months, without explaining that they are really talking about antibodies, which is not the same thing. This is frustrating because if you read the University’s press release, it is clear the researchers are talking about antibodies decreasing and not immunity. The sensationalist headlines will mean that the many people who have already been infected will undoubtably be concerned about what this really means for them.

Almost all the articles we read made claims that the researchers themselves did not make – particularly in their headlines or the first paragraphs. The Guardian suggested ‘the virus could reinfect people year after year, like common colds’. The Herald Scotland said ‘immunity to coronavirus in recovered patients may only last a few months’. The BBC was more accurate, saying ‘antibodies fall rapidly after infection’ but the Metro said ‘immunity to coronavirus may only last a few months’.

Points to remember

Immunity is a complicated process. The researchers do not discuss other mechanisms of immunity, namely cytotoxic T cells in their pre-print. They also only detected IgG antibodies, and as you can see, there are multiple types, although IgG is the dominant type. You would expect that antibody levels decrease over time after infection, but they would increase again if the person encounters the virus for a second or third time.

One thing to note is that these results of this study are, for now, a pre-print, which is a full draft research paper that is shared publicly before it has been peer-reviewed. Pre-prints allow rapid data and information sharing, which is particularly important in helping researchers to understand how SARS-CoV spreads, causes disease, and how the body responds to infection. However, this means that the results have not been submitted for peer-review and have not been scrutinised to ensure the research has been conducted to the highest quality standards.

The bottom line

Currently we don’t know how antibody levels relate to protection from re-infection of this novel coronavirus. Until researchers unpick all the complex components of the immune system and their roles, everyone should play it safe and follow the government guidelines on social distancing, hand washing and wearing face coverings, and getting a test if you have symptoms.

Does having irregular periods increase your risk of early death?

This blog was written by Rocío Martínez Aguilar (Post-doctoral Research Fellow) and Jacqueline Maybin (Senior Research Fellow and Consultant Gynaecologist). Both work at the MRC Centre for Reproductive Heath at the University of Edinburgh.

This month the media reported an increased risk of early death in women who have irregular periods, based on the findings from a recent study from Harvard University published in the British Medical Journal. This study is a very welcome addition to the medical literature, adding much needed data about menstruation and its impact on women’s lifelong health. However, media reports may also have caused distress for the millions of women experiencing irregular menstruation. In addition to the negative physical, social, mental and economic effects of having problematic periods, these women may now be worried that they are going to die earlier than those with trouble-free menses. The concern such headlines cause is exacerbated by the stigma and shame surrounding menstruation that prevents open, honest conversations. Here we explore the science behind the headlines and decode the language used regarding menstruation to give context to these findings.

What did this study do?

In this study, 79505 women were asked to report the regularity and frequency of their periods during three timepoints in their life: at 14 to 17 years old, 18 to 22 and 29 to 46. The frequency of menstruation is defined as the usual length of time from the first day of one period to the first day of the next period. Regularity is the amount of variation that occurs in this time from one period to the next. Women in the study described the regularity of their periods as either: very regular (occurring within 3-4 days of the expected date), regular (within 5-7 days), usually irregular, or always irregular/no periods. The frequency was categorised as 25 days or less, 26-31 days (considered ‘normal’), 32-39 days, or more than 40 days (too irregular to estimate).

The researchers then examined the number of premature deaths (that is, a death below the age of 70 years old) in each group and found this was greater in women with ‘always irregular/no periods’ than in women with ‘very regular’ menstruation. In addition, women with very infrequent periods ( more than 40 days/too irregular to estimate) had a small but statistically significant increased rate of premature death. This association remained when the data were corrected for factors such as BMI, physical activity or smoking. These relations were strongest for deaths due to cardiovascular disease (e.g. heart attack, stroke).

