The next generation of weight-loss drugs

It’s no exaggeration to say that the past decade has revolutionized how we think about and treat obesity. Drugs like semaglutide (Wegovy) and tirzepatide (Zepbound) have dominated headlines, enabling significant weight loss at speeds once considered unthinkable. The market for innovative weight loss medications is booming, with pharmaceutical companies investing heavily in hopes of developing the next blockbuster drug.

However, amid this race for market dominance, many experts are questioning whether the amount of weight loss alone is the best measure of these drugs’ usefulness. How can the next generation of obesity treatments meaningfully improve upon the powerful options already available?

Joining The Lancet editors Callam Davidson and Miriam Sabin to discuss this question is Professor Steven Heymsfield from the Pennington Biomedical Research Center. This wide-ranging conversation covers exciting pharmaceutical advances and limitations of these treatments, including the significant disparities in access, and why these breakthroughs may have broader societal implications.

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Transcript

This transcript was automatically generated using speech recognition technology and may differ from the original audio. In citing or otherwise referring to the contents of this podcast, please ensure that you are quoting the recorded audio rather than this transcript.

Callam: Hello and welcome to The Lancet Voice. It's July, 2025. And I'm Callum Davidson, your host for this episode. I'm joined by Miriam Saban, the Lancets North American Executive Editor, and we're talking to Professor Steven Heim, field Director of the Body Composition Metabolism Laboratory at the Pennington Biomedical Research Center of the Louisiana State University System in Baton Rouge.

Professor Himes Fields's research focuses on pharmacological aspects of weight loss medications and developments of new imaging technologies for the assessment of human body composition. He's also been a key investigator involved in the development of the drug. Biab is just one of the many drugs we discuss in today's episode, which focuses on next generation obesity therapeutic.

It is no exaggeration to say that over the past five to 10 years, drugs like semaglutide and Tirzepatide, soldiers Wegovy and zep bound have revolutionized the way that obesity is treated, perhaps even the way in which it's conceptualized. With many emerging drugs now achieving staggering weight loss at pace, many experts feel we're entering an era in which weight loss alone is no longer the sole consideration when designing the perfect drug.

Join us as we discuss weight loss, drugs, past, present, and future, and the implications these drugs could have, not just for the field, but for our societies. Let's get started.

Miriam: So I was just really interested in hearing about what got you interested in working in this area in particular and in studying next generation obesity, drugs, and what excites you about this work? 

Steven: When I was early in my training I got very interested in the problem of cachexia, the wasting states that occur in people with chronic diseases like congestive heart failure.

And I developed methods of evaluating cachexia and feeding patients who are malnourished in the hospital. And that technology and interest brought me into the area of obesity. At the time, obesity was not a major global problem that it is today, but I became very interested in obesity and I eventually joined up with the team in New York at Rockefeller University and Columbia University where the hormone leptin was discovered.

I was right in the center. It wasn't my personal discovery, but a colleague discovered leptin and that allowed me to be the investigator who first tested leptin in humans for its effects on promoting body weight loss. And that was the entry to a very wide and ranging career in my life. 

Callam: It's always nice to hear about the coincidences that can lead to these things.

It's rarely planned. 

Steven: Yes. That's absolutely right. I think about all of the serendipitous events in my career and that was clearly the major one, 

Miriam: a clearly very exciting one as well. 

Steven: It was a watershed in the evaluation of obesity because prior to that, obesity was thought primarily to be a problem, a lack of willpower or some psychological derangement, poor upbringing.

And it transitioned it to a metabolic, hormonal genetic disorder that we now understand it today. But that was the pivotal moment that occurred. 

Callam: It's funny that you mentioned that the way Obesity's conceptualized, it's still a kind of battle that's being fought today to some extent, right? I think there's more and more meaningful efforts to transition away from that individual responsibility, disease of lifestyle.

'cause although there is obviously a, an aspect of that, it's so much more complicated. But it's really only in the last few years that I feel we've started to see a, this conversation being had across the board. Would you agree with that? 

Steven: I completely agree, and we have to think of these things as pendulums and it swung all the way to the metabolic genetic.

It's not your fault. And I think it has to swing back to some extent. There always has to be some level of individual understanding and control behavior. We can't. Totally put this on your genes and absolve you of any responsibility in your weight. 

Callam: I think as well it comes down to, who's controlling the narrative to use a sort of in vogue phrase, there's lots of different people who have different vested interests in how to conceptualize obesity. But that's probably a, an entirely separate podcast. 

