COVID-19: Pandemics and ‘Infodemics’

Posted on September 7, 2021September 6, 2021 by lindsey.pike

Drs Luisa Zuccolo and Cheryl McQuire, Department of Population Health Sciences, Bristol Medical School, University of Bristol.

The problem

Soon after the World Health Organisation (WHO) declared COVID-19 a pandemic on March 11th 2020, the UN declared the start of an infodemic, highlighting the danger posed by the fast spreading of unchecked misinformation. Defined as an overabundance of information, including deliberate efforts to disseminate incorrect information, the COVID-19 infodemic has exacerbated public mistrust and jeopardised public health.

Social media platforms remain a leading contributor to the rapid spread of COVID-19 misinformation. Despite urgent calls from the WHO to combat this, public health responses have been severely limited. In this project, we took steps to begin to understand and address this problem.

We believe that it is imperative that public health researchers evolve and develop the skills and collaborations necessary to combat misinformation in the social media landscape. For this reason, in Autumn 2020 we extended our interest in public health messaging, usually around promoting healthy behaviours during pregnancy, to study COVID-19 misinformation on social media.

We wanted to know:

What is the nature, extent and reach of misinformation about face masks on Twitter during the COVID-19 pandemic?

To answer this question we aimed to:

Upskill public health researchers in the data capture and analysis methods required for social media data research;
Work collaboratively with Research IT and Research Software Engineer colleagues to conduct a pilot study harnessing social media data to explore misinformation.

The team

Dr Cheryl McQuire got the project funded and off the ground. Dr Luisa Zuccolo led it through to completion. Dr Maria Sobczyk checked the data and analysed our preliminary data. Research IT colleagues, led by Mr Mike Jones, helped to develop the search strategy and built a data pipeline to retrieve and store Twitter data using customised application programming interfaces (APIs) accessed through an academic Twitter account. Research Software Engineering colleagues, led by Dr Christopher Woods, provided consultancy services and advised on the analysis plan and technical execution of the project.

Cheryl McQuire, Luisa Zuccolo, Maria Sobcyzk, Mike Jones, Christopher Woods. (Left to Right)

Too much information?!

Initial testing of the Twitter API showed that keywords, such as ‘mask’ and ‘masks’, returned an unmanageable amount of data, and our queries would often crash due to an overload of Twitter servers (503-type errors). To address this, we sought to reduce the number of results, while maintaining a broad coverage of the first year of the pandemic (March 2020-April 2021).

Specifically, we:

I) Searched for hashtags rather than keywords, restricting to English language.

II) Requested original tweets only, omitting replies and retweets.

III) Broke each month down into its individual days in our search queries to minimise the risk of overload.

IV) Developed Python scripts to query the Twitter API and process the results into a series of CSV files containing anonymised tweets, metadata and metrics about the tweets (no. of likes, retweets etc.), and details and metrics about the author (no. of followers etc.).

V) Merged data into a single CSV file with all the tweets for each calendar month after removing duplicates.

What did we find?

Our search strategy delivered over three million tweets. Just under half of these were filtered out by removing commercial URLs and undesired keywords, the remaining 1.7m tweets by ~700k users were analysed using standard and customized R scripts.

First, we used unsupervised methods to describe any and all Twitter activity picked up by our broad searches (whether classified as misinformation or not). The timeline of this activity revealed clear peaks around the UK-enforced mask mandates in June and September 2020.

We further described the entire corpus of tweets on face masks by mapping the network of its most common bigrams and performing sentiment analysis.

We then quantified the nature and extent of misinformation through topic modelling, and used simple counts of likes to estimate the reach of misinformation. We used semi-supervised methods including manual keyword searches to look for established types of misinformation such as face masks restricting oxygen supply. These revealed that the risk of bacterial/fungal infection was the most common type of misinformation, followed by restriction of oxygen supply, although the extent of misinformation on the risks of infection decreased as the pandemic unfolded.

Extent of misinformation (no tweets), according to its nature: 1- gas exchange/oxygen deprivation, 2- risk of bacterial/fungal infection, 3- ineffectiveness in reducing transmission, 4- poor learning outcomes in schools.

Relative to the volume of tweets including the hashtags relevant to face masks (~1.7m), our searches uncovered less than 3.5% unique tweets containing one of the four types of misinformation against mask usage.

A summary of the nature, extent and reach of misinformation on face masks on Twitter – results from manual keywords search (semi-supervised topic modelling).

A more in-depth analysis of the results attributed to the 4 main misinformation topics by the semi-supervised method revealed a number of potentially spurious topics. Refinements of these methods including iterative fine-tuning were beyond the scope of this pilot analysis.

Our initial exploration of Twitter data for public health messaging also revealed common pitfalls of mining Twitter data, including the need for a selective search strategy when using academic Twitter accounts, hashtag ‘hijacking’ meaning most tweets were irrelevant, imperfect Twitter language filters and ads often exploiting user mentions.

Next steps

We hope to secure further funding to follow-up this pilot project. By expanding our collaboration network, we aim to improve the way we tackle misinformation in the public health domain, ultimately increasing the impact of this work. If you’re interested in health messaging, misinformation and social media, we would love to hear from you – @Luisa_Zu and @cheryl_mcquire.

Note:

This blog post was original written for the Jean Golding Institute blog

Metadata errors: an under-appreciated source of bias in Mendelian randomization studies

Posted on August 20, 2021 by lindsey.pike

Dr Philip Haycock

In two-sample Mendelian randomization (MR), a type of epidemiological method, we combine the results from different genetic studies to study the causal relationship between human characteristics and disease. For example, we might take results from a genetic study of smoking and a different genetic study of cancer. We can combine their results to understand whether smoking might be a cause of cancer. If the same position in the genome is associated with smoking in the first study and with cancer in the other study, this can provide evidence that smoking is a causal factor in cancer. However, it’s also possible that this position in the genome could be related to smoking and cancer via separate pathways. This phenomenon is known as “horizontal pleiotropy” and is a common source of bias in Mendelian randomization research.

Another, often under-appreciated, source of bias are errors in metadata. To understand this we need to understand what genetic results look like in practice. Below is an example of a genetic results file with 5 rows and 6 columns (a typical file might actually have several million rows).

Each row refers to a single position in the human genome that varies between people. These positions are referred to as “genetic variants” (also known as polymorphisms). The particular type of variant that an individual carries is known as their allele.

Below is an example of metadata. The metadata helps us understand the contents of the results file. It tells us what the columns represent.

Some columns in the results file will describe the relationship (“effect” column) between the genetic variant and some human characteristic (e.g. smoking) and there will be additional columns that help researchers interpret this relationship. These additional columns include things like the identity of the allele that is used to model the relationship (e.g. if people have allele “A” they may be more likely to smoke compared to people without this allele) or information on how common the allele is in the population. These columns are also known as the “effect allele” and “effect allele frequency” columns. Metadata errors refer to mistakes in how these columns are reported. For example, maybe allele1 is reported as the effect allele column when in fact it should have been allele 2 that is described in this way. Sometimes the information provided in metadata is ambiguous. For example, the metadata tells us that the “freq” column represents allele frequency but there are two alleles. Is this the frequency of allele1 or allele2? We can’t be sure. Another type of error refers to mistakes in the reported results, for example reporting that a genetic variant increases the probability that a person smokes when in reality it has no effect (in other words the effect is zero). This is known as a summary data error. Failure to identify these errors can lead to mistakes in Mendelian randomization analyses, such as finding that smoking protects against cancer (when we know the opposite is true).

