Okay. So could you start by telling me your name and your current title?
So I'm Naomi. Evan. I'm professor of epidemiology here at University of Oxford, and I'm chief scientist for UK Biobank.
Okay, thanks very much. And without telling me your entire life story, but just to give me a bit of background,
just tell me how you got from your first interest in science to where you are now.
How did your career unfold? Well, like most people, it's quite a circuitous route.
I actually did Environmental Science at Universe, my undergraduate university and graduated in a recession, was unemployed, couldn't get a job.
And then just after a year of not doing very much thought, actually,
I read I really need to go back to education and do something that I'm really interested in.
And the only thing that I was really passionate about at university was we did a module on epidemiology and public health.
So I went back and I did a master's in epidemiology at the London School of Hygiene and Tropical Medicine in London.
And I felt like I've come home.
It was just I just absolutely loved it. And I haven't really looked back since then.
I came here in Oxford to do my dphil in the late nineties and became a cancer epidemiologist
with a focus on breast and prostate cancer and how diet and hormones influences cancer.
And then in 2011, I also started to work with the UK Biobank as their senior epidemiologist,
and that was really different because rather than just doing research and analysing data and writing papers,
you actually thinking about how can I help to set up and improve cohort studies?
How can I engage the participants in collecting more valuable data for the global research community?
So it's all about enabling others to use this fantastic resource, which I find hugely satisfying.
Hmm. Well, we'll talk a bit more on that later, but I've got this question I've been asking everybody.
If you could say if there was one question that you could say really kind of get you out of bed in the morning, what would it be?
Oh, for me, it would.
It would be, how can we better measure our lifestyle and particularly our environment to find out more about how that impacts health?
That's what gets me out of bed. And what are the methods, the main methods that you use.
So the main methods for finding out about people's lifestyle factors, we is simple.
We ask them questionnaires about their diet, physical activity, how did they sleep?
And of course, more recently we can now use fancy devices like Fitbits and apps on phones to find out more about their sleeping habits,
their physical activity, and even down to having sleep monitors on their head to measure the activity in
their brain and MRI machines to to to measure that volume of their heart chambers.
I mean, it's just astonishing the amount of information you can collect on individuals now.
So it's very much about data. Oh, it is. I mean, the more data we can collect on individuals and how they interact with their environment,
couple that with information on their genetic profile.
Then suddenly you could open up this wonderful box and find out how your people's genetic profile together with
exposures to their lifestyle and why broader environment interacts to influence disease many years later.
So that's really brought us very neatly to Biobank. So let's for the benefit of people who don't know about it, go back to the beginning.
What is UK Biobank, how was it set up and what's it setting out to do?
UK Biobank is arguably the world's most flexible and accessible biomedical resource
for the global research community to use to perform health related research.
It's in the public interest. So we recruited half a million individuals in the UK about 15 years ago aged 40 to 70,
and we collected all sorts of information on them lifestyle factors, physical measures,
we took biological samples from them and then we're following them up over many decades through linkage
to the medical records and through asking them through questionnaires to find out about their health.
And from that, we've made this huge database available for approved researchers worldwide to access this incredibly valuable dataset to.
For the world's best imaginative minds to mine this dataset to find out about the causes and determinants of a whole range of diseases.
So that's what you can buy books about, in essence. And what's your role as chief scientist?
So my role is I'm largely responsible for making sure we follow up the health of all harmony participants through linkage
to a broad range of medical records and other health related records to make that available to the worldwide community.
And also to talk to the researchers about what would make UK Biobank better.
What's over the next 510 years? So the technology is changing so rapidly.
How can we make the resource even better in the future?
Is that through more different measures that we can perform in the blood samples?
Is that through doing repeat measures on the participants?
Is that through slightly different measures now that the cohort or ageing?
What can we do to better enhance the study to make it really valuable to to
enable researchers to answer the most important research questions in the day?
And this is just a kind of slide thing to cover, but how is it funded?
So it's largely funded by the Wellcome Trust and the Medical Research Council in the UK.
And it was set up and it had when it was set up, it had some additional funding from local governments as well.
And but over the last five years we've also received industry funding to do specific enhancements to the resource.
So for example, a consortium of pharmaceutical companies have funded whole exome sequencing,
which measures the the genome that encodes for the proteins.
And again, a consortium of pharmaceutical companies, together with government and charity, have funded whole genome sequencing.
We have a pharmaceutical consent companies invested in UK Biobank to fund measuring circulating proteins in the blood,
measuring circulating metabolites in the blood. So really, industry is starting to invest in this study to measure proteins,
metabolites and genes in order to really accelerate their drug discovery work.
And all those data are made available to the global research community to further enhance scientific discoveries.
So academic and commercial research, the resources available to both academic and commercial research, it is, yeah.
And it's available in exactly the same terms.
So academic academics and researchers from the commercial world can access the data at the same cost, the same terms and conditions.
