Dr James Galloway, an Academic Rheumatologist and Senior Lecturer at King's College London
AUTHORS: Dr Sanketh Rampes and Dr Anvarjon Mukhammadaminov
In this series the Medspire team interviews doctors about their career, their specialty, the choices they have made and their advice for doctors and medical students.
Here the subject is Dr James Galloway, an academic rheumatologist and senior lecturer at King's College London. His research is focused on clinical epidemiology, especially relating to pharmacovigilance. Throughout the pandemic, Dr Galloway has been closely involved in COVID-19 research, including the TACTIC and Novavax clinical trials.
A podcast of this interview is available here:
How did you get to where you are today?
I'm an academic rheumatologist employed by King's College London (KCL). I do my clinical work as a consultant at Denmark Hill, King's College Hospital. I qualified 20 years ago in Bristol. I did postgraduate training - which was a slightly roundabout sort of training in those days.
There weren't the same sort of run-through posts as today, so I did a scattered series of junior doctor posts - senior house officer posts - in the internal medical specialties.
I realised quite early on I was probably not going to be a surgeon. I had various mishaps trying to stitch people up in emergency departments and realised I didn't have a steady hand. I liked puzzles, so I sort of meandered through various medical specialty jobs, settling upon rheumatology because it was a specialty that was full of puzzles.
I then went to Manchester to do my postgrad training and took a PhD there. I got into research through training with the epidemiology unit in Manchester. I never realised how much fun statistics could be. It was while I was working in Manchester, I also started to get more involved in clinical trial work.
I came to London and carried out postdoctoral work in London, doing Phase I clinical trials with some of the ‘greats’ of clinical trial medicine: Tim Mant and Jim Ritter. (Some of you may have come across the textbook Rang, Dale and Ritter.) Jim Ritter taught me a lot about clinical trial medicine, and then I gradually developed a research group here at King's.
What drew you towards your PhD in epidemiology?
I was very fickle about my choices of research. There are a few things that have massively influenced me in my career. One of the most important things has been people, and having mentors who I’ve worked with and thought that what they did was interesting.
When I was looking at research ideas, it was because during my postgrad training in rheumatology I did a master's in rheumatology, and as a component of that there was an epidemiology course. I listened to lectures by one of the teachers on the course - a very eminent professor now at Oxford in epidemiology called Alan Silman.
I found it fascinating hearing about the way he would interpret information, look at data, look at information at population level, as well as understanding how you can then take that data, interrogate it, and learn something that changes how you practise medicine. And it gave me a real passion for wanting to do it.
I didn't actually do a PhD with him, I had other supervisors. I’ve been very fortunate with the people I've been trained by. Deborah Simmons, who was head of the unit that I worked in and was my PhD lead supervisor, was similarly very passionate, very good at detail, and about looking at a dataset and being able to say: 'Have you looked at this aspect of it?’ ‘Have you looked at this question?’ ‘Have you asked the right question?'
I'd say what drew me to research and to doing research within epidemiology, were my mentors. They opened a door to me. Another thing - and this was I think something that was a big bit of luck - was that I came into rheumatology at a time when there was an advent of biologic therapies.
Now, if you are learning about rheumatology, biologics is the ‘bread and butter’ of rheumatic disease management. There's all these new drugs with long names that end in 'mab' or 'cept' - they all do subtly different things - and there's also a myriad of cytokines you have to learn about.
When I studied rheumatology there was steroid, methotrexate and a few other drugs, but the cytokine blocking drugs were only just emerging on the market. When I was at medical school they didn't even exist, they weren't licensed.
When I was looking at research there was an enormous question: ‘We've got these drugs that are very different in how they work - are they safe?’ That was the overarching question to my PhD, looking at pharmacovigilance, and trying to understand the short and long-term harms that were associated with this new class of therapies for rheumatoid arthritis.
It ‘paired up’ - seeing some mentors who were very inspiring with a question that seemed really relevant and, clinically, something that was crucial to understand. You’re prescribing for patients where you really don't know what the long-term safety is.
And yet we know that in rheumatoid, for example, when you prescribe someone a TNF inhibitor, the disease gets amazingly better until you stop the drug, and then it comes back again. So you're talking about leaving people on drugs for decades, potentially.
Is there one paper that you have published in particular that you're most proud of?
It’s really difficult to talk about pride in publishing a paper. You have to be very humble in research, recognising that it's not a one-man show, and you have to recognise that research is about working in teams.
