Podcast transcript: Leeds Voices - Episode 11 Cystic Fibrosis Trust's Dr Keith Brownlee
Transcript for Leeds Voices podcast episode 11. Return to the news article: Transforming cystic fibrosis care.
Alex Regan: Hello and welcome to Leeds Voices, the weekly podcast brought to you by the University of Leeds. I'm Alex Regan and a few weeks ago you will have heard a real treat as we spoke to Olympic triathlete Jonny Brownlee, a name synonymous with Leeds. And this week we're speaking to another Brownlee. Obviously, you assumed that it's going to be his brother, Alistair. Well, in fact, it's not. It's the patriarch of that family. It is, in fact, Alistair and Jonny's dad, Dr. Keith Brownlee, as well as being a Leeds alum. Dr. Brownlee is director of medical affairs at the Cystic Fibrosis Trust. Since graduating with a medical degree from Leeds in 1984. He's gained over 30 years experience caring for children and families with cystic fibrosis.
We learn more about the disease, the development of life changing treatments, the work of the cystic fibrosis trust, and the impact Leeds has had on improving outcomes for the disease across the world. Ed Newbold spoke to him this week and as the father of two of Leeds's most successful sporting alumni, he also asked him about his experience of being a parent, watching their children compete on the world stage.
Ed Newbould: For for anyone who might listen who has only heard of the nam, can you give a sort of a a brief description of what cystic fibrosis is and the impact that it has?
Keith Brownlee: Yeah, certainly it's it's a genetic condition. So it's there at birth and there's around about 11,000 people in the UK with cystic fibrosis, but about one in 25 people in the UK carry the gene that causes cystic fibrosis and you need two of those genes to actually develop the condition. So you need to inherit one from mum and one from dad. Basically people with cystic fibrosis are missing a channel and ion channel or gate on their cells that allow salt and water in and out of the cells. Now the result of that is that they have very sticky secretions and those sticky secretions are particularly a problem in some organs, particularly the lungs, which means that very vulnerable to certain infections and those infections over the years cause lung damage and scarring.
And most people pass away as a result of respiratory failure due to the chronic scarring and damage caused to their lungs due to infections as a result of that sticky mucus. But people also get problems with sticky mucus in their pancreas, and that means that they have difficulty absorbing fats in particular, and that causes nutritional problems and also stomach symptoms of bowel symptoms.
Now, various other organs are affected as well, but it's mainly the lungs and the pancreas and guts that cause the problems. Cystic fibrosis is often considered to be an invisible disease. So people often to their colleagues, look completely normal. And some people don't even tell their work colleagues that they've got C.F., you know, they want to be treated as everybody else. And yet there's a lot that goes on behind that. So we are desperate to increase awareness of cystic fibrosis as a, you know, relatively common genetic condition that has a massive impact on people with CRF and that there's still a lot of work to be done.
I was offered a place at Leeds Medical School in 1979, okay? And I've been in or about Leeds pretty much ever since, to tell you the truth. Yeah. And the course itself was really full on, you know, it was 24/7 really with lectures and studying and exams and, and it was quite old school medical course and with the basics sciences for the first couple of years.
But Leeds itself, being a city, provided loads of opportunities and I must admit took advantage of a lot of those opportunities. This fantastic places to visit, you know, some great had pubs and some great restaurants as well. So it was really enjoyable. And being a student in Leeds as I say, I met my wife there and started going out in the third year of medical school and the last two years, you know, we had a really good time.
I graduated in 84, did a year of house jobs, I did a surgical job in Wakefield and then a medical job at St James in Leeds at Beckett Wing. And, and then I went into pediatrics. I was determined to try and pursue a career in pediatrics, and I was really fortunate to be offered a rotation in pediatrics at St James’s University Hospital as it was then, and that's when I first really became involved in the care of people with cystic fibrosis.
And, and, you know, I did my pediatric training for the next nine, ten years or whatever it was, and in Leeds, in Sheffield, in Huddersfield, and eventually came back to St James's to work in as a pediatrician and in a permanent post and initially general pediatrics. But I worked with somebody called Jim Littlewood, you know, who's a massive figure in cystic fibrosis in the UK. He really did develop health center care and multidisciplinary team care. He brought it. You travel the world looking how cystic fibrosis care was delivered in places like Canada and and the US and brought the best of it back to Leeds and really developed a superb set up and and I together with colleague sort of inherited that mantle and provided care from around about 200 250 kids with CRF in Leeds and around the north of England.
