From the mysteries of space to the secrets of the microbiome, from the science of pain to extraordinary stories of resilience and discovery — 2025 was a year to remember. Join Conor, Dodi and the team as they reflect on the highlights on Discovery Matters.
Best of 2025
DODI: Welcome back to Discovery Matters, everybody. It is that time of year again…
CONOR: That's right. As 2025 comes to a close, we are taking a step back to revisit some of our favorite moments, insights, and conversations with guests across the year. Think of this as our greatest hits for life sciences.
DODI: The absolute collection.
CONOR: That's it. The Spotify Wrapped and the chance to reflect on what surprised us, inspired us, and maybe even challenged us. Actually, it challenged us a lot because a lot of it was really complicated.
DODI: Thank goodness we're not doing any of this alone. We have invited our very own, former producer, Bethany Armitt Brewster.
CONOR: Who has gone on to great things.
DODI: Great things, yes, so she's going to share.
CONOR: And we've also invited podcast editor Tom Henley, who's going to tell us about his favorite moment from this year, plus offer a little of the behind the scenes at how he has shaped these episodes into the stories that you heard over the last, goodness me, is it six years.
DODI: Is it six? It has crept up on us.
CONOR: But we released our first episode all the way back in 2019. Wow.
DODI: And we must keep going. So, whether you are a scientist, a student, or simply someone who marvels at how tiny molecules can change the world, this episode is our way of saying thank you. Not just for 2025, but for all the years this podcast has existed. Thank you for listening. Thank you for your curiosity and thank you for letting us bring these stories of discovery into your world.
THEME TUNE
CONOR: Let's dive in.
DODI: Beginning with our former producer, Bethany Armitt Brewster. Conor, you said she's gone on to greater things and that means she's still working with us at Cytiva. She is now the sustainability marketing and communications leader.
CONOR: Yes, indeed. She's got a longer title that must mean she's much more important, so good luck to Beth. And what is Beth's favorite moment of 2025?
DODI: Beth chose an episode that looked at space not just as something full of rockets and distant planets, but as a living laboratory shaping the very biology of the human body. So here she is sharing the episode that captured her imagination the most, and she has also chucked in a few heartfelt words about her journey with Discovery Matters. Over to you, Beth.
BETHANY: “How Space Affects the Body” was categorically my favorite episode of the year. It sort of took us beyond, you know, the idea of rockets and planets into sort of the biology of survival in space. You know, we can imagine our bodies aging faster. Muscles shrinking. DNA rewriting itself because of microgravity and cosmic radiation.
SPACE CLIP 1: We know that space flight is this hugely negative environment for our health at least, and we can see that muscle mass and strength can decline by about 20 to 40% in a six month stay. If you spend one year in space, you lose the same amount of muscle mass in that time that you would do on Earth over 40 years’ worth of aging. What it gives us is this accelerated aging environment for us to study muscle loss that we hope we can then translate down to earth and try to help us maintain healthier muscle mass for longer with aging. Because when we think about aging on earth, we know that our skeletal muscle declines after the age of 40, and that can be anywhere roughly around 8% per decade. And we know that although it declines and how important muscle is to our metabolic health and our functional health, we still don't have fully effective non-pharmacological treatments to stop that. So, what we do is try and research muscle health in space to try and improve muscle aging on earth.
BETHANY: The NASA twin study really blew my mind. You know, two identical brothers, one on earth, one orbiting, showing how space literally changes us at a genetic level.
SPACE CLIP 2: All of us care about aging and maintaining health span as long as we possibly can. So, as we learn more and more about space flight and how that influences aging, the more that we'll be able to actually think about ways to manage it better or things we can do to intervene.
BETHANY: And so, what was even cooler was that these discoveries aren't just for astronauts up in space, there aren't so many of them. There are a lot of us down here. We could actually use these learnings to help us… almost teach us how to fight aging and chronic disease here on Earth. The idea of personalizing space medicine for the future of Mars missions, that's sort of science fiction turning into science fact.
SPACE CLIP 1: We've seen that in one of the space flight recently that collaborators have done experiments they actually sent up to space a C. elegan that's very similar to a muscular dystrophy that we have on Earth, known as Duchenne muscular dystrophy. So, they sent up this worm. It's called a d dys‑1 worm, but it looks like the dystrophy worm significantly loses strength in this space flight environment. And actually, a lot of the reasons for the genes that were associated with this decline were related to the neuromuscular aspects. So that might give us a promising avenue for looking at dystrophy research on earth. So we might be able to find, for example, neuromuscular nutrients or drugs and trial them in the dystrophy context.
BETHANY: On a personal note, I think this has been such a joyous experience being a producer of Discovery Matters, and as I go on to other opportunities, I will stay close to Discovery Matters. I enjoy every second of it, and I hope that you, our listeners, really enjoy listening. So, thank you for the time that I've had to produce this podcast. It means the world to me.
CONOR: That was just lovely from Beth.
DODI: We also enjoyed every second with Beth behind the wheel. It is funny that Beth chose episode 103 about space because here's a little peek behind, behind the scenes or backstage, if you will, because the idea to look into that episode actually came from Tom Henley, our mixer and editor. Tom and I occasionally meet at a cafe in the south of Stockholm. I do bring Peter Barker along. Sometimes we meet on purpose. Sometimes I am just walking the dog and there's Tom and I usually stop and say, Tom, let's go get a cup of coffee. So, we get the opportunity to discuss podcast ideas. What more we could do during the year, and he brought up this twin study, and we thought, yes, let's do it. And this is the way a lot of our episodes come alive, and sometimes we get an email from our listeners, and we go chasing a scientist who's an expert on that study. So, keep up the ideas coming to us.
CONOR: Bring them in. Yeah.
DODI: Yes. In the meantime.
CONOR: And there's nothing quite like a twin study is there? I mean, that's a lot of fun.
DODI: Gotta love it. Gotta love it. Yeah. Toms’ favorite episode was actually, another example of something that was born out of one of our cafe chats. Here he goes.
TOM: Yes, thank you Dodi, and thanks Conor. Indeed, the episode that I've chosen from this year is actually number 110. It's a recent episode, and as Dodi mentioned just there, this episode was actually born from one of our chats in our local cafe. In fact, it was Dodi who brought up the idea. After I mentioned that I would just love a deep dive episode on one person, one scientist. Because you see, apart from editing and sound scaping, this podcast, I am a rookie, a self-proclaimed rookie. It is Dodi and Conor. They're the ones that know about life sciences and so often my favorite part of an episode when I'm editing it, when I'm putting it all together, is when I hear something human, something really personal that can help zoom out and show the big picture of what we're talking about. And so, as I said this, Dodi stood up and shouted out Dr. Rex Spendlove, and I was like, wow, what a name. We have to do an episode with him.
BRAD: He loved science. He wanted to talk about science. He wanted to talk about technology. He wanted to talk about serum. And every time I went to his house and we would have conversations, he would talk about his family. He would talk about his business and legacy, and not from the standpoint of wanting to hear what he accomplished, but from the standpoint of wanting to talk science, going into his bedroom because that's often where I would meet. He had this makeshift bed. It was in essence a gurney, that was one of the inventions. And his intent was, look, in order to buy one of these, it costs somebody that needs it $120,000. We think we can make this for $6,000. And it was interesting to see the prototype right there that he was actually using and his intent was to not make money per se, but his intent was to help mankind.
TOM: As you can hear from that clip, Brad really took us closer to Rex Spendlove as a human and as a scientist.
BRAD: What I realized is he understood the customer's need, and he was asking the questions to get us ultimately to solve the customer's need while we were just trying to solve a scientific problem. And so, he was really putting it together.
TOM: And finally, what I loved the most about this episode was the fact that Dr. Rex Spendlove seemed to have lived his life in pursuit of science, and that's just a great legacy to leave.
BRAD: And his belief is that there was no invention. His belief was all you're doing is finding out something that's already known, and we don't know it. Somebody else does, but we're trying to discover it and we're doing that for the improvement of mankind. And it was more about the journey for him than it was about really the end recognition or what he was going to get out of it. His hope was to learn throughout the journey, improve life for individuals and do so in a way that was an honorable and positive way. He did not care about the accolades that he was going to get in the end. He just cared about helping. To me, he was the epitome of what you look for in a leader, especially a scientific leader that understands the sciences, but cares about the individual and cares not only the growth of the business and the project, but the growth of the people. And that's, to me, that's who Rex Spendlove was.
CONOR: Yeah, that was a great episode. Looking at the people behind all of science, the people making all those discoveries that actually matter.
DODI: Over to you Conor. What has been your favorite episode of the year?
CONOR: My favorite episode kind of turned things upside down. It was the episode on vaccines, the inverse vaccines versus the traditional vaccines. I just love the idea of vaccines being something that we know and love, of course, because they've had such a huge impact on human health by training the immune system to recognize pathogens, but also that vaccines could be used the other way to suppress the immune system to ensure that that drugs and interventions can have the effect that they would. And for me, that was just this aha moment that, you know, whilst we always think we're trying to promote something, in some ways, sometimes we're trying to suppress something to make it work.
DODI: The off button.
CONOR: That’s exactly right.
DODI: So what clips are you going to play for us?
CONOR: First, I wanted to play the section of the episode where Professor Lawrence Steinman, who's an expert in inverse vaccines, refers to the immune system as our Department of Defense.
PROF LAWRENCE STEINMAN: The immune system is our Department of Defense. As a neurologist, I'm interested not only in diseases that are caused by a virus like polio, but in diseases that result in an attack by the human immune system against one's own tissue, often the brain tissue. So current therapies for multiple sclerosis, is to use very effective drugs that suppress the immune system quite widely. And as we learn more and more about these diseases, we come to know that there are very specific immune attacks against very specific molecules in the nervous system. So, the thought was, what if we could just throw the off switch for those unwanted immune responses and leave the immune system available to attack things that we need to attack, like polio and other viruses that might come our way. So, this would be an inverse vaccine. Let's make an inverse vaccine, but make it very limited to just shutting down unwanted immune responses and leave the rest of the immune system ready to do its job and fight viruses that can harm us.
CONOR: I also loved it when he talked about how human and viral proteins often share similar structural segments.
DODI: Ah, I remember that phenomenon called molecular mimicry.
PROF LAWRENCE STEINMAN: In the 1900s we tried to build a myelin mimic that had a few variations. Individuals in the clinical trial started getting immunity to their own myelin proteins. 10 years later, we made what we called an inverse vaccine by encoding the antigen in its DNA sequence, injecting the DNA into a person's arm and then watching to see whether there was an attenuation of immunity to myelin, and there we did a little better. We saw a reduction in the MRI activity and a reduction in the antibodies that were being made to myelin, but the effect was very mild. Could we do this more effectively and still get the precision we would want in an inverse vaccine? So, precision means we only want to attenuate immunity to unwanted immune responses. The trick is getting it strong enough without making it too strong. But what we did not know back in 1999 going into 2000 was what exactly is being attacked in multiple sclerosis. Recent research that was published first in 2022 showed that we were missing something very important, that everybody who has MS has been infected with a virus called the Epstein Barr virus, EBV. Research for the eight years previously showed that there was a molecular mimic between a piece of the Epstein Barr virus and a piece of a molecule that forms our myelin sheath, called glialCAM.
CONOR: And the final clip I wanted to share is from when Professor Steinman talked about his surprise at how the human immune system responds to environmental factors and pathogens and how these effects can resurface just years later.
PROF LAWRENCE STEINMAN: As we understand it now, there's a lot of components of nearly every virus that do have some structural similarity with our own proteins. We have a number of different genes that we're born with that decide what part of a molecule our immune system is going to attack. So, you can make a perfectly effective response against a virus like EBV, if you don't happen to have one of those genes that homes in on this region of similarity, and so those genes have been known for a long time. They're called human leukocyte antigens, and they are one of the reasons why we can't transplant organs from people on this podcast willy nilly, we have to find a good match. So those HLA molecules help decide for the immune system what part of a target to attack. So, it gets splendidly complex, but for our own good. By being aware of exactly what part of self-antigen mimics a virus, we can then attempt to make these precision inverse vaccines just to shut down that one unwanted response, and you could leave the immune system able to attack the rest of the virus because we'd like to be immune to that virus. We just don't want to be immune to that part of the virus shared with ourselves or our self-antigens.
CONOR: Right Dodi, we've heard from Beth. We've heard from Tom, and we've heard from me. Now it's time for you. Which episode are you choosing?