And the only thing that we we really are obliging researchers to do in return is to return all of their results back to UK Biobank.
So whether that's results from assays that they performed on the blood samples or whether they've derived a new variable from the MRI scans,
all that data, plus the research data that they've done on the resource is returned back to you
could Biobank so that others can build on the findings that have been made.
So it's one of the first studies in the world actually to really enforce this really collaborative,
open way of performing science and kind of building on what others have already achieved.
And what's a bit if you had to pick out,
you probably do talk sometimes some of the the more impressive achievements of people who've been using the resource.
What would you pick on? So I would say over the last couple of years,
what we're finding is coming out to the UK Biobank resource is in 2017 we made available genetic
data on half a million participants in the world's largest study at that time to do so.
That led literally overnight to an explosion of research into the genetic determinants of disease.
From that work, that's led to a concept called polygenic risk pools.
So this is where you look at all the genetic variants across an individual's genome, each of which only has a very small increased risk of disease.
But when you add them all together, what you find is the people say in the highest, unfortunately in the highest,
fifth percentile of genetic risk across variants, all their genome have substantially increased risk of,
say, breast cancer or prostate cancer, heart disease.
And you can say the same about pretty much every condition, and that's actually equivalent to many diseases that are monogenic in in order.
And what we found is that if you can use this polygenic risk score idea.
So that is really starting to galvanise the whole area of precision medicine.
So you can imagine, for example, going to your GP, having a blood test done, they'll look at your genetic sequence and they'll say,
well, you've got, you know, a 10% risk of developing heart disease by the age of 30, 75.
Based on your genetic predisposition alone,
we might want to think about perhaps taking preventative measures like taking statins to reduce your cholesterol or doing lifestyle advice.
So you can see how this idea of knowing an individual's genetic profile and how that may influence risk can then start to tailor either
screening programs or targeted treatments or preventative advice to those individuals who are increased genetic risk of a certain disease.
So I think that's by far being today anyway.
And the biggest broad achievement of the resource.
Mm hmm. So let's finally arrive at a kind of boot camp.
Can you remember where you were, what you were doing, or how.
How you first heard that there was a pandemic in the offing?
I remember being in a meeting in London, and it must have been February of 2020, and everybody was whispering and did that before the meeting started.
There was all of you seen the news app, you seen this, and there was somebody show me something on Twitter.
And it was this graph that was just just just going upwards.
And it was it was a number of people in Wuhan who had been diagnosed with this with this strange virus.
And there was all this talk about, oh, well, you know, it might not come over here and we might be alright and then all.
But no it's already happening in Italy and Italy's really if it can happen in Italy it can happen anywhere.
So there was this sense of unease about the rapid spread of something that was
very unknown and we were kind of sitting ducks and there was a real sense that,
Oh my God, there is this wave of infection that is killing people rapidly.
And it was it. I remember it very well.
It was a sense of like cold shivers down your spine, like, oh, my God, this is going to really change things in this country and we are not prepared.
Right? Yes. So having got over the shock,
how soon was it before you and your colleagues felt that this was something that by a bank could contribute to a straightaway?
So it must have been end of March 2020.
So just as we were entering the first lockdown, yeah, the Department of Health and Social Care got in touch with us and said,
could you could you set up a study to find out what's going on in the UK?
You know, we want to know the spread of infection across the UK, different population,
subgroups, disease, how is it by age, by sex, by region and so on.
And more importantly, how long once people who had been infected with the virus, how long do their antibodies last?
Over time. And that was a crucial at that point.
That was a crucial question because nobody knew that once you'd been infected, were you immune forever after that, how long were you protected for?
And knowing the answer to that question had a real impact, of course, on vaccine rollout and how long in space the the vaccine.
So we very quickly mobilised all our resources to set up this Seroprevalence study to find out the extent
of infection across the UK and how long antibodies last full just just using the UK Biobank participants.
Well, so that was another I mean,
I've interviewed Derek Crook and I think I'm beginning to get and I've interviewed Sarah Walker and I I'm beginning to get slightly confused.
It is quite confusing things in Sarah for the first time because you wanted to find
out what was the rate of past infection across different age groups and so on.
All of our participants are now in the sixties, early seventies.
For the first time ever. We got the kids and the grandkids of the part of the existing participants involved
and we were absolutely bowled over with willingness to contribute to the study.
I would think within five days of putting out an email to the participants and saying,
If you've got children who want to you want to involve, let them know.
We had over 100,000 people volunteer to join the study.
We only needed 20,000 to find out really what was going on across the country.
So we were bowled over with support. And yeah,
hopefully it means that the the value of doing this type of epidemiological study was not not just in the forefront in the mind of the participants,
but also their wider families. And, and you must have needed to collaborate with other organisations because you needed that test results presumably.