Other things to keep in mind

First, it is  is crucial to remember that irregular periods are a symptom (something you experience) rather than a diagnosis (something that causes the symptom). If irregular periods really did cause premature death, correction of the irregular menstruation should reverse the risk of dying early. The most common way of regulating menstruation is to take the oral contraceptive pill. However, in this study women who took the oral contraceptive pill during adolescence were actually more likely to have an early death. Therefore, it is possible that an underlying cause of irregular bleeding results in the increased risk of premature death, rather than having irregular periods, per se. We already know that women with polycystic ovarian syndrome (PCOS), a leading cause of irregular periods, have an increased risk of diabetes, high blood pressure and cancer of the womb. There are ways to reduce these risks and it is important that women with PCOS speak with their doctor. 

Second, in 2011 the International Federation of Gynaecology and Obstetrics (FIGO) first published guidance to standardise the language used for menstruation and introduce a classification system for abnormal periods. They recommended that doctors and scientists should assess menstrual duration, frequency, regularity, and volume. This study examined just two of these criteria but used a slightly different definition of regularity and frequency. This is likely to be due to the timing of data collection in this study, perhaps commencing prior to 2011. However, it is important to standardise such terms so that global data can be combined to find important conclusions regarding the impact of menstruation on health.

Lastly, the characteristics of the women who took part in this study were not representative of the diversity frequently seen in most societies, making it more difficult to apply the study findings to individual women seeking medical advice.  The majority  participants were white and they all worked as nurses. Some nurses work irregular hours, including nightshifts. This will have a significant impact on the natural body clock and previous studies have shown a link between shift work,  irregular periods and poor health. This was not accounted for in the study.

How well did the media cover the findings?

The study was covered in media outlets such as The Guardian, Daily Mail and CNN. Overall, the articles clearly described the key points of the study. The headlines summarised the most attractive findings but did not fall into the trap of confusing association with causation. The body of most articles clearly stated that there was an association between irregular periods and early deaths but explained that this does not mean that early deaths are caused by irregular periods. The importance of emphasising an association is not necessarily causal is an issue we have advised on within our Top Tips series at Research the Headlines. Most of the articles used quotes from independent experts alongside quotes from those who performed the study, an issue we have also previously highlighted. This provides a balanced overview and assessment of the research and highlights the positives of the study as well as the limitations that may otherwise go unnoticed by a non-scientifically trained audience.

The balanced reporting of these important findings highlights the benefits of good communication between scientists and the media. For researchers, engagement with the media facilitates an active role in public discourse about science, giving context to new discoveries, preventing sensationalism and limiting misconceptions. Perhaps it should be viewed as a moral duty for researchers to help society understand the latest scientific findings. Creating a media profile as a researcher is also an opportunity to inspire the next generation. As the saying goes, ‘if you can’t see it, you can’t be it’ and researchers who represent society in all its shapes and forms can, and will, have a significant positive impact on diversity and excellence in academia.


This study is a real step forward to close the huge data gap that exists regarding menstruation and its impact on lifelong health. As with all good research studies, it throws up many questions and areas of further study. It is imperative that we delineate how the menstrual cycle may affect, predict or be impacted by other diseases. Use of FIGOs standardised terminology and classification system will facilitate such research. After all, menstruation affects over 50% of the population and its relative invisibility in current scientific literature needs to be addressed. It is time to obtain good data on women and their menstrual cycles to improve their health across the lifespan.

Useful links

HOPE. Healthy Optimal Periods for Everyone.

Latest guidance on the language used for menstruation and the classification of causes for abnormal periods.

Does trauma lead to faster ageing in children?

This blog was written by Julie Cameron, Associate Director for Mental Health Foundation (Scotland and Northern Ireland).

Improving our understanding of how experiences of trauma and adversity in childhood impact on health outcomes as adults is of increasing interest and importance.  Trauma and adversity would include a wide range of factors including the experience of abuse, neglect, sudden death or abandonment, parental alcohol or drug misuse, parent being in jail, divorce, poverty, violence within the family unit and wider community. This sits within the broader context of the significant health inequalities in our society where people living in poverty are more likely to experience mental health problems, physical health problems, and die younger than those from more affluent backgrounds.