But if you had to ask me about a paper that I most enjoyed contributing to and driving, we did a paper looking at infection risk with various biologics in people with rheumatoid. It was a really interesting question, which was that a lot of the time in these studies, when we see infections associated with drugs it's to do with confounding.
One of the major reasons we give people these drugs in registers - these are not trials, this is people who are chosen to be given the drug in routine care - is that we give them to people with the more severe disease, so you see more side effects and more adverse events.
That's not due to the drug, that's due to the type of person given the drug, but I had thought for some infections this might not be the case.
For example, shingles and the reactivation of varicella zoster. If we saw that shingles was more increased with these drugs, that might suggest an immunological change specific to the drug, rather than just a general marker that these people had more severe disease.
I wanted to demonstrate this by not just saying how - in the analysis, we can adjust for disease severity. What I wanted to do was adjust for disease severity over time, showing potentially that people who are given the drug and whose disease gets better, would still be at greater risk of this one particular infection called shingles, but that the overall infection could be explained by disease severity.
I'm not sure if I explained that very clearly, and I know that in hindsight - having published the paper and talking to people who read it - a lot of people didn't quite capture what we did, and the finesse of what we did.
We stole some methodology from economics - from some people who had done some stats modelling of looking at economic outcomes over time, called ‘marginal structural modelling’.
It took months of working to get the code to run and to work, but we basically showed that in this massive dataset of 20,000 people, skin infections overall were increased in those given TNF inhibitors, compared to people treated with standard rheumatoid therapies like methotrexate. That difference was all explained by comorbidity - disease severity.
With shingles, the risk was elevated to a similar extent and it wasn't explained by all the comorbidities. In the complex adjusted model - with this marginal structural modelling accounting for disease severity, disease activity over time - that didn't take away the association for shingles.
We were able to say that some of the infections are confounded, but some are genuinely causal associations, so these drugs increase your risk of reactivation of shingles. It's not my most cited paper, and to this day I remain convinced that some people have entirely misunderstood what we did in the analysis.
But in terms of hours spent looking at code and trying to get a massive dataset pulled together, anda model applied to it which worked, it is one of my greatest achievements.
That's maybe from a slightly selfish perspective, because it's also perhaps the paper which I spent the most hours in a darkened room trying to do. Most of my more recent papers are spent with my team in darkened rooms.
What are the biggest changes within rheumatology during your career?
These are almost indescribable. I started rheumatology where you had a 40-bed ward with patients in hospital with rheumatoid arthritis, and diseases like vasculitis - half the people who were diagnosed with ANCA vasculitis would die during admission.
The outcomes were very different. A rheumatoid arthritis clinic was frequently done jointly with an orthopaedic surgeon, because it was about knowing when to operate, which joints to operate on, and which procedures for which patients.
I barely know the orthopaedic surgeons at King's anymore, because we don't send people for joint replacements. Rheumatology has been completely transformed. The headline has been the move away from corticosteroid as being our mainstay of therapy, so that's massively reduced side effect burden.
We knew that corticosteroids on their own didn’t seem to modify disease outcomes. In the advent of initially the TNF inhibitor class, drugs like adalimumab, infliximab, etanercept - which were the first ‘big three’ - they gave us this glimpse that you could have a very different goalpost.
Your goal post isn't about keeping people a little bit more comfortable. It’s about getting people into a state of disease remission where they will not need joint replacement surgery later in their life, where they will be able to continue working, bring up a family and have a quality of life that while not normal, is definitely much closer to the general population - to healthy people.
If you were to fast forward, in 2017 and early 2018, the UK saw the first licensing of a JAK inhibitor. The JAK inhibitors were unlike all the other drugs we had between 2001 when TNF was licensed and then, all of the drugs we had for rheumatoid were biologics. They have to be given parenterally, by injection, because they're proteins.
If you took them by mouth, you would just digest them. They're biologics and you store them in the fridge - there's a cold chain - and they have a cost attached to them. Even at generic cost you're still talking about thousands of pounds a year, whereas with a small molecule you could take it as a tablet, and when it's off patent its cost will potentially come down enormously to £100 a year.
The advent of the JAK inhibitors is so exciting because they're tablets - they're small molecules. They appear to work as well, if not better, than the TNF class, and once they come off patent then you could envisage that they will become a standard of care globally. In the UK we do great for rheumatoid, but is that the same everywhere in the world? Definitely not.