Yes. So what we did was we sent a a blood,
a tiny blood sampling device which literally you prick the end of your finger and you squeeze it to get a drop of blood into a little test tube.
You wrap it up, pop it in the post. So it was dead simple for people to use.
And then that went to one of our collaborating labs, which is just over the way here in Oxford,
and they set up in double quick time and assay that could measure the main antibody to the spike protein of the corona virus.
So that was very close. That was Derek. Yes. Outfit.
Yeah. So all the samples were first sent to our co-ordinating laboratory.
So a Royal Mail van came every day with these 20,000 samples and we collected samples every single month for six months from 20,000 individuals.
So it was an awful lot of samples that we had to we had to unpack adequate put into little place,
put them on dry ice curry, carrying them down to Oxford's Derek Crookes lab.
They then had to unpack the measured them. It was a huge, huge effort all round.
But we got fantastic data on how long antibodies to coronavirus so we could tell who would be previously infected with the virus,
how long antibodies last lasted over a six month period.
And what we found was, was really clear data actually, that almost everybody had been infected in the first wave.
So March, April, May in 2020, nearly everybody still had antibodies three months later and the vast majority,
88% still had antibodies six months later.
So what we're doing now is we've just sent a final sample and the back end of last year,
so December of 21 to again to all of these 20,000 individuals to find out if their antibodies persist 12 to 18 months after infection,
because that's still an outstanding question. We know antibodies wane because people get reinfected.
But we don't actually know. Does that vary by age?
Does that vary by ethnicity? And just what does that trajectory look like in terms of the waning of of protection, likely protection from infection?
So that's something that we're looking at now. Mm hmm. So that I mean, I, I assume the the awareness study was also looking at serology.
How did your results compare with this? And I mean, is there a difference in your approach?
Well, they're very complimentary. I mean, they they own study looked at households again across the UK and they but they
didn't look at they didn't have intense repeat measures like UK Biobank had.
So we were able to collect multiple blood samples from 20,000 individuals, Onassis, a larger Subsample.
But they did collect blood samples as frequently as we did.
So that's a main difference. But they're they're complementary.
And it's it was really useful when we were going through there in the teeth of the pandemic, if you like,
talking to Onassis and the React study and our study about just,
just how complimentary our findings were, particularly around the spread of the virus across the UK.
You know, the higher rates in elderly people, higher rates in ethnic minorities,
higher rates in urban areas, and the possible reasons why that might be.
So presumably because you're connected to people's health records, you know,
you would get sort of as people in the study became infected, you would you would see that.
Were you able to use that data along with all your environmental and and genetic data to try and answer questions about who was getting infected?
So the short answer was yes, but with some difficulty.
So before the pandemic, we usually obtain health record data on an annual basis cancers, deaths, hospital admissions and so on.
When the pandemic first started, we thought, Hang on a minute.
This is nowhere near frequent enough to enable research into COVID into the determinants of severe COVID 19.
So researchers were coming to us saying, Well, we could look at the what's the genetic predisposition to severe COVID 19?
What are the lifestyle factors related to, you know, a smoking a risk factor?
Is obesity a risk factor? Is ethnicity a risk factor? We could answer all these questions using UK Biobank.
In order to enable that, we had to have rapid updates of health data, including COVID 19 testing data and critical care data from hospitals.
So we we worked very, very well with all the data providers, and we managed to get monthly updates of these data.
And our poor data finally came in. UK Biobank literally worked around the clock to make hospital inpatient data, death data, COVID 19 test data.
And we were able to there was emergency legislation that was introduced called a coping notice that enabled us to obtain primary care data,
so data from GP practices solely for the purposes of COVID 19.
So we had to rapidly put in pipelines in place to process these millions and millions of rows of data from
primary care records and make that available to researchers on a regular basis for COVID 19 research.
And all our hard work was, was we felt vindicated in all of our hard work because, I mean, I think within the first six months,
there were 200 odd papers looking at the genetic determinants and the lifestyle and environmental determinants of COVID 19.
And it made a real difference to our understanding of actually what were the
main risk factors for severe COVID and what were some of the key findings?
So, I mean, obviously, there's genetic predisposition to developing severe COVID 19.
Ethnic minorities have an increased risk of contracting COVID 19 in the first place.
And research that we've done in the Seroprevalence study, because we also found that rates were much higher in black and ethnic minorities.
We then sent out a questionnaire asking about their behaviour.
You know, do do you work in a public facing role? Do you have public transport?
Whereabouts do you live? How many people live in your household? All those questions we thought might be relevant to see if we could.
That could explain why ethnic minorities were more likely to catch COVID.
And what we found was that actually it was the type of job that you had, particularly whether you worked in the NHS or whether.
In a public facing role and where you lived.
So whether you lived in an urban area, and particularly if you lived in the London area of the UK, you're much more likely to develop COVID 19.
And that and that explained two thirds of the excess risk in black and ethnic minorities.