The role of adversity and trauma within this picture came to prominence following the US Adverse Childhood Experience (ACEs) survey which found that as the number of ACEs increased so did the risk of experiencing negative health conditions in adulthood.  This included mental health problems such as anxiety and depression, as well as physical health conditions like cardiovascular disease, diabetes, and cancer.  The relationship between mental health and physical health conditions is not fully understood.  Studies exploring this association have cited the impact of trauma on wider behavioural and relational factors, experiences of stigma, and discrimination, as well as neurobiological research on the impact of ‘toxic stress’ on brain development.  A recently published study provides further insight into the association between childhood trauma and later life experiences of poor physical and mental health.

What did this study do?

The study, led by Dr Katie McLaughlin at Harvard University, reported that children who suffer trauma from abuse or violence biologically age faster than children who have never experienced adversity. The study built on previous mixed findings on whether childhood adversity is linked to premature ageing.  The authors more clearly defined adversity into two categories (1) threat-related adversity of violence or abuse, and (2) deprivation related adversity of neglect and poverty. The study also used three signs of biological aging – early puberty, cellular aging, and changes in brain structures – to undertake a meta-analysis of almost 80 studies.  A meta-analysis is a systematic approach to the review of findings from multiple studies, which explore the same question or area of interest, to identify whether there are statistically significant common findings or conclusions that can be drawn. The study found that threat-related trauma was associated with all three signs of premature biological aging, but deprivation-related adversity was not significantly associated with premature aging.

How well does the media describe the study?

The study was covered in many media reports, including The Guardian and science news outlets.  Although the ‘science’ behind the association was reported in varying levels of detail what is interesting to note is the strong inequalities focus within the reporting.  This was clearly led by the author who highlights in her quotes the implications this study has for understanding health disparities and the need to focus prevention in the early years.  However, there are gaps in how these findings are presented.  Overall, there is a strong emotional detachment from the findings and little clarity into whether particular sub-groups are more or less impacted

This study provides evidence that exposure to violence makes children grow up faster, not only emotionally but biologically.  The severity of this situation within the articles is at times hidden behind terms such as trauma and adversity with little insight into the human cost.  There is no clarity within the reports as to whether particular sub-populations, particularly girls, are more or less impacted.  This is interesting as two of the media reports mention early onset of puberty in girls.  

The findings are also emphasised within a medical model, with little discussion on the implications of the findings on public mental health – the art and science of improving mental wellbeing and preventing mental health problems via organised efforts and informed choices of society, organisations, public and private, communities, and individuals. This is evident in the reporting of the lead author’s view of the findings. Quotes from Dr. McLaughlin frame implications of the study as the need to use existing evidence-based treatments to improve mental health in children experiencing trauma to slow down the pattern of accelerated biological aging.  There is no reporting into what this means from a public mental health perspective.  In particular,  for breaking cycles of violence and abuse so that fewer children and young people are exposed to these in the first place.  This would move the analysis and implications of the study from a very individualised approach to one that explores the policy and community supports required to create strong family units and thriving communities. 

Another important point to keep in mind is that the results of the meta-analysis were of a small effect, rendering them as potentially trivial. Even the authors themselves acknowledge that the findings are preliminary and so further research will be needed in the area before it can be stated that ‘Children who suffer violence or trauma age faster’. Additionally, the meta-analysis only focused on combining results from studies that have been published. Publishing non-significant findings (i.e. where results don’t show a strong relationship) can be more difficult to publish. As such, it cannot be ruled out that including unpublished scientific data could have changed the results.

Useful links:

Adverse childhood experiences in context briefing paper (Aug 2019) Public Health Scotland:

Tackling Social Inequalities to reduce mental health problems: how everyone can flourish equally (Jan 2020) Mental Health Foundation: