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Looking back on Research the Headlines in 2021

2021 was another challenging year for evidence-based media reporting of research. Daily exposure to health related research has again 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 2021 we posted about media coverage of both COVID-19 and non-pandemic topics. Back in March we wrote a myth busting post about COVID-19. This post was very much needed at the time with all the inaccuracies about the virus that were going around. The post is still highly relevant now we have reached the end of the year as it covers issues like vaccines and variants. We also recently posted about the association between dementia and COVID-19 and were pleased to highlight there was balanced accurate reporting in the media about the research.

We blogged about other cases of accurate reporting of research over the last year. We saw examples of good reporting in posts about diet and brain health. Most journalists were careful to acknowledge 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 including linking to relevant charities such as our post about maternal health and obesity back in September. In a recent post about antimicrobial resistance we also highlighted excellent use of the views of an independent academic to support interpretation of the study.

Some media reports of research weren’t quite so accurate. Use of technology and its impact on health is frequently discussed in the media. Back in March we blogged about media coverage of ‘excessive’ smart phone use and highlighted how the media had exaggerated the findings of studies. 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.  Other examples of inaccurate reporting again related to risk reported in relation to a percentage format. We have regularly advised caution when interpreting the significance of a reduction or increase of something reported in percentage format. In this recent post about Vitamin D and bowel cancer, the media had reported that ‘eating just half a serving of salmon a day can slash your risk of getting bowel cancer by 50%, study claims’ in reference to the findings of the study.  In our ‘How to Research the Headlines’ tips series we have described the importance of referring to the absolute risk or benefit when describing results, so including the benefit with and without eating this portion of food.

We will continue with our range of activities in 2022 and look forward to continue working with early career researchers and offering them opportunities to develop their blogging skills!

Vitamin D and the Risk of Bowel Cancer 

This blog was written by Dr Issraa Al-Obaidi (University of Strathclyde)

Colorectal cancer is the most common type of cancer in the UK. It is also known as bowel cancer, colon cancer and rectal cancer. The main symptoms of this disease are diarrhoea or constipation, abdominal pain, blood in the stool, unexpected weight loss and fatigue. A recent report for England indicates that this disease has increased in younger adults under the age of 50. 

A study conducted by Hanseul Kim and colleagues at Harvard found that young people (women in this particular study) were recorded at risk of early onset colorectal cancer due to vitamin D deficiency.  This vitamin is formed naturally under our skin when we are outside exposed to sunlight, so it is called sunshine vitamin. It keeps our bones, teeth, and muscle healthy by working together with calcium and phosphorous (a mineral found in foods like beer, cheese, beans, and fish). Vitamin D is available in our daily food such as milk, fish (salmon, tuna, trout), egg yolk, cheese, some cereals and liver. Any deficiency in vitamin D can cause muscle cramps, bone pain, fatigue, and mood changes such as depression. Your GP can order a blood test for you to check any deficiency of vitamin D in your body.

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Beyond social distancing and the need for care: Do Alzheimer’s Disease and COVID19 share genetic risk too? 

This piece was written by Dr Fiona Kerr (Edinburgh Napier University).

The COVID19 pandemic has impacted young and old both due to poor outcomes from the disease itself and through negative impacts on well-being due to lockdown and poor access to healthcare systems. One group that quickly emerged as being particularly vulnerable are people living with dementia, with almost 25% of those who died from COVID19 in 2020 also having Alzheimer’s Disease (AD) or other forms of dementia (COVID19 and Dementia Mortality, Alzheimer’s Society). Much of this disproportionate impact has been attributed to challenges for people with dementia to adhere to the social distancing and hand hygiene mitigations put in place to prevent infection, and their over-representation in care homes, which were particularly hard hit by COVID19 (Science Media Centre). In October this year, a new study in the journal Brain, by Magusali N et al., 2021, identified that a genetic variant may confer risk for both AD and severe COVID19. This suggests that there may also be molecular reasons to explain why people with dementia are particularly vulnerable to this infectious disease. 

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Science in The Media Vs. The Wonderdrug Valley of Death

This blog was written by Dr Delma Childers from the University of Aberdeen.

Antibiotics were the game-changing wonderdrugs that revolutionized medicine in the early 20th century. In fact, their impact stretches far beyond medicine – antibiotics also revolutionized agriculture and livestock practices to usher in an era of relatively cheap and plentiful food in industrialized nations. However, decades of antibiotic misuse, overuse, a lack of drug discovery investment, and the resilient evolution of microorganisms have led to a concerning state of antimicrobial resistance and to a very real threat of society facing a world where the antibiotics don’t work.

18-24 November was World Antimicrobial Awareness Week which is part of a campaign by leaders at the World Health Organization (WHO) to bring attention to the problem of drug resistance. The WHO have listed antimicrobial resistance as one of the biggest global threats to health, food security, and development. There are two main solutions that current research efforts around the globe are testing: 1) find/design new drugs or 2) adapt current drugs to overcome microbial resistance strategies. A recent study (1) demonstrating an outside-the-box solution has been covered by The Daily Mail and Express. How did the media coverage of this study go?

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A balanced diet: can wine and cheese be good for your brain?

This piece was written by Reece Thompson (University of Strathclyde) and Dr Fiona Kerr (Edinburgh Napier University).

As part of the RSE Young Academy Scotland (YAS) Robertson Trust mentoring programme, YAS members mentor Robertson Trust Journey to Success Scholars who have talent, but perhaps not the financial means or guidance, to reach their potential through higher education. Often first in family to undertake a degree, scholars are supported by YAS members to develop their communication, learning, and employability skills. During this year’s programme, Reece Thompson, a third-year student in Biochemistry and Pharmacology at the University of Strathclyde, worked with Dr Fiona Kerr, a YAS member from Edinburgh Napier University, to develop his understanding of how research is reported in the media and to communicate the findings of a complex research study to the public through this Research the Headlines post. 

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Weighing up the risk: The relationship between maternal obesity and bowel cancer risk

In the past week a number of media outlets (The Guardian, The Herald) have covered the findings from research investigating the link between maternal obesity and the rise in numbers of bowel cancer cases in younger adults (aged <50 years).

According to the World Health Organization obesity is a global issue affecting all nations, which has tripled since 1975. Obesity, which is the abnormal accumulation of body fat, has been linked to many illnesses including cancer.

Researchers have shown a clear link between obesity and cancer, but there has been little research investigating the evidence linking maternal obesity with the risk of their children developing cancer later in life.

Researchers at the University of Texas Health Science Centre (Texas, USA) have attempted to answer this very important question on the association between maternal health and health outcomes for their babies later in life. In this study, they focused on the link between maternal obesity and the risk of bowel cancer developing in their children. This work was published on August 21st 2021 in the British Medical Journal Gut.

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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.