We're very fortunate with our access to therapies, and the movement of new therapies is exciting. The biggest question that hangs over them is their long-term safety, which is something I'm very interested in because it's my research area. But I think it's a tough question we're going to struggle to answer going forward.
What research questions do you hope to answer in the future?
It's a huge subject. On the cusp of discovery in rheumatology is our patient profiling and biomarker identification to predict treatment response. The ‘golden chalice’ of what we want is that we've now got a dozen different therapeutic options.
We've got to where we can block IL-6, or we can block IL-23 or the JAK pathway. But it's about how do we pick the right one for the right patient, the first time around? How do we get that precision medicine where we can say: ‘Let's get someone the right drug first off?’ Part of that is about understanding that rheumatoid arthritis, for example, or systemic lupus erythematosus, are ‘disease baskets’ that actually encapsulate many subsets within them.
People who have very different phenotypes and probably different biological signatures and drivers of their disease. Although we tend to lump rheumatoid all into a single disease, there are undoubtedly different subsets. Some people need TNF inhibition, some need IL-6 inhibition, and so forth, and which subset they fit into may evolve over time.
In recent years, what has massively changed is our ability to deep phenotype people's immunological profile. There’s the rapidity that we can now get biomarker profiles, measure cytokines in the peripheral blood, measure cytokine profiles in the joint, even things like RNA signatures to look at transcript change.
To genotype someone it used to be that you would send a sample off, it would cost you £20,000 and you would wait nine months for a result. However, at the start of the pandemic the NHS launched its first commercially available whole exome sequencing service, which runs at a cost of just half a thousand pounds a patient to sequence their entire protein encoding genome.
And that is revolutionising what we can do in terms of disease phenotype. That's one of the great things we’re facing.
There's also some really cool bits of immunology we're just starting to take the lid off, one of them being complement cascades. In February 2021 there was a paper in the New England Journal of Medicine by David Jayne - who’s a friend of mine actually.
He was published on a drug called avacopan, which is a complement C5a inhibitor, which was compared in ANCA vasculitis to either avacopan or steroids alongside standard of care. The difference is astonishing.
I've been watching this trial and talking to David about this for quite a while, because the trial results are basically paving the way for almost a steroid-free induction regime for an ANCA vasculitis. So we've got a new, really ground-breaking treatment for the most severe form of vasculitis.
So how does complement therapy work? A complement is a protein cascade that forms the membrane attack complex, which causes cell death - it kills invading bacteria. Except avacopan doesn't stop the formation of membrane attack complex, it blocks one of the subsidiary proteins.
You have on the complement cascade the main bits, what we call C1, C2, C3 down to C9, and when they activate they each split in half - so there's an 'a' and 'b' component. The 'b' component goes on to do the work, if you like, and the membrane attack complex is made up of C5b, C6b, C7b, and so forth, so you get this nice pentameric rim.
The 'a' components are generally thought of as being autoregulatory. They go back and just tell the complement to slow down a bit. No one quite followed these 'a' proteins to see what they did, except we've discovered that the C5a protein appears really important in neutral activation.
It's opened this door about understanding what complement does and what it can do, which is so exciting. Understanding complement immunology is another really interesting aspect of immunology.
What advice would you give to people who would like to get more involved in research?
An involvement in research, if it can lead to a publication, can improve your chances of getting jobs and get your points up on applications to the foundation programme. There's no doubt, once you start working full-time as a doctor in your foundation programme, your chances of getting a publication drop down, because you've got your day job to do.
There is an advantage to getting involved in research as an undergraduate. However, I would say that 90 per cent of the students who contact me about research never actually do any research. It's a tiny fraction who actually engage.
Why would you want to get involved in research? If the answer is: 'I'd like to get more points’, that probably isn't the best reason to get involved in research. But it might be because you want a career one day that is not doing just clinical medicine, but doing research as well.
You might want to get a taste of what that involves. But it's not about having a chat with someone, or writing a paper over a few weekends. It's about putting in a large number of hours to get involved, and committing, in your spare time, to a substantial piece of research. It would be a mistake to say it's not a lot of work.
Someone who gets a paper on their CV by the end of medical school has usually put in a hell of a lot of work to do that. That's why these papers do set people apart.
Thinking about why you want to get involved in research is about trying to understand what research involves. What is a career that takes in research, and why is it different from just doing clinical? Anyone who is interested in how to do research should start by having conversations with clinicians that they do placements with, or with those whose lectures they attend.