Steven: Yes, I agree. The sort of overall model of obesity we have is so complicated and has so many nodes on it that any one scientist can stake out a whole territory in the field.

Miriam: What's so interesting about this subject too is that this is exactly what's involved in it. It's discussed very much in terms of the current drugs that are available for obesity and managing weight and what the role of the person is in that process as well is discussed in some quarters, maybe not enough in others.

For example, like in patient testimonials and so forth. You tend to hear a little bit more of that. So it's a very interesting area to explore. 

Steven: It is. And I think now that we have extremely potent drugs, that discussion is going to come center forward. 

Callam: So that's a great opportunity to segue onto the drugs.

It's a increasingly complicated field. As subject ambassador at Lancet for Diabetes and Metabolism. I find it it's a full-time day job, just keeping on top of all the different options and the different points they're at in clinical development, maybe. To simplify things for listeners and to give people a kind of good steer on the field.

Could we start with what. Therapies are currently approved for treatment of obesity. Maybe you could just let us know what they are and their mechanisms of action. And importantly, the major limitations that they have. 

Steven: The mainstream of drugs that we have are called the GLP one agonists, glucagon, like peptide agonists.

And those go back many years. And over time. At least two major drug companies, Lilly and Novo Nortis have perfected that molecule so that the molecule exists a long time after you inject it up to a week and has actions then to reduce your food intake primarily, and suppress appetite. So the two drugs are semaglutide is one and.

Tirzepatide is the other, and both those drugs are approved under various brand names for a treatment of obesity. 

Callam: And so in terms of what they are well targeting, you've already talked about, so GLP one is the central receptor. This is the target of semaglutide, is just GLP one on its own Tirzepatide.

It's a slightly different story, right? There's a couple of targets there. 

Steven: There's natural hormone in blood glucagon and thi this glucagon-like peptide is the natural hormone in blood that acts to promote release of insulin after you eat a meal. And the target of that is, is a receptor.

The glucagon-like peptide one receptor. And when you activate that receptor, it affects the motility, the movement of your stomach. It increases it, it helps empty food after you eat a meal and. If you activate this hormone naturally it aids in digestion and mobilization of blood sugar and other effects like that.

That's the natural effect, the remarkable change in that molecule brought about by the two drugs I just mentioned. Semaglutide and Tirzepatide is that scientists were able to make them last longer in your blood. Na, normally they last just a few minutes at the most, and they're digested by other actions in your body.

The artificial ones, semaglutide and tirzepatide last days, and what the effect that has then is this effect on gastrointestinal. Function last a much, much longer time than naturally. That was the innovation 

Callam: and in practice. How would that make an individual taking this drug feel then in terms of both the positives and the negatives, 

Steven: it makes them basically feel like they're full, much longer. It suppresses appetite and extreme. They can vomit and have other gastrointestinal effects. Those are usually transient and go away after a period of days or weeks, but that's the main effect. It affects your gastrointestinal function. Now people think that it also may affect parts of the brain that recognize how hungry you feel and your appetite for certain types of foods and impulsive behavior.

Things that we didn't really appreciate when these molecules were first being studied. 

Callam: This is one of the really interesting questions, isn't it? Because we don't have this long-term data yet. I suppose there must be all sorts of potential effects that might emerge as we accumulate this kind of real world data in decades to come.

You already alluded to a few things we didn't necessarily anticipate these drugs doing, but there're affecting people's kind of desires beyond just eating behaviors.

Steven: For one thing people use food to socialize. Some people miss that when they go on these drugs and partially relapse because of it.

But the other thing we don't clearly know is what are the really long-term effects? It only requires a year or two of evaluation in, studies that get approval for the drug. So the studies have been intensively studied for at least two years, sometimes a little longer, but we don't know what 20 years on these drugs would do.

And there are two parts to that question we have. One is simply what happens to people over a long-term weight loss and weight maintenance? That's one question. 'cause they're losing a lot of weight. And the other question is, will these drugs specifically have effects? On the people that we don't really know.

For example, simply losing weight and keeping it off for 20 years has adverse effects that we now recognize. For example, people are more prone to certain types of fractures. Bones are affected when we lose a lot of weight, that's simply weight loss. Doing that. Then we have the drug on top of that, and we don't really know.

When we put the drug into millions of people and they go for 20 or 30 years on the drug, we don't really know what that drug will do when we have many examples in the obesity field where long-term effects we're not clearly recognized at the outset when the drugs were approved and later became very serious as time went on.

Callam: That, that's interesting. Would you be able to give us a previous example? 

Steven: Absolutely. The most famous one, and there, there are many by the way, but the most famous one was Fen. The combination of phentermine and fenfluramine. Two decades ago it was when millions of people went on, that combination of very rare side effect popped up and that was it.

One of the drugs seemed to. Be active on one of the cardiac valves. And these people went into heart failure and required replacement of some of their cardiac valves. And when it was looked at much deeper, it turned out that one of those drugs fenfluramine. Had unknown effects on cardiac valves in a small percentage of people, but a very lethal condition.

The drug had been proved for many years and since the appearance of that complication was very rare until you got a million people on the drug, you didn't see it and it brought. The drug combination fend down with a crash overnight. 10 or so cases were published in New England Journal and it stopped instantly.

The FDA got very involved and I could give you many more examples of drugs that were out there where the adverse events were not clearly known in the beginning. 

Callam: I'm sure there'll be a lot of people very anxiously watching for the long-term data on these GLP ones for that exact reason. 

Steven: Yes, they will.

And that's one of the reasons we need good surveillance systems adverse events, reporting. Very important. 

Callam: So you are talking there about the long-term potential adverse outcomes. That will take a long time for us to fully understand. We do know in the sort of immediate term that there are downsides to these drugs that are already available.

You already mentioned gastrointestinal adverse effects, which are very common as well. We also have the issue that a lot of people, as I understand it, after stopping on the drugs, tend to rebound and put that weight back on, which obviously isn't ideal for them. There's now a kind of development pipeline for drugs that operate on a similar.

Sort of incretin based model targeting the same sorts of things. GLP one or similar, but there's so many of them. It will be really helpful to hear from an expert like you on what the key players are and what their major advantages over what's available would be. 

Steven: Apparently this molecule can be.

Reshaped in many different ways, and that leads many companies to create their own version of this mechanism. I can't keep up with all of the molecules in the pipelines of many companies and. What determines success of one or another? Right now, I'm sorry to say the benchmark is weight loss, magnitude of weight loss and safety.

They all have very similar safety profiles so far. We know them very well, but the war is on efficacy. Weight loss. And when I did do drug development the adage was either you're the first in the class or you're the best in the class. And so the first in the class here was Ozempic.

Semaglutide was the first one out, and that became what we now know as wegovy, that's the brand name. And that was the first in class. And then out came, tirzepatide is the next one that ca came forward that, that's called Zep Bound, that has greater efficacy than semaglutide. And so now they can claim to be best in class.

I'm not saying that for the company. I'm saying that's the, a street wisdom. It's now we've got the best in the class. So that's usually how this war is fought. But then there are many other variables, pricing, and, but as we move forward what we're going to see.

And I may be preempting what you're going to ask me later a little bit is we're going to see versions of these drugs that either you can take every day as a pill or you only need to inject once a month. So we're going to see many variations on the theme of this whole class, the GLP one agonists. 

Miriam: So that's probably a good segue into this discussion about what's coming down the pipeline.

And aside from the frequency or dosage of these various drugs you've been involved in the development of Mima, I believe we'd be very interested in hearing about. It's being discussed recently and we're curious how it works and how others that might be similar in the pipeline work as well. 

Steven: That's a very interesting question.

First, just a brief background of how I got involved with that. I was very interested, as I mentioned earlier in kikexia, the wasting that people get and there's a more benign version of that. Called sarcopenia, age related muscle loss. And I was very interested in that early in my career. And one of my colleagues went into the drug industry to develop drugs for sarcopenia loss in muscle mass with aging.

And he spent many years, he developed a monoclonal antibody, an antibody called biab. And that drug was tested in sarcopenia and muscle diseases like AM Myotrophic, lateral Sclerosis, Parkinson's Disease many other wasting diseases. And then as the drug got tested further, it became clear that some of the people were losing weight when they got the drug.

And it turned out the drug works primarily on muscle mass. It blocks a hormone called myostatin and other hormones that regulate muscle mass. And when you administer this drug, it increases your muscle mass. You become a bodybuilder so to speak with this drug. And it was a class that the drug company developing it, they didn't see much benefit functionally in people with the drug.

They couldn't run faster or lift more weights, and they. Got lost interest in until they realized that in addition to working on muscle mass, the drug also seemed to have an action on fat cells that had not originally been appreciated. And so that's when I got involved is they said, should we try this in obesity?

Let's see what happens. And we did a clinical trial with the company, which was Novartis, and it turned out, now I just presented the a DA meeting that it had very powerful effects in people with obesity and mobilizing body fat while preserving muscle mass or even increasing muscle mass. And what that effect had was then suddenly.

Weight loss was no longer the primary outcome. It was mobilization of body fat, improving what people would call the quality of weight loss. And just as a background, when you lose weight, you typically lose some muscle. Also, that's part of the weight loss process. Very common. You lose a little bone and other factors like that are part of being obese, and it turns out you can prevent that loss of muscle and bone, largely bone also, with these drugs.

Now that's shifting the focus from weight loss to quality of weight loss, primarily fat loss. And what we don't really know yet is, will that matter in any way, will people be able to run faster, climb the stairs better, or will they have lower blood levels of adverse hormones? Or I guess, where is it going?

I would say. Stay tuned. 

Callam: I wonder as well, one of the groups you'd imagine would be particularly vulnerable to detrimental lean weight loss that you're talking about. There would be o older individuals who are often excluded from the very clinical trials that are looking at these drugs. So is that a problem in your view?

Is there anyone addressing that problem? 

Steven: I think now it's coming on the radar. First of all, I'm that age bracket, so I ha have to be a little careful. But people who are 60, 70, 80 and who are obese still many still wanna lose weight and improve their function because as you get into that age bracket, you have the combination of loss and muscle mass, which is natural and excess body fat, and that really impairs function.

That's what we call sarcopenic, obesity, muscle loss and excess body fat. And people in that age bracket now are taking these drugs. And the question is, for example, GLP one agonist, can you tolerate more muscle loss in that age group? Will that further impair your function? And again, here, we're in uncharted territory, but that question is hanging in the air and many people are asking it can I treat my 70-year-old patients who are obese with GLP one agonists?

Is it safe? Will they lose too much bone and too much muscle? That's where these drugs really come into play that preserve muscle mass. And there are several, not just Bim AgroMax. 

Callam: It's a super exciting story and we'll definitely be monitoring it very closely. I know it will be unreasonable to expect you to have an encyclopedic knowledge of all the various sort of next generation therapies.

But another one that did catch my eye when I was at a DA recently where we met in person, the Ortho Laron, the Achieve one trial that was presented. So this is a non peptides oral. GLP one small molecule inhibitor, which is quite a mouthful, and I might ask you to expand slightly on that if you're able just to tell us a little about what the advantage of this compound would be over existing therapies.

It's quite different to Bimm. 

Steven: First of all, as you mentioned these other drugs like semaglutide and ammad, they, they're all molecules built up of amino acids. They're proteins and peptides. They're big molecules. This drug that you mentioned are for. Let's see there. I can, I pronounce it right.

O Aron is a small molecule. It doesn't have that kind of molecular structure, and it can be given by mouth every day. You take it by mouth and. So far it seems to have the same effectiveness in promoting weight loss as the injectable drugs. So now we would go from a weekly injection or even a monthly injection to a daily pill.

As you can imagine, there are several implications of that. One is the cost comes way down. These are much less expensive drugs to make and to market. And second, you don't have to take a shot. You can just take the pill. And in some ways pills can be used more expeditiously in patients. For example, if you skip a dose you don't have to worry.

You just take. The next day or whatever, when you take the injectable, if you miss your weekly dose, it's a little different or even a monthly dose. It's pills have more flexibility, I think is what I'm getting at. 

Callam: I suppose that's a double-edged sword in some respects.

'cause by the same token, it would be easy to accidentally double up on your dose. If people are taking these drugs, if I accidentally took two pills that seems easier to do them with an injection, which I imagine could be quite. Quite dangerous with such a powerful drug. 

Steven: You raise a great point.

One of the problems when you do a clinical trial, everything's very regimented. For example, we count pills and we count injectables and we do blood tests to make sure people are taking the right amount. When you get into the real world, what happens is people don't always behave as the label tells them to.

And what happens is you often. People say, oh, I'm not losing enough weight. I'm gonna double the dose or triple the dose. And that's when, as I mentioned, Fen, that's when the adverse events really showed up, was people were saying, oh, this is amazing. I'm doing great. I'm gonna. Take twice as much and nobody will know and they take twice as much.

And that's when you go beyond where the drug was tested. You're right that doubling the dose could be accidental, but more commonly it's voluntary and people really can get in trouble when they do that. 

Callam: Again, it comes down to this monitoring the real world kind of data, doesn't it? I feel like right now so much of the media retention, perhaps rightly falls to the exciting trials and all the kind of innovation that's occurring, but at the same time, there's this kind of background story which could potentially, it would only take one unexpected major adverse event emerging to really bring the whole story crashing down.

Steven: That's exactly what I was getting at. Usually it's the canary in the coal mine. And again, when I did drug development the drug I worked on had an adverse effect. It affected mood. People got a little anxious and depressed on the drug, and I never thought it was much of a problem. But when we went to the FDA Federal Drug Administration, the us they said it's only gonna take one person jumping off a bridge and killing themselves with a suicide to bring.

And then to this billion dollar drug that is the case. It only takes, for example, we know these drugs so far don't cause suicidality. That is, the risk of suicide. But that's what regulators are always looking for, is that even the small events that are very serious. 

Miriam: As you said, this is where surveillance becomes important, and also perhaps developing some standards around, not just in this area of drugs, but in other areas.

It applies too, of course, for how to best conduct surveillance, in various countries too, because everybody has their own definitions, their own lists of adverse events and so forth. So it'll be interesting to see how that. Develops. This gets me thinking about some of the broader global public health implications in general that we're talking about here.

So we're talking about a size of the population. If we look globally, we look at the epidemiologic shifts that have, been changing in countries worldwide that can lead with certain risk factors to greater obesity. There could potentially be. Large populations that will benefit from these drugs.

And so we're really curious what your thoughts are about that. Are you feeling optimistic about that? Where this area is going? Do you have any concerns about it? And also, we're thinking about in terms of equity, the ability of people to also access these medications in places outside of, for example, high income countries.

Steven: Obviously the global population who are candidates for these drugs is enormous. That's a sizable fraction of the world population. And so we have to think in those terms. And there are a number, obviously those people who can afford it are the first wave that are going to get this drug. And that leaves out many people who can't afford it or don't have access to good healthcare.

And I think over time we will see that neutralized to some extent as the cost of these drugs come down. And they will come down because they do have natural patent lives. Those patents will expire. We're going to see generics come on the market. They'll be far less expensive. Plus we'll see the oral versions again, which, where cost will come down.

So generally we'll see more diffusion into populations that originally couldn't afford these drugs. So I think that will be a major shift. We're in the glow phase of this GLP one revolution. Now we're right in the middle of it the crest of the wave, but I think go 10 years forward, it'll be like statins.

I'd say 75% of my friends in my age group are taking statins for one reason or another, and they're generic. I take generic statin. And so I think you go down the line years you're going to see that, that happen with these drugs. And as you probably know, there are a counterfeit versions of them being made all over the world.

India, China have factories that make these drugs. So I think there's some meeting of demand through all these activities, but I we'll see this area mature, but I can't help but think that. We need to prevent obesity to begin with, and we need a global movement to improve the quality types of foods we eat and how foods are marketed.

And public health experts have spent years trying to get this under control with, I'd say only modest success. They've put in place food taxes in certain cities. States in the US and around the world. And that seems to help a little bit if you charge enough it work with cigarettes. But I think that given the cost of obesity, the world will have to take on a really serious posture and getting it under control.

Callam: That is the focus of a recent editorial. We had Inance actually in our I think it was our June 28th this year. It's such a fundamental philosophical question, isn't it? The role of pharmaceuticals and kind of your classical public health policy, preventative approach, how those two approaches can be married in such a way that at one end of the spectrum you have the quite credible argument that many previous public health interventions have, as you say, only.

Really scratch the surface of getting the problem under control. It's not a problem that can be solved overnight. And obviously with time, these public health approaches may show more benefits, but certainly the drugs are a very welcome addition to the kind of armory we have against obesity. But then at the other end of the spectrum, you risk.

Over medicalizing this problem that has really complex social and economic roots, right? I feel as though there's a little bit of discomfort around the idea of mass medicalization, which possibly you share or maybe you are more optimistic. 

Steven: No I completely agree. As you probably know right now in the US there's an emphasis on eliminating chronic disease.

That's a big focus, and making foods healthier and attacking ultra processed foods. And, foods with sugar in them added sugar. And so there's a focus on that. But the complexity is enormous. How you bring that under control and you have to accept people's rights to the eat the foods they want to eat.

There's a lot of unrest when people are told to eat foods that they don't perceive as tasting good or so I think it's very difficult, there's a very interesting question about if you go forward 50 years, I think we might have talked about this call. If you go forward 50 years and the limit obesity has been eliminated, what happened in the meantime?