It struck me as a, you know, a fascinating condition, and I was very massively impressed by how the families and the children dealt with the condition and the ability to be involved in that and see the same people over a prolonged period of time and build up a relationship with them. There's something that really appealed to me and I really enjoyed. And, you know, you're almost in it together to try to make life as, as as good as possible for the families and the children. And always with an eye on the future and the prospect that a new treatment would come along, which would transform the outlook for people with care. And, you know, in the early days that was we were thinking gene therapy would make a difference.
But these modulators have come along before gene therapy and they've definitely made such a transformational difference. You know, when I first started, it was unusual to, you know, for adults to have cystic fibrosis because most people with CF died as children. But now there's almost 60% of the population in the UK over the age of 18.
So it's gone from being a pediatric condition to an adult condition in my lifetime. And it's going to improve even more with the advent of new medications and new treatments. And, you know, I remember in the early days when I was first involved, there was pediatric wards with several children with horrendous coughs, producing pots full of thick, green, sticky sputum every day, requiring intravenous antibiotics for 2 to 3 weeks in order to try to dry up the secretions.And you just don't see that these days.
Ed Newbould: For you, what's kind of the most exciting development there has been?
Keith Brownlee: Cystic fibrosis care and treatment has always been traditionally aimed at trying to treat the consequences of that thick, sticky mucus. So treatment has traditionally been antibiotics to treat the infection. We try to help cough up the secretions to stop blockage of the airways. But research has developed a new class of drugs which actually interact with that ion channel.
I was talking about the channel that allows salt in and out of cells because of the genetic abnormalities informed properly if you have cystic fibrosis. So the channel is produced within the endoplasmic reticulum in the cell but doesn't get to the cell surface. So those cells can transmit chloride and sodium normally. Now there's a whole family of small molecule have been developed here called correctors and potentiated, which interact with that channel.
So they attach to the channel and reconfigure the protein so that it gets to the cell surface and the channel works more effectively. So it actually treats the fundamental cause, the fundamental problem that abnormal channel. And they have been truly transformational. There's a drug called kaftrio, which works particularly on the communist mutation that causes cystic fibrosis. And those people benefit remarkably from the drug. Yeah. One of the most amazing things is that it converts the sweat test, which is the diagnostic test for cystic fibrosis to normal. And so, you know, we diagnose cystic fibrosis by collecting sweat on people and measuring the amount of chloride in that sweat. And if it's high, you are likely to have cystic fibrosis. If it's below a certain limit, you're unlikely. But once you start taking this drug, it converts that test back to normal values. But in addition to that, it improves lung function significantly. It reduces the rate of decline of lung function, it reduces the number of exacerbations or flare ups of infection, reduces hospital admissions, reduces the need for IV antibiotics, you know, by a very significant amount across a population level.
And almost certainly it will improve life expectancy and very significantly for people with CF.
Ed Newbould: Why has CF have come on in such leaps and bounds? I mean, I'm not sure what it's like compared to other illnesses, but it feels like the development of these drugs and the research going into is really significant.
Keith Brownlee: I think the reason and that's a really important question, you know, is that the cystic fibrosis charity funds research and research is incredibly expensive. So we are eternally grateful for our supporters. And when you consider there's only 11,000 people with C.F. in the UK, it's remarkable that we get the support that we do to fund the research that we do.
But that's true all over the world as well. And in the in the States, the CF Foundation has had a very productive research pipeline as well. And I think partly because CF is caused by mutations to that channel. So it's relatively straightforward. You know, if you can correct that channel, you can correct the problem, whereas lots of other disease sources have multiple causes too.
So see, it is relatively simple from the genetic perspective, but I think you can't underestimate the importance of the likes of the trust and the foundation for investing in basic science research and investing in, you know, treatments to to address the condition. And then pharmaceutical companies have taken them on. And then the community has come together as well to trial those those drugs that have been developed.
So this research networks in the UK, in Europe and the US, which have really pushed through the trials of the new compounds to see if the benefit people receive. So it's been a massive collaborative effort, you know, between people with C F in terms of the, you know, volunteering to participate in clinical trials of new drugs from the charities like the CF Trust, a foundation that funded a lot of that research and the pharmaceutical companies as well.
It's been a superb success story. Having said that, you know, these drugs treat the majority people with CF, but there's still a significant minority in whom the drugs don't work. There's a subclass of people where the mutation means that they don't produce any of that in general. So these compounds can't interact with the ion channel and stop making function normally if you don't produce any.
So the so called class one mutations do not respond to these modulators as they are called. Leeds has been a powerhouse of delivery of care over the years. Going back to Jim Lockwood, the person I mentioned to you earlier on, but it's also had a strong a very, very strong history of clinical research. So and that's you know, it's that's been very, very impressive going back to my time as well, but particularly in the adult unit.