So, you know, it's and it was less to do with the number of people in the household and so on.
So that that was quite interesting. The social and economic determinants of of clothing.
So I overturned a lot of assumptions people had been making about multigenerational households.
Exactly. Exactly. Yes.
And then research coming out from the broader research community, looking at all of the data that we had in UK Biobank, you know,
found, you know, put, put to bed the fact that Vitamin D was protective for COVID 19, that was a big hypothesis that was out there.
And actually there was no real evidence to suggest that it found that obesity was a
strong risk factor for developing severe COVID 19 and also underlying health condition.
So if you had diabetes or depressed or even depression and cardiovascular disease,
you're more likely to develop severe COVID 19 and subsequent complications.
And also, if you had previous vaccines, too, like diphtheria or tetanus, whether they were more likely to protect you from subsequent COVID 19.
So some really interesting research into the determinants of the disease coming out of the resource.
Mm hmm. And were any of those findings converted into policy changes on the fly, as it were?
Well, I think it certainly led to a greater understanding of the likely causes of COVID 19.
And there was, I think, in the general public consciousness, people were aware that if you were A, B, C,
and if you were ethnic minority and if you had underlying co-morbidities that you were somehow more vulnerable to COVID 19,
whether that led to direct changes in policy in real time is is less clear.
I mean, the policy work that came out of our Seroprevalence study in the 2000, I think really did lead to some changes because it helped to influence.
Okay.
Well, if we know antibodies last for at least six months in majority people, that actually has an impact on how often you're going to vaccine people.
So that was, I think, a main contribution of in terms of policy and what people were doing on the ground.
Mm hmm. So another study you did was one that you call the antibody self-test or self-testing.
Yes. So once we'd we finished our seroprevalence study, we were making all the electronic health records available to the research community.
They would get in on doing this fantastic research into finding the determinants of COVID 19.
We then moved our attention to think about what about long COVID, you know, and quite early on in the pandemic,
there were growing anxieties that this wasn't just a respiratory illness, but it had real systemic in some people,
real systemic effects, brain fog, complete exhaustion as what are the risk, the cough and the fever, you know,
muscle aches that lasted for months, loss of sense of taste and smell that lasted that did last for months in some individuals.
So it seemed to be a more systemic virus with with with with wider health consequences.
So we thought UK Biobank would be the ideal resource to look at that because it's a longitudinal study that follows that people over time.
So what we did was we wanted to find out can objectively is possible who had developed covi who had been exposed to
the virus because we knew from our serology work that about 25% of the population had antibodies to coronavirus,
but they never thought they'd had COVID as many as 25.
Yes, yes. And 40% of those who were positive didn't have the three main symptoms that were eligible for testing way back in the first wave.
So there were there's thousands of people walking around, certainly in 2020, who had contracted the virus,
but either weren't eligible for testing because it didn't have the main symptoms or they didn't have any symptoms at all.
So we then sent out a self-test antibody lateral flow tests.
So these were little devices you sent in the post,
you just put a finger prick of blood onto the little cassette and within 15 minutes it tells you whether you got.
Antibodies to to the virus or not.
And so these were provided by the Department of Health and Social Care.
And Amazon kindly donated, distributing all the kits for free.
How did that relationship come about? Well, we already had an a kind of an ongoing relationship with Amazon for some of our other projects.
So and they just wanted to help. There was a real sense of what can we do to help figure out what's going on with COVID, particularly long COVID.
And so Amazon were like, Yeah, we'll deliver we'll deliver your your kits to half a million participants.
So we developed a really close working relationship with them.
About every participant got one as well. So we invited every participant for to have one of these case and over 200,000 actually had a kit,
did the test and gave us a result which was which was fantastic.
Unfortunately for us, this was all this all happened in 2021, just as the first vaccines were starting to be rolled out.
And the kits that we sent out, they test for antibodies to the virus.
They couldn't distinguish between antibodies produced from infection and antibodies produced from the vaccine.
So we were we were really up at the clock was ticking to get these kits out before people would react.
And I won't bore you with the details, but we had huge delays getting MHRA approval to use these tests in the home for research purposes.
It has to go through a long bureaucratic. Because it involves blood.
Because it involves blood. It's a medical device.
So it needs to be approved by the the authorities.
And it was being used it wasn't being used by a health professional. It has been used by Joe Bloggs in the home for research purposes.
That took months to get approved. Meanwhile, people are starting to get jabbed and we knew that the test couldn't differentiate between the two.
So what we had to do was ask people, have they been vaccinated?
If so, when and if they had a positive antibody result.
We then had to send them a another test that got sent to a different laboratory,
which could tell whether the antibodies was from the vaccine or from previous infection.
So it was a hugely complex and frustrating project,
but at the end of it we've got data back from over 200,000 individuals on whether they were previously infected with the virus,
irrespective of whether they had symptoms or not. Incorporating that data into UK Biobank that will enable really large scale
epidemiological research into the long term health effects of being infected,
regardless of whether you had symptoms or not. So some individuals were completely asymptomatic, others were hospitalised.