When people email me, I always try to reply to say, 'Let's meet'. The ones that come and meet me, spend some time with me. I then say: 'Well, why don't you do something? We'll do a bit of work together’.
The way you get involved in research as a student is to show interest, to pitch up at an academic's door and say: 'I heard you give a talk’,' or, 'I sat in a clinic with you and I'm really interested. I want to learn more. Is there any opportunity?' But know that it's not a one-way street. When you come to an academic they know if it's because you want to get your name on a paper.
That isn't appealing to an academic. Someone saying: 'I just want my name on a paper' - that doesn't ring any bells for me. That's not something I want to invest time in. I want to help people who want research to be a part of their career and who want to learn about the subject.
How can students and doctors become the best clinician possible?
I was given this advice by a mentor of mine: ‘The more you know, the more enjoyable medicine is.’ A large part of this is about reading. It's about pitching up to the lectures - both postgraduates and undergraduates alike. It's about turning up to an education opportunity, and never getting bored of it.
Everyone has a different way of learning. Some people do better with a textbook, some with a screen, and some people do better with a podcast. But whatever you do, it's about being diligent that every week you will put in time to learn, consolidate and acquire new knowledge relating to your field of interest.
I was told that you cannot underestimate how much reading you need to do, and I believe that's true. The point at which you get bored of reading about your subject is the point at which you should be looking for a different subject.
When you get your foundation job, IMT job or specialty training job, and you see a case in clinic of whatever diagnosis, whether or not you’re familiar with it, when you get home reflect on what you've seen. Look it up and read about what you've done.
The more you read, the more you challenge your knowledge, the more you say: ‘I think I've seen this before, I've treated it before, but I'm just going to check and look again’. ‘Are there new guidelines?’ ‘Has something else come out?’ ‘Do I understand why I definitely do this?’ Say you’re a foundation doctor and someone has been admitted to hospital with pneumonia.
How are we going to treat that pneumonia? So we're going to give them this antibiotic regime and we're going to put them on anticoag prophylaxis. But you think: ‘There's that CURB-65 score’. Do you know where all this comes from? Have you read the studies that underpin those decisions? Have you read about the CURB-65? Have you read any of the antibiotic trials?
That knowledge you sometimes superficially take for granted - it's about learning to delve deeper. You learn the basics when you qualify in medicine, then as you become more senior, the skill is then to build depth to that knowledge, to start to really understand the rationale behind decisions. Then you can question them, and reasonably say: ‘Hold on, maybe this isn't the best way of doing things’, or ‘maybe I've got the diagnosis wrong’.
Like many clinicians and researchers, you were redeployed to help with COVID. What was that like?
It was interesting. I've done a few things with COVID. The first thing was the beginning of March 2020 when I was running a COVID ward. It was before redeployment happened. One of the chest consultants - a friend - said: 'I was just wondering if you might be able to help on a ward.'
I said that I could pop up for an hour to see a patient with a painful knee. And they said: 'No. We thought you might like to come and do the ward round.’ It was okay, because at that time it was ‘turn the oxygen up’, ‘turn the oxygen down’, ‘call ICU’. It wasn't ‘rocket science’ initially, because the disease was brand new.
I've seen a fair amount of disease and I'm curious. I'm interested in seeing clinical patterns of disease, and this was very distinct. I don't recall ever seeing a disease where people come in looking like they need to be ventilated, but with a normal pulse and blood pressure. That's not a thing.
Normally by the time you've got severe enough pneumonic disease to need to be tubed, your pulse is racing, your blood pressure is in your boots, you're filling up with fluid, you're thinking about putting them on norad. But COVID pneumonia was very different. From a clinician perspective, it was really interesting.
From a personal perspective, it was a very unsettling time. I remember not sleeping for days. You would not sleep for several days, then you would crash out and sleep really well, and then it would start again. Conversations with relatives were awful - talking to people and saying you can't visit.
People asking: 'What's likely to happen?', and you saying: 'Well, people are going to die.' Having that same conversation that someone is likely to die, particularly with elderly people who weren't suitable to go to be ventilated. There was just that déjà vu sense of having that conversation so many times.
The juniors were amazing. There was an immense, very emotional sense of feeling indebted to the junior team, who were just brilliant - they were absolutely tireless in what they did. Back in the first wave of COVID, people became fairly blasé about personal risk, because PPE was not being used in the way we now use it - there was much less access to FFP3.