And that's been very strong. But over recent years. Daniel Peckham, one of the adult physicians at the Leeds Adult Cystic Fibrosis, has done some phenomenal basic research looking at the the fundamental problem and trying to understand and see it as an inflammatory condition and how the modulators impact on that and how that may impact on all sorts of other co-morbidities associated with cystic fibrosis.
And that's been world leading research. My particular role as Director of Medical Affairs is more a advisory role, and I help bridge the gap between the clinical community and the Trust, you know, so that there's a good flow of information and and joint objectives and that the trust is informed by the issues that affecting people with CF. We're very fortunate in that we have really strong involvement groups.
So we do involve people with CF in virtually all of the decisions that occur in the trust. And it's a genuine partnership and it works really well and the trust has done some fantastic reas funded some fantastic research into some of the, you know, the characteristics of the channel that I've been talking about and the properties of the channel, but also, you know, it helped with the delivery of the clinical trials and it's funding a lot of research into and infections, identification of infection, treatment of infections, new new drugs to try to combat some of the gram negative infections.
The people we see at the particularly vulnerable to. But there's a whole host of different projects that the trust is funded. One particular one that I should mention is gene therapy. Several years ago, the trust invested a lot of money into gene therapy and on the back of that, an awful lot of science was sort of discovered and that's helped develop the therapies for CRF, including the modulators, because it's increased the background and understanding of, you know, why people get CRF and what the channels do and how you can interact with the cross infection as well, so one of the things that we were very, very interested in, you know, people with CF get infections with these gram negative bugs and over the last 40 years it's become increasingly apparent that they can pass one of these bugs between people with CF and therefore it's highly recommended that people receive avoid cross-infection avoid coming into contact with each other to try to avoid cross-infection between people. It does make the condition rather isolating. If you can get in the same room with other people at CRF. Cystic fibrosis trust is quite unique in that it works with the community of people with CRF and the clinical community to hold a database on everybody with CRF in the UK, and that includes all of the a lot of the clinical data as well.
And that data is used to leverage support for people with CF and also for research as well, and to gain access with policy and public affairs to the high cost treatments that we've been talking about. It's incredibly effective with the with new treatments. People are going to be living a lot older with CF and therefore they're going to potentially suffer from some of the co-morbidities that we all suffer from which people with CF haven't done in the past because, you know, the median age of death has been in the thirties, and that will be challenging. We produce information for people with CF in families about issues. We produce guidelines and consensus statements for clinical teams and we help produce standards of care and specifications for the delivery of care for people with CF.
The support is providing advice and help to families and people who care about issues like schooling, employment and, you know, access to government support. And we provide direct support ourselves financially, to the people and families with CF who are struggling. There's the research element that we've talked about quite a lot, but there's also the Clinical Trials accelerator program, which is the the Network for Delivering Pharmaceutical Studies, which has been incredibly effective and supported by a grant from the Foundation.
And then there's all the policy and public affairs work of the trust to make sure that CF remains a priority and people with CF get access to the treatments that we know work as soon as they possibly can so they can benefit from them as soon as they possibly can. So that's the sort of spectrum of work the trust is involved.
And you didn't ask me anything about Alastair and Jonny.
Ed Newbould: I wanted to avoid that. I thought you might get that a lot. Do you get to go and watch them a lot?
Keith Brownlee: Over the years we have gone quite a lot. We've travelled, you know, in the UK and in Europe and occasionally for the big, big competitions abroad. So, you know, we've been fortunate to go to the Olympics in Beijing and Commonwealth Games in Australia and Olympic Games in Rio de Janeiro and obviously went to the London Olympics as well.
So we have travelled. Yeah, and it's been you know, it's been a really fascinating journey, to tell you the truth. It went from one from a hobby to a profession almost overnight. Yeah, it is not been easy in some ways because, you know, I don't know if you know, but some races have ended up with heat exhaustion and collapsing and also intensive care and they’ve been all over the place. And when you sit at home and you see them collapsing and, you know, clearly struggling, it's a worrying thing to see.
Ed Newbould: And there was that one race, that famous footage of Alistair carrying Jonny over the line.
Keith Brownlee: That was in Mexico. Yeah, that was just after Rio. Cathy and I had been out in South America following Rio and we didn't know that they were planning to race in Mexico. So we'd gone home and we just got home and then we sat late at night watching that race on the television. It's a bit scary.
Alex Regan: Thanks very much for listening to this episode of Leeds Voices. It was presented by me, Alex Regan. It was edited and produced by Ed Newbold. Leeds Voices is a podcast brought to you by the University of Leeds Advancement Team. You can follow us on social media @LeedsAlumni or you can contact us on email at alumni@leeds.ac.uk