So it will enable research into the effects of long COVID across the full disease spectrum.
So obviously this research will take months, years, as you know, long COVID plays out over the ensuing months.
But that data, coupled with the vaccination data, which we just put it into the resource, will be, I think,
a unique biomedical dataset for people to work on the effects of corona virus infection for months and years to come, actually.
Mm hmm. And now you mentioned that it's very much a systemic condition.
And one of the things it affects when it affects multiple organs.
And you've got scans of some of your partners. We have, yeah.
So another way that we thought we could enable research into Long-covid was by taking advantage of our ongoing imaging study.
So before the pandemic, where we're embarking on a hugely ambitious programme to perform MRI scans on 100,000 participants,
of which we're halfway through. So by the end of 2019, we'd imaged 50,000 participants.
So this involves MRI of the brain heart body optimum full body, DEXA scan, carotid ultrasound is a four hour visit,
is very intensive for the participants, but it provides just unique, invaluable data on the physiology and the structure and function of organs.
So 50,000 participants had already undergone an image, an assessment before the pandemic.
So we thought, well, why not bring some of these participants back for a repeat scan, half of who we know have been infected with coronavirus.
And we can tell that either from the self-test and lateral flow antibody kit that we sent
to them or that they been diagnosed with COVID from linkage to medical health records.
And then we'll bring back. So there are cases, if you like, cases with COVID 19 and will match them to controls.
So matched similarly to age sex where they have that imaging assessment when they have their imaging assessment done.
And we managed to invite back 2000 individuals.
So this is the largest study in the world of the effect of coronavirus on internal organs.
And it's the only study in the world that's got imaging scans of participants before
they were infected with the virus and after they were infected with the virus.
So it enables research into the likely direct effect of coronavirus on changes in internal organs.
So for example, you could look at the effect of corona virus in changes in the heart,
in the heart structure or the or the or the heart function in some way.
Actually, SARS is unique because it's the only state in the world that's got imaging
scans before and after infection and again across the full disease spectrum.
Most of the studies they have, lots of studies have looked at the effect of COVID on imaging internal organs,
but they tend to recruited people who are hospitalised with the disease and of course they've only got the scans after they were infected.
So you can't see severe cases and they're particularly severe cases.
So that's right. So it is impossible to look at the effect of all of of the virus because you don't know what the baseline was.
So you don't know what their function was before they were infected.
So we we were thrilled to be able to to perform this study last year.
And as I said, we we managed to get 2000 individuals come back despite all the COVID restrictions.
They were willing to come back for a second visit. And now that data is available to the research community.
And already some really interesting findings are starting to come out of that.
Can you pick back a few of them? Yes.
So that the first finding to come out of this unique study is the effect, the likely effect of corona virus infection on the brain.
So what researchers in based here in Oxford have shown is that those individuals who are infected with coronavirus,
most of whom developed mild symptoms,
they had a greater decline in grey matter in the brain, in all different areas of the brain, but particularly in the olfactory region.
So the region of the brain related to sense of smell and taste.
So this decline in grey matter volume, the significance of grey matter.
So the significance of grey matter is,
is this is a part of the brain that's really responsible for how it works or the neural connections in the brain.
So if you've got a reduction in in in that part of the brain,
it suggests that your connections are perhaps even perhaps slower or or that there's that then there may be,
at least over the short term, some reduction in in how that area of the brain works.
So the fact that one of the main symptoms is loss of sense of taste and smell,
it was quite interesting to see that actually there was a corresponding reduction in the volume of the brain in this in this area.
And also the researchers found that there was there was likely to be an increase
in the time it took participants to perform some cognitive function tests.
So as well as having an MRI, they also performed a range of different tests to measure thinking and memory and so on.
And while these differences were not big, they they were there.
So, of course, what we don't know is how long these these differences will last in the brain is usually plastic.
It can recover. We know that.
So the good news is that we hope that these are not permanent reductions in the brain and not permanent changes in cognitive function.
And, of course, you know, only further MRI scans will really be able to answer that.
But very interesting that you can actually see the effect of the virus.
Even in mild cases, it really does seem to have an effect on the structure and possibly the function of the brain,
at least over a couple of months period.
And I'm wondering whether that's something you might repeat to see whether the electron variant and that the H2 variant.
Act any differently from the previous variants that people have?
Yeah, I mean, at the moment we don't have that granular information about variants.
Maybe it's not everybody who has a PCR test for for COVID has their virus sequenced.
Oh, I see. Yeah. And actually, we don't yet have half the information in the UK Biobank resource.
There are there are work underway to try and marry the two different data sets up.
So at the moment, that type of research is impossible.
But there's there've been waves of the different variants on this side just from the time a person becomes infected.