When we met outside of the clinical space or the bedside, we all took our masks off, and there was huge amounts of staff transmission. That was very interesting - a sort of blend of emotions.
On the research front, we've done a lot of clinical trial work. We set up a national platform trial, TACTIC. We've been involved in several other trials. We've recruited seriously large numbers of people to clinical trials over the last year. I ran the Novavax trial here at King's - I've done vaccine trials before.
When I did Phase I work a decade ago I did vaccine trials then, so I've been an investigator on vaccine trials. But when we were doing the COVID vaccine trials we randomised 250-odd patients into a vaccine trial in three weeks. It was astonishing. As soon as we got them in through the first wave - which we did October/November time - then COVID started to hit on the wards.
My trial investigators and the research nurses I have working with me, they were worked to the bone doing the COVID vaccine trial. Then we got on to the wards, back in to re-recruit to TACTIC. We recruited 140-odd people. One individual physician of mine, he personally recruited over 100 patients to the various different trials we've got on the go. It was a very humbling experience being part of that team.
Can you give more details about the TACTIC trial, and how you got involved?
It's one of the national platform trials - a UPH badged trial. I got involved in March. I was having phone calls with a lot of people in a fairly short space of time saying we needed to get trials up and running. We knew RECOVERY was opening up, but that it had a very heavy focus on antiviral therapy.
We thought we needed drug trials that were going to look at immune modulation rather than antiviral. What I really wanted was a combination therapy trial. I spent hours on the phone to Gilead, trying to convince them to give us remdesivir, because I wanted a trial that was going to compare an antiviral strategy to an immune modulatory strategy to a combination strategy.
But through politics and life, that wasn't to be. We ended up having remdesivir licenced and available anyway, so it became standard of care before our trial really took off.
It was a strange journey, because we at King’s set up in partnership with Cambridge. There was myself, Andy Cope - he's my boss, a KCL professor who's an absolute legend in T-cell immunology, and a rheumatologist. We partnered with colleagues at Cambridge including David Jayne, who did the avacopan trial. He’s a great trialist and a nephrologist by training.
There was Frances Hall, a rheumatologist and the overall senior investigator for the trial. She’s been really passionate about looking at immune modulation in COVID. Then there’s Joe Cheriyan and Ian Wilkinson, who are both pharmacologists and also trial designers by trade. We formed this core team of people that would get together.
It was an enormous battle to get UPH badging, to get funding, to get the trial pulled together. We're probably, I hope, going to have some answers very soon. We've recruited over 400 people.
It's a very different trial to RECOVERY, which is run out of Oxford and is an astonishing feat. If you had another pandemic, RECOVERY is the way to do it. It has recruited enormous numbers of people to some very pragmatic designed intervention studies, where you get randomised to an arm and then you collect the outcome data through NHS Digital.
You don't have clinicians spending hours filling in data sheets. Contrast that with TACTIC, which is a very different study. It's a really detailed trial where we are collecting biomarker data. We're taking samples of blood at every time point, and closely monitoring people and following them up to look at not only drug efficacy, but safety as well.
One of the challenges we were concerned about was the equipoise of immunosuppressing someone with active infection. They're very different studies and they will answer different pieces of the COVID puzzle. It's been a labour of love and a lot of hours and time and effort have gone into the study . And it's a Bayesian adaptive design - which I won’t explain.
What advice would you give to your younger self?
That’s a really difficult question. I'm a reasonably positive person and I generally see the bright side of life. I don't think I'd want to be anywhere else. I would be slightly worried to go back and tell myself to do something different, and to end up somewhere different.
I'm actually quite pleased with where I've ended up. I've had a lot of luck along the way. I don't think it's all been through choice - there's been a lot of support, good colleagues and good fortune. There’s one thing that I would tell my younger self not to do though.
Recently, I saw a photo of me at medical school in my second year where I had grown a goatee. That was a huge error, and it's unfortunately on a number of photographs of me at medical school. I could probably have got rid of that goatee and it wouldn't have adversely affected where I would end up today. That probably wasn't the sort of advice you were hoping for.
Are there any habits that have helped you succeed?
Keep reading. If you sit down for more than a few minutes, pick up a book or read a journal. Reading is so important - you can't read enough.
There's also a couple of habits that are so important in terms of behaviour, team-working and working as a collegiate group. Whether you're clinical or academic, or even just in a household at home with family outside of medicine, learning how to communicate well and effectively is really important.