And you can think of all the measures that would've taken place, but I spoke to a very distinguished colleague about this and he had the same thought as I did when we traveled to parts of Asia and we saw people who were. Perfectly normal weight in the population as a whole, not this enormous amounts of obesity we see, for example, where I live here.

What's the difference between those two places? What. Differences in the foods they eat and in their cultural values. And you know that's what we have to ask is what's happened in between where people have become so obese in terms of our up. Culture, the foods we eat and try and reverse that.

But I, I think it's an enormous undertaking. 

Callam: I think what you just said is reflected in the sort of epidemiological shifts that Miriam mentioned. I mean it, the parts of the world that are experiencing the greatest increases in obesity are these ones experiencing an economic and a cultural transition.

It's actually, that's exactly right. We're almost seeing the kind of obesity rates plateau in places like the us right? Where it's the kind of, the problem has. Arisen in the sort of eighties through nineties and naughties, and now we're at the peak of the issue. And it makes me think as well about this very interesting, one of the reasons that public health interventions, like the fiscal interventions like taxes you were mentioning have failed or rather, at least being heavily constrained, is because of the fight back and the lobbying from big food, right?

Steven: That's right. Whereas 

Callam: now you have this very interesting situation where these drugs, presumably people in the world of. Big foods have. A lot of concerns around these drugs, which are putting people off, consuming and buying these foods. And there's a sort of a vying of commercial interests. I'm not oversimplifying the problem.

Obviously pharmaceutical industry, big food people need these things, but there is a really complex interplay, and I don't know how that's gonna play out in the decades to come. Presumably there's a lot of people in the food industry who are talking about how they're gonna respond to this potentially game changing drug that may put people off their products.

Steven: That's exactly right. I think some industries are already feeling it. I haven't seen the latest data, but my understanding is some foods are already experiencing reduced sales because of these drugs. So we'll see. I think, I'm not an expert on food science, but it must be very hard to make foods that are.

Palatable and very healthy and leave out the salt and the sugar and the saturated fat to, to leave out those ingredients that we know are unhealthy. It must be very hard to do that or else they would've done it. That's my only thought about the. 

Callam: We're moving towards the end of the time we've got, but another question I wanted to ask you.

When you start looking really down into the sort of distant future of therapies for obesity, there's people to, I think Novo have devoted some huge proportion of their research budget to looking at gene therapies and RNA interference approaches to almost. Eradicates obesity as a health issue is the way it's portrayed in the articles I've read at least.

And that kind of gets me thinking about a really ingrained problem in the field of obesity, which is that of stigma. So I'm not entirely sure how. It would make someone feel to have their kind of body type referred to as something that we want to eradicate with medication. I dunno if you have any thoughts.

Do you think we should be talking about obesity as something that needs to be eradicated or do you find those terms unhelpful? 

Steven: I'm very interested in evolutionary biology and we have body fat for a reason. And the reason is that is our energy store. And I think when we're playing with genetic mechanisms that might alter the amount of body fat you have, for example, during pregnancy, body fat increases.

That's a biological adaptation. It's essential for nursing and carrying a fetus. And I think when we're playing with those mechanisms, we get into a whole different set of. Ethical and moral questions. In other words, can we permanently change someone's set point? A wait set point. Do we wanna do that?

If you get sick, you develop cancer. Do you want to block their ability to eat, compensate for whatever treatment they're getting? I think there's another set of questions, but I guarantee it's coming. The reason I'm sure that is we're already seeing drugs that have one month. Injectable at times. Meritide iss another one of these GLP one agonists that's coming on board.

And you may only have to inject it once a month, and I've heard even you could put in pumps that you would only have to change once a year, subcutaneous pumps. And so now we're getting into another whole territory, and I think it brings forward a set of ethical and medical questions that will have to be answered.

Callam: We need a modern day, Mary Shelley, to come and write an excellent science fiction novel about all of this. I feel like there's echoes of Frankenstein concerns coming through in what you're saying. Yes. Yes.

Miriam: What's so wonderful about discussing all of this is that, sometimes we don't.

Think, we think of science in its own place, but it really belongs very much and is part of the worlds of these philosophical ideas and some of the points that you've talked about and you've really illustrated that so beautifully today. Yeah. Thanks. I think it's been really fascinating. Yeah.

Yeah.

Callam: Thanks very much for listening to this episode of Lancet Voice. You can find all of our podcast offerings alongside infographics and videos by heading to lancet.com/multimedia. As always, if you haven't already, please consider subscribing to Lancet voice wherever you normally get your podcasts, and we hope to see you again next time.

Thanks for listening.