You've got to you've got a good guess at what you've got. You've got a good guess.
Yeah. So as you say, there are you could depending on when they contracted the disease or when they were infected,
you've got a pretty good guess at what variant they most likely had.
Yeah. So it would be very interesting to see whether Long-covid work as to when people were infected.
Does that. Well, we know it changes the symptoms that they get acutely.
Does that change the downstream long COVID consequences as well?
And that's something that we don't know yet and that hopefully over the coming months and years, we'll will be able to answer that.
Mm hmm. So do you have any in-house research programmes, or is this all other people coming to you and saying, Can we use your data?
The answer is this is well. So our job at UK Biobank is to build the resource to enable other researchers to use it.
So by and large, we don't do the research ourselves.
We have a small epidemiological and analyst team here.
And, you know, sometimes we do do our own research, but we're we're we're treated as researchers just like anybody else.
So we have no preferential or exclusive access to the data.
So if we're particularly interested in some research question, we might ourselves put in an application to use the data and answer that.
But essentially our job but you could buy a case is is to build the resource.
So, yes, I think I've got all those.
I've covered that. We've talked about health data linkage and we talked about Non-covid.
Um. Yeah. So.
So how do you think this work will help to plan future strategy for this pandemic?
And I guess we I think we have to expect there will be future pandemics.
I think. What? Well, I'd like to think maybe we didn't do that.
Oh, I'm so sorry. Thank you. To not me along the way.
Okay. So what? I think the pandemic, if there's any silver lining to the pandemic,
is that everybody became familiar with epidemiology and the importance of epidemiology.
I couldn't believe that people were talking on the dinner table about the R number and T cells.
And to me, having a wider public discourse about science can only be a good thing.
I mean, everybody became armchair epidemiologist overnight.
And I just think that's wonderful. And I just really hope that stays in the public consciousness and the govt and you know,
the government as well about the importance of large scale population based epidemiological studies because they're very expensive to run.
They take 20, 30 years to really come to maturity because you're following people over decades.
But actually they're crucial to find out about the determinants of disease and particularly find determinants of of of pandemics.
So when, you know, coronavirus came along, you could buy it and was already up and running.
If we had to build a study from scratch, we'd still be there recruiting people two years later.
So being able to tap into existing resources and existing studies to suddenly focus on on trying to understand the distribution
of the disease and then the determinants of the disease can only really be done with existing large scale population studies.
So I hope the epidemiology has kind of earned its its place at the table now and is is
recognised as being absolutely crucial to public health in this country and globally.
I suppose one thing we didn't talk about is another potential consequence of having a dataset
like this is that it may actually point to where the particular the genetic information,
where there might be targets that pharmaceutical companies or researchers can focus on to try and try and make some new treatments.
Absolutely. I mean, the whole reason why pharmaceutical industry have invested and it's millions of dollars to perform whole
exome and whole genome sequencing on half a million participants is to accelerate drug discovery work.
Because if if you find it an association between a particular genetic variation variant and a disease,
you're you've got a good bet that that genetic variant is somehow related.
So if you can find a drug target, then that's good.
That's built around that function of the gene that that's going to massively accelerate your drug discovery work.
So absolutely. I mean, the resource is already those data already finding that there are genetic variants that are
related from the exome sequencing data that relates to a much lower risk of developing obesity,
which is kind of the holy grail of drug companies.
They of course, you want a magic bullet to produce a drug to reduce rates of obesity.
And so the exome sequencing data has really shone a light as to potential drug targets that can do exactly that.
And the same is true for, you know, all sorts of diseases, including COVID and the diseases that will come in the future for sure.
Now, you talked about the incredible public awareness. Where you personally involved in media appearances?
Yes. Yes. It was very interesting because the the media obviously want to want to have an individual story.
And epidemiology is all about the population.
And so there's a little bit of tension between actually what you find on a population level and may not be directly relevant to an individual.
And of course, the media, what very simple messages and what we found with the pandemic, it's not so straight forward.
You know, even even with the public messaging around COVID, when they try to really drill it down to.
Three words, you know, face both hands.
You know, it, you know, it makes you realise that in order to get across a public health message, it really needs to be very simple.
And everybody needs to follow the rules.
And start as soon as you start introducing nuance or error margins or maybe they switch off, that's not what they want to hear.
So there is a natural tension between scientists wants to err on the side of uncertainty
and models and predictions with some caveats to the media who want it in black and white.
This is going to happen or this isn't going to happen with safe or we know. So that's been quite an interesting journey.
Hmm. Yes. I mean, I could have gone away from what you said earlier and said. Everybody's brain is going to decline.
We'd all be vegetables. But yes.
And I think the message there was really actually, you know, the reduction in in the grey matter, the brain is actually pretty small.
On average, it was about 2%, which in the grand scheme of things is quite small.