A big part of that is having insight into how you communicate and getting feedback. Part of that you can do through reflective practice and a portfolio. Sadly, probably a substantial majority of people - and this is probably no different at undergrad level - see them as a tick box exercise and not as a useful way of actually trying to reflect upon your communication, and your ability to interact.
My first tip would be to treat portfolios - which you will carry with you for your entire career that you stay GMC registered - with respect and dignity. Portfolios are not for someone else to read and tick off, but for you to look at and reflect upon yourself. I have found the ability to reflect on my strengths and weaknesses - it's not something that comes naturally.
I actually stop and look at my portfolio over the last year and say: ‘These are some things I need to do better. This is what I can evolve and learn from’. That's really important. Just realising in the moment something has not gone well doesn't actually lead you to want to change and do better. If you want to continue to strive to do better, keeping a record of it helps.
What you agree to do for other people is also really important. There are some people who say ‘You've got to learn to say no’. I know a lot of people who are told that when you start out in life, when you get a new job, you must learn to say no. But I would challenge that. It's not so much about learning to say no, it's about trying to learn to say yes as often as you sensibly can.
During your career you work out that there's people you will work with and collaborate with - whether that's clinicians or otherwise - and they will be the ones who will help and support you, and who generally say ‘yes’. Recently, I went to the wards, and saw a patient for whom, on reflection, I had probably not done my best.
I had been to see them several times but they either weren’t by their bed, or I hadn’t spent long with them because there were other people at their bedside. I didn't pay attention. The last time I saw them I regretted this because I may have missed a trick. I missed a diagnosis and I could have done better. So I’ll reflect on that and that reflection will go in my portfolio.
Recently, I phoned a dermatology friend and said: 'I've got a really difficult case, I wonder if you would help'. I knew before I phoned her that she would say yes, and when she answered the phone she said, 'No problem. I'll come now'. She dropped what she was doing and she pitched up - and I know that she had had a busy day.
She's like me, she has a busy timetable, but she dropped it to come and help. Colleagues like that, they are what make the difference between success in a career, and also our happiness at the end of the day.
So my advice is: value your ability to reflect on your performance, use the portfolio, and try and say yes most of the time. You've got to stay sane and you have a finite number of hours in the day, but that positive and supportive attitude to colleagues, to teammates, is so vital.
Do you have a healthy work-life balance?
I think I do. I would say I work a lot of hours, but I enjoy work. I don't have kids, but if I did I would have a different balance of work and life outside of work. What is very important though is that while our personalities and who we are in life is inevitably dependent upon our work, the people that are generally most valuable to us in life are often our families.
As soon as you get married you have a partner, you have kids, or it may be that there’s just your own family, your parents - these are such important bonds and it can sometimes be easy to lose sight of this. You turn up to work, you leave work and you get very stressed by it, not realising that the most important bits you have are the bits that you leave work for. You get home, you relax, you exercise, you laugh.
I have a good work-life balance, not because I don't work lots of hours, but because the time I have outside of work is really good. I'm very fortunate with whom I spend my time with. I also believe having a good sense of humour has carried me through a lot of painful years of study. Moments like some of the ‘lows’ of your PhD, where two years in you've not published anything yet, you can't see an end in sight and the analyses won't run.
Several months into his PhD, my husband realised that the strain of mice that he was studying were genetically not the strain he thought they were. You have to remember that life goes on outside of work, and that's really important to value.
Finally, what's your favourite book?
I've got lots of favourite books. I'm going to have to say it's not a single book, but a series. The name of the first in the series is Master and Commander. A guy called Patrick O'Brian wrote a series of books based on actual events of naval history. There's 21 books in the series - I read one book a year, and I'm on about the 17th now.
I've been slowly working my way through them. There's nothing quite like being on a beach, looking out to the ocean - perhaps some exotic location like Tenerife - and reading about life aboard. The great thing about these books is that I would genuinely recommend them to anyone with a medical history, because the protagonists are the ship's captain and the ship's doctor.
The ship's doctor is modelled on sort of a ‘Darwin style’ doctor, so he's a botanist and he's interested in nature. These books also beautifully describe health and disease aboard a ship in the late 17th and early 18th century.
Medspire podcasts are produced by Dr Sanketh Rampes and Dr Anvarjon Mukhammadaminov, both full-time junior doctors. They aim to inspire the next generation of doctors and scientists by exploring the career journeys of leading clinicians and researchers.