As research complexity increases, so does the potential for errors

These types of errors were fairly easy to avoid during the early years of Mendelian randomization research, when studies tended to be hypothesis-driven and focused on small numbers of relationships (although errors still occurred). Mendelian randomization study designs are, however, increasingly complex and hypothesis-free, sometimes assessing relationships amongst 100s or even 1000s of characteristics and diseases. New online platforms and databases that collate genetic results from many different sources, and provide tools that can automate analyses, make these studies easier to undertake than ever before. The downside is that they probably make meta and summary data errors more likely.

Maximising metadata quality to reduce errors

We address this issue in a new pre-print: “Design and quality control of large scale Mendelian randomization studies”. We present an R package and set of quality control tools that identify meta and summary data errors, which we developed for the Fatty Acids in Cancer Mendelian Randomization Collaboration (FAMRC). The FAMRC is a pan-cancer MR study that seeks to evaluate the causal relevance of fatty acids for risk of major cancers. We wanted to maximise the quality of the genetic study results we collected from the cancer studies, to ensure the integrity of our Mendelian randomization analyses. After implementing our tools, we found major meta and summary data errors in 7 (13%) of 55 genetic studies in the FAMRC.

What types of metadata errors did we find?

The basic principle of our quality control approach is to identify errors through

comparison of the results of individual studies in the FAMRC to external studies
comparison of reported to expected results.

For example, we identified genetic variants that are known to cause cancer and checked that the same variants had the expected relationship in the FAMRC. In the figure below, every data point represents a single genetic variant that is known to increase cancer risk. The horizontal or X axis shows the known relationship in the GWAS catalog (this is a database of known genetic associations with 1000s of human characteristics in 1000s of genetic studies) and the vertical or Y axis shows the relationship in one of the studies in the FAMRC. Each axis shows the Z score, which is basically a standardised measure of how each genetic variant affects cancer risk (positive values mean that the variant increases risk of cancer and negative values indicate they decrease risk). As you can see, in the FAMRC study on the vertical Y axis, almost all the variants have negative Z values (indicating they reduce cancer risk), when in fact they are known to increase risk (the true relationship is represented by Z scores in the GWAS catalog). This discrepancy was caused by a metadata error, where the effect allele column was incorrectly labelled. We also found that the “frequency of the effect allele” was wrong. How common the allele is in the population was opposite to what we’d expect, based on comparison with other studies, confirming the presence of metadata errors.

Various other types of errors were identified, including one study reporting that 100s of genetic variants had very strong effects on fatty acid levels when in fact they had no effect at all. For example, in the figure below, the many red data points refer to genetic variants in the FAMRC that had a very large effect on fatty acids but were not reported in the GWAS catalog, suggesting a potential problem with the genetic results.

We also compared the reported results (how the genetic variants affected fatty acids in the FAMRC) to predicted results (how we would expect the genetic variants to affect fatty acids). In the figure below we see a “fanning-out” pattern, when what we should see is a strong linear relationship (i.e. the data points lying on a single straight line). This relationship can be summarised with the “slope” metric. We should see a slope of 1 (this means if the reported result increases by 1 the predicted result will also increase by 1), which is not the case. We confirmed with the data provider that low quality genetic variants had not been excluded from their study. Once the low quality variants had been excluded, the discrepancies disappeared.

Avoiding metadata errors: recommendations for researchers

When conducting Mendelian randomization analyses using results from genetic studies, researchers can avoid metadata and other errors by:

Requesting results for genetic variants that are known to affect their disease of interest. Researchers should check that these variants have the expected effect in their dataset.
Comparing the frequency of genetic variants to expected frequencies in a reference dataset. We created a special reference dataset that can be used for this purpose (accessible via the CheckSumStats R package).
Not assuming that results have had low quality variants excluded, but instead seeking confirmation of this with data providers. Our quality control tools also provide a way to check this.

Further attention is needed to address the growing diversity of GWAS

One issue we only partly addressed was the “two-sample assumption”: that the studies being compared come from the same population. In our own analyses, we found that the frequency of genetic variants was very similar across European-origin studies, indicating satisfaction of the assumption. On the other hand, our tools were not really optimised for this purpose. The need to assess the “same population” assumption is becoming more urgent with the growing diversity of genetic studies.

In conclusion, meta and summary data errors are an under-appreciated source of bias in MR research, especially in complex study designs. We developed an R package and set of tools that can be used to flag meta and summary data errors in the results of genetic studies, which in turn can be used to enhance the integrity of Mendelian randomization analyses. Our tools and methods are available to other researchers via the CheckSumStats R package.

Contact the author

philip.haycock@bristol.ac.uk

Does testosterone drive success in men? Not much, our research suggests

Posted on August 3, 2021August 3, 2021 by lindsey.pike

Not quite what the science says.
UfaBizPhoto/Shutterstock

Amanda Hughes, University of Bristol; Neil Davies, University of Bristol, and Sean Harrison, University of Bristol

There’s a widespread belief that your testosterone can affect where you end up in life. At least for men, there is some evidence for this claim: several studies have linked higher testosterone to socioeconomic success. But a link is different to a cause and using DNA, our new research suggests it may be much less important for life chances than previously claimed.

In previous studies, male executives with higher testosterone have been found to have more subordinates, and financial traders with higher testosterone found to generate greater daily profits. Testosterone has been found to be higher among more highly educated men, and among self-employed men, suggesting a link with entrepreneurship. Much less is known about these relationships in women, but one study suggested that for women, disadvantaged socioeconomic position in childhood was linked to higher testosterone later in life.

The beneficial influence of testosterone is thought to work by affecting behaviour: experiments suggest that testosterone can make a person more aggressive and more risk tolerant, and these traits can be rewarded in the labour market, for instance in wage negotiations. But none of these studies show definitively that testosterone influences these outcomes because there are other plausible explanations.

Rather than testosterone influencing a person’s socioeconomic position, it could be that having a more advantaged socioeconomic position raises your testosterone. In both cases, we would see a link between testosterone and social factors such as income, education and social class.

There are plausible mechanisms for this too. First, we know that socioeconomic disadvantage is stressful, and chronic stress can lower testosterone. Second, how a person perceives their status relative to others in society might influence their testosterone: studies of sports matches, usually between men, have often found that testosterone rises in the winner compared to the loser.

Older man holds head in front of a computer. — Chronic stress can lower your testosterone.
Shutterstock

It’s also possible that some third factor is responsible for the associations seen in previous studies. For instance, higher testosterone in men is linked to good health – and good health may also help people succeed in their careers. A link in men between testosterone and socioeconomic position could therefore simply reflect an impact of health on both. (For women, higher testosterone is linked to worse health, so we would expect an association of higher testosterone and lower socioeconomic position.)

Look at it this way

It is very difficult to pick apart these processes and study just the effects of testosterone on other things. With this goal in mind, we applied a causal inference approach called “Mendelian randomisation”. This uses genetic information relevant to a single factor (here, testosterone) to isolate just the effect of that factor on one or more outcomes of interest (here, socioeconomic outcomes such as income and educational qualifications).

DNA visualisation with coloured bars — DNA can tell us a lot about our relationship with testosterone.
Zita/Shutterstock

A person’s circulating testosterone can be affected by environmental factors. Some, like the time of day, are straightforward to correct for. Others, like somebody’s health, are not. Crucially, socioeconomic circumstances could influence circulating testosterone. For this reason, even if we see an association between circulating testosterone and socioeconomic position, we cannot determine what is causing what.

This is why genetic information is powerful: your DNA is determined before birth and generally does not change during your lifetime (there are rare exceptions, such as changes which occur with cancer). Therefore, if we observe an association of socioeconomic position with genetic variants linked to testosterone, it strongly suggests that testosterone is causing the differences in socioeconomic outcomes. This is because influence on the variants of other factors is much less likely.

In more than 300,000 adult participants of the UK Biobank, we identified genetic variants linked to higher testosterone levels, separately for men and women. We then explored how these variants were related to socioeconomic outcomes, including income, educational qualifications, employment status, and area-level deprivation, as well as self-reported risk-taking and overall health.

Similar to previous studies, we found that men with higher testosterone had higher household income, lived in less deprived areas, and were more likely to have a university degree and a skilled job. In women, higher testosterone was linked to lower socioeconomic position, including lower household income, living in a more deprived area, and lower chance of having a university degree. Consistent with previous evidence, higher testosterone was associated with better health for men and poorer health for women, and more risk-taking for men.

However, there was little evidence that genetic variation related to testosterone affected socioeconomic position at all. In both men and women we detected no effects of genetic variants related to testosterone on any aspect of socioeconomic position, or health, or risk-taking.

Because we identified fewer testosterone-linked genetic variants in women, our estimates for women were less precise than for men. Consequently, we could not rule out relatively small effects of testosterone on socioeconomic position for women. Future studies could examine associations in women using larger, female-specific samples.

But for men, our genetic results clearly suggest that previous studies may have been biased by the influence of additional factors, potentially including the impact of socioeconomic position on testosterone. And our results indicate that – despite the social mythology surrounding testosterone – it may be much less important for success and life chances than earlier studies have suggested.

Amanda Hughes, Senior Research Associate in Epidemiology, University of Bristol; Neil Davies, Senior Research Fellow, University of Bristol, and Sean Harrison, Systematic Reviewer, University of Bristol

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

Study collecting the views of young people, parents of children with long COVID, and doctors, finds that long COVID in children is poorly understood by doctors

Posted on July 21, 2021July 20, 2021 by lindsey.pike

Dr Katharine Looker

‘Enhancing the utilization of COVID-19 testing in schools’, is a study which will look at the characteristics of long COVID and COVID-19 infection in children. ‘Long COVID’ is commonly used to describe signs and symptoms that continue or develop after acute COVID‑19. The study is being funded as a result of a rapid funding call by Health Data Research UK (HDR UK), the Office for National Statistics (ONS) and UK Research and Innovation (UKRI). The study forms part of the larger Data and Connectivity National Core Study, which is led by HDR UK in partnership with ONS.

The COVID-19 testing in schools study is related to the CoMMinS (COVID-19 Mapping and Mitigation in Schools) study being undertaken by the University of Bristol in partnership with Bristol City Council, Public Health England [PHE] and Bristol schools. CoMMinS aims to give us an understanding of COVID-19 infection dynamics centred around school pupils and staff and onward transmission to family contacts, using regular testing. Our study will jointly analyse data from CoMMinS, along with information from Electronic Patient Records, and data from the COVID-19 Schools Infection Survey (SIS; jointly led by the London School of Hygiene & Tropical Medicine [LSHTM], PHE, and ONS). The SIS is a study similar to CoMMinS but carried out nationally.

To help inform research questions and methods for the study, members from the University of Bristol study team gathered views about long COVID in children between 9 March and 30 April 2021 from:

seven young people from the NIHR Bristol Biomedical Research Centre Young People’s Advisory Group (YPAG)
five families whose children have long COVID or suspected long COVID, recruited through two online UK campaign groups for long COVID, and
a survey completed by four GPs and one paediatrician, and an online meeting with two paediatricians.

It is important to note that the opinions gathered were based on small samples which may not be representative.

Through the meeting and survey with the doctors, the study team found that clinical understanding of long COVID in children is currently very limited.

The doctors said that it may be hard to distinguish between long COVID and other conditions with similar symptoms. Many of the symptoms of long COVID, like fatigue and feeling sick, aren’t very specific, and are common to many different conditions. Long COVID in children currently lacks a clinical definition, making diagnosis difficult. It isn’t yet properly understood whether long COVID is a new condition in itself, or a group of conditions like post viral fatigue, which is already recognised.

Young people, and families of children with long COVID or suspected long COVID, who were also asked for their opinion, said that feeling sick or stomach pain, extreme tiredness, and headaches were the symptoms they would rank as most ‘harmful’. For young people, this was based on them imagining having the symptoms. For the families, this was based on their first-hand experience.

The families also said that the symptoms their children were experiencing were numerous, often very severe, and more wide-ranging than those currently listed on the NHS website for long COVID. It is not yet clear what is causing the unusual symptoms.

The families said that they had struggled to get a diagnosis and treatment for their children. They also said that long COVID symptoms were having a significant impact on their children’s day-to-day lives both physically and psychologically, and that some of the children had missed school because of the symptoms. Some of the families also found fevers difficult to manage because their children had to miss school to self-isolate every time they had a fever. They wanted to know why the set of symptoms were being experienced, and why their children in particular had developed them.

It is not known how many children have or will develop long COVID. So far, studies which have tried to measure the rate of long COVID in children suggest it is rare. However, quantifying the number of cases is made difficult by a lack of clinical understanding of long COVID including the lack of an agreed clinical definition. The opinions collected suggest that relying on clinical diagnoses alone will under-estimate cases. On the other hand, there needs to be a cautious approach to estimating the number of cases based on non-specific symptoms, as other conditions which cause similar symptoms may be counted as well.

Caroline Relton, Professor of Epigenetic Epidemiology and Director of the Bristol Population Health Science Institute at the University of Bristol, joint lead for CoMMinS and one of the lead authors of the report, said: “The opinions we gathered further highlight that it is difficult to count the number of children with long COVID on the basis of diagnoses alone while long COVID in children remains poorly defined.

“There are added complications of studying long COVID in children, when it is sometimes difficult to disentangle what might be the result of experiencing infection from what might result from the wider impact of experiencing the pandemic. Isolation, school closures, disrupted education and other influences on family life could all have health consequences. Defining the extent of the problem in children and the root causes will be essential to helping provide the right treatment and to aid the recovery of young people who are suffering.”

The findings highlight that examining GP and hospital visits, and school attendance, might currently be a more useful and feasible way of assessing how COVID-19 has affected children, rather than relying only on diagnoses of long COVID. However, the study researchers also need to be aware how often healthcare is accessed according to need, and absence from school due to self-isolation, which will affect what is being measured.

Feeling sick or stomach pain, extreme tiredness, and headaches will be important symptoms to consider in the study.

Read the full report

Find the full report on the CoMMinS study news page.

How can your gut microbiome affect risk of cancer?

Posted on June 3, 2021 by lindsey.pike

Dr Kaitlin H. Wade^1,2,3

¹Population Health Sciences, Bristol Medical School, University of Bristol, Bristol, BS8 2BN

²Medical Research Council (MRC-IEU), University of Bristol, Bristol, BS8 2BN

³Cancer Research UK (CRUK) Integrative Cancer Epidemiology Programme (ICEP), University of Bristol, Bristol, BS8 2BN

The causes of cancer are often preventable

Cancer, a disease that has a profound impact on the lives of individuals all over the world, also has an ever-increasing burden. And yet, evidence indicates that over 40% of all cancers are likely explained by preventable causes. One of the main challenges is identifying so-called ‘modifiable risk factors’ for cancer – aspects of our environment that we can change to reduce the incidence of disease.

Photo by Chloe Russell for ‘Up Your A-Z’, an encyclopaedia of gut bacteria

The gut microbiome could influence cancer risk

The gut microbiome is a system of microorganisms that helps us digest food, produce essential molecules and protects us against harmful infections. There is growing evidence supporting the relationship between the human gut microbiome and risk of cancer, including lung, breast, bowel and prostate cancers. For example, experiments have shown that changing the gut microbiome (e.g., by using pre- or pro-biotics) may reduce the risk of developing colorectal cancer. Research also suggests that people with colorectal cancer have lower microbiota diversity and different types of bacteria within their gut compared to those without a diagnosis.

As the gut microbiome can have a substantial impact on their host’s metabolism and immune response, there are many biological mechanisms by which the gut microbiome could influence cancer development and progression. However, we don’t yet know how the gut microbiome can do this.

Human studies in this context have used small samples of individuals and measure both the microbiome and disease at the same time. These factors can make it difficult to tease apart correlation from causation – i.e., does variation in the gut microbiome change someone’s risk of cancer or is it the existence of cancer that leads to variation in the gut microbiome? This is an important question because the main aim of such research is to understand the causes of cancer and how we can prevent the disease. We want to fully understand whether altering the gut microbiome can reduce the burden of cancer at a population level or whether it is simply a marker of cancer itself.

I’m inviting feedback on your knowledge and understanding of the gut microbiome and cancer – please take this 5-minute survey (click here for survey) to contribute your thoughts.

People are interested in their gut microbiome

Even though we don’t yet know much about the causal relevance of the gut microbiome, there is still a growing market for commercial initiatives targeting the microbiome as a consumer-driven intervention. This usually involves companies obtaining a small number of faecal samples from consumers and prescribing “personalised” nutritional information for a “healthier microbiome”. However, these initiatives are very controversial given uncertainty in the likely relationships between the gut microbiome, nutrition and various diseases. What these activities do highlight is the demand for such information at a population level. This shows there is an opportunity to improve understanding of the causal role played by the gut microbiome in human health and disease.

Microbiome and variation in our genes

Using information about our genetics can help us find out whether the gut microbiome changes the risk of cancer, or whether cancer changes the gut microbiome. Genetic variation cannot be influenced by the gut microbiome nor disease. Therefore, if people who are genetically predisposed to having a higher abundance of certain bacteria within their gut also have a lower risk of, say, prostate cancer, this would strongly suggest a causal role of those bacteria in prostate cancer development. This approach of using human genetic information to discern correlation from causation is called Mendelian randomization.

Studies relating human genetic variation with the gut microbiome have proliferated in recent years. They have provided evidence for genetic contributions to features of the gut microbiome including the abundance or likelihood of presence (vs. absence) of specific bacteria. This knowledge has given the opportunity to apply Mendelian randomization to better understand the causal impact of gut microbiome variation in health outcomes, including cancer. There are, however, many important caveats and complications to this work. Specifically, there is a (currently unmet) requirement for careful examination of how human genetic variation influences the gut microbiome and interpretation of the causal estimates derived from using Mendelian randomization within this field.

This is exactly what I will be looking at in my new research funded by Cancer Research UK. For more details on the nuances of this work, please see my research feature for Cancer Research UK and paper discussing these complexities.

What’s next for this research?

This research has already shown promise in the application of Mendelian randomization to improve our ability to discern correlation from causation between the gut microbiome and cancer. It has importantly highlighted the need for inter-disciplinary collaboration between population health, genetic and basic sciences. Thus, with the support from my team of experts in microbiology, basic sciences and population health sciences, this Fellowship will set the scene for the integration of human genetics and causal inference methods in population health sciences with microbiome research. This will help us understand the causal role played by the gut microbiome in cancer. Such work acts as a new and important step towards evaluating and prioritising potential treatments or protective factors for cancer prevention.

Acknowledgements

The research conducted as part of this Cancer Research UK Population Research Postdoctoral Fellowship will be supported by the following collaborators: Nicholas Timpson, Caroline Relton, Jeroen Raes, Trevor Lawley, Lindsay Hall and Marc Gunter, and my growing team of interdisciplinary PhD students and postdoctoral researchers. I’d also like to thank the following individuals for comments on this feature: Tom Battram, Laura Corbin, David Hughes, Nicholas Timpson, Lindsey Pike and Philippa Gardom. Additional thanks go to Chloe Russell, a brilliant photographer with whom I collaborated to create “Up Your A-Z” as part of Creative Reactions 2019, who provided the photos for this webpage.

About the author

Dr. Wade’s academic career has focused on the integration of human genetics with population health sciences to improve causality within epidemiological studies. Focusing on relationships across the life-course, her work uses comprehensive longitudinal cohorts, randomized controlled trials and causal inference methods (particularly, Mendelian randomization and recall-by-genotype designs). Kaitlin’s research has focused on understanding the relationships between adiposity and dietary behaviours as risk factors for cardiometabolic diseases and mortality. Having been awarded funding from the Elizabeth Blackwell Institute and Cancer Research UK, Kaitlin’s work uses these methods to understand the causal role played by the human gut microbiome on various health outcomes, such as obesity and cancer. Since pursuing a career in this field, Kaitlin has already led and been key in several fundamental studies that with path the way to resolve – or at least quantify – complex relationships between genetic variation, the gut microbiome and human health. In addition to her research, Kaitlin is actively involved in organising and administering teaching and public engagement activities as well as having many mentorship and supervisory roles within and external to the University of Bristol.

Key publications:

Hughes, D.A., Bacigalupe, R., Wang, J. et al. Genome-wide associations of human gut microbiome variation and implications for causal inference analyses. Nat Microbiol 5, 1079–1087 (2020). https://doi.org/10.1038/s41564-020-0743-8.

Kurilshikov, A., Medina-Gomez, C., Bacigalupe, R. et al. Large-scale association analyses identify host factors influencing human gut microbiome composition. Nat Genet 53, 156–165 (2021). https://doi.org/10.1038/s41588-020-00763-1.

Wade KH and Hall LJ. Improving causality in microbiome research: can human genetic epidemiology help? [version 3; peer review: 2 approved]. Wellcome Open Res 4, 199 (2020). https://doi.org/10.12688/wellcomeopenres.15628.3.

Breastfeeding research improves lives and advances health, but faces conflicts

Posted on March 16, 2021 by lindsey.pike

Research shows the breast milk of women who have recovered from COVID-19 offers a source of COVID-19 antibodies.
(Shutterstock)

Meghan Azad, University of Manitoba; Katie Hinde, Arizona State University; Lars Bode, University of California San Diego; Luisa Zuccolo, University of Bristol; Merilee Brockway, University of Manitoba; Nathan C. Nickel, University of Manitoba, and Rafael Perez-Escamilla, Yale University

Breastfeeding and breast milk provide big opportunities to support maternal, infant and population health. This is especially true during the current pandemic because breastfeeding can help alleviate food insecurity, and research shows the breast milk of women who have recovered from COVID-19 offers a source of COVID-19 antibodies.

Breastfeeding saves lives and prevents illness. It is environmentally friendly and profoundly important to children’s long-term development. After all, breast milk is the only food that has evolved specifically to feed humans.

Breastfeeding matters

Beyond supplying nutrition, breast milk provides personalized immune protection and shapes the developing microbiome. Scientists have discovered enzymes, hormones, antibodies and live cells in breast milk, and these bioactive components could hold the key to developing new therapies — not only for COVID-19, but also autoimmune diseases, diabetes and cancer.

Yet, remarkably, we still don’t fully understand the composition of breast milk, or the biological basis for its many health effects. In fact, more scientific papers have been published on headaches than breastfeeding, and more federal research dollars from Canadian Institutes of Health Research and the Natural Sciences and Engineering Research Council of Canada have been invested to study corn than breast milk.

The act of breastfeeding also supports mother-infant bonding and helps to prevent breast and ovarian cancer in mothers. Unfortunately, most mothers do not even meet their own breastfeeding goals, let alone achieve recommendations of exclusive breastfeeding for six months, followed by 18 months of breastfeeding along with other foods.

This is particularly concerning during this pandemic, when mothers infected with COVID-19 may be separated from their newborns (despite World Health Organization guidance to the contrary) and breastfeeding support is often unavailable because public health visits are being cancelled and lactation services have been suspended in many places.

Tensions abound

Every parent knows that infant feeding is a complex issue, often evoking strong emotions based on personal experience. Difficult or negative breastfeeding experiences can fuel a defensive “breastfeeding denialism” attitude.

A woman with tattoos breastfeeding her infant — Breastfeeding support such as public health visits may not be available during the pandemic.
(Pexels/Anna Shvets)

Conversely, some breastfeeding advocates refuse to acknowledge that for some families, formula is necessary for medical, personal, societal or socioeconomic reasons. These extreme attitudes cause a tense and unproductive environment for researchers working to generate inclusive evidence-based guidance for infant feeding.

Industry partnerships also cause tension in this field because the infant feeding industry frequently violates the World Health Organization code for marketing of breastmilk substitutes, and transgressions have worsened during the pandemic. However, due to lack of funding for breastfeeding research, scientists are often faced with choosing between industry funding or no funding at all.

Unfortunately, these tensions often detract from the energy and resources that breastfeeding advocates, researchers, health professionals and policy-makers could be using to advance their shared goal of supporting maternal and child health.

What can be done

Of course, members of the diverse breastfeeding advocacy and research communities will not always agree — but we should aim to find common ground and work together. There are many stakeholders involved, each with a role to play:

Governments and non-profit funding organizations should acknowledge the importance of breastfeeding and breast milk and invest more resources into this field.

Researchers should build interdisciplinary teams to study breast milk as a biological system and think broadly about “breastfeeding challenges” in the context of complex social systems – including social inequities, parental leave policies, lactation difficulties and donor breast milk.

Companies, researchers and advocacy groups should co-develop a conflict of interest framework for research on breastfeeding and breast milk and reporting of results.

Messaging is key to achieving these goals. All groups need to communicate effectively with each other, and with the health-care, research and public sectors. This means providing or sharing clear resources to convey scientific evidence free of conflict of interest, targeted to each audience, such as fact sheets for policy-makers, engaging videos for the public and infographics for health-care providers.

Stakeholders also need to actively discredit unfounded claims and misinformation, such as unsubstantiated health claims made by infant nutrition companies, or rumours about the transmission of COVID-19 via breastfeeding, when there is no evidence of this occurring.

Looking forward

A woman breastfeeding a baby — COVID-19 has highlighted both the importance and fragility of breastfeeding support systems.
(Shutterstock)

Progress in breastfeeding, breast milk and lactation research is being hampered by tensions among researchers, advocates and industry.

As breast milk scientists, breastfeeding researchers and lactation specialists, we are concerned about these tensions and their potential to impede or delay discoveries in our field. Last year, we held a workshop to discuss these concerns and develop solutions.

Our workshop paper was written before the pandemic, but its recent publication is timely. The pandemic has brought researchers together in ways that seemed impossible before.

Breast milk research that would normally take years has been completed in months with unprecedented efficiency. A global network of human milk banks was established in a matter of days to share information about safe operations during the pandemic. Milk scientists and breastfeeding researchers are meeting monthly with the WHO to speed up the transition from discovery to policy.

We hope these trends will continue beyond the pandemic and become the new standard for doing and sharing research.

COVID-19 has also emphasized both the importance and fragility of breastfeeding support systems, which have suffered considerably due to current restrictions. The pandemic has also highlighted the potential of breast milk to inform new avenues of biomedical research, such as milk antibodies as potential therapeutics.

We hope this added urgency will encourage researchers, advocates, funders and policy-makers to work together to accelerate progress in supporting breastfeeding and breast milk research.

Meghan Azad, Associate Professor of Pediatrics and Child Health; Canada Research Chair in the Developmental Origins of Chronic Disease, University of Manitoba; Katie Hinde, Associate Professor, School of Human Evolution and Social Change, Arizona State University; Lars Bode, Professor of Pediatrics and Director of Mother-Milk-Infant Center of Research Excellence, University of California San Diego; Luisa Zuccolo, Senior Research Fellow, Health Sciences, University of Bristol; Merilee Brockway, Post-doctoral Fellow, Department of Pediatrics and Child Health, University of Manitoba; Nathan C. Nickel, Associate Professor of Community Health Sciences; Co-Director MILC; Associate Director, Manitoba Centre for Health Policy, University of Manitoba, and Rafael Perez-Escamilla, Professor of Public Health, Yale University

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

Underestimation of Drug Use: A Perennial Problem with Implications for Policy

Posted on February 22, 2021February 22, 2021 by lindsey.pike

by Olivia Maynard

Follow Olivia on Twitter

Photo by Louie Castro-Garcia on Unsplash

In a paper recently published in the journal Addiction, Hannah Charles and colleagues suggest that the prevalence of illicit drug use among 23-25 year olds in a Bristol-based birth cohort (ALSPAC) is over twice that reported in the Crime Survey for England and Wales (CSEW). The team propose that these figures reflect under-reporting in the CSEW, although they note that they may reflect higher levels of illicit drug use in Bristol. Here I present some preliminary data supporting their view that the CSEW underestimates illicit drug use.

In March 2020, I recruited 683 UK university students to participate in a short survey on drug use via the online survey platform Prolific which has been shown to produce reliable data. I recruited only students aged 18 to 24 years who reported using alcohol in the past 30 days, and participants reported whether they had used any of MDMA/ecstasy, cocaine or cannabis in the past two years.

Table 1. Prevalence of self-reported illicit drug use across three surveys of young people in the UK

	University students via ProlificAged 18-24	Bristol, ALSPAC Aged 23-25		CSEW Aged 23-25
	2 years	1 year	Lifetime	1 year	Lifetime
Any illicit drug use^a	52.7 (360)	36.7	62.8	16.4	40.6
Cannabis	50.2 (343)	29.2	60.5	13.8	37.3
MDMA/ecstasy/amphetamines^b	23.3 (159)	17.0	32.9	3.6	11.1
Cocaine	21.1 (144)	19.6	30.8	4.8	13.9

Notes: Values represent percentage of participants (number of participants). Percentages for CSEW and ALSPAC are taken from Charles et al (1) and are weighted percentages.
^{a ‘}Any illicit drug use’ refers only to the illicit drugs assessed in the respective surveys (only cannabis, MDMA and cocaine in our survey), more drugs in ALSPAC and CSEW – see Charles et al (1).
^bOur Prolific survey asked about ‘MDMA / ecstasy’ use, ALSPAC categorised ecstasy/MDMA use along with other ‘amphetamine’ use and CSEW asked about ‘ecstasy’ use.

Over half of my sample reported using at least one of cannabis, cocaine or MDMA in the past two years (Table 1). This is markedly higher than the CSEW’s estimates of either past year or lifetime use, and more in line with those reported in ALSPAC. Comparing across drugs, past two-year use of the three drugs is higher in my survey than either past year or lifetime use in the CSEW, and higher than past year, but lower than lifetime use in ALSPAC. Perhaps of more interest than ever use of the drugs over the past two years, I also examined the combinations of drugs students in my survey were using (Table 2). I find that the majority of students who report using illicit drugs have only used cannabis in the past two years (25% of all students), although the second largest group (15%) have used all three of cannabis, MDMA and cocaine.

Table 2. Prevalence of self-reported illicit drug among UK university students

	Qualtrics survey of university students (past two years)
	All (n=683)	Female (n=336)	Male (n=312)	Other (n=35)
Illicit drug use
Cannabis	50.2 (343)	48.5 (163)	53.5 (167)	37.1 (13)
MDMA / ecstasy	23.3 (159)	19.3 (65)	29.2 (91)	8.6 (3)
Cocaine	21.1 (144)	17.6 (59)	26 (81)	11.4 (4)

Illicit drug use profiles
Alcohol only (no illicit drug use)	47.3 (323)	48.2 (162)	44.6 (139)	62.9 (22)
Any illicit drug use^a	52.7 (360)	51.8 (174)	55.4 (173)	37.1 (13)
Cannabis only	24.5 (167)	27.4 (92)	21.5 (67)	22.9 (8)
Cannabis + Cocaine + MDMA	15.4 (105)	11.3 (38)	20.8 (65)	5.7 (2)
Cannabis + MDMA	6.3 (43)	6 (20)	7.1 (22)	2.9 (1)
Cannabis + Cocaine	4.1 (28)	3.9 (13)	4.2 (13)	5.7 (2)
Cocaine only	0.9 (6)	1.2 (4)	0.6 (2)	0 (0)
MDMA only	0.9 (6)	0.9 (3)	1 (3)	0 (0)
Cocaine + MDMA	0.7 (5)	1.2 (4)	0.3 (1)	0 (0)

Notes: Values represent percentage of participants (number of participants).
‘Illicit drug use’ refers to participants reporting any use of the three drugs in the past two years.
‘Illicit drug use profiles’ refers to the combinations of drugs participants report using in the past two years.
^{a ‘}Any illicit drug use’ refers only to use of cannabis, MDMA and cocaine.

There are some important differences between my sample and both the CSEW and ALSPAC samples. Some differences may mean that my figures are overestimates, including sampling university students who are more affluent than the general population (although drug use is not necessarily higher among students than non-students) and only including those who reported drinking alcohol (although according to the study authors, over 95% of the ALSPAC participants report past year drinking). Other differences may mean my figures are underestimates, including only asking about use of three drugs (thereby underestimating ‘any illicit drug use’), and the younger average age of my sample. I also report on past two-year use, rather than either lifetime or past year use as per CSEW and ALSPAC. Given these differences, I would like to run a larger, more representative sample on the Prolific platform (Prolific allows researchers to recruit a sample which is representative of the general population), to get an estimate of illicit drug use which is more comparable to ALSPAC and CSEW.

Despite these differences, my data support those reported by Charles and colleagues. Indeed, I find it unsurprising that illicit drug use is under-reported in the Home Office’s CSEW. The validity of self-reports for sensitive issues has long been a concern. Over-reporting of illicit drug use is not considered to be a concern and numerous methods have been developed for preventing under-reporting (see a 1997 NIDA report on this issue, as well as more recent techniques for estimating prevalence of use such as the crosswise method). It is important to consider the context in which surveys are administered, including participants’ perception of who is asking the questions and for what reason. It seems that if drug use is asked about in a research context, (e.g., with a clear research objective, informed consent and no possibility of repercussions), the validity of responses may be higher than when questions are asked by organisations that are perceived to be involved in the punishment of people who use drugs (e.g., governments, universities).

While the CSEW recognises that it does not reliably measure problematic drug use, my data and that of Charles and colleagues provide evidence that CSEW’s claim that it is a ‘good measure of recreational drug use’ may be wrong. Although it may be convenient to believe that only a small subset of the population uses illicit drugs, accurate information may galvanise policy makers (both nationally and locally, including at universities) into developing drugs policies that reflect reality and which support, rather than criminalise, the large proportion of the population who choose to use drugs. Indeed, this is what we’re doing at the University of Bristol, where it has been accepted that drug use is relatively common among our students and we’re providing support and education to those students who need it.

This blog posted was originally posted on the Tobacco and Alcohol Research Group blog

Using genetics to understand the relationship between young people’s health and educational outcomes

Posted on January 22, 2021January 21, 2021 by lindsey.pike

Amanda Hughes, Kaitlin H. Wade, Matt Dickson, Frances Rice, Alisha Davies, Neil M. Davies & Laura D. Howe

Follow Amanda, Kaitlin, Matt, Alisha, Neil and Laura on twitter

Young people with health problems tend to do less well in school than other students, but it has never been clear why. One explanation is that health problems directly damage educational outcomes. In that case, policymakers aiming to raise educational standards might want to focus first on health as a means of improving attainment.

But are there other explanations? What if falling behind in school can affect health, for instance causing depression? Also, many health problems are more common among children from less advantaged backgrounds – for example, from families with fewer financial resources, or whose parents are themselves unwell. These children also tend to do less well in school, for reasons that may have nothing to do with their own health. How do we know if their health, or their circumstances, are affecting attainment?

It is also unclear if health matters equally for education at all points in development, or particularly in certain school years. Establishing how much health does impact learning, when, and through which mechanisms, would better equip policymakers to improve educational outcomes.

Using genetic data helps us understand causality

Genetic data can help us answer these questions. Crucially, experiences like family financial difficulties, which might influence both a young person’s health and their learning, cannot change their genes. So, if young people genetically inclined to have asthma are more absent from school, or do less well in their GCSEs, that would strongly suggest an impact of asthma itself. Similarly, while falling behind in school might well trigger depression, it cannot change a person’s genetic propensity for depression. So, a connection between genetic propensity for depression and worse educational outcomes supports an impact of depression itself. This approach, of harnessing genetic information to better understand causal processes, is known as Mendelian randomization.

To find out more, we investigated links between

health conditions in childhood and adolescence
school absence in years 10 & 11
and GCSE results.

We used data from 6113 children born in the Bristol area in 1991-1992. All were participants of the Avon Longitudinal Study of Parents and Children (ALSPAC), also known as Children of the 90s. We focused on six different aspects of health: asthma, migraines, body mass index (BMI), and symptoms of depression, of attention-deficit hyperactivity disorder (ADHD), and of autism spectrum disorder (ASD). These conditions, though diverse, have two important things in common: they affect substantial numbers of young people, and they are at least in part influenced by genetics.

Alongside questionnaire data and education records, we also analysed genetic information from participants’ blood samples. From this information, we were able to calculate for each young person a summary score of genetic propensity for experiencing migraines, ADHD, depression, ASD, and for having a higher BMI.

We used these scores to predict the health conditions, rather than relying just on reports from questionnaire data. In this way, we avoided bias due to the impact of the young people’s circumstances, or of their education on their health rather than vice versa.

Even a small increase in school absence predicted worse GCSEs.

We found that, for each extra day per year of school missed in year 10 or 11, a child’s total GCSE points from their best 8 subjects was a bit less than half (0.43) of a grade lower. Higher BMI was related to increased school absence & lower GCSE grades.

Using the genetic approach, we found that young people genetically predisposed towards a higher BMI were more often absent from school, and they did less well in their GCSEs. A standard-deviation increase* in BMI corresponded to 9% more school absence, and GCSEs around 1/3 grade lower in every subject. Together, these results indicate that increased school absence may be one mechanism by which being heavier could negatively impact learning. However, in other analyses, we found a substantial part of the BMI-GCSEs link was not explained by school absence. It’s unclear which other mechanisms are at play here, but work by other researchers has suggested that weight-related bullying, and negative effects of being heavier on young people’s self-esteem, could interfere with learning.

*equivalent to the difference between the median (50^th percentile) in population and the 84^th percentile of the population

Diagram showing the pathways through which higher BMI could lead to lower GCSEs; either through more schools absence aged 14-16, or other processes such as weight-related bullying. — Our results suggest increased school absence may partly explain impact of higher BMI on educational attainment, but that other processes are also involved.

ADHD was related to lower GCSE grades, but not increased school absence.

In line with previous research, young people genetically predisposed to ADHD did less well in their GCSEs. Interestingly, they did not have increased school absence, suggesting that ADHD’s impact on learning works mostly through other pathways. This is consistent with previous research highlighting the importance of other factors on the academic attainment of children with ADHD, including expectations of the school environment, teacher views and attitudes, and bullying by peers.

We found little evidence for an impact of asthma, migraines, depression or ASD on school absence or GCSE results

Our genetic analyses found little support for a negative impact of asthma, migraines, depression or ASD on educational attainment. However, we know relatively little about the genetic influences on depression and ASD, especially compared to the genetics of BMI, which we understand much better. This makes genetic associations with depression or ASD difficult to detect. So, our results should not be taken as conclusive evidence that these conditions do not affect learning.

What does this mean for students and teachers?

Our findings provide evidence of a detrimental impact of high BMI and of ADHD symptoms on GCSE attainment, which for BMI was partially mediated by school absence. When students sent home during the pandemic eventually return to school, the impact on their learning will have been enormous. And while all students will have been affected, our results highlight that young people who are heavier, who have ADHD, or are experiencing other health problems, will likely need extra support.

Contact the researchers

Amanda Hughes, Senior Research Associate in Epidemiology: amanda.hughes@bristol.ac.uk

COVID19 – should schools close early for Christmas?

Posted on December 15, 2020December 16, 2020 by lindsey.pike

Sarah Lewis, Marcus Munafo and George Davey Smith

We have previously written about the limited risk posed to pupils, teachers and the community by schools being open during the Covid19 pandemic. Schools have now been open for almost a full academic term (3 months), so it is time to take another look at the evidence.

School re-openings have coincided with an increase in Covid19 infection rates across all UK nations. This rise in infection rates was anticipated, given the annual pattern of rising respiratory infections in the autumn term. There was also a rapid increase in Covid19 testing rates as children returned to school and presented with mild symptoms. Rates of positivity among children were very low at first, but a rise was observed over the autumn. This corresponded with an increase in rates among adults, and there seems to be a strong correlation between Covid19 positivity in schools and rates in the local community.

But has transmission of Covid19 in schools driven the second wave? And should schools be closed again to reduce infection in the community?

This post argues that there is little case for closing schools, as

Schools don’t seem to drive transmission in the community
The risk of the virus to most school children is very low
The harms of school closures are wide ranging.

Infection rates among children have been low

Since September children with COVID19 symptoms have been asked to stay at home and have a test before returning to school. Tests equating to 10% of the school pupil population were carried out during first half term in Scotland; only 0.2% of pupils tested positive during this period. Similarly high volumes of testing have been carried out in Wales, but only 0.6% of pupils tested positive between 1^st September and 9^th December 2020. Pupils made up 3.5% of cases in Wales over that period, despite making up 16% of the population.

However, the weekly Covid19 incidence among 12-16 year olds in Wales was similar to the national average for the week ending 9^th December 2020, suggesting a change in the age demographic of cases.

Transmission levels in school have been low

It is unclear what proportion of children who tested positive contracted the infection in school – many children have similar social circles both in and out of school. When infections are found in schools, most schools have only 1 or 2 cases within a 2-week period (unless levels in the local community are high). This suggests low levels of transmission in schools.

Children and adults have different symptoms

Comparisons of rates of infection between children and adults should be treated with caution. Cases are diagnosed using recognised Covid19 symptoms, and are influenced by the volume of testing in the community. Younger children seem to be less likely to have symptoms – around 50% of infected children tend to be completely asymptomatic. They also may have somewhat different pattern of symptoms to adults – fatigue, gastrointestinal symptoms, and changes in sense of smell or taste, but only rarely a cough. Therefore, studies relying on symptoms in children may be unreliable.

Random testing is the best way to find out level of infection

Surveys show that while young adults had the highest levels of infection in September, secondary school pupils now have the highest rates.

Studies which test individuals at random in the community are more reliable indicators of the levels of infection among children compared to adults. The UK Office of National Statistics (ONS) infection survey has been randomly testing people from the community since early May. It showed that young adults (school year 11 to age 24) had the highest positivity rates in September. This became more pronounced in early October when universities re-opened to students. By the end of October, rates among secondary school pupils were similar to those in young adults, at around 2%. Secondary school pupils now have the highest rates. Covid19 positive rates among primary school children are about half those in secondary school children and have barely changed since the beginning of the academic year.

Infection rates among teachers

There is no evidence that teachers are more at risk of death from COVID19, and infection rates among teachers do not seem higher than other professions.

ONS data from the first wave of the COVID19 epidemic in the UK showed that teachers were not at increased risk of death from the disease compared to other professionals. Based on ONS data, during October those working in the education sector had an antibody positivity rate of 8.1% (95% CI 5.9-10.8) compared with 6.5% (95% CI 5.9-7.3) among those working in other professions. This suggests perhaps slightly higher infection rates, but this is estimated with uncertainty.

Infection positivity rates – also measured by the ONS survey – from 2^nd September to 16th October showed that teachers were no more likely to test positive than other professions, although again there was a lot of uncertainty in these estimates*. The Swedish Public Health Agency have linked data on Covid19 infection to occupational data and found no increase in infection rates among teachers, although there was some evidence of an increase in infection rates among teaching assistants, school counsellor and headteachers. However, infection rates may have been inflated relative to other profession if there is increased testing among asymptomatic people in the education sector.

Could infections in schools be driving community infection rates?

The evidence suggests this is unlikely.

Infection rate increases appear to coincide with school openings, but the R-number was increasing in Scotland and England before school openings. Hospital admissions due to Covid19 had also started to rise before this point. In September, positivity rates were initially highest among young adults, not among children of school age, suggesting that perhaps infections among school children were not driving community rates. The ONS data showed infection rates levelling off over October half term, and climbing again among young adults and secondary school children after half term. However, this trend was not as marked in primary school children, and was not observed in adults, even amongst the 35-49 year age group, to which many parents of school aged children belong. Another study of community-based testing – the REACT-1 study – found a greater decrease in infections among younger children compared with older children following the October half term holiday, but again there was a lot of uncertainty in this estimate.