We don't really know how clinically relevant that is in terms of your longer future health,
because obviously we need to follow people up to find out that out.
And also, given how plastic we know the brain is, you know, is it may be that in six months time that difference is no longer there.
So this year, you could make a big splash of a headline going, Oh my God, everybody who's got COVID has got smaller brain.
Whereas actually, the realities is quite different.
Mm hmm. And Adam, did you have any help with Make It work did you do get have any training or some time ago?
Yes. So few years ago, you know, we talked to the media quite a lot about UK Biobank more broadly.
Yeah. So I'm just well through it now.
Yeah. So how does this work? Raised new questions that you're interested in exploring in the future?
Well, for me, it's really raised the importance, something I've always been interested in,
but it is even made it higher on my priority list, if you like, is about how important infectious diseases still are.
You know, we've been focus I've been focusing on cancer all my career.
You think of cancer. Cardiovascular disease is the two main important things.
And actually, because we can we've got linkage to cancer registries and linkage to hospital inpatient data,
they're quite easy to study other diseases like COVID, but also things that you go to your GP about but don't make it into hospital.
So things like, you know, arthritis, asthma, diabetes, actually eczema,
they've been relatively under-researched because as epidemiologists we haven't had access to the data about who's got all of these things.
So in my mind, one thing what I'm trying to say is,
is I've become very much more interested in the role of infectious diseases and how that impacts chronic disease.
So in terms of long-covid, it may be that, you know, coronavirus in some individuals may lead to longer term health consequences.
We know other viruses cause cancer, HPV, Epstein-Barr virus, hepatitis C, we know that they cause cancer.
And, you know, we now know that EBV can cause multiple sclerosis.
So the role of infections is not just in their wacky infectious disease symptoms is actually they may cause chronic longer term disease down the line.
So I become very interested in the role of infections and in longer term chronic disease.
And I think coronavirus has just kind of made me more aware that actually we
need to look at these as exposures as well as outcomes in their own right.
Yes, yes. Yep. So things like just think of things like urinary tract infections, which are incredibly common but regarded as a bit trivial.
Yeah. Exactly. Yeah. So what other health what are the health impacts of those?
You've had duties five, ten years later, and it's only by having thousands and thousands of people,
you can really try to tease out those small effects because they will be small.
And how did the first lockdown impact on what you were able to do?
So we haven't really talked before. And you said your colleagues were very busy, but it must have changed your life as well.
Well, it's changed all of our lives, didn't it? I mean, we it was it was quite interesting.
We had a new member of staff and her first day in the office was the end of March.
It was it was our last day in the office was her first day in the office.
And she came to work because, you know, she wanted to work in a big team and lots of group chats.
And actually, when you do that for a day, because we're we work from home and literally overnight,
we all had to be set up with, you know, VPN systems that we can log in and do our work.
We all had our Microsoft teams and you're suddenly I was working from, you know, a tiny box room or spare bedroom.
And, you know, suddenly you're working for 14 hours a day on calls.
And but actually it was.
I look back on it quite fondly because we were all working frenetically towards a common goal that we got to set at this studying.
We've got to do it in double quick time. And it was all hands on deck.
And we all felt we were doing something important.
And it kind of we all pooled together across the whole organisation and we all worked really, really,
really well together because normally in your day to day things, you don't have that real sense of urgency.
You've done your work in a slightly different things, slightly different timelines.
And it was the first time I've ever experienced this kind of all hands on deck mentality.
And we were all working silly hours and things, you know, messages flying around everywhere as to how to do things.
And it was it was hugely rewarding. It was exhausting, but it was hugely rewarding for all of us, I think, involved.
And do you think it helped to support your own wellbeing, the fact that you knew you were doing something?
Oh, for sure. For sure. I mean, you know, lots of my friends who were on furlough who, you know, picking up hobbies that they that they,
you know, put down years ago and and worrying about money and having to homeschool their children.
And I think if your your we were lucky in that we were focussed on one task and it was
just down the rabbit hole with that and everything else was kind of pushed to one side.
So I think that kind of bunker mentality kind of did you didn't have time to think about anything else or how scary it was or or what have you.
But I mean, some call it I mean, these, you know, millions of people were were affected,
both in terms of loved ones being really ill, but also having to homeschool young children while they're trying to work.
You know, I can't tell you the amount of times we had Zoom calls and there were little kids,
you know, under the desk or popping up to say hello and hugely challenging, but good fun.
Mm hmm. And one thing a number of people I spoke to said is that, I mean, academic life can be quite competitive.
And you it you know, you're constantly worrying about getting on it's paper out and so on.
I mean, you already work in a fairly collaborative way, but was this noticeably more collaborative?
And do you think that's a lesson for. Well, it's definitely more collaborative.
I mean, the fact that I mean, we've been trying to get access to primary care data for years.
And overnight it happened because there was emergency legislation to copy notes that basically told the
system's suppliers to make the primary care data available for UK Biobank for COVID 19 research only.