DODI: I have chosen episode 106 about zoonotic diseases and their growing impact on global health. That was really good. And one of my favorite moments from that episode was when our guest professor Clare Bryant talked about how she got into the whole topic of zoonotic disease in the first place.
PROF CLARE BRYANT: I was really gripped by the excitement of science and trying to understand how things happen at a molecular level. And I did my veterinary degree, and I realized very quickly that I really couldn't get to grips with those questions unless I specialized in research. I then went to work in a Nobel laureate lab, actually, in London. And that was really exciting. And I really started to think about, ‘Well, let's think about the fundamental science here, and let's start to understand what happens in people. Why is it different in animals?’. What's really very exciting recently is that for years and years and years I could hardly do any research in cells from any animal, and then suddenly, CRISPR Cas9, which is an incredible technology for gene editing. Now I can say, ‘Okay, if, if this gene is important, if I take it out of humans, does that mean I don't get infection anymore? Or if I put a gene back into a bird, does that mean it suddenly becomes inflamed in response to a pathogen?’
DODI: Something else that Professor Bryant mentioned, which I couldn't stop thinking about afterwards, was how we might change the narrative around Africa, which as you know, Conor has, historically been at the forefront of zoonotic outbreaks.
CONOR: Indeed, it has.
PROF CLARE BRYANT: Had we rolled out the vaccines to various places in Africa, there's a chance we might not have got Omicron, because Omicron arose in South Africa. The South Africans were brilliant, absolutely brilliant, because they told us about it, and because we knew about it, we were able to respond accordingly, but it was massively infectious. Imagine if Omicron had never emerged, my epidemiology friends tell me the rest of the pandemic would have been curtailed much sooner. And part of that was due to the vaccine inequality. It makes me concerned, because, for example, America decided they don't want to be in the WHO anymore, and that to my mind, I find that terrifying, because WHO is one of the organizations that globally watches what happens, and then they need to be funded in order to do this work to protect all of us. Ebola, the Oxford group had actually managed to use their technology to generate a vaccine, and we didn't get to the point where that had to be rolled out globally. But that's a terrifying virus. So far, we've survived a global pandemic with a pathogen that at least some people didn't die from.
CONOR: And what about the last clip?
DODI: When Clare talked about how effective data work depends less on having lots of information and more on proper training, cleaning, and validating models, because a mistake early on or a mistake at that foundational level can lead to unstable systems and harmful real-world decisions.
PROF CLARE BRYANT: One of the things that's assumed is that all databases are equal. As a veterinarian, I could probably cure a mouse of most of the diseases on the planet, frankly. We know quite a lot less about humans. Point number one is that we need to really develop serious databases to try and understand about the immune system and various genes in different animals in order to inform what we're doing and to really understand the basis of zoonotic disease. I need to understand what's happening to pathogens across the globe, and I need to understand how the human immune system, which is not the same, so most of our data comes from a certain cohort of people, but we need to understand globally, the immune system and how that differs. How that then impacts on pathogens and their evolution, and then how we then manage to generate vaccines and drugs to interfere with those processes. Only by having that kind of global understanding can we protect the planet, and that's on a human level and at an animal level.
DODI: So that's been our “Best of”; a few listens back to highlights of our program during 2025.
CONOR: What I would love to learn from the audience, is like, what was your favorite episode? Drop us a note.
DODI: Oh, please do.
CONOR: Drop us in the comments. Which episodes this year have you enjoyed the most? And who should we go and speak to next? Send us your interesting, send us your crazy. Send us your marvelous science. And we'll get in touch and try and find the little secrets that keep discovery mattering for everybody all around the world all year in 2026.
DODI: And you do that by writing to discovery.matters@cytiva.com. C-Y-T-I-V-A. And we do know CYTO comes from the Greek for cell.
CONOR: And -IVA comes from the Latin for life. Put those two things together and get Cytiva. Our producer, mixer, and sound magician and sprinkler of fairy dust is Tom Henley. My name is Conor McKechnie.
DODI: I'm Dodi Axelson. Please do give us a rating on Spotify or whichever platform you use to listen to Discovery Matters brought to you by Cytiva. Bye for now.
CONOR: Happy holidays.