Contact mixing patterns show that people tend to have the most contacts within the same age group, followed by the age group closest to them. Children have more opportunities to pass on the infection to other children and young adults, and are not significantly influencing rates in older adults.

The current R-number in England is currently estimated to be slightly below 1 despite schools being open. This shows that it is possible to drive down infection rates in the community whilst keeping schools open. Furthermore, when everything else but schools are closed – such as in the case of the national lockdown which occurred in England in November, school children will have more contacts than anyone else and schools will contribute to relatively more transmissions in the community even if transmission rates are low overall.

Closing schools is not the answer

Rates have recently fallen among adults in England, despite schools remaining open and secondary school rates increasing. The evidence suggests low levels of virus transmission within schools. First Minister of Wales Mark Drakeford recently said that behavioural evidence suggests closing schools could place some children “in even riskier environments”. Children being looked after by their grandparents rather than being in school would be more dangerous in terms of the virus being transmitted to a higher risk group.

Any public health intervention should consider the costs as well as the benefits. We know that school closures have wide ranging adverse consequences for children and families as outlined by UNESCO, and such costs are particularly pronounced for the poorest and most vulnerable children in society. Children:

who do not have access to technology to participate in online learning
whose parents who do not have the resources or the educational background to help

have been shown to fall further behind following school closures. Evidence suggests that children’s mental health deteriorated during the first lockdown, and that vulnerable children were at greater risk of violence and exploitation. School closures can also cause economic hardship due to parents being unable to work. This has prompted Robert Jenkins Global Chief of Education at UNICEF to issue a statement over the last few days saying:

“Evidence shows that schools are not the main drivers of this pandemic. Yet, we are seeing an alarming trend whereby governments are once again closing down schools as a first recourse rather than a last resort. In some cases, this is being done nationwide, rather than community by community, and children are continuing to suffer the devastating impacts on their learning, mental and physical well-being and safety”.

If schools being open are not major drivers of transmission in the community (which they don’t appear to be), given that the risk of the virus to most school children is very low, there is very little case for closing them given the potential harm this could cause.

Footnote: Secondary schools in Wales were closed early for Christmas on the 11^th December 2020

*(estimates ranged from 0.2% (95%CI=0.07-0.53) for primary school teachers to 0.5% teachers of unknown type (95% CI=0.36-0.69) compared with 0.4% (95%=0.39-0.49) for all other professions)

Drinking in pregnancy: the right to record, or the right to privacy?

Posted on October 21, 2020 by philippa.gardom

Luisa Zuccolo , MRC Integrative Epidemiology Unit and Department of Population Health Sciences, Bristol Medical School, University of Bristol

Cheryl McQuire, School for Public Health Research/Centre for Public Health and Department of Population Health Sciences, Bristol Medical School, University of Bristol

Follow Luisa and Cheryl on Twitter

What’s the issue?

Drinking alcohol during pregnancy continues to stir passionate and polarised reactions. The issue has once again come into sharp focus. In England, the National Institute for Health and Care Excellence (NICE) is proposing to measure all alcohol use in pregnancy and transfer this information to a child’s health records, without explicit agreement from the mother. The aim of the proposal is to ensure better diagnosis and support for those with lifelong conditions caused by drinking in pregnancy that can include problems with learning, behaviour and physical abnormalities, known as Fetal Alcohol Spectrum Disorders (FASDs). However, the NICE proposal has been met with strong opposition from some organisations, which say that this breaches pregnant women’s right to medical privacy.

A balancing act

Benefits of introducing the proposed FASD NICE Quality Standards

It’s important to remind ourselves why measuring and sharing information on drinking in pregnancy could be worthwhile, and who will benefit.

Information – the key to understanding

Official guidance recommends that it is safest not to drink at all during pregnancy, or when trying for a baby. But a quarter of people in the UK are not aware of this guidance and the UK has the fourth highest rate of drinking in pregnancy in the world. The new NICE quality standards propose to rectify this by making it compulsory for midwives (or other health care professionals) to have conversations about alcohol with pregnant women. The idea is to help women to make informed choices about drinking in pregnancy.

Information is in everyone’s interest. We still don’t know enough about the effects of different levels of alcohol use in pregnancy. This is a tricky area to study, in large part because we don’t have enough information. If we don’t measure, we can’t fully understand the effects of alcohol in pregnancy (not even to confirm whether small amounts are safe). This has been our area of research for a number of years, and it is important both because many pregnant women drink alcohol, and because they should have the right to be better informed. Current abstinence guidelines are largely (but not solely) based on the precautionary principle. Our research has provided some evidence that even low levels of use (two drinks a week or fewer) can have negative effects, including smaller babies and preterm birth. We need more information to find out about the full extent of these risks – including whether the risks are genuinely there – to ensure that women can make informed decisions based on the best possible evidence.

Diagnosing fetal alcohol spectrum disorders (FASD)

Fetal alcohol spectrum disorders are severely underdiagnosed. They are characterised by lifelong problems with learning, behaviour and, in some cases, physical abnormalities. Contrary to what many think, these are common disorders. Our recent research suggests that between 6 and 17% of children in the UK could have symptoms consistent with FASD. Without good information on exposure to alcohol in pregnancy, many of these children remain ‘invisible’ to services and do not get the support that they need.

Concerns about the Quality Standards

Despite the potential benefits of these proposals, there are several unresolved issues that need tackling urgently.

Stigma and trust

If women feel stigmatised, they might lie about their drinking, invalidating any data collection. If they can’t trust their healthcare providers, then we can’t trust the data – so what would be the point of collecting it?

Tradeoffs

What would women be offered, in exchange for volunteering this information? What’s in it for them? It would be unbalanced and probably unethical to request information about drinking in pregnancy, at the risk of stoking maternal anxiety, without explaining the reasons, or offering support if so desired. The treatment of pregnant women who smoke provides an appropriate model – information is recorded on antenatal notes, and support to quit is offered at the same time. We need to guarantee a non-judgmental and supportive approach to listening when it comes to alcohol too.

Confidentiality

Women should be able to opt out. For those opting in, it should be made clear that the same high levels of confidentiality will apply as are already in place for current information from maternity notes and child health records. These new data on alcohol use should be no different and must be covered by existing guarantees.

Finding the right balance

So, where is the balance between the benefits and risks of the proposed changes? We often talk about burdening pregnant women with anxieties, but we neglect to talk about the lifelong consequences of emotional and behavioural problems arising from exposure to alcohol in pregnancy – these pose real everyday challenges for families, for many years to come. If on the one hand, maternal health is child health, then on the other child health is maternal health.

As we hear in these COVID-19 times, health is a marathon not a sprint

We need to continue shifting the focus from ‘healthy pregnancies’ to ‘healthy families’. The former can be met with resistance by those evoking the dangers of the surveillance state and policing women’s ‘baby-making’ bodies. The latter reminds us of the many individuals involved, all equally important, all of whom need support for the long term beyond those initial nine months. We believe that NICE should listen to the plurality of women and families’ voices. The debate on recording alcohol in pregnancy will lead to constructive health gains that will benefit all.