So you know where there's a will, there's a way.
And so, yeah, huge collaboration at all levels and a real sense of working on it together.
And everybody from the Department of Health and Social Care, from Amazon, from other academic colleagues,
just wanted to do anything to help and really cut through the red tape to try and speed things up.
So I really hope that, you know, translates into more cooperation in the future.
And I think that having pushed that primary care data door open, you might be able to hang on to it.
I really hope so. I really hope so.
You know, I mean, it's silly, really, because the government made the primary care data available only for COVID 19 research because it's a pandemic.
And yet we've got this more people died of cardiovascular disease than COVID.
We've got pandemics of cancer and pandemics of cardiovascular disease and dementia going on all the time.
So the fact that they made these data available only for COVID 19,
because we been in an emergency where we're in a dementia emergency, we were in a cancer emergency.
So why can't you make the data available for that? To me, it just doesn't make any sense.
And I'm hoping that once we've shown that the data can be used responsibly,
that it is of real scientific added value to find out the determinants of disease.
Then they will be will have an easier path to try and make the data available for research into all conditions, not just COVID 19.
Mm hmm. So were you also involved in or involved in any way in the in the kind of safety regime for the department
deciding when it was safe to come back and had to come back and that kind of thing for UK Biobank.
Yeah. I mean, we have, you know, a chief operating officer and health and safety, you know, that was really.
They're very mixed. But yeah, you know, we're we're we're we'll have a say in what works for us,
how we feel safe when we should be going back in kind of with safety measures,
particularly for participants who are, you know, some of whom are quite elderly,
coming in for imaging assessments, how to really make sure they feel safe and that is safe for them.
So we just have a lot of work around that.
I didn't have a problem getting PPE and that kind of thing that you needed in order to keep everybody safe knowing the image and sensor.
Yes. No, that was that was that was fine.
But I think that was because we actually we did the co-lead imaging study in 2021 when the PPE was the the pipeline scan setup.
It was really in the first wave of the pandemic. Then getting your hand on gloves and masks and and gowns and stuff was a real problem.
Right. And so as an FDA epidemiologist, you deal with risk all the time.
And we were obviously very aware of the risks that were around to do.
Did you personally feel threatened by that, by by the risk of actually getting the vaccine?
Did you get the disease? I've never had never had COVID, although it's as we speak, the rates are probably the highest they've ever been.
Um, and I've, I've been very, very fortunate in no one in my immediate family has been really ill with.
I haven't lost anybody to it unlike others.
So I think I recognise a very creepy when I've had a very easy time of it.
Um, and I've also noticed that those of us who've had an easy time of it may get a bit blasé about it and you know,
individuals who've lost loved ones who have been really ill before, I say like no put your mask on.
No, you know, two metres. So I think you just have to be mindful that everybody's had slightly different experiences in their,
their personal experiences may actually be very, very different to your own.
But so far, personally, I've been very, very fortunate.
So, yes, this is the last question. Has your experience of the pandemic and everything with it changed your attitude or your approach to your work?
And how would you like things to change in the future?
Well, so obviously we overnight we had to move to Homeworking and it was more collaborative.
We were talking to many more people than we would otherwise do. Everybody wanted to help.
And now that we're we're kind of coming out the other side.
It has been hugely complicated about what does New Normal look like for not just us here,
but across the country, about working from home, coming into the office?
It's a very emotional subject and, you know, really having to think about, well, what is optimal for our team.
And we're still figuring out what works best.
You know, we, we recognise that actually getting everybody into the office five days a week is maybe not,
not best, for it is not optimal for everybody's way of working.
They've got long commutes. Most of us don't live in Oxford, you know, most of us have some caring responsibility.
So actually, can we get the best? Can we learn from COVID and get the best out of our staff by having some flexibility and reaching a new normal?
That looks a little bit different.
But quite what that looks like and making sure this seems to be fair for everybody is more difficult than we originally thought.
So there's no question of just going back to how everything was before.
I think the world's moved on. I think you're right. I don't think we should be saying right.
It's over now.
Everybody back to coming into the office five days a week, because I think we've all recognised that we can be just as productive working from home.
And actually sometimes if you want to focus on something and you don't want distractions,
it's better to work from home no matter what your job title is and you can have a better quality of life.
You don't have to sit in a car for 2 hours a day to get to the office.
And yes, we recognise that we,
we have to come in for meetings and have more days and the collaboration and don't undervalue the importance of a quick chat around the cattle.
But equally there is just as much value as putting aside a day to really focus on a specific task, and you can do that at home just as well.
So it's managing those. I think people expect very different things now post COVID, they expect to be able to have some flexibility.
They expect to be able to work from home a bit more. And I totally understand that.
And I think we should be trying to optimise the way people work and think a bit more creatively about what's best for people.
It's lovely. Thank you very much